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 -eL SUOISNTOUOD SUIMOT[OF OT AJSul YoryA spunoss ay? ayerooidds 04 lapvor oy} opquue ATquqoad [IM sosed Surpooaad atyy Jo s}uaqu0e any “MIT DNIWNG GAZITVOOT Ad AVN NIVUT AHL Ao SNOISHT HOIHM AMT SWOLdUWAS OILSONDVIG AHL JO AUWVWWOS V "ToYV] POSSNOsIp oq ][LA WA o199 dy} Jo sJoury Surperoosse oy. 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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 Co-ordination . Pulse eas icts ques serragtai wits ce etorepreeseereonss te Tem peratures ¢csnmactaua acavaias tome heanamtaneae Respiration.... Tibi leary tae ine Sh sx csraisca claiggarete sian s Sadana Land Waiting ks Gusas iswaiar dated era merece DeeeneN Condition of arteries.......+-.0 of urethra... of bladder. of urine... ‘Of heart. ccc scuewntosanornsiensnitee 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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ST Ue came NC ESS tTe tal SHTOSATY JO THNALOVALNO,) Aq peapedarid yon) | “postop pruen aq SBT SAPD pd RQ PIpIIaT 7719 ‘Aappuovagy RAD WIE | WOLPEULLO TUL of ee eo OORRTOPUL SOT USTLUL wippipd pu} “PVA VATG WIAPFO PL es ww go seta opou, sucagdiuls PUMA | TE Saoysty Peoturp: 24 Je fen OL at : ‘paaAToOA | | “UL SE wwn)o0o 4 Baio . fe Sicet (| H.1375] 9A FL} DIDI DCE popooPvu, popoayeuyy t -VIIBSUXI Ih Tea | | \ ! i “[VLOVTI IO i | ‘sissqered ; TROVE aq, AVY 3 jo Apuepuodep ‘ ‘sts dpuaud omy : “ysIxXo ; Meso teL (UE to sistyured =f royse sdopoaoy bi joa AvUI 10 AVY | LaqygZu sdopaar i | i “ATT ( : | -waayxa readdu “(quosaud Jt) ou} UT Ay etvadsa recs . TRAVILTLULL OCy sew) “SqUEp oy Fo Lan PWISKLY queasy | -ULIOFap OTYSLIEy | | L DIL B sasuy,) ‘op SsIOurnayy : 2 ‘SHOWIN “SISOMI 10S \ “‘O2UO.LY,D oqnNopy inwidy aydayynyy | ‘SISONA IOS Ph a ete TVUELVT : oe f | ‘SNOISHET TVOOK | SEE AO SLORY SILITHANOITON “SISOUATIS IVNIdS TVXRLVT 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. 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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. 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Spas . ‘ si i WAIT ani ev ani & = 4 passer eal speotante = ‘ TOTAL JON MOI Oy OTL EL \ IO patives Jo [se ‘uaqIq JON |se ‘uazaIq ION i UIAION) io pativog { SD SOL L potavos 4o NJ = g . . 3 | . Ie 9yelIp i “ e é . eee ee eee 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