COLUMBIA LIBRARIES OFFSITE 
 
 HEALTH SCII MCI '. MANDARD 
 
 HX641 23952 
 RC341 -St22 1 891 Familiar forms of ne 
 
 RECAP 
 
 Hi 
 
 wSBm 
 
 mmm 
 
 Ural 
 
 ,w3BbSk^8&5i 
 
\Kcm 
 
 -St M. 
 
 Columbia (Bntoraiitpl^ 
 
 in tl) f Cttp of itogmft 
 
 Collcgf of $f)psictans! anb ^urgeonei 
 Hibrarp 
 
 -CD. 
 

 yv^s/r. 
 
 ^ H **m 
 
Digitized by the Internet Archive 
 
 in 2010 with funding from 
 
 Open Knowledge Commons 
 
 http://www.archive.org/details/familiarformsofnOOstar 
 
FAMILIAR FORMS 
 
 OF 
 
 NERVOUS DISEASE 
 
FAMILIAR FORMS 
 
 OF 
 
 Nervous Disease 
 
 BY 
 
 M. ALLEN STARR, M.D., Ph.D. 
 
 Professor of Diseases of the Mind and Nervous System, College of Physicians and 
 Surgeons, New York 
 
 WITH ILLUSTRATIONS, DIAGRAMS, AND CHARTS 
 
 -SECOND EDITION 
 
 NEW YORK 
 WILLIAM WOOD & COMPANY 
 
Copyright, 1890, 
 
 WILLIAM WOOD AND COMPANY. 
 
 1811 
 
PREFACE. 
 
 ADVANCES in knowledge in the department of neurology 
 have been of late more rapid than in any other branch of 
 medicine. The result has been to render diagnosis in many 
 affections, previously obscure, both more precise and less 
 difficult; and to open to successful surgical treatment many 
 diseases formerly considered fatal. It is the object of this 
 volume to make available to the general practitioner some of 
 the results of later investigations which have a direct and 
 practical bearing upon the commoner forms of nervous disease. 
 The facts which have been chiefly emphasized are those which 
 enable one to make an accurate diagnosis of the nature and 
 of the location of lesions in the central nervous system; for it 
 is evident that such a diagnosis is the essential preliminary 
 both to medical and to surgical treatment. 
 
 This work is not a treatise upon nervous diseases. It is a 
 series of clinical studies of the more familiar types. The 
 chief source of all medical knowledge is the careful study of 
 groups of cases by those who have at their disposal a large 
 supply of clinical material. The data which have been utilized 
 in the preparation of these studies have been selected from 
 American sources, chiefly from the Nervous Clinic of the Col- 
 lege of Physicians and Surgeons. My assistants in that Clinic 
 have joined heartily in the work of collecting and analyzing 
 the material, and have prepared several of the most valuable 
 chapters. I take pleasure in acknowledging my indebtedness 
 
vi PREFACE. 
 
 to Dr. Frederick Peterson, the Chief of Clinic; and to Dr. 
 Walter Vought, Dr. Winslow W. Skinner, Dr. Edwin E. 
 Swift, and Dr. M. L. Goodkind, the clinical assistants, for their 
 
 co-operation. 
 
 The eases which are recorded have been carefully chosen 
 from a large number because they present typical features 
 and indicate the possibilities of surgical as well as of medical 
 treatment. It is hoped that as a contribution to clinical 
 neurology they may be useful and that these studies may 
 stimulate similar work in other large clinics of this country. 
 
 M. Allen Stark. 
 \ i w York, .May ist. 1S90. 
 
CONTENTS. 
 
 CHAPTER I. 
 THE LOCALIZATION OF CEREBRAL FUNCTIONS. 
 
 PAGE 
 
 The development of the doctrine of cerebral localization. — A 
 statement of the facts now established. — The proofs of the doc- 
 trine derived from anatomy, embryology, pathology, experimental 
 atrophy, comparative anatomy, and recent exact researches in 
 physiology. — Its application to cerebral surgery, . . . i-io 
 
 CHAPTER II. 
 THE FUNCTIONS OF THE CEREBRAL CORTEX. 
 The general functions of the brain cortex ; perception ; association 
 of perceptions into mental images ; memory ; expression ; self- 
 control. — The special functions of the brain cortex. — Criteria of 
 evidence. — General vs. local symptoms. — The brain fissures and 
 convolutions. — The cortical areas. — Cranio-cerebral topography, I I-2I 
 
 CHAPTER III. 
 THE MOTOR AREA AND ITS AFFECTIONS. 
 The limits of the motor area. — The functions of the motor area. 
 Jacksonian epilepsy or localized spasms ; symptoms and cases. — 
 Case I. Brachial spasm and aphasia. — Case II. Brachial and 
 facial spasms with aphasia. — Case III. Brachial monospasm. — 
 Case IV. Crural monospasm. — Case V. Crural monospasm. — The 
 diagnosis of the location and nature of the disease. — Surgical 
 treatment of Jacksonian epilepsy, 22-38 
 
 CHAPTER IV. 
 THE MOTOR AREA AND ITS DESTRUCTION. 
 Cortical paralysis. — Monoplegia and hemiplegia. — Case VI. Cor- 
 tical hemorrhage producing aphasia and hemiplegia, removal of 
 the clot, recovery. — The centres of muscular sense. — The tactile 
 centres, 39~47 
 
viii CONTENTS. 
 
 CHAPTER V. 
 THE VISUAL AREA AND ITS AFFECTIONS. 
 
 TAGE 
 
 The limits of the visual area.— Hemianopsia; the visual tract. — 
 Sensory epilepsy from irritation of the visual cortex. — Cases VII. 
 and VIII. Visual hallucinations and temporary hemianopsia. — 
 Case IX. 1 lemianopsia of cortical origin 48-56 
 
 CHAPTER VI. 
 THE CORTICAL AREAS GOVERNING LANGUAGE. 
 The varieties of aphasia. — Mental images or concepts and theii 
 physical bases. — Apraxia; inability to recognize objects. — Case 
 with successful operation. — The musical sense and its loss. — The 
 seat of the lesion in apraxia. — Word images and their physical 
 basis. — Aphasia ; inability to recognize or to use language. — 
 Word deafness; word blindness; motor aphasia ; agraphia. — Par- 
 aphasia. — The tests for aphasia. — Illustrative cases, . . 57-83 
 
 CHAPTER VII. 
 
 THE CORTICAL REGIONS WHOSE FUNCTION IS 
 
 UNDETERMINED. 
 
 The frontal convolutions ; mental defects. — The parietal convo- 
 lutions. — The temporo-sphenoidal convolutions. — The uncinate 
 convolution and the sense of smell. — The median cortex of the 
 hemispheres, 84-88 
 
 CHAPTER VIII. 
 
 THE TRACTS WITHIN THE BRAIN AND THE DIAGNOSIS OF 
 
 SUBCORTICAL LESIONS. 
 
 The projection tracts : frontal ; motor ; tactile ; visual ; auditory. — 
 The commissural tracts; mirror writing. — The assocation tracts : 
 memory. — Diagnosis of subcortical lesions, . . . 89-104 
 
 CHAPTER IX. 
 AFFECTIONS OF THE BASE OF THE BRAIN. 
 I. Paralysis of the ocular nerves. — II. Unilateral cranial nerve paraly- 
 sis. — III. Staggering to one side as a symptom, . . 105-125 
 
 CHAPTER X. 
 THE LOCALIZATION OF SPINAL CORD DISEASE. 
 The functions of the spinal segments. — The relation of the seg- 
 ments to the vertebrae. — Diagnostic symptoms of local spinal 
 lesions at various levels ; (1) extent and character of the paralysis; 
 
CONTENTS. . 
 
 IX 
 
 (2) condition of reflex action ; (3) distribution of sensory disturb- 
 ance ; (4) position assumed by the limbs. — The localization of 
 the functions of the segment, 126-143 
 
 CHAPTER XI. 
 THE LOCALIZATION OF SPINAL CORD DISEASE (continued). 
 Cases of lesion at various levels of the cord. — Lower sacral. — Sacral 
 and lower lumbar. — Upper lumbar. — Cases of lesion of the cauda 
 equina, contrasted with those of the lower segments of the spinal 
 cord. — Brown-Sequard paralysis. — Case of Brown-Sequard paral- 
 ysis ; lesion at the ninth dorsal level ; operation ; improvement. — 
 Cases of transverse lesion in the ninth and sixth dorsal region. — 
 Cases of transverse and unilateral lesions at the lower and upper 
 cervical levels, 144-166 
 
 CHAPTER XII. 
 LOCOMOTOR ATAXIA— WITH SOME REMARKS ON THE TREAT- 
 MENT BY SUSPENSION. 
 BY WINSLOW W. SKINNER, M.D. 
 
 Clinical study of twenty-four cases, 167-177 
 
 CHAPTER XIII. 
 THE PARALYSES OF INFANCY. 
 I. Traumatic paralysis of the brachial plexus ; Erb's paralysis ; birth 
 palsy. — II. Infantile spinal paralysis ; atrophic paralysis. — III. In- 
 fantile cerebral paralysis, 178-205 
 
 CHAPTER XIV. 
 MULTIPLE NEURITIS. 
 The discovery of the disease. — Pathology. — Etiology. — Symptoms: 
 sensory, motor, electric changes, deformities, vaso-motor, tro- 
 phic, mental. — Course and duration. — Diagnosis. — Types of the 
 disease. — Beriberi. — Prognosis. — Treatment, . . . 206-221 
 
 CHAPTER XV. 
 
 PARALYSIS AGITANS. 
 
 BY FREDERICK PETERSON, M.D. 
 
 Analysis of twenty-three cases. — Etiology. — Symptoms. — The varie- 
 ties of tremor. — Rigidity and contractures. — Gait and its peculiari- 
 ties. — Treatment, ......... 222-234 
 
 CHAPTER XVI. 
 
 CHOREA. 
 
 BY WALTER VOUGHT, M.D. 
 
 Analysis of one hundred and twenty-four cases. — Etiology. — Month 
 
v CONTENTS. 
 
 of onset. — Relapses. — Relation to rheumatism, endocarditis, and 
 malaria. -Duration of attacks. — Treatment, . . . 235-244 
 Note on paramyoclonus multiplex by Dr. Starr, . . 244 ^1 
 
 CHAPTER XVII. 
 EPlLErsv. 
 A classification of epileptics. — The causes of the disease. — The fre- 
 quency of attacks. — The aura. — Psychical epileptic equivalents. — 
 Reflex neuroses of an epileptiform type and their diagnosis. — The 
 treatment of epilepsy 252-274 
 
 CHAPTER XVIII. 
 SOME PAINFUL FUNCTIONAL AFFECTIONS AND THEIR 
 TREATMENT. 
 Trigeminal neuralgia. — Tic convulsif. — Reflex or transferred pains. 
 — Headaches, their varieties and treatment, . . . 275-2S5 
 
 CHAPTER XIX. 
 THE TREATMENT OF NEURASTHENIA. 
 The vaso-motor origin of neurasthenic symptoms. — Mental recrea- 
 tion. — Overfeeding. — Baths. — Vascular stimulation. — Exercise. — 
 Tonics vs. Sedatives. — Alkalies, 286-290 
 
 CHAPTER XX. 
 
 THE ORDINARY FORMS OF INSANITY. 
 
 BY FREDERICK PETERSON, M.D. 
 
 Analysis of seventy-one cases. — A practical grouping of cases of 
 insanity. — I. Defective brains. — II. Diseased brains. — Varieties of 
 each group. — Home vs. Asylum care, ..... 291-30O 
 
 CHAPTER XXL 
 ELECTRICITY AS A THERAPEUTIC AGENT. 
 
 Elementary physics. — I. Static electricity. — II. Voltaic electricity 
 or galvanism. — Catalytic effects. — Cataphoric effects. — Electro- 
 tonic effects. — III. Faradism or the induced current. — Summary, 
 
 307-321 
 
 CHAPTER XX 1 1. 
 Prescriptions in use in the nervous department of the Vanderbilt 
 Clinic. Register of cases treated at the clinic, . . 322-330 
 
 Index 33' 
 
INDEX OF ILLUSTRATIONS. 
 
 1. The lateral surface of the left hemisphere (Eberstaller), 
 
 2. Fissures and convolutions of convexity (Ecker), 
 Fissures and convolutions of median surface (Ecker), 
 Relations of sutures to convolutions, . 
 Cranio-cerebral topography, guiding lines (Reid), 
 The motor area, convex surface, . 
 
 7. The motor area, median surface, . 
 
 8. Diagram of motor areas on monkey's brain (Horsley), 
 Diagram of lesion in Case I., 
 Diagram of lesion in Case II., 
 Diagram of lesion in Case III., 
 Diagram of lesion in Case IV., 
 Diagram of lesion in Case V., 
 Diagrams of cortical lesions, 
 
 15. Diagram of lesion in Case VI., 
 
 16. The visual area, ..... 
 
 17. The optic and visual tracts, . 
 
 18. The visual fields in Case IX., 
 
 19. Diagram of lesion in Case IX., ! 
 
 20. Diagram to illustrate the Concept " Bell," 
 
 21. The situation of lesions causing word deafness, 
 
 22. The situation of lesions causing word blindness, 
 
 23. The situation of lesions causing aphasia, 
 
 24. The unknown areas, .... 
 
 25. The projection fibres within the brain, 
 
 26. The motor tract, . . . 
 
 27. The association fibres within the brain, 
 
 28. The base of the brain (Allen Thompson), 
 
 29. The cerebral axis, lateral view (Edinger), 
 
 30. The nuclei of the ocular nerves, . 
 
 31. Photograph of a patient with ophthalmoplegia externa, 
 
 32. The lesion on the base of the brain in Case XVI. (Henle), 
 
 33. The lesion in the pons Varolii in Case XVII., . 
 
 34. The relation of the vertebrae to the spinal segments (Gowers) 
 
 PAGE 
 
 16 
 
 17 
 17 
 
 20 
 
 21 
 
 22 
 
 23 
 26 
 
 30 
 31 
 
 33 
 34 
 35 
 
 40 
 
 44 
 48 
 
 • 5o 
 55 
 55 
 58 
 66 
 
 67 
 68 
 
 35 
 92 
 
 94 
 98 
 106 
 107 
 109 
 109 
 121 
 123 
 127 
 
INDEX OF ILLUSTRATIONS. 
 
 35. Diagram of the spinal segment (Bramwell). 
 
 36. Lateral sclerosis 1 Gowers) 
 
 37. Anterior Poliomyelitis, 
 
 38. Area of anaesthesia in lesion of V. and IV. sacral segments, 
 
 39. Area of anaesthesia in lesion of V., IV., III. sacral segments 
 
 40. Area of anaesthesia in lesion at V. lumbar segment, . 
 
 41. Area of anaesthesia in lesion at III. lumbar segment (back), 
 
 42. Area of anaesthesia in lesion at III. lumbar segment (front), 
 
 43. Area of anaesthesia in lesion at VI. dorsal segment, . 
 
 44. Area of anaesthesia in lesion at VII. cervical segment (Thorburn). 
 
 45. Area of anaesthesia in lesion at VII. cervical segment (Herter), 
 
 46. Area of anaesthesia in lesion at VI. cervical segment, 
 
 47. Diagram of section of cervical spinal cord (Gowers), 
 
 48. The spinal cord, spinal nerves and cauda equina (Ferrier) 
 
 49. Ascending degeneration in Case XXIV 
 
 50. Ascending degeneration (Gowers) 
 
 51. Diagram of lesion causing Brown-Sequard paralysis, . 
 
 52. Areas of anaesthesia and hyperesthesia in Case XXVI., 
 
 53. Area of sclerosis in locomotor ataxia, 
 
 54. Area of sclerosis in locomotor ataxia (Gowers), 
 
 55. Photograph of infantile spinal paralysis of arm, 
 
 56. Photograph of infantile spinal paralysis of arm, 
 
 57. Diagram of extent of spinal cell groups, 
 
 58. Photograph of infantile spinal paralysis of hand, 
 
 59. Photograph of infantile spinal paralysis of leg, 
 
 60. Photograph of infantile cerebral paralysis of arm, 
 
 61. Photograph of infantile cerebral paralysis of arm, 
 
 62. Photograph of infantile cerebral paralysis of arm, 
 
 63. Athetoid motions of hand (Striimpell), 
 
 64. Lesion of multiple neuritis (Mayer) 
 
 65. Lesion of multiple neuritis (Mayer) 
 
 66. Lesion of multiple neuritis (Joffroy), . 
 
 67. Tracings of tremor in paralysis agitans (Peterson), . 
 
 68. A comparative series of myograms of tremor (Peterson), 
 
 69. Diagram to show month of onset in chorea (Vought), 
 
 70. Diagram of situation of reflex pains (Dana), 
 
 71. Diagram of situation of reflex pains (Dana), 
 
 72. Composite photograph of melancholia (Noyes), 
 
 73. Composite photograph of dementia paralytica (Noyes), 
 
 74. Photograph of a paranoiac (Field) 
 
 75. Diagram of cranial measurements of a paranoiac (Peterson) 
 
 76. Shape of cranium of a paranoiac (Peterson), 
 
 77. Photograph of a melancholiac (Peterson), 
 
Familiar Forms of Nervous Disease. 
 
 CHAPTER I. 
 THE LOCALIZATION OF CEREBRAL FUNCTIONS. 
 
 The development of the doctrine of cerebral localization. — A statement 
 of the facts now established. — The proofs of the doctrine derived 
 from anatomy, embryology, pathology, experimental atrophy, com- 
 parative anatomy, and recent exact researches in physiology. — Its 
 application to cerebral surgery. 
 
 The theory of the localization of brain functions is now- 
 established. It is no longer a matter of doubt that each part 
 of the organ has its own work to do. And already the prac- 
 tical application has followed, and cerebral surgery has its 
 accepted place in therapeutics. The brain is no longer an 
 organ exempt from surgical interference. 
 
 It becomes, therefore, a necessity for every physician to 
 be in possession of those facts which are essential to the diag- 
 nosis of local cerebral disease; to be able to decide upon the 
 possibility of surgical interference; to be able to direct the 
 surgeon where to trephine. 
 
 The facts which must be known are not difficult to under- 
 stand, and, when they are brought together, the conclusions 
 which they warrant are evident at once. It is the collection 
 of the facts which is necessary. But they are scattered 
 through medical literature and are not easily accessible to 
 those who are far from libraries. Their study is tedious, yet 
 the conclusions to be reached are of the* greatest importance. 
 
 In the present chapter, the progress of the discovery of 
 
 the facts of localization, the various proofs of the doctrine, and 
 i 
 
2 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 its chief data arc presented for the purpose of bringing into 
 
 general knowledge the results of the special work of neurolo- 
 gists during the past ten years. 
 
 Physiological experiment has led the way to much of this 
 knowledge. But it is only in so far as it has been supple- 
 mented and confirmed by clinical and pathological observa- 
 tion on man, that the facts which are of practical importance 
 can be utilized. Hence, greater attention is paid here to 
 cases of disease than to the supposed effects of experiments 
 upon animals. And illustrative cases of the various cortical 
 lesions are presented, in order to demonstrate the possibility 
 of diagnosis and of surgical treatment. 
 
 THE DEVELOPMENT OF THE DOCTRINE OF CEREBRAL 
 LOCALIZATION. 
 
 While it was known in the first century of this era that 
 each hemisphere of the brain is in functional relation with the 
 opposite half of the body, the first facts which had a bearing 
 upon the modern theory of the localization of the functions 
 of the brain were not observed prior to 1822. At that time 
 Thomas Hood, in England, and three years later Bouillaud, in 
 France, recorded cases to show that disturbances of speech 
 were produced by disease in the frontal lobes of the brain. 
 In 1836, Marc Dax published a case of aphasia caused by a 
 lesion in the left hemisphere ; but this excited little notice 
 until, in 1861, Broca attempted to locate more definitely the 
 faculty of language. This he assigned to the left third frontal 
 convolution, basing his assertion upon two cases of loss of 
 speech, and supporting his position, two years later, by fifteen 
 cases, in fourteen of which aphasia was due to disease in that 
 region. The subsequent publication of numerous cases of 
 aphasia with autopsies, and the discussion of the subject 
 before the French Academy of Medicine in 1864, did much 
 to stimulate the study of cerebral diseases, and to bring to 
 notice the causal relation between certain nervous symptoms 
 and certain brain lesions. 
 
 Up to that time the teachings of Flourens, that the brain 
 
LOCALIZATION OF CEREBRAL FUNCTIONS. 3 
 
 acts as a whole, its various parts not possessing different 
 powers, had been widely accepted. But the facts regarding 
 aphasia threw doubt on these teachings ; and when, between 
 1862 and 1867, Hughlings Jackson and Meynert advanced the 
 opinion that the anterior part of the brain only was concerned 
 in motor acts, the one reaching this conclusion from the study 
 of localized spasms, the other from the observation of the 
 lesions of general paresis, the authority of the French physi- 
 ologist was seriously undermined. It was evident that the 
 physiological experiments of Flourens needed confirmation ; 
 and in 1869 and 1870, Fritsch and Hitzig, of Berlin, under- 
 took their verification. From the beginning of their experi- 
 ments, the modern doctrine of" the localizaton of functions 
 may be said to date ; for by those experiments it was proven 
 that in animals the anterior portion of each hemisphere is 
 motor, its irritation by electricity causing co-ordinated move- 
 ments, and its removal causing paralysis in the limbs of the 
 opposite side. These conclusions were confirmed by Ferrier, 
 in 1873, who enlarged them greatly by his experiments: for 
 he showed that the posterior portions of the brain are sensory 
 and distinguished between various sensory areas assigning 
 each sense to a cortical region. 
 
 It is not necessary to enter here upon the discussions be- 
 tween different physiologists to which their discoveries gave 
 rise. Nothnagel (1877), Munk (1881), Luciani and Seppilli 
 (1884), Ferrier (1887), Francois Franck(i887), Beevor, Horsley, 
 and Schafer (1888), and Thompson and Brown (1889) have 
 published conclusions based upon experiments upon different 
 animals, with somewhat varying results as regards the exact 
 localization of the different functions. But whatever minor 
 differences may be noticed, all agree upon the principle that 
 the functions of the brain are localizable. Even the strongest 
 and almost sole remaining opponents of the theory, Goltz, of 
 Strassburg, and Brown-Sequard, of Paris, admit that the re- 
 sults of destruction of various parts of the brain are different. 
 On all sides, therefore, the doctrine of Flourens has been dis- 
 carded and the modern view has prevailed. 
 
 The physiological discussions have, from the first, stimu- 
 
4 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 latcd clinical and pathological observations. For it was at 
 once evident that in the case of man it is only by the care- 
 ful collation of symptoms and lesions that conclusions regard- 
 ing cerebral localization can be reached. From 1864 until 
 the present time, the publication of more or less careful 
 records of cases of cerebral disease in the medical journals of 
 every country has gone on. From time to time, these cases 
 have been collected and analyzed ; special symptoms being 
 brought into relation with limited lesions, and general con- 
 clusions being reached from the numerous data. From time 
 to time, previous conclusions have had to be modified, finer 
 distinctions between local functions have appeared to be war- 
 ranted, and obscure phenomena have been cleared up by the 
 observation of some rare case, or by the insight of some gifted 
 observer. 
 
 The work* of Charcot, Pitres, Boyer, Brissaud, Fere, and 
 Bernard, in France; of Ferrier, Ross, Bastian, and Gowers, in 
 England ; of Nothnagel, Exncr, Wernicke, Benedikt, Petrina, 
 Vetter, Wilbrand, Lichtheim, and others in Germany; of Lu- 
 ciani and Seppilli in Italy; of Scguin, Mills, Dana, and the 
 author in America, warrants mention in any historical sum- 
 mary; though to these names others might well be added. For 
 by the careful collection and comparison of individual cases — a 
 work which requires much laborious research and much criti- 
 cal insight — in pursuance of a strictly inductive method of in- 
 vestigation, these observers have reached well-founded conclu- 
 sions regarding the application of the doctrine of cerebral 
 localization to man. 
 
 THE FACTS OF LOCALIZATION NOW ESTABLISHED. 
 
 It has, by this method, been fully established that various 
 powers of perception, memory, and volition can be definitely 
 assigned to various parts of the brain ; that each sense has its 
 corresponding area in the cortex and each voluntary move- 
 ment its point of departure from the cortex. 
 
 It has been proven that perceptions leave behind them a 
 physical trace inseparably connected with the area in which 
 
LOCALIZATION OF CEREBRAL FUNCTIONS. 
 
 they were originally received ; that irritation of this area pro- 
 duces a renewal in consciousness of the original perception 
 as a memory, which may be so vivid as to appear real, being 
 then a hallucination; that destruction of this area causes a 
 loss of the power of recalling the previous perception or of 
 recognizing it when repeated. 
 
 It has been proven that movements which are acquired by 
 practice, and are therefore the result of conscious effort, are 
 always initiated from a definite area; that this area is insepa- 
 rably related to movements ; since its irritation, by any cause, 
 results in the production of forcible movements of the nature 
 of spasms, and its destruction produces a loss of the power of 
 movement or paralysis of voluntary action. 
 
 It has been proven that the use of language involves both 
 the recollection of auditory and visual symbols and the initi- 
 ation of impulses of speech and writing, thus calling into play 
 not only the motor portion of the brain, destruction of which 
 therefore causes a loss of speech, as Broca held, but also the 
 sensory portion of the brain, a lesion of which will also cause 
 aphasia, as the opponents of Broca clearly proved by the 
 cases which they cited in opposition to his theory. The 
 progress of the investigation, therefore, has helped to recon- 
 cile facts supposed to be incompatible, while it has added 
 definiteness to diagnosis. 
 
 THE VARIOUS PROOFS OF THE DOCTRINE. 
 
 While thus from the investigations of clinical observers 
 and of pathologists facts have been accumulating which place 
 upon a sure and reliable basis the doctrine of cerebral locali- 
 zation as relating to man, in other lines of research further 
 evidence, in favor of this doctrine, has been elicited. 
 
 The study of brain anatomy, as well as that of physiology, 
 has been revolutionized during the past twenty years. By the 
 introduction of new methods of research, the complex struc- 
 ture of the cerebral hemisphere has been gradually brought to 
 light. In the adult brain, as it is seen when removed from the 
 body, the structure of the white matter lying beneath the cor- 
 
6 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tex is not suggestive of its functions. But the microscopic 
 
 stud)' of this portion oi the brain lias shown it to be made up 
 of nerve fibres passing in various directions, and the admitted 
 function oi such fibres is the transmission of nervous impulses. 
 In the health)' adult brain it is impossible to separate these 
 fibres from one another or to detect the existence of bands of 
 fibres functionally related and running together in tracts. 
 But. in 1877, Flechsig made the important discovery that such 
 tracts could be differentiated from each other in fcetal life, 
 by the fact that fibres which were functionally related devel- 
 oped simultaneously and in the definite direction in which 
 the\- were destined to transmit impulses; each tract having 
 its own time and direction of development. It thus became 
 possible to separate different tracts from one another and to 
 trace their exact course and destination; and in the hands of 
 Flechsig, Bechterew, and Edinger this work has yielded a 
 brilliant confirmation of the doctrine of localization. 
 
 It had already been observed by Tiirck, in the study of the 
 spinal cord, that as a result of transverse lesions, certain col- 
 umns degenerated downward and others upward. The re- 
 searches of Flechsig showed that these separate columns, dis- 
 tinguished from one another by the degenerative method of 
 Tiirck, corresponded in situation to the separate tracts which 
 developed at different times in the foetus. Thus the develop- 
 mental and degenerative methods combined to show the ex- 
 istence of separate tracts in the white matter of the spinal 
 cord. It was but a step to apply these methods to the exam- 
 ination of the brain: and, in 1878, Brissaud showed that after 
 certain limited brain lesions, certain tracts in the white matter 
 showed evidences of degeneration. These tracts coincided, ?n 
 situation, with the functional tracts simultaneously differen- 
 tiated by the method of Flechsig, which thus received an im- 
 portant verification. 
 
 The differentiation of tracts through the white matter was 
 also aided by the application of the atrophy method of von 
 Gudden to the investigation of brain anatomy. Von Gudden 
 had discovered, in 1870, that when an organ, like the eye, is 
 extirpated from an animal at birth, the nerve connected with 
 
LOCALIZATION OF CEREBRAL FUNCTIONS. 7 
 
 the organ fails to develop, and hence, by its atrophic appear- 
 ance in the grown animal, can be distinguished from the cor- 
 responding nerve of the opposite side, and the course of each 
 can thus be traced. Von Gudden also investigated the re- 
 sults of natural atrophies from deficient development of cer- 
 tain parts in idiots. It remained for his pupils to apply the 
 method fully to the tracing of intra-cerebral tracts. This 
 was done by von Monakow (1884 and 1889) in some experi- 
 ments which resulted in tracing the visual tract and showing 
 its connections; and it has been applied by Babinsky (1886), 
 by Spitzka (1886), and by Forel (1889) to the tracing of the 
 auditory tract. Tracts thus traced are found to correspond 
 to those whose situation had already been determined by the 
 other methods mentioned. And hence the harmony in the re- 
 salts of these totally different methods of investigation carries 
 conviction that the doctrine of localization is absolutely true. 
 
 It is found that areas of the brain whose function is estab- 
 lished by the clinico-pathological method, may be shown by 
 these anatomical methods to be joined to the organs with 
 which they are functionally related. Hence the results of 
 these parallel lines of research harmonize. 
 
 And further, the results of a series of observations made 
 by Gegenbaur, Spitzka, Osborn, Zuckerkandl, Herve, and 
 Edinger upon the comparative anatomy of the brain have al- 
 ready furnished an independent mass of testimony regarding 
 the localization of function. This last-named method is as 
 yet in its beginning; but it has produced the evidence needed 
 regarding the course of the auditory tract in the brain axis 
 (Spitzka, 1886), and has confirmed the hypothesis of the loca- 
 tion of the olfactory sense (Zuckerkandl, 1887) and of the 
 motor region concerned in speech (Herve, 1888). It may be 
 said to be the correlative of the atrophy method of von Gud- 
 den. For in that the loss of an organ was associated with a 
 deficient development of its related cerebral parts ; while in 
 this the excessive development of certain parts is associated 
 with an extraordinary power and use of some special organ. 
 And in the future this line of research will doubtless furnish a 
 mass of facts of the greatest value. 
 
8 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Lastly, it may be mentioned, that exact methods of elec- 
 trical measurements have been applied to the solution of 
 questions of localization by Horsier, Beevor, and Gotch 
 (1888). When an electric current is applied at one end of a 
 nerve tract its arrival at the other end can be detected and 
 the time oi its passage can be measured. If its passage is 
 direct, the time will be short; if indirect, longer. It is thus 
 found that an electric message sent from the motor area of 
 the brain travels in the motor tract and never spreads to 
 other tracts ; that the message starting from the motor area 
 of the arm does not pass below the upper dorsal region of 
 the cord; while a message from the motor area of the leg 
 reaches the lumbar part of the cord; a valuable confirmation, 
 therefore, of the respective locations in the cortex of the 
 areas for arm and leg. Again, it had been found that electric 
 excitation of various areas of the cortex might produce the 
 same movement; thus, the application of currents to two 
 widely separated regions gave rise to a turning of both eyes to 
 one side ; and it was impossible to determine in which of these 
 areas the motor centre' for conjugate movements of the eyes 
 was located. The investigation of the time elapsing between 
 the irritation and the movement has shown that after irrita- 
 tion in the anterior of these two regions the reaction-time was 
 less than that after irritation of the posterior region. Hence 
 it is argued that the actual motor impulse starts from the 
 anterior region ; and that when it is the sensation which in- 
 duces the movement, as by the attraction of a light both eyes 
 turn to the side, the impulse starts from the posterior region, 
 but must go first to the anterior region before it passes to the 
 oculo-motor centres. Thus the more exact methods of re- 
 search in physiology are being used to confirm or to correct 
 the earlier statements and to finally determine disputed ques- 
 tions. 
 
 It is therefore evident, from the summary of the results 
 reached by different independent methods of investigation, 
 that cerebral localization is no longer a tentative theory. It 
 is an established fact. 
 
