ee
CORNELL UNIVERSITY.
34! es
PE eel, ge ThE
He oy Rca
Roswell P. Flower Library
THE GIFT OF
ROSWELL P. FLOWER
FOR THE USE OF
THE N. Y. STATE VETERINARY COLLEGE.
1897
CORNELL UNIVERSITY LIBRARY
Niiuiiiiigg
1924
at liom
_ LIBRA! ay
LO rTUuURES a
ep
Nate « aa %
ON
NERVOUS DISEASES
FROM THE STANDPOINT OF CEREBRAL AND SPINAL LOCALIZATION,
AND THE LATER METHODS EMPLOYED IN THE DIAGNOSIS
AND TREATMENT OF THESE AFFECTIONS.
BY
AMBROSE L. RANNEY, A.M., M_D.,
Professor of the Anatomy and Physiology of the Nervous System in the New York Post-Graduate
Medical School and Hospital; Professor of Nervous and Mental Diseases in the Medical
Department of the University of Vermont ; Late Adjunct-Professor of Anatomy in the
Medical Department of the University of the City of New York; Member
of the Neurological Society of New York; Resident Fellow of the
New York Academy of Medicine; Member of the New
York County Medical Society; Author of «The
Applied Anatomy of the Nervous System,”
** Practical Medical Anatomy,”
«*Electricity in Med:
icine,”’ etc.
PROFUSELY ILLUSTRATED WITH ORIGINAL DIAGRAMS AND SKETCHES IN COLOR BY THE
AUTHOR; CAREFULLY SELECTED WOOD-CUTS, AND REPRODUCED
PHOTOGRAPHS OF TYPICAL CASES,
PHILADELPHIA:
F. A. DAVIS, PUBLISHER,
1888,
4b Qinrser, Luke,
Ne & 14
a PN,
~~
es
Entered according to Act of Congress, in the year 1888, by
F. A, DAVIS,
In the Office of the Librarian of Congress at Washington.
All rights reserved.
as
34 /
~ i ed
Stor oe
The Medical Bulletia Printing House,
No. 1231 Filbert Street,
Philadelphia.
I DEDICATE THIS VOLUME
TO MY FRIEND,
ERRATA.
Page ls. Fig. 6. Text. For shaded portions read gray and red masses.
Page 156, 25th line. For musculo-spinal, read museculo-spire’.
Page 166. 26th line. For hyprocephalus, read hydrocephalus,
Page 248. No. (5) occurs twice in the diagram. The lower (5) should be (6).
Page 350. Under the * FUNCTIONAL DISeAshs OF THE Corp,” read Thomsen's
Disease for Thomson's Disease.
B02 UA YU ee ee
“CAUSATION AND CURE OF FUNCTIONAL
NERVOUS DISEASES.
1 DEDICATE THIS VOLUME
TO MY FRIEND,
GEORGE TT. STEVENS, M:D., Pu.D.,
AS A TRIBUTE TO
HIS PERSONAL INTEGRITY AND GENERAL sce,
AND, ABOVE ALL, TO
HIS ORIGINAL INVESTIGATIONS RESPECTING THE
CAUSATION AND CURE OF FUNCTIONAL
NERVOUS DISEASES.
PEP Co.
WaHatever of merit or demerit this course of lectures
may possess in the opinion of its readers or erities, it must be
conceded that it differs radically in arrangement and plan
from others published upon this department of medicine.
The first section treats of those facts (anatomical, physio-
logical, aud pathological) upon which the science of cerebral
and spinal localization of to-day is, of necessity, based.
The second section discusses more completely than most
works in this field the various steps which should be taken
by an aspirant in neurology during the clinical examination
of a patient; and the deductions which may be drawn from
the faets thus elicited. In many instances, authors have
given avery incomplete résumé of this field or have omitted
it entirely.
The third and fourth sections treat of individual diseases
of the brain aud spinal cord. Each is discussed from the
clinical standpoint indicated in the first section, viz., the
localization of. the lesions described, as well as the recognition
of the type which is encountered.
The section which treats of “functional” nervous diseases
will, I trust, receive the careful attention it deserves. It
comprises a full résumé of the researches of Dr. George T.
Stevens respecting the bearings of ‘“eye-defect” and “ eye-
(v)
vi PREFACE.
strain” upon the causation and cure of these imperfectly
understood conditions. My own observations in this field
have been quite extensive. They lead me to fully indorse
all that has been claimed by this author. I can bear strong
testimony to the value of the new methods of examination
and treatment suggested by him for these distressing and
obstinate maladies. Like other delicate procedures, they can
only be intrusted to skillful hands, well versed in their
intricacies and careful in respect to minute details. No
other treatment has ever yielded me such satisfactory results
in severe forms of epilepsy, hysteria, chorea, neuralgia,
headache, insanity, and functional visceral derangements.
As no drugs were employed by me in many of these cases,
the relief obtained must be attributed solely to the method
of treatment referred to.
The final section treats of electricity,—an agent which
is to-day invaluable in neuro-therapeutics, but which is
seldom if ever discussed in neurological manuals. To this
subject the author has given much attention for some
years past.
A glossary of neurological terms has been added, in
order that the reader may not grope in the dark when
uncertain respecting the meaning of a word which is new
to him.
Much time has been devoted to the condensation of the
matter presented within reasonable limits. To deal with
an extremely difficult and somewhat new field in medicine
in such a way as to bring it within the grasp of those who
have devoted little or uo attention to it, and at the same
PREFACE. vii
time to avoid, from those more familiar with the field, the
eriticism of superficiality, has been no casy task. The
author does not expect that his attempt will prove acceptable
to all. An experience of fourteen years, however, in teaching
medicine has governed the author in the presentation of
this field as he deems most wise.
‘To those who have attended the author’s lectures, deliv-
ered from year to year before his classes (either in the
Medical Department of the University of the City of New
York, the New York Post-Graduate Medical School and
Hospital, or the Medical Department of the University of
Vermont), much of the matter here contained will certainly
be familiar, and he trusts acceptable.
The labor of preparing this volume from scattered
lecture-notes has been greater than might appear on a cursory
examination. Many of the illustrations are from the author’s
pencil, while others are from original photographs of his
eases. Most of the colored diagrams incorporated are
similar to those drawn by him upon the blackboard before
his classes. Colors are of great service in making a diagram
clear and easy of comprehension. ‘To the author’s mind,
diagrams in this special field of medicine are of greater
utility to the busy practitioner than microscopic sections,
because very intricate mechanisms are discussed and inter-
preted which cannot always be shown.
‘Portions of this work embody extracts from two chapters
upon Diseases of the Brain and Spinal Cord in the third
edition of the author’s treatise on “Surgical Diagnosis.”
Some other portions have appeared in print from time to
Vili PREFACE.
time, in the following journals: New York Medical Journal,
Medical Record, Archives of Medicine, Journal of Nervous and
Mental Diseases, Medical News, Harper’s Monthly, Medical
Bulletin, and Medical Register.
In elosing, the author would acknowledge his great
indebtedness to the original investigations of those who
by their researches have been the source of much valuable
information incorporated by him in this work. This ac-
knowledgment must act as a poor substitute for frequent
reference-notes, which are precluded on account of a want
of space. A bibliography of some of the more important
works and monographs on this field to which the author is
indebted is, however, appended for the benefit of the reader.
Special care has been exercised in selecting these, as far
as possible, from sources which are easily accessible to
American readers.
AMBROSE L. RANNEY, A.M., M.D.
156 Mapison AVENUE,
New Yor City, May, 1888.
TABLE OF CONTENTS.
SECTION I.
ANATOMICAL, PHYSIOLOGICAL, AND PATHOLOGICAL DEDUC-
TIONS RESPECTING THE NERVE-CENTRES OF MAN, . 2 1
SECTION IT.
THE CLINICAL EXAMINATION OF PATIENTS AFFLICTED WITH
NERVOUS DISEASES, AND THE STEPS EMPLOYED AS
AIDS IN DIAGNOSIS, é : , é : i . 107
SECTION IIL.
DISEASES OF THE BRAIN AND ITS ENVELOPES, . ; e 21F
SECTION IV.
DISEASES OF THE SPINAL CORD AND ITS ENVELOPES, . . 347
SECTION V.
FUNCTIONAL NERVOUS DISEASES, , : é : ‘ . 449
SECTION VI.
TOXIC AND UNCLASSIFIED NERVOUS DISEASES, : . ood
SECTION VII.
ELECTRICITY IN MEDICINE, . . ; ‘ i s . 605
GLOSSARY OF NEUROLOGICAL TERMS, . 5 i . . 745
BIBLIOGRAPHY, . ‘ ‘ ; ; 1 ‘ . . 7538
INDEX, . : ‘ 5 ‘ 2 Y 3 ‘ : . 163
(ix)
LIST OF ILLUSTRATIONS.
SOURCE OF ILLUSTRATIONS, PAGE
I pouiiey ‘am of Component parts of Brain,
2—- * Cortical Cell.
8. — a “ Cortical Centres, r
co “Cerebral Convolutions, . é wz
a oY * Cortical Areas,
6.— ob * Cerebral Fibres,
iL cd ss om + 5
8.— as “ Centres of Thalamus,
9.—Section of Cerebral Hemispheres,
w- « « “ “
11.—Diagram of the Crura Cerebri,
12.— He “ Fibre-Tracts of Brain and Gora:
13.—Section through the Pons, .
14,—Diagram of the Fibre-Tracts of Cer aniline,
15.— ne ee i “ Medulla,
16.— oe ue Nuclei of the Medulla,
17.— ne ae Fibre-Tracts of the Spinal Cord,
18,— fe se Pyramidal Fibres of Medulla,
19.— a ah Nerve-Tracts of Spinal Cord,
20.— oe ep Motor Centres of Cerebrum,
2h.— + ae Optic Fibres, .
on “ 4“ 4G a
“ “i “ “ce
24— ee ue Cerebral Mechanism of Speech,
‘© of Motor and Sensory Cerebral Tracts,
—Base of Cerebrum (partial), zi ‘ “ é %
27.—Diagram of a Cross-Section of the Medulla, .
28.—Base of Skull and Cranial Nerves,
29.—A Diagram of Fibre-Tracts of Spinal eu d,
30,—A Spinal Segment,
31.—Diagram of Relations of Spinal Segments to Ver ae e,
32.— aR “ Fibre-Tracts of Spinal Cord, i
33— st “ Spinal Gray Substance,
34.— ee * a Reflex Arc;
35,.— ne “ Cerebro-Spinal ‘Ae nitartaiee.
36.—Scheme of Cerebro-Spinal Nerve-Tracts,
37.— te “ “
38.—Diagram of Refractive Errors of Eye,
39.— ef “ Ciliary Action, S cat ©
40.—The Ophthalmoscope, . a a i ,
—Sketch of Facial Paralysis, ; ‘ é “ ‘
42,—Syphilitic Teeth, . . ; a C , : "
43.—The Claw-hand, . é s 2 é z : ‘ é
44.—Ulnar Paralysi fs ;
46.—Median Paralysis (two es . si .
46.—Musculo- Spiral Paralysis, :
47.—Athetosis, : z
48.—Paralysis ‘Agitans, ‘ . %
49.—Pseudo-hy per tenphie Paralysis, i é : ‘
50,.— te Fi : 7 . . é
Original.
Modified fram Luys.
eb “Ferrier,
we Datton.
Original.
“
“
Modified from Lays.
ce “ Flechsig.
Schucfer.
“ “
Original.
“
Modified from Erb.
Original
Medved es om Erb.
“ “
Original,
ed ified from Ierb.
“ Flechsig.
Original.
“
Modified from Seguin.
Original,
Modified from Spitzku,
Original ©
Morlified from Branwcll,
Original,
LOE ou Gowers.
Bramwell,
“ eh Er vb.
th “Bramwell.
ss Ter Mer,
Aeby.
“
Original
Modified from Fick.
Loring.
Original,
Hutchinson.
Original,
Modified from Bramwell,
Original,
+
Modified from Hammond.
me “Charcot,
pe “Duchenne,
es “Gowers.
eX)
5
97
102
103
125
127
14)
lal
154
156
157
Jas
15!)
161
168
164
167
LIST OF ILLUSTRATIONS.
73.—Miliary .Ancurism of the Cerebr: a Gor igs:
TA, —Diagram of Cerebral Sinuses in Profile,
73.— Hs ** the Venous Sinuses of the PueacMates at
76.— a an Embolic Infarction, .
TT a “ the Mechanism of the Speech Koaaraties
73.— ee “a Transverse Vertical Section of the Left
Cerebral Hemisphere, showing the Arterial
Distribution, . “+ 3
719: —Diagram of the Effects of c ‘ortical and X Von- Cortical
Lesions of the Cerebrum,
80.—Diagram of the Motor Tracts and the Etfects as
Lesions of the Crus Cerebri, Pons Varolii, and,
Medulla Oblongata upon Motility,
81.—Diagram of the Sensory Tracts and the Effects ae
Lesions involving the same within the Crus
Cerebri and the Medulla Oblongata,
82. ~Diagram of a Horizontal Section through the C erebral
TIemispheres and the Basal Ganglia, .
83.—One of the Attitudes of a Hand caused by Post-
Hemiplegic Contracture, ; 7 : : -
84.—Chronie Hydrocephalus, —. & s " % . -
85,—Softened Brain-Tissne, . i e ie
86.—The Fundus of the Normal Eye,
87.—The Appearance of the Fundus wt the pe in,
“Choked Disk,” 2 5 : . =
§8.—Cerebral Sclerosis, : ‘ ‘ 2 g 3 a o
89,—Cerebral Glioma, . a * 4 2 “ ‘ . ig
90.—Syphilis of the Brain, . ¥ 3
91,—Diagram of Nerve-Fibre Trac te in the Spinal € aid;
92,— “ the Secondary Effects of a Lesion of the
Entire Spinal Cord, :
93. —Diagram to show Distribution of Gusseatl Py aii
Fibres to Spinal Seyments,
94.—Diagram of the Secondary Sclerosis following a Lesiiine
of the Left Cerebral Hemisphere, . é -
95.—Diagram of Multiple Spinal Sclerosis,
96.—Case of Poliomyelitis Anterior, followed by TRtanesre
Atrophy of Right Side.
97.—Case of ** Wing-Scapula,” from Atrophy cue SRE
98.—Protile View of same case, showing Atrophy of Deltoid,
Van Schaick.
Original,
te
Modified from Weber.
Original.
Modifie@ rom Westbrook.
Original.
wWodificd from Starr.
Original,
a
Modified from Fox.
Loss.
“
. Modified from Far.
“ es te
“ wok
Be S Flechsig.
Erb,
Original.
Erb.
cr
Original,
“
be
SOURCE OF ILLUSTRATIONS, PAGE
- 51.—Pseudo- enypertrophie Paralysis, S ch w «gee Maiaes tr oe Gers: 167
a— eR Be ae 167
a3) il <3 ue oe ¥ ae ee “ee 167
54.—Attitude te om Atrophy of ‘sade Migselei, ‘ - _ & Duchenne. 168
55, ee “ Abdominal Muscles, th . _ 169
56. a casechaanes ; & ¥ & & & Fs Instrument-maker. 177
57.—Dynamograph, : “ = 178
58.—Curves of Polar Muscular Gantenction (three aivts), Erb. 188
59.—Author’s Spring Electrode, Original. 191
6O— “ Tinganshic Key-board, a a Hs 192
6— * i (inaction), . 2. . te 198
62,.—Electrode, Erb. 198
63.—Diesmeter, ‘ : 5 ‘ ‘ : . A di « Beard. 199
64.—yEsthesiometer, Hammond. 200
65,.— ee Carroll. 201
66,— nr . Ntevcking. 201
67.—Diagram of Effects ofa an Unilateral Aptnal fede, . Modified from Erb, 205
65.— uo “ Relations of Certain Cranial Nerves, Original au
ith ss te fs * Optic Nerves, Modified from Seguin, 209
70.—Surface Thermometer, Seguin, 210
71.—Ditferential Thermo-Electric Calorimeter, instrument-maker. 211
72.—Duchenne’s Trochar, “ 212
219
2a
313
318
822
Boe
332
339
340
351
Fic,
“
a
LIST OF ILLUSTRATIONS.
SOURCE OF ILLUSTRATIONS,
99.—Poliomyelitis Anterior Acuta, ‘
100.—F ull View of same case, showing the Atri sake of Faia,
101 and 102.—A Case of Infantile Paralysis, with Involve-
ment of the Medullary Nuclei,
1038.—Hand in Amyotrephic Lateral Sclerosis,
104.—Fibres from the Diaphragm in Tlealth,
_ 105.—Same taken from a Case of Progressive Musentte
a\trophy affecting the Diaphragm,
106.—Two Views of the Hand of a Patient suffering fron
Progressive Muscular Atrophy, 3
107.—Progressive Muscular Atrophy of all the Tanhe. ‘
108.—Expression due to Implication of the Nuclei of the
Medulla governing the Mouth, —e and
Throat,
109.—Profile of Patient ainiilanty: affected,
110.—Hemiatrophy of the Face, ‘ s c
liL— BS “ Tongue and Palate,
112.—Side View of Pseudo-Hyper o opine Par. alysis, a &
113.—Rear “ a
1l4.—A Diagram of the Lesion of the Sensitive Tracts i in an
Unilateral Lesion of the Right Side,
115.—A Transverse Section of the Spinal Cord of an Agate
Patient,
116.—A Diagram of the Pathological Lesion of ne Cord
observed in Locomotor Ataxia, . % i 4
117.—Extensive Joiht-Changes in Locomotor Ataxia, . .
118 and 119.—‘‘ Charcot’s Disease” of Left Knee-Joiut fol-
lowing Locomotor Ataxia, . s
Cavities within the Substance of the pina tara,
constituting the condition known as ‘Syringo-
myelia,” . . . < is . . 3
121.—Hystero-Epilepsy, . . . . . . és
120.—
12 Another Attitude of same case, * = 2 ei 5
123.—Third Ke ne a oe s) é a % a
124.—Convulsion of Hystero-Epilepsy, . 2 2 S
125.—Case of Catalepsy, &
126.—A Cataleptic Patient, eanner ted by Titi andl Feet,
127,—A Marked Paroxysm of Tetanus, . ‘ ie ‘ e
128.—Paralysis Agitans, or Shaking Palsy,
129.—Morbid Appearances presented in Hereditary Ataxia
130.—Photograph of Case of Ataxia, 3 7 é
131,—Second Photograph of Case of Ataxia, . ‘“ a ‘
132:—Section of Dorsal Region of epinal Cord op te fs
BB | wo “ “ : €
134.—One of the Many Forms of Faradaic Machines, a Ss
135.—Diagram of the Construction and Action of a Fara-
daic Machine, . . s % * =
136.—A Static Machine in Use, . A é x 3
137.—A Simple Galvanic Element, . ‘a s ‘ “ e
138.—A Compound Chain, . < ‘ .
139.—A Schematic Representation of the Intr duc tion of a
Human Body into the Circuit of Closure of a
Galvanic Chain, ‘ Si th val +G> “<
140,—Six Cells Connected for Latenaty, S = 2 &
141.— “ He me & Quality, .* 5 3 fs
142.—Smee's Cell, . 5 n 5 ‘ 7 * ‘ a é
143.—Leclanche’s Cell, . . a . s . . ’
144.—Grenet’s Cell, . o . - = q ‘
145.—Fuller’s Cell,. j . - 3 .
146.—Siemens and Halske’s Cell, A A 3 < A é
147.,—Hill’s Gravity Cell, . ‘ ni % as a é
148.—Grove’s Cell, . m . c #£ « . oe @
Original.
“
“
Chareot.
ue
Original,
Fricdreich,
Hanrmone,
a
Original.
‘“
Duchenne,
“
Erb,
Van Schaick,
Erb.
Charcot.
Original,
Original.
va
Bell,
Charcot.
Privdreich,
Smith,
“
“e
Instrument-maker.
Original.
Instrument-maker.
firb,
“a
“
De Watteville,
“
Instrwment-maker.
ae
Bo
Sil
611
612
614
619
620
621
21
625
624
624
625
625
626
X1V
LIST OF ILLUSTRATIONS.
SOURCE OF ILLUSTRATIONS. PAGE
Fig. 149.—Bunsen’s Cell, . 2. 2...) Instrument-maker. 627
“* 150.—A Galvanometer Dial, De Watteville. 628
“ 151.—A Diagram of the Method of Tangent Cotilinaiiiers, Original. 629
““ 152.—A Horizontal Milliampére-meter, . . . . » Instrument-maker, 629
“ 153,—"* Dead-beat”’ Milliampére-meter, . . 2 we 2 se 630
“ 154.—A Fluid Rheostat, se » & e “ “ 631
* 155.—Rosebrugh's Fluid Rheostat, z 3 ei é Canada Pract. 632
“ 156.—Thermo-Electric Differential Calorimeter, Instrument-maker. 633
“ 157.—A New Form of Current Selector, “ “ 634
“ 158.—A Skeleton Drawing of the Pin eee of "Portable
Galvanic Battery, . . . oe 8 « eh ee 635
“ 159.—Various Forms of Electrodes, . . . ..s Erb. 637
“ 160.— se te ** Special Electrodes, Instrument-maker. 638
“ 161.—The Physician’s Handy Cabinet Battery, 5 » Original, 640
‘““ 162.—The Perfected Office Cabinet Battery, . . . . AInstrument-maker. 642
“ 163.— " WallCabinet, .. » 4 4 Original. 6H
“ 164.—Hawksbee's Original Electrical Machine, Nollet. 647
“ 165.—Ramsden’s Electrical Machine, Appleton & Co. 648
“ 166.—Nairne’s bs as e @ % - Re 649
“* 167.—Nicholson’s “‘ Electric Doubler,” . A ‘ New Royal Encyclop. of
Arts and Sei. 650
“ 168.—Same machine, New Royal Encyclop. of
Arts und Sei. 650
“ 169.—An Apparatus for Generating Frictional Electricity
by Steam, % ‘ » Armstrong. 651
“ 170.—Old Model of Gpindeicdi Static Mativiae: és New Royul Encyclop, of
: Arts and Sci. 651
“ 171,—Holtz’s Induction Machine, . ® “ . . Appleton & Co. 632
“ 172.—Stationary Plate of the Original eralie 5 ee ee 653
“ 173.—Holtz’s Static Induction Machine, . z ee a 654
“ 174.—Imnproved Holtz Induction Machine, Original. 657
“ 175.—Electrodes Employed with an Induction } Ach ie dnstrument-maker, 662
“ 176.—The Indirect Spark, . é 5 4 s * < . Original. 666
“* 177,—The Direct Spark, eo. z . a - = CGS
“ 178.—Shock with Leyden-Jar Tisehared ‘ te 669
“* 179.—An Application of the Leyden-Jar Shock duri a the :
Highteenth Century, « . « + New Royal Encyclop. of
Arts and Sci. 669
** 180.—Static Insulation, 4 é - 8 is ; ‘i . Original. 670
“ 181,—The Indirect Static erect i ‘ a i @ re 671
“ 182.—The Direct te Se 8 Se ee ee 671
“ 183.—The Electrical Head-Rath, z ‘ = “ é oR 672
“ 184.—The Static Induced Current, . 3 e é ' 673
** 185.—Morton’s Pistol- Electrode, : a é % Instrument-maker, 674
“ 186.—Electrode for Electrolysis, a . . ‘ ‘ ce ee 694
“ 187.—An Electrode for Electrolysis, . ‘ 3 % a : as, ey 694
“* 188.—Piffard’s Cautery Battery,. . iby, “ ™ 698
* 189.—Schemutie Representation of the Distribution of an
Electric Current applied eli to the
Head, . Erb. 714
* 190.—Schematic Repr aseniakiea: of the Caine se of Rieeric
Currents sent Transversely through the Head, * 714
* 191.—Schematic Representation of the Tistribution and
Density of Threads of Mlectric Currents during.
Applications to the Spinal Cord, 2 * ae 716
192. —Schematic Representation of the Density of the Cum
rent upon Application of the Electrodes to the
same Surface and in Close Relation to Each
Other, is ‘i i . “ : % . i
SEOlION 4
ANATOMICAL, PHYSIOLOGICAL, AND PATHOLOGI-
CAL DEDUCTIONS RESPECTING THE
CEREBRO-SPINAL AXIS
OF MAN.
SECTION I.
ANATOMICAL, PHYSIOLOGICAL, AND PATHOLOGICAL DEDUCTIONS
RESPECTING THE CEREBRO-SPINAL AXIS OF MAN.*
Some thirty-six years ago, by a premature explosion of gunpowder,
an iron bar three and a half feet long, one and a quarter inches in diameter,
and weighing thirteen and a quarter pounds, was shot completely through
a man’s head and perforated his brain. This man walked up a flight
of stairs after the accident, and gave his account of how it happened.
Although his life was naturally despaired of for some time, he developed
no paralysis, nor did marked impairment of his intellectual faculties
follow convalescence. Eventually he recovered his health. Twelve years
elapsed before his death; during which time he worked as a laborer on
a farm.
The “ American crowbar case” at once became famous, It startled
the minds of the reading public, and confounded the medical fraternity.
No satisfactory explanation of the remarkable features of the case could
be given. Some prominent medical men pronounced it ““an American
invention,” and laughed at the possibility of such an occurrence. The
skull was exhumed, however, after death, and is to-day in the medical
museum of Harvard University.
This case may be said to have been the starting-point of a new epoch
in medical science. It rendered untenable all previous hypotheses that
had been advanced regarding the organ of the mind. It proved con-
clusively that little, if anything, was known at that time respecting the
architecture of the brain of man, and the functions of its component
parts. F
Since then, a large number of observers have published the results
of various forms of experiments upon animals, made with a view of deter-
mining the physiology of the brain; but for some years the conclusions
drawn from such investigations were contradictory, and nothing was
definitely established.
We now are aware that serious defects existed in the early methods
of research. By great ingenuity these have been gradually eliminated.
We owe, however, to the discoveries of Turck, Fritsch and Hitzig,
Waller, Flechsig, and Gudden, most of our knowledge of new methods
*The first ten pages of this chapter are quoted (with many important modifications
and additions) from an article contributed by the author to Harper’s Monthly, March,
1885.
1
2 LECTURES ON NERVOUS DISEASES.
of research which have simplified the study of the nervous system during
life and after death. These methods of investigations have settled many
points in dispute. They have also made our knowledge more accurate,
and in accord with clinical observations.
The last decade has enabled us to bring many of the results obtained
by vivisection into perfect harmony with pathological data. Those who
have claimed that conclusions drawn from experiments upon animals are
not applicable to man are, to-day, confronted with certain unanswerable
facts to the contrary. Nature, through the agency of disease processes,
is constantly performing experiments upon human brains; and the symp-
toms so produced may be recorded during life, and compared with the
changes found in the brain after death. Physiology and pathology have
thus proven valuable lines of research in this field *
To-day, the “crowbar case” is no longer a mystery to specialists
in neurology. Bullets have been shot through the brain since then
without loss of motion, sensation, or intellect; and, in some cases, they
have been known to remain buried in the brain substance for months
without apparent ill effects. Five years ago a breech-pin of a gun, four
and three-quarter inches long, was forced into the brain of a boy nine-
teen years old, through the orbit, and its presence was not suspected
for some five months. It was discovered during a surgical attempt to
repair the facial deformity that resulted from the accident. Death fol-
lowed the removal of the foreign body from the brain in consequence of
inflammation created by the piece of iron, or possibly by its extraction.
This case is quite as remarkable as the crowbar case, but it excited less
interest in neurological circles because we are in possession of new facts.
We know, to-day, that if even a needle be thrust into one region of
the brain (the medulla oblongata, Fig. 1), immediate death may follow;
while a crowbar may traverse another portion of the organ, and recovery
be possible. The effects of injury to the brain depend rather upon its
situation than its severity.
In the light of our present knowledge the brain must be regarded
as a composite organ; whose parts have each some special function, and
are, to a certain extent, independent of each other.
* There are at the present time three distinct schools among the experimental phy-
siologists respecting the subject of cerebral localization. Ferrier and Munk represent a
faction which strenuously hold the view that the cortical gray substance can be mapped
out into areas whose limits, as well as their individual functions, are clearly defined.
Goltz stands at the head of a school which denies the accuracy of these views, and supports
the conclusion, originally advanced by Flourens, that the brain can only act as a whole.
Exner and Luciani (in common with their followers) occupy a ground which opposes very
sharply-defined boundaries to cortical areas, functionally associated with the various senses,
They believe that these areas overlap each other to a greater or less extent. At present,
the latter view seems to be most perfectly in accord with clinical and pathological data.
THE CEREBRO-SPINAL AXIS OF MAN» a.
One limited part is essential to vital processes; hence its destruction
causes death. Another part presides over the various movements of the
body ; hence paralysis of motion is the result of destruction of any
portion of this area. A third part enables us to appreciate touch, tem-
perature, and pain; and some disturbance of these functions will be
apparent when this region is injured or diseased. A fourth region pre-
sides over sight ; disturbances of vision may follow disease or destruction
of this area, in spite of the fact that the eyes escape. In the same way,
smell and hearing are governed by distinct portions of the brain, and also
the sense of taste. When a combined action of different parts is demanded
—as in the exercise of the reason, judgment, will, self-control, ete.—the
knowledge gained by means of the special senses can be contrasted and
become food for thought.
The skilled neurologist can determine to-day, in many cases, by the
symptoms exhibited during life, the situation'and extent of disease pro-
cesses that are interfering with the action of certain parts of the brain.
So positive is the information thus afforded, in some cases, that surgical
operations are now performed for the relief of the organ. A patient
who had lost the power of speech from an accumulation of pus within
the brain, was lately cured by the removal of a button of bone from the
skull over the seat of the pus, and its prompt evacuation. Epileptics
who suffer in consequence of brain-irritation may sometimes be cured of
their fits by the mechanical removal of the cause. Paralysis can occn-
sionally be alleviated by a removal of blood or pus from the surface of the
brain through a hole in the skull. Only a few months ago a bullet, which
had been shot into the head during an attempt at suicide, was removed
from the skull, in one of our hospitals, by means of a counter-opening.
The labors of such men as Meynert, Nothnagel, Ferrier, Flechsig, Wer-
nicke, Munk, Luciani, Exner, Charcot, and others, have made neurology
a science that would exceed the comprehension of its founders. Our
ability to localize disease within the substance of the spinal cord is even
more positive than in the case of the brain.
When we consider that it is by means of our nervous system that we
move, feel, see, hear, smell, taste, talk, and swallow; that in our brains
are stored all the memories of past events; that we digest and assimilate
our food partly by the aid of nerves; and that, in fact, we perform every
act of animal life by the same agency,—the utility of the latest infor-
mation regarding the brain becomes apparent at once.
he nerves are but telegraphic wires that put the brain and spinal
cord in direct communication with the muscles, the skin, and the various
organs and tissues of the body.
The nervous centres may therefore be compared to the main offices
of a telegraphic system, where messages are being constantly received
4 LECTURES ON NERVOUS DISEASES,
and dispatched. Every message sent out is more or less directly the
result of some message received. So it is with our nerve centres. We
are constantly in receipt of impressions of sight, smell, taste, hearing,
touch, and other conscious sensations. These are called afferent im-
pulses. As the result of the information so gained, we are constantly
sending out efferent or motor impulses to the muscles. These create
movements of different parts of the body. Respecting this view, Michael
Foster expresses himself as follows: “ All day long, and every day, mul-
titudinous afferent impulses, from eye, and ear, and skin, and muscle,
and other tissues and organs, are streaming into our nervous system ;
and did each afferent impulse issue as its correlative motor impulse,
our life would be a prolonged convulsion. As it is, by the checks
and counter-checks of cerebral and spinal activities, all these impulses
are drilled and marshaled and kept in hand in orderly array till a move-
ment is called for; and thus we are able to execute at will the most com-
plex bodily manceuvres, knowing only why, and unconscious or but dimly
conscious how, we carry them out.”
Sometimes, however, the motor impulses sent out by the brain in
response to sensory impressions take place in spite of our volition. Let
us cite an instance in the way of illustration: a timid person sees per-
chance some accident in which human life is possibly sacrificed, or the
sensibilities are otherwise shocked. His feelings overcome him, and he
faints. How are we to explain it? Let us see what takes place. The
impression upon the brain made by the organ of sight creates (through
the agency of special centres in the organ of the mind) an influence upon
the heart and (by means of vaso-motor nerve filaments) upon the blood-
vessels of the brain. This results in a decrease in the amount of blood
sent-to the brain, and causes a loss of consciousness. In the same way
persons become dizzy when looking at a water-fall, or from a height,
through the effects of the organs of sight upon the brain.
Again, if a frog be deprived of only the upper part of the cerebral
hemispheres, he is still capable of voluntary movement, breathing, swallow-
ing, croaking, and all the other manifestations of frog-life. But when we
observe such an animal with attention, we shall see that he is only a pure
automaton, and that he differs from the normal frog in his behavior when
left to himself and when disturbed. He will swim when placed in water,
but only until he reaches a spot where he can safely repose. Then he re-
lapses into quietude, evincing no desire to hop (as a normal frog would
do) or to escape from his tormentor. Everytime that his back is stroked
the frog will croak. The same irritation will produce the same result
over and over again. Such a frog, if placed upon a board which can be
tilted, will climb up the board (in case he perceives that his equilibrium
is endangered) in a direction necessary to render his position secure.
THE CEREBRO-SPINAL AXIS OF MAN.
Otherwise he remains motionless.
the normal attributes of that animal in health.
escape. He experiences no apparent alarm at surrounding objects.
movements can be predicted and repeated again and again at the will of
the experimenter. He has been transformed into a machine in which
every muscular movement can be traced directly to some stimulating
influence from without.*
WHITE SUBSTANCE
OF THE CERESRAL HEMISPHERE
(FORMER OF NERVE FIBRES)
Fic. 1.—A D1acramM DssIGNED BY THE AUTHOR TO ELUCIDATE THE CHIEF COMPONENT
Parts oF THE Human Brain.—The lettering upon the figure will be explained in the text.
-C. Q. the corpora quadrigemina. The lines within the white substance of the cerebrum or
in the ‘‘crus’’ are not intended to convey any impression to the reader of the actual arrange-
ment of the fibres; nor are the colors employed selected with special reference to the elucida-
tion of the functions of the component parts of the organ thus diagrammatically shown.
Before we go farther, let us examine in a cursory way the anatomi-
cal elements of which the brain is composed. These are practically the
same in all animals of the higher grades. We can then review the group-
ing of these elements, and study some of the structural details of that
organ in man. Many of these have baffled all attempts at investigation
until of late.
*The distinction between “ instinctive’? or automatic acts (which are governed by
the spinal and cerebral ganglia) and ‘‘ conscious volitional acts” (which are always of cor-
tical origin) is not properly recognized by some experimental physiologists. Dr. M. Allen
Starr has very happily shown in a late article on speech (Princeton Iteview) that this dis-
tinction helps materially to reconcile the antagonistic views now held by the opponents
and supporters of cerebral localization.
He is no longer a frog endowed with
He does not attempt to
His
6 LECTURES ON NERVOUS DISEASES.
We may start with the statement that the brain consists of two dis-
tinct anatomical elements,—brain cells and nerve fibres.
The number of brain cells in the cerebrum alone may be estimated
at many thousands. Hach cell, by means of its nerve fibres and the pro-
cesses that spring from it, may be considered as a central station of an
clectric system. It can receive messages from parts more or less distant.
It can dispatch messages in response to those received. Finally, it can
store up such information as may be carried to it from time to time for
future use, affording us, at the same time, memories of past events. It -
will simplify description if we consider each of the anatomical elements
of the brain separately.
THE BRAIN CELLS.
These are placed chiefly upon the exterior of the organ, which is
thrown into alternating ridges and depressions, somewhat like a fan when
half closed. The ridges are called the “ convolutions,” and the depres-
sions are termed “sulci;” or “ fissures,” in case they are deeper than the
rest. The gray matter upon the exterior of the brain is called the
“ cortex.”
_ The cerebral cortex is alone associated with consciousness and voli-
tion. Like gray matter found in other regions of the organ, the cortex
consists of brain cells and a cement (formed of connective-tissue elements)
that binds them together. This is called the “neuroglia.”
Masses of brain cells are found imbedded within the substance of
the organ; but their functions are less well determined than those of the
cortical gray matter. The corpus striatum* and the optic thalamus are
certainly the largest and perhaps the most important of these ganglionic
masses.
If we study the appearance of the brain cells under the micro-
scope, we find that different convolutions of the brain are peopled with
cells that have individual characteristics of form and construction;
hence we are justified (from an anatomical stand-point alone) in attrib-
uting different functions to individual areas of the cortex. This view is
sustained, furthermore, by physiological and pathological investigation.
We may consider each cell within the brain as possessing an individ-
uality. Each is intrusted with and controls some particular function.
Hach is in telegraphic communication with other cells, and participates
constantly in the growth and development of some special region of the
body, acting in harmony with its fellows. Luys, who has carefully in-
vestigated the structure of these minute bodies, says of them: “ Imagina-
*I apply the term “corpus striatum” throughout this work to its two halves (the
caudate and Icnticular nuclei, Fig. 6) collectively. Many of the German authorities em-
ploy it as synonymous with the caudate nucleus alone.
THE BRAIN CELLS. t
tion is confounded when we penetrate into this world of the infinitely
little, where we find the same infinite divisions of matter that so vividly
impress us in the study of the sidereal world; and when we thus behold
the mysterious details of the organization of an anatomical element, which
only reveal themselves when magnified seven hundred to eight hundred
diameters, and think that this same anatomical element repeats itself a
thousandfold throughout the whole thickness of the cerebral cortex, we
cannot help being seized with admiration, especially when we think that
Fic. 2.—Corticar Cait oF THE Deeper Zones AT ABOUT ErGHT HunDRED Diameters. (After .
Luys.) A section of the cell is made through its greater axis, its interior texture being thus
laid bare. A, represents the superior prolongation radiating from the mass of the nucleus
. itself. B, lateral and posterior prolongations. C, spongy areolar substance, into which the
structure of the cell itself is resolved. D, the nucleus itself, which seems only to be a thick-
ening of this areolar stroma; it sometimes has a radiated arrangement. E, the bright
nucleolus, which is itself decomposable into secondary filaments. The colors are only em-
ployed to aid in recognizing the various parts of the cell.
each of these little organs has its autonomy, its individuality, its minute
organic sensibility, that it is united with its fellows, that it participates
in the common life, and that, above all, it is a silent and indefatigable
worker, discreetly elaborating those nervous forces of the psychic
activity which are incessantly expended in all directions and in the most
8 LECTURES ON NERVOUS DISEASES.
varied manners, according to the different calls made upon it, and set it
vibrating.”
In the cortex of the brain we find the brain cells arranged in super-
imposed strata: The number of these strata varies in different areas of
the brain surface.
Each stratum is composed of cells that have identical shapes, and
whose structure is apparently the same. Delicate, hair-like processes
are given off from the body of each cell, many of which subdivide like
the branches of a tree, and become closely intermingled with those given
off from neighboring cells, Nome of these processes unquestionably
serve to connect the cells that compose the various strata of the cortex ;
others serve as a means of attachment of nerve fibres to the cells. By
means of these processes, molecular movements generated within any
individual cell can probably be transmitted to other cells in the same
stratum of the cortex, or to those composing other strata. Thus the
different layers of cells can probably act independently, or in conjunction
with others.
We may generalize respecting the purposes for which these minute
bodies have been constructed, as follows :—
1. Some cells are unquestionably capable of generating nerve force;
just as the electric battery, for example, generates electricity for the
purpose of telegraphy.
2. Some are designed to promote muscular contraction, and thus
to cause voluntary movements. They are enabled to do this by the
nerve fibres. These conduct the current from the cells to detinite
muscles of the body. When, therefore, from any cause the generating
power of motor cells, or the conducting power of motor fibres is inter-
fered with, we have a symptom produced known as * motor paralysis.”
Tumors, or inflammatory deposits sometimes press upon the motor
cells to such an extent as to impair their function; intlammatory con-
ditions may affect them directly, and cause their disintegration; blood
may escape into the brain substance and plough up the delicate fibres
that convey the impulses to the muscles (the condition known as ‘“ apo-
plexy”); and many other pathological conditions may derange or de-
stroy this elaborate system of wires and batteries. Let me impress upon
the reader that paralysis of motion is not a disease, as most people sup-
pose. It is but one of the manifestations of disease.
3. Some cells of the cerebral cortex serve as receptacles for nerv-
ous impressions.* Let us cite some examples. At birth the brain may
be likened to the sensitized photoeraphie plite before it has been ex-
* Disturbances of the memory may often prove a valuable aid in localizing the seat
of a cerebral lesion, This fact has only been utilized of late; as new facts in cerebral phy-
siology have been brought to light.
THE BRAIN CELLS. 9
posed to the action of the lenses of the camera. Nothing has yet
been recorded upon it. It may subsequently be beautified or disfigured
by the impressions that are to be made upon it from without. At first
the child stares stupidly about, unable to appreciate or properly interpret
the pictures that are constantly being formed upon the retina by light.
Loud noises frighten it, and softer sounds fail to attract its attention.
It has not yet learned to determine the direction from which a sound
comes. The appreciation of distance has not yet been acquired. The
tiny hands are stretched ont alike at remote and near objects.
Now mark the change that occurs when suflicient time has elapsed
to allow the brain cells to accumulate memories of past events in num-
bers sufficient to admit of comparison with each other, and to form the
basis of judgment.* ‘The child soon begins to recognize familiar faces.
It learns to discriminate between the voice and touch of the mother
or nurse and that of a stranger. When only a few weeks old it begins
to estimate distance, and to make voluntary efforts to grasp surrounding
objects. Gradually its brain learns the meaning of articulate sounds. and
by associating such sounds with definite objects it acquires a knowledge
of language. The power of speech is developed later than the knowl-
edge of language, because the complicated movements of the tongue,
lips, and palate are difficult to perform properly, and also because articu-
lation must of necessity be based upon a memory of the various sounds
employed. Thus for many months the brain of a child is simply re-
ceiving and storing up in these wonderful receptacles, the brain cells,
the impressions of the external world, that reach it chiefly by mcans of
the organs of sight, smell, hearing, taste, and touch.
These facts become even more mysterious than they might at first
appear to the reader when we reflect that the eve, for example, telegraphs
the outline, coloring, and other details of every picture (focused by its
lenses upon the retina) to the cells in the cortex of the occipital lobes of
the cerebral hemispheres; and that these cells retain these impressions
in such a manner that they can be recalled by a voluntary effort again
and again as memories of what we have seen. The eve can thus go on
taking photographs of external objects forever without fear of losing
what it so elaborately duplicates. We have positive evidence to prove
the accuracy of these statements. If the occipital lobes of both hemis-
pheres be destroyed in animals, the sense of sight is lost immediately,
in spite of the fact that the eyes have not been injured by the operation.
I have had under my care several patients who have been rendered
* Clinical observation, as well as pathological statistics go to show that in right-
handed subjects the left cerebral hemisphere is more intimately connected with the storage
of memories than the right hemisphere. This is well illustrated in the reported cases of
ataxic aphasia, paraphasia, word-blindnees, and word-deafness.
10 LECTURES ON NERVOUS DISEASES.
totally blind in a lateral half of each cye by brain-disease ; the other
half retaining its normal power of vision. It is equally well proven that
the memories of our conscious perceptions of odors, sounds, taste, and
touch, are stored within the cells of ditferent areas of the cerebral cortex,
whose limits are already determined with approximate accuracy. These
memories, as we all know, can be recalled at will with unimpaired vivid
ness, just as picture after picture can le struck off the same negative
when once made indelible upon a vlass plate.
F0
907 qwiain00 3
=
Fic. 3.—Sipgz View oF THE Brain oF MAN SHOWING THE AREAS OF THE CEREBRAL CON-
votutions, (Modified slightly from Ferrier.) R, Fissure of Rolando, §, Fissure of Syl-
vius, divided into its two branches. 1 (on the postero-parietal [superior parietal] lobule).
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; @, 4, c, d@ (on the ascending parietal [posterior central] convolution), individual
and combined movements of the fingers and wrist of the opposite hand; prehensile move-
ments. 5 (at the posterior extremity or the superior frontal convolution). Extension for-
ward of the opposite arm and hand. 6 (on the upper part of the antero-parietal or ascend-
ing frontal {anterior central] convolution). Supination and flexion of the opposite forearm.
7 (onthe median portion of the same convolution) Retraction and elevation of the oppo-
site angle of the mouth by means of the zygomatic muscles. 8 (lower down on the same con-
volution). Elevation of the ala nasi and upper lip with depression of the lower lip on the
opposite side. 9, 10 (at the inferior extremity of the same.convolution, Broca's convolution).
pening of the mouth with 9, protrusion; and 10, retraction of the tongue,—region of aphasia,
bi-lateral action, 11 (between 10 and the inferior extremity of the ascending parietal convo-
lution). Retraction 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). The eyes
open widely, the pupils dilate, and the head and eyes turned toward the opposite side. 13,13
(centres of vision in the occipital lobes). 14 (of the infra-marginal, or superior [first] tem-
poro-sphenoidal ee nee Pricking of the opposite ear, the head and eyes turned to the
opposite side, and the pupils dilate largely (centre of hearing). Ferrier, moreover, places
the centres of taste and smell (15) at the extremity of the temporo-sphenoidal lobe, and that
of touch in the gyrus uncinatus and hippocampus major.
Professor Ferrier, of London, has mapped out, by means of a series
of experiments upon the monkey tribe (the nearest approach to the type
of man),a chart of the brain which shows the situation of certain groups
THE CEREBRAL CORTEX. 11
of cells or “centres” in the cortex that preside over particular functions.
The cut introduced (Fig. 3), and its descriptive text, will make some of
the conclusions of this author intelligible to the reader.*
Most of the conclusions of this investigator (excepting those relating
to the visual centres, in which I think he is in error) have been partially
verified upon man. It may interest the reader to know how these con-
clusions have been verified, since vivisection upon the human race is, of
course, impossible.
In the first place, a careful study has been made of cases where
Nature has performed the experiment of destroying or imperfectly de-
veloping portions of the brain, and where an opportunity of examining
that organ after death has been afforded.t The clinical records of such
cases have been collected from all reliable sources, and critically ana-
lyzed by competent medical men (Charcot, Ferrier, Nothnagel, Wernicke,
Broadbent, Luys, Exner, Spitzka, Starr, Seguin, and many others).
Again, a large number of subjects who have suffered amputation of
limbs, and who have survived the operation for some years, or who haye
manifested arrested development of limb, have been made to bear indirect
testimony to the accuracy of the facts gained by vivisection and patho-
logical research. When any part of the body is deprived of exercise,
it will waste gradually from disuse. On this basis of reasoning, Bourdon
and others have sought to determine the centres of motion of the limbs,
by examining the cortex of the cerebral hemispheres of such subjects
after death, with a view of determining the existence and exact seat of
atrophy of definite groups of brain cells.
A third line of investigation, which has yielded brilliant results,
consists in tracing the origin, course. and ultimate distribution of sepa-
rate bundles of nerve fibres within the brain and spinal cord (Meynert,
Flechsig, Gudden, Wernicke, Spitzka, Aeby, Roller, Starr, and many
others). Some important discoveries have been made of late, which
enable us to do this with accuracy,—-a feat that was impossible by the
older methods employed. A knowledge of the peripheral connections
of certain groups of brain cells has shed much light upon their probable
functions.
Finally, much has been learned by a microscopical study of the dif-
ferent layers of the cortex and the nerve-nuclei with reference to the
*The view upheld by Ferrier and Munk that the cortical areas have distinct lines of
demarcation has been opposed by Luciani and Exner, who believe that the edges of these
areas merge gradually into each other, and manifest less prominently than do their cen-
tral portions the individual peculiarities of each. :
} The study of microcephalic specimens, which bears somewhat upon this field, bids
fair to become a very important line of investigation respecting the relations of certain
parts of the brain to definitely recognized bundles of fibres within the crus, pons, medulla,
and spinal cord. It is as yet in its infancy.
12 LECTURES ON NERVOUS DISEASES.
character of cells that compose them. It has been proven that the form
and arrangement of the brain cells afford some elue to the special fune-
tions over which each preside (Luys, Arndt, Betz, Stephany, Spitzka,
and others). Comparative anatomy has aided in this line of research,
Now, when we find that all of these methods lead us to an identical
conclusion concerning any point in cerebral physiology, that conclusion
becomes a fact beyond the possibility of dispute. Unfortunately for
science, much still remains to be determined regarding this mysterious
mechanism; but, on the other hand, much has been positively proven.
Perhaps the day may never come when the human mind can fathom all
of its mysteries.
SAR Er ay
Fic. 4.—A Diacrammatic Figure, SHOWING THE CEREBRAL CoNnvoLutions. (Modified
. from Dalton.) S, Fissure of Sylvius, with its two branches, a, and 4, 6, 6. Kk, Fissure
of Rolando. P, Parieto-occipital fissure. 1,1, 1, ‘he first, or superior frontal convolution.
2, 2,2, 2, The second, or middle frontal convolution. 3, 3, 3, The third frontal convolution,
curving around the ascending limb of the fissure of Sylvius (centre of speech movements).
4,4, 4, Ascending frontal (anterior central) convolution. 5,5, 5, Ascending parietal (posterior
central) convolution. 6, 6, 6, Supra-Sylvian convolution, which is continuous with 7, %. 7%
the first or superior temporal convolution. 8, 8, 8, The angular convolution (or gyrus), which
becomes continuous with 9, 9, 9, the middle temporal convolution. 10, The third, or inferior
temporal convolution, 11,11, The superior parietal convolution. 12. 12, 12, The superior,
middle, and inferior occipital convolutions, called also the first, second, and third (the centres
of vision). It is to be remembered that the term ‘“gyrus’’ is synonymous with ‘* convolu-
tion,” and that both terms are often interchanged.
Before we pass to the consideration of the second anatomical clement
of nervous tissues—the nerve fibres—let me call the attention of the reader
to the general form of the brain, and to a classification of the convolutions
THE CEREBRAL CORTEX. 13
that is now generally adopted. This will enable him to gain a clear in-
sight into the functions of different ureas of the cerebral cortex. Fig. 4
should be compared with Fig 5, as each will help to interpret the other.
The lobes of the cerebrum are named respectively the frontal, parie-
tal, occipital, and temporal, from the bones with which they lie in con-
tact. They are demarcated from each other hy fissures or clefts that are
clearly defined and more definitely placed than the sulci.
The fissures of Rolando and of Sylvius and the parieto-occipital
fissure are of special importance. (Fig. 4.)
The diagram shows that the frontal and. parietal lobes have four
convolutions cach, and the occipital and temporal lobes three each.
It must be remembered that the cerebrum has two hemispheres—a
right and a left—only one of which is seen in profile. The right hemis-
phere is associated chiefly with the left lateral half of the body, and the
left hemisphere with the right lateral half. Disease of one hemisphere
of the brain may produce, therefore, a disturbance of some or all of the
functions of the opposite side of the body below the head. There are ex-
ceptions to this rule, but it is a safe one to follow in the majority of cases.
Another diagram (Fig. 5) will be introduced later to show certain
areas of the surface of the brain that are believed, in the light of our
present knowledge, to preside over special functions, as, for example,
those of speech, muscular movements of the extremities, sight, hearing,
smell, and touch.
In summary, we are justified in drawing the following conclusions
respecting the cells of the cerebral cortex from the results obtained by
experimentation, clinical experience, and pathological data :—
1. The surface of the brain is the seat of all conscious mental
action. It is the receptacle of all impressions made upon the organs of
smell, sight, taste, hearing, and the tactile organs of the skin. Here,
and only here, do such impressions become transformed into a conscious
appreciation of external objects.
2. The mental powers are the result of different combinations of
memories of past events stored in the cells connected with the special
senses, and the activity of other groups of cells that are probably situ-
ated in the frontal lobes. Although the integrity of the entire organ
is necessary to the unimpeded action of the higher mental faculties
(such as judgment, will, self-control, reason, ete.), the cells of that por-
tion of the frontal lobes that lies in front of the motor centres are per-
haps more closely associated with these faculties than those of any other
area. (Fig. 5.)
3. The central convolutions* of the brain (a part of the frontal and
* Chiefly the precentral gyrus. The post-central gyrus appears to be associated with
both motion and sensation to a greater extent than the precentral.
14 LECTURES ON NERVOUS DISEASES.
parietal lobes of each hemisphere) preside over motion and the mewory
of all motor acts of the limbs and body. The upper part governs the
legs chiefly, the middle part controls the upper extremity, while the
lower part presides over the complex movements of the tongue and lips
necessary to specch. The memories of muscular acts are probably stored
within the cells of the motor area. It is also probable that some forms
of sensation are appreciated by the smaller cells of this area (Moeli,
Tripier, and others).
Mo 7 AREA
SYVLVIAN
FISSURE
Fic. 6—A DiaGram Desicnep By THE AUTHOR TO ILLUSTRATE THE PROBABLE FUNCTIONS
or DirreRENT AREAS OF THE CEREBRAL CORTEX.
The limits of these areas must not be interpreted too literally by
the reader as a basis for diagnosis, Each area probably merges almost
imperceptibly into those which lie adjacent to it. The central portion
of cach are more clearly related to special functions than the peripheral
portions.
The so-called “motor area” is probably connected not only with
voluntary muscular contractions, but also with the conscious apprecia-
tion of all sensory impressions connected with the muscles. It might,
therefore, be more properly designated as the “muscular area.”
THE CEREBRAL CORTEX. 15
4. The occipital lobes* preside over the sense of sight and the memo-
ries of sight-pictures (Munk, Wernicke, and others). The recognition
of familiar objects by the eyes depends on the activity of the cells in the
cortex of these lobes. Hallucinations of vision point strongly toward a
disturbance of the function of these cells. .An inability to recognize
familiar objects, such as faces, letters, words, etc., is one of the promi-
nent symptoms of disease of the occipital region, provided the eyes are
capable of performing their norma! functions. Colored perceptions of
objects and other ocular spectra often accompany irritation of these
lobes. If the whole of the occipital lobe be not destroyed, the unim-
paired part may slowly accumulate new sight memories, and the sense
of vision may thus be slowly regained. This has been proven upon the
dog by Munk.
5. That part of the parietal lobes which is not occupied by special
centres of motion is probably associated with the conscious perceptions
of various tactile impressions and the associated memories of touch,
temperature, degrees of pressure, and pain.
6. The temporal lobes are the probable seat of our conscious appre-
ciation of sounds, odors, and taste (Ferrier, Kussmaul, Gudden, and
others). When these lobes are diseased, the memory of spoken words
may be obliterated, and hallucinations of hearing or deafness may be de-
veloped. I once encountered an interesting case where hallucinations of
sinell (imaginary odors) existed in consequence of disease involving the
apex of this lobe. Persons who have heen suddenly deprived of their
ability te appreciate a question when spoken, but who would reply
promptly to the same question if written before their eyes, have been
reported. In such the memories of sound have been obliterated by dis-
ease of the temporal lobe, but the memories of the form and meaning
of letters have remained intact, because the occipital lobes were not
involved. These patients can sometimes be made to repeat mechanically
word upon word, in a parrot-like way, but the memory of their meaning
has gone forever.
1. The power of speech (when regarded as a merely mechanica: per-
formance) seems to be governed by the inferior frontal convolution and
the area adjacent to it around the lower part of the fissure of Sylvius,
* Ferrier origiually placed the visual centres in the angular convolution of the parietal
lobe (Fig. 4). Iam led to believe that this is an error. This seems to be proven by an
analysis of cases collected and published by Starr and Seguin. Wernicke has also lately
shown that the visual fibres pass beneath the cortex of the angular gyrus in order to reach
the occipital cortex. This discovery helps to explain the effects of destruction of the
angular gyrus upon sight, as observed by Ferrier, Dalton, and others. Sight was de-
stroyed by these observers, probably, by damage done to tracts of fibres lying beneath
the cortex, rather than by a destruction of the cortical cells alone.
16 LECTURES ON NERVOUS DISEASES,
(Fig. 24.)* Butit must be remembered that our remarks are usually
called forth by some form of excitation, such as a spoken question, an
impression upon the eye, or some form of irritation of the sensory
nerves, as in the case of pain, tickling, etc., for example. Disease of
this limited area of the brain surfice causes patients to frequently
interpolate wrong words in conversation, in spite of the fact that they
grasp the meaning of all that transpires about them, and have the
memories of past events perfectly at their command. Such a subject
could write a reply to any spoken or written question with perfect
accuracy, although he might speak it incorrectly. If he were asked
to repeat words selected as a test of codrdinated movements of the
tongue and lips, he would probably fail to do so with his accustomed
facility. This subject will be discussed in subsequent pages.
8. That we are endowed with memories of muscular movements is
well illustrated by a case observed by Professor Charcot, of a gentleman
who was rendéred incapable, by disease of his brain, of recognizing either
printed or written language, but who could grasp the meaning of both
with ease by tracing out the curves with his fingers. The habit of
writing had impressed the mind with the symbols of thought, through
the agency of the muscles.
9. Some collections of cells within the deeper parts of the brain
(the corpus striatum and optic thalamus of each cerebral hemisphere)
are probably distributing centres for all impulses that pass either to or
from the cerebral cortex.
They act as “‘middle-men,” as it were. They are capable, as illus-
trated in the case of the mutilated frog previously referred to, of an au-
tomatic control over movements; but, as far as we know, there is no
reason to think that they are associated in any way with the attribute of
consciousness.
10. The functions of the cerebellum, the pons Varolii, and the me-
dulla oblongata (see Fig. 1) are too complex to be fully discussed here.
Their cells are called into action in a reflex manner, rather than by voli-
tion. There is reason to believe that the cerebellum is an “informing
depot” for the cerebrum (Spitzka), and a ‘store-house for nerve force”
(Mitchell). The medulla oblongata presides over acts that are chietly
outside of the domain of the will; such as the beating of the heart, the
worm-like movement of the intestine, the regulation of the calibre of the
* Destruction of the centre of Broca and the island of Reil, seems to deprive the indi-
vidual of those memories which are associated with the proper cobrdination of the apparatus
of speech. Such patients cannot pronounce words which they may be able either to recog-
nize by sight or to understand perfectly when spoken. The substitution of wrong words
in conversation (paraphasia) is more commonly encountered than true ataxic aphasia
when the island of Reil is involved. This subject will be more fully discussed later,
THE NERVE FIBRES. 17
blood-vessels to the wants of the different organs, the modifications of
blood-pressure, and other functions that are essentially vital.
THE NERVE FIBRES.
We now come to the second anatomical element of nervous tissues.
If we pull a brain apart so as to expose its central portions, we shall be
able to see that distinct bundles of extremely delicate white threads com-
pose each “crus cerebri,” or the leg of the hemisphere (Fig. 1), and
that the thousand filaments which form each bundle diverge within the
hemisphere and pass to its surface. We have grounds for the belief that
each of these threads becomes united to a cell.
These are the nerve fibres. Each of these threads is insulated by
a protective covering so as to prevent the diffusion of its currents to
other fibres. The white substance of the brain is composed exclusively
of fibres.
Of those that constitute the central portion of the cerebrum, one set
serves to connect the cells of different areas of the cortex of each hemis-
phere (the “associating fibres”). These do not cross the mesial line of
the skull. ‘They allow of comparison of different memories, etc., and are
probably essential to the higher mental faculties. The areas of sight,
hearing, smell, motion, general sensibility, and taste, of each cerebral
hemisphere, are thus brought into communication with each other.
These fibres will be discussed at a greater length in connection with
aphasia.
A second set serves to join the cortical cells of homologous parts
of the two hemispheres of the cerebrum. They are evidently designed
to promote a simultaneous action of the two hemispheres upon corre-
sponding parts of the body, as illustrated in rowing a boat with two
hands, swimming, etc. These are called “ commissured fibres.” (Fig. 6.)
A third set comprises those fibres that pass from each hemisphere
into the spinal cord. These are known as the “ peduncular fibres,”
because they help to form the stem of the brain, or the crus cerebri (see
Figs. 1 and 6). :
A fourth set may be said to comprise those fibres that are associated
directly with the organs of special sense, the nose, eye, ear, tongue, and
skin. Some of these belong to the peduncular group.
Finally, a fifth set, known as the fornia, serves to connect the corti-
cal cells of the temporal lobe of each cerebral hemisphere with a mass of
cells buried deeply within the corresponding hemisphere, known as the
optic thalamus. The function of these peculiarly arranged fibres is not
yet determined with positiveness.
We have already discussed the réle which the nerve fibres play in
connection with the brain cells. They are the channels of transmission
9
al
18 LECTURES ON NERVOUS DISEASES.
of nerve impulses. Some carry impressions of a sensory character ;
hence their currents travel from peripheral parts to the cells of the brain.
Others convey motor impulses from the brain cells to the muscles.
eo
some 2
Fic, 6—A DIAGRAM DESIGNED BY THE AUTHOR TO SHOW THE GENRRAL ARRANGEMENT OF
Tur Fires OF THE CEREBRO-SpINAL System. (Modified from Landois.) The shaded
_portions represent the collections of gray matter. Qn the left side of the diagram, the sea-
sory fibres of the crus are traced upward from the spinal cord to different portions of the
cerebrum; onthe right side, the »zofor fibres are similarly represented. Numerals are used
in designating the sexsory and commissural fibres; the motor fibres are lettered in small
type. The cortical layer is shown at the periphery of the cerebral section, with commis-
sural fibres (1) connecting homologous regions of the hemispheres, and associating fibres
(a.s.) connecting different convolutions of each hemisphere. c¢.#., Caudate nucleus of the
THE NERVE FIBRES. 19
corrus sreratum; L.N., lenticular nucleus of the same; O, T., OPTIC THALAMUS of
each hemisphere, united to its fellow in the median line; ¢. g., CORPORA QUADRIGEMINA }
c, 2., CLAUSTRUM, lying to the right of the letters; c.¢., CORPUS CALLOSUM, with its commis-
sural fibres; S, FISSURE OF SyLviuS; /’, LATERAL VENTRICLE, the fifth ventricle being shown
between the two layers of the sepévan lucidum, C,the motor tract of the CRUS CEREBRI (Jas7s
cruris—crusta); 7, the sensory tract of the CRUS CEREBRI (¢eg7entum cruris); C/, the
cerebellar fasciculus; e,the point of decussation of the motor fibres of the spinal cord; /, the
course of the decussating motor fibres of the spinal cord below the medulla, showing their
connection with the cells of the anterior horns of the gray matter, and their continuation into the
anterior roots of the spinal nerves (g); a, fibres which radiate through the caudate nucleus; 4,
fibres of the “‘¢xternal capsule ;’’ ce, fibres which radiate through the lenticular nucleus; ¢@,
fibres of the “external capsule; 2, 3, 4, 5, 6. 7, 8, 9, sensory fibres radiating from the
tegumentum cruris to the cortex by means of various nodal masses of gray matter; 11, course
of the sensory fibres of the spinal cord (shown by dotted lines), intimately connected with
the posterior root of the spinal nerve (12), and decussating at or near to the point of entrance
into the spinal cord. This diagram may be studied in connection with Figs. 12, 15, 16, 36,
and 37, with possible benefit to the general reader. In this diagram, the direct pyramidal
fbres are not shown (see Fig. 29), nor the gray matter of the pons.
Different observers have been able to trace the course and termina-
tions of the separate bundles with exactness hy means of methods lately
discovered. Nature, under certain conditions, makes the dissections
during life; and we, after death, can study out the details of her work.
In this way we have learned facts that no human dissection could have
determined. The discovery of Tiirck that nerve fibres degenerate (as a
result of malnutrition) when severed from the nerve cells, enables us to
investigate the results that follow destruction of ccrtain limited areas
of the cortex of man by disease or mechanical injury. When sections
across such a brain are made and examined under a glass (proper stain-
ing reagents being employed) the area of the degenerated fibres be-
comes as clearly depicted from that of healthy brain fibres as would
an ink-spot upon a table-cloth. An examination of successive sections
enables us to trace the course of the fibres that were originally connected
with the cells of the diseased area to their peripheral connections. Some
years after Turck’s original paper, Flechsig opened another field of inves-
tigation. Heshowed that during the development of the embryo, certain
bundles of nerve fibres in the brain and spinal cord became completely
formed before others. By means of sections of embryotic brains, he and
his followers have been able to confirm many of the facts made known to
us by Turck’s method. Finally, Gudden has lately proven that extirpa-
tion of the eye and some other organs, as well as the divisions of some
nerve-tracts, in the newly-born animal, are followed by a proximal degen-
eration. of the fibres connected with the organ removed.
Let me remark here that every nerve impulse sent to the brain does
not travel along a continuous fibre to reach the cell of the cortex that is
capable of receiving it; and the same holds true of all motor impulses dis-
patched from the brain to the muscles. All impulses are passed from cell
to cell by means of connecting fibres. In this way they eventually reach
the cerebral cortex, just as water-buckets are passed up a ladder, in case
of fire, to use an illustration borrowed on account of its aptness. The
object of this arrangement is to allow of an independent action of certain
collections of cells (that are subservient to the cortical cells of the cere-
20 LECTURES ON NERVOUS DISEASES,
brum) in case the required response does not necessitate volition or con-
sciousness. Many of the vital processes (such as the beating of the heart)
are governed by what is known as ‘reflex action.” We cannot check
them by the will, and, as a rule, we are unconscious that they are con-
stantly going on.
THE GANGLIA AT THE BASE OF THE CEREBRUM.
Buried within the substance of each cerebral hemisphere, isolated
gray masses (composed of nerve-cells) exist. They may be revealed by
vertical or horizontal cross-sections of the hemispheres.
Among these may be prominently mentioned : (1) the caudate and
lenticular nuclei of the corpus striatum (so named from the striped appear-
ance which they present); (2) the optic thalamus (a term which signifies
the “bed” of the optic fibres); (8) the geniculate bodies, connected with
the optic tracts (Fig. 21); (4) the amygdale, each being formed by the
tail-like prolongation of the caudate nucleus of the corresponding hemi-
sphere (Fig. 9); and (5) the basal ganglia of Meynert.
The limits of this chapter will preclude more than a hasty and very
imperfect summary of the functions of the corpora striata and the optic
thalami.
In the Journal of Nervous and Mental Diseases, | published some
years ago two lectures delivered by me upon these ganglia. In some
respects, I have changed my views relating to a few disputed points con-
cerning the structure and probable functions of these bodies since these
lectures were published. I shall quote, howevcr, some paragraphs from
these articles from time to time, with modifications in the phraseology.
THE CORPUS STRIATUM.
Within each cerebral hemisphere, two nodal masses of cells are im-
bedded, known as the corpus striatum and the optic thalamus (Fig. 1).
Because these bodies lie near to the base of the cerebrum, they are col-
lectively called the ‘ basal gangliu” of the hemispheres.
Each corpus striatum is divided (hy the fibres which constitute
the so-called “internal capsule” of each hemisphere) into two distinct
portions ; one of which projects into the Interal ventricle, while the other
does not. These are known as the ¢ntra-ventricular portion, or the
“ caudate nucleus,” and the exrtra-ventricular portion, or the “ lenticular
nucleus.” Fig. 6 will make this apparent to the reader.
The two nuclei of the corpus striatum become jotned both anteriorly
and posteriorly ; hence the separation of these masses is only partial.
Horizontal and vertical cross-sections of the cerebrum show these nuclei
as distinct from each other, as a rule.
Space will not allow of an anatomical description of these bodies.
THE CORPUS STRIATUM. Sl
I quote, therefore, a few paragraphs from two monographs of mine, re-
lating to these nuclei :—*
“The clinical results of lesions of either nucleus are attributed by
Afferent fibres of
corpus striatum
“‘cortico-striate
group.”
|
Efferent fibres : \ |
of corpus striatum, | |
\ | Cerebellar fibres to
, | \ corpus striatum
ise Date a abil A Peed | A secouding to
a ii c Uys).
B
Fic. 7.—A Diacram DESIGNED BY THE AUTHOR TO SHOW THE AFFERENT AND EFFERENT
FIBRES OF THE CoRPUS STRIATUM. C.J, “caudate nucleus,’’ or ventricular portion of
corpus striatum; Z, WV, ‘lenticular nucleus,’’ or extra-ventricular portion of corpus stria-
tum; d—S, median line, separating cerebral hemispheres; P—/’, psycho-motor regions of
the cortex; a, peduncular fibres connected with Z, 4; 4, fibres of the so-called “internal
capsule ;”’ ¢, fibres connected with C. NV; O, olfactory fibres. (Luys.)
most authors to pressure effects upon the motor fibres of the internal
capsule. In no instance, to my knowledge, has the destruction of these
nuclei produced psychic manifestations.
* Journal of Nervous and Mental Diseases, 1883.
22 LECTURES ON NERVOUS DISEASES.
The hemiplegia, which follows injury to the corpus striatum, is
confined chiefly to the side opposite to the lesion; in cases of extreme
rarity, paralysis of motion on the same side has been clinically recorded.
Flechsig has proved that such cases are to be interpreted as the result
of an individual peculiarity in the relative number of decussating and
direct pyramidal fibres (Fig. 29).
“The corpus striatum, like the optic thalamus, may possibly (as Luys
suggests) be considered, as a territory in which cerebral, cerebellar, and
spinal activities are brought into intimate communication. It probably
acts as a ‘halting place for voluntary motor impulses’ emitted from the
cerebral cortex. It enables these impulses to ‘become modified and pos-
sibly reinforced by currents derived from the cerebellum; and, by its
efferent fibres, it transmits centrifugal motor impulses along the projec-
tion system to different groups of cells within the spinal gray matter,
whose individual functions they tend to evoke,’”
Luys states that this ganglion probably acts as a condenser and
modifier of all motor acts which are the result.of volition ; and manifests,
through the agency of its satellites (the cells of the anterior horns of the
gray matter of the spinal cord), the outward expressions of our person-
ality. Without the influence of the cerebral hemispheres, it is also
capable, by means of cerebellar innervation, of governing all the complex
muscular movements required in maintaining equilibrium (coérdinated
movements). Finally, it may be presumed to “ possess the power of
analysis of cerebral and cerebellar currents received simultaneously, and
of materializing them by the intervention of its nerve-cells, projecting
them in a new form, amplified and incorporated with the requirements
of the general organism.”
Experiments made upon the caudate and lenticular nuclei can hardly
be said to have afforded results which can be made the basis for positive
deductions respecting the functions of each. Nothnagel employed injec-
tions of chromic acid into the substance of each, and also destroyed them
by means of an instrument devised for that purpose, but he arrived at no
positive conclusions, save that the lenticular nucleus seemed to have a
more decided influence upon motion than the caudate nucleus, when the
nuclei of both sides were simultaneously destroyed. Observations in
comparative anatomy seem to show a relationship of the caudate nucleus
with the fibres of the leg and of the lenticular nucleus with those of the
arm.
Some observers claim to have destroyed the entire ganglion without
any marked disturbance of sensory or motor phenomena. Collected
cases of lesions confined to cither nucleus fail to show that any perma-
nent symptoms have been produced which are diagnostic of such lesions.
THE OPTIC THALAMUS. 23
THE OPTIC THALAMUS.
Efforts have been made by some of the later anatomists and physi-
ologists who have specially investigated the brain, to subdivide the gray
matter of the thalamus into circumscribed masses or nuclei, and to trace
the fibres which appear to arise from these nuclei to special regions of the
brain and spinal cord. Among the most attractive of these attempts may
be mentioned that of Luys, whose views will be subsequently given in
detail. Whether clinical research and physiological experiment will con-
firm all of these attractive theories, and place them upon a ground as
worthy of credence as the deductions of Broca, Munk, and Ferrier re-
garding the functional attributes of other parts of the brain, time alone
Fic. 8.—A DraGeam or tHe Nuciet or THE Optic THALAMUS AND THE CONVERGING Freres
ASSOCIATED WITH THem. (After Luys.) 1, converging fibres of posterior convolutions;
2, same, of middle convolutions; 3, same of posterior convolutions; 4, 4’, 4/’, cortical
periphery as related to the central gray masses; 5, optic thalamus; 6, corpus striatum; 7,
anterior (o¢/actory) centre; 8, middle (oftzc) centre; 9, median (sexsztive) centre; 10, pos-
terior (acoustic) centre; 11, central gray region; 12, ascending gray fibres of visceral inner-
vation: 13, gray optic fibres; 14, ascending sensitive fibres; 15, ascending acoustic fibres;
16, series of antero-lateral fibres of the spinal axis going to be lost in the corpus striatum.
can decide. They are opposed to many of the conclusions of Meynert,
Flechsig, Wernicke, Spitzka, Starr, and others.
“According to the researches of Luys, four isolated ganglions may
be demonstrated in the thalamus. Arnold, in common with some other
anatomists, has recognized three of these, and the fourth is now added
by the author quoted. This author states that these ganglia are arranged
in an antero-posterior plane, and form successive tuberosities upon the
thalamus, giving that body the appearance of a conglomerate gland.
24 LECTURES ON NERVOUS DISEASES.
“The anterior ganglion of Luys (corpus album subrotundum) is
especially prominent. It is said by this author to be developed in ani-
mals in proportion to the acuteness of the sense of smell. By means of
the ‘ tenia semi-circularis,’ this ganglion (according to this author) may
be shown in the human species to be connected with the roots of the
olfactory nerve. Respecting it, he says: ‘Direct anatomical examination
shows that there are intimate connections between the anterior centre
Fic. 9.—A TRANSVERSE SECTION OF THE Human BRAIN FROM Berore Backwarp. (After
Flechsig.) MC, caudate nucleus; N C’, the tard of N-C, cut across (the amygdala);
L WN, lenticular nucleus, with its three subdivisions (/, //, ///); TH, optic thalamus; F,
frontal lobe; 7S, temporal sphenoidal lobe; Q, occipital lobe; Cls, c/austrum,; IK,
thalmo-tcnticular portion of internal capsule; K, knee ofsame; /A’, caudo-lenticular
portion of same; EA, extermsl capsule, lying between the lenticular nucleus and the claus-
trum; 4, fornix cut across; /n, insula, or island of Reil; Op, depth of Sylvian fissure
beneath the operculum; sc, middle commissure of the thalamus; #/, posterior horn of
lateral ventricle; a4, anterior horn of same; SZ, septum lucidum.
and the peripheral olfactory apparatus. On the other hand, in confirma-
tion of this, in the animal species, in which the olfactory apparatus is
very much developed, this ganglion itself is proportionally very well
marked. Analogy has thus led us to conelude that this ganglion is
THE OPTIC THALAMUS. Ds
in direct connection with the olfactory impressions, and that this marks
it as the point of concentration toward which they converge hefore being
radiated toward the cortical periphery.’
“The second or middle centre is in apparent continuity, according
to Luys, with the fibres of the optic tract. JIe considers it on the
same grounds as those previously quoted respecting the anterior centre,
asa seat of condensation and radiation of visual impressions.* There
seems to be undisputable grounds for the belief that the thalamus, the
outer geniculate bodies, the anterior corpora quadrigemina, and the cor-
tex of the occipital lobes are, in some way, associated with the percep-
tions atforded by the retina. (Munk, Wernicke, Monakow, and others. )
“We know that extirpation of the eye is followed by more or less
complete atrophy of the outer geniculate body of the opposite side,
although the inner geniculate body scems to remain unaffected. The
experiments of Longet, who destroyed the optic thalami upon both sides
without being able to note any impairment of vision, or influence upon
the movements of the pupil; and those of Lussana and Lemoigne, who
found that blindness of the opposite eye followed unilateral destruction of
the thalamus, may suggest the possibility, in the former, of the escape of
this centre, and, in the latter, its destruction. It is diflicult to devise any
experiment which will positively settle the bearings of the thalamus upon
vision; because it is almost impossible to destroy special portions with
accuracy, or if this were insured, to avoid injury to adjacent. structures.
Fournié claims to have effected the separate annihilation of the special
senses of smell and vision by injections made into different parts of
the thalamus of animals; and his experiments, if subsequently verified,
will tend to confirm some of the theories advanced by Luys.
“ Ritti has pointed out that irritation of the thalamus may play an
important part in the development of hallucinations.
“The third centre (‘median ganglion’ ‘of Luys) is described as
about the size of a pea, and situated mathematically in the exact centre
of the thalamus. To it, the discoverer ascribes the function of presiding
over and condensing all sensory impressions.
“The fourth posterior centre is stated to act as a halting place and
condenser of auditory impressions. Two instances where the brains of
deaf mutes were found to present a localized lesion of this centre are
reported by Luys.
“The views here expressed are quoted on account of their origi-
nality; and because the author of them ranks high as an authority upon
*Luys states that it is scarcely visible in those animals (the mole as an example)
where the optic nerves are rudimentary. The view is now more generally accepted that
the posterior tubercle of the thalamus (the pulvinar) is functionally associated with the
optic fibres.
26 LECTURES ON NERVOUS DISEASES.’
the subject of which he speaks. ‘The numerous cases of cerebral hemor-
rhage which have been reported, where the thalamus was apparently the
seat of localized injury, are too often accompanied with a clinical history
which points toward pressure upon the internal capsule, to be of value
as confirmatory evidence of the existence of special centres in the thala-
mus.* The effort of Luys to adduce cases of hemianesthesia in support
of his views regarding the function of the ‘median centre’ of the thala-
mus, merely because a lesion of that ganglion was found in an area
defined by him as the normal limits of that special centre, must not be
deemed conclusive; because the same effect might have been produced
by pressure upon the fibres within the posterior third of the internal
capsule of the cerebrum, There is reason to hope, and possibly to be-
Fic. 10.—Srction Across THE Optic THALAMUS AND CoRPUS STRIATUM IN THE REGION
oF THE MippLe Commissure. (Shafer after a preparation by Mr. S. G. Shattuck ) Natu-
ralsize. ¢/., thalamus; a., é., z.,its anterior, external, and internal nuclei respectively ; w, its
latticed layer; 7. c., middle commissure ; above and below it is the cavity of the third ven-
tricle; ¢. ¢., corpus callosum ;_/, fornix, separated from the third ventricle and thalamus by
the velum interpositum. In the middle of this are seen the two veins of Galen and the choroid
plexuses of the third ventricle; and at its edges the choroid plexuses of the lateral ventricles ;
z.s., tania semicircularis; cv., forward prolongation of the crusta passing laterally into the
internal capsule, 7. c.; s. t. »., subthalmic prolongation of the tegmentum, consisting of
(1) the dorsal layer, (2) the zona incerta, and (3) the corpus subthalamicum ; s. 2., substantia
nigra; #. ¢., nucleus caudatus of the corpus striatum; #. 2., nucleus lenticularis ; ¢. ¢., e2-
ternal capsule; cé., claustrum; J, island of Riel. : 7
lieve, that sooner or later isolated ganglia within the optic thalamus will
be demonstrated to exist by normal and pathological anatomy, as well
as by physiological experiment; but the conclusions even of so promi-
nent an author should not be fully accepted without further testimony
to substantiate their accuracy. Some of the later observations respecting
the optic fibres, seems to disprove the view of Luys. ,
“A few interesting cases have, however, been brought forward, which
certainly seem to sustain the views advanced.. A case reported by Hun-
*If permanent symptoms remain after a lesion of the thalamus is suspected to exist,
the internal capsule is probably indirectly involved. (See subsequent pages relating to the
internal capsule. )
THE OPTIC THALAMUS. 27
ter,* where a young woman successively lost the senses of smell, sight,
sensation, and hearing, and who gradually sank, remaining a stranger to
all external impressions, disclosed at the autopsy a fungus hamatodes
which had gradually destroyed the optic thalamus of each side, and the
optic thalami alone, if the drawing given is reliable. Again, Fourni¢’s
experiments on living animals points strongly to the existence of local-
ized centres in the thalamus. Three instances of unilateral destruction
of smell, observed by Voisin and reported by Luys, have been found to
be associated with a destruction of the anterior centre of the thalamus.
A hemorrhagic effusion into the thalamus, on a level with the soft com-
missure (the situation of the optic centre of Luys), produced (in the ex-
perience of Serres) a sudden loss of sight in both eyes. Later observa-
tions seem, however, to point toward a relationship between the poste-
rior extremity of the thalamus (the ‘pulvinar’) and the optic fibres.
“Ritti's paper upon the effects of irritation of the thalamus upon
the development of hallucinations, lends strength to the view that that
ganglion in some way regulates the transmission of sensory impressions
of all kinds to the cerebral cortex; and confirms the opinion that ‘the
optic thalami are to be regarded as intermediary regions which are inter-
posed between the purely reflex phenomena of the spinal cord and the
activities of psychial life.’
“The view taken by Lussana and Lemoiegne, that the optic thalami
contained motor centres in animals for the lateral movements of the fore-
limbs of the opposite side, seems to be completely overthrown by patho-
logical statistics in the human race. The results obtained by these ex-
perimenters are also at variance with the belief, which has now become
general among neurologists, that the thalami are intimately connected
with the sensory tracts of the cerebrum and cord; since they concluded
that no evidence of pain or any loss of sensibility resulted from injury
to these bodies.
“The effects of all experiments on animals, however, agree entirely
with the general experience of pathologists, that lesions of both the
thalamus and corpus striatum produce results upon the opposite side of
the body; whether the symptoms produced point to a disturbance of the
kinesodic (motor) or ssthesodic (sensory) tracts. The view originally
advaneed by Carpenter and Todd, that the thalami are concerned in the
upward transmission and claboration of sensory impulses, in contradis-
tinction to the corpora striata, which are concerned in the downward
transmission and elaboration of ‘motor impulses, seems to be gaining
ground, and many facts may be urged in its favor.”
The experiments of Monakow on rabbits lead him to views not en-
tirely dissimilar to those advanced by Luys. He places the cortical
* Medico-Chirurg. Trans., London, 1825, vol. xiii.
28 LECTURES ON NERVOUS DISEASES.
connections of centres in the thalamus, somewhat differently, however,
from the conclusions already mentioned. According to this observer,
the posterior tubercle (the pulvinar) is related to the visual tracts, as is
also the external geniculate body; the internal geniculate body is related
to the auditory fibres, and the cortical centres of hearing in the first
temporal convolution; and the anterior tubercle and median nucleus
are related to the frontal lobes.
The pillars of the fornix seem to unite the thalamus with the cor-
tical centres of smell and taste; and, according to Ferrier, with the cor-
tical centres of tactile sensibility.
Hemichorea and hemiathetosis have been observed in connection
with lesions of the thalamus; but they must, to my mind, be regarded as
an evidence of irritation of the motor fibres of the internal capsule
(which lie closely adjacent to the thalamus). Fig. 9 will make this rela-
tionship clear to the mind of the reader.
THE CAPSULAR FIBRES OF THE CEREBRUM.*
Vertical and horizontal cuts made through the cerebrum exhibit a
well-defined tract of fibres in each hemisphere which separates the len-
ticular nucleus from two other gray masses of the same hemisphere,
viz., the caudate nucleus and the thalamus.
This tract of fibres (inclosed between these nodal masses of cells)
is termed the “internal capsule,” because it bounds the lenticular nucleus
on its mesial aspect. ; that Goll’s columns increase in size from below upward; that the direct cerebellar col-
umns appear in C, and increase in size in B and A; that the crossed pyramidal columns
reach the surface in D; and that the shape of the gray substance differs in all the sections.
The numerals employed in the cuts indicate the order of development of the various parts
designated. It will be seen that the motor-tracts of the cord are the last to attain their com-
‘plete development.
47
of
If in the brain, the
48 , LECTURES ON NERVOUS DISEASES.
uated in (1) the coverings of the brain, (2) the external gray matter that
invests it like a cap (the cerebral cortex), or (3) in parts more or less dis-
tant from its exterior. It is important, from a standpoint of prognosis
and treatment, that he comes to some definite conclusion also regarding
the character of the trouble. If the disease he confined to the spinal
cord of the patient, it becomes necessary for the physician to discrimi-
nate again between affections that follow separate bundles of nerve fibres
' (systematic lesions of the cord) and those that spread transversely from
column to column (focal lesions of the cord); and to decide also as to the
height of the lesion, its pathological character, and the special regions
that are affected by it. Finally, if the paralysis be due to some spinal
nerve, the possibility cither of brain or spinal disease must be excluded,
and the cause must be sought for along the course of the nerve whose
function is impaired.
Betore I discuss the clinical tests of nervous diseases in detail, I
direct. the attention of the reader to some extracts from the chapters on
the Disenses of the Brain and Spinal Cord that are embodied in the third
edition of my work on ‘Surgical Diagnosis.’
MOTOR PARALYSIS.
Anything which tends to impuir the generating power of the nerve
centres or the conducting power of nerve fibres may produce paralysis
of motion or sensation.
“Motor paralysis (when due to a lesion affecting the cerebro-spinal
axis) can result, therefore, from any condition which interferes with the
motor conyolutions of the brain, or the nerve fibres which start from
them and are continued «as the so-called ‘motor tract.’ The latter aid
in all voluntary movements of the ertremities, They pass through the
following parts successively: (1) The white substance of the cerebral
hemispheres; (2) the corpora striata; (8) the crura cerebri; (4) the pons
Varolii; (5) the medulla oblongata; and (6) down the motor columns of
the spinal cord.
“ The disturbing lesions may be therefore classified as: (1) Those of
the gray matter of the convolutions of the brain (cortical lesions) ; (2)
those of the central mass of the cerebral hemispheres, including lesions
of the ‘‘ internal capsule ;” (3) those of the corpora striata; (4) those of
the crura cerebri; (5) those of the pons Varolii; (6) those of the medulla
oblongata; (7) those of the spinal cord.
“The various tests which are employed to determine the existence
and extent of a loss of muscular power will be given later.”
CORTICAL PARALYSIS OR SPASM. 49
CORTICAL PARALYSIS OR SPASM.
These may be dependent upon some lesion of the gray matter of the
cerebral convolutions (the cerebral cortex). They may occur in con-
nection with abscesses, blood-clots, spots of softening, tumors, depressed
bone, meningeal thickenings and exudations, embolism, thrombosis, etc
The researches of Ferrier, Luciani, Exner, Horsley, Beevor, and
others have lately taught us the situation of special motor centres scat-
tered over the convolutions of the so-called “motor area” of the cere-
brum. From this standpoint we are often enabled to judge of the seat
of the lesion by the aid of the groups of muscles which exhibit the
paralytic state (monoplegia). Hughlings-Jackson and Brown-Séquard
have added to our knowledge of the relative effects of destructive and
irritative lesions of the cerebral cortex.
“ Trritative lesions of the cerebral cortex are usually ushered in by
convulsive attacks, which leave the subject paralyzed in some special
group of muscles (monoplegia); or, if hemiplegia ensues, some parts of
the body are more affected than others. The paralysis is usually tran-
sient, and returns again after subsequent convulsive attacks. These irri-
tative lesions are particularly liable to be of syphilitic origin.
“ Destructive lesions of the cerebral cortex are characterized by
paralysis of special groups of muscles (monoplegia, or mono-anesthesia),
as was the case with the irritative lesions. This is in marked contrast to
the hemiplegia, or hemianzsthesia which follows lesions of the central
portions of the brain. If the lesion be very extensive coma may be pro-
duced, but consciousness is not usually lost unless the attack be accom-
panied by convulsions. Pain ofa local character within the head is often
complained of, and percussion over the seat of the lesion frequently elicits
it, if it should be absent. The sensibility of the paralyzed parts is not
impaired unless more or less sensory paralysis exists as a complication.
The paralyzed muscles exhibit the normal electro-contractility. As is
the case with all cerebral lesions, the paralysis is developed on the side
opposite to the exciting cause (except in very rare instances). In cor-
tical lesions of the motor area, the muscles frequently exhibit a state of
post-paralytic rigidity in the early stages of the disease. The various
types of monoplegia and the surgical guides for trephining over special
motor centres have been discussed in the Author’s work upon the anatomy
of the nervous system.
Iforsley has lately added a valuable contribution to the subject of
cortical localization, based upon experimentation on monkeys, and also
on observations in ten cases where the diseased area was successfully
determined in the human subject prior to operative procedure. IIis con-
clusions are therefore worthy of note. They may be summarized as
follows :— 4
50 LECTURES ON NERVOUS DISEASES.
1. Sulct, or fissures, are not to be regarded as accurate boundaries to
cortical areas, although they constitute valuable landmarks for operative
procedures upon the cortex.
9. The motor centres, according to this observer, are capable of
further subdivision than those described by Ferrier, and they overlap
each other at their borders.
3. The face area, taken as a whole, embraces the lower third of
both central convolutions (Fig. 4). This is subdivided into (a) an upper
and anterior portion, which controls the upper part of the face and the
angle of the mouth; (b) the anterior half of the lower portion, which
governs the movements of the vocal cords ; and (c) the posterior half of
the lower portion, which governs the lower part of the face and the floor
of the mouth.
4. The area for the upper limb occupies the middle third of both
central convolutions, and also the base of the superior and middle frontal
convolutions. It joins, and also merges with, the area for movements of
the head and neck in the middle frontal gyrus, and with that of the leg
in the superior frontal gyrus.
In the area described as pertaining to the upper limb, the uppermost
part is thought to control the muscles of the shoulder; below, and pos-
teriorly, the elbow is represented; still further below and somewhat an-
teriorly, the wrist; next in order, anteriorly, the finger-movements are
placed, and lowest of all, and posteriorly, the thumb-movements are
located. These views he substantiates by observations made in cases of
cortical tumors, where spasm was developed and appeared first in ar
isolated region of the upper limb.
5. The area for the lower limb is described by this observer as em-
bracing the upper portions of the two central convolutions; also the
whole of the superior parietal, the base of the superior frontal convo-
lutions, and the para-central lobule. This description is not materially
different from that of Ferrier (Fig. 3).
The subdivisions of this area are as yet incompleted, but the points
given are of interest to the surgeon. The movements of the big toe are
referred to the para-central lobule; those of the leg alone to the middle
part; those of the leg and arm combined to the most anterior portion.
Most of these conclusions agree in the main with those of Ferrier
(Fig. 3).
6. The area for movements of the head and neck, and also for con-
jugate deviation of the eyes, is placed by this observer (in common with
Ferrier and Munk) in the bases of the three frontal gyri (see 12, in Fig. 3).
“'. Respecting the steps required to locate the fissures of Rolando
and Sylvius upon the human subject during life (as a basis for surgical
procedures) the following conclusions are reached :—
CORTICAL PARALYSIS OR SPASM. 51
(a). The method first described by Thane for locating Rolando’s
Jissure is adopted. A careful measurement is first made along the mesial
line of the skull, starting from the root of the nose and extending to the
occipital protuberance. This distance is then halved. The fissure of
Rolando at its upper part lies one-half inch posteriorly to its central
point. A strip of flexible iron (with a movable arm placed at an angle of
sixty-seven degrees to it) is now laid upon the middle line of the head;
the point of junction of the movable arm with the mesial strip being
carefully located at the point previously determined as overlying the
upper end of Rolando’s fissure. When this is accurately done, the
movable arm marks the course of the upper two-thirds of the fissure of
Rolando, but, as the lower third tends to bend slighty backward, it does
not as clearly define the lower third of that fissure.
(b). To accurately locate the fissure of Sylvius upon the skull no
little precision is required. A few points in the bones of ‘the skull have
first to be accurately determined. These are as follows:°(1) The point
where the temporal ridge crosses the coronal ‘suture (the “stephanion”).
This can usually be felt with the finger, the coronal suture appearing to
the touch either as a depression or as a ridge lying between two grooves.
(2) Exactly midway between the stephanion and the upper border of the
zygoma, ona line drawn vertical to the zygoma toward the stephanion,
lies another point known as the “ pterton.” (3) To determine the highest
point of the suture which exists between the squamous portion of the
temporal bone and the inferior border of the parietal bone (the “ squamo-
parietal” suture) a measurement has to be made, because that suture
cannot be felt beneath the temporal muscle.
In front of the temporo-maxillary articulation, an upright upon the
line C-D in Fig. 20, would cross the zyzoma. The junction of the upper
and middie thirds of the measurement made upen such a vertical line
between the upper border of the zygoma and the ridge formed by the
temporal muscle, indicates the situation of the highest point of the
squamo-parietal suture.
The anterior limb of the Sylvian fissure starts from a point which
lies from one-half to one line (one-twenty-fourth to one-twelfth of an
inch) in front. of the “pterion.” It runs anteriorly and upward from
that point. The posterior limb passes backward and slightly upward
from the same point.
8. The sulci of the frontal lobe, and also the inter-parietal sulcus
(which limits the so-called “motor area” of the cortex posteriorly), are
next to be located upon the exterior of the skull, in order to map out
the convolutions. The guides to the sulci are as follows :—
The precentral sulcus lies somewhat behind the coronal suture and
parallel to it. It extends to about the middle of Rolando’s fissure.
52 LECTURES ON NERVOUS DISEASES,
The inferior frontal sulcus diverges from the precentral at about
the level of the temporal ridge.
The superior frontal sulcus starts at a point in the precentral gyrus
somewhat posterior to the line of the precentral sulcus if continued
upward. The exact point is about midway between the fissure of Ro-
lando, and an upward continuation of a line in the direction of the pre-
central sulcus. Its altitude in the cerebrum is slightly above the level
of a point (midway between the mesial line of the skull, and the centre
of the parietal eminence) which designates the lower nes of the superior
parietal convolution.
The inter-parielal sulcus in its ascending course starts from a point
on a level with the junction of the middle and lower thirds of Rolando’s
fissure. It turns backward on a level situated midway between the
mesial line of the skull (marked by the longitudinal fissure) and the
centre of the parietal eminence.
HEMIPLEGIA.
This condition is characterized by a paralysis of motion in one
lateral half of the body. It is often associated with more or less anzs-
thesia, but it may exist independently of it. I quote from a previous
article of my own, as follows :—
“ Hemiplegia may be produced by any lesion which interferes with
the free action of the ‘motor tract’ of fibres during their passage from
the motor convolutions of the cerebrum to the columns of the spinal cord;
and lesions of the spinal cord itself (if sufficiently high up and restricted
to a lateral half of the cord on the side which corresponds to the paral-
ysis) may also induce it.
“Tf the lesion be within the cavity of the cranium the hemiplegia
will be on the opposite side of the body; if it be spinal the hemiplegia
will be upon the same side.*
“ Hemiplegia from intracranial lesions may be the result of embolism,
thrombosis, apoplexy, softening, abscess, tumors, compression of the
brain from traumatic causes, destruction of limited portions by injury,
general pressure from inflammatory exudations, etc.
“Consciousness is generally lost when cerebral hemiplegia is de-
veloped. Convulsive attacks are not usually present at the onset of
the paralysis. The paralysis is more profound, as a rule, than that of
cortical lesions, and of longer duration. The special senses are not
infrequently involved to a greater or less degree. Other cranial nerves,
which are not associated with the special senses, may also give evidence
of being implicated by the lesion. The facial nerve is most frequently:
affected.
*This rule is not absolutely true, but the exceptions to it are so rare that it is a safe
one to follow in clinical deductions.
CROSSED AND COMPLETE PARALYSIS. D3
“By means of anatomical guides the seat and extent of an intra-
cranial lesion may often be determined with positiveness. The co-exist-
ence of impairment of sensation with motor paralysis is a valuable
diagnostic sign that the exciting lesion is within the substance of the
brain and not upon its surface. The exceptions to this rule are ex-
tremely rare.
“ The localization of non-cortical lesions is more difficult and some-
what less certain than those which are confined to the cortex. A careful
study of all the symptoms presented (when combined with «a knowledge
of modern cerebral and spinal anatomy) will often, however, lead to the
most positive deductions. It should be remembered that accuracy of
diagnosis often leads to- success in treatment of disease, and in no case
is it better exemplified than in the nerve centres.”
CROSSED PARALYSIS.
A condition in which the face or some organ of special sense gives
evidence of an impairment of a cranial nerve, while the body is simul-
taneously rendered hemiplegic on the opposite side, is termed “ crossed
paralysis ”"—the “ paralysie alterne” of the French authors. We owe
much of our knowledge of this subject to Professor Romberg, of
Berlin, who has written extensively upon it.
‘‘The more common forms of crossed paralysis are named from the
cranial nerve which exhibits an impairment of its functions. They are
as follows: First cranial nerve (olfactory) and body type; third cranial
nerve (motor oculi) and body type: fifth cranial nerve (trigeminus) and
body type; seventh cranial nerve (facial) and body type. They will be
discussed later.
“It may be well to remark in this connection that ‘crossed paral-
ysis’ is of special clinical importance, because it often imparts the most
positive information to the surgeon in regard to the seat of the intra-
eranial lesion which has produced it.”
COMPLETE PARALYSIS.
When a lesion is situated at the base of the brain, and is sufli-
ciently large to involve the motor fibres of both hemispheres, the body
may be completely paralyzed below the head.
“Various cranial nerves—chiefly the third, fifth, sixth, and seventh
—are liable to then exhibit the effects of simultaneous pressure upon
them; hence the general paralysis of the body is apt to be associated
with paralytic symptoms confined to the face.
“ Bilateral spinal lesions when situated high up in the cervical
region, may also cause a form of complete paralysis of the body—the so-
called ‘cervical paraplevia.’”
Dt LECTURES ON NEKVOUS DISEASES.
SENSORY PARALYSIS.
The sensation of special parts of the body may be so modified by
lesions of the nerve centres as to constitute a type of paralysis. The
various forms of this condition may exist independently of motor paral-
ysis, or may co-exist with it. The tests commonly employed to detect
the limits and degree of sensory paralysis will be given later.
“Sensory paralysis may be classified as follows: (1) Paralysis of
those cranial nerves which are not endowed with motor attributes; (2)
paralysis of sensory nerves below the head. The latter subdivision
comprises hemiansthesia, general anvesthesia, and local anesthesia.
Fic. 20.—A DiaGram J)ESIGNED BY THE AUTHOR TO ILLUSTRATE THE REGIONS OF THE
Cortex or THE Brain ASSOCIATED WITH SpeciaL PARTS oF THE Bopy, as a GuiIDE
TO THE SEAT oF Destructive Processes IN CONNECTION WITH MoToR PARALYSIS OR
Spasm.—A, 8&, dotted line to indicate the relative depth of the brain in the anterior, middle,
and posterior fossz of the skull; C, D, a line running from the cusps of the teeth of the upper
jaw to the tip of the mastoid process of the temporal bone, ‘This is useful as a base line from
which to erect vertical lines, by careful measurement during life, which shall intersect the
different centres of the brain. Trephining for the relief. of #zonoplegia and afphas7ya can
thus be performed with scientific accuracy. The circle designated in the diagram as the
speech area is related only to the wofer acts required in speech. It has no relationship to
the various forms of sensory aphasia.
The views lately advanced by Horsley (p. 49), seem to suggest that this diagram might
be modified somewhat,
“Among the various clinical evidences of lesions which affect the
sensory nerve tracts of the brain and spinal cord, the folowing may be
mentioned: (1) hypervwsthesia, or an excitation of sensibility ; (2) numb-
ness; (38) formication, or a sensation like the creeping of ants; (4) aboli-
tion of sensation, or complete anresthesin—this condition may be general
or local; (5) anosmia and hemianopsia; (6) delayed sensation, as is
evidenced hy a perceptible interval of time between the contact of a
foreign body with the skin and its conscious ‘appreciation hy the patient
HEMIANZSTHESIA—NUMBNESS AND FORMICATION, 55
when the eyes are closed. The pricking of the skin with a needle is a
test commonly employed to determine the latter condition.
“Some of these conditions will be now considered in their more
important aspects. Others will not be separately described, as they
would require too much space, provided such a résumé was attempted.”
HEMIAN HSTHESIA.
This condition is characterized by a loss only of sensation (not of
motion) in one lateral half of the body. It is often associated with more
or less marked hemiplegia. When hemiplegia and hemianesthesia exist
upon the same side a cerebral lesion may be strongly suspected; when
upon opposed sides, a spinal lesion probably exists.
The tests employed to determine the existence of this state and its
degrees of intensity are the same as those employed in any form of sen-
sory paralysis. They will be described later.
“ Wemianzesthesia (when not due to hysteria or spinal lesions) indi-
cates that the exciting lesion has impaired the conducting power of the
fibres associated with the so-called ‘sensory area’ of the cerebral convo-
lutions (Fig. 5). There is strong clinical evidence to sustain the opinion
that these fibres run in the posterior third of the ‘internal capsule.’
Lesions of this latter region are not infrequently the cause also of more
or less impairment of sight, smell, hearing, and taste, in addition to their
effects upon general sensation. Charcot, Ferrier, Rendu, Raymond, and
others who have studied the effects of lesions of the posterior third of
the internal capsule of the cerebrum concur in this statement.
“ Hemianesthesia is frequently accompanied by the development of
choreiform movements after the paralysis has developed. These may
assume the type of athetosis, true ataxia, or tremor. The same may
also be said of that type of hemiplegia which occurs as the result of
lesions of the internal capsule of the cerebrum. Finally, in cerebral
hemianesthesia there is usually more or less insensibility to touch, pain,
and temperature, and also abolition of muscular sensibility with complete
retention of electro-motor contractility. The mucous membranes of the
eye, nose, and mouth, are also frequently rendered anesthetic. Aphasic
symptoms have been observed to co-exist with hemianzsthesia (see
page 68).”
NUMBNESS AND FORMICATION.
In connection with sensory paralysis, a condition of numbness,
which the patient describes as feeling as if some special part was “fast
asleep” is often experienced. In others, a sensation which has been com-
pared to the “creeping of ants” over some special region is complained
of. The latter has been termed “formication.”
56 LECTURES ON NERVOUS DISEASES.
“These abnormal sensations are confined exclusively to those parts
in which the sensory nerves are more or less impaired. This impairment
may result from some lesion of the nerves after their escape from the
brain or spinal cord, or from lesions of the nerve centres which involve
their fibres of origin.
“By a careful study of the symptoms, a skilled anatomist is often
enabled to decide whether the lesion is cerebral, spinal, or confined to
special nerve trunks. This field is too extensive, however, to be consid-
ered in detail here.”
HYPERASTHESIA.
In connection with lesions of the brain and spinal cord. a condition
of excessive sensibility is sometimes encountered. It is termed “ hyper-
zesthesia.”
“Tt may exist independently of motor or sensory paralysis; or, again,
it may co-exist with them. Its clinical significance depends upon its seat
and extent and the other evidences of disturbed nervous functions which
co-exist. It will be discussed from a clinical point of view in subsequent -
pages.”
HEMIANOPSIA.
A loss of vision in one lateral half of each retina is termed * hemi-
anopsia” and “ hemianopia.” It is called “ hemiopia” hy some authors:
although incorrectly so, as that term means ‘ half-vision,” while the two
others mean what they are intended to express.
The following steps are commonly employed to detect the existence
of this symptom: Request the patient to close one eye by pressing the
lid down with the finger, and to so direct the open eye as to concentrate
its gaze upon some fixed object near to it. [I usually hold up the fore-
finger of my own hand within a foot of the patient’s open eve, and tell
him to look steadily at it.] Having donc this, take some object which is
easily seen (such as a piece of white paper) in the unemployed hand, and
move it to the right and left of the object upon which the patient is
gazing, and also above and below the object, asking the patient, in each
case, if the two objects are seen simultaneously and with distinctness,
and notice upon which side of the fixed object the patient cannot perceive
the moving object. It is self-evident that the retina is blind upon the
side opposite to that upon which the moving object is lost to sight.
The most common form of hemianopsia is that in which the nasal
half of one eye and the temporal half of the other is blind. This condi-
tion is termed homonymous hemianopsia. It is the result of pressure
upon, or actual destruction of one of the optic tracts, the pulvinar of
the thalamus, the cortex of the occipital lobe (probably the cuneus), or
the fibres that connect it with the optic tract. (This seems to be proven
by the late researches of Munk, Wernicke, Starr, Seguin, and others.)
HEMIANOPSIA. 57
Optic Ne res
RIED Saas Optic
‘ chiasm.
pulvinar.
Corpora quadri-
piece gemina or the
1 \ i
tea ml es St \ fRight tract
2 i | 4 —_—- 0.
Wernicke / . lw ernicke.
,
D
Cortical visual
area of right
cerebral hemi-
sphere.
Cortical visual
area of left
cerebral hemi-
sphere.
Fic. 21.—A D1iaGRAM By THE AUTHOR ExpLicaTive oF HemianopsiA. The lines (.4 and
B) indicate the fibres associated with the left cerebral hemisphere. Those of the right
hemisphere (C and 7) appear as separate lines. Both will be seen in the diagram to
pass from the retina through the following parts: The optic nerves; the crossing fibres
through the optic chiasm ; the optic tracts ; the external geniculate body ; the corpora quad-
rigemina or the ‘ pulvinar”’ of the optic thalamus ; and the internal capsule. The fibres are
shown to end in the cortex of the occipital lobes.
A lesion situated at the points designated as 1, 2, 3, 4, and 5, will cause homonymous
hemianopsia. Lesions of the right hemisphere of the cerebrum produce blindness of the
right half of each eye, and vice versa
58 LECTURES ON NERVOUS DISEASES.
Lesions at the base of the skull frequently produce this variety of
hemianopsia, if they le posteriorly to the optic chiasm. In this situa-
tion, the lesion usually produces the symptoms which are referable to
pressure upon, or destruction of the bundles of motor or sensory fibres
found in the crus and below it, or some of the nerves which escape from
the base of the. skull. Fig. 21 will aid the reader in appreciating the
clinical value of this suggestion.
‘Whenever the chiasm is affected, we meet the binasal type. Regions
ec and 6, in Fig. 21, would then be deprived of visual perceptions.
There is still one more form of hemianopsia which is occasionally
encountered, viz., the bitemporal type. This has been interpreted by
F
VISUAL AREA
MEDULLA.
Fic. 22.—A DraGram DesiGNED BY THE AUTHOR TO SHOW. THE GENERAL COURSE OF FIBRES
OF THE ‘Sensory’? anp *Moror Tracts,’’ AND THEIR RELATION TO CERTAIN Fas-
CICULI OF THE (pric NERVE TRACTS. Grodines from Seguin.) S, Sensory tract in posterior
region of mesocephalon, extending to O P and T, occipital, parietal, and temporal lobes of
hemispheres ; M, motor tract in basis cruris, extending to P and F, parietal and (part of)
frontal lobes of hemispheres; C Q, corpus quadrigeminum; © T, optic thalamus; N L,
nucleus lenticularis; NC, nucleus caudatus; 1, the Fibres forming the ‘‘tegmentum cruris’’
(Meynert); 2, the fibres forming the ‘basis cruris’’ (Meynert); a, fibres of the optic nerve
which become associated with the ‘‘optic centre’’ in the optic thalamus, and are subse-
quently prolonged to the * visual area”’ of the occipital convolutions of the cerebrum; 6,
optic fibres which join the cells of the “ corpora quadrigemina,"’ and are then prolonged to
the visual area of the cerebral corten.
an autopsy made upon a case intrusted to the eare of Professor H.
Knapp, of this city. It must be evident that the chances would, of
necessity, be extremely small of ever encountering a bilateral lesion
which would affect only those fibres of the optic chiasm or optic tract
which supply the temporal half of each retina. and at the same time
leave the decussating fibres intact. How, then, are we to account for
the fact that this form is sometimes met with? I would call attention
to a peculiar arrangement, of the arteries in the region of the optic
chiasm as a factor in causing this condition. It has been shown that
atheromatous degencration of the “circle of Willis” (a peculiar arrange-
HEMIANOPSIA. 59
ment of blood-vessels at the base of the brain) so impairs the elasticity
of the arteries as to create through their pulsation a type of injury to
the chiasm, so limited in its extent as to impair only the fibres dis-
tributed to the temporal halves of the retinz, and thus to create bi-
temporal hemianopsia.
Hemianopsia will be more fully discussed in connection with the
effects of lesions of the optic nerve. The diagrams introduced will, I
trust, make the facts stated clear to the mind of the reader.
MEDULLA
Fic. 23,—A D1racram DesIGNED BY THE AUTHOR TO SHOW SOME OF THE RELATIONS OF THE
Oprric AND OLFAcTORY NEkVE Figres ro SURROUNDING Parts. F, Frontal lobes of cere-
brum; P, parietal lobe; T, temporo-sphenoidal lobe; S$, fissure of Sylvius; R, fissure of
Rolando; O, occipital lobe; C, cerebellum; M, medulla oblongata; 1, olfactory nerve; 2,
optic chiasm ; 3, motor-oculi nerve; 4, corpora quadrigemina; 5, trigeminus nerve; a, basis
cruris; 4, tegmentum cruris. The diamonds in the occipital lobe, the cortical visual centres
of Munk, ‘The cerebellum and pons Varolii are shown as if separated from the cerebrum,
in order to made the relations of the crus to the optic tracts apparent. This diagram should
be compared with the preceding ones (Figs. 21 and 22) to make its bearings upon cerebral
localization apparent.
We may, therefore, summarize the clinical significance of this peculiar
form of blindness as follows: (a) The homonymous variety indicates
lesions affecting the optie tract or its continuation backward ; or, possibly
a lesion of the cortex of the occipital lobe of the same side. (6) The bi-
nasal variety indicates a lesion pressing upon the central portion of the
chiasm. (c) The bitemporal variety indicates atheromatous degene-
ration of the circle of Willis. Symmetrical lesions of the outer part of
the chiasm might possibly (?) also canse it.
60 LECTURES ON NERVOUS DISEASES.
APHASIA.
An impairment of the idea of language or its expression (inde-
pendent of paralysis of the tongue) constitutes this condition.
It is commonly described as of two varieties—the sensory or ‘am-
nesic form,” in which the memory of words or of symbols is more or less
effaced, and the motor or “ataxic” variety, in which the memory is per-
fect, but the subject cannot properly pronounce words, from an inability
to perfectly cobrdinate the muscles concerned in articulation.
The symptoms of this malady in either of its forms are always of
great clinical interest, because some peculiarity in each case causes it to
differ from others which may have been previously encountered.
I quote from the third edition of my work on “ Surgical Diagnosis,”
some selected paragraphs relating to this symptom, with occasional
changes in their phraseology :—
“In the amnesic variety the most familiar objects are commonly
misnamed; the subject being oftentimes aware that the error has been
committed, and yet is not able to correct it. The form which this loss
of memory takes is liable to vary with each case. As an illustration of
this, some forget only names; others only numbers. In certain reported
cases, the names of things only in dead or foreign languages were re-
tained; in others, the reverse had been observed, the patient losing all
memory of acquired tongues. Again, the sound of words often will not
be recognized when the letters which form them will; and the reverse of
this condition is not infrequently met with in aphasie subjects.
“We owe to Broca the credit of the discovery that the centre for
the codrdination of the movements of the tongue, lips, and palate, neees-
sary to articulate speech, could be located in the posterior portion or base
of the third frontal convolution; and to many of the later pathologists
the debt of overthrowing what once was the popular view, viz., that this
centre is not confined exclusively to the left cerebral hemisphere. Sub-
sequent pathological observation seems to have added strength to the
view that lesions of the ‘island of Reil,’ as well as the medullary sub-
stance which intervenes between it and the centre of Broca, must be in-
cluded in the so-called ‘motor speech area.’ The amnesic form may be
dependent likewise upon lesions of the so-called ‘sensory areas’ of the
cortex.
“ The ‘centre of Broca’ is supplied with blood by the middle cere-
bral artery. An embolus within that vessel will tend, therefore, to arrest
the circulation, of that important area, and, at the same time, it will in-
terfere more or less with the nutrition of the motor area of the cortex
and the corpus striatum—the ganglion which probably modifies all motor
impulses sent out from the brain to the muscles of the opposite side of
APHASIA. 61
the body. Now we know clinically that embolism is a frequent cause
of aphasia, and that hemiplevia almost always accompanies it. We also
know that the middle cerebral artery of the left side is the most frequent
seat of embolic obstruction. This fact helps us to interpret the devel-
opment of right hemiplegia in connection with aphasia, as is found to
exist in the large proportion of such cases. Seguin found two hundred and
forty-three cases in which right hemiplegia existed out of a total of two
hundred and sixty—left hemiplegia being present in but seventeen cases.
“Tn the ataxic variety of aphasia, the patient can usually write what
cannot be spoken, thus proving that the memory of words seen or heard
is not effaced, but rather the ability to so codrdinate the muscles of speech
as to properly pronounce them. This condition must not be confounded
with aphonia (loss of voice). Several cases have been reported where the
amnesic form has given place to the ataxic, and the lesion has been found
over the centre of Broca. It would seem, therefore, that the third frontal
convolution (although placed in close relationship with the oral and
lingual centres of Ferrier) has some imperfectly understood connection
with the memory of words, as well as with the codrdinated movements
of the apparatus of speech.
“Tf irritative or destructive lesions of the cerebral cortex exist as
the exciting cause of the aphasia, convulsions may be associated with its
development.
“Tf numbness or anesthesia co-exist with hemiplegia and aphasia, it
indicates that the ‘motor and sensory tracts’ which connect the cere-
brum with the extremities are involved, as well as the centre of speech,
or the ‘speech tract.’”
We have reason to believe that the cortical cells of the so-called “ sen-
sory area” of the cerebrum not only enable us to appreciate the many
facts telegraphed to them by the organs of smell, sight, hearing, taste,
and touch; but that each cell is able furthermore to store up such impres-
sions as it is specially designed to take cognizance of, and to recall them
at the command of the will as memories of past events.
Munk has lately demonstrated that the cortical cells of the oecipital
lobes preside over vision; and that a permanent loss of sight follows the
total destruction of these lobes. The same observer has shown, also,
when a circumferential ring of cells in the occipital lobes were not in-
cluded in the experiment (the central portions only of the lobes being
removed), that an animal will slowly regain its familiarity with surround-
ing objects through the sense of sight. A dog, for example, will learn
to again recognize faces, can be taught anew to fear the lash, to recognize
food by sight, ete. The only explanation of such facts is that the new
sight-memories are formed in place of those that were obliterated by the
operation.
62 LECTURES ON NERVOUS DISEASES,
Experimental investigation and pathological facts lead us to the
conclusion that the various forms of memories recognized are stored up
in those cortical cells which were originally thrown into activity by the
fact remembered. Thus, for example, the cells of the area of hearing
- give to us our memories of sound; those of the sight area our memories
of visual impressions; and those of the smell area our memories of odor.
Some remarkable clinical facts sustain the view that the cells of the motor
area even are capable of giving to us memories of muscular efforts. These
are totally distinct from other forms of memory. Professor Charcot lately
reported a case where a gentleman could read by tracing the lines with
his finger, when a lesion of the brain had deprived him of his ability
to recognize written or printed characters by sight. He could write with
ease, but could read what he had written only by retracing the lines, or
going through the motions necessary to reproduce the letters.
Dr. M. A. Starr has lately written two popular articles,* in which
the physiology of speech is discussed at some length. It is illustrated
with some admirable diagrams. This author cites many interesting cases
which illustrate the various types of aphasia, and he supports the view
that the parietal convolutions, which are not related to muscular move-
ments, are the seat of our conscious appreciation of tactile impressions
and of touch-memories. Ross, Hughlings-Jackson, Bastian, Broadbent,
Kussmaul, and others, have written extensively upon this subject.
Much light has been shed by recent investigations upon those cases
of aphasia where the ability to respond to spoken questions has been
destroyed by focal lesions of the brain, and the patient has still been
able to appreciate written interrogations and to reply to the same. Cases
also where the reverse has been observed, are now understood.
The condition known as “ word-deafness” is to be clinically regarded
as a symptom of a lesion affecting the superior temporal convolution, in
which the centres of hearing are situated. The condition known as
“ word-blindness”’ indicates a lesion of the occipital lobes.
The centre of Broca must, therefore, be regarded as related exclu-
sively to motor speech memories, which can be called into activity by the
different parts of the cortex in case any impression received by them
demands a verbal response.
We are in possession of facts to-day that render it certain that the
nuclei of origin within the medulla oblongata of the nerves which preside
over the tongue, lips, and palate, are connected with those cortical cen-
tres that are functionally related to speech by the fibres of the so-called
“speech tract.” Wernicke has lately traced the course of these fibres by
a study of reported cases which bear upon this field. He places them in
the posterior part of the internal capsule (Fig. 24), and states that they
* Popular Science Monthly, Sept., 1884; Princeton Review, May, 1886.
PARAPHASIA—-TRUE MOTOR APHASIA. 63
pass also through the external capsule to reach the third frontal convo-
lution, This discovery enables us to explain the co-existence of aphasia
with hemianzsthesia and hemianopsia, which has been observed. It also
clears up those cases where lesions of the crus, pons, and medulla have
produced aphasic symptoms. The “speech tract”? must not be con-
founded with the cerebral extension of fibres of the hypoglossal nerve,
which have a different course.
Clinically, we may be called upon to recognize the following varie-
ties of defective speech produced by brain lesions :—
(1) Moror or “ Araxic” APHastA. Paraphasia.
(2) Sunsory or “ AMNESIC” APHASIA. . et ocemne teens
Word-blindness.
Agraphia.
PARAPHASIA.
This is a condition where the substitution of wrong words or symbols
occurs in conversation or during attempts at writing. The patient is
conscious of this error, but is unable to correct it. Nouns are more
frequently lost than verbs. Patients of this type often exercise great
ingenuity in avoiding, during conversation or writing, the words which
they are liable to fail in properly recalling. By means of oddly-con.
structed sentences they will often hide this defect in speech from
strangers. A good test often for such cases is to request the patient
to say his alphabet, and to count until requested to cease. These pa-
tients will probably substitute wrong letters or figures for the proper
ones.
Paraphasia is due to a lesion of the island of Reil. On the left side
of the brain in right-handed subjects, or vice versa.
TRUE MOTOR APHASIA.
This condition is due to a lesion in the centre of Broca (third
frontal convolution).
These patients cannot articulate correctly. They are painfully con-
scious of this defect; hence they frequently become mute rather than
to expose themselves to criticism or ridicule. I have known such
patients to be deemed a melancholiac because they could not be induced
to talk.
In case certain words are retained or regained after the attack, these
words or expressions are used in a peculiarly automatic way by the
patient in reply to any question asked. It is not uncommon for a
patient with motor aphasia to use some absurdly irrelevant phrase as an
answer to any question which may be propounded. Occasionally, this
phrase may be traced to some peculiar expression which existed in the
64 LECTURES ON NERVOUS DISEASES.
mind of the patient at the time when the attack occurred. As examples,
a case is reported by Hammond where a patient would reply “hell to
pay ” under all cireumstances; and another by Hughlings-Jackson where
the unyarying reply was, “1 want protection.”
AGRAPHIA.
This term is applied to a condition where, from cerebral disease or
other causes, the power of writing is suddenly or gradually lost.
The explanation of this condition rests in the fact that the patient
has lost certain memories which previously enabled him to make the
necessary finger movements for placing upon paper results obtained by
his mental processes.
Such a person might be able to perform any or all movements of
the fingers (that are not connected with the writing of letters or figures)
with his accustomed delicacy. He cannot write from dictation, or copy
from a printed or written slip. He is not paralyzed, nor is he affected
with “ writers’ cramp.” The memory is alone at fault; hence this con-
dition is a variety of ‘amnesic aphasia.”
In some instances, delicate finger movements required in the me-
chanical trades, the use of musical instruments, ete., have been known to
be suddenly taken away from a similar loss of motor-memories, Such
cases are not included under the term “agraphia.”
WORD-DEAFNESS.
This is a form of sensory aphasia which is dne to a lesion of the first
temporal convolution. These patients cannot be made to understand
spoken language, because their centres of hearing have been impaired.
They are not deaf to sound, but they fail to appreciate the meaning of
certain sounds. Their own tongue is as unintelligible to them as a
foreign language.
This condition prevents the patient from speaking correctly, because
of an inability on his part to recall the proper sound of many words pre-
viously employed by him. Their efforts to talk or to read aloud, result
in an “ unintelligible jargon” which the patient does not recognize as in
any respect unnatural or inexpressive of ideas he desires to commnu-
nicate to you, because his ear does not properly interpret his own
utterances.
You may test such a patient, therefore, by asking him to read aloud
some printed selection, or to write at your dictation. With neither of
these tests will he be able to fully comply.
Starr quotes from Broadbent the following illustrative case:—
“One such person was asked to read the sentence, ‘You may receive
a report from other sources of a supposed attack on a British consul-
WORD-BLINDNESS. 65
general. The affair is, however, unworthy of consideration.’ He rend it
slowly, and in a jerky manner, as nearly as could be taken down, thus:
‘So sur wisjee coz wenement apripsy fro freuz fenement wiz a seconce
coz foz no Sophias a the freckled pothy conollied. This affair eh oh
cont oh curly of consequences.’ It was evidently an effort to rend aloud,
requiring close attention, and he read seriously and steadily, apparently
unconscious of the shinrdiity of his utterances, till interrupted by
laughter, which it was impossible to restrain. He was never able to
write at dictation, but he signed his name quite well, and could copy
accurately, though as he wrote each letter he would attempt to name it
aloud, but always pronounced a wrong letter.”
WORD-BLINDNESS.
This is another form of sensory aphasia. It is due to a lesion of
the visual centres in the occipital lobes. It is accompanied by a loss of
memory of the meaning of prinied or written symbols. Such patients can
generally recognize familiar. objects or faces, but they cannot read cor-
rectly.
When asked to read a printed selection or a written slip, their inter-
pretation is an incorrect one. They can often write from dictation, but
they cannot read what they have written. Their conversational powers
are not impaired unless “ word-deafness ” is also present.
The following illustrative case is quoted by Starr, from a contri-
bution of Ross upon this condition :— :
““One man who had suttered from this affection seemed at first un-
conscious of his actual condition. When asked to read he would make
very elaborate preparations, putting on his spectacles and moving the
paper or book backward and forward until he seemed to get it into a
position where he could see well. He would then read aloud, uttering a
few sentences which had not the remotest connection with anything that
was before him on the printed page. He was handed a note which read
as follows: ‘Dear Sir, I shall be much obliged if you will let me know
whether or not you consider it likely that A. B. will recover.’ He looked
at it carefully, and seemed to glance it through, and then read slowly
and deliberately, and without much hesitation: ‘Dear Sir, You are re-
quested to bring this note with you the next time you come to the in-
lirmary;’ and then he added, ‘that is what I make of it; I don’t know
whether it is right or not.’ He often tried to read a newspaper aloud,
and his wife said that he ‘read a lot of stuff all made up out of his own
head.’ On one occasion she took the paper and read it to him. He was
very quiet for a time, and then asked, ‘Is that what it says in that paper?’
and when she assured him that it was, he said,‘ Well, then, I must be an
idiot.’ At that time he would remark, ‘I don’t know what is the matter
5
66 LECTURES ON NERVOUS DISEASES.
with the newspapers nowsdays, they are filled with such silly stuff.’
Soon, however, he began to maalize that the trouble lay in himself rather
than in the papers, and then he gave up attempting to read.”
It ig not uncommon to encounter this form of aphasia in conjunction
with word-deafness, a fact which is easily explained by the close prox-
imity of the visual and auditory centres (see Fig. 5).
GENERAL DEDUCTIONS RELATIVE TO APHASIA.
In summary, the following deductions relative to disorders of speech
may be given :—
1. The cortex of the posterior part of the third frontal convolution,
and possibly the island of Reil also, presides over the codrdination of such
muscular acts as are necessary to speech. It also stores the memories of
such acts, so that any combination of articulate sounds can be voluntarily
seitoduend when the proper form of excitation is furnished (chiefly in
response to sight or sound-impressions).
This centre is connected by “ associating fibres” with the centres of
hearing (first temporal convolution) and those of sight (the occipital con-
volutions). It is also put in communication with the nuclei of the facial,
hypoglossal, pneumogastric, and glosso-pharyngeal nerves (within the
medulla) by means of two distinct tracts of fibres, viz., the ‘ hypoglossal
cerebral tract,” and the so-called ‘‘speech tract.”
Thus, this cortical centre of codrdinated speech-movements is ca-
pable of receiving excitation from the centres of hearing, when replies
to spoken language are demanded; and from the centres of sight, when
written or printed language calls for a verbal response. It is also put in
direct communication with the nerves which preside over the apparatus
of speech (whose nuclei of origin are situated within the medulla).
2. The form of amnesic aphasia, known as ‘* word-deafness” (Kuss-
maul) indicates the existence of a lesion of the first temporal convolu-
tion* of the left side, which has impaired the memories of spoken lan-
guage. Hearing may not be impaired, in spite of the fact that the appre-
ciation of words, music, etc., may be totally absent.
3. The condition known as “ word-blindness” (Kussmaul) indicates
the existence of a lesion of the left occipital convolutions, which has im-
paired the memories of written or printed symbols of language, numerals,
familiar objects, etc.
4. The condition termed “ paraphasia” by Kussmaul (in which the
amnesic and ataxic varieties of aphasia seem to be peculiarly combined)
may be excited by a lesion which interferes with the action of the asso-
*In right-handed subjects the left hemisphere, and in left-handed subjects the right
hemisphere, secnis to monopolize the function ef sound-interpretation to the speech centre.
GENERAL DEDUCTIONS RELATIVE TO APHASIA. 67
ciating tracts of fibres between the areas of hearing or sight and the
motor speech centre of Broca (Wernicke).
5. The condition of imperfect speech, termed “ anarthria,” is pro-
duced by a lesion of the medulla, which interferes with the functions of
the nuclei of the cranial nerves associated with’speech. It is occasionally
observed in connection with focal lesions of the floor of the fourth ven-
tricle. These cases are to be differentiated from aphasia of cortical origin
by the co-existence of other symptoms produced by the medullary lesion
(see subsequent page).
6. In order to properly pronounce any word, it is essential that
both the cortical centre of speech, and also the nuclei of the medulla,
which are associated with it, must be called into action.
ASSOCIATING-~
TRACT
THE SO-CALLED --—-|
"SPEECH TRACT“
»)-~1 > WUCLE! OF ORIGIN
—[--- OF NERVES
-“EMPLOYED JN SPEECH
Fic. 24.—A DiaGcram DESIGNED BY THE AUTHOR TO ILLUSTRATE THE MECHANISM OF THE
APPARATUS REQUIRED IN SPEECH.—The reader must not regard this diagram as intended
to accurately portray the anatomical relations of the various centres and tracts to each other.
7, The peculiar course which the fibres of the “ speech tract” take
within the cerebral hemisphere, sheds light upon those reported cases of
aphasia where the lesion was situated posterior to the centre of Broca,
These fibres run from the third frontal gyrus close to the surface of the
hemisphere, and in an antero-posterior direction (passing in the external
capsule) to reach the posterior part of the lenticular nucleus. They dip
at this point into the posterior part of the internal capsule. They then
pass through the middle part of the crus and pons to the medulla
“SUOISO[ UIVAG [vOOJ JO sIsOUSvIp oy} Suroods
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“MIT DNIWNG GAZITVOOT Ad AVN NIVUT AHL Ao
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"ToYV] POSSNOsIp oq ][LA WA o199 dy} Jo sJoury Surperoosse oy. Jo
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puy SuLIwaT JO arjuad ayy Useayoq sauqy’ Busporo0ssy oy} UIA, “ET
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09 0} 9IG¥IT 9 pom ‘vison seuviMy 10 ‘eisdouvtutay ‘aznsdpo pousay
“ut ayy fo worsa, B Jo yNser v sv ‘padoteasp eq visvqde prnoyg °s
‘qov1y ATosuas at} JO oso}
pue saiqy odo oq} waemjaq (aaadasO stg} 0} Surpso998) AIT .,40¥r4
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“SUSVESIG SQOAWAN NO SAUNA LOgT 89
CORTICAL LESIONS OF THE CEREBRUM. 69
Frequent references will be made in subsequent sections of this
volume, to these clinical deductions ; hence the importance of a thorough
mastery of the closing pages of this section cannot be too strongly im-
pressed upon the reader.
CORTICAL LESIONS OF THE CEREBRUM.
Lesions of the motor convolutions, when of small size, produce some
form of monoplegia, or mono-anesthesia; when of large size, a hemi-
plegia may be produced.
Consciousness ix not necessarily lost at the time of the attack. Asa
rule, the patient is not rendered totally unconscious.
Early rigidity of the paralyzed muscles is often present. This is
probably due to irritation of the cortex. .
Cortical hemianesthesia will be produced when the entire parictal
cortex is involved by a cortical lesion, and, in addition, the balance also
of the motor area, which lies outside of the parietal lobe. Such an ex-
tensive cortical lesion is rarely, if ever, encountered. We, therefore, do
not observe co-existing hemiplegia and complete hemianesthesia in cor-
tical disease.*
Localized pain in the head is a symptom which is often present in
connection with cortical lesions. If it be absent, percussion over the
lesion will generally tend to excite. This step will also tend to incréase
the pain, in many cases, where it exists prior to this test.
* The experiments of Munk, made with a view of determining the area of common sen-
- sation in the cerebral cortex, lead to the conclusion that the entire parietal cortex must. be
destroyed, and the ascending frontal convolution as well, before complete and permanent an-
zsthesia is produced on the opposite side of the body below the head. These results make
the motor area overlap the sensory area to some extent, and tend to refute the deductions
of Ferrier, who places the centre of tactile sensations in the temporal lobe, and to confirm
the views held by Luciani and Exner. Ifa partial destruction of the sensory area of Munk
be produced in animals, the anesthesia persists only for a few weeks, because the adjacent
regions learn to perform vicariously the functions of the part destroyed.
Tripier, of Montpellier, France, has lately affirmed the conclusions of Munk, respect-
ing the existence of sensory centres in the central convolutions, as has, also, Moeli, of
Berlin. | These three observers support the view that the motor and sensory centres of any
one limb coincide. This view was advanced theoretically by Luys some years ago.
Exner has collected from European journals all cases of cortical disease that have
been associated with disturbances of sensation, and M. Allen Starr has lately performed
the same labor in American literature. An analysis of the cases so collected seems to
justify the conclusions of Munk and his followers, and to add some clinical suggestions of
value. These cases demonstrate (1) that the cerebral cortex of each hemisphere appreci-
ates sensory impressions from both sides of the body, but are chiefly associated with the
sensory tracts of the opposite lateral half of the body; (2) that the sensory area includes
the central convolutions (Fig. 4) and the posterior part of the parietal lobe; (3) that the
sensory centres coincide to some extent with the motor centres of similar parts; (+) that
no disturbances of geueral sensation have been known to result from lesious continued to
the frontal, temporo-sphenoidal, or occipital lobes.
70 LECTURES ON NERVOUS DISEASES.
Convulsions, when followed by transient attacks of paralysis (Jack.
sonian epilepsy), indicate an irritative lesion of the cortex. They are
frequently encountered in connection with syphilitic disease of the brain.
- Subjective sensations (paresthesie) may also be excited in limited por-
tions of the limbs.
Blindness of that half of each retina, which corresponds to the cere-
bral hemisphere affected, occurs when extensive cortical disease of the
euneus in the occipital lobe is present. ‘“ Word-blindness” may also be
produced by lesions of these lobes (especially if upon the left side).
Abolition of hearing, and also the condition known as ‘“ word-deaf-
ness” occur from lesions of the first temporal convolution (chiefly upon
the left side).
Abolition of the sense of smell, or of taste, may result from lesions of
the tip of the temporal lobe. The memories of taste-and-smell-percep-
tions may also be impaired or lost.
Alaxie aphasia and paraphasia may be developed as a result of cor-
tical lesions, which involve respectively the speech centre of Broca and
the island of Reil.
The face is never rendered totally hemiplegic by cortical lesions;
as far as my clinical observation and research among reported cases goes
to show.
The conditions known as “ mono-anesthesia,” by which we mean an
impairment, or total arrest of sensation in some distinctly localized part,
as, for example, the hand, arm, leg, etc., and, also, the condition known
as “ mono-paresthesia,” which signifies the existence of subjective sensa-
tions of a definitely localized character, are particularly diagnostic of
cortical lesions lying posterior to the fissure of Rolando. The former
indicates a destructive lesion, the latter an irritative lesion.
The muscular sense is liable to be impaired (when a cortical lesion
of the motor area exists) in the parts functionally associated with the
limits of the part diseased.
Monoplegia and monospasm are pecularly diagnostic of a cortical
disease anterior to the fissure of Rolando,
The memories of sensory impressions are more frequently impaired
by cortical lesions of the left hemisphere than of the right (as shown, for
example, in ataxic aphasia, word-blindness, word-deafness, paraphasia,
etc).
Motor memories may be impaired by cortical disease affecting the
motor area. Subjects may thus lose a dexterity with the fingers, arm,
hand, leg, ete., which they had acquired previous to the development of
the lesion. A knowledge of this fact may sometimes aid in the locali-
zation of a lesion.
Irritative lesions of the cortex of the cuneus (a part of the occipital
CORTICAL LESIONS OF THE CEREBRUM. 71
lobes) may cause hallucinations of vision. If one hemisphere only is
affected, the objects seen will appear to lie on the side opposed to the
lesion, and to move with the eyes as they are turned from side to side.
Lesions of the “island of Reil,” or “ insula” of the left side (Fig. 9),
seem to create (in some instances) symptoms of ataxic aphasia, and also
paraphasia (the substitution of wrong words). The motility of the face
and arm of the opposed side may occasionally be impaired from cortical
lesions of this region.
Lesions of the cortex confined to the apex of the temporal lobe (Fig.
3) are liable to cause an impairment of the sense of smell or of taste (if
destructive in character); or subjective odors and tastes (if irritative in
character).
2);—M-—_——_
Se
._ MEDULLA
Fic. 25.—A Dracram Desicnep To ILLUSTRATE THE GENERAL CouRSE AND DISTRIBUTION
oF tHE Motor AND SENSORY TRACTS OF THE CEREBRUM. (Modified slightly from Seguin.)
P, Parietal lobes, F, frontal lobes, T, temporal lobes; O, occipital lobes ; M, motor bundles ,
S, sensory bundles, N C, nucleus caudatus ; N L, nucleus lenticularis ; O T, optic thala-
mus, C Q, corpora quadrigemina , 1, sensory (posterior) bundles of the medulla, pons, and
crus; 2, motor (anterior) bundles of the same. Note that the motor fibres are associated with
the frontal and parietal lobes; and the sensory fibres with the parietal, temporal, and oc-
cipital lobes
Destructive lesions of the cortex of the motor convolutions (Fig. 5)
are followed by a descending degeneration of the fibres which arise from
these gyri. This may account (?) for the late rigidity of the muscles
paralyzed, which is occasionally observed after such lesions.
Cortical lesions of the base of the brain are especially liable to pro-
duce vomiting, choked disc, bilateral paralysis, and symptoms of impair-
2 LECTURES ON NERVOUS DISEASES.
ment of some of thé cranial nerve trunks. The crus, pons, and island of
Reil may also be involved and give additional symptoms.
Cortical disease of those frontal gyri which lie anteriorly to the
motor centres (Fig. 5) is often attended with no marked symptoms of a
diagnostic character. The higher mental faculties may occasionally give
signs of more or less impairment. Connected thought, the control of
the emotions, accurate reasoning, and concentration of the attention are
particularly difficult under such circumstances.
The memories of sound- or sight-impressions, as well as those of
smell, taste, muscular movements, etc., may be separately annihilated by
cortical disease (see Fig. 5).
NON-CORTICAL LESIONS OF THE CEREBRUM.
Many of the clinical facts pertaining to non-cortical cerebral lesions
may be thus summarized :—
Profound coma is more often encountered in non-cortical lesions
than in cortical; possibly because the cerebro-spinal fluid is more liable
to be displaced from the ventricles (Duret).
Hemiplegia commonly exists in combination with more or less hemi-
anesthesia, and paresis of the lower part of the face. These symptoms
are observed, as a rule, upon the side of the hody opposed to the cere-
bral lesion.
Pain, when present in the head, is less circumscribed than in cor-
tical disease ; and is not increased by percussion; or, when absent, elicited
by that step.
Muscular rigidity in the paralyzed muscles develops late. Typical
monoplegia is probably never observed.
Tremor, hemichorea, and athetosis are not uncommon sequele of
non-cortical cerebral lesions.
The senses of sight, smell, hearing, and tactile sensibility are occa-
sionally impaired to a greater or less extent by non-cortical lesions. The
seat of the lesion will modify the evidences of such impairment, because
the fibres of some of the cranial nerves may be involved by the lesion,
while others may escape injury.
Typical attacks of Jacksonian epilepsy do not occur; although gen-
eral convulsions may be excited,
LESIONS OF THE EXTERNAL CAPSULE.
These may cause (if within the left cerebral hemisphere) the con-
dition of paraphasia, which has been previously described. This is due
to the fact that the “speech tract” probably passes through it before it
enters the internal capsule
LESIONS OF THE INTERNAL CAPSULE, ETC. 73
LESIONS OF THE INTERNAL CAPSULE.
These often result in the development of hemiplegia, hemianaes-
thesia, or a combination of the two. Hemiparalysis of the lower half of
the face may be produced. The nerve fibres of sight, hearing, and smell,
and the so-called “speech tract” may be implicated. Conjugate deviation
of the head and eyes is not infrequent. ‘“Choked disc” may accompany
this condition, because it is a clinical evidence of an excess of intra-
cranial pressure, The different forms of tremor already mentioned are
most common when the internal capsule is implicated, Paraphasia may
be induced, if the “ speech tract’ is involved.
LESIONS OF THE CAUDATE NUCLEUS.
These are seldom, if ever, associated with hemianzsthesia. Hemi-
plegia, if developed, is probably due to pressure upon the motor fibres
of the internal capsule. The face may develop paralysis in its lower part
upon the opposed side for the same reason.
Many of the symptoms enumerated above (as indicative of a cap-
sular lesion) may exist also when the caudate nucleus, the lenticular
nucleus, or the thalamus, are individually attacked by any lesion which
' markedly increases their size, and thus creates pressure upon the fibres
of the internal capsule (see page 22).
LESIONS OF THE LENTICULAR NUCLEUS.
- These chiefly affect motility. Hemianzsthesia may occur if the pos-
terior capsular fibres be pressed upon.
Hallucinations are very common in connection with disease of the
thalamus (Ritti). The senses of sight, hearing, smell, and tactile sensi-
bility are perhaps more liable to be affected than motility.
: LESIONS OF THE CRUS CEREBRI.
The symptoms which point to a lesion of the crus (Fig: 11) may be
summarized as follows :—
Crossed paralysis of the “third nerve and body type” never occurs
except from a lesion of the crus.
If the lesion be confined to the legmentum cruris (the sensory por-
tion), hemianesthesia of the opposite side will ensue, and the third and
fifth cranial nerves of the same side may possibly be paralyzed. Inco-
érdination may be developed; provided that the fillet (lemniscus) is in-
volved.
If the crusta cruris (the motor portion) be alone suciiivedl, paralysis
of the third nerve will generally co-exist with hemiplegia on fhe opposed
side. The lower part of the face may be rendered paretic, in some in-
stances, showiug that filaments of origin of the facial nerve are impaired.
74 LECTURES ON NERVOUS DISEASES.
Symptoms referable to lesions of the corpora quadrigemina may
be developed in connection with lesions of the teqgmentum cruris (Fig.
11). Among these, the following may be prominently mentioned: Inco-
drdination of movement; sbolition of the pupillary reflex; nystagmus ;
and strabismus. Blindness may be found to exist independent of the
presence of a choked disc, atrophy of the optic nerve, or an optic neu-
ritis.
ass } Line of Gubler.
(3
MEDULLA
Fic. 26—A Dracram oF THE Base oF THE Brain, DesicNep To SHOW THE Parts Ap-
JACENT TO THE OPTIC NERVE TRACTS AND CHIASM,—The nerves are represented by
their respective numbers. , optic; III., motor oculi's- 1V., trachlearis; V. » trigeminus ,
VI., abducens; C, crus ca of each hemisphere ; 3b, infundibulum, the pituitary body
being cut off to'show the optic chiasm; a, the corpus albicans (mamillary tubercle) ; 4, ex-
ternal geniculate body ; z, internal geniculate body. The dotted line which crosses the pons
Varolii, connecting the roots of the fifth nerves, is Gubler’s line, an important guide, since
lesions of the pons in front of it cause ‘ crossed facial paralysis.” Lesions in the region of
thecrwsmay involve the third and second nerves simultaneously, Lesions about the chiasm
may press upon the corpus striatum within the mass of the cerebrum, ‘lhe crus comprises
both the motor and sensory tracts of the cerebrum,
LESIONS OF THE PONS VAROLII,
Apoplectic clots and foci of softening are not infrequently met with
in this region (Fig. 18), and tumors are sometimes encountered. Certain
clinical deductions of value can be drawn from a study of reported lesions
of the pons, as follows :—
The imaginary line that connects the apparent origin of the tri--
geminal roots (line of Gubler) marks the level of decussation of the
fibres of the facial nerves that pass cephalad.
Lesions above the line of Gubler are liable to produce facial palsy and
hemiplegia upon the same side of the body (the one opposed to the lesion).
LESIONS OF THE PONS VAROLII. 75
Lesions below the line of Gubler produce * crossed paralysis of the
seventh nerve and body type,” the face being paralyzed upon the same
side as the lesion, while a hemiplegia is developed upon the opposed side
of the body.
The trigeminus nerve may be paralyzed by lesions of the pons, if it
lies within the inner two-thirds of the reticular formation (according to
the researches of Starr).
If such a lesion be situated high up in the pons, trigeminal paralysis
will co-exist with a hemianesthesia of the opposed half of the body; if
situated low in the pons, the trigeminal paralysis and the hemianesthesia
will be upon the same side. The point of union of the ascending and
descending roots of the fifth nerve is nearly at the level at which the fifth
nerve escapes from the pons (line of Gubler).
Difficulties of articulation may often be considered as diagnostic
of lesions of the pons or medulla, provided the presence of aphasia of
cerebral origin can be excluded by the history of the case. There is
unquestionably a tract of fibres (the motor speech tract) that serves to
connect the centres in the medulla with the cortical centres for the move-
ments of the face and tongue.
Conjugate deviation of the eyes may accompany a lesion of the pons.
This symptom is not pathognomonic, however, because it may occur also
with cortical lesions of the cerebrum and lesions of the internal capsule.
The motor, sensory, and vaso-motor effects of lesions within the
pons are manifested in the extremities, chiefly, but not exclusively, upon
the side opposed to the lesion. This is not the case with those cranial
nerves whose fibres of origin probably traverse the pons (the fifth, sixth,
seventh, eighth [7], eleventh [7], and twelfth). The effects of intrapon-
tine disease upon some of these nerves, at least, are modified by the seat
of the lesion, as has been shown in preceding ‘paragraphs.
Contraction of the pupils during an apoplectic attack is to be re-
garded as strongly diagnostic of a clot within the pons.
Hemorrhage into the pons is usually followed by coma and sudden
death, if the clot be large or if the blood escape into the fourth ventricle.
The diagnostic points mentioned above apply, therefore, more particularly
to foci of softening and destructive lesions of small size and slow devel-
opment. When blood escapes into the fourth ventricle, convulsions are
observed, and death is liable to follow rapidly.
Disturbances of the circulatory and respiratory functions may occur
in connection with lesions of the pons; but they are to be regarded rather
as evidences that the medulla oblongata is directly implicated or sub-
jected to pressure.
76 LECTURES ON NERVOUS DISEASES.
LESIONS OF THE CEREBELLUM.
The functional attributes of this ganglion are as yet imperfectly
determined, and the effects of lesions (tumors, hemorrhage, softening,
atrophy,and sclerosis) which involve its different regions vary with their
seat. The following deductions are chiefly those of Nothnagel, who has
devoted special attention to diseases of this ganglion. Seguin has also
lately contributed to this field a valuable article.
Lesions of one of the cerebellar hemispheres are often incapable of
diagnosis, especially if only one hemisphere be involved.
Lesions of the vermiform process are generally attended with symp-
toms of a more decided character.
Incoérdination af movement, an intense vertigo (identical with that
of Ménitre’s disease), and a ‘“ titubating gait,’ are the more common
effects of cerebellar lesions; but these are not in themselves pathogno-
monic of cerebellar disease, because they may he produced by lesions of
other parts of the brain. The consideration of all the morbid phe-
nomena of each case (both of a positive and negative character) is
required to render the diagnosis certain.
A staggering qait is especially liable to be developed in case the
“worm” of the cerebellum is directly involved, or is pressed upon by
lesions of adjacent parts. It only exists when the subject is in the upright
posture, and the ataxic symptoms rarely affects the delicate movements
of the fingers.
Gastric crises (chiefly exhibited by persistent vomiting) are a diag-
nostic feature of lesions of the cerebellum, in many cases. When de-
structive lesions of the cerebellum exist, vomiting is less frequently
observed than when that ganglion is encroached upon by lesions of other
parts.
Atrophy of the cerebellum has been observed to produce imperfec-
lions of speech (ANARTHRIA). The difficulty seems to be confined ex-
clusively to the motor apparatus, The memory of words is not disturbed.
It is probably to be attributed to interference with the “speech tract”
(Fig. 24).
Pain in the occipital region is often present in cerebellar disease. It
may exist also in the frontal region, or be entirely wanting.
The organ of vision may be affected. Occasionally, the eyes may
exhibit, incodrdination of movement and nystagmus; and also the evi-
dences of choked disc, amblyopia, and amaurosis.
Hemorrhage into the cerebellum is sometimes associated with a loss
of facial expression, due toa slight paresis. The patient may also ex-
hibit a tendency to assume one position, and to return to it when moved
by the attendants. Should hemiplegia oceur, in such a case, it indicates
’
LESIONS OF THE MEDULLA OBLONGATA. 77
that the lesion exerts pressure-effects upon the pyramidal tracts, either in
the crus, pons, or medulla.
Irregularity of the heart’s action, which is sometimes observed in
connection with a cerebellar lesion, indicates a pressure upon the cardio-
inhibitory centre of the medulla.
Abnormal mental symptoms are generally absent in connection with
cerebellar lesions. When atrophy of the organ is present, or when other
parts of the brain are diseased simultaneously with the cerebellum, mental
derangements may be observed.
When the middle crura of the cerebellum (going to the pons) are
affected by lesions which create irritation, rotary movements of the body
and a lateral deflection of the head and eyes may be developed. As
a rule, these rotary movements are toward the healthy side; but this is
not invariably the case, as they sometimes are toward the side upon
which the lesion is situated. It is a curious fact that most of the effects
of cerebellar lesions are attributable to a greater or less extent to irrita-
tion of the crura.
Lesions of the superior peduncle of the cerebellum are liable to in-
duce paralysis of the motor oculi nerve, as shown by the development of
ptosis, external strabismus, and dilatation of the pupil. Hemianzsthesia
and more or less ataxia may be induced by pressure upon the tegmentum
and the fillet tract (lemniscus) respectively.
“ Bulbar symptoms” may develop late in the course of a cerebellar
lesion. Such phenomena are usually attributable to obliteration of the
vertebral and basilar arteries and their branches, as a result of arteritis
obliterans (Seguin).
LESIONS OF THE MEDULLA OBLONGATA.
The size of this ganglion almost precludes the existence of lesions,
even if small, which do not influence to a greater or less extent the nerve
nuclei contained within it.
An implication of the cranial nerve roots (Figs. 16 and 26) may
cause disturbances of respiration, circulation, phonation, deglutition,
and articulation.
The sensory and motor tracts to the extremities may be simulta-
neously involved; and thus anesthesia (7) and paralysis of motion may
occur upon the side of the body opposed to the lesion. The fillet tract
(Fig. 11) may be also affected by the lesion, in which case evidences of
ataxia will be developed in the extremities. Finally, the lower part of
the face may be rendered paretic.
Of the above-mentioned symptoms, aphonia and the impairment of
the respiratory and circulatory symptoms are particularly diagnostic of
medullary lesions.
78 LECTURES ON NERVOUS DISEASES.
The symptoms of Duchenne’s disease are present only when chronic
progressive degeneration of the nuclei of the medulla exists.
Suddenly developed lesions of the medulla are liable to cause in-
stantaneous death.
Diabetes and albuminuria may be excited by lesions of the medulla,
When the pneumogastric nerves are implicated, dyspnoea, irregu-
larity of the action of the heart, and gastric or intestinal derangements
are encountered. ,
Fic. 27.—A TRANSVERSE SECTION OF THE MEDULLA (PARTLY SCHEMATIC) MADE THROUGH
THE Mippie oF THE OLivary Bony. (Modified from Spitzka.) A, and 4, nuclei of origin
of the hypoglossal nerve (twelfth cranial); #. &., reticular formation, with its cell masses ;
O, olivary body; P, pyramid; a, . /., antero- median fissure; G and Pu, masses of cells
probably associated respectively with the glosso-pharyngeal and pneumogastric nerves; Ja,
ascending root of fifth cranial nerve; 2, restiform column; a. /., arcuate fibres; 7, fibres
passing through the inter-olivary tract; ¢ and @, bundles of ‘fibres from the posterior ‘spinal
tracts, cut across on their way to the inferior cerebellar peduncle after decussation; 7, the
“trincural fasciculus’’ of Spitzka; ‘‘solitary’’ or ‘‘round’’ bundle of other authors. Note
that the solid masses represented in the cut in red and yellow are composed of cells; the black
areas are designed to represent conducting fibres running ‘vertical to the plane of the section;
the white lines represent fibres which run in the plane oF the section; and, finally, that some
of the conducting strands are left uncolored (as, for example, 7, l’a, F, ¢ “and ays
In a few instances, tumors and foci of softening in the medulla have
been known to exist and create no symptoms of a diagnostic character.
Dysphasia, and the loss of the power of protrusion of the tongue,
points to an implication of the hypoglossal and glosso-pharyngeal nuclei.
FOCAL LESIONS INVOLVING CRANIAL NERVES.
In the third edition of ny work upon “ Surgical Diagnosis,’* I have
incorporated some axioms which bear upon the diagnosis of focal lesions
of the brein that affect cranial nerves,
* William Wood & Co., New York, 1883.
LESIONS AFFECTING THE OLFACTORY NERVE. 79
Some of the axioms there given require modification, when viewed
from the standpoint of our present knowledge. Many of the suggestions
referred to had been selected by me from some of my earlier writings
on this field, and, if taken literally, would now be in conflict with later
observations of an anatomical and clinical character published since that
date by others. Some other points given by me in that work are more
or less imperfect, although perhaps technically accurate. I have, there-
fore, seen fit to alter the wording of certain parts of this work, which
I shall now repeat in substance :—
Fic, 26.—Tue Base oF THE SKULL wiTH THE NERVES WHICH ESCAPE FROM ITS ForA-
MINA. The cranial nerves are numbered in their customary order,
LESIONS AFFECTING THE OLFACTORY NERVE.
Anosmia (loss of smell) may occur from :any lesion which involves
the first cranial nerve. It is usually unilateral.
Whenever it occurs in connection with hemiplegia, the body pa-
ralysis is on the side opposite to, and the anosmia on the same side as
the lesion. This condition is known as crossed paralysis of the “ first
cranial nerve and body” type. Anosmia indicates the existence of a
lesion situated in the anterior fossa of the cranium, or a destructive
lesion of the cortex of the temporal lobe near to its apex.
80 LECTURES ON NERVOUS DISEASES.
Crossed paralysix of the “olfactory nerve and body type” may
occur whenever a localized pressure is exerted chiefly upon parts within
the anterior fossa of the skull. The fibres of the so-called “ motor tract”
(Fig. 12) are involved by an upward pressure upon the caudate or lentic-
ular nucleus; or the fibres of the internal capsule are directly affected by
the lesion. This accounts for the hemiplegia of the opposite half of the
body. The olfactory nerve (which lies near the optic chiasm) is affected
by pressure in the downward direction, and the optic chiasm or tract may
be simultaneously involved; hence, a loss of smell in the nostril on the
same side as the lesion may co-exist with some form of hemianopsia, as
well as with a crossed hemiplegia.
LESIONS AFFECTING THE OPTIC NERVE.
Hemianopsia may occur when the optie chtasm, the optic tracts, the
thalamus, the posterior part of the internal capsule, or the corter of the oc-
cipital lobes (chiefly the cuneus) are pressed. upon or destroyed. It is
evident, therefore, that the trephine cannot aflord relief of this symptom
in most cases, because the lesion is commonly situated at the base of
the cerebrum. When syphilitic gummata may be suspected, the prog-
nosis is extremely favorable if active treatment be employed.
The variety of hemianopsia may indicate the seat of the lesion with
great exactness. Fig. 21 will make this apparent.
If paralysis (in any of its forms) co-exists with hemianopsia, a valu-
able guide may often be afforded in determining the extent of the lesion.
The binasal, and also the bitemporal varieties of hemianopsia are
due (as a rule, at least) to lesions confined to the anterior fossa of the
cranium; hence we sometimes find the olfactory nerve (of the side cor-
responding to the seat of the lesion) simultaneously affected, and creating
anosmia (loss of smell) with or without subjective odors.
If the lesion be situated within the middle fossa of the cranium, the
optie tracts may be affected, thus causing homonymous hemianopsia
(Fig. 21). The motor nerves of the eye may be simultaneously pressed
upon, as they pass through that fossa on the way to their foramen of
exit from the cranium (the sphenoidal fissure), and thus more or less
impairment of the movements of the eyeball of the same side may be
created.
The value of these complications cannot be over-estimated, when
they exist, because they may be of the greatest aid in diagnosis. They
may often enable the skilled anatomist to positively determine the seat
of the lesion.
Hemiplegia may occur in connection with hemtanopsia, provided
that the lesion is of sufficient size to affect any part of the so-called “ motor
tract” of fibres simultaneously with the optic nerve fibres (Fig. 23).
LESIONS AFFECTING THE OPTIC NERVE. 81
Motor paralysis is, under such circumstances, developed chiefly if not
exclusively on the side opposite to the lesion, because the fibres of the
motor tract decussate, to a greater or less extent, at the lower part of
the medulla. Flechsig has shown that, in rare cases, exceptions to this
rule are to be explained by an abnormality in the decussation of the
motor fibres.
Hemiplegia is seldom observed in connection with hemianopsia alone.
The olfactory, motor oculi, trigeminus, or facial nerve roots are
especially liable to be simultaneously involved. This explains the
mechanism of the four varieties of ‘crossed paralysis” which are
clinically encountered. The hemiplegia being developed on the side
opposite to the lesion as a rule, while the symptoms produced by pa-
ralysis of the cranial nerve are confined to the side corresponding to
the lesion.
Homonymous hemianopsia, when it occurs without any impairment
of mobility or sensibility, points strongly toward a lesion of the cuneus.
Ataxie manifestations, occurring in connection with evidences of
impairment of the sense of sight, open a wide field for speculation. The
proximity and intimate structural relations of the cerebellum with the
optic lobes, basal ganglia, crus, and medulla, suggest the possibility of
cerebellar lesions when these two symptoms are present to a marked
degree, and the patient can stand with the eyes closed.
Hemianesthesia may occur in connection with hemianopsia and
other disturbances of vision. It indicates some disturbance of the
nerve fibres of the so-called “sensory tract; the loss of sensation being
confined to the lateral half of the body opposite to the lesion which
causes it, because the sensory fibres decussate in the spinal cord.
In cerebral hemianesthesia, there is more or less insensibility to
touch, pain, and temperature, and also an abolition of muscular sensi-
bility with complete retention of electro-motor contractility. The mu-
cous membranes of the eye, nose, and mouth are also anesthetic. If it
be due to hysteria, the special senses are cither abolished or rendered defi-
cient, and Ayperesthesia over the ovaries exist (Ferrier). These facts
will often enable the diagnosis to be made between hysterical and cere-
bral hemianzsthesia of organic origin.
Choked disc is a common symptom of lesions situated at the base
of the cerebrum, and also of any intra-cranial disense which produces a
gradually increasing pressure. It is especially diagnostic of cerebral
tumors.
It is not associated with impairment of vision until late, so that it
is often unsuspected when present. The ophthalmoscope is necessary
for its detection. It may co-exist with hemianopsia, and is always bi-
‘lateral. It is a positive contra-indication to trephining.
6
82 LECTURES ON NERVOUS DISEASES.
Lesions at the base of the skull may cross the mesial line, and still
involve only one optic tract. If this occurs, the hemianopsia will he
accompanied by other symptoms of diagnostic importance, no longer
confined to one side. Double anosmia, general paresis or complete pa-
ralysis, general anaesthesia, and paralytic symptoms referable to both eye-
balls might be thus produced. Lesions of this character are more liable
to affect the chiasm of the optic nerves than the optic tracts; in either
case, however, hemianopsia would result, and its type would be a reliable
guide to the seat of pressure. ;
Motor aphasia sometimes co-exists with hemianopsia. I have met
with two instances of this kind. In one there was slight paresis of the left
side, tending to prove that aphasia can occur with lesions involving the
right hemisphere. Both were cured with specific treatment. We must
attribute the development of this complication to pressure upon parts in
the neighborhood of Broca’s centre.
LESIONS AFFECTING THE MOTOR OCULI NERVE.
The nucleus of origin (Fig. 12) of the third cranial nerve of each
side seems to be capable of subdivision into groups of cells which pre-
side over movements of special muscles of the orbit.
_ Thus we may clinically recognize the existence of a special nucleus
for visual “accommodation,” for pupillary movements, and for the
internal rectus, the superior rectus, the levator palpebre, the inferior
oblique, and the superior oblique muscles.
This fact probably explains how the existence of “external oph-
thalmoplegia” and other distinct forms of orbital paralysis may occur
from organic lesions in the region of the tegmentum.
Paralysis of this nerve is indicated by the following symptoms: (1)
a falling of the upper eyelid (ptosis); (2) external strabismus; (3) dila-
tation of the pupil; (4) a slight bulging of the eye forward, on account
of muscular relaxation ; and (5) a loss of accommodation of vision, .
When the third cranial nerve is paralyzed from cerebral lesions
the lower part of the face is often paretic on the same side as the lesion.
This is not the case when a lesion involves the nerve after it escapes
from the crus cerebri, viz., within the middle fossa of the cranium or the
orbital cavity.
Crossed paralysis of the “motor oculi nerve and body” type, indi-
cates a lesion situated within the crus cerebri. We find that the eye on
the same side as the lesion can no longer be turned toward the nose,
or made to act in parallelism with the opposite eye; that the pupil is
dilated; and that the upper eyelid droops over the eyeball, giving it a
sleepy appearance. On the side opposite to the lesion the body is hemi-
plegic. There are few conditions which are of greater clinical importance '
LESIONS AFFECTING THE CRANIAL NERVES. 83
than this type of crossed paralysis, because the seat of the lesion is posi-
tively indicated.
If the optic tract, which lies in close relation with the crus be
simultaneously affected by the lesion, the evidences of “ homonymous
hemianopsia,” will be superadded, viz., the eye on the same side as the
lesion will be blind in its temporal half, and that of the opposite side
in its nasal half,
One half of the pupil may fail to react to light when hemianopsia
exists. This is known as the “hemiopic pupillary reaction.”
LESIONS AFFECTING THE FOURTH AND SIXTH CRANIAL NERVES.
The nerves which are associated with the movements of the eyeball
—the third, fourth, and sixth cranial—pass through the middle fossa of
the cranium in company with the fifth cranial nerve. For this reason,
lesions situated at the base of the brain are liable to involve any of
these nerves separately, or all simultaneously, according as its pressure-
effects are felt in one direction or another.
In addition to cranial causes, lesions of the orbdié may also create
impairment of the third, fourth, ophthalmic branch of the fifth, or sixth
cranial nerves—all of which pass through the sphenoidal fissure into the
orbit. ,
Impairment of the sixth cranial nerve is indicated by the develop-
ment of internal strabismus; the extent of which varies with the degree
of the paralysis.
If this nerve be affected by lesions within the cranium, other nerves
are liable to be simultaneously involved; and an impairment of the cere-
bral motor tract may also be evidenced by a co-existing hemiplegia or
paresis of the side of the body opposite to the seat of the lesion.
LESIONS AFFECTING THE FIFTH CRANIAL NERVE.
The following propositions will cover the diagnostic points which
relate to lesions of the trigeminal nerve (after it escapes from the pons),
Peripheral lesions cause anesthesia of special parts supplied by
small branches or single filaments of the nerve.
The co-existence of paralysis of other cranial nerves with anes- -
thesia of the face, indicates a lesion in the vicinity of the base of the
cerebrum.
If a part of the face and the corresponding facial cavity (orbital,
nasal, or buccal) are simultaneously affected with a loss of sensation, the
lesion is within the cranium, and so situated as to involve one of the
three main divisions of the nerve.
If the anesthesia extends over the entire area supplied by all of
the branches of the nerve, and evidences of disturbance in the nutrition
84 LECTURES ON NERVOUS DISEASES.
of the parts are also present, the lesion affects the ganglion of Gasser or
its immediate neighborhood.
If the muscles of mastication are paralyzed, and no anesthesia
exists, the lesion is outside of the cranium and involves only the motor
root of the inferior maxillary branch of the nerve.
The anterior two-thirds of the tongue, the mucous lining of the
floor of the mouth, and the integument of the chin will be rendered
anesthetic simultaneously if the sensory trunk of the inferior maxillary
nerve is involved; and taste may be affected also on the same side as the
sensory paralysis.
Neuralgia of the various branches of the fifth nerve may exist in
place of anesthesia, whenever the lesion simply zrritates the nerve trunks,
but does not impair their power of conduction of sensory impulses.
All late authorities agree in the statement that the deep trigeminal
fibres may be traced as two roots: the so-called descending root (which
comes from the cerebrum), and the ascending root, which is apparent in
cross-sections at different levels of the medulla. ‘The view of Mcynert,
that the fibres of the descending root cross within the substance of the
pons, is sustained by clinical facts, as shown by Starr. This author
draws the following deductions, respecting the clinical significance of
facial anesthesia :—
1. Lesions affecting the ascending root-of the trigeminus produce
anwsthesia of the face upon the same side as the lesion.
2. Lesions affecting the descending root of the trigeminus produce
anesthesia of the face upon the side opposed to the lesion.
3. Disturbances of sensibility in the face indicate a lesion situated
within the medulla or pons, and in the external lateral part of the for-
matio reticularis (provided it be not due to neuritis of the trigeminus or
a cerebral lesion).
4. If the face be rendered anesthetic upon one side, and the body
upon the opposite side (the condition known as “crossed sensory pa-
ralysis’’), the lesion affects the entire extent of the formatio reticularis,
and lies, in the medulla or pons, below the point of union of the ascend-
ing and descending roots of the trigeminus.
5. If the face and limbs be rendered anesthetic upon the same side.
the lesion lies in the brain at a point higher than the junction of the two
roots of the trigeminus. It may, therefore, be found within the formatio
reticularis of the upper part of the pons and crus, or, if cephalad of the
crus, it may affect the posterior third of the internal capsule of the cor-
responding cerebral hemisphere, the centrum ovale of that hemisphere,
or the sensory area of the cerebral cortex, in which all the sensory tracts
terminate,
LESIONS AFFECTING THE CRANIAL NERVES. 85
LESIONS OF THE SEVENTH CRANIAL NERVE.
The following propositions will cover the diagnostic points of lesions
which induce facial paralysis (Bell’s palsy) :—
If the paralysis be limited to distinc! parts of one lateral half of
the fuce, the lesion affects only individual branches of the nerve, and is
outside of the cranium. An apparent exception to this rule is sometimes
smet with in connection with lesions of the internal capsule and of the
crus cerebri—paralysis of the lower half of one side of the face being
clinically observed to occasionally accompany hemiplegia, and also pa-
ralysis of the motor oculi nerve on the same side as the lesion,
If the fauces and palate exhibit-paralytic changes the lesion is within
the cranium or in the temporal bone.
If the sense of taste be lost in the anterior two-thirds of the lateral
half of the tongue (on the same side as the general facial paralysis), the
lesion is either within the cranium, or in the temporal bone above the
origin of the chorda tympani branch.
If the sense of hearing is rendered very acute upon the same side
as the facial paralysis, the lesion is probably within the temporal bone
and involves the ganglionic enlargement found. upon the nerve in the
aqueduct of Fallopius.
Facial paralysis (when dependent upon cerebral lesions, or those
of the crus cerebri or the pons) is commonly associated with hemiplegia,
which may be upon the same side as the lesion or on the opposite side.
Crossed paralysis of the “facial nerve and body type” indicates a
lesion of the pons Varolti posterior to the line which connects the
trigeminus nerve with its fellow at their escape from the pons. (Gubler.)
The reader is referred to Fig. 2.
If the lesion be situated in front of Gubler’s line, the facial pa-
ralysis and the hemiplegia will be on the same side.
LESIONS AFFECTING .THE CRANIAL NERVES ARISING FROM THE
MEDULLA OBLONGATA.
The facial, auditory, glosso-pharyngeal, pneumogastric, spinal ac-
cessory, and hypoglossal uerves have their apparent origin from the
medulla, and are more or less imperfectly understood in regard to their
connection with different parts of the encephalon.
Labio-glosso-pharyngeal paralysis (“ Duchenne’s disease” or “ bulbar
paralysis ’’) is associated with successive destruction of the nerve nuclei
in the floor of the fourth ventricle and a secondary degeneration of the
nerve trunks connected with them.
The nerve which exhibits the first evidences of paralysis will often
afford. clinical data from which some deductions respecting the original
86 LECTURES ON NERVOUS DISEASES.
seat of the lesion may be drawn. The more coimmon lesions of the
medulla include arteritis, thrombosis, traumatism, softening, hemorrhage,
sclerosis, and tumors.
The development of ‘ bulbar paralysis’ is associated, as a rule, with
neuralgic pains, muscular spasms, anesthesia, and disorders of special
senses.
Compression of the medulla oblongata has been shown to cause the
respiratory phenomena termed “ Cheyne-Stokes respiration,” and also
albuminous and diabetic urine. In the former, the frequency and char-
acter of respiration constantly changes in some regular order—gradually
increasing to a certain maximum, and then gradually decreasing in fre-
quency till they cease, when they begin again to increase in frequency
and in depth.
The vaso-motor centres, which are situated within the medulla. help
to explain many other visceral phenomena which are observed when it is
diseased. These are too numerous and complex in their nature to be
discussed here.
The differential diagnosis of suddenly-developed lesions of the
medulla, which are not immediately fatal, must rest upon the co-exist-
ence of certain functional disturbances. Among these may be chiefly
mentioned: 1, epileptiform attacks, occurring at the onset or later; 2,
hemiplegia or paraplegia; 3, loss of consciousness; 4, hyperesthesia or
circumscribed anesthesia; 5, dysphagia, vomiting or hiccough, and
Cheyne Stokes respiration, from interference with the pneumogastric
nerve; 6, embarrassment of speech, from interference with the hypo-
glossal nerve; 7, deflection of the velum palati and uvula, from interfer-
ence with the facial nerve; 8, hydruria, from interference with the centre
of renal circulation; 9, diabetes, probably from interference with the
centre of the vaso motor nerves of the liver; 10, normal electro-mus-
cular contractility in the paralyzed parts.
If the lesion be very erlensive and of sudden advent, death may
occnr without the bulbar symptoms being well defined.
A SUMMARY OF THE MORE IMPORTANT PHYSIOLOGICAL AND PATHO-
LOGICAL FACTS PERTAINING TO THE SPINAL CORD.* :
Much of an anatomical nature relating to the spinal cord might he
introduced at this point with profit to the reader if space would permit.
It is hoped, however, that by the aid of the diagrams incorporated, the
various “ tracts”? or bundles of fibres which compose the cord will be
comprehended. Additional information of an anatomical kind may be
* Some parts of this section have already appeared in the chapter upon the Diseases
of the Spinal Cord in the last edition of the Author’s work, ‘ A Practical ‘Tea on Sur-
gical Diagnosis.”’ William Wood & Co., N. Y., 1884.
SUMMARY OF FACTS PERTAINING TO THE SPINAL CORD. ST
a
seesseearvan ane.
By
a
Baia caacawsvasuverdl sen aedhcovaeseastaOyQanekentinrexedanvaauets
a
\¢
wyly
De GP oe
Q
Fic, 29.—A DrAGRAMMATIC REPRESENTATION OF THE CONDUCTING TRACTS OF THE SpinaL
Corp. (Modified from Bramwell.) 7, fibres of Tiirck’s coliimn (direct pyramidal bundle) ;
C. P., crossed pyramidal fibres;’’ G, fibres of the column of Goll (postero-median column) ;
D. C., fibres of the ‘‘ direct cerebellar column.’’ Note that the arrows show the direction of
the impulses carried by each tract of fibres, Also that the motor fibres of the lateral column
decussate at the dower part of the medulla, Each of the ‘‘anterior pyramids’ of the
medulla is composed of the motor fibres (direct and decussating) above the lower limits of
the medulla.
88 LECTURES ON NERVOUS DISEASES.
gained by the reader (in case the diagrams prove insufficient) by refer.
ring to the introductory pages of a subsequent section which treats of
diseases of the spinal cord. :
1. The anterior and lateral pyranudal columns of each side con-
tain only motor fibres. Those in the former (Turck’s columns) are con-
nected with the corresponding cerebral hemixphere, while those of the
latter (the “crossed pyramidal tracts”) are connected with the opposite
cerebral hemisphere. (Fig. 29.)
2. The posterior column of each side (comprising two portions—
that of Goll and Burdach) serves to convey sensory nerve fibres appa-
rently connected with the tactile sense, and also commissural fibres (?)
which connect different segments of the cord; hence they are physiologi-
cally associated both with tactile sensation and the codrdination of mus-
cular movement, (Fig. 29.)
3. The lateral column of exch side (exclusive of the crossed pyra-
midal fibres and those of the direct cerebellar column) probably conveys
vaso-motor fibres and possibly those of sensation also. It has been proven
also to convey fibres directly to the cerebellum (the “direct cerebellar
column ”), The crossed pyramidal tract occupies a distinct area of this
column.
4. The multipolar nerve cells in the anterior horn of the spinal
gray matter possess a ‘trophic function.” When they are destroyed,
the nerve fibres arising from them, and the muscles also which are sup-
plied by those fibres, undergo atrophy. (Fig. 33.)
5. The fibres of the anterior and lateral pyramidal columns have
their “trophic centre” in the motor area of the cerebral cortex. Any
lesion which tends to sever these fibres from this centre creates a de-
scending degeneration of all the nerve fibres so disconnected, as far as
their ultimate distribution, viz., to segments of cord below the lesion.
6. The spinal nerves may be regarded as guides to the various
segments of the spinal cord; each segment ‘consisting of a disc of the
cord of sufficient thickness to include a separate pair of spinal nerves
which are attached to it. (Fig. 31.)
1. Each spinal seqment, with its attached nerves, may be figura-
tively regarded as a distinct spinal cord for that limited portion of the
body to which its nerves are distributed, viz., the mascles to which the
anterior roots of the spinal nerves proceed, and the parts supplied with
sensation by means of the posterior roots of the same.
8. The super*mposed segments of the cord are hound together by
tracts of nerve fibres. Some of these are continued into the brain, while
others are purely commissural tn type. We can attribute to the former
group (the “ motor” and “sensory tracts”) the conduction of motor im-
pulses from the brain to the various spinal segments, and of impressions
SUMMARY OF FACTS PERTAINING TO THE SPINAL CORD. 89
of a sensory character from the periphery of the body to the brain itself
The other group mentioned (the “associating fibres”) serves to assist the
different spinal segments in the performance of all acts where a har-
monious and simultaneous action of sevrral segments of the spinal cord
is demanded. :
9. The two lateral halves of each segment of the spinal cord are
not totally distinct from each other, because « connecting band of the
gray substance of the cord (the gray commissure), and also one of
white substance (the white commissure), bind them together. The
white commissure lies at the bottom of the anterior median fissure; the
gray commissure fills the remaining space between the anterior and
posterior median fissures (Fig. 30).
10. The anterior horns of the spinal gray matter contain cells of
large size which are connected (1) with motor nerve fibres, joining each
spinal segment with the brain (somewhat indirectly), and (2) with the
fibres of the anterior root of the spinal nerve (associated with the muscles
controlled by each segment). Thus these nerve cells are interposed be-
ANTERIOR
ROOT
SPINAL, |
© NERVE H gf MUSCLE
MOTOR
BRANCH
POSTERIOR
ROOT
GANGLION
SENSORY
RANCH
Fic. 30.—A SPINAL SecmENT. The two roots of the spinal nerve are shown; also the sensory
and motor fibres of which each is composed.
tween the fibres which pass from the brain to the cord and those dis-
tributed to the muscles, an arrangement which permits of an automatic
action of the cord, irrespective of cerebral influences.
The cells of the anterior horns appear to control also the nutrition
of the muscles, connected with them by means of the nerve fibres.
ll. The cells of the posterior horns and central portion of the spinal
gray matter are probably connected more or less intimately with the
fibres of the posterior or sensory roots of each spinal segment, and
possibly also with the paths of conduction of pain ful impressions to the
brain. They do not exert any apparent influence upon the nutrition of
the parts associated with them by means of the spinal nerve fibres.
12. The spinal refleres are probably performed }y means of un
anastomosis of the processes of the cells of the anterior and posterior
horns of each lateral half of a spinal segment. This enables a sensory
90 LECTURES ON NERVOUS DISEASES.
| Ni
lll v MOTOR. | SENSORY. REFLEX,
c Neck and scalp
St.-Mastoid
rapezius
Y { Neck and shoulder
T
{ Diaphragm
=
'
'
-
awe
|
@ Serratus
5 fo H | 5) Cerra Shoulder _Shoulder
6c 6 6) ----7 Arm mus. Arm | Scapular
CF |
7 1 /.2) BER ds Hand || ‘Hand '
h (ulnar lowest) ; |
D.! GET j pe ie i - J
4 Hh |
64 5) Oat egmonneee 5 | ¢ Front of thorax
Ol | ‘_ Intercostal | |
VA @ Peete eiciat= 6 Muscles | Epigastric
3 Ensiform area
OOO NM ... ----- 7
oI
e ~- --------8
0
9 Y Nl 1Q\ fie amie ta 1 ie Abdominal Abdomen
; omina) oi
fe : Umbil 10th
10 | BB Laseee | Mupcles one ) Abdominal
11 A
2 Fe pele Buttock, upper
12 s "| part
tl J) 4 =. ----- iL | ? Groin and scrotum
+ 4j 35 front
i 21 5 il ( outer side
2 Gl —. —- C Flexors, hip | | | | ee
3 fe os ene it i een knee ail front j Hee amie
is { navetors al |
|
| Lhiy ‘Buttock, lower
f Adductors pare Gluteal
ob ssi eel
Flexors, knee (?) 2 |
Leg
and
Foot
except
Muscles of leg inner part
i
cl moving foot Foot clonus
| Back of Thigh
Plantar
{ Perineal and Anal
Muscles
J
inner side
Leg, inner side
|
|
| |
!
} |
\
Perinzum and Anus
Skin from coccyx to
Anus
1
4 i
Fic. 31.—A DiaGcram DesiGNED TO SHOW THE RELATIONS OF THE VERTEBRA TO THE
SpinAL SEGMENTS, AND OF THE SPINAL Nerves To THE Movor, Srnsory, AND REFLEX
FUNCTIONS OF THE SPINAL CORD. (GOWERS.)
SUMMARY OF FACTS PERTAINING TO THE SPINAL GORD. 91
impression, which is conveyed to the spinal segment by means of the
fibres of the posterior root of the spinal nerve, to become transformed
into motor impulses in the cells of the anterior horn. These are then
transmitted to the muscles hy the fibres of the anterior root of the spinal
nerve.
13. The sense of touch may be destroyed, in parts below the point
of injury, by section or disease of the posterior columns. The sense of
pain and the appreciation of temperature are apparently still conducted,
provided the gray matter escapes injury.
14. The sense of pain is destroyed when the gray matter is rendered
incapable of transmitting such sensations. The sense of touch apparently
remains unattected, if the posterior columns escape.
15. The sensation of pain and of touch may be independently re-
tarded by lesions of the cord that impair, but do not totally destroy the
conductivity of the paths for such sensations. The amount of such
retardation depends upon the extent of the destructive process within
the cord. Cases have been reported where thirty or more seconds would
elapse between each painful contact on the periphery of the body and its
appreciable sensation.
16. Destruction of a posterior root of a spinal nerve, or the net-
work of fibres formed by it within the substance of the cord, must affect
the transmission of all sensations of touch, pain, and temperature from
the peripheral area of distribution of the nerve so affected (Fig. 31).
li. Destruction of « posterior nerve root causes anesthesia to pain,
temperature, and touch. Trophic disturbances of the skin are also liable
to follow, particularly if the nerve-root is injured outside of the gang-
lionic enlareement developed upon it (Fig. 30).
18. Destruction of the columns of Burdach and Goll is followed
by tactile ansesthesia of definite areas, that correspond to the spinal seg-
ments affected, and sometimes in parts below the injury. Anesthesia of
the arms is especially characteristic of a lesion in Burdach’s column;
when in the legs, of Goll’s column.
19. When the posterior columns of the cord are affected with dis-
eased conditions that create ¢rritation of the parts, the so-called “ girdle
pain,” or » vincture-feeling” is developed in-‘those nerves that traverse
the disease area of the cord. Below the level of the spinal lesion, sub-
jective sensations of touch (such as formication, numbness, abnormal
sensations of heat or cold, etc.), and more or less hypersthesia are
usually created.
20. Lesions of the sensory tracts (the so-called “ sesthesodic sys-
tem”) cannot induce paresis, paralysis, spasm, or muscular atrophy.
They can only create sensory manifestations (such as anesthesia, hyper-
esthesia, numbness, formication, abnormal sensations of heat and cold,
92
LECTURES ON NERVOUS DISEASES.
*,
oS
Puss oneweunceeesanees,
i i
;
i)
i
Sea
wee B
acl lap Gizrie op
Fic, 32.—A Dracram Desicnep To ILLUSTRATE THRE CONNECTIONS OF THE MoToR AND
Sensory ConpuctinG TRAcTS OF THE CORD WITH THE SprnAL Nerves. (Modified
from Bramwell.) AZ, motor fibres of the anterior root of a spinal nerve; 5S, S’, sensory fibres
of the posterior root. Note that the course of S and S’ are not the same. Some sensory
fibres pass directly through the posterior horn of the spinal gray substance, and others through
Burdach’s column to read the gray substance. ‘The direct cerebellar column is composed of
fibres which start in Clarke's column of cells (Fig. 33). The fibres of the two pyramidal
tracts become united to the motor cells in the anterior horns of the spinal gray substance.
SUMMARY OF FACTS PERTAINING TO THE SPINAL CORD. 93
and pain), and, in addition, an inability to properly codrdinate muscular
movements (ataxic symptoms).
21. Sensory phenomena are manifested, as a rule, upon the side of
the body opposed to the seat of the lesion. If they occur upon the same
sie, either the posterior nerve roots are directly involved, or the sensory
tracts are affected during their ascent in the posterior columns belore
their decussation.
22. The so-called “cincture feeling” or “girdle pain” may be taken
as a valuable guide in deciding as to the probable limits of a focal lesion
of the cord.
23. Pain in the region of the spine is a rare symptom of disease of
the spinal cord. When it exists, it commonly indicates a disease pro-
cess that is confined to the vertebre or the spinal meninges.
24.0 Destructive lesions of the posterior coliimns (if bilateral) are
commonly associated with a band of complete anesthesia that corre-
sponds to the area of distribution of nerve roots affected by the lesion.
Below this girdle of anesthesia, sensations of touch are usually impaired
or absent, and sensations of pain are localized with difficulty, but are still
trausmitted by the gray matter of the cord.
26. Lesions that cereale vrritation of the cervical gray substance are
accompanied by dilatation of the pupil. If destructive processes are
subsequently developed, the pupil becomes contracted (Argyll Robert-
son’s pupil).
26. Lestans of the posterior columns that irritate primarily and
subsequently destroy the spinal substance tend, as a rule, to progress
upward. As they advance, the girdle of pain travels upward and leaves
behind it a girdle of anesthesia that’ steadily increases in width. In
parts situated below the level of the lesion, the sense of touch is usually
lost, although subjective sensations of touch, such as formication, ting-
ling, numbness, etc., may exist.
27. The existence of a girdle pain, without any impairment of the
sense of touch in parts below it, or the presence of motor paralysis,
points strongly to some lesion that involves the posterior nerve roots
only.
28. Lesions that affect only the motor tracts (the so-called “ kine-
sodie ‘system ) may induce paresis or paralysis, spasm, and atrophy of
muscles, They never cause sensory symptoms (such as marked and per-
manent pain, hyperesthesia, anesthesia, numbness, formication, etc).
29. Paralysis of motion and muscular atrophy, when due to spinal
lesions, develop upon the same side of the body as the lesion. The same
is generally true of the symptoms referable to incodrdinalion of move-
ment,—the so-called “ataxic” symptoms. The fibres that convey the
“ muscular sense” do not decussate until they reach the medulla.
94 LECTURES ON NERVOUS DISEASES.
80. Alrophic changes in muscles notes strongly toward a degen-
erative change in the motor nerve-cells of the anterior horns of the spinal
eray matter. These cells are the trophic centres for the fibres of the
anterior nerve roots. (Fig. 33.)
31. Contracture, or a permanent shortening of paralyzed muscles,
is strongly diagnostic of a lesion that involved the “ crossed pyramidal
tract’? within the lateral column of the cord. (Fig. 29.)
32. Symptoms referable to special organs (when dependent upon a
spinal lesion) indicate that some of the special centres of the cord are
involved. Such symptoms may be of value in determining the extent
and situation of the lesion.
Fic. 33.—Srmi-DiaGkamMMaTic TRANSVERSE SECTION OF THE GRAY SUBSTANCE OF THE
Cervicay (4) ann Lumbar ENLarGemenr (2) OF THE Srinat Corp. (Erb.) 4. a,
median group of cells; 4, antero-lateral group; ¢, postero-lateral group; @, vesicular column
of Clarke, 2B, a, median group; @’, group that appears first in the lumbar region, possibly,
belonging to a; 3, antero-lateral group} c, postero-lateral group. Note that the cells are
few and scattered in the posterior horns, and also that the shape of both horns differs
markedly in 4 and 2.
33. Lesions of the so-called “ motor tracts” of the cord (the “ kine-
sodi¢ system”), if destractive in character and sufliciently large to sever
the connection of the motor fibres from their connection with the cells of
the cerebral cortex, produce complete paralysis of motion below the level
of the lesion on the corresponding side of the body. The paralyzed
muscles will probably undergo subsequent contracture, and the deep or
tendon-retlexes will become exagecrated.
me
SUMMARY OF FACTS PERTAINING TO THE SPINAL CORD. 99
34. Lesions of the anterior horn of the spinal gray matter are liable
to produce paralysis in the areas of distribution of the related nerves,
without disturbance of sensibility, but with marked trophic¢ disturbances.
35. Slight pressure upon the cord may induce moderate paralysis
(paresis) of the extensor muscles and secondary contracture of the
flexors.
36. Lesions of one lateral half of the cord produce complete motor
paralysis, vaso-motor disturbances, incodrdination of movement, and
hypereesthesia on the corresponding side below the level of the lesion,
and a loss of sensibility on the opposite side with more or less paresis
in some cases. 0), comprise
ehietlt the so-called substantia nigra and the ‘red nucleus of the teg-
mentum.” The fibres associated with them (2. 2.8. $e. So 10,
2icand 72), constivute, collectively, the dasés and fegmentum eruris of
Mey neit. whieh are separated by the substantia nigra. The red nucleus
lies beneath the corporn quadrigemina in the feymenéwm (the sensory
portion of the crus). and is in intimate relation wich the fibres of the
~coorior eerebellar peduncle (3). The corpora quadrigemina (not shown
in the diagram) should be also included among the ganelioniG masses of
this region. The third eranial nerve is represented as) structurally
related to the mesencephalon. The optie nerve has also intimate rela-
tions with some of its parts. Fibres ef many of the eranial nerves. which
spring from the medulla, aro prolonzed through the pons and crus to
reach the cerebrum.
100 LECTURES ON NERVOUS DISEASES.
The functions of the mesencephalic centres are too complex to
justify any generalizations. All of the complex forms of muscular
activity which are more especially clicited in response to some form of
impression received from without by means of the nerves of special
sense, Such as locomotion, emotional expression, etc., are to be attributed
partly, if not wholly, to these ganglionic centres. The special attributes
of the red nucleus of the tegmentum and the substantia nigra are, as yet,
somewhat conjectural.
THE MEDULLA OBLONGATA.
5. Within this ganglion, the nuclei of origin of many of the cranial
nerves have been found, and special centres which preside over important
physiological functions have also heen demonstrated. The circles (.W’”’)
and ($’’’) in the diagram are supposed to represent the sensory and motor
collections of gray matter, which give to this portion of the central
nervous system its peculiar powers. The motor centres (J/'’) are repre-
sented as in communication with certain cranial nerve roots, and also
with motor fibres which serve to connect the medulla to the corpus
striatum and the ganglionic masses of the mesencephalon above, and the
seements of the spinal cord below. The sensory centres (S’’’) are shown
to be in relation with the sensory cranial nerve roots (the term “sensory”
being used in its broadest sense to include all fibres bearing atterent
impulses), as well as with the paths of cerebral and cerebellar sensory
conduction (6 and ZO). Thus it is that the cerebellum as well as the
cerebrum probably is made cognizant not only of tactile sensations and
of other varieties of sensory impulses transmitted along the spinal tracts,
but also of other facts which our special senses reveal to us. The view
that the cerebellum acts in part as an “informing depot” (Spitzka) for the
cerebral hemispheres can be comprehended by a study of this diagram.
The fibres which are drawn in the diagram between the motor and
sensory centres of the medulla help us to comprehend the probable
inechanism of many forms of complex coirdinated reflex actions, of
which the medulla is capable when all the nerve centres above it have
been removed. It is apparent that each of the segments of the nervous
system here depicted is capable (by means of. associating fibres) of an
action of its own which is independent of those centres above it, but
which may be controlled or overpowered by the higher centres when they
are called into action.
THE SPINAL CORD.
6. The diagram shows the cells of the anterior horns of the spinal
gray matter Cd. C.) to be in connection with the fibres of the direct motor
tract which we have now traced from the cerebral cortex downward
(although some have lheen deflected from the direct path ly the cells of the
SUMMARY OF CEREBRO-SPINAL ARCHITECTURE. 101
mesencephalon :nd medulla). These motor fibres of the spinal cord are
prolonged by means of the interposed cell (4.C.) as fibres of the anterior
or motor roots of the spinal nerves, The cells of the posterior horns
of the spinal vray matter (2. C.) are likewise shown to receive the afferent
impulses conveyed to them from without by the posterior or seusory
roots of the spinal nerves (as shown ly the arrow), and to transmit then
upward by means of fibres which connect them with higher ganglionic
masses (6,6,and 7), The exact paths of motor aud sensory conduction
through the spinal cord are not positively settled. The antero-lateral
columns of the cord are commonly regarded ‘as the chief motor paths,
although all observers are not in agreement respecting the anterior
columns. The sensory tracts probably run partly in the central gray
matter of the cord, and partly in the lateral and posterior columns. Sen-
sory impulses travel on tlie side opposite to that on which the nerves
enter, with the exception of impressions of the so-called muscular sense
(Starr). The views held respecting the functions of the spinal columns
have been given in preceding pages.
Finally, it will be observed that the motor and sensory cells of the
spinal cord communicate. This arrangement allows of an automatic
spinal action. Beheaded animals can be made to exhibit definite mus-
cular invvements when any irritation of the sensory nerves of the skin
is employed to call them forth. A frog so mutilated will scratch with
the opposite foot a spot on the leg which has-been touched with an acid.
Robin has observed similar phenomena in a beheaded criminal. These
movements are purely reflex in type, because all parts which we know to
be essential to consciousness or volition have been taken away, They
can only be attributed, therefore, to a communication (not yet well un-
derstood) between the sensory and motor cells of the spinal segment.
Many of the acts which constant and long-continued practice enable us
acquire during life—as, for example, the running of scales upon a piano
—are unquestionably performed automatically by the spinal cord, with-
out assistance of the higher ganglia in many instances.
In closing this section, the Author feels that much has of necessity
been omitted; and that some of the views advanced are apt to be
modified or possibly overthrown hy subsequent investigation.
He trusts, however, that the difficulties of the task will not be lost
sight of by the reader; and that the chapter, 1s a whole, may prove of
material assistance in fathoming the mysteries of obscure neuroses.
The two diagrams which follow are copied from Aeby. They pre-
sent, to the Author’s mind, the main points in cerebro-spinal architecture
with singular lucidity.
LECTURES ON NERVOUS DISEASES.
FIG. 36.
eer TTT Spl
ir
Figs. 36 and 37.—A DiAGRAM oF THE Course or THE Nexve Fisxes iy THE SUBSTANCE
OF THE BRAIN AND SPINAL Corp. (After Aeby.) I, view of a transverse section; II, Pro-
file view; II], the nuclei of the medulla (partly after Erb). The crosses of color corre-
sponding to the lines upon which they are placed, designate the point of section of each tract
as it passes through different levels (the crus and pons). C i, ¢aferual capsude, with
radiating fibres (in yellow), pyramidal fibres (red), and fibres going to the pons (in purple):
C, the crwra cereéré, with the pyramidal fibres and the.fibres going to the ganglia of the
pons anteriorly, and posteriorly, the substantia nigra, the fillet tract (in dotted lines), the
fibres of the superior peduncle of the cerebellum (in blue); Pc, the peduncles of the cere-
écllum, showing the fibres going to the cerebrum, the pons, and the medulla; P, jaws
Varolii, with its ganglia on either side (in purple). In III, the 2uclet of the cranial nerve
roots are numbered to correspond with the nerves. Red is used for the motor nuclei, and
SUMMARY OF CEREBRO-SPINAL ARCHITECTURE.
Fia. 37.
blue for the sensory nuclei. The ¢vacts im the cord are designated by the area similarly
colored in the cross-section of the cord beneath, c’, Column of Tiirck; c, crossed pyramidal
column; a, anterior horn; a’, anterior root zone; e, direct cerebellar column; b, posterior
horn; b’, column of Burdach; d, column of Goll. Higher up are seen b’’, the inferior
peduncle of the cerebellum; d’, the fillet or lemniscus tract; f, the fibres connecting the
ganglia of the pons with the cerebrum and cerebellum, b’’’, the fibres of the superior cere-
bellar peduncle; h, the caudo-lenticular and thalmo-cortical fibres ; i, the commissural fibres
(see Fig. 6); Th, optic thalamus; nc, nucleus, caudatus; nl, nucleus lenticularis ; gc, central
convolutions.
In this diagram, the course of b/’ seems to be in error in not undergoing a decussation
(Author’s note).
103
LON aL,
PRACTICAL HINTS REGARDING THE CLINICAL
EXAMINATION OF PATIENTS AFFLICTED
WITH NERVOUS DISEASES, AND THE
VARIOUS TESTS WHICH MAY
BE EMPLOYED AS AIDS
IN DIAGNOSIS.
SECTION II.
THE METHODS OF EXAMINATION EMPLOYED IN THE DIAGNOSIS OF
NERVOUS DISEASES.
#
THE majority of practitioners apparently join in the feeling (which
happily conduces largely to the benefit of specialists in neurology) that
nervous anatomy and physiology is “too complex a subject for them to
master,” and that they must be, therefore, given over to those who are
devoting themselves particularly to the department of nervous diseases.
While this may be true in part, I believe that it is not only possible
but comparatively easy for any medical practitioner (who is willing to
make the necessary effort) to grasp certain general principles which are
applicable to the examination of cases afflicted with nervous diseases.
These can be applied without expensive apparatus, and with decided
benefit both to himself and his patients. They will tend to render his
diagnosis more scientific and accurate. They will aid him in properly
directing his treatment. Finally, they will often save him the humiliation
of seeing his patient seek advice from other hands.
The intelligence of laymen is always strongly impressed by evidences
on the part. of the physician of great care and marked skill, as shown in
the first examination. The impressions left upon the patient’s mind by
the results of the first interview are of the greatest importance to both
parties. While the doctor is studying the patient, the patient is, as a
rule, studying the doctor with even greater interest.
Every step which is taken by the physician, as a means of forming a
positive and final judgment, is watched with an earnestness on the part
of the patient that invariably accompanies mental anxiety. Hach ques-
tion that is asked regarding the previous history of the patient, the pos-
sibility of similar troubles in his parents or blood-relations, the origin
and course of the more important symptoms, ete., are even more indelibly
impressed upon the mind of the patient than upon that of the physician,
who keeps the written record.
When, later in the examination, the power or electrical reactions of
the muscles, and the sensibility of different regions of the body to touch,
temperature, and pain are being tested in various ways, and the results
of such tests are being recorded in the case-book of the physician, the
reasoning faculties of the patient are even more keenly alive, and seek to
penetrate (as far as his intelligence will permit him to do) into the mys-
teries of the science, and to draw conclusions regarding the clinical
(107)
108 LECTURES ON NERVOUS DISEASES.
sionificance of certain symptoms, of which, perhaps, he was unconscious
up to that time. It will often be necessary, therefore, for the physician to
quiet evidences of alarm on the part of the patient, from time to time, as
the examination of the symptoms proceed, by judicious explanation or
words of encouragement.
It should ever be remembered by the physician that any omission
on his part to investigate the condition of the motor or sensory nerves,
the pulse, the respiration, the temperature, the spinal reflexes, etc., in
each and every case, will sooner or later be remarked by some patient,
who has either read extensively or had, from time to time, different
metical advisers. Moreover, interested friends (sometimes very intelli-
gent from past experiences of their own) may often drop hints to the —
patient which will tend to strengthen or weaken his or her views that
have previously been formed of the accuracy and care of the first exami-
nation of the symptoms.
It is my intention to give here, with some detail, the description of
the various steps that are commonly employed by specialists in neurology
in the examination of their patients; and to suggest a simple method of
recording symptoms, as a basis for the diagnosis and subsequent treat-
ment of nervous affections.
I shall discuss the subject under the following heads :—
First—The clinical history of the patient, and how to record the
chief symptoms of each case.
Second.—The symptoms revealed to the physician by his sense of
sight.
Third.—The symptoms revealed to the physician by instruments of
various kinds, and other tests.
I,
THE CLINICAL HISTORY OF THE PATIENT.
Every physician should be provided with a case-book. In it the
main features of each patient’s case should be first recorded, and a memo-
randum of the treatment and modifications of the symptoms should be
subsequently jotted down at each visit. In this way only can the results
of an extended experience be made useful for scientific purposes at some
later date. It will furthermore aid the doctor in utilizing his leisure
hours by studying the cases which he meets during the busy routine of
his office work. One case well studied is worth a hundred casually
glanced at and hastily prescribed for.
-1t will help to economize time if the case-book is printed in sucha
way as to have the more important symptoms already upon the page;
spaces being left blank to allow of a record of any modifications of these
THE CLINICAL HISTORY OF THE PATIENT. 109
that may exist. This plan adds to the legibility of the notes, and also
admirably adapts them for comparison with those of previous or subse-
quent cases. Hach physician may alter the arrangement of the pages of
his case-book to suit his individual practice, but it is best for a general
practitioner to have it adapted for all classes of patients.
In.a subsequent portion of this chapter I will suggest a form of case-
book which seems to me to be well adapted to the requirements of a
specialist in nervous diseases.
Let us now suppose that 2 patient enters the office of a physician for
medical advice relating to a nervous malady. After the usual questions
have been asked the patient regarding the name, the age, the condition
as to marriage, the nationality, and the occupation, and the answers
recorded, the patient should be brought rapidly to a concise statement of
the more important symptoms for which he seeks medical relief. This
can be usually accomplished by a little tact; and much valuable time is
saved by so doing. These symptoms can then be separately recorded
upon a page in your case-book.
With these especially marked symptoms as a starting-point, ques-
tions may then be asked regarding certain of them which the physician
deems the most important from a clinical aspect; seeking in each instance
to learn all about the present and past history of one symptom at a time,
and the modifieations which have been observed concerning it, so far as:
the patient’s memory will prove of assistance.
Now, the ability on the part of the doctor to ask questions that are
pertinent to each symptom will depend entirely upon the knowledge
which he himself possesses of the subject. J have often tested medical.
students and young practitioners in this regard, and have been amused
to see how rapidly their stock of pertinent inquiries became exhausted.
In order to intelligently ask about pain, for example, the physician
must know all the axioms of nerve-distribution which Hilton so ably
advanced; he must be a master, in the second place, of the course of
separate nerves which enable definite regions to tell the doctor (by
the presence of the sense of pain) of disease that is sometimes far re-
mote from the painful area; again, he must be able to correctly trace
the course of affected nerves, and thus to seek for abnormal condi-
tions along the line of each nerve which might produce local pressure
upon them; he must be familiar, in the fourth place, with the individual
peculiarities of pain in special diseases, as, for example, the characteristic
pains of rheumatism, neuralgia, locomotor ataxia, etc.; finally, he must
be familiar with all the possible causes of pain in different regions of the
body or extremities.
When we shall have discussed the various symptoms revealed by
inspection of the patient, as well as the tests employed to determine ab-
110 LECTURES ON NERVOUS DISEASES.
normal states of the motor or sensory nerves, and the reactions of muscles
to different electric currents, many points will have been given that may
prove of assistance in suggesting pertinent questions, to be employed in
obtaining the clinical history of patients so afflicted; but it will require
continued practice, much study, and close observation to excel in the art
of quickly and accurately gathering pertinent facts, from which con-
clusions can be drawn regarding the diagnosis and treatment of nervous
diseases,
A few general hints may, however, be thrown out here as to special
lines of inquiry, each of which may afford us valuable information re-
specting nervous maladies.
Tur Duration or Extstrna Symproms.—It is important to ascertain
the exact date of the commencement of the symptoms for which the
patient seeks relief, or of others which may be detected by the physician
at the first interview.
This will often decide as to the acuteness of the attack, and also
afford in some instances information respecting the seat and type of the
disease.
In the chronic varieties of spinal disease (as, for example, progressive
muscular atrophy, locomotor ataxia, disseminated sclerosis, etc.), the
patient cannot, as a rule, fix the date at which the symptoms commenced
because the development has been extremely ‘slow and gradual.
On the other hand, a hysterical fit may be followed immediately by
an attack of hysterical paralysis; a hemorrhage into the brain or spinal
cord, that has ploughed up the substance of these organs, causes paralytic
symptoms that develop instantly; inflammatory changes of the brain or
cord are usually attended by a more gradual onset, although it may be
comparatively rapid.
As an illustration of the clinical bearing of the duration of symptoms,
let us take the following: Two patients present a deformed hand from
atrophy of the muscles of the thumb and interossei. The one has been
slowly developed, and is probably the result of progressive muscular
atrophy; the other has been very rapidly developed, and is probably due
to some disease or local injury of the ulnar nerve. Should the deformity
have occurred in years past, and have shown no evidences of steady pro-
gression, the existence of progressive muscular atrophy could be then
safely excluded.
Tue Excitina Cause or Existinc Symproms.—If there has been any
external violence received, it is important to ascertain the exact nature,
seat, und severity of the injury.
Concussion of the spine may cause severe and often fatal disease of
the spinal cord. Violence to the head may depress the inner tablet of the
skull without any evidence of depression upon the exterior. The brain
THE CLINICAL HISTORY OF THE PATIENT. 111
may be seriously injured, when the bones that encase it may escape.
Some of the spinal nerves may be implicated in a wound or bruise, and
thus paralysis may be induced independently of the nerve centres.
Mental anxiety or overwork is a frequent cause of brain diseases,
Eye-defect acts very frequently as an etiological factor in many cases of
headache, neuralgia, hysteria, epilepsy, chorea, and some obscure visceral
derangements. Some defects in the eye are inherited (as are peculiarities
in feature and mental traits). This field will be discussed later in this
chapter.
A family tendency to gout or rheumatism, etc., may suggest the
possibility of an abnormal blood-condition as an important factor in
creating nervous disturbances.
The urine should always be carefully examined, as well as the heart,
to exclude the possibility of renal or cardiac disease as a factor in the
nervous derangement.
Tue AGE or THE Patient.—Much may be suggested to the mind of
the physician by the age of the patient; because some diseases are
more common at one period of life than at another.
During early childhood we are particularly Hable to encounter the
symptoms of idiocy, epilepsy, and chorea, as well as those of an inflam-
mation of the anterior horns of the gray matter of the spinal cord, the so-
called “ poliomyelitis anterior.” The acute variety of the latter disease is
most common between the ages of one and four, and it is seldom devel-
oped except in childhood. In the vast majority of cases, the condition
termed “pseudo-hypertrophie paralysis” (because the muscles are over-
grown like those of an athlete) is developed during the first few years of
life. Again, the tubercular form of inflammation of the meninges, both
of the brain and spinal cord, occur in the young child. Among the rarer
forms of disease of the spinal cord, a congenital variety of the so-called
“spastic paralysis,” and also of ‘locomotor ataxia,” is encountered in
young children. Reflex paraplegia is also occasionally seen in very
young subjects. Cases of disseminated sclerosis of the spinal cord have
been reported in the child.
Between the ages of puberty and the fully developed adult, Pott’s
disease of the vertebra may develop and create compression of the spinal
cord; and attacks of rheumatism may render the development of embolic
hemiplegia and aphasia possible. Meningitis of the brain and spinal
cord are not uncommon during this interval. Hysterical paraplegia
occurs in young females in connection with uterine disturbances. Be-
tween the ages of twenty and thirty, cerebro-spinal sclerosis is most
commonly developed.
In the adult, progressive muscular atrophy, myelitis, meningitis of
the cord, locomotor ataxia, the chronic form of poliomyelitis, and amyo-
112 LECTURES ON NERVOUS DISEASES,
trophic lateral paralysis are among the spinal diseases often encountered.
Cerebral meningitis, and softening, tumors, and embolism of the brain
are frequently recognized. Shaking palsy seldom occurs except in ad-
vanced life. The symptoms of Duchenne’s disease, and the paralysis of the
insane are most commonly developed between the ages of thirty and sixty.
Linked with adult life, also, comes apoplexy associated with paralysis;
and a late rigidity of the paralyzed muscles is developed whenever the in-
jury excites a descending degeneration of the fibres that are torn across by
escaping blood, or deprives the cerebrum of its power of control over the
cerebellum. Excessive indulgence in eating and drinking, coupled with
the absence of proper physical exercise, and the possibility of acquired
syphilis, render males more subject to paralysis than females.
Tus Sex.—Males suffer much more frequently from organic nervous
affections than females.
This fact is to be accounted for partly by the liability of that sex to
injury, exposure to cold or dampness, and excessive mental or physical
labor. But habits of indulgence in alcohol and venery, with its danger
of syphilitic infection, are also far more common in males than in females,
and are often prominent factors in the causation of morbid conditions of
the nerve centres. Certain occupations, tending toward great muscular
strain, or lead, arsenic, and mercurial poisoning, may be exciting causes
of serious nervous affections. Prolonged exposure to compressed air (as
in the case of divers) is often followed by paralysis. Many such cases
have occurred among workmen in submarine excavations,
Tue Ierepiry,—After you have exhausted the special lines of
inquiry indicated by the prominent symptoms that each patient seeks
relief for, questions should then be propounded to the patient touching
upon the possibility of hereditary predisposition to nervous affections
or of some hereditary ‘diathesis.”
Some nervous affections exhibit a marked dependence upon a heredi-
tary predisposition, either to the disease actually present, or to some
allied disorder. Epileptics, for example, are frequently the offspring of
tubercular or syphilitic parents, or of epileptics. Again, chorea and
hysteria may be developed from the most trivial excitement (even from
imitation of others so affected) in subjects predisposed to nervous ex-
citability or debility. Apoplectic subjects not infrequently beget. off-
spring who manifest in adult life a decided tendency to vascular disease.
Certain spinal affections seem to be particularly associated with heredity.
A predisposition to cancer and tuberculosis is unquestionably transmitted,
and these conditions are not infrequently found in the brain and spinal
cord, or their envelopes.
A marked hereditary tendency toward some spinal affections seems
to be well established, Pseudo-hypertrophic paralysis is transmitted
THE CLINICAL HISTORY OF THE PATIENT. 113.
through the mother. Locomotor ataxia occasionally runs in families, and
progressive muscular atrophy is markedly hereditary. Quite a lar ge pro-
portion of hysterical women can be shown to haye sprung from ancestry
in which tuberculosis, epilepsy, or insanity has existed; and idiotic
children and epileptics sometimes owe their disease to a so-ealled “hys-
terical temperament” on the mother’s side. I believe that, in many cases,
this predisposition can be traced to an inherited defect in the ocular
muscles, or a refractive error in the eye itself, which creates eye-strain
when binocular vision is attempted. This view is based upon an exami-
nation of quite a large number of such cases.
: Hasirs or tHE Parient.—These should be the next subjects of
inquiry.
Alcoholic subjects are always surrounded by dangerous possibilities.
Inflammation, when once started in such patients, is liable to be of a
severe and fatal form. ‘Trivial injuries often excite serious complications
in such subjects, and hereditary or acquired diseases, which have been
comparatively dormant for some time, may be kindled into activity by a
“spree.”
Again the habitual use of drugs for nervousness, sleeplessness, and all
the other ailments with which the laity often experiment at the suggestion
of friends, but without the knowledge of their doctor, may be a factor in
nervous symptoms that have become aggravated or actually developed
by their injudicious use. Some patients can use tobacco without ap-
parent injury, while it is a rank poison to others; tea and coffee are like-
wise injurious to many patients. The long-continued use of chloral, the
bromides, opium, or other drugs may result in nervous affections of a
serious character.
THE OccuPATION OF THE PatiENT.—This may be a possible factor
in the development of nervous diseases.
Sewing-girls frequently develop ulceration of the stomach from the
pressure exerted upon that organ by stooping. Painters are peculiarly
liable to lead-poisoning; and in some arts, where mercurial, phosphoric,
and arsenical preparations are extensively employed, symptoms of these
forms of poisoning may be developed. Constant or prolonged exposure
to cold or dampness is very often an exciting cause of spinal affections.
Excessive exercise or occupations demanding an unusual strain upon the
muscles may induce actual disease of the muscles, peripheral nerves,
spinal cord, or brain. Extreme mental labor or anxiety is a frequent
cause of brain inflammation and changes within the coats of the blood-
vessels of that organ.
Tue AcqgurreD Drsrases.—Finally, the previous history of the
patient in respect to acquired diseases is especially important as an aid
in deciding as to the probable cause of the existing symptoms.
8
114 LECTURES ON NERVOUS DISEASES.
All attacks of illness which have been passed through should be
carefully inquired into.
The presence or absence of latent syphilis should always be investi-
gated as perhaps one of the most common causes of nervous aftections.
The presence or absence of tubercular deposits in the lungs, or of cancer
in the breast or viscera, should be decided by a physical examination,
because similar deposits may exist elsewhere in the body. Some of the
fevers often cause sequel that create impairment of the senses of sight
and hearing, as well as other nervous phenomena, Cerebro-spinal men-
ingitis may leave after-effects upon the nerve centres that last for an in-
definite period. Kidney diseases may result in serious changes in the
blood-vessels, and thus be a factor in the development of brain troubles.
Diphtheria is frequently followed by paralysis of the throat and limbs.
Diabetes may itself indicate an existing brain disease; or, as the result
of imperfect performance of the digestive processes, create, in turn,
symptoms referable to the nervous mechanism. In point of fact, few, if
any of the more common diseases are entirely exempt from a more or
less direct association with nervous phenomena.
There is a prevalent opinion among the laity (and unfortunately,
with some of the profession also) that the nervous system is a distinct
and separate part of the human organization; an entity entirely inde-
pendent of the other organs and having functions peculiarly its own.
They seem to forget that it is nourished by the same source as muscle,
bone, organs, etc., e.g., the blood; also that every part of the body is
capable of sending telegraphic communications to the brain and spinal
cord by means of the sensory nerves; and, finally, that these organs
are called into action rather as the servants of the other parts of the
body than as independent organisms, by the various impressions which
they receive from without. All the mental processes are based, of necessity
upon some impressions of the outer world gained by means of the organs
of sight, smell, hearing, touch, taste, or the nerves of general sensibility.
The apparent disassociation which exists between the nervous cen-
tres and the viscera often misleads the practitioner of medicine, and
causes him to disregard the importance of a complete examination of the
various organs before a final judgment is expressed concerning nervous
phenomena that are brought to his notice.
Some of the more common forms of nervous affections are purely
functional. Text-books abound in cases where some disease of the intes-
tine, ovaries, uterus, kidneys, bladder and urethra have been the exciting
cause of paralysis, and of serious effects upon the nerve centres. The
eye is also a very frequent factor in functional nervous diseases—although
the fact is not generally recognized by authors, This field will be dis-
cussed later. Iysteria is often associated with an attack of paralysis
THE CLINICAL HISTORY OF THE PATIENT. 115
that is not easily differentiated from the types of paralysis produced by
destructive processes within the brain and spinal cord. Epilepsy and
St. Vitus’ dance are purely nervous diseases, and yet they may sometimes
be the indirect result of a defective assimilation of food, general de-
bility, some poverty of the blood, and many other causes that are not
directly associated with the nervous system proper.
‘On the other hand, diseased conditions of the nervous centres may
induce so-called trophic changes, or changes of nutrition, not only in the
muscles—as is evidenced by atrophy of a more or less complete kind—
but also in the skin, the various organs, the joints, and even in the bones.
The peripheral nerves preside, not only over the muscles to which
they give the power of contraction, and the tactile organs of the skin, to
which they contribute the ability to perceive all varieties of impressions,
such as the tactile sense, the sense of cold and of heat, the feelings of
pain, etc., but they have another equally important function, which they
exercise chiefly by means of the so-called vaso-motor filaments, viz., the
regulation of the blood supply to the viscera, organs of special sense.
muscles, bones, joints, and skin. Now, when the nerve centres become
involved by any form of destructive process that cuts off these so-called
“trophie fibres” from connection with certain parts of the spinal cord or
brain, definite regions of the body may waste away without exhibiting
paralysis, the eye and ear may lose their marvelous functions, and the
skin may develop different forms of eruptions, bed-sores, etc.
Finally, the spinal cord and the medulla oblongata (which is its
uppermost portion) contain certain collections of nerve cells or “reflex
centres” that preside over the more important functions, or those essen-
tial to life.
By means of an excitability which is present in these collections of
cells, the heart is kept pulsating; the respirations go on, even in spite of
any voluntary efforts made to arrest them; the pupil dilates and con-
tracts when exposed to different degrees of light; and the bladder and
rectum expel the excretions that accumulate within them. In the same
way the sexual act is rendered possible in the male; the stomach and
intestine keep up a perpetual worm-like movement; swallowing is per-
formed in such a way that the food does not enter the ar-passages or pass
upward into the nose; the calibre of the blood-vessels is constantly altered,
so as to meet the demands of different parts of the body when active or
at rest; and the acts of vomiting, hiccough, sneezing, sighing, laughing,
etc., are rendered possible, and often involuntary.
In closing this section of the chapter, I take the liberty of presenting
a sample page of my own case-book, specially designed for the recording
of the results of the first examination of patients afflicted with any form
of nervous malady. Some of the headings will be discussed in subsequent
116
pages.
Their bearings upon diagnosis will then be made clear.
LECTURES ON NERVOUS DISEASES.
The
page which faces the printed one is left blank to allow of subsequent
record of the treatment and any new symptoms that may arise.
Namem........ ALN ee i AGH siiaicianieis e OCCUPATION, os cceeoseccees es DATEssseees nets ate aren TOS steve
Clinical history:
Acquired diseases— ©
HeVCES esciunssaeipicie recs sie
LUM gS seidictes Aer
Kidneys ........
Pelvic organs....
Vernereal.....sccceeccencecercccoes siemieaiotetiaiciers
Habits, as to dict...05. ceccesee sa cnee ce eendeoe ete
es © -aleoholl 1g asaiaeeseeweleis eels
ee « ‘tobacco or drugs... sss eee sera een
“ “© -venery. sneeeeareesesane
Motor PHENOMENA... cee ciecreesenneeeceneeneseeee
SCNSOVY PHENOMENA, ce rgevererercesceceeccens aerate
Allitude sc sssceaccs tence cesses eesssccees ease aNeg
Cath aunhenoastaw send eeeni iat eeGeeess, ace
Senseof Siell came meinen + eater sana eetaiahaw
Eye:
Pupils ..
Lar:
DGfOrmMiti eS ccewis caecameunaeearne texans
Mauth:
Articulation s
Deglutition....
Attitude of lips......
Movements of tongue.........00..eeseeee Hamels
Brain:
Memory ......
Emotions......
Logical powers
Sleep ... 046%
Vertigo...3--+-
Spinal cord:
Superficial. reflexes
Deep: reflexessuviss
Delayedisensatson gps casi tote Ges eee arenes ae
ANaSthesia.cceeecccees cere ecueneeseeeratsenres
Hyperesthesia
Pain...eeeseees
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LI,
SYMPTOMS OF NERVOUS DISEASES REVEALED
TO THE PHYSICIAN
BY HIS SENSE OF SIGHT.
When a patient and his medical adviser meet for the first time there
are many medical facts which may be detected simply by a glance, with-
out a question being asked. Sometimes information thus gained is in-
valuable to the doctor, and of the greatest importance in diagnosis. To
become skillful in this line, however, both study and practice are requisite.
SYMPTOMS REVEALED BY THE SENSE OF SIGHT. 17
Some years since I published, in the New York Medical Journal, a
contribution to the study of medical physiognomy which has been
honored by two foreign translations; and, in my late work on “ Medical
Anatomy” (Wood's Library for 1882), I have devoted an entire chapter
to the subject. In this article, however, I shall only touch upon such
points as are related to the diagnosis of nervous diseases,
This section of my article I shall discuss under the following heads:
1, The study of the features and general appearance of the patient. 2,
The study of the gait and the attitude of the patient, when sitting, stand-
ing, or reclining.
Tue FEATURES AND GENERAL APPEARANCE OF THE Parient.—
One glance at a face affected with such striking alterations as those
produced by Bell’s paralysis, Duchenne’s palsy in its advanced state,
marked atrophy of the facial muscles, and some other nervous conditions
which are associated with extreme facial deformity, would be sufficient
with even an inexperienced practitioner fora diagnosis. But all diseases
of the nervous centres, or of the cranial nerves themselves, independently
of the brain, are not so forcibly evidenced in the face. Something of value
can, however, usually be learned by a careful study of each of its parts,
especially the forehead, eye, lips, tongue,and ear. It has been my custom
for some years to have impressions from untouched photographic nega-
tives made of many of my patients before any mode of treatment was
commenced, J have found them very useful in many ways; and they
certainly constitute the easiest and most reliable method of recording
some medical facts.
A prominent and tortuous artery upon the temple may catch the
eye of the doctor. It is well to know that such a condition often accom-
panies kidney disease.
A scanning of the face will show whether the complexion is ruddy,
as in health, or pale from some cachexia; clear and free from eruptions,
or sallowed and dingy; waxy and transparent, as in Bright’s discase, or
tinged with blue from imperfect oxygenation of the blood.
In children, certain lines or wrinkles may possibly exist that point
strongly to some complicating disease of the brain, lungs, heart or
digestive organs, the presence of persistent pain, and other valuable data.
In adults, or the aged, these lines are of less clinical importance. I have
discussed them in other articles, previously referred to.
A collar loosened or open may suggest some difficulty in breathing.
An untied shoe may cover a dropsical foot; a slit in the region of the
“oreat-toe” joint may have been made as a relief to gouty inflammation;
one shoe badly worn at the toe may tell of an existing hemiplegia, Pa-
tients with enfeebled mental powers and drunkards are particularly liable
to have their clothing wrongly or incompletely buttoned; the pants im-
‘
118 LECTURES ON NERVOUS DISEASES.
perfectly closed or open; the shoe down at the heel; the hair uncombed,
and to present other evidences of indifference to neatness of appearance,
Good, strong hair in abundance, and teeth that are free from defects,
are evidences in the adult of a naturally vigorous constitution. Broad
shoulders and deep chests are likewise an indication of inherited strength
both of the organs and muscles.
Tue Diarnesis.—The general appearance of the patient may afford
some valuable information respecting an hereditary diathesis. Laycock
has admirably described them.
Patients of the ‘ gouty” diathesis usually have a heavy frame, well-
developed muscles, a large head and jaw, strong hair and teeth, a robust
appearance, and an erect carriage. They are peculiarly susceptible, in
adult life, to diseases of the blood-vessels, apoplexy, aneurism, and heart
troubles,
In contrast to this type, those of the well-marked “ strumous” dia-
thesis have a light, bony framework, which is often characterized by an
enlargement of the ends of the long bones. The hand is sometimes un-
shapely from this peculiar defect, or the rings which will pass the joints
are too large for the finger. The chest of such subjects is also small.
The glands of the neck tend to become enlarged at about the age of
puberty.
The hair of strumous subjects is apt to be thin and fine. The eye-
lashes are usually long and silken, although the lids may sometimes be
diseased and the lashes more or less disfigured. As children, they
are liable to be unusually precocious. The teeth are crowded into a
narrow arch and are liable to decay early. The under jaw is light. Evi-
dences of rickets in childhood may exist during adult life. Scrofulous
children inherit “ either a velvety skin, dark-brown complexion, dark hair,
dark brilliant eyes and long lashes, with the lineaments of a face finely
drawn and expressive; or a fair complexion, thick and swollen nose,
broad chin, teeth irregular and developed late, inflammation of the Mei-
bomian glands, scrofulous ophthalmia, eruptions of the head, nose, and
lips, and enlarged cervical glands.” These subjects are often ‘“chicken-
breasted” and “bow-legged.” The “strumous diathesis” entails a pecu-
liar liability to defective nutrition, glandular. enlargements, and “con-
sumptive” changes within the lungs during early manhood. Epilepsy
and hydrocephalus often develop in such subjects during infancy or
childhood.
The so-called “nervous” diathesis is commonly associated with small
but perfect bones, an absence of fat, a well-formed cranium, small features,
quick intelligence, and an active frame. They usually have a bright eye
and small abdominal organs. They bear fatigue well, but are peculiarly
susceptible to nervous excitability and depression. In adult life they
'
SYMPTOMS REVEALED BY THE SENSE OF SIGHT. 119
become the more common victims to neuralgia, epilepsy, hysteria, dipso-
mania, and many other nervous diseases,
Dark-haired and swarthy subjects are often of the so-called “ bilious”
temperament. They commonly possess large frames, strong muscles, and
a tendency to moderate obesity. They are active rather than lethargic.
The digestive organs are often disturbed by habits of over-indulgence at
the table or excessive mental efforts. Such subjects commonly suffer
from “sick-headaches” from early childhood, and often develop gouty
symptoms in early adult life. They are not infrequently victims to vas-
cular changes, kidney disease, and apoplexy, after the age of fifty years.
The “lymphatic” diathesis is generally met with in sluggish, lazy,
and large subjects. They are commonly addicted to alcohol (because
they suffer from fatigue) and to excessive eating. They have heavy
bones, but soft and flabby muscles. They are often pale. They usually
thrive best in invigorating climates.
Now, it must be remembered that it is ‘seldom that.the physician
meets either of these types unadulterated. A man of the gouty diathesis,
with a wife of the “nervous” type, will probably have children that ex-
hibit certain characteristics of both. Hence it is often desirable, before
making a diagnosis, to inquire into the peculiarities of build and tem-
perament of the ancestors of patients afflicted with nervous diseases, as
well as to their duration of life and the causes of their death.
Tue CacHExtA.—These are diseased conditions. The ones which
are most frequently recognized by the neurologist are those of syphilis,
cancer, gout, mercurial or lead-poisoning, and malaria. In all of these
there is poverty of the blood, because the red corpuscles are more or less
destroyed and the constituents of the blood-plasma are altered. If a
cachexia is superimposed upon some special form of diathesis, a double
danger to the patient is the result A strumous subject, for example,
may have his tubercular tendencies materially hastened, if not actually
developed, by malaria, syphilis, and mercurial or lead-poisoning.
Spectra, Puystognomy.—As the physician scans the features of his
patient, it is best to inspect different parts of the face separately, as it
were. Let us note what he should particularly observe.
The Forehead.—If the forehead be well developed, the “nervous
diathesis”’ is liable to be present. If protuberant and overhanging a
small and imperfectly-developed face, rickets, hereditary syphilis, or
hydrocephalus have probably existed in childhood. If hereditary
syphilis has conduced toward the cranial deformity, the teeth will be
found to be defective. Ulceration upon the forehead, unless it be due to
a wound, is invariably syphilitic. Scars of this region or copper-colored
spots are equally significant and suggestive. Depressed fractures over
the frontal region are not necessarily associated in the adult with injury
120 LECTURES ON NERVOUS DISEASES.
to the brain, even if extensive, because the frontal sinuses are deyel-
oped after puberty, and the front wall of the sinus may be then crushed
in without disturbing the back wall or the underlying brain. A very
small cranium and a retreating forehead are often present in imbeciles.
The Eye.—In the aged, if the cornea be cloudy, you should lift the
upper eyelid and seek for an are of a lighter shade—the so-called “ arcus
senilis.”
If it exist, and its edges are indistinctly defined, there is reason to
suspect that the tissues of the body (especially the heart) are under-
going fatty degeneration.
The pupils should be examined to see if they are equal in size, and
if their movements are in any way impaired.
There is one condition, called from its discoverer the ‘“ Robertson
pupil,” that is of the greatest significance to the neurologist, because it
indicates a hardening, or “sclerosis,” as it is called, of the spinal cord. It
occurs only when this disease has involved the “cilio-spinal centre” of
the cord. This condition is indicated in the eye by preternaturally small
pupils that do not respond to light, but which still move when efforts to
accommodate the vision to near objects (7.e., within a radius of twenty
feet) are demanded.
To test this fact, place the patient at a window and instruct him to
look fixedly at some abreet more than twenty feet off whenever his eyes
are open, so that the pupil need not contract in order to focus the vision.
Now tell him to close the eyes and keep them closed until instructed to
open them. After sufficient time has elapsed for the pupils to have be-
come dilated, tell him to open his eyes. Watch carefully at this moment
for a response in the pupils, as they will contract instantly in health. If
they fail to do so, the existence of spinal sclerosis is almost positively
indicated.
Abnormalities of the pupils may afford the practitioner material aid
in diagnosis,
The pupils are found to be dilated dur ing attacks of dyspnea and
after excessive muscular exertion, in the later stages of anwsthesia, and
in cases of poisoning from bell: damon and other drugs of similar action.
A contracted state of the pupils exists during aleoholic¢ exvitement, in the
early stages of anaesthesia from chloroform, and in poisoning by morphia
or other preparations of opium, physostigmine, chloral, and some other
drugs. Paralysis of the third cranial nerve ‘creates a dilated condition
of the pupil of the same side, since that nerve controls the circular fibres
of the iris.
Again, one pupil may dilate irregularly in a weak light. This sug-
gests the existence of adhesions of the iris, as.a result of past inflamma-
tion. Ivitis is often syphilitic, and this symptom may tell of past
SYMPTOMS REVEALED BY THE SENSE OF SIGHT. 121
infection. The inner surface of the eyelid is a valuable guide to detect the
presence of anemia, as it shows a pallor that is in marked contrast, to the
redness of health. Alcoholic subjects are apt to have a vascular redness
of the eyeball. Bright’s disease often causes a drop of' fluid beneath the
conjunctiva that might be mistaken for a tear. It can be moved, how-
ever, while a tear cannot without causing its disappearance.
In connection with hemianopsia (see previous section) there may be
an absence of pupillary movement upon one lateral half of each eye——
the so-called “ hemiopic pupillary reaction.”
The movements of the eye should be a subject of special inquiry.
Brain diseases sometimes manifest their existence very early by some
form of paralysis of the ocular muscles. Strabismus or cross-eye may
exist when the third or sixth cranial nerves are impaired. We meet it
chiefly in connection with hydrocephalus, apoplectic clots, brain-tumors,
cerebral meningitis, growths within the orbit, and as a congenital or ac-
quired deformity. This subject will be fully discussed later.
It is a fact well known among oculists, and one which often helps
them materially in diagnosis, that the defects of vision occasioned by a
serious impairment in the power of some of the muscles which control
the eyeball, cause the patients. unconsciously to assume an abnormal
position of the head, which tends to assist them in the use of the affected
eve. So diagnostic are some of the attitudes assumed by this class of
afflicted people, that the condition which exists may be told at « glance,
as the patient enters a room, by one thoroughly familiar with diseases
of this important organ. The explanation of this tendency on the
part of this class of patients lies in the fact that a loss of power in the
ocular muscles nay immediately show itself in the perception of every
object, as it were doubled; and it is to overcome these double images
that patients almost instantaneously discover their ability to get rid of
the annoyance by some special attitude, which, of course, depends upon
the muscle that is weakened or paralyzed.
It will be necessary, in order to clearly understand the mechanism
of this peculiarity, that the separate action of the six muscles which
directly act upon the globe of the eye be considered.
The action of each of the ocular muscles may be given, then, as fol-
lows, with the proviso that many of the motions of the eye are not the
result of the contraction of any single muscle, but often of a number
acting either in unison or successively.
The superior oblique muscle turns the eye downward and outward;
the inferior oblique muscle turns the cye upward and outward; the
superior rectus muscle turns the eye downward and inward; the internal
rectus muscle turns the eye directly inward; the external rectus muscle
turns the eye directly outward,
122 LECTURES ON NERVOUS DISEASES.
This statement as to the above muscles reveals nothing which would
not be immediately suggested by the insertion of each, with the exception
of the superior and inferior recti muscles, which, besides the action that
their situation would naturally suggest, tend also to draw the eyeball
inward, on account of the obliquity of the axis of the orbit, and the same
obliquity of the muscles, since they arise at the apex of the orbit. The
action of the oblique muscles is, as any one familiar with their origin
and insertion would naturally surmise, to control the oblique movements
of the eyeball.
Now, as soon as any one of these six muscles becomes pressed upon
and weakened by the presence of tumors, inflammatory exudation,
syphilis, or other causes, the patient at once perceives double images,
and, in order to get bis eye into such a relative position with that of the
healthy side as to enable them both to focus upon the same object ina
natural manner, the patient soon learns to so move his head as to compel
the two eyes to look in parallel directions.
A very simple rule can be suggested by which the physician may he
enabled not only to tell in what direction a patient would move his head
in case any special muscle be rendered weak or utterly useless, but also to
diagnose the muscle affected, when he looks at the patient, without any
knowledge of his history. The rule may be thus stated: In paresis of any
of the ocular muscles, the head is so deflected from its normal position that
the chin is carried in a direction corresponding to the action of the af-
fected muscle.
Thus, in paresis of the external rectus,* the chin would be carried
outward toward the affected muscle; while in paresis of the internal
rectus muscle the head would be turned away from the side on which the
muscle fails to act. In case the superior oblique muscle is impaired, the
chin would be carried downward and outward; while in case of the inferior
oblique muscle, the chin would have to be moved upward and outward to
benefit the vision of the patient. The superior and inferior recti muscles,
when impaired by disease or other causes, would likewise create a de-
flection of the head in a line corresponding to that of their respective
actions.
Paresis of the external and internal recti muscles occasionally causes,
in addition to the facts already described, another point of very great
value in diagnosis, viz., an alteration in the apparent size of the objects
seen from what they would be in health. The condition of vision
*While this statement would be absolutely true in theory in all cases, we must ac-
knowledge, as a clinical fact, that paticnts learn to utterly disregard the image in the
affected eye when the internal or external rectus is the seat of paresis, and to use the
normal eye only for the purposes of vision, thus rendering this attitude of the head less
diagnostic than when the oblique muscles are affected.
ea ee
THE EYE AS A WHOLE. 123
termed by oculists “ megalopsia,” or “macropsia,” often signifies paresis
of the external rectus; while the opposite condition, called “ micropsia,”
‘may indicate a loss of power in the internal rectus muscle,
In the former of these conditions, the objects seen by the patient
seem to be greater in point of size than the intelligence of the patient
assures him is the case; while in the latter, objects seem smaller to the
patient than they really are.
THE EYE AS A WHOLE.
I take the liberty of inserting, in this connection, an extract respect-
ing the eye from my brochure on medical physiognomy :—
The intimate communications between the fifth, the seventh, and
the sympathetic nerves, through the media of the ciliary, optic, and
Meckel’s ganglia, would lead us to expect that the eye should exhibit in
its altered appearance the derangement of internal structures. ‘“ When a
glance of this organ is caught, what a field of mute expression is open to
the mind! This silent or instructive index of the whole man may be
bright or dull, heavy or clear, half-shut, or unnaturally open, sunken or
protruded, fixed or oscillating, straight or distorted, staring or twinkling,
fiery or lethargic, anxious or distressed; again, it may be watery or dry,
of a pale blue, or its white turned to yellow.”
The pupils may be contracted or widely dilated, insensible to or
intolerant of light, oscillating or otherwise, unequal in size, or changed
from their natural clearness of outline. “The noble arch of the brow
speaks its varied language in every face of suffering humanity. It may
be overhanging or corrugated, raised or depressed; while the lid of the
eye, animportant part of this vault, exhibits alternations of puffiness or
hollowness, of smoothness or unevenness, of darkness or paleness, of
sallowness or brown discoloration, of white or purple. Lines intersect
this region, and the varied tints are perpetually giving new color, new
feature, new expression, by their shadows.” If the frontal muscle acts in
connection with the corrugator supercilii, an acute deflection upward is
given to the inner part of the eyebrow, very different from the general
action of the muscle, and decidedly expressive of debilitating pain, or of
discontent, according to the prevailing cast of the rest of the countenance.
An irreeularity of the pupils of the two eyes indicates, as a rule, pressure
upon nerve centres or upon the optic nerve itself. In adynamic fevers
the eyes are heavy and extremely sluggish, and are, as a rule, partially
covered by the drooping eyelid; while in certain forms of mania they
are seldom motionless. This latter peculiarity is also often noticed in
idiocy.
In the so-called ‘“ Bell’s paralysis,” due to failure of the facial nerve,
the eyelids stand wide open, and cannot be voluntarily closed, since
124 LECTURES ON NERVOUS DISEASES.
the orbicularis palpebrarum muscle is paralyzed. This condition may be
further recognized, if unilateral, by a smoothness of the affected side,
since the antagonistic muscles tend to draw the face toward the side
opposite to the one in which the muscular movement is impaired; an
inability to place the mouth in the position of whistling, because for this
act the two sides of the face must act in unison; loss of control of saliva,
which dribbles from the corner of the mouth ; and a tendency to accumu-
lation‘ of food in the cheek since the buccinator muscle no longer acts.
When the third pair of nerves are affected upon either side, the upper
eyelid: cannot be voluntarily raised, for the levator palpebre muscle fails
to act; and the eye is caused to diverge outward, because the external
rectus muscle, not being supplied by the third pair and having no counter-
balancing muscle, draws the eye from its line of parallelism with its
fellow. In photophobia, attempts to open the eye create resistance on
the part of the patient, since the entrance of light causes pain; while, as
death approaches; or in the state of coma (save in a few exceptions), the
eyes are usually open. In cardiac bypertrophy, an unusual brilliancy of
the eye is perceived, since the arterial system is overfilled from the
additional power of the heart. A peculiar glistening stare exists during
the course of scarlet fever, which is in marked contrast with the liquid,
tender, and watery eye of measles. Many diseases of the eye itself tend
to greatly alter the normal expression of the face. Prominently among
these may be mentioned cataract, glaucoma, cancer, staphyloma, exop-
thalmus, iritis, conjunctivitis, amaurosis, etc., but the special peculiarities
of each need not be here described.
THE EYE AS A FACTOR IN THE CAUSATION OF SOME COMMGN
NERVOUS SYMPTOMS. ,
Although something has been written within the past few years in
relation to the deleterions effects of errors of refraction and accommeda-
tion of vision and the condition known as “ muscular insufficiency ” upon
the functions of the nervous system and the viscera,* the profession at
* Priority in this field (save in respect to ocular defect as a cause of headache, which
has been recognized in a somewhat imperfect way for many years) is justly claimed, as far
as I know, by Dr. George T. Stevens of New York. Although his views have been regarded by
some as extreme and untenable, those who have carefully and accurately investigated the
eyes of nervous subjects cannot, I think, deny that defects in refraction and accommoda-
tion, and insufficiency of the ocular muscles, are very important and generally neglected
factors of causation. Authors cannot afford to-day to utterly discard all mention of the
tests for muscular insufficiency from neurological works, as they have done in the past.
In point of fact, even the tests for errors in refraction are not described in the standard
works on nervous maladies. Mcst authors secm to have been content with showing a cut
of some opbthalmoscope and dismissing the subject with a few lines. It is safe to infer
that such writers are either not familiar with the field here discussed, or not in the habit
of employing the tests herein described upon their patients. Iam sure (if this is not the
case) they could not remain so apathetic and apparently indifferent to the results obtained.
THE EYE AS A FACTOR IN NERVOUS SYMPTOMS. 125
large is not yet thoroughly awakened to the importance of the detection
and correction of such errors. J deem it of the greatest importance,
therefore, to call attention to it again in this connection, and to give a
full description of the testing of vision and of ‘the eye muscles.
Most of you know that some persons can be made dizzy by looking
‘from a height or inspecting a water-fall; you have doubtless seen laymen
suffer pains in the head and be made “sick at the stomach” by trying on
a pair of spectacles which gave relief to a friend.* You doubtless know
that a “squint” in the eyes is very often due to some defect in the refrac-
tion of the eye or a weakness of its muscles; but possibly some of you do
not know that a squint will occasionally disappear at once when the
proper glasses are given to such a patient, without recourse to cutting
the muscle. Perhaps it has never occurred to most of you that sight is
the only special sense which. we use constantly except during the hours of
sleep. There is not a moment of the day or evening when we are not
acquiring visual impressions of some kind.
ee ee ica Tie ck fake, th cooler ar an tine e
eye; H, represents the Aypermzetopic eye; M, the myopic eye.
Fortunately for our nervous system, the normal eye takes pictures of
surrounding objects without any muscular effort when the object is more
than twenty feet away; hence, during the larger part of each day, the
normal eye is passive, and is practically at rest, although performing its
functions. How different is the condition of the far-sighted or “byper-
metropic” eye, however, from the normal! For this eye (since it is (oo
short in its antero-posterior axis) all objects have to be focused by mus-
cular effort, irrespective of their distance from the eye. Such an eye is
never passive. It has no rest while the body is awake. It is always
straining more or less intensely to bring properly upon the retina the
images of objects seen.
* Let a healthy child try on its grandfather’s spectacles and wear them for a time, and
the effects of ‘‘eye-strain’’ will be very clearly exhibited by distressing symptoms in u few
minutes. :
126 LECTURES ON NERVOUS DISEASES.
THE HYPERMETROPIC EYE.
The “hypermetropic” condition of the eye, or ‘‘far-sightedness,” as
it is called, is a very common defect. It is especially frequent in persons
of tubercular parentage.* It is well, therefore, to suspect the existence
of this defect in children or adults whose ancestors have died of “con-
sumption.” ;
Hypermetropia cannot be corrected too early in life. It is unquestion-
ably one of the most frequent causes of “ sick-headache,” which, as you
know, runs in families. It is commonly encountered also (among other
optical defects) in subjects afflicted with chorea and epilepsy.f Itisa
congenital defect, and will never be “outgrown,” as many people think.
A hypermetropic child, from the days of babyhood, suffers (unconscious
perhaps of the fact) from a variety of symptoms which indicate the
“strain” to which it is subjected in consequence of its efforts to see dis-
tinctly. Its eyes are liable to become easily suffused when it plays or
looks steadily at near objects. A slight cast in the eye is sometimes
developed. Jt occasionally “sees double” after it learns to read. It
usually prefers and excels in out-of-door sports, which require only
slight efforts at accommodation of vision. It finds that study and close
application to books bring an indescribable sense of weariness and dis-
comfort; hence, study becomes irksome and play brings a sense of pecu-
liar relief. Some years ago Dr. Loring, of this city, wrote an article for
Harper’s Monthly which treated of hypermetropia and myopia in a
charmingly lucid and popular manner.
* This is probably due to the shallowness of the orbits.
} Dr. George T. Stevens was the first, so far as I know, to advance the general propo-
sition that ocular defect was an important factor in causing functional nervous diseases,
that muscular insufliciency (chiefly of the externi) was particularly apt to cause such dis-
turbances, and that they could be relieved by tenotomy. I haye an epileptic child under
my care at the present time whose attacks have averaged four a day for several years. The
fits will cease at once when the child is at sea, possibly because efforts of accommodation are
almost entirely dispensed with when on deck. Hypermetropia, astigmatism, and external
insufficiency exist in this patient. The use of atropine causcd a complete cessation of the
fits for several days. Why cannot the eye act as a disturbing element as well as phimosis,
sexual excesses, ovarian irritations, etc., concerning which so much has been written?
fIt is a well recognized fact that people who are victims to sick-headuches early in
life tend, as a rule, to suffer less {rom such attacks after the age of forty. This is not
generally attributed (as in my opinion it should he in many cases) to the enforced use of
glasses. in writing, sewing, reading, and other forms of near eye-work. Most of this class
of sufferers are hypermetropic to a marked degree; hence they are compelled to relieve
their “accommodation”? by a glass earlier than most adults.
These subjects, therefore, do not “ outgrow their malady ;”’ nor does the eye improve
in regard to its refractive error as age advances. They simply aid the eye at last with a
glass, which it has too long needed ; not voluntarily in most instances. but from compul-
sion, because the focusing muscle of that organ is unable after a while to continue to work
under the strain which the refractive error has entailed wpon it.
THE HYPERMETROPIC EYE. 127
Now, one peculiar fact should be noticed here—viz., that Ayper-
melropic subjects often have remarkable acuteness of sight. They are very
apt (when young adults) to boast of their power of vision. They can often
read all the test-types made for distance (twenty feet or more) without
anerror. If the defect exists in a child, the parents will frequently tell
you how the child can see things with distinctness which possibly they
themselves cannot see at all; how they have tested its eyes from time to
time; how absurd the idea seems to them and their friends that the vision
of the child is defective; and how unnecessary the use of glasses seems
to them (even if the eye is abnormal) so long as the child can get along
without them. In some cases no amount of explanation or pleading will
persuade the parents to have atropine used upon the echild’s eyes in
order.to positively decide the question of the existence of “latent”
far-sightedness.
Fic, 89.—Srcrion or THE Front Part or tHe Eyn, SHowinc THE Mrcnanism oF Ac-
commopaTion, (Fick.) The left side of the figure (7°) shows the lens adaptel to vision
at distances of over twenty feet; the right side of the figure ()} shows the lens adapted to
the vision of near objects, the ciliary muscle being contracted and the suspensory ligament of
the lens consequently relaxed.
Some years ago I pleaded with a medical man to allow some oculist of
reputation to examine his children’s eyes, all of whom had weekly attacks
of sick-headache, inherited from both the mother and father, and in whom
a tubercular tendency was strongly marked. Iwas refused, and the state-
ment was made that never, while the father lived, should a child of his
wear glasses with his consent. One of these children wears to-day a con-
vex glass with a twelve-inch focus for distance; another wears the same
glass with five degrees of prisms added. These only partially correct an
insufficiency of the muscles which exists in addition to the Lyperme-
tropia, A third child is highly hypermetropic and astigmatic. In every
one of these subjects immense relief has been afforded by the correction
of an optical defect which had rendered their early life one of suffering.
This is not an uncommon experience. I could cite many more, if I
deemed it necessary to prove what is already accepted by ophthalmolo-
gists as proved—viz., that hypermetropia and eye-defect of other forms
may prove to be fruitful sources af headache.
128 LECTURES ON NERVOUS DISEASES.
There is a prejudice among laymen and some medical men that
classes are an injury when they can be avoided, because, as they say, “a
person becomes so dependent upon them when he once puts them on.”
This argument should be exactly reversed, and construed as follows:
Because nature becomes dependent upon a glass which gives relief and
corrects an existing strain upon the eye, no time should be lust in afford.
iny this relief.
Should a hip-splint be avoided (when the pain in the joint is arrested
hy it) because the patient feels his dependence upon the splint? Should
a child be allowed to go through life with a deformed eye simply because
the defect is not apparent to himself or his friends on account of an un-
naturally-developed ciliary muscle (see Fig. 39), which for a time renders
the eye capable of getting along tolerably well in spite of its deformity?
More harm is beine done to-day to the community at large by this
fallacious argument than it is possible to compute. Thousands of suf-
ferers from sick-headache and neuralgia are to-day struggling along
through life with an optical defect uncorrected, and, in many instances, -
after costly experimentation with drugs and doctors, are left in despair
of cure.
I speak strongly upon this point because I believe that the gastric
symptoms which accompany typical attacks of sick-headache are not to
be explained (as they commonly are) on the ground that the “liver is
inactive,” or that “dyspepsia exists,” or that “the gastric juice is weak,”
or that “the patient uses tobacco to excess,” or that “he has been living
too high.”” Every one who has suffered for years with these attacks knows
that they often occur without explainable cause; that they are cured some-
times by eating, drinking, and smoking, and made worse at other times
by similar indulgences or excesses; that every known reinedy is spt,
sooner or later, to prove inoperative, and that a sure specific for them is
unknown among the drugs of our Pliarmacopeia. These subjects also
know that life is rendered almost unendurable by the attacks at times.
They are tractable patients, and will try anything, live in any way
specified, and bear any privation without a murmur, if it will insure a cure.
I believe, from a personal experience of my own of this kind (which
it is unnecessary to relate here), and from some experience also in exam-
ining the eyes of this class of sullerers, that the symptoms of sick-head-
ache are reflex in character to a larve extent, and are due primarily in
almost every case to some ocular defect, We can easily demonstrate
that disturbed brain-action from “eye-strain”’ may produce in a healthy
child and in some adults all of the symptoms of these attacks in a few
minutes. Why is it irrational, therefore, to affirm that a brain (disturbed
by the constant efforts made to use eyes which are abnormal in respect
to the refraction, accommodation, or the equilibrium which should exist
THE MYOPIC YE. 129
between its various muscles) may manifest its disturbed state by nausea,
headache, vomiting, dizziness, constipation, and other evidences of im-
perfect performance of the functions of the viscera? Does not our cen-
tral nervous system regulate and directly control those functions? Is it
not as probable that the master when upset disturbs the servants under
him, as to advance the argument that the servants themselves are the all-
important factors in causation ?
THE MYOPIC EYE.
When the eye is too long from before backward, the patient is said
to be “ myopic,” or near-sighted. Distant objects are more or less indis-
tinct to such an eye in proportion to the excessive length of the antero-
posterior axis of the eye over the normal standard. No amount of mus-
cuiar effort can overcome or improve this defect in vision; hence these
individuals are not subjected to the muscular strain which far-sighted
persons constantly and unconsciously exert in order to see at a distance.
Again, the near-sighted eye can read or perform any of the functions
required of it (when brought sutliciently close to the object) without any
muscular effort of an unnatural character. In contrast, the far-sighted
eye has to exert a still greater muscular effort to see near objects dis-
tinctly than when employed upon distant objects; hence the fatigue, the
blurring of letters upon a printed page, the watering of the eyes, the pain
in the eyes and head, and the many other ills previously described.
Near-sighted subjects are generally conscious of an eye-detect, be-
cause they cannot see across a room with distinctness or recognize
familiar faces on the street. They are apt to become very fond of occu-
pations which brings the eye close to their work, because they have no
difficulty in seeing the object. Near-sighted children are liable to be con-
sidered precocious beyond their years, because they prefer to read rather
than to play out-of doors. It is generally safe to conclude that a child is
near-sighted when it avoids out-of-door amusements in order to gratify a
taste for reading or in-door occupations.
Near-sightedness is less liable to induce nervous disturbances than
far-sightedness, provided it is not accompanied by astigmatism or mus-
cular insufficiency. Yet it should be remembered that myopic subjects
are more frequently sent to the oculist for relief than hypermetropic
subjects are, because the defect in vision is very apparent to all in the
former class, and is more often unsuspected than recognized in the latter.
THE ASTIGMATIC EYE.
You may find, in the third place, when you have examined the eyes
of patients or friends who suffer from headache, persistent neuralgic
attacks, ete., that a condition of the eye known as “astigmatism,” may
9
130 LECTURES ON NERVOUS DISEASES.
be detected, co-existing with far- or near-sightedness, or independent of
these refractive errors. In such subjects the cornea or the lens of the
eye (see Fig. 39) has a greater curvature in some meridians than in
others; hence the images of all objects seen are more or less distorted
when they fall upon the retina. To this class of sufferers some letters in
the tests employed will be distinct, while others will not. If a number
of dots are made upon a blackboard or a sheet of paper, some will appear
as ovals, with a hazy border, or as lines, while others will more closely
resemble the normal appearance of the dots. Finally, if a card, with .
lines running from its centre to its periphery (the “ clock-face test”), is
used, some of the lines will appear blacker than. the rest and more clearly
defined. Now, there can be no comfort to such subjects in their visual
efforts. They learn by practice and experience to properly interpret,
after a while, the imperfect images of objects seen, and they are aided in
so doing by the fact that the outlines of letters, ete., become clearer in
some positions, as regards the eyes, than in others; but, in spite of all
that may be said to the contrary, the strain of using imperfect eyes tells
upon most astigmatic persons sooner or later, and tends to excite reflex
nervous phenomena of various kinds. To properly correct astigmatism
by glasses is often an extremely difficult matter. It requires experience,
a thorough knowledge of optics, and a familiarity with the practical use
of the ophthalmoscope. There are comparatively few physicians (outside
of the specialists in ophthalmology) who are capable of managing a bad
case of this kind with perfect success. You ean, however, easily detect
its existence in most cases. When you discover it, I would advise you
to intrust its correction to skillful hands,
Certain abbreviations are employed by oculists to designate various
forms of astigmatism which may be detected. These are of use in re-
cording the results of an examination :—
Ah stands for simple hypermetropic astigmatism.
Am stands for simple myopic astigmatism.
H + Ah stands for compound hypermetropic astigmatism,
M + Am stands for compound myopic astigmatism.
M+ Ah, or H + Am, stands for mixed astigmatism.
THE ASTHENOPIC EYE.
Finally, it is very important that you determine (in each patient
whose eyes are examined by you) the condition of the muscles of the eye.
The term “asthenopia” is commonly applied to that condition of the
visual apparatus which entails suffering in consequence of a defective
“equilibrium” in the muscular power exerted upon that organ when a
fixed ‘position of the eye is maintained for any length of time. When a
state of perfect equilibrium is impaired from a weakness in some muscle
THE ASTIIENOPIC EYE. 131
of the eye, the effects become manifested sooner or later by pain and ereat
discomfort after the eyes are used for any length of time. I have scen
patients who could not attend a place of amusement, or read or sew, for
even a short time, without great distress from this cause. These patients
may or may not have a refractive error. In some instances, no glasses
but prismatic ones will benefit them.
A high-couraged horse feels the will, as well as the support, of his
driver through the reins by means of the wits Although his course and
rate of speed are changed from time to time at the will of the driver, the
reins are never slackened. The horse becomes acquainted with the de-
sires of his master by a sense of increased or diminished tension upon the
reins. He is guided to either side by a difference in the tension of the
two, although the driver does not entirely relax his hold upon the op-
posing rein while he uses the guiding one, and the difference in tension
may be very slight.
So it is with the normal eye. It is both controlled and supported
while performing ite movements within the orbit by the eye muscles (which
are its reins). The brain is the driver. At its command the eye revolves
or remains stationary at any desired point. The tension of muscles,
opposed to any movement of the eye required,.is so modified by the brain
as to insure the requisite support to the eyeball, and to steady it as it
moves. Thus a perfect equipoise is constantly established between op-
posing forces, adjusted with the nicest care to meet the full requirements
of the organ under all possible circumstances. ‘The normal eye does not
tremble or wabble when it moves or the attempt is made to hold it in any
fixed attitude. It is a piece of machinery, perfect in all its parts, relinble
in its movements, perfectly controlled by its master.
The eye with “muscular insufficiency” is like a horse with an inex-
perienced and incompetent driver; the proper teusion upon the reins is
not maintained at all times, as it should be; there is no equilibrium be-
tween antagonistic muscles; fixed attitudes are maintained with difficulty
for any length of time; the brain becomes more or less disturbed by its
inability: to properly control the eye movements, and exhausted by the
continual strain imposed upon it by the efforts required to do so even
imperfectly.
Asthenopic subjects are very frequently encountered in the practice
of a neurologist. The oculist, perhaps, sees them still oftencr, because
they are generally conscious that something is wrong with their eyes.
Still, there are exceptions to this rule. I have examined patients who
showed, in response to appropriate tests, very high degrees of muscular
“insufficiency,” that came to me for the relief of symptoms which had
never been referred by themselves or their physician to any possible eye
detect. I recall the case of an epileptic who was p:aced under my charge.
132 LECTURES ON NERVOUS DISEASES.
His family assured me he had “wonderful eyes;” and they were sur-
prised when I examined them with care. The results of this examination
showed, however, that twenty-five degrees of external insufficiency ex-
isted (as measured by the vertical diplopia test), and that he was hyper-
metropic and astigmatic to a marked degree.
Insufliciency of ocular muscles seems to me to bea congenital defect
in most cases—possibly in all. It is encountered in very young subjects.
It is not a paralysis or a true paresis. It is not uncommon to note wide
variations in the same case, if examinations are made from time to
time. Possibly this fact helps to explain why competent observers do
not always estimate the degree of insufficiency in a given case alike,
even when similar tests are employed and equal care is given to the case.
We have no way as yet of determining “latent” insufficiency,* as we
*Because this term was used by me, ina prior publication, I have received several
communications from oculists of prominence denying the existence of ‘“‘latent”’ or hidden
insufliciency, and taking me to task for the use of such an expression. I would state,
therefore, that there are, to my mind, most positive evidences that the condition thus de-
scribed does exist in some cases; in fact, I would go so far as to assert that it is the rule,
rather than the exception, to find a certain amount of masked insufficiency, in connection
with ‘‘functional’”’ nervous maladies, that cannot be elicited by any means yet known to
the science of opties.
My expericuce in relieving ocular ‘‘insufficiencies’’ by tenotomy of the recti muscles
has shown me that the amount of tissue divided is almost always greatly in excess of the
apparent defect to be overcome. Again, after the eyes have been perfectly balanced by a
tenotomy (as shown by careful tests made after the operation), it is very frequently found
that more “insufficiency” develops within a short time than was detected before surgical
interference was resorted to as a step for its correction. In the third place, I have found
that repeated tenotomies (performed as often as indicated by the tests described) eventu-
ally bring the patient to a point where the eyes remain permanently corrected—a fact that
proves quite conclusively the error of supposing that the tenotomy was in any way re-
sponsible for the lack of equilibrium which developed later. In the fourth place I have
found it to be advisable in some cases to cut the muscles to excess, so as to over-correct an
error in equilibriwm—knowing that by so doing I anticipate a certain amount of “latent”
insufficiency, which will assist in making the results more satisfactory to the patient
within twenty-four or forty-eight hours.
If it were necessary, in my opinion, to argue this question at greater length, I might
add (1) that a persistent wearing of prisms for the correction of insufficiency almost in-
variably results in the development of a latent weakness‘of the muscles not discovered at
first; (2) that persistent daily exercise of the eyes by prisms usually accomplishes the
same result; and (3), that my views are in accord with all who have had much experience
in the use of prisms—irrespective of partial tenotomies, which demonstrate the facts even
more satisfactorily.
I take the liberty of quoting from the late work of Prof. H. D. Noyes (pp. 87 and 89)
the following passages :—
“Give due opportunity for disclosure, and what at first seemed to be a moderate de-
gree (referring to insuficiency) may at length declare itself in much larger proportions.”
“While great advantage is gained by Graefe’s test, it is not true that latent insuf-
ficiency is always thus brought to view.”’
Again, I may quote from a late article by Dr. G. T. Stevens as follows: ‘‘ Muscular
anomalics of the orbit may be totally or partially latent.”
THE TESTS OF VISION AND OCULAR MOVEMENTS. 133
do latent hypermetropia by atropine. Should a patient show us an
insufficiency counteracted by a prism of a certain angle to-day, it only
proves that he has aé least that amount, not that he has no more. This
statement can, I think, be demonstrated. It is an important fact to
remember when the results of examinations of such patients made by
yourself are at variance with the observations made by another.
Without further preparatory remarks, I pass to the consideration of
the steps commonly taken to determine if the eye (regarded purely as a
piece of mechanism) is perfect or imperfect. The study of the eye, when
any of its component parts become the seat of disease, has no hearing
upon the subject under discussion. ‘his field is properly relegated to
oculists.
THE TESTS OF VISION AND OCULAR MOVEMENTS.
The steps which should be employed in examining the eye for errors
in refraction and accommodation, as well as those employed to detect
defect in the power of ocular muscles, have not thus far been discussed.
J expect to offer nothing new, but I hope to make the detuils of such an
examination simple and within the comprehension of all.
The importance of this department of diagnosis ean hardly be over-
estimated in nervous maladies. It has been my custom for three years past
to examine the vision of nearly every patient sent to me, as my experience
has shown me many times that remarkable cures may be made by the light
thus shed upon the causation of obscure nervous symptoms.
Unfortunately for the sick, in many instances, physicians in general
seem to think that the examination of the eye is too difficult a field for
them to intrude upon without some special preparation for it. While
this is undoubtedly true, in case the ophthalmoscope is to be employed,
it is by no means a difficult matter for a person acquainted with physics
to acquire a practical and satisfactory knowledge of the few tests here
described in a comparatively short time, and with but a limited number
of patients, provided that he works faithfully and intelligently. The
healthy (?) as well as the sick can often be used to familiarize the be-
ginner with the practical adjustment of prismatic, spherical, and cylin-
drical glasses, and also with the tests employed to detect “asthenopia”
or anomalies of the eye-muscles.
Defective vision does not always produce ill health; hence among
your friends or in your immediate family you may find a field for inves-
tigation and practice.
Now, in the first place, it is not necesssary to have a complete
Nachet case of lenses. Such a case is very expensive. By selecting a
limited assortment of lenses and prisms, different combinations can be
made to meet the needs of alinost every eye-defect encountered in medical
practice.
134 LECTURES ON NERVOUS DISEASES.
There is furnished, with the various small cases designed by
prominent oculists, a sheet of Snellen’s test-types for distance, and also
one contsining several paragraphs printed in an assortment of types of
various sizes to be used as a test for reading power. Each paragraph is
numbered so that a record can be kept of the one read by the patient as
a test. These test-type slips can be purchased separately, however, of
any optician. It is best to have each mounted on card-board, and it is
well to have the one used in testing for distance a double one with dif-
ferent letters on the opposed sides. If you suspect that the patient is
using his memory during the tests employed rather than his sight, the
board can then be exposed upon different sides at various periods of the
examination.
You will find that the letters are mathematically made for testing
distant vision. Above each linea numeral or Roman character is placed
to designate the number of feet at which the normal eye should read the
line with ease, Thus, the large letter on the top line will be designated
usually by 200, or C C, while small letters of the lower line will be marked
10,or X. This shows that the top letter should be read easily at two
hundred feet by the normal eye, and the lower line at ten feet. After
you have provided yourself with a good trial-case,a set of prisms, and
the necessary test type, let us see how you should proceed with an exami-
nation of a patient’s vision. We may illustrate the steps by using one
of the class as a patient.
I first hang upon the wall, as you see, the test-tvpe card; and
I place the patient with his eye on the same level and at a distance from
it of exactly twenty feet. J then take the triple-grooved spectacle frame
from the trial case and insert a plate of metal in the left rim of the frame,
so that when itis used by the patient the left eye will be covered. I
then place this frame upon the patient, and ask him to read aloud the
letters on the testing card from the top downward, line by line. This
act tests his vision in the right eye. I note (while he reads) the following
facts: (1) If he calls all the letters properly; (2) if he reads without ap-
parent effort; (3) at what line he fails to read. I then make a record
, 20 (feet)
as follows: O. D. (oculus dexter, or right eye) V = — Cece The dash
in the fraction is filled with the number which indicates the last line which
the patient reads. Wuhen the vision is normal, the fraction will be as
20 20
follows: V. == — or If the patient fails at the line next above the
20 XX
: 20 20
normal point the fraction would be expressed by — or —-. Remember
30 XXX ‘
that the numeralor represents the distance (in feet) between the patien
THE TESTS OF VISION AND OCULAR MOVEMENTS. 135
and the test-type, and that the denominator represents the numeral on
the test card placed above the last line of type read by the patient
(which indicates the normal distance in feet at which it should be legible
to the normal eye. Now, if the vision of the right eye is found to be
defective, try and improve it, and, if possible, to rendcr it normal, or
as nearly so as possible, by testing the effects of concave or convex
glasses. upon it as the case seems to indicate, beginning with the weakest
lenses-and gradually increasing their strength until the vision reaches its
highest acuteness. This takes some little practice and experience. If
conver glasses are found to be indicated, note the strongest which gives
the best vision to the patient; if concave, record the weakest glass that
overcomes the defect.
In some cases you may find yourself unable to obtain normal vision
in either eye by means of cylindrical or spherical glasses. I presuppose
.a certain degree of acquired facility on your part with glasses of the
forms specified, and a carefully made effort to overcome the existing
defect.
In such a case it is well to consult some expert oculist (if near at
hand), and thus to ascertain the results of an ophthalmoscopic examination.
The patient may have some mechanical impediment to vision, such as an
opaque lens within the eye (cataract), or an opacity of the cornea; or he
may have a high degree of astigmatism, which can often be estimated
with some accuracy by the ophthalmoscope. Again, he may be found to
be suffering from morbid changes within the optic nerve or the retina.
When it is found that a patient is so blind in an eye as to be unable
to recognize any of the letters on the testing-card at any distance, jou
should note (before sending him to an oculist) if he can recognize with
accuracy the number of fingers which you hold before the eye, and record
the results of such investigation. You should make this test with the
fingers in all possible positions in reference to the diseased eye (directly
in front, above, below, and to either side of it). ;
We might record the results of an examination of a suppositious case
up to this point as follows :—
20 20
O.D. V. = —— (manifest) made — by + 30 glass.
XXX XX
The word “ manifest” in this record means that the far-sightedness or
“hypermetropia,” which apparently exists, is overcome by a convex or
(+) glass which focuses at thirty inches. After the use of atropine, any
increase over this amount which may be developed is recorded as ‘ latent”
farsightedness. I use here the old style of numbering glasses for the sake
of perspicuity, althoueh I personally prefer the metric system (dioptre),
as it allows of more rapid combinations when the trial-case contains only
a limited supply of lenses.
136 LECTURES ON NERVOUS DISEASES.
You will understand, when I exhibit the method of recording such
observations more fully to you, why it is that the right and left eyes have
to be separately examined and corrected (as already described) before
the binocular vision is tested with and without the needed correction. I
usually make upon the page of my own case-book a note relating to each
eye of the patient, prior to the use of atropine somewhat as follows:—
20 20
0. D, (right eye) V. == —~ (manifest) made — by + 30.
Sx XX
20 20
0.8. (left eye) V. = — made — by — 30
xl xX
20 20
Brnocunar V. = —- made — by this combination.
XXX XX
Such a record of a suppositious case would show that the patient was
far-sighted or “hypermetropic” in the right eye, and near-sighted or “nuy-
opic” in the left eye. It would lead me to believe also that the right eye
(when under the influence of atropine) might show a still greater defect,
which is now rendered “latent,” or hidden, by an excessive development
of the muscle of accommodation.
In all far-sighted eyes Nature tries from the date of birth to com- ~
pensate for the congenital defect (an eye which is too flat) by a hyper-
trophy or enlargement of the ciliary muscle (see Fig. 89); hence, when
this muscle is temporarily paralyzed by atropine, the true refractive con-
dition of the eye is no longer masked. Far-sighted patients, therefore,
lose their clearness of vision more or less at once when atropine is used.
The normal or the “myopic” eye, on the contrary, is but little affected
(as regards the outline of objects seen at twenty or more feet from the
eye) by the use of atropine, although excessive light may annoy the eye
in any case.
Let us now suppose that during the examination of a patient we first
have examined each eye separately, carefully corrected all existing error
20
found, and succeeded in getting —, or normal vision, for each eye sepa-
XX
rately; that we have then tried both eyes together with the glasses best
adapted for cach, and found the patient able to read the normal type for
distance without fatigue or conscious effort; and, finally, that we have made
acareful record of each point noted during our observations. Are we now
prepared to order glasses for the patient? Have we noted all that is im-
portant to note? To both of these inquiries I would say to the beginner,
emphatically, “No.” Several steps still remain to be taken, even before
the use of atropine (which it is generally best to employ before a final
decision is arrived at).
THE TESTS OF VISION AND OCULAR MOVEMENTS. 137
This brings us to the tests for the detection of muscular anomalies
in the orbit. :
Until within a comparatively few years ‘the necessity of carefully
measuring the power of adduction and of abduction of the eyes, and
of determining the presence or absence of muscular insufficiency in
“nervous” subjects, seems to have been practically disregarded even by
oculists. Even to-day this defect (which probably is, as a rule, con-
genital) seems to be omitted from prominent mention among the
enumerated list of ztiological factors of nervous symptoms by almost
all authors of note. In some cases I have known it to be overlooked
even by opthalmologists of world-wide reputation, simply on account of a
careless and hasty examination for the defect. It is an extremely
common defect of the eye; and may prove a very serious one to the
patient. It is an important factor in many subjects afflicted with head-
ache; it often exists to a high degree in epileptics ; it is frequently found
among children who suffer from chorea; it may unfit a patient for
sewing, reading, attending places of amusement, or using the eyes in
any way for any length of time. I have known it to cause vomiting and
so-called periodical “‘bilious attacks” by exciting a reflex irritability of
the central nervous system. One patient of mine (a close student) was
completely cured of chronic dyspepsia by the use of prisms which cor-
rected an insufficiency of 6° of the external recti muscles. He sub-
sequently had tenotomy performed and now uses his eyes without
fatigue. All bodily ailments have disappeared without the use of drugs.
In order to properly determine the condition of the ocular muscles,
several tests have to be made. I do not personally regard any of these
alone as sufficient for diagnostic purposes. The tests which I advise you
to invariably employ are as follows :—
1. Direct the patient (as you see me do with a member of the class)
to look fixedly with both eyes at some small object (say the end of a
pencil), and to follow it with the eyes as I move it before the face of the
patient at a distance of about ten inches. I watch both eyes carefully at
the same time and note if a tremulous movement in either eye is present
in any position of the eye as it moves about, and if the two eyes act in
perfect unison with each other.
2. While the patient is instructed to fixedly gaze at the same object,
I next shield one eye with a card or sheet of paper so as to exclude
the object from view. Now I shift the card rapidly from one eye to the
other, and I observe at the same time any deflection or trembling of the
covered eye, which may show itself as I shift the card. If deflection or
trembling occurs, it indicates a weak muscle.
3. Deviations of the visual axis ofan eye in a vertical direction are
not always revealed by the two tests previously mentioned, nor are they
1388 LECTURES ON NERVOUS DISEASES. .
always apparent to a careful observer of faces. They are of the
greatest clinical importance, however, and should be looked for early
in the examination. A pair of prisms of five or more degrees each are
placed in a spectacle frame with their bases inward* in order to overcome
the power of fusion of images by the externi, and the patient is directed
to look through them at a candle flame placed twenty feet from the pa-
tient’s eyes and on the same level, The head is placed in natural position
for distant vision and steadied by a photographer’s head-rest. If either of
the two candle flames (seen by the patient in consequence of the prisms)
be higher than the other, « prism is selected, which, with its base upward
or downward, when placed before one eye overcomes the defect. The
angle of this prism (in degrees) is then noted and recorded in the case-
book.
4. I next place upon the patient a spectacle-frame previously ar-
ranged with a disc of ordinary glass, tinted red, to cover one eye, and
a prism of 5°, with its base directed accurately upward or downward,
before the other eye. I then direct the patient’s vision upon a candle-
flame at a distance of twenty feet. The prism causes two candles to
appear (one being colored red by the glass of that hue), both of which
to the normal eye should be scen as if in a vertical line. If the red
image is seen to the same side of an imaginary vertical line dropped.
through the white image as the eye covered with the red glass, the
external recti are insufficient; if the red image is seen on the opposed
side of the vertical line, the internal recti muscles are weak.t
5. Any deviation of the candle which exists can be remedied easily
by placing a prism with its base outward before one eye for external in-
sufficiency, and with its base inward for internal insufficiency. The
strongest correcting prism that can be worn without an over-correction
marks the degree of the “ manifest” insufficiency only ;{ hence we will
* Dr. Stevens had devised an rectangular and elongated form of glass for this pur-
pose. Its great adyantages must be apparent to all who have worked in this field.
+ I have lately employed in my consultation room a device which seems to me to be
of great assistance to patients while their eye-muscles are being tested. It consists of two
pieces of white tape which are stretched upon a dark background at right angles to each
other ; so that one lics exactly vertical and the other horizontal. The flame from a small
gas burner at the tip of a porcelain candle lies directly opposite to their point of intersec-
tion and between them and the eye of the patient, all of which should be on the same
level.
During the tests described, the patient can tell at once if either line appears double
as well as the image of the candle flame.
t My experience with tenotomy, as a means of producing an equilibrium between
opposing forces in the orbit, has convineed me that the amount of insufficiency detected by
prisms is but a small proportion of what actually exists in some cases, A persistent use of
prismatic glasses will often develop a degree of insufficiency which the patient did not at
first apparently possess. In my experience this is the rule rather than the exception. Itis
comparatively rare for me to encounter a case where a full correction of an existing insuff-
THE TESTS OF VISION AND OCULAR MOVEMENTS. 1389
note variations from time to time, I usually note both the weakest and
the strongest prism which corrects the candle-deflection.
6. I next test and measure the power of adduction and abduction
(convergence and divergence) of the eyes by means of prisms. To do
this I set a lighted candle twenty feet from the patient on a level with his
vision when seated. I then hold before one eye a prism, with tts base di-
rected oulward, of sufficient angle to cause two images of the candle to
appear when both eyes look at the object. I then instruct the patient to
make an endeavor to draw the images together and to fuse the two into one
image. This is the test for adduction or convergence. The normal eye
should overcome a prism of at least 23° to 25°. It may overcome 60°
in some instances.
In the same way a prism with its base directed inward is used to
test the power of abduction or divergence. The external recti muscles
should not fail to overcome a prism of at least 8°. By combining
prisms of varying angles, one of the requisite angle can be easily ob-
tained with but a few prisms in your trial-case.
The power of abduction and adduction should always be recorded
when accurately determined. One fact should be stated, however, in
this connection—viz., that several sittings are usually required before
the patient learns to use his eye-muscles to the best advantage; hence
the records of daily tests should be kept for purposes of comparison
fora short time (when practicable to do so).
7. The power of convergence and divergence of the eyes can be
estimated for near objects by means of a stereoscope modified by Pro-
fessor Henry D. Noyes, into which prisms may be dropped at will. I
have used it of late with some satisfaction. I find that the accommo-
dation often modifies the power of ocular muscles (as determined by
the previous test at twenty feet distance). Prisms vary, moreover,
according to the glass used in their construction.
8. The power of fusing images of the test-object at twenty feet
when a prism is placed with its base up or down before each eye is next
determined. This is recorded as the “sursumduction” test for the right
or left eye. This test should not be employed successively upon the two
eyes without some minutes of rest have been given the patient. It aids
us in determining the relative strength of the superior and inferior recti
of the two cyes, and offers suggestions regarding the proper muscle to
divide for the relief of vertical deviations of the visual axis (see test 3).
ciency of the ocular muscles by prismatic glasses insures a perfect equilibrium of the eyes
for any great length of time. When we attempt to correct this peculiar muscular defect in
the eye by weakening the stronger muscle (as I am constantly doing with brilliant results)
the existence of ‘‘latent”’ insufficiency cannot, in my opinion, be doubted. Unfortunately
for science, we have as yet no way of fully developing it, as we do ‘‘latent’”’ hypermetropia
by the aid of atropine.
140 LECTURES ON NERVOUS DISEASES.
9. It is well to exercise the muscles of the eye with prisms before
the results of the diplopia tests are finally recorded. I have found
that, after a flexibility of the eye muscles has been obtained by the aid
of prisms, an insufliciency of the internal or external rectus muscle will
sometimes manifest itself where it was not apparent at first. That this
is not simply the result of fatigue seems proved by the fact that the insuf-
ficiency remains more or less apparent during subsequent examinations.*
I have lately adopted some new terms suggested by my friend Dr.
George T. Stevens, in recording the results of my tests made to deter-
mine the condition of ocular muscles.
I quote the article referred to in full, because I deem it of great
practical value. Dr. Stevens says :—
“The relations of the eyes to each other, in the act of vision, exercise important in-
fluences, not only in occasioning the condition known as asthenopia, but in the causation
of many other important nervous disturbances.
“Tf this statement is admitted, it will be evident that the subject of irregularities in
the actions of the ocular muscles must assume a greater importance than when disturb-
ances of equilibrium were regarded as only occasional factors of asthenopia, and when
these disturbances were looked for mainly in a single direction, in case they were not en-
tirely disregarded. It is true, even at the present time, that ‘insufficiency of the interni’
is the only disturbance of the ocular muscules, excluding strabismus or some of the results
of paralysis mentioned in the majority of the text-books upon the eye. Indeed, the im-
portance of even this defect is hardly dwelt upon at any considerable length in many of
these works, and it is not at all uncommon for the oculist to overlook the condition in his
practical work,
“Defects which result in lasting difficulties and perplexities in the performance of
binocular vision are not to be ignored; and the réle of the ocular muscles in the causation
of many nervous disturbances is undoubtedly of very considerable importance.
“As the investigator in this department of ophthalmology proceeds in his researches,
or attempts to record his observations, he is met by the fact that the terms now in use are
not only frequently inaccurate and misleading, but wholly inadequate to describe many
of the states observed.
‘To illustrate the two factors of the proposition just made, a few ordinary conditions
may be adduced :—
“1, The expressions employed to designate the deviations from the state of physio-
logical equilibrium are often incorrect and misleading.
“The term ‘insufficiency of the interni’ is used to express a state of the muscles of
the eyes which is shown by the equilibrium test of Graefe at reading distance. In this
test. the images seen by the two eyes are separated by a prism held vertically, with its
base exactly up or down before one of the eyes. If, under these circumstances, the images
deviate laterally in directions opposite to the two eyes—that is, if the image of the right
eye deviates to the left, and of the left eye to the right—there is said to be ‘insufficiency
of the interni’ of as many degrees as equals the strength of a prism which, with its base
toward the nose, will bring the two images in a vertical line. The expression, ‘insufficiency
of the interni,’ in this relation, is used to indicate the fact that the internal recti muscles
are ‘insufficient’ to counterbalance the external recti; and it also carries the idea
that tho externi are, in proportion to their physiological state, stronger than the
* This fact also confirms the views expressed in the previous foot-note (p. 138).
THE TESTS OF VISION AND OCULAR MOVEMENTS. 141
interni, or that the interni are, proportionally to the others, abnormally weak; tending
thereby to balance the eyes outward, so as to cause an unusual and excessive demand
upon the internal recti in close work.
“The fact that a great many cases, in which the equilibrium test of Graefe shows the
conditions described, are really ‘insufficiency of the externi’ and not of the interni, must
occur to any careful observer. Such a one will often find that, if he makes his test of
equilibrium while the ocular muscles are in a comparative state of repose, as when looking
at an object at a distance of six metres or more, he may find very marked ‘insufficiency
of the externi,’” He may even observe that, if a screen is passed before one of the eyes
while the other continues its gaze, at the distant object, the covered eye will deviate ina
marked manner inward. If the screen is quickly changed to the opposite eye, he will see
the lately covered eye move outward in order to fix the object. He may make various
other tests which will demonstrate beyond a doubt that the real balance of the eyes is in-
ward, and yet, when he makes the test of the dot and line of Graefe, or any similar test, at
near point, he has marked ‘insufficiency of the interni.’
“Tt is manifestly incorrect to say of such a muscular arrangement that the interni
are ‘insufficient,’ and especially when by such a term it is generally understood that the
outer are the stronger of the two opposing sets of muscles.
“Again, in certain cases of what is known as ‘insufficiency of the interni,’ one of the
eyes actually deviates inward while the other deviates outward, while in a still greater
number an apparent ‘insufficiency of the interni’ results from irregularities in the superior
or inferior recti.
“Many other illustrations of the truth that this term as employed is misleading
might be cited, but, without further expenditure of time or space, we may pass to the other
factor of the proposition.
“2. The term ‘insufficiency’ is quite inadequate to express the conditions of devia-
tion from the equilibrium as they may be observed.
“ Graefe, as one of the great pioneers in modern cphthalmology, and as the greatest
authority on the subject of muscular asthenopia, recognized some of these deviations, and
not only regarded ‘insufficiency of the interni’ as a condition of notable importance, but
wrote also of the ‘insufficiency of the externi’
“ Notwithstanding his remarkable observations, much remained to be learned in
this department of ophthalmology. While Graefe’s great authority is to be fully recog-
nized, the knowledge of these important conditions may yet be greatly extended.
“A class of deviations not at all uncommon, and one which induces great nervous
perplexity, is that in which the tendency is for the visual line of one eye to deviate above
that of the other.
“In examining some thousands of cases of ‘insufficiencies’ I have found a very im-
portant proportion of such tendencies. There is no term now in use which definitely ex-
presses this condition. We cannot say that it is insufficiency of one or other superior or
inferior rectus, for it is, in the great majority of cases, impossible to determine through
what special influence the equilibrium is lost. We have not here, as in paralysis of the
muscles, the definite guides of restricted motions by which we may determine the exact
location of the trouble. Indeed, the defect. may include an inclination on the part of the
one eye to deviate upward, and on the part of the other to deviate downward. We might,
perhaps, call such a condition ‘insufficiency in a vertical direction,’ with the right (or left)
line of vision inclined to deviate upward.
“This would be a descriptive and somewhat extended expression. It would still be
inaccurate, for it implies a weakness of some muscle, when the actual state may be an ex-
cess of tension on the part of some other muscle.
142 LECTURES ON NERVOUS DISEASES.
' “Again, there may and often does exist a combination of faulty tendencies in more
than one direction. The eyes may incline to deviate in both the vertical and the hori-
zontal planes, the result of which will be a tending of the visual lines to deviate in an
oblique manner. It must be apparent that the term ‘insufficiency’ is inadequate to
express all these tendencies.
“There may be some propriety in using the expression ‘insufficiency of the interni’
in many cases, but in these just cited it would be impossible for us to speak of insufficiency
of this or that oblique muscle without more accurate information than we are likely to
possess. Indeed, in the majority of vases these muscles may not be influential factors in the
condition described.
“Some term better adapted to express just what is intended, and nothing more, is
needed. It is after much hesitation and doubt whether a suggestion involving the use of
new terms in connection with a subject which has already engaged the attention of many
able investigators might not be regarded as needless and presumptuous, that I have ven-
tured to propose such an innovation. If, however, a change is to be made at any time in
the classification and nomenclature of these defects, such change should be made before the
literature becomes still more extended.
“The first need in a scientific classification of these muscular defects is the possession
of such terms as, with proper modifications, shall justly express the conditions described.
“The terms which have already been employed are all unsatisfactory, and are not
uniformly employed by different writers to describe precisely similar conditions. No terms
now in common use occur to me as being in all respects desirable.
“We may, therefore, select some word which shall convey the general idea and which,
with its proper modifications, will express our meaning. with specific variations. Such a
term should not, like the word ‘insufficiency,’ attempt to describe the exact nature of the
muscular conditions, for this is often, if not generally, a subject of uncertainty. It should
rather indicate the resultant facts as shown by the tendency of the visual lines to deviate
from the physiological equilibrium. Nor should the term convey the idea of an actual
turning, or deviation of one of the visual lines from what should be the common point of
fixation. It should express a tendency to such deviation of such character that, should the
force of the will be removed, this actual turning would result.
“The visual lines, in the conditions under consideration, are held in such relations to
each other as to permit of more or less perfect binocular vision, but at an expense of a cer-
tain excess of nervous effort. In this we have the distinction between these conditions
and those known as strabismus; for, while in these there is habitual binocular vision, in
strabismus there is habitual diplopia, either conscious or unconscious. It is true that a
fusion of images is possible in many cases of strabismus, and that slight diplopia may be-
come to a certain degree a habit, in the conditions under consideration. Nevertheless, a
condition of habitual diplopia should in general be regarded as distinguishing strabismus
from these conditions.
“The Greek word ¢époc (a tendency) seems to fulfill the conditions required, and
accurately expresses our meaning in regard to this class of defects. With this for our
central idea we may easily express every variety of tendency to deviation, as well as
the absence of such tendency. Thus the two generic: terms orthophoria (ope, right,
déopoc, a tending) and heterophoria (érepoc, different) would express respectively a ten-
caine straight forward and a tendency in some other direction.
“In order that these terms should possess precise signification, the relation of the
visual lines to which they are apphed should be determined under the uniform conditions
which are here given.
‘The eyes should be directed toward an object situated at a given distance from
THE TESTS’ OF VISION AND OCULAR MOVEMENTS. 143
them, and the head should be in the position known as the ‘natural’ or ‘ primary’ posi-
tion. The most convenient distance for the object is that at which tests for refraction
are commonly made; that is, twenty feet, or six metres. This distance is, therefore, chosen
as the standard for the determination of orthophoria and heterophoria. The best object
for use in these determinations is a lighted candle against a dark background. It should
be on a level with the eyes and at a distance of twenty feet. . If ametropia exists, the eyes
should be supplied with suitable correcting glasses. In the ‘natural position’ the body
and head are erect, the eyes are in the same horizontal,plane, and the median line (a
horizontal line at right angles with the line connecting the two ‘eyes) is directed exactly
toward the object. Under these circumstances there should be in orthophoria the minimum
of muscular innervation.
“These conditions being observed, we may ascertain the existence of muscular equi-
librium. or its absence by means of prisms in the manner familiar to all oculists,
“The determination of the muscular conditions at near points will occupy our atten-
tion as we proceed. It is to be remembered that the results in such examinations are by
no means absolute. Heterophoria may, like hypermetropia, be partly or entirely latent.
Indeed, as in actual hypermetropia, we sometimes have apparent myopia, so with an actual
inward tendency an apparent outward tendency may be observed.
“The different relations of the visual lines which may be now found may be defined
and arranged as follows, a state of the most complete relaxation of muscular effort attain-
able being always supposed :—
“T. Generic Terms —Orthophoria: A tending of the visual lines in parallelism.
Heterophoria: A tending of these lines in some other way.
“TL. Specific Zerms—Heterophoria may be divided into:—
“1. Esophoria: A tending of the visual lines inward.
“9. Exophoria: A tending of the lines outward.
“3. Hyperphoria (right or left): A tending of the right or left visual line in a direc-
tion above its fellow.
“This term does not imply that the line to which it is referred is too high, but that it
is higher than the other, without indicating which may be at fault.
“III. Compound Terms.—Tendencies in oblique directions may be expressed as
hyperesophoria, a tending upward and inward; or hyperevophoria, a tending upward and
outward, The designation ‘right’ or ‘left’ must be applied to these terms.
“In recording the respective elements of such compound expressions I have employed
the sign L.. For example, if it is desired to indicate that the right visual line tends above
its fellow 3°, and that there is a tending inward of 4°, the facts are noted thus: Right
hyperesophoria, 3° L- 4°.
“Tn the absence of any means of producing a uniform state of relaxation of the long
ocular muscles, such as we possess in atropine for the ciliary muscles, we must resort to
every known device to ascertain as nearly as possible the true relations of the muscles.
Methods other than that of measuring the deviation when diplopia is produced should,
however, be regarded as auxiliary, and the record of ortho- or heterophoria should be
made from the diplopia test.
“The powers of the different pairs of muscles to overcome prisms should next be de-
termined. Some confusion has existed in the use of terms to express this power. Thus,
the words adduction and abduction have been employed by Graefe and succeeding writers
to express the power of the eyes to overcome respectively a prism with its base out or in.
They have, however, been employed to express this power both when the object of fixa-
tion has been at a considerable distance, and when at the ordinary reading distance.
The same words are also used to express: the limits of excursion of the eyes outward.
or inward in the act of fixation,
144 LECTURES ON NERVOUS DISEASES.
“The words convergence and divergence have similarly been employed to express
different classes of phenomena. As the words adduction and abduction are necessary to
express the power of moving outward and inward of either eye singly, and as the terms
convergence and divergence must in all cases imply the approach or the separation of the
axis of the two eyes, whether in the act of overcoming a prism or otherwise there might
be an advantage in employing the word convergence to indicate the highest degree of power
of blending images ata distance of twenty feet when a prism with its base out is inter-
posed; and the term divergence to indicate the limit of power to overcome a prism with its
base in. This latter would also be less liable to objection for the reason that, while each eye
is habitually directed in abduction and adduction, the two are rarely by voluntary effort
caused to diverge except by the influence of a prism. The fact, however, that Graefe in
his classic treatise on muscular asthenopia employed the words abduction and adduction
to indicate the ability to overcome prisms must, beyond a doubt, determine the point, and
these words should, therefore, represent the diverging and converging power with prisms.
The standard of distance should, however, be uniform with that for the test for ortho- and
heterophoria.
“Tt often happens that images can be united when a prism is placed before an eye
with its base up or down, but that diplopia is produced if the prism is reversed, or if it is
placed in the first position before the other eye. In other words, the tendency of one
visual line being higher than the other, the power to blend images is greater when the
prism is placed in one than when placed in the opposite direction.
“This condition is one of great importance, and no examination of muscular equi-
librium should be regarded as complete in which its presence or absence is not determined.
The ability to overcome a prism with its base down may‘be called sursumduction, and the
eye before which the prism is placed is indicated by the word ‘right’ or ‘left.’
“Tt remains to consider the relations of the muscles when the eyes are directed to
objects at the usual reading distance,
‘‘These relations may be uniform with those manifested at a distance, or they may
vary in degree or in the direction of greatest apparent energy. To these conditions it
might at first appear best to apply the familiar terms ‘insufficiency of the interni’ or
‘externi.’
‘The objections are that the terms have already been employed to express the rela-
tions of the eyes in accommodation and also in repose, and that only two of many con-
ditions can be described.
‘The relations of the visual lines in accommodation do not always depend upon the
comparative strength or weakness of the opposing muscles, but upon a peculiar state of
innervation of the muscles.
“The habit of maintaining an excessive tension upon the outer muscles in order to
overcome esophoria frequently manifests itself in the near test as ‘insufficiency of the in-
terni’
“ These considerations render it desirable that a uniformity in the descriptive terms for
the near and distant tests should be maintained. The tertns already employed for distance
may, therefore, be properly used if the modifying phrase ‘in accommodation’ is added.
Thus we should have for insufficiency of the interni exophoria in accommodation, ete.
“The relations of the ocular muscles should, as Graefe has shown, occupy a prominent
place in the record of all examinations of the eves for asthenopia or kindred troubles.
“Tf the system of words here introduced at first appears to be superfluous, and, there-
fore, unnecessary, a careful consideration of the subject w ill be likely to convince a candid
observer that new and more definite terms are needed to convey uniform meanings, and to
express more conditions than are described by terms now in use. The terms here proposed
ASTIGMATISM AND ESTIMATION OF THE VISUAL FIELD, 145
are explicit in meaning, and the system, by arranging the various deviating tendencies
into classes, suggests to the examiner the conditions concerning which he should inform
himself.”
Thus far, then, in the examination, our record page in blank would
stand as follows :—
Name............ Residence............ DSC cicescnguny
Ra ees Wadendsyaier ed corrected by ...... glass
lp Se ah vsaanseatess a a a
ASTIGMATISM ........0..04. e SS amenity sand eamaniete’
Hsophoria................. in accommod...............0.
Exophoria................. in accommod..............00.
ABOUCEss cosuseve ced Leptin AUG asters. sae ttunneteat aa acai
Hyperphoria, R............ Livcsisserstavsc teiaeaca trtracdahiaxareaalinines
Sursumduct, R...... 2.2... Noi ccivarn caterer a penaunciAana tp aedaetaes
Reading power at fourteen inches, eonractal DY cawawss glasses
VISUAL FIELD OPTHALMOSCOPE
Pe ee ee eee ee ee ee wm wee | we ee ee ee ee ee beer ete eet eee
Cc ey
All the data indicated for record in this table, excepting the esti-
mation of the degree of astigmatism and the outline of the visual field,
have been referred to, and the tests for each have been given with some
detail.
The estimation and correction of astigmatism is a difficult matter for
a novice, and sometimes for an expert. It will be better understood by
reference to and close study of the standard text-books on ophthal-
mology. Moreover, the ophthalmoscope is often required to properly
estimate the degree and kind of astigmatism which exists. I would say,
in passing, that a high degree of astigmatism should never be disregarded
or left uncorrected, especially if present in connection with abnormal
“nervous phenomena. It is a very common cause of headache and as-
thenopic symptoms.
In estimating the visual field, an instrument specially designed for
that purpose (the perimeter) greatly simplifies the step, and gives us at
the sume time an accurate representation of its outline for subsequent
reference. A drawing can be roughly made, however, of the visual field
of any patient, by means of a blackboard and a piece of chalk, through a
simple method described in most of the text-books. In some nervous
cases it is very desirable that a register of the visual field be taken from
time to time and preserved for reference.
10
146 LECTURES ON NERVOUS DISEASES.
Now, when we have carefully examined our patient respecting all
the data indicated in the preceding table, are we safe in passing an
opinion respecting the condition of the eyes? I would again say,
4 No. ” y
We have now reached a point where we should administer atropine
to the patient. I usually employ a solution of gr. iv of sulphate of atro-
pine to an ounce of distilled water. This can be kept constantly in your
office in a phial with a rubber-top dropper substituted in place of a cork,
A drop or two in each eye will suflice in most subjects to dilate the pupil
widely and to paralyze the power of accommodation of vision for near
objects in about three hours. In occasional instances it becomes neces-
sary to keep the patient under its influence for several days, but this is
not the rule. A :
It is well to caution the patient, after using this drug, that he may
possibly suffer from the sunlight, and that colored glasses will relieve him
of this-annoyance. It is also best to tell him that his vision may becume
very blurred for distant objects in case he is far-sighted; and that, in any
case, he will be unable to read or to write by the aid of vision without
glasses for several days. I- have known hypermetropic patients to be-
come greatly alarmed at the rapid loss of vision which has followed the
use of atropine; all of which could easily have been avoided had they
been prepared for it by timely words of explanation. It is always well
to explain to far-sighted subjects the difference between ‘manifest ” and
“latent” hypermetropia, and to make them intelligent as regards the
effect of atropine upon the ‘focusing’ muscle before you administer it.
If they are forced by their business to use their eyes for near-work while
under the influence of atropine, a pair of cheap glasses may be given
them for temporary use while under its influence.
I cannot impress too strongly upon you the necessity of using atro-
pine upon a patient (if young) for diagnostic purposes when an error of
refraction or of accommodation is suspected. Personally, 1 do not regard
an examination as complete without it. It solves the question of the pres-
ence of “latent”? hypermetropia—a very common defect and a very im.
portant one (from the standpoint of the neurologist) if allowed to go
unrecognized. It reveals the existence of a previous ciliary spasm.
It ‘often arrests headache as if by a magic touch, and solves the nervous
origin of many other similar symptoms.
Patients who boast of their acuteness of vision, and who apparently
justify their statement by reading test-type at a distance without the aid
of glasses, are often astonished and sometimes alarmed at the immediate
loss of this power which is brought about hy the use of atropine, ‘This
surprise is heightened when (by the use of proper lenses) their power of
vision for distance is immediately restored, and they become conscious
LATENT ERRORS OF REFRACTION. 147
for the first time of the muscular effort which they have been compelled
in the past to exert in order to see without them. I shall never forget, per-
sonally, the sensation which I experienced of “ seeing without effort ” when
a latent hypermetropia was discovered in my own eye, and corrected by
glasses.
These experiences are well-known fhinlis among oculists, but to the
profession at large aay often occasion as much of a surprise as to the
patient.
I could point to case after case in my own practice where the cause
of neuralgic attacks, excruciating headache, vomiting, extreme nervous-
ness, and many other symptoms (not apparently connected with eye-de-
fect) would have remained unrecognized if atropine had not been em-
ployed. There is a rule given by most oculists—viz., to give to a hyper-
metropic patient the strongest conver glass* with which he can comfortably
read the normal test-type (xx) at a distance of twenty feet. It is impos-
sible in many cases to decide this fact without atropine or an ophthal-
moscope. The former method is unquestionably the most accurate one,
because the accommodation of the oculist, as well as that of the patient,
has to be excluded in the latter; and it has the advantage, moreover,
that it can be employed by the general practitioner as well as by the
specialist. +
Now, after the patient returns to you with widely dilated pupils, you
should carefully repeat each step of the previous examination. You
should record the results of these tests and then compare them with those
obtained before atropine was employed. If the eye is a normal one, the
20
vision will be — after atropine has been used, as it was on the first ex-
SK :
amination; but, when an error of refraction or accommodation exists,
changes of a greater or less degree may be noted. You may find, more-
over, that the power of adduction and of abduction of the eve will be mod-
ified in some patients by the action of the drug upon the accommodation of
vision, and that a different degzee of muscular insufficiency may be detected.
You can now decide intelligently as to the glass which is best ndapted to
restore vision for distant and near objects in each eye of the patient, and
you are prepared to advise the patient respecting the use of the glasses
* The advisability of a full correction by glasses of existing hypermetropia can only be
decided after the condition of the patient, his age, his susceptibility to reflex irritation from
eye-strain, etc., have been carefully considered. It is not usually advisable to force a
young subject to wear a glass which fully corrects the latent hypermetropia. I am in the
habit of correcting all latent hypermetropia in excess of one dioptre.
t Personally, I have of late discarded the ophthalmoscope as a means of estimating
errors in refraction, except in children and feeble-minded persons. It cannot always be
relied upon, even in the hands of an expert, for this special object.
148 LECTURES ON NERVOUS DISEASES.
selected. You can decide also respecting the question of the utility of
prisms or of tenotomy if the patient has marked insufliciency of the
muscles. You can judge more accurately respecting the proper angle of
the prism required in case their use is indicated. I would caution you,
however, against deciding this latter point before the error of refraction
(if such exists) is corrected, and not until the “diplopia tests”
have been employed, after such lenses as are required to correct it have
been placed before the patient’s eyes. I have seen patients who gave
evidence of marked insufficiency (5° to 8°), when the refractive error was
uncorrected, exhibit no such defect when glasses which corrected that
error were worn. Prisms in such a case would inflict injury upon the
patient rather than afford relief.
In closing, | would remark that views which I have advanced respect-
ing the dependence of abnormal nervous phenomena upon eye-defect are
not new. They are in antagonism, however,.to those of some authors,
and have been more or less actively combated of late, especially in regard
to eye-defect as a cause of chorea and epilepsy. I do not think the re-
lationship between “eyestrain” and attacks of headache or neuralgia
can be denied, although it is only hinted at by Anstie and is omitted
by most authors who have written on the causes and cure of these dis-
tressing maladies. Some of our best neurologists, as well as most oculists,
are now investigating with renewed interest not only the ametropie con-
ditions of the eye, but also the eye with “insufficient” muscles. Facts
are being daily substantiated beyond dispute which met with ridicule
some years since. Every day, in my own experience, I am strongly im-
pressed with the curative effects of glasses and partial tenotomies of the
ocular muscles in various forms of functional nervous disturbances. In
my opinion, the neurologist of to-day who fails to familiarize himself
thoroughly with the examination of the eye omits an evident line of
duty both to himself and his patients. No neurologist can send all of
his cases to an oculist for an opinion, and, even if he could do so, he
should at least be able to verify the opinion thus gained respecting the
refractive errors found and the state of the eye-muscles. He requires
a case of lenses. and prisms in his office as much as an electrical outfit,
and he should know how to use both—the one as an aid in diagnosis,
and the other as a means of cure. Personally, I have come to regard
the examination of any patient sent to me as incomplete until I have
tested the state of refraction and accommodation, and examined with
care the condition of the ocular muscles. This view has not been
hastily formed, and my daily experiences confirm me in it. I believe
the time will come when the tests employed in eye-examinations will
rank in importance in neurology with the knee-jerk test, which for
generations, as Gowers remarks, simply “amused school-boys.”
THE USE OF THE OPHTHALMOSCOPE. 149
THE OPHTIALMOSCOPE,—In connection with the eye, it may be well
to mention the instrument which is employed to detect abnormalities of
that organ, viz., the ophthalmoscope.
All forms of this instrument consist (1) of a concave mirror which
is perforated at its centre, in order that the observer may look directly
into the illumined field; (2) a series of lenses by which it is possible to
correct errors of refraction in the eye of the patient or observer; (8) a
bi-convex lens, which brings the deeper parts of the eye into prone,
and enables the observer to-inspect them minutely.
Hutchinson (as quoted by Hamilton) gives some concise and prac-
tical suggestions respecting the use of this instrument, which will bear
repetition. Ile says :—
Fic. 40.—Tue OpntHatmoscorg. (Loring’s Pattern.)
“Having placed the patient’s head in such a manner that the light (a
lamp, candle, or gas-light) is on a level with his temple, and slightly he-
hind it and his face, as a consequence, in shadow, the observer sits in
front.and applies the ophthalmoscope mirror to his own eye. He should
keep both eyes open that he may sce where the light falls, and then move
the mirror until the light falls full upon the pupil of his patient. Ina
moment he will perceive the first fact which this instrument reveals, that
the fundus is not black, as it has always appeared to be before, but that
it is of a brilliant fire-red. He will, however, see nothing of the fundus
distinctly, only a genera) reflex Now at this point the student must
150 LECTURES ON NERVOUS DISEASES.
stop awhile and use his mirror to inspect first the transparency of the
cornea, and next, that of the lens and vitreous, and to do this he must
make the patient move his eye in various directions. After a little prac-
tice he will be able to manage his light well, and to throw it with pre-
cision wherever he may wish, and to keep it steadily on any given part.
At a first lesson, he may even with advantage practice for awhile by illu-
minating the second button of the patient's waistcoat. Tact in directing
the light having been obtained, we may now proceed further. Instruct
the patient to look, not full in your face, but’ over one shoulder; if you
are inspecting his rzght eye, over your /e/t shoulder. You will, when he
does this, notice at once that the tint of the light reflected from the
fundus is changed, that it is no longer fire-red, but canary yellow. The
reason of this is, that a different part of the fundus is exposed to view,
that, namely, of the optic disk itself, which is much lighter in color than
the rest. The area of yellow is very large,—occupies, indeed, the whole
of the field, while we know that the disk itself is very small. This proves
that the objects thus distinctly seen are immensely magnified. Magnified
by what? By the patient’s own eye, which, as we have said, is equivalent
to a lens of one-inch focus.
“Hitherto we have seen nothing distinctly, but if the observer now
brings his head very close to the patient’s face, he will be able with more
or less facility to observe the details of the bottom of the eve, the trunks
of the vessels of the retina, the optic disk, ete. What he sees is now
equivalent to type looked at through a one-inch lens, placed exactly one
inch in front of it.”
; In the ophthalmoscope now generally employed, a revolving disk
containing a series of lenses is placed behind the mirror. These are in-
tended for the purpose of correcting any error of refraction in the eye of
the observer or patient. It is important that such error be determined
first with accuracy and properly corrected, before the fundus is examined.
The ophthalmoscope is an important and valuable aid to those who
are skilled in its use in detecting changes in the deep parts of the eye,
chiefly those of the optic nerve and the vessel of the retina, by means of
the sense of sight.
Dr. William C. Ayres has lately published in The American Journal
of the Medical Sciences (1881) an exceedingly valuable and complete
article upon this branch of diagnosis
By means of the ophthalmoscope the neurologist determines the
presence or absence of 2 neuro-retinitis, or a “ehoked disk” as it is called,
which is peculiarly suggestive of some brain lesion, that is creating a
gradually increasing pressure within the cavity of the skull. Again, the
vessels of the retina are derived from the same source as those of the
brain; hence chanves in the one are liable to be associated with similar
chanves in the other.
THE EYELIDS AND MOUTH IN DIAGNOSIS. 151
Tue Eyeirps.—These may atford valuable aid in diagnosis. The
upper lid sometimes drops over the eyeball and cannot be raised, con-
stituting the condition termed “ptosis.” This indicates a paralysis of
the third cranial nerve. Again, when the facial nerve is paralyzed, the
eyelids of the attected side cannot be closed. Pufliness of the lower
eyelid, especially in the morning after rising, suggests the possibility of
kidney disease. Alcoholic patients often exhibit a quiver of the mus-
cular fibres of the eyelids. Spasm of the lids produces the peculiar
winking so often seen in St. Vitus’ dance and other nervous affections.
In imbeciles and cretins the lids are often obliquely placed.
The expression of the eye is influenced to a large extent by the eye-
lids and may often be characteristic of certain nervous diseases. Melan-
choliacs exhibit the downcast eye. Maniacs may look excited, suspicious,
or distrustful. A vacant stare is often present in dementia. Some forms
of brain disease exhibit in the eye an air of exaltation. Masturbators
seldom direct their gaze at the questioner, but look furtively about as if
to avoid scrutiny.
Tue Movuru.—The lips are sometimes paralyzed. The pronunciation
of the labials is then rendered indistinct or impossible, and a facial de-
formity is also created. The various diseases in which the mouth is
affected may be considered separately with advantage.
A, In Bell’s paralysis the lips are rendered incapable of movement
on one side only and the mouth is drawn toward the opposite side ly
muscles which are no longer antagonized, on account of the facial
paralysis. The act of whistling is rendered impossible, hecause * pucker-
ing” of the lips requires a contraction of the symmetrical muscles of the
face. The saliva is no longer retained, and the patient ‘‘drools.” All
expressions except that of repose are those of a face alive on one side
and dead and motionless on the other; hence, they would be particularly
grotesque and striking (were it not so frightful and distressing) even to
a casual observer.
In those rare cases where the facial nerve of both sides is impaired,
symptoms similar to those mentioned above exist, except that the tongue
has its normal capabilities of movement, save in the perfect articulation
of the labial consonants only, and that a complete absence of facial ex-
pression is present.
Certain rules, which prove of value in making a diagnosis of the seat
of the exciting cause of the condition have been given in the preceding
chapter (p. 85). They are based entirely upon anatomical facts, and are
therefore very important, because they admit of no exceptions :—
B. The lips and tongue are particularly affected also in that disease
of the medulla called Duchenne’s disease (glosso-labio-laryngeal pa-
ralysis), So marked is this loss of power, in severe cases, that a most
152 LECTURES ON NERVOUS DISEASES.
characteristic facial deformity is induced. As this disease is commonly
bilateral, the lips usually hang apart from each other and cannot be
approximated. The tongue lies trembling and immovable in the floor of
the mouth, if the paralysis be complete; but if paresis only exists, it can
be imperfectly protruded with difficulty, and is tremblingly and slowly
retracted. If the paralysis be unilateral, the healthy side of the tongue
becomes full and prominent, in comparison with the affected side, when
called into action. Speech and mastication are seriously embarrassed.
The saliva is constantly expectorated, because swallowing is performed
with extreme difficulty.
C. The facial muscles, as well as the tongue, exhibit a peculiar
tremor in paralytic dementia. Small bundles of fibres composing parts
Fic. 41.—Be’s Paratysis. (After a Sketch from Life by the Author.)
of the tongue, or the delicate muscles of the face, are thrown into non-
rhythmical contractions hy emotion, or the performance of any voluntary
movement, as when showing the tongue or teeth. These fibrillary tremors
may sometimes exist even in the quiescent state of the muscles. The
tongue occasionally exhibits coarser movements of a convulsive character,
Late in the disease it may become atrophied or shriveled.
The effects of this form of tremor upon speech are aggravated by an
imperfect codrdination of the muscles of the tongue and lips, which is
simultaneously developed. Long or difficult words are omitted in con-
versation by these patients in a half-unconscious way, and the terminal
syllable of other words is commonly left off. The speech becomes thick,
and of a tremulous character. The shortest words possible are employed
THE LIPS, GUMS, TEETH, AND TONGUE. 1538
by the patient to convey his ideas. A distinct pronunciation of conso-
nants and polysyllabic words, such as ‘‘constitution,” “inrallibility,”
“prognostication,” etc., is impossible; hence, a test is thus atlorded
between carelessness of utterance and a physical inability to articulate.
An unnatural quietude of the muscles of the face and a slight dis-
parity of the pupils are prominent features of its stage of development.
It is well to note, in this connection, a test which is of some value
in deciding as to the existence of this special form of disease. Extend
the patient’s fingers and place them between your own, and a delicate,
“parchment-like” fremitus will be felt, which is due to an otherwise imper-
ceptible tremor of the hand muscles.
D. The lips participate to a marked degree in severe types of facial
spasm. In the clonic form of the muscles on one side of the face, are
violently contracted and as suddenly relaxed. The eye is commonly
affected simultaneously with the angle of the mouth. The spasms are
marked by distinct paroxysms, whose duration varies from a few seconds
to an hour or so. If the spasm is of atonie variety, mastication and
articulation are interfered with, and the paroxysms are of longer duration.
It is always well to search carefully for carious teeth in these cases ;
but the spasms may be due to cold, wounds, injuries to the trigeminal
nerve, or chorea.
E. The lips may indicate some form of defect in the heart's action
if blue or purple in color.
Sears at the corners of the mouth are strongly suggestive of previous
syphilitic ulceration, a point of importance in the treatment of some
forms of nervous disease.
F. The gums should always be inspected. If pale, anaemia exists.
If blue along the line of junction with the teeth, lead poisoning is
present. If the teeth are loosened and the gums are soft and bleed easily,
mercurial poisoning may be suspected; this is rendered positive if the
breath has the “mercurial odor” and the saliva is excreted in very large
quantities. Various cachexias, phosphorus poisoning, purpura, and
scurvy, produce marked and often characteristic changes in the gums.
G. The teeth may afford much valuable information respecting the
possibility of hereditary syphilis. Hutchinson has described the char-
acteristics of such teeth with accuracy and detail. It is impossible to
quote his deductions here, but the peculiarities of syphilitic teeth are
now generally well recognized, and are often-a valuable aid to the neu-
rologist, both in diagnosis and treatment.
H. The tongue. Some diagnostic points regarding the tongue have
been touched upon already. When the face exhibits any form of pa-
ralysis, it should be always carefully noted if the tongue exhibits fibril-
lary tremors; also whether it can be protruded in a straight line and
154 LECTURES ON NERVOUS DISEASES.
moved freely in all possible directions. In testing speech those words
should be employed that require the normal power of movement of the
lips (the labials) and of the tongue (chiefly the consonants). It should
be also noted whether the words are clearly, rapidly, and distinctly
articulated, or if the utterance of words is slow, thick, or slurred.
Ragged edges in the tongue indicate epilepsy, because it is frequently
bitten during the paroxysms.
Imperfect mastication of food and difficulty in swallowing may be
due to loss of power in the tongue.
A “furred condition” ‘of one lateral half of the tongue indicates
some irritation of the branches of the fifth cranial nerve; hence. the
presence of decayed teeth, disenses of the gums, or the maxillary bones.
etc., should be carefully searched for. The tongue may be paralyzed on
one side or on both. This condition is not infrequently due to hemor-
rhage, softening. or tumors of the brain, and it occurs in connection with
embolixm or the general paralysis of the in A. 0. Co> aA. C. CC. 0. C.
NORMAL MUSCLE-REACTION.
C. 0. C2>A. C. C25 A. 0. C0. 0. 6.
The final contraction (C. O. C.) of each of these series is seldom seen,
because the current required to produce it is too painful to be endured.
Fewer cells are required to cause muscular formule than those of a
nerve-trunk,
In recording the results of an electrical examination of nerve-trunks
and muscles it is best to arrange the record-page so that the two sides
of the body may be easily contrasted. The number of galvanic cells em-
ployed or the number of milliamperes of current (as shown by a galva-
nometer) should also be specified, and the faradaic reaction of homologous
nerves or muscles should be stated for the purpose of comparison and for
clinical deduction. We may follow with advantage some such plan as the
following :-—
THE PRINCIPLES OF ELECTRO-DIAGNOSIS, 191
NAME.......... DATE scaaunws AGE,
History or Case. See page .... of Caser-Boox.
FARADAIC TESTS.
2 | Extent of secondary
Right side. Left side. coil employed, (In| Nerve tested.
centimetres, )
Nerve reactionS..cccasscaceeseces
Muscle tested.
{
Muscle reactionS.........--+.56-- |
GALVANIC TESTS.
Right side. cameron pro- Left side. Mews ar anescle
Cells or miliam- Cells or milliam-
péres, péres.
f cee |
Nerve-reactions..... ayainiaeiaks aaa daese 7 a c a nerve,
Cc. 0. C.
c.c. C.
Muscle-reactions....++-.seseeeeeeee - @ muscle:
iG Oz Gs
Slips of this character may be printed and kept on hand, They can
be pasted into the case-book of the physician when filled out. The tests.
made at different dates can this be compared with each other and the
progress of each case determined.
Fic. 59.—Tue Autuor’s Sprinc Erecrrope.—QJ, the binding-post for attaching the rheophore
which connects it with the battery, or with the diagnostic key-board when that instrument is
employed. The motor point of the electrode is represented as enveloped in chamois-skin.
Jt must be thoroughly dampened in salt-and-water before it is applied to the nerve or muscle
to be tested. ‘I'he other end of the electrode is designed to prevent slipping of the instru-
ment after its proper adjustment. z
For the purpose of demonstrating the special action of individual
muscles and nerves before classes of students, as well as the study of
muscle- and nerve-reactions in disease, I have devised small electrodes
which may be made stationary upon any desired part of the head, limbs,
or trunk, by means of straps, strips of adhesive-plaster, or insulated
springs. By means of these I have been enabled to make many points
clear to a large audience which would be extremely difficult to show by any
192 LECTURES ON NERVOUS DISEASES.
other method. Furthermore, it is often desirable to refer from time to
time during an examination ofa patient to the effects of currents of known
intensity upon certain nerves and muscles for the sake of accurate
comparison,etc. Small electrodes of the type described may be accurately
placed upon a patient and allowed to remain upon the spot selected during
the entire examination. To each of these a separate rheophore may be
attached, and, by a simple device of my own, each may be controlled by
touching a key upon a board, without movement of the operator. I can
thus observe simultaneously the reactions of corresponding muscles or
nerves upon the two sides, those of the leg and arm of the same side; and
any other comparisons which may be required in diagnosis. The “ motor-
points” of the body are not always exactly where charts depict them;
hence it is sometimes necessary to hunt for them within a radius of an
inch or two of the normal point. When they are found with exactness,
a small electrode may be fastened over the spot (with moistened ab-
sorbent cotton beneath it) and allowed to remain stationary during the
Fic. 60.—THe AutHor’s DiaGnostic Kry-soarv.—A, the rheophore which connects it with
one of the binding-posts of a galvanic battery; B, rheophores connecting its binding-posts
with spring electrodes previously placed upon the body of the patient so as to influence the
“nerves or muscles to be tested; C, buttons and springs which make a circuit to the body of
the patient when the knob on the spring is pressed downward so as to impinge upon the
button. The number of rheophores which may be employed depends upon the necessities
of the case; the cut shows an instrument capable of six.
entire sitting. Whenever it becomes necessary to refer to the reactions
of that point, it can be called into action by touching the key connected
with it by its individual rheophore. The cuts introduced show the ar-
rangement of my device for this purpose. I have given a more com-
plete description of the advantages of this method over others previously
employed, in the New York dMledical Journal of May 9, 1885.
Now, from such a table of record it is apparent that the faradaic
current should first be employed upon the patient (the poles of the sec-
ondary coil being used), The extent of the overlap of this coil (in centi-
metres) necessary to produce muscular contractions when the nerve- and
muscle-reactions are being separately tested should be recorded. In case
no muscular contractions ensue, the extent of the overlap which produces
THE PRINCIPLES OF ELECTRO-DIAGNOSIS. 193
an unbearably painful current should be ascertained and noted. This
may be compared with that necessary to produce contractions upon the
healthy side.
The next step in the examination consists in changing the rheophores
to the binding-posts of a galvanic battery. We can now ascertain the
number of cells or milliamperes (which is preferable) required to produce
the different varieties of contractions (enumerated in the table designed
for record) of muscles in homologous regions of the right and left sides.
Each nerve which is impaired should be tested first; and the muscles
ma
err i
Kis ! iy
cg
Fic. 61.—Tue AutHor’s Diacnosric Key-soarp aS APpirep in AcTUAL Use.—The spring
electrodes are represented in the cut (for the purpose of illustration) as applied to the facial,
ulnar, and musculo-spiral nerves of each side. Jf he so chooses, the operator can have his
case-book on a stand at his right, for recording his observations as they are made.
supplied by it should be tested afterward. The strength of the current
employed should be ascertained by throwing a galvanometer into the
circuit (when extreme accuracy is desired); by so doing, a comparison
of the nerve- and muscle-reactions of the two sides can be based upon
conditions which are exactly alike.
When we have completed the steps indicated by the chart prepared
for the assistance of the practitioner (page 191) we are in possession of
certain facts which may be of great practical value as regards both diag-
nosis and prognosis :—
18
194 LECTURES ON NERVOUS DISEASES.
1. Suppose a case of localized paralysis is examined, and the fara-
daic and galvanic reactions of both a nerve and its muscles are normal
and exactly alike on the two sides. We have reason then to believe that
the exciting cause is either hysteria, a lesion of a higher spinal segment
than that from which the nerve arises, or a lesion within the brain, pro-
vided the possibility of deception on the part of the patient respecting
his paralytic condition can be excluded.
2. If the nerve-reactions of the affected side to both currents are
exaggerated (i.¢., if the contractions occur in their proper sequence, but
under a weaker current than in health), the probability of an existing cen-
tral lesion is heightened, although hysteria may possibly still exist as the
exciting cause of the paralysis.
3. If the faradaic current applied Hinoaglh the nerve fails to pro-
duce contractions of the affected muscles as readily as upon the healthy
side (¢.¢., ifa stronger current is demanded to call any one of the para-
lyzed muscles into action indirectly through the nerve which supplies it,)
then we know that the nerve filaments within the spinal cord or those of
the trunk of the nerve itself are atiected by a lesion which has impaired
but not entirely destroyed their usefulness.
4. If no current from a faradaic machine (which can be endured by
the patient) causes muscular contractions, we know positively that the
motor cells of the anterior horns of that spinal segment which controls
the paralyzed muscles are impaired, or that the nerve itself has been sev-
ered from its connection with the spinal cord, or is undergoing degen-
eration.
5. When the MUSCLE-REACTIONS to the faradaic current have been
tested, the previous deductions (based on the nerve reactions) still hold
good. The electrode should, however, be placed over the “motor point”
' of each muscle thus tested. These are shown in plates at the end of this
volume.
6. If the formule obtained by the galvanic current are normal, all
questions regarding the existence of degenerative changes in the nerve-
or the muscle-plates can be excluded. When the normal order ts altered,
degenerative changes in the nerve- or the motor-cells of the spinal cord
are present.
7. The history of a case in which motility 7s impaired is never
complete without a record of an electrical examination of the nerve- and
muscle-reactions to hoth the faradaic and galvanic current. When doubt
exists respecting the existence of a ccrebral lesion or hysteria, the facts
obtained by other methods of examination (fully described by me in the
preceding pages) will clear up all doubts.
8. Patients afflicted with paralysis from a cerebral lesion generally
exhibit normal electro-nerve and electro-muscular reactions in the para-
lyzed parts, In some instances the reactions may even be exaggerated.
DETECTION OF FEIGNED DISEASES. 195
9. Hysterical patients afflicted with paralysis may exhibit either
normal or exaggerated electro-muscular reactions to faradism or gal-
vanism. The sensitiveness of the muscles to faradism is generally de-
ercased ; in some cases it may be totally wanting (Duchenne).
10. In rheumatic paralysis the electro-muscular contractility is, as
a rule, markedly increased; this may be shown by a comparison of the
reactions of the two sides of the body. In exceptional cases this is not
found to be so,as I have seen the reactions follow only the strongest
currents.
ll. In pertpheral paralysis the faradaic and galvanic reactions are
altered after ten days have elapsed. The muscular contractility to the
faradaic current is lost early to a greater or less extent; and the formula
of degenerative changes is developed later by the employment of the
galvanic current.
12. .
Orie mot
©
Fre, 64.—Hammonp’s AEsTHESIOMETER.— When closed it can be conveniently carried in the pocket.
(b) The appreciation of pressure, as suggested by Weber, may be
tested by placing weights of varying sizes upon the skin of some part,
that has previously been supported in order to avoid the so-called “ mus-
cular sense” being a factor in the patient’s decision. Dr. Beard has de-
vised an instrument for this test that answers all purposes very well.
(ec) Again, the various forms of esthesiometers are used to detect
the minimum distance which can exist between two points of simple
contact with the skin without destroying the distinct perception of both
points by the patient. This distance varies in health between extremely
wide limits, because some regions are abundantly supplied with sensory
TESTS FOR TACTILE SENSIBILITY. 201
nerves and tactile corpuscles, while others are not. For this reason, the
following measures* can be used as the healthy standard for comparison
in any given case. They are given in inches, lines, and millimetres so
as to meet the requirements of any scale:—
1. Pointof tongue ...... gyinch = $line = llm
2. Palmar surface of finger tips. py “ = 1“ = 22 %
3. Mucous surface of ips. ... § “ = 2lins= 42 *
4. Palm of hand and tip of nose. }$ “ = 3 “ = 63 “
5. White partof lips ..... 3% = 4 “ = 84 *
6. Lower part of forehead ... 8 “ =10 “ =211 *
7. Backofhand ....... 18 “ =14 “ =202 *
8. Dorsumof foot. ...... 1) * =18 " = 375 *
9. Forearm. ......... 18% =19 “ =396 «
10) (Stemant ¢a 2a Goaweee de s2b ety
ll. Middle of thigh ...... 2hinches=30 “ =62.5 “
V2 Baths ogee ead eee 2E- 8h e660. *
Fic. 63.—Carroi’s AisTHESIOMETER —The instrument has two points upon each leg of the
compass, one blunt and the other sharp. It is a convenient instrument to determine the con-
dition of the sensory nerves in respect to contact sensations and those of pain. This is ac-
complished by simply substituting the blunt for the sharp points, of vice versa.
Various forms of esthesiometers have been devised, but a simple
pair of compasses, such as are used by artists, will answer all purposes.
Fig. 66.—Srevexine’s Aistuestomrter.—A modification of the ordinary beam compass ems
ployed vy carpenters, but graded in inches and tenths of an inch. Its points are not sharp.
The distance between the points can be ascertained by a rule graded in
inches, lines, or millimétres. The points should not be sharp, as they will
cause pain if so, and thus defeat the object of this test.
* More complete tables than the one offered may be found in many of the later works
on physiology and nervous diseases,
202 LECTURES ON NERVOUS DISEASES.
The suggestions previously made respecting the definite instructions
to the patient, the use of blank experiments, and the employment of a
bandage over the patient’s eyes, apply to this test as well as to those pre-
viously described.
The following rules must be observed in case the xsthesiometer is
to be used :—
1. The two points of the instrument must be made to touch the skin
simultaneously; otherwise the patient will detect the two points of con-
tact more readily than if both meet the skin at the same moment,
2. The contact should be a gentle one; otherwise the impression
upon the skin becomes a painful sensation.
3. The relative position of the two points should always bear the
same relation to the axts of the limb or median line of the body, because
the sensibility of a part is affected differently when the points are directed
transversely or longitudinally. This is essential to the accurate com-
parison of the sensibility of different regions of the body, or of corre-
sponding regions of either side.
4. The table which has been previously given should be employed
asa standard of comparison only when the sensory functions of the skin
are impaired upon both sides. When the derangement is one-sided, the
healthy side will be the satest guide for comparison.
ABNORMAL CONDITIONS OF SENSATION.
We are now prepared to consider the significance of the disorders
of cutaneous sensibility, viz., anesthesia or loss of sensibility; hyper-
zesthesia, or increased sensibility; the existence of pain; and the lack of
appreciation of varying degrees of temperature.
ANZSTHESIA.—Certain regions of the body may be deprived of
cutaneous sensibility (either totally or partially) (1) by diseased con-
ditions of the brain or spinal cord, and (2) by any abnormal state of the
nerves themselves that tends to impair or destroy their ability to conduct
sensations to the nerve centres.
In the latter case, the loss of sensation is liable to be associated
with an impairment also of motion, because the cerebro-spinal nerves are
composed, as a rule, of both motor and sensory fibres. The fact that
sympathetic nerve fibres are also present in the majority of nerves, helps
us to explain certain disorders in the nutrition of the skin that some-
times accompany motor or sensory paralysis dependent on injury or de-
struction of some individual nerve.
The regions of the spinal cord and brain that are functionally asso-
ciated with sensation, have been already touched upon in Section lL. It
may be stated in a general way that the nerve fibres that conduct sensory
impressions from the peripheral parts of the body to the brain travel
ABNORMAL CONDITIONS OF SENSATION. 2903
chiefly through the posterior columns of the spinal cord and tts gray matter
in order to reach the brain—the seat of intelligent perception of such
sensations. Within the substance of the brain itself, these fibres pass
through the outer part of the formatio reticularis and the posterior part
of the so-called “internal capsule” of that organ. We are justified, I
think, in drawing the following clinical deductions as regards the exist-
ence of cutaneous anesthesia :—
1. Lesions of the cerebral hemispheres produce anesthesia when
they involve the posterior one-third of the internal capsule.
If the sensory cranial nerves are affected by such a lesion, the loss
of sensation is commonly on the same side as the lesion, except in case
of the optic nerve (the condition known as hemianopsia). The anzs-
thesia of parts below the head, if due to cerebral causes, is confined to
the side opposite to the hemisphere in which the lesion exists.
2. Anzesthesia from lesions of one lateral half of the substance of
the spinal cord exists, as a rule, on the side opposite to the spinal
lesion.
3. Lesions which involve both lateral halves of the spinal cord
create anesthesia on both sides of the body, provided the destructive
process affects the so-called “sensory tract” of the cord, viz., the pos-
terior columns, or the gray matter around its central canal.
4. Anzsthesia may exist on the same side as a spinal lesion, pro-
vided the posterior roots of the spinal nerves be pressed upon or de-
stroyed by it, or in case the sensory nerves be affected by the spinal
lesion before they cross to the opposite side of the cord.
5. Anesthesia, unlike motor paralysis, is not necessarily present in
parts of the body supplied by those nerves that are given off from the
cord below the seat of the lesion. Anesthesia is often associated with a
_ condition of increased sensibility or “hypersesthesia” of parts below the
seat of the spinal lesion, and on the side opposite to it.
6. Anzesthesia may often co-exist with other sensory symptoms,
such as pain, incodrdination of movement, the peculiar sensation known
as “formication,” numbness, tingling, and other subjective sensations.
7. Anesthesia of spinal origin is generally bilateral and symmet-
rical, because lesions of the cord commonly affect both lateral halves.
8 Tactile sensibility may be destroyed by spinal lesions, and yet
the sensibility to pain and temperature may occasionally be retained.
9. Unilateral anesthesia of the face and of the opposed arm and
leg indicates a unilateral lesion of the formatio reticularis.
In rare cases, sensibility to temperature may be lost, and the sensi-
bility to pain and touch may be normal. It is not extremely infrequent
for the neurologist to record an absence of sensibility to pain, when
tactile sensibility remains unaffected, and accurate perceptions of tem-
204 LECTURES ON NERVOUS. DISEASES.
perature are still experienced by the patient. These subjects can detect
a needle thrust into the muscles from a simple sensation of touch. These
clinical facts seem to confirm the view that has been advanced by late
physiologists,* viz., that the paths of conduction of sensations of touch,
pain, and temperature probably lie in different parts of the spinal cord.
Hyrenastures1a.—The skin may be rendered extremely sensitive in
certain diseased conditions. This abnormal state of the nerves is termed
“hyperesthesia” in contradistinction to ‘“‘anmwsthesia” or a loss of sen-
sation.
When the “sensory tracts” of the spinal cord are involved by a
localized lesion, the parts below the regions that are rendered anesthetic
by the cutting of the sensory nerves are sometimes affected with hyper-
zsthesia. The cause of this is not yet definitely known.
A narrow band of hyperesthesia is also developed, as a rule, at the
upper level of the spinal lesion. If in the dorsal region, this zone of
hypereesthesia generally encircles the body. When in the lambar region,
it is more or less vertical over the limbs in accordance with the particular
spinal segment which happens to be affected.
Hyperesthesia probably indicates, according to our present knowl.
edge, some irritation of the nerve fibres distributed to the regions so
affected. The cut introduced is admirably adapted to illustrate the
effects of a one-sided spinal lesion upon the sensory functions of the skin.
In the disease known as locomotor ataxia, after a paroxysm of
“stabbing pains” has subsided, the seat of previous pain becomes
markedly sensitive to the touch, while the rest of the body is not simi-
larly affected.
Hyperesthesia may be of service in diagnosis. It may afford valu-
able information respecting the spinal segments that are irvztated by some
destructive process within adjacent regions of the spinal cord. Again,
*The lateral columns (Fig. 84) and the posterior columns are probably concerned
(as well as the gray substance of the cord in the region of its central canal) in the trans-
mission of sensory impressions to the brain.
Woroschiloff, Ludwig, and Ott have apparently demonstrated by careful and appar-
ently conclusive experiments that, in the lower animals, the lateral columns in the dorsal
region ‘of the spinal cord are physiologically associated with the transmission of sensations
from the legs. Whether this is true of man is not yet determined, although Gower’s re-
ported case of a crushed cord in man gave evidence of ascending degeneration, both in
the postero-internal columns (Goll’s columns) and also in the lateral columns in front of
the ‘‘ crossed pyramidal tract” (Fig. 29), Unfortunately, this case stands alone as yet.
This view is directly opposed to the older one that has been generally accepted by
standard authors, viz., that sensations of pain travel along the gray matter of the cord,
and those of touch, and perhaps of temperature, pass up the posterior columns of the
spinal cord.
The late researches of Starr seem to prove that impressions of muscular sense from
the upper limbs are transmitted by Burdach’s column, and from the lower limbs by Goll’s
column of the corresponding side of the cord,
ABNORMAL CONDITIONS OF SENSATION. 205
if limited to the area of distribution of some individual nerve, it may
point most suggestively toward the existence of some local cause of irri-
tation of that nerve itself. Finally, Valleix has pointed out the situation
of certain regions in the course of the more important nerves of the
hody where extreme sensitiveness to pressure or touch exists in con-
Fic. 67.—D1aGRamMaTiIc REPRESENTATION OF THE SKIN SYMPTOMS IN UNILATERAL LESION
OF THE Dorsat Portion OF THE SrrnaL Corp on THE Lert Sipr. (After Erb.) The
diagonal shading (a) signifies motor and vaso-motor paralysis; the vertical shading (¢@ and
o signifies anesthesia of the skin; the dotted shading (c) indicates the hyperzsthesia of
the skin.
nection with neuralgic attacks. These are known as the “puncta dolo
rosa.” They have been separately described by the author in his work
entitled “The Applied Anatomy of the Nervous System.”
Hyperesthesia may be functional or organic. If functional, it is
often due to some form of general spinal irritation; if organic, it is com-
206 LECTURES ON NERVOUS DISEASES.
monly associated with more or less anesthesia. We meet the organic
variety chiefly in connection with spinal meningitis, compressa of the
sensory nerve roots, and locomotor ataxia.
DELAYED SENSATION.—To the beginner in medicine as well as to the
laity, nothing strikes the intelligence so forcibly as this symptom when
well marked. Imagine a patient stuck with a pin, when unaware of its
occurrence, and an interval of time (varying from one to thirty seconds)
to elapse without any consciousness of the wound. Imagine the patient
then suddenly becoming conscious of the injury with all the evidences
of pain that should have occurred without any perceptible interval of
time in a healthy subject. This is delayed sensation. It occurs chiefly
in connection with the disease known as “locomotor ataxia.”
This symptom is to be interpreted as an evidence of imperfect con-
duction of sensation to the brain by means of the sensory nerves and the
so-called ‘sensory tracts” of the spinal cord. The sensation is not ar-
rested “in toto;” it is simply delayed. Complete abolition of sensation
or “anesthesia” is liable to be developed later—when the nerves or sen-
sory tracts are so extensively involved as to be no longer able to perform
the functions.
SENSIBILITY TO TEMPERATURE.
In testing this variety of sensibility, the precautionary steps pre-
viously mentioned in connection with sensory disturbances must be
carefully observed.
Test-tubes holding water of different degrees of temperature are then
applied to the different regions of the body which have given previous
evidences of sensory disturbances, and the patieut’s ability to discrimi-
nate between them with accuracy should be noted. The temperature of
the test-tubes should be greater or less than that of the skin (983°) and
of a uniform size. This prevents the confusion of simple “tactile” sen-
sations with those of temperature. Breathing upon the surface of the
patient answers as a rough test for the appreciation of heat.
SENSIBILITY TO PAIN.
The tests for this variety of sensibility comprise (1) pinching or
pricking of the skin; (2) the application of extreme heat to the skin;
and (3) the use of a powerful faradaic current upon the skin with dry
electrodes. The patient should never be prepared for this test,as he may
fail to give external evidences of pain from an assumed fortitude. Sen-
sitiveness to pain and temperature may sometimes be affected when
tactile sensations are not impaired.
THE SPECIAL SENSES. 207
THE SPECIAL SENSES.
These comprise smell, sight, hearing, taste, and touch, The latter
has already been discussed, and the tests employed to detect abnormalities
of the eve or its muscles have been quite fully described.
SmeLLt.—The abolition of smell, or “anosmia,” is to be detected Wy
the following methods: (1) Use the same test upon the nostrils alter-
nately; (2) avoid all irritating substances, such as ammonia, acetic acid,
snuff, etc.; (8) employ both agreeable and disagreeable odors (cologne,
camphor, musk, etc.,on the one hand, and valerian, turpentine, asafcetida,
sulphuretted hydrogen, etc., on the other); (4) employ odoriferous sub-
R e
Fic. 68.—A Diacram DeEsiGNepD BY THE AUTHOR TO SHOW -SOME OF THE RELATIONS OF
THE Optic AND OLeacrory Nerve Fisres ro SurrounpinG Parts, F, Frontal lobes
of cerebrum; P, parietal lobe; ‘I’, temporo sphenoidal lobe; 5, fissure of Sylvius; R,
fissure of Kolando; O, occipital lobe; C, cerebellum; M, ‘medulla oblongata; 1, corpora
quadrigemina; 2, optic tracts; 3, optic chiasm; 4, optic nerves; 5, olfactory nerve; 6,
motor-oculi nerve; 7,trigeminus nerve ; @, basis cruris ; 6,tegmentum cruris. ‘The diamonds
in the occipital lobe represent the cortical visual centres of Munk, ‘he cerebellum and
‘pons Varolii are shown as if separated from the cerebrum, in order to make the relations of
the crus to the optic tracts apparent.
stances on the tongue (coffee, wines, cheese, etc.), so that the nose may
perceive them by means of the throat, rather as imaginary taste percep-
tions than as true olfactory impressions.
The abnormal acuteness of smell, or ‘“hyperosmia,” may indicate
brain disease that creates irritation of the olfactory nerve. Nauseating
208 LECTURES ON NERVOUS DISEASES.
odors to the healthy subject may become agreeable to such patients.
Pleasant odors, such as those of flowers, may cause nausea, headache, or
possibly convulsions.
Anosnvia has been observed to accompany a congenital defect in the
olfactory nerve, Bell’s paralysis, tumors at the base of the brain, absence
of the pituitary body, syphilitic disease of the nose, hysteria, insanity,
paralysis of the fifth cranial nerve, meningitis, typhoid fever, injuries to
the nose or skull, and nasal catarrh.
Hyperosmia is commonly met with during convalescence from some
exhausting disease, and in connection with hysteria, insanity, meningitis,
tumors of the frontal lobes, softening of the brain, epilepsy, and adhesions
of the olfactory bulbs to the dura mater.
Siaur.—In connection with vision, in addition to errors of refraction
and accommodation, and the condition known as “ ocular insufficiency ”
(which have been already discussed at some length), the neurologist is
chiefly called upon to detect the following conditions: (1) Paralysis of the
eye muscles; (2) the Robertson pupil; (3) the condition known as “ hemi-
anopsia,” or, less correctly, “‘hemiopia;” (4) the condition of the retina
known as “choked disk;” (5) the conditions known as “amblyopia” and
“amaurosis.”
Paralysis of the Eye JMuscles.—The attitudes assumed by the
patient as a result of defective power in some of its muscles have been
discussed in the second portion of this chapter.
Hemianopsia.—This condition is characterized by a blindness of one
lateral half of each eye; the unaffected half of each eye retains its power
of sight. The forms of this condition that are observed, and the tests
employed to detect it, have been referred to already.
Choked disk.—This condition is also known as “neuro-retinitis,”
because the optic nerve and retina both participate in the changes that
ensue. It has been discussed already (page 150).
Robertson’s Pupil—This condition is characterized by extremely
small pupils that contract for the focusing of vision upon near objects
(within a radius of twenty feet), but do not respond to varying degrees
of light. The tests employed to determine this point have been pre-
viously mentioned in the second section of this chapter.
Amblyopia and Amaurosis.—These terms are commonly used to
cover all the various conditions of blindness where no organic changes
in the cye itself can be seen to account for them. The term “amblyopia”
is frequently used to denote a mild degree of “amaurosis.”
The more common causes of these two conditions comprise (1)
poisons, such as lead, tobacco, and urea; (2) exposure to a prolonged
glare, 1s in snow-blindness; (3) concussion of the eye; (4) irritation of
the fifth cranial nerve, as in severe neuralgia; (5) certain brain diseases.
THE SPECIAL SENSES. 209
The latter are of special interest in this connection. Several diagrams
incorporated in this work may prove of aid in explaining certain ana-
tomical points that bear directly upon the subject.
The following diagram (Fig. 69) shows that the optic nerve fibres
eventually pass to those regions of the gray matter on the surface of the
brain (the cerebral cortex) that are associated with the intelligent percep-
tion of the images focused upon the retina. But-it will be also observed that
the optic nerve fibres (a and 5) first pass through certain collections of
gray matter or “centres”? within the optic thalami and the corpora quad-
rigemina before they radiate to the so-called ‘visual area” of the con-
yolutions,
Let us now compare this diagram with another (Fig. 21), which will
make some of these statements more intelligible to the general reader.
VISUAL vei \
MEDULLA.
Fic. 69.—A DiaGram DESIGNED BY THE AUTHOR TO SHOW THE GENERAL COUKSE OF
Fisres IN THE ‘SENSORY’? AND “ Moron TRACTS’’ AND THEIR RELATION TO CERTAIN
Fascicuti OF THE Optic Nerve Tracts, (Modified from Seguin.) 5, Sensory tract in
posterior region of mesocephalon, extending to O and T, occipital and temporal lobes of
‘hemispheres: M, motor tract in basis cruris, extending to P and F, parietal and (part of)
frontal lobes of hemispheres; C Q, corpus quadrigeminum; O T, optic thalamus; N L,
nucleus lenticularis ; N C, nucleus caudatus; 1, the fibres forming the ‘tegmentum cruris’’
(Meynert); 2, the fibres forming the ‘basis cruris'’ (Meynert); @, fibres of the optic nerve
which become associated with the ‘‘ optic centre’ in the optic thalamus, and are subsequently
prolonged to the ‘visual area’ of the convolutions of the cerebrum ; 4, optic fibres which
join the cells of the “ corpora quadrigemina,”’ and are then prolonged to the visual area of the
‘cerebral cortex.
It will help to explain why it is that pressure upon the optic tracts, as
they are called, causes hemianopsia or blindness of one lateral balf of
each retina.
Tasre.—This special sense is presided over by the gustatory branch
of the fifth cranial nerve, the glosso-pharyngeal nerve, and the cherda
tympani branch of the facial nerve. Taste may be affected, therefore, by
any diseased condition that can cause either irritation or destruction of
14
210 LECTURES ON NERVOUS DISEASES,
the fibres of these nerves. Certain functional diseases, in contradis-
tinction to organic lesions of the brain, may also cause modifications of
taste.
An abnormal sensitiveness of taste is known as “hyperquesia.” It
may be developed in connection with hysteria; with melancholia and
some other types of insanity; and with facial paralysis of rheumatic
origin. Such subjects can often detect extremely small quantities of
sapid substances in solution, which in health would be unperceived.
They may perceive gustatory sensations when the electric current is
applied over the spine in the region of the neck or upper dorsal verte-
Inve. They may develop a loathing of certain dishes which have pre-
viously been their delight, from some imaginary taste of a disagreeable
character. Again, this condition may express itself in an unnatural
enjoyment of food. Finally, sweetish, sapid, or sour tastes within the
mouth may be constantly present.
A loss of the sense of taste is known as “aguesia.” It may be com-
plete or partial. Some regions of the tongue may be affected, and others
‘retain the sense of taste. In some instances, the tongue may be sensible
to certain substances, and insensible to others. -It may be associated
Fic. 70 —SEGUIN’s SURFACE THERMOMETER.
with a sense of burning and bitterness within the mouth, as in a case
reported by Béttcher, where a tumor at the base of the brain was its
exciting cause,
This abnormal state has, been observed to follow the development of
tumors of the brain or its coverings; paralysis of the fifth cranial nerve;
sclerosis of the medulla oblongata; injuries to the glosso-pharyngeal
nerves; atrophy of the nerves associated with taste; and ear disease
causing pressure upon the chorda tympani branch of the facial nerve.
Hearinc.—The mechanism of the ear is so complicated that defects
in hearing are commonly due to some abnormal condition of the ap-
paratus itself, rather than of the nerve of hearing or the brain. Perhaps
the most reliable test to determine the presence of the latter condition is
the employment of the tuning-fork. If this instrument be set in vibration
and applied to the teeth, or the bones of the skull, the transmission of
the sound-waves through the bones will enable them to reach the nerve
filaments of the internal ear, and afford the patient perceptions of sound.
If the patient is unable to perecive sound when thus conducted to the
verve filaments, it is strongly suggestive of some diseased condition
within the eavity of the skull.
CEREBRAL THERMOMETRY. 211
CEREBRAL THERMOMETRY.
Within a few years much attention has been given to the temperature
of limited portions of the skull in health and disease (Broca, Hammond,
Seguin, Amidon, Gray, and others). Many forms of instruments may be
employed for this purpose. Probably the simplest and least expensive is
the surface thermometer devised by Seguin, which has « large flattened
bulb well adapted to insure close contact with the scalp. Any number
of such thermometers may be fastened to a shaven scalp by means of per-
forated straps (Gray) or an India-rubber cap similarly perforated. The
effect of the temperature of the air upon the mercury may be avoided
by coating the parts not in contact with the scalp with shellac.
Fic. 71.—THERMOo-xLECTRIC DIFFERENTIAL CALORIMETER.—Connect the two thermostats as
shown in figure, viz.: connect by means of one of the metal tipped cords one binding-post of
each of the thermo-piles to the two binding-posts on base of the galvanometer. Then con-
nect the two remaining posts, one on each of the thermo-piles with each other, After so
doing, place the thumb on the face of one of the thermo-piles and observe the direction of the
deflection of the galvanometer needle, then place thumb on face of the other thermo-pile,
leaving the first uncovered, and, if the deflection is in the opposite direction to that first ob-
tained, the instruments are properly connected. If, however, the second deflection is in
same direction as obtained by pressing thumb on first thermo-pile, disconnect the two cords
from either thermo-pile and interchange them, viz.: take cord from right-hand post and
place in left, and cord from left post and place in right-hand post; the deflections will then
be as first alluded to, one pile turning needle in one direction and the other in the opposite
direction.
More delicate tests of temperature may be obtained by the thermo-
electric calorimeter devised hy Lombard. One or two minutes is only
required by this instrument to detect variations in the temperature of
homologous regions of the scalp, but it is expensive and only available
for use in the office.
212 LECTURES ON NERVOUS DISEASES.
It is essential that two thermometers at least be employed when the
thermometry of the scalp is being tested, in order that the temperature
of homologous parts of the two hemispheres may be simultaneously taken,
thus insurine the same conditions of vascular supply. A comparison
should always be made between the results so obtained, before any
clinical deductions can be drawn from them.
The temperature of the scalp seems to be somewhat below the
normal standard of health (98.5° Fahr.) in all of its parts.
Amidon has shown that willed muscular movements if continued for
some time are associated with an increase of heat over the cortical centres
which are called into action. He has thus confirmed some of the dedue-
tions obtained by physiological experiments upon animals. Gray and
Mills report the diagnosis of a tumor of the brain by the detection of a
localized elevation of temperature over the area involved. The differ-
ence between the healthy and unhealthy side was about one degree and a
half. Hamilton reports a case where a difference of three degrees ex-
isted, and persisted at repeated examinations; the case was living at the
date of this statement, so that the diagnosis of tumor had not been posi-
Fic, 72.—Ducuenne’s TROCHAR. a, Open; 4, closed.
tively verified, From my own experience, I am led to believe that an
unilateral deviation of one and a half or two degrees above or below the
normal point, within a circumscribed area of the scalp, which is per-
sistent and unattended with as marked a rise or fall in temperature in
adjacent areas, must be regarded asa valuable diagnostic symptom of
disease within that area. If it be a cerebral tumor, I should expect to
find by the ophthalmoscope the characteristic evidences of nenro-retinitis,
known as the “choked disk.”
Sometimes it is very important to decide as to the existence of or-
ganic changes in the muscular tissue of different parts of the body. By
means of this very ingenious and useful instrument we are enabled to
extract with little pain, and no danger, small pieces of any muscle which
can be examined microscopically at your leisure. This instrument is
introduced (with the slide open) into the substance of the muscle; sub-
sequently the slide is closed and the instrument is then withdrawn, A
small piece of the muscle will be found to have been removed and re-
tained within the instrument.
CEREBRAL THERMOMETRY. 213
In closing this chapter, the author feels that he has perhaps over-
taxed the patience of his readers. If he has erred in this direction, it is
because he has endeavored to cover a large field within the limited com-
pass of a single chapter, and to so interpret the symptoms of nervous
diseases as to bring them within the grasp of the general practitioner of
medicine. It must not be inferred that all of the tests described are of
necessity demanded in each individual case that is brought to the notice
of the neurologist. As Gower happily remarks, ‘To know our enemy is,
if not ‘half the battle,’ at least an important part of it.” When once the
symptoms of nervous
io
a ace
r
(
=
a a
{
He
Fig. 91.—DraGram ILLUSTRATING THE RELATIONS OF THE NERVE-FIBRE TRACTS IN THE
Spina Corp.—The section is supposed to be taken transversely through the lower part of
the cervical enlargement (slightly modified from Flechsig): A, Anterior median fissure ;
B, posterior median fissure; C, intermediate fissure; D, anterior gray cornu; E, posterior
gray cornu; F, gray commissure, with central canal; G, “uncrossed pyramidal tract (Flech-
* sig), or column of Tiirck; H, fundamental part of the anterior column (anterior root-zones
Charcot and his pupils) ; 1, anterior part of lateral column; Kk, crossed pyramidal tract
of lateral column; L, direct tract from lateral column to cerebellum ; M, column of Burdach,
posterior root-zones “of Charcot and his pupils; N, column of Goll: S, sensory tract of
Gowers. The posterior columns of descriptive anatomy include the fields M and N extending
on the surface from Bto R. The antero-lateral columns extend on the surface from R to A.
Their anterior division includes the fields G and H; their lateral division, the fields K, L,
and!. Similar colors are supposed to indicate in this plate a similarity of function.
4. Trophic and vaso-motor filaments. These connect the cells of
the cord (by means of the spinal nerve-roots) with the blood-vessels and
the organs related to motion and sensation.
We can therefore draw the following conclusions, which bear upon
diagnosis :—
Interference with the function of the first and second of these
352 LECTURES ON NERVOUS DISEASES.
groups of spinal fibres will result in a disturbance (more or less pro-
found) of the patient’s capabilities either of motion or of perceiving and
recording sensory impressions of various kinds (those of touch, pain,
temperature, muscular sense, and electrical stimulation).
Destruction of the third group of fibres will cause symptoms of
incodrdination of movement.
Impairment of the functions of the fourth group may create abnor-
malities in the calibre of blood-vessels, and an unhealthy state of the
skin, hair, nails, muscles, ete. The etiects of spinal lesions upon the
pupil (p. 411) are probably attributable to the vaso-motor fibres,
The arrangement of the cells and fibres of the spinal cord are very
clearly shown, from a physiological standpoint, in a table which I have
prepared (p. 355). It is somewhat similar to one lately published by
M. A. Starr.
It is well to know that there are certain symptoms which are pecu-
liarly apt to be encountered in connection with spinal diseases. These
may be separately discussed with advantage to the reader prior to the
description of the separate Cliseases.
It is also important that a beginner in this field of diagnosis
should grasp certain general axioms that will materially aid him in
discriminating between focal or systematic spinal lesions which may be
creating an impairment of the functions of one or more of the groups of
fibres just described or the horns of the spinal gray matter.
The following paragraphs and table may possibly shed some light
upon the diagnosis of spinal diseases :—
1. CONTRACTURE OF MUSCLES, when present in a case afflicted with
paresis or paralysis, points strongly to a lesion of the motor fibres in the
lateral column of the same side (the “crossed pyramidal fibres”).
2. EXAGGERATION OF TIIE TENDON-REFLEXES is a symptom which
points to the same conclusion.
3. RAPID ATROPHY OF MUSCLES (either as an independent affection or
as a sequel to paralysis) points to a diseased condition of the cells of the
anterior horn of the spinal gray substance. A piece of muscle (when
bitten out by means of Duchenne’s trocha and subjected to a micro-
scopical examination) will quickly show whether atrophy is occurring
as a result simply of disuse or of organic disease of the nervous
mechanism.
4. ABNORMAL SENSORY PHENOMENA (such for example as pain, hyper-
xsthesia, smeusthesia, analgesia, formication, numbness, tingling, etc.)
point to the existence of a lesion which affects either the posterior
nerve-roots or the esthesodic portions of the cord (p. 98).
5. DIMINUTION OR ABOLITION OF THE REFLEXES (p. 96) points to lesion
which affects a reflex-are (Fig. 95).
DISEASES OF THE SPINAL
CORD.
303
A Tasie or Some or tHE More Important Diacnostic SyMProMs OF SPINAL Lestons.
PART OF,SPINAL CORD
AFFECTED.
CoNTRACTURE (tonic
shortening of muscle,
of a persistent type).
Arropuy oF MuscLes
(due to fatty degen-
eration of the sarcous
elements).
EXAGGERATED RE-
FLEXES.
Diuinution orn ABO-
LITION oF SPINAL
REFLEXES.
Tropuic DisruRBANCES.
ABNORMAL SENSORY
PHENOMENA.
( (1) Generally due to an im-
| pheation of the ‘crossed-
pyramidal fascicult” (Fig.
32
(2) day possibly follow (?)
implication of the fibres of
Turck’s column (Fig. 32).
(1) Is generally due to a
esion confined to the cells
of the anterior horn.
(2) It may follow a severance
of the motor fibres which
compose the anterior nerve-
L roots.
Occurs from implication of
the motor bundles of the
lateral column, as a rule.
(1) Usually occurs with
esions of the posterior
columns of the cord (loco-
motor ataxia).
(2) Lesion of the posterior
nerve-roots may also cause
| this symptom.
( Lesions of the gray substance
of the cord are particularly
liable to cause symptoms
of this variety.
(1) May indicate either an
arritative or a destructive
lesion of the cord.
(2) The posterior columns or
posterior nerve-roots are
enerally involved.
(3) The posterior horns of
spinal gray substance may
be implicated. .
L
|
|
ONSET.
(1) May occur simultaneous
with paresis or paralysis
(primary contracture),
(2) May follow paralysis of
motion (post-paralytic con-
tracture), if the lateral scle-
rosisis asecondary affection.
(1) Rapid, and preceded by
motor paralysis, if the lesion
be an inflammatory or trau-
matic one.
(2) Slow, and not associated
with motor paralysis, if the
lesion be ae degenerative
kind (progressive muscular
atrophy).
When complete paralysis of
motion exists in a limb, this
test cannot be employed.
(1) Usually occurs indepen-
dently of motor impairment.
(2) Abnormal sensory phe-
nomena generally coexist
with it.
Are apt to accompany symp-
toms of vesical or rectal
impairment (myelitis).
(1) May develop slowly or
ramdly. ;
" Are often accompanied
ry inco-urdination of move-
ment, or trophic disturb-
ances, or impairment of the
bladder or rectum.
(2) Spinal reflexes are apt to
e diminished or abolished.
Let us now examine some of the symptoms, which have been already
referred to, more in detail.
Moror Paratysis (of spinal origin) may assume one of four varieties:
(1) Hemiplegia—where one lateral half of the body is affected with
motor paralysis.
(2) Paraplegia—where the lower half of the body is affected with
motor paralysis.
(3) Hemi-paraplegia—where the lower half of one lateral half of
the body is affected with paralysis of motion.
23
LECTURES ON NERVOUS DISEASES.
(4) Paralysis of special nerve-roots (spinal-nerve paralysis).
1
Fic. 92.—A DIAGRAMMATIC
REPRESENTATION OF THE
SgeconpDary EFFECTS OF A
LESION OF THE ENTIRE
SPINAL CorD_ ar (5),
(After Erb.) Note the as-
cending degencration of
the sexsory tracts in sec-
tions 4, 3,2 and 1; and the
descending degeneration
in the motor tracts in sec-
tions 6, 7 and 8,
The SENSORY PHENOMENA, which may be pro-
duced by lesions of the spinal cord, or of the posterior
nerve-roots, include the following :—
(1) Pain—usually of a. peculiar kind (see loco-
motor ataxia, and the various focal lesions of the cord),
(2) Hyperesthesia, or increased sensibility of parts.
(3) Numbness, or a sense of tingling (as if “the
part. were asleep”’).
(4) Sense of culdness or of heat in some part of
the body.
(5) Anesthesia, or loss of sensibility. It may be
complete or partial and be limited to the apprecia-
tion of pain, touch, or temperature by the patient.
(6) Delayed sensation (see locomotor ataxia).
(1) Formication, or a feeling likened to the
crawling of ants over the body.
Among the remaining symptoms which are of value
in the diagnosis of spinal lesions may be mentioned :—
(1) Incoérdination of muscular movements.
(2) Diminution, abolition, or increase of the spinal
reflexes (see Section II of this volume).
(3) Abnormal — electro-muscular
Section IT).
(4) Contracture of muscles—often preceded by
stiffness (see lateral spinal sclerosis).
(5) Atrophy of muscles (see poliomyelitis and
progressive muscular atrophy).
(6) Vaso-motor phenomena (see myelitis, ataxia,
etc.).
(7) Symptoms which are indicative of destruction
or wrritation of some of the special physiological cen-
tres of the spinal cord (see focal lesions of the cord).
(8) Lremor or some other form of spasmodic
movement.
Fig. 67 exhibits in a diagrammatic way several
of the above-mentioned abnormal conditions which
may coexist as a result of an unilateral lesion of
the dorsal segments of the spinal cord. It will
serve to aid the reader in mastering the statements
made in subsequent pages,—chiefly those which
refer to the symptomatology of focal spinal lesions.
The methods which should be followed in dnves-
reactions (see
DISEASES OF THE SPINAL CORD.
300
tigating each of the above-mentioned symptoms (prior to a diagnosis) have
been fully described in Section II., to which the reader is referred.
Before we pass to the consideration of the separate spinal diseases,
I would call attention to a carefully prepared summary of the functions
of special spinal segments, which differs but slightly from one compiled
and tabulated by Starr.*
table of Gowers (p. 90), as each will explain the other.
It should be compared with the diagram and
A TABLE SHOWING THE ARCHITECTURE AND FUNCTIONS OF THE VARIOUS
COMPONENT PARTS OF A SPINAL SEGMENT.
r
1, ‘ANTERIOR MEDIAN COLUMN.” (‘' Tiirek’s
column’ — direct pyramidal column,” )
2.
“ANTERIOR ROOT-ZONE.”
umn.«)
(Anterior col-
(a) Un-named
portion.
3. LATERAL COLUMN (con-
sisting of three subdivi-
sions).
(b) “Crossed
pyramidal col-
UA wamnn.”*
THE WHITE
MATTER OF
THE CORD.
(c) “Direet cere-
L bellar column.”
4d. “ PosTERO-LATERAL COLUMN.” (“Column
of Burdach’—“ posterior root-zone” — SLUS-
ciculus cuneatus’? — postero-external col-
uinn.)
Ny, “Column
5. “\POSTERO-MEDIAN COLUMN, (‘Co
of Goll’— fasciculus gracitis” — “ postero-
internal column.”’)
!
|
|
Fibres of conduction of
Motor fibres from the
“motor area” of the
cerebral hemisphere
of the same side (figs.
5 and 29).
(1) Fibres of associa-
tion between differ-
ent segments of the
spinal cord (vertical
in direction).
(2) Motor fibres passing
from the cells of the
anterior horn of the
spinal gray matter in-
to the anterior nerve-
roots (horizontal in
direction),
(1) Associating fibres
etween spinal seg-
ments.
(2) Fibres of the sensory
tract of Gowers (°).
(3) Vaso-motor sibres(?).
(1) Motor fibres from
the ‘‘motor area” of
the opposite cerebrul
hemisphere (vertical
in direction).
(2) Fibres passing from
the cells of the col-
umn of Clarke to form
the direct cerebellar
column (horizontal in
direction).
Fibres passing from the
cells of Clarke’s col-
umn to the cerebel-
lum. The “vegeta-
tine-tract” of Starr.
(1) Sensory fibres from
posterior nerve-roots
to spinal cells (except
those associated with
the ‘superficial’ or
“skin reflexes’) (hori-
zontal in direction).
(2) Associating fibres
between spinal seg-
ments (vertical in di-
rection).
3) Fibres of conduc-
tion of sensations of
touch and the museu-
lar sense, from the
arms and neck, up-
ward (vertical in di-
rection).
sensations of touch
and the muscular
sense, from the legs
and lower half of the
trunk, upward.
* Am. Jour. Neurol. and Psychiatry, November, 1884.
306 LECTURES ON NERVOUS DISEASES.
A TABLE SHOWING THE ARCHITECTURE AND FUNCTIONS OF THE VARIOUS
COMPONENT PARTS OF A SPINAL SEGMENT (continued).
fi
(
(2) Lateral groups in the extension of the limbs
(possessed by all verte-
brates).
a.
1) Mesial group of cells. Presiding over flexion and
cervical and lumbar en-
largements.
Presiding over move-
ments of the hand and
fingers(peculiar to man)
and the act of walking
erect.
Motor cells, whose peculiar functions are not deter-
mined.
d. Trophic centres for the motor nerves and the muscles
supplied by them. ;
e. Motor mechanism necessary to spinal automatism and
zB. L reflex spinal action.
THE GRAY (a. Anterior part. Trophic centres for the skeleton.
. 1) Trophic centres for the skin
pa aro i CELLSOF THE | y Posterior purt. f ae pindder, joints. ?
THE CORD. CENTRAL 4 (2) Vaso-motor centres.
GRAY ec. Automatic centres of a complex nature, and the asso-
MATTER. ciating fibres necessary to their peculiar functions
L (sexual, vesical, rectal, cilio-spinal, etc).
Trophic centres for sensory conducting-tracts.
Paths of conduction of sensations of pain, and tem-
perature from all parts below. :
ce. Clarke's column of cells (vesicular column) which are
CELLS ORTH apparently associated with the fibres of the “direct
POSTERIOR « cerebellar column.”
lL FIORE: d. Posterior group of cells; related to sensations of all
kinds.
The sensory mechanism necessary to spinal automatism
and spinal reflex action.
(2) Central group of cells
in the cervical and lum-
{
(1) Middle group of cells.
{ bar enlargements.
ANTERIOR 7
CELLS OF THE b.
Horn.
a
rP
The size of the multipolar cells of the anterior horns seems to depend upon two factors:
(1) the size of the muscle supplied by the cell, and (2) the length of the nerve-fibre which
connects the cell with the muscle (Spitzka).
We are now prepared to discuss the separate lesions enumerated in
the table of diseases of the spinal cord. The scattered hints which have
been already given in a previous section will possibly help us to grasp
the salient features of each, and their physiological interpretation.
In examining a case of paralysis of spinal origin, the following points
should be ascertained with great care :—
(1) The area of distribution of the paralysis (be it sensory or motor
in character). ,
(2) The degree of the paralysis; by separately testing the motor
power of different sets of muscles, and also the skin for sensory paralysis
by means of the esthesiometer.
(3) The state of nutrition of the paralyzed muscles (see pages which
treat. of poliomyelitis and progressive muscular atrophy).
(4) The electrical reactions of the paralyzed muscles; noting all
abnormal formule and the intensity of the current required to produce
muscular contraction (see section on electricity).
(5) The presence or absence of rigidity in the paralyzed muscles
(see pages which discuss sclerosis of lateral columns).
(6) The condition of the superficial and deep spinal reflexes of the
two sides. These have been discussed in Section IT.
SCLEROSIS OF THE ANTERIOR COLUMNS. 357
(7) The presence or absence of symptoms of incodrdination of
muscular movements (see locomotor ataxia),
SCLEROSIS OF THE ANTERIOR COLUMNS.
The anterior columns of the cord are frequently called “the columns
of Tiirek” and “the direct pyramidal fasciculi.”
The first of these names was given in honor of a distinguished
pioneer in pathological research relating to spinal lesions. The latter is
employed because the bundles which compose these columns pass directly
from the hemisphere of the cerebrum to the ultimate spinal seements
without decussating in the medulla,—the anterior pyramids of which they
help to form.
Several diagrams have been introduced in Section I of this volume
to illustrate the formation of these columns; as well as their physiologi-
cal association with the motor bundles of the opposite lateral column of
the cord (see Figs. 29 and 82).
Morbid Anatomy.—Sclerosis of these bundles of nerve fibres usually
coexists with similar changes in those which compose a part of the lateral
column of the cord,—the so-called “ crossed pyramidal fasciculi.” It may
occasionally exist as an independent lesion; but it usually follows the
development of some brain or cord lesion and travels downward. It is
then unilateral. The symptoms which are peculiarly characteristic of
its development are unknown. Its existence is to be inferred when
secondary sclerosis of the postero-lateral columns is manifested by
symptoms which are clinically well determined. The pathological changes
of sclerosis of the cord do not differ from those of that condition else-
where. They have been described in the preceding chapter, in connection
with the brain.
The discovery, made by Flechsig, that the relative proportion of the
direct and decussating pyramidal fibres differs in individuals, helps us
to properly interpret those rare cases where a lesion of the cerebral
hemisphere has been known to produce a hemiplegia of the same side
_ (instead of the opposed side); as well as those cases of greater frequency
where a paresis of the corresponding side coexists with a hemiplegia
of the side opposed to the cerebral lesion. In one case in sixty, no
decussation of the pyramidal tracts occurs.
SCLEROSIS OF THE MOTOR FIBRES OF THE LATERAL COLUMN.
(Lateral Spinal Sclerosis—Tetanoid Paraplegia—Spastic
Paralysis—Spasmodic Tabes.)
Within the lateral columns of the cord, we encounter a bundle of
motor fibres which decussate anteriorly in the medulla at its lowest
part. They are, therefore, associated with the opposite cerebral hemis-
358 LECTURES ON NERVOUS DISEASES.
phere. These fibres occupy only a portion of each lateral column, and
lie adjacent to the posterior horn of the spinal gray matter. They are
known as the “ crossed pyramidal ” fibres. They are separated from the
periphery of the spinal cord (in some of the spinal segments, although
MOTOR FIBRES
OF LATERAL COLUMN
mu
MUSCLES | | |
CONTROLLED BY |
EACH SPINAL | 1
Tee bh
1]
|
CELLS OF THE
ANTERIOR HORNS
OF SUCCESSIVE
SPINAL SEGMENTS
Fic. 93.—A DIAGRAM DESIGNED BY THE AUTHOR TO SHOW THE DISTRIBUTION OF THE
** CROSSED PYRAMIDAL FIBRES’’ (OF ONE SIDE) TO THE CELLS OF THE ANTERIOR HORN
or Successive SpinAL SzeGments.—Note that the motor fibres of the lateral column can
act upon the muscles only indirectly (through the cells of the anterior horn); also that each
segment of the cord receives from the lateral column certain fibres which put the muscles
associated with that particular segment in the circuit of cerebral influence (volition). In
this diagram, the circles represent groups of cells,and not a single cell. Eachred fibre
represents a dundle of fibmes having similar termination. The blue lines represent bundles
of motor fibres, which form the anterior nerve-root of successive spinal segments. The
terminal muscles (in red) represent the ex¢/re group controlled by each spinal segment,—
not individual muscles. Figs. 19 and 32 will help to further interpret this diagram. ‘Ihis
diagram illustrates the reason why the motor columns of the spinal cord grow smaller in size
as they reach the terminal segment.
not so in all) by the so-called “direct cerebellar column.” (Fig. 19.)
The size of this motor bundle decreases gradually (by the giving off of
fibres to the various spinal segments) from the cervical enlargement of
the cord till it ends in the lumbar enlargement.
Morbid Anatomy.—Sclerosis of this tract may exist as a-primary
disease; and also as a secondary result, occasioned by the development
of a lesion higher up in a cerebro-spinal axis.
SCLEROSIS OF MOTOR FIBRES OF LATERAL COLUMN. 309
When the disease is of the primary variety, sclerosis is usually
found on both sides of the cord in the lateral column. When it is of the
secondary variety, the sclerotic process in the cord (if due to a cerebral
lesion) is usually detected in the lateral column of one side and the
anterior column of the opposite side. Fig. 32 will make the reason of this
fact apparent to the reader.
In some cases, sclerosis of the posterior columns and the morbid
changes of poliomyelitis anterior may coexist with lateral spinal sclerosis.
Whether this is due to an extension of the morbid process or not is
as yet not thoroughly determined.
Etiology.—Sclerosis of this tract of fibres, when it occurs as a
primary aftection, is rarely encountered before the twentieth or after
the fiftieth year of age. It may follow exposure to cold or dampness
and injuries of various kinds. In many cases, its causation is very
obscure. Some authors believe that it starts as a transverse myelitis.
The secondary variety occurs as the result of any morbid process
which tends to cut off the fibres of the so-called “ motor tracts ” from
their trophic centres in the motor area of the brain. It is commonly
known, therefore, as “ secondary degeneration ” of the spinal cord. We
are apt to encounter this condition as a sequel to any form of cerebral
disease which affects the motor fibres or “ will-tract.” It may also be
due to any spinal lesion which has involved the motor fibres of the
cord above the seat of the sclerosis.
Secondary degeneration of nerve fibres travels, as a rule, in the
direction of the impulses conveyed by the fibres affected (downward in
the motor, and upward in the sensory bundles).
PRIMARY LATERAL SCLEROSIS.
(Primary Spastic Paraplegia— Tetanoid Paraplegia.)
This condition is usually present upon both sides of the spinal cord.
It is most frequently encountered in adults between the ages of thirty
and fifty, although it may exist in children. It seems to be more fre-
quent among males than females, and to attack individuals in apparently
robust health. It has been suggested that any excessive muscular exer-
cise or strain may predispose to its development. Among children, this
form of paralysis may be traced, apparently, in some instances, to an
Injury received upon the spinal column, to the head during birth, or to
some congenital defect in the development of the motor apparatus.
In the opinion of Bramwell, lateral sclerosis of the primary variety
is very rarely observed. He attributes the frequency of those cases
(which are usually considered as of the primary type) to a transverse
myelitis unassociated with disturbances of sensation, and usually present
360 LECTURES ON NERVOUS DISEASES.
in the dorsal segments of the spinal cord. In this view he is supported
by Leyden,
Irrespective of the relative frequency of this condition as a primary
disease or its etiology, the bilateral character of its symptoms is in
marked contrast to the unilateral character of the form which is com-
monly regarded as secondary.
Symptoms.—In this form of spinal sclerosis, the patient is attacked
by a paresis of a progressive character. This develops slowly and
attacks, as a rule, the lower limb of both sides simultaneously. Subse-
quently the upper limbs may exhibit similar symptoms. There is in
almost every case a marked increase of the spinal reflexes. The paralyzed
muscles tend to become rigid to a greater or less extent when sitting, rising
or walking. This accounts for peculiarities in the gait of these patients.
No evidences of atrophy in the paralyzed muscles, more than would
be accounted for by disuse, are observed. Sensation is preserved in the
affected limbs, and there are few if any well-pronounced clinical evidences
of disturbed sensory functions. Pain is infrequent, there is little numb-
ness, tingling, or other subjective phenomena, and the viscera of the
pelvis are not usually affected, as they are liable to be in myelitis.
The stiffness in the legs which accompanies the development of
paresis compels the patient to use two canes early in the disease when
attempts at walking are made. Subsequently crutches, and possibly an
attendant, are rendered necessary. The patient moves with the most
extreme difficulty. When an advance step is made the feet appear to he
glued to the ground, and are scraped or dragged alone rather than lifted.
The pelvis and the limb asa whole is lifted in order to allow of the scraping
of the foot forward, because little if any flexion is made at the knee.
The knees frequently tend to become locked together during the act
of walking, because the foot is apt to cross its fellow as it is brought
forward. This is an evidence of spasm of the adductor muscles.
As a rule, these patients are inclined to stand upon the toes, rather
than on the entire sole of the foot, when walking.
Occasionally the muscles of the calf are affected with spasm during
attempts at walking, and the foot is then suddenly raised from the
ground irrespective of the will of the patient (hopping gait). This pecu-
liarity in gait closely resembles that of a horse when affected with what
is known as the “string-halt.” Again, the patient may be lifted suddenly
upon the toes when endeavoring to walk, by contraction of the extensor
muscles acting upon the foot.
A peculiar attitude of the back and chest is observed as the patient
leans heavily first on one cane and then on the other in order to raise
the weight of his body hy the arms. The dack is strongly arched and
the chest is thrown very much forward.
SECONDARY LATERAL SCLEROSIS. 361
Whenever the muscles are manipulated they become more or less
tense and rigid. This is due to the fact that the spinal reflexes are very
much. exaggerated in this disease.
The knee-jerk is markedly intensified and an “ankle-clonus” can
gencrally be elicited. Sometimes a blow upon the patella-tendon causes
a response in the opposite limb. This is known as “vadialion of the
reflex.”
The superficial reflexes are sometimes decreased or abolished; but
in exceptional instances they may be exaggerated.
The tests employed to determine the condition of the spinal reflexes
have been already described in the second section of this work.
After a lapse of several months or years, these patients are obliged
to remain in bed from an inability to walk. The legs then tend to
remain stiffly extended; and the thighs are closely approximated, as the
result of spasm of the adductor muscles. The feet are usually inverted.
Ultimately, the upper extremities may become affected with contracture,
in which case flexion predominates over extension.
The electrical reactions of the affected muscle are normal or slightly
decreased. Those of the nerves may be diminished, both to the fnradaic
and galvanic currents.
Cerebral complications are rarely if ever developed; the viscera are
apparently healthy ; and the pelvic organs are not, as a rule, affected.
In somewhat rare instances, one leg alone, or one leg and one arm
may be attacked. Such cases are to be diagnosed from. hemiplegia or
monoplegia of cerebral origin.
Diagnosis.—This condition is to be distinguished from the secondary
form of lateral sclerosis; from poliomyelitis; from amyotrophic lateral
sclerosis; and from focal lesions of the spinal cord. A subsequent
table (p. 364) will make the points of discrimination more apparent than a
verbal description.
SECONDARY LATERAL SCLEROSIS.
(Descending Spinal Sclerosis.)
This morbid condition is due to a degeneration of the motor fibres
of the cord from any cause which tends to separate them from their
trophic centres (which are situated within the cortical motor centres of
the cerebrum). Whenever a nerve fibre is separated from its trophic cell,
it tends, with few exceptions, to degenerate in the direction of the
impulses which it is designed to transmit. Hence motor fibres usually
exhibit under such circumstances a progressive degeneration downward,
and the sensory fibres a similar alteration in an wpward direction.
The CEREBRAL LESIONS which are liable to produce this form of spinal
disease may affect one of the following parts: (1) those convolutions of
the brain which are chiefly associated with motion; (2) the motor
LECTURES ON NERVOUS DISEASES.
bundles of the ‘corona radiata” or of the “internal capsule,” (3) the
Fic. 94.—A DIAGRAM DESIGNED Yo
ILLustRATE THE SECONDARY SCLE-
ROSIS WHICH WOULD FOLLOW A
Lesion or THE Lerr CEREBRAL
HemispHEre, (After ot Note
the involvement of the column of
‘Tiirck is seen on the left side in
sections 1, 2, 3, 4, 5 and 6 (where its
fibres end). That of the crossed
pyramidal tracts extends throughout
the entire length of the spinal cord.
caudate nucleus or lenticular nucleus; (4) the
crusta cruris; (5) the motor fibres of the
pons; or (6) the anterior pyramids of the
medulla, above the point of decussation of
the pyramidal fibres. Figs. 36 and 79 will
make this apparent to the reader.
Secondary degeneration of the spinal
fibres, which occurs after cerebral disease,
tends, 1s a rule, to progress downward both
in the column of Turck on the same side,
and in the lateral column of the opposite
side of the cord.
Although, in the majority of cases, this
results in a bilateral spinal lesion, the pre-
ponderance of the symptoms are due to the
sclerosis of the lateral columns. They are,
therefore, most marked upon the side of the
body which is opposed to the cerebral hemi-
sphere primarily attacked.
If, on the other hand, the primary lesion
is confined fo one side of the cord, secondary
sclerosis of the lateral column will occur only
below the level of the primary lesion on the
corresponding side of the cord.
Finally, when a transverse spinal lesion
which affects both sides of the cord exists,
or when a lesion of both cerebral hemi-
spheres or one which crosses the median line
cuts off both motor tracts, it may induce
secondary sclerosis of a descending charac-
ter in both of the lateral columns. In the
latter case, the symptoms exhibited hy the
patient during life would be of a markedly
hilateral type.
Secondary sclerosis produces, as a rule,
about the same train of symptoms as the
primary form, with the exception that the
symptoms are most marked upon one side;
provided they are not exclusively confined
to it.
Symptoms.—In this disease, paresis or
paralysis, contracture of muscle, and ez
SECONDARY LATERAL SCLEROSIS. 363
aggeration of the tendon reflewes are the chief symptoms which are to
be expected.
The paralysis or paresis precedes the de-
velopment of contracture. The paralytic symp-
toms are usually of a very marked character;
and they may have developed suddenly. The
pelvic organs sre liable, moreover, to be affected.
The skin, hair and nails may also exhibit
trophic disturbances.
All of these symptoms are usually observed
either upon one side only; or, if on both sides,
one will be more markedly affected than the
other. Whenever the exciting lesion is of a
bilateral type, the symptoms will be identical
with those described under the primary variety’.
Diagnosis.—This form of sclerosis is to be
distinguished chiefly from a chronic myelitis
which involves one lateral half of the spinal cord
in its anterior and lateral portions; and also
from those diseases which tend to produce a
gradual compression of the spinal cord, such as
meningitis, tumors, etc. It is far more frequent
than the primary variety; and cannot, as a rule,
he confounded with it. Moreover, the history of
the case will usually point toward some cerebral
or spinal lesion as its exciting cause. A sub-
sequent table will aid the reader in making the
necessary discriminations between it and other
spinal lesions which might be mistaken for it.
Something has already been said regarding
the discrimination of the primary and second-
ary forms of this disease from other spinal
affections. The chief diagnostic points by which
lateral spinal sclerosis can be distinguished from
all other spinal diseases (provided it be itself
uncomplicated) are: (1) the development of
paralysis with contractures and rigidity of the
muscles; (2) the absence of atrophy; and (8)
the marked increase in the tendon reflexes.
When no cerebral symptoms or those of a
on
Fic. 95.—A DiaGrammatic RE-
PRESENTATION OF THE CORD IN
MULTIPLE SPINAL SCLEROSIS.
(After Erb.) This condition,
as will be seen, affords a marked
contrast with systematic scle-
rosis shown in Figs.92 and 94.
lesion of the upper part of the cord (bulbar symptoms) have preceded
the development of the contractures and paresis, it is safe to infer that
the primary variety exists.
364
LECTURES ON NERVOUS DISEASES.
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INFLAMMATION OF CELLS OF ANTERIOR HORNS. 364
Prognosis —Cases of apparent recovery from this affection have
been recorded ; and in many instances a period of indefinite duration, in
which no advance of the symptoms takes place, seems to be developed.
I believe that a few cases may be cured by proper treatinent, and that
-ahnost all can be materially helped if seen sufliciently early.
When it results fatally, the nuclei of the medulla are usually first
atfected, thus producing the symptoms of the so-called “ glosso-labio-
laryngeal paralysis,” or Duchenne’s disease.
Treatment.—It is my custom to administer large doses of ergot to
these patients very early in the disease,—before the paresis or contract-
ures become very apparent. This drug alone will occasionally arrest
the disease, in my opinion.
To syphilitic patients in the active stage, or those who have been
infected with that discase at any time, I administer the treatment sug-
gested on page 291.
I usually employ the galvanic and static currents to the paralyzed
muscles from the onset ; and, as a tonic, I am in the habit of giving cod-
liver oil and quinine. he nitrate of silver in combination with the
extract of belladonna may prove of service. Hot water (as recom-
mended on page 248) has helped some of my caxes.
I am satisfied that I have obtained marked and permanent improve-
nent by the use of the cauwery and severe static sparks when applied on
each side of the spinous process of the vertebra and the contractured
muscles every other day, or less often, for several weeks consecutively.
The spasms may be relieved by daily hypodermic injections of
er. yi, of atropine to begin with, and gradually increasing the dose.
The eflicacy of static electricity (administered chiefly by the
“spark ”) in relieving contracture and spasm of muscles is now quite
well established to my mind. I have had quite an extended experience
with this agent; and I know of nothing that will give such immediate
relief. to patients so afflicted.
The great disadvantage which most static machines labor under (in
the hands of those who own them) is their lack of power. A machine
which gives but a feeble and thin spark is practically useless for medical
purposes. Personally, I cannot recommend revolving plates of less than
24 inches in diameter ; and several such plates are needed to generate the
quantity which is requisite to a satisfactory use of the induction machine.
INFLAMMATION OF THE CELLS OF THE ANTERIOR HORNS.
(Poliomyelitis Anterior, of Infants and Adults—Atrophic Spinal
Paralysis—Infantile Paralysis.)
This condition sometimes coexists with lateral sclerosis. It fre-
quently occurs, however, as an independent affection, especially during
childhood.
366 LECTURES ON NERVOUS DISEASES.
The cells of the anterior horns are affected by an inflammatory
process in this disease; which, if sufficiently severe, leads to their atrophy
or destruction.
Morbid Anatomy.—W hen these cells become inflamed, their function
is at once arrested; hence sudden paralysis is developed, provided the
inflammatory action be of the acute type. If the gray matter be so
affected beyond the possibility of recovery, acute pigmentary degenera-
tion of the cells so attacked apparently follows. The name poliomyelitis
Fie. 96.—PoLiomyvevitis ANTERIOR (ACUTE) FOLLOWED BY EXTENSIVE ATROPHY, CHIEFLY OF
tHE Ricut Sipe, (From a photograph in the possession of the author. )
(MtoALds, gray, and (LvEAdS, marrow) expresses the seat of the lesion, 2s
well as its inflammatory character.
Asa result of inflammatory and degenerative changes within the cells
of the anterior horns, the spinal nerve-fibres (which serve to connect the
inflamed cells with the muscles) degenerate as a result of defective nutri-
tion; and the muscles connected with those fibres also undergo rapid
fatty deeeneration and atrophy. The symptoms of this disease tend to
confirm the view that the eanelion-cells of the anterior horns preside not
only over muscular movement, but that they also serve to regulate the
nutrition of the muscles connected with them by means of the fibres which
INFLAMMATION OF CELLS OF ANTERIOR HORNS. 367
compose the anterior nerve-roots. It is believed hy some observers,
however, that some of the cells found in this locality have a peculiar
trophic function.
The inflammatory changes observed in the spinal cells during an
attack of poliomyelitis must not be confounded with a non-inflammatory
degeneration of the cells in the anterior horns. This is probably the spinal
cuuse of “ progressive muscular atrophy ” (in which there is no paralysis).
The changes observed in poliomyclitis anterior are commonly con-
fined to a few spinal segments. It is not uncommon for the horn of one
il WS QQ NY SVE S
Fic. 97—Back View or SamE CASE, SHOWING THE SO-CALLED “WinG-scaPpuLa” (xS-
PECIALLY ON RIGHT SIDE) FROM ATROPHY OF THE MUSCLES.
side to escape while the other is seriously involved. Whenever the
attack has been a severe: one, the anterior horn of the affected segments
will appear after death to be more or less distorted from atrophy of its
cells and the development of newly formed connective-tissue.
The form of paralysis which develops in any given case will be
modified by the spinal segments attacked; and also by the character of
the attack, whether unilateral or bilateral. One of my cases exhibited
an attack confined to the right horn of the cervical segments and the left
horn of the lumbar segments. He had paralysis and extensive atrophy
368 LECTURES ON NERVOUS DISEASES.
of the right arm and paralysis of the left leg, which passed away after a
lapse of a few weeks.
If the inflammatory process is not sufticiently severe to prevent the
recovery of the cells attacked, the spinal cord may exhibit no evidences
after death of destructive processes.
Etiology.—This disease is commonly deseribed as of three varieties,
—the acute, subacute, and chronic. It is more common in children than
in adults, although the chronic variety is less frequently observed during
childhood than the acute.
Fic. 98.—PRroFiLE VIEW OF SAME CASE, SHOWING ATROPHY OF DeLtoin REGION, THE
ALTERED POSITION OF THE RIGHT SCAPULA, AND THE WASTING OF THE Richt ARM.
The infantile variety has been known to follow exposure to cold or
dampness, overfatigue of the muscles, some forms of blood-poisoning
(such as eruptive fevers, diphtheria, lead-poisoning, etc.), dentition, and
traumatism. Some cases develop from imperfectly understood causes.
It generally occurs before the second year,—seldom later than the seventh
year. It is most common among boys.
The adult variety seems to be excited chiefly by exposure to cold or
dampness and overexertion. Lead-poisoning is said to sometimes excite
it. Debility, convaleseenee from fevers, malaria, pneumonia, etc., are
INFLAMMATION OF CELLS OF ANTERIOR HORNS. 369
mentioned by authors as among its factors of causation. It inay develop
between the ages of twenty and fifty years. One of my patients (Figs.
99 and 100) was so affected (after severe exertion and excessive in-
dulgence in alcohol) from sleeping on the ground during a summer
shower. The paralysis in this case attacked the muscles which were
chiefly employed by him in his occupation.
Symptoms.—The three forms of this disease will he described
separately, as they should be distinguished at the bedside.
Acute Form. (lnfantile Spinal Paralysis—Acute Spinal Paralysis of
Adults.) —The onset of this form is usually marked by a sudden elevation of
Fic. 99,—Pouromveitis ANTERIOR ACUTA, OCCURRING IN THE ADULT FROM SLEEPING ON
Wer Grounp. (From a photograph in the possession of the Author.) Note the extensive
atrophy of deltoid region, forearm, and hand.
temperature. The febrile symptoms may be either continued or remittent
intype. The fever may last from twenty-four hours to several days. It
is not uncommon to observe pains in the limbs, muscular twitchings,
tremors, convulsions, delirium, and occasionally a sense of numbness in
connection with the stage of fever.
Sudden paralysis of a marked character soon follows, and with ts
appearance the febrile symptoms disappear. The paralysis usually attains
its height at the onset.
The seat and type of the paralysis vary with the spinal segments
affected and with the character of the attack,—whether unilateral or
24
370 LECTURES ON NERVOUS DISEASES.
bilateral. All the Lmbs may he aifected in some cases. (Complete
paralysis.) Again, it may be confined to one lateral half of the
body. (demuplegia.) When the lesion is bilateral and confined to the
dorsal or lumbar segments, paraplegia may develop. Finally, if the
lesion be unilateral and confined to the cervical or lumbar seg-
ments, monoplegia may occur. I have personally reported an unique
case, where the right upper and left lower limb were simultaneously
paralyzed.
The paralysis of motion is usually quite complete at the onset. It is
not accompanied by any disturbances of the sensory function as a rule,
\i
Fic. 100.—Furt View oF sami CASE, SHOWING THE DEFORMITY AND ATROPHY OF Hanp.
(From a photograph in the possession of the Author. )
although a slight numbness may be complained of by the patient. The
pelvic organs are not affected.
In infants, the existence of paralysis may be overlooked. Sooner or
later, the nurse or mother may notice that the child does not move its
arm or leg. When this disease is suspected during infancy, the move-
ments of the limbs should he very carefully observed. Nurses are often
unjustly blamed by physicians as well as parents for the development of
paralysis in infants intrusted to their charge. The misfortune is in
many cases erroneously attributed to some blow or fall which the child
may have received. The fever which precedes the development of the
INFLAMMATION OF CELLS OF ANTERIOR HORNS. dtl
paralysis is, therefore, a very important and valuable point in the
diagnosis of this affection,
Soon after the onset of the paralysis, the affected muscles of the
limb (some usually escape) cease to respond to the faradaic current.
They also contract slowly and with abnormal formule when the galyanic
current is used (thus exhibiting evidences of nerve degeneration and
muscular degeneration. (Fig. 58.) Later on, they exhibit a marked
increase of galvanic excitability, with abnormal formule.
Whenever the cells are not sufliciently impaired to produce a
permanent arrest of their function, the paralyzed muscles begin in a
short time to show a return of power. In such.a case, the normal formule
of muscular reaction to galvanism returns, and faradaic currents begin
to cause muscular contraction.
After several weeks have elapsed, signs of atrophy will begin to be
apparent in those muscles whose cells have been most seriously injured.
In all such cases, the muscular atrophy is markedly progressive and
more or less permanent. If a piece of such a muscle be removed by
Duchenne’s trocha, evidences of extensive fatty degeneration could be
discerned under a microscope. This step is sometimes a valuable one in
making a diagnosis or a prognosis.
This variety is commonly described as “infantile spinal paralysis,”
because children are more often affected than adults. Nevertheless, it
is still encountered in adult life, but rarely in old age. Prévost and
Charcot were the first observers to discover the exact morbid changes
which occur in the anterior horn in this type of disease.
Subacute Form.—This is a rare type of disease, and never affects
children. It differs from the acute variety in the gradual onset of the
paralysis, the total absence of all cerebral symptoms, the presence of
only slight febrile symptoms, and the fact that it attacks adults
exclusively. It may closely resemble lead-paralysis and progressive
muscular atrophy.
Chronic Form.—A chronic type of inflammation confined to the
anterior horns causes symptoms which may closely resemble those of
multiple neuritis and “progressive muscular atrophy.” It is a com-
paratively rare form of disease. It may attack children or adults.
This condition may be recognized from the other forms of polio-
myelitis chietly by its chronicity. The presence of severe neuralgic pains
and other abnormal sensory phenomena, which exist for weeks or months
prior to the development of atrophic changes in the muscles, points
rather to multiple neuritis. The type of muscular atrophy which occurs
in this affection differs from that observed in progressive muscular
atrophy, in that it affects entire groups of muscles simultaneously. In
the latter disease, separate bundles in the affected muscles may be
372 LECTURES ON NERVOUS DISEASES.
destroyed, while others may remain unchanged. The reactions of the
affected muscles to the faradaic and galvanic currents are similar to
those of the acute variety.
Diagnosis.—Acute poliomyelitis in the infant may be mistaken for
lowie neuritis, progressive muscular atrophy, rickets, the wasting diseases
of childhood, pseudo-hypertrophic paralysis, hemiplegia from cerebral or
spinal lesions, and (during its initial stage) with the exanthemata or some
of the inflammatory disorders.
In the adult, the acute form might be confounded with multiple
neuritis, progressive muscular atrophy, amyotrophic lateral sclerosis,
hemipleyia, monoplegia, myelitis, and the subacute variety of polio-
myelitts.
It. does not seem to me possible for the reader to err in the recog-
nition of this affection, provided the essential facts pertaining to this
disease are firmly fixed in his memory.
It should be remembered that the acute form of the disease begins
with a stage of febrile excitement, which ceases in a short time; that —_.
paralysis develops suddenly, and reaches its height at once; that the
paralysis begins to improve ulmost immediately after its appearance;
that atrophy of some of the muscles previously paralyzed also begins
soon after the attack; that noe cerebral symptoms will have existed
previous to, during, after the attack; and that the child or adult has
usually been in perfect health up to the commencement of the disease.
The paralysis is at first generally extensive; but it soon becomes
limited to a greater or less extent. Rare exceptions to this rule have
been recorded, however, where the reverse has occurred. Atrophy of
the muscles follows the paralysis. There is usually a diminution of
reflex spinal irritability. Bed-sores do not ‘occur, nor are the bladder
and rectum affected. Disturbances of sensibility are absent, as a rule.
The distinctions between the acute, subacute, and chronic types of
poliomyelitis are those of degree rather than of kind. The respiratory
muscles are never involved in true spinal paralysis, according to Seguin.
In this respect he draws a line of distinction between the so-called
“acute ascending paralysis” and poliomyelitis. To my mind_ this
clinical distinction is questionable.
From progressive muscular atrophy acute poliomyelitis is to be
distinguished hy the rapid development of the paralysis, the febrile
stage which precedes its development, its appearance before the seventh
year of age, and the fact that the faradaic current fails to create a
response in the paralyzed muscles; whereas in progressive muscular
atrophy the uninvolved fibres of the affected muscles respond to
faradaism. The insidious advent of progressive muscular atrophy and
the effects of electric tests (p. 189) would decide between it and
INFLAMMATION OF CELLS OF ANTERIOR HORNS. B73
poliomyelitis in the adult. Furthermore, by means of Duchenne’s
trochar (p. 212), the fibres of the muscles attacked may be examined
microscopically.
Pseudo-hypertrophic paralysis can be easily distinguished from
poliomyelitis by the absence of a febrile stage, the increase in size of
Fics. 101 and 102.—A_Casr of INFANTILE PARALYSIS, WITH INVOLVEMENT OF THE MEDUL-
Lary Nucrer (From two photographs in the possession of the Author), The deformity of
the left side of the patient and the facial atrophy of the left side is wellshown. Several years
had elapsed between the date of the attack and the taking of the photographs.
the muscles, the locality affected, the normal electro-muscular phenomena,
the characteristic gait (p. 164), the late development of symptoms in the
extremities, the peculiar curve of the vertebral column, and the micro-
scopical examination of the muscles.
Rickets never produce paralysis, alterations in the normal electro-
muscular reactions, nor a stage of well-marked fever.
old LECTURES ON NERVOUS DISEASES.
Hemiplegia vf cerebral origin can be diagnosed from poliomyelitis
by the history of the case, the presence of symptoms of impairment
of the intellect or speech, by paralysis of some of the cranial nerves,
the development of hemiplegia and hemianesthesia upon the same
side [if the lesion be non-cortical (p. 72)], the presence of normal electro-
muscular formule, the absence of a febrile stage, and abnormalities in
the pupil.
Myelitis commonly causes more or less trophic disturbances; but it
is very liable to create symptoms referable to the genito-urinary tract
as complications, and to present all forms of combinations of motor and
sensory symptoms, which do not exist in poliomyelitis.
Some other points in the differential diagnosis of this affection have
been given in a table when discussing sclerosis of the lateral column of
the cord. (P. 364).
The condition of multiple neuritis has been very frequently mistaken
for poliomyelitis. There seems to be little, if any, doubt that many
cases reported in the past by authors of note as those of poliomyelitis,
were improperly classed.
The development of abnormal sensory phenomena, such as pain,
anesthesia, parasthesiw, etc., in connection with motor disturbances and
muscular atrophy, should always lead to the suspicion of the existence
of multiple neuritis.
Prognosis.—In cases afflicted with poliomyelitis, partial or complete
recovery usually takes place. Some of the muscles may undergo per-
manent atrophy. Deformities muy ensue from -post-paralytic contracture,
in some cases. As arule, the electro-muscular phenomena return to the
normal standard in the muscles which are the least affected. The power
of motion is regained with greater or less rapidity and completeness ;
and the reflexes tend to return to the condition of health. If the muscles
continue to respond at all to the faradaie current during the height of
the attack, it is safe to predict a total recovery. I have never seen a
muscle undergo permanent atrophy when it constantly preserved even a
trace of faradaic excitability. Ifthe disease creates interference with the
action of the respiratory nerves, it is possible for a fatal termination to
take place. Happily, such instances are uncommon,
Treatment.—There exists experimental as well as clinical evidence
to show that a regeneration of the cord may sometimes take place after
a scrious injury. Hence we are justified in devoting particular care and
attention to the medicinal and mechanical treatment of the peripheral
manifestations of spinal disease with the hope that the cord itself may
he stimulated and eventually regain its functions.
The administration of large doses of evyot early in the acute variety
of poliomyelitis (as first suggested by Hammond) often tends to check
INFLAMMATION OF CELLS OF ANTERIOR HORNS. 30)
the inflammatory process. Ten drops of the fluid extract ma y be given
with safety three times a day to a six-months-old infant. It should not
be given after evidences of muscular atrophy appear.
Strychnia by the mouth, or by injection into the paralyzed muscles,
is sometimes of benefit to these subjects later in the disease. The dose
must be graded to the age of the patient. I never give over one-
hundredth of a grain at a dose to a child under one year of age. Der-
sonally, I prefer the hypodermic method of administration.
Daily immersion of the limbs in hot salt water (110°-120°) for thirty
minutes, friction (made by the hand ora rough towel several times a
day), massage, and passive movements all tend to excite a determination
of blood to the paralyzed muscles, and are of great utility in these cases.
I do not believe in the use of Jounod’s boot, as I have known of serious
harm being done by it. It isa dangerous instrument in the hands of
inexperienced persons.
To adults J often recommend the internal administration of hot-
water drinking. If administered to children, a competent nurse must
supervise its use. JI have given the rules for its administration in a
preceding section (p. 248).
Hlectricity is an extremely valuable adjunct to treatment in these
eases. It must be kept up for a long period of time, and the parents or
the patient must be prepared for slow results, When the faradaic
current fails to create responsive contractions of the muscles, the
galvanic or static current must be substituted for it. The strength of
the current must be sufficient to create muscular contractions. It
should not be used oftener than on alternate days, as a rule. Months,
and even years, may elapse before the muscles are brought back to the
standard of health.* Pieces of the affected muscles may be removed
from time to time (through the aid of Duchenne’s trochar) and examined
microscopically. In this way we can decide regarding the progress of
the muscular atrophy. If the disease is progressing favorably, the
percentage of oil-globules scattered throughout the muscular fibres will
show a decrease.
During the acute stage, the patient should be kept in bed. After all
febrile symptoms have disappeared this is not, necessary.
The tonic plan of treatment—iron, quinine, cod-liver oil, arsenic,
phosphorus, etc.—may be combined with hypodermics of strychnia when
deemed necessary. The diet should be nutritious and adapted to easy
digestion and assimilation.
* One of my cases made a perfect recovery under electrical treatment and massage, in
spite of the fact that the lower limbs had been almost completely paralyzed for over three
months previous to my examination of the child. She moved about the room by the aid
of her hands only when I made my first examination of the patient.
376 LECTURES ON NERVOUS DISEASES.
AMYOTROPHIC LATERAL SCLEROSIS.
In connection with two systematic spinal conditions which have been
already described, viz., lateral sclerosis and changes in the anterior
horns, it may be well to consider another systematic affection of the
spinal cord where the two are combined. This has been named by
Charcot, who first recognized the pathological changes which tended to
produce it, “amyotrophic sclerosis.” The term “amyotrophic” (signi-
fying an absence of muscular nutrition) expresses well the chief morbid
change which characterizes this form of spinal sclerosis.
Morbid Anatomy.—The lesion is not confined necessarily to the
spinal cord, for it tends to extend throughout the medulla oblongata
and even into the peduncle of the cerebrum. Hence the nuclei of the
hypoglossal, spinal accessory, and facial nerves are involved, as a rule,
late in the disease. The changes in the anterior horns in this disease are
apparently identical with those which exist in connection with progres-
sive muscular atrophy. The morbid process seems to start first in the
cervical enlargement of the spinal cord; for that reason the muscles of
the upper extremity are first attacked.
From these segments the sclerotic and degenerative processes gen-
erally extend both upward and downward. Bands of dense, newly-formed,
connective tissue are often detected between the sclerosed lateral
columns and those portions of the anterior horns which are involved.
In the atrophied muscles, the perimysium undergoes a marked
hyperplasia. Inflammatory changes are more apparent than in pro-
gressive muscular atrophy.
When the medulla becomes involved, the cells which constitute the:
motor nuclei within the gray matter of the floor of the fourth ventricle
undergo a rapid degeneration.
The deformities of the limbs which result from muscular contracture
are extreme in this type of spinal sclerosis.
Etiology.—The causes which conduce to the development of this
condition are apparently similar to those mentioned in connection with
poliomyelitis and primary sclerosis of the lateral columns. Exposure to
cold or dampness seems to be a prominent cause. In one of my cases,
it developed after prolonged and intense mental anguish following the
death of a child. :
Charcot, who has investigated this disease, divides its manifestations
into three distinct phases. These are as follow :—
1. The first stave is manifested only in the muscles of the upper
extremities. 2. During the second stage, the muscles of the lower
extremities are attacked. 3. In the third stage, the morbid process
extends to the medulla oblongata.
AMYOTROPHIC LATERAL SCLEROSIS. 377
Although this clinical distinetion is generally truc, there may be
exceptional instances in which the disease attacks the medulla first, and
gradually extends downward. Again, cases in which the disease first
attacks the lower limbs and gradually extends upward, have been reported.
First Staye—The duration of this stage varies from four months to
ayear, During this time tremors of the upper limbs appear early, and
paresis or paralysis subsequently develops. There is no alteration in
the electric tests of the muscles. Fibrillary twitchings are commonly
observed in the muscles of these patients.
An extensive sorm of atrophy follows the paralysis, and the muscles
tend to develop a state of rigidity and contracture which creates
permanent deformities. The characteristic deformity of this discase is
chiefly observed in the hand, the wrist and fingers being permanently
Fic. 103.—Hanp in Amyorropuic LATERAL ScLerosis. (Charcot.)
flexed to a greater or less extent, and more or less rigid. Fig. 103
illustrates this attitude.
Sometimes the muscles of the neck and jaw are thrown into a state
of spasm, which is more or less persistent. After atrophy has progressed
to a marked extent in the forearm, this rigidity of the neck and jaw
usually tends to disappear. Several months usually elapse between the
first and second stages, during which time the disease appears to remain
stationary.
Second Stage.—As this disease advances, after it has apparently
remained stationary for a time, the muscles of the lower limbs begin
to exhibit evidences of paralysis, and, at the same time, tonte or clonic
spasms (or both forms) may simultaneously develop. Gradually the
state of permanent rigidity or contracture appears in some of the affected
muscles,
378 LECTURES ON NERVOUS DISEASES.
The spinal refleres, chiefly the knee-jerk, are very much increased,
and in some cases an ankle-clonus may be detected.
Aiter a considerable lapse of time has occurred, the muscles of the
lower limbs tend to become less rigid and give place to atrophy and
jibrillary twitchings.
The pelvic organs are not usually disturbed, nor is there any
tendency toward the development of bed-sores which are so commonly
observed in connection with myelitis.
The muscular atrophy in the upper limbs increases to a very marked
extent during this stage.
Third Stage-—In many patients aftlicted with this disease, the
development of ‘“ bulbar” symptoms are superadded to the symptoms of
the second stage.
When these occur the disease has extended to the mnedulla, and has
involved the nuclei of origin of the cranial nerves which arise from the
medulla. These nuclei are situated in the gray matter of the fourth
ventricle. (Fig.16.) In this stage, we are Hable to encounter evidences
of paralysis in the muscles of the tongue, lips, larynx, and pharynx.
The patient experiences difficulty in articulation, in swallowing, and in
controlling the escape of saliva from the mouth. During the act of
swallowing the food is liable to be expelled in part through the nose, and
it is with great difficulty that some patients are able to get the bolus of
food into the pharynx. This distressing condition is commonly known
as Duchenne’s disease. Its physiognomy is shown in Figs. 108 and
109.
Serious disturbances of the circulation and respiration are apt to
occur during this stage from paralysis of the pneumogastric nuclei.
These symptoms may prove the cause of death.
Amyotrophic lateral sclerosis usually proves fatal within two years
after its initial symptoms make their appearance.
Diagnosis.—This disease can hardly be confounded with any other
spinal affection, in spite of the fact that some of its manifestations
closely resemble those of progressive muscular atrophy and poliomyelitis.
When we review the symptoms of the three we may easily make the
necessary discrimination. (Sce table on p, 364.)
From progressive muscular atrophy this disease can be distinguished
by the following facts: The atrophy follows the paralysis and attacks
groups of muscles, rather than individual fibres. Contractures develop,
resulting in characteristic deformities of the limbs. The progress of
the disease is rapid. The lees are attacked soon after the arms. The
medulla becomes implicated in almost every case. The disease is rapidly
fatal.
From poliomyelitis (adult variety) the diagnosis is made by the fact
PROGRESSIVE MUSCULAR ATROPHY. 379
that the reflexes are impaired, but the farado-muscular excitability not
decreased. Moreover, the atrophy is more rapid and permanent in this
form of spinal sclerosis. The contractures of muscles are conducive to
greater deformity ; the medulla is implicated; fibrillations are present ;
improvement in the symptoins is rare; and the ciscase is always fatal.
Prognosis.—I am not aware that a case of cure has ever been
reported. Death usually results from an embarrassment of the circu-
latory and respiratory functions, in consequence of an extension of the
morbid changes to the nuclei of the medulla. It is uncommon for these
patients to live over two or three years.
Treatment.—Nothing can be said under this head which will aid the
reader in curing this disease. Its advent deprives the patient of all
hope of cure, and places the fatal termination at no very distant date.
I have, however, apparently succeeded, by employing static sparks daily
to the spine and limbs, in greatly relieving the contracture of the
muscles and holding the progress of the disease in check for many
months.
PROGRESSIVE MUSCULAR ATROPHY.
The close analogy which this disease bears in some instances to
“poliomyelitis anterior” in the adult as regards its symptoms will help
to explain the fact that such cases are sometimes erroneously regarded
asa variety of progressive muscular atrophy.
This disease is essentially one of adult life, although the so-called
“pseudo-hypertrophic paralysis” of children bears some resemblance to
it. It affects males more frequently than females, and usually appears
between thirty and fifty years of age.
Morbid Anatomy.——A slow degeneration of the ganglion cells of the
anterior horns of the spinal gray matter, probably independent of
inflammatory changes, exists in this disease. It is one of the most
chronic and incurable of all spinal affections, and is comparatively
common. By some authors, this disease is believed to start in the
muscular tissue, in some instances,—and possibly in all.
The vessels of the cord are often abnormally dilated. The arterioles
may be sclerosed, and an inflammatory exudation sometimes surrounds
the larger arterial trunks.
The neuroglia is excessively developed. Sometimes the anterior
roots of the spinal nerves exhibit atrophic changes and discoloration.
The anterior horns of gray matter are altered both in their size and
appearance. The ganglionic cells within them are atrophied or com-
pletely obliterated.
The affected muscles are shrunken and pale in color to the naked
eye. The microscope reveals 4 disappearance of the transverse strie in
380 LECTURES ON NERVOUS DISEASES.
the fibrille; and in those bundles most diseased all traces of muscular
tissue may have disappeared. The muscular tissue has been replaced
hy oil-globules. This process of muscular disintegration does not
appear to affect whole muscles at once; it seems to attack only individual
bundles, or even fibrilla. Eventually, an entire muscle may thus be
destroyed, bundle by bundle, or fibre by fibre.
I am personally inclined to believe that this disease is primarily
one of the spinal cord, and that the muscular changes are a result of
trophic disturbances dependent upon the morbid process within the
spinal gray matter.
Etiology. —.\ mong the exciting causes of this affection, which have
been reported by authors of note, may be mentioned: (1) a hereditary
Fic. 104,—Fiares From THE DIAPHRAGM IN Fic. 105.—SAME TAKEN FROM A CASE OF PRo-
Heattu. (Charcot.) GRRSSIVE MuscuLtaR ATROPHY AFFECTING
tHE DiarpHracm. (Charcot.) The muscular
fibres (a) are greatly atrophied but preserve
their transverse striz. The connective tissue
intervals (4) are enlarged.
tendency; (2) excessive muscular efforts: (3) traumatic injuries of
peripheral parts of the body ; (4) lead poisoning; (5) certain blood
conditions, such as rheumatism, measles, typhoid, ete. ; (6) exposure to
cold and dampness ; (7) excessive venery and masturbation.
There seems to he no doubt regarding an etiological relationship
between certain occupations (demanding an excessive and continual use
of the fingers and hand) and progressive muscular atrophy in some of
the cases reported.
Symptoms.—The chief clinical feature of this disease is the develop-
ment of erfensive and progressive atrophy of certain muscles.
PROGRESSIVE MUSCULAR ATROPHY. 381
The wasting of the muscle may not be detected hy the patient for
some time after its onset. It is unattended with any symptoms of
paralysis, and there are no febrile manifestations to mark its advent.
The patient usually first perceives that certain muscles are appar-
ently wasting, and that some loss of power has occurred in the diseased
part in consequence of the diminution in size of the affected muscles.
This loss of power is always proportionate to the extent of the
atrophy. In this respect, this disease differs from those spinal affections
in which paresis occurs independently of alteration in the muscular
structure.
As a rule, progressive muscular atrophy commonly affects the upper
extremities first; and, in many cases, homologous regions on both sides
are successively attacked.
Patients commonly first observe a wasting of the muscles of the
hand and of the shoulder. A considerable lapse of time usually occurs
before any evidence of atrophic changes in the lower limbs can be
detected.
In the hand, certain muscular groups are generally attacked ,—chietly
those of the thenar and hypothenar eminences, and the interossei muscles.
These patients complain early of more or less stiffness in the fingers
and an inability to perform delicate manipulation with the hand. Cold
tends to increase this difficulty, and warmth to diminish it. The ball of
the little finger and thumb becomes very much wasted as the disease
progresses, and the bones of the metacarpus tend to become unduly
prominent.
Sooner or later the hand assumes a characteristic deformity on
account of a predominance of power in the extensors and abductors of
the thumb (the so-called ‘“ape-hand”). Marked atrophy of the interossei,
combined with the unopposed action of the lumbricales, may give rise
to a condition commonly known as the “claw-hand.” Fig. 106 well
illustrates this deformity.
Flattening of the palm is occasionally observed as the result of
atrophy of the lumbricales.
‘When the muscles of the shoulder become involved, the movements
of the arm are more or less interfered with, and the deltoid region is
markedly flattened. Atrophy of the scapular muscles may also occur; in
which cage movements of the arm are still more seriously embarrassed,
In the forearm, the extensor muscles undergo atrophy more
frequently than the flexors. The supinators usually escape atrophy.
Asarule, the right hand is attacked before the left. The muscles
of the scapula and trunk are not generally attucked until the arms
exhibit very marked atrophic changes.
When the muscles of the back or abdomen undergo atrophy, a
382 LECTURES ON NERVOUS DISEASES,
characteristic posture during the erect attitude is developed. (See Figs.
54 and 55.)
In very rare instances the diaphragm may undergo atrophy, and
create difficulties in respiration.
The lower limbs are usually attacked late in the disease. I have
observed one very striking case, in which the muscles of the thigh were
very extensively wasted, in spite of the fact that the arms and trunk
remained unaffected. Generally, the flexors-of the legs are the first to
exhibit atrophy when the disease has extended to the lower extremities.
The electrical reactions of the muscles undergoing atrophy are
normal in their formula. They are, however, impaired (as is the power
of the muscle) in a direct proportion to the number of fibres which are
Fic. 106.—Two Views of THE Hanp oF a PATIENT SUPFERING FROM PROGRESSIVE
MuscuLar Arropny.
involved in the muscle tested. The faradaic current, as well as the
galvanic, will produce contractions of the affected muscle so long as any
of its individual fibres escape atrophy. The “ reaction of degeneration ”
is not observed in this disease.
In the carly stages of this disease the spinal reflexes may be more
or less increased, this heing the rule for many of the so-called “ wasting
diseases.” They are of course abolished whenever all the fibres are
destroyed, and they tend to diminish proportionately to the extent of
the atrophy whenever it becomes established.
Some diagnostic symptoms are frequently observed in connection
with the clinical evidence of muscular atrophy. Among these the
following may be mentioned as prominent :—
PROGRESSIVE MUSCULAR ATROPHY. B83
1. Fibrillary Twitchings.—These are more apparent perhaps in this
disease than in any other. They are confined to the atrophied
muscles. They consist in repeated and brief contractions of
individual parts of the museles. They are apt to be most marked
when the muscles are tapped with the finecr, subjected to a current
of cold air, or faradized. They are often observed by the patient
while disrobing. Occasionally, involuntary movement of the
fingers, arm, or leg, may be caused by them. It is difficult to
detect them whenever the integument is fatty.
peaertniasis
Fic-107.—Procressve Muscurar ATRopHY OF ALL THE Limps. (After Friedreich.) The
3.
=
age of the patient was 45 years.
Diminished Temperature in the Affected Parts.—A peculiar sensi-
tiveness to cold on the part of the patient is perhaps attributable
to this fact.
Pains in the muscles and in the neighboring joints are occasionally
observed.
Deformities.—These are due to shrinking of the muscles and the
unantagonized action of unaffected muscles. The joints of the
fingers may become enlarged.
The skin may appear mottled or of a bluish-red color over the
wasted muscles. The epidermis may become sealy, the nails may
384 LECTURES ON NERVOUS DISEASES.
thicken, the growth of hair diminish, the secretion of perspiration
become unnaturally excessive, and eruptions may occasionally be
detected.
6. Changes in the Pupils—The pupils may be unnaturally small on
one or both sides, dilate imperfectly, and react slowly to light.
7, Bulbar Symptoms.—These indicate an extension of the spinal
lesion to the medulla. Whenever the pneumogastric nerve
becomes involyed, death may occur from a disturbance of the
heart and the function of respiration.
Diagnosis.—This disease cannot well be confounded with any other
spinal affection, except perhaps one of three forms of poliomyelitis which
have been described. induce it.
Diagnosis.— Locomotor ataxia may be, and too frequently is, mis-
taken in its initial stage for rheumatism and neuralgia. Occasionally
the abdominal crises of ataxia may cause the physician to suspect the
existence of visceral derangements. The points by which the pains of
ataxia may be distinguished from those of other affections of a painful
character have been given already (p. 397).
In its second stage, locomotor ataxia must be distinguished from
motor paralysis, spinal meningitis, cerebellar ataxia, hysterical mani-
festations, chronic myelitis, and multiple sclerosis of the cord.
The symptoms known as those of “Charcot’s disease” must. be
diagnosed from those of chronic rheumatic arthritis.
Motor paralysis can readily be distinguished from ataxia by the
gait (p. 164) and by testing the power of individual muscles. Ia ataxia
there is no diminution of motor power, as may be demonstrated when
the muscles are subjected to proper tests. There is no incodrdination of
movement when motor paralysis exists. The nutrition of paralyzed
muscles is generally impaired. This is not the case in ataxic subjects.
Spinal meningitis can be recognized ly the existence of pain on
motion of the spine and when pressure is made over the spinous pro-
cesses, both of which tests are negative in ataxia. Moreover, febrile
disturbances and more or less motor paralysis are liable to accompany
meningitis. The reflexes will be normal or exaggerated in meningitis;
ocular symptoms will not be discovered; no incodrdination of move-
ment will be developed; nor will the clini¢al history. of the two diseases
be alike,
Hysterical ataxia may be recognized by the history of the case and
the condition of the reflexes. If the patient be a male, hysteria can
gencrally be excluded.
Cerebellar lesions produce a peculiar gait and attitude which closely
resembles that of ataxia in some respects. It has been described on 4a
previous page (p.165). Vertigo is a symptom of cerebellar lesions, and
gastric crises which are attended with vomiting are frequent. Rotary
movements may be developed. The reader is referred to page 46 for
further information respecting cerebellar lesions.
SCLEROSIS OF THE POSTERIOR COLUMNS, 405
Chronic myelitis is to be distinguished from ataxia by peculiar
combinations of sensory and motor phenomena, which are developed
during the progress of the inflammatory affection; by the usual absence
of incodrdination of movement; and by the presence of spasms, con-
tractures, bed-sores, cystitis, vesical paralysis, febrile disturbances, ete.
The pupils are seldom aflected, nor are typical ataxic pains’ ever
encountered in myelitis.
Prognosis.—It is my belief that some cases of ataxia may be cured.
The majority are usually capable of being greatly relieved by proper
treatment, although some are not. If it proves fatal, it gencrally
does so by the aid of an intercurrent affection, The duration of the
disease can hardly be estimated. I have one patient now under my care
who gives a clear history of ataxie pains for the past thirty years.
Sometimes the second stage of the disease is never reached. In rare
instances, the progress of the disease may be rapid. In one of my
cases, general paresis set in after fifteen years of suffering. He is now
in an insane asylum.
Treatment.—In: the early stayes of locomotor ataxia, it is my custom
to place the patient upon the internal administration of hot water (p.
248), and to give ergot in large doses (one drachm of the fluid extract
three times a day). I sometimes administer the bromides of potash,
sodium, or calcium, in place of the ergot. Three times a week or more
T usually employ heavy static sparks to the spine and muscles, and I
employ also the actual cautery to the spine very actively at intervals.
In this way, I have repeatedly caused a total arrest of the pains, which
had been very frequent and severe up to the date when this treatment
was begun. In a few instances a cure seems to have been accomplished.
The kneejerk has returned, and all symptoms of the disease have
disappeared.
During the parorysms of intense pain, hypodermic injections of
morphine, or the internal administration of codeine are of service.
When a distinct syphilitic history can be obtained from the patient,
I give the iodides and mercurial baths as an adjunct to some of the other
agents mentioned. :
When the stage of incotrdination has been reached, the treatment
must be somewhat modified. The bromides are of no service. The
ergot may be continued, but the nitrate of silver in one-third grain
doses should be administered in conjunction with it three times a day.
Care should be exercised against continuing the administration of this
agent long enough to cause staining of the skin. The electrical* and
cautery applications should be regularly employed. Belladonna is of
benefit when the bladder becomes affected. Hammond recommends the
* My experience with galvanism has not been as satisfactory as with the static spark,
406 LECTURES ON NERVOUS DISEASES.
hypodermic use of atropia in doses of one hundred and twentieth of a
grain at first, the dose being gradually increased until one-thirtieth of a
grain is administered.
The employment of crutches when walking, in order to prevent
excessive use of the muscles, has produced beneficial results in the
experience of some authors. I am inclined to think that the suggestion
is a good one. They certainly aid the patient in walking.
The question of the utility of stretching the sciatic nerves, as first
suggested by Langenbeck in 1879, for the relief of incoUrdination and
the pains of ataxia is still undecided. Some remarkable results have
been accomplished by this procedure, and also some remarkable failures.
The nerve is exposed by an incision made above the popliteal space,
The finger should then be introduced beneath it, and the limb raised
by means of the nerve, thus subjecting it to a tension sufficient to
stretch it.
By means of the different methods of treatment suggested, inco-
drdination of movement and the paroxysms of pain may be very
markedly decreased in the majority of cases. One patient, for example,
was lately placed under my care. He came to my office at first in a
carriage, and was able to ascend the steps of my residence only by the
aid of two canes and a body servant. In less than three months he
walked alone to my house with only one cane, the servant having been
dispensed with. Another had his pains (which were typical and of daily
occurrence) arrested for nearly six weeks by six applications of the
static spark.
Incontinence of urine is sometimes a serious complication of ataxia.
As a rule, it is properly an overflow from a highly-distended bladder,
rather than a true incontinence. It is always well to remember this
fact, and to introduce a catheter into the bladder at once when this
symptom is presented by an ataxic patient If the bladder be found to
be distended with retained urine, catheterization should be employed
several times each day at regular intervals, and the bladder washed out
with care each day. This can be easily done by the patient himself by
attaching a soft-rubber catheter to a fomntain syringe. Raising the
fountain fills the bladder, and lowering it siphons the fluid back into the
rubber bag.
T recall a case, which was sent to me some three years ago, in which
the patient (an ataxic) had worn a urinal in his trowsers-leg for many
months, at the advice of a physician. When IJ introduced a catheter,
over a quart of urine was taken from the over-distended bladder. The
treatment mentioned above cured this symptom in less than a month,
and the patient was relieved of a source.of great annoyance and mortif-
cation.
7 CENTRAL MYELITIS. 407
CENTRAL MYELITIS.
Ina previous table, I have seen fit to classify inflammation of the
central gray matter of the spinal cord as a systematic lesion. I am at
variance with some authors in so doing. The other varieties of myelitis,
with the exception of poliomyelitis, should unquestionably be included
under the head of focal spinal lesions, because they tend to spread
transversely and to involve, as they progress, one column of the cord
after the other. In this respect central myelitis seems to be an excep-
tion. It tends to spread chiefly both up and down the cord, and
transversely to a limited extent only.
Morbid Anatomy.—This form of myelitis 1s a rare one. It has been
known to extend throughout the entire length of the spinal cord. It
may extend also to the anterior or posterior horns of the spinal gray
matter. Its pathology does not differ from that of ordinary myelitis.
Etiology.—Little is positively known respecting the exciting causes
of this peculiar form of myclitis, or the physical condition which par-
ticularly predispose to it. The remarks which I shall make later relative
to the causes of myelitis are probably applicable to this condition.
Symptoms. —These will be moditied (as might be inferred from the
statements made in the early pages of this section) by the extent of the
lesion. The combination of symptoms which the patient is liable to
present may be an exceedingly complex one. All the disorders of
sensibility mentioned on a preceding page (p. 854), as well as paralyses
of motility of various types and degrees, with or without contracture,
may be observed. Whenever the anterior horns are attacked, more or
less atrophy of muscle may accompany or follow the clinical evidences
of impaired motility.
The disease is essentially 2 chronic one; hence, sufficient time is
afforded to carefully observe and study the development of the various
symptoms. The inflammatory process may gradually extend to portions
of the spinal cord which are diametrically opposed in their functions.
As in all inflammatory processes, a stage of irritation first exists.
We observe, therefore, this train of symptoms early, but usually for
only a short duration. The effects of irritation upon the motor and
sensory apparatus have already been discussed.
Whenever destructive changes occur, a totally different set of
abnormal nervous phenomena from those of the irritative stage are
produced.
Finally, these destructive changes may become an exciting cause of
a secondary degeneration of those bundles of nerve-fibres which are cut
off by the destructive changes from association with certain cells in the
cord which act as regulators of their nutrition (trophic centres).
408 LECTURES ON NERVOUS DISEASES.
The symptoms of irritation may be manifested by disturbances of
sensibility, such as pain, numbness, paresthesie, hyperesthesia, ete. ;
and also by disturbances of motility, such as motor spasm, exaggerated
spinal reflexes, contracture, and changes in the pupils.
Destruction of the spinal gray matter may result in a total loss of
sensation, marked paresis or paralysis, marked atrophy of muscles,
paralysis of the pelvic organs, the development of bed-sores or other
atrophic disturbances of the skin, and Robertson’s pupil (p. 120),
Diagnosis.—This disease cannot be confounded with any of the
systematic spinal diseases previously described, because a combination
of motor and sensory phenomena of an abnormal character is clinically
observed.
Focal lesions of the cord closely resemble it in many respects.
They can usually be recognized, however, by certain evidences which the
patient presents during the progress of central myelitis of a progressive
destruction of superimposed spinal segments. When the symptoms of
focal lesion shall have been discussed, this distinction will be better
understood.
Prognosis.—In the majority of instances, this disease is a fatal one.
Active treatment, if commenced sufficiently early, may possibly arrest
the morbid process in some cases.
Treatment.—This will be discussed under that of myelitis.
*NON-SYSTEMATIC” OR “FOCAL LESIONS” OF THE SPINAL CORD.*
By reference to a table on page 350, it will be seen that these lesions
differ in their character from the systematic diseases which have been
described. .
The clinical features which they present differ in each individual case;
because they are modified hy the situation of the lesion, in respect to the
different columns of the cord involved, as well as its height in the cord.
The height of the lesion is determined partly by the region to which
- the so-called “ cincture ” or “ girdle sensation” is referred ; partly by the
extent of the motor paralysis or sensory phenomena; again, by the
superficial spinal reflexes which are found to be unimpaired ; and, finally,
by the history of the case, when the seat of the exciting cause can be
well defined. -
Focal lesions differ from the systematic or non-focal lesions in that
they. tend to spread laterally from column to column. They often
extend to the gray matter of the cord, and sometimes involve the entire
structures of both lateral halves of the organ. At first such a lesion may
be small and affect only a limited area; in such a case the symptoms may
* Several pages which relate to focal lesions of the cord are quoted from the Author’s
work, entitled ‘‘ The Applied Anatomy of the Nervous System.”’ D. Appleton & Co., N.Y.
“FOCAL LESIONS” OF THE SPINAL CORD. 409
be confined exclusively to either motor or sensory phenomena, depending
upon the column which is attacked. As it spreads to adjacent columns,
the symptoms are modified, new ones being added ‘which indieate the
direction of its growth. Phy siological and anatomical knowledye can
alone aid in deciding as to the height of the lesion in the cord, or
the portions which are destroyed by it, provided that the cause of the
symptoms is not of a traumatic character.
Before we pass to the consideration of lesions confined to special
seoments of the cord, it may be well to refer again to a few general state-
ments which have heen made on page 352.
Focal lesions commonly give rise: (1) to paresis or paralysis of the
extremities ;, (2) to anesthesia or paresthesize—such, for example, as
numbness, formication, etc.; (8) to modifications of the superficial and
deep spinal reflexes; (4) to paresis or paralysis of the bladder and
rectum; and (5) to a tendency to bed-sores.
The spinal cord may be regarded from a physiological stand-point
as composed of numerous segments which are superimposed; each of
which is capable of an automatic action. In some of these are placed
special centres which govern the action of the viscera, the sexual organ,
and the calibre of blood-vessels.
The segments of the cord may be controlled, when necessary, by the
ganglia of the brain which are of a higher order; but when this con-
trolling power is interrupted from any cause, as in spinal lesions, for
example, the spinal segments may still continue to act automatically.
This is one of the many explanations that have been advanced to explain
the etaggeration of the spinal reflexes (which often exists when focal
lesions of the spinal cord are present), as well as the fact that the bladder,
rectum, sexual apparatus, and the skin are sometimes affected by such
lesions, and again are not.
It is often possible and of great practical importance to the diag-
nostician to tell in what region of the cord a lesion is situated, and to
estimate the height to which it has progressed. Of course, this is much
easier in focal lesions than in the systematic, because the different
columns of the cord then simultancously furnish symptoms which can
be compared, and thus aid in the diagnosis. In the table, to which
I some time ago directed attention, you will perceive that the focal
lesions include traumatisms (of all forms); compression of the cord
(chiefly by inflammatory exudation, bone, and tumors) ; transverse
sclerosis of the cord ; transverse softening of the cord; hemorrhage into
the substance of the cord; and, finally, certain tumors which involve the
cord itself. There are many other causes which might excite some local
lesion, but these are the ones which will most frequently come under the
notice of the practitioner.
410 LECTURES ON NERVOUS DISEASES.
A few anatomical points are suggested in this connection as of value
in spinal diagnosis; (1) the hypoglossal and pneumogastric nerves arise
from the medulla, which lies above the level of the axis; (2) the phrenic
arises on a level with the spine of the axis; (3) the brachial pleaus and
the ulnar nerve are connected with the cord in the region of the neck
(third and sixth cervical spines); (4) the cilio-spinal centre is situated
between the fifth cervical and the second dorsal vertebrie ; (5) the lumbar
enlargement of the cord gives off the crural and sctalic nerves at different
points, and the space between the eleventh dorsal and the second lumbar
spines includes the point of origin of both; (6) the spinal cord ends at
the second lumbar spine, although the nerves continue to escape from the
spinal canal much below that point.
Before we discuss the various conditions siuaneoated in a previous
table.as “focal lesions” of the cord (page 350) as separate diseases, it
may be advisable to consider in a general way the effects of focal lesions
of the cord at different levels. These may be made use of in diagnosis,
We have already studied the effects of systematic lesions, both of
the kinesodic and esthesodic systems, and have noticed how perfectly
the physiology of the spinal cord is confirmed by lesions affecting
the anterior or posterior portions of the cord separately. We are now
called upon to investigate those lesions which, by extending in a trans-
verse direction, are liable to be accompanied by symptoms referable to
both the sensory and motor portions of the cord.
Of course, the symptoms will be modified by the extent of the lesion
in a transverse direction, so that they may be mostly sensory or motor;
but the presence of both sensory and motor symptoms is strongly
diagnostic of focal lesions, irrespective of :a predominance of either,
and is never produced by any systematic lesion of the cord, with the one
exception of central myelitis.
We may start with a general statement in our study of focal lesions,
as follows: Focal lesions usually give rise to paralysis of motion; to an
alteration in the reflex excitability of the cord (usually an increase) ; and
to more or less anesthesia, numbness, and pain. The bladder and rectum
are often paralyzed, and a tendency to bed-sores is frequently produced.
The first two of these effects, and also the last, are due to alteration
in the kinesodie system; the remaining ones are the result of some
disturbance to the esthesodic system.
‘In studying focal lesions situated in different regions of the spinal
cord, we must adopt some system if we expect to grasp the fine distine-
tions which can be drawn between the results of lesions of the upper
cervical region, the cervical enlargement, the mid-dorsal region, the
region just above the lumbar enlargement, and, finally, the lumbar
enlargement itself.
“FOCAL LESIONS” OF THE SPINAL CORD. 411
FOCAL LESION IN THE UPPER CERVICAL REGION.
Hemiplegia will be produced if one lateral half of the cord be alone affected ;
while paraplegia will be present if the lesion extends transversely to both lateral halves
of the cord. The hemiplegia or paraplegia will be complete below the head, and the
entire body may be rendered anesthetic. Since the phrenic nerve arises at this point,
the act of respiration will be interfered with, creating dyspnea and hiccough; but
respiration will not be arrested, since the pneumogastric nerves continue to excite it, and
the auxiliary muscles of respiration can expand the chest without the action of the
diaphragm, Should the lesion be a surgical one (as it usually is), the respiratory centre
of the medulla may be affected, and death take place fromm asphyxia; but I do not think
such a result can be explained as a simple effect of paralysis of the phrenic nerves alone.
The involvement of the cilio-spinal centre in the lower cervical region may cause the
pupils to show an irregularity, and the face and neck may manifest a marked increase of
temperature. The pulse may be rendered variable, from irritation of or pressure upon
the acceleratory centre of the heart.
Now, as I have before said, this type of lesion is almost always a surgical one, com-
prising pressure from fracture, dislocation, caries, tumors of the vertebra, etc. These
cases seldom live long enough for us to study the effects of such a lesion with much detail.
In those rare instances where the lesion is non-traumatic and slowly developed, the
effects of irritation have been shown in a hiccough (probably due to irritation of the
phrenic nerve), acceleration of the pulse (from irritation of the acceleratory centre of
the heart), and dyspncea (from some interference with the phrenic nerve or the nucleus
of the pneumogastric nerve in the medulla); while the paralysis has first appeared as a
paretic condition of the arms, then of the chest, and, finally, of the lower limbs.
FOCAL LESIONS OF THE CERVICAL ENLARGEMENT,
This type of lesion differs in its effects if developed suddenly or gradually, and also
when situated in the upper or the lower part of the enlargement. If the lesion be so
situated as to create only irritation of the cilio-spinal centre, or the acceleratory centre for
the heart (both of which are in that vicinity), the effects will differ from those due to
actual pressure upon or destruction of those centres, In the first instance, the pupils will
usually be dilated and the face pale, while the heart will be accelerated; in the latter, the
pupils will generally be contracted, the face and neck flushed, and the pulse retarded.
The effects will also differ if the lesion affects both lateral halves of the cord or only one.
Wherever the lesion be situated within the cervical enlargement, the arms and legs
will gradually become paralyzed; the-arms and hands usually becoming first numb and
paretic, and the lower limbs exhibiting, for some time, only a sense of weakness and
evidences of an increased reflex excitability. A sense of constriction around the chest
(the so-called “cincture feeling”) is generally present, the seat of which varies with that
of the exciting lesion. ;
When the lesion is situated at the upper part of the enlargement, the motor and
sensory symptoms will be manifested in the lower extremities, the trunk, and in nearly all
the regions of the upper extremities. The constricting band around the thorax is
referred to the devel of the clavicles, and dyspnea is often excessive,
The brachial plexus is associated with the upper part of the cervical enlargement,
and the ulnar nerve with the lower part; hence, the paralysis of the arms in this case
would naturally be manifested in almost all of the regions of the upper extremity, and
also in those parts supplied by the brachial plexus above the clavicle.
412 LECTURES ON NERVOUS DISEASES.
If the lesion be situated in the lower part of the cervical enlargement, the symptoms
exhibited will include a loss of faradaic reaction of those muscles which are supplied by
the ulnar nerve (rather than' those of the arm and the extensors of the forearm), and
atrophy of these muscles will often be developed, chiefly in the flexors of the wrist and
the small muscles of the hand. The sense of constriction (cincture feeling) experienced
in most spinal lesions of a local character will exist, but it will be referred to the upper
part of the chest. A paralytic condition of the muscles of the trunk (the intercostals,
triangularis sterni, and the accessory muscles of respiration), as well as of the abdominal
muscles, will be detected in severe cases, rendering both inspiration and expiration
embarrassed, and thus adding to the danger to life. The lower limbs may exhibit evi-
dences of numbness, anesthesia, paresis, or complete paralysis, depending upon the extent
of the lesion and the destruction done to the tissues of the cord. A condition of paralysis
may also exist in the upper extremity.
In surgical injuries to the upper portion of the cord, a peculiarity is often noticed in
the temperature of the body, which is sometimes greatly elevated. This clinical feature
may be associated with a marked retardation of the action of the heart (apparently
confirming the situation of an acceleratory centre for that organ in the spinal cord).
FOCAL LESIONS OF THE MID-DORSAL REGION OF THE SPINAL CORD.
In the early stages of these conditions the lower limbs become paretic, and a
condition of increased reflex excitability is manifested by a rigidity and stiffness of the
impaired muscles whenever the patient attempts to stand or walk. As the disease
progresses, the muscles become paralyzed and contractured* (probably on account of
changes of a secondary character in the lateral columns of the cord). In some cases the
_ reflex ‘movements assume the type of spasms, so as to exhibit both tonic and clonic con-
tractions. It was this symptom which suggested to Brown-Séquard the name of “spinal
epilepsy,” since it occurs when the patient is exposed to the slightest peripheral irritation,
and often when in the recumbent posture.t The sense of constriction around the body is
referred to the region of the navel, or that of the lower ribs, or possibly as high as the
axilla, since it may be taken as a relative guide to the highest limit of the lesion. A
peculiarity exists in this condition as regards the bladder and the rectum; although they
may be paralyzed, they are often enabled by the aid of reflex action to expel their
contents, thus apparently having regained their function. In the early stages the urine
and faeces may be too hastily expelled for the comfort of the patient, often compelling the
performance of either act before a proper place can be reached; but, in the advanced
stages the urine is retained to such an extent as to cause an “overflow,” which is often
mistaken for an actual incontinence, since a constant dribbling is present. This symptom
is always an indication for the regular use of a catheter. The sexual function seems to be
often unimpaired, as coition is frequently possible. It is seldom that the paralyzed
muscles exhibit a tendency to atrophy, and the electrical reaction of the affected parts is
either normal or exaggerated. The chief seat of weakness is usually first detected in the
feet; subsequently the paralysis gradually involves the entire lower limbs.
FOCAL LESIONS ABOVE THE LUMBAR ENLARGEMENT OF THE SPINAL CORD.
In this situation, a focal lesion of the cord produces about the same sensory and
motor’symptoms as those described in connection with a lesion of the mid-dorsal region,
* A term used in contradistinction to the word ‘ contracted,” to designate a permanent
shortening rather than a temporary response to a motor impulse.
} The presence of urine in the bladder or of faces in the rectum may often create
these spasms.
‘FOCAL LESIONS” OF THE SPINAL CORD. 413
with the exception that the reflex spasms, present in the paralyzed muscles, are perhaps
somewhat less violent than when the lesion is higher up-the cord. These tonic and clonic
spasms are, however, sufliciently well marked to constitute a. prominent symptom,* and
they indicate an increased reflex excitability of the gray matter of the’cord below the seat
of the lesion. An ingenious explanation of this increased reflex has been advanced by
Professor Seguin, of this city, which seems to merit respectlul consideration. I quote
from a paper of his upon affections of the spinal cord, as follows :—
“The classic theory of the physiology of contracture in hemiplegia is thal it is due to
the secondary degeneration; ie., actively caused by the lesion of the postero-lateral
column, Seven years ago (sce Archives of Scientific and Practical Medicine, vol. i,
p. 106, 1873,) I rejected this hypothesis, and suggested a different one, which I have since
elaborated and taught in my clinical lectures. This hypothesis, which I intend shortly to
publish in detail, is briefly that the spasm is due, not to direct irritation from the
sclerosed (?) tissue in the postero-lateral column, but to the cutting off of the cerebral
influence by the primary lesion, and the consequent preponderance of the proper or
automatic spinal action—an action which is mainly reflex. This theory explains the
phenomena observed in cases of primary spinal diseases with descending degeneration,
and can be reconciled with results of experiments on animals (increased reflex power of
spinal cord after a section high up, Brown-Séquard; inhibitory power of the encephalon
on the spinal cord, Setchenow).” j
The urinary and rectal organs are affected in about the same way as in lesions of the
dorsal region. Coition is often possible, and erections are normally frequent. The rectum
is paralyzed, as a rule, and constipation is usually present on that account. Micturition
becomes slow and interrupted, as the bladder grows paretic, and retention and overflow are
produced later on in the disease.
The paralysis of the extremities is first noticed in the feet, which have long before
exhibited a sense of weakness and easy fatigue. Numbness and anesthesia usually
accompany the motor paralysis, and extend as high as the groin or the waist. The sense
of a constricting band around the body is present here, as in lesion of other localities, and
is referred to the waist, below the level of the umbilicus, or at the level of the hips.
FOCAL LESIONS OF THE LUMBAR ENLARGEMENT.
The lower portion of the lumbar enlargement gives origin to the sciatic nerve; hence,
it is reasonable to expect that a lesion situated in the lower part of this enlargement
would be manifested by symptoms of an incomplete paraplegia, in which the muscles
supplied by the sciatic nerves would be the most affected. Now, this fact seems to be
confirmed by clinical experience, since the feet, legs, posterior aspect of the thighs, and the
region of the nates are chiefly paralyzed when the lesion is so situated. The bladder is
unaffected, but the sphincter ani muscle is often rendered paretic, or it may be entirely
paralyzed. The portions of the limbs which are to become the seat of paralysis usually
exhibit a sense of numbness before the effects of the lesion are fully developed, and, in case
the posterior columns of the cord be involved, complete anesthesia may also exist in the
parts supplied with motor power by the sciatic nerve. The condition of the paralyzed
muscles, as to their electrical reactions, and the presence or absence of the evidences of
increased reflex excitability will depend greatly upon how much damage has been done
to the gray matter of the lumbar enlargement. If the gray matter be so destroyed as to
impair its function, the reflex movements will be absent; and, if the trophie function of
the cord be affected by changes in the ganglion cells of the gray matter, the paralyzed
* These reflex spasms have been called by Brown-Séquard ‘‘ spinal epilepsy.”
414 LECTURES ON NERVOUS DISEASES.
muscles will undergo atrophy. The sense of constriction, or ‘‘band feeling,” will usually
be referred, in this lesion, either to the ankle, leg, or thigh.
FOCAL LESIONS CONFINED TO THE LATERAL HALF OF THE SPINAL CORD.
In discussing the focal lesions of the cord, we have described the clinical points which
are afforded by destruction, to a greater or less extent, of the substance of the cord in both
of its lateral halves; hence the motor and sensory symptoms have been usually referred
to both sides of the body. It was necessary to thus describe them, since focal lesions,
unless traumatic, are seldom confined to one lateral half of the cord; but, in some cases
which may be presented to your notice, where a tumor, a fractured vertebra, a hemorrhage,
a severe contusion, or some other localized lesion exists, the injury done to the spinal cord
may be confined exclusively to one lateral half, resulting in one of two named conditions,
viz., ‘spinal hemiplegia” and “hemi-paraplegia.” :
Any lesion of a lateral half of the spinal cord must produce anesthesia on the
opposite side of the body, since all the sensory nerves decussate and enter the gray matter
of the-cord, which serves as a conducting medium for sensory impressions, while the motor
symptoms produced by the same lesion must be confined to the same side of the body as the
lesion, since no decussation probably occurs in the spinal cord (these fibres decussating
only in the medulla oblongata).
Lateral lesions, as well as those which affect the entire cord, are modified, as regards
their symptomatology, by the height of the lesion in the cord; since the motor nerves, and
the special centres which are situated in the cord itself, will only be affected when they lie
below the seat of the lesion, or are directly involved in the destructive process,
When the focal lesion is placed high up in the substance of the spinal cord, the motor
paralysis affects one side only of the body (provided the lesion is confined to a lateral
half), and the term “spinal hemiplegia” is applied to this form of paralysis in contra-
distinction to a hemiplegia of cerebral origin. If the spinal lesion be situated in the
dorsal region and be confined to the lateral half of the cord, a motor paralysis of one
half of the same side of the body below the seat of the lesion is developed,—a condition to
which the term “hemi-paraplegia” is commonly applied. In closing the clinical aspects
of lesions of the spinal cord, it will be necessary, therefore, for us to consider the essential
features of these two remaining conditions.
SPINAL HEMIPLEGIA.
In order to produce a typical case of this condition, it is necessary to have a lateral
focal lesion of the cord in its uppermost part (in or above the cervical enlargement of the
cord). If we suppose, then, that such a lesion be present, let us see what we might
reasonably expect, on purely physiological grounds, would be the result. We can then
examine the clinical records of such cases, and either confirm our deductions or gain some
additional information. Snch a lesion would, in the first place, shut off all motor impulses
sent out from the brain to parts below the lesion, on the same side as the lesion, since the
decussation of the motor fibres has already taken place in the medulla; hence, motor
paralysis should, theoretically, occur in the arm and leg of the side of the body corre-
sponding to the seat of the exciting lesion, and the trunk should also be paralyzed upon
that side. This we find clinically to be true,* with the exception that the intercostal
nerves often retain their motor power when the nerves of the arm and leg are no longer
* The researches of Brown-Séquard, as early as 1849, and his published memoirs (1863-
65, and 1868, 1869) have probably done more to clear up this field and to place it upona
positive foundation than those of any other observer.
SPINAL MENINGITIS. 415
capable of carrying motor impulses. In the second place, we should expect to find that
the sensation of the side of the body opposite to the seat of the lesion would be destroyed
or greatly impaired, since the sensory nerves decussate throughout the entire length of the
cord, This we also find confirmed by clinical facts; and so perfect is this anesthesia that
the line can often be traced to the mesial line of the body exactly, and upward to the limit
of the exciting lesion. In the third place, the situation of the cilio-spinal centre in the
cervical region of the cord would naturally suggest some effects upon the pupil, and the
circulation and temperature of the face, neck, and ear of the same side, This is also
confirmed, as the pupil does not respond to light, but it still acts in the accommodation
of vision for near objects, and the skin of the regions named becomes red and raised in
temperature, Finally, the presence of vaso-motor centres in the cord might occasion a
rise in temperature in the paralyzed muscles; and, strangely confirmatory of this fact, we
often find the temperature of the paralyzed side of the body hotter than that of the
anesthetic side.
In some exceptional cases, the face, arm, and trunk are alone paralyzed, the legs seem-
ing to escape, and often giving evidence of reflex spasm (perhaps most commonly on the
anesthetic side). ‘his must be explained as the result of incomplete destruction of the
lateral half of the cord.
HEMI-PARAPLEGIA.
This condition is the result of some focal lesion of the spinal cord in the dorsal region,
which involves only its lateral half. The results of such a lesion differ but little from those
of one causing spinal hemiplegia, as regards the motor and sensory symptoms, excepting
that the situation of the exciting cause is below the cervical enlargement, where the nerves
to the upper extremity are given off, and where the cilio-spinal centre is situated. For
that reason the muscles of the upper extremity are not paralyzed, nor are the effects upon
the pupil and the skin of the face, ear, and neck (mentioned as present in spinal hemiplegia)
produced. The muscles below the seat of the lesion are paralyzed on the side of the body
corresponding to the exciting cause, and the skin is sometimes rendered hyperesthesic upon
that side ;* while the integument of the side opposite to the lesion is deprived of sensibility.
The bladder and rectum may be paralyzed in some instances. The sense of constriction,
or “band feeling,” will vary with the seat of disease in the spinal cord. The amount of
reflex irritability and the presence or absence of muscular atrophy in the parts paralyzed
will depend upon the depth of the lesion in the spinal cord and the changes which have
been produced in the gray matter. The same increase of temperature in the paralyzed
limb, which was mentioned as occurring in spinal hemiplegia, may also be present in this
variety of paralysis.
Should the side affected with anesthesia give any evidence of motor paralysis or
muscular weakness, or symptoms of anesthesia appear upon the side where the motor
paralysis is present, you may regard either one as conclusive evidence that the exciting
lesion is progressing, and that the opposite lateral half of the cord is being involved to a
greater or less extent.
SPINAL MENINGITIS.
(Pachymeningitis Spinalis—Leptomeningitis Spinalis.)
The membranes of the spinal cord may become inflamed inde-
pendently of, or in conjunction with, similar changes in the cerebral
envelopes. I shall discuss the former variety here.
* This is probably due to some irritation of the gray matter of the cord.
416 LECTURES ON NERVOUS DISEASES.
Spinal meningitis may be of two forms: (1) pachymeningitis
(internal and external varieties), and (2) leptomeningitis (acute and
chronic varieties). I have chosen to include both of these conditions
among the focal lesions of the cord, because their effects upon the
functions of that organ are due chiefly to pressure. The pressure so
produced is liable to spread in a lateral direction from column to column
of the cord.
Although the acute variety of leptomeningitis (inflammation of the
pia and arachnoid) is generally diffused over a much larger area than
the chronic, the distinction drawn on a previous page between systematic
and focal lesions of the cord (see table on p. 350) clearly justifies the
classification adopted.
When the symptomatology of this disease is reached, many of the
hints given in connection with the diagnosis of focal lesions (p. 411 to
415) will prove of great assistance to the reader.
branes (chiefly the pia) are rendered thicker than normal, more or less
opayue and oedematous, sometimes ecchymotic, and often adherent to
each other, The meshes of the pia are filled with a turbid exudation,
which may be tinged with blood. It is sometimes clear, but generally
more or less filled with floceuli of lymph. The consistency of this
exudation varies. It may be fluid, or of the density of jelly. It is
usually most abundant at the posterior part of the cord and around the
posterior nerve-roots ; but it may envelop the entire circumference of
the cord.
Tn the arachnoid, hard cartilaginous plates are occasionally detected.
The size of the plates may reach a quarter of an inch in diameter, but
they are usually much smaller,
The dura may become involved in conjunction with the arachnoid
and pia; or it may be separately affected, as is’ also the case with the
dura lining the cavity of the cranium. We may thus have an énternal
and external variety of spinal pachymeningitis, as well as leptomeningitis
(inflammation of the pia).
The external form of spinal pachymeningitis is primarily an
affection of the dura. The other membranes may, however, occasionally
become involved by an extension of the inflammatory process. Its most
common seat is in the cervical region, and it seldom extends beyond the
limits of two vertebrie, Several such foci of inflammation may coexist.
The membranes hecome hypertrophied and encroach upon the spinal
canal. This may result in a compression of the spinal cord. Myelitis
may be thus induced. Again, the roots of the spinal nerves may be
compressed by the changes in the membranes through which ihey pass,
thus causing disturbances of sensibility and motility.
SPINAL MENINGITIS. 417
The external variety of pachymeningitis spinalis is confined to the
loose connective tissue between the dura and the vertebral canal. This
is more abundant in the posterior part of the spinal eanal than elsewhere ;
a fact which helps to explain the circumscribed character of its morbid
changes, as well as the tendency of these changes to become most
marked posteriorly. /
Swelling and redness are generally to be detected at the seat of the
extra-dural cellulitis. Abscesses may develop in exceptional instances.
In other cases the dura is simply thickened and adherent; or dry, cheesy
masses of considerable size may be detected.
The pains, which are a prominent symptom of the first stage of this
affection, are probably due to a slight compression of the posterior nerve-
roots. Rigidity of muscles may also occur from a similar condition of
the anterior nerve-roots. Later on, the compression of the cord may
induce paralysis, contracture, and atrophy of muscles (chiefly those
supplied by the median and ulnar nerves), anaesthesia of limited areas
of the body, and possibly symptoms of incodrdination of movement.
We owe most of our knowledge of this affection to the publications of
Charcot.
The internal form of spinal pachymeningitis (the hemorrhagic
variety) was first fully described by Meyer, although it was partially
recognized by Albers. A laminated sac enclosing » hemorrhagic con-
dition of the spinal membranes exists in this disease, which is identical
with that described in connection with the dura of the cranium. It
seems to occur in connection with alcoholism, some cases of insanity,
general paralysis, caries of the bones, and syphilis.
This form of spinal pachymeningitis usually runs a chronic course.
It is not always of the hemorrhagic variety. The dura presents in rare
cases upon its inner surface a series of concentric lamelle of a fibrous
character, while the arachnoid and pia have become similarly affected,
constituting the so-called “ hypertrophic internal spinal pachymeningitis.”
In this disease, the spinal cord is constricted by a ring of fibrous
tissue (with numerous interstitial spaces) whose concentric lamelle: may
exceed one-twentieth of an inch in thickness. This ring is generally
situated in the lower half of the cervical enlargement of the cord. It
tends to compress the spinal nerve-roots, and later the substance of the
cord itself. When the latter occurs the spinal gray matter is apt to
suffer. Frequently newly-formed canals are detected near to the gray
commissure, which are lined with a membrane and contain fluid.
When spinal meningitis is developed in connection with syphilis,
the lesion is usually of the type of gummata, and is more or less circum-
scribed. The antero-lateral portions of the cord are more often involved
than the posterior; hence, we are more apt to encounter disorders of
27
418 LECTURES ON NERVOUS DISEASES.
motility than of sensation or codrdination. When these gummata are
not multiple, they are commonly found in the region of the lower dorsal
and upper lumbar segments of the cord. If multiple, they may occa-
sionally be detected higher up.
In the chronic variety of spinal leptomeningitis, the membranes
are excessively thickened and puckered. The adhesions are also
abundant and very firm. Finally, the opacity of the membranes is
greater than in the acute form. In some cases pigmentation exists.
Caleareous plates within the membranes are not uncommon. The
amount of fluid within the subarachnoidean space is increased, and may
contain flocculi of lymph, with pus, or blood. The cord is generally
anemic and frequently sclerosed. The nerve-roots are usually more or
less degenerated and atrophied.
Etiology. Among the predisposing causes, bad hygienic surround-
ings, an excessive use of alcohol and tobacco, indulgence in narcotics,
exposure to cold or dampness, rheumatism, venereal excesses, scrofula,
wasting diseases, tuberculosis, and general debility may be mentioned as
prominent.
The exciting causes comprise injuries to the spine of all kinds,
operations for spina bifida, syphilis, aleoholismus, some of the diseases
of the cord, tumors of the cord or its meninges, caries of the vertebra,
tetanus, hydrophobia, cancer, spinal concussion, infectious febrile
diseases, and rheumatism.
External pachymeningitis is almost always a secondary disease.
Among the primary conditions which may induce it by extension
through the intervertebral foramina, may be mentioned caries of the
vertebre, suppurations in the neck or pharynx, tuberculosis, pleurisy,
empyema, peritonitis, pelvic suppuration, syphilitic ulceration, ete.
Youth and early adult life are more prone to this disease than old
age. It is most frequent in males. The acute form is liable to be
followed by the chronic. Spinal pachymeningitis is a very common
complication of Pott’s disease.
Leptomeningitis is most frequently met with during the winter
months. Sun-stroke is said by some authors to induce it, but I think
such instances must be very rare, The chronic variety generally coexists
with locomotor ataxia, multiple spinal sclerosis, myelitis, and other
organic spinal diseases.
Symptoms.—The most important and marked symptom of the onset
of leptomeningitis is pa‘. This may be localized in the back, or it may
shoot into those parts which are associated with the seements of the cord
nearest to the seat of inflammation. The pain is generally constant,
but it may often be intensified by movements of the spine, pressure
over the spinous. processes, or the application of an electric current to
SPINAL MENINGITIS. 419
the spine. Like some other symptoms which occur early, it may be
regarded as a clinical evidence of irritation of the posterior nerve-roots.
A chill or severe rigor may usher in this disease in some cases. It,
is often followed by nausea, vomiting, a moderate rise in temperature, and
a sense of weakness. The pulse is seldom greatly accelerated : it inay
even be below the normal standard.
Soon a rigidity of the muscles of the spine appears. Opisthotonos
is developed in some cases, especially when the cervical region is in-
volved. The patient generally maintains a fixed position, since move-
ment intensifies the pain.
Convulsive twitchings of the muscles may be developed. They are
exceedingly painful.
The spinal reflexes will be found, as a rule, to be exaggerated; this
symptom indicates an irritation of the lateral columns of the cord.
Sensory and motor symptoms gradually develop. The skin may
become intensely hyperzesthesic, and, as a rule, the motility of the
hyperesthesic parts is more or less impaired. It is common to encounter
an incomplete form of paraplegia, or anzesthesia when the cord or nerve-
roots are seriously affected.
Some of the other symptoms of this disease depend upon the seat
and extent of the lesion. There may be frequent micturition or retention,
whenever the vesical centre of the cord is involved. Dyspncea may be
produced when the lesion is high up. Sweating of a profuse type indi-
cates an impairment of the vaso-motor nerves or centres. The pupils
may be irregular from defective innervation of the cilio-spinal centre.
Bed-sores may be produced on account of trophie disturbances. It is
unnecessary to repeat here all that has been ‘discussed when the effects
of focal lesions of the cord were described. (Pages 411 to 415.)
Chronic spinal leptomeningitis generally follows an acute attack.
There are exceptions to this rule, but they are infrequent. The extreme
pain of the acute stage usually gives place to a sense of dull aching,
Soreness, or an itching and burning of the limbs. The “cincture
feeling” is well marked, and is a guide to the height of the lesion. The
intestinal, vesical, and sexual centres of the cord may be affected and
cause marked disturbances of their functions, We are apt to have
constipation or incontinence of fieces, incontinence of urine, impotence
or priapism, bed-sores, etc. The lower limbs are particularly liable to
become partially paralyzed. Hyperesthesia is also a common symptom.
In the external variety of pachymeningitis spinalis, the symptoms
closely resemble those of leptomeningitis. A stiffness in the back when
the patient rotates the spine (or when sitting or standing for any length
of time) is noticed early. The application of heat, cold, pressure, or the
negative pole of a galvanic battery increases the pain at the seat of the
420 | LECTURES ON NERVOUS DISEASES.
morbid changes. The “cincture feeling” is generally experienced
around the body at a level approximating closely to the height of the
lesion. The pain is apt to be more paroxysmal than in leptomeningitis,
Sometimes the spine may present evidences of the primary disease which
has induced the morbid changes in the extra-dural connective tissue,
The neck is not usually rigid, because this condition is infrequent in the
cervical region.
In the internal variety of pachymeningitis spinalis, the symptoms
run amore chronic course, and more closely resemble those of spinal
and meningeal tumors.
In the “hypertrophic” form, the stage of irritation is followed
(after a lapse of a few months) by paralysis and atrophy of the muscles,
These later symptoms are due to compression of the spinal cord or
the spinal nerve-roots. The stage of irritaticn is characterized by
paroxysms of severe neuralgic pain in the shoulders, the occiput, the
cervical region of the spine, and the large joints of the upper extremity.
It is not usually affected by pressure upon the spinous processes.
Hyperzsthesia and pareesthesie are frequently observed early in these
subjects. The skin of the upper limbs may show trophic disturbances,
chiefly by desquamation, vesicular eruptions, or a roughness of the
epidermis. The hand may assume the typical attitudes depicted by
Charcot and Ross.
Diagnosis.—The different forms of spinal meningitis previously
described are not always easy of diagnosis. The best clinicians have
been misled in cases where the autopsy has revealed very marked lesions
of the spinal meninges. As a rule, however, it is well to suspect the
existence of spinal meningitis whenever we encounter a persistent and
severe pain in the back which is aggravated by movement, and which
oceasionally shoots along the spinal nerves (those associated with the
diseased area). Our suspicions are strengthened if we observe also a
tendency toward muscular rigidity, distortions of the spine, or an
exaggeration of the spinal reflexes, together with marked clinical
evidences either of irritation or impairment of the motor or sensory —
functions.
The presence of marked febrile symptoms at the onset of any attack
associated with spinal symptoms should lead us to suspect the develop-
ment either of a meningitis or a myelitis. It may be justly said, how-
ever, that these two conditions usually go hand in hand, and that one or
the other simply predominates. The existence of a “girdle pain” ora
“eincture feeling” is rather diagnostic of myelitis; as is also the
presence of exavyerated reflexes, with bladder and rectal complications,
changes in the pupils, contractures, or trophic disturbances.
The difficulties in diagnosis are to be attributed chiefly to the fact
SPINAL MENINGITIS. 491
that it makes very little difference clinically whether the spinal cord is
actually diseased or subjected to pressure, and that we cannot always
discriminate between lesions of the cord and those which involve the
spinal nerve-roots.
The table on the following page will possibly prove of value to the
reader in making the diagnosis of the different types of spinal meningitis
from each other, and in discriminating between them and other conditions
which resemble them in many respects.
Prognosis.—In the external form of pachymeningitis spinalis, the
prognosis is always grave. Recovery is very rare and seldom complete.
In the internal variety recovery is possible.
In leptomeningitis spinalis, the acute variety is apt to coexist with a
myelitis, and the proguosis is grave. It is especially so if paralysis and
atrophy are developed, or if the sphincters are involved. A bad con-
stitution, a high range of temperature, dysphagia, an extension to the
medulla, and extreme youth or old age are all unfavorable to the patient.
Relapses are very common, even if the case progresses favorably.
In the chronic variety, death is apt to occur from cystitis, bed-sores,
an acute exacerbation of the disease, or an extension to the medulla. It
is apt to last for years, and to lead to permanent paralysis and atrophy
of muscles.
Treatment.—The cause of the morbid condition, as well as the
symptoms which it creates, must necessarily modify the treatment of
each case.
Irrespective of syphilitic origin, some authcrs advise calomel by the
mouth, Personally, it seems to me a dangerous and unscientific way of
‘controlling (?) inflammatory processes.
If syphilis exists, mercurial inunctions or fumigation may be
employed with benefit, and the iodides may be given in conjunction
with mercury. This subject is quite fully discussed on page 291.
Applications of ice-bags, wet-cups, leeches, or the actual cautery
may be made to the spine over the painful regions.
Bed-sores may be prevented by extreme care respecting the patient
and the bed, and by a change in posture (preferably upon the side or
abdomen). Bathing the skin daily in alcohol, and applying diachylon
plaster over any inflamed spots, may prove of service as preventative
measures. Air-cushions are often employed to remove pressure from
tender surfaces. If sores actually occur, they may be treated by the
permanent water bath or by ordinary surgical dressings.
If the bladder becomes involved, and exhibits incontinence, over-
flow or retention, it is advisable to introduce a catheter at regular and
short intervals, and to thoroughly cleanse the bladder daily by attaching
the catheter to the pipe of a fountain syringe filled with water and
LECTURES ON NERVOUS DISEASES.
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TUMORS OF SPINAL CORD AND ITS COVERINGS. 423.
raising and lowering the bag. This alternately distends and empties
the organ and affords great relief to many patients. The patient can
regulate the pressure by having a string which is attached to the
fountain run through a pulley in the ceiling directly over the side of
the bed, so that he can raise or lower the bag without changing his
posture in bed.
The pain is best controlled by opiates in full doses. I usually
administer it by the hypodermic method. The stomach is less affected
by so doing, and you can control the dose better than by trusting it to
the patient or the attendants. If nausea is created, add one grain of
atropia to one ounce of Magendie’s solution of morphia in preparing
the hypodermic solution. Acid should not be used in dissolving the
morphia, as it increases the danger of abscesses.
Ergot and iodide of potash are commonly employed in full doses
by most authors who have written upon this disease and myelitis. I
have not much faith in the beneficial effects of the latter, and I scldom
push ergot to extremes.
As the patient becomes able to walk it is best to insist on very
gradual exercise, care being taken to avoid over-exertion. In this con-
nection, sexual intercourse should be interdicted.
Paralyzed and atrophied muscles may be subjected to massage,
faradization, galvanization, or static sparks of a mild character. I
think that strong currents are generally detrimental in these patients.
Finally, strychnia, arsenic, iron, and a well-regulated diet are of
service in building up the strength during convalescence, or in prolong-
ing the life of the patient.
TUMORS OF THE SPINAL CORD AND ITS COVERINGS.
Within the substance of the cord, glioma is most often found among
the tumors; and sarcoma comes next in frequency. Tubercle and gum-
mata, as well as fibro-sarcoma and myxo-sarcoma, may likewise be
detected at an autopsy. Tumors may also spring from the meninges
and the vertebra and affect the spinal cord indirectly.
Morbid Anatomy.—Glioma most often affects the cervical and
lumbar enlargements. If extremely vascular (as it sometimes is) the
tumor may be infiltrated with blood and contain blood-cysts. It
probably starts from the neuroglia. Mixed varieties of glioma are
sometimes found in the substance of the cord (chiefly glio-sarcomata).
In the meninges of the cord, we may encounter all the varieties of
tumors mentioned excepting glioma; and, in addition, carcinoma,
psammoma, parasitic growths, fibromata, and myxomata.
The bones of the vertebral column and their periosteum may be the
starting point of intra-spinal growths. These may compress the cord.
424 LECTURES ON NERVOUS DISEASES.
Finally, aneurisms of the spinal arteries or of the thoracic or
abdominal aorta may interfere with the functions of the cord. The latter
can only do so by first causing absorption of the vertebra.
Etiology.— Wounds, injuries, and the results of tubercular, cancerous,
and syphilitic cachexiz are the only definitely known causes of these
morbid growths.
Symptoms—Tumors of the spinal canal cause symptoms either by
irritation or compression of the cord or the spinal nerve-roots or by
inducing changes in the bones. Even when of large size they may
produce no symptoms. In some cases we may encounter all the clinical
evidences of a myelitis, or of spinal meningitis. The general remarks
made in reference to focal lesions of the cord (pages 411 to 415) are
applicable to spinal tumors.
Diagnosis.—Although it is often impossible to recognize a spinal
tumor and its seat during life with certainty, there are some symptoms
which should lead to a suspicion of this condition, These comprise:
(1) an excess of motor paralysis on one side of the body over that
observed on the other, with an excess of anwsthesia on the side where
motility is least affected; (2) a clinical history which would lead to the
suspicion of tubercle, cancer, or syphilis in the patient; and (8) the long
duration of the disease (usually from six months to several years) and
the gradual development of the spinal symptoms. Moreover, the ability
on the part of the patient to recognize with closed eyes the position of
the limb during passive movements (muscular sense) is apt to be more
affected on one side (that corresponding to the tumor) than on the
other.
When more than one tumor exists, the diagnosis ig even more
uncertain than if the growth were single. It might then simulate
multiple spinal sclerosis. I lately treated a case of this description.
By a careful study of the symptoms I was enabled to recognize during
life a multiple lesion of the cord and the seat of the morbid processes
with some exactness, and I suspected either multiple sclerosis or multiple
tumor. The autopsy confirmed the latter view, as sarcomata of the
mcainges were discovered.
Prognosis.—This depends upon the nature of the growth. If it is
syphilitic, recovery under the treatment indicated on page 291 may be
expected, provided the spinal cord has sustained no permanent injury
from compression. Tubercle may, in exceptional cases, be recovered
from, Asa rule, however, spinal tumors are fatal.
Treatment.—lodide of potash, arsenic, cod-liver oil, phosphatic
salts, etc., may be employed as symptoms arise which seem to demand
them, unless the case be clearly of syphilitic origin. In the latter
form the most active specific treatment is indicated.
= SPINAL HEMORRHAGE. 425
SPINAL HEMORRHAGE.
Blood is rarely extravasated into the substance of the spinal cord.
It is generally poured out into the spinal meninges. We can therefore
divide spinal hemorrhage into the intra-medullary variety or “spinal
apoplexy,” and the extra-medullary variety, or ‘ meningeal hemorrhage.”
SPINAL APOPLEXY.
( Hematomyelia.)
Etiology.—This condition is somewhat rare. It may occur from
changes inthe coats of the blood-vessels or from excessive blood-
pressure. Probably the latter cause is not alone sufficient to induce it
in health.
Morbid Anatomy.—We encounter intra-medullary hemorrhage in
connection with gliomatous tumors, acute myelitis, and traumatisms.
The clot is usually small in size, seldom exceeding that of an almond.
In exceptional cases, the blood may escape through the pia into the
subarachnoidean cavity.
The age of the clot will modify its appearances at an autopsy. If
recent it will be red or blackish-red. Older clots become brown or
yellow in color. If sufficient time has elapsed to allow of still further
changes, the clot may be found to be encapsulated by a fibrous deposit,
or possibly an apoplectie cyst or a pigmented cicatrix may be all that
remains of the original lesion.
Symptoms.—These depend upon the seat and extent of the lesion.
Asarule, the patient is attacked with sudden paraplegia, accompanied
by severe pain in the back. The pain usually subsides within twenty-
four hours. Occasionally, the symptoms will indicate a unilateral lesion
of the cord. (Fig. 67.) Again, the effects of disease confined to the
posterior or anterior horns will be evidenced at the onset.
Prodromata are very infrequently observed. Consciousness is not
lost except when the lesion is situated near the medulla, A slight fever
is apt to follow the attack after a lapse of some hours. A high range of
temperature only occurs as the result of complications, such as cystitis,
bed-sores, ete.
The ‘pavalyeis may be of the type of monoplegia, hemiplegia, or
paraplegia,
The sensory functions may be disturbed, causing anesthesia, anal-
gesia, hypereesthesia, parsesthesie, ete.
The bladder and rectum may be affected.
The reflexes may be abolished or exaggerated.
Vaso-motor and trophic disturbances have been observed, and also
hematuria and albuminuria.
426
LECTURES ON NERVOUS DISEASES.
The effects of focal lesions of the cord at different levels may he
studied in this connection with benefit.
(Pages 411 to 415.)
Diagnosis.—Some of the more important symptoms of this affection
can be contrasted with those of other spinal diseases (which closely
simulate it) as follow :—
RAPIDITY OF
ONSET .scecssoee
FEVER. scssecevers
PAIN, ccvcccceecees
HYPERASTHESIA
ANJZESTILESIA «206
CoNTRACTURE
AND SPASM.....
SPHUINCTERS OF
BLADDER AND
RECTUM ....48.-
BED-SORES .....06
ATROPHY oF
MUuUS¢LES
ELECTRICAL
TESTS
PROGNOSIS......:
. SPINAL
sna oee: MENINGEAL
Eee HEMORRHAGE.
(Heematomyetia.) (rematorrhachis)
!
{
Rapid or instan-
Rapid. May be
taneous.
instantaneous. |
Absent at onset,
Occurs on second
Absent at onset. | {
or third day.
Occurs on second.
or third day.
Severe in back at
onset and gradu-
ally subsides.
Marked in back
and limbs, and
are of consider-
aoe ™ | able duration.
May be wanting. | Generally present.
May exist in | (Usually imper-
arts below j fectly devel-,
esion. Appears 1 oped and ap-}
at onset. pears late.
Occur at onset
(if at all) as a
rule,
Are strongly di-
agnostic.
Z
{
Frequently de-!
veloped.
{
potten paralyzed.
Unaffected until
late in the dis-;
ease. |
Oceurs rapidly,
only in those
muscles con-
nected with af
fected spinal
segments.
|
} May not occur.
l
Reaction of de-
generation in
steeped jane
cles associated) > Ma: .
with tot | pee OTEE
cord.
Often fatal. Re-
covery always| | Complete recov-
segments of
{
incomplete. ery is possible.
' { Not developed.
POLIOMYELITIS
ANTERIOR
ACUTA.
Never instanta-
neous.
| Preeedes pa-
f ‘ralysis,
+ Vo pain.
J
Absent.
1
i Absent.
i Absent.
format
Not developed.
{
Rarely fatal.
Occurs rapidly in
all the para-
lyzed muscles.
Reaction of de-
generation in
all paralyzed
muscles.
MYELITIS.
Never instanta-
neous. Compar-
atively slow, as
a rule.
Not prominent
as asymptom,
May be absent,
Is generally
marked,
May be totally
absent.
Not marked.
{
!
An early sign,
and is generally
well marked.
Not usually very
prominent,
Peculiarly liable
to be affected.
Extremely com-
mon.
pry not exist.
exaggerated, or
May be normal,
abolished.
Generally un-
favorable.
Prognosis.—The situation of the clot modifies the prognosis, as well
as the amount of blood which is extravasated into the substance of the
cord. Hemorrhages into the dorsal segments cause less serious symp-
toms than if present in the cervical segments (where the respiration may
be disturbed by interference with the phrenic nerve), or in the lumbar
segments (where the centres for the vesical and rectal sphincters are
probably situated).
The rapid development of bed-sores is an unfavor-
SPINAL MENINGEAL HEMORRHAGE. 427
able sign. In any case, a complete recovery is impossible, and a long
duration of life improbable.
Treatment.—To arrest danger to the patient from a further escape
of blood, ice-bags should be applied to the spine as soon after an attack
as possible, and large doses of ergotine should be given by the mouth or
hypodermically. The patient should be placed in a horizontal posture,
and absolute rest and quiet should be insisted upon. All undue excite-
ment should be carefully guarded against. The subsequent treatment
does not differ materially from that already recommended for myelitis.
~ SPINAL MENINGEAL HEMORRHAGE.
(Hematorrhachis.)
This morbid condition is not commonly encountered. It is more
frequent among males than females. It may be secondary to a spinal
apoplexy which has perforated the pia, or to an aneurism.
Etiology.—No cause can be discovered in some cases. In others, a
history of traumatism, tuberculosis or cancer of the spine, violent
excitement, suppressed menstruation, cardiac hypertrophy, attacks of
spasmodic diseases, purpura, a hemorrhagic diathesis, some infectious
disease, or the presence of an aneurism (which has at last burst into the
spinal canal), may be detected. It may occur in the infant from the
use of forceps. A cerebral hemorrhage has been known to be suf-
ficiently severe to flow into the spinal canal.
Symptoms.—These are dependent upon the extent and seat of the
hemorrhage. They are largely due to irritation or compression of the
spinal nerve-roots at first, and possibly, later’on, to spinal compression
or myelitis.
The character of the onsct depends to a great extent upon the
rapidity of the effusion. A large clot will cause at once very severe
shooting pains in the back and the limbs, with more or less muscular
twitchings, cramps, spasms and rigidity.
The onset is unaccompanied by fever; and the paralysis and anas-
thesia are not very pronounced at first. On the second or third day
reactive fever sets in to a moderate extent.
There is apt to be a“ cincture feeling ” around the chest or abdomen.
If the bladder or rectum show any impairment, or when bed-sores
occur, it indicates that the spinal cord is compressed.
Whenever the nerve-roots become seriously impaired by pressure
of the clot, the functions of motion or sensation, as well as the spinal
reflexes and the electrical tests of nerves and muscles begin to show a
progressive deterioration. ;
Prognosis.—This disease lasts from two weeks to an indefinite
period. It is possible for death to occur from shock, soon after the
428 LECTURES ON NERVOUS DISEASES.
onset, provided the clot be near the medulla. Spinal hemorrhage may
induce a complicating meningitis ; and the extension of this inflammation
to the medulla may cause death. Permanent paralysis and atrophy of
muscles may be induced by pressure upon the anterior nerve-roots,
although the spinal cord may have entirely escaped injury.
The published records of these cases go to show that quite a large
percentage tend to ake a recovery without any very serious impairment
of motion or sensation.
Treatment.—This is similar to that given for spinal apoplexy.
MYELITIS.
Inflammation of the substance of the spinal cord has been partially
studied already under the heads of two systematic spinal diseases, viz.:
poliomyelitis anterior, and central myelitis.
We now approach the consideration of structural changes in the
cord of an inflammatory type which assumes the character of a focal or
“non-systematic ” spinal disease.
We shall discuss this morbid condition as of two varieties, the acute
and chronic.
ACUTE MYELITIS.
This disease may be primary or secondary. It is comparatively a
rare affection; more frequent in males than in females, and is generally
observed during middle life.
Etiology.—The causes of this disease vary with its type; although
a predisposition to it may be engendered by excesses in alcohol, bad
hygiene, overwork, venereal excesses, and exposure to dampness.
The primary variety may be developed as the result of rheumatism,
traumatism to the spine, severe emotional excitement and certain poisons.
Among the latter causes, lead, arsenic, mercury, phosphorus, alcohol,
and carbonic oxide have been known to induce it. Some of these
poisons may be taken into the system while following certain manu-
facturing pursuits.
The secondary variety may be induced by diseases of the vertebre
and the spinal meninges; either by extension of inflammatory processes
or as the result of compression of the cord. Again. it has been known
to follow pneumonia, phthisis, syphilis, diphtheria, pyzmia, the eruptive
fevers, and malarial poisoning.
Morbid Anatomy. — Myelitis of the acute form most commonly
attacks the dorsal segments; occasionally the cervical and lumbar
enlargements of the cord. The extent and seat of the inflammation
varies. It may attack the central gray matter (central myelitis); again,
it may traverse the entire spinal segment (transverse myelitis); finally,
ACUTE MYELITIS. 429
it may be distinctly circumscribed and contined to one lateral half of the
cord (circumseribed myelutis).
A very rare condition, known as “ pertmyelitis” or “myelo-
meningitis (in which only the periphery of the cord is inflamed) has been
observed.
The appearance of spots of myelitis must not be confounded with
post-mortem changes which are commonly detected during the warm
months in subjects which have been kept some time,
When myelitis is present, we may encounter the sewnatedee
appearances of red, white, or yellow softening. These have been
described in connection with the brain (page 317).
The formation of a distinct abscess of the cord is sometimes
observed in myelitis of the acute form. It is most often found in
pyemic and traumatic cases. i
The meninges, especially the pia, are generally more or less reddened,
softened, and infiltrated with pus. The nerve-roots may be markedly
swollen and appear redder than normal. Finally,evidences of ascending
or descending spinal degeneration (see Fig. 92) are generally to be
detected.
Symptoms.—The onset of an acute myelitis may or may not be
preceded by prodromata. If so, they are poorly defined and are those
of slight febrile disturbance.
The onset may be accompanied by convulsions in children; and, in
adults, by a chill and marked fever.
Within a short space of time the patient: begins to notice abnormal
sensory symptoms, such as pain in the back, a cincture feeling around
the chest or abdomen, formication and shooting pains in the limbs,
pains in the joints or cardialgia. The pain in the back is not increased
by movement, unless a spinal meningitis coexists.
The muscles may exhibit twitchings or temporary contractures
early. The bladder may be affected almost: from the onset; causing
either retention, overflow, or incontinence of urine.
Later in the disease, paralysis of the muscles of a complete or
partial character develops. Complete anesthesia may be observed in
other parts.
The muscles begin to waste rapidly whenever the anterior horns of
the spinal gray matter are attacked ; and the “reaction of degencration ”
is then developed in the nerves and muscles associated with the spinal
segments thus affected.
Tf the muscles of the abdomen or chest are paralyzed, respiration
becomes markedly interfered with, and slight pulmonary complications
become a source of danger to the patient. Asphyxia develops suddenly
when the phrenic nerve-roots are attacked.
430 LECTURES ON NERVOUS DISEASES.
In some cases delayed sensation (page 398) is observed. In rare
instances, circumscribed stimulation of the skin, as in the case of a pin-
thrust, is followed by a vibration of the limb. This is known as
“ dysasthesia.”
The vaso-motor nerves generally give clinical evidence of their
impairment quite early in the disease. The paralyzed limb may cease
to perspire. The joints may swell from cedema, and become cold and
peculiarly pale. Eruptions may develop, usually of the vesicular type.
Over the bony points which sustain the weight of the patient, the skin
is peculiarly liable to become reddened, and to undergo a rapid form of
gangrenous destruction. We encounter bed-sores of this type chiefly in
the region of the sacrum, and over the trochanters, malleoli, and the os
calcis.
Cerebral symptoms are generally absent. In rare cases, atrophy of
the optic nerve has been observed.
The urine may become ammoniacal, bloody, albuminous, and sac-
charine. Indications for regular catheterism are often clearly pro-
nounced. Involuntary evacuations of the bowels may follow a paralysis
of the sphincters.
The condition of the reflexes varies with the seat and extent of the
lesion. Ifthe lateral column is alone affected, they will be exaggerated.
If the “reflex arc” (Fig. 34) is injured anywhere in its course, they
will be decreased or abolished.
Diagnosis.—Acute myelitis is apt to be confounded with spinal
meningitis, spinal apoplexy, spinal meningeal hemorrhage, hysterical
paralysis, and multiple neuritis.
From the first three of these diseases, the distinguishing points are
clearly shown in a diagnostic table on page 426.
From true hysterical paralysis, without organic spinal changes,
acute myelitis is to be told by its rapid course, its febrile symptoms, its
bladder and rectal complications, its trophic disturbances, and the sex
affected.
From multiple neuritis, myelitis is to be differentiated in many cases
by the absence of severe pains in the limbs, an imperfect history of
excess in alcohol, the pain in the back, and the retention of normal
electrical formule, both of nerves and muscles. In a few cases, the
diagnosis is difficult. While it is not always easy to make the distine-
tion, it must be remembered that bed-sores and a disturbance of the
bladder and rectum are peculiarly characteristic of myelitis.
Prognosis.—If the myelitis is not of the hemorrhagic variety,
the duration of the acute form is usually from one to several weeks.
The patient may die of ammonizmia, septiceemia, pyemia, exhaustion,
paralysis of the respiratory or cardiac centres, or some pulmonary
CHRONIC MYELITIS. 431
complication (chiefly pneumonia). Some patients pass into a subacute
or chronic variety of myelitis. A few are said to have recovered
completely.
Treatment.—The steps indicated in connection with the treatment
of spinal meningitis are applicable to that of myelitis.
CHRONIC MYELITIS.
_ Under this head some authors place all inflammatory conditions of
the substance of the spinal cord which are focal in type, run a pro-
tracted course, and are unattended with febrile symptoms. Some of’ the
“systematic ” diseases already described are but special forms of chronic
myelitis; as, for example, primary lateral sclerosis, locomotor ataxia,
amyotrophic lateral sclerosis, poliomyelitis anterior acuta, ete. .
Etiology.— A congenital or acquired hereditary predisposition to
this form of myelitis is more pronounced than in the acute variety.
The exciting causes are similar to those of the acute form of the disease.
Morbid Anatomy.—The eye will usually detect a flattening or
depression of the spinal cord, with an unnatural firmness of its substance,
at the seat of the disease. The pia may be adherent over the diseased
area; and it, as was the dura, may be markedly thickened. In
exceptional cases softening of the cord is observed; possibly, also, the
formation of cavities in its substance (syringomyelia) may be detected.
The microscope will usually show an increase of Deiter’s cells,
which are often enlarged and present numerous nuclei; a marked
increase of the neuroglia; a thickening of the coats of the blood-
vessels; a dilatation of the lymphatic sheaths of the blood-vessels ; an
enlargement of the axis-cylinders (chiefly at the periphery of the lesion);
a disappearance of the medullary sheaths; and the presence of granulo-
fatty cells.
Chronic myelitis may in exceptional cases be confined to one lateral
half of the cord. It more often tends to spread transversely to both
jateral halves. It may also assume a multiple form.
The abdominal and thoracic viscera may exhibit evidence of existing
somplications of myelitis.
Symptoms.—These are modified somewhat by the seat and extent
of the lesion,—a statement which is true of all focal spinal lesions. In
a general way, they resemble those of the acute variety of myelitis, save
in the fact that their approach is more gradual and unattended with
‘fever.
Hyperesthesia, numbness, formication, and occasional severe pains
in the limbs are commonly observed. These are followed or accom-
panied by a steadily increasing weakness of the lower limbs, usually
associated with imperfect micturition and defecation.
432 LECTURES ON NERVOUS DISEASES.
Paraplegia is more frequent than unilateral paralysis in this disease.
Whenever the lateral column of the cord is attacked, the gait of spastic
paralysis may be induced (p. 163), We are particularly apt under these
circumstances to encounter, in addition to the progressive paresis of the
legs, contracture, muscular spasms, and exaggeration of the tendon
reflexes.
The later symptoms of this affection are similar to those of the
acute form already described. In some instances, “ bulbar symptoms”
(p. 384) may be added to those already mentioned.
Diagnosis.— All forms of paraplegia must be differentiated from
each other. Whenever this symptom is clinically encountered, the
differential tables given on pp. 422 and 426 will assist the reader in doing
so; and the light thrown upon the symptomatology of diseases of the
spinal cord in the first section, together with the general remarks on
“focal” spinal lesions will aid in localizing the exact seat of the lesion
which has induced paralysis.
It is very important in all focal spinal lesions (1) that the exact
limits of both the motor and sensory paralyses be accurately mapped out
in each individual case; and (2) that the vertical extent of the lesion be
determined by testing each of the spinal reflexes. This can be done by
the methods already described in Section II of this work. Those only
are abolished which depend upon a reflex arc in the diseased segments.
If a bed-sore develops it is clinical evidence, as a rule, that the nerves
which supply that particular area of skin are involved directly in the
spinal lesion.
Prognosis.—Syphilitic cases may make a complete recovery; pro-
vided treatment be begun before spastic symptoms become developed.
The course of the other varieties of chronic myelitis is very protracted
(often ten to twenty years), but is usually fatal.
Treatment.—The treatment suggested for spinal meningitis is
applicable to this disease. Erb extols the effects of the “cold-water
cure” in Ziemssen’s Encyclopedia, and gives some directions for its use.
I have never tried it personally.
If spastic symptoms are prominent, ergot and the nitrate of silver
act better than strychnia, in my experience. When the paralyzed
muscles are relaxed and flaccid, strychnia, iron, arsenic, phosphorus and
quinine are of benefit.
I have obtained very beneficial results in several cases by the
withdrawal of heavy static sparks from the spine and the paralyzed
muscles. This treatment certainly surpasses any other form of electrical
application. The machine must have large plates to generate suflicient
quantity to yield good results.
SYRINGOMYELIA AND HYDROMYELIA. 433
SYRINGOMYELIA AND HYDROMYELIA.
Cavities in the substance of the spinal cord muy exist either as a
congenital or acquired condition. Their extent, situation, and contour
vary in different cases. They usually contain a serous or hemorrhagic
fluid, and occasionally a hyaline material.
These cavities may be single or multiple. They are most common in
the posterior white columns of the cervical and dorsal segments of the
cord. They may be totally independent of the central canal of the cord,
but they usually communicate with it. The anterior horns are occasion-
ally found to be the seat of such cavities.
Morbid Anatomy.—The wall of these cavities
is generally composed of a firm fibrous tissue
(which is apt to be friable and highly vascular),
or of myxomatous tissue. Its inner surface may
or may not be lined with epithelial cells of the
cylindrical variety.
Acquired cavities may result from the soften-
ing and degeneration of clots or of spinal tumors
(chiefly glioma), and from spinal compression.
Chronic myelitis may possibly induce cavities
within the cord. Meningeal adhesions have been
considered by some authors as a possible factor
in their development.
Symptoms.—Large cavities in the cord may
exist without causing any symptoms during life.
If they are created by the morbid conditions
mentioned above, the symptoms will be those of
the exciting cause.
The situation of these spinal cavities being,
as a rule, confined to the anterior horns, the
Fic. 120.—CAVITIES WITHIN THE
central gray matter and the posterior columns — Sunstance or THE Sprvat
Corb, CONSTITUTING rHE Con-
of the cord would naturally suggest the Co- bimon Known as “Svrinco-
existence during life of interference with the ae
sensory, vaso-motor, and trophic functions of the
spinal segments involved, as well as more or less atrophy of the muscles,
and possibly motor paralysis. The reported cases, where post-mortem
observation hag confirmed the diagnosis, seem to sustain such a
conclusion.
Among the abnormal sensory phenomena noted by various observers,
we find the following mentioned: Analgesia, an imperfect perception
of varying degrees of temperature, and occasionally anzesthesia and im-
perfect localization of touch-impressions. The seat of these abnormal
28
434 LECTURES ON NERVOUS DISEASES.
sensory phenomena depends upon the spinal segments attacked. (See
tables on pages 411 and 415.)
The abnormal trophic or vaso-motor phenomena may comprise any or
all of the following conditions: Eruptions (chiefly of the bullous type),
defective secretion of perspiration in some localized form, abscesses or
intractable ulceration, fragility or atrophy of bones, lowering of the
temperature of some parts, cyanosis, etc.
The abnormal muscular phenomena may comprise all the symptoms
enumerated when describing the clinical history of poliomyelitis.
Diagnosis.—This disease may be confounded during life with mul-
tiple neuritis, amyotrophic lateral sclerosis, poliomyelitis, multiple
sclerosis, and spinal tumors outside of the cord,
From multiple neuritis, it is told by the fact that impressions of
touch, temperature, and pain are not equally and simultaneously im-
paired, as they are when a nerve-trunk is undergoing extensive degenera-
tion. The history of the patient might also exclude the exciting causes
of neuritis.
From amyotrophic lateral sclerosis, this affection is told by its being,
as a rule, a unilateral spinal affection, and by the absence of the peculiar
rigidity of the muscles and the characteristic deformity of amyotrophic
spinal sclerosis. Moreover, the duration of life is much longer in
syringomyelia.
From poliomyelitis anterior, it differs in that sensory symptoms
generally coexist with paralysis and atrophy, and also in that the vaso-
motor and trophic disturbances are quite marked.
From multiple spinal sclerosis, it may be told by the absence of
tremor, and the limited number of spinal segments involved in syringo-
myelia.
From spinal tumors, pressing upon one lateral half of the cord, this
disease is to be distinguished chiefly by the absence of all symptoms
pointing to an implication of the vertebra.
Prognosis.—Syringomyelia seems to follow a somewhat uncertain
course. It may progress slowly, or become stationary for long periods
of time. Occasionally it causes a sudden fatal termination.
FUNCTIONAL DISEASES OF THE SPINAL CORD.
In a preceding table (p. 850) we have included under this head the
conditions of spinal irritation, functional paraplegia, spinal neurasthenia,
writers’ cramp or paralysis, and tetany.
Some of these will be discussed under the general head of functional
nervous disease, to whose special consideration the sixth section of this
work will be devoted. Others demand some passing notice in this.
section.
SPINAL IRRITATION: 435
SPINAL IRRITATION.
(Anzemia of the Posterior Columns.)
Notwithstanding the opinions of many writers to the contrary, it is
questionable to my mind whether it is proper to regard this condition as
a special form of disease. The symptoms which are generally enumer-
ated under this head are very often nothing more than manifestations of
the hysterical or neurasthenic states. It is probably a purely functional
derangement, and affects young adults (from fifteen to thirty-five years
of age), chiefly of the female sex.
Etiology.—F or information on this subject, I would refer the reader
to my remarks relating to the causes of neurasthenia and hysteria.
Symptoms.—Pain in the region of the spine and marked tenderness
over the spinous processes of the vertebra and adjacent skin are the
prominent symptoms of this affection.
The pain is of a most distressing kind, usually described by patients
as a severe “ache.” It is very commonly experienced between the
shoulder-blades and in the lumbar region; but it may extend into the
thighs and down the area of distribution of the sciatic nerves.
Nausea and vomiting may coexist with tenderness confined to the
cervical spines.
The hyperesthesta is often of an extreme kind. It exists over the
vertebral spines. The slightest pressure along the spine may call forth
evidences of acute suffering on the part of the patient.
The general health is usually below par. The urine may be loaded
with phosphates, the digestive functions poor, the eyes asthenopic, and
the mental condition sluggish and apathetic.
No evidences of impairment of motility are observed, nor is there
any anesthesia. The bladder or rectum is never paralyzed.
Treatment.—The reader is referred to my remarks on the treatment
of spinal neurasthenia and hysteria.
FUNCTIONAL PARAPLEGIA.
The lower limbs may sometimes be paralyzed without an organic
cause, We encounter this condition chiefly in women and children,
Etiology. Among the causes of this condition may be mentioned
hysteria, anemia, blood poisons (malaria, lead, arsenic, phosphorus,
ergot, alcohol, etc.), ovarian irritation, phimosis, and many other forms
of reflex irritation. I believe that “ eye-strain ” is a factor in these cases
too commonly overlooked.
Symptoms.—When hysteria exists, Drummond thinks that an in-
sensibility to pain, but not to touch or temperature, is peculiarly char-
acteristic. Duchenne, on the other hand, regards the loss of muscular
436 LECTURES ON NERVOUS DISEASES.
sensibility as of great diagnostic importance. Todd has describe
certain facial changes (p. 170) as of value in recognizing this condition
Reynolds has described a type of functional paraplegia “ dependen
purely upon idea,” in which the patient is strongly impressed with th
fact that voluntary movement is impossible. He claims that this stat
is not necessarily hysterical.
In malarial paraplegia, the paralysis is said to be intermittent ir
type. I have never observed a case of this kind.
In reflex paraplegia, the bladder, external genitals, urethra, ovaries
and the eye may act as the exciting cause.
In alcoholic paraplegia, the symptoms of “ multiple neuritis” are
apt to be encountered ; hence this condition is not purely functional in
many cases. Pains in the limbs and the coexistence of the “ reaction of
degeneration ” (p. 189) are diagnostic of the latter condition.
Treatment.—The removal of the cause and steps judiciously directed
toward the improvement of the general health are indicated. Electricity,
massage, tonics, etc., are beneficial. In my opinion, a correction of
“ eye-strain ” will generally prove of immediate service to a large pro-
portion of adult cases.
WRITERS’ CRAMP.
(Professional Cramp ; Mogigraphia; Graphospasm ; Chetrospasm.)
Writers, pianists, violinists, telegraphers, the counters of paper
bills, ete., often become unable to pursue their vocations from a peculiar
form of weakness and pain, ora tendency toward sudden spasm of the
muscles of the hand and forearm.
Etiology.—Any occupation which requires incessant use of a certain
set of muscles of the forearm or hand may lead to this distressing con-
dition. It is doubtful to my mind if injuries, sprains, or exposure to
cold ever induced this morbid state. - I regard causes of that character
as mere coincidences. ,
Symptoms.—This condition develops gradually. The patient feels
at first a peculiar sense of distress or ‘fatigue in performing for any
length of time the vocation which has induced it. This sense of distress
may be in the fingers or forearm. It is accompanied sooner or later by
a peculiar awkwardness in the finger-movements, a sense of stiffness in
the fingers, or a tendency to uncontrollable spasm of the fingers when
these acts are persisted in.
Gradually these symptoms increase in severity. The fingers become
more and more uncontrollable when used by the patient in lis vocation.
For example, when writing, the pen may be flung from the hand or
pressed violently upon the page. A pain becomes marked along the
arm, often as highas the shoulder. After ceasing all attempts at writing,
TETANY. 437
the limb affected may feel relieved by rubbing it and kneading the
muscles for some time. In many cases, the vocation which has occa-
sioned the cramp has to be abandoned.
Strange as it may seem, these patients can use their affected hand
for any other purpose with their accustomed facility. I have seen cases
where the patient could draw for hours but could not write for one
minute without distress. Some sufferers learn to use the left hand, so
as to.avoid using the afflicted member. If the left hand is then over-
taxed, the condition tends to become bilateral.
This disease is very persistent, after it is well-developed. I per-
sonally suffered from it for many years; and am still unable to write
continuously with a pen for any length of time without severe distress,
T can use a type-writer, however, for hours without the slightest symptom
of cramp.
Respecting the morbid anatomy of this disease, many theories have
been advanced. Althaus regards it as an exhaustion and abnormal
irritability of the codrdinating centres in the upper part of the cord.
Some authors consider it an affection of the muscular system only or of
the terminal plates of the nerves. Ross claims that he can locate the
disease by the electrical reactions of the affected muscles. He places it
in the ganglionic spinal cells, when the reactions are diminished; and in
the cortex, when the reactions are intensified.
Treatment.-—Entire rest from the occupation that causes distress is
the first step in the treatment. This must be ensured for many months,
if possible,
Some patients who cannot do this are benefited by wearing a rubber
band around the forearm; others by holding the pen in an unusual way ;
afew, by employing a‘cork pen-holder of an extreme size (often over an
inch in diameter); while many have recourse to a type-writer for corre-
spondence.
Showering the arm in hot and cold water alternately, and using
friction, percussion of the affected muscles, and massage (Wolft’s
method) after the water application is often very beneficial.
Blisters and the actual cautery over the median nerve is of service
in many cases. It must be kept up for some weeks
Static sparks to the cervical spinal segments and to the affected
forearm and hand often give immediate relief.
TETANY.
This condition is characterized by paroxysms of tonic muscular
spasm confined to groups of muscles. It is also known as “ intermittent
tetanus” and ‘intermittent cramp.”
The upper extremities are most often attacked. Generally the
438 LECTURES ON NERVOUS DISEASES.
spasms are bilateral in character. In exceptional cases they may be
unilateral. Sometimes the spasins are confined to the legs, and occa-
sionally the muscles of the back, thorax, and-abdomen may be involved.
Cases where the attacks have been general in character, affecting the
limbs, trunk, and even the face, have been reported.
Etiology.—This disease is most frequently encountered in children
at the time of dentition, and at the age of puberty. It is rare in
advanced life.
Heredity seems to be apparent in some cases. Several of one
family have been so afflicted, according to Murdoch, and the researches
of Bouchut seem to show a history of neurotic affections in the ancestral
line of many so afflicted.
A state of low vitality is generally present in these subjects. Rickets,
acute infectious diseases, impaired digestive functions, etc., are among
the predisposing causes.
Among the exciting causes may be mentioned a marked exposure to
cold or dampness, rheumatism, peripheral irritation of all kinds, and
violent mental excitement.
Morbid Anatomy.—Little is positively known respecting the morbid
changes which probably exist in the nerves or the nerve-centres. Weiss
believes that diseases of the sympathetic system exists and induces
circulatory changes in the spinal cord.
Symptoms.—These may be grouped into two classes, the prodromal
and the actual.
The prodromal symptoms may include pains in the limbs, formica-
tion, coldness of the extremities, vertigo, a sense of confusion in the
head, and tinnitus aurium. They may exist for days or weeks prior to
the attack. .
The symptoms of an attack may occur after mental excitement or
excessive muscular effort. They may occur at night or during the day.
When the upper limbs are attacked, the flexors of the fingers
(usually of each hand) and also the flexors of the wrist cause the
attitude of the hand to assume a position which Trousseau very aptly
compares to that of an obstetrician when about to pass the hand into
the vagina. Occasionally the forearms are flexed, and the arms are
drawn to the chest to an extent suflicient to cause a crossing of the
distorted hands over the epigastrinm. In very exceptional instances
the spasm is unilateral and the extensors may be attacked. During the
paroxysm the muscles are very prominent and firm, and are sensitive to
pressure,
When the lower limbs are attacked the foot is distorted at the ankle by
spasm of the calf-muscles, the leg is extended upon the thigh, the big toe
is drawn beneath the adjacent toe, and the thighs are strongly adducted.
TETANY. 439
When the trunk is attacked the back muscles may cause opis-
thotonos or pleurosthotonos. Again, the spine may be bent anteriorly.
The chest-muscles may cause disturbances of respiration of an alarming
kind. The muscles of the neck may create cyanosis, prominence of the
jugulars, and protrusion of the eyeballs.
During the paroxysm the contractures may be partially overcome
by a voluntary effort, but the deformity returns at once when the effort
issuspended. The contractures may even persist during sleep. Fibrillary
contractions are often observed during the paroxysm.
The duration of the attacks varies from a minute to several days.
They may return with great frequency or at long intervals.
The attacks are not excessively painful, as a rule. They are
generally accompanied by a sense of tingling, formication, coldness, or
slight neuralgic pains of a shooting character. Fever and sweating may
be observed in some cases.
Trousseau lays much stress upon the diagnostic importance of a
test to be employed during the intervals between the paroxysms, which
consists in the ability to enduce these attacks at will by pressing upon the
arteries or nerve-trunks of the arm. After such pressure of two or more
minutes the spasm occurs. It rapidly disappears when the pressure is
removed. The same test can be applied to the crural artery and the
sciatic nerve, but with more uncertainty.
The electrical irritability of the affected motor nerves is markedly
increased. The nerve responds to abnormally weak faradaic currents.
Applications of galvanic currents to the nerve-trunk by the polar
method show the following conditions: C.C.C. and A.O.C. occur very
early; cathodal-closure-tetanus and anodal-closure-tetanus are rapidly
developed ; finally, anodal-opening-tetanus is produced in almost. every
case with ease, and cathodal-opening-tetanus in some cases,
Diagnosis.—This disease may be confounded with tetanus, hys-
terical contractures, and ergotism.
In tetanus, there is an inability to use the muscles of mastication,
more pain, a traumatic history, and a general rigidity and abnormal
posture of the limbs and trunk.
In hysterical contractures, the test of Trousseau is inoperative, there
is no increase of the mechanical and electrical irritability of motor
nerves, children and males are seldom attacked, and the history of the
case is suggestive of hysteria. :
In ergot poisoning, the history of the case would point clearly to the
exciting cause of the attacks.
Prognosis.—These sufferers usually recover perfectly after a lapse of
time. The disappearance of Trousseau’s phenomena, and the abnormal
irritability of the motor nerves, is indicative of a favorable change in
440 LECTURES ON NERVOUS DISEASES.
the patient. Recurring paroxysms are to be anticipated for some
months after the first attack.
Treatment.—If a history of rheumatism or a rheumatic tendency
_can be elicited, it is well to give iodide of potassium, salicylic acid, or
the oil of wintergreen. Ice-hags, wet-cupping, and blisters to the spine ;
the application of the actual cautery, and galvanism to the spine have
been recommended by different authors,
The general health of the patient should be restored by all judicious
means. Tonies, massage, good hygiene, nutritious food, stimulants in
moderation, and moderate exercise will conduce toward that end.
Among the electrical applications, static sparks to the limbs and
spine, general faradization, the polar action of the anode to tender
points applied by the stabile method, and labile applications of the
anode to the peripheral nerves (stroked slowly from the distal extremity
of the nerve toward the proximal end) have proven of service in many
cases.
TIIOMSEN’S DISEASE.
(Myotonia Congenita—Congenital Dluscular Spasm.,
In this disease, a tendency of the muscles to tonic spasm during
attempts at voluntary movement is the characteristic feature.
By such spasms, the execution of intended movements of the limbs
is always more or less delayed, and sometimes entirely prevented.
This disease is also known as “ Myotonia Congenita,” because it is
seldom, if ever, observed except in patients who are not predisposed to
it by heredity. Dr. Thomsen, who first described this affection, noted
its occurrence in five generations of his own family. He suffered from
it himself, as did also one of his sons. A very complete monograph on
this subject has been published by Erb, who has collected and analyzed
all cases reported to that date. Jacoby and Dana have lately added to
the literature of this affection. .
Etiology.—As has already been stated; heredity plays a very im-
portant part in this disease. In one reported case, fright seems to have
acted as an exciting cause. It is questionnble, however, if this disease
ever occurs without some congenital defect either in the spinal cord or
in the muscles themselves. A late monograph upon this subject by
Dr. G. W. Jacoby seems to show conclusively that muscular anomalies
were present in the case reported by him.
Morbid Anatomy.—Although this disease has been classed by me as
a functional disease of the spinal cord (because no spinal changes have
ever been shown to exist in connection with it), it must be said that the
muscles appear to show characteristic conditions which are probably
congenital. The individual muscular fibres are greatly augmented in
THOMSEN’S DISEASE. 441
point of size, and the number of their nuclei is in excess of that observed
‘in healthy muscle.
The muscles are generally unnaturally large in this disease. This
gives to the patient an appearance of strength, which is in marked
contrast to the actual power of contraction which the patient possesses.
The anomalies of muscular construction which have been referred to
necessarily add to the size of each individual muscle. But, on the other
hand, such a muscle appears to be more liable to become tetanic when
called into play by the act of will. .
Symptoms.—Typical cases of this disease exhibit in very early
youth, to a moderate degree, the disorder of movements, which becomes
more pronounced later in life. A history of a similar affection can be
found upon inquiry to have existed in some of the patient’s ancestry.
After a period of rest the patient experiences a peculiar tension and
stiffness of the muscles when any voluntary movement of the limbs is
attempted. This stiffness may be so marked in some cases as to com-
pletely arrest. the intended movement for a time. It gradually dis-
appears, however, and, by the aid of continued movements, the patient
after a time regains complete control over his muscles.
In addition to this peculiar muscular state, the patient is also
rendered unable to voluntarily relax the muscles quickly.
The muscles of the lower limbs are more frequently affected than
those of the upper. In some cases, the muscles of the tongue, face, eyes,
and also those of mastication, are affected. Involvement of the tongue
by spasms of this character gives rise to a peculiar hesitancy in speech.
Awkwardness in the mastication of food is observed whenever the
muscles which move the lower jaw are attacked.
When the muscles of the lower limbs are affected with this disease
the patient is very apt to experience great difficulty in attempting to
rise and walk, after a prolonged recumbent or sitting posture. Such sub-
jects have been known to fall as soon as efforts to walk were attempted.
Fibrilary contractions of the muscles may occasionally be detected.
Continued movement and the application of heat tend to diminish the
spasm, while mental excitement and cold usually aggravate it.
Again, the muscles in these patients show an abnormal excitability
to mechanical and electrical stimuli. Artificially produced contractions
are apt to be very much prolonged. Erb describes peculiar “ wave-like
contractions” in the muscles of the limbs, whenever galvanic currents
of sufficient intensity are employed upon the patient by the stabile polar
method. These contractions, according to this author, always tend to
pass toward the anode. After a time they subside “like waves of water
produced by a falling stone.” Any increase of the strergth of the
current, however, tends, as a rule, to reproduce them.
449, LECTURES ON NERVOUS DISEASES.
To test this reaction in the upper extremities, one pole may be
placed at the nape of the neck and the other in the palm of the hand or
at the annular ligament of the wristjoint on its palmar aspect. To test
it in the lower extremity, one pole should be at the neck and the other
may be placed adjacent to the patella or upon the tendo-Achilles. The
strength of the current employed varies from six to twenty milliampéres.
Jacoby has observed an absence of any fixed relationship of Ca.C.C.
and An.C.C, to each other, as exists in healthy muscle (page 190).
The duration of this disease is limited by the life of the patient;
although remission and exacerbations have been described by different
observers.
Diagnosis.—This disease is to be distinguished from muscular
hypertrophy by the presence of the spasms, and the peculiar electrical
phenomena already described. The reflexes give evidence, also, of an
unusually prolonged muscular response.
Treatment.—Gymnastic exercises, warm baths, and judicious electri-
cal treatment may possibly afford some relief.
ACUTE ASCENDING SPINAL PARALYSIS.
(Kussmaul-Landry’s Paralysis.)
This disease, as far as we at present know, is not associated with
anatomical changes in the nervous system. It consists of a tendency
toward progressive paralysis, which slowly creeps from below upward
in a more or less irregular way. There is an absence of atrophy; and
no sensory or trophic disturbances are observed. There is no paralysis
of the bladder or rectum. The irritability of the paralyzed muscles is
retained.
Etiology.—This disease is a rare one. It is more common among
males than females; and, as a rule, it affects middle life.
Its exciting causes are very obscure. It has been observed to follow
mental excitement, exposure to cold, suppressed menstruation, acute
infectious diseases, coitus in the standing posture. The syphilitic history
may be detected in a certain proportion of persons so afflicted.
Morbid Anatomy. — Little if anything is known respecting the
changes which occasion this disease. Westphal concludes from his
investigations that it is the result of some unknown infection; because
he detected changes in the intestinal follicles and the mesenteric glands
in a numher of cases.
Symptoms.—The paralysis may develop suddenly; or it may be
preceded by slight fever, pain in the back and limbs, tingling and other
forms of abnormal sensation. The paralytic symptoms do not always
follow a strictly ascending course. They may begin in one or both feet
and then skip to the upper extremities, the neck, chest, or abdomen.
ACUTE ASCENDING SPINAL PARALYSIS. 443
This, however, is not always the case. In rare instances, the impairment
of motion has apparently pursued a descending course; and, in one case
reported by Westphal, the nuclei of the medulla were alone iunplicated
and * bulbar” symptoms appeared at the onset.
In most cases, a paresis first appears; this subsequently deepens
into complete paralysis. A sense of fatigue in the limbs is first noticed
by the patient, and walking soon becomes extremely difficult. For this
reason these patients usually take to bed early.
When the back muscles become paralyzed, it is impossible for the
patient even to sit up. Paralysis of the muscles of the abdomen renders
coughing, sneezing, expiration, defecation and micturition difficult.
When the intercostal muscles are paralyzed, inspiration is seriously
disturbed, and the most marked difficulty in breathing may occur when-
ever the phrenic nerve becomes affected. Sooner or later the movements
of the upper extremities are rendered difficult or are totally lost.
Whenever the medulla is implicated, speech becomes very much impaired,
and the act of swallowing may be attended with great difficulty. It is
very rare to observe any paralysis in the nerves of cerebral origin,
No atrophy is detected in the paralyzed muscles, and they retain
their normal irritability to electrical stimulation.
In very exceptional instances only do the sensory functions give
any evidence of serious impairment. Cases have been reported, however,
where the sensations of pain and temperature have been imperfectly
conducted, and where the muscular sense has been somewhat diminished
Anesthesia and hyperesthesia have also been observed, There seems
to be a tendency to diminution or abolition of the skin and tendon
reflexes late in the disease.
In some cases a marked enlargement of the spleen and clinical
evidences of albuminuria have been detected.
Diagnosis.—This disease may he confounded with an ascending
myelitis, poliomyelitis anterior acuta, and acute multiple neuritis.
From myelitts of the ascending type, it may be recognized by the
absence of fever and sensory disturbances, by the fact that bed-sores
do not occur, and by the non-occurrence of vesical and rectal com-
plications.
From poliomyelitis, it may be told by its progressive character, and
the absence of rapid atrophy in the paralyzed muscles. The “ reaction
of degeneration ” is present in poliomyelitis ; while it is generally absent
in ascending paralysis.
From acute multiple neuritis, it differs in that marked pain and
sensory disturbances are usually absent, and in the fact that the affected
nerves and muscles do not rapidly lose their irritability to electricai
_ currents.
444 LECTURES ON NERVOUS DISEASES.
Prognosis.—This disease usually runs an acute and progressive
course; hence the prognosis is naturally grave, although recovery has
been observed. The development of “bulbar” symptoms generally
indicates the approach of a fatal termination. The more rapid the
development of paralysis of a complete kind, the more serious is the out-
look for the patient. The duration of the disease is generally a short
one. It may prove fatal in from four days to as many weeks.
Treatment.—If the disease can be shown to be connected with any
of the clinical manifestations of syphilitic infection, the remedies sug-
gested on page 291 should be administered. It is well to make use of
the actual cautery, dry cups, or ice-bags to the spine. The internal
remedies suggested by authors comprise the iodide of potash, full doses
of ergot, belladonna, and strychnia, The galvanic current may be applied
to the spine, preference being given to the polar action of the cathode.
ABNORMAL VASCULAR CONDITIONS OF THE SPINAL CORD AND ITS
COVERINGS.
Under this head I have included, in a previous table, spinal con-
gestion, spinal ansemia, spinal embolism, atheroma of the spinal vessels,
fatty degeneratian of the vascular coats, and aneurismal dilatations.
Of these, only the first two can be described as conditions which are
clinically recognized. The other four are pathological states which tend
when present to induce structural changes within the substance of the
spinal cord. They are more directly concerned, therefore, with the
etiology of organic spinal diseases than with their symptomatology.
One form of spinal anzemia has been already considered under the head
of ‘ spinal irritation.”
SPINAL CONGESTION OR HYPERMIA.
The distinction between congestion and hyperemia is one of degree
rather than of kind. In both conditions we encounter dilatation of the
vessels with an excess of blood. In hyperemia, the current is unusually
rapid; in congestion, it is unnaturally slow.
Clinically, the line of distinction between hypersemia and inflamma-
tion is very difficult, if not impossible, to draw. One may be simply
a precursor of the other. As the vessels of the pia are the chief
sources of supply to the spinal cord, hyperemia of the cord and me-
ninges usually go hand in hand. Its symptoms must, therefore, be of
necessity closely allied to those of spinal meningitis and myelitis.
When the pia is diseased, the spinal cord is almost invariably affected
simultaneously to a greater or less degree.
Etiology.—A sudden checking of the perspiration by draught of cold
air, bathing, etc., is generally regarded as tending to excite this condition.
SPINAL CONGESTION OR HYPERZMIA. 445
Excessive fatigue, violent excitement, unnatural indulgencies in
venery, suppression of the menstrual discharges, the effects of com-
pressed air, prolonged physical or mental exertion, blows and falls, ete.,
have also been mentioned by some authors as apparent causes of spinal
hyperemia.
Personally, I am inclined to believe that most of the symptoms
usually attributed by authors to this morbid state are dependent upon a
neuropathic tendency whose exciting causes will be discussed in full in
the section which relates to functional nervous diseases.
Symptoms.—These are to be attributed in a general way cither to
irritation or a state of depression of the spinal functions. They may,
therefore, vary with each case, and closely simulate the first symptoms
observed in spinal meningitis, spinal tumors, and myelitis.
Hammond, Browne-Séquard, Radcliffe, Ollivier, and others, who
have written upon this condition, describe among the symptoms many
clinical features which, in my opinion, are not always distinguishable
from those occasioned by the organic diseases mentioned. Thus, for
example, pain, disturbances of motility and sensation, the cincture-
feeling, a lowering of the temperature in parts below the lesion, inter-
ference with breathing and the action of the heart, a loss of control of
the bladder and rectum, a diminution of the electro-muscular con-
tractility, the development of bed-sores, etc., are what we are apt to
observe whenever the spinal cord is subjected to irritation or when its
functions are in any way interfered with. The clinical history of each
case, combined with prolonged observation of the patient, can alone
enable us to exclude organic spinal changes.
Respecting the pain of spinal congestion, it is claimed that the
recumbent posture increases it; and also that the standing posture adds
to the distress when the congestion is localized in the lower spinal
segments. This is attributed to the effects of gravity. It is also stated
that a sudden blow or shock, as a false step, for example, adds to the
pain in the spine.
Anesthesia, or a sense of tingling and formication, may exist in the
feet (chiefly in the plantar surface of the toes) whenever the dorsal or
lumbar segments are locally congested.
Paresis of the legs, or actual paraplegia, may be developed. The
patient can usually move the limbs when sitting or in bed, although
they may be incapable of supporting the body.
According to Hammond, the symptoms of spinal congestion are
always more marked on rising than as the day advances.
Diagnosis.—This condition may be confounded with spinal anzemia,
myelitis, spinal meningitis and spinal tumors.
In spinal anemia, the bladder, when aftected, is impaired before the
446 LECTURES ON NERVOUS DISEASES.
development of motor weakness in the legs, while the reverse order is
observed in spinal congestion. UHyperesthesia is developed in place
of anesthesia and formication. The effects of a recumbent posture tend
to cause an improvement in the symptoms.
In myelitis, the urine is apt to become alkaline, irrespective of
decomposition from retention within the bladder. Moreover, the
paralysis is more decided, the development of bed-scres more frequent,
the cincture feeling is more decidedly marked, and the pain in the cord
is more severe.
In spinal meningitis, the tendency to muscular spasm, the pain on
movement of the spine and of the paralyzed limbs, the febrile symptoms,
the muscular twitchings, and the tendency toward muscular rigidity are
all in contrast to the symptoms of simple congestion.
In spinal tumors, the loss of motility is most marked upon one side,
and sensory disturbances (anesthesia) upon the other. There is also a
history of tubercle, cancer, or syphilis. The spinal symptoms develop
very gradually, as a rule,
Prognosis.—There is a tendency in all cases of spinal congestion for
the disease to progress along the cord. Moreover, the development of
structural disease of the cord is liable to be a result of excessive vascu-
larity. The prognosis is not unfavorable, if the case be one of a
localized type and unaccompanied by organic or inflammatory disease of
the cord or its membranes.
Treatment.—In cases of an acute character, where the symptoms
develop rapidly, leeching the anus will indirectly deplete the cord, and
dry-cups over the spine may also tend to relieve the congestion.
Hammond also suggests the daily use of three drachms of the sulphate
of magnesia in divided doses to cause watery stools, which require a
determination of blood to the intestinal canal.
irgot should be administered in large doses. I have given it in
doses of a drachm of the fluid extract after each meal for many weeks at
a time to patients without any symptoms of ergot poisoning. Bella-
donna, in doses of fifteen drops of the tincture, may be given with
benefit three times a day.
The employment of the hot douche to the spine—the water being
poured froma height of two feet upon the bare back for five minutes
daily—is highly recommended by Hammond.
Electricity is of service in the treatment of this disease. I prefer’
the withdrawal of static sparks from the spine to galvanism or faradism.
I have also employed the same treatment to the paralyzed muscles with
good results.
Strychnia and phosphorus are strongly contra-indicated, according
to Hammond,
SPINAL ANZZMIA. 447
SPINAL ANEMIA.
One form of this condition has already been discussed under the
head of “ spinal irritation.” This disease is believed by some observers
to depend upon an anemia of the posterior columns of the spinal cord.
Another varicty is thought to affect the antero-lateral columns of the
spinal cord (Fig. 91). If this condition be recognized as a distinct
disease, the symptoms will be of necessity connected with motility ; and
possibly with exaggerated reflexes, contracture, and atrophy. It will
also cover all of the so-called “ functional paralyses ” whose pathology is
now unknown.
_ I cannot express my full concurrence with these views; but, with
deference to those advanced by others, I shall here give the main features
of the disease as generally taught.
Etiology.— Extreme cold, sleeping on damp ground, exhausting
diseases, spinal embolism, thrombosis or atheroma, and interference with
the circulation through the abdominal aorta; from compression, throm-
bosis or aneurism of that vessel, may cause spinal anemia. Moreover,
the spinal vessels may be influenced to contract through the agency of
the vaso-motor nerves, as an indirect result of peripheral irritation from
any cause, such as the ovaries, intestine, genitals, eye-strain, injuries to
nerves, etc.
Symptoms.—The affected segments of the cord give evidence of
deficient blood-supply early by paresis of certain muscles. It is claimed
that the anterior tibial muscles and the peronei seldom escape. The
paresis rarely prevents walking, although the gait is generally feeble and
the patient’s endurance slight. The upper limbs are seldom paretic,
The sphincters of the bladder and rectum are seldom affected ; and
the paresis of the limbs is not usually progressive in type.
Sensory disturbances are infrequent. The cincture feeling is not
developed.
The reflexes may be normal or exaggerated slightly. They are
never abolished.
Prognosis.—If the exciting cause can be removed, the chances for
a complete recovery are good; if not, the spinal cord may undergo
softening.
Diagnosis.—The chief points, which relate to the discrimination -
between this disease and spinal congestion, have already been given
(page 445).
Treatment,—The utmost care should be exercised in ascertaining
the cause. My remarks concerning the effect of “eyestrain” in a
preceding section should be carefully considered, and all necessary tests
Should be made early to determine the condition of this organ and its
448 LECTURES ON NERVOUS DISEASES.
muscles. In the light of late researches made in this direction, I am
inclined to discredit the value generally placed by the profession upon
many of the other reflex causes enumerated, although more than one
cause may exist in any individual case.
The general treatment should be directed toward improving the
vitality of the patient.
SRL Vs
- FUNCTIONAL NERVOUS DISEASES.
29 (449)
SECTION V.
FUNCTIONAL NERVOUS DISEASES.
Unper this heading I propose to discuss certain abnormal conditions
of body, in consequence of which some special form of disturbance or
derangement of the nervous functions may be exhibited, which has not,
as yet, been shown to depend upon any positively recognized pathological
state.
Among this class of conditions may, in my opinion, be included a
certain percentage of epilepsy, chorea, hysteria, and hystero-epilepsy. In
this percentage, the existence of organic lesions can be excluded. Again,
neurasthenia (with its endless variety of manifestations), typical attacks
, of migraine or * sick headache,” certain obstinate types of neuralgia,
and, in some cases, evidences of imperfect performance of some of the
functions of the abdominal and thoracic viscera, are unquestionably to
be regarded as functional neuroses. :
JT am aware that I am at variance with the majority of authors in
thus grouping so many diseased conditions that are apparently dis-
cordant under one head. I may be severely criticised possibly by some
for so doing. I may even be taken to task for the selection of the term
“functional nervous disease,” which is rejected by many enthusiasts in
pathological research.
To show, however, that I am not alone in the position taken, I take
the liberty of quoting the following paragraphs from the preface of a late
work* upon this special field :-—
“Pathological anatomy has exercised such an enormous influence
upon the advances made in practical medicine within the last twenty-five
years, that many pathologists sneer at the term ‘ functional ’ disease, and
deny its very existence.
“While we fully agree that there can be no morbid manifestations
without a change in the material structure of the organs involved, we
are nevertheless fully convinced, in view of the fruitless search of
pathological anatomists, that the diseases which we have considered in
this work present no primary anatomical changes which are visible to
the naked eye or the microscope; in other words, that the changes are
of a molecular nature.”
While the truth of this statement appears to me self-evident, I have,
moreover, other reasons than those urged by this author for including
* Putzel—‘ Functional Nervous Diseases,”’ 1880.
(451)
452 LECTURES ON NERVOUS DISEASES.
under the term “functional” nervous diseases, the abnormal states
specified by me, as will appear later. These will be more apparent when
I call attention to what I regard as of vital importance in some of these
cases.
THE RELATIONSHIP BETWEEN FUNCTIONAL NEUROSES AND
ANOMALIES OF THE VISUAL APPARATUS.
The study of defects in the adjustment of the eye-muscles and the
relationship which exists between such defects and nervous diseases, has
not been generally regarded as of very great practical importance until
of late. Many of our best text-books upon the eye do not deal with any
such muscular defects, except in relation to strabismus. Some give
directions for testing the ocular muscles, that are in direct opposition to
the views which are here advanced. A few are positively misleading ;
chiefly on account of errors of statement concerning points where
physiological optics come into play.
I may be pardoned, therefore, if I review, in a general way, a few
points which have a practical bearing upon a method of examination and
treatment of the visual apparatus, which is to-day exciting considerable
attention among scientific medical men, especially among those whose
interest centres in the study of nervous diseases and in ophthalmology.
What I have to say here includes the discussion of the following
points of inquiry —
(1) What steps may be deemed as essential to success in the diag-
nosis and treatment of certain anomalies of the visual apparatus.
(2) Why it is that observations in this direction, when too hastily
or imperfectiy made, are peculiarly apt to be untrustworthy.
The limits of a few pages will hardly suffice for me to cover more
than a few of the more important points comprised under these headings.
What I have to say will, therefore, be as condensed as seems to me per-
missible. A personal experience, derived from several years of
continuous research in this field upon a class of patients afflicted
exclusively with nervous derangements, and from more than five hundred
graduated tenotomies upon the recti muscles of the orbit, justifies me,
I think, in expressing positive convictions.
‘The views which I shall discuss here constitute the basis of a
systematic method of examination for and treatment of certain ocular
defects, whose relationship to functional nervous diseases seems to me
to be now established beyond dispute.
Since these views were first advanced by Dr. George T, Stevens,
they have attracted no small amount of professional attention. In spite
of the fact that his contributions in relation to this subject are
remarkably clear and succinct, considerable misapprehension still appears
FUNCTIONAL NEUROSES AND VISUAL APPARATUS. 453
to exist in the minds of the profession at large relative to the views
advanced by him.
I may be pardoned, therefore, if, as an exponent of these views, I
repeat in substance much that has already appeared in print. By so
doing, I hope to concentrate attention upon certain steps employed in
the examination of the visual apparatus, whose order is deemed by no
means unimportant, and in some of which the observer should exercise
no small amount of care.
The following statements are, therefore, deemed by me as worthy
of your attention :— :
(1) The view is held that errors of refraction (by which I mean
near-sightedness, far-sightedness, or astigmatism) often modify apparent
muscular anomalies to.such an-extent as to render the early detection and
correction of refractive errors imperative.
This point is of vital importance in the treatment of many patients.
Clinical observation has conclusively shown that one of the most
important steps in correcting what is commonly known as a “squint,” or
“ cross-eye,” is first to properly detect any existing error in refraction and
to properly correct it. Such defects should always be sought for early,
and the effect of a proper glass upon the deviation of the axes of vision from
their normal position which demands relief should first be carefully noted.
Many cases are observed by oculists where spherical glasses alone have
corrected a marked “squint.” The neglect of this important step may
prove to be a serious omission, as it may lead to an error in diagnosis
or treatment, Let me impress upon you the fact that each eye of every
patient must be separately examined for refractive errors, and rendered
as nearly emmetropic as possible, before any test relating to the ocular
muscular conditions can be considered as reliable. It is not enongh,
therefore, for a neurologist to provide himself simply witha set of prisms
with which to examine his patients’ eyes for suspected muscular errors.
Any tests so crudely made are certainly unscientific, and probably
inaccurate.
. (2) The view is held that errors of refraction can only be positively
determined after the full effects of atropine; hence the step of dilating
the pupil is deemed of importance in most cases.
‘There are two sources of error which are possible in all oph-
thalmoscopic examinations as a step toward the determination of
. tefraction.
The first of these is that the observer may not be able to perfectly
relax his own “accommodation” while using the instrument. Most
oculists of large experience believe that-they can do this with cer-
tainty,—a belief which, in my opinion, is perhaps not always well
founded. The second source of error lies in the “ accommodation ” of
454 LECTURES ON NERVOUS DISEASES.
the patient. This cannot always be relaxed by instructing the patient to
look at an object twenty or more feet distant from the eye.
I am satisfied that mistakes in the determination of refractive errors
by the ophthalmoscope are far more frequent than are generally supposed.
For the past four years I have examined the eyes of every patient
intrusted to my care by the aid of test-type both before and after the
pupils have been fully dilated by atropine. I am not aware that I have
ever lost a patient by the use of this drug. In my experience, intelligent
persons are always willing to submit to a temporary inconvenience for
the purpose of obtaining positive information respecting any point that
is deemed of scientific value in relation to themselves. I have personally
come to regard the ophthalmoscope as an unreliable instrument for the
determination of refraction. Its use is rendered compulsory, however,
in very young children, and in ‘those who, from ignorance or feeble-
mindedness, are unreliable in their reading of test-type.
It is generally accepted, furthermore, among our best oculists that
astigmatism (a recognized source of nervous perplexity) is always esti-
mated more accurately with the pupil widely dilated by atropine than
with the normal pupil.
The reasons which I have already given must suffice to explain why
the use of atropine constitutes a most important preliminary step to the
detection and estimation of any error in the eye-muscles, although many
other arguments might be brought forward to prove its advisability in
some subjects.
(3) The view is held that no examination for suspected muscular
error in the orbit should be regarded as conclusive for diagnosis, or as a
basis for any surgical procedure, until the eye has been proven to be free
from refractive error, or rendered as nearly emmetropic as deemed
advisable by properly selected glasses.
It is, of course, advisable during the first interview with each
patient to note and record any “ manifest” defect in sight. If such
exists, each eye should be provided with the glass which gives the best
vision for each eye (the two eyes being always tested independently of
each other). After such correction, the different tests employed to
detect muscular anomalies should then be made, and the results of each
test should be recorded as the “‘ manifest muscular error.”
At the second interview, with the pupils fully dilated by atropine,
the sine steps should be repeated. We thus learn, in many cases, the
existence of refractive conditions which the first interview did not reveal.
We record such as “ latent ” refractive conditions, By the aid of suitable
glasses, any latent refractive error found is then to be corrected ; subse-
quently, at this interview, the muscular movements are to be tested with
each eye temporarily adjusted to distant vision by suitable glasses.
FUNCTIONAL NEUROSES AND VISUAL APPARATUS. 455
(4) The view is held that all tests employed to detect muscular
anomalies must be made with the test-object (preferably a candle flame) at
a distance of at least twenty feet from the eye. In this respect, the
method of conducting examinations advocated here is somewhat at
variance with that commonly described in most text-books.
In the practical office work of many oculists the so-called “line and
dot” test is generally employed (at a distance of fourteen inches from
the eye).
It is usually advisable to employ this test in addition to the
“candle flame” test at twenty feet; but, when it is employed, the results
obtained by each test should be separately recorded, The words “in
accommodation”? have been suggested by Dr, Stevens as a suflix to
designate the results obtained when the test-object is placed at fourteen
inches from the eye.
While it is deemed desirable in most instances to record the results
of both tests described above, all operative procedures are invariably
based upon the results obtained by placing the test-object at a distance
of twenty feet from the eye.
To a lack of uniformity in the tests made by oculists to detect mus-
cular anomalies in the orbit many of the discrepancies frequently met
with between observations made by different men upon the same patient
are unquestionably due. For example, a patient may exhibit an in- -
sufficiency of the externi at twenty feet, and of the interni at fourteen
inches, in spite of the fact that all precautions have been taken to
previously rectify existing refractive errors. This field is too large to
discuss here, but it is a very important one.*
(5) The view is held that observations made for muscular anomalies
in the orbit, when the test-object is within the limits of accommodation, are
not usually reliable as a basis for operative procedure undertaken for the
relief of such anomalies.
Experience goes to show that deviations of the visual axes observed
when the test-object is placed at twenty feet from the eye more correctly
represent the muscular error which needs correction in any given case
than when made at a nearer point.
I have encountered several interesting cases where extremely
satisfactory results upon functional nervous phenomena of a distressing
type have followed an operative procedure upon the eye-muscles, which
/ would have been strongly contra-indicated if I had attached as much
importance to the results of tests made with the test-object at fourtecn
_ inches from the eye as the statements found in most of the text-books
* See articles by G. T. Stevens, in New York Medical Journal, December, 1886, and in
Archives of Ophthalmology, June, 1887; also a. paper read by the same author before the
Toternational Medical Congress at Washington, D. C., September, 1887.
456 LECTURES ON NERVOUS DISEASES.
would justify. These cases impressed me very strongly at the time.
They bear the strongest testimony in favor of the view that convergence
of the eyes is a factor which should be eliminated as far as possible in
searching for muscular anomalies of the orbit.
(6) The view is held that muscular anomalies in the orbit may be
partially or totally “latent.”
The amount of muscular error detected in any given case does not
necessarily indicate the full amount of error that actually exists,
The results of ordinary tests simply tell us how much eye-tension
exists which the patient cannot overcome by any effort of which he is
capable.
Upon this one point too great stress cannot be laid, as it sheds much
light upon the clinical history of many patients who suffer from eye-
strain. :
All authorities recognize the fact to-day that a patient may have a
very marked congenital shallowness of the eye, and apparently have
normal yision, or possibly appear to be even near-sighted, prior to the
use of atropine. Subsequently to its use, the same patient will, however,
show a high degree of far-sightedness (hypermetropia), because the ciliary
muscle (temporarily paralyzed by the atropine) cannot overcome, or (to
speak more technically) compensate for the abnormal shallowness of
the eye.
Unfortunately for science, we have as yet no drug which aids us in
determining the existence of a “latent” muscular error in the orbit.
Yet, are we justified in concluding that latent muscular anomalies do
not exist? Most assuredly not. There is the strongest clinical evidence
to the contrary.
Only a few weeks ago, I examined the eyes of a prominent physician
on three consecutive days, and I was unable to detect (either before or
after prismatic exercise of his eye-muscles) any change in his ocular
condition from the one noted at the first examination. His symptoms,
however, led me to believe that a greater muscular error existed than he
showed, although the anomaly detected was a very marked and im-
portant one.
I therefore instructed him to wear a prism, which nearly corrected the
error then detected, until the next examination. Less than two hours
later, I accidentally had the opportunity of again examining his eyes.
His muscular error was then exactly double what it originally appeared
to be. He was again given almost a full prismatic correction for the
defect detected. Twenty-four hours later he was examined for the fifth
time, and he still showed an excess of two degrees over the record of
the day previous. He was again given a further prismatic correction;
but from that time he failed to exhibit any further alteration in his ocular
FUNCTIONAL NEUROSES AND VISUAL APPARATUS. 457
tests. The relief afforded by prisms was so instantaneous and permanent
(while they were worn) as to prove conclusively that the prisms were
wisely selected, and that the “latent” insufficiency, which was developed
after and by means of their use, more accurately represented his true
condition than did the original observations made at the first interview.
I mention this case, not because it is at ‘all unique (for many such
instances have been observed) but because it illustrates admirably the
existence of latent insufliciency, which happened in this case to be
developed rapidly by the temporary use of correcting prisms.
In the second place, it is not at all uncommon to observe the
development of latent muscular anomalies in the orbit after a graduated
tenotomy has been satisfactorily and scientifically performed for the
correction of a ‘“‘manifest’”’? muscular error. Sometimes, quite a long
interval elapses before latent insufficiency shows itself. Again, it shows
itself almost immediately.
An epileptic, upon whom I operated for eye-defect, ane who has
now been free from attacks for over one year.and a half, in spite of the
cessation of all drugs, showed me originally only one degree of esophoria.
This defect would, I think, have been heretofore regarded’ by most
oculists as hardly worthy of correction—even by a prism. , The sub-
sequent treatment of this case demanded repeated partial tenotomies
upon both of the interni; and proved not only that I had a high degree
of “latent” trouble to correct (which a one-degree prism would not have
helped), but also that the attacks have thus far been totally arrested by
the relief of abnormal eye-tension.
In the third place, it has been proven that systematic daily exercises
of the various eye-muscles (accomplished by teaching the patient to fuse
images which have been rendered momentarily double by a prism held
before the eyes) will in some cases develop latent muscular anomalies of
the orbit.
In other words, a patient, after a week’s muscular drill, will often
show a greater flexibility of the eye-muscles and the existence of a lack
of equilibrium in the eye-movements, which they did not exhibit at the
‘earlier examinations. JI am aware that an injudicious use of such
prismatic tests in’ the hands of a novice might cause “asthenopia,”
and seriously affect muscular conditions; but this fact can hardly be
used, I think, by fair-minded critics, to explain the phenomena alluded
to here.
Finally, it may be stated, in this connection, that one examination
of the various eye-movements is not, as a rule, sufficient for a positive
diagnosis respecting muscular anomalies. Repeated tests have often to
be made before a complicated problem may be satisfactorily solved, even
by an expert in this line of examination.
458 LECTURES ON NERVOUS DISEASES.
(1) The view is held that prismatic glasses are not only inadequate
as satisfactory remedial agents in most cases, but that they may be posi-
tively injurious to certain classes of patients.
Few, if any, of our prominent oculists have perhaps ordered as
many prismatic glasses as has the chief advocate of the method now
under discussion. Yet, in spite of this fact, strict limitations upon their
field of usefulness (not generally taught) seem to be rendered probable
by late investigations.
A careful study of the different movements of the eyeball, and of
the combination of muscles required to produce some of them, must
impress even the most casual reader with the idea that an agent (such,
for example, as a strong prism) which tends to restrict the movements
of any one muscle, may do harm if persistently worn.
Some patients are peculiarly susceptible to such influences. I have
encountered a large number of patients whose eyes refused to tolerate a
prismatic glass. Their symptoms were at once made worse whenever
they attempted to correct an existing muscular anomaly by wearing a
prismatic glass.
On the other hand, many patients are benefited at once by the use
of prisms, and suffer no inconvenience of any kind from them.
What are we to infer from this statement? Are we to surmise that
the prisms were either injudiciously selected or improperly placed,
simply because the patient could not tolerate them? Ithink not. Such
might possibly be the case in the hands of a novice, but presumably it
is not the case in the experience of one skilled in eye-examinations.
My own experience in several such instances has shown me that a
properly graduated tenotomy of the muscle exhibiting the greatest tension
has been followed by a complete cessation of the nervous symptoms for
which the patient sought relief, in spite of the fact that prisms prescribed
to correct the same error have proved intolerable to the patient, and
have markedly aggravated the symptoms.
There is, however, a practical atid important field for prismatic
glasses. It is well to keep, as a part of a physician's office equipment, a
large number of prisms of different angles. These can be slipped into’
a frame with the base inward, outward, upward or downward, as the
exigencies of any case seem to demand. They may be loaned from time
to time to patients, for the purpose either of verifying a diagnosis or, by
giving relief to a “manifest”? ocular tension, of developing a latent
muscular error which the physician may be led (by repeated examinations
of the patient) to suspect. When they are well-tolerated, the physician
may often learn a great deal by their protracted influence. When they
are not well borne, it is advisable, as a rule, to discontinue their use at
once.
FUNCTIONAL NEUROSES AND VISUAL APPARATUS. 459
It is often wise to prescribe prismatic class, also, for a class of
patients who are unable (for one reason or another) to submit at the
time to a graduated tenotomy.
Sooner or later, I find that such patients usually return. Asa rule,
they do so for one of the following reasons: (1) because they have
developed an additional “latent” muscular error, which the prisms
naturally failed to correct; (2) because they do not tolerate them well,
and are made decidedly worse by their use; (3) because they prefer a
tenotomy to the inconvenience of a glass which has to be constantly
worn; and (4) because they suffer from eye-fatigue, on account of the
disturbance to codrdinate movements of the eyeball.
’ There is no doubt that very many cases of nervous diseases are
materially helped (if not radically cured) by the aid of prismatic glasses;
but the question naturally arises to my mind in this connection, “ Would
they not have been more rapidly benefited and permanently relieved with
far less inconvenience to the patient by tenotomy ?”
(8) The view is held that a graduated tenotomy is the only way of
satisfactorily and permanently relieving abnormal tension of a muscle in
the orbit.
There are only two ways of overcoming an abnormal tendency of
the visual axes to deviate from parallelism whenever the eyes are directed
upon an object more than twenty fect off. One of these is by the aid of
a prism; the other is by a graduated tenotomy of the muscle, which
directly aids in producing and perpetuating the deviating tendency.
Whenever prisms are prescribed, they afford relief practically in the
same way as a “rubber muscle” does in orthopedic surgery; in other
words, they compel the muscle which is opposed to the base of the prism
worn by the patient not only to overcome the antagonistic muscle, but
also to so adjust the eye as to compensate for the refractive effect. of
the prism. They practically act, therefore, as a “ pulley-weight ”—
mechanical device seen in all gymnasiums.
Now, if the wearing of prisms had no deleterious action upon those
particular muscles, which, in each case, are not at all at fault, and if
they invariably exerted only beneficial effects, this principle of treatment
could be more generally applied with benefit. Even then, the existence
of latent insufficiency might, unfortunately, remain unrecognized for a
greater or less period of time, possibly to the serious detriment of the
patient. On the other hand, if it be satisfactorily demonstrated that
the operation termed “graduated tenotomy ” has been rendered a safe
and accurate method of correcting muscular anomalies in the orbit, a
fact has certainly been noted that opens a new and shorter route to relief.
Such a step enables us, moreover, to decide the question of “ latent ”
mingealar defects in any given case.
460 LECTURES ON NERVOUS DISEASES.
(9) The view is held that the difficulties previously experienced in
attempting to correct so-called ‘muscular insufficiencies” in the orbit by a
surgical procedure upon the stronger muscles have now been satisfactorily
overcome.
Space will not permit of a discussion here of the demerits of oper-
ations previously devised for this purpose. Suffice it to say that the
operation first suggested and performed by my friend, Dr. G. T. Seevens,
preserves the normal line of traction of the muscle.
This igs a point of vital importance to the patient, and one which
cannot be claimed, in my opinion, for any other operation previously
devised for this purpose with which I am familiar.
Any disturbance in the proper adjustment of the eye-muscles, which
must ensue from an alteration in the line of traction of any one or more
of the six muscles which move the eye, cannot help but be a serious
matter.
The full details of the operation alluded to have sean been
published.* I quote from an article lately read before the Neurological
Society of New York by the chief advocate of this method :—
“In the main it consists of making a small opening through the
conjunctiva, exactly over the insertion of the tendon, when the tendon
is seized by extremely fine forceps, and divided in each direction,
‘preserving the extreme outer fibres, or, at least, the reflection of the
capsule of Tenon, which serves as an auxiliary attachment.”
It may be stated in this connection that this operation is absolutely
painless when done under the influence of cocaine; that stitches are
never employed; that no subsequent dressings are rendered necessary ;
and that patients frequently go from the operating chair directly to their
business, A slight amount of redness and irritation about the wound,
and occasionally some sub-conjunctival hemorrhage (both of which tend
to rapidly disappear) are all the inconveniences which this operation
commonly entails. I have personally performed this operation about
six hundred times up to the present date, and I have never known
suppuration to occur, or any complications to be induced which caused
me serious perplexity.
(10) The view is held that “eye-strain” from any cause (be it
refractive or muscular) 7s @ serious matter, and that its tendency is to
predispose to nervous derangements and to perpetuate them when once
developed so long as this factor exists.
This is one of the most important, if not the chief claim made.
It is substantiated by many carefully made and collected observations,
It is chiefly in those cases where, in spite of a muscular error, the
images of the two eyes can be blended by a great effort that the patient
* Archives of Ophthalmology, June, 1887.
FUNCTIONAL NEUROSES AND VISUAL APPARATUS. 461
begins to experience the deleterious physical influences of abnormal
muscular tension in the orbit. Placing a plain red glass before one eye
of a patient suspected of having a slight degree of strabismus will often
reveal to a patient a diplopia of which he or she may have been un-
conscious. Such cases do not belong to the class discussed here as
those of “ insufficiency of the ocular muscles.”
It is not hard to understand why it is that an animal too heavily
laden is unable to rise after a fall has occurred until the load is taken
from it.
So it is with many nervous patients. The incessant efforts made to
fuse the images perceived by the two eyes into a single image (when a
muscular defect renders such an act possible, yet one of extreme difli-
culty) are liable sooner or later to exhaust the nervous force of the patient
and to excite some form of functional nervous disturbance.
This is the line of argument, which apparently seems difficult to
understand. It is a train of reasoning which many enthusiastic patholo-
gists naturally prefer to discard, because it puts an end to a search fora
pathognomonic lesion which no human eye (even with the aid of a
microscope) has ever yet been able to detect in many hopeless and
chronic cases of chorea, epilepsy, insanity, neuralgia, headache, hysteria,
and neurasthenia. Itis a view which will probably be opposed by some,
because it comes into direct antagonism with the prolonged administration
of the various bromide salts; in spite of the fact that the injurious effects
of such administration are too frequently encountered to be ignored. It
is a principle relating to functional neuroses which is naturally combated
on general grounds, because it is new, and opposed to preéxisting views.
Respecting the views here advanced, I take the liberty of quoting a
few selected paragraphs from a singularly lucid paper lately read by the
pioneer in this field before the Neurological Society of New York.* 1
do so because they appear even yet to be misunderstood by some who
listened to the paper quoted from. The author of that paper says :—
“A doctrine so much at variance with ordinary beliefs must. of
necessity excite suspicion that the proposition has been based upon
insufficient data, or that observations have been imperfectly made. That
neither of these suspicions is correct it is hoped may be shown to the
satisfaction of reasonable inquirers. If the proposition appears extreme,
and tending at best to the recognition of a single class of causes to the
exclusion of others, let me recall the fact that the proposition fully
recognizes any and all causes of nervous irritation, and that the influ-
ences indicated are held to be preéminent, but not exclusive permanent
causes, If greater importance is conceded to the influences mentioned
in the proposition than to others, it is from no unmindfulness of the
* New York Medical Journal, April 16, 1887.
462 LECTURES ON NERVOUS DISEASES.
possibility of other conditions acting as irritating influences, or that cer-
tain known or unknown influences may give character to the results of
irritation arising from the causes mentioned. Let it be remembered
that it has been universally conceded that the nature of the neuropathic
tendency is unknown. If one preéminently important element is de-
monstrated, it is not to be rejected because it may not include the
whole.
“In the explanation of the etiology and treatment of disease, neither
settled thcorics nor novel doctrines are to be accepted only as they are
confirmed by undoubted facts. Nor can isolated facts, nor facts divested
of their natural environments, be accepted as valid evidence in support
of theories, old or new. The facts must be uniform, occurring so regu-
larly as sequences as to demonstrate that they are consequences.
Unless the skilled observer is able to predict, with a reasonable degree
of accuracy, the result of certain combinations of circumstances, such
result, when occurring, must be considered accidental.”
“The principle of ocular irritation is of wide application, and is not
to be compared with the occasional irritation set up by such accidental
and usually secondary causes as phimosis is, the presence of calculus, the
existence of a stricture of a passage, the effects of decayed teeth, and of
many other peripheral irritations which might be mentioned. All these
are of importance, and are not to be overlooked.
“The conditions to which I have especially called attention are,
however, in general, commensurate with the life of the patient, and exist
in a vastly greater number of instances than either or all of the condi-
tions belonging to the other class just mentioned. Not only are those
painful or irregular conditions, usually described as neuroses, in great
proportion responsive to the relief from ocular tensions; but a great
variety of conditions, commonly regarded as local affections, yield as
readily, and prove that they are in faet reflex phenomena.
“Tf it be said that the origin and prevention of nervous diseases is
to be found in a great variety of circumstances, I reply, let us find them
all, and adapt our measures to them all, but let us not neglect this
because there may be others.
“For myself, I do not think that another as important class of
causes of nervous disturbance will be found as that which attends the
anomalies of the parts engaged in the performance of the visual function.
In any case, our aim is to prevent the evils of nervous derangement by
the early removal of any known mischievous tendency, and our duty is,
when such nervous derangement actually occurs, to remove every per-
plexing cause. In the observance of such a principle, we may leave to ~
superstition and to ignorance the practice of expelling nervous diseases
by means either fashionable or obsolete.”
FUNCTIONAL NERVOUS DISEASES AND REFLEX CAUSES. 463
ARE FUNCTIONAL NERVOUS DISEASES FREQUENTLY REFLEX
MANIFESTATIONS ?
The view that a direct relationship exists in many subjects between
epileptic seizures (that are apparently not associated with organic lesions
of the brain) and abnormal muscular tension within the orbit seems to
have received most valuable indirect confirmation in the startling
experiments published by Drs, F, X, Dercum and A. J. Parker, of the
University of Pennsylvania,* According to these observers, convulsive
seizures were artificially induced in apparently healthy subjects by
prolonged muscular tension of a single muscle or groups of muscles in
the limbs.
I regard these experiments as perhaps the most important ones that
have yet been brought forward in support of the general view that
epileptic seizures are, in the large proportion of cases, simply one of the
many types of manifestation that a reflex cortical disturbance is capable
of exhibiting.
It is unquestionably true also that such reflex causes are too
. often not sought for by the profession with sufficient care or in the
proper way.
The methods of examination that have been generally regarded until
of late as conclusive, when defects in adjustment of the eye-muscles
have casually been sought for, were certainly most crude and unscientific;
and a modification of them appears to be most timely.
I take the liberty of quoting from the published experiments of
Drs. Dercum and Parker the following paragraphs :—
“The subject being seated, the tips of the fingers of one or both hands were so
placed upon the surface of a table as to give merely a delicate. sense of contact, 2.e., the
fingers were not allowed to rest upon the table, but were maintained, by a constant muscular
efort, barely in contact with itt Any other position involving a like effort of constant
muscular adjustment was found to be equally efficient. Any one object in the room was
now selected, and the mind fixed upon it, or some subject of thought was taken up and
unswervingly followed.
‘After the lapse of a variable period of time, extending from a few minutes to an
hour, and depending upon individual peculiarities to be noted, .... the subject was
frequently thrown violently to the ground in a general convulsion, preceded by tremors
which rapidly hecame more violent.
“Seizures equalling in violence a general convulsion were by no means induced in all
subjects, and were generally the result of experiments repeated many times during the
same evening. In the experimenters the convulsions became so easily induced that it was
thought advisable to desist for a long period.”
* Jour. of Nervous and Mental Diseases, 1884, pp. 579 and 636,
{ Italics my own.
464 LECTURES ON NERVOUS DISEASES.
Dr. Chas. H. Thomas, of Philadelphia, when speaking of these
experiments in a late contribution to this subject,* says :—
“The effort of constant muscular adjustment here spoken of appears not unlike
the condition found in the eyes in cases of insufficiency of the ocular muscles; and
it seems not unreasonable to infer that if such strain of the muscles of the forearm
would produce results of the kind reported by the authors just named, that the strain
upon ill-balanced ocular muscles (which must be continuous during the whole of the
time that the eyes are opened) should be productive of even more serious, and, indeed,
permanent results.”
Within the past year, an extremely valuable paper respecting
one of the much neglected and perhaps not infrequent causes of
epilepsy has been also published by Dr. A. P. Brubaker,t of Phila-
delphia, entitled “Dental Irritation as a Factor in the Causation of
Epilepsy.” The following extracts from this paper have an impor-
tant clinical bearing, and possibly shed some light upon the proper
treatment of convulsive diseases and other forms of reflex nervous
conditions :—
“In all the wide divergence of view as regards the nature of epilepsy there is a
general consensus of opinion that its essential feature is of the character of an explosive
discharge from the higher nerve-centres, the nerve-force: thus liberated bearing down upon
the centrifugal distributions of the motor nerve-tracks with such an excess of energy that
incodrdination of movement reaches the stage of convulsion and spasm. Owing to the
periodicity of the convulsive seizures, it has been assumed that in individuals predisposed
to epileptic attacks the higher nerve-centres are in a state of high tension, of unstable
equilibrium, and that it only requires a stimulus of a definite quantity or intensity to
excite the explosive discharge.
“The object of this paper is to direct the attention of physicians to a cause of epilepsy
which has not hitherto been estimated at its full value, inasmuch as in none of the standard
works upon neurology is the subject even alluded to,—viz., pathological states of the dental
structures. That dental inflammations and disorders are more often provocative of
epileptic seizures than is commonly supposed appears quite certain from the following
cases, and also from the character of the cause and its effect. Many reasons might be
given why dental disorders are peculiarly adapted to call forth this periodical discharge,
and why these disorders are habitually overlooked by the physician, but they need not be
detailed here. As exemplifying these phenomena, some interesting and instructive cases
are adduced.
“The interest aroused by the result of the preceding case led to an examination of
medical literature for reports of similar cases. I find that no less than sixteen cases,
entirely and immediately cured by the removal of an irritating tooth, have been
recorded by different observers, and which are here arranged in chronological order.
It is not supposed that this collection embraces all the recorded cases, but it is hoped
that it will elicit references to many others, and, what is more important, the reporting
of many new cases.”
* Trans. Phila. Co. Med. Soc., Mar. 14, 1888.
t Jour. of Nervous and Mental Diseases, 1888, p. 117.
FUNCTIONAL NERVOUS DISEASES AND REFLEX CAUSES. 465
In the light shed upon this subject chiefly by recent contributions
to medical literature,* the view is gradually being accepted by many in
the profession that certain nervous diseases (whose pathology, to say the
least, is still in doubt) are possibly not dependent in every case upon an
unrecognized organic lesion; and they are being led to coincide with
the statement that the term “functional” nervous disease may be
properly applied, in some instances at least, to the graver nervous
conditions,—such, for example, as epilepsy, chorea, hysteria, or other
manifestations of nervous exhaustion, and insanity. In other words,
the professional mind seems more willing now than in the past to discard
an apparently fruitless search for a pathognomonic lesion for each
intractable nervous condition, and to look more calmly upon tangible
clinical facts, even if they are radically opposed to preéxisting views.
If the view that eye-strain, dental irritation, or other causes of reflex
disturbance may be a frequent cause of functional nervous derangements
proves to be the correct one, beyond the possibility of doubt or cavil,
it is not difficult to see that a hope of marked relief or of ultimate
recovery is practically extended to many hopeless sufferers upon whom
drugs have exerted little or no benefit.
In order that those of my readers who have possibly not given
much attention to the views which most of my incorporated cases are
particularly selected to illustrate may properly understand the train of
reasoning that offered a solution to my mind of the symptoms here
recorded, I take the liberty of quoting a few paragraphs from a paper
which I lately read before the International Medical Congress at
Washington, entitled “ Does a Relationship Exist between Anomalies of
the Visual Apparatus and the So-called ‘ Neuropathic’ Predisposition ?”+
This paper was based upon a carefully tabulated analysis of the records
*The reader is referred to the articles by Dr George T. Stevens on ‘‘ Chorea”’
(Medical Record, 1876); on ‘“‘ Anomalies of the Ocular Muscles”? (Arch. of Ophthalmology,
June, 1877); and on ‘Ocular Irritations and Nervous Diseases”? (New York Medical
Journal, April, 1877); also to his work on ‘‘ Functional Nervous Diseases” (D. Appleton
& Co., N. Y., 1887); also toa contribution by Dr. H. D. Noyes, on ‘‘ Tests for Muscular
Asthenopia and Insufficiency of the External Recti,’’ read by him before the International
Medical Congress, Copenhagen, 1884; also to papers by the author on ‘“ The Eye as a
Factor in the Causation of Some Common Nervous Symptoms (New York Medical Journal,
February 27 and March 15, 1886); on ‘“ Eye-strain in Neurology”? (New York Medical
Journal, April 16, 1887); on ‘ Eye-strain in its Relations to Functional Nervous Diseases”
(Medical Bulletin, September, 1887); and an abstract of an essay read before the
Tuternational Medical Congress at Washington, entitled ‘Does a Relationship Exist
Between Anomalies of the Visual Apparatus and the So-called ‘Neuropathic Predisposi-
tion?” (Medical Register, November 19, 1887). The articles by Drs. Dercum and Parker,
Dr. C. H. Thomas, and Dr. A. P. Brubaker, of Philadelphia (already quoted), are worthy
of special notice in this connection,
tAn abstract of this paper was published in the Medical Register, Ncvember 19,
1887,
30
466 LECTURES ON NERVOUS DISEASES.
of one hundred consecutive cases of typical neuroses taken from my
private case-book.
In this paper I say :—
Until there is a uniformity in the methods employed for testing the eye-muscles,*
and of terms for the recording of anomalies so detected, the profession must unfortunately
continue to be more or less embarrassed in this line of research, I do not feel justified in
personally discussing this subject here, as it has only an indirect relationship with this
paper; but I can not refrain from saying, in this connection, that to defective methods of
examination, made venerable chiefly by their antiquity, we owe to-day, in my opinion,
much of our ignorance of anomalies of the ocular muscles.
Some time ago I was struck, on looking over a children’s magazine, with an illustra-
tion designed to teach the reader the dependence of the various organs of the body upon
the brain. It represented the brain as the head of a manufacturing establishment sitting
at his desk, and around him were the various departments,—as, for example, the liver-
department, the stomach-department, the eye-department, etc. These departments were
connected with the head of the establishment (the brain) by telegraph-wires, through
which each could make its wants known and receive information regarding them.
Probably the designer of this sketch (made for the purpose of illustrating to the
child the dependence of the organs upon the brain for their successful operation, as well
as their actual support) built ‘better than he knew.” He embodied in his drawing a
graphic representation of certain fundamental principles of physiology which are not
clearly understood even by many adult minds in their. bearings upon the general health,
The lungs do not make us breathe; except in an indirect way, by asking the brain
to start the necessary muscles into action, The stomach does not perform its functions
until ‘after the brain has been requested by it to turn on the blood-supply in sufficient
quantities to produce the requisite quantity of gastric juice. The intestine performs its
incessant worm-like movements by no inherent power of its own, The heart keeps up its
rhythmical beating only when permitted to do so by the great centre of nerve-force.
Now, is it at all inconsistent with physiological principles to advance
the view that any excess of nervous expenditure to one organ over the
normal amount which should be furnished ‘is done at the expense of
the others sooner or later?
No one can draw incessantly upon his reserve capital of nerve-force
without incurring a risk of ultimately exhausting it. A bankruptcy in
the reserve capital of nerve-force entails untold ills to the individual.
The day of reckoning is postponed in any given case in direct
proportion to the drafts made upon the reserve and the amount of the
reserve. This may help us to explain why some escape it indefinitely,
while others are precipitated into indescribable distress when life is
hardly begun.
In case the bearing of eye-strain upon the problem of nervous
expenditure is not very clear to some of my readers, I deem it wise to
quote here some extracts from a late brochure of mine upon this subject
(N. ¥. Medical Journal, Feb. 27 and March 13, 1886).
* See article by Dr. G. T. Stevens in the Archives of Ophthalmology, 1887 and 1888.
FUNCTIONAL NERVOUS DISEASES AND REFLEX CAUSES. 467
Speaking of hyperopia, I say :—
Fortunately for our nervous system, the normal eye takes pictures of surrounding
objects. without any muscular effort when the object is more than twenty feet away; hence,
during the larger part of each day the normal eye is passive, and is practically at rest,
although performing its functions. How different is the condition of the far-sighted or
“hyperopic” eye, however, from the normal! For this eye (since it is too short in its
antero-posterior axis) all objects have to be focused by muscular effort, irrespective of
their distance from the eye. Such an eye is never passive. It has no rest while the
body is awake. It is always straining more or less intensely to bring properly upon the
retina the images of objects seen.
The “hyperopic”’ condition of the eye, or ‘ far-sightedness,” as it is called, is a very
common defect. It is especially frequent in persons of tubercular parentage. It is well,
therefore, to suspect the existence of this defect in children or adults whose ancestors
have died of “ consumption.”
Again, speaking of muscular anomalies, I use the following illus-
tration :—
A high-couraged horse feels the will, as well as the support, of his driver through the
reins by means of the bit. Although his course and rate.of speed are changed from time
to time at the will of the driver, the reins are never slackened. The horse becomes
acquainted with the desires of his master by a sense of increased or diminished tension
upon the reins. He is guided to either side by a difference in the tension of the two,
although the driver does not entirely relax his hold upon the opposing rein while he uses
the guiding one, and the difference in tension may be very slight.
‘ So it is with the normal eye. It is both controlled’ and supported while performing
its movements within the orbit by the eye-muscles (which are its reins), The brain is the
driver. At its command the eye revolves, or remains ‘stationary at any desired point.
The tension of muscles, opposed to any movement of the eye required, is so modified by
the brain as to insure the requisite support to the eyeball, and to steady it as it moves.
Thus, a perfect equipoise is constantly established between opposing forces, adjusted with
the nicest care to meet the full requirements of the organ under all possible circumstances.
The normal eye does not tremble or wabble when it moves or the attempt is made to
hold it in any fixed attitude. It is a piece of machinery, perfect in all its parts, reliable
in its movements, perfectly controlled by its master.
The eye with “muscular insufficiency” is like a horse with an inexperienced and
incompetent driver; the proper tension upon the reins is not maintained at all times, as it
should be; there is no equilibrium between antagonistic muscles; fixed attitudes are
maintained with difficulty for any length of time; the brain becomes more or less
disturbed by its inability to properly control the eye-movements, and exhausted by the
continual strain imposed upon it by the efforts required to do so even imperfectly.
A point may now be raised concerning which some misapprehension
seems to exist among medical men (judging from remarks which I
occasionally hear expressed). I refer to the relationship of actual
squint to nervous disturbances.
No one can deny that people frequently live for long periods of
time in houses impregnated with sewer-gas and in the most malarious
regions without apparently suffering in consequence. Yet no intelligent
468 LECTURES ON NERVOUS DISEASES.
man would attempt to prove to-day that sewer-gas poisoning and
malarial infection were delusions simply because some people had escaped
their influence.
The argument has been advanced that, because some cross-eyed
people have escaped epilepsy, chorea, insanity, and functional neuroses
of the milder types, it is erroneous to maintain that eye-strain has any-
thing to do with these conditions. This is absurd upon its face. The
hint might, perhaps, be pertinently dropped in this connection that
cross-eyed people practically suffer but little from their muscular error,
simply because they have habitual double vision, which no effort on their
part can correct, These subjects learn very quickly to practically
discard one image (the one seen by the crossed-eye) and to use one eye
only for ordinary vision. In other words, they never try to blend the
images of the two eyes, except in certain attitudes of the head, which
result in a single visual image without an effort on the part of the
patient.
It is only in those cases where (in spite of a muscular error) the
images of the two eyes can be blended by a great effort that the patient
begins to experience the deleterious physical influences of abnormal
muscular tension in the orbit.
If we admit the proposition that eye-defects, or anomalies of the
ocular muscles, are liable to become causes of impaired nervous energy
(because they demand an excess of nervous expenditure), we are forced
to the conclusion that the earlier this source of physical depression is
removed the better are the prospects of the person so relieved of
escaping diseases which impaired nervous energy necessarily tends to
hasten or develop. We are naturally led to question if the so-called
“neuropathic predisposition” is not dependent (in a certain proportion
of cases, to say the least) upon “eye-strain.’ We might possibly also
be led to think that the so-called “tubercular tendency” (which is
present, as far as my observation goes, in nearly 50 per cent. of all cases
of marked functional nervous disease) might, in some cases, be modified,
controlled, or perhaps arrested before its physical results become
apparent by taking from the life of such subjects a load which their
small reserve capital of nervous energy particularly unfits them to
endure.
It is hard to give up the view, so universally conceded, that a
predisposition to disease means a “constitutional taint.” Yet, in many
cases, we are absolutely unable to demonstrate that any evidence of
physical weakness or disease has appeared until sufficient time had
clapsed from the date of birth for the development of a serious impail-
ment of nervous energy. What has caused it? Has it been deficient
nourishment, a lack of maternal care or solicitude during childhood,
FUNCTIONAL NERVOUS DISEASES AND REFLEX CAUSES. 4469
gross violations of the rules of hygiene, ora lack of prudence on the
part of the individual when of matured experience ? The history of
case after case answers ‘‘no” to such surmises, These, then, sre not the
all-important factors in every case. Phthisis, epilepsy, chorea, headaches,
neuralgias, hysteria, dyspepsia, obstinate constipation, nervous prostra-
tion, inebriety, and many other evidences of the neurasthenic state are
markedly hereditary. What is the load (if any) which many sufferers
of this type are carrying through life? Have they a congenital burden—
which is, perhaps, too often unrecognized? I leave these questions for
future research to solve.
In this section I will call attention to a few cases selected from my
own case-book where the relief of ocular defects produced remarkable
and unexpected benetit after all hope of recovery had practically been
abandoned by the patient.
I bring these cases prominently forward in the interest of science
only; because the improvement made by these patients is attributable
not to drugs, but solely to Nature, when a burden of which she could
not rid herself was taken away and recuperation beeame possible.
Did you ever see a tired horse fall prostrate under an excessive
burden? How long would he remain so, were the burden not removed ?
Now, it should constantly be borne in mind that no two cases
exhibit identical manifestations of nervous depression or irritation.
Some patients who are suffering from such conditions manifest the effects
in physical, others in mental disturbances. The heart’s action may be
alone disturbed in some cases, the stomach may give out in others,
some may complain alone of spasmodic muscular troubles, some may
notice its effects in the eyes, some are rendered sleepless, many suffer
from more or less persistent pains, a few complain alone of skin
disturbances, and so on throughout the different parts of the entire
human organism. :
‘We can understand how these apparently discordant facts may be
reconciled when we recall the fact that by means of the brain and spinal
marrow, and the nerves which unite these centres to the different parts
of the body, we are enabled to see, hear, taste, smell, appreciate touch,
swallow, breathe, and perform voluntary muscular acts. It is by means
of our nerves alone that the heart beats; the digestive processes go on
without our knowledge or control through the same agencies; the blood-
vessels contract and dilate in accordance with the demands for blood
telegraphed to the nerve-centre by different organs and tissues; and
every process pertaining to life is thus automatically regulated.
It requires no medical knowledge to see at once how a disturbance
of so complicated an electric mechanism as the nerve-fibres and the
herve-cells of a living animal are can upset all or any one of the
470 LECTURES ON NERVOUS DISEASES.
individual functions enumerated. Many of our houses are furnished
to-day with electric bells by means of wires distributed in the wails. In
some houses we light the gas-jets, and even the rooms themselves, by
means of the same subtle fluid. When the battery becomes weak, or when
the wires are disarranged or broken, what may be the results? Some of
the bells may cease to ring when the button is touched, while others
work properly. Perhaps the electric light may fail in some rooms and
burn with its accustomed brilliancy in others. The gas-jets may not he
properly ignited. So it is with the nervous apparatus of man. From
the same cause one patient may have nervous dyspepsia, another sleep.
lessness, a third headache or neuralgia, a fourth weakness of the muscles,
a fifth disturbances of sensation, a sixth hysteria, chorea or epilepsy. It
is needless to multiply illustrations.
The nervous system of man has been very aptly compared to a
mountainous region where any atmospheric disturbance calls forth a
“ series of echoes” at distant points. So it is with many of the so-called
“functional diseases.” They may be simply the manifestations of a
disturbance of the nervous system, entailed by causes which have been
overlooked or imperfectly relieved.
Before I leave this subject it is but proper to say that a few cases
reported by me in this chapter (while not a large number in the aggre-
gate) were, without exception, well-marked cases of typical and intractable
neuroses, The improvement noted in each case after well-directed
treatment of the eyes or the eye-muscles tends to cast a doubt upon the
existence of any organic disease. No other causes of reflex nervous
disturbances outside of the eyes were detected after a careful search in
any of these cases; otherwise it would have been my manifest duty to
relieve all that were found in my efforts to benefit the symptoms
manifested by each patient.
It is not to be expected, nor do I anticipate, that views so radically
opposed to the ordinary methods of treatment by medication, now gen-
erally advocated for functional nervous diseases, will be accepted at once
by the profession at large, even if correct and satisfactorily demonstrated.
No great advance in science has ever been made until time has tempered
prejudice and modified the prevailing tendencies of thought.
Of late years we, as a profession, have had our attention drawn,
however, more seriously than ever before to the clinical importance and
the necessity of detection of remote sources of irritation to the nervous
centres. We have already learned that the ovaries, the womb, the pre-
puce, the urethra, the rectum, the alimentary canal, ete., can, in some
instances, induce serious nervous conditions which closely simulate the
evidences of organic disease. Complete paralysis of both legs has been
known to be cured in a child by circumcision. The operation devised
FUNCTIONAL NERVOUS DISEASES AND REFLEX CAUSES. 471
by Battey for the removal of the ovaries in subjects attacked with
hystero-epilepsy is to-day sustained by the profession, and often
performed with the view of removing a merely suppositious source of
reflex disturbance. This supposition, in many cases, is based, unfortu-
nately, upon tests much less scientific and therefore less reliable than the
tests employed to detect anomalies of the visual apparatus. It is safe to
question, therefore, if the source of reflex irritation in many patients of
this class has been carefully sought for, and if it does not lie more in the
eyes than in healthy ovaries,* which are not infrequently sacrificed.
Personally, I should not feel justified in taking so serious a step with
any patient until every other possible cause of reflex disturbance had
been carefully sought for in vain.
There is no doubt that many physicians of prominence are devoting
more attention to-day in their practical office work to the determination
of latent refractive errors in the eye and disturbances of equilibrium in
the eye-muscles than was their habit in years past.
This long-neglected but important element in the “neuropathic
tendency ” (and perhaps also in the “ tubercular predisposition ”’) is now
receiving from many sides the most thoughtful consideration. Sooner
or later, in my opinion, our views of the causes of functional nervous
disease will no longer be those now advanced in most of the works
devoted to that field. We shall in time more elearly recognize the fact
that drugs do more harm in functional neuroses than good whenever any
exciting cause of such a morbid condition persists and can be removed;
just as we to-day rely, in case of a joint-disease, more upon mechanical
separation of the surfaces of the inflamed joint than upon anodynes to
relieve the pain. We shall learn to search more carefully and intelligently
for obscure causes of reflex disturbances, and ‘to try the effect of their
removal before we resort to drugs. Medication must eventually, in my
opinion, become the dernier ressort of the physician, in this particular
class of nervous diseases, rather than the haven of refuge.
We are now prepared to discuss some of the various forms of
functional nervous disturbances commonly encountered in medical
practice.
The term “disease” can hardly be applied to a condition whose
morbid anatomy is unknown (as is the case with epilepsy, chorea,
hysteria, hystero-epilepsy, migraine, and certain forms of peripheral
paralysis, and neuralgia). These abnormal states are, properly speaking,
but symptoms, the exciting cause of which may often be involved in
obscurity, and the removal of which must, of necessity, form a very
important factor in the treatment.
* Cysts in the ovary are seldom, if ever, wanting ; hence, they can scarcely be pro-
nounced (when small) an evidence of disease.
472 LECTURES ON NERVOUS DISEASES.
EPILEPSY.
Of all the so-called “functional” nervous diseases, this condition
merits attention first, because it is the most grave. It consists of
periodical convulsive attacks, associated, in typical cases, with a loss of
consciousness.
The paroxysms may vary in regard both to their frequency and
severity.
The extent of the coma, the duration of the fit, the parts con-
vulsed, the mental aberration, and the constitutional effects which follow
the attack vary also in different subjects. Among the ancients, this
condition was regarded with peculiar horror, and was attributed to the
“possession of a devil.”
Varirties.—Custom has established a classification of this con-
dition into types, as follows :—
(1) The “Granp MaL” or typical attack, where consciousness is
totally absent during the convulsive stage.
(2) The “petit MaL” or mild attack, in which consciousness may be
wholly or partially retained, and the convulsive movements may
‘be slight or absent.
(3) To these, may be added a condition known as “IRREGULAR
EPILEPSY.” :
These distinctions are not clinically accurate. Cases do occasionally
occur where consciousness may be wholly lost, and yet the convulsive
movements may be partial rather than general. Again, general con-
vulsions of a severe type have been observed in rare cases where con-
sciousness has been perfectly retained. I have encountered, moreover,
a few cases of petit mal where certain peculiar attitudes of the ex-
tremities and face have taken the place of convulsive movements and
consciousness has been only imperfectly lost.
I have frequently seen patients have an epileptic attack in my office
while sitting upon a chair without falling from it. One patient now
under my charge has had numerous attacks while walking in the street,
which, as his attendant assures me, did not demand any aid on his part
toward supporting the patient.
Etiology.—Heredity plays an important part in the history of many
cases. A record of epilepsy, hysteria, insanity, chorea, migraine, or
phthisis is commonly found to exist in some branches of the ancestral
line. Tnebriety may also have been frequently observed on the father’s
or mother’s side.
Some adults are apt to trace their first fit to masturbation; or
to excessive venery, some great mental excitement or strain, or some
infectious disease (prominently syphilitic infection).
EPILEPSY. 473
Most epileptics also give a history of some severe injuries received,
to which they attribute (too often erroneously) their convulsive attacks.
Investigation will usually show that these injuries are apt, however, to
be the result of an attack rather than cause, or to be a mere coincidence.
Traumatism may, unquestionably, in rare cases, prove an exciting cause
of epilepsy, but I believe the frequency of such cases to be greatly over-
estimated. ‘The same remark would apply to some organic brain-lesion.
In the third place, any condition which creates marked reflex
trritation—such, for example, as eye-defect, dental irritation, phimosis,
gastric or intestinal disturbances, cicatrices involving nerve-filaments,
foreign bodies or wax in the ear, ovarian irritation, uterine or rectal
diseases, the first menstruation or coitus, ete.—may, in some subjects,
induce epileptic seizures. A large proportion of the epileptic attacks
of infancy are unquestionably brought about by trivial reflex causes.* In
adults, however, the reflex causes enumerated (with the exception of
“eyestrain” and bad teeth) are, in my opinion, less apt to induce true
epilepsy than the profession generally suppose.
It is very uncommon, in my experience, to meet with male or female
adults (in whom attacks of epilepsy have commenced after the seventh
year) which fail to show some abnormality of refraction, or in whom the
condition known as ‘“ ocular insufficiency ” is not found to exist toa
marked degree.
Ihave one patient under my care at present who, for years, had
always been seized with an attack on suddenly going from the light into
darkness. Another (who, happily, has apparently about recovered after
partial tenotomies performed upon the eye-muscles) had the first two
attacks when exposed to the dazzling reflection of the bright sun upon
a rough sheet of water, and was rescued from drowning twice in conse-
quence. A third patient of mine, who had several attacks daily when
on land, would, strange as it seems, skip many wecks without a fit when
on shipboard, where his efforts to accommodate vision for near objects
were infrequent. He had very serious refractive and muscular anomalies.
Finally, it must be conceded that organic changes within the brain-
substance or irritative lesions of the cortex may, in a certain proportion
of cases, induce epileptic attacks. A depressed fracture of the cranium
or an exostosis, for example ; a meningeal thickening; an abscess within
the skull; parasitic deposits ; gummata, etc., have been shown to have
induced attacks of this character.
We may assume in cases of epilepsy that, as a rule, the condition
becomes more grave after the seventh year than in early childhood,
—especially if no well-ascertained cause of reflex irritation can be
* Worms, indigestion, phimosis, teething, etc., are often accompanied by epileptic
attacks in infancy or early childhood.
474 LECTURES ON NERVOUS DISEASES.
discovered. It is impossible as yet to express any definite knowledge
regarding the relative freyuency of such causes to the total number of
epileptics encountered ,—because the published records of such cases are
singularly imperfect in reference to the examination of the eye. The
following statistics (taken from Dr. Stevens’ prize essay) will, however,
prove of interest in this connection :—
Total number of cases reported, a ae ae include all cases up to
Total taken from the author's private practice, . 1882,
An analysis of 100 consecutive cases of typical epilepsy, from number
above mentioned, shows the following refractive errors to have existed :—
Hyrerorra or Hyprropic ASTIGMATISM, . . . present in 59 cases, or . per cent.
Myopra on Myopic ASTIGMATISM, . . . .. ee 23: a
Refractive errors of less than 1 dioptre, . . . e 1g © i3 “i
Total, 100
The condition of the eye-muscles was not sufliciently well reported
in many of these eases to allow of percentages being given in reference
to this important factor.
My own examinations up to 1887, of a much smaller number, show
that my private cases possess a much larger percentage of hyperopic
abnormalities (in excess of 1 dioptre), and a smaller proportion of
myopic defects. In fourteen cases carefully observed, prior to 1887,
nine were markedly hyperopic, four were myopic in excess of one dioptre,
and only one was emmetropic. In every case but one, a marked condi-
tion of esophoria was found. In five, hyperphoria existed in addition to
esophoria. In the remaining case, a hyperphoria of about 4 degree was
all that was detected. The following summary of these cases may shed
possibly some additional light upon this new field of inquiry :—
Total cases, 14. (All of the severe type.)
FREQUENCY OF THE AT- EXAMINATION ‘OF
7
MENTAL |
TACKS (IN SPITE OF; ioe 2 EYES: peteoep STATE t REMARES.,
ACTION OF BROMIDES) © Refractive Muscular | OF PATIENT.
WHEN FIRST SEEN. | | "2pyor. hrven
Seer ty ftp a ey hag
” Beophor ia, | Markedly af. | One of these cases
13cases. _ fected in 5 cases. had 52 convulsions
| in 8 honrs, after
Huperphoria, ‘Slightly affected : stopping the use of
ATER of over five ‘fits | H., 7 cases.
each day, 1 case.
Average of three per day, ‘Ha., 4 cases,
4 cases | 5 cases. In 8 cases. | the bromides.—each
Average of two per day, M., 4 cases. Exophoria, Unaffected in | fit lasting 3 min-
2 cases. ‘ 0 case. 6 cases. | utes.
4
Average a one per week, Ma., 1 case. | Heterophoria. | In all of these cases
cases, 14 cases, the frequency of
Average of one per! Em.,1 case. | Orthophoria, Pe ny
month, 3 cases. 0 case. ae th
discontinued the
Occasional attacks, 2 use of the bromides.
cases. “|
Total cases=11 | Total= 1 * * __ Total=lt at
*Some of these wvatlantis showe ‘la au more fan: one eye-defect ; Tene: these two columns
cannot be tallied.
+ The symbols used in this table are explained on p. 130.
EPILEPSY. 475
Morbid Anatomy.—In spite of the fact that much has been written
upon this subject, no primary changes of an anatomical character can be
asserted to be pathognomonic of epilepsy.
In this view, I think that most of the later authorities stand
agreed,
The view of Schroeder Van der Kolk (1859) that the vessels of the
posterior half of the medulla (those affecting chiefly the roots of the
vagus and hypoglossal nerves and the fourth ventricle) were unnatu-
rally dilated is not now accepted. That of Kroon (asymmetry of the
olivary bodies); of Solbrig (constriction of the spinal canal, with second-
ary atrophy of the medulla); of Lélut (sclerosis of Ammon’s horn); of
Cooper (compression of the carotid arteries) ; of Landois (venous hyper-
wmia of the brain and spinal cord); of Nothnagel (irritation of the
“convulsive centre ” in the region of the medulla and pons); and many
other equally fanciful hypotheses have been proven to be more or less
fallacious. .
The exhaustive paper of Hughlings-Jackson (1873), in which he
advocates the theory of “explosive discharges ” of the cells of the brain
in epileptic attacks, is rather physiological than pathological in its scope.
If, as he believes, a mal-nutrition of the brain-cells exists as a primary
state (which predisposes to these paroxysmal explosions) the importance
of the detection and removal of its cause becomes the more apparent.
The paper referred to aids us more in localizing an intra-cranial lesion
of an irritative type than in explaining the occurrence of genuine epilepsy
as we commonly encounter it.
In the light of later researches, it is, in the opinion of the
author, not necessary to discuss at length the view of Lasegue
(1877) that epilepsy proceeds from cranial asymmetry or mal-
formation.
Brown-Séquard has shown that animals can be made epileptic by
injuries to the spinal cord and peripheral nerves; but, as some weeks are
required to induce this result, these experiments seem to show that some
secondary changes in the nerve-tissues had probably developed as a
result of the injury inflicted.
Eccheverria claims to have discovered serious changes in the
cervical sympathetic ganglia and the sympathetic fibres in connection
with epilepsy. Similar changes have been observed, however, by Mayer
and others in connection with diseases of the brain associated with
vascular disturbances.
Symptoms.—The general character of a severe epileptic attack has
been partially described already in a previous section (page 155). Jt
will simplify description to consider certain features of the attack
separately.
476 LECTURES ON NERVOUS DISEASES.
GRAND MAL.
PremMonitory Symproms.— Most epileptics affected with “orand
mal’? have some peculiar sensations (the aurexe ) which indicate the
approach of an attack. Some subjects experience a marked change in
temperament for a day or two prior to the fit. They become either
gloomy, sullen, inclined to anger, or, in exceptional instances, more
cheerful than usual, Again, the skin of the face and neck may assume a
a dusky hue some hours before the attack, In others, headache, cardiac
palpitation, pain in the precordium, a sense of distension of the ab-
domen, a diarrhwa, attacks of vomiting, sensitive spots on the limbs,
attacks of agraphia, giddiness, unnatural loquacity, etc., have been
reported as forerunners of an epileptic fit.
Aure connected with the special senses are not uncommon. Some
patients perceive an unnatural color (usually red or green or blue) in
the field of their vision. Some patients of this class habitually see
objects enlarged or diminished in size—an evidence of eye-defect. Others
see a rising mist or various unnatural objects (as in a dream). To smell
bad odors, to hear strange or unnatural noises, to taste unexpectedly
obnoxious things, or to feel numbness, etc., are not infrequently a note
of warning to epileptics to seek a recumbent posture.
The muscular aure observed comprise an unexpected and un-
controllable spasmodic movement in some part of the limbs or body,
a sudden activity in the facial muscles, a sudden tendency to rotate the
body, or to break into a run while walking, and a sudden stiffness or
immobility of a part.
Vaso-motor aure are not uncommonly observed. They comprise
spots of pallor or flushing upon different portions of the skin, an
unnatural heat or coldness in some part, a tendency to. sudden local
perspiration, and flashes of heat or of cold shooting over the whole
body.
Psychical aure are occasionally exhibited in the form of delusions,
hallucinations, and illusions,
The Epileptic Cry.—In a certain proportion of cases, a peculiar cry
precedes the fit. It may be a shriek, or again it may be scarcely audible.
IT have known it to awaken all the patients in a hospital ward from deep
slumber. The patients are usually unconscious of having uttered it,
and it is probably due to a very forcible expiration through a partially
closed and rigid glottis.
Indications of Alarm.—Some epileptics have a facial expression of
great alarm just preceding the fit. This is more common in children
than in adults. In rare instances, the attitude of the hands and arms
express the same mental state.
GRAND MAL. 477.
Actua Symrtoms.—At the approach of the fit, it is common to
observe a marked facial pallor. KEyen in “petit mal” this is generally
present. In exceptional cases the face may appear congested.
The Stage of Rigidity.—If the fit is a severe one, the body
becomes at first as rigid as a board. The limbs are extended,
the feet inverted, the fingers and toes are commonly flexed, and
the head is thrown back and usually turned to one side. The
whole body may be twisted backward or laterally. The eyes are
fixed during the tonic stage, and the pupils are, as a rule, widely
dilated. The breathing is partially or totally arrested. Sensibility
is abolished. :
The Stage of Clonic Spasms.—After the tonic stage has lasted
for a short time (about two minutes or less), convulsive movements
begin, the whole body being alternately thrown into violent contraction
and relaxation. The face is distorted by terrible grimaces and assumes
a purplish hue. The breathing gradually becomes loudly stertorous ;
the saliva escapes from the mouth as froth, and is often bloody from
wounds inflicted by the teeth upon the tongue. ‘The urine, semen,
and feces are often passed involuntarily. The clonic spasms generally
subside by degrees, growing less and less violent until they entirely
cease, As the convulsions subside the face becomes less dusky. During
this stage the eyes may stand open and seem to protrude from the
socket; but they are generally turned upward, so that the white of
the eye only shows beneath the blinking eyelids. They sometimes
become intensely congested, so as to give the eye a resemblance to
raw beef.*
The pulse cannot be satisfactorily observed in this stage on account
of the muscular movements. ;
Stage of Recovery.—When the convulsive movements have entirely
ceased, and the breathing has resumed its normal character, the patient
lies limp and helpless for a short time and gives evidence of a desire to
sleep. If aroused, he acts as if dazed and stupid; answers questions
with reluctance or imperfectly ; looks about him in a semi-conscious or
frightened way; mutters to himself some unintelligible sentences; and
relapses into a lethargic sleep. Cases where complete epileptic coma
has lasted forty-eight hours have been reported. As a rule, however, a
sleep of a few minutes suffices to enable the patient to walk with slight
assistance.
The fit usually leaves a sensation of dull headache for several hours
and great muscular fatigue.
* Serious difficulties may occasionally arise from this intense congestion after a partial
tenotomy of the eye-museles has been performed. I have had two patients intensify the
effect desired from a graduated tenotomy by a fit occurring soon after the operation.
478 LECTURES ON NERVOUS DISEASES.
In very severe fits, the teeth, and even the jaw itself, have been broken
by the violent muscular movements, the tongue completely divided, the
clavicle fractured, and muscles torn across. One of my patients worked
his way through the ash-door of a furnace (12x16 inches) during an
epileptic fit, and the brick-work had to be removed to extricate him.
Fortunately no fire was in the furnace.
Many epileptics fall very violently when the fit comes on, because
of insufficient warning. It is very common, therefore, to encounter
scars on different portions of the body in these subjects. The edges of
the tongue usually give more or less evidence of previous attacks of
“orand mal.” They are badly scarred, or ragged, from imperfect union
of old wounds.
PETIT MAL.
The milder forms of epilepsy may assume a variety of types.
Personally, I do not regard any attack as one of true epilepsy unless
consciousness is more or less completely lost; hence, I do not usually
include among this particular class those subjects who suddenly have
some of the premonitory symptoms of grand mal, already described, and
still retain a perfect knowledge of their surroundings.
Subjects afflicted with petit mal often assume a fixed attitude without
any premonition of an attack, and stare unconsciously for a few seconds.
I once had a patient who would frequently do this at a card-table without
dropping a card or losing the run of the game. He played for very
heavy stakes and was usually a winner.
Occasionally, these subjects will stop in the middle of a sentence,
grow pale or red, and remain motionless for half a minute or more with
the eyes staring into vacancy. They will then finish the sentence and
be unaware of the intermission which had possibly alarmed the rest of
the company.
Facial grimaces or slight twitchings of the muscles may occur in
more severe attacks of this character, and the urine may be voided
unconsciously, ,
Some attacks of this type are exhibited by the patient walking about
in an aimless way, with inarticulate mutterings, as if in search of some-
thing.
Petit mal is usually associated with some ill-defined aura, which
leads the patient to suspect that he has had an attack accompanied by a
temporary loss of consciousness. Some subjects compare these attacks
to “a dream;” others feel dizzy or nauseated; a few suffer an in-
describable physical distress. I have had several patients of this class
who have told me that they “became blind” for a moment. An uncon-
trollable dancing of the eyes (nystagmus) occurs during these attacks
in one of my patients, of which he is conscious.
IRREGULAR EPILEPSY. 479
Momentary strabismus is not infrequently observed in epileptics.
It may occur independently of a fit or in conjunction with one.*
IRREGULAR EPILEPSY.
These attacks are of a peculiar kind, which are indicative of a
condition designated by Hughlings-Jackson as “mental automatism.”
Hammond classes them as aborted paroxysms.
Such attacks are characterized by acts on the part of the patient of
an impulsive and unnatural character, of which he is unconscious. ‘They
simulate in some cases attacks of momentary insanity. There are no
muscular twitchings, as a rule. These attacks may occur in subjects
who have never had either grand mal or petit mal. They are usually of
short duration (a few minutes only, as arule). Acts of violence are not
uncommon in these attacks. Patients often wander without proper
preparation through crowded streets, commit acts of immodesty or
indecency, utter lewd expressions, etc., during these attacks, without a
knowledge of doing so. Some suddenly find themselves standing or
sitting in unexpected places (as in a closet), or committing some act
which they had no will and often no motive to perform. These attacks
may occur at any time of the day or night, and cannot usually be traced
to any special cause. Kleptomania and other unconscious acts of crime
may be attributed (in some cases) to this particular form of epilepsy.
Diagnosis.—The various types of epilepsy may be confounded with
comatose states and with other convulsive attacks; such, for example,
as those of cerebral congestion ; alcohol- or opium-poisoning; the con-
vulsions of uremia, hysteria, apoplexy, cerebral organic lesions, and
feigned epilepsy. The table on the following page will aid the reader
in the diagnosis of some of the more important conditions mentioned.
COMPLICATIONS OF EPILEPSY.
Various forms of mental disturbance may develop in connection
with epilepsy. I have observed several cases where such disturbances
have assumed the condition of permanent insanity; but they are, as a
rule, of short duration. The condition described as “irregular epilepsy ”
is particularly liable to manifest itself in this way. It is stated by
Reynolds that one-tenth of all cases of epilepsy develop epileptic mania.
This proportion seems to me to be somewhat excessive.
* In this connection I may remark that the constant efforts which epileptics
commonly and unconsciously make to avoid being cross-eyed is, in my opinion, one of
the causes of their attacks. If they were actually cross-eyed, they would learn soon to
disregard the visual image of the distorted eye, and their diplopia would be clinically of
no account. As it is, they suffer in many cases from. a very high degrce of “latent 7
insufficiency, which they instinctively endeavor to overcome in order to prevent diplopia.
This subject has been discussed on a preceding page.
LECTURES ON NERVOUS DISEASES.
480
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Saas. een Nn Irregular or scanty menstruation. It may be suppressed (amenorrhea),
: * | 6. Vicarious menstruation by the lungs or the rectum.
7, Retention of urine. (Requiring the regular use of a catheter.)
8. Abolition of sexual excitement.
[ 9. Increase of sexual excitement. (Nymphomania.)
Morbid desire for sympathy or for attracting attention.
¢ Premonitory Apathy to external surroundings, e
manifestations Obstinaey to all influences exerted upon the patient.
Sudden transition from gayety to sadness, or vice versa.
Hallucinations.
D Acute manifes- | Delirium.
Psy. CHT can 4 tations. { Ecstasy.
DISTURBANCES, Mania,
Melancholia.
Ecstasy. : .
Somnambulism (usually followed by convulsions, if the
Chronie mani- patient is awakened while out of bed).
festations. Nymphomania. .
Lethargy or stupor. (Has béen known to last for months
without any interruption. )
Trance, (It may simulate death very closely, in some cases.)
Elevation of temperature. (Sometimes preceded by a chill.)
BR Salivation, (erocably due to irritation of the central origin of the chorda
Vaso-MorToR tympani nerves. )
D Polynria. (The urine being very light in color and deficient in salts.)
ISORDERS. | edema: (Usually appearing suddenly without cause and disappearing as
suddenly.)
After a perusal of this table, the thought may occur to the reader
that it would have been easier to mention the symptoms which do not
occur in hysteria than those that may be encountered. It is safe to say
that no nervous