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THE LIBRARY
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THE UNIVERSITY
OF CALIFORNIA
LOS ANGELES
i
This book is DUE on the last date stamped below
UNlViiiv ...u^ORNIA
LUb AInGELES
LIBRARY
HANDBOOK
DISEASES OF THE NERVOUS SYSTEM.
BY
JAMES ROSS, M.D., LL.D.,
FEM.OW or THE ROYAL roM.EGE OF PHYSICIANS OF LONDON, AND SENIOR ASSISTANT PHYSICIAN TO THE
MANCHESTER ROVAI. INFIRMARY.
WITH ONE HUNDRED AND EIGHTY-FOUR ILLUSTRATIONS.
4B 8-^
PHILADELPHIA:
LEA BROTHERS & CO
1885.
k
•3193
a
i
Entered according to the Act of Congress, in the year 1885, by
LEA BEOTHEES & CO.,
In the Office of the Librarian of Congress. All rights reserved.
7 48
PHILADELPHIA :
nORNAK, PRINTER,
634 Filbert Street.
R73Bh
PREFACE.
This Handbook is intended for the use of students, and such of
my medical brethren as are so fully occupied in practice that little time
is left to them for reading lengthy treatises, and monographs on special
subjects. The work is divided into two parts — a general and special
neurology. In the former I have endeavored to give a brief outline of
the evolution and dissolution of nervous structures and functions, adding
a chapter on the general principles of treatment. In approaching a
new subject our capacity to master it may be measured by the ease and
thoroughness with Avhich the mind assimilates with its previous stock of
knowledge the new facts and relations presented to it. The student
may, indeed, acquire much information concerning diseases or any other
new subject of study without assimilating the new fiicts, which come
under his notice, with well-established principles, but the knowledge
thus obtained — if it deserves the name of knowledge — is not ])roperly
organized, and will be found to be both Meeting and ill-adapted for
\^ guidance in emergencies. Keeping these considerations in view, it has
\^ been my endeavor in this part to arrange tlie anatomical and physio-
logical facts, with which the student is already more or less familiar, in
^ such a way that his mind may be prepared readily to comprehend the
multiform phenomena of disease, and to associate them with the funda-
mental laws of development. In the special part my great aim has
been to make the work thoroughly practical. With this A^iew I have
adopted, as far as possible, a clinical classification, so that the diseases
wliich are most apt to be mistaken for each other will be found described
in close proximity, and the reader can thus note the various features
which differentiate nervous diseases clinically allied. My rule of
VI ■ PREFACE.
selection lias been to give the clinical descriptions with tolerable
fulness, and to leave out the details of morbid anatomy and physiology,
and almost all reference to the opinions and theories of different authori-
ties. But although want of space has prevented me from quotino-
authorities, I am none the less grateful to men like Hughlings-Jackson,
Wilks, Terrier, Charcot, Westphal, Leyden, and the other great masters
who have placed our knowledge of nervous diseases upon a secure and
unshakable foundation.
JAMES ROSS.
Manchester, November, 1885.
LIST OF ILLUSTRATIONS.
FIG.
1.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
Diagram of the Distribution of the Bloodvessels, and Grouping of
Ganglion Cells in the Spinal Cord
Section of the Medulla Oblongata, showing the Distribution of the
Vessels ............
Diagram of the Distribution of the Vessels at the Base of the Cerebrum
View of the Brain from below ........
Inner Surface of Right Hemisphere .......
Outer Surface of the Left Hemisphere .....
Transverse Section of the Cerebral Hemispheres, about 1 cm. behind the
Optic Commissure ....
Diagram showing the relation of the Spines of the Vertebrae to the Origin
of the Nerves .........
Lateral View of the Human Skull ......
Diagram showing the Relations of the Convolutions to the Skull
Horizontal Section of the Brain of a Child nine months of age, the righ
side being at a somewhat lower level than the left half
Prefrontal Section ....
Pedunculo-frontal Section .
Frontal Section .....
Parietal Section .....
Pedunculo-parietal Section
Occipital Section ....
The Anterior Surface of the Spinal Segment, the Anterior Root of the
Right Side being Divided
Section from the Middle of the Cervical Enlargement of the Spinal Cord
at the Third Month of Embryonic Life
'I Sections of the Spinal Cord of a Five-months' Human Embryo, from 1
/ Middle of the Cervical and Lumbar Enlargements, respectively . >
\ Sections of Spinal Cord of a Nine-months' Human Embryo, from the )
i Middle of the Lumbar and Cervical Enlargements, respectively *
■) Sections of the Adult Spinal Cord from the Middle of the Lumbar and \
J Cervical Enlargements, respectively ...... i
■) Sections of the Adult Human Spinal Cord, from the Upper Cervical \
i and Dorsal Regions, respectively .......'
Section of the Medulla Oblongata on a level with the Superficial Origin
of the Acoustic Nerve ..........
22
23
25
27
28
29
30
32
33
35
37
38
39
39
40
40
41
41
42
42
43
43
44
46
viii LIST OF ILLUSTRATIONS.
FIG.
PAGE
29. Transverse Section of the Cervical Part of the Spinal Cord of a Human
Embryo of Six Weeks 47
30. Transparent Section of a Furrow of the Third Cerebral Convolution of
Man 50
31. Pyramidal Giant-cell 51
32. Schema of the Cerebro-spinal System 52
33. Schema of the Cerebello-spinal System 55
34. Cord of Human Embryo at Five Months 56
35. Diagrammatic Kepresentation of Embryological Tracts .... 57
36. Diagram of the Gray Masses of the Spinal Cord and Brain, showing the
course of the Conducting Paths 59
37. Diagram of Transverse Section of the Spinal Cord in upper half of the
Dorsal Kegion ........... 00
38. Diagram of the Spinal Segment as a Centre and Conducting Medium . 61
39. Diagram of the Course of the Principal Conducting Paths within the Cord 66
40. Upper Surfoce of the Brain of the Monkey 71
^2 I Side and upper Views of the Brain of Man I 73
43. Schema of Encephalo-spinal Action 76
44. Diagram Illustrating the Attachments of some of the most important
Muscles which keep the Body in the Erect Posture .... 78
45. Horizontal Section of the Basal Ganglia and Internal Capsule of a
Nine-months' Embryo .......... 86
46. Transverse Section of the Crus Cerebri on a level with the Anterior Pair
of Corpora Quadrigemina, from a Nine-months' Embryo ... 87
47. Transverse Section of the Pons on a level with the Abducens and Facial
Boots, from a Nine-months' Embryo ....... 88
48. Ganglion Cells of the Anterior Gray Horns of the Spinal Cord . . 97
49. Alterations in Nerve Fibres after Section ....... 98
f Transverse Section of the Spinal Cord, from the Middle of the Cervi- ]
50- I cal Enlargement, Dorsal Region and Lumbar Region, respectively, I
rn ^ showing Ascending Degeneration of the Columns of Goll, and of
I the Direct Cerebellar Tract .......
53. Horizontal Section of the Right Hemisphere Parallel with the Fissure
of Sylvius . . . . . . . . . . . .11.5
54. Horizontal Section of the Crura Cerebri in a case of Secondary De-
generation . . . . . . . . . . . .116
Transverse Section of the Spinal Cord from the Middle of the Cer- ]
vical Enlargement, Dorsal and Lumbar Regions, respectively, I
showing Descending Sclerosis of the Pyramidal Tract in the !'
I Lateral Column Secondary to a Cerebral Lesion ...
114
58.
r Transverse Sections of the Spinal Cord, from the Middle of the T
J Cervical Enlargement, Dorsal and Lumbar Regions, respectively, I
! showino- Primnrv T.ntprnl ."-ii^lorricic r\f tVio O.^i'A /-v^ ^inr^r^-r^A.^-.,,-, *„ C
gQ* j showing Primary Lateral Sclerosis of the Cofd, or Secondary to f
a Lesion high up in the Cord or Medulla Oblongata
61. Recent Softening of the Frontal Lobe, Island of Reil, and Middle
Third of the Lenticular Nucleus . .117
119
140
142
1
1
164
165
_,
LIST OF ILLUSTK ATIONS,
62. Diagram of Lesions found in the Anterior Half of the Lenticular Nucleus,
Anterior Segment of the Internal Capsule, and the Internal Third of
the Crusta . . . . . . . . . . _ .118
63. Diagram of the Optic Thalami, Tegmentum, and Superior Peduncles of
the Cerebellum •-........
64. Atrophy of Muscular Fibres from a case of Infantile Paralysis
65. Appearance of Muscle in Infantile Paralysis .....
66- f Diagrams representing the General Kelations of Motor Power,
go" -{ Electrical Excitability and Structural Changes of the Nerves and
gg I Muscles present in Different Stages of Paralysis
70. Diagram and Table showing the Approximate Eelation to the Spinal
Nerves of the Various Sensory and Keflex Functions of the Spinal
Cord 174
71. Diagram of the Keflex Functions of the Spinal Cord .... 180
72. Schema explaining Conjugate Deviation of the Eyes and Kotation of the
Head and Neck 186
73. Superior Cervical Ganglion of the Sympathetic: its Connections and
Branches ............ 195
74. Nervous Mechanism of the Iris . ........ 197
75. Schema of the Action of the Cardiac Nervous Mechanism . . . 205
76. Diagram showing the Probable Plan of the Centre for Micturition . . 213
77. Sensory Nerves of the Head and Face ....... 246
78. Diagram of the First and Second (Superior Maxillary) Divisions of the
Fifth Nerve : its Connections and Chief Branches .... 248
79. Diagram of the Third (Inferior Maxillary) Division of the Fifth Nerve
its Connections and Chief Branches ......
80 ">
> Cutaneous Nerves of the Trunk ; Upper Extremity
250
251
259
261
271
275
81./
82. Cutaneous Nerves of the Lower Extremity .....
83. Distribution of Keddened Surface in Neuralgia Plantaris .
84. Diagram of Glosso-pbaryngeal Nerve: its Connections and Branches
85. Diagram showing the Fields of Color Vision in a Normal Emmetropic
Eye on a Dull Day
86. Horizontal Section through the Optic Nerve at its Point of Insertion in
the Globe, and its Passage through the Membranes of the Eye
87. Diagram of Decussation of the Optic Tracts ....
88. Section of the Medulla Oblongata on a level with the Largest Diameter
of the Diseased Focus, which is represented by the Shaded Part on the
Left Half of the Diagram ......
89. Spasm of the Trapezius .......
90. Spasm of Splenius ........
91. Contraction of the Khomboid Muscles ....
92. Position of the Hand in Spasm of the Interosseous Muscles
93. Diagram showing Position of Body in Tetanus
94. Diagram showing Lesion in Crural Monospasms
95. Diagram showing Lesion in Brachial Monospasm
96. Diagram showing position of Eyeballs in a case of Oculo-motor Mono-
spasm ............. 326
280
284
285
308
305
306
308
316
324
325
X LIST OF ILLUSTRATIONS,
FIG.
97. External Convex Surface of the Human Brain
98. Diagram of the First or Ophthalmic Division of the Fifth, showing also
the Third, Fourth, and Sixth Cranial Nerves
99.1
. [:
360
867
372
374
100. [- Disorders of Movements of Eyelids
101. J
102. Kelations of the False to the True Image
108. Diagram of the Facial Nerve: its Connections and Branches
104. Diagram of the Hj'poglossal Nerve : its Connections and Branches
105. Diagram of the Pneumogastric and Spinal Accessory Nerves : their Con
nections and Branches .........
106. Distortion of the Uvula in a case of Peripheral Paralysis of the Eight
Side of the Face
107. Schema of a Horizontal Section through the Larynx
108. Schema of a Horizontal Section through the Larynx, showing the
Action of the Arytenoid Muscles ......
109. Schema of Horizontal Section through the Larynx, illustrating the
Action of Crico-arytenoidei Laterales Muscles ....
110. Laryngoscopic Appearances of the Interior of the Larynx
111. Laryngoscopic Appearance of the Larynx during Quiet Breathing
112. The Laryngoscopic Appearance of the Larynx during Vocalization
113. The Laryngoscopic Appearance of the Larynx during Deep Inspiration
showing the Bifurcation of the Trachea .....
114. Nerves of the Cervical Plexus ........
115. Nerves of the Brachial Plexus . .......
116. Paralysis of the Serratus Magnus .......
117. Distribution of the Sensory Nerves on the Back of the Hand
118. Showing the Distribution of the Anaesthesia in a case of Division of the
Musculo-spiral Nerve in the Arm .'....
119. The Dorsal Aspect of the Hand two weeks after Kesection of the Kadial
Nerve ............
121 [Cutaneous Nerves of the Trunk and Upper Extremity .
122. ■) Pvadial Border and Dorsal Aspect of one Hand, showing the Distri
l-^^- i bution of Aniesihesia in a case of Division of the Median Nerve
124. Showing the Distribution of the Aniesthesia on the Back of the Fingers
in a case of Injury of the Median Nerve 39-5
125. Main en GritFe 3<I6
127! J -^^^ion of Aniesthesia in Paralysis of the Ulnar Nerve . . . 397
128. Attitude of the Hand in Pachymeningitis Cervicalis Hypertrophica,
when the Disease is situated on a Level with the Lower Half of the
Cervical Enlargement of the Spinal Cord 399
129. Region of Anteslhesia in a case of Cervical Pachymeningitis .
130. Region of AnsBsthesia in a case of Tubercular Spinal Tumor .
131 1
J32; I ^distribution of Anaesthesia in Rupture of the Brachial Plexus
133. Region Unaffected by Rupture of the Brachial Plexus
134. Lumbar Plexus
135. Sacral and Coccygeal Nerves
PAGE
348
357
3-58
375
378
378
379
380
380
380
380
384
386
390
392
392
392
393
394
400
40O
401
401
404
406
LIST OF ILLUSTRATIONS. xi
PAGE
13(3. Cutaneous Nerves of the Lower Extremity ...... 410
137. Case of Infantile Paralysis (Genu RecurvHtum) 432
138. Main en Griffe 438
.\^' > Lesions in Acute Spinal Atrophic Paralysis / ^'3'^
141. Transverse Section of the Spinal Cord and Medulla Oblongata at dif-
ferent levels, from a case of Chronic Atrophic Spinal Paralysis, show-
ing the Disappearance of the Ganglion Cells 4.j7
142. Transverse Section of the Spinal Cord from the Middle of the Cervical
Enlargement, from a case of Syringomyelia, showing a Cavity behind
the Posterior Commissure, and Destruction of a large portion of the
Ganglion Cells of the Anterior Gray Horns ...... 4.58
143. Transverse Section of the Cervical Enlargement of the Spinal Cord,
showing a Central Cavity which has destroyed considerable portions of
the Anterior Gray Horns ......... 4.j8
144. Transverse Section of the Cervical Region of the Spinal Cord, from a
case of Progressive Muscular Atrophy ....... 4-59
145. Transverse Section from the Middle of the Cervical Enlargement of
the Spinal Cord, from an advanced case of Progressive Muscular
Atrophy 460
146. Transverse Section of the Spinal Cord from the Middle of the Cervical
Enlargement, showing that the Central Column and a large portion
of the Anterior Gray Horns are Diseased . . . . . .461
147. Portion of the Gray Substance on the Floor of the Fourth Ventricle on
a level with the Middle of the Hypoglossal Nucleus, from a case of
Progressive Muscular Atrophy with Bulbar Paralysis, showing the
Destruction of the Ganglion Cells of the Nuclei of the Hypoglossal
and Pneumogastric Nerves ......... 462
148. Muscular Fibres from a case of advanced Infantile Paralysis withdrawn
hy Leech's Trocar ........... 464
149. Muscular Fibres in Various Stages of Degeneration, from a case of
Pseudo-hypertrofhic Paralysis ........ 466
150. Attitude of the Hand and Forearm in Amyotrophic Lateral Sclerosis . 475
151 1
1 r:,o f Spasmodic Paraplegia of Infancj' ■ 484
153. Transverse Section of the Medulla Oblongata on a level with the Middle
of the Nucleus of the Hypoglossal 490
154. Horizontal Section of the Basal Ganglia and Internal Capsule in an
Embryo of Nine Months 491
155. Vertical Section of the Brain a little behind the Knee of the Internal
Capsule, showing the Effects of Rupture of the Lenticulo-striate Artery 492
156. Vertical Section of the Brain on a level with the Posterior Part of the
Internal Capsule, showing the Effects of Rupture on the Lenticulo-
optic Artery (Hemianissthesia) ........ 494
157. Crura Cerebri. Transverse Section of the Crura Cerebri on a level with
the Anterior Pair of the Corpora Quadrigemina, from a Nine-months'
Human Embryo ........... 495
158. Diagram showing Decussation of Fibres of Pyramidal Tract at the
Middle of the Pons 496
Xll
LIST OF ILLUSTRATIONS.
159.
160.
161.
162.
163.
164.
165.
166.
167.
168.
169.
170.
171.
172.
173.
174.
175.
176.
177.
178.
179.
180.
181.
182.
183.
184.
Dia:;rftni of Defect of Parietal Bone in a case of Congenital Paren-
cephalus ..........
Appearance of Brain in a case of Congenital Parencephalus
i Diagram of Lesion in Crural Monoplegia
Diagram of Lesion in Brachio-crural Monoplegia .
Diagram of Lesion in Brachio-facial Monoplegia .
Diagram of Lesion in Facial Monoplegia
Diagram of Lesion in Unilateral Oculo-motor Monoplegis
[-Diagram of Lesion in Hemiplegia from Cortical Disease
Transverse Section of the Lumbar Region, from a case of Locomotor
Ataxia, complicated with Muscular Atrophy
Region of Anaesthesia in a case of Hemorrhage into the Upper Dorsal
Region of the Right Side of the Cord
Diagram of the Cutaneous Symptoms in Unilateral Lesion of the Dorsal
Portion of the Spinal Cord on the Left Side ......
Section of the Middle of the Cervical Enlargement of the Spinal Cord
from a case of Central Myelitis ........
Diagram of the Course of the Principal Conducting Paths within the
Cord
Distribution of Aniesthesia in Pacliymeningitis Cervicalis Hypertrophica
Attitude of the Hand in Pachymeningitis Cervicalis Hypertrophica,
when the Lesion is situated on a level with the Upper Half of the
Cervical Enlargement ..........
Diagram of Lesion in a ca.se of Aphasia .......
Diagram showing the Area of Distribution of the Middle Cerebral
Artery .............
Diagram of Lesion in a case of Word-deafness .....
Attitude of the Hand in Paralysis Agitans ......
Attitude of the Hand in Paralysis Agitans simulating that of Arthritis
Deformans ............
Section of Anterior Gray Horn of the Cervical Enlargement of the
Spinal Cord, from a case of Chorea that died on the Fourth Day of
Scarlet Fever ............
Section of the Cervical Region of the Spinal Cord, from a case of Chorea
View of the Posterior Surface of the Medulla
Transparent Lateral View of the Medulla
498
499
500
501
501
502
503
505
505
506
532
544
559
563
566
572
573
644
645
646
672
673
684
685
697
698
CONTENTS.
CHAPTER I.
ANATOMICAL INTRODUCTION.
Formation of Nervous Constituknts
Formation of Nervous Tissues .
Formation of a Nervous System
Encephalo-spino-neural System
■ PACK
18
19
19
21
CHAPTER II.
PHYSIOLOGICAL INTRODUCTION.
1. Functions of the Spino-neural System 65
2. Functions of the Encephalo-spinal System 67
3. Functions of the Cerebro-spinal System 68
4. Functions of the Cerebello-spinal System 75
5. Cooperation of the Cerebro-spinal and Cerebello-spinal
Systems 76
CHAPTER III.
GENERAL MORBID ANATOMY AND PHYSIOLOGY OF THE
NERVOUS SYSTEM.
I. General Morbid Anatomy ......... 90
1. Defects of Development ......... 90
2. Dissolution of the Nervous System ....... 93
3. Dissolution of the Nervous System (continued) 108
II. General Morbid Anatomy and Physiology 122
CHAPTER IV.
GENERAL SYMPTOMATOLOGY.
A. The .^Esthesioneuroses ......
I. The Primary ^Esthesioneuroses ....
II. The Secondary or Compound .^Esthesioneuroses
125
125
135
XIV
CONTENTS.
CHAPTEK V.
GENERAL SYMPTOMATOLOGY {continued)
B. Tkoi'iioneurosks
I. Neurotic Atrophy of Muscle .
II. Cutaneous Trophic Affections .
III. Trophic Disorders of the Nails and Hair
IV. Bedsores and other Destructive Processes
V. Nutritive Affections of the Joints, Bones, and Teeth (Articular
and Osseous Trophoneuroses) ......
VI. Nutritive and Secretory Affections of the Glandular Apparatus
VII. Nutritive Affections of the Viscera (Visceral Trophoneuroses)
PAOE
140
140
143
145
146
151
15.3
1.56
CHAPTER yi.
GENERAL SY:MPT0MAT0L0GY' (continued).
C. The Elementary Kinesioneuroses 158
T. The External Kinesioneuroses
158
CHAPTER VII.
GENEPvAL SY'MPTOMATOLOGY {continued).
C. The Elementary Kinesioneuroses {continued) .
II. The Visceral Kinesioneuroses ......
III. Vascular Kinesioneuroses or Angioneuroses
CHAPTER VIII.
GENERAL TREATMENT
1. Prophylactic Treatment
2. Removal of the Exciting Cause .
3. Removal of the Anatomical Cause .
(a) Internal Remedies ....
{b) External Remedies ....
4. To Allay or Remove Serious Symptoms
194
194
21()
222
223
223
223
225
234
SPECIAL PATHOLOGY OF THE NERVOUS SYSTEM.
CHAPTER I.
GENERAL DISEASES OF THE PERIPHERAL NERVES.
1. Hyper.emia or Congestion of the Nerves 237
2. Inflammation of Nerves (Neuritis and Perineuritis) . . . 237
o. Atrophy of Nerves 239
4. Hypertrophy of Nerves 240
5. Nkuromata . „.„
240
CONTEXTS. XV
CHAPTER II.
DISORDERS OF COMMON SENSATION AND OF SPECIAL SENSE.
PAGE
I. Anaesthesia and Analgesia in thk Region of Distribution of
Individual Nerves and Plexuses 243
II. Hyper.esthesia and Hyperalgesia in the Region of Distribu-
tion of Individual Nerves and Plexuses .... 244
III. Neuralgia in the Region of Distribution of Individual Nerves
AND Plexuses . 24")
1. Neuralgia of the Fifth Nerve (Trigeminal Neuralgia) . . 24')
2. Cervico-occipital Neuralgia ......... 2-")2
3. Phrenic Neuralgia 252
4. Cervico-brachial Neuralgia ........ 253
5. Dorso-intercostal Neuralgia . . ..... 254
6. Lumbar Neuralgia 255
7. Neuralgia of the Sacral and Coccygeal Nerves ... 257
8. Visceral Neuralgia .......... 2()2
IV. Disorders of the Nerves of Si'f.cial Skxse 2G7
1. Diseases of the Olfactory Nerve 2G7
2. Diseases of the Acoustic Nerves ... .... 269
3. Diseases of the Gustatory Nerves 270
4. Diseases of the Optic Nerves 273
V. Disorders Caused by Disease of the Cerebro-Spinal Sensory
Conducting Paths 284
VI. Disorders Caused by Disease of the Cortical Sensory Centres. 288
1. Cutaneous and Muscular Hemiantcsthesia 288
2. Disorders of the Sense of Smell .....•■■ 288
3. Disorders of the Auditory Sense 289
4. Disorders of the Visual Sense -Bft
CHAPTER III.
SPASMODIC DISORDERS
I. Spino-neural Spasms
1. Local Spasms
2. General Spino-neural Spasms
3. Myopathic Spasms
CHAPTER IV.
SPASMODIC DISORDERS {coniinned).
295
295
313
321
323
II. Cerebro-spinal Spasms
1. Spasms from Organic Disease of the Cortex of the Brain (Monospa.sms
and Unilateral Convulsions) '^23
2. Spasmodic Atfections from Functional Disease of the Cortex of the
Brain .....•••■•••
327
CONTENTS.
CHAPTER V.
ATROPHIC PARALYSES.
Simple Nkural Paralyses
1. Paralysis of the Oculo-motor Nerves
2. Masticatory Paralysis
3. Paralysis in the Area of Distribution of the Seventh Nerve (Mimetic
Paralysis, Hemiplegia and Diplegia Facialis, Prosopalgia, Bell's
Paralysis) ....•••••••
4. Paralysis of the Muscles Supplied by the Hypoglossal Nerve (Glosso
plegia)
5. Paralysis of the Pneumogastric Nerve
(j. Paralysis of the Spinal Accessory Nerve .
7. Paralysis of the Muscles Supplied by the Cervical Plexus
8. Paralysis of the Muscles Supplied by the Brachial Plexus
9. Paralysis of the Muscles Supplied by the Dorsal Nerves
10. Paralysis of the Muscles Supplied by the Lumbar Plexus
11. Paralysis of the Muscles Supplied by the Sacral Plexus
PAGE
356
356
363
365
371
373
383
385
389
402
403
408
CHAPTER VI.
ATROPHIC PARALYSES {continued).
II. Multiple Neural Paralyses .
1. Idiopathic Progressive Multiple Neuritis
2. Lead Paralysis .....
3. Alcoholic Paralysis ....
4. Diphtheritic Paralysis ....
III. Reflex Atrophic Paralyses
412
412
413
415
418
422
CHAPTER VII.
ATROPHIC PARALYSES {continued).
lY. Spinal Atrophic Paraly'ses (Poliomyelopathies) . . . 425
1. Paralysis Ascendans Acuta (Acute Ascending Paralysis, Landry's
Paralysis) ............ 425
2. Poliomyelitis Anterior Acuta (Kussmaul) (Acute Inflammation of the
Anterior Gray Horns, Acute Atrophic Spinal Paralysis) . . 426
3. Poliomyelitis Anterior Chronica (Chronic Atrophic Spinal Paralysis) 434
4. Periependymal Myelitis (Syringomyelia, Hydromyelia) . . . 436
5. Progressive Muscular Atrophy 437
6. Primary Labio-glosso-laryngeal Paralysis (Chronic Progressive Bulbar
Paralysis (Wachsmuth)) 442
7. Ophthalmoplegia Externa vel Progressiva 447
V. Myopathic Atrophic Paralysis 448
Pseudo-hypertrophic Paralysis and Erb's Juvenile Form of Progressive
Muscular Atrophy 448
Morbid Anatomy and Physiology of the Atrophic Paralyses . . . 4-54
CONTENTS. xvii
CHAPTER VIII.
THE SPASMODIC PARALYSES.
I'AOE
I. Paraplkgi^e 471
1. Primary Lateral Sclerosis (Tabes Dorsalis Spasinodica (Charcot), Spas-
modic Spinal Paralysis) . . . . . . . . .471
2. Amyotrophic Lateral Sclerosis ........ 474
3. Secondary Lateral Sclerosis ......... 470
II. Hemiplegia: 476
L Ordinary Hemiplegia .......... 470
2. Hemiplegia and Hemiansesthesiu ........ 477
3. Hemiplegia, Heinianuesthesia, and Hemianopsia ..... 477
4. Crossed Hemiplegia . . . .• . . . . 477
5. Hemiplegia and Post-hemiplegic Spasms ...... 478
III. Special Consideration of Post-hemiplegic Spasms as they occur
IN Infancy (the Spasmodic Paralyses of Infancy) . . 482
1. Spastic Hemiplegiae of Infancy 482
2. The Spasmodic Paraplegiije of Infancy ...... 484
IV. Monoplegia 485
V. Paralyses from Functional Disease ...... 485
1. Post-epileptic Paralysis ......... 485
2. Hysterical Paralysis • . . 486
3. Toxic Paralyses 488
Morbid Anatomy 489
I. Paraplegia 489
II. Hemiplegia ........... 491
III. Special Consideration of Lesions of the Pyramidal Tracts as they
occur in Infants .......... 497
IV. Monoplegia 499
CHAPTER IX.
DISORDERS OP MOTOR COORDINATION.
1. Meniere's Disease (Aural or Labyrinthine Vertigo) . . . 509
2. Primary Sclerosis of the Columns of Goll 510
3. Secondary Sclerosis of the Columns of Goll and of the Direct
Cerebellar Tracts 511
4. Progressive Locomotor Ataxia (Tabes Dorsalis, Gray Degenera-
tion or Sclerosis of the Posterior Columns of the Spinal
Cord) 511
(1) The Preataxic Stage 512
(2) The Ataxic Stage 521
(8) The Paralytic Stage 526
5. Combined Sclerosis of the Posterior ajsd Lateral Columns . 528
6. Diseases of the Cerebellum 528
PAGE
CONTENTS,
CHAPTER X.
VASCULAR DISEASES OF THE SPINAL CORD.
I. Anemia, Thrombosis, and Embolism of the Spinal Cord (Myelo-
malacia, Vascular Spinal Sclerosis) 539
II. HYPERiEMIA and HEMORRHAGE OF THE SPINAL CORD . . . 540
L Spinal Uyperaemia 540
2. Spinal Apoplexy (Hajmatorayelia) 541
CHAPTER XI.
MYELITIS.
Varieties of Diffused Myelitis 551
1. Central Myelitis 551
2. Bulbar Myelitis • .552
3. Transverse Myelitis 552
4. Wounds of the Spinal Cord 554
5. Compression Myelitis (Tumors in the Vertebral Canal) . . . 556
6. Spinal Hemiplegia and Hemiparaplegia (Unilateral Lesion of the
Spinal Cord) 557
7. Meningo-myelitis ........... 500
8. Universal Progressive Myelitis 560
9. Disseminated Myelitis .......... 561
CHAPTER XII.
DISEASES OF THE SPINAL MEMBRANES.
I. Vascular Diseases of the Spinal Membranes .... 569
1. Hj'peraemia .........'... 569
2. Hajmatorrhachis (Meningeal Apoplexy) ...... 569
II. Inflammation of the Spinal Dura Mater (Pachymeningitis
Spinalis, Perimeningitis) 570
1. Pachymeningitis Spinalis Externa (Peripachymeningitis) . . . 570
2. Pachymeningitis Interna . . .571
III. Inflammation of the Spinal Pia Mater and Arachnoid (Lepto-
meningitis Spinalis; Perimyelitis and Arachnitis) . . 574
1. Leptomeningitis Spinalis Acuta ........ 574
2. Leptomeningitis Spinalis Chronica ....... 575
CHAPTER XIII.
CERTAIN FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
1. Spinal Irritation 578
IL Neurasthenia 579
III. Headache (Cephalalgia) 584
Hemicrania 586
CONTENTS.
XIX
CHAPTER XIY.
saocK, coxcussioisr, and allied conditions.
I. Shock .
II. Concussion of the Spinal Cord (Commotio Spinalis)
Varieties of Spinal Concussion .....
III. Concussion of the Brain
IV. Contusion of the Brain ......
V. Compression of the Brain
PAGE
594
596
596
598
599
600
CHAPTER XY.
VASCULAE DISEASES OF THE BRAIN.
I. Anemia and Occlusion of the Intracranial Vessels . . 603
1. Universal Cerebral Anaemia ........ 603
2. Partial Cerebral Anemia (Occlusion of the Intracranial Ves«els . 604
II. C0NGE.ST10N of the Brain 608
III. Intracranial Hemorrhage 610
1. Cerebral Hemorrhage (Apoplexy) ....... 610
2. Meningeal Hemorrhage ......... 615
CHAPTER XYI.
ENCEPHALITIS.
Diffused or General Encephalitis 620
Partial or Local Encephalitis 620
1. Poliencephalitis Acuta Infantium ....... 621
2. Traumatic Local Encephalitis ........ 621
3. Acute Pyiemic Encephalitis ........ 622
4. Encephalitis Complicating Preexisting Lesions of the Brain . . 623
CHAPTER XVII.
ATROPHY, HYPERTROPHY, AND TUMORS OF THE BRAIN.
I. Atrophy of the Brain 630
1. Atrophy of the Corpus Callosum ....... 630
2. Atrophy of the Cerebellum ........ 630
3. Atrophy of the Cerebral Hemispheres ...... 630
II. Hypertrophy of the Brain 631
1. General Hypertrophy of the Brain ....... 631
2. Partial Hypertrophy or Heterotopia of the Brain Substance . . 631
III. Intracranial Tumors 632
CHAPTER XYIII.
APHASIA.
Motor Aphasia
Sensory Aphasia (Amnesic Aphasia)
Mixed Motor and Sensory Aphasia ....
638
640
643
CONTENTS.
CHAPTER XIX.
DISEASES OF THE MEMBRANES OF THE BRAIN.
PAGE
I. DrSKASES OF THE DuRA Mater 651
(I.) External Pachymeningitis 651
(II.) Internal Heniorrnagic Pachymeningitis (Hjematoma of the Dura
Mater) 651
II. Diseases of the Pia Mater. 653
(I.) Tubercular Meniningitis (Acute HydrocephHliisj .... 653
Chronic Hydrocephalus ......... 658
(II.) Meningitis of the Convexity of the Brain 660
(III.) Simple Meningitis of the Base of the Brain (Basilar Meningitis) 663
(IV.) Metastatic Meningitis 664
(V.) Traumatic Meningitis 665
CHAPTER XX.
PAPvALYSIS AGITANS, MULTIPLE SCLEROSIS, AND CHOREA.
I. Paralysis Agitans 670
II. Multiple Sclerosis of the Brain and Spinal Cord (Dissemi-
nated OR Insular Sclerosis) 674
III. Chorea 679
CHAPTER XXI.
GENERAL DIAGNOSIS.
1. Clinical Diagnosis 690
2. Topographical Diagnosis 691
3. Pathological Diagnosis 699
Syphilis of the Brain ... . .... 705
DISEASES OF THE NERVOUS SYSTEM.
/4387
CHAPTEK J.
ANATOMICAL INTRODUCTION.
Before entering upon the study of the nervous system it is desirable
to lay down a foAV general principles, to which all nervous structures,
with their corresponding functions, must conform. The key to the
interpretation of the form assumed by the constituent parts of the ner-
vous SA'Stem, and of the actions performed by each part, is best obtained
by a close study of the order of development of nervous structures and
functions as manifested in passing from the lower to the higher animals,
and from the initial to the adult stages of animals. The knowledge
obtained by these studies constitutes the comparative anatomy and em-
bryology of the nervous system. The great law to Avhich all developing
organisms and organs, as well as all developing functions, must conform
is the law of evolution. This law may be defined as a progressive
integration of structure and function, during which there is a passage
from the uniform to the multiform, from the simple to the complex, and
from the general to the special.
In the lowest organisms, which consist of individual cells, or of an
aggregation of cells without definite parts, each part performs all the
vital functions. Each part possesses the fundamental property of irrita-
bility, and is capable of initiating movement, or, in other words, is
automatic and contractile, and each is likewise metabolic, excretory, and
reproductive. But on ascending in the scale of organization it is found
that certain parts of the organism acijuire the power of performing
more perfectly a few functions, and ultimately one special function,
while losing to a greater or less extent the power of performing the
general functions. One part or tissue, for example, becomes adapted
to the performance of the functions of contraction, while at the same
time it gives up the functions of initiating movement and reproduction.
18 ANATOMICAL INTRODUCTION.
and only performs the metabolic and excretory functions in a very subor-
dinate degree. This process has been named a " physiological division
of labor," or a "specialization of function," when regarded from the
point of view of the actions of the organism, and its anatomical counter-
part in development is to be found in what is known as the "differen-
tiation of structure."
FORMATION OF NERVOUS CONSTITUENTS.
The first beo-inning of a differentiation of the nervous from the other
elements of organisms is well illustrated in Hydra. In this organism
the internal end of an ectodermic cell is prolonged into a process,
which, being shielded from external influences, tends only to contract
when it receives a stimulus through the external end. In other words,
the internal end performs the work, and the external determines when
the work shall be done : the one is operative, the other regulative.
This differentiation of structure is carried still further in Beroe, where
the internal and external ends of the ectodermic cells are represented
by two different cells connected by a thin fibre. The changes set up
in the external or sensitive cell are conducted through the fibre to the
internal cell, which it excites to contract. This new arrangement of
fibre introduces us to a new specialization of function. The regulative
or automatic cell and the work cell are separated from each other by a
considerable distance, but the molar contraction of the one is coordinate
with the molecular motion of the other by the internuneial function of
the fibre. The property the fibre possesses of transmitting the state of
activity from one end to the other is called its conductivity.
The next step in development consists in the differentiation of the
external or sensitive cell into two : one of which becomes adapted to
responding to external stimulation alone, and the other to modifying
the impulses which are sent to it from the external cell and trans-
mitting them to the work cell. The nervous mechanism now consists
of an external sensory cell, an afferent fibre connecting it with a cen-
tral regulating cell, and an efferent fibre or fibres connecting this last
with work cells. This mechanism constitutes a rejiex loop, and its
function is named rejiex action. One other complication of this simple
mechanism may be mentioned : When an automatic or reflex cell is
already engaged in action, a new stimulus brought to it by means of a
second afferent fibre may check, instead of still further exciting that
action, so that this function introduces us to inhibitory as well as excito-
motor fibres. The inhibitory fibres are either afferent, or connect one
central cell with another central cell, being then intercentral, and prob-
ably never connect a central cell directly with a work cell.
FORMATION OF A NERVOUS SYSTEM. 19
FOKMATION OF NEEVOUS TISSUES.
On looking at a simple nervous system, the greatest contrast in
structure is manifested between certain knots termed ganglia and
certain cords termed nerves, and, since these parts exhibit the greatest
structural contrast existing in the nervous system, they may also be
expected to exhibit the widest functional contrast. The ganglia are
composed of nerve cells, with their connecting processes, held together
by a fine connective tissue ; and the nerves are composed of nerve fibres
arranged side by side in a bundle — these being also held together by a
firm connective tissue and by a fibrous sheath.
Functionally regarded, the ganglia are originators of motion, and, to
some extent, conductors also ; while the nerves are mainly conductors,
although it is probable that they are also in some small degree origin-
ators of motion. A still further examination shows that the afferent
fibres are provided Avith peripheral end-organs, which are adapted for
receiving impressions from environing agents and objects ; while the
efferent fibres are provided with arrangements by means of which the
molecular motion of the nervous system is transmitted into the molar
motion of the work organs.
FOKMATION OF A NERYOUS SYSTEM.
It has just been seen how the cells and fibres which constitute the
nerve elements integrate so as to form the simple tissues, and now we
must follow this progressive integration to still higher stages. In the
higher animals, the ganglia, instead of appearing as small knots, have
come, by approximation and fusion, to form a continuous mass, which,
from its color, is termed the gray substance; and the fibres, instead of
always appearing as cords connecting separate ganglia, also form a con-
tinuous mass called the white substance. Now, this fusion of nerve
centres and nerve strands takes place when the functions are integrated
in corresponding degree, and fails to take place when the functions
remain in large measure independent of one another.
The internal organs of the body which are derived from the hypo-
blast of the embryo are much more independent of one another in
their actions than are the external organs derived from the epiblast ;
and the functions of the former are regulated chiefly by means of the
ganglia of the sympathetic system, which are only connected by small
cords, while those of the latter are regulated by means of large masses
of gray and white substance, which constitute the encephalo-spino-
neural system.
20 ANATOMICAL INTEODUCTION.
■ The parts of tlie body which are derived from the mesoblast form a
system of organs which serve to connect the external and internal
or<^ans ; and fn so far as the intermediate tissues subserve the functions
of ''the external organs their actions are regulated from the encephalo-
spinal and the spino-neural centres ; and when they subserve the func-
tions of the internal organs their actions are regulated by the sympa-
thetic system ; while in so far as their function is intermediate between
the internal and external organs, but partially independent of them,
their actions are regulated by an intermediate and partially inde-
pendent system, termed the vaso-motor.
A plane passing longitudinally and from behind forwards through a
human being bisects the body into two bilaterally symmetrical divisions,
and this statement is equally true of the nervous system as of the body
as a whole. The sympathetic system of each half of the body is rep-
resented by a gangliated cord, which is situated along the side of the
vertebral column ; while the encephalic and spinal systems of each side
are represented by the cerebral and cerebellar hemispheres, the crus
cerebri, and the lateral halves of the pons, medulla oblongata, and spinal
cord. Although the two lateral halves of the body are more or less
symmetrical, the organs of the one side are to a considerable extent
dependent upon those of the other in their functions, and consequently
the actions of the organs of the two sides must be duly coordinated.
The structural counterpart of this interdependence is to be found, in
the case of the sympathetic system, in the plexus of fibres and small
ganglia which pass in front of the vertebral column and connect the
ganghated cords of the two sides with one another ; and in the en-
cephalic and spinal systems by the commissures of the spinal cord, the
median raphe of the medulla oblongata and pons, the middle peduncles
of the cerebellum, the commissures of the third ventricle, and the
coi'pus callosum.
The body is composed of segments placed end on end, and there is
a similar distribution of the nervous system. That this is the case
with the greater part of the sympathetic is readily recognized. Each
segment of the body is represented by a vertebra and its appendages,
and most of the vertebrae have a corresponding ganglion for each
lateral half, although fusion of two or more ganglia in the successive
segments of the cervical region and in those of the coccyx prevents the
correspondence from being altogether perfect.
In the spinal cord the analogous ganglia of the same segment and
the homologous ganglia of successive segments have become so com-
pletely integrated that they form a closed tube of gray matter, which
extends from the conus medullaris up through the whole length of the
ENCEPIIALO-SPINO-XEURAL SYSTEM. 21
cord, the floor of the fourth ventricle, the aqueduct of Sylvius, and the
gray matter of the third ventricle, to terminate at the tuber cinereum.
One consequence of the fusion of homologous ganglia is that the parts
of the cord which correspond to the diiferent segments of the body have
undergone considerable displacement. The cord usually ends at the
lower border of the body of the first lumbar vertebra- ; but the nerves
which descend to pass out through the remaining lumbar intervertebral
foramina and through the sacral and sacro-coccygeal foramina, show
that the lower part of the cord presides over the functions of the lower
segments of the body, although it has by the fusion and approximation
of the homologous centres suffered considerable displacement.
A still further integration has taken place in the cephalic centres, and
the highest ganglia — the cerebrum and cerebellum — consist of large
aggregations of gray and white matter, in which it is diflBcult to find
any trace of the separate ganglia and the conducting paths of which
they are composed. The cephalic ganglia, spinal cord, and peripheral
nerves form one functionally indivisible system which may be named
the encephalo-spino-neural system.
Encephalo-spino-neural System,
We shall now make a few general remarks on (1) the arterial supply
of this system ; (2) its topography ; (3) its relations to the skeleton ;
(4) the topography of the internal parts of the cerebrum, as being the
part of the system in which this knowledge is most generally required
for practical purposes; and (5) the internal structure of the system.
1. Tlie Arterial Supply,
a. The Spinal Arteries.
(1) The spinal branches enter the intervertebral foramina along with
the roots of the spinal nerves, and are distributed to the vertebrae,
spinal membranes, and spinal cord. These arteries are derived from
the lateral sacral, ilio-lumbar, lumbar, aortic intercostal, the ascending
cervical branch of the inferior thyroid, and vertebral arteries.
(2) The anterior spinal artery is a small vessel derived from the
vertebral artery near its termination in tlie basilar. This vessel joins
with its fellow of the opposite side to form a single vessel which de-
scends along the anterior aspect of the spinal cord, and is continued to
the lower end of the cord as the anterior median artery.
(3) The posterior spinal artery is derived froui the inferior cerebellar
22
ANATOMICAL INTKODUCTION
artery ; it winds round the medulla oblongata to reach the posterior
aspect of the cord, when it is continued onwards to the cauda equhia.
(4) The nutritive arteries of the spinal cord are sufficiently indicated
in the annexed diagram (Fig. 1).
Fig. 1.
la
ea a \ m
Diagram of the Distribution of the Bloodvessels, and Gbovping or Ganglion Cells in the
Spinal Cord. (Young. )
Anterior median artery.
(if, Arteries of the anterior median fissure.
<ic, Artery of the anterior commissure.
1, Anterior branch.
1', Median branch.
1", Posterior branch.
ca, Central artery.
2, Anterior branch.
2', Median branch.
2", Posterior branch.
pa, Posterior root arteries.
6' 6", Arteries of posterior horns.
«Vt, Internal anterior root artery.
CO, External anterior root artery.
n V. Internal and external branch.
Antero-lateral branch.
4, Anterior branch.
4', Bledian branch.
4", Posterior branch.
, Median lateral artery.
.5 5', Anterior and posterior branches
Posterior lateral arteries.
Internal posterior arteiy.
Kxtcrnal posterior arteiy.
Arteries of the column of Goll.
Artery of the posterior commissure.
Vesicular column of Clarke.
Internal group of cells.
Anterior group.
Antero-lateral group.
Postero-lateral group.
Central group.
Median area.
ENCEPHALO-SPINO-NEUEAL SYSTEM
23
b. The Arteries of the Medulla Oblongata, Pons, Crura Cerebri, and
Cerebellum.
(1) The vertebral artery/ winds backwards round tlie articulating
process of the athis, and, after piercing the dura mater, enters the skull
tlirough the foramen magnum, and terminates at the lower border of
the pons Varolii bj uniting with the corresponding vessel of the oppo-
site side to form the basilar artery. Besides the spinal branches already
pia
Section of the Mebulla Oblongata, showing the Distribution of tiik Vkssels.
K, Artery of the Median Kapbe.
Ill, Branches to the formatio reticularis.
V, Branch to the olivary body.
1", Branches to the liypoglossal nucleus.
1'", Branches to the floor of the fourth ventricle, and to the internal inferior nuclei of the
facial [if).
24 AXATOMICAL INTRODUCTION.
p. Pyramidal arteries,
or, Anterior root artery (hypoglossal).
2', Branch to the olivary body.
2", Branches to the formatio reticnUris. It terminates in branches to the hypoglossal nucleus.
Ir, Lateral root artery (vagus).
.5, Branch to the restiform body and the inner division of the inferior cerebellar peduncle,
o', Branches to the nucleus of the vagus. Also gives branches to the ascending root of the
tifth and the Jirrmidio reticularis.
ala. The anterior lateral artery of the medulla oblongata. It supplies branches to the formutio reti-
cularis, olivary body, anterior nucleus of the lateral column {olc\ and terminates in branches
to the hypoglossal nucleus.
mla. The middle lateral artery of the medulla oblongata. It supplies branches to the formatio reli-
mlaris, the posterior nucleus of the lateral column {pic), and terminates in branches which are
distributed to the external accessory nucleus of the facial (ef).
phi, The posterior lateral arteries of the medulla oblongata. They supply the restiform bodies.
C, Central artery.
:S :i' 3", Branches to tlie liypoglo-ssal and external accessory facial nuclei.
mp, Median posterior artery.
4 4' 4", Branches to tlie external accessory facial and pneumogastric nuclei.
ep, External posterior artery. It supplies branches to the internal division of the inferior peduncle
of the cerebellum and restiform body.
i. Internal group of cells of the hypoglossal nucleus.
al, Antero-lateral " "
pi, Postero-lateral " "
a. Anterior "
ale, Anterior nucleus of the lateral column.
pic. Posterior " "
viii, Inferior portion of the posterior median acoustic nucleus.
if, Internal accessory facial nuclei.
ef, External accessory facial nucleus.
/, Fasciculus rotundus.
XII, Ilypoglossal nerve.
X, Pneumogastric nerve.
G, Column of GoU.
pr. Posterior root-zone. The direct cerebellar tract forms a thin band lying external to the column of
GoU and posterior root-zone.
CM, Clavate nucleus.
In, Triangular nucleus.
0, Olivary body.
po, Parolivary body.
vp, Nucleus of the pyi'ainid.
pn, Nucleus of the arciform fibres.
P, Anterior pyramid.
al, Ascending root of the trigeminus.
ng. The substantia gelatinosii.
described, tlie vertebral gives rise to the inferior cerebellar artery, as
well as to meningeal and muscular branches.
(2) The basilar artery runs forwards in the groove on the anterior
surface of the pons Varolii, and divides at the anterior border of the
pons into two terminal branches, which will be found to form part of
the circle of Willis. The branches of the basilar artery are the trans-
verse arteries of the pons, the middle and superior cerebellar arteries,
and the posterior cerebral artery. These branches are sufficiently indi-
cated in the annexed diagram (Fig. 2).
(3) The nutritive arteries of the medulla oblongata and pons are
shown in the annexed diagram (Fig. 2).
ENCEPH A LO-S PINO- NEURAL SYSTEM.
25
c. The Arteries of the Cerebrum.
(1) The posterior cerebral arteries are the terminal branches of the
basihxr trunk, and each artery winds round the crus cerebri to reach the
occipital lobe.
(a) The posterior median group (Fig. 3, 2), which pierce the poste-
rior perforated space and supply the internal surface of the optic thala-
nius and the walls of the third ventricle.
Fig. 3.
P-^
Diagram of the Distribution of the Ves^sels at the base of the Cerebrum. (After Charcot.)
CA, Anterior cerebral artery ; S, S, Sylvian arteries ; V, V, Vertebral arteries ; B, Basilar ; CP, CP,
Posterior cerebral arteries; 1, 2, 3, 3, 4, 4, Groups of nutritive arteries. The line limits the
ganglionic vascular area.
(h) The poster 0-lateral group (Fig- 3, 4) enter the brain beliiiid the
border of the crus cerebri and pass into the optic thalamus and corpora
quadrigemina.
(e) The cortical branches, consisting of the anterior temporal, the
posterior temporal, and the occipital arteries.
(2) The anterior cerebral artery/ (Fig. 3, CA), derived from the
internal carotid artery, runs forAvards in tlie longitudinal fissure, and,
26 ANATOMICAL INTKODUCTION.
turning round tlie cm-pus callosum, is distributed to the anterior part of
the cerc'bruni. The arteries of the two sides are united at their com-
menceuient by a short transverse branch, the anterior communicating
artery.
(a) The anterior median group (Fig. 3, 1) supply the anterior part
of the head of the caudate nucleus.
(6) The cortical branches.
(8) The middle cerebral or Sylvian artery (Fig. 3, S) is the most
important branch, and the direct continuation of the internal carotid.
(a) The antero-lateral group (Fig. 3, 3) pierce the anterior perforated
space, and supjdy the corpus striatum and anterior part of the optic
thalamus.
{h) A choroid branch Avhich winds round the crus to reach the choroid
plexus.
(c) The cortical branches, consisting of the inferior frontal, the
ascending fi-ontal, the ascending parietal, the parieto-sphenoidal and
sphenoidal branches.
(4) The posterior communicating artery is a long and slender vessel
which connects the internal carotid with the posterior cerebral arteries.
These two arteries, Avith the posterior communicating artery, connect
the anterior and posterior arterial systems of the brain, and complete
the anastomosis round the circle of Willis (Fig. 3).
A survey of the arteries of the brain shows that they may be divided
into (1) the vessels which are distributed to the cortex of the brain —
the cortical system of arteries; and (2) those which pierce the base of
the organ to supply tlie basal ganglia — the ganglionic system.
(1) THE CORTICAL SYSTEM OF ARTERIES.
The arteries of the cortical or nutritive system are of two kinds : (a)
the long or medullary arteries., and (b) the short or cortical arteries.
(a) The long or medullary arteries pass into the substance of the
centrum ovale without communicating with one another, except by fine
capillaries, and consequently each constitutes a small, independent
vascular territory. These vessels extend as far as the ganglionic sys-
tem, but do not appear to anastomose with it.
(b) The cortical or nutritive arteries arise from the vascular network
of the pia mater, and most of them terminate in the gray matter ; but
a few of them send capillaries to the centrum ovale.
The distribution of the cortical arteries is shown in the annexed
diagrams (Figs. 4, 5, and 6).
EXCEPHALO-SPINO-NEURAL SYSTEM. 27
Fig. 4.
View of the Brain fkom below. (After Ecker and Duret.)
Distribution of Vesseh.
The region bounded by the line ( ) represents the territory over which the Internal and Inferior
Frontal Branches of the Anterior Cerebral Artery are distributed.
The regions bounded by the line ( ) represent the territories over whicli the branches of
the Posterior Cerebral Artery are distributed
I. Is the region of tlie Anterior Temporal Artery.
II. " " Posterior Temporal Arlerij.
III. " " Occipital Artery .
Fissures and Convolutions.
Fl, Gyrus Eectus. ti. Sulcus occipito-temporalis inferior.
J^2, Middle frontal convolution. t3, Sulcus temporo-sphenoidalis inferior.
FS, Inferior frontal convolution. 12, Sulcus temporo-sphenoidalis medialis.
fi. Sulcus olfactorius. x>o, Parieto-occipital fissure.
/5, Sulcus orbitalis. oc, Calcarine fissure.
T2, Second or middle temporo-sphenoidal convolution. H, Gyrus hippocampi,
rs, Third or inferior temporo-sphenoidal convolution U, Gyrus uncinatus.
Ti, Gyrus occipito-temporalis lateralis (lobulus fusi- Ch, Optic chiasma.
formis). fc, Corpora albicantia.
T5, Gyrus occipito-temporalis medialis (lobulus lin- KK, Crura cerebri,
gualis . C, Cori)us callosum.
28
ANATOMICAL INTRODUCTION
(2) THE CENTRAL OR GAKGLIONIC SYSTEM OF ARTERIES.
The ganglionic system form six main groups, which are named the
anterior' an'd posterior median (Fig. 3, 1 and 2) ; the right and left
antero-lateral (Fig. 8, 3, 3) ; and the right and left posterolateral (Fig.
8, 4, 4). An imaijinary line passing round the circle of Willis, at a
distance of two centimetres, would completely surround all these ves-
sels, and the area so limited may be called the ganglionic vascular area.
Fig.
Inner Surface of Riuht Hemisphere. (After Ecker anJ Dueet.)
Distribution of Vessels.
Tlie regions bounded by the line ( ) represent the territories over whicii the branches of the Ante-
rior Cerebral Artery are distributed.
I. Is the territory of the Interior mid Ankriur Frontal Artery.
II. " " Internal and Middle " "
III. " " Internal and Posterior " "
The regions bounded by the line ( ) represent the territories over which the branches of
the Posterior Cerebral Artery are distributed.
II. Is the territory of the Posterior Temporal Artery.
Ill- " " Occipital ilrtery .
Fissttres and Convolutions.
CC, Corpus callosum, longitudinally divided ; Gf, Gyrus fornicatus ; H, Gyrus hippocampi ; h, Sulcus
hippocampi ; U, Uncinate gyrus ; cm, Sulcus calloso-marginalis ; Fj, Median aspect of the first frontal
convolution ; c, Terminal portion of the sulcus centralis, or fissure of Rolando ; A, Anterior ; B, Posterior
central convolution ; Pj", Precuneus ; Oz, Cuneus ; Po, Parieto-occipital fissure ; o, Sulcus occipitalis
transversus ; oc, Calcarine fissure ; oc', Superior, oc". Inferior ramus of the same ; D, Gyrus descendens ;
T4, Gyrus occipito-temporalis lateralis (lobulus fusiformis); T5, Gyrus occipito-temporalis medialis (lobulus
lingualis).
EISrCEPHALO-SPINO-XEUEAL SYSTEM,
29
All these vessels are terminal arteries. Some of these branches are of
sufficient importance to have been specially described and named.
Fig. 6.
Outer Surface of the Left Hemisphere. (After K<kek and Duret.)
Distribution of Fes.sefe.
The region bounded by the line ( ) represents the territory over wliicli branches of tlie Anterior
Cerebral Artery are distributed.
The anterior regions bounded by the line ( ) represent the territories over which
branches of the Middle Cerebral Artery are distributed.
I. Is the region of the External and Inferior Frontal Artery.
II. " '■ Anterior Parietal Artery.
III. " " Posterior Parietal Artery .
IV. " " Parielo-sphenoidal Artery
Tlie posterior and inferior region bounded by the line ( •- ) represents the territory
over which branches of the Posterior Cerebral Artery are distributed.
Fissures and Convolutions.
F, Frontal lobe. P, Parietal lolx-. 0, Occipital lobe. T, Temporo-spheuoidal lobe. S, Fissure of
Sylvius, S' Horizontal, S" Ascending ramus of the same, c, Sulcus centralis or fissure of Eolando. A
Anterior central or ascending frontal convolution. B, Posterior central or ascending parietal convolution
Fi Superior, r2 Middle, and F^ Inferior frontal convolutions, /i Superior and /» Inferior frontal sulcus
fs Sulcus prjecentvalis. Pj Superior parietal or postero-parietal lobule ; Po Inferior parietal lobule, viz.
Po Gyrus supra-marginalis, Pj' Gyrus angularis. ip, Sulcus intra-parietalis cm, Termination of the
calloso-marginal fissure. Oj First, Oj Second, O3 Third occipital convolutions, po, Parieto-occipital fis
sure, o. Sulcus occipitalis transversus ; oj Sulcus occipitalis longitudinalis inferior. Tj First, To Second,
T3 Third temporo-sphenoidal convolutions. <i First, t« Second temporo-sphenoidal fissures.
50
ANATOMICAL INTRODUCTION,
Branches of the Middle Cerebral Artery.
(a) The lenticular branches are two or three small twigs which are
distributed to the two inner divisions of the lenticular nucleus and the
adjoining portion of the caudate nucleus (Fig. 7, 5).
(b) The lenticulo-striate artery ascends between the external capsule
and lenticular nucleus, and supplies the outer division of the lenticular
nucleus, the internal capsule, and the caudate nucleus (Fig. 7, 4).
Fro. 7.
Transverse Section of the Cerebral Hemispheres, about 1 cm. behind the Optic Commissure.
(From Buret.)
Arteries of the Corpus Striatum. — Ch, Chiasnia; B, Section of the optic tract ; L, Lenticular nucleus;
I, Internal capsule ; C, Caudate nucleus ; E, External capsule ; T, Claustrum ; B, Island of Reil ; F,
V, Section of the lateral ventricle ; P, P, Anterior pillars of the fornix ; 0, Gray substance of the
third ventricle.
Vascular Areas. — I, Anterior cerebral artery; II, Middle cerebral artery; III, Posterior cerebral
artery. — 1, Internal carotid artery ; 2, Sylvian artery ; 3, Anterior cerebral artery ; 4, 4, External
arteries of the corpus striatum (lenticulo-striate artery) ; 5, 5, Internal arteries of the corpus striatum
(lenticular arteries). The opto-striate artery is not represented in the figure.
(c) The lenticulo-optic artery also ascends between the external cap-
sule and the lenticular nucleus, and supplies branches to the posterior
part of the nucleus and of the internal capsule, and terminates in the
anterior and external part of the optic thalamus.
Branches of the Anterior Cerebral Artery.
The anterior median group supplies the anterior part of the caudate
nucleus.
Branches of the Posterior Cerebral Artery.
(a) The jJosterior internal artery of the optic thalamus is distributed
to the internal surface of that oranglion.
ENCEPHALO-SPIXO-NEURAL SYSTEM. 31
(b) The posterior external artery of the optic thalamus is distributed
to the posterior and external portion of that ganglion, and also sup-
plies the external geniculate bodies.
2. Topography of the Encephalo-spino-neural System.
The fissures and convolutions of the cerebrum are suflSciently indi-
cated in Figs. 4 to 6 -without further description. The cerebellum,
pons, and medulla oblongata lie at the base of the skull below the
tentorium, the spinal cord occupies the vertebral canal as low as the
inferior border of the body of the first lumbar vertebra, the cranial
peripheral nerves issue through various foramina at the base of the
brain, and the spinal nerves pass through the intervertebral foramina.
3. Relation of the Different Parts of the Encephalo-spino-neural
System to the Skeleton,
a. Kelations of the Spinal Cord and Nerves to the Vertebral Canal.
The annexed diagram (Fig. 8) shows the position of the spinal cord
in relation to the vertebral canal in which it lies. The tips of the
cervical spines correspond nearly to the lower borders of the correspond-
ing vertebrae. Each of the upper three dorsal spines corresponds nearly
to the upper border of the body of the vertebra below. The ninth,
tenth, and eleventh spines slope less, and their tips again correspond to
the upper borders of the next vertebrae below, while the rest of the
spines are opposite the bodies of their own vertebrae.
b. Kelations of the Cerebral Convolutions to the Skull.
The convolutions and fissures of the surface of the brain have just
been described, and we must now give a brief account (1) of the topog-
raphy of the surfiice of the skull ; and (2) of the relations existing
between the different areas of the skull and the respective convolutions
and fissures of the brain.
(1) topography of the external surface of the skull.
The topography of the external surface of the skull has been studied
by Broca, Fere, Turner, and others, with the view of connecting defi-
nite points and areas on the surface with the respective convolutions
and fissures of the brain. We shall adopt the divisions and descrip-
tions of Turner in this place :
Definite Landmarks on the Surface of the Skull. — The following
structures and markings are easily recognized on the skull. The ex-
ternal occipital protuberance (Fig. 9, o), the parietal (P) and frontal (F)
32
ANATOMICAL INTRODUCTION,
eminences, and tlie external angular process of the frontal bone (A),
the coronal {c) and lambdoidal (Z), squamous (s), squamoso-sphenoid
Fig. 8.
Diagram showing the Relation of the Spines of the
Vertebr.t: to the Origin of the Nerves.
(After GowEits.)
The first three cervical spiues are upiiosite the origins of
the od, 4th, and 5th cervical nerves. The 6th and 7th pairs
arise opposite the intervals between the 4th and 5th and the
5th and 6th cervical spines respectively The 6th cervical
siiine corresponds to the origin of the 8th cervical nerve,
and the 7th cervical spine to the first dorsal nerve. The
first four dorsal spines vary. The 1st spine corresponds to
the interval between the 2d and 3d pairs, or to the origin of
tlie .3d pair. The 2d spine is between the 3d and 4th pairs,
or opposite the 4th pair The 3d spine is opposite the 5th,
or the interval between the 5th and Gth pairs. The 4th
spine is opposite the lower part of the origin of the 6th
pair, or even below it The 5th spine always corresponds
to the origin of the 7th pair; the 6th spine to the 8th pair ;
the 7th to the 9th pair ; the 8th to the ui)per part of the
loth pair ; the 9th to the 11th pair ; and the 10th to the
12th pair. The 1st lumbar arise opposite the 11th dorsal
spine ; the second lumbar opposite the interval between the
11th and 12th spines ; the 3d and 4th ojiposite the 12th
spine ; the 5th lumbar and the 1st sacral opposite the inter-
val between the 12th dorsal and 1st lumbar spines, while
the remaining sacral nerves arise nearly opposite the 1st
lumbar spine.
The cervical enlai-gement of the cord corresponds nearly
to the bodies and spines of the cervical vertebrae, while the
lumbar enlargement corresponds to the bodies of the 11th
and 12th dorsal and 1st lumbar vertebras, and to the lower
three dorsal and 1st lumbar spines.
ENCEPHALO-SPINO-NEURAL SYSTEM. 33
(ss), and parieto-splienoid sutures (ps), and the curved line of the tem-
poral ridge (t).
Primary Areas of the Skull. — The coronal suture (c) forms the
posterior boundary of the frontal area. A vertical line (Fig. 9, 2)
drawn from the squamous suture (s) upwards through the parietal emi-
nence (P) to the sagittal suture lies almost parallel to the coronal suture,
Fig. ;i.
Latkral View ui' the Hujian Skull. (Feuriee. )
A, The external angular process of the frontal bone. F, The frontal eminence. P, The iiarictal emi-
nence. 0, The occipital protuberance, c, The coronal suture. I, The lambdoidal suture s, The squa-
mous suture, t, The temporal ridge, /s, The fronto-sphenoid suture, ps, The parieto-sphenoid suture.
ss, The squanioso-sphenoid suture, pm, Tlie parieto-mastoid suture 1, Frontal line. 2, Parietal line.
SF, MF, IF, The supero-, mid-, and infero-frontal subdivisions of the frontal area. SAP, Tlie supero-
antero-parietal area. lAP, The infero-antero-jjarietal area. SPP, The siipero postero-parietal area.
IPP, The infero-postero-parietal area. 0, Tlie occipital area. Sq, The sijuamoso-tem])oral area. AS,
The ali-sphenoid area.
and subdivides the parietal region into an antero-parietal (Fig. 9,
SAP-f lAP) and a postero-parietal area (Fig. 9, SPP + IPP).
The occipital region lies between the lambdoidal suture (l) and the
occipital protuberance (o), with the superior cui'ved line extending from
it (Fig. 9, o).
Secondary Areas of the Skull. — These four primary divisions of the
skull may be subdivided into secondary areas. The temporal ridge
34 ANATOMICAL INTEODUCTION.
(Fig. 9, t). Starting from the external frontal process, curves backwards
across the frontal (A), antero-iiarietal, and post-parietal areas to the
internal angle of the occipital bone, and subdivides each of these re-
gions into an upper and a lower area. The upper frontal area, which
includes all the frontal regions above the temporal ridge, is again di-
vided by a line drawn vertically upwards and backwards from above the
orbit through the frontal eminence to the coronal suture (Fig. 9, c).
This line divides the upper frontal area into a supero-frontal (SF) and
a mid-frontal area (MF).
Two other areas remain to be described. These are concealed by the
temporal muscle, and are limited superiorly by the squamoso-parietal,
sphenoido-parietal, and fronto-sphenoidal sutures. The lines of the
sutures naturally divide this area into a squamoso-temporal (Sq) and
ali-sphenoidal area (AS).
The following, then, are the secondary areas of the skull : Superior
Frontal (SF), 3Iiddle Frontal (MF), Inferior Frontal (IF), Upper
Antero-parietal (SAP), Lozver Antero-parietal (lAP), Ujjper Postero-
parietal (SPP), Lower Fostero-jyarietal (IPP), Occipital (0), Squa-
moso-tem^joral (Sq), and Ali-sphenoidal (AS).
(2) RELATIONS OF THE DIFFERENT AREAS OF THE SKULL TO THE RESPECTIVE
CONVOLUTIONS AND FISSURES.
The fissure of Sylvius (Fig. 10, SS) commences behind the posterior
border of the lesser wing of the sphenoid, and courses upwards and
backwards below the greater wing of the sphenoid, where this articu-
lates with the anterior inferior angle of the parietal bone, and then
appears in the lower part of the inferior antero-parietal region. The
fissure of Rolando (Fig. 10, R) lies in the antero-parietal region, both
in its superior and inferior divisions, its upper extremity being as much
as two inches and its lower an inch and a half behind the respective
ends of the coronal suture. The coronal suture does not, therefore,
correspond to the boundar}- between the frontal and parietal lobes of
the brain.
The parieto-occipital fissure (Fig. 10, PO) is situated on an average
about 0.7 to 0.8 inch in front of the apex of the lambdoidal suture.
Contents of the Respective Areas.
The frontal area is occupied by the frontal lobe, but does not cover
the whole of it, the posterior extremities of the three frontal convolu-
tions lying behind the coronal suture. The frontal area, therefore,
corresponds to the part of the frontal lobe supplied by the anterior
cerebral artery, and which is not excitable to stimulation. The supe-
EXCEPIIALO-SPINO- NEURAL SYSTEM,
35
rior, middle, and inferior frontal areas of the skull correspond respec-
tively to the superior, middle, and inferior frontal convolutions, with
the exception of their posterior extremities.
The uppe7' antero-parietMl area (Fig. 10, SAP) contains the upper
two-thirds of the ascending frontal (AP) and ascending parietal (S)
Fig 10.
DiAGKAM showing; the Relations of the Convolutions to the Skull. (Turner.)
K, The fissure of Rolando, which separates the frontal from the parietal lobe. PO, The parieto-occipi-
tal fissure between the parietal and occipital lobes. SS, The fissure of Sylvius, which separates the tem-
poro-spheuoidal from the frontal and parietal lobes. SF, MF, IF, The supero-, mid-, and infero-froutal
subdivisions of the frontal area of the skull : the lettei-s are placed on the superior, middle, and inferior
frontal convolutions SAP, The superoantero parietal area of the skull : S is placed on the ascending
parietal convolution, AP on the ascending frontal convolution. lAP, The infero-antero-parietal area of
the skull : I is placed on the ascending parietal, AP on the ascending frontal convolution. SPP, The
supero-postero-parietal area of the skull : the letters are placed on the angular convolution. IP?, The
infero-postero-parietal area of the skull : the letters are placed on the mid-teraporo-sphenoidal convolu-
tion. Xj The convolution of the parietal eminence, or supra-marginal gyrus. 0, The occipital area of
the skull : the letter is placed on the mid- occipital convolution. Sq, The squamoso-temporal region of
the skull : the letters are placed on the niidtemporo-sphenoidal convolution. AS, The ali-sphenoid
region of the skull : the letteis are placed on the tip of the supero-temporo-s])henoidal convolution.
convolution, and the posterior extremities of the superior (1.2 in.) and
middle frontal (1.3 in.) convolutions. At the upper posterior angle of
this area part of the postero-parietal lobule is visible, and below this
part of the supra-marginal lobule may appear.
The lower antero-parietal area (Fig. 10, lAP) contains the lower
36 ANATOMICAL INTRODUCTION.
third (if tlie ascending parietal (1 in.) and ascending frontal (AP) con-
volutions, and the posteriin- extremities (1 in.) of the inferior frontal
convolution. A small portion of the supra-marginal gyrus is visible at
the upper posterior angle of this area, and below it a small portion of
the sujierior temporo-splienoidal convolution.
The upper poster o-parletal area (Fig. 10, SPP) contains the greater
part of the postero-parietal lobule. Below it lies the upper portion of
the angular gyrus (SPP), and part of the supra-marginal gyrus (X)
Posteriorly the annectant gyri blend with the occipital lobe.
The loiver postero-parietal area (Fig. 10, IPP) contains part of the
supra-marginal gyrus, and behind it part of the angular gyrus, and
below this the posterior or upper ends of the temporo-sphenoidal con-
volutions.
The occipital area (Fig. 10, 0) indicates the situation of the occipital
lobe, but is not coextensive with it, inasmuch as a portion extends
anteriorly beyond the lambdoidal suture into the postero-parietal area.
The squamoso-temporal area (Fig. 10, Sq) contains the greater por-
tion of tlie temporo-sphenoidal convolutions, but the superior temporo-
sjjhenoidal convolution ascends into the lower parietal areas.
The ali-sphenoidal area (Fig. 10, AS) contains the lower or anterior
extremity of the temporo-sphenoidal lobe.
The central lobe, or Island of Reil, does not come to the surface, but
lies deep in the fissure of Sylvius, and is concealed by the convolutions
which form the margin of that fissure anteriorly. It lies opposite the
ui)per part of the great wing of the sphenoid and its line of articulation
with the anterior inferior angle of the parietal and the squamous part
of the temporal.
The convolutions situated on the internal aspect of the hemisphere
are altogether out of relation to the surface of the skull.
The deep-seated position and direction of the hippocampal region are
superficially indicated by the convolutions of the temporo-sphenoidal
lobes, contained chiefly in the inferior postero-parietal, squamoso-tem-
poral, and ali-sphenoidal areas.
4. TopjOLirapliy of tlie Internal Parts of the Cerebrum.
The anatomy of the cerebrum is most conveniently studied by suc-
cessive horizontal and vertical sections.
Centrum Ovale.
A horizontal section made half an inch above the corpus callosum
displays the white matter of each hemisphere surrounded on all sides
E X C E P H A L O - S P I N O - X E Tj R A L S Y S T E :N F ,
37
by the giay matter of the convolutions. The white central mass in
each hemisphere was named by Vicq. d'Azyr the centrum ovale minus.
A section made at the level of the corpus callosum shows that the white
substance of that part is continuous with the central white substance of
Fig. 11.
Hdrizom AT, Section of the Brain of a Child nine months of aue, the right side being at a
SOMEWHAT lower LE\T:L THAN THE LEFT HALF. (After FLECHSIG.)
F,- Frontal, TS, Temporo-sphenoidal, and 0, Occipital lobes; Op, Operculum; In, Island of Kei! ; CU,
Clanstrum ; /", Third frontal convolution ; Th, Optic thalamus ; NC, Caudate nucleus ; iVC, Tall of cau-
date nucleus ; LN, Lenticular nucleus ; I, II, III, First, second, and third divisions of the lenticular
nucleus ; EK, External capsule ; IK, Posterior division, IE', Anterior division, and K, Knee of the inter-
nal capsule ; ah, ph. Anterior and posterior horns respectively of the lateral ventricles ; gcc, Knee of the
corpus callosum ; sp, Splenium ; mc, Middle commissure ; f. Fornix ; si, Septum lucidum ; a, Cornu
Animonis.
each hemisphere. The large, white medullary mass thus displayed is
named the centrum ovale majus. The corpus callosum connects the
convolutions of one cerebral hemisphere with corresponding points in
38 ANATOMICAL INTEODUCTION .
the convolutions of the other. It consists of bundles of nerve fibres,
almost the whole of which pass transversely between the two hemispheres,
although a few fibres run longitudinally on its surface, named the strice
longitudinales or nerves of Laneisi.
A horizontal section nearer to the base of the brain reveals the basal
ganglia and the internal capsule, as represented in Fig. 11.
A svstematic nomenclature of the various parts of the centrum ovale
has been devised by Pitres. His system consists in making vertical
sections of the brain at definite points, and naming the various parts of
the medullarv sidjstance exposed in each section. A vertical section of
the hemisphere at right angles to its longitudinal axis in the pra-frontal
region gives the prcefrontal sectmi(F\g. V2). The next section is made
Fig. 12.
Pe KFEONTAL SECTION. (After PiTRES.)
1, 2, 3, First, second, and third frontal convolutions. 4, Orbital convolutions. 5, «'onAi)Uitioii3 on the
internal aspect of the frontal lobe. 6, Prsefrontal fasciculi of the centrum ovale.
two centimetres in front of the fissure of Rolando and passes througli
the bases of the three frontal convolutions, and is named the pedunculo-
frontal section (Fig. 13). The medullarv substance in this section is
subdivided into a superior, middle, and an inferior pedunculofrontal
fasciculus, corresponding with the respective frontal convolutions.
The next section is made through the ascending frontal convolution,
parallel with the fissure of Rolando, and is named the frontal section.
It also passes through a small portion of the sphenoidal lobe. The
medullary substance of this section is also subdivided into sujjerior,
middle, and inferior frontal fasciculi (Fig. 14). The fourth section
is carried through the ascending parietal convolution, and is named the
parietal section. It is subdivided into superior, middle, and inferior
ENCEl'IIALO-SPINO-XEURAL SYSTEM. 39
parietal fasciculi (Fig. 15). The next is the j^cdunculo-panetal sec-
tion, made by dividing the hemisphere three centimetres behind the
Fig. 1?,.
lO
y
■""■'*
n
V
m
12
/3
ff-
-:■ ^W
9
\^
:^;^
■A 8
1^3
Peduncui-o-fuumai, Skction. (Aftei- Pitees.)
1, 2, 3, Fii-st, second, and third frontal convolutions. 4, Anterior extremity of the insular lobe. .5,
Posterior extremity of the orbital convolutions. 6, Superior pedunculo-frontal fasciculus. 7, Middle
pednnculo-frontal fasciculus. 8, Inferior pedunculo-frontal fasciculus. 9, Orbital fasciculus. 10, Corpus
callosum. 11, Caudate nucleus. 12, Internal capsule. 13, Lenticular nucleus.
Fig. 14.
Feontal Section (After Pitres.)
1, Ascending frontal convolution. 2, Insular lobule. 3, Sphenoidal lobe, i, 5, 6, Superior, middle,
and inferior frontal fasciculus. 7, Sphenoidal fasciculus. 8, Corpus callosum. 9, Caudate nucleus. 10,
Optic thalamus. 11, Internal capsule. 12, Lenticular nucleus. 13, External capsule. 14, Claustrum.
40 ANATOMICAL INTRODUCTION,
Fig. 15.
Tarietat, Section. (After Pitres.)
1. Ascending iiarietal convolution. 2, Insular lobe. 3, Sphenoidal lobe. 4, Superior parietal fas-
ciculus. 5, Middle parietal fasciculus. 0, Inferior parietal fasciculus. 7, Sphenoidiil fasciculus. >S, 9,
10, 11, 12, 13, 14, as in the preceding figure.
Fig. 10.
PEnUNCULO-PARIETAL SECTION. (After PlTRES.)
1, Superi( r parietal lobule. 2, Inferior parietal lobule. 3, Sphenoidal lobe. 4, Superior pedunculo-
parietal fasciculus. 5, Inferior pedunculo-parietal fasciculus 0, Sphenoidal fasciculus. 7, Coi pus cal-
losum. 8 and 10, Caudate nucleus, ii, Optic thalanui:^.
EXCEPH ALO - SPIXO - X K U R AL SYSTEM ,
41
fissure of Rolando, and cutting the superior and inferior parietal lobules.
It is subdivided into superior and inferior pedunculo-parietal and
sphenoidal fasciculi (Fig. 16).
The last is the occipital section (Fig. 17), in which no separate fas-
ciculi are distinguished.
Fig. 17.
l>(CIPirAI, Sfctiiin. { MtCI rilRES )
1, Occiiiital convolutions, i, Occipital fasciculi of the centrum ovale.
5. The Internal Structure of the Eneephalo-spino-neural System.
The internal structure of the encei)halo-spino-neural system must
now be briefly described, and for this purpose we shall divide the sys-
tem into (1) the spino-neural, and (2) the encephalo-spinal systems.
(1) The Spino-neur-vl System.
A spinal segment consists of a disk of nervous matter to each lateral
half of which a nerve is attached by an anterior and posterior root, the
The Anteriok Surface of the Spinal SEfiMENT, the Anterior Eoot of the Eight Side being
Divided. (After Allen Thomson, from Quain.)
1, The anterior median fissure ; 2, Posterior median fissure ; 3, Anterior lateral depression, over which
the anterior nerve roots are seen to spread ; 4, Posterior lateral groove into which the posterior roots are
seen to sink ; 5, Anterior roots passing the ganglion ; 5', The anterior root divided ; 6, The posterior
roots, the fibres of which pass into the ganglion, 6' ; 7, The united or compound nerve ; 7', The posterior
primary branch seems to be derived in part from the anterior and in part from the posterior root.
latter being furnished with a ganglion (Fig. 18). The gray substance
which represents the gangliated structure occupies the central parts of
4-2
ANATOMICAL INTllODUCTION
the cord in the well-known shape of the letter H. The median part of
the orav substance contains the central canal and the central gray
nucle'us of Kolliker, the anterior gray and white commissure lying in
Fig. ]0
Section from the Midpi.e of the Cervical Eni-aroemknt ..f the Sri>Ai. Cokd at the Third
Month of Embryonic Life.
C, Central canal. The other lettei-s indicate the same as tlie conespomling lettei-s in Fig 1.
Fig. 20
i, internal ;
ganglion cells
group.
Spinal Cord of a Five-months Human Embryo, from the Middle ok the Cervk.al
and Lumbar Enlargements Respectively. (YouNfi )
a, anterior ; a\ antero-lateral ; p/, postero-lateral, c, central, and m, median groups of
: 1, ganglion cell of the centre of the antero-lateral group; 2, ganglion cell of the median
E X C E P H A L O - S P I N O - X E U R A L S Y S T E :^r
Fig. •_'•_'. Fig. 23.
Sf.itioks of Spinal Curd of a Xine-moxths Human- Embryo, from tHf, Middle of the Lumbar
AND Ceevk'al Enlargements Respectively. (Young.)
A, anterior, and P, posterior horns. Tlie small letters indicate the same as in Figs. 20 and 21. The
normal size of the .•action from which the di-awing was made is shown above each figure.
Fig. 24.
Fig. 25.
Sections of the Adult Spinal Cord from the Middle of the Lumbar and Ckrvical Enlargements
Kespectively. (Young )
The letters indicate the same as those in Figs. 20 and 21.
u
ANATOMICAL INTRODUCTION.
front, and the posterior commissure behind it. The hiteral parts or
coluimis consist of an anterior, middle, and posterior part, the first of
them representing the anterior, and the Last the posterior gray horn,
and the middle chiefly the vesicular column of Clarke.
The anterior horns contain large ganglion cells, each of which is
furnished with numerous branched processes by means of which it
forms definite connections with other cells and fibres. One of these
processes is unbranched, and it becomes continuous with the axis-cylin-
der of an efierent fibre which passes out through the anterior root and
nerve to the periphery. The ganglion cells of the posterior horn are
much smaller and less branched than those of the anterior horns, and
this horn receives afferent fibres from the periphery of the body.
Fio. 20.
Fio. 2^
Sections of the Ahui.t Uimax Simnal Cord, from the Upper Cervicai, axd 1J"R.s.vi. Keoioxs
Respectively. (Young.)
A, anterior, and P, posterior liorns; aa, anterior roots; cc, central canal; ml, the meilio-lateral area.
The other letters indicate the same as the corresponding ones in Figs. 20 and 21 The size of the sections
from which the drawing was talcen is indicated above each. In Fig. 27, vc represent;* tlio vesicular
column of Clarice.
In the development of the gray matter of the cord, the groui)S of
ganglion cells appear first in the anterior and lateral margins of the
anterior horn (Fig. 19), where they form several distinct groups, which
are as far as possible removed from the central canal. The gray matter
surrounding the central canal represents the growing or embryonic por-
ENCEPIIAT.O-SPINO-NEUEAL SYSTEM. 45
tion of tlie gray luuttor, and every new ganglion cell which develops
becomes su])eradded at the margins of the first forward groups. The
groups of ganglion cells are i)retty constant for the same portions of the
c<»rd, but the arrangement varies considerably when sections at different
elevations are compared. These groups are represented in the annexed
diagrams (Figs. 20-27), and are named the |)Ostero-lateral {pt), the
antero-lateral {at), the anterior (a), the internal (/), and the central (c)
groups respectively. Another area — the median (m) — contains in tlie
adult human cord a considerable number of caudate cells of small size,
although they are not aggregated into a distinct group. The cells
of the median area, and of the margins of the groups, representing the
latest evolved structures, will be the counterpart of the latest evolved
functions. The last evolved purely spinal function (not taking into
account those regulated from the medulla oblongata) are the complicated
movements of the hand, and it may therefore be expected that the
median area and the marginal cells will be more fully developed in the
cervical enlargement than in any other part of the cord, in the adult
cord than in the embryo, and in the hunuin cord than in the cord of
animals. This expectation is fully borne out by these facts. A very
distinct grouj)ing of ganglionic cells lies in the posterior gray horn near
the posterior commissure, named the vesicular column of Clarke (Fig. 1,
ve). So far we have only spoken of one segment of tlie cord, but the
gray matter of the different segments has become integrated to such an
extent that it forms, not a series of ganglia like the sym])athetic sj^stem,
but a continuous tube. The central gray tube opens at the calamus
sci'iptorius into the fourth ventricle, while higher up it is represented
by the aqueduct of Sylvius, and then opens into the third ventricle.
In the medulla the groups of ganglion cells ha\'e undergone an exten-
sive rearrangement. The main grouj) of the anterior horns is repre-
sented by the nuclei of origin of the hyi»oglossal nerve (Fig. 2, ^', a,
ah pi), but a portion of the antero-lateral and ])ostero-lateral groups
have become detached from the rest of their groups, and are aggregated
in the formatio reticularis in two tolerably distinct groups, the anterior
and posterior nuclei of the lateral column of the medulla (Fig. 2,
ale, pic). The median area and the nuirginal cells are represented by
a much larger ao-o-regation of cells than anything to be found in the cord,
and constitute groups which may be named the internal accessory
(Fig. 2, if) and the external accessory nuclei (Fig. 1, ef) of the facial
nerve. These groups of cells are probably the structural counterparts
of mimetic facial and articulatory movements.
The vesicular column of Clarke is only represented in the dorsal
region of the spinal cord. It contains bipolar ganglion cells, and cells
46
ANATOMICAL INTRODUCTION.
of similar character are to be found in the nuclei of the vagus (Fig.
2, nv) and glosso-pliaryngeal nerves, and it is therefore probable that
the nuclei of these nerves are, to some extent at least, the representa-
tives of the vesicular column of Clarke in the medulla.
Fig. 28.
Section of the Meduli,.\ Obuin(:.\ta on a levkl with the supbrfici.\t. orkmn of the Acoustic Nerve.
(Modified from Flechsig.)
E vm, Boot uf the acoustic nerve.
VIII, Posterior median acoustic nucleus
Tin", Posterior lateral acoustic nucleus.
H, Nucleus of the hypoglossal nerve.
ip, Internal division of the inferior peduncle of the cerebellum.
ep, External division of the inferior peduncle of the cerebellum.
frs, Forniatio reticularis.
a, Arciform iibres.
The posterior gray horn is represented in the medulla by the sub-
stantia gelatinosa (Fig. 2, sg). In addition to the sensory nuclei of
common sensation represented by the substantia gelatinosa, the medulla
oblongata contains special sensory nuclei. It is probable that part of
ENGEPHALO-SriNO- NEURAL SYSTEM.
47
the nuclei of the gh)8so-i)haryiige!il nerve, and probably also of the fifth
nerve, reiiresent the special nerves of taste; four nuclei, namely, the
posterior median (Fig. 28, Viii), the posterior lateral the anterior median,
and the anterior lateral acoustic nuclei, represent the auditory nerve;
Avhile the corpora quadrigemina and the internal geniculate body repre-
sent the nuclei of origin of the optic nerve. The spinal ganglia, situ-
ated in the })Osterior roots of each pair of nerves, belong to the spinal
system. The casserian ganglion is the representative of these ganglia
in the cranial end of the spinal system. The middle sensory nucleus of
the trigeminus is also in structure very similar to the ganglia of the
posterior roots, and it also is probably the homologue of the spinal
ganglia. The external geniculate hody likewise contains cells which are
very like those of the ganglia of the posterior roots, and it must possibly
be regarded as a ganglion for the optic nerve homologous with the
spinal ganglia.
«/*
Transversje Section of the Cervical Part or the Spinal Cord of a Human Embryo of six weeks.
(From KoLLiKER.)
c, Central cuiial ; e, e', Its eiiithelial lining ; g, Gray substance ; ar, Anterior roots ; pr, Posterior roots ;
a, Anterior root-zones ; p, Posterior root-zones.
The white substance of a sjiinal segment is divided anatomically by
the anterior and posterior median fissure, and the nerve roots into an
anterior, lateral, and posterior column for each lateral half. A small
portion only of this white substance really belongs to the spinal system,
the remainder representing conducting paths between the portions of
the cord below, or posterior to the segment examined, and the encephalic
ganglia. This purely spinal portion of the white substance consists of
the portions named the anterior and jyosterior root-zones. As might
be expected, these areas are the first portions of the white substance to
48 ANATOMICAL INTRODUCTION. |
appear in the development of the cord, an<l they are consequently least
distinguislied at an early period of embryonic life. During the first
Aveeks'^of embryonic life the cord consists entirely of gray matter in
the form of a tube, Avhich, by the appearance of lateral slits, is imper-
fectly divided into anterior and posterior portions. Toward the end of
the first month a zone of white substance appears on the surface of the
anterior and posterior portions of the gray tube, and there constitute
respectively the anterior and posterior root-zones (Fig. 29, a,p). Tliese
zones are supposed to consist of short looped fibres, the posterior one
coordinating the functions of the gray substance on the sensory or
ino-oing side, and the anterior on the motor or outgoing side.
The most important fact with regard to the distribution of these
zones is that, at any level of the cord, they correspond in size to that
of the gray substance, these zones being, like the gray substance, of
comparatively large size in the lumbar and cervical enlargements.
The jjosterior root-zone (Fig. 2, pr), on being followed upwards
into the medulla oblongata, will be found to terminate in the gray
nucleus of the cuneate fasciculus, the triangular nucleus ; but the tracts
of Avhite substance known as the ascending root of the fifth nerve (Fig.
2, at), the fasciculus rotundus (Fig. 2, /), and the descending root
of the fifth nerve are the homologues, in the cranial portion of the
spinal system, of the posterior root-zones of the cord. i
The anterior root-zone, on being followed upwards into the medulhi
oblongata, is seen to be separated up into bundles by the arcuate fibres
of the medulla, and the interlacement of the two systems of fibres
forms what is knoAvn as the formatio reticularis (Fig. 28, frs). The
anterior root-zone consists of two portions : an internal (Fig. 37, ar),
which lies to the inner, and an external (Fig. 37, ar'j, which lies to
the outer side of the anterior roots.
The internal portion of the anterior root-zone is puslied aside in the
lower part of the medulla by the decussating fibres of the pyramidal
tracts ; but above the level of the decussation it is thrust backwards
behind the anterior pyramid of the medulla, and is situated between
the median raphe and the fibres of the hypoglossal nerve (Fig. 2, ar)
In the spinal cord the internal portion of the anterior root-zone main-
tains a close relationship with the internal group of ganglion cells, and
this portion of the root-zone is most probably represented in the
medulla oblongata, pons, and crura cerebri by the bundle of fibres
named the posterior longitudinal fasciculus (Fig. 2, ar). This fas-
ciculus is said by Wernicke to be connected with the first division of
the lenticular nucleus by the fibres which form the anterior portion of
the collar of the crus cerebri.
EXCEPIIALO-SPIXO-XEURAL SYSTEM. 49
The external jjortion of the anterior root-zone of the spinal cord is
continued upwards into the formatio reticularis of tlie medulla oblon-
gata (Fig. 28, ar'). This portion lies behind the olivary body, and
comes to the surface of the medulla in its lateral column ; while it is
bounded internally by the root-fibres of the anterior motor nerves, ex-
ternally by the root-fibres of the nerves of the lateral mixed svstem,
and posteriorly by gray matter. The interlacing fibres of the pons
(Fig. 47, Tr) pass in front of this portion {ar'), and in the crus it
comes again further forwards, so that it is only separated from the crusta
by the locus niger (Fig. 40, ar').
The Fillet. — The portion of the anterior root-zone which lies next
to the inner and posterior surfaces of the olivary body in the medulla,
an<l to the interlacing fibres of the pons, is named the fillet. It is
divided into an internal and an external portion corresponding to the
internal and external divisions of the anterior root-zone. The internal
portion lies to the inner side of the olivary body, a part of it even
coming in front of that body, and between it and the anterior pyramid
(Fig. 28, ar). Above the line of the olivary body this last portion is
pushed backwards so as to join the external portion, and both divisions
now lie behind the transverse fibres of the pons. The fibres of the
internal division of the fillet seem to pass upwards to become connected
with the optic thalamus, while those of the external division (Fig. 36,
x' and x) subdivide into an outer and inner bundle, the former of Avhich
terminates in the posterior, and the latter in the anterior tubercle of
the corpora quadrigemina.
(2) The Encephalo-spinal System.
The encephalo-spinal system consists of a, the gray substance of the
cerebellum ; 6, the gray substance of the cerebrum ; and c, the con-
ducting paths which connect these gray masses with one another and
with the central gray tube.
a. THE GRAY SUBSTANCE OF THE CEFvEBRUM.
(1) The Cortex Cerebri. — By far the greater portion of the gray
substance of the cerebrum is disposed up the surface of the cerebral
hemispheres. The cortical substance consists of cells and fibres em-
bedded in a matrix similar to the neuroglia of the spinal cord.
The cells are of various forms, the most usual forms being spherical,
stellate, pyramidal, and fusiform. The fibres radiate into the gray
4
50
ANATOMICAL INTRODUCTION,
Fig. 30
Transparent Sfxtion of a Furrow of
THE Third Cerebral Convolution of
Man. Magnified 100 decimetres. (After
Meynert.)
1, Layer of the scattered small cortical
corpuscles ; 2, Layer of close-set, small
pyramidal corpuscles ; 3, Layer of large
pyramidal cortical corpuscles i formation
of the coruu Ammonis) ; 4, Layer of small,
close-set, irregular-shaped cortical corpus-
cles fgranule-like formation) ; 5, Layer of
fusiform cortical corpuscles (claustral
formation) ; m, the medullary lamina.
cortex from tlie wliite centre of each con-
volution, their course being vertical to
the free surfoce of the convolution. They
are arranged in bundles as they pass
through the gray substance, and this
o:ives to the nerve-cells a columnar ar-
rano-ement. The radiating fibres are
wanting in the sulci between the convo-
lutions, but the internal layer of the
gray substance of the cortex generally
contains fibres which ])ursue an arciform
course and connect adjacent convolutions.
Fibres pass in all directions through the
gray substance connecting its several
layers, and forming a dense network,
like that described by Gerlach in the
spinal cord.
Layers of the Cortex. — The cortex of
the cerebrum is divided into several
layers, each of which possesses a definite
histoloo-ical character. The most com-
monly distributed form of structure is
what Meynert has called the "five
laminated type." The external layer con-
sists of neuroglia and a layer of delicate
nerve-tubes,- along with a few scattered
small nerve-cells which are destitute of
processes. The next layer is composed
of small angular or pyramidal nerve-cells
with branching processes. The third
layer contains large and small pyramidal
cells Avith branching processes, arranged
with their pointed extremities towards
the surface of the convolutions, and
separated into groups by bundles of the
radiating fibres. In the innermost por-
tion of this layer the pyramidal cells are
larger than in the remaining portions,
and it has therefore been described as a
separate layer by Dr. Lockhart Clarke.
In the cortex of the occipital lobe the
encephalo-spino-np:ural system. 51
deeper cells of the third layer are pyramidal in form, with their bases
turned inwards towards the medullary substance, but their basal pro-
cesses are directed laterally so as to connect adjacent cells, and none
of them appear to be directed inwards to connect the cells with the
fibres of the medullary substance. In the anterior portion of the
frontal convolutions the disposition of these cells is somewhat similar,
but a distinct basal process has occasionally been observed, which is
directed towards the medullary substance of the convolution, and which
afterwards becomes continuous with one of the fibres of the centrum
ovale.
In the central convolutions of the brain, Betz and Mierzejewski
have discovered cells which are tAvo or three times the size of the pvra-
FiG. 31.
Pyramidal Giant-cell.
», Nucleus ; «, «, «, Branched processes ; c, UnbraDched basal process.
midal cells of the other regions of the cortex, and they have conse-
quently named them giant cells. In addition to the branched proto-
plasmic processes (Fig. 31, a, a) which connect neighboring cells with
one another, these cells possess a distinct axis-cylinder process (Fig. 31, c).
The latter is always unbranched, and after becoming surrounded by a
medullary sheath it forms the axis-cylinder of a nerve-fibre of the
52
ANATOMICAL INTRODUCTION,
centrum ovale. Giant cells have been observed in the paracentral
lobule and in a portion of the postero-parietal, as well as in the ascend-
ScHEiviA (IF THE CEREDRo-sriNAL SYSTEM. (From Landols's Phijuiologie.)
C, C, Cortex of the Brain ; s, Corpus Striatum ; X I, Lenticular Nucleus ; T o, Optic Tlialanms ;
V, Corpora Quadrigemina ; P, Crura Cerebri; H, Tegmentum; j), Crusta; 1 1, Eadiate Filires of the
Corpus Striatum ; 2 2, those of the Lenticular Nucleus ; 3 3, those of the Optic Tlialamus ; 4 4, those of the
Corpora Quadrigemina and Tegmentum; 5 5, the Pyramidal Tract; fi G, Fibres connecting the Corpora
Quadrigemina and Tegmentum ; m, their further co\irse ; 8 8, Fibres connecting the C'orpus Striatum and
Lenticular Nucleus with the Crusta; M, their further course ; S S, course of the Sensory Fibres, 11, Trans-
verse Section of the Spinal Cord ; v W, Anterior, and h W, Posterior Hoots of the Nerves, a a, associat-
ing Fibres ; c c, Commissural Fibres. II, Transverse Section through the Crura Cerebri of Man on a
level with the posterior pair of the Corpora Quadrigemina (after Meynert) ; p, Crusta ; S, Locus Niger;
V, the posterior pair of the Corpora Quadrigemina with the A(iueduct of Sylvius. Similar sections from
the Crura of — III, Dog ; IV, Monkey ; V, Guinea-pig.
ENCEPHALO-SriXO-NEURAL SYSTEM. 53
ing frontal and parietal convolutions, and posterior extremities of the
three frontal gyri. These cells are disposed in groups, and correspond
in position to the motor centres of physiologists. The giant cells vary
greatly in size, the largest being found, as we have already seen, in
the paracentral lobule, Avhich may be regarded as the upper extremity
of the ascending frontal and parietal convolutions. Large pyramidal
cells are also met with in the upper part of the ascending frontal con-
volutions, and Dr. Bevan Lewis has found that they diminish in size
from the upper extremity until at the lower extremity they are but half
the size. The pyramidal cells of the posterior extremities of the frontal
convolutions are on the whole smaller than those of the ascendino-
frontal, and the cells also diminish from above downwards, those in
Brocas convolution being the smallest.
The fourth layer consists of closely set angular corpuscles with fine
processes, placed irregularly and not distinctly separated into groups.
The fifth layer consists of medium sized, fusiform, and bipolar cells.
The long diameters of these cells run parallel to the layers of the
cortex, and are associated with the system of fibres which connects dif-
ferent convolutions of the same hemisphere with one another.
(2) The Basal 'or the Intermediate Cerebral Cranglia. — Several
masses of gray matter are situated at the base of the cerebral hemi-
spheres, there occupying an intermediate position between the cortex
cerebri and the central gray tube. These ganglia are the caudate
nucleus (Fig. 32, C s), the lenticular nucleus (Fig. 32, N T), the optic
thalamus (Fig. 32, T o), the locus niger, the corpora quadrigemina
(Fig. 32, V), and the internal geniculate body. The corpus striatum
is sometimes used to designate the caudate nucleus alone, wdiile at other
times it is used as a generic term for both the caudate and lenticular
nuclei. Although we have included the corpora quadrigemina amongst
the intermediate cerebral ganglia, we have already seen some reason to
regard them as being the homologues of the posterior gray horns of the
spinal cord.
b. THE GRAY SUBSTANCE OF THE CEREBELLUM.
(1) The Cortex CerehellL — The greater portion of the gray sub-
stance of the cerebellum is also disposed on the surface, Avhere it forms
numerous lartiince or folia, which are separated by fissures or sulci of
different depths.
(2) The Intermediate Cerebellar G-anglia. — Occupying the central
part of the lateral lobe of the cerebellum is a folded mass of gray
matter named the corpus dentatum ; and Stilling has described two
small masses of gray matter which are situated in the anterior end of
the inferior vermiform process, and which he named roof nuclei.
54 ANATOMICAL INTRODUCTION.
These, then, are the only masses of gray matter which are to be found
in the' cerebellum itself; but the inferior, middle, and superior pedun-
cles are connected with other aggregations of gray substance in the
medulla oblongata, pons, and crura cerebri, and these must also be
regarded as belonging most probably to the cerebellar system. The
chief of these masses of gray matter are the olivary bodies, which are
connected with the inferior peduncle of the cerebellum of the opposite
side (the late researches of Flechsig appear to cast some doubt upon
this statement) ; the red nucleus of the tegmentum, which is connected
with the superior peduncle of the cerebellum of the opposite side ; and
the <n-ay matter interposed between the transverse fibres of the pons,
and which is connected with the middle peduncle of the cerebellum also
of the opposite side. The parolivary body, the superior olivary body,
and the nucleus of tie pyramid are other small aggregations of gray
matter having a structure somewhat similar to that of the corpus den-
tatum of the cerebellum, the olivary body, and the red nucleus of the
tegmentum, but their connections are not yet made out. In addition
to these are, in the lateral and posterior part of the medulla oblongata,
the triangular nucleus, in which the posterior root-zones, and the
clavate nucleus, in which the column of Goll, to be immediately de-
scribed, terminate.
C. THE ENCEPHALO-SPINAL CONDUCTING PATHS.
The purely spinal portion of the spinal cord consists, as we have
seen, of the central gray tube, with its commissures and attached
nerves, and the anterior and posterior root-zones. Now these portions
of the cord form more or less direct connections with the encephalic
ganglia. The central gray tube is directly connected with the optic
thalamus by means of the gray matter which lines the third ventricle.
The anterior root-zone is connected with the lenticular nucleus by
means of the posterior longitudinal fasciculus, with the optic thalamus
by means of the internal portion of the fillet, and with the corpora
quadrigemina through the external portion of the fillet. The greater
portion of the posterior root-zone terminates in the triangular nucleus
(Fig. 33, tn) of the medulla oblongata, and this nucleus is connected
by means of arcuate fibres (Fig. 33, 11) with the olivary body (Fig.
33, 0) of the same side, which in its turn is connected with the inferior
peduncle of the cerebellum of the opposite side.
We must now pass on to describe the special conducting paths which
connect the central gray tube with the higher ganglia, and a knowledge
of these is best obtained by a study of the development of the cord.
At the end of the first month of embryonic life the spinal cord con-
E X C E 1' H A T, O - S 1' I X u - X E L' R A T, SYS T E M
Fkj. 33.
55
Schema of the Cekebellospinal System.
C, (', Cortex of the Cerebellum. D, D, Corpora Deutata. 0, 0, Olivary Bodies. E, Ked Xucleus of
Tegmentum P, Gray matter interposed between transverse Fihi-es of the Pons. CR, Crura Cerebri. C,
Ci-usta. .S, Substantia Nigra. T, Tegmentum. A, A(iucduct of Sylvius. 1, Fibres which connect the
cortex of the Cerebrum and that of the Cerebellum on the opposite side. 2, 2, Fibres connecting the
Cortex of Cerebellum and Red Xucleus of the opposite side. 3, 3, Fibres connecting the Corpus Dentatum
of the Cerebellum with the Red Xucleus of the opposite side. 4, 4, Fibres connecting the Cortex of the
Cerebellum with the Corpus Dentatum 5, Fibres connecting the Cortex of the Cerebellum with Gray
substance interposed between the transverse Fibres of the Pons on the opposite side. G, Fibres connect-
ing the .Corpus Dentatum with the Olivary body of the opposite side. 7, Fibres connecting the Cortex of
the Cerebellum with the Olivary body of the opposite side. 8, 8, Fibres connecting the Red Xucleus.
9, !l, those connecting the interposed Gray substance of the Pons, and 9", those connecting the Olivarj'
l(ody respectively with the anterior Gray Horn of the Spinal Cord. M, The Anterior Column of the cord
through which the fibres piiss. g, Column of GoU terminating in en the Clavate Xucleus 10, Arcuate
Fil)res connecting the Clavate Xucleus with the Olivary body of the same side, p r, The Posterior Root-
zone terminating in tu, the Triangular Xucleus 11, Arcuate Fibres connecting Triangular Xucleus and
Olivary body of same side, dc, dc, Direct Cerebellar Fibres ascending in the lateral column of the cord
and connecting the vesicular column of Clarke with the Cortex of the Cerebellum.
5(3 ANATOMICAL IXTRODUCTION .
sists of a tube of gray matter with a layer of white substance on its
anterior and posterior aspects, a portion of the lateral surface of the
tube being uncovered. At the end of the sixth week a thm layer of
white substance appears on each lateral surface, and, as the fibres of
this layer are found to pass to the cerebellum, they have been named
the direct cerebellar fibres of the lateral column. At the end of the
eidith week of embryonic life still further changes are observed to
ocair in the cord. Two bundles of longitudinal fibres, one for each
side, are intercalated between the direct cerebellar fibres and the pos-
terior gray horns. These bundles, on being traced upwards, are found
to pass forwards at the lower end of the medulla, and after decussating
with one another, they push aside the anterior columns and form the
inner and larger portion of the anterior pyramids of the medulla, and
consequently these fibres are called the lateral pyramidal tracts (Fig.
34^ P^ P'y Contemporaneously with the formation of the lateral pyra-
FiG. 34.
Cord op Human Emukyo at Fivi; Months.
'tjTi
ah, ah', Anterior Horns of gray substance ; j)/i, j)7(', Posterior Horns of gray substance; ar, ar', .\n-
terior Root-zones; pr, pr', Posterior Koot-zones ; P, P, Pyramidal Fibres of lateral columns; T, t'ol-
umns of Tiirck ; G, Columns of Goll ; dc, dc', Direct cerebellar fibres ; c. Anterior Commissure.
niidal tracts an analogous formation appears in the anterior columns,
one of these being formed on each side of the anterior median fissure.
These tracts have been called the columns of Tiirck, or of Lockhart
Clarke, or the anterior pyramidal tracts (Fig. 34, T). At the same
time that these changes are occurring in the lateral and anterior col-
umns, two bundles of longitudinal fibres make their appearance in the
posterior columns, one being situated on eacli side of the posterior
EXCEPHALO-SPIXO- NEURAL SYSTEM.
57
ft P
en G
f M vm ^P
T ar
Fig. 35.
(After FLECiisin )
G, The column of Goll.
J))-, the posterior root-zone.
J), the posterior root.
r, the posterior gray horn.
A, the anterior gray horn.
dc, the direct cerebellar tract.
j)t, the lateral pyramidal tract
T, the anterior pyramidal tract
fr, the formatio reticxilaris.
or', the external portion of the
anterior root-zone.
ar, the internal portion of the an-
terior root-zone.
(it, the ascending root of the fifth
nerve.
Sg, the substantia gelatinosa.
tn, the triangular nucleus
en, the clavate nucleus.
P and P', the anterior pyramids of
the medulla oblongata.
//, the jillet.
po, the parolivary body,
o, the olivary body,
e/i, the external division of the
inferior peduncle of the
cerebellum.
ip, the internal division ot the in-
ferior peduncle of the cere-
bellum.
ale and j.)?c, anterior and pot^terior
nuclei of the lateral column.
/". fasciculus rotundus.
VIII, posterior median nucleus of
the auditory nerve
XII, the micleus of the hypoglos-
sal nerve.
G P^
58 ANATOMICAL INTKODUCTION .
median fissure. These fibres are called the coluiims of Goll, or tlie
postero-medimi columns (Fig. 34, Gf). The anterior white commis-
sure also appears about the eighth week. A most important fact to
notice in connection with the development of the white substance is
that the fibres when first developed are destitute of a medullary sheath,
and only become mcdullated at a late period of development. When
the cord of a human embryo is examined at the end of the fifth month,
it will be found that the pyramidal fibres of the lateral columns, the
fibi-es of the columns of Tiirck, and the columns of Goll are non-medul-
lated, while the fibres of the anterior and posterior root-zones, and
those of the direct cerebellar tracts are medullated. When a transverse
secti(m of the cord is examined in glycerin after hardening in chromic
acid, the bundles composed of the non-medullated fibres Avill be found
to transmit the light more readily than those composed of the medul-
lated fibres, and consequently a section of the cord of a hunuin embryo
at the fifth month presents in the cervical region the appearances repre-
sented in Fig. 34. The embryological tracts are represented diagram-
raatically in Fig. 35. The portion of the lateral column which adjoins
the gray matter is named, from its i-eticulated appearance, the formatio
reticularis (Fig. 35, fr). This part of the cord is composed chiefly of
longitudinal fibres of small diametei', and the reticulated appearance is
given to it partly by the passage through it of a considerable number
of horizontal fibres from the vesicular column of Clarke to reach the
direct cerebellar tract, and from the ganglion cells of the anterior gray
horns to reach the lateral ])yramidal tract, and ])artly by the hmgitudi-
iial fibres being separated by comparati\ely wide septa of neuroglia.
The formatio reticularis appears indeed oidy to be a better developed
part of the anterior root-zone, and it is not known to perform any
special functions. The spinal part of the encephalo-spinal conduct-
ing paths then consists of the columns of dioll, tlie direct cerebellar
tracts, and the pyramidal tracts, and Ave must now attend to their
longitudinal distribution. The most noticeable feature with regard
to the longitudinal distribution of these tracts is that all of them
increase steadily in size from below upwards, thus showing that
they must be regarded as conducting paths between the central gray
tube and the higher ganglia. It is impossible, within the limits
of this work, to describe in detail the encephalo-spinal conducting
paths, but a general view of their course and connections may be
obtained from the annexed diagrams. These paths may be divided
into (1) the cerebro-spinal and (2) cerebello-spinal conducting paths.
E N C E P H A L - S P I N O - N E U R A r . SYSTEM
59
Diagram of the Gray ^Masses of the Simnal Cord and Brain, showinc the course of Tiir.
Conducting Paths (After Flechsig.)
i?, Fissure of Eolaiulo
P" P, Tand Pt, Course of the fibres of the pyraiiiiilal tract from their origin in the central convolutions
to their termination in the anterior gray liorns (a, a').
I, IT, III, First, second, and third portions of the lenticular nucleus (NL). NC, Caudate nucleus.
Th, Optic thalamus.
D, O, B, A, Points from which fibres issue connecting the cortex of the brain and basal ganglion, and
also the gray substance of the pons {PO} Bd, Fibres connecting the cerebellum and optic thalamus ;
and Ottji, those connecting the cerebellum and the gray substance of tlie pons.
aq, and pq, Anterior and posterior pair of corpora (juadrigemina respectively.
X, Upper, and x', lower fibres connecting the olivary body and the corpora quadrigemina.
FR, Formatio reticularis of the medulla oblongata, formed by fibres from the optic thalamus (Th), the
internal division of the inferior peduncle of the cerebellum Hep), from the spinal cord (/r, ar, and ar'),
and probably also from the clavate nucleus (Nc).
0, Olivary body ; ecp, fibres of the restiforni bodies connecting the olivary bodies and cirebcUum ;
other fibres connect it with the triangular (Npr) and clavate (Nc) nuclei.
dp, Decussation of the pyramids.
pr', Fibres of the posterior roots whicli pass upwards and downwards into the gray substance, and pursue
only a short course.
a, a', a", a'", anterior roots.
p, pr, pr", O, Fibres of the posterior roots
60
ANATOMICAL IXTRODUCTION
(1) The Cerebrospinal Conducting Paths.
The cereljro-spinal contlucting paths are represented in Figs. 32
and 36.
{a) The Pyramidal Tract (Fig. 32, 5, 5, m).— The fibres of this tract
issue from the gray matter of the central convolutions of the brain,
DiAGUAM OF Transverse Section of the Spinal Cord in cppek iiai.k of the Dorsai, Re(;ion.
(After Flechsii;.)
C, Anterior commissure.
dc'. Fibres which pass from the vesiculur column of Clarke (cc) to the flirect cerebellar tract.
P, Posterior horn .
Figs. Si; ami 37. — Letters cuminon to both.
I't, Pyramidal tract of the lateral column.
T, Columns of Tiirck.
dc, Direct cerebellar tract.
«r, Internal portion of the anterior root-zone.
ar', External portion of the anterior root-zone.
pr. Posterior root-zone.
fi, CJoir.s columns.
/)•, Reticular formation of the spinal cord.
(I, Anterior gray horns of the spinal cord.
the axis-cylinder processes of the giant cells already described being
continuous with the axis-cylinder of the fibres of this tract. These
fibres form at first more or less separate bundles, which descend in the
centrum semiovale of the hemisphere, and come together on reaching
EXCEPHALO-SPIXO-XEURAL SYSTEM.
(U
the basal ganglia to form a bundle, ^vhich occupies the anterior t^vo-
thirds of the posterior segment of the internal capsule. The fibres lie
Fig. 38.
DiAljRAM OF^THE SPIXAL SEGMENT AS A CeNTKE AM) COXDVCTIXG MedUM (After BrAMWELL )
B, right, and B', left liemispheres of the brain ; M 0, lower end of the medulla oblongata ; 1, the
niotor tract from the right hemisphere ; it divides at M 0, and the larger portion crosses over to the oppo-
site side and passing down the lateral column it supplies the muscles M and M' on the left side of the
body. The supply to HI is given off at 1'. The smaller portion passes down the anterior column of
the same side, and supplies the muscles m and m' on the right side of the body ; 2, the motor tract on
the left side of the body ; the larger portion crosses over to the opposite side and supplies the mus-
cles yi- and 313 on the right side of the body, wliile the lesser portion i>asses down the same side and
supplies the muscles m^ and m^ on the left side of the body S, S', sensory areas on the left side of the
body ; 3', 3, the main sensory tract from the left side of body ; it passes up on the opposite side (right) of
the cord in the postero-external column, and proceeds to the right hemisphere of the biain ; S-, S^, sensoi'y
areas of the right side of the body ; •!', 4, the main sensory tract from the right side of the body, proceed-
ing up the left side of the cord to the left hemisphere of tlie brain The arrow;^ indicate the direction of
the conductiim.
between the caudate nucleus and optic thalamus on the inner, and the
lenticular nucleus on the outer side, but without forming any connec-
62 ANATOMICAL INTRODUCTION.
tions with these ganglia, and pass still as one bundle through the
middle third of the crusta of the crus cerebri. On reaching the pons
the fibres become separated into several bundles by the transverse fibres
of the middle peduncle of the cerebellum, but on reaching the medulla
oblono-ata they come together again and form the anterior pyramid of
the medulla, and it is from this circumstance that they are named the
pyramidal tracts. At the lower end of the medulla by far the largest
portion of the anterior pyramid crosses over to the lateral column of
the opposite side after decussating with the corresponding fibres of
the anterior pyramid. A few of the fibres which lie on the external
aspect of the anterior pyramid pass onwards in the anterior column of
the spinal cord without crossing, and these form the columns of Tiirck.
(b) The Sensory Conducting Paths. — The fibres of the posterior nerve-
root diverge like a fan immediately on entering the spinal cord (Fig.
37, pr', pr"), and most if not all of them cross over to the opposite
side (Fig. 38, S S'^), and then ascend to reach the cerebral cortex
chiefly of the occipital and temporo-sphenoidal lobes. The course of
these fibres is not well ascertained at all the intermediate points.
It is probable that in the spinal cord some of these fibres ascend in
the posterior gray horn, and others in the postero-external column.
Some anatomists believe that a portion of the sensory conducting path
ascends in the cord on the same side as the root from which it is
derived, and that a supplementary decussation of sensory fibres takes
place in the medulla oblongata (Fig. 32, S). It is, however, very
doubtful whether such a supplementary decussation exists, and patho-
logical observations would at least seem to indicate that the sensory
conducting paths belonging to the opposite side of the body pass
through the restiform body of the medulla oblongata. These fibres
pass upwards in posterior and external bundles of the longitudinal
fibres of the pons and come together to form one bundle in the ex-
ternal third of the crusta (Fig. 32, ps). The fibres ascend as one
bundle on the posterior third of the posterior segment of the internal
capsule, and at this point they are joined by fibres which ascend from
the optic tracts through the geniculate bodies and anterior tubercle of
the corpora of the quadrigemina around the optic radiations of Gratiolet,
and also by fibres from the olfactory tracts of the opposite side, which
reach them most probably through the anterior commissure of the third
ventricle and the optic thalamus. The sensory fibres of the internal
capsule now radiate backwards, outwards, and upwards to reach the
cortex of the occipital and temporo-sphenoidal lobes, and to a less
extent <lhat of the parietal lobe.
The connections of the intermediate ganglia with the central gray
ENCEPIIALO-SPINO-NEURAL SYSTEM. C,;;
tube have already l)een described, and tliest- are also connected with
the cortex cerebri by fibres whicli ascend in the corona radiata.
(2) The CerebeAlo-spinal Conducting Paths.
(a) The Direct Cerehellar Tracts. — The fibres of this tract appear
to take their origin from the ganglion cells of the vesicular column of
Clarke (Fig. -^7, dr), and then to pass out^vards to reach the surface
of the lateral column. The tract makes its first appearance in the
upper lumbar or lower dorsal region, and it gradually increases in size
from below upwards, by the addition of new fibres. It lies on the
surface of the cord to the outer side of the lateral pyramidal tract, and
on reaching the medidla oblongata it occupies the surface of the resti-
form body (Fig. 35, dc\ and finally the fibres pass through the in-
ferior })eduncle to reach the cortex of the cerebellum (Fig. 38, dc).
{b) The Columns of GoU. — The columns of Goll begin as an insig-
nificant bundle of fibres in the lumbar region of the cord, and gradually
increase in size from below upwards (Fig, 35, G). The inferior origin
of the fibres is not well ascertained, but it is probable that they are
directly derived from the jjosterior roots. On reaching the medulla
the fibres terminate in the cells of the clavate nucleus (Fig. 33, en).
This nucleus is connected l)y arcuate fibres (Fig. 33, 10) with the olivary
body of the same side, Avhich in its turn is connected, by means of the
inferior peduncle of the cerebellum, with the cortex of the cerebellum
(Fig. 33, 7) and with the corpus dentatum (Fig. 33, 6) of the opposite
side. The interiHediate (janglia of the cerebeUo-spinal system are con-
nected with one another and with the cortex of the cerebellum in vari-
ous Avays. The transverse fibres of the middle peduncle of the cere-
bellum (Fig. 33, 5) connect the cortex and the interposed gray matter of
the pons of the opposite side (Fig. 33, P). The superior peduncle
contains fibres which connect the cortex (Fig. 33, 2) and the corpus
dentatum (Fig. 33, 3) with the red nucleus (Fig. 33, R) of the opposite
side, and fibres (Fig. 33, 1) which pass near the red nucleus and through
the optic thalamus to connect the cortex of the cerebellum with the
cortex of the opposite hemisphere of the brain.
The connections of the cerebellar system with the anterior gray
horns or the motor part of the spinal cord, are not well ascertained,
but as the upward continuation of the anterior root-zone of the spinal
cord almost surrounds the olivary body and the red nucleus, and passes
near to the interposed gray matter of the pons, it is not improbable that
connections may be formed between them. These supposed connec-
tions are represented in Fig. 33 by the lines 8, 8 ; 9, 9, and 9''.
CHAPTER II.
PHYSIOLOGICAL INTRODUCTION.
The law of evolution is, as the student has already learned, as
applicable to the function as to the structure of the nervous S3^stem.
It is, indeed, manifest that there must be a determinate relation between
these two factors in development. The most general expression of
this relationship is that unlike functions entail unlike structures ; and,
inversely, that unlike parts assume activities of unlike kinds. The
whole of scientific pathology may be said to rest upon this law, for we
assume that deranged nervous functions are caused by disorders, either
molar or molecular, of nervous structures ; and, inversely, that injured
or diseased nervous structures are, or were, accompanied by correspond-
ino- disorders of nervous functions. In tracing the development of the
structure of the nervous system, therefore, it was found impossible to
avoid continual reference to its functions, and now in briefly discussing
the functions of the system constant reference Avill have to be made to
its structure.
The nervous system is, as we have seen, composed of cells and fibres.
The cells are originators of motion, and, to some small extent, con-
ductors also, while the fibres are conductors, and only in a very small
degree originators of motion. But the unit of composition of a ner-
vous system, which has assumed even a minor degree of complication,
is a cell with a nerve fibre connecting it Avith a muscular fibre or work
organ, or a cell with one fibre connecting it with the periphery of
the body and another with a muscular fibre or work organ. In the
first arrangement the cell gives out energy or discharges at periodi-
cal intervals, and the liberated energy being conducted by the effer-
ent fibres to the work organ, gives rise to rliythmical contractions
of the muscular fibre. This constitutes automatic action. In the
second arrangement an impression made on the surface of the body
sets up a disturbance which is conducted by an afferent fibre to the
nerve-cells, where it liberates a store of energy which is now con-
ducted outwards to the muscular fibre, secreting cell, or other work
organ. This constitutes reflex action. Of these two mechanisms, the
latter is by far the most important. The ganglia and strands of the
sympathetic system appear to be simply an aggregation of reflex mech-
anisms connected together in various ways, and Ave shall, therefore,
SPINO-NEUEAL SYSTEM. 05
at once proceed to discuss the functions of the spinal and encephalic
systems.
1. FUNCTIONS OF THE SPINO-NEURAL SYSTEM.
(1) Reflex Action. — The ganglion cells of the anterior gray
horns of the spinal cord are centres for reflex actions. The afferent
fibres of the reflex loop start from the periphery of the body and pass
upwards along the peripheral nerves and through the posterior roots
and posterior gray horns to join the ganglion cells of the anterior
horns, while the efferent fibres pass outwards through the anterior
roots and peripheral nerves to reach the muscles. Two forms of reflex
action maybe distinguished, {a) the superficial and (b) the deep reflexes.
(a) The superficial reflexes are excited by stimulation of the skin
and accessible mucous membranes.
(b) The deep reflexes consist of muscular contractions evoked bv
striking the muscles themselves, stretching their tendons, or tapping
certain parts of the periosteum, and probably some of the fascise.
Some physiologists believe that the tendon reactions are caused not by
reflex, but by direct action, being supposed to be due to the sudden
stretching of the muscular substance itself. It is, however, admitted
by all that the integrity of the reflex loop is necessary for the jn'oduc-
tion of these reactions, and we shall consequently speak of them in
these pages as if they were proved to be of reflex origin. The various
forms of the superficial and deep reflexes will be described in detail
when the disorders of the reflex functions are under consideration.
(2) Automatic Actioji. — The spinal cord contains a considerable
number of what have been regarded as automatic centres, but it is
probable that many of them act in a reflex manner. The lumbar
portion of the cord contains centres for the regulation of the acts con-
nected with micturition, defecation, erection and ejaculation, and par-
turition. The medulla oblongata contains numerous centres which are
more or less automatic in their actions. The following may be men-
tioned : (a) the respiratory centre, {b) the cardiac centre, (c) the vaso-
motor centre, [d) the diabetic centre, or more probably a centre for the
regulation of the nutrition of the liver and the other abdominal viscera,
(e) the centre for deglutition, (/) the centre for the movements of the
stomach and oesophagus, {g) the centre for the regulation of the secre-
tion of saliva, and (A) the centre for the dilation of the pupil.
(3) Tropliic Functions of the Cord. — The ganglion cells of the
anterior horns exercise a trophic influence on the muscles with which
thev are connected bv efferent fibres. It is also probable tliat these
66
PHYSIOLOGICAL INTRODUCTION.
cells exercise a controlling influence upon the nutrition of the bones
and j(.ints, while the cells of the posterior gray horns constitute trophic
centres for the skin and its appendages.
(4) Vaso-motor and Secretory Functions. — Vaso-motor centres exist
in the cord, by means of which tonus of the muscular coat of the
vessels is maintained. The secretions of the glands are also controlled
by the spinal centres, and the peristaltic movements of the oesophagus,
stomach, and intestines are regulated from the cephalic end of the
central o-ray tube. Little is known, beyond conjecture, of the localiza-
FiG. 39
/■!■ 3 3 2 1
It t t u
X A
Diagram of the Course of the Peixiipal Condvctinh Paths within the Cord. (Aftor Erh. i
1 and 1', The motor and vaso-motor tracts passing througli the anterior root («), and remaining on tlie
same side of the cord ; 2 and 2', Tracts which conduct the muscular sensibility, also passing thruugh the
anterior roots, and remaining oh the same side of the cord ; 3 and ',i', The tracts which conduct sensory
impressions of touch, temperature, pain, and tickling. These enter the cord through the posterior roots,
and cross to the other side, and pursue their course upwards on that side. Section of the right half of the
cord {«) must interrupt conduction through the motor, vaso-motor, and musculo-sensory tracts (1 and 2)
on the right side, and the cutaneous sensory tracts on the left side (3').
tion in the cord of the centres of visceral innervation. That they are
not situated in the anterior gray horns is rendered certain by the fiict
that the visceral movements, and the automatic actions of defecation,
micturition, erection, and parturition, are unaffected in those diseases
in which the lesion is limited to the anterior gray horns. The vesicu-
lar column of Clarke, the ganglion cells of which are bipolar like those
of the sympathetic ganglia, may possibly contain the centres of visceral
innervation.
(5) Fmictions of the~ Cerebrospinal Conducting Paths. — A trans-
verse lesion of the cord, if complete, gives rise to loss of sensation and
ENCEPHALO-SPINAL SYSTEM. 67
voluntarv motion in all parts of the body which are innervated from
the i)art of the cord which is below the level of this disease. If the
lesion is limited to one lateral half of the cord, the sensations of touch,
pain, temperature, and tickling are lost on the opposite side to the
disease, while muscular sense and voluntar}^ motion are lost on the same
side. The annexed diagram (Fig. 39) will afford a sufficient explana-
tion of this statement.
((J) Functions of the Cerehello-spinal Conducting Paths. — A trans-
verse lesion of the spinal cord must doubtless arrest conduction through
the cerebellar spinal conducting paths, but the symptoms which might be
caused by injury of these paths are altogether obscured by the presence
of voluntary paralysis. The cerebellar afferent conducting paths are,
however, most probably interfered with when the posterior columns of
the cord are separately diseased, and it is probable that the incoordina-
tion of movements, to be subsequently described under the name of
ataxia, is caused by injury of these paths. Disease of the cerebello-
spinal efferent conducting paths is not known as a separate affection.
2. FUNCTIONS OF THE ENCEPHALO-SPINAL SYSTEil.
All recent researches have, in my opinion, tended to confii-m Mr.
Herbert Spencer's hypothesis : "• That the cerebellum is an organ of
doubly compound coordination in space, while the cerebrum is an organ
of doubly compound coordination in time." According to this theory,
which has been adopted and elaborated by Dr. Hughlings Jackson, the
cerebellum regulates the muscular contractions necessary for the main-
tenance of all our attitudes in space, while the cerebrum regulates the
contractions necessary to effect all the changes of attitude which are
made in response to the successive impressions made upon the organism
in time. Now, so long as a particular attitude is maintained in oppo-
sition to gravity or other forces, the contractions of the various groups
of muscles concerned must be continuous and in equilibrium with one
another ; Avhile each change of attitude necessitates the overthrow of
this equilibrium by the contractions of some groups of muscles pre-
ponderating over those of others, and thus change of attitude involves
alternate muscular contractions and relaxations. Speaking broadly,
then, the cerebellum regulates continuous or tonic muscular contrac-
tions, while the cerebrum regulates alternate or clonic contractions. It
will be seen, therefore, that every compound muscular adjustment
necessitates the cooperation of both these organs. No change of atti-
tude can be effected by the cerebrum except in so far as a certain atti-
tude was previously maintained by the cerebellum, and no steady move-
ment can be produced by the alternate contractions of some groups of
QS PHYSIOLOGICAL IXTR ODUCTIOX.
muscles except in so far as other groups of muscles are maintained in
a state of continuous contraction, and it may consequently be inferred
that all the movements of the body are coordinated both in the cere-
bellum and cerebrum. But although the functions of the cerebellum
and cerebrum are to a considerable extent coordinate, yet it is manifest
that the former must act in subordination to the latter.
The degree of development to which an animal has attained may,
indeed, bemeasured by its power of effecting multitudinous changes of
attitude, and, were it only possessed of the power to maintain one un-
varying attitude, its degree of organization would not require to be
more complicated than that of a vegetable. But, in effecting these
changes of attitude, the alternate contractions, under the guidance of
the cerebrum, must take the lead, and any change Avhich is produced
in the relative strength of the continuous contractions, although regu-
lated by the cerebellum, must be in strict subordination to the action
of the cerebrum.
3. FUNCTIONS OF THE CEREBRO-SriNAL SYSTEM.
The central gray tube, with the peripheral nerves, constitutes, as Ave
have seen, a system of simple coordination in time (reflex action), and
Ave must noAv point out that the basal ganglia, when acting upon the
central gray tube and peripheral nerves, form a system of compound
coordination in time (instinctive action), and the cortex of the brain,
when acting on the inferior centres, forms a system of doubly compound
coordination in time (conscious action). Both conscious and instinctive
subconscious movements are comprised under the name of psychical
actions. Reflex actions consist, as Ave have seen, of three factors : (a)
conduction to a nerve centre of an impression made on the surface ; (b)
reduction to order of these impressions in the centre ; and (e) conduc-
tion of these outwards, with ^ the muscular contractions resulting from
them. But, as has been frequently stated by Mr. Herbert Spencer,
four factors may be distinguished in every psychical action. To quote
Mr. Spencer's own language: " There is (a) that property of external
objects which primarily affects the organism — the taste, smell, or
opacity ; and, connected Avith such property, there is in the external
object that character (l>) Avhich renders seizure of it or escape from it
beneficial. Within the organism there is (c) the impression or sensa-
tion Avhich the property a produces, serving as stimulus, and there is
connected Avith it the motor change {d) by which seizure or escape is
effected. Now, psychology is chiefly concerned <\ith the connection
between the relation ab and the relation cd, under all those forms
which they assume in the course of evolution. Each of the factors
CEREBRO-SPINAL SYSTEM". 69
and each of the relations grows more involved as organization advances.
Instead of being single, the identifying attribute a often becomes, in
the environment of a superior animal, a cluster of attributes, such as
the size, form, colors, motions, displayed by a distant creature that is
dangerous. The factor 5, with which this distant combination of attri-
butes is associated, becomes the congeries of characters, powers, habits,
which constitute it an enemy of the subjective factors ; c becomes a
complicated set of visual sensations coordinated with one another and
with the ideas and feelings established by experience of such enemies,
and constituting the motive to escape ; while d becomes the intricate,
and often prolonged, series of runs, leaps, doubles, dives, etc., made in
eluding the enemy."
The account first given of reflex and psychical action shows that the
former consists of a muscular adjustment made in response to ?l pi-esent
impression ; while the latter is a muscular adjustment excited by a
present impression, but made to attain or avoid an anticipated impres-
sion. In reflex action the muscular adjustment is effected by means of
afferent and eff'erent fibres and one centre, while in psychical action this
mechanism must consist of at least afferent and efferent fibres, a recep-
tion and an emission centre with some means of intercentral communi-
cation. In the purely unconscious psychical actions, or the instinctive
actions, the optic thalamus is supposed to be the central receptive organ,
and the corpus striatum the central emission organ, the two being con-
nected 1)7 white fibres which interlace with the longitudinal filires of the
internal capsule. The cortex of the cerebrum with its afferent and
efferent fibres appears to be the organ for the regulation of the con-
scious psychical actions, although the fact that individuals sometimes
sing songs or recite long passages of poetry during the unconscious
stage which follows an epileptic attack, or that which results from the
mesmeric state or from chloroform narcosis, seems to show^ that all ac-
tions, which, like spirits, are regulated from the cortex of the brain, are
not necessarily attended by consciousness. A glance at the structure
of the cortex of the brain (Fig. 30) will show that the small cells of
the outer layers are best adapted to act as a receptive organ, while the
caudate cells of the inner layers are best adapted to act as an emissive
centre. The structure of the outer layers of the cortex in comparison
with the inner layers, forcibly reminds one of the structure of the pos-
terior gray horn of the spinal cord in comparison with that of the
anterior horn. In the outer layers of the cortex, as in the posterior
gray horn, the afferent fibres terminate without forming definite con-
nections with the cells, which are in both cases, small, round, and desti-
tute of processes, while in the inner layers of the cortex and in the
70 PHYSIOLOGICAL INTEODUCTION .
anterior gray horns, the cells, which are large and furnished with
numerous processes, are definitely connected with the axis-cylinders of
efferent fibres.
Now, although it is probable that the outer layers of the cortex of
the whole cerebrum constitute a receptive organ, and the inner layers
an emissive organ, yet, the outer layers of certain districts of the cortex
have become specially adapted to act as receptive organs or sensory
centres, and the inner layers of other districts have become specially
adapted to act as emissive organs or motor centres.
(1) The Sensory Cortical Centres. — From his first experiment,
Ferrier concluded that the centre for vision was situated in the angular
gyrus and surrounding gray matter; the auditory centre in the superior
temporo-sphenoidal convolution ; the centres of taste and smell at the
extremity of the temporo-sphenoidal lobe, and that of touch in the
uncinate gyrus and the hippocampus major, Munk believes that the
visual centre or area is of much larger extent than that assigned to it
by Ferrier, and that it is situated in the occipital lobes. He maintains
that removal of this area causes Ijlindness, and that extirpation of small
portions of it gives rise to blindness of localized areas of the retina. He
beheves that there are three visual spheres in the cortex corresponding
to three visual areas in the retina. The external part of the retina of
the left eye is connected with the external part of the cortical visual
centre in the left hemisphere, while the internal and central portions of
the retina of the right eye are respectively connected with the internal
and central portions of the visual centre of the left or opposite hemi-
sphere. The upper portion of the retina is connected with tlie front,
and the lower part with the posterior aspect of the visual centre of the
opposite hemisphere.
Removal of both visual centres causes, according to Munk, complete
or absolute blindness, while partial removal of these areas causes incom-
plete, or what Munk calls psycliical blindness, a state of vision first
observed by Goltz, in which the animal sees and avoids objects, but
fails to recognize the special properties of a piece of meat, for example,
which renders it food to be eaten instead of an obstacle to Ije avoided.
Munk regards the whole superior and internal surface of the cerebral
hemisphere as constituting a sensory area, and the annexed diagrams
(Fig. 40) indicate the manner in which he believes these centres to be
distributed. Very elaborate experiments have been conducted by Drs.
Ferrier and Yeo, to determine the exact seat of the centre of vision, and
the most important conclusion they come to is that " destruction of both
angular gyri and occipital lobes causes total and permanent blindness
in both eyes without any impairment of the other senses or of motor
CEREBRO-SPIXAL SYSTEM. 71
])Ower." Blindness or heniiopia Avas caused by less extensive injuries,
but partial or complete recovery ahvays ensued. The experiments of
Luciani show that visual disturbances follow extirpation, not only
of the occipital, but also of the parietal, temporal, and frontal lobes.
It may therefore be concluded that the localization of sensory centres
is a diffused one, and that the whole surface of the cortex is possessed
of more or less of sensory functions.
Fig. 40.
Upper Sueface of the Brain of the Monkey. (After Munk.)
Senxory Areas : A, of the eyes; B, of the ears ; C, of the sensibility of the lower extremitj' ; D, Anterior
extremity ; E, Head ; F, Ocular mu.scular apparatus ; G, Region of ears ; H, Neck ; I, Body.
(2) The Motor Qortical Centres. — The experiments of Hitzig and
Fritsch, Terrier, and others have shown that stimulation of certain
po'-tions of the cortex of the cerebral hemispheres by electrical currents
is followed by associated muscular movements of the opposite half of the
body. The portion of the cortex which is thus excitable is named the
motor area. This area corresponds generally with the ])art supplied
by the Sylvian artery, and also with the area in which the giant cells,
already described, have been discovered. The portions of the cortex —
the areas supplied by the anterior and posterior cerebral arteries — which
do not respond to electrical excitation are called latent areas. It has
also been found that extirpation of a localized portion of the motor
area causes paralysis of the muscles which are thrown into a state of
spasm by electrical excitation of this portion. The annexed diagrams
(Figs. 41 and 42) show the topographical distribution of these motor
centres on the outer and superior surfaces of the cerebral hemispheres
without further description. The experiments of Schafer and Horsley
72 PHYSIOLOGICAL INTRODUCTION.
have shoAvn that a p(3rtion of the cortex of the internal surface of the
cerebral hemisphere is excitable. The excitable portion is limited to
the marginal convolution, and extends as far forwards as the junction
of the middle and posterior thirds of the superior frontal convolution,
and as for backwards as a point opposite the centre of the parietal
lobule. Speaking in general terms, stimulation induces contractions of
the muscles of the trunk and of the large muscles inserted in the
j^houlder-blade and shoulder, and those inserted about the hip-joint.
Fig. 41.
Figs. 41 and 42.— Sihe and Upi'eu Views of the Bkain of Max. (After Ferkier )
These figui'es are constructed by marking on the brain of man, in their respective situations, the motor
areas of tlie brain of the monkey as determined by experiment, and the description of the effects of stimu-
lating the various areas refers to tlie brain of the monkey.
1 (On the posterior-parietal lob\ile\ Advance of the opposite hind limb as in walking.
2, 3, 4 (Around the upper extremity of the fissure of Rolando), Complex movements of the opposite leg
and arm, and of the trunk as in swimming,
a, 6, c, d (On the ascending parietal convolution). Individual and combined movements of the fingers
and wrist of the opposite hand. Prehensile movements,
o (At the posterior extremity of the superior frontal convolution\ Extension forward of the opposite
arm and hand.
6 (On the upper part of the ascending frontal convolution). Supination and flexion of the opposite
forearm.
7 (On the median portion of the ascending frontal convolution >, Retraction and elevation of the oppo-
site angle of the mouth by means of the zygomatic muscles.
8 (Lower down on the same convolution), Elevation of the ala nasi and upjier lip with depression of
the lower lip on the opposite side
C E R E 1 5 R - S P I N A L S Y S T E :N[ .
rs
(o) Tlw Intireentral Connections. — The central ends of the indi-
vidual sensory mechanisms are unified 'bf a collective centre — the sen-
sormm commune — which is the general centre of nervous connections
on the afferent side. It may also be supposed that the individual
motor centres are unified by a general centre of nervous connections
which may be regarded as a motorium commune. Between the sen-
FiG. 42.
0, 10 (At the inferior extremity of the ascending frontal and posterior extremity of the third frontal
convolution), Opening of the mouth with (9) protrusion and (10) retraction of the tongue.
Region of Aphasiu.
11 (At the inferior extremity of the ascending parietal convolution), Eetraction of the opposite angle
of the mouth, the head turned slightly to one side.
12 (On the posterior portions of the superior and middle frontal convolutions), Eyes opening widely,
pupils dilating, and the head and eyes turning towards the opposite side
13, 13' (On the supramarginal lobule and angular gyrus). The eyes moving towards the opposite side-
with an upward (13; or downward (13') deviation. Pupils generally contracting. (Centre of
Vision.)
14 (On the inframarginal or superior temporo-.sphenoidal convolution), Pricking up of the opposite ear,
head and eyes turning to the opposite side, and pupils dilating largely. (Centre of hearing.)
Ferrier, moreover, places the centres of taste and smell at the extremity of the temporo-sphenoidiil
lobe, and that of touch in the gyrus uncinatus and hippocampus major.
74 PHYSIOLOGICAL INTRODUCTIOX .
sorium commune and the motorium commune there is no distinct line
of demarcation, nor is there any definite boundary between these
hio-hest centres and the individual sensory and motor centres. All of
them run indistinguishably into one another, and all of them are rep-
resented bv the cortex. The activity of the individual sensory centres
is the con-elation of sensation and feeling, and of the highest sensory
centre of perception — emotion, and the highest operation of the intel-
lect, while the activity of the motor centres is the correlation of con-
scious exertion and the will. But although the molecular activity of
the cortex of the brain is the correlative of consciousness, all parts of
the cortex do not stand in e(iual relation with feeling. It seems to me
that consciousness is correlated in a special manner with the activity of
the small cells, which are destitute of processes and definite connections.
When an unaccustomed impression is made upon the surface of the
body the impulses are conducted inwards to the small cells of the outer
layers of the cortex, and the energy set free by the unusual disturbance
is in great part expended in producing a new organization amongst these
cells, and it is during the progress of this organization that psychical
action is attended by the highest consciousness. But in proportion as
this impression becomes frequently repeated in experience, the organi-
zation of the cells becomes more and more complete by the establish-
ment of new connections, and after a time the channels of communica-
tion between the receptive and emissive organs become so open that the
muscular adjustment follows the impression promptly and in almost a
wholly unconscious manner. The degree of consciousness which
attends a particular operation may, therefore, be regarded as an expres-
sive indication of the resistance offered to the molecular movements or
impulses in passing from the central receptive to the central emissive
organs. Nor is this all. It is very probable that the part of the
centre which is most remote from both the sensory and motor centres
will, durintr its activity be correlated with the highest consciousness.
This part is what is called the praefrontal area of the coi'tex, and the
fact that consciousness is lost at a much earlier period in epileptiform
attacks caused by lesions of this area than in the attacks which are
caused by lesions in other areas of the cortex, speaks much in favor of
the supposition just advanced.
The different cortical sensory and motor centres are connected with
one another in various ways by systems of white fibres. These SA'stems
are the longitudinal or collateral fibres, consisting of the arcuate fibres
or fibrse proprise, fibres of the gyrus fornicatus, longitudinal septal fibres,
tlie fasciculus uncinatus, the longitudinal inferior fasciculus, the longi-
tudinal fibres of the corpus callosum, and the perpendicular occipital
CEREBELLO-SPINAL SYSTEM. 75
fasciculus described by Wernicke, and the transverse or commissural
fibres, wliicli connect similar points of the convolutions of the two
hemispheres, and which consist of the transverse fibres of the corpus
callosum, and the fibres of the anterior and posterior commissures of
the third ventricle.
4. FUNCTIONS OF THE CEREBELLO-SPINAL SYSTEM.
The cerebellum must, like the cerelirum, act on the muscular svstem
through the spinal cord and peripheral nerves. The central gray tube,
as we have seen, forms with the peripheral nerves a system of simple
coordination in time, and we now find that it likewise forms a system
of simple coordination in space (reflex tonus) ; the intermediate ganglia
of the cerebello-spinal system acting on the central gray tube and
peripheral nerves form a system of compound coordination in space
(maintenance of unvarying attitudes), and the cortex of the cerebellum
acting on the inferior centres forms a system of doubly compound
coordination in space (the adjustment of the tonic contractions of the
muscles rendered necessary by changes of attitude). If now tlie cere-
bellum is an organ for producing a balanced state of contraction of the
muscles in the maintenance of attitudes, it may be expected that injury
of this organ will cause a loss of this balance and a conse(|uent diffi-
culty in maintaining complex attitudes. Flourens was the first to
observe the effect of injuries of the cerebellum on the maintenance of
attitudes, or on equilibration, as it is called. He found that when a
small portion of the cerebellum was removed from a pigeon, the animal's
gait became unsteady, and that when larger portions were taken away,
the movements became very disorderly. Experiments on animals have
also shown that section of the middle peduncle of the cerebellum is
followed by a forced movement of the body in which the animal rolls
round its longitudinal axis, the rotation being generally towards the
side operated upon. Injury of the lateral lobe of the cerebellum, and
probably of the fibres of the peduncle as they pass transversely through
the pons, produces the same kind of forced moyeiaent as section of the
middle peduncle. Nothnagel concludes from experiments on rabbits
that lesions which injure the fibres uniting the two sides of the organ
occasion the greatest amount of motor disturbance. Ferrier found
that electrical stimulation of the cortex of the cerel)ellum in animals
caused movements of both eyes with associated movements of the head,
limbs, and pupils. Our relations to the external objects in space are
largely determined by the sense of vision, which is better adapted than
any of the other senses for conducting a large number of simultaneous
impressions from the periphery to the centres, and it may consequently
7(3
PHYSIOLOGICAL INTKODUCTION .
be expected that the organs of vision will stand in a peculiarly intimate
relation to the chief organ for regulating the attitudes of the body.
The semicircular canals, with the portion of the auditory nerve which
supplies them, appear to form a special peripheral organ for determining
the attitudes of the body through the cerebellum.
5. COOPERATION OF THE CEREBRO-SPINAL AND CEREBELLO-
SPINAL SYSTEMS.
According to the theory which has just been advanced the multitu-
dinous adjustments of the body, both in time and space, are regulated by
the combined action of the cerebrum and cerebellum acting through the
spinal cord and peripheral nerves. The cooperation of these organs in the
regulation of motor actions is, however, generally of an antagonistic
Fig. 43
CL" a' a
Schema of Encephalo-spixal Action.
8, Motor ganglion cell of spinal cord ; c, Ganglion chH of cortex of cerebrum, and d , of cortex of cere-
bellum ; o, o', a", Afferent fibres to the spinal cord, and to the cortices of the cerebrum and of the cere-
bellum respectively ; e, e, Efferent fibres from the spinal ganglion cell to m, »n', the muscles ; e' and e",
Fibres from the cerebral and cerebellar cells respectively to the spinal ganglion cell ; i, Intercentral filire
connecting the cerebral and cerebellar cells. The arrows indicate the direction of the conduction.
kind. The cerebellum tends to maintain an unvarying attitude, Avhile
the cerebrum, in initiating a change of attitude, must act by overthrowing
the balance of the muscular contractions which maintain this attitude.
The overthrow of this eciuilibrium can Ije effected by the cerebrum in
CEREBKO-SriNAL AXD CE R E BE LLO - SP IX AL SYSTEMS. 77
either of two ways, either positively by an increase of nervous impulses
to certain groups of muscles, or negatively by arresting or inhibitino- in
the spinal centres the cerebellar influx to their antagonists. Now it is
manifest that the latter method would be much more economical than
the former, and consec^uently there is every reason to believe that the
cerebrum does act largely by inhibiting the action of the cerebellum,
although it is also certain that it must exercise a positive control over
the various muscular contractions. The conjoint action of the central
gray tube, the cerebrum, and cerebellum is represented in the accom-
panying diagram (Fig. 43) under the simplest conditions. A ganglion
cell of the spinal cord is represented by s, of the cerebrum by c, of
the cerebellum by c'. The afferent conducting paths from the periphery
to the spinal cord, cerebrum, and cerebellum are represented by a, a\ a"
respectively. The efferent conducting path between the cerebrum and
spinal cord is represented by e', between the cerebellum and cord by e",
and lietween the cord and muscles l)y e, while m m represent the mus-
cles themselves, and the arrows indicate the direction of the currents.
Now, when an impression is made upon a, it is conveyed to .s, and
reflected through e e to m m, this constituting a simple reflex action.
When an impression is made upon a", the impulse is conveyed to c'
and through e" to s, and through e e to m m, producing a continuous
contraction of the muscles. But when an impression is made upon a',
an impulse is conveyed to c and dowuAvards, through e to s. Now, the
impulses conveyed through e' to s may produce, Avhen of a certain
degree of intensity, only an arrestive or inhibitory action on the im-
pulses conveyed to s through a and e", while an additional degree of
intensity enables it to pass through s and e <? to m m, and to produce
clonic muscular contractions. It is also probable that the cerebrum
may exercise both an inhibitory and excitative action on the cerebellum
through the intercentral fibres (i), which connect the centres directly
with each other. This hypothesis was first stated by Dr. Hughlings
Jackson, and he has since applied it, with his usual subtle and gen-
eralizing power, to the explanation of various pathological phenomena.
As this is an exceedingly important theory, it Avill be as well to illus-
trate the actions of the cerebrum and cerebellum by reference to the
muscular contractions necessary for the maintenance of the erect
posture and for locomotion.
(a) The E^^ect Posture. — In the erect posture the weight of the body
is borne by the plantar arches, and the body is maintained by a series of
muscular contractions in such a position that the line of gravity falls
within the area of the feet. In this position the line of gravity of the
head falls in front of the occipital articidation, that of the combined
PHYSIOLOGICAL INTRODUCTION.
Fig. 44.
Diagram Illustrating the
Attachments of some of the
MOST Important Muscles
WHICH KEEP THE BoDY IN THE
Erect Posture. (After Hux-
ley.)
I. Muscles of the Calf.
II. Those of the back of the
Thigh. III. Those of the
Spine, which tend to keep the
body from falling forwards.
1, the Muscles of the front of
the Leg ; 2, those of the front
of the Thigh ; 3, those of the
front of the Abdomen ; 4, 5,
those of the front of the Neck,
which tend to keep the body
from falling backwards. The
arrows indicate the direction
of action of the muscles, the
foot being fixed.
head and trunk passes behind a hne joining the
two hip-joints, that of the com1)ined head, trunk,
and thighs falls a little behind the knee-joints,
and the line of gravity of the whole body passes
in front of the line drawn between the two
ankle-joints. This statement of the direction of
the line of gravity shows that when the foot is
made the surface of support, the body would
fall forwards unless prevented by contraction of
the muscles of the calf (Fig. 44, I). " But
this action," says Prof. Huxley, "tends to bend
the leg, and to neutralize this and keep the leg
straight the great muscles in front of the thigh
(Fig. 44, 2) must come into play. But these,
by the same action, tend to bend the body for-
ward on the legs ; and if the l)ody is to be kept
straight they must be neutralized by the action
of the muscles of the buttocks and of the back
(Fig. 44, III)." It will be seen, however, that
since the centre of gravity of the combined
head and trunk falls a little behind the line
joining the hi]>s, the muscles of the buttocks,
although stronglv contracted in effecting the
erect position, do not require to contract in
order to maintain it.
The muscles of the calf, those of the front of
the thigh, and the erector spinne are therefore
the most active muscles in maintaining the erect
posture, and these are, according to the hypothe-
sis, maintained in a state of tonic contraction,
mainly by the cerebellum.
(b) Walking. — At each step in w'alking there
is a moment at which the body rests vertically
on the foot of one leg (say the right), Avhich is
then called the '■'■active leg." The other (left),
which is now called the ^'■passive leg," is at this
time inclined obli(^uely, Avith the heel raised and
the toe resting on the ground. The left leg,
slightly flexed to avoid contact with the ground,
is now swung forwards like a pendulum, the
length of the swing or step being determined
CEREBRO-SPINAL AND CEEEBELLO - SPIN AL SYSTEMS. 79
by the length of tlie leg, the left toe is brought to the ground, and the
step is finished. The left leg, Avhich was previously passive, now
gradually becomes straight and rigid, and the body is moved forwards
<»n the left toe as a fulcrum ; while the right leg, which was previously
at-tive, assumes an inclined position, with the heel raised and the toe
resting on the ground, so that it is ready to swing forwards, and then
once more to assume the role of activity, while its fellow becomes in its
turn passive again. During the forward movement the centre of
gravity of the body describes a curve, the convexity of which is up-
ward ; hence in successive steps the centre of gravity, and with it the
{(>]) of the head, describes a series of curves, with their convexities
upwards.
In standing on Ixjth feet the line of gravity falls betAveen them, )jut
in walking it must be alternately shifted from one foot to the other, in
order to balance the body on the active leg. While the left leg, for
instance, is passive and swinging, the line of gravity falls within the
area of the right foot, and passes through the right lateral half of the
pelvis, and as the left foot becomes active the centre of gravity is
shifted to the op])osite side, and the line of gravity passes through the
left lateral half of the pelvis to the left foot. In walking, therefore,
the centre of gravity describes not only a series of vertical but also a
series of horizontal curves, so that the curve described by the head is
composed of vertical and horizontal factors. In slow walking there is
an appreciable time during which both feet are on the ground ; the one
being planted so as to become active before the other has ceased its
activity. In fast walking this period is very short, the one leaving the
ground the moment the other touches it, while in running there is an
interval during which neither foot is on the ground.
Let us now attend to the muscles, the contraction of which effects the
changes of attitude necessarily involved in walking. Suppose that we
start with the right leg in the vertical position, with the line of gravity
passing within the line of the right foot, and the left partially raised
from the around. The first indication of a forward movement must be
eff"ected by a contraction of the flexors of the foot on the leg, which,
as the toe is fixed, bends the leg and with it the whole body forwards.
This contraction fixes the upper end of the tibia, the leg being bent
forwards at an acute angle with the foot, and the femur is kept extended
on the tibia by a rigid contraction of the muscles of the front of the
thigh. The lower end of the femur and upper end of the tibia are
now rendered fixed points, the line of gravity is rapidly passing forwards
from the middle of the foot to the toe, the weight is thus taken off" the
heel, and contraction of the muscles of the calf causes its elevation.
}iO PHYSIOLOGICAL IXTRODUCTIOX.
But tlie line of gravity is now passing through the toe, in front of the
knee, and in front of the centre of the hip-joint, so that the muscles of
the back of the thigh and those of the buttocks must contract strongly
or the body would be flexed on the thighs, while the erectors of the
spine must be sufficiently contracted to keep the different segments of
the body in a rigid condition. It is manifest that as soon as the line
of p-ravity passes in front of the centre of the hip-joint and through
the toe, although muscular action may maintain the different segments
of the body extended, no muscular action can prevent the body as a
whole from falling forwards on the toe as a pivot, and the body would
fall unless the left foot were now in a position to be planted on the
o-round in front of the line of gravity, and ready to assume the role of
the active leg. Before, however, the left leg can become active, the
line of gravity must be transferred to the left foot, and before the right
foot can be made to swing it must be shortened so as to avoid contact
with the ground. These operations are so im])ortant as to require care-
ful study.
(c) The transference of the centre of gravity from the passive to
the active leg is largely effected by the contraction of the abductors of
the thigh, especially by the gluteus medius, contraction of which, the
left thigh being fixed, causes the pelvis to rotate vertically on the hip-
joint; so that the centre of gravity, and with it the head, describes
a curve to the left, with its convexity upAvards, a movement which at
the same time slightly elevates the pelvis and Avith it the hip-joint of
the opposite side. The slight elevation of the right hip-joint not only
transfers the centre of gravity to the left, but also increases the distance
of the centre of movement (hip-joint) of the passive leg (right) from
the ground, and thus prepares for the forward SAvinging of the right
leg. The contraction of the abductors is accompanied by a contraction
of their antagonists — the adductors, Avhich not only gives steadiness to
the pelvis but holds the latter in I'eadiness to counteract at once any
tendency to overaction on the part of the former, by Avhich the line of
gravity Avould be carried beyond the middle of the foot. The curve
described by the head OAving to contraction of these muscles Avould
indeed be much greater than \l is Avere it not compensated by contrac-
tion of other muscles. At the time that the abductors of the left leg con-
tract, and thus rotate the pelvis, the centre of gravity, and head to the
left, the erector spinee of the right side enter into a somcAvhat additional
contraction producing a compensating curve to the right, so that the
head does not deviate to the left during the transference of the centre
of gravity to the left foot to anything like the extent that might l)e
expected.
CEEEHRO-SPIXAL AXD C E 1! E 15ELL0 - S ]' 1 X AL SYSTEMS. bl
(d) Sivinginti of the Passive Leg. — It lias just been said tliat Avlien
the left leg becomes active the pelvis rotates vertically on the left hip,
so that the opposite hip-joint is slightly elevated to an extent sufficient
to take the weight of the body from the right toe, but inasmuch as the
right foot is, at the time it is about to become passive, extended ob-
liquely, with the toe depressed, while the left is placed nearly vertically,
the former is much too long to swing past the other without touchino-
the ground, and the slight vertical rotation of the pelvis just described
does not give the requisite elevation for this purpose. In order to
swing forwards, therefore, the right leg is still further shortened bv
flexion of its various segments on the body and on one another. The
thigh is slightly flexed on the body, the leg on the thigh, and the foot
on the leg. Of these movements the slight elevation of the toe caused
by dorsal flexion of the foot is by far the most important and special ;
it is this movement which distinguishes the walk of the adult from that
of the infant, the latter advancing the passive foot not by a pendulum
motion, but by a voluntary eifort in which the leg and foot are raised
from the ground by the flexion of the thigh on the body. It may also
be mentioned that the adductors of the thigh manifest a very special
action in assisting to cross one leg over the other — an action which
cannot be effected by the lower animals, or by the human inflint, and
hence these muscles must also be regarded as being in an esjiecial
manner under cerebral influence. The cerebro-spinal influence is
therefore manifested in the active leg during locomotion by securino- a
strong contraction of the anterior flexors of the foot, and of the flexors of
the leg on the thigh along with the abductors so as to fix and rotate the
pelvis vertically, while it is manifested in the passive leg partly by con-
traction of the flexors of the thigh on the body, partly by contraction
of the flexors of the leg on the thigh, and partly by flexion of the foot
on the leg, the flexion in all these instances being ])robably due less to
active contraction than to relaxation of the antagonistic muscles. The
transference of the line of gravity to the active leg also takes part in
this action by removing the fixed point, from which the muscles of the
passive leg act, from the foot to the pelvis.
(e) The Act of Acquiring the Erect Posture. — Now, if the changes
of position which take place in walking are due to the predominance of
cerebro-spinal over cerebello-spinal action, this is no less true with
respect to the successive changes of posture requisite to raise the body
from the recumbent to the erect posture. Suppose a man is lying in
the prone position, and then gets up on his hands and knees. When
the knees are raised by muscular action, so that the body is supported
by the tips of the fingers and the toes, while the centre of gravity falls
6
<S2 PHYSIOLOGICAL INTRODUCTION.
midway between the anterior and posterior extremities, this constitutes
what I may call the quadrupedal position: In this position the toes
constitute the fixed point for the posterior extremities, and the muscular
strain rests upon the flexors of the phalanges, their contraction being
necessary to maintain the rigidity of the plantar arch. The extensors
of the foot on the leg must contract to prevent flexion of the leg at the
ankle, the extensors of the leg on the thigh must contract in order to
prevent the thigh being flexed on the leg, and the extensors of the
body on the thigh must also contract in order to prevent the former
being flexed on the latter. A further contraction of these same muscles
drags the centre of gravity of the body upwards and backwards, the
Aveight is taken off" the anterior extremities, and the body assumes the
semibipedal posture, in which the line of gravity passes between the
feet in the line which joins the toes, considerably in front of the line
which joins the ankles, behind that which joins the knees, and in front
of that joining the hip-joints. It is manifest that the contractions of
the muscles of the sole, those of the calf, front of the thigh, those of
the gluteal region and the erectors of the spine, must largely predomi-
nate over their antagonists in order to maintain this position, and that
this predominance must be maintained until such time as the heel
touches the ground, when the line of gravity passes from the toes to
the centre of the plantar arch, and behind the line joining the centre
of the two hip-joints. The vertical position is then maintained mainly
by means of the bones and ligaments, aided only by a slight degree of
muscular contraction. Now, the bipedal erect posture has only been
attained from the recumbent position by passing through an infinity of
intermediate postures, and according to the hypothesis the cerebello-
spinal system has had to maintain each posture attained by striking a
balance between the tensions of the extensors and flexors of the body,
the latter being aided by gravity ; while the cerebro-spinal system con-
tinually changes each attained posture by overthroAving this balance in
favor of the extensors. In passing from the bipedal erect posture
through the semibipedal and quadrupedal to the recumbent posture a
reverse process takes place, the cerebro-spinal system at each new posi-
tion ac(|uired, inhibits the action of the cerebello-spinal system on the
extensors, so that contraction of the flexors assisted by gravity is
allowed gradually to predominate.
But if this hypothesis of the joint, although opposite, action of the
cerebrum and cerebellum acting through the spinal cord be true at all,
it must be accepted in its fullest extent. If, for instance, it be true
that the passage from what I have called the quadrupedal to the
bipedal posture in the human subject is due in the individual to the
I
CEREBRO-SPINAL AND CER EBELLO - SPIN AL SYSTEMS. 83
predominance of cerebral influx to the extensors over their antagonists,
thL^ is no less true with respect to the race. In the gradual develop-
ment of man from the lower animals the same forces have been at work.
From the seniibipedal position assumed hj a dog attempting to stand
on its hind legs, and the imperfect bipedal attitude of the monkey to
the perfect bipedal posture of man, the transition must have been
effected l)y the gradual j)redoininance of the extensors over their antago-
nists through cerebro-spinal influence. In all these processes it will be
seen that the flexors of the body are aided in their action by the force
of gravitation, while the extensors have to overcome this force bv their
action, hence the latter must be capable of much more powerful con-
traction than tilt' former, and are consequently more liable to have
more j)Owerful discharges sent to them both from the cerebro-spinal
and cerebel]o-s])inal systems.
When, therefore, both the extensors and flexors of the head, trunk,
and lower extremities are contracted to their utmost capacity, the action
of the former must predominate over that of the latter ; so that the
segments of the lower extremities will be extended upon one another,
and the body will be arched with tlie concavity directed backwards, as
occurs during the paroxysms of tetanus. But the hand being mainly
an organ of })rehension, the principal functions of the anterior limbs of
man is to pull objects towards the trunk, the latter being the fixed
point during their activity, hence the flexors of the upper extremities
must be more strongly developed than the extensors. And when the
hands become fixed, as in climbing, the most powerful contractions are
obtained when they are in a ])osition to drag the body towards the
fixed ])Osition, and not, as in the case of the lower extremities, when
the body is thrust upwards and away from it ; hence, when the muscles
of the upper extremities are contracted to their utmost capacity, flexion
will predominate over extension.
[f) Fundamental and Accessory Portions of the Nervous System. —
Before leaving this })orti()n of our subject I should like to establish one
more distinction. Structure being the correlative of function, the mul-
tiplicity and complexity of the movements which distinguish man from
the lower animals must be accompanied by a corresponding degree in
the intricacy ;ind variety of the structui'al arrangements of his nervous
system. The main movements which distinguish man from the lower
animals are tjiose concerned in attaining and maintaining the erect
posture, the varied movements of the hands as organs of prehension,
the movements of voice and articulation concerned in speech, and those
which are active in the production of facial expression. All these
movements must, therefore, be represented in the human nervous system
34 PHYSIOLOGICAL IXTRODUCTIOX .
by structural arrangements superadded to those Avliich man possesses in
common with the highest of the lower animals. Indeed, all the cgm-
plex movements first mentioned are accjuired considerably after the
birth of the human infant, and we may conse(iuently expect that the
structural arrangements corresponding to them eitlier do not exist at
birth or exist only in an embryonic condition.
The portions of the nervous system which man possesses in common
with the lower animals, and which are well developed in the human
embryo at nine months, I shall call the fundamental part, and the
portions which have been superadded in the course of evolution, which
differentiate the nervous system of man from that of the highest of the
lower animals, and which are either absent in the human eml)ryo, or
exist only in an embryonic condition, I shall call the accessory part of
the nervous system.
The fundamental portion of the human nervous system coordinates
the fundamental functions which man possesses in common with the
lower animals, but the accessory portions can only l>e said to regulate
the accessory functions in a peculiar sense. The accessory structure
constitutes indeed a new complexity of mechanism superadded to that
already existing, a complexity rendered necessary for the regulation of
the intricate and multiform actions Avhich distinguisli man from the
lower animals. In the develo])ment of the accessory system, small
round cells and non-medullated fi])res appear at a comparatively late
period in the development of the embryo, and the presence of these
simple elements may be regarded as the structural counterpart of a
new modification or specialization of function. Specialization of func-
tion has hitherto been connected with the gradiuil development of
medullated from non-medullated fibres, and of large caudate fi'om small
round cells ; but now it appears that specialization of function is to be
connected with the development of embryonic cells and fibres. There
is, however, no contradiction between the two statements. The em-
bryonic cells and fibres of the accessory system do not of themselves
indicate any specialization of function. I'hese cells and fibres are,
indeed, mere complications of an already existing mechanism, and it is
this alone which entitles them to be regarded as true indicators of a
newly acquired specialization of function ; they are, in short, mere
modifications of an already existing structure corresponding to newly
acquired modifications of previously existing muscular adjustments.
There can 1)e no doubt that the fundamental and accessory portions of
the nervous svstem will be so min";led together that it will be almost
impossible to separate the two, but whether they can be distinguished
from one another morphologically or not, the mental distinction is a
CKRl-:i?R()-SI'IXAI, AXD CE R EBELLO - SP IN AL SYSTEMS. 85
valuable one, and it -will Ije found of importance to remember that in
man the cephalic ganglia, the central gray tube, the conducting paths,
and even the peripheral nerves, Jimst contain fundamental and accessory
cells and fibres.
A comparison of the brain of man Avith that of the monkey will
afford a rough test by which we may distinguish the accessory portions
of the former of the two. Passing over such obvious considerations as
distinctions of size and weight, the first important difference we note is
the great relative increase in the size of the frontal lobe in the brain of
man. The relative increase of this lobe causes the posterior lobes to
be thrust further backwards over the cerebellum, the fissure of Rolando
to slant upwards and backwards instead of being vertical, as in the
brain of the monkey, and the posterior limb of the Sylvian fissure to
become longitudinal instead of slanting upwards, as in the Simian
brain. It is likely that the large relative size of the frontal lobe in
num is connected with his mental superiority over the monkey. The
next difference we observe is the depth of the fissures in the brain of
man as compared with that of the monkey. In the course of develop-
ment the summits of the convolutions are first formed, and they alone
are directly connected with the incoming and outgoing fibres of the
cerebro-spinal conducting paths. The infolding of the cortex, which
forms a sulcus, is a later result of development, and, as the superficial
extent of the cortex becomes greater and greater, the deeper the sulci
become, so the depth of the sulci may be taken to some extent as a
measure of the development of the brain. The next point we note is
the great complexity of the arrangement of the convolutions in the
brain of man as compared with that of the monkey. The convolutions
of the human brain are divided into primary or fundamental and
st'condary or accessory. The fundamental convolutions in man are
distributed along the margins of the great longitudinal fissure and other
primary fissures, like the Sylvian fissure and the fissure of Rolando,
and their disposition corresponds closely with the arrangement of the
convolutions in the brain of the monkey. The accessory convolutions
of man, which are rather irregular in their distribution, may be re-
garded as structures superadded in the course of evolution. These
convolutions are connected with the primary convolutions by arcuate
fibres, and are not directly connected with the ascending and radiating
fibres of the internal capsule, and consequently their activity is likely
to be correlated with mental operations. Another remarkable feature
in which the human brain diff"ers from the brain of animals is the
manner in which the Island of Reil is completely surrounded and
hidden out of view by deep convolutions. This is brought about by
80
PHYSIOLOGICAL INTRODUCTION,
the large development of the posterior extremity of the inferior frontal,
of the Inferior extremities of the ascending frontal and parietal convo-
lutions, and of the supra-marginal, angular, and temporo-sphenoidal
gvri. The consequence of the large development of these convolutions
is that the cortex is deeply folded over the Island of Reil, this fold
forming a kind of hood, which has been named the operculum. It ap-
pears to me that the cortex of the Island of Reil, starting from the
gray matter of the anterior perforated space, is the embryonic part of
the cortex of the brain, just as the central gray column is the embryonic
Tig. 4;'!.
Horizontal Section ok the Basal Ganglia and Inteksal C'apsvle of a Nine .Months' Kmbrvo.
II, in, Second and third segments of the nucleus respectively ; NC, Caudate nucleus ; TH, Optic
thalamus ; IN, Island of Keil ; ps, Peduncular sensory tract and optic radiations of Gratiolet ; P, Fnndii-
mental, P', Mixed, and^), Accessory portion of pyramidal tract ; C, Fibres from the corpus callosum i?).
portion of the gray matter of the spinal cord. On the supposition that
the portion of the Island of Reil which lies in the line of distribution
of the Sylvian artery is the embryonic portion of the convolutions of
the motor area of the cortex, it may be expected that the earlier formed
portions of these convolutions will be thrust upwards towards the great
longitudinal fissure, while the later formed pin-tions will approach nearer
and nearer to the root of the artery. According to this supposition,,
therefore, the fundamental portions of the convolutions supplied by the
Sylvian artery Avill be found near the great longitudinal fissure, and the
("KRKBKO-SPIN AL A X D (' K R K ]5ELL0 - S P 1 N A L SYSTEMS. 87
accessory portion low down near the root of the artery, the hast portion
being formed by the o))erculum. This opinion corresponds closely with
the topoii-raphical distribution of the motor centres as determined l)v
experiment and i)atliological observation. The movements of the mus-
cles of the trunk, which must be regarded as the fundamental move-
ments, are regulated from the marginal convolutions of the longitudinal
Fio. 4)).
P/ —
Tkansveksf, Section oi- iHh < ui:- Cerebri on a level with the anterior pair of Corpora
QUADRKiEMINA, FROM A NINE MONTHS' EMBRYO. (Modified froill KraUSE.)
ff, cnista ; P, pyrnniidal tract ; p, accessory portion of tlie pyramidal tract ; LN, locus niger ; BK, reil
nuclous of the tegmentum ; L, posterior longitudinal fasciculus ; or and ar', upward continuation of the
internal and external portions respectively of the anterior root-zone of the spinal cord ; iii, third nerve ;
in', nucleus of the third nerve ; iv, fourth nerve ; iv', nucleus of the fourth nerve : iv", crossing of the
fibres of the fourth nerve to opposite sides; rf/, descending root of the trigeminus; cc, aqueduct of
Sylvius ; X, crossing of the fibres of the superior peduncles of the cerebellum ; pf, fasciculus of meduUated
fibres proceeding from the fillet tn the anterior pair of corpora i|uadrigemiiia.
sulcus ; while the movements of the lips and tongue, and those of the
small muscles of the hand, Avhich are the chief accessory movements,
are regulated from the operculum.
In endeavoring to discriminate ])etween the fundamental and acces-
sory portions of the C(mducting paths, the most efficient practical test
ss
PHYSIOLOGICAL INTRODUCTIOX
is to regard all those fibres which are fully medullated at birth as be-
lonsing^to the fundamental system ; and those which are non-meduUated
at birth, but afterwards acquire this sheath, as belonging to the acces-
sory system.
In following the course of the pyramidal tract downwards from the
cortex, its fibres come together to form one bundle in ihe anterior two-
thii-ds'of the posterior segment of the internal capsule. When the
internal capsule is examined at birth the pyramidal tract consists of a
Fig. 47.
Tr.vxsvkrsf. Sectiiin of the Pons on a i.f.vel with the Ahuucens akd Kai'iai. Hoots, ekom a sine
months' embryo. (Jlotlified from Kuu. )
The right lialf repi'esents a section made a little lower thau the left P, jiyramidal tract ; ji, accessory
jiortiou of the pyramidal tract; JV and TV', transverse fibres of the pons; so, superior olivary body; nlc
and^^c, anterior and posterior nuclei of the lateral column respectively, representing the nucleus of the
facial nerve; rvii, root of the facial nerve ; vi', nucleus of the sixth nerve ; rvi, root of the sixth nerve ;
at, ascending root of the trigeminus. B, The internal division of the peduncle of the cerebellum as it
passes from the cerebellum ; L, posterior longitudinal fasciculus ; ar anil ar", the upward continuation of
the internal and external divisions of the anterior root-zone of the spinal cord ; I, fasciculus teres.
posterior portion (Fig. 47, P) in which all the fibres are medullated, a
middle portion (Fig. 45, P') in which medullated and non-medulla ted
fibres are mixed, and an anterior portion (Fig. 45, p) in which all the
fibres are non-medullated. In the crusta the medullated fibres lie in
the outer portion of the middle third (Fig. 4(^ P), the mixed fibres in
the inner portion of the middle third (Fig. 4(!, P'), and the non-medul-
lated fibres in the inner third (Fig. 4(5, p). In the pons the medullated
C E K K 15 K O - S P 1 X A L A N I) C K E E B E L L O - S P 1 X A L SYS T E :^I S . 89
Hbres lie in the anterior and external longitudinal bundles (Fig. 47, P),
and the non-niedullated lie in the anterior and internal bundles (Fif,
47, p), while the bundles of mixed fibres lie between these. In the
anterior pyramid of the medulla the medullated fibres occupy the pos-
terior and external parts of the pyramid (Fig. 28, P), and the non-
medullated the anterior and inner side (Fig. 28, j))^ while the area of
mixed fibres lies between them. It is probable that the fibres of the
medullated area form the conducting paths of the moA'^ements of the
muscles of the trunk and of those of the lower extremities, the fibres
of the mixe<l area tlie conducting paths of the movements of the hand,
and the fibres of the non-medullated area the conducting paths of the
movements of articulation and facial expression, movements which are
not orL'anized until some time after birth.
CHAP TEE III.
GENERAL MORBID ANATOMY AND PHYSIOLOdY OF THE
NERVOUS SYSTEM.
I. GENEKAL MOKBID ANATOMY.
Disease of the nervous system is caused (1) by defects in its devel-
opment or evolution; or (2) by a reversal of the process of evolution, or,
in other words, by dissolution.
1. Defects of Dkvei-op.mhnt.
a. Congenital Defects of Nerves.
When portions of the body are incompletely formed, the ner\es are
defective or absent. When, for example, the nose is arrested in its
development, and when no eyes have been formed, not only are tlic
optic nerves absent, but the third, fourth, and sixth pairs are also deti-
cient. In a Cyclops, in which the face was almost entirely wanting, no
facial nerve could be found, and when the ton<rue is wanting the lingual
brandies of the fifth and the liyj)oglossal nerves are absent. In
monsters in which one or more of the extremities are imperfect, there is
a corresponding deficiency in the nei'ves of that limb or limbs.
h. Congenital Defects of the Spinal Cord.
(1) Amyelia, or absence of the spinal cord. Only met with when
the brain is also absent.
(2) Atelomyelia, or imperfect development of the spinal cord. The
upper end of the cord is lacking or imperfectly develoj)ed, the brain
being also absent {anencephalia), or the head defective (acephalia). The
medulla oblongata is absent or exists only in a rudimentary form.
(3) Diastematomyelia is a condition in which the two lateral halves
of the cord either do not unite, or unite only throughout a portion of
their extent. This malformation occurs with anencephalia.
(4) Diplomyelia, or duplication of the spinal cord, appears in the
various foi-ms of double monsters.
DEFECTS OF 1) E VELO P M EN 'J' . <U
(5) Aiioiiialies in the leiic/th and thickness oi' the cord are sometimes
ohscrved the organ being sometimes thick and voluminous, and at'
other times thin and small. It descends at times to the third lumbar
\crtcbra. and ends at other times opposite the eleventh or twelfth
dorsal. A small si/e of the spinal cord has been met Avith in hered-
itarv ataxia.
((')) Asymmetry of the (jray substance has been oljserved in cases of
i iseudo-hypertrophic paralysis, and more especially in cases of con -
Lienital absence of one or more of the extremities.
(7) The pyramidal tracts are absent in anencephalous monsters,
and imperfectly developed in some cases of congenital parencephalus.
Each anterior ])yramid of the medulla may also send the mass of its
libi'es into the spinal cord, either entirely crossed or only partially
crossed, or down the anterior columns almost entirely uncrossed.
(8) Hydromyelus congenitus, or hydrorrhachis interna, is a condition
in which thei-e is a congenital enlargement of the central canal of the
lord, which is converted, in the slighter degrees of the aftection, into a
i-avitv vai'vino- from the size of an ordinarv knittincr-needle to that of
a crow's (piill. The dilated canal may extend the whole length of the
i-ord, be restricted to certain portions, assume a moiiiliform appearance,
> >r present the appearance of a double canal by the growth of adhesions
lietween the anterior and posterior walls. In the higher grades of con-
genital hydromyelus the spinal cord either disappears entirely, or be-
comes split into two halves for a greater or less distance, while the
cavity of the central canal communicates freely with the cavity of the
-])inal arachnoid: the hydrorrhachis interna is then merged into
liydrorrachis externa, as not infrequently happens in spina bifida.
(9) Spina bifida consists of an abnormal accumulation of fluid within
rhe cavity of the sj)inal arachnoid, associated with a greater oi' less
lefonnity of the s])inal canal.
c. Gonyenital Malformations of the Skull and Brain.
(1) Anencephalia. — The upj)er portion of the skull and Ijrain is
entirely absent, and ip occasionally associated with amyelia.
(2) Heniicrania. — The anterior portion of the skull is absent, and
the brain deficient.
(o) Heniicephalia. — The lateral half of the liraiii and skull is de-
ficient.
(4) Notmccphalus. — The upper part of the skull is deficient, and
the vertebral column is not entirely closed in, the brain develoi)ing in
the vertebral canal instead of in the skull.
92 MORBID ANATOMY OF THE NERVOUS SYSTEM.
(;')) ffydrencephalocele.— The bones of the skull are deficient, an
opening being left through which a soft fluctuating tumor projects.
The walls of the tumor consist of the soft coverings of the skull and
the distended membranes of the brain. The tumor c(mimunicates
with the general ventricular cavity of the brain, and can generally l)e
emptied on steady pressure.
(<!) Uncephalocde. — The bones of the skull are deficient, and through
the oi)ening thus caused a portion of the brain projects, forming a
broad, flat, solid tumor. The tumor frequently occupies the fu-ehead,
orbit, or side of the nose.
(7) Parencephalus. — A portion of the hemisphere is deficient, but,
as it is not always caused by a congenital arrest of development, it will
be subsequently described.
(8) Microcephalus is a condition in which the brain as a whole, and
probably the nervous system generally, is arrested in its development.
It occurs in idiots, and the brain is not only small in size, but its con-
volutions also retain the simplicity of arrangement which characterizes
the Simian brain.
(9) Neuropathic constitution is a condition in which the nervous
inheritance of the subject is shown to be defective b}" a functional
incapacity to respond adequately to the ordinary conditions of life, but
without this defect being apjwrent to our means of investigation in the
structure of the nervous system. The predisposition to a particular
disease may be sjyecial and direct, or general and indirect. Migraine,
for example, may be transmitted directly from a mother to her daughtei",
and the attacks of headache generally appear in both al)Out puberty.
In such a case the transmission is direct from mother to daughter, and
the transmitted disease is limited to a particular aflFection. But the
inheritance in this case is also immediate as well as direct and special,
inasmuch as the disease is directly transmitted from parent to child.
But, in a large number of diseases, the inheritance is remote^ the
transmitted affection being derived not immediately from the parent,
but from a grandparent, or a still more remote ancestor. The ])he-
nomena of atavism or reversion, as the remote inheritance is called,
are, indeed, very conspicuous in the transmission of a large nundjcr of
nervous diseases.
In other cases a vulnerable nervous system, named a neurotic or
neuropathic disposition, is transmitted, which favors tlie appearance of
nervous disease. In such cases the tendency to any particular disease
is indirect; and it is also general, inasmuch as one member of a family
may suffer from neuralgia, another from chorea, paralysis, hysteria,
epilepsy, or insanity, while others mav manifest a tendencv to uncon-
DISSOLUTION OF THE NEKYOUS SYSTEM. 03
trollablo alcoholic excesses. At other times the predisposition to ner-
vous disease is still more indirect. One man dies of disease of the
brain, as his father did before him, at a particular age, but it is because
both have inherited gout, which has induced early arterial degeneration,
whieh in its turn has ended in rupture of a bloodvessel in the brain.
In another family several children die about the same age after convul-
sions and coma, but it is because they have inherited a strong tendency
to tubercular disease, and not from inherent weakness of the nervous
system. The inherited tendency to certain nervous diseases is strongly
influenced by age, sex, and race ; but this point need not detain us at
in-esent.
2. Dissolution of the Nervous System.
The law of dissolution is the converse of evolution, and may be
enunciated as a progressive disintegration both of structure and func-
tion, in which there is a passage from the complex to the simple, from
the multiform to the uniform, and from the special to the general.
Before discussing further the application of the law of dissolution to
the phenomena of the diseases of the nervous system, it will be useful
to classify the lesions to which the nervous system is liable — the term
lesion being used hei'e as a generic expression to indicate any morbid
alteration of tissue, whether this alteration be or be not attended by
such structural chan^-es as can be recoo-nized after death by our means
of research.
Classification of Lesions of the Nervous System.
Lesions of the nervous system may be classified (1) according to their
nature ; (2) according to their form : (3) according to the functional
disturbances they produce.
(1) Classification According to the Nature op the Lesion.
(1) lyiflatnmation. — Every part of the nervous system is subject to
inflammation, which, like inflammation of other tissues, may be acute,
subacute, or chronic, -with respect to its course and development. When
the affection is acute it generally ends in complete disintegration of the
affected tissue, which, on being mixed up with fluid and morphological
elements eff"used from the bloodvessels, ])resents a i)ulpy mass technically
called softening. When the inflammatory process is clironic the tissue
undergoes degeneration ; but, inasmuch as degeneraticm may occur
independently of inflammation, ])oth kinds may be included in one
group.
il4 MORBID ANATOMY OF THE NERVOUS SYSTEM.
(i^) Degenerations. — Degenerations of nervous tissues are of various
kinds ; ))ut inasmuch as in all of them the nervous tissue, instead of
undero-oino- softenino- as in acute inflammation, becomes somewhat denser
than usual, they are called scleroses. From the color of the altered
tissue, it is sometimes called gi-ay dcfiencration. Both inflammations
and degenerations include afiectious which have begun in the connective
tissues or neuroglia, the vessels and their adventitite, or the blood itself,
as well as those which are primarily of parenchymatous origin.
(3) Vaseular Lesion.^. — Besides the vascular lesions which accom-
pany all inflammatory and degenerative processes, other very important
diseases in connection with the vessels must be mentioned.
{a) Hypcrcemia and Ancemia. — The vessels are at times actively
dilated so that an undue quantity of blood is sent to portions of the
nervous system, while they are at other times contracted so that the
normal quantity is diminished. The hyperaemia may at times be active
and due to high arterial tension and active dilatation of the ai'terioles.
while at other times it is passive, and is then caused by some obsti-uc-
tion of the blood along the large veins of the body. The ani^mia to
wliich the nervous system is subject does not differ from the anaemia of
other organs, and may, therefore, be due to an alteration of the quality
as Avell as the ([uantity of the blood.
[h) Hemorrhage. — Ru})ture of vessels with consequent hemorriiage
is a very common cause of disease of the central nervous organs, and
especially of the cerebrum. The rupture may at times be due to acci-
dental injury, but more freiiuently it occurs in the degenerative period
of life, and is then caused by various degenerations of the coats of the
vessels, such as atheroma and the fibrosis which accompanies Bright">
<lisease.
(c) Emholism and Thronhosis. — The morbid processes of embolism
and thrombosis, when they occur in the nervous system, are essentially
the same as in any of the other organs of the body. The sudden arrest
of the circulation, caused by obliteration of an artery, causes intense
anaemia and loss of function of the part to which its branches are dis-
tributed. The centre of the ischaemic region usuallv underjjoes necro-
biosis, and its substance becomes altered into a soft pulpy mass closely
resembling inflammatory softening.
(4) Toxic Lesions. — Various chemical agents circulating in the blood
induce morbid alterations of the nervous tissues.
(5) Traumatic Injuries. — Wounds, contusions, and other traumatic
influences cause so many alterations of nervous tissues that their results
deserve to be mentioned amongst the morbid lesions of the nervous
system.
DISSOLUTION OF THE NERVOUS SYSTEM. 95
(6) Compression of Nervous Tismes. — The ner\()us tissues are fre-
(|uently subjected to sudden or gradual compression from various causes.
One of the most frequent causes of compression is the gradual encroach-
ment on the tissues of new formations, no matter whether the growth
l)e outside the nervous tissues or extra-neural, or in the substance of the
tissues or intra-7ieural. Other causes of compression are fractures of
the cranium, dislocations, fractures and curvatures of the vertebrae, the
formation and subsequent enlargement of abscesses and aneurisms, and
the growth of cjsticerci and other jiarasites. Inflammatory effusions
and thickenings of the membranes of the brain or cord, or of the sheaths
of nerves, also injure the nerve tissues by compression as well as by
extension of the morbid process to the nervous tissues themselves.
(2) Classification According to the Form of the Lesion.
(1) Circiimserihed or Focal and Diffused Lesions — Systematic Dis-
eases. — When a lesion is circumscribed within definite limits it is called
•A. focal lesion, and when it extends over an iiidefinite area with irregular
limits it is called a diffused lesion. "When the lesion is limited to a
portion of the nervous s^^'stem which possesses a distinct functional unity,
it is called a system-disease or a systematic lesion; and when several
physiological tracts are implicated, it is called a mixed disease, or indis-
criniinate lesion. A lesion limited to the pyramidal tract in the sj)inal
cord is a good example of a systematic lesion, and a transverse myelitis
of an indiscriminate lesion.
(2) 3folecular, Molar, and Histological Lesions. — In order to study
these diseases under the simjdest conditions, let us suppose that the
sciatic nerve of a frog is isolated, with the gastrocnemius muscle at-
tached. On being stimulated by a strong faradic current, the muscle
immediately contracts ; but a second shock through the nerve is poAver-
less to induce a contraction — the nerve is paralyzed. During the pas-
sage of the nerve from almost perfect health to complete, though tem-
porary, paralysis, the change which it has undergone is such as cannot
be detected by the most refined chemistry, or by the aid of the highest
powers of the microscope. In such case we assume that the molecules
of the axis-cylinder have come to a condition of stable equilibrium ;
hence the cause of the loss of function may be described as a molecular
lesion. It need scarcely be added that a molecular lesion may also give
rise to excess, as well as diminution, of functional activity. The lesion
which I have called 7nolecular has also been termed functional, from
the fact that the part affected, while giving rise to definite functional
disturbances, does not present any apparent structural changes.
But if a portion of the sciatic nerve be crushed or cut, the conductivity
96 MORBID ANATOMY OF THE NERVOUS SYSTEM.
of the nerve is destroyed at tlie point of injury, and a faradic current
applied to the nerve on the central side of the injury Avill not cause the
muscle to contract. The loss of function in this case is caused by a
lesion, which can l)e recognized by the naked eye ; hence it may be
called a molar lesion. Dr. Hughlings Jackson has proi)OSed to call the
molar lesion 1)y the name of " coarse disease," and the molecular lesion
by the name of "fine disease"— names which, at least, possess the merit
of explaining themselves. Between the fine or the molecular lesion on
the one hand, and the coarse or molar lesion on the other, another
variety may l)e interposed. When the morphological elements of tlie
nervous tissues themselves, or of the tissues by which the nervous
elements are surrounded, undergo alterations wliich can l)e recognized
by the aid of the microscope, the morl)id change of structure may l)e
called a Jnstological lesion.
(3) Classification according to the Alterations of Function Produced
BY THE Lesion.
(1) Irritative and Depressive Lesions. — Wlien the morI>id alteration
is attended during life with excess of functional activity, it is inferred
that the lesion is one of an irritative character; or, in other words, it is
inferred that the irritability of the cells and fibres of the part affected
is increased. The opposite condition, in wliicli the irritalulity is dimin-
ished or abolished, deserves a special name and may be called a de-
pressive lesion.
(2) I)is<-har(iing and I>estroying Lesions. — Tlie morbid alterations
which are attended by paroxysmal and excessive liberations of energy
have been called by Dr. Hughlings Jackson discharging lesions. AVi-
have seen that the nerve cells are the main generators and accumulatoi-s
of energy, hence these lesions always im])licate the gray substance,
although it is not always easy to draw a shar]» line of distinction between
discharges of eneruv from f^rav substiince and those which result from
irritation of nerve fibres. When the affection is accompanied by a
distinct destruction of nerve tissue, such as occurs in hemorrhage into
the substance of the brain, Dr. Hughlings Jackson has named it a
destroying lesion.
(1) Dissolution of JVerve Cells and Fibres.
a. Morbid Changes of the Ganglion Cells.
(1) Hypertrophy. — In acute inflannnation the ganglion cells become
swollen, their contents are cloudy and granular, and often pigmented,
and their processes also participate in the same changes (Fig. 48, 2).
DISSOLUTIOX OF THE XERVOUS SYSTEM.
97
(-2) Shrinking. — In the acute diseases of the f,nay suhstance of the
cord the fluid contents of some of the ganglion cells appear to escape,
I he cell-wall shrinks around the nucleus and a small quantity of yel-
l(.Av pigment, and the cell is contracted into a shrivelled mass, which
only presents slight traces of its former structure (Fig. 48, 4). At a
Fig 48.
Ganglion Cells of the Anterior Gray Horns of the Spixal Cord. (Young.)
1, Healthy caudate cell; 2, Hypertrophied cell; 3, Yellow degeneration (the yellow color cannot be
represented here) ; 4, Shrivelled cell ; 5, Chronic atrophy, a group of cells from a case of pseudo-hyper-
trophic paralysis, C, Pigmentary atrophy; 7, Vacuolation, from a case of canine chorea (Gowers) ;
8, ( iironic atrophy, I'lum a case of progressive muscular atrophy — "yellow atrophy."
subsequent period these cells lose their processes and become converted
into small angular masses, in which even a nucleus can scarcely be
detected.
(3) Multiplication of the Nucleus and Nucleolus. — Tlie nucleus
and nucleolus may at times be observed either to have divided into two,
or to exhibit an hour-glass contraction indicating that the process of
division has commenced.
98
MORBID ANATOMY OF THE NERVOUS SYSTEM.
Fig. 49.
Alterations in Nerve Fibres after Section. (After Ranvier.)
1 and 2. Two nerve fibres from the peripheral segment of the sciatic nerve of a hare fifty hours after
section, examined after maceration for twenty-four hours in a solution of perosmic acid; (n) nucleus of
interannular segment, swollen and detached from the sheath of Schwann ; (p) mass of protoplasm, in
which fat granules and drops of myeliue {g and my) may be observed. The medullary sheath is com-
pletely interrupted at the level of the nucleus, while at a it has undergone strangulation.
DISSOLUTION OF THE NERVOUS SYSTEM. 1)9
;i. Ap|iearance presented by the peripheral fibres four days after section of the sciatic nerve of a
hare, originally hardened in a solution of bichromate of ammonia and stained by picrocarmine ; (cy) frag-
ments of the axis-cylinder retracted, somewhat tortuous and embedded in a mass of myeline (my) ;
tp) protoplasm swollen and granular.
4. Fibre same as 3, but originally colored by picrocarmine after maceration in perosraic acid ; (h) nucleus
compressing and partially interrupting the medullary sheath and the axis-cylinder ; p, protoplasm.
5 and 6. Fibres from the peripheric portion of the sciatic nerve of a pigeon three days after section
(same method of preparation as 4). 5. Jledian portion of an interannular segment presenting a single
swollen nucleus (») surrounded by a mass of protoplasm (p). 6. Presents four nuclei (n" n" n" n") in a
single interannular segment. The protoplasm {p) which surrounds them is not segmented, but contains
masses of myeline in its interior.
7 Fibres from the central end of the sciatic neive of a hare ninety days after section (same method of
preparation as 4). Dark upper portion represents primitive nerve fibre surrounded by the sheath of
Schwann (s), and terminating by a knobby enlargement of its medullary sheath (h). From the extremity
of this termination a second tube (l') issues, which divides and subdivides until it forms a bundle of verj-
fine medullary fibres (F), surrounded by a secondary sheath (s*) emanating from the sheath of Schwann;
m, drops of myeline derived from the old nerve fibre.
8. .\ large nerve fibre of the central extremity of the pneumogastric nerve of a hare seventy-two days
after section — maceration in perosmic acid. The medullary sheath (t) terminates by a knobby extremity
(6), and from this extremity secondary medullated nerve tubes (<'<"; issue, as well as fibres without
myeline ; (s) the sheath of Schwann of the primary fibre forming secondary nerve sheath (s') for the
nerve fibres which issue from it.
9. A nerve tube of the peripheric segment of the pneumogastric of a hare six days after section. The
portions a a, which are neither occupied by drops of myeline nor by nuclei, are collapsed, and the tube is
contracted at this level, n n, nuclei of the interannular segment, having undergone proliferation ;
m m, drops of myeline.
(4) Vacuolation. — Two or tliree large .spherical air-space.s named
vacuoles^ may sometimes be observed in ganglion cells which have
undergone a granular degeneration (Fig. 48, 7).
(")) Colloid Dejjeneration. — The hjpertrophied cells of the early
stage of inflammation may subsequently undergo colloid degeneration.
Their processes become transparent, glistening, and brittle, while a
large portion of them are broken off so that the cells assume a rounded
form. The cell-wall has a glassy appearance, and assumes brilliant
tints when stained by various aniline dyes. The colloid appearance
may be the result of post-mortem changes, and consequently con-
siderable cauti(m must be exercised in accepting them as evidence of
disease.
(6) Pigmentary Dcijcneration. — The best examples of pigmentary
degeneration are seen in the chronic diseases of the spinal cord. The
cell-wall becomes contracted around a mass of dark granular pigment,
the nucleus and nucleolus are indistinct or obliterated, the processes are
atrophied, and many of them have disappeared (Fig. 48, 6).
(7) Atrophy. — In chronic diseases the cell-wall becomes dense and
contracted, the processes are broken oif, and the remnant of the cell is
contracted into a small angular mass, without recognizable nucleus or
nucleolus, and finally all traces of the cell may be lost (Fig. 48, 5 and 8).
(8) Calcareous Degeneration. — This form of degeneration is ob-
served on rare occasions.
100 MORBID ANATOMY OF THE XERVOUS SYSTEM.
Although tlic iUustnitions of the morbid alterations of ganglion cells
have been^taken from disease of the caudate cells of the anterior gray
horns of the spinal cord, yet essentially the same changes are met Avith
in the ganglion cells of other parts of the nervous system, and notably
in thos'e of the cortex of the brain. It is scarcely necessary to point
out how these various alterations conform to the law of dissolution.
These alterations, taken as a whole, are a passage from the complexity
and nudtiformity of the caudate cells with their numerous processes and
well-defined connections to the simplicity and uniformity of the round
cell without processes or definite connections.
b. Morbid Changes of Nerve Fibres.
(1) Wallerian Degeneration. — The most notable morbid alterations
of nerve fibres are best studied in the peripheral ends of divided nerves.
"When the ])eripheral portion of a divided nerve is examined two days
after section, the medulla of the divided fibres is found to be coagulated,
opaque, granular, and broken up into cylindrical masses (Fig. 49, 1, 2).
The imcleus (?() of the interannular segment has l)ec()me increased in
size, and contains a large and well-marked nucleolus. The protoplasm
which surrounds the nucleus becomes so al)undant and well develo])ed at
the level of the nucleus, that it fills the calibre of the nerve tube, and
completely interrupts the medullary sheath. The protoplasm at this level,
and at other points where it also accumulates, becomes filled with fine
fat "Tanules into which the myehne has been converted, and a similar
granular debris may be observed outside the sheath of Schwann, and
in the substance of the cells of the endoneuriuni. Duririij; the next
two or three days the segmentation of the medullary sheath proceeds,
and the cylindrical masses become broken up into globular masses
(Fig. 49, 5, 6), which, at the end of the first week after section, are
converted into drops of variable size, amongst Avhich a progressively
increasing nuniljer of fine fat grainiles may be observed. At this
period the altered medulla occupies a larger space than in health, so
that the fibies appear broader than usual, but their outlines are some-
what irregular and wavy. As the morbid processes advance the me-
dulla becomes gradually converted into fat granules, which are finally
absorbed. The axis-cylinder is said by some observers to persist for a
long time after the medullary sheath has disapi)eare(l, l)ut Ranvier
asserts that the protoplasm collects at the level of the interannular
nucleus to such an extent that it compresses, and finallv intersects the
axis-cylinder (Fig. 49, 3, ;? <•?/), which may also at a subsequent period
be cut across by the accumulation of protoplasm at other levels. On
the fourth day after section the nucleus, which is situated neai- the
DISSOLUTION OF THE XERVOUS SYSTEM. 101
middle of an interaniiular segment, contains a large and distinct nucleo-
lus (Fig. 41t, ."), n), which may present an hour-glass contraction, or be
divided into two. After a time the nucleus exhibits a similar trans-
formation, and ends by becoming completely divided into two nuclei,
each of which may subsequently undergo subdivision, and these four
nuclei may l)e found in one interannular segment (Fig. 49, 6, n" n" n" n").
At a later ])eriod of the degenerative process the greater portion of the
medulla is absor1)ed, although some globular masses may accumulate at
certain points in the length of the fibre (Fig. 49, 6, in), the process of
multiplication of nuclei ceases, and even the axis-cylinder disappears
from considerable portions of the length of the fibre. The result of
this process is that the sheath of Schwann is completely empty of its
contents at certain points, and collapses so that the degenerated fibre
appears very slender (Fig. 49, a a). The calibre of the tube is dis-
tended at intervals by elongated nuclei arranged in a series (Fig.
49, 9, n n), by fragments of the axis-cylinder, or by globular masses of
altered myeline (Fig. 49, 9, »?), and the degenerated nerve tube now
appears as a delicate pale band with irregularly undulating contour.
With the disappearance of the medullary sheath the degenerated nerve
loses its white color and assumes a gray appearance, the fibres shrink,
and the nerve looks small and wasted. This process is probably accom-
panied Ijy proliferation of the cells of the endtmeurium, or even of the
perineurium, and in long-standing cases the newl}" found tissue under-
goes cicatricial shrinking, or cirrhosis, rendering the texture of the de-
generated nerve denser and adding to its atrophied appearance.
(2) Regeneratvni of Nerves. — Under favorable circumstances, the
process of dissolution is arrested and a new evolution begins. If the
ends of the divided nerve are maintained in apposition during the repa-
rative process, it is probable that the axis-cylinders of the central and
peripheral ends may become connected before any serious degenerative
changes have occurred in the latter of the two segments. But when
the ends are not in apposition, the nerve tubes of the peripheral seg-
ment become degenerated in their entire extent, and the subsequent
regeneration is eifected by an active growth of the nerve tubes of the
central segment. Several ways are described by Ranvier in which the
central ends give rise to new nerve fibres, but only one or two of the more
common of these will be mentioned here. The central tube terminates
by a slight enlargement of one of the nodes (Fig. 49, 7), and from this
extremity a nerve tube {t') issues, which, although thin, is furnished by
a medullary sheath {s') and interannular nucleus. This tube subdivides
into two others of almost the same size as itself, and each of these in
its turn subdivides into two new nerve tubes, so that the old sheath
102 MOEBID ANATOMY OF THE NEKYOUS SYSTEM.
of Scliwann becomes distended by a bundle of new fibres (Fig. 4<J, 7,
F). Rounded masses of altered myeline {m) are often observed to lie
at intervals between the old sheatli and the young fibres. At other
times several nerve tubes (Fig. 49, 8, t t' t"), some of them possessing
distinct medullary sheaths, while others consist of naked axis-cylinders,
issue from the extremities of the central fibres, and these also extend
towards the pei-iphery. These new fibres, on reaching the peripheral
segment, penetrate for the most part into the interior of the degenerated
tubes; but some of them, according to Ranvier, insinuate themselves
between the old sheath and the substance of the endoneurium. The
duration of the process of regeneration varies according as there is
simple division of the nerve or a portion is resected. It is also influ-
enced by numerous other circumstances, the most important of which
is the length of the peripheral part of the divided nerve, restoration
being so much the slower the longer that portion of the nerve is.
Schiif found complete reunion of divided nerves in young animals in
from seven to fourteen days, and Paget found in two cases of complete
division of nerves traces of returning sensibility in fifteen days. Sen-
sory functions are, however, restored considerably sooner than motor
functions, and, after division of the fiicial nerve, the return of motor
power in the facial muscles only takes place after the lapse of two or
three months. If a portion of the nerve is resected the process of
repair takes a much longer time, and if tlie ])ortion of nerve removed
exceeds two inches regeneration is not likely to take place. The nei've
fibres of the white substance of the spinal cord and brain are found to
undergo a degeneration essentially similar in kind to that just described
as occurring in peripheral nerves. That degeneration of nerve fibres
conforms to the law of dissolution, and their regeneration to that of
evolution, is too obvious to require pointing out in detail.
(3) Hyjyertnyphy of the Axis-cylinder. — In myelitis the axis-cylin-
ders of many of the fibres appear on transverse section two or three
times the normal size, but it is seen on longitudinal section that the
swelling does not extend the Avhole length of the axis-cylinder, the
fibre now presenting a varicose appearance.
(4) Calcareous degeneration of the fibres of the spinal cord has
been exceptionally observed.
(2) Dissolution of the Nervous Tissues.
The morbid changes of the nervous tissues manifest themselves in
(1) the parenchymatous elements; (2) the connective tissue or neu-
roglia ; (3) the bloodvessels ; and (4) the blood.
DISSOLUTION OF THE NERVOUS SYSTEM. 103
(1) Morbid Changes of Parenchymatous Elements.
The morbid changes of the i)arenchyma of the nervous system are
the .^^anie as those ahvadv descril)e(l as occurring in the cells and fibres,
the kind of alterations -which take place depending upon whether the
process is acute or chronic, or it be caused by an irritative or degenera-
tive lesion, or upon various other circumstances.
(2) Morbid Changes or the Neuroglia and Connective Tissue.
(a) Hypertrophy and Hyperplasia of the Connective Tissue. — In
intiammation of nervous tissues the septa of the connective tissue
become swollen, while its nuclei and those of the neuroglia are largely
increased in number. It is also probable that the leucocytes, which
have migrated from the vessels, may subsequently ])ecome organized,
and thus increase the volume of tlie connective tissue.
(h) Interstitial Sclerosis. — When hyperplasia of the connective tissue
has once taken place, the newly formed tissue may undergo cicatricial
contraction, and thus lead to the destruction of the nervous elements,
by a kind of cirrhosis or interstitial sclerosis.
((') G-l'dye's Corpuscles. — These corpuscles ai-e large globular cells
which are distended with granular contents ; they are met in the
nervous system of the embryo in considerable numbers, but are only
sparsely distributed in that of the adult, except in cases of disease, and
then are sup})Osed to be derived from fatty degeneration of the cells of
the connective tissue and neurcjglia, the white corpuscles of the blood,
and the endothelial cells of the capsules of the ganglion cells of blood-
vessels.
{d) Amyloid Corpuscles and Colloid Bodies. — Amyloid corpuscles
(corpora amylacea) are small, round, concentrically laminated bodies,
most of which turn blue or bluish-gray when acted on by iodine, and
assume a l)eautiful blue tint on the addition of sulphuric acid. Colloid
bodies are irregular masses, consisting apparently of changed myeline,
and assuming beautiful tints on being stained with logwood or some of
the aniline dyes. Neither of these bodies affords trustworthy evidence
of disease, inasmuch as they may probably result from post-mortem
mortem changes.
(e) Deiters cells appear to be much increased in number in inflam-
matorv diseases of the nerve centres.
(3) Morbid Alterations of the Vessels.
(a) Intravascular Changes. — The vessels are at times greatly dis-
tended with blood, but this distention may have occurred from the mode
of dying, or from hypostatic congestion after death.
1(14 MOUHIl) AXATOMY OF THE XERVOUS SYSTEM.
{(>) Capillar^/ Extravasations.— In the early stage of inflammation
of nervous tissues the affected part assumes a reddish color, and lie-
comes studded hx a number of capillary extravasations, each about the
size of a pin's head, these being sometimes so numerous that the part
presents the appearance of a hemorrhagic infarct.
{<-) Thirkemn;/ of the walls of the vessels of the nervous system is
found in cln-onic Bright's disease similar to that which occurs in the
vessels of the body generally in that disease.
(d) Perivascular Changes. — The most important perivascular changes
observed in disease of the nerve centres are caused by migration of the
white corpuscles of the blood into the perivascular lymph spaces and
surrounding tissues. The number of leucocytes surrounding a vessel
may sometimes be so great as to constitute what has been called a
miliary ahsress.
(e) Atlieroina and Aneurism. — The vessels of the brain are as sub-
ject to atheromatous changes as those of the body generally, and these
changes are very prone to occur in syphilitic subjects at a comparatively
early age. When the cerebral arteries are diseased the smaller branches
often undergo saccular dilatations, which have been named by Charcot
)inliary aneurisms. They are said to lesult from a kind of arterial
sclerosis of the nature of a chronic periarteritis, consisting of multijdi-
cation of the nuclei of the lymph sheaths and adventitia, with atrophy
of the muscular coats. These aneurisms ai-e liable to rupture, and
thus give rise to massive hemorrhages in the brain. Atheroma of the
vessels may also lead to aneurisms of the medium sizeil and larger
arteries of the brain, which may compress and desti-oy the nervous
substance like other tumors, or cause sudden destruction of large })or-
tions of it by rupturing and giving rise to massive hemorrhages.
(/) Occlusion of Bloodvessels. — In valvular diseases of the heart a
fibrinous mass may be washed off from the left cavities of the heart or
their valves, or from the pulmonary veins, or an atheromatous aorta,
and may be lodged in one of the arteries of the brain, the left middle
cerebral artery being the one most liable to be occluded. This process
is termed cmholis)n. The embolus sometimes consists of a cancerous
nodule washed from the pulmonary vessels in cancer of the lungs, or of
a syphilitic nodule which had projected into the interior of one of the
arteries of the neck or brain. A cerebral vessel may be occliuled l)y
the locid formation of a clot, a process which consti^ites thrombosis.
(4) Morbid Changes of the Blood.
In cases of pysemia, morbid products are conveyed in the blood, and
metastatic abscesses may form in the brain and other parts of the ner-
nSSOLUTION OF THE NERVOUS SYSTEM. 105
vous system, and morbid changes are apt to occur in the nervous tissues
in blood diseases like anaemia, leucocythfemia, and the specific fevei's,
and in those cases in -which the blood contains a chemical poison like
strvchnine, lead, and alcohol.
(")) Nem- Formations.
(a) Neuromata. — Growths in nerves may be divided into (j ) true
and (jj ) false neuromata.
( j ) True neuromata consist of a growth of nerve fibres mixed with
a connective-tissue formation. True neuromata have been divided into
two varieties according to the character of the nerve fibres found in
them. In one form the fibres are medullated, and consequently it has
been called by VirchoAv neuroma myelinirum ; whilst in the other form
the fibres are non-medullated, and the tumor has been named by the
same author neuroma amyeliniewn. True neuromata have also been
divided into several varieties according to the amount and character of
the connective-tissue basis and to the degree of vascularity, the more
usual names applied to them being Jibro-neuroma, glio-ncuroma, myxo-
neuroma., and neuroma tcleangiectodes. True neuromata occur most
fre([uently in spinal nerves, rarely in sympathetic nerves, and still more
rarely in one of the cerebral nerves. They vary from the size of a
millet-seed to that of the closed fist. Neuromata consisting of both
gray and white matter have occasionally been found in the brains of
lunatics, being situated on the surfiice of the ventricles.
(jj ) False neuromata consist of tumors of various kinds, but in
which there is no formation of nerve fibres, these fibres Ijeing indeed
injured or destroyed by compression. The following false neuromata
are met with : fibroma., often forming small knots luimed tubercula
dolorosa; myxoma, frequently met with in nerves, and sometimes con-
taining cysts, when they are called neuroma cysticum ; ylioma, found
in the auditory nerve ; sarcoma occurs in nerves, and transitional
varieties between it and fibroma and myxoma are not unfrequently
observed : carcinoma occurs occasionally as a primary, but much more
frequently as a secondary growth ; syphilitic gumma, most frequently
found in the cerebral nerves ; and lepra nervorum appears as a difliised,
more or less fusiform swelling of the nerves.
The size of neuromata is extremely variable, being sometimes not
larger than a mustard-seed, and at other times as large as a man's head ;
the majority range between the size of a bean and that of a hen's egg.
The number of the tumors is as variable as their size. In some cases
there is only a solitary tumor, while at other times a large number may
100 MORBID ANATOMY OF THE NERVOUS SYSTEM.
be present, either at a circumscribed spot or distributed over the body,
the number in some cases being as high as from eight hundred to sevei-al
thousands.
The nerve sometimes passes on one side of the tumor ; at other times
tlie tumor occupies the centre of the nerve ; while in other cases the
nerve runs directly into the tumor, the fibres breaking up into a kind
of brush or pencil.
(h) Gh'oiiiata form tumors which vary in size from a cherry-stone
to that of the closed fist ; they may be localized in any part of the
brain or spinal cord, but are most frequently found in the hemispheres
of the brain. Gliomata consist of a matrix and an abundant admixture
of round, oval, or stellate cells with granular contents and one or two
nuclei, the structure of the tumor being like that of the neuroglia.
When the cells are abundant the tumor is soft, vascular, of a grayish-
red color, and infiltrates into the nervous tissues : l)ut when the cells
are relatively few, and the matrix, which is fi)rmed of fine fibrillge or a
dense reticulum, is abundant, the tumor is Jiard, not very vascular,
white in color, and it is more or less cii'cumscribed, although never
encapsulated. The hard gliomata are allied in general characters to
the fi])romata, and intermediate forms are met with which are termed
jibro-jiUoiimta. Transitional forms are also observed between gliomata
and sarcomata, named olio-sarcomata. \X other times jjliomatous
tumors undergo a mucoid degeneration, and they then reseml)le myxo-
mata; Avhile some of them are so richly sui)plied by bloodvessels that
they have been named telangiectatic gliomata, these being of great
importance from their liability to hemorrhage.
(c) Hyjjerplasia of the 'pineal (/land is very similar to gli»mm. It
forms a solid, grayish-red, slightly lobulated tumor, which may grow to
the size of a walnut, or larger. In old persons the tumor generally
contains a large number of sand-like bodies.
(d) Myxomata take their origin, like gliomata, from an overgrowth
of the neuroglia, but are }-arer in the brain tlian in the spinal cord and
periphei'al nerves.
{e) Solitary tuhcrde forms a hard, rounded nodule, which varies from
the size of a pea to that of a pigeon's egg, and, on section, the interior
IS seen to be yellowish and cheesy ; while the outer cortex, which is
only about a line in thickness, is of a reddish-gray color, and very
vascular. These tumors are met with in all parts of the brain, but
then- favorite seat is the cortical substance of the cerebrum and cere-
bellum, close upon the cortico-medullary boundary. It is also one of
the most fre(|uent forms of tumor met with in the spinal cord. Tliis
DISSOLUTION OF THE XERVOUS SYSTEM. 107
ruiiiov is often imilti])le, but Avlieii it is solitary it may attain a consider-
able size.
(f) CarcinoiUKtd may gioAv on the outer surface of tlie dura mater,
and, ultimately perforating the bones of the skull, form fungus lucma-
todes of the dura mater. It may also grow from the under surface of
the pia mater, and the growth may then be primary or secondary ; but
primary cancer in this situation is the more common of the two. Can-
cerous tumors of the brain may be single or multiple. They destroy
the neighboring tissues by pressure and infiltration, and are usually
suri'ounded by a zone of softened tissue, of about a line in breadth, in
which active growth proceeds.
(//) Cholesteatoma, or })earl cancer, appears to be derived from the
l)ia mater, and is usually situated in some hollow at the base of the
brain. The tumor, on section, is hard, pearly, non-vascular, and com-
posed of epidermic cells, arranged in concentric layers, which have
undergone partly horny and partly fatty degeneration. The tumor is
enclosed in a delicate fibrous capsule, and its surface presents a beautiful
mother-of-])earl lustre. These tumors grow very slowly, and may remain
for a long time without giving rise to symptoms.
(//) Papilloma of the cere])ral pia mater is occasionally met with.
(^) Syp1nlomat(( may reach the size of a walnut or of a hen's egg,
and are usually found near the surface of the brain, developing from
the perivascular sheaths. They are only met with in the cord on rare
occasions.
{k) Sarco)nata aj)j)ear as hard, slightly vascidar, round, somewhat
nodulated tumors. Every variety of sarcoma is found in the brain,
and transitional forms between sarcoma and other tumors are named
fflio-sarcoma, myxosarcoma, etc. In some of the spindle-celled sar-
comas the cells are arranged in concentric layers or nests, and conse-
quently this form has been named "nested sarcoma."
(?) Melanoma is a pigmented sarcomatous tumor Avhich springs from
the pigment cells of the pia mater.
(m) Lipoma has occasionally been met with on the inner surface of
the dura mater, and the raphe of the corpus callosum, and the fornix.
in) Psammomum is a tumor with a basis of connective tissue, or
sometimes of mucoid tissue, which is distinguished by containing calca-
reous concretions. It appears to be a calcareous deposit in tumors of
widely different structure, the most frequent of these being nested
sarcoma.
(o) Osteomata are the rarest of all intracranial growths.
(p) Cystic growths are caused 1:)y a portion of the posterior cornu
of the lateral ventricle l)eing cut off from the general cavity by dropsy
108 MORr.ID ANATOMY OF THE XERVOUS SYSTEM.
of the septum lucidum, and cystic degeneration of the pineal gland
and pituitary body, and gliomatous tumors.
(r) Angiomata generally occur in the l)rain as a complication of
other tumors such as glioma. Pachymengitis hc\?morrhagica belongs to
this class.
(6) Ankurism.
Aneurisms of the larger cerebral vessels are not very rare, and when
they attain to a considerable size they give rise to the usual symptoms
of an intracranial growth.
(7) Parasites or thp: Brain.
[a) Cysticcrcus cellulosa is met with in the parts of tlie l)rain which
are richly supplied with blood, and the parasite is sometimes found in
other parts of the body as well as in the brain. Cerebral cysticerci
are usually enclosed in a soft capsule, in which the animal may be seen
with the naked eye as a small tubercle, and its neck, with the charac-
teristic booklets, may be discovered on microscopic examination.
(b) Echinococcus hominis form cysts Avhich often attain to a large
size in the brain. In a case reported by Dr. Morgan the cyst Aveighed
eighteen and a half ounces, and contained eighteen ounces of serum.
They reach their greatest size in the hemispheres and the ventricles,
especially in children before the foutanelles are closed. The cyst is
composed of an external fibrous membrane, which encloses the para-
sites ; its internal surfice is lined l)y small l)uds, each about the size of
a millet-seed, which are provided with the characteristic ring of booklets.
o. Dissolution of thk Nervous System {continued).
a. 3fassive HcmorrJiagcs.
Massive hemorrhages generally destroy a considerable portion of the
nervous system. In the recent condition the apoplectic focus forms a
dark red soft clot, which is frequently mixed wdth the debris of the
brain substance. The internal surfiice of the cavity is irregular and
consists of torn shreds of cerebral tissue, and it is surrounded ])y a
zone of variable thickness in which the tissue is softened by the inhibi-
tion of serum, and in which numerous punctiform hemorrhages are
observed. If the patient survives, the tissues surrounding the blood-
clot become softened partly by the imbibition of serum and partly from
a retrograde fatty metamorphosis of the torn fragments of brain tissue,
and the softened tissues, when mixed up with the blood clot, form a
DISSOLUTION OF THE NERVOUS SYSTEM. 109
dark cliocolate-i-olored mass of the consistence of gruel. The hcematin
uoAv becomes grachially absorbed, and the substance filling the cavity
changes to a brighter red or saffron color. After a time a fibrous cap-
sule forms round the clot, and the solid constituent becoming absorbed,
a cyst is formed -which contains at first a turbid, and subsequently a
clear, limjjid, or straAv-colored fluid, having frequently suspended in it
a film of loose spongy connective tissue. When the cyst is small, and
the fluid is absorbed, the opposite walls may come in contact and
mlhere by a connective tissue, -which usually contains a considerable
amount of pigment, and gives rise to the appearance known as the
a|)()plectic or hemorrhagic cicatrix.
h. Jlorbid Changes caused by Occlusion of Bloodvessels.
^Vhen a terminal artery becomes occluded the arterioles and vessels
of the ])art are imperfectly nourished, and consequently their walls
dilate and fre<|uently rupture, the former causing redema and the latter
hemorrhage. The softened tissues are named red, yellow, or white
softening according as a considerable amount, a moderate amount, or
no 1)lood is extravasated from the vessels.
e. Morbid Clianges caused by Thickening of the Walls of the
Arterioles.
The walls of the Ijloodvessels of the nerve centres become thickened
in Brights disease, and the nervous tissues surrounding the altered
vessels undergo, in some cases, morbid changes more or less similar to
those of chronic inflammation, and consisting of an increase of connec-
tive tissue and destruction of nerve cells. This condition may be
named vascular sclerosis.
d. Inflammation of the Nervous System.
(1) Acute inflammation of nervous tissues is characterized in its first
stage by congestion, capillary extravasations, and some oedema of the
tissues. If the ju'ocess proceeds further, it causes softening of the
inflamed part. Inflammatory softening may be divided into (a) red,
{b) yellow, (c) white, {d) gray, and ie) green or purulent softening.
[a) Red Softening. — The spot affected with red softening is soft,
and swells up aljove the level of the surrounding surface on section.
The aflected tissue may be washed away by a gentle stream of water,
or it may be diflHuent. Numerous capillary hemorrhages may be ob-
served, and the aflected part assumes a tint which varies from rosy to
deep red, reddish-broAvn, or chocolate.
11(1 M(.KIUI) ANATOMY OF THE XEKVOUS SYSTEM.
(//) Yellow Softenhu/.—A^ tlie disease progresses the affected parts
l.t'coiiie i)aler and softer, and the color changes to veHow. partly from
diffusion and alteration of the coloring matter of the Idood, and partly
from degeneration of the medullary sheath.
{<■) White Softniinij. — Owing to the continued process of fatty de-
generation the color hecomes progressively whiter, and the diseased
portions assume a creamy oi- milky appearance, and on section the
medulla swells up ahove the surface of the surrounding tissues.
{d) Gray Softening. — In consequence of the absorption of fat gran-
ules and nerve substance, the affected part gradually assumes a grayish
eolor, and finally becomes smaller and more depressed than normal.
{e) Green Softenim/. — The white blood-corpuscles may migrate in
such large numbers that the affected ])art is converted into a cavity
containing a greenish purulent fluid, and constituting an abscess.
Microscopical Cha)u/es. — In the early stage of inflammation the
arterioles and capillaries are dilated and distended with blood, while
they may be enveloped in layers of migrated white and red blood-
corpuscles. As the disease advances the walls of the vessels become
tliiekened and studded with fat granules and granule cells, Avhile the
lymph sheaths are tilled with granular or cellular exudation. The reti-
culum of the neuroglia is swollen and thickened, and filled with nuclei,
lymphoid cells, and granule cells, while Deiters cells are increased in
number. The nerve fibres present irregular contractions and enlarge-
ments, the medullarv sheath becomes broken down into globules and
is finallv absorbed, and the axis-cvlinders are greatly swollen, while in
the second stage the medullarv sheaths are in a state of fattv degenera-
tion, and the axis-cylinders are altered or destroyed. The ganglion
cells are first swollen, the nucleus and nucleolus may l)e observed in
process of division, while at other times they undergo vacuolation, the
cell processes are swollen, cloudy, irregular in shape, and partly de-
stroyed, and at a later period the cells lose their processes, and shrivel
so as to become- reduced to small angular masses without structure.
When a cicatrix has formed, the affected spot is occupied by a dense
connective tissue containing many nuclei and neuroglia cells, and numer-
ous Deiter's cells. When cijsts are formed they are surrounded by a
more or less dense layer of connective tissue, and are generally trav-
ersed by a loose connective-tissue network.
The morbid appearances just described apply more particularly to
those occurring in the spinal cord and termed' ctcute myelitis, and in
the brain and named acute encephalitis, l)ut essentially the same
changes are met with in acute inflammation of nerves. When the
inflammation begins in the nerve fibres the process is named neuritis,
DISSOLUTIOX OF THE NERVOUS SYSTEM. lU
and when in the slieath of the nerve it is named perineuritis. In acute
neuritis or periaeuritis the vessels become enhu-ged and distended, and
the nerve-trunk is swollen from serous, gelatinous, or fibrinous exudation.
If the inflammation subside at ari early date the effusion is absorbed
l)efore there is any destruction of the nerve fil)res, and the healthy
condition is reestablished. If the inflammatory action is very acute
and severe, both white and red corpuscles escape from the vessels, the
color of the nerve l)ec()mes yellow or brownish-red, its tissues are infil-
trated with sanguineous pus, abscesses may form around its trunk, and
the entire structure may l)ecome completely disintegrated.
(2) Chronic inpmimation causes the aifected part, as a rule, to be
atrophied, and unusually dense or in a state of sclerosis. When the
white substance is the subject of chronic inflammation it assumes a gray
color, and consequently the condition is sometimes called (p'iiy degene-
ration. When the inflammation spreads over a considerable area of
tissue it is named diffused sclerosis ; when it is limited to the embrvo-
logical tracts of the cord it is named an ascending or a descending
sclerosis, according as the process extends from below upwards oi- from
above downwards ; when it is limited to certain spots or foci it is named
circumscribed or insular sclerosis ; and when these spots are numerous
and distributed in diff"erent parts of the nervous system, it is named
multiple or dissoninated sclerosis. The terms insular, multiple, and
disseminated are applied indiff'erently to the same disease, because, when
the sclerosis is limited to circumscribed spots, the spots are also mul-
tiple and widely distributed over the nervous system. When the
sclerosis is more or less restricted to the embryological tracts the
morbid process is supposed to begin in the nervous elements themselves,
and consequently some anatomists have called this form of chronic
inflammation parencliymatous sclerosis. This distinction is admissible
theoretically, l)ut it is not always easy to maintain it practically. A
microscopical examination of a part in a state of sclerosis shows that
the connective-tissue septa are thickened, and that the cells of the neu-
roglia are swollen and their nuclei multiplied. Deiters cells are also
increased in size and number, and in long-standing cases the neuroglia
becomes converted into a dense fibrillated connective tissue in which a
large number of nuclei are observed. The nerve fibres undergo changes
more or less similar to those which occur in secondary degeneration of
the fibres of the peripheral nerves. The medullary sheath undergoes
granular and fatty degeneration, and is finally absorbed ; but the axis-
cylinder persists a long time, although it becomes swollen at certain
points, and, on being viewed longitudinally, presents spindle-shaped
enlargements. After a time the axis-cvlinders also Avaste and disappeai\
[[•1 MOHHID AXATOMY OF THE NEEVOUS SYSTEM.
and nothing- remains l»ut a dciise fil)i'illate(l connective ti^^ue. The
ualls of the small arteries and veins become thickened, and their calibre
is diminished in size. The lymph spaces are destroyed, or contain fat
and jiigment granules, while granule cells and corpora amylacea are
found scattered through the diseased tissue.
The morbid apjiearances just described are met with in the nervous
centres, but essentially similar alterations occur in nerves. In chronic
neuritis and perineuritis the trunk of the nerve becomes irregularly
vascular, and is enlai-ged in some places and atrophied in others. The
sheath of the nerve is thickened, fibrous, and resisting, while it is fre-
(|uentlv adherent to the adjacent tissues. In cases of perineuritis the
nerve filtres are compressed by the exudation and disappear after a
time, so that tlie sti'ucture of the nerve is supplanted by a band of
connective tissue.
Segmental periaxillary neuritis, induced l)y Gombault in the perij)h-
eral nerves of guinea-pigs, is a parenchymatous neuritis in which only
a part of the nerve fibre is implicated. A segment lying between two
of the nodes of Ranvier is diseased, while those on each side of it may
remain healthy. Several seginents may, however, be affected in the
course of one fibre. The medullary sheath and the protoplasm of the
fibre are at fii-st alone implicated in the morbid change, while the axis-
cylinder remains for a long time uninterrupted. After a time the
diseased segment may either be restored by the growth of a new medul-
lary sheath, or the axis-cylinder becomes ruptured, and the ])eripheral
end of the nerve then undergoes the Wallerian degeneration.
e. Degenerations of the Nervous System.
(1) Primary Degeneration.
Tlie gray substance of the nervous system may apparently undergo
a primary chronic degeneration in addition to the degeneration which
is consecutive to inflammation. In the primary degeneration the nerve
cells undergo atrophy and various forms of ])igmentarv defeneration.
This form of degeneration occurs most probably in the gray substance
of the anterior horns of the spinal cord in progressive muscular atrophy,
and in the cortex of the brain in the chronic forms of insanity. It is
possiVde that the white substance may also undergo a primary chronic
degeneration, and the disease known as progressive multiple neuritis
appears to be a primary degeneration of the peripheral nerves. The
morbid changes which have been found in the nerves in this disease
consist of partial or complete destruction of many of the nerve fibres.
The perineurium of the individual bundles has also been found thick-
DISSOLUTION OF THE NERVOUS SYSTEM. 118
ened, and Levden has observed an accumulation of fat cells between
the bundles, and a deposit of pigment around the bloodvessels. Lev-
den regards this pigment as a hemorrhagic inflammation of the tissues
between the nerve fibres, and he believes that the absence of any sio-n
of multiplication of nuclei proves that the nerve fibres had become
atrophied through the compression caused by the congestion of the
tissues surrounding them.
(2) Secondary Degenerations.
The Wallerian degeneration of peripheral nerves has already been
described, but we have now to point out that essentially the same pro-
cess occurs in the conducting paths of the nerve centres. It has
already been stated that Waller observed that when a mixed nerve is
divided the peripheral portion degenerates throughout its whole course
in a few weeks, Avhile the portion attached to the cord does not degen-
erate. This statement, however, is only a portion of the truth. He
also found that while the efferent fibres degenerate their whole length
on division of the anterior root, that the peripheral portion of the
afferent fibres do not degenerate on division of the posterior roots. On
division of the posterior roots what takes place is that the peripheral
portions which are attached to the spinal ganglion remain healthy, but
the small central portion which is attached to the cord soon wastes.
From these facts Waller concluded that the efferent fibres receive their
nutritive influence from the caudate cells of the anterior horns, and the
afferent fibi'os from the ganglia of the |)OSterior roots, and he then
formulated the general law that nen'e fibres ilegenerate when they are
se])arated fi'om their trophic centres.
The central conducting paths also undergo degeneration in one direc-
tion after division or injury of them, and it may be confidently asserted
that the degeneration occurs along the line of conduction of the fibres, some
paths undergoing an ascendinf/ and others a di'scending degeneration.
(a) ASCENDING DEGENERATIONS.
The trophic centres of the columns of (roll and of the direct cere-
bellar tracts are situated at their inferior extremities, the ganglia of
the })osterior roots or the gray substance of the posterior horns forming
the trophic centres of the former, and the cells of the vesicular colunms
of Clarke probably those of the latter. The lower limit of the de-
generation of these columns will depend upon the position of the lesion
of the cord which interrupts the continuity of the fibres, and the
deoeneration of the columns of Goll may extentl from the lumbar
8
114 MORHII) ANATOMY OF THE XERVOUS SYSTEM,
region of the cord up to tlie termination of the fibres in the cuneate
nucleus, while the degeneration of the direct cerebellar tracts may
extenil from the inferior part of the dorsal region up to the external
surface of the restiform bodies. In both of these degenerations the dis-
eased area increases progressively in size from below upwards (Figs.
50, 51, 5:2). A case is reported by Dr. Gowers in which the lower
Fig. 50.
Fig. 51.
TnANSVERsE Sections op the Spinal Cord, fro-ai the middle of the Cervical Enlargement,
MIDDLE OF THE DoRSAL RF-GION, AND MIDDLE OF THE LUMBAB EEGION, RESPECTIVELY, SHOWING ASCEND-
ING Degeneration of the Cdlvmns of Goi.L(g), and op the direct Cerebellar Tract (dc).
extremity of the spinal cord was crushed by a fracture of the spine,
and in which, in addition to the ascending degeneration of the columns
of Goll, a small area of degeneration w^as observed in each anterior
root-zone in front of the lateral pyramidal tract, the latter being
healthy on each side. Dr. Gowers suggests that these areas constitute
a part of the sensory conducting paths. In lesions of the cauda
equina, and sometimes after severe traumatic injuries of the sciatic
nerve, the posterior root-zones as well as the columns of Goll undergo
ascending degeneration in the lumbar and greater portion of the dorsal
regions, but the degeneration becomes limited to the columns of Goll in
the upper dorsal and cervical regions. In transverse lesions of the
cord the posterior root-zones may also be found degenerated for a short
distance above the lesion, but the evidence of degeneration soon ceases,
probably because the fibres of these columns soon tei-minate in gray
matter.
{()) DESCENDING DEGENERATION.
(j) Sclerosis of the Pyramidal Tract.
Lesions of the cortex of the brain, provided the whole thickness of
the gray substance is implicated, are followed by descending degenera-
tion of the fibres of the pyramidal tract Avhich may be followed tiirough
the internal capsule, crusta, longitudinal fibres of the pons, anterior
pyramids of the medulla oblongata on the anterior column of the same
side as the lesion, and in the lateral columns of the cord on the side
opposite the lesion. A descending degeneration of this kind has also
been found in animals after extirpation of portions of the motor area
of the cortex of the brain.
DISSOLUTIOX OF THE NERVOUS SYSTEM.
115
A focal lesion limited to the middle third of the internal capsule
(F\<s. 08, F) is followed by descending degeneration of the fibres of the
middle third of the crusta (Fig. 54, D), and of a portion of the longi-
tudinal fibres of the pons and the anterior pyramid of the medulla on
the same side. The greater part of the degenerated fibres cross over
at the lower end of the medulla oblongata to reach the lateral column
f)f the opposite side of the cord (Figs. 55, 56, 57), while a few of them
pass doAvn the column of Tiirck on the same side.
Fio. 53.
H'liiizoxTAL Section of the Eight Hejiisphere Parallel with the Fissuke of Sylviu;s. (Charcot.)
Xc, Caudate nucleus ; Sa, Anterior segment of the internal capsule ; Nl, Lenticular nucleus ; G, Knee
of the internal capsule ; Sp, Posterior segment of the internal capsule ; Co, Optic thalamus ; F, A focal
lesion in the middle third of the posterior part of the internal capsule.
In diseases of the spinal cord the degeneration is generally bilateral
and symmetrical, and the positions occupied by the diseased areas at
different levels of the cord are represented in Figs. 58, 59, 60. When
the disease reaches to the medulla oblongata, the areas of degeneration
are limited to the anterior pyramids.
The portions of the pyramidal tracts which belong to the nuclei of
lie. MORBID ANATOMY OF THE NERVOUS SYSTEM.
the medulla ol)l()ngata ami pons are sometimes diseased in the absence
of any affection of the spinal pyramidal tracts.
(jj ) De<ieneration of the Fillet and Superior Peduncle of the Cerebellum.
In a case reported by Homen, a focus of softening was found in the
lateral half of the upper part of the pons, and the pyramidal tract of
Fig 54
F L n
Horizontal Section of the Crura Cerebri in a case or Secondary Degeneration. (Charcot )
T, Tegmentum ; F, Crusta of the healthy side ; L, Locus uiger ; D, The degenerated fibres, occiii),viug
alidut the middle third of the crusta ; P, The fibres which undergo secondary degeneration imly when the
fibres (if the anterior segment and the knee of the internal capsule are diseased
that side was degenerated below the seat of the lesion as far as to the
lower end of the medulla oblongata, the streak of deo;eneration being
Fig. 55.
Fig. 5fi
Transverse Sections oe the Spinal Coed, from the middle of the Cervical Enlargement,
MIDDLE of the DoHSAL EEGION, AND MIDDLE OF THE LUMBAR KEGION, RESPECTIVELY, SHOWING DE-
SCENDING Sclerosis of the Pyramidal Tract in the L.a.teral Column Secondary to a Terebral
Lesion. (Charcot )
.\, .\, A, Degenerated pyramidal tracts.
found in the part which lies to the inner side of the olivary body. In
a case reported by Meyer, a focus of softening was found in the lateral
half of the lower part of the pons, which embraced tlie nucleus of the
DISSOLUTIOX OF THE NERVOUS SYSTEM.
117
sixth nerve, the foniiatio reticularis, and the superior olivary body.
Below the level of the lesion the internal division of the fillet and the
olivary body were degenerated. The degeneration of the fillet could
Fig. 58
Fig. 50.
Fig. 60.
Traxsveuse Sections of the Spinal Cord, from the middle of the Cervical Enlarokment, middle
OF THE Dorsal Region, and middle of the Lumbar Region, respectively, showing Primary Lateral
Sclerosis of the Cokd, or Secondary to a Lesion high up in the Cord or Medulla Oblongata.
(Charcot.)
A, A, A, Pegenerated pyramiilal tracts.
be traced as far as the level of the decussation of the pyramidal tract,
and it was represented immediately below this level by a small spot of
degeneration near the periphery of the external division of the anterior
Fig. 61.
Recent Softening of the Frontal Lobe, the Island op Reil, and Middle Third of the
Lenticular Nucleus. (Brissaud )
D, GUI focus of softening occupying the knee of the internal capsule ; A, Caudate nucleus ; B, Optic
thalamus ; C, Anterior, and E, Posterior division of the internal capsule.
root-zone, immediately behind the anterior nerve roots. Above the
level of the lesion a secondary degeneration of the fillet could be traced
as far as the posterior tubercle of the corpora quadrigemina.
118 MOKBU. ANATOMY OF THE NEEVOUS SYSTEM.
A case lias been described bv Brissaud in whicb, along with exten-
sive recent softening of one hemisphere, an ohl focus of softening was
observed limited exactly to the knee of the internal capsule (Fig. bl,
D) A streak of degeneration was observed lying between the internal
and middle thir.ls of the crusta, being the anterior portion of the area
which has alreadv been described as the mixed area of medullated and
non-medullated fibres in a nine months' embryo. According to Bris-
saud, degeneration occurs in the knee of the internal capsule in cases
of long-standing aphasia.
Fig. r,2.
A, Caudate nucleus; B, Optic thalamus; C, Posterior iiml licaltliy part of the lenticular nucleus; D,
Posterior segment of the internal capsule ; E, Lesion of the anterior segment of tlie capsule ; F, ( 'yst
presenting the form of the lenticuhir nucleus ; P, Degeneration of the internal fibres of the crusta.
(Brissaud.)
Another important case has been observed by Brissaud, in Avhich an
old focus of softening was found in the anterior half of the lenticular
nucleus, destroying also the anterior segment of tlie internal capsule
(Fig. 62, F), A streak of degeneration was observed in the internal
third of the crusta (Fig. 62, P), but all the fibres of this area were not
implicated in the degeneration, a small bundle of tlie innermost fibres
DISSOLUTION OF THE XERVOL'S SYSTEM.
119
remaining normal. The degenerated fibres in this case corresponded
very nearly to those which we have described as the accessory fibres of
the tract. Degeneration of the internal tract of the crusta, accordin^j;
to Brissaud, appears to beahvays connected with intellectual disorders.
It is important to remember that a fcAv cases have been reported of
destructive lesions localized in the motor area of the cerebral hemi-
spheres, but in which no secondary degenerations Avere discovered in
the internal capsule, crura, pons, medulla oblongata, or spinal cord.
Fig. C,?,.
Th.o.^
Herd
DiAiiEAM OF THE Ol'TK TlIALAMI, TEGMENTUM, ANT) SvPEaiOR PehUXCLES OF THE ( 'EHEBEI.LVM.
(After Mendel )
3V., The third ventricle; Th.o., The optic thalamus; S.t, The red nucleus of the tegmentum; B.,
Superior peduncle of the cerebellum : C.d., Corpus dentatum of the cerebellum ; Herd, The diseased
focus. The dark line between the diseased focus and the corpus dentatum of the opposite side represents
the streak of degeneration.
The following bundles of fibres may, therefore, be distinguished in
the internal capsule :
(1) A posterior or sensory fasciculus (occupying the external third
of the crusta), Avliich is never the seat of secondary degeneration.
■ (2) A middle fasciculus (occupying the middle third of the crusta).
which is the usual seat of secondary degeneration.
(3) A geniculate fasciculus (occupying the point of union of the
middle and internal thirds of the crusta), which has erroneously been
regarded as incapable of degeneration. This fesciculus contains fibres
which are distributed to the bulbar centres, and are concerned in the
])rotluction of the voluntary movements of the face and tongue.
1-J(I MOHBTl) ANATOMY OF THE NERVOUS SYSTEM.
(4) An (interior fa^ekuhts (occupying the internal third of the
cnistii), degeneration of which appears only to be associated Avith
intellectual disorders.
A descending degeneration of a fcAv of the fibres of the superior
peduncle of the cei-ebclluni has been observed. In a case reported by
Menilcl, in which the patient had suffered, after a slight apoplectic
attack, from right-sided hemiparesis and transitory right-sided henii-
anivsthesia, Avith left-sided heraiopia, a hemorrhagic focus about the size
of a pea Avas found in the pulvinar of the left optic thalamus, close to
tlic internal capsule. Slight evidences of descending degeneration of
the pyramidal tract on both sides of the cord Avere found, and, in addi-
tion, a streak of degeneration was followed downwards to the internal
aspect of the red nucleus of the same side ; it then ascended in the
tegmentum and crossed over to the superior peduncle of the cerebellum
of the opposite side, and was followed as far as the corpus dentatum of
the right hemisphere of the cerebellum (Fig. 63).
(c) DKOENERATIONS OF NERVE CENTRES AND CONDUCTING PATHS FROM DISEASE.
( j ) Secondary Degeneration of the Spinal Cord after Amputation.
In cases of long-standing amputation of limbs, the posterior roots of
the nerves are found slightly diminished in size. The posterior gray
horn on that side is also relatively diminished in size, Avhile some of
the ganglion cells of the anterior horns completely disappear, and
others are diminished in size and shorn of their processes.
( jj ) Degeneration of Sensory Ganglia and Conducting Paths.
The facts so far knoAvn with regard to degeneration of sensory con-
ducting paths in human pathology are very scanty. Wlien unilateral
blindness has existed for a long time the optic nerve on the lilind side
has been found atrophied, but the tract of the oi)posite side is aifected
to a greater degree than that of the same side. The external genicu-
late l»ody and the anterior tubercle of the corpora quadrigemina on the
side oi)posite the blind eye have also been found smaller than the corre-
si)onding i)arts on the same side. Similar phenomena have been found
by Gudden after extirpation of one eyeball in young animals. Tlie
parieto-occipital convolutions of the left hemisphere of the brain were
extirpated by Gudden in a young dog, and he afterwards found that
the external geniculate l)ody and the optic tract of the same side were
atrophied. Experiments of this kind have recently been cai-ried out
systematically by Monakow, and he finds that extirpation of circum-
scribed portions of the cortex is followed by atrophy of strictly defined
DISSOLUTION OF THE NERVOUS SYSTEM. 121
parts of the optic thalamus and adjoining ganglia. The author distin-
guishes the folloAving areas of the cortex : (1) Tlie zone of the rorpm
geniculatum externum, so named because extirjjation of it caused atrophy
of this ganglion. This area is situated in the posterior superior part
of the hemisphere ; it forms about one-third of the hemisphere and
corresponds to Munk's visual sphere. In addition to the external
geniculate body, the posterior third of the internal capsule with the
part of the corona radiata which lies between it and the injured cortex,
the lateral layer of the optic thalamus, the stratum zonale in part, the
optic tract, and in a less degree the tractus peduuculus transversalis,
the anterior tubercle of the corpora quadi'igemina, and the optic nerves
were also atr()[)hied. (2) The zone of the internal genieulate hody,
which is situated below the first area and corresponds to Munk's audi-
tory sphere. Extirpation of this area was folloAved Ijy atrophy of the
posterior inferior portion of the internal capsule, along with the portion
of the corona radiata which joins the atrophied part of the cajisule with
the injured portion of the cortex, and in a less degree the posterior
part of the stratum reticulatum, (3) The zone of the lateral nucleus
of the optic thalamus, which lies in front of the first zone or visual
s})here. Extirjiation of it was followed by atrophy of the external
nucleus of the optic thalamus, the outer portion of the crusta, and to a
less extent the formatio reticularis, the middle peduncle of the cere-
bellum, and the corpus trapezium. (4) The zone of the stratum reti-
culatiun (Gitterschicht) lies to the outer side of the last zone. Extir-
pation of it causes atrophy of the third fifth of the internal capsule, a
part of the lateral portion of the crusta, the anterior part of the stratum
reticulatum, and to a less degree of the portion of the tegmentum Avhich
lies between the external geniculate body and the posterior tul;)ercle of
the corpora quadrigemina. (5) The zone of the anterior tubercle of
the optic thalamus is situated in front of the third zone. Extirpation
of it causes atroj)liy of the anterior tubercle of the optic thalamus, the
anterior part of the internal capsule, a part of the pyramidal tract, and
to a less degree of the lamin;e medullaris of the anterior tubercle,
and the bundle of Vic(i( d'Azyr. ((')) The zone of the internal nucleus
of the optic thalamus occupies the anterior area of the cerebral cortex.
Extirpation of it causes atrojjhy of the most anterior portion of the
internal capsule, and partial atrophy of the pyi-amidal tract aiul the
internal nucleus of the optic thalamus. (7) External to the zone of
the anterior tubercle lies another zone, extirpation of which causes
atrophy of the anterior portion of the internal caj)sule, and of a tract
which runs direct to the crus cerebri, which is suppose<l by Monakow
to contain fibres of the fjicial and hypoglossal nerves.
1:^-2 GEXEEAL MOKHID AXATOMY AXD PHYSIOLOGY.
11. GENERAL MORBID ANATOilY AND PHYSIOLOGY'.
Tlie i)i-ol>lem of morbid physiology is to interpret morbid functions
by morbid .structures, and the hiw ^vhich underlies all our conclusions
is that every disordered function is the correlative of a diseased struc-
ture : and, invensely, that every diseased structure has for its counter-
pnrt a derangement of function. It may be laid down as a general
law that, when the irritability of a nervous structure is increased, it
will manifest increased functional activity.
It may be supposed that a free arterial sui)ply to a part, or a flushed
condition of the arterioles, is the necessary correlative of increased
irritability ; and, conversely, that a diminished arterial supply, with
an empty and contracted condition of the arterioles, is the necessary
correlative of diminished irritability. This statement, however, can
only be accepted as true within certain limits and with numerous (piali-
fications. When the brain, for instance, is very freely supplied with
blood so that its substance becomes congested, the irritability of the tis-
sues is no doubt at first increased. It must, however, be remembered
that the cranium is unyielding, and its contents practically incompressi-
ble, so that no additional (juantity of blood can enter into the intra-
cranial vessels except Ijy displacing a corresponding (piantity of some
other fluid. When, therefore, the vessels become dilated beyond certain
nari-ow limits the nervous tissue becomes compressed, the material e.x-
changes within the cranium become less than when the circulation passes
in normal (juantity and under normal pressure, and the functional
activity of the organ is diminished or abolished. A similar process no
doubt occurs in the spinal cord and nerve trunks. Congestion in them,
when carried beyond certain limits, is also attended with diminution of
function, due, no doubt, to compression of the nerve tissues by the
dilated vessels. The irritative lesion is attended with increased nutri-
tive activity, and C()nse(iuently with free arterial supply ; but this lesion
is exceedingly apt to terminate in the opposite condition of diminished
nutrition and functional activity. The first stage of inflammation, for
instance, is an irritative lesion, and it is attended by excess of func-
tional activity, manifesting itself by symptoms of hyperesthesia and
hyperkinesis ; Init when the nervous tissues become partly compressed
by effiised pi-oducts and partly disorganized by internal changes, the
lesion becomes depressive, and the symptoms of excess give place to
those of diminution of function; in other words, the symptoms of
hyperaesthesia and hyperkinesis give place to those of anesthesia and
akinesis.
GENERAL MORBID AXATOMY AXD PHYSIOLOGY. 123
But if excess of nutrient activity is not always accompanied bv
increased functional activity, neither is diminished nutrient activity
always accompanied by diminution of functional activity, When the
nutrition of a nerve fibre is gradually lessened its irritability becomes,
indeed, increased instead of diminished. The stock of irritable matter
which the nerve fibre possesses is no doubt less under these circum-
stances, but an increased readiness to discharge the energv is mani-
fested : and it is notorious that feeble and angemic persons manifest an
undue readiness to respond to the action of stimuli of all kinds, a
condition which is correctly designated nervous irritahUity. One other
important consideration must be taken into account before the amount
of nourishment supplied to an organ or a tissue can be accepted as in
any way a measure of the functional activity of the latter. When a
strong faradic current is sent through the sciatic nerve of a frog, the
gastrocnemius muscle contracts strongly ; but a subsequent current
])assed through the nerve is followed by no reaction until the irritability
of the nerve is restored by the absorption of more nourishment. A
similar process doubtless occurs in disease of the nervous system.
\yhen a part is supplied with an excessive amount of nourishment, the
tissues become so irritable that they discharge readily, either sponta-
neously, or in response to stimuli which would not affect them under
normal conditions. Under these circumstances, excessive discharges of
nervous energy readily take place, and these are followed by temporary
loss of irritability, and the tissue becomes incapable for a time of per-
forming its normal functions. The excessive liberations of energy
from the cortex of the brain, which occasion epileptic attacks, for
instance, are accompanied by loss of consciousness, which lasts for a
considerable time, and the convulsive phenomena are not unfrequently
followed by temporary motor paralysis. When the energy of the
dischargbui lesion is once liberated, the part affected becomes incapable
of performing its functions, until its irritability is restored by the
absorption of a fresh stock of irritable matter. The primary effect of
almost all chemical agents on the nervous system is to stimulate it, and
to increase its functional activity, Avhile their secondary effect is to
depress or abolish its functional activity. The stimulant action of
alcohol on the brain, for instance, is followed by a stage of depression,
which may amount to complete abolition of the cerebral functions or
coma. Strychnine increases the irritability of the gray substance of
the spinal cord ; but the reflex actions, which are at first greatly exag-
gerated, become ultimately abolished, and the animal poisoned by
strychnine often dies from paralysis. Curara, which may be taken as
the type of nervous sedatives, paralyzes the terminations of the motor
124 GENERAL MORBID ANATOMY AND PHYSIOLOPxY.
nerves, yet Bernard i)rove(l that it first increases the irritability of the
fibres.
Tlie direct tendency of all destroying lesions is to abolish function.
It 111 list, however, be remembered that these lesions are frequently sur-
rounded by a zone of nervous tissue Avhich is in a state of irritation,
and the prominent symptoms of the affection are often produced by tliis
zone, consequently the symptoms may be indicative of excess of func-
tional activity. A gummatous tumor, for instance, in the cortex of the
brain is generally declared by epileptoid convulsions ; yet the direct
tendency of the tumor, in so far as it has destroyed and replaced ner-
vous tissue, is to abolish function. In such cases, both the direct and
indirect effects of the tumor are often manifested : the former by para-
lytic and the latter by convulsive symptoms. Even the ischa?mic soften-
ing, caused by plugging of vessels, is often surrounded by a congestive
zone of tissue, and the latter may give rise to symptoms of irritation.
CHAPTER lY.
GENERAL SYMPTOMATOLOGY.
Disease of the nervous system gives rise to disorders (A) in the
feelings of the patient — the a'sthesio7ieuroses, (B) in the nutrition of
the various tissues of the body — the trojjJwneuroses, and (0) in the
movements of the body as a Avhole and of its various parts — the
kinesioneui'oses.
A. THE .ESTHESIONEUllOSES.
The assthesioneuroses may be divided into disorders (i) of the primary
or elementary feelings — the prima)'!/ ajsthesioneuroses, and (ii) of the
secondare/ or compound feelings — the secondary nesthesioneuroses, while
each of these divisions may be subdivided into (1) disorders of the
common subjective or emotional feelings (pleasures and pains), and (2)
the s})ecial. objective, or intellectual sensations.
1. TjIE PkI.M.VUY .ESTIIESIOXEUROSES.
The general disorders of the feelings consist, first, of excess of the
normal sensation caused by a stimulus, which is named hypera'sthesia
when the objective feelings are increased in acuteness, and hypcrahiesia
when the common sensation of pain is increased ; secondly, of diminu-
tion of the normal sensation evoked by a stimulus, which is named
awcsthesia when the objective feelings are diminished, and analgesia
when the subjective feelings are diminished in acuteness : tJiirdly, of
l)aroxysms of pain in the region of distribution of a sensory nerve in
the absence of external stimulus or active inflammation of the nerve,
named neurcdgia ; fourtldy, of abnormal sensations, such as )iunil)ness,
tickling, crawling, itching, and feelings of heat and cold, also felt in
the absence of external stimulus, and grouj^ed togetlier under the name
of parcesthesiCB ; and fifthly, a diminution or increase of the interval
wliich elapses between the instant at which a stimulus is applied to a
sensory surface and the moment at wliich the suliject makes a voluntary
effort to indicate that the sensation has l)een perceived, named accelera-
tion or retardation of sensory perception respectively.
Disorders of the primary or elementary feelings may be divided
y2i] GENERAL SYMPTOMATOLOGY.
■iccordin- to the tissues and organs implicated into sensory afiections :
1 of the" skin and exposed parts of the mucous meml.ranes : 2. the
voluntary muscles; 3, the bones and joints; 4, the viscera; 5, the
special senses. The anatomical division is traversed at right angles by
a physiological division into sensory disorders of (1). the common or
subjective feelings, and (2) the special or objective feelings.
1. Cutaneous ^Esthesioneuroses.
Sensory disorders are known through the statements and gestures of
the patient, and the information obtained by this means must be
checked by a systematic examination.
The foilowino- tests of the various forms of cutaneous sensory dis-
orders may be used at the bedside :
[a) Common cutaneous sensations may be tested by the i»rick of a
pin, application of heat and cold, i)inching, and firm pressure, or the
application of the faradic current.
(7;) The rapidity of sensory conduction may be tested by getting the
patient, with closed eyes, to give a signal by voice or by a tap on a
table immediately on feeling the prick of a pin, and noting the interval
which elapses between the prick and the signal.
(c) The sense of pressure may be tested by Weber's method, which
consists of the superimposition of weights to determine the smallest
difference which can be perceived. To exclude the muscular sense the
part to be tested should be at rest on a table, and the sensation of tem-
perature may be excluded by the interposition of a bad conductor like
a wooden disk.
(d) The sense of locality may be tested by touching some part of the
surface with the finger or point of a needle whilst the j)atient"s eyes
are closed, and asking him to indicate the point touched. A better
plan is to ascertain to what distance the points of a compass must be
separated from one another before they are felt as two. The distance
to which the points of the compass must be separated varies for differ-
ent regions of the body, so that the observer must know the normal
scale of difference before drawing any conclusions from the results
obtained, but in many cases valuable information may be obtained by
comparing the anaesthetic area with the corresponding part on the
opposite side, which may be normal.
{e) The sense of temperature is tested by applying hot and cold
bodies to the surface when the patient's eyes are closed, and asking
him to indicate each time whether the temperature of the touching
body was hot or cold. Two test-tubes, one filled with cold aii.l the
THE PEIMARY .ESTHESIOXEUROSES. 127
Other with hot water, aiiSAver the purpose of testing very well, or two
silver spoons, one clipped in hot and the other in cold water, are
e([ually efficient and often more convenient.
(/) 'i'lie sense of touch is a compound sensation, but it may be
roughly tested by means of a light touch with a featlier, and asking
the patient to indicate with closed eyes each time he is touched.
a. Cutaneous Hyper.esthesi.e.
(1) Hyperpselaphesia, or abnormal acuteness of tactile sensibility,
declares itself by excessive reaction to the various tests for the senses
of pressure and locality. A smaller difference than usual in the in-
crease of pressure is perceptible, and the diameters of the areas of
sensibility are unusually small.
(2) Foli/ccsthesia is the condition in which one point of the compass
on being placed on the skin is felt as two, three, or five points.
(3) AllocJdria is a condition in Avliich the patient is not sure, and is
often in error when the eyes are closed, as to w^hich side of the bodv is
touched, even though the cutaneous sensibility is more or less normal
in other respects.
(4) Girdle seiisations consist of a subjective perception Avhich pro-
duces the impression of having a girdle or a broad bandage tied about
the trunk or limbs.
(o) TJierj7io-Jti/pe)restJiesia consists of an alniormal acuteness of the
sense of temperature, so that differences in temperature so slight as to
be inappreciable in health are recognized.
(0) Causalgid is a name given by Dr. S. Weir Mitchell to a distress-
ing pain which appears to belong to the thermo-hypersesthesiee. It is
described by patients as an intensely burning sensation, and is compared
to that caused by a mustard plaster, or by '' a red-hot file rasping the
skin.'" It is generally associated with " glossy skin,"' but often pre-
cedes the trophic changes of the skin.
(7) Dy^cesthnia is a term introduced by Charcot to indicate a sensa-
tion of a peculiarly distressing and vibratory character, which ascends
towards the central end of a limb and descends towards its extremity.
The sensation is excited by the slightest touch or the application of a
cold body to the surface, and it persists from several minutes to a
quarter of an hour after the exciting cause has ceased to act. After a
short time an analogous sensation may be felt at a corresponding point
of the limb, opposite to the one primarily excited.
(8) Hyperce-'sthetie spots consist of circumscribed patches of skin
which are exquisitely painful to touch, and which are subject to attacks
of spontaneous pains of a burning character.
l-)s genp:ral symptomatology.
(!)) Cutaneous hyperalgesia consists of an increased sensibility of
the common sensations, and is much more frequent tlian increase of
tactile sensibility. In this condition, stimuli, Avhich in health give rise
to touch, or even to pleasant sensations like the minor degrees of tick-
liiiii-. noAV become i)ainful. Thermo-hjperahjesia may be applied to
desiijnate the condition in which contact Avith a hot or cold body gives
risernot to a feeling of temperature, but to a i)ainful sensation.
I). Cutaneous An^esthesi.e.
(1) Distribution of Ancesthesia. — Anaesthesia or sensory paralysis is
sometimes distributed in limited patches or in the area of distribution
of particular nerves, and it is then termed cirrumscriht'd anaesthesia.
At other times it appears in the form of a zone of variable Avidth sur-
rounding the bodv on one or both sides, and it is then named anaesthesia
in the form of a girdle. When it is distributed over the lower half of
the body and the lower extremities it is tei'med parana'sthesia ; and
when over the lateral half of the body, including half tlie face and the
extremities, it is named heiiiiana'sthesia.
(2) Total anaesthemi is a diminution or loss of every form of cuta-
neous sensibility, and partial anaesthesia a diminution or loss of certain
forms of sensibility while others are preserved.
(8) Api^elapliesia or tactile ancesthesia denotes a diminution or h)ss
of the acuteness of tactile sensibility, a condition which is fre([uently
associated with hyperalgesia. Severe pain is sometimes felt in anes-
thetic parts, and the condition is then called anaesthesia dolorosa.
(4) Thermo-ana'Sthesia means insensibility to heat or cold, a condi-
tion which sometimes occurs as an isolated affection.
(")) Analgesia diQiioie^ a diminution or loss of the sensation of i»ain.
Analgesia, with preservation of the tactile sensibility, is the most fre-
(pient form of partial sensory paralysis.
(6) Retardation vf sensory conduction may be employed as a test of
any form of auBesthesia, and gives rise in the partial varieties to the
following anomalous phenomena :
(a) Separation of Tactile and Painful Impressions. — In locomotor
ataxia the prick of a needle causes a prompt feeling of touch, which is
often followed in two or three seconds by a feeling of pain. In cases
of thermo-ansesthesia, a test-tube holding hot water may at first give
rise to an immediate feeling of touch, to be followed in two or three
seconds by a sensation of temi»erature.
(h) Double Painful Sensations.— In some cases of locomotor ataxia,
pricking the skin on the back of the foot with a needle is sometimes
THE PRIMARY .ESTHESIONEUROSES . 129
followed bv a first painful sensation, and, when this subsides, bv a
sec(»nd painful sensation, which is usually of greater intensity and more
prolonged than the first. The first is felt after a lapse of two and a
half to three seconds subsequent to the prick, but the second is not
felt until after another interval of from two to five seconds.
{(■) Persistent After-sensations. — In some cases of partial ansesthesia,
pinching the skin or pricking with a needle gives rise to a sensation
which begins slowly, but gradually increases in intensity, and is much
more severe than the i)ain which occurs in health.
{d) Inability to Count Successive Impressions. — Closely connected
with these persistent afiter-sensations is the inability of the patient to
count correctly several imi)res.sions made in quick succession. Enume-
ration of successive impressions presupposes an interval to elapse
between the sensation caused by each ; but, when the conduction is
retarded, each sensation is unusually prolonged so that the first does not
fade before the second begins, and so counting Ijecomes impossible.
c. Cutaneous Par.esthesi.e and Paralgesia.
(1) Pruritus is a sensation caused l)y aluiormal irritation of the
nerve-ends of the papillae of the skin, or by a state of undue irrita-
bility of these nerve terminations themselves. Pruritus is related to
such sensations as tickling and to burning and stinging pains, but an
irresistible tendency to scratch is its characteristic symptom.
('2) Formication does not amount to pain, but is described as a feel-
ing of creeping or pricking, or is compared to the crawling of ants.
Formication occurs as a transitory symptom in minor mechanical in-
juries of nerve-trunks, and is felt in the foot as a sensation of " pins
and needles," numbness, or ''sleepy sensation," Avhen the sciatic nerve
is compressed for some time.
d. Neuralgia and Neuralgiform Pains.
(1) Neuralgia consists of periodic attacks of severe pain, occurring
suddenly and spontaneously in the course of one of the larger nerve-
trunks, and ramifying in a few or all of its sensory branches.
The character of the pain in cutaneous neuralgia will be described
when the special forms of it are under consideration, but we shall here
refer to some of the more prominent phenomena of the affection.
During the height of the neuralgic paroxysm there is an irradiation
of the jMin to other sensory nerves, generally to branches of the same
trunk or to neighboring nerves, but occasionally to more or less distant
nerves, and the neuralgic pain is accompanied by various parsesthesiae,
hyperaesthesia, or sometimes anaesthesia.
130 GENERAL SYMPTOMATOLOGY.
Painful Points.— These points were first described by Yalleix under
the name of jyoints douloureux. An examination of the part during
an attack of superficial neuralgia will reveal one or more points which
are extremely sensitive to the pressure of the tip of the finger. The
sensitiveness of these points stands almost in a direct relation with the
severity of the paroxysms, but they may be present occasionally during
the period of remission, and in some cases pressure upon them induces
an attack. These tender spots are found at various points in the
course of the affected nerves, when their trunks pass from a deeper to
a more superficial level, and especially where they emerge from bony
canals or pierce fibrous fascia?, or even where a nerve lies on a hard
bed so that it may be easily compressed.
Point Apophymire. — Trousseau believed that in all forms of neural-
gia the spinous processes of the vertebrae corresponding to the origin
of the painful nerve, and which he calls points apophysaire or spinous
points, are painful on pressure, but these points are also present in
spinal irritation and in myalgia. The concomitant symptoms of
neuralgia will be described along with the special forms of neuralgia.
(2) Lightning-like Pains. — In locomotor ataxia patients often suffer
from spontaneously occurring paroxysms of distressing pains, which
are compared by them to forked lightning darting through the body,
and have been described under the name of general neuralgia, or
neuralgic rheumatism.
2. Sensory Affections of the Voluntary Muscles
{^Muscular ^-Esthesioneuroses) .
a. Muscular Hyper^esthesia and Hypkralgesia.
The feeling of unrest and desire for constant change of position,
called the ''fidgets,"' appears to be due to muscular hypene^thesla. In
spasmodic wry-neck, and in "cramps" the hyperiesthetic condition is
often very great, and causes intense pain. The excessive feeling of
fatigue and prostration which occurs on slight exertion in the prodromal
stage of acute diseases, is probably due to an increasing muscular sen-
sibility, and consequently this condition may be regarded as a muscular
hyperalgesia. Painful conditions of the muscles are called myalgia or
myodynia. Pain is most frequently met with in the muscles of the
neck and of the lumbar region, and inasmuch as it corresponds to
cutaneous neuralgia and arthralgia, it may be called muscular neuralgia
or myoneuralgia.
THE PRIMARY .ESTHESIONEUROSES. 131
h. Muscular Ax^sthesia.
Muscular aniiestliesia consists of diminution or loss of the common
sensibility and of the sense of muscular effort. When muscular sensi-
bility is lost, as tested by the faradic current, while the muscular sense
is retained, the condition is termed muscular analgia, or muscular
analf/rsi((. When there is a diminution or loss of the capacity of rec-
ognizing small weights, or of perceiving small differences by means of
muscular effort with closed eyes, the condition is called ancesthesia of
the muscular sense.
(1) Tests of Muscular Sensibility. — The state of muscular sensi-
bility is best tested by the faradic current. When a healthy muscle is
made to act, a dull feeling accompanies the contraction, this feelino-
being much increased in muscular hyperalgesia and diminished or lost
in muscular analgesia.
(2) Tests for Muscular Sense. — To test the muscular sense the
patient should be made to lift various weights, and to form an estimate,
with closed eyes, of the weights and of the differences of successive
Aveights. In order to eliminate the cutaneous sense of pressure, the
weights should be placed in a cloth and suspended from the limb to be
tested. The patient may also be made to move the limb into certain
prescribed positions, with closed eyes ; he may be asked to touch a
particular part of the body, such as the tip of the nose, with the index
finger, to take hold of a ticking watch held before him, or to describe
an imaginary circle on the floor with the big toe. The patient fails to
accomplish these actions with precision when there is muscular
ancesthesia.
8. Sensory Affections of the Joints and Bones
{Articular and Osseous jEsthesioneuroses).
a. Osteoneuralgia.
The bones are sometimes the seat of severe pain, and when the pain
is not caused by recognizable anatomical changes the condition is re-
garded as a neuralgia, and named osteoneuralgia.
Neuralgia of the bones differs from cutaneous neuralgia in not radiat-
ing along the course of the principal Ijranches of the affected nerves.
It is probable that the sensory nerves of the Ijones reach them along
with the sympathetic plexus which surrounds the vessels.
2^32 GENERAL SYMPTOMATOLOGY.
6. Arthroneuralgia.
Arthroneuralgia consists of severe neuralgiform pains in a joint in
the absence of any recognizable anatomical alteration of it. The pain
occurs in paroxysms which come on spontaneously, and which are sep-
arated by intervals of complete or comparative freedom from pain.
The pain is sometimes described as tearing, or shooting through the
joint like lightning, and at other times as a boring or stabbing pain.
The patient may also complain of numbness and formication about
the joint, or of sensations of heat and cold, and the skin over the joint
is often hyperjesthetic in the early stages of the affection, and anaes-
thetic when it is of long standing. The pain is much increased when
tlie patient's attention is directed to it, while it is diminished under the
influence of general fatigue, and does not prevent the patient from
sleeping. Pressure increases the pain, but, as occurs in cutaneous
neuralgia, slight and superficial pressure may produce intense pain,
while deep, continuous, and uniform compression produces no effect, or
even relieves the pain. Painful points may be obtained on pressure,
but their position is somewhat indefinite. Neighboring nerve-trunks
may also be found painful on pressure, and the spines of some of the
vertebra may likewise be tender to pressure. In some cases spastic
contraction of the muscles surrounding the joint occurs, while in other
cases the limb is feeble and lie]i)less, owing, perhaps, to the fear of
inducing a paroxysm of pain by movement at the joint rather than to
any muscular paralysis.
The vaso-motor disturbances consist of redness, heat, and increased
secretion of sweat in the neighborhood of the affected joint, and a cir-
cumscribed dough or fluctuating swelling is sometimes observed in the
skin over the joint, which was compared by Brodie to an unusually
large urticaria wheal. Swelling of the joint from serous effusion within
the capsule may occasionally take place, and is apt to be regarded as of
inflammatory origin, and when effusion takes place in the tissues sur-
rounding the joint as the result of irritating applications, the diagnosis
is still further obscured.
4. Sensory Affections of the Internal Organs
( Visceral ^sthesionniroses).
The visceral sensations belong to the common or subjective sensa-
tions, and consequently excess of a normal visceral feeling may be
regarded as a hyperalgesia, while an altogetlier abnormal visceral feel-
ing belongs to the parmsthesim ; but it is by no means easy to draw a
distinction between these two kinds. Diminution or loss of the visceral
THE PRIMARY .ESTHESIOXEUROSES . 133
feelings constitutes a visceral ancesthcsia, or, more correctly, a visceral
a. Visceral Hyperalgesi.e and Paralgesia.
(1) Titillation is a sensation induced by irritation of the sensory
brandies of the vagus, especially the superior laryngeal branch, or by
undue irritability of the ends of the nerve, and corresponds with pru-
ritus of the external skin ; and as pruritus leads to an irresistible ten-
dency to scratching, so titillation leads to the reflex respiratory move-
ments Avhich produce coughing.
(2) G-Iobus is a sensation which gives the feeling of a ball ascending
from the epigastric region to the throat. It is a frequent symptom of
hysteria, and occasionally forms the aura of an epileptic attack. Globus
is supposed by some to be caused by spasm of the oesophagus and
pharynx, and it has consequently been called oesophagismus, but the
explanation is not a satisfactory one.
(3) Pyrosis or water-brash is a painful sensation in the epigastrium,
consisting of a sense of burning, which is generally attended with the
rising of a ((uantity of clear watery and strongly alkaline fluid into the
mouth. An attack of pyrosis may last from a few minutes to many
hours, with alternating remissions and exacerbations, and is most prob-
ably caused by a spasm of the cardiac end of the stomach when its
contents are very acid, thus arresting the secretion of saliva in the
oesophagus.
(4) Bulimia is a feeling of hunger, which is abnormal in its period
of occurrence or in its intensity, and which is appeased only for a short
time by taking food.
(5) Polydipsia is an excessive feeling of thirst, and is a constant
symptom of polyuria and diabetes, and is an occasional symptom in
hysteria.
(6) Excessive voluptuous feelings arise without any exciting cause in
both sexes, and are associated with the erections and ejaculations which
accompany normal coitus. These sensations may be caused by a local
irritation of the genitals, or by a central disease like tabes dorsalis.
(7) Feeling of oppt'ession arises, when general, from overwork or
deficient nourishment of the nervous system. It is described by the
patient as a feeling of heaviness, dulness, and depression of spirits. A
more specific form of oppression occurs in connection with cardiac
aff'ections, which will be subsequently described as angina pectoris.
b. Visceral Anaesthesia and Analgesia.
Very little is known with regard to diminution or loss of visceral
feeling. The normal functions of the viscera are performed without
134 GENERAL SYMPTOMATOLOGY.
definite sensibility, although a diffused visceral sensibility contributes
greatly to our feeling of comfort and well-being, and it is probable that
diminution of visceral sensations contributes in a corresponding degree
to our o-eneral feeling of bodily discomfort. Visceral anaesthesia is best
defined'^in the organs which are most in relation with external forces,
such as the larynx, stomach, sexual organs, and rectum.
(1) Ancestliesia of the laryngeal and bronchial branches of the vagus
renders titillation and the consequent reflex act of coughing impossible.
In this condition catarrhal secretions fail to be expelled, and may by
their accumulation cause suffocation.
(2) Ancesthrsia in the territorg of the gastric branches of the vagus
gives vise to polgj^hagia, & condition in which an unusual quantity of
food must be taken before the feeling of hunger is appeased, or in which
the feeling of repletion is never obtained however much food is taken.
The experiments of Brachet, Arnold, and others have proved that, on
section of the vagi, animals continue to eat until the oesophagus is
filled with food.
(3) Ancesthesia of the sexual feelings is most frequently observed in
the female sex. Complete absence of voluptuous feelings in hysterical
females, along with diffused or circumscribed cutaneous angesthesia, is
most probably due to anaesthesia of the mucous membrane of the
vagina. Anaesthesia of the genitals is observed in the male sex as a
result of sexual excesses or onanism, or as a symptom of chronic affec-
tions of the spinal cord, such as spinal meningitis and tabes dorsalis,
or in the absence of any appreciable cause. In such cases the electrical
sensibility of the glans penis and of the external genitals is diminished,
and the power of erection is lost, constituting impotency ; or the loss of
reflex irritability arrests the secretion of semen and abolishes the power
of ejaculation, a condition named asperinatisin.
(4) Ancesthesia of the mucous membrane of the rectum, which is a
frequent symptom of grave organic diseases of the spinal cord, permits
the stools to pass unconsciouslv.
(5) Ancesthesia of the mucous membrane is probably present in the
early stages of many cases of locomotor ataxia, and causes great toler-
ance of the bladder to its contents. The bladder may become greatly
distended without giving rise to the desire to micturate. Anaesthesia
of the mucous membrane of the urethra produces a condition in which
the urine may pass in a full stream without the knowledge of the patient.
5. Sensory Disorders of the Special Senses.
The consideration of this part of the aesthesioneuroses is reserved for
special mention in a later part of this work.
SECONDARY OR COMPOUXI) J^STHESIOXEUROSES . 135
II. The Secondary or Compound ^Esthesioneuroses.
The sensory conducting paths unite with each other for the first time
on reaching the common centre of sensory connections — the scnsorium
commune; and molecular change in this centre is the correlative of
the compound feelings and cognitions, while an abnormal molecular
discharge from this centre is the correlative of the disorders of the
compound feelings comprised under the name of the secondary aesthesio-
neuroses. But we have seen that the cortex of the brain forms also a
common centre of motor connections, a motorium commune, and that
there is no clear dividing line between the common sensory and common
motor centre ; and it may, therefore, be expected that the disorders of
the compound feelings will not be separated by a sharp line of demar-
cation from the disorders of the compound movements of the body. As
a matter of fact, the disorders of the elementary feelings, of the com-
pound feelings, of the compound movements, and of the elementary
movements merge into one another by insensible gradations, and it is
impossible to draw anything like a clear-cut division between them.
We shall, therefore, describe briefly in this section a few of the disorders
of the compound feelings and movements under the name of psychical
disorders, and without attempting to differentiate clearly between the
two sets of phenomena :
(1) Pseudo-cesthesia is a generic name given to sensations and per-
ceptions experienced in the absence of any adequate irritation of the
peripheral end-organs or of the conducting paths, the condition of their
production being a molecular discharge from the common sensory centre.
When a sensation of this kind is experienced, and gives rise to an
erroneous perception of external objects and relations, it is named an
illusion; when it gives rise to an objective sensation in the entire
absence of an external cause, it is termed a hallucination ; and when
the patient forms such a distorted conception of the properties and
relations of things actually existing that he is led to a false conclusion
with regard to them, the condition is called a delusion.
(2) Unconsciousness. — The molecular activity .of the sensorium
commune is intermittent, and under normal conditions it is suspended
for several hours every night, and during this time consciousness is
abolished. This constitutes sleep. If the subject cannot be aroused
to consciousness by the application of ordinary stimuli, the condition is
called somnolence or stupor ; and if the unconsciousness become so
profound that the subject cannot be aroused by the strongest external
stimuli, the condition is called coma.
136 GENEKAL SYMPTOMATOLOGY.
(8) Subconscious and Semiconscious Psychical Actions. — Between
the active consciousness of a healthy person after being restored l.y
sleep and complete insensibility there are all degrees of diminution of
sensibility. It is well known that a person whose attention is strongly
directed to a particular subject is insensible to ordinary stimuli. A
more advanced degree of diminution of the activity of consciousness is
manifested by persons suffering from great fatigue and loss of sleep.
Under such circumstances a person may walk about in a half-conscious
state, and a similar dazed condition is frecjuently observed after epileptic
seizures. The patient may perform complicated motor actions Avhile in
a totally unconscious condition, as is seen in somnambulism, the mes-
meric state, or the narcosis caused by chloroform and similar agents.
Unconscious conditions are, indeed, frequently associated with motor
disturbances. When the inliil)itory action of the highest coordinating
centre is removed, the functional activity of tlie lower centres may be
increased. Many atrocious murders are committed during the period
of semiconsciousness which sometimes follows an epileptic seizure, and it
is well kuoAvn how fierce and brutal many men ))ecome during the semi-
conscious condition induced by alcoholic excess. In delirium^ again,
the highest form of consciousness is in abeyance, while the lower, earlier
organized forms are abnormally active. The patient, for instance, is
unable to sleep, and yet he is only partialh^ conscious of surrounding
objects and events ; he is subject to illusions, hallucinations, and delu-
sions, and motor disturbances are manifested bv great restlessness and
incoherent speech. It is probal)le that in delirium the stock of irritable
matter in the gray substance of the cortex is much exhausted, and that
what remains manifests an undue degree of irritability, so that the
protoplasm gives out energy either spontaneously or on the application
of slight stimuli, while functionally there is a dissolution from the later
to the earlier acquired feelings and experiences.
But although the patient is only semiconscious in delirium, yet his
mental experiences during that time may be subsequently remembered
with painful intensity. This also occurs in dreams. The patient is
wholly unconscious of external impressions at the time, but he is par-
tially conscious of a succession of feelings and images, cither of a
joyful or a painful kind, which may be subsequently revived in memory
with greater vividness than almost any of his mental experiences during
waking hours. Dreams are frequently accompanied by motor disturb-
ances, such as vocalization and articulate sounds. The most prominent
feature of the night-terrors of children is the outward expression of
extreme terror by which the attack is manifested. The partial uncon-
sciousness which precedes or follows an epileptic seizure is often asso-
SECONDARY OK COMPOUXD .ESTH ESIONEUROSES . 137
ciated with the (nitward manifestations of one of the emotions, and
sometimes by a corresponding inward feeling. The aura of an epileptic
attack may be a guilty expression, and the patient may subsequently
be able to remember that innnediately before the attack he experienced
a feeling as if he had been guilty of an infamous action. What appears
to be an increase of consciousness often results from a diminished activity
of the higher sentient centres. Increase of the normal desires and
appetites sometimes results from a ])eripheral irritation, but a person is
liable to an illegitimate indulgence of the passions when the moral
feelings are weakened, and tem])tation is apt to be strongest during
states of mental enfeel)lement from cerebral exhaustion. It is then
also that remorse for previous indulgence is liable to become (|uite dis-
proportionate in its intensity to the degree of guilt, and may be experi-
enced in the absence of any guilt to atone for. The depressing emotions,
such as fear and anger, are also liable to become excessive during states
of nervous exhaustion, and it is a nuxtter of common ol)servation that a
person who is in feeble healtli is often very irascible, while others are
easily excited to laughter or tears. Experiments on animals have show n
that a nerve whose nutrition is lowered discharges its energy more
readily than one whose nutrition is perfect, and similarly when the
nutrition of the sensorium commune is defective it responds to stimuli
of less intensity than Avhen its nutrition is normal.
(4) Double Consciousness! ; Periodic Amnesia. — Closely allied to
somnambulism and the mesmeric sleep is the curious condition which
has been called double consciousness, or periodic amnesia. In this con-
dition the subject is liable to periodic seizures, which may last from
some hours to as many days, and during which there is complete for-
getfulness of the feelings and events of ordinary existence, although
rational thou<>;lit and action still remain.
(5) Abnormal States of Conscious7iess. — There are some abnormal
elementary feelings which must be regarded as qualitative rather than
quantitative alterations of consciousness. As examples of these, may
be mentioned ('/) headaclie, (b) vertigo, and (c) fainting. To the con-
sideration of these nuiy be added a few remarks on {d) abnormal appe-
tites and emotions.
(a) Headarhe. — Although headache is an excess of painful feeling,
yet it cannot as a rule be regarded as an excess of any normal feeling,
or of any feeling which can be excited by the application of external
stimuli. From this statement neuralgic, rheumatic, and pro])a))ly
some other forms of headache must be excepted, but what is generally
known as a nervous headache is a truly abnormal feeling, and must be
experienced by a person before he can form an adequate idea of it.
138 GENERAL SYMPTOMATOLOGY.
Such headaches are caused by changes of circulation in the brain, the
circulation of poisons in tlie blood, or they may arise spontaneously at
recurrino- intervals. It is probable that in all of them there is an
alteration of tlie irritability of the cells and fibres of the sensorium.
Recurring headaches are generally associated with vaso-motor phe-
nomena in the regions of distribution of the cervical sympathetic
nerves, but it is probable that these are the results and not the cause
of the sensorial disturbance. Such headaches are regarded by Dr.
Hughlings Jackson as a sensory epilepsy and as being dependent upon
a discharge from the sensory portion of the cortex of the brain.
{!)) Vertigo is a sensation of swimming in the head, during which
surrounding objects appear to oscillate before the eyes, or rotate in a
definite direction, and which is also accompanied by a sense of stag-
gering or of rotation of the body. A^ertigo a})pears to be the subjec-
tive correlation of want of coordination between the various muscular
contractions necessary for adjusting the body to the different objects
which surround it in space. It is a prominent symptom of those dis-
eases in which the automatic mechanism for maintaining the erect
posture is deranged, such as affections of the cerebellum and Meniere's
disease. The position of the body in space is largely determined by
the association of objects seen with the appreciation of the position of
the eyes and head. Displacement of the positi(m of the eyes, such as
occurs in paralysis of one or more of the recti muscles, or of the posi-
tion of the head, such as occurs in rotation of the head with conjugate
deviation of the eyes, and in the compulsory movements to be subse-
quently described, is also accompanied by severe vertigo. This symp-
tom frequently attends visceral disease, as dyspepsia, and it is then
probably caused by vaso-motor changes influencing the cerebral circula-
tion. This opinion is rendered all the more probable from the fiict
that vertigo is a troublesome symptom both of ansemia and congestion
of the brain. Vertigo is usually accompanied by a motor phenomena
in the region of distribution of the pneumogastric, such as feeble and
irregular pulse, irregular respiration, and vomiting.
(f) Fainting is a deadly feeling caused by sudden anaemia of the
brain occasioned by severe loss of blood or cardiac failure. It also
is attended by gasping respiration, and frequently accompanied by
vomitino;.
{d) Ab>ior)nal Appetites, Amotions, and Impulses. — Drunkenness
may be regarded as an abnormal appetite, especially when it assumes
the aggravated form of dipsomania ; but the most remarkable example
of an abnormal appetite is afforded by the condition described by
Westphal and others as perverted sexual instinct (contrare sexualemp-
SECONDAET OR COMPOUND .ESTHESIONEUROSES . 139
fimlung). This condition is defined by Westphal as "a congenital
perversion of the sexual instinct with retained consciousness of the
morbid nature of the condition," and the recorded cases show that
some pei'sons are attracted in their sexual desires exclusively by indi-
viduals of their own sex. The most remarkable of the abnormal
emotions consist of a morbid dread experienced in the absence of any
circumstance or event which could l)e thought in the remotest deoree
capable of inducing such a feeling. Some persons experience an un-
conijuerable feeling of dread when they are alone in an open space
[am/oraphohia) ; others have the same feeling when in a narrow lane
between two Avails {claustrophobia). Some people have a morbid dread
of society (anthrophohia), while there are some men who only experi-
ence an aversion to the society of women {(lynephohia). Some persons
are totally unable to sign their names in the presence of a witness. A
gentleman in business once told me that while able to keep accounts
and attend to his business as well as ever, he found himself totally
unal)le to sign a check if his clerk made a sudden demand for one.
Suicidal, homicidal, and other morbid impulses are liable to become
uncontrollable during periods of great nervous exhaustion, and when
the highest manifestations of consciousness are in abeyance. Atrocious
crimes are usually committed by persons during the period of depres-
sion which follows a prolonged carouse, or when the individual. is in
a state of semi-stupefaction, either from alcohol or as a sequel to an
epileptic seizure.
CHAPTER Y.
GENERAL SYMPTOMATOLOGY {continued).
B. TKOPHONEUROSES.
The degenerations of the nervous system having ah-eady been con-
sidered, we shall now proceed to describe the degeneration of muscles
which result from nervous disease.
I. Neueotic Atrophy of Muscle.
Neurotic atrophy of muscle may be divided into three stages,
namely: 1, Simple atrophy; 1, Atrophy with nuclear proliferation;
3, Cirrhosis of muscle.
1. Simple Atrophy.
In simple atrophy and the early stage of the severer forms of
atrophy, the muscular fibres undergo a simple diminution in size,
t ■ c
Atrophv of Muscular Fibres from a Case of Infantile Paralysis. (After Havem.)
«, Fibres of normal size, showing multiplication of nuclei ; 6, simple atrophy, with granular degenera-
tion ; c, advanced granular degeneration, with atrophy.
without presenting any degenerative changes. The longitudinal and
transverse striations are at times as well preserved as in health (Fig.
NEUROTIC ATROPHY OF MUSCLE. 141
G4, a), and not a trace of fatty degeneration can be discovered. It
would appear that the fibrilhe of which the fibre consists are diminished
in number, but those which remain do not seem to be sensibly dimin-
ished in size. At other times the striation becomes less marked and
more delicate than in health, probably owing to a diminution in the
length of the sarcous elements of the contractile disks (Fig. G-t, h).
The substance of the contractile^ disks may also present a finely granu-
lar aspect, which appears to be the first indication of the profound
chemical change which this substance subsequently undergoes.
2. Atrophy with Xud'ar Proliferation.
When the muscle is examined from three to five weeks after the
injury the contents of the fibre are now seen to have undergone a finelv
granular degeneration (Fig. 64, c). The granules at first consist of
altered protein, but they soon become distinctly fatty. The primitive
fibrils now disappear, and only small fragments of the fibre present,
here and there, either transverse or longitudinal striation. In addition
to these changes the nuclei or muscle corpuscles are multiphetl. and in
the later stages of atrophy the sarcolemma may become almost filled
Avitli masses of nuclei Avhich are surrounded by granular and fatty
detritus, while the contents of the fibres are completely disintegrated
(Fig. 65, h h). The nuclei of the endomysium also seem to be more
numerous than in health.
3. Cirrhosis of Muscle.
The nuclei of the endomysium, now greatly increased in number,
elongate into fibres which form narrow bands of fibrous tissue running
parallel to the direction of the muscular fibres, and cicatricial contrac-
tion of this tissue completely destroys the remnants of muscular fibre
and gives rise to organic shortening of the l)and of fibrous tissue which
now represents the muscle. These bands of filirous tissue contain
many oat-shaped nuclei and connective-tissue cells (Fig. 65, a a) which
may become distended with flit, and these fat cells may become so
abundant that the original volume of the muscle may be maintained or
even exceeded.
It is now fully ascertained that active neurotic atrophy of muscle
never occurs except when the spino-neural mechanism is injured, either
by disease of the ganglion cells of the anterior horns of the cord and
the corresponding cells in the medulla oblongata and pons, or of the
efferent fibres which connect these with the muscles. A moderate
142
GENERAL SYMPTOMATOLOGY,
decrree of muscular atrophy may also be caused by irntation of the
afferent fibre of the reflex arc. Whether the same cell exercises both
trophic and motor functions, or there exist separate cells for each func-
tion is as yet undetermined. It would appear that a destructive lesion
of the cranglion cells, or of the efferent fibres which connect these with
the muscle, causes both motor paralysis and active atrophy, while in
Fig. 65.
Infantile Paralysis. (After Havem.)
a a, Excess of connective tissue, containing a large number of conuective-tisBue and fat cells ; 6 b, atro-
pliied muscular fibres, containing a large number of nucli^i ; c, simple atrophj- of muscular filjre
severe cases there is also rapid loss of the faradic contractility. A.
certain degree of wasting may occur in paralyzed muscles Avhen the
lesion is restricted to the cerebral mechanism, but this form of atrophy
arises simply from disease of the muscle, and differs entirely from the
active atrophy which has just been described.
CUTANEOUS TROPHIC AFFECTIONS. 143
II. Cutaneous Trophic Affections.
1. Ciititneous Eruptions in Lesions of Peripheral Nerves.
Erythematous patches are often observed on the extremities after
traumatic lesions of the peripheral nerves, on the root of the nose and
forehead in trigeminal neuralgia, and on the hand in cases of brachial
neuralgia. Erythema often arises in the course of digestive disorders,
and it is then most probably of reflex origin. The urticaria which is
caused by the stings of insects and nettles, and that which arises in the
neighborhood of the puncture in subcutaneous injections, seems to
indicate that this eruption is often, if not always, of nervous origin.
Vesicular eruptions are often observed after injury to nerves. Ecze-
matous eruptions are often associated with neuralgic pains in the area
of distribution of an injured nerve, and eczema of the whole side of
the face has been observed to accompany a severe attack of trigeminal
neuralgin. Herpes zoster often accompanies a severe attack of neuralgia.
Its favorite seat is the skin covering one or more of the intercostal
spaces, and the neuralgia which accompanies it generally begins and
terminates with the eruption ; but, in aged people, the pain, which is
very intractable, continues long after the eruption has disappeared.
Herpes zoster of the face occurs in trigeminal neuralgia. It may
appear on any part of the face, but is most frequent on the forehead.
When the palpebral nerves are affected the eruption spreads over the
upper eyelid, and the conjunctiva is inflamed ; and when the frontal and
its nasal branches are likewise involved, the iris and other structures
within the eyeball are inflamed, and the disease may then cause serious
damage to the eye. Herpes zoster has also been observed in the area of
distribution of various spinal sensory nerves when the nerve is com-
pressed by aneurism, cancer of the vertebra, or other tumors. Evidences
of neuritis of the aifected intercostal nerves have been found in cases that
died whilst the patients were suffering from intercostal herpes zoster.
Pemphigus bulh^ sometimes develop with great rapidity over various
parts of the surface supplied by the cutaneous branches of an injured
nerve. After section or injury of nerves, the skin frequently becomes
dry, harsh, and scaly ; and a case is reported by Eulenburg in which
several branches of the brachial plexus were injured and compressed in
consequence of a dislocation of the humerus, and in which ichthyosis
of the skin of the affected extremity had supervened.
After traumatic injuries of nerve-trunks the skin often undergoes
atrophy, loses its Avrinkles, and becomes smooth and glossy, and conse-
144 GENEKAL SYMPTOMATOLOGY.
quently this condition has been named " glossy skin " by Paget. " In
well-marked cases," this author says, '' the fingers Avhich are affected
(for this appearance may be confined to one or two of them) are usually
tapering, smooth, hairless, almost void of wrinkles, glossy, pink or
ruddy, or blotched as with permanent chilblains. They are commonly
also very painful, especially on motion, and pain often extends from
them up tlie arm." Glossy skin is often met with in injuries of the
ulnar nerve of the brachial plexus and in the upper extremity ; the
palm of the hand is the part which usually suffers, while in injuries of
the nerves of the lower extremity the dorsum of the foot appears to be
the part most liable to be attacked. Patches of leucoderma, with
aneesthesia of the affected skin, have been observed on the face in
trigeminal neuralgia, and over other parts of the body after injuries to
large nerve trunks. Patches of highly pigmented skin, with anaesthesia,
have also been found scattered irregularly, but symmetrically, all over
the body ; these also being doubtless of nervous origin.
The early occurrence and the severe degree of anaesthesia in the
tubercular variety of leprosy, as well as the manner in which it pro-
gresses from the periphery towards the central parts of the affected
limbs, Avould alone indicate that disease of some part of the nervous
system is a prominent part of the affection, and characteristic anatomical
changes have been found in the nerve-trunks. Morbid changes have
also been discovered in the spinal cord and brain, but it is probable
that disease of the nerve-trunks takes the most active part in causing
the local symptoms.
2. Cutaneous Eruptions in Diseases of the Spinal Cord.
Cutaneous eruptions of various kinds occur in cases of chronic mye-
litis, but they are most frequently met with during attacks of lightning
pains in tabes dorsalis. These eruptions consist of patches of urticaria,
vesicular eruptions of which herpes is the most common, and papular
eruptions like lichen planus, and they ai-e always limited to nerve terri-
tories affected with neuralgic and lightning pains. Several cases of pem-
phigus in connection with spinal disease have been recorded by Chovstek
and olhers. A case is recorded l)y Balmer in which an attack of pem-
phigus occurred in the course of progressive muscular atrophy.
3. Cutaneous Eruptions in Diseases of the Brain.
Herpes is not infrequently associated with hemiplegia, but it is
doubtful whether there is anything more than an accidental connection
between them. Two cases are reported bv Dr. Duncan, in each of
TROPHIC DISORDERS OF THE XAILS AXD HAIR. l-i.")
Avliich an eruption of herpes appeared on the affected side simulta-
neously with the motor paralysis. Several cases are reported in which
a pemphigus eruption appeared on one of the paralyzed extremities in
hemiplegia of central origin.
III. Trophic Disorders of the Nails and Hair.
1. Trophic Disorders of the Nails and Hair in Lesions of the
Nerve-trunks.
Traumatic lesions of nerve-trunks in which the nerve is not com-
pletely divided, are followed by various deformities of the nerves. The
nails become greatly curved — both laterally and longitudinally — fur-
rowed, dry, and cracked at their extremities, and of a yellowish-brown
color. These deformities may also occur in connection with neuralgia
and idiopathic neuritis of sensory nerve-trunks. Local affections of
the hair often occur in man after traumatic lesion of nerve-trunks, or
in connection with idiopathic neuritis and neuralgia. The hairs over
the region of distribution of a nerve affected with neuralgia have some-
times been observed to be hypertrophied and even increased in number ;
but, as a rule, the effect of neuralgia upon the hair is to make it brittle,
and to cause it to fall out in considerable quantities. Localized gray-
ness of the hair is often associated with ophthalmic neuralgia, and it
may also involve the eyebrow of the affected side. This grayness
sometimes assumes an intermittent character, increasing during and
sometimes after an acute attack of pain, the color becoming partially
restored in the interval between the paroxysms. In glossy skin the
surface becomes hairless.
2. Trophic Disorders of the Nails and Hair in Spinal Disease.
The nails may become deformed in cases of acute and chronic
myelitis, but the most remarkable change to which they are liable in
spinal diseases occurs in locomotor ataxia. In the course of this disease
the nails of the great toes sometimes fall oft" spontaneously, and are then
rapidly replaced by a new and perfectly normal nail, which may In its
turn ftill off a few months later, and this process may occur in the
same nail several times in succession. The falling off of the nail may
be preceded for some weeks by a dull pain, or by a feeling of uneasi-
ness in the toe, and then the nail falls oft' without being accompanied
either by suppuration or by apparent ulceration of the matrix. In
other cases the patient observes that the nail of one great toe, and a
few days later that of the other, suddenly become of a dark blue color
10
146 GENERAL SYMPTOMATOLOGY.
from subungual effusion of blood, and a few days afterwards the nail
falls off, witliout being preceded or accompanied by pain or other warn-
ing. The nails have also been known to fall off in sclerosis in patches.
An* increased growth of hair has occasionally been observed in cases of
chronic myelitis.
3. Trophic Disorders of tJie Nails and Hair in Cerebral Diseases.
In cases of hemiplegia the nails become curved and cracked, but the
trophic disorders to which they and the hair are liable in cerebral dis-
ease are by no means so well marked as in spinal affections and lesions
of nerve-trunks.
IV. Bej)Sores and other Destructive Processes.
1, Decubitus Aeutus. — Some days or even hours after the occurrence
of a severe spinal or cerebral lesion, or aftei- a sudden exacerbation of
these affections, one or several erythematous patches appear over the
sacrum and gluteal regions, the trochanters of the femur, ankles, or
other parts subjected to pressure. In -these patches, which are of
variable extent and irregular form, the skin assumes a rosy hue, or
becomes dark red or violet, but the color disappears momentarily on
pressure with the finger. After a period which varies from twenty-
four to forty-eight hours, the central part of the erythematous patch is
covered with vesicles or bullae, the contents of which, at first colorless
and transparent, become more or less opaque, reddish, or brown colored.
Under favorable circumstances the vesicle may wither, dry u]), and dis-
appear, and the part recover without further change; but in most cases
the vesicles burst, and leave ill-looking ulcers, the bases of which are
composed of the true skin in a state of ])hlegmonous inflammation, and
infiltrated with blood. The base of the ulcer soon perishes by gan-
grene, the neighboring skin becomes inflamed to a greater and greater
extent, and the gangrenous destruction extends deeper and deeper,
laying bare and including in its destructive operation muscles, tendons,
fiiscise, hgaments, and even the subjacent bones. One of the most re-
markable characteristics of the affection is the extreme rapidity of its
development, the entire cycle of changes being completed in a few days.
Cystitis and hsematuria are not infrequent complications of this condi-
tion, and the muscles of the lower extremities become the subjects of
rapid atrophy. Metastatic abscesses now occur in the kidney, lungs,
and other viscera, the accompanying fever assumes a remittent type,
and the patient dies of septic fever. In some cases the gangrenous
process extends to the sacral bones, and with the destruction of the
BEPSdRES AND OTHER DESTRUCTIVE PROCESSES. 147
sacro-coccygeal ligament the vertebral canal is opened, and thus the
ichorous discharges find access to the fatty cellular tissue which sur-
rounds the dura mater, and by penetrating this membrane they may
even make their Avay to the arachnoid cavity. This grave accident is
followed by a simple purulent or an ichorous ascending meningitis,
which rapidly reaches the base of the brain, and is soon fatal.
2. Chronic Decubitus. — In chronic diseases of the spinal cord the
portions of skin subjected to pressure in the recumbent posture assume
a dark red color, and at times become covered with superficial ulcera-
tions. After a time a black spot appears on the reddened portion of
skin, and, if i)re8sure is contiimed, it enlarges rapidly, and the afiected
skin dries up into a hard leathery mass. In a short time a boundary
line of inflamniation forms around the gangrenous portion of skin, and
the latter may, under proper treatment, be thrown oif, leaving a more
or less healthy granulating surface, which may sometimes cicatrize.
But if the pressure be continued, or if the primary disease of the ner-
vous system undergo a fresh exacerbation, the ulcerated surface assumes
a dark violet color, the gangrene spreads rapidly, and all the destructive
changes characteristic of acute bedsore make their appearance and soon
lead to a fatal result.
3. SyrtDiietrical Gangrene and Local Asphyxia. — This disease,
which was first described by Raynaud, generally involves the fingers,
and less frequently the toes, tips of the nose, and external ear. The
affected parts become suddenly white, cold, bloodless, and insensible,
and motor power is diminished. The skin is wrinkled and shrunken,
the ends of the fingers appear thin and conical, and, when the whole
exti-emity is affected, the pulse is feeble or imperceptible. After some
months reaction sets in : the parts then become congested, of a violet
or livid color, intensely painful, and the seat of troublesome itching,
while vesicles form which are filled with a sero-purulent fluid, and, on
bursting, leave the cutis excoriated. Even at this stage recovery
may take place, but the attack usually recurs, and ultimately the parts
undergo a true nmmmification and the last phalanges of the fingers drop
off". The disease occurs usually in chlorotic and nervous persons, and
is seldom met with in children and old people. It appears to be caused
by a spastic ischtemia of the arterioles.
4. Perforathig Ulcer of the Foot. — This aff"ection, as seen in the
foot, is less like an ulcer than a sinus. It usually presents itself as a
small aperture, which leads directly by a narrow channel to exposed
and diseased bone. From this opening there is little or no discharge ;
the skin surrounding the orifice is greatly thickened by superimposed
layers of epidermis, and, indeed, the formation of a large corn appears
148 GENERAL SYMPTOMATOLOGY.
always to precede the destructive process. The ulcer is, as a rule,
insensible to ordinary stimuli, and there is no pain when the patient is
at rest ; but considerable pain may be caused by pressure on the sole
during locomotion, and the patient often suffers from severe lightning
painsln the lower extremities. Not only are the tissues surrounding
the wound insensible, but there is also, as a rule, more or less complete
cutaneous anaesthesia and analgesia of the whole of the sole of the foot,
and sensation may be diminished in the region of distribution of one
or more of the cutaneous nerves as far up as the calf or knee. The
surfiice is usually cold in the anaesthetic area, and the extremity is
likewise apt to become livid on slight exposure, Avhile it is prone to
attacks of inflammation or of eczema. These inflammatory attacks
sometimes implicate the subcutaneous tissues ; the limb then becomes
greatly swollen and oedematous, and the attack occasionally termin-
ates in suppuration. Lesions of the articulations of the foot fre-
quently accompany this affection, and not only is the joint in direct
relation with the wound diseased, but it is also not uncommon to meet
with more or less complete ankylosis of all tlie phalangeal, metatarso-
phalangeal, and tarso-metatarsal articulations, while sul)luxations of these
joints may take place in other cases. It is, however, pr()l)ab]e that
extensive disease of the bones and joints of the foot o»ily occurs when
perforating ulcer is a symptom of locomotor ataxia. The nails assume
a brownish color ; they become greatly thickened, curved longitudinally
and laterally, furrowed, dry, and cracked. The skin of the leg be-
comes at times pigmented, and there is an increase in the growth of
the hair, while the foot is bathed in sweat which has a permanently
fetid odor. The ulcer is generally situated over the metatarso-phalan-
geal articulations, most frequently over those of the big and little toes.
There may be as many as three ulcers on one foot, and when both feet
are affected the disease is generally symmetrical. Perforating ulcer
has on rare occasions been met with in the hands. The disease is
essentially chronic; the ulcers may, under favorable circumstances,
remain stationary for a long time, and may even heal under prolonged
rest, but a relapse readily occurs Avhen the patient begins to walk.
The most recent observations on perforating ulcer of the foot show
that it is very frequently, if not always, associated with other symptoms
of locomotor ataxia. It was known a long time ago that this form of
ulcer was often accompanied by shooting pains and anaesthesia in the
lower extremities, while strabismus and other ocular troubles Avere also
mentioned as being present in such cases. It is now found that patients
with perforating ulcer also suffer from gastric crises, arthropathies,
swaying movements on closing the eyes, tottering or unsteady gait, and
BEDSORES AND OTHER DESTRUCTIVE PROCESSES. 149
absence of the patellar-tendon reactions. Perforating ulcer is associated
with the neuralgic form of locomotor ataxia, and motor disorders do
not form prominent features of such cases. It may be one of the
earliest symptoms of the disease, and may even precede the anesthesia
of the loAver extremities, so that its association with locomotor ataxia
is not always readily made out. In a case wliich was under the care
of my colleague, Mr. Hardie, there was some degree of anaesthesia of
the lower extremities, but the patellar-tendon reactions were exagger-
ated, and I was about to conclude that the case was not one of loco-
motor ataxia, A closer examination, however, showed that the patient
had suffered from diplopia, and that the pupils failed to react to light,
but reacted to accommodation. The presence of these symptoms ren-
dered it very probable that the patient was in the early stage of loco-
motor ataxia, notwithstanding the patellar-tendon reactions were ex-
aggerated. Dengenerative lesions of the nerves have been found, on
microscopical examination, in several cases of perforating ulcer.
5. Unilateral Profiremive Atrophy of the Face {Heniiatrophia
Facialis Progressiva). — This disease has been observed about twice as
often in women as in men, and it generally begins between 10 and 15
years of age, although it has occasionally been observed as early as 2
and as late as 30 years of age. The characteristic phenomena of this
disease may be preceded for some time by such symptoms as a local
herpetic eruption, toothache, tearing pains in the head and superior
maxillary region, ei)ileptiform attacks in which the spasms are some-
times more or less limited to the side of the face, an attack of hemi-
plegia, spasms of tlie masticatory muscles, and hypersesthesia with
parsesthesia in the side of the face, which is afterwards the subject of
atrophy.
The first definite symptom to attract notice is a peculiar discolora-
tion of circumscribed areas of the skin. Small spots of a white color
and slightly depressed appear on the side of the face, and these gradu-
ally spread so as to coalesce into a patch of considerable size. The
affected area may now assume a yellowish or brownish tint like that
often observed in cicatrices after burns, the skin over them becomes
thin and emaciated, the subcutaneous fat disappears, and the side of
the face becomes deformed by pits of greater or less size and depth.
On the affected side the eyeball often sinks back into the orbit from
disappearance of the orbital fit, the palpebral fissure is narrowed, tiie
beard, eyelashes, and hair of the head become gray and undergo
other structural changes, and the secretions of the sebaceous follicles is
arrested, but the functions of the sweat glands appear to be normally
l^Q GENEKAL SYMPTOMATOLOGY.
performed. lu advanced cases the affected skin feels irregular and
atrophied, and it may assume the form of a cicatrix, but does not
become adherent to the underlying structures. Cutaneous sensibility
is not, as a rule, much affected, hut patients sometimes complain of
various parfesthesise in the atrophied portions of skin, and others have
suffered from neuralgiform attacks, while in one case partial ani^sthesia,
and in a few others hypertesthesia was present.
The muscles are not usually implicated in the atrophy, but in a case
observed by Eulenburg and Guttmann the masticatory muscles on the
affected side were relatively feeble and emaciated, in a few cases
atrophy of one half of the orbicular of the mouth w^as observed, and
in other cases one half of the tongue, the veil of the palate, and the
uvular were found atrophied, but the muscles always gave normal elec-
trical reactions. Romberg reports a case occurring in an unmarried
woman, aged twenty-eight years. The left side of her face had gradu-
ally atrophied as the result of extensive suppuration on the left side of
the neck, which had burst through the tonsil. Every feature, including
the brow, eye, nostril, lips, cheek, and chin, as well as the left half <»f
the tongue and left arch of the palate, was smaller than those on the
opposite side.
The large arteries of the face are generally unaltered in size, and
the tone of the small arteries is retained or increased. The atrophied
parts are generally capable of blushing, and also redden under local
electrical excitation. The temperature is the same on both sides.
The bones of the face liave been found decidedly diminished in
volume. The upper and lower maxillary Ijones and the cartilages of
the nose are often atrophied, especially Avhen the disease begins at an
early age. Romberg was the first to give an accurate description of
this affection, and he classified it amongst the trophoneuroses. The
trophic fibres are not likely to run in the motor branch of the fifth
nerve, inasmuch as paralysis and atrophy of the masticatory muscles,
although occasionally present, are never prominent symptoms. Cases
have been described by Seeligmiiller and Brunner, in which the symp-
toms appeared to have been caused by disease of the cervical sympa-
thetic, but it is probable that, as suggested by Miiller, the lesion is
situated in the medulla oblongata. This disease is, with occasional
long pauses and recommencements, a progressive one, and no treatment
has hitherto been of any avail.
6. Neuroparalytic Ojjhthahnia.—Tlm affection begins with conges-
tion of the conjunctiva, which is followed by profuse secretion of mucus
or pus, nisensibility and opacity of the cornea, and a pseudo-mem-
branous exudation of the iris. In a few days ulceration and perfora-
ARTICULAR AXD OSSEOUS AFFECTIONS 151
tion of the cornea may oecuv, -which is followed by escape of the
humors and collapse of the eye.
Several hypotheses have been advanced to account for this destruc-
tive inflammation of the eyeball, but the most probable is that it is
due to irritation of the trophic fibres which descend from the casserian
tranulion to the eyeball.
7. Simple Glaueovia. — Experiments on animals have shown that
irritation of the nucleus of the trigeminus in the medulla, or of the
nerve itself, is foUow^ed by increase of the intraocular pressure, caused
by augmented secretion of the aqueous humor. As a result of the
high tension the iris and lens are pushed forwards, and the internal
membranes are stretched. It is supposed by many pathologists that
glaucoma is produced by a similar mechanism, although this opinion is
not accepted by all.
V. Nutritive Affections of the Joints, Bones, and Teeth
(Articular and Osseous Trophoneuroses).
1. Affections of Peripheral Oruiin. — Traumatic injuries of nerves, in
which the nerves are not completely divided, are often followed, any
time after the first few days, by disease of the joints, which consists of
a painful swelling like that of subacute articular rheumatism. This
swelling may attack any or all of the articulations of a limb, and often
begins in the joints remote from the injury, so that it cannot be caused
by direct extension of inflammation from the wound. After the acute
stage is over, the tissues about the affected articulations become thick-
ened, and partial ankylosis results, Avhich may ultimately destroy the
mobility of the joint. The bones also may become swollen and thick-
ened after injuries of nerve-trunks, and in young people the same
bones may, at a later period, be arrested in their development. In
progressive unilateral atrophy of the face the bones participate, to some
extent, in the wasting.
2. Affrctions of Spinal Origin. — Attention has been directed by
Charcot and his scholars to the great fre(j[uency with which nutritive
changes occur in joints in spinal diseases. These joint affections may
be divided into acute or subacute, and chronic arthritis.
The acute or subacute form is accompanied hj more or less severe
pain, tumefaction, and redness, just as occurs in acute rheumatism.
This form occurs in Pott's curyature, traumatic lesions of the cord,
idiopathic myelitis, progressive muscular atrophy, acute and chronic
poliomyelitis, and disseminated sclerosis.
Chronic arthritis is irenerallv observed in association with locomotor
ir,2 GENEEAL SYMPTOMATOLOGY.
•ifixia Tl.e knee, liip, shoulder, and elbow-joints are most frequently
'attacked, although the fingers and toes are also liable to be affected.
When the tarsal bones are affected a characteristic deformity is pro-
duced which is named the tabetic foot. The joint disease usually
betrins about the same time as the locomotor incoordination, and its
onset is accompanied or preceded by severe paroxysms of lancinating
pains. The symptoms begin suddenly in the absence of any apprecia-
ble external cause, generally witliout pain or febrile reaction, and the
joint may be enormously swollen within twenty-four hours from the com-
mencement. The general tumefaction disappears after a few days, but a
more or less considerable local swelling remains, caused by the accumu-
lation of serous fluid in the joint and the periarticular serous bursa-.
The fluid, however, disappears from the joint in a few weeks from the
onset. In tlie bimigyi form of the affection the joint may recover com-
pletely, but in the inalignant form the articular surfaces become greatly
altered and so roughened that cracking sounds are heard on movement.
After a time the heads of the bones become atrophied and worn, the
ligaments become relaxed, and the surrounding muscles ai'e so much
atrophied and enfeebled that spontaneous laxations may occur.
Fractures. — Spontaneous fractures occur not infrequently in the
course of locomotor ataxia. The period of fracture is generally pre-
ceded by two or three severe paroxysms of lancinating pains, the limb
is then found swollen and presenting all the symptoms of osteo-perios-
titis, and it then becomes fractured on the slightest movement, or in
the absence of any movement or external cause. The femur is more
frequently fractured than any other bone, the seat of fracture being
generally the neck, but the bones of the leg, arm, foreai*m, and indeed
almost every bone in the limbs and trunk, includinjr those of the
vertebral column, have been found fractured. The spontaneous fract-
ures of ataxics often reunite very readily and rapidly, with an enormous
formation of callus. The earthy phosphates are diminished in the
bones which undergo spontaneous fractures, forming sometimes ordy
sixty instead of eighty per cent, of the bone as in health, while tlie
fatty constituents are enormously increased in amount.
3. Osseous Affections of Cerebral Origin. — In the spastic hemiplegia
of infoncy the bones on the paralyzed side are arrested in their devel-
opment, being smaller and shorter than tlie corresponding Ijones on the
opposite side. In hemiplegic patients arthroi)athies of the joints of
the hand and foot are met with which -are like the acute arthropathies
of spinal origin. The affection begins with a slight swelling and local
increase of temperature, either witli or without pain in the joint, and
at times tumefaction and redness are so marked as to resemble the
AFFECTIONS OF THE GLANDULAK APPAEATUS. 158
articular affections bf acute rheumatism. The sheaths of the tendons
are sometimes implicated along with the joints. These arthropathies
occur, as a rule, simultaneously with late rigidity, although it may
begin a few days after the attack or at a much later period.
4. Osseous Lesions in the Insane. — In insane patients the bones
may either become so soft that they yield readily to pressure, and thus
l)roduce various deformities, or so fragile that they are liable to undergo
spontaneous fracture, and may be found to crumble readily under the
finger and thumb after death. Out of 100 post-mortem inspections of
the insane made by Gudden, evidences of fracture were found in 16
cases, and cliiefly in men who had suffered from general paralysis. In
three-fourths of these cases there were multiple fractures ; in one case
as many as 14, in another 23, and in another 36 fractures. The
morbid changes which occur in the bones of the insane are closely
related to those observed in the spontaneous fractures of locomotor
ataxia.
5. Trophic Affections of the Teeth. — The teeth are not very liable
to undergo changes in diseases of the nervous system. They have
been known to fall out after an attack of herpes affecting the maxillary
branches of the fifth nerve, probably more from necrosis of the bone
than from disease of the teeth themselves. Attention has, in recent
years, been directed to the fact that the teeth sometimes fall out sud-
denly in the course of locomotor ataxia, and in the al^sence of pain or
caries of the bone. They have also been observed to fall out in a case
of sclerosis in patches.
VI. Nutritive and Secretory Affections of the
Glandular Apparatus.
1. Cutaneous Secretory Disorders.
Various pathological facts appear to prove the existence of cutaneous
secretory nerve fibres independently of the vaso-motor nerves. Dimi-
nution or absence of the secretion of sweat may at times exist side by
side with local increase of temperature and redness, indicating vaso-
motor paralysis; and, conversely, the secretion may be increased in
amount along with local diminution of temperature and pallor of the
surface, indicating vaso-motor spasm. Recent experiments show that
peripheral irritation of a divided sciatic nerve in animals induces an
increased secretion of sweat in the paralyzed part.
The cutaneous secretory neuroses consist of excessive sweating or
hi/peridrosis, diminution or absence of secretion or anidrosis, and
151 GENERAL SYMPTOMATOLOGY.
qualitative changes which may be grouped under the name o^ paridrosis.
The profuse sweating of acute disease, that which results from the
action of various toxic agents, and the partial sweats which occur dur-
ing hysterical and epileptoid attacks, are doubtless of nervous origin.
StTu more striking examples are to be found in the unilateral perspira-
tions which have ))een described under the name of Iniperidrosis uni-
lateraUs. This affection is sometimes limited to one-half of the head,
and at other times extends to the arm of the same side, or even extends
over one-half of the body, and is usually associated with severe nervous
affections, such as hemicrania, Graves's disease, dialietes mellitus, tal)es
dorsalis, and general paralysis of the insane. It is probably caused by
lesion of the sympathetic or of the cerebro-spinal centres, with which
it is united.
Anidrosis is a symptom of fever, diabetes mellitus, chronic 13right"s
disease, and of certain skin diseases, and is often associated with grave
nervous diseases like general paralysis of the insane. The diminution
of ])erspiration caused by various toxic agents like atropine is evidently
due to action on the nervous system. A good example of local dryness
of the skin occurs in unilateral atrophy of the face, an<l a similar local
condition may also be found on the extremities in the course of most
of the different cerebral, spinal, and ])eripheral chronic nervous affections.
Paridroscs of various kinds have been observed in diseases of the
nervous system. In some nervous affections the secretion emits a
peculiar, generally very offensive, odor — nsmidrosis. S. Weir Mitchell
observed excessive sweating, Avith stronjr odor of vinegar, after severe
contusion of peripheral nerves, and in one case the smell resembled
that of a bad drain. The secretion at other times becomes changed to
a black, blue, red, or green color, chromidrosiH. Colored ])erspiration
generally occurs in hypochondriacs, in women with uterine disorders
of various kinds, or as the result of severe emotional disturbance. In
some few cases extravasation of blood takes place into the sweat glands,
giving rise to bloody sweating or Jicematidrosis. This condition ajjpears
to be occasionally vicarious menstruation, but it is usually associated
with hysteria and other central nervous affections. It is probable that
in most of the cases described as ha^matidrosis the coloring matter of
the blood alone escapes.
2. Secretory Disorders of the Salivary G-Iands.
Secretory disorders of the salivary glands may occur, in connection
with lesions of the peripheral fibres of the trigeminus, the facial nerve,
or the cervical sympathetic. An increased secretion of saliva is not
AFFECTIONS OF THE GLANDULAK APPAEATUS. 155
an unusual symptom of trigeminal neuralgia, caused by irritation of the
lingual branch of the fifth as the afferent, and the chorda tympani as
the efferent channel. Stimulation of the glosso-pharyngeal nerve also
causes an increased flow of saliva. In peripheral paralysis of the
facial nerve, caused by lesion of the nerve in the Fallopian canal, where
it is accompanied by the chorda tympani, the secretion of saliva is
deficient on the paralyzed side, because the secretory fibres of the sul)-
maxillary and sublingual glands pass through the chorda tympani. In
paralysis of the cervical sympathetic the salivary secretion is diminished
in quantity because tlie ])arotid gland receives a portion of its secretory
fibres through the cervical sympathetic. Irritation of the sensory
nerves of the stomach, especially great acidity of the gastric secretions,
causes an increased flow of saliva, which appears to be an automatic
action, by means of Avhich the gastric acidity becomes neutralized.
Certain poisons, like atropine, paralyze the secretory fibres of the
chorda tympani, and lead to a diminution or arrest of the salivary
secretion : whilst others, like digitalis, physostigmin, nicotin, and
jaborandi, irritate the secretory fibres and cause an increased flow of
saliva. The secretion of saliva may be influenced by direct or reflex
action on the intracerebral secretory paths. Bernard found that an
increased flow of saliva is produced by ])uncture of the floor of the
fourth ventricle behind the origin of the trigeminus, and it is probable
that the increased flow of saliA a observed in bulbar paralysis may at
times be due to irritation of this point. An enormously increased flow
of saliva has been observed by Eulenburg in dogs, after destruction by
the actual cautery of portions of the cortex of the brain lying in front
of the cruciate sulcus. The saliva flowed out in a constant stream from
the angle of the mouth on the opposite side to the injured hemisphere,
and was of the same thin watery character which is observed after
irritation of the chorda tympani.
3. Secretory Disorders of the Lachrymal G-lands.
Trio-eminal neuralgia gives rise to an increase in the amount of
lachrymal secretion both by reflex and direct action, the secretory fibres
of this gland being contained partly in the lachrymal and partly in the
subcutaneous malar nerve. After traumatic injury of the cervical
sympathetic there is an increased flow of tears on the affected side,
probably from vaso-motor paralysis, and the free flow of tears which
often takes place towards the termination of an attack of hemicrania is
probably caused by a similar mechanism. Many anomalies in the flow
of the lachrymal secretion are doubtless of central origin, such as the
15(3 GENERAL SYMPTOMATOLOGY.
copious fl(jw Avhich occurs in hysterical attacks ami in connection with
emotional disturbances.
4. Secretory Disorders of the Crlands of the Digestive Tract.
An increase in the flow of the secretions of the stomach and intes-
tines appears to be caused by affections of the vagus, or of the sympa-
thetic plexuses and ganglia. Diarrhoea and vomiting are often caused
by emotional disturbance, and they may also accompany hysterical
attacks, Avliile apepsia and constipation are frequent accompaniments of
numerous cerebral diseases. Paroxysms of vomiting, and less fre-
([uently of diarrhoea, are also prominent symptoms of locomotor ataxia.
5. Secretory Disorders of the GUnds of the Crcnito-urinary Apparatus.
The influence of the nervous system on the secretion of urine is very
great, but the various channels by means of which it is conveyed are
not accurately ascertained. The most notable examples are polyuria
and diabetes mellitus. Various anomalies may occur in the secretions
of the vagina, uterus, and mannn?e in hysterical females, although it
is doubtful whether they are due to affections of vaso-motor or secretory
nerves. In tlie condition known as irritable uterus there are often, in
addition to the sensory disturbance, numerous anomalies of circulation
and secretion, which are probably of reflex origin. Similar phenomena
may be associated with ilio-lumbar neuralgia. Attacks of hysteria are
often followed by an abundant secretion of mucus from the vagina, and
erotic thoughts may give rise to an obstinate discharge in the absence
of any organic lesion. In "irritable testis" the organ and the sper-
matic cord are often swollen, and many cases of spernuit«nThcea, pollu-
tions, and aspermatism may probably be caused by functional disturb-
ances of secretory or motor nerve fibres issuing from the lumbar portion
of the spinal cord. Pollutions may be caused by reflex irritation, or
by an increased excitability of the centre of ejaculation in the spinal
cord in such diseases as tabes dorsalis, while spermatorrhoea is caused
most probably by debility of the vesiculse seminales,
VII. Nutritive Affections of the Viscera
(Visceral Trophoneuroses),
It has not been found possible to separate the vaso-motor and trophic
fibres of the viscera, either with regard to their anatomical distribution
or their fiinctions. It is very likely that the congestion, ecchymoses,
NUTRITIVE AFFECTIONS OF THE VISCEEA. 157
and extravasations which occur in various central nervous diseases are
caused '»y implication of vaso-motor nerves. Cerebral hemorrhage is
frequently accompanied by i)ulmonary apoplexy or pneumonia of the
lung on the side opi)osite to the lesion ; while lesions of the nuclei of
the origin of the pneumogastric, or of tlie nerve itself, may give rise
to pneumonia and fatty degeneration of the heart. The most frequent
consequences of extirpation of the cteliac and mesenteric plexuses in
animals are congestion of the liver, congestion and extravasations in
the stomach and intestines, and diabetes — all of them symptoms wliicli
are likely to be caused by vaso-motor paralvsis.
CHAPTER YI.
GENERAL SYMPTOMATOLOGY [continued).
C. THE ELEMENTAKY KINESIONEUROSES.
The movements of the body and of its different parts are caused by
muscular contractions, the muscle being stimulated to act by impulses
received through the nervous system, when a nervous stimulus gives
rise to a muscular contraction. Elementary motor disorders admit of
a double classification — the one anatomical, the other physiological, the
two traversing each other at right angles.
Anatomical Classificatio7i. — Elementary motor disorders may be
divided into those which affect (i) the muscles of external relation —
the external Jcine8ioneuro.^es, (ii) the muscles of the internal organs —
internal or visceral kinesioncuroses, and (ill) the muscular fibres of
the vascular system — the vascular kincsicmcuroses, or the angioncuroscs.
Physiological Classification. — Motor disorders may be divided into
(1) the conditions in which there are excessive muscular contractions —
spasms or hyperkineses, (2) those conditions in Avliich there is a dimi-
nution or loss of the power of exciting the muscles to contraction —
paralyses or akineses, and (3) various anomalous muscular contractions
which may be comprised under the name of the synkineses. The
hyperkineses and akineses may be subdivided, according to the func-
tion of the nervous apparatus which is the seat of the lesion, into three
classes, namely : a, the voluntary, 6, the reflex, and c, the automatic
kinesioneuroses.
I. The External Kinesioneuroses.
Methods of Examining the Motor Apparatus.
As an introduction to this part of the subject it will be useful to
describe briefly the various methods employed for discovering the pres-
ence or absence of motor disorders of the external muscular apjiaratus.
The striped muscles are, for the most part, connected with the skeleton,
and by their contractions they move the bones to which they are
attached, and thus constitute the active agents in maintaining tlie
various attitudes of the body. The graceful form of the body is also
THE EXTERNAL KINESIONEU ROSES. 159
in great measure due to the rounded bellies of the muscles which help'
to fill up the si)ace between the bones and the skin and the subcutane-
ous tissues. In subjecting the neuro-muscular mechanism of external
relation, therefore, to a methodical examination we must attend (1)
to the form of the body during repose, and (2) to the attitudes of the
body during actual or attempted movements.
1. Examination of the Body during Repose.
The 1)ulk and consistence of a muscle as felt through the skin may,
as a rule, l)e accepted as a more or less adequate sign of the degree of
its nutrition and motor power, and consequently an examination of the
exposed body by inspection and palpation affords much valuable in-
formation with regard to the motor mechanism. If, for instance, the
outer surface of the shoulder is seen to be flattened and the head of
the humerus can l)e felt immediately underlying the skin, it is known
that the deltoid is wasted, and if the opposite shoulder is at the same
time plump and rounded, it is inferred that the deltoid of the affected
shoulder is Avasted from a special and not from a general cause. But
if the deltoid, instead of being wasted, is unduly prominent and tense,
and the elbow is held })ermanently removed from the trunk, it is at
once a])parent that the muscle is the subject of spasm. Distortion of
the limbs often shows at once that certain groups of muscles must be
paralyzed, or that their antagonists are in a state of spasm, and pei'-
formance of passive movements will generally decide this question,
showing directly whether a particular group of muscles is relaxed or
tense. In the case of spasm valuable information may be obtained by
producing a corresponding deformity on the healthy side by means of
the faradic current, and in the case of paralysis, by exciting the
antagonists of the affected muscles to contraction by means of fara-
dization.
2. Examination of the Body during Movement.
The muscles of external relation may be excited to contraction by
(a) voluntary, (b) reflex, (c) automatic, (d) mechanical, and (e) electrical
stimuli, and the response of the muscles to one or more of these stimuli
may be wanting, excessive, or otherwise disordered.
(a) Voluntary Movements. — The student should make a careful
study of the different forms of disordered locomotion, and be able to
distinguish at a glance the hemiplegic walk, the spastic gait, and the
loose and dangling limbs of the various forms of atrophic paralysis.
The patient should be asked to perform special movements, such as
standing on one leg, standing with feet touching along their inner
1(50 GENERAL SYMPTOMATOLOGY.
1 .orders (tlic eyes being closed), ascending a stair, writing, speaking,
and mimetic facial movements, in order that any deviation from the
normal may be carefully observed. Attention should be directed to
ascertain whether incapacity to perform a particular movement is caused
bv ])aralysis of a group of muscles or spasm of their antagonists. An
approxiiiiate estimate can be formed of the degree of paralysis present
by comparative testing of the resistance which can be opposed by i)as-
sive movements, while a more accurate test of motor power which
can be increased by certain groups of muscles is afforded by the various
forms of dynamometers. It is also important to observe whether the
muscular contraction can be maintained for some time without inducing
exhaustion, and whether the intended movement is executed with pre-
cision and steadiness, or is interrupted by tremors and antagonistic
secondary movements. Slowness in executing certain movements is a
sign of diminished motor i)Ower, and feebleness of the muscles of the
liaiid, for instance, may sometimes be more readily detected by asking
the patient to write his name or to perform the " devil's tattoo " on the
tal)le, than by estimating the strength of the grasp.
(b) Heflex movements may be tested by tickling, pricking, pinching,
and faradic excitation of the skin and accessible mucous meml.ranes.
The reflexes of the special senses nnist be tested by their special exci-
tants, while it is most important to examine the deep reflexes by ta])-
ping tendons, fascige, and the periosteum.
(c) Automatic Movements. — The movements of respiration and of
the iris, and the action of the sphincters, may be mentioned as examples
of automatic actions which ought to be carefully observed. In ordinary
locomotion, the observer ought to be able to distinguish at a glance the
ataxic walk, the cerebellar reel, the staggerinir gait of ^Meniere's disease,
and the uncertain, tremulous walk of sclerosis in patches.
(d) Mechanical Stimuli. — A moderately strong blow over almost
any muscle induces a contraction of the fasciculus struck, especially if
the blow fall near the point of entrance of the motor nerves. In ex-
hausting diseases like phthisis, when the nutrition of the muscles is
greatly diminished, a sharp blow causes the formation of a wheal which
lasts several seconds, and from which small waves of contraction run in
l)oth directions towards the extremities of the muscle, this reaction
l)eing called idio-muscular contraction.
(e) Electrical Stimuli.~T\\e electrical currents usually employed for
clinical investigation are (1) the faradic and (2) the galvanic currents.
(1) The faradic current consists of a series of isolated currents, each
of momentary duration, and of very rapid development and decline,
following each other in (piick succession and flowing alternately in
THE EXTEEXAL KIXESIONEU ROSES . 161
oi)posite directions. Faradic exeitahility or irritability is tlie term
used to designate the kind and strength of the reactions exhibited hy
muscles and nerves under the influence of the faradic current. Mus-
cuLir contraction may be induced by the direct application of the faradic
current to the muscles themselves, or indirectly through excitation of
the motor nerves. The cathode of the secondary induced current is
usually employed as the exciting pole, while the anode may be placed
upon some indifferent part of the body, as the sternum or patella.
Direct excitation of accessible muscles is best performed when the poles
are applied over the points at which the motor nerves enter the muscles,
which may be ascertained by reference to Ziemssens diagrams. The
faradic excitability of both nerves and muscles in diseased conditions
admits only of quantitative changes. It may remain normal or be
slightly increased in cases of muscular spasm, in that form of muscular
paralysis which is attended by tension, and in hysterical pai-alysis ;
while it is diminished or lost in that form of paralysis which is attended
by wasting of the muscles, with the exception of the active stage of
progressive muscular atrophy, in which it may be increased. The
degree of the excitability runs a more or less parallel course in the
nerves and muscles.
(2) The galvanic current is continuously produced and runs in the
same direction, and with the same intensity, but by means of the com-
mutator the current may be interrupted at pleasure, or even quickly
reversed, a change which induces a very powerful contraction.
G-alvanic excitability or irritability is a term used to express the
reactions obtained in response to opening and closing the circuit, and
to the continuous passage of the current. The law of contraction
both of motor nerves and muscles rests upon the facts that the cathode
produces contraction chiefly on closure of the current, the anode chiefly
on opening the current, and that the stimulus of the cathode is stronger
than that of the anode.
The law of normal contraction may be expressed by the following
formulae.
Let An = anode, Ca = cathode, C =^ medium contraction, c =
feeble contraction, C = strong contraction, S =^ closure of current,
= opening of current, Te = tetanic contraction, thus:
Weak currents produce CaSc.
Medium currents produce CaSC, AnSc, AnOc.
Strong currents produce CaSTe, AnSC, AnOC, CaOc.
In diseased conditions the law of contraction may remain (a) normal,
or deviations from the normal law may occur by way of {h) increase or
11
1^2 GENERAL SYMPTOMATOLOGY.
{c) diminution of the excitability, or by changes in (d) the quality of
the various reactions.
(a) A normal degree of the galvanic excitability is obtained in cases
of muscular spasm, in hysterical paralysis, and in paralysis attended
by muscular tension.
(h) Simple increase of the galvanic excitability occurs in certain
forms of spasmodic paralysis, tabes dorsalis, and as a transient symptom
in a few cases of peripheral paralysis. Increase of the excitability
gives rise to the following deviations from the normal law :
Weak currents produce CaSC, AnOC.
Medium currents produce CaSTe, AnOC, CaOC.
Strong currents produce CaSTe, AnOTe, CaOC.
(c) Simple diminution of the galvanic excitability occurs in all those
cases in which paralyzed muscles undergo a minor degree of atrophy.
The following formulae express simple diminution of excitability :
First degree, strong currents produce CaSC, AnSc, AnOc.
Second degree, strong currents produce CaSc.
(d) Qualitative as ivell as quantitative alterations of the excitability
are found in all those cases in which paralyzed muscles undergo a con-
siderable or a profound degree of atropliy, and this kind of reaction
has consequently been called the "atrophic test," or the "reaction of
deo-eneration." The alterations in the reaction of the nerves and the
muscles do not run a parallel course, so that the two must be separately
described.
(j) Reaction of the Affected Nerves. — The reaction in the afiected
nerves begins on the second and third day after a severe attack of that
form of paralysis which will be subsequently described as atrophic
paralysis, and a continuous uniform diminution of the galvanic as of
the faradic excitability is observable without any qualitative change, and
in rare cases only is it preceded by slight increase. The diminution
begins in the part nearest the lesion, and extends rapidly to the
periphery. At the end of the first, or in the course of the second
week (from the seventh to the twelfth day), the excitability wholly dis-
appears. In incurable cases the loss of the excitability is permanent,
but if repair of the diseased tissue takes place, the excitability, after
being lost for a variable period, is restored. The reactions to both cur-
rents appear simultaneously, beginning first in the central segments of
the nerve and spreading slowly to the periphery.
(jj) Reaction of the Affected 3Iuscles. — The reactions obtained by
the application of the faradic current directly to the muscles are
quite similar to those obtained from the application of the current to
the degenerated nerves. When the electrode is placed over the para-
THE EXTERNAL KINESIONEUROSES. 163
Ivzed muscle a diminution of the excitability is observed to\^ards the
end of the first week, and in severe cases there is complete extinction
of it towards the end of the second week. When the case is incurable
the foradic contractility of the muscle is permanently abolished, but in
curable cases it reappears along with the restitution of voluntary power,
although usually somewhat later than in the nerves. As recovery pro-
ceeds the faradic excitability increases gradually but slowly, and o-en-
erally remains for a long time abnormally low, especially if the paralysis
has been of long duration.
The galvanic excitabiUf// falls slightly during the first week, but in the
course of the second week it becomes enormously increased and con-
tinues to increase until about the end of the fourth week. The aifected
muscles now respond to currents much too feeble to act upon healthy
muscles. The character of the contractions is also changed, and
instead of appearing suddenly and being of short duration, as in
health, they now develop gradually and slowly, are protracted in dura-
tion, and readily pass into tetanus even when produced by feeble
currents.
The law of muscular contraction also becomes qualitatively altered, so
that anodal closing contraction soon equals or exceeds cathodal closing
contraction (AnSC = or> CaSC), and cathodal opening contraction soon
equals or exceeds anodal opening contraction (CaOC = or > AnOC).
The following formulge express the qualitative changes in the reaction
of degeneration:
Weak currents produce during stage of increase CaSC, AnSTe,
AnOC, CaOC.
^ledium currents produce during stage of gradual decrease CaSc,
AnSTe.
Strong currents produce during final stage prior to abolition AnSc.
The following diagrams, borrowed from Erb, represent graphically
the general relations of motor power, electrical excitability and struct-
ural changes of the nerves and muscles which are present in the differ-
ent stages of paralysis. The first tliick vertical line or ordinate indi-
cates the sudden appearance of paralysis ( IBD )» and the period of
return of motor power is indicated by a ( * ), whilst the succeeding
ordinates represent intervals of one or more weeks dating from the
occurrence of the attack. The undulations in the line representing
the galvanic excitability of the muscles indicate qualitative changes in
the reactions. In the first degree of the reaction of degeneration
(Fig. 66), the electrical excitability of both nerve and muscle falls
during the first week, the nerves lose all their electrical reactions
during the second week, but the muscles lose only their faradic con-
164
GENERAL SYMPTOMATOLOGY
tractility during tliis period, wliilst the galvanic excitability becomes
greatly increased and manifests the qualitative changes already de-
scribed. At the end of the sixth week there is a gradual return of
Degeneration
of the Nerve.
Fig. 06.
Recovery Rapid.
Atrophy and
Multiplication of Nuclei
in the Blusciilar Fibres
Regeneration
Motility.
i ( Galv.
I 1 Farad.
g ("Galv. and
tj -; Farad. Excit-
|z; (ability.
10. U 12. Week.
motor power, and at the end of the seventh week there is a gradual
return of the electrical reactions of the ner\'e and of the faradic con-
tractility of the muscle, while the galvanic reactions of the muscle
gradually sink, and the (iualitati\e changes disaj)pear until gradually
the normal reaction is established.
In ''the second degree of the reaction of degeneration the faradic
Degeneration
of the Nerve.
FlO. 67.
Recovery Slow
Atrophy, etc ,
of jrviscles.
]{egeneration.
1. 2. 4. i;. 111. 15. 20. 2.'>. :?(i
Motility.
Galv.
Farad.
g ( Galv. and
•g •< Farad. Excit-
>5 (ability.
and galvanic excitability of the nerve does not appear until the thirtieth
week (Fig. 67), while in the third degree (Fig. 68) the excitability of
the nerve never returns, but the galvanic excitability of the muscle
THE EXTERNAL KINESIONEUROSES.
165
only becomes finally lost after a pi-olonged period, in some cases extend-
ing over a period of two years.
A "partial reaction of degeneration" (Fig. 69) has been described
by Erb, in which the faradic and galvanic excitability of the aifected
4 \ Galv.
^ ( Farad.
=■ (Galv. and
^ - Farad. Excit-
5^ (ability.
Degeneration
of the Nerve.
Fig. (58.
No Recovery.
Atropliy,
Jlultiplication of Nuclei, Cirrhosis
t'omplete
Disappearance.
1 3. 1(1. 211.
o. 80. till. 1(1(1. Week.
nerve is diminished, but not abolished, the diminution beino- sometimes
only to a slight degree. The faradic excitability of the paralyzed
muscle undergoes a diminution corresponding to that of the nerve, but
the galvanic excitability of the muscles manifests the quantitative and
([ualitative changes which are so characteristic of the severer form of
the reaction of degeneration.
Fig. G9.
Atrophy and
Degeneration of Multiplication of Nuclei
the Nerve (?) in the Muscular Fibres.
KeKeneratiou
Motility.
1
fGalv.
(Farad.
(Galv.
^ Farad,
(ability.
and
Excit
1. Hypcrkinesis of the 3Iuscles of External Relation.
Hyperkinesis of the voluntary muscles consists of abnormal contrac-
tions called spasms. Muscular spasms consist of contractions which
IQQ GENERAL SYMPTOMATOLOGY.
are disproportionate to the degree of external stimulus, or which arise
in the absence of external stimulation as the result of morbid irritation.
Spasmodic affections may be divided into, a, clonic spasms, in which
the muscles are in a state of rapidly alternating contractions and re-
laxations ; and, b, tonic spasms, in which the affected muscles are
maintained in a state of persistent and equable contraction.
a. Clonic Spasms.
(1) Tremor is the mildest form of clonic spasm. It consists of slight
contractions of groups of muscles by means of which a peculiar
rhythmical oscillation of the limbs and trunk is produced. The higher
degrees of tremor cause manifest trembling of the limbs and trunk,
while fibrillary contractions consist of alternate contractions and re-
laxations of individual bundles of muscular fibres which are visible as
wavy oscillations under the skin, but do not give rise to any movement
of the limb. There are two chief varieties of the severer form of
tremor which moves the limbs : one of which persists during repose,
and is met Avith in paralysis agitans ; and the other which appears only
when the patient makes a voluntary effort, and is observed in sclerosis
in patches,
(2) Convulsion is the severest form of clonic spasm. It consists of
energetic contractions and relaxations of particular muscles or groups
of muscles which produce a rapid succession of vigorous movements,
and give rise to twitchings of the face, startings of the limbs, and
movements of the head and body. If the majority of the muscles of
the body are affected with alternating contractions and relaxations, so
that extensive and irregular movements of the trunk and limbs are
produced, the condition is termed general convulsion, which forms the
most prominent feature of epilepsy, uraemia, eclampsia, and hysterical
attacks.
h. Tonic Spasms.
(1) Cramp is the simplest form of tonic spasm, and consists of a
persistent painful contraction of a muscle or of a group of muscles.
Cramp of the calf is the most common variety of this affection when it
IS limited to a single muscle, while tetanus may be taken as the best
example when the majority of the muscles of the body are affected.
A peculiar modification of cramp is met with in"^ catalepsy. The
muscles are moderately contracted, but the resistance they "offer to
passive movements may be readily overcome, and the limbs may be
made to assume constrained positions which thev retain. From the
THE EXTERNAL KINESION EUROSES. 167
manner in which the limbs can be moulded into various positions this
condition has been caWed Jiexibilitas cerea.
(2) Muscular tension is a state of moderate contraction of muscles
which occurs either when they are stretched by passive movements or
by a voluntary contraction of their antagonists. This condition is
always associated with a certain degree of loss of voluntary power over
the affected muscles.
(3) Contracture is meant to express any persistent shortening of a
muscle, whereby its points of origin and insertion are permanently
approximated. The varieties of contraction are myopatliic contracture,
when the shortening occurs as a result of disease in the muscle itself;
imralytic or secondary contracture, when it occurs in healthy muscles
which have their ends permanently approximated owing to paralysis of
their antagonists ; and primary or neuropathic contracture, when the
muscles are persistently rigid and shortened from abnormal innervation,
a condition which is always associated with a certain degree of paralysis.
In the last variety the rigidity of the muscle usually disappears during
sleep and gradually returns on awakening, and it is almost always in-
creased by voluntary and passive movements.
Pressure points are frequently observed in spasmodic affections.
Pressure upon certain points puts a stop at times to the convulsion
when present, and consequently these points may be called pressure-
arresting points. In other cases the convulsions are brought on by
pressure on particular points, and these may, therefore, be called pres-
sure-exciting points. Pressure points of the first kind have been par-
ticularly observed in facial spasm, and they correspond, like the painful
points in neuralgia, to the various branches of the trigeminus, and are
not unfrequently sensitive to pressure.
Spasms are caused by increased irritability of some part of the motor
nervous mechanism. When the spasm, Avhether it be clonic or tonic,
is limited to the area of distribution of particular nerves, the lesion is
most probably situated in some part of the spino-neural system, either
in the centre or efferent fibre, or in some afferent fibres, the last con-
stituting rejlex spasms. Paroxysmal clonic convulsions are caused by
irritation of the cortex of the brain, and certain forms of tonic and
clonic spasms are caused by irritation of the fibres of the pyramidal
tracts. Paroxysmal tonic contractions are most probably caused by
irritation of the cortex of the cerebellum. Persistent muscular tension
and contracture are caused by disease of the pyramidal tracts, and are
associated with paralysis. Dr. Hughlings Jackson explains the pres-
ence of tension under such circumstances by supposing that the with-
drawal of the cerebral influence allows the tonic action of the cere-
1(38 GENERAL SYMPTOMATOLOGY.
bellum to become predominant. Against this theory it is urged that
tension is present in cases of transverse myelitis, in Avhich both the
cerebral and cerebellar influences are withdrawn. It is therefore prob-
able that muscular tension is caused by the removal of the inhibitory
action of the cerebrum, owing to disease of the pyramidal tracts, per-
mission being thus given for the predominant action of the reflex
nervous mechanisms of the spinal cord.
2. Akinesis of the Muscles of External Relation.
By akinesis or paralysis of the muscles of external relation is under-
stood the diminution or abolition of the power to contract the affected
muscles by voluntary effort. The term paresis is used to denote tlie
diminution of motor power. Some authors have endeavored to restrict
paralysis to its complete abolition, but this term Avill be employed hei-e
in a generic sense as embracino; both conditions.
Classification.
Paralyses of the muscles of external relation are susceptible of being
classified according to the nature, cause, and situation of the lesion, the
distribution of the paralysis, and the functional disorders of the muscles
which accompany paralysis of them. Tliese divisions constitute the —
I, pathological, ii, etiological, ill, topographical, iv, clinical, and, v,
physiological classification.
I. THE PATHOLOGICAL CLASSIFICATION.
The diff'erent varieties of paralysis are arranged, according to the
nature of the lesion, into rheumatic, syphilitic, inflammatory, and other
forms. They may also be divided into organic and functional lesions,
according as the morbid changes which underlie the paralysis are or are
not capable of being recognized by our present means of research.
II. THE ETIOLOGICAL CLASSIFICATIOX.
The functional paralyses are not susceptible of being arranged
according to the situation of the lesion, and they are therefore usually
classified according to tlie cause of the aff"ection. They are usually
divided into (1) toxic, (2) febrile and post-febrile, (3) reflex, (4) post-
epileptic, and (5) hysterical paralysis.
III. THE TOPOGRAPHICAL CLASSIFICATION.
The organic paralyses lend themselves readily to a classification
according to the situation of the lesion. They may be divided into (i)
THE EXTERNAL KINESIONEU ROSES. 169
myopathic paralyses, or those in Avhicli tlie primary disease is situated
in the muscles themselves, and (ii) neuroiyathic paralyses, or those in
Avhich the primary disease is localized in some part of the nervous
system.
The neuropathic paralyses, with which we have to do chiefly here,
may be subdivided into (1) cerebral, (2) spinal, and (3) neural or
peripheral i)aralyses, according as the lesion is situated in the brain,
spinal cord, or peripheral nerves respectively. But although this divi-
sion is very convenient, a much more important distinction is that which
divides them into (1) cerebrospinal and (2) spino-neural paralyses.
In the cerebrospinal variety the lesion is situated either in the motor
centres of the cortex of the brain or in the pyramidal tracts.
In the spino-neural variety the lesion is situated in the anterior gray
horns of the spinal cord and their upward continuations in the medulla
oblongata, pons, and crura cerebri, or in the fibres of the })eripheral
nerves which connect the ganglion cells of these horns with the muscles.
It will immediately be found that this topographical division corresponds
more or less closely with the divisions of the physiological classification,
and this constitutes its chief advantage.
It may here be noticed that when the lesion is restricted to one of
the physiological tracts of the spinal cord the affection is called a
system-disease, and when several of them are simultaneously implicated
the affection is called a mixed or indiscriminate disease. Amongst
the mixed diseases we shall also include complicated cases of cerebral
paralysis.
IV. THE CLINICAL CLASSIFICATION.
Various names have been given to a paralysis according to its extent
and distribution. The paralysis is sometimes limited to a single muscle
or group of muscles, or all the muscles supplied by a single nerve or
plexus of nerves may be implicated ; when all or almost all the muscles
of a single extremity are paralyzed, the condition is called a monoplegia.
In other cases the paralysis afi'ects both halves of the body symmetri-
cally, and then it generally begins in the lower extremities, and spreads
to the trunk and upper extremities. This is the usual form of paralysis
Avhich results from disease of the spinal cord, and is termed paraplegia.
In other cases the paralysis afi'ects the lateral half of the body, impli-
catino; the face, arm, and le<z of the same side, and it is then termed
hemiplegia. The lesion which causes this form of paralysis is usually
situated in the opposite hemisphere of the brain ; hemiplegia of spinal
origin is named hemiparaplegia. When the upjier and lower extremi-
ties on both sides are paralyzed, the condition, when due to spinal dis-
170 GENEEAL SYMPTOMATOLOGY.
ease, has been named paraplegia cervicalis, and when caused by cerebral
disease, bilateral hemij^legia, or pamplegia. When the ocular or flicial
muscles on one side, and the limbs on the opposite side, are paralyzed,
the condition is called crossed or alternate hemiplegia.
V. THE PHYSIOLOGICAL CLASSIFICATION.
A much more important distinction than those depending upon the
extent and distribution of the affection is that which divides the various
forms into (1) atrophic, and (2) spastic or spasmodic paralysis. This
division does not embrace every form of paralysis, inasmuch as in some
paralytic affections the muscles neither undergo active Avasting, nor are
affected by spasm. This distinction is, nevertheless, a very important
one, and ought to be kept in view in the clinical examination of every
case of paralysis. Both atrophic and spasmodic paralyses embrace
some forms of myopathic paralysis, but, when these are due to an
organic disease of some part of the nervous system, they correspond
respectively to the spino-neural and cerebro-spinal paralyses of the
topographical classification.
The different methods of classification are combined into one scheme
in the following tables :
THE EXTERNAL KINESIONEUROSES.
171
T-ABLE I. — Hetiropathie Paralyses.
A. ORGANIC PARALYSES.
, Spino-neural or Atrophic Paralyses.
I. Neural or Peripheral Paralysis.
II. Reflex Atrophic Paralysis.
1. Acute Atrophic Spinal Paralysis of Infants.
2. Acute Atrophic Spinal Paralysis of Adults.
3. Paralysis Ascendens Acuta.
4. Chronic Atrophic Spinal Paralysis.
III. Spinal Atrophic Paralyses. -{ 5. Peri-ependymal Myelitis— Syringomyelia.
6. Progressive Muscular Atrophy.
7. Primary Labio-glosso-laryiigeal Paralysis.
8. Ophthalmoplegia Externa.
t 9. (Pseudo-hypertrophic Paralysis.)
II. Cerebro-spinal or Spasmodic Paralyses.
1. Primary Lateral Sclerosis.
2. Compound Lateral Sclerosis.
a. Amyotrophic Lateral Sclerosis.
6. Combined Posterior & Lateral Sclerosis.
3. Secondary Lateral Sclerosis.
a. Compression Myelitis.
b. Transverse Myelitis.
1. Tonic Spasm. I " j ^ >r> J-
(. b. Late Rigidity.
f a. Intermittent Tremor.
I b. Choreiform Movements.
2. Tonic & Clonic ' i. Pre-hemiplegic Chorea,
ii. Post-hem iplegic Chorea.
iii. Spastic Hemiplegia of
Infancv.
I. Spinal Spasmodic Paralyses.
(paraplegia.)
II. Cerebral Paralyses.
(hemiplegia.)
Spasm.
3. Clonic Spasm.
I
f a. Continuous or Remittent
! Tremors.
J
j b. Athetosis.
[ c. Post-heniiplegic Hemiataxia.
III. Mixed Paralysis.
B. FUNCTIONAL PARALYSES.
(1) Toxic Paralysis.
(2) Febrile and Post-febrile Paralysis.
(3) Reflex Paralysis.
(4) Post-epileptic Paralysis.
(.5) Hysterical Paralysis.
172
CxENEKAL SYMPTOMATOLOGY.
Table II.— Paralyses from Organic Disease of the Nervous System.
TOPOGRAPHICAL DIAGNOSIS.
I. Spino-neural Lesions.
I. LESIONS OF EFFERENT NERVE FIBRES.
II. LESIONS OF AFFERENT NERVE FIBRES.
III. LESIONS OF THE ANTERIOR GRAY
CLINICAL DIAGNOSIS.
I. Atrophic Paralyses.
I. NEURAL or peripheral PARALYSES.
II. REFLEX ATROPHIC PARALYSIS.
III. SPINAL ATROPHIC PARALYSES.
1. Acute Atrophic Spinal Parah'sis
of Infants.
2. Acute Atrophic Spinal Paralysis
of Adults.
3. Acute Ascending Paralysis.
4. Chronic Atrophic Spinal Paralysis.
.5. Peri-ependymal Myelitis. "]
6. Progressive Muscular Atrophy. i
7. Primary Labio-glosso-laryngeal
Paralysis.
8. Ophthalmoplegia Externa.
9. (Pseiido-hypertrophic Paralysis.)
II. Spasmodic Paralyses.
I. spinal spasmodic paralyses.
1. Primary Spinal Spasmodic Paralysis.
2. Compound Spinal Spasmodic
Paralysis.
3. Secondary Spinal Spasmodic
Paralysis.
II. CEREBRAL PARALYSES.
1. Ordinary Hemiplegia.
2. Alternate Hemiplegia.
3. Hemiplegia and Hemianc^sthesia.
4. Hemiplegia, Hemianaasthesia, and
Hemianopsia
5. Pre-hemiplegic Chorea.
6. Post-hemiplegic Chorea.
7. Athetosis.
8. Post-hemiplegic Continuous
Tremor and Hemiataxia. j
9. Spastic Hemiplegia of Infancy.
10. Unilateral Convulsions and
Hemiplet
HORNS. (POLIOMYELOPATHIES.)
Poliomyelitis Anterior Acuta
Infantium.
Poliomyelitis Anterior Acuta
Adullorum.
Poliomyelitis Acuta.
Poliomyelitis Anterior Chronica.
Degeneration of the Ganglion Cells of
the Anterior Horns of the Spinal
Cord and Motor Cells of the Me-
dulla Oblongata.
(Primary Muscular Disease.)
II. Cerebro-spinal Lesions.
(PYRAMIDAL TRACT.)
. LESIONS OF THE LATERAL COLUMNS.
Primary Lateral Sclerosis.
Amyotrophic Lateral Sclerosis.
Combined Posterior and Lateral
Sclerosis.
/ Compression Myelitis.
l Transverse Myelitis.
II. LESIONS OF THE CEREBRAL PYRA-
MIDAL TRACT AND MOTOR AREA OF
CORTEX.
r Lesions of Lenticular Nucleus.
I Area of Lenticulo-striate Artery.
Lesions of Crura and Pons.
Lesions in Area of Opto-striate Artery.
Lesions in the Area of the Posterior
External Optic Artery.
f Unilateral Atrophy of the Motor
Area of Cortex.
Porencephalus.
Lesions of Motor Area of Cortex.
THE EXTERNAL KINESIONEU ROSES. 173
3. Reflex Central Kinesioneuroses.
The disorders which occur in the reflex mechanisms which are situ-
ated in the different parts of the nervous system are almost infinitely
numerous, but we shall here mention only a few of the more usual dis-
orders of the spinal reflexes. The spinal reflexes may be divided
into (1) the superficial, and (2) the deep reflexes, while disorders of the
reflex mechanisms may declare themselves by way of an excessive reac-
tion, constituting (</) reflex hyperkinesis^ or by diminution or loss of
reaction, constituting (h) reflex akinesis.
(1) The Superficial Reflexes.
The superficial reflexes are excited by stimulation of the skin and
accessible mucous membranes. The tests employed for estimating the
various degrees of these reflexes are tickling, pricking, pinching, or
gently scratching the surface, or the application of the faradic current
to the surface by means of dry electrodes or the faradic brush.
The following superficial reflexes may be distinguished (Fig. 70) :
(ji) The plantar reflex, obtained by tickling the sole of the foot and
depending upon the integrity of the reflex loops through the lower end
of the cord (conus meduUaris).
[b) The gluteal reflex, consisting of contraction of the gluteal mus-
cles caused by stimulating the skin over the buttock, and depending
upon the integrity of the loops through the fourth and fifth lumbar
nerves.
(c) The cremasteric reflex, by which the testicle is drawn up when
the skin on the inner side of the thigh is stimulated, and demanding
the integrity of the first and second pairs of lumbar nerves.
{d) The abdominal reflex, consisting of a contraction of the abdominal
muscles, chiefly the rectus, caused by stroking the skin on the side of
abdomen from the edge of the ribs downwards, and requiring the integ-
rity of the arc throusrh the nerves from the eighth to the twelfth dorsal
nerves,
(g) The epigastric reflex, producing a dimpling of the epigastrium
on the side stimulated. It is induced by stimulation of the side of the
chest in the sixth, fifth, and sometimes fourth intercostal spaces. This
dimpling probably depends upon contraction of the highest fibres of
the rectus abdominis, and its presence requires the integrity of the cord
from the fourth to the sixth or seventh pairs of dorsal nerves.
(/) The erector spinal reflex, consisting of a local contraction of
these muscles, caused by stimulation of the skin along their edge from
174
GENERAL SYMPTOMATOLOGY.
<
Fig 70.
a
)0..
^.■.
Motor.
Sterno-mastoid ....
Trapezius ... . .
Khomboids and rotators of
humerus . . . .
Diaphragm ...
Deltoid, biceps, brachalis,
supinators.
Serratus.
Triceps, extensors of
wrist and fingers, and
pronators
Flexors of wrist and long
flexors of fingers . .
Intrinsic muscles of hand
• Sensory.
Neck and scalp.
Neck and shoulder.
Reflex,
Intercostal muscles
Outer aspect of arm and
forearm.
Anterior and posterior as-
pects of arm, forearm,
outer half of hand, and
•iy,2. fingers.
Inner aspect of arm, fore-
arm, innerhalf of hand,
and iYi fingers.
Front of thorax
Ensiform cartilage ,
" Scapular.
Epigastric.
(- Abdominal muscles
Abdomen ....
Umbilicus . . .
J- Buttock, upper part
Abdominal
)!
Flexors, hip
Extensors, knee
Adductors 1
Abductors ■ Hip
I
Extensors (?) J
Flexors, knee(?)
Muscles of leg moving
foot.
J Groin and scrotum (front)
{Outer side
Front side
Inner side
. J Thio-h I Front side
Cremasteric
Knee-jerk.
Leg, inner side . . . . i
Buttock, lower part . . r Gluteal.
" Back of thigh ....
Leg and foot, except "I Foot-chmns.
inner part .... J Plantar.
Perineal and anal muscles Perineum and anus.
Skin from coccyx to anus
DI.1GKA.M AM, TaIILE SHOWING THE APPROXIMATE RELATION TO THE SPINAL NERVES OF THE VARIOUS SENSORY AND
Reflex Functions of the Spinal Cord. (After Gowers.)
THE EXTERNAL KINESIONEUROSES. 175
the angle of the scapula to the iliac crest, and demanding the integrity
of the reflex arcs in the dorsal region of the spinal cord.
[y) The scapular reflex, consisting of a contraction of some, or
nearly all, of the scapular muscles according to its degree, and demand-
ing the integrity of the cord at the level of the upper two or three
dorsal and lower two or three cervical nerves.
(A) Ti\Q palmar reflex consists of a contraction of the flexors of the
fingers induced by tickling the palm of the hand. It requires the
integrity of the reflex arcs through the greater part of the cervical
enlargement. This reflex is not readily induced during waking hours
and consequent cerebral activity, probably because the hand is much
more under cerebral influence than the foot. During sleep, however,
and in young infants, when the cerebral influence is suspended, or not
yet fully established, this reflex is as readily induced as the reflex of
the sole of the foot.
{{) Cranial Reflexes. — The chief reflexes of the cranial nerves are
the contraction of the palatal muscles caused by irritation of the fauces ;
the facial contortions caused by irritation of the fifth nerve ; the
sneezing and lachrymation caused by irritation of the mucous mem-
brane of the nose ; the cough caused by irritation of the mucous mem-
brane of the larynx ; the closure of the eyelids caused by irritation of
the conjunctiva ; and the reflex contraction of the iris caused by light.
Some of these reflexes are absent in healthy individuals more especi-
ally the reflexes of the back and abdomen, so that the diminution or
absence of these must not be taken as a sure sign of disease. Their
presence, however, is a proof that the respective paths through the
cord are not seriously interrupted.
a. HTPERKINESIS OF THE SUPEKFICIAL REFLEXES.
Increase of the reactions obtained from reflex stimulation indicates
that the irritability of the reflex arc is increased in some portion of its
course, or that the inhibitory influence of the cerebrum is withdrawn.
Exaggerated reflex reactions are obtained by increased irritability (j)
of the afferent portion of the arc ; (jj) of the efferent portion of the
arc ; ( jjj ) of the gray matter of the cord, as in tetanus and strychnia
poisoning ; (iv) by arrest of the functions of the pyramidal tracts (Fig.
71, 6, 7). The condition of the cutaneous reflexes in cerebral paral-
ysis, however, appears to be an exception to the rule that withdrawal
of the cerebral influences causes excess of the reflex actions, inasmuch
as the cutaneous reflexes are diminished or lost on the paralyzed side
in hemiplegia. The diminution of the cutaneous reflexes under such
17(3 GENEKAL SYMPTOMATOLOGY.
circumstances is caused probably by a loss of tone of the muscular
fibi-es distributed to the skin, which prevents the papillae from being
ijroperly exposed to the irritation of tickling and other cutaneous
stimulants.
b. AKINESIS OF THK SUPERFICIAL REFLEXES.
When stinnilation of the surface produces either feeble or no reac-
tions, it indicates that there is diminution or loss of the irritability (j)
of the afferent portion of the arc — examples of which are met with
in destructive lesions of the sensory branches of the fifth nerve ; (jj)
of the efferent fibres — examples being afforded by lesions of the facial
nerve and the anterior roots of the spinal nerves ; (jjj) of tlie gray
matter of the anterior horns — examples of which are afforded by the
spinal atrophic paralyses, and by the diminution of the reflexes which
is observed after large doses of l^romide of potassium ; and (iv) by
increased cerebral action conveyed through the pyramidal tracts — an
example being afforded by the inhiliition of reflex actions by means of
voluntary control.
(2) The Deep Keflexes.
a. tendon reactions.
If a man in health sits with one leg crossed upon the other, and the
ligamentum ])atellae be then smartly struck immediately below the knee-
cap, the extensor muscles in front of the thigli Ijecome suddenly con-
tracted, and the foot is jerked forwards to a variable extent according
to the degree of contraction. The jerk is named the patellar-tendon
reaction, knee-phenomenon, or knee-jerk. The blow is usually deliv-
ered by the inner edge of the hand ; but an ordinary stethoscope,
held loosely by the small end Avhile the blow is struck by the edge of
the ear-piece, is a convenient instrument for the purpose, and a Win- •
terich percussion hammer is a still more efficient instrument. It is
also desirable to uncover the knee that the blow may be delivered on
the bare skin. In stout people, Avho cannot cross one leg over the
other in a sitting posture, the operator may pass his hand beneath the
patient's thigh just above the knee-joint, and, grasping the opposite
knee, support the extremity to be examined by his forearm. Another
convenient ])osition is to get the patient to sit on a table or on an
elevated seat with the legs hanging freely. Similar reactions may be
obtained by striking the tendons of the upper extremity, but these are
not well marked except under certain diseased conditions. The reac-
tions are best elicited by striking Avith the edge of the stethoscope the
tendon of the triceps at the elbow, and those of the supinator longus
and extensor muscles at the wrist.
THE EXTEENAL K INESI OXEU ROSES . 177
b. VARIOUS FORMS OF CLONUS.
Ankle-clonus^ or Achilles-tendon reaction, consists of a rhytlimical
clonic spasm, which can be obtained under certain circumstances at the
ankle-joint. When the necessary conditions are present, the reaction
is most readily elicited if the operator will support the lower extremity
of the patient by placing his hand behind the knee-joint, the leg being
slightly bent upon the thigh, while with the right hand he seizes hold
of the toes lightly between the fingers and thumb and puts the tendo
Achillis suddenly upon the stretch by producing a quick and enero-etic
dorsal flexion of the foot, and then maintaining pressure against the
toes for some time. When the tendon is first stretched, the sastro-
cnemius immediately contracts and the toes are depressed; the muscle
now relaxes, and, the pressure of the hand being still continued, the
toes are once more elevated, when the muscle again contracts and de-
presses the toes a second time ; and thus the contractions and relaxa-
tions are continued in rhythmic sequence so long as the tension of the
tendo Achillis is maintained. This series of rhythmic contractions
constitutes ankle-clonus, and, so long as the movement continues,
between eight and ten contractions of the gastrocnemius take place in
a second of time.
Toe-clonus. — In cases of increased tension of the foot, rhythmical
contractions of the big toe may be obtained by producing sudden pas-
sive extension of the first phalanx, flexion being produced by contrac-
tion of the abductor and flexor brevis pollicis.
Wrist-elonui^. — Movements like those of ankle-clonus may be ob-
tained in the hand, in cases of late rigidity of hemiplegia, by grasp-
ing the tips of the fingers and pressing the hand backwards so as to
produce hyperextension at the wrist.
C. PERIOSTEAL AND FASCIAL REACTIONS.
The best known of these movements are the contraction of the quad-
riceps femoris muscle, induced by gently tapping the front of the tibia
near its middle ; that of the biceps on tapping the lower end of the
radius with the edge of the stethoscope ; and that of the triceps on
tapping the lower end of the ulna, in cases of muscular rigidity with
contraction. When the muscles of the shoulder and arm are impli-
cated in the rigidity, contractions of the pectoralis major, deltoid, and
biceps may be obtained by a gentle tap on the sternal end of the clavi-
cle, and even a crossed reaction may be obtained by a tap on the cla\i-
cle of the opposite side. Under similar circumstances a considerable
12
j^Yg GENERAL SYMPTOMATOLOGY.
number of the muscles of the scapula and shoulder contract on tap-
ping the spine of the scapula. Contractions of the erector muscles of
the spine may, under certain circumstances, be induced by tapping the
lumbar fascia.
d. SPINAL EPILEPSY.
The paroxysms of violent tremors which occur in certain affections
of the spinaf cord, and which Brown-Sequard named spinal epilepsy
from a fancied similarity to an epileptic convulsion, are of a compound
nature. These movements appear, indeed, to be caused by contrac-
tions produced by simultaneous and successive stimulations of the
superficial and deep reflexes. A painful cutaneous impression causes
reflex contractions of both lower extremities, which predominate in the
flexors ; but when the anterior flexors of the legs contract the Achilles
tendons are put upon the stretch, and ankle-clonus results. These
actions and reactions, reverberating for a time through all the muscles,
maintain the lower extremities in a state of tremor, which may be so
violent as to shake the bed on which the patient reposes. When these
tremulous movements are proceeding, if the toes of one foot be grasped
by the hand and brought suddenly and powerfully into plantar flexion,
the muscles iu^mediately relax and the tremors cease for a time.
e. PARADOXICAL CONTRACTION.
Some muscles may, under certain circumstances, be made to contract
by suddenly approximating their points of origin and insertion. I'he
curious fact that a sudden relaxation of a muscle causes it to contract
has led Westphal, who was the first to direct attention to this phenome-
non, to name it paradoxical contraction. This symptom is best studied
in the tibialis anticus, which may, in certain nervous diseases, be made
to contract by producing a sudden, or sometimes a gradual, dorsal
flexion of the foot. When the patient is laid on his back in l)ed, and
the muscles are relaxed, the feet occupy the position of extensor or
plantar flexion. If dorsal flexion of the foot be now produced, the
tibialis anticus, under certain not well-ascertained circumstances, enters
into contraction, its tendon becomes prominent, and the foot is main-
tained for some minutes in the position of dorsal flexion and adduction.
Distinct resistance is also offered to the production of plantar flexion of
the foot by passive movements. After a variable interval of time the
muscle relaxes, either gradually and continuously or with several inter-
missions, and the foot falls by its own weight to the position of plantar
flexion. The paradoxical contraction sometimes extends to the extensor
THE EXTERNAL KINESIONEUROSES. 179
communis digitorum and extensor brevis pollicis. It is possible that
this anomalous reaction is caused by an impression upon the sensory
nerves of the joints, and not by the sudden relaxation of the muscle.
/. HTPERKIXESES OF THE DEEP REFLEXES.
(j) It is probable that increased irritability of both the aflFerent and
efferent portions of the reflex arcs will increase the activity of these
reactions, but no crucial examples of this kind have as yet been de-
scribed. When, however, the irritability of the muscular fibres them-
selves is increased in degree, as in phthisis and other exhausting diseases,
the tendon reactions are much more readily induced than in health.
(jj) Irritation of the posterior roots, and of the efferent fibres as
they pass through the inner radicular fiisciculus of the posterior col-
umns, probably also increases the activity of the tendon reactions, but
direct evidence upon this point is as yet wanting.
(jjj) Increased irritability of the gray substance of the spinal cord
causes increase of the activity of the tendon reactions. The patellar-
tendon reaction is, for example, exaggerated by the administration of
strychnia, and probably also by such diseases as tetanus and hydro-
phobia.
(iv) The tendon reactions are increased in activity when the cerebral
influence is withdrawn from the spinal cord by disease of the pyramidal
tracts, and consequently all these reactions are exaggerated in all forms
of sj)asmodic paralysis, unless, indeed, the reflex arc is at the same
time arrested by a local spinal disease like chronic spinal pachymenin-
gitis.
g. AKINESES OF THE DEEP REFLEXES.
(j) The tendon reactions are diminished or lost in disease of the
afferent portion of the reflex arc. The disease may be situated in the
tendon itself; in such a case the movements of the joint are generally
interfered with by an ankylosis, and the conditions are not favorable
for applying the test. The reaction may be lost when the lesion is
situated in the peripheral course of the nerve (Fig. 71, 1), but the
motor and sensory fibres are then interfered with, and under such
circumstances it is not possible to prove that disease of the afferent
fibres takes any part in the arrest of the reaction. This reaction may,
however, be lost in spinal meningitis affecting the posterior roots
(Fig. 71, 2), when the absence of any atrophic paralysis of the cor-
responding muscle shows that the afferent portion of the reflex arc is
intact. The patellar-tendon reaction is, for instance, often absent in
180
GENERAL SYMPTOMATOLOGY
(ii) This reaction is lost when the afferent fibres are diseased in
their passage through the inner radicular fasciculus (Fig. 71 3) of the
pachymeningitis affecting the lumbar region in the absence of any atro-
phic paralysis of the quadriceps femoris muscle.
Fig. 71.
Diagram of the Keflex Functions of the Spinal Coed. (Young.
C, skin and, T, tentlon with their afl'erent nerve fibres, both terminating in the ganglion cell of the anterior
gray horn, from which issues an efferent fibre which connects the cell with the muscle M. B B, the cor-
tices of the cerebral hemispheres, with their attached pyramidal tract fibres connecting the cortical giant
cells with the ganglion cells of the anterior gray horns. 1, lesion of the peripheral nerve, causing atrophic
paralysis, loss of sensation, and abolition of both kinds of reflexes ; 2, lesion of the posterior root (pachy-
meningitis), causing loss of sensation and abolition of both kinds of reflexes, but no paralysis ; 3, lesion
of the posterior root-zone (tabes dorsalis), causing loss of the tendon reflex only ; 4. lesion of the anterior
gray horns (poliomyelitis), causing atrophic paralysis and loss of both kinds of reflexes, but no sensory
disorder ; 5, lesion of the anterior root (pachymeningitis), causing the same symptoms as 4 ; C, transverse
lesion of the spinal cord, causing a spasmodic paralysis of the lower extremities, with excess of both
kinds of reflexes ; 7, focal lesion of the cerebral hemisphere, causing hemiplegia of the opposite side, with
excess of the tendon reflexes on the paralyzed side, but with diminution of the cutaneous reflexes. The
dotted lines indicate descending sclerosis of the pyramidal tracts
spinal cord, this being the essential anatomical change in locomotor
ataxia. It will hereafter be found that loss of the patellar-tendon
reaction is the earliest and most constant symptom of locomotor ataxia.
THE EXTERXAL KI XESIONEU ROSES . 181
(jjj) Tlie tendon reactions are diminished or lost in depressive and
destructive lesions of the gray anterior horns. Large doses of bromide
of potassiinn and of opium diminish the activity of the tendon reaction
and it is very probable that a poison circulates in the blood which
diminishes or abolishes these reactions in certain cases of diabetes.
Destructive lesions (Fig. 71, 4) of the anterior gray horns abolish
the tendon reactions, but the loss of the reactions is accompanied by
paralysis with atrophy of the corresponding muscles.
(iv) The tendon reactions are likewise lost in destructive lesions of
the efferent portion of the reflex arc (Fig. 71, 5), and in this case, also,
the abolition of the reaction is accompanied by paralysis with atrophy
of the muscles. Disease of the muscle itself abolishes the reflex, the
early loss of the patellar-tendon reaction in pseudo-hypertrophic paral-
ysis being a good example.
(v) Increase of cerebral influence on the gray substance of the spinal
cord diminishes the activity of the tendon reactions. The patellar-
tendon reaction can, for instance, be arrested by voluntary eifort, and
it is diminished or lost during the convulsive stage of an epileptic
attack. The conditions under which paradoxical contraction is ob-
tained are not well ascertained.
h. AUTOMATIC KINESIONETJROSES.
The groups of symptoms which may be included under automatic
aff'ections of the muscles of external relation, cannot be distinctly
separated from the reflex and voluntary afi'ections of these muscles.
There are, however, disturbances of muscular adjustments in which the
simple reflex actions of the spinal cord, the sensory mechanisms, and
the voluntary mechanisms are normal, and yet in which complex mus-
cular adjustments either fliil to be efiected in spite of all voluntary
efforts to accomplish them, or are effected in spite of all voluntary
efforts to prevent them, the last kind of adjustment being named com-
pulsory ov forced movements. It is such movements as these Avhich
are meant to be included under the name of automatic kinesioneuroses
of the muscles of external relation. These movements are, in all proba-
bility, coordinated in the cerebellum and basal ganglia of the cerebrum.
(1) Peripheral Auicnnatlc Disorders.
Disorder of LahjrinfMne Impressions. — Disease of the peripheral
nerves generally involves either the sensory or the voluntary motor
fibres, or both together, so that disorder of muscular coordination
becomes thus obscured by the more prominent symptoms caused by
Ig2 GENERAL SYMPTOMATOLOGY.
disorder of the voluntary mechanism. There is, however, a growing
conviction that ataxia is frequently, if not always, caused by a periph-
eral lesion, but we shall at present adhere to the more classical view
that it is caused by a spinal lesion. It would seem, however, that the
seventh pair of nerves contain afferent fibres which are not subservient
to the conduction of sensory impressions, and yet disease of which
gives rise to the phenomena of motor incoordination. These fibres are
involved in disease of the internal ear or of the semicircular canals, and
in such cases the patient suffers from a staggering and uncertain gait,
which will be subsequently described as Meniere's disease. The dis-
orderly and incoordinate movements of animals after division of one or
other of the semicircular canals are described in manuals of physiology.
(2) Spinal Automatic Disorders.
Ataxia is a very characteristic kind of motor incoordination observed
in diseases of the spinal cord, and constitutes the most prominent
feature of tales dorsalis. It is characterized by inal>ility to make
combined or complicated movements with certainty and precision, and
in advanced cases all movements requiring intricate and delicately
balanced muscular adjustment become impossible. The motor incoor-
dination usually presents itself in tlie most marked manner during
locomotion and station, these being respectively named dynamic and
static ataxia. These forms of muscular incooi'dination will be more
fully described when locomotor ataxia is under consideration.
(3) Encephalic Aiiiornatlc Disorders.
[a) Reeling is the well-known gait of a di'unken man. It is caused
by irregular swaying movements of the trunk, from side to side and
from before backwards, requiring the legs to be moved irregularly in
various directions in order to maintain their position vertically under
the trunk. Staggering is a slighter degree of motor incoordination
than reeling, and vertigo is the subjective correlation of this form of
motor disorder.
(5) OerebeUar rigidity consists of i-igidity of the muscles of the
neck, which in aggravated cases extends to those of the back and
extremities, so that complete opisthotonos is induced. This form of
rigidity is frequently associated with tumor of the middle lobe of the
cerebellum.
i. COMPULSORY OR FORCED MOVEMENTS— COORDINATE CRAMPS.
These movements are best seen in animals after experimental injury
to various parts of the medulla, pons, and crura cerebri, but most of
THE EXTERNAL K IX ESTON E U ROSES . 183
them are probably caused by injury to one or other of the peduncles of
the cerebellum. The usual forms of these movements are, that in which
the animal rolls around the longitudinal axis of its OAvn body, that in
which it moves round and round in a circle, and that in which it rotates
round the transverse axis of the body, tumbling head over heels in a
series of somersaults. INIovements of this kind are never so marked
in man as in animals, but less degrees of these movements are some-
times observed in disease in the neighborhood of the peduncles of the
cerebellum.
All the automatic disorders just described are caused by the over-
throw of the delicate balance of the tonic muscular contractions, which
is necessary for the maintenance of complicated adjustments in space.
Irritative lesions of the cortex of the cerebellum, which is the organ
for regulating these tonic contractions, gives rise to excessive tonic con-
tractions of certain muscles, which destructive lesions cause paralysis
of them, Avhich, however, is not recognized as a paralysis, because the
cerebi-al influence on the muscles is still intact. In other cases the
cerebellum itself is healthy, but false intelligence is sent to it owing to
disease of the cerebello-afferent conducting paths, and this leads to a
loss of the balance of the tonic contractions of the body, or to loss of
equilibration, as it is called.
k. SYNKINESIS.
Under this term are generally included certain involuntary move-
ments of paralyzed parts, but we shall also include under it certain
motor disorders which occur in muscles aifected with spasm, as w^ell as
certain anomalous movements which occur in muscles that in health
are associated in their actions Avith those primarily affected.
(1) Associated Movements of Paralyzed Parts.
In facial paralysis of cerebral origin the muscles of the paralyzed
half of the face may occasionally perform the movements necessary to
changes of expression in association with those of the opposite side,
although in most cases the contrast between the actions of the two sides
is rendered all the more evident under changes of expression. In cases
of hemiplegia automatic movements may occur in a completely para-
lyzed arm. When the patient sneezes, and under the influence of
emotional excitement, the paralyzed extremities may be strongly flexed,
while the unaffected limbs remain passive. A voluntary movement of
the healthy side is often accompanied by a contraction of the corre-
sponding muscles on the paralyzed side.
184 GEXEEAL SYMPTOMATOLOGY.
(2) Relative Immuniiy of some Muscles from Paralysis, and their Relative Liability
to Convulsion.
In ordinary cases of severe hemiplegia some muscles are completely
paralyzed, while others are little if at all affected. The muscles which
are most paralyzed are those of the extremities and the lower muscles of
the face, and those which escape are the muscles of the trunk, and the
upper muscles of the face. In unilateral convulsions, however, the
spasm keeps limited to one-half of the body in the extremities and
lower half of the face, while it often extends to both sides in the trunk
and upper part of the face. Looking broadly at the muscles which
are most liable to be completely paralyzed in hemiplegia, it may be sai<l
of them that they are the muscles which are most engaged in executing
special movements, while those least liable to be paralyzed are engaged
in effecting the most general movements. The muscles of the hand,
for. instance, which are so peculiarly liable to be paralyzed, effect the
special movements of writing, while those of the trunk, which generally
escape, are those which are engaged in carrying on respiration and
other automatic actions. But the laryngeal muscles are engaged in
effecting the very special movements of articulation, and yet they are
by no means liable to be affected in hemiplegia, and consequently the
rule just laid down is not of universal application, and we may, there-
fore, be certain that the muscles which remain comparatively free from
paralysis have some other common characteristic. This characteristic
is to be found in the fact, first pointed out by Dr. Broadbent, that tlie
muscles wliicli have a relative immunity from paralysis are those which
are hilaterally associated in their actions. The thoracic, abdominal,
and laryngeal muscles, and even those of the eyelids and eyebrows are
brought into simultaneous action on both sides of the body, while those
of the limbs, and, to a less extent, those of the lower part of the face,
act more or less independently of one another on the two sides. This
bilateral association of the functions of certain groups of muscles Avould
lead us to expect that there will be a corresponding bilateral a-ssociation
of the nervous mechanisms by which their movements are regulated.
Dr. Broadbent has suggested that in bilaterally associated actions the
muscles of each side are connected with the cortical centres in both
hemispheres. He believes that this connection is effected by means of
spinal commissural fibres, and has happily enunciated the principle
as the bilateral association of the nerve nuclei of muscles hilaterally
associated in their actions. In Fig. 72, for instance, d', representing
the spinal nuclei of the dorsal nuclei of the left side, is connected with
the cortex of the opposite side by fibres (5 5) which ascend in the
THE EXTERNAL KIX ESI OX EU ROSES . 185
pyiamidal tract, and also with that of the same side througli the com-
raissural fibres which connect the two spinal nuclei (<?'"), and the fibres
(")' 5') which connect the nuclei of the right side (d) with the left
cortex {c'). Suppose now that the fibre 5 5 is ruptured and the nucleus
d' is thus severed from the cortex of the opposite hemisphere, Avhich
usually controls its function, it can still obtain impulses from the cortex
of the same side through 5' 5' and c'". When, however, the muscles
of the opposite sides act independently of each other, such as those of
the right and left hands, commissural fibres are not established between
their nerve nuclei. In the nucleus (a) of the right upper extremity,
as represented in the figure, rupture of fibre 6' severs the connection
with the cortex of the opposite side, and no channel is established l)y
means of which it can obtain impulses from the cortex on the same side.
The effect which this bilateral fusion of the spinal nerve nuclei of
various nerves produces in certain spasmodic affections is as striking as
that produced by it in hemiplegia. In unilateral chorea, for instance,
while the spasmodic action is limited to one side in the extremities and
lower muscles of the ftice, it extends to the muscles of both sides of
the trunk and of the eyelids and eyebrows, these being muscles which
are habitually associated in their actions. This rule is also true with
respect to other forms of convulsion, so that in hemispasm the muscles
which are habitually associated in their actions are affected on both
sides ; while in hemiplegia these muscles are comparatively preserved
from paralysis. The reason of this is so plain that it is scarcely neces-
sary to add another word by Avay of explanation. Suppose that ex-
cessive impulses are sent down from the cortex of the brain through
the fibres 6' and 5', the former will reach a and pass out through hn
to the muscles of the arm on the opposite side ; while the latter will
i-each d and pass both through dn and c'", d', and dn' to reach the
muscles of the trunk on both sides. But the muscles which are habit-
ually associated in their actions are not always symmetrically placed
on the two sides of the organism, nor are their actions always analogous.
It is only necessary that their actions should concur to produce a defi-
nite result : and the commissural fibres often connect, not two nerve
nuclei on the same spinal level, but nuclei at different levels, thus form-
ing an oblique crossed connection as in Fig. 72, e^.
(3) Conjugate Deviation of the Eyes, and Roraiion of ihe Head and Neck.
The actions of the external rectus of one eye and of the internal of
the other is a good example of muscles having quite opposite actions,
and yet concurring to produce a harmonious result. It is evident that
186
G E N E E A L SYMPTOMATOLOGY.
if commissural connections exist anywhere they must exist between the
nucleus of the sixth nerve of one side and the portion of the nucleus
of tiie third nerve which presides over the action of the internal rectus
of the opposite eye ; and as these nuclei are placed at different levels
in the pons and crura, the connection between them must be oblique
and crossed. In Fig. 72, let r and r' represent respectively the nucleus
of the portion of the third nerves (3w and 3w') supplied to the right
and left internal recti, and er and or' be respectively the nuclei of the
Fig. 72.
( ', (", corte.x of ii<;lit and left cereliral hemi-
spheres respectively ; 1, 2, 3, 4, 5, 0, fihrcs of the
pyramidal trart uniting (', tlie cortex of the right
}iemi8i>Iiere, and r', e'r, v', u', d', I', the respective
spinal nuclei of the internal rectus, and the e.\-
ternal rectus muscles of the eye, the muscles of
articulation and vocalization, those of the upper
e.xtremity, the dorsal muscles, and those of the
lower extremity, all of the left side ; 1', 2', 3', 4',
5', C, fibres of the pyramidal tract, connecting
the corte.x of the left h('mis]ihere with r, et; v,
a, d, 1, the spinal nuclei of the right side cor-
responding to those already enumerated on the
left side ; c, e, fihres of the corpus callosum
uniting identical regions of the two hemispheres;
c', comnn'ssural fibres connecting the spinal nu-
cleus of the internal rectus muscle of one eye with
that of the external rectus muscle of the opposite
eye ; c", those connecting the spinal nuclei of the
muscles of vocalization and articulation of tho
two sides; c'", those connecting the special nuclei
of the muscles of the trunk: c*, those connecting
the spinal nuclei of the posterior extremity of
one side witli the anterior extremity of the oppo-
site side. The arrows indicate the direction of
the conduction.
right and left sixth nerves {6n and G>i/) : while c' represents the cross-
mg of the commissural fibres. The external rectus of one eye and the
mternal of the other eye acting simultaneously rotate both eves so as
to direct the axes of vision to lateral objects. When the object is
placed to the right it is manifest that the right eye is in a better posi-
THE EXTKRNAL KINESIONE Ul? OSES 187
tion than the left to catch the first glimpse of it, hence the external
rectus, Avhich rotates the right eye outwards, takes the lead in the action.
But the internal rectus of the opposite side rotates at the same time the
left eye inwards : and to effect this movement it will be a clear gain of
time, as well as economy of force, if it were to receive its impulses to
action through the short commissural fibres which connect the two
nuclei, and not from the cortex of the cerebrum of the opposite side.
When, therefore, the eyes are directed by a voluntary effort to the
right, the impulse to action may be supposed to come from the cortex
of the brain (C) on the opposite side, to pass out through the fibres
(2') of the pyramidal tract which connect the cortex with the nucleus
of the sixth nerve {er'), and then to pass on through the commissural
fibres (c') to the part of the nucleus (r) of the opposite third nerve
concerned in the action. According to this statement, therefore, in
directing the eyes laterally, say to the right, both the right external
rectus and the left internal rectus receive the impulse to action from
the cortex of the left hemisphere, the impulses of the nucleus of the
third nerve being received through the commissural fibres which con-
nect it with the nucleus of the sixth nerve of the opposite side. So
far, Ave have only spoken of the two recti muscles; but when these
muscles are contracting so that the eyes are directed laterally, the
muscles which rotate the head also become contracted in such a way
that the head is turned in the same direction as the eyes, this movement
being frequently observed when a man looks over his shoulder. Rota-
tion of the head, say to the right, is produced mainly by contraction of
the right inferior oblique muscle of the neck, although the left sterno-
mastoid, and probably other muscles, cooperate in the movement, and
these muscles also receive their voluntary impulses to action through
commissural fibres which connect their nerve nuclei with the nucleus of
the sixth nerve of the right side. According to this supposition, when
a strong impulse is sent from the left cortex (C) of the brain through
the fibres ('2') which connect it with the nucleus {er) of the sixth nerve
of the opposite side, these impulses will also pass through commissural
fibres to the nuclei of the nerves which supply the internal rectus and
sterno-cleido-mastoid muscles of the opposite side, and of the inferior
oblique muscle of the neck of the same side ; and the eyes and head
will consequently be strongly rotated to the right, and away from the
hemisphere from which the impulses originated. But this lateral devi-
ation or conjugate deviation of the eyes, as it is called, occurs fre([uently
in disease, and it is then associated with rotation of the head and neck
to the same side as the eyes are directed. This position of the eyes
and head is almost a constant accompaniment of convulsions of cereljral
188 GENERAL SYMPTOMATOLOGY.
orio-in, and, when the convulsions are unilateral and due to disease of
the cortex of one hemisphere, the rotation always takes place towards
the convulsed side and away from the seat of the lesion. Unilateral
convulsions are often associated with a certain degree of hemiplegia,
the convulsions being then limited to the paralyzed side ; and when,
under these circumstances, conjugate deviation of the eyes occurs, the
rotation is always towards the paralyzed side. This, then, constitutes
spasuiodic lateral deviation of the head and eyes. But Graux has
drawn attention to the fact that this lateral deviation is often of para-
lytic origin. Let us now suppose that the fibres (2') which connect
the left cortex (C) and the right nucleus of the sixth (er) are suddenly
interrupted, the cerebral impulses to the nucleus are arrested, the ex-
ternal rectus of the right eye becomes paralyzed, and that eye is rotated
to the left. But the impulses through the commissural fibres which
connect the nucleus of the right sixth, and those of the left internal
rectus, and of the rotators of the head to the left must also be arrested,
so that the latter muscles likewise become paralyzed ; hence the left
eye and the head become, rotated to the left, the rotation now taking-
place awai/ from the paralyzed side and towards the hemisphere of the
brain in which the disease is situated. The rotation of the eyes in
this direction has been facetiously described as an attempt on the part
of the patient to inspect the cerebral lesion which is the cause of the
paralysis. The rotation of the eyes, head, and neck is not now due to
spasm of the muscles engaged in producing the action, but to paralysis
of their antagonists. This symptom is usually associated with all
sudden and severe attacks of hemiplegia ; it is generally absent in the
slighter forms of the attack, and in all cases in which the paralysis is
more or less gradual in its onset. The ])henomenon is also, as a rule,
a very transitory symptom in hemiplegia, and usually disappears in
from four days to a week. The rotation of the head generally disap-
pears first, and then the deviation of the eyes improves; but it not
unfrequently happens that a temporary s(iuint may be observed during
the progress of the rotation of the eyes towards recovery.
The reason of the temporary character of the paralytic form of con-
jugate deviation of the eyes and rotation of the head and neck — say
towards the right— appears to be that although the nucleus of the left
third {r') usually receives its impulses to action through the commis-
sural fibres which connect it with the nucleus of the right sixth nerve (er),
and consequently from the cortex of the left hemisphere, yet channels
of communication (1) still exist between the nucleus of the left third
and the cortex of the right liemisphere. There is no congenital defi-
ciency of the channels which connect the cortex of the ri^^ht hemi-
THE EXTERNAL KIN ESI OX EU ICOSES . 189
sphere and the nucleus of the tliird nerve of the opposite side, nor
indeed of the oblique commissural fibres -which connect the latter with
the nucleus of the right sixth nerve ; and now that the more usual
channels are interrupted by disease, impulses begin to pass through the
k'ss used channels. In a few days, then, the channel (1) between the
right cortex and the nucleus of the left third nerve becomes patent,
and some days later the commissural fibres (c) between the two nuclei
liecome so for open as to convey impulses from the nucleus of the left
third to that of the right sixth, so that the paralysis of the muscles
supplied l)y these nerves disappears. A destroying lesion in the pons
situated above the nucleus of origin of the sixth nerve, but below the
upper crossing of the fibres of the pyramidal tract, causes a conjugate
deviation, Avhich is directed away from the side of the lesion and
towards the paralyzed limbs. It has also been shown by Graux that
whereas disease of one of the sixth nerves produces an internal squint
of the eye on the side of the lesion, and no affection of the other eye,
disease of the nucleus of origin of one of the sixth nerves produces a
conjugate deviation of the eyes, the external rectus on the side of the
lesion and the internal on the opposite side being thus more or less
' ])aralyzed. But the internal rectus is not completely paralyzed, although
it does not act when the eye has to be directed to lateral objects, it
contracts quite well in association with the internal rectus of the oppo-
site eye when the eyes are converged on a near object in front. These
facts prove that the internal rectus muscle is innervated by fibres
issuing from, or at least passing near the nucleus of origin of the sixth
nerve of the opposite side, as Avell as by fibres from the third nerve of
the same side. As we have seen, conjugate deviation of the eyes is, as
a rule, a transitory symptom in hemiplegia, but if a lesion in the pons
• interrupts the commissural fibres (c) so as to prevent impulses passing
from one nucleus to another, a second lesion situated in any posi-
tion which will interrupt the fibres of the pyramidal tract will then
produce a paralytic conjugate deviation of the head and eyes which
remains permanent.
(4) Secondary Deviation of the Sound Eye.
In paralysis of one of the ocular muscles, say of the external rectus
of the right side, the eye is of course subject to internal s(piint. Now,
if durino- recovery from this condition, when the conduction through
the sixth nerve (6») is still delayed, the eye of the sound side be
closed and the patient be directed to look at an object with his right
eye in such a way as to strain the external rectus nuiscle, this strain is
190 GENERAL SYMPTOMATOLOGY.
accompanied by a strong voluntary effort, but owing to the diminished
conductivity of the nerve only a relatively small amount of the volun-
tary impulses will pass to the muscle. But the impulses generated by
the strong voluntary effort will pass through the commissural fibres {(■')
to the nucleus of the left third nerve {r') in undiminished degree, so
that the internal rectus of the left eye becomes strongly contracted.
The energetic contraction of the internal rectus of the left eye induces a
secondary squint in it, the extent of Avhich is much in excess of that
of the squint of the paralyzed side. But although this secondary
deviation is more apparent in the case of paralysis of the ocular than
in paralysis of other muscles, yet essentially the same phenomenon
occurs in the extremities. If the common extensor muscle of the toes
is partially paralyzed, a voluntary effort to extend the toes is followed
by flexion of them. A simple movement like flexion at the elbow-joint
is not caused by contraction of the flexors only, but by the predominance
of their contractions over the contraction of the extensors simulta-
neously induced. During recovery from an attack of hemiplegia it
often happens that when the patient makes an effort to flex the forearm
the flexor muscles may be observed to contract, yet either no movement
or movement in the opposite direction occurs, because the balance of
the innervation to the antogonistic muscles is equal to, or the innerva-
tion to the extensors is in excess of, that to the flexors.
(5) Disorders of the Associated Movements of the Extremities.
We have seen that the movements of the limbs, and especially of
the hand of one side, are largely independent of those of the other,
and consequently that the spinal nuclei of the nerves which supply the
limbs are not intimately connected by transverse commissural fibres.
But in walking, the movement of the right leg is always associated
with swinging of the left arm; and, conversely, that of the left leg with
swinging of the right arm. It may be inferred, therefore, that the
nuclei of the nerves of the upper [a a') and lower extremities (/ V) are
connected by oblique and crossed commissural fibres. In man the
movements of the leg of one side are not very intimately associated
with that of the arm of the opposite side, hence the commissural fibres,
which connect their respective nerve nuclei, are represented by dotted
lines (e" ). In quadrupeds, however, the crossed association between
the movements of the anterior and posterior extremities of opposite
sides IS much more intimate than in man, and consequently the oblique
commissural fibres are patent in a corresponding degree.
Let us now suppose that the fibres (4' and (J') which connect the
coitex (C) of the left hemisphere with the spinal nuclei {a, I) of the
THE EXTEENAL KIN ESIONEU ROSES . 191
light extremities are ruptured. Rupture of these fibres would produce
hemipk-gia in man ; but in the dog only a certain amount of paresis
results, inasmuch as the right hind limb receives impulses through the
open commissural fibres which connect the spinal nuclei of its nerves
with the nuclei of the nerves of the left anterior limb. The right
anterior limb likewise becomes innervated through the commissural
fibres which connect the nuclei of origin of its nerves with those of
the nerves of the left posterior extremity. All the limbs of the dog,
therefore, become innervated from one hemisphere when the other
hemisphere is injured, so that, although disease of one hemisphere
causes a certain amount of paresis, no true paralysis or hemiplegia
results as in the case of man. This condition has often been induced
by experimental lesions of one of the hemisplieres in the dog, and it is
always associated with conjugate deviation of the head and eyes, show-
ing that both phenomena are induced by disease of the same mechanism.
But although the dog does not manifest complete paralysis of the mus-
cles of the side opposite the lesion — say the right side, the lesion being
in the left hemisphere — yet, on standing, a slight degree of pressure on
the left side pushes the animal over to the right, the vertebral column is
arched with the convexity towards the right, showing a predominance
of the action of the left erector-spin^ over their antagonists, and the
eyes and head are rotated to the left, a position whicli indicates paresis
of the muscles which produce rotation of them to the right. Under
these circumstances, Avhen the dog endeavors to advance he begins to
move round his tail, a movement which has been called " mouvement
de manege^' and Avhich is the equivalent of hemiplegia in man. It is,
therefore, probable that some of the compulsory movements described
as automatic kinesioneuroses really belong to the synkineses, as at
present defined.
(6) Disorders of the Associated Movements of Articulation.
But when the muscles which are bilaterally associated in their action
are small, and when minor nervous discharges only are re(i[uisite to
throw them into action, the connection of the muscles of the two sides
with one hemisphere may be brought into such habitual use that the
connection with the other hemisphere, although still existing, is held
practically in abeyance. The muscles concerned in executing the
movements of articulation, for instance, are bilaterally associated ; the
necessary adjustments demand great delicacy of execution, but no great
muscular exertion ; the muscles engaged in executing the most delicate
192 GENEEAL SYMPTOMATOLOGY.
of these adjustments are small, and consequently these muscles fulfil
all the conditions just mentioned.
It is now a matter of almost daily observation that the muscular
adjustments concerned in articulate speech are regulated from the left
hemis[)here ; but it by no means follows that the regulation of all the
functions performed by these muscles is similarly restricted. The con-
tractions of the laryngeal muscles concerned in vocalization, for instance,
are not necessarily interfered with, because the delicate adjustments
required in articulate speech are abolished ; hence complete loss of the
power of articulate speech is perfectly compatible with entire absence
of voluntary paralysis of any of the muscles engaged in articulation.
It is not the power of producing voluntary contractions of these mus-
cles which is lost, but the power of producing highly complex coml)i-
nations of these contractions. If we suppose that v and v' are the
spinal nuclei of the nerves {v n, v n') which supply the muscles of
articulation, the two nuclei are practically fused into one by transverse
commissural fibres {c") ; and consequently impulses which start from
the left cortex (C), and pass through the fibres (3') to the spinal
nucleus {v) of the right side, readily reach the left nucleus (y') through
the commissural fibres [c"). But as the muscles concerned in articu-
lation act always bilaterally and symmetrically, the channels of com-
munication between the spinal nuclei of their nerves and the cortex of
one hemisphere are brought into habitual use ; while tlie channels of
communication between these nuclei and the opposite hemisphere
become partially obliterated from disuse, and prol)ably not thoroughly
developed from the first. The channels of comnmnication between the
right cortex (C) and the nuclei v and v', for instance, are represented
by the dotted line (3 3), and the commissural fibres which convey
impulses from the left to the right nucleus by the dotted line {c"), in
order to indicate that these channels are only partially open. De-
struction of the communication (3') between the left cortex (C) and
the right nucleus {v) is followed by loss of articulate speech, a condition
Avhich is called aphasia.
If the lesion destroy the portion of the cortex of the left liemisphere
—the posterior part of the third frontal convolution— from which the
fibres of communication spring, this condition is permanent, except
perhaps in young people, in whom the corresponding part of the right
hemisphere becomes educated and develoi)ed for the purpose. But if
the lesion involve only the channel of communication (3') between the
left cortex and the right nucleus, the loss of speech is only temporary.
The corpus callosum consists of fibres {c c) which connect symmetrical
parts of the two hemispheres; and the portion of it which connects
THE EXTERNAL KINESIONEUROSES. 193
the third frontal convolution of the two sides is represented in Fig. 72
by the dotted line to show that, although the connection exists it is
l)artially closed through disuse. When, however, the communication
through (3') is interrupted, impulses generated in the third left frontal
convolution make their way through the fibres of the corpus callosum
to the corresponding part of the right hemisphere, and after a time
through the dotted line (8) which connects the latter with the left
nucleus, and, after another interval, through the partially open com-
missural fibres Avhicli connect the left (v) with the right nucleus (v'). so
that the power of speech is gradually reac(|uired. A lesion, however,
which destroys both the channel of communication (3') between the
third left frontal convolution and the spinal nuclei, and the fibres of
the corpus callosum [a r, dotted line) connecting tlie right and left third
frontal convolutions, Avill influence speech as powerfully and perma-
nently as disease of the gray substance of the third left frontal convo-
lution itself. Such a lesion effectually cuts off the third left frontal
convolution, in which the higher mechanism which regulates the mus-
cular adjustments concerned in articulation is organized, from the spinal
nuclei ; and the only means by which speech can be then restored is
the organization of a new mechanism in the corresponding part of the
right hemisphere, a method which must always be slow, and which can
onh^ take place, at least to any considerable extent, in the plastic tissues
of young people.
13
CHAPTER YII.
GENERAL SYMPTOMATOLOGY [contmued).
II. The Visceral Kinesioneuroses.
The motor affections of internal organs present many peculiarities
in comparison with those of the organs of external relation. These
peculiarities depend in great part upon the fact that the muscular
apparatus of" the internal organs is formed of unstriated muscular
tissue, which differs from the striated muscle in its mode of contraction,
and in several other respects. An unstriated muscular fibre does not
respond to mechanical and electrical stimuli by a prompt contraction of
short duration, but a long latent period precedes the contraction, which
itself lasts for a considerable time, while relaxation takes place only in
a slow and gradual manner. Another peculiarity of the contractions
of unstriated muscles is the rhythmic and automatic manner in which
they occur ; these characteristics being well exemplified by the peri-
staltic action of the intestines and ureters. It is very ])robable that
these movements depend upon the presence of local ganglia on the
walls of the organs, although there are not wanting facts to show that
the power of undergoing such contractions is an inherent property of
the unstriated muscular fibres themselves. The functions of these
intramural ganglia are regulated by means of accelerating and retard-
ing nerve fibres from centres situated in the cerebi'O-spinal system, so
that arrest of the contractions of unstriated muscles may be caused by
a destructive lesion of the accelerator or an irritative lesion of the in-
hibitory fibres, while spasm may be caused by an irritative lesion of
accelerator fibres or a destructive lesion of inhil)itory fibres.
The movements of the internal organs are regulated chiefly by the
ganglia and plexuses of the sympathetic system, but these are so inex-
tricably connected with the cerebro-spinal system that it is impossible
to draw any line of demarcation between the two nervous mechanisms.
The sympathetic system of nerves consists of a vertebral and pre-
vertebral portion. The vertebral portion is composed of a series of
ganglia, united by a longitudinal cord (Fig. 78, I C to C) which de-
scends along each side of the vertebral cofumn from the head to the
coccyx. The prevertebral portion consists of the numerous ganglia
THE VISCEEAL KINESIOXEUEOSES.
195
Superior Cervical Ganglion of the Sympathetic: its connections andbrakciies.
(Reduced from Flower.)
IC to IVC, Branches of communication to four upper cervical nerves
PS, " " petrosal ganglion.
Vr, " " ganglion of root of pneumogastric.
V', " " ganglion of trunk of pneumogastric.
H, " " hypoglossal nerve.
CP, Carotid plexus.
C'P, Cavernous plexus.
CA, Branches accompanying internal carotid artery.
OG, " to ophthalmic ganglion.
X96 GENEEAL SYMPTOMATOLOGY.
Ih, To tympanii; branch of glosso-pbaryngeal. g|
3, to third nerve. -
4, to fovirth nerve.
5, to fifth nerve.
e, to sixth nerve. ^
V, Vidian nerve to spheno-palatine ganglion. ''
S p, Large superficial petrosal from facial nerve.
E.\0, Accompanying branches of external carotid artery.
PP Pharyngeal plexus, formed by union with branches of vagus and glosso-pbaryngeal nerves.
SG, Superior cardiac nerve.
The Middle Ceritical, or Thyroid Ganglion.
IVC to VIC, Branches of communication with fourth, fifth, and sixth cervical nerves.
IT, Inferior thyroid branches.
MC, Middle cardiac nerve.
RL, To recurrent laryngeal.
The Inferior Cervical Ganglion.
VIIC to Vine, Branches of communication with seventh and eighth cervical nerves.
IC, Inferior cardiac nerve.
CP, Cardiac plexus.
GW, Ganglion of Wrisberg.
LCP, Posterior, or left coronary plexus.
KCP, Anterior, or right coronary plexus.
CRL, Cardiac branches from pneumogastric or recurrent laryngeal nerves.
APP, To right anterior pulmonai-y plexus.
LPP, To left anterior pulmonary plexus.
ID to IID, Branches of communication from the first to the twelfth doi-sal nerves.
a, a, To aorta, vertebrae, cesophagus, and posterior pulmonary plexus.
GSN, Great splanchnic nerve.
SSN, Small splanchnic nerve.
SSN', Smallest splanchnic nerve.
D, Diaphragm.
PN, Phrenic nerve.
SP, Epigastric, or solar plexus.
CLP, ('celiac plexus.
Cs, Cystic plexus.
GSD, Gastro-duodenal plexus.
C s P, Gastric or coronary plexus.
Vy, Pyloric plexus.
SpP, Splenic plexus.
LGsE, Left gastro-eplploic plexus.
Po-, Pancreatic plexus,
HjjP, Hepatic plexus.
V", Branches from pneumogastric.
DmP, Diaphragmatic plexus.
SG, Semilunar ganglion.
SK«P, Suprarenal plexus.
BkP, Renal plexus.
SpV, Spermatic plexus.
SMP, Superior mesenteric plexus.
Mce, Middle colic.
Kce, Right colic.
Ice, Ileo-colic.
AP, Aortic plexus.
IMP, Inferior mesenteric plexus.
LCI, Left colic plexus.
Sz, Sigmoid plexus. I
SHni, Superior hemorrhoidal plexus. I
IL to VL, Branches of communication with the five lumbar nerves.
IS to VS,
five sacral nerves.
IHP, Pelvic, or inferior hypogastric plexus, giving branches to all the pelvic visceni.
' ' coccygeal ner\'e.
HP, Hypogastric plexus.
THE VISCERAL K INESIONEUROSES.
197
and plexuses of the head, chest, abdomen, and pelvis. The cerebro-
si)inal nerves communicate with the cord of the sympathetic at their
exit from the cranium and vertebral canal. The fourth and sixth
cranial nerves communicate with the sympathetic in the cavernous sinus
tlie olfactory in the nose, and the auditory in the meatus auditorius
internus. The sympathetic branches of distribution accompany the
arteries, so that all the organs of the body are supplied by sympathetic
nerves.
1. Disorders of the Nervous Mechanism of the Iris and other
Associated Mechanisms.
The nervous mechanism of the iris (Fig. 74) consists of a (1) con-
tractor centre in the crus cerebri (C), which forms part of the nucleus
A A, psychical impression ; B, centrum optici ; C, oculo-motor centre ; D, dilator centre (spinal) ; E,
iris ; G, optic nerve ; H, oculo-motor (sphincter) ; I, sympathetic (dilator) ; K,*L, anterior roots ; M N 0,
posterior roots; /^, seat of lesion causing reflex pupillary immobility ; *, probable seat of lesion causing
myosis. (After Erb.)
of the third nerve ; (2) a cortical contractor centre (A), situated prob-
ably in the angular gyrus ; (3) a dilator centre in the medulla (D) ;
and (4) a cortical dilator centre (A), situated probably in the posterior
part of the first frontal- convolution. The cortical centres are connected
with the contractor and dilator spinal centres by centrifugal fibres which
descend in the pyramidal tract ; the spinal contractor centre is con-
198 GENERAL SYMPTOMATOLOGY.
nected with the sphincter of the iris (E) by efferent fibres (H) which
pass in the third nerve ; and the dilator nucleus with the dilator muscle
by means of efferent fibres which descend in the cervical region of the
cord, emero-e along with the anterior roots of the eighth cervical (K)
and first dorsal (L) nerves, ascend in the cervical sympathetic, and
ultimately find their way to the dilator fibres through the cavernous
plexus, the lenticular nucleus, and the ciliary nerves. The contractor
nucleus is connected with the surface by afferent fibres which pass from
the retina (F) in the optic nerves and tracts (G) to the corpora quadri-
gemina (B), and then bend down to join the contractor nucleus in the
floor of the aqueduct of Sylvius. The afferent and efferent fibres of
the contractor nucleus form a reflex loop, so that when light falls on
the back of the eye the iris contracts. The dilator nucleus appears to
be connected with the surfiice of the body generally by afferent fibres
(M N 0), so that strong irritation of any part of the surface of the
body causes the iris to dilate. It will be seen that only part of this
mechanism belongs to the sympathetic system, but it will conduce to
clearness if all the disorders of the })U])ils are considered in this place.
The cervical sympatlietic also contains vaso-motor fibres for the
corresponding half of the head, and trophic and secretory fibres for
the salivary glands. The orbital muscles of iSIiiller are also innervated
from the cervical sympathetic. Irritation of the fibres supplying these
muscles causes the eyeball to protrude (exophthalmos), and the jialpe-
bral aperture is consequently widened ; while paralysis of them allows
the eyeball to fall back into the orbit, and the palpel)ral aperture is
then narrowed. The eyeball appears also to undergo trojihic change,
which increases the intraocular pressure and renders the cornea more
convex in irritation of the fibres, and diminishes the intraocular pres-
sure and renders the cornea flatter in paralysis of the fibres.
a. Disorders of the Movements of the Iris.
The disorders of the movements of the iris may be divided into the
following varieties, namely, (1) contraction of tlie pupil, or myosis ;
(2) dilatation of the pupil, or mydriasis ; (3) immobility of the pupil
with normal size ; (4) clonic spasm of the muscles of the iris ; and (5)
reflex disorders of the pupil.
(1) Myosis.— Three forms of myosis may be distinguished, namely,
(a) spastic or spasmodic myosis caused by spasm of the sphincter ;
{h) paralytic myosis, caused by paralysis of the dilator fibres ; and
(c) combined spasmodic and paralytic myosis, caused bv simultaneous
spasm of the sphincter and paralysis of the dilator fibres. In the first
THE VISCERAL KINESIONEUROSES . 199
two of these varieties the i)upil is in a medium degree of contraction
and movable, and consequently they may be named the medium or
labile mijoses. In the last of the three the pupil is in the hio-hest
degree of contraction and immovable, and conse(|uently it may be
named maximum or stabile mi/osis.
(a) Spastic myosis, if in high degree, prevents the pupil contracting
to light or during efforts at accommodation. The pupil does not dilate
by shading the eyes, but a moderate degree of dilatation is caused bv
all excitants of the dilator centres or fibres, such as a strong sensory
impression or emotional disturbance. A minimum dilatation is produced
by mydriatics, and a maximum contraction by myotics.
{b) Paralytie nii/osis does not prevent the pupil contracting to the
stimulus of light or during efforts at accommodation, but dilatation
does not occur in irritation of the dilator centres or fibres. A medium
degree of dilatation is produced by mydriatics and a maximum contrac-
tion by myotics. The pupil is more contracted, as a rule, in spas-
modic than in paralytic myosis.
(c) Combined spastic and paralytic myosis causes a maximum de-
gree of contraction of the pupil, which is also completely immovable to
the stimulus of light and accommodation, as well as to those which act
on the dilator centres and fibres. Mydriatics cause a medium degree
of dilatation, but myotics have no effect on the size of the pupil.
(2) Mydriasis. — Three forms of mydriasis may^ also be distinguished,
namely, {a) spastic or spasmodic mydriasis, (b) paralytie mydriasis,
(e) combined spasmodic and paralytic mydriasis. In the spastic and
paralytic form the pupil is in a medium degree of dilatation, and
movable to certain stimuli, and conse(piently they may be named
medium or labile mydriasis ; while in the combined form it is in a con-
dition of maximum dilatation and immovable, and consequently it may
be called maximum or stabile mydriasis.
(a) Spasinodic mydriasis is characterized by a medium degree of
dilatation of the pupil, which contracts slightly to light and during
efforts at acconnnodation, but does not dilate on irritation of the dilator
centre either through sensory nerves or psychical impressions. The
pupil is difficult to contract by myotics, but a maximum dilatation is
readily produced by mydriatics.
{b) Paralytic mydriasis is characterized by a medium degree of dila-
tation of the pupil, which fails to contract to the stimulus of light or
during efforts at accommodation, but dilates further on sensoi-y or
psychical irritation of the dilator spinal centre. A maximum dilatation
is readily produced by mydriatics, but a medium contraction alone is
produced by myotics.
200 GENEllAL SYMPTOMATOLOGY.
((•) Oomhined spasmodic and 'paralytic mydriasis is cliaructerized by
the pupil being in a maxinium degree of dilatation, and eorai)letely
reactionle.ss to all kinds of stimuli. It is not possible to ol)tain a
further dilatation of the pupil by mydriatics, but a medium degree of
contraction is produced by myotics.
(8) Complete immohllity of the pupil with normal size is caused by
paralysis of both the dilator and contractor muscles of the iris. When
the muscles of the iris are alone affected the condition is named (<i) Iri-
doplegia, but when all the internal muscles of the eye are paralyzed
the condition is named (b) ophthalmoplegia interna.
(a) Tridoplci/ia is characterized by the pupil being midway between
dilatation and contraction, and being innnovable to every form of
stimulus. Hutchinson states that the power of being acted upon by
myotics and mydriatics is only completely lost Avhen the substance of
the iris itself is disorganized.
(b) Ophthalmoplegia interna is characterized by the pupil being
midway between dilatation and contraction, and completely reactionless,
while in addition the power of acconnnodation to near vision is lost.
(4) Clonic spaf<m of the inuseles of the ii'is is named hippus or
chorea of the iris; it consists of (juickly alternating contractions and
dilatations of the pupil, which depend probably upon a clonic spasm of
the sphincter. It sometimes accompanies nystagnms, while at other
times it is observed during the regressive period of paralysis of the
third nerve.
(5) Disorders of the reflex movements of the iris may be divided
into those of (a) the irido-dilator, and (6) the irido-contr actor reHex arc.
{a) Disorders of the irido-dilator reflex arc may be subdivided into
those caused l)y lesion (j) of the efferent and ( jj) of tlie afferent por-
tion of the reHex arc.
(j) Disorder of the efferent portion of the reflex dilator arc is met
with in locomotor ataxia. A strong sensory irritation of any part of
the body is followed in healthy persons ])y dilatation of the i)U])ils, but
this reaction fails to take place in many cases of locomotor ataxia, the
reflex arc being interrupted by lesion of the efferent fibres of the
ddator centre in their descending course through the cervical portion of
the cord.
(jj) Disorder of the Aferent Portion of the Reflex Dilator Are. —
When there is complete anaesthesia of the lower part of the hotly from
spinal disease, irritation of the anesthetic area is not followed by dilata-
tion of the pupils, but in cerebral anaesthesia, simulated anesthesia, and
probably, also, in hysterical anagsthesia, the reaction is not interfered
I
THE VISCERAL KINESIONEU ROSES. Wl
Avitli. This reaction, tlicrefoiv, may be found a useful test in distin-
<^uis]iing spiiuil anesthesia from the other forms.
(b) Disorders of the irido-rontractor rcjlcx arc may he di\ided into
those which are caused by disease of (j) the efferent fibres of the arc
which pass in the third nerve, the short root of the lenticuhir fan^rlion,
and the ciliary nerves; (jj) the afferent fibres of the arc, which pass
from the retina through the optic nerves and tracts to the corpora
((uadrigemina; and (jjj) the loop which joins the corpoi-a, ((uadrigemina
with the nucleus of tlie third nerve.
(j) Disordn- of the ^ffererit Portion of the Irido-contraetor llejit'x
Arc. — When the j)upil fails to react to the stimulus of light from lesion
of the eflerent fibres of the reflex arc, the sphincter of the iris is found
to be paralyzed, and the other symptoms which indicate partial or com-
plete paralysis of the third nerve are generally present.
(jj) Disorder of the Afferent Portion of the Irido-contr actor Reflex
Arc. — In atrophy Avith blindness of the optic nerves the sphincters of
the iris lose their tone, and, provided the sympathetic mechanism be
free from disease, the pupils dilate, and they fail to contract to the
stimulus of light, Init still retain the power of contracting when the
eyes are converged. In unilateral atrophy with blindness both pupils
fail to contract when light is admitted to the affected side, but both
contract readily when light is admitted to the sensitive eye, because
the central cord of the contractor reflex arc is coimected with its fellow
of tiie opposite side by commissural fibres. In blindness from a lesion
situated above the corj)ora quadrigemina, contraction of the pupil to
light is retained, because the reflex arc is unaflected and consecpiently
the presence or absence of reflex contraction of the pupil to light in
cases of blindness is a valuable diagnostic sign in determining the
localization of the lesion.
(jjj) Reflex Dmiiohility of the Pupil {the Argyll- Robertson Pupil).
— In this condition there is absence of reflex contracticm of the pupil
to lifiht, while the associated contraction with accommodation is re-
tained, and vision may be normal. The absence of any paralysis of
the sphincter and of blindness, shows that the efferent and afferent
fibres of the reflex ai-c are unaffected, and consequently the lesion must
be situated in the fibres which connect the corpora quadrigemina with
the nucleus of the third nerve (Fig. 75); the interruption taking place
most probably near the descending root of the fifth nerve. This symp-
tom is met Avith almost exclusively in locomotor ataxia and general
paralysis of the insane.
202 GENEKAL SYMPTOMATOLOGY.
b. Disorders of the Vaso-motor and Other Mechanisms or the Cervical
Sympathetic and Cilio-spinal Kegion of the Spinal Cord.
The symptoms caused bv disease of the cervical portion of the sym-
pathetic differ according as the lesion is (1) an irritative or (2) a de-
pressive one.
(1) Irritative Phenomena. — When the sympathetic centres in the
medulla oblongata, or the efferent fibres -which connect them with the
periphery, are irritated, the pupil becomes dilated (spasmodic mydri-
asis) ; the palpebral aperture is increased in size ; the eyeball becomes
slightly protruded (exophthalmos) ; the temporal artery is contracted,
and feels like a hard cord under the finger ; the skin of the half of the
face and the ear on that side is pale and cold to the touch ; and the
temperature in the external meatus, and probably in the cavities of the
mouth and nose on that side, is lowered as compared with that on the
opposite side. The phenomena of irritation of the sympathetic are
somewhat transient, so that we do not possess any very accurate infor-
mation with regard to the state of the secretions in such cases ; but I
have observed, in cases of cervical pachymeningitis with dilated pupils,
that the face has often an oily appearance, as if the secretion of sweat
were not so much increased in (piantity as altered in quality. There
are no very accurate observations with regard to the condition of the
secretion of tears, saliva, or of that from tlie mucous membrane of the
nose.
(2) Depressive Pheno)nena. — When the sympathetic centres in the
medulla, or the fibres which connect tliem with the periphery, are
paralyzed, the pupil is contracted (paralytic myosis) ; the intraocular
tension is diminished and the cornea flattened ; the eyeball is retracted
or falls back into the orbit, and its pressure against the eyelids being
thus lessened, the palpebral fissure becomes narrower ; the temporal
artery is dilated and tortuous ; the skin of the face and side of the
head on the affected side may be congested, especially at first ; the
temperature in the external meatus, the mouth, and the nostril is in-
creased on the diseased as compared with corresi)onding ])arts on the
healthy side ; and the secretions of tears, saliva, and sweat, as well as
that from the mucous membrane of the nose, are diminished on tlie
side of the lesion ; while the skin of the face looks, in long-standing
cases, more flabby and wrinkled and older than tliat of the opposite
side. When the disease has become chronic, the vessels on the affected
side of the face may cease to be dilated ; and when the patient exerts
himself so that the cutaneous vessels of the bodv generally become
ddated, the healthy side of the face becomes flushed and covered with
THE VISCERAL KIXESIONEU ROSES. 203
perspiration, while the aftected half retains its normal appearance and
remains free from moisture. The diseased side may also remain dry
when the patient takes a hot bath. Bilateral paralysis of the sympa-
thetic centres in the medulla oblongata, such as sometimes occurs in
progressive muscular atrophy, is attended by a great flow of viscid
saliva corresponding to the paralytic secretion obtained by experiments
on animals.
Morbid Anatonry and Physiology. — Organic lesions of the sympa-
thetic may be divided into those which implicate (1) the centres in the
medulla oblongata or the conducting fibres in their descending course
through the cervical portion of the spinal cord (Fig. 74, D to K, L) :
and (2) the fibres in their course through the rami communicantes of
the eighth cervical and first dorsal nerves (Fig. 74, K. L) and the
cervical sympathetic.
(1) Lesioxs of the 3IeduUa Oblongata and of tlie Cervical Portion
of the Spinal Cord. — Oculo-pupillary phenomena are not mentioned as
being present in reported cases of lesions of the medulla oblongata, but
a case is under my care just now in which there is decided paralytic
myosis and diminution of the palpebral fissure of the right eye, and in
which the accompanying symptoms would seem to indicate that the
lesion is situated in the medulla. The patient had an apoplectic attack
four or five weeks ago, and he is now suffering from left-sided hemi-
plegia and crossed hemianaesthesia, the right half of the face and the
left half of the body being anaesthetic. In addition, the patient is
(piite unable to maintain the erect posture, although he is not com-
pletely paralyzed even on the left side of the body ; and when he is
placed on his legs between two attendants he staggers from side to side,
and throws his legs about in the most irregular manner when he
attempts to move. The staggering and incoordination are most prob-
ably caused by implication of the fibres coming from the inferior
peduncles of the cerebellum. The crossed hemianesthesia is likewise
best explained by supposing that the lesion is situated in the medulla,
causing simultaneous injury of the sensory conducting paths in their
passage through the medulla, and of the ascending root of the fifth
nerve. The excessive flow of saliva which is present in advanced cases
of bulbar paralysis is most probably caused by paralysis of the sym]ia-
thetic centres in the medulla oblongata. Dilatation of both pupils,
along with paralysis of the four extremities, and a remarkably small
and slow pulse (48 per minute), was observed by Rosenthal in a person
who had been stabbed in the neck in the neighborhood of the sixth
cervical vertebra. Oculo-pupillary phenomena, sometimes of the irri-
tative and at other times of the depressive variety, have been frequently
204 GENERAL SYMPTOMATOLOGY.
observed in cervical spinal pachymeningitis and in fractures of the
cervical spine ; and the fact that these phenomena are also fre(|uently
present in locomotor ataxia would seem to indicate that the efferent
fibres pass downwards through the posterior columns of the cord, while
the absence of these symptoms from cases of progressive muscular
atrophy and acute spinal atrophic paralysis shows that the efferent
fibres are not likely to pass through the gray anterior horns.
(2) Lesions of the Rami Coinmunicantes and of the Cervical
Sympathetic. — The rami communicantes are sometimes implicated in
cases of cervical pachymeningitis as they emerge from the spinal cord
with the anterior roots of the eighth cervical and first dorsal nerves,
and in the early stages of such cases the irritative phenomena may be
present, but these soon give place to the depressive symptoms. The
rami communicantes are divided in cases of rupture of the brachial
plexus, and in these cases the paralytic oculo-impillary, vaso-motor,
and secretory phenomena are ahvays well marked. These symptoms
are also frequently met with in aortic aneurisms and mediastinal tumors
from pressure on the inferior ganglion of the cervical sympathetic, in
compression of the cervical sympathetic from goitre and other tumors,
and in these cases the irritative symptoms may be present ; but the
paralytic plienomena are much more frequently met with. The de-
pressive phenomena may also be caused by division of the cervical
sympathetic from gunshot wounds. The irritative and depressive
phenomena of the sympathetic are also met with in certain functional
diseases, such as hemicrania.
The explanation of these symptoms is to be found in the facts, estab-
lished by experiments on animals, that the cilio-spinal region of the
cord and the cervical sympathetic contains not only dilator fibres for
the iris, but also vaso-motor fibi-es for the bloodvessels of the side of
the face, and secretory fibres for the lachrymal, salivary, and nasal
secretions. It would also appear that the cervical sympathetic contains
trophic fibres for the eyeball, as, after section of it, Brown-Sequard
found gradual atrophy of the eye to take place on the side operated
upon. The diminution of the intraocular tension and the flattening of
the cornea which occur in paralysis of the sympathetic filjres in man is
probably caused by lesion of these trophic fibres. The cervical sympa-
thetic also contains fibres which regulate tlie contractions of the muscles
of Miiller in the orbit ; and when these fibres are irritated the muscles
are maintained in a state of contraction, and the globe is protruded ;
and when they are paralyzed the muscles relax and allow the globe to
fall back into the orbit, and the palpebral fissure is diminished.
THE VISCERAL KIXESIOXEU ROSES .
205
2. Disorders of tJc Ncrvom Meclianhm of the Heart.
a. The Cardiac Nervous Mechanism.
The nervous centres which preside over the movements of the heart
consist of intracardiac ganglia, centres in the meduHa oblongata, and
centres in the cortex of the brain. The positions of these centres may
be illustrated by the annexed diagram (Fig. To). The cardiac muscle
Fig. 75.
0' \e
(^^ MA
U k"
1 1 ! ^^\-
I I I
Schema of the Action of the Cardiac Neevous Mechanism.
CA, intramural motor ganglia of the lieart ; CI, intramural inhibitory ganglia; MI and MA, centres
in the niedulla oblongata, the former being inhibitory, the latter motor; B, centre in cortex of brain ; <i,
afterent filire to intramural ganglion cell ; a', afiferent-motor or excito-motor tibre ; a", afferent inhibitory
or excito-inhibitoi-y fibre; a'", afferent fibres connecting periphery with cortex of brain; e', effero-motor
fibre ; e" and e'", effero-inhibitory fibres ; e, e, efferent fibres of the reflex arc of the motor intramural
ganglia ; c, c', fibres connecting the cortex of the cerebrum with the centres in the medulla oblongata.
The arrows indicate the direction of the conduction.
is represented by H, and the endocardium by E ; CA represents the
intramural ganglia ; MA and MI the motor accelerating and the motor
inhibitory centres respectively ; and B the cortical centre, which is
206 GENEEAL SYMPTOMATOLOGY.
represented not only as a motor centre, but also as receiving sensory
fibres from the heart and from the periphery of the body. These cen-
tres are connected with the periphery and with one another and the
heart in various ways : Firstly. Afferent fibres (not represented in the
diao-ram) connect the endocardium and the muscuLar fibres with a car-
diac sensory cortical centre. These fibres pass from the heart through
the cardiac plexuses, and the great cardiac nerve to the middle ganglion
of the cervical sympathetic ; but their subse^juent course through the
spinal cord and brain is not known. Irritation of these fibres in any
part of their course causes cardiac pain or angina. Secondly. Afferent
fibres (a') connect the endocardium Avith the intramural motor ganglia
(CA), and from the latter issue fibres (e) which are distributed to the
cardiac muscle (H). This constitutes a simple reflex mechanism.
Thirdly. Afferent fibres {a") connect the periphery of the body with
the cardiac accelerator centre in the medulla, and irritation of these
renders the action of the heart more frequent. These fibres are called
excito-motor, but affero-accelcratiny fibres would best characterize tlieir
functions. Fourthly. Afferent fibres (a'") connect parts of the peri-
phery with the cardio-inhibitory centre in the medulla, and irritation of
these renders the action of the heart slower. These fibres are called
exeito-inhibitory, but affero-inhihitory would best characterize their
functions. It is possible that each of the centres in the medulla is
connected by afferent fibres with the endocardium and the muscular
fibres of the heart, but these are not represented in the diagram.
Fifthly. Afferent fibres {a"") connect the surface of the body, either
directly or indirectly, with the cortical motor centre (B). Sixthly.
Intercentral fibres {e') connect the motor accelerating centre (MA) in
the medulla and the intramural cardiac ganglia (CA); they convey
efferent impulses which increase the activity of the heart, and are con-
sequently called acecleratinji JihrcH. Seventhly. Intercentral fibres {e'^
and e'") connect the inhibitory centre (MI) in the medulla and the
intramural ganglia (CA) ; they carry impulses which arrest the action
of the heart, and are therefore called cardio-inhibitory fibres. Various
physiological facts seem to indicate that between the cardio-inhibitory
centre in the medulla (MI) and the intramural motor ganglia (CA)
intermediate ganglia (CI) are interposed, which, from their action, are
called intramural cardio-inhibitory ganglia. Eighthly. Intercentral
fibres (c and c') connect the cortex of the opposite hemisphere of the
brain with the cardio-motor and cardio-inhibitory centres in the me-
dulla. These fibres may respectively be called centrifugo-motor and
centrifugo-inhibitory fibres.
THE VISCERAL KI NESIONE U ROSES . 207
b. Disorders of the Cardiac Nervous Mechanism.
(1) disorders of the sensory nerves of the heart (angina pectoris).
Angina pectoris occurs in paroxysms which are separated from one
another by longer or shorter intervals. The attack begins by a sudden,
shooting, tearing, or burning pain, which is felt at the lower part of
the sternum and shoots over the left side of the chest and neck, or
along the sternum and down the left or botli arms. At the same time
a feeling of oppression or constriction is felt across the chest, which is
accompanied by a sense of suffocation and inability to breathe. Dur-
ing the paroxysm the arteries feel like cords, and the pulse is small and
wiry, or feeble, irregular, and intermittent ; the surface of the body is
pale and cold ; the face is pale, sunken, and covered with sweat ; and
tlie expression is one of great alarm and fear ; while it has an unac-
countable feeling of anxiety and fear of impending death. At the end
of the attack the pulse becomes full and soft ; the skin becomes warm,
red, and covered with abundant perspiration. The paroxysm is gener-
ally of short duration, lasting only a few minutes ; but sometimes the
attack is made up of a series of paroxysms, each being followed bv a
remission or a complete intermission of the distressing symptoms. The
paroxysms recur, as in epilepsy, at extremely variable intervals, and
the course of the disease is always chronic. The spinous and trans-
verse processes of the cervical and upper dorsal vertebrae and the region
of the inferior angle of the scapula are sometimes tender to pressure,
either during the attacks or continuously.
It would appear that the essential condition which underlies angina
pectoris is loss of the balance which ought to be maintained between
the propulsive powers of the heart and the resistance to be overcome,
the conditions being altered in such a way that the muscular walls of
the heart are subjected to strain. This state may result from all con-
ditions which weaken the muscular power of the heart, such as the
auc^mia caused by calcification of the coronary arteries, and fatty
degeneration of its muscle ; and from all conditions which cause an
obstruction to the onward flow of blood, such as aortic obstruction, and
diminution of the calibre of the arterioles generally, either by disease
of their walls or spasm of their muscular coats. It will, therefore, be
apparent that the symptoms of angina will accompany many, probably
most, of the organic disorders of the heart.
(2) disorders of the simple reflex cardiac mechanism.
The heart may be thrown into action after it has been removed from
the chest by stimulating the endocardium, a fact which shows that the
208 GEXEKAL SYilPTOMATOLOGY.
afferent fibres connect this membrane with the intramural ganglia,
Avhich in their turn are connected by efferent fibres with the muscular
fibres. Poisons which act on the muscular substance of the heart, as
the salts of potassium, lactic acid and its salts, destroy this mechanism
bv rendering the muscle incapable of responding to a nervous stimulus.
Such poison's arrest the action of the heart in diastole. Landois has
shown that weak solutions of these agents, when injected into the endo-
cardium of the frog, stimulate this reflex mechanism, and accelerate
the action of the heart, while stronger solutions paralyze it. Irrita-
tion of this reflex mechanism in disease accelerates the action of the
heart, while all depressive influences upon it render the action of the
heart slow and feeble, and angina is found associated with the last state.
(3) DISORDERS OF THE CARDIO-INHIBITORY MECHANISM.
{a) Disorders of the Inhibitors/ Fibres of the Vagus. — The beat of
the heart may be checked or stopped in diastole by stimulating the
peripheral part of the divided vagus nerve. The inhibitory fibres (e")
of the vagus are paralyzed by curara, the action of the heart is then
accelerated, and is not rendered slow by stimulation of the vagus.
Electrical stimulation of the sinus venosus will, however, still inhibit
the cardiac beats, and to account for this action the existence of intra-
mural cardio-inhibitory ganglia are assumed. Nicotine stimulates the
same fibres which curara paralyzes and consequently the action of
these drugs is strictly antagonistic. But atropia paralyzes the intra-
mural inhibitory mechanism, while physostigma stimulates, so tliat
these drugs are also antagonistic in their action on the heart. But
although atropia and nicotine, and curara and physostigma have
opposite effects on the cardiac rhythm, yet they are not mutually
antagonistic. Atropia and physostigma will check the action of nico-
tine and curara respectively, but the latter drugs have no effect in
checking the action of the former. Muscarin and jaborandi produce
standstill of the heart which may be removed by atropia, yet neither of
the former drugs has any influence ui)on the action of the hitter.
From this it is inferred that muscarin and jaborandi stinmlate the
inhibitory fibres of the vagus, but do not affect the intranmral cardio-
inhibitory mechanism.
Irritation of the vagus is indicated by a full, hard, retjirded pulse,
increased force of the cardiac beats, disorders of phonation and deglu-
tition, and sometimes temporary arrest of the heart's action. Paralysis
of the vagus is indicated by increased rapidity of the pulse, which
may beat as high as from 216 to 240 times in a minute. This form of
THE VISCERAL KIN ESI ONEU ROSES . 209
accelerated action of the heart is sometimes associated with attacks of
bronchial asthma.
(b) Disordci's of the Cardio-inliihitory Centre in the Medulla. — In
acute and chronic diseases of the base of the brain the rhythm of the
heart is greatly changed, and this is probably due to irritation or paral-
ysis of the cardio-inhilutory centre in the medulla. In tubercular
meningitis, for instance, the pulse, which is at first very slow, becomes
very quick towards the terminal period of the disease. Great accelera-
tion of the pulse is also met with in the various forms of bulbar paral-
ysis, and in cases of locomotor ataxia with gastric crises and other
symptoms indicative of disease of the medulla.
[(■) Disorders of the Reflex-inhihitory Mechanism. — It would appear
that powerful stimulation of any part of the body will produce reflex
inhibition of the heart. Crushing of a frog's foot will, for instance,
stop the cardiac beats, and in man the fainting which occurs during
severe pain is caused by an inhibitory action on the heart. Injury of
the intestines, however, appears to exercise a more powerful effect on
the heart than that of any other part of the body. If the abdomen of
a frog be laid bare and the intestines be sharply struck, the heart will
stand still in diastole, and the same effect is produced by strong stimu-
lation of the mesenteric nerves, but this action fails in both cases if the
vagi are previously divided. Disease of the abdominal organs often
gives rise, by reflex irritation of the vagi, to a kind of angina, which
Landois has named angina pectoris rejlectoria.
(4) DISORDERS OF THE EXCITO-MOTOR OR ACCELERATOR MECHANISM.
Stimulation of certain parts of the spinal cord, and of certain fibres
of the sympathetic, causes acceleration of the heart's action, but section
of these nerves does not render the action of the heart slower, and
consequently the accelerator and inhibitory fibres are not to be re-
garded as antagonistic, this view being still further confirmed by the
tact that simultaneous stimulations of these fil)res do not neutralize each
other. When the accelerating fibres are irritated bv disease the svmp-
toms are the same as are caused by stimulation of the simple reflex
motor mechanism.
(5) ANGINA PECTORIS VASO-MOTORIA.
The symptoms of angina are sometimes caused by irritation of the
vaso-motor nerves, but this condition will be considered with the angio-
neuroses.
14
210 GENEEAL SYMPTOMATOLOGY.
3. Disorders of the Nervous 3Iechanism of Respiration.
a. The Kespiratory Nervous Mechanism.
The nervous mechanism of respiration consists of nerve centres and
their connection with one another, with the muscles of respiration, and
with the periphery of the body.
The respiratory nerve centres are situated in the spinal cord and
medulla oblongata, and in the cortex of the brain. The spinal centres
are the nuclei of origin of the thoracic, phrenic, and spinal accessory
nerves, and to these may be added the nuclei of origin of the nasal
branches of the facial nerve, and of some of the fibres of the superior
laryngeal nerve. The respiratory centres in the medulla are situated
beneath the fourth ventricle, at the nuclei of origin of the pneumo-
gastric and spinal accessory nerves. This centre controls and regu-
lates the spinal centres, inasmuch as destruction of it arrests all respira-
tory movements. The cortical motor respiratory centres appear to be
situated on the internal surface of the hemisphere. The following are
some of the conducting fibres of the respiratory mechanism : Firstly.
Afierent fibres from the surface of the body generally influence the res-
piratory cortical centres, and consequently any sudden impression upon
the surface of the body interferes with the resj)iratory rhythm. Secondly.
Afferent fibres from certain parts of the body influence the respiratory
centre in the medulla. Breathing is arrested in inspiration by cold sud-
denly applied to the surfjice of the body, and it is temporarily arrested
in expiration by a sudden irritation of the mucous membrane of the nose,
the irritation being conveyed through the branches of the fifth nerve.
Thirdly. Affero-acerlerating fibres to the respiratory centre are con-
tained in the trunk of the vagus. If tlie vagi are divided respiration
becomes much slower, fuller, and deeper than normal, but if the central
end is stimulated the respiration is again quickened, and a strong
stimulus arrests it in the position of deep inspiration. Fourthly. Affero-
inhibitory fibres to the respiratory centre pass in tlie superior and in-
ferior laryngeal nerves, and proljably, also, in the splanchnic nerves,
and powerful stimulation of these fibres produces respiratory arrest in
expiration. Fifthly. Efferent fibres connect the cortical motor centres
with the respiratory centres in the medulla, and probably also directly
with the spinal centres. Sixthly. The respiratory centre in the medulla
is connected with the spinal centres probably by cells as well as by fibres,
and the former of these centres is probably only the upper expanded
termination of a continuous gray column which forms the spinal nuclei.
Seventhly. The spinal nuclei are connected with the muscles of respira-
THE VISCERAL KIXESIOXEU ROSES . 211
tion by the thoracic, phrenic, and spinal accessory nerves, and by the
nasal branches of the facial, and some of the fibres of the superior
laryngeal nerve. Eighthly. It is probable that there is no localized
sensory cortical centre for respiration, but the distress caused by
obstruction to the breathing is a complex sensation caused by irritation
of the afferent fibres of the respiratory muscles and various other
afferent fibres.
The rhythmical action of the respiratory centre is probably auto-
matic and not reflex in its nature, although its action is variously
modified by afferent impulses. The exciting cause of the respiratory
movements is the presence of a certain amount of oxygen and carbonic
acid in the blood, respiration becoming stronger the less the quantity of
oxygen and the more of carbonic acid it holds. The rhythm of res-
piration is, however, modified and regulated by impulses passing through
the afferent inhibitory and accelerating fibres. Brener and Herinof
believe that distention of the lungs acts as an excitant to the inhibitory
fibres, and thus induces an expiratory act, and that contraction of the
lung excites accelerating fibres and thus initiates an inspiration. It is
also probable that we must assume the existence of an inspiratory and
an expiratory centre in the medulla.
b. Disorders of the Respiratory Nervous Mechanism.
(1) Accelerated Breathing. — When the blood is deficient in oxygen
and charged with carbonic acid, the respiratory centre in the medulla
is stimulated and the respiratory rhythm is accelerated. The breathing
is also often accelerated in hysteria and other nervous disorders, and
in febrile diseases.
(2) Dyspncea. — When respiration is accompanied by a distressing
consciousness of want of breath, arising from undue irritability of the
nervous mechanism, as in hysteria, or from insufficient aeration of the
blood, as in organic diseases of the heart, the accessory muscles of res-
piration are thrown into action, and the condition is called dyspnoea.
When there is an obstruction to the passage of air to and from the
lungs, the limits of distention and contraction are reached slowly and
Avith effort, and consequently the dyspnoea is declared not so much by
the frequency of the respiratory movements as by the increasing effort
required to accomplish the act and by an alteration in the ratio of the
various stages of the respiratory rhythm.
(3) Apnoea. — By blowing air into the lung or by forced voluntary
breathing the blood becomes saturated with oxygen and poor in car-
k
212 GENERAL SYMPTOMATOLOGY.
bonic acid, and the respiratory movements are temporarily arrested.
This condition is termed apnoea.
(4) Asphyxia.— ^\\en the deficiency of oxygen in the blood is very
o-reat the excitability of the respiratory motor centre in the medulla
becomes destroyed, and the respiratory movements are arrested. This
condition is termed asphyxia.
(5) Cheyne-Stokes Respiration. — In various cerebral, cardiac, and
renal affections the breathing becomes intermittent. After a prolonged
pause the respiratory rhythm becomes established, and the respiration
gradually increases in depth and frequency up to a certain point,
beyond which they become gradually shallower and slower until the
pause, which may last from one-half to three-quarters of a minute.
The duration of the whole cycle is usually from one to two m.inutes.
This peculiar kind of breathing, with its gradually ascending and de-
scending intensity and periodical pause, is named the Cheyne-Stokes res-
piration, after the observers who first described it. The usual explanation
of this phenomenon is that when the excitability of the respiratory centre
is greatly diminished the blood must become surcharged with carbonic
acid in order to excite it, the increased inspiratory efforts thus induced
diminish the venous state of the blood, and the respiration becomes
less powerful, until it is finally arrested for a time until the blood
becomes again surcharged with carbonic acid. Langendorffs experi-
ments prove that arrest of the flow of blood to the medulla will induce
this kind of breathing in animals, and it is, therefore, likely that an
alteration in the nutritive quality of the blood, or a spasm of the
arteries of the medulla, may help to cause it.
(6) Asthma nervosum consists of paroxysmal attacks of difficulty of
breathing, which are caused by a spasmodic contraction of the muscular
tissue of the bronchial tubes. The expectoration of frothy mucus
which generally accompanies an attack would seem to indicate that the
symptoms are also in part caused by an oedematous swelling of the
mucous membrane of the smaller bronchi. Those who are subject to
nasal catarrh will readily understand the suddenness with which such a
swelling may appear, and the degree of obstruction and discomfort to
which it may give rise. The asthmatic paroxysm may be excited by
direct irritation of the trunk of the vagus, in other cases it is caused
by reflex irritation of the sensory nerves of the lungs themselves, or of
those of remote organs, such as the stomach, intestines, or uterus. An
attack sometimes results from central irritation, and it is then generally
associated with hysteria. In some cases an asthmatic attack is accom-
panied by a feeling of great oppression and great acceleration of the
pulse, which may beat from 132 to 148 in the minute, and in these
THE VISCEKAL KINESIOXEUROSES. 213
cases it is probable that there is a simultaneous irritation of the pul-
monary and paralysis of the cardio-inhibitory fibres of the vagus.
Sneezing, coughing, respiratory spasm, and respiratory paralysis
will be considered hereafter.
4. Disorders of the Nervous Mechanism of tlw Bladder and Rectum.
a. The Nervous Mechanism of the Bladder and Rectum.
The walls of the bladder and rectum contain muscular fibres to
expel their contents, while at the mouth of each there is a sphincter
which is maintained in a state of tonic contraction, and thus prevents
Fig. 76.
Diagram Showing the Probable Plan of the Centre for JIictirition. (After Gowers.)
5IT, Motor tract, ST, Sensory tract in the spinal cord ; MS, Centre, and m s, 3Iotor nerve for spliincter ;
MD, Centre, and m d, Motor nerve for detrusor ; s, Afferent nerve from mucous membrane to S, sensory
portion of centre ; B, Bladder. At r the condition during rest is indicated, the sphincter centre in action,
the detrusor centre not acting. At a the condition during action is indicated, tlie sphincter centre
inhibited, the detrusor centre acting.
the continual escape of their contents. It is probable that the nervous
arrangements for the regulation of both the urinary and rectal func-
tions are the same, and it will consequently suffice if we describe the
nervous mechanism of the bladder.
This nervous mechanism consists of nerve centres and their connec-
tions with one another and with the viscus. It is probable that two
centres exist in the spinal cord — an automatic centre (Fig. 76, MS)
214 GENEEAL SYMPTOMATOLOGY.
situated in the segments corresponding with the second, third, and fourth
sacral nerves, and maintaining the tonic contraction of the sphincter,
and a reflex centre (Fig. 76, MD) situated on a little higher level for
the expulsion of the urine by inducing a contraction of the detrusor
vesicae. Another centre is situated in the cortex of the brain, and by
its means the automatic and reflex lumbar centres are brought under
voluntary control. The cortical centre is connected Avith the lumbar
centres by means of centrifugal fibres (MT), and the lumbar automatic
and reflex centres are connected with the bladder by eff"erent fibres,
some of which [m s) connect the automatic centre (MS) with the
sphincter and others {m d) connect the reflex centre with the detrusor.
These centres are also connected with the periphery by means of
afierent fibres, some of them being reflex and othei'S sensory. The
reflex afierent fibres (s) ascend from the mucous membrane of the
bladder, to reach the lumbar centres through the posterior gray horns
(S), while other afi'erent fibres ascend along the centripetal conducting
paths (ST) to reach the cortex of the brain, and then to become con-
nected with the cortical centre.
When the bladder is empty or only })artially full the S])hincter is
maintained in a state of continuous contraction by tlie action of the auto-
matic centre (MS). But when it becomes distended a strong impression
is made upon the afferent nerves of the mucous membrane and impulses
are conveyed to the lumbar centre and to the brain. Now the effect of
afferent impulses upon an automatic centre is to inhibit its action, while
afferent impulses conveyed to a reflex centre find vent along eff"erent
channels. When, therefore, afferent impulses are conveyed to the
lumbar centres, the action of the automatic centre is inhibited and the
sphincter relaxes, while that of the reflex centre is increased and the
detrusor vesicae contracts. The action of the local automatic and reflex
mechanisms is rendered more definite and certain when the afferent
impulses reach the brain. A desire to urinate is excited ; voluntary
impulses are then conveyed by centrifugal cliannels to the inferior cen-
tres, the action of the automatic centre is either increased and that of
the reflex centre inhibited so as to check tlie reflex tendency to urinate,
or the action of the automatic centre is inhibited and that of the reflex
increased, and urination is accomplished.
b. Disorders of the Vesical ^^ekvous Mechanism.
The nervous mechanism of the bladder may be aff"ected in various
ways, but those disorders generally declare themselves either by incon-
tinence or retention. Affections of the nervous mechanism of the
I
L
THE VISCERAL KIXESIONEUROSES . 215
bladder may be divided into those caused ])y (a) spino-periplieral and
(b) those caused by cerebro-spinal lesions.
(a) Spino-periphcral Lesions. — A destructive lesion of the automatic
centre of the sphincter, or of its efferent fibres, gives rise to parahjtir
or atonic incontinence, while irritative lesions occasion spasmodic reten-
tion. A destroying lesion of the reflex centre causes paralytic or
atonic retention, and irritative lesions of the reflex arc, generally
caused by peripheral irritation of the afferent fibres, as in cystitis, give
rise to spasmodic incontinence.
(h) Cerebrospinal Lesions. — Destroying lesions of the cortical cen-
tre or of the centrifugal conducting paths arrest voluntary control over
the bladder the urine is discharged at irregular intervals, and cannot
be restrained : but if the spino-peripheral apparatus is free from disease
the urine does not escape in a continuous stream. If the centripetal
cerebral conducting paths are also aff'ected, the patient is unconscious
of the act of uriiuition. Irritative lesions of the cerebro-spinal appa-
ratus may give rise at one time to spasmodic incontinence, and at other
times to spasmodic retention. The disturbances of the functions of the
bladder met with in cases of hysteria and during epileptic attacks are
probal)ly caused b}^ cerebral discharges along the cerebro-spinal con-
ducting paths.
o. Disorders of the Nervous Mechanism of the Gfenital Organs.
a. The Nervous Mechanism of the Genital Organs.
Sexual Functions. — The sexual functions are governed by a cortical
centre, a reflex centre situated in the upper part of the lumbar enlarge-
ment, and local automatic ganglia connected with the bloodvessels of the
corpora cavernosa. It is not necessary to describe in detail the connec-
tions of these centres with one another and with the periphery. The
lumbar reflex centre is stimulated to action by («) irritation of the
sensory nerves of the glans penis, and (b) discharge from the cortex of
the brain with its associated emotional excitement. On stimulation of
the reflex centre efferent impulses are conveyed along the nervi eric/entes,
which cause vascular dilatation and erection by inhibiting the action of
the local automatic ganglia. A still more prolonged irritation of the
lumbar centre produces ejaculation.
b. Disorders of the Nervous Mechanism of the Genital Organs.
The sexual functions may be disordered by (a) spino-peripheral, or
(b) cerebro-spinal lesions.
(a) Spino-peripheral Lesions. — Destroying lesions of the lumbar
centre or of the nervi erigentes cause impotence, while irritative lesions
216 GENERAL SYMPTOMATOLOGY.
of the reflex arc, generally stimulation of the afferent portion of the arc,
cause erection without sexual desire, named priapism, or partial erec-
tions with strong sexual desire, named satyriasis. In the latter condi-
tion the cortical centres are also stimulated either directly from the
original source of irritation or indirectly from the erections produced.
This condition is met with in cases of locomotor ataxia.
{h) Cerebrospinal Lesions. — Destroying lesions of the cortical cen-
tres or of the centrifugal conducting paths render the patient impotent,
but erections and ejaculations may still occur so long as the reflex
mechanism in the cord is intact. If the centripetal paths are inter-
rupted the subject is insensible of an erection. The act of coition for
instance, affords no pleasure to many hysterical Avomen, and it is proba-
ble that in them there is a functional arrest of centripetal impulses to
the cortex of the brain. Irritati\'e lesions of the cortical centre or of
the centrifugal conducting path may give rise to satyriasis, nympho-
mania, or to priapism. Satyriasis in the male, ov nymphomania in the
female, are not unfrequently observed in the insane, caused probably
by irritation of the cortex ; and irritation of centripetal fibres is also
likely to give rise to the same condition. But although irritation of
centrifugal channels occasions priapism, it is not likely to cause satyria-
sis. Lesions in the upper dorsal and lower cervical regions of the
cord are often accompanied by })riapism, doubtless caused by irritation
of centrifugal conducting paths.
6. Disorders of the Nervous 3Ii'chanisnis of Other Viscera.
It would occupy too much space to enter upon an analysis of the
motor affections of the other viscera, such as the various segments of
the intestines and the uterus with its a[)pendages. Complicated dis-
orders of these and other organs occur from lesions of the centres of
innervation in the cortex of the brain, medulla oblongata, and spinal
cord, as well as from lesions of the intramural ganglia, and the fibres
which connect these different centres with one another and the peri-
phery. These lesions give rise to atony or hypertony, spasm or
paralysis, or want of motor coordination, similar in principle to the
disorders of the nervous mechanisms we have just been considering.
Iir. AVASCULAR KiNESIONEUROSES OR AnGIONEUROSES.
1. The Vaso-motor Nervous Mechanism.
The calibre of the bloodvessels throughout the body appears to be
regulated by means of a nervous mechanism which is essentially similar
to those which regulate the movements of the hollow viscera. Tlie
THE VASCULAR KINESIO^'EUROSES. 217
centres consist of local ganglia in the walls of the arteries, spinal cen-
tres, vaso-motor centre in each lateral half of the medulla, and cortical
luotor centres which are situated in the motor area of the cortex. The
vaso-motor centre in the medulla is probably only the upper expanded
end of a column of gray matter which represents the spinal centres.
The following are some of the conducting fibres of the vaso-motor
mechanism : Firstly. Afferent fibres from the periphery of the body
generally alter the arterial tonus. A medium degree of irritation of
the sensory nerves causes an increase, but strong irritation causes great
diminution of the vascular tone. Secondly. Afferent fibres which run
in the vagus, and which, on being irritated, cause a diminution of the
vascular tone, and these are consequently named depressor fibres. In
the rabbit these fibres arise from the heart, and form a separate branch
which runs alongside the carotid artery and the cervical sympathetic.
Thirdly. Afferent fibres which run in the superior laryngeal nerve and
the sympathetic, and excitation of which causes a marked increase of
vascular tone, and conse(|uentl_y these fibres are named pressor fibres.
Fourtldy. Afferent fibres connect the muscular fibres of the middle
coat of the arteries with the intramural gano-lia, and excitation of these
causes first contraction and then dilatation of local vascular areas.
Fifthly. Centrifugal fibres connect the cortical centres of one hemi-
sphere with the vaso-motor centre of the opposite half of the medulla.
Sixthly. Efferent fibres connect the vaso-motor centre in the medulla
with the spinal centres, but it is probable that the connection between
these centres is in considerable part effected by means of gray matter.
Seventhly. Efferent fibres connect the vaso-motor fibres in the medulla
and the spinal vaso-motor centres with the intramural ganglia, these
fibres passing outwards partly through the rami communicantes and the
sympathetic, and partly through the anterior roots and the spinal nerves.
These fibres are of two kinds : excitation of one set of fibres causes
the arteries to contract, and these are consequently named vaso-con-
strictor fibres; but excitation of the other set causes the arteries to
dilate, and these are consequently named vaso-dilator fibres. In many
parts of the body the vaso-dilator fibres run in separate channels from
the vaso-constrictor fibres. Stimulation of the chorda tympani, for
example,, causes dilatation of the bloodvessels of the submaxillary
glands and of the anterior part of the tongue. In the extremities the
nerve trunks contain both kinds of nerve fibres; Eighthly. Effei-ent
filjres connect the local ganglia with the muscular fibres of the middle
coat of the arteries.
The centre in the medulla oblongata is the general vaso-motor centre
for all the arteries of the body, and by its action, which is probably of
218 GEXEEAL SYMPTOMATOLOGY.
a reflex nature, it maintains all the arteries of the body in a medium
state of contraction, constituting arterial tonus.
2, Disorders of the Vaso-motor Nervous 3fechanism,
Spasm of the vessels — angiospasm or vascular hypertony — may be
caused by irritation of vaso-constrictor or paralysis of vaso-dilator
fibres ; while dilatation of vessels — angioparalysis or vascular atony —
may be caused by paralysis of vaso-constrictor or irritation of vaso-
dilator fibres. Both irritation and paralysis of vaso-motor fibres may
be direct from lesion of the fibres or of the centres, or reflex from lesion
of aff"erent fibres. Alterations of the calibre of the vessels of the sur-
foce of the body may be caused by (a) ]ieriplieral, (/>) spinal, and (/•)
cerebral lesions : while special mention will be made {d) of the vaso-
motor disorders of the viscera.
a. Peripheral Ancjioneuroses
Reflex vascular disorders may be produced by lesions of the afferent
fibres which pass from the vessels to the local ganglia, or of afferent
fibres which pass to the ganglia situated higher up. These reflex dis-
orders may consist of spasm or dilatation, although it is not known
under what conditions the one or the other state is caused. Dilatation
of the vessels of the conjunctiva, for example, is caused by neuralgia
of the first division of the trigeminus, but it is not known whether the
action is reflex or direct, or whether the vascular dilatation is caused
by paralysis of vaso-motor constrictor or irritation of vaso-dilator fibres.
Division of large nerve trunks is followed by redness and increased
temperature of the parts supplied by the injured nerve, which is caused
by paralysis of the vaso-constrictor nerves. But degeneration of the
nerve fibres induces trophic changes in the affected extremity, which
causes the material exchanges to be diminished and the circulation to
be less active, and consequently less heat is generated, while more is
radiated owing to the dilatation of the vessels, and the temperature falls
below the normal. Paralysis of the vaso-motor nerves of an extremity
occurs sometimes in the absence of any other symptom of nervous
disease.
b. Spinal Anoioneuroses.
Lesions of the vaso-motor centres in the medulla and spinal cord, or
of their respective conducting paths, may increase or diminish the
arterial tone either locally or generally. Injuries and diseases of the
spmal cord which cause paraplegia are generally associated by a pri-
THE VASCULAR KINESIONEUROSES. 219
maiy increase of temperature of the paralyzed limbs. In hemipara-
plegia of spinal origin there is a primary increase of temperature in
the paralyzed as compared with the non-paralyzed limb.
Injuries of the cervical portion of the cord near the medulla oblon-
gata cause a remarkable elevation of the temperature of the body, and
in these cases the temperature may continue to rise after the injurv.
and may even increase considerably after death. This remarkable rise
of temperature probably depends upon sudden paralysis of the vaso-
motor system, or upon interference with the action of a heat-regulating
centre in the medulla oblongata. In locomotor ataxia, again, which is
a disease of the afferent or sensory portion of the spinal cord, the lower
extremities are often cold from vascular spasm, and in some cases of
this disease a local alteration of the vessels occurs Avhich is so remark-
able as to require special mention.
Tabetic JEcchi/Dioscs. — In the course of locomotor ataxia, patches of
discolored skin are found scattered irregularly over the lower extremi-
ties and lower part of the trunk. These patches are at first of a bright
red color, but soon become purple, and pass, like ordinary ecchymoses,
through various shades of brown, green, and yellow, until they finally
fade from the circumference to the centre, and disappear in from four to
six days from the commencement. These ecchymoses appear suddenly
towards the termination of severe paroxysms of lancinating pains and
gastric crises. They are irregularly circular in form, and vary in size
from a few lines to more than an inch in diameter. Several of these
patches are found at the same time, as many as three or four of them
being observed on each lower extremity.
The local asphyxia of Renaud belongs probably to the angioneuroses,
but, as it often terminates in gangrene, its description will be found
amongst the trophoneuroses.
c. Cerebral Angioneuroses.
Vaso-motor disorders are daily observed under the influence of
various emotions, the most familiar of these being the blush of shame
and the pallor of fear. Fainting is associated with pallor of the sur-
face, and alternatincr conditions of pallor and redness are often observed
in various neuroses, such as hysteria and epilepsy. At other times the
vascular alteration, instead of being diffused, occurs in patches — what
has been observed under the name of cerebral maculae.
Taches cerebrales consist of red blotches and mottlings on the chest
or abdomen of epileptics, and those suffering from Graves's disease and
other neuroses. When the affected portion of skin is rubbed, or, ni
strongly marked cases, is merely touched by the finger, the surface soon
220 GENERAL SYMPTOMATOLOGY.
becomes suffused ^vitll bright red marks, which spread to some distance
around the point touched, and persist for several minutes.
d. Visceral Axgioneuroses.
The vaso-motor nerves of the thoracic viscera are derived from the
inferior cervical and superior tlioracic ganglia, and from the spinal
cord bv communicating branches from the third to the seventh dorsal
vertebrge. The vaso-motor nerves of the abdominal viscera exist
chiefly in the splanchnic nerves. Section of the splanchnic nerves
occasions a great diminution of the arterial pressure from dilatation of
the vessels and engorgement of the abdominal viscera. Irritation of
the distal end causes contraction of the vessels and conseciuent eleva-
tion of the blood pressure. A part of the vaso-motor nerves of the
abdominal viscera probably passes in the vagus. Experimental in-
jury of the lumbar portion of the spinal cord in animals has been
found to cause congestion and even extravasation of blood in the
suprarenal capsules, and hemorrhagic foci have been found in these
organs in cases of acute myelitis. Crushing of the pons and basal
ganglia in animals has l^een found to cause congestion and ecchy-
moses in the lungs, pleura, kidneys, and nmcous membrane of the
stomach and bowels, and Eulenburg found intestinal hemorrhage after
bruising the cortex of the occipital lobe of the brain. Congestion
and extravasations of blood in the internal organs are not uncom-
mon as complications of cerebral apoplexy. The various menstrual
disorders which are so frequently associated with emotional disturb-
ances are no doubt the result <)f functional disorders of the vaso-motor
nerves, and the vicarious hemorrhages of the stomach, intestines, lungs,
and other organs probably also depend iijjon disorder of vaso-motor
innervation. Both quantitative and (pialitative anomalies in the con-
dition of the urine probably de])end upon disorder of the vaso-motor
nerves of the kidneys. Bernard found that injury of the upper part
of the floor of the fourth ventricle causes polyuria and albuminuria,
while injury of the lower part of the floor of the fourth ventricle
causes temporary glycosuria. Injuries of the spinal cord, in the cervi-
cal and thoracic ganglia, or of the large nerve-trunks, such as the
sciatic nerve, are also followed by glycosuria. If the pneumogastric
nerve is divided in the neck, stimulation of the upper end is followed
by dilatation of the vessels of the liver, and the appearance of sugar
in the urine. The most reasonable explanation of these phenomena is
that vaso-motor paralysis of the hepatic artery causes engorgement of
the hepatic vessels, which gives rise to an increased production of
THE VASCULAR KUSTESIONEUROSES. 221
sugjir. Certain forms of enlargement of the liver and spleen are
l^robably caused by paralysis of vaso-motor nerves. Section of tlie
cfterent fi))res of the semilunar and splenic plexuses in animals causes
enlargement of the spleen, while ii-ritation of these fibres reduces its
size and renders the organ paler. Extirpation of the coeliac and
mesenteric plexuses causes, besides other phenomena, congestion and
enlargement of the liver, and it is probable that the congestion of this
organ which takes place during attacks of migraine is of vaso-motor
oriirin.
CHAPTEK YIII.
GENERAL TREATMENT.
Nervous diseases must be treated according to the same general
principles as all other diseases, and it is therefore unnecessary to entei-
upon a detailed description of treatment in this place. The treatment
of nervous diseases may be divided into that which is directed : (1) to
prevent disease ; (2) to remove the exciting cause of the disease ; (3)
to remove the anatomical cause ; and (4) to allay or remove serious
symptoms.
1. PROPHYLACTIC TREATMENT.
Prophylactic treatment consists of a special application of hygienic
rules to the cases of those who manifest inherited or acquired proclivi-
ties to diseases of the nervous system. The children of parents who
have suffered from severe nervous diseases, like hysteria, epilepsy, or
neuralgia, ought to be specially guarded against being subjected to
severe mental strain and emotional excitement in youth, and especially
during the period of sexual development. The children of such parents
are generally quick in their perceptive ficulties and are possessed even
of great intellectual activity, and they ought not to be allowed to enter
upon competitive examinations at schools except under the strictest
precautions. Parents and teachers ought to pay great attention to such
symptoms as headache, sleeplessness, horrible dreams and night starl-
ings, and loss of flesh and appetite, Avhich are the more usual symptoms
of an overstrained nervous system. Of these symptoms, sleeplessness
is probably the most important as a danger signal, inasmuch as, on the
one hand, it is generally caused, especially in the absence of pain, by
exhaustion of the nervous system, and, on the other hand, it becomes a
powerful cause of further exhaustion, because the nervous energies used
up during the day fail to be restored at night. Plenty of muscular
exercise, so long as it is thoroughly enjoyed and stops short of inducing
fatigue, is the most powerful means we possess of fortifying the nervous
system in young people. Those who inherit a predisposition to nervous
disease also require an abundance of plain and nourishing diet, and a
due exposure to sunlight and fresh air.
REMOVAL OF THE ANATOMICAL CAUSE. 228
2. REMOVAL OF THE EXCITING CAUSE.
When a disease of the nervous system has been induced by unfavor-
able circumstances of climate, exposure to variations of temperature,
or excessive fatigue, these conditions must, if possible, be corrected •
and Avhen the disease has been caused by wounds, contusions, or com-
pression of nervous tissues, these causes must be removed, and the
damage done to the tissues repaired as much as possible by suro-ical
interference. If the disease is caused by a morbid poison like syphilis,
malaria, gout, rheumatism, or the metallic poisons, the treatment must
be directed to remove these poisons from the system or to neutralize
their action.
3. REMOVAL OF THE ANATOMICAL CAUSE.
The nutrition of diseased nervous tissues may be favorably influenced
by agents which act directly on the nervous tissues themselves, the
connective tissues which surround the nervous tissues, the vaso-motor
nerves and centres of the bloodvessels themselves, and the blood. The
agents by which nutrition can be influenced may be divided into (a)
internal and [b) external remedies.
(a) Internal Remedies.
Internal remedies produce their action after gaining admission into
the circulation either by being absorbed through the mucous membranes,
skin, or subcutaneous tissues after injection, or by direct injection into
a vein. The following are some of the remedies of this class : Strychnia
and the preparations of nux vomica increase the irritability of the gray
substance of the sj^inal cord and diminish its specific resistance, and
they are usefully administered when the irritability is depressed.
Strychnia is a powerful remedy in atonic dyspepsia, constipation with
flatulence, paralysis of the sphincters, nocturnal incontinence of urine,
and sexual debility ; but does not possess much value in the treatment
of organic diseases of the spinal cord, being valueless in chronic spinal
affections and positively injurious in all acute organic aff'ections.
Conium depresses the irritability of the spinal cord and of the motor
nerves, and its use has been recommended by Dr. Crichton Browne in
acute mania, and it has likewise been found useful in tetanus. CaJahar
bean lessens and ultimately destroys the irritability of the gray sub-
stance of the spinal cord, causing anaesthesia, loss of reflex excitability,
and paralysis. It has been found useful in tetanus and in hemicrania.
224. GENERAL TEEATMENT.
Its alkaloid, physostig)>ia, iucreases the irritability of the terminal fibres
of the vagus, and kills by paralyzing the respiration. Belladonna and
its alkaloTd, atrojnne, increase the irritability of the gray substance of
the spinal cord, and stimulate in a special manner the respiratory and
vaso-motor centres, the cardiac acceleratory nerve or its centre, and the
pupillary fibres of the sympathetic to the eyes. It paralyzes the motor
nerves, first aifecting those of the trunk, the terminations of the vagi
both in the heart and lungs, the terminations of the secretory nerves of
the salivary glands and of the sweat glands, the terminations of the
inhibitorv fibres of the splanchnics, and the terminations of the nerves
supplying the iris. In large doses it depi-esses the functions of the
afferent nerves. This drug has been found useful in cliecking profuse
sweating, especially the night sweats of phthisis, and the secretion of
milk. It is also useful in habitual constipation, Avhooping cough,
incontinence of urine, and nocturnal emissions; and its use has been
recommended bv Brown-Sequard in chronic organic spinal diseases on
the grounds that it contracts the arterioles of the cord. It is also
useful in allaying pain, but is inferior to opium. JEr(/ot is given in
chronic spinal affections, being supposed to have the power of contract-
intr the arterioles. Opium lessens the irritability of the sensory con-
ducting paths and of the perceptive centres. Small doses first increase
the irritability, but the primary increase is soon followed by a secondary
stage of depression, and if a large dose be administered the first stage
of increased irritability is so transitory that it may be overlooked.
Opium may be administered in small doses so as to obtain tlie primary
or stimulant action, and given in this way it is foun<l useful in the
treatment of nervous exhaustion caused by mental anxiety and over-
work. It is, however, most frequently given in large doses, and is the
most powerful remedy we possess for allaying pain and procuring sleep.
Hydrate of chloral in small do^es induces sleep, and in large doses
profound coma. It paralyzes sensation and reflex action and causes
arrest of respiration, or paralyzes the heart. Chloral and allied agents
are given in relatively large doses with the view of depressing the
irritability of the sensory mechanism and ])rocuring sleep. Chloral
has been found useful in the treatment of tetanus and of poisoning by
strychnia, and as a sedative and hypnotic in cases in which the irrita-
bility of the nervous mechanism is increased. Bromide of potassiimi
and its allies depress the irritability of the gray matter of the brain
and spinal cord, and in large doses diminish sensibility and reflex
excitability. They are very valuable remedies in epilepsy and various
other spasmodic affections. Preparations of zi7ic, arsenic, and phos-
2)horus appear to exercise a fovorable influence on the nutrition of the
REMOVAL OF THE ANATOMICAL CAUSE. 225
nervous system, and they have consequently been named " nervine
tonics."' These agents have been found useful in cases of neurasthenia,
ejiilepsy, chorea, liysteria, and various spasmodic affections. Silver
salts also belong to the same class of agents, and they have been
employed in the treatment of epilepsy and tabes dorsalis. Iron, bv
imjjroving the quality of the l)lood, is a most useful remedy in various
nervous affections, and large doses of the carbonate are particularly
efficacious in neuralgic affections. Quiniyie is a specific against all
nervous affections which result from malaria, but it is also useful in the
treatment of neuralgia, and especially in neuralgia of the supra-orbital
branch of the fifth nerve. Milk, whey, and grape '■^ cures," and
courses of mineral ivaters, act beneficially in many nervous diseases by
exercising a favorable influence on general nutrition. Iodide of potas-
sium has probably no special action on the nervous tissues themselves,
but its well-known action in quickening the absorption of inflammatory
effusions renders it an invaluable agent in the management of many
nervous diseases, and it is an indispensable agent in the treatment of
syj)hilitic nervous diseases. Mercurial preparations are also useful in
tlie treatment of inflammatory diseases, more especially when the mem-
branes of the brain or spinal cord or the sheaths of nerves are affected.
Mercurial treatment is, however, chiefly directed against syphilitic
nervous diseases.
(b) External Remedies.
Cold steadily applied lowers the irritability and retards the conduc-
tivity of the nervous tissues, and consequently it is used as a remedy
in the acute stage of all inflammatory affections of the nervous system.
Chapman's vaso-motor therapeutics is founded on the assumption that
cold applied to the spine lowers the irritability of the vaso-motor, along
with the other centres of the spinal cord, and thus causes dilatation of
the bloodvessels whose nervous supply is derived from the portion of
the cord over which the cold is applied. Chapman's ice-bag is the best
method of applying cold to the spine, and very convenient bags are
made for applying ice to the head or any other part of the body.
Warmth increases the irritability and accelerates the conductivity of
the nervous tissues, and when combined with moisture it relaxes the
tissues, and thus exercises a soothing influence in painful and spasmodic
affections. Warmth may be applied by means of hot-water fomenta-
tions, poultices, Priessnitz's compresses, hot sand-bags, and India-rubber
bags filled with liot water.
Cold baths tend directly to lower the irritability of the nervous tis-
15
226 GENERAL TREATMENT.
sues and to depress the nervous functions, and, when their use is attended
with benefit, it is due to their indirect action, or to the reaction of the
tissues. This reaction is aided by the presence of salt in the water,
and consequently the sea bath is less depressing than the ordinary bath.
The cold bath is a powerful therapeutic agent in neurasthenia, hysteria,
and various other functional afiections, and it may occasionally be found
useful in chronic organic aflFections. SJiowcr, douche, and sponge baths
produce powerful nervous stimulation by the impact of Avater on the
body, in addition to the effects of the cold immersion. Shower and
sponge baths are useful in the treatment of functional nervous affec-
tions ; while the douche is employed for its local effects on paralyzed
parts, and in rousing a patient from drunkenness or opium poisoning.
TFarm baths act as a sedative to the cutaneous nerves, and through
them to the nervous system generally.
If the temperature be indifferent (90° to 97° F.) the bath acts
mainly as a nervous sedative, while warm and hot baths (97° to 108° F.)
produce great vascular excitement and act as powerful nervous stimu-
lants. If the symptoms of irritation preponderate the indifferent baths
should be selected, and if the symptoms of depression are prominent
the warm and hot baths are to be preferred. Brine, vapor, hot-sand,
hot-air, gaseous, and chalybeate baths all act on the same ])rinci])le as
hot baths, and are to be used when powerful stimulation is required.
The needle bath is also a powerful stimulant and is used when the
symptoms of depression predominate.
Mud baths act like warm baths, but are much less exciting than
warm-water spring baths, and they are consequently adapted for the
treatment of spinal irritation and of the various forms of spasmodic
paralysis.
The Turkish bath combines many of the properties of the hot and
cold bath. The great heat to which the body is subjected tends doubt-
less to induce debility, but the subsequent free application of cold
water excites the cutaneous nerves and braces the system, so that the
tonic effects of the cold bath are secured. The systematic kneading to
which all the muscles of the body are subjected promotes their own
nutrition and that of the nerves which supply them, and thus the
effects of the bath are combined with those which result from careful
and regulated exercise, and systematic gymnastics. The Turkish bath
is, indeed, a powerful therapeutic agent, and has a wide range of use-
fulness in the treatment of various nervous affections.
Experience has shown that certain climates and regions exercise a
favorable influence on various nervous diseases, especially on those of
functional origin. Sea air has a very invigorating effect on the system,
REMOVAL OF THE ANATOMICAL CAUSE. 227
and it is well adapte<I for the cure of nervous exhaustion from overwork
in those who are otherwise strong and healthy, Feehle and irritable
people, however, obtain greater benefit from residence in a mountainous
district. Mountain exercise has a very enlivening effect upon the ner-
vous system, and the higher and drier the district the more marked are
the tonic effects. The Engadine and Davos Platz are favorite moun-
tain residences, and the Scottish mountains, the English lake district,
and Ilkley, in Yorkshire, are also favorite places of resort, although
they have neither the elevation nor the dry atmosphere of the Swiss
mountains.
Bhodletting ayid counter-irritation are as useful in the treatment of
inflammatory affections of the nervous system as in those of other
organs, but as they present nothing special in their action or mode of
application when employed in the treatment of nervous diseases, they
do not require further consideration at present. The counter-irritants
usually employed are cutaneous faradization, sinapisms, vesicants,
issues, moxge, and the actual cautery. External frictions are carefully
employed in various nervous affections. Frictions with soothino- lini-
ments, warm oil, and ointments containing opium or belladonna, are
used to allay pain in neuralgic and other painful affections. Frictions
with spirituous liniments, either alone or combined with other stimu-
lants, such as ammonia and camphor, are used in the treatment of
various forms of paralysis.
Seclusion of patients from their friends is of great value in the
treatment, not only of the graver psychoses, but also of many cases of
hysteria, neurasthenia, melancholia, and other functional affections.
With reference to the treatment of neurasthenia. Dr. S. Weir Mitchell
says: "Once separate the patient from the moral and physical sur-
roundings which have become part of her life of sickness, and you will
have made a change which will be in itself beneficial, and will enor-
mously aid in the treatment which is to follow." One of the most
frequent questions which the physician has to decide in the treatment
of nervous diseases is whether a patient is to take exercise or rest.
This question is readily decided in most cases of organic disease, the
general rule being that physiological rest should be enjoined in all
acute, and a certain amount of graduated exercise in chronic affections.
In the minor deg-rees of neurasthenia and melancholia a moderate de-
gree of exercise may be prescribed, but it should be always short of
fatigue, and in aggravated cases the most absolute rest should be
enjoined, while the place of exercise is to some extent supplied by
massage.
Massage is a general term which includes methodical rubbing, strok-
228 GENEKAL TKEATMEJSTT.
ing, kneading, and clapping the surface of feeble and paralyzed parts—
a "method which is often successful in the treatment of organic and
functional paralyses. Massage has been extensively used in the Man-
chester Royal Infirmary by my colleague, Dr. Morgan, and with very
gratifying results. The directions for carrying out the process as
practised by Dr. Morgan are briefly the following :
1. Pinch the surfiice of the skin from below upwards, with the view
of stimulating the cutaneous nerves. Suppose the lower extremities to
be paralyzed, the skin of the foot is first drawn up into successive folds
and lioh'tly pinched. The skin over the Avhole of the leg, and finally
that of the thigh is gone over in the same way.
2. Give passive movements to the joints, first moving each of them
separately and then all together.
3. Shampoo the limb well. This is done by lubricating it with some
bland oil, which is well rubbed into the surface by the tips of the
fino-ers passing from l)elow upwards, the spaces between the muscular
groups being specially selected for rubbing.
4. Work the muscles well with the fingers. Each muscle, or group
of muscles, is grasped between the ball of the thuml) and the fingers,
and well kneaded and rolled. During this process the limb nnist be
placed in a position to appi'oximate the ends of the muscles operated
upon, and thus relax them to the utmost.
5. Slap the muscles well with the ulnar border of the hand.
6. Grasp the lower portion of the limb between the hands, and then
draw them slowly and firmly upwards. This movement should be
repeated some twelve or fifteen times. In this manner the veins are
emptied and the circulation quickened.
The IFciV Mitchell treatment., which has been carried out so success-
fully l)y Dr. Playfair, of London, in the treatment of neurasthenia, is
a combination of seclusion, rest, massage, and hyperfeeding. With
regard to the carrying out of this treatment Dr. Playfair remarks :
" The removal of the patient from her home surroundings, and lier
complete isolation in lodgings with only a nurse in attendance, is a
matter of paramount importance. This is a point on which I am most
anxious to lay stress, since it is the great crisis to the patient and her
friends, and constant appeals are made to modify this, which I look
upon as an absolute sine qua non. I attribute much of the success
which I have been fortunate enough to obtain in my cases, to a rigid ad-
herence to this rule." Great care must be exercised in the selection of
a suitable nurse, and if the case is not going on favorably much advan-
tage is often obtained by a change of nurse. The patient is ordered to
bed for from six weeks to two months, and during the greater part of
REMOVAL OF THE ANATOMICAL CAUSE. 229
this period such actions as sewing, reading, and writing are strictly-
forbidden. In aggravated cases the patient is not allowed even to turn
over in bed without aid. She is fed by the nurse, and even the calls
of nature are obeyed in the recumbent posture. With regard to the
use of massage and feeding, Dr. Playfair says: "Massage consists in a
systematic and thorough kneading and movement of the whole muscu-
lar system for about three hours daily, the result of which at first is to
produce great fatigue, and subsequently a pleasant sense of lassitude.
Subsidiary to this is the use of the faradic current for about ten to
twenty minutes, twice daily, by which all the muscles are thrown into
strong contraction, and the cutaneous circulation is rendered excessively
active. The two combined produce a large amount of muscular waste,
which is supplied by excessive feeding, and in consequence of the in-
creased assimilation and improved nutrition we have the enormous gain
in weight and size which one sees in these cases, it being quite a
common thing for a patient to put on from one to two stones in weight
in the course of five to six weeks. The feeding at regular intervals
constitutes a large part of the nurse's work. At first from three to
five ounces of milk are given every few hours, and the first few days
the patient is kept on an exclusively milk diet. By this means dys-
peptic symptoms are relieved, and the patient is prepared for the
assimilation of other food. This is added by degrees, pari passu with
the production of muscular waste by massage, which is commenced on
the third or fourth day. By about the tenth day the patient is sham-
pooed for an hour and a half twice daily, and by this time she is able
to take an amount of food that would appear almost preposterous did
not one find by experience how perfectly it is assimilated and how
rapidly flesh is put on. It is the usual thing for patients to take, when
full diet is reached, in addition to two quarts of milk daily, three full
meals, viz., breakfast, consisting of a plate of porridge and cream, fish
or bacon, toast and tea, coffee and cocoa; a luncheon, at 1 p.m., of
fish, cutlets or joints, and a sweet, such as stewed fruit and cream, or a
milky pudding; dinner at 7 p.m., consisting of soup, fish, joints, and
sweets, and in addition a cup of raw meat soup at 7 a. m. and 11 p. m.
It is really very rare to find the slightest inconvenience from this enor-
mous dietary. Should there be an occasional attack of dyspepsia, it is
at once relieved by keeping the patient for four and twenty hours on
milk alone."
The results obtained by means of this treatment have been so striking
and remarkable that not the slightest detail in the method of carrying
it out is unimportant. After the first few days of treatment a consider-
able quantity of soup made from raw beef is added to the milk diet.
230 GENERAL TREATMENT.
The following is Dr. Mitchell's formula for this soup : " Take one
pound of raw fillet of beef, chop it finely, and place it in a bottle with
a i)int of water and five drops of hydrochloric acid. Stand the mixture
in ice all night, and in the morning set the bottle in a pan of water at
110° F., and keep it two hours at this temperature. It is then to l^e
thrown on a stout cloth, and strained until the remaining mass is nearly
dry. The filtrate is given in two or three doses in the course of twenty-
four hours. If the raw taste prove very objectionable, the beef to be
used may be quickly roasted on one side, and then the process is com-
pleted in the manner above described. The soup thus made is for the
most part raw, but has also the flavor of cooked meat."
Swedish gymnastws are a mere modification of ordinary gymnastics,
the object being to aid the recovery of paralyzed or rather paretic parts
bv bringing the muscles into methodical exercise. The patient is
instructed to make systematic voluntary efforts to move the paralyzed
muscles, and when a certain degree of voluntary movement is attained
the effect is increased by the opposition of a practised assistant. If,
for example, the flexors of the forearm are to be exercised, the forearm
is first extended, and the patient endeavors to flex it "whilst the assistant
opposes flexion with more or less force. In the case of associated
movements it is often necessary to aid the contraction of one grouj) of
muscles so as to overcome the contraction of their antagonists, which
are also excited to action during the voluntary effort to contract the
paralyzed group. The assistant must then aid the paralyzed muscles
by passively extending the healthy antagonist muscles. The action of
the healthy antagonist muscles can be weakened, not only by the hands
of an assistant, but also by fixing elastic bands or spiral wires to the
limb so as to aid the action of the paralyzed groups. In the Swedish
system great attention is paid to the development and strengthening
of the extensors of the body.
Ordinary gymnastic exercises are also useful in the treatment of
various nervous affections. By their use the nutrition of the muscular
system is improved, the heart propels the blood more eflSciently through
the organism, the blood itself becomes of better quality, and the nervous
system participates in the general improvement.
Mechanical Vibrations. — Some years ago, Dr. Mortimer Granville
was led to try the effects of rapidly tapping the skin over the fiftli
nerve in a case of facial neuralgia by means of a Bennett's percussion
hammer, using the pleximeter as a shield. The results obtained were
so encouraging that he gradually extended the application of mechani-
cal vibration as a therapeutic remedy to various other nervous diseases.
With the view of better regulating the number and strength of the
REMOVAL OF THE ANATOMICAL CAUSE. 231
l)lows which can be delivered in a given time, Dr. Granville had an
instrument constructed Avhich he names "percuteur." The newest
and most efficient percuteur is worked by electricity, but it is important
to remember that no electricity passes through the patient ; the elec-
tricity is converted into mechanical motion, and its only use is to enable
the performer to deliver a regulated number of blows on any desired
l)art, just as was done more roughly by means of Bennett's percussion
hammer. Dr. Granville believes that by means of mechanical vibra-
tions he can relieve a considerable number of cases of neuralgia ; that
much amendment occurs by its use in the early stages of locomotor
ataxia and lateral sclerosis ; and that by it he can even arouse torpid
nerve centres to action, and consequently that it is of great use in the
treatment of neurasthenia.
Electricity in the forms of the galvanic and induced currents is one
of the most useful remedies we possess in the treatment of the diseases
of the nervous system. Only the briefest possible account can here be
given of the methods of application and uses of electricity in the treat-
ment of disease, and the student is referred for further information to
books specially devoted to this subject, the valuable work of Dr. De
Watteville on "Medical Electricity" being particularly recommended
to the English reader.
In selecting the position upon which the electrodes are to be placed,
two methods of application have been adopted, viz., the direction and
poJcir methods. In the direction method one rheophore is placed over
the plexus and the other over the trunk of the nerve. When the posi-
tive pole or anode is centrally placed the current is called a deseending
current, and Avhen the cathode occupies that position the current is
called an ascending current. In the polar method one rheophore is
placed on an indifferent part of the body, such as the sternum, and the
other is placed over the nerve or muscle which it is desired to stimulate.
It does not appear that there is any essential diiference in principle
between these two methods. When the cathode is used as the exciting
pole in the polar method, the same kind and degree of contraction is
obtained as when the cathode is peripherally placed in the direction
method ; and, conversely, when the anode is used as the exciting pole
in the polar method, the reactions obtained are the same as those pro-
duced when the anode is peripherally placed in the direction method.
In practice, therefore, it appears to be indifferent whether the polar or
direction method be employed, but those positions should be chosen
Avhich will best insure that the tissue or organ which it is desired to
influence shall be thoroughly permeated by the current. With refer-
ence to the size of the electrodes, the general rule is that, when a
2-^2 GENERAL TREATMENT.
purely local effect on a nerve or muscle is Avanted for diagnostic pur-
poses, the electrodes should be small ; but when an alterative effect on
deeply seated organs is required large electrodes, thoroughly moistened,
should be employed. The current, instead of being passed through
the skin, may be sent directly to a nerve or muscle which it is desired
to stimulate by means of needles introduced into its substance. This
method, which is only of limited application in therapeutics, is called
electric acupuncture.
aalvanhation.— There are three methods of applying the galvanic
current, according as it is desired to obtain its sedative, alterative, or
stimulant action. According to the first method the rheophores are
maintained immovable on the skin, or the affected extremities are placed
in tepid salt water, with which the conducting wires of the battery are
in contact. This is the stabile method of application. In the second
or labile method of application the cathode is made to glide over the
skin in the direction of the nerves and muscles to be acted on. The
third or interrupted method is based upon the fiict that the constant
current acts as a stimulus to both nerves and muscles at the moment of
making and breaking contact. In using this method one pole is held
immovable on one point, whilst the other is made repeatedly to touch
the part to be stimulated. The current may also be interrupted by
means of a commutator. A still more powerful effect is produced l)y
suddenly reversing the direction of the current by means of the com-
mutator — a descending current, for instance, being suddenly changed
for an ascending current. This method has been called by Remak,
who introduced the practice, voltaic alternatives.
Faradization. — When it is desired to limit the current to the skin
the rheophores must be used dry, and the skin should also be dusted
with toilet powder or some other absorbent powder so as to diminish its
conductivity. The electrode used should be metallic, either in the form
of a cylinder, disk, or wire brush, and the useful method of application
is what is known as the electric hand. A moist rheophore is applied
over the sternum or other indifferent part of the body, and the other is
held in one hand of the operator while he passes the back of the dis-
engaged hand over the part which it is desired to excite. When the
deeper tissues are to be reached through the skin the rheophores should
consist of well-moistened sponges in cylinders, or metallic disks covered
with wet leather, and the skin itself should be thoroughly moistened
with a mixture of warm water and salt. In order to electrize a muscle
completely the rheophores should be applied over its fleshy body, and
they should either cover its whole surfoce or be applied in succession
to all points of its surface. When the body of the muscle is thick a
REMOVAL OF THE ANATOMICAL CAUSE. 288
Strong current should be used ; otherwise the superficial layers alone
are excited. The easiest way to apply the current to a muscle is to
hold the handles of the rheophores in the right hand, one between the
thumb and index finger, and the other between the middle and rino-
fingers. The two electrodes are then moved up and down over the
whole surface of the muscle so as to secure a thorough contraction of
every part of it. The faradic current is passed through a nerve in order
to obtain contraction of the muscle or group of muscles Avhich it sup-
plies. The polar method is adopted for this purpose, one electrode
being placed over the sternum or some indifferent part of the body,
and the other over the course of the nerve at the motor points, as indi-
cated in Ziemssens diagrams.
Central galvanization aims at bringing the whole of the central
nervous system under the influence of the current. The cathode is
held immovable over the epigastrium, while the anode is passed over
the forehead and top of the head, along the inner border of the sterno-
mastoid, over the course of the pneumogastric and sympathetic in the
neck, over the nape of the neck, and along the whole length of the
spine.
G-cneral faradization aims at bringing the whole muscular system
under the influence of the current. One pole, usually the negative, is
placed on some insensitive part of the body or fixed to a copper plate
upon which the soles of the feet are placed, while the other is either
sponged over the whole body or kept stationary at certain points.
G-alvano-faradization is obtained by joining the induction coil and
the galvanic battery in one circuit. The negative pole of the one is
connected by means of a wire with the positive of the other, while the
electrodes are attached to the two extreme poles. I have had repeated
opportunities for observing the excellent results which are obtained by
this method in the practice of my colleague. Dr. Morgan, who was the
first to devise this method. Dr. De Watteville, who appears to have
adopted this method independently of Dr. Morgan, speaks very higlily
of its power as a therapeutic agent.
Uses of Electricity. — The faradic current is a powerful stimulant to
both nerves and muscles, and when a simple stimulant effect is alone
desired this current is, as a rule, more applicable than the galvanic
current. This current may, therefore, be used as a stimulant either to
act on the skin directly in cases of anaesthesia, or to act indirectly on
remote organs in a reflex manner ; or it may be used as a jiowerful
neuro-muscular stimulant in the various forms of paralysis. The gal-
vanic current acts as a stimulant to nerves and muscles both on making
234 GEXERAL TREATMENT.
and breaking contact, and, in addition, produces a profound alteration
of nutrition during the time the current is interruptedly passing through
an oro-an. The latter action has been called by Remak its catalytic
action^nd it is to it probably that the constant current owes the many
advantages it possesses over the faradic current in the treatment of
many of the diseases of the nervous system. The stimulant action of
the constant current is, however, very important both as a means of
diao-nosis and in the treatment of paralysis. We have seen that while
paralyzed muscles manifest the reaction of degeneration, they are more
sensitive to the action of the galvanic than of the faradic current, and
in these cases the constant current should be selected to stimulate the
nutrition of the affected muscles. With this exception, however, the
faradic is a more powerful agent in the direct treatment of paralyzed
muscles than the constant current. But the catalytic action of the
constant current renders it an exceedingly valuable agent in modifying
the nutrition of the nerves and trunks of the central organs of the
nervous svstem, and it may even be used in the treatment of cases
where the irritaljility of portions of the nervous system is increased,
and to which, therefore, the faradic current is wholly inapplicable. As
examples of the numerous applications of the constant current may be
mentioned its emi^oyment for the relief of pain in neuralgia and the
assuaging of various forms of spasm, not to speak of its numerous
applications, both locally and generally, in the treatment of chronic
diseases of the brain, spinal cord, special senses, and viscera.
4. TO ALLAY OR REMOVE SERIOUS SYMPTOMS.
The fourth indication of treatment is to allay or remove serious
symptoms, and of these the distressing symptom of pain is by far the
most prominent and important. Opium is the most powerful remedy
Ave possess for the alleviation of pain, and it acts most effectually when
administered in the form of subcutaneous injection of morphia. Brom-
ide of potassium, chloride of ammonium, chloral hydrate, croton chloral,
atropia, quinine, and various other agents may at times be used in pref-
erence to opium in cases of neuralgia. The constant current is also a
valuable agent for assuaging pain, and when it succeeds it should be
preferred to all other remedies, inasmuch as its use is unattended by
any evil after-consequences. Cold, continuously applied, has been used
as a palliative for the removal of pain in neuralgia, while at other times
the local application of warmth aff"ords greater relief, acting, probably,
by relaxing the tissues in which the nerve fibres are embedded. Con-
TO ALLAY OK REMOVE SERIOUS SYMPTOMS. 235
tinuotis pju'ssiire over a nerve is often useful in neuralgia and in cases
of motor spasm, the action being produced by arrest of the conduc-
tion through the nerve. Ointments and liniments of aconite, veratrine,
opium, or atropine are useful as local applications for the removal of
pain.
Surgical operations have been successfully undertaken for the re-
moval of pain or spasm. These operations are performed with the
view of arresting the conduction of nerves in cases of neuralgia or in
local spasms. The operations are neurotomy, in which the nerve is
simply divided ; neurectomy, in which a portion of it is dissected out ;
and nerve -stretching, in which the nerve is powerfully stretched. The
conditions under which each of these operations ought to be under-
taken, will be mentioned in another part of this work.
V
f
i
SPECIAL PATHOLOGY OF THE NERVOUS SYSTEM.
CHAPTER I.
GENERAL DISEASES OF THE PERIPHERAL NERVES.
1. HYPEE.EMIA OK CONGESTION OF THE NERVES.
CoxcESTiox of the nerves is caused by exposure to great cold, as
lias been proved by S. Weir Mitchell, who found that exposed nerves
■which had been frozen became congested and SAvollen on thawinii-.
Sy)iq}toms. — The symptoms caused by freezing of nerves were first
studied by Waller, who froze the ulnar nerve by placing the elbow in a
freezing solution. The first symptoms are pain, anaesthesia, paralysis,
and increase of temperature in the region of chstribution of the nerve.
In the thawed portion a very painful sensation is felt which spreads
backwards to the brachial plexus, and may even produce vertigo and
faintness. The symptoms wliich follow the thawing of the nerve are
hyperi^sthesia, numbness, formication, and partial loss of power, but
no elevation of temperature in the area of distribution of the aflected
nerve.
2. INFLAMMATION OF NEEVES— NEURITIS AND PERINEURITIS.
Etiohiiy. — Inflammation of peripheral nerves is caused by wounds,
contusions, rupture, laceration, or sudden compression of the nerve, or
by exposure to cold and wet. Neuritis may also be caused by exten-
sion of inflammation from the surrounding tissues and organs. The
most notable diseases which set up neuritis are caries of bones, inflamed
tendinous sheaths, acute and chronic inflammation of joints, abscesses,
and malignant growths. It is also frequently developed after acute
diseases such as the acute exanthemata, typhoid fever, and diphtheria,
and after chronic diseases like rheumatism and syphilis. Inflammation
of nerves is also met with in lepra an;\?sthetiea, herpes zoster, and van-
238 GENERAL DISEASES OF THE PERIPHERAL NERVES.
ous other cutaneous affections, and it may appear in the absence of any
recognizable cause, being then called idiopathic neuritis.
Symptoyns. — The symptoms of neuritis differ according as the in-
flammation is (a) acute or {h) chronic.
[a) Acute neuritis comes on soon after exposure of the nerve to one
or other of the causes of the disease. It is ushered in by a well-
marked feeling of chilliness, or by an actual rigor, which is accom-
panied by headache, sleeplessness, and smart fever. In inflammation
of a mixed or sensory nerve the patient experiences a severe and almost
intolerable pain in the region of the affected nerve, and Avhich often
radiates into the areas of other branches of the same plexus, or into
more remote nerve territories. The pain is deep-seated, tearing, boring,
or burning, and it is described as being almost continuous, although
there may be remissions and paroxysmal exacerbations, the latter
being specially apt to occur at night. Every movement of the limb
augments the sufferings of the patient, and pressure over the affected
nerve causes intense pain, which radiates from it in all directions. The
tract of the inflamed nerve is sometimes indicated by a red line like that
which occurs in inflammation of a superficial lymphatic vessel. I'he skin
over the whole area of distribution of the nerve is at first extrenielV" sen-
sitive to the slightest contact, and the patient complains of numbness
and formication of this area, but the hyperesthesia soon gives place to
anaesthesia. In the early stage of the disease muscular spasms and
twitchings may be present, but these are soon replaced by paralysis of
the muscles supplied by the nerve. The degree of paralysis varies
according to the severity of the inflammation, but in all aggravated
cases the muscles undergo rapid atrophy, and manifest "the reaction of
degeneration." In excitable patients an attack of acute neuritis may be
attended by slight delirium, and an emotional condition is sometimes
induced which may be mistaken for an attack of hysteria.
(h) Chronic neuritis occurs either as a sefjuel of an acute attack, or
it arises insidiously with obscure symptoms, which gradually or sud-
denly attain great intensity. Pain is the earliest and most constant
symptom ; it varies considerably in character and intensity,' being some-
times dull and tensive, at other times of a lancinating, tearing char-
acter, and radiating towards the periphery. The pain is continuous,
although it is frequently interrupted by paroxysmal exacerbations,
which generally occur at night and prevent sleep. It is increased by
every kind of exertion and movement, and by everything which excites
the activity of the heart. In the first stages of the disease the patient
complams of numbness an(J of formication, and of unpleasant pricking
sensations when the skin is touched or struck, but in the later stages of
ATROPHY OF NERVES. 239
the disease anaesthesia is established, which may vary in degree from a
slight blunting of sensibility up to complete loss of all forms of sensi-
bility.
Symptoms of motor irritation, such as tension, sudden contractions,
cramps, or persistent contractures of the muscles, are present in the
early stage of the disease, but these are succeeded by paralytic phe-
nomena. Tlie muscular spasms are sometimes direct and sometimes
reflex. Reflex spasms are met with in the facial muscles when the
fifth nerve is affected, and the sphincter of the iris and ciliary muscle
may be the subjects of spasm when the ophthalmic branch is impli-
cated ; and even in neuritis of mixed nerves reflex spasms are some-
times so violent that, for example, the finger-nails may become buried
in the skin of the palm from spasm of the flexors.
The affected nerve is swollen, and when it occupies a superficial
position it can be felt as a continuously thick cord. In other cases the
thickening occurs at certain intervals, and then fusiform or moniliform
swellings may be felt in the course of the nerve — a condition which
has been named neuritis nodosa. The nerve is always sensitive to
pressure, and compression of the swollen portions gives rise to eccentric
pains and formication.
The electrical reactions of the affected nerves and muscles may
remain normal or be even increased in slight cases ; but in rheumatic
and syphilitic cases, and, indeed, in all aggravated forms of the disease,
the muscles undergo atrophy and manifest the " reaction of degenera-
tion."
Trophic disorders of the skin and nails and swelling and stiffiiess
of the joints are frequently observed in chronic neuritis ; hysterical
or epileptic convulsions and tetanus frequently result from neuritis.
3. ATEOPHY OF NEEVES.
Atrophy of nerves may, as we have already seen, be con<ienital in
those cases where portions of the body are incompletely formed, idio-
pathic when there is a simple wasting of the nerve fibres, as occurs in
atrophy of the optic nerves in tabes dorsalis, and secondary when the
nerve fibres are separated from their trophic centres.
Symjotoms. — It may be laid down as a general rule that whenever
atrophy of a nerve exists its function is lowered or lost. Secondary
atrophy of motor nerves may be distinguished by electrical examina-
tion, and primary atrophy of the optic nerves may be recognized by
an ophthalmoscopic examination.
■940 GENERAL DISEASES OF THE PEKIPHERAL XERVES.
4. HYPERTROPHY OF NERVES.
Hvpertropliy of nerves is a mere anatomical curiosity, and is not
known to be connected with any definite symptoms.
5. NEUROMATA.
Etiolof/i/. Some individuals appear to be predisposed to the forma-
tion of neuromata, and phthisical and scrofulous persons seem to be
particularly liable to their formation. Isolated neuromata are more
common in women than in men, while multiple neuromata are almost
exclusively met with in men. They occur at all ages, and are often
congenital.
The best known of the exciting causes are blows, intermittent press-
ure, penetration and retention of foreign bodies, and various injuries.
JS'euromata are also frequently found in the cicatrices formed after nerves
have been divided or injured, and swellings of the ends of the nerves
.are often met with in the stumps of amputated limbs. Chronic neu-
ritis, syphilis, lepra, and elephantiasis may lead to the formation of
tumors in nerves, and in a large number of cases no definite cause can
.be traced.
Syinptoms. — The symptoms of neuromata are variable, many of them
being quite painless, and others causing intense and persistent suftering.
Isolated neuromata give rise to severe and incurable neuralgia, and
they have consequently been called tubcrrula dolorosa. The pain may
be tearing, lancinating, aching boring, or burning ; it is almost always
remittent or completely intermittent, but when the paroxysm comes on
the pain gradually increases in intensity, and radiates from certiiin
points towards the periphery. The })ain is increased by cohl and <lanip
weather, by pressure, or the slightest movement of the affected limb,
and in women frequently by the return of the menses or by pregnancy.
It may often be made to disappear temporarily by firm pressui-e on the
nerve above the tumor. The pain is generally more severe in small
tumors of cutaneous branches than in larger tumors of deeper nerve-
trunks. In addition to pain, feelings of numbness and formication,
and sensations of heat or cold, are often felt in the area of distribution
of the afiected nerve. In some cases aniiesthesia may be present, and
appears not infrequently in the form of ancesthesia dolorosa.
Motor disorders are rare, but sometimes occur in the form of tremors,
spasms, and contractures, and these may ultimately give place to com-
plete paralysis. The course of the disease is very variable. True
neuromata may remain stationary for many years without causing any
1
NEUROMATA. 241
serious symptoms, and multiple neuromata are sometimes so free from
l)ain tliat they are only discovered accidentally during life or at the
autopsy. In other cases active symptoms, present for a time, may
remit and ultimately cease, and in a few cases the tumor disappears.
In other cases the tumor gives rise to persistent paralysis, and tumors
of the Cauda equina cause anaesthesia of the lower extremities of
variable distribution, paraplegia, and various trophic disorders. In
other cases the symptoms are such as to give rise to the greatest suffer-
ing, and to cause sleeplessness, cachexia, and even death from ex-
haustion.
Treatment. — The treatment must be directed to remove the cause,
and surgical interference is frequently necessary in cases of injury.
At other times the treatment must be directed against articular
rheumatism, inflammation of tendons, syphilis, and other morbid con-
ditions.
In simple connestion the steady application of ice along the track of
the nerve, elevation of the part, and absolute rest suffice to arrest the
disease.
In aciiti' neuritis energetic antiphlogistic treatment nnist be a<lopted.
consisting of local dei)l('tion, application of ice, purgatives, favorable
position of the parts, and absolute rest. Large doses of quinine may
prove useful, and large doses of morphia or atropia are necessary to
allay pain.
In suharute and clironic neuritis cold may be applied in the first
stages, but depressing treatment must soon be changed for counter-
irritation by means of the faradic brush, painting with iodine, or blis-
tering. In very chronic and obstinate cases recourse may be had to
energetic counter-irritants, such as the moxa and the actual cautery.
Hot baths, such as those of Wilbad, Gastein, Teplitz, and Wiesbaden,
as well as mud and strong saline baths, have been found useful in the
treatment of chronic neuritis. The galvanic current is a most effectual
remedy, and the best method of applying it appears to be the steady
application of the anode for a few minutes each day, over the affected
spot. In severe cases the part must be kept at absolute rest in
an appropriate position, and the patient should be warned against
taking active exercise, or exposing himself to cold and wet. When all
active symptoms have subsided the return of motion to paralyzed mus-
cles may be promoted by massage and the faradic current.
In congenital atrophy no treatment is of any avail, and in idioi)athic
atrophy a simple delay in the progress of the disease is all that can be
expected from treatment. Secondary atrophy may be arrested, and
16
2-i2 GENERAL DISEASES OF THE PERIPHERAL XERVES.
even complete recovery may take place, provided the primary disease
can be removed.
The only successful treatment of neuromata is afforded by the ex-
tirpation or the destruction of the tumor. Extirpation succeeds best
when the growth can be removed whilst the nerve is left intact. When
extirpation is impracticable the tumor may be destroyed by caustics or
electrolysis, but these methods are not very successful. "When the
tumor cannot be removed, palliative treatment to alleviate the suffer-
ings of the patient must be adopted.
CHAPTER II.
DISORDEES OF COMMON SENSATION AND OF SPECIAL
SENSE.
I. ANAESTHESIA AND ANALGESIA IN THE REGION OF DISTEI-
BUTION OF INDIVIDUAL NERVES AND PLEXUSES.
AVhen a purely sensory or mixed nerve is divided a certain degree
of anaesthesia is generally produced in the cutaneous area supplied by
it, but the extent and degree of this anesthesia are very variable, and
by no means correspond with the anatomical distribution of the sensory
filaments of the nerve. Arloing and Tripier found that section of one
of the four nerve branches by which the digit of a dog or cat is sup-
plie<l caused no recognizable diminution of its cutaneous sensibility,
section of two branches caused only slight general diminution of sensi-
bility, section of three branches caused decided diminution of sensibility,
but complete amTesthesia of any part of the digit was only estaldished
when the four branches were divided. They also found that on the
fifth digit of the dog, which is supplied from branches from the ulnar
and radial nerves, partial anaesthesia only is caused by section of one or
other of these nerves, while on the fifth digit of the cat, which is sup-
plied by branches of the ulnar nerve alone, section of the nerve caused
complete anoesthesia. It would seem, therefore, that the skin is not
mapped out into functionally independent territories corresponding to
the anatomical distribution of the filaments of the sensory nerves.
This functional intercommunication between neighboring nerve terri-
tories is explained by the free anastomosis which is known to take
place, first, between branches of different nerves of considerable size,
and second, between those nerves in the terminal networks described
by Jacobowitsch and Beale. Arloing and Tripier have described a
third method by means of which nerve fibres from one nerve district
may be distributed to another territory. After division of one of the
branches of the median nerve of the dog or cat, for instance, they
found that the animal gave manifest evidence of pain when the periph-
eral portion of the divided branch was pinched, and even division of
the whole nerve did not entirely prevent these manifestations of sensi-
bility. The peripheral portion of the divided branch was cut out and
examined microscopically a few days after section, and it was found
I
244 DISORDERS OF MIXED NERVES.
that although by far the greater number of fibres were degenerated,
yet a few of them had remained healthy. A portion of the proximal
end of the divided nerve was also examined microscopically, and a few
degenerated fibres were discovered amongst a large number of healthy
ones. From these observations the authors concluded that the few
fibres which remained healthy in the peripheral portion of the nerve
still retained their connection with their trophic centres, while the few
which were degenerated in the proximal portion were .severed from
their centres. As the trophic centres of these fibres must have been
situated in the spinal ganglia or in the gray matter of the cord, they
must have reached the divided branch from the peripheral side of the
point of section, and have been pursuing a centripetal course, and the
authors justly assume that these fibres conferred recurrent sensibility
upon the peripheral part of the nerve. They also believe that these
fibres, after ascending a short distance in the nerve, are distributed to
the skin, and tlms take an important part in supplying one district
with nerve fibres from neighboring nerve territories. It has also been
suggested by Jacobi that the spinal ganglia form a centre in which an
anastomosis takes place between fil)res from different cutaneous nerve
territories. But whether these explanations be satisfactory or not, it is
at least certain that, after division of a principal nerve trunk, complete
angesthesia is either absent or is limited to a very small portion of skin,
while the area of partial anaesthesia is much less than that of the ana-
tomical distribution of the sensory branches of the nerve. A detailed
description of the distribution of ansesthesia in diseases and injuries of
individual nerves will be given when we come to discuss paralysis of
peripheral nerves, because the presence of anesthesia serves to distin-
guish peripheral paralysis from the atrophic paralysis of spinal origin.
The distribution of angesthesia in disease of individual nerves may also
be gathered in a general way from the distribution of neuralgia of the
same nerves, and it is therefore unnecessary to pursue the subject
further at present.
II. HYrEK^ESTHESIA AND HYPERALGESIA IN THE REGION OF
DISTRIBUTION OF INDIVIDUAL NERVES AND PLEXUSES.
The most characteristic feature of the hyper?esthesia and hyperal-
gesia caused by disease of peripheral nerves is that they are apt, by
radiating to neighboring nerve territories, to extend over a much wider
area than the anatomical distribution of the sensory branches of the
affected nerve. The distribution of hypernesthesia in disease of indi-
vidual nerves may, however, be gathered from the distribution of the
pain in neuralgia without further description.
XKUHALGIA OF IXDIVIDUA]. XEEYES AXD PLEXUSES. 245
III. NEURALGIA IN THE KEGION OF DISTKIBUTION OF
INDIVIDUAL NERVES AND PLEXUSES.
1. NElRALlilA OF THE FlFTH NeRVE (TRKiEMIXAL NeURAL(;IA).
Etiology. — Trigeminal neuralgia occurs with unusual frequency in
epileptic families, and in the female sex. The passage of the nerve
through long bony canals renders it liable to be implicated in various
aflections of the bones and periosteum. Aneurism of the internal
carotid artery, exostoses of the petrous portion of the temporal bone,
and tumors at the base of the skull give rise to intractable neuralgia
by pressure on the Casserian ganglion, or on the nerve itself. The
important special causes of facial neuralgia are peripheral irritations,
such as the presence of carious teeth, retarded appearance and false
development of the wisdom teeth, disease of the nasal and frontal
sinuses, and overexertion of the eyes. It may also be caused by remote
irritation, such as that caused by intestinal worms, genital excitement,
and uterine disease, or may result from injury of other nerves, exces-
sive mental strain, and emotional disturbance. The ophthalmic branch
of the nerve is more liable than any other nerve to malarial neuralgia.
Ani>?mia, arterial degeneration, wounds, cicatrices, and diseases of
neighborini: tissues exercise the same influence in neuralgia of the fifth
as in the neuralgine of other nerve territories.
SymjJtoniH. — Facial neuralgia consists of attacks of pain in the area
of distribution of the fifth nerve (Fig. 77) or of one of its branches,
which are apt to recur on the slightest exposure to the exciting cause,
or even in the absence of such cause. Each attack is made up of
recurring paroxysms of severe pain, separated by intervals of com-
parative but not entire freedom from pain. The actual outburst of
severe pain may be preceded by obscure feelings of discomfort, itching
or formication in the side of the face, flying pains about the teeth, or
by a feeling of general malaise and shivering, but at other times a
severe dart of pain shoots along the course of one of the branches of
the nerve without being preceded by any warning.
Each paroxysm consists of a succession of quick lightning-like darts
of pain, which emanate from one or two foci and radiate toAvards the
[)eriphery. At first one or two of these flashes may be followed by a com-
paratively free interval, but they recur with increasing severity and
(juickness, until they at last blend into an uninterrupted pain of great
intensity, during the continuance of which the patient sufters indescrib-
able agony. After one or two minutes the intensity of the shooting pain
246
DISOKDERS OF MIXED NERVES,
abates, but the patient continues to suffer during the interval from a
dull achinc^ pain, which occasions great discomfort and prevents sleep.
The character of the pain during the paroxysm varies ; it may be
burning, boring, cutting, crushing, or stabbing, although the lightning-
like shocks are most frequently met with. The intensity of the disease
may vary from an attack which consists of a few darts of pam or a
Fig. 77.
Skn^ory Nerves of the Head and Face. (At'ter Fi.oweu.)
First division of the fifth :
SO, Supraorbital.
ST, Supratrochlear.
IT, Infratrochlear.
L, Lachrymal.
N, Nasal.
Second division of the fifth :
10, Infraorbital.
T3I, Temporo-malar.
Third division of the fifth :
B, Buccal.
M, Mental.
AT, Auriculo-teniporal.
Branches of the cervical plexus
GO, Great occipital.
S'O', Small occipital.
GA, Great auricular.
SC, Superficial cervical.
IIIC, Third cervical.
little tinghng of the face, and manifests no tendency to recur, up to
a disease of the most obstinate character, that recurs repeatedly and
with great severity during the whole of life, and in which an attack
may be determined by such a slight exciting cause as a current of cold
air on the cheek, or such actions as chewing, coughing, washing the
face, or slight emotional disturbances.
Painful points are observed during the attacks, and sometimes even
in the periods of intermission, corresponding generally to the localities
Avhere the nerve becomes more superficial, either in issuing from a bony
canal or in penetrating fascias.
NEURALGIA OF INDIVIDUAL NERVES AND PLEXUSES. 247
The ronroinitant symptoms of trigeminal neuralgia are very numer-
ous. During a severe paroxysm the pain often radiates to other nerve
territories, extending to the other branches of the fifth, when one only
is primarily affected, or to the occipital, cervico-brachial, or intercostal
sensory nerves. The skin is generally hypersesthetic in the early
stages of the disease, and often anaesthetic in chronic cases. Disturb-
ances of special sense have occasionally l^een observed in facial neural-
gia, consisting of photophobia, amblyopia, or even amaurosis, and dis-
orders of the senses of hearing, tasting, and smellino-.
Motor disorders are almost always present in aggravated cases, and
consist of clonic and tonic spasms of all the muscles of the affected side
of the face, or of a few only of them, such as those of the eyelid or
the angle of the mouth, while the muscles of mastication and of the
tongue are sometimes attacked.
Vaso-motor disturbances are manifested by pallor and coldness in
the early stage of the attack, but these are quickly followed by intense
redness and elevation of temperature, and then the skin 1)ecomes glossy
and oedematous. The redness extends to the mucous membranes sup-
plied by the affected nerve, the conjunctiva being specially liable to
become red and congested; the carotid, facial, and temporal arteries of
the affected side may be seen to pulsate strongly, and the side of the
face is covered by beads of perspiration.
Seeretory disorders are represented by an increased flow of tears,
by arrest or increase of the secretion of the mucous membrane of the
nose, and occasionally by augmented salivary secretion.
The tropldc disturbances consist of swelling of the face, changes in
the color and texture of the hair, herpes zoster frontalis, erysipelas,
subacute inflammation of the periosteum and of the fibrous membranes
in the neighborhood of the painful points, neuroparalytic ophthalmia,
iritis, and glaucoma. In aggravated and long-continued cases the inces-
sant pain and its attendant sleeplessness undermine the constitution,
the general nutrition becomes impaired, and at last the patient suffers
from marasmus and nervous exhaustion.
The psychical disorders present are mental irritability and despon-
dency, and hysterical seizures, whilst occasionally patients have com-
mitted suicide to escape from their sufferings.
Varieties of Trifjeminal Neuralgia,
a. Ophthalmic or Supraorbital Neuralgia.
In this form several branches of the first division of the fifth nerve
(Fig. 78) are all aftected, or the pain is limited to some particular
branch.
248
DISORDERS OF MIXED NERVES.
The painful points are :
(1) The supraorbital point, at or near the supraorbital foramen :
(2) the palpebral, in tlie upper eyelid ; (3) the nasal, at the point of
Fig. 78.
DiAfiRAM OF THE FiRST AND SfxOND (SUPERIOR MaXILLARY) DIVISIONS OF THE KlFTH XeRVE, ITS
Connections and Chief Branches. (From Hermann's " Phj'siology.")
V, Placed over Casserian ganglion.
a, First or ophthalmic division, with d its frontal, e its lachnjmnl, and/ its miml branches
6, Second or superior maxillary division, branches of wlilch are marked as follows :
1, Its terminal branches, nasal, labial, and palpebruL
2, Itecurrent branch to the ckira mater, and middle metdiujeid artery.
3, Oibital branch.
4 is placed between the two spheuo-palatiue branches (which descend to Meckel's ganglion)
.5, Dental branches.
MG, Meckel's ganglion.
6, The Vidian nerve (constituting the motor and sympathetic root of Jleckel's ganglion).
7, The ijreat svperficinl pttruml nerve, from the geniculate ganglion of the facial nerve, joining
the Vidian.
8, The sympatlu'lic branch from the plexus on the carotid artery, joining the ijreat sKperficial
petrosal, and forming with it the Vidian nerve
9, Ascending branches of Meckel's ganglion.
10, Descending palatine branches.
11, Naso-palatine branch.
12, Upper nasal branches.
13, Pharyngeal liranch
F, Facial nerve. CA, Carotid artery. IF, Infraorbital foramen.
emergence of the long nasal branch at the junction of the nasal bone
with the cartilage ; (4) the ocular, a some-what indefinite focus 'vvithin
NEURALGIA OF INDIVIDUAL NERVES AND PLEXUSES. 249
the globe of the eye when the ciliary nerves are aftected ; (5) the
trochlear, at the inner angle of the orbit. The characteristic features
of ophthalmic neuralgia are pain in the forehead, extending down-^-ards
to the upper eyelid and root of the nose, hyperemia of the conjunctiva,
lachrymation, and a painful spot at the supraorbital foramen. Malarial
neuralgia almost ahvays assumes this form ; the attacks recur with
great regularity, and are very intense.
b. SUPRAMAXILLARY NEURALGIA.
"When all the branches of the second division of the fifth nerve
(Fig. 78) are affected the pain is situated in the cheek, eyelid, lateral
portion of the nose and upper lip (infraorbital nerve), in the zygomatic
arch and anterior temporal region (orbital nerve), in the upper row of
teeth (dental branches), and in the nasal cavities and gums (naso-pala-
tine and posterior palatine nerves).
Infraorbital neuralgia is the most common variety of the second
division of the nerve, and the characteristic pain is localized in the
cheek, upper lip, upper row of teeth, and the neighborhood of the
zygomatic arch. An ol)stinate form of neuralgia has been described
by Gross which appears to have its seat in the remnants of the alveolar
processes or the overlying gum in elderly persons who have lost their
teeth.
The painful points of supramaxillary neuralgia are : (1) The infra-
orbital, corresponding to the emergence of the nerve from its bony
canal; (2) the maJar, on the most prominent part of the malar bone;
(3) an indeterminate focus somewhere in the line of the gum of the
upper jaw ; (4) the superior labial, also indeterminate ; (5) the palatine,
rare, but occasionally the seat of intolerable pain.
c. Inframaxillary Neuralgia.
When all the branches of the third division of the fifth nerve are
affected the pain is localized in the region of the lower jaw and lower
roAv of teeth (inferior dental nerve), in the chin (mental branch), in the
tongue and mucous membrane of the mouth (lingual nerve), in the cheek
(buccal nerve), and in the temporal region, anterior part of the auricle
of the ear, and external auditory meatus (auriculo-temporal nerve).
The painful points are: (1) The temporal, a little in front of the
ear; (2) the inferior dental, opposite the point of emergence of that
nerve; (3) the lingual, on the side of the tongue; (4) the inferior
labial. The parietal point, a little above the parietal eminence,
250
DISOEDEES OF MIXED XEEVES.
corresponds to the inosculation of various branches of the nerve, and
may occur in all forms of trigeminal neuralgia.
Fig. 79.
DlAGK.VM OF THE THIRD (INFERIOR JIaXILLARV) DiVI.SION OF THE FiFTH NeRVE, ITS CONNECTIONS .*ND
Chief Branches. fFiom Hermann's " Pliysiologj-.")
V, Fifth nerve. (;, Its largest S(?nsory root, with Ciisserian ganglion.
a, Its smaller motor root joining e, the thiril division of the Casserian ganglion, to fi>nii the inferior
maxillary nerve.
A, Anterior division of inferior maxillary nerve (mainly motor) supplying branches to the muscles
of mastication, and a terminal hnccnl liranch to the mucous membrane of the mouth.
B, Posterior division (mainly sensory) ; its branches are marked —
1, Lingual nerve ; 1', Branches to the tongue.
2, Inferior dental nerve ; 2' Its twigs to the teeth ; 2", Incisor branch ; 2'", Mental branch.
3, IVIylohyoid branch to digastric and mylohyoid.
4, Auriculo-temporal nerve.
F, Facial nerve, ct, Its chorda ti/mp^ini branch, joining the lingual and running to the submaxillary gan-
glion SG, of which it forms the motor root.
OG, Otic ganglion :
ssp, Ismail superficial petrosal nerve, connecting otU: ginglion and facial nerve.
M, Middle meningeal artery, from the plexus upon which sympathetic filaments pa.ss to the oUc ganglion
esp, External superficial petrosal nev\e, connecting the plexus on the middle meningeal artery with
the facial nerve ;
gsp. Great superficial petrosal nerve, connecting the facial with Meckel's ganglion.
FA, Facial artery, from the plexus upon which sympathetic filaments pass to the submaxillary
ganglion.
FO, Foramen ovale. MF, ilental foramen
SG, Submaxillary ganglion
XEURALGIA OF IXDIVIDUAL XEEVES AXD PLEXUSES. 251
d. Epileptiform Neuralgia.
In this form of facial neuralgia lightning-like pains of the most
violent nature succeed each other with the gi-eatest rapidity for a few-
seconds or minutes, and then suddenly vanish. These short attacks
Fig. 80.
Fig. 81.
Figs. 80 and 81.— Cutaneous Xerves of the Trunk, Upper E.xtremitv. (After Flower.)
Sa, Supraclavicular nerve.
IID, Second dorsal.
PS, Posterior branches of the spinal nerves.
LI, Lateral branches of the intercostal nerves
AI, Anterior branches of the intercostal nerves.
II, Iliac branch of ilio-ingiiinal nerve.
I'H', Ilio-hypogastric nerve.
C, Circumflex nerve.
IH, Intercostal humeral
AV. Xerve of Wrisberg
I'CB, Internal cutaneous branch of musculo-spiral nerve.
ECB, External cutaneous branch of musculo-spiral nerve.
ICB, Internal cutaneous nerve.
MC, Musculo-cutaueous nerve.
K, Kadial nerve.
U, Ulnar nerve
M, Median nerve.
252 DISORDEES OF MIXED NERVES.
may, however, recur and follow each other in quick succession for a
period of hours, days, or even weeks, when a respite follows, and the
paroxysm disappears for days, weeks, or even years, although relapses
are sure to recur after a longer or shorter time. This form of neural-
gia is of centric origin, and occurs in families with a strongly marked
neuropathic tendency, while it is often accompanied by epilepsy.
2. Cervico-occipital Neuralgia.
Etiology. — Cervico-occipital neuralgia is usually excited by exposure
to cold, and occasionally results from disease of the upper cervical
vertebne.
Symptoms. — The area of distribution of the great occipital nerve
(Fig. 77, GO) is the region usually affected, but the pain may radiate
widely into the area of distribution of the other branches of the cervical
plexus, and even over the brows, temples, cheeks, or lower part of the
ftice, so that the affection may be mistaken for trigeminal neuralgia.
The most usual concomitant symptoms are hyperf^sthesia or an;v?stliesia
of the occipital region, spasm of the cervical muscles, and considerable
irritation and swelling of the cervical glands.
The painful points are : (1) the occipital point, about midway be-
tween the mastoid process and the spinous processes of the upper cer-
vical vertebra; (2) the parietal point, over the parietal eminence.
The track of the nerve over the occiput is often painful, and the
spinous processes of the upper cervical vertebra are generally tender
on pressure.
o. Phrenic Neuralgia.
It is believed by Peter that the phrenic is a mixed instead of being a
purely motor nerve. The symptoms of phrenic neuralgia, as described
by this author, are severe pains at the point where the nerve descends
over the scalenus anticus muscle in its course through the chest, at
the anterior and lower part of the thorax, and along the line of attach-
ment of the diaphragm. Pain in the shoulder is a constant and charac-
teristic symptom. Phrenic neuralgia is usually a symptom of epilepsy,
hysteria, and angina pectoris, and is met with occas'^ionally as a sei)arate
affection.
The painful points are: (1) The spinous processes of the upper
cervical vertebrae; (2) the phrenic nerve in its course along the sub-
clavicular fossa ; (3) the line of attachment of the diaphragm, especially
anteriorly between the seventh and tenth ribs ; (4) a point over the
cartilage of the third rib.
NEURALGIA OF INDIVIDUAL NERVES AND PLEXUSES. 253
4. Cekvico-brachial Xeiraloia.
Etiology. — The most important exciting causes are the various in-
juries to which the upper extremities are so peculiarly exposed. It
may also be caused by lead-poisoning and malaria, and may be a
symptom of central diseases, as tabes hemiplegia and proc^ressive mus-
cular atrophy.
Si/rnptoms. — Cervico-brachial neuralgia occurs in the area of distri-
l)Ution of the sensory branches of the brachial plexus (Figs. 80 and 81)
and the posterior branches of the four lower cervical nerves. The pain
is more or less continuous, and is of a dull, boring, or burnino- char-
acter, interrupted by paroxysms of lancinating pains, which shoot
through the arm along the course of the nerves. It often occurs in
nocturnal paroxysms which last through the night and may disap])ear
during the day. The pain may have its seat in the upper arm or fore-
arm, or may extend into the hand and fingers, but it is generallv
widely distrifented, and the intimate interweaving of the various nerve
trunks in the plexus renders it difficult to determine what nerve roots
or l)ranches of the plexus are implicated. When the pain is situated
near the periphery it may be limited to one branch of a nerve. The
violent burning pain described by S. Weir Mitchell under the name of
'"causalgia" is often present in the neuralgiie which result from gun-
shot injuries of the nerves.
The pcmiful points, which are somewhat indefinite, are: (1) an
axillafy pointy corresponding to the brachial plexus; (2) ^ scap)ular
^^o/n^, corresponding to the lower angle of the scapula; (3) a shoulder
point, corresponding to the emergence through the deltoid of the
cutaneous branches of the circumflex; (4) a mrdian cephalir jjoint, at
the bend of the elbow ; (5) an external humeral point about three
inches above the elbow; (6) a superior ulnar point, over the ulnar
nerve in its course between the olecranon and the epitrochlear ; and
(7) a radial point, where the nerve becomes superficial at the lower and
external aspect of the forearm. Painful points may occasionally be
developed by the side of the lower cervical vertebrtie, corresponding to
the posterior branches of the lower cervical nerves.
The concomitant symptoms consist of cutaneous hypersesthesia, numb-
ness, and formication, or a considerable degree of ana?sthesia. Radiat-
ing pains are felt in the region of distribution of the cervical plexus,
and of the upper dorsal and intercostal nerves.
The motor disorders consist of twitchings of the muscles of the
upper extremities, and in aggravated cases they may be maintained m
2o4 DISOEDEES OF MIXED NEEVES.
:i State of persistent spasm. In chronic cases some of the muscles may
he enfeebled or completely paralyzed, but neuritis is then probaldy
present.
The vaso-motor disorders are coldness and pallor, or redness and
heat of the affected extremity.
The trophic disorders consist of eruptions of herpes, Ijut the aggra-
vated cases which are caused by gunshot and other injuries of the
nerves are complicated by pemphigus, obstinate ulcers, glossy skin,
and changes in the groAvth of the nails and hair.
5. DORSO-INTERCOSTAL NeURAL(;IA.
Etiology. — Women are especially liable to this form of neuralgia.
It comes on usually between the ages of twenty and forty years, in
nervous, hysterical, and anemic subjects, and its usual exciting causes
are oversuckling, menorrhagia, and leucorrhoea.
The exciting causes of dorso-intercostal neuralgia are exposure to
cold, injuries of various kinds, neuritis, neuromata, disease of the ver-
tebnie or ribs, aortic aneurisms, pulmonary phthisis, dilatation of the
venous plexus in the interior of the vertebral canal, and diseases of
the spinal cord, such as transverse myelitis, spinal meningitis, spinal
and meningeal tumors, and locomotor ataxia.
Symptoms. — The pain of intercostal neuralgia is seated in the area
of distribution of the sensory branches of the twelve pairs of dorsal
nerves; it is of a dull, and tensive character, and is usually continuous,
but it is occasionally interrupted by tearing, lancinating, or burning
pains. The pain is aggravated by all violent respiratory movements,
and by slight pressure on the skin, but it is often relieved by firm and
steady pressure. The pain not infrequently radiates tOAvards the back
and arm, or into the loins or lower extremities, and this form of
neuralgia may be associated with brachial and lumbo-abdominal neural-
gia, or with angina pectoris. The seat of true intercostal neuralgia is
the skin of the anterior and lateral wall of the thorax and abdomen as
far down as the symphysis pubis, and when the first two nerves are
attacked the pain extends to the axilla and inner surface of the arm.
When the posterior branches are affected the pain is seated in the back
an<l loins as fiir down as the crista ilii. Dorso-intercostal neuralgia is
generally unilateral except when it is a symptom of spinal disease, and
the area of distribution of one or two branches on the left side from
the fifth to the ninth nerve is the part most usually affected.
The concomitant symptoms consist of hypersesthesia of the affected
skin, while a circumscribed patch of antesthesia has occasionally been
XEURALCxIA OF INDIVIDUAL NERVES AND PLEXUSES. 255
Ulg
met Avith. Spasm of the intercostal muscles, givinf rise to catclii
breathing like that of pleurisy, is often present. Of the vaso-motor
and trophic disorders, herpes zoster is the most common ; it may be
present without neuralgia in young persons, but the neuralgia precedes
and outlasts the eruption in old persons.
The painful points are: (1) a vertebral point, close to the vertebral
column over the point of emergence of the nerve from the intercostal
foramen ; (2) a lateral point, over the spot in which the lateral per-
forating branch becomes subcutaneous ; and (3) an ajiterior or sternal
point, over the spot where the anterior perforating branch pierces the
muscle close to the sternum, and in the abdomen over the rectus muscle.
The whole length of tlie intercostal nerves is often sensitive, and
several of the spinous processes of the corresponding vertebra tender to
pressure.
Mastodynia.
Etiology. — Neuralgia of the female breast forms a special variety of
intercostal neuralgia. It may appear at puberty in persons having a
strong neurotic tendency, while aniiemia, chlorosis, and hysteria act
as predisposing causes. It is also liable to come on during pregnancy,
although a large proportion of the pains felt in the gland during this
period are caused by mechanical distention. The exciting causes of
mastodynia are irritation of cracked nipples, shrinking of the nipples
during lactation, injuries of the gland, and neuromata and painful
tubercles of the nerves.
Symptoms. — The pain of "irritable breast" is very violent; it is
described as tearing, cutting, boring, and lancinating, and appears in
paroxysms which are usually of short duration, but may last several
hours. The breast feels heavy, and the patient cannot lie on the
affected side, while the slightest contact, even the pressure of the
clothes, is unbearable. There is generally a great deal of hyperfesthesia,
and the paroxysms are sometimes accompanied by vomiting. The pain
radiates into adjoining regions, and the severity of the paroxysm is
increased during the catamenial ])eriod.
Painful points may be found on the nipple or on the sides of the
breast, but they are indefinite. The spinous processes of the second
to the sixth dorsal vertebra are generally tender to pressure.
6. Lumbar Neuralgia.
Etiology. — The special exciting causes of lumbar neuralgia are com-
pression of the nerves by hernia, accumulation of feces, cancer in the
pelvis or in the vertebral column, diseases of the uterus and vagina.
256 DISOEDERS OF MIXED NERVES.
coitus, ])Soas abscess, chronic spinal diseases, and diseases of tlie ver-
tebral column.
Symptoms. — Lumbar neuralgia includes all forms having their seat
in the area of distribution of the sensory branches of the first four
pairs of lumbar nerves. The pain is usually limited to one or two of
the branches of the plexus. Lumbar neuralgia may be divided into
(1) lunibo-abdominal and (2) femoral neuralgia, while it will be conve-
nient to describe in this place (3) neuralgia of the external generative
organs, even although these organs and the neighboring parts are sup-
phed by branches from the sacral as well as from the lumbar nerves.
a. Luinho-nhdominal Neuraliiia.
The \n\m in this variety is seated in the loins, hypogastrium, mons
venei-is, and scrotum or labia majora, and extends over the crista ilii as
far as the buttock, while the inguinal region may bo occasionally
affected. The usual concomitant symptoms are spasm of the cremaster,
vomiting, herpes, and increased sexual desire with priapism and ejacu-
lation of seminal fluid.
The painful points are: (1) Vertebral points, corresponding to the
posterior branches of the respective nerves ; (2) an iliac point, at the
middle of the crista ilii ; (3) an ahdo in inal point, at the side of the linea
alba above the symphysis pubis; (4) an inguinal point, in the groin
near the exit of the spermatic cord ; (5) a scrotal or labial point, in
the scrotum or labium majus. The pain frequently radiates into
neio-hborino; nerve territories.
b. Femoral Neuralgia.
(j) Neuralgia of the lateral cutaneouff nerve of the tliigh is situated
in the outer and part of the posterior aspect of the thigh as far as the
knee.
The painful points are: (1) Spot over anterior superior spinous
process, which is constant; (2) spots along the outer aspect of the
thigh, which are less constant.
(jj) Crural neuralgia is situated in the middle and inner part of the
anterior surface of the thigh, the anterior surface of the knee, and
the inner surface of the leg, and of the foot as far as the great toe.
Tlie concomitant symptoms are hyperiesthesia or anesthesia of the skin,
especially in the vicinity of the knee-joint, a feeling of numbness or
formication in the region of distribution of the saphenous nerve, and a
feeling of weariness on exertion, or paresis of the muscles of the thigh.
NEURALGIA OF INDIVIDUAL NERVES AND PLEXUSES. 257
The painful points are: (1) One in the fold of the groin, where the
nerve emerges from the pelvis ; (2) one at the inner side of the patella,
Avhere the saphenous nerve becomes subcutaneous; (3) one in front of
the ankle-joint; and (4) one at the base of the great toe.
(jjj) Obturator neuralgia is situated in the inner side of the thio-h,
and extends as far as the knee-joint. It is associated with obturator
hernia, and the concomitant symptoms are formication on the inner
surface of the thigh, and a feeling of stiffness and immobility of the
adductors of the thigh.
c. Neuralgia of the External Organs of Greneration.
(j) Neuralgia of the Penis or Clitoris. — The pain has its seat in the
glans and extends to the root of the penis. The pain is violent, lan-
cinating, and burning, and may be unilateral or bilateral ; it is in-
creased by sexual intercourse and urination, and it may be accompanied
by priapism and frequent ejaculations. The clitoris is sometimes the
seat of ])ainful erections in the early stage of tabes dorsalis.
(jj) Neuralgia scrotalis vel labialis is a common symptom of lumbo-
abdominal neuralgia. The scrotum or lal)ium majus is often tender to
touch.
7. NEUIlAL(iIA OF THE SaCRAL AND COCCYGEAL NeRYES.
Neuralgia affecting the sensory branches of the sacral and coccygeal
nerves may be divided into (a) sciatica, (b) plantar neuralgia, and (c)
coccygodynia.
a. Neuralgia Ischiadica {Sciatica).
Etiology. — Heredity does not appear to exercise much influence in
the production of sciatica. The largest number of cases occur between
forty and fifty years of age or during the period of commencing bodily
degeneration, and after the age of thirty years males are much more
frequently attacked than females. The exciting causes are exposure
to cold, gunshot wounds, and injuries of the nerve by blows, fixlls on
the buttock, or by compression of the nerve in difficult labors, especially
wdien the forceps is used. Other causes are mechanical pressure on the
nerve from sitting on hard seats, enlargements and displacements of
the uterus, pregnancy, accumulation of feces in the sigmoid flexure,
and pelvic tumors. Portal congestion, habitual constipation, and all
conditions which g-ive rise to congestion of the hemorrhoidal and other
pelvic veins may cause sciatica, while it may also result from the poisons
of rheumatism, gout, and syphilis.
17
258 DISORDERS OF MIXED NERVES.
Symptoms. — The pain is seated in the area of distribution of the sen-
sory branches of the small and great sciatic nerves (Fig. 82). An
attack of sciatica is generally preceded by premonitory symptoms, such
as a sensation of fluid trickling over the skin, or a feeling of cold or
heat, formication, and a sense of stiifness and dragging. The symptoms
of true neuralgia now make their appearance, and consist of lightning-
like pains which increase in intensity and recur with greater and
o-reater frequency, until a violent paroxysm of almost continuous pain
is established. After a time the violence of the pain abates and the
patient has an interval in which he is comparatively but not completely
free from pain, but after a longer or shorter period he is seized with
another violent paroxysm. The pain is usually superficial, but at times
it may be felt in and between the muscles, or even in the bones ; it
proceeds from one or more fixed points, and generally shoots along the
branches of the nerve to the periphery, while a nocturnal exacerbation
is frequently experienced. It is aggravated by all movements of the
limb, and such actions as coughing, sneezing, straining at stool, or
even simple contact of the bedclothes may bring on a paroxysm, and
consequently the limb is maintained in a fixed position with all the
joints slightly flexed.
The pain is most commonly felt in the posterior surface of the thigh,
commencing in the neighborhood of the sciatic foramen, and extending
to the popliteal space and calf of the leg. The next part most fre-
quently aftected is the peroneal region, including the anterior and
external surface of the leg and the dorsum of the foot. Sometimes
the whole area of distribution of the sciatic nerves is affected, and the
violence of the pain may shift from one region to another. Violent
pains are also felt in the sacrum and loins from implication of the pos-
terior branches of the sacral nerves, while the pain may also shoot into
the lumbar nerves and their branches, into the sciatic nerve of the
opposite side, or into more remote nerve territories.
The concomitant symptoms are hypen\?sthesia, or partial anaesthesia,
and diminution of the electric sensibility of portions of the skin,
cramps of particular groups of muscles, which are especially severe at
night when the patient is falling asleep, and in long-standing cases
considerable diminution of motor power, which renders the gait limp-
ing. Complete paralysis only occurs when there is neuritis. The
most usual vaso-motor and trophic disorders are pallor and coldness,
or redness and heat of the surface, increased secretion of sweat, wast-
ing or occasionally hypertrophy of some of the muscles.
The painful points are : (1) a series of points reaching from the
lower end of the sacrum up to the crista ilii, representing the posterior
NEUEALGIA O P^ INDIVIDUAL NERVES AND PLEXUSES. 259
Fig. 82.
CUTANEC<JS XERVES OF THE LoWER EXTREMITY. (After FlOWER.
Lumbar Plexus.
IH, Ilio-hypogastric nerve.
II, Ilio-inguinal.
IIL, Second lumbar nerve.
GC, Genito-crural.
EC, External cutaneous.
MC, Middle cutaneous.
IC, Internal cutaneous^
IS, Internal saphenous.
PP, Plexus patellw. ^
Sacral Plexus. ^^
DP, Dorsalis penis of pudiifr.
IP, Inferior hemorrhoidal of pudic.
P, Superficial perineal of pudic and inferior pudendal of small sciatic.
IG, Inferior gluteal of small sciatic.
SS, Small sciatic. '
EP, Branches from external popliteal. *
ES, External saphenous.
5It'S, Musculo-cutaneous.
AT, Branches of anterior tit^al.
PT, Branch of posterior tibial.
/^
260 DISORDERS OF MIXED NERVES.
branches ; (2) a point opposite the emergence of the great and small sciatic
nerves from the pelvis ; (3) a point opposite the spots where the ascend-
ino- branches of the small sciatic become subcutaneous ; (4) several points
at'the posterior aspect of the thigh corresponding to the emergence of the
cutaneous nerves; (5) -a fibular point at the head of the fibula; (6) an ex-
ternal maUeolar point behind the ankle ; (7) an internal malleolar point.
The sacral plexus is frequently tender on pressure when examined
through the anus or vagina.
h. Neuralgia Flantaris {Erythemomegalalgia).
The first accurate account of this aft'ection was given by Dr. S.
Weir Mitchell, under the title of '' A rare vaso-motor neurosis of
the extremities," or "Erythemomegalalgia," but inasmuch as the vaso-
motor disorders are preceded and accompanied by severe paroxysms of
pain, I see no reason why the affection should not be regarded as
plantar neuralgia, or as a neuritis of the plantar nerves.
Etiology. — This disease occurs nearly always in the male sex, and
comes on after some constitutional disease as a low fever, after pro-
lono-ed exertion, or as a sequel of an attack of gonorrheal rheu-
matism. It is, indeed, probable that the cases of obstinate pain in
the sole of the foot, described by Dr. EUiotson as folloAving gonorrhoeal
rheumatism, belong to this category.
Symptoms. — The pain usually begins in the ball of the great toe, or
in the heel, and often extends over a great part of the sole, and may
reach the dorsum of the foot, and the leg. It is felt at first towards
night, and is relieved by the night's rest, while it is increased by walk-
ing, the erect posture, or even by allowing the foot to hang down.
The pain in the early stage of the disease consists of a deep-seated
aching, but after a time it becomes of a burning character, and is then
aggravated by warmth and relieved by cold and the recumbent posture.
The most characteristic symptom of the affection, however, is a flushing
of the painful area, which comes on with exertion or when the feet are
allowed to hang down, and is accompanied by swollen veins and violent
throbbing of the arteries. The shaded part in the annexed diagram
shows distribution of the reddened surface in one of Dr. Mitchell's
cases. In the worst cases the extremity is pale and cold when the
patient is at rest. In aggravated cases the pain is so severe as to
render walking all but impossible, and when persisted in intense redness
and swelling are occasioned, the patient sleeps with his feet uncovered,
and may even be reduced to crawl on his hands and knees, or is obliged
to be carried about in order to avoid placing his feet on the ground.
XEL'RALGIA OF INDIVIDUAL NERVES AND PLEXUSES. 261
The feet are generally bathed in sour-smelling sweat, and the skin of
the sole mav have a sodden appearance, becoming somewhat glazed
during the paroxysm of pain and redness. The disease is sometimes
progressive, and in its later stages may be associated with evidences of
spinal disease, such as girdle pains and partial paralysis with atrophy
of some of the muscles of the leg, while the fliradic contractility has
been found diminished in the muscles of the limb most affected. The
Fig. 83.
disease is generally bilateral, and in one case observed by Dr. Mitchell
the hands were attacked as well as the feet. In each of several cases
which came under my observation a tender spot was present in the
centre of the heel, the whole course of the external plantar nerve was
tender to pressure, and painful points were found between the heads of
the metatarsal bones, over the bifurcation of the brandies of the plantar
nerves for the digits.
c. Neuralgia of the Coccygeal Nerves [Qoccygodynia).
Etiology. — This affection occurs generally in women in consequence
of injury to the coccyx fi'om a fall, or during labor. It may also be
caused by exposure to cold, or may originate spontaneously.
Symptoms. — The chief symptom of coccygodynia consists of pain
in the region of the coccyx when the patient sits or walks, and it is
often felt during micturition and defecation, especially if there be much
straining. Pressure on the coccyx, by the finger, aggravates tliis pain.
262 DISORDEES OF MIXED NERVES.
Diagnosis.— Scintkai may be mistaken for myalgia of the thigh or
leo-, but the pain in myalgia has a diffused localization, so that the
patient indicates its seat with his Avhole hand, whilst in neuralgia he
points to it Avith his finger. Sciatica may also be mistaken for chronic
hip-joint disease or hysterical coxalgia, but an error will be avoided by
a careful observation of the movements of the joint, of the presence or
absence of pain Avhen the head of the femur is pressed against the ace-
tabulum, or of painful points, and the concomitant symptoms of neuralgia.
A valuable diagnostic sign of sciatica is afforded by passively flexing
the affected extremity at the hip-joint, whilst the leg is extended on the
thigh which is affected, when the patient is lying on his back, by grasp-
ino- the heel and raisino; it from the bed. This movement causes the
nerve to be stretched over the trochanter, and to be likewise pressed
upon by the tense muscles, and the consequent irritation of the nerve
induces a reflex spasm of all the muscles, Avhich renders the limb as
rigid as a bar of iron, and arrests the movement when the heel is
raised about a foot from the bed. If the patient is standing, essentially
the same test may be applied by asking him to bend down and touch
the toe of the affected limb with the tips of the fingers of the corre-
sponding hand, while keeping the legs extended at the knees. The
nerve is thus put upon the stretch and the movement is arrested long
before the fingers reach the toe.
Plantar neuralgia is most liable to be mistaken for an affection
described by Gross, which is peculiar to tailors, and named ])odyni(i.
It appears to depend upon subacute inflammation of the periosteum,
and consists of a burning pain in some part of the sole, but there is
no redness. A painful spot on the heel may be observed after syphilis,
but careful examination will reveal a node on the os calcis.
8. Visceral Neuralgia.
The various plexuses of the lymphatic system are liable to be
afi"ected by severe attacks of neuralgia.
a. Neuralgia of the Pharyngeal and (Esophageal Plexuses.
Neuralgia of the pharynx and soft palate occurs in young girls, and
occasionally in married women between thirty and forty years of age.
Patients complain of pain in the soft palate, which is generally limited
to one side.
XEURALGIA OF INDIVIDUAL XERVES AND PLEXUSES. 263
b. Neuralgia Mesenteriea {Colic, Unteralgia, Colica Saturnina).
Etiology. — The causes of colic are local irritation of the mucous
membrane, such as is produced by the presence of worms or undigested
food in the intestines, by increased irritability of the nerves, occa-
sioned by disease of the intestines, by indirect irritation from disease of
the uterus, ovaries, or remote organs ; spinal diseases, like tabes dor-
salis, central affections like hysteria, and poisons circulating in the
blood, like the poison of gout and rheumatism, or mineral poisons,
the chief of them being lead, which produces the most obstinate and
severest form of colic.
Symptoms. — In colic the patient is suddenly attacked with severe
twisting or griping pains in the abdomen, which begin and are most
severe about the umbilical region, but may spread over the entire abdo-
men, and are liable to change their position. The pains occur in
paroxysms, which are followed by periods of remission or complete in-
termission. The bowels are usually constipated, and distended with
flatus, so that a very tympanitic note is afforded on percussion, and
when the hand is placed upon the abdomen the bowels can be felt roll-
ing about with flatus, Avhile the abdominal muscles are felt contracted,
hard, and knotty. Colic may occasionally be associated with diarrhoea.
In lead colic the abdomen is retracted, and there are obstinate constipa-
tion, nausea, vomiting, eructations, and hiccough, while the blue line
on the gums will indicate the presence of the poison in the system. In
colic uniform pressure of the abdomen almost always affords relief, and
the patient usually bends forwards, or lies with the face downwards, and
presses it with both hands. During the attack the face and extremities
are pale and cold, and the action of the heart becomes slow and feeble,
and if the attack be prolonged, there may be symptoms of more or less
complete collapse, and the patient feels faint and weak, and experiences
a sense of impending death just as is felt in angina pectoris. The
action of the heart is universally weak in lead colic, and the pulse,
although occasionally quickened, is, as a rule, slow.
c. Neuralgia G-astrica vel Coeliaca {Cardialgia, Gfastralgia,
G-astrodynia).
Etiology. — Gastralgia is more common in youth than in old age and
in women than in men. It is often associated with anaemia and chlorosis
and is not an unfrequent manifestation of hysteria. A very severe
form of gastralgia, coming on in spontaneously recurring paroxysms,
264 DISORDEES OF MIXED NERVES.
named gastric crises, is a very frequent and distressing symptom ot
locomotor ataxia.
>,SV///^;>fo;»«.— Gastralgia is characterized by paroxysmal attacks of
pain in the epigastric region which may radiate upwards to the back
between the shoulders, or to the middle of the sternum. The attack
comes on suddenly, without premonitory symptom, and the pain, whicli
is very severe, generally intermits after a few minutes, but soon recurs
with greater intensity, and after repeated intermissions and recurrences
it finally disappears. Pressure over the cartilages of the false ribs on
the left side, or on the corresponding intercostal spaces, may cause pain,
and the spinous processes of some of the dorsal vertebrae may be tender
on pressure. Tlie pain of gastralgia is relieved by firm and uniform
pressure, and tenderness of the epigastrium is generally absent. The
upper portions of the recti muscles are strongly contracted during the
attack and the abdominal walls are rendered tense and unyielding, whilst
the epigastric region is usually retracted. The pulse is generally slow
and feeble; the arterial tension is low; the extremities are cold and
pale ; and towards the end of the attack the patient may suffer from
chilliness and a feeling of oppression and faintness like that of angina
pectoris reflectoria. The attack often terminates by copious vomiting,
the food contained in the stomach is first ejected, and then large quanti-
ties of watery fluid mixed with bile and blood, and in aggravated cases,
mucus; while if the urine be examined during or soon after the attack
it is often found to contain a small (piantity of albumen.
Tabetic gastric crisis is a variety of gastralgia which ])egins during
an attack of the lancinating pains of locomotor ataxia. The jiatient
complains of pain which starts from the groins, and passes up each
side of the abdomen to become fixed in the epigastrium, while at the
same time severe lightning pains dart from between the shoulders and
radiate round the base of the thorax. Severe vomitincr now sets in,
just as occurs in all severe cases of gastralgia. The patient suffers
during the attack from a profound malaise ; the action of the heart is
accelerated, and the lightning pains are unusually severe. The attack
may last without respite for two or three days, and may recur every two
or three weeks although the usual interval betAveen them is not less than
a month.
d. Neuralgia Hepatica {Hepatalgia).
Etiology. — Hepatic colic is usually the result of the passage of biliary
calculi through the cystic and common ducts, but colic of similar char-
acter sometimes occurs in neurotic subjects in the absence of any signs
of biliary obstruction and it is regarded as of purely neuralgic origin.
NEURALGIA OF INDIVIDUAL NERVES AND PLEXUSES. 265
Symptoms. — The symptoms of hepatic colic are more or less severe
pain which comes on suddenly and lasts with irregular intermissions and
exacerbations from a few hours to a few days. The pain is often very
severe, and of an aching, cutting, or tearing character, and is usually
attended with a feeling of constriction or cramp. It is o-enerallv
referred to the pit of the stomach or to the umbilicus, whence it radiates
to the back and between the shoulders, but never downwards. The
patient suffers during a severe attack from faintness, nausea, and vomit-
ing ; the action of the heart is Aveakened, the surface of the body is
cold, and in severe cases there are symptoms of collapse.
(\ Neu7'algia Hypog<(strica.
Hyposastric neuralgia mav be divided into the followino- varieties
according to the branches of the plexus affected,
(1) Neuralgia Ani.
Etiology. — Neuralgia of the rectum generally results from fissures of
the anus, but it may occur in the absence of any recognizable local
cause ; and it is a common symptom of locomotor ataxia.
Symptoms. — The symptoms consist of severe paroxysms of cutting
pains coming on suddenly and si)ontaneously after exposure to cold.
The pains are situated an inch within the anus, and they are much in-
creased by defecation. The pain is associated with hypersesthesia or
an;esthesia of the skin of the perineal region, spasm of the sphincter
ani and bladder, and difficulty of micturition.
(2) Neuralgia Uteri (Hysteralgia).
Etiology. — The causes of uterine neuralgia are prolapse of the uterus,
uterine tumors of all kinds, ulceration of the cervix, profuse and in-
tractable leucorrhoea, ascarides in the rectum, scybala impacted in the
rectum, and calculus in the ureter or kidney. Sometimes the source of
irritation may be in a remote part of the body, and in some cases
paroxysms of uterine neuralgia may occur in the absence of any dis-
coverable disease of the pelvic organs.
Symptom,s. — The patient complains of paroxysmal attacks of intense
pain situated deeply in the pelvis which is aggravated by movement,
by the maintenance of the erect posture, and by pressure on the cervix.
The pain often radiates to the inguinal and lumbar regions of one si<le,
and it is often, although not always, worse at the menstrual period.
2(36 DISORPERS OF MIXED NERVES.
Vaginismus is a condition of excessive sensibility of the vaginal
orifice which renders coitus impossible. It is often associated with
spasm of the constrictor vagina and of the levator ani, and attempts at
coition may induce general hysterical convulsions.
(3) Ovarian Neuralgia axd Hyper.esthesia (Ovarialgia).
Miolof/i/.—OvaYian neuralgia may be caused by any of the sources
of irritation already enumerated as the causes of uterine neuralgia.
The left ovary is the one usually aflFected. It is frequently associated
-with o-rave hysterical symptoms, and it is difficult to determine whether
the ovarian pain is to be regarded as the cause or an effect of the
hysteria.
St/mptoms. — The symptoms of ovarian neuralgia consist of pain,
which is sometimes so acute that the patient cannot tolerate the slightest
touch, and which is localized partly in the hypogastrium and partly in
the iliac fossa. In many cases there is more or less complete anesthesia
of the abdominal walls and pain is only elicited on deep pressure over
the affected ovary, which c-in generally be felt by the hand in the other
variety of ovarian neuralgia. Pressure exaggerates this iliac pain, and
causes it to radiate towards the epigastrium and throat. The radia-
tion of the pain towards the epigastrium is often accompanied by nausea
and vomiting, and, if the pressure be continued, palpitations of the
heart, increased frequency of the pulse, and a sensation of " globus
hystericus" supervene. If the pressure be continued, the patient,
according to Charcot, suffers on the affected side, in addition to the
symptoms just described, from l(»ud sibilant sounds in the ear, obscurity
of the sight of the eye, and a sensation as of blows from a hammer on
the temporal region.
(4) Neuralgia Testis.
Etiology. — Neuralgia of the testis may be caused by morbid growths
in the organ, and calculus in the ureter, while it is not uncommon in
neurotic subjects as the result of self-abuse.
Symptoms. — The symptoms of neuralgia of the testis consist of
spontaneously arising paroxysms of severe pain which is situated partly
in one testicle and partly in the epididymis and cord. The organ is
tender to pressure and contact, and the patient complains of a dull
aching pain in the intervals between the paroxysms. During the
paroxysm the testicle is strongly retracted from spasm of the cremaster
muscle, and the patient suffers from fainting and vomiting. The affec-
tion is usually very obstinate, and it is often accompanied by great
DISORDERS OF THE NERVES OF SPECIAL SENSE. 267
mental depression which may end in confirmed hypochondriasis or
melancholia.
(5) Cystalgia.
Etiology. — Neuralgia of the bladder usually results from the presence
of calculus, or malignant disease, but it occasionally results in -women
from long-continued menorrhagia combined Avith anaemia.
Symptoms. — Neuralgia of the bladder consists of severe paroxysms
of pain, which is situated at the neck of the bladder, and is accompanied
by a frequent desire to micturate.
(d) Neuralgia Urethralis.
Etiology. — Neuralgia of the urethra may occur in the absence of any
local source of irritation, and is then generally a symptom of locomotor
ataxia.
Symptoms. — Neuralgia of the urethra consists of paroxysms of severe
pain in the course of the urethra. The pain is accompanied by an
urgent desire to pass water, probably caused by spasm of the detrusor
muscle, but the patient frequently experiences difficulty in voiding the
urine, probably because the sphincter is also spasmodically contracted.
IV. DIKOEDERS OF THE NERVES OF SPECIAL SENSE.
1. Diseases of the Olfactory Nerve.
The sense of smell is excited by the contact of odoriferous particles
with that part of the mucous membrane of the nose to which the olfoc-
tory nerves are distributed. The smell induced by simple diffusion of
odoriferous particles is very imperfect, but the sensation is much in-
tensified by the forcible impact of those particles against the mucous
membrane which is obtained by the process of sniffiyig.
Tests. — In testing the sense of smell care should be taken not to
irritate the fifth nerve, and conse(iuently substances having a pungent
odor should be avoided. The best substances are volatile oils, the fetid
gum resins, and other substances having a penetrating odor like cam-
phor and musk. Our perception of flavors being due to the sense of
smell and not to that of taste, it is necessary to get the patient to par-
take of substances possessing a delicate aroma or bouquet, such as roast
beef, cheese, or wine. Electricity is not of much use in testing the
sense of smell.
208 DISORDERS OF CRANIAL NERVES.
a. Hyperosmia or Olfactory Hyperesthesia.
The acuteness of the sense of smell may, like that of the other
senses, be increased by education, and hysterical patients are often able
to discriminate smells which are quite inappreciable to others.
h. Hyperalgesia of the Sense of Smell.
The sense of smell is fre(iuently perverted in insanity, and other
grave diseases of the nervous system. Hysterical subjects may mani-
fest a decided aversion to perfumes which are agreeable to most people,
or a predilection for odors, like that of asafoetida, which are repugnant
to others. An unaccountable aversion to a particular perfume is some-
times one of the earliest symptoms of locomotor ataxia.
Illusions or hallucinations of smell, which are generally of a repug-
nant kind, are often complained of by the insane. The most usual
odors complained of are those of sulphur and putrid substances, and
these patients are often led to believe that they arc surrounded Ijy dead
and decaying bodies. A bad smell sometimes constitutes the aura of
epileptic and epile|)tiform seizures, and it may likewise be a symptom
of an intracranial tumor.
c. Anosmia or Olfactory Ancesthesia.
Anosmia consists of a diminution or complete loss of the sense of
smell, and when both sides are affected the sense of taste is likewise
impaired. The sense of smell is diminished in disease of the fifth
nerve owing to nutritive changes occurring in the mucous membrane
of the nose, and it is also diminished in fiicial paralysis l)ecause the act
of sniffing becomes impossible, owing to the paralysis of the dilators of
the alas nasi. It is likewise impaired by local disease, such as constric-
tion of the nostrils, nasal polypi, acute and chronic inflammation of the
mucous membrane, strumous and syphilitic oz8ena, and occlusion of
the nasal and pharyngeal cavities. The sense of smell is frequently
blunted in old age, and loss of smell is occasionally observed as an early
and persistent symptom of locomotor ataxia. Loss of smell is some-
times caused by injuries of the head, the affection being thus described as
traumatic anosmia. The most frequent injury to cause anosmia, in the
absence of fracture of the cranium, is a blow or fall on the occiput, and
a blow on the forehead is sometimes followed by loss of smell. Anos-
mia of the left nasal cavity is sometimes associated with right hemi-
plegia and aphasia, the result of embolism of the middle cerebral artery.
'
DISORDEKS OF THE NEEVES OF SPECIAL SENSE. 269
In Other cases left-sided anosmia is associated Avith aphasia in the
absence of any paralysis, and in some of these cases at least the dis-
order of speech Avas a sensory aphasia. In cerebral hemiana-sthesia,
Avhether of hysterical origin or caused by organic disease, smell is lost
on the same side as the other sensory disorders. Loss of smell is also
caused by tumors in the anterior fossa of the skull, or in the anterior
cerebral lobes, and by basal meningitis, exostoses, or caries of the bones.
It is at other times a congenital affection, and then usually results from
absence of the olfactory bulbs.
3Iorhid Anatomy and Physiology. — Diminution or loss of smell may
be caused by disease of the local olfactory organ, the peripheral end-
oi'gans, the olfactory' nerves, the conducting apparatus through the
olfactory bulbs and hemispheres of the brain, or of the cortical centres
themselves. With regard to local disease it Avill suffice to say, that it
is very probable the ramifications of the olfactory nerves themselves
become secondarily affected in chronic inflammation and other diseases
of the mucous membrane. Loss of smell may, however, be caused by
disease of the peripheral end-organs of tlie olfactory nerve in the
absence of disease of the mucous membrane. Smell is sometimes
permanently lost in consequence of the impression of a very powerfid
stench, and Prevost found degeneration of the olfectory nerves and
atrophy of the bulbs in old people in Avhom the sense of smell Avas
diminished. The anosmia Avhich accompanies locomotor ataxia is caused,
most probably, by a neuritis of the olfactory nerves, AN'hile that Avhich
accompanies cerebral tumors is most frequently caused by compression
of the olfactory nerves and bulbs. Traumatic anosmia is generally
caused by bloAvs on the occiput ; the elastic bones of the cranium yield
to some extent to the bloAv; the Avhole of the encephalon above the ten-
torium is thus pushed forAvards ; the anterior margins of the temporo-
sphenoidal lobes impinge against the great Avings of the sphenoid bones :
and the olfactory bulbs are apt to suffer damage at these points of junc-
tion ANitli the brain near the anterior perforated space, or some of the
olfactory nerves may be ruptured in their passage through the cribriform
plate of the ethmoid bone.
2. Diseases of the Acoustic NERyES.
a. Auditory Hypercesthesia or Hyperacusia. — In this condition the
sensibility of the auditory sensory mechanism is increased, so that
sounds too faint to be detected in the normal state are heard distinctly,
A\hile the poA\'er of discriminating differences in sounds is unusually
acute. Hyperacusia is often observed in hysterical patients, in con-
270 DISORDEES OF CRAXIAL NERVES.
(litions of ecstacy, and sometimes even in somnambulism. Auditory
hypergesthesia, however, generally declares itself, not by an increased
power of discriminating tones, but an increase of the pleasant or painful
feelino-s which accompany sound, and this condition may be called audi-
tory hyperalgesia. In disease the painful feelings which accompany
sound predominate, and in cases of acute disease, general debility, hys-
teria, and various mental affections, the slightest sound becomes exceed-
ingly distressing to the patient. Auditory hyperaesthesia is often accom-
panied by subjective sensations, illusions, and hallucinations. Tinnitus
is the most common form of subjective sensation, and it may assume the
form of whistling, humming, and various other noises. This symptom
is generally caused by disease of the external or middle ear, changes in
the circulation of the brain, large doses of quinine or salicin, and
forms a prominent feature of Meniere's disease. Auditory illusions
are frequently observed in mental disease, more especially in melan-
cholia and dementia ; in the former they assume the form of abusive
or threatening words or commands to do acts of violence, and in the
latter they take the form of heavenly messages or revelations. Audi-
tory illusions are sometimes unilateral, and in some cases there are
alternating illusions of different senses, such as right-sided optic and
left-sided auditory illusions. Auditory hallucinations sometimes con-
stitute the aura of an epileptic attack. The galvanic current affords
valuable aid in the diagnosis of the various conditions of the auditory
nerve, but for information on this subject the reader is referred to
special treatises.
h. Auditory anaesthesia consists of abnormal diminution or abolition
of the sense of hearing. The cause of deafness may be either lesion
of the local apparatus of hearing and of the peripheral nerve-endings,
of the conducting apparatus, or of the central terminal organ. Func-
tional deafness is observed in hysteria, and after toxic doses of quinine,
lead, and other agents.
3. Diseases of the Gustatory Nerves.
The gustatory nerves are derived from the glosso-pharyngeal nerve
(Fig. 84) which supplies fibres to the posterior third of the tongue, the
palate, and the walls of the pharynx ; and from the lingual branches
of the fifth nerve, which are distributed to the tip and anterior two-
thirds of the tongue. It has been proved by experiment and by an
analysis of clinical observations that most, if not all, of the gustatory
fibres of the lingual nerve are derived from the chorda tympani ; this
nerve joins the fiicial in the Fallopian canal, but on reaching the genicu-
DISORDERS OF THE NERVES OF SPECIAL SENSE. 271
late ganglion the gustatory fibres leave the facial and return by means
of the petrosal nerves to the trigeminus, with which they enter the
cavity of the skull and brain. Gowers believes that the gustatory fibres
of the glosso-pharyngeal are also derived from the fifth nerve.
Fig. 84.
GP,
1,
To
DiAGRA^M OF Glosso-pharyngeal Xerve, its Connections and Branches.
(From Hermann's "PLj'siologj-.")
Glosso-pharyngeal nerve. JG, Its jugular ganglion. PG, Its petrous ganglion.
Tympanic branch, or nerve of Jacobson, the branches of which are as follows :
2, Filaments to plexus on carotid artery ; 3, To Eustachian tube ; 4, To fenestra rotunda ;
fenestra ovalis.
6, Twig of union with small superficial petrosal n.
7, Twig of union with great su^yerficial petrosal n.
S, Pharyngeal branches of glosso-pharyngeal n.
9, Muscular branches to stylo-pharyngeus and constrictors (?).
10, Tonsillitie branches.
11, Terminal lingual branches.
P, Pneumogastric nerve, from the ganglion of the root of which, branches pass to the petrous ganglion.
S, Superior cervical ganglion with an ascending branch to the petrous ganglion.
MG, Meckel's ganglion. OG, Otic ganglion. F, Facial nerve. CA, Carotid artery.
Tests of the Sense of Taste. — The patient should be directed to put
his tongue out, with the mouth widely open and the eyes closed, and then
272 DISORDEES OF CKAKIAL NERVES.
the sapid substance is applied, with a glass rod or small lirush, to the
part to be tested. The tongue ought not to be withdrawn into the
mouth until time is given for the taste to be perceived.
Bitter tastes are most distinctly perceived at the root of the tongue,
and they may be tested by a solution of quinine or infusion of quassia.
Sweet tastes are best perceived at the tip of the tongue and are tested
by syrup or honey. Acids and salines are most readily perceived at
the sides of the tongue and are tested by vinegar and solution of common
salt. Galvanization of the tongue by means of special electrodes is
also a valuable method for testing the sense of taste.
a. Ilypera^sthesia of the Gustdtory Nerves.
Hypen^sthesia of the sense of taste may manifest itself as an increase
in the delicacy of taste. Hysterical patients, for example, often detect
certain ingredients in food or medicines which are quite inappreciable
to healthy persons. It may again express itself as an increase in the
enjoyment or loathing of food, certain substances causing a more agree-
able or disgusting taste than they do in the case of the healthy palate.
Amongst the parcesthesia must be mentioned the subjective sensations
of taste perceived on the anterior half of the tongue in some cases of
facial paralysis, and when certain drugs have been taken. The subjec-
tive gustatory sensations of insane patients are, doubtless, of centric
origin, and consist partly of hallucinations, and i)artly of illusions of
taste.
b. Ancesthesia of the Gustatory Nerves.
(xustatory anaesthesia may be complete or incomplete in its degree,
circumscribed or diffused in extent, and partial or total as regards the
forms of sapid qualities interfered with.
Gustatory anaesthesia maybe caused by catarrh or other local disease,
or by lesion of the glosso-pharyngeal, lingual, chorda tympani, facial,
or trigeminal nerves. When the glosso-pharyngeal nerve is affected taste
is weakened or lost on the root of the tongue, palate, and pharynx on
the corresponding side, but no uncomplicated case of this kind is yet
recorded. Little is known with regard to disease of the cortical centres
of taste. If the lesion is situated on the lingual or chorda tympani
nerves, or in certain sections of the facial or trigeminal nerves, the
gustatory aneesthesia affects the anterior or lateral half of the tongue
along with its border and apex. When loss of taste in the areas of dis-
tribution of the lingual and glosso-pharyngeal nerves of one side is
associated with hemianeesthesia of the same side of the body, it may be
DISORDERS OF THE NKRVES OF SPECIAL SEXSE. "JTS
inferred that the lesion is central, such a combination of symptoms
being- generally met with in hysteria.
4. Diseases of the Optic Nerves.
<i. Functional Affections of the Sense of Si(//tt.
(1) Optic Hypkr.esthksia ano Hyperalgesia.
Optic hypersesthesia consists of those conditions in which external
objects are distinctly seen in an obscure light, or in which the acuteness
of vision is greater than in ordinary sight. But disease usually drives
rise to painful feelings or to abnormal psychical visual sensations, such
as sparks of light and luminous disks, and these may be comprised
under the name of optic hyperalgesia. Illusions and hallucinations of
sight occur in insanity, epilepsy, and vai-ious other cerebral affections.
(2) Optic An.esthe.sia.
Optic anaesthesia is characterized by diminution of vision or Kinbly-
opia., or ])y abolition of vision or atnaurosix.
Etiologij — The forms of amblyo{)ia and amaurosis which occur in the
absence of any apparent lesion of the fundus of the eye on ophthal-
moscopic examination are those which interest us at present. Amblyopia
or even amaunjsis is sometimes caused Ijy exposure to cold, venereal
excesses, exhaustion, hsematemesis, profuse menorrhagia, or other severe
loss of blood, irritation of the sensory branches of the trigeminus, and
irritation of the abdominal organs by the presence of worms, constipa-
tion, tumors, pregnancy, or uterine disease. An epileptic attack may
be succeeded by a temjiorary enfeeblement of sight, which usually dis-
appears rapidly, but may become more or less pennanent when the
attacks are frequently repeated. Unilateral blindness, lasting only for
a few minutes, may occur in paroxysms in the midst of perfect health,
and it may possibly be regarded as a vaso-motor epilepsy. Amblyopia
may result from toxic agents such as lead, alcohol, tobacco, opium,
belladonna, quinine, and santonin, or it may be a se([uel of acute
diseases, like typhus fever, scarlet fever, and pneumonia.
Symptoms. — The symptoms of functional amblyopia and amaurosis
are the same as those which are observed in organic diseases of the optic
nerves, except that in the former no changes are found in the fundus
on ophthalmoscopic examination.
Vision presents four distinct alterations in amblyopia : {a) Diminution
in the acuteness of vision; (6) Alterations in the field of vision; {>■)
18
274 PISOBDERS OF CRAXIAL XERVES.
Disorders in the perception of light ; and {d) Disorders in the percep-
tion of colors.
(a) Diminution in the Acutenes^ of Vision.— "iXie patient sees objects
through a mist ; he has difficulty in distinguishing minute objects, or
at times may observe a dark spot in the centre of vision.
Tests of the Acuteness of Visio?!.— The acuteness of vision is usually
tested by asking the patient to read print of a certain size of type, and
at definite distances. In Snellen's scale the size of type is numbered
according to the distance in feet at which the print can be read by the
normal eye in a good light. The acuteness of vision is expressed by a
fraction of which the denominator is the number of the test type, and
the numerator the distance in feet at which it can be read. The sight
of each eye must always be tested separately.
(b) Alterations in the Field of Vision. — The field of vision may be
altered in several ways, but the form usually observed in functional
amblyoi)ia begins at the margin of the field and progresses concentri-
cally until only a small central area is left. The first loss of vision
may appear in the centre of the field, constituting a central scotoma,
while at times the whole field of vision is covered with scotomata. The
blindness may sometimes be surrounded by spectral appearances and
then it is named a scintillatinc) scotoma. In their simplest form they
consist of a blind area which is surrounded more or less completely l)y
a luminous border, the latter Avidening as the former expands. This
luminous arc is subject to a rapid oscillatory movement which has been
variously described by different observers. In the more pronounced
forms the luminous border assumes a zigzag outline which has been
compared to the outlines of a fortification. It is also fringed l)y gorgeous
colors which are in continual trembling movement, or appear to ''corus-
cate," or to emit a "shower of sparks." The phenomenon lasts from
a quarter to half an hour and then passes off".
Tests of the Field of Vision. — The most ready test of the field of Aision
is to direct the patient to fix one eye, the other being closed, on the
corresponding eye of the operator, and the latter then moves his hand
to the right, left, above, and below, and at a certain distance from the
fixed point as a centre. If the field of vision be limited in any particu-
lar direction, the observer will have to approach his hand nearer and
nearer to the point on which the patient's eye is fixed before it is seen,
and thus any serious departure from the normal limit can be readily
detected. If greater accuracy be required, the field must be measured
by means of the " mapping system " or by the perimeter, for a descrip-
tion of which the reader is referred to ophthalmological works.
DISORDEKS OF THE XERVES OF SPECIAL SKX3E. 27."
::LiO
(c) Disorders of the Perception of Light. — There are several
varieties of partial anaesthesia in which the ophthalmoscopic appearance
may be negative. Sometimes the patient cannot see at night, a condi-
tion which is called henwralopia ; at other times sight is deficient in
daylight, and this condition is called nyetalopia.
(d) Disorders of the Pereeption of Colors {Dyschromatopsia, Achro-
matopsia). — The perception of colors may be defective when the acutencss
of vision is very little impaired, and, conversely, color vision may be
little aflected when there is considerable limitation of the field of vision.
The area of the field of vision varies for each color, green havino- the
smallest and yellow and blue the largest visible areas (Fig. 85).
Fig. 85.
DiAiiRAU Showing the Fiklds of Color Vision in a Normal Emmetropic Eye on a Dim. Day.
(After GowERS.)
Tlie fields are each ratliei- smaller than on a bright day. The asterisk indicates the fixing- point, the
black dot the position of the blind spot. (U.sually the blue field is larger than the yellow.)
Tests of Color Vision. — A scale of colors is submitted to the patient
and it must be ascertained whether he can identify and name each ; or
the patient is asked to match a given color from a number of others
presented to him.
In amblyopia the order in which the percej)tion of colors is lost is
usually that in which the fields are arranged on the retina, the first
defect beino; for o-reen, then red, while yellow and blue are the last to
be lost. The condition in which central vision for the perception of one
or more colors is much restricted is named dyschromatopsia, while total
color blindness is named achromatopsia.
Color blindness is sometimes a congenital defect, and of tins form
there are three varieties; namely, (1) Red blindness, (2) (irecii blind-
276 DISOKDEKS OF CRANIAL NERVES.
uess, and (^J) Violet blindness. Dalton suffered from red-blindness ; he
imagined that diluted ink gave a color much resembling a florid com-
plexion ; blood appeared to him not unlike in color to that called bottk--
areen • and he could not distinguish between the color of a ripe cherry
and that of a leaf.
b. Orjiiinic Bisi'ases of the OjJtic JVcrvc^.
Optic Neuritiif: and Atrophy.
Etiology. — Ojitic neuritis may l)e caused by tumors of the brain,
hydrocephalus, basal meningitis, meningeal hemorrhages, and throm-
bosis of the cavernous sinus, but it only rarely results from abscess of
the brain, and softening from occlusion of vessels, and in the few cases
in Avliich it was associated with hemorrhage it may be suspected that a
tilioma was jjresent. Optic neuritis is occasionally observed in cases
in which the symptoms point to intracranial disease, but in which the
])ost-mortem examination reveals no lesion. It may also be caused by
extracranial causes, such as orbital tumors, and inflammation of the
bones, periosteum, or cellular tissue of the orbit, and hyperostosis nar-
roAving the optic foramina. Optic neuritis sometimes follows injuries
of the cervical spine, while it has occasionally been observed in caries
of the cervical vertebrit;, witli transverse myelitis of the cervical and
dorsal regions of the cord.
Double optic neuritis is sometiuics caused by acute diseases, suc-h as
the specific fevei's and pneumonia. I'Xposure to C(dd or to a very bright
light, suppression of the menses, or chronic blood-poisoning from lead,
syphilis, diabetes niellitus, or chronic liright's disease.
Varieties. — The diseases of the optic nerves may divided as follows :
(1) Congestive and inflammatory affections :
(a) Simple congestion of the disk.
{b) Congestion with swelling of the disk (optic neuritis).
((') Albuminuric retinitis and neuritis.
(2) Atrophic affections:
(a) Simple or primary atroj)hy.
{b) Secondary atrophy.
(1) Inflammatory Affections of thk Optic Nerve.
{'() Simple congestion is characterized by an increased redness of
the disk, Avhich is the more readily recognized when it is greater in
one eye than in the other. The redness invades the })hysiological cup
and may entirely obscure it; the sclerotic ring and the edge of the
choroid are rendered indistinct, and the disk loses its sharpness of
outline.
DISORDERS OF THE XEKVES OF SPECIAL S K X S E . 277
(/>) Optic neuritis is characterized b}' (edema as well as congestion of
the disk, which becomes enlarged, swollen, red, and cloudy, the physio-
logical cup is obscured, the sclerotic ring and the edge of the choroid
are concealed, and the edges of the disk are l)adly defined and hazv.
As the disease advances the disk becomes more swollen, it assumes a
reddish-grav color, and its periphery becomes distinctly striated, partly
owing to the swelling and opacity of the nerve fibres and partly to an
enormous development of minute vessels. The veins are enororored
tortuous, and often varicose, while the arteries are reduced in size, and
a])pear paler than the veins, ^Vhen exudation takes place the vessels
become veiled and lost to sight at the boi'der of the disk, but reappear
partially as they proceed inwards, and disappear again l)efore reaching
the lamina cribrosa.
The inflammaticm may now subside, the swelling gradually dimin-
ishes, the edge of the choroid becomes apparent, and the only indica-
tion of the previous inflammation which remains may be a narrow zone
of atmphy adjacent to the disk and along the edge of the choroid.
(j) I:J)i;/07yed or Choked Disk. — If the inflammation continues the
<lisk becomes still more swollen, and its margins becoming steeper, the
vessels which pass over the side become concealed by the edge of the
swelling, and reappear in a different position in the fundus. The
arteries are reduced to small threads and are often invisible, but the
veins ai-e visible towards the edge of the tumor and often appear dis-
tended and tortuous for a long distance fi'om the disk. Hemon-hages
are now frequent and extensive, and generally ajjpear at the edge
rather than on the surface of the swelling. Sight becomes, as a ride,
rapidly impaired during this stage of strangulation. This form of
neuritis has been called the choked <>r engorged disk.
(jj) Subsidence of Optic Neuritis. — After the strangulation has
existed for some time the veins become less distended, the swelling loses
its intense red color and becomes pale and less prominent, hemorrhages
cease, the extravasated blood is absorbed, leaving pigmented or white
spots on the retina, the edges of the choroid and the sclerotic ring
become dimly apparent after a time, and then the (hsk assumes a
whitish or grayish color, its edges being generally irregulai- and sur-
rounded by a zone of choroidal atrophy.
(jjj) Descending Neuritis or Neui-o- retinitis. — It is not often pos-
sible to distinguish during life between neuro-retinitis and the slighter
decrees of eno-orored disk. In neuro-retinitis there is only a slight
r5 c o 111
deo-ree of swellincr, the changes are more marked towards the edge
than in the centre of the disk, hemorrhages are absent, white spots
278 DISORDERS OF CRANIAL XERYES.
may be seen scattered over the disk or along the edges of the vessels,
and the disk has a striated appearance from atrophy of the nerve fibres.
(iv) Retrobulbar Neuritis and Perineuritis. — In retrobulbar neu-
ritis the primary congestion soon passes on to atrophy with narrowed
vessels. It is met with in periostitis of the orbit and in cases where
the optic nerves are constricted by thickening of the cranial bones.
Optic perineuritis results from chronic inflammation of the sheath of
the nerve, which gives rise to thickening and purulent infiltration of
the trabeculse, and it generally ends in optic neuritis.
(v) Albuminuric Retinitis and Neuritis. — In diseases of the kidneys
the arteries of the retina become diminished in calibre like the arterioles
of the body generally. As the disease advances the retinal arteries are
reduced to small lines, and when swelling is present they may be invisi-
ble beyond the edge of the disk, while the thickening of their walls
causes white lines to appear along their edges. The arteries are liable
to undergo aneurismal dilatations, and retinal hemorrhages form a
marked feature of the affection. Albuminuric retinitis ])resents several
varieties, viz., (a) degenerative, {b) hemorrhagic, and [<■) inflammatory
retinitis, to which may be added, according to ( Jowers, {d) albuminuric
neuritis.
(a) Begenerative Albuniinurie Retinitis. — This form, which is the
most common, begins by the appearance of white spots on the retina;
they are small and rounded at first, but after a time increase in size
and become irregular in outline, while neighboring spots sometimes
coalesce to form large white patches. Small white spots are generally
to be seen around the macula lutea; they are sometimes so small as to
be seen only on careful direct examination, but are at other times large
and well marked, and arranged end to end, so as to form ladiating
streaks irregularly disposed around the macula, and giving to the
retina at this part a silvery appearance.
{b) Hemorrhagic AJbuminurir Retinitis. — The chief characteristic
of this variety is the large number of hemorrhages which occur, and
white spots only appear around the macula lutea at a late stage of the
affection.
{c) Inflammatory Albuminuric Retinitis. — In this variety there is
general swelling of the retina, the disk is obscured, the arteries are
thready and numerous, the veins are distended and tortuous, with
irregular outline, and large hemorrhages often occur, while the white
spots are often numerous and well marked. On the subsidence of the
inflammation the optic nerve may undergo secondary atrophy.
[d) Albumhiuric Neuritis.~ln this affection inflammation of the
optic nerve predominates over the retinal changes, the ed^es of the
DISORDERS OF THE NERVES OF SPECIAL SEXSE. 279
disk are indistinct and veiled under a grayish-red swelling, and the
arteries are small and often hidden, while even the veins may be con-
cealed in the swelling, and form curves over the sides of the swollen
disk. White spots may be seen on the surface of the swollen disk, on
the retina, and around the macula lutea, and small hemorrhages may
be observed about the fundus, but are rare over the swollen disk.
When the inflammation subsides a consecutive atrophy of the optic
nerve may be left. Albuminuric neuritis cannot often be distinguished
from ordinary optic neuritis.
General Symptoms. — Sight may remain unimpaired in advanced
cases of optic neuritis, and when amblyopia is present its degree is by
no means proportional to the amount of change observed on ophthal-
moscopic examination. Vision is likely to fail sooner in descendino-
neuritis than in cases of engorged disk, while a high degree of uni-
lateral or bilateral amblyopia may precede for some time anv changes
in the fundus in retrobulbar neuritis.
The cerebral symptoms most likely to be associated with optic neu-
ritis are headache, vertigo, vomiting, loss of memory, unilateral epi-
lepsy, hemiplegia, and paralysis of some or all of the ocular muscles.
3Iorbid Anatohiy. — In order to understand the mechanism by which
the swelling of the disk is caused in optic neuritis, the anatomy of the
nerve must be kept in mind. The annexed diagram (Fig. 86) will
suffice to remind the reader of the structure of the nerve. Inflamma-
tion of the optic nerve gives rise to a serous infiltration which augments
its volume and diminishes its consistence. The sheath of the nerve is
often distended with fluid, the connective tissue of the pial sheath and
of the trabeculge surrounding the nerve bundles becomes thickened and
infiltrated with nuclei and cells, a considerable number of leucocytes is
found surrounding the vessels, and the nerve fibres undergo degen-
erative changes, while in advanced cases the tissue of the lamina
cribrosa is distended and its structure altered. The veins are large and
tortuous, but the arteries are abnormally small.
Various theories have been advanced to account for the different forms
of optic neuritis. Descending neuritis and perineuritis of the nerve
are caused by a local disease and need not be further discussed. But
the double optic neuritis, or choked disk, which is caused by the presence
of an intracranial tumor does not find a ready explanation. It was
suggested by Von Graefe that the increase of intracranial pressure
which results from the presence of a tumor within the skull caused an
obstruction to the flow of blood from the eyes by compressing the cavernous
sinus. ]Many objections have been urged against this theory, and it
was finally abandoned when Sesemann showed that the supraorbital vein
280
DISORDERS OF CRANIAL NKRVES.
anastomoses so freely with the f^u-ial veins, that pressure on the cavernous
sinus would only produce a very temporary effect. When it was dis-
covered l)v Schwalbe that the subvaginal space around the oi)tic nerve
was continuous witli the subdural space around the brain, Schmidt
sufTo-ested that any increase of intracranial pressure would tend to dis-
tend the sheath of the optic nerve with fluid, and consequently Avould
produce strancrulation of the nerve fibres in tlieir passage through the
sclerotic ring and Inmin;! cribrosa. Tliis theory is by no means free
Fk;. 86.
~^^'
/
r'J.HllTiMllltQirlrlAiaiaill'XA.
inn A ti
/>
HoHi/.oNTAi, Section through thk utth Nkrve at its Point ok Insertion in thk »;i,obf,, anh it.<
Passage through the JIembranes of the Eye. (P'rom Landois's " Ph.vsiologie "l
a, Internal ; ft, External layers of the retina ; c, Choroid ; d, Sclerotic ; e. Physiological cup ; f. Central
artery of the retina; </, Point of its bifurcation ; h, Lamina crihrosa ; 7. Dnral sheath ; m, sulidural space ;
n, Suharachnoidal space ; r Arachnoidal sheath ; j), Pial sheatli : i i, Bundles of nerve tilm-s: /. /., Connec-
tive-tissue trabeculaj.
from objections. Optic neuritis may be absent in very large tumors
and in chronic hydroce]:)halus when the increase of intracranial pressui-e
must be very great, while small cortical tumors which can scarcely be
supposed to increase the pressure to any appreciable extent, often give
rise to the most marked swelling of the disk. Dr. IIuo-hlino;s-.Iackson
suggested that intracranial tumors act like foreign bodies, and jjroduce
optic neuritis by their irritating effects. Benedikt elaborated this theory
still further. He supposed that the irritation of the tumor acts on the
])TSORI)ERS OF THE NERVES OF SPECIAL SENSE. 281
Optic nerves through the vaso-motor nerves, and this opinion is now
known as the hj])othesis of reflex vaso-motor action. In a later pub-
lication. Dr. Hughlings-Jackson maintains that the irritation of the
tumor causes a discharge from the cortex of the 1)i-ain, the first result
of which is to occasion spasm of the vessels of the optic nerves, which
is followed by a secondary paralysis of these, just as occurs in voluntary
muscles su1)ject to unilateral spasm from intracranial disease. He
believes that the nutritive change which constitutes optic neuritis is
caused by this secondary paralysis. I have myself suggested that optic
neuritis is a trophic change caused by irritation of the external geniculate
bodies which I believe to be the homologues of the spinal uano-lia.
(2) Atrophic Affkctioxs of tue Optfc Nervks.
In atrophy of the optic nerve the intraocular extremity of the
nerve becomes slowly and progressively transformed into a pure white,
or grayish-Avhite disk. There is complete cessation of the capillary
circulation of the disk and consequently its healthy rosy tint disappears.
(a) Pritnary Atrophy. — This form of atrophy is generally associated
with other symj)toms of locomotor ataxia, and consequently Charcot
called it tahetlc amaurosis, or parenchyiiiatous atrophy ; on ophthal-
moscopic examination the optic disk is seen to be of a pearly Avhite
color (white atrophy), occasionally mixed with a slight tinge of blue or
of gray (gray atrophy). The contour of the disk is sharply defined,
and it may maintain its normal size and round form for a long time,
although its outline is occasionally iri'egular, and its size reduced. The
central artery and vein maintain their normal volume and direction, but
the lateral branches of the disk are in great part atrophied. White
atroph\' is usually bilateral, but it may sometimes remain limited for
many years to one eye. The retina is quite normal throughout. The
onset of the affection is usually sIoav, and the patient observes for months
or years that his sight is becoming progressively enfeebled. The field
of vision becomes concentricall}- contracted but in a very in-egular
manner, and a central scotoma may occasionally be associated with the
peripheral limitation. Dyschromatopsia or achromatopsia is present at
an early period of the atrophy, and the acuteness of vision becomes
progressively diminished, but the diminution is not always in direct
proportion to the degree of change in the optic nerve, inasmuch as the
patient can sometimes read the smallest type when the atrophy is very
advanced. The patient may experience various subjective sensations
such as sparks or flashes of light (photopsia), or a play of colors (chro-
matopsia). The mode of locomotion is characteristic ; the head is
retracted and the chin elevated, the gait is shuflling, the eyes are directed
2S'2 DISORDERS OF CRANIAL NERVES.
upwards, and the expression of the countenance is vague because the
eyes are not fixed on any object. White atrophy is generally associated
with various disorders of the pupil, of which paralytic myosis is the
most fre(|uent. The pupillary disorders are independent of the white
atrophy, being caused by an extension of the lesion which underlies
locomotor ataxia, to the cilio-spinal region of the cord.
(b) Secondary atmphy of the optic nerve is caused in various ways.
The following varieties may be distinguished :
[c) Atrophy by Compression of the Fibres of the Optic Nerve. — This
form may be caused by pressure on the chiasma or on the optic nerve
in any part of its course through the base of the brain, optic foramen,
or orbit. It is often preceded by a stage in which the disk is congested,
but when atrophy is established the ophthalmoscopic appearances of the
disk are the same as those of white atrophy. A lesion of one optic
tract causes, but only after some years, pallor of the corresponding halves
of the disk. The disease is steadily progressive and the prognosis is
most unfavorable.
(j) Atrophy Secondary to Optic Neuritis. — The main features of
this form of atrophy have already been described, when the subsidence of
neuritis was under consideration. The disk is at first yelloAv or dull
white, its contour is completely hidden under an exudation, and the
vessels are varicose ; but as the exudation becomes absorbed the disk
becomes whiter and whiter, its capillaries undergo atrophy, and the
central vessels themselves become smaller although they preserve their
tortuous course. The disk is larger than normal, and its edge is irregular
and broken and remains to some extent obscured by exudation, while
patches of exudation are often seen around the disk and in the neighbor-
hood of the macula. This form of atrophy is not always followed by
blindness, and patients after becoming blind during the acute stage may
recover some degree of vision.
(jj) Atrophy Secondary to Obliteration of Vessels. — This form of
atrophy is caused l)y embolism or thrombosis of the central artery of
the retina. The disk is of a pearly white color ; its margin is covered
Avitli a Avhite veil which extends to the retina, and the arteries are so
small as to be scarcely perceptiljle and are often surrounded by a whitish
and more or less opaque exudation. After the exudation has been
absorbed this form of atrophy is distinguished from every other by the
small size of the arteries of the disk and retina.
(jjj) Choroiditic Atrophy. — This form of atrophy is very similar to
that which is consecutive to obliteration of the central artery ; the retinal
vessels are greatly atrophied, but the disk has a peculiar reddish or
yellowish tint and its edges are slightlv blurred.
I
\
DISORDERS OF THE XERVES OF SPECIAL SENSE. 2«8
( iv) Atropliij Secondary to Betinitis Pigmentom. — In tins variety
of atroi)hY the retinpe become studded by pio:inentary spots from mitn-a-
tiou of the choroidal pigment, and the central vessels are atrophied,
-while their collateral branches disappear, after a time, altogether. The
capillary vessels derived from the ciliary arteries of the optic nerve are,
however, not affected to the same extent, and consequently the disk
generally preserves a well-marked rosy tint.
( v) Atrophy hy Exravation. — This optic atrophy is caused by increase
of intraocular pressure in such diseases as glaucoma and hydroi)hthalmia,
and it is characterized by the deep excavation of the optic disk. A
certain degree of excavation may occur in the other forms of atropliv
from wasting of the fibres of the optic nerve and cicatricial contraction
of the newly formed connective tissue.
Morbid Anatomy. — The anatomical changes in atrophy of the disk
extend through the optic nerves. In primary atrophy the nerve is
much reduced in size ; it is gray and gelatinous in appearance; the con-
nective-tissue trabeculcTe are hypertrophied, and the nerve fibres are pro-
gressively destroyed, so that the nerve is ultimately reduced to a cord of
connective tissue. In atrophy from pressure the nerve is much reduced
in size and the connective tissue is much increased. In the various
forms of atrophy the disk presents a superficial depression which does
not usually pass beyond the limits of the choroid ; the lamina cribrosa
is only covered by a thin layer of the debris of the disk, but does not
itself undergo displacement ; and the ganglionic layer and the nerve
fibres of the retina undergo atrophy, but the other layers are unaffected.
The degeneration always ascends to the chiasma, and the optic tracts are
atrophied, in long-standing cases, as far as the external geniculate bodies.
c. Diseases of the Optic Commissure and Tracts.
The lesions which usually affect the optic tracts and commissure are
circumscribed affections of the bones and membranes of the brain or
injuries of the base of the skull.
Symptoms. — The characteristic symptom of disease of the optic tract
is an enfeeblement or abolition of sight of one lateral half of the
retinse. The blind half of the retina is separated from the sensitive
half by a sharply defined vertical line, but central vision is preserved
in both eyes. When this condition is described with reference to the
field of vision it is called hemianopsia, and to the retina, hemiopia. If
the left optic tract be compressed by a tumor (Fig, 87, K), the two left
halves of the retinie — the outer of the left and the inner of the right —
are cut off from the cortex and consequently there is blindness of the
H
284
DISORDERS OF CRANIAL NERVES
ri<'-lit halves of the fields of vision, a condition named right lateral
hcmianopda. The affected portions of the retin;^ are associated in their
actions, and this condition has, therefore, been also named equilateral
or homonymous hemianopsia. When both the inner or both the outer
halves of the retime are blind, the condition is called crossed hemianopsia.
When the lesion is situated over the centre of tlie commissure (Fig.
ST, T) the inner halves of both retinae' are affected. AVith reference to
Fig. 87.
F THi: iimir Tk.vcts. (After Charcot. t
T, Semidecussation in the cliiasma ; TQ, Decussation of fibres posterior to the external geiiiciilate hoUii>ti
(CG) ; a' b, Fibres which do not decussate in the chiasma; b' a', Fibres coming from the right eye, and
coming together in the left hemisphere (LOG) ; K, Lesion of the left optic tract producing right lateral
hemianopsia ; A, Lesion in the left hemisphere (LOG), produces crossed amblyopia (right eye). T, Lesion
producing temporal hemianopsia: NX, Lesion producing nasal hemianopsia.
the fields of vision this condition is called double temporal hemianopsia.
In- this defect patients experience difficulty in walking, but they are
often able to read the smallest print. Douhlc nasal hemianopsia is rare,
and can only result from a double lesion (Fig. 87, N N).
Y. DISOKDEKS CAUSED BY DISEASE OF THE CEREBRO-SPINAL
SENSORY CONDUCTING PATHS.
Various sensory disorders are caused by disease of the fibres of the
posterior roots after they join the spinal cord, but inasmuch as these fibres
are affected most frequently in posterior sclerosis, the resulting dis-
orders will be considered along with tabes dorsalis.
Parancesthesia. — In transverse lesions of the spinal cord the part
of the body which is innervated from that portion of the cord which
lies below the level of the lesion is more or less anaesthetic, according to
the completeness of the destruction of the cord produced. A hyper-
])ISEASh: OF CEREBKO-SFIXAL SENSORY PAl'irs. -iS.")
iVi^sthetic belt is tiequently met Avitli suirounding the body on a level
Avith the iipi)er limit of the lesion, caused by irritation of fibres descend-
ing from the posterior roots which are situated immediately above the
level of the lesion.
Hejiiiparancesthesia. — In destructive lesions of one hiteial half (.f
the spinal cord there are, on the side of the lesion, motor paralysis and
loss of muscular sense below the level of the lesion from destruction of
the fibres of the pyramidal tract, cutaneous hypemesthesia of the parts
below the level of the lesion from irritation of the sensory conducting
paths of the opposite half of the spinal coitl, an anaesthetic belt on a
level with the lesion from implication of the posterior roots, and u hypcr-
sesthetic belt above this level from irritation of fibres descending from
the posterior roots immediately above the lesion. On the side opposite
to the lesion there is anaesthesia of the sensations of touch, pain, tem-
SeCTION 01' THE MeDI I.LA OllLliXr.ATA nX A LEVEL WIT}I THE LAEGEST lHAMETEi; OF THE DISEASED FOCUS,
WHICH IS KErRESENTED BV THE SHADED PART ON THE LEFT HALF OF THE DIA(iRAM. (After SENATOR. )
P, pyramids ; ol, olivary bodies ; Voir, ascending root of tlio fifth m-rve ; A7.-, nucleus of the vagus ;
Xiuk, motor nucleus of the vagus; lib, fasciculus rotundus ; x, the vagus; xii, the hypoglossal nerve.
perature, and tickling of the parts supplied from beloAv the upper
limit of the lesion, from destruction of the sensory conducting ])aths
after thev have crossed over to the opposite side of the cord, and a zone
of hypersesthesia immediately above the level of the upper limit of the
lesion caused by irritation of fibres descending from the posterior roots
immediately above the lesion, and some of which jirobably cross over to
the diseased side of the cord. In unilateral lesions of the lumbar or
the cervical enlargements a zone of anaesthesia is found in the lower
or upper extremities wdiich varies in its position according to the level
of the lesion, and the root or roots which are involved in it.
280 DIS<^Kl)EPiS OF CEREBRO-SPINAL SENSOEY PATHS.
Crossed HemianCBstheda. — In this affection there is ansesthesia of
the face on one side of the body, and of the trunk and extremities on
the opposite side. In a case of this kind reported bv Senator the
lesion consisted of a spot of softening in the restiform body, and impli-
cated the ascending root of the fifth nerve (Fig. 88). It must be re-
membered that this root begins as low down as the third cervical nerve,
so that some det^ree of anaesthesia of the side of the face ma}' be observed
in unilateral lesions of the upper portion of the cervical region of the
cord.
Hemiancesthesia. — In this affection there is loss of sensibility of the
whole of one-half of the body, face, and extremities, including the
accessible mucous membranes as well as the skin. The abolition of
sensation is sometimes incomplete, and then cutaneous analgesia or
thermo-aniesthesia may be present, while tactile sensibility remains
unaffected. At other times the anaesthesia of the skin and mucous
membranes is complete, and even muscular sensibility and muscular
sense are abolished. The patient, for instance, does not feel deep pressure,
strono- contraction of the muscles may be produced by the faradic current
without causing pain, and Avhen his eyes are closed he is unable to
describe the position in which the affected extremities may be placed by
passive movements, and is not aware when his attemjjted voluntary
movements are forcibly prevented. The patient can walk Avithout
difficulty Avhen his eyes are closed, but by slight pressure upon the
affected side he may be easily induced to walk in a circle while under
the impression that he is walking in a straight line. One hnlf of the
mucous membrane of the tongue, mouth, veil of the palate, and the
conjunctiva of the same side are insensitive, but the cornea retains its
sensibility. The affected side feels cold to the touch, and the ])rick
of a pin does not bleed so readily as on the opposite half of the l)ody.
The cutaneous reflex actions may be lost on the affected side Avhile
the deep reflexes are retained.
The senses of taste and smell are abolished on the affected side.
The sense of hearing is diminished, and in some cases there may be
complete unilateral deafness.
The sense of sight is impaired, l)ut not abolished. There is concen-
tric restriction of the field of vision, and the perception of colors is
diminished or lost [dgsehronuitopsia), these defects being present in both
eyes, but most marked on the side opposite the lesion.
Hemiancesthesia as just described occurs in its most typical form in
hysteria and occasionally in epilepsy, chorea, neurasthenia, and other
grave neuroses. It also occurs in organic diseases Avhen the lesion is
situated in or near the posterior third of the posterior segment of the
DISORDEES OF C EREBE O - SP I X AL SEXSORY PATHS. 287
internal capsule. Hemiansesthesia is generally present in hemichorea
and athetosis, the lesion being situated in these diseases either in tlie
external and posterior part of the optic thalamus or in the posterior
part of the lenticular nucleus. In these diseases the posterior part of
the internal capsule is only partially injured and the degree to wliich
sensory conduction is impaired varies greatly in different cases. When
the lesion is situated on the lenticular nucleus the various forms of
cutaneous and muscular sensibility are aifeeted, but the special senses
often remain intact. The special senses may also remain unaffected
Avhen the posterior part of the internal capsule is compressed bv the
growth of a tumor in the optic thalamus, probably because the slow
growth of the tumor enables the fibres of the optic radiations of Gi-atiolet
to be pressed aside without rupture.
Hystei-ical hemianfesthesia is associated, as Ave have just seen, with
concentric restriction of the fields of vision of both eyes, and especiallv
with amblyopia of the eye on the same side as the other sensory dis-
orders. In order to account for this fact, Charcot assumed that all the
fibres which come from one eye are connected with the cortex of the
opposite hemisphere, and he supposed that for the fibres w^hich did not
cross in the commissure there was a suj)plementary crossing in the corpora
quadrigemina (Fig. 87, T Q). But that part of the scheme which relates
to the supplementary crossing is now, I believe, abandoned by its distin-
guished author, because a considerable number of cases are now recorded
in which homonymous lateral hemianopsia has been caused by disease
of one cerebral hemisphere, the lesion being situated in such cases on
the pulvinar of the optic thalamus, the white substance of the occipital
lobe, or the cortex of the occipital lobe as far forwards as the angulai-
gyrus. From an analysis of recorded cases it would appear that the
fibres of the optic tract pass through the geniculate bodies and anterior
tubercle of the corpora ((uadrigemina, and are continued upwards through
the pulvinar of the optic thalamus, the posterior part of the internal
capsule, and the posterior part of the corona radiata, to reach the cortex
of the occipital lobe. In homonymous hemianopsia caused by disease
of one optic tract, central vision is retained in both eyes, a fact Avhich
proves that the macula lutea of each eye must be connected with the
corticles of both hemispheres. As the organs of vision are bilaterally
associated in their functions, it is pi-obable that the cortical visual centres
are connected by commissural fibres through the corpus callosum.
288 DISORDERS OF CORTICAL SKXSORY CENTRES.
VI. DISORDERS CAUSED BY DISEASE OF THE CORTICAL
SENSORY CENTRES.
1. Cutaneous and Muscular 1Ie.ml\n.ksthesia.
Ferricr localizes the centre of tactile sensibility in the hippocanijial
region, but unilateral lesions of these convolutions are not known to
o-ive rise to anesthesia. Disease of the temporo-sphenoidal lobe some-
times causes loss of tactile sensibility of the opposite side, but it is most
probably caused by interference with the sensory fibres of the internal
capsule. Cutaneous aniesthesia and loss of muscular sense have occa-
sionally been found associated with hemiplegia in cases of extensive
softening of the cortex of the parietal lobe, and it is, therefore, probable
that the cortical centre of general sensil»ility is widely diffused over the
so-called motor area of the cortex.
2. DlSOUDKKS OF THF SeNSE OF S.MKl.L.
a. Hnlluritiations of Smell. — The case of a woman is reported by
Dr. McLane Hamilton, Avho had for nearly thirty years suffered froih
occasionally recurring e]tile[)tiform attacks which were always ushered
in by an aui-a of a disagreeable (jdor. The patient died of phthisis,
and at the autopsy the pia mater was found adherent over the right
uncinate gyrus and adjacent convolutions, while the subjacent gray
matter was atrophied and in a state of sclerosis. The olfactory neives
were not involved in the lesion.
/'. Anosmia. — FeiTier found that destruction of iXw.sahtcuhini cornu
amnionis in monkeys caused loss of smell on the side of the injury.
but in heiJiiancesthcsio from disease of the fibres of the posteri<»r part of
the internal capsule the loss of smell is on the side opposite the lesion.
Anosmia of the left nostril is S(»metimes met Avith in cases of right
hemiplegia and aphasia, but the loss of smell is most probably caused
by softening of the external root of the olfactory tract and not from
disease of the cortex. A case of abscess of the temporo-sphenoidal
lobe is reported by Dr. Glynn, in which the most prominent symptom
was complete anosmia, l)ut the loss of smell was most prol)ably caused
by compression of the olfactory tracts at their points of junction with
the brain. On the whole, our clinical information with regard to the
localization of the cortical centre of smell is exceedingly scanty and
will not bear a critical investio;ation.
I
DISEASES OF THE COKTICAL SEXSOKY CEXTEES. 289
•S. Disorders of the Auditory Sense.
a. Hallucinations. — Ferrier places the auditory cortical centre in
the first and second convolutions of the temporo-sphenoidal lobe, and
irritative lesions of these convolutions give rise occasionally to hallucina-
tions of hearing. A man, under my care, received a blow over the
head a little above the left ear, and at the seat of injury, which was
opposite the first and second temporo-sphenoidal convolutions, a slight
depression in the bone could be detected. After the injury the patient
suffered from recurring epileptiform attacks which were ushered in by
loud rattling noises, caused most probably by a discharging lesion havin^
its origin in the auditory cortical centre.
h. Psyehical Deafness. — In this condition, which was first described
by Goltz as occurring in dogs after portions of the cortex of the brain
had been washed away, the animal is not deaf, but fails to recognize
the significance of the usual calls. He does not, for example, respond
to the call of his name, and is not cowed by angry threats, and yet
distinct evidence is obtained that he hears noises. This defect was
named psychical deafness by Munk. The state in man most nearly
approaching to it is word-deafness., which will be subsequently described
along with the disorders of speech.
c. Absolute Deafness. — Unilateral destructive lesions of the first
and second temporo-sphenoidal convolutions do not give rise to complete
deafness of one ear, because the sense of hearing is bilaterally associated,
and so long as one hemisphere is unaffected the auditory sense remains
unimpairevl or only slightly weakened. The condition which will be
subsequently described as word-deafness is, however, associated with
disease of the first and a portion of the second temporo-sphenoidal con-
volutions. But if the first and second tem})oro-si)henoidal convolutions
contain the auditory centres, bilateral lesions of these ought to give rise
to complete deafness. A case is reported by Wernicke in which the
patient first suffered from word-deafness and subsequently became com-
pletely deaf, and after death the first temporo-splienoidal convolution
was found softened in each hemisphere. A careful dissection of the
ears proved the absence of any local disease of the peripheral organ of
hearing.
4. Disorders of the Visual Sense.
a. Halluei7iations of Sight. — Tumors of the occipital lobe give rise
to hallucinations of sight such as colored vision, and the images of animals
and of variously dressed men, and when the growth causes epileptiform
convulsions the attacks are often preceded by a visual aura.
19
290 DISORDEES OF THE VISUAL SENSE.
b. Psychical Blindness.— Ti\\& condition was, like psychical deafness,
first observed by Goltz in dogs after portions of the cortex of the brain
were washed away. The dog, after the operation, sees and avoids
obstacles, thus recognizing resistance and the other fundamental prop-
erties of matter, but he has lost the power of appreciating the special
properties of matter to so great an extent that he does not recognize his
food as such. A more or less similar condition has been descril:)ed hx
Fiirstner as occurring in some cases of general paralysis of the insane.
The patient, for example, recognizes that a piece of money placed in
his hand is a metal, but has lost all knowledge of the special properties
which constitute it a coin. Word-blindness is a more or less similar
condition. Subsequent dissection has proved that in the dogs operated
upon by Goltz, it was the posterior lobes of the brain which were chiefly
denuded of cortex by his method of procedure, and in Fiirstner"s cases
the cortex of the occipital lobes was always found diseased when a
post-mortem was obtained. It will be hereafter seen that in word-blind-
ness the disease is limited mainly to the cortex of the angular gyrus.
c. Homonymous Bilatcnd Hemianopsia. — Man^^ cases are now re-
corded in which this defect of sight was caused by softening of the cortex
of the left angular gyrus, and the condition is frequently associated with
word-blindness.
d. Absolute Blindness. — Disease of the cortex of one hemisphere
of the brain does not usually give rise to complete blindness. The case
of a boy, however, is reported by Dr. Abercombie, who, after an injury
which caused a depressed fracture of the right parietal bone, suftered
from hemiplegia of the left side and amaurosis of the left eye, from
which he made a quick recovery on the depressed part being removed.
The position of the fracture rendered it probal)le that the angular gyrus
was injured. A case is reported by Dr. Glynn, of Liverpool, in which
the patient became suddenly and completely blind, and in which a clot
was found occluding the posterior cerebral artery of the left side, causing
extensive softening of the left occipital and temporo-si)henoidal lobes.
The case of a woman is reported by Dr. Shaw, of Brooklyn, who had
become suddenly aphasic and perfectly deaf and blind. At the autopsy
the angular gyri and superior temporo-sphenoidal convolutions of both
hemispheres were found completely atrophied, and no other lesions could
be discovered in the brain or peripheral organs. This case Avould seem
to indicate that bilateral disease of the angular gyri will alone suffice to
cause complete blindness. Berger has recently recorded two cases of
complete blindness with normal or almost normal reaction to light of
the pupils and in which extensive softening was found in the occipital
lobes.
DISEASES OF THE CORTICAL SEXSOEY CENTRES. 291
Nothing is known of disorders of the sense of taste from cortical
disease.
Treatment. — Inasmuch as anaesthesia and hyperjesthesia are generally
associated with other important phenomena such as motor paralysis, the
treatment of these symptoms does not require to be specially cfiscussed
in this place. In the treatment of neuralgia the first indication is to
remove the exciting cause. An endeavor must be made to remove every
source of external irritation such as carious teeth, foreign bodies pressino-
upon the nerves, cicatrices, tumors, and neuromata. It is manifest that
in order to fulfil this indication great scope is afforded the exercise of
surgical skill. At other times the exciting cause of a neuralgia is to
be found in remote irritation such as when the presence of intestinal
worms or uterine disease gives rise to facial neuralgia. Venous conges-
tion of the pelvic organs from constipation and portal obstruction is
sometimes the cause of sciatica, and in these cases benefit is likely to be
obtained from purgatives and the use of natural saline waters like those
of Kissingen, Marienbad, and Harrogate. A turpentine enema has
also been strongly recommended in such cases. The early stages of
neuralgia which arises in rheumatic and gouty subjects must be treated
by absolute rest, diaphoresis, the milder counter-irritants, the vapor or
Turkish bath, and salicylate of soda or alkalies with colchicum, and by
iodide of potassium either alone or in combination with guaiacum, when
the acute symptoms have subsided. When the patient is suffering from
anpemia, as often occurs in trigeminal neuralgia, large doses of carbonate
of iron, with or without cod-liver oil, have a very beneficial effect. In
such cases arsenic either alone or combined with iron is a useful remedy,
and it is also useful in ophthalmic neuralgia of malarial origin. In
malarial neuralgia, however, large and repeated doses of quinine are the
most trustworthy remedy and it also may be employed in the treatment
of other forms of neuralgia, and is especially useful in trigeminal
neuralgia. In neuralgia of syphilitic origin large doses of iodide of
potassium must be given, and this drug will also be useful whenever there
is reason to suspect the presence of neuritis. Zinc, nitrate of silver,
chloride of gold and sodium, and strychnia, are other drugs which have
occasionally been found useful in the treatment of neuralgia. Gelse-
minum sempervirens, best given in the form of tincture, and croton
chloral hydrate, either in one large dose of a scruple or in four grain
doses every four hours, have been found useful in the treatment of
trigeminal neuralgia, and Dr. Ringer speaks favorably of a liquid extract
of tonga prepared by Messrs. Allen k Handbnry, given in drachm
doses every four hours. In sciatica, rectified oil of turpentine has
been found useful. It is best administered in gelatine capsules each of
292 TKEATMENT.
which contains fifteen drops of the oil, and two or three of these may
be given at meal-time. Copaiba has succeeded in the hands of Dr.
March, of Rochdale. The local treatment of neuralgia consists of the
application of hot fomentations and poultices in the early stages, while
flying blisters may be applied along the course of the painful nerve
when the acute symptoms have subsided. When the nerve is deep-'
seated like the sciatic its course may be painted Avith tincture of iodine,
or the actual cautery may be used in chronic and obstinate cases. In
such cases a very effectual but very severe remedy consists in the sub-
cutaneous injection over the seat of severest pain of a few minims of a
strong solution of nitrate of silver (gr. x to 5j)- An injection, by
means of a subcutaneous syringe, into the substance of tlie nerve of a
one per cent, solution of perosmic acid has been favorably reported upon
by Eulenburg and others. Ointments containing opium, veratria,
aconitia, or equal parts of chloral and camphor, may be rubbed into the
skin over the painful nerve, or the course of the nerve may be painted
with aconite or belladonna liniment, or rubbed with narcotic and sooth-
ing liniments. Chloroform is also found useful as a local application,
and its inhalation may be advisable to allay the pain of very violent
paroxysms of neuralgia. Chloral and camphor when rubbed together
in a mortar form a clear solution Avliich is an excellent local application
in neuralgia of superficial nerves.
The constant current has been found very successful in the treatment
of obstinate neuralgia. /In neuralgia of isolated superficial branches
the direction method may be employed and a descending stahilr current
passed through the painful nerve. AYhen the polar method is used, the
anode is to be placed on the specially painful points and held stationary
there, whilst the cathode rests on the back of the neck, sternum, or on
any other indifferent part of the body. When the deeper-seated nerves
are affected, the anode may be placed on some indifferent part of the
body and the cathode over the point of emei'gence of the affected nerve.
In order to reach the main divisions of the fifth nerve at the base of
the cranium, and after their emergence through the foramen of the
sphenoid bone, the current may be conducted transversely through the
base of the skull at the appropriate spots, the anode being placed on the
painful side. /Benedict recommends that in severe cases of trigeminal
neuralgia galvanic currents should be passed longitudinally and trans-
versely through the skull, and along the sympathetic nerve. Faradiza-
tion occasionally answers better than the constant current, the moist
poles being applied to the painful points and along the nerve trunks.
The electric hand is sometimes very soothing and agreeable to the
patient.
DISEASES OF THE CORTICAL SENSORY CENTRES. 293
In the treatment of sciatica the anode should be placed over the sciatic
foramen or upon the sacrum, and the cathode upon the specially painful
parts. Remak advises that successive portions of the nerve, from six
to eight inches in length, should be successively brought under the
influence of tlie current, beginning at the sacrum and passing down to
the feet. Another method recommended by Remak, under the name
of circular current, consists in the stabile application of the anode upon
the painful points and over the trunk of the nerve; broad electrodes
and strong currents being used. In severe cases Benedict recommends
that one electrode should be introduced into the rectum and the other
placed over the sacrum, so that the current may pass through the
plexus. Ciniselli recommended a zinc and copper plate connected by
a wire, to be applied to the aifected limb and worn continuously. In
chronic cases I have obtained excellent results by introducing several
acupuncture needles over the course of the nerve as it emerges from the
sciatic foramen, and passing a feeble galvanic current through them,
the positive pole being in contact with the needles and the negative
placed over the sacrum. (The faradic current gives the best results
when the pain has in great measure disappeared and the subsequent
muscular feebleness has to be treated, or if more or less antesthesia be
present the faradic brush may be employed.
(tnoi'dpr to nft' nrd immediate relief to the pain the administration of
narcotics forms an indispensable part of treatment. The most generally
effectual narcotic is morphia administered by subcutaneous injection.
Another useful method of employing morphia is to dust from one-sixth
to one-third of a grain every three or four hours over the raw surface
left when the cuticle is removed by the application of a blister over the
course of the painful nerve. It may also be useful to change some-
times from morphia to stramonium, hyoscyamus, or atropine. In
the treatment of epileptiform trigeminal neuralgia Trousseau recom-
mended the use of large doses of opium or morphia, and in some cases
he prescribed as much as a drachm of morphia, or two or three of
opium in the course of the day ; but this treatment ought only to be
resorted to -when every other method fills. Large doses of bromide of
potassium, either alone or in combination with tincture of opium or
chloral, act beneficially sometimes in this form of neuralgia. In intrac-
table cases of neuralgia relief for the pain, when all other methods fail,
is only to be obtained by means of surgical operations. Resection of the
painful nerve, and even amputation of the affected limb, have been resorted
to in intractable cases, but such serious operations ought only to be
resorted to under the most pressing necessity. Stretching of the affected
nerve is a much less serious operation, and several cases of neuralgia
294 TREATMENT.
of different nerves are now on record in which the operation has proved
successful. Lange procured relief of pain in sciatica by producing
forcible flexion of the thigh, and thus stretching the affected nerve
over the neck of the femur.
The form of plantar neuralgia described by S. Weir Mitchell has
hitherto proved intractable to every kind of treatment. The posterior
tibial nerve was stretched in one of ray patients by my colleague,
Mr. Southam, but the relief which followed was not lasting.
Coccygodynia, in addition to the usual remedies, must sometimes
be treated by means of a surgical operation. The usual operations are
extirpation of the coccyx, and separation of the bone from all the nerves
connected with it by means of a tenotomy-knife introduced subcu-
taneously.
Disorders of the special senses come under the care of the physician
as symptoms of other diseases of the nervous system, and the treatment
must be directed against the chief lesion, whatever it may be. 'I'he
possibility of the sensory affection being of syphilitic origin should
never be forgotten. Local electrical treatment is sometimes found
useful in those cases in which the acuteness of any of the special senses
is diminished.
The treatment of those sensory disorders which are caused by disease
of the sensory conducting paths and cortical centres, must vary accord-
ing to the nature and locality of the lesion. Local treatment is seldom
of any use.
CHAPTER III.
SPASMODIC DISORDERS.
The general characteristics of the various forms of spasm have ah-eady
been considered and we shall now describe in detail (I.) the spasms
which are caused by reflex or direct irritation of the reflex spinal
mechanisms and which may be named spino-neural spasms, and (II.) the
spasms which are caused by irritation of the cortical motor centres or
of the fibres of the pyramidal tracts, and which may be named cereljro-
spinal spasms. It is not always possible to make a trenchant division
between these two forms of spasm. Some fornas of writer's cramp, for
instance, belong probably to the spino-neural, and others to the cerebro-
spinal paralyses, and even some local spasms like masticatory spasm
may be caused either by reflex irritation or by irritation of the cortex
of the brain, but it will be found convenient to describe all forms of
these affections in the same place. Notwithstanding the difficulties
which present themselves in carrying out this division of spasm, the im-
portance of the distinction Avliich underlies the classification must be our
justification for adopting it.
I. SPINO-NEURAL SPASMS.
The spino-neural spasms may be divided into : 1, local spasms affect-
ing muscles supplied by particular nerves or their branches ; 2, general
spasms caused by excessive irritability of the spinal reflex mechanisms ;
and 3, spasms of myopathic origin. Amongst the spino-neural spasms
tetanus and tetany are here included, but we are by no means sure that
a more extended knowledge of the pathology of these affections will
justify their retention in this category.
1. Local Spasms.
a. Spasms of the 3Iuscles of the Eyeball.
The external muscles of the eyeballs are subject to both tonic an<l
clonic spasms.
(1) Tonic spasm of the internal rectus is more frequent than spasm
of any other muscle of the eyeball, and it is usually associateil with
296 SPASMODIC DISORDERS.
blepharospasm. It gives rise to homonymous diplopia similar to that
which occurs in paralysis of the sixth nerve, but in the latter the squint
is permanent and the relative positions of the true and false images
fixed, while in the former there is a constant oscillation between the two
images which alternately approach and recede from each other. All
easel of spasmodic strabismus are accompanied by paroxysms of neuralgia,
and by photophobia and lachrymation. Tonic spasm of the internal
rectus may be caused by long-standing paralysis of the external rectus.
(2) Tonic sjjasm of the external rectm, which is rare, causes diver-
gent squint, and gives rise to diplopia with crossed images, but contrary
to what occurs in paralysis the two images never remain fixed, but
alternately approach and recede from each other.
(3) Nystagmus consists of a clonic spasm of the muscles of both
eyeballs, giving rise to continual lateral oscillatory or rotatory move-
ments which are entirely beyond the control of the patient. When the
patient looks at a remote object the trembling liecomes very pronounced,
but the eyes become more and more fixed in proportion as they are
directed to near or small objects. Nystagmus may be caused by con-
genital cataract, corneal opacities, and other local diseases, but it is ver}'^
generally due to central changes and is a prominent symptom in sclerosis
in patches, and in Friedreich's hereditary form of locomotor ataxia,
while it may arise in connection with meningitis, hydrocephalus, and
other intracranial diseases. It is often present in albinos, and colliei's
are frequently affected.
h. Masticatory Spasm {Trismus).
Etiology. — Bilateral masticatory spasm is often a symptom of general
spasms, such as tetanus, epilepsy, hysteria, and chorea. When it occurs
as a separate affection it may be caused by disease of tlie motor nerves
themselves, or be a symptom of basal meningitis, apoplexy, intracranial
tumors, and other central diseases. It may also result from reflex
irritation either of the sensory branches of tiie fifth nerve or of some
remote part of the body.
Symptoms. — The spasm is generally bilateral and it may be either
tonic or clonic.
In the tonic variety the lower is approximated to the upper jaw, and
when the teeth are so firmly clenched that they cannot be separated from
one another by force the condition is named lock-jaws or trismus. The
muscles of the jaw are then tense, rigid, often painful, and mastication
is impossible. In the clonic variety the lower jaw is moved either in a
vertical or horizontal direction, the former giving rise to chattering of
SPIXO-NEURAL SPASMS. 9i)7
the teeth, as in the cohl stage of ague, and the hitter to grinding and
munching of the teeth. The teeth are much ^vorn hy the constant
grinding against each other, and they may even be broken l)y the vio-
lence of the spasm.
c. Spasm in the Area of Distribution of the Facial Nerves (Histrionic
Spasm, Mimic Convulsion, Convulsive Tic).
Etiologij. — Convulsive tic sometimes appears to be inherited, and it
may occur in neuroi)athic subjects from emotional causes, or in tlie
absence of any recognizalde cause. It is caused frequently by direct
or indirect irritation of the facial nerve. The direct causes are often
only a slighter degree of those which occasion paralysis of the nerve,
such as exposure to cold, tumor of the base of the brain or in the
lower end of the pons, aneurism of the vertebral artery, inflamed
glands in the neighborhood of the stylo-mastoid foramen, abscess of the
parotid gland, caries of the petrous portion of the temporal bone, and
otitis. Reflex irritation is often conveyed through the fifth nerve and
the causes of irritation are trigeminal neuralgia, carious teeth, an<l irri-
tation of the eyeball and conjunctiva. The source of irritation is,
however, sometimes remote, the spasm having been caused by such
diseases as cervico-brachial neuritis, and intestinal or uterine disease.
Symptoms. — Facial spasm may be clonic or tonic, the former being
by far the more frequent.
The clonic form is characterized by periodically recurring attacks of
spasm, each paroxysm consisting of sudden and violent contractions
and relaxations of some of the muscles of the face. The duration of
each paroxysm varies from a few seconds to a few minutes, and the
interval between them is generally brief, except during sleep, when the
spasms entirely cease. The spasm is generally unilateral, and thus
the contortions and grimaces of the affected side contrast strangely
with the calm expression of the healthy side. The contortions pro-
duced are extremely varial)le and consist mainly of elevation and
depression of the occipital and frontal muscles, corrugation of the eye-
brows, twitching or winking of the eyelids, elevation of the cheek and
of the nostril, and distortion of the angle of the mouth, these symp-
toms being present either singly or in every imaginable combination.
The spasm is sometimes partial, being limited to the muscles supplied
by single branches of the nerve. The palpebral twigs alone are some-
times affected, and the spasm then manifests itself by a rapid winking
called nictitating spasm. In some cases there is only slight twitching
movements of one of the eyelids, the lower being the one uiost usually
298 SPASMODIC DISORDERS.
affected. At other times the spasm gives rise to a paroxysmal closure
of the evelids which may last from a few minutes to a feAv hours, and
mav occasionally extend over a period of weeks or months, this form
beiiag named blepharospasm. This form is accompanied by photo-
phobia, and is generally caused by reflex irritation of the fifth nerve.
In some other cases the spasm is limited to the area of distribution of
the malar and labial branches, and then it gives rise to a convulsive
orin on one or both sides, resembling laughing, and consequently this
form is called the sardonic laugh, risus eaninus, or ct/nic spasm. All
the muscles supplied by the fecial nerve, including the platysma
myoides, may be involved, and the spasm sometimes extends to the
territories of other nerves, such as the fifth, hypoglossal, spinal acces-
sory, and upper branches of the brachial plexus.
Sensory disorders never form a prominent feature of the disease,
but the patient may occasionally suffer from numbness or even a slight
deuree of pain in the side of the face, and he may also complain of
headache and tinnitus aurium. Vaso-motor and secretory disorders
are never present, the electrical reactions of the affected muscles are
normal, and all the voluntary movements of the face can be executed
with undiminished power. Certain points may be discovered, pressure
on which will arrest the spasm ; these, when present, correspond with
the pressure point in trigeminal neuralgia.
The tonic form of facial spasm was first clearly recognized by Dr.
Marshall Hall. In this form the muscular contraction is persistent,
the tip of the nose, the angle of the mouth, and the chin are drawn to
the affected side, and the furrows and dimples of that side are rendered
deeper. The contracted muscles render the tissues too scanty for cov-
ering the orifices, so that when the eye is closed a tightness is induced
at the angle of the mouth, and when the angle of the mouth is moved
further from the. eye, as in speaking, it is difficult to keep the eye closed,
articulation is rendered indistinct, and tlie bolus of food tends to collect
between the teeth and the affected cheek, causing slight trouble during
mastication, but there is no difiiculty of deglutition.
d. Spasm of the 3Iuscles Supplied hy the Hypoglossal Kerve
{Lingual Spasm, Aphthongia).
Etiology. — Lingual spasm is rare as an independent affection, but is
a common symptom of hysteria, chorea, epilepsy, and eclampsia, while
it often accompanies spasm of the muscles supplied by the fifth nerve.
Spasm of the tongue may also result from meningitis, and lesions of its
cortical motor centre, and it is frequently met with in bilateral athetosis
SPINO -NEURAL SPASMS. 299
and the spasmodic paralyses of infancy, while tremor of the tono-ue is a
symptom of progressive bulbar paralysis, and disseminated sclerosis.
Symptoms. — In lingual spasm the muscles innervated by the hypo-
glossal nerve are thrown into a state of clonic or tonic convulsions
when the patient attempts to speak, the affection being more or less
similar to writer's cramp, and the spasms implicating groups of other
muscles engaged in effecting special movements. In some cases the
tongue becomes fastened to the hard palate by a tonic spasm whenever
the patient tries to speak, but in other cases it is attacked with clonic
spasms, and the sterno-hyoid, thyro-hyoid, and sterno-thyroid may like-
wise be implicated in the convulsion.
c. Spasm of the Muscles Supplied hij the Vagus and
Pharyngeal Plexus.
(1) Spasm of the Soft Palatk, Pharynx, and (Esophagus.
('/) Spasm of the soft palate and Eustachian tuhe is not well known
as a natural disease, but noises in the ears can be induced in healthy
persons by the application of the faradic or galvanic current to the end
of the Eustachian tube, which are caused most probably by contraction
of the tubal muscle. Twitching movements of the palate have occa-
sionally been observed in advanced cases of paralysis agitans.
(h) Spasm of the constrictors of the pharynx usually accompanies
acute pharyngitis and spasmodic stricture of the oesophagus, while it is
a prominent symptom of hydrophobia.
(c) (Esophagismus, or spasmodic stricture of the oesophagus, is fre-
quently met Avith in hysterical women, and some believe that globus
hystericus is the subjective correlative spasm of the oesophagus. It
may be so severe and persistent in some cases of hysteria as to simulate
organic stricture, and the patient may be reduced to the verge of death
by inanition. It is sometimes caused by irritation in the peripheral
course of the nerves, or in a reflex manner in cases of ulcer of the tube,
but it is rare as a result of central disease.
(2) Spasmodic Affections of the Larynx.
(a) SPASM or the glottis in infants or internal convulsions
(laryngismus stridulus).
Etiology. — The predisposing causes of spasm of the glottis in inftmts
are the same as those which tend to produce eclampsia, and, indeed,
the two diseases frequently coexist. Spasm of the glottis usually
attacks children between four and ten months of age : it is more fre-
300 SPASMODIC DISORDEES.
([uent in boys than in girls ; and badly nourished, cachectic, or rachitic
children are almost exclusively affected. The exciting causes are expo-
sure to cold, the irritation of teething, or the presence of parasites or
other irritating substances in the alimentary canal. It may sometimes
be caused by direct irritation of the laryngeal mucous membrane from
excessive crying.
Sympt07m. — The attack generally begins suddenly without premoni-
tory symptoms, and inasmuch as the action of the adductors predominates
over that of their antagonists the glottis is completely closed during
the continuance of the spasm. The attack is characterized by a sudden
arrest of respiration ; the chest becomes fixed : the face is turgid and
of a blue color; the countenance expresses great anxiety: the mouth is
widely open, as if to make a deep inspiration ; the head is drawn back-
wards ; the eves are staring ; the action of the heart is tumultuous and
irregular; and the infant appears to be on the verge of suffocation,
then the spasm relaxes. The paroxysm lasts from two to twenty sec-
onds, and the end is announced by a series of sonorous inspirations, as
if air were drawn through a narrow reed. The last inspiration becomes
longer and more sonorous than the rest, and then the respirations
assume their natural rhythm. During the paroxysm the spasm involves
the extremities, causing flexion of the hand and extension of the feet,
and occasionally the infant is seized with general epileptiform convul-
sions at the end of the attack. The disease may be limited to a single
paroxysm, but it usually consists of a series of paroxysms, coming on at
irregular intervals for many days or weeks. The mortality of the dis-
ease is very great, death occurring suddenly .by suffocation during an
attack, or from nervous exhaustion from frequently repeated attacks.
(6) SPASM OF THE GLOTTIS IN ADULTS.
Spasm of the glottis in adults may be caused by local disease of the
larynx, the inhalation of irritating gases, tlie entrance of morsels of
food into the larynx, or irritation of one of the recurrent laryngeal or
pneumogastric nerves. It may also be caused by centi-al diseases of the
nervous system, like hysteria. Paroxysms of hysteria generally culmi-
nate in a deep stridulous inspiration and opisthotonos. On laryngo-
scopic examination during an attack of spasm the mucous membrane
may be found to be healthy or slightly congested, and the vocal cords
may be seen separating for an instant, and then becoming spasmodically
closed.
SPINO-XEUEAL SPASMS. gOl
(c) SPASM OF THE TENSOKS OF THE VOCAL CORDS (APHONIA SPASTICA).
This condition does not interfere with the respiratory function, but
the voice is rendered feeble, jerky, and intermittent. The patient may
speak a few words in a normal voice, but the current of the voice is
soon partially interrupted, and the sound becomes like the suppressed
voice of a jjcrson engaged in some act requiring a straining effort, like
the act ()f defecation.
(d) SPASMODIC LARYNGEAL COUGH.
The cough caused by spasm of the laryngeal muscles is a shrill or
barking cough of metallic quality, which comes on in paroxysms and
lasts for many hours, only ceasing when the patient sleeps. This
cough occurs in young girls, but is occasionally met with in hojs. The
paroxysmal cough of whooping-cough is caused by a direct or reflex irri-
tation of the laryngeal nerves. The attack begins with a deep inspira-
tion, which is followed by a succession of short and frequently repeated
coughs with no intervening inspirations. When the chest is contracted
to the utmost, and the patient seems on the verge of asphyxia, another
deep inspiration is taken, during Avhich the air, rushing through the
spasmodically closed glottis, makes a characteristic whistling, crowins,
or whooping noise.
(e) TABETIC LARYNGEAL CRISES.
The course of locomotor ataxia is liable to be complicated by parox-
ysms of spasmodic cough, not unlike those of whooping-cough, and which
have been named laryngeal crises. These attacks may be divided into
three varieties according to their degree of intensity : (a) the mild ; (h)
the medium ; and (c) the severe crises.
(a) The mild attacks are like paroxysms of whooping-cough, the dura-
tion of each varying from a few seconds to about ninety.
[h) The medium form is characterized by a more violent cough and
a louder and more difficult inspiration, the duration of the attack being
from five to ten minutes.
(c) The severe form is manifested by symptoms of asphyxia, uncon-
sciousness, and epileptiform convulsions, and the attack may last from
half an hour to several hours.
The attacks vary greatly in their periods of recurrence ; they are
more frequent during the day than during the night, and they may
sometimes be repeated as often as fifty times in the twenty-four hours.
The attack mav be excited by a current of air, sudden exertion, or a
302 SPASMODIC DISOEDERS.
slight catarrli, or it may come on suddenly, and without warning, in
the middle of a conversation or during sleep. At other times the
patient may feel a scalding sensation, or a feeling as if a foreign body
were lodged in the larynx, immediately before the attack.
( f) CLONIC SPASM OF THE LARYNGEAL MUSCLES (CHOREA OF THE LARYNX).
In some cases the laryngeal muscles contract and relax, during attempts
at phonation in such a way that the glottis is alternately closed and
opened in an irregular manner, so that the power of inflecting the voice
is diminished. Gerhardt reports the case of a flutist who was not able
to play his instrument without a continuous noise being caused in his
throat, and he believes that the aff'ection is analogous to professional
spasms in the hand. The laryngeal muscles are subject to clonic
spasms in chorea, and in bilateral athetosis, while they are occasionally
aifected by incoordinate movements in ataxia.
/. Spasm in the Region of the External Branch of the Spinal
Accessory Nerve ( Wry-nech, Caput Ohstipum Spasticum).
Etiology. — The relatives of those suffering from wry-neck are often
subject to hysteria and other nervous affections ; the male sex is rather
more frequently affected than the female, and adults than young or old
people. The most usual exciting causes are excessive exertion, emo-
tional excitement, exposure to cold, irritation of remote organs, while
it sometimes comes on suddenly Avithout assignable cause.
Symptoms. — Spasms of the muscles supplied by this nerve may be
divided into, a, tonic and, 6, clonic wry-neck.
(a) The tonic form is almost exclusively confined to one of the sterno-
cleido-mastoid muscles, but a part of the trapezius is sometimes aff'ected.
In this form of the disease the head is rotated so that the occiput is
approximated to the shoulder of the aff'ected side ; the ear of the same
side is drawn towards the clavicle ; and the chin is turned upwards and
towards the opposite side. In chronic cases a spinal curvature with its
convexity to the sound side occurs in the cervical region, and compensa-
tory curves in the dorsal and lumbar regions.
When the trapezius alone is the seat of the spasm the head is drawn
strongly backwards and is inclined to the opposite side ; there is no turn-
ing of the chin ; the point of the shoulder is elevated ; and on any
attempt being made to bend the head forwards the muscle becomes tense
and painful (Fig. 89).
{h) The clonic form of the disease may be either unilateral or
bilateral.
S P I K O - X E U R A L SPASMS,
803
The unilateral variety begins with uneasiness in the neck, and it is
soon noticed by the patient or his friends that the head is not stniio-ht.
As the disease advances the patient comphiins of a dull achino- pain in
the course or at the insertion of the muscle, and when the spasm is
limited to one of the sterno-cleido-mastoid muscles, the head becomes
rotated obliquely to one side by a succession of jerks, the occiput beino-
turned towards the shoulder and depressed, and the chin elevated in the
opposite direction. The muscles on the side to -which the head is
drawn are hard, contracted, and frequently hypertrophied. When the
trapezius is affected, the head is bent back and the shoulder raised in
the manner already described. At the end of a short time, generallv a
Fig. 89.
Spasm of the Tkapezius. (Fioni Dlchexxe )
few seconds, the muscle relaxes and the head returns to the normal
position, but this is soon followed by a second contraction and a second
rotation. At first there may be a considerable interval between the
contractions, but as the disease advances the interval is shortened, and
ultimately the contractions may number twenty or thirty in the minute.
In an early stage the patient may arrest the spasm by a voluntary
effort, or counteract it by a voluntary contraction of the muscles of the
opposite side, but in long-standing cases the voluntary is overpowered
by the involuntary contractions, and the head is habitually twisted to
one side, except, indeed, when the patient counteracts the deformity by
holding his head between both hands, or placing it against a resisting
;304 SPASMODIC DISORDERS.
object. Patients are distressed by wakefulness caused by constant move-
ments of the head against the pillow, but as sleep is approaching they
feel the movements becoming gradually less, and the spasm generally
ceases entirely during sleep.
The disease is rarely confined to the muscles supplied by the spinal
accessory nerve, and it is even probable that the splenii and obliqui
capitis are often the first attacked, and they are at least generally impli-
cated. When the scaleni are affected oedema and some degree of anes-
thesia of the corresponding arm may be present from compression of
the brachial plexus and veins. Facial tic and masticatory spasm may
be associated with clonic spasmodic torticollis, and in aggravated cases
the spasm extends to the muscles supplied by the cervical and brachial
plexuses. The clonic form of the disease is generally unilateral, but
occasionally the spasm invades both sides, and then the head is rotated
first to the one side, and after a time to the other, according as the
action of the muscles of one side or of the other predominates. Occa-
sionallv the two muscles may hai)pen to contract simultaneously, and
the head is then bent forwards and the chin drawn to the sternum.
The faradic irritability of the affected muscles, and the faradic sensi-
bility of that side are increased. A constant current of moderate
strength may relax the spasm for a moment, but it soon returns when
the current is Avithdrawn. Points of arrest are frequently found in the
course of the nerve or over the affected muscles.
The bilateral clonic Avry-neck (eclampsia nutans, salaam convulsion)
is almost exclusively met with in children from the first period of den-
tition to puberty. The spasm comes on in paroxysms, each of which
lasts only from a few seconds to some minutes, but generally recurs
two or three times, or many times in the course of the day. During
the attack the body and head are bent slightly forwards, and this is
followed by almost instantaneous relaxation, to be succeeded after an
interval of a few seconds, by a second bowing of the head, and so on
until the paroxysm ceases after from twenty to one hundred alternate
contractions and relaxations. The spasm in the neck has frequently
associated with it some degree of facial spasm, Idepharospasm, strabis-
mus, or a slight convulsive movement of one or other arm, and at other
times attacks of general convulsions intervene, so that the case becomes
manifestly one of ordinary epilepsy. During the attack the child
seems bewildered, but there is no complete loss of consciousness, and
as soon as the movements cease the patient may be ([uite bright and
happy, but occasionally the attack is followed by exhaustion and
<lrowsiness.
SPIXO-NEURAL SPASMS.
305
(J. Sjyasm of the Musdes supplied by the Cervical Plexus.
(1) Spasm of the Muscles of the Neck.
(a) Spasm of the splenius capitis causes the head to be drawn back-
wards and towards the affected side (Fig. 90), and the chin to be some-
FiG. no.
Spasm of Splenus
what depressed and directed towards the aftected side, Avhile a hard
ridge can be felt at the point where the splenius appears beneath the
anterior l)order of the trapezius. The spasm is generally tonic with
remissions and occasional more energetic contractions.
(h) Spasm of the ohliquus capitis inferior causes either intermittent
or persistent rotation of the head around its vertical axis without eleva-
tion of the chin or depression of the mastoid pi'ocess.
(e) Spasm of the deep muscles of the neck is characterized by
stronor backward rotation of the head when the affection is bilateral, or
towards the affected side Avhen it is unilateral.
(2) Spasm of the Diaphragm.
{a) Tonic spasm of the diaphragm causes so much dypsnoea that the
patient is threatened with asphyxia. The lower half of the chest is
expanded and immovable, and the epigastrium is made to project
strongly, whilst rapid and superficial respirations are effected with the
20
806
SPASMODIC DISORDERS,
upper part of the chest. There is severe pain in the epigastrium and
alon(^ the attachments of the diaphragm, the voice becomes feeble and
muffled, there is Avell-marked cyanosis, and the attack proves fetal if it
last beyond a short time.
{b) Qlonic spasm of the diaphragm, singultus or hiccough consists of
short energetic contractions of the diaphragm accompanied by an inspira-
tory sound, which is usually suddenly arrested by closure of the glottis.
The contractions may succeed each other at tolerably long intervals or
may occur in rapid succession, and the attack may last from a few
minutes to many hours, or, in aggravated cases, for weeks, and they
may recur more or less fre([uently for years. Hiccough is caused by
reflex irritation from neighboring or remote organs, and it is to be
regarded as an ominous sign in cancer of the abdominal viscera and
in cachectic conditions. It is often of hysterical origin, and it may be
caused by direct irritation of the roots of the phrenic nerves from cer-
vical pachymeningitis.
h. Spasm of the 3Iusc/cs supplied by the Brachial Plexus.
(1) Spasm of the Muscles of the Neck and Trunk.
(a) Spasm of the rhomboidci manifests itself by the peculiar position
of the scapula (Fig. 91). Its inner border assumes an oblique position
ViG. 91.
Contraction of Rhomboid Muscle.s. (Duchenne.)
A, Levator scapulae ; B, Ketracted rhomboid ; C, Fibres of serratus magnus ; D, Abnormal position of
the inferior angle of the scapula ; E, Inferior angle on the healthy side.
SPINO-NEUEAL 8PASMS. ;-507
from above dowiuvanls and from within outwards, the lower an-de is
drawn upwards and approximated to the vertebral column, the m'uscle
can be felt as a firm swelling between the scapula and spinal column,
and it offers a distinct resistance when an attempt is made to raise the
arm to a vertical position.
{b) Spasm of the Levator Anguli Seapuke. — The upper and inner
angle of the scapula is strongly elevated, the head is slightly inclined
to the same side, the shoulder is drawn somewhat forwards, the supra-
clavicular fossa is increased in depth, and the contracted muscle projects
distinctly beneath the anterior liorder of the trapezius, which can easily
be isolated from it by faradization.
(c) Spasm of the serratus magnus, latissimus dorsi, the teres major
and minor, the supra- and infraspinati, the subsrapularis, or the pee-
toralis major, is rare. It may be readily recognized by the position
assumed by the scapula and arm, and the kind of interference with
their movement, along with the hardness and fulness felt over the
affected muscle. The diagnosis is aided by a comparison with the
deformity produced by faradization of the corresponding muscles of the
opposite side.
(2) Spasm of the Muscles of the Upper Extremity.
(a) Spasm of the Muscles Supplied by the Circumflex Nerve. — In
the tonic form of spasm the arm is held out from the body, and it is
also directed backwards in those cases in which the j)Osterior fibres of
the deltoid and teres minor are aff"ected. The lower angle of the scapula
is pressed backwards towards the vertebral column, as in paralysis of
the serratus magnus. In cases of clonic spasm of the deltoid the arm
is thrown upwards and moved convulsively in various directions, but
other muscles are usually implicated at the same time.
(b) Sjjasm of the muscles supplied by the musculo-cutaneous nerve
causes some resistance to passive abduction of the arm, and strong
flexion of the forearm.
(c) Spasm of the muscles supplied by the musculo-spiral nerve causes
extension of the forearm at the elbow, of the hand at the wrist, of the
fingers at the metacarpo-phalangeal articulations, and of the thumb at
both the metacarpo-phalangeal and phalangeal articulations, as well as
supination of the forearm.
(d) Spasm of the Muscles Supplied by the Median Nerve. — In spasm
of these muscles the forearm is strongly pronated ; the hand is bent
towards the radial side ; the fingers are flexed ; and there is apposition
of the thumb. Spasm of the muscles of the hand supplied l)y the
308 SPASMODIC DISOEDEKS.
median produces apposition of tlie thumb, Avith approximation and slight
flexion of the first phalanges of the index and middle fingers.
(e) Spasm of the 3Iusdes Supplied by the Ulnar Nerve.— In spasm
of these muscles the hand is rendered concave ; the thumb is adducted ;
the little finger is strongly flexed and opposed ; and the remaining
fingers are moderately flexed at the metacarpo-phalangeal and extended
at the phalangeal articulations. The position assumed by the hand in
spasm of the interossei is shown in Fig. 92.
Fig. 92.
Position of the Hand in Spasm of the Interosseous Muscles. (After riowEas.)
(/') Writer s Cramp and Allied Affections {Graphospasmus, Mogi-
l/raphia. Professional Hyperkiyieses). — Writer's cram]) is only one of
a large group of aftections which have been called professional hyper-
kineses. This name has been given to them because the spasm aff"ects
muscles engaged in delicate associated and acquired actions, such as
those required for writing, piano-forte playing, sewing, etc.
Etiology. — Writer's cramp is most frecjuently met with in men, while
piano-forte player's spasm occurs most frequently in women. Profes-
sional spasms of all kinds are liable to occur in nervous subjects and
neuropathic families. The spasm may be caused by exposure to cold,
injuries of nerves or muscles, and foreign bodies in the fingers, or it may
be caused in a reflex manner by periostitis of the external condyle of
the humerus. The main cause, however, of writer's cramp is excessive
writing, and consequently it is most frequently observed in secretaries,
clerks, and merchants. The other professional cramps are also caused
in the same way by the excessive use of particular groups of muscles.
Symptoms. — Writer's cramp may be divided into (1) the spastic,
(2) the tremulous, and (3) the paralytic forms.
(1) In the spastic form of the disease some of the muscles of the
hand are seized with tonic or clonic spasms whenever the patient tries
to use the pen and this gives rise to an irregular stroke in the writing.
The patient may, indeed, be quite unable to write Avhile holding his
pen in the usual position, but he is often able to do so tolerably well by
holding it in a new and more or less grotesque manner. After a time
SPINO-NEUEAL SPASMS. 309
the spasm becomes stronger ; the thumb and first finger may be sud-
denly extended so that the pen drops, or there is a spasmodic action of
the opponens pollicis, with abduction and flexion of the index-finc^er
and the pen is thus rapidly moved away from the paper. At other
times there is spasmodic flexion of the first three fingers, which then
become pressed tightly against the pen, so that it cannot be moved fur-
ther onwards ; or there may be movements of pronation and supination
in the forearm, and the pen is raised from the paper, and moved back-
wards and forwards in the most irregular manner. The faradic con-
tractility of the affected muscles is sometimes increased, and at other
times diminished, the former probably indicating an early, and the
latter a late stage of the affection.
(2) In the tremulous form of the disease the hand and forearm, or
even the whole arm, are the subjects of Avell-marked tremors on any
attempt at writing, so that the pen only makes undulating or angular
strokes. The writing is altered in character ; the strokes are coarse,
imperfect, and unequal, and numerous irregularities and false strokes
are to be observed, while in the highest degrees of the aftection the
writing becomes a mass of undulating and zigzag strokes, and wholly
illegible.
(3) In the paralytic form the patient experiences great fatigue and
weakness of the hand and forearm on attempting to write, but as soon
as the pen is laid down the feeling of weakness and exhaustion disap-
pears, to reappear when it is taken up again.
In those who suffer from writer's cramp the movements requisite for
sewing, piano-forte playing, embroidery, buttoning-up the clothes, and
all actions requiring delicate manipulation are also impaired ; and if
the patient has learned to write with his left hand, the spasm, to his
great disappointment, frequently extends to it also.
The most common sensory disorder is an undefined feeling of strain-
ing and fatigue, a sensation of pressure in the affected muscles, a pain-
ful drawing of the nerves in the direction of the trunk, or a feeling of
coldness in the whole arm.
The pain frequently extends to the shoulder and back, and some of
the spinous processes of the cervical and dorsal vertebrpe may be tender
to pressure.
Other spasmodic disorders are not infrequently associated with
writer's cramp, the most frequent of these being strabismus, stammer-
ing, and spasms of the face, throat, and other parts of the body, while
weakness and tremors of the lower extremities occasionally occur. In
addition to the mental depression caused by failure of the hand the
patient is often of an anxious disposition, and subject to general nei-v-
310 SPASMODIC DISORDERS.
ousness, which makes tlie writing worse when executed in the presence
of a spectator.
The following are a few of the other professional hjperkineses :
Piano-forte player s spasm is not uncommon in professional players,
especially women, and the spasm is in every respect similar to that of
writer's cramp.
Telegraphist's cramp has been met in France with the use of Morse's
machine, in which the letters are represented by an association of dashes
and dots.
Violin-player's spasm occurs either in the form of painful exhaus-
tion and stiffness, or as a convulsive spasm of some of the muscles of
the hand, arm, or shoulder. It may attack the right or left hand, and
it renders playing impossible.
Tailor s and shoemaker s spasw is of the same kind as the other
professional spasms, and as soon as the patient begins to Avork, tonic or
clonic spasms, or functional debility of the muscles of the hand and
arm, are experienced.
Spasmodic movements have been described as occurring in smiths,
milkers, painters, makers of artificial flowers, harp-players, turners,
and watchmakers.
i. Spasms of the Muscles supplied hy the Dorsal Nerves.
(1) Spasms of the Kespikatory Muscles.
{a) Inspiratory spasni differs considerably from hiccough, although
the latter frequently complicates the former. The essential feature of
the affection is that many or all of the muscles particii)ate in the
spasm, and that a true inspiration, unbroken by sudden closure of the
glottis, takes place. The spasm consists of a more or less rapid suc-
cession of deep inspirations, whilst the intervening expirations are per-
formed in the usual noiseless way. The chest is powerfully expanded,
the epigastrium is protruded, the auxiliary muscles of respiration are
excited to action, the pectoral and sterno-cleido-mastoid muscles are
brought into strong relief, the shoulders are raised, the head is drawn
backwards, and the respiratory muscles of the face, ala nasi, and eye-
lids enter into strong contraction. Inspiration is noisy, and often
accompanied by eructations of gas from compression of the stomach.
The spasm usually occurs in paroxysms of variable duration, the ab-
domen is generally tympanitic, and there are, as a rule, other symptoms
of nervous derangement, especially those characteristic of hysteria.
{b) Attacks of sneezing {sternutatio eonvulsiva) occur in a parox-
ysmal and spasmodic form, so that the patient will sometimes sneeze
SPTNO-NEURAL SPASMS. 311
several hundred times in succession. Ordinary sneezino- is a reflex
act excited by irritation of the nasal filaments of the fifth nerves.
Attacks of sneezing are generally accompanied by a profuse watery
secretion from the nose, and, when of long duration, they are produc-
tive of great misery.
{(■) Attacks of y<iwning {osredo, chasme) consist of a succession of
yawns following one another with greater or less rapidity, and are
accompanied l)y the well-known phenomenon of gaping, flow of saliva,
increased flow of tears, and diminution in the acuteness of hearing,
with dull tinnitus aurium.
(d) Spasmodic cough comprises all those paroxysmal attacks of
coughing Avhich are accompanied by a loud ringing sound. Such
attacks of coughing may last for a variable ])eriod, and may also recur
frequently for months or years.
{e) Fits of laughin;) or crying are a form of expiratory spasm, the
former consisting of a succession of loud expirations accompanied by
vocal tones, and the latter of long-drawn expirations, often interrupted
by sobs and generally by a profuse secretion of tears. These actions
are accomjianied by well-known mental states, and by characteristic
fecial expressions. In pathological conditions they may be independent
of emotional disturbances, and they then constitute subordinate symp-
toms of several general neuroses, such as hysteria, or are produced by
disease of the central nervous system.
(/) Spasm of the Dorsal and Abdominal Muscles. — The dorsal
muscles are the subjects of a strong tonic spasm in tetanus, and some-
times in hysteria, wdiile they are affected by both tonic and clonic
spasm in attacks of epilepsy and eclampsia. They may also be affected
by spasm in cases of lateral spinal sclerosis, and various other central
aff'ections. The abdominal muscles are also ;iffected by spasm in cen-
tral nervous affections, and they are the subjects of spasm in l)iliary
calculi and all ])ainful affections of the abdominal organs. In spasm
of the muscles of the l»ack the body is strongly arched backwards, a
condition which has been named opisthotonos, or when the action of
the muscles of one side predominates it is arched backwards and to
one side, a condition named pleurosthotonos.
In spasm of the abdominal muscles the walls of the abdomen become
hard, tense, and resisting,- and as it is generally accompanied by spasm
of the dia})hragm, the breathing is of the upper costal type, and be-
comes accelerated and shallow.
312 SPASMODIC DISORDERS.
h. Spasm of the Muscles supplied hy the Lumbar and Sacral Nerves.
(1) Spastic contracture of the hip consists of a tonic spasm of the
psoas and iliacus, the quadratus lumborura, and occasionally of one or
two of the muscles of the front of the thigh. The extremity is flexed
at the hip-joint, the tendon and muscular belly of the ilio-psoas muscle
project strongly, the pelvis appears to be raised on the aftected side,
the limb is shortened, and the patient inclines to the afiected side in
walking. Any attempt to extend the limb causes acute pain in the
tense muscles and in the knee. This aifection is caused by disease of
the lumbar vertebrae with psoas abscess, and by reflex irritation in
disease of the hip-joint.
(2) Spasm of the quadriceps extensor femoris gives rise to rigid
extension of the leg on the thigh, and is observed in tetany and neu-
ralgia of the knee-joint. Clonic spasm of the extensors of both sides
was observed in a case in which no obvious cause could be traced.
The spasms recurred at brief but irregular intervals, and gave a pecu-
liar hopping character to the gait.
(3) Contracture of the adductors of both thighs approximates the
knees together, and is a symptom of lateral sclerosis of the spinal cord.
It also occurs in tetany, and is probably caused sometimes by reflex
irritation from disease of the hip-joint, or from genital irritation.
I. Spasm of the Muscles supplied hy the Sciatic Nerves.
(1) Spasm of the flexors of the leg causes the leg to be flexed on
the thigh, and in aggravated cases the heel is brought in contact with
the buttocks. It occurs in hysteria, diseases of the knee-joint, and
spinal diseases.
(2) Spasm of the anterior muscles of the leg is of rare occurrence.
A painful contracture of the tibialis anticus, peroneus longus, and gas-
trocnemius is described by Dr. S. Weir Mitchell as occurring in young
people after long standing, and leading to deformity of the feet.
Spasm of the peroneus - longus plays an important part in the produc-
tion of certain forms of club-foot, and is, according to Duchenne, of two
kinds, the first consisting of persistent contraction of the muscle ; the
second of a functional spasm which occurs only when the leg is brought
into use. The latter form is particularly liable to occur in congenital
spasmodic aflections.
(3) Spasm of the muscles of the calf produces talipes equinus, in
which the heel is strongly elevated and the toes depressed. The well-
SPINO-NEURAL SPASMS. 813
known "cramps" of the calf belong to this variety, and it occurs in
sciatica and painful affections of the knee-joint.
(4) Diffused spasm of the muscles of the lower extremity of one or
both sides occurs in hysteria, as a motor aura in epilepsy, and in spinal
diseases.
2. General Spino-neural Spasms.
a. Saltatory Spasm.
Etiology. — In all cases of this disease either a decided neuropathic
disposition has been clearly traceable or the patients themselves have
been subjected to depressing influences before the attack. The male is
as frequently attacked as the female sex, and the ages of those aftected
range from ten to seventy years.
Symptoms. — In this affection singular spasms of the muscles of the
lower extremities arise when the sole of the foot is placed upon the
ground, which have the effect of throwing the patient repeatedly in the
air. These spasms continue so long as the patient maintains the erect
posture, and they cause the patient to hop and jump on the floor, and
render him quite unable to stand still for an instant. In some cases
the feet are thrown oft' the ground at every spring, and in others the
hopping movements are caused by quickly alternating elevations and
depressions of the heel, while in one of two cases reported by Gowers,
the springing movements w^ere made from the hip and knee-joints.
The movements disappear when the patient sits or lies down, but in
most cases they can be made to reappear by pressing on the soles of the
feet. The onset of the symptom is, as a rule, more or less sudden, but
in a few cases premonitory symptoms such as a sense of w^eight, tearing
pains, or slight tremors, have been observed. The spasms may disappear
in a few days or last for many weeks, and they may recur after a per-
fectly free interval. The distribution of the spasms varies greatly, they
are at times limited to the legs, while at other times they extend to the
muscles of the back, face, neck, and pupils, but the arms always remain
unaffected. Emotional excitement has sometimes been found to aggravate
the spasm and at other times to arrest it.
h. Tetanus.
Etiology. — Tetanus may be of traumatic or idiopathic origin. Trau-
matic tetanus, which is by for the more important and frequent variety,
is caused by punctured, lacerated, or contused wounds, and may even
;->14 SPASMODIC DISORDERS.
result from contusions without external abrasion, but is rare after incised
wounds. The extent and severity of the wound do not appear to bear
any direct relation to the frequency of tetanus, and in some cases the
primary wound is healed and forgotten when the symptoms make their
api>eai-ance. The interval between the injury and the development of
tetanus varies ; the average duration is from four to fourteen days, but
the symptoms may begin in a few hours or be delayed many weeks after
the injury. Various causes may cooperate with the external wound in
the production of tetanus, the most potent of these being exposure to cold
and damp after the patient has undergone great excitement and fatigue
like that caused l)y a great battle. The absence of antiseptic dressings
and other improper treatment seem to increase the liability to tetanus.
The most usual cause of idiopathic tetanus is exposure to cold and
damp, more especially when the patient is warm and perspiring. It may
occur in the course of pleurisy, peritonitis, and other acute diseases.
Malaria appears to give rise occasionally to an intermittent tetanus which
may be cured by quinine. Strychnine and other toxic agents cause
symptoms resembling tetanus.
Symptoms. — Premonitory symptoms are generally observed in tetanus,
consisting of shivering or a distinct rigor, sensation of dragging in the
neck, stiffness in certain muscles, difficulty of articulation and degluti-
tion, and yawning. In traumatic cases the wound may become sensitive,
and the patient complain of shooting pains radiating from it. These
symptoms may occur a few hours or even a few days before the charac-
teristic tonic spasms make their appearance.
The spasms, as a rule, begin in the muscles of the jaw. At first the
jaws can be separated, and the movements of cheAving and swallowing
be accomplished, although with difficulty. Soon, however, the jaws
become firmly clenched, constituting the condition called trismus ;
swallowing of even a small quantity of fluid is difficult and fatiguing
owing to spasm of the <x\sophagus ; while articulation is indistinct, and
the voice altered, partly from the difficulty of moving the toncrue, and
partly from implication of the muscles of tlie larynx.
Spasm of the facial muscles gives to the countenance a characteristic
expression. The angles of the mouth are drawn outwards, being at the
same time depressed or elevated, and the lips are often drawn apart and
expose the set teeth, so that the face assumes a sneering expression,
named the "n-SMS sardonicus." The nostrils are dilated ; the eyes are
staring and motionless ; the pupils are generally contracted ; the brow
IS wrinkled ; and all the lines of the face become strongly marked, and
give to the patient an aged appearance.
The spasm rapidly extends to the muscles of the back of the neck,
SPINO-NEUKAL SPASMS. 315
causing retraction of the head ; while the erectove spinae soon become
implicated, and the vertebral column is then arched backwards; the
chest is projected forwards and rendered very broad ; and the body rests
on the back of the head and sacrum, constituting the condition called
opisthotonos. The epigastrium is sunk, and the abdomen flattened,
while the hardness assumed by the abdominal muscles is characteristic.
On rare occasions the body is said to be bent forwards, the convexity of
the arch being directed backwards, a condition named emprosthotonos.
In a few cases the bodv is maintained in a rigid attitude without beino-
curved in any direction, a condition named orthotonos ; and in some
rare cases it is curved laterally — plcurosthotonos.
The muscles of the extremities are usually not affected to so great
an extent as those of the trunk, neck, lace, and jaws. The muscles of
the lower extremities are, however, generally implicated to a greater or
less extent ; and extension, as a rule, predominates over flexion during
the spasmodic attack, although flexion at individual joints has occasionally
been observed. During the attack the varioris segments of the lower
extremities are extended upon one another and upon the trunk, so that
the patient rests on the head and heels ; the toes are extended and
spread out ; and the feet are everted. Even in severe cases the muscles
of the upper extremities may remain comparatively unaffected, but if
passive motion of the forearm be attempted, increased muscular resistance
is readily perceived. When the spasm extends to the muscles of the
upper extremities, flexion predominates over extension ; and during the
paroxysms the arms are drawn close to the chest ; the forearm is flexed
upon the arm ; the hand is flexed at the wrist; and the fist is closed,
the palm being directed towards the upper arm (Fig. 93).
In some cases the spasm persists continuously from the beginning to
the termination of the disease ; but, as a rule, the spasmodic rigidity
of the muscles occurs in paroxysms with intervals of comparative, but
never complete muscular relaxation. Each paroxysm lasts from a few
seconds to several minutes, or with slight remissions for hours ; while
the duration of the free interval varies from ten minutes to hours, but
at other times the spasms recur and remit with such frequency that they
assume a more or less clonic character. As the disease progresses, the
paroxysms of spasm recur with greater frequency, and muscular con-
traction is sometimes so violent that teeth are broken, long bones frac-
tured and powerful muscles torn across. The paroxysms recur spon-
taneously, but they are induced by the most trivial external cause, such
as a draught of air, a sudden noise, or an attempt to swallow or to
administer an injection. Attempts at swallowing may, indeed, provoke
an attack so readily that the disease may bear a certain resemblance to
516
SPASMODIC DIS0EDEE3.
hydrophobia. The spasm occasioned by the attempt may be in the
pharynx, gullet, or in the cardiac end of the stomach, as the oesophagus
passes through the diaphragm. But wherever it may be situated, all
attempts at swallowing are rendered impossible, and fluids introduced
are ejected through the nose and mouth, so that the patient can neither
be fed in the usual way nor by the stomach pump. During the paroxysm
the action of the inspiratory preponderates over that of the expiratory
muscles, so that the act of coughing is rendered impossible, and mucus
accumulates in the bronchi. In severe paroxysms the chest becomes
fixed ; the countenance is livid ; the eyes are suffused ; the patient foams
Fig. 93.
Taken from the okiginal painting by Sir Charles Bell. (From Spence's "Surgery").
at the mouth ; and he is tormented with a feeling of dread and suffoca-
tion. Arrest of respiration may sometimes be caused by spasm of the
glottis ; but, as a rule, it is the result of spasm of the thoracic muscles
and diaphragm. In the intervals respiration is only slightly changed
in freciuency, but it is accompanied by a painful sensation of increased
resistance, requiring effort. Motor paralysis is a rare symptom of
tetanus. Rose observed paralysis of the muscles of one side of the
face in two cases, and in one of them the tetanus was caused by a deep
wound over the upper jaw, so that the lesion was situated in the area of
distribution of the facial nerve. Similar cases have been recorded by
others. General muscular weakness, and paralysis of certain groups
of muscles are observed as terminal phenomena, and strabismus is,
according to Wunderlich, a precursor of death.
The sensory disturbances in tetanus are such as are usually produced
by intense muscular cramp in the muscles of the calf. Some observers
SPINO-NEURAL SPASMS. 317
liave noticed an increase of the sensibility to pain independently of the
spasms, while at other times the acuteness of the senses of touch and
temperature may be diminished. Pargesthesife, such as numbness,
tickling, and tingling, have occasionally been observed. Pain at the
epigastrium, piercing through to the back, is, according to some authors,
a pathognomonic symptom of tetanus. It is present during both the
tetanic paroxysms and the intervals, and depends most probably upon
spasm of the diaphragm.
PsyeJiical disturbance is generally absent in tetanus. The mind is
almost always clear from the lieginning to the end of the disease
although delirium or coma may supervene a short time before death,
often due to the remedies used. Sleeplessness is one of the most
troublesome symptoms of acute cases of tetanus, and even in subacute
cases sleep is only obtained at broken intervals. The spasms cease
during sleep and the narcosis of opium or chloroform. The skin is hot
and bathed in perspiration, having a peculiar pungent smell, while the
surface may be covered by sudamina as in other cases of profuse sweat-
ing. In the majority of cases the temperature ranges from 101° F. to
103° F., and may even rise suddenly to 105° F. in cases which re-
cover, although it is not maintained long at this level except in fatal
cases. In many cases there is hyperpyrexia immediately before death,
the temperature rising to 108° F. or even 112° F., and it may continue
to rise for some hours after death.
The pulse may remain normal during the first stage of tetanus, but
there is a considerable increase in its frequency during the tetanic
seizure, and in the last stage, especially Avhen there is elevation of tem-
perature, it may beat as often as 180 in a minute. Listen observed in
a case of amputation during tetanus the vessels so contracted that not a
drop of blood had escaped.
The daily quantity of urine passed in tetanus is usually below the
average in health; the reaction is strongly acid; the specific gravity is
high ; and there is generally an abundant deposit of urates on cooling.
Sugar in the urine in tetanus was first discovered by Demme, and its
presence has since been detected by others. Senator found that the
excretion of nitrogen was not increased in tetanus as compared with
the amount excreted by a person fasting. He also states that the crea-
tinine is not increased. There may be retention of urine, caused prob-
ably by spasm of the sphincter, while at other times dribbling may
occur during the paroxysm. The bladder is, however, never affected
to so great an extent as it is in acute spinal meningitis. Spasm of the
sphincter ani is often present, as is proved by the difficulty of intro-
ducing an enema pipe.
31^ SPASMODIC DISOKDEKS.
The general liealth of the patient suffers greatly during the course of
the disease. The distorted position of the body, the persistent sleep-
lessness, the difficulty of respiration, and the impossibility of swallowing
combine to render the state of the patient extremely distressing. The
bowels are constipated, the tongue is generally coated, a tenacious viscid
saliva accumulates in the mouth, and the patient may be excessively
hungry and tormented with thirst, yet can swallow neither food nor
drink.
The intensity of the disease is variable. The symptoms in slight
cases may consist only of trismus and some stiffriess of the neck ; in
other cases they develop rapidly and prove fatal in a few days, or occa-
sionally in a few hours from the commencement. Death may take
place during a paroxysm from asphyxia caused by respiratory spasm ;
from sudden arrest of the heart's action : or from a gradual cessation of
the heart's action during a paralytic stage.
In cases of recovery the convulsive attacks become lighter and less
frequent, but a considerable degree of muscular rigidity persists long
after the paroxysms have disappeared. Recovery takes place in from
one to eight weeks, or even longer, and a certain degree of weakness
and stiffness may remain in the muscles for a long time.
In the tetanus of strychnia the masticatory muscles are rarely attacked
first, and may possibly escape altogether ; the symptoms are well marked
at the commencement, and reach their full development in a few minutes:
opisthotonos is a very early symptom. There are usually intervals of
complete intermission ; and death occurs commonly in three hours, or
else recovery is very rapid.
c. Tetany (Tetanilla).
Etiology. — Tetany occurs most frequently between the ages of seven-
teen and thirty years, but it is not unfrequent in children from the
fourth to the sixth years of age. Amongst the predisposing causes of
the affection may be mentioned disordered menstruation, the puerperal
state, and pregnancy, and persons are particularly liable to be attacked
at the age of puberty. Tetany has sometimes been observed as one of
the sequelae of typhoid and other fevers, and either obstinate constipa-
tion or exhausting diarrhoea appears to predispose to the disease, while
it is probable that many cases are of rheumatic origin. Of the existing
causes the most frequent are exposure to cold, fright or other emotional
disturbance, Avhile it may occasionally occur as an epidemic amongst
girls at school.
SPINO- NEURAL SPASMS. ::;i9
Symptoms. — The affection generally begins by tingling and feelincrs
of heat and cold in the hands, or by decided pains in the forearm and
hand or in the calves of the legs. Soon afterwards the fingers feel stiff"
and after a time this feeling increases to the decided spasm which consti-
tutes the chief feature of the disease. The spasm occurs in paroxysms,
each of which begins with rigidity of the hands and fingers ; the thumb
is strongly adducted ; the fingers are approximated and flexed at the
metacarpo-phalangeal and often extended at the phalangeal joints ; and
the palm is made hollow by the approximation of its outer and inner
borders, so that the hand assumes, as Trousseau remarks, the peculiar
conical form which the accoucheur gives to it when about to undertake
the operation of turning. At other times the second, third, and fourth
fingers are strongly flexed at the phalangeal as well as the metacarpo-
phalangeal articulations, while the index-finger is only slio-htly flexed
and all the fingers are firmly applied to the thumb, while the hand is
usually strongly flexed at the wrist and directed to the ulnar border,
although occasionally it is hyper-extended. The different positions
assumed by the fingers and thumb may, indeed, be imitated by a pow-
erful faradic excitation of the ulnar nerve, or by a simultaneous excita-
tion of the ulnar and median nerves. When the spasm extends upwards
the upper arms are strongly adducted, and the forearms are semi-flexed
and are thus crossed upon the epigastrium. The spasms frequently
extend to the lower extremities ; the toes are then drawn towards one
another and strongly flexed ; the sole is hollowed out in the same man-
ner as the hand ; the dorsum of the foot is strongly arched ; the heel
is drawn strongly upwards by the contracted muscles of the calf: and
the lea; and thio;h are in a state of rigid extension.
From the extremities the spasm extends to other portions of the
body, but it is only very rarely that a large portion of the muscles of
the body is simultaneously attacked, although in aggravated cases
the spasm may invade the abdominal muscles and the bladder, as well
as the muscles of the face, eyeballs, tongue, jaws, neck, and larynx.
Extreme and dangerous symptoms may occasionally be caused by spasm
of the muscles of respiration, including the diaphragm.
During the continuance of the spasm the affected muscles feel hard,
tense, resisting to passive movements, and although the degree of con-
traction undergoes considerable variations during the attack, yet the
muscles never become entirely relaxed. Each paroxysm may last for
a few minutes or a quarter of an hour only, but in some cases it may
continue for some hours ; its violence then gradually abates, but a
painful feeling of fatigue and a certain amount of rigidity of the mus-
cles are generally felt for some time after the active spasm has ceased.
y-jJO SPASMODIC DISORDERS.
After u variable period of time the paroxysms recur, and although the
interval between them may, in some cases, extend over some days or
even weeks, yet it is, as a rule, only a feAV hours in duration, and the
attack then recurs several times in the same day. In severe cases the
attacks may follow one another so rapidly that the patient only remains
free from spasm for a few minutes at a time. Erb found a great in-
crease of the electrical excitability in the nerves of the extremities
which supplied the affected muscles, while the galvanic irritability of
the nerve was not only increased, but a tetanic contraction was also
obtained by a feeble current during cathodal closure and even with
anodal opening.
The attacks are preceded and accompanied by tingling, formication,
numbness, and other abnormal feelings, while, in addition to the pain
felt in the tense muscles, a tearing sensation is experienced in the
course of some of the nerve trunks. The sense of touch is impaired,
and the patient foils to appreciate the size and hardness of objects
grasped, which feel as if they were wrapped in some thick material,
and when the lower extremities are affected the subject feels as if he
■were Avalking on carpet. The paroxysms of tonic spasm are said by
Trousseau to be preceded and accompanied b}^ loss of muscular power :
'•movements of extension," he says, ''are not the only ones abolished
by the convulsive contraction of the muscles ; those of flexion are
equally so. The fingers, for instance, Avhen half flexed, no longer obey
the will, and the patient cannot close them further," and Buzzard has
made a similar observation. The joints, especially the small joints of
the hand, may be red, swollen, and painful, and during the acme of the
attack the body may be bathed in perspiration, so that the patient may
seem to be affected with acute rheumatism, and this appearance has,
indeed, led many pathologists to believe that the disease is of rheumatic
origin. Disorder of the general health, although frequently present as
predisposing to tetany, does not appear to be an essential ])art of the
disease ; but in severe cases a certain degree of fever may be present,
and the patient may complain of headache, giddiness, and humming
noises in the ears. The mental faculties are ahvays unimpaired, except
in those severe and exceptional cases in Avhich the respiratory troubles
become so aggravated that the patient is threatened with asphyxia.
The symptoms of tetany generally appear suddenly on exposure to
one of the exciting causes of the affection. Such paroxysm is generally
of short duration, but the attack is liable to recur for a period of weeks
or even months. The disease almost always terminates favorably,
although a case is mentioned by Trousseau which terminated fatally
from respii'atory spasm.
SPIXO-NEUEAL SPASMS. 321
8. Myopathic SPAS.Mr
a. Local Myopathic Spasviis.
A large number of spasms are caused by local disease of the affected
muscles. The stiffness which accompanies muscular rheumatism, and
the temporary spasm of the muscles of the neck which is caused b\
exposure to cold, are examples of a local affection of the muscles,
although it is possible that even in these affections the intra-muscular
nerve-endings may take a chief part in the production of the spasm.
h. General Myopatlik Spasms {Thomsens Disease).
Etiolony. — This disease, which was first described by Thomsen, who
is himself a sufferer, is often inherited, and may appear in several
members of the same family, as well as in successive generations. In
all cases in which a decided hereditary tendency to the disease was
manifested the symptoms appeared in early infancy, but in other cases
the characteristic spasm did not appear until from the fifth to the tenth
year of age. The exciting causes are any slight injury, sucli as a fall
from a carriage, which is accompanied by a severe fright.
SynqJtonis. — The most characteristic symptom of this affection is a
peculiar stiffness and rigidity of the muscles on voluntary movement,
which may increase to a persistent tohic spasm which prevents all
intended actions. When the patient performs a voluntary movement
the muscles contract slowly at first, but when the contractions are once
begun they persist for a long time and only terminate very gradually,
so that patients cannot readily let go articles they have once seized.
The spasms are increased by cold, during the incubation stage of fevers,
after severe and exhausting muscular exertion, and by emotional dis-
turbances. The stiffness is also increased by rest, and the patient ex-
periences great difficulty in beginning any voluntary action, but when,
by a great effort, the intended movement is once begun, it is effected
with increasing freedom, and when the body becomes Avarm by exercise
the actions of the patient are scarcely to be distinguished from those of
healthy persons. The muscles are well developed or even hypertrophied,
the electrical reactions are normal or only slightly diminished, Init a
tetanic contraction is more readily obtained than in health. The nmscles
of the extremities are always affected with the spasm ; in many cases
the erector spinse are implicated, so that the patient suffers from
spasmodic lordosis ; the movements of the tongue are often interfered
with, givino- rise to difficulties of articulation ; the muscles of the neck
21
322 SPASMODIC DISORDERS.
are sometimes also aifectecl, so that on rotation of the head it is liable to
be fixed for some time in a distorted position : and in some cases the
patient experiences difficulty in opening his mouth owing to spasm of
the masticatory and lower facial muscles, while in a case reported by
Ballet and INIarie the patient observed at one time of his life that when
he looked upwards his eyes became fixed and he experienced consider-
able difficulty in bringing them to the horizontal position. In one
reported case the phenomena of this disease coexisted with all the char-
acteristic symptoms of pseudo-hypertrophic paralysis. There are no
sensory disorders in this disease, but these patients are liable to suffer
from attacks of giddiness. Passive movements of the limbs do not pro-
voke muscular tension, and the tendon reactions are normal. The
patients are irritable, suspicious, and reserved, Avhile, as a rule, tliey
are morbidly sensitive with regard to their condition.
CHAPTER lY.
SPASMODIC DISORDERS [continued).
II. CEREBRO-SPINAL SPASMS.
Inflammation in or near the pyramidal tracts in their course through
either the brain or spinal cord gives rise to spasmodic jerkings of the limbs,
but in such cases paralysis is soon established. The paralysis caused
by disease of these tracts is attended by muscular tension and contrac-
tions, but these symptoms will be subsequently described under the name
of the spasmodic paralyses. In post-hemiplegic chorea and athetosis,
clonic spasm is present unaccompanied by much paralysis, but both
these affections are preceded by an attack of hemiplegia, and they will
be more conveniently described along with the spasmodic paralyses.
There now remain for consideration the spasms caused by : 1, organic
disease ; and 2, by functional disease of the cortex of the brain.
1. Spasms from Organic Disease of the Cortex of the Brain
(Monospasms and Unilateral Convulsions).
Organic disease of the cortex of the brain gives rise to attacks of
spasm which may be limited to one limb or to one side of the head
(monospasm), or which begin in one limb or the side of the head
(protospasm), and extend to the other limb or to the one side of the
head, and to half the body or to both sides of the body. The charac-
teristics of these spasms are that they are gradual in their appearance
and deliberate in their progress, and that they are not attended by loss
of consciousness, or the spasm begins before the patient becomes un-
conscious, so that he is afterwards able to describe a motor aura.
Another characteristic of these convulsions is that an attack is followed
by a transitory or permanent paralysis of the affected muscles. The
clinical varieties of unilateral convulsions may be divided into — (1)
crural, (2) brachial, (3) facial, (4) oculo-motor, and (5) masticatory
monospasm or protospasm.
324
SPASMODIC DISOKDEES.
(1) Crural Monospasm or Protospasm.
In crural monospasm the spasm is limited to tlie leg, while in proto-
spasm it begins in the leg, often in the toes, and ascending to the muscles
of the trunk the arm is next attacked, and the face last. The spasm
extends to a greater or less extent to both sides when it affects muscles
which are bilaterally associated. In a case of crural protospasm which
was recenth^ under my observation the spasm, which began in the toes
of the left foot, affected the abdominal and thoracic muscles on both
sides, but was wholly limited to one side in the extremities, while
the muscles of the face were not much affected. In the same case the
spasm of the arm began in the muscles of the shoulder, and descended
gradually to those of the hand. The tendon reactions were exaggerated
on the side affected with spasm, and a certain degree of permanent
hemiplegia existed, the paralysis being most marked in the left leg, which
was the part in which the spasm always began. Several cases of crural
monospasm and protospasm have been reported in Avhich a post-mortem
examination was obtained, and the lesion has always been found in or
near the upper part of the ascending parietal convolution, the superior
Fig. 94.
parietal lobule, and the paracentral lobule. Bourneville describes a case
of the hemiplegia of infancy, in which the convulsions began by tremors
or twitching in the left or paralyzed leg. The cortex of the right
hemisphere was found atrophied in front of the fissure of Rolando, the
superior half of the ascending frontal, the posterior extremities of the
first and second frontal (Fig. 94), and the whole extent of the para-
central lobule.
(2) Brachial Monospasm or Protospasm.
In brachial monospasm the convulsions are limited to the arm, while
in protospasm they begin in the arm, the face is next attacked, and the
C E R E B R O - S P I X A L SPASMS.
825
leg last. The spasms often begin in the small muscles of the hand and
gradually ascend to those of the shoulder, this being the opposite order
to that followed by the spasms when the convulsions begin first in the
lower extremity. A case of brachial protospasm has been recorded by
Dr. Dreschfeld in which the attack began "by sudden clenching of the
fist, flexing of the wrist, and pronation of the forearm on the left side,
the corresponding angle of the mouth being at the same time drawn
downwards." At the autopsy the dura mater was found adherent to
the brain on the right side over the greater part of the ascending
parietal convolution and the supra-marginal lobule (Fig. 95). Several
Fig. 9-1.
other cases of brachial protospasm with post-mortem examinations are
on record, and the lesion has always been found in or near the ascending
parietal and frontal convolutions. In a case recorded by Dr. Hughlings-
•Jackson the spasm began in the shoulder and went down the arm, and
in this case a tumor was found in the posterior extremity of the first
frontal where it joins the ascending frontal convolution. When, how-
ever, the spasm begins in the hand the lesion is situated near the lower
end of the fissure of Rolando.
(3) Facial Monospasm or Protospasm.
In facial monospasm the convulsion is limited to the muscles of the
face, while in protospasm it begins in them, extends next to the arm,
and attacks the leg last, if at all. In the reported cases of facial pro-
tospasm, with post-mortem examination, the lesion has always been
found in the cortex in the inferior part of the ascending frontal and
parietal convolutions upon a level with the posterior part of the third
frontal convolution. The case of a French soldier, for example, is
reported by Hitzig, who, two months after a bullet wound on the right
326
SPASMODIC DISOEDERS,
side of the head, suffered from clonic spasms followed by paralysis of
the left side of the face and tongue. An abscess was found in the
cortex of the right hemisphere, situated in the inferior part of the
ascending frontal on a level with the third frontal convolution.
(4) Oculo-motor Ilonosjyasm or Frotospasm.
Many cases of unilateral epilepsy begin by a conjugate deviation of
the eyes and rotation of the head and neck, the eyes and head being
directed towards the side affected by spasm. In some cases the patients
are able to give an accurate description of the head being forcibly
twisted to one side, but in other cases they state that the attack is
ushered in by an apparent rotation of surrounding objects, this feeling
being the subjective correlation of the rotation of the eyeballs and head.
A case has been reported by my friend Dr. Thomson, of Oldham, in
which the eyeballs were persistently rotated towards the right (Fig. 06)
Fig. 96.
by a spiculum of bone which projected towards the cortex of the brain
near the angular gyrus of the left side from a depressed portion of the
skull over the infero-postero-parietal area. On removal of this spiculum
CEREBEO-SPIXAL SPASMS. 327
of bone by means of an operation the rotation of the eyeballs almost
immediately ceased.
(5) 3Iasticatori/ ^lonospasm or Protospasm.
Masticatory spasm from cerebral disease is not very common, but
several cases are now recorded. Lepine has reported a case of apo-
plexy in which the masticatory muscles Avere in a state of persistent
spasm up to the time of death. At the autopsy the chief lesion Avas
found to consist of a hemorrhagic focus which occupied the claustrum,
external capsule, and lenticular muscles of the right hemisphere, and
had separated from the white substance a portion of the gray matter of
the Island of Reil, and of the inferior part of the ascending frontal
convolution the latter Ijeing the part in which Ferrier places the centre
for the movements of the jaws. Cases in which trismus was caused by
disease in or near the cortex of the brain have also been recorded by
Petrina, Seeligmliller, Senator, and Oulmont and Charcot.
2. Spasmodic Affectioxs from Functional Disease of the
Cortex of the Brain.
a. Epilepsy.
Etiology. — A hereditary taint may be distinctly traced in rather
more than one-third of all cases of epilepsy, but a neurotic constitution
is met with in a much larger number of cases. The disease appears to
be transmitted rather more frequently through the mother than the
father, and the female sex is rather more frequently attacked than the
male sex. With regard to age Dr. Gowers found that out of 1450
cases analyzed by him the disease began in 29 per cent, under ten years
of age; in 4(3 per cent, between ten and twenty years ; in lo.T per
cent, between twenty and thirty years ; in 6 per cent, between thirty
and forty years ; in 2 per cent, between forty and fifty years ; and in
IJ per cent, above fifty years. Anaemia, chlorosis, scrofula, rickets,
chronic alcoholism, and chronic lead-poisoning, appear to beget a certain
instability of the nervous system which predisposes to the production
of epilepsy.
The exciting causes of epilepsy are profound emotional disturbance,
intestinal irritation from the presence of worms, overloading of the
stomach, the . passage of gall-stones, over-exertion, sexual excess, ex-
posure to cold, acute febrile diseases, sunstroke, injuries to the head,
and injuries to the principal nerve trunks.
328 SPASMODIC DISORDERS.
Symptoms. — The ■premonitory symptoms of an epileptic attack may
be divided into remote and immediate warnings, the Latter forming the
aurce epilepticce. The remote warnings may extend over hours or days
before the attack ; they usually consist of such symptoms as headache,
dizziness, confusion of thought, or some mental change, the patient
becomino- depressed or morose, or excited, lively, and irritable.
Epileptic aurce, or the immediate warning of the paroxysms, consist
of the subsequent account which the patient is able to give of the feelings
he experienced immediately before the attack. The aura may consist of
(a) motor, {h) sensory, (c) vaso-motor and secretory, or (d) psychical phe-
nomena.
{a) Motor Aurce. — It is not always easy to distinguish between a
motor and a sensory aura, because the patient, instead of describing a
spasm in objective language, often describes the sensations which accom-
pany the spasm in subjective language. When, for instance, the con-
vulsion begins in the hand, the patient, instead of describing the thumb
as being drawn into the palm, says that he felt a dragging sensation in
the thumb, or a feeling of creeping or numbness in the hand which
gradually passed up the arm. And when the convulsion begins in the
lower extremity the aura usually begins as a creeping sensation in the
big toe which passes up the leg and may extend to the arm before con-
sciousness is lost. Conjugate deviation of the eyes and rotation of the
head and neck, which frequently usher in an epileptic attack, are often
regarded by the patient as an apparent rotation of surrounding objects.
At times patients see objects recede from them and appear smaller, ov
approach them and become larger, and these sensations are pi'obably
caused by variations in the tension of tlie muscles of accommodation.
The motor aura often begins in the side of the face, and it is then
described as a feeling of " the face being drawn,"' or it may begin in the
side of the tongue, and be described as a feeling of something crawling
over it. In many cases the aura consists of a sudden inability to speak,
or a transient aphasia. At other times it consists of a sensation of
shivering or of trembling in the muscles of the back, while at othei'
times there may be a general tremor or a jerking of particular limbs,
and Romberg mentions "a sudden relaxation and loss of mobility '"
as being sometimes the forerunner of an attack. In some cases the
aura consists of complicated coordinated movements, such as running
forwards or backwards, or turning round.
{h) Sensory Aurce. — The sensory aura sometimes consists of a feeling
of general heat or cold, while at other times it is distinctly localized.
Besides various sensations such as tingling, numbness, or pain in the
extremities, it may consist of a localized pain in any part of the head,
or of a general feeling of pressure in the head. Patients complain of
CEREBRO-SPINAL SPASMS. 829
dizziness and vertigo before an attack, more frequently perhaps than
any other form of aura, but these symptoms are most probably but
subjective accompaniments of the derangement of the adjustments of
the body to surrounding objects in space, which is caused by commenc-
ing motor discharcres.
The aur(E of the special sensations may consist of undeveloped or
crude sensations, or of more elaborate sensory representations. The
crude sensations consist of sparks, flashes of light, and various colors :
hissing, ringing, or explosive noises ; metallic or other abnormal sensa-
tions of taste, or unpleasant smells. In some cases the attack is ushered
in by sudden blindness of one or both eyes, or by a sensation of unusual
stillness. The elaborate sensory representations consist of spectral
faces, visions of beautiful places or more commonly of disagreeable
objects and scenes, vocal utterances or strains of music, and other com-
plicated perceptions.
Visceral sensations sometimes constitute epileptic aurse, and probablv
one of the most common of all sensory warnings are sensations which
are referred to the pit of the stomach. The epigastric aura sometimes
consists of pain, coldness, or burning at the pit of the stomach and some-
times it is spoken of as a vague and indescribable sensation, which ascends
to the throat and causes a feeling of choking, or rises to the head, and
then immediate loss of consciousness ensues. In some cases a feeling
of suffocation constitutes the warning, and in others there may be nausea
with rumblino; in the bowels, retchino;, a feeling of intense hunger,
bronchial asthma, or palpitation with or without angina.
(c) Vaso-motor aurcB are often described as a sensation of coldness
or numbness in the fingers and toes, and the affected part becomes pale
and cold to the touch. At other times spots in various parts of the
body assume a red color, and become the seat of feelings of transient
heat. Of the secretory aurce^ an excessive flow of saliva is probably the
most commonly observed.
{d) Psyehical aurcE are frecjuently experienced in the form of a feeling
of intense horror or alarm, and the patient may look startled, guilty, or
frightened. In other cases the patient feels as if he were suddenly in
a strange country, and in many cases the aura is what Dr. Hughlings-
Jackson has named " a dreamy " or "voluminous " mental state similar
to that experienced by persons in the act of drowning, during which all
the past events of life are said to crowd upon the memory.
It is very important to study the order in whicli the phenomena of
the aura succeed one another. The motor aura generally begins in small
muscles, which are organized for special actions, and other muscles
become involved in the spasm in a determinate manner, but the succes-
330 SPASMODIC DISORDERS.
sions of these motor plienomena Avill be best studied in cases of unilateral
epilepsy. A crude sensation of sight, such as a red light, is often
followed by a developed perception, such as the image of a man : a
confused noise may be succeeded by strains of music ; and a subjective
sensation of smell may be followed by efforts to prevent the effluvia from
gaining admission to the olfactory chambers, showing that the sensation
had become objective. A visual is not unfrequently associated with an
aural sensation, sometimes the one and sometimes the other taking
precedence. In some cases the epigastric aura is followed by an emotion
of fear or of anguish, and the patient may have a facial expression cor-
responding to the emotion.
The epileptic paroxysm may be divided for the purposes of descrip-
tion into {a) epilepsia mitior or U petit mal, {h) epilepsia gravior or le
Jiaut mal, and (<?) epileptiform seizures.
(a) Epilepsia mitior or le petit mal consists of paroxysms of momentary
confusion of thought, or transitory unconsciousness. The patient, for
instance, may be attacked while speaking ; he becomes suddenly uncon-
scious, there is a pause, probably in the middle of a sentence, but in a
few seconds speech is resumed at the point where it was interrupted and
the sentence is finished. At times the attack may consist of a feeling
of fainting with slight confusion of mind, and, indeed, any of the
numerous aurse just described may, along Avith slight confusion of mind,
constitute a minor attack of epilepsy. Most of these attacks are accom-
panied by minor degrees of muscular spasm. At the outset of the
seizure the countenance becomes ghastly pale ; the pupils contract ; the
eyes are fixed and staring or squint ; and the mouth is slightly drawn ;
or there may be partial rotation of the head and eyes, chewing move-
ments, or rolling about of the tongue. An involuntary discharge of
urine or feces during the attack frequently occurs. Sometimes the
patient utters a shriek and reels, or walks hurriedly round the room and
then recovers. At other times the patient is unconscious for a con-
siderable time, but goes on with the work in which he was en^ajxed as
if he were conscious. Minor attacks are very liable to be followed by
'' epileptic mania."
(6) Epilepsia gravior or le haut mal may for the purposes of descrip-
tion be divided into three stages.
(j) '^^e first stage is ushered in by three prominent symptoms which
occur simultaneously ; namely, loss of consciousness, sudden falling, and
great pallor of the face, while a fourth symptom is often present in the
form of a loud and piercing cry. The loss of consciousness is sudden
and complete, and every form of sensibility and mental operation is
completely abolished. The patient often falls, as if struck by lightning,
CEREBRO-SPIXAL SPASMS. 331
either forwards on his face. Ijackwards on his occiput, or hiterallv, and
so instantaneously that he has no time to select a place or attitude, and
may consec^uently fall into fire, water, or from a height. At other times
the patient has sufficient warning of the impending attack to enable him
to sit or lie down. Pallor of the flice is probably always present at the
beginning of the attack, although the symptom is sometimes so transient
that it may pass unobserved. The epileptic cry which the patient often
utters immediately l)efore or during the fall is loud and piercing and
alarms, according to Komberg, both man and animals. It is probably
produced by spasm of the expiratory muscles with closed glottis. Wheia
the patient falls to the ground he remains for a period of from two to
forty seconds in a rigid condition caused by a tonic, although unequal,
contraction, of all the muscles of the body. Various distortions are
thus produced ; there is conjugate deviation of the eyes with rotation
of the head and neck ; the pupils are dilated and insensible to light ;
the countenance is variously altered ; the jaws are firmly closed and the
tongue may be severely bitten ; there is opisthotonos, and the different
segments of the lower extremities are extended upon one another and
upon the trunk, the foot being rotated inwards and the toes widely
separated ; while- the segments of the upper extremities are usually
flexed upon one another, the thumb being bent upon the palm, the
fingers closed, and the hand pronated. The respiratory muscles are in
a state of tonic spasm and the breathing is arrested. The pallor of the
face is soon replaced by a dull red or dusky hue ; the veins of the head
and neck become greatly distended ; the carotids throb violently, and
the action of the heart is forcible, but the pulse at the w^rist is small
or imperceptible.
(jj) The second stage begins after a variable period of from two to
forty seconds, and then the tonic gives place to clonic spasms which are
usually more pronounced on one side of the body. The muscles of the
foce, tongue, pharynx, and larynx are usually first affected by clonic
spasm, and those of the extremities and trunk are afterwards invaded.
The patient now presents a hideous appearance ; the head is alternately
drawn laterally, or forward and backward ; the eyes are convulsively
rotated in various directions, but upward and outAvard rotation pre-
dominates, so that the pupils are hidden and only the whites of the eyes
are visible under the blinking, half-closed lids : the face is variously
distorted ; the jaws are violently convulsed and the tongue being severely
bitten, the blood oozes through the clenched teeth as a sanguineous froth ;
the trunk and limbs are variously thrown about ; and the contents of
the bladder, rectum, or vesiculae seminales may be evacuated.
The venous hyperi^mia reaches its maximum just as the spasms are
332 SPASMODIC DISORDERS.
beginning to abate in severity, and the skin is bathed in sweat which
sometimes has a fetid odor. The heart beats tumultuously, the carotids
throb ; and the pulse, if it can be felt, is fuller and more labored than
during the period of tetanic contractions. The pupils are alternately
contracted and dilated and are said to be slightly sensitive to light.
This stage may last from a few seconds to five or ten minutes, the average
duration being from two to three minutes.
(jjj) The third strnje is characterized by a gradual return to conscious-
ness and voluntary power. The convulsions either cease suddenly or
wear off gradually, the period of transition being marked by partial
jerkings of some muscular groups, or by a diffused tremor of the body.
The patient soon attempts to change his position ; he opens his eyes and
looks around him with a bewildered expression, and may even attempt
to speak. The respiratory movements are now more natural in rhythm,
although still somewhat irregular; the pupils are contracted; the pulse
is quieter and fuller than in the previous stage ; the conjunctivae are
injected and petechiae are often observed on the eyelids, forehead, and
temples; the muscles are relaxed and powerless, and the patient is
exhausted and disposed to sleep. The attack is often followed by
vomiting, and a large quantity of pale urine is often passed.
(iv) The/ow^/i or after stage is very variable in the duration, severity,
and nature of its sym])toms in different cases. In some cases the patient
recovers in half an hour and resumes his usual occupation, but, as a
rule, recovery is delayed for a much longer period. In many cases the
general muscular relaxation is interrupted by clonic spasms, or fibrillary
contractions, and the patient suffers from lassitude and stupor, from
which he is aroused with difficulty, and, if awakened, he is peevish and
irritable. The average duration of the stupor is about an hour when
the attack occurs during the day, but when it occurs in the evening or
during the night it passes insensibly into the ordinary nocturnal sleep.
Complications. — Various mental disturbances are by far the most im-
portant of the complications of epilepsy. The patient sometimes exhibits
marked mental derangement immediately before as well as after the
paroxysm, and a maniacal condition sometimes constitutes the principal
feature of the attack. After an attack of epileptic vertigo a person
may continue for some seconds, minutes, or even hours in a dull, half
stupid condition. He may mutter a few incoherent words or some lewd
expressions, no matter how foreign to his habits; he may unbutton his
clothes and expose his person, urinate in a public assembly, exhibit
himself naked to his domestics, or even walk in public naked unless
prevented, and on recovery he has only the vaguest recollection of
what has occurred. These, however, are a few of the minor actions
CEREBRO-SPINAL SPASMS. 333
Avhicli may be done by individuals subject to epileptic vertio-o, imme-
diately after the attack. The most motiveless and atrocious crimes
are sometimes committed in this condition, so that some medical jurists
are of opinion that no epileptic is responsible for his actions. Epileptics
sometimes have a Avarning of the approaching maniacal attack and can
then caution their friends, but generally the seizure is more or less
sudden. There is every variety of intermediate form between the milder
and severer cases. Reynolds says that epileptic mania occurs in about
one-tenth of all cases of epilepsy, including the minor attacks of
epileptic vertigo, and having occurred in the case of any one individual
it is apt to recur frequently, especially when several fits have followed
in rapid succession. Epileptic delirium is not always furious and
dangerous. It may appear in the form of preternatural gayety or illu-
sions of the senses before the attack, or during the intervals. Menini:;itis
has been known to follow epileptic paroxysms, but it is frequently the
result of an injury inflicted by the fall, and both apoplexy and permanent
paralysis are rare complications of idiopathic epilepsy.
The fre(|uency of recurrence of the epileptic paroxysms varies within
wide limits, some patients only having one seizure a year, others having
thousands ; but Reynolds states that half the cases are found to have a
rate of recurrence ranging from one attack in fourteen to one in thirty
days. Sometimes the mode of recurrence is what has been termed
"serial." The patient suffers from two or more attacks in a day and
then there is a free interval of from one to several weeks.
Each group of seizures may be composed of from two to a hundred or
more single seizures in twenty-four hours. This condition may extend
over a much longer period, and Delasiauve saw in a boy of fifteen, within
one month, a " collective seizure " which was composed of 2500 " frag-
mentary seizures." The French have designated this condition etat de
maJ epiJeptique (status epilepticus), and Bourneville has recently drawn
attention to the great increase of temperature Avhich characterizes this
condition. The patients lie in a profound coma, and the temperature
may rise to 107.6° F., and still higher in fatal cases. In favorable cases
the temjierature gradually falls, but in other cases a subsequent rise
takes place, coma becomes profound, and the patient dies, often with
symptoms of collapse associated with the formation of acute " bedsores."
b. Eclampsia.
Etiology. — Convulsions are frequent during the first two years of life,
but become rare after the fifth and exceptional after the seventh year.
The influence of hereditary predisposition in the production of convul-
33i SPASMODIC DISOKDEKS.
sions is shown by the fact that successive infants of one family are liable
to be attacked with convulsions in the absence of any definite cause.
The children of parents with neuropathic constitutions are more liable
to be attacked than the children of healthy parents. All debilitating
causes increase the tendency to convulsions, and children suffering from
rickets are specially lialjle to be attacked : of sixty-five infants attacked
Avith convulsions, Dr. Gee found that no less than fifty-six of the number
were suffering from rickets.
Eclampsia has been divided into several varieties according to the
exciting cause of the convulsions. These are («) idiopathic, {b) reflex,
(r) febrile, (d) asphyxia, (e) urtemic, (/) puerperal, and (,</) toxic con-
vulsions.
(a) In idiopathic convulsions children are so predisposed to these
seizures that an attack supervenes from the slightest exciting cause or
even in the absence of any such cause.
{b) Reflex convulsions are caused by irritation of the extremities of
peripheral nerves. Amongst the more usual causes of irritation are
pricking by pins, wounds and burns on the surface of the body, reten-
tion of urine, the presence of a calculus in the kidney, foreign bodies
in the external auditory meatus, and irritation of the digestive canal
from the presence of worms or undigested food, and of the gums during
painful dentition.
(f) Febrile convulsions often usher in severe acute diseases such as
pneumonia and the eruptive fevers. They appear to correspond to rigors
in the adult.
{d) Convulsions due to asphyxia occur in the course of diseases of
the respiratory organs.
{(•) Urcernic convulsions in childrofi generally result from scarlatinal
nephritis, and they may arise from most forms of Bright's disease in the
adult.
(/) Puerperal eclampsia is, as a rule, merely a form of uremic con-
vulsion.
{g) Toxic convulsions are caused by such agents as prussic acid,
nicotine, picrotoxine, oenanthe, crocata, carbonic oxide, and carburetted
hydrogen.
Symptoms. — An attack of eclampsia cannot be distinguished from a
true epileptic seizure, and it is therefore unnecessary to give a minute
description of it. Infantile convulsions have been divided into internal
and external, the muscles of the glottis and the respiratory muscles being
chiefly aff"ected by spasm in the former and the muscles of external
relation in the latter.
The symptoms caused by spasm of the glottis have already been
CEREBRO-SPIXAL SPASMS. 335
•lescribed, aiul we shall consequently limit our further remarks to the
external convulsions of children. An attack of eclampsia may occur
either with or without premonitory symptoms ; but when present, these
usually consist of sleeplessness and restlessness, or drowsiness for a day
or two before the attack ; while immediately before it the pulse is often
hard and wiry, the countenance assumes a frightened expression, or the
child starts up frightened from a fitful and uneasy sleep. The convul-
sion usually begins by conjugate deviation of the eyes, and slight jerkin^
contractions of the muscles of the angles of the mouth. The natural
look of the infant is noAv exchanged for a fixed stare, followed soon
afterwards by an upward rotation of the eyeballs, the latter being in its
turn followed by a fixed stare, and that again by an upward rotation of
the globes. The eyeballs are often rotated to the right or left as well
as upwards, and the two are generally moved unequally, so that a con-
siderable degree of strabismus may occur. The pupils are sometimes
dilated, sometimes contracted, and when they are completely concealed
by the superior lids, the whites of the eyes being alone visible, the
countenance assumes a frightful and characteristic aspect.
Clonic spasms of the facial muscles produce a series of grimaces and
contortions, in which the laljial commissures are drawn outwards, and
at each successive jerk a peculiar sucking noise is made by the passage
of air through the mouth, the lips being covered by a frothy, and often
slightly sanguinolent mucus. The superior lip is sometimes drawn
upwards, so as to expose the teeth, and the countenance then assumes
an almost savage expression. The inferior jaw is sometimes agitated by
clonic spasms, while at other times there is trismus, interrupted from
time to time by grinding of the teeth. The head is usually strongly
retracted, and sometimes rotated to one side. The thumb is flexed into
the palm, and the fingers are flexed over the thumb ; the forearm is
bent upon the arm and is constantly agitated by slight movements of
semiflexion and semiextension ; the hand is alternately pronated and
supinated ; and the segments of the superior extremities are contorted
into every imaginable shape. The inferior extremities are affected in a
similar manner, although to a less degree than the superior. The
muscles of the trunk occasionally participate in the clonic convulsions,
but as a rule the trunk is maintained rigid by tonic contraction of its
muscles. The contractions of the muscles of one-half the body may
predominate over those of the opposite side, and then the child is arched
laterally in such a way that he may be projected out of bed by the
convulsion. The spasmodic contractions of the diaphragm and of the
muscles of the larynx produce a peculiar and characteristic noise when
air is drawn into the chest during inspiration. Involuntary evacuations
336 h^PASMODIC DISOKDEKS.
occasionally take place during convulsions. Deglutition is rarely im-
possible, although attempts to get the infant to swallow during the con-
vulsion are attended with danger.
There is complete loss of consciousness during the attack, but reflex
excitability is partially retained. When the convulsion is prolonged
the face becomes of a violet color and bathed in perspiration ; the head
is hot and the extremities cold ; the skin is moist ; the pulse is frequent
and difficult to count, owing to jerking of the tendons ; and the respira-
tions are accelerated, but stertorous only in aggravated cases.
The ocular muscles and those of facial expression are usually the fiist
to be affected with clonic spasm, and then the muscles of the fingers and
forearm. In the more severe convulsions the muscles of the shoulders
are affected, but those of the Ijack and loAver extremities are only impli-
cated in aggravated cases. The great tonic contractions which form the
first stage of the epileptic attack fail altogether in eclampsia. The
duration of an attack of eclampsia is very variable. The convulsions
cease in some cases in a fcAv minutes, while in others they recur for
hours or days, Avith only short intervals of calm. The terminal con-
vulsions of asphyxia are generally partial, incomplete, and alternate
with coma. The initial convulsions of fever are intense and generalized,
but are usually limited to a single attack. Urcemie convulsions are
characterized by their violence, the ftxMjuent re]jetition of the jiaroxysm,
and the profound coma which alternates with or succeeds the spasm.
Convulsions caused by meningeal hemorrhage or other organic lesion
generally assume a unilateral character and are followed by paralysis
with contractures, choreiform movements, aphasia, or idiocy. Essential
convulsions sometimes terminate fatally, either after a single violent
seizure, or after a series of seizures which occur in rapid succession,
death being caused by spasm of the glottis or by coma.
c. Hysterical Spasmodic Affections.
Etiology. — Hereditary predisposition exerts a poAverful influence in
the production of hysteria, the transmission being sometimes direct from
the mother to the daughter and at other times indirect through in-
heritance of a general neuropathic constitution. Hysteria occurs with
preponderating frequency in the female sex, and the first symptoms
usually make their appearance about puberty, but it also occurs in the
male sex and is by no means unfrequently met with in children of both
sexes. All causes which lower the nutrition of the nervous system,
such as hemorrhages, insufficient nourishment, impaired digestion, and
anaemia, predispose to hysteria. It is also frequently induced by the
CEREBRO-SPINAL SPASMS. 337
depressing passions, such as fear, jealousy, and remorse, as well as by
anxiety, especially when combined with overwork. Hysteria may be
acquired, by those who are predisposed to it, by imitation, and young
susceptible girls are not unfrequently seized after being witnesses of an
attack in another. An actual epidemic of hysteria may occur in
public institutions, and the convulsive diseases of the middle ages appear
to have spread in this manner. All uterine derangements and ovarian
diseases are apt to be attended by hysteria, and it may also be caused
by local irritation of the other viscera, such as intestinal irritation from
the presence of worms. A slight contusion or other insignificant injurv
may cause hysteria in those who inherit a strong predisposition to the
disease, but a severe injury, such as a gunshot wound of a large nerve
trunk, may induce in the strongest men an emotional condition very
similar to hysteria in the female.
S'i/))ipto)ns. — The spasmodic affections of hysteria may be divided
into (1) general hysterical attacks, and (2) local spasms.
(1) Hysterical Attacks
(a) Simple Hysterical Attack. — The attack is preceded by the sen-
sation of globus along with a feeling of suffocation, a painful dragging
in the extremities, pain and giddiness in the head, singing in the ears,
or darkening of the field of vision. It is often preceded by a fit of
crying or laughing, or a combination of both ; the patient suddenly
screams or makes a spluttering noise, and falls down in a state of ap-
parent unconsciousness. The head and extremities become affected with
general rhythmical clonic convulsions, the breathing is accelerated and
exaggerated, irregular, or temporarily arrested. The loss of conscious-
ness is more apparent than real. The hysterical patient generally hears
what is said by those around her, and she has almost always time to find
a suitable place upon Avhich to fall ; she often throws herself on a couch
or reclines on a sofa, and not unfrequently appears to bestow some degree
of attention upon the propriety and gracefulness of her attitude.
Another peculiarity of the hysterical attack is that the facial expres-
sions and attitudes assumed are not devoid of meaning, but are repeti-
tions of those occurring in health under varying emotions. Sometimes
the expression is that of great terror, at other times there is a frown as
if of anger, and at still other times it becomes imploring or beseeching.
Hysterical attacks rarely last more than a few minutes, but they may
recur in quick succession, so that they seem to form an almost con-
tinuous paroxysm, extending over a considerable period. The hysterical
seizure frequently ends in a fit of crying and sobbing, there is no sub-
22
338 SPASMODIC DISORDERS.
sequent coma, and on recovery the patient generally passes a large
quantity of clear and limpid urine of low specific gravity. Hysterical
attacks always occur when some one is present to witness them, and never
during sleep or when the patient is alone.
(b) Cataleptic attacks are liable to occur in hysterical patients : they
are of variable duration, disappearing sometimes in the course of a few
hours, and being prolonged at other times, with slight intermissions, for
a period of months. Cataleptic rigidity is sometimes limited to par-
ticular hmbs ; but, as a rule, the whole body is implicated, and then all
voluntary movements are suspended and reflex action is diminished.
All the forms of general sensibilit}' are usually lost, but one or more of
the special senses, especially hearing, may be retained.
{(■) Hysteria in Boys. — Boys, at the approach of puberty, not un-
frequently suffer from hysterical symptoms resembling those observed in
the female sex. Sometimes the symptoms may assume the form of
globus along with attacks of causeless weeping and sobbing ; at other
times there may be partial spasm of the glottis, a barking cough, attacks
of dyspnoea or some local sensory or motor disturbance. l*sychical
phenomena often predominate. In a case which came under my obser-
vation, the boy was sometimes found creeping on his hands and knees
and barking like a dog; another time he jumped like a frog from the
floor on to the table. The depraved form of hysteria named chorea
major is often met with in boys. In this variety of the disease the
patients run, dance, jump, or climb with much greater readiness and
dexterity than similar actions could be performed in health, or they may
sing or recite poetry, even in a foreign language.
(2) Local Spasms.
In hysteria both tonic and clonic spasms may occur in every muscle
and group of muscles of the head, trunk, and extremities. Every one
of the spasms already described as occurring in the area of distribution
of the peripheral motor nerves may appear in hysteria, but it is un-
necessary to describe these in detail. The facial muscles are incessantly
active in many hysterical patients, so that the countenance has a restless
and unsettled expression, and, indeed, the "facies hysterica " constitutes
one of the main characteristics by means of which the practised physician
is enabled to diagnosticate the disease. It is "characterized," accord-
ing to Dr. Todd, " by a remarkable depth and prominent fulness, with
more or less thickness of the upper lip. There is also a fulness and
obviously drooping condition of the upper eyelids. This drooping con-
formation of eyelids is at once a mark of beauty, and of that from
CEREBRO-SPINAL SPASMS. 339
■which many beautiful women suffer very much, namely, the hysterical
state of constitution."
Spasmodic closure of the glottis may produce alarming dyspnoea, and
the patients are liable to attacks of convulsive laughter and weepino-,
which often arise apparently in the absence of any emotional disturbance.
During hysterical attacks loud screams are commonly emitted, and in
that form of hysteria named chorea major the patients often imitate the
cries of animals by mewing, liarking, or howling. Hysterical patients
often suffer from a temporary acceleration and exaggeration of breathing
without there being any feeling of embarrassed respiration, and at other
times they suffer from temporary spasmodic pauses in the respiratory
rhythm. Hiccough and yawning are frequent and sometimes very dis-
tressing symptoms.
The pharyngeal muscles are sometimes spasmodically contracted, so
that swallowing becomes difficult or impossible. Spasm of the tongue
is not unfrequently associated with that of the pharyngeal muscles, and
at every attempt to move the organ it becomes distorted in various direc-
tions, so that articulation and swallowing become greatly impeded. The
sensation of choking in the throat, named globus hystericus^ is supposed
by some to be caused by a spasm of the oesophagus, while at other times
the spasm may be so persistent as to resemble organic stricture.
The stomach is liable to undergo spasmodic contractions, which give
rise to persistent and distressing vomiting. The patient vomits almost
immediately after food is taken, and the latter is usually consequently
ejected in an undigested condition. Some of the food is, however,
probably retained, as the nutrition of the patient rarely suffers in pro-
portion to the apparent violence and persistency of the vomiting.
Irregular peristaltic movements occur in various parts of the intestines,
and these may be so energetic that they can be felt through the abdominal
wall, and the patient may become convinced that a movable body is
present in the abdomen. Spasm of certain portions of the intestines
may be so persistent as to cause temporary- stricture, and the bowels
above the constricted portion become so distended with gas, as to give
rise to what has been called a " phantom tumor ; " or a real obstruction
of the bowels may sometimes be caused by accumulation of feces behind
the constricted portion. Eructations, borborygmi, and griping pains
may also be caused by irregular peristaltic movements of various por-
tions of the digestive canal.
Spasmodic retention of urine, generally combined with increased in-
clination to micturate, occurs in many hysterical patients, and this
condition is sometimes, but not always, associated with a painful condi-
tion of the genitals.
340 SPASMODIC DISORDERS.
Vaginismus, caused by spasm of the constrictor vaginae, sometimes
renders coitus difficult or impossible ; it is generally associated with
hyperfesthesia of the vaginal orifice, and the spasm is induced by reflex
action.
Hysterical patients are also liable to suff"er from attacks of palpitation,
and during these the pulse is small and hard and the skin pale and
cold, owing to spasm of the small arteries of the body. Patients suffer-
ing from hysteria are also subject to fainting fits, and these are most
probably caused by sudden anemia of the brain from spasm of its
vessels.
d. Hystcro-epilepsy.
In hystero-epilepsy the patient suffers in the intervals between the
attacks from various hysterical symptoms, the most usual of which are
complete or incomplete hysterical hemianjvisthesia associated with
ovarian hypersesthesia. The paroxysm is always preceded by an aura,
consisting of a sensation which proceeds from the region of the hyper-
iesthetic ovary and ascends successively to the epigastrium, throat, and
head, and on reaching the last the patient utters a loud shriek and falls
to the ground. All the muscles of the body now become the subjects
of tonic spasm ; the head is retracted, and the body and limbs are
arched backwards and rigid ; the respirations are stertorous and infre-
quent ; and foam, sometimes bloody from the tongue being bitten,
generally issues from the mouth. The tonic stage is followed by a few
clonic convulsions, but these soon cease, and a state characterized by
general muscular relaxation, stertorous breathing, and coma, terminates
that portion of the attack which resembles the epileptic paroxysm.
The second stage, or what the French call the '■'■phase des grand
mouvements," now makes its appearance. The body is arched back-
Avards in a state of opisthotonos, or bent forwards or laterally ; while at
other times it is maintained in a rigid position, with the lower extremities
extended and the upper stretched out. This stage, according to Richer,
" consists of movements Avhich may be executed with a certain rhythm,
or in the most complete disorder, and often with excessive violence. In
addition to screaming, there is a disposition to bite and to tear, and
sometimes the patient becomes furious. At other times the attack of
the grand movements is in no way frightful and consists almost exclu-
sively of salutations, jumping, and somersaults, which recall to mind
the performance of acrobats, and justify the name of " attaques de
clownisme " that has been given to it.
The third stage, or stage of emotional attitudes {phase des attitudes
passionelles), now appears, and during its continuance the patient
CEREBRO-SPINAL SPASMS. 3-il
assumes in rapid succession attitudes and gestures expressive of various
emotions. The first attitude assumed by the patient is usually a threaten-
ing one ; she raises herself in a half-sitting posture ; the brows frown ;
the fists are clenched ; and the face presents an angry and menacino-
expression. This attitude, however, soon gives place to an expression
of abject fear, which in its turn makes room for a look of intense happi-
ness and beatitude. But the expression of beatitude is also fleetino' in
character, and is succeeded by one of intense voluptuousness, followed
by gestures which lead to this stage being called the phase of luhricity.
Terror now seizes the patient ; she sees rats and other odious animals that
ev^oke from her passionate exclamations of dread and disgust, and this is
followed by a stage in which she appears to be laboring under the idea
that she committed a great oifence, and sues for mercy. The patient
now hears strains of music, she looks pleased and may join in hummino-
the tune, but her singing is soon followed by weeping, broken bv re-
proaches addressed to her parents as the cause of her misery. This
last phase constitutes the phase of recovery, but hallucinations may
persist for some time. The patient can always describe afterwards the
hallucinations to which she was subject, and each of the attitudes is
found to have corresponded to an hallucination.
An attack of hystero-epilepsy may be provoked at any time by various
manipulations, such as suddenly gripping the skin of the breast on
both sides, on a level with the fifth rib, and midway between the anterior
and posterior boundaries of the axillae. An attack is also readily
induced by pinching a fold of the skin of the sub-inguinal region, or by
slight pressure on the region of the hyperiesthetic ovary. Sudden and
firm pressure exerted on the affected ovary, however, instantly arrests
the paroxysm at any stage. When such compression of the ovary is
made, the patient's mouth opens Avidely, the tongue is spasmodically pro-
truded, and the convulsions cease. Attacks of hystero-epilepsy are not
often seen in this country in the typical form described by French
authors.
Hystero-epileptic attacks may occur in series like epileptic attacks,
and each group of attacks may consist of from several hundreds to over
a thousand separate seizures, while group after group of these attacks
may follow each other day by day for weeks. This status hystericus
is, however, unlike the status epilepticus in the facts that the tongue is
not bitten, that there is no elevation of temperature, and that it is never
fatal.
342 SPASMODIC DISOEDEES.
e. Catalepsy.
Etiology. — Catalepsy often occurs as one of the many manifestations
of hysteria, while at other times it is caused by chronic cerebral dis-
ease,"^ such as softening, tubercular meningitis, and tumors. In some
cases the cataleptic condition appears to be premonitory of epilepsy,
Avhile in other cases attacks of catalepsy recur at certain intervals, and
thus appear to take the place of epileptic seizures. Some cases, how-
ever, cannot be traced to any external cause, and then catalepsy may
be called idiopathic or essential, cases of this kind being observed in
families who inherit a decided neurotic disposition. The disease is
most frequently observed about the age of puberty, but it has been
met with as early as eight years of age, or even earlier, and occasion-
ally in advanced life. The two sexes appear to be equally liable to
the idiopathic variety, but the hysterical is almost exclusively observed
in the female. The exciting causes of idiopathic catalepsy are gastric
and intestinal irritation, and great emotional disturbance. Malarial
infection is said to have caused typical attacks of catalepsy.
Symptoms. — The cataleptic attack is sometimes preceded by pre-
monitory symptoms, such as headache, vertigo, trembling of individual
muscles, and an undefined sense of discomfort. As a rule, the attack
begins abruptly ; the movements of the patient are suddenly arrested,
it may be while he is speaking or performing some action ; the face
becomes deadly pale; the respirations are slow and tranquil; the pulse
is soft ; and, although consciousness is lost, the attitude of the patient
at the time of the seizure is retained. The muscles in action at the
beginning of the attack appear to be the first to become rigid, but in
most cases the spasm rapidly extends to all the voluntary muscles,
although occasionally it is partial or unilateral. The affected mus-
cles feel firm, and offer resistance to passive movements of the limbs,
which is sometimes so great as to amount to tetanic rigidity, but when
once this resistance is overcome the limbs, head, and neck, or features
may be placed in constrained positions, which they retain for a com-
paratively long period. After the first resistance of the muscles has
been overcome the limbs possess a flexibility and pliability, Avhich has
been compared to that of soft wax, and the condition has consequently
been named flexihiUtas cerea. The resistance of the muscles enables
the limbs to be moulded in any position compatible with the rigidity of
bones and inextensibility of ligaments, and the constrained attitudes in
Avhich the limbs may be placed are maintained without change during
the whole course of the attack. But even during the cataleptic condi-
CEREBKO-SPIXAL SPASMS. 843
tion the muscular stiffness does not persist in its full intensity for a
lengthened period. After some minutes the stiifness diminishes some-
what, so that the arm, for instance, when raised horizontally falls lower
by its own weight, and the limb undergoes a slight trembling, indicat-
ing the approaching exhaustion of the muscles.
Consciousness is usually al)olished, but not in all cases. A certain
amount of consciousness may be retained in the early stage of the
attack or be present throughout, so that strong peripheral irritation
may cause pain Avhich will be remembered by the patient. Reflex
irritability is sometimes lost; at other times certain reflex actions, such
as closure of the eyelids on touching the conjunctiva, are retained.
The electric contractility of the muscles, according to Benedikt, is
somewhat diminished during the attack, but soon becomes normal, and
in a case observed by Rosenthal the electrical reaction of the nerves to
both currents was perfectly normal, in another it was increased.
The organic functions are not usually seriously interfered with. The
respiration may be normal, but is generally slow and shallow. The
pulse is slow, soft, and compressible. The temperature is generally
lowered, and at times the surface of the body becomes icy cold. When
the surface of the body is cold, and the pulse at the wrist and respiration
are almost imperceptible, the condition may be mistaken for real death.
The attack of catalepsy is sometimes very brief, lasting only a few
minutes, at other times several hours or days. Attacks described as
being very protracted are in reality made up of a succession of these,
separated from one another by intervals in which the patients recover
either wholly or partially. The seizures sometimes disappear quite
suddenly, and the patients at once recover full consciousness and im-
mediately resume the actions which had been interrupted. As a rule,
however, recovery is gradual, patients at first being stupefied as if
awaking from a profound sleep, a certain amount of muscular stiffness
remaining for some time, which renders motion difficult and slow.
In simple catalepsy no mental disorder is observed in the intervals
between the attacks, but when it is merely a symptom of profound ner-
vous disease the intervals may be characterized by the occurrence of
hysterical convulsions, delirium, maniacal attacks, and hallucinations, or
the catalepsy may be associated with ecstasy and somnambulism.
The course of catalepsy is usually chronic, extending over many
years. Some individuals suffer only from a small number of attacks
separated by intervals of many years. Others, again, have frequent
periodical attacks. In hysterical catalepsy the slightest external influ-
ence may suffice to provoke a paroxysm. Cataleptic attacks are hardly
ever fatal of themselves.
PA-i: SPASMODIC DISORDERS,
f. Trance.
In trance the patient lies for days together without eating or drink-
inc', there is apparent insensibility, and the pulse and respiration are
imperceptible, but the limbs remain flexible and the tonic rigidity of
catalepsy is absent. The state of complete insensibility is not, how-
ever, continuous, inasmuch as there occur periods during which the
patient may see, hear, and remember all that goes on about him, and
may partake of small quantities of food. The condition of the patient
is not, indeed, unlike that of a hibernating animal. In the state of
trance the patient usually lies in a warm room, Avell covered with
clothing, so that little heat is lost by radiation ; the mental functions
are in abeyance, indicating that the molecular changes which are the
correlatives of mental actions have ceased, and all muscular movements
are suspended with the exception of the cardiac contractions, and
slight respiratory movements, and under such circumstances the amount
of waste must be small. The physician must, of course, be on his guard
against deception in cases of trance.
g. Ecstasy.
This condition is closely allied to trance, the patient being insensible
to outward impressions in both. In ecstasy the mind is absorbed with
some fixed idea, generally of a religious character, and the patient
becomes oblivious of surrounding events and objects. The limbs are
motionless, and often fixed in maintaining a particular attitude, the
breathing is slow and feeble, the pulse is almost imperceptible, the eyes
are often bright and animated, and the countenance has an expression
of rapture.
h. SomnambuUsm and Hypnothm.
In somnambulism the patients appear to be wholly unconscious, yet
they walk, climb, and avoid obstacles, and may manifest greater strength,
agility, and precision of muscular adjustments than during waking
hours.
Hypnotism or mesmerisyn is, as Maudsley remarks, a kind of artifici-
ally induced somnambulism. The subject, who is probably always of a
neurotic temperament, is induced to look steadily at the operator, the
latter attracting his attention by making a few gentle "passes" with
his hand. Mr. Braid, of Manchester, directed the person to look upon
a disk or some bright object held in front of and a little above the level
of the eyes. After a short time there is a slight tremor of the eyeballs
CEREBRO-SPINAL SPASMS. 345
of the subject, bis pupils dilate, and be falls into the mesmeric condi-
tion. In this state the mental functions are abolished, and all the
actions of the subject are afterwards determined by the suggestions of
the operator. Under the influence of these suggestions, the subject mav
sing, recite poetry, and perform the most absurd and outrageous actions.
He may be made to eat a raw cabbage, amidst all the outward sions of
enjoyment, to appease a suggested hunger; he may spit out pure water
given him to drink with all the signs of disgust, on the suggestion that
it is bitter and nauseous, or drink infusion of wormwood with apparent
relish on being told that it is an agreeable beverage ; or he may be made
to sneeze violently on being asked to take a pinch of snuff from an
empty box. Hysterical patients may be thrown into a condition of
trance or of catalepsy, or one half of the body may be thrown into
trance and the other half into catalepsy, by being made to look upon a
brio;ht lif^ht.
Morhid Anatomy and Physiology. — Morbid anatomy has not yet
thrown much light upon the nature of local spasms. These spasms are
most liable to occur in muscles which are engaged in special actions,
such as the facial muscles, the rotators of the head and neck, and the
small muscles of the hand. These local spasms are most probably
caused by irritation of some part of the reflex loop. The irritation is
probably sometimes direct, but it is undoubted that it is frequently of
reflex origin. The reflex nature of these spasms is well illustrated in
some cases of facial tic. When motor-arresting points are obtained in
such cases they are observed not in the course of the facial nerve, but
over certain points of the trigeminal nerve. The nature of these
spasms will, however, be best illustrated by a detailed reference to the
pathology of the professional hyperkineses. The combinations of
muscular contractions concerned in writing are exceedingly complex,
but some of these combinations are more special than others. The
operation of writing is divisible into the acts of (1) prehension of the
pen, (2) moving the pen, (3) poising the hand and forearm. Of thes&
acts the first and the third are the most special, and they are certainly
the most liable to be affected in writer's cramp. The act of prehension
is mainly effected by the muscles of the ball of the thumb and the in-
terossei, and spasm, weakness, and incoordination of the movements
of these muscles are the more frequent symptoms of the disease.
Poising of the hand and forearm is effected chiefly by the pronators and
supinators of the forearm, and as the hand is always held in a position
in which gravity aids the pronators, the most delicate part in preserving
the attitude is thrown upon the supinators, and a sudden jerking of the
latter muscles causing the hand to roll outwards is not an unfrequent
3J:6 SPASMODIC DISOEDERS.
symptom of the disease. Professional cramps are doubtless caused by
a functional or molecular lesion of some part of the nervous mechanism
■which reo-ulates the actions of the muscles executing the movements
which are disordered. It is very likely that professional cramps are
sometimes caused in the same way as cramp of the calf by irritation of
the intramuscular nerve endings, or the end ])lates in the muscular
fibres. It is possible that at other times the seat of the lesion is the
mechanism of cells and fibres in the anterior gray horns of the spinal
cord which regulates the movements concerned in writing, while in still
other cases the lesion is probably situated in the cortical centre, or in
the course of the centrifugal conducting paths Avhich connect it with
the spinal cord. We should say that the chief lesion is situated in the
ganglion cells of the spinal cord, or in the fibres which connect them
Avitli the muscles in all those cases in which the electrical reactions of
the muscles are diminished, and that it is situated either in the cortex
or in the cerebral conducting path above the spinal level in all those
cases in which the electrical reactions are increased, especially if this
increase is maintained when the disease is of long standing.
Saltatory spasm is here placed amongst the spino-peripheral spasms,
because a case recorded by Bamberger appears to indicate that the
excess of reflex action in such cases originated in the skin. The spasms
are, however, regarded by Frey as being caused by undue tension and
stretching of the muscles, and it is, therefore, possible that some of
of the recorded cases are caused by exaggerated tendon-reactions. A few
of the recorded cases appear to have been of liysterical origin, while in
others the presence of contractures shows that the affection was caused
by some form of lateral sclerosis. It is, indeed, very probable that very
different aff'ections have been grouped together under this name.
Tetanus is here placed amongst the spino-j)eriplieral spasms because
there can be little doubt that increased irritability of the gray matter
of the spinal cord plays a very important i)art in the production of
the symptoms of idiopathic and traumatic tetanus as well as of the tetanic
spasms which are caused by strychnine and other poisons. Lockhart
Clarke found great hypercemia of the spinal cord and its memliranes
as Avell as foci of softening in the gray and white substance of the cord
in cases that died from tetanus, and these observations have been con-
firmed by numerous other investigators. Similar changes have also
been found in the medulla oblongata. It is, however, po.ssible that the
changes which have been discovered were caused by the great conges-
tion of the cord and membranes which must have resulted from the
violent attacks of spasm. Some pathologists believe that tetanic seizures
are caused by an increased irritability of the gray matter of the spinal
CEREBRO-SPIXAL SPASMS. 347
cord and of the medulla oblongata. This increased irritability of the
.spinal centres not only raises the irritability of the i-efle.x arcs, but also
gives rise to spontaneous discharges of energy, and both of these con-
ditions are doubtless present in tetanus. I am, however, inclined to
believe with Dr. Hughlings-Jackson that discharges of nerve energv
from the cortex of the cerebellum are the main cause of the paroxysms
of spasm in tetanus, although these discharges may to some extent be
determined by the instability of the centres in the medulla oblongata
and spinal cord. Tetany is believed by many authors to be also caused
l)y an increased irritability of the spinal centres, but pathological
anatomy has not thrown much light upon the question. The theory of
cerebellar discharge is probably as applicable to tetanus as it is to tetany,
Init it must be admitted that the question is one which can hardly be
determined in the present state of our knowledge.
Thomsen's disease would appear to be, according to the latest re-
searches of Erb, a primarily muscular disease. If this view should
turn out to be correct, this disease will hold the same relation to the
spino-neural spasms that pseudo-hypertrophic paralysis bears to the
spino-neural paralyses.
It has been found most convenient to describe the morbid anatomy of
the cortical monospasms and protospasms along with the clinical descrip-
tion of the different varieties of these spasms. The most important
characteristic of these lesions is that they are what Dr. Hughlings-
Jackson has called "coarse disease,"' that is, a disease which can be
recognized by the naked eye. It now remains for us to connect the
morbid changes Avith the symptoms. When an irritative lesion is situated
in or near the motor area of the cortex of the brain the surrounding
parts are more freely supplied with blood and the gray substance, after
absorbino; a lar^e stock of nourishment, discharges its accumulated
energy at periodical intervals, thus giving rise to paroxysms of convul-
sions of the muscles whose actions are regulated from that part of the
cortex. Every excessive discharge of energy is followed by exhaustion
of the motor centres near the irritative lesion, and consequently each
convulsive paroxysm is followed by a transient paralysis of the affected
muscles. The lesion may destroy a portion of the cortex Avhile main-
taining the neighboring portions in a state of irritation, and consequently
cortical monospasms are often accompanied by a permanent paralysis
of some groups of muscles, and the convulsive paroxysm always begins
in the neighborhood of the paralyzed muscles. The annexed diagram
(Fig. 97) will readily explain the order in which the spasm progresses
in the chief varieties of unilateral convulsion. If the lesion is situated
near the longitudinal fissure between the fissure of Rolando the spasm
348
SPASMODIC DISORDERS,
will beo-in in the leg, and as the wave of molecular disturbance extends,
the arms are next involved and the i\ice last. If the lesion is situated
near the frontal convolution the spasm will begin in the muscles of the
face, those of the hand are next involved, and those of the leg last. If
the lesion is situated about the sulcus of Rolando, the spasms will begin
in the muscles of the arm and hand, those of the face are involved
Fig. 97.
External Convex Surface of the Human Brain.
Fissures: R, Fissure of Kolando ; S/, Fissure of Sylvius; pf. Parallel fissure ; ipf, Interparietal fissure :
pof, External parieto-occipital fissure. Couvobiliotis and Lobules : A, Ascending frontal ; B, Ascending
parietal convolutions; Fj, Fo, F3, First, second, and tliird frontal convolutions; Pj, Superior parietal
lobule ; Po, Supra-marginal gyrus ; P3, Angular gyrus ; 0], Oo, O3, First, second, and third occipital cim-
volutions ; Tj, To, T3, First, second, and third temporo-sphenoidal convolutions. Mnlor Centres: ], Move-
ments for rotation of head and neck ; 2, Movements of the upper facial muscles ; 2', Jlovements of the
lower facial muscles ; 3, Movements of the tongue and jaws ; 4, Jlovements of 8ui)erior extremity ; 5,
Jlovements of inferior extremity ; 6, Movements of the ocular muscles ; 7, Movements in relation with
the sense of hearing.
next, and those of the leg last. When the lesion is situated wholly in
the motor area consciousness is either not much affected, or it is lost at
a comparatively late period of the spasm, but when it is situated in the
prefrontal area of the cortex, consciousness is lost Ijefore the commence-
ment of the spasm or soon after it begins. And when the lesion is
situated in the occipital or temporo-sphenoidal lobes, the spasm is pre-
ceded by some disturbance of sight or of hearing respectively.
In idiopathic epilep.sy no constant anatomical changes have been
found in the nervous system, but such changes as have been discovered,
like atrophy of one of the hippocampi majores, have generally affected
CEREBRO-SPINAL SPASMS. 349
the cortex of the brain. The lesion of idiopathic epilepsy is, therefore,
regarded as a molecular disturbance.
Dr. Todd was the first to suggest that epilepsy was caused by an
explosion of nerve force, but this theory has assumed a definite shape
in the hands of Dr. Hughlings-Jackson, who advanced the opinion
that all convulsions which are attended by loss of consciousness are
caused by discharging lesions of the cortex of the brain. This hy-
pothesis has received a considerable amount of experimental verifica-
tion. Hitzig Avas able to determine epileptic paroxysms by various in-
juries to the cortex of the brain, and Ferrier obtained a similar result
by passing a faradic current of moderate intensity through the cortex,
the electrodes being widely separated, so that a large portion of the
cortex was included in the circuit. According to this theory, the con-
vulsions are caused by a large discharge of nervous energy from the
cortex of the brain along centrifugal nerve paths, and the loss of con-
sciousness is caused by the temporary exhaustion which succeeds to an
excessive nervous discharge. But we have seen that the paroxysm of
unilateral epilepsy is alwaj^s followed by a temporary paralysis of the
convulsed limbs, and it may be asked why it is that the paroxysm of
general convulsions is not likewise followed by a temporary paralysis?
The reply is that it is so followed. After an epileptic attack there is
complete muscular relaxation, but as the patient is at the same time in
an unconscious condition the degree of paralysis which is present cannot
be estimated, and even after consciousness is regained general muscular
feebleness often remains for a time, Avhich although not called paralysis is
really paralytic in nature. The unseemly and apparently immoral actions
performed, and the atrocious crimes often committed by patients after
minor attacks of epilepsy, may be explained on the supposition that
the inhibitory influence of the highest centres is temporarily suspended,
thus permitting the centres which preside over automatic actions and
animal instincts to spring into greater activity.
Many of the spasmodic phenomena of hysteria are best explained
on the supposition that the irritability of the cortex of the brain is
increased, whilst others are best explained by supposing that the irrita-
bility of the cortex diminishes. Hysterical attacks are caused by a dif-
fused discharge of energy from the cortex of the brain, while local
spasms are sometimes caused by a local discharge from one of the
motor centres, and at other times, especially Avhen they assume the
form of persistent contracture, by paralysis of one of these centres,
removing the inhibitory action of the brain, and thus permitting the
unrestrained action of inferior ganglia. Very little beyond conjecture
is known with regard to the pathology of catalepsy, trance, ecstasy,
350 SPASMODIC DISORDERS,
somnambulism, and hypnotism, but there can be but little doubt that
these curious conditions are caused by a molecular disturbance of the
cells and fibres of the cortex of the brain, or of the conducting paths
which lead from the surface of the body to the cortex. Hysterical
hemianesthesia, for example, is best ex})lained by supposing that the
conduction of the centripetal fibres in their ascent through the internal
capsule is temporarily arrested. Suppose that a complete bilateral
hemianesthesia exists, what would be the condition of the patient?
There would be complete loss of every form of cutaneous and muscular
sensibility as well as of sensation in the bones and joints, there would
be loss of taste on both sides of the tongue, and of smell in both nos-
trils, and instead of there being amblyopia and partial deafness on one
side as in hemianaesthesia, there would be complete blindness and deaf-
ness on both sides, inasmuch as, according to the hypothesis, the sen-
sory centres in both hemispheres either have ceased to act, or the
impressions made upon the peripheral sense organs fail to be conducted
to them. But impressions made on the periphery would, however,
reach the cortex of the brain through the optic thalamus, and the
subject of bilateral hemiansesthesia, although effectually cut off from
the external world so far as the anatomical substratum of consciousness
is concerned, would perform various complicated actions in response to
peripheral impressions, but without being attended by consciousness.
The state of the patient would, indeed, be very similar to that observed
in somnambulism, the mesmeric state, and various post-epileptic and
allied conditions.
Treatment. — The first aim of treatment is to Avithdraw the excitin"-
cause of the spasm, and with this view all sources of direct irritation
such as tumors in the vicinity of the nerve, of reflex irritation such as
conjunctivitis in blepharospasm, carious teeth in facial spasm, and irri-
tating substances in the atmosphere in sneezing, and of remote irritation
such as uterine disease in facial spasm or spasmodic torticollis, must be
removed. The source of irritation may be found in impure blood, and
if the patient be rheumatic salicylate of soda or iodide of potassium,
and if scrofulous, carbonate of iron and cod-liver oil should be admin-
istered. When the local spasm is a mere expression of a more general
nervous disease such as hysteria or chorea, the treatment appropriate
for the central disease must be adopted. The most likely internal
remedies for such cases are arsenic, bromide of zinc, and bromide of
potassium. The local application of chloroform and ether spray, and
the subcutaneous injection of morphia, will be found useful in many
cases to allay the distress caused by the spasm. The best local treat-
ment, however, is afforded by the application of the constant cur-
CEREBRO-SPINAL SPASMS. 351
rent. A descending current of moderate intensity may be passed
along tlie affected nerve, and when points of arrest are obtained the
anode shoukl be phaced over one of these. The antagonists of the
affected muscles may be strengthened by the use of the ftiradic current,
but the interrujjted current should never be applied directly to muscles
Avhich are the subjects of spasm. Some cases of spasm are benefited
by the application of a strong galvanic current over the vertebi'al column,
the part of the cord from which the affected nerve is derived beino- in-
cluded in the circuit. Continuous pressure over the affected nerve bv
means of a compress or suitable mechanical appliance at a point at
which it emerges from a bony canal or becomes superficial has been
found useful in the treatment of spasm. In some cases the pressure is
more successful when applied over one of the "spasm-arresting points'"
of the fifth nerve in fecial spasm, in the length of the affected muscles
in other cases.
Various surgical operations have been resorted to for the cure of local
spasms. Subcutaneous division of muscles and of tendons is most likely
to be of use in the tonic form of spasm. Division of the spinal accessory
nerve has been successful in several cases of spasmodic torticollis, but
section of the facial nerve causes paralysis of such a large number of
important muscles that it is hardly a justifiable operation. Stretching
of the nerve has, however, been attended with very favorable results in
several cases. In spasms of groups of muscles of the extremities various
mechanical contrivances may be employed in order to force and maintain
the limb in a normal position. In spasmodic torticollis the head may
likewise be maintained in the normal position by means of a Sayre's
jacket with jury-mast. Another method is to surround the head and
the trunk each by a plaster-of-Paris bandage, and to connect the tAvo by
a strong India-rubber band passing obliquely from one side to the other
in such a position as to counteract the spasm of the affected muscle.
Professional cramps must be treated on the same general principles as
other forms of local spasm. In slight and recent cases rest for a period
of from two to three months will alone suffice for a cure, but this period
must be prolonged to from six to twelve months in severe cases.
The most successful treatment of writer's cramp appears to be that
practised by Wolff, which is a combination of gymnastics and massage.
The gymnastic exercis.es consist of both active and passive movements.
In the active form of exercise the patient is instructed to execute, three
or four times a day, a series of vigorous movements with the affected
extremity, the hand being opened and closed in quick succession. The
number of these movements, and consequently the duration of each
exercise, is progressively increased until a duration of about half an
352 SPASMODIC DISOKDERS.
hour is attained for each sitting. In the passive movements the operator
makes forcible traction three or four times a day upon each of the
affected muscles separately in the direction of its length. This appears
to be the most delicate part of the treatment, inasmuch as if too little
strength is employed the cure is delayed, and if too much the disorder
is aggravated. When the spasm is notably diminished, which usually
occurs in a short time, the patient is encouraged to take slow and grad-
uated exercises in writing. The operator practises daily massage of the
affected extremity, particular stress being laid upon percussion over
the affected muscles with the ulnar border of the hand. When no
amelioration of the symptoms is produced in four or five sittings, Wolff
believes that the treatment maybe abandoned as not likely to prove
useful. The treatment by massage is applicable to spasms of other
muscles, and several cases of spasmodic torticollis in which I prescribed
it, were much benefited.
3Iechaniecd means have been resorted to in severe cases. The simplest
method of this kind is to insert the pen into a cork or thick piece of
wood, or to fasten it by means of a ring to the first or middle finger.
Many patients are relieved by applying a narrow bandage or a strip of
court-plaster firmly-round the wrist.
Tenotomy of the affected muscles has been performed, but the results
obtained have not been very encouraging. The treatment of other
professional spasms must be conducted on essentially similar principles.
Very little is known with regard to the treatment of saltatory spasm,
but the agents most worthy of trial are morphine, bromide of potassium,
calabar bean, ergotine. conium, and atropine.
In tetanus the great aim of treatment is to diminish the irritability
of the gray matter of the spinal cord. The agents which have been
used for this purpose are chloral hydrate, bromide of potassium, calabar
bean or cannabis indica, nicotine, chloroform, and morphine. The cold
bath and cold douche may be used Avhen there is a sudden elevation of
temperature, and under these circumstances the patient may be placed
in a bath of about 90° F., and the temperature should be gradually
reduced to 60° F. by the addition of cold water. In ordinary cases a
warm Ijath is soothing to the patient. The patient should be protected
from every source of irritation, such as noises, strong lights, changes
in temperature, and sudden contact. His strength should be well
supported, and when he is unable to swallow liquids, owing to the
spasm, food should be introduced by means of a tube passed through
the nose after the patient has been brought under the influence of
chloroform.
In tetany the causes of the disease must be carefully inquired into
CEREBRO-SPIXAL SPASMS. 353
and removed when possible. The diet should be full and generous, and
Avhen the spasm is allayed change of air is indicated. Durino- a severe
paroxysm it may be necessary to use chloroform inhalations, opiates, or
belladonna, and bromide of potassium, either alone or in combination
with chloral, may be a useful adjunct to treatment. The galvanic cur-
rent to the contracted muscles has often proved useflil.
In unilateral convulsions the treatment must be directed against the
primary disease, and the possibility of syphilis should never be for-
gotten. In the treatment of functional spasmodic affections the greatest
care must be taken to discover and remove any source of peripheral
irritation, and in hysteria great attention must be paid to the treatment
of ovarian and uterine disorders.
In the treatment of epilepsy, it has been found that la-omide of
potassium is the most useful drug, and to do good it must be given in
doses ranging from ten to forty grains three times daily. Large
doses of this salt are apt to produce an eruption of acne, Avhich
soon subsides when the drug is discontinued, and it may possibly be
prevented by combining arsenic with the bromide. The bromide of
sodium or of ammonium may be used instead of the potassium salt, as
being less depressing in its effects. Chloral hydrate is sometimes a
useful adjunct to the bromide of potassium. The salts of zinc have also
proved useful in the treatment of epilepsy, and they appear to be more
eflBcient with patients under twenty years of age than with those of
maturer years. The oxide may be given in doses of from two to five
grains three times daily, or the sulphate may be administered at first
in doses of three grains, and progressively increased to scruple doses
three times daily. The bromide of zinc has been given in gradually
increasing doses until a scruple is taken three times a day. The oxide
of zinc may be combined with extract of belladonna or hyoscyamus,
or with the powdered root of valerian. Iklladonna, or atropine and
digitalis have been found useful in the treatment of epilepsy, either
alone or in combination with one of the bromide salts.
The treatment of eclampsia must vary according to the cause of the
convulsion, but during the attack the inhalation of chloroform is the
most generally useful method of treatment for arresting the spasm.
The general treatment of hysteria is too wide a subject to be dis-
cussed fully in this place. Bromide of potassium is found very useful
in the treatment of hysterical spasms, but the administration of iron
and other tonics, with attention to the health of the patient, is much
more generally useful than any special remedies. The most important
part of the treatment, however, consists of the moral management of
tlie patient, and hysterical patients are treated with much greater
23
;^5J: SPASMODIC DISORDERS.
success in the wards of a hospital than in their own homes. In
aggravated cases, therefore, the patient shoukl be removed from her
home and relations, and placed for a period of some months either in
a public institution or under the care of complete strangers. Tlie
method of seclusion from her friends was first, so for as I know, strongly
insisted upon by Dr. R. Brudenel Carter, and it forms a principal factor
in the treatment of hysterical neurasthenia, which has been elaborated
by Dr. S. Weir Mitchell, and which has already been described. "The
attacks," says Dr. Carter, ''Avill, in all probability, occur during a
meal, or when there are strangers present, or at some most inconvenient
time and place, and it may, on this account, be necessary to have the
patient removed to her bedroom. In such case she should be carried
there as quickly as possible, placed upon the floor, and immediately
left quite alone, the door being shut, and no one being suffered to open
it on any pretext whatever until the patient does so herself. But if
the room in which the attack takes place can be spared for a few hours,
it should be closed and shut up in the same manner, and in either case
especial care must be taken not to give utterance to a single expression,
either of sympathy or alarm. After the lapse of a longer or shorter
time, often at a meal, and sometimes not until the next morning, she
will present herself as usual, and will perhaps offer some apology or
express some regret for her illness. This should be graciously received,
and then every attempt on her part to return to the subject must be
carefully and industriously foiled, no inquiries being made about her
health, and all complaints being interrupted by the introduction of
ordinary conversational topics." Treatment by isolation is only to be rec-
ommended in very aggravated cases, and after other measures have failed.
In ordinary hysterical attacks the patient takes care not to injure her-
self, but it is often necessary to prevent respiration being impeded by
clothing. In my experience it is often desirable to prevent a hysterical
woman from tossing about violently in all directions. The best method
of preventing the patient's struggles is to place an attendant on each
side of her, and to direct each to grasp one wrist with one hand, and
to hold the shoulder firmly down to the bed or floor with the other, and
if necessary the legs must be held down by a third attendant. It is
remarkable how soon a hysterical patient ceases to struggle when she
finds that she is held as in a vice. So long as the patient can shake herself
free from her attendants, so long is the struggle likely to be maintained,
but when once she feels that she is thoroughly restrained, and that her
efforts do not find outward expression, she generally ceases to struggle.
The most usual remedy for arresting the attack is to dash cold water
on the face and neck, and the plan suggested by Dr. Hare, of forcibly
CEREBRO-SPINAL SPASMS. 355
holding the mouth and nose of the patient so as to prevent her from
breathing, is still more effectual. An emetic of sulphate of zinc is also
very successful in arresting the attack.
Local spasms in hysteria are best removed by general treatment and
moral management, although local treatment and special remedies are
occasionally found useful. The most useful local remedies are the cold
douche and faradic current.
In the treatment of catalepsy and allied conditions the best results
have been obtained by the use of iron and other tonics, ergot, the cold
douche, and the faradic current. In protracted cases artificial feeding
by the stomach pump and nutritious enemata must be employed.
CHAPTER Y.
ATROPHIC PARALYSES.
It has already been shown that the various forms of paralysis may be
divided into spino-peripheral or atrophic, and cerebro-spinal or spasmodic
paralyses. The spino-peripheral paralyses with which we have to do at
present may be divided into (I.) simple neural paralyses caused by local
disease or injury of individual motor or mixed nerves ; (II.) multiple
neural paralyses caused by disease affecting many of the peripheral
nerve branches and often assuming a progressive character; (HI.)
reflex paralyses caused by iiiitation of afferent nerve fibres ; (IV.)
spinal atrophic paralyses caused by disease of the ganglion cells of the
anterior gray horns of the spinal cord, and to these may be added (Y.)
certain forms of myopathic paralysis.
I. SIMPLE NEUKAL PARALYSES.
1. Paralysis of the Oculo-motok Nerves.
The oculo-motor nerves are the oculo-motorius, trochlearis, and
abducens, and the subjoined diagram (Fig. 98) Avill suffice to remind
the reader of their course and distribution.
a. Disorders of the Movements of the Eyelids.
(1) The lev( ^^ palpehrce superioris is but seldom affected by tonic
spasm as an isolated affection, and hardly ever by clonic spasm. Tonic
spasm of this muscle causes the lid to be drawn upwards, and there is
consequent inability to close the eye, either by voluntary effort or during
sleep. The orbicular muscle is supplied by the fiicial nerve, and spasm
of it will be subsequently described.
(2) Paralysis of the levator palpebrce superioris, or ptosis, may occur
as a separate affection, but it is usually associated Avith paralysis of the
superior rectus, both muscles being supplied l)y the superior branch of
the oculo-motor nerve. The upper lid hangs motionless, the palpebral
aperture is greatly narrowed, the lid remains motionless when the eye is
directed upwards, and the horizontal wrinkles of the upper lid are
effaced.
SI.MPLE XEURAL PARALYSES. ;—
357
(3) Disorder of the Associated and Mechanical Movements of the
Muscles of the Eyelids. — When the eyes are directed upwards in health
there is an associated contraction of the elevators of the lids and the
upper eyelids are Tetracted, and when the eyes are directed downwards
there is a simultaneous downward movement of the upper eyelids, and
Fig 98.
DiAORAM OF THE FiRST OR OPHTHAI.MIC DiVISIiiX OF THE FiFTlI, SHOWING ALSO THE TuiRD, KlIURTH,
AND Sixth Cranial Xerves. (From Hermann's "Phj'siology."')
V, Sensory root of fifth nerve.
GG, Gasserian ganglion on larger ruot of the fifth nerve.
a, Ophthalmic division of the fifth nerve.
1, Frontal nerve. 2, Lachrymal nerve. 3, Xasal nerve.
LG, Lachrj'mal gland.
.3', Infra-trochlear branch of nasal nerce.
3", Long ciliary branches of nasal nerve.
3'", Branch of nasal nerve to ophthalmic ganglion.
OG, Ophthalmic ganglion.
6, Second division of the fiftli cut across, c, Third division of fifth cut across.
III, Third nerve (motorius oculi).
4, Upper division of third nerve. 5, Lower division of third nerve, near point where it gives
the short root to the ophthalmic ganglion.
IV, Fourth nerve (n. trochlearis).
7, Its fibres passing to the superior oblique.
VI, Sixth nerve (n. abducens).
0, Its fibres passing to external recttis.
CA, Carotid artery.
E, Vertical section through anterior part of eyeball ; conjunctiva indicated by dotted line.
^^
to a less extent of the lower lids also. The downward movement of the
upper eyelid is most probably caused by an inhibitory cerebral influence
being sent to the elevator of the eyelid and superior rectus muscles
simultaneously with the impulse to contraction sent to the inferior
rectus, while the depression of the lower eyelid is probably caused by
pressure of the cornea against it. It has been shown by Dr. Gowers
that these movements are disordered in partial paralysis of the third
358
A'TEOPHIC PAR-
nerve. In a case of the kind under my care tne i^atient in looking
forwards manifests a slight external squint of the right eye (Fig. 99),
while the palpebral aperture on that side is a little smaller than the other
Pig. 99.
Fig. 100.
one. When the patient looks up (Fig. 100) the left or healthy eye is
rotated upwards, and there is a simultaneous upward movement of both
eyelids on that side, but, as usual, the eye has gained on the lower lid,
Fig. 101.
so that a considerable portion of the sclerotic between the lower margin
of the cornea and the « edge of the lid is uncovered. The right eye,
however, has scarcely moved, and the lids have also remained stationary.
SIMPLE NEURAL PARALYSES. 359
But the most striking deformity occurs wlien the patient looks down.
The left upper eyelid moves downwards in association with the down-
ward rotation of the eyeball, but the right eyelid and eyeball remain
comparatively stationary, and the patient presents the singular appear-
ance of looking Avith the left eye at an object lying at her feet, while
the right eye seems to be looking at an object almost on a level with
the eye (Fig. 101). This disorder in the movements of the eyelids of
the right side is caused neither by spasm of the levator nor by paralysis
of the orbicular, because the patient can close that eye with as much
readiness and firmness as the left one. The immobility of the right
eyelids must, therefore, be caused mainly by an arrest of the associated
contraction and relaxation of the levator palpebrpe, which respectively
occurs during upward and downward rotation of the eyeball.
h. Paralysis of the Exteryial Muscles of the Eyeball.
General Etiology.
Paralysis of one or more of the ocular muscles may be caused by
cold, exposure of the eye to strong impressions of light, excessive
smoking, alcoholic excess, blows on the eye, penetrating wounds of
the orbit, fracture of the skull, and compression of the nerves by
tumors. But the most frequent and important causes are syphilitic
deposits and the degeneration wdiicli is the anatomical substratum of
locomotor ataxia. Ocular paralysis is also caused by diphtheria, and
may occasionally be a sequel of other acute diseases.
General Symptoms.
Diplopia. — If, when the visual axis of one eye is directed to an
object, the direction of the other deviates from it, the image in the dis-
torted eye falls on an eccentric portion of the retina, and two objects
instead of one are seen. The image seen on the healthy eye falls on
the macula, and is therefore distinct, but the image seen on the distorted
eye forms upon a more or less peripheric region of the retina, and is
therefore faint and more or less confused ; the former is consequently
called the true, and the latter the false image.
Neutralization of the False Image. — When the paralysis is of old
date the patient learns to perceive objects only with the healthy eye
and the diplopia disappears, whilst the distorted eye, from long-con-
tinued disuse, suffers consecutive amblyopia. The diplopia may, how-
ever, be made to reappear by placing before the healthy eye a colored
glass, which differentiates the true image and permits that of the dis-
torted eye to be perceived.
360
ATROPHIC PARALYSES.
Relation of the Images to One Another. — The false image ahvays
occupies, with reference to the axis of vision, an opposite position to
the distortion of the eye. Assuming the left eye to be aftected, the
false imaiT-e is displaced horizontally to the patient's right in outward
squint (Fig. 102, 1), horizontally to the patient's left in inward squint
(Fig. 102, 2); the false is above the true in downward (Fig. 102,
Fig. 102.
In the above diagram the thick cross represents the true image, tho thin cross the/i(/«e image. The left
eye is supposed to be affected in all of them. (After Bristow.)
3 and 4), and below it in upward squint (Fig. 102, 5 and 6). In out-
ward or inward squint the images are vertical and parallel Avith one
another, but in all other forms of squint the oblique muscles rotate the
distorted eyeball and the false becomes tilted with reference to the true
image (Fig. 102, 3, 4, 5, and 6), the false image being tilted in the
opposite direction to the rotation of the globe. The distance between
the images becomes greater as the object is moved in the direction of
the action of the paralyzed muscles.
Vertigo. — Diplopia causes considerable embarrassment to the patient
whilst walking, which disappears in great part when the distorted eye
I
SIMPLE NEURAL PAEALY.SES. 3H1
is closed. In ascending a stair, for instance, he sees two steps for
every one, and not knowing upon which to place his foot becomes con-
fused and stumbles. Perception of distance is defective, and the patient
becomes confused on endeavoring to grasp objects. This constant con-
fusion causes great fatigue, vertigo, and sometimes vomiting.
Compensating Attitudes. — The patient instinctively neutralizes the
perception of double images by placing the head in such an attitude
that the paralyzed muscle does not require to act, and then the visual
axes can be converged upon objects.
Secondary Deviation of thr Sound Eye. — This condition has already
been described.
False Projection. — When a person looks at an object Avith one eve
only, a judgment of its position in space is formed by the sense of
effort made to fix the object. If a patient with paralysis of the ex-
ternal rectus of the left eye be asked to touch an object coming before
him from the left or paralyzed side, he misses it by carrying his finger
too far to the left, or to the side of the object corresponding to that
of the paralyzed muscle. The difficulty of immediately recognizing
the position of objects in space, called false projection., is caused by
the fact that it is necessary to make an increased effort with the affected
eye, so that the amount of rotation is overestimated, and consequently
an erroneous judgment of the position of the body in space is formed.
Secondary contraction of the antagonistic muscles often occurs ; it
increases the extent of the duration, and augments the distance of the
double images from one another.
Symptoms of Special Forms of Paralysis.
(1) Complete paralysis of the oculo-motorius gives rise to paralytic
exophthalmos, ptosis, divergent strabismus, dilatation and immobility
of the pupil, and impairment of the power of accommodation. Every
effort to move the eye in any direction causes it to rotate outwards
and downwards, and it gradually becomes fixed in this position by the
secondary contraction of the external rectus and superior oblique.
Double images appear over almost the Avhole field of vision : the folse
image is to the right when the left eye is affected, the two images are
on a level when the object is in the horizontal position, and the false
appears below- the true image when the object is below, and above it
when the object is above the horizontal line. Fixation is only possible
in an outward and downward direction, the compensating attitude of
the head is a very oblique position backwards and towards the healthy
side, and secondary deviation of the eye takes place in all directions
except in that towards the affected eye.
362 ATROPHIC PAEALYSES.
(2) Incomplete Paralysis of the Oculo-motorius. — {a) Paralysis of
the superior rectus gives rise to strabismus dorsum vergens, in which
the affected eye is rotated dowiiAvards and a little outwards. The
false is seen above the true image and tilted to the patient's right
when the left eye is affected (Fig. 102, 3) ; the vertical distance be-
tween the images increases according as the eyes are directed upwards
and outwards, while the false image disappears at the horizontal line,
provided there be no secondary contraction of the inferior rectus.
When the eyes are directed downwards objects are seen single, and the
head is thrown back in order to counteract the paralysis.
(6) Paralysis of the internal rectus gives rise to strabismus diver-
gens, and the eye cannot be rotated inwards beyond the middle line.
The images are vertical, parallel, and on the same plane; the lateral
distance between them increases as the object is moved towards the
sound side, and the false image is to the patient's right when the left
eye is affected (Fig. 102, 1). There is secondary deviation of the sound
eye outwards, and in fixing an object the head is turned towards the
healthy side.
ic) Paralysis of the inferior rectus gives rise to strabismus sursum
veryens, in which the affected eye is directed upwards and slightly out-
wards. The false is below the true image and tilted to the patient's
left when the left eye is affected (Fig. 102, 5). The false image dis-
appears when objects are held above the horizontal line, but double
vision reappears whenever the line of vision is lowered, and conse-
quently this form of paralysis is very troublesome in walking and in all
kinds of handiwork.
(d) Paralysis of the inferior oblique gives rise to a squint in which
the eye is turned slightly down-svards and inwards. The false image is
above the true and tilted to the patient's right when the left eye is
affected (Fig. 102, 4). Double images appear when the eyes are
directed upAvards and disappear at the horizontal line, while the images
become more and more separated, l)oth vertically and laterally, and
the tilting of the false image becomes more pronounced according as
the object is carried upwards and outwards. In the compensatory
attitude the head is thrown backwards and the chin turned a little
towards the healthy side.
(3) Paralysis of the trochlear nerve gives rise to a moderate squint in
which the eye is slightly rotated upwards and inwards. Double images
appear when the eyes are directed dowuAvards, and become more and
more separated both vertically and laterally according as the olyect is
carried downwards and outwards. The images are vertically superim-
posed, the flilse being the lower and the more remote of the two, and
SIMPLE NEUEAL PARALYSES. 363
Tilted to the patient's right when the left eye is affected (Fig. 102, 6).
The secondary deviation is usually straight downwards. There is false
projection of the field of vision downwards and a little outwards, and
the head is inclined forwards and turned towards the healthy side. The
feeling of giddiness is often well marked.
(4) Paralysis of the abdueens nerve gives rise to strabismus ron-
vergens, and the eye cannot be rotated outwards beyond the middle
line. Double images are seen when the eyes are turned horizontally to
the paralyzed side, the distance between them increases according as
the object is moved to that side ; the images are vertical and parallel,
and the false one is to the left of the patient when the left eye is
affected (Fig. 102, 2). Secondary deviation occurs to the inner side,
there is false projection of the field of vision towards the outer side,
and the head is turned towards the affected side. The feeling of o-iddi-
ness is severe, and may be accompanied by nausea and vomiting.
(5) Paralysis of the ciliary muscle, (cycloplegia) renders the patient,
if not myopic, unable to focus small objects or- read small print, and he
forms an incorrect estimate of the size and' distance of small objects.
It is often complicated by mydriasis, although it may occur as an inde-
pendent affection.
2. Masticatory Paralysis.
Etiology. — Paralysis of the trigeminus is rare as a result of lesions
of the nerve in its extracranial course, but generally results from intra-
cranial lesions such as periostitis, exostoses, caries, extravasations, and
tumors, which compress the nerve at the base of the skull. It is also
caused by lesions of the pons and occasionally by lesions of the cortex
of the brain.
Symptoms. — "When the paralysis is unilateral there is difficulty or
impossibility of masticating food on that side, and the lateral move-
ments towards the sound side are rendered impossible by paralysis of
the pterygoids. The affected muscles are often felt to be wasted, and
they remain flaccid during mastication, while those of the opposite side
feel rigid at each contraction. The paralyzed muscles may occasionally
manifest the "reaction of degeneration." The tensor veli palati is
supplied by the fifth nerve, but paralysis of this muscle has not been
observed along with masticatory paralysis. The tensor tympani is also
supplied by the fifth nerve, and it is probable that disorders of hearing
may accompany masticatory paralj'^sis in the absence of any lesion of
the auditory nerve, consisting of noises in the ears, and a diminished
power of appreciating deep tones. The paralyzed muscles may become
atrophied, and they then, as a rule, manifest the reaction of degeneration.
8(34 ATROPHIC PARALYSES. ^
When the aflfection is bilateral the patient suffers great fatigue during
mastication, and he is forced to eat only fluid and pulpy nourishment.
When the paralysis is complete the lower jaw falls down with its own
weight ; at other times the jaw is fixed by secondary contraction of
the paralyzed muscles. Bilateral masticatory paralysis is generally met
with as a part of labio-glosso-laryngeal paralysis.
Sensoty disorders usually accompany unilateral masticatory paralysis,
and the sensory branches of the nerve are often implicated in the absence
of any paralysis of the motor branch. When all the branches of the
nerve are affected, one side of the face, part of the ear, the skin of the
temple and forepart of the head, conjunctiva, cornea, nasal and oral
mucous membranes, tongue, gums, and part of the pliarynx are all
rendered more or less completely insensitive on the affected side,
but violent eccentric pains may be felt in the anaesthetic area (anics-
thesia dolorosa). When the patient puts a cup to his lips it gives him
the impression of being broken, as he can only feel with one-half of
the lip.
On the affected side the skin of the face is cold and often of a bluish
color ; the gums are spongy ; the mucous membrane of the mouth and
nostril may ulcerate and bleed ; and neuroparalytic ophthalmia is apt
to occur. Irritation of the nasal mucous membrane by ammonia or
snuff, on the affected side does not excite sneezing, and the sense of smell
on that side is diminished owing partly to dryness of the Schneiderian
membrane and partly to the nutritive changes which take place in it.
The sense of taste in the anterior two-thirds of the anaesthetic side of
the tongue is lost in those cases only in which the lesion is situated at
the base of the skull, or in the lingual branch of the nerve. When the
anaesthesia is of peripheral origin, reflex actions are abolished. The
extent of the anaesthesia will of course vary according to the seat of
the disease, and it may sometimes be limited to the area of distribution
of a single branch of the nerve.
Diagnosis. — The chief difficulty in diagnosis is to discover the locality
of the primary lesion, and for the determination of this point the fol-
lowing rules modified from Romberg may be of use :
(a) The more the anaesthesia is confined to slight filaments of the
nerve the more peripheral Avill the seat of the lesion be.
(b) If the loss of sensation affect a portion of the face together with
the corresponding facial cavity, one of the divisions of the nerve is
affected before or immediately after its passage through the cranium.
(c) When the entire area of the fifth is more or less anaesthetic, and
there are nutritive disorders in the affected pai-ts, the Gasserian ganglion
or the nerve in its immediate vicinity is the seat of the disease.
.SIMPLE NEURAL PAEALYSES. 365
(d) If the antesthesia of the fifth nerve is complicated with disordered
function of adjoining nerves, it may be assumed that the disease is seated
at the base of the brain.
(f) If sensation is lost in the face on one side, and in half of the
body and limbs on the other side, the lesion is probably situated in the
lateral part of the upper end of the medulla.
(f) If sensation is lost in the face, half of the body, and the limbs on
the same side, the lesion is situated in the opposite hemisphere of the
brain, most })robably in or near the posterior third of the posterior seg-
ment of the internal capsule.
3. Paralysis in the Area of Distribution of the Seventh
Nerve (Mimetic Paralysis, Hemiplegia and Diplegia
Facialis, Prosopalgia, Bell's Paralysis).
Paralysis of the facial nerve, ■which from the long course of the nerve
and its exposed position is frequently observed, may be (a) unilateral or
(6) bilateral. The branches and connections of the nerve are shown in
Fig. 103.
a. Unilateral Facial Pai^alysis [Honiplegia Facialis).
Etiology. — Exposure of one side of the face to cold is one of the
most frequent causes of facial paralysis, it is then called rheumatic
paralysis although most probably resulting from a slight neuritis. Facial
paralysis, although appearing at all ages, is most frequent between
twenty and forty years of age, and sex does not seem to exert any
influence on its production, and each side of the face is about equally
liable to be afiected. It frequently results from injury such as a severe
blow on the ear, gunshot and other wounds, and fractures of the temporal
bone, wdiile in association with paralysis of the auditory nerve it is one
of the most common signs of fracture of the base of the skull. It also
occurs after extirpation of the parotid gland and other surgical opera-
tions about the face and ear, and may be caused in newborn infants by
pressure of the forceps. Disease of the parotid gland or of neighboring
parts may cause facial paralysis either by pressure on the nerve or by
extension of the morbid process to it. Various diseases of the ear may
cause facial paralysis, and of all the causes suppurative otitis interna,
followed by destructive changes in the temporal bone, is probably the
most frequent. Bony tumors, and neoplastic formations of all kinds
in the internal ear may lead to compression and destruction of the nerve.
Primary disease of the facial nerve is occasionally observed as a com-
plication or sequel of acute febrile diseases such as diphtheria or variola,
366 ATllOPHIC PAKALYSES.
but is much more frequent as a secondary result of these affections from
disease of the temporal bone. Syphilitic periostitis, meningitis, and
exostoses, or gummata at the base of the skull, brain, temporal bone,
or in the sheath of the nerve itself, may produce paralysis by com-
pressing the nerve. Some persons appear to be predisposed to facial
paralysis. Eulenburg mentions the case of a young man who suffered
twice from right-sided, and thrice from left-sided facial paralysis. Facial
paralysis may occur as a rare symptom of some diseases of the spinal
cord when the morbid process extends upwards to the medulla, and it
may occur occasionally in tabes dorsalis, and as a rare complication in
tetanus.
Symptoms. — Premonitory symptoms consisting of pain, noises in the
ear, deafness, and abnormal sensations of taste on the side which is
subsequently attacked with paralysis may be experienced for some days
before the loss of motor power declares itself. The symptoms of com-
plete unilateral facial paralysis are very characteristic. The affected
side loses its wrinkles and furrows and appears smooth, flaccid, and
expressionless ; while it appears puffy and falls to a lower level than the
healthy side. The patient cannot wrinkle his forehead or elevate his
eyebrow on the paralyzed side ; he is also unable to close his eye and
on attempting to do so the eyeball rolls upwards and inwards or occa-
sionally upwards and outwards. The power of winking is lost and
the eye remains open during sleep (lagophthalmos), and being no longer
protected from the contact of foreign particles it often becomes irritated
and inflamed. Owing to paralysis of Horner's muscle, the tears cannot
enter the lachrymal canal, and, therefore, flow over the cheek. The
nostril on the paralyzed side flills in during inspiration instead of expand-
ing as it does in health, the tip of the nose is sometimes drawn to the
healthy side, and the naso-labial fold is obliterated. The mouth is
drawn obliquely over to the healthy side, and the distortion becomes
more pronounced during all mimetic movements, such as crying, laugh-
ing, and speaking. Paralysis of tlie buccinator causes the cheek to puft'
out in speaking, and during other expiratory actions ; the pronunciation
of the labial consonants is impaired ; attempts at blowing or whistling
fail because the air escapes through the paralyzed fissure of the lips ;
the saliva dribbles from the affected side ; and food is apt to accumulate
between the inner surface of the cheek and the teeth. The external
muscles of the ear are also paralyzed, but since these muscles are not
usually under voluntary control, impairment of movement in them is
not readily detected. Signs of paralysis of the platysma, the posterior
belly of the digastric, and the stylo-hyoid muscles can sometimes be
<liscovered. If the lesion of the nerve is situated above the geniculate
SIMPLE NEURAL PARALYSES,
367
ganglion, the levator palati and azygos uvulfB become paralyzed, but the
symptoms of this condition will be fully described -when the various
forms of paralysis of the soft palate are under consideration. If the
nerve is diseased above the point where the branch to the stapedius is
Diagram of the Facial Nerve, its connections and branches. (From Hermann's "Physiology."";
F, The facial nerve. A, Auditory nerve.
1, The geniculate ganglion.
gsp, Great superficial petrosal nerve connecting the facial ami Meckel's ganglion.
sxp, Small superficial petrosal nerve connecting the facial with the Otic ganglion and with the
tympanic hranch of the glosso-pharyngeal.
exp, External supei-ficial petrosal connecting the tacial with the plexus un the middle meningeal
artery.
"2, Chorda tympani, joining lingual nerve.
3, Nerve to stapedius muscle.
4, Communicating branch with the ganglion of the root of the vagus.
5, Posterior auricular nerve.
6, Branch to the stylo-hyoid and digastric muscles.
TF, Temporo-facial division )
,',„ rt ■ c ■ ^ ^■ ■ ■ r to muscles of expression.
CF, Cervico-facial division J ^
V, Fifth nerve. oJ, Auriculo-temporal branch.
id, Inferior dental nerve. I, Lingual nerve.
MO, Meckel's ganglion.
iiG, Otic ganglion.
SG, Submaxillary ganglion.
IM, Internal maxillary artery.
MM, Middle meningeal artery.
P, Pneumogastric nerve.
GP, Glosso-pharyngeal nerve.
I, Its tympanic branch (nerve of .Jacobson).
given oif (Fig. 103) that muscle becomes paralyzed, and the membrana
tympani is rendered unduly tense by the unantagonized action of the
tensor tympani, a condition which causes an abnormal acuteness for
3(58 ATROPHIC PARALYSES.
hearing musical tones, especially deep notes, and which is often accom-
panied by a subjective sound of high pitch.
The auditory and facial nerves are simultaneously affected when the
lesion is situated at the base of the brain, in the meatus auditorius
internus, or in the middle ear and the adjoining parts of the temporal
bone, and then the patient is completely deaf on the affected side.
If the lesion is situated anywhere between the geniculate ganglion
and the point where the chorda tympani leaves the facial, the sense of
taste in the lateral half of the anterior two-thirds of the tongue is lost,
and the patient often complains of abnormal dryness of that side of the
mouth.
The sense of smell is occasionally diminished on the aiffected side
partly from dryness of the nostril from the tears not getting into the
lachrymal sac, and partly from interference with the access of air to the
olfactory chambers from paralysis of the nasal muscles.
The tongue is never paralyzed in lesions of the facial nerve, but there
is an apparent deviation or protrusion because the mouth is drawn over
to the healthy side. Sensory disorder.^ are usually absent, but when the
peripheral divisions are affected, branches of the fifth are often impli-
cated and then there are corresponding disturbances of sensibility.
The reflex movements are lost in peripheral paralysis of the facial.
There are no manifest secretory disorders of the face, but it has been
found that subcutaneous injection of pilocarpine does not cause sweating
of the paralyzed side in cases of peripheral lesions of the nerve. The
electrical reactions of the paralyzed nerve and muscles remain normal
in slight and transitory cases, but in all aggravated forms they manifest
the " reaction of degeneration."
Spontaneous movements may occur in the muscles during recovery,
and at times the twitching may be so marked that the disease looks like
facial tic. At other times associated movements occur in the paralyzed
muscles. "When, for instance, an attempt is made to close the eye, the
angle of the mouth is drawn outwards and upwards, and conversely,
when an attempt is made to draw the angle of the mouth to one side,
the eyelids contract ; the zygomatici contract when an attempt is made
to elevate the eyebrow. The paralyzed eyelid moves or falls to a lower
level than the other during downward rotation of the eyeballs. Reflex
contraction may occur in the paralyzed muscles, either through the fifth
nerve by touching the skin or eyelashes, or through the optic nerves by
making a rapid movement towards the eyes.
SIMPLE NEURAL PARALYSES. 369
h. Bilateral Facial Paralysis {Diplegia Facialis).
Etiology. — BiLateral facial paralysis often results from simultaneous
lesion of both facial nerves, such as compression of them by a tumor
where they lie close together at the base of the skull or in the course of the
fibres through the medulla oblongata and pons, bilateral otitis interna, or
caries of both temporal bones. It is, however, more fre(juentlv observed
in connection with progressive bulbar paralysis, and it may occasionally
result from lesions in the cerebral hemispheres, but these cases will Ije
subsequently described.
Syynptoms. — In facial diplegia the immobility which is present on the
one side in the unilateral affection now appears on both sides, but the
oblique position of the mouth, nose, and chin is absent. The face is
smooth, fixed, and expressionless, even when the emotions ai'e powerfullv
excited, and the patient, in the apt language of Romberg, " lau<dis and
cries as from behind a mask." When all the branches of both nerves
are implicated the patient is unable to wink or close either eye, and the
tears flow over both cheeks. The saliva dribbles when the head is bent
forwards ; taste is abolished in the anterior two-thirds of the tongue :
and the mouth may be abnormally d]y ; paralysis of the stapedii muscles
may occasion disorders of hearing, and paralysis of the soft palate gives
to the voice a nasal quality and allows fluid to escape through the nose
during attempts at deglutition, which is rendered still more difficult by
paralysis of the stylo-hyoid and digastric muscles. The nostrils fall in
during inspiration, a condition which gives rise to considerable discomfort
and difficulty in breathing, and articulation is impaired, as is manifested
by the patient being unable to pronounce the vowels o and u, and the
labial consonants.
Diagnosis. — The discrimination of facial paralysis from other dis-
eases presents no difficulty except in the slighter forms of the affection,
and the want of symmetry between the two sides may be detected by
paying careful attention to the play of the features under varying
emotions, or by getting the patient to execute complicated movements,
such as whistling, showing the teeth, and pronouncing difficult words.
The principal signs by which the disease is recognized in infants are
distortion of the face or crying, difficulty of sucking, and lagophthal-
mos during sleep. The most difficult part of the diagnosis is to de-
termine the exact position of the lesion. We must, in the first i)lace,
decide Avhether the lesion is situated in the fibres which connect the
facial nuclei in the pons with the muscles — peripheral paralysis, or in
370 SPASMODIC DISORDERS.
the fibres Avhich connect the facial cortical centres Avith the nuclei in the
pons — central or cerebral facial paralysis.
Peripheral facial paralysis is characterized by the presence of paral-
ysis of both the upper and lower branches of the nerve, lagophthalmos
durino- sleep, atrophy with the reaction of degeneration of the paralyzed
muscles, external wounds or disease in the vicinity of the nerve, and
disease of other nerves which lie near to it at the base of the brain or
in its course, while there is an alisence of hemiplegia and other cerebral
symptoms.
Cerebral facial p)aralysis is, characterized by the presence of paralysis
of the lower branches of the nerve combined with hemiplegia and other
cerebral symptoms, but the power of closing the eye and reflex actions
are retained, and the muscles neither undergo atrophy nor manifest the
reaction of degeneration. The following rules will enable the reader
to determine the exact position of the lesion in cases of peripheral
paralysis of the nerve:
(1) If the lesion be situated external to the Fallopian canal, the
muscles of the face are alone paralyzed.
(2) If the lesion be situated in the Fallopian canal, but below the
point at which the chorda tympani leaves the facial, the muscles of tlie
external ear are paralyzed in addition to those of the face.
(3) If the lesion be situated between the point at which tlie chorda
tympani is given off and the point of origin of the small branch to
the stapedius, there are, in addition to the symptoms already men-
tioned, abolition of taste on the lateral half of the anterior two-thirds of
the tongue, and diminution of the salivary secretion on the affected
side.
(4) If the lesion be situated between the point of origin of the nerve
to the stapedius and the geniculate ganglion, the same symptoms are
present, along Avith abnormal acuteness of hearing.
(5) If the geniculate ganglion itself is diseased all the previous signs
are present, and in addition paralysis of the soft palate and distortion of
the uvula.
(6) If the lesion be situated in the nerve above the geniculate gan-
glion, all the previous signs are present except the disorder of the sense
of taste, but the auditory nerve is frequently implicated, and then there
is dulness of hearing on the affected side.
(7) If the lesion be situated in the pons on a level with tlie facial
nerve, paralysis of the facial muscles is accompanied by one or more of
the following symptoms, namely: Hemiplegia of the opposite side,
paralysis of the sixth, auditory, and branches of the fifth nerves on
SIMPLE NEURA]. PARALYSES. 371
the same side, and a staggering gait iitli tendency to fall towards the
side affected with facial paralysis.
The diagnosis of the seat of the lesion in cerebral facial paralysis will
be subse(|uently considered.
4. Paualysis of the Muscles Supplied by the Hypoglossal
Nerve (Glossoplegia).
Etiology. — Paralysis of half of the tongue occurs in hemiplegia,
and of both sides in the various forms of bulbar paralysis. Injury of
the upper part of the vertebral column, such as fracture of the atlas,
may implicate the hypoglossal nerve, and unilateral paralysis with
atrophy of the tongue may occur in the advanced stages of tabes dorsalis
and in secondary descending sclerosis when the ganglion cells of the
hypoglossal nuclei are implicated. The nerve may be injured in its
peripheral course by tumors and other lesions at the base of the brain,
or by extracranial growths and wounds.
Symptoms. — In unilateral paralysis very little is observed when the
tongue is in a state of repose, but when it is protruded the tip is seen
to deviate to the paralyzed side in consequence of the predominance of
the action of the healthy genioglossus, which directs the tip of the
tongue to the opposite side. The various movements of the tongue
can only be imperfectly or not at all performed on the aifected side.
When the paralysis is bilateral and complete, the tongue lies immova-
ble on the floor of the cavity of the mouth ; it is relaxed, often atrophied,
with its surface wrinkled, and frequently presenting slight fibrillary
contractions on the dorsum. When the patient lies on his back the
paralyzed tongue falls backwards in the cavity of the mouth, and by
partially closing the glottis it contributes to the production of stertorous
breathing in cases of apoplexy, and may even cause asphyxia. If
the paralysis is incomplete, the tongue can be protruded, but the patient
is unable to execute complicated movements, such as raising the tip
towards the roof of the mouth, directing the tip towards the nose after
protrusion, or rolling it into a tubular form. In bilateral paralysis
mastication becomes seriously interfered with, because the food can
no longer be rolled about in the mouth and placed between the teeth,
whilst deglutition is impeded because the bolus cannot be properly
collected on the dorsum of the tongue and pushed backwards into the
pharynx, and consequently food and fluid regurgitate into the mouth,
and the patient is annoyed by the constant accumulation of saliva.
Articulation becomes indistinct, difficulty being first experienced in
572
SPASMODIC DISORDERS,
singing and in pronouncing the letters s, sh, I, e, i, and, at a later
period, k, g, r, etc., while if the paralysis be bilateral, complete, and
associated with atrophy, vocal speech becomes quite inarticulate and
unintelligible, this condition being named anartheca.
Fig. 104.
DiAGEAM OF THE HYPOGLOSSAL NeKVE, ITS CONXECriONS AND BRANCHES.
H, Hypoglossal nerve. p, Pneumogastric nerve.
S, Superior cervical gauglion of the sympathetic. L, Lingual nerve.
IC, lie, IIIC, The three upjier cervical nerves.
1, Communicating branches from hypoglos-sal to ganglion of the trunk of the vagus.
2, Connecting filaments with the loop of first and second cervical nei ves.
3, Branch to the sympathetic.
4, Descendens noni.
5, Branch from second and third cervical nerves (conimunicantes noni).
fi, Branch to thyro-hyoid.
7, Terminal muscular branches.
8, Communicating branch to lingual branch of the fiftli.
SIMPLE NEURAL PARALYSES. 373
Dicupiosis and Prognosis. — The best method of testing the condition
(if tlie lingual muscles, according to Hutchinson, is to take each side of
the tongue between the finger and thumb of each hand, and then to
re(|uest the patient to put his tongue out. If half is paralyzed,
that side remains soft and flaccid, while the healthy side becomes firm
and stiff". Paralysis of the tongue is, however, readily detected by
asking the patient to protrude it or to perform complicated movements
with it, such as turning the tip towards the nose after protrusion, and
rolling it into a tube.
The situation of the primary lesion must be determined from the
concomitant symptoms. Unilateral paralysis of the organ associated
Avith hemiplegia is caused by a cerebral lesion, while bilateral paralysis
in association with paralysis of the lips and soft palate is caused by a
l)ulbar lesion. The prognosis will depend upon primary lesion.
5. Paralysis of the Pneumogastric Nerve.
The distribution of the pneumogastric nerve is represented in
Fig. 105.
a. Paralysis of the Soft Palate.
The soft palate is supplied by branches from the pharyngeal plexus,
which is composed not only of branches from the vagus, but also of
the seventh, the glosso-pharyngeal, and the sympathetic nerves. The
levator palati and the azygos uvul?e are supplied from the seventh
nerve, but the part Avhich the branches of the other nerves take in the
innervation of the palate has not yet been determined, and it will,
therefore, be more convenient to group together all the motor and sen-
sory disorders to which the palate is liable.
Etiology. — Paralysis of the soft palate occurs in connection with
Ijulbar paralysis, and in the course of many diseases of the spinal cord,
Avhile partial paralysis of it occurs in certain cases of peripheral lesions
of the seventh nerve.
Sy7nptoins. — The symptoms differ according as the paralysis is partial
or complete.
(1) Paralysis of the levator palati causes the velum on the affected
side to hang loosely downwards, and to occupy a lower position during
rest than the sound side. Tickling does not cause the uvula to be
arched upwards, but it is rendered tense transversely by the action
of the tensor palati, while its posterior edge is drawn slightly down-
wards by the action of the palati pharyngeus.
374
SPASMODIC DISORDERS,
Fig. 105.
Diagram of the Pneumogastric and Spinal
Accessory Nerves, their connections and
BRANCHES. (From Hermann's "Physiology."')
P, Pneumogastric neire.
SA, Spinal accessory ner\e.
H, Hypoglossal nerve.
GP, Glosso-pbarjiigeal nerve
r, Facial nerve.
S, Superior cervical ganglion of the sympatlietic.
yr, Ganglion of the root of the vagus.
i/t, Gdvglion of the tniii]; of the vagus.
1, Auricular branch of the vagus (Arnold's
nerve).
'Z, Pharyngeal branch.
3, (,'onvergence of nerves to form phanjngtul
plexus.
4, Superior laryngeal nerve.
4', Internal bi-auch of superior laryngral
nerve
4", External branch Vf superior laryngeal
nerve.
5, Inferior laryugeal nerve (recurrent).
5', Cardiac branch of inferior'' laryngeal
nen-e.
6 fi G, Cardiac branches of the vagus.
7, Convergence of branches of vagus to form
cardiac plexuses.
.*<, Pulmonarj' branches.
9, (Esophageal branches.
10, Gastric branches.
11, Splenic branches.
12, Hepatic branches.
SA, Spinal accessory nerve.
id, Internal division of spinal accessory.
ed, External division of spinal accessory.
IC, IK", IIIC, IXC, Cervical nerves.
SIMPLE NEURAL PARALYSES,
375
I
(2) Combined paralysis of the levator palati and azygos wnsch-
occurs in lesions of the seventh nerve situated in or above the (genicu-
late ganglion. In addition to the symptoms of paralysis of the levator
the uvula is distorted, being arched obliquely forwards and usually
towards the healthy side. In many cases, however, the tip of the
uvula is directed not to the healthy but to the paralyzed side, the con-
vexity of the arch Ijeing then turned to the healthy side (Fig. 1(J6).
Fig. lOi;.
'*«/j)W»W*i""'^^
Distortion of the L'vila ix a case of peripheral paralysis of the right sihe of the face.
{After Sanders.)
Sanders thought that the last form of distortion was caused by the
action of the palato-pharyngeus exerting a greater effect on the uvula
on the affected side than it can exert on the sound side, Init this ex-
planation is not very satisfactory.
(3) Combined paralysis of the levator and tennor j^^^lttti causes the
velum to hang doAvn deeper than when the levator is alone paralyzed,
and the velum is likewise displaced laterally owing to the unopposed
action of the tensor of the opposite side, while there is no contraction
on the affected side on reflex irritation. Speech has a more nasal (puility
and fluids regurgitate more freely through the nose than when the
levator is alone affected.
(4) Paralysis of the palato-pharyngeus is recognized by the altered
appearance of the isthmus of the fauces, the posterior pillars of these
being widely separated from one another, and immovable.
(5) Bilateral paralysis of all the muscles of the soft palate causes
the palate to hang loose and flapping from tlie roof of the moutli, and
its activity is not called forth during deep inspiration, or during the
376 SPASMODIC DISORDERS.
movements of deglutition and phonation. The speech has a strongly
nasal quality ; while fluids are ejected through the nose. Deglutition
is rendered still more difficult when paralysis of the soft palate is asso-
ciated, as frequently happens, with paralysis of constrictors of the
pharynx.
The sensory disorders Avliich accompany paralysis of the soft palate
consist of hypera^sthesia or amTesthesia, and various par;\?sthesicV of the
mucous membrane of the soft palate and pharynx. Increased sensitive-
ness of these parts is often met with in nervous and hysterical subjects,
while anesthesia is always pi-esent in diphtheritic and progressive
bulbar paralysis, and is frec^uently met with in the insane. Par<^s-
thesi» of the pharynx, consisting of feelings like that caused by the
presence in the throat of foreign bodies, such as a fish-bone, hair, or
some hard substance, are often experienced by nervous and hysterical
subjects.
h. Faralyns of the Pharynx {Dysphagia Paralytica).
Etiology. — Partial paralysis of the superior constrictors may bo
associated with paralvsis of the soft palate after diphtheria and syphilis,
but paralysis of all the muscles of the pharynx and the muscular coat
of the tx:sophagus generally results from compression of the nerves at
the base of the skull by tumors, local diseases of the pons and medulla,
or as a terminal phenomenon in apoplexy.
Symptoms. — When the muscles of the pharynx are alone paralyzed
the only symptom present is difficulty in deglutition : the morsel passes
to the back of the mouth, but remains on the root of the tongue in the
glosso-epiglottidean fossa, or even over the epiglottis, and must, on
account of the dyspnoea to which it gives rise, be removed by means
of the finger. Fluids run along the dorsum of the tongue, and, passing
readily into the larynx, give rise to attacks of suflbcative cough ; whilst
the patient instinctively makes strenuous effi:>rts to pass the fluid over the
epiglottis by throwing the head backwards, and by an endeavor to bring
the root of the tongue as near as possible to the upper end of the
oesophagus. Paralysis of the superior constrictor allows fluids to re-
gurgitate through the nose during deglutition, inasmuch as contraction
of this muscle is necessary to complete the division which the soft palate
forms between the buccal and nasal portions of the pharynx during
swallowino;.
c. Paralysis' of the (Esophagus.
In isolated paralysis of the oesophagus the morsel of food passes from
the pharynx into the oesophagus, but it remains fiist in the cervical por-
SIMPLE XEURAL PARALYSES. 377
tion of the tube or regurgitates into the mouth. "When it remains fast
in the oesophagus it may produce compression of the larynx and cause
dyspnoea and the other symptoms which indicate the presence of a foreign
body. In paralysis of the oesophagus a sound can be passed readily
into the stomach.
d. Paralysis of the Laryngeal Branches of the Vagus {Aphonia
Paralytiea, Paralysis of the Larynx).
Etiology. — The more usual causes of paralysis of the larynx are gun-
shot wounds and surgical injuries of the vagus or recurrent laryngeal
nerves, or compression of these nerves in the neck or mediastinum by
various tumors, such as enlarged lymphatic glands, aneurism of the
arch of the aorta or of the carotid and subclavian arteries, and cancer of
the oesophagus, trachea, and thyroid gland. Laryngeal paralysis results
occasionally from bilateral compression of the spinal accessory nerves
in their passage through the foramen lacerum by cancerous infiltration
at the base of the skull. It may also be caused by exposure to cold,
and excessive speaking, or it may be a sequel of acute diseases like diph-
theria. As a symptom of central disease it is met with most frequently
in hysteria, but it sometimes occurs in the course of tabes dorsalis,
insular sclerosis, and progressive bulbar paralysis. Unilateral paralysis
of the vocal cords may result from an apoplectic seizure when the lesion
is situated in the medulla oblongata and more rarely from injury of the
cerebral conducting path above the medulla.
Symptoms. — If paralysis of the laryngeal muscles gives rise to vocal
and respiratory disorders it is named (1) mixed laryngeal paralysis, but
if disorders of respiration are alone present it is named (2) respiratory
paralysis, while if disorders of vocalization are alone present it is named
(3) phonetic paralysis. Paralysis of the laryngeal muscles may also
be divided into unilateral and bilateral, complete and incomi)lete
paralysis, according to its extent, and each of these may be divided
into total and partial paralysis, according to its degree. Before \)vo-
ceeding to describe the symptoms it may be as well to mention the
various positions assumed by the glottis under different circumstances.
Passing from the middle line outwards, these positions are: (1) Com-
plete closure of the glottis (Fig. 108, LI, LL), produced by the com-
bined action of the arytsenoidei and crico-arytnenoidei muscles; (2) the
cadaveric position, in which the glottis is slightly open, as it is found in
the dead body; (3) the position of quiet breathing, in which the glottis
878
SPASMODIC DISOKDERS.
is more open than in tlie last position, but still only moderately dilated
(Fig. 107, J, I): (4) the j^osition of deq) inspiration, in which the
Fig. 107.
Schema of a Horizontal Section thkouoh the Lakvnx.
/ /, The position of the arytjenoid cartilages and vocal cords during cjuiet breathing. The arrows
indicate the direction in which the crico-arytsenoidei postici muscles act. // //, Position of the arytenoid
cartilages in consequence of contraction of these muscles.
Fui. 108.
Schema of a Horizontal Section through the Larynx, showing the action or the Aryt.enoid
Muscles. (From Landois's "Physiologie.'")
1 1, Position of the arytenoid cartilages during quiet breathing. The arrows show the direction of th.>
action of the muscles. // U, Position of the cartilages when the muscles are contracted.
SIMPLE NEURAL PARALYSES. 879
glottis is widely dilated (Fig. 107, //. 11): (5) the position in wliicli
the glottis vocalis is closed and the glottis respiratoria open (Fio-
109,/,/). ^ *■
Fig. 100.
Schema of Horizontal Section through the Larynx, illustrating the action of Crico-aryt.enoidei
Laterales Musci.es. (From Landois's " Physiologie " )
II II, Position of the arytsenoid cartilages during quiet breathing. The arrows show the direction in
which the muscles act. 1 1, Position of the cartilages when the muscles are contracted.
(1) Mixed Laryngeal Paralysis.
Mixed laryngeal paralyses are caused by disease of the recurrent
laryngeal nerves, and the muscles which dilate the glottis as well as
those which render tense and approximate the vocal cords, are para-
lyzed, giving rise to disorders of vocalization and respiration. The
muscles become atrophied as in other forms of peripheral paralysis,
and lose their faradic contractility.
(a) In complete bilateral paralysis of the laryngeal muscles the
glottis assumes the cadaveric position, and is immovable during attempts
at phonation. The relaxed cords are drawn somewhat downwards
during inspiration, and pushed slightly upwards, and probably slightly
removed from one another during expiration, but these slight move-
ments are very different from the active movements caused by contract-
ing muscles. The voice is weak and may be reduced to an almost
inaudible whisper. Respiration is not much interfered with when the
patient is at rest, but dyspnoea and stridulous inspiration are readily
induced on slight exertion (Figs. 110-113).
(h) In complete unilateral paralysis of the laryngeal muscles the
vocal cord of the corresponding side is motionless, its free edge is
slightly removed from the middle line, and the vocal cord of the sound
380
SPASMODIC DISOKDERS,
side alone vibrates during attempts at phonation. The voice is com-
pletely lost, but more frequently it is harsh and discordant, and is
liable"^to break into falsetto tones on the slightest strain.
(c) In incomplete paralysis, whether unilateral or bilateral, the power
of excursion of the vocal cord is merely diminished and not entirely
lost.
Fio. 110.
LAKVXtiOscoi'ic Ai'PEAiiAxi'Es OF THE iNTEitiOR OF THE i-ARYNx. ( From Landois's " rbysiologie." )
L., The root of the tongue; V. V., Glosso-epiglottidean ligament; E., The epiglottis; H., Glottis;
L. r., The time vocal cord; ,S. M., Opening into the sinus of Jlorgagni ; L. v. »., The false vocal cords ;
S. S., The projection of the cartilages of Santorini ; P , Pharynx wall ; 11'. »'., The cartilages of Wrisbrrg
in the ary-epiglottidean ligament ; N. p., The sinus pyriformis.
Fig. 111.
Fig. 11 -J.
Fig. 113.
Flii. lU. — LaUYXOOSCOPIC appearance of the LAltVXX lU'RI.VG VUIET HRKATHINa.
Fir, 112. — ThF, LARYNGOSrOPIC APPEARANCE OF THE LARYNX DURING VOCALIZATION.
Fic;. 113 — The laryngo.«copic appearance of the larynx dvring deep inspiration, siiowini; the
BIFURCATION OF THE TRACHEA.
(2) Kespiratory Laryngeal Paralysis.
Respiratory laryngeal paralysis occurs when the muscles which
widen the aperture of the glottis — the crico-aryt?enoidei postici — are
paralyzed. In such cases the voice is unaffected, but serious disorders
of respiration may be present. Bilateral compression of the recurrent
laryngeal nerves by aneurism or other tumor causes paralysis of the
abductors of the vocal cords, while frequently leaving the adductors
unaffected.
SIMPLE XEUHAL PARALYSES. 381
{a) 111 coDiph'te fiirali/sis of the crico-aryt£enoi(lei postici the vocal
cords assume the cadaveric position, just as in complete paralysis of all
the laryngeal muscles. But in isolated paralysis of the abductors of
the larynx the approximation and parallelism of the vocal cords can
gtill he accomplished, and the voice is unaffected, but the glottis does
not dilate during deep inspiration, and the cords cannot be separated
beyond the cadaveric position. The respiratory function is at first
only slightly interfered with, but after a time the healthy adductors
undergo "paralytic contracture" and drag the vocal cords towards the
middle line, so that the glottis is almost completely closed. The glottis
is then converted into a narrow slit, and is quite inadequate to carry
on ordinary respiration. The breathing now becomes laborious and of
the "forced costal type," inspiration is prolonged and noisy, as in
croup, but expiration is comparatively easy and quick, and in conse-
quence of the difference of atmospheric pressure above and behnv the
constricted part the larynx moves up and down considerably durin<T
each respiratory act. On laryngoscopic examination it is seen that the
vocal cords are approximated so that only a. narrow linear chink is left
between them, and during forced inspiration the cords approach each
other so closely as almost to close the glottis completely instead of
separating from each other as in health. The cords are slightlv sep-
arated during each expiratory act. During phonation the vocal cords
and aryto?noid cartilages approach each other in a perfectly normal
manner.
[h) Incomplete 7'espiratory larynfieal paralysis may exist for a long
time without giving rise to difficulty of breathing or any manifest
symptoms, but the condition could doubtless be detected in laryngo-
scopic examination.
(3) Phoketic Laryngeal Paralysis.
Plionetic paralyses occur when the muscles which render tense and
approximate the vocal cords are paralyzed, and the affection of voice
may vary from slight hoarseness to complete aphonia, according to the
degree and extent of paraljisis.
\a) In bilateral paralysis of the adductors the glottis is partially open,
and both the arytenoid cartilages and the vocal cords are immovable
during attempts at phonation. The glottis cannot be closed in cough-
ing, on making an effort, or during deglutition, while there is complete
aphonia.
{h) In unilateral paralysis of the adductors the vocal cord of the
affected side is removed from the middle line, and cannot be apju-oxi-
382 SPASMODIC DISOEDERS.
mated to its fellow. Tlie affected vocal cord can only vibrate with its
edge, and consequently the voice is feeble, and readily assumes the
falsetto character.
{(') In incomplete phonetic laryngeal paralysk the tensor and cou;
strictor muscles of the vocal cords are separately paralyzed. Aphonia
is a symptom of paralysis of all these muscles, but it is most marked
in those cases in which the space between the cartilages remains open,
because the blast of air escapes through the patent glottis respiratoria.
The voice may not be much affected in those cases in which the carti-
lages close and the ligamentous portion remains open, because the blast
of air must pass through the glottis vocalis, and a certain degree of
vibration of the cords induced.
(j) In paralysis of the eric o-ihy void muscles, which occurs when
the superior laryngeal nerve is implicated, either directly or through
the spinal accessory nerve, the vocal cords cannot be rendered tense,
and consequently the voice becomes hoarse and deep, Avhile the produc-
tion of high notes is difficult or impossible. The absence of tension of
the crico-thyroid muscles during vocalization may sometimes be per-
ceived by placing the finger over the crico-thyroid space. Disease of'
the superior laryngeal nerve also paralyzes the thyro-arytasno-epiglot-
tidei, and the epiglottis, being drawn towards the tongue, fails to be
depressed over the aperture of the glottis during deglutition, and con-
sequently food and drink obtain entrance into the larynx. Aniesthesia
of the larynx is also present, and consequently the reflex act of cough-
ing is not set up until the foreign substance has passed below the level
of the vocal cords, and thus an attack of pneumonia is likely to be
provoked. On laryngoscopic examination the glottis is seen to be rep-
resented by a wavy line, and in unilateral paralysis the vocal cord on
the affected side remains on a higher level than its fellow. The crlottis
closes completely during strong expiratory efforts like coughing, and
the arytgenoid cartilages are quite movable during attempts at phonation.
(jj) Ii^ paralysis of the thyro-arytcenoidel the ligamentous part of
the glottis remains open, while juxtaposition of the arytsenoid cartilages
takes place. Rheumatic laryngeal paralysis often assumes this form,
but occasionally all the muscles may be affected.
( jjj ) In paralysis of the crico-arytcenodei laterales the glottis remains
open in the form of a tolerably broad ellipse.
(iv) In paralysis of the arytoenoidei the ligamentous portion closes
almost completely, while the space between the arytenoid cartilages
assumes a triangular form. This is the kind of paralysis which gener-
ally causes hysterical aplionia.
SIMPLE NEURAL PARALYSES. 383
The senson/ disorders which occur in diseases of the laryngeal
nerves consist, in addition to neuralgia, of hypergesthesia, anesthesia,
and various parsesthesise. Hyperaesthesia of the laryngeal mucous
membrane gives rise to excessive reflex actions on slight provocation.
Anaesthesia of the larynx occurs in diphtheritic paralysis, and may be,
in association with anaesthesia of the pharynx, one of the earliest
symptoms of bulbar paralysis. The pari»sthesi;3e consist of abnormal
feelings as if a hair, fish-bone, or morsel of food had lodged in the
larynx, while a laryngoscopic examination shows the absence of any
foreign body.
{d) Paralysis of the trunk of the vagus aiid of the //astrie and
cardiac plexuses has already been considered.
6. Paralysis of the Spinal Accessory Nerve.
Etiology. — Paralysis in the region of distribution of the spinal acces-
sory nerve is generally of peripheral origin, and is caused by traumatic
injuries of the nerve or by compression by tumors, abscesses, or dis-
eased bones of the skull. Paralysis may also be caused by exposure to
cold or by neuritis in wliatever way produced, and it may likewise arise
as a part of progressive muscular atrophy. Partial paralysis of the
nerve may be caused by disease of the four or five upper cervical
vertebrae.
Symptoms. — Paralysis of the sterno-cleido-mastoid or trapezius mus-
cles may be unilateral or bilateral, and the muscles may be separately
or simultaneously afiected.
(1) In unilateral j^aralysis of the sterno-cleido-mastoid the head is
held in an oblique position, the chin is elevated and turned towards
the affected side, the prominence of the healthy muscle on its move-
ments being resisted is absent, and the head can only be moved in the
direction of the affected muscle with difiiculty and by the aid of the
other muscles, but passive movements can be readily jjerformed. In
chronic cases the healthy muscle becomes contracted, and the head is
made to assume a permanently oblique position.
(2) In bilateral paralysis of the sterno-cleido-mastoid muscles the
head is held straight, but rotation of it can only be performed with
difficulty, especially when the chin is elevated. The prominences of
the muscles are absent, the neck looks wasted, and a slight depression
is produced between the mastoid process and the sternum.
(3) In unilateral paralysis of the trapezius the scapula of the affected
side is drawn somewhat downwards and forwards, and its inner border
384
SPASMODIC DISORDEES.
Fig. 114.
\P
Nerve.s of the Cervkwl Ple.xis.
IC, lie, IIIC, IVC, First, second, third, and fourth cervical nerves.
1, Muscular branch to rectus capitus posticus major and minor.
1', Muscular branch to obli(iuus superior.
1", Muscular branch to coniplexus.
2, Muscular branch to oblii|Uus inferior.
2', Muscular branch to coniplexus and traclielo-mastoid.
2", JIuscular branch to splenius.
3, Muscular branch to muscles of the neck.
4, Muscular branch to muscles of the neck.
G 0, Great occipital nerve, cutaneous to posterior part of scalji.
CO, Cutaneous branch to posterior part of scalp and back of neck.
5, Muscular branches to rectus capitis lateralis.
5', jMuscular branches to rectus capitis anticus major and minor.
■y", Commuuicating branches with hypoglossal and pneumogastric nerves.
SO, Small occipital nerve
Ti, Musculur branch to occipito-froutalis mu.scle.
SIMPLE NEURAL PARALYSES. 385
is separated from the vertebral column and assumes an oblique position
the inferior angle being nearer than the superior to the vertebral column.
The acromion process falls downwards and forwards, the projectino-
clavicle makes the supraclavicular fossa deeper than natural, and the
posterior and superior angle of the scapula can be felt with .unusual
distinctness. Paralysis of the upper portion of the trapezius alone
renders elevation of the arm above the horizontal line difficult.
(4) In bilateral paral^/ns of the trapezius the symptoms are present
on both sides, both shoulder-blades fall outwards and forwards, the head
readily sinks on the chest, and some difficulty is experienced in main-
taining it in an upright position.
(5) In combined jjaralysis of the sterno-eleido-)na8toid aiid trapezius
muscles the symptoms of the separate paralyses are combined, and then
the laryngeal muscles are not infrequently paralyzed.
7. Paralysis of the Muscles Supplied by the Cervical Plexus.
(1) Paralysis of the Posterior Muscles of the Neck.
Paralysis of the posterior muscles of the neck occurs occasionally in
infantile atrophic paralysis and progressive muscular atrophy, but it is
not easy to distinguish separate paralysis of the individual muscles.
When all the muscles of both sides of the back of the neck are paralyzed
the head can no longer be carried erect, but the patient usually carries
it inclined backwards and supported only by the anterior muscles of the
neck. When the head is moved forwards beyond the vertical line it falls
forwards until the chin rests on the sternum, and the patient is unable
to raise it in opposition to the slightest resistance, but can do so by a
peculiar swinging movement.
(2) Paredysis of the Diaphragm.
Etiology. — Paralysis of the diaphragm may occur as a late symptom
of progressive muscular atrophy ; it is occasionally observed in hysterical
patients, and Duchenne met with it in lead poisoning. It may also be
caused by exposure to cold, compression of the nerve by tumors, and in
cervical pachymeningitis on a level with the body of the fourth vertebra.
Symptoms. — Diaphragmatic paralysis is most commonly bilateral aiid
the symptoms are then highly characteristic. During inspiration the
epigastrium and hypochondria are drawn inwards instead of being
curved outwards, and if the hand be placed upon the epigastrium the
protrusion caused in health by the descending diaphragm during inspira-
25
38(5
ATROPHIC PARALYSES.
Fig. 115.
Nerves of the Brachial Plexus. (After Flower.)
VC, VIC, VIIC, Vine, ID, IID, HID, Fifth, sixth, seventh, and eighth cervical, an I first, sycund, and
third dorsal nerves.
CB, Communicating- brancli from tlie fourtli cervical nerve.
P, Phrenic nerve.
SIMPLE NEURAL PARALYSES. 387
r, c, Dorsal cutaneous branches from the tilth cervical to the thinl ilor«al nervi'.
M, Jl, Branches to the muscles of the neck and back.
B, Branch to the scalenus medius.
S', Branch to the subclavius muscle.
I, I', Branches to rhomboideus major and rhomboideus minor.
SS, Suprascapular nerves :
2, Branch to supraspinatus muscle.
2', Branch to infraspinatus mtiscle.
sj, Branch to shoulder-joint.
PT, Posteiior or long thoracic (external respiratory of Bell) supplies serratus magnus.
EAT, External anterior thoracic supplies pectoralis major.
lAT, Internal anterior thoracic to pectoralis major and pectoralis minor.
II, First intercostal nerve.
21, Second intercostal nerve.
IH, Intercosto-humeral joins nerve of Wrisberg.
AC, Anterior cutaneous nerves of the thorax.
31, Third intercostal nerve.
LC, Lateral cutaneous :
a, Anterior branch.
p, Posterior branch.
OC, Outer cord of brachial plexus.
PC, Posterior cord of brachial plexus.
IC, Inner cord.
MC, Musculo-cutaneous nerve.
4, Branches to coraco-brachialis.
5, Branches to biceps.
5', Branches to brachialis anticus.
6, Anterior cutaneous branch l
U', Posterior cutaneous branch r" ""*'''■ '''^<' "*" fo'earm.
IC, Internal cutaneous nerve.
E, Anterior or external branch.
I, Posterior or internal branch to inner side of forearm.
SIC, Small cutaneous nerve (nerve of Wrisberg) to inner side of arm.
SSS, Subscapular nerves :
21, Long subscapular nerve to latissimus dorsi.
21', Muscular branches to subscapularis and teres major
21", Muscular branches to subscapularis.
C, Circumflex Nerce.
sJ', Branch to shoulder-joint.
s, Superior division.
7, Cutaneous.
"', Muscular to deltoid.
1, Inferior division.
7", Cutaneous.
7'", Muscular to teres minor.
3IS, Muscitlo-qnral Nerve.
S, Muscular to brachialis anticus.
8', Muscular to triceps.
8", Muscular to anconeus.
8"', Muscular to supinator longus.
8"", Muscular to supinator brevis.
SX, Muscular to extensor carpi radialis longior.
icb, Internal cutaneous branch to inner side of arm.
iiec, Upper external cutaneous branch to outer side of arm.
lee, Lower external cutaneous branch to outer side and back of forearm.
E, Radial nerve cutaneous to dorsal surface of thumb and two outer fingers.
PI, Posterior Interosseous.
9, Muscular branch to extensor carpi radialis brevior.
9', Muscular branch to extensor ossis metacarpi poUicis.
9", Muscular branch to extensor primi internodii pollicis.
388 ATEOPHIC PARALYSES.
10, Muscular branch to extensor secundii interuodii poUicis.
10', Muscular branch to extensor indicis.
10", JIuscular branch to extensor carpi ulnaris.
(• digitorum communis and extensor
10'", Muscular branch to extensor | mjuin^i digiti.
uj, Branch to wrist-joint.
M, 3Iedian Nerve.
11, Muscular branches to pronator radii teres.
11', Muscular branches to flexor profundus digitonim.
11", Muscular branches to flexor longus poUicis. '
AI, Anterior interosseous branch to pronator quadratus.
12, Muscular branch to flexor carpi radialis.
12', Musciilar branch to flexor sublimis digitorum.
12", Muscular branch to palmaris longus.
13, Muscular branch to opponens poUicis.
13', Muscular branch to abductor pollicis.
13", Muscular branch to flexor breyis pollicis (outer half).
14, Muscular branch to first lumbricalis.
14', Muscular branch to second lumbricalis.
pc, Palmar cutaneous branch.
D to D4, Digital cutaneous branches.
U, Ulnar Nerve.
ej, Branch to elbow-joint.
15, Muscular branch to flexor profundus digitorum (inner part).
15', Bluscular branch to flexor carpi ulnaris.
DC, Dorsal cutaneous branch. To dorsal surface of two inner fingers.
2)' e'. Palmar cutaneous branch.
c'. Communicating to median.
D3 to D4, Cutaneous to little finger and inner side of ring finger.
16, Muscular branches to palmaris brevis.
16', Muscular branches to abductor minimi digiti.
10", Bluscular branches to opponens minimi digiti.
16"', Bluscular branches to flexor brevis minimi digiti.
17, IMuscular branches to fourth dorsal interosseous.
17', Muscular branches to third dorsal interosseous.
17", Muscular branches to second dorsal interosseous.
17'", Muscular branches to first dorsal interosseous.
18, Muscular branches to third palmar interosseous.
18', Muscular branches to second palmar interosseous.
18", Muscular branches to first palmar interosseous.
19, Muscular branches to fourth lumbricalis.
19', Muscular branches to third lumbricalis.
20, Muscular branches to adductor i)ollicis.
20', Muscular branches to flexor brevis pollicis (inner half).
I
tion cannot be perceived, but the epigastrium may be felt to protrude
slightly during expiration. When the jjaralysis is unilateral these
signs can only be recognized on one side. The breathing, even in com-
plete paralysis, is not much accelerated during rest, but dyspnoea begins
with the slightest exertion, and the respirations frequently rise from
forty to fifty in the minute. The contents of the bladder and rectum
are expelled with difficulty, because the patient is unable to strain, the
action of the abdominal muscles being; rendered ineffective bv the
absence of the counter-pressure afforded by the contracted diaphragm.
simple neural paralyses. 389
8. Paralysis of the Muscles Supplied by the Brachial Plexus.
The paralyses of the brachial plexus may be divided into those, a,
of the muscles of the neck and trunk, and, 6, those of the upper
extremity.
a. Paralysis of the 3Iuscles of the Neck and Trunk.
(1) Paralysis of the Pectoralis Major and Pectoralis Minor . — When
these muscles are paralyzed the power of adducting the arm to the
thorax or of resisting passive abduction of it is impaired ; the patient is
unable to seize the opposite shoulder with the hand ; and if the muscles
are likewise atrophied the anterior wall of the axilla is reduced to a
flaccid fold of skin, the superior ribs and intercostal spaces are well
marked, and the subclavicular fossa is deepened.
(2) Paralysis of the rhomboid muscles of the levator anguli scapulce
renders forced elevation of the scapula without rotation impossible.
(3) Paralysis of the latissimus dor si diminishes the power of adducting
the arm, or of resisting passive abduction of it, and makes it difficult
to move the hand to the buttock.
(4) Paralysis of the outward and inivard rotators of the upper arm
is readily recognized by the inability of the patient to produce out-
ward or inward rotation of the arm respectively.
(o) Paralysis of the serratus magnus is often preceded by neuralgic
pains in the neck and round the shoulder-blade; the scapula, when the
arm is hanging b}^ the side, is somcAvhat raised and approximated to the
vertebral column, and it is so rotated on its axis that its inner border is
directed obliquely upwards and outwards, and its inferior angle, which
stands out slightly from the thoracic wall, is drawn close to the vertebral
column (Fig. 116). The patient experiences difficulty in raising the
extended arm beyond the horizontal level because the usual forward
rotation of the inferior angle of the scapula is not affected, but by
instinctively leaning the body to the opposite side he can raise the arm
to a point midway between the horizontal and vertical positions, but not
further. If the observer rotates the scapula forwards and fixes the bone
in that position, the patient is enabled to raise the arm to a vertical
position. When the arm is raised to a horizontal position the inner
border of the scapula is drawn inwards to the vertebral column while
pushing a mass of muscle before it, and if the paralysis be bilateral the
inner borders of the scapula may actually touch one another. If the
raised arm be brought forwards, the inner border of the scapula becomes
more and more separated from the costal wall, so that a deep fossa is
390
ATROPHIC PARALYSES,
formed in which the hand may easily be laid so as to feel the inner
surface of the bone, and if the paralysis be bilateral the scapulae enclose
a deep hollow in which the muscular bellies of the rhomboid muscles
may be seen to project. The patient experiences difficulty in crossing
the arms in front of the chest, and in moving the apex of the shoulder
Fig. 116.
forwards as in delivering a blow in fencing, and he offers less resistance
than in health to forcible retraction of the shoulder. The chest expands
less and the digitations of the serratus magnus with the external oblique
are not so marked on the paralyzed as on the healthy side during forced
inspiration.
b. Paralysis of the Muscles of the Upper Extremity.
(1) Paralysis of the Circumflex Nerve. — The circumflex ner\e
supplies the deltoid and the teres minor muscles, but the symptoms are
almost exclusively those of paralysis of the deltoid. The arm cannot
be raised outwards or forwards, and during attempts to raise it the
deltoid remains quite relaxed, and the arm hangs helpless along the side
SIMPLE NEURAL PAEALYSES. 391
of the thorax. The muscle frequently undergoes atrophy, and the
slioulder-joint becomes so loose that a deep groove can be felt throucrh
the atrophied muscle between the head of the humerus and the glenoid
cavity. There may be pain in the shoulder-joint and in the substance
of the muscle, but other sensory disturbances in the region of distribu-
tion of the nerve are rare. Lesions of the circumflex nerve do not give
rise to any very manifest disorders of sensibility, but there may be a
slight degree of 1)lunting of sensibility on the outer surface of the
shoulder (Figs. 120, 121).
(2) Paralysis of the MuscuJo-cutaneous JVerve. — Paralysis in the
region of distribution of this nerve greatly diminishes the power of
flexing the forearm upon the arm, especially when the forearm is supi-
nated so that the flexor action of the supinator longus can no lon»er
come into play. Paralysis of the musculo-cutaneous nerve is accom-
panied by anaesthesia along the radial border of the forearm (Fio-s. 120,
121).
(3) Paralysis of th' Musculo-spiral N<rve. — Paralysis of this nerve
is frequently caused by injury of the nerve as it winds round the
humerus. The most frequent cause of injury is compression of the
nerve between the bone and some hard substance during the deep and
prolonged sleep which follows intoxication. The nerve may also be
subjected to pressure in the axilla by means of improperly constructed
crutches. AVhen the nerve is completely paralyzed the hand is main-
tained in a flexed position, and hangs helpless when the forearm is
extended and pronated. The patient is unable to raise the hand or
extend the fingers at the metacarpo-phalangeal joints; the thumb is
flexed and adUucted, and the fingers are flexed over the thumb. When
the hand is placed on a table it cannot be raised or moved laterally, but
the lateral movements of the fingers remain unimpaired. The patient
is unable to supinate the forearm, especially when it is extended so as
to exclude the action of the biceps* Paralysis of the supinator longus
is readily recognized by requesting the patient to make a powerful effort
to flex the arm against a resisting object when the forearm is maintained
in a half-flexed position and midway between pronation and supination :
it is then found that the muscle does not enter into contraction but
remains flaccid and soft. In lead paralysis the supinator longus is
always spared unless the paralysis implicates the deltoid and biceps :
Avhen the lesion is situated in the nerve as it winds round the humerus
the triceps muscle is spared, but in crutch paralysis it is paralyzed and
the patient cannot extend the forearm upon the arm. The action of
the flexor muscles is apparently weakened, but this is due to the fact
that the flexed position assumed hx the hand approximates the points
392
ATROPHIC PARALYSES.
of origin and insertion of these muscles. Disease of the musculo-spiral
nerve when situated high up gives rise to anaesthesia in the areas of
distribution of the superior and inferior external cutaneous branches
(Figs. 120, 121, I'CB, ECB) ; but when the lesion is situated low
Fig. 118.
Fig. 119.
Fig. 117. — Distrirutiok op the Sensory Nerves on the Back ok the IlAvn. (After Kr.^vse )
r, Radial ; m, median ; and u, ulnar nerve.
Fig. 118.— Showing the Distribution of the Anj:sthesia in a Case of Division of the JIusi.ulo-
SPIRAL Nerve in the Arm. (After LiTifcvANT.) A, Deeply shaded, to show the area of greatest anaes-
thesia ; B, shaded in a medium degree, to show the area of partial anaesthesia ; C, faintly shaded, to show
the area of slight anjesthesia.
Fig. 119.— The Dorsal Aspect of the Hand Two Weeks after Resection of the Radial Nerve.
(After Mitchell.) A B and A C, the length of the portion removed. The light shading represents the
area in which tactile sensibility was diminished ; the deep shading the area in wliich it was lust.
down, the dorsal surfaces of the thumb and of the inde.x and half of the
middle finger as far as to the second phalanx and the corresponding
parts of the back of the hand are alone affected (Fig. 117, r). A slight
SIMPLE XEURAL PARALYSES,
393
degree of anesthesia may sometimes be found over the back of all the
fingers, including the little finger, which is supposed to be entirely
Fig. 120.
Fig. 12 L
Figs. 120 and 121.— Citaneous Nerves of the Trunk .\nd Upper Extremity. (After Flower.)
Su, Supraclavicular nerve.
IID, Second dorsal.
PS, Posterior branches of the spinal nerves.
LI, Lateral branches of the intercostal nerves.
AI, Anterior branches of the intercostal nerves.
II, Iliac branch of ilio-inguinal nerve.
I'H', Ilio-hypogastric nerve.
C, Circumflex nerve.
IH, Intercostal humeral.
AV, Nerve of Wrisberg.
I'CB, Internal cutaneous branch of musculo-spiral nerve.
ECB, External cutaneous branch of musculo-spiral nerve.
ICB, Internal cutaneous nerve.
MB, JIusculo-cutaneous nerve.
R, Radial nerve.
U, Ulnar nerve.
M, Median nerve.
innervated by the ulnar nerve. This fact is well illustrated by a ca.se
reported by Letievant, in which the nerve was divided in the inferior
894
ATROPHIC PARALYSES.
and internal aspect of the left arm, and the distribution of the anaesthesia
two and a half years after the injur}^ is shown in Fig. 118. In most
cases, however, the area of anesthesia is much more limited than the
anatomical distribution of the nerve would lead us to expect. A case
is reported by S. Weir Mitchell in which three inches of the radial nerve
were removed in the back of the forearm, and the distribution of the
anesthesia as it was found two weeks after the operation is shown in
Fig. 119.
(4) Paralysis of the median nerve abolishes the power of pronating
the hand and of closing the hand to grasp an object, with the exception
of the two ulnar fingers, which can still be partially flexed, because the
Fig. 123.
Figs. 122 and 12S. — Radial Bokher and Dorsal Aspect hfthe Hand, showing the Distkibl'tiov ok
An.esthesia in a Case of Division of the Median Nerve. (After LfeTifevANT.)
A, Deep shading representing more or less complete anaesthesia ; B, E, and H, light shading, and
C, medium shading, representing a slight and medium degree of antesthesia respectively.
flexor profundus digitorum is in part supplied by the ulnar nerve. The
patient is unable to abduct, oppose, or perform any of the more delicate
movements of the thumb, which is permanently extended and adducted.
while its metacarpal bone is drawn backwards so that it lies on a plane
SIMPLE XEURAL PARALYSES.
395
with the metacarpal bones of the fingers, as in the hand of the monkey.
Flexion at the wrist is accompanied by adduction, owinor to the un-
opposed action of the flexor carpi ulnaris. Flexion of the first with
extension of the second and third phalanges of the fingers can be effected
by means of the interossei ; and, indeed, the last two phalanges may
be hyperextended owing to the unopposed action of these muscles. The
muscles of the forearm and ball of the thumb become atrophied in
severe cases.
The sensory disorders are, according to Letievant, distributed over
the palmar surfaces of the thumb, index, and radial border of the middle
finger, the thenar eminence, and the radial half of the palm, and over
the dorsal surfaces of the ungual and middle phalanges of the index
and middle fingers and occasionally the ungual phalanx of the thumb
(Figs. 122, 123). The anaesthesia is partial everywhere except over
the palmar surface of the whole of the ungual phalanx of the index
Fig. 124.
SHOWING THE DISTRIBUTION OF THE An.BSTHESIA ON THE BaCK OF THE FiNGEBS IN A CaSE (jF
Injtjry of the 3IEDIAN Xerve. (After Bernhardt.)
finger, and part of the dorsal surfiice of the same phalanx. The different
degrees of shading in Figs. 122 and 123 represent the varying degrees of
anaesthesia, the very deep shading at A representing complete anaesthesia.
A case is reported by Bernhardt in which the median nerve was para-
lyzed as the result of an injury. Four months after the injury the
sensibilitv of the skin of the ball of the thumb and the i-adial half of
896
ATROPHIC PARALYSES,
the palm was somewhat diminished, whilst that of the palmar aspect of
the thumb, index, middle, and radial border of the ring finger was
greatly lessened, the loss of sensibility becoming progressively greater
from the basal to the ungual phalanges. On the dorsal aspect the sen-
sibility of the skin of the thumb and little finger was intact over all
the phalanges, but was much diminished over both borders of the middle
and ungual phalanges of the index and middle fingers, and over the
radial border of the corresponding phalanges of the ring finger (Fig. 124).
In many cases of paralysis of the median nerve, however, the distribu-
tion of the anaesthesia is by no means so extensive as it was in the cases
of Letievant and Bernhardt.
(5) Paralyds of the ulnar nei've limits the power of ulnar flexion
and adduction of the hand, and abolishes the power of completely
flexing the last two fingers, of moving the little finger, of separating
the fingers from and compressing them against the middle finger, and
Fig. 12.).
1- Main en Griffe. 2.
(1) Hand, Palmar Surface. (2) Dorsal Surface. (After Dvchexxe.)
A, Wouml of the ulnar nerve ; B, Ends of the metacarpal bones ; D, Tendons of the flexor
sulilimis ; (', Muscles of the ball of the thumb.
of flexing the first and extending the second and third phalanges of all
the fingers. The patient is also unable to adduct the thumb and apply
It firmly to the metacarpal bone of the index finger. If the interossei and
lumbricales are alone paralyzed, the combined traction of the extensors
.SIMPLE NEURAL PAKALYSES.
597
and flexors of the fingers produces hyiDerextension of tlie first and
flexion of the last two phalanges, and the hand assumes the chiAv-like
appearance which is so characteristic of paralysis of the ulnar nerve
above the wrist, and of certain cases of progressive muscular atrophv.
In severe and protracted cases the first phalanges are dislocated backr
wards upon the metacarpal bones by the unantagonized action of the
extensors of the fingers ; the second phalanges become dislocated for-
wards on the first, and the third on the second from the unantagonized
action of the flexor digitorum sublimis and profundus, respectively, and
then the most characteristic form of the claw-hand (warn en griffe) is
produced (Fig. 125). The accompanying atrophy of the muscles gives
to the hand some of its chief characteristics. The hypothenar eminence
is flattened from atrophy of the muscles of the little finger, deep furrows
Fig. ]2(j.
Fig. 12
A, Deep shading, representing complete anwstliesia ; B, liglit shading, represents slight, and
C, medium sliading, represents a medium degree of anaesthesia. (After L£ti£va.nt.)
appear between the metacarpal bones from atrophy of the interossei :
the metacarpal bone of the index finger may be felt immediately under-
lying the skin from disappearance of the abductor indicis : and when
the mass of tissue Avhich lies between the metacarpal bones of the thumb _
398 ATROPHIC PARALYSES.
and index finger is grasped by tlie observer it is felt to consist of little
more than a fold of skin, owing to atrophy of the adductor pollicis and
inner head of the adductor brevis pollicis.
The senso7-y disorders appear on the palmar and dorsal aspects of the
little and half of the ring finger, and the corresponding part of the
palm and back of the hand, but the aniesthesia is only complete over
a very limited portion of the ulnar border of the hand (Figs. 126, 127).
All severe lesions of the ulnar nerve are apt to give rise to glossy fingers,
and various other trophic phenomena.
(6) Combined Paralysis of the Nerves of the Brachial Plexus. —
Various kinds of paralysis occur after dislocation of the shoulder-joint.
In suhcoracoid luxations the subjacent nerve trunks are especially
liable to injury, and the Avhole of the nerves may be compressed or
lacerated.
In fracture of the humerus one or more nerve trunks may be injured,
or may afterwards be implicated in the formation of callus. The mus-
culo-spiral is the most frequently paralyzed, then the ulnar, and more
rarely the median nerve.
In dislocations and fractures near the elbow-joint the ulnar and
median nerves are liable to be affected.
Tight bandaging may also give rise to a widely distributed and
obstinate paralysis.
In all these forms of paralysis recovery is slow, the reaction of degen-
eration is manifested in the affected nerves and muscles, and many of
them prove incurable.
(7) Paralysis of the Muscles Supplied by the Fifth Cervical Nerve.
— The root of the fifth cervical nerve is liable to suffer injury from
various causes as it descends over the transverse processes of the fifth
and sixth cervical vertebrae to join the brachial plexus! It may be
compressed by a tumor in this course, but more frequently the nerve is
suddenly injured by accident at this point. In accidents which have
given rise to this injury, the upper extremity has been directed forwards
and upwards to break a fall, and in such a position that when the col-
lision comes the clavicle is thrust upwards and backwards, and conse-
(juently the root of the fifth nerve may receive a ^'iolent blow as it
passes over the transverse processes of one of the vertebrae. The first
suggestion of this exijlanation came from Mr. Williamson, one of the
house physicians at the Royal Infirmary, and the proljabilities of it
were subsequently verified on the dead subject by Mr. Collier, Demon-
strator of Anatomy at Victoria University. The muscles which are
paralyzed after this injury are the deltoid, biceps, brachialis anticus,
and supinators of the forearm, and to a less degree the outward rotators
SIMPLE NEURAL PARALYSES,
899
(.f the humerus. The sensory disorders consist of formication and
numbness in the outer surfaces of the arm, forearm, thumb, and index
finger. The same muscles are paralyzed in the form of paralysis de-
scribed by Duchenne under the name of obstetrical infantile paralysis
of the superior extremities. It is caused by turning or some other
operative procedure during delivery.
(8) Paralysis of the Inferior Roots of the Brachial Plexus.—
Paralysis of the roots of the eighth cervical and first dorsal nerves is
observed in cases of pachymeningitis cervicalis hypertrophica when the
lesion is situated on a level with the junction of the cervical and dorsal
regions of the cord. The muscles supplied by the ulnar and median
nerves are then paralyzed, while those supplied by the musculo-spiral
nerve remain comparatively free, and consequently the hand, especially
when the patient tries to grasp, assumes the claw form shoAvn in Fio-.
128. In most cases the second dorsal nerve is likewise implicated in
Fig. 128.
Attitude of the Hand ix PACHiMrMM.iii^ iii\iiaii> Il^rERTKOPHicA, when the disease is
SITUATED ON A LEVEL WITH THE LOWER HALF OF THE CERVICAL ENLAEOEJIENT OF THE SPINAL CORP.
(.\fter Charcot.)
the lesion and consequently the anaesthesia caused by implication of
the posterior roots is found in the area of distribution of the intercosto-
humeral, the nerve of Wrisberg, the large internal cutaneous, and the
terminal cutaneous branches of the ulnar nerve. In pachymeningitis
the sensory conducting paths are often implicated, and the whole of
the body below the level of the lesion is then anaesthetic, as is shown
in Fig. 129. In a case of tubercular tumor of the sninal membranes
which involved the roots of the seventh and eighth cervical and first
dorsal nerves — the posterior root of the seventh cervical was not much
implicated — the anaesthesia was distributed as is shown in Fig. 130.
(9) Rupture of the Brachial Plexus. — Rupture of the brachial plexus
has generally been caused by the patient falling from a height and grasp-
400
ATROPHIC PARALYSES.
ing some object during his fall, by severe pulling of the arm, or by the
fall of a heavy weight on the shoulder. Immediately after the accident
all the muscles of the upper extremity are paralyzed. The latissimus
dorsi and the lower two-thirds of the pectoralis major are also paralyzed ;
but the upper third of the pectoralis major, the pectoralis minor, and
the internal and external rotators of the humerus are unaffected, but
Fig. 130.
Fig. 120. — The shaded portion shows the distribution of iiiuvsthesia in u cajse of cervical pachymeningitis,
in which the lesion was situated on a level with the eighth cervical and first and second dorsal nerves.
Fig. 130 — The shaded portion shows the distribution of anesthesia in a case in which a tubercular
tumor was situated on a level with the roots of the seventh and eighth cervical and first dorsal nerves.
the serratus magnus may be relatively feeble, although not completely
paralyzed. In a case under my care, however, the latissimus dorsi, the
deltoid, biceps, brachialis anticus, and the supinators of the forearm
were found to have completely recovered when the i)atient Avas exam-
ined eighteen months after the accident, although these muscles were
known to have remained completely paralyzed for eight months. Oculo-
pupillary phenomena are always observed in rupture of the brachial
plexus. On the affected side there are paralytic myosis, diminution of
SIMPLE NEURAL PARALYSES.
Fig. L3L Fig. 132.
401
Figs. 131 ami 132. — Posterior and anterior aspect respectively of the arm in a case of rupture of the
brachial plexus, the shaded area showing the distribution of the anasothesia. By an oversight the right
arm is represented as being affected instead of the left.
Fig. 133.
The line a a a, ou the outer surftice of the arm, marks the lioundary above and outside of which sensation
is preserved. The dotted line 6 6 marks the same for the inner surface of the arm. (After Maurv and
Dtjhring.)
26
402 ATROPHIC PARALYSES.
the palpebral fissure, and often relative elevation of temperature in the
external meatus of the ear. The area of absolute anaesthesia in the
case observed by me is shown in Figs. 131 and 132. There was a rela-
tive diminution of tactile sensibility over the whole of the skin of the
upper arm. The sensation to the inner surface of the arm would be
probably supplied by the intercosto-humeral nerve, which would remain
uninjured in this affection. In a case of excision of the brachial plexus
by Maury and Duhring the sensations of pain and touch were absent,
six months after the operation, over the whole of the hand and forearm,
and over the anterior aspect of the arm as represented in Fig. 133, a a.
In this case the communicating branch from the fourth and the fibres
derived from the fifth cervical root would be divided, while in rupture
these fibres had been uninjured from the first or had recovered.
9. Paralysis of the Muscles Supplied by the Dorsal Nerves.
a. Paralysis of the Respirdtory Muscles.
(1) Complete paralysis of the respiratory muscles occurs when the
respiratory centres in the medulla oblongata are affected, or when the
motor tracts proceeding from these centres, and which run in the lateral
columns of the cord, are interrupted. In these cases rapid death is
inevitable.
(2) Unilateral paralysis of the respiratory muscles does not imme-
diately endanger life. This fi)rm of paralysis may be caused by
unilateral lesions of the spinal cord, but cerebral disease does not inter-
fere much with the respiratory process.
(3) Peripheral paralysis of the respiratory muscles only affects indi-
vidual muscles or a group of muscles, and paralysis of one or two of
the intercostal muscles is not readily distinguished.
h. Paralysis of the Dorsal and Abdominal Muscles.
The extensors of the back are not infrequently more or less para-
lyzed. Spinal curvatures are often caused in young people by a rela-
tive feebleness of the dorsal muscles of one side. Paralysis of these
muscles may be caused by rheumatism and injuries of the back, and
by spinal disease, such as acute atrophic spinal paralysis and all the
forms of ascending myelitis and progressive muscular atrophy, while it
gives to pseudo-hypertrophic paralysis one of its most characteristic
features.
SIMPLE NEURAL PARALYSES. 403
(1) Bilateral paralysis of the extensors of the dorsal region gives
rise to a large and equable curve of the vertebral column ; the patients
are bent and doubled up as in old age, and are unable to hold them-
selves erect, but passive straightening of the vertebral column can
easily be effected, and this distinguishes paralytic kyphosis, as the con-
dition is called, from the kyphosis which results from muscular con-
tracture or disease of the vertebrae.
(2) Unilateral paralysis of the dorsal muscles gives rise to the
various forms of paralytic scoliosis.
(3) Bilateral paralysis of the extensors of the lumbar region pre-
sents very characteristic features — the lumbar vertebrae are arched for-
Avards, forming a hollow in the back which is increased by the upper
part of the body being thrown backwards in order to compensate for
the incurvation of the lumbar portion. A plumb line allowed to drop
from the most prominent spinous process of the dorsal vertebra clears
the sacrum generally by one or two inches.
(4) Paralysis of the abdominal muscles is rare as an isolated affec-
tion, but is common as a symptom of spinal paralysis, and occurs occa-
sionally in progressive muscular atrophy. Bilateral paralysis of the
abdominal muscles renders all expiratory efforts like coughing and
singing ineffective. The power of compressing the abdomen is im-
paired, and consequently diflSculty is experienced in evacuating the
contents of the bladder and rectum. The abdomen is large and protu-
berant, its walls are relaxed, and the patient is unable to raise the upper
part of the body from the recumbent position, or to sit up in bed without
being propped up with the hands. In walking or standing the upper
part of the body is bent slightly forwards and balanced exclusively by
the lumbar muscles, and consequently each backward movement of the
centre of gravity renders the patient liable to fall on his back, because
the abdominal muscles are incapable of drawing the body forwards. A
plumb line let fall from the most prominent of the spinous process of
the vertebrae falls well within the sacrum. If the lower extremities are
paralyzed, this symptom cannot be determined.
In unilateral paralysis of the abdominal muscles the umbilicus is
carried to the sound side with each movement of forcible expiration,
and during the act of straining.
I'O. Paralysis of the Muscles Supplied by the Lumbar Plexus.
a. Paralysis of the anterior crural nerve (Fig. 134, AC) arises from
injuries of the vertebral column and pelvis, tumors, and extravasation
of blood in the cauda equina, inflammation of the knee-joint, psoas
404
ATEOPHIC PARALYSES.
abscess, fracture of the thigh, dislocation of the hip-jomt, wounds
and injuries of the lower abdominal and crural regions, pelvic and
crural tumors, and neuritis, while it is a frequent symptom of all forms
of spinal paralysis.
Fig. 134.
LusiBAR Plexus.
XL, IIL, IIIL, and IVL.— The first, second, third, and fnurth hiiuliHr nerves, respectively.
D, Communicating branch from the last dorsal nei-ve.
CCCC, Posterior cutaneous branches.
mmmni, Branches to the muscles of the back.
IH, Ilio-hypogastric nerve.
I, Iliac branch, cutaneous, to surface of gluteal region.
H, Hypogastric branch, cutaneous, to surface of hypogastric region.
1, Muscular branch to obliquus internus.
T, Rectus abdominis.
simpi.p: neural paralyses. 405
II, lliu-iDguinal nerve, cutaneous, to inguinal region ami scrotum.
UC, Genito-crural nerve.
6, (Jenital branch to spermatic cord or round ligament.
2, Muscular branch to cremaster.
C, Crural branch, cutaneous, to surface of upper part of front of thigh.
EC, External cutaneous.
P, Posterior brancli, cutaneous, to upper and outer part of thigli.
A, Anterior branch, cutaneous, to front of thigh.
ps, 3Iuscular branches to psoas muscle.
AC, Anterior crural nerve.
3, Muscular branches to iliacus.
3' 3Iuscular branches to sartorius.
3", 3Iuscular branches to pectineus.
fa, Branch to femoral artery.
3IC, Middle cutaneous to front of thigh.
IC, Internal cutaneous to inner part of thigh and leg.
LS, Internal or long saphenous.
0, Cutaneous over inner ankle.
/', Cutaneous to inner side of foot.
4, 3Iuscular branch to rectus femorls.
4', Muscular branch to vastus externiis.
4", Jluscular branch to crureus.
4'", Muscular branch to subcrureus.
4"", JIuscular branch to vastus internus.
Kj, Branch to knee-joint.
0, Obturator nerve.
hj, Branch to hip-joint.
c'. Communicating with branches of internal cutaneous and internal saphenous.
5, Muscular branch to pectineus.
5', Muscular branch to obturator externus.
6, Muscular branch to adductor longus.
6', Muscular branch to gracilis.
C", Muscular branch to adductor brevis.
6'" 6"", Muscular branch to adductor magnus.
Kj', Branch to knee-joint.
L, Communicating branch to fifth lumbar nerve.
Symptoms. — The patient is unable to flex the leg at the hip-joint or
raise the body from the recumbent position. He cannot extend the
leg, and when sitting he is unable to move the leg forwards. Standing
and sitting upright are rendered insecure, while walking, jumping,
and running are difficult or impossible, and the difficulty is much
increased when both nerves are affected.
The sensory disorders extend over the lower two-thirds of the thigh,
the reo-ion of the knee, and the inner side of the leg and foot.
h. Paralysis of the obturator nerve (Fig. 134, 0) may be caused by
strangulated obturator hernia, and the pressure of the head of the
child, or of obstetric instruments, in difficult deliveries.
Symptoms. — The patient is incapable of adducting the thigli, of
pressing the knees together, or of crossing one leg over the other. Out-
ward rotation of the thigh is rendered difficult, and the affected leg soon
tires in walking. A slight degree of anaesthesia extends down the inner
side of the thigh as far as the knee.
406
ATROPHIC PAEALYSES.
c. Paralysis of the gluteal nerves (Fig. 135, SG) is caused by tumors
and lesions of the cauda equina, fractures of the sacrum and pelvis, and
various diseases of the spinal cord.
Fig. 135.
Sacral and Coccygeal Nerves.
VL, IS, IIS, HIS, IVS, VS, VIS.— Fifth hiinbar, and fiist, sccoml, third, fourth, fifth, and .sixth
sacral nerves.
LS, Lumbo-sacral cord.
c, c. Posterior cutaneous nerves.
TO, Branches to muscles of back.
1, Branches to pyriformis muscle.
3, Muscular branches to obturator internus.
SIMPLE XEURAL PARALYSES. 407
3', JIuscular branches to gemellus superior.
3'', Muscular branches to gemellus inferior.
3'", Muscular branches to quadratus femoris.
SG, Superior gluteal nerve.
2, Muscular branches to gluteus medius.
2', Sluscular branches to gluteus minimus.
2", Muscular branches to tensor vaginte femoris.
12, Muscular branches to gluteus maximus.
I G, Inferior gluteal nerve (cutaneous).
I P, Inferior pudendal nerve, cutaneous, to perineum and scrotum, or external labium.
C, Cutaneous branch to back of thigh and upper part of leg.
P, Pudic.
lip, Dorsalis penis sen clitoriilis.
13, Muscular brauch to transversus jjerinaii.
13', Muscular branch to erector penis.
13", Muscular branch to compressor urethras.
13'", Muscular branch to accelerator urinoe.
13"", Branch to the Inilb.
asp, Anterior superficial perineal to perineum and scrotum, or external laliiuni.
psp, Posterior superficial perineal to perineum and scrotum, or external Uil>ium.
I H, Inferior hemorrhoidal.
IVS, Fourth sacral nerve.
14, Muscular branch to levator ani.
14', Muscular branch to sphincter ani.
14", Muscular branch to coccygeus.
Great sciatic nerve.
hj, Branch to hip-joint.
4, Muscular branches to semi-teudinosus.
4', Muscular branches to semi-membranosus
5, Muscular branches to adductor magnus.
5', Muscular branches to biceps.
IP, Internal popliteal.
0, Muscular branch to gastrocnemius (inner head).
6', Muscular branch to gastrocnemius (outer head).
(V, IMuscular branch to popliteus.
6'", Muscular branch to soleus.
PT, Posterior tibial nerve.
7, Muscular branch to tibialis posticus.
7', Muscular Ijranch to flexor longus digitorum.
7", Muscular branch to flexor longus pollicis.
pc, Plantar cutaneous.
Int. P., Internal plantar nerve.
8, Muscular branch to abductor pollicis.
8', Muscular branch to flexor brevis pollicis.
8", Muscular branch to first lumbricalis.
8'", Muscular branch to second lumbricalis.
8X, Muscular branch to flexor brevis digitorum.
tl to t'i. Digital branches.
Ext. P. External plantar.
li and (.5, Digital branch to fifth and outer half of fourth toe.
10', Muscular branch to flexor accessorius muscle.
10", Muscular branch to abductor minimi digiti.
9, Mu.soular branch to flexor minimi digiti.
9', JIuscular branch to fourth lumbricalis.
DB, Deep branch of external plantar nerve.
9", Deep branch of external transversalis pedis.
9'", Deep branch of external third lumbricalis.
2>S,p2,pl, Deep branch of external third, second, and first plantar intcrossei muscles.
d4, d3, d-2, dl, Deep branch of external fourth, third, second, and first dorsal interossei
muscles.
10, Deep branch of external adductor pollicis.
ES, External or short saphenous to outer side of foot
408 ATROPHIC PARALYSES.
EP, External popliteal.
CP, Communicaus peronei.
C, Cutaneous to outer side of leg.
MC, Musculo-cutaneous uerve.
11, Muscular branch to peroneus lougus.
11', Muscular branch to peroneus brevis.
AT, Anterior tibial nerve.
11", Muscular branch to tibialis anticus
11'", Muscular branch to extensor lon^us digitoruni.
11"", Muscular branch to extensor longus pollicis.
IIX, Muscular branch to extensor brevis digitoruni.
Kj, Muscular branch to knee-joint.
at, Articxilar branch to tarsus.
Symptoms. — The power of rotating the leg botli inwards and out-
wards is interfered with, and that of abduction is impaired. Some
uncertainty is felt in standing : the patient experieni-es great difficulty
in ascending stairs, and when the body is inclined forwards it is difficult
to raise it to the erect posture. The characteristic rotation of the pelvis,
produced by the contraction of the gluteus niedius during locomotion
is not effected, and the muscle is not felt rigid on the side of the active
leg, as in health, when the hand is laid over the pelvis above the
trochanter. Disorders of sensibility are only present when other nerves
are coincidentlv affected.
11. Paralysis of the Musclks Sii'I'ijed nv the Sackal Plexis.
Etiology. — Paralysis of the sciatic nerve or of one of its branches
may be caused by injuries of various kinds, and compression of the
nerve by tumors ; by injury of the plexus during the extraction of the
child by means of the forceps, tumors and abscesses on the pelvis, or
compression of the gravid uterus, and by fractures of the vertebral
column and tumors of the cauda equina. Paralysis of the nerve may
also be caused by a rheumatic inflammation of its sheath, and by neuritis
from extension of inflammation to it from neighboring diseased textures,
while it sometimes occurs after acute diseases and as a symptom of
hysteria. Paralysis in the region of distribution of this nerve is an
almost constant symptom of disease of the spinal cord, and of many cases
of cerebral paralysis.
a. In partdysis of the vmsculo-cutaneous and anterior tihial nerve i<
(Fig. 135, MC and AT) the foot cannot be flexed or abducted, and can
only be incompletely adducted. It hangs down in a flaccid condition,
and in walking the toes, being depressed, are apt to trip the patient at
every inequality of the ground. The necessary elevation is given to
the foot in advancing during locomotion by flexion of the limb at the
hip- and knee-joints, and the point of the foot is the last part to leave
SIMPLE NEURAL PARALYSES. 40!)
tlie grouiul and on planting it doAvn the outer border of the foot and
the toes touch the ground first. This mode of progression is frequently
observed in cases of infantile paralysis, and is very characteristic.
(1) In parah/sis of the tibialis anticus the power of producino- dorsal
fiexion and adduction of the foot is limited, and the inner border and
the point of the foot can no longer be raised, though these movements
may in part be vicariously executed by the extensor digitorum communis
and the extensor longus pollicis.
(2) In paralysis of the extensor digitorum communis the power of
producing dorsal flexion of the foot, and abduction of it in the flexed
position is diminished, and extension of the basal phalanges of all the
toes cannot be effected.
(3) In paralysis of the extensor longus -pollicis the power of pro-
ducing dorsal flexion is diminished and that of extendino- the great toe
abolished.
(4) In paralysis of the peroneus longus abduction of the foot in the
extended position is impossible, the arch of the foot becomes flattened,
and the inner border no longer touches the ground because the head of
the first metatarsal bone is no longer drawn downwards, and a peculiar
kind of flat foot is thus produced.
(5) In paralysis of the peroneus hrevis pure abduction of the foot is
rendered impossible, although it may be effected along with dorsal flexion
by means of the extensor digitorum communis and along with plantar
flexion by means of the peroneus longus.
(6) In paralysis of the extensor digitorum communis hrevis the power
of extending the basal phalanges of the last four toes is impaired. These
forms of paralysis may be combined in various ways and then the affected
muscles can only be recognized by the most careful and prolonged ni-
vestigation.
The sensory disturbances are limited to the anterior and external
part of the leg, the dorsum of the foot, and the greater part of the toes
(Fig. 136, MCS).
h. In paralysis of the tibial nerve the patient is unable to extend the
foot, or produce flexion or lateral movements of the toes.
(1) In paralysis of the gastrocnemius and soleus the foot cannot be
extended and the patient cannot stand upon the toes, and when secondary
contraction of the anterior muscles of the leg ensues the foot assumes
a hook-like position in which the heel alone touches the ground, forming
talipes calcaneus.
(2) In paralysis of the tibialis posticus the power of abducting the
foot and of raisinjr its inner border is diminished.
410
ATEOPHIC PARALYSES.
Fig. 136.
i-.^^r^
iL' .A
Cutaneous Nerves of the Lower Extremity, (.\fter Flower.
Lumbar Plexus
IH, Ilio-hypogastric uerve.
II, Iliu-inguiual.
IIL, Second lumbar nerve.
GC, Geuito-Crural.
EC, External cutaneous.
31C, Middle cutaneous.
IC, Internal cutaneous.
IS, Internal saphenous.
PP, Plexus patellie.
Sacral Plexus.
DP, Dorsalis penis of pudic.
IP, Inferior hemorrhoidal of pudic.
P, Superficial perineal of pudic and inferior pudendal nf small sciatic.
IG, Inferior gluteal of small sciatic.
SS, Small sciatic.
EP, Branches from external popliteal.
ES, External saphenous.
MCS, Musculo-cutaneous.
AT, Branches of anterior tibial.
PT, Branch of posterior tibial.
SIMPLE XEURAL PARALYSES. 411
(o) In paralijsis of the flexor communis digitorwn flexion of the two
distal phalanges of the toes is impossible.
(4) In paralysis of the flexor loncjus polUck flexion of the great toe
is incomplete.
(.")) In paralysis of the abductor and adductor poUicis the power of
moving the great toe laterally is lost.
(6) In paralysis of interossei the patient is unable to flex the first or
to extend the two distal phalanges of the toes, or to effect separation of
them. The first phalanges become hyperextended on the metatarsal
bones and the distal phalanges are strongly flexed, so that the toes no
longer touch the ground with their bulbous extremities, and a claw-like
position is thus produced, as occurs in the hand from paralysis of the
corresponding muscles.
The sensory disorders are limited to the posterior surface of the leg,
the sole of the foot, and the plantar surface of the toes (Fig. 136, PT).
c. In paralysis of the trunk of the sciatic nerve all the muscles of
the leg and foot are paralyzed, and, in addition, the patient is unable to
flex the leg upon the thigh, to approximate the heel to the gluteal
region, or to offer any resistance when an attempt is made to extend
the leg.
The region of the knee, the back part of the thigh, and ultimately
the buttock and perineum are successively affected by anaesthesia, ac-
cordincr as the lesion is situated at hio-her levels in the trunk of the
nerve. If the lesion is situated in the hollow of the sacrum or in the
Cauda equina the anaesthesia affects the whole sacral region, the scrotum
or labia, and penis, urethra, bladder, and rectum.
The vaso-motor disturbances consist of cyanosis, mottling and cold-
ness of the skin of the paralyzed leg. Increase of temperature has
occasionally been observed as a transitory symptom.
The trophic disturbances are muscular atrophy, ulceration of the
skin, eruptions of herpes and pemphigus, and liedsores on the sacrum,
ankles, and heels.
CHAPTER YI.
ATROPHIC PARALYSES {continued).
II. MULTIPLE NEURAL PARALYSES.
1. Idiopathic PiiOdREssivio Mri/rii>i,i-; Nkuritis.
This affection is usually ushered in by more or less fever ; the patient
soon complains either simultaneously or successively of tingling pains
and feelings of coldness and numbness in the feet and hands, the terri-
tory of the ulnar nerve being peculiarly liable to be affected at an early
period of the disease. Pressure over circumscribed spots of the nerves
causes great pain, which radiates towards tlie periphery, and both the
skin and the muscles in the area of distribution of the affected nerves
are so extremely sensitive to pressure that the patient avoids any move-
ment of the limbs, and complains bitterly of the slightest touch or of
passive movements. Alongside this hypencsthesia to pressure there is
well-marked anjesthesia of certain forms of sensibility. Tactile sensi-
bility is indistinct, and the patient is unable to localize accurately, with
closed eyes, a point touching the skin, or to distinguish two points as
separate until they are far removed from one another. In the early
stage of the disease it is somewhat difficult to distinguish whether the
motionless condition of the limbs arises from the reluctance of the
l)atient to move them for fear of provoking pain, or from decided
motor paralysis. Soon, however, distinct paralysis sets in, and the
affected muscles undergo rai)id atrophy and manifest the '' reaction of
degeneration." The paralysis begins in the small muscles of the hands
and feet, gradually spreads upwards, and successively invades the larger
muscles of the limbs and those of the trunk, while in some cases the
muscles of the bladder and rectum are involved. The small muscles of
the hands and the extensors of the forearm are usually affected to a
greater degree than the other muscles of the upper extremities, and,
consequently, the fingers and hands assume distorted positions similar
to the claw-hand of progressive muscular atrophy. Some of the cutaneous
reflexes may be normal, while others are variously altered. The plantar
reflex is absent in the advanced stage of the disease ; even at first it is
absent to slight stimulation, but a strong stimulus is said to provoke an
MULTIPLE NEURAL PARALYSES. 413
exaggerated reaction. The tendon-reactions, and more especially the
patellar tendon-reaction, appear to be abolished at an early period of
the disease. The affected nerves are, as already mentioned, painful on
pressure of particular ])oints, and at times the nerve may be felt to be
distinctly swollen at these points ; while in some cases it may be the
seat of an oedematous swelling of considerable size. The trophic dis-
orders consist, besides the atrophy of the muscles already described, of
alterations of the nails, which sometimes become brittle, cracked,
strongly curved, and of a yellowish or brownish color : and of an in-
creased develojunent of hair, or in some cases disappearance of the hair
from some spots of the skin, the skin of the fingers being especially
liable to become hairless and glossy. Patches of the skin are liable to
become of a red or bluish color from vaso-motor changes, and the sub-
cutaneous tissue may also become decidedly a?dematous.
In its onset progressive multiple neuritis is essentially an acute affec-
tion, considerable sensory and motor disturbances beincr established in
the course of a few days. In its further progress the affection becomes
chronic, and any change which takes place either by way of amend-
ment or extension of the disease may occupy many weeks. After from
nine to eighteen months, complete recovery may take place or the
recovery may be partial, the muscles supplied by the ulnar nerve re-
maining sometimes permanently disabled. The disease sometimes termi-
nates fatally from implication of the intercostal and bulbar nerves, but
the fatal result is often caused by a complication like chronic nephritis,
or an intercurrent affection like pneumonia or tiiberculosis.
2. Leau Paralysis.
Almost all the muscles of the body may be affected by an atrophic
paralysis in chronic lead-poisoning, although certain groups are attacked
by preference. In partial paralysis the extensor muscles of the fore-
aiTii are more frequently affected than any other group, and consequently,
Avhen the arms are held out horizontally, with the hands in a state of
pronation the hands hang powerless, this condition being graphically
called ivrist-drop. The common extensors of the fingers are the first
to be attacked, then the extensors of the index and little fingers, the
extensor secundii internodii pollicis, the extensors of the wrist, the
extensor primi internodii pollicis, and the extensor ossis metacarpi pollicis
are successively invaded. The supinator longus is spared until a com-
paratively late period of the disease and it is never invaded unless the
paralysis extend to the muscles of the upper arm. Occasionally the
paralysis may begin in the muscles of the upper arm and then the
41-i ATROPHIC PARALYSES,
deltoid, biceps, brachialis anticus, and supinator longus are almost simul-
taneously attacked. When the muscles of the inferior extremities are
paralyzed, the anterior muscles of the leg are generally the first to be
attacked, and the extensor muscles of the thigh are the next most
likely to be invaded. In some cases all the muscles of both upper and
lower extremities are paralyzed, whilst on rare occasions the muscles of
the thorax and back, those of phonation and speech, the intercostal
muscles, and even the diaphragm have been implicated. Paralysis of
the muscles of the glottis has been observed by Trousseau in horses
employed in red lead factories. The sphincters remain always unaffected
in the paraplegic form. The paralyzed muscles undergo rapid atrophy,
and lose their faradic contractility before voluntary power is completely
abolished, while the galvanic degeneration reaction appears in them at
an early period. The patellar tendon-reaction is often lost in cases in
which there is no perceptible atrophy of the muscles of the lower ex-
tremities, but I have found this reaction present in several cases in
which the wrist-drop was very pronounced.
Tremor is sometimes observed in lead-poisoning ; it is often limited to
the upper extremities, but may become general in aggravated cases.
Ataxic symptoms have occasionally been observed along with anaesthesia.
Sensory disorders are often absent in cases of wrist-drop, but when
the paralysis extends to the muscles of the lower extremities a good
deal of anaesthesia may be present, especially in the area of distribution
of the cutaneous branches of the external popliteal nerve. In some
cases, however, the skin over the back of the hands and forearms is
more or less aniesthetic, and a certain degree of loss of feeling may Ije
observed over the surface of the chest and abdomen, whilst in a few
cases the veil of the palate and uvula, and even the conjunctiva, may be
completely ansesthetic. Symptoms of sensory irritation are also often
present in chronic lead-poisoning. Cutaneous hypertvsthesia may
accompany attacks of pain, while drthralgia, occurring in paroxysms
and situated either in the extremities or in the jaws, is often a promi-
nent symptom.
Lead colic is one of the most frequent and important symptoms of
the disease ; the pains, which are chiefly referred to the umbilical region,
are more or less continuous, but they are liable to paroxysmal exacerba-
tions of great severity. The special senses are sometimes aflfected.
Diminution of taste on one-half the tongue and of smell in one nostril
has been observed, but deafness is said to result only from local disease
of the ear. But visual disorders are more frequent and more important
than those of the other special senses. These consist of transitory
amblyopia without ophthalmoscopic changes; persistent amblyopia
MULTIPLE NEURAL PARALYSES. 415
passing on to amaurosis of both eyes and rarely of one only, attended
by atrophy of the optic nerve : amblyopia with double optic neuritis,
and amblyopia with albuminuric retinitis in association with oranular
kidneys.
Psychical disorders are often present in aggravated cases. Before
the outbreak of pronounced cerebral symptoms the patient generallv
suffers from headache, vertigo, and drowsiness during the day with
sleeplessness at night ; or there may be a state of agitation, or complete
apathy. The psychical disorders consist of hallucinations of sight and
hearing, with a quiet delirium, or the patient may have an attack of
furious delirium. Convulsions are frequently present, and they may be
partial, being then limited to the muscles of the face or to one or more
of the hmbs, or they may assume the form of an attack of eclampsia.
These convulsions are generally followed by a stage of profound un-
consciousness with stertorous breathing. Apoplectiform attacks are
liable to occur in the last stage of lead paralysis, and inasmuch as the
patient often recovers motor power quickly these attacks cannot always
be due to hemorrha£:e.
3. Alcoholic Paralysis.
Persons who have indulged too freely in the use of alcohol are liable
to suffer fi'om a progressive paralysis which is accompanied by more
or less rapid atrophy of the affected muscles. The affection generally
begins, so far as the paralysis is concerned, by a gradually increasing
weakness of the lower extremities. The patient, after suffering from
numbness, tearing pains, and often also from distressing cramps in the
lower extremities, experiences a progressively increasing difficulty in
maintaining the erect posture, and on attempting to walk the legs are
spread asunder in order to widen the base, while the gait is uncertain,
or walking may be impossible Avithout the support of tAvo sticks or of
an attendant. The movements of the hands are also sometimes irregu-
lar and uncertain and when an arm is stretched out to perform an in-
tended movement the object may only be reached after numerous slight
lateral and vertical jerking interruptions. At this stage of the disease
the alcoholic subject, provided the person be sober during examination,
appears to be in a moderately advanced stage of locomotor ataxia, and
the similarity between the two diseases is rendered still more striking
by the fact that the patellar tendon-reaction is absent in the alcoholic
disease as well as in ataxia. A closer examination, however, will show
that the alcoholic affection is, from the first, a paralytic one. Provided
the patient is able to walk, it Avill be seen that the toe of the advancing
4:16 ATEOPHIC PARALYSES.
foot ahvays drops, just as occurs in cases of infantile paralysis ^vllen the
extensors of the foot and toes are paralyzed, and when the legs of the
patient are uncovered in bed it will be seen that the feet assume the
position of paralytic talipes equinus. or rather talipes equina varus,
because the tibialis anticus is not paralyzed to the same degree as the
extensors and peronei muscles. It will also be found that the extensors
of the front of the thigh are very feeble. A methodical examination of
the upper extremities proves equally instructive. The patient on holding
his arms out horizontally, the forearms being in a state of pronation, may
be able to hold the hands and fingers extended, Init the slightest pres-
sure on the backs of the fingers causes flexion at the metacarpo-phalan-
geal joints, on the back of the hand causes flexion at the wrist, and in
many cases the little finger is seen to drop, the patient being unable to
maintain it fully extended at the metacarpo-phalangeal joint. On
electrical exploration the faradic contractility will ]je ascertained to be
much diminished or completely lost in the extensors of the leg and
those of the front of the thigh, and considerably diminished in the
extensors of the forearm, while the galvanic excitability of these mus-
cles manifests the qualitative changes of the " reaction of degeneration."'
After another deep carouse the whole clinical picture of the disease
changes. The patient now lies helpless in bed, being unable to stand,
and possibly not even to sit up in bed. But the most remarkable
feature of this stage of the disease is presented by the upper extremi-
ties. The extensors of the forearms are completely paralyzed and a
double wrist-drop results just as in lead paralysis, and to render the
similarity between the two diseases more striking the supinator longiis
is comparatively spared in the former as in the latter disease. The
flexors of the fingers and wrist and the intrinsic muscles of the hand
are also very feeble, but I have not seen them completely paralyzed.
In the upper arm the triceps is much more feeble than the biceps, and
consequently the forearm is maintained during repose at a right angle
to the arm, but when the patient moves the extremity the forearm becomes
flexed at an acute angle to the arm, and the curled-up attitude now
assumed by the extremity may appear to a superficial observer to be
imposed upon it by an active spasm and not by a paralysis, so that the
disease has a certain resemblance to tetany. The movements at the
shoulder are not much interfered with. On electrical exploration it will
now be found that, speaking generally, the extensors of both lower and
upper extremities give the complete, and the remaining muscles of the
limbs Erb's partial, "reaction of degeneration."
If the disease advances further, the diaphragm becomes paralyzed
and the abdomen sinks as the chest expands and protrudes slightly as
ML'LTIPLE NEURAL PARALYSES. 417
the chest contracts. At a still later period the intercostal muscles
become paralyzed, and the patient after a short interval, in which the
breathing is maintained by the upper thoracic muscles, dies from
asphyxia. The order in Avhich the various muscular groups are
attacked is important, because in all the ascending forms of spinal
paralysis the intercostal muscles are affected before the diaphragm, and
the intrinsic muscles of the hand before the extensors of the forearm.
The cutaneous reflexes and the mechanical irritability of the affected
muscles are diminished or absent, Avhile the tendon reactions are nearly
always lost at an early period of the disease.
Sensory disturbances are always present. The patients suffer from
tearing pains in the lower extremities which are apt to become pecu-
liai'ly distressing at night, and they complain of a distressing burning
of the feet, as well as of numbness and various other parjesthesite.
Cutaneous hypersesthesia is occasionally present, but it is by no means
in so marked a degree as muscular hypersesthesia, which forms one of
the most characteristic features of the disease. The slightest pressure
on the muscle calls forth loud cries from the patient, and suffices to
induce in females a prolonged attack of hysterical sobbing. The
hvpersesthesia of the lower extremities, most probably that of the mus-
cles, is indeed sometimes so great that the weight of the bedclothes is
intolerable to the patient, and the feet have to be protected by cradles.
The sense of temperature is sometimes perverted in such a way that all
objects feel cold on contact. In the more advanced stages of the dis-
ease, the hypertBsthesia gives place to more or less ansesthesia, sensory
conduction is retarded, the tactile sense is diminished, and Remak's
double sensation may be observed. At times, the spine is tender to
pressure, but pain and stiffness of the vertebral column are not promi-
nent symptoms.
Vaso-motor disorders are generally present in the form of redness of
the feet, and of oedema of the ankles and backs of the feet and hands.
The oedema of the lower extremities is sometimes present to so great a
degree as to suggest the presence of a cardiac complication, but a
physical examination negatives this idea.
The trophic disorders consist of local asphyxia, and even gangrene
of the extremities has been occasionally observed as a complication.
Psychical disturbances are by no means rare ; they consist of restless-
ness, sleeplessness, marked loss of memory with diminished intelligence
and a stupid and stolid expression, delusions or hallucinations, and
delirium, these being present either separately or in various combnia-
tions. The girdle sensations, disorders of the movements of the pupils
and eyeballs, disturbances of the functions of the bladder and rectum,
27
418 ATROPHIC PARALYriES.
and arthropathies, which are so frequently observed and so characteristic
of tabes dorsalis, are absent in alcoholic paralysis.
Alcoholic paralysis is said to occur Avith greater frequency in women
than in men, but without questioning the truth of this statement, I am
convinced that it is more frequent in men than is generally supposed.
Out of eight well-marked cases of the disease which I have seen within
the last six months, four were men and four women, and of these, two
men and two women had complete double wrist-drop. One man died
from respiratory paralysis and a woman from cerebral complication ; of
the remaining six", one has almost completely recovered and five are still
under treatment.
The symptoms of the pronounced form of alcoholic paralysis in which
double wrist-drop occurs begin more or less acutely, generally after an
unusually deep carouse, but as a rule the affection assumes a chronic
course, although a few cases are rapidly fatal from respiratory paralysis.
In chronic cases death may take place from a cerebral complication or
from an intercurrent disease such as cirrhosis of the liver. Most cases,
however, recover completely, provided the use of alcohol is wholly pro-
hibited, but a relapse is liable to take place on recurrence to the old
habit, and when through long indulgence the affection becomes very
chronic, the paralysis may prove incurable.
4. DiPHTTiKRiTic Paralysis.
Diphtheritic paralysis begins occasionally towards the close of the
febrile attack, but in most cases it does not declare itself until from eight
days to three weeks or more after the disappearance of the false mem-
brane from the throat. The first symptom to attract attention is a nasal
quality of voice and the ejection of fluids through tlie nose, caused by
paralysis of the veil of the palate, and when the back of the throat is
examined it is seen that the soft palate hangs loose and flap])ing from
the roof of the mouth, and that it is not retracted on reflex irritation
or during phonation, deep inspiration, and attempts at deglutition. The
patient can swallow solids better than fluids, inasmuch as the latter are
more readily ejected through the nose than the former, but when the
pharyngeal muscles become paralyzed, as they frequently do, the diffi-
culty of deglutition becomes greater, and the patient is in danger of
being starved from inability to swallow sufficient food, or of being suf-
focated by the bolus becoming impacted in the pharynx, or finding its
way into the air-passages, the latter accident being much facilitated by
the fact that anaesthesia of the mucous membrane of the superior part
of the larynx is often superadded to the palatal and pharyngeal paralysis.
MULTIPLE XEUKAL PARALYSES. 419
Difficulty of respiration may be caused by paralysis of the abductors of
the vocal cords, or the voice may be altered from a slight deo^ree of
hoarseness up to complete aphonia, owing to paralysis of the muscles
which render tense and approximate the vocal cords. The tongue, the
lips, and the masticatory muscles may likewise be more or less paralyzed,
and the symptoms then are very like those of progressive bulbar paralysis.
But the ocular muscles, and especially the internal muscles of the eye
are those which are most frequently attacked after the muscles of the
throat. The patient is unable to read small print and cannot accom-
modate the eye for near objects, this defect being due to paralysis of
the ciliary muscle, and mydriasis has occasionally been observed from
paralysis of the sphincter of the iris. Paralysis of one or more of the
external muscles of the eye is declared by the presence of diplopia or
strabismus, while ptosis on one or both sides reveals paralysis of the
elevator muscle of the eyelid. Complete paralysis of the facial muscles
has not been observed in diphtheritic paralysis, but a certain degree of
immobility of the face is often present, which, when conjoined to the
defect of vision, gives to the patient an idiotic expression, although
psychical disturbances are absent during the whole course of the disease,
except perhaps some degree of apathy and a disinclination to make any
intellectual effort. The paralysis now extends to the muscles of the
limbs, and the inferior extremities are usually the first to be attacked,
but in most cases the muscles of the superior extremities are subsequently
implicated, and ultimately those of the trunk, including the muscles of
respiration, may be invaded.
In most cases the motor disorder simply amounts to a certain degree
of feebleness of the limbs, which manifests itself in an uncertain and
staggering gait that may be mistaken for ataxia, the similarity between
the two aftections being rendered still closer by the presence in diph-
theritic paralysis of certain sensory disorders, which will be immediately
described, and absence of the patellar tendon-reflex. The paralysis
after a time increases in intensity and extent, and the feebleness of the
lower extremities may become so great that the patient is unable to
maintain the erect posture and becomes confined to his bed, while the
upper extremities are so much affected that the patient is unable to
button his clothes, or to carry a spoon to his mouth, and the difficulty
of seizing small objects is greatly increased by the presence of sensory
disorders. The muscles of the neck may be paralyzed even before
those of the extremities. After a time the erector muscles of the spine
are invaded, and the patient may then be unable even to sit up in bed.
In some cases the paralysis assumes the hemiplegic form, but a care-
ful examination shows that the side which is presumed to be healthy is
420 ATROPHIC PARALYSES.
enfeebled, and that the hemiplegic distribution of the paralysis arises
from the fact that there is a disproportion between the degree to which
the motor weakness has attained on each side of the body. The dia-
phragm may ultimately be paralyzed, and should the intercostal muscles
be simultaneously attacked the danger of death from asphyxia is great.
Sensory disorders always accompany the loss of motor poAver in
diphtheritic paralysis. The mucous membrane of the soft palate and
pharynx is anaesthetic, and the tactile sensibility of the mucous mem-
brane of the lips, cheeks, and tongue is often diminished. The motor
disorders of the extremities are accompanied, or possibly preceded, by
sensory phenomena, the patient complains of numbness and tingling
pains in the feet and hands, and of a feeling of cold and of weight in
the limbs, the tactile sensibility is blunted, and in some cases there is
complete anesthesia. The inferior extremities are usually the first to
be affected, and patients cannot then feel the ground on which they
tread, or feel it only imperfectly ; they often state that it seems as if
they were walking on cotton, wool, or some other soft substance, and
they are unable to walk with closed eyes without danger of falling,
just as occurs in locomotor ataxia. AVhen the hands are attacked the
patients feel as if their fingers were covered with gloves, and tactile
sensibility may be so blunted that the person is unable to seize and
hold small objects without tlie aid of sight. The disorders of cutane-
ous sensibility are very variable in their extent and distribution, as
well as in their degree of intensity. The anaesthesia begins in the
periphery of the limbs and extends towards the trunk ; it often remains
limited to the distal segments of the extremities, but sometimes becomes
general, and Trousseau mentions a case in which the patient had almost
no consciousness of the passage of the urine and feces, although mic-
turition and defecation Avere voluntarily performed. In a few cases the
anaesthesia has been limited to the superior extremities, and in excep-
tional cases cutaneous hypertesthesia, accompanied by articular pains,
has been observed. The special senses are also sometimes affected in
diphtheritic paralysis. We have already seen that vision is rendered
indistinct by paralysis of the ciliary muscles, but in other cases ambly-
opia, proceeding to complete amaurosis, may result from insensibility of
the retinae. Taste has occasionally been found diminished, probably
never abolished, but loss of smell and deafness have been more fre-
quently observed.
The reflex action of the palate is diminished or lost at an early
period of the disease, but there are not very accurate statements with
regard to the reflex actions of the extremities. The patellar tendon-
reactions are lost even before paralysis of the lower extremities becomes
MULTIPLE NEURAL PARALYSES. -i21
very pronounced and consequently the liability to mistake diphtheritic
paralysis, at a certain stage of its development, for locomotor ataxia is
very great. The paralyzed muscles manifest the reaction of degenera-
tion on electrical exploration.
Visceral disorders are numerous and important in this form of paral-
ysis. We have already seen that the respiratory muscles may be
attacked, and that the disease may terminate fatally by arrest of res-
piration. In other cases the heart becomes affected with paralysis.
The cardiac disorder is manifested by an excessively slow, irregular,
and feeble pulse, and by paroxysms of palpitation, accompanied by
precordial anxiety and dyspnoea. The nervous disorders are sometimes
ushered in by a remarkable slowing of the pulse, attacks of syncope,
and vomiting, all of these being symptoms which are to be referred to
interference Avith the functions of the pneumogastric nerve, and at a
late period of the disease the patient may suffer from prsecordial agony,
and the pulse becomes slow, irregular, and so small as to be almost
undistinguishable, while death by syncope is not uncommon. I have
known glycosuria to occur after an attack of diphtheria, and the patient
has since made a complete recovery. Obstinate constipation is a fre-
(juent symptom of diphtheritic paralysis ; it is usually a late symptom,
and generally appears after the extremities are invaded, but in the last
stage of the disease the rectum may be paralyzed, and then constipa-
tion is succeeded by an involuntary discharge of feces. After a time
the urinary organs may become affected ; the bladder becomes greatly
distended, and unless the catheter be used, dribbling of urine occurs
from overdistention ; but this is succeeded by paralysis of the sphincter,
with incontinence. The patient likewise loses his virile power, and in
some cases there is complete impotence.
The duration of diphtheritic paralysis is very variable. When the
veil of the palate alone is affected the paralysis disappears, as a rule, in
from ten days to three weeks, but when the paralysis is widely distributed
over the body it lasts from two to four months, but rarely persists beyond
six months. Diphtheritic paralysis usually terminates in complete re-
covery or death, and only very exceptional cases are recorded in which
the recovery was incomplete. About twelve per cent, of all cases
terminate fatally, death taking place by asphyxia from respiratory
paralysis or from food getting into the glottis, inanition from inability
to swallow, nervous exhaustion, or syncope.
422 ATEOPHIC PARALYSES.
III. EEFLEX ATPvOPHIC PAEALYSES.
Etiology. — The most characteristic examples of this form of atrophic
paralysis are to be found in chronic diseases of the joints, Avhilo the
extensor muscles are often found to be feeble and emaciated. It is a\ ell
known to surgeons that the deltoid is often feeble and wasted in chronic
disease of the shoulder-joint, while Hunter and more recently Adams
directed attention to the flattening of the gluteal region which is
observed in chronic disease of the hip-joint. The extensors of the
thigh are liable to become feeble and emaciated in diseases of the knee-
joint, and the extensors of the fingers and thumb, and to a less extent
the flexors also, are similarly afl'ected in cases of rheumatoid arthritis.
In some cases a slight and transitory synovitis gives rise to a degree of
paralysis and wasting of the extensor muscles which is altogether dis-
proportionate to the severity and duration of the joint affection.
The aflection described under the name of reflex or urinary para-
plegia does not differ in its causation from the paralysis of joint
diseases, being set up by irritation of one of the viscera, such as the
urinary organs, uterus, or intestinal canal. The cause of the paralysis
is sometimes an injury or neuritis of a peripheral nerve. In severe
cases of neuritis from injury the inflammatory process may pursue an
ascending course and set up an acute or subacute myelitis, but in the
cases under consideration at present it is probable that the symptoms
are caused by irritation of the gray matter in the absence of serious
structural changes.
Symptoms. — In paralysis of the extensors secondary to diseases of
the joints, the affected muscles become soft and flabby, and emaciated,
while their motor power is greatly diminished. The mechanical irrita-
bility of the afl'ected muscles is increased, the reaction of their tendons is
normal or slightly exaggerated, and lively contractions are said Ijy Charcot
to be obtained by passing sparks of static electricity through them, but
the faradic and galvanic excitability is diminished without qualitative
changes. In cases of rheumatoid arthritis the muscles of the body often
undergo a diffused atrophy which predominates in the extensors. The
deltoid, the triceps, the extensors of the wrist, fingers, and thumb, the
gluteal muscles, the extensors of the thigh, and the extensors of the toes
are feeble and emaciated, and although the flexors are likewise implicated,
yet the paralysis in them being to a less degree they undergo adapted
contractions and the limbs become then fixed in flexed positions. The
mechanical irritability of the partially paralyzed muscles is in excess,
the tendon-reactions are exaggerated, and even ankle clonus may be
elicited in both ankles.
REFLEX ATROPHIC PARALYSES. 423
111 urinary paraplegia the lower extremities are paretic, but never
completely paralyzed : the reflexes are said now to be increased ; and
there is complete absence of pains in the loins, girdle pains, dys^sthesiic.
anassthesia, muscular tension and contractures, paralysis of the bladder,
and bedsores and other trophic disturbances. The gait corresponds to
the well-known shuffling gait of old age and is never of the spastic
variety. The paralysis is very variable in its degree and extent and
rapid improvement may take i>lace if there be an amelioration of the
peripheral lesion. This affection is generally met with in old people
with prostatic disease, and it may be associated with symptoms caused
by aiuemia of the cord from disease of the bloodvessels — vascular
sclerosis — so that it is not always easy to determine the share each lesion
takes in the production of the symptoms. The paraWtic symptoms are
sometimes caused by remote irritation. The most striking examples
of paralysis from remote irritatiiin are afforded by those cases in which
a paraplegia, or even a paralysis of the upper extremities suddenly
disappears on the expulsion of a tape, or of lumbricoid worms. The
paralyses which result from injury of remote parts are well illustrated
by several cases which occurred during the American war. The case
of a soldier is reported by S. Weir Mitchell, who had received a bullet
wound on the right side of the neck, which wounded the pharynx and
fractured the hyoid bone, but did not implicate any important nerve
trunk. The injury was immediately followed by paralysis of both
upper extremities ; the left extremity recovered rapidly, and the right
improved considerably but remained feeble.
In another case reported by the same author, a wound in the soft
parts of the thigh which did not injure any large nerve trunk, was
followed by right-sided hemianalgesia and paralysis of all the four ex-
tremities. The left arm recovered rapidly, but the improvement in the
other limbs was only slow, and the hemianalgesia persisted.
Neuritis sometimes gives rise to paralysis not only of the muscles
supplied by the affected nerve itself, or by nerves derived from the same
plexus, but also to paralysis of muscles supplied by nerves derived from
the plexus of the opposite side or from a different plexus altogether.
This form of paralysis is caused by a secondary myelitis set up by tlie
diseased nerve. This condition is well illustrated by a remarkable case
reported by Charcot and Fere, in which the sciatic nerves Avere injured
by a severe blow over the point of their emergence from the pelvis.
At first the patient suffered from the usual symptoms of inflammation of
the sciatic nerves. At the end of three months after the injury, lioth
lower extremities were so feeble that the patient was unable to maintain
the erect posture, and then there was also an involuntary passage of the
424 ATROPHIC PARALYSES.
urine and feces and loss of virile power. A careful examination of the
patient ten months after the injury showed that all the muscles supplied
by the left sciatic nerves were paralyzed and atrophied, and manifested,
to a marked degree, the " reaction of degeneration," these muscles being
probably affected by in^jury of the different fibres of the nerves. In addi-
tion to paralysis of these muscles on the left side, the corresponding
muscles of the right limb were also feeble and emaciated, but they only
gave the slightest form of the "reaction of degeneration," while the
muscles supplied by the left superior gluteal nerve, which received no
direct injury, were also paralyzed and atrophied and manifested the
" reaction of degeneration." The muscles supplied by the anterior
crural and obturator nerves were not paralyzed on either side. The
presence in this case of paralysis of the sphincters, of the muscles of
the right lower extremity, and of the gluteus medius and minimus of
the left side shows conclusively that a consecutive myelitis of the gray
substance was set up by the local injury to the nerves. The excess of
the patellar tendon-reaction on the right side is explained by Charcot
by supposing that the ganglion cells connected with the anterior crural
nerve were maintained in a state of irritation.
CHAPTER YII.
ATROPHIC PARALYSES [contiaued).
IV. SPINAL ATROPHIC PARALYSES (POLIOMYELOPATHIES).
1. Paralysis Ascendens Acuta (Acute Ascending Paralysis,
Landry's Paralysis).
Etiology. — Acute ascending paralysis often begins in the absence of
any recognizable predisposing cause, but it is thought likely that syphi-
litic infection and rheumatism may develop a liability to it. Men are
more frequently attacked than women, and the majority of cases have
occurred between twenty and forty years of age. The exciting causes
are exposure to cold, suppression of menses, and convalescence from
acute disease, such as typhoid fever, variola, and pleurisy.
SymiJtoms. — Premonitory symptoms consisting of slight fever, shoot-
ing pains in the back and limbs, formication and numbness in the feet
and finger-tips, and a feeling of great weariness, debility, and general
discomfort may be present several days before the occurrence of paral-
ysis. The characteristic symptoms of the disease now declare them-
selves by a paralysis which begins in the muscles of the feet and spreads
upwards to those of the thigh. The paralysis progresses with so much
rapidity that in a few days the lower extremities may be completely
paralyzed, and the limbs lie flaccid and pow^erless in any position in
which they may be placed, and without offering the slightest opposition
to passive movements.
The paralysis continues to advance steadily upwards, the muscles of
the trunk are invaded, and the patient is unable to sit up in bed ; the
small muscles of the hand are probably the next to be attacked, and
delicate manipulations, like those of writing, become impossible ; the
muscles of the upper arm and shoulder are successively invaded; the
acts of urination, defecation, and respiration are now rendered increas-
ingly difficult by the progressive paralysis of the abdominal and inter-
costal muscles; and when the muscles of the tongue, lips, pharynx,
and oesophagus become implicated a fatal termination is near.
A considerable degree of emaciation may occur in this disease as in
other acute affections, but the paralyzed muscles do not undergo n
426 ATEOPHIC PARALYSES.
rapidly progressive atrophy, and with rare and doubtful exceptions the
electric excitability of the paralyzed nerves and muscles remains
normal. Reflex action, -which is preserved or occasionally increased
during the first few days of the disease, becomes diminished and finally
extinguished. The patellar tendon-reactions have been found absent
at an early period of the disease in those cases in which the state of
these reactions has been tested.
The sensory disorders consist merely of numbness and tingling in
the fingers and toes, but, as a rule, the cutaneous sensibility is found to
be normal on objective examination, although occasionally a slight
diminution of tactile sensibility has been observed at the periphery of the
extremities. The pupils are sometimes unequal, and towards the end
the pulse is very frequent. The functions of the bladder and rectum
are usually unaffected, there are no bedsores, the general health is often
good, and the intellect is clear throughout the whole course of the
disease. The disease, as Ave have seen, generally begins in the lower
extremities, but in some cases it begins in the upper extremities, or,
rarely, in the region of distribution of the bulbar nerves, and then it
pursues a descending course.
The duration of the affection is somewhat variable. In some cases
it terminates fatally in the course of two or three days, while occasion-
ally it lasts from two to four weeks, the average of fatal cases being
from eight to twelve days. Death is caused by arrest of res])iration
subsequent to implication of the bulbar nerves. The disease may end
in recovery. It may cease to progress at any stage of its development,
and even after the cranial nerves are implicated the case must not be
regarded as altogether hopeless. In favorable cases improvement begins
at an early period of the disease, the parts last attacked being the first
to recover.
2. Poliomyelitis Axterior Acita (Kiss.maul) (Acute Inflam-
mation OF THE Anterior Gray Horns, Acute Atrophic
Spinal Paralysis).
Etiology. — This affection is most frequently met with in childhood,
the disease appearing between the ages of six months and three years
in thirty-two out of forty-four cases observed by West. It may, how-
ever, occur at so early an age as ten days, and a disease essentially
the same occurs in the adult. Heine asserts that the disease occurs in
the healthiest children, and that neither sex nor hereditary predisposi-
tion appears to exercise any influence in its causation. " It appears,
SPIXAL ATROPHIC PARALYSES. 427
according to Drs. Bai-low and Wharton Sinklcv, to be more common
during the summer than the winter months.
Injuries of various kinds are often said to be the cause of tlie disease,
and nurses are fi-equently blamed unjustly by parents who, unalde to
believe that such a striking phenomenon as paralysis can occur sud-
denly without appreciable cause, imagine that the child has been lamed
by a fall through the carelessness of its attendant. The most usual
exciting causes are painful dentition, and exposure to cold, more espe-
cially when the body is overheated, and the affection often occurs in
children, and occasionally in the adult, during or soon after an attack
of measles, scarlatina, smallpox, typhus, and other acute affections.
Syyiqjtoms. — Although this disease is essentially the same in children
as in adults, yet the symptoms differ so much in the tAvo as to demand
separate description. The disease will be first described as it occurs in
children.
a. Infantile Sjnnal Atrophic Paralym.
It Avill conduce to clearness if, like Laborde, we divide the clinical
history of this affection into the periods of (1) invasion ; (2) remission :
(3) regression of paralytic ])lienomena ; (4) atrophy with deformities.
It must, however, be remembered that these ])eriods overlap, and that
this subdivision is merely adopted for the sake of convenience.
(1) The Period of Invasion. — The disease is commonly ushered in
by a more or less intense fever, which is often preceded l)y general
malaise, pain in the head or in the back, mental irritaljility, fretfulness,
and startings of the limbs. As a rule, the fever is of short duration,
lasting only from one to two days. In some cases it passes off in a
few hours, while in others it continues from fourteen to sixteen days,
or even longer. As the fever increases the cerebral symptoms become
more pronounced, confusion of ideas and slight somnolency are ob-
served, and the child may become unconscious, or delirium of varying
degrees of intensity may supervene. The disease^ was ushered in by
convulsions in thirty out of seventy cases collected by Duchenne. these
convulsions being, most probably, the ordinary eclamptic attacks which
so frequently precede every acute febrile disease in childhood. All
general symptoms are sometimes absent ; the child is put to bed appar-
ently in good health, and is found paralyzed in the morning.
(2) The Period of Remission. — After the initial symptoms have sub-
sided it is observed that the patient is unable to move one or more of
his limbs, or the paralysis may not attract attention until the child is
428 ATKOPHIC PARALYSES.
taken out of bed for some purpose and then the relaxed and helpless
condition of the affected extremities can hardly fail to be noticed. The
paralysis is probably never fully developed at once ; it increases gradually
and reaches its maximum extent and degree in the course of a few
hours, in a day or two, and occasionally not until a longer period has
elapsed. Relapses sometimes occur. After a first attack one limb is
paralyzed and a few days afterwards, during which rapid improvement
has been taking place, the child is seized with a second febrile attack
and other limbs become paralyzed. A case is reported by Laborde in
which the paralysis did not become permanently established until the
third attack.
The distribution of the paralysis is very variable. It often involves
not only the four extremities, but also the muscles of the vertebral
column, and even the intercostal muscles and those of the neck are not
always spared. Sometimes the lower extremities alone are paralyzed,
but the upper extremities are seldom exclusively affected. The paralysis
assumes in some cases the form of a hemiplegia, and in these the side
of the neck, of the face, and of the tongue may be implicated at first
and may on rare occasions remain permanently paralyzed.
Sensory disorders are almost entirely absent during the whole course
of the disease. At the outset patients may complain of pains and
various parc^sthesicTe,but these symptoms are of short duration. A certain
degree of cutaneous hypertesthesia or rather hyperalgesia has been
described as being present during the febrile stage, but this tenderness
to touch probably depends upon affections of deeper structures, such as
rheumatic inflammation of joints. The cutaneous sensibility is some-
times blunted in the paralyzed extremities in old standing cases, but
this probably depends upon underlying nutritive and vascular changes.
Reflex action is completely lost in all the muscles Avhich are severely
paralyzed and it is much lowered or temporarily extinguished in the
muscles which are slightly affected.
The tendon-reactions are also absent in the paralyzed muscles.
The functions of the bladder and rectum are rarely affected. During
the first days there may be retention, but more frequently there is in-
continence, and the stools may be passed involuntarily. These disorders
disappear in from three to eight days from the commencement, except
in young children, in whom a slight incontinence of urine may remain
for some time.
(3) The Period of Regression. — After a certain time, which varies
from a few days to a few weeks, some of the paralyzed muscles begin
to improve, and in a few cases complete recovery takes place. The
cases which recover have been described by Kennedy under the name
SPINAL ATEOl'HIC PARALYSES. 429
temporary spinal 2)arali/sis. But, as a rule, only some of the muscles
are completely restored, while the rest remain permanently paraly/.ed.
When the paralysis is general it often happens that the upper half of
the body is the first to shoAv signs of amendment, the paralysis disap-
pearing rapidly from the neck, upper extremities, and trunk, and
becoming restricted to the lower extremities. This improvement, which
Laborde calls the period of first regression, is followed after a variable
interval of time by a second period of amendment, which the same
author calls the period of second regression. During the second re-
gression some of the muscles of the lower extremities undergo a pro-
gressive improvement and one limb may be restored to full motor power,
while one or more of the muscular groups of the other limb may remain
permanently affected, particularly the anterior and external group of
the leg. In some cases improvement takes place from below upwards
instead of from above downwards, and then the paralysis becomes
permanently localized in a superior extremity, or occasionally in the
trunk or neck. The permanently paralyzed muscles are implicated in
groups according as they are associated in their action, and not in accord-
ance with the peripheral distribution of their motor nerves.
(4) Tlu- Period of Atrophy <md Deformities. — All the muscles
which are severely paralyzed become the subjects of a rapidly p>ro-
gressive atrophy, and even those which are but slightly affected Avaste
to some extent, but soon recover. The atrophy becomes well marked
in the course of a few weeks, in the muscles which are severely affected,
and after a time they become so attenuated that the bones seem to under-
lie the skin. Sometimes the muscular atrophy is masked by the accu-
mulation of fat in the connective tissue, and consequently the loss of
volume is not always a trustworthy test of the degree to which the
muscle has become atrophied.
The electrical reactions of the affected nerves and muscles may vary
from a simple diminution of the normal reactions to the partial or the
complete reaction of degeneration. It was first shown by Duchenne
that the faradic irritability of both nerves and muscles sinks quickly in
those which are severely attacked, and becomes lost in them on the
seventh day or during the course of the second week. He laid it down
as a rule that all the paralyzed muscles in which the faradic irritability
is only more or less diminished during the course of the second week
do not remain permanently paralyzed, and that the restoration is the
more prompt and complete the less the faradic irritability is diminished.
Arrest of development of the osseous system often occurs, and it may
be altogether out of proportion to the degree in which the muscles arc
paralyzed. The greater part of the muscles of a limb nay. indeed, be
480 ATROPHIC PARALYSES.
lost while the bones are almost entirely unaffected, and, conversely, a
limb may be considerably shortened while only one or two muscles are
atrophied. The paralyzed lower extremity may be found from two to
six inches shorter than the corresponding healthy limb, and the upper
extremity may be similarly affected, although not generally to the same
degree. The long bones are thinner than normal ; they are porous,
friable, and yielding ; their epiphyses and processes grow smaller and
less distinct ; the paralyzed hand or foot is shorter, narrower, and thinner
than the sound one ; and even the pelvis may be arrested in its develop-
ment.
The joints become unusually movable, partly from disappearance of
the articular extremities of the bones and partly from relaxation and
stretching of their ligaments, and occasionally the changes undergone
are so great that the patient is able to dislocate a joint without experi-
encing any discomfort.
The shin of the affected extremity is flabby an<l so inelastic that it
retains for a long time slight pressure marks, such as that made by the
stocking. The surface of the limbs is of a mottled or bluish color, it
is remarkably cold to the touch, and in old cases its tem})erature may
be from 5° to 12° F. lower than that of the corresponding healthy
limb. The skin is liable to chilblains, and indolent ulcers form on
slight provocation, these nutritive changes being accompanied, and
probably caused by a diminution in the calibre of the arteries.
The deformities occurring in the affected limbs give to this disease
some of its most characteristic features. Some pathologists believe
that the deformities are produced by the predominant action of the
healthy muscles, the normal tonus being destroyed in the affected
muscles, but Volkmann asserts that the deformity is produced mainly
by the weight of the limb itself, because the position generally assumed
by the foot is only a higher degree of that which it assumes when un-
supported and left free from the action of the muscles. The influence
of gravity on the position of the limb ought certainly not to be ignored,
but the position assumed by the foot in talipes calcaneus when the
muscles of the calf are paralyzed shows that gravity is not the only,
perhaps not the chief, force which is operative in the production of
these deformities. Two other factors, at least, must be taken into
account. The first is that the paralyzed muscles often permit the limb
to assume a position in which the ends of their healthy antagonists are
more or less permanently approximated, and the latter consequently
become permanently shortened by undergoing "adapted atrophy."
The second factor is that the paralyzed muscles themselves may become
permanently shortened either from arrested development or from pro-
SFIXAL ATROPHIC PARALYSES. 431
liferation and subsequent retraction of their connective tissues. Of all
the deformities which occur in infantile paralysis, talipes e(iuinus and
e([uino-varus are the most frequent, because the muscles most frequently
paralyzed are the long extensors of the toes, the tibialis anticus, the
extensors of the great toes, and the peronei muscles. When the anterior
group and the adductors of the foot are affected at the same time talipes
equino-valgus, and when the muscles of the calf alone are affected talipes
calcaneus is produced, but this form is exceedingly rare, and simple
talipes varus is of still rarer occurrence. Another common deformity
is the "'pes cavus" — "talus pied creux" of the French, in which the
sole is hollowed and the instep is rendered prominent. Duchenne thinks
it is caused by a more or less complete paralysis of the muscles of the
calf, along with simultaneous contraction of the flexors of the foot, either
the long flexors of the toes or the long peroneus. The great laxity of
the ligaments allows the foot to become bent upon itself from the trans-
verse tarsal joint when the foot is unsupported, but when it is place<l
upon the ground it assumes the form of ''flat-foot."
Various deformities occur in the inferior extremity, according to the
extent and localization of the paralysis. The anterior and internal
muscles of the thigh are those most usually affected above the knee,
and then the predominant action of the flexors of the leg on the thigh
maintains the leg in a permanent condition of partial flexion (genu
recurvatum), while the thigh is likewise abducted. This deformity is
always associated with flexion of the thigh on the body, and talipes
equino-varus (Fig. 137). All the muscles of both legs are sometimes
paral^'zed, so that the patient is compelled to walk on his knees, drag-
ging his small, thin legs after him. In still more aggravated cases the
muscles of both legs and thighs are permanently paralyzed, so that the
small, flexible limbs dangle about like the limbs of a doll (jambe de
polichinelle). Curvatures of the vertebral column generally result in
infantile paralysis from the attitudes imposed by other deformities, but
occasionally the curvature is caused more or less directly by the paral-
ysis. Of the direct curvatures lordosis is the most frequent and
important; it is caused by partial paralysis of the sacro-spinal muscles,
and in order to prevent the permanent bending forwards of the body,
by the predominant action of the flexors, the patient voluntarily throws
the trunk backwards, so that the weight of the trunk is borne by the
flexors, while the tension is taken off the partially paralyzed extensors.
In this form of lordosis the pelvis is pushed forwards, and the buttocks
become less prominent than in health.
The deformities of the upper extremities are much less frequent and
serious than those of the lower extremities. The muscles of the
432
ATEOPHIC PARALYSES.
shoulder, and particularly the deltoid, are the most usual subjects of
paralysis and atrophy in the upper extremity. In the severer forms of
paralysis of the muscles about the shoulder-joint the humerus becomes
separated from the glenoid cavity, so that a dislocation is readily pro-
duced or may occur spontaneously, the arm hangs powerless by the
Fig. 137.
Case of Ixkaxtile Paralysis (genu becvbvatum). (After Laumitii).
side, and, to use the apt comparison of Heine, dangles about like the
loose end of a flail. The distortions of the forearm and hand are not
so frequent or important as to require description.
The general health of the patient is not interfered with in this dis-
ease; the organic functions are "well performed and the patient may
live to extreme old age.
b. Acute Atrophic Spinal Paralysis of Adults.
Acute atrophic spinal paralysis of adults is essentially the same
disease as acute atrophic spinal paralysis of infants. The differences
SPIXAL ATROPHIC I'ARALYSES. 433
between the clinical features of the two affections result from the fact?
that the brain of the adult does not respond so readily to the acute
symptoms of the initial stage as that of the infant ; that the adult
organism is not so liable to fever as that of the infant ; and that in the
adult the ligaments and joints being fully developed offer greater resist-
ance to the resulting deformities than do those of infants. The disease
begins by pain in the back and extremities, parnesthesia, and more or
less fever. In addition there may be headache, vomiting, somnolency,
or even slight delirium, but convulsions have never been observed.
The paralysis is developed more or less rapidly, generally in the
course of a few hours ; and, as in the case of children, it is more or less
widely spread, complete, and associated with more or less flaccidity of
the paralyzed muscles. Reflex action is either much lowered or abolished
in the paralyzed muscles, but may be retained in those which are slightly
affected. Temporary weakness of the bladder may be present at first.
The initial general symptoms pass off" in a fcAV days ; soon afterwards
the paralytic symptoms begin to improve, and complete restitution of
motor power may take place in the course of some weeks or occasionally
not until the lapse of nine months, these cases forming the temporary
spinal paraJi/sis of adults. But the restoration of motor power is, as
a rule, partial, the muscles which remain permanently paralyzed suffer-
ing a rapidly progressive atrophy as in the case of children and affording
the usual evidences of the reaction of degeneration. The skin becomes
loose, flabby, and inelastic, and the affected extremities are cold and
cyanotic.
Paralysis of one extremity is most commonly met w'ith in infants,
but, according to Miiller, paralysis of the four extremities, or of Ijoth
the lower extremities, occurs more frequently in adults. Out of forty-
seven cases collected by him tlie paralysis implicated all the extremities
in twenty-two, both lower jextremities in eleven, both upper extremities
in three, an upper and lower extremity of the same side in one, ami an
upper and lower extremity of opposite sides in one. The right upper
extremity was paralyzed in one, the left in two, the right inferior in two,
and the left inferior in one case.
The sensory disorders which may have existed at the beginning soon
subside, and the sensibility becomes normal ; the sexual functions are
throughout unaffected : there are no bedsores, and the general health is
good.
Paralytic contractions supervene with their resulting deformities, but
never attain the same degree as in children, because the joints and
ligaments in adults are resistant and the long bones have attained their
full development.
28
434 ATROPHIC PARALYSES.
3. Poliomyelitis Anterior Chronica (Chronic Atrophic
Spinal Paralysis).
Etiology. — The causes of this disease are exceedingly obscure ; it
was thought that adults were alone attacked, but it is now known that it
occurs in" children. The most frequent exciting causes are injuries,
such as a fall on the back or hip, exposure to severe cold, damp dwellings,
and alcoholic and sexual excesses.
Symptoms. — The disease usually begins with a feeling of lassitude
and fatigue in walking, pain and stiffness in the loins and lower ex-
tremities, slight fever, gastric disturbance, headache, and various par-
lesthesiffi, such as tingling and formication of the feet and hands. After
a time distinct muscular weakness is felt in one or both lower extremities,
which gradually increases until complete paralysis is established. The
intrinsic muscles of the foot, and the extensors of the toes and foot are
the first to be affected, and subsequently the muscles of the calf, the
flexors of the thigh on the trunk, the flexors and extensors of the leg
on the thigh, and the extensors of the thigh on the body become suc-
cessively invaded. The disease pursues its ascending course and the
muscles of the back and abdomen become paralyzed, so that the patient
is no longer able to sit up in bed, and expiratory acts like coughing and
sneezing, as well as urination and defecation, are rendered difficult and
inefiective. As the intercostal muscles are gradually attacked, it is seen
that the breathing becomes more and more diaphragmatic, and at the
same time the small muscles of the hand show signs of atrophy while
the grasp is feeble from paralysis of the long flexors of the fingers.
The flexors of the forearm, the extensors of the forearm, the supinators,
and the muscles of the arm and shoulder are next attacked in succession.
It is important to observe that in this disease the intercostal muscles
are attacked before the diaphragm, and the intrinsic muscles of the
hand and the flexors of the fingers before the extensors of the forearm,
this mode of invasion being the reverse of what occurs in alcoholic and
lead paralysis and other forms of multiple neuritis. But, although the
disease usually begins in the lower extremities and pursues an ascending
march, it sometimes begins in the upper extremities and pursues a
descending course, or rather pursues an ascending and a descending
course, inasmuch as the bulbar nuclei are liable to be invaded as well as
the motor cells of the dorsal and lumbar rejrions. Althoudi the two
lower and the two upper extremities are usually affected, the paralysis
is frequently more pronounced on one side of the body than on the
other. The paralyzed muscles are soft and flaccid, tension is not pro-
SPINAL ATROPHIC PARALYSES. 435
voked in them by passive movements of the affected extremities, and
they undergo rapid atrophy. The calves of the legs become converted
into loose and flabby sacs, the muscles of the thighs and gluteal regions
grow thin and soft, and the bones of the lower extremities may ulti-
mately be felt immediately underlying the skin, while scarcely a trace
of the muscular masses is left. The patient now lies on his back with
the various segments of the lower extremities extended upon one another ;
the upper extremities lie immovable by his side in any position in which
they may be placed ; the arms and forearms become greatly emaciated
from disappearance of their muscular masses ; the thenar and hypo-
thenar eminences are flattened ; and the hands assume characteristically
distorted positions.
Fibrillary contractions may be present in the early stages of the
atroph}^, but these soon disappear. Reflex action is lost at an early
period of the disease, and the tendon-reactions are likewise soon abolished.
The electrical reactions of the paralyzed nerves and muscles are, on the
whole, the same as those met with in acute atrophic spinal paralysis,
lieing only modified to some extent in correspondence with the slow
development of the former disease as compared with the latter. A case
of this disease came under my observation in which the faradic con-
tractility of the paralyzed nerves and muscles was at first much increased
during the early stage, but it was completely lost after a few weeks, and
then the galvanic reactions manifested the qualitative changes which
characterize the "reaction of degeneration."
The sensory disorders consist of tingling and formication, but the
cutaneous and muscular sensibilities are found to be normal on objective
examination.
The skin of the paralyzed limbs may become of a blue color and
the surface may be cold, while the lower extremities may be oedema-
tous, but there are no bedsores nor cutaneous eruptions, the functions of
the bladder, rectum, and sexual organs remain unaffected, and the
general health is satisfactory. During the course of the disease the
small joints of the hand are liable to become swollen, red, and painful,
and the patient may be covered with an abundant sour-smelling per-
spiration like that of acute rheumatism. The acute symptoms subside,
but the joints are apt to remain, to some extent, permanently deformed
like those of rheumatic arthritis. The course of the disease is variable,
the paralysis may supervene suddenly or be preceded for some time by
premonitory symptoms, and when the lower extremities are the first to
be attacked, the upper extremities may be implicated in a few weeks or
not until the lapse of months or years. In fatal cases death is usually
caused by implication of the bulbar nuclei and respiratory paralysis, but
436 ATROPHIC PARALYSES.
occasionally it results from exhaustion. Very frequently the disease
becomes arrested in its upward course, and, after a stationary period of
variable duration, improvement takes place in the muscles which Avere
the last to be invaded. During recovery the electrical reactions return
slowly and gradually to the normal formula. Recovery from this dis-
ease is not often complete. Groups of muscles, especially the anterior
and external muscles of the legs, remain paralyzed and atrophied, and
the patient is partially disabled for life.
4. Periependymal Myelitis (Syringomyelia, Hydromyelia).
Etiology. — The causes of this disease are the same as for other forms
of myelitis.
Symptoms. — This affection begins somewhat abruptly by paralysis of
some muscular groups, the patient finding suddenly that he is unable
to move the fingers, hands, or more rarely an entire limb. The muscles
lose their faradic contractility, and become atrophied at an early period
of the disease, and the affected extremities assume distorted positions.
In the early stage of the disease the uniscles may manifest fibrillary
contractions, and occasionally involuntary movements of a limb or of
the trunk have been observed. Patients often complain of vague pains
along the vertebral column, but in most cases there are no other sensory
disorders. In some cases, however, the patient suffers from numbness
and tingling of the lower extremities, and there may be an extensively
diffused anaesthesia, as in a case recorded by Schiippel, which was fre-
quently exhibited during life in Niemeyer's clinic. An ataxic gait has
never been observed, and the bladder and rectum always remain
unaffected.
The course of the disease is slow, and it may be temporarily arrested,
or may even regress, and then the atrophied muscles gradually regain
their motor power and volume, but relapses are liable to occur. Tlie
muscles of the lower extremity most fre(|uently affected are the flexors
of the foot on the leg, and of the thigh upon the pelvis ; and of the
upper extremities, are the extensors of the fingers and of the hand; then
the small muscles of the hand, and lastly the flexors of the forearm,
and the muscles of the arm and shoulder. The disease pursues an
ascending course when the lower extremities are the first to be para-
lyzed, and both an ascending and a descending course when the upper
extremities are attacked first, and bulbar paralysis is ultimately liable
to supervene, and to cause death. In some cases the paralytic symp-
toms pursue a rapidly ascending course, and the disease may then be
mistaken for an acute ascending paralysis.
SPINAL ATROPHJC PARALYSES. 437
5. Progressive Muscular Atrophy.
Etiolotjjj. — Hereditary predisposition is generally supposed to play a
very important part in the production of progressive muscular atrophy,
but it is most probable that the cases in which the disease appears in
numerous members of the same family really belong to the group which
Erb has described under the name of the "juvenile form of progressive
muscular atrophy," a group which is more allied to pseudo-hypertrophic
paralysis than to genuine progressive muscular atrophy, and until the
two groups of cases are separated from one another by a rigid analysis,
we are not in a position to estimate the part which heredity plays in
the production of progressive muscular atrophy. The disease attacks
males more frequently than females, the proportion, according to Fried-
reich, being one hundred and forty-three males to thirty-three females.
The disproportion between the sexes probably depends on men being
more exposed, than women, to the exciting causes of the disease.
Progressive muscular atrophy is often developed during convalescence
from acute diseases, such as typhus fever, measles, acute rheumatism,
and cholera, and it occasionally begins in Avomen soon after parturition.
Of the exciting causes of the disease the most usual are excessive
muscular exertion, exposure to cold and damp, injuries of various
kinds, and sexual and other excesses.
Symptoiiis. — The invasion of progressive muscular atrophy is slow
and insidious, and the disease is usually in existence some weeks or
months before its presence is discovered. The patient first experiences
some difficulty in performing certain movements, and on attention
being directed to the aifected limbs, some of the muscles are found to
be more or less wasted. At other times, especially when the disease
has been caused by exposure to cold, the mode of invasion is attended
l)y more prominent symptoms. Paroxysmal pains, like those of rheu-
matism or of neuralgia, are felt in the affected limb several weeks or
months before the atrophy of the muscles is noticed, and when once
the atrophy begins in these cases it proceeds more rapidly, and becomes
more generalized than in the painless variety.
The disease usually begins in one of the upper extremities, more
commonly in the right, and. the first muscles to be attacked are either
those of the thenar or hypothenar eminences, the interossei, or the
muscles about the shoulder. It will be shown hereafter that the cases
in which the atrophy begins in the muscles of the loAver extremities
and the lumbar muscles are most probably not examples of true pro-
gressive paralysis. Dui'ing the progress of the disease certain muscles
438
ATROPHIC PARALYSES.
or groups of muscles are attacked while their neighbors are spared, and
the healthy and less atrophied muscles overcome the resistance of the
more diseased, and thus produce distortions, which are rendered more
characteristic by the wasting of the muscles. The disappearance of
the interossei is shown by the deep furrows which appear between the
metacarpal bones ; the thenar and hypothenar eminences are flattened,
and the disappearance of the muscles of the palm brings into view the
diverging flexor tendons which are stretched between the wrists and the
bulging bases of the fingers. The deformity produced by paralysis of
the interossei gives to the hand the appearance of the talons of a bird
of prey, and consequently it has been called the claw-shaped hand, or
main en griff e (Fig. 138). This deformity, however, is not peculiar to
Fig 138.
1- Main en Guiffp:, 2.
(1) Hand, Palmak Surface. (2) Dousal Surface. (After Duchenne.)
A, Wound of the ulnar nerve ; B, Ends of the metacarpal bones ; D, Tendons of the flexor
subllmis ; C, Muscles of the ball of the thumb.
progressive muscular atrophy, inasmuch as it may be caused by injury
of the ulnar and median nerves.
Atrophy and paralysis of the opponens and abductor pollicis cause
the thumb to be extended and abducted when the flexors of the hands
and fingers are afl'ected, the anterior and internal aspects of the fore-
arm are flattened, and when the extensors of the hands and fingers are
SPINAL ATROPHIC PARALYSES. 439
attacked the posterior aspect of the forearm presents a thin and wasted
appearance. Atrophy of the supinator longus gives rise to a flattening
of the external border of the forearm. When the disease begins in
the small muscles of the hand and ascends gradually towards the trunk,
the supinator longus is often the only muscle of the forearm which
retains its plumpness, but when the disease begins in the muscles of
the shoulder and extends to the periphery, the external border of the
forearm becomes flattened at an early period from implication of the
supinators.
When the muscles of the shoulders are affected the arms may hano-
by the side and rather in front of the patient and seem as if they were
merely attached to him by strings and did not belong to him ; the
natural rounded configuration of the shoulder is replaced by a hollow
in which the palm of the hand may be lodged under the projecting
acromial and coracoid processes of the scapula, which stand out in
relief The biceps and the other muscles of the arm may also waste,
so that the limb loses its roundness and becomes flattened, and the
humerus appears to be surrounded merely by a bag of skin. When
the abdominal muscles are affected, the lumbar curve is greatly ex-
aggerated by the unopposed action of the erectors of the spine, and
the abdomen is loose and protruding, but the thorax is held well for-
wards, so that a plumb-line let drop from the most prominent of the
spinous processes of the vertebra will pass well within the sacrum.
When the atrophy is unequally distributed oh both sides of the body,
scoliotic or kyphotic bending of the vertebral column is produced.
When the erectors of the spine and the extensors of the thigh are
simultaneously affected the resulting deformities and the gait are similar
to those observed in pseudo-hypertrophic paralysis and need not be de-
scribed here.
Implication of the muscles of the lower extremities is rare except in
the later stages of the disease, but when they are attacked the various
forms of paralytic club-foot may appear.
The accessory respiratory muscles, such as the pectoralis major,
serratus magnus, and trapezius, are frequently invaded ; and although
the wasting and loss of power of these muscles do not directly endanger
life, yet they may do so indirectly, inasmuch as a slight intercurrent
attack of bronchitis may lead to asphyxia from the inability of the
patient to make a strong expiratory effort to clear the tubes of mucus.
In the later stages of the affection the diaphragm and the intercostal
muscles become attacked, expectoration fails, mucus collects in the tubes,
and the patient dies asphyxiated. In other cases a progressive bulbar
paralysis^ is superadded to the atrophy of the other muscles, and the
440 ATKOPIIIC PARALYSES.
disease is then generally fatal from arrest of respiration caused by
paralysis of the centre in the medulla. The loss of muscular paralysis
keeps pace with the atrophy, and is, as a rule, directly in proportion to
the degree of the latter, and so long as any muscular fibres are left, they
can be made to contract by voluntary efibrt. For a long time, indeed,
the various movements are capable of being perfonned, although with
diminished poAver, and it is only in the last stage of the disease that
complete immobility of the limb is produced. When once a muscle is
attacked, it wastes, as a rule, in a perfectly uniform manner, but in
some cases a portion only of the length of the muscle undergoes atrophy,
while the remainder maintains its volume, and to a considerable degree
its power also.
The jihrUlary contractions of the affected muscles, consisting of
vibratory tremors or quivering of the fibres, are frequently observed
throughout the whole active stage of the disease. They occur spon-
taneously, but may be ])rovoked by gently tapping the surface, by
exposing to air parts which are usually covered, by electrical excitation,
and by active or passive movements of the affected muscles. These
fibrillary contractions arc sometimes the earliest symptom of a fresh
advance of the disease, and they disappear altogether when the atrophy
has reached an extreme degree, or when its progress is arrested.
Tonic or clonic contractions of entire muscles or of groups of muscles
may occasionally occur, which are accompanied by an intense pain
like that of cramp at the calf. During the stage of active fibrillary
contractions the idio-muscular contractility may be so much increased
that the slightest tap on the tendons, fasciic, neighboring bones, or
on the bellies of the muscles themselves occasions widely diffused con-
tractions, such as are frequently observed in advanced cases of acute
phthisis. When the muscles of the upper extremity, for instance, are
undergoing active atrophy a slight tap on the lower end of the radius
may cause almost the whole of the muscles of the forearm and arm,
as w^ell as the pectoral muscles, to enter into contraction, and the
forearm may be jerked upwards just as occurs in cases of spasmodic
paralysis ; and when the atrophy invades the muscles of the lower
extremities the knee-jerk may be so lively as to give rise to considerable
difficulty in diagnosis.
The cutaneous reflex actions are often exaggerated during the active
stage of atrophy, and this renders still greater the similarity of the
affection to a spasmodic paralysis. As the atrophy advances, the
cutaneous reflexes and tendon-reactions become diminished and finally
disappear.
The electrical reactions of the paralyzed muscles may also be at first
SPIXAl. ATROPHIC PARALYSE/ \ 441
/
increased. During tlie active stage of atrophy fee]fl^ , //ctrical currents
either passed through the nerve or the muscle inttu^^fe very active con-
tractions, ahhough their energy is diminished according to the decree
of atrophy. iVs the atrophy advances the strength of current required
to produce a minimum contraction becomes greater and greater, and
after a time the qualitative changes in the galvanic reactions -which
characterize the " reaction of degeneration " ar,e observed.
The sensory disorders of progressive mupcdlar atrophy are of sub-
ordinate importance. In some cases the raiiscular disease is preceded
by paroxysms of pain in tlie affected parts, which sometimes radiate
along the branches of certain nei'^es, and at other times appear to have
their origin in the sensory nerves of the muscles, the pain being then
aggravated by compression of the affected muscles or by passive move-
ments of them. A moderate degree of anaesthesia may be present in
the hands and tips of the fingers in the later stages of the disease, -while
complete analgesia of circumscribed areas of the skin is not uncommon,
and in some cases the area of analgesia is much more extensive than
that of the atrophied muscles. The farado-cutaneous sensibility may
also be diminished, and the patient often complains of sensations of
cold, numbness, formication, and other parfesthesise in the hands and
feet.
The vaso-motor disturbances consist of a local spasm of the blood-
vessels giving rise to coldness and pallor of the affected parts, -v\'hicli is
apt to be followed by relaxation of the vessels and consequent warmth
and redness. In the early stages of the disease the temperature of the
affected extremities is increased, according to Frommann, by 0.2° or
0.3° C, Avhile in the later stages it may sink 3° or 4° C. below the
normal. In the later stages of the disease the patient is sometimes
covered -\yith a profuse sweat (hyperidrosis) which is probably due to
vaso-motor paralysis.
Tro-pliie disorders may sometimes occur in addition to the muscular
atrophy. The skin is sometimes the subject of atrophy, but never to a very
pronounced degree. In the early stages of the disease the patient may be
attacked with painful swellings of the phalangeal joints (arthritis nodosa),
which are most probably related to the arthropathies of tabes dorsalis.
Oculo-piqnllarij symptoms, consisting of paralytic myosis and diminu-
tion of the palpebral fissures, have occasionally ))een observed ; but it is sur-
prising how rarely these phenomena are met with when it is considered
how frequently the lesion is localized in the spinal cord on a level Avith
the cilio-spinal region. In the early stage of progressive muscular
atrophy the patient may complain of chills, and there may be a con-
tinuous, though slight, increase of temperature, wliich lasts for days
\
\
442 ^ ATROPHIC PAEALYSES.
or months. T^S^Vebrile condition may probably be due at times to an
accompanying art?iritis nodosa. In the later stages of the disease tran-
sitory or permanent elevations of temperature may occur, which are,
perhaps, due to such complications as diseases of the lungs or acute
bedsores. No constant changes have been found in the urine. The
course of progressive muscular atrophy is essentially chronic, but its
duration is ver}' variable.and uncertain. In twenty-eight cases analyzed
by Dr. Roberts the mean, duration was thirty-eight months ; of these
four recovered and their mean duration was fourteen months ; the
disease was arrested in thirteen c-ases with a mean duration of twenty-
seven months, and the remaining eleven cases died with a mean duration
of upwards of five years. The disease may progress steadily until
nearly all the voluntary muscles are implicated, and the unfortunate
patient is reduced to such utter helplessness that he is quite unable to
feed himself or turn in bed. The advance of the disease is, however,
seldom continuous, even when it is progressive. Its course is often
interrupted by remissions which may last for weeks, months, or even
years, or its progress may be permanently arrested after some groups of
muscles have been irretrievably destroyed. In a few cases the atrophied
muscles may be restored by treatment to tlieir former volume.
6. Primary Labio-glosso-laryngeal Paralysis (Chronic
Progressive Bulbar Paralysis (Wachsmuth)).
Etiology. — It does not appear that heredity exercises much influence
in the production of labio-glosso-laryngeal paralysis. The disease
occurs most frequently between the ages of forty and seventy years,
although it occasionally attacks younger people. The cases described
as occurring in children are probably examples of insular sclerosis in
which the first diseased patches are localized on a level with the bulbar
nuclei and nerves. The disease attacks men twice as frequently as
women, and all ranks of society appear to be equally liable to it.
The exciting causes of progressive bulbar paralysis are exposure to cold,
blows on the back of the neck, emotional excitement, excessive mental
activity, straining of the affected muscles in singing and speaking, and
bad and insufficient food. Syphilis is a frequent cause of the disease.
Symptoms. — The disease is generally preceded by slight premonitory
symptoms, such as pain in the head and back of the neck, slight dizzi-
ness, and great diminution or complete loss of the reflex irritability of
the larynx, oesophagus, and phar^mx.
The symptoms of chronic progressive bulbar paralysis begin stealthily
SPINAL ATROPHIC PARALYSES. 448
and creep on gradually. A slight affection of speech is usually the
first symptom to attract attention, articulation becomes indistinct, and
the pronunciation of certain letters presents special difficulty, while the
tongue and lips are soon fatigued, so that prolonged reading aloud or
speaking is impossible. The articulatory difficulties are followed bv a
gradual weakness of the lips, and of the palate. The expression of
the face is altered, the voice becomes nasal, and the muscles of masti-
cation and deglutition are so readily fatigued that the patient is soon
compelled to eat only pulpy food, and is unable to swallow much at a
meal.
The initial debility and fatigue of the muscles may extend over a
period of years before the stage of distinct paralysis is reached, but
when once decided paralysis is established the disease assumes a more
progressive character, and advances steadily and surely to a fatal
termination.
When the tongue becomes more or less paralyzed the patient experi-
ences an ever-increasing difficulty in pronouncing the dental and gut-
tural sounds, and inasmuch as the vowel i requires the greatest raising
of the tongue for its production, its pronunciation is the first to suffer,
and then the pronunciation of the consonants r, s, ?, ^, g, t, and lastly
d and n become difficult, imperfect, and finally impossible. After a
time the patient is unable to effect the coarser and less complicated
lingual movements. He may at first be able to protrude the tongue,
but not to raise the tip towards the hard palate or tow-ards the nose
after protrusion, while inability to move the tip laterally indicates a
still greater degree of paralysis. As the paralysis increases the tongue
cannot be lengthened into a point or rolled into the form of a tube,
and ultimately the patient is unable to protrude the organ, which now
lies behind the lower row of teeth completely helpless, and motionless,
or maintained in constant vibration by fibrillary tremors. The tongue
may maintain its normal aspect, or it becomes large and flabby, or
more frequently it is sodden, grooved longitudinally, wrinkled, and
shrunken, while simultaneous atrophy of the papillae give a glazed
appearance to the surfoce.
Deglutition is rendered difficult in the early stages of the disease by
the weakness of the tongue alone. The patient experiences a difficulty
in collecting the food so as to form it into a bolus, and in pressing it
back against the soft palate and into the pharynx. In order to over-
come this difficulty the patient, after chewing his food well, takes a
drink and throws his head backwards, while at other times he assists
the imperfect movements of his tongue with his fingers, using them to
extract the food which has lodged between the teeth and cheeks, and to
444 ATROPHIC PARALYSES.
push the bohis to the back of the tongue till it is caught by the retiex
movements of the pharyngeal muscles.
The glottis is not completely closed during deglutition, even at this
early stage, because the root of the tongue cannot be sufficiently ele-
vated during; the second stao;e of the act in order to allow the bolus to
glide over the depressed epiglottis. The closure of the glottis is also
rendered still more imperfect by the presence of paralysis of the muscles
which pass from the inferior maxilla to the hyoid bone, a defect which pre-
vents the larynx from being raised as in health during the second stage of
deglutition, and consequently the glottis fails to be closely applied to the
epiglottis. The imperfect closure of the glottis causes food and fluids
to find their way into the trachea, and these give rise to distressing
paroxysms of cough and dyspnoea. The saliva cannot be swallowed,
and accumulates in the mouth, and, owing to the paralysis of the
orbicularis oris, flows from it in a continuous stream.
The facial muBcles are implicated soon after, or sometimes before
the muscles of the tongue, the orbicularis oris being the first to suffer.
With the increasing Aveakness of the orbicular muscle the patient be-
comes unable to Avhistle, blow, compress his lips, or kiss; he experi-
ences difficulty in pronouncing the vowels o and w, and with the ad-
vance of the paralysis the labial consonants p, /, i, and m become
increasingly difficult to articulate.
Paralysis of the palate renders the formation of the explosive labial
consonants still more difficult, because the current of air necessary to
force the lips suddenly asunder escapes through the nose, and the con-
sonants p and h are consequently turned into me and ne. If the
patient's nose be closed, these letters are better pronounced. Paralysis of
the palate also gives a nasal resonance to the voice, and permits food
and fluids to escape readily through the nose during efforts at degluti-
tion. When the muscles of the tongue, lips, and palate are simulta-
neously paralyzed, speech becomes more and more indistinct, and the
patient can only give utterance to inarticulate and grunting sounds, but
the vowel a, being independent of the articulatory movements, can still
be pronounced.
The other facial muscles most liable to be implicated are the quad-
ratus and levator menti, the muscles of the palpebral and nasal regions
are never affected, and even the elevators of the superior lips and the
buccinators are only occasionally paralyzed. The paralyzed muscles
are almost always distinctly atrophied, and consequently the lips look
thin, sharp-edged, and furrowed, and fibrillary contractions are not
infrequently observed in them. The patient now presents a very strik-
ing and characteristic appearance. The lower lip hangs loose and
pendulous, the mouth is somcAvhat increased in breadth and cannot be
SPIXAL ATliOPHIC PARALYSES. 445
closed, and tlio naso-labial folds become deepened and give to the
patient a laclin-mose expression. During states of emotional excite-
ment the lower part of the face remains comparatively motionless, and
contrasts strongly -with the vivacious movements of the upper half of
the face, and with the brightness and activity of the eyes.
The saliva now flows from the mouth in a continuous stream and
causes much annoyance to the patient, inasmuch as it soaks through the
pillow at niglit, and requires to be constantly wiped from the lips with
a handkert-hief during the day. The saliva is sometimes unchanged in
quality, while at other times it becomes so viscid that it may be drawn
out of the mouth in long ropes. It appears to be generally secreted in
normal quantity, but sometimes it is increased to six or eight times the
(juantity secreted in healthy persons.
Mastication is indirectly impaired from paralysis of the tongue and
facial muscles, but after a time it becomes still further interfered with
by direct implication of the masticatory muscles. The pterygoid
muscles are the first of the masticatory muscles to be attacked, and Avith
paralysis of these the power of effecting the lateral movements of the
lower jaw is lost, and with the progressive feebleness of the remaining
muscles of mastication the power of chewing the food becomes increas-
ingly difficult, feeble, and finally impossible.
^\\e pharyngeal muscles are now invaded and portions of food lodging
in the pharynx increase the risk of foreign particles entering the larynx,
Avhile at other times the whole bolus sets impacted on a level with the
glottis and causes imminent danger of suffocation.
The constrictors of the glottis are paralyzed soon after or simul-
taneously with the pharyngeal muscles, and the danger of swallowing
either solids or fluids is now much intensified, and solid particles freely
entering the trachea not only cause distressing paroxysms of cough and
dyspnoea, but are also apt to pass into the bronchi and give rise to a
fatal pneumonia.
The oesophagus becomes ultimately paralyzed if the patient survive
so long ; the power of deglutition is now completely lost, and the patient
must starve unless he is fed with the stomach pumj).
The laryngeal muscles are sometimes found paralyzed : the laryngo-
scope reveals paresis or paralysis of the vocal cords, and the voice
becomes hoarse and feeble, until finally there is complete aphonia.
The circulation is variously affected according to the stage of the
disease. There is no trustworthy record of retardation of the pulse
which could with probability be referred to irritation of the vagus, but
a pulse rising before death to from 130 to 150 per minute, or even
higher, has been frequently recorded, and is prol)ably caused by paralysis
446 ATROPHIC PARALYSES.
of the vagus. In the terminal period of the disease patients often suffer
from fainting fits, accompanied by great anxiety and a sensation of
impending death, and, indeed, death may result from an attack of syncope.
These phenomena are probably caused by disease of the cardiac centres
of innervation.
When the respiratory mechanism is affected a fatal termination is
near. The respiratory movements become feeble, and owing to the im-
plication of the spinal accessory nerves the auxiliary muscles of res-
piration are paralyzed, and superior thoracic breathing is impossible.
The inefficiency of the respiratory movements renders the breathing
shallow, and all attempts at coughing or blowing the nose are weak and
powerless. After a time the pneumogastric nuclei are invaded, and
spontaneous paroxysms of dyspnoea with a tendency to syncope super-
vene. The attacks of dyspnoea become more and more frequent as the
disease advances, while the breathing power becomes feebler and feebler
until ultimately the patient dies from asphyxia. But the patient often
dies before this advanced period of the disease is reached, the fatal issue
being generally caused by an attack of bronchial catarrh or of pneu-
monia.
Atrophy of the paralyzed muscles is usually most marked in the
tongue and lips, these parts being likewise kept in constant movement
by fibrillary contractions. The apparent loss of volume and the degree
of paralysis do not always run a parallel course, and the tongue some-
times retains its normal volume while completely paralyzed, but a sub-
sequent microscopical examination will show that the muscular fibres
have undergone extensive degeneration.
The electrical excitability is said by most authors not to undergo any
noteworthy changes, but Erb states that he lias met with the most marked
"reaction of degeneration" on direct irritation of the muscles of the
chin, lips, and tongue. The electrical irritability of the nerves was
normal or but slightly diminished.
The sensibility generally remains unaffected throughout the whole
course of the disease. Buzzing in the ears and deafness have occasionally
been present, and in some cases various parsesthesijB, or even a consider-
able degree of anaesthesia of one or both sides of the face, loss of
common sensation on the tongue, and pain in the occipital and upper
cervical regions have been observed.
The intelligence remains quite clear to the last, but the temper is
somewhat excitable, and patients often manifest an inclination to laugh
or weep on slight provocation.
Reflex irritability is often much diminished or lost in the tongue, soft
palate, pharynx, and even in the larynx before the appearance of any
SPINAL ATROPHIC PARALYSES. 447
Other symptom, but it is sometimes retained in these parts until a late
period of the disease.
Vaso-motor disturbances have not been recorded, and there is no
fever during the whole course of the disease.
G-eneral nutritive disorders occur sooner or later in the course of this
disease, owing in great part to the insufficient quantity of food which the
patient is able to take. The patient becomes after a time greatly ema-
ciated, and, unable to get up, he sits in bed with the upper part of the
body propped up, and with the head resting on pillows and inclined to
one side in order to let the saliva flow out of the mouth. When this
condition is reached death soon supervenes, either from a paroxysm of
dyspnoea, or suddenly and quietly from arrest of the heart's action.
The course of this form of bulbar paralysis is always slow and chronic,
but surely progressive. There is seldom a remission of long duration
and recovery has never been observed Avhen the diagnosis of the primary
disease was beyond question. The disease is usually fatal in from one
to five years.
Complications. — Progressive muscular atrophy is the most important
and frequent complication of bulbar paralysis, the latter disease being
sometimes the primary afiection, and at other times a terminal phenome-
non supervening in the course of the former. The two affections are,
indeed, essentially the same disease, both as regards the clinical symp-
toms and the anatomical changes formed after death.
Amyotrophic lateral sclerosis is another important complication of
progressive bulbar paralysis. In the cases which concern us at present
the phenomena of bulbar paralysis are primary, but in the course of the
disease the lower extremities become the subjects of a gradually increas-
ing paralysis which is characterized by the muscular tension, and ex-
ag-gerated tendon-reactions which are held to indicate disease of the
lateral column of the cord.
7. Ophthalmoplegia Externa vel Progressiva.
Etiology. — The two known causes of the disease are syphilis and
rheumatism.
Symptoms. — The first symptom to attract attention is usually a
drooping of the eyelids, which gives to the patient a peculiar sleepy
appearance. Soon afterwards all the muscles of the eyeballs manifest
signs of weakness, the aff"ection is usually bilateral, and every possible
combination of paralysis may occur, but the muscles are always attacked
in groups and not singly. The pupils are in a medium state of dilata-
448 ATROPHIC PARALYSES.
tion, and their reflex contraction to light is either sluggish or lost. The
condition of accommodation has not always been tested, but in some
cases it was found normal. White atrophy of the optic disks, with
blindness, was present in one-third of the cases reported by Hutchinson.
In some cases the fifth nerves, and in others the facial nerves were
involved in the disease, while in one case reported by Hutchinson the
palate was affected and smell was lost. In some of the recorded cases
the patellar tendon-reaction was absent, and other symptoms indicative
of locomotor ataxia were present. It seems, indeed, likely that a con-
siderable number of the reported cases Avere examples of locomotor
ataxia in which the ocular troubles were unusually well marked.
Y. MYOPATHIC ATROPHIC PAPvALYSES.
PSEUDO-HYPERTIIOPHIC PARALYSIS AND Erb'S JuVENILE FoRM OF
Progressive Muscular Atrophy.
Etiology. — Pseudo-hypertrophic paralysis was supposed to begin
almost always in infancy, but if we include Erb's juvenile form of
muscular atrophy, it will be seen that adults are frequently attacked,
although in these cases the symptoms make their appearance between
five and thirteen years of age. The disease is much more common in
boys than in girls ; out of two hundred and twenty cases collected by
Gowers one hundred and ninety Avere boys and thirty girls. Hereditary
predisposition to the disease can often be traced. Two children in the
same family are often attacked, and Meryon met with a family in which
eight children were the subjects of the disease, while other equally
striking examples have been reported by others. It is very probable
that all the cases of supposed progressive muscular atrophy in which
numerous members of the same family were attacked, such as the cases
reported by Hemptenmacher, Friedreich, Hammond, and Naunyn, really
belong to Erb's juvenile paralysis, and Avill therefore have to be trans-
ferred to this group. A remarkable circumstance about the heredity
of this disease is that it is mainly confined to the male sex, yet the
descent, so far as is known, is always through the mother's side. The
disease is not, as a rule, transmitted directly from parent to offspring,
inasmuch as the majority of its victims are attacked at an early age,
and they do not, therefore, become parents. For the same reason the
disease cannot be regarded as an example of atonism. It must, there-
fore, be inferred that a certain predisposition is transmitted which, with
the concurrence of other unfavorable circumstances, such as an eruptive
fever, develops the disease.
MYOPATHIC ATROPHIC PARALYSES. 449
The exciting causes of the disease are not well known. Exposure
to cold and damp appears to be occasionally the determining cause,
while at other times it has followed an eruptive fever, variola, or
measles, and several cases have been ushered in by convulsions.
Symptoms. — When pseudo-hypertrophic paralysis begins in infancy
the parents do not notice that anything is wrong until the child arrives
at the age when he ought to begin to walk. At this period it is noticed
that when the child is placed on his feet he does not instinctively move
his legs to walk, but they double helplessly under him, or the child
may have begun to walk, but it is observed that he is soon fatigued,
and that he is unable to stand steadily or walk without stumblino-.
The parents are not readily alarmed at the inability of the child to
walk, because the lower limbs appear to be unusually well developed.
The appearance of muscular strength is caused by an increase in
volume of some of the muscles, but this increase is due, as we shall
hereafter see, to morbid changes occurring chiefly in the connective
tissue of the muscle, and which are always attended by a diminution of
its power. The apparent hypertrophy of the muscles generally begins
by enlargement of one calf, the other soon becoming affected. The
gluteal muscles are soon invaded, and then the disease successively
attacks the lumbo-spinal muscles, the muscles of the thigh, trunk,
shoulders, and upper arms, while the muscles of the neck, face, tongue,
forearms, or hands may occasionally be attacked, but only, as a rule, at
a late period of the disease. The aftected muscles may attain an
enormous volume, and stand out so prominently under the skin that
Duchenne uses the term "hernial protrusions" to describe their ap-
pearance. The muscles feel hard and resisting to the touch, so that the
whole appearance of the patient often suggests the idea of Herculean
strength instead of the great feebleness Avhich really exists. But even
in the midst of all this apparent development of muscular power there
are not wanting visible indications of the real nature of the malady,
inasmuch as some of the muscles are always found atrophied and their
wasted condition contrasts strongly with the excessive size of the others.
In the majority of cases the gastrocnemii and the gluteal muscles are
increased in size, while those of the thigh often undergo some degree of
atrophy, and consequently the slender thighs afford a marked contrast
to the enlarged calves and buttocks. In the upper part of the body
the atrophy frequently predominates. The deltoids are usually enlai-ged,
but the remaining muscles of the arm and the pectoral muscles undergo
atrophy, while those of the forearm and hand are often spared until a
late period of the disease. Of the muscles which move the shoulder
the rhomboids and the serrati are the most liable to be :itt:icked, and
29
450 ATROPHIC PARALYSES.
these are generally atrophied instead of being enlarged. In a large
majority of cases, therefore, the uj^per part of the body is contrasted by
its slenderness with the unusual development of the lower extremities,
and perhaps the greatest contrast is afforded by the thin arm, which
often consists of scarcely anything more than the humerus surrounded
by skin, and the normal condition of the forearm on the one hand, with
the prominence of the enlarged deltoid on the other.
The relative distribution of the hypertrophied and atrophied muscles
just described is that usually met with in the cases named by Erb "the
juvenile form of progressive muscular atrophy," but I can see no
essential difference between these cases and those in which the muscular
hypertrophy is more widely distributed. Pseudo-hypertrophy of muscles
does not, indeed, appear to be a necessary part of the diseases Avhich
mav be grouped together as myopathic atrophic paralyses. In the cases
described by Leyden under the name of " hereditary muscular atrophy,"'
the slight degree of increase of volume observed in some of the muscles
is quite subordinate to the widely diffused atrophy of others. Cases
have been described by Zimmerlin which appear to belong to the myo-
pathic atrophic paralyses, and in which the muscles of the shoulders
and arms were atrophied without any admixture of pseudo-hypertrophy,
and cases have been described by Landouzy and Dejerine which must
also apparently be included in this category, and in which the symptoms
began in infancy by atrophy of the muscles of the face, the muscles of
the shoulders and arms being invaded about the age of eleven years.
In short, the group of myopathic atrophic paralyses presents several
varieties, but we shall at present proceed with the more usual form of
the disease as represented by the affection known under the name of
pseudo-hypertrophic paralysis.
The relative degree of paralysis of groups of muscles gives rise as
usual to certain deformities, and one of the most notable of these occurs
in the foot. The gastrocnemius muscle undergoes progressive shorten-
ing, partly perhaps owing to the internal changes it is undergoing, and
partly owing to the increasing paralysis of the anterior muscles of the
foot. But whatever may be the cause, the result of this shortening is
that the patient experiences difficulty in bringing the heel to the ground,
and as the disease advances a permanent condition of talipes ecjuinus
or equino-varus is established. The foot also becomes more hollow and
the plantar arch increased, while paralysis of the interossei causes the
first phalanges to be maintained in a state of exaggerated extension on
the metatarsal bones, and the distal phalanges to be flexed, so that the
toes assume the peculiar claw-like appearance which Duchenne has
called griffe des orteils. A remarkable curvature of the spine in the
MYOPATHIC ATROPHIC PARALYSES. 451
lumbo-sacral region, named by Duchenne lordosis or saddle-hack, is one
of the most constant symptoms of the disease. This deformity is not
seen until the patient stands or walks ; the shoulders and the upper part
of the vertebral column are then carried backwards, so that a plumb-
line let fall from the most prominent spinous process of the vertebral
column falls behind the sacrum. This deformity is produced by com-
parative feebleness of the extensors of the pelvis and the erector muscles
of the spine. Weakness of the extensors allows the pelvis, and with it
the loAver vertebra, to incline forwards when the patient assumes the
erect posture, and a compensatory backward inclination of the dorsal
spine is rendered necessary in order to keep the centre of gravity in the
normal position. The posterior displacement of the upper part of the
body also causes the line of gravity to fall behind the trochanters of the
femur and takes off all strain from the enfeebled erector muscles of the
spine and the gluteal muscles. The attitude of the patient on assum-
ing the erect posture is quite characteristic of the disease. The feet
are kept widely apart, and the patient cannot approximate them without
risk of falling. In the early stage of the disease the heels are brought
to the ground, but after a time the patient has to balance himself upon
his toes, and at the same time the dorsal curve becomes very pronounced,
and in consequence of these deformities the power of the patient to
maintain the erect posture becomes very precarious and the slightest
push suffices to throw him down.
The gait of the patient is no less characteristic than his attitude in
the erect posture. We have seen that the feet are held apart, and in
walking the body is inclined first to one side then to the other, so
that the gait resembles the Avaddling of a duck. When the feet are
kept widely apart the centre of gravity must be carried at each step
well over to the side of the active leg, in order that the line of gravity
may pass through the centre of the arch of the foot planted on the
ground. Duchenne thought that the oscillation of the body in walking
was an instinctive movement on the part of the patient in order to avoid
putting a strain upon the paralyzed gluteus medius. But in a case of
muscular atrophy observed by myself the gluteus medius was completely
paralyzed on each side, yet instead of the waddling gait so characteristic
of pseudo-hypertrophic paralysis, the head and body were moved for-
Avards during locomotion almost in a straight line, and without the
lateral inclinations being at all equal to those observed in healthy per-
sons. From an examination of several cases of this disease it appears
to me that the lateral inclinations, instead of being caused by paralysis
of the gluteus medius, are mainly effected by alternate contractions of
these muscles, and are rendered necessary partly by the legs being held
452 ATEOPHIC PAEALYSES.
widely apart, and partly by the inability of the patient to clear the toes
of the advancing foot from the ground by producing dorsal flexion of
the foot. As the disease advances the patient, as we have seen, becomes
unable to bring the heel to the ground, and at each step the body must
be delicately balanced in order that the line of gravity may pass through
or a little behind the ball of the active foot, and the slightest displace-
ment of the centre of gravity will cause the patient to fall. It is,
therefore, necessary that at each step the body should be inclined well
over to the side of the active leg, and the patient aids himself in main-
taining the centre of gravity vertically above the ball of the foot on the
ground by moving his arms about like a rope dancer.
The manner in which the patient attains the erect posture is equally
characteristic. When he is laid down, or falls, he drags himself up
with the aid of his arms if a chair or other article of furniture is
sufficiently near for him to lay hold of. But when he has to get uj)
without extraneous aid, the body is first raised on the hands and feet.
In this attitude the feet are planted on the ground, the different seg-
ments of the lower extremities are slightly flexed upon one another,
the body is flexed on the lower extremities, and more or less horizontal,
the head is directed downwards, and the tips of the fingers of both
hands rest on the ground in front of the toes. The patient next raises
his hand, say the left, and places it above the left knee. The body is
now drawn over to the opposite side so that its weiglit rests mainh^ on
the right leg, and by one vigorous push of the left arm the left knee is
thrust backwards, and the leg and thigh are thus extended upon one
another, while the body is at the same time thrust upwar<ls. Simulta-
neously with this action the weight of the body is transferred from the
right to the left leg, and the right hand is elevated and planted above
the knee on the corresponding side, and a backward push on that knee
causes the different segments of that limb also to become extended upon
one another. The patient has now attained the second posture, and in
this position his feet are planted on the ground, the lower extremities
are directed upwards or backwards, and the body is inclined upwards
while the arms prop up the trunk by passing from it to the knees
where the hands are placed. The fact that the weight of the upper
part of the trunk is directed through the arms to the knees redis-
tributes the force in such a way that the knees are pushed backwards,
and thus the thighs and legs tend to become extended upon one another,
the heels are forced downwards, and so the patient is fixed firmly to the
ground, and the trunk is maintained in its upward and forward attitude
without any strain being placed upon the enfeebled extensors of the
body. The next great effort of the patient is directed to attain the
MYOPATHIC ATROPHIC PARALYSES. 453
erect posture, and in accomplishing this object it is said that he thrusts
his body upwards by gradually chmbing up his thighs. This de-
scription is very graphic, but it is only partially accurate. The
movement by which the pelvis is elevated upon the thighs is, indeed, a
very complicated one, and is effected not by simple extension, but bv a
kind of screw movement.
The patient experiences great difficulty in getting up steps, owino- to
the feebleness of the gluteus maximus. He lays hold of the railing with
one hand, say the right, and drags his body upwards at each step.
The right arm is, however, assisted by the left. The left hand is
planted above the knee upon the same side, and each time the left leg is
raised a step the body is thrust upwards by the various segments of
the left arm being extended upon one another. The disease now be-
comes stationary for two or three years, and sometimes for a much
longer period, and as the general health is good and the muscular
development apparently very powerful, the parents cannot believe that
the affection is incurable. This illusion is, however, after a time des-
tined to be dispelled. The feebleness of the lower extremities gradu-
ally increases, so that the child cannot maintain the erect posture,
while the muscles of the superior extremities also become both para-
lyzed and atrophied, and even the hypertrophied limbs begin to waste.
The patient, now arrived at adolescence, may live on for several years
in a condition of almost complete paralysis, until finally death takes
place from exhaustion, implication of the respiratory muscles, or, more
usually, from some intercurrent affection.
The patellar tendon-reaction is lost at a comparatively early period
of the disease, and the electrical reaction of the muscles remains normal
so long as any muscular fibre is left. The skin over the affected parts
often presents a mottled appearance, and the superficial temperature of
the inferior extemities has sometimes been found higher than that of
the trunk.
The disease is associated with a certain amount of mental incapacity.
Patients are sometimes slow in acquiring speech, others are obtuse in
intelligence, and some are idiots. The disease is unaccompanied by
suffering, there is no alteration of sensibility, and the functions of the
bladder and rectum are unaffected, while the general health is not in-
terfered with until the terminal period of the disease.
The course of the disease is always chronic. It begins insidiously,
and consists of a first stage, in which there is progressive enfeeblement
of the lower extremities, saddle-back, and waddling gait, and which
may last from a few weeks to some years before the commencement of
the next stage. This second period is characterized by apparent hyper-
454 ATROPHIC PARALYSES.
trophy of a certain number of muscles usually beginning in those of
the calf, and extending gradually to other muscles of the trunk and
upper extremities. The stage of hypertrophy attains its maximum
extent and intensity generally eighteen months from the beginning of
the second stage. The symptoms now remain stationary for two or
three or for many years. Some of the cases described by Erb under
the name of "the juvenile form of progressive muscular atrophy," live
to a moderately old age, and the disease may then remain more or less
stationary for from ten to twenty or more years.
The third stage of the disease is now ushered in by a still furtlier
enfeeblement of the affected muscles, and by the extension of the paral-
ysis to the superior extremities. Abduction and elevation of the arm are
at first rendered difficult, and by and by the paralysis gradually impli-
cates the other movements of the arm.
The last stage of the disease generally begins about puberty, although
it is sometimes deferred until a moderately mature age. The slight
power of movement of which the patient was capable becomes gradually
lost, so that he can only sit in a chair or recline on a couch. The
patient may continue to live for a long time in this condition, but
eventually death supervenes from exhaustion or some intercurrent
malady.
Morbid Anatomy and Physiology of the Atrophic Paralyses.
1. Changes in the Nervous System. — Paralysis of the muscles sup-
plied by individual nerves is caused by a local neuritis, by injuries of
the nerve from external wounds, or by compression of it from tumors
growing in the nerve or in neighboring structures. When a nerve is
seriously injured in any part of its course, the peripheral part under-
goes the Wallerian degeneration, and the muscles supplied by it are not
only paralyzed, but also undergo atrophy.
The morbid anatomy of progressive multiple neuritis has already
been described. The most important changes observed in lead paral-
ysis have been found in the intramuscular nerve fibres, and in the
musculo-spiral nerve. The connective tissue and the sheath of the
primitive fibres are thickened, while the axis-cylinders are sometimes
distinctly visible, and at other times disappear altogether. Vitreous
degeneration and atrophy of the ganglion cells have been found by
some observers, while others failed to detect any change in the spinal
cord.
In diphtheritic paralysis the nerves of the palate have been found
altered in the same manner as occurs in the peripheral end of a nerve
MYOPATHIC ATROPHIC PARALYSES,
-i55
after section, and Dejerine found similar alterations in the anterior roots
of the nerves on a level with that portion of the spinal cord from which
the paralyzed muscles are innervated. Changes have also been ob-
served in the anterior gray horns of the spinal cord, but they are
slight, and the balance of evidence appears to favor the idea that the
primary lesion is situated in the course of the nerves. In alcoholic
paralysis also the most recent observations seem to prove that the paral-
ysis is caused by a neuritis of the peripheral nerves. No anatomical
changes have as yet been discovered in those cases of reflex paralysis
which are attended with w'asting of the extensor muscles of the in-
flamed joint.
In the spinal atrophic paralyses the chief lesions have been found in
the anterior gray horns of the spinal cord.
In acute ascending paralysis post-mortem examinations have yielded,
for the most part, completely negative results, no morbid changes
whatever having been detected in the spinal cord, peripheral nerves, or
Fig. 139.
The letters o, h, c indicate respectively tlie central, antero-lateral, and postevo-Iateral groups of ganglion
cells On the left side the group h has almost entirely disappeared, causing a marked falling in of the
circumference of the gray matter. The groups a and c are fairly well represented on the left side, but the
cells composing them are not so numerous as on the right. The internal group lias disappeared from l.iotli
sides. (After Humphreys.)
muscles. In other recorded cases, which apparently were examples of
the disease, the usual signs of an acute myelitis were discovered, while
in a case reported by Dejerine and Goltz decided evidences of a degen-
erative neuritis were found in the anterior roots of the spinal nerves.
It is very probable that some of the cases recorded as examples of
Landry's paralysis really belong to the group of progressive multiple
neuritis.
4:66
ATROPHIC PARALYSES.
Acute spinal atrophic jjaralt/sis appears to be an acute inflammation
which remains more or less limited to the anterior gray horns of the
spinal cord (Fig. 139). The antero-lateral columns may also manifest
a greater or less degree of sclerosis, while the anterior roots and the
efferent fibres of the peripheral nerves give evidence of having under-
gone a degenerative atrophy. In old-standing cases the anterior horn
of the affected side, when the disease is unilateral, undergoes marked
atrophy as compared with the healthy one (Fig. 140).
Fig. 140.
Tr.insverse Section of the Spinal Cord
taken from the cervical region of a woman, aged fifty years, who died in the Salpetritre, of general paral-
ysis of the insane, and who was the subject ot infantile spinal paralysis of the right superior extremity.
There was fibroid atrophy of the right anterior cornu, and atrophy of all the white columns of the corre-
sponding side. (From Charcot.)
In eli7'onic atrophic spinal paralysis the post-mortem examinations
hitherto obtained have been few, but cases have been recorded by
Cornil, Webber, Aufrecht, Dreschfeld, and myself. The chief changes
were found in the anterior gray horns, and consisted in disappearance
and atrophy of the ganglion cells, destruction of their processes, thick-
ening of the walls of the bloodvessels, and exudation of the white and
of a few red blood-corpuscles into the perivascular spaces. The case
recorded by myself was that of a young girl aged fifteen years, who
had died from respiratory paralysis after having the typical symptoms
of the disease for seven months. The ganglion cells had almost com-
pletely disappeared from the anterior horns throughout the entire
MYOPATHIC ATROPHIC PARALYSES.
457
length of the spinal cord (Fig. 141, 1 to 4), while the upward contin-
uation of the anterior horns in the medulla was similarly affected but to
a less degree (Fig. 141, 5). Slight changes were observed in the columns
of Goll, which showed that the lesion was not strictly limited to the
anterior horns, although they were the portions which chiefly suffered.
Fig. 141.
Tkansverse Sections of the Spinal Cord and JIedulla Oblongata at different levels, fuom a case
OF CHRONIC atrophic SPINAL PARALYSIS, SHOWING THE DISAPPEARANCE OF THE GANGLION CELLS.
(Young.)
1, Jliddle of the lumbar enlargement ; 2, Middle of the dorsal region ; 3, Middle of the cervical enlarge-
ment ; 4, Section on a level with the origin of the second cervical nerve ; 5, Section of the medulla oblon-
gata on a level with the middle third of the olivary body.
In 'periependymal myelitis the gray column which surrounds the
central canal is the seat of inflammatory changes. These changes con-
sist in some cases of a proliferation of the epithelioid cells which line the
central canal, while in other cases the morbid process appears to begin
in the neuroglia which surrounds the canal, and the central grav column
becomes converted into a solid mass of fibroid tissue which grows from
within outwards, and invades the remaining parts of the gray matter.
The central core may be solid throughout the whole extent of the cord,
but in most cases a portion of the interior undergoes softening and a
cavity is formed which is filled with serous fluid. The cavity varies
greatly in its dimensions ; it sometimes extends the whole length of the
cord, while at other times it is only a few lines in length ; and on trans-
verse section it is sometimes large enough to admit the tip of the finger,
while at other times it is only large enough to be visible to the naked
eye. The cavity is usually situated, not in the position of the central
canal, but in that part of the posterior columns which adjoins the pos-
terior commissure, and the central canal can generally be found lying
in front of it. The cavity is always surrounded by a ring of fibroid
tissue, which grows from within outwards, and invades the gray sub-
458
ATROPHIC PARALYSES.
Stance of the cord, and which may even extend to the white substance,
especially to the lateral columns. In some cases the cavity forms the
predominating feature of the morbid change, while in others the cavity
is insignificant and almost the whole of the central gray column is con-
verted into a dense mass of sclerosed tissue. In the annexed woodcut
(Fig. 142) borrowed from Leyden, a section of the cervical enlargement
Fig. 14-2.
Transverse Sf.ction of the Spinal Cord from the Middle of the Cekvical Enlargement, from
A CASE OF Syringomyelia, showing a cavity behind the posTERioa commissure, and destruction of a
LARGE portion OF THE GANGLION CELLS OF THE ANTERIOR GRAY HORNS. (FrOIlI LeYDEN.)
of the spinal cord, from a case of syringomyelia, is represented : the
central gray column is changed into a substance of a gelatinous con-
sistence, Avhich became softened into cavities at certain points. In a
case observed by Sir W. Gull a considerable dilatation of the spinal
canal (Fig. 143) was found in the cervical region, and on this level the
FiQ. 143.
Transverse Section of the Cervical Enlargement of the Spinal Cord, showing a central cavity,
WHICH has destroyed consideuable portions of the anterior GRAY HORNS. (After Gull )
gray substance of the cord was so much compressed as to have almost
disappeared. In a case recorded by Westphal the cavity was said to
have resulted from the softening of a gliosarcomatous tumor, but in a
later paper by the same author it is admitted that the tumor was most
probably a mass of inflammatory tissue.
I
MYOPATHIC ATROPHIC PARALYSES,
4:59
Treatment. — The treatment is the same as that foi' the subacute
ascending general paralysis of Duchenne.
In progressive muscular atrophy the spinal cord has, according to
Eulenburg, been examined in forty-nine cases, and out of these, morbid
changes have been found in thirty-four, while the cord was healthy in
fifteen cases. But too much importance must not be attached to the
cases in which the results were negative, inasmuch as changes may have
been present in many of them, and been overlooked for want of the
requisite skill on the part of the person who conducted the examination,
while it is certain that cases have been included in these statistics which
must be transferred from the group of progressive muscular paralvsis
to the juvenile form of muscular atrophy described by Erb.
Fig. 144.
Transverse Section of the Cervical Region of the Spinal Cord, from a case of progressive
muscular atrophy. (charcot.)
A, Left anterior gray horn ; the ganglion cells have persisted, but are much altered in appearance.
B, Eight anterior graj' horn, almost complete atrophy of the cells, one group only (6) having persisted.
Attention was first directed by Luys to the morbid changes of the
gray substance of the spinal cord in cases of progressive muscular
atrophy. In a case of advanced progressive muscular atrophy he found
the capillary vessels of the gray substance of the anterior horns increased
in number, the walls of the vessels thickened and surrounded by granu-
lar exudation, numerous corpora amylacea scattered through the gray
substance, and disappearance of a considerable number of the ganglion
cells and disintegration of others. The degeneration affected the left
4(>0
ATROPHIC PARALYSES.
anterior cornu principally, this localization being the counterpart of the
fact that the atrophy was most pronounced on the left side. The spinal
cord has been examined in six cases of the disease by Lockhart Clarke,
and the observations of Luys have been confirmed by him in all essential
respects, and similar observations have been made by Dumenil, Hayem,
Charcot and Joffroy, Pierret and Troisier, and others.
In a case reported by Charcot the ganglion cells of the left anterior
o-ray horn (Fig. 144, A) could still be distinguished, but were observed
to be in an advanced stage of atrophy. In the right anterior horn
(Fig. 144, B), however, the cells could only be distinguished in one
group — the postero-lateral (Fig. 144, b) — while the cells of the remain-
incp oroup were completely destroyed. But it has appeared to me that
too little attention has hitherto been paid to the condition of the central
gray column. In this diagram (Fig. 144) the left central column is
seen to be intersected by enlarged vessels, and that of itself affords some
evidence that this column was not free from disease in the section from
which the drawing was taken. It seems to me likely that the morbid
Fig. 145.
TnANSVERSE Section from the Middle of the Cervical Enlahgemest of the Spinal Coud, from an
ADVANCED CASE OF PROGRESSIVE MUSCULAE ATROPHY. (YOUNO.)
cc. Central canal ; i, Internal ; al, Antero-lateral, nmXpl, Postero-lateral groups of ganglion cells.
process begins on each side of the central canal, probably in tlie tissues
immediately adjoining the central artery, and that it extends outwards
and forwards, as well as upwards and downwards from this point as a
centre. In a transverse section of the middle of the cervical enlarge-
MYOPATHIC ATEOPHIC PARALYSES,
461
uient in my possession, which I owe to the kindness of Dr. Dreschfeld,
it was unmistakable that the central gray column Avas more diseased
than any other part of the section. This column was traversed bv en-
larged vessels, and almost all structure was obliterated, while the various
groups of ganglion cells on the anterior horns Avere still distinctly
recognizable. The cells of the median area and the marginal cells of
the other groups were destroyed, but considerable traces of the laro-e
cells of the groups were still distinctly visible (Fig. 145). I have also
observed in one of my sections a streak of degeneration to pass alono-
the posterior branch of the central artery and into the substance of the
posterior horn, and this may explain why patches of cutaneous Anal-
gesia are sometimes met with in progressive muscular atrophy. In the
accompanying woodcut (Fig. 146) borrowed from Leyden's work on
the diseases of the spinal cord, it is also distinctly represented that the
most diseased portions occupy the central column of the cord, and that
thence the disease extends laterally to the anterior gray horns and
])etween the groups of ganglion cells.
Fig. 14ti.
Transverse Sectkix of the Spinal Cord from the 31iddle of the Cervical ExLARiiEMEXT, siiowi.st;
THAT THE CENTRAL COLUMN AND A LARGE PORTION OF THE ANTERIOR GRAY HORNS ARE DISEASED.
(From Leyden. I
The anterior roots of the nerves were first observed to be diseased by
Cruveilhier in the case of the shoAvman Le Compte, who died of a pro-
gressive muscular atrophy of five year's duration, and similar observa-
tions have since been made by others. The peripheral nerves have
likewise been found diseased by Virchow, Hayem, Charcot and Joft'roy,
Bamberger, and many others. The changes observed consisted of hyper-
plasia of the neurilemma, multiplication of nuclei, and a fibrillary
thickening of the sheath of Sclnvann.
462 ATROPHIC PARALYSES.
In addition to the aflfection of the anterior horns and peripheral fibres,
the posterior columns, the posterior horns, the posterior roots, and the
intervertebral ganglia have been found in a state of degeneration. The
cervical sympathetic was found diseased in a case examined by Schnee-
voo-t, the cervical ganglia were almost entirely changed into fat cells,
while the cords of the cervical and thoracic sympathetic abounded in
fat cells which compressed the nerve fibres. More or less similar obser-
vations were made by Jaccoud, Swarzenski and Dumenil.
In progressive bulbar paralysis the essential morbid changes appear
to consist of a degenerative atrophy of the ganglion cells of the gray
nuclei in the floor of the fourth ventricle. The cells shrink and become
filled with yellow or brown pigment, their nuclei disappear, and finally
the ceils themselves are only represented by angular, glistening, and
pigmented masses. The connective tissue is found to be increased and
to contain Gllige's corpuscles ; the nuclei and Dieter's cells are multi-
plied, and the vascular walls are hypertrophied or have undergone
fatty degeneration.
Fig. 147.
NH w-' - -... '" t?^^' J - NH
<«■
H
R
Portion oi- the Gray Substance on the floor op the fourth ventricle on a level with the middle
or THE Hypoglossal Nucleus, from a case of Progressive Muscular Atrophy with Bulbar Paralysis,
SHOWING the destruction OF THE GANGLION CeLLS OF THE NUCLEI OF THE HYPOGLOSSAL AND PnEU.MOOA.S-
tric Xerves (NH). (From Leyden )
R, Jledian raphe ; H, H, Filires of the hypoglossal nerves. The accessory nuclei have evidently
disappeared .
The nuclei of the hypoglossal nerves appear to be the starting point
of the disease, and the nuclei of the spinal accessory and pneumogas-
tric nerves are afterwards invaded, but the disease does not always
extend to the nuclei of the glosso-pharyngeal nerves. The nuclei of _
the fiicial nerves are attacked at a very early period of the disease, and ■
MYOPATHIC ATROPHIC PARALYSES. 463
the nuclei which are connected with the inferior branches of the nerves,
and which I have named the accessory nuclei, are especially liable to
be invaded. The motor nuclei of the fifth nerves have been found
affected, but the nuclei of the sixth and acoustic nerves and the tri-
geminal sensory nuclei seem never to suffer. The annexed diagram
(Fig. 147), borrowed from Leyden, represents the morbid changes
observed in the medulla oblongata in bulbar paralysis. Remnants of
the fundamental cells of the hypoglossal nuclei may still be observed,
while no traces of the accessory nuclei are left. This would seem to
indicate that the morbid process begins in the embryonic tissue which
immediately underlies the ependyma of the fourth ventricle, and that
with advance of the disease the changes extend deeper and deeper into
the gray matter and among the oldest formed cells. Other changes
have been described, but they appear to be secondary to the alterations
in the ganglion cells. Atrophy of the roots of the hypoglossal, facial,
and spinal accessory nerves was discovered by the earlier observers
with the naked eye, and degenerative atrophy of the nerve fibres was
subsequently observed on microscopic examination. The muscles are
found to undergo essentially the same degenerative changes which are
observed in progressive muscular atrophy. The anterior pyramids of
the medulla oblongata have often been found diseased, and the morbid
changes were generally traced upwards into the pons and downwards
into the antero-lateral columns of the spinal cord. It is probable that
in all these cases the lower extremities were affected during life with a
spasmodic paralysis. The bulbar affection is often associated with
lesions of the anterior gray horns of the spinal cord, indicating a com-
plication during life with progressive muscular atrophy.
In a fatal case of ophthalmoplegia externa reported by Mr. J.
Hutchinson, degeneration of the roots of the oculo-motor nerves and
disappearance of the cells from their nuclei were found, at the post-
mortem, by Dr. Gowers. In a case of locomotor ataxia complicated by
ophthalmoplegia externa, reported by Dr. Buzzard, extensive changes
were discovered by Dr. Bevan Lewis in the nuclei of the sixth nerve
and in the ascendino; root of the fifth nerve, and in a case of this
kind which died recently under my care, I noted the disappearance of
cells fi'om the nuclei of the third pair of nerves, and degenerative
changes in the ascending and descending roots of the fifth nerve and
in the fasciculus rotundus. It appears likely that two kinds of cases
are included in this group. In the one the ganglion cells of the nuclei
of the ocular nerves undergo a primary degeneration just as occurs in
bulbar nuclei in progressive bulbar paralysis, while in the other, the
primary disease is found in the cranial homologues of the posterior
464
ATEOPHIC PARALYSES,
root-zones, the ascending and descending roots of the fifth nerve and
the fasciculus rotundus, and the ganglion cells of the oculo-motor
nerves are only implicated secondarily.
In pseudo-hypertrophic paralysis and the juvenile form of progres-
sive muscular atrophy the spinal cord and peripheral nerves are normal
or show only minor changes, which must be regarded as secondary to
the changes in the muscular system.
2. Changes in the Muscles. — When a peripheral nerve is divided or
injured the muscle supplied by it undergoes a progressive atrophy, the
various degrees of which have already been described. Essentially
similar changes occur in the muscles in the various forms of progressive
multiple neuritis, but in reflex paralysis the muscular fibres only undergo
a simple wasting Avithout proliferation of nuclei or destruction of the
Muscular Fibues from a case of advanced Infantile Paralysis withdrawn bv Leech's trocar.
(Young.)
a, Muscular fibres presenting a more or less healthy appearance ; h, muscular fibres, soniewliat atroi)liieil,
and with granular contents ; c, muscular fibres greatly atrophied, but presenting faint traces of transverse
striation, and having their surfaces thickly studded with nuclei.
fibres. In Landry's paralysis, also, the muscular fibres may undergo
some degree of wasting, but they have not been found much altered in
their structure. In the acute atrophic spinal paralysis of infants and
adults the muscles undergo essentially the same changes as after severe
injury of a peripheral nerve. When a portion of a muscle which has
undergone advanced atrophy is withdraAvn by means of Leech's trocar,
it will be found, as shown in Fig. 148, that some of the fibres are
J
MYOPATHIC ATROPHIC PARALYSES. 465
more or less healthy (a) ; that others have lost their normal striation
and present granular contents, but are not much diminished in size (6) ;
that a large number are reduced to slender, transparent filaments, while
still others retain a faint degree of their transverse striation, but have
their surfaces thickly studded with nuclei (c). The nuclei may be ob-
served to project distinctly from the surface of its atrophied fibre, and it
is, therefore, probable that they have been derived from either the nuclei
of the sarcolemma or of the endoraysium. In chronic atrophic spinal
paralysis the changes in the muscles are never so well marked as they
are in the acute variety, while in periependymal myelitis the muscles
have not been carefully examined.
In progressive muscular atrophy the muscles have been found vari-
ously altered. The affected muscles are generally of a pale red or rose
color, while at other times they may be bufl" or ochre, and streaks of
adipose tissue may be seen to run in lines between the fibres. The
muscles are wasted in various degrees, and different parts of the same
muscle may present differences in the degree to which the atrophy is
carried, a portion being sometimes normal while the rest is reduced to
a fibrous band.
A microscopical examination of the muscle at different stages of the
atrophy shows that the changes begin in the perimysium internum as a
hyperplastic groAvth of the interstitial connective tissue in its finest
ramification among the single primitive fibres. The muscle corpuscles
are increased in number, and swollen, their nuclei are multiplied, and
the transverse striation becomes faint, while the fibres present a granu-
lar cloudiness. Wasting of the muscular substance goes on side by
side Avitli increase of the interstitial tissue, a process which ultimately
leads to a true cirrhosis of the muscle.
In pseudo-hypertrophic paralysis and the juvenile form of progressive
muscular atrophy the hypertrophied muscles appear as yellow fatty
masses of tissue, Avith scarcely a trace of muscular structure left, Avhile
those which have undergone extreme atrophy may appear as fibrous
bands.
The first muscular change which takes place in this disease consists
of an increase of the connective tissue which separates the muscular
bundles from one another, so that the sheaths of the muscular bundles
become greatly thickened. There is also a corresponding increase of
the connective tissue which passes betAveen the fibres themselves. The
comparatively thick masses of tissue Avhich noAv separate the fibres from
one another consist of fibres arranged parallel to the long axes of the
muscular bundles, mixed Avith a considerable number of embryonic
cells (Fig. 149, e). In this early stage the muscular fibres themselves
30
466
ATROPHIC PARALYSES.
do not undergo any manifest changes, except that, according to Du-
chenne, their transverse striation becomes fainter, while their longi-
tudinal striation becomes more marked (Fig. 149, a). The second
stage of the change consists of the development of fat cells in the
connective tissue and also in the newly formed fibrous tissue, whereby
the muscular fibres become widely separated from one another. The
muscular fibres now become atrophied and begin to disappear. They
become narrower, and, indeed, a single fibre varies in diameter at
Muscular Fibres in various stages of degeneration, from a case of Pseudo-hypertroi-hic Paralysis.
(Young.)
a, Muscular fibres only slightly changed, showing increase of the muscle corpuscles, and indistinctness
of the transverse striation in certain parts of its length ; h, the same as a, Imt more atrophied ; c, muscu-
lar fibre greatly atrophied, and presenting nuclei at intervals; d, atrophied muscular fibre, with its
transverse striation unusually distinct ; e, atrophied fibre surrounded by a fibrillated connective tissue rich
in nuclei ; /and g, muscular fibres from the erector spina-, which manifested the greatest changes to the
naked eye. These fibres appear to have undergone a hyaline change, but their transverse striation is still
faintly visible. The fibres often tapered to a point, sometimes at one and sometimes at both ends.
different points in its length. The transverse striation may disappear
in the narrower fibres and be replaced by granules distributed uniformly
through them. The fibrous tissue surrounding the fibres contains oat-
shaped nuclei which are supposed by some pathologists to be derived
from the empty sheaths of muscular fibres. After a time both the
muscular fibres and the newly formed fibrous tissue completely disap-
pear, and the entire muscle is represented by fat cells like those of an
MYOPATHIC ATROPHIC PARALYSES. 467
ordinary lipomata, but may subsequently be absorbed, and all that is
left of the muscle is connective tissue with, perhaps, a few traces of
muscular fibres.
The fact that this disease is accompanied by a progressive paralysis
and atrophy of muscles has led authors to believe that the essential
morbid changes would be found in the anterior gray horns of the spinal
cord, and slight changes have been discovered in some of the cases
Avhich have been examined post mortem. These changes have not
always been the same in different cases and are likewise so slight in
degree that they are not likely to be essential to the disease. A con-
siderable number of cases are now reported in which the spinal cord
and peripheral nerves were found quite healthy after being examined
by the most competent observers and with the aid of the most approved
methods of research. Under these circumstances it must be assumed
that the muscular atrophy is either primary, or results from disease of
the intramuscular nerve fibres and endings, and whatever changes are
met with in the cord are either secondary to the muscular disease, or
accidental. And if the cases which have been described by Erb under
the name of "the juvenile form of progressive muscular atrophy" be
transferred from the group of progressive muscular atrophy, in which
many of them have hitherto been included, to that of pseudo-hyper-
trophic paralysis then we have on the one hand a primary disease of the
ganglion cells of the spinal cord, and on the other a primary disease of
the muscles or of the intramuscular nerve endings.
The tendons, joints, and hones are liable to undergo morbid changes
in some of the forms of atrophic paralysis. These changes are probably
best marked in the acute atrophic paralysis of infants. In this affection
the tendons appear as thin, narrow bands, and are found to be much
atrophied when compared with corresponding healthy structures. The
hones are retarded in their growth when the disease occurs in childhood ;
the protuberances and processes are little developed, and the epiphyses
are shortened. The external lamella of the long bones is thin and friable,
while the medullary portion is increased, and its fiitty contents more
abundant. The ligaments are thin and loose, while the articular ex-
tremities of the bones are atrophied, eroded, and their cartilages atten-
uated. The arteries are said to be diminished in calibre. The skin
and the circulatory and digestive organs are normal or only show changes
which have no necessary connection with the spinal disease. Essentially
similar changes occur in disease of the peripheral nerves.
Morhid Physiology. — The ganglion cells of the anterior gray horns
of the spinal cord are the trophic centres for the efferent fibres of the
peripheral nerves and muscles, and they also appear to produce an
468 ATROPHIC PARALYSES.
influence upon the nutrition of the bones, tendons, and joints. A
destructive lesion of a peripheral nerve severs the ganglion cells of the
anterior horns from the distal portion of the nerve and from the tissues
to which the efierent fibres are distributed, and consequently the nutri-
tion of tissues becomes impaired. In reflex paralysis an irritation is
conducted through afferent fibres to the motor ganglion cells and reflected
by them outward to the muscles ; or, as suggested by Charcot, the
peripheral irritation may exercise an inhibitory influence upon the func-
tions of the ganglion cells, and a diminished functional activity on the
part of these cells will lead to a lessened nutrition in the muscles.
Ligature of the hilus of the kidney in animals was observed by Brown
Sequard to cause spasm of the spinal vessels, and from the results of
this experiment he argued that urinary paraplegia is caused by anj^niia
of the spinal cord. Jaccoud supposes that in such cases the paralysis
is caused by the exhaustion which follows over-excitement, while S.
Weir Mitchell adopts a view which appears to be a combination of the
theory of reflex vascular spasm, and that of exhaustion. It has been
found by Lewisson that when the uterus, one kidney, or a fold of the
intestine of the hare is strongly compressed, after exposure, a paralysis
of the inferior extremities results, which persists so long as the pressure
is maintained and disappears immediately on its being removed. This
experiment shows that the paralysis is caused by a functional lesion of
the cord, consisting most probably of an inhibitory influence exerted
upon the motor ganglion cells. When myelitis occurs it is an ascending
myelitis.
Acute atrophic spinal paralysis is one of those diseases the morbid
anatomy of which lias largely contributed to clear up our knowledge of
the functions of the anterior gray horns. The multipolar cells probably
constitute ganglionic centres both for reflex action and for the trans-
mission of impulses received from the cortex through the pyramidal
tracts, and when they are destroyed both reflex actions and voluntary
actions are impaired or abolished according as the destruction of the
cells is incomplete or complete. Destruction of the ganglion cells is
also followed by various trophic changes in the muscles, bones, tendons,
and joints. The ganglion cells which constitute the spinal centre for
the regulation of the movements of a muscle appear also to form its
trophic centre. But most muscles are connected with fundamental and
accessory cells and it is only when the connection, between the former
and the muscle, is severed that its motor power and nutrition suffer pro-
foundly. The acute nature of the lesion in acute atrophic paralysis is
well calculated to sever the muscles from their connections with the
fundamental cells, even if the latter were to remain themselves entirely
MYOPATHIC ATROPHIC PARALYSES. 469
unaffected, and consequently the clinical features of the paralysis are
very similar to the paralysis which results from severe lesions of the
peripheral nerves.
The case is wholly different when we have to do Avith a chronic and
progressive affection like progressive muscular atrophy, in which the
accessory cells are first attacked, and the disease invades by slow and
successive steps the fundamental cells. In such a disease the symptoms
of paralysis and atrophy may be expected to pursue a totally different
course from that which obtains in acute atrophic spinal paralysis.
In progressive muscular atrophy fibre after fibre of the muscles
attacked become diseased in correspondence with a similar progi-essive
invasion of the ganglion cells and their processes, and the consequence
is that so long as the healthy fibres predominate over the diseased
fibres so long Avill the muscle give normal reactions to electrical examina-
tion. But in acute atrophic spinal paralysis all the fibres of a muscle
are more or less simultaneously attacked and consequently the muscle
gives the reaction of degeneration at a very early period of the disease.
Treatment. — In the treatment of the various forms of atrophic paral-
ysis the first indication is to remove the exciting cause. In carrying
out this indication in cases of paralysis of peripheral nerves consider-
able scope is afforded for various kinds of surgical interference, such as
bringing together by means of suture the ends of divided nerves, the
removal of tumors and diseased bones which compress or otherwise
injure nerve trunks. When the paralysis is of rheumatic origin anti-
phlogistic treatment must be adopted in the early stages of the disease,
and when it is caused by the presence of lead, alcohol, or other poison,
means must be taken for withdrawing the patient from the influence of
the deleterious agent, and for eliminating it from the system. If the
paralysis is of syphilitic origin, mercury and iodide of potassium must
be prescribed either separately or combined. In the early stage of every
form of acute spinal atrophic paralysis a mild antiphlogistic treatment
must be adopted.
If the nature of the disease be detected at an early period, an ice
bag may be applied to the spine. In the early stage of the atrophic
paralysis of infancy ergotine has been employed subcutaneously in doses
of one-fourth of a grain for a child from one to two years of age, one-
third of a grain for one from three to five years, half a grain for children
from five to ten years of age, and a grain for patients upwards of ten
years of age, the dose being repeated either daily or twice a day.
Belladonna has also been employed with apparent benefit in this stage
of the affection. After the fever has subsided iodide of potassium may
be administered in appropriate doses with the view of promoting the
470 ATEOPHIC PARALYSES.
absorption of effused products, while mild counter-irritants might be
applied along the spine.
In the latter stages of acute cases and in all chronic cases of atrophic
paralysis stimulating treatment must be adopted. A nutritious and
abundant diet should be prescribed along with prolonged sojourn in the
open air, mountainous or sea-air being especially useful. The thermal
springs of Wildbad, Teplitz, and Gastein, have been specially recom-
mended, and sulphur baths have also been found useful.
Electrical treatment is more useful in the treatment of the various
forms of atrophic paralysis than in that of any other variety of paralysis.
In the spinal atrophic paralysis the constant current should be made to
pass through the diseased area of the cord immediately after the fever
has subsided. If the leg alone be affected, the current should be applied
over the lumbar enlargement; if an arm only be affected, the cervical
enlargement should ))e acted upon, and if the muscles of the trunk
suffer likewise, the whole dorsal region of the cord should be included
in the circuit. In order to reach the cord it is better to place one pole
on the spine, and to apjily the other to the anterior surface of the trunk.
The electrodes should be large, the one placed over the back being large
enough to cover the entire diseased area. The force of the current
should be gentle, and the application continued for from three to ten
minutes according to the extent of the lesion. The local application of
electricity to the diseased nerves and muscles is useful in all cases in
which degenerative changes have occurred in the muscles. So long as
the muscles and nerves have not entirely lost their faradic contractility
the local application of the faradic current will be of service. But as
a rule the constant is superior to the interrupted current, being in
most cases the only agent which will evoke nuiscular response. Appro-
priate gymnastic exercises of the affected muscles when they are not
completely paralyzed, and shampooing and friction, with or without
stimulating liniments, may be employed as adjuncts to the electrical
treatment. After the chronic stage of atrophic paralysis is fully estab-
lished internal remedies do not appear to do much good. The most
usual remedies for chronic cases are phosphorus Avith cod-liver oil,
arsenic, and tonics like iron and quinine, but these agents probably do
good only in so far as they help to improve the general health. The
use of strychnine has been advocated in cases of infantile atrophic
paralysis, especially in the form of subcutaneous injection, but I have
never seen any good results attend its employment. When serious
deformities result from paralysis of certain groups of muscles the case
should be placed under the care of the orthopaedic surgeon.
CHAPTEE YIII.
THE SPASMODIC PARALYSP:S.
I. PAPxAPLEGI^.
1. Primary Lateral Sclerosis (Tabes Dorsalis Spasmodica
(Charcot), Spasmodic Spinal Paralysis).
Etiology. — A hereditary tendency to the disease can occasionally be
traced. Dr. Morgan records the case of a man suffering from the
typical symptoms of lateral sclerosis, whose brother was similarly
affected, while a sister of his was said to have died of the same disease.
Primary lateral sclerosis appears to occur rather more frequently in
males than in females. By far the larger number of cases begin between
the ages of thirty and fifty years. A spasmodic paralysis of the lower
extremities of congenital origin is frequently met with in children,
but the symptoms in these cases are caused most probably by a cere-
bral lesion.
The exciting causes are unknown, although it is very probable that
exposure to cold, injuries of the spine, lead poisoning, and syphilis
may cooperate as factors in the production of the disease. It seems to
be caused sometimes by the use of a species of vetch — the lathyrus
cicera — as a chief article of diet.
Symptoms. — The first symptom is a paresis of the inferior extremi-
ties, which may be equal in both or more pronounced in one than in
the other, and the only effect of which is to render walking somewhat
difficult, especially on getting out of bed in the morning. The patient
complains that he is soon fatigued, and that his limbs are heavy, while
his o'ait becomes drao-gino; and difficult. On lying down at night,
especially after being fatigued, the legs begin to shake, and as the dis-
ease advances the tremors may be so extensive and violent as to throw
the whole body into a convulsive trembling, which has been named
spinal epilepsy. These tremors may be readily excited by pushing
against the toes so as to produce dorsal flexion of the foot. Muscular
tension is developed at an early period of the disease; at first the ten-
sion, which is only present when provoked by passive movement of the
lower extremities, may be overcome by increasing the pressure, and it
472 THE SPASMODIC PARALYSES.
can be considerably diminished by repeated movements, but after a
time the muscles become tense during voluntary efforts ; the paresis
then seems to be greater than it is in reality, and the movements of
the affected limbs become stiff and difficult.
As the disease advances the muscular tension increases to permanent
rigidity, and a high degree of contracture results. The lower extremi-
ties are maintained in a position of rigid extension, the thighs are also
held rigidly together by contracture of the adductors, the feet are in a
position of extreme talipes equino-varus, but the toes are generally
strongly flexed. The rigid immobility of the foot is now and then
interrupted by attacks of trembling, which are excited by every move-
ment of the extremity.
The Spasmodic Gfait or Spastic Walk. — The gait of the patient is
rendered quite characteristic by the combined paresis, stiffness, and
tremors of the lower extremities. The foot seems to cling to the
ground, from which it is detached Avith difficulty, and it is made to slide
forwards, and the toes produce a characteristic scraping noise. The
presence of lateral sclerosis may, indeed, be sometimes recognized
without seeing the patient by listening to the scraping or shuffling
noise which accompanies each step, the "shuffle" in hemiplegia being
only heard during alternate steps. Owing to the rigidity of the lower
extremities in extension the necessary elevation of the passive leg is
usually obtained by an upward rotation of the pelvis, W'hich causes the
body to be strongly inclined to the side of the active leg, and the
alternate inclination of the body from one si<le to the other during suc-
cessive steps gives rise to a '• waddling gait." In other cases the
necessary elevation of the passive foot is obtained partly or wholly by
an unusual degree of elevation of the heel of the active leg, and in these
cases the gait has a peculiar hopping character. When the body is in-
clined from one side to the other in locomotion, the passive foot advances
not directly forwards, but forwards and outwards in a semicircular man-
ner, and on being brought to the ground it is dragged over to the
opposite side in front of the other leg by the predominant action of
the adductors over their antagonists, while the foot is also often in-
verted by overaction of the inward rotators of the thigh. In long-
standing cases the patient experiences great difficulty in disentangling
the toes of the foot about to be advanced from the heel of the one
which has just been brought to the ground, and in the effort to accom-
plish this the calves of both legs become strongly contracted, the patient
is elevated on tiptoes, and a degree of ankle-clonus may be induced
which suffices to give rise to alternate elevations and depressions of the
body, and when at last the toes of the posterior are disengaged from the
PARAPLEGIA. 473
heel of the anterior foot, and the passive leg is being moved forwards
in the semicircular manner already described, the foot is seized with a
trembling which may extend to the trunk and be so violent as to agitate
the whole body. In aggravated cases of this kind the patient is quite
unable to maintain the erect posture unsupported. On standing the
patient rests on the tips of his feet, the body is inclined forwards, and
the arms are propped up by crutches, or are supported by two sticks
which are held well in front of the patient, and Avith an outward inclina-
tion. As the disease gradually extends upwards the abdominal muscles
become prominent and tense, and at the same time a kind of lordosis
is produced by spasm of the lumbar muscles.
When the upper extremities are affected the paretic condition of the
hands manifests itself by the inaptitude of the patient to seize small
objects. The digits are at times forcibly flexed into the palm, while a
successive invasion of the muscles of the hands, forearms, and arms
causes the upper extremity to become rigid and immovable in positions
of extension and pronation, and to be strongly drawn to each side of
the body.
Although the disease usually begins in the lower extremities and
pursues an ascending course, yet occasionally the symptoms are de-
veloped in a different order. In some cases the paresis passes from a
lower extremity to the upper one of the same side, and this hemiplegic
condition may persist for many years before the other loAver extremity
is attacked. In a few cases the disease begins in the upper extremities
and pursues a descending course.
The tendon and periosteal reactions are much exaggerated in this
disease. The patellar tendon-reaction and ankle-clonus are elicited with
undue readiness in the usual way, and the tremors induced may become
diffused over the whole body. The quadriceps femoris and the adductors
of the thigh may be excited to contract by tapping the broad end of the
tibia, and the contractions may extend to the adductors of the opposite
thigh. The adductors of the thigh may often be made to contract by tap-
ping over the region of the lumbar vertebrtB, and the tibialis posticus,
semitendinosus, and other muscles by striking their tendons. The ten-
don reactions are in like manner increased in the upper extremities when
once they are implicated. They can be elicited in the biceps and
triceps by striking their tendons, and the former may be made to con-
tract by tapping the lower end of the radius, and the latter by tapping
the lower end of the ulna. The posterior portion of the deltoid often
contracts along with the triceps when the lower end of the ulna is
lightly struck. The flexors of the wrist, the extensors of the wrist,
and the supinator longus can each be made to contract by ta))ping
474 THE SPASMODIC PARALYSES.
their tendons at the wrist, while the interossei may sometimes be made
to contract by striking the ends of the metacarpal bones.
The cutaneous reflexes appear to be occasionally increased, but they
are generally normal or diminished. The electrical excitability of the
motor nerves may manifest slight quantitative but never qualitative
changes; the excitability of the muscles is slightly diminished to both
currents.
Sensory disorders are absent throughout the whole course of the
disease ; the functions of the bladdei-, rectum, and sexual organs are
unaffected ; and there are no vaso-motor disturbances or nutritive aflfec-
tions of the muscles or skin, and no bedsores.
The course of the disease is ahnost always very chronic, and months
or years may elapse before it can even be recognized with certainty.
The disease occasionally ends in recovery, but in uncomplicated cases
the symptoms slowly and gradually progress until after many years the
patient is rendered quite helpless, but even then death generally occurs
from accidental causes or intercurrent diseases.
2. Amyotrophic Lateral Sclerosis.
Etiology. — Very little is known Avith regard to the causation of this
disease, but persons of middle age are most frequently attacked. Seelig-
miiller, however, met with the typical form of the disease in four children
of the same family, and in all of them the symptoms appeared for the
first time in early childhood.
Symptoms. — In this disease the symptoms of primary lateral sclerosis
are complicated by a progressive muscular atrophy. The symptoms
are, indeed, more allied to those of the latter than to those of the former
disease, but as it would not be possible to understand the significance of
the spastic phenomena until the clinical features of primary lateral
sclerosis had been described, it has been found convenient to consider
amyotrophic lateral sclerosis in this place.
The disease often begins with premonitory symptoms of formication
and numbness in the upper extremities, but it is soon observed that these
extremities are feeble, and that their muscles are undergoing a rapid
and uniformly distributed atrophy, which is accompanied by fibrillary
twitchings. Muscular tension and contractures are soon superadded to
the paresis and atrophy, and the affected extremities are brought into
permanently deformed positions. The arm is applied to the trunk ; the
forearm is semiflexed and pronated ; the hand is flexed on the foreann ;
and the different segments of the fingers are flexed upon one another
I
\
PARAPLEGIA. 475
and upon the metacarpal bones (Fig. 150) ; while any attempt to give
passive movements to the limb at any of the articulations provokes
muscular tension and resistance. When the patient elevates the arm
by a voluntary effort, the extremity becomes agitated by tremors, not
unlike those which occur in sclerosis in patches. In advanced cases the
thenar and hypothenar eminences become flattened ; the palm of the
hand becomes excavated ; the forearm and arm may be reduced almost
to a skeleton, but the spasmodic rigidity becomes less pronounced,
Fig. 150.
Attitude of the Hand and Forearm in AMVOTROPiirc Lateral Sclerosis. (After Charcot.)
although even now the limbs may maintain the forced attitudes in which
they have been held so long.
In some patients the head is fixed by spasmodic rigidity of the muscles
of the neck so that it cannot be moved in any direction. The contrac-
ture may also extend to the temporal muscles, and then the mouth can
only be opened to a limited degree.
After a period of from two to six or nine months the lower extremities
become affected by paresis, which may be preceded or accompanied for
a longer or shorter period by formication and numbness of the limbs.
The paresis of the lower extremities is not at first accompanied by
muscular atrophy, but the symptoms are those of a pure lateral sclerosis,
and consist of muscular tension, contractures with the limbs held rigid
in the position of extension, tremors on voluntary or reflex movements
of them, ankle-clonus, and exaggerated tendon-reactions. The rigidity
of the muscles of the lower extremities soon become so great that walk-
ing is impossible, and the patient becomes helpless and bedridden. After
a time even the muscles of the lower extremities undergo a diffused
atrophy with fibrillary twitchings, the contractures diminish, and the
limbs become flaccid and powerless, and lie immovable in any position
in which they may be placed. The third stage of the disease is char-
4:76 THE SPASMODIC PAEALYSES.
acterized by the appearance of bulbar paralysis which pursues the usual
progressive and fatal course, and the patient ultimately dies from the
circulatory and respiratory disorders caused by implication of the nuclei
of the pneumogastric nerves.
But altliough the symptoms usually begin in the upper extremities a
few cases are reported in which the phenomena of bulbar paralysis took
the precedence, and the muscles of the upper extremities became para-
lyzed and atrophied at a subsequent period, while those of the lower
extremities remained the subjects of a spasmodic paralysis only until
the terminal period of the disease.
Amyotrophic lateral sclerosis develops rapidly, and generally causes
death in from one to three years, differing in this respect from progres-
sive muscular atrophy, which may extend over a period of from eight to
twenty years.
3. Secondary Lateral Sclerosis.
Lateral sclerosis occurs as a secondary disease in transverse myelitis
and in various diseases of the medulla oblongata, pons, and brain.
The symptoms of secondary degeneration of the pyramidal tract of the
spinal cord will be described in detail when the primary lesions from
which it results are under discussion. It will suffice at present to say
that if, to the motor symptoms of lateral sclerosis already described, any
sensory disorders, muscular atrophy, or disturbances of the functions of
the bladder and rectum be superadded, then the case is not an exam])le
of the primary disease,
II. HEMIPLEGI.E.
1. Ordixary Hemiplegia.
Hemij)legia consists of paralysis of one half of the body, although
many of the muscles are either not implicated or only temporarily
weakened. The paralysis is, as a rule, limited to the arm, leg, part of
the face, and half of the tongue. The muscles chiefly aff'ected in facial
paralysis of cerebral origin are the buccinator, orbicularis oris, and the
straight muscles which pass to the angle of the mouth and nose on the
paralyzed side ; while the occipito-frontalis, corrugator supercilii, and
orbicularis oculi remain almost entirely unaff'ected. Paralysis of the
hypoglossal nerve is manifested by a difficulty in executing certain
movements of the tongue, and by a deviation of the point to the sound
side on protrusion, because the base is dragged further forwards on the
healthy than on the paralyzed side. It is often stated that the muscles
HEMIPLEGI^E. 477
of the trunk are unaffected in hemiplegia, but in severe cases the inspira-
tory muscles act much less freely on the paralyzed than on the healthy
side for the first few days of the attack.
2. Hemiplegia and Hemian.t.sthesia.
It has for some time been observed as a clinical fact that those cases
of hemiplegia in Avhich the leg is more paralyzed than the arm are
^associated Avith hemianivsthesia. In such cases, however, the special
senses are not very seriously implicated.
3. Hemiplegia, Hemianesthesia, and Hemianopsia.
Some cases of hemiplegia in which the arm is more paralyzed than
the leg are accompanied by hemiannesthesia. In these cases the para-
lyzed limbs are often affected by choreoid movements and the cutaneous
sensory disorders are accompanied by disturbances of the special senses.
The sense of sight is variously affected ; in some there is a restriction
of the fields of vision on both sides, but it is most marked on the side of
the paralyzed limbs, while in others a well-defined bilateral homonymous
hemianopsia is present, the blind portions of the fields of vision being
on the side of the paralyzed limbs. In certain cases of hemiplegia and
hemiaUcTesthesia which come on with severe apoplectic symptoms, one
eyeball may be directed downwards and outwards, and the other upwards
and somewhat outwards. Such cases may live for many days or weeks
without the patient regaining a sufficient degree of consciousness to
render it possible to determine whether hemianopsia is or is not present.
Another curious symptom which is sometimes present is that the pupils
may be found to dilate to light and to contract when shaded ; but as the
eyeballs are almost constantly moving, it is probable that the changes in
the diameter of the pupils are to be regarded as an associated move-
ment and not as a reflex action. In these cases repeated paroxysms of
Cheyne-Stokes breathing may occur, and all of them that have come
under my observation have proved fatal.
4. Crossed Hemiplegia.
In cro.ssed hemiplegia the muscles supplied by one or other of the
cranial motor nerves are paralyzed on one side and the limbs on the
opposite side of the body. The cranial nerves most frequently affected
in this form of paralysis are the seventh and the third nerves ; when
the first of these is affected the face is paralyzed on one side and the
478 THE SPASMODIC PARALYSES.
limbs on the other, and when the last of these is attacked the muscles
supplied by the oculo-motor nerve are paralyzed on one side and the limbs
on the other side of the body.
5. Hemiplegia and Post-hemiplegic Spasms.
In hemiplegia the paralysis is accompanied by spasm of the affected
muscles. These may be either a, tonic, 6, combined tonic and clonic,
or c, clonic spasms. In addition Ave must specially consider d, spasm
as it occurs in the various forms of the spasmodic paralysis of infancy.
a. Tonic Spasms.
These spasms may be divided into (1) carhj, and (2) late ru/iditi/.
(1) Early rigidity consists of a tonic spasm of the paralyzed muscles,
which may either occur at the time of the hemorrhage or a few days
subsequently during the inflammatory reaction. Early rigidity is some-
times so slight as only to be manifest when passive movement of the
paralyzed extremity is made, while at other times it maintains both
extremities in fixed positions of flexion, and any attempt to extend the
limbs only increases the spasm. This form of rigidity generally dis-
appears soon, but it occasionally persists for weeks or months.
(2) Late rigidity corresponds in its essential features to the spasmodic
rigidity of primary lateral spinal sclerosis, and, like it, is attended with
exaggeration of the tendon-reactions and periosteal reflexes. When the
lower extremities are affected the patellar tendon-reaction is in excess,
ankle-clonus is readily elicited, and corresponding phenomena may be
obtained in the upper extremity when it is the subject of contracture.
When the loss of voluntary power is complete the rigidity is more or
less constant, although it is in most cases diminished during sleep and
increased during voluntary efforts and emotional disturbances. The
attitudes assumed by the limbs affected with late rigidity differ consider-
ably in different cases, but on the whole they conform to the rule observed
in almost all spasmodic affections ; namely, that flexion predominates
in the upper, and extension in the lower extremity.
The Hemiplegie Cfait. — When the muscles of the paralyzed lower
extremity have acquired a certain degree of rigidity, the patient is able
to walk by the aid of a stick, even if the voluntary paralysis of the
affected side remain complete. The patient on standing leans towards
the healthy side, but is prevented from falling over to that side by the
support of the stick, w^hile the pelvis and hip-joint of the paralyzed
side are elevated by contraction of the abductors of the healthy thigh,
so that the weight is taken off the paralyzed extremity. When the
HEMIPLEGI.E. 479
paralyzed loAver extremity, say the right, is the active one, the line of
gravity is carried over to a slight extent to that side, but instead of
reaching the centre of the paralyzed foot it remains midway between it
and the end of the stick, so that the weight of the body is maintained
partly by the paralyzed lower extremity and partly by the healthy arm
through the stick. The healthy or left lower extremity is now moved
forwards a step, an unusual degree of flexion of the thigh upon the
body taking place in order to avoid the necessity of carrying the line
of gravity too far to the paralyzed side. The left leg now becomes
active and the paralyzed one must be moved forwards. The manner in
which this movement is executed depends upon the degree of paralysis
and of muscular rigidity present. If the paralysis be almost complete,
and the rigidity not great, the extremity is partly swung and partly
dragged round mainly by contraction of the inward rotators of the
healthy limb. Contraction of these muscles causes the pelvis to rotate
forwards on the hip-joint of the healthy side, and consequently the
opposite hip-joint, dragging after it the paralyzed leg, is moved forwards.
This forward movement is aided by a further elevation of the right
hip-joint caused by contraction of the abductors of the opposite thigh,
and sometimes by a slight backward inclination of the trunk by means
of which the distance between the points of origin and insertion of the
flexors of the thigh on the body is increased. If a high degree of con-
tracture with talipes equinus be present, the paralyzed lower extremity
is moved forwards much in the same manner as has already been de-
scribed in the case of primary lateral spinal sclerosis. When once the
weight of the body is taken ofl' the paralyzed extremity the heel becomes
elevated, and the toe during the forward movement, which takes place
in a semicircular manner, makes a characteristic scraping noise. If
tremors or choreoid movements be present in the paralyzed lower ex-
tremity, the hemiplegic walk may become modified in such numerous
ways as to render it impossible to compare the different varieties which
may be presented in a single description.
b. Combined Tonic and Clonic Spasms.
In the combined tonic and clonic forms of post-hemiplegic motor
disorders the muscular contractions are at first quite like those which
occur in late rigidity, but after a time some of the muscles implicated
become the subjects of clonic spasm. The combined tonic and clonic
spasms of hemiplegic limbs may be divided into (1) intermittent tremor
and (2) choreiform movements.
(1) Intermittent tremor is produced when the muscles are put upon
the stretch by passive movements or voluntary effort. This kind of
480 THE SPASMODIC PARALYSES.
tremor is similar to that described as "spinal epilepsy" in primary
lateral spinal sclerosis, and, like the tremor of multiple sclerosis, it is
absent during repose. The muscles of hemiplegic limbs are also liable
to be affected with fibrillary contractions similar to those which occur
in progressive muscular atrophy and amyotrophic lateral sclerosis, but
in these cases it is probable that the descending changes of the pyra-
midal tract have extended to the ganglion cells of the anterior gray
horns of the cord.
(2) Choreiform movements of the extremities may either precede or
follow an attack of hemiplegia, the former being named pre-hemipJegie
clwrea^ and the latter post-hemiplegic chorea. In pre-hemijiJegic chorea
the patient complains of a feeling of numbness and feebleness of the
extremities of one side, his gait becomes hesitating and irregular, and
the upper extremity of the affected side is attacked by choreiform
movements. These symptoms may continue for some days, when com-
plete hemiplegia, usually associated with hemiangesthesia, is either sud-
denly or gradually established. Post-hemiplegic chorea occurs in par-
tially but never in completely paralyzed limbs, and usually appears
simultaneously with a marked diminution of the paralytic symptoms.
The clonic spasms become, as a rule, gradually established as motor
power returns, but they sometimes appear suddenly during a voluntary
effort on the part of the patient to move the paralyzed limb. Clonic
spasms appear more frequently in the arm than in the leg, and when
they exist in both they ai'e generally more severe in the former than in
the latter, while if they exist exclusively in the leg, the arm is com-
pletely paralyzed. The movements affected by choreiform spasms are,
in their increasing order of frequency, the special movements of the
fingers and thumb, pronation and supination of the forearm, extension
and flexion at the elbow-joint, and movements at the shoulder-joint.
The interossei are particularly liable to be affected by choreiform spasm,
and consequently the movements most frequently observed consist of
varying degrees of flexion and extension at the metacarpo-phalangeal
articulations, associated respectively with extension and flexion at the
phalangeal articulation. The movements induced by these spasms are
of wider range than those of the hemiplegic tremor, resembling in this
respect the movements of chorea rather than the tremors of primary
lateral spinal sclerosis. The movements are disorderly and irregular,
and may or may not continue during repose ; they cease during sleep,
and become much aggravated during voluntary efforts to perform a
definite movement with the affected hmb, such as that of raising a glass
of water to the mouth. Post-hemiplegic chorea of adults is always
accompanied by some degree of antesthesia, which extends over the
HEMIPLEGI^E. 481
lateral half of the body on the side aiFected with spasm, and affects all
forms of cutaneous and muscular sensibility as well as the special senses.
c. Clonic Spas)iis.
The post-hemiplegic motor disorders which consist of clonic spasms
unaccompanied by tonic contractions of the muscles, are (1) continuous
or remittent tremor, (2) choreiform movements (athetosis), and (3)
jerking movements on voluntary effort (hemiataxia).
(1) Continuous or re7nittent tremo?' is continuous during wakino-
hours, and instead of being exaggerated by voluntary effort like the
tremors of lateral spinal sclerosis and that of sclerosis in patches, it
may be diminished or arrested for a short time by a voluntary effort,
being in this and other respects like the tremor of paralysis agitans.
The tendon-reactions are not sensibly exaggerated in this form of
tremor.
(2) Athetosis is a condition in which the patient is unable to main-
tain the fingers and toes in fixed positions. The fingers and toes are
maintained in continuous slow movement, and are made to assume
various distorted positions. In some cases these movements extend to
the hand and foot, and occasionally even to the muscles of the neck
and face. No motor weakness has been observed, the muscles do not
become tense on passive movements, and the tendon-reactions are not
sensibly exaggerated. The appearance of the clonic spasm is in almost
all cases preceded by a distinct attack of hemiplegia, and when no
decided paralysis can be ascertained to have been present, the historv
of the case shows that the patient has suffered from an attack of con-
vulsions and unconsciousness. Hemianaesthesia is described as having
been present in a considerable number of the reported cases, and a
certain degree of numbness of the affected side is frequently mentioned,
Avliile it is possible that diminution of sensibility would have been found
in all cases had special attention been directed to this point. The
affected extremity usually presents vaso-motor disturbances, being red
or livid, moist, and colder than the corresponding extremity. The
affected hand or foot is also frequently smaller than the corresponding
part of the opposite extremity, although the muscles affected by spasm
may undergo a certain degree of hypertrophy. The electric contrac-
tility of the affected muscles varies in different cases, being sometimes
normal, at other times enfeebled or increased. The ligaments and
joints of the affected extremities may occasionally be found considerably
relaxed.
(3) Hemiataxia consists of disorderly or incoordinate movements of
the limb on voluntary effort, coming on in the absence of paralysis,
31
482 THE SPASMODIC PARALYSES.
permanent rigidity, or spontaneous spasm. The ataxic movements
become most marked when the patient is asked to execute a complicated
movement with the afiected limb when his eyes are closed. This con-
dition is associated with a slight degree of anesthesia, tactile sensibility
beino- sometimes found diminished, while the sensibility to pain is
normal.
III. SPECIAL CONSIDERATION OF POST-HEMIPLEGIC SPASMS AS
THEY OCCUR IN INFANCY (THE SPASMODIC PARALYSES OF
INFANCY).
The spasmodic paralyses of infancy may, from the clinical standpoint,
be divided into (1) paralysis of hemiplegic and (2) paralysis of para-
plegic distribution, and in addition we shall consider in this place (3)
the cases of tonic spasm of voluntary muscles described by Thomsen.
It is possible that some of the paraplegiie of infancy are of spinal
origin, but many of them are probably to be regarded as bilateral
hemiplegite rather than as true hemiplegio?.
1. Spastic Hemiplegle of Infancy.
The spastic hemiplegite of infancy may be divided into a, acquired^
and 6, coyigenital spastic liemiplegia?. In addition we shall consider in
this place e, double athetosis.
a. Acquired spastic hemiplegia of infancy dates from birth or begins
at any time between that date and four or five years of age. The child
is unconscious and convulsed for the first few days after birth (as})hyxia
neonatorum), or if attacked after birth it is suddenly seized with con-
vulsions and unconsciousness which may last from a few hours to a few
days. The convulsions are limited to, or at least most pronounced on
one side of the body, and this side becomes subsequently paralyzed.
In the cases Avhich recover the hemiplegia pursues the usual course, con-
tractures become established, and choreiform movements may or may
not make their appearance, and if these movements once make their
appearance they remain permanent. So far, then, these cases present
nothing peculiar except that the disease dates from childhood, that it is
ushered in by convulsions and profound unconsciousness, and that the
motor paralysis is not accompanied by hemiangesthesia. But as the
patient advances in age the bones of the paralyzed limbs, and even those
of the paralyzed half of the face, are somewhat arrested in their develop-
ment as compared with the corresponding bones of the healthy side, so
that the former are found to be smaller in all their dimensions than the
THE SPASMODIC PARALYSES OF INFANCY. 483
latter. Each of the long bones of the limbs may be from one-fourth of
an inch to one inch shorter than the corresponding bones of the healthy
side, and even the clavicle of the [laralyzed side may be from one-fourth
to one-half of an inch shorter than the opposite clavicle. The diminu-
tion in size of the half of the face may extend to all the features, in-
cluding the eyebrow, eyelids, half of the nose, the cheek, and half the
mouth. At from seven to fifteen years of age the patient is attacked
with epileptic convulsions, which- recur at periodical intervals of greater
or less duration during the rest of life. These convulsions are at first
limited to the paralyzed half of the body, and they are not always ac-
companied by decided loss of consciousness. After a time, however, the
convulsions become general, but even then they often retain a unilateral
character at the beginning of the attack, and the patient usually de-
scribes a unilateral aura. The aura is often described as a numbness or
other sensation beginning in the paralyzed arm, and ascending along
the arm to the shoulder and then to the side of the face, when un-
consciousness supervenes. At other times the sensation begins in the
leg and ascends successively to the arm and side of the head, or in the
side of the face and descends to the arm and leg. The intellectual
faculties almost always suffer in this disease, and the patient is usually
more or less idiotic, but in some cases this defect of intelligence amounts
only to a certain degree of imbecility, which becomes established only
after a frequent recurrence of the epileptic attacks.
h. Congenital sjjastie hemiplegia presents numerous varieties, and all
of them are generally associated with imbecility or idiocy. In some
cases the paralysis is limited to one-half of the body, while at other
times both sides are affected. In these cases there is absence of a
history of convulsions and unconsciousness occurring at birth or during
childhood, and the spasmodic rigidity of the affected limbs is accom-
panied, as a rule, by disorders of articulation, wry neck, or strabismus,
while the skull is often of comparatively small size and unsymmetrical.
(2. Bilateral athetosis is generally of congenital origin, and is always
associated with more or less idiocy, and of articulatory disorders, while
aphasia is sometimes present. The muscles of the face are more liable
to be implicated in the spasm of the bilateral than in the unilateral
disease. In cases of bilateral athetosis sensory disorders have not been
observed, and there is no history of an apoplectic attack or convulsions
having occurred during infancy, and consequently the affection is most
probably of congenital origin.
484
THE SPASMODIC PARALYSES,
2. The Spasmodic Paraplegia, of Infancy.
Children are liable to be affected with a spasmodic paraplegia from
disease of the vertebral column or from any other lesion which causes a
consecutive transverse myelitis ; but the cases which are under discus-
sion at present occur at birth, or are of congenital origin. In this
affection the muscles of the lower extremities are in a condition of
spasmodic rigidity, the patellar tendon-reactions are exaggerated, and
the feet are generally maintained in a condition of talipes equinus
(Figs. 151 and 152) oAving to the predominance of the actions of the
Fig. 151.
Fig. 152.
muscles of the calves, while the gait of the patient is like that of lateral
spinal sclerosis. The upper extremities are not affected, but the patient
often suffers from difficulties of articulation, and the head is often rather
smaller than is usual in healthy children of the same age. In other
cases the head is large with projecting forehead, showing that the patient
has suffered in infancy from hydrocephalus or rickets. When the spasm
is limited to the lower extremities the patient is often quite bright and
PARALYSES FROM FUNCTIONAL DISEASE. 485
intelligent, and feebleness of intellect is only present in occasional
cases, but the patient never appears to sufier from epileptic convulsions.
IV. MONOPLEGI^E.
The clinical features of the monoplegioe do not require lengthened
description. The paralysis, which is restricted to one limb or to certain
groups of muscles on one side of the body, is accompanied by the same
kind of muscular tension and excess of the tendon-reactions which are
met with in hemiplegia. The clinical varieties most usually observed are
crural, brachio-crural, brachial, brachio-facial, facial, labio-glosso, and
unilateral oculo-motor monoplegise.
The monoplegitfi derive their chief interest not so much from their
clinical features as from the localization of the lesions which give rise
to them, and consequently they will be more minutely described when
we come to discuss the morbid anatomy of the spasmodic paralyses.
Sensory disorders sometimes accompany the paralyses caused by
disease of the cortex of the motor area of the brain. The tactile sen-
sibility and the muscular sense are specially liable to be diminished in
the paralyzed limbs in cortical disease. Vaso-motor and trophic dis-
orders, consisting of elevation of the temperature of the paralyzed limbs
and acute bedsores, have also been observed in cases of disease of the
cortex of the brain, but these symptoms do not possess any value in
determining the localization of the lesion.
V. PARALYSES FROM FUNCTIONAL DISEASE.
1, Post-epileptic Paralysis.
Attacks of unilateral epilepsy are always followed by a temporary or
permanent paralysis of the convulsed limbs, which is attended by some
degree of exaggeration of the tendon-reactions, showing that this form
of paralysis belongs to the spasmodic or cerebro-spinal variety. The
general convulsions of idiopathic epilepsy are followed by a general
resolution of the limbs which is not usually spoken of as a paralysis
because all the limbs are affected 'in an equal degree. This muscular
feebleness sometimes predominates on one side of the body or in one
limb, and then it is recognized to be of a distinctly paralytic nature,
and there can be little doubt that the general muscular relaxation which
follows an epileptic attack ought also to be regarded as a paralysis.
486 THE SPASMODIC PARALYSES.
2. Hysterical Paralysis.
Partial or complete loss of muscular power is a frequent symptom of
hysteria. The loss of motor power may begin with mere weakness and
heaviness of the limbs, and these symptoms may gradually increase until
complete paralysis is established, but at other times complete paralysis
is suddenly established after a hysterical attack. The paralysis may
assume the form of paraplegia, hemiplegia, monoplegia, or it may be
limited to one or more motor nerves or to particular branches of a nerve.
Hysterical hemiplegia often supervenes after an attack of convulsions
Avith partial loss of consciousness, so that in its mode of onset as well as
in its clinical features it resembles the hemiplegia which results from an
apoplectic seizure, and the fact that contractures become developed in
the former as well as in the latter, renders the similarity between them
still more striking.
In some cases the contracture appears simultaneously with the paral-
ysis, while in other cases a paralysis with flaccidity is established and
continues for some tinie and then contracture develops gradually or
suddenly after a fresh attack. In the upper extremity the forearm,
hand, and fingers are spasmodically flexed, and the muscles may be so
rigid that it is impossible to obtain complete extension or to increase the
flexion. The lower extremity is strongly extended upon the pelvis and
the leg upon the thigh, while the foot assumes the position of extreme
talipes equino-varus. In hysterical paraplegia both lower extremities
assume the position just described, and the knees are drawn inwards
and strongly pressed against each other by contraction of the adductors
of the thighs. In hysterical paralysis with contracture, tremor is some-
times observed on attempting any movement. The patellar tendon-
reactions are often exaggerated and even ankle-clonus may sometimes
be elicited, these being the symptoms which are so characteristic of the
paralysis which results from sclerosis of the lateral columns of the cord.
Hysterical hemiplegia diff'ers from hemiplegia due to organic disease of
the brain in the following respects : It is usually accompanied by hemi-
anaesthesia, and by emotional disturbances, and other well-marked
hysterical phenomena ; the paralysis is scarcely ever complete, the face
and tongue almost never being aftected ; the leg is generally more para-
lyzed than the arm, and the diminution of motor power is liable to
sudden variations of intensity under the influence of diff"erent emotions.
Hysterical paralysis may be distinguished from atrophic paralyses by
the facts that in it the electrical reactions of the muscles remain normal,
and the muscles do not undergo active wasting. These tests, however.
PARALYSES FKOM FUNCTIONAL DISEASE. 487
fail in distinguishing hysterical paralysis from Landry's paralysis, and
as a matter of history the latter has freijuently been mistaken for
hysterical paralysis. The most trustworthy diagnostic sign between
the two affections is afforded by the patellar tendon-reaction, which is
generally exaggerated in hysterical paralysis and absent in Landry's
paralysis.
For purposes of diagnosis the student should pay particular attention
to the features Avhich distinguish the gait of a person suflFering from
hysterical paralysis and that of one suffering from a spasmodic paralysis
caused by organic disease. In organic spasmodic paralysis, whether of
the hemiplegic or paraplegic variety, when the affected extremity is to
be moved forward in walking the heel becomes strongly elevated and
the toes depressed ; the necessary elevation to clear the toes off the
ground is obtained chiefly by elevation of that side of the pelvis ; and
the foot is projected forward by a movement of circumduction, the toes
making a scraping noise on the ground. In hysterical paralysis there
is little or no elevation of the heel or depression of the toes during the
forward movement of the foot ; the necessary elevation to clear the foot
off the ground is obtained by flexion of the limb at the hip- and knee-
joints, and consequently rotation of the pelvis is not a marked feature
of the walk ; there is no movement of circumduction, and the toes do
not scrape the ground. In hysterical paralysis the foot is maintained
throughout the whole forward movement at right angles with the leg,
and as it is made to glide forwards the sole is held close to and almost
parallel with the ground.
The relative feebleness of the extensors of the toes in comparison
with those of the heels in spastic paralysis from organic disease, may
be tested in another way. If the patient be placed with her back
against a wall, so as to prevent her from inclining the body forwards, it^
will be found that when she attempts to elevate the toes a spasm of the
muscles of the calf supervenes, which fixes the anterior part of the foot still
further to the ground, but in hysterical paralysis the patient may often,
although not always, be coaxed to elevate her toes just like a healthy
person, and even when she refuses to make the necessary effort it will
be found that the anterior part of the foot does not become so strongly
fixed to the ground as in organic paralysis. In organic spasmodic
paralysis of the lower extremities the reflex of the sole is exaggerated,
while it is often absent when the paralysis is hysterical. In spasmodic
paralysis of the lower extremities from organic disease the patient fixes
her eyes steadily on the ground, but the hysterical patient either looks
about her, or, while pretending to look at the ground, she casts stealthy
488 THE SPASMODIC PARALYSES.
glances from tlie corners of her eyes to see what effect she is producing
on the surrounding observers.
Of the paralyses which occur in the region of distribution of par-
ticular nerves, hysterical aphonia is probably the most frequently met
with. In hysterical aphonia the loss of voice appears suddenly after
some mental excitement, and may disappear with e(pial celerity, and it
is not attended by a persistent cough like laryngitis. A laryngoscopic
examination reveals the signs of paralysis of the glottis, sometimes on
one and at other times on both sides. DiflRculty of moving the tongue
is sometimes associated with the laryngeal paralysis, and the patient is
no longer able to articulate in a Avhisper, but has to resort to pantomime
in order to make herself understood. Paralysis of the muscles of the
pharynx and oesophagus is not an uncommon symptom of hysteria,
and swallowing then becomes difficult or impossible. In such a case
the oesophageal tube passes into the stomach without encountering any
obstruction. Inspiratory dyspnoea is a frecjuent symptom of hysteria,
and it is possible that it is sometimes caused by a temporary paralysis of
the diaphragm. Paralysis of the muscular coat of the stomach is partly
the cause and partly the effect of the general tympanites which is so
frequently met with in hysterical patients. The obstinate constipation
which is so frequent a s^'mptom of hysteria is probably caused by
paralysis of the muscular coat of the l)owel. Retention of urine is
common in hysteria, but it is not often of paralytic origin. Hysterical
women have been known to drop down dead after a great shock, and
in these cases death is doubtless caused by paralysis of the heart.
Various phenomena occur in hysterical patients from paralysis of the
vaso-motor nerves. The excessive menstruation, and even the haemop-
tysis and haematemesis which are occasionally observed are most prob-
ably caused by paralysis of vaso-motor nerves.
3. Toxic Paralyses.
Various poisons give rise, as we have already seen, to paralysis by
causing organic disease of the nervous system. Clironic poisoning l)y
lead and by alcohol, as well as the poison of diphtheria, cause a paral-
ysis which we have reasons for believing is due to a progressive multi-
ple neuritis, and it is very probable that arsenic and many other metallic
salts act in a similar manner. Other poisons cause paralysis by induc-
ing a molecular or functional change in peripheral nerves, such as
curara, which acts upon the intramuscular nerve-endings, and atropine,
which paralyzes the terminations of the vagi and the nerves which
MOEBID ANATOMY. 489
supply the ciliary muscle and the sphincter of the iris. Some of the
methyl compounds of conium produce parah^sis by depressing the irrita-
Itility of the gray matter of the spinal cord and of the motor nerves.
This subject is, however, so wide that were it to l)e fully discussed we
should have to go over nearly the whole field of toxicology.
Some poisons appear to act on the fibres of the pyramidal tracts.
Cases of spasmodic spinal paralysis investigated by Dr. Brunelli render
it probable that the symptoms were caused by a species of vetch —
lathyrus cicera — which was used by the patients as a chief article of
diet.
A case I saw a short time ago along with my friend, Dr. Niven,
would seem to show that the symptoms of spastic spinal paralysis may
be caused by malaria. The patient came home an invalid from South
America some weeks before I saAv him. When I examined him he was
suffering from the usual symptoms of a primary lateral sclerosis, con-
sisting of stiiFness and feebleness of the lower extremities, muscular
tension, exaggerated patellar tendon-reaction, ankle-clonus, and decided
spastic gait. Iodide of potassium was ordered, but the symptoms did
not improve much. Dr. Xiven uoav ascertained that the patient was
suffering from well-marked attacks of airue, and he was accordingly
treated with large doses of quinine, and not only did the febrile symp-
toms disappear, but the spinal symptoms also improved rapidly, and the
patient left for South America, two months afterwards, with scarcely a
trace of the stiffness or exaggei'ated tendon-reactions of the lower
extremities to be detected.
MORBID ANATOMY.
I. Paraplegia.
Some pathologists doubt whether such a disease as a primary sym-
metrical sclerosis of the lateral columns has yet been proved to exist.
Cases have been reported in which the symptoms attributed to primary
lateral sclerosis were present during life, but which proved on post-
mortem examination to have been examples of sclerosis in patches, or
tumor of the medulla oblongata, or of the cerebellum. The most
notable case of primary lateral sclerosis so far reported is that of a
man under the care of my colleague, Dr. Morgan, in the Manchester
Royal Infirmary. The patient died from some intercurrent disease,
and Dr. Dreschfeld, who conducted the microscopical examination,
■ found symmetrical sclerosis of the pyramidal tracts of the spinal cord
490
THE SPASMODIC PAKALYSES.
from the medulla oblongata to the conus medullaris, and, with the ex-
ception of slight atrophy of the ganglion cells of the anterior gray
horns, an entire absence of any other lesion. The presence of some
atrophy in the ganglion cells in this case has led Westphal to suggest
that it was an example of amyotrophic lateral sclerosis, but having
watched the symptoms during life, and examined sections of the spinal
cord, I do not concur in this view. A secondary symmetrical sclerosis
of the lateral columns is caused by all transverse lesions of the spinal
cord. Transverse and compressive myelitis are followed by a descend-
ing sclerosis of the antero-lateral pyramidal tracts below the level of
the lesion, and an ascending sclerosis of the columns of Goll and direct
cerebellar tracts, but these conditions have already been sufficiently
described.
Fig. 153.
Transverse Section of the Medulla Oblojigata on a level with the middle of the Nucleus of
THE Hypoglossal. (From Charcot.)
E, R', median raphe ; A, B, represents the normal condition, and A', B', the parts as they appear in
amyotrophic lateral sclerosis ; C, C, the floor of the fourth ventricle ; V, a vessel which bounds the
nucleus of the hypoglossal anteriorly and externally ; D, fasciculus teres? and D', the corresponding part
on the diseased side ; A, healthy nucleus of the hypoglossal ; and A', the diseased nucleus. B, the healthy
nucleus of the pneumogastric nerves ; and B', the nucleus on the diseased side, which is seen not to be
much affected.
Morbid Anatomy. — In amyotrophic lateral sclerosis Charcot and
others have proved the presence of symmetrical sclerosis of the pyra-
midal tracts of the antero-lateral columns of the cord, and of the
anterior pyramids of the medulla oblongata, along with degenerative
atrophy of the anterior gray horns and of the motor nuclei in the
medulla oblongata, and loss of the motor ganglion cells. The condi-
tion of the bulbar nuclei is represented in Fig. 153, borrowed from
MORBID ANATOMY.
491
Charcot, the diseased nuclei being shown to the left of a fictitious line
(R E/), and the healthy one for the sake of comparison to the right of
that line. The part which Charcot calls the fasciculis teres really con-
sists of a group of small cells which I have called the external acces-
sory nucleus of the facial. It is seen to be diseased on the left side
(D'") of the figure.
II. Hemiplegia.
1. Ordinary Hemi'plegia.
The fibres which issue from the motor ganglion cells of the cortex
form separate bundles in the centrum semiovale, and descending in the
corona radiata come together in the internal capsule. Speaking some-
what broadly, it may be said that the fibres of the middle third of the
posterior segment of the internal capsule (Fig. 154, P) are concerned
Fig. 154.
Horizontal Section of the Basal Ganglia and Internal Capsule in an embrto of nine months.
KC, Caudate nucleus ; TU, Optic thalamus ; IX, Island of Reil ; //, III, Second and third segments of
the lenticular nucleus ; ps, Sensory peduncular tract ; P, Fundamental, and P', Mixed portion, and p,
Geniculate fasciculus of the pyramidal tract.; c. Anterior segment of the internal capsule.
in regulating the actions of the trunk, lower extremities, and probably
the general actions of the upper extremities; that the fibres of the
anterior third of the posterior segment (Fig. 154, P') are concerned in
492
THE SPASMODIC PARALYSES.
regulating the special movements of the hand as an organ of prehen-
sion, and probably also the movements of the rotation of the head and
neck along Avith the associated ocular movements; and that the fibres
of the knee (Fig 154, P) and the adjoining part of the anterior segment
of the capsule are concerned in the regulation of the movements of facial
expression, articulation, and the most special movements of the hand,
such as those of writing. The posterior third of the posterior segment
of the capsule contains the sensory conducting paths, and injury of these
Cls-
Vertical Section of the Bkain a little behind the Knee of the Internal Capsule, showing the
EFFECTS OF RUPTURE OF THE LENTICULO-STRIATE ARTERY. (Modified from CHARCOT.)
NO, Head, and NC, Tail of the caudate nucleus ; Ch, Chiasma, NL, Lenticular nucleus ; IK, Internal
capsule; Cls, Claustrum ; 1, The most frequent position in wliich the lenticulo-striate artery is ruptured;
1', 1", V", Progressive extension of the hcmorrliage producing compression and rupture of the fibres of
the pyramidal tract (liemiplegia) ; 2, Primary focus in the internal capsule ; 2', 2", 2'", Successive extension
of the clot.
causes hemiansesthesia. Of all the arteries of the brain, the lenticulo-
striate artery is the one most liable to rupture. If the hemorrhage be
small, it may lodge between the external cap.sule and the lenticular nucleus
and give rise to no symptoms. The vessel, however, is a comparatively
large one, and the hemorrhage usually extends beyond these limits. It
is sometimes directed upwards between the external capsule and the
lenticular nucleus, and it may then extend for a considerable distance
with the centrum ovale, the fibres of the internal capsule become rup-
MORBID ANATOMY. 493
tared at tlie point -where they form the foot of the corona radiata, and the
hemorrhage may then be so extensive as to extend upwards to the
summits of the ascending frontal and parietal convolutions, and out-
wards so as to compress the Island of Reil, but the external capsule is
only rarely ruptured. At other times the hemorrhage is directed
inwards through the gray matter of the lenticular nucleus, and if it
remain limited to the nucleus the patient will recover almost completely
from the hemiplegia which follows the attack. But if the clot is large
enough to rupture the internal capsule (Fig. 155, 1"), the fibres below the
seat of the lesion undergo descending sclerosis, and the paralysis remains
more or less permanent. In descending sclerosis the morbid changes
are observed in the middle third of the crusta, the longitudinal bundles
of the pons, the anterior pyramid of the medulla oblongata and the
column of Tiirck on the side of the lesion, and in the lateral column
of the cord on the side opposite to the lesion. In some cases a large
hemorrhage may I'upture into the lateral ventricle and then death takes
place in a few hours.
Rupture of the lenticulo-striate artery gives rise to a hemiplegia in
which the arm is more paralyzed than the leg or face. If one of the an-
terior branches of the artery is the seat of rupture the anterior segment
of the capsule may be injured to a greater degree than the posterior seg-
ment, and then paralysis of the face predominates. Hemorrhage of
the caudate nucleus may, by pressing on the internal capsule, cause a
hemiplegia in which the face is more paralyzed than the arm or leg.
2. Hemiplegia and Hemiancesthesia.
Hemorrhage of the lenticulo-optic artery (Fig. 154) impinges against
the posterior part of the posterior segment of the capsule, and causes
hemiplegia in which the leg is more paralyzed than the arm or face,
and which is accompanied by hemiansesthesia.
3. Hemiplegia^ Hemiancesthesia, and Hemianopsia.
The internal capsule may be injured by lesions of the optic thalamus.
Hemorrhage of the posterior internal optic artery, if small, does not
give rise to any definite symptoms, but if large it ruptures into the
lateral ventricles and causes death in a short time. Hemorrhage from
the posterior external optic artery does not usually give rise to pro-
nounced hemiplegia, but it causes hemiansesthesia of the opposite side
from injury of the sensory peduncular fibres of the optic radiations of
Gratiolet. When the lesion occurs in the pulvinar the external geni-
culate body is apt to be implicated and then bilateral hemianopsia of the
494
THE SPASMODIC PARALYSES.
opposite side results along with hemiplegia and hemianaesthesia, and the
same symptoms have occasionally been observed when the lesion is
situated too far forwards to injure the external geniculate body.
When a large hemorrhage occurs in the area of distribution of the
posterior external optic artery, the effused blood ruptures the posterior
part of the internal capsule, either wholly or partially, and makes its
way inwards and backwards so as to tear up a considerable portion of
the anterior tubercle of the corpora quadrigemina. It is in such cases
Fio. 156.
Cls
Vertical Section of the Brain ox a level with the Posterior Part of the Internal Capsule,
SHOWING THE EFFECTS OP RUPTURE OF THE LENTICULO-OPTIC ARTERY (hEMIAN.ESTHESIA). (Modified from
Charcot.)
NC, NC, Head and Tail of the caudate nucleus ; NL, Lenticular nucleus ; TH, Optic thalamus ; Cls,
Claustrum ; 1, Primary focus in the posterior part of the external capsule (hemiansesthesia) ; 1', 1", 1'",
Progressive extension of the primary focus causing compression or destruction of the internal capsule ;
2, Primary focus in the internal capsule (hemian;esthesia) ; 2', 2", 2'", Successive extension of the focus.
that the hemiplegia and hemianresthesia with the peculiar disorder of
the movements of the eyeballs already described have been observed.
The clot in these cases is only separated from the general ventricular
cavity by a thin layer of tissue, consisting chiefly of the ependyma of
the ventricle, and under such circumstances it is very probable that some
serous exudation will take place into the ventricles. The passage of
this fluid through the aqueduct of Sylvius into the fourth ventricle may
possibly explain the presence of Cheyne-Stokes respiration in these cases.
MORBID ANATOMY,
495
4. Crossed or Alternate Hemiplegia.
When the lesion is situcated in the crus cerebri the fibres of the third
nerve in their passage from the nucleus to their point of emergence
are damaged, while the fibres of the pyramidal tract in the middle third
of the crusta are ruptured or compressed (Fig. 157, p). The conse-
quences of a lesion in this position are that the muscles innervated by
the third nerve are paralyzed on the side of the lesion, while the limbs
sf-i^: ^rc< ^ /?^jl'--:v-- i^^-^;'^:- -^ti^;?>pi^ Sf
\--^' -^.-^V ':••■•?.<'•■>. >vi«»3>>-:-^ -~ ■ 'r'\^^y
Crura Cerebri. Transverse Section of the Crura Cerebri on a level with the anterior pair
OF the Corpora Quadrigemina : from a nine-months human embryo. The dark portions represent
Medullated Fibres.
s, Aqueduct of Sylvius ; g, q', Anterior pair of Corpoi-a Quadrigemina; pf, pf, Fasciculi of Medullated
Fibres proceeding to the anterior pair of Corpora Quadrigemina; L, L', Posterior Longitudinal Fasciculi ;
V, V, portions of these Fasciculi which join the posterior commissure of the third ventricle ; g, g', External
Geniculate Bodies ; af, af. Anterior portion of Fillet ; n, n', Substantia Nigra ; R, R', Red Nuclei ; p, p',
Pyramidal Tract ; c, c', Crustae ; 3, 3', Third pair of nerves ; x, Decussation in front of the Aqueduct of
Sylvius, which is part of the interlacement of the Tegmentum.
are paralyzed on the opposite side of the body, because the pyramidal
tract is injured above the crossing of the fibres of the two sides in the
medulla oblongata.
If the lesion is situated in the lower part of the lateral half of the
pons there is well-marked facial paralysis on the side of the lesion, and
a more or less complete motor and sensory paralysis of the limbs on the
opposite side. In order to account for these phenomena it is necessary
496
THE SPASMODIC PARALYSES.
to assume that the fibres of the pyramidal tract, which connect the
cortex of the opposite hemisphere with the nucleus of the facial nerve
in the upper part of the medulla, cross over about the middle of the
pons, as represented in Fig. 158.
5 — V-
L, Left,
if, Right.
P, Pons.
M, Medulla oblongata.
(From XoTiiNAGEi..)
DP, Decussatio pyramidiini.
E, Nerve fibres for the extremities.
F, Fibres destined for the facial nerve.
X, Lesion in the upper part of the pons.
y, Lesion in the lower part of the pons.
5. IlemijAegic and Post-hemiplegic Spasn^s.
It is in the area of distribution of the posterior external optic artery
that the lesion has almost always been found in cases of post-hemiplegic
chorea. The lesions which have been found in hemichorea are the
remains of old hemorrhages, or softening from occlusion of the posterior
external optic artery, although choreiform movements have occasionally
been observed during the groAvth of tumors in this region. It is evident,
therefore, that the symptoms depend not upon the nature of the lesion,
but upon its localization. In three cases of unilateral athetosis observed
by Charcot the lesion was situated in the posterior extremity of the
optic thalamus in one, the posterior extremity of the caudate nucleus in
the second, and the posterior part of the corona radiata in a third. In
a case observed by Landouzy an old focus of softening was found in
the portion of the lenticular nucleus which adjoins the internal capsule,
and in one reported by Ringer a focus of softening Avas found in the
posterior part of the lenticular nucleus near to the internal capsule. In
a case observed by Gnauck the coexistence of sensory disturbances in
the region of distribution of the fifth nerve on the side opposite to the
spasmodic movements rendered it probable that the lesion was situated
MORBID AXATOMY. 497
in the lateral half of the pons. It is, therefore, probable that the lesion
in athetosis may occupy different positions in the vicinity of the pyra-
midal tract. In all the cases hitherto examined after death the posi-
tions occupied by the lesion render it pro))able that the fibres of the
pyramidal tract are never completely ruptured and that there are no
descending changes in the coixl, but the fibres of the tract are likely to
haA'e suffered partial damage.
III. Special Consideration of Lesions of the Pyramidal
Tracts as they Occur in Infants.
1. Unilateral or JJiffused Atropliy of the Brain. — The lesions in
the acquired spastic hemiplegia of infancy have been found situated in
the motor area of the cortex of the brain. The primary lesion appears
to consist of a local hemorrhage, softening from occlusion of a vessel
or a local encephalitis. As a general rule q, puckered cicatrix forms at
the seat of the primary lesion, and the surrounding portion of the
cortex undergoes a diff"used sclerosis with retraction, so that the motor
area of the cortex of that side becomes much smaller than the corre-
sponding area of the opposite hemisphere, and consequently such cases
have been named unilateral atrophy of the brain. In addition to the
changes occurring in the cortex, the fibres of the jtyramidal tract con-
nected Avith the diseased area undergo a descending sclerosis, and con-
sequently the crusta of the crus cerebri, the longitudinal fibres of the
pons, and the anterior pyramid of the medulla oblongata on the side of
the lesion are found atrophied, while a microscopical examination reveals
a patch of sclerosis in the lateral column of the spinal cord on the side
opposite to the lesion. In a considerable number of the reported cases
the lateral lobe of the cerebellum on the opposite side to that of the
cerebral lesion has been found atrophied.
2. Parencephalus is a name first given by Heschl to the condition in
which a loss of substance is found in the brain, and which is usually
filled with serous fluid. The cavity is generally situated on the surface
of the cerebral hemisphere ; on one side it may open into the arach-
noid sac, or be separated from it by the viscei'al arachnoid, and on the
other side it may penetrate the whole extent of the medullary sub-
stance so as to reach the ependyma or to communicate freely with the
lateral ventricle. The defect may be only of small extent, but it is
sometimes associated with hydrocephalus, and it may then extend over
the whole mantle of the hemispheres as far as the basal ganglia, while
all intermediate sizes may be found between these extremes. The
498
THE SPASMODIC PARALYSES.
cerebral defect may be acquired or congenital. The ac(|uired varieties
may occur at alf ages, and they are chiefly caused by embolism or
hemorrhage, although they may occasionally result from injury. Tlie
lesion may be situated in any area of the cerebral hemisphere, but in
the majority of cases it occupies the area of the Sylvian artery, and it
is then accompanied by descending degeneration of the corresponding
pyramidal tract. Congenital parencephalus may be caused either by a
destructive lesion or by an arrest of development.
When the cavity has been caused by a destructive lesion its Avails
are formed of cicatricial tissue, and it is probable that evidences of
sclerosis of the pyramidal tracts of the cord will be found on micro-
scopical examination, but this point has not been fully investigated in
the recorded cases. In the congenital variety, caused by arrest of
Fig. 150.
development of the brain, the Avails of the cavity are formed by the
ependyma of the lateral ventricles, and by the gray matter, which to
the naked eye has all the appearance of the healthy cortex, but showing
deficiency of the motor ganglion cells on microscopical examination.
In some cases a defect in the parietal bone is present immediately over the
defect in the brain. A case of this kind was examined at a post-mortem
by Meschede, and I have recorded a case of defect of the parietal bone
(Fig. 159) associated with congenital hemiplegia of the opposite half
of the body, and in which a parencephalous defect most probably existed
MORBID ANATOMY,
499
immediately underlying the osseous defect. In parencephalus from
arrest of development a cavity often exists at symmetrical points in
each hemisphere, and the antero-lateral columns of the cord, instead of
being in a state of sclerosis, are small in size and defective in develop-
ment, as in a case recorded by myself (Fig. 160). When the paren-
cephalous defect is unilateral the anterior colmnn of the cord on the
same side and the lateral column on the opposite side are much less in
size than the corresponding columns the fibres of which are derived
Fig. 160.
from the healthy side. This fact was well illustrated in a case of paren-
cephalus shown b}^ Dr. Shuttleworth, of the Albert Asylum, at a meet-
ing of the Manchester Medical Society. It is very likely that bilateral
athetosis, and other cases of infantile motor disorders associated with
idiocy, are caused by a parencephalous defect of one or both hemi-
spheres of the brain.
Very little is known with regard to the morbid anatomy of the spastic
paraplegias of infancy. In most of these cases the spastic condition of
the extremities is cono-enital, and cvenerallv associated with difficulties
of articulation and other evidences of disordered cerebral function, and
consequently it is probable that the symptoms are caused by a small
parencephalous defect in each hemisphere of the brain.
IV. MOXOPLEGIA.
It has just been seen that ordinary hemiplegia is caused by destruc-
tive lesions in or near the fibres of the pyramidal tract, as they lie
600
THE SPASMODIC PARALYSES.
near together in the internal capsule. In the corona racliata these
fibres form more or less separate bundles corresponding to the motor
centres in the cortex, so that destructive lesions of the centrum semi-
ovale or of the cortex, provided the whole thickness is destroyed, may
injure one of these bundles whilst leaving the others intact, and conse-
quently localized lesions in these positions give rise to a monoplegia.
It must, however, be remembered that extensive lesions of the cortex
of the motor area of the brain will cause a comi)lete hemiplegia whicli
differs scarcely in any respect from the hemiplegia which results from
disease of the internal capsule.
1. Crural Monoplegia.
A few cases of disease of the cortex of the brain are recorded in
which the paralysis was limited to the leg. In a case reported by Dr.
Huddon the paralysis was limited to the left leg for five months, but
after a time the left arm also became paralyzed. After death a tumor
three inches in diameter was found connected with the dura mater; it
Fi(i. 161.
was situated to the right of the middle line and compressed the sub-
jacent hemisphere, and destroyed the upper extremities of tlie ascend-
ing frontal and parietal convolutions and the i)ostero-parietal lobule
(Fig. 162) as well as the paracentral lobule (Fig. 161).
2. Brachio-crural Monoplegia.
Paralysis of the leg and arm are frequently associated in disease of
the cortex. A case of paralysis, with rigidity of the leg and arm, of
three years' duration, is reported by Charcot and Pitres, in which a
patch of softening was found at the upper extremity of the fissure of
Rolando on the convex surface of the right hemisphere. Pitres de-
MORBID ANATOMY,
501
scribes a case of paralysis with unilateral convulsions of the left ex-
tremities, in which a focus of softening was found not in the cortex, but
Fig. 162.
Fig. 163.
in the centrum ovale, immediately beneath the posterior extremity of
the first frontal convolution (Fig. 163), and extending backwards under-
neath the superior parietal lobule.
602 THE SPASMODIC PAEALYSES.
3. Brachial Monoplegia.
A large number of cases of brachial monoplegia from cortical disease
have been collected and analyzed by Decaisne, but it would occupy too
much space to quote them here. The lesions have been found in the
ascending frontal and parietal convolutions.
4. Bracliio'facial Monoplegia.
Paralysis of the face and arm is not infrequently associated in dis-
ease in or near the cortex, and when the left hemisphere is the seat of
lesion the paralysis is accompanied by aphasia. In these cases the
lesion has been found near the inferior part of the fissure of Rolando
on a level with the posterior part of the third frontal convolution. In
Fig. 164.
other cases the lesion is situated in the white substance. A case, for
example, is reported by Anton Frey in which the left arm and the left
side of the face were paretic, and in which a focus of softening was
found in the white substance at the junction of the middle frontal with
the ascending frontal convolutions (Fig. 104).
5. Facial Monoplegia.
Facial paralysis of cerebral origin is generally complicated by aphasia
and paralysis of the arm, but a few uncomplicated cases of this form of
paralysis have been observed. Hitzig relates the case of a soldier
who had received a bullet wound on the right side of the head, and
became aiFected two months subseiiuently by clonic spasm of the left
side of the fiice, followed by paralysis of those muscles and of the
left half of the tongue. After death an abscess was found correspond-
ing to the seat of the injury in the ascending frontal convolution be-
MORBID ANATOMY. 503
tween the paracentral fissure and the fissure of Rolando (Fig, 165).
This case and others show that the lesion in facial monop^.eoia of corti-
FiG. ^p>'
cal origin is situated in or near the posterior extremity of the third
frontal convolution,
6, Labio-glosso-Iari/m/eal Paralysis of Cerebral Origin.
The symptoms of a progressive labio-glosso-laryngeal paralysis are
sometimes closely simulated by lesions of the hemispheres of the brain.
Dr, Barlow reports the case of a boy, aged ten years, who was
suffering from aortic regurgitation, and had an attack of right hemi-
plegia and aphasia, from which he made a good recovery. Four months
afterwards he had an attack of left hemiplegia with aphasia, and in
addition the muscles of mastication and articulation and those concerned
in the first act of deglutition, were paralyzed. The patient died of
the aortic disease, and at the autopsy evidence of an embolus was
found in both Sylvian arteries, A focus of softening, about the
size of a shilling, was found in the cortex of each hemisphere, involving
the inferior extremity of the ascending frontal, and the posterior
extremities of the second and third frontal convolutions. In a case
reported by Magnus and (pioted by Romberg, not only were the symp-
toms of bulbar paralysis ])resent, but the upper fixcial muscles were
likewise paralyzed, and after death only one hemorrhagic cyst, which
was about the size of a small walnut, was found, the situation of this
cyst evidently being the centrum semiovale of the right hemisphere
immediately underlying the posterior part of the third frontal convolu-
tion. Several cases of bulbar paralysis of cerebral origin have now
been reported in which the lesions were found in the lenticular nucleus
of both hemispheres. Bulbar paralysis occurring in sclerosis in patches
is sometimes caused by a patch of sclerosis in each lenticular nucleus,
504 THE SPASMODIC PARALYSES.
but these symptoms Avhen of cerebral origin usually occur in those who
are suffering from granular kidney, or from syphilis of the cerebral
vessels. The general history of such cases is that the patient has an
attack of right-sided hemiplegia with aphasia, the aphasia rapidly dis-
appears and recovery takes place from the hemiplegia to such an extent
that the paralysis is scarcely perceptible, but the tendon-reactions are
slightly exaggerated. Some months after the first attack the patient
suffers from an attack of left-sided hemiplegia with aphasia ; the aphasia
soon disappears after this attack also, and the limbs recover, so that there
is only a slight diminution of the motor power remaining, but the
tendon-reactions remain exaggerated, and noAV the patient is found to be
suffering from all the usual symptoms of bulbar paralysis. In these
cases the lenticular nucleus in each hemisphere is found to contain a
cyst filled with serous fluid, the result of hemorrhage or of softening.
The symptoms are, however, caused, probably not by the disease of the
lenticular nuclei themselves, but by partial damage of the fibres of the
pyramidal tract which pass on each side through the knees of the
internal capsule and which connect the posterior part of the third frontal
convolution witli the bulbar motor nuclei.
7. Unilateral Ofulo-niotor Blonoplcgia.
It has already been mentioned that conjugate deviation of the eyes
and rotation of the head and neck are frequent symptoms both of con-
vulsions and hemiplegia, and that the deviation in the former is directed
away from and in the latter towards the hemisphere in whicli the lesion
is situated. In the brain of the monkey Ferrier localizes a centre in
the posterior extremity of the second frontal convolution, irritation of
Avhich causes elevation of the eyelids, dilatation of the pupils, conjugate
deviation of the eyes and turning of the head to the opposite side ; and
he also found that extensive movements of the eyeballs, along with asso-
ciated movements of the head and neck result from irritation of the
supramarginal and angular gyri. One or two cases are recorded which
render it probable tluit lesion of the posterior extremity of the second
frontal convolution will cause conjugate deviation of the eyes and
rotation of the liead and neck in man, but the recorded cases are not
conclusive upon this point. Numerous cases, however, have been re-
corded in which this symptom was caused by a lesion in or near the
angular gyrus. Grasset has collected much evidence upon this point
and he has recorded a case of his own in which the patient suffered
from left-sided hemiplegia and a conjugate deviation of the eyeballs
with rotation of the head directed to the right, and in which the disease
MORBID ANATOMY.
505
consisted of lesion of the pli courh of the right hemisphere (Fig. 166).
Many cases are also reported in which conjugate deviation of the eyes
was caused by disease of the centrum ovale and in these cases the lesion
was, as a rule, situated between the internal capsule and the supra-
Fio. 166.
marginal and angular gyri. It would also appear that disease in the
neighborhood of the angular gyrus and supraniarginal lobule produces
at times paralysis of the levator palpebrfe superioris of the opposite
side, without the other muscles supplied by the third nerve being im-
plicated.
8. Hemiplegia from Cortical Disease.
A case of complete hemiplegia of the right side, of six years' dura-
tion is described by Lepine in which there was total destruction, caused
Fig. 167.
by yellow softening, of the ascending parietal convolution, and partial
destruction of the Island of Reil, ascending frontal convolution, and the
506
THE SPASMODIC PARALYSES,
anterior part of the superior and inferior parietal lobules of tlie left
hemisphere (Fig. 167). Secondary degeneration was traced in the left
half of the pons and in the pyramid of the medulla. Several similar
cases are reported by others. Dussaussay describes a case, quoted hj
Pitres, of right hemiplegia with conjugate deviation of the eyes to the
left, and in which a cavity Avas found in the centrum ovale of the left
hemisphere containing dark coagulated blood (Fig. 168). This cavity
Fig. 168.
was limited internally by the gray substance of the paracentral lobule ;
superiorly and externally by the gray substance of the ascending frontal
and parietal convolutions : in front it extended to the pnuceiitral fissure :
and behind to the posterior border of the ascending parietal convolu-
tions ; while inferiorly it was separated from the corpus striatum by a
thin layer of white substance.
Morbid Physiology. — In primary lateral sclerosis conduction through
the fibres of the pyramidal tracts, which convey voluntary impulses from
the cortical motor centres to the spinal cord, is wholly or partially
arrested, and consequently voluntary paralysis results. The spinal
centres with the reflex arcs are, however, uninterfered with, and as they
are now set free from the inhibitory influence of the cerebrum the
reflexes and tendon-reactions become increased. Dr. Hu2hlin<:rs-Jack-
son has suggested that the muscular tension and contractures are caused
by the unantagonized influence of the cerebellum on the paralyzed
muscles, but this theory is not free from difficulty.
Amyotrophic lateral sclerosis is caused, according to Charcot, by a
primary lateral sclerosis to which disease of the anterior gray horns
MORBID ANATOMY. 507
becomes superadded, the lesion beginning in the cervical region and sub-
sequently extending upwards to the medulla oblongata and downwards
to the lumbar region. The presence of lateral sclerosis explains the
facts that the paralysis often precedes the atrophy, and is associated with
muscular tension, contractures, and exaggerated tendon-reactions ; Avhile
the presence of disease of the ganglion cells explains the muscular
atrophy which becomes associated with the paralysis. But the paralysis
of the upper extremities is sometimes of the pure atrophic variety, and
I cannot help thinking that in some cases at least the lesion begins in
the gray matter and extends outwards to the lateral columns.
In disease of the substance of the cerebral hemispheres and of the
basal ganglia, hemiplegia is caused by arrest of conduction through the
fibres of the pyramidal tract. If the clot simply compresses these
fibres without rupturing them, recovery takes place when the eflPused
blood is absorbed, but if these fibres are ruptured the hemiplegia
becomes permanent. It is very probable that early rigidity occurring
at the time of the hemorrhage is caused by rupture of these fibres,
while the rigidity which begins a few days after the attack is caused
by an inflammation of the fibres excited by the presence of the clot,
which acts as a foreign body. Late rigidity comes (in about the same
time as the descending changes in the pyramidal tract, and is produced
by the same mechanism as the spastic rigidity of the limbs in primary
spinal lateral sclerosis. It is not easy to give reasons why choreiform
movements are so liable to occur wdien the lesion is situated in the area
of the posterior external optic artery. Two probable explanations of
these clonic spasms suggest themselves to my mind. The first is that
fibres connecting the cerebrum with the cerebellum are injured by these
lesions, so that the normal proportion between the outgoing discharges
which regulate the tonic (cerebellar) and the clonic (cerebral) actions of
the body is lost. The second is that the spasms are caused by partial
injury of the fibres of the pyramidal tract which regulate the funda-
mental actions. The fundamental actions are regulated from the con-
volutions near the longitudinal fissure, and the special actions from the
convolutions which border the Sylvian fissure, :ind it is manifest that
the fibres which descend in the corona radiata from the former will pass
on the optic thalamus side of the internal capsule, while those which
descend from the latter Avill pass on the lenticular nucleus side of it.
Injury of the optic thalamus will, therefore, be likely to damage the
fundamental fibres of the pyramidal tract, while leaving the accessory
fibres unaff'ected. The eifect of impairment of the fundamental actions
might well be to cause the voluntary and special actions to be effected
with irregularity and want of harmony. The only interpretation which
508 THE SPASMODIC PARALYSES.
the spastic paralyses of infancy admit of, is that the cerebral motor
mechanism in one or both hemispheres is either destroyed by a lesion
after its development, or that the development of the motor mechanism
is defective from the first or completely arrested.
The morbid physiology of the functional paralyses is somewhat obscure.
Post-epileptic paralysis is most probably induced by the exhaustion of
the motor cortical centres caused by a previous excessive discharge, just
as the sciatic nerve of a frog is paralyzed for a time by passing a strong
faradic current through it. Hysterical paralysis is also best explained
by supposing that the molecules of the cells of the motor centres of
the cortex are in a state of stable equilil)rium, and consequently im-
pulses from the cortex fail to be conducted outwards to the muscles
through the fibres of the pyramidal tract. It is still more difficult to
give an explanation of the toxic paralyses. It is impossible for us to
tell why curara acts on the intramuscular nerve endings, atropine on
the vagi, and lead on certain peripheral nerves ; we must accept the
facts as they are disclosed by experiment and observation and generalize
them as best we can.
Treatment. — The treatment of the spasmodic paralyses will depend
upon the primary lesion which causes the sclerosis of the lateral columns
which underlies the paralysis. Primary sclerosis of the lateral columns
of the cord must be treated internally like other cases of chronic
myelitis by iodide of potassium, while the galvanic current is the most
trustworthy local remedy. A carefully conducted hydropathic treat-
ment may sometimes be beneficial, and gaseous thermal springs have
been employed with advantage. Local stimulating treatment by means
of the faradic current and massage must be avoided in all forms of
spasmodic paralysis. Amyotrophic lateral sclerosis must be treated on
the same general principles as other forms of chronic myelitis. In
secondary sclerosis of the lateral columns of the cord the case must be
carefully investigated with a view to discover whether the primary lesion
is situated in the vertebrae, membranes, or cord itself, and then the
nature of the lesion, whether inflammatory, scrofulous, or syphilitic,
should be determined, and the treatment must be conducted accordino-lv.
In hemiplegia and monoplegia the locality of the lesion must first be
investigated and then an endeavor must be made to determine whether
the lesion is likely to be a hemorrhage, embolism, thrombosis, or a
tumor. The treatment of these morbid conditions Avill be subsequently
described. The local treatment of the paralyzed limbs consists of the
application of the galvanic current, and a moderate degree of rubbing
of the surface, but deep kneading of the muscles, and the application
of the faradic current or any other stimulating measures, must be avoided.
CHAPTER IX.
DISORDERS OF MOTOR COORDINATION.
1. MENIERE'S DISEASE (AURAL OR LABYRINTHINE VERTIGO).
Etioloiji). — Aural vertigo, as described by Meniere, comes on suddenly
and Avithout apparent cause. Acute and chronic catarrh of the middle
ear and inflammation of the labyrinth are often accompanied by deaf-
ness and severe vertigo, and transient vertigo may be caused by the
impulsion of air or fluids through the Eustachian tube into the tym-
panic cavity, by external pressure on the drum-head, by wax or other
accumulation in the meatus, or by the passage of a galvanic current
through the ears. Aural vertigo with deafness is sometimes one of
the earliest symptoms of locomotor ataxia.
Symptoms. — The characteristic symptoms of Meniere's disease are
sometimes preceded by partial deafness, earache, and other indications of
a local disease, but in other cases the patient is suddenly attacked with
deafness, noises in the ears, and a feeling of giddiness, Avhich is attended
by fainting, nausea and vomiting. The attack passes off in a few
seconds or minutes, but recurs after a variable period, the paroxysms
becoming more aggravated, and more frequently repeated as the dis-
ease advances. The noise is sometimes heard in both ears, but is
probably always more pronounced on one side than the other ; it is
compared to the loud whistling of a steam engine or to a succession of
explosions, or is described as a continuous humming or buzzing. The
noise ceases with the attack in recent or slight cases, but continues to
distress the patient during the interval in long-standing and severe
cases.
The attack of vertigo varies in duration and intensity. In slight
cases it consists of a momentary feeling of swimming in the head, but
in severe cases each paroxysm may extend over a period of ten or more
minutes, Avhile in still more aggravated cases tlie feeling of uncertainty
and giddiness is never absent during waking hours, and every effort on
the part of the patient to assume the erect posture determines a parox-
ysm of vertigo, nausea, and vomiting. During the paroxysm the
patient feels as if he were rotating round a vertical or liorizontal axis,
or as if he were falling forwards, backwards, or laterally : he staggers
510 DISORDERS OF MOTOR CO - RDIX ATIOX .
and clutches at surrounding objects, or actually flills in the direction in
which his abnormal sensations would lead him to expect. The patient
also feels faint, and occasionally actual syncope may occur; the skin
then becomes pallid, cold, and covered with sweat, pulse is feeble and
flickering, the patient suffers from confusion of ideas, and in aggravated
cases there may be a transitory loss of consciousness, and there is an
intense feeling of nausea Avhich often terminates in vomiting, when the
attack usually comes to an end. Oscillatory movements of the eyeballs
have in some cases been observed during the attack, and in these cases
there was an apparent displacement of objects with reference to the
patient. When one ear is exclusively aff"ected w^ith noises and deafness
the i)atient may experience a constant tendency to walk to the opposite
side. It was shown by Hinton that perception of musical notes is often
faulty in this disease; in one case observed by him G- of the third
octave was heard as C of the octave below, or twelve notes below the
normal pitch, and more or less similar results were obtained with other
notes.
The course of the disease is a steadily progressive one until complete
deafness is established, when, fortunately, all the distressing symptoms
of the disease cease. The paroxysms of vertigo come on at first at
irregular intervals; they increase gradually in frequency and intensity,
and in aggravated cases the patient suffers continuously from some
degree of vertigo, while he is liable to paroxysmal exacerbations of
great severity. The noises in the ears may cease at first during the
intervals, but after a time they are constant during waking hours until
the patient is completely deaf.
2. PRI3IARY SCLEROSIS OF THE COLUMNS OF GOLL.
Only a few cases which can ho regarded as a primary affection of
the columns of Goll are recorded. In a case recorded by I'ierret the
symptoms consisted of a girdle sensation passing round the body, light-
ning pains and various other sensory disorders in the lower extremities,
and inability to maintain the erect posture with closed eyes, while on
wishing to advance the patient felt as if she were drawn backwards, but
once started she was impelled forwards by an uncontrollable force. The
patient died at the age of thirty years from an attack of acute pneu-
monia, and at the autopsy Pierret discovered the presence of sclerosis
of the columns of Goll. The posterior root-zones were, however, im-
plicated in the lesion to some slight extent in the dorsal region, and,
judging from the drawings which accompany the report of the case, in
PEOGRESSIVE LOCOMOTOR ATAXIA. oil
tlie lumliar region also. The case cannot, therefore, be regarded as a
typical example of sclerosis of the columns of Goll. A case of primary
sclerosis of the columns of Goll has been reported by DuCastel and
another by Gowers, but in neither were there symptoms durino- life
Avhich could -with probability be attributed to disease of these columns.
3. SECONDAKY SCLEROSIS OF THE COLUMIS'S OF GOLL AKD OF
THE DIRECT CEREBELLAR TRACTS.
These affections are only of anatomical interest inasmuch as they do
not give rise to any recognizable symtoms.
4. PROGRESSIVE LOCOMOTOR ATAXIA (TABES DORSALIS, GRAY
DEGENERATION OR SCLEROSIS OF THE POSTERIOR COLUMNS
OF THE SPINAL CORD).
Etiology. — Locomotor ataxia often occurs in individuals whose nearest
relatives have suffered from other nervous diseases, such as monomania,
hypochondriasis, epilepsy, migraine, mental disease, or violent fits of
anger and drunkenness. In other cases the heredity is direct from
parent to offspring. Friedreich met with three different ftimilies in
which several brothers and sisters were attacked with the disease about
the same age, while the parents themselves were healthy, and Carre
was informed by an ataxic patient that eighteen other members of her
family were affected by the same disease. Locomotor ataxia, according
to the statistics of Eulenburg, attacks males in the proportion of one
hundred and twenty-eight to twenty-one females. It is essentially a
disease of youtli and middle age, by fiir the larger number of cases
occurring between the ages of twenty and fifty years, although it has
been observed occasionally in children.
The exciting causes of locomotor ataxia are exposure to cold and
damp, severe bodily and mental exertion, emotional disturbances, sexual
excesses, and injuries of various kinds, such as a fracture of the thigh
or concussion of the spinal cord. It is sometimes the sequel of acute
disease, such as typhus, articular rheumatism, acute pneumonia, and
diphtheria, and of repeated abortions and the puerperal state.
But of all the antecedents of locomotor ataxia, syphilis is the most
frequent and most important factor in its genesis. Fournier stated, in
1876, that syphilis had preceded locomotor ataxia in twenty-four out of
thirty cases observed by him. and soon afterwards "N^ilpian asserted
512 DISOEDEES OF MOTOE CO - OEDIN ATIOX.
that about seventy-five per cent, of patients suffering from locomotor
ataxia are old syphilitic subjects. In the more recent statistics of Erb,
Fournier, and others, the frequency with which ataxia attacks syphilitic
subjects is placed as high as from eighty-nine to ninety-one per cent, of
all cases, while Fischer, Westphal, and others do not find the propor-
tion higher than from fourteen to twenty per cent. My own experience
agrees with the higher rather than the lower percentages. Locomotor
ataxia is one of the tertiary manifestations of syphilis, but Fournier
met with a case in which the symptoms of tabes began twenty-tA\o
months after the primary infection, and during the secondary symptoms;
in other cases an interval of upwards of twenty years elapsed between
the infection and the first ap})earance of the tabetic symptoms, but the
majority of cases of syphilitic ataxia occur between the sixth and twelfth
years after infection. It is important to notice that locomotor ataxia
succeeds with much greater frequency to the milder than to the severer
forms of syphilitic infection, and Fournier has shown that an efficient
mercurial treatment during the early period of syphilis greatly dimin-
ishes the liability to ataxia.
Symptoms. — The course of locomotor ataxia may, for the i)urposes
of description, be divided into three stages : (1) The premonitory or
preataxic stage ; (2) the ataxic stage ; and (3) the paralytic stage, or
the period of the generalization of the ataxia.
(1) The Pkkataxic Stage.
The symptoms of tlie preataxic stage may be subdivided into dis-
orders of (a) general sensibility ; {b) the general motor functions apart
from ataxia ; {c) the special senses ; (d) the cranial motor and mixed
nerves with the cilio-sj)inal region of the cord : (/) the nutritive func-
tions ; and (//) the cerebral and psychical functions.
(a) Disorders of G-eneral Sensibility. — The most constant of the
premonitory symj)toms of locomotor ataxia -ayc pains of a peculiar and
often distressing kind, which may precede l)y many years all other
symptoms, and generally last throughout the whole course of the disease.
These pains are compared by the patient to forked lightning darting
through the body, and are consequently named lightning-like or lancinat-
ing pains. The lightning pains are, as a rule, not very urgent at first
and are believed b}'^ the patient to be of rheumatic origin. They con-
sist of a single dart which shoots suddenly into some j)art of the lower
extremities, or occasionally of the back of the head or side of the face,
and disappears as suddenly as it came, but only to return at no distant
PROGRESSIVE LOCOMOTOR ATAXIA. 513
date. As the disease advances the shooting pains recur at shorter
intervals, and after a time a number of tliem follow each other so quickly
as to constitute a paroxysm of almost continuous pain. The paroxvsm
may last only a few minutes at first, but by and bye its duration is pro-
longed to some hours or even days, during which the patient suffers the
most excruciating agony. The duration of the interval between the
paroxysms is also very variable ; in some cases the paroxysm recurs
every few weeks, but in the interval the patient is comparatively free
from pain, Avhile in other cases the patients never know what it is to
have a perfectly free interval from pain, and they are liable to suffer
every few weeks from exacerbations of great severity. The character
of the pain also varies ; it is sometimes described as burning, gnawino-, or
dragging, and during the paroxysm the pain is said to shoot like light-
ning through the limbs, or to be like that which would be caused by a
sharp knife or red-hot iron passing quickly through the tissues. The
lancinating pains are usually deep-seated in the soft tissues or in the
bones, but in addition to these, true neuralgic pains, which are limited
to the area of distribution of a particular nerve, may supervene in the
course of the disease. These neuralgic pains sometimes shift from one
nerve territory to another, and do not invade the same region during
successive paroxysms of pain, but at other times the pain becomes
localized for a long time in a particular nerve like the sciatic, and obsti-
nately resists all treatment.
Pain along the vertebral column, Avhich is generally situated in the
loins or between the shoulders, is another symptom of tabes. This pain
is dull, aching, and more or less continuous, but presents alternating
periods of remission and exacerbation, and it is only on rare occasions
that it rises to any great intensity, and then it may be suspected that
the disease is complicated by a spinal meningitis.
The girdle pain which is so frequently met with in many spinal affec-
tions is an almost constant symptom of locomotor ataxia, and the patient
feels as if a rope were drawn tight around his body, or as if it were
encircled by an unyielding iron ring. This sensation is usually situated
on a level with the lower thoracic or upper abdominal region, although
it may occasionally be felt at the lower part of the body and it may
then reach to the neck of the bladder. A pain of similar character
may likewise be felt around the joints of the lower extremities, and
patients then describe it as a feeling like that caused by a garter tied
tightly below the knee.
Cutaneous hypemesthesia is not an uncommon symptom of the early
stage of tabes, and it may be present in several forms. At times there
may be hypersesthesia to impressions of temperature and anaesthesia to
33
514 DISORDERS OF MOTOR CO - ORDIX ATION.
touch, while at other times anaesthesia to touch may be accompanied by
a high degree of hypertesthesia to impressions of pain. The hyper-
ffisthetic condition is distributed in patches, which are often found on
the lower extremities of patients suffering from severe paroxysms of
lancinating pains. Circumscribed areas of skin then feel exquisitively
sensitive to the slightest contact, such as a light touch or the rubbing
of the clothes, and a slight touch on one of these spots appears to be
capable of determining an attack of the lancinating pains. These
hyperresthetic areas are also subject to attacks of spontaneous pain,
which is generally of a scalding or burning character ; a patient once
compared this pain to that Avhich might be caused by rubbing into the
skin a burning vesuvian match.
Various paraesthesiae are also experienced in the preataxic stage of the
disease. The patient suffers from the sensation popularly known as
" the fidgets " ; in other cases, from a feeling of heat which may be so
intense as to compel him to uncover his feet at night ; and in still
other cases he is troubled with cold feet from vaso-motor spasm. The
patient often complains of numbness and tingling of the extremities,
the soles of the feet being, as a rule, the parts first attacked. Patients
feel as if they were Avalking on wool, cork, or felt soles, or upon bladders
of water, and in aggravated eases they have a sensation as if the ground
were passing from under their feet, or as if they were walking on air.
When their hands are affected they feel as if their fingers were covered
with gloves, and are then unable to discriminate the primary qualities
of objects which they grasp.
(b) Disorders of the General Motor Functions apart from Ataxia.
— The patellar tendon-reactions are usually absent at a very early period
of the premonitory stage of locomotor ataxia, and whenever these re-
actions are wanting in a person who has for some time been suffering
from recurring lancinating pains, and who is not the subject of an
atrophic paralysis of the quadriceps femoris muscle or of diabetes, there
is a very strong presumption that he has already entered upon the first
stage of this progressive disease. It is possible that these reactions may
be absent in a fcAV persons who are otherwise healthy, while, on the
other hand, they may be present or exaggerated in a very few cases, in
which other symptoms strongly point to locomotor ataxia ; but with
these slight reservations absence of the patellar tendon-reaction is one of
the most certain and valuable signs of the early stage of locomotor ataxia.
The cutaneous reflexes are usually unaffected in the early stage of
locomotor ataxia, but as the disease advances the normal interval between
the cutaneous excitation and the resulting contraction may become
greatly prolonged. In a few cases the cutaneous reflexes are greatly
PROGRESSIVE LOCOMOTOR ATAXIA. 515
exaggerated even at an advanced period of the disease. Paradoxical
contraction has been observed by Westphal as a symptom of tabes, and
its presence may possibly be taken as a sign that the lesion of the pos-
terior columns is extending to the lateral columns, and that the paralytic
stage of the disease is approaching.
Transitory paresis of some muscular groups is an occasional symp-
tom of the early stage of tabes ; whilst walking, the legs may suddenly
give way at the knees so that the patient falls to the ground. This
sudden failure of motor power appears to be comparable to the transitory
diplopia which is so common a symptom of the preataxic stage. In
other cases the disease is ushered in by the occurrence of a sudden
paraplegia, and it is only after the patient has recovered from the
paralytic symptoms that the motor incoordination becomes apparent.
It is probable that in these cases the primary lesion had extended trans-
versely so as to have affected the lateral columns, and that under treat-
ment it has receded so as to become limited again to the posterior columns.
Uncertainty of gait and station when the eyes are closed, or when in
the dark, is a motor symptom frequently observed before true ataxia is
established. This is, indeed, frequently the first symptom to attract the
patient's attention. When he puts his hands over his face whilst wash-
ing, in the morning, he may feel as though he were swaying from side
to side, or he may totter, and he may be compelled to steady himself by
propping his knees against the washstand, while his uncertainty of gait
becomes very troublesome when he ascends a flight of stairs in the
dark, or enters an unlighted chamber. On careful observation of
the patient it may be noticed that he has a slight tendency to stagger
when he rises suddenly after sitting for some time, or when he is asked
to turn suddenly round or to walk backwards, but so long as he walks
straight forwards with open eyes and in daylight there is no staggering
nor uncertainty of gait. The patient is also troubled at this period
with attacks of vertigo, which is the subjective correlative either of
diplopia or of the uncertainty of gait. Vertigo is a prominent symptom
of the cases of congenital ataxia described by Friedreich.
(c) Affections of the Special Senses. — Amaurosis is a frequent and
distressing symptom of locomotor ataxia. Interference with sight is in-
dicated by a slowly or rapidly advancing diminution in the acuteness of
vision, and by a restriction of the field of vision, first, for the perception
of colors, and finally for the recognition of objects ; the patient may
become blind at the end of a few weeks, or years may elapse before the
loss of sight is complete, and occasionally the affection ceases to pro-
gress after it has lasted for a comparatively long time. The blindness
516 DISORDERS OF MOTOR CO-ORDINATION.
is caused by white atrophy of the optic disks, which is said to appear
in about thirty per cent, of all cases of tabes.
Hemiopia has been met as a transitory symptom of the preataxic
stage, but its occurrence is rare. Deafness is not an infrequent accom-
paniment of locomotor ataxia, but it is only in a certain number of
these cases that the loss of hearing can be regarded as forming a part
of the disease, and in such cases the deafness is probably caused by a
parenchymatous atrophy of the auditory nerve analogous to that of
the optic nerve. Deafness, with vertigo and the other symptoms of
Meniere's disease, has occasionally been observed in the early stage
of tabes.
The olfactory sense is also occasionally lost, a case being described
by Althaus in which the patient complained at first of a subjective
smell of phosphorus, and ultimately lost all sense of smell.
The gustatory sense has not, so far as I know, been found aifected,
although slight disturbances of the sense of taste may be present when
the trigeminus is implicated.
[d) Disorders of the Cranial Motor and Mixed Nerves, and of the
Cilio-spinal Region of the Cord. Paralysis of the Ocular Muscles. —
The symptoms of locomotor ataxia are fre(iuently ushered in by paral-
ysis of one or more of the ocular muscles, the paralysis ])eing at first
generally transient. After a longer or shorter time, however, the
paralysis recurs and becomes permanent toAvards the later stages of the
disease. The transient paralyses of the first stage are generally so slight
that they declare themselves not by the presence of a perceptible squint,
but by the sudden appearance of diplopia, which is either constantly
present or only when the eyes are turned in particular directions.
Distinct squint and ptosis are, however, occasionally present in the
early stage, and very frequently in the later stages of the disease.
Out of sixty-four cases of tabes collected by Eulenburg twenty-five
had strabismus ; of these twenty-five cases nineteen had divergent
strabismus, and four had in addition paralytic ptosis, while six had
convergent strabismus.
Disorders of the pupils are frequently present in a very early stage of
locomotor ataxia. Of the sixty-four cases collected by Eulenburg nine
had mydriasis, the dilatation being double in three, single in four, and
accompanied by myosis of the other in two cases, while twenty-eight had
myosis, the contraction being double in twenty-one and single in seven
cases. Inequality of the pupils is common in the early stage of the
disease, and on the side on which the contraction of the pupil is the
more marked there may be redness of the cheek, congestion of the
conjunctiva, local elevation of temperature, and relative diminution of
PROGRESSIVE LOCOMOTOR ATAXIA. 517
the palpebral aperture, while in a few cases unilateral hyperidrosis of
the side of the face has been observed.
The Argyll-RoherUon pupil is frequently present in the early stage
of locomotor ataxia, and it is generally, although not invariably associ-
ated with myosis.
Nystagmus is a very rare symptom of locomotor ataxia, and is prob-
ably never present except in the hereditary form of Friedreich.
The trigemmus is not unfrequently implicated in tabes. The most
prominent symptoms in the area of distribution of this nerve are pains,
which may either be neuralgiform in character or of the same kind as
the lancinating pains of the lower extremities. Both kinds of pain
may be felt in the forehead, face, parietal region, external auditory
meatus, and the lancinating pains are particularly liable to be felt in
and around the orbit. Paroxysms of these pains may sometimes be
mistaken for hemicrania, more especially as the attack is often accom-
panied by redness of the conjunctiva, photophobia, and an increased
flow of tears. The attacks are usually followed by cutaneous hyperaes-
thesia, but as the disease advances the increased sensibility gives place
to anaesthesia which is said to occupy most frequently the conjunctivae
and the nasal fossae, but may implicate the mucous membrane of the
mouth, tongue, and pharynx on one or both sides.
The motor branch of the trigeminus is not so frequently affected as
the sensory branches, but occasionally cases have been observed in which
the masticatory muscles were the subjects of ataxia, or were so feeble
that the patient was obliged to live upon pulpy food.
1^\\Q facial nerve is also occasionally implicated in the disease, and
then the face may be contorted by grimaces when the patient speaks,
from ataxia of the facial muscles. The muscles of the face, tongue,
and larynx may be simultaneously affected with motor incoordination,
and then the speech becomes ataxic ; the articulation is hurried, stutter-
ing, and becomes so indistinct in advanced cases that the patient's
speech is almost incomprehensible. One side of the face may become
suddenly more or less paralyzed, and paralysis of the veil of the palate,
implicating the muscles supplied by either the facial or glosso-pharyn-
geal nerves, has occasionally been observed, while the symptoms of
bulbar paralysis have been known to occur suddenly in the early stage
of ataxia. These paralyses are, like the corresponding affections of the
ocular muscles, generally of a transitory character.
The disorders in the area of distribution of the tenth and eleventh
nerves are very numerous, and give to the disease some of its char-
acteristic featuies.
Laryngeal crises, consisting of paroxysms of spasmodic cough like
518 DISORDERS OF MOTOR CO - ORDINATION .
those of whooping cough, are liable to complicate the early stage of
tabes, while paralysis of the adductors, or more rarely of the abductors,
of the vocal cord is occasionally present.
Cardiac crises, consisting of paroxysms of angina with irregular
and frequent pulse, are occasionally present, and Charcot believes that
in ataxia the pulse is permanently accelerated, often beating from 100
to 130 in a minute. Aortic regurgitation has so frequently been found
associated with locomotor ataxia that some authors have been led to
believe that the two diseases are related by some causal connection.
The twelfth nerve is only rarely affected in locomotor ataxia, but it
is implicated with the facial and laryngeal nerves when there is ataxic
speech. Several cases of tabes are recorded in which the lateral half
of the tongue was paralyzed and atrophied, this symptom being gener-
ally associated with some degree of atrophy of the muscles of the hand.
{e) Disorders of the Visceral Functions. — G-astrahjic attacks or gas-
tric crises are frequently observed in the premonitory stage of tabes.
The attack begins suddenly during a paroxysm of the lancinating pains.
It consists of severe epigastric pain, which radiates in different directions,
and is accompanied by distressing vomiting of a large quantity of
watery mucus, which ultimately becomes mixed with bile and blood.
The patient suffers during the attack from a profound malaise and
vertigo, while in addition to the gastric pains the lancinating pains in
the extremities are unusually severe and agonizing. These attacks
may last for two or three days, and may recur every two weeks, but
usually the interval between them is not less than a month.
Enteralgic attacks are occasionally present in tabes, but much less
frequently than the gastric crises. These attacks consist of paroxysms
of unusually severe colic, which are often accompanied l)y diarrhocic
crises, or painful discharges from the bowels of large quantities of
watery mucus often mixed with blood.
Nephralgic attacks, the symptoms of which are almost in every respect
similar to those of renal colic have been observed in tabes in the
absence of calculi, gravel, or blood in the urine.
Affections of the Bladder and Rectum. — During the early stage of
the disease the patient often suffers from fre(iuent and painful micturi-
tion along with neuralgic pains in the depth of the pelvis, the perineum,
the neck of the bladder, or along the urethra. At other times the
bladder manifests great tolerance of its contents, most probably from
some degree of anaesthesia of the mucous membrane, and the patient
may then go a whole day without feeling any desire to evacuate his
bladder, and when he empties it at night as a matter of routine he is
surprised at the large quantity it contains. At a later stage of the
PROGRESSIVE LOCOMOTOR ATAXIA. 519
disease paresis of the bladder makes its appearance, so that emptvino-
the bladder takes an unusually lono; time, and there is some dribbling
afterwards, or there may be a moderate degree of incontinence, but
complete paralysis of the bladder only occurs in the last stage of the
disease. Dr. Buzzard has suggested that a phosphatic calculus may
readily form in tabes with bladder troubles, and he believes that many
cases of atony of the bladder, for which surgeons are consulted, are
examples of talies.
Patients complain in the early stages of tabes of peculiar sensations
in the rectum ; they sometimes feel as if a large foreign body were being
forcibly introduced in the anus, and this sensation is accompanied by a
strong desire to evacuate the contents of the bowel, while occasionally
there may be an involuntary discharge of fecal matters. Anaesthesia
of the anus and paralysis of the sphincter are, however, only present in
the later stages of the disease.
The disorders of the sexual functions consist at first of the phenomena
of irritation, but even from the beginning the voluptuous sensations are
often accompanied by slight dribbling of urine, spermatorrhoea, and
involuntary seminal emissions, while the erections are often imperfect
and accompanied by premature ejaculation. Locomotor ataxia in women
is sometimes ushered in by symptoms of genital irritation arising in the
absence of the usual sexual excitants, and consisting of erections of the
clitoris followed by a discharge of mucus.
(/) Vaso-motor and Trophic Disturbances. — Yaso-motor disorders
are not prominent features of locomotor ataxia. They are manifested
by the presence of hot or more frequently cold feet, a tendency to the
formation of cutis anserina^ mottling of the skin, increased or diminished
cutaneous secretion, and the occurrence of patches of ecchymoses on
the lower extremities during paroxysms of severe lancinating pains.
The most common trophic affections are cutaneous eruptions, such
as herpes, lichen, or bullre like those of pemphigus, these eruptions
sometimes appearing during or after every aggravated attack of lancinat-
ing pains. The nails of the great toes are liable to fall off spontaneously
during the course of tabes, and are replaced in a few weeks by ncAv and
perfectly normal nails, which may in their turn be shed a few months
later, and this process may be repeated several times in succession. All
the teeth have been known to fall out w^ithin a period of a few weeks in
the course of tabes. Perforating ulcer of the foot is most commonly
met wuth in subjects who are suffering from the earlier symptoms of
tabes. The nutrition of the muscles is usually preserved until a late
period of the disease, but occasionally some muscular groups may undergo
active atrophy in the preataxic stage. The intrinsic muscles of the
520 DISORDERS OF MOTOR CO-ORDINATION,
hand are particularly liable to be attacked, and then the hand presents
the well-known claw-form, but the muscular atrophy which complicates
tabes does not pursue the progressively invading course of that observed
in progressive muscular atrophy. Atrophy of the muscles of the hand
in tabes has several times been found associated with hemiatrophy of the
tongue.
Disorders in the Nutrition of Joints and Bones. — The arthropathies
des ataxiques of Charcot is the most remarkable trophic affection which
is met with in tabes. The joint affections always appear in the loAver
extremities during the early stage of tabes, and also in the upper ex-
tremities during the early invasion of the symptoms in them, although
the symptoms may be long established in the lower extremities, and they
also begin, almost always, during an unusually severe paroxj^sm of lan-
cinating pains. The knee-joint is the one most frequently affected, and
then in a descending order of frequency the shoulder, elboAV, hip-joint,
wrist, and the small joints of the feet and hands. Various luxations
of the joints ensue, which produce notable deformities which need not be
described here. The bones sometimes become abnormally friable, so
that spontaneous fractures are liable to occur.
[g) Cerebral and Psychical Disorders. — Vertigo is a common symp-
tom of the early stage of ataxia. This symptom is sometimes the
subjective correlative of diplojiia, or is associated with aural troubles,
but occasionally it comes on in the absence of apparent cause. Essential
vertigo is frequently accompanied by confusion of mind, an involuntary
turning of the head and eyes, and an eml)arrassment of speech which
sometimes consists of a difficulty of articulation and at other times of
a decided aphasia. These attacks are doubtless of the nature of minor
attacks of epilepsy, and we shall now see that locomotor ataxia is occa-
sionally ushered in by more decided epileptiform attacks.
Epileptiform Attacks. — The symptoms of tabes may be ushered in
by unilateral epileptiform attacks with subsequent transitory paralysis
of the convulsed limbs, while at other times the seizures are like the
petit mal or occasionally like the haut nial of idiopathic epilepsy.
Apoplectiform Attacks. — Locomotor ataxia may also be preceded or
accompanied by apoplectiform attacks similar, in every respect, to those
which are met Avith in sclerosis in patches and general paralysis of the
insane. In some of these attacks there is only a transitory loss of con-
sciousness from whicli the patient recovers without any other symptom ;
in other cases the seizure is accompanied by embarrassment of speech,
facial paralysis, brachial monoplegia, or complete hemiplegia with or
without hemianeesthesia. In these cases the recovery takes place in a
few hours or at most in a few weeks, the transitory nature of the paral-
PROGRESSIVE LOCOMOTOR ATAXIA. 521
ysis showing that it must have resulted from a functional lesion and not
from a hemorrhage or other gross lesion of the brain. Locomotor
ataxia may also be complicated with a permanent hemiplegia, and in
such cases care should be taken lest the ataxia may not be entirely over-
looked.
Psychical disorders are occasionally observed in the early stao-e of
locomotor ataxia ; the patient becomes irritable and moody and towards
the end of the disease he may suffer from hallucinations, illusions, and
weakness of memory. At other times his moral character undergoes a
great change ; he is sometimes grossly indecent, and may be guilty of
making lascivious gestures, or leaving his clothes unbuttoned in the
presence of his family. The symptoms of progressive paralysis of the
insane are frequently associated with those of tabes, and sometimes those
of the former and sometimes those of the latter take the precedence in
the order of development.
(2) The Ataxic Stage.
After one or more of the premonitory symptoms which have just
been described have been in existence for some time, the phenomena
which characterize the ataxic period of the disease make their appear-
ance. The duration of the preataxic stage varies greatly in different
cases ; in exceptional cases the ataxic gait begins at once, while in
other cases lightning pains, amaurosis, absence of patellar tendon-
reactions, and other symptoms of the disease may be in existence for a
period of from twenty to thirty years before the motor incoordination
is fully established.
Static Ataxia. — The motor disorders of tabes almost always begin
in the lower extremities, and are at first so slight that they can only be
recognized by the application of special tests. If the patient be asked to
stand up and keep his feet closely applied along their inner edges, he
may manage to maintain the erect posture with moderate steadiness Avhen
his eyes are open, but when they are closed the patient immediately
oscillates from side to side, and will fall unless he is supported or open
his eyes. A still severer test is afforded by asking the patient to stand
on one leg, first with eyes open and then closed.
As the muscular incoordination increases standing Avithout support,
even when the eyes are open, becomes increasingly difficult and finally
impossible. When the patient now stands with the aid of two sticks
it may be observed that all the extensor muscles of the body are in a
state of powerful muscular contraction. The muscles of the calf are
strongly contracted, and extend the leg upon the foot so tliat they form
522 DISORDERS OF MOTOR CO-ORDINATION.
an obtuse angle with one another, the extensors of the thigh are con-
tracted and extend the thigh upon the leg, the flexors of the thigh are
also contracted, and the foot being fixed they tend to extend the trunk
on the thigh, this tendency being greatly increased by contraction of
the gluteal muscles and of the erector sp'mx. The tendency of the
patient to fall backwards, caused by contraction of the extensor muscles,
appears to be counteracted by a voluntary contraction of the muscles
which flex the body upon the thighs. The body is thus bent forwards
so that the line of gravity falls in front of the line joining the centres
of the arches of the feet, and the tendency to fall forwards is counter-
acted by the support of the two sticks. The attitude assumed by the
patient under these circumstances is characteristic. The feet are kept
widely apart in order to widen the base, the legs are drawn backwards
so as to form an obtuse angle with the feet, the thighs are extended on
the legs, and a plumb-line let fall from each trochanter fiills considera-
bly behind the heel, the body is inclined well forwards in order to keep
the line of gravity in front of the arches of the feet, and the buttocks
project well backwards.
Ataxic G-ait. — In the early stage of tlie disease the patient nuiy
continue to walk, when once he has started, without the slightest diffi-
culty or sign of motor disorder, but he may be observed to stagger a
little on getting up suddenly from a chair, especially after sitting for
some time. X little uncertainty of gait may also be observed when he
is asked to stop walking at a given signal, and he may manifest a de-
cided stagger when in the course of a brisk walk he is asked to turn
abruptly around. The uncertainty of gait is also increased when the
patient walks in the dark or closes his eyes, when he is made to ascend
or descend stairs, or when he walks backwards.
But when the ataxia becomes more j)ronounced the gait is so charac-
teristic that it can be readily recognized without the application of
any special tests. The patient has now to direct his eyes to the ground
and to his feet while walking, and were he to close them the movements
of the legs would become disorderly, and walking would be impossible.
The attitude already described, with the tonic contractions of the ex-
tensors of the body, renders it impossible for the foot to advance Avith the
usual pendulum movement of healthy locomotion ; the passive foot is
flung forwards and outwards in one piece with a rapid jerk by a simul-
taneous contraction of the flexors of the thigh on the body and the
abductors of the thigh, and it is subsequently brought to the ground
with a thump. During the advance of the foot the heel is said by
some observers to be the last to leave the ground and the first to touch
it as the forward movement is being completed, but this mode of pro-
PROGRESSIVE LOCOMOTOR ATAXIA. 523
gression must be rare if it ever occurs. "When the foot is about to be
advanced a certain degree of flexion occurs at the knee-joint and the foot
is raised oft' the ground: the foot is then suddenly projected forwards
and outwards, and the heel is afterwards brought down with a thump
in the manner ah-eady described. In order to enable the passive leo- to
clear the ground during its forward movement, the abductor muscles of
the thigh on the side of the active leg enter into strong contraction,
and the pelvis on the side of the passive leg is thus well elevated.
The elevation of the pelvis on the side of the passive leg is indeed so
well marked that the patient is in some danger of carrying his centre
of gravity too far to the side of the active leg. In order to counteract
this tendency the upper part of the body is curved to the opposite side
by contraction of the erector spinse, and when the patient is able to
walk without the aid of sticks the arm on the side of the passive leg is
thrust out laterally, and, in order to maintain his equilibrium during
the transference of the line of gravity from one foot to the other in
walking, the trunk is strongly inclined from one side to the other, and
the arms are flung about like those of a rope-dancer. When the patient
walks by the aid of sticks, the tendency to too great a displacement of
the line of gravity towards the side of the active leg is instinctively
counteracted by an outward inclination being given to the sticks, so
that they aff'ord a lateral support.
Patients have been known to walk long distances after being; aifected
with a high degree of ataxia, but after a time the incoordination
becomes so great that the maintenance of the erect position and walking
become impossible. If the patient be now supported by two persons
under the arms whilst he tries to walk, the legs are thrust backwards
and forwards, to the right and to the left in the utmost disorder, and
are incapable of giving the least support to the body : they move, as
Trousseau remarks, like those of a puppet or a marionette. The
muscles of the trunk now become affected, and the body makes irregular,
swaying movements when the patient sits in a cliair, but even in these
advanced cases the patient when laid doAvn may be able to resist passive
movements of the limbs, and to perform the simple movements of flexion
and extension w'ith scarcely diminished poAver. When the patient now
attempts to touch an object with the tip of the foot, the line of motion
is irregular and zigzaw, and disturbed by lateral movements, while he
is quite incapable of exerting more complicated movements, such, for
•instance, as are required in describing an imaginary circle with the tip
of the great toe.
At a late period the ataxia appears in the upper extremities ; in the
cases of hereditarv ataxia described by Friedreich, the motor inco-
524 DISORDEES OF MOTOR CO - ORDINATION .
ordination appears in the npper simultaneously with, or soon after its
first manifestation in the lower extremities, but in the more usual form
of the disease ataxia of the upper extremities is rare and belongs to the
later manifestations of the disease. In ataxia of the upper extremities,
complicated and special movements, such as those required for writing
or playing the piano, are uncertain, and the irregularity becomes greater
if an attempt is made to perform them Avith closed eyes. The slighter
degrees of ataxia of the upper extremities may be tested by instructing
the patient to touch with closed eyes some part of the surface of the body,
such as the tip of the nose or lobule of one ear with the point of the fore-
finger of each hand alternately, Avhen the ataxia declares itself by the
inability of the patient to touch the intended spot until after repeated
trials. A similar uncertainty is observed when the patient is asked to
transfer a small object from one hand to the other. At a later period
of the disease the simpler movements become irregular and ataxic,
the patient fumbles in buttoning and unbuttoning his clothes, the act of
grasping is performed in an uncertain and spasmodic manner, and the
patient can only reach the object in a roundabout way and with jerky
interruptions. Static ataxia may be revealed in the upper extremities
by the inability of the patient to hold out his arms horizontally, especi-
ally when the eyes are closed. In a still more advanced stage of the
disease patients can no longer dress or feed themselves, inasmuch as
they cannot perform such simple movements as are requisite for carry-
ing a spoon to the mouth, but even under these circumstances they
may be able to exert great muscular power in resisting passive move-
ments. The ataxy may invade, as we have seen, the muscles of the
trunk, and ultimately the muscles of the neck may also be implicated,
and the head is the subject of irresular and shakinjr movements.
The electrical reactions of the muscles are not of much value in the
prognosis or diagnosis of locomotor ataxia. It is probable that in the
earlier stages of the disease there is an increase and in the later stages
a diminution of the electric contractility.
Sensory Disorders. — The girdle pains and the lightning pains of
the premonitory period are continued, as a rule, through the ataxic
stage, and often, indeed, become increased in severity as the disease
advances. The hyperaesthetic spots, however, now give place to anaes-
thesia, and an;^sthetic patches may be found on the soles of the feet,
the toes, and the back of the feet, and they may become widely diffused
over the thighs and trunk before the patient is aware of their presence.
After a time, however, the patient finds that he no longer feels the floor
distinctly, that all articles which he touches have a velvety feel, and
that he cannot hold small objects in his fingers. Every variety of
PROGEESSIVE LOCOMOTOR ATAXIA. 525
paralysis of sensation and every combination of these are met with in
the late stages of the affection, but probably analgesia is the most
frequent. Occasionally, however, the sensibility to pain is retained, or
even increased, while there is a diminution of sensibility to some or all
\arieties of touch, and again, partial paralysis of the sense of touch
may be combined with analgesia and hyperalgesia, or with hypera;s-
thesia towards impressions of temperature. At a late period of the
lisease a distinct retardation of the conduction of sensations, especialh^
■A' impressions of pain, is observed, and this may also be found in the
earlier stages. The prick of a pin frequently gives rise to a double
sensation, the first of touch and the second of pain, and the sense of
temperature may also be retarded. The sensation of pain continues
fi)r a relatively long time, even when its cause has only been of
momentary duration, and the highest degree is not reached until several
seconds after the pain has begun. In circumscribed areas of the skin
of the foot the patient may feel two points when only one is touching
the skin, and when two points are in contact four or five may be felt.
In some cases the patient is not sure which side of the body is touched
when the eyes are closed, even although the cutaneous sensibility is
more or less completely retained. In the early stage of the disease
the disorders of the muscular sensibility and muscular sense declare
themselves by a feeling; of fatigue and the sensation termed the
"fidgets," but as the disease advances the muscular sense becomes
diminished, and consequently the power of recognizing what muscles
are thrown into action is lessened in a corresponding degree. After a
time the patient, when his eyes are closed, cannot tell the position of
his lower extremities, and has lost the power of recognizing small
weights, and of discriminating the differences of Aveights.
Visceral Disorders. — The gastralgise are seldom so distressing in the
second as in the first stage of the disease, but the genito-urinary symp-
toms become much more urgent and troublesome. The sexual weak-
ness of the early stage now advances to complete impotence, and the
dribbling of urine, which was at first an occasional symptom, now
becomes habitual, while in some cases there is so much antesthesia of
the urethra that the urine may pass in a full stream without the patient's
knowledge. In other cases the patient is unable to evacuate the l)lad-
der, Avhich becomes so distended as to require the use of the catheter.
The tenesmus and neuralgiform pains about the rectum, which were
present in the first stage of the disease, now give place to anaesthesia,
and then there may be an unconscious passage of the stools, which,
indeed, would be a much more frequent symptom if it was not for the
high degree of constipation which is usually present.
526 DISORDERS OF MOTOR CO - O RDIN ATIOX .
Trophic disorders are not liable to occur in this stage of the disease,
but the skin of the lower extremities may become dry and covered by
furfuraceous scales, and patches of ichthyosis may form over the toes
and metatarsal bones, and the muscles of the lower extremities may
noAV undero-o diffused Avastino-.
(3) The Paralytic Staue.
In the terminal period of locomotor ataxia the motor incoordination
has increased to such an extent that the patient is quite unable to walk,
and he is consequently obliged to sit propped up in an armchair, or to lie
helplessly in bed ; but even when he is quite unable to stand, the indi-
vidual movements of the lower extremities may be performed with
scarcely diminished power. But after a time even the power of per-
forming separate movements is diminished, and the muscles undergo
diffused atrophy, are soft and flaccid, and no tension is provoked on
passive movements of the limbs. The anaesthesia to pain and touch is
now complete, the patient is quite unable to tell the position of his limbs
in bed without the aid of sight ; but the sense of temperature may still
remain nearly normal. The patient also suffers from incontinence of
urine ; the stools pass unconsciously ; bedsores appear on the sacrum ;
chronic cystitis supervenes ; and the patient dies in a state of great
marasmus, as in other forms of myelitis. In other cases the disease ma}''
progress ujiwards and implicate the medulla oblongata, and the patient
dies from respiratory troubles, or diflSculties of deglutition. At other
times cerebral symptoms may supervene, and the patient, after being
delirious for a few days, dies comatose. But the disease runs its full
course only on rare occasions, and in the majority of cases the patient
dies from an intercurrent disease such as acute pneumonia, phthisis,
or cardiac complication. The course of locomotor ataxia is usually slow
and chronic ; it often extends over a period of many years, and even the
initial stage, with lancinating pains, may last more than twenty years. In
the majority of typical cases the average duration of life appears to be
from eight to twelve years, but a few cases run a rapid course, these
having been described under the name of acute ataxia.
Varieties. — The following clinical varieties of locomotor ataxia may
be distinguished :
(1) The typical form of tabes, which begins with lancinating and girdle
pains, loss of patellar tendon-reactions, and disorders of the oculo-
motor nerves, and runs through the preataxic, ataxic, and paralytic
stages which have been described.
PEOGRESSIVE LOCOMOTOR ATAXIA. 527
(2) Hereditary Tabes. — This form of tabes was first described by
Friedreich. The disease begins between the ages of twelve and eighteen
years ; it is usually remarkably protracted, extending sometimes over a
period of thirty years ; several members of the same family are liable
to be affected, and the female members appear to be attacked by prefer-
ence. Lancinating pains and other sensory disorders are never well
marked and are often absent ; the ataxia begins at an early period and
attacks the upper extremities simultaneously with or soon after the lower
extremities. Disorders of articulation, and ataxic nystagmus are
generally present, and the tendon-reactions are lost ; but static ataxia,
bedsores, psychical disorders, tremor, and amaurosis are generally absent ;
while muscular atrophy, paresis, contractures, 'and weakness of the
bladder appear only in the last stage. The symptoms of this group
are very variable and the cases included in it are probably more allied
to sclerosis in patches than to locomotor ataxia.
(3) Anomalous Form. — This variety comprises the form in which
are present arthropathies, muscular atrophy, tremors of the upper ex-
tremities, psychical disorders, or any other prominent symptom which
does not belong to the typical disease.
(4) Paraplegic Form. — In some cases the symptoms of tabes are
obscured by the presence of paraplegia. The presence of paralysis
with muscular tension may lead the observer to believe that the case is
one of ordinary paraplegia, but in such cases the patellar tendon-reac-
tions are usually absent, instead of being exaggerated, as in ordinary
paraplegia. These cases will be subsequentl}^ described under the name
of posterior and lateral sclerosis.
(5) Neuralgic Form. — The lancinating pains are very violent and
distressing in this form, and these pains and the absence of the patellar
tendon-reactions may be the only symptoms present for upwards of
twenty years, and consequently this variety has been named " tahes
dolorosa'' or "abortive locomotor ataxia." Amaurotic tahes belongs
to this variety, inasmuch as white atrophy with blindness may exist for
very many years without any other symptom except absence of the
patellar tendon-reactions.
(6) Hemiataxia. — The ataxic symptoms may in rare cases be much
more pronounced on one side of the body than on the other.
(7) Meningitic Form. — When locomotor ataxia is complicated with
spinal meningitis the typical symptoms of tabes are apt to be compli-
cated by pain in the back, and along the vertebral column, spinal
tenderness, and diffused or circumscribed cutaneous hyperaesthesia.
528 DISOEDEKS OF MOTOR CO-ORDINATION,
5. COMBINED SCLEROSIS OF THE POSTERIOE AND LATERAL
COLUMNS.
Symptoms. — The symptoms of locomotor ataxia and of primary
lateral sclerosis may be present in every possible combination, those of
the former disease predominating at one time and those of the latter at
another.
The symptoms Avhich indicate that the lateral columns are being
gradually invaded in cases of locomotor ataxia are spontaneous jerkings
in the lower extremities, gradual loss of power to perform simple move-
ments of extension and flexion, muscular tension, and contractures.
When the symptoms of lateral sclerosis predominate, the signs ])y which
a complication of locomotor ataxia may be suspected are the presence
of lancinating pains, girdle pains, and other sensory disturbances, vesical
Aveakness, slight swaying on closing the eyes, and, above all, the absence
of the patellar tendon-reaction and ankle-clonus. Two cases came
under my observation in Avhich the symptoms of pure lateral sclerosis
Avith exaggerated tendon-reactions present in the lower extremities were
accompanied by extreme myosis of both pupils, and it is probable that
there was a combination of sclerosis of the lateral columns, and of the
posterior columns in the upper segment of the cord.
6. DISEASES OF THE CEREBELLUM.
The diseases of the cerebellum consist of hemorrhage, abscess, and
tumors.
Symptoms. — The general symptoms of cerebellar disease consist of
headache, Avhich is more frequently situated in the occiput and only
occasionally in the forehead, vomiting, vertigo, unsteadiness on stand-
ing Avhich increases Avhen the eyes are closed, and a reeling gait. In
hemorrhage the symptoms come on suddenly, and when a large clot
forms the patient suffers from apoplectic symptoms, and death may occur
rapidly from pressure on the pons and medulla oblongata. Abscess of
the cerebellum generally results from disease of the middle ear, Avhile a
tumor declares itself by the gradual onset of the symptoms or by the
presence of double optic neuritis, Avhich is frequently accompanied by
amblyopia or even complete blindness.
Stationary lesions in the cerebellum may be of large size without
giving rise to any recognizable symptoms. Progressive lesions cause
different symptoms according to the situation of the lesion. When the
lesion is situated in the upper part of the middle lobe the patient has a
DISEASES OF THE CEREBELLUM. 529
Staggering gait, and manifests a tendency to fall backwards, and when
it is situated in the inferior part of the middle lobe it is probable that
the tendency is to fall forwards, or to revolve round a horizontal axis.
Tumors situated near the upper part of the middle lobe give rise to a
tonic contraction of the muscles of the neck which causes retraction of
the head. The muscles of the trunk and extremities may likewise be
implicated in the spasm, and the patient then suffers from tetaniform
seizures, during which the head is retracted, the body arched backwards,
the lower extremities extended, and the upper strongly flexed as in teta-
nus. All lesions attended with an increase of size, like abscesses and
tumors, must exert pressure forwards on the pons, inasmuch as the or^an
is limited above by the unyielding tentorium and behind and below by
the occiptal bones. The consequence is that abscesses and tumors of
the cerebellum are often attended by slight weakness of the limbs with
increase of the tendon-reactions. The long course of the sixth nerves
in front of the pons to reach the cavernous sinus renders one or other
of them liable to be paralyzed in tumors of the middle lobe. Cases of
tumor of the middle lobe are met with in which the patellar tendon-
reactions are absent without any disease being found in the spinal cord.
It is possible that in these cases there is an increase of the spinal fluid,
owing to obliteration of the foramen of Magendie, which forms the com-
munication between the spinal and cerebral subarachanoid spaces.
Tumors of the cerebellum are also sometimes attended by numbness and
tingling of the trunk and extremities, but only rarely by amTesthesia,
and one or more of the cranial nerves may be more or less paralyzed.
Movements of the eyeballs are frequently observed in cases of tumor
of the middle lobe of the cerebellum. These movements may be ver-
tical, horizontal, or oblique, and are generally parallel. At times they
are only observed during a tetaniform seizure, but Avhen there is per-
manent rigidity the eyes may be rotated in one direction and fixed, or
slight parallel oscillatory movements may be present. When the lesion
is situated in one of the lateral lobes or in one of the middle peduncles,
there is a tendency to fall towards the side of the lesion. If a tumor
is growing slowly, the tendency to fall to one side is counteracted by
cerebral action to such an extent that this symptom is not readily
elicited, but when the patient turns suddenly round, especially with
closed eyes, a slight stagger may be observed, or the statement of the
patient may indicate to which side he has a tendency to fall. A tumor
of one lateral lobe may also encroach upon the middle lobe, and then
the tendency to stagger to one side is accompanied by a tendency to
fall backwards, so that the patient now manifests an inclination to fall
backwards and to one side in a diagonal direction. If the tumor grows
34
530 DISORDERS OF MOTOR CO-ORDINATION.
forwards so as to encroach upon the hiteral half of the pons, some of
the cranial nerves become paralyzed, while the sensory and motor tracts
may be more or less compressed. In such a case paralysis of the sen-
sory and motor branches of the trigeminus may be present either separ-
ately or combined, along with more or less hemiplegia of the opposite side.
Much more frequently the patient becomes completely deaf on the side
of the lesion from compression of the auditory nerve, facial paralysis is
then established, and the external rectus of the eyeball is the last to be
affected. If the growth begins in the pons the sixth or seventh nerves
are the first to be affected, and the auditory nerve last. If the growth
encroaches upon the pyramidal tract hemiplegia of the opposite side,
with or without some degree of anaesthesia, accompanies deafness and
peripheral facial paralysis on the same side as the lesion. The para-
lytic phenomena may be preceded by spasmodic contractions of the
masticatory, facial, or ocular muscles. Instead of paralysis of the
external rectus of the eyeball on the side of the lesion, there may be a
conjugate deviation of the eyes, which is directed towards the diseased
side when the lesion is irritative, and away from it when it is destructive.
The symptoms caused by lesion of the inferior peduncle of the cere-
bellum are not well ascertained. In a case in which I suspected a
hemorrhage of the restiform body where it joins the inferior peduncle,
the symptoms were paralytic myosis and diminution of the palpebral
fissure, and partial anaesthesia of the face on the side of the lesion,
and partial hemiplegia with well-marked hemianesthesia on the opposite
side. Although the patient could move the partially paralyzed limbs
pretty freely in bed, he was totally unable to stand without support ;
he had, indeed, to be supported on both sides in order to be kept erect,
and it seemed as if he had an equal tendency to fall backwards, for-
wards, and to either side. On attempting to walk the head was drawn
slightly backwards, and the eyes were directed upwards, the body was in-
clined to the paralyzed side until it was at an angle of about sixty degrees
to the floor, and as each foot was moved forwards it was raised about
eighteen inches from the ground, and the patient had the greatest diffi-
culty in disentangling it from the leg which was planted on the ground.
Sometimes he raised the feet alternately in the most ridiculous manner
without moving forwards at all. When he attempted to lie down, after
being placed sitting on the edge of the bed, his head became rotated
towards the side of the lesion, and by the time his body reached the
bed his face was directed towards the pillow. On some occasions the
patient on making a semi-revolution round his longitudinal axis, worked
his way back, but not without considerable difficulty, until he got on his
back, while at other times he only got on his back after making a com-
DISEASES OF THE CEREBELLUM. 531
plete revolution. He never manifested a tendency to revolve on his
longitudinal axis when once laid on his back.
The symptoms caused by lesion of the superior peduncle of the cere-
bellum are also not well known. The proximity of these peduncles to
the corpora quadrigemina renders it probable that they would give rise
to unilateral or bilateral disorders of vision, and it is not unlikely that
the eyeballs might be found on different levels, the one being directed a
little upwards and outwards, and the other a little downwards and out-
wards. Lesions in this situation might also be expected to give rise to
disorders of the third nerve.
Morbid Anatomy. — In aural vertigo the lesion was thought by
Meniere to be limited to the semicircular canal and vestibule, but
Knapp thinks that all parts of the labyrinth are involved. The dis-
ease of the labyrinth may be primary or secondary to affections of the
tympanic or cranial cavity. The primary affections of the labyrinth
are (1) hemorrhage from suppression of the menses, severe attacks of
fever, or fractures of the petrous portion of the temporal bone ; (2) serous
effusion in specific forms ; and (3) the formation of pus as a complica-
tion of purulent meningitis. When aural vertigo is an early symptom
of locomotor ataxia the lesion is most probably a parenchymatous
neuritis of the auditory nerve. The secondary diseases of the labyrinth
are set up by an extension to it of inflammation in cases of acute and
chronic catarrh of the middle ear. All that is known of the morbid
anatomy of primary sclerosis of the columns of Goll has been men-
tioned along with the description of the symptoms, while the secondary
sclerosis of these columns and of the direct cerebellar tracts has already
been considered.
In locomotor ataxia the spinal pia mater, especially in the posterior
aspect of the cord, is often thickened, cloudy, and connected to the
dura mater by numerous adhesions, while the spinal fluid is increased.
The cord is generally of an increased consistence, although it has occa-
sionally been found softened, and it is often flattened from before back-
wards owing to the atrophy of the posterior columns, while a grayish-
yellow discoloration may be observed extending the whole length of
the cord along the posterior median fissure. On making transverse
section the posterior columns are seen to be of a grayish color and
diminished in size, and the posterior gray horns and posterior roots
have also Ijeen found atrophied. The degeneration is not, as a rule,
uniformly distributed over the whole transverse area of the posterior
columns. The intensity and extent of the lesion, in long-standing cases,
are greatest in the upper lumbar and dorsal regions, when it occupies
the whole transverse section of the posterior columns. In the inferior
532
DISORDEKS OF MOTOR CO - ORDINATION
portion of tlie lumbar region there is frequently only a slight gray dis-
coloration in the external half of the posterior columns, while in the
upper dorsal and cervical regions the area of the lesion becomes again
restricted, and in the upper cervical region the columns of Goll are
alone affected. In long-standing cases the posterior gray horns may be
found shrivelled and distorted, and the posterior roots wasted, while the
direct cerebellar tracts may likewise be affected, and in a few cases the
anterior gray horns have been implicated. In very protracted cases
the whole transverse area of certain portions of the cord may be found,
on section, transformed into a gray translucent mass. But when a
Fig. 169.
V^v
A ^
Teassverse Section of the LxniBAR Region, from a Case of Locomotok Ataxia, (.omplicated
WITH MuSCDLAtt ATROPHY. (CHARCOT and PlERRET.)
A, A, Sclerosis of tlie posterior root-zone ; C, Left anterior gray horn, healthy ; D, Right anterior
gray horn in a state of atrophy
patient, suffering from lancinating pains and other symptoms of abor-
tive tabes, dies from some intercurrent disease, the sclerosis is limited
to the root-zones of the posterior columns, and the columns of Goll
are free from disease (Fig. 1(39).
On microscopical examination of the portions of the cord which have
undergone sclerosis, the interstitial tissue is found increased in amount,
the nuclei and Deiter's cells are increased in number, the walls of the
vessels are thickened, and corpora amylacea and granule cells are scat-
DISEASES OF THE CEREBELLUM. 533
tered tliroughout the tissue, the nerve fibres are thin and wasted, and
many of them have disappeared, while in the later stages of the disease
the tissue is converted into a firm fibrillary, often wavy connective
tissue, in which only a few traces of nerve fibres are left.
The ganglion cells of the posterior gray horns are often found pig-
mented, but the ganglion cells in Clarke's columns are unaffected although
a number of fine, apparently degenerated, nerve fibres may be seen to
pass through and around them. The degenerative process sometimes
extends to the anterior gray horns, and the motor ganglion cells and
anterior roots are then seen to be atrophied. Degenerative changes
have likewise been discovered in the peripheral nerves and the posterior
roots, and cases have recently been recorded which render it probable
that the morbid changes of tabes begin in the afferent fibres of the
peripheral nerves. The optic nerves are sometimes found atrophied,
and morbid changes have occasionally been found in the ocular motor
and hypo-glossal nerves, while the roots of the pneumogastric nerves
have been found atrophied in cases of tabes Avith laryngeal crises. The
nuclei of origin of the cranial nerves on the floor of the fourth ventricle
and the floor of the aqueduct of Sylvius are occasionally involved in
the disease. When arthropathies form part of the disease the articular
cartilages of the affected joints are destroyed, while the articular ends
of some of the bones are eroded. In cases of combined lateral and
posterior sclerosis the lateral as well as the posterior columns are in a
state of sclerosis. In some cases the posterior sclerosis does not reach
downwards as far as the lumbar region and in these the patellar tendon-
reactions are exaggerated.
The diseases of the cerebellum consist of hemorrhage, softening,
abscesses, and morbid growths ; but inasmuch as their morbid anatomy is
the same as that of other parts of the brain it is unnecessary to consider
them further at present. The tumors most frequently met with, especially
in young people, are tubercular growths and glioma.
Morbid Physiology. — Meniere's disease is caused by a primary or
secondary disease of the semicircular canals, and the most consistent
theory of their functions is that they are peripheral end-organs of
afferent fibres, Avhose central end-organ is the cerebellum. As we have
seen, the cerebellum is an organ for adjusting the body to space relations,
and disease of the peripheral end-organs throws the whole of this
mechanism into disorder, and consequently the patient is unable to effect
those delicately coordinated muscular contractions which are required
for maintaining various attitudes in space, and vertigo is the subjective
correlative of this objective fact.
The case of primary sclerosis of the columns of Goll, recorded by
584 DISORDERS OF MOTOR CO-ORDINATION.
Pierret would seem to indicate that these columns take some part in the
function of equilibration in space. The fact that these columns and the
direct cerebellar tracts undergo an ascending sclerosis proves that they
are centripetal conducting paths, and the fact that the former terminates
indirectly and the latter directly in the cerebellum appears to show that
both tracts consist of cerebello-afferent fibres. It is, therefore, likely that
the columns of Goll and the direct cerebellar tracts conduct centripetal
impulses to the cerebellum, but Avhen sclerosis of these tracts is caused
by a transverse myelitis, the symptoms which might be caused by disease
of them are obscured by the paralysis which is caused -by arrest of con-
duction through the pyramidal tract.
In locomotor ataxia the primary lesion is most probably situated in
the posterior root-zones of the spinal cord, and in the homologues of
these tracts in the medulla oblongata, pons, and crura cerebri ; namely,
the fasciculus rotundus, and the ascending and descending roots of the
fifth nerves. It is, indeed, supposed by Dejerine that the primary
changes begin in the peripheral nerves and ascend through the posterior
roots to the spinal cord, and it is at least certain that the nerves of
special sense are primarily affected in this peripheral manner. But eyon
if the primary changes begin in the peripheral nerves, there can be little
doubt that those portions of the posterior columns through which the
afferent fibres pass to reach the posterior gray horns are involved in the
disease at a very early period. As the disease of the posterior root-
zones extends horizontally towards the posterior median fissure, the
columns of Goll become implicated, and when once the fibres of these
columns are interrupted in any part of their course the portions above
the seat of the lesion undergo degeneration, and in advanced cases these
columns are always found in a state of sclerosis throughout their entire
length. The direct cerebellar tracts are also found in a state of degenera-
tion in long-standing cases, and in some cases the morbid process is
observed to have extended to the posterior gray horns, the anterior gray
horns, and the lateral columns. The lancinating pains may be ex-
plained by the irritation of the fibres of the posterior roots in their
passage through the posterior columns, while the subsequent anjiestliesia
may be supposed to be caused by destruction of these fibres. Irritation
of the posterior gray horns causes the cutaneous trophic changes, while
destructive lesions of these horns causes retardation of painful impres-
sions and analgesia. Extension of the lesion to the lateral columns
causes the paraplegia which sometimes complicates tabes, while impli-
cation of the anterior gray horns causes the muscular atrophy and
probably also the arthropathies of locomotor ataxia. Disease of the
automatic centres in the lumbar region causes the vesical and sexual
DISEASES OF THE CEREBELLUM. 535
disorders. Parenchymatous atrophy of the optic nerves causes blindness
and white atrophy of the optic disks, and it is pr()bal)le that the disorders
of the other special senses, occasionally observed, are caused by degenera-
tion of the respective nerves. Absence of the patellar tendon-reaction
is caused by disease of the afferent portion of the reflex arc in its
passage through the posterior columns; while reflex pupillary immo-
bility is caused by lesion of the fibres of the reflex loop which connect
the afferent fibres in the optic tract with the efferent fibres in the third
nerve. The fibres of this reflex loop proceed from the anterior tubercle
of the corpora quadrigemina to the nucleus of the third nerve, and in
their course they pass through or near the descending root of the fifth
nerve, which is as we have seen the honiologue of the posterior root-
zone of the cord. The other symptoms which are observed in the region
of the cranial motor nerves may be explained by sclerosis of the fasciculus
rotundus and ascending root of the fifth nerve and by an extension of
the morl>id process from these bundles of nerve fibres to the nuclei
themselves. The sympathetic oculo-pupillary symptoms are caused by
irritation, or more frequently by paralysis, of the fibres which proceed
from the dilator nucleus through the cervical portion of the cord to
emerge with the eighth cervical and first dorsal anterior nerve-roots.
These fibres descend most probably in the posterior root-zones of the
cervical region of the cord, and are consequently liable to be implicated
in the disease at an early period.
It now remains for us to explain the phenomena of static and dynamic
ataxia. Leyden first suggested that the ataxia was the result of the
disorders of sensibility which are present in this disease, but this theory
fails to account for the well-ascertained clinical fact that, on the one
hand, a slight degree of ataxia may be present in the almost entire absence
of sensory disorders, while, on the other, there may be an absence of
ataxia with a high degree of anaesthesia. It was suggested by Erb and
others that the ataxia was caused by disease of motor or centrifugal
paths, but this view is not supported by any well-ascertained physiological
or pathological facts. It seems probable that the ataxia is caused by
disease of afferent subconscious paths. These paths consist of afterent
spinal, afferent cerebellar, and afferent subconscious cerebral tracts.
The posterior root-zones themselves constitute, most probably, afferent
spinal paths for coordinating various reflex movements, but it is prob-
able that static ataxia is never present until the columns of Goll, or the
direct cerebellar tracts are implicated in the disease. It has been
suggested by Althaus that dynamic ataxia is caused by disease of the
afferent conducting paths of the basal cerebral ganglia, but the tension
of the extensors of the body which is present in tabes, when the patient
536 DISORDERS OF ilOTOR CO - 0RDI:N^ ATION.
assumes the erect posture, would seem to take an active part in the pro-
duction of the ataxic gait. This tension is caused most likely by irrita-
tion of cerebello-afferent paths and consequently irritation of these
paths is likely to be one of the main causes of the ataxic gait. When
the patient is unable to maintain the erect posture the extensors of the
body have lost their tension, and it may then be presumed that these
paths are more or less destroyed and that cerebellar paralysis is estab-
lished for lack of communication with the external world. All that
can be said with regard to the manner in which disease of the cerebellum
causes the symptoms, is implied in what has already been said respecting
the physiology of the organ.
Treatment. — When Meniere's disease depends upon morbid changes
in the middle ear the patient should be placed under the care of the
aural surgeon, and when the local disease is not accessible to treatment
relief may be obtained by rest in the recumbent posture. The adminis-
tration of quinine in doses of from ten to twelve grains three times a
day for some days appears to have produced great amelioration of the
symptoms in some cases. At first the subjective aural sounds caused
by the quinine are superadded to those of the disease, and the symp-
toms are intensified, but if the quinine be omitted for eight or ten days
the sounds and the vertigo undergo notable diminution. If the quinine
be readministered for a period of eight or ten days the symptoins arc
again aggravated, to be followed by a second amelioration on its cessation,
and after "a time the attacks of vertigo may be completely arrested.
Large doses of salicylate of sodium have also proven useful in the treat-
ment of the disease.
Primary sclerosis of the columns of Goll requires to be treated by
rest in the recumbent posture along with the remedies used for other
forms of chronic myelitis, while secondary sclerosis of these columns
and of the direct cerebellar tracts does not admit of treatment ai)art
from the primary disease of the cord which has caused the sclerosis.
Locomotor ataxia is so frequently preceded by syphilitic infection
that in all cases of the disease the most careful investigation should be
instituted with the view of discovering any indication 'of the presence
of this poison. In every case in which a history of syphilis can be
detected, and in all doubtful cases, iodide of potassium in ten grain
doses three times a day should be given, and if there are any active
syphilitic symptoms present other than the ataxia, the patient should
have a mercurial course. Cases of locomotor ataxia which are comj)li-
cated by spinal meningitis are also benefited by the administration of
iodide of potassium. But even when locomotor ataxia is of syphilitic
origin the nervous disease pursues, after a time, an independent course,
and consequently when the patient has been subjected to a thorough
DISEASES OF THE CEEEBELLUM. 537
antisyphilitic treatment, or when the absence of syphilis has been
proved from the first, other methods of treatment must l)e adopted.
Of internal remedies nitrate of silver, given in doses of one-sixth to
one-third of a grain three times a day is probably the most generally
useful. It may be continued for three weeks at a time, and then after
an interruption of two Aveeks its use may be resumed for another three
weeks. The use of the remedy may be continued in this way with
repeated interruptions for many months without producing deleterious
effects. If the skin shows the slightest discoloration, the medicine
must, of course, be interrupted for a longer period. Belladonna, arsenic,
chloride of gold and sodium, and chloride of barium have also been
employed in the treatment of tabes, but not apparently with much
success. The administration of ergot is sometimes beneficial, but it
ought to be given with caution, as diseased rye is known to cause scle-
rosis of the posterior columns of the cord. Phosphorus, either alone or
with cod-liver oil, has sometimes been found useful. Strychnine is
always useless and dangerous.
Thermal baths may be soothing to the patient during severe attacks
of lancinating pains, but they do not appear to exercise a favorable
influence over the course of the disease.
Saline thermal baths appear to act favorably, and those of Rheims
and Nanheim have been favorably reported upon. Sulphur, chaly-
beate, and mud baths have been employed, but it is doubtful whether
they do any good except by improving the general health of the patient.
Hydr other a'peutics, as carried out in well-conducted hydropathic
establishments, is a very useful adjunct in the treatment of many cases
of tabes. The institution should be situated in an elevated region, so
that the patient may have the advantage of a pure mountain air. This
treatment answers best in the summer season. The wet pack should
be used with caution, beginning with a temperature of 88° F. and
going down to 77° F. Wet rubbings are useful, beginning Avith a
temperature of 77° F. and going down to 65° F.
Electrical treatment exercises a favorable influence on the progress
of the disease. The constant current is usually employed, and both
electrodes should be placed on the vertebral column — one in the lumbar
region and the other at the nucha. One pole, say the lower, should be
fixed and the other slowly moved along the back so as to come in
contact with every part of the vertebral column ; then the upper pole
should be fixed, and the lower one slowly moved along tlie back. The
direction of the current is of no consequence. The current should be
applied daily, but each sitting should not be for more than from three
to six minutes' duration. Strong currents should be avoided, especi-
538 DISOEDERS OF MOTOR CO - O R DIN ATIOX .
ally in irritable persons with severe pains. The application of the
fai-adic brush to the surface of the body is useful when there is marked
anaesthesia. The positive pole should be placed on the sternum, and
the negative pole, with the brush, drawn repeatedly along the vertebral
column and then along the extremities.
Favorable results have been obtained by Dr. Mortimer Granville by
means of nerve vibration, I have given a trial to this treatment in
some cases, and found it very grateful to the patients, although I cannot
say that it appeared to be of much use in other respects.
Nerve-stretching has been used as a means of treatment in locomotor
ataxia. It is possible that the lancinating pains may be rendered more
tolerable by this treatment, but after witnessing the effects of the treat-
ment in a few cases, I am not disposed to hazard further trial of it
myself or to recommend it to others.
The treatment of tabes b}" complete rest in the recumbent position,
which was first reconun ended by Dr. S. Weir Mitchell, appears to be
one of the most successful methods which can be adopted, but it is only
in exceptional cases that patients can be induced to lie in bed for any
considerable period of time so long as they are able to move about at all.
Amongst various remedies which have been used against the lancinat-
ing pains may be mentioned sinapisms, blisters, Avarmth, Priessnitz's cold-
water compresses, belladonna plasters, chloroform and other liniments,
faradization or galvanization of the hypeniesthetic spots (stabile anode),
subcutaneous injections of morphine, and large doses of the bromide of
potassium, or of the hydrobromate of quinine, and large doses of iodide
of potassium when the symptoms indicate the presence of meningitis.
One patient told me that he found most relief from the lancinating
pains by hot ironing the painful joints. AVhen antesthesia is present
cutaneous faradization may be employed with benefit.
In vesical weakness faradization of the bladder, either with or with-
out the aid of the bladder electrode, may be usefully employed. Cystitis
must be treated in the same way as in chronic myelitis.
Constipation must be combated by mild aperients, enemata, and
regulation of diet, or by fiiradization.
The treatment of the diseases of the cerebellum must depend upon
the nature of the lesion. In hemorrhage the treatment is the same as
for cerebral hemorrhage, and it seems to me that there may be a possi-
bility of our being able, in some cases, to evacuate the pus through the
temporal bone. In tubercular growths, glioma, and other tumors, little
can be done beyond palliative treatment, unless, indeed, the growth be
of syphilitic origin, when an energetic antisyphilitic treatment may
procure partial or, on rare occasions, more or less complete recovery.
CHAPTER X.
VASCULAR DISEASES OF THE SPINAL CORD.
I. ANEMIA, THKOMBOSIS, AND EMBOLISM OF THE SPINAL
CORD (MYELOMALACIA, VASCULAR SPINAL SCLEROSIS).
Etiology. — The predisposing causes of spinal antemia are congenital
narrowness of the calibre of the vessels, weakness of the heart, and
undue excitability of the vaso-motor nerves giving rise to vascular
spasm. Anaemia of the cord is often only an expression of general
anjBmia caused by hemorrhages, and dyscrasic conditions like chlorosis,
pernicious anaemia, and other cachectic diseases. Spinal ansemia occurs
much more frequently in the female than in the male sex. In some
cases the anaemia is caused by extensive atheromatous changes of the
spinal bloodvessels, or by the arterio-capillary fibrosis which accompanies
chronic interstitial nephritis. When the vessels are extensively changed
by atheroma, thrombosis may take place to such an extent that softening
occurs, a condition Avhich has been named myelomalacia, but arterio-
capillary fibrosis is more likely to give rise to sclerosis of the walls of
the vessels and of the tissues in their immediate vicinity, a condition
which may be named diffused vascular sclerosis. The anastomosis of
the spinal vessels is so free that embolism of them is not likely to give
rise to extensive softening, but the multiple embolism which occurs in
cases of chorea sometimes gives rise to small spots of necrotic softening
in the cord. The greatest degree of ansemia of the spinal cord is
caused by compression, thrombosis, or embolism of the abdominal aorta
above the point of origin of the lumbar arteries.
Symptoms. — When the abdominal aorta is suddenly obliterated by a
large embolus the lower extremities become quickly paralyzed, and
every form of sensibility is lost in them ; the reflex excitability and the
tendon-reactions are also abolished, and the bladder and rectum are
paralyzed. If the obliteration of the aorta takes place more slowly
the symptoms develop gradually and are less severe; they consist of
a feeling of numbness in the lower extremities, which also feel weak
and easily tired on slight exertion. Nothing is known of the symptoms
caused by ischsemia of the cervical region of the spinal cord. The
ischaemia caused by vaso-motor spasm is characterized by the same
540 VASCULAR DISEASES OF THE SPINAL CORD.
kind of symptoms as those resulting from aortic obstruction, although
they are much less severe in the former than in the latter. In this
form of anaemia some source of peripheral irritation can usually be
discovered, and the paralytic symptoms generally disappear if the
source of irritation be removed.
In the spinal ansemia which results from general causes the most
constant symptoms are motor weakness, first in the lower and subse-
quently in the upper extremities, and tremor on the slightest exertion,
and in some cases complete paralysis may be developed. The sensory
disorders consist of various parsesthesije, pain, hyperesthesia, and, on
rare occasions, a slight degree of amvsthesia. The cutaneous reflexes
and tendon-reactions are often exaggerated, and the sphincters are not,
as a rule, affected. It is said that the symptoms improve on lying
doAvn, and on the contrary are made worse when the patient assumes
the erect posture. The spinal symptoms are associated with the usual
symptoms of general anaemia or of chloi'osis.
In myelomalacia the symptoms are very obscure. The patient first
complains of numbness and feebleness of the lower extremities, and
these symptoms gradually increase in intensity until ultimately anaes-
thesia and complete paralysis of the lower extremities are fully estab-
lished. The cutaneous reflexes are also diminished and finally abol-
ished in the loAver extremities, but the patellar tendon-reactions may
be retained for a long time. As the disease advances the spliincters of
the bladder and rectum become gradually paralyzed, and ultimately the
patient dies from bedsores, marasnms, and pyaemia. Hypemesthesia,
spasms, or increase of the cutaneous reflexes, are said to be absent
throughout the course of the disease.
In diffused vascular sclerosis the symptoms pursue a chronic course,
and are for a long time like those of a primary lateral sclerosis, with
an admixture of indefinite sensory disorders. The sphincters are not
affected until a late period of the disease.
II. HYPEK.EMIA AND HEMORRHAGE OF THE SPIXAL CORD.
1. Spinal Hyper/EMIa.
Etiology. — Hyperaemia of the cord is produced by excessive func-
tional activity, such as occurs in severe exertion or violent sexual ex-
citement. Congestion being present in the early stages of inflamma-
tion, all the causes of myelitis likewise give rise to hyperaemia. It
may also be caused by various toxic agents, such as strychnine, carbonic
HYPER.EMIA AND HEMORRHAGE OF SPINAL CORD. 541
oxide, and alcoholic excess. Passive hypersemia- is caused by those
conditions which flivor general venous congestion, such as diseases of
the heart and lungs, or convulsive diseases like tetanus, epilepsy, and
eclampsia.
Symptoms. — The most prominent symptoms of spinal hypersemia
are pains in the loins, and along the spine, of a dull oppressive char-
acter, and which are not increased on pressure. The patient com-
plains of tingling, formication, and tearing pains in the lower extremi-
ties, and a slight degree of hyper?esthesia of the skin, a girdle sensation,
and a moderate increase of reflex activity may be present. The motor
symptoms consist of transitory jerking of the muscles and trembling of
the limbs, and Rosenthal says that the electrical excitability is increased.
In severer cases the patient complains of numbness in the lower ex-
tremities, the limbs feel heavy and feeble, and the patient feels tired on
slight exertion, but complete paraplegia probably never occurs. The
sensory and motor disorders may occasionally implicate the upper
extremities, and in those cases respiration is said to have been disturbed.
The symptoms are said by Brown-Sequard to be aggravated by lying
on the back with the head and legs raised, while they are relieved by
lying on the ftice, standing or walking, and the patients are said to feel
worse before getting up in the morning. If the congestion is sufficiently
intense to give rise to serous effusion the patients feel better in the
horizontal position. There is no fever, and the pulse may be either
quick or slow if the hypera^mia extend to the spinal centres of cardiac
innervation. Passive must be distinguished from active congestion by
the presence or absence of general venous congestion. Spinal hypere-
mia ends in recovery unless the case prove fatal from a cardiac or some
other complication.
2. Spinal Apoplexy (H.ematomyelia).
Etiology. — Spinal apoplexy is more common in youth and middle
age than in old age, attaining its greatest frequency between twenty
and thirty-five years of age. Men are more subject to the disease than
women in the proportion of about four to one. Amongst the exciting
causes are traumatic injuries, suppression of accustomed discharges,
active congestion of the cord, and the presence of a rapidly growing
tumors like glioma.
Symptoms. — The disease may be preceded by obscure premonitory
symptoms like those of congestion of the cord, which may last from a
few hours to several days, but even in those cases the onset of the
542 VASCULAR DISEASES OF THE SPINAL CORD.
characteristic symptoms is always sudden, and complete paraplegia
develops in the course of a few minutes or at most an hour. During
the development of the paralysis the patient often complains of a violent
pain, which is either localized at a particular spot, extends along the
spinal column, or shoots in the form of a girdle round the l)ody ; but
when the paralysis has become complete the pain usually disappears,
although the spinous processes of the vertebrae over the seat of the lesion
may remain tender to pressure, or to the cathode of a galvanic current,
for a considerable time. When the lower cervical region is implicated
the paraplegia extends to the upper extremities, the respiratory muscles
are paralyzed, and the breathing is diaphragmatic. The paralyzed
muscles are at first flaccid, and the reflexes and tendon-reactions are
absent in the lower extremities, from the shock, even in the cases in
Avhich the lesion is situated high up.
In the early stage there is more or less complete aniTesthesia of every
form of sensibility, having in most cases the same distribution as the
motor paralysis, but when the lesion is unilateral there may be hyper-
sesthesia of one of the lower extremities and anaesthesia of the other
even although both limbs may be paralyzed. Ketention of urine may
be present from the first from interference with the conducting paths,
or the shock may give rise to a transient incontinence, but permanent
incontinence of urine and feces only occurs when the automatic centres
of the bladder and rectum are invaded by the hemorrhage or are
secondarily implicated by the inflannnatory reaction. Priapism is a
frequent symptom during the first few days, and the temperatui-e of the
paralyzed extremities may be raised from 0.2° to 2° C. above that of
the axilla. In the course of a few days the symptoms of secondary
myelitis may be superadded to those caused by the primary lesion, and
then the patient may suff"er from pains of various forms, and twitching
movements and jerkings of the extremities. If the myelitis extends
downwards so as to reach the level of the upper lumbar region of the
cord the sphincters become paralyzed, cystitis and bedsores appear, and
the patient dies from septic fever ; and if it ascend to the upper cervical
region the patient dies from asphyxia.
If the patient survive the stage of secondary myelitis signs of im-
provement begin to show themselves. In those cases in which there is
hypenesthesia of one lower extremity and anaesthesia of the other, the
anaesthetic extremity gradually regains its motor power and it may
ultimately be almost completely restored, but the hyperaesthetic extremity
becomes the seat of a permanent spasmodic paralysis with exaggerated
reflexes and tendon-reactions. If the upper extremities are paralyzed
the one on the anaesthetic side may also recover, while the paralyzed
HYPEK.EMIA AND HEMORRHAGE OF SPINAL CORD. 543
muscles of the opposite upper extremity remain permanently paralyzed
and undergo atrophy, being innervated from the level of the lesion.
The sensory disorders also undergo some improvement. The hyper-
8esthesia may gradually disappear from the lower extremity which is
permanently paralyzed, but the anaesthesia often remains more or less
permanent in the lower extremity which has recovered motor poAver,
and it also extends over the half of the body on that side up to the area
of distribution of the sensory nerves derived from the upper limit of the
lesion. On the paralyzed side, although the sensibility has become
normal below the level of the lesion, yet a band of anaesthesia extends
round the half of the body corresponding to the vertical extent of the
lesion.
The immediate and permanent symptoms will, of course, vary accord-
ing to the extent and situation of hemorrhage, and in cases which make
a partial recovery the lesion is generally limited to one-half of the cord.
In small hemorrhages it may not be possible to make a certain diagnosis
of the nature of the lesion. When, for example, the hemorrhage remains
limited to the anterior eornua the chief symptom will be the sudden
occurrence of an atrophic paralysis and the case should be regarded as
very acute anterior poliomyelitis.
If the lumbar region of the cord be the seat of the hemorrhage the
symptoms of paralysis and anaesthesia are limited to the lower extremities ;
the muscles of the lower extremities undergo a diffused atrophy and
manifest the reaction of degeneration ; the patellar tendon-reactions are
lost, but the reflex of the sole may still be retained ; the bladder and
rectum are paralyzed ; cystitis and bedsores appear at an early period,
and the patient dies from septic fever. If the lesion is, however, very
limited and situated below the level of the automatic centres of the
bladder and rectum gradual recovery may take place, the paralysis of
the sphincters which was present at first disappears, the sensory dis-
orders improve, but the muscles of the lower extremity on the side of
the lesion undergo a diff'used atrophy, and one or more groups may
remain permanently paralyzed, but the other lower extremity often gives
signs of a slight degree of spasmodic paralysis.
If the dorsal region be the seat of the hemorrhage the patient recovers,
unless a secondary myelitis supervene and prove fatal. The permanent
symptoms will be a spasmodic paralysis of the lower extremity on the
side of the lesion and an atrophic paralysis of the dorsal, abdominal, or
intercostal muscles supplied from the level of the lesion. There will be
anaesthesia of the lower extremity and of the half of the body on the
opposite side to that of the inner paralysis, and a band of amijsthesia
64:4: VASGULAE DISEASES OF THE SPIRAL COED.
surrounding the body on the side of the lesion and corresponding to the
vertical extent of the lesion.
If the lower cervical or upper dorsal regions are the seat of the
hemorrhage the permanent symptoms will be a spasmodic paralysis of
the lower extremity and an atrophic paralysis of groups of muscles of
the upper extremity and of the upper intercostal muscles on the side of
the lesion, hemiansesthesia on the opposite side of all points below the
level of the upper limit of the lesion, and on the side of the lesion a
band of anaesthesia encircling half the body and an area of aniTesthesia
of variable distribution in the upper extremity. In addition to the
motor and sensory disorders, oculo-pupillary phenomena are found on
the side of the lesion. In a case of spinal hemorrhage which has been
under my observation for many years the permanent symptoms are a
spasmodic paralysis of the right lower extremity and an atrophic paral-
ysis of the intercostal muscles from the ninth upwards, and of the small
muscles of the hand and the flexors of the fingers and wrist. The hand
assumes the well-known claw-form met with in cervical pachymeningitis
IIYPER^EMIA AND HEMORRHAGE OF SPINAL CORD. 545
when the lesion is situated on a level with the eighth cervical and first
dorsal nerves. On the left side, the lower extremity and the half of the
body up to the level of the clavicle are almost completely anaesthetic, the
skin of the right lower extremity and of the half of the body up to the
level of the tenth rib, which was at first hypenesthetic, is now normal,
but above the tenth rib a band of anaesthesia encircles half the body up
to the level of the clavicle, while the anaesthetic area extends down the
inner aspect of the arm and forearm, the ulnar half of the palm and
back of the hand and two and a half fingers (Fig. 170). The oculo-
pupillary symptoms are well marked in the right eye.
If the lesion extends further up in the cervical region other groups
of muscles will be paralyzed in the upper extremity and the area of
distribution of the anaesthesia will also be different from that of the case
just described. If the hemorrhage occur above the origin of the phrenic
nerves, rapid death by asphyxia is inevitable.
Morbid Physiology. — Ancemia of the spinal cord had been experi-
mentally produced in animals by Stenon as far back as 1667, and since
that time by various other physiologists, but the most complete and
conclusive experiments of this kind were performed by Kussmaul and
Tenner. These experimentalists first tied the subclavian arteries, and
so arrested the circulation through the vertebral arteries. Compression
upon the descending portion of the arch of the aorta now caused more or
less complete arrest of the circulation in the cord, and after a minute and
a half the animals operated upon became paralyzed in their posterior
extremities, but the paralysis soon extended upwards, and death re-
sulted from paralysis of respiration. Inert powders have been injected
into the aorta of animals by Panum and A\dpian, with the result of
obliterating a large number of the small bloodvessels of the abdominal
organs and of the lower part of the si»inal cord. The operation Avas
almost immediately followed by paralysis of both sensation and motion
of the posterior extremities, and after death foci of softening were
found in the spinal cord. These experiments show that arrest of the
circulation through the cord, either by occlusion of the large vessels
from which the cord derives its arterial supply, or of a large number of
the vessels of the cord itself, is followed by a cessation of the spinal
functions.
Hypercemia of the spinal cord gives rise at first to slight irritative
sensory and motor phenomena, but these soon give place to depressive
symptoms. The primary irritative symptoms are caused by the free
supply of nourishment conveyed to the cord by the well-filled vessels,
but as the vessels become greatly distended the nervous tissues are com-
35
54:6 VASCULAK DISEASES OF THE SPINAL CORD.
pressed, the material exchanges are in great part arrested, and the irri-
tation gives place to depressive s^^mptoms.
Hemorrhage of the spinal cord is said by Hayem and Charcot to
be always a secondary result of hyperacute myelitis or of some other
disease of the spinal cord. It is probable that hemorrhagic infiltration
is always the result of a very acute central myelitis, and a hemorrhagic
clot sometimes occurs as a grave and generally fiital complication of a
chronic spinal disease like progressive muscular atrophy. In other cases,
however, the sudden onset of the disease and the absence of all irritative
symptoms as well as of power, seem to indicate that the henmrrhage
is primary, and that any evidence of myelitis which may be present in
the cord after death is caused by a secondary myelitis. The character
of the symptoms will depend upon the extent and localization of the
hemorrhage, the degi'ee of secondary myelitis, and the tracts of the
cord which have been destroyed.
Treatment. — In the treatment of spinal ancemia the causes must be
removed by a tonic and stimulating treatment. In aggravated cases
the patient should be laid on his back and his legs raised, and this
position should be maintained during the night and for a considerable
portion of the day. Strychnine may be administered in spinal antijmia,
and the constant current should be applied daily to the vertebral
column, while the faradic current may be applied to the paralyzed
muscles if the reflexes are not in excess. Chapman's spinal bag, filled
with hot water, or hot sand-bags, may be applied along the back. The
diet should be generous and moderately stimulating.
In spinal hyperceinia leeches may be ap}»liod along the spine, especi-
ally when the affection is caused by the suppression of accustomed dis-
charges. A saline purgative may be of use by unloading the vessels
and lowering the arterial tension. Ergotine and belladonna arc the
favorite internal remedies. The patient should be directed to lie on
his side, or in the prone position, and Chapman's ice-bag may be
applied to the spine. The cold effusion, douches, cold packing, and
sea baths may take the place of the ice-bag. The diet siiould be plain,
nourishing, and unstimulating, and everything which might increase the
hypereemia, such as sexual and alcoholic indulgence, must be avoided.
Spinal hemorrh<(;/e mii^t be treated ^at first like spinal hyperaemia,
and after a time like an ordinary case of myelitis.
CHAPTER XI.
MYELITIS.
The forms of myelitis which affect exclusively the embryological
systems of the spinal cord have already been considered, and conse-
quently there remain for discussion only those kinds in which the gray
and white substances are indiscriminately attacked, and in which the
symptoms of atrophic and spasmodic paralysis, along with various dis-
orders of sensation and of the functions of the bladder and rectum, are
associated in the same case. When inflammation affects several of the
embryological systems of the spinal cord it may be named diffused or
indiscriminate myelitis.
Etiology. — Many cases of myelitis begin in the absence of any rec-
ognizable exciting or predisposing cause. Males appear, to be more
liable to myelitis than females, and the majority of cases occur between
ten and thirty years. Sexual excess and severe bodily exertion act as
predisposing causes.
The most usual exciting causes are wounds, fractures, and contusions
of the vertebral column, extension of inflammation to the cord from
disease of the membranes or vertebrfB, and exposure to cold when the
body is overheated. jNIyelitis may also be caused by an ascending
neuritis set uj) by irritative lesion of the joints and internal organs,
especially the genito-urinary organs. It may also occur as a complica-
tion or sequel of the acute specific fevers, acute rheumatism, and severe
puerperal diseases, and a very acute form of myelitis is liable to occur
in syphilitic subjects.
Any condition, indeed, which narrows the spinal canal and leads to
compression of the cord may become a cause of myelitis. Of these
causes caries of the vertebrae is the most frequent and important. The
cord may be subjected to compression by the bodies of diseased verte-
brae, displaced fragments of bone, or protruding intervertebral carti-
lages. More frequently, however, the cause of compression is to be
found in the accumulation of inflammatory products around the mem-
branes, or secondary inflammatory thickening of the dura mater itself.
Amongst other diseases of the vertebrae which occasionally cause com-
pression of the cord may be mentioned exostosis, syphilitic new forma-
tions, dry arthritis of the vertebrge, and thickening of the odontoid
548 MYELITIS.
process of the axis. External tumors of all kinds, such as carcinomata,
sarcomata, and echinococci may, by effecting an entrance into the ver-
tebral canal, occasion more or less sudden compression of the cord, or
even give rise to a secondary myelitis in the absence of compression.
Intramedullary, meningeal, and perimeningeal tumors of all kinds give
rise to myelitis by compression, and of these it is important to remember
that syphilitic deposit is the most frequent.
Symptoms. — The spinal phenomena, in acute cases, are often pre-
ceded by premonitory symptoms consisting of general malaise, slight
pyrexia, chilliness, headache, general depression, loss of a])petite, and
aching of the limbs. The spinal symptoms generally manifest them-
selves by sensory disturbances consisting of girdle pains ; numbness,
and various other paraesthesije, along with shooting, burning, and other
sensations in the limbs : by pain in the back over the vertebral column,
which is accompanied by tenderness on pressure of the spinous pro-
cesses, and by superficial sensitiveness that can be elicited by passing a
hot sponge or the cathode of the galvanic current over the part. Patients
complain at times of painful, dragging sensations in tlie l)laddcr and
rectum, gastralgic attacks, and neuralgic pains in other viscera. As the
disease advances the parjesthesiie and pains give place to an;estliesia,
Avhich may be partial or complete, although even when sensation is
wholly lost to objective examination the patient may complain of severe
pains in the i)art — anceHthenia dolorosa. In most severe cases the
amesthetic lower ])art of the body is se])arated from the normal skin by
a pretty sharply defined line.
The motor symptoms consist at first of twitchings of individual
muscles or of entire extremities, and occasionally the spasm may increase
to a condition of tetanic rigidity. But the symptoms of motor irrita-
tion soon give place to paralysis, and loss of motor power is sometimes
developed Avith so much rapidity that we speak of apoplectiform myelitis.
When paralysis is rapidly developed the muscles are perfectly flaccid,
and when the limbs are raised they fall like inert and lifeless masses.
If the patient survive, symptoms of motor irritation may reappear in
the affected limbs, consisting of spontaneous twitchings of the paralyzed
muscles, Avhich are generally accompanied by severe shooting pains.
The muscles now become tense, and the tension is increased by passive
movements of the limbs, while contractures become established which
fix the lower extremities generally in positions of extension and only
occasionally in flexion. The most common forms of paralysis are para-
plegia and hemiparaplegia, while complete paralysis of all four ex-
tremities occurs occasionally.
The reflex excitability and tendon-reactions vary according to the
SYMPTOMS. 549
seat of the disease. When the disease involves the lumbar enlargement
l)otli the reflex of the sole and the patellar tendon-reaction are abolished ;
-when it involves the upper end of the lumbar enlargement the reflex of
the sole is exaggerated, but the patellar tendon-reaction and the cremas-
teric reflex are lost ; and when the lesion is situated in the dorsal region
the reflexes of the sole, of the cremaster, and of the patellar tendon are
exaorserated.
The bladder, rectum, and sexual organs are generally affected in acute
myelitis. At first there may be spasmodic closure of the sphincter of
the bladder, so that a catheter has to be used, but incontinence of
urine soon supervenes, vesical paralysis being, indeed, sometimes one
of the earliest symptoms of the disease. In severe cases the urine
becomes alkaline and sometimes bloody after the seventh or eighth day ;
it then contains numerous crystals of the triple phosphates and putrefac-
tion bacteria, and there is considerable muco-purulent deposit. The
bowels are obstinately constipated, and the abdomen becomes distended
with flatus, while soon the stools are passed involuntarily. Priapism is
not an uncommon symptom of acute myelitis, the erection being usually
incomplete, but generally persisting for days.
The vaso-vwtor disturbances are variable. The paralyzed limbs are
often oedematous, and generally cold, although occasionally elevation of
temperature has been observed in them. The perspiration is sometimes
increased, sometimes diminished.
The trophic disorders consist of acute bedsores, which may make
their appearance as early as from the second to the fifth day and are
situated over the sacrum, trochanters, and other exposed situations ;
they often pursue a rapid course and prove fatal by pyaemia. When the
disease is situated in the lumbar region the paralyzed muscles undergo
a diff"used atrophy, and then the affected nerves and muscles manifest
the " reaction of degeneration." When the lesion is localized in the
dorsal region the muscles retain their nutrition and the electrical reac-
tions are normal.
Psychical symptoms are not often present in acute myelitis, although
in children the symptoms may be ushered in by headache, delirium, and
general convulsions ; when cerebral symptoms occur in the adult they
are probably due to the accompanying fever.
When the erector muscles of the spine are paralyzed the patient is
unable to sit up in bed, and when the abdominal muscles are paralyzed
all forcible expiratory acts are rendered feeble, and consequently the
air-passages cannot be cleared of mucus, a difficulty which is still further
increased when the intercostal muscles are paralyzed. When the
cervical portion is implicated some or all of the muscles of the upper
550 MYELITIS.
extremities are paralyzed and various sensory disorders appear in them.
In addition oculo-pupillary symptoms are present, and double optic-
neuritis lias been observed on rare occasions ; while the pulse may either
be much accelerated or retarded, and the patient suffers from palpitation,
irregularity of the heart's action, and unpleasant sensations in the pre-
cordial region.
As the disease ascends the movements of the diaphragm become
feebler, and as inspiration is now carried on chiefly by means of the
cervical muscles death by asphyxia is imminent; when the medulla
oblongata becomes involved articulation and deglutition are interfered
with, and the patient dies from respiratory paralysis.
In acute myelitis the early stage of the disease is accompanied by
fever, and the temperature may remain persistently high throughout the
whole course of the disease, while there may be hyperpyrexia at death.
In other cases the fever is slight and may disappear entirely in the
course of the disease, but in the tei'minal stage a fever of remittent
type appears which is caused by septic infection from the cystitis, bed-
sores, and pyelo-nephritis.
Acute myelitis is always rapidly developed, but when the acute
symptoms have subsided the disease may pass into a chronic myelitis,
and the symptoms may then remain stationary for months or years.
In other cases acute myelitis pursues an ascending course and becomes
quickly fatal. When the lumbar region of the cord is the chief seat of
the disease it proves fatal after many months from the exhaustion caused
by septic fever. In some cases complete recovery may take place and
a favorable termination may occasionally result even after the formation
of bedsores. In most cases, however, recovery is only partial, and one
or more groups of muscles remain permanently paralyzed and atrophied.
Chronic myelitis is sometimes a sequel of acute myelitis, but in most
cases the disease begins slowly and is gradually developed. The symp-
toms often begin by parsesthesia in the lower, and occasionally in the
upper extremities, and a girdle sensation, and at the same time the
patient complains of a feeling of weakness and heaviness of the limbs,
and probably suffers from jerkings of the legs in bed at night. He
also complains of a sensation of stiffness of the legs, which is worse in
the morning and at starting to walk than when the limbs have been
moderately exercised. As the disease advances the stiffness and weak-
ness of the legs become worse, and after a time the paralysis assumes
the typical form of spastic paraplegia, or occasionally of a spinal hemi-
plegia, and now the lower half of the body is also more or less anges-
thetic. The course of chronic myelitis is very variable. When the
disease reaches a certain degree of intensity it may remain stationary
VARIETIES OF DIFFUSED MYELITIS. 551
for mail}' years, or periods of improvement may alternate Avith relapses
and exacerbations. The disease may, indeed, last a lifetime without
producing dangerous symptoms. Complete recovery is, however, rare
and the majority of cases terminate fatally either from bedsores, cystitis
and pyiemia, occasionally from bulbar paralysis, or more frequently
from pneumonia or other intercurrent disease.
VARIETIES OF DIFFUSED MYELITIS.
The following varieties of diffused myelitis may be distinguished:
1, Central myelitis; 2, bulbar myelitis; 3, transverse myelitis; 4,
wounds of the spinal cord; 5, compressive myelitis; 6, unilateral
myelitis; 7, meningo-myelitis; 8, universal progressive myelitis; and
9, disseminated myelitis. The various inflammations of the spinal cord
may be subdivided into acute and chronic myelitis.
1. Central Myelitis.
Symptoms. — This affection begins suddenly by parsesthesise and
other sensory disturbances, which are soon followed by complete anaes-
thesia and paralysis with flaccidity of the lower extremities, and by
paralysis of the bladder and rectum. The reflex excitability is abol-
ished, and the paralyzed muscles undergo rapid atrophy, and manifest
the "reaction of degeneration" at an early period. The further prog-
ress of the disease is marked by acute bedsores, cystitis with ammoni-
acal urine, oedema of the paralyzed limbs, arthropathies, more or less
intense fever, and progressive advance of the paralysis upwards, so
that the intercostal muscles and those of the upper extremities become
successively paralyzed, and ultimately the muscles of articulation and
deglutition are invaded, and the patient dies from respiratory paralysis.
The course of acute central myelitis is very similar to that of acute
ascending paralysis, but in the latter the bedsores as well as the vesical
and rectal disorders of the former disease are absent. In other cases
the symptoms become more or less chronic, and the disease may then
be mistaken for chronic atrophic spinal paralysis, but in the latter dis-
ease the sensory disorders and the bedsores of the former affection are
wanting. In some cases the symptoms develop with almost apoplecti-
form rapidity, the lower extremities becoming completely paralyzed in
the course of a few minutes, or, at most, in the course of an hour or
two. In such cases the gray matter of the cord has been found soft-
552 MYELITIS.
ened and mixed with red blood-corpuscles, and the disease has conse-
quently been named hcematomyeUtis. It may also be named hypei--
acute central myelitis.
2. Bulbar Myelitis.
Symptoms. — Acute bulbar myelitis begins suddenly with violent
headache, giddiness, vomiting, distressing hiccough, various pariTesthesijv?,
and difficulty of articulation and deglutition, but, contrary to what
occurs in an apoplectic attack, consciousness is retained. After a short
time the inferior muscles of the face, the muscles of tlie tongue, soft
palate, and pharyngeal muscles become paralyzed in various degrees
and combinations, and in some cases the ocular muscles, especially the
external recti, may be implicated. Disorders of respiration appear at
an early period, the respirations are hurried and irregular, and there
may be an intense feeling of oppression, dyspnoea, and cyanosis.
The pulse is small, quick, and irrc'gular or intermittent. One, two, or
all the extremities may be paralyzed, or paralysis of the limbs may be
absent. The patient may complain of pain and formication in the
limbs, but there is anesthesia. The bladder and rectum may become
paralyzed towards the terminal period of the disease. Tlie disturb-
ances of circulation and respiration now increase, the patient becomes
unconscious, and death from asphyxia results.
Chronic projjressive bulbar paralysis has already been described.
A chronic form of bulbar paralysis may also result from necrotic pro-
cesses, and from inflammation set up by tumors and other morbid
processes in the neighborhood of the meduHa, but this form of bulbar
myelitis does not demand separate description.
3. Transverse Myelitis,
Symptoms. — Tlie symptoms of transverse myelitis will vary accord-
ing as its course is acute or chronic, and according a.s it is caused by
wounds and other injuries of the cord, by the growth of tumors, or by
the extension of inflammation from other tissues, or as it begins as an
idiopathic affection. In this place, however, we have to do cliiefly with
the localizing symptoms, and for the purposes of description the affec-
tion may be divided into a, dorso-lumbar ; 6, dorsal; and c, cervical
transverse myelitis.
a. Dorso-lumbar transverse myelitis may begin more or less sud-
denly by fever, par?esthesia of the lower extremities, retention of urine,
VARIETIES OF DIFFUSED MYELITIS. 553
and startings of the lower extremities, but tliese symptoms soon give
place to sensory and motor paralysis of the limbs and paralysis of the
sphincters of the bladder and rectum. The lower extremities become
(edematous, and their muscles may undergo a diffused atrophy, and
may manifest the reaction of degeneration. The patellar tendon-reac-
tions, which were possibly at first exaggerated, now become lost, and
the cremasteric reflex is also lost, but the reflex of the sole is often
exaggerated. The neck of the femur is occasionally the subject of
spontaneous fracture, and arthropathies of other joints may appear.
In acute cases of this kind the patient generally dies at an early period
of the disease from the usual cystitis, bedsores, and septic fever.
The ehronif form of the disease begins gradually by girdle pains in
the region of distribution of the ilio-hypogastric and ilio-inguinal nerves,
while the patient complains of shooting pains, and various par^esthesise
in the lower extremities. The patient suffers from cramps in the calves
of the legs, and is soon fatigued, while the movements are stiff" and
constrained. After a time the lower extremities become rigid by con-
tractures, the cutaneous reflexes and tendon-reactions are exaircrerated
in them, and the gait is of the spastic variety. As the disease advances
the sensory disorders become more profound, and anaesthesia of the
lower extremities becomes established, while the patient becomes com-
pletely paraplegic. The lesion now usually invades the lumbar enlarge-
ment, and when it creeps down to the level of the second or third
lumbar nerves the cremasteric reflex is lost, the extensor muscles of
the knee undergo atrophy, the patellar tendon-reaction is abolished,
and the sphincters are soon afterwards paralyzed. AVith a still further
downward extension of the lesion all the muscles of the lower extremi-
ties undergo a diffused wasting and lose their tension : the limbs become
oedematous, the reflex of the sole may, after a time, be lost ; bedsores,
which have, indeed, already appeared over the sacrum, now form over
the trochanter and other points subjected to pressure; the urine is
alkaline and contains pus ; and the patient dies from pyaemia.
b. Dorsal Transverse 3Iyelitis. — In this form of myelitis both the
sensory and motor paralysis extend higher than in the dorso-lumbar
variety, but the condition of the lower extremities, with regard to paral-
ysis, contractures, spastic gait, exaggerated reflexes, and tendon-reac-
tions, is the same as in the early stage of that disease. When the
lesion is situated in the upper part of the dorsal region the muscles of
the back and abdomen are liable to be paralyzed, and paralysis of the
abdominal muscles renders urination, defecation, and forcible expiratory
acts difficult, and consequently the patient is troubled with constipation,
and being; unable to clear the bronchial tubes thorougldv from mucus
554 MYELITIS,
he is liable to succumb to a slight bronchial catarrh. Double optic
neuritis has occasional^ been observed. The level at which the cord
is diseased may be determined by the level of the girdle pains and
anaesthesia, and by an examination of the cremasteric, gluteal, abdomi-
nal, epigastric, dorsal, and scapular reflexes.
c. Cervical Transverse Myelitis. — This form of myelitis generally
begins with pain in the back of the neck, and the muscles of the neck
become rigid, while owing to the predominant action of those of the
back, often of one side, the head is generally rotated and retracted.
The upper extremities now become subject to shooting pains and muscular
startings, provided the lesion involves the origin of the brachial plexus,
but these symptoms of irritation soon give place to sensory and motor
paralysis. The paralysis of the upper extremities is of the atrophic
variety, and its distribution, with the consequent deformities, will de-
pend upon the level of the lesion, while it may be accompanied by
oedema and arthropathies. The lower extremities become affected with
a spasmodic paralysis with exaggerated reflexes and tendon-reaction.
There may also be complete or incomplete anaesthesia of the body and
lower extremities below the level of the lesion, and of the upper ex-
tremities on a level with the lesion, the distribution of the last depend-
ing upon the posterior roots which are implicated. The pupils arc, in
some cases, dilated, in others contracted, or often first dilated and then
contracted; the size of the palpebral fissure may be increased or dimin-
ished; and the face may be unusually pale or flushed, and it is often
covered by perspiration. In some cases oculo-pupillary symptoms are
absent. The establishment of paralysis may be preceded by anoma-
lous symptoms like cough, dyspnoea, sweats, wasting of the muscles of
the arm and neck, pains between the shoulders or at the back of the
neck, severe attacks of vomiting, hiccough, difficulty of deglutition, and
great slowness of the pulse. The inflammatory process is liable to
ascend to the medulla oblongata, and death results from respiratory
paralysis.
4. Wounds of the Spinal Cord.
Symptoms. — The symptoms caused by wounds and injuries of the
cord may be divided into (a) those caused by comparatively slight
nijuries of the cord, such as simple incised and punctured wounds,
and {h) those caused by the more serious lesions, such as sudden com-
pression and tearing of the cord.
a. The symptoms which indicate that an injury by cutting or stal)-
bing in the neighborhood of the spine has penetrated the cord will
at first be those caused by loss of conduction to and from the brain
VARIETIES OF DIFFUSED MYELITIS. 555
in the portions situated below the seat of the injury. At the moment
the injury is received paraplegia, hemiparaplegia, or general paralysis
is suddenly developed. If the cord is completely divided, there is com-
plete anaesthesia of the paralyzed parts ; but if only one-half of the
cord is divided the anaesthesia is situated on the side opposite to the
lesion, Avhile girdle pains may be present on a level with the lesion.
If the injury be of considerable extent paralysis of the bladder and
rectum occurs, and there is also vaso-motor paralysis with increased
temperature and redness of the region affected by the motor paralvsis.
The reflex actions are usually abolished at first, owing to the shock, but
if the lesioii is situated in the dorsal or cervical region, they may,
subsequently be exaggerated. After a time the symptoms of secondary
traumatic myelitis complicate those caused by the primary lesion, and
then the symptoms will be more or less like those caused by acute
idiopathic transverse myelitis.
h. The symptoms which indicate that the cord is crushed or torn in
severe injuries of the spine are, in addition to the evidences of local
injury of the spine, complete paralysis and anaesthesia of the portion of
the body which lies below the seat of the injury. The other symptoms
are abolition of the reflex actions, retention of urine and constipation,
with meteorism or involuntary evacuations of urine and feces, priapism,
in which the organ is turgid but still flexible, and elevation or some-
times depression of the temperature of the body.
When the cervical region is injured the temperature of the body is
generally much increased, and often rises still further for some hours
after death. In a case of fracture of the fifth and sixth cervical ver-
tebr;:©, reported by Quincke, the temperature at death was 42.3° C,
and eight hours after death it was 43,2° C, and in a case of compres-
sion of the cervical region he found the temperature 42,7° C, at death,
and 43.6° C, eight hours afterwards, A case of fracture of the spine
on a level with the body of the fifth cervical vertebra is recorded by
Mr, Jonathan Hutchinson, in which the temperature, which was 99,3° F.
in the urethra twent^^-four hours after the injury, rose to 106.3° F. at
death, thirty-eight hours after the injury, and Mr. F. Churchill has
recorded a case of fracture of the same vertebra in which the tempera-
ture in the axilla was 110° soon after death. In some cases the tem-
perature undergoes great variations, being in one case as low, at one
time, as 94.2° F., and soon afterwards as high as 106.4° F., these varia-
tions being apparently independent of bedsores and septic fever. In
some cases of fracture of the cervical spine the temperature of the
body falls after the injury, and remains low till death.
Another symptom of injury of the cervical region is afforded by a
556 MYELITIS.
very feeble, slow, and infrequent pulse, which beats in some cases only
forty- eight times in the minute, and it is in these cases, according to Mr.
Jonathan Hutchinson, that the temperature flills and the surface is cold
to the touch. When the injury is situated in the dorsal or lumbar
region the pulse is not affected except by the shock, just as occurs
after other severe accidents. The severer forms of injury to the cervi-
cal spine are rapidly fatal by paralysis of respiration, but when the
patient survives for a few days the symptoms of acute transverse mye-
litis are superadded to those caused by the injury.
5. Compression Myelitis, Tumors in the Vertebral Canal.
Symptoms. — The symptoms of compression myelitis nuiy be divided
into a, extrinsic, and h, intrinsic sym])toms.
a. The extrinsic or prodromal symptoms consist of severe girdle
pains, hypersesthesia of the skin corresponding to the distribution of
the pain, eccentric neuralgiform pains generally fixed to one spot, severe
pain in the back, local stifiness, and tenderness of the spinous processes.
The neuralgic pains are sometimes accompanied by herpetic or bullous
eruptions of the skin. Phenomena of motor irritation are superadded
to the sensory disturbances in the distribution of the nerves whose roots
were first implicated. These consist of twitchings, spasms, and con-
traction of the muscles supplied by the affected nerves. The irritative
motor symptoms are soon followed by weakness and paralysis of single
muscles or groups of muscles, the affected muscles undergo a diffused
atrnpliy, the cutaneous reflex actions and the tendon reactions are lost
in them, and they may manifest the partial " reaction of degeneration,"
but not often the severest form of that reaction. As the second stage
of the disease approaches the patient complains of pan\?sthesia3 in the
lower half of the body, consisting of tingling, numbness, and sensations
of heat or of cold, and after a time more or less ansesthesia is established,
but complete anesthesia is rare in vertebral caries. The motor symp-
toms consist at this stage of startings of the lower extremities, especially
at night, and a sense of weariness and heaviness of the limbs, while the
patellar tendon-reactions will often be found exaggerated, unless the
lesion is situated in the lower dorsal and lumbar regions, when they may
be lost.
When cancer of the vertebral column makes its way into the spinal
canal it gives rise to the most agonizing pains. These consist of severe
girdle pains, and of pains which radiate along the distribution of
certain nerves, such as the crural and sciatic nerves, when the lumbar
vertebrae are affected. The skin to Avhich the affected nerves are dis-
VARIETIES OF DIFFUSED MYELITIS. 557
tributed is intensely hyperresthetic, so that the slightest touch is painful.
The pains never intermit, but they are liable to paroxysmal exacerba-
tions of great severity, which are difficult to allay even by laro-e doses
of narcotics. Patches of angesthesia may be observed in the skin to
-which the affected nerves are distributed, but the pain still continues
unabated, this condition being named ancesthesia dolorosa, and when
the symptoms of transverse myelitis are after a time superadded to these
sensory disorders, the condition is called paraplegic dolorosa.
In all cases in which the premonitory symptoms of compression or
transverse myelitis are present a careful examination must be made to
determine the level of the girdle sensations, or the upper limit of the
pan^sthesia or anaesthesia if any be present, and when once this point
has been ascertained the vertebral column on a level with the upper
limit of the sensory disorders must be subjected to careful examination.
In cases of angular curvature, and in those cases in which an external
tumor has made its way into the vertebral canal, decided evidence of the
nature of the disease may be at once obtained. And even in those cases
in which there are no enlargements or other deformities it may be found
that one or two of the spinous processes are tender to pressure or percus-
sion, or sensitive to a hot sponge drawn along the vertebral column, or
to the cathode of the galvanic current.
b. The intrinsic syinptonis are generally the same as those of trans-
verse myelitfs, and are ushered in by paralysis of the lower extremities,
Avhich may begin at first as a hemiparaplegia, and afterwards develop
into complete paraplegia. The symptoms of acute and chronic trans-
verse myelitis need not be described a second time. In intramedullary
tumors the phenomena of atrophic paralysis may predominate, but they
are often associated with a spasmodic paralysis with exaggerated reflexes
in one of the limbs or in one or more groups of muscles. Multiple
tumors are sometimes found in the cord, consisting of sarcoma, tubercle,
or syphilis, and the symptoms may then manifest themselves at dif-
ferent elevations, as in acute and chi'onic disseminated myelitis. In
addition to the variable character of the purely spinal symptoms, one
or more of the tumors may appear in the medulla oblongata and
pons, and the symptoms caused by these tumors may help to clear the
diagnosis.
6. Spinal Hemiplegia and Hemiparaple(!Ia (Unilateral Lesion
OF THE Spinal Cord).
Symptoms. — The symptoms of unilateral spinal paralysis may be
developed insidiously and gradually, or (juite suddenly, the mode of
558 MYELITIS.
invasion depending upon whether the lesion consists of a slowly invad-
ing disease like the growth of a tumor, or upon a sudden injury like
a stab from a sharp-pointed instrument. The most prominent symptoms
are a motor paralysis on the side of the lesion which may involve only
one leg (hemiparaplegia), or the leg and the arm of the same side (spinal
hemiplegia), and a sensory paralysis on the opposite side of the body.
The paralyzed muscles undergo early and rapid atrophy when the
lesion is situated in the lumbar enlargement, but when it is situated at
a higher level the lower extremity on the side of the lesion undergoes
spasmodic paralysis, provided the patient survive sufficiently long for
secondary degenerations to occur in the cord, while groups of the muscles
of the upper extremity are the subjects of atrophic paralysis if the
lesion is on a level with the roots of origin of the In-achial plexus. In
some cases well-marked ataxia has been observed in the paralyzed leg
after return of motor power,
Vaso-motor paralysis is declared, on the side of the lesion, by an
elevation of the temperature of the paralyzed limb to the extent of
from 1° F. to 3.6° F., but the temperature may be lower than normal
when the disease has existed for some time.
Muscular sense and muscular sensibility are also usually diminished
on the side of the lesion, but all forms of cutaneous sensibility are
increased. Impressions of touch, temperature, and pain are felt with
unusual acuteness, and there is an increased power of localizing tactile
sensations. At times, however, the hypersesthesia is limited to a few
forms only of cutaneous sensibility. The hyperjesthetic area of the
skin is usually bounded by an anesthetic zone which corresponds with
the level and longitudinal extent of the lesion of the spinal cord, and a
narrow hypertesthetic belt which extends to the opposite side may some-
times be detected above the anaesthetic zone (Fig. 171). The reflex
actions on the side of the motor paralysis vary, but they are generally
increased below the seat of the lesion.
On the side opposite the lesion there are no motor disorders or they
are only slight in degree, and both the muscular sense and the electro-
muscular sensibility are retained on that side ; however, there is more
or less complete anesthesia of the skin, although some forms of sensi-
bility may be involved to a greater extent than others. The anesthesia
extends nearly to the median line of the body and it is often bounded
above by a slightly hyperesthetic region, corresponding to a similar
zone on the opposite side. Near the median line anteriorly and pos-
teriorly there is a vertical space of about one inch in breadth in which
hyperesthesia is absent on the side of the lesion, and a similar space
on the front and back in wdiich there is an absence of any great degree
VARIETIES OF DIFFUSED MYELITIS,
559
of anaesthesia, these phenomena finding a sufficient explanation in the
well-known anatomical fact that the sensory nerves of the two sides
overlap. There are no vaso-motor disturbances on the anaesthetic side,
and reflex action is usually normal, but has occasionally been found
increased. The patient sometimes complains of a feeling of constriction
and neuralgiform pains on a level with the lesion, and these may at
times be more prominent on the anaesthetic and at other times on the
hyperaesthetic side. In acute traumatic cases retention or incontinence
Diagram of the Cutaneous Symptoms in Unilateral Lesion of the Dorsal Portion of the
Spinal Coed on the Left Side. (After Erb.)
The diagonal shading (a) signifies motor and vaso-motor paralysis; the vertical shading (6, d) signifies
cutaneous antesthesia; the dotted shading (a, c) indicates hyperesthesia of the skin.
is always present at first, but after a time recovery takes place, so that
at most only a certain degree of weakness of the sphincters remains.
The sexual functions are at times unaffected and at other times more or
less weakened.
The trophic disorders consist of acute bedsores which appear on the
anaesthetic side, and inflammation of the knee-joint, which appears on
the paralyzed side.
560 ' MYELITIS.
Varieties. — The symptoms differ according to the level at Avhich the
lesion is situated in the cord.
(1) Unilateral lesion of the lumbar eiilargement causes an anaes-
thetic zone, on the paralyzed side, in the area of distribution of one or
more of the sensory branches of the sacral or lumbar plexuses, in addi-
tion to the other characteristic unilateral symptoms, but there is no
belt round the body. The muscles of the paralyzed limb undergo
atrophv when the lesion occupies a considerable portion of the lumbar
enlargement in A'ertical extent.
(2) Unilateral lesions of the dorsal re<jion of the cord give rise to
the most characteristic symptoms of the disease, as already described.
(3) Unilateral lesions of the cervical 2>ortion give rise to different
symptoms according to the level at which the lesion is situated. The
motor and sensory disorders are the same in the trunk and lower ex-
tremities as when the dorsal region is affected, but when the lesion is
situated on a level with the brachial plexus the muscles of the upper
extremity undergo atr()i)hic jiaralysis, while hyperaesthesia of certain
parts of the skin is mingled with anaesthesia of other regions, or for
certain varieties of sensation. On the side opposite the lesion there is no
paralysis, but there is complete anaesthesia of the parts below the level
of the lesion. In addition to these symptoms oculo-pupillary phenomena
and vaso-motor paralysis of the side of the face are present on the
side of the lesion. If the lesion is situated in the upper part of the
cervical region, the neck and head on the side of the lesion manifest
annesthesia and hypenvstliesia of certain areas of the skin, and paral-
ysis of the vaso-motor and oculo-pupillary fibres, while on the opposite
side there are usually an«sthesia of the neck and a narrow zone of
hyperiTSSthesia, with a normal condition of the face and eye.
7. Meninoo-myelitis.
Myelitis is sometimes complicated by the symptoms of meningitis.
The symptoms Avhich indicate meningitis are pain and stiffness in the
back of the neck, pronounced hyperesthesia, diffused pains in the back
and lower extremities, pain along the vertebral column, and tenderness
on pressure of some of the spinous processes of the vertebrae. In some
chronic cases the posterior are more involved than the lateral columns,
and then ataxic symptoms predominate over those of paralysis.
8. Universal Progressive Myelitis.
This form of myelitis embraces the whole transverse area of the cord,
and is characterized by a progressive weakness of the lower extremities
VARIETIES OF DIFFUSED MYELITIS. 561
-which develops into complete paralysis. The disease usually begins in
the lower extremities and pursues an ascending course, but occasionally
it begins in the upper extremities and pursues a descending course.
The muscles may be in a state of contracture at first but as the gray
matter becomes involved they undergo gradual atrophy. The cuta-
neous reflexes, tendon-reactions, and faradic contractility also gradualh^
diminish and gradually disappear. There may be more or less violent
pains in the back, trunk, and extremities, the patient complains of
paraesthesiae and dysaesthesiee, and after a time there is complete anaes-
thesia, paraplegia, paralysis of the sphincters, and bedsores.
9. Disseminated Myelitis.
Symptoms. — There are two forms of disseminated myelitis, a, the
acute; h, the chronic.
The symptoms of the acute form are very variable, but sensibility is
usually more or less impaired, and there is a spasmodic paralysis of the
lower extremities with its attendant phenomena, although in some cases
one or more groups of muscles may suffer from an atrophic paralysis.
The state of the electrical sensibility and of the cutaneous reflexes is
variable, but they are generally diminished. The grouping of the
symptoms may show that several centres of disease exist, and the diag-
nosis is rendered more probable if the symptoms of acute myelitis
supervene during an attack of variola, or if they develop suddenly in
phthisical patients.
Chronic disseminated myelitis is a part of a disease which is widely
distributed in the spinal cord and brain, and will be subsequently de-
scribed under the name of multiple sclerosis.
Morbid Anatomy and Physiology. — The morbid anatomy of the
various forms of myelitis has already been sufficiently considered, and
we shall now make a few remarks to connect the morbid changes with
the principal alterations of function observed in this disease.
Acute myelitis gives rise to the various forms of softening of the
spinal cord which have already been described. The initial symptoms
of irritation, which are present in the early stages of acute myelitis, must
be ascribed to the increased irritability of the nerve cells and fibres,
occasioned by increased nutritive activity during the early stages of the
inflammatory process, while the later symptoms of paralysis ai-e caused
by the destruction of these elements and their compression by inflam-
matory exudation. The girdle pains are caused by implication of the
posterior roots of the dorsal region in the inflammatory process, while
the partesthesiae and neuralgic pains of the inferior half of the body
36
562 MYELITIS.
result from irritation of the sensory conducting paths situated in the
gray matter and posterior cokimns of the cord. The motor symptoms
are caused first by irritation and subse(][uently by loss of the function of
the motor centres and conducting fibres in the cord. When the anterior
gray horns are diseased the resulting paralysis is of the atrophic and
when the pyramidal tracts are affected the paralysis is of the spasmodic
variety.
When the myelitis affects the lumbar region the bladder and rectum
are involved, the sphincters being first closed by spasm, and subsequently
incompetent from paralysis. Priapism must be regarded as a sign of
irritation produced either by interference with the conducting paths
passing from the brain to the lumbar portion of the cord, or by reflex
irritation proceeding from the bladder or skin. The trophic affections
of the muscles and bones are caused by lesion of the ganglion cells of
the anterior horns, while the cutaneous trophic affections and bedsores
appear to be caused by disease of the posterior horns. The vaso-motor
disturbances are caused by interference with the centres in the cord,
but the spinal mechanisms which preside over these functions are not
yet clearly ascertained.
In acute central myelitis the softening affects principally the gray
substance, which often flows out or becomes depressed under the surface
of section Avhen the cord is divided transversely. On microscopic ex-
amination the disease is seen to extend in the lumbar region forwards
from the central column into the anterior gray horns, the ganglion cells
of which may be entirely destroyed and also backwards into tlie posterior
gray horns, while in some cases the white substance, especially the
pyramidal tracts, may be implicated in the disea.se. In the cervical and
upper dorsal regions of the cord and in the medulla oldongata the disease
is restricted to the central gray column and the accessory cells of the
anterior gray horns and their continuations through the medulla, while
the fundamental cells in these regions may be entirely unaffected.
Hcemato myelitis is like acute central myelitis in every respect except
that in the former of the two the central softened mass assumes a
hemorrhagic character. In the cases of acute bulbar myelitis observed
by Leyden, small indefinite centres of softening were found in the
medulla oblongata.
In acute transverse myelitis the part of the cord in which the chief
lesion is localized is found in various stages of softening, and if the
case has assumed a more or less chronic form the usual ascending and
descending degenerations are observed above and below the primary
seat of the disease. In rapidly fatal cases evidences of inflammation
are discovered in the gray matter above and below the seat of the chief
VARIETIES OF DIFFUSED MYELITIS.
563
lesion. In the neighborhood of the primary lesion all the ganglion cells
of the anterior horns may be destroyed, but in the remote portions of
the cord the disease becomes more and more limited to the central o-ray
columns and to the margins of the groups of ganglion cells in the
anterior horns. The annexed diagram (Fig. 172) illustrates this condi-
tion, and although it was taken from a somewhat protracted case of
myelitis, I have observed similar appearances in the cervical region from
a case of fracture of the vertebral column in the dorsal region which
Fig. 172.
Section of the Middle or the Cervical Enlargement of the Spinal Cord from a Case of
Central Myelitis. (After Young )
i, The internal ; a, the anterior; al, the antero-lateral ; &nd pi, the pustero-lateral group. The median
area was completely destitute of cells, and a large number of the marginal cells of the different groups of
the anterior horn were destroyed or diseased.
proved fatal in five days. The continuation of the central column into
the medulla olilongata and its accessory nuclei are generally implicated.
In simple incised or punctured wounds of the spinal cord the cut edges
project at first beyond the pia and the wound is closed. In a few days
the membranes are reddened and covered with fibro-purulent matter,
while the neighboring parts of the cord are more or less softened. Crush-
ing of the cord causes softening and disintegration of the cord itself, and
congestion and hemorrhage into the membranes. If the patient survive
a kind of cicatrix is formed which may enclose cystic cavities containing
564 MYELITIS.
clear fluid. In acute myelo-meningitis the usual signs of meningitis
will be found along with those of myelitis, and in sections of the cord
tinted with carmine a highly stained border is observed which extends
more or less deeply into the substance of the cord and consequently this
form of disease has been called peripheric or cortical myelitis. Acute
disseminated myelitis occurs in small spots scattered through the sub-
stance of the cord. The morbid change appears to consist chiefly of
an increase of the interstitial tissue, which becomes unusually dense and
rich in nuclei.
. Chronic myelitis gives rise to gray degeneration or sclerosis of the
aff"ected parts, although the cord is sometimes found softened in the
main focus of disease. The connection between the morbid changes
and the symptoms is the same as in acute myelitis. In chronic cen-
tral myelitis the disease appears apparently as an acute central myelitis,
and then assumes the chronic form. It may pursue an ascending
course, but it is not so surely invading as Landry's paralysis. The
morbid appearances are the same as those found in other forms of cen-
tral myelitis, but in addition the white substance is invaded in the
lumbar region, the columns of Goll and the direct cerebellar tracts
undergo an ascending sclerosis, and the lateral columns in the lumbar
region a descending sclerosis. This disease may be set up by an injury
of the sciatic nerve or by the pressure of a tumor on the cauda equina,
and then the posterior root-zones in the dorsal region are implicated in
the sclerosis as well as the columns of Goll. In chronic transverse
myelitis the whole thickness of the spinal cord is implicated at the level
of the chief focus of disease, and at this point the cord may be found
softened. Above the level of the main lesion the columns of Goll and
the direct cerebellar tracts undergo an ascending, and below this level
the lateral columns undergo a descending sclerosis. Evidences of a
central myelitis are also frequently observed, the motor ganglion cells
are completely destroyed immediately above and below the main focus,
while in the parts which are remote from this lesion the morbid changes
are restricted to the central columns and the accessory nuclei. In
compression myelitis the primary disease may consist of caries, cancer,
or some other disease of the vertebral column, but it is unnecessary to
describe all these diseased conditions in this place. It may also consist
of some forms of meningitis, of an accumulation of pus between the
dura mater and vertebrae, or hematoma of the spinal dura mater, but
these aff'ections will subsequently be described. The following peri-
meningeal and meningeal tumors have been found in the vertebral
canal, namely: Lipoma, originating either from the tissue outside the
dura mater or from the pia mdiiev; fibroma ojid fibrosarcoma, vihxch.
VARIETIES OF DIFFUSED MYELITIS. 565
may be situated either within or without the sac of the dura mater*
sarcoma, myxoma, and psammoma, originating from the pia mater
or arachnoid ; enchondroma, springing from the vertebrae and dura
mater; osteoyna, appearing as disks in the arachnoid, and as a diffused
ossification of the dura mater; multiple fibrous melanoma, exception-
ally found in the spinal canal ; carcinoma, almost always met with as a
secondary growth from the mammae or vertebra; miliary tubercles,
which are always found on the soft membranes; and syphiloma, which
appears as gummata of the dura or pia mater. Neuromata, either
true or false, have been found on the roots of the spinal nerves, and
are most frequently situated on the cauda equina. Parasitic growths
are rarely met with in the vertebral canal, but echinococcus has been
occasionally met with, and Westphal has reported a case of cysticercus"
cellulos?e of the spinal cord.
The following are the intramedullary tumors which have been ob-
served, namely: Glioma, which may form a rounded tumor or may
infiltrate the gray matter throughout the whole length of the spinal
cord; myxoglioma, which is only a variety of glioma; gliosarcoma,
myxosarcoma, sarcoma, and carcinoma are rare in the substance of the
cord; nested sarcoma, with calcareous deposit at parts of the growth
forming psammoma, may infiltrate considerable portions of the cord
and replace the nervous tissues while retaining the form of the cord ;
solitary tubercles, which may be situated either in the gray or white
matter; syphilotna, which in the form of gumma is only rarely found
in the substance of the cord; and the cystic dilatation described as
syringomyelitis.
The substance of the spinal cord is rendered more or less flat and
thin at the point compressed, so that it may be reduced to the size of a
small quill, and in chronic cases the usual ascending and descending
changes occur above and below the level of the lesion.
In hemiparaplegia the chief lesion and the secondary changes are
restricted to one-half of the cord. Interruption, with subsequent de-
scending sclerosis of the fibres of the lateral column, produces a spas-
modic paralysis of the muscles, vaso-motor paralysis, and loss of the
muscular sensibility and the muscular sense of the parts innervated
from below the level of the lesion, while destruction of the posterior
horns and the posterior columns, causes loss of the sense of touch and
temperature, and of common sensation on the side opposite the lesion
(Fig. 173). The anaesthetic belt which surrounds the half of the body
on a level with and on the same side as the lesion, is caused by impli-
cation of the posterior root-fibres, and the narrow hyperaesthetic zone
which is frequently observed on both sides above the level of the anses-
566
MYELITIS.
thetic belt, is supposed by Brown-Sequard to be caused by irritation of
descending fibres of those posterior roots which are situated immedi-
ately above the level of the lesion. In uiiiversal progressive myelitis
the whole of the transverse area of the cord is diseased in the lumbar
and lower dorsal regions, but in the upper dorsal and cervical regions,
the sclerosis may be limited to the columns of Goll and the direct cere-
FiG. 173.
It t t tl
Diagram of the Gouhse of the Piunxipai. (,'oxdu(-tino Paths within the f'oRD. (After Krb.)
1 and 1', The motor and vaso-motor tnicts, passing through tlie anterior root (i;), and remaining on the
eame side of the cord ; 2 and 2', Tracts which conduct the muscular sensibility, also passing through the
anterior roots, and remaining on the same side of the cord: 3 ami 3', The tracts which conduct sensory
impressions of touch, temperature, pain, and tickling. These enter flic cord through the posterior roots,
and cross to the other side, and pursue their course upwards on that side. Section of the right half of the
cord (n) must interrupt conduction through the motor, vaso-motor, and musculo-sensory tracts (1 and 2)
on the right side, and the cutaneous sensory tracts on the left side (3').
bellar tracts, while associated with them may sometimes be found a
certain degree of chronic central myelitis.
In chronic myelo-menim/itis the spinal cord is surrounded by a ring
of sclero.sed tissue, and consequently this form of myelitis has been
named by Yulpian peripheric or cortical myelitis, or ring-shaped scle-
rosis. Chronic disseminated myelitis will be subsequently described.
Treatment. — In acute myelitis active antiphlogistic treatment must
be adopted during the febrile stage and Chapman's ice bag should be
applied along the spine, while the patient should lie as much as possible
on his side or abdomen. It is also desirable to place the patient on a
water bed and the parts exposed to pressure should be sponged with
brandy or whiskey, and dusted with an absorbent powder in order to
prevent, if possible, the formation of beds<ores. In the very acute stage
VARIETIES OF DIFFUSED MYELITIS. 567
of myelitis a saline mixture may be given in order to maintain the
activity of the skin and kidneys, and the bowels should be freely acted
on by mineral waters containing sulphate of magnesia, or bv senna
rhubarb, or castor oil. Belladonna and ergot are supposed to contract
the capillaries of the spinal cord and either one or other may be ad-
ministered in the early stage of myelitis, and when the fever has sub-
sided iodide of potassium may be given to promote absorption of effused
products. When myelitis is developed in the course of syphilis large
doses of iodide of potassium should be administered, while mercury
should also be given either in combination with the iodide salt, by in-
unction, or by subcutaneous injection. Counter-irritation and electrical
treatment should not be used until the disease has become more or less
chronic. Great care should be observed in introducing the catheter for
fear of setting up or aggravating cystitis, and every precaution should
be taken to prevent the introduction of bacteria into the bladder along
with the instrument.
Chronic myelitis must be treated in the earlier stages of the disease
on the same general principles as are applicable to the acute disease.
The patient should be kept in the recumbent posture, the usual pre-
cautions against the appearance of cystitis and bedsores must be taken,
and ergot, belladonna, or iodide of potassium should be given internally.
Counter-irritation to the vertebral column should only be used with
caution, but in transverse myelitis Corrigan's button may be applied
at two or three points on each side of the vertebral column opposite the
seat of the lesion. The application of a water douche at a temperature
of from 98° to 104° F. over the back is sometimes very soothing.
When all acute symptoms have sul;)sided and the disease is more or less
stationary arsenic or phosphol'us with cod-liver oil may be found useful,
but strychnine should on no account be administered.
Baths of various kinds are found useful in the treatment of chronic
myelitis, and Erb recommended the use of the thermal brine baths Avith
a temperature of from 88° to 78° F., while ordinary brine baths,
chalybeate, and mud baths are recommended by others. The temper-
ature in most cases should in my opinion be considerably above that
recommended by Erb, but this point must be largely determined by the
feelings of the patient.
Hydropathic treatment is also useful, but great care should lie taken
not to use a too exciting method, and consequently cold douches and
slappings should be avoided.
The galvanic current is one of the most useful therapeutic agents for
the treatment of chronic myelitis. The poles should be placed over the
vertebral column in such positions that the diseased portion of the cord
568 MYELITIS.
is included in the circuit, and either a stabile or a slowly labile current
may be employed. The currents should not be strong and each appli-
cation should be of short duration. This treatment should be continued
for months, being occasionally interrupted but only to be recommenced
after a brief pause.
The patient should avoid all overexertion, or mental excitement, and
should lead a very regular life, Avhile the diet should be simple, nutritious,
and easy of digestion. Alcoholic drinks, tea, coffee, and tobacco should
only be used very sparingly, and sexual intercourse should be confined
within the strictest limits or absolutely prohibited. Residence in a
mountainous region at a moderate elevation, or at the seaside, will be
useful, and it is often advisable for the patient to spend the winter in
the South. When completely paraplegic the patient should be allowed
to enjoy the fresh air in a wheeled chair, and when bedridden care
should be taken that the patient is made to lie alternately on either side
or in the prone position in order to avoid as long as possible the forma-
tion of bedsores, the appearance of which would be accelerated were
the patient permitted to be always in the recumbent posture.
Pain must be relieved by narcotics, such as the subcutaneous injection
of morphia. The faradic brush, Preissnitz's compresses, applications of
chloroform, and frictions with veratrine ointment and soothing liniments
will be found useful in the treatment of many of the sensory disorders
which arise in the course of a chronic myelitis, while electrical currents
form the best local application for the removal of the paralyses, atrophies,
and anaesthesia which persist after the disease has run it course.
CHAPTEK XII.
DISEASES OF THE SPINAL MEMBRANES.
I. VASCULAR DISEASES OF THE SPINAL MEMBRANES.
1. Hypek^mia.
Hyperj^.mia of the spinal membranes has already been considered
along with hyperpemia of the spinal cord.
2. H.EMATORRIIACHIS (MENINGEAL ApOPLEXY).
Etiology. — Very little is known with regard to the predisposing causes
of hsematorrhachis, but it occurs more frequently in men than in women.
The most usual exciting causes are injuries of the spinal column, caries
of the vertebrfe, excessive bodily exertion, the spasms of convulsive
diseases like epilepsy, and the sudden suppression of accustomed dis-
charges. It may also occur in such diseases as scorbutus, purpura
hemorrhagica, smallpox, typhoid fever, and other acute infectious diseases.
Aneurisms have been known to rupture into the vertebral canal, and
blood effused into the l^rain or cerebral membranes may sometimes pass
down into the spinal canal.
Symptoms. — The patient is suddenly attacked with violent pains and
falls down, but generally without loss of consciousness. The severest
pain is localized at a spot over the spinal column corresponding to the
seat of the hemorrhage, but this pain is associated with eccentric sensa-
tions such as formication, burning, and tingling, which radiate along the
distribution of the nerves the roots of which are first implicated, while
an objective examination reveals anaesthesia or hypersesthesia of these
nerve-territories. The early motor symptoms consist of spasmodic
jerking and trembling of the extremities, or of a tonic spasm of various
groups of muscles which causes the extremities to be forcibly flexed or
the head to be retracted or rotated towards one shoulder. The vertebral
column is likewise stiff" and painful and the patient is unable to raise
himself in bed or to assume the sitting posture.
The irritative symptoms give place after a time to those of sensory
and motor paralysis, but complete paraplegia is rare, and the anaesthesia
570 DISEASES OF THE SPINAL MEMBKAXES.
also is seldom complete on objective examination, but the patient com-
plains of subjective sensations of SAvelliug and heaviness of the limbs
and trunk, and of feelings of numbness and tingling.
The reflex excitability is said to be depressed in some cases, but
probably this only occurs in the region supplied by fibres derived from
the nerve roots directly aifected ; weakness of the bladder and rectum
is present only in severe cases, and fever is absent at first, but may
occur on the second or third day. The symptoms remain stationary
for some time, but Avhen the disease is uncomplicated it often runs a
favorable course and a tolerable recovery may take place in a few Aveeks
or months.
Varieties. — (1) If the lumbar region is affected there are pains and
stiffness in the loins, tearing pains in the loAver extremities, perineum,
bladder, and genitals, well-marked paralysis of the lower extremities,
loss of the reflexes, and paralysis of the bladder and rectum.
(2) If the dorsal region is affected there are pains in the back and
abdomen, girdle-pain, stiffness in the dorsal part of the spine, paralysis
of the legs and abdominal muscles, and retention of the reflexes in the
lower extremities.
(3) If the cervical region is affected there are pains in the arms and
shoulders, stiffness of the neck, and pain in the occiput. The anaes-
thesia and paralysis are most marked in the upper extremities, and
oculo-pupillary symptoms, difficulty of breathing, and a retarded and
feeble pulse may be present. When the upper cervical region is affected
sudden death from respiratory paralysis may occur.
II. INFLAMMATION OF THE SPINAL DURA MATER
(PACHYMENINGITIS SPINALIS, PERIMENINGITIS).
Pachymeningitis may be divided into inflammation of 1, the external
layers of the dura mater and the surrounding cellular tissue, or external
pachymeningitis ; and 2, the internal surface of the membrane with
deposition of morbid products between the dura mater and arachnoid,
or internal piachy meningitis.
1. Pachymexingitis Spinalis Externa (Peripachymeningitis).
Etiology. — Various diseases in and about the vertebral column, such
as vertebral caries and bedsores, constitute the most fre(j[uent causes of
this disease, but it may possibly arise occasionally as an idiopathic
affection.
1
INFLAMMATION OF THE SPINAL DURA MATER. 571
Symptoms. — The symptoms of external spinal pachymeningitis may
develop in an acute or chronic form. In the acute purulent forms the
prominent symptoms are caused by irritation and consist of pain and
rigidity of the back, great tenderness on pressure, shooting pains in the
lower extremities, and pain in the joints, while there may he consider-
able elevation of temperature, diarrhoea, and other general symptoms.
In the acute form the sym])toms of transverse myelitis may be more or
less suddenly developed. In the chronic fibrinous form of the disease
the premonitory symptoms are obscure and the symptoms of slow com-
pression of the cord or of a chronic transverse myelitis with secondary
degenerations predominate. These symptoms comprise both sensory
and motor paralysis below the level of the lesion, muscular tension,
increased cutaneous reflexes and tendon-reactions, and after a time
paralysis of the sphincters and bedsores.
2. Pachymeningitis Interna.
Internal pachymeningitis may be divided into a, the hypertrophic,
and h, the hemorrhagic varieties.
a. Pachymeningitis Interna Hypertrophica.
Etiology. — The causes usually assigned to the hypertrophic variety
are exposure to cold and damp, and the excessive use of alcohol.
Symptoms. — The hypertrophic form usually occurs in the cervical
region and it generally begins by neuralgiform pains in the neck and head
which shoot into the shoulders and arms, and by a painful girdle sensa-
tion in the upper part of the chest. The muscles of the neck are in
a state of spasmodic rigidity, the patient often complains of formication
and numbness of the upper extremities, and vesicular herpetic eruptions
may make their appearance on the upper extremities.
The transition to the second stage is characterized by the gradual
development of paralysis, which is usually of the atrophic variety in
the upper extremities, and of the spasmodic in the lower. When the
lesion is situated on a level with the eighth cervical and first dorsal
nerves, both hands are maintained in the position of exaggerated ex-
tension, and the segments of the thumb are also extended, while the
phalanges of the fingers are partially flexed on the metacarpal bones
and upon one another, the fingers being thus held like claAvs (Fig. 175).
In a case o^ pachymeningitis on the level of the eighth cervical and first
and second dorsal nerves which was under my care, the hands were
only hyperextended when the patient endeavored to grasp, while the
572
DISEASES OF THE SPINAL MEMBEANES.
distribution of the anaesthesia is seen in Fig. 174. Oculo-pupillary
phenomena, first of the irritative kind, and as the disease advances of
the paralytic kind, are always present Avhen the eighth cervical and
first dorsal nerve roots are implicated, and they may also be present
when the lesion is situated on a higher level if the cord undergoes
considerable compression, or if there be transverse myelitis. When
the lesion is situated above the level of the eighth cervical nerve the
Fig. 174.
distended position of the hand, and the distribution of the anaesthesia
differ from those just described. In a case under the care of my col-
league, Dr. Leach, in which the lesion was situated on a level with the
fifth, sixth, and probably the seventh cervical nerves, the arm was held
close to the side, the forearm was extended on the arm and strongly
pronated, the hand was strongly flexed on the arm, the fingers were on
a line with or only slightly extended on the metacarpal bones, and the
phalanges were extended upon one another, while the thumb was flexed
into the palm. All the muscles of the forearm and hand were doubt-
INFLAMMATION OF THE SPINAL DURA MATKR. 573
less more or less paralyzed, but the muscles supplied by tlie musculo-
spiral nerve were, on the whole, more aftected than those supplied by
the ulnar and median nerves, contrary to what takes place when the
lesion is situated on a level with the junction of the cervical and dorsal
regions of the cord. In another case under my care, in which the
spinous process of the fourth cervical vertebra was tender to pressure
and the skin of that region sensitive to the cathode of the galvanic
current, the symptoms were slight spasmodic paralysis of the lower
extremities; feebleness with diffused wasting of all the muscles of the
Fig. 175.
Attitude of the Hand in Pachymeningitis Cekvicalis HypERTRorHirA, when the Lesion is
SITUATED ON A LeVEI, WITH THE UPPER HALF OF THE CERVICAL ENLARGEMENT.
upper extremities, most marked in the deltoid, biceps, and supinator
longus; arthropathies of the small joints of both hands; dilatation of
the pupils, with widening of the palpebral apertures, most pronounced
on the left side; and troublesome hiccough, which persisted continuously
during waking hours for about ten days after the patient was laid on
her back in bed, and which, after abating, could be readily excited
again by any movement of the head. The sensory phenomena con-
sisted of stiff"ness of the neck, and pains on a level with the fourth
cervical vertebra, which radiated on both sides of the neck and down
the shoulders, but there was no anaesthesia. The patient recovered.
h. Pachymeningitis Interna Hemorrliagica.
The symptoms of internal hemorrhagic pachymeningitis are very
obscure, and are usually complicated with those of coexisting cerebral
disease. They consist of pains in the loins and back, tearing pains in
the extremities, stiffness of the vertebral column, increasing muscular
574 DISEASES OF THE SPINAL MEMBRANES.
weakness which may gradually develop into complete paraplegia with
contractures, various degrees of cutaneous hyperpesthesia or anaesthesia,
and weakness of the bladder. If a patient with these symptoms is at
the same time suffering from chronic alcoholism and cerebral paralysis,
internal hemorrhagic pachymeningitis may be suspected.
III. INFLAMMATION OF THE SPINAL PIA MATER AND ARACH-
NOID— LEPTOMENINGITIS SPINALIS ; PERIMYELITIS AND
ARACHNITIS.
Spinal leptomeningitis presents many varieties, but for practical
purposes it will suffice to divide the disease into the acute and the
chronic forms.
1. Leptomeningitis Spinalis Acuta.
Etiology. — The predisposing causes of acute meningitis are a scrofu-
lous or tubercular constitution, insufficient food, damp dwellings, and
sexual or other excesses. The disease attacks by preference children,
young persons, and the male sex. The most important of the exciting
causes are exposure to cold, wounds and injuries of the vertebral column,
and extension of inflammation from neighboring structures. Spinal
meningitis may occur along with or during convalescence from pneu-
monia, acute articular rheumatism, and febrile and infectious diseases,
and it is a very usual complication of tul)ercular basal meningitis.
Epidemic cerebro-spinal meningitis is an infectious disease, and its
consideration is beyond the scope of this work.
Symptoms. — Acute spinal meningitis is generally complicated by a
simultaneous affection of the cerebral pia mater, and it is not always
easy to separate the spinal from the cerebral symptoms. The outbreak
of the characteristic symj)toms of si)inal meningitis may be preceded
by premonitory symptoms consisting of general heaviness and depres-
sion, slight chilliness, gastric disturbances, transitory pains in the head
and back, restlessness, and sleeplessness. 'I'he characteristic symptoms
of the disease are ushered in by a rigor followed by fever of irregular
type, and, if the pia mater of the brain be affected, vomiting and other
severe cerebral symptoms are present. The patient now complains of
an intense, deep-seated, boring pain in the loins, back, or nape of the
neck, corresponding to the seat of the lesion. The pain radiates from
the vertebral column round the trunk, and shoots in all directions
through the extremities, while it is aggravated by all movements of the
spine, and by pressure on the spinous processes. It may abate for a
time, but a remission is generally folloAved by an exacerbation of great
severity.
INFLAMMATION OF SPINAL PIA MATER. 575
The muscles of the back are in a state of spasmodic rigidity, which
may sometimes extend the whole length of the spine so as to resemble
a tetanic seizure, but at other times is limited to a part of the vertebral
column corresponding to the seat of the lesion. The muscles of the
extremities are also tense and contracted, and the limbs are then rigid
and immovable or the subjects of painful twitchings.
Cutaneous and muscular hyperesthesia are often present in the ex-
tremities and trunk, the distribution corresponding to the areas supplied
by fibres derived from the posterior roots of the part affected. The
reflex actions are increased at first, but they are liable to be diminished
or lost in the later stages of the lesion.
Disorders of the function of the bladder occur at an early period of
the disease, caused, most probably, by spasm of the sphincters, and
when the cervical region is affected the respiratory muscles become
rigid and painful, giving rise to a difficulty of breathing, which may
increase to such an extent as to cause asphyxia.
As the disease progresses cutaneous sensibility becomes diminislied
and complete anaesthesia may be established, while the extremities
manifest various degrees of motor weakness up to complete paralysis.
The pupils may be contracted, dilated, or unequal, and if the inflam-
mation extends to the medulla oblongata or to the base of the cranium,
the patient suffers from vertigo, headache, paralysis of ocular muscles,
and delirium, which soon terminates in unconsciousness and fatal coma
with hyperpyrexia. At other times deceitful signs of temporary im-
provement appear, but paralysis and bedsores supervene, and the
patient dies from septic fever. In slight cases recovery may take
place, but convalescence is slowly established, and the symptoms of
sensory and motor irritation disappear only after a long period. In
many cases incurable defects are left behind, consisting of anaesthesia,
some degree of ataxia, atrophic paralysis of some groups of muscles,
and spasmodic paralysis of other gi-oups.
2. Leptomeningitis^ Spinalis Chronica.
Etiology. — The disease frequently develops from the acute form and
is produced from the same causes.
Symptoms. — The disease begins more insidiously than the acute
variety. The patient complains of a gradually increasing pain and
stiffness in the back, various parajsthesiae in the lower extremities, and
a feeling of weakness and heaviness of the limbs. Eccentric pains
are felt in the areas of distribution of the nerves Avhose roots are impli-
576 DISEASES OF THE SPINAL MEMBRANES.
cated in the lesion, consisting of shooting pains in the lower or upper
extremities or a girdle sensation round the body according to the situation
of the lesion. Hypersesthesia of the skin of the lower extremities is
frequently present, but anaesthesia is rare, and when present it consists
mostly of blunting of the sensibility of the feet and lower part of the
legs. The motor symptoms consist of stiffness of the back and neck,
and an involuntary drawing up or extension of the extremities, but the
phenomena of motor irritation are never very prominent in this disease.
After a time the limbs become heavy and feeble, but complete paraplegia
is rare. When, however, the lower extremities are more or less com-
pletely paralyzed the muscles become tense, and contractures with flexion
of the limbs or flexion of one limb and extension of the other are estab-
lished, but the patellar tendon-reactions are often absent under such
circumstances. If there be a considerable effusion of spinal fluid, the
paralysis becomes augmented when the patient stands, but at other times
it is most marked when the patient is lying on his back, probably because
the cord becomes passively congested. In severe cases the paralyzed
muscles may undergo atrophy ; aniesthesia is developed ; the cutaneous
reflexes and the tendon-reactions are lost ; bedsores and cystitis appear
and the patient dies from pyaemia.
Morbid Physiology. — The morbid anatomy of hemorrhage and in-
flammation of the spinal membranes has already been sufiiciently con-
sidered. In connecting the morbid process with the symptoms the
chief points to notice are that the most j)rominent pheiiomena of the
various affections are caused by irritation or paralysis of the posterior
and anterior loots on a level with the lesion, and irritation or paralysis
of the sensory and motor conducting paths below the level of the lesion.
In disease of the membranes tliere are two causes of sensory disorder —
disease of the posterior roots and of the conducting paths in the posterior
columns and posterior gray horns ; and two causes of spasm or paralysis
— disease of the anterior roots and of the motor conducting paths in
the lateral columns. It is important to remember that disease of the
anterior root gives rise to an atrophic, and of the lateral column to a
spasmodic paralysis. In cases recovering from an attack of meningitis
ataxic symptoms may be present from the persistence of the disease in
the posterior columns, and when the posterior columns are affected on
a level with the upper part of the lumbar enlargement the patellar
tendon-reactions will be absent from interference with its reflex loop,
whether paralysis be present or not. When the lesion is on a level
with the cilio-spinal region, oculo-pupillary symptoms, and when on a
level with the upper part of the lumbar enlargement, disorders of the
hladder and rectum will be present.
INFLAMMATIOX OF SPINAL PIA MATEE. 577
Treatment. — In meningeal hemorrhage the patient should be main-
tained at rest on his side or face and an ice bag applied to the vertebral
column, and ergot may be given internally. Leyden recommends the
use of mercurial inunction and repeated small doses of calomel during
the period of reaction, but when this stage has passed absorption may be
promoted by the administration of iodide of potassium. The vertebral
column may be painted with iodine, and the galvanic current will also
be found useful in promoting recovery.
In external pachymeningitis the treatment must be directed ao-ainst
the primary lesion, and when vertebral caries is present the patient ought
to be placed on his back on a water bed until the acute symptoms have
subsided, and the subsequent treatment must be conducted with a Sayre's
jacket or other form of spinal support. The actual cautery applied in
the vicinity of the diseased vertebrae is often a very useful remedy, and
iodide of potassium, iodide of iron, or friction with mercurial ointment
may each be advantageously employed according to the nature of the
case. When the primary disease has been arrested and the symptoms
have become chronic, galvanic treatment Avill be found to promote re-
covery from the sensory and motor disorders.
In internal pachymeningitis and leptomeningitis the same general
principles are applied to the treatment of both diseases. In the early
stage of acute meningitis cold must be applied to the spine by means of
Chapman's ice bag, while leeches may be applied to the vertebral
column and a smart saline purgative administered. When the temper-
ature has fallen blisters or some other form of counter-irritation should
be applied along the spine, and when the acute symptoms have subsided
a mercurial treatment Avill prove useful, inunction being probably the
most efficient method of administration. The patient should lie on his
face or side, and when hyperaesthesia, pain, or sleeplessness are urgent
symptoms sedatives must be given, the best form of administration being
a subcutaneous injection of morphia. Warm baths afford great relief,
and moist packing of the whole body often soothes and induces sleep.
In chronic spinal meningitis repeated blisters may be applied along
the vertebral column, while moderate doses of iodide of potassium are
given internally. Mercury should not be administered unless the
presence of syphilis is suspected, while ergot and belladonna have not
been found so useful as in myelitis. Warm baths and douches are very
soothing to the patient, and a galvanic current of moderate strength
may be employed, either applied to the spine or in tlie course of the
nerves which are the subjects of eccentric pains.
CHAPTEE XIII.
CERTAIN FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
I. SPINAL IRRITATION.
Etiology. — The female sex predispose to this disease, although men
are occasionally affected. The members of neuropathic families are
o-enerally attacked, and most of the cases occur between fifteen and
thirty years of age.
The exciting causes are emotional disturbances, sexual excesses,
exhausting diseases, and everything which weakens the nervous system.
Symptoms. — The symptoms begin with headache, sleeplessness, in-
creased nervous irritability, ill-defined pains in the back, neuralgiform
pains in the face or extremities, and general feebleness, these symptoms
gradually increasing in intensity until the disease is fully developed.
The patient now complains of pain in the back, which is aggravated
by exertion, and is situated most frequently between the shoulder-
blades, or in the back of the neck, and less frequently in the loins.
The spinous processes of some of the vertebmc are excessively tender
to pressure, and over these processes the surface is found to be very
sensitive when a hot sponge or the cathode of a galvanic current is
applied. Tenderness of the vertebrpe to pressure is, indeed, the most
constant and important symptom of spinal irritation, and this sign is
rendered all the more valuable from the fact that spinal tenderness is
never a prominent symptom of myelitis and other organic diseases of
the cord.
The patient complains of various parsesthesiae and neuralgiform pains
in the upper and lower extremities, occiput, face, pelvic region, bladder,
genitals, or viscera ; the slightest exertion occasions great fatigue and
exhaustion ; and walking soon becomes impossible owing to the exces-
sive pain caused by it.
The motor symptoms consist of fibrillary twitchings, spasms of some
muscles, choreic movements, hiccough, and even permanent contrac-
tures in rare cases. Epileptic attacks ai'e said to have been occasionally
observed, but it is more likely that these general convulsions were
Ijysterical seizures. A certain degree of muscular weakness may be
present in some cases, but real paralysis has never been observed.
NEUKASTHEXIA. 579
The vaso-motor disorders consist of coldness of the hands and feet
and the patients are apt to turn pale or red on the slightest provocation.
The most common visceral disorders met with are eructations, nausea,
vomiting, palpitations, asthmatic breathing, cough, vesical spasm, and
polyuria. The patient also complains of noises in the ears, dizziness,
muscae volitantes and other disorders of vision, sleeplessness, and great
mental depression or irritability. The brothers Griffin divided the
disease into several varieties, and endeavored to connect the symptoms
present in each case with the localization of the spinal tenderness in
the cervical, dorsal, or lumbar regions, but the symptoms first enumer-
ated are frequently met with in cases of hysteria in the entire absence
of spinal tenderness. I have never been able to assure myself that
the divisions of the brothers Griffin are borne out by clinical facts.
Spinal irritation is never a fatal disease, although it may last for months
or years and cause great suffering to the patient.
II. NEUKASTHENIA.
Etiology. — Neurasthenia consists of exhaustion of the cerebro-spinal
centres, and generally occurs in neuropathic families, and the male is
more liable to the disease than the female sex. Neurasthenia may be
a sequel of any exhausting disease, but it is generally caused by over-
work and worry, or by sexual and other excesses.
Symjjtoms. — The symptoms vary according as the weakness declares
itself in the spinal or cerebral centres, although in most cases both
groups of symptoms are variously combined.
In spinal neurasthenia the patient complains of weakness of the
lower extremities, which may sometimes be so great as to amount to a
slight degree of paralysis. The arms also are readily fatigued, but
the weakness in them never reaches the same degree of intensity as in
the legs. The sensory disturbances consist of pains in the back and
neuralgiform pains in the extremities, which may sometimes be so
intense as to simulate the pains of locomotor ataxia, although in the
former disease they are never so acute and darting as in the latter.
The patient also complains of numbness and formication in the lower
extremities, the hands and feet are cold, and the body is apt to be
bathed in sweat at night, and during the day on slight exertion. The
sexual power is generally diminished, and the act of coition is followed
by great prostration, disturbed sleep, and a fidgetty, restless feeling in
the lower extremities. The functions of the bladder are usually normal,
although a little dribbling of urine may occasionally be present.
580 FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
In cerebral neurasthenia one of the most constant symptoms is a dif-
fused tenderness of the scalp, which is exquisitely sensitive to a slight
touch, such as that caused hy a comb or by a slight ruffling of the hair
over the part, but the pain is relieved by deep and steady pressure.
The patient also complains of a sense of pressure over the vertex, Avhich
is sometimes compared to the feeling that might be caused by a mailed
hand being laid heavily over the head. This pain, which is distinct
from the sense of tenderness, is most proba,bly caused by the ani^emia
which so frequently accompanies the affection. Neurasthenic patients
are also liable to suffer from migraine headaches, and facial neuralgia,
but the only connection between it and these affections appears to be
that all of them are liable to occur in neuropathic families.
The motor disorders of cerebral neurasthenia are jerkings of the
limbs, which are particularly troublesome when the patient is about to
fall asleep ; tremors of the hand ; and slight clonic spasms of the facial
muscles, which may be limited to the orbicular muscle of the eye, or
to the angle of the mouth, or implicate a large number of the muscles,
so as to constitute a decided facial tic. The patient complains of heavi-
ness of the limbs and is soon fatigued, and decided paralysis is common
in females but not in males. The sensory disorders are very numerous
in cerebral neurasthenia. In addition to the sensory disorders already
described as belonging to the spinal disease, patients are liable to suffer
from numbness and tingling in the extremities from slight pressure on
the nerves.
Pressure by the edge of a chair over the sciatic nerve causes numb-
ness of the foot, while tingling of the hand is readily caused if the
arm rests for a short time over a chair. Sleep is frequently disturbed
by feelings of " pins and needles " in one hand and arm, caused doubt-
less by a slight pressure exerted on the brachial plexus or some of its
branches. Hemiansesthesia is a common symptom of neurasthenia in
women, and men sometimes complain of abnormal sensations in one-
half the body but in them they usually assume the form of a hyper-
algesia rather than loss of feeling. Tlie nerves of special sense are
almost always affected. The patient complains of a sour or bitter taste,
and may have subjective sensations of the smell of phosphorus or other
odors, while his perception of flavors and relishes is much diminished.
The patient is also troubled with various noises in the ears, and on
lying down at night he is so much disturbed with rushing sounds and
hearing the beating of his heart with unusual distinctness that he is
obliged to lie on his back to avoid his ear coming in contact with the
pillows, while in the morning there is decided deafness which is accom-
panied by distressing attacks of yawning. Sight is affected in various
NEURASTHENIA. 581
ways ; the patient suffers from muscae volitantes, colored vision, and
spectral illusions, the latter being specially liable to appear when the
eyes are closed for sleep at night. Vision may be impaired either from
defective nutrition of the sensory nervous mechanism, or from feebleness
of accommodation and of the internal recti muscles.
The vaso-motor disorders of neurasthenia are numerous. One of the
most common is blushing, which may spread not only over the face, but
also over the neck and other parts of the body, or pallor may take the
place of a blush owing to vaso-motor spasm. Neurasthenic patients
are very liable to suffer from cold hands and feet, which are sometimes
bathed in a clammy sweat and at other times abnormally dry ; they
also complain of coldness of the knees and other joints, and chills
passing along the spine, all of them being symptoms which may be
attributed to disorder of the vaso-motor system.
The organic functions are profoundly affected in cerebral neurasthenia.
The heart is irritable, its action is often tumultuous, and the patient is
painfully sensible of its beatings. The pulse is compressible, irregular,
and increased in frequency, and may on slight exertion beat one hundred
times or more in the minute. Some of the most distressing symptoms
are caused by nervous dyspepsia (apepsia nervosa). The patient may
take a fair quantitity of food at a meal although he is never really
hungry and scarcely ever feels as if the stomach were quite empty. It
seems as if a portion of the food were always retained owing to the
inability of the stomach to empty itself from simple inertia, and a certain
degree of dilatation of the organ may be discovered on physical ex-
amination. The introduction of fresh food into the stomach often brings
a sense of relief and comfort, but it is only of short duration, and soon
after a meal the patient experiences a painful feeling of distention in
the epigastrium, a sensation of fulness in the head, confusion of thought,
an indisposition to undertake any work, and a sense of profound and
indescribable misery. The bowels are constipated, or attacks of diarrhoea
alternate with constipation, and the patient is much distressed with
flatulent distention of the abdomen Avhich often becomes blown up
suddenly in the most unaccountable manner. The urine is sometimes
abundant and of low specific gravity, at other times it is unusually acid
and contains an excess of urates, while oxalic acid crystals are often
found in it.
The psycJiical disorders are numerous and variable. One of the
most constant is sleeplessness. Some patients sleep soon after going to
bed, but awake with a start in the early morning, and are unable to fall
asleep again. This start is often very painful, the patient sometimes
experiencing a feeling as if he had received a blow with a heavy mallet
582 FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
on the top of the head. In other cases the subject lies awake for hours
after going to bed and sleeps best in the morning. In almost all cases
the sleep is disturbed by dreams which are always of a disagreeable
character, and in the morning the sufferer rises unrefreshed and with a
dull aching head.
The patient is liable to suffer from morbid fears, which may assume
various forms in difterent cases. The chronic hypochondriacal patient,
who goes from physician to physician and from hospital to hospital wich
the fixed idea that he is the subject of every imaginable disease, is well
known, but many other varieties of morbid fear are met with in neuras-
thenia. The following morbid fears have received separate names :
Astrophobia, fear of lightning ; topophobia, fear of places, including
agoraphobia, fear of open, and claustrophobia, fear of narrow places ;
anthrophobia, fear of men and of society generally, mcin^xng gynephobia,
a special fear of women ; monophobia, fear of being alone ; pathophobia,
fear of disease ; photophobia, fear of light ; and mysophobia, fear of
contamination. In addition to these many other unreasoning fears
might be mentioned, such as a dread of poverty, which, even in cases
in which the fear is not altogether groundless, becomes morbidly ex-
aggerated. Another fear Avhicli haunts the neurasthenic patient is an
intense dread of not fjilling asleep on going to bed, a dread which in
many cases becomes the cause of the sleejdessness which is so much
feared. In some cases this fear is so overpowering that the patient sits
in an armchair the whole night rather than risk jroino; to bed, while at
other times he will not go to bed without having a glass of whiskey or
some narcotic. Such patients are, indeed, liable to develop a morbid
craving for stimulants or narcotics. The power of self-control is
diminished, and if once a neurasthenic patient give way to an illegitimate
indulgence or to excess in a legitimate one the vice is apt to acquire an
overpowering mastery over him. In neurasthenia, therefore, the patient
is apt to give way to alcoholic and sexual excesses, and many are prob-
ably tempted to overstep the line which divides vice from crime.
< The intellectual condition of those suffering from neurasthenia is very
interesting. The first indication of commencing nervous exhaustion
may be an unwonted difficulty in recalling the names of individuals.
In a further stage of this amnesia the patient forgets the names of
familiar objects and he has frequently to indicate his meaning by a
jDaraphrase; for example, he may have to call a "chair," "the thing
yon are sitting upon." I have known a person suffering from neuras-
thenia who had the greatest possible difficulty in completing a simple
sentence, owing to his forgetfulness of the names of objects, and to
maintain a conversation for a brief period required an intense effort
NEURASTHENIA. 583
which was followed by profound exhaustion. In other cases the patient
is able to converse freely, but is unable to write a letter without dan-
ger of misspelling simple words and committing mistakes in grammar
and diction. But a man who is apt to forget the name of his most in-
timate friend, who is exhausted by having to carry on a brief con-
versation, who is unable to write a simple business letter, and who can-
not concentrate his attention for more than a few minutes at a time
upon any ordinary subject, may be quite capable of grasping as Avell as
ever the profoundest speculations of philosophy. Educated men, indeed,
have a tendency, when their nervous systems become exhausted, to brood
over such questions as the relation between mind and matter, the doc-
trines of free will and necessity, the existence of evil, the nature of the
first cause, and the other great insoluble problems of the universe. And
it may be taken as one of the first indications of recovery when the
patient is able to set his mind free from these all-absorbing questions
and becomes again interested in the practical details of life.
In disposition the patient is shy, and to strangers he is reserved, but
he is apt to exhaust the patience of his friends by interminable com-
plaints of his morbid feelings and suiferings. The degree of shyness
which the patient manifests may vary from simple coyness to a condition
in which he is utterly unable to enter any kind of society, and avoids
converse with anyone except a few intimate friends. We have already
seen that the patient blushes or becomes pale on the slightest provocation,
and when conversing with a stranger he averts his eyes, or he may be
unduly watchful and have a slight staring expression as if he were try-
ing to read what is being thought of him. In manner he is fidgetty
and frequently changes his position ; his hands are in constant move-
ment and he either nervously pulls his beard or seizes and displaces
small objects which may be near him ; his expression is changeable but
always self-conscious ; his voice is feeble, in aggravated cases the patient
experiences difficulty in articulating polysyllabic words ; and even the
manner in which he shakes hands is lacking in energy.
The symptoms of neurasthenia usually make their appearance between
the sixteenth and fiftieth year of age, and the attack generally super-
venes when the mind is subjected to some unusual strain or worry. The
symptoms are exceedingly variable and it is impossible to draw the line
which separates neurasthenia from hysteria on the one hand and melan-
cholia on the other. The duration of the affection depends greatly
upon the circumstances and surroundings of the patient. If the symp-
toms have been induced by overwork, and it be possible for the patient
to suspend work and take a long holiday, the improvement usually
appears early and proceeds to complete recovery. But even in such
584: FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
circumstances it is not always easy to shield the patient from family
troubles and anxieties, and it may be still less possible to protect him
from the consequences of previous imprudence and immorality. But,
although the aiFection is very variable in its duration, it nearly always
terminates in recovery, and neurasthenic patients are often long-lived,
being less liable than others to the degenerative changes of the blood-
vessels and other tissues which indicate age and shorten life.
III. HEADACHE (CEPHALALGIA).
Headache is so important a sign of nervous disease and arises from
so many different causes that it demands separate consideration. The
following varieties may be distinguished :
(1) Ancemic headache usually affects the temples and brow, or ex-
tends along the sagittal suture. It is aggravated by long maintenance
of the erect posture, and by all causes which exhaust the nervous
system, such as anxiety, night watching, and sexual excess ; while it is
relieved by rest in the recumbent posture.
(2) Hypercemic or conyemtive headache usually affects the Avhole head ;
the eyes are suffused ; the carotids pulsate strongly ; and the headache
is accompanied b}^ throbbing, agitation, hypemcsthesia with illusions of
the special senses, and sometimes by redness and heat of the brow and
vertex.
(3) ITysterical headache occurs in females and is generally accom-
panied by other symptoms of hysteria. The pain is sometimes diffused
and deep-seated, but it is more frequently localized in one spot, and feels
as if a nail were being driven through the skull ; hence it is called
clavus. Hysterical headache is increased in severit}^ during the men-
strual period and by mental worry, whilst it is removed by amusement
and anything which engages the attention.
(4) Toxic headaches are caused by poisons in the circulation. One
of the best known examples of this form of headache is that which
follows alcoholic intoxication. In the morning after a carouse a severe
headache is experienced, which is chiefly localized in the deeper parts of
the eyes and at the base of the brain, and is accompanied by a feeling of
pressure and weight. Severe headaches also follow the use of narcotics
and anaesthetics, and the inhalation of various gases, such as carbonic
oxide, sulphuretted hydrogen, the impure atmosphere of crowded rooms,
and sewer gas. Obstinate cephalalgia is likeAvise one of the most
common symptoms of uraemia, and in many cases of granular con-
HEADACHE. 585
tracted kidney, headache is the chief symptom complained of when the
patient seeks medical advice for the first time.
(5) Pyrexia! headache is probably a variety of the congestive or
hyperaemic headache, but it is accompanied by elevation of temperature
and the other symptoms which indicate the onset of an acute disease
such as the specific fevers and acute inflammatory diseases like pneu-
monia. The headache is generally moderate in intensity, dull and
deep-seated, and is accompanied by a feeling of lightness in the head,
and not infrequently by delirium. This form of headache ceases, ac-
cording to Jenner, when delirium begins.
(6) Neurasthenic headache occurs when the nervous system is ex-
hausted by mental anxiety and worry, night Avatching or other depress-
ing circumstances. The pain varies considerably in its character, but
it is generally deep-seated, heavy, dull, and oppressive. It is often
attended by a feeling of pressure and tension above the occiput, and
often by great sensitiveness to touch in that region.
(7) Rheumatic headache consists of a violent and tearing pain local-
ized in the muscles of the head, or in the fascia of the occipito-frontalis
muscle. It is often attended with marked tenderness of the scalp, and
is usually brought on by exposure to cold.
(8) Gouty headache takes the form of a dull, heavy pain in the
forehead, and is generally attended by great depression of spirits, gid-
diness, pain and fulness in the right hypochondrium, flatulence, and a
high-colored urine loaded with lithates. Intense neuralgiform head-
aches, which are often termed gouty, are probably in most cases an
expression of commencing granular changes in the kidneys.
(9) Sympathetic headache may supervene on disease of almost all
the peripheral organs, although it is commonly associated with diseases of
the digestive and sexual organs. The most common form of this variety
is the brow-ache of gastric catarrh, but headache may accompany irrita-
tion of the intestinal canal or of the uterus and ovaries. This is probably
the place in which to mention the headache caused by excessive strain-
ing of the eyes. This form of headache is often accompanied by
vertigo, insomina, and sickness, and occasionally by vomiting. Head-
ache may be caused by excessive use of the normal eye, but it is much
more liable to be induced when the eye is deficient as an optical instru-
ment, and is especially liable to occur in disorders of accommodation.
In cases of headache of obscure origin, and more especially when it is
found to supervene or to become intensified when the patient begins to
read or write, the state of vision should be carefully investigated by an
ophthalmologist.
(10) Syphilitic headache is characterized by a deep-seated and in-
586 FUNCTIOXAL DISEASES OF THE NERVOUS SYSTEM.
tense pain, Avhich is either attended by a feeling of weight on the
vertex or a sense of constriction as if the head -were held fast in a vice.
The patient compares it to that which might be caused by successive
blows on the head with a heavy mallet. The pain is at times distinctly
circumscribed, at other times it is diffused, and may then occupy either
the frontal, temporal, or occipital regions. In some cases it is diffused
and invades the whole head. The headache never completely intermits,
but it is liable to paroxysmal exacerbations of great severity, which
are particularly intense during the night. There is, indeed, no other
form of headache in which a nocturnal exacerbation is so characteristic
as the syphilitic variety, and it is alwaj's accompanied by a degree of
sleeplessness which is often out of proportion even to the intensity of
the headache.
(11) Organic headache occurs as one of the symptoms of structural
disease within the cranium, and is especially characteristic of intra-
cranial growths. The pain is persistent and continuous, but liable to
paroxysmal exacerbations of great severity. It may be frontal or
occipital, and it is generally deeply seated in one spot, although it may
extend over the whole head. Tenderness of the scalp often attends
the headache, and pain may be elicited on percussing the skull over the
seat of the tumor. An ophthalmoscopic examination often reveals the
presence of optic neuritis.
(12) Hemicrania.
Etiology. — The predisposing causes of hemicrania are inheritance,
generally from mother to daughter; a neuropathic disposition; the
female sex, and the ages of fifteen to thirty years, while the exciting
causes are digestive disorders, constipation, exhaustion from want of
food, fatigue, sleeplessness, and excessive mental exertion.
Symptoms. — Hemicrania consists of paroxysms of headache which
are separated by free intervals of shorter or longer duration. The
attack is frequently preceded by premonitory symptoms, the patient
has a sense of pressure in the head, and feels chilly, nauseated, de-
pressed, Aveary, and indisposed to work. Other interesting symptoms
often precede the attack. The most usual of these are transitory im-
pairment of cutaneous sensibility, which is accompanied by tingling,
numbness, and formication. At other times there may be, separately
or in various combinations, deafness, tinnitus aurium, a bitter taste,
loss of taste, embarrassment of speech, momentary incoherence, drowsi-
HEADACHE. 587
ness, transitory paresis of one of the limbs, vertigo, indistinct vision,
muscre volitantes, scintillating scotoma, or hemiopia.
The characteristic pain comes on by degrees in the course of the day,
but almost never with the lightning rapidity of the pain of neuralgia. The
patient often feels great drowsiness and weariness in the evening, and
awakens with headache in the morning. It often begins with a dull
pain over the forehead, and as it increases in severity it passes down to
one eye and remains fixed over the temple. Occasionally it is localized
at the top or back of the head. The left is more frequently attacked
than the right side, but occasionally successive attacks occur on alter-
nate sides, these cases being named hemicrama alternans by Eulenburg.
Patients describe the pain as being dull, burning, or bursting, and it is
frequently associated with an intense feeling of sickness. Every beat
of the heart is felt as a throb of pain, and the slightest movement, even
raising the head from the pillow, or the exertion of talking, augments
the throbbing pain to an almost unendurable pitch by exciting the cir-
culation. The patient suffers from continuous nausea, the appetite is
lost, there may be more or less jaundice, and the attack often terminates
by free vomiting, first of the usual contents of the stomach and after-
wards of bile. The skin over the forehead, temples, and parietal region
is often sensitive to a light touch during an attack of migraine, but
deep diffused pressure affords relief Berger has shown that the sense
of touch may become morbidly acute (ht/perpselaphesia), the circle of
perception being sometimes only one line in diameter on the affected,
and four lines on the sound side of the forehead. He also found that
variations of temperature of 0.4° C. were perceived on the affected, and
only of 0.8° C. on the sound side. The electro-cutaneous sensibility was
likewise increased on the affected side. Deep pressure over the superior
or middle cervical ganglion of the sympathetic, and over the spinous pro-
cess of the cilio-spinal region of the cord is painful, and a small spot is
sometimes found over the parietal protuberance which is painful on pres-
sure, but the painful points of genuine neuralgia are never present.
The vaso-motor phenomena of migraine are exceedingly important,
and the disease has been divided into (1) hemicrania spastica or sym-
pathico-tonica, (2) hemicrania angioparalytica or neuroparaJytica, and
(3) hemicrania mixta, according as the phenomena of vascular con-
traction, dilatation, or first contraction and then dilatation, are present
respectively.
1. Hemicrania Spastica or Sympathico-tonica. — On the affected
side, at the height of the attack, the eye is prominent ; the pupil is
dilated ; the temporal artery feels like a hard cord ; the side of the face
and the ear are pale ; and the temperature in the external meatus is lower
588 FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
by 0.4° C. or 0.6° C. than that of the meatus of the opposite side.
The pain is aggravated by every circumstance which excites the circu-
lation and increases the arterial tension, and compression of the carotid
on the aifected side augments, and of that on the unaffected side dimin-
ishes the pain. The salivary secretion is much increased in quantity and
becomes very viscid. Towards the end of the attack the affected side
of the face and ear become red and hot, the conjunctiva is injected,
there is a copious flow of tears, the pupil becomes contracted, a diffused
feeling of Avarmth spreads over the body, and the paroxysm terminates
by palpitations, vomiting, a free discharge of limpid urine, and some-
times a watery evacuation from the bowels.
2. Hemicrania Angioparalytica or Neuroparalytica. — On the affected
side, at the height of the attack, the eye is retracted ; the palpebral fissure
is narrowed; the pupil is contracted; the conjunctiva is injected; there
is an increased flow of tears ; the side of the face and ear are red, hot,
and turgid; the temporal artery is large, tortuous, and beats with
unusual force; and the temperature in the external meatus is higher
by from 0.2° C. to 0.4° C. than on the opposite side; and compres-
sion of the carotid on the affected side and of that on the opposite
side aggravates the pain. The radial artery is sometimes small and
contracted, and the pulse is slow, beating only from forty-eight to fifty-
six times a minute. Towards the end of the attack the face becomes
paler and the other phenomena pass off. Vomiting is not so urgent a
symptom in the paralytic as in the spastic variety, and the course of
the former is, on the wliole, milder than that of the latter,
3. Hemicrania Mixta. — In this form the phenomena of the spastic
variety are present at first, but these are soon followed by those of the
paralytic variety.
An attack of hemicrania usually lasts from a few liours to half a
day, but may, at times, continue a whole day or even several days.
If the pain be present on waking it often wears off gradually towards
evening, and the patent falls into a sleep from which he usually awakes
free from pain. But if it should come on during the day, it gradually
increases in severity, and the patient is unable to sleep. The headache
is generally most tolerable when the patient is laid down in a darkened
room, but at other times it is aggravated by the recumbent position,
and the patient can best endure his suflerings in the sitting or upright
posture. The paroxysms often recur with great regularity at intervals
of three or four weeks, and females are frequently attacked during the
catamenial period, although this rule is not without numerous excep-
tions. Those who are liable to migraine often enjoy excellent health
during the intervals between the attacks. Migraine headaches fre-
HEADACHE. 5§9
quently cease to recur after the climacteric jDeriod in women, and after
the fiftieth year of age in men, and in persons Avho do not inherit a
strong tendency to the disease they may cease at an early ao-e, either
spontaneously or under the influence of remedies.
3Iorhid Physiology. — In sjnnal irritation there is an excessive irrita-
bility of the spinal cord, but the brain also must participate in this dis-
order, inasmuch as the spinal symptoms are usually associated with an
emotional condition, such as is met with in hysteria. It must be remem-
bered that the inci'eased irritability of the nervous tissues in spinal
irritation is a paralytic irritability and therefore the afiection is allied
to exhaustion of the nervous system or to neurasthenia.
Neurasthenia is, as its name implies, caused by exhaustion of the
nervous system, those portions of it which are the last to be developed
being more profoundly afiected than the earlier evolved parts. Ex-
haustion of the latest evolved tissues implies diminution or temporary
abolition of the latest evolved functions, and consequently the control
of the conscience is diminished, and the animal instincts and propensi-
ties become more urgent and active. But although the stock of energy
of the nervous system is diminished ^the irritability is increased, just as
occurs in the nervous tissues of animals after prolonged starvation.
The consequence is that stimuli which produce little or no effect in
health have now widespread results. This excessive irritability of the
nervous tissues explains the great mental excitability of neurasthenic
patients, as well as their sensitiveness to changes of weather and other
external stimuli.
Hemicrania is the only form of headache, the morbid physiology of
which we shall discuss in this place. The chief symptoms which re-
quire explanation are (1) the vaso-motor and oculo-pupillary symptoms,
(2) the disorders of the general circulation, and (3) the pain.
(i) The vaso-motor and oculo-piqnllary disorders which are observed
in hemicrania spastica are explained by supposing that the cilio-spinal
region of the spinal cord and the cervical sympathetic are in a state of
irritation, those of hemicrania paralytica by supposing that the same
nervous mechanism is paralyzed, and those of mixed hemicrania by
supposing that this mechanism is first irritated and then paralyzed.
(2) The retardation of the pulse which is often observed is supposed
by Landois to be due to direct irritation of the vaso-motor centre in
the medulla. Other symptoms which show that this centre is in a state
of irritation are coldness of the hands, chilliness, suppression of per-
spiration, contracted state of the radial artery, and increased arterial
tension. Towards the end of the attack symptoms of vascular dilata-
tion, such as increased secretion of saliva and urine, and watery stools
590 FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
indicate that the irritation of the vaso-motor centre has been followed
by exhaustion and temporary paralysis.
(3) The pain in migraine has been variously explained. Romberg
thought it due to a hyper?esthesia of the brain, and he called it " neu-
ralgia cerebralis " in order to distinguish it from peripheral neuralgia.
Others suppose that the pain is caused by a neuralgia of the intra-
cranial and meningeal branches of the trigeminus and the other nerves
which accompany the bloodvessels, and not of the cerebrum itself as
Romberg supposed. But when once the vaso-motor and oculo-pupillary
symptoms of hemicrania attracted attention the supposition that the
pain was secondary to vascular disturbances in the brain lay near at
hand. Du Bois-Reymond suggested that the pain was caused by a tonic
spasm of the muscular coat of the vessels and was thus similar to the
pain felt in cramp of the muscles, or to that felt in the uterus during
labor. Others have suggested that the pain is caused by the anaemia
which results from spasm or the hypememia which results from dilata-
tion of the vessels of the brain; this view being supported by the well-
known fact that anaemia or hyperaemia of the peripheral nerves is one
of the most frequent causes of various neuralgias. But some pathol-
ogists believe that hemicrania is allied to genuine epilepsy. The facts
in fiivor of this opinion are the paroxysmal character of the disease, its
occurrence in members of neuropathic families, and the attack being
often preceded by symptoms, like scintillating scotoma, resembling an
epileptic aura and occasionally accompanied by embarrassment of speech
or a slight degree of aphasia. Observing the resemblances between
certain forms of headache and epilepsy Dr. Sieveking proposed to name
the periodical headaches of nervous peoi)le cephalalgia epileptica, while
Dr. Liveing for the same reason came to the conclusion that hemicrania
was caused by " nerve storms." But Dr. Hughlings-Jackson has given
a more scientific expression to this theory by attributing the headache
of migraine, especially the form which is associated with ocular phe-
nomena, to a discharging lesion from the cortex of the posterior lobes
or the sensory area of the brain, or in that part of the sensory area
which is the anatomical correlative of the sensation of pain in the head.
But during the attack the nervous discharge does not remain limited to
the sensory area, since some is directed outwards to the medulla oblongata
and cilio-spinal region of the spinal cord, causing irritation or inhibition
of some of these centres, and giving rise to the vaso-motor and oculo-
pupillary phenomena of the disease.
Ti'eatment. — The treatment of spinal irritation must first be directed
to remove the cause, while an endeavor is made to improve the general
nutrition by a full diet including the moderate use of wine, and much
HEADACHE. 591
exposure to the open air and to sunlight. The patient should rest fre-
quently in the recumbent posture, and all causes of fatigue should he
avoided. Change of air to a dry mountainous district or to the seaside,
or a moderate hydropathic treatment may be found useful.
The internal remedies which are found most generally useful are
quinine, iron, zinc, and strychnine. The galvanic current should be
passed through the vertebral column, and the painful portions should be
included between the poles. Each sitting should be short and the
strength of the current moderate. The negative pole placed directly
over the painful vertebra appears to be a good method of applyin<T
galvanism, and general faradization or central galvanization is said to
be useful. Counter-irritation applied directly over the painful portion
of the spine is a most effectual method of treatment and Corrio-an's
button gives very favorable results.
Neurasthenia must be treated on the same general principles as spinal
irritation. The means to be adopted are complete mental rest, generous
diet, and much exposure to fresh air and sunlight, but with only a
moderate amount of active exercise. It is almost incredible what a
small amount of exercise suffices to induce great fatigue followed by
profound mental depression in such patients, even when the subject
of the disease appears to be possessed of great muscular strength. In
aggravated cases the treatment introduced by S. Weir Mitchell of rest,
seclusion, over-feeding, electricity, and massage, should be adopted.
The treatment of headache may be directed against the cause, or
against the symptom of pain. In order to fulfil the first indication the
remedies for anaemia, hyperasmia, hysteria, syphilis, nervous exhaustion,
Bright's disease, or for allaying local irritations must be employed ac-
cording to the nature of case.
It is scarcely possible to adopt a casual treatment against migraine,
inasmuch as so little is known of the circumstances which concur to
induce an attack. An emetic may sometimes arrest an impending
attack, but it appears to act less by removing indigestible substances
than by the impression it produces upon the nervous system.
The direct treatment of migraine may be divided into that which is
appropriate during the intervals and for removing or palliating the
paroxysm. In the intervals between the attacks the preparations of
iron, especially the carbonate, have been found useful in feeble and
amemic subjects. Arsenic is another very useful drug during tlie
intervals, and other periodic remedies, such as quinine, quinoidin, and
salicin, have been tried, but they appear to act better in arresting an
impending attack than during the interval. Strychnine, nitrate of silver,
sulphate of nickel, bromide of potassium, chloride of ammonium, oil of
592 FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
turpentine, and lupulin have been tried during the interval, but with
doubtful success. Chalybeate springs, mud and sea baths, hydropathy,
and residence in lofty mountainous regions, have all been found bene-
ficial, but they appear to influence the disease favorably by improving
the general health. Dr. Ringer believes that cannabis indica in doses
of from one-quarter to one-half a grain, or ten minims of the tincture
three times a day, is one of the best remedies we possess for preventing
the attack. In the treatment of the attack every source of external
irritation should be removed, the room should be moderately darkened,
and all noises should be prevented. In spastic hemicrania the patient
should lie flat on the back with the head a little raised, Ijut in the
paralytic variety the patient usually prefers to maintain a sitting posture,
and to rest the head against some hard substance. Firm compression
of the head by a handkerchief bound round it is an old remedy and
appears to give temporary relief. The application of cold to the head
by means of an evaporating lotion or ice bag is often grateful, while a
warm fomentation to the forehead and temple is sometimes more soothing
than the cold. Quinine given in doses of from five to fifteen grains
two or three times in succession often arrests an attack, and half drachm
doses of the liquid extract of ergot are often useful in the angioparalytic
variety.
Coffee is another remedy which appears to act by stimulating the
vaso-motor nerves, and may be given in the form of a strong infusion,
but its alkaloid, caffeine, is more eff'ectual. The citrate of caffeine may
be ordered in doses of one grain every four hours for some time before
the expected attack. Guarma powder in half drachm doses every four
hours till relief is obtained is sometimes very effectual. The inhalation
of the nitrite of amyl has been found useful in the spastic form of
hemicrania, but it acts only as a palliative, its effect being transitory.
Croton chloral hydrate is a very useful remedy for arresting the attack.
It may be administered in five grain doses every four hours or in one
dose of from fifteen to twenty grains. The late Dr. Austin thought
the best means of arresting a sick headache was to give twenty grains
of chloral and make the patient plunge his feet into very hot water and
mustard while breathing the steam. A full dose of bromide of potas-
sium either alone or in combination Avith chloral or Avith tincture of
opium, or better still nepenthe, is also very efficacious. Chloride of
ammonium in half drachm doses is another useful remedy. Morphia
and other narcotics may be employed in aggravated cases, but they are
not so useful in migraine as in neuralofia.
The galvanic current when properly applied is one of the most power-
ful remedies we possess for hemicrania. Hoist recommends that one
HEADACHE. 593
electrode be placed at the inner edge of the sterno-cleido-mastoid muscle,
and the other on the palm of the hand. The pole on the neck is made
l)0sitive in hemicrania spastica, and from ten to fifteen elements are
used for two or three minutes, while the negative pole is used at the
neck in hemicrania angioparalytica and powerful excitations are pro-
duced by re})eated closures and openings, or by reversals. Other authors
recommend that a weak current should be passed continuously through
the head. The induced current has been recommended by Frominhold ;
he applies one of the poles high up the back of the neck in the median
line, and the other upon the forehead or over the superciliary arch.
Fieber employs the " electric hand," and the application is certainly
grateful to the patient, but I have not found that it produces a marked
effect upon the duration of the attack.
In dealing Avith the various forms of headache, other than hemicrania,
the treatment must be directed against the cause of the pain. In the
anaemic form, iron and sustaining diet ; in the hypersemic, saline pur-
gatives and low diet ; in the febrile, ice to the head ; in the hysterical,
iron and moral management of the patient, are the means of treatment
which must be chiefly relied upon. In symptomatic headache the
stomach or other organ which is the source of irritation must be sub-
jected to treatment ; in gouty headache with hepatic derangement saline
purgatives bring relief; and in the neuralgiform variety saline diuretics
and agents which lower the arterial tension are indicated. In rheumatic
headache salicylate of soda may be given, but iodide of potassium is, as
a rule, the most effectual remedy for such cases. In syphilitic headache
an energetic antisyphilitic treatment must be adopted.
38
CHAPTEK XIY.
SHOCK, CONCUSSION, AND ALLIED CONDITIONS.
I. SHOCK.
Etiology. — Shock is more easily produced in persons inheriting an
irritable and unstable nervous system than in robust persons, in Avomen
than in men, and in young than in old people. The exciting causes of
shock are sudden and severe or extensive injuries of any part of the
body, and strong emotional excitement, especially the depressing pa.ssions.
Symptoms. — Cases of shock may be divided clinically into two, (1)
torpid shock or those in Avhich the symptoms of depression predominate,
and (2) erethismic shock or those in which the symptoms of prostration
are associated with those of excitement.
(1) Torpid SJiocJc. — In the torpid form of shock the patient lies
utterly prostrate, the surface of the body is pale, cold, and covered by
a clammy sweat, which collects in drops on the forehead and eyebrows ;
the lips are bloodless, the nostrils dilated, and the countenance of a
dull aspect and shrunken ; while the eyes have lost their lustre, are sunk
in their sockets, and partially concealed by the drooping lids. There is
complete muscular relaxation, which may even extend to the sphincters.
If the patient be conscious he may complain of feeling cold and faint,
and the whole body may tremble. The pulse is frequent, unequal, and
feeble or imperceptible at the Avrist, but the fluttering action of the heart
may be heard on auscultation. The respiratory movements are irregular
and gasping, or short and feeble, the respirations being sometimes so
feeble that they are scarcely visible, although a slight movement of the
diaphragm may generally be discovered by careful observation. The
temperature of the body is depressed. The patient suffers from vertigo
and dimness of vision, while in the less severe cases there are nausea,
vomiting, and hiccough. The psychical symptoms consist of mental
depression, restlessness, confusion of thought, incoherence, or drowsiness,
but the patient generally gives rational replies to definite questions. At
other times the patient appears singularly calm and rational, while the
various senses remain unaffected, hearing being sometimes unusually
acute.
SHOCK. 595
(2) Erethismie Shock. — This form of shock is rare, the majority of
cases in which symptoms of prostration are mixed with those of excite-
ment being preceded by a distinct, though it may be transient stance of
collapse. The skin is at first hot and dry ; the pulse is quick and
bounding, but always compressible ; the respirations are hurried, imper-
fect, and interrupted by sighs ; the tongue is tremulous ; the patient
complains of thirst ; rigors are occasionally present ; and vomiting is a
frequent and sometimes obstinate symptom. The mental and bodily
prostration of collapse is succeeded by tremor and twitchings of the
muscles, and the patient suffers from restlessness, jactitation, prsecordial
anxiety, and delirium. At times the patient merely presents a peculiar
irritability of manner with an increased disposition to talk, sometimes
rationally, occasionally incoherently. At other times the patient has
strange illusions attended by a peculiar dread of impending evil.
In some cases, however, there is fierce maniacal raving, which is most
pronounced during the night, or the delirium may assume all the charac-
teristics of that observed in delirium tremens. The patient obtains no
sleep, or it is partial, interrupted, and unrefreshing. As the exhaustion
increases the skin is covered by a cold, clammy, and often profuse
sweat; the face becomes pale; the expression haggard; and the pulse
is frequent, irregular, fluttering, and uncontrollable. Towards the end
subsultus and slight convulsions supervene and the patient dies coma-
tose. In the severest form of shock the functions of the nervous
system are suddenly abolished and the heart ceases to beat; in the
mild forms of the affection the symptoms are more or less similar to
those of an ordinary fainting fit, while between these two kinds in-
numerable transitional forms are observed. The medium degrees of
shock are named collapse. In the intermediate forms of shock the
symptoms of collapse give place to those of excitement, this stage
being called the period of reaction. The period of reaction is charac-
terized by improved pulse and respiration, restoration of muscular
power, and increase of temperature. These symptoms often merge
quickly into health, but in some cases relapses occur, and convalescence
is then protracted. In other cases the torpid may be replaced by the
erethismie form of the disease. Recovery after shock is often partial
only, the irritability of the nervous system remains permanently in-
creased, so that slight exciting caases suffice to give rise again to the
phenomena of shock.
696 SHOCK, CONCUSSION, ANT) ALLIED CONDITIONS.
II. CONCUSSION OF THE SPINAL COED (COMMOTIO SPINALIS).
Etiology. The most usual causes of spinal concussion are falls upon
the feet or buttocks, blows over the back, and railway collisions, those
who sit with their back in the direction from which the shock comes
being most liable to suffer. Lightning passing through the body causes
a general shock in which the spinal cord participates, and violent
mental excitement appears to l)e able to produce the symptoms of spinal
concussion occasionally.
Symptoms. — The most usual symptoms of spinal concussion are
feebleness or, on rare occasions, paralysis of the extremities; paraes-
thesise of various kinds; pain in the neck, loins, or along the spinal
column; tenderness on pressure of some of the spinous processes;
some deforce of cutaneous hypergesthesia or, more often, anaesthesia,
weakness of the bladder, and considerable emotional disturbance.
Varieties of Spinal Concussion.
(1) Severe Forms of Shock causing Rapid Death. — The patient,
after the injury, is found more or less paralyzed in all his extremities:
the surface of the body is distinctly anaesthetic; the pulse is small,
weak, and slow ; the skin is cold and pale or slightly cyanotic ; the res-
piration is disordered and sometimes the difficulty of breathing may
amount to dyspnoea; the mind is confused or there may be complete
loss of consciousness; the stools and urine are passed involuntarily;
and the patient dies in a few hours or days from general prostration
and paralysis of respiration.
(2) Slight Shock causing Severe Symptoms at first., hut soon ending
in Recovery. — Immediately after the accident the patient is found more
or less paralyzed and anaesthetic in the lower, and occasionally in the
upper extremities, but the bladder is not usually affected, while im-
provement begins in a few days, and recovery is complete in a few
weeks or months.
(3) Severe Symptoms at first., followed hy a Protracted Illness from
ivhich the Patient usually Recovers. — Soon after the accident the
patient complains of a motor Aveakness, which gradually increases until
the extremities are paralyzed. He also complains of pains in the back
of the neck, loins, or along the vertebral column, which is often exces-
sively sensitive and tender to pressure, and various parsesthesise, but
aneesthesia is not well marked. Vomiting and loss of consciousness
may be present at first, the extremities are cold and livid, and occasion-
COXCUSSION OF THE SPIXAL CORD. 597
ally there is retention of urine, while patients often manifest a high
degree of mental irritability for a long time. Gradual improvement
now occurs, but the patient complains of great weakness, and even
slight atrophy of some of the muscles may occur, and complete recovery
from the paralysis may not take place for several years, while patients
may remain irritable and sensitive long after all the paralytic symptoms
have disappeared.
(4) Very Slight Symptoms at first, but subsequently a Severe Pro-
gressive Spinal IHsease develops, and the result is doubtful. — This
form of concussion is usually caused by railway collisions, and immedi-
atel}' after the injury the symptoms are insignificant. At first, indeed,
the patient is unusually calm and self possessed, and he may busy him-
self for some hours in assisting his less-fortunate fellow sufferers, but
on reaching home he becomes talkative and excited, and is now apt to
burst into tears. On the following day he complains of feeling shaken
or bruised all over, but it is not until the lapse of from a few days to a
week or more that he finds himself unfit for exertion and unable to
attend to business. When the patient is examined some Aveeks after
the injury, the back is found painful on movement; some of the spinous
processes are found tender on presure; the patient holds himself stiff"
and erect in walking, as if the various vertebrae were soldered into one
piece, and he is unable to bend forwards to pick anything off" the
ground, to move the spine backwards or laterally, or to raise himself
from the horizontal position without the aid of bis hands. Girdle sen-
sations, parresthesiee of all sorts, and anaesthesia or hyperesthesia in
varying degrees and in diff"erent situations may be present, while weak-
ness of the bladder and diminution of the sexual power are frequently
observed. After a time marked atrophy may take place in individual
muscles and groups of muscles, and at times it may be extensively dis-
tributed. The extremities are cold and bluish, the general nutrition is
impaired, and the expression of the countenance changes to one indi-
cating great anxietv and nervousness. Patients often suff'er from
muscse volitantes and spectral images, intolerance of light, or diplopia
and strabismus, while they are often annoyed by deafness, noises in the
ears, or great intolerance of sound. The patient is irritable and timid,
suffers from a feeling of constriction in the head, sleeplessness, con-
fusion of thoughts, weakness of memory and intelligence, impaired
power of work, and his friends observe that his whole character has
undergone a serious change. In cases of this kind the patient may die
from bedsores and pypemia, become permanently paralyzed in the lower
extremities, or gradually recover.
598 SHOCK, CONCUSSION, AND ALLIED CONDITIONS.
III. CONCUSSION OF THE BKAIN.
Etiology. — The exciting causes of cerebral concussion are severe
injuries, such as falls from a height or blows on the head, which cause
the whole mass of the brain to be jolted or shaken. Concussion may
be complicated by fracture of the skull, and in such cases the effects of
the concussion are often less severe than in uncomplicated cases, ap-
parently because a certain amount of the applied force is expended in
producing the fracture.
Symptoms. — Concussion is a special form of shock and its s^'mptoms
may be described under four stages : (1) the stage of collapse; (2) the
stage of rallying or vomiting ; (8) the stage of reaction; and (4) the
stage of gradual convalescence.
(1) The Stage of Collapse. The symptoms of this stage are some-
what variable. In the slighter forms the patient suffers from transient
confusion of ideas, and slight giddiness. He may feel weak and faint
and be unable to maintain the erect posture. In the more severe forms
the symptoms are those of collapse, with loss of consciousness ; but
paralysis, such as occurs in comi)ression of the brain, is never present.
The patient is semi-conscious or insensible, most reflex actions are
abolished, the skin is cold and pallid, the respirations superficial and
shallow, the pulse feeble or imperceptible at the wrist, whilst the pupils
may either be contracted, dilated, or unequal.
(2) The Stage of Rallying or of Vomiting. After a period varying
from a few minutes even up to days, according to the severity of the
attack, the patient usually begins to show signs of rallying. This stage
is often ushered in by vomiting, or very occasionally by an e})ileptiform
attack ; the pulse improves in strength, the respirations become less
shallow and more perceptible, the body becomes warmer, reflex actions
can be excited, and the patient gives evidence of returning sensil>ility,
while he may exhibit signs of mental distress.
(3) The Stage of Reaction. The symptoms of the stage of rallying
are succeeded by those of reaction. In this stage the phenomena of
febrile reaction manifest themselves by the usual symptoms — hot and
dry skin, quick and hard pulse, and scanty urine ; while the patient is
drowsy, yet quite conscious when roused by a question addressed to him.
In some cases these symptoms gradually develop into those of com-
pression and the patient dies comatose, while in other cases the symp-
toms of reaction give place to those of inflammation of the brain. This
stage may continue from three to twelve days in cases which recover.
(4) The Stage of Convalescence. Reaction is followed by a pro-
CONTUSION OF THE BRAIX. 599
gressive subsidence of the symptoms, and either by a gradual restora-
tion of the patient to health, or the establishment of one or other of
several chronic affections of the nervous system.
Cerebral Irritation. — In another form of nervous disturbance follow-
ing injuries of the head, and described by Erichsen under the name of
cerebral irritation, the phenomena of cerebral excitement are associated
with those of loss of function. The patient assumes a peculiar attitude :
he lies with the body bent forwards, the knees drawn up on the abdomen,
the legs bent on the thighs, the forearms flexed on the arms, and the
hands drawn. The patient is restless, and frequently changes his posi-
tion, but never stretches himself out or assumes the supine posture.
The eyelids are firmly closed : the pupils are contracted : the surface
of the body is pale and cold ; and the pulse is small, feeble, and slow,
being seldom more than seventy beats per minute. The sphincters
remain, as a rule, unaffected.
The patient is indifferent to everything around him, and is only
partially conscious. He may, however, be roused when addressed in a
loud voice, and then looks up, mutters indistinctly, or frowns and turns
hastily away. His sleep is not stertorous.
After a period of from one to three weeks the pulse improves, the
body becomes warmer, the flexed attitude is abandoned, and the mental
irritability gives place to mental feebleness and torpidity.
The course of concussion is variable. Some patients die during the
stage of collapse, and others from compression or encephalitis following
an excessive reaction. Even after apparent recovery the patient often
suffers from persistent headache ; his mental powers are impaired : his
speech may be indistinct and stuttering, his special senses may be per-
manently impaired ; and he remains excitable and is apt to give way to
uncontrollable bursts of passion.
IV. CONTUSION OF THE BEAIN.
Whenever the skull undergoes a change of form as the result of injury
the substance of the brain may be contused or lacerated. The contusion
may be situated immediately beneath the portion of the skull where the
injury was inflicted, or on the opposite side of the brain as the result
of contrecoup, or both these places may be simultaneously affected.
The symptoms of contusion are always complicated by those of con-
cussion and of compression. The diagnosis of contusion must be made
by the presence, in addition to the symptoms caused by a general
injury to the brain, of ]ihenomena like monospasms or monoplegia which
indicate a local lesion in the absence of any signs of fi-acture of the skull.
600 SHOCK, coxcussioN, AjSTd allied conditions.
V. COMPRESSION OF THE BRAIN.
Compression of the brain may occur after injuries from the pressure
of a fractured portion of the bones of the skull, the presence of ex-
travasated blood, pus formed within the skull, or of a foreign body
lodged there.
The patient becomes unconscious, the l)reathing is slow, deep, ?^nd
stertorous, wliile the cheeks are puffed out during respiration. The
surface of the body is cool at first, but soon becomes hot and bathed in
perspiration. The pupils are dilated or unequal, the pulse is slow and
full, the feces pass involuntariW, and there is retention of urine. This
condition of stupor sometimes alternates with paroxysms of delirium,
while local spasms or j^aralyses are sometimes observed, but it is prob-
able that in these cases the motor area of the cortex is not often lacerated
or contused.
For further information with regard to contusion and compression of
the brain the reader is referred to surgical works.
Morbid Anatomy. — In shock all the cavities of the heart are usually
distended with blood and the veins of the body, especially tlie abdominal
veins, are engorged. No changes have been discovered in the nervous
system. In cases of concussion which have terminated fatally at an
early period, small extravasations of blood have been found, in the spinal
variety, in the cord and its membranes ; and in the cerebral variety, in
the brain and its membranes. In rapidly fatal cases of spinal concussion,
fractures of the vertebrae, laceration of the membranes, or meningeal
or spinal hemorrhage have been observed, Avhile in the cerebral variety
the morbid changes discovered consist of superficial lacerations, minute
hemorrhagic extravasations either studded on the surface of the brain or
in its substance, and occasionally of a difiiised ecchymosis of the pia
mater. In cases of spinal concussion which give rise to a protracted
illness or to progressive spinal disease the symptoms are caused by
secondary meningo-myelitis. It is probable that death is caused suddenly
in some cases of cerebral concussion from injury of the roots of the
pneumogastric nerves.
In contusion of the brain capillary hemorrliagic extravasations have
been found either limited to the cortex or diff"used through the substance
of the brain. When the injury is localized the extravasations may be
so closely aggregated that the part aff"ected presents the appearance of
a hemorrhagic infarction. The extravasations are more diffused when
the substance of the brain is contused. Compression of the brain is
COMPRESSION OF THE BRAIX. (501
caused by depressed fractures, extravasated blood, tbe formation of pus,
or the lodgement of a foreign l^ody within the cavity of the skull.
3Iorhid Physiology. — The most striking phenomena of shock are
those which cluster around the organs of circulation. The experi-
ments of Goltz and Brunton show that shock results probably from
cardiac paralysis combined with vaso-motor paralysis of the laroe vas-
cular trunks of the abdomen. Brunton states that moderate blows on
the abdomen of frogs produce in some stoppage of the heart without
dijatation of the abdominal vessels, and in others vascular dilatation
without arrest of the cardiac pulsations, while severe blows produce
both effects simultaneously. The vessels of the alxlomen are so large
that when fully relaxed they are capable of containing almost all the
blood in the body, and consequently the condition resulting from this
rapid dilatation is equivalent to a sudden hemorrhage. This double
condition of cardiac failure and vascular dilatation produces amemia of
the nerve centres, and this accounts for the pallor and coldness of the
surface of the body, and the w^eak, compressible, and fluttering pulse.
It must not, however, be forgotten that the injury which has disordered
the functions of the cardiac and vaso-motor centres in the medulla
oblongata must also have produced a directly deleterious effect upon
the nerve centres. The disorders of respiration, the cries of pain, and
the various bodily contortions which are caused by bodily injuries or
severe mental excitement show that excessive stimuli occasion powerful
outgoing discharges from the higher nerve centres. But a powerful
discharge from a nerve centre is followed by temporary impairment or
abolition of its functions, and it is probable that the arrest of the func-
tions of the higher nerve centres, caused by the application of a sudden
and powerful stimulus, is the most important factor in the production
of the phenomena of shock. The symptoms of erethismic shock may
be explained partly on the supposition that the nervous tissues are in
the irritable condition frequently observed when they are imperfectly
nourished, and partly on the supposition that the phenomena of excite-
ment are in great part due to the abolition of the functions of the
higher nerve centres, thus permitting a greater activity of the loAver
nerve centres to take place.
The symptoms of spinal and cerebral concussion have both been
attributed by one set of authorities to vascular spasm, and by others to
vascular paralysis, but they are most probably caused by molecular dis-
turbance of the gray matter of the spinal cord and brain respectively,
which is of such a character that it is attended by impairment or loss of
the functions of the nerve cells and fibres. In contusion of the brain
the part that is the chief centre of the injury is more or less permanently
602 SHOCK, CONCUSSION, AND ALLIED CONDITIONS.
damaged and its functions destroyed, while a widely diffused molecular
disturbance occurs in the remaining parts of the brain. In compres-
sion of the brain the functions of the organ are abolished partly because
the whole brain is rendered antemic by the pressure to which the organ
is subjected owing to the diminution of the cranial cavity, and partly
by the molecular disturbance produced by the suddenness of the injury.
Treatment. — The great aim of treatment is to excite reaction, but it
must be borne in mind tliat when once reaction appears it is apt to
become excessive. If the threatened arrest of the heart's action is of
purely nervous origin, Savery recommends that blood should be imme-
diately drawn from the external jugular vein, but if it be caused by
hemorrhage then transfusion of l)l()od appears to afford the best chance
of success. In every case of shock the patient should be well Avrapped
up in warm blankets and surrounded by hot bottles. Stimulants must
now be given internally, brandy being generally the readiest and best.
If the patient be unable to swallow, ammonia or ether may be injected
subcutaneously or into a vein, or a stimulating enema may be given.
Tincture of digitalis may be administered in half drachm doses, but its
action is too slow to be of much use in urgent cases.
The treatment of concussion consists of absolute and prolonged rest.
One of the most important rules of treatment is to abstain from giving
stimulants during the stage of collapse except in unusually severe cases.
In this stage the patient should be surrounded by warm blankets and
hot bottles, and absolute rest in a dai'kened room should be enjoined
until the stage of reaction is passed. During the stage of reaction a
moderate purgative may be given, and ice may be applied to the head
if agreeable to the patient, while the diet should be plain and unstimu-
lating consisting chiefly of milk. Spinal concussion must be treated
on the same general ])rinciples as the cerebral variety. The patient
should be made to lie on his face or side, or on his back, as recom-
mended by Erichsen, on a couch Avhich is tilted a little at its foot.
When the case has become chronic the usual remedies for meningo-
myelitis must be employed. Contusion and compression of the brain
from external injury come under the care of the surgeon.
CHAPTER XY.
VASCULAR DISEASES OF THE BRAIN.
I. AN^^MIA AND OCCLUSION OF THE INTRACRANIAL VESSELS.
Etiology — Cerebral ansemia may be divided into 1, Mmwers«? anaemia,
Avhicli results from the same causes as anaemia of the body generally :
and 2, partial anaemia, which is caused by obstruction of one of the
cerebral vessels.
1. Universal Cerebral Anaemia.
Symptoms. — The universal form of the disease may be divided into
a, acute; and h, chronic universal cerebral ana?mia.
a. Acute Universal Cerebral Ancemia. — The initial symptoms of the
ansemia which is caused by severe hemorrhage, are obscuration of the
senses; buzzing in the ears; dizziness; contraction, followed by dilata-
tion of the pupils ; imperfect reaction to external stimuli ; and loss of
consciousness. The surface becomes cold and pale, the respiratory
movements, accelerated at first, become slow, and this condition is fre-
quently followed by general convulsions and coma. In an ordinary fam^-
ing fit or syncope there is at first some degree of mental incoherence
manifested by the inability of the patient to direct his attention to a
particular object, a feeling of oppression in the chest, along with a ten-
dency to yawn. The face becomes pale, a cold perspiration breaks out
on the forehead and sometimes over the entire body, and there are gen-
eral muscular relaxation, ringing in the ears, dimness of sight, nausea,
and sometimes vomiting. The pulse is small, compressible, but regular.
The patient may noAV recover or fall insensible to the ground, and after
a few moments in the recumbent position he begins to rally.
h. Chronic Universal Cerebral Anaemia. — In these cases the patient
is fretful and restless, his sleep is disturbed by dreams, while he suffers
from intolerance of light and sound and great mental irritability. These
symptoms are frequently succeeded by the phenomena of depression,
and sometimes the latter predominate from the first. The patient
suffers from almost constant headache, vertigo, nausea, and faintness.
604 VASCULAR DISEASES OF THE BRAIN.
The pulse is small and compressible, the cardiac impulse feeble, and
tliere is great disinclination for either mental or physical exertion.
In the severe forms of chronic or subacute cerebral antemia, such as
that produced by starvation, or that Avhich arises during the course of
exhausting fevers, delirium becomes a prominent symptom. During
the delirium of cerebral anaemia the patients are excited and sometimes
maniacal; there are illusions of sight and hearing, and delusions of
persecution. The duration of this condition is variable; it may last a
few hours or days only, but it sometimes continues for weeks, and occa-
sionally passes into permanent insanity.
Cerebral anaemia is seen in infants after severe diarrhciea, or other
exhausting disease ; and as this is the form Avhich was called by Marshall
Hall liydroceflialoid or hydrenccphaloid disease, it demands special
notice. The affection may be divided into two stages — that of irri-
tability, and of torpor. In the first stage, the infant is irritable and
restless, with flushed face, Avarm skin, and frequent pulse : the patient
starts on being touched or on hearing any sudden noise, and sleep is
disturbed and interrupted by sighs, moans, or screams. During the
second stage the countenance becomes pale, the cheeks and extremities
cold, the eyelids are half closed, the eyes sunk iii their sockets, there is
frequently slight strabismus, and the pupils are dilated and do not con-
tract to light. The breathing is irregular and sighing, the voice husky,
and there is sometimes a teasing cough with rattlini; in the throat. A
most important symptom which distinguishes this disease from liydro-
cephalus is that the fontanelle, instead of being tense as in tlie latter
disease, is depressed. The child inclines almost constantly to fall into
a sleep, which may pass into coma and death, but under appropriate
treatment gradual recovery usually takes place.
2. Partial Cekeijral An.emia (Occlusion ok thk Intracranial
Vessels).
Occlusion of the cerebral vessels may take place in a, the arteries ;
h, the veins and sinuses ; and t\ the capillaries of the brain.
a. Occlusion of the Cerebral Arteries.
Etiology. — The arteries of the brain may be occluded by a substance
carried from a distant part of the circulation, constituting embolism ; or
by a clot formed on the spot, constituting thrombosis.
An embolus consists of a fibrinous mass washed away from the left
cavities of the heart, the mitral or aortic valves, or the arch of the
AN.EMIA AND OCCLUSION OF INTRACRANIAL VESSELS. 605
aorta. In cases of cancer of the lungs, a nodule of the growth may
possibly be carried from the pulmonary veins, and pass into the cerebral
vessels.
Thrombosis of an artery occurs most frequently when the internal
surface of the vessel is rendered rough and uneven by arterial degenera-
tion. The predisposing causes of thrombosis are all those conditions
which tend to diminish the force of the heart's action and to alter the
<|uality of the blood, and thrombosis is particularly liable to occur when
these general causes and local arterial degeneration are conjoined. Em-
bolism occurs most frequently in young, and thrombosis in old people.
Symptoms. — The symptoms of embolism of a cerebral artery are
almost identical with those of cerebral hemorrhage in their mode of
onset and general characters, but the unconsciousness caused by embolus
is, as a rule, more transient than that caused by hemorrhage. In some
cases the patient is suddenly attacked with dizziness and utters an in-
voluntary cry, or complains momentarily of headache and immediately
loses consciousness, but in other cases the patient ovAj complains of
dizziness and slight confusion of mind for a minute or two and becomes
suddenly paralyzed and often aphasic, but without loss of consciousness.
In still other cases the attack is ushered in by an attack of convulsions,
which may be general like an ordinary epileptic attack, or limited to
one-half or to a part of one-half of the body. When general convulsions
are present they occur simultaneously with the loss of consciousness and
are immediately followed by paralysis, while unilateral and partial con-
vulsions may recur repeatedly before paralysis is fully established. In
many cases sudden speechlessness constitutes the only symptom of em-
bolus of a cerebral artery and in these cases this symptom may disappear
when collateral circulation is established, but, as a rule, the aphasia is
associated with right-sided hemiplegia. The state of the pupils varies
during the attack.
The sympto))is of thrombosis are, as a rule, more gradual in their
development than those of embolus. The more usual premonitory
symptoms of thrombosis of a cerebral artery are headache, dizziness, a
sense of general confusion, numbness, coldness, or formication of one
extremity or of one-half of the body, and considerable mental disturb-
ance, especially, marked loss of memory.
Convulsive movements occasionally precede the appearance of paral-
ysis, but, as a rule, the loss of motor power begins gradually, and its
progress is marked by successive remissions and exacerbations until
ultimately a more or less extensive paresis is established. The duration
of the prodromal stage may vary from a few days to a few months, and
occasionally apoplectic symptoms may come on suddenly as in embolism.
606 VASCULAR DISEASES OF THE BRAIX.
When once the vessel has become completely occluded the further prog-
ress of thrombosis is like that of embolus of a corresponding vessel.
When softening occurs either from embolus or thrombosis, the temper-
ature, according to Bourneville, begins to rise on the second or third
day of the attack and in two or three days it may reach 40° C. (104° F.).
After a few days longer the temperature sinks rapidly, its decline being
more rapid than after the period of inflammatory reaction in cases of
hemorrhao-e. When once softening has become thoroughly established
the symptoms are generally the same as those of other localized cerebral
diseases, while the sensory, trophic, and vaso-motor disorders, and the
aifections of the special senses are the same as those occurring in cerebral
hemorrhao-e. In some cases of embolism, however, the ophthalmic
artery is occluded, and the patient l)ecomes suddenly blind on that side,
while an ophthalmoscopic examination reveals the usual signs which
indicate occlusion of the central artery of the retina.
In cases of embolism the signs of valvular disease of the heart or of
disease of the large arteries are detected on physical examination, and
in cases of thrombosis the signs of degeneration of the arteries are
present.
In some cases of occlusion of cerebral arteries the symptoms begin to
improve at an early period and the patient may ultimately recover com-
pletely. In these cases it is evident that collateral circulation has
become established before softening has taken place. In cases in which
recovery has taken place the patient is liable to be suddenly attacked
by occlusion of other vessels.
h. Thrombosis of the Cerebral Sinuses.
Etiology. — Thrombosis is prone to occur in the cerebral sinuses
because they are traversed by bands of connective tissue, are destitute
of muscular walls, and are rigid tubes incapable of collapsing. Throm-
bosis of the sinuses is particularly liable to occur in infants during the
collapse induced by severe diarrhoea, while in adults it occurs in cases
of profuse sujjpuration, cancer, senile marasmus, and other diseases
associated with great debility. In other cases inflammation of the
sinuses is produced by disease or injury of the cranial bones, which is
followed by the formation of purulent thrombi. Erysipelas of the head
and face, furunculus of the face, and purulent inflammation of the deep
muscles of the neck, are other causes of thrombosis of the sinuses.
Symptoms. — The symptoms of thrombosis of the sinuses in children
consist of convulsions or paralysis in addition to the collapse, and som-
nolence caused bv the cerebral anaemia which results from an exhaust-
AX.EMIA AXD OCCLUSIOX OF IXTRACRAXIAL VESSELS. 607
ing diarrhoea. The motor symptoms most commonly observed are
rigidity of the muscles of the neck and sometimes also of those of the
limbs, nystagmus, strabismus, ptosis, and paresis of the facial muscles.
The fontanelles are at first depressed as in the hydrencephaloid disease
described by Marshall Hall, but as the disease advances either effusion
of serum or extensive meningeal or intra-cerebral hemorrhages may
take place and the fontanelles become less tense and the cranial bones
pushed apart.
Thrombosis of the sinuses from marasmus in adults give rise to very
indefinite symptoms, and at times a slight degree of apathy and general
depression are the only symptoms present. At the outset the patient
may complain of headache, nausea, and vomiting, but these soon give
place to coma, and in a few cases loss of consciousness is preceded by
delirium, which occasionally assumes a maniacal character. The most
usual motor disturbances are strabismus, trismus, tremors and con-
tractures, epileptiform convulsions, or paralysis, which may involve one-
half or both sides of the body. At other times paralysis and contrac-
tures may be associated, one extremity being the seat of contractui-e
and the other of paralysis. Swelling of the veins outside the skull
affords a valuable sign of thrombosis of the sinuses. The superior
longitudinal sinus communicates directly with the veins of the nasal
cavities and with those on the upper surface of the skull, and conse-
quently thrombosis of it may give rise to epistaxis, or to distention of
the veins which run from the temples on both sides to the anterior fon-
tanelle, and there may also be cyanosis of that part of the face which
is supplied by the anterior facial veins.
The lateral sinus communicates with a small vein which traverses
the mastoid process, and in thrombosis of the sinus localized oedema
behind the ear occasionally may make its appearance. Simultaneous
thrombosis of both lateral sinuses gives rise to the same symptoms as
occlusion of the superior longitudinal sinus.
The cavernous sinus communicates with the ophthalmic vein, and in
thrombosis of the sinus, venous hypersemia of the fundus oculi has been
observed, along with cedema of the eyelids and conjunctiva, and promi-
nence of the eyeball caused by congestion of the retrobulbar frontal
veins. Interference with the nutrition of the nerves which pass along
the floor of the sinus may also give rise to paralysis of the oculo-motor
nerves, trigeminal neuralgia, and neuroparalytic ophthalmia.
The phlehitie variety is generally complicated with meningitis and
cerebral abscess, and it is not, therefore, always possible to distinguish
between the symptoms caused by each of these morbid conditions. In
the few cases in which suppurative thrombosis was alone present, the
608 VASCULAK DISEASES OF THE BRAIN.
symptoms Avere the same as those of septiciiemia with pronounced cere-
bral symptoms. The attack generally begins with chilliness, which
recurs repeatedly during the course of the disease, and the jiatient
has a characteristic typhoid look, with dry tongue, loss of appetite, and
mental confusion. After a time the patient flills into a somnolent con-
dition which gives place to coma, which soon terminates fatally. Wlien
suppurative thrombosis is complicated with meningitis, more pronounced
sensory and motor symptoms are present, consisting of headache, hyper-
algesia, paresis, paralysis, or convulsions. The disease sometimes
pursues a latent course, and is only discovered after death.
c. Occlusion of the Cerebral (Japillaries.
Etiology. — In severe cases of intermittent fever the cerebral capillaries
are liable to be obstructed by dark colored masses which have been called
'pigment embolism. The cerebral capilhiries may also be obstructed by
oil globules, constituting fat embolism. The cerebral capillaries are
said to be sometimes occluded by linie Ijccoming deposited on tlieir walls,
a process named by Virchow lime metustasis. (Japillary embolism is sup-
posed to give rise to chorea, but this subject will be discussed hereafter.
Synqotoms. — If the embolic masses are few in number they do not
give rise to symj)tonis which can be recognized during life, but if a con-
siderable part of the brain is deprived of its nourishment the patient
suffers from dift'used cerebral symjitoms such as dizziness, headache,
nausea, trembling, Aveakness of the extremities, and loss of memory
with other signs of mental decay. If the circulation is suddenly
arrested in a large portion of the brain the symptoms of a localized
destructive disease of the cerebrum may be produced.
Morbid Anatomy. — Capillary occlusion can only be discovered with
the aid of the microscope. The first effect of these emboli is to cause
anoemia, and subsequently the various stages of necrobiosis up to com-
plete softening are produced.
Treatment. — The treatment will depend upon the cause of the emboli
and must be conducted on general principles.
II. CONGESTION OF THE BKAIN.
Etiology. — Congestion of the brain may be either active or passive,
and is produced by the same general causes as congestion of other
organs. It is, indeed, asserted by Moxon that congestion of the brain
does not give rise to symptoms which can be set up as a distinct disease.
CONGESTION OF THE BRAIN. 609
but apoplectiform attacks occur in the course of such diseases as loco-
motor ataxia, general pai-alysis, and sclerosis in patches, for which it is
difficult to assign any other cause than congestion, and although it is
probable that congestion has been often assumed to exist without due
warrant, Ave do not feel ourselves justified in rejecting the condition as
a cause of a distinct and separate disease.
Symptoms. — Congestion of the brain gives rise to symptoms which
vary widely in different cases, but for clinical purposes three varieties
may be described: (a) the slight, {h) the severe, and (c) the apoplectic
form.
(a) In the slifiht form of congestion the prominent symptoms are
sensory disorders. The patient complains of severe headache, either
deep-seated or lancinating, aggravated by movement, light, sound, or
heat, while all intellectual efforts become impossible. Patients at the
same time complain of dizziness, tinnitus aurium, and optical illusions.
Sleeplessness is an early and important symptom. It is accompanied
by restlessness and agitation, and if sleep do supervene, it is disturbed
by horrible dreams, and the patient awakes unrefreshed without relief
to the headache.
In venous hypersemia the phenomena of mental depression are usually
more marked than those of excitement. There is a dull sense of oppres-
sion in the head, the face is livid, there is mental torpor with a ten-
dency to sleep, and a certain amount of confusion of ideas, especially
on awaking after a short sleep.
(h) In the severe forms other symptoms are added. The patient
suffers so much from vertigo that he is unable to maintain the erect
posture, and sudden vomiting may occur in the absence of any gastric
irritation to account for it. The pulse is slow, full, and hard; the
arteries of the head and neck beat forcibly; the face is frequently,
although not always flushed, and may at times be livid, while a sensa-
tion of flying heat shoots over the head and neck. The pupils are
generally contracted, and there is some degree of intolerance of light
and sound. The patient complains of intense headache, and is the
subject of hallucinations and illusions which pervert the judgment,
and may lead to strange and disorderly acts. He sometimes endeavors
to quit his bed, and to pursue or run away from imaginary objects; he
is loquacious or bursts into a flood of tears, and struggles with and tries
to escape from his attendants. After some hours of excitement and
struggling the skin becomes covered with sweat, the pulse is accelerated,
the face of a deep red color, and the patient presents the leading symp-
toms of encephalitis; the thermometer shows that the temperature, if at
all altered, is only slightly above the normal. If these symptoms
39
610 VASCULAR DISEASES OF THE BRAIX.
persist for some time, the phenomena of excitement are succeeded by
those of depression, the delirium gradually gives place to mental
torpor, the muscular agitation is replaced by muscular relaxation, the
respiration becomes stertorous, there are involuntary evacuations, and
the patient falls into a state of coma. An abundant secretion from the
conjunctivae and mucous membrane of the mouth is said to be a frequent
symptom of congestion of the brain in old people. It is very probable
that many of the cases which have been described as examples of cere-
bral congestion ought to be regarded as the delirium or mania which
so frequently follows a slight epileptic attack.
The symptoms of cerebral congestion in infancy are somewhat simi-
lar to those of meningitis. Both are attended with partial or general
convulsions, headache, contraction of the pupils, vomiting, and consti-
pation. The course of the two affections, however, enables them to be
readily distinguished. In congestion the child has been in good health
up to the beginning of the attack, there is little or no elevation of tem-
perature, and the disease terminates in recovery in two or three days
at most.
(e) The ajyojjlectic form is characterized by sudden and total loss of
consciousness and complete resolution of the limbs, but reflex excita-
bility is preserved. The patient recovers consciousness in a few hours,
and after a short time — two or three days at most, all the symptoms
disappear without leaving a trace behind. Sometimes, however, after
complete restoration to consciousness, a certain amount of muscular
paralysis remains in one limb, or it assumes the hemiplegic form and
persists for some time. Apoplectiform attacks of this kind are liable
to occur in the course of locomotor ataxia, sclerosis in patches, and
general paralysis of the insane. Patients suffering from these diseases
are sometimes seized with general convulsions and die comatose in a
fcAV hours, and at the autopsy no coarse lesion of any kind is discovered
in the brain.
III. INTRACRANIAL HEMORRHAGE.
Intracranial hemorrhage may be divided into 1, cerebral; and
2, meningeal hemorrhage.
1. Cerebral Hemorrhage (Apoplexy).
Etiology. — Some families exhibit a predisposition to cerebral hemor-
rhage, but this tendency is only an indirect result of an inherited ten-
dency to a general arterial degeneration. Cerebral hemorrhage is rare
IXTEACRANIAL HEMORRHAGE. 611
before the fortieth year of age, and it occurs more frequently in men
than in women, but age, sex, as well as occupation and climate, seem
to predispose to it only in so far as they tend to induce degeneration of
vessels. The chief circumstances which predispose to cerebral hemor-
rhage are (1) diseases of the bloodvessels, (2) increase of the arterial
tension, (3) disease of the tissues surrounding the vessels, and (4) cer-
tain diseases of the blood.
(1) Diseases of the Vessels. — The great majority of massive hemor-
rhages into the substance of the brain are due to degeneration of those
branches of the Sylvian artery which pass through the anterior perforated
space to reach the corpus striatum. By far the most frequent cause of
intracerebral hemorrhage is that condition of the arterioles which has
been described by Charcot and Bouchard as miliary aneurisms. These
aneurisms are of a reddish color, and vary from the size of a millet
seed to that of a pin's head. Sometimes a few only are found in the
neighborhood of the ruptured vessel, while at other times they are scat-
tered in large numbers throughout the whole brain. The parts of the
brain in which they are situated, in the order of decreasing frequency,
are the lenticular nucleus, the optic thalami, the pons, the convolutions,
the caudate nucleus, the cerebellum, the medulla oblongata, the middle
peduncles of the cerebellum, and the centrum ovale. Miliary aneu-
risms result, according to Charcot and Bouchard, from a kind of arterial
sclerosis of the nature of a chronic periarteritis. Atheroma of the
vessels may also lead to aneurisms of the larger and medium sized
arteries of the brain, and although rupture of these are apt to give rise
to hemorrhages on the surface of the brain, yet the hemorrhage passes
into the substance of the brain more frequently than is generally sup-
posed. Atheromatous degeneration may also cause hemorrhage indi-
rectly by rendering the walls of the larger vessels rigid, so that the
pulse-wave reaches the arterioles without being modified by the normal
elasticity of the arteries.
Primary fatty degeneration of the cerebral bloodvessels occurs at all
ages, and Paget believes that it sometimes predisposes to cerebral hem-
orrhage in young people.
(2) Vascular Tension. — It is doubtful whether increase of the arte-
rial tension ever gives rise to cerebral hemorrhage in the absence of
disease of the vascular walls, but when arterial degeneration is present
any increase of tension becomes a powerful predisposing cause of hem-
orrhage. Sudden exposure to cold may increase the arterial tension
by inducing extensive contraction of the cutaneous arteries. During
the winter months it is very common for individuals to be found in a
comatose condition on the streets and taken up by the police on the
612 VASCULAR DISEASES OF THE BRAIX.
supposition that they are drunk. Such accidents usually occur in per-
sons of middle age ; the breath may smell of alcohol, and the person
attacked may be known to have been drinking during the evening.
The evening has been spent in a heated apartment, when, under the
conjoined influence of a high temperature, alcohol, and emotional ex-
citement, the cutaneous vessels have become dilated, the skin bathed in
perspiration, and the cardiac action accelerated. On going out into the
cold air the surface becomes suddenly chilled, and the arterial tension
is rapidly augmented ; the internal organs become gorged with blood :
and if, as is frequently the case, the Avails of the cerebral vessels are
weakened by disease, rupture of one of them is apt to occur.
The hypertrophy of the left ventricle, which takes place in contracted
kidney, taken along with arterio-capillary fibrosis, which invariably
accompanies it, is a frequent cause of cerebral hemorrhage.
(3) Condition of the Tissues. — The theory that cerebral hemor-
rhage is generally preceded by softening of the cerebral tissue, was
advanced by Rochoux, and he gave to this supposed process the name
of ramollisseDtent hemorrhagfpare, but it is now generally admitted that
when the softening is not caused by occlusion of vessels, it is secondary
to the hemorrhage.
(4) The State of the Blood. — Cerebral hemorrhage has been occa-
sionally observed in the course of diseases of the blood, like scorlmtus,
purpura, chlorosis, leucocythemia, pernicious ansemia, icterus, typhoid
and other specific fevers.
Symptoms. — An attack of cerebral hemorrhage may begin suddenly
Avithout any warning, but in many cases premonitory symptoms are
present some days or even weeks before the actual onset of the attack.
The usual forerunners of an apoplectic attack are dizziness, headache,
ringing in the ears, muscae volitantes, numbness in the hand or foot,
muscular tAvitchings of the face or some portion of the extremities, mis-
takes in talkino; or Avritino;, vomitincj, mental irritabilitv, and drowsiness.
These symptoms, either separately or in various combinations, are to be
regarded as warnings of apoplexy only in old people, or in middle-aged
people Avith evidences of arterial degeneration. The mode of onset of
an attack of cerebral hemorrhage may be divided into (1) the apo])lecti-
form, (2) the epileptiform, and (3) the simple mode of onset.
(1) Apoplectifoi-m Onset. — This mode of onset is characterized by
sudden loss of consciousness and resolution of the limbs, either Avith
or without warning, constituting what is popularly called apoplexy.
When the apoplectic attack is Avell marked the patient lies in a state
of profound coma, and is insensible to all kinds of stimuli. The face
is usually flushed and SAvollen, although it may occasionally be pale
INTRACRANIAL HEMORRHAGE. 613
and clammy; the lips are livid; the head and neck feel warm and
bathed in persi)iration ; the carotids and other arteries throb violently;
the eyelids are closed; the conjunctivae are ingested; the eyeballs are
fixed; the pupils are sluggish to light; the respiration is usually deep,
Avith or without stertor and protrusion of the cheeks during expiration ;
the pulse is generally full and slow ; and there is either complete mus-
cular resolution, so that the limbs when raised drop like inert bodies,
or the resolution is more marked on one side of the body than on the
other. In the severer cases there is not only complete absence of vol-
untary motion, but all reflex movements are lost, with the exception of
the cardiac and respiratory movements and those concerned in the
second act of deglutition. In such cases the patient may die after a
few minutes, a few hours, or a few days. In cases which are less severe
from the first or in which some degree of recovery has taken place,
powerful irritation causes reflex movements, and in still less profound
cases the patient, when loudly spoken to, raises his eyelids for a moment
or two, and may even reply in a monosyllable when loudly pressed with
any question. In such cases a difierence can be detected between the
two halves of the body ; the extremities of one side offer some degree
of resistance to passive movements, while those of the other side sink,
when unsupported, like inert masses, and the corner of the mouth is
lower on one side than on the other.
(2) The Epileptiform Onset. — In this mode of onset the patient,
either with or without prodromata, drops down insensible in a kind of
epileptic fit, and after a time it is discovered that he is paralyzed on
one side of the body. The convulsions may be limited to one-half of
the body, and this side is subsequently paralyzed ; but if the convul-
sions occur after paralysis has become established the non-paralyzed
side is the one which is attacked with clonic spasms. In some of the
cases initiated by convulsions the patient may remain in a somewhat
lethargic condition, with eyes closed or only half open, for a period of
from three to six weeks and yet recover, but if deep coma continues for
forty-eight hours the case generally terminates fatally.
(3) Simple Mode of Onset. — In the simple onset the patient may
suddenly fall from paralysis, but without loss of consciousness. He
generally complains of a feeling of " numbness " of the paralyzed side,
but does not suffer pain.
The temperature is lowered immediately after an apoplectic attack,
reaching in some cases 96.5° F., and in the fulminating foi'ms it remains
low until death. If life continue for from ten to twenty hours the
initial sinking gives place to an elevation of temperature. In fatal cases
the secondary rise may reach 108° F. or even higher before death, but
614 VASCULAR DISEASES OF THE BRAIX.
in favorable cases it continues to oscillate for some clays between 99° F.
and 100.5° F. If the case is to terminate favorably the temperature
now gradually sinks to the normal, but if a fatal termination is to take
place the more or less stationary temperature of the first few days is
followed by a rapid and continuous rise, just as occurs after the period of
initial lowering.
Conjugate deviation of the eyes, with rotation of the head and neck.
occurs as a temporary symptom in all cases of severe cerebral hemor-
rhage, the deviation being directed away from the paralyzed side when
the lesion is situated in the hemisphere and towards it when it is situated
low down in the pons. The eyes are usually fixed, but occasionally
exhibit slight nystagmus. The rotation may completely disappear when
the patient falls asleep and the symptom usually lasts only a few days.
The permanent symptoms of cerebral hemorrhage are the various
forms of hemiplegia with rigidity of the paralyzed muscles which will
be subsequently described.
Vaso-motor disorders are generally observed in the paralyzed limbs
soon after the attack ; the paralyzed limbs are redder and warmer than
the corresponding healthy limbs, the difference in temperature var^nng
from a fraction of a degree to 2° F., and they may also become swollen
from a slight degree of subcutaneous oedema. The temperature of the
paralyzed limbs gradually decreases and is eventually lower than that
of the sound side, and when the oedema disappears the skin becomes
dry and scal3^ Congestions and even hemorrhage of the lungs, and
extravasations into the pleura, endocardium, mucous membrane of the
stomach, the suprarenal capsules, and the kidneys frequently accom-
pany cerebral hemorrhage, and are often limited to the paralyzed side
of the body.
The trophic disorders consist of acute bedsores, which may appear on
the gluteal region of the paralyzed side soon after the attack. Acute
inflammation of one or more of the large joints, or chronic arthritis of
the small joints, may begin on the paralyzed side generally in from
three to six weeks after the onset. In some cases the patient complains
of pain on pressure in the paralyzed limb, which is especially well
marked along the course of the principal nerve trunks, and Cornil
has shown that it is most probably caused by an inflammatory hyper-
trojihy of the nerves or of their sheaths. In some exceptional cases
the paralyzed muscles undergo early and rapid wasting, and when the
hemiplegia occurs in childhood, the affected limbs grow more sloAvly than
the corresponding healthy ones, and the former are consequently smaller
in all their dimensions than the latter. The skin on the paralyzed side
sometimes feels thicker than on the healthy side, while the hair some-
IXTRACRANIAL HEMOERHAGE. 615
times grows better on the affected than on the unaffected side. The
nails on the paralyzed side become yellowish, marked with ridges, brittle,
and curved.
The mental condition of the patient is seldom fully restored. In most
cases the intellectual condition is permanently enfeebled, so that the
patient feels unequal to any unusual intellectual effort, wdiile in other
cases the intellect undergoes progressive declension, and the patient is
reduced to a state of childishness or pronounced dementia. At other
times the patient becomes peevish, whimsical, irritable, and gives way
to outbursts of passion. The disorders of speech which occur in cerebral
hemorrhage will be subsef{uently described.
2. Meningeal Hemorrhage.
Etiology. — The most frequent causes of meningeal apoplexy are in-
juries of the skull producing rupture of arteries, veins, or sinuses,
rupture of aneurisms of larger arterial branches, and thrombosis of the
sinuses. Meningeal hemorrhage may occur in the course of acute
infectious diseases, chronic dyscrasise, and progressive paralysis of the
insane, while the meningeal apoplexy of newborn children is caused by
certain accidents attending childbirth.
Symptoms. — Meningeal hemorrhage caused by rupture of an aneurism
forms the least complicated form of the disease, inasmuch as hemor-
rhages of traumatic origin are usually complicated by other cerebral
symptoms. In severe cases of uncomplicated meningeal hemorrhage
the patient becomes suddenly apoplectic without any warning, or with
only slight premonitory symptoms, such as headache, dizziness, and
vomiting. The paralysis commonly affects all four extremities, and
hemiplegia is only rarely met with. The onset is often marked by
epileptiform convulsions and vomiting, profound coma supervenes, and
the patient dies in a few hours or at most in a few days. In less severe
cases the patient may recover consciousness after a few hours, and he
then complains of headache and is often delirious, and after a short period
of somnolence he finally becomes comatose. In a few cases the symp-
toms creep on gradually ; the patient complains at first of headache,
dizziness, and numbness or weakness of the extremities on one or both
sides, and after a time he falls into a condition of stupor and ultimately
dies comatose.
If an aneurism of considerable size has existed for some time before
the occurrence of hemorrhage, it may give rise to the symptoms of an
intracranial tumor, which will be subsequently described.
616 VASCULAR DISEASES OF THE BRAIX.
In the meningeal hemorrhages of the newborn, the children are either
born dead, or in a condition of asphyxia, and often die soon afterwards.
If respiration is established the infant lies in a comatose condition for
some days or weeks, and during this time he suffers from frequent attacks
of convulsions, which are generally most pronounced on one side of the
body. In such cases the disease may prove fatal by coma or the patient
may gradually recover so far as life is concerned, but he remains the
subject of one or other of the forms of spastic paralysis of infoncy
already described.
Prognosis. — The case will terminate fatally at an early period if the
patient cannot be roused at all, and if the reflex action of the conjunctiva
is abolished, the urine and feces are passed involuntarily, and there is
well-marked stertor, while the persistence of even a slight degree of
these symptoms without abatement is a sign of great gravity. A (|uick,
irregular pulse with labored respiration, and decided diflSculty of deglu-
tition and articulation, are also very unfavorable signs. A marked
and persistent depression of the pulse is of fatal significance, while a
marked and persistent rise of temperature is an almost equally grave
sign. A sudden depression of temperature with increase or renewal of
a preexisting comatose condition is also of serious import, indicating, as
it does, the occurrence of a fresh hemorrhage. Acute bedsores on the
buttock of the paralyzed side is a fatal sign.
Treatment. — The treatment of cerebral antr'mia must vary according
as the disease is acute or chronic, and as it is limited to the brain or
affects the entire body. In an ordinary faintinf/ fit tlie patient should
be as speedily as possible placed in the recumbent posture, and recovery
usually takes place without further treatment. If the symptoms are
more persistent, some form of local irritant must be employed, such as
sprinkling the face with cold water, or flecking it with the corner of a
towel dipped in cold water, the apj)lication of the faradic current to the
surface by means of the metallic brush, the inhalation of ammonia to
stimulate the olfactory and trigeminal nerves, or a stimulating enema.
As soon as the patient can swallow, stimulants, such as coffee or brandy,
must be given, especially if the heart's action be feeble. In severe
cases of cerebral ansemia, after profuse hemorrhage, the body of the
patient ought to be covered with warm clothing and surrounded by
bottles containing hot water, and in order to increase the flow of blood
towards the brain the head ought to be kept in a low position, while
pressure is maintained over the abdominal and axillary arteries. In
cases of severe and prolonged anaemia from loss of blood transfusion
ought to be tried as a last resort. The cerebral anaemia which arises
during the course of acute diseases must be treated by the judicious use
INTKACEANIAL HEMOERHAGE. 617
of wine and nourishing diet, and if the ease admit of it by such tonics
as quinine, iron, and arsenic. When delirium or other form of cerebral
excitement accompanies the aniBniia, the great aim of treatment should
be to procure sleep, and a full dose of chloral or better still an opiate
should be administered. Hydrocephaloid disease should be treated on
the same general principles as other forms of cerebral anaemia and in
addition the diarrhoea or other disease which has caused the ant^mia
must be attended to.
Occlusion of cerebral vessels must be treated on the same general
principles as hemorrhage from them, but in embolus the cardiac compli-
cation must be subjected to treatment, while in thrombosis the presence
either of syphilitic endarteritis or of atheromatous degeneration of the
arteries must be borne in mind and the appropriate treatment adopted
for each.
Congestion of the brain must be treated by rest in the recumbent
position with the head raised, ice to the head, and active purgation.
The diet should be plain and unstimulating, but nourishing. Moderate
doses of ergot are supposed to have a favorable influence on the disease.
In cerebral hemorrhage the aims of treatment are (1) to avert a
threatened attack ; (2) to treat the apoplectic condition ; (3) to allay
excitement during the inflammatory reaction ; and (4) to improve the
permanent symptoms.
(1) Prophylactic Treatment. — When a person complains of any of
the usual premonitory symptoms of apoplexy the treatment must vary
according to the state of the general health. The condition of the heart
and bloodvessels must be carefully explored, and the urine must be
tested for albumen and sugar, and the treatment must be adapted to meet
any disorder of the general health which may be discovered. Saline
purgatives are generally useful by lowering the arterial tension, and
during the continuance of threatening symptoms the patient should be
kept quiet in a darkened room and cold applied to the head.
(2) The apoplectic attack must be treated by absolute rest, and cold
to the head, and if the arterial tension be high a moderate bleeding may
do good, but the severe general bleeding practised a few years ago is
quite inadmissible. When there are signs of cardiac failure, or when
the breathing is intermittent or assumes the Cheyne-Stokes character,
then a stimulating treatment must be adopted, but the common practice
of applying blisters to the shorn scalp or to the nape of the neck, or
mustard plasters to the calves of the legs, is useless and ought to be
strongly condemned.
If the attack is preceded or accompanied by recurring epileptiform
attacks, or if the patient is restless and there is more or less of delirious
618 VASCULAR DISEASES OF. THE BRAIX.
Avandering, bromide of potassium nia}^ be given. If the. bowels are
constipated an enema containing castor oil or oil of turpentine should
be administered, or two drops of croton oil may be given in a suitable
vehicle or placed on the back of the tongue. The state of the bladder
should be carefully examined and a catheter used if necessary.
(3) If the patient survive the first shock of the apoplectic attack,
the less we interfere during the first days the better. He must be kept
as quiet as possible both in body and mind, his diet should consist
of liquid nourishment, and the state of his secretions and excretions
should be carefully regulated. Cold should be applied when the symp-
toms of inflammatory reaction appear, and if the patient complain of
headache, or there be persistent wakefulness or delirium, a full dose of
bromide of potassium, or even an opiate or chloral should be given.
During this period great care must be taken to prevent bedsores on the
paralyzed side by paying constant attention to the state of the bedding
and securing extreme cleanliness. In severe cases the patient should,
when practicable, be placed from the first on a water bed.
(4) The most effectual method of promoting the improvement of the
paralyzed nerves and muscles is a thorough attention to the general
health of the patient, and tlie treatment pro})er for each case will depend
upon his age, habits, and constitution, and on the presence or absence
of any concomitant disease. The general principles of treatment
are to take care that the patient has a sufficiency of easily digestible
and nutritious food ; tliat all circumstances which might cause mental
excitement are avoided ; and that he has a due amount of repose and
sleep. In the hemiplegias of elderly people, in which miliary aneu-
risms may be presumed to exist, care must be taken that the circulation
is not subjected to any sudden strain, and it is, therefore, necessary to
keep the bowels moderately open lest straining at stool should induce
another attack. The patient should take open air exercise by walking
on level ground, or in a chair or carriage, and much good may be done
by sponging with salt water. When there is advanced arterial degenera-
tion or high arterial tension the water ought to be tepid, and heniiplegic
patients, as a rule, should only use baths of moderate temperature.
Iodide of potassium is the most likely drug to promote the absorption
of the clot, and its administration may be commenced immediately after
the febrile symptoms of the inflammatory reaction have subsided. In
ordinary cases, from three to five grain doses three times a day will
suffice ; but if the hemorrhage is caused by premature degeneration of
the arteries from syphilis, it Avill be advisable to give from fifteen to
twenty grain doses three times a day, and in some cases it will be neces-
sary to give mercury in some form along with the iodine salt.
INTHACRANTAL HEMORRHAGE. 619
The local treatment of the paralyzed limbs consists of passive move-
ments, and friction of the skin by means of a flesh brush, flannel, or
the palm of the hand. After a time the patient should be directed to
move the paralyzed limbs by voluntary effort, and various gymnastic
exercises may be adopted to bring the paralyzed muscles into separate
and combined action. The constant current may be employed by
placing one electrode on each mastoid process, or one on a mastoid
process and the other on the nape of the neck, but in this method only
feeble currents should be used, and the duration of the application
should not exceed three minutes. According to another method, the
current is passed through the paralyzed nerves and muscles in the
usual way. The faradic current has been employed in contractures
for the purpose of acting, not on the contracted muscles, but upon their
antagonists, but this method has not been productive of much good.
The methods used to promote the recovery of the paralyzed muscles
are also the best remedies for the sensory disorders which are often
present in cases of hemiplegia.
CHArXER XYT.
ENCEPHALITIS.
Etiology. — The most freciuent cause of acute inflammatiou aud
abscess of the brain is recent injury. When air gains access to the
interior of the skull through an open wound, encephalitis becomes com-
plicated with meningitis, but contusion of the brain may give rise to it
in the absence of any perforating wound. Encephalitis may be set up
by diseases of the bones of the skull, such as caries, or inflammatory
action may be transmitted to the brain from diseases of the nose,
antrum of Highmore, and orbit, while abscess of the brain frequently
results from disease of the middle or internal ear. Multiple cerebral
abscesses occur in connection with acute febrile affections, such as
typhoid and scarlet fevers, and in putrid bronchitis and bronchiectasis,
ulcerative endocarditis, and other pytrmic affections. Focal diseases of
the brain like tumors, hemorrhage, thrombosis, and embolism, often set
up surrounding inflammation in the brain, and in some cases enceph-
alitis may be of idiojjathic origin.
DIFFUSED OK GENERAL ENCEPHALITIS.
Cases of uncomplicated general encephalitis are not very common,
most of the cases Avhich have l)een reported as examples of this disease
being examples of cerebral meningitis, or, more strictly speaking, of
meningo-encephalitis. The symptoms of simple encephalitis are pyrexia,
a busy and talkative but not violent delirium, passing on to somnolence
and finally to coma. The presence of spasms Avould seem to indicate
a complication with meningitis, while the appearance of partial or com-
plete hemiplegia Avould shoAv that the disease is more pronounced on one
side than on the other, and therefore that the inflammation is partial.
PARTIAL OR LOCAL ENCEPHALITIS.
Local encephalitis may occur as 1, an idiopathic affection in children,
when it has been named poUencephalitis acuta infantium; 2, as the
result of an injury; 3, as a consequence of pyaemic infection; and
PARTIAL OR LOCAL E XC E P H ALl TIS . 621
4, as a secondary result of a focal disease like (a) abscess, [b) hemor-
rhage, (c) softening from occlusion of vessel, and [d) tumor.
1. POLIEXCEPHALITIS AcUTA InFANTIUM.
Acute inflammation of the brain occurs in infancy between the ages
of one and six years. The attack may follow measles or scarlet fever,
or be set up by a blow on the head, but in the majority of cases no
exciting cause can be assigned, and the subjects of the disease do not
even seem to belong to neuropathic families. The attack begins sud-
denly with fever, vomiting, and convulsions, and the child falls into an
apoplectic condition which may last two or three days, occasionally
one or two weeks, or even longer. The spasms are generally more
pronounced on one side of the body than on the other, and are often
strictly unilateral ; after a longer or shorter time the convulsed limbs
become more or less completely paralyzed. It is possible that many
of these cases are fatal, but in other cases the child gradually re-
covers, except that he is the subject of a permanent hemiplegia. The
further progress of this aff'ection has been already described under the
name of spasmodic hemiplegia of infancy, of Avhich unilateral atrophy
of the brain is the anatomical counterpart.
2. Traumatic Local Encephalitis.
When a contusion in the interior of the brain has taken place, the
patient first suffers from the usual symptoms of concussion, and it is
only when these have disappeared that the usual symptoms of a local
encephalitis can be recognized. The patient lies in a semiconscious
condition, and when roused complains of headache and dizziness, and
staggers on attempting to walk. The pupils are variable in size, but
they are generally equal and react slowly to light. The countenance
is usually suffused, but at times it turns pale, and the pulse, which was
frequent and irregular during the stage of concussion, sinks to sixty or
seventy beats, but the thermometer may indicate the existence of fever
of remittent type. When the encephalitis is situated in the frontal,
temporal, or occipital lobes, the symptoms may be so slight that the
patient feels quite well in a few days, or suffers for a week or two from
very indefinite symptoms. Suddenly, however, more pronounced symp-
toms become manifest; the fever, which still continues of irregular
type, becomes more intense; dizziness and headache become more
marked ; vomiting is not infrequently present : the pupils are dilated
622 ENCEPHALITIS.
and fixed ; the pulse is slow ; and the patient fells into a condition of
stupor, which may be accompanied by delirium, or may pass directly
into complete unconsciousness.
As the case progresses the symptoms of a localized disease may
appear, consisting at first of spasmodic phenomena, such as rolling of
the eyes, twitchings of the face or hands, or more decided clonic con-
vulsions of the limbs, or even a general convulsion, but these are soon
followed by paralysis of the abducens, motor oculi, or facial nerve, and
in a few cases by hemiparesis or hemiplegia. The stupor now grows
deeper, the urine and feces are passed involuntarily, the previously slow
pulse becomes quick and irregular, and death takes place in coma.
The course of the temperature is variable, but a continuous elevation
until death is exceptional.
The duration of local encephalitis varies greatly, and an abscess of
the brain has occasionally been found as early as the fifth day after the
injury, and when air gains access to the brain through an open wound,
and suppuration occurs, the disease may terminate fatally at a much
earlier period. The patient may occasionally be restored to compara-
tive health after an attack of traumatic encephalitis. The inflamma-
tory focus may be transformed into a relatively innocuous condition,
but even in those favorable cases chronic changes of a diffused character
are occasioned which give rise to more or less permanent symptoms.
The symptoms consist generally of some form of mental deterioration,
such as melancholia, chronic mania, or a condition resembling general
paralysis. Injuries of the skull are often followed by epilepsy, and
may be the starting-point of intracranial growths, while a fall on the
back of the head sometimes gives rise to diabetes.
3. Acute Py.emic Encephalitis.
Acute pycemic encephalitis is frequently ushered in by rigors, but
these being symptomatic of the general disease, do not indicate the
approaching complication. The first signs of the brain affection are
afforded by severe headache, which is usually frontal; dizziness; deli-
rium or somnolence ; unilateral convulsions ; and formication or numb-
ness of the extremities. The disease makes rapid progress and the
headache now becomes intense, the dizziness is so gi*eat that the patient
is unable to sit up in bed, the mind is confused, and the delirium or
somnolent condition of the first stage soon gives place to profound
coma, which proves rapidly fatal. The intensity of the febrile symp-
toms is variable, but in many cases there is a considerable elevation of
temperature.
partial or local e xcep ii alitis. 623
4. Encephalitis Complicating Pre-existing Lesions of the
Brain.
a. Acute Abscess 2cnth Encephalitis.
The symptoms caused by the acute encephalitis which accompanies
caries of the petrous bone are often obscured by coexisting meningitis
and thrombosis of the lateral sinuses. An abscess in the temporal
lobe may attain a considerable size, and cause general symptoms of
compression before giving rise to symptoms of local disease, inasmuch
as this lobe does not contain any direct sensory or motor conducting
tracts. Acute abscesses of the temporal lobe are consequently seldom
recognized during life. The symptoms of acute abscess, from otorrhoea,
or from caries of the other bones of the skull, begin with severe headache,
vomiting, ringing in the ears, confusion of ideas, loss of memory, and
delirium. As the disease advances the headache becomes more and more
intense, the delirium gives place to stupor, epileptiform convulsions
supervene, and the case soon terminates fatally amidst profound coma.
Fever of variable type is usually present, the pulse is slow, and the
pupils are contracted and sluggish. In some cases of abscess of the
temporal lobe the general symptoms are complicated by those of a
localized disease, and in these cases the abscess, which has rapidly
attained to a considerable size, compresses the fibres of the internal
capsule or the cerebral peduncle, and thus causes an incomplete hemi-
plegia with various sensory disorders, as well as paralysis of the oculo-
motor nerve, and occasionally of the facial. A few cases are associated
with acute meningitis or thrombosis of the lateral sinus.
h. Chronic Abscess with Encephalitis.
Chronic abscess of the brain may be divided into {a) primary, and
(b) secondary chronic abscess.
{a) Primary Chronic Abscess.
Primary chronic abscess is usually caused by some injury of the
brain. All the symptoms, or nearly all, may disappear soon after the
injury, and a period relatively free from symptoms may follow, forming
the latent stage of chronic abscess. The average duration of the latent
stage is, according to Lebert, from one to two months, but the period
may vary in individual cases from a few days to years. When once a
chronic abscess is formed, the symptoms caused by it are more or less
624 ENCEPHALITIS.
similar to those of cere1)ral tumor, and when the former is situated in
the motor areas of the cortex and centrum ovale, or injure the sensory
peduncular fibres, the symptoms of a local lesion are present from the
beo-innintr. The symptoms may be divided into those of (1) the latent,
and (2) the tei'minal stages.
(1) Sy7nptoms of ihe Latent Period.
The symptoms of the latent stage are those of a moderate degree of
intracranial pressure. These consist of constant headache with parox-
ysmal exacerbations, and slight febrile disturbance, dizziness, nausea,
and occasionally vomiting. The headache may be limited to the spot
where the injury was received, or correspond to the part of the brain
where the abscess is situated, the latter being often at a point of the
brain exactly opposite the seat of injury. l*aroxysmal exacerbations
of the headache are indicative of congestion around the abscess, and
when these frequently recur the abscess is likely to prove fiital within a
l)rief space of time. In some cases monospasms, monoplegia, or other
indications of a local disease in the brain are superadded to the general
symptoms just described.
In other cases the patient has intervals of comparative freedom from
all cerebral symptoms, but in the midst of comparative health he may
suddenly complain of intense headache, and soon fall into a deep but
transitory coma of several hours" duration, from which he rapidly re-
covers, such attacks being probably due to sudden pressure on the
brain from congestion.
("2) Symptoms of the Terminal Period.
When once the terminal period begins, abscess of the ])rain generally
leads to death in a few days. The symptoms of this period differ widely
in individual cases, and the following groups may be distinguished :
(a) TerniinaJ oedema of the brain is the most usual mode of termina-
tion of chronic abscess. In the majority of cases the tissues of the
brain are compressed to such an extent that death by coma results in
two or three days, while in a few cases the course of the symptoms is
characterized by temporary improvements and aggravations, so that the
fatal issue may be delayed for some time. In some cases there may be
a transitory initial stage of irritation, characterized by mental irritability,
restlessness, illusions, violent delirium, and a slight elevation of temper-
ature. The irritative symptoms soon give place to those of depression,
the patient complains of headache, the temperature falls, the pulse is
slow, the pupils are dilated and react feeblv to light, there is mental
i
PAKTIAL OR LOCAL ENCEPHALITIS. 625
confusion, and the patient falls into a somnolent condition, from Avhich
he may be roused temporarily when pressed by questions ; but in a
short time coma supervenes, and the case soon terminates fatally, the
pulse becoming small, quick, and irregular before death.
The symptoms of local disease which may have been present during
the latent stage of the abscess are variously modified in the terminal
stage. Partial convulsions, which may have been present, become more
violent and are soon followed by paralysis, or they may become trans-
formed into a series of epileptiform attacks terminating in coma.
General convulsions are sometimes caused by abscess situated in the
latent regions of the hemisphere, and these are usually followed by pro-
found coma.
(b) Rupture of the Abscess on the Surface of the Brain. — When
abscesses make their way to the surface of the brain, an acute and
rapidly fatal meningitis generally results. The symptoms of irritation
are at first predominant, but the patient soon becomes unconscious, and
dies comatose in a short time.
(c) Perforation of the Abscess into the Ventricle. — This occurrence
causes a group of symptoms which may be recognized, if the existence
of an abscess have been previously suspected. A sudden cerebral
attack, attended by bilateral, but more or less partial convulsions, such
as spasms of both legs, or of the facial muscles on both sides, is an
indication of rupture into the ventricles, provided the patient be not
already in an unconscious condition. General convulsions have some-
times been observed. Clonic spasms of the ocular muscles soon appear,
caused probably by irritation of the corpora quadrigemina. The patient
becomes rapidly unconscious, hemiplegia and death in profound coma
take place generally in from four to twenty-four hours after the rupture
of the abscess.
(d) Abscess of the cerebellum may terminate suddenly from arrest of
the respiratory functions produced by pressure on the medulla oblongata.
(e) Occasionally the brain is found in a condition of remarkable
antemia, and in such cases the immediate cause of death is not evident.
(b) Secondary Chronic Abscess of the Brain.
Secondary chronic abscesses are generally caused by affections of
the inner ear. The diagnosis of the presence of chronic abscess of the
brain is difficult, inasmuch as only a small proportion of such cases give
rise to characteristic symptoms. When the abscess is encapsulated it
may remain latent for a long time, so that no disease of the brain is
suspected until the terminal period. Even the terminal symptoms pre-
sent varieties which tend to obscure the diagnosis, these symptoms
40
626 ENCEPHALITIS.
sometimes resembling those of diffuse meningitis, and at other times
those of thrombosis of a sinus.
Varieties. — The following varieties of chronic abscess secondary to
disease of the ear may be distinguished : (1) Chronic abscess with
distinct typical course ; (2) Chronic abscess Avith terminal stage alone
distinct ; (3) Chronic abscess with thrombosis of the lateral sinus ; (4)
Chronic abscess complicated during the terminal period by meningitis.
(1) In affections of the inner ear abscess may form in the temporo-
sphenoidal lobe. In a long-standing case of disease of the internal ear,
where ric^ors and other general inflammatory symptoms are associated
with severe pain in the head, vomiting, convulsions, and other cerebral
symptoms, the formation of an abscess in the brain may be suspected.
These symptoms may pass off, and the patient enjoy apparent health
for months, with probably occasional headaches. The terminal stage is
announced by intense headache and dizziness soon followed by loss of
consciousness and stertorous breathing. Consciousness may be partially
restored in a few hours, and the patient then suffers from intense head-
ache and vomiting. After a short time the patient lapses a second time
into a semiconscious condition, and convulsions, generally unilateral,
supervene. Spasm followed by paralysis of the ocular muscles is not
an unfrequent symptom, and when the abscess is so large that it extends
to the lenticular nucleus and compresses the internal capsule, or the
fibres of the pyramidal tract in the crusta, a certain degree of hemi-
plegia may be present.
(2) Chronic abscess of the brain is sometimes observed in cases of
caries of the petrous bone, in which the terminal symptoms have not
been preceded by those indicative of irritation or encephalitis.
(3) Chronic abscess of the brain sometimes precedes, at other times
succeeds to thrombosis of the lateral sinus. The chief initial symp-
toms are, besides those of the ear affection, dizziness, intense headache,
and occasionally transitory delirium, followed by somnolence. The
patient suffers from frequently repeated rigors if the temperature of the
body be raised, and the fever assumes a remittent type. In the further
progress of the case the symptoms may pursue either of two directions.
The symptoms may be those of progressively increasing pressure upon
the brain, ending in coma, or the general symptoms indicative of com-
pression may be associated with those of localized disease, provided the
abscess has attained a sufficient size to press upon the internal capsule.
General convulsions may occur immediately before death.
(4) Chronic abscess of the brain may be complicated during the
terminal period by meningitis, and when the initial stage of the former
is latent, the terminal symptoms may be so similar to those of primary
PARTIAL OR LOCAL ENCEPHALITIS. 627
acute meningitis that the two aiFections cannot be distinguished from
one another during life.
e. Encephalitis Secondary to Hemorrhage.
The patient may have made a good recovery from the early symptoms
of an apoplectic attack, but several days afterwards there is a secondary
elevation of temperature, and the pulse becomes hard and frequent.
The patient complains of headache, or he may suflFer from slight wander-
ing and confusion of ideas or fall into a somnolent condition. The
general are soon followed by local symptoms, consisting usually of the
well-known secondary contractures. Some patients may manifest only
a slight tremor of the paralyzed limbs ; in others the flexors are in a
state of contracture ; and in a third series of cases these conditions
alternate. The temperature of the paralyzed side is often considerably
elevated, and anomalies in the secretion of sweat are observed. The
somnolence may now increase to a deep sopor which lasts several days,
and may pass into a profound or fatal coma. In cases that recover
symptoms frequently persist Avhich show that a chronic encephalitis is
established. The patient suffers from persistent headache, and frequent
attacks of dizziness, while he is subject to congestive attacks each of
which may cause new convulsions in the paralyzed limbs. The para-
lyzed limbs are generally subject to pains of variable character, which
may be situated in the joints, bones, skin, or muscles. Secondary en-
cephalitis is also the chief cause of the atrophy of the brain found in
many of these patients and which is always associated with profound
psychical disturbances.
d. Encephalitis Secondary to Thrombosis and Embolism.
After the formation of softening from occlusion of a vessel in the
brain, a febrile condition, attended by a drowsy delirium or somnolence,
often continues for some time, and either develops into permanent
imbecility, or gives place to partial restoration of the mental faculties.
When partial recovery takes place the patient is affected with weak-
ness of memory, irregular and causeless outbursts of temper, and a
disposition to shed tears or to laugh without adequate cause. The
patient is liable to congestive attacks which cause temporary uncon-
sciousness, and during these new foci of softening may be developed in
the brain.
In senile encephalomalacia the symptoms of secondary encephalitis
are caused by an increase of the intracranial pressure on the one hand
and irritation of the surrounding parts on the other. The symptoms
of inflammatory reaction are slight, and when a certain degree of senile
628 ENCEPHALITIS.
atrophy of the brain had existed previous to the occurrence of the attack,
the mental fimctions become progressively abolished without being pre-
ceded by symptoms of active irritation or by those which indicate a
gradual compression of the brain.
e. Encephalitis Secondary to Tumor.
The symptoms which may, with probability, be ascribed to encephalitis
durino- the growth of a cerebral tumor, are the occurrence of sudden
apoplectiform attacks, the rapid conversion of slight muscular weakness
into complete paralysis, partial convulsions followed by paralysis, general
convulsions, the sudden appearance of sensory disorders in the para-
lyzed or partially paralyzed limbs, and the gradual development of coma.
When, however, coma is suddenly developed it is more likely to be
caused by hemorrhage or sudden oedema than by ence])halitis. Every
attack of encephalitis is attended by violent headache, but the symptom
may be caused by a congestive swelling of the tumor itself.
Morbid Anatomy. — In encephalitis the affected tissue assumes a
reddish color, and is studded with a num1)er of capillary extravasations,
which are followed by more or less oedema. The affected portion of the
brain becomes voluminous and the cut surface rises above the level of
the surrounding tissues. An encephalitis of slight intensity and small
extent may undergo complete repair. At other times the focus under-
goes destructive changes and its contents become converted into a thick
emulsion, colored brownish or yellowish by blood pigment. After a
time a focus of yellow softening forms which gradually becomes more
colorless, and at last may be transformed into a cavity which is filled
Avith a thin milky fluid. Later, the focus manifests a delicate stroma
consisting of connective tissue supplied with fine bloodvessels, and
the interspaces of which are filled by a thin turbid fluid. In other
cases a local encephalitis leads to the production of a firm sclerotic
cicatrix. These cicatrices are situated usually near the surface of the
brain and only rarely in its interior ; they are of a dirty white color,
tough and firm, and the tissue surrounding them becomes atrophied so
that the affected hemisphere is less th;in the other. In a large number
of cases the encephalitic focus is transformed into a collection of pus,
forming either an acute or chronic abscess. An acute abscess has a
tendency to spread in every direction, and presents an irregular cavity
in the substance of the brain, the walls of which have a rough and
shaggy surface. As the pus in the central cavity accumulates, so much
pressure is exerted on the surrounding tissue that the circulation is
arrested and this leads to further destruction and to advance of the
abscess. Chronic abscesses of the brain possess a fibrous capsule which
PARTIAL OR LOCAL ENCEPHALITIS. 629
may attain to a thickness of several millimetres. The internal surface
of the limiting membrane is smooth, and has an opaque yellowish-white
appearance owing to a continuous layer of cells Avhich are in a state of
fatty degeneration. The pus of the abscess is of a greenish color, greasy
consistence, odorless, and gives an acid reaction. After a time the
abscess enlarges so as to raise considerably the general intracranial
pressure, and extensive yellow softening may occur in the surrounding
tissues from arrest of their nutrition. Both acute and chronic abscesses
may give rise to perforations on the surface of the brain and into the
ventricles, extensive oedema or anaemia of the brain from increase of
the intracranial pressure, and chronic internal hydrocephalus when the
abscess is situated in the cerebellum in such a position that it lessens
the cavity of the fourth ventricle or of the Sylvian aqueduct.
Morbid Physiology. — Acute encephalitis gives rise to general symp-
toms like headache, dizziness, and vomiting, most probably through an
interference with the general circulation of the brain. Local irritative
symptoms like monospasms and unilateral convulsions form by no means
so prominent a feature of acute encephalitis as of acute meningitis, and
in the former the symptoms which indicate a general compression of the
brain, such as somnolence and coma, appear at an earlier period than in
the latter. The clinical course of chronic abscess of the brain is similar
to that of an intracranial tumor, and the symptoms which are present
in the former depend like those of the latter upon the locality of the
lesion.
Treatment. — The physician's advice may be sought to determine
questions of cerebral localization and other delicate points of diagnosis
which are likely to arise in the progress of abscess of the brain, but
the decision with regard to the treatment to be adopted must rest with
the surgeon.
The secondary inflammation which is liable to supervene in the course
of necrotic softening, cerebral hemorrhage, and intracranial tumors, is
the form of encephalitis which is most likely to come under the care of
the physician. This form of encephalitis is best treated by complete
rest in a darkened room, mild purgation, and cold applied to the head.
Active measures like bleeding and blistering are worse than useless.
In chronic abscess of the brain the general health of the patient must
be attended to, and if definite localizing symptoms be present the pus
ought to be removed by operation. Paroxysms of severe headache may
sometimes be relieved by chloride of ammonium, while more active
symptoms like delirium may be combated by bromide of potassium,
either alone or in combination with chloral, and an opiate or cannabis
indica may sometimes be found useful.
CHAPTER XYII.
ATROPHY, HYPERTROPHY, AND TUMORS OF THE BRAIN.
I. ATROPHY OF THE BRAIN.
1. Atrophy of the Corpus Callosum.
The corpus callosum may be arrested at any period of its develop-
ment so that it may be entirely wanting, or union may fail to take
place in the middle line, either wholly or partially. Deficiency of the
corpus callosum has generally been found associated with idiocy or
imbecility, but the mental defects do not present anything character-
istic, and some cases have ])een reported in which there was no mental
defect, and consequently the condition cannot be recognized during life.
2. Atrophy of the Cerebellum.
Atrophy of the cerebellum has sometimes been met with as a primary
disease from arrest of development, but atroj)hy of one lateral lobe ol
the cerebellum occurs most fre({uently as a secondary result of acquired
atrophy of the opposite hemisphere of the brain. The symptoms most
frequently observed in the primary disease are a staggering gait, along
with a tendency to fall backwards ; persistent or temporary disturbances
of speech ; analgesia and other sensory disorders ; epileptiform convul-
sions; and weakness of mind, or idiocy.
3. Atrophy of the Cerebral Hemispheres.
The cerebral hemispheres are arrested in their development in cases
of microcephalic and other forms of idiocy, and partial defects of the
brain, either from arrest of development or from destructive lesions,
are met with in parencephalus and unilateral atrophy of the brain,
already described as giving rise to some forms of the spasmodic paral-
ysis of infancy.
IIYPERTEOPHY OF THE BRAIX. 631
II. HYPERTKOPHY OF THE BRAIN.
1. General Hypertrophy of the Brain.
Etiology. — General hypertrophy of the brain usually appears to be
congenital. Several of the reported cases were associated with periph-
eral multiple neuroma, and both of these conditions are frequent accom-
paniments of idiocy or delayed mental development. A few cases
appear to have developed subsequently to an injury to the head, while
the disease appears to have been a result of chronic lead poisoning.
Symptoms. — The symptoms almost always appear soon after birth or
in early infancy, and consist of epileptiform convulsions, local spasms,
attacks of laryngismus stridulus, and tremors. The pulse is usually
retarded, but it may occasionally be much accelerated. The affection
in children is sometimes associated with premature development, but
in other cases there is more or less weakness of mind, amountino;
even to the highest degree of idioc3^ The tongue is often so much
increased in size that it protrudes from the mouth. Drowsiness
is an occasional but by no means constant symptom. Some of the
affected children are liable to fall fre({uently, being overbalanced by the
great weight of the head. Disturbances of the nerves of the general or
special senses are comparatively rare. Death results from • an attack
of convulsions, from cerebral compression with coma, or from an inter-
current disease.
2. Partial Hypertrophy or Heterotopia of Brain Substance.
This condition was first described by Virchow, and has hitherto been
principally of interest to the morbid anatomist. Virchow observed in
one case an apparently new formation of gyri within the white sub-
stance of the posterior lobe, and a hyperplastic malformation of the
caudate nucleus, while Simon met with small accessory gyri on the
summit of the convolutions. Klob found a mass of white cerebral sub-
stance, the size of a bean, hanging from a pedicle between the optic
nerves.
These conditions have hitherto been found in epileptics, idiots, or in
persons otherwise mentally affected, but their clinical significance is
somewhat doubtful. All authors regard these malformations as con-
genital. ■
632 ATROPHY, HYPERTROPHY, AND TUMORS OF BRAIN.
III. INTRACRANIAL TUMORS.
Etiology. — Tumors of the brain arise from similar causes to those
which originate tumors in other localities, and these need not be de-
scribed here.
Symptoms. — Headache is one of the earliest and most striking of
the initial symptoms of intracranial growths, and it is present in about
two-thirds of all cases. The headache of intracranial tumor consists
of an acute lancinating or severe boring pain which is very violent,
and may continue for many weeks Avithout intermission, although it is
liable to paroxysmal exacerbations of great severity. The pain is
aggravated by light, noises, and all movements of the head, and it may
occupy the occipital, frontal, or temporal regions, but its seat has no
necessary relation to the situation of the tumor. The skull may, how-
ever, be found tender to percussion at a point corresponding to the
situation of the tumor. The profound headache of cerebral tumor may
also be accompanied by neuralgic headache caused by irritation of the
fifth nerve in its course along the base of the brain. The pain of
trigeminal neuralgia occurs in paroxysms, and it is usually associated
with numbness, formication, itching, a feeling as if the part was
swollen, or neuroparalytic ophthalmia. When sensation is diminished
on the painful side, or when all three branches of the nerve are simul-
taneously affected, the presence of tumor may be suspected, and the
diagnosis is rendered more certain if disorders of other cranial nerves
are present.
Another frequent initial symptom of intracranial tumor is dizziness.
which may, along with paroxysms of violent headache, be the only
symptom of a growth which presents itself for many months. Vomit-
ing is, however, apt to be associated with headache and dizziness in the
early stages of a cerebral growth, and it is often a very distressing
symptom.
Sensory disorders are generally ushered in by liypemesthesia or some
other irritative symptoms, which are, after a time, followed by anaes-
thesia. Wandering pains, formication, tingling, and numbness alter-
nate with one another before there is a distinct diminution of sensation,
and they do not entirely cease until complete aniestliesia is established.
The motor disorders consist at first of tremor of one extremity or of
one-half of the body, or of cramps which may vary from slight spas-
modic twitches of a special group of muscles to persistent tonic, clonic,
or choreiform spasms of the muscles of some of the extremities. The
clonic spasm is liable to assume the form of unilateral epileptiform con-
INTRACRANIAL TUMORS. 633
vulsions which may or may not be accompanied by unconsciousness.
After a longer or shorter time the irritative motor symptoms give place
to paralysis, which often creeps on gradually and may not ])e complete
for a comparatively long time. The most usual form of paralysis in
cerebral tumor is hemiplegia, which only diifers from that of cerebral
hemorrhage by the fact that it creeps on gradually in the former, instead
of being suddenly produced as in the latter, and that the spastic con-
dition of the limbs is not generally so pronounced in the hemiplegic
tumor as in that of hemorrhage.
One or more of the cranial motor nerves may be compressed at the
base of the brain or at their point of origin in the crus cerebri, pons,
and medulla oblongata. Paralysis may be preceded by spasmodic
twitchings of the muscles supplied by these nerves.
Various forms of reeling and staggering may be present when the
tumor is situated near the cerebellum or its peduncles, but these dis-
orders belong to the localizing symptoms and will be subsequently
described.
The sense of sight is frequently affected in the course of intracranial
growths, Calmeil having found amblyopia in two-fifths, and Ladame
amaurosis in one-fifth of the cases analyzed by them. The field of
vision may be altered in various ways and it is very important for
regional diagnosis to examine for the diiferent varieties of hemiopia.
On ophthalmoscopic examination the fundus of the eye may present
the usual signs of optic neuritis or of the " choked disk," the latter
being by far the most important sign of cerebral tumor, inasmuch as it
is seldom present except when the intracranial pressure is increased in
degree by a solid growth. The pupils may be contracted or unequal,
but as the intracranial pressure becomes great by the increasing size of
the tumor the pupils are dilated and react feebly to light.
The disorders of the sense of hearing consist of rustling noises in
the ears, and dulness of hearing, but complete deafness is only occa-
sionally observed. Paralysis of the labyrinthine fibres of the auditory
nerve mav cause vertigo and motor disorders similar to those observed
in Meniere's disease.
The disorders of the sense of sjnell consist of subjective sensations
or loss of smell in one or both nostrils, but this sense is not often affected.
The disorders of the sense of taste consist also of subjective sensa-
tions or loss of taste, but Ladame found that this function was only
mentioned as having been affected seven times out of all the cases he
had collected.
The organic functions are always impaired in the course of intra-
cranial growths. The intense headache from which the patient suffers
634 ATROPHY, HYPERTROPHY, AXU TUMORS OF BRAIN.
occasions a continued wakefulness which reacts upon the general health,
and when vomiting recurs frequently the general nutrition is greatly
impaired. The patient often suffers from constipation, but this condition
may alternate with diarrhoea. Polyphagia is an occasional symptom of
cerebral tumor, but it does not prevent the progressive emaciation. This
symptom is occasionally accompanied by diabetes mellitus. Polyuria
with or without saccharine urine is not an infrequent symptom of cerebral
tumor. In the early stages of cerebral tumor the action of the heart
may be irregular and slow from irritation of the vagus, but towards the
end the pulse becomes extremely frequent from ])aralysis of that nerve.
Respiration is not often affected, but its rhythm may be quickened by
irritation and rendered slower by pressure of the brain.
Fever, although not a usual symptom of cerebral tum^or, may be
present during complicating attacks of encephalitis.
The psychical disturbances Avhich are present in greater or less
degree in about one-half the cases, consist at first of mental excitement
and emotional displays like those of hysteria, ideas of grandeur, hallu-
cinations, delusions, and outbursts of passion which may amount to
maniacal fury. The irritative symptoms, however, give place after a
time to those of depression, which consist of drowsiness, apathy, loss of
speech, and imbecility. The terminal symptoms consist of extreme
emaciation, widely spread anaesthesia, blindness and impairment or loss
of one or more of the other s|)ecial senses, motor paralysis which often
implicates all the extremities, imbecility, and deep and enduring coma.
Morbid Anatomy. — The morbid anatomy of the atrophy and hyper-
trophy of the brain is a wide subject, which cannot be further discussed
here. With regard to intracranial tumors, it Avill suffice to remind the
reader that the brain is surrounded by unyielding osseous walls and
that consequently all growths which gradually encroach upon the space
occupied by the brain must give rise to nearly the same kind of symp-
toms. The tumors themselves being so variable in their nature, possess
no affinity with each other and the symptoms to which they give rise
from their situation afford the only grounds for grouping them together.
Intracranial tumors may be divided into, </, ncAV formations ; 6, vascular
tumors ; and c?, parasites.
Morbid Physiology. — The tumor at first may give rise to few or
no symptoms, but as it gradually increases in volume the whole brain
is subjected to pressure, the cerebro-spinal fluid is first displaced, the
blood is then squeezed out and the whole brain becomes anaemic ; the
functions of the brain become gradually diminished aiul ultimately lost,
and the patient dies comatose. But in addition to this general pressure
the tissues surrounding the growth are subjected to a special pressure
INTRACEANIAL TUMORS. 635
Avbicli soon leads to their destruction. Destruction of tissue is at other
times caused by ischaemic softening from the compression of an artery,
while loss of function may be caused by effusion of serum from com-
pression of veins. But although the direct tendency of a tumor is to
destroy the surrounding tissue, its indirect effect is often irritation, and
consequently the depression symptoms are often preceded or accompanied
by phenomena of irritation. Still greater complications in the symp-
toms are caused by the fact that on the one hand irritation of a higher
centre may produce an inhibitory action on a lower centre, while on the
other hand destruction of a higher centre may leave the functional
activity of a lower centre more unrestrained. The symptoms which
are caused by the localization of the tumor do not differ essentially from
those caused by other focal diseases, and these will be afterwards con-
sidered. The intensity of the symptoms depends to some extent upon
idiosyncrasies of the patient, the locality of the lesion, and in still
greater degree upon the rapidity of the growth of the tumor, slow grow-
ing tumors often attaining great size before giving rise to any distinctive
symptoms, and fast growing tumors causing very active symptoms at an
early period.
Treatment. — In the earlier stages of cerebral tumors the symptoms
of irritation and local congestion predominate, and these must ])e treated
by cold to the head, purgatives, the use of flying blisters, and bromide
of potassium either alone or combined with chloral hydrate. The
intense headache of cerebral tumor must be treated by the application
of cold to the head, and subcutaneous injection of morphia. Chloride
of ammonium in half drachm doses may occasionally be found useful.
Epileptiform convulsions must be treated by large doses of bromide of
potassium. With the view of promoting the absorption of the growth
iodide of potassium has been given in large doses, and as much as from
half a drachm to a drachm may be given three times a day. In ])ro-
gressive growths like cancer, sarcoma, and glioma this treatment cannot
of course lead to any permanent benefit, but it may be useful in aneurism,
and is by far the most hopeful treatment in parasites. If syphilis is
suspected, an energetic antisyphilitic treatment by means of mercury
and iodide of potassium must be undertaken. It is possible that here-
after surgeons will be able to undertake the removal of a considerable
number of cerebral tumors ; even already a few successful cases have
been reported.
V
CHAPTER XYIII.
APHASIA.
Aphasia comprises certain disorders of the faculty of language, but
inasmuch as every form of disorder is not to be included under the
term it is necessary to subject the faculty itself to a preliminary analysis
in order to determine which belong and wliicli do not belong to this
group. Language, taken in its evident sense, consists of the various
means by which animals indicate mental states to one another, this
faculty comprising a power of expressing one's own states and of ap-
preciating the states of others. Mental states may be divided into
feelings, cognitions, and volitions. In one sense language may be said
very often, if not always, to indicate volitions, but inasmuch as volun-
tary actions are always determined by motives, or, in other Avords, by
the feelings and cognitions, the language of volition merges into that of
the other two mental states. Language may, therefore, be divided into
that of the feelings, or emotional language, and that of the cognitions,
or intdJectual language, or speech. The distinction between the lan-
guage of the emotions and speech is by no means clear and trenchant.
When a man delivers an oration, for instance, only a small part of his
utterances and gestures are to be regarded as belonging to intellectual
language. All the variations of tone, the melodious voice, the graces
of attitude and gesture, the charm of elegant and rhythmical language,
and the thousand other ways by which a great orator knows how to
sway and influence his audience, belong to emotional and not to intel-
lectual language. The pleasure we derive from looking at a clearly
printed volume, and especially from looking at an illuminated text, or
at a picture rather than at a diagram, shows that there are different
means whereby the feelings may be engaged, and even such methods as
accents, italics, and notes of exclamation, by means of which inflection,
emphasis, and wonder are indicated, the rhythm of metrical language,
and the diction and imagery of poetry, all belong to emotional and not
to intellectual language. The language of emotional and of intellectu.al
gesture are also by no means readily separated. The gestures of those
who retain the full use of spoken and written language are in great part
indicative of the feelings, but that gestures can be made subservient to
intellectual expression is shown by the importance it assumes in the
APHASIA. 637
training of the deaf and dumb. But although it is not always easy to
discriminate between emotional and intellectual language, we must
repeat that it is disorders of speech or intellectual language alone that
are comprised under the term aphasia.
But we shall now see that aphasia does not include every form of
disorder of intellectual language. Speech is the instrument of the
social state, and that it may be the means of communication between
animals it must possess to each a subjective and an objective value, or
must fulfil an impressive and an expressive function. Each individual
of a social community, in order to become an eftective member, must be
able to comprehend the mental state of others from watching their
gestures and listening to their various vocalizations, and must also be
able by his gestures and vocalizations to render his own mental state
intelligible to the others. The subjective or impressive function of
speech may be divided into receptive and regulative functions.
The receptive department is represented structurally by the various
peripheral sense-organs and the centripetal fibres Avhich conduct impres-
sion upon these sense-organs upwards to the cortex of the brain.
Complete loss of speech from disease of the receptive apparatus is
unknown. The vocal speech of a person born blind is almost entirely
unaffected either in its subjective or objective aspects, while the patient
may, by the device of raised letters, be taught to understand wa-itten
language. The deaf-mute is taught both to understand and to give
expression to a complicated speech by gestures, and in recent times
such patients have been taught not only to use their vocal organs for
expression in speech, but also to understand the vocal speech of others
by closely observing the movements of the muscles of articulation.
The structural counterpart of the regulative function consists of
that part of the cortex of the brain in which the centripetal impulses
are reduced to such order as is necessary to render them the corre-
latives of the cognitions. Now^ the cognitions express the relations
between our feelings, and every cognition must be expressed in a
proposition. The mode of expression may not always assume a distinct
prepositional form, but it must at least possess a prepositional value if
it convey distinct knowledge. If I pronounce the word "orange" in
the hearing of another, it may or may not convey to him distinct in-
formation, but if any information be imparted the word must convey to
the listener the idea that the object named "orange" belongs to a class
of objects already known to him under that name, and the word in this
sense possesses the value of a distinct proposition. If the listener has
never had any experience with the object named "orange," it is clear
that the utterance of the name Avill convey no meaning, but if he has
638 APHASIA.
liad experience of fruits and colors, distinct information may be con-
veyed to him with regard to the object by saying "an orange is a
yellow fruit." The listener will be able to associate the general prop-
erties of fruit and a distinct color with the Avord in future, but the
information has been imparted by means of a formal proposition. The
activity of the regulative cortical centres of speech has for its func-
tional correlative the arrangement of the prescntative and representa-
tive cognitions into the form of distinct mental propositions.
The objective or expressive function of speech may be divided into
emissive and executive departments.
The emissive department is represented structurally by that organiza-
tion in the cortex of the brain in which the regulative impulses are
finally coordinate before being conducted to tlie executive department.
The executive department is represented structurally by groups of
nerve cells in the central gray tube, and by the nerves and muscles
concerned in vocalization, articulation, the manual operations of Avriting,
and various gestures. Complete loss of speech from disease of the
executive apparatus is probably unknown. The patient, for instance,
may lose his voice in different diseases of the larynx, but he can still
articulate ; he may lose both voice and power of articulation in bulbar
paralysis, but he is generally able to make his wants known in writing,
and when unable to write from want of a previous education, he can
make his ordinary recjuirements known by gesture.
Our further remarks must be limited to the derangements of speech
caused by disease of the cortex of the brain, and which are grouped
together under the name of aphasia. These disorders consist of affec-
tions of the regulative department of the impressive function, and of
the emissive department of the expressive function ; the former of these
being named sensory and the latter motor aphasia. In addition to these
two chief varieties there are cases in which the ingoing and outgoing
functions of speech are both affected, and inasmuch as the lesion in such
cases is situated between the sensory and motor cortical centres Wernecke
proposes to group them under the name of commissural aphasia, but
here Ave shall treat of them under the name of )tnxed sensory and motor
aphasia. As motor aphasia is the simplest form of the affection, we shall
deal with it first.
MOTOR APHASIA.
In cases of motor aphasia the patient is unable to communicate his
thoughts by words (motor aphemia), or by writing (motor agraphia),
wliile there is loss or impairment of his intellectual pantomime (motor
MOTOR APHASIA. 039
amimia). The patient can often utter words, but they do not, if the
motor aphasia is complete, possess any intellectual value ; in the lanffuao-e
of Dr. Hughlings-Jackson, the patient is speechless but not wordless.
The words which the patient can utter continue, as a rule, the same for
the same patient — " recun-ing utterances," or the patient may under
excitement swear, or even utter a phrase appropriate to the surroundino-
circumstances, such as " good-bye " when a friend is leaving. It will
be readily seen that "■ recurring utterances" like'" yes " and " no,"
Avhich are repeated on all occasions whether appropriate or not, do
not possess any intellectual value, while of the occasional utterances
swearing is a purely emotional expression, and even the phrase " o-ood-
bye" must be regarded as expressing a state of mental regret rather
than a purely intellectual appreciation of the surrounding conditions.
In some cases, in addition to the usual recurring utterances of "yes"
and " no," the patient repeats such phrases as " come on to me, ' or
" I want protection." The man whose recurring utterance was " come
on to me " was a railway signalman, and had been taken ill on the rails
in front of his box, while the man who could only say " I Avant protec-
tion," had his left cerebral hemisphere injured in a brawl. Dr. Hughlings-
Jackson makes the very probable supposition that in these cases the
recurring utterances constituted the last words spoken, or which were in
a state of mental preparation for utterance when the damage occurred
to the brain. It is not improbable that words uttered or about to be
uttered during a period of great excitement may leave permanent
traces on the ororanization of the brain which will render them liable
to be subsequently uttered as interjectional phrases during emotional
states. That all these words and phrases must be regarded as expressive
of emotional rather than intellectual states is shown by the fact that the
patient is frequently unable to repeat his favorite oath or his formula of
leave-taking, or perhaps " yes " or " no," when asked to do so.
The patient is not always completely speechless ; he may, for instance,
retain the full use of the words " yes " and " no," and even when he
uses " no " to express assent as well as dissent he may be able, by the
aid of pantomime, to make it known in which sense he intends the word
to be understood. All forms of intellectual expression are not affected
to the same degree. A patient may have lost the use of vocal speech
completely and yet retain to a greater or less extent the power of
writing, and conversely a patient may retain or reacquire the full use of
vocal speech while the power of writing is permanently lost ; in other
Avords, motor aphemia may be present without agraphia, or agraphia
without aphemia. The fliculty of intellectual pantomime is also often
reacquired long before that of vocal speech in cases of motor aphasia ;
640 APHASIA.
but none is known, so far as I am aware, in wliich the former was per-
manently lost while the latter was regained.
In motor aphasia the patient understands all that is said to him and
remembers what is read to him or what he reads himself; his vocal
organs act normally ; the muscles of mastication and deglutition are not
paralyzed, and he can sing, laugh, smile, and frown as usual. He
will point to objects named and recognize drawings of them, provided
they were known to him before his illness. He is able to play at
cards and other games, and recognizes handwriting. He can copy
Avriting, provided his hand is not paralyzed, but in aggravated cases the
patient copies printed words in printed characters and written words in
written characters. If the right hand is paralyzed, the patient on
attempting to use his left hand Avrites from right to left instead of from
left to right as usual, the result being Avhat is known as " mirror-writ-
ing," so named because it looks like ordinary writing only on being
reflected from a mirror.
SENSORY APHASIA (AMNESIC APHASIA).
The purest examples of sensory aphasia consist of the aftections
known as word-hlindiicss and word-deaf nesx.
In word-blindneas the patient is totally unable to comprehend written
or printed language, but he is at the same time not blind, inasmuch as
he avoids obstacles in walking, and takes notice of everything that
passes around him. His sight is, however, sometimes defective, right-
sided bilateral homonymous hemianopia being often if not always present,
but this defect does not prevent the patient from reading fairly well
when the lesion is situated in the optic tract. The patient can write
spontaneously or to dictation, but he cannot copy printed or written
words and is quite unable to read what he has himself just written.
The patient is not only totally unable to read aloud, but singularly
enough he may also be quite unconscious of his disability. A patient
of mine on being presented with a letter which I had just received
making in(|uiries about a patient attending as an out-patient at the
infirmary, read without much hesitation : " Manchester Royal Infirmary.
Dear Sir : You are requested to bring this paper with you the next
time you come to the Infirmary." Not a single word of this corre-
sponded with the note which he pretended to read. His wife told me
that at home he pretended to read the newspaper aloud, but she added
"it's all stufi" out of his own head." One night he stopped in the
midst of a paragraph in which he was apparently interested ami asked
I
SENSORY APHASIA. (Ul
his Avife to finish the remainder of it. She read the paragraph aloud
as it was printed, and in great surprise he asked, " Is that what it says ? "
and on being assured that such was the case he added, " Well ! I must
be an idiot."
In ivord-deafness the patient is unable to understand the vocal speech
of others. The subjects of this disorder hear as Avell as ever a knock-
ing at the door or the tick of a watch, but are totally unable to com-
prehend the language of others, or, in other words, spoken words fail to
call up in the mind of the patient the images correspondino- to the
persons, things, events, and relations indicated by the words. When
word-deafness is complete, the subject of it fails to do anything requested
of him. But even in such cases the patient is quick at interpretino-
signs, and if the physician ask him to put out his tongue he may do so
not because he understands the spoken request, but because he notices
that the eyes of the observer are directed to his mouth. In most cases,
however, the disorder is partial, and the patient is then able to compre-
hend ftimiliar words and phrases, and may put his tongue out, close the
door, and perform a number of other simple and common actions when
asked. A very good test of word-deafness is the one proposed by Dr.
Hughlings-Jackson, namely: Ask the patient some absurd question,
such as "Are you a hundred years of age?" If the patient compre-
hends the question it will excite astonishment and amusement. A patient
of mine when asked the question says readily, "No, I don't think I am
so old as that," and evidently the question does not cause him any sur-
prise, but when 100 is presented to him in written figures he then
bursts into laughter and says, "Pooh! Nothing like it."
Word-deafness is almost always associated with a certain degree of
word-blindness. Speech is organized for the first time in connection
with the sense of hearing, and when some time afterwards written speech
comes to be organized, the visible characters are understood through the
medium of the already organized audible characters. The connection
between the written and spoken words varies greatly in difterent cases.
In uneducated persons written speech is only understood by being read
aloud or translated into spoken speech, and in such cases word-deafness
would entail complete word-blindness. Educated persons, however,
understand the meaning of written words directly, so that injury of the
auditory centre would not damage much the understanding of written
speech. A patient of mine, who has received a tolerable education, is
suffering from word-deafness, and he can read aloud without committing
many mistakes, while he apparently understands what he reads, but he
is unable to name a single object presented to him. The sight of the
object does not call up its name, and yet there is every ground for be-
41
642 APHASIA.
lieving that the lesion is situated in the auditory cortical centre, and
that the visual centre is free from disease. In this case the patient is
totally unable to name his own fingers, but when the word is written
down he immediately identifies it as indicating the finger of his own
hand. Another patient with hemiopia and word-blindness, fails to rec-
ognize the written word, but readily names his finger or any other
object when presented to him. The disorder of the expressive faculty
of speech in word-deafness is (piite as interesting as the disorders of the
impressive faculty. When the patient speaks he misplaces words, as
calling the "window" a "fender," or he uses a word kindred in its
meaning with the one intended, as "Avorm powder" for "cough medi-
cine," or in its sound, as "parasol" for "castor oil." This condition,
which has Ijeen named by Kussmaul paraphasia, may be present in
word-blindness as well as in word-deafness, and possibly also in the
incomplete form of motor aphasia. A condition Avhich may be named
paragraphia is also often present.
A patient of mine on being asked to write his own name, "William
Abson," wrote down "Wuagageag Abreaghrer," and on being asked
to copy a passage beginning "with deep feeling," he wrote with great
care and deliberation, and in a good hand, "weeth deap flneearer."
As the patient wrote each letter he named one aloud, but the written
and spoken letter never corresponded with one another. AVhen asked
to read a passage beginning with "Oh, those dreams of my childhood
and my youth," he read "On througli depth of my shouded and my
youth." This condition has been called para?('«/a.
A profounder degree of disorder than paraphasia is found in those
cases just mentioned, in which the presentation of persons and things
to the patient fails to call up their names. The patient already men-
tioned as being unable to name his own finger, has only the use of
three or four concrete nouns, which he employs on all occasions, yet
he has a large vocabulary of words expressive of events, dates, and
relations, as well as the use of some abstract nouns. On being pressed
for the name of his thumb, he called it "the public house," the index
finger "the first one," and on being pressed still further for a name,
"the first halfpenny;" the middle finger, "the second halfpenny;" the
ring finger, "threepence;" and the little finger, "the fourth half-
penny." Asked the name of a watch, he called it "a glass of beer,"
and to indicate his appreciation of the diff'erence between a gold and
silver watch presented to him, he pointed to the first as being "the best
beer." The only names of things in his possession are public house,
glass of beer, and the names of the coins in ordinary circulation, but
which he seldom uses correctly. He can count up to any number
i
MIXED MOTOR AND SENSORY APHASIA. 643
when he begins from one, but it is only on rare occasions that he is
able to break in on the series and begin Avith, say six. This patient is
almost completely word-deaf, but will show his appreciation of most
requests and statements made in writing. A still more aggravated
disorder of the expressive faculty of speech is found in those cases in
which the vocal speech of the patient is an unintelligible jargon. Such
patients fail to comprehend either written or spoken language, and it is
probable that the sensory aphasia is also accompanied by a motor
aphasia. A patient of mine takes a book in his hand and begins to
read aloud with much apparent relish, and uses variations of accent,
inflection, and pauses to give emphasis to his reading, but his vocaliza-
tions are quite unintelligible, and consist of such sounds as "pluf, plon,
lep," etc. The intervals between his pauses seem to depend upon his
breathing capacity, and to have no relation to the length of the sen-
tences on the printed page before him. When, however, the page is
presented to him upside down he immediately turns it the right side up,
and Avith an expression of great impatience.
MIXED MOTOR AND SENSORY APHASIA.
In cases of right-sided hemiplegia Avith aphasia the patient is fre-
quently unable either to express a single word or to comprehend any
question addressed to hiui in Avritten or spoken language. There is at
first total motor aphasia and total sensory aphasia. In cases of this
kind, however, gradual recovery takes place, and after a time either the
motor or the sensory aphasia greatly diminishes or Avholly disappears.
A young boy Avas recently under my care Avho, after an attack of right-
sided hemiplegia, sufiered from complete motor and sensory aphasia.
The presence of a systolic murmur at the apex of the heart showed
that the apoplectic attack which caused the paralysis was of embolic
origin. After a time a gradual improvement took place ; the patient
began to obey such ordinary requests as "put out your tongue," and
" close your eyes," and a few months after the attack the sensory aphasia
completely disappeared, and only slight traces of the hemiplegia could
be detected, but the motor aphasia still persists six months after the
attack. In some cases of this kind the improvement appears to take
place on the motor side. Those aggravated cases of word-deafness
and word-blindness in which the speech is mere jargon are fre(|uently
if not always accompanied by hemiplegia, and in such cases the motor
as well as the sensory aphasia is at first more or less complete, and
even when partial recovery takes place it is probable that these cases
644 APHASIA.
are to be recognized as a mixed motor and sensor}'-, rather than a pure
sensory aphasia.
Morbid Anatomy and Physiology. — The. faculty of language was
placed by Gull in the supra-orbital lobes of the brain, but the first
serious attempt to determine the localization of this faculty by means of
morbid anatomy was made by Bouillaud, who, in 1825, came to the
conclusion that the faculty of speech was situated in the anterior cerebral
lobes. In 1836, Marc Dax advanced the opinion that the organ of
language was situated in the left hemisphere of the brain near to the
Island of Riel, but this opinion was neglected and almost forgotten
until 1861, when Broca localized the faculty of language in the third
left frontal convolution. In the subsequent two years Broca collected
seventeen cases of aphasia with post-mortem examinations, and of these
the lesion Avas situated sixteen times in the posterior part of the third
left frontal convolution and once in the temporal lobe and Island of Riel.
Soon afterwards cases were published by Parrot, Fernet, and Charcot,
in which a destructive lesion of the jiosterior part of the third right
frontal convolution had not given rise to any disorder of speech, these
cases affording the negative side of the proof that the faculty of language
is organized in the left hemisphere. It was suggested by Bouillaud and
Broca that the faculty of speech is organized in the same hemisphere
of the brain as the mechanism which regulates the special movements of
the hand, and in proof of this supposition it has been found tliat aphasia
Fia. 17(1.
does coexist with left-sided hemiplegia in left-handed people, several
cases of this kind being now recorded by different observers. The lesion
in aphasia may consist of a growth, of a depressed bone, or of a hemor-
rhage, but occlusion of the Sylvian artery or of one of its branches is
by far the most frequent cause of aphasia.
MOKBID ANATOMY,
645
Lesions of the centrum semiovale which damage the fibres of the
corpus callosum Avhich connect the third frontal convolutions of the two
hemispheres, and the fibres which connect the third left frontal convolu-
tion with the internal capsule, occasion an aphasia which is as permanent
as that caused by destruction of Broca's convolution itself (Fig. 176, L).
In sensory aphasia the lesion is localized in the area of distribution of
the parieto-sphenoidal and sphenoidal branches of the Sylvian artery
(Fig. 177, 4 and 5). In Avord-deafness the lesion is situated in the first
Fig. 177.
Diagram Showing the Area of Distribution of the Middle Cerebral Artery.
S, Sylvian or middle cerebral arterj' ; P, Perforating branches ; 1, Inferior frontal branch ; 2, Ascending
frontal branch ; ?•, Ascending parietal branch ; 4 and 5, Parieto-sphenoidal and sphenoidal branches; A,
Ascending frontal convolution; B, Ascending parietal couvolntion ; Fj, Fo, Fj, First, second, and third
frontal convolutions ; Pj, Po, P3, First, second, and third parietal convolutions ; Tj, To, T3, First, second,
and third temporo-sjihenoidal convolutions ; OL, Occipital lobe.
and second temporo-sphenoidal convolutions (the acoustic centre), and
in word-blindness in the angular gyrus and adjacent parts of the occipital
lobe (the visual centre). The shaded portion in Fig. 178 shows the
position of the lesion in a case of word-deafness reported by Wernicke.
The lesion may also be situated in the white substance subjacent to
these convolutions. In mixed sensory and motor aphasia the Sylvian
artery is occluded immediately outside the nutritive arteries which pass
into the anterior perforated space, and consequently the circulation is
arrested through all the cortical branches of the vessel. The result of
occlusion of the vessel at this point is that hemiplegia is associated
with aphasia, and the sensory as well as the motor centres are partially
646
APHASIA.
damaged. It must, however, be remembered that the temiinal cortical
branches of the Sylvian artery anastomose to some extent with the
terminal branches of the anterior and posterior cerebral arteries, and
occlusion of the vessel is not always followed by extensive softening,
especially in young people. A young girl came under my observation
who was suffering from mitral disease, and who died a fortnight after
an attack of right-sided hemiplegia with complete motor and sensory
aphasia. At the autopsy an embolus was discovered in the left Sylvian
artery immediately outside the nutritive arteries to the anterior per-
FiG. 178.
forated space, but not a trace of softening could be discovered in the
hemisphere. The whole brain was very amemic and the cortex of the
left hemisphere was particularly pale, and it is probable that the cells
had undergone fattv degeneration, but there was no .softening, and it is
possible that had the patient lived the cortex of the central convolutions
would have completely recovered. In older people, however, softening
of some portion of the cortex always takes ])lace after occlusion of the
Sylvian artery. The softening may sometimes take place in the area
of the posterior, and more frequently in the area of the anterior
branches, while at times the intt-rvening portion of the cortex is more
or less disorganized, and thus it is that a disorder of speech which at first
is a complete motor and sensory aphasia may recover, so that it becomes
a simple motor or a simple sensory aphasia, according to the locality
which is permanently softened, or may remain permanently a combined
motor and sensory aphasia in case a wide area of the cortex undergoes
softening.
Motor aphemia is caused by destruction of the posterior part of the
third left frontal convolution for the same reason that paralysis of the
right hand is caused by destruction of the ascending frontal and parietal
MORBID ANATOMY. 647
convolutions. It may be objected that in motor aphemia the muscles
of articulation are not paralyzed, inasmuch as there is no sign of a local
paralysis of the tongue or lips. But notwithstanding that the general
movements of the tongue and lips are unaffected, there is a paralysis of
the special combination of muscular movements which are required to
produce articulate sounds, and in motor agraphia there is a paralysis of
the particular combination of movements by which writing is effected,
although the general movements of the hand may be unimpaired. The
reason that motor aphemia and agraphia are so frequently associated is
that the centre for the special movements of the tongue and lips, and
that for the special movements of the hand lie near together; the one
being organized in the posterior portion of the third frontal convolution,
and the other in the adjoining inferior part of the ascending frontal
and parietal convolutions. But although these two centres lie near
together, the fact that they still form separate centres explains why
it is that the one kind of disorder may be present without the other,
and that the two are only seldom present in any one case in an
equal degree. The reason that the general movements of the tongue
and lips are not paralyzed in lesion of the left hemisphere is that they
are organized in both hemispheres, and that when the organization in
the left hemisphere is destroyed the right hemisphere takes up the
action and maintains the general movements of both sides. It may,
therefore, be presumed that the recurring utterances which are met
with in cases of complete motor aphasia are also like the general move-
ments of the tongue and lips, organized in both hemispheres of the
brain. But if motor aphasia is caused by destruction of a motor
centre in the cortex of the left hemisphere of the brain, why is it that
aphasia is not caused by destruction of the conducting path which con-
nects this centre with the bulbar nuclei ? The answer is, that injury of
the conducting path in the knee of the internal capsule does cause an
aphasia, although it does not remain permanent. A right-sided hemi-
plegia caused by hemorrhage into the lenticular nucleus is accompanied
by a motor aphasia at first, but the disorder of speech passes off in a few
weeks or months at most. The explanation which Dr. Broadbent has
given of this fact is generally accepted. He believes that when the
direct conducting path which connects the third left frontal convolu-
tion with the bulbar nuclei is interrupted, a new path is gradually
opened first from the third left to the corresponding third right frontal
convolution, through the corpus callosum, then through the pyramidal
tract of the right hemisphere to the bulbar nuclei. But when the
right pyramidal tract is injured subsequently to an injury of the left
tract, there not only is then more or less aphasia, but the general move-
648 APHASIA.
ments of the lips and tongue become paralyzed, and the patient presents
all the phenomena of a bulbar paralysis. But if motor aphasia is a
paralysis of certain special movements, we shall now see that sensory
aphasia is an anaesthesia to certain properties of matter, while the ap-
preciation of the general properties is retained. The condition of
patients who are word-deaf and word-blind is comparable to the mental
state to which Goltz reduced dogs by washing out lai-ge portions of the
cortex of the brain. The animal operated upon recovers to a greater
or less extent from the paralysis which follows immediately upon the
injury, but it is found that the psychical capacity is very seriously im-
paired. He is not blind, because in walking about the laboratory he
avoids obstacles, but he fails to recognize his usual food as such, and
the vessel in which it is contained is avoided as an obstacle.
The (log still retains the knowledge which connects the falling of a
shadow upon the eye with the near proximity of a resisting body, which
is the most general of all knowledge, but he has lost the knowledge which
is only a little less general tlian it, that a particular substance possesses
the specific properties of taste and smell, which constitutes its food to
be eaten and not an obstacle to be avoided. On the side of the audi-
tory sense the dog is equally deficient; he is, indeed, like the word-
deaf: he still hears noises, but fails to respond to his own name. 'J'o
make the similarity between the dogs operated upon by (loltz and the
word-deaf and word-blind more complete, a post-mortem examination
of the dog exhibited at the International Medical Congress at London,
showed that the cortex was chiefly injured in the occipital and temporo-
sphenoidal lobes, or in the sensory areas of the cortex. A more or less
similar mental condition to that of the dog operated upon, so far as
regards sight, was observed by Fiirstner in cases of general paralysis
of the insane, in which the occipital lobes were specially involved in
the disease. The patient could still see large objects and avoid them
as obstacles, but was unable to count correctly small objects, and lost
all knowledge of the special properties of matter. A coin, for instance,
he recognized as made of metal, and as liaving a certain form and size,
but he had no knowledge of the special properties which gave it value
as a money tender. The word-deaf and tlie word-blind are not reduced
to so low a condition of intelligence as this, but their disability is the
same in its essential features ; there is a loss of the more special and
least organized knowledge, and a preservation of the more general and
best organized knowledge. To elaborate this idea would reijuire much more
time and space than 1 can aflbrd, but it will suffice to say that, speaking
generally, the best organized knowledge is that which is most frequently
repeated in the experience of any individual, and of the race. As I
MORBID ANATOMY. 649
look around me, I see a number of objects which I recognize as books,
and one would think that the association between the sight of a book
and its name is well organized in me, and so no doubt it is. But of
each book I can say that its color, its size, its weight, and all its other
innumerable properties, is the same as the color, size, weight, and other
properties which I know in other objects. Wherever I turn, and what-
ever object I look at, I cannot get rid of the fundamental relations of
sameness and difference, and consequently the name of these simple
relations must be much more profoundly organized than the names of
things.
In dissolution of the impressive faculty of speech, therefore, the
names of things disappear first and of the simple relations last. Now
of all words the individual names are the least organized, and it is
within the experience of every one how very easy it is to forget the
names of one's friends, while such simple predicates as is, may, and shall,
or being, go, run, and know ; adverbs like here, there, now, before,
and after; adjectives like good and bad, and hard and soft, are un-
doubtedly much more frequently repeated in speech than the names of
persons and things, and the former are, therefore, more likely to be
preserved than the latter in cases of dissolution of the impressive faculty
of speech. In those cases of aphasia in which the names of persons
and things are almost entirely lost, let it not be thought that the other
parts of speech have suffered no damage. The patient whose case I
have already mentioned, who named every object presented to him,
including his own fingers, " public house," "glass of beer," or "half-
penny," was accustomed to describe his previous occupation in the
following terms : " When gentlemen got into trouble I brought an action
against them and they were all right then." He was a messenger in
the bankruptcy court and had to serve processes on defaulting debtors.
He must, therefore, have been very familiar with such words as " to
liquidate," and with such phrases as " to compound with one's creditors,"
but he now never uses such complex words and does not give any evi-
dence that he understands them when uttered in his presence. It must,
therefore, be presumed that in him all other parts of speech as well as
the nouns have suffered damage, inasmuch as he is only able to make
use of those words and phrases which express the simplest relations,
and qualities, and the events most frequently repeated in his experience.
In dissolution of the nervous mechanism of the impressive faculty of
speech the names of persons and things disappear first because they are
the least organized. The facility with which proper nouns are lost has
been experienced by most of us in the readiness with which we forget
the names of our most intimate friends when the brain is fatigued by
650 APHASIA.
overwork or loss of sleep. Most educated men have also experienced
the strong tendency which the technical language of a newly acquired
science has to fade from the memory. But although the loss of the
nouns is the most marked feature of sensory aphasia it must be ad-
mitted that this disability is accompanied by the loss of all words which
express complex relations and qualities, and the Avords which remain to
the last are those which express the relations and qualities which have
been most frequently repeated in the experience of the race, and the
events which have been most frequently repeated in the experience of
the individual. It must, however, be remembered that frequency of
repetition is only one factor in producing degrees of organization in
speech. The strength of the impression Avhich formed the association
between the word and the thing signified by it, as well as various other
circumstances, must be taken into account. " Burnt children dread the
fire," and doubtless the word fire becomes deeply fixed in the organiza-
tion from a very limited experience of its action. But as it is impossible
to pursue the subject further in this ])lace, the student must be left to
think it out for himself. That word-deafness, and word-blindness are
examples of partial anaesthesia is well illustrated by recorded cases in
which a person, while suffering from one of these affections, suddenly
becomes completely deaf or blind without having any local disease in
the ear or eye, and at the autopsy a spot of softening is found symmetri-
cally pkced in each hemisphere of the brain on a level with the first
and second temporo-sphenoidal convolutions, or with the angular gyn.
CHAPTEE XIX.
DISEASES OF THE MEMBRANES OF THE BRAIN.
I. DISEASES OF THE DURA MATER.
Inflammation of the dura mater may be divided into (I.) external,
and (II.) internal pachymeningitis.
(I.) External Pachymeningitis.
Etiology. — The chief causes of external pachymeningitis are injuries
which detach the dura mater from the skull and give rise to hemorrhage
between the membrane and bones ; perforating injuries of the skull :
and extension of inflammation from neio-hborinof tissues, as from the
temporal bone in caries of the petrous portion. The external layer of
the dura mater is .subject to chronic thickening in old age.
ST/inptoms. — In traumatic external pachymeningitis the patient may
recover from the immediate effects of the injury, but at the end of two
or three weeks he suffers from pain in the head and is feverish, and
should there be an external w^ound it assumes an unhealthy aspect. If
the inflammation spread further the headache increases in intensity, and
the patient suffers from vertigo, nausea, and vomiting, while mono-
spasms, or unilateral convulsions may occur if the motor area of the
cortex is affected. As the inflammatory process extends inwards through
the pia mater to the cortex the previously convulsed limbs become para-
lyzed, delirium supervenes, and the patient soon dies in coma.
When an abscess forms between the bones of the skull and the dura
mater the symptoms may be those of gradual cerebral compression.
In the pachymeningitis of old age the symptoms consist of a persistent
dull headache, and in many cases the presence of the disease is only
discovered post mortem.
(II.) Internal Hemorrhagic Pachymeningitis (Hematoma of
the Dura Mater).
Etiology. — Hsematoma of the cerebral dura mater is generally met
with in old age, and is either caused by internal injury, or results from
652 DISEASES OF THE MEMBRANES OF THE BRAIN.
cachectic diseases like scorbutus, chronic alcoholism, general paralysis,
and senile atrophy of the brain.
Symptoms. — The symptoms are variable, but the most constant is a
dull headache, which is generally diffused, but may be more pronounced
on one side than the other. The motor disturbances consist of unilat-
eral or bilateral muscular twitchings, which are followed by a persistent
rigidity. In other cases paresis, first of the one and then of the other
extremity of the same side occurs, which gradually increases until a
decided hemiplegia is established. In some cases the paralysis extends
to the other side, showing either that the inflammatory action has
spread to the other side or that a fresh hemorrhage has occurred, form-
ing a new focus of disease. The gait is often uncertain, and the patient
experiences difficulty in Avriting and speaking, while a conjugate devia-
tion of the eyeballs towards the side of the lesion is not infre(juently
present. Patients sometimes complain of formication and numbness of
the paralyzed side, but impairment of sensation in the absence of paral-
ysis never occurs.
Psychical disturbances are sometimes present as part of the primary
disease, as when hematoma occurs in general paralysis, but at other
times they result directly from the luematoma. These disorders con-
sist at first of great mental irritability, abnormal sensitiveness to light,
and ringing in the ears, but as the disease advances the signs of in-
creased irritability give place to those of a gradual compression. In
other cases drowsiness is the chief psychical symptom observed, and
when it is present in old people in conjunction with chronic headache
and contracted or dilated j)upils, luematoma should be suspected. The
pupils are contracted and unirritable to liglit during the irritative stage
of the disease, but dilatation predominates when the symptoms of
compression supervene. In most cases the pulse is slow during the
early stages of the disease, but becomes frequent and irregular before
death. The course of the disease is very variable. It usually begins
witli more or less acute symptoms, which are followed by an interval of
comparative health; after a time a fresh acute attack occurs, which may
cause death or is followed by another interval. The majority of cases
terminate fatally, although it is not impossible that partial recovery
may occasionally take place.
DISEASES OF THE PIA MATER. 653
II. DISEASES OF THE PIA MATER.
(I.) TuBERCUi«vE Meningitis (Acute Hydrocephalus).
Etiology. — Most of those ■who suffer from tubercular meningitis
belong to families in which the tubercular diathesis is distinctly marked.
The largest proportion of cases of tubercular meningitis should occur
in croAvded populations and large cities, and amongst the poorest and
most neglected part of the population. Season does not appear to
exert any influence in the production of the disease. Tubercular men-
ingitis may set in at any age, but it is much more frequent between
the ages of two and seven years. The numbers diminish from the
seventh to the tenth, and in still greater proportion from the tenth to
the fifteenth year. In adults it is most common between the ages of
tAN'enty and forty, and occurs very exceptionally after the forty-fifth
year. The male sex appears to be more frequently affected than the
female. In adults the proportion is 51.5 men to 48.5 women, and the
proportion of males affected in children is still greater.
Symptoms. — Premonitory s}'mptoms manifest themselves for a varia-
ble period of weeks or months before the development of the distinctive
phenomena of tubercular meningitis, the most constant of these being
a gradual loss of flesh without perceptible cause, which is more noticea-
ble in the trunk and limbs than in the face, loss of appetite, constipa-
tion or diarrha^a, and an undefined feeling of illness and weariness.
As the invasion approaches the patient, Avhen a child, loses his
vivacity, becomes sad, fretful, taciturn, irritable, and Avants to be left
alone, and in the midst of play leaves his companions in order to give
vent to his distress in tears. He sleeps with eyes half open, and grinds
his teeth, while his sleep is disturbed by muscular twitches and horri-
ble dreams, so that he frequently starts and cries out.
On awakening he complains of headache, and after a time a slight
febrile accession is observed towards evening without obvious cause.
In some cases the brain symptoms make their appearance without
any warning, and the first symptoms Avhich indicate an affection of the
pia mater may be violent headache, vomiting, or facial paralysis, fol-
lowed quickly by unconsciousness.
The disease itself presents [a) an initial period in which symptoms may
be referred to excitation of the cortex; {h) a period in which symptoms
caused by excitation are mixed with those due to progressive pressure
caused by effusion and to lesions at the base of the brain ; and {c) a
651- DISEASES OF THE MEMBRANES OF THE BKAIN.
final period in -which symptoms due to pressure caused by the ventricu-
h\r effusion greatly predominate.
{a) The Period of Invasion. — In some cases the invasion is ushered
in by a chill, accompanied by a rapid rise of temperature, while in
others there are distinct shiverings, violent headache, and attacks of
giddiness. Vomiting is, however, the most common special symptom
of the period of invasion. It varies greatly in frequency, but as a
rule occurs only twice in twenty-four hours during the first two or
three days of the disease. In some few cases, however, the child
vomits incessantly, Avhether food is taken or not, but when once the
tendency to vomit has ceased for twenty-four hours, it does not ordi-
narily recur. Constipation is present, as a rule, throughout the whole
course of the disease. Although there are occasional exceptions, the con-
stipation is not often obstinate, and it is generally easy to procure
action of the bowels by ordinary means.
Headache, of a dull, heavy, or lancinating character, is usually an
urgent symptom while consciousness is retained, and its temporary
exacerbations are made known by moaning or shrieks, while even after
unconsciousness has set in the patient puts his hand to his head, wrinkles
his forehead, and distorts his face as if from pain. Vertigo is always
present. Patients feel as if they were falling in bed, or as if surround-
ing objects were revolving around them, and the gait is often reeling
and unsteady, but the rapid development of severe symptoms soon pre-
vents all attempts at station and locomotion.
The motor disturbances consist of spasmodic movements in the form
of partial convulsions, giving rise to tremor and conjugate deviation of
the eyeballs, with rotation of the head and neck, strong convergent
and divergent S({uints, grinning contortions of the muscles of the face,
and grinding of the teeth. It is probable that the hydrocephalic cry,
which so commonly occurs during this period of the disease, Avhich Trous-
seau says is '"single and loud, like the cry of a person frightened by
some sudden danger," is due to spasmodic action of the respiratory and
laryngeal muscles, and is quite independent of consciousness. The
muscles of the neck and back are often persistently contracted, and
the abdomen is retracted, owing to spasm of its muscles, so that it
presents a characteristic boat-shaped depression. In children epilepti-
form convulsions are not uncommon, but they are rare in adults, and
towards the end of this stage slight paralysis of the ocular and facial
muscles may be present, as declared by inequality of the pupils, ptosis,
strabismus, or slight facial paralysis.
The sensory disturbances are often obscured by loss of consciousness,
but at times a general or partial hyperpesthesia of the surface of the
DISEASES OF THE PI A MATER. 655
body may be observed at the beginning of the disease, while general or
partial anaesthesia is not infrequent at an advanced period of the dis-
ease, and has occasionally been observed as a premonitory symptom.
Intolerance of sound and light is a prominent symptom; the child is
impatient of the slightest noise, and avoids the light by lying with the
face buried in the pillow or turned towards the wall, with the knees
drawn up towards the abdomen, and the eyelids firmly closed.
Psychical disturbances are not always present in the early period of
the affection. The patient cannot, however, form consecutive trains of
ideas, and children soon become somnolent, lie with their eyes closed,
and reply to questions curtly or merely by a nod. When raised up,
they complain much, knit their brows, throw back their heads, and slip
down in bed ; they cannot bear the slightest disturbance, and will clench
their teeth against food. Delirium is of frequent occurrence when the
patient is half asleep; and, in the case of children, the hydrocephalic
cry is not infrequently heard at this time, being accompanied by start-
ing up in terror. At other times the patient may spring from bed, or
make defensive movements in consequence of hallucinations of sight
and hearing. The somnolence soon increases, tbe eyes stare without
expression into vacancy, and the patient ceases to speak to his atten-
dants, but he talks senselessly with himself, or laughs, sings, whistles,
or shouts, and performs meaningless movements, such as plucking at
imaginary objects, picking the bedclothes, blowing, spitting, and grim-
acing. After a time these disturbances cease, and the mental faculties
may again become completely or partially clear, but after a longer cr
shorter period, new and more profound disturbances supervene, which
increase until the fatal termination.
Disorders of vision are seldom absent in this stage so long as the
patient is tolerably conscious, and an ophthalmoscope may reveal the
presence of double optic neuritis, or tubercles of the choroid.
The pulse is, as a rule, slow and full during the early stage of the
affection, but it is subject to rapid variations during muscular exertion
of every kind and psychical excitement, especially in the case of children.
The temperature is very inconstant, and does not conform to any type.
The skin is usually dry, and even in those cases where the tubercular
meningitis is associated with phthisis, the sweats of the latter disease
usually cease when the meningitis manifests itself. It has also been
observed that the cough, dyspnoea, and expectoration of phthisis cease,
and in the case of intestinal tuberculosis the diarrhoea is arrested. The
injection of the face and conjunctiva varies frequently without obvious
cause; lividity of the face belongs to a later period, or is dependent on
lung complications.
656 DISEASES OF THE MEMBRANES OF THE BRAIN.
The average duration of the first stage is about eight days, but it
varies from two days to two or three weeks, and is not unfrequently
followed by a remission which leads the friends of the patient to hope
for a favorable termination.
(b) The second stage is now ushered in with the evidences of loss of
functional activity. The signs of excitement become less frequent, and
somnolence and mental torpor more prominent, but even in the midst
of sopor adults give evidence of suffering from severe headache by
groans and gestures, while in children the hydrocephalic cry is frequently
heard at this stage.
The presence of muscular spasms is declared by combined movements
of the eyeballs or nystagmus, iiie(iuality of the pupils, winking and
facial contortions, and grinding of the teeth with munching movements
of the jaws, Avhile in some cases one or more of the limbs are agitated
by tremors or choreic movements, and in rare cases the muscles of the
trunk and limbs are maintained in a state of cataleptic rigidity.
The stiffness of the muscles of the nape of the neck becomes more
intense, so that the head is drawn back and thrust into the pillow. The
rigidity may also extend to the muscles of the trunk, and the body is
maintained in a condition of tetanic rigidity, the opisthotonos either
appearing in paroxysms and lasting only a few minutes at a time, or
remaining continuous until death. Paralyses of various extent and
distribution now make their appearance. Paralysis of the oculo-motor
nerve is common, and gives rise to divergent squint, ptosis, and dilata-
tion, with fixity of one or both pupils. The trochlear nerve may be
paralyzed along with the third, but is never affected alone. Paralysifs
of the abducens may, however, occur as a separate affection. The
paralytic form of conjugate deviation of the eyes and rotation of the
head and neck may appear at this ])eriod of the disease, and decided
paralysis of one side of the face is often present, while the tongue is
drawn towards the paralyzed side on protrusion. It is not uncommon
for aphasia to occur, especially in adults, in this stage of the disease.
The disorder of speech may either be a sensory or a motor aphasia, or
a sensory aphasia may appear first, then there is a ra])id im])rovement,
but soon a motor aphasia is superadded and in a few days the patient
dies comatose after suffering probably from severe general convulsions.
Hemiplegia and hemiparesis are rare, but monoplegias are frequent.
At times one arm or one leg is paretic or completely paralyzed ; while
occasionally the paralysis assumes the paraplegic form, or a considerable
diminution of strength may occur in all four extremities.
The sensory disorders consist of partial anaesthesia which may be
limited to one or other extremity or to the side of the face, but as the
DISEASES OF THE PIA MATER. 657
disease progresses the anaesthesia becomes more profound, and distributed
over the whole body. The optic disks are markedly swollen in this
stage, and retinal hemorrhages are a frequent complication.
Vomiting is an occasional symptom of this stage, the constipation
continues, and the urine is generally passed in bed or there is complete
retention. The pulse becomes less frequent, and may sink to sixty or
still lower, and is at the same time fuller ; but the slightest excitement
may raise the number of beats to more than one hundred per minute,
and it is apt to become irregular. The temperature varies, and although
it usually conforms to the remittent type in children which is so charac-
teristic of tuberculosis of other organs, yet it should be remembered that
in adults it may remain almost completely normal throughout this stage
of the disease.
The respiration is sometimes normal, at other times irregular, and it
occasionally assumes the character of the Cheyne-Stokes respiration.
Neuro-paralytic oedema of the lungs is liable to occur at this period of
the disease. This period may last about a week, and then the third
stage of the disease is ushered in by the appearance of persistent coma.
{c) The Third Stage. — The patient is now completely insensible to
most external excitants, and most reflex actions are extinguished, al-
though he may still respond to a loud voice close to the ear.
Isolated paralyses are not now so readily observed, inasmuch as there
is general relaxation of the whole muscular system, but rigidity of the
masticatory muscles and of the muscles of the back and extremities is
sometimes still present. Convulsions are rare in adults ; but in children
partial convulsive spasms may occur, and immediately before death the
patient may be seized with general convulsions. The electric excit-
ability of the muscles to both constant and induction currents is normal.
Every form of sensibility is now completely abolished. The pupils are
dilated and fixed, the upper lids fall inert and paralyzed over the eye-
balls, and an ophthalmoscopic examination reveals signs of marked
oedema of the optic disks. The pulse during this period becomes more
and more frequent and may be irregular, and in the case of children
the pulsations of the fontanelles become weaker and weaker, and may
disappear before death.
The respiration is irregular, and at times so superficial and feeble
that it may escape observation, while at other times it is forced and deep.
Kapid emaciation occurs, especially in the case of children ; the skin
is generally dry and rough, and it may become slightly livid with the
decreasing force of the heart ; and occasionally a bedsore a})pears. The
temperature during this period varies greatly. In some cases it is below
normal, and immediately before death may sink as low as 95° F. or
42
658 DISEASES OF THE MEMBRANES OF THE BRAIN.
even 93° F. In another series of cases a state of moderate fever con-
tinues up to the time of death ; while in a third group the fever greatly
increases before death, and may even continue to increase for some time
afterwards.
The urine is generally scanty with high specific gravity ; its quantity
may be increased or normal ; the proportion of chlorides varies greatly ;
and the phosphates are said to be increased. A small quantity of
albumen is frequently present, but sugar is rare. The duration of
the paralytic stage is generally three or four days, and seldom reaches
a week.
The course of tubercular meningitis is very variable. In some cases
it runs a rapid course and terminates fatally in five or six days. In
other cases the disease is very protracted ; the invasion is slow and
insidious, and the disease may last from thirty to fifty or even sixty days.
Chronic Hydrocephalus.
The etiology of chronic hydrocephalus is not well known ; but hered-
itary predis})Osition appears to exert some influence in its production,
for more than one child may be affected in the same family. Congenital
syphilis is probalily the most important predisposing cause, and it is
possible that too much importance lias been attributed to rickets in its
production. The disease is always congenital or acquired soon after
birth, except when it results from intracranial tumors or from occlusion
of one or more of the lateral sinuses. Of the exciting causes little is
known. Chronic hydrocephalus is sometimes preceded by an attack
resembling acute hydrocephalus.
Symptoms. — In congenital hydrocephalus cerebral symptoms, such
as daily recurring convulsions, strabismus, or rolling of the eyeballs,
are apparent from the infant's birth, while in a few days or weeks the
head is observed to undergo progressive enlargement.
Impairment of the general nutrition is one of the first symptoms;
the child may seem eager for food and sucks well, yet it loses flesh and
strength, and the skin hangs in loose folds on its attenuated limbs.
The bowels are generally constipated, or diarrhoea may alternate with
constipation, and the evacuations are always unhealthy. The child is
restless and may be drowsy during the day, but wakeful and fretful
during the night. The fontanelles and sutures are now unusually open,
the anterior fontanelle is tense and pulsates strongly, and the child is
subject to paroxysms of restlessness, during which there is increased
heat of the head.
DISEASES OF THE PIA MATER. 659
The sutures become gradually Avicler with the increase of effusion,
the fontanelles increase in size, the head assumes a globular form, and
the physiognomy of the child soon acquires the characteristic features
of chronic hydrocephalus. As the fluid accumulates within the cranium
it presses equally in all directions, and the cavity of the skull must
enlarge in the direction of least resistance. The greatest increase in
the size of the head is effected chiefly by enlargement of the anterior
fontanelle and by widening of the sagittal suture, these being the points
which are the last to be ossified, and at which the bones of the skull
are less firmly fixed. The frontal bones are consequently pushed for-
wards, rendering the forehead round and prominent, the parietal bones
are pressed backwards and outwards, and the occipital bone downwards
and backwards, sometimes even so far that it assumes an almost hori-
zontal position. The head is, as a rule, globular and flat at the top,
although it occasionally assumes a conical form. Its size varies, and it
has been known to measure two or even three feet in circumference. The
orbital plates of the frontal bones are pushed from the horizontal to an
oblique, or it may be almost vertical position, and thus encroach upon
the cavities of the orbits. The eyeballs are consequently pressed for-
wards and rendered prominent ; they are at the same time rotated down-
wards, so that the sclerotic coat appears below the upper lids, while the
pupils are half hidden beneath the lower lids. On placing the hand
over the open fontanelles and sutures they are felt tense and fluctuating.
The hair grows scantily over the head, and the skin is tense and shining,
differing in this respect from the wrinkled condition of that of the rest of
the body ; distended veins ramify over the scalp ; and the enlarged head
contrasts strikingly with the small infantile face. The child has a dull
and stupid expression, and being unable to hold his head up he is obliged
to remain in the recumbent posture or to assume a half-sitting position,
while his head is supported with his hands or propped up with pillows.
The most usual cerebral symptoms which appear during the progress of
the case are convulsions ; attacks of laryngismus stridulus ; paralyses
with contractures of varying distribution ; rolling of the eyeballs ; and
amblyopia progressing to amaurosis. Hearing, as a rule, remains un-
affected until near the fatal termination. Chronic hydrocephalus lasts
usually from one to two years, but in exceptional cases the patient has
been known to live to middle or even old age. The disease is almost
always fatal, death being caused by laryngismus stridulus, general con-
vulsions, or some intercurrent disease.
660 DISEASES OF THE MEMBRANES OF THE BRAIN.
(II.) Meningitis of the Convexity of the Brain.
Etiology. — Simple primary meningitis of the convexity of the brain
is a rare affection. It may occur at all ages, but chiefly attacks infants
under two years of age, when it is named leptomeningitis infantium.
It occurs with decreasing frecjuency from this age to puberty, when it
becomes more frequent, but it is only very rarely met with in advanced
ao-e. In adults men are more frequently attacked than women. The
exciting causes of the disease are not well known.
Secondary meningitis of the convexity may be produced by inflam-
mation of the bones of the skull, the usual causes of the latter being
external injury, scrofula, and syphilis. Gummata may also give rise
to this inflammation. Otorrhtiea, especially when complicated by caries
of the temporal bone, is one of the most frequent causes of purulent
menino-itis, and the affection may result from puriform softening of a
thrombus in one of the sinuses, erysipelas of the head leading to osteo-
phlebitis of the bones of the skull, carbuncles of the face and neck,
suppuration of the eyeball, and all intracranial diseases like tumors,
abscesses, or necrotic softening.
Symptoms of Primary Meningitis of the Convexity. — The course of
acute meningitis may be divided into three stages: (1) The period of
excitement, (2) the period of transition, and (3) the stage of collapse.
(1) The Period of Excitement. — Obscure premonitory sym])toms
are sometimes observed, consisting usually of a feeling of heaviness in
the head along with paroxysms of violent cephalalgia, sleeplessness,
irritability of temper, and general malaise. As a rule, however, the
disease begins suddenly by a well-marked rigor, intense headache,
vomiting, fever, and delirium, while in children it is ushered in by an
attack of general convulsions.
The headache may be diffused or referred to the forehead, temples,
vertex, or occiput; it is intensified by light and sound, and by all
movements of the head. The patient consequently shuns the light,
and holds his head between his hands, in order to prevent it from
moving. The headache is continuous, but is marked by exacerbations
of intense severity, during which the patient, especially if a child, may
utter a loud and piercing cry.
Vomiting is a very constant symptom of meningitis, and is, like the
vomiting symptomatic of other cerebral diseases, unattended by nausea,
and epigastric pain or tenderness. It recurs frequently during the first
forty-eight hours, and may then cease or occur at intervals throughout
the course of the affection.
DISEASES OF THE PIA MATER. 661
The motor disturbances in this stage consist of strabismus, slight
twitching of the muscles of the face and limbs, and tonic spasms of those
of the neck and back, Avhile the patient staggers if he attempts to walk.
The pupils are usually contracted or unequal, but react readily to lio-ht.
The sensory disturbances consist of buzzing in the ears, flashes
before the eyes, and intolerance of light and sound. Cutaneous hyper-
aesthesia is not infrequently present, so that the slightest touch on the
skin may cause pain, and the reflex excitability is increased.
The psychical disturbances are well marked from the first. The
patient is extremely iri-itable, and fierce delirium is apt to occur, the
patient shouting and violently struggling with his attendants. At
other times he is morose, and buries his head under the bedclothes,
obstinately refusing to answer questions. The temperature of the
body is elevated, the pulse beats from one hundred and twenty to one
hundred and forty or more, and the respirations are increased to thirty
or forty in the minute. .
(2) The Period of Transition. — During this period the furious
delirium of the first stage becomes quieter, the patient lies on his back,
with his fingers picking at the bedclothes or catching imaginary flies in
the air.
The motor symptoms of this period consist of strabismus, conjugate
deviations of the eyeballs, with rotation of the head and neck, twitch-
ings of the face; grinding of the teeth and trismus; distortions of the
tongue; the hydrocephalic cry; subsultus and tremor of the hand;
convulsive movements of the limbs, and retraction of the head and
neck with opisthotonos.
These convulsive symptoms are followed by paralysis, which is very
variable in its distribution, some groups of muscles being paralyzed
while others continue convulsed.
The sensory disturbances consist of dimness of vision and of hearing,
ending in blindness and deafness, while the general cutaneous hyper-
aesthesia of the first stage is replaced by anaesthesia. The bowels ai'e
constipated throughout, and the abdominal walls are often retracted as
in tubercular meningitis. The respirations are irregular, the pulse fre-
quent and thready, and there is retention of urine.
(3) The Stage of Collapse. — The third stage of the afl'ection now
becomes established, the convulsive phenomena give place everywhere
to paralysis, and the patient passes into a profound and fatal coma.
Symptoms of Secondary Meningitis. — The symptoms of secondary
meningitis differ considerably according to the cause of the inflamma-
tion, but, inasmuch as inflammation from caries of the petrous bone is
the most usual form of the affection, it will be useful to describe it first.
662 DISEASES OF THE MEMBRANES OF THE BRAIN.
The affection may be ushered in by chilliness or a distinct rigor and
feverish symptoms, but intense headache, either continuous or marked
by remissions and exacerbations, is the first symptom to direct attention
to the brain. The headache may be fixed to a point in the vicinity of
the diseased ear, or shoot from one ear to another, while at other times
it is diffused over the whole head. If the local affection be attended
by pain, the commencement of the meningitis is marked by a great
increase of its intensity, and the onset of the latter may sometimes be
completely masked by an increase of the local inflammation in the ear.
Attacks of dizziness now supervene, accompanied by nausea and vomit-
ing ; the patient complains of noises in the head, general painful sensa-
tions diffused over the body, and obscuration of the special senses, while
he often becomes actively delirious.
The motor symptoms are rigidity of the muscles of the nape of the
neck, convulsive twitching of the facial muscles on the affected side,
trismus, grinding of the teeth, and occasionally .spasms of the extremities.
The spasmodic phenomena, however, soon give place to paralysis
affecting first the facial, hypoglossal, and glosso-pharyngeal nerves, and
should the inflammation extend forwards along the base of the skull,
the third, fourtli, sixth, and probably the fifth nerves on the same side
as the lesion. The state of the pupils is variable, and liable to frequent
changes during the course of the disease, being generally contracted or
unequal at first, and dilated and fixed wlien effusion has taken j)lace.
Paralysis of the extremities is rare, but the patient has an unsteady,
staggering gait.
The sensoty disturbances consist of marked hyperaesthesia of the
skin, joints, bones, and muscles, so that every movement is painful.
Vomiting generally continues throughout the whole course of the
disease, the bowels are constipated, and the abdominal muscles are
tender to the touch and retracted. The temperature in acute cases is
usually high, but remits in the morning, although it remains constantly
high in some cjises.
The pulse, as a rule, rises and falls in frequency along with the tem-
perature, except in the cases where symptoms of compression of the
brain occur during the first days of the disease.
The urine is often albuminous, and this may or may not be associated
with amyloid disease of the liver, spleen, and kidneys.
The optic disks usually present the same ajipearances as those observed
in tubercular meningitis. The psychical symptoms are very variable,
consisting of jactitation, restlessness, and confusion of ideas, especially
towards evening, when the temperature rises. After a time the patient
falls into a somnolent condition, from which he can at first be readilv
DISEASES OF THE PIA MATER. 663
roused by a loud question, but this state soon gives place to profound
and fatal coma.
(III.) Simple Meningitis of the Base of the Brain (Basilar
Meningitis).
Etiology. — Inflammatory processes at the base of the brain are caused
by fissures, tumors, abscesses and other lesions at the base of the brain,
but the form to be described at present arises spontaneously, and occurs
in persons from sixteen to thirty years of age.
S'i/Diptoms. — When primary basilar meningitis is diffused and general,
the affection begins by languor, mental depression, chilliness or even
rigor, thirst, and the usual symptoms of fever. The patient complains
of intense cephalalgia and giddiness, and these are followed by severe
attacks of vomiting.
Motor disturbances may be completely absent throughout the whole
course of the affection, but when present they consist of spasmodic
rigidity of the muscles of the back of the neck, with retraction of the
head, and rarely of rigidity or clonic twitchings of certain groups of
the muscles of the extremities. The patient grinds his teeth during
sleep, and in the later stages of the affection trismus and hiccough have
been observed. Paralysis of the abducens is not uncommon, but paral-
ysis of the oculo-motor nerve is rare. Paresis of the facial or hypo-
glossal nerves may occur temporarily during the course of tlie affection,
and subse(|uently disappear, but complete paralysis of them has not
been observed. The power of deglutition may be impaired during the
course of the affection and be afterwards regained, or it may increase
to complete dysphagia before death. Paresis of the extremities is occa-
sionally observed, but never complete paralysis.
The sensory disturbances consist of cutaneous hyper?esthesia, espe-
cially in the region of distribution of the fifth nerves, ringing in the
ears, scintillations before the eyes, and occasionally hallucinations. The
psychical disturbances are more variable than in any other form of
meningitis. In some cases the mental faculties are unaffected through-
out the whole course of the disease, while in others they are early in-
volved. The mental symptoms usually consist of a mild delirium ; but
in exceptional cases this may be more active, the patient being restless,
quarrelsome, capricious, and irascible. Active delirium is usually tem-
porary and soon gives place to a milder form ; the patient after a time
becomes somnolent, but may be temporarily aroused by a loud (juestion
addressed to him ; in a short time he fails into a state of complete in-
664 DISEASES OF THE MEMBRANES OF THE BRAIN.
sensibility, during which the urine and feces are passed involuntarily.
Vomiting continues to distress the patient throughout the course of the
disease, the bowels are constipated, but the abdomen is not retracted as
in tubercular meningitis.
The temperature may rise in the first stage as high as 104° F. in the
evening and approach to the normal in the morning, but in the later
stages the temperature remains low, being sometimes subnormal. The
pulse, as a rule, follows the temperature, being very frequent in the
initial period, and sinking in the course of the disease to below sixty
beats in the minute. Towards the end of life it again increases, and
becomes very frequent, irregular, and intermittent ; the patient is covered
with bedsores, much emaciated, and dies in a state of marasmus.
The chronic forms of basilar meningitis may give rise to localized
inflammatory products at the base of the brain, which cause symptoms
scarcely to be distinguished from those of tumors occupying the same
situation. The symptoms are variable in such cases, the most charac-
teristic being paralyses of the various cranial nerves. In addition to
the headache and dizziness, there are anosmia, amaurosis, or hemianopsia,
ptosis, paralysis of the motor nerves of the eyeball, sensory disturbances
in the region of distribution of the fifth nerve, masticatory paralysis,
paresis of the seventh nerve, and occasionally paresis of one or more of
the extremities. If the inflammation extend to the lower end of the
pons, bulbar paralysis, dysphagia, and dyspnoea may be present.
(IV.) Metastatic Menixiutis.
Metastatic meningitis comprises certain varieties of the affection,
which occur as terminal phenomena in the course of acute diseases.
The diseases with which meningitis is most fre(iuently associated are
pneumonia, ulcerative endocarditis, acute rheumatism, purulent pleurisy,
pericarditis, diphtheria, and the acute exanthemata. Although chronic
Bright's disease is liable to be complicated by inflammation of the serous
membranes, meningitis is rare.
Symptoms. — The extent and intensity of the inflammation vary
greatly in different cases ; in some there is little or no effusion into the
ventricles, and the symptoms of compression are absent ; the inflamma-
tion is sometimes limited to the convexity, and at other times extends
to the base and upper part of the spinal cord ; and in the meningitis
of acute febrile diseases the symptoms are obscured by the cerebral dis-
turbance usually observed in all grave acute affections.
DISEASES OF THE PIA MATER. 665
Varieties of Metastatic Meningitis.
Meningitis ivith Pneumonia. — Meningitis may appear in the course
of pneumonia from the third to the eighth day, or even later. The most
usual symptoms are chilliness, intense headache, rapidly developed and
mild, or occasionally furious delirium, a fresh accession of fever, and
hyperpyrexia before death. The delirium gives place at an early period
to somnolency, ending in coma. A slight degree of rigidity and pain
in the neck is always a valuable sign of meningitis, and vomiting is a
frequent occurrence. The pupils are generally contracted at first, and
may subsequently become unequal. If the base of the brain be affected,
paralysis of the oculo-motor and other nerves at the base of the skull
renders the nature of the complication more apparent.
Meningitis ivith Ulcerative Endocarditis. — The cerebral symptoms
in ulcerative endocarditis are caused by multiple hemorrhagic infarctions
of the cortex of the brain or of the pia mater, and the symptoms pro-
duced are more or less like pyeemic encephalitis.
Rheumatic meningitis has been described, but post-mortem evidence
of its existence is wanting.
(V.) Traumatic MENixiiiTis.
Etiology. — This form of meningitis or of meningo-encephalitis may
appear during the period of reaction from concussion, or follow a con-
tusion of the brain. Injury of the scalp, with subsequent inflammation
of the bones of the skull and dura mater, may also give rise to inflam-
mation of the pia mater and brain. At other times the inflammatory
process is set up by a perforating injury of the skull either with or
without extravasation of blood between the dura mater and the bone,
the effects in such cases being intensified by the admission of air con-
taining germs into the open wound. In other cases the meningitis is a
secondary result of osteitis, thrombosis of the sinuses probably playing
an important part in its production in such cases. The meningitis at
other times may result after necrosis of the bone has taken place.
Hutchinson thinks that in fractures of the petrous portion of the
temporal bone the inflammation extends along the sheath of the seventh
nerve, and in this way gains access to the subarachnoidal spaces.
Symptoms. — This affection may be divided into two varieties : (a)
acute, and {h) chronic or subacute traumatic meningo-encephalitis.
{a) Acute Traumatic Meningo-encephalitis.— The symptoms of the
onset of the acute form of the affection are modified by the fact that
()()() DISEASES OF THE MEMBRANES OF THE BRAIN.
the inflammatory process usually attacks a patient already suffering
from the symptoms of concussion, compression, or contusion of the
brain. It is impossible to distinguish between the symptoms of the
reaction period of concussion and those of the early or congestive stage
of true inflammation, so that we are unable to determine when the
symptoms of the former terminate and those of the latter begin. At
the onset of the inflammatory attack the patient complains of severe
and continuous cephalalgia ; the carotids beat forcibly ; the face is
suffused and the scalp hot ; the pupils are contracted ; and there are
intolerance of light and sound, spectral illusions, noises in the ears, and
general hyperesthesia to external impressions. The patient likewise
suff"ers from the usual symptoms of pyrexia ; the pulse is full and
boundinij. and there are restlessness and wakefulness with delirium of a
violent character. These symptoms may, under proper treatment,
gradually subside until health is reestablished ; but more commonly the
symptoms of the stage of irritation develop into those of the stage of
compression.
During the transition period between the early stage of excitement
and that of comj)ression of the brain, the symptoms of a localized
disease may make their appearance. Clonic or tonic spasms, followed
by paralysis, may occur in particular groups of muscles. Rigidity of
the muscles of the nape of the neck, Avith retraction of the head, is
usually present at this period, and may also extend to the muscles of
the back and give rise to tetanic seizures. Hemiplegia of the side
opposite to tlie injury is, according to Hutchinson, a constant symptom
of direct traumatic meningo-encephalitis. Tlie abdominal muscles are
usually retracted and the bowels constipated. When the meningitis is
situated at the base of the brain, the cranial nerves in their passage
along the base of the skull may become imj)licated. The most usual
symptoms produced are ptosis, strabismus, paralysis of the facial muscles
or of half of the tongue, and difficulty of deglutition.
The symptoms of compression of the brain now become rapidly
developed; the delirium is replaced by stupor, from which the patient
is roused Avith difficulty ; the pupils are dilated and insensible to light ;
the breathing is slow and stertorous ; the pulse, retarded at first, becomes
feeble and frequent towards the end ; the skin is hot and bathed in
perspiration ; and convulsive twitchings or jerkings of the limbs are
observed ; but these soon give place to general muscular relaxation, and
the patient dies in profound coma.
{b) Subacute Traumatic Menhujo-encephalitiH. — This form of men-
ingo-encephalitis may come on a few days after the injury or not until
months have elapsed. The patient has often apparently recovered from
DISEASES OF THE PIA MATER. 667
the original injury, but, as a rule, some of the consequences of con-
cussion remain. The patient in the interval has complained of head-
ache, impairment of sight and hearing, confusion of ideas, or mental
in-itability. The symptoms of the inflammatory attack may be ushered
in by an aggravation of the symptoms which have persisted during the
interval, or by an epileptic attack. The pupils are contracted, dilated,
or unequal ; there are intolerance of light and sound, convulsive twitch-
ings of the limbs and face, strabismus, delirium, and the ordinary
phenomena of symptomatic fever. After a time the symptoms of com-
pression supervene, and the patient dies comatose.
Morbid Anatomy. — In external pachymeningitis the dura mater is
at first congested and presents punctiform extravasations, while at a
more advanced stage the membrane becomes swollen and infiltrated with
numerous white blood-corpuscles. If the disease has been acute, the
white corpuscles become more numerous and make their way inwards,
so that a purulent internal pachymeningitis is superadded to the external
pachymeningitis. If, however, the disease has been chronic, the Avhite
blood-corpuscles become transformed into spindle-cells and ultimately
develop into connective tissue. In long-standing cases portions of the
membrane may become calcified.
HemorrJiagie pachymeningitis appears to begin with hypergemia of
the dura mater in the 'area of distril)ution of the middle meningeal
artery. The inner surface of the dura mater assumes a rosy color, and
after a time a loose yellowish coating or false membrane forms, which
is dotted with a number of confluent or separate hemorrhagic points.
The false membrane become very vascular and from time to time some
of them rupture, giving rise to hemorrhages of variable quantity. The
clots which form become partially organized and the delicate capillaries
which develop in them become the source of new hemorrhages, so that
in this way a large quantity of blood may be poured out between the
thickened membranes. Haematoma is most frequently found in the
upper part of the brain along the falx cerebri and thence it spreads
down the curved portion of the frontal and occipital lobes and later-
ally towards the Sylvian fissure. The bones of the skull have been
found sometimes abnormally thin and at other times unusually thick,
and the brain itself is compressed by the hnematoma, while it is often
the subject of atrophy independently of the disease in tlie membranes.
In tubercular meningitis the changes in the pia mater are (1) those
which are directly connected with the formation of tubercles, (2) those
caused by the inflammation surrounding them, and (3) those which arise
from the effusion into the ventricles.
668 DISEASES OF THE MEMBRANES OF THE BRAIN.
(1) The pia mater is studded with tubercles which appear as grayish-
white granulations distributed along the course of the vessels, the terri-
tory supplied by the Sylvian artery being particularly liable to be
affected.
(2) The inflammatory changes in the pia mater vary greatly accord-
ing to the amount of effusion which has been present. Evidences of
suppuration are found at the base of the brain, and cloudy streaks of
exudation may be observed passing along the vessels. In some cases a
purulent or fibrinous effusion is observed in the pia mater of the con-
vexity, which may extend backwards over the anterior surface of the
pons and medulla and find its Avay over the entire surface of the cere-
bellum. In some cases the choroid plexuses and the velum interpositum
are covered with a yellowish purulent exudation.
(3) The ventricles are generally distended with serous or sero-puru-
lent fluid, and the brain is compressed, so that the cortex and white sub-
stance are dry and ansemic, but when effusion is absent those parts are
congested and oedematous.
The cortex is often studded by punctiform hemorrhages caused, accord-
ing to Rindfleiscli, by tubercular degeneration of the nutritive arteries.
AVhen the exudation sj)reads along the base of the brain the cranial
nerves are implicated in the disease, and even the spinal cord is not
unfrequently affected.
Essentially the same phenomena are met with in the other forms of
acute meningitis as in the tubercular variety, so far as the appearances
of inflammation and the effusion are concerned, and it is, therefore,
unnecessary to describe the morbid changes of these diseases in detail.
In chronic hydrocephalus the general ventricular cavity of the brain
contains serous fluid, which varies in quantity from a few ounces to many
pounds, and conse([uently the hemis])heres of tlie brain are compressed
and flattened, so that the sulci and convolutions almost entirely disappear.
Morbid Physiology. — The premonitory symptoms of all the acute
forms of meningitis are such as are met with in all severe inflammatory
affections, and the purely nervous phenomena of the period of invasion
are caused by irritation of the cortex of the brain, and the student who
is acquainted with the physiology of the cortex will be able readily to
explain the various sensory disorders and the spasmodic affections which
occur at this period of the disease. In the second stage of the disease
portions of the structure of the cortex are being destroyed, so that the
hyperaesthesias and spasms of the first period become mixed up with
various forms of anaesthesia and paralysis. Direct implication of the
cranial nerves in the inflammatory process at the base of the brain
explains some of the local forms of anaesthesia and paralysis which
DISEASES OF THE PIA MATER. 669
occ'iu- at this period. As the eftusion increases in quantity the brain is
subjected to compression and its functions are gradually or suddenly
abolished, and the patient dies comatose.
Treatment. — The treatment of all the acute forms of meningitis must
be conducted on the same general principles, by the application of ice
to the shaven scalp, rest in a darkened room, and moderate evacuation
of the bowels by a saline purgative. Local bloodletting often relieves
the severe headache and gives at least temporary relief.
In external pachymeninyith the question of trephining will arise
Avhen an abscess forms or an extravasation of blood takes place between
the dura mater and bone, but such cases come under the care of the
surgeon.
In licematoma the treatment will depend greatly upon the underlying
affection, and a careful examination must be made into the habits of the
patient, and of all the other organs, in order to discover upon what
disease the meningeal affection depends.
In all the acute inflammations of the pia mater mercury may be given
in frequently repeated small doses ; in the tubercular disease this treat-
ment can do no harm, and in the simple varieties it may do good. Iodide
of potassium has also been given with the view of promoting absorption
of the effusion but the results of this treatment are doubtful. When
the headache is very severe, morphia in suitable doses should be admin-
istered subcutaneously, and chloral hydrate and l)romide of potassium
either separately or combined will be found useful when the convulsive
symptoms are severe. Blisters or croton oil liniment to the shaven
scalp have been much used in the treatment of meningitis, but I cannot
too strongly condemn this practice.
In chronic hydrocephalus partial success has been obtained by with-
draw^ing a few ounces of fluid at a time by means of an aspirator, while
the skull is at the same time supported by bandages.
CHAPTEE XX. j
PARALYSIS AGITANS, MULTIPLE SCLEROSIS. AND CHOREA.
I. PAEALYSIS AGITANS.
Etiology. — Paralysis agitans occurs generally in advanced age,
although a few cases have been observed in young people. Men are
more frequently attacked than women. The disease is frequently met
with amongst persons living in damp and unhealthy situations, and
some authors believe that there is a causal relation between it and
rheumatism. It is sometimes caused by great emotional disturbance,
and many cases follow wounds and other injuries.
Symptoms. — The clinical history of paralysis agitans may be divided
into three stages: (1) The period of invasion; (2) the stationary
period; and (3) the terminal period.
(1) The Period of Invasion. — Paralysis agitans may begin in a
slow and progressive manner, or more or less suddenly. In the sloiu
mode of invasion the characteristic jihenomena of the disease are pre-
ceded by premonitory symptoms, consisting of sleeplessness, mental
irritability, rheumatoid or neuralgic pains, a remarkable feeling of
fotigue, and a transitory feeling of Aveakness in the limbs. After a longer
or shorter time the disease declares itself by a trembling in one of the ex-
tremities, generally in the small muscles of one hand. At first the tremor
is only occasionally })resent, but as the disease advances it becomes per-
sistent during w'aking hours, but ceases with sleep, and it can be arrested
by a strong voluntary effort. When the hand is the first part affected,
the "patient," to quote Charcot, "closes the fingers on the thumb, as
though in the act of spinning wool, at the same moment the wrist is
bent by rapid jerks on the forearm and the forearm on the arm.' As
the disease advances, the tremor increases in intensity and persistency,
and invades by degrees parts which have hitherto remained sound.
The order in which the tremor invades the different groups of muscles
is somewhat variable. In some cases the tremor is restricted for a long
time to one-half of the body, the tremor begins in the right hand, and
after months or years the lower extremity on the same side becomes
affected, and after another variable i)eriod the left hand and foot are
SYMPTOMS. 671
successively invaded. In other cases both lower extremities are first
aftected, and in a few cases the upper extremity of the one side, (gener-
ally the right, is first attacked, and then the lower extremity of the
opposite side.
In the sudden mode of invasion the tremor appears suddenly either
in one extremity or in all the limbs at once; it may soon diminish or
disappear, but soon recurs, and after a series of alternate exacerbations
and remissions, becomes permanent. The duration of the initial stage
varies from one to three years.
(2) Stationary Period. — When the disease is fully developed the
trembling becomes almost incessant, although it varies in intensity.
It is aggravated by emotional excitement, cold, and voluntary efi'ort,
and becomes less during repose, and ceases during sleep. The diiferent
segments of the fingers and hand undergo involuntary and rh^^thmical
oscillations, which closely resemble voluntary movements. "Thus in
some patients," says Charcot, "the thumb moves over the fingers as
when a pencil or paper ball is rolled between them; in others the
movements are more complicated, and resemble what takes place in
crumbling a piece of bread." The handwriting now assumes special
characteristics. At an early stage of the disease the writing at the first
glance presents little change, but when examined with a magnifying
glass slight inequalities are perceived, and as the disease advances the
up-strokes become markedly tremulous.
The muscles of the head and neck, as already stated, usually remain
unaffected. The muscles of the eyeballs are also exempt from tremor,
and consequently nystagmus, Avhich is so prominent a symptom of dis-
seminated sclerosis, has no existence in paralysis agitans. Tlie move-
ments of the eyeballs are, however, often executed with great slowness.
The muscles of the face, instead of trembling, are motionless ; the features
become fixed; and the face assumes a mournful, stolid, or vacant ex-
pression. The utterance is slow, jerky, and accomplished with great
apparent effort, soon inducing weariness, and if the tremor of the body
be intense it becomes tremulous and broken, while in old-standing
cases the saliva may dribble from the mouth to some extent.
After a longer or shorter time the muscular power becomes gradually
weakened. In many cases, however, motor weakness is more apparent
than real, the phenomena depending upon the great slowness with
which voluntary movements are executed, the immense effort which all
voluntary actions, even speaking, entail, and the readiness with which
fatigue is induced. But although the muscular power, when measured
by the dynamometer, is often retained much longer than might be
expected, yet after a time motor power becomes gradually diminished, and
672 PARALYSIS AGITANS.
paralytic symptoms supervene. The paralysis, however, almost always
remains partial, and is irregularly developed in different groups of
muscles, and, as in various other forms of paralysis, the extensors of
the limbs are affected to a greater extent than the flexors. The trem-
blino- often abates in the muscles as paralysis increases. The bladder
and rectum are only very exceptionally involved in the paralysis. The
muscles react normally to both the faradic and galvanic currents.
After a time the muscles of the extremities, trunk, and neck become
the subjects of rigidity, at first temporary, but ultimately becoming
permanent, the flexors being affected to a greater extent than the ex-
tensors. The rigidity of the muscles produces characteristic alterations
in the attitudes of the body. The rigidity of the anterior cervical
muscles causes the head to be strongly bent forwards, and the patient
cannot raise it or turn it to either side without great difiiculty. The
body is also inclined forwards Avhen the patient is standing. The
elbows are habitually held somewhat removed from the chest, the fore-
arms are slightly flexed on the arms, and the hands are sometimes
flexed, sometimes slightly extended on the forearms, and rest on the
epigastrium. The fingers are flexed at the metacarpo-phalangeal articu-
lations, the index and middle fingers are extended, but the remaining
fingers are slightly flexed at the phalangeal articulations, all of them
are slightly inclined to the ulnar border of the hand, and the thumb is
extended and opposed to the index finger, so that the attitude of the
hand and fingers closely resembles that assumed by tliem in holding a
pen (Fig. 179). In some cases the fingers are alternately flexed and
Fig 170.
Attitude ok the IIand in I'arai.ysis Aoitans. (After ('iiaucot.)
extended at their several articulations so as to resemble the distortions
of arthritis deforinans (Fig. 1(S0). In paralysis agitans, however, the
joints are not swollen and stift", and passive movement of the articula-
tions does not give rise to the creaking sounds observed in the rheumatic
affection. The rigidity of the muscles of the lower extremities is some-
times so great as to resemble paraplegia with contracture. The spasm
SYMPTOMS. 673
of the adductors of the thighs and muscles of the calf predominates
over their antagonists, so that the knees are drawn inwards, the leo- is
slightly flexed on the thigh, and the foot assumes the well-known posi-
tion of talipes equino-varus. The toes are extended at the metatarso-
phalangeal and flexed at the phalangeal articulations [Griff e des Orteih).
Fro. 180.
Attiti'de or THE }1am) IX Paralysis Agitans simvlating that of Authritis Deformans.
(Alter Charcot.)
In the advanced stage of this disease the patients move all of a piece,
as if their joints were soldered together, and the head and body are
kept inclined forwards, a position which no doubt largely contributes
to produce that tendency to fall forwards manifested when walking.
The gait is now characteristic. The patient gets up sloAvly and with
difficulty from his seat, and hesitates for a few moments before starting;
Avhen once he has begun to walk, he is compelled to run forwards, in
order to save himself from falling. In the language of Trousseau, he
looks as if pursuing his own centre of gravity. This gait has been
called parali/sis festinans or procursoria, or slmiplj propulsion.
The forward running or propulsion is the usual gait of paralysis
agitans, but some patients manifest a strong tendency to run or to fall
backwards, although their bodies are inclined forwards, a tendency
which has been named retropulsion. Graves mentions the case of a
patient who, if arrested in his forward movement, immediately began to
run backwards, and Chai'cot could excite the impulse to move back-
wards in a female patient by slightly pulling her back by the dress
when slie was standing. It has already been mentioned that a few
cases of paralysis agitans are ushered in by rheumatoid or neuralgic
pains, but in the majority of cases pains are absent. The patient is,
however, distressed by disagreeable sensations," such as cramps and sensa-
tions of tension and traction in the muscles, along with a general feeling
of weariness and discomfort. These sensations render the patient restless,
and cause him to seek frequent changes of posture. He complains of
a constant sensation of excessive heat, although the thermometer shows
that the temperature of the body is normal. In order to relieve this
43
674 MULTIPLE SCLEROSIS.
feeling the patient throws off the bedclothes at night, and only retains
the lightest garments in the daytime. This sensation of heat is espe-
cially felt in tlie epigastrium and back, but may affect the face and
limbs. It is liable to remissions and exacerbations, and seems to attain
its maximum after a paroxysm of trembling ; it is often accompanied by
profuse perspiration.
(3) Terminal Period. — The course of the disease is very protracted,
and may extend over a period of many years. As the tremors and
muscular rigidity increase in intensity, the patients are compelled to
remain the whole day seated on a chair, or confined to bed. The general
nutrition suffers, the muscles become atrophied, and the paresis of the
second stage of the disease gives place to pronounced paralysis. The
memory and intellect are weakened, general prostration sets in, the
urine and feces are passed unconsciously, bedsores appear on the sacrum,
and the patient dies from nervous exhaustion and marasmus. The
tremors disappear entirely a few days before death, and paralytic symp-
toms become predominant. In the majority of cases, however, death
results from some intercurrent disease, sucli as pneumonia or pleurisy.
II. MULTIPLE SCLEROSIS OF THE BKAIN AND Sl'INAL CORD
(DISSEMINATED OR INSULAR SCLEROSIS).
Etiology. — Hereditary transmission has been traced in several re-
corded cases of multiple sclerosis, although it is always indirect rather
than direct. It is commonly observed in youth and middle age, and a
considerable proportion of the cases recorded in p]ngland have been in
children under ten years of age. It is probably more frequent in
women than in men, but the disproportion between the sexes is probably
not great. The exciting causes are exposure to cold and damp, excessive
mental or bodily exertion, profound emotional disturbances and trau-
matic influences, as blows on the head and concussion from railway
accidents.
Symptoms. — Multiple sclerosis may be divided into three varieties:
(1) the cerebrospinal, (2) the cerebral, and (3) the spinal form. Of
these the cerebro-spinal variety is by far the most fre(iuent and important.
(1) The Cerebro-spinal Form. — This form of multiple sclerosis may
develop gradually and insidiously or suddenly. In cases, the develop-
ment of Avhich is gradual, the initial symptoms are very obscure, and
may be referred either to the spinal cord or brain. The spinal symp-
toms which usher in the disease consist of paresis of the lower extremities,
with a slow and trembling gait, or ataxia with various parsesthesioe,
neuralgic pains, other disturbances of sensibility in the limbs, and
SYMPTOMS. 675
cardialgic attacks accompanied by urgent vomiting. The more usual
cerebral symptoms observed in the beginning of the disease are vertigo,
headache, staggering gait, tremors on voluntary effort, impairment of
speech, vision, or hearing, paresis of the muscles supplied by one or
more of the cranial motor nerves, and various psychical disturbances.
When the disease begins abruptly, the symptoms are ushered in by a
convulsive or apoplectiform attack, followed by diplopia, amblyopia,
nystagmus, and disturbances of speech.
The first motor symptom to attract attention is usually paresis or
paralysis of certain muscular groups. Weakness generally begins in
one leg, and subsequently extends to the other leg and to the arms, but
the order in which the paralysis of the difterent muscular groups is
developed presents every imaginable combination.
The gait is usually of the spastic variety, muscular contractures set
in, and the legs are held like rigid bars in the position of extension and
adduction, just as in primary lateral sclerosis. In the later stages of
the disease flexion of the different segments of the lower extremities
may predominate over extension. The paralysis rarely becomes so well
marked in the upper as in the lower extremities. When the upper
extremities are, however, affected with paralysis and contracture, they
are maintained in a position of forced extension, and closely applied to
the sides of the body. The affection sometimes begins with ataxia, but
in these cases it may often be noticed that characteristic symptoms of
true locomotor ataxia are absent, while others are present which do not
usually belong to it.
Intermittent muscular tremor constitutes one of the most character-
istic symptoms of this affection, although it has been found absent in a
few isolated cases. This tremor appears almost exclusively during
voluntary movements, and disappears during repose. So long as the
patient remains seated quietly the tremor is either entirely absent, or
at most there is only a trifling shaking movement of the head, or a slight
oscillation of the trunk. As soon, however, as he attempts to seize
anything with his hand the tremor begins, and increases in violence in
proportion to the effort made to execute the movement. Several devices
may be used in order to bring into prominence the characteristic tremor
(if multiple sclerosis, such as asking the patient to seize small objects
with his fingers or to stretch out his arms horizontally before him.
The tremor of this affection differs from that of paralysis agitans,
not only in being intermittent instead of continuous, but also in having
a much wider sweep than that of the latter affection. It holds an
intermediate position between the extensive jerking movements of
chorea, and the small and frequent oscillations of paralysis agitans.
676 MULTIPLE SCLEROSIS.
The true characteristic of the tremor of multiple sclerosis is best elicited
by asking the patient to convey a glass of water to his mouth. As the
glass is being carried to the mouth it oscillates from side to side in the
patient's hand, these oscillations appearing to increase in extent and
frequency as the mouth is approached. In aggravated cases the con-
tents of the glass are spilt in every direction ; but in milder cases the
patient is able, by moving his head downwards in ordei" to meet the
glass, to apply it to his lips, and then the trunk, head, and arms begin
to tremble violently, so that the edge of the glass rattles against the
teeth, and the contents are spluttered over the patient's face. When
the patient rises and attemj)ts to walk the tremor involves the entire
body, which may be shaken with such violence that he is unable to pro-
ceed or even to remain standing. As soon as the voluntary effort is
relaxed the tremor diminishes, and as long as the patient is in tlie
recumbent posture no trace of it can usually be detected ; occasionally
the tremor has been known to persist during repose.
The sensory disturl)ances are somewhat variable and not always well
marked. They may assume the form of facial neuralgia, lancinating
or diffused pains in the extremities, hyperesthesia or anaesthesia of
variable distribution, girdle jtains. and various j)arpestliesiic felt in dif-
ferent parts of the body, the latter being the most frequent of all the
sensory disorders.
The reflex actions are variously affected in different cases. The
cutaneous reflexes remain for a long time unaffected: but the tendon-
reactions are usually exaggerated, especially in the lower extremities.
In consequence of the increase of the tendon-reactions in the lower ex-
tremities, the knee-phenomenon and ankle-clonus are usually exaggerated,
and the limbs may be thrown into the state of trembling named spinal
epilepsy. This condition must, however, be carefully distinguished from
the characteristic tremor of multiple sclerosis.
Trophic disturbances are generally wanting for a long time, but in the
later stages various nutritive disorders usually make their appearance.
The sclerotic nodules may encroach on the anterior gray horns of the
spinal cord, and then muscular atrophy results as in progressive muscular
atrophy. Muscular atrophy may present itself in the upper or lower
extremities, neck, face, tongue, or indeed in any part of the body. The
electrical reactions of the nerves and muscles remain normal until the
muscular atrophy begins, and then the electric irritability of both
becomes gradually diminished.
During the terminal period of the disease bedsores appear over the
sacrum and other parts subjected to pressure, and general nutrition fails.
The bladder and rectum, as a rule, remain unaffected for a compara-
SYMPTOMS. 677
tively long time, but their functions are ultimately interfered with as in
chronic myelitis. The disorders of the sexual functions are somewhat
variable. In some patients sexual desire appears to be increased at an
early period of the disease, while in others it is completely abolished.
In the majority of cases the sexual functions remain normal for a com-
paratively long time.
Bulbar Symptoms. — Some of the phenomena caused by implication
of the pons and medulla oblongata in the morbid process are amongst
the most important and characteristic symptoms of the disease. The
speech is slow and hesitating, while each syllable is separately pro-
nounced, presenting a mode of articulation which has been named the
syllabic or scanning. The voice is weak, low, sometimes whispering,
and monotonous, while it breaks readily when forced efforts are made.
Laryngoscopic examination shows that the vocal cords move normally,
but their tension is diminished and frequently changes. The acts of
laughing and crying are often represented by peculiar noisy inspirations.
After a time symptoms of true bulbar paralysis supervene, the move-
ments of the lips and tongue are impaired, and by-and-by mastication
and deglutition become increasingly difficult, the velum palati is para-
lyzed, speech becomes inarticulate, and the mouth remains permanently
paralyzed, while the saliva dribbles out.
Diplopia with strabismus is a not unfrequent symptom, although it
may subsequently disappear as in locomotor ataxia.
Nystagmus is, however, the most important of all the ocular symp-
toms, being present, according to Charcot, in about half the cases.
The movements of the eyeballs may be persistent or occur only during
forced accommodation, or when movements are performed by the ex-
tremities. At other times the nystagmus may not be apparent during
the ordinary movements of the eyeballs, but when the patient is asked
to look upwards and outwards so as to strain the ocular muscles, slight
oscillatory movements may be observed.
Amblyopia or amaurosis is a frequent symptom. Of fifty cases
observed by Guanck, defects of vision were found in twenty-eight cases,
and of these cases various degrees of amblyopia were present in eight,
amblyopia and restriction of the field of vision with dyschromatopsia in
five, and amblyopia and defects of the field of vision, with morbid changes
in the optic disks, in fifteen cases. Of the fifteen cases in which the optic
disks were found altered, complete white atrophy of both disks with blind-
ness was found in two cases. Such cases are rare, the rule being that
atrophy of the optic nerve in multiple sclerosis is unilateral. In ten
cases partial white atrophy was observed, the change in color was strictly
limited to the temporal halves of the fields of vision in four cases, while
678 MULTIPLE SCLEROSIS.
the nasal halves were affected, but in a much less degree than the tem-
poral halves, in six cases. In the remaining three cases hypersemia of
the disks with optic neuritis was present, caused, most probably, by a
retrobulbar neuritis. The senses of smell, taste, and hearing are im-
paired in some cases, but these disorders are rare.
Psychical disorders are always observed in multiple cerebro-spinal
sclerosis. They consist of mental irritability, emotional excitement
causing the patient to laugh or to shed tears without apparent motive,
and impairment of memory and intelligence. At other times the
mental disorder assumes the form of distinct unsoundness of mind.
In such cases there may be melancholia, monomania, with ideas of per-
secution or of grandeur, and tlie patient may fall into a state of com-
plete dementia.
In the course of the disease, the patient suffers from attacks of
vertigo. This symptom usually comes on at an early period, and con-
tinues to distress the patient throughout. The patients feel as if they
themselves were being turned round, or as if surrounding objects were
whirling around them. They suffer greatly from sleeplessness and
violent headache.
Apoplectiforin or epileptiform seizures have been observed in a small
number of cases ; they are apparently analogous to the apoplectiform
attacks which occur in general paralysis of the insane. They are
characterized by the development of grave cerebral symptoms, and are
accompanied by a considerable elevation of temperature. After slight
premonitory symptoms, such as a feeling of pressure in the head, there
is a partial loss of consciousness, which in a few hours may develoj)
into coma. The face is red and hot, the pulse is quick, and the tem-
perature of the body rises to 104° F. or 105° F. In most cases hemi-
plegia with muscular flaccidity, and on rare occasions rigidity, is
present from the outset of the seizure. After one or two days the
temperature falls, the patient sinks into a quiet sleep from which he
may be readily roused, and he feels, on awaking, comparatively well.
Hemiplegia, hov/ever, persists for a few days longer, and then gradu-
ally disappears. These attacks may be repeated several times in the
course of the disease, recurring in some cases every few months, but
each is followed by an aggravation of the general symptoms, and death
sometimes occurs during an attack.
(2) Cerebral Multiple Sclerosis. — In this form of the disease, which
is rarely observed, the psychical disturbances are predominant. The
tremor is said to precede the paralytic manifestations, but in other
respects the course of the affection does not differ greatly from the
cerebro-spinal variety.
C H O K E A . 679
(8) Spinal Multiple Sclerosis. — The spinal fonii of the affection is
characterized by absence of the cerebral symptoms, particularly nys-
tagmus, tremor on voluntary effort, vertigo, apoplectiform attacks, and
psychical disturbances. The symptoms of the spinal form of multiple
sclerosis often simulate those of a primary lateral sclerosis, amyotrophic
lateral sclerosis, or locomotor ataxia, but in the first disease symptoms
are usually superadded Avhich do not belong to the symptoms of the
classical forms of the last three diseases. The course of multiple
sclerosis is somewhat variable, the average duration being from five to
ten years. The first stage extends from the commencement of the
symptoms up to the appearance of marked paralysis with contractures.
This stage occasionally begins Avith cerebral symptoms, consisting of
headache, vertigo, and unsteady gait, but most commonly it commences
■with paresis of the lower extremities like that caused by a primary
lateral sclerosis, and in such cases the nature of the disease may not be
recognized until the appearance of the characteristic tremor. In other
cases the disease begins by an apoplectiform attack or gastralgic dis-
turbances, while paralyses, disorders of coordination, tremor, and other
symptoms are added in (juick succession. The progress of this stage is
often interrupted by remissions or improvements, but the nature of the
disease is essentially progressive, and at the end of from two to six
years the second stage of the disease is constituted by the appearance
of marked and persistent paralysis with contractures. During the
second stage, which lasts from four to six years or more, the nervous
symptoms remain more or less stationary, and the general nutrition is
but little impaired. In the third stage of the disease the patient loses
his appetite and becomes emaciated, the bladder is paralyzed, cystitis
and bedsores appear, and the patient dies from septic fever. In other
cases death is caused by a bulbar paralysis, or by some intercurrent
disease like pneumonia, pleurisy, or phthisis.
Ill, CHOREA.
Etiology. — Heredity plays an important part in the production of
chorea, but the transmission is probably always indirect. The disease
chiefly attacks children, often occurring about puberty, although chil-
dren at the breast and young women are sometimes attacked. Girls
are much more frequently affected than boys. Everything which aug-
ments the excitability of the nervous system during the period of sexual
develoimient, such as premature excitement of the sexual passion, onan-
ism, or any undue emotional disturbance, increases the tendency to
680 CHOREA.
chorea. But the most usual predisposing causes in adults are preg-
nancy and menstrual disorders, and chlorosis. That some causal rela-
tionship exists between articular rheumatism and chorea has been known
since the beginning of the century, but the true nature of this relation-
ship is not yet accurately ascertained. Out of two hundred and four-
teen cases of chorea analyzed by Dr. Moury, thirty-three had suffered
from rheumatic fever and twenty-three from rheumatic jjains, while in
nine cases the history of rheumatism was very doubtful, tliese figures
o-iving from twenty-nine to thirty-two per cent, of cases in which a
rheumatic history could be traced. Chorea occurs frequently after
scarlet fever, a fact which may probably be explained by the frequency
with which scarlet fever is followed by rheumatism. Chorea sometimes
occurs during pregnancy. It is mt>st frequent during first pregnancy,
but it is sometimes repeated in the same patient in subsequent pregnan-
cies. It appears more frequently during the first than the second half
of pregnancy, but it sometimes begins in the later months, and may
continue up to the time of delivery or beyond it. The majority of
those affected are from twenty to thirty years of age. The disease is
more prevalent in large cities tlian in the country, and race appears to
influence the production of the disease, inasmucli as in South America
the black is much less frequently attacked than the white population.
Of the exciting causes of cliorea, the most frecjuent and important are
emotional disturbances, such as fright, sorrow, and discontent. Hys-
terical girls and those who are strongly predisposed to chorea, or wlio
have already suffered from an attack, may acquire the disease from
imitation of others suffering from it.
Symptoms. — The development of tlie characteristic phenomena of
chorea is generally preceded for a variable period of days or weeks by
various premonitory symptoms. The most usual of these are afforded
by changes in the character and disposition of the patient, who becomes
forgetful, inattentive, fretful, and discontented or apathetic, while the
intellectual powers are impaired. The irregular spasmodic muscular
contractions of chorea are not unfrequently ushered in by a slight
dragging of one of tlie lower extremities, with a tendency to walk in a
curved line and liability to let objects fall from the hand. Tbese mani-
festations of the approaching disease are probably due, in some degree,
to irregular muscular contractions, but are largely dependent upon
muscular weakness, and in some cases paralysis may be so pronounced
that the case may be mistaken for hemiplegia. The characteristic
choreic movements generally begin in the small muscles of the face and
in those of a hand. They consist at first of grimaces and other con-
tortions of the face, and slight jerking movements of the fingers and at
SYMPTOMS. 681
the wrist-joint, with pronation of the forearm, Avhen the patient is con-
scious of being observed or is excited from any other cause ; these soon
increase in intensity and persist during repose.
The irreguLar contractions soon extend so as to involve all the voluntary
muscles, when the affection may be called f/eneral chorea, or they remain
more or less limited to the muscles of one-half of the body, when the
disease is called unilateral chorea or hemichorea.
G-eneral Chorea. — When once the disease is fully established the
symptoms are quite characteristic, and it would be difficult to find
phrases more expressive of the disorderly muscular movements than
'• insanity of the muscles," adopted by Bellingham, and " folic muscu-
laire" by Bouillaud.
The features undergo every variety of contortion. The brow is knit
and immediately expanded ; the eyebrows are elevated and the next
moment depressed, or one may be elevated while the other is lowered ;
the eyelids open and close alternately ; the eyeballs are quickly rotated
in different directions ; and the labial commissures are suddenly drawn
outwards, and as quickly retracted. These opposite movements succeed
one another with such rapidity that the fiice presents in quick succession
the most contradictory expressions, such as those of delight, vexation,
and anger.
The tongue is thrust out of the mouth, and quickly retracted and
rolled about from side to side ; the jaws are separated and closed, it may
be with so much violence that teeth are broken, or the tongue and cheeks
are severely bitten ; lateral displacements of the lower jaw are frequently
observed, and the head is jerked suddenly from one side to the other,
while the facial grimaces by which the movements of the jaws, tongue,
and head are accompanied add to the comical appearance presented by
the patient. The pupils are usually dilated and their reaction to light
is diminished.
The superior extremities execute every variety of movement, the
shoulders are elevated, then lowered, and immediately afterwards drawn
backwards or forwards ; the arm and forearm are moved at the shoulder-
and elbow-joint in every possible direction ; the hand is alternately pro-
nated and supinated, flexed and extended ; and the fingers are at one
moment extended and spread apart and at the next flexed. These
movements are combined in such varied ways that a gesticulatory agita-
tion is produced which defies description.
The muscles of the trunk are implicated, and their unequal disorderly
contractions produce sudden lateral and antero-posterior deviations of
the vertebral column, which in certain cases may be so violent that
the patient is thrown from his chair or out of bed. The muscles of the
682 CHOREA.
lower extremities also undergo irregular contractions, causing eversion
and inversion of the foot and various contortions of the toes, as well as
movements at the larger articulations. The respiratory j-hvthm becomes
irregular and jerky, and on laryngoscopic examination the vocal cords
have been observed to act in an irregular and disorderly manner.
Choreic movements may persist during repose, and are much ex-
aggerated during voluntary effort and when the patient is under obser-
vation or excited in any way, but they cease during sleep, and also
under the influence of chloroform, in all but very aggravated cases. In
cases of moderate intensity delicate manual operations, such as those
required for writing, sewing, and playing upon musical instruments,
become alone impossible ; while operations, like eating, requiring less
complicated adjustments for their performance, are still effected, although
in an imperfect and roundabout manner, and after frequent interrup-
tions from the involuntary contraction of antagonistic muscles.
In aggravated cases it becomes impossible to execute almost any in-
tended movement. When the patient endeavors to carry anything to
his mouth, such as a glass of water, the progress of his arm is arrested
by a series of jerks and contradictory movements which may scatter
the contents of the glass in every direction ; the patient cannot button
or unbutton his clothes ; the maintenance of the erect posture is
difficult or impossible; and even in the recumbent posture he is not
free from the danger of being thrust out of bed ; his clothes and linen
become worn out by constant rubbing; and the skin over the prominent
bones becomes erythematous and may ulcerate.
On the patient's being asked to show the tongue, he protrudes it with
a jerk, the mouth being opened to an unnecessary extent; the tongue
is immediately withdrawn, while the mouth and jaws close upon it with
violence. When the patient endeavors to speak, the convulsive action
of the facial muscles becomes aggravated ; his articulation is irregular,
jerky, drawling, or stammering; his voice is monotonous; and in
aggravated cases his speech is so disordered as to be almost if not
entirely unintelligible. Spasmodic contraction extends to the muscles
of mastication and deglutition, and consequently these functions are
performed imperfectly and with difficulty,
Hemichorea. — The spasmodic phenomena are sometimes limited to
the muscles of one-half the body, the unilateral variety occurring in
about one-fifth of all cases. Disorders of speech are usually more
marked when the right than when the left side is affected with spasm,
although speech is sometimes disordered Avhen the left side is solely
affected. Broadbent asserts that the muscles bilaterally associated in
their actions, and which are comparatively spared in hemiplegia, are
SYMPTOMS. 683
aftected to some extent on both sides in liemichorea. The other symp-
toms of hemichorea are the same as those of general chorea, and do not
require separate description.
Although spasmodic motor disturbance constitutes the most charac-
teristic feature of chorea, it must not be forgotten that a certain decree
of muscular weakness is always present, this being easy of recognition
in cases of hemichorea. Indeed, towards the termination of the affec-
tion or during its course, the choreic movements may be replaced by a
more or less complete hemiplegia or paraplegia, and we have already
seen that paralytic symptoms may precede the development of the char-
acteristic movements.
The electric excitability of the nerves and muscles is said to be in-
creased to both currents, a fact more readily proved in hemichorea than
in the bilateral variety.
The reflex excitability is said by some authors to be increased and
by others to be diminished.
Sensory disturbances are not frequently observed in chorea. Painful
points have been found at times in the course of the nerve trunks of
the affected region, while tenderness on pressure over the spinous pro-
cesses of some of the vertebrae is occasionally met with. At other times
cutaneous hyperaesthesia or hyperalgesia distributed over half or the
whole of the body has been observed, but anfesthesia of like distribution
is more common,
Vaso-motor and secretory disturbances are wanting, there are no
special trophic changes, and the general health does not suffer, except
in aggravated and chronic cases, in which the constant agitation and
want of sleep induce a condition of angemia and general marasmus.
Psychical disturbances are invariably observed in chorea. The
mental depression and irritability with which the disease begins usually
increase during its course. The patient is obstinate, taciturn, and even
violent towards parents and attendants. He suffers from impairment of
memory, incapacity for thinking, and general intellectual weakness.
At times there may be hallucinations of sight, especially at night, suc-
ceeded by a maniacal delirium, and according to the observations of
Marce, half of the cases in which this delirium supervenes terminate
fatally.
The pulse may be irregular, and the patient suffers from palpitation,
while a physical examination of the heart generally reveals the presence
of endocardial murmurs, either arising from disease of the valves or of
functional origin. Chorea is not usually accompanied by pyrexia, but
in severe cases, when there is violent muscular action, elevation of tem-
684
CHOKEA,
perature is not uncommon. When chorea is associated Avith acute rheu-
matism more or less fever is necessarily present.
Chorea usually runs a chronic course, the majority of cases lasting
from six to eight weeks, and aggravated cases four to five months.
Chorea frequently recurs, a fresh attack being excited by a slight emo-
tional disturbance, pregnancy, or the presence of an acute disease.
Chorea usually terminates in complete recovery. The disease is not
often fatal in children, but a fiital termination may occur from a com-
plication of rheumatism and endocarditis, or from cerebral symptoms,
consisting of collapse with complete muscular relaxation and involuntary
evacuations, and a final coma.
Morbid Anatomy. — Post-mortem investigation has not thrown much
light upon the nature of paralysis agitans. The chief changes which
have been discovered consist of obliteration of the central canal of the
spinal cord from increase of the epithelium of the ependyma, and pig-
mentation of the <2;ano;lion cells of the column of Clarke, anterior horns,
olivary body, and corpus dentatum of the cerebellum. Slight evidences
of sclerosis were found in the lateral columns of the cord as well as in
the corpora striata and the hemispheres of the brain.
Multiple sclerosis consists of a chronic infiammation which appears
in well-defined nodules, and is widely distributed throughout the
Fi<». 181.
Section ok the Anterior Oray Horn of the Cervical Enlargement of the Spinal Cord from a
Case of Chorea that died on the Foirtii Day of Scarlet Fever. (Bury.)
cc, Otntral canal ; nc, Anterior commissure ; A, Anterior horn.
nervous system. In the spinal cord these nodules vary from the size
of a hemp seed to that of a bean, but they often become confluent and
appear to attain a much larger size in the brain. On section the
MO K BID ANATOMY.
685
nodules appear gray or grayish-yellow, and when exposed to the air
change to a salmon color ; they are translucent or opaque, irregular or
oval in shape, generally isolated and circumscribed, but occasionally
confluent, and are in consistence dense, tough, even cartilaginous, but
on rare occasions semifluid and gelatinous. The distribution of the
nodules is very variable. On making successive transverse sections of
the cord the nodules will appear in one or both the lateral columns at
one level, in the posterior columns at another, in the gray substance at
a third, and in the whole transverse area of the cord at a fourth. The
Fig. 182.
Section of the Cervical Region of the Spinal Cord from a Case of Chorea. (Young )
cc, Central canal ; A and P, Anterior and Posterior horns respectively.
fjivorite sites in the cerebral hemispheres are the Avhite substance of the
centrum ovale, the septum lucidum, the corpus callosum, the basal gan-
glia, and the walls of the lateral ventricles. In the cerebellum the
nodules are generally found in the white substance. The cortices of
the cerebellum and cerebrum are singularly free from nodules. The
anterior and posterior roots of the spinal nerves have been found dis-
eased, and the cranial nerves, in tlieir passage along the base of the
skull, are particularly liable to be affected. The number of nodules
which are present in one case is very variable, a few only being ob-
served in some cases, while in others hundreds may be counted*.
In most fatal cases of chorea which have been examined after death,
small fibrinous vegetations have been found studded along the edges of
686 CHOREA.
the mitral valve. Various changes have been described by different
observers as having been met with in the nervous system. These
changes, according- to Dr. Dickinson, consist of dilatation of the medium
sized arteries and veins throughout the substance of the brain and
spinal cord, exudation, small hemorrhages, and patches of necrotic
softening, or, in chronic cases, of sclerosis in the neighborhood of the
vessels. These changes were more pronounced in the corpora striata,
optic thalami, the anterior perforated spaces, and at the junction of
the posterior gray horns and central column of the spinal cord (Fig.
181). In a fatal case of chorea examined by myself, all the vessels
of the spinal cord were found more or less distended with red blood-
corpuscles, and in some sections a fibrinous plug, which distended
the vessel, was observed in the anterior or antero-lateral arteries
(Fig. 182). Spots of necrotic softening were also observed in the
basal ganglia.
3Iorhid Physiology. — The tremors of paralysis agitans are most
probably caused by a loss of the balance normally existing between the
regulative functions of the cerebrum and cerebellum. The attitude of
paralysis agitans is, as lias been pointed out by Dr. Hughlings-Jackson,
the opposite of that of tetanus. During a tetanic seizure the action of
the extensors of the trunk and lower extremities predominates, and the
body is arched backwards ; iji paralysis agitans the action of the flexors
predominates, so that the dift'erent segments of the trunk and extremi-
ties are flexed upon one another. In tetanus the muscles, the actions
of which must have gradually prcdominateil in the course of evolution
so as to attain the erect posture, are excited to increased activity,
while in paralysis agitans the same muscles, speaking broadly, become
relatively paralyzed, and there is a gradual reduction of the human to
the animal posture. In the stage of propulsion the attitude of the
patient is very similar to that of a dog attempting to walk on his hind
legs. The phenomena of propulsion are caused partly by the forced
attitude of the patient and partly by the great slowness with which his
movements are executed. When once the heel is raised from the
ground by contraction of the muscles of the calf, the patient on getting
up must balance himself on his toes, but in walking the forward in-
clination of the body tends to make the line of gravity pass in front of
the active leg. The position is to some extent the same as that assumed
by a person in running. But a healthy runner is able to take rapid
and long strides with the passive leg, and by the time it is brought to
the ground it is well in advance ef the line of gravity, and the body is
thus kept from falling.
In paralysis agitans, however, the rigidity of the muscles prevents
MORBID PHYSIOLOGY. 687
the patient from taking a long j^tride, and the slowness with which the
movements are executed renders it impossible for him to plant the leo-
that is about to become active in front of the line of gravity, and con-
sequently the patient tends to fall forwards at every step. In retropul-
sion the line of gravity ever tends to fall behind the ball of the toe of
the active leg, and the other leg cannot be moved backwards with suffi-
cient celerity to enable the patient to place it far enough behind the
retreating centre of gravity in-order to ari-est the backward movement.
It is difficult to connect the chief symptoms of paralysis agitans with
the morbid changes which have been discovered after death, but it must
be remembered that these changes are not limited to the spinal cord,
but are widely diffused over the encephalo-spinal centres and conduct-
ing paths. There is at least nothing in the changes which have been
discovered after death incompatible with the idea that paralysis agitans
is a dissolution of those nervous mechanisms whose action must have
gradually predominated in passing from the quadrupedal position of
animals to the bipedal position of man.
In multiple sclerosis the nodules are widely distributed over different
parts of the nervous system, and the implication of different parts of the
nervous system, having different functions, affords a ready explanation
of the chief symptoms of the disease. Implication of the lateral columns
explains the paresis, contractures, excess of the tendon-reflexes, and the
phenomena grouped under the name of spinal epilepsy, of the posterior
columns, the ataxia; of the anterior horns, the muscular atrophy; and
of the bulbar nuclei, the labio-glosso-pharyngeal paralysis which may
be present in different cases, while the student who is tolerably w^ell ac-
quainted with the physiology of the nervous system will be able to con-
nect the remaining symptoms with the appearance of those nodules in
different parts of the cerebrum, cerebellum, pons, and crura. Charcot
attributes the characteristic tremor of multiple sclerosis to the long per-
sistence of the axis-cylinders in the nodules of sclerosis. Conduction will
take place through the nerve fibres long after they are involved in the
nodules of the disease, but when once the medullary sheath is destroyed
the conduction will be so retarded that the impulses from the cortex do
not pass in a sufficiently quick succession to cause a continuous con-
traction. It has, however, been pointed out by Erb, that the charac-
teristic tremors are absent in purely spinal cases, and that in all cases
in which tremors were present during life nodules were discovered after
death in the medulla oblongata, pons, crura cerebri, and other parts of
the brain. It Avould seem, therefore, that in this disease again the
tremors are caused by a loss of balance between the regulative functions
of the cerebrum and cerebellum.
688 CHOREA.
In chorea the lesions are supposed, by Broadbent and Hughlings-Jack-
son, to be localized in the corpus striatum, optic thalamus, and cortex of
the brain, but they are still more widely distributed over the nervous
system. It was first suggested by Kirkes that chorea is caused by mul-
tiple embolism of the vessels of the brain and spinal cord, produced by
fibrinous particles being Avashed off from the valves of the heart after
endocarditis. This theory, which has been elaborated by Dr. Hughlings-
Jackson and others, has many facts in its favor, and now there can
scarcely be a doubt that chorea is often caused by multiple embolism.
Choreiform movements have, indeed, been produced in animals by Dr.
Angel Money, by injecting inert powders into the circulation. At the
same time, it must be remembered that chorea may occur in persons who
are free from suspicion of a cardiac complication, and it seems likely,
therefore, that the affection may be caused by other conditions besides
multiple embolism. It seems likely, indeed, that the symptoms of
chorea may be caused in the cliildren of neuropathic families by condi-
tions which lower the nutrition of the nervous system.
Treatment. — Paralysis agitans being a progressive disease, its treat-
ment can only be palliative. The internal remedies which have been
used are carbonate of iron, chloride of barium, hyoscyamus, strychnine,
ergot, belladonna, quinine, zinc, nitrate of silver, chloride of gold,
arsenic, and phosphorus, and of these probably the last two are the
most deserving of trial. Morj)hia and other narcotics are necessary
adjuncts of treatment in the later stages of the disease, when the patient
is harassed by restlessness and sleeplessness, and both chloral and
bromide of potassium may then be of use.
Multiple sclerosis must be treated on the same general principles as
chronic myelitis. The most promising method of treatment appears to
be the persistent application of the galvanic current to tlie spine, hydro-
pathy, nitrate of silver, phosphorus, cod-liver oil, and nourishing but
unstimulating diet. The greatest improvement that I ever saw take
place in this disease was in the case of a man who, acting on my advice,
changed the sedentary occupation of a clerk in a factory for that of a
farmer.
Ohorea should be treated by the careful regulation of the diet, and
by the removal of every source of reflex irritation, such as intestinal
worms. If anaemia be present, iron may be given, and if rheumatism
complicates the case, salicylate of sodium must be administered, while the
hot vapor bath may be of service. The child should in all cases be
removed from school, and all intellectual work ought to be suspended.
Of internal remedies, arsenic and zinc are the most useful. Arsenic is
best given in the form of the ordinary liquor arsenicalis, and of this
MORBID PHYSIOLOGY. 689
preparation the dose should be from two to five minims gradually in-
creased up to from five to ten minims three times a day, according to
the age of the patient. The sulphate is the most convenient salt of
zinc to employ. A dose of two or three grains may be given at first,
three times a day, and the. dose should be gradually increased daily until
the almost incredibly large quantity of from fifteen to twenty grains is
taken three times a day. If nausea or vomiting is produced, the dose
should be slightly diminished for a few days until tolerance is established.
Bromide of potassium or chloral hydrate are useful when psychical dis-
turbances and sleeplessness are prominent symptoms, but they do not
appear to exercise a decided influence on the course of the disease. At
the Cheadle Convalescent Hospital Dr. Wausburgh Jones is having
marked success in the treatment of chorea, by rest in bed, seclusion,
overfeeding, and massage, or by the S. Weir-Mitchell treatment.
44
CHAPTEK XXI.
GENERAL DIAGNOSIS.
Before brinerino; the work to a close, it will be desirable to make a
few remarks on diagnosis, and although much of what we shall have to
say will be a mere repetition, yet it will prove useful to discuss the
general principles of this important subject disencumbered from the
details of clinical descriptions. The diagnosis of the diseases of the
nervous system may be divided into: 1, the clinical; 2, the topo-
graphical; and 3, the pathological diagnosis.
1. CLINICAL DIAGNOSIS.
With the view of arriving at a satisfactory clinical diagnosis, which
must form the basis of the other kinds of diagnosis, the patient must be
subjected to a methodical examination. The various tests which have
already been described must be systematically aj)plied in order to dis-
cover the sensory, motor, vaso-motor, trophic, and psychical disturbances
which may be present. At the end of the examination the observations
which have been made are systematized, when it is concluded that the
patient is suifering from local anfesthesia, paranesthesia, hemianaes-
thesia, local spasms, monospasms, unilateral convulsions, general con-
vulsions, atrophic paralysis, spasmodic paralysis, jiaraplegia, hemiplegia,
and monoplegia, either separately or in various combinations. It should
also be noted whether the disease is, in its mode of onset, fulminant, acute,
or chronic, and its origin idiopathic, traumatic, syphilitic, or arises from
any other cause. Our knowledge of many diseases is, indeed, so slender
that they admit of only a clinical diagnosis. When, for example,
general convulsions occur at irregular intervals and in association with
various emotional manifestations, we call them hysteria ; when they recur
at regular intervals in the absence of such manifestations, we call them
epilepsy ; when they occur as an acute affection without showing a
tendency to periodical recurrence, we call them eclampsia, these being
subdivided according to the cause of the symptoms into toxic, puerperal,
uraemic, febrile, and reflex convulsions ; and when no cause for them
can be assigned, we call them idiopathic convulsions.
TOPOGRAPHICAL DIAGNOSIS. 691
2. TOPOGRAPHICAL DIAGNOSIS.
In a large number of cases we are enabled to pass readily from the
clinical to the topographical diagnosis. In order to determine the
locality of the lesion, it is all important to remember the course of the
sensory conducting paths from the periphery up to their termination in
the sensory centres of the cortex of the brain, and of the motor con-
ducting paths from their origin in the motor centres of the cortex to
their termination, first in the spinal nuclei and then in the various
muscles. In reference to the sensory symptoms, it may be said that
when the disorder is more or less limited to the area of distribution of
the afferent branches of a particular nerve the lesion is situated in the
peripheral course of the nerve, when it is distributed pretty uniformly
over the lower half of the body and the lower extremities the lesion is
situated in the spinal cord, and when it is distributed over one lateral
half of the body the lesion is situated in the brain, the posterior third
of the posterior segment of the internal capsule being the part usually
affected. Similar remarks apply to the motor symptoms. When a
paralysis, for example, is limited to the muscles supplied by the
branches of a particular nerve, the lesion is likely to be situated in the
peripheral course of the nerve; when the paralysis is pretty uniformly
distributed over the lower half of the body the lesion is situated in.
the spinal cord, and when it is restricted to a lateral half of the body
the lesion is localized in the brain. The division of the various forms
of loss of motor power into atrophic and spasmodic paralyses is a most
important one for diagnostic purposes. In atrophic paralysis the lesion
is situated in the anterior gray horns of the spinal cord, in the fibres
which connect the ganglion cells of these horns with the muscles, or in
the affected muscles themselves. In the spasmodic paralyses the lesion
is situated in the motor centres of the cortex or in the conducting
paths which connect these centres with the motor ganglion cells of the
anterior gray horns of the spinal cord. Loss of the reflexes indicates,
as a rule, that the lesion is situated in the spinal reflex loops, Avhile
excess of them generally shows that it is situated in the motor centres
of the cortex, or in the conducting paths which connect these with the
spinal nuclei. General symptoms like headache, vomiting, optic
neuritis, incoherence, delirium, and loss of consciousness, indicate that
the brain is implicated, but they are of no further value in locahzing
the disease. Before proceeding further with our subject, it will be well
to mention some general difficulties which present themselves in local-
izing the lesion. The first is that the degree of the symptoms does not
692 GENERAL DIAGNOSIS.
by any means always correspond to the size and extent of the lesion.
A hemorrhage may, by suddenly rupturing some of the fibres of the
conducting paths and compressing others, give rise to sensory and
motor disorders out of proportion to the extent of the lesion, while a
slow growing tumor may, by gradually displacing and stretching the
fibres of the conducting paths, come to occupy the usual situation of
these paths without causing but a slight degree of motor or sensory
disorder. It may, indeed, be laid down as a general rule that acute
lesions are often much smaller, and chronic lesions much larger than
the degree and character of the symptoms would lead us to expect.
The second difficulty is that a lesion not only causes direct symptoms
from irritation or destruction of the nervous tissues in its immediate
vicinity, but often produces marked indirect symptoms by excitation or
inhibition of remote parts, Goltz, for example, found that section of
the spinal cord in the cervical region in dogs causes immediate paralysis
of the power of erection of the penis, but if the animal survive for a
few days this function recovers, and an erection may be obtained by
reflex excitation. Indirect symptoms, having a similar import, are fre-
quently met with in disease, and this is particularly apt to be the case
when the lesion is situated in the brain. A small irritative lesion,
when situated in the cortex of the brain, may set up widely diffused
discharges, and thus give rise to extensive unilateral spasms or even to
general convulsions. A small hemorrhage in the substance of the
brain may, partly through the shock communicated to the whole organ
from the suddenness of the onset, and partly from the compression it
exercises upon the nervous tissues by encroaching upon the volume of
the cranial cavity, suddenly arrest all the functions of the organ, so
that the patient lies in an unconscious condition, and with almost com-
plete muscular relaxation. When the indirect symptoms are so pre-
dominant as in the example just given, it will not be found possible to
recognize the direct symptoms or to interpret their significance. But
in most cases the indirect symptoms tend to pass off in a few days, and
then the localization of the lesion may be detemiined. Having come
to the conclusion that the lesion is situated in the brain, the case must
now be approached with the view of determining its exact seat. Ordi-
nary hemiplegia, when persistent, is caused most frequently by disease
of the anterior two-thirds of the posterior segment of the internal
capsule or of the area of the lenticulo-striate artery. In the most
usual form of hemiplegia tlie arm is more paralyzed than the leg, but
in those comparatively rare cases in which the leg is more paralyzed
than the arm, the motor paralysis is unaccompanied by hemianaesthesia,
and the lesion is then situated in the posterior two-thirds of the pos-
TOPOGRAPHICAL DIAGNOSIS. 693
terior segment of the internal capsule or in the area of the lenticulo-
optic artery. In some cases the arm is more paralyzed than the leo-
and yet the hemiplegia is accompanied by hemianesthesia, and the
lesion is then situated in the optic thalamus and partially involves the
posterior part of the internal capsule. If the hemiplegia is transient
the lesion is situated near the motor tract without causing permanent
damage to its fibres, most commonly in the lenticular nucleus. Mono-
plegia? are caused by lesions in the motor area of the cortex, or in the
centrum semiovale between the motor centres and the internal capsule.
If the paralysis in such cases be preceded or accompanied by unilateral
convulsions, the lesion is situated in or near the cortex. Monopleo-ie
caused by disease of the motor cortex or of the underlying white sub-
stance, are often accompanied by considerable diminution of the mus-
cular sense and cutaneous sensibility of the affected limb. The exact
situation of the disease when the cortex or underlying white substance
is its seat, may be determined by reference to Terrier's diagrams and
Pitre's vertical sections of the cerebral hemispheres. In persistent
motor aphasia the lesion is situated in the posterior part of the third
frontal convolution or in the white substance immediately underlying
it ; but if recovery takes place in a few weeks or months, it is in or
near the knee of the internal capsule. In sensory aphasia the lesion is
situated in the angular gyrus or first and second temporo-sphenoidal
convolutions, while in mixed motor and sensory aphasia, which is accom-
panied by hemiplegia, it is widely distributed over the motor area of the
cortex. A transient aphasia may precede an attack of migraine head-
ache, or follow a minor attack of epilepsy. Hemiansesthesia, with
implication of the special senses, is caused by disease of the posterior
part of the internal capsule. In some of these cases the visual affec-
tion consists of an amblyopia of the eye on the opposite side to the
lesion, whilst in others it consists of a bilateral hemianopsia. In hemi-
anaesthesia, with bilateral hemianopsia, the lesion, which is always
situated in the optic thalamus, reaches sometimes so far back as to
implicate the external geniculate body, but at other times it is situated
opposite the middle part of the posterior segment of the internal cap-
sule, and much too far forwards to reach that body. A tumor in any
of the basal ganglia may cause hemianopsia by compression of the
underlying optic tract. Homonymous hemianopsia may also be caused
by a lesion in the white substance or in the cortex of the occipital lobe.
Cortical or centrum ovale hemianopsia may be suspected rather than
tract hemianopsia if the blind is not separated from the sensitive area
of each retina by a sharply defined straight line, if a quadrant only of
each field is lost, or if there is a considerable restriction of the pre-
694 GENERAL DIAGNOSIS.
served halves of the fields of vision, especially on the side opposite the
lesion. When the lesion is situated in the left hemisphere the hemi-
anopsia is often accompanied by word-blindness. In convulsive attacks
which begin with a visual aura consisting of colored vision or hallucina-
tions of sight, it may be inferred that an irritative lesion is situated in
or near the cortex of the occipital lobe. If the convulsion begins with
rattling noises in the ears or hallucinations of sound, an irritative lesion
is situated in or near the cortex of the first or second temporo-con-
volutions.
It is possible that a destructive lesion in this area may give rise to
some degree of deafness of the ear on the opposite side, but this sign is
not to be much depended upon. If the lesion, however, is situated in
the left hemisphere the patient suffers from word-deafness, which is
often accompanied by loss of smell in the nostril on the side of the
lesion from softening of the external root of the olfiictory tract. If a
person who is suffering from word-deafness suddenly becomes absolutely
deaf without there being any evidence of local disease of the ears, there
are symmetrical lesions in both temporo-sphenoidal lobes on a level with
the first and second convolutions.
Lesions in the remaining parts of the cortex of the temporo-sphenoidal
lobe and in the underlvincr white substance do not give rise to definite
localizing symptoms, A tumor of this lobe may by compressing the
optic tract give rise to hemianopsia, and the internal capsule to hemi-
plegia. The Island of Riel is, as we have seen, the embryonic area of
the cortex, and lesions of it are often unaccompanied by any localizing
symptoms, but when situated near the junction of this lobe with the
operculum they give rise to a motor aphasia. IJut to return to the
internal capsule ; disease of the anterior segment does not give rise to
any definite symptoms. Charcot found softening of this segment in a
case in which there was considerable psychical disturbance during life.
Disease of the cortex of the prefrontal area of the brain with which the
anterior segment of the internal capsule appears to be connected, is
also often found in cases in which there had been considerable mental
disorder during life. If a patient with the general symptoms of a
cerebral disease lies in a somnolent condition without giving evidence
of localized sensory or motor disorder, the lesion is most probably situ-
ated either in the cortex or the white substance of the prefrontal lobe.
In cases of unilateral convulsions which begin by spasm of the side of
the face, if loss of consciousness precedes the spasm, the lesion is most
probably situated in the prefrontal lobe.
If paralysis of the limbs on one side is associated with paralysis of
one of the cranial nerves on the other, the lesion is situated in or near
TOPOGRAPHICAL DIAGNOSIS. 695
the pyramidal tract of the side opposite the paralyzed limbs somewhere
in its course between the internal capsule and the crossing in the medulla
oblongata. When the third nerve of one side and the limbs on the
other are simultaneously paralyzed, the lesion is in the crus cerebri ;
when the fifth is the cranial nerve affected, the lesion is situated about
the middle of the pons ; when the sixth or seventh, the seat is about
the lower or posterior end of the pons ; and Avhen the twelfth, it is
localized in the medulla, but the last occurs only very rarely. In apo-
plectic lesions of the upper part of the pons the pupils are often strongly
contracted from irritation of the nuclei of the third nerve. In partial
anaesthesia of one side of the face and anaesthesia of the trunk and
limbs on the opposite side, the lesion is situated in the restiform body in
or near the ascending root of the fifth nerve. Unilateral lesions of the
pons implicate the transverse fibres coming from the middle peduncle
of the cerebellum, and consequently give rise to a tendency to fall to
the side of the lesion.
Disease of the basal ganglia do not give rise to very definite symp-
toms, except when they are sufficiently large to compress or rupture the
fibres of the internal capsule. If a patient has sufiered from a slight
apoplectic attack with right hemiplegia and aphasia, from which recovery
takes place in a few weeks leaving only a slight exaggeration of the
tendon reflexes at the wrist, the lesion is most probably a hemorrhage
limited to the left lenticular nucleus. If the same patient has, some
time afterwards, a second apoplectic attack with left-sided hemiplegia
and aphasia, from which recovery also takes place in the course of a few
weeks, leaving, in addition to a slight exaggeration of the tendon-reflexes
at the left-wrist, bulbar symptoms like those of progressive labio-glosso-
pharyngeal paralysis, both lenticular nuclei will most probably be found
to have been destroyed by hemorrhage. Lesions strictly limited to the
caudate nucleus or to the inner half of the optic thalamus cause no
localizing symptoms. If, however, a person has a slight apoplectic
attack which is at first attended with little or no loss of consciousness,
and becomes after a few minutes or hours suddenly profoundly comatose
with complete resolution of all the limbs, or paralysis of the limbs on
one side and spasmodic contraction of those on the other, dilated and
fixed pupils, and a great initial lowering followed by a rapid rise of tem-
perature, a hemorrhage of the caudate nucleus or of the inner part of
the optic thalamus has ruptured into the general ventricular cavity.
When an apoplectic attack causes hemiplegia with hemianaesthesia,
which is followed by post-hemiplegic chorea or athetosis, the lesion is
situated in the area of the posterior external artery of the optic thalamus,
but it is not known whether the mobile spasms are caused by the damage
696 GENERAL DIAGNOSIS.
done to the ganglion itself or by partial injury of the internal capsule.
Bilateral athetosis and the choreic movements which attend some of the
spasmodic paralyses of infancy are caused by a parencephalus or uni-
lateral atrophy of the motor area of the cortex of the brain. If a
severe apoplectic attack, followed by a prolonged period of partial un-
consciousness and death after a few weeks, is attended by hemiplegia
and hemiangesthesia, rotation of one eyeball downwards and outwards
and of the other upwards and outwards, dilating pupils on exposure to
light, and paroxysms of Cheyne-Stokes breathing, the lesion Avill be
found to have been a hemorrhage which has completely destroyed the
whole of the pulvinar of the optic thalamus with the posterior part of
the internal capsule, and to have made its way inwards so as to be only
separated from the cavity of the third ventricle by a thin layer of tissue,
and backwards so as to have undermined and partially destroyed the
anterior tubercle of the corpora quadrigemina. Lesions which are
more or less limited to the corpora quadrigemina do not probably give
rise to distinctive symptoms, and the same remark applies to lesions of
the corpus callosum, although cases of tumor in this situation have been
recorded by Erb and Bristow.
Loss of one or more of the functions of the cranial nerves suggests
the possibility of an intracranial growth at the base of the brain, or a
basal meningitis. Complete loss of smell with the presence of double
optic neuritis, or other symptoms of a chronic intracranial disease, indi-
cates a growth in the anterior fossa of the skull. Complete loss of
sight of one eye, with atrophy of the optic disk and paralysis of the
oculo-motor nerves and of the ophthalmic division of the fifth, indicates
most probably a chronic meningitis with much thickening around the
optic foramen and temporo-sphenoidal fissure. If, in addition to these
symptoms, there is temporal hemianopsia of the other eye, the lesion is
a tumor situated over the cavernous sinus and coming as far forwards
as the optic foramen. The presence of double temporal liemianopsia
shows pressure on the centre of the optic commissure either by tumor of
the sella Turcica or rarely by distention of the third ventricle by fluid.
As the lesion increases in size complete blindness may result, but most
frequently it grows to one side and gives rise to blindness of one eye,
with temporal hemianopsia of the other.
When hyper?esthesia or anaesthesia in the area of distribution of the
fifth nerve is accompanied by neuroparalytic ophthalmia, with or without
masticatory paralysis, the lesion is likely to be situated in the middle
fossa of the skull, and when both third nerves are paralyzed in associa-
tion with some degree of single or double hemiplegia, and the general
symptoms which indicate an intracranial growth or abscess, the lesion
TOPOGRAPHICAL DIAGNOSIS.
697
is situated in the interpeduncular space. When the fifth and sixth,
the seventh and eighth, or the eleventh and twelfth nerves are simul-
taneously paralj^zed, the lesion is likely to be in the posterior fossa of
the skull rather than in the substance of the pons and medulla ob-
longata. When a tumor is situated near the cortex of the brain the
skull is often tender to percussion at the the point at which the growth
comes nearest to the surface.
View of the Posterior Surface of the Mepulla (after Erb),
the roof of the fourth ventricle being removed to show the rhomboid sinus clearly. The left half of the
figure represents: On, funiculus cuneatus, and g. funiculus gracilis; 0, obex; sp, nucleus of the spinal
accessory ; p, nucleus of pneumogastric, p + sp, ala cinera ; R, restiform body ; XII', nucleus of the
hypoglossal; t, funiculus teres; a, nucleus of the acousticus ; m,, strife meduUares ; 1, 2, and 3, middle,
superior, and inferior cerebellar peduncles respectively ; /, fovea anterior ; 4, eminentia teres (genu nervi
facialis) ; 5, locus coeruleus. The right half of the figure represents the nerve nuclei diagrammatically ;
V, motor trigeminal nucleus ; V, median, and V", inferior sensory trigeminal nuclei ; VI, nucleus of
abducens ; VII, facial nucleus ; VIII, posterior median acoustic nucleus ; VIII' anterior median,
VIII" posterior lateral, VIII'" anterior lateral acoustic nuclei ; IX, glosso-pharyngeal nucleus ; X, XI,
and XII, nuclei of vagus, spinal accessory, and hypoglossal nerves respectively. The Roman numerals
at the side of the figure, from V to XII, represent the corresponding nerve roots
When the lesion is situated in the spinal cord below the crossing of
the pyramidal tracts, it gives rise to a spasmodic paralysis of all muscles
innervated from below the level of the disease, as well as to more or
less anaesthesia of the inferior part of the body. The muscles supplied
from the level of the lesion suffer from atrophic paralysis, the reflexes
698
GENERAL DIAGNOSIS,
of the affected segment of the cord are abolished, and a line of hyperaes-
thesia passing round the body generally sepai'ates the anaesthetic and
sensitive areas.
In the various forms of atrophic paralysis the situation of the lesion
must be inferred from the grouping of the affected muscles. In oph-
thalmoplegia externa the lesion is situated in the nuclei of the third
Fig 184.
Transparent Lateral View of the Mediila (alter Erb),
showing the relative positions of tlie most important nuclei ; right half of the medulla, seen from the
surface of section ; the parts that lie closer to this surface are deeiH'r shaded. Diagrammatic. Vy, pyra-
midal tract; Py, Kr, decussation of pyramids; 0, olivary body; 0», superior olivary body; V, motor,
V, middle sen.sory ; V", inferior sensory nucleus of trigeminus; VI, nucleus of abducens; c.f, genu
facialis nervi ; VII, nucleus facialis ; VIII, posterior median acoustic nucleus ; IX, glosso-pharyngeal
nucleus; X, nucleus of vagus; XI, nucleus of the acrcssorius ; XII, hypoglossal nucleus; Kz, nucleus
of the funiculus gracilis; Rv, trigeminus root; RVI, roof of the abducens ; KVII, root of facialis
and sixth nerves; in progressive labio-glosso-laryngeal paralysis and
the acute form of the affection caused by occlusion of a branch of the
basilar artery, the lesion is situated in the inferior part of the floor of
the fourth ventricle (Figs. 183 and 184); and in the usual forms of
acute atrophic spinal paralysis of infants and adults the lesion is situated
in the anterior gray horns of the spinal cord, the exact level of the
PATHOLOGICAL DIAGNOSIS. 699
lesion in the longitudinal extent of the cord being indicated by the
particular muscles attacked as well as by the reflexes which are found
abolished.
When an atrophic paralysis is restricted to the muscles supplied by
a particular nerve, and Avhen there is at the same time more or less
anaesthesia in the area of distribution of the sensory branches, the
lesion is situated in the peripheral course of the nerve. In atrophic
paralysis from disease of nerves the muscles are affected according to
the distribution of the branches of the diseased nerve, but in spinal
atrophic paralysis they are affected in groups according as they are
associated in their functions. If the motor disorder consists of an
incoordination and not of a spasm or paralysis, the disease is likely to be
either tabes dorsalis, Meniere's disease, sclerosis in patches, or a cere-
bellar lesion. In tabes the patellar tendon-reflexes are absent, and the
gait is ataxic; in Meniere's disease the patient is deaf and suft'ers from
whistling noises in the ears ; in multiple sclerosis the patellar tendon-
reactions are generally exaggerated, and the patient manifests the
tremor, scanning speech, and other characteristic phenomena, while in
cerebellar disease the patellar tendon-reactions are generally exaggerated,
and the salt is a reel and not a true ataxia.
3. PATHOLOGICAL DIAGNOSIS.
The aim of pathological diagnosis is to determine the nature of the
lesion no matter where it may be situated. It may be laid down as a
general rule, but one requiring numerous qualifications in practice, that
the diseases which develop the symptoms of depression in the course of
a few minutes or a few hours, and without being set up by traumatic or
toxic causes, are of vascular origin ; that the diseases which take from
a few days to a few weeks for the full development of the symptoms,
and in which the symptoms of depression are preceded by those of
irritation, are of inflammatory origin; and that the diseases which take
from two to six months for the full development of their symptoms,
and in which the primary symptoms of irritation are either absent or
obscured by the more prominent symptoms of depression, are of degen-
erative origin, or are due to a slow and gradual compression of nervous
tissue by the growth of a new formation.
(1) Vascular Lesions. — The vascular lesions Avhich are the most
frequent causes of disease of the nervous system are rupture with hem-
orrhage, embolism, and thrombosis. If a patient suddenly becomes
profoundly comatose without premonitory symptoms, and with or with-
700 GENERAL DIAGNOSIS.
out evidence of the presence of hemiplegia, the lesion is more likely to
be a hemorrhage rather than embolism or thrombosis. If the coma
passes off in a few hours or days Avithout leaving a trace of hemiplegia
or other grave symptoms, the lesion has probably been a cerebral conges-
tion, but if the coma has been somewhat prolonged, and if hemiplegia
persists, the lesion has been a hemorrhage. Hemorrhage is to be sus-
pected rather than embolism if an apoplectic attack occurs during the
degenerative period of life or after forty-five years of age ; if the arteries
at the wrist and temples are hard and knotty; if the left ventricle of
the heart is hypertrophied ; if the second sound of the heart is much
accentuated at the base; if the urine is abundant and of low specific
gravity, and if it contains a small quantity of albumen ; if the arterial
tension is high ; and if a well-marked arcus senilis and other signs of
degeneration of tissue are present. Ingravescent apoplexy is almost
always caused by hemorrhage, and when this form of hemorrhage
occurs in comparatively young people it may be suspected that an
aneurism has burst. If an apoplectiform attack, with or without hemi-
plegia, occur in a young or middle-aged person who is suffering from
valvular disease of the heart, the lesion is likely to be eml)olism. This
supposition is strengthened if the onset of the disease was not attended
by a profound loss of consciousness, and if a more or less persistent
aphasia is established. Embolism is, indeed, more probable than hem-
orrhage if the attack has supervened during the course of acute rheuma-
tism, chorea, or scarlet fever, even when no signs of valvular disease
can be discovered. Valvular disease may give rise to an aneurism of a
cerebral vessel and to subsequent rupture, and conseijuently the signs of
cardiac disease are only of value in determining the question of em-
bolism or hemorrhage when taken in conjunction with other symptoms.
Thrombosis of the arteries of the brain occurs in old aije from atheroma
and in middle age from syphilitic endarteritis.
Occlusion of a cerebral artery by thrombosis gives rise to an apoplectic
attack like that caused by an embolus, but in the former the attack is
preceded by premonitory symptoms which are wanting in the latter, and
the attack itself is often more gradual in its development in thrombosis
than either in embolus or hemorrhage. The premonitory symptoms
of thrombosis consist of headache, dizziness, loss of memory, and
general confusion, together with numbness and formication of one of the
limbs or of one-half the body. Syphilitic thrombosis is often preceded
by severe headache with nocturnal exacerbations, while other evidences of
syphilis may be obtained.
If an apoplectic attack supervenes in the puerperal state, or in the
course of exhausting diseases like phthisis and cancer, and in children
PATHOLOGICAL DIAGNOSIS. 701
after severe diarrhoea, the cause is most likely a thrombosis of one of
the cerebral veins or sinuses. It is also probable that the condition
known as asphyxia neonatorum, and which is followed by a spasmodic
paralysis with idiocy, is caused by thrombosis of one of the cerebral
veins occasioned by injury to the head during delivery.
Hemorrhage of the spinal cord occurs in comparatively young subjects.
It is liable to be mistaken for acute spinal atrophic paralysis, from which
it may be distinguished by the fact that the atrophic paralysis caused by
the local lesion is in hemorrhage accompanied by sensory disorders and
by spasmodic paralysis caused by implication of the posterior horns and
the sensory and motor conducting paths.
(2) Inflammatory Lesions. — The inflammatory nature of the lesion
must be determined by the mode of onset being more gradual than in
vascular lesions ; the symptoms of depression being preceded by. those
of irritation, and the presence during the development of the disease of
elevation of temperature and other febrile sym.ptoms. When once it is
concluded that the lesion is inflammatory the further classification of
the disease must be determined from the grouping of the symptoms and
the localization of the lesion.
(3) Degenerative Lesions. — It is difiicult to draAv any definite line of
demarcation between the secondary degenerations, which result from
chronic inflammation, and those diseases which are of degenerative orio-in
from the commencement. The development of the disease may be
chronic and progressive in both, and the chief reliance in diagnosis
must be placed upon the presence of symptoms of irritation and slight
elevation of temperature in the former and their absence in the latter.
Multiple cerebro-spinal sclerosis is a chronic degenerative disease,
probably of inflammatory origin, which, from the variability of its symp-
toms, is liable to be mistaken for various other diseases. It would be
difficult to believe that paralysis agitans and multiple cerebro-spinal
sclerosis were confounded with one another, were it not a matter of
history that the two diseases were only separated from one another
clinically for the first time by Charcot only a few years ago. Multiple
sclerosis is a disease of youth and middle age, and paralysis agitans
most commonly of advanced age. The tremor of paralysis agitans
consists of fine rapid oscillations, which persist during repose ; it may be
temporarily arrested by voluntary effort, and seldom implicates the
muscles of the head ; while the tremor of multiple sclerosis has a some-
what extensive sweep, ceases during repose, is excited or aggravated by
voluntary movements, and almost always implicates the muscles of the
head. In paralysis agitans decided loss of motor power is not developed
until long after the appearance of tremor, but in multiple sclerosis
702 GENERAL DIAGNOSIS.
paralysis precedes or soon follows the tremor. The nystagmus, scanninfr
speech, and other cerebral symptoms of multiple sclerosis are wanting
in paralysis agitans.
Multiple sclerosis, especially in its early stages, may be mistaken for
some one or other of the system diseases of the spinal cord, such as
locomotor ataxia, primary lateral sclerosis, amyotrophic lateral sclerosis,
or progressive labio-glosso-laryngeal paralysis, and it is not always
possible to be sure of the diagnosis until symptoms like nystagmus,
scanning speech, and tremor appear in the course of the disease, which
are more or less characteristic of multiple sclerosis, and never form jiart
of the system diseases. The hereditary form of locomotor ataxia de-
scribed by Friedreich is probably more allied to nmltiple sclerosis than
to the tabes dorsalis of adults. Mercurial tremor is sometimes so like
a moderately advanced case of multiple sclerosis that the former can
only be recognized from the latter by the history of exposure to its
cause. Hysterical tremor persists during repose, provided the patient is
conscious of being observed ; it may disappear for a long time and then
recur, and general hysterical symptoms are usually present. The dis-
orderly movements of chorea differ considerably from the tremor of
multiple sclerosis, but the diagnosis is not always easy when, as may
occasionally happen, choreiform movements complicate those proper to
multiple sclerosis.
The early stage of general paralysis of the insane may very readily
be mistaken for the early stage of multiple sclerosis. The hesitating
and indistinct speech of general paralysis is very like the scanning
speech of multiple sclerosis, and the tremors of the tongue and angle of
the mouth and of the hands in the former, may be mistaken for the
tremor which is so characteristic of the latter disease ; wiiile the patellar
tendon- react ions may be either exaggerated or absent in both diseases.
The age at which patients are attacked affords some help in diagnosis,
multiple sclerosis being most common in the first three, and general
paralysis in the fourth decade of life. Inequality of the pupils and loss
of the light-retlex are common in general paralysis, and ])robably never
occur, especially together, in multiple sclerosis. When the characteristic
expansive delirium with grand ideas, of general paralysis is well marked,
the diagnosis is easy, and even in the man}' cases in which it is absent
the patient has a peculiar air of contentment and self-satisfaction which
is wanting in multiple sclerosis. The diagnosis becomes more easy with
the advance of these diseases. In general paralysis the ])atient mani-
fests distinct signs of loss of memory and decided mental failure, while
in multiple sclerosis the mental condition is generally one simply of
emotional excitability, and only rarely of pronounced mental failure.
PATHOLOGICAL DIAGNOSIS. 703
and in these occasional eases other characteristic symptoms, like nystag-
mus and a widely diffused tremor, are present to make the nature of the
disease sufficiently clear.
(4) Neiv Formations. — When a patient suffers from a severe and
persistent headache, dizziness, and vomiting, the existence of an intra-
cranial growth ought to he suspected, and the presence of double optic
neuritis places the diagnosis almost beyond question. The localizing
symptoms met with in cases of cerebral tumor are the same generally
as those caused by hemorrhage and focal diseases, but these symptoms
creep on gradually and progressively in tumor, and not suddenly as in
the vascular diseases. Paralysis and other localizing symptoms may,
however, occur in the course of a tumor from a complicating hemor-
rhage, or oedema of the brain, or occlusion of a vessel from compression.
When once it is concluded that a foreign body is encroaching upon
the cranial cavity, the next question to be determined is the nature of
this growth. If the symptoms of an intracranial growth are found in
a young person of tubercular diathesis, and especially if the presence
of cavities in the chest, of enlargement of glands, or of a chronic dis-
charge from the ear indicate tubercular disease of other organs, then
the cerebral disease is likely to be a tubercular tumor. This supposition
is strengthened if the symptoms indicate that the tumor is situated in
the pons, cerebellum, or cortex of the brain; if the progress of the
case is somewhat rapid ; and if there are signs of the presence of
multiple lesions.
If the symptoms of an intracranial growth, indicating the same
localization as that of the tubercular tumor, occur in an otherwise healthy
young person who is free from syphilitic taint, the tumor is likely to be
a glioma. This supposition Avill be strengthened if the development of
the symptoms had been preceded by an injury to the skull, and if tlie
progress of the disease is comparatively slow. If the chief symptom
of an intracranial growth is caused by compression of the nerves at the
base of the skull, the tumor is likely to be a sarcoma. This supposition
is strengthened if the progress of the disease is slow and progressive,
and the diagnosis is rendered almost certain if a sarcomatous growth
is discovered in any other organ. If a patient about middle age
suffering from the symptoms of an intracranial growth, has a cachectic
appearance, if the disease makes rapid progress, and, above all, if there
is evidence that cancer is deposited in other organs, then the growth is
likely to be cancer.
If the symptoms of an intracranial growth are attended by marked
psychical disturbances, and convulsions, which are at first unilateral
and occasionally become general and frequently repeated near the fatal
70-i GENERAL DIAGNOSIS.
termination, and if these symptoms occur in a butcher or pork-dealer,
or in one who has suffered from tapeworm, then the tumor is likely to
be cysticercus cellulosce. The diagnosis of the presence of echinocoeci
in the brain must be made from the general symptoms of intracranial
tumor appearing and disappearing alternately, a'dema of the eyelids,
an opening in the cranial bones through which a fluctuating tumor pro-
jects, or exploratory puncture.
Abscess of the brain occurs as the direct consequence of an injury,
such as fracture of the skull and contusion of the brain, or is associated
with some other disease, such as caries of the petrous portion of the
temporal bone, and oz?ena, and the presence of suppuration is often
indicated by rigors and fever. A cerebral abscess may remain more or
less latent for a long period, and then the patient is suddenly attacked
Avith symptoms like those of meningitis or becomes rapidly comatose.
If a person beyond middle life is the subject of heart disease, extensive
arterial degeneration, or syphilis, and is at the same time suffering
from the symptoms of a tumor situated at the base of the brain, an
aneurism of one of the arteries of the brain may be suspected, and this
suspicion will be confirmed provided a murmur is audible on auscultation
of the skull. It is probable that aneurisms cause more pronounced
symptoms of irritation than otlier growths, consisting of intense cepha-
lalgia, paroxysms of severe and intractable trigeminal neuralgia, and
attacks of mania and other grave psychical disorders. If a patient who
has been suffering from the symptoms of a basal tumor die suddenly
from an attack of ingravescent apoplexy, it may be conjectured that the
tumor has been an aneurism. If a patient suffering from a tumor in
the anterior fossa of the skull die suddenly after a copious hemorrhage
from the nose, it may be assumed that an aneurism of the anterior cerebral
artery has perforated the cribriform j)late of the ethmoid bone. If
pulsation and a murmur on auscultation be observed in the orbit in)ine-
diately after an injury to the skull, it is probable that a communication
has been established between the internal carotid and cavernous sinus.
The localizing symptoms of intracranial aneurisms are the following:
aneurisms of the anterior cerebral and anterior communicating arteries
cause loss of smell and probably also unilateral blindness ; aneurism of
the internal carotid causes intractable facial neuralgia, paralysis of the
motor nerves of the eyeball, blindness of one eye and temporal hemi-
anopsia of the other. It may also cause complete facial paralysis, Avith
distortion of the uvula and complete deafness on the side of the lesion.
Aneurism of the posterior communicating artery causes paralysis of
the third nerve with or without hemianopsia ; aneurism of the posterior
cerebral artery or of the superior cerebellar artery causes paralysis of
PATHOLOGICAL DIAGNOSIS. 705
the third nerve of the sanae side and hemiplegia of the opposite side.
Aneurism of the upper part of the basilar causes paralysis of the fifth
and sixth nerves with bilateral weakness of the limbs, and aneurism of
the lower part of the basilar or of the vertebral artery causes symptoms
of bulbar paralysis with unilateral or bilateral weakness of the limbs.
Occipital pain is also a symptom of aneurism of the basilar artery.
Tumors of the vertebral canal and spinal cord, and of the peripheral
nerves, have already been sufficiently considered, and we shall now make
a few general remarks on syphilis of the nervous system, a subject which
we have purposely reserved to the last. There is scarcely any orcranic
disease of the nervous system but may be simulated by syphilitic lesions.
Syphilis may cause periostitis, osteitis, exostoses, and caries of bones,
which will first irritate and subsequently destroy neighboring nervous
structures. When the vertebrae or bones of the skull are afi'ected, the
spinal or cerebral dura mater becomes thickened, and thus a chronic
pachymeningitis is constituted which damages the roots of the nerves as
they pass outwards to the intervertebral foramina, or along the base of
the skull. Gummata may form in the dura mater, where they become
encapsulated and injure the spinal cord or brain only by pressure; or
in the subarachnoid space, and then the nerves, bloodvessels, and the
nervous structures themselves are involved in the growth. Gummata
may also grow in the sheaths of the peripheral nerves, and the cranial
nerves are often implicated at their points of origin and before they
have become covered by a prolongation of the dura mater. In other
cases gummatous tissue forms a diffused infiltration in the substance of
the nervous tissues, instead of forming a circumscribed growth. In
many cases this infiltration undergoes a partial organization, and it
then gives rise to a chronic sclerosis which may alFect one of the phy-
siological tracts of the spinal cord, or a localized portion of the brain,
or it is disseminated in patches throughout the brain and spinal cord.
When the syphilitic infiltration occurs in the membranes it renders the
tissues, on being partially organized, dense, inelastic, and opaque, and
causes adhesions between the dura and pia mater, and between the
latter membrane and the brain. In such cases the neighboring nervous
tissues are imperfectly nourished owing to the retraction of the lumen
of the bloodvessels. The arteries of the body, as a whole, arc liable to
undergo chronic changes in syphilis, caused by an endarteritis, which
may ultimately lead to the formation of aneurisms in various parts and
occlusion of arteries by thrombosis, or even by embolism, or to rupture
and hemorrhage. Syphilitic diseases of the bones and gummata may
act like foreign bodies and set up a more or less acute inflammation
of neisrhborino; nerve structures, and thus extensive inflammatory affec-
45
706 GENERAL DIAGNOSIS.
tions which are not at all syphilitic in their own nature, may be origi-
nated by this poison, and when once a sclerosis of nervous tissue is set
up by a syphilitic lesion, it is probable that the process will pursue a
progressive course independently of the syphilitic poison. Syphilis
appears also to favor the appearance of acute diseases of the nervous
system without the presence of any lesion which is distinctively syphilitic.
Acute ascending paralysis, for example, has been observed with prepon-
derating frequency in syphilitic subjects, but an examination of the
nervous tissues has not led to the discovery of any characteristic syphi-
litic lesion.
In the peripheral nerves syphilis gives rise occasionally to acute,
more frequently to chronic neuritis, and to compression of both spinal
and cranial nerves by the formation of gummata. In the spinal cord
it tends to produce acute ascending spinal paralysis and probably acute
spinal meningitis and acute myelitis, and it likewise causes, with varia-
ble frequency, chronic spinal meningitis, chronic myelitis, lateral spinal
sclerosis, progressive locomotor ataxia, progressive muscular atrophy,
labio-glosso-laryngeal paralysis, and ophthalmoplegia externa. In the
brain it may be the cause of acute and chronic meningitis, hemorrhage,
thrombosis, and even embolism of the arteries; thrombosis of one of
the sinuses in cases of chronic pachymeningitis ; a defined gummatous
growth; and a chronic degeneration in which the symptoms are very
similar to those of general paralysis of the insane, while it may also be
the direct or indirect cause of functional cerebral lesions like epilepsy,
hysteria, and chorea.
Inherited syphilis, besides giving rise to various local diseases in the
peripheral nerves, spinal cord, and brain, or their membranes, is often
the cause of imbecility in childhood, which progresses, if unchecked,
until the mental faculties are destroyed. The disease appears to begin
as a chronic meningitis of the convexity, and it leads to a progres-
sive destruction of the cortex of the brain. When the change spreads
over the motor area of the cortex it gives rise to a bilateral sclerosis
of the pyramidal tracts, and corresponding to this change there is,
during life, a spasmodic paralysis of the legs first, and ultimately of all
the extremities. The growth of the brain may also be arrested by
thickening of the cranial bones from syphilitic osteitis, or from narrow-
ing of the arteries from syphilitic endarteritis. It asserted by Virchow
that syphilis is sometimes a cause of congenital myelitis and encepha-
litis, and hydrocephalus appears to be frequently met with in the chil-
dren of syphilitic parents.
Nervous affections belong, as a rule, to the later manifestations of
syphilis, and make their appearance long after the more prominent phe-
PATHOLOGICAL DIAGNOSIS. 707
nomena of constitutional syphilis have ceased to exist. Search must
then be made for cicatrices on the genitals or on the groins ; circular
pigmented spots on the skin ; depressed and irregular cicatrices over
the forehead and front of the legs, with the integument adhering to the
subjacent bones; radiated cicatrices on the mucous membranes, especi-
ally of the mouth ; circular depressions on the arches of the palate or
tonsils, which look as if a piece of tissue had been punched out ; irregu-
lar protuberances on the surfaces of the bones; a moderate degree of
hard swelling of the occipital, cervical, or cubital lymphatic glands;
enlargement and knobby induration or atrophy of one testicle; cicatrix
on the penis ; and the existence of iritic adhesions. An inquiry into
the history of a case may throw great light on its nature. If the patient
be a man, it may be asked whether lie has ever suffered from syphilitic
infection. In the case of a married woman, valuable information may be
obtained by ascertaining whether or not she has had miscarriages, if
some of her children were stillborn or died soon after birth, or if those
living manifest any of the characteristic symptoms of congenital syphilis.
It is probable that nearly one-half of the cases of paralysis of the third,
fourth, fifth, and sixth nerves, when one nerve only is affected, are of
syphilitic origin, and curable by antisyphilitic treatment. The paral-
ysis of the ocular nerves which occurs in the course of locomotor ataxia,
is likewise, in the large majority of cases, an indirect result of syphilis.
When a gummatous deposit takes place into the spinal pia mater, or
into the substance of the spinal cord, the clinical features of the case
often present more or less of the form of a hemiparaplegia, but the
symptoms are never strictly unilateral, and there is an absence of the
definite phenomena which are observed on a level with the upper limit
of the lesion in other forms of spinal tumor. An outburst of cerebral
syphilis is often preceded for tAvo, three, or more weeks, by a deep-
seated headache, with intense nocturnal exacerbations and sleeplessness.
If a person after suffering from a headache of this kind is attacked with
recurring unilateral convulsions, each of which is followed by a slight
degree of paresis of the muscles affected by spasm, the case is one of
local syphilitic cerebral meningitis of the convexity, either primary or
secondary to disease in the bones, or a gummatous growth in or near
the cortex. The presence of double optic neuritis in such a case points
to a gimima rather than meningitis. An apoplectic attack occurring
before forty-five years of age in a person who is free from cardiac or
renal disease, points strongly to syphilis, thrombosis if tlie attack be
slight, or hemorrhage from the bursting of an aneurism if it assume
the form of ingravescent apoplexy.
708 GENERAL DIAGNOSIS.
The manner in whieli the symptoms are associated may help us in
recognizing the presence of syphilis even in the absence of other evi-
dence. Syphilitic lesions are, as Dr. Broadbent expresses it, often
"multiple, seldom symmetrical." Peripheral paralysis of one of the
ocular motor nerves of one side is probably never associated with a
similar paralysis of the corresponding nerve of the opposite side, but is
frequently accompanied by a unilateral epilepsy, or by a hemiplegia on
one or other side, from syphilitic thromltosis. Syphilitic affections of
the fifth nerve are also probably never bilateral, and if both of these
nerves are paralyzed by a tumor at the base of tlie bi-ain, the growth is
likely to be cancer. The succession of the symptoms may also aftbrd
important aid in diagnosis. The lesions of syphilis being multiple,
appear at difteient times and in Avidely different j)arts of the nervous
system, and thus a grouj) of symptoms, such as that caused by paralysis
of a cranial nerve, is apt to be followed after a time by a convulsion
from a deposit of gummatous tissue on the surface of the brain, or by
hemiplegia from thrombosis of a vessel. In nervous affections supposed
to result from inherited syphilis, it is imj)ortant to observe the general
conformation and physiognomy of the patient, and to examine the long
bones for evidence of periostitis, and the fundus of the eye for choroi-
ditis disscminatd, besides making minute inquiries into the family
history.
INDEX.
* BDOMINAL reflex, 173
A Abducens nerve, paralysis of, 363
nerves, spasm of, 296
Abscess of brain, 623
Accelerated breathing, 211
Accessory portions of the nervous system,
83
Achilles-tendon reaction, 177
Achromatopsia, 275
Acoustic nerves, diseases of, 269
Acute ascending paralysis, 425
atrophic spinal paralysis, 426
pathology of, 456
atrophic spinal paralvsis of adults,
482
decubitus, 146
hj'drocephalus, 653
pysemic encephalitis, 622
^sthesioneuroses, 125
articular, 131
cutaneous, 126
muscular, 130
osseous, 131
primar\', 125
secondary, 125
visceral, 132
Agraphia, 638
Akinesis of the muscles of external re-
lation, 165
of the deep reflexes, 179
of the superficial reflexes, 176
Albuminuric neuritis, 278
perineuritis, 278
retinitis, 278
degenerative, 278
hemorrhagic, 278
inflammatory, 278
pathology of, 279
S3'mptoms of, 279
Alcoholic paralysis, 415
AUochiria, 127
Alternate hemiplegia, 477
pathology of, 495
Amaurosis, 273
Amblyopia, 273
Amima, 639
Amnesic aphasia, 640
Amyelia, 90
Amyloid corpuscles, 103
Amyotrophic lateral sclerosis, 474
Anaemia of the brain, 603
of the spinal cord, 539
patholog\' of, 545
treatment of, 546
Anaesthesia, 125
in region of the distribution of
nerves, 243
in region of the distribution of
plexuses, 243
of the gustatory nerves, 272
of the mucous membranes, 134
of the olfactory nerves, 268
of the sexual feelings, 134
of the vagus, 134
Ansesthesia? dolorosa, 128
muscular, 131
visceral, 133
Anal neuralojia, 265
Analgesia, 125, 128
in region of distribution of nerves
and plexuses, 243
visceral, 133
Anatomical introduction, 17
Anencephalia, 91
Aneurism, intracranial, 104
Angina pectoris, 207
reflectoria, 209
vaso-motoria, 209
Angiomata, 108
Angioneuroses, 216
cerebral, 219
peripheral, 218^
spinal, 218
visceral, 220
Angoraphobia, 139
Anidrosis, 153
Ankle-clonus, 177
Anosmia, 268, 288
Anterior gray horn, 44
poliomyelitis, 426, 434
pathology of, 455
treatment of, 469
pyramidal tracts, 56
root zone, 48
Anthrophobia, 139
Aphasia, 192, 63*^
710
INDEX.
Aphasia, amnesic, 640
mixed, 643
motor or ataxic, 638
pathology of, 644
sensory or amnesic, 640
Aphemia, 638
Aphonia paralytica, 877
Aphthongia, 298
Apncea, 211
Apoplexy, cerebral, 610
treatment of, 617
Apselaphesia. 128
Arachnitis, 574
Argyll-Kobertson pupil, 201
Arteries, 21
anterior cerebral, 25
branches of, 80
spinal, 21
antero-lateral cerebral, group of, 26
antero-median cerebral, group of, 26
atheroma of, 104
basilar, 24
central system of, 27
choroid, 26
circle of Willis, 25
cortical, 25
system of, 26
ganglionic system of, 27
lenticulo-striate, 30
middle cerebral, 26
branches of, 30
nutrient of medulla and pons, 24
posterior cerebral, 25
branches of, 30
communicating, 26
median cerebral, group of, 25
spinal, 21
postero-lateral cerebral, group of, 25
spinal, 21
nutrient, 22
Sylvian, 26
vertebral, 23
Arthroneuralgia, 132
Articular iijsthesioneuroses, 131
Articulation*, disorders of, 131
Ascending degeneration of the nervous
tissues, 113
Aspermatism, 134
Asphyxia, 212
local, of llaynaud, 147
Associated movements of paralyzed parts,
183
Asthma nervosum, 212
Ataxia, jtrogressive locomotor, 511
Ataxic gait, 522
Atelomyelia, 90
Atheroma, 104
Athetosis, 481
bilateral, 483
Atrophic paralysis, 356
Atrophy of the cerebellum, 630
of the cerebral hemispheres, 630
Atrophy of the corpus callosum, 630
of the face, 149
of the nerves, 239
of the optic nerves, 281
progressive muscular, 437
Attacks of sneezing, 310
of yawning, 311
Audition, loss of, 288
Auditory hallucinations, 288
hypera^sthesia, 269
hyperalgesia, 269
nerves, diseases of, 269
Aura? epilepticie, 328
Aural vertigo, 509
Automatic action, 65
kinesioneuroses, 181
movements, 160
Azygos uvula>, paralysis of, 373
BASAL ganglia, 53
Basiilar meningitis, 663
13aths, 226
brine, 226
hot air, 226
hot sand, 226
mud, 226
needle, 226
shower, 226
sponge, 226
Turkish, 226
vapor, 226
warm, 226
Bedsores, 146
Bell's paralysis, 365
Bilateral athetosis, 483
facial jiaralysis, 369
Bladder, nervous disorders of, 215
Blepharospasm, 298
Bloodletting in nervous diseases, 227
Bones, nutritive affections of, 151
Brachial monospasms or protospasms,
324
plexus, diseases of, 306
Brain, 91
abscess of, 623
ansemia of, 603
atrt)phy of, 630
compression of, 600
concussion, 598
congenital malforn)ations of, 91
congestion of, 608
contusion of, 599
disease of membranes of, 651
hemorrhage of, 610
hypertropiiy of, 631
parasites of, 108
syphilis of, 705
tumors, 682
unilateral atrophy, 497
Bulbar mj-elilis, 552
treatment of, 566
INDEX.
711
Bulbar paralysis, chronic progressive, 442
See labioglosso-laryngeal paralysis.
Bulimia, 138
CALCAREOUS degeneration of nerve
fibres, 102
Carcinomata, 106
Cardiac nervous mechanism, 20-5
disorders of, 207
plexus, neurosis of, 263
Cardialgia, 263
Catalepsy, 342
etiology of, 342
symptoms of, 342
treatment of, 355
Cataleptic attacks, 338
Causalgia, 127
Central galvanization, 233
myelitis, 551
pathology of, 562
treatment of, 566
Centrum ovale, 30
Cephalalgia, 584
Cerebellar diseases, 528
Cerebello-spinal conducting path^, 63
functions of, 67
system, functions of, 75
Cerebral abscess, 628
aniemia, 603
partial, 604
treatment of, 61G
universal, G03
angioneuroses, 219
apoplexy, 610
concussion, 598
congestion, 608
convolutions, relations of, to skull,
31
embolism, 605
facial paralysis, 370
hemorrhage, 610
treatment of, 617
sinuses, thrombosis of, 606
thrombosis, 005
tumors, 632
Cerebro-spinal conducting paths, GO
functions of, 66
multiple sclerosis, 674
system, functions of, 68
Cervical portion of the cord, lesions of,
203
sympathetic, depressive lesions of,
202
disorders of, 202
irritative lesion of, 202
lesions of, 204
morbid anatomy of, 203
physiology of, 203
Cervico-brachial neuralgia, 253
Cervico-occipital neuralgia, 252
Chasme, 311
Cheyne-Stokes respiration, 212
Choked disk, 277
Cholesteatoma, 107
Chorda tympani, lesions of, 272
Chorea, 679
of iris, 200
of the larynx, 302
pathology of, 686
post-hemiplegic, 480
prehemiplegic, 480
treatment ol", 688
Chromidrosis, 154
Chronic arthritis, 152
atrophic spinal paralysis, 434
decubitus, 147
hydrocephalus, 658
inflammation of nervous tissues, 111
progressive bulbar paralysis, 442
Ciliary muscle, paralysis of, 302
Circle of Willis, 25
Circumscribed anesthesia, 128
Cirrhosis of muscle, 141
Classification according to the alterations
of function produced by lesion, 96
according to the form of the lesion,
95
of lesions of nervous system, 93
Claustrophobia, 139
Clinical diagnosis, 090
Clonic spasms, 166, 481
Clonus, various forms of, 177
Coccygeal nerves, neuralgia of, 261
Coccygodynia, 261
Colica saturnina, 268
Colloid bodies, 103
Color blindness, 275
Columns of Clarke, 56
of Goll, 57, 68
of Tiirck, 56
Combined tonic and clonic spasms, 479
Compound testhcsioneuroses, 185
Compression mj'elitis, 556
pathology of, 564
treatment of, 506
of the brain, 600
of nervous tissues, 95
Compulsory movements, 182
Concussion of the brain, 598
treatment of, 602
of the spinal cord, 596
Congenital defects of nerves, 90
of spinal cord, 90
malformations of the skull and brain,
91
Congestion of the brain, 608
treatment of, 617
of the optic nerves, 276
of the nerves, 237
treatment of, 241
Conjugate deviation of the eyes and ro-
tation of the head and neck, 185
Continuous tremor, 481
712
INDEX.
Contracture, 167
myopathic, 167
paralytic or secondary, 167
primary or neuropathic, 167
Contusion of the brain, 699
Convulsions, internal, 299
Convulsive tic, 297
Coordinate cramps, 182
Corpus dentatum, 53
Cortex cerebelli, 53
cerebri, 49
Counter-irritation in nervous diseases,
227
Cranial reflexes, 175
Cremasteric reflex, 173
Crises, cardiac, 518
tabetic gastric, 518
laryngeal, 517
Crossed hemiplegia, 477
Crural monospasms or protospasms, 324
neuralgia, 250
Crutch paralj-sis, 391
Cutaneous ana;sthesia, 128
eruptions in diseases of the brain, 144
in diseases of the spinal cord, 144
in lesions of peripheral nerves,
143
hemiana?sthesia, 288
hyperoesthesire, 127
hyperalgesia, 128
pariBsthesiiP, 129
paralgesia', 129
trophic affections, 143
Cycloplegia, 363
Cystalgia, 267
Cystic growths, 107
Cysticercuscellulosa, 108
DECUBITIS acutus, 146
chronic, 147
Deep reflexes, 176
Defects of development, 90
Degeneration of fillet and superior
peduncle of the cerebellum, 116
of the nerves, 100
of the nerve centres and conducting
paths, 120
of sensory ganglia and conducting
paths, 120
Degenerative albuminuric retinitis and
perineuritis, 278
Deiter's cells, 103
Delusion, 135
Depressive lesion of cervical sympathetic.
202
Descending degeneration of the nervous
tissues, 114
optic neuritis, 277
Deviation, secondary, of sound eye, 189
of the eyes and rotation of the head
and neck, 185
Diagnosis, clinical, 690
general, 690
pathological, 699
topographical, 691
Diaphragmatic paralysis, 385
spasm, 305
clonic, 306
tonic, 305
Diastematomyelia, 90
Dill'used atrophy of the brain, 477
Diphtheritic paralysis, 418
Diplegia facialis, 369
Diplomyelia, 90
Dipsomania, 138
Diseases of motor coordination, 509
of the acoustic nerve, 269
of the cerebellum, 528
of the cerebrum, 603
of the gustatory nerves, 270
of the membranes of the brain, 651
pathologj- of, 667
treatment of, 669
of the olfactory nerve, 267
of the optic commissure and tracts,
283
of the optic nerves, 273
of the pia mater, 653
of the spinal membranes, 669
Disorders of common sensation, 243
of special sense, 243
of the associated movements of artic-
ulation, 191
of the associated movements of the
extremities, 190
of the cardiac accelerator mechan-
ism, 209
of the cardio-inhibitory centre in
medulla, 209
of the cardio-inhibitory mechanism,
208
of the inhibitory fibres of the vagus,
208
of the nerves of special sense, 267
of the nervous mechanism of the
bladder, 214
of the heart, 205
of respiration, 210
of the reflex-inhibitory mechanism,
209
of the sense of smell, 288
of the simple reflex cardiac mechan-
ism, 207
of the visual sense, 289
Disseminated myelitis, 561
sclerosis, 674
Dissolution of nerve cells and fibres, 96
of the nervous system, 93
law of, "93
Dorso-intercostal neuralgia, 254
Double consciousness, 137
Dysesthesia, 127
Dyschromatopsia, 275
INDEX.
718
D3'Spliagia paralytica, t37C
Dyspnoea, 211
ECHINOCOCCUS hominis, 108
Eclampsia, 333
asphyxic, 334
etiology <if, 334
febrile, 334
idiopathic, 384
puerperal, 334
reflex, 334
symptoms of, 334
toxic, 334
treatment of, 353
urtemic, 334
Ecstasy, 344
Electric acupuncture, 232
Electrical reaction of afiected muscles
162
of nerves, 162
Electricity, 231, 233
Embolism, 104
of the spinal cord, 539
Encephalitis, 620
abscess with, 623
complicating other lesions, 623
infantile, 621
pathology of, 628
pyasmic, 622
secondary to embolism, 627
to thrombosis, 627
to a tumor, 628
traumatic, 621
treatment of, 629
Encephalic automatic disorders, 182
Encephalo-spinal conducting paths, 54
system, 49
functions of, 67
Encephalocele, 92
Encephalo-spino-neural system, 21
arteries of, 21
internal structure of, 41
relation of, to skeleton, 31
topography of, 31
Engorged disk, 277
Enteralgia, 263
Epigastric reflex, 173
Epilepsy, 327
aursB, 328
complications of, 332
etiology of, 327
grave, 330
minor, 330
morbid anatomy of, 348
symptoms of, 328
treatment of, 353
varieties of, 330
Epileptic mania, 333
Epileptiform neuralgia, 251
Erect posture, 78
Erector spinal reflex, 173
Erythemomegalalgia, 260
Examination of the body during move-
ment, 159
of the body during repose, 159
External cerebral pachymeningitis, 651
kinesioneuroses, 158
remedies in nervous diseases, 225
Eyeballs, paralysis of the muscles of, 359
Eyelids, disorders of the movements of
the, 356 . /
Eyes, conjugate deviation of the, 185
secondary deviation of sound, 189
IjiACIAL atrophy, 149
monospasm or protospasm, 325
nerve, paralysis of, 370
spasm of, 297
Fainting, 138
Faradic excitability, 161
Faradization, 232
general, 233
Fascial reactions, 177
Femoral neuralgia, 256
Fibroma, 105
Field of vision, 274
alterations in, 274
diminution in acuteness of, 274
tests of, 274
acuteness of, 274
Fifth nerve, neuralgia of, 245
Fillet, 49
degeneration of, 116
Forced movements, 182
Formation of a nervous system, 19
of nervous constituents, 18
of nervous tissues, 19
Formatio reticularis, 48, 58
Formication, 129
Fractures, trophic, 152
Functions of the cerebello-spinal con-
ducting paths, 67
system, 75
of the cerebro-spinal conducting
paths, 66
system, 68
of the encephalo-spinal system, 67
I Fundamental portions of the nervous
system, 83
GAIT, ataxic, 522
hemiplegic, 478
spastic, 472
Galvanic excitability, 161
Galvanization, 2^2
central, 233
Galvano-faradization, 233
Ganglion cells,
atrophy of, 99
calcareous degeneration of, 99
colloid degeneration of, 99
714
INDEX.
Ganglion cells, hypertrophy of, 96
multiplication of the nucleus
and nucleolus in, 97
pigmentary de«ceneration of, 99
shrinking of, 97
vacuo lation of, 99
Gangrene, symmetrical, 147
Gastralgia, 263
Gastric crises, tabetic, 518
Gastrodynia, 263
General diagnosis, 690
diseases of the perijiheral nerves, 237
faradization, 233
morbid anatomy and physiology, 122
of the nervous system,
90
myopathic spasms, 321
symptomatology, 125
treatment of nervous disea:<es, 222
medicinal, 223
prophylactic, 222
Genital organs, nervous disorders of, 215
Giant cells, 51
Girdle anicsthesia, 128
sensation, 127
Glaucoma, 151
Gliomata, 106
Globus, 133
Glossoplegia, 371
Glossy skin, 143
Gliige's corpuscle.', 103
Gluteal reflex, 173
Grapliospasmus, 308
Gray degeneration of the posterior col-
umn, 511
softening, 110
substance of tlie cerebellum, 53
of cerebrum, 49
Green softening, 110
Gustatory nerves, anivsthesia of, 272
diseases of, 270
hyperipsthesia of, 272
Gynephobia, 139
H.EMATIDROSIS, 154
Haematoma of the dura mater, 651
Htematomyelia, 541
Hamiatorrhachis, 569
Hair, trophic changes in, 145
Hallucination, 135
of hearing, 289
of sight, 289
of the sense of smell, 288
Headache, 137, 584
anaemic, 584
congestive, 584
gouty, 585
hyperiemic, 584
hysterical, 584
neurasthenic, 585
organic, 586
Headache, pyrexia), 585
rheumatic, 585
sick, 586
sympathetic, 585
syphilitic, 585
toxic, 584
treatment, 591
Hearing, disorders of, 289
Heart, nervous mechanism of, and its
disorders, 205
Hemeralopia, 275
Hemian:osthesia, crossed, 128, 286
cutaneous, 288
muscular, 288
Hemianopsia, 283, 284
crossed, 284
double nasal, 284
temporal, 284
equilateral, 284
homonymous, 284
Hemiataxia, 481
Uemiatrophia facialis progressiva, 149
Hemicephalia, 91
Hemicrania, 91. 586
pathology of, 589
Heiniparanicsthesia, 285
Heniiparaplegia, 557
Hemiplegia, })athology of, 476, 491
and iiemiana'sthcsia, 477
pathology of, 493
facialis, 365
from cortical disease, 505
liemianaistliesia, and hemianopsia,
477
pathology of, 493
Hemiplegia^, spastic, of infancy, 482
Hemiplegic gait, 478
Hemorrhage, cerebral, 610
into the S|)inal cord, 541
pathology of, 546
Hemorrhagic alliuminuric retinitis and
perineuritis, 278
Hepatalgia, 264
Herpes zoster, 143
Heteroto|tia of brain substance, 631
Hiccough, 306
Hippus, 200
Histrionic chasm, 297
Homonymous hemianopsia, 284
Hydrencephalocele, 92
Hydrocephalus, acute, 653
chronic, 658
Hydromyelia, 436
Hydromyelus congenitus, 91
Hydrorrhachis interna, 91
Hyperacusia, 269
Hyperaemia of brain, 608
of the nerves, 237
of the spinal cord, 540
pathology of, 545
treatment of, 546
of the spinal membranes, 569
INDEX.
715
Hyperesthesia, 125
in region of distribution of nerves
and plexuses, 244
muscular, 130
of the auditory nerve, 269
of the gustatory nerves, 272
of the olfactory nerve, 208
of the ovary, 260
Hyperifisthetic spots, 127
Hyperalgesia, 125
in region of distribution of nerves
and plexuses, 244
muscular, 130
of the sense of smell, 268
visceral, 132
Hyperidiosis, 153
unilateralis, 154
Hyperkineses of the deep reflexes, 179
of the muscles of external relation,
165
of the superficial reflexes, 175
Hyperosmia, 268
Hyperplasia of the Pineal gland, 106
Hyporpselaphesia, 127
Hypertrophy of axis-cylinder, 102
of the brain, 631
of the nerves, 240
Hypnotism, 844
Hypogastric neuralgia, 265
Hypoglossal nerve, paralysis of, 371
Hysteralgia, 265
Hysteria in boys, 338
Hysterical attacks, 337
treatment of, 353
paralysis, 486'
spasmodic affections, 836
morbid anotomy of, 349
Hystero-epilepsy, 340
TLLUSION, 135
± Impotency, 134
Infantile paralysis, 427
spinal atrophic paralysis, 427
atrophy, 429
deforinity of, 429
invasion of, 427
regression of, 428
remission of, 427
Inflammation of the nerves, 237
treatment of, 241
of the spinal dura mater, 570
of the spinal pia mater and arach-
noid, 574
Inframaxillary, 249
Insular sclerosis of brain and cord, 671
Intercentral connections, 73
Intermediate cerebral ganglia, 53
ganglia of the cerebello-spinal
S3'stem, 63
Internal cerebral pachymeningitis, 651
Intestinal colic, 263
Intracranial tumors, 632
pathology of, 634
treatment of, 635
Iridoplegia, 200
Iris, chorea of, 200
disorders of movement of, 198
nervous mechanism of, 197
Irritative lesion of cervical sympathetic,
202 J F .
J
OINTS, nutritive affections of, 151
KINESIONEUKOSES, 176
automatic, 181
classification of, 168
clinical, 169
etiological, 168
pathological, 168
topographical, 168
elementary, 158
external, 158
reflex central, 173
vascular, 210
visceral, 194
Knee-jerk, 170
Knee-phenomenon, 176
T ABIO-GLOSSO-LARYNGEAL
Jj paralysis, 442
pathology of, 503
Labyrinthine vertigo, 509
Landry's paralysis, 425
Larj'ngeal crises, 301, 517
disorders, 301
Laryngismus stridulus, 299
Lateral pj'ramidal tracts, 56
sclerosis, 528
Layers of the cortex, 50
Lead colic, 414
paralysis, 413
Lenticulo-striate artery. 30
Leptomeningitis spinalis acuta, 574
chronica, 575
Lesions of the cervical poi'tion of the
cord, 203
of the medulla oblongata, 203
of the rami communicantL'S, 204
Lightning-like pains, 130
Lingual spasm, 298
Lipoma, 107
Local asphyxia, 147
hysterical spasms, 338
myopathic spasms, 321
spasms, 295
Locomotor ataxia, 511
affections of special senses in,
515
anosmia in, 516
716
INDEX.
Locomotor ataxia, apoplectiform attacks
in, 520
Argyll-Kobertson pupil in, 517
ataxia of facial muscles in, 517
ataxic stage of, 521
sensory disorders in,
524
trophic disorders in, 526
visceral disorders in,
525
bladder affections in, 518
bone affections in, 520
cardiac crises in, 518
cerebral disorders in, 520
deafness in, 516
disorders of the pupils in, 517
epileptiform attacks in, 520
etiology of, 511
facial paralysis in, 517
gait in, 522
gastric crises in, 518
hemiopia in, 516
joint affections in, 520
laryngeal crises in, 517
loss of taste in, 516
nephralgia attacks in, 518
nystagmus, 517
paralysisof ocular muscles in, 51 6
paralytic stage of, 526
pathology of, 531
preataxic stage, 512
psychical disorders in, 520
rectal affections in, 518
symptoms of, 511
treatment of, 536
trigeminal neuralgia in, 517
trophic affections in, 519
varieties of, 526
anomalous, 527
hemiataxic, 527
hereditary, 527
meningitic, 527
neuralgic, 527
paraplegic, 527
typical, 526
vaso-niotor disorders in, 519
vesical affections in, 518
Lordosis, 431
Lumbo-abdominHl neuralgia, 256
Lumbar neuralgia, 255
MAINE en griffe, 396
Massage, 227
Massive hemorrhages, 108
Masticatory monospasms or protospasms,
327
paralysis, 363
diagnosis of, 364
etiology of, 363
symptoms of, 363
spasms, 296
Mastodynia, 255
Mechanical vibrations, 230
Median nerves, paralysis of, 394
Medulla oblongata, lesions of, 203
Melanoma, 107
Meniere's disease, 509
etiology of, 509
pathology of, 531, 533
symptoms of, 509
treatment of, 536
Meningeal apoplex}^ cerebral, 615
spinal, 569
hemorrhage, cerebral, 615
treatment of, 617
spinal, 569
treatment of, 577
Meningitis, basilar, 663
metastatic, 664
of the convexity of the brain, 660
rheumatic, 665
simple, 663
traumatic, 665
tubercular, 653
with pneumonia, 665
with ulcerative endocarditis, 665
Meningo-myelitis, 560
Mesenteric neuralgia, 263
Metastatic meningitis, 664
Methods of examining the motor ap-
paratus, 158
Microcephalus, 92
Microscopical changes in inflammation
of nervous tissues, 110
Migraine, 586
Mimetic paralysis, 365
Mimic convulsion, 297
Mixed aphasia, 643
Mogigraphia, 308
Monojilegia, 485
pathology of, 499
Monospasm, 323
bracliiai, 324
pathology of, 500
crural, 324
pathology of, 500
facial, 325
pathology of, 502
masticatory, 327
oculo-motor, 326
Motor aphasia, 638
cortical centres, 71
Motorium commune, 73
Morbid anatomy and physiology of the
atrophic paralyses, 451
Multiple neural paralyses, 412
sclerosis of the brain and cord, 674
pathology of, 684, 686
treatment of, 688
Muscular £Bsthesioneuroses, 130
anaesthesia, 131
atrophy, progressive, 437
with nuclear proliferation, 141
INDEX,
717
Muscular cirrhosis, 141
hemiansesthesia, 288
hyperaesthesia, 130
hyperalgesia, 130
sense, 131
sensibility, 131
tension, 167
trophoneuroses, 140
Musculo-spiral nerve, paralysis of, 391
Myalgia, 130
Mydriasis, 199
paralytic, 199
spastic, 199
Myelitis, 547
etiology of, 547
pathology of, 561
symptoms of, 548
treatment of, 565
varieties of, 551
acute, 551
pathology of, 561
bulbar, 552
central, 551
compressive, 556
disseminated, 561
meningo-, 560
periependymal, 436
transverse, 552
traumatic, 554
unilateral, 557
universal, 560
Myelomalacia, 539
Myoneuralgia, 130
Myopathic spasms, 321
etiology of, 321
pathology of, 847
svmptoms of, 321
Myosis, 198
paralytic, 199
spastic, 199
3Iyxomata, 106
NAILS, trophic changes in, 145
Xerve, abducens, paralysis of, 363
diseases of pneumogastric, 299
Xerves, anaesthesia in region of distri-
bution of, 243
analgesia in region of distribution
of, 243
atrophy of, 239
congenital defects of, 90
congestion of, 237
degeneration of, 101
general diseases of, 237
hypenemia of, 237
hyperfesthesia of, 244
hyperalgesia of, 244
hypertrophy of, 240
inflammation of, 237
regeneration of, 100
Nerves, stretching of, 235
Nervous asthma, 212
constituents, formation of, 18
disorders of the bladder, 214
of the genital organs, 215
exhaustion, 579
mechanism of the bladder and
rectum, 213
of the genital organs, 215
of the iris, 197
system, anaemia of, 94
classification of lesions of, 93
degenerations of, 94,112
dissolution of, 93
embolism of, 94
formation of an, 19
hemorrhage, 94, 108
hyperemia of, 94
inflammation of, 93, 109
syphilis of, 705
thrombosis, 94
toxic lesions of, 94
traumatic injuries of, 94
vascular lesions in, 94
tissues, ascending degeneration of,
113
capillary extravasations in, 104
chronic inflammation of, 111
compression of, 95
degenerations of, 112
descending degeneration of, 114
dissolution of, 102
formation of, 19
hypertrophy and hyperplasia of
neuroglia and connective
tissues of, 103
interstitial sclerosis, 108
microscopical changes in acute
inflammation of, 110
primary, 112
secondarv, 113
Neuralgia, 125, 129, 244
anal, 265
cervico-brachial, 258
etiology of, 253
symptoms of, 253
cervico-occipital, 252
etiology of, 252
symptoms of, 252
treatment of, 252
coccygodynia, 261
cceliaca, 268
cystic, 267
dorso-intercostal, 254
epileptiform, 251
facial, 251
femoral, 256
gastric, 263
hepatic, 264
hypogastric, 265
inframaxillary, 249
718
INDEX.
Neuralgia in the region of distribution
of nerves and plexuses, 245
ischiadica, 257
lumbar, 255
femoral, 25G
genital, 257
liimbo-abdominal, 256
mastodynia, 255
mesenteric, 268
muscular, 130
oesophageal, 262
of mons veneris, 257
of the bladder, 267
of the clitoris, 257
of the fifth nerve, 245
of the penis, 257
of the urethra, 267
ophthalmic, 247
ovarian, 266
phar3^ngeal, 262
phrenic, 252
plantar, 260
diagnosis of, 262
etiology of, 260
symptoms of, 260
treatment of, 294
sciatic, 257
diagnosis of, 262
etiology of, 257
symptoms of, 258
treatment of, 293
supraorbital, 247
supramaxiHary, 249
testicular, 266
trigeminal, 245
etiology of, 245
symptoms of, 245
varieties of, 247
epileptiform, 251
inframaxiliary, 251
ophlhalmic, 247
sup-amaxillary, 249
supraorbital, 247
treatment of, 291
urethral, 267
uterine, 265
Neuralgiform pains, 129
Neurasthenia, 579
cerebral, 579
etiology of, 579
spinal, 579
symptoms of, 579
treatment of, 591
Neurectomy, 235
Neuritis, acute, 237
chronic, 112
Neuromata, 240
etiology of, 240
false, Y05
motor disorders in, 240
symptoms of, 240
Neuromata, treatment of, 242
true, 105
Neuroparalytic ophthalmia, 150
Neuropathic constitution, 92
paralyses, 171
Neuro-retinitis, 277
Neurotic constitution, 92
Neurotomy, 235
Nictitating spasm, 297
Ninth nerve, paralysis of, 371
Notencephalus, 91
Nutritive affections of the glandular
apparatus, 153
Nyctalopia, 275
Nystagmus, 296
OBTURATOR neuralgia, 257
paralysis, 405
Occlusion of cerebral capillaries, 608
Oculo-motor monospasm or protospasm,
32G
paralysis, 356
symptoms of, 360
OEsophagcal neuralgia, 262
paralysis, 376
spasm, 299
ffisophagisnius, 299
Olfactory nerve, ana)sthesia of, 268
diseases of, 267
hyperajsthesia of, 268
morbid anatomy of, 269
physioloiry of, 269
Olivary bodies, 54
Operculum, 86
Opisthotonos, 311
Ophthalmia, neuroparalytic, 150
Ophthalmic neuralgia, 247
Ophthalmoplegia externa vel progressiva,
447
pathology of, 463
interna, 200
Optic ana-thesia, 273
hj'penesthoia, 273
hyperalgesia, 273
nerves, aiia'.<thesia of, 273
congestion of, 276
diseases of, 273, 276
hyperesthesia of, 273
hyperalgesia of, 273
inflammation of, 276
primarv and secondary atrophy
of, 276, 281, 283
neuritis, 277
Ordinarv hemi|)legia, 476
Oscedo, 311
Osmidrosis, 154
Osseous affections of cerebral origin,
152
lesions in the insane, 153
('steomata, 107
^
INDEX.
19
Osteoneuralgia, 131
Ovarian neuralgia, 266
PACHYMENINGITIScerebralis,6.51
external, 651
internal, 651
interna hemorrhagica spinalis, 573
treatment of, 577
hypertrophica spinalis, 571
treatment of, 577
spinalis externa, 570
treatment of, 577
Painful points, 130
Palate, paralysis of, 373
Palmar reflex, 175
Papilloma, 107
Paradoxical contraction, 178
Parsesthesia?, 125
visceral, 132
Paralgesia?, visceral, 133
Paralysis, 356
acute ascending, 425
acute atrophic spinal, in adults, 432
in children, 426
agitans, 670
alcoholic, 415
Bell's, 365
cerebral facial, 370
chronic atrophic spinal, 434
progressive bulbar, 442
diphtheritic, 418
from functional disease, 485
hemiplegic, 476
hypoglossal, 371
hysterical, 484
in locomotor ataxia, 526
labio-glosso-laryngeal, 442
Landry's, 425
lead, 413
levator palati, 378
masticatory, 363
myopathic atrophic, 448
oculo-motor, 356
of ciliary muscles, 363
of the abdiicens, 363
of the diaphragm, 385
of the muscles supplied by the
brachial plexus, 389
by the cervical plexus, 385
by the dorsal nerves, 402
by the hypoglossal, 371
by the hmibar plexus, 403
by the median nerve, 394
by the sacral plexus, 408
of the cesophagus, 376
of the pharynx, 376
of the respiratory muscles, 402
of the sixth nerve, 363
of palate, 373
peripheral facial, 370
Paralysis, phonetic laryngeal, 381
pneumogastric, 373
post-epileptic, 485
primary labio-glosso-laryngeal, 442
pseudo-hypertrophic, 448
reflex atrophic, 422
spasmodic, 471
spinal accessory, 383
atrophic, 425
toxic, 488
Paralytic mydriasis, 199
myosis, 199
Paranesthesia, 128, 284
Paraplegiie, 471,489
pathology of, 490
Parasites of the brain, 108
Parencephalus, 92, 497
Paridrosis, 154
Partial aniesthesia, 128
hypertrophy of brain, 631
Patellar-tendon reaction, 176
Pathological diagnosis, 699
Perforating ulcer of the foot, 147
Periependymal myelitis, 436
pathology of, 457
Perimeningitis, 570
Perimyelitis, 574
Perineuritis, 112,237
Periodic amnesia, 137
Periosteal reactions, 177
Peripachymeningitis spinalis, 670
Peripheral angioneuroses, 218
automatic disorders, 181
of the larynx, 377
facial paralysis, 370
Perverted sexual instinct, 138
Pharyngeal neuralgia, 262
Phrenic neuralgia, 252
Physiological introduction, 64
Physiology of the spas-modic paralyses,
506
Piano-forte player's spasm, 310
Pineal gland, hyperplasia of, 106
Plantar neuralgia, 260
reflex, 173
Pleurosthotonos, 311
Pneumogastric nerve, diseases of, 299, 377
Podynia, 262
Points apophysaire, 130
douloureux, 130
Poliencephalitis acuta infantium, 621
Poliomyelitis anterior acuta, 426
chronica, 434
Poliomyelopathies, 425
Polyaosthesia, 127
Polydipsia, 133
Post-epileptic paralysis, 485
Posterior gray horn, 46
longitudinal fasciculus, 48
root zone, 48
sclerosis, 511
720
INDEX.
Postero-median columns, 57
Post-hemiplegic spasms, 478,482
Pressure-arresting points, 167
Pressure- exciting points, 167
Primary assthesioneuroses, 125
areas of si<ull, 33
degeneration of the nervous tissues,
112
labio-glosso-laryngeal paralysis, 442
lateral sclerosis, 471
sclerosis of the columns of G^ll,
510
Professional hyperkineses, 308
Progressive bulbar paralysis, 442
pathology of, 462
locomotor ataxia, 511
muscular atrof)hy, 437
treatment of, 459
pathology of, 4(i4
Prosopalgia, 365
Pruritus, 129
Protospasms, 328
brachial, 324
pathology of, 500
crural, 324
pathology of, 500
facial, 325
pathology of, 502
masticatory, 327
oculo-motor, 326
Psammomum, 107
Pseudo-ajsthesia, 135
Pseudo-hypertrophic paralysis, 448
pathology of, 465
Psychical blindness, 290
deafness, 289
Puj)il, Argyll-Robertson, 201
Pupil, reflex immobility of, 201
Pyramidal giant cell, 51
tract, 60
sclerosis of, 114
Pyrosis, 133
REACTION of degeneration, 164
*Ked softening, 109
Reflex action, 65
akinesis, 173
atrophic paralj'sis, 422
etiology of, 422
symptoms of, 422
central kinesioneuroses, 173
Reflexes, abdominal, 173
akineses of the deep, 179
cranial, 175
cremasteric, 173
deep, 176
epigastric, 173
erector spinal, 173
* fascial, 177
gluteal, 173
hyperkineses of the deep, 179
Reflexes, palmar, 175
periosteal, 177
plantar, 173
scapular, 175
Reflex hyperkinesis, 173
immobility of the pupil, 201
movements, 160
spasms, 167
Regeneration of nerves, 100
Relation of cerebral convolution to skull,
31
Relative immunity of some muscles from
paralysis, 184
liability of some muscles to convul-
sions, 184
Remittent tremor, 481
Respiration, Cheyne-Stokes, 212
Respiratory nervous mechanism, dis-
orders of, 210
Retrobulbar neuritis and perineuritis,
278
Rupture of the brachial plexus, 399
SACRAL plexus, disorders of, 257
Saint Vitus 's dance, 679
Saltatory spasm, 313
morbid anatomy of, 346
Sarcomata, 107
Scapular reflex, 175
Sciatica, 257
Sclerosis, amyotrophic lateral, 474
cerebro-spinal, 674
disseminated, 674
insular, 674
multiple, 674
of the posterior and lateral columns,
528
of the posterior columns, 511
of the pyramidal tracts, 114
primary lateral, 471
primary, of columns of Goll, 510
secondary, of columns of Goll, 511
of direct cerebellar tracts, 511
lateral, 476
Scotomata, 274
Seclusion in the treatment of nervous
diseases, 227
Secondary ajsthesioneuroses, 125
areas of, 33
degeneration of the nervous tissues,
113
deviation of the sound eye, 189
lateral sclerosis, 476
sclerosis of the columns of Goll, 511
Secretory functions, 66
affections of glandular apparatus,
153
disorders of the glands of the diges-
tive tract, 156
of the genito-urinary ap-
paratus, 156
INDEX,
721
Secretory disorders of the lachrymal I Spasms of the glottis in adults, 300
;lands, 155
of the salivary glands, ISi
Segmental periaxillary neuritis, 112
Sense of locality, 126
of pressure, 126
of temperature, 126
Sensorium commune, 73
Sensory aphasia, 640
conducting paths, 02
cortical centres, 70
disorders of the special senses, 134
Shock, 594
erethismic, 595
pathology of, 601
torpid, 594
treatment of, G02
Shoemakers' spasm, 310
Sick headache, 586
Simple basilar meningitis, 663
glaucoma, 151
muscular atroph}^, 140
Singultus, o06
Sixth nerve, paralysis of, 363
spasm of, 296
Skull, primary areas of, 33
secondary areas of, 33
Smell, disorders of, 288
hallucinations of, 288
hyperalgesia of, 269
illusions of, 269
loss of, 288
Sneezing, attacks of, 310
Soft palate, paralysis df, 373
Solitary tubercle, 106
Somnambulism, 344
Spasmodic atiections of the larynx, 299
cough, 311
disorders, 295 .
gait, 472
laryngeal cough, 301
spinal paralysis, 471
paralysis of infancy, 484
Spasms, 165, 295
cerebro-spinal, 323
clonic, 160
from organic disease of the cortex
of the brain, 323
general myopathic, 321
hemiplegic, 478
pathology of, 496
histrionic, 297
hysterical, 337
in area of distribution of the facial
nerve, 297
inspiratory, 310
lingual, 298
local myopathic, 321
masticatory, 296
mimic, 297
of the abducens nerve, 296 .
of the diaphragm, 305
in children, 299
of the laryngeal muscles, 302
of the muscles of the eyeball, 295
of the neck, 305
of the upper extremity, 307
sui)plied by the hypoglossal
nerve, 298
supplied by the lumbar :ind
sacral nerves, 312
by the sciatic nerves, 312
by the vagus and pharyn-
geal plexus, 299
of the obliquus capitis inferior, 305
of the oesophagus, 299
of the respiratory muscles, 310
of the sixth nerve, 296
of the soft palate, 299
of the splenius capitis, 305
of the trapezius, 302
of the vocal cords, 301
piano-forte players', 310
post-hemiplegic, 478
saltatory, 313
shoemakers', 310
tailors', 310
telegraphers', 310
tonic, 166
toxic, 478
and clonic, 479
Spastic gait, 478
hemiplegia of infancy, 482
mydriasis, 199
myosis, 199
walk, 472, 478
Special pathology of the nervous system,
237
Spina bifida, 91
Spinal accessory, paralysis of, 383
angioneuroses, 218
atrophic paralysis, 425
automatic disorders, 182
concussion, 596
treatment of, 602
cord, anajmia of, 539
apoplexy, 541
concussion of, 596
congenital defects of, 90
embolism of, 539
hemiplegia of, 557 '
hemorrhage of, 541
hypenemia in, 540
irritation of, 578
relations of vertebra) to, 31
syphilis of, 705
thrombosis of, 539
tumors of, 564
epilepsy, 178
irritation, 578
Spino-neural spasms, 295
Splenius capitis, spasms of, 30")
Status epilepticus, 333, 341
46
722
INDEX.
Slernutatio convulsiva, 310
Strabismus, 362
Stretching of nerves, 235
St. Vitus's dance, 679
Subconscious and semiconscious psych
cal actions, 136
Superticial reflex, 173
Superior peduncle of cerebellum, 116
Supramaxillary neuralgia, 249
Supraorbital neuralgia, 247
Surface of skull, landmarks on, 31
topography of, 31
Swedish gymnastics, 230
Symmetrical gangrene, 147
Synkinesis, ltt3
Syphilis of the brain, 705
of the cord, 705
of the nervous system, 705
Syphilomala, 107
Syringomyelia, 436
T
ABES dorsalis, 511. See locomotor
ataxia,
spasmodic, 471
Tabetic amauroses, 281
ecchymoses, 219
foot, 152
gastric crises, 518
laryngeal crises, 301
Tactile anjesthesia, 128
Tailors' spasm, 310
Teeth, nutritive attections of, 151
trophic aliections of, 153
Telegraphers' cramp, 310
Tendon reactions, 176
Tenth nerve, diseases of, 299, 377
Testicular neuralgia, 266
Testis, irritable, 266
Tetanilla, 318
Tetanus, 313
etiology of, 313
morbid anatomy of, 346
symptoms of, 314
treatment of, 352
Tetany, 318
etiology of, 318
morbid anatomy of, 347
symptoms of, 319
treatment of, 352
Thermo-ana2Sthesia, 128
Thermo-hyperajsthesia, 127
Thermo-hyperalgesia, 128
Third nerve, monospasm or protospasm
of, 326
paralysis of, 356
Thomsen's disease, 321 ^^ \
Thrombosis, 104
of the cerebral sinuses, 606
of the spinal cord, 539
Tic, convulsive, 297
douloureaux, 245
Tinnitus aurium, 509
Titillation, 183
Toe clonus, 177
Tonic and clonic spasms, 479
spasms, 166, 478
early rigidity in, 478
lalerigidity in, 47?
T<^pographical diagnosis, 691
Topography of external surface of the
skull, 31
Torticollis, 302
Total anaesthesia, 128
Toxic paralyses, 488
Trance, 344
Transverse myelitis, 552
pathology of, 562
treatment of, 566
Trapezius, spasm of, 302
Traumatic local encephalitis, 621
meningitis, 665
myelitis, 554
treatment of, 566 .
Treatment of the spasmodic paralyses,
508
Trigeminal neuralgia, 245
Trismus, 296
Trophic attections of the teeth, 153
disorders of the nails and hair in
cerebral affections,
146
in lesions of nerve-
trunks, 145
in spinal disease, 145
functions of the cord, 65
Trophoneuroses, 140, 151
articular, 151
muscular, 140
of bones, 151
of joints, 151
of teeth, 151
osseous, 151
visceral, 156
Tubercular meningitis, 653
pathology of, 667
Tumors of the brain, 632 •
of the spinal cord, 564
Twelfth, spasm of, 371
ULCP^K, perforating, 147
Ulnar nerve, disease of, 396
Unconsciousness, 135
Unilateral atrophy of the brain, 477
facial paralysis, 365
myelitis, 557
pathology of, 655
treatment of, 656
oculo-moior monoplegia, 504
progressive atrophy of the face, 149
myelitis, 560
Urethral neuralgia, 267
Uterine neuralgia, 265
INDEX,
723
VAGUS, diseases of the. 299,377
Vaginismus, 266
Vascular diseases of the brain, G03
of the spinal membranes, 569
spinal sclerosis, 539
Vaso-motor functions, 66
nervous mechanism, 216
disorders of, 218
Vertigo, 138,160
aural, 509
lab_yrin thine, 509
Vesicular column of Clarke, 44
Violin-players' spasm, 310
Visceral angioneuroses, 219
kinesioneuroses, 194
neuralgia, 262
paralgesia, 133
Voluntary movements, 159
Vdluptnous feelings, excess of, 133
WALK, hemiplegic, 478
Walking, 78
"Wallerian degeneration, iOO
White softening, 110
Wrist clonus, 177
Writers' cramp, 308
morbid anatomy of, 345
treatment of, 351
Wry-neck, 302
YAWNING, attacks of, 311
Yellow softening, 110
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