 As long ago as 1876, the practical bearings of the doctrine 
 
LOCALIZATION OF CEREBRAL FUNCTIONS. 9 
 
 of localization were appreciated by the early investigators, 
 especially by Ferrier. It was even then evident that if dis- 
 ease in the brain could be exactly located during life, and was 
 of a nature to be removed by surgical means, diagnosis might 
 lead the way to therapeutics. It has only been within the 
 last five years, and chiefly in America and England, that this 
 great result has been attained ; and even now the application 
 of the doctrine to the development of cerebral surgery meets 
 with hesitating acceptance upon the Continent of Europe. 
 Caution cannot be excessive, and there are indeed still but 
 few parts of the brain which can be said to be open to surgi- 
 cal treatment. But the continuous progress of discovery in 
 the past, and the actual success of well-conducted aseptic 
 surgical interference in appropriate cases, warrants the expec- 
 tation of future results in the domain of cerebral surgery, 
 which will rival in brilliancy those of any other department of 
 that most practical art. 
 
 BIBLIOGRAPHY OF LOCALIZATION. 
 
 Hood : Phrenological Transactions, vol. iii., 1822. 
 
 Bouillaud : Traite de l'Encephalite, 1825, p. 281. 
 
 Dax, Marc : Bull, de l'Acad. de Mc'd., 1863, quoted by G. Dax. 
 
 Broca : Bull, de la Soc. Anat., 1863. 
 
 Hughlings Jackson : Med. Times and Gaz., 1861-64. 
 
 Meynert : Vierteljahrsch. f. Psych., 1867. 
 
 Fritsch and Hitzig : Reichert und Du Bois Reymond's Archiv f. Physiol., 1870. 
 
 Ferrier : Functions of the Brain, 1876. 
 
 Localization of Brain Disease, 1878. 
 Nothnagel : Virchow's Archiv, lviii. 
 Munk : Verhand. d. Physiol. Gesell. zu Berlin, 1878. 
 
 Verrichtungen der Gehirns, 1881. 
 Luciani and Seppilli : Die Functions-Localization — Deutsch. Aufgabe, 1886. 
 Francois Franck : Lecons sur 1. Funct. du Cerveau, 1887. 
 Ferrier : Functions of the Brain, 2d ed., 1887. 
 Broadbent : Med. Chir. Trans., 1872, 1878, 1884. Brain, vol. i. 
 Beevor and Horsley : Philosoph. Transactions, 1888, B. 28. 
 Horsley and Schafer : Philosoph. Transactions, 1888, B. 20. 
 Horsley: Trans. Cong. Amer. Phys. and Surgs., 1888. 
 
 Thompson and Brown : Report of the Loomis Laboratory, New York, 1890. 
 Goltz : Pfliiger's Archiv f. Physiol., 1878-87. 
 Charcot et Pitres : Revue de Med., 1879, 1883. 
 Boyer: Recherches Clinicales sur les Mai. Cerebrales, 1S79. 
 
10 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Brissaud : 1 esions en Foyer, 1S77. 
 
 i;i us aki> : De I'Aphasie, 1885. 
 
 Ross : Diseases of the Nervous System, 1883. 
 
 Aphasia, 1SS7. 
 Bastian : Paralysis, Cerebral and Spinal, 1886. 
 GOWERS : Diseases of the Nervous System, 1888. 
 Nothnagei. : Topische Diagnosiik der Gehirnkr., 1879. 
 EXNER: Untersuchungen u. d. Local, d. Funct. i.d. Grosshirn, 1881. 
 WERNICKE : Lehrbuch d. Gehirnkr., Bd. ii., iii., 1883. 
 Benemkt: Wiener Klinik, 1883. 
 rKTKiNA : Vierteljahr. f. Tract, lleilk., 1S79. 
 
 Zeitsch. f. Ileilkunde, 1S81. 
 Kahler and Tick: Zeitsch. f. Heilkunde, 1879. 
 Vettek: Deut. Arch. klin. Med., 1S83. 
 W11 BRANDT : Ueber Hemianopsie, 1881. 
 LlCHTHElM : Aphasia, Brain, 1887. 
 SEGUIN : Jour. Xerv. and Ment. Dis., 1886-90. 
 
 Amer. Jour. Med. Sci., i88«. 
 Dana : Jour. Ment. and Nervous Dis., 1889. 
 Mills : Pepper's System of Med., vol. v. 
 
 Trans. Cong. Amer. Phys. and Surg., 1888. 
 Starr: Cortical Lesions, Amer. Jour. Med. Sci., 1884. 
 
 Sensory Tract, Jour. Nerv. and Ment. Dis., 1884. 
 Pathol, of Sensory Aphasia, Brain, 1889. 
 Flechsig : Leitungsbahn im Gehirn u. Riicken, 1877. 
 
 Neurol. Centralbl., 1890. 
 Bechterew: Neurol. Centralbl., 1885-90. 
 Edinger : Zvvolf Vorlesungen, 1889. 
 
 Untersuch. u. d. Vergleich. Anat. d. Gehirns, 1889. 
 Von Gudden : Gesammelte Arbeiten, 1888. 
 Von Monakovv : Arch. f. Psych., 1884-89. 
 Babinsky : Virchow's Archiv, vol. cv. , 1886. 
 Spitzka: N. Y. Med. Jour., 1886. 
 
 Jour. Compar. Anat.. 1887. 
 
 Architecture of the Brain, Ref. Handbook Med. Sci., vol. viii. 
 Forel: Arch. f. Psych., 1889. 
 Zuckerkandl : Ueber das Riechcentrum, 1887. 
 Herve : La Convolution de Broca, 1888. 
 
CHAPTER II, 
 THE FUNCTIONS OF THE CEREBRAL CORTEX. 
 
 The general functions of the brain cortex ; perception ; association of 
 perceptions into mental images ; memory ; expression ; self-control. 
 — The special functions of the brain cortex ; criteria of evidence ; 
 general vs. local symptoms.— The brain fissures and convolutions ; 
 the cortical areas. — Cranio-cerebral topography. 
 
 There is a unanimity of belief among physiologists and 
 psychologists that all conscious mental activity has its physical 
 basis in the cerebral cortex. Reflex and automatic acts may 
 be performed in response to sensory impulses by the agency 
 of the masses of gray matter collected in the spinal cord, in 
 the cerebral axis, or in the basal ganglia ; and some automatic 
 action, such as acts of somnambulism and in a state of hyp- 
 notism, may possibly be cortical yet unconscious. But con- 
 scious perceptions of sensation and conscious efforts require 
 for their performance the existence and activity of the gray 
 matter spread out in a thin layer upon the surface of the cere- 
 bral hemispheres. This is proven not only by the facts that 
 the degree of development of the cortex in extent, thickness, 
 and condition of nutrition and blood supply varies directly as 
 the mental powers of the animal, as the capacity of the race, 
 and as the mental status of the individual ; but also by the 
 facts that its deficient development leads to idiocy, and its 
 actual disease produces mental as well as physical symptoms. 
 
 GENERAL FUNCTIONS OF THE CORTEX. 
 
 The general functions of the cortex of the brain may be 
 enumerated as follows: 
 
 (i) It receives impressions from the various sensory organs 
 of the body as conscious perceptions. 
 
12 FAMILIAR I'ORMs OF NERVOUS DISEASE. 
 
 It is true that every impression is not consciously per- 
 ceived, as is shown by the familiar fact of one's reading down 
 a page without knowing what has been read. Yet all impres- 
 sions are received and semi-consciously preserved, as is proven 
 by the fact that one may become conscious that the clock has 
 struck and be able to recall the hour, even though the striking 
 has been apparently unnoticed. Impressions which are con- 
 sciously perceived come in through different senses and hence 
 reach different parts of the cortex, since each organ is joined 
 to its own area by a distinct tract. Hence the conscious per- 
 ception of impressions may be arrested by cortical disease, 
 and the location of the disease will determine which set of 
 perceptions is cut off. 
 
 But impressions are not exclusively sensory. They may 
 be motor. For motion is performed reflexly at first, is then 
 perceived consciously as motion, is remembered, and finally 
 imitated by effort. The impression of a motion made, ac- 
 quired through muscular sense, is therefore one of the con- 
 scious perceptions of the cortex; and hence it too maybe ob- 
 literated by disease. It must be held that motor memories lie 
 at the basis of all adaptive movement. These are acquired 
 by observation and practice. The combination of known 
 efforts into new adaptations, like the combination of various 
 perceptions into a single concept, or the combination of mem- 
 ories into imaginative fancies, is a power of the cortex depen- 
 dent upon but additional to its power of conscious perception. 
 (2) The association of various perceptions into mental 
 images is also a function of the cortex. Perceptions rarely 
 come singly. As one looks at a rose one perceives its delicate 
 color and its fragrance, one handles it and gets the sensation 
 of its soft, velvety leaves and thorny stem. These various 
 perceptions are associated together into a mental image of the 
 rose, which is a thing of parts' and not a simple perception. 
 The various perceptions occur in various regions of the cortex, 
 and these regions are joined with one another both by a fine 
 network of fibres within the cortex and by bands of associa- 
 tion fibres running beneath the cortex. It is by means of 
 these fibres that various cells, whose function it is to receive 
 
THE FUNCTIONS OF THE CEREBRAL CORTEX. 13 
 
 the impressions, are joined together. Hence, the physical 
 basis of the mental image of an object is a complex set of cor- 
 tical cells joined together by fibres. 
 
 (3) This physical basis of each mental image remains after 
 the object ceases to be perceived. It is, therefore, the func- 
 tion of the cortex to retain perceptions as memory pictures so 
 that consciousness may recall them and recognize them when 
 they appear again. Such recollection may occur of only one 
 perception, but this is likely to lead to the recollection of the 
 entire mental image, or of other images associated with the 
 first. Disease of the cortex will, therefore, impair the powers 
 of recognition and of recollection either by depriving the 
 mental image of some of its parts, or by interfering with the 
 process of association which is necessary to its completeness. 
 
 (4) It is also a function of the cortex to give expression to 
 thought in action and in speech. Thought may be considered 
 as the play of consciousness among the mental images along 
 the lines of association, in part voluntary, in part automatic. 
 Such thought leads eventually to expression either in sign 
 language, in speech, or in action. Each of these is at first 
 imitative but eventually voluntary ; and each is directed by its 
 appropriate cortical area. If these areas are diseased, arrest 
 of the powers of expression ensues, as in all cases of paralysis. 
 
 (5) But thought does not lead immediately to expression 
 in all cases. Expression may be restrained ; the impulse may 
 be arrested. This restraint of the flow of thought outward in 
 expression has been termed inhibition ; and inhibition, or the 
 act of control, is the highest of all cortical functions. 
 
 In this summary of cortical action, it will be noticed that 
 no mention has been made of the higher mental acts, of judg- 
 ment, reason, imagination, or of those qualities which deter- 
 mine talent and character. These cannot, as yet, be assigned 
 to any particular region of the cortex, and no physical basis, 
 no mechanism for such purely mental acts can, as yet, be pic- 
 tured to the mind. As Hughlings Jackson has well said, 
 " Psychical states are not functions of any centre but are sim- 
 ply concomitant with functioning of the most complex ner- 
 vous arrangements." It is certainly true that all mental activ- 
 
I 4 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 ity has a physical basis in the brain; but there are numerous 
 problems regarding the mutual relation of thought and cere- 
 bral action upon which physiology has thrown no light. 
 
 SPECIAL FUNCTIONS OF SPECIAL AREAS OF THE CORTEX. 
 
 It is possible, from the evidence of clinical cases and of 
 pathological examination, to assign special functions to differ- 
 ent parts of the cortex. These are motion, tactile, tempera- 
 ture, pain and muscular sensations, sight, hearing, smell and 
 taste, and the use of language. 
 
 But, in reviewing this evidence, it seems necessary to con- 
 sider critically its value; and to exclude all questionable facts, 
 so as to make conclusions reliable. 
 
 According to Nothnagel, 1 those cases only are of use in 
 determining the function of limited areas of the cortex in 
 which there is a single lesion of small extent, accurately located 
 and of considerable duration. If lesions are multiple, it is im- 
 possible to assign different symptoms to each. If the lesion is 
 of large extent, the functions of two or more areas involved 
 cannot be distinguished. If the patient dies soon after the 
 invasion of the disease, especially if that disease be a cerebral 
 hemorrhage, it is impossible to separate temporary symptoms 
 due to shock, from permanent symptoms due to the destruc- 
 tion of brain tissue. If, however, the function of limited areas 
 is fairly determined by such carefully-weighed evidence, cor- 
 roborative proof furnished by multiple and extensive lesions 
 may be admitted. 
 
 Cases of brain disease afford two distinct kinds of informa- 
 tion regarding the function of cortical areas which have been 
 termed by Exner" positive and negative, and each is of value. 
 The positive evidence is the symptom produced by the lesion 
 of a definite area. The negative evidence is the lack of symp- 
 toms referable to other organs. Thus if a lesion in one region 
 produces uniformly a special form of blindness but never 
 causes any disturbance of motion, it is allowable to conclude 
 positively that this region has a functional relation to sight ; 
 
 1 " Topische Diagnostik der Gehirnkrankheiten," p. 6. 
 
 - " Localisation der Functionen in der Grosshirnrinde." p. 4. 
 
THE FUNCTIONS OF THE CEREBRAL CORTEX. 15 
 
 and, negatively, that it has no functional relation to motion. 
 Each of these lines of evidence is important. 
 
 In the study of cases of cortical disease, it is necessary at 
 the outset to distinguish general from local symptoms, for it 
 is the latter only which enable one to locate the lesion. Gen- 
 eral Symptoms are those which are common to various kinds 
 of brain disease in whatever region they are located. They 
 are headache, vertigo, digestive disturbances, general convul- 
 sions, optic neuritis, with or without blindness, delirium, and 
 coma. These are due either to an increase of the intra-cranial 
 contents (as by the growth of a tumor) and consequent pres- 
 sure, or to some other interference with the normal condition 
 in the brain. They give no evidence as to the exact region 
 of the brain which is affected. They merely indicate that the 
 brain is diseased. 
 
 Local Symptoms, on the other hand, depend entirely for 
 their production upon the region of the cortex which is in- 
 vaded. They are disturbances of motion and of sensation of 
 various kinds, and of sensory perception; disturbances of 
 memory; and loss of speech. They may be divided into 
 symptoms of irritation and symptoms of destruction ; and it 
 is not infrequently the case that the former precede the latter 
 in the course of a disease. An irritative lesion produces symp- 
 toms due to an increased activity of the area affected ; e.g., 
 spasms, pain, tingling and numbness, flashes of light, sounds, 
 or hallucinations of smell and taste. A destructive lesion 
 produces symptoms due to a loss of function in the area in- 
 volved ; e.g., paralysis, anaesthesia, blindness, deafness, loss of 
 smell and taste and of the use of language. Each of these 
 points to a different location of the disease, and is essential 
 to its localization. 
 
 THE BRAIN FISSURES AND CONVOLUTIONS. 
 
 Before proceeding to study the special functions of differ- 
 ent parts of the cortex in detail, and the symptoms of their 
 diseases, a brief recapitulation of the fissures and convolutions 
 may be given for reference. 
 
i6 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Brains differ widely from one another in their appearance 
 on the surface, great variety being the rule. Even the two 
 hemispheres rarely resemble each other exactly either in the 
 arrangement of fissures or of convolutions. Hence no one 
 figure or diagram is satisfactory. It is necessary to establish 
 certain landmarks on the brain surface, and this may be done 
 by means of the chief fissures. The convolutions which are 
 separated by these fissures may be small or large, or may 
 
 Fig. i. — The Lateral Surface of the Left Hemisphere. (Eberstaller.) S, fissure of Sylvius; 
 c, fissure of Rolando, or central fissure; pet, sulcus prae-centralis inferior; pes, sulcus pra;-centralis 
 superior; rtc, sulcus retro-centralis; s/r, sulcus sub-frontalis;/i,/2,y3, sulcus frontalis, sup., inf. et 
 medius; ip, interparietal fissure; pa, parieto-occipital fissure; occ. ant., occ. Int., sulcus occipitalis, 
 ant. et lat.; ti, ti, t$, sulci temporales; A,B,ant. and post, central convolutions; F\, F2, ^3, Frontal 
 convolutions, sup., med., infer.; Pi, P2, parietal convolutions, super, and infer.; G. spm, gyrus 
 supra-marginalis; G. ctng., gyrus angularis; O, occipital lobe; 7*i, 7*2, 7*3, temporal convolutions. 
 
 even be reduplicated, presenting by the indentation of very 
 small fissures, the appearance of two or even more irregular 
 convolutions. Yet, however complex the folding, it is, in 
 every case, possible to distinguish the chief primary fissures 
 easily; and this being done, the convolutions can be assigned 
 to their diagrammatic equivalent and named. 
 
 The figure (Fig. i) is drawn from a photograph of the 
 brain by Eberstaller. 
 
THE FUNCTIONS OF THE CEREBRAL CORTEX. 
 
 17 
 
 The diagrams (Figs. 2 and 3) are those of Ecker — which 
 are widely known. The prominent features of the convexity 
 
 P-o 
 
 Fig. 2. — Fissures and Convolutions of the Left Hemisphere. (Ecker.) .J, fissure of Sylvius; R, 
 fissure of Rolando; /, Interparietal fissure; Fo, parieto-occipital fissure; Fi, Fi, F3, frontal convo- 
 lutions; A,B, ant. and post, central convolutions; Oi, O2, O3, occipital convolutions; 7*i,72, T-j, 
 temporal convolutions. 
 
 are the fissure of Sylvius (Figs, i and 2, S); the fissure of 
 Rolando (Figs. 1, c; 2, R); the interparietal fissure (Figs. 1 
 and 2, I); and the pa- 
 rieto-occipital fissure 
 (Figs. 1 and 2, P-O), 
 which is seen on the 
 median surface to run 
 downward to join the 
 calcarine fissure (Fig. 
 3, C). On the median 
 surface the calloso- 
 marginal fissure is the 
 most prominent (Fi^-. 
 
 1 \ o riG. 3. — lne rissures and Convolutions of the Brain. 
 
 3, M) and the OCCip- The median surface of the right hemisphere. M, Calloso-mar- 
 
 -. . 1 /XT" ginal.fissure; F-O, parieto-occipital fissure; C, calcarine fissure 
 
 ltO temporal {tig. 3, to ^ temporo-occipital fissure (inferior); i% frontal convolu- 
 
 T-O) is also deep. SeC- t i° n ; P-C, paracentral lobule; Q, quadrate lobule; Cu, cuneus; 
 
 , , . U «, uncinate convolution. 
 
 ondary and tertiary 
 
 fissures may be distinguished from these primary fissures by 
 
 their shortness and shallowness. 
 
 2 
 
1 8 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 The convolutions of the convexity are divided into five 
 groups. The frontal convolutions, whose general direction is 
 from before backward, are three in number: superior or first, 
 middle or second, inferior or third (Figs, i and 2, F,, F . 
 
 F 3 ). Behind these and lying on each side of the fissure of 
 Rolando are the anterior and posterior central convolutions 
 (Figs. 1 and 2, A, B), which join together at the vertex in the 
 para-central lobule (Fig. 3, P-C). These arc of the chief im- 
 portance surgically, as they contain the motor centres. Pos- 
 terior to the central motor convolutions, lie the superior and 
 inferior parietal lobules (Figs. 1 and 2, P., P~), separated from 
 one another by the inter-parietal fissure. The superior parie- 
 tal lobule presents a square appearance on the median surface 
 of the brain, and hence is there named the quadrate lobule 
 (Fig. 3, Q). The inferior parietal lobule has numerous short 
 convolutions, the chief of which lies just above the fissure of 
 Sylvius and is known as the supra-marginal convolution. The 
 angular gyrus is at its posterior limit. At the posterior ex- 
 tremity of the hemisphere lie the short occipital convolutions 
 (Figs. 1 and 2, O., O?, 3 ); and on the median surface, the 
 cuneus (Fig. 3, Cu), which is a part of this region, is seen. 
 These convolutions receive the visual impressions and are also 
 of surgical interest. 
 
 Below the fissure of Sylvius, the convolutions of the tem- 
 poral lobe run from before backward, being numbered from 
 above downward (Figs. I and 2, T,, T,, T 3 ). This region is 
 of importance in the left hemisphere, since in the first two 
 temporal convolutions, speech memories are located. Its 
 function on the right side is unknown, though somewhere near 
 this region lie the centres of hearing. In the apex of the 
 temporo-sphenoidal lobe and on its median surface are the 
 convolutions which receive impressions of smell and taste (Fig. 
 3, Un). There are several convolutions lying on the under 
 surface of the hemisphere and passing from the occipital to 
 the temporal region whose function is not known. And the 
 small convolutions of the basal part of the frontal lobe which 
 lie on the orbital plate, are also unimportant physiologically 
 in view of our present knowledge. 
 
THE FUNCTIONS OF THE CEREBRAL CORTEX. ig 
 
 It must be distinctly understood that the cerebral fissures 
 are not real boundaries of cortical areas, since the gray corti- 
 cal layer is not cut through anywhere by a fissure, but is 
 merely thrown into folds by its existence. In referring, there- 
 fore, to functional areas, it is not possible to refer to different 
 convolutions as synonymous with these areas. Thus the fron- 
 tal convolutions make up portions of three distinct functional 
 areas: the frontal, the motor, and the speech areas. While, 
 therefore, precision of description of lesions is attained by the 
 naming of convolutions, the facts of localization prove that 
 functional areas are not bounded by cerebral fissures, or lim- 
 ited to particular convolutions. 
 
 In considering diseases of the cortex, therefore, the func- 
 tional areas are considered successively, rather than the ana- 
 tomical lobes of the brain. 
 
 CRANIOCEREBRAL TOPOGRAPHY. 
 
 The fact that the brain may be exposed for the removal of 
 diseased parts in appropriate cases has made it necessary to 
 ascertain the relation of its different fissures and convolutions 
 to the cranial sutures, or to certain landmarks upon the sur- 
 face" of the head. These relations are well shown in the figure 
 (Fig. 4), which is a photograph of a cast of a head made imme- 
 diately after death by Dr. Cunningham, of Dublin. 1 Numerous 
 rules have been laid down for the determination of the location 
 of various parts of the convex surface of the hemisphere upon 
 the head. The most important are the following, which may 
 be compared with the diagrams of Reid (Fig. 5). To find the 
 fissure of Rolando, lay down a line from the root of the nose 
 to the occipital protuberance over the top of the head, and 
 take a point 0.557 °f the distance back upon this line. This 
 point will correspond to the upper end of the fissure. The 
 fissure makes an angle of 6y° with the median line just meas- 
 ured. Hence if two strips of metal fixed to one another at 
 
 1 See Dublin Journ. Med. Sci., 1888, p. 157. Foran opportunity of photograph- 
 ing this cast I am indebted to Dr. F. Ferguson, Curator of the Museum of the New- 
 York Hospital. 
 
20 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 this angle be placed on the head with their junction upon the 
 upper end of the fissure, when one strip is on the median line, 
 the other strip, pointing forward and downward, must lie over 
 the fissure of Rolando. In its lower third the fissure becomes 
 a little more vertical than the strip. The fissure is about 
 
 Fig. 4. — Photograph of a Cast of the Head showing Relation of Cranial Sutures to the Cerebral 
 Fissures and Convolutions. F, Frontal; /^parietal; O, occipital; T, temporal lobes; S, fissure of 
 Sylvius; /?, fissure of Rolando; /, interparietal fissure; P,0, parieto-occipital fissure; A,B ant. and 
 post, central convolutions. 
 
 three and a half inches long. To find the fissure of Sylvius, 
 lay down a base line from the lower margin of the orbit to 
 the auditory meatus. Lay down a second line parallel to the 
 base line from the external angular process of the frontal 
 bone backward one inch and a quarter; this gives point one. 
 Find the most prominent part of the parietal eminence and 
 
THE FUNCTIONS OF THE CEREBRAL CORTEX. 21 
 
 from it draw a line downward perpendicular to the base line, 
 and on this take a point three-quarters of an inch below the 
 eminence; this gives point two. Join these two points and 
 the line will lie over the fissure of Sylvius. The anterior limb 
 of the fissure will be two inches behind the external angular 
 process. The fissure of Sylvius is about four inches long. To 
 find the parieto-occipital fissure, continue the line of the fis- 
 sure of Sylvius to the median line. At their junction lies this 
 fissure. Since all areas now open to surgical operation can 
 
 Fig. 5. — Guiding lines Reid and Relations of the Lines to the Fissures, (Reid.) (See text for ex- 
 planation. 
 
 be located with a definite relation to these three fissures, no 
 further rules are necessary. Since in opening the skull it is 
 customary to make a fenestrum of at least an inch in diame- 
 ter, and it is frequently necessary to enlarge the opening much 
 more, a procedure in no way dangerous under aseptic condi- 
 tions, there is no difficulty in recognizing the fissures and con- 
 volutions exposed if the rules are closely followed. Prior to 
 the large incision of the scalp it is well to mark certain points 
 upon the skull by the sharp point of a scalpel, so that when 
 the bone is laid bare surface landmarks may still be kept in 
 view. 
 
CHAPTER III. 
 THE MOTOR AREA AND ITS AFFECTIONS. 
 
 The limits of the motor area. The functions of the motor area. — Jack- 
 sonian epilepsy or localized spasms; symptoms and cases. — Case I., 
 Brachial spasm and aphasia. — Case II., Brachial and facial spasm 
 with aphasia. — Case III., Brachial monospasm. — Case IV., Crural 
 monospasm. — Case V., Crural monospasm. — The diagnosis of the 
 nature of the disease and of its location. — Surgical treatment of 
 Jacksonian epilepsy. 
 
 THE MOTOR AREA. 
 
 The situation and limits of the motor area are now accu- 
 rately determined and are shown in Figs. 6 and 7. This has 
 
 been done by the study 
 of two independent series 
 of phenomena — spasm 
 and paralysis. 
 
 Electrical stimulation 
 of the cortex in monkeys, 
 within certain limits, pro- 
 duces spasmodic con- 
 traction of groups of 
 muscles. If the stimula- 
 tion be very weak, the 
 resulting movement is 
 limited in extent. If the 
 
 Fig. 6.— The Motor Area on the Lateral Surface of stimulation be increased 
 the Hemisphere. This includes the anterior and posterior . , 
 
 central convolutions (^4, B) on each side of the fissure of or kept Up, the ITlOVe- 
 
 Roiando(R). ment becomes greater. 
 
 Thus weak stimulation of a given spot will cause the hand to 
 close. Increase the stimulus and the wrist and arm will be 
 flexed. Increase it again or continue it for some time, and 
 the entire limb will be moved and even face and leg may be- 
 
THE MOTOR AREA AND ITS AFFECTIONS. 23 
 
 come tense and give evidence of slight motion. It is thus 
 established that each cortical district presides over and ini- 
 tiates some movement, so that definite movements can be 
 assigned to different areas within the motor region. 
 
 Very precise statements now appear to be warranted, based 
 upon the recent physiological experiments of Horsley, 1 
 Schafer, and Beevor and on the careful clinical studies of cor- 
 tical spasms by Rolland. 2 
 
 If we study actions as they are performed, we find that 
 every act involves a succession of movements by different 
 joints, each movement being produced by a number of motions 
 in different muscles. The act of carrying a glass of water to 
 the mouth, may involve ^^ ^^^^-^ 
 
 perhaps the same muscles y^^ — \^ ^_/V 
 
 as $he act of lifting a t\ s-* ' "" *""">«— S ~vs. 
 heavy vase from a high f ' f y ^ ;: ^ : T !s »s S!a!! ^_ — \ \ 
 shelf and placing it on the f — <v V V§^<C ^^^\ "^X^s 
 floor; but there is a great ^v-^ s> ^^^' ~"^il§lr ^/^JI"^ ) 
 difference between the ^- — -y — fJ ^^^^^ ^ </ j^ ^^^5 ( 
 
 order and sequence of 1 ~~ -ZL/ 
 
 movements in the two _ ^/^ \ u ». *■ c c 
 
 Fig. 7. — The Motor Area on the Median Surface. 
 CaSeS and the relative This includes the paracental lobule {PC) into which the 
 r r ,1 a central convolutions run. 
 
 force or these movements. 
 
 In the first, the delicate balancing of the glass by the fingers 
 and thumb is the most noticeable: in the second, it is the 
 firm action of the arm and shoulder which is necessary to 
 support the weight, and the act is aided by balancing move- 
 ments of the entire body and legs to maintain the equili- 
 brium. In both acts the entire muscular system of the upper 
 extremity is involved, but in each there are some muscles 
 whose action is greater in degree and precedent in time 
 than in the other. It seems necessary, in view of recent re- 
 searches, to adopt the view that the motor centres of the cor- 
 tex govern motor acts rather than special muscles; that it is 
 the act of grasping, or of opening the hand, or of separating 
 the fingers, or of pointing at an object, which is produced by 
 
 1 Philosophical Transactions, 1888, B. 20, B. 28. 
 
 2 " L'Epilepsie Jacksonienne," Paris, 18SS. 
 
24 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 cortical action, rather than the contraction of the flexors or 
 of the extensors as separate muscles of the hand. When any 
 act is carefully examined it is found to involve a large number 
 of muscles in its production. One cannot point one's finger 
 quickly and forcibly at an object without feeling that almost 
 the entire muscular system of the body is really being called 
 into play. The motor area of the upper extremity is to be 
 thought of, therefore, as containing an enormous number of 
 centres of action, arranged in groups, so that it cannot be 
 divided by sharp lines or circles into flexor or extensor cen- 
 tres, since flexor and extensor action occur simultaneously in 
 many different acts; as, for example, in suddenly closing the 
 hand. If it be divided at all, it must be into regions for vari- 
 ous acts, each having a predominate feature." Those acts in 
 which the shoulder movements take the chief part are repre- 
 sented in the upper forward part of the arm area ; those in 
 which the thumb and finger movements take the chief part 
 are represented in the lower hinder part of the arm area, and 
 the elbow acts may be placed between these: so that if, in a 
 motor spasm, the first thing which occurs is a motion of the 
 thumb and a closure of the hand, and then pronation and 
 flexion of the wrist and elbow and forcible adduction of the 
 arm follow, while finally the shoulder is raised as if to aid the 
 act of forcible seizure of an object, it is proper to conclude 
 that the cortical irritation began far back in the thumb region 
 of the arm area and gradually increased in intensity. While 
 if the spasm comes on in the reverse order, the point of initial 
 irritation must be located in the shoulder region at the ante- 
 rior part of the arm area. In both of these areas all of the 
 muscular movements performed are represented ; but in the 
 hinder one, it is the hand motions which predominate, or may 
 be said to be primary: in the forward one it is the shoulder 
 motions which are prominent and the others are quite secon- 
 dary. 2 
 
 1 Jackson says, " The convulsion is a brutal development of a man's own 
 movements. A severe fit is nothing more than a sudden, excessive and temporary 
 contention of many of the patient's familiar movements, such as winking, articulat- 
 ing, singing, manipulating, etc." 
 
 2 Philosophical Transactions, 15. 20. 
 
THE MOTOR AREA AND ITS AFFECTIONS. 25 
 
 If, therefore, a very slight irritation occurs in the anterior 
 part of the motor area, it will cause only a shrugging of the 
 shoulder; if it becomes more intense the arm and forearm 
 may begin to move; and if it is at a maximum, the hand par- 
 ticipates in the convulsion. If very slight irritation occurs in 
 the posterior part of the motor arm area, the fingers only may 
 twitch, or the thumb be turned in ; and as the intensity of the 
 irritation increases, the number of motions made by the ex- 
 tremity as well as their force increases. The spasm does not 
 cease in the muscles first set in motion as other muscles be- 
 come involved, but continues in all till a maximum of motion 
 is reached. Examples of these varieties of spasm, and of the 
 order of extension of the motions, are found in the first three 
 cases of brachial spasm, soon to be studied. In one of these 
 cases both of these forms of spasm were observed, indicating 
 clearly that the lesion was not a small focus of irritation, but 
 a wide one covering a considerable area, or else that these 
 were two separate foci of disease. 
 
 The area governing the movements of the head and the 
 conjugate motion of the eyes, is thought to lie in front of the 
 arm and face areas. Distinctions in the order of centres in 
 the face area are not yet well established clinically, though 
 the upper forward part is known to govern the upper facial 
 muscles, the lower part the muscles of the mouth and tongue. 
 The motions of the legs are so few and simple in man, as com- 
 pared with monkeys on whom physiological experiments are 
 made, that little need be said regarding them except to note 
 that the centres of movement for the foot and great toe lie 
 farthest back, those for the knee and hip further forward, and 
 those for the trunk and back appear to be limited to the 
 median surface of the hemisphere in the para-central lobule. 
 If a spasm, therefore, begins in the abdominal muscles — as in 
 Case V. — the lesion causing irritation is to be sought on the 
 median surface of the brain, and here it was found at the ope- 
 ration on this case; if it begins in the toes and advances up 
 the leg, the irritating lesion lies in the convexity far back in 
 the motor area. 
 
 Electrical stimulus has been frequently applied to the brain 
 
20 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 of man, with the result of producing the same effect in respect 
 to motion, which is produced in monkeys. Hence it is inter- 
 esting to observe the result of such stimulus in monkeys. 
 The accompanying figure (Fig. 8) shows the various areas of 
 the motor zone mapped out by Horsley on the monkey's 
 brain ; the subdivisions of the motor area being thus demon- 
 strated. The phenomena of spontaneous spasms in man are 
 identical in kind with those produced by electrical stimulation 
 of the cortex. In both the movement is of the voluntary 
 character; that is, it occurs in harmoniously related muscles. 
 
 Fig. 8.— Diagram of Monkey's Brain. (Horsley and Schafer). The motor area and its 
 various functions. 
 
 acting together for an end. In both it may be limited to a 
 small movement, as the turning inward of the thumb upon 
 the hand.' In both it may be increased in intensity, involving 
 more and more groups of muscles, producing more and more 
 complex acts. In both it may extend to parts of the body 
 represented in adjacent areas. In both opposing movements 
 may be alternately excited, giving rise to what Horsley calls 
 confused movements, such as are seen in a severe convulsion. 
 
 JACKSONIAN EPILEPSY — LOCALIZED SPASMS. 
 
 It was the study of localized spasms which led Hughlings 
 Jackson long ago to the conclusion that a portion of the 
 
THE MOTOR AREA AND ITS AFFECTIONS. 27 
 
 brain cortex is excitable and is motor; and that in the motor 
 area distinct divisions for the control of different movements 
 exist. Such limited spasms have been termed Jacksonian epi- 
 lepsy; and the study of cases has shown that the location of 
 the source of irritation is the determining element in the form of 
 spasm. 1 
 
 The symptoms of Jacksonian epilepsy are as follows: 
 
 1. A sensation of numbness or tingling, or a feeling of motion 
 in some particular part of one side ; usually the side of the 
 face, or the thumb and fingers, or the great toe. This has 
 been called the " Signal symptom " by Seguin, as it ushers in 
 the attack. It remains during the attack. It is of the great- 
 est value in the diagnosis of the seat of the lesion, and may 
 determine the point at which the trephine is to be placed, if 
 an operation be undertaken. Its situation is usually the same 
 in all the attacks of one patient. 
 
 2. A spasm or convulsion beginning uniformly in one part 
 of the face or of an extremity and slowly invading other parts. 
 The eyes or face may begin to twitch ; or the thumb may turn 
 in and the fingers close; or the toes may move and the ankle 
 become stiff. The spasm commences soon after the signal 
 symptom and increases in intensity. It continues sometimes 
 for three or four minutes, or longer when the convulsion ex- 
 tends to other parts. The movements performed are usually 
 complex movements out of their natural order and sequence 
 and with an irregular degree of force; both tonic and clonic 
 spasms occur. 
 
 3. The spasm extends from the part in which it begins to 
 other parts in a definite order of extension. Thus if it starts 
 in a part of the face, the entire face is involved and then the 
 shoulder, arm, forearm, and hand, possibly the leg also from 
 the trunk down to the toes. Or if it starts in the hand, the 
 
 1 Hughlings Jackson's early articles are to be found in Medical Times and 
 Gazette, 1861-1863; Aug. 13th, 1864; May 28th, 1868; Aug. 26th, 1871; Jan. 6th, 
 1872; March to August, 1873; January and October, 1874. May to September, 
 1875; J an - Ist - l8 7°- Lancet, May 16th, 1868; Dec. 13th, 1873. Brit. Med. Jour- 
 nal, May 10th, 1873. His latest lectures have appeared as this volume was in 
 press. The Lumleian Lectures on Convulsive Seizures, Brit. Med. Jour., March 
 25th and April 5th, i8go. 
 
28 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 forearm, arm, and shoulder become successively affected, then 
 the face or the leg. If it starts in the trunk, the thigh and leg 
 and foot follow in the motions. Or it may begin in the foot 
 and gradually creep up the bod)-. As it extends, the muscles 
 first affected become more and more convulsed until the en- 
 tire limb or the entire side is working. Occasionally the op- 
 posite side of the body is affected and if this occurs conscious- 
 ness may be finally lost. 
 
 4. Consciousness is almost always perfectly preserved during 
 the attack. 
 
 5. After tJie convulsion ceases the parts convulsed, and espe- 
 cially the part in which the spasm began, and consequently 
 continued longest, are found to be partially paralyzed and very 
 awkward, and not infrequently the numbness persists for a 
 time and is found to be associated with a moderate degree of 
 tactile or thermal anaesthesia. This partial paralysis may re- 
 main from a few minutes to several hours, depending on the 
 severity and duration of the convulsion. If it remains perma- 
 nently, it is evidence of organic destructive changes in the 
 cortex. Thus a growing tumor may cause local spasms at 
 first ; then local spasms with temporary paralysis ; then the 
 duration of the attacks of post-epileptic paralysis increases, 
 and finally the paralysis becomes total and permanent with 
 partial anaesthesia. Usually, if the lesion is only one of irri- 
 tation, the patient is free from symptoms between the attacks.' 
 
 These symptoms are absolutely characteristic of Jackso- 
 nian epilepsy, and when they occur are absolute evidence of a 
 source of irritation of some kind in the motor area. The ex- 
 act location in that area is indicated by the " signal symptom " 
 in each case. 
 
 The following cases, seen at the Vanderbilt clinic, illus- 
 
 * Hughlings Jackson explains the attack as due to a liberation of energy by 
 the nervous elements during rapid decomposition of some material in or a part of 
 the motor cells, probably due to chemical changes. As glycerine may become ex- 
 plosive by the addition of nitric acid forming nitro-glycerine, so he thinks the cells 
 may become ready to discharge by imperfect nutritive changes. For an interesting 
 presentation of this theory and many acute observations, the reader is referred to 
 the Lumleian lectures for 1890. Brit. Med. Jour., March and April, 1890. 
 
THE MOTOR AREA AND ITS AFFECTIONS. 
 
 2( J 
 
 trate the phenomena of Jacksonian epilepsy in several of its 
 forms, and the localization of the lesion is shown in each 
 case: 
 
 CASE I. — JACKSONIAN EPILEPSY. 
 
 Aphasia and Brachial Monospasm. — The patient, a man of 
 32 years, who had had a chancre in 1882, suffered from ver- 
 tigo, headache, and insomnia during November and December, 
 1885, and on December 15th while at work, suddenly felt a 
 numbness in his right hand and let fall a pail which he was 
 carrying. At the same time, he found himself unable to 
 speak. He did not lose consciousness; he understood what 
 his companions said to him, but he could not reply and he 
 could not move his arm. These symptoms passed off in half 
 an hour. Two days later another attack occurred, beginning 
 with a numb feeling at the tips of the fingers; then this ex- 
 tended up the hand and arm ; then the fingers became flexed 
 and stiff, though he found that by effort he could straighten 
 them. There were no clonic spasms of the fingers or hand or 
 arm ; but the numbness and stiff feeling extended up the arm, 
 shoulder, and neck to the face, which was drawn to the right 
 side, and then speech was lost. This attack lasted twenty 
 minutes without loss of consciousness. Similar attacks oc- 
 curred every day or two for three weeks, and during this time 
 his headache and insomnia increased. The attacks were not 
 all alike in their commencement. Sometimes they began with 
 aphasia; sometimes with brachial numbness; but in' all the 
 distribution of the symptoms was finally the same. The leg 
 and trunk were never involved. The hand often felt cold 
 during the attack, though it was warm to the touch, and was 
 always weak for some hours after an attack. On examina- 
 tion January 3d, 1886, there was no aphasia or facial paresis, 
 but there was slight tactile, and temperature anaesthesia in 
 the hand, some paresis and slight ataxia of movement. He 
 was put at once upon inunctions of mercury and large doses 
 of iodide of potash. The attacks ceased after a week of treat- 
 ment; and in the course of a month all symptoms had sub- 
 
^o 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 sided. Six months afterward he reported that on the day 
 previous he had felt a tingling in the right side of his face for 
 a few moments; and had had, for a few days, some headache. 
 He was again put upon specific treatment and no further 
 symptoms developed. He was shown at the clinic in Octo- 
 ber, i888, having then been two years without treatment and 
 in good health. All paresis and anaesthesia had disappeared. 
 The diagnosis in the case was a syphilitic gumma in the men- 
 inges over the lower posterior part of the second frontal con- 
 volution, causing occasional cortical " discharges of energy," 
 
 resulting in the brachial, 
 facial, and aphasic symp- 
 toms. The fact that these 
 symptoms never extended 
 to the leg showed that the 
 area affected was not ex- 
 tensive and did not include 
 the upper third of the mo- 
 tor area. The fact that 
 the symptoms began oc- 
 casionally with aphasia 
 and occasionally in the arm 
 showed that the lesion was 
 at a point about equidis- 
 tant between speech and 
 arm areas. The greater frequency with which attacks began 
 with aphasia, and the very slight anaesthesia permanent for a 
 time in the arm showed that the middle third of the motor 
 area was not involved to as great a degree as the aphasic area. 
 The pathological condition was probably a thin, flat, and 
 rather diffuse infiltration of the membranes over the area (Fig. 
 9). A very similar case was reported by Seguin ' in which a 
 limited meningitis was found in this area after death (Fig. 14, 1). 
 The co-existence of tactile and temperature sensations with 
 the spasm and the subsequent blunting of these senses with 
 the existence of ataxia is interesting as an indication of the 
 mixed function of the motor area. 
 
 Fig. 9. — Diagram of Left Hemisphere. Situation 
 of lesion in case I. 
 
 •Jour. Xerv. and Ment. Dis., June, 1S87. 
 
THE MOTOR A RICA AND ITS AFFECTIONS. 
 
 3' 
 
 CASE II. — JACKSONIAN EPILEPSY. 
 
 Brachial Monospasm Extending to the Face and followed by 
 Aphasia. — Five years ago, when 43 years old, this woman had 
 a carbuncle on her back which was opened. A short time- 
 afterward her attacks began, and have continued ever since, 
 sometimes at intervals of several weeks, sometimes as fre- 
 quently as several in a day. She first notices a prickling sen- 
 sation in the right hand, which then begins to jerk, and the 
 spasm extends up the arm and involves the right side of the 
 face. As soon as the prickling begins she becomes speechless, 
 and recovers her speech 
 very slowly after the at- 
 tack passes off . Occasion- 
 ally her right leg is stiff 
 during the spasm, but it 
 rarely jerks. She some- 
 times loses consciousness 
 but not as a rule. She 
 suffers from severe occipi- 
 tal and frontal headaches, 
 which are not, however, 
 constant, and at times has 
 a very intense itching in 
 the right side of the face. 
 There are no symptoms 
 of paresis or anaesthesia between the attacks, and the only 
 objective signs are an increase of the tendon reflexes on the 
 right side and slight lateral nystagmus. Her optic discs 
 are normal. She passed the menopause at 37 and is not hys- 
 terical. She was not benefited by treatment, and soon ceased 
 to attend. 
 
 The probable diagnosis was a chronic pachymeningitis 
 over the left hemisphere, affecting the middle of the anterior 
 and posterior central convolutions. The supposed situation 
 of the meningitis is shown in Fig. 10. The lesion is located 
 in this case posterior to that in Case I., because the spasm 
 uniformly began in the hand, speech being lost later. 
 
 Fig. 10. — Lateral Surface of Left Hemisphere. 
 Situation of lesion in Brachial Monospasm. Case II. 
 
j2 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 CASE III. — JACKSON IAN KHI.KPSY. 
 
 Brachial Monospasm.- The patient, a man of 34 years, had 
 a chancre thirteen years ago, but had been in good health until 
 April, 1887, when attacks began for which he applied to the 
 clinic in April, 1888. These attacks began by a trembling and 
 numb sensation, usually in the fingers of the left hand, but oc- 
 casionally in the left shoulder. This was followed at once by 
 spasm of the entire left upper extremity. When the tingling 
 began in the fingers the spasm began in the hand and ex- 
 tended up the arm, the wrist and elbow being successively in- 
 vaded, and finally reached the muscles of the left side of the 
 neck. When it commenced in the shoulder the neck was 
 moved first, and then the spasm extended down the arm to the 
 fingers. Several attacks were observed of both varieties, last- 
 ing from one to four minutes, never producing any disturb- 
 ance of consciousness or extending beyond the muscles of the 
 left upper extremity and neck. The rate of muscular con- 
 traction was four per second. Just before the spasm power 
 was 1 1 5 . Just after, it was 90 . There was some awkward- 
 ness of movement after an attack not noticed before it ; but 
 sensation was never impaired. When he applied he had been 
 having as many as five attacks daily. There were no other 
 symptoms at first; but under observation a gradually in- 
 creasing weakness of the left hand and awkwardness of move- 
 ment developed, with a sensation of numbness, until power 
 was reduced to 6o°, one-half that of the right hand, and 
 finer movements, such as buttoning his clothing, were done 
 clumsily. He had no headache, no tenderness of the head, no 
 optic neuritis, and no cerebral sensations. Under treatment 
 by inunctions of mercury and increasing doses of iodide of 
 potash with bromide of potash his attacks diminished in fre- 
 quency, so that he had but four during May. In June, after 
 drinking hard and neglecting treatment, he had a return of 
 the attacks, having forty-one in five days. He was sent into 
 Roosevelt Hospital, and the same treatment was carried out 
 with more care than he had probably given it when at work. 
 He was kept in the hospital till August, when he was dis- 
 
THE MOTOR AREA AND ITS AFFECTIONS. 
 
 33 
 
 charged, as he had had no attacks for three weeks. In Octo- 
 ber he reported at the dispensary that there had been no re- 
 turn of his attacks. Power was then found to be perfect, 145" 
 to 165 in both hands; sensation perfect, but a slight tremor 
 of the left hand was noticed, and he admitted that he was a 
 little awkward in using it, 
 but said that he had no 
 numbness. 
 
 The diagnosis was a 
 syphilitic tumor of the 
 meninges pressing on the 
 middle third of the right 
 anterior and posterior cen- 
 tral convolutions, which 
 was absorbed by the spe- 
 cific treatment. The lo- 
 cation of the tumor was 
 
 thought tO be at the point Fig. h.— Lateral surface of Brain. Situation of lesion 
 • ]■ . 1 • tt' , ,, tt 1 in Brachial Monospasm with Paresis. Case III. 
 
 indicated m .big. 1 1. Had 
 
 the specific treatment failed, an operation would have been 
 undertaken. In a very similar case reported by Dr. Keen, 1 
 the removal of a portion of the hand centre was followed by 
 a recovery from attacks whose frequency had been six a day. 
 
 CASE IV. — JACKSONIAN EPILEPSY. 
 
 Crural Monospasm. — For a year and a half prior to his 
 appearance at the clinic (March, 1889) the patient, a man of 50 
 years, had been subject to attacks of the following kind. He 
 felt a tingling and numbness in the left foot followed imme- 
 diately by twitching of the muscles of the toes, which then 
 extended up the leg to the hip until the entire limb felt numb 
 and was in motion. Sometimes this ceased after a few min- 
 utes; at other times he felt it ascend the left side of his body 
 to his arm and then he would lose consciousness; and on 
 coming to his senses was told that he had had a general con- 
 vulsion, in which, however, he never bit his tongue. These 
 
 1 Keen, Med. News, April 12th, 1S90, vol. lvi., p. 3S3. 
 ■ 3 
 
34 
 
 FAMILIAR FORMS OF NERVOUS DISEASE, 
 
 attacks occurred at first at intervals of a month, then became 
 much more frequent, and then again subsided so that he had 
 had but one in three months prior to March 8th, 1889, when 
 his last attack occurred. Early in his illness he had had ver- 
 tigo, headache, especially in the right parietal region, and in- 
 somnia; but these symptoms subsided after a few months. In 
 February, 1889, he had noticed a beginning weakness and numb- 
 ness in his left hand ; he wou2d let things fall unless he watched 
 his hand. A month later he noticed some difficulty in talking, 
 his articulation being indistinct for a few days; but both these 
 symptoms had passed off when he was examined. On March 
 
 8th he was not found to 
 present any abnormal 
 symptoms excepting a 
 slight increase of knee- 
 jerk on the left side. It 
 being probable that he 
 had had a chancre, he was 
 put upon mercury and 
 iodide, and this treatment, 
 with occasional tonics, has 
 been continued for a year, 
 during which time he has 
 
 Fig. 12.— Lateral surface of Right Hemisphere. Situ- had IIO attacks and has 
 ation of lesion in Crural Monospasm. Case IV. . . . . T 
 
 been in good health. It 
 is therefore probable that the attacks were due to a small fo- 
 cus of irritation in the paracentral lobule, either a small gumma 
 or a localized syphilitic meningitis, which had at one time ex- 
 tended downward along the fissure Rolando; and that this 
 was absorbed under the antisyphilitic treatment. The slight, 
 transient paresis of the arm and tongue were probably due to 
 the formation of thrombi of small extent in cortical arteries 
 having free anastomoses but in a state of endarteritis syphi- 
 litica ; they could hardly have been due to the slight pressure 
 of the syphilitic exudation. The situation of the lesion is 
 shown in Fig. 12. In a very similar cases reported by Hun' 
 
 •Henry Hun, Amer. Jour. Med. Sci., January, 1887, Case IV. 
 
THE MOTOR AREA AND ITS AFFECTIONS. 35 
 
 and Seguin ' a tumor was found in this region. Fig. 14, 4 
 shows the situation of the tumor in Seguin's case. 
 
 CASE V. — JACKSONIAN EPILEPSY. 
 
 Monospasm of Trunk and Leg. — The patient, a man of 46 
 years, had suffered from attacks of a peculiar character for 
 several years. He felt a numbness and tingling in the great 
 toe of the left foot, followed by a twitching of the muscles. 
 This sensation and spasm then extended up the leg, usually 
 stopping at the hip, but occasionally invading the muscles on 
 the left side of the abdomen, which would then contract rhyth- 
 mically causing him much _ ^^^ 
 discomfort. It never ex- ^-* W Blv^W 
 tended to the arm, and jf ^ ■ — ■ — ^ ^ ^ /jK 
 never produced a loss of / ' J _^^ -Oif \ 
 
 consciousness, but was r~\ V F^V ~~^ !5;S:! \ y^y^\ 
 
 always followed by a sen- VV^^" ^"""Si^l) f^C \ 
 sation of weakness in the ^ — ^^^^ — ^ / 
 leg. There were no other ( — "~~~- ~"" J ~~^^ / 
 symptoms. This patient ' ^ > "" - '^ 
 
 Continued tO have Spasms FlG -^.-Median surface of Right Hemisphere. Situ- 
 r ation of lesion in Spasm of T runkand Leg. Case V. 
 
 once a week, or oftener, 
 
 for months. He put himself under the care of Dr. Seguin 
 and was finally induced to go to the New York Hospital and 
 was operated upon by Dr. Weir, who found a local focus of 
 meningitis over the right para-central lobule, with adhesions 
 between the falx, the pia, and the brain on the median sur- 
 face of the hemisphere; thus establishing the diagnosis of a 
 focus of irritation in the cortical centres for the leg and trunk. 
 The case will be reported in full elsewhere. The situation of 
 the lesion is shown in Fig. 13. 
 
 The location of the lesion in these cases is very evident in 
 the light of the experience of the past ten years, numerous 
 cases exactly similar to these being on record where an ope- 
 ration or an autopsy revealed the exact seat of the disease. 
 It is impossible to cite such cases here, but in the articles of 
 x Jour. Merit, and Nerv. Dis., June, 18S7. Case II. 
 
36 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Hughlings Jackson, to which reference has already been made, 
 and in the books of Rolland on Jacksonian epilepsy and of 
 Bastiah on Paralysis, cerebral and spinal, as well as in a recent 
 article of Lowenfeld,' numerous illustrations of the same form 
 of spasm with autopsies may be found. It is with these cases 
 and those already cited in view that the lesion in each of the 
 preceding cases has been definitely located. 
 
 The Nature of the Lesion in these Cases. — In three of the pre- 
 ceding cases the diagnosis of a syphilitic exudation upon the 
 meninges was made. It is well known that the most frequent 
 syphilitic affection producing cerebral symptoms is an oblite- 
 rating endarteritis, and it is certain that on the occurrence of 
 a thrombosis within such a diseased artery sudden mono- 
 plegia may occur, temporary in character, owing to the fact 
 that the anastomosis of the arteries supplying the cortex is 
 so full that a collateral circulation is soon set up and prevents 
 permanent softening. Such a monoplegia is rarely preceded 
 by monospasm ; hence in the cases here recorded, since there 
 was a spasm, the lesion was probably not endarteritis with 
 thrombosis. The diagnosis made was meningitis syphilitica. 
 The most convincing point of differentiation between menin- 
 gitis and thrombosis is the recurrence in the former of the 
 same form of spasm in the same extremity over and over 
 again. When the lesion is the formation of a thrombus, on 
 each occasion of the attack the situation of the spasm and 
 of the subsequent paralysis differs. For when a syphilitic 
 endarteritis invades the vessels it is scattered widely through 
 them and is not confined to one alone. It seems evident, 
 therefore, that in these cases the nature of the lesion was 
 a syphilitic exudation in the meninges or a gumma. That 
 the exudation was not of sufficient thickness to produce much 
 pressure is seen by the very slight symptoms remaining be- 
 tween the attacks And its comparatively small amount is 
 also proven by the rapid response to treatment in all of the 
 cases. 
 
 In the second of these five cases the probable diagnosis 
 was a slowly increasing pachymeningitis with adhesion to the 
 1 Arch. f. Psych., xxi., s. I., s. 411, 1890. 
 
THE MOTOR AREA AND ITS AFFECTIONS. 37 
 
 cortex not syphilitic in origin. This diagnosis could not be 
 established as the patient was not under observation, for a 
 sufficient time. 
 
 In the last case the nature of the lesion was obscure, but 
 on operation a limited meningitis with adhesion of dura, pia, 
 and brain surface was found. Such localized meningitis has 
 been found after death in a number of cases as the cause of 
 the epilepsy. 
 
 There are numerous cases of Jacksonian epilepsy in which 
 it is impossible to determine the nature of the disease, and in 
 which, even after death, no gross changes are found. It is 
 well known that a uraemic convulsion may simulate a local- 
 ized spasm. Therefore some caution is to be exercised in the 
 diagnosis of this disease. When, however, the symptoms oc- 
 cur in the order named, and attacks are repeated, each resem- 
 bling the others, and no other cause is found, a diagnosis of a 
 source of irritation in the cortex in a particular area is proper. 
 This source of irritation is most frequently tumor, next a 
 small area of softening or of sclerosis, lastly meningeal adhesion. 
 
 SURGICAL TREATMENT OF JACKSONIAN EPILEPSY. 
 
 Many operations . have been performed for the relief of 
 Jacksonian epilepsy with varying success, and it is still too 
 soon to make any definite statements regarding the advisa- 
 bility of surgical interference, although the safety of the ope- 
 ration under antiseptics makes it legitimate in any severe case 
 where the spasms occur frequently. If this is undertaken, the 
 trephine should be applied over the part of the motor area 
 which presides over the movements with which the spasm be- 
 gins. If on exposing the dura or pia mater, or the brain sur- 
 face, some lesion is found, such as a localized meningeal thick- 
 ening, a tumor, an adhesion between membranes and brain, or 
 an abnormal appearance of the gray matter, it is proper to 
 remove it. If nothing is found, it is proper to apply to the 
 cortex exposed the irritation of a faradic current of electric- 
 ity, by means of two poles made of blunt-pointed probes, held 
 within a quarter of an inch of one another, the current being 
 
38 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 increased gradually until motions are elicited in the limb of 
 the opposite side. When the point of the cortex is found 
 whose irritation causes a motion similar to that with which 
 the spasm begins, a small wedge-shaped piece of the cortex 
 may be excised. 1 
 
 This surgical treatment has been carried out successfully 
 in a number of cases by various operators; among whom 
 Macewen, Horsley, Bergmann, Weir, Keen, and Park may be 
 mentioned. In a number of cases the spasms have ceased, the 
 patient has remained well, and has not suffered from perma- 
 nent paralysis. In some of the cases, however, the spasms 
 have returned subsequently to the operation, so that it is not 
 possible to promise a cure in any case. 2 
 
 * For successful cases see Mills: Trans. Cong. Amer. Thys. and Surg., vol. i., p. 
 223, 1888. Lloyd : Jour. Nerv. and Ment. Dis., vol. xiv., p. 350, 1889. Keen : 
 Medical News, vol. lvi., p. 381, April 12th, 1890. 
 
 2 For an account of the surgical procedure the reader is referred to the follow- 
 ing articles upon cerebral surgery: 1. Brain Surgery, V. Horsley, M.D., Brit. 
 Med. Jour., Oct. 9th, 1886, April 23d, 1887; also Amer. Jour. Med. Sci., April, 
 
 1887. 2. Cerebral Surgery, by W. Macewen, M.D., Brit. Med. Jour., Aug. nth, 
 
 1888. 3. A Contribution to the Diagnosis and Treatment of Tumors of the Cere- 
 brum, by R. F. Weir, M.D., and E. C. Seguin, M.D., Amer. Jour. Med. Science, 
 1888, July, Aug., and Sept. 4. Three Successful Cases of Cerebral Surgery, by 
 W. W. Keen, M.D., Amer. Jour. Med. Science, 1888, Oct. and Nov. 5. Surgery 
 of the Brain, by Roswell Park, M.D., N. Y. Med. Jour., 1888, Nov. 3d, 10th, and 
 17th. 6. Die Chirurgische Behandlung von Hirnkrankheiten, by E. von Berg- 
 mann, Berlin, 1889, 2te Auflage. 7. Cerebral Surgery, by W. W. Keen, M.D., 
 Ref. Handbook Med. Sci., vol. viii., 1889. 
 
CHAPTER IV. 
 
 THE MOTOR AREA AND ITS DESTRUCTION. 
 
 Cortical Paralysis. — Monoplegia and Hemiplegia. — Case VI., Cortical 
 Hemorrhage producing Aphasia and Hemiplegia; Removal of the 
 Clot; Recovery. — The Centres of Muscular Sense. — Tactile Centres. 
 
 CORTICAL PARALYSIS. MONOPLEGIA AND HEMIPLEGIA. 
 
 When any portion of the motor area is destroyed by dis- 
 ease, paralysis results. The extent of this paralysis is deter- 
 mined by the location of the destruction. If this is in the 
 lower third of the motor area, the face (except the act of clos- 
 ing the eye) will be paralyzed. If it is in the middle third, it 
 will be the movements of the upper extremity which are im- 
 paired. If it is in the upper third, it will be the lower ex- 
 tremity which is rendered useless. 
 
 Hemiplegia does not often occur from a cortical lesion. 
 For such a lesion must be very extensive to involve the areas 
 for face, arm, and leg. The ordinary form of hemiplegia is 
 due to a small lesion tearing through the motor tract in the 
 internal capsule, where the fibres from the separate areas are 
 collected in a narrow band, as seen in the diagram, Fig. 26. 
 
 Cortical paralysis is usually in the form of a monoplegia, 
 one part only being paralyzed. Hence, in tumors of the cor- 
 tex, monoplegia rather than hemiplegia is the rule. In Fig. 
 14 the situation of four such tumors is shown which pro- 
 duced monoplegia in arm or leg. As a tumor becomes 
 larger the paralysis may extend gradually from one limb to 
 another, giving rise to associated monoplegia? (as in Case II., 
 Fig. 14): the face and arm or the arm and leg are associated 
 together in such paralysis: the face and leg are never para- 
 lyzed together when the arm escapes. The diagnosis of a brain 
 tumor can usually be made from the general symptoms, and 
 
4Q 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 when it is localized in the motor area it should be removed. 
 For examples of such cases in which tumors were successfully 
 extirpated, the reader is referred to the articles mentioned at 
 the end of the last chapter. 
 
 In small areas of softening in the cortex, due to emboli or 
 to thrombi forming in vessels which are diseased or obstructed 
 by syphilitic deposits, the paralysis is almost always limited to 
 
 Fig. 14. — Diagrams of Lateral Surface of Brain showing Lesions. 1, Situation of tumor pro- 
 ducing brachial spasm and paralysis, successfully removed by Weir, Amer. Jour. Med. Sci., xcvi.; 
 2, Situation of tumor producing brachial paralysis, and finally hemiplegia, successfully removed by 
 Keen, Amer. Jour. Med. Sci., xcvi., p. 337 ; 3, Situation of adhesion of membranes producing 
 brachial spasm and paralysis successfully removed by Keen, Amer. Jour. Med. Sci., xcvi., p. 330; 
 4, Situation of tumor producing crural spasm and paralysis, with autopsy; Seguin, Jour. Nerv. and 
 Ment. Dis., June, 1887. 
 
 one limb. These do not admit of relief. Hemorrhages in the 
 meninges causing paralysis, though common in children, are 
 rare in adults. They are usually due to traumatism, as in the 
 remarkable case soon to be studied, which illustrates the char- 
 acter of cortical paralysis when this is very extensive. They 
 may also be due to chronic pachymeningitis. The lesion in 
 chronic pachymeningitis is permanent and progressive; and 
 
THE MOTOR AREA AND ITS DESTRUCTION. 4 j 
 
 when a hematoma forms, the condition of the patient is, as a 
 rule, such that operative interference could not arrest the dis- 
 ease or result in permanent benefit. 
 
 The prospects of recovery in cases of cerebral hemorrhage 
 are so bad, and the utility of medical treatment by drugs, 
 electricity, or apparatus is so doubtful, that in any case where 
 surgical interference is possible it affords the only definite 
 hope. When a hemorrhage has occurred within the cerebral 
 hemisphere, lacerating the tracts and destroying the tissue, 
 operative interference is out of the question. For tissue once 
 destroyed in the brain is not repaired by nature, and even 
 were repair possible, the surgeon could not reach and remove 
 the clot without producing a further laceration of very im- 
 portant cerebral structures or serious cerebral hemorrhage. 
 It is, therefore, in cases of cortical or surface hemorrhages 
 only that operations can be done. When such hemorrhages 
 occur as a complication of depressed fractures, they may be 
 treated coincidently with the fracture, and when the cranial 
 bone is elevated the hemorrhage may be stopped and the clot 
 removed. 1 When, however, there is no external evidence of 
 injury, the propriety of trephining becomes a problem of a 
 most serious character. If the symptoms point to a hemor- 
 rhage upon the base of the brain, involving by pressure the 
 cranial nerves, the clot cannot be reached by the surgeon. If, 
 however, it is upon the external surface of the hemisphere 
 and produces symptoms of aphasia, hemiplegia, or hemi- 
 anopsia, it can be removed. 
 
 Soon after the onset of an apoplexy, it is rarely possible 
 to determine whether a clot lies upon or within the brain. It 
 is only by observing the character and order of the onset of 
 symptoms, by watching their progress, and determining which 
 are permanent direct local symptoms and which are tempo- 
 rary indirect general symptoms, that a definite diagnosis can 
 be reached. It becomes evident, therefore, that in but a few 
 cases of cerebral hemorrhage can the surgeon accomplish 
 
 1 In an article by Turner, Lancet, r887, i., p. 116, maybe found a number of 
 cases of aphasia produced by wounds and fractures of the skull, and relieved ty 
 removing clots, or pieces of bone. 
 
4 j FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 anything, and that only after some careful observation of a 
 patient is he warranted in making an attempt. 
 
 In the following case [ior the opportunity of seeing and 
 recording which I am indebted to Dr. Chas. McBurney) the 
 conditions for success seemed favorable and the result demon- 
 strates the propriety of the course taken : 
 
 CASE VI. — CORTICAL HEMORRHAGE AFTER INJURY. 
 
 Right Hemiplegia. Aphasia. Operation. Partial Recovery. 
 — A physician was thrown from his carriage on the 17th of 
 August, 1889. He was slightly stunned by the fall, but was 
 able to help his wife, who seemed badly hurt, to reach home. 
 For some hours he appeared to be suffering merely from 
 bruises, and though lying down was able to converse with a 
 patient and give him a hypodermic injection. In the course 
 of the evening, however, he became delirious and excited, 
 then rather stupid, and regarding the occurrences of the three 
 following days, he has no recollection ; though he was able 
 during all this time to recognize his wife. On the morning 
 of the 1 8th he was found to be completely hemiplegic on the 
 right side and completely aphasic ; although the power of un- 
 derstanding what was heard was never lost. The condition of 
 hemiplegia with complete motor aphasia remained until De- 
 cember, 1889, at the time of the operation. At that time he 
 was able to move his leg a little and to drag it forward when 
 held up by two persons. He could not move his arm or hand 
 at all. His face was slightly flat on the right side, but his 
 tongue protruded straight. The only sounds he could make 
 were the vowel sounds; no formed words were possible. The 
 right pupil was one-third smaller than the left one. Sensa- 
 tions of touch and pain and of location were somewhat im- 
 paired, but not lost on the affected side. To cold and hot 
 objects he seemed extremely sensitive. The tendon reflexes 
 were extremely exaggerated, wrist and finger clonus, as well 
 as patella and ankle clonus, being easily elicited ; and ankle 
 clonus could not be stopped and often persisted for hours 
 when once started. The hand was flexed and pronated ; the 
 
THE MOTOR AREA AND ITS DESTRUCTION. 43 
 
 leg extended; both were rigid. He controlled his sphincters 
 perfectly. Mentally, he appeared to be less active than pre- 
 vious to the accident; though understanding what was said, 
 it was difficult to determine the reliability of his assent or 
 dissent in the sensory tests. He was emotionally unstable, 
 laughing very easily and being at times depressed. Sometimes 
 the laughter was like that of a demented person, causeless 
 and silly. Sight was good, and the optic discs appeared nor- 
 mal. Hearing was unaffected. 
 
 The chief and most permanent symptom was, therefore, 
 the motor aphasia. The hemiplegia had somewhat improved 
 during three months, but the arm was still totally helpless. 
 The inequality of the pupils, the mode of onset, and the per- 
 manence of the symptoms pointed to the occurrence of a 
 cerebral hemorrhage in or upon the left hemisphere. The 
 total aphasia could not be explained by a lesion in any other 
 position than in the posterior part of the third frontal convo- 
 lution; for while aphasia may occur as a temporary symptom 
 in lesions of the left internal capsule, it is not one which per- 
 sists. The paralysis, greater in the arm than in the leg, was 
 consistent with the idea of a cortical lesion in the middle half 
 of the anterior central convolution. The escape of face and 
 tongue from the paralysis would not have been possible had 
 the lesion causing the aphasia and brachial paralysis lain in 
 the internal capsule, or in fact anywhere within the brain, be- 
 cause the speech tract and motor arm tract are separated 
 from each other by the motor tract to the face and tongue : 
 and the three, as a rule, are injured together. The hemor- 
 rhage was, therefore, thought to be cortical and to lie in 
 the position indicated in Fig. 15, with two areas of greatest 
 intensity and an area of less intensity between them. Inas- 
 much as the aphasia was the most prominent symptom and 
 had shown no tendency to subside, it was thought that the 
 posterior part of the third frontal convolution was the point 
 of greatest pressure. 
 
 Operation. — On December 13th Dr. McBurney undertook 
 the operation of trephining. The trephine was applied at a 
 point one inch and seven-eighths behind and seven-eighths of 
 
44 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 an inch above the external angular process of the frontal 
 bone ; the line backward being parallel to the zygoma. The 
 dura did. not pulsate, and when it was incised the pia was 
 found to be cedematous, and the surface of the brain was seen 
 to be without pulsation and to be covered with a clot of blood 
 over the posterior part of the area laid bare, which was the 
 third frontal gyrus. 
 
 The opening in the skull was accordingly enlarged back- 
 ward and upward by the use of rongeur forceps. As the lower 
 part of the anterior central gyrus was exposed, it was seen to 
 be also covered by the clot of blood, which was continuous 
 
 with a thicker layer 
 which extended into the 
 fissure of Rolando. This 
 fissure was consequently 
 laid bare by an increase 
 in the cranial opening, 
 and was followed up to 
 the junction of its mid- 
 dle and upper thirds, 
 where the clot was found 
 to cease. The pia was 
 then incised as the clot 
 lay beneath it, and the 
 clot was gently removed 
 It w a s 
 found to fill up and 
 greatly distend the fissure of Rolando, and in the ail-de-sac 
 at the lower limit of the fissure a mass of blood had collected, 
 making pressure forward as well as inward, thus adding to 
 the compression of Broca's speech centre by the thin sur- 
 face clot already described. The clot was partly organ- 
 ized and came away in small shreds upon the fine aseptic 
 sponges used. The brain cortex was slightly discolored, and 
 at no point of the area exposed was it seen to pulsate. The 
 veins in the pia, which had been cut, were tied, drainage- 
 tubes were put in place, the dura was stitched, the scalp- 
 wound was united by sutures, and the bandages were adjusted. 
 
 Fig. 15. — Diagram of Lateral Surface of Left Hemi- 
 sphere. Situation of clotssuccessfully diagnosticated and by SpOIiglllg 
 removed. Case VI. 
 
THE MOTOR AREA AND ITS DESTRUCTION. 
 
 45 
 
 The entire operation was conducted according to the most 
 strictly aseptic method, with success, as the subsequent lack 
 of suppuration and the normal temperature demonstrated. At 
 the third dressing, on the fourth day, the brain was seen to 
 pulsate under the entire opening. The drainage-tubes were 
 removed in a week, and in the course of a month the wound 
 had entirely healed. 
 
 From the first day after the operation, a decided change 
 was noticed in the mental condition of the patient. He was 
 much more intelligent and no longer silly or emotional. In 
 the course of the first week, it was evident that an improve- 
 ment in his power of movement was beginning. At the end 
 of three months, he was able to walk with the aid of a cane 
 and to perform many of the larger motions of the arm and 
 forearm, and flexion but not extension of the fingers. Speech 
 had been also returning slowly under instruction and con- 
 stant practice. At present, six months after the operation, 
 he can repeat many words after another person ; can say all 
 the letters of the alphabet and reply simply to ordinary ques- 
 tions. It appears as if he were learning, like a person study- 
 ing a foreign tongue, to articulate strange and unfamiliar 
 sounds. But his efforts now are successful, while formerly 
 they could not be begun. It is very evident that the removal 
 of the clot has been followed by an improvement in his men- 
 tal condition, motor power, and speech. The irregularity of 
 the pupils subsided after three months; the rigidity of the arm 
 and leg and the increased tendon reflexes remain, but his gen- 
 eral condition is certainly far better than prior to the opera- 
 tion, and there is every reason to hope for recovery. A 
 marked deficiency of tissue and depression of surface remain 
 partly filled by dense connective tissue; but as the hair covers 
 this completely it is not very noticeable and is easily concealed 
 by a cap. 1 
 
 1 C. B. Ball (Brit. Med. Jour., April, 1888, p. 748) and Mouisset (Lyon Medical, 
 Oct., 18S9, p. 204) report successful operations for aphasia, with removal of a 
 cortical clot and recovery of speech. 
 
46 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 IHK CENTRES OF MUSCULAR SENSE. 
 
 The localization of tlic centres appreciating t lie position of a 
 limb (the so-called muscular sense) has been a matter of con- 
 troversy. It ma)' therefore be interesting to note that in the 
 preceding case, in which the clot compressed the motor cen- 
 tres, muscular sense was impaired. This was more strikingly 
 evident in another patient, also seen with Dr. McBurney. In 
 this man a bolt had been driven through the left parietal bone 
 over the hand centre and had produced an almost complete 
 paralysis of the right hand and arm, with only partial affection 
 of the face and leg. In this patient, tactile and pain and tem- 
 perature senses were slightly impaired, and muscular sense 
 was markedly deficient. He could locate accurately the point 
 touched upon the hand, but was unable to place his left hand 
 in positions given to the right hand with his eyes closed. If 
 the right hand was placed in a fist position and he was told 
 to put his left hand in the same position, he was just as likely 
 to open as to close it ; and other positions also were not ap- 
 preciated nor imitated. An operation was performed to ele- 
 vate a depressed portion of skull in this man, and extensive 
 injury of the parietal cortex was found, with an abscess under 
 the depressed bones. The exact location of the lesion was 
 therefore certainly in the posterior central region. These two 
 cases would therefore appear to indicate a coincidence in sit- 
 uation of the motor and muscular sense centres in the cortex. 
 
 THE TACTILE CENTRES. 
 
 The existence of slight anaesthesia in both of these cases 
 and the uniform occurrence of sensations of numbness in cases 
 of Jacksonian epilepsy when the irritation occurs in the motor 
 area seems to show quite clearly that the tactile and motor 
 centres coincide. Horsley has suggested that in the three chief 
 layers of cells which make up the motor cortex the three 
 functions of motor power, muscular sense, and tactile sense 
 are located, so that each part of the motor area has a sensory 
 function as well. When one considers how nicely muscular 
 
THE MOTOR AREA AND ITS DESTRUCTION. 47 
 
 and tactile impressions regulate motor efforts, this theory 
 gains in probability. The efforts to lift a bit of cotton or a 
 lump of lead differ greatly, and are directly determined by 
 the perception of weight and contact. 
 
 Whether there are tactile centres separate from the motor 
 area in the hippocampal region, as Ferrier alone holds, is not 
 yet determined for man. Dana has shown ' by a large collec- 
 tion of cases that lesions in the motor area are very frequently 
 associated with anaesthesia. And since the sensory tract in 
 the internal capsule lies just behind the motor tract, it is not 
 unlikely that tactile centres do lie (as I showed in 1884 2 ) in the 
 parietal region just behind the motor area or else coincide 
 with it. It is certain that lesions in the posterior half of the 
 motor area are frequently productive of anaesthesia, while 
 lesions in the anterior half of the motor area are rarely pro- 
 ductive of anaesthesia. In the posterior part lie the motor 
 centres of the smallest joints, fingers, and toes, and, since the 
 finer movements of these are guided by touch, it is not un- 
 likely that about these centres tactile areas lie. The question 
 of the localization of tactile temperature and pain senses is 
 still an open one; and more precise statements are not yet 
 warranted. 
 
 1 Dana: Jour. Nerv. and Ment. Dis., 1888, p. 650. 
 
 2 Starr: Jour. Nerv. and Ment. Dis., July, 1884. 
 
CHAPTER V. 
 
 THE VISUAL AREA AND ITS AFFECTIONS. 
 
 The limits of the visual area. — Hemianopsia ; the visual tract. — Sensory 
 epilepsy from irritation of the visual cortex. — Case VII., Visual hal- 
 lucinations and temporary hemianopsia. — Case VIII., Visual halluci- 
 nations and temporary hemianopsia. — Case IX., Hemianopsia of 
 cortical origin. 
 
 THE VISUAL AREA. 
 
 THE visual area of the brain is located in the occipital 
 
 convolutions and the 
 cuneus. The limits of 
 this area are shown in 
 Fig. 16 (i and 2) and 
 are no longer a matter 
 of dispute. Since 1884, 
 when I was able to col- 
 lect ' 27 cases of lesion 
 in the occipital lobes, 
 and to prove by their 
 analysis that the visual 
 area was located in this 
 region, about 20 addi- 
 tional cases have been 
 published. These seem 
 to confirm the conclu- 
 sion reached by Scguin, 
 in 1886, 2 that the cuneus 
 is the part of the occip- 
 ital lobe in which the 
 
 Fig. 16.— i. Lateral Surface of Hemisphere; 2, Median visual tract ends. That 
 Surface of Hemisphere. The shading shows the visual area. fU P anrrnlar rryniS lllS 
 
 1 Starr: " Visual Area of the Brain," Amer. Jour. Med. Sci., Jan., 1884. 
 
 2 Seguin: " Hemianopsia," Jour, of Nerv. and Ment. Dis., Jan., 1886. 
 
THE VISUAL AREA AND ITS AFFECTIONS. 49 
 
 nothing to do with vision in man (whatever its function in 
 monkeys) is not only proven by these cases of lesion in the 
 occipital region, but is also determined by a collection ' of 23 
 cases of lesion in the angular gyrus without disturbance of 
 vision. The visual area is therefore limited in man to the 
 convolutions of the occipital lobe. 
 
 The character of the blindness produced by the destruc- 
 tion of this cortical area is peculiar. It is termed bilateral 
 homonymous hemianopsia, that is, a blindness in the like- 
 named halves of both visual fields. When the right occipital 
 lobe is affected the patient cannot see any objects lying to 
 the left side of the middle line as he looks forward. When 
 the left occipital lobe is affected the patient can see nothing 
 to the right side of the middle line. This peculiar form of 
 blindness is easily understood by a consideration of the anat- 
 omy of the visual tract as shown in the diagram (Fig. 17). It 
 is seen that each optic nerve divides into two parts at the 
 optic chiasm. The larger part crosses to the opposite optic 
 tract ; the smaller joins the optic tract of the same side. 
 Each optic tract then contains fibres from both eyes. It is 
 found that the fibres from the temporal half of the retina, 
 which receives impulses from the nasal half of the visual 
 field, do not decussate. Hence a lesion of the right optic 
 tract will cause blindness in the nasal half of the visual field 
 of the right eye. Fibres from the nasal half of the retina, 
 which receives impulses from the temporal half of the visual 
 field, do decussate with those of the opposite side. Hence a 
 lesion of the right optic tract will cause blindness in the tem- 
 poral half of the visual field of the left eye. Therefore a le- 
 sion of the right optic tract causes a loss of function in the 
 right half of both retinae, and as a consequence the blind- 
 ness is limited to the left half of both visual fields. Both eyes 
 are affected, the blindness is bilateral; it is but one half of 
 the vision which is lost, the blindness is therefore called hemi- 
 anopsia; and like-named halves of the two visual fields are 
 blind, hence the term bilateral homonymous hemianopsia. 
 
 1 Starr: " The Lesions of Sensory Aphasia." Brain, July, 1SS9. 
 4 
 
50 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 B.tg r 
 
 Fig. 17. — The Optic and Visual Tracts. A r , Lesion causing nasal hemianopsia, unilateral; T, 
 lesion causing temporal hemianopsia, unilateral ; //, lesion causing bilateral heteronymous hemi- 
 anopsia. Any lesion lying behind the chiasm causes bilateral homonymous hemianopsia; A"A r , red 
 nucleus of tegmentum; S.V, substantia nigra of crus ; L, lemniscus; /C, inter, geniculate body; 
 77/, third nerve exit; /, infundibulum; CM, corpora albicantla. 
 
THE VISUAL AREA AND ITS AFFECTIONS. 51 
 
 From the optic chiasm, each optic tract passes around 
 the crus cerebri and terminates in the external geniculate 
 body, in the optic thalamus, and in the anterior corpus quad- 
 rigeminum, as seen in the diagram. From these three masses 
 of gray matter new fibres start out which issue from the outer 
 side of the optic thalamus, enter the internal capsule, and 
 curve backward through the occipital lobe, lying on the outer 
 side of the posterior horn of the lateral ventricle, and thus 
 reach the occipital convolutions, ending chiefly in the cuneus. 
 It is evident that a lesion anywhere in the course of the visual 
 tract from the optic chiasm to the cuneus will cause bilateral 
 homonymous hemianopsia. This is the only form of blind- 
 ness produced by a lesion of the visual area, or caused by dis- 
 ease of one cerebral hemisphere. Blindness in one eye alone 
 is not produced by cortical disease. When it occurs it is 
 usually either from disease in the eyeball or in the optic 
 nerve, or it is hysterical. 
 
 Since the visual tract is a long one, it is desirable to be able 
 to locate a lesion in its various parts. This can easily be 
 done by a study of the symptoms associated with the hemi- 
 anopsia. Thus if the optic tract is involved, as it curves 
 around the crus cerebri, the same lesion which causes hemi- 
 anopsia will be likely to affect the motor tract in its passage 
 through the crus, or to involve the third nerve at its exit from 
 the crus (compare the diagram Fig. 17 with the diagram Fig. 
 26). In this case hemianopsia and hemiplegia of one side 
 will be combined with oculo-motor paralysis of the other side. 
 If the optic tract is involved at its termination in the thalamus, 
 the lesion, unless very small, will affect the sensory tract 
 from the opposite side of the body in its passage along the 
 internal capsule at the side of the thalamus; and in this case 
 hemianaesthesia will be found as well as hemianopsia. If the 
 visual tract in the internal capsule is involved by disease of 
 the capsule or basal ganglia, the proximity of both sensory 
 and motor tracts may render a combination of hemianopsia, 
 hemianaesthesia, and hemiplegia possible. If the visual tract 
 is invaded within the occipital lobe or in the cortex, none of 
 these other symptoms will be present ; hence their absence is 
 
5 j FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 an aid to the localization of the lesion. As will be shown later 
 (Chapter VII.), when the left visual tract is invaded in the 
 occipital lobe, word-blindness may be found. Such a condi- 
 tion docs not occur when the right hemisphere is diseased. 
 
 SENSORY EPILEPTIC SEIZURES FROM IRRITATION OF THE 
 VISUAL AREA. 
 
 Since " nervous discharges " occurring in the sensori-motor 
 area give rise to spasm followed by paralysis distinctly limited 
 to a single limb, it is not surprising that attacks of an homo- 
 logous nature should be observed when other regions of the 
 cortex are invaded." The two following cases indicate the 
 existence of " discharges " in a purely sensory area of the cor- 
 tex; namely, in the visual area, which lies in the occipital 
 lobes. The initial symptom in both cases was the sudden 
 appearance of a bright light to one side of the middle line in 
 both eyes, followed by a blindness in the corresponding visual 
 field. The hallucination of light may be regarded as homo- 
 logous to the motor spasm; the blindness as homologous to 
 the paralysis. The situation of the initial irritation must have 
 been in the occipital convolutions, since they receive impres- 
 sions from the eyes ; each occipital lobe being functionally 
 related to one half of both eyes, so that the hallucination or 
 blindness was necessarily one-sided. These cases are of im- 
 portance, as they might be easily mistaken either for migraine 
 or for ordinary epilepsy of the: petit vial type. But a consid- 
 eration of the symptoms shows that either of these diagnoses 
 would be erroneous. 
 
 CASE VII. — CORTICAL DISCHARGE IN THE LEFT OCCIPITAL 
 
 LOBE. 
 
 Visual Hallucination followed by Temporary Right Hemi- 
 anopsia. — The attacks from which the patient suffered began 
 in 1886, when he was 39 years old, after a day of severe in- 
 
 1 Hughlings Jackson: Brit. Med. Jour., Jan. nth, 1879 < Charcot : Lecons, Pro- 
 gris Med., 1887; Pitres : Revue de Med., Aug., 1888; Lowenfeld: Arch. f. 
 I'svch.. xxi., p. 423 ; Anderson: Brain, 1S86, p. 385. 
 
THE VISUAL AREA AND ITS AFTECTIONS 
 
 53 
 
 tellectual work. While reading he felt a queer sensation in 
 his head and found himself blind in the right half of both 
 visual fields. He called his wife to apply cold water to his 
 head, and thus arrested the attack at once. Similar attacks 
 recurred at intervals of six or eight weeks for two years. 
 Sometimes the hemianopsia is preceded by an aura of blue 
 or red light or of " smoke " in the right visual field, and then 
 the blindness follows. The attacks last from three to ten 
 minutes and are not attended by loss of consciousness or fol- 
 lowed by headache. There is no vertigo with them, but his 
 head feels full and sometimes his right upper eyelid twitches. 
 He is a physician and observes and describes the attacks 
 intelligently. He has no other symptoms. Bromide reduces 
 the frequency of the attack. His V = |£ ; pupils are equal and 
 react normally; he has no insufficiency of the ocular muscles; 
 his visual fields are normal to light and colors; but his optic 
 discs are rather pale. When relieved of a condition of ex- 
 treme neurasthenia the attacks become less frequent but they 
 still occur. 
 
 CASE VIII. — CORTICAL DISCHARGE FROM THE OCCIPITAL 
 
 LOBES. 
 
 Visual Hallucinations follotved by Hemianopsia. — The pa- 
 tient has had attacks since the age of 21. They begin with a 
 sudden vision of yellow sparks or flashes of light in one half 
 of the visual field of both eyes, either to the right or to the 
 left, never in the middle line, and then in a few seconds the 
 entire half of the visual field in which he has seen the flashes 
 becomes dark for a few minutes. He feels dizzy and bewil- 
 dered at the time, and as if about to faint, but he has never 
 lost consciousness or fallen or had a twitching of the muscles. 
 The attacks are often followed by severe unilateral headache. 
 During the attacks his face flushes and his head feels full. 
 He can arrest the attack by putting his feet in hot water. 
 Bromides diminish the frequency of the attacks, which ordi- 
 narily come about once a week. He has no other symptoms. 
 V = f g ; pupils are dilated and react normally ; insufficiency of 
 
54 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 theexterni, ' _. c ; adduction, 9 ; abduction, 6°; visual fields nor- 
 mal and discs clear. 
 
 In the first case the left cuneus (Fig. 16) must have been 
 irritated, since the hallucinations and blindness were uni- 
 formly in the right half of the visual field. 
 
 In the second case the irritation affected sometimes one 
 side and sometimes the other. Since the cunei lie adjacent to 
 one another, separated only by the falx cerebri, it seems prob- 
 able that in this case the irritating focus of disease may have 
 been in the falx between the cunei, and variations in the cere- 
 bral circulation caused the irritation to be manifested at times 
 on one side and at times on the other. It is well known that 
 hemorrhages in the falx at this point, by pressing simultane- 
 ously on both cunei, have caused total blindness by produc- 
 ing double hemianopsia. Such cases have been recorded by 
 Chauffard and Bouveret (1888).' 
 
 The following case, which was referred to me by Dr. John 
 E. Weeks, Chief of the Ophthalmic department of the Clinic, 
 and the history of which he has kindly prepared, well illus- 
 trates the form of blindness due to cortical lesion: 
 
 CASE IX.— LEFT HEMIANOPSIA. 
 
 A woman was forced to fly from a burning house within a 
 week of her confinement, and on reaching the street became 
 weak and noticed a sudden blindness in both eyes. She stum- 
 bled but did not fall or lose consciousness, and she had no 
 convulsion. For a few hours subsequently she felt a weak- 
 ness in her left side, but this soon passed off. The blindness 
 remained. Seven months after the onset she was found to 
 have no symptoms of paralysis or anaesthesia, but a well- 
 marked left homonymous hemianopsia. She was blind in the 
 left half of both visual fields; the blindness, however, not in- 
 volving the point of distinct vision, but passing, as the diagram 
 (Fig. 18) shows, 3 around it. When she looked straight for- 
 ward she saw everything to the right side, nothing to the left 
 side. Her optic nerves were normal, and vision was ■§£ + in 
 
 1 Revue de Medecine. 
 
THE VISUAL AREA AND ITS AFFECTIONS. 
 
 55 
 
 both eyes. There were no symptoms of cranial nerve paral- 
 ysis to indicate a lesion of the optic tract on the base. There- 
 was neither hemiplegia nor hemianesthesia, one or both of 
 which would have been present had the lesion been in the 
 
 Fig. 18.— The Visual Fields. The shading shows the blind field in Case IX. 
 
 optic thalamus or internal capsule. The lesion, therefore, 
 must have lain in the right occipital lobe or its cortex (Fig, 
 19). 
 
 The diagnosis of the nature of the lesion was as evident as 
 that of its location. A sudden cerebral apoplexy in a puer- 
 peral woman is almost 
 certainly due to the 
 lodgment of a clot in 
 some artery of the 
 brain, and the origin 
 of such a clot, acting 
 as an embolus is al- 
 ways from a venous 
 thrombus in the uterus 
 when, as in this case, 
 there is no cardiac dis- 
 ease or phlebitis elsewhere. The only artery which supplies 
 the occipital convolutions exclusively is the posterior cerebral, 
 and although thrombi and emboli in this artery are rare, there 
 is a sufficient number of cases on record in which they have 
 been found to warrant the diagnosis in this case. 
 
 Fig. 19. — Median Surface of Hemisphere, 
 left hemianopsia. 
 
 Lesion causing 
 
56 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 There are a number of cases upon record in which lesions 
 of a destructive character have been removed from the occi- 
 pital lobe. In 1882 Wernicke and II aim reported ' a case of 
 abscess of this region successfully diagnosticated and evacu- 
 ated. In 1887 Birdsall diagnosticated a tumor in the occipi- 
 tal lobe which Weir removed by trephining.-' Other cases of 
 this nature might be cited. In such cases, when hemianopsia 
 has been produced the removal of the disease does not result 
 in restoration of vision. But when the lesion is one which is 
 progressing, such as an abscess or tumor, its removal may 
 save the patient's life. The diagnosis of a tumor in the visual 
 area is to be made from the presence of general symptoms 
 combined with hemianopsia, and the situation of the lesion in 
 the visual tract can be ascertained if the differential indica- 
 tions already described are regarded. Tumors anywhere in 
 the visual tract, excepting in the cortex, cannot be reached. 
 
 1 Virchow's Arch., vol. lxxxvii , p. 335. 
 3 Med. News, April 16th, 1887. 
 
CHAPTER VI. 
 THE CORTICAL AREAS GOVERNING LANGUAGE. 
 
 The varieties of aphasia. — Mental images or concepts and. their physical 
 bases. — Apraxia ; Inability to recognize objects; Case with success- 
 ful operation. — The musical sense and its loss. — The seat of the lesion 
 in apraxia. — Word images and their physical basis. — Aphasia ; Ina- 
 bility to recognize or to use language. — Word deafness ; Word 
 blindness; Motor aphasia ; Agraphia. — Paraphasia. — The tests for 
 aphasia. — Illustrative Cases. 
 
 Before entering upon the study of aphasia, it may be of 
 service, in understanding affections of speech, to look at the 
 mental and physical mechanism which regulates the use of 
 language. 
 
 The accepted notion to-day is that every word in ordinary 
 use has a complex mental substratum, which may be termed 
 the word-image, made up of a number of memory-pictures. 
 The memory of the sound of a word as spoken, the memory 
 of the appearance of the word as printed, the memory of the 
 muscular movements needed to write the word or to pro- 
 nounce it, are known to be distinct from one another and yet 
 to be associated together. Loss of one of these memory- 
 pictures, or disturbance in their association, impairs the integ- 
 rity of the word-image, and produces such defects in its use 
 as are indicated by the names given to the respective varie- 
 ties of aphasia. For the division of disturbances of speech 
 into the two great classes of sensory and motor aphasia — the 
 first due to defect in the receptive and the second due to im- 
 pairment of the emissive functions of the brain — has been fol- 
 lowed by a further subdivision into several varieties. These 
 ^re word-deafness, word-blindness, agraphia, motor aphasia, 
 and paraphasia. But, before considering these defects, let us 
 look at the physical basis of the thought which lies back of 
 
58 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 the word. For the word is only a convenient means of ex- 
 pressing a thought, and thinking precedes language, as every 
 intelligent observer of animal life or of the education of a 
 child knows. 
 
 MENTAL IMAGES AND THEIR PHYSICAL BASIS. 
 
 Objects and actions are the chief subjects of thinking, 
 and their mental substratum is not difficult to discover. 
 
 Take an example. A steel 
 pen has a certain shape and 
 size and consistence which I 
 see and feel. The shape and 
 hardness perceived by eye 
 and finger are associated and 
 are remembered, and the 
 mental substratum or idea of 
 the pen consists of these two 
 memory-pictures joined to- 
 gether. Other pens have 
 forms of their own, and of 
 them, too, I have a series of 
 memory-pictures. But the 
 idea of the object is only 
 made complete when its use 
 is known. And so to the 
 memory-pictures of the pen 
 
 Fig. 20.— Diagram to illustrate the Concept IS added another of the act 
 " Bell," and to show the Varieties of Apraxia and „r ...„:4.;„„. :4-„„lf „ „„™„1 
 
 . , . „, , H . of writing; itself a complex 
 
 Aphasia. 1 he memory pictures are relics of past ° * 
 
 perceptions received through different senses, image, for that act has been 
 Their association makes up the mental image bell. j. i_ j j *.-■ J 1_ 1 
 
 -r. ,■ . , . . t watched and practised before 
 
 I he word image is made up of the memories of •»«•••»««»»« >».u ^.uv.i.^v.u ^>_i^iv. 
 
 the sound and appearance of the word, and o; the bein°" aCQuired and its recol- 
 
 uttering and writing-effort memories; these are , ^. . , ^. ... 
 
 joined together. The mental image and the word leCtlOll involves the recalling 
 
 image are also joined with one another, making f those memories of activ- 
 
 up the concept "bell." . r . . . T . , 
 
 ity of which I have been a 
 spectator or a participant. The mental image of the action 
 is associated with the various mental images of different 
 kinds of pens, so that it forms a common basis for the for- 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 59 
 
 mation of a general idea of a pen as an object used for writing. 
 And this idea, complex as it is, made up. of numerous mem- 
 ory-pictures, is acquired by the mind through observation long 
 before language is used. The baby may try to write before 
 it can say " pen," or before it can describe the act of writing. 
 The words, then, are added to the mental image to make it 
 communicable to others, but are not essential to the idea. 
 
 A bell has, as its mental basis, four distinct memory-pic- 
 tures; it has weight, form, a cold smooth surface, and sound; 
 in fact, every object, if thus analyzed, will be found to vary 
 from every other in respect of the memory-pictures which 
 form its mental substratum. The figure shows the various 
 kinds of memory-pictures and word-images making up the 
 concept " bell." What is true of these single words will be 
 found to be true of every other, if the trouble be taken to 
 analyze one's subjective knowledge of them — an analysis full 
 of interest. 
 
 APRAXIA. 
 
 It is a fundamental position involved in the accepted 
 theory of cerebral localization that memories are the residua 
 of perceptions and are therefore localizable in the regions of 
 the brain concerned in perception. It follows that these 
 memories forming the idea of an object or an action, being 
 distinct from one another, may be lost by disease of the brain 
 having a limited extent, and that the character of the memories 
 lost will depend on the location of the disease. Now, cases 
 have been recorded in which persons acted as if they no longer 
 possessed such object-memories, for they failed to recognize 
 things formerly familiar. A fork, a cane, a pen may be taken up 
 and looked at by such a person, and yet held or used in a 
 manner which clearly shows that it awakens no idea of its use. 
 And this symptom, for which at first the term blindness of 
 mind was used, is found to extend to other senses than that of 
 sight. Thus the tick of the watch, the sound of a bell, a 
 melody of music, may fail to arouse the idea which it formerly 
 awakened, and the patient then has deafness of mind; or an 
 
60 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 odor or taste no longer calls up the notion of the thing smelt 
 or tasted; and thus it is found that each or all of the sensory 
 organs, when called into play, may fail to arouse an intelli- 
 gent perception of the object exciting them. For this gen 
 eral symptom of inability to recognize the use or import of 
 an object the term apraxia is now employed. And since 
 apraxia is a symptom which is very frequently associated with 
 aphasia and which, in fact, may lie at the basis of aphasia, it 
 should always be looked for in a patient. To test for apraxia 
 it is only necessary to present various objects to a person in 
 various ways and notice whether he gives evidence of recogni- 
 tion. Have him watched by his friends, and they will be able 
 to tell whether he still chooses his articles of food at the table 
 intelligently; whether he still knows how to put on his clothes, 
 to use various toilet articles; to sew or knit or embroider if 
 the patient is a lady; to admire pictures, or flowers, or per- 
 fumes, as before the illness began. The patient may or may 
 not be able to name these objects; that, at present, is not the 
 question. But is it evident that the object awakens an idea 
 in the mind ? 
 
 The variety of apraxia known as blindness of mind is the 
 one most commonly found, and it may not be uninteresting 
 to recount one case of it, especially as that case affords the 
 first example of its successful treatment by operation. 
 
 It is a case recorded by Macewen, 1 of Glasgow, and is as 
 follows : 
 
 A man who had received an injury a year previously to his 
 applying for treatment suffered from deep melancholy and 
 strong homicidal tendencies which were relieved by parox- 
 ysms of pain in the head. There were no motor phenomena, 
 but it was discovered that immediately after the accident, and 
 for two weeks subsequently, he had suffered from psychical 
 blindness. Physically he could see, but what he saw conveyed 
 no impression to his mind. An object presented itself before 
 him which he could not make out, but when this object 
 emitted sounds of the human voice he at once recognized it 
 to be a man. In attempting to read, he saw what he consid- 
 ' British Medical Journal, Aug. nth, 1888. 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 6 1 
 
 ered must be letters and words, but they were unknown sym- 
 bols to him ; they conveyed no impression of their meaning ; the 
 memory of their signs was gone ; the book was a sealed book to 
 him. These phenomena gave the key to the hidden lesion in 
 the brain. On operation the angular gyrus was exposed, and 
 it was found that a portion of the internal table of the skull 
 had been detached from the outer and had produced pressure 
 on the posterior portion of the supra-marginal convolution, 
 while a corner of it had penetrated and lay embedded in the an- 
 terior portion of the angular gyrus. Removal of the bone 
 resulted in complete recovery from the pain and mental 
 symptoms. 
 
 The variety of apraxia known as deafness of mind has 
 recently been studied by Oppenheim, 1 of Berlin. He noticed 
 that while some aphasics retain their musical faculties, others 
 may lose the power to follow melodies, to appreciate music, 
 or to hum or sing the tunes which they formerly knew. 
 Thus, he relates that a patient of Finkelnburg, a flutist, no- 
 ticed an impairment and finally a loss of power to follow 
 notes, to play or to write notes, at the same time that he lost 
 his speech. Ballet relates the case of a musician who sud- 
 denly lost his power to read music, and Kast one of a musi- 
 cian who suddenly became note-deaf; and Oppenheim gives 
 histories of eleven such patients seen by him. That this is 
 not a part of aphasia in any sense is proved by the fact that 
 in many patients no such loss of musical power accompanies 
 aphasia; and in many cases of aphasia, it is expressly stated 
 that the musical faculties were unimpaired. Granet tells of a 
 patient who could say only one word, " pardi," and yet who 
 could follow music, and not only sing the tune of the Marseil- 
 laise, but, while singing, pronounce several words, "patrie," 
 " enfant," etc., which he could not say voluntarily; and Proust 
 relates the case of a musician who could neither speak nor 
 write, yet who could write a musical melody which he heard 
 sung. 2 
 
 In view of these observations, it is worth while to test in- 
 telligent patients as to their musical faculties — their power to 
 
 1 Charite Annalen, xiii., 18S8. - L'Encephale, iSSS, No. 5. 
 
62 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 recognize tunes, hymns, melodies, their power to sing or hum 
 a tune, and to read or write music or play on various instru- 
 ments.* 
 
 Investigations of the power of a person to recognize and 
 name an object by touch or taste or smell would be interest- 
 ing, but have not often been undertaken. The loss of the 
 muscular sense and consequent inability to perform delicate 
 motions of the hands has rendered deaf and dumb persons 
 who use their peculiar language of motion incapable of con- 
 veying their ideas; and if cases of this kind were more closely 
 investigated, some light might be thrown on the exact location 
 of muscular sense. But all of us, by the feeling of many ob- 
 jects, can recognize them at once with our eyes closed, and 
 thus arouse the memory-pictures of an object through this 
 channel of sensation. Recently a case has been recorded by 
 Farjes, in France, of a gentleman afflicted with aphasia, who, 
 though unable to name an object when he saw it, could do so 
 when he felt it, thus proving that when one association is 
 broken another may persist and be put to use. And in this 
 connection mention may be made of cases, now several in 
 number, of persons who, though unable to read letters which 
 they saw, w 7 ere at once able to name these letters correctly 
 when they traced the shape of the letter with the finger, the 
 muscular sense thus acting for sight and arousing the idea, 
 and enabling the person to read, though he had true " blind- 
 ness of mind." ~ 
 
 All of these facts are of great interest, not only as throw- 
 ing light on mental processes of association, but as indicating 
 that those processes are carried on in definite areas of the 
 brain and in tracts which connect those areas, and can be ar- 
 rested by disease in these parts; for in some of these forms of 
 apraxia the situation of the lesion has been found. It is as 
 yet too soon to make definite statements regarding such le- 
 sions. It seems likely that they lie in that terra incognita, the 
 
 1 A patient of my own, suffering from pure motor aphasia and agraphia, but 
 without any paralysis, had lost her power of playing on the piano though she could 
 read and enjoy music. She could sew perfectly well. 
 
 2 See Bernard : " De l'Aphasie." 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 63 
 
 white matter beneath the cortex. And if the problem of the 
 differentiation of cortical from subcortical lesions is ever to 
 be worked out, it will only be after a number of cases, thor- 
 oughly examined as to all these processes, have been recorded, 
 with autopsies to supplement the clinical record. 
 
 One fact, however, of great interest, not previously men- 
 tioned to my knowledge, has been brought out by a study of 
 the cases of apraxia which T have been able to collect and 
 which are here tabulated, namely that the lesion has always 
 been found in the left hemisphere in right-handed and in 
 the right hemisphere in left-handed persons ; in other words, 
 in the same hemisphere lesion of which has produced aphasia. 
 It is true that apraxia, like aphasia, has been noticed in 
 cases of paretic dementia in which the disease is diffuse 
 and is situated on both sides. This fact would not, however, 
 imply that a unilateral lesion alone was insufficient to produce 
 the symptom, and the nine cases with autopsy here brought 
 together for the first time seem to establish the statement 
 made. 
 
 Apraxia has as many varieties as there are organs of sen- 
 sation. The variety which existed in the nine cases tabulated 
 was that of psychical blindness, and accompanied the form of 
 aphasia known as word-blindness. In all the cases the lesion 
 involved the cortex of the supra-marginal and angular gyri, or 
 the tracts posterior to these parts in the white matter beneath 
 them. It is probable, from the association of psychical deaf- 
 ness with word-deafness, that it is due to lesions in the upper 
 temporal convolution, but autopsies are wanting. It is notice- 
 able, however, that this symptom of apraxia is always associ- 
 ated with some form of aphasia. Hence all cases of aphasia 
 should be examined for apraxia. It is well known that lesions 
 in the right hemisphere in right-handed, and in the left hemi- 
 sphere in left-handed persons do not produce aphasia. In the 
 accounts of cases of such lesions, I have not been able to find 
 any account of the discovery of any form of apraxia. It 
 seems, therefore, that at present we must locate our memory- 
 pictures of objects on one side of the brain, and on the same 
 side which presides over speech. This appears to be very 
 
6 4 
 
 FAMILIAR FORMS OF NERVOUS DISEASE, 
 
 £• 
 ^ 
 
 ^ 
 
 - 
 
 
 I 
 
 
 
 . 34 
 
 J, 
 
 
 c 5 
 •-j= 
 
 df 
 
 ■- E 
 n « 
 §•" 
 
 
 — C - Jj S; E 
 j§ -°.2 ; - 
 
 1) 
 
 
 9 H 9 " 05 
 
 .£ • '-.= .= - * 
 
 u "2 « ■ 
 
 
 is < . - '£ jc c w 
 
 ? a. u; > ? 
 
 
 
 ■a Mho 
 
 ti ti u ti ti 
 
 ti« 
 
 c 
 
 p 5 e 
 
 e = c c c 
 
 C k 
 
 _o 
 
 " r'S 
 
 c = 3 c c 
 
 'S S 
 
 
 
 V u u u u 
 
 
 
 
 
 
 -' 
 
 
 "c "; *c 'c "c 
 ir.ir.u.v.w 
 
 t/)^ 
 
 
 •O T3 
 
 
 
 J< 
 
 U 0) 
 
 d 
 
 d 
 
 fl 
 
 u u 
 
 
 
 
 
 Q. 
 
 
 
 x*J! ShS"d -dM-d-d 
 
 be 
 
 
 EoE 
 
 - r c *o 
 
 •a 
 
 £ 
 
 
 sOC^CO 
 
 HO 
 
 ■s 
 
 >- <- 
 
 5 
 
 "3 
 
 
 
 '5 '5 
 
 H 
 
 H 
 
 
 ^- U. 
 
 
 
 -c 
 
 
 
 
 o c . 
 
 -d 
 
 •d 
 
 
 Z S-* 
 "It 
 
 * - s 
 
 o~ £• 
 c = * 
 
 3 
 
 -a u 
 
 f .j ^ j « 
 
 • 3 ur tr tr ^3 
 
 ■OTJ 
 
 1 I 
 
 '3 O O O 2 
 
 O O 
 O O 
 
 CO 
 
 jj 
 
 
 
 
 
 •a 
 
 
 
 
 
 
 
 
 
 * 
 
 -d 
 
 V 
 
 
 
 
 c 
 3 
 
 
 
 
 
 
 
 
 o 
 
 
 
 
 
 u 
 
 
 
 o rt 
 
 c 
 
 
 
 
 
 
 
 j s- 
 
 h)h 
 
 
 ►J 
 
 
 
 u 
 
 E 
 
 
 
 
 
 
 £ 
 
 
 
 
 
 V 
 
 
 o 
 
 
 
 
 
 15 
 
 
 o 
 
 •a 
 
 
 
 
 
 
 4) 
 
 
 
 
 
 irfo 
 
 
 
 
 
 
 J> « 
 
 : « 
 
 
 
 
 c 
 
 
 
 0. 
 
 : 1 
 
 
 J 
 
 ~-J 
 
 ►J J 
 
 oX> . 
 
 
 
 
 U c 
 i- a) 
 
 -6 T3 
 
 *0 *C "D *U *C 
 
 •d-d 
 
 
 4) V 
 
 u ai u 1; 
 
 OJ <L> 
 
 o u " 
 
 '3 '3 
 
 U L. 1- U U 
 
 '5'3 
 
 
 
 O, — 
 
 a a 0. a a 
 
 D.& 
 
 £ o.S. 
 
 S J 
 
 E £ E E E 
 
 E E 
 
 
 
 
 o 
 
 
 
 
 0- 
 
 
 
 
 
 
 
 1 
 
 
 
 
 j= 
 
 
 
 
 
 
 
 m N ->o ■ 
 
 O h 
 
 
 
 ~ co'Soo 
 
 ~ .CO 
 
 1^4-. 
 
 u 
 
 
 
 d=i 
 -5 
 
 CO 3 
 
 c 
 
 
 '"S 'C 
 
 00< 
 
 w 
 
 M * 
 
 d ~ '5 c» M 
 
 
 u 
 
 CO 
 O CO 
 
 CO *• 
 
 1 i si"° 
 
 2"" > 
 
 
 ■d 
 
 .no 5 
 J: «= .£>-•' • 
 
 
 
 
 g S 
 
 
 < x 
 
 u "^ c u u 
 
 3 u 
 
 
 C u 
 
 >- • 3 u u 
 
 U 'C 
 
 
 O < 
 
 izt.<i 
 
 Za 
 
 
 
 • • |J 
 
 c 
 
 o 
 
 < 
 
 3 "3 
 
 t: C C c J; 
 
 si 
 
 IJ 
 
 
 2: S3 
 
 U < -jr. ~ a 
 
 JS 
 
 "°N 
 
 " « 
 
 " 
 
 ■^ ■*• " 
 
 
 r~ 
 
 CO c 
 
 
 ^ 
 
 ft, 
 
 V 
 
 
 
 V 
 
 TS -° 
 
 
 c u 
 
 « B.C 
 
 
 eg" 
 
 H ^^ 
 
 
 •2| 
 
 u « * . 
 
 
 
 •c u^ 
 
 
 
 t> ti: u bi si be 
 
 
 c 
 
 3 C C C C C 
 
 
 
 c c c c c c 
 
 « 4; V V V V 
 
 
 
 
 
 hJ 
 
 000000 
 
 C/3 X trt t/; X t/3 
 
 
 
 :-d 
 
 
 
 . u 
 
 
 n 
 
 
 
 
 
 
 
 . . . c . . 
 
 
 
 
 •CO . 3T3"0 
 O C .3 C O 
 O O ■ OO 
 
 
 - 
 
 U >•- U 
 
 
 S 
 
 
 
 
 
 
 e- 
 
 :io 
 
 
 •0 
 
 
 
 c c . 
 
 
 
 Z 2-* 
 
 •O T3 i- T3 *D 13 
 
 
 V w 4J 
 
 O O -3 O O 
 
 2 
 CO gOOO 
 
 
 
 
 0*0 D. 
 
 
 C- c " 
 3 
 
 
 
 
 
 2 
 
 
 
 
 ? 
 
 •d 
 
 ■ jm" c c 
 
 
 
 
 
 . aii P " « 
 
 
 
 O 
 
 "^ U t. O DT3 
 
 : > , ~ t a. % 
 
 c 
 
 
 : Zo 1 " 
 
 IS 
 
 
 
 
 
 
 
 
 
 
 
 " « 
 
 § 
 
 
 
 j^j^^;^ 
 
 
 Ch 
 
 
 
 ux 
 
 
 
 4) 
 
 
 
 O OJ 
 
 
 
 
 000000 
 
 
 
 000000 
 
 
 u *C% 
 
 cooooo 
 
 
 $ o.Si. 
 
 
 
 
 
 
 
 Cu 
 
 
 
 
 ri 
 
 
 
 -i" 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 o-^s s; 
 
 
 
 ^^3=2: 
 
 
 u 
 
 fic£- S '"?d a 
 
 
 
 
 
 
 
 
 
 e r t/: 00 00 
 
 
 
 
 
 
 
 
 u 
 
 C tfiX'g M _T 
 
 
 « 
 
 \ a g c g "S 
 
 .i S J £ ^ £ 
 
 
 u 
 
 F.5 S ■« 
 
 
 J= 
 
 £ g-S i-d 
 
 
 
 
 
 3 
 
 5-33-03 
 
 
 < 
 
 £ « 1 :.- a 
 
 oa >-sE s ? u5 
 
 
 ■°N 
 
 MS 
 
 m ■*■ m>o 
 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 65 
 
 strange, since the bilateral connection of each sensory organ 
 with both hemispheres is proved. There appears to be no 
 reason why the appearance of things, their sounds, tastes, 
 odors, etc., should not be received and remembered in both 
 hemispheres instead of in one. But, as a fact, they are not. 
 And the fact remains as mysterious as the corresponding fact 
 regarding speech-memories. 
 
 APHASIA AND ITS VARIETIES. 
 
 Turning now from this investigation as to the condition of 
 the memory-pictures of objects in the brain which together 
 form the idea of a thing, let us look at the second set of 
 memory-pictures which make up the word-image. As already 
 stated, the word makes the idea available for thought and for 
 its communication. The word "pen" or "bell" brings to a 
 focus a number of various sensory images. But the word 
 itself, in its ordinary use among intelligent persons, involves 
 several of the senses. Words are heard, read, spoken, and 
 written ; and each of these processes goes on in its own brain- 
 area, in which area, therefore, distinct residua of the process 
 or memory-pictures of the word lie. Hence each word is 
 composed, as far as its own image goes, of four separate mem- 
 ories, each of which may be lost separately. 
 
 1. If the memory of the sound of the word is lost, the 
 word cannot be called to mind and cannot be recognized 
 when heard. Show the patient a watch and he is unable to 
 name it ; tell him it is a stone, a match, a watch, and notice 
 whether he dissents from the former and gives signs of satis- 
 faction at the last. If he does, he has only auditory amnesia 
 but not word-deafness. If not, he is word-deaf, and is unable 
 to understand what is said to him. The lesion lies in the pos- 
 terior half of the first and second temporal convolution in the 
 left hemisphere in right-handed ; in the right, in left-handed 
 persons 1 (Fig. 21). This is one variety of aphasia whose le- 
 sion is well known, though it rarely occurs alone. 
 
 1 I have collected 50 cases of pure sensory aphasia with autopsies on which this 
 statement is based. Brain, partxlv., July, 1SS9. 
 
 5 
 
66 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 2. If the memory of the appearance of the word is lost, 
 the visual image of it cannot be called to mind or recognized, 
 and then the patient will be unable to write spontaneously, 
 for he cannot remember how the letter looks which he wishes 
 
 Eichhorst. ^V ^ Hitzig. 
 
 Fig. 21. — The Situation of Lesions causing Word Deafness only. 
 
 to write; and he will be unable to read because the shapes of 
 the letters and words seen arouse no recollection. As a mat- 
 ter of fact, words are forgotten more easily than letters, and 
 if a patient is to relearn to read he must begin with letters 
 and go on to words. Figures are sometimes recalled when 
 
THE CORTICAL AREAS GOVERNING LANG U AG I:. C,j 
 
 words are forgotten, and many a patient can do mathematical 
 calculations on paper who cannot read or write ordinary 
 words. I have seen a case in which the reverse was true: the 
 patient being able to read and write, but being unable to un- 
 derstand figures or calculate. Such patients may also play cards 
 
 Hun. \. ^"^ Macewen. 
 
 Fig. 22. — The Situation of Lesions causing Word Blindness only. 
 
 or other games if they are not psychically blind. It is not infre- 
 quently the case that persons who are thus word-blind can read 
 aloud, can write at dictation, or copy, and yet show no evidence 
 of understanding what has just been read or written. A dis- 
 tinction must be made between those who can and cannot do 
 
6S 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 these things, though its pathological basis is still obscure. 
 The condition of visual amnesia with word-blindness is due to 
 a lesion involving the inferior parietal convolutions and an- 
 gular gyrus, and is often associated with psychical blindness, 
 but may occur independently of it (Fig. 22). It was present 
 in all the cases of psychical blindness enumerated in Table I. 
 Word-deafness and word-blindness frequently occur together, 
 and then the lesion is found involving both the temporal and 
 the angular convolutions. About forty cases are now on record, 
 with autopsies, which prove this assertion. Two of the cases 
 
 here recorded illus- 
 trate this combina- 
 tion. 
 
 3. If the mem- 
 ory of the effort 
 needed to pro- 
 nounce a word is 
 lost, a true paraly- 
 sis of active speech 
 occurs, though the 
 muscles may not be 
 
 Fig. 23.— The Situation of Lesions causing Aphasia, i, Lesion WeaKenea. 1 IllS IS 
 of word deafness; 2, lesion of word blindness; 3, lesion of motor the Ordinary form 
 aphasia; 4, supposed lesion of agraphia. 
 
 of motor aphasia, 
 due to a lesion of Broca's centre (Fig. 23, 3). It is to be 
 noted that such a loss of speech involves a loss of the power 
 of repeating words after another, as well as of voluntary 
 speech, and is not accompanied by any inability to under- 
 stand spoken or written language. In the uneducated, as 
 in children, the acts of talking and writing are closely joined, 
 as may be seen by watching the lips, which move in the 
 act of writing. But among those accustomed to write much 
 these acts are independent, and it is probable that many edu- 
 cated aphasics may be able to answer questions in writing 
 when their efforts at speech fail. Reading aloud will also be 
 lost in motor aphasia, for here, too, the inability to articulate 
 hampers the patient. 
 
 4. The independence of the effort-memory necessary for 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 69 
 
 writing and connected with movements of the hand from the 
 effort-memories of speech has been alluded to. When these 
 are lost alone the condition is known as agraphia. In such a 
 state the pen cannot be used. Copying, writing at dictation, 
 and voluntary writing are all lost. It has been noted already 
 that when a word cannot be called to mind it of course cannot 
 be written. But words can often then be written at dictation, 
 if the person is one who writes much. Hence sensory agra- 
 phia and motor agraphia must be distinguished; the former 
 being a part of word-blindness, the latter not at all associ- 
 ated with inability to read. The lesion of motor agraphia is 
 unsettled, though a few facts point to the posterior part of 
 the second frontal convolution as the probable seat of this 
 function (Fig. 23, 4). It is not unlikely, however, that the 
 more exact localization of fine movements of the thumb and 
 fingers in the posterior central convolution by Horsley may 
 be followed by the discovery of the writing centre in this 
 vicinity. As it is still unsettled, it becomes incumbent to test 
 every patient as to his powers of writing voluntarily and at 
 dictation and of copying. 
 
 These forms of aphasia are due to a loss of distinct mem- 
 ory-pictures. These several memory-pictures which are united 
 in the word-image may thus be reasonably regarded as separate 
 from one another in their location in the brain. But since 
 they are joined together to form the word-image, it follows 
 that the association-fibres joining the various areas are as 
 necessary to the use of even a single word as the various areas 
 with their memories. It is really by association only that an 
 object or a word becomes a subject of thought or use. To a 
 man who understands English only, the word " cloche," as 
 seen or heard, conveys no idea. Form an association with 
 that word by telling him that it is the French for " bell," and 
 he at once possesses an idea. Or, to put it in another way. 
 cut off from the auditory word-memory " bell " all its connec- 
 tions with sight, sound, feeling, and effort-memories — isolate 
 it completely — and when the word bell is heard it no longer 
 means anything. Such complete severance of association- 
 fibres is the probable explanation of some cases of psychical 
 
JO FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 blindness and deafness, including word blindness and deafness. 
 And when the condition is complete it will, of course, be im- 
 possible to distinguish between a loss of the memory-picture 
 and an isolation of the memory-picture. The condition may, 
 however, be incomplete. A man suddenly unable to read at 
 sight is able to recognize letters by tracing them with his fore- 
 finger. What does this mean? It is evident that he has a 
 visual memory of the letter, for he can. under certain circum- 
 stances, arouse that memory and recognize the word. But he 
 cannot arouse it directly by sight. He has to do so indirectly 
 through muscular sense. Is it not evident that the association 
 of the visual memory-picture with the general visual area is 
 cut off, but its connection with the muscular sense area is 
 preserved; and so, byway of the latter, it can be reached? 
 The association with the word-hearing and word-writing mem- 
 ories in these cases is commonly preserved, for the man could 
 write at dictation or write spontaneously, yet was unable to 
 read what he had just written. All the associations with that 
 visual memory, then, were intact but one, and that one the one 
 commonly used in reading, namely, from the common sight 
 centre in the occipital lobe to the angular gyrus. Thus ana- 
 lyzing the condition subjectively we reach the conclusion that 
 in such a case some defect in definite associations was pres- 
 ent. In four such cases now on record a deep-seated lesion 
 within the occipital lobe underneath the cortex has been found 
 after death,' lying in such a position as inevitably to affect 
 seriously the association-fibres passing to the angular gyrus. 
 
 Again, it has been noted that the power to recall the name 
 of objects was often lost when the patient was able to recog- 
 nize that name when heard. It is in a serious and permanent 
 degree the same trouble which we are all liable to when we 
 fail to recall the name of a man whom we know. In such a 
 condition of auditory amnesia the memory or mental echo of 
 the word is not lost, because when the word is heard it is rec- 
 ognized. The memory-picture remains, but is inaccessible by 
 the ordinary way. The sight of the object does not call it 
 1 Wilbrand: " Seelenblindheit," p.180; Claus: Irrenfreund, 1883, p. 82; Dejerine: 
 Progres Medical, July 31st, 1SS3 ; Broadbent : Med. Chir. Trans., 1872, p. 162. 
 
THE CORTICAL AREAS GOVERNING LANGUAGE, yi 
 
 up. But, in such a case, if the object be handled or smelt or 
 tasted — or heard, if that is possible — the name may come to 
 mind. Thus the voice of the man may cause us to recall his 
 name when his face has not done so. In other words, if one 
 association-tract is impervious others may be open, and be- 
 fore it can be stated that the memory-picture is lost all the 
 ways to it must be tried. The theory that auditory amnesia 
 is due to lesion in the association-tracts from the occipital to 
 the temporal convolutions, in distinction from word-deafness 
 due to lesion in those convolutions, has a pathological basis. 
 There are eight cases on record with autopsies in which this 
 effect has resulted from a 'lesion of the occipital-temporal as- 
 sociation-tract. 1 In collecting facts we are met with the diffi- 
 culty that previous examinations of cases have been incom- 
 plete even when autopsies have been secured, hence the im- 
 portance of more careful examination of patients with aphasia. 
 5. There is one form of aphasia in which the lesion is 
 known to affect a great association-tract, viz., paraphasia, or 
 the aphasia of conduction of Wernicke. In this condition the 
 word-hearing and word-uttering process is perfect, but their 
 connection is broken. The patients can understand what is 
 said to them and can pronounce many words well. But they 
 misplace words, use one word for another, e.g., call, as one of 
 my patients did, the card four of spades the " five of tele- 
 phone." Such patients may even talk jargon. In such a 
 case it is impossible for the person to repeat a word after an- 
 other, yet he may be able to speak the word, like the patient 
 who, after trying in vain to say no at the request of the phy- 
 sician, finally gave it up and, shaking his head sadly, said, 
 " No, no." The lesion in these cases usually involves the 
 island of Reil and severs the fibres beneath it which join the 
 temporal and frontal lobes with one another. 2 This power 
 of repetition should, therefore, be tested invariably. A some- 
 what similar condition of defective writing and copying, in 
 
 1 See Brain, partxlv., 1. c. 
 
 2 Cases of Wernicke, Aphas. Sympt. Compt. 1874; Dejerine : Revue de Med., 
 1885, p. 174 ; Starr : Amer. Jour, of the Med. Sci., 18S4, Case 99. 
 
7- 
 
 1 AMI LIAR FORMS OF XERVOUS DISEASE. 
 
 which words are misspelled or are unintelligible, has been rec- 
 ognized clinically, but its lesion is not yet known. 
 
 It is, therefore, evident that the processes of association 
 should be most carefully tested. Such acts as reading aloud, 
 writing at dictation, or copying, ma)- be mentioned as involv- 
 ing the function of a few of the association-tracts, and these 
 should be investigated, as well as those already named. 
 
 In many cases of aphasia the symptoms are not such as 
 to point to one of these pure forms of aphasia; a combina- 
 tion of the characteristics of these forms will be found. The 
 patient then has a mixed form of aphasia in which both sen- 
 sory and motor elements are combined. But in such cases a 
 thorough examination will demonstrate that one or the other 
 pure form is present in excess, and this will indicate in which 
 direction the lesion lies. The fact that all the various speech 
 areas are supplied with blood by the middle cerebral artery, 
 and the frequency with which an embolus lodges in this artery 
 instead of plugging a small branch of it, explains the frequency 
 of mixed aphasia and the rarity of pure forms — which are due 
 to small areas of softening. 
 
 To examine an aphasic thoroughly it is necessary to test — 
 
 i. The power to recognize objects seen, heard, felt, tasted, 
 or smelt, and their use. 
 
 This will determine whether the condition of apraxia is 
 present. 
 
 2. The power to recall the spoken name of objects seen, 
 heard, handled, tasted, or smelt. 
 
 3. The power to understand speech and musical tunes. 
 
 4. The power to call to mind objects named. 
 
 This will test the integrity of the auditory speech area and 
 of the association-tracts between other sensory areas and the 
 temporal convolutions. 
 
 5. The power to understand printed or written words. 
 
 6. The power to read aloud and to understand what is read. 
 
 7. The power to recall objects whose names are seen. 
 
 8. The power to write spontaneously, and to write the 
 names of objects seen, heard, etc. 
 
 9. The power to copy and to write at dictation. 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 73 
 
 10. The power to read understandingly what has been 
 written. 
 
 These tests will determine the condition of the visual word- 
 memories in the angular gyrus, and of the connections be- 
 tween this area and surrounding sensory and motor areas. 
 
 11. The power to speak voluntarily, and if it is lost, the 
 character of its defects. 
 
 12. The power of repeating words after another. 
 
 This will test the integrity of Broca's centre and its associa- 
 tion-tracts. 
 
 The practical application of the localization of lesions in 
 aphasia hardly requires more than a mention. It is obvious. 
 
 The regions of the brain concerned in speech are especially 
 accessible to the surgeon, and experience has shown that sub- 
 cortical tumors and abscesses are as open to operation as cor- 
 tical lesions. 1 It is evident that in cases of sensory aphasia 
 the trephine should be applied, not over Broca's centre in the 
 frontal region, but over the temporo-parietal region ; in word- 
 deafness over the posterior temporal region ; in word-blind- 
 ness over the angular gyrus ; in both combined over the infe- 
 rior parietal region, especially if verbal amnesia is present. 
 
 When aphasia is purely motor, the understanding of lan- 
 guage being preserved but the power of talking being lost, the 
 lesion is in Broca's centre and the trephine should be applied 
 over the posterior part of the third frontal convolution, as in 
 Case VI., already described. 
 
 The lesion of agraphia is not yet so absolutely determined 
 as to warrant its surgical treatment when it is the only symp- 
 tom present. 
 
 The following cases illustrate some of the varieties of 
 aphasia here described, and present interesting features: 
 
 CASE X. — WORD-DEAFNESS AND WORD-BLINDNESS. 
 
 S. B., aged sixty-five, right-handed, was suddenly seized 
 with aphasia during the night of April 20th, 1888. His wife on 
 
 1 See cases of Seguin and Weir: Amer. Jour. Med. Sci., iSSS ; Ferrier and 
 Horsley : Brit. Med. Jour., 1888, i., p. 530 ; Roswell Park : Trans. Cong. Amer. 
 Phys. and Surg., 188S. 
 
74 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 waking found him on the floor, acting strangely, saying, 
 
 " What is the matter with me?" and in distress, but conscious 
 and not paralyzed. For the next three days his wife thought 
 that he was out of his head, for he paid no attention to what 
 she said, and could only say one word — "hook." Then the 
 use of words began to return, and he talked better and better. 
 He complained of numbness in the right side, and said that he 
 could not understand her. He seemed himself, but she was 
 unable to get him to answer questions, as he could not com- 
 prehend what she said to him. His general health has been 
 about as usual, but he has kept quiet, as going about among 
 people bewilders him. He is always worse in the morning on 
 rising. 
 
 Examination on May 14th failed to reveal any sensory or 
 motor disturbance, excepting a slight deviation of the tongue 
 to the right. Reflexes equal on both sides; pupils equal and 
 react normally. The existence of hemianopsia could not be 
 determined, as he could not be made to understand what was 
 sought, and experiments were ambiguous in results, as he was 
 very watchful of all tests. Hearing good; central vision good. 
 Loud aortic direct murmur, with hypertrophy and dilatation 
 of the heart, which was rapid and irregular. The aphasia 
 was tested carefully. As far as the power of articulation and 
 of the spontaneous use of words was concerned he had no 
 loss. He talked freely and rapidly when he could be made 
 to talk at all, and often made remarks of his own accord ; e.g.,. 
 while I was testing his sensation to cotton, he said, " I feel 
 you touch me, if that is what you want to know." As far as 
 the power of writing spontaneously or handling the pen was 
 concerned there was little loss, for he wrote his name clearly. 
 He therefore did not present the symptoms of motor 
 aphasia nor of agraphia. 
 
 His power of understanding spoken or written language 
 was, however, almost entirely abolished. He had a bewildered 
 look, and turned to his wife constantly for aid when spoken 
 to, though he did not seem to understand her any better than 
 me. To all such commands as " Shut your eyes," " Show 
 your tongue," " Stand up," " Sit down," " Put on your glasses,"' 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 75 
 
 he remained wholly indifferent, listening attentively, but not 
 obeying until the idea was conveyed by gestures, when he at 
 once understood and acted accordingly. To ordinary ques- 
 tions he gives no appropriate answer; sometimes, however, 
 when he sees that a reply is awaited, he says, " I don't under- 
 stand you ; " "I would answer you if I knew what you wished 
 to know." The only method of arousing any comprehension 
 is to repeat a single word over and over, when he sometimes 
 understands. Thus when the word " name " is repeated he at 
 last seems to get the idea, and says, "Oh, my name; yes, my 
 name is S. B." To several subsequent questions he gives 
 the same reply, and seems puzzled that I should ask, as he 
 supposes, the same question again. The word " age " re- 
 peated, elicits the answer, " Sixty-five, sixty-seven," and he 
 appears uncertain as to the exact number. When asked his 
 address he does not reply, but when it is repeated gives his 
 name again, then his age, and only when the words " Long 
 Island " are repeated several times does he get the idea. Then 
 he gives his full address at once correctly. There is, there- 
 fore, almost total word-deafness. His auditory memory of 
 the names of objects is also impaired, for when various ob- 
 jects were shown him he failed to name any of them, though 
 after several attempts he occasionally succeeded. He ap- 
 peared much perplexed at his failure to name objects, and so 
 much distressed that tests were not pursued. The power to 
 recall names, as well as the power to recognize words, was 
 therefore much impaired. Since it was impossible to obtain 
 replies to spoken questions, written questions were put to 
 him. And this elicited a remarkable symptom. He read to 
 himself or aloud all that was written, easily and rapidly, but 
 failed utterly to understand what he read. To very few of 
 the written questions did he show any evidence of intention 
 to reply. In one or two, a single prominent word read several 
 times aloud awakened an idea; thus, " When did this begin ? " 
 was answered by, " I don't know whether I can tell you ; it 
 • was the twentieth of April, I think." " Where do you live ? " 
 he read three times aloud, and then answered by giving his 
 name. Other questions were equally lost to his understand- 
 
j6 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 ing. It was evident that word-blindness as well as word-deaf- 
 ness was present, and in about an equal degree. This condi- 
 tion of word-blindness appeared to prevent his writing freely. 
 The only thing he could be got to write was his name; and 
 this he wrote again and again when attempts were made to 
 make him write at dictation or copy. In fact, he could do 
 neither of the last two even when the idea was conveyed to 
 him by gestures. He succeeded a week later in copying a few 
 figures, but was unable to add them up, though formerly a 
 good accountant. The word-blindness was therefore associ- 
 ated with visual amnesia. 
 
 The condition was therefore one of pure sensory aphasia, 
 word-deafness and word-blindness being combined, but no 
 disturbance of utterance, no misplacing of words, no hesitancy 
 in reading aloud being present. 
 
 The diagnosis of embolism of the terminal branches of the 
 left Sylvian artery, producing anaemia and loss of function in 
 the first temporal and angular convolutions and the interven- 
 ing cortex, seemed justifiable in view of the existence of a 
 cardiac obstruction at the aortic valve, and in view of the post- 
 mortem findings in similar cases in the brain (Fig. 23, 1, 2). 
 
 During the following months he improved slowly but 
 steadily, the irregular cardiac action being corrected by the use 
 of digitalis. He soon recovered the power to name objects 
 and to write after a copy, but was still unable, in July, to 
 write at dictation or to add and divide. His wife thought that 
 he understood many things he heard, but she admitted that 
 he did not comprehend what he read, for he had given up 
 reading his Bible on this account. It was evident that he 
 understood much that was said to him. Thus it became pos- 
 sible to test his visual field, which was found to be intact on 
 all sides though slightly contracted in the right eye. Ophthal- 
 moscopical appearances were normal from the first. 
 
 In October he was very much better. He now understood 
 what was said to him, if it was said slowly, but it was difficult 
 for him to follow conversation, as the change from one topic 
 to another confused him. He would go on talking on a pre- 
 vious subject even when questions on a new one were asked, 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 77 
 
 and his wife says that she has to indicate to him that the sub- 
 ject is changed by clapping her hands. He is able to name 
 objects quickly and correctly and speech is as fluent as ever. 
 He reads without hesitation aloud and says that he understands. 
 His wife says that he now reads the papers and tells her the 
 news. So she is sure that he does understand what he reads 
 if he reads very slowly. Rapid reading, like rapid speaking, 
 he is still unable to follow, and for this reason he cannot yet 
 go to church. 
 
 His writing is still, at the end of two years, imperfect. He 
 figures and calculates perfectly, but makes mistakes in writing 
 at dictation and in copying. During an attempt to write he 
 stopped and said, " I can't think how that letter looks." It 
 was a capital H which he wanted; and a little later in the 
 test, when a word beginning with it was given him to copy, 
 he failed to make it properly, writing Nurrison for Harrison. 
 And it is this lack of memory of the appearance of words 
 which prevents his writing with any freedom. There is there- 
 fore still a moderate degree of sensory aphasia, the word-blind- 
 ness being now more prominent than the word-deafness. 
 
 CASE XI. — WORD-DEAFNESS AND WORD-BLINDNESS; TEMPO- 
 RARY APRAXIA. 
 
 T. D. C, aged forty-two, right-handed, suddenly became 
 unconscious on March nth, 1888, and on coming to him- 
 self a few minutes later felt bewildered, did not recognize his 
 surroundings or his wife or father, and could not talk intelli- 
 gibly or understand what was said to him. He therefore pre- 
 sented symptoms of aphasia with psychical blindness. His 
 alarm led him to desire to see his physician, Dr. Walker, to 
 whom he at once wrote the following note, which he appar- 
 ently read over after it was written, and sent off with the idea 
 that it was a request for an immediate call. The note is writ- 
 ten in his natural handwriting and reads : " Please person me 
 personally per me Dr. personally me personally me. My love. 
 T. D. C." Dr. Walker saw him on the following day and 
 found a condition of almost total aphasia. He tried 'to talk, 
 but could not be understood, the words used being discon 
 
;S FAMILIAR FORMS OF NERVOUS DISEASE, 
 
 nected. He said, " Crazy, I am era/.}! " and he was unable to 
 reply to questions, as he could not understand anything said 
 to him; He was slightly-paralyzed on the right side of the 
 faee, not elsewhere, and he had pain over the left eye and in 
 the forehead and head on the left side. For a week this con- 
 dition remained and then he began to improve rapidly, recog- 
 nized his family and friends, regained the use of words, and 
 on March 24th wrote a letter of some length quite correctly 
 to Dr. Walker. I saw him March 25th. He then talked freely 
 and rapidly, so that no one would have noticed any difficulty 
 of speech, articulation being distinct and words used correctly. 
 He was able to write spontaneously freely, but has difficulty 
 in writing at dictation and in copying. The words dictated 
 had to be repeated if more than three words were given, and 
 in copying he scanned closely each letter and word. But 
 writing thus slowly he made no mistake. There was, there- 
 fore, no motor aphasia or agraphia. 
 
 There was, however, marked impairment in his power of 
 understanding what he heard or read. My questions were 
 only understood when spoken very slowly and repeated, and 
 any sudden change of subject caused evident bewilderment. 
 His wife had found it very difficult to make him understand, 
 and as she spoke to him in French it was evident that this, as 
 well as his English memory of words, was impaired. He had 
 been to the theatre and occupied a front seat the day before 
 I saw him, but had been unable to understand the words of 
 the play, so that, as he said, " The actors might as well have 
 spoken in Greek." Unfamiliar words were not as readily un- 
 derstood as common ones, an.d the bewilderment increased as 
 he was examined ; so that at the end of half an hour he did 
 not understand as quickly as at first. He was able to repeat 
 single words after me, but if more than two or three were 
 given him at a time he failed, and in a long phrase only occa- 
 sional words were remembered. His recollection of familiar 
 sentences — e.g., " Peter piper " — was, however, good. The same 
 trouble was noticed in writing at dictation as in repetition. 
 He recalled the name of various objects shown to him readily. 
 He therefore had partial word-deafness. 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. j<j 
 
 When asked to read he did so to himself and aloud accu- 
 rately. But he only understood short sentences, and if long 
 ones were read through they conveyed no idea to him. He 
 was spending most of the time in reading, but confessed that 
 he only got an indefinite idea of what he read. The single 
 words, if dwelt upon long enough, were understood, but when 
 combined into sentences were not fully comprehended. He 
 remembered having read the note to Dr. Walker, and supposed 
 it was written correctly. When given paragraphs of a news- 
 paper to read he was never able to tell subsequently the con- 
 tents of the paragraph when he had read it rapidly. In writ- 
 ing from a copy he could only recollect the appearance of a 
 word or two of the copy and had to consult it frequently. There 
 was therefore partial word-blindness. 
 
 Hearing and sight were perfect, the visual field being 
 equally extensive in both eyes and normal. No trace of the 
 psychical blindness remained. He had a systolic murmur, 
 heard at the apex and conveyed to the back. The lesion in 
 this case was probably like that in Case X. He did not re- 
 cover from his sensory aphasia, but went abroad, and died in 
 Paris of acute encephalitis about the middle of April. 
 
 In both of these cases the power to speak, the power to 
 write spontaneously, the power to read aloud were preserved ; 
 the power to understand spoken or printed language was lost, 
 and the power to repeat sentences, to write at dictation, or 
 to copy was impaired. In both, the power to recall the names 
 of objects seen was much better than the power of recogniz- 
 ing those names when heard. In both, the things which were 
 read aloud correctly were nevertheless not comprehended. 
 In both, the condition present was pure sensory aphasia with- 
 out any affection of articulation, or of the use of the pen; and 
 in both a very marked degree of recovery had followed the 
 attack. In both, the word-deafness and word-blindness were 
 about equally marked. In neither was motion, sensation, 
 sight, or hearing markedly impaired. 
 
8o FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 CASK XII. — PARAPHASIA PROGRESSING TO TOTAL APHASIA. 
 
 H. A. T., aged fifty-four, right-handed, after a severe 
 mental strain gradually developed a difficulty of speech dur- 
 ing a period of three weeks preceding the time when I saw 
 him, in consultation with Dr. O'Dwyer, on January 9th, 1885. 
 He first misplaced words, using one word when he meant to 
 use another, both in speech and in writing, and this increased 
 until his speech became almost unintelligible. At the same 
 time mental failure was thought to be present, as he seemed 
 less able to understand what was said to him than formerly, 
 and had forgotten many words and names. On examination 
 it was found that he understood fairly well all words and short 
 sentences, but failed to follow long sentences or complex 
 orders. When told to walk, to stand still, etc., he did so; but 
 when told to pick up a pack of cards and put them on another 
 table, he did not catch the idea until it was repeated slowly. 
 His power to recall the names of objects was very much im- 
 paired, but he dissented from wrong names and recognized 
 the right names when told. He often recognized the fact that 
 he had not said the word which he meant to say, but he did 
 not succeed in this always ; so that he often became indignant 
 with his wife because she failed to understand him. He could 
 not recall the names of presidential candidates, of the day of 
 the week or month ; and even when told he forgot them at 
 once. There was, therefore, considerable auditory amnesia 
 and word-deafness. There was also some word-blindness. He 
 read single words, but sentences seemed to convey no idea. 
 When he attempted to read aloud he uttered jargon. When 
 he attempted to write, either voluntarily or at dictation, or 
 after a copy, he only succeeded in making a series of badly- 
 formed letters, few words being properly spelled and the re- 
 sult being illegible. Though an expert accountant, he failed 
 to add or to subtract correctly, putting down and saying out 
 loud the wrong figures every time. There was evidently a 
 considerable degree of word-blindness. That his mental powers 
 were not impaired was evident from the fact that he would 
 not allow me to take the paper on which these attempts at 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 8 1 
 
 writing had been made until I tore off and gave to him the part 
 containing his name. 
 
 His power of articulation was good, words being well pro- 
 nounced and his speech rapid and fluent. Like the power of 
 handling the pen, the power of forming words was unimpaired. 
 There was no motor aphasia and no motor agraphia. 
 
 But the chief defect consisted in a substitution of some 
 word for the one which he wished to use. Thus when asked to 
 name the card of a pack with which he had been playing, he 
 called the four of spades " five of telephone ; " " trying to do " 
 he pronounced " trayling to dool." His alphabet was said 
 as follows : " a, m, vv, x, w, m, x, y, w," the constant recur- 
 rence to " m " and " w " being noticed ; he also substituted m 
 for four in counting from one to ten. The days of the week 
 were not said correctly, Friday coming next to Tuesday, but 
 this he noticed and corrected after saying them all over from 
 the first. He made mistakes in repeating words after me, as 
 well as in talking and in reading aloud. This difficulty of 
 speech became worse when he was excited, and then not a sin- 
 gle sentence of a long harangue could be comprehended. This 
 was especially unfortunate, as he was anxious to give directions 
 regarding financial affairs and about his will; and though he 
 knew what he wished, it was impossible for others to learn his 
 desires, either by his speech or in writing. 
 
 Vision and hearing good; slight paresis of right side of face 
 and tongue, none elsewhere; no anaesthesia; optic discs nor- 
 mal; no cardiac disease. Syphilis was suspected, but no history 
 was obtainable, and specific treatment, on which he was placed, 
 failed to modify the course of the disease, which progressed 
 to total aphasia and right hemiplegia, and he died comatose 
 on February 9th, 1885. No autopsy was obtained. 
 
 In this case a partial degree of word-deafness and word- 
 blindness was accompanied by a very marked condition of 
 paraphasia with paragraphia. 
 
 CASE XIII. — PARAPHASIA AND PARAGRAPHIA. 
 
 W. E. V., aged forty-five, right-handed, became uncon- 
 scious suddenly in March, 1884, an d on recovering conscious- 
 6 
 
82 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 ness was unable to talk, had much tingling and numbness in 
 his entire right side, but no paralysis. For a month he could 
 only say, " How man)-," but then the use of words returned, 
 and improvement has been stead}- until February, 1885, when 
 I saw him. He is an intelligent physician and interested in 
 his own case. He understands perfectly whatever he hears 
 or reads, and has no evidence of psychical blindness or deaf- 
 ness, though for a few weeks after the attack he could not play 
 cards or enjoy music as he had formerly done. His pronun- 
 ciation and his power of using the pen are perfect, and his only 
 complaint is that both in speaking and in writing he uses wrong 
 words. In talking he chooses his words carefully and speaks 
 slowly, but makes occasional mistakes — e.g., "when" for "well," 
 " lant " for "lance," "misplate" for "misspell." He says his 
 alphabet and counts perfectly. He says that when unable 
 to say the word he is thinking of, if he calls up to his mind 
 the appearance of the word as written he can usually pro- 
 nounce it correctly; and it is found that he makes fewer mis- 
 takes in reading aloud than he does in talking. In writing he 
 often misspells words, e.g., " unforable " for "unfavorable," 
 " sencotts " for " senate," but he copies freely, remembering 
 several words easily, and he writes well at dictation. He says 
 that he has sometimes written the name of one drug in a pre- 
 scription for another, and that he is also apt to write the quan- 
 tities wrong, so that he never fails to read his prescriptions 
 several times. He finds much difficulty in keeping accounts, 
 addition and subtraction being very much impaired, and the 
 results being very apt to be wrong. The condition is there- 
 fore one of paraphasia with paragraphia. He has cardiac 
 disease, which makes it probable that the lesion is embolic in 
 origin. Vision and hearing unimpaired. Six months subse- 
 quently a slight improvement had taken place, but he never 
 recovered entirely, and died of cerebral embolism three years 
 later. 
 
 Such an uncomplicated condition of paraphasia is rare, 
 and it is especially interesting to notice that conduction of 
 impulses from the word-hearing centre to the word-uttering 
 centre was more interfered with than from the word-seeing 
 
THE CORTICAL AREAS GOVERNING LANGUAGE. 83 
 
 centre to the word-uttering centre. He therefore got over the 
 obstacle by calling to mind the appearance of the word, and 
 then could say it when the recollection of its sound was insuffi- 
 cient to initiate the movement. The lesion therefore affected 
 the association-tract between the temporal and frontal lobes 
 more seriously than the one between the angular gyrus and 
 the frontal lobe. 
 
 For a good illustration of the symptoms in pure motor 
 aphasia, the reader is referred to Case VI., already described, 
 in which the condition was relieved by a surgical operation. 
 
CHAPTER VII. 
 
 THE CORTICAL REGIONS WHOSE FUNCTION IS 
 UNDETERMINED. 
 
 The frontal convolutions ; mental defects. — The parietal convolutions. — 
 The temporo-sphenoidal convolutions. — The uncinate convolution 
 and the sense of smell. — The median cortex of the hemispheres. 
 
 THE REGIONS OF THE CORTEX WHOSE FUNCTION IS UNDE- 
 TERMINED. 
 
 If diagrams of the two hemispheres are prepared in which 
 the motor, visual, and speech areas are laid down (Fig. 24), 
 it will be seen that there remain extensive regions of the cor- 
 tex to which, as yet, no function can be ascribed. 
 
 There is (1) the frontal region, including all the cortex of 
 the frontal convolutions, except the posterior half of the third 
 frontal on the left side. 
 
 In lesions of this region mental symptoms are quite likely 
 to be prominent. These do not conform to any type of in- 
 sanity. They are rather to be ascribed to a loss of self-con- 
 trol and a decided change of character. The mind exercises 
 a constant inhibitory influence upon all action physical or 
 mental ; from the simple restraint upon the lower reflexes, such 
 as the knee-jerk and the action of the sphincters, to the higher 
 control over what may be termed psychical reflexes, such as 
 emotional impulses and their manifestation in expression, 
 speech, and conduct. This action of control implies the rec- 
 ognition of the import of an act in its relation to other acts, 
 and involves the highest mental powers, judgment and reason. 
 By inhibiting all but one set of mental acts, it enables one to 
 fix the.attention on a subject and to hold it there. 
 
 It is the possession of these mental powers which chiefly 
 
CORTICAL AREAS OF UNKNOWN FUNCTION. 
 
 85 
 
 distinguishes a normal man from an imbecile or an idiot. And 
 the brain of a normal man differs from that of the lower ani- 
 mals and from idiots chiefly in the greater and more perfect 
 development of the frontal lobes. It seems probable, there- 
 fore, that the frontal lobes have 
 some necessary relation to the 
 highest mental powers. In 
 about half of the cases on 
 record of destruction of the 
 frontal convolutions by disease, 
 the patients have manifested 
 mental symptoms, such as an 
 inability to fix the attention, to 
 follow a continuous train of 
 thought, or to conduct higher 
 intellectual processes; to exer- 
 cise the power of judgment and 
 reason and to maintain that self- 
 control which regulates con- 
 duct. Various forms and de- 
 grees of dementia have been 
 observed after such lesions. 1 
 And when such mental symp- 
 toms are present, the diagnosis 
 of lesion in the frontal lobes is 
 warranted when lesions else- 
 where can be excluded. Un- 
 fortunately such cases are not 
 
 yet Open tO Surgical treatment, F f ,G> ^.-TheUnknown Areas, r Lateral 
 
 J 1 ° surface of left hemisphere; 2, lateral surface 
 
 for any precise localization Of of right hemisphere; 3, median surface of 
 
 r , ■ .1 1 c 1 1 right hemisphere. T, Talking; W, writing; 
 
 iunctions in the large frontal 
 
 regions is impossible ; and in 
 
 the absence of symptoms of 
 
 aphasia or paralysis we have not even a clue as to which 
 
 hemisphere is diseased. 1 
 
 1 See " Cortical Lesions," Amer. Jour. Med. Sci., April, 1SS4, where 23 cases 
 are collected. Compare the remarks On Psychical Epileptic Equivalents in chap, 
 xvii. 
 
 M, motor; V, visual; R, reading; H, hearing; 
 .S", smelling areas. The functions of the un- 
 shaded areas are unknown. 
 
86 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 There is (2) the region of cortex lying between the poste- 
 rior central convolution and the occipital convolutions, and 
 including the parietal convolutions except the left inferior 
 parietal lobule. 
 
 It has already been stated, in discussing the motor area, 
 that lesions of the posterior central convolution are more likely 
 to produce disturbances of tactile and muscular sensations 
 than lesions in the anterior central convolution alone. In 
 1884 I attempted to show that in the parietal convolutions 
 were the centres of tactile sense, and Dana's collection of cases 
 gives some support to this theory. I am now inclined to be- 
 lieve that the sensory and motor areas coincide, including the 
 cortex of the posterior central convolution, and that lesions 
 of this convolution are found to be associated with anaesthesia 
 in the paralyzed part, rather because the motor and sensory 
 centres for the parts in which the appreciation of sensations is 
 most acute (viz., the thumb, fingers, and hand, the toes and 
 feet) lie in this region, than because this region contains tac- 
 tile centres only. 
 
 It is an open question whether the muscular sense percep- 
 tions occur in the motor centres, as I am inclined to believe. 
 A few cases on record would indicate their location in the 
 parietal region. But these cases are open to the same expla- 
 nation which has been offered for the anaesthesia observed 
 after lesion in the posterior central convolution. 
 
 It may therefore be stated that we do not know the func- 
 tions presided over by the superior and inferior parietal lobules, 
 except in so far as the latter on the left side is concerned in 
 the memory of the appearance of printed words. 
 
 There is (3) the region lying in the entire temporo-sphe- 
 noidal lobe on the right side, and in the temporo-sphenoidal 
 lobe on the left side, not concerned in speech. Abscesses in 
 this regi'on are very common after otitis media, and are often 
 successfully operated upon. But the diagnosis in such cases 
 has to be reached entirely by the existence of otitis, together 
 with the discovery of the general symptoms of brain disease 
 (see page 15); as no distinctively local symptoms are pro- 
 duced by lesions in this area. It is to this region that physi- 
 
CORTICAL AREAS OF UNKNOWN FUNCTION. 87 
 
 ologists assign the function of hearing. There are two cases 
 on record, in which bilateral destruction of the three temporal 
 convolutions has been followed by total deafness. But deaf- 
 ness of cerebral origin is an exceedingly rare symptom, and 
 there is not as yet a sufficient number of facts to warrant 
 any localization of the auditory sense, or to determine the 
 exact functions of the temporo-sphenoidal convolutions. 
 There are several cases on record of tumors in this area pro- 
 ducing convulsions preceded by an aura of sound. These, 
 however, do not prove this region to be auditory. The same 
 lack of knowledge regarding the regions of the cortex lying 
 on the base of the temporo-sphenoidal lobe must be admitted. 
 
 There is (4) the apex of the temporo-sphenoidal lobe, includ- 
 ing the uncinate convolution (Fig. 24, S). To this region the 
 olfactory tract has been traced, and in it physiologists located 
 the sense of smell. Three cases are recorded which favor this 
 localization, by Hamilton, 1 by Anderson, 2 and by Hughlings 
 Jackson. 3 In Hamilton's case there were symptoms of epi- 
 lepsy, and each fit was preceded by a sensory aura of a bad 
 smell. The lesion was a meningitis and sclerosis of this con- 
 volution. In the other cases there were epileptiform attacks 
 preceded by an aura of a bad smell, and this region was de- 
 stroyed by a tumor. In neither case had smell been tested. 
 The* theory that this area governs the sense of smell has 
 therefore some pathological facts in its favor, and though it is 
 hardly allowable to draw a definite conclusion from three 
 imperfectly observed cases in man, the conclusions of anatom- 
 ical, physiological, and pathological evidence, taken together, 
 make it probable that the sense of smell is perceived in the 
 uncinate convolution. 
 
 There is (5) the entire median surface of the hemispheres 
 with the exception of the paracentral lobule (motor) and the 
 cuneus (visual). With regard to the functions of this region 
 nothing is known (Fig. 24, 3). This includes the gyrus forni- 
 catus and the hippocampal cortex, no cases being on record 
 
 1 Allan McL. Hamilton : N. Y. Med. Jour., June, 1882. 
 
 2 J. Anderson: Brain, 1S86, p. 385. 
 
 3 Brain, part xlvii., 1889. 
 
88 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 to support the theory derived from physiological experiment 
 that the tactile sense is located in the hippocampus. 
 
 When, the extent of these regions is contrasted with the 
 extent of those regions whose functions are determined, it is 
 found that the}' include about two-thirds of the entire cortical 
 area. It becomes evident, therefore, that as yet but a third 
 of the cortex is open to surgical interference — since in this 
 extent only can an exact diagnosis of a lesion be made. 
 
 The functions of the brain, whose situation is still unde- 
 termined, are hearing and taste. 
 
CHAPTER VIII. 
 
 THE TRACTS WITHIN THE BRAIN AND THE 
 DIAGNOSIS OF SUB-CORTICAL LESIONS. 
 
 The projection tracts ; frontal; motor; tactile; visual; auditory. — The 
 commissural tracts. — Mirror writing. — The association tracts. 
 
 THE TRACTS WITHIN THE BRAIN. 
 
 The diagnosis of lesions involving the mass of white sub- 
 stance lying beneath the cortex of the brain and above the 
 level of the basal ganglia has been hitherto almost impossible. 
 Such authorities as Nothnagel, 1 Charcot, 2 and Striimpell 3 ad- 
 mit that few rules for guidance can be given, and at present 
 there are few definite symptoms assigned to diseases of the 
 centrum semi-ovale. 
 
 The subject of lesions of this part of the brain has an im- 
 mediate practical bearing. In the journals of the past few 
 years are recorded several cases of operations upon the brain 
 for the evacuation of cerebral abscesses, and the excision of 
 tumors, some of which were sub-cortical. This is, doubtless, 
 but a beginning of a brilliant advance in the department of 
 cerebral surgery. But unless the diagnosis of sub-cortical 
 disease can be made with some degree of accuracy, such opera- 
 tions cannot be safely undertaken. 
 
 The natural manner of approaching a subject of this nature 
 is to follow the inductive method, and, by a collection of cases 
 in which an autopsy has demonstrated the existence of a 
 lesion, to cbllate the common symptoms and thus arrive at 
 
 1 Nothnagel : " Topische Diagnostik der Gehirnkrankheiten," 1879. 
 
 2 Charcot : Revue de Medecine, 1883, " Localisations cerebrales." 
 
 3 Striimpell : " Lehrbuch der inneren Krankheiten," 1884. 
 
90 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 the diagnostic conclusions. But while this method does afford 
 i certain number of facts of importance, it is by no means as 
 satisfactory as in the case of cortical lesions, in the investiga- 
 tion of which it has given such brilliant results. For lesions 
 of the centrum ovale are not very common, and, therefore, 
 are not often suspected during life. An examination directed 
 toward the symptoms which such lesions might cause is there- 
 fore frequently omitted, and hence facts are wanting in the 
 recorded histories which would serve to establish a sympto- 
 matology of these diseases. There are many symptoms in 
 every case which must be sought for by the examiner, as the)' 
 are of a character to escape the notice of the patient. Dis- 
 turbances of the temperature sense, of vasomotor activity, of 
 the power of locating the position of the extremities, or of 
 the exact limitation of the visual field, are all instances in 
 point. It is evident, therefore, that some of the symptoms of 
 lesions in the centrum ovale may have escaped notice because 
 they were not properly investigated. And it follows that we 
 must ascertain the probable nature of those symptoms from 
 other data than those furnished by the recorded cases. 
 
 It seems to have been a constant fact in the history of 
 progress in clinical medicine that, just in proportion to our 
 knowledge of the anatomy and physiology of a part, does our 
 knowledge of the symptomatology of its diseases advance. To 
 bring symptoms into connection with lesions is the aim of 
 scientific investigation, and this has been done chiefly along 
 the lines of anatomy and physiology. 
 
 Hence, in investigating lesions of the centrum ovale, we 
 may turn from pathology to anatomy for the information 
 needed to establish the symptoms of such forms of disease. 
 
 The anatomy of the centrum ovale can be studied to the 
 best advantage upon torn brains which have been properly 
 hardened in alcohol. A dissection made in this manner with 
 care enables one to establish the fact that this part of the 
 brain is made up of fibres only, and to distinguish easily three 
 sets of fibres passing through it. These three sets have been 
 named the projection, commissural, and association systems of 
 fibres. 
 
THE TRACTS WITHIN THE BRAIN. 91 
 
 THE PROJECTION FIBRES. 
 
 The projection system includes those fibres which join a 
 definite area of the cortex with parts of the nervous system 
 lying below it. It therefore follows that but one termination 
 of a projection fibre is found in the cortex, and hence the 
 fibre, in passing through the centrum ovale, is either on its 
 way to, or on its way from, some nervous mechanism in the 
 basal ganglia, brain axis, or spinal cord. Indirectly, through 
 the medium of such mechanisms, the external world is pro- 
 jected upon the brain and reaches consciousness, and volun- 
 tary impulses originating in the brain are sent to the muscles. 
 , A dissection of the centrum ovale, prepared so as to show the 
 projection system, demonstrates the existence of fibres from 
 the entire cortex passing downward and gathering together 
 within the hemisphere at the upper level of the basal ganglia, 
 and either ending in the optic thalamus, or going on between 
 these ganglia to the brain axis and spinal cord. 
 
 The majority of these fibres end in the optic thalamus, 
 which is thus connected with all parts of the cortex of the 
 brain. They are not shown in Fig. 25. Of the function of 
 these we know very little. Two large bundles, however, are 
 separable from the mass. One of these passes inward and 
 forward from the occipital lobe, and joins the pulvinar of the 
 thalamus and the external geniculate body (Fig. 25, D). This 
 is now known as the visual tract, and conveys impulses re- 
 ceived by the optic thalamus from one-half of each retina to 
 the like-named occipital lobe, as has been already described 
 (page 51). A second bundle passes from the temporal lobe 
 upward to the thalamus, internal geniculate body, and poste- 
 rior corpus quadrigeminum, in which the auditory tract from 
 the acoustic nucleus ends (Fig. 25, E). This probably conveys 
 impulses of sound from both ears to each temporal lobe, as 
 the investigations of von Monakow T and Babinsky 2 by the 
 atrophy method, and of Spitzka 3 by the method of compara- 
 
 1 Arch. f. Psych., xii. 2 Virchow's Arch., cv., 28. 
 
 3N. Y. Med. Journal, Sept. i-Sth, 1S86. 
 
9 2 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tive anatomy have shown. These arc the only bundles of the 
 thalamic radiations whose function is determined. 
 
 Some of the projection fibres pass on through the internal 
 capsule without communicating with the basal ganglia, and of 
 these we know three distinct bundles. 
 
 The first is collected from the three convolutions of the 
 
 Fig. 25. — The Projection Fibres within the Brain. Lateral View of the Internal Capsule. A, 
 Tract from frontal convolutions to pons nuclei thence to cerebellum; /?, motor tract; C, sensory 
 tract for touch; Z>, visual tract; £, auditory tract; F, superior cerebellar peduncle; C, middle cere- 
 bellar peduncle; //, inferior cerebellar peduncle; _/, tract from auditory nucleus to corp. quad, inf., 
 A", motor decussation in medulla; A', red nucleus of tegmentum; O, olivary body; O T, optic thal- 
 amus: C A*, caudate nucleus; / V, fourth ventricle; numerals refer to cranial nerves. 
 
 frontal lobe, and passing between the caudate and lenticular 
 nuclei in the anterior division of the internal capsule, descends 
 in it to the base of the brain, and issuing in the inner third of 
 the foot of the crus cerebri, passes down to the pons, where 
 it terminates in nuclei lying in the ventral half (Fig. 25, A). 
 The nuclei thus reached by these fibres are also joined by 
 
THE TRACTS WITHIN THE BRAIN. 93 
 
 other fibres from both hemispheres of the cerebellum, which 
 enter the pons, at its lateral surfaces in the middle peduncles 
 (Fig. 25, G). Thus it is evident that a connection exists be- 
 tween each frontal lobe and both cerebellar hemispheres, the 
 crossed connection being greater than the direct one. In 
 Flechsig's case of deficient cerebellum, the pons nuclei and 
 the fibres to them from the frontal lobe were found.' In my 
 case of deficient cerebrum the pons nuclei and the fibres to 
 them from the cerebellum were found. 2 Therefore each half 
 of this tract, if it is a continuous tract, may develop independ- 
 ently of the other. 
 
 Of the function of this tract we know nothing, and of the 
 functions of the frontal lobes and cerebellar hemispheres we 
 know very little. Therefore we cannot as yet connect any 
 symptoms with its destruction. 
 
 The second bundle of the projection system is the motor 
 tract. It comes from the posterior part of the third frontal 
 convolution, the two central convolutions, and from the para- 
 central lobule, and passes out of the base through the middle 
 third of the crus cerebri. Its fibres collect at the middle por- 
 tion of the upper surface of the internal capsule, those from 
 the lower parts of the cortex passing straight inward, those 
 from the upper parts curving outward and downward to pass 
 around the side of the lateral ventricle. Thus within the cen- 
 trum ovale these fibres, if looked at from in front (Fig. 26), 
 appear like the sticks of a fan, and like those sticks their rela- 
 tive position is altered in the point of junction, where those 
 passing inward from the lowest part of the cortex lie in front 
 of those which pass downward from its upper part (Fig. 26). 
 Thus in the capsule the order from before backward is, first, 
 the fibres conveying speech impulses to the pons and medulla; 
 second, the fibres conveying facial motor impulses to the pons; 
 third, the fibres destined to the arm centres of the cord ; 
 fourth, the fibres transmitting impulses to the leg centres in 
 
 1 Flechsig: " Plan des Mensch. Gehirns," Leipzig, 1884. 
 
 - Starr : " Sensory Tract in Central Nervous System," Jour, of Nerv. and Ment. 
 Dis., July, 1884. 
 
04 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 the cord. The fibres conveying impulses to the muscles of 
 the trunk probably lie behind those to the leg. 
 
 This is the great motor tract, whose course through the 
 anterior half of the posterior division of the capsule is well 
 known, and which can be traced through the middle third of 
 each crus, through the pons (where the division to the facial 
 
 Fig. 26.— The Motor Tract. .?, Fissure of Sylvius; N L, lenticular nucleus; O T, optic thala- 
 mus; N C, caudate nucleus; C, crus; P y pons; M, medulla; O, olivary body. The tracts for face, 
 arm, and leg gather in the capsule and pass together to the lower pons, where the face fibres cross to 
 the opposite VII. nerve nucleus, while the others pass on to the lower medulla where they partially 
 decussate, to enter the lateral columns of the cord; the non-decussating fibres pass from the ante- 
 rior median columns. The effect of a lesion situated at three points in the tract is shown on the 
 left side of the figure; at x,y, z. 
 
 nucleus crosses to the opposite side and ends), and thence by 
 way of the pyramids of the medulla to the crossed pyramidal 
 and anterior median columns of the spinal cord. It is evident, 
 however, that the concentration of this tract is much greater 
 in the capsule than in the centrum ovale, where the individual 
 fibres are scattered among the other systems and occupy but 
 
THE TRACTS WITHIN THE BRAIN. 95 
 
 a small area from before backward. Lesions beneath the 
 third frontal convolution of the left side produce motor aphasia. 
 Lesions beneath the central convolutions in the centrum ovale 
 produce paralysis, which will vary according to the position of 
 the lesion. The nearer the lesion lies to the cortex the more 
 will the symptoms resemble those of cortical disease, mono- 
 plegia being the rule (Fig. 26, x). The nearer the lesion to 
 the point of junction at the capsule the more will the symp- 
 toms resemble those of capsule lesion, hemiplegia being the 
 rule (Fig. 26, y). There are numerous cases recorded which 
 support this statement. When the motor tract is injured by a 
 lesion in the lower half of the pons (Fig. 26, z) the result is 
 paralysis of the face on the side of the lesion and of the arm 
 and leg on the opposite side (alternating paralysis). 
 
 The third set of fibres of the projection system includes 
 those which lie just posterior to the motor tract, and which 
 pass inward from the parietal convolutions (Fig. 25, C). These 
 take a similar course to those of the motor tract, and fill up 
 to a considerable extent the space between it and the radia- 
 tion of the visual tract, toward the occipital lobe. They are 
 mingled with fibres which pass to the optic thalamus, but are 
 separable from them in fcetal brains, 1 as Edinger has shown, 
 and may be traced down through the capsule to the tegmen- 
 tum of the crus, where they divide into a portion going to the 
 lemniscus, and a portion going to the formatio reticularis. 
 The fibres can be traced through these tracts downward to 
 the medulla and through the sensory decussation to the pos- 
 terior pyramids of the medulla in which the posterior columns 
 of the spinal cord begin. This set of fibres conveys the sen- 
 sations of touch, pain, temperature, and muscular sense, 2 and 
 lesions in its course will cause disturbance of these sensations. 
 Like lesions in the motor tract, the rule obtains that the nearer 
 the cortex the more likely is the lesion to cause an affection 
 of a single limb, while the nearer the capsule the more likely 
 is the symptom produced to be hemianaesthesia. 
 
 1 Edinger : " Vorlesungen liber den Bau der Nervosen Cetitralorgane," Leipzig, 
 18S9. 
 
 2 Starr : " Sensory Tract," loc. cit. 
 
9 6 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Looking, then, at the dissection of the projection system 
 of fibres, it is evident that a lesion which lies in the centrum 
 ovale at any point posterior to the praecentral fissure of the 
 frontal lobe, may produce recognizable symptoms, for it must 
 affect either the motor, or the sensory, or the visual, or the 
 auditory tracts, or individual fibres of those tracts. In the 
 latter case it will be necessary to examine carefully for symp- 
 toms, as they may escape a superficial examination. 
 
 THE COMMISSURAL TRACTS. 
 
 The second system of fibres in the centrum ovale is the 
 commissural system. This joins corresponding areas of the 
 two hemispheres with one another. The commissural fibres 
 between the frontal, parietal, and occipital lobes of the two 
 sides pass in the corpus callosum ; the view of Hamilton, of 
 Aberdeen, that these fibres are not commissural being dis- 
 proved by the researches of Spitzka and Beevor. 1 Those from 
 the temporal lobes pass in the anterior commissure. The func- 
 tion of these fibres is to harmonize the action of the two hem- 
 ispheres. This may be proven with regard to the fibres which 
 join the central convolutions with each other, and harmonize 
 motor acts (Fig. 26). Every one knows that simultaneous 
 movements of like nature can be made with great facility with 
 both upper extremities. An attempt to swing Indian clubs is 
 more difficult if each hand is executing a different motion. 
 So, too, movements which are difficult when attempted with 
 the left hand alone become easy when associated with corre- 
 sponding movements of the right hand — as, for example, draw- 
 ing a circle, writing one's name. But the motion, in order to 
 be associated by the commissural fibres, must involve the cor- 
 responding muscles on both sides of the body. Hence, if the 
 right hand moves to the right the left must move to the left 
 to a similar degree in order to bring into play the aid of com- 
 missural association. Hence, such writing with the left hand 
 will be backward, and can only be read by the aid of a mir- 
 
 1 See Hamilton : Brain, July, 1885: Beevor: Brain, Oct., 1885; Spitzka: Amer. 
 Jour. Neurol., Aug., 1884. 
 
THE TRACTS WITHIN THE BRAIN. 
 
 97 
 
 ror. Now, it is a very simple thing to test this power of sym- 
 metrical movement in persons, but I venture to state that it 
 is very rarely done; so that no clue is usually obtained as to 
 the condition of conducting power in the commissural fibres 
 in cases of brain disease. It is the commissural fibres joining 
 the motor convolutions only which can be thus tested. Fail- 
 ure to perform easily corresponding bilateral motions in face, 
 hands, or feet would indicate some obstruction to conduction 
 in them. With regard to the fibres lying in the anterior part 
 of the corpus callosum and joining the frontal lobes, little can 
 be said except that in numerous cases of idiocy these fibres 
 have been wanting. The cases of Mc Bride (Amer. Jour. Neu- 
 rol., May, 1884) and of Erb (Virchow's Arch., Bd. 98) of lesion 
 of the corpus callosum presented no peculiar local symptoms. 
 Nor have we any power of testing the integrity of commissu- 
 ral fibres lying posterior to the motor tract, though a theo- 
 retical statement may be made, that those between the occipi- 
 tal lobes are very important, inasmuch as each occipital lobe 
 receives impulses from but one-half of each retina. Hence, 
 integrity of both occipital lobes and simultaneous, connected, 
 and harmonious action in both is necessary to the perfect per- 
 ception of the whole of any object when the eyes are fixed 
 upon one point of that object. The function of the anterior 
 commissure which connects the apices of the temporal lobes 
 is probably that of conducting sensations of smell and taste, 
 but this is not certain. Theoretically, a lesion of the commis- 
 sural fibres should produce a lack of harmony in the simulta- 
 neous action of the two hemispheres, and if the lesion in the 
 centrum ovale lay opposite to the two central convolutions, 
 this could be detected by appropriate tests. 
 
 THE ASSOCIATION TRACTS. 
 
 The third system of fibres in the centrum ovale is the as- 
 sociation system (Fig. 27). 
 
 It can be shown by careful dissection that each convolu- 
 tion is joined to the two adjacent convolutions by fibres which 
 pass around the separating fissures. Also, that bundles of 
 7 
 
9 8 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 fibres exist which pass from each convolution to the convolu- 
 tion next but one, and so on (Fig. 27, A). Hence, it may be 
 stated that each convolution has a possible connection with 
 every other. Besides this association of convolutions by small 
 bundles .of fibres, it is possible to find a distinct set of associ- 
 ation tracts which pass between more or less distant regions. 
 One such tract passes from the frontal lobe, collecting its 
 bundles from all three convolutions, backward to the occipital 
 
 Fig. 27. — The Association Fibres. A, Between adjacent convolutions; B, between frontal and 
 occipital areas; C, between frontal and temporal areas, cingulum; D, between frontal and temporal 
 areas, fasciculus uncinatus; E y between occipital and temporal areas, fasciculus longitudinalis infe- 
 rior; C iV, caudate nucleus; O T, optic thalamus. 
 
 lobe (Fig. 27, B). Another tract joins the occipital with the 
 anterior part of the temporal lobe (Fig. 27, E). Another 
 passes from the upper two temporal convolutions forward to 
 the third frontal convolution, passing beneath the island of 
 Reil (Fig. 27, D). And a tract from the frontal to the poste- 
 rior temporal area may also be found (Fig. 27, C). 
 
 What can be the function of these association fibres ? 
 Without going very deeply into the subject of psychology, it 
 may be suggested that they form the physical basis for the 
 association of concrete memories and of psychical acts. 
 
THE TRACTS WITHIN THE BRAIN. cjcy 
 
 Our concrete memories are reproductions of former sensa- 
 tions. But if the sensations are received in various areas of 
 the brain, as we must admit from the facts already stated re- 
 garding the function of the projection fibres, it is evident that 
 the reproduced sensation which depends on the revival of the 
 original sensation will occur in the same part of the brain in 
 which the original sensation was received. A sight memory 
 is located in a different part of the brain from a sound, or 
 touch, or motor, or speech, or writing memory. And this fact 
 will be readily admitted by those who have seen cases in which 
 a single set of memories have been lost while others remain. 
 The symptoms of apraxia, word-deafness, word-blindness, 
 aphasia, agraphia, alexia, are all dependent upon loss of a 
 definite set of memories. And they are due to definite lesions 
 of the cortex in different areas, as has already been stated in the 
 discussion of aphasia (Chap. VI.). But no concrete memory 
 can be said to exist without associations. The sight of a dog 
 leads us at once to think of the form and appearance of other 
 dogs, of animals resembling dogs, and of quadrupeds in gen- 
 eral. Thus the impulse received in a memory area excites 
 other memories of a like quality. Further, the sight of a dog 
 might easily lead us to think of his bark, or, if we had once 
 felt it, of his bite ; and that because originally the simultane- 
 ous occurrence of the sight and sound of the animal had asso^ 
 ciated the two memories forever. Thus an impulse received 
 in a memory area may excite other memories of an unlike 
 quality. In fact, any one of our concrete ideas may be said 
 to be made up of a number of associated memory pictures, 
 all of them united into a definite whole. My idea of an orange 
 is made up of my memory of the appearance of the orange, 
 its color and form, of the memory of its odor and taste, of the 
 peculiar feeling of its surface, of the sound which I know as 
 its name, of the motion necessary in my throat and lips to 
 pronounce the word which designates it, and of the movements 
 necessary to write the word orange. And further, each one 
 of these memories is joined not only to the next, but also to 
 all the others, for if you show me an orange and ask me to 
 say or to think or to write its name, I can do either at your 
 
IOO FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 will, and need not say it before I write it, or taste it before I 
 can call to mind its odor. 
 
 These facts of concrete memory gained by introspection 
 show how intimate is the connection between our various kinds 
 of memories, and demonstrate <> priori the need of just such 
 sets of association fibres in the brain as may be found by an- 
 atomical dissection. It may be stated, therefore, that the as- 
 sociation fibres of the centrum ovale have as a function the 
 harmonizing of the activities of the various cortical areas. 
 They are necessary to the union of different memories in a 
 whole, to the formation of a concrete idea. I do not now 
 allude to abstract ideas, or to processes of reasoning. I have 
 spoken only of concrete ideas, for it is only regarding these 
 that our investigation of cases of localized brain disease will 
 allow us to speak. But if these association fibres pass through 
 the centrum ovale, it is evident that the integrity of the cen- 
 trum ovale is necessary to their proper action, and that lesions 
 of the centrum ovale will lead to a separation or failure of asso- 
 ciation of ideas and memories formerly joined. If the fibre is 
 broken which joins my memory picture of a familiar face with 
 my memory picture of the sound or name associated with that 
 face, I cannot call the person by name on seeing him. If I 
 have lost the power of copying a page that is placed before 
 me and which I can see, it is possibly because I no longer as- 
 sociate the sight of a letter with the motion of my hand neces- 
 sary to write that letter, an association originally made by 
 practice. If I can understand what is said to me, and can 
 pronounce words distinctly, but talk jargon or replace one 
 word by another, it is because the fibres which join corre- 
 sponding auditory and motor speech memories are unable to 
 perform their function. 
 
 Instances of such loss of function in the association fibres 
 between the temporal and occipital lobes have already been 
 given in the chapter on aphasia. 
 
 It is evident, therefore, that we have not only a knowl- 
 edge of the anatomy and physiology of the association fibres 
 of the centrum ovale, but also a set of symptoms referable to 
 their destruction. But here, again, it must be emphasized 
 
THE TRACTS WITH IN THE BRAIN. \o\ 
 
 that careful examination of cases in a proper way is necessary 
 in order to detect a lesion of such fibres. 
 
 Brill has recorded ' a case of lesion of the cuneus associated 
 with color-blindness to green, and he states that the patient 
 had difficulty in naming various colors on account of the pres- 
 ence of a slight degree of amnesic aphasia. This aphasia was 
 most marked in regard to names of colors, not in regard to 
 contours, for he would compare colors to the tints of com- 
 mon objects. The aphasia was limited to the names of those 
 colors which were imperfectly perceived — green and violet. 
 
 These facts seem to emphasize the importance, already in- 
 sisted upon, of careful examinations, especially in cases of 
 aphasia. 
 
 THE DIAGNOSIS OF SUB-CORTICAL LESIONS. 
 
 It is evident, therefore, that a lesion of the centrum ovale 
 may give rise to three sets of symptoms, referable to projec- 
 tion, commissural, and association fibres. The important fact 
 at once appears that these symptoms will be inevitably asso- 
 ciated in any case of its occurrence. It is upon the fact of 
 such association of symptoms that the diagnosis of lesions of 
 the centrum ovale must depend. Monoplegia alone may be 
 caused by cortical or centrum ovale disease. Hemiplegia 
 may be caused by capsular or centrum ovale disease. But if 
 in either case it is the centrum ovale which is diseased, there 
 will be in addition to the paralysis a suspension of action of 
 commissural and association fibres. The commissural fibres 
 being destroyed, simultaneous bilateral symmetrical motions 
 will be suspended. The association fibres being destroyed, 
 certain mental associations will be affected. Take as an ex- 
 ample a lesion in the centrum ovale of the occipito-temporal 
 region. Such a lesion will produce hemianopsia because it 
 involves the visual tract of the projection system. It may also 
 produce word-blindness, the patient being no longer able to 
 associate a word or letter seen with its corresponding sound, 
 or with the motion necessary to write it. Charcot has re- 
 
 1 Amer. Jour, of Neurology, Feb., 1SS3. 
 
102 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 ported .t case of this kind, and as I had an opportunity to see 
 and examine the patient under his direction, I maybe excused 
 for mentioning it in detail. The man, who was a very intelli- 
 gent merchant, was suddenly seized with right hemianopsia 
 while playing billiards, and was surprised to find that he saw- 
 but one-half of the ball and of the table. Soon after he had 
 occasion to write a letter, and after writing it was surprised 
 to find that he could not read what he had just written. He 
 found, however, that on tracing individual letters with the 
 pen or fingers he became conscious of the letter — a few let- 
 ters (r, s, t, x, y, v. i, however, being exceptions to this rule. 
 When a book was given him to read, he would trace out the 
 forms of the letters with some rapidity and thus manage to 
 make out the words. If his hands were put behind him and 
 he was asked to read, he would still be observed to put his 
 fingers in motion and to trace the letters in the air. Speech 
 was in no way interfered with, but reading aloud was only ac- 
 complished, like reading to himself, by the aid of muscular 
 sense. Here, then, was an example of a lesion which had 
 separated entirely the tract associating sight with speech, viz., 
 the occipito temporal tract; but had left intact the tracts as- 
 sociating sight with muscular sense and muscular sense with 
 speech. 
 
 The first tract, the occipitotemporal, lies side by side with 
 the visual, and its implication in the lesion which caused the 
 hemianopsia is not to be wondered at. The second tract, 
 the occipito-central, lies much higher in the centrum ovale 
 and evidently escaped. Now, had this patient been an un- 
 intelligent laborer, seldom called upon to read or write, such 
 a peculiar symptom might have escaped notice, and although 
 it might have been discovered that he had alexia, the pos- 
 sibility of his being able to read by means of his muscular 
 sense would only have been elicited by proper investiga- 
 tion. This case also illustrates a possible point of differential 
 diagnosis between lesions of the centrum ovale and lesions of 
 the cortex. If the lesion is in the cortex, some one of the 
 cortical functions — e.g., sight or motion — will be suspended 
 tog-ether with their memories; while in lesion of the centrum 
 
THE TRACTS WITHIN THE TRAIN. 
 
 103 
 
 ovale it is only the association of two or more memories which 
 will be impaired. It is possible that in cases of word-blind- 
 ness the symptoms are due to such a break of the association 
 tracts when sight and speech are preserved. Certainly, in 
 numerous cases of word-blindness and in the condition of 
 dyslexia x — i.e., a great reluctance with some inability to read 
 — the lesion found was in the centrum ovale just beneath the 
 cortex, at the posterior end of the Sylvian fissure, and involved 
 the centrum ovale where the occipito-temporal tract lies. 2 
 
 There is a psychological deduction which occurs naturally 
 from the study of the case just related. The man could see 
 the letter so as to be able to trace its form, and yet the sight 
 alone conveyed to him no idea. We have already seen, in 
 studying apraxia, that a concrete idea must be considered as 
 a complex collection of memory pictures. Is it not evident 
 from this case that a single one of these pictures isolated from 
 the rest is incapable of awakening a concrete idea ? The pa- 
 tient only obtained the idea when he put into action the motor 
 memory, whose connections with sight and sound and speech 
 were all intact. We have spoken only of concrete ideas. If 
 we conceive of abstract ideas as made up of a numerous as- 
 semblage of concrete ideas, as they may possibly be, brought 
 into consciousness as a single concept by the aid of the name 
 or word, is it not probable that lesions of the centrum ovale 
 will give rise to a confusion of abstract as well as of concrete 
 ideas ? And is it not possible that the symptoms of mental 
 confusion of that peculiar kind which occurs in diseases of 
 the frontal lobes of the brain, may be ascribed to a suspension 
 of action of association and commissural fibres which pass in 
 all directions through the frontal lobes ? 
 
 Nothnagel, in his great work, " Topische Diagnostik," has 
 said that there are no diagnostic local symptoms of lesion of 
 the centrum ovale. Such symptoms as headache, vertigo, 
 vomiting, mental inactivity, and optic neuritis being general 
 rather than local symptoms, and common to affections in any 
 part of the brain, are frequently present in disease of the cen- 
 
 1 Berlin: " Ueber Dyslexic" - Brain, part xlv., p. 91. 
 
104 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 trum ovale. It is not to these that reference is made, but 
 rather to symptoms whose presence would lead inevitably to 
 the diagnosis of disease below the cortex and above the basal 
 ganglia. Nothnagel's assertion may be repeated to-day, not- 
 withstanding the labor that has been expended since 1879 on 
 the study of localized brain disease. It is evident to me that 
 the way to soke the problem here is to reason from anatomy 
 and phyisology to the probable results of lesion in the centrum 
 ovale, and then in every case to examine for the symptoms 
 which theoretically might occur. In that manner it will be 
 evident that no latent symptoms will be overlooked, and it is 
 not impossible that, after a time, so many new symptoms now 
 unsuspected maybe educed and brought into connection with 
 lesions found by post-mortem examination, as to warrant the 
 formulation of certain diagnostic signs of diseases of the cen- 
 trum ovale. 
 
CHAPTER IX. 
 AFFECTIONS OF THE BASE OF THE BRAIN. 
 
 I. Paralysis of the ocular nerves.- — II. Unilateral cranial nerve paralysis. 
 — III. Staggering to one side as a symptom. 
 
 I. PARALYSIS OF THE OCULAR NERVES. 
 
 In affections of the parts of the brain which lie upon 
 the base, one of the most common symptoms is some form of 
 paralysis of the ocular muscles. There are a number of forms 
 of such paralysis, each of which implies a lesion in a different 
 position. 
 
 Internal strabismus with inability to turn the eyeball out- 
 ward and. an accompanying contraction of the pupil is most 
 frequently seen. This implies an affection of the sixth or 
 abducens nerve, which has the longest course upon the base 
 of any cranial nerve, and hence may be affected by a lesion 
 anywhere from the sphenoidal fissure in front to the junction 
 of the pons and medulla behind (see Fig. 28). 
 
 External strabismus, with inability to move the eyeball 
 upward or downward, and with ptosis, as well as dilatation 
 of the pupil and loss of pupil reflexes, is also often observed. 
 These symptoms together imply an affection of the third 
 nerve or oculo-motorius. This nerve issues from the inner 
 side of the crus and passes forward to the orbit. A lesion in 
 its course implies that the disease producing it lies in front of 
 the pons Varolii. If the disease is a tumor or meningeal thick- 
 ening situated between the two crura, both third nerves are 
 often involved together, as they there lie side by side. 
 
 Paralysis of the fourth nerve is extremely rare and is only 
 to be detected by a careful examination for double images 
 with a red glass over one eye. The upright image is then 
 
io6 
 
 I'AMILIAR FORMS OF NERVOUS DISEASE. 
 
 seen to be upright by the normal eye, but appears to be dis- 
 placed downward and turned obliquely by the affected eye. 
 Such a conditon indicates disease upon the back of the cere- 
 
 cl La 
 
 Fig. 28.— The Base of the Brain and the Cranial Nerves. Crura, Pons and Medulla (Allen 
 Thompson;, /to XII, the cranial nerves; T/i, optic thalamus; h, pituitary body; /c, tuber cine- 
 reum; a, corpora albicantia; /', pes pedunculi; i, interior, and e, exterior, geniculate body; PV, 
 pons Varolii; /a, anterior pyramid of medulla; 0, olive; a', decussation of anterior pyramids; ca y 
 anterior column of spinal cord; c/, lateral column of spinal cord; C>, cerebellum; y7, flocculus of 
 cerebellum. 
 
 bral axis or in the anterior part of the cerebellum, since the 
 fourth nerve does not pass out on the base but curves around 
 the outer side of the crus lying between the corpora quadri- 
 gemina, and the cerebellum (see Fig. 29). In a case present- 
 
AFFECTIONS OF THE BASE OF Till': BRAIN. 
 
 107 
 
 ing the symptoms of cerebellar disease, the existence of fourth- 
 nerve paralysis shows that the anterior portion of the cerebellar 
 hemisphere on the side of the paralysis is the part of the 
 cerebellum affected. This statement is based on a case with 
 autopsy seen in Meynert's clinic in Vienna. 
 
 It is very common to find the sixth and third nerves of one 
 
 Fig. 29. — The Cerebral Axis, Lateral View (Edinger). The exit of the ocular nerves are 
 shown; N. III., N. IV., N. VI. Fuss = pes pedunculi. Bindearra = superior peduncle of cere- 
 bellum. Corp.g. = Corpora geniculata. 
 
 or both sides affected together in varying degrees in basilar 
 affections, especially in the forms of syphilitic disease of the 
 base. 
 
 It may be laid down as a rule that when one of the ocular 
 nerves is affected all of its functions are about equally im- 
 paired. This condition is not, however, always found. There 
 are cases observed in which a single ocular muscle or two 
 
IOS FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 muscles become weak, the others not being affected. Under 
 these circumstances the conclusion is warranted that the 
 lesion does not lie in the course of the nerve supplying the 
 muscles, but is located in the group of cells from which vari- 
 ous sets of fibres making up the nerve arise. If it is the ex 
 ternaJ rectus which is paralyzed alone, a lesion of the sixth 
 nucleus can be diagnosticated from one of the sixth nerve by 
 the fact that conjugate movement of the eyes toward the side 
 of the lesion is impossible. An analysis of twenty cases of 
 such affection of individual ocular muscles has enabled me ' to 
 locate the relative situation of the groups of cells governing 
 the ocular muscles. The following table displays the situation 
 of these groups, each group being named for the muscle which 
 it governs : 
 
 ARRANGEMENT OF THE GROUPS OF CELLS GOVERNING THE OCULAR MUSCLES. 
 
 Left. 
 I Ciliary muscle. 2 Sphincter iridis. 
 
 Right. 
 
 2 Sphincter iridis. I Ciliary muscle. 
 
 5 Levator palp. sup. 3 Rectus internus. 
 
 6 Rectus superior. 
 
 7 Obliquus infer. 4 Rectus inferior. 
 
 8 Obliquus super. 
 
 9 Rectus externus 
 
 3 Rectus internus. 5 Levator palp. sup. 
 
 6 Rectus superior. 
 
 4 Rectus inferior. 7 Obliquus infer. 
 
 8 Obliquus super. 
 9 Rectus externus. 
 
 The cells making up these groups lie in the gray matter of 
 the floor of the aqueduct of Sylvius and of the fourth ventri- 
 cle, all but the last group being underneath the corpora 
 quadrigemina (see Fig. 30). Disease of a single group results 
 in the permanent paralysis of its muscle, just as the disease of 
 a single group of cells in the spinal cord in infantile paralysis 
 results in the paralysis of a single muscle. A number of 
 groups may be affected together, and Wernicke has named 
 such a disease when it occurs suddenly polio-encephalitis su- 
 perior, and he considers it quite homologous to polio-myelitis. 
 When all the groups except the sphincter iridis are simultane- 
 ously or successively diseased, the disease is named ophthal- 
 moplegia externa. The result is a double ptosis, inability 
 to move the eyes in any direction, but preservation of sight 
 
 '"Ophthalmoplegia Externa Partialis," Jour. Nerv. and Ment. Dis., May, 
 1888. 
 
AFFECTIONS OF THE BASE OF THE BRAIN. 
 
 [09 
 
 and of the pupil reflex to light. The appearance of the patient 
 suffering from ophthalmoplegia externa in its terminal stage 
 Cdf , 
 
 Fig. 30. — Sagittal Section through the Cerebral Axis to show the Nuclei of the Ocular Nerves 
 in the Floor of the Aqueduct of Sylvius and Fourth Ventricle and the Course of the Nerves to 
 their Exit. The various groups of cells from which the III. N. arises are seen. R N, Red 
 nucleus of tegmentum; Z,, lemniscus (sensory tract); C C, motor tract in the crus cerebri seen to 
 traverse the pons and enter the ant. pyramid of the medulla. 
 
 Jw 
 
 \ 
 
 - M 
 
 V 
 
 Wj 
 
 
 1 
 
 
 Fig. 31. — Photograph of Patient with Ophthalmoplegia Externa. Double ptosis, external stra- 
 bismus. The muscles of mastication are also atrophied. 
 
 is shown in Fig. 31, a photograph of a patient under Dr. 
 Peterson's care at Ward's Island Hospital. I am indebted to 
 
1 1 o /•". XMILIA R /■'( WAfS ( V' NER VOL 'S DISE. ISE. 
 
 him for the use of the photograph. The great effort of the 
 patient to open the eyes by contracting the frontal muscles 
 in place of the levatores palpebral is well shown. Such a dis- 
 ease is usually progressive and cannot be arrested by treat- 
 ment. 
 
 Ophthalmoplegia interna, in which the movements of the 
 iris alone are paralyzed, the external muscles of the eye not 
 being affected, is a rare condition seen occasionally as a symp- 
 tom in hydrocephalus ami paretic dementia, and due to a 
 thickening of the ependyma of the third ventricle with impli- 
 cation of the two anterior groups of cells just mentioned, which 
 lie at the entrance of the aqueduct of Sylvius into the ventri- 
 cle. Paralysis of the pupil reflex to light, while the contraction 
 in accommodative effort is preserved, is called the Argyll Rob- 
 ertson pupil, and is due to some interference with the passage 
 of impulses along the fibres from the corpora quadrigemina to 
 the cells controlling the iris and not to disease in the group of 
 cells governing the iris. It is a symptom of locomotor ataxia 
 and of multiple sclerosis. 
 
 It is evident from this review of symptoms referable to the 
 ocular muscles, that it is not difficult to distinguish between 
 lesions on the base affecting the ocular nerves and lesions 
 within the cerebral axis affecting their nuclei in the floor of 
 the fourth ventricle. 
 
 The following cases illustrate the latter condition, and ex- 
 amples of the former will be considered subsequently. 
 
 CASE XIV. — PARTIAL OPHTHALMOPLEGIA EXTERNA — SOFTEN- 
 ING IN THE CRUS CEREBRI DUE TO EMBOLISM. 
 
 S. D., a Frenchman, aged fifty-six, a painter by occupation, 
 and a resident of Providence, R. I., was brought to the clinic 
 April 1 8th, 1887. He had been a healthy man all his life, 
 with the exception of occasional attacks of rheumatism and 
 frequent attacks of migraine. He had never contracted 
 syphilis, and denied all symptoms of pulmonary, cardiac, gas- 
 trointestinal, and renal disease, although a physical examina- 
 
AFFECTIONS OF THE J! ASF OF THE BRAIN, \\\ 
 
 tion revealed the existence of slight aortic obstruction pro- 
 ducing a systolic murmur heard at the base and associated 
 with slight ventricular hypertrophy. 
 
 He stated that about the 1st of April, 1887, he had been 
 seized very suddenly with double vision and vertigo, objects 
 appearing to move up and down constantly, so that he was 
 much bewildered and unable to stand or to walk alone. He- 
 managed with help to reach his home, but has no recollection 
 of what occurred during the three following days, during 
 which, according to the statement of his family, he lay in a 
 somnolent condition, but not comatose nor paralyzed. He 
 was then able to get up, but felt stupid, dizzy, and walked with 
 difficulty, it being impossible for him to fix any object with 
 his eyes; all objects being seen double and in motion. These 
 symptoms have improved slightly, but he still feels weak, 
 has vertigo and double vision. He has never had headache, 
 nor has he felt any sensation of numbness or cold or pain in 
 his body, and he has had no paralysis, tremor, or spasm. He 
 staggers in walking and the staggering is not increased by 
 closing his eyes. 
 
 Examination shows a well-nourished, intelligent, active 
 man, whose facial expression is rendered peculiar by the posi- 
 tion of his eyes. When at rest, they diverge slightly, and the 
 right eye is turned upward, and the right pupil is slightly larger 
 than the left. When the eyes are moved it becomes apparent 
 that the motion is defective. The eyes can be turned from 
 side to side together perfectly, but such motion soon produces 
 lateral nystagmus of the right eye. They cannot be converged 
 to an object nearer than two feet, because of slight weakness 
 of the right internal rectus muscle. They cannot be turned 
 downward below the horizontal line either together or when 
 tested separately. When asked to look up, the right eye fol- 
 lows the object above the horizontal line, but the left eye 
 does not. Both eyes, however, turn up and in, though this 
 motion produces rotary nystagmus. The reaction of the 
 pupils to light and in accommodation is prompt, though the 
 right pupil contracts in accommodation more slowly and less 
 completely than the other, and remains slightly larger. Tests 
 
112 FAMILIAR FORMS OF NERVOUS JUS EASE. 
 
 by secondary deviation and double images confirm the con- 
 clusion reached by this examination, viz., that in the right eye 
 there is paralysis of the inferior rectus and paresis of the in- 
 tern. d rectus; and that in the left eye there is paralysis of 
 the inferior rectus and superior rectus. There is no ptosis. 
 There is no paralysis of the oblique muscles or of the exter- 
 nal recti. One week later the paresis of the right internal 
 rectus, the difficulty in convergence, and the difference in the 
 size of the pupils had disappeared, but all the other conditions 
 remained, and persisted for fourteen months. He then had a 
 stroke of apoplexy due to embolism of the right middle cere- 
 bal artery with left hemiplegia, which still remains. He is still 
 suffering from general weakness, vertigo, and double vision, 
 although the latter symptom no longer troubles him except- 
 ing when he tries to read. Attempts to turn the eyes up or 
 down, or upward or inward, produce nystagmus of a rotary 
 kind, more marked in the right eye, and this always makes 
 him dizzy. The diagnosis made at first was embolism, from 
 the aortic valve, in the small arteries entering the posterior 
 perforated space between the crura cerebri, and resulting in 
 one or more small foci of softening in the tegmentum cruris; 
 a diagnosis which the subsequent development of hemiplegia 
 confirmed. 
 
 This diagnosis was reached by exclusion ; for it is impossi- 
 ble for the symptoms to have been caused by a tumor or a 
 meningitis upon the base of the brain in the course of the third 
 nerves. Such a lesion would not have come suddenly or have 
 remained stationary, and would have involved the oculo-motor 
 nerve as a whole, impairing all its functions and not affecting 
 merely a part. Nor is a condition of acute inflammation with 
 hemorrhage in the floor of the aqueduct of Sylvius possible, nor 
 such a condition as occurs in a true ophthalmoplegia externa; 
 for there is no tendency manifest toward an extension of the 
 symptoms, or to complete immobility of the eyes. 
 
 It is true that a hemorrhage in the same region is with 
 difficulty distinguished from an embolism, but in hemorrhage 
 some evidence of pressure upon the adjacent sensory or motor 
 tracts is usually shown which was wanting here at first; and 
 
AFFECTIONS OF THE BASE OF 77/ E HRAIN. 
 
 "3 
 
 in this case the existence of an aortic murmur and the subse- 
 quent occurrence of hemiplegia make embolism probable. 
 
 CASE XV. — THROMBOSIS OF AN ARTERY IN THE TEGMENTUM 
 OF THE CRUS CEREBRI. 
 
 Henry B., aged forty, applied for examination at the New 
 York Polyclinic February 27th, 1886, complaining of numb- 
 ness in the right side of his body and of double vision. He 
 denied syphilis, but admitted having had gonorrhoea twice, 
 and having suffered from severe sore throat and nocturnal 
 headache. Has never had any eruption. No scars on geni- 
 tals. It is, therefore, uncertain whether he has had syphilis. 
 
 He was fairly well until five months ago, when, on waking 
 one morning, he noticed that he saw everything double, and 
 had a peculiar sensation of numbness in his entire right side. 
 This condition has been permanent. 
 
 Examination shows a well-nourished man, able to walk nat- 
 urally. There is slight ptosis of the left eye, and a marked 
 sinking downward of the eyeball when at rest. The pupil is 
 slightly dilated, but reacts to light and during accommodation. 
 Voluntary motion of the eyeball is good, except upward, the 
 superior rectus being weak. When his eyes are at rest, he sees 
 double, the new object appearing just above the old one. 
 From the consequent misinterpretation of the position of 
 objects, he lifts his feet higher than necessary in walking or in 
 going up-stairs. When he turns both eyes to the right or to 
 the left, the double vision persists, but the two images main- 
 tain the same relative position. There is no apparent devia- 
 tion to either side, and no secondary lateral deviation can be 
 noticed when one eye is covered. Examination by Dr. Web- 
 ster : R.V. §#, L.V.ff . Hm -gV in both eyes. No insufficiency at 
 20' nor at i\ Ophthalmoscopic examination negative. The 
 condition of the eye is one of paresis of the levator palpebrae 
 and superior rectus muscles; all other muscles of the left eye 
 and all muscles of the right eye being normal. 
 
 He complains of a constant feeling of numbness and tin- 
 gling in the right half of the body; face, arm, body, and leg 
 
114 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 being equally involved. Examination shows a slight degree 
 ^i tactile anaesthesia in the entire right half of the body, ex- 
 cepting a small area back of the ear and on the neck, where 
 sensation is normal. There is also a difference between the 
 perception of temperature sensations in the two halves, heat 
 and cold being perceived less intensely on the right side. 
 The sense of pain is also somewhat impaired on the entire 
 right side. These sensations are not delayed in transmission. 
 Muscular sense is normal. There is no incoordination, all 
 motions being accurately and promptly performed. The re- 
 flexes are normal and equal on both sides. There is no loss 
 of power. There are no other symptoms. Vertigo and head- 
 ache are absent. Hearing normal. The examination indi- 
 cates a lesion in the course of the sensory tracts of touch, 
 temperature, and pain from the right half of the body, not 
 sufficient in extent to destroy completely that tract, but only 
 to impair its action. 
 
 Since the sensory and ocular symptoms began simultane- 
 ously, it is probable that they were due to one cause. The fact 
 that but two of the branches of the left third nerve were in- 
 volved pointed to a lesion in the nucleus of the nerve rather 
 than to a lesion in the nerve trunk. In this case, the fifth 
 and sixth groups of cells (page 108) were affected. But just 
 at the side of the gray matter lining the aqueduct of Sylvius, 
 in which these groups lie, the formatio reticularis of the crus 
 cerebri is situated. In the formatio reticularis, the tracts con- 
 veying touch, temperature, and pain pass from the opposite 
 side of the body toward the internal capsule. A lesion lying 
 in the formatio reticularis on the left side of the tegmentum, 
 if small in size, might at once interfere with the transmission 
 of sensations from the right side of the body, and affect the 
 nuclei of the left third nerve. The lemniscus, lying outside 
 of the formatio reticularis, would not be affected if the lesion 
 were a small one, and hence no ataxia or incoordination would 
 be present. A lesion, therefore, in the formatio reticularis of 
 the tegmentum of the left crus cerebri would explain perfectly 
 the symptoms present in this case (see Figs. 17 and 30J. 
 
 As to the nature of the lesion, its sudden onset and the 
 
AFFECTIONS OF THE BASE OF THE BRAIN. \ \ 5 
 
 stationary character of the symptoms indicated that tumor and 
 hemorrhage were equally improbable. If a small thrombus 
 had formed in one of the twigs of the posterior cerebral artery 
 which supplies the crus cerebri, it would have led to a small 
 area of softening, the symptoms of which would have been 
 sudden in onset and stationary in character. An embolus 
 would produce the same effect, but the patient's freedom from 
 cardiac disease threw doubt on the hypothesis of embolism. 
 The diagnosis of thrombosis was strengthened by the fact that 
 syphilis was suspected, a specific endarteritis being the usual 
 cause of thrombosis. 
 
 The case is interesting, as it demonstrates the possibility 
 of local diagnosis from the peculiar combination of symptoms 
 present; and also as it is rare to find an affection of but two 
 of the nuclei of origin of the third nerve. The failure of the 
 patient to return a second time prevents any statement regard- 
 ing the termination of the case. 
 
 II. UNILATERAL CRANIAL NERVE PALSIES. 
 
 The diagnosis of affections of the base of the brain is 
 rarely difficult, and cases of these affections are very fre- 
 quently met with. From before backward upon the base the 
 cranial nerves lie in a definite order, and no serious lesion can 
 be present there without involving them. In any case, there- 
 fore, in which the cranial nerves are affected, attention is at 
 once directed to the base of the brain as the seat of the dis- 
 ease. Very frequently the nerves upon both sides are in- 
 volved in the lesion, especially when this is a syphilitic menin- 
 gitis or gumma, or some other form of tumor. Such cases 
 are so common as to need no special description. For in 
 addition to the general symptoms of brain disease, such as 
 headache, vertigo,- insomnia, restlessness, or even convulsions, 
 the local symptoms of cranial nerve lesion enable a diagnosis 
 to be reached at once. 
 
 The lesion may also be strictly unilateral, the cranial nerves 
 upon one side only being affected. And as such unilateral 
 cranial nerve palsies are rare, some of the cases on record are 
 here collected for comparison with those presented. 
 
n6 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 I. Bamberger {Wien. Medicin, Wockensckr., 1883, P- ll 4^> 
 reports the following case: 
 
 A woman, aged fifty-three, previously healthy and without 
 syphilis or tubercular disease, began to suffer in the spring of 
 1SS0 from pain in the entire right side of the head and face 
 which was sufficiently intense to keep her awake. In the fall 
 a right-sided facial paralysis developed, and soon after an in- 
 ternal strabismus of the right eye. During the following year 
 the right eye became inflamed, and ulceration of the cornea 
 rendered sight imperfect. She came under observation in 
 1S82, and was shown by Bamberger at the Medical Society of 
 Vienna in January, 1883. It was then demonstrated that the 
 right eyeball was completely immovable, and the upper lid 
 could not be raised ; that the entire right side of the face, in- 
 cluding the conjunctiva and mouth, was anaesthetic, and that 
 the cornea had become ulcerated and opaque; that the right 
 half of the face was completely paralyzed, taste being affected 
 on the right anterior part of the tongue and the uvula also be- 
 ing paretic ; the muscles of mastication were also weak. The 
 patient could not hear a tuning-fork placed upon the mastoid 
 process as well on the right side as on the left ; although the 
 watch held before the ear'was heard better on the right side, 
 a fact which Bamberger explained by supposing an increased 
 tension of the drum membrane due to the facial paralysis. 
 There was anaesthesia of the right half of the fauces and paraly- 
 sis of the right vocal cord, also paralysis of the trapezius and 
 sterno-mastoid muscle. There were no symptoms of vagus 
 paralysis and the hypoglossal nerve was not involved, as the 
 tongue was freely movable. 
 
 Bamberger concluded that the lesion was one of the nuclei 
 of these nerves along the floor of the fourth ventricle. 
 
 II. In February, 1884, Nothnagel presented to the Vienna 
 Medical Society a patient with paralysis of the fifth, sixth, 
 seventh, eighth, ninth, tenth, eleventh, and twelfth nerves, on 
 the left side. She had paralysis of the tongue, of the left trape- 
 zius and sterno-mastoid; difficulty in breathing, swallowing, 
 and talking, the left vocal cord being paretic ; loss of taste and 
 anaesthesia of mouth and face and eye on the left side; a cen 
 
AFFECTIONS OF THE BASE OF THE BRAIN. 117 
 
 tral deafness of the left ear; internal strabismus as well as left 
 facial paralysis, including the muscles of mastication. There- 
 was neuro-retinitis, but no paresis of the extremities. The 
 third and fourth nerves escaped. Nothnagel thought the lesion 
 was a unilateral chronic tubercular meningitis, or a tubercular 
 tumor involving the cranial nerves after their exit from the 
 side of the cerebral axis {Ccntralblatt fiir NervenJieilk., 1884, 
 p. 147). 
 
 III. Briere reports a case in the Gazette des Hopitaux, 1884, 
 p. 883, of paralysis of the fourth, fifth, sixth, and seventh 
 cranial nerves on the right side which occurred in a girl aged 
 twenty-one, who had been infected with syphilis a year pre- 
 viously. She had a growing tumor in the mouth, and it was 
 supposed that a similar tumor on the base of the brain had 
 caused the symptoms. She died a year later. 
 
 IV. Dr. Hughlings Jackson reported a case in the Med. 
 Times and Gazette for January 8th, 1870, of a male, aged 
 twenty-eight, who had had syphilis and who was found to 
 have paralysis of the fifth, sixth, seventh, and twelfth nerves 
 on the left side and paralysis of the vocal cord also on that 
 side. He was slightly deaf in the left ear. There was marked 
 weakness and anaesthesia in the right limbs, which led to the 
 diagnosis of a syphilitic affection of the base involving these 
 nerves and compressing the pons. 
 
 V. Mader, of Vienna, reports in the service of the Rudolph 
 Hospital for 1882, a case of sudden paralysis of the right face 
 with anaesthesia, loss of taste, and paresis of the right half of 
 the tongue. The electric reactions of the facial nerve were 
 those of degeneration. The patient recovered. 
 
 VI.-IX. Mobius recounts five cases of multiple cranial 
 nerve paralysis in the Centralblatt fiir Nervenheilkunde, 1887, 
 in four of which the paralysis was unilateral, and in all of 
 which recovery followed specific treatment. 
 
 X. A case was reported by Dr. Ramskell, seen at the Lon- 
 don Hospital in May, 1868 (Med. Times and Gazette, May 23d, 
 1868), of a man aged twenty-seven, syphilitic, who had suffered 
 from ptosis and paralysis of the fifth, sixth, seventh, and eighth 
 nerves on the left side. Taste was destroyed on the left side. 
 
ilS FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 The cornea was ulcerated. There was no paralysis of the 
 limbs and no difficulty of speech or of swallowing. He suf- 
 fered much from nocturnal headache, and after some months 
 developed optic neuritis. The termination of this case was 
 not reported. 
 
 XL A most remarkable and indeed unique case is reported 
 in the Fortschritte der Med., December 15th, 1887, of a gradu- 
 ally advancing total paralysis of all the cranial nerves on both 
 sides, without other cerebral symptoms. The autopsy failed 
 to reveal, at first sight, any lesion ; but careful examination 
 showed a sarcomatous growth beneath the dura covering the 
 base of the brain in the bone, which had narrowed all the 
 foramina of the skull and had thus compressed all the cranial 
 nerves at their exit. 
 
 These cases demonstrate the possibility of an affection of 
 the base of the brain producing unilateral cranial nerve para- 
 lysis. When the lesion lies outside of the cerebral axis, the 
 motor and sensory tracts passing through it are less likely to 
 be affected than when— as in Case XV. — the lesion lies within 
 it. In the latter condition the characteristic symptom is the 
 alternating character of the paralysis or anaesthesia, which 
 can only occur from lesions in the pons Varolii or crus. 
 
 III. STAGGERING TO ONE SIDE. 
 
 In the following cases an additional symptom of a unilat- 
 eral affection of one part of the brain lying on the base has 
 been noticed, viz., a persistent tendency to stagger tozvard one 
 side in walking, or to fall toward one side in standing. This 
 symptom is not very often mentioned, but it is not infrequent 
 and is of great value in determining the exact location of the 
 seat of the disease, for, as the cases here collected show, it in- 
 dicates that the lesion has involved the fibres of the pons 
 Varolii as they pass off into the cerebellum. Since several 
 of the cranial nerves pass out of the side of the pons, it is not 
 to be wondered at that the symptoms of unilateral cranial 
 nerve palsy and staggering should occur together. 
 
 The new cases here recorded for the first time show three 
 
AFFECTIONS OF THE BASE OF THE BRAIN. 119 
 
 phases or degrees of this symptom of staggering. In one case 
 the. patient fell to one side on attempting to stand. In all 
 three the patient staggered to one side in attempting to walk. 
 In one the patient ran around in a circle when he walked, and 
 in his epileptic attacks he ran about in a circle at the begin- 
 ning of an attack, a symptom which has received the name of 
 procursive epilepsy. It is interesting to observe that in all 
 these cases the staggering was toward the side of the lesion — 
 that side being indicated by the side of the cranial nerve palsy. 
 In the two cases of procursive epilepsy with autopsy reported 
 by Bricon, 1 the lesion was found in one half of the cerebellum, 
 and in a recently published case of Mairet 2 a sclerotic patch 
 was found in one hemisphere of the cerebellum. 
 
 CASE XVI. — UNILATERAL MULTIPLE CRANIAL NERVE 
 PARALYSIS. 
 
 Syphilitic Basilar Meningitis or Gumma — Staggering Toward 
 One Side. — The patient, a man of thirty, has been under my 
 observation since February, 1884, and has presented very in- 
 teresting symptoms. When first seen he was suffering from 
 severe headache in the occipital region, worse at night, from 
 insomnia, from vomiting, and from paresis of the right abdn- 
 cens and facial nerves. In the course of three months the right 
 trigeminus had also become involved, so that there was some 
 anaesthesia, analgesia, and disturbance of temperature sense in 
 the entire right half of the face, as well as slight paresis, and 
 internal strabismus with contraction of the right pupil. Then 
 vision began to be affected and a slight swelling of the optic 
 discs was seen with marked venous congestion, a beginning 
 optic neuritis. Under mercurial inunctions and one hundred 
 and fifty grains of iodide of potash daily these symptoms en- 
 tirely disappeared in three months, but after six months of 
 good health he again began to suffer from insomnia and head- 
 ache, and soon after a paresis of the right third nerve with ex- 
 ternal strabismus, dilatation of the pupil and slight ptosis, and 
 slight left hemiplegia developed. At this time the knee-jerk 
 
 1 Bourneville et Bricon: " Recherches Cliniques sur l'Epilepsie," Paris, 1888. 
 
 2 Mairet : Revue de Med., 18S9, pp. 147, 641. 741. 
 
120 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 was absent from the left knee and exaggerated in the right 
 knee, and the right half of his face was numb, but not anaes- 
 thetic. A. renewal of the treatment produced a subsidence of 
 the symptoms, so that in two months his eyes were straight 
 and the left half of his bod)- was as strong as the right. But 
 three months after this he again applied for treatment, this 
 time complaining of very great difficulty in walking owing to 
 vertigo, with a marked tendency to stagger and fall to the right 
 side, and almost total deafness in the right ear. The intensity 
 of the symptoms increased, and at the end of a month it was 
 found that the right third, fifth, seventh, and eighth nerves 
 were all paretic, and polyuria had developed so that he was 
 passing nearly three quarts of urine daily, which was, however, 
 free from sugar. At this time there was a slight weakness of 
 the left arm and leg, a very typical cerebellar gait, and a con- 
 tinued tendency to fall to the right. Specific treatment was 
 again prescribed, and in the course of two months all the 
 symptoms, except the polyuria and the tendency to stagger 
 toward the right side, had disappeared. Since November, 
 1886, he has had no return of the cranial nerve symptoms. In 
 January, 1890, when shown at the clinic, he still had a stagger- 
 ing gait w r ith marked turning toward the right side when walk- 
 ing with his eyes closed, a loss of knee-jerk in the left side 
 and exaggeration on the right side, and he complained of poly- 
 uria. All the cranial nerves were found to be normal, and 
 there was no evidence of hemiplegia. The urine was free from 
 sugar or albumin. The optic discs were clear. He had no 
 headache and he slept well. 
 
 The Situation and Character of the Lesion. — This man must 
 have had a syphilitic exudation upon the base of the brain 
 limited to the right side, advancing from one part to another 
 and invading at the outset the sixth and seventh, and later 
 the sensory part of the fifth and the third nerves; and lastly, 
 after subsiding in these two localities, appearing further back 
 and involving the eighth nerve, and affecting the right middle 
 peduncle of the cerebellum (Fig. 32 ). The fourth, motor fifth. 
 
AFFECTIONS OF THE BASE OF THE BRAIN. 121 
 
 ninth, tenth, eleventh, and twelfth, nerves were at no time in- 
 volved. The entire recovery from all cranial nerve symptoms 
 shows that the mass has been entirely absorbed. And the 
 permanence of the symptoms of polyuria and staggering gait 
 indicate rather a permanent destruction of tissue in the 
 medulla and middle peduncle of the cerebellum than the exist- 
 ence of continued pressure. Such a destruction of tissue, lim- 
 ited in extent, might easily have been produced by the ob- 
 
 Fig. 32.— The Base of the Brain. Unilateral syphilitic meningitis causing cranial nerve 
 paralysis in Case XVI. 
 
 struction of one or more branches of arteries entering the 
 lateral surface of the medulla in close contiguity with the sev- 
 enth and eighth nerves and resulting in an area of local anaemia 
 and softening. Such a condition was found post-mortem in 
 cases reported by Eisenlohr 1 and by Dr. Delavan, 2 the local 
 softening in the latter case having been limited to a small area 
 of the lateral part of the medulla, and causing in that case a 
 unilateral paralysis of the vocal cord. 
 
 1 Eisenlohr : Arch. f. Psych., xix., p. 314. 
 
 2 N. Y. Med. Rec, 1885, Feb. 14th (autopsy subsequently). 
 
[22 FAMILIAR FORMS OF NERVOUS DISEASE.. 
 
 Polyuria may be due to lesions in the middle third of the 
 medulla, near the floor of the ventricle and in the lateral part 
 of the formatio reticularis, Dr. Flatten having collected eleven 
 cases of this kind.' It has been observed frequently by Op- 
 penheim a as a complication of cerebral syphilis. Staggering 
 gait may be due to lesions of the cerebellar peduncles, as well 
 as of the middle lobe of the cerebellum in which these pedun- 
 cles terminate. It is interesting to note that the tendency to 
 stagger was toward the side of the lesion. This was also ob- 
 served in a case reported by Buzzard 3 in which a tumor in 
 the right side of the pons invading the right middle and infe- 
 rior peduncles caused a staggering toward the right side. It 
 was also present in a patient with brain tumor seen by me with 
 Dr. Peabody at the New York Hospital, in which the autopsy 
 showed the tumor to be located on the side of the pons. 
 
 In the following case a marked tendency to fall and to 
 stagger toward the left side was present, and the concomitant 
 symptom of alternating anaesthesia proved that here again the 
 lesion was in the pons Varolii on the side toward which the 
 staggering occurred. 
 
 CASE XVII. — HEMORRHAGE IN THE LEFT MIDDLE CERE- 
 BELLAR PEDUNCLE AND PONS. 
 
 Tendency to Turn and Fall Toward the Left Side — Alter- 
 nating Anaesthesia. — A healthy but hard-working engineer was 
 suddenly seized with vertigo, headache, and vomiting, and 
 with double vision, difficulty in swallowing and speech, and 
 numbness in the left side of the face and right side of the body 
 and right limbs. These symptoms gradually passed off to 
 some extent, but when seen two weeks after the attack, he 
 was found to have partial anaesthesia of the left half of the 
 face, and of the entire right side of the body from the level of 
 the neck downward, and paresis of the left sixth nerve causing 
 a partial internal strabismus. These symptoms seemed suffi- 
 cient to locate the lesion in the lower half of the pons Varolii 
 
 1 Arch, for Psych., xiii., 671. 
 
 - Oppenheim : Berl. klin. Woch., 1889, No. 48. 
 
 3-Brain, 1888. 
 
AFFECTIONS OF THE I! ASF OF THE BRAIN. 123 
 
 upon the left side, and in the absence of cardiac or arterial 
 disease the lesion was thought to be a hemorrhage' (Fig. 3.3). 
 The chief feature of interest was the disturbance of his 
 gait and equilibrium, a symptom which had been present from 
 the onset. He staggered much in walking, although not par- 
 alyzed, and he turned toward or fell toward the left side when- 
 ever he started to walk. He had no vertigo, but on rising 
 from a seat would fall over to the left unless supported. This 
 
 Right Cms. 
 
 R. V. N 
 
 Pons. 
 
 Middle Cerebellar I ^' r >^ 
 
 Peduncle. \ 
 
 V. N. Nucleus 
 
 Sensory Tract C 
 
 Fig, 33. — The Crura Cerebri, Pons, and Medulla showing the Sensory Tracts, and a Lesion 
 producing Alternating Anaesthesia and Staggering toward the Left. Case XVII. 
 
 symptom did not appear to be increased by the closure of 
 his eyes. There was no ataxia of the limbs. In the course 
 of two months after the attack the diplopia had disappeared; 
 the anaesthesia, though present, was less; but the gait was still 
 very unsteady, with a marked tendency to stagger to the left. 
 At present, a year after the onset, he is able to walk, but has 
 still some traces of the anaesthesia and a tendency to stagger 
 to the left. 
 
 1 A case almost identical with this one is reported by Senator: Arch. f. Psych., xi. 
 
[24 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 In this connection the following case ma)' be recorded, as 
 it presents the same feature prominent in the preceding case 
 viz., a tendency to turn to one side in walking, but in a much 
 more marked degree. It also offers an example of procursive 
 epilepsy. 
 
 CASE Will. — PROCURSIVE EPILEPSY IN A DEAF-MUTE. 
 
 Rotation to the Left in Walking. — A boy now (January, 1890) 
 aged seven years was apparently a healthy baby until the age 
 of seven months, when he suddenly had a series of convulsions, 
 since which time he has been deaf and dumb. For a month 
 after the convulsions he was paralyzed upon the left side of 
 his body, but this hemiplegia passed off within two months, 
 and no trace of it now remains except that the arm and leg 
 upon the left side are smaller and not as well developed as 
 those on the right, all movements, however, being perfect, 
 without rigidity or increase of reflexes. He still has occa- 
 sional attacks of epilepsy, and these are of the procursive 
 variety; for he runs forward and to the left in an attack. He 
 is still deaf and dumb and is manifestly wanting in intelligence, 
 though he has not the appearance of an imbecile. He no- 
 tices everything about him, but puts everything he can get 
 hold of into his mouth, eating all sorts of things without re- 
 gard to taste. He cannot be taught to keep himself clean. 
 The feature of particular interest, however, is his tendency to 
 move about in a circle whenever he is not held. If put down 
 on the floor he begins at once to run around toward the left 
 side. Even when standing he will turn about toward the left 
 from time to time. This tendency is so uniform that at home 
 he is kept tied to a chair. It has been present ever since he 
 began to walk. The condition is very similar to that observed 
 in animals after a unilateral operation upon the cerebellum. 
 
 The nature and position of the lesion in this case cannot 
 be determined, there being no other symptoms of a localizing 
 nature, but when compared with other cases it seems proba- 
 ble that the symptom of turning to the left indicates that the 
 left middle peduncle of the cerebellum is diseased. 
 
AFFECTIONS OF THE BASE OF THE BRAIN. 125 
 
 In concluding this chapter upon affections of the base, one- 
 additional set of symptoms, sometimes overlooked, may be 
 mentioned. They are due to a disturbance of vaso-motor 
 control. 
 
 The vaso-motor centre lies in the medulla and lesions in 
 the upper half of the medulla produce marked vaso-motor 
 symptoms. They consist of a general vaso-motor paralysis 
 with flushing of the surface and sensation of heat, and of ab- 
 normal sweating. Polyuria and glycosuria may also be caused 
 by its destruction. The vaso-motor centre is bilateral, and 
 each centre controls the circulation on its own side of the 
 body. Lesions in its area are so likely to cause sudden death 
 that but few cases can be found in which it was affected. But 
 the symptoms of a vaso-motor character are to be looked for 
 in any case of medullary lesion, and when such symptoms are 
 limited to one lateral half of the body, and are associated with 
 other symptoms of bulbar disease, they are valuable as signs 
 of the situation of the lesion. 
 
 There are a few general symptoms which have been not 
 infrequently observed in disease of the base which require 
 mention. General convulsions is the most constant of these. 
 The majority of sudden lesions (hemorrhage, embolism) in 
 the pons are ushered in by general convulsions, followed by 
 coma. Nothnagel established the fact that in animals irrita- 
 tion of the pons produces general convulsions, and hence 
 authors have spoken Of a convulsive centre in the pons. This 
 centre will be alluded to in discussing epilepsy. When the 
 lesion is a tumor or a sclerosis — i.e., a gradually increasing 
 lesion — convulsions rarely occur. Headache, disturbance of 
 vision, vertigo, and psychical changes have been frequently 
 observed in connection with diseases of the pons and medulla, 
 but they are to be ascribed to changes in the circulation or 
 internal cranial pressure, and not to any special local lesion. 
 Hemiplegia and hemianesthesia often occur in lesions on the 
 base when the motor or sensory tracts which pass through the 
 cerebral axis are affected. Such lesions have already been 
 considered in Chapter VIII. 
 
CHAPTER X. 
 
 THE LOCALIZATION OF SPINAL CORD DIS- 
 EASES. 
 
 The functions of the spinal segments. The relation of the segments to 
 the vertebrae. — Diagnostic symptoms of local spinal lesions at various 
 levels; (i) extent and character of the paralysis; (2) condition of 
 reflex action ; (3) distribution of sensory disturbance ; (4) position 
 assumed by the limbs. 
 
 THE FUNCTIONS OF THE SPINAL SEGMENTS. 
 
 The localization of the functions of the gray matter of the 
 spinal cord has been determined within the past six years. 
 The first observations upon the subject were made by Gowers 
 and Ross in England, and by Erb and Remak in Germany; 
 they were based on but a few cases of disease. The numer- 
 ous facts bearing upon the accurate localization of functions 
 were first collected in 1884. 1 The careful microscopic study 
 of the structure of each spinal segment in man, as compared 
 with the structure of corresponding segments in fishes, birds, 
 rabbits, dogs, oxen^ and monkeys, furnished much valuable in- 
 formation. The review of the physiology of the various seg- 
 ments as investigated by Ferrier and Yeo, offered another set 
 of facts. The study of numerous cases of congenital malfor- 
 mation of the cord and of the atrophy occurring in it after 
 amputation produced a further line of evidence. And lastly, 
 the pathological data derived from a collection of forty cases 
 of anterior poliomyelitis, with autopsies, and of a still larger 
 number of cases of syringo-myelitis and of transverse lesions 
 at different levels, afforded ground, when compared with the 
 
 1 Starr : Amer. Jour, of Neurol, and Psychiatry, August, 1884. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 127 
 
 data furnished by these other meth- cfjJn 
 
 ods of investigation, for some defi- ^^Sta^ft^ 
 
 nite conclusions which were em- C1 <\z\x 'J 
 
 bodied in a table. 2 (^^ll „ 4 
 
 The accuracy of these conclu- 3 /^ lEl-« 
 
 sions has been attested by a large 6 ^JpQ.. 
 
 number of cases published during 6 £^etK "7 
 
 the last six years in various coun- 7 C^J ^^) -a 
 
 tries by different observers. 1 In c» <^J z M^i-- 
 
 only a few particulars has it been g (/J^WJ^^ ** 
 
 necessary to modify or to correct _ /^f*^p^.... 
 
 them. Such corrections have been YM j|j^ 
 
 embodied in the table presented on y I w.54 - -5 
 
 pages 128 and 129. 5 wYW&i 
 
 <> (a&&L — f 
 
 RELATION OF SEGMENTS TO VER- V /\^S^ ""9 
 
 TEBR.E. 8 C^ l0 |Os. 
 
 The relation of the various seg- , ^'^ar^ 
 ments of the cord to the bodies i\Jlf:'lli22n ' 
 and spines of the various vertebrae, . /li\™LJL-~ 
 must be known as a preliminary to r^TOSHLHj 
 the consideration of spinal surgery. L1 \^|fl||r^' 
 As the cord extends only to the 2 L^M|lt£r^~ 
 level of the second lumbar vertebra, 3 f\J& flL^j. 
 its various segments do not lie oppo- ' 
 site to the vertebrae from which they ZWIIlllit^— 
 are named. The accompanying dia- 
 gram of Gowers displays the mutual S L W~S^ -|s 
 
 relation between the segments and 
 their nerves, and the bodies of the 
 vertebrae, and no further description 
 
 is needed. VfflN 
 
 - co. 
 
 1 The table has been reproduced in Pep- 
 per's System of Medicine, in Schmidt's Jahr- 
 
 buch, in Edinger's Vorlesungen, 2d edition, in FlG ' 34--The Mutual Rel; 
 
 ,,.,,, ' . . the Vertebral Bodies and Spines to the 
 
 Mills Monograph on Spinal Localization, and Segments of the Cor d and to the Exit 
 
 elsewhere. of the Nerves. (GoweFS.) 
 
[28 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 LOCALIZATION OF THE FUNCTIONS OF THE SEGMENTS OF 
 THE SPINAL CORD. 
 
 Segment. 
 
 Muscles. 
 
 Keflex. 
 
 Sensation. 
 
 II. and 
 
 Sterno- mastoid. 
 
 Hypochondrium (?). 
 
 Back of head to 
 
 III. C. 
 
 Trapezius. 
 
 Sudden inspiration pro- 
 
 vertex. 
 
 
 Scaleni and neck. 
 
 duced by sudden pres- 
 
 Neck. 
 
 
 Diaphragm. 
 
 sure beneath the lower 
 border of ribs. 
 
 
 IV. C. 
 
 Diaphragm. 
 
 Pupil. 4th to 7th cervical. 
 
 Neck. 
 
 
 Deltoid. 
 
 Dilatation of the pupil 
 
 Upper shoulder. 
 
 
 Biceps. 
 
 produced by irritation 
 
 Outer arm. 
 
 
 Coraco-brachialis. 
 
 of neck. 
 
 
 
 Supinator longus. 
 
 
 
 
 Rhomboid. 
 
 
 
 
 Supra and infra spinatus. 
 
 
 
 V. c. 
 
 Deltoid. 
 
 Scapular. 
 
 Back of shoulder and 
 
 
 Biceps. 
 
 5th cervical to ist dorsal. 
 
 arm. 
 
 
 Coraco-brachialis. 
 
 Irritation of skin over the 
 
 Outer side of arm 
 
 
 Brachialis anticus. 
 
 scapula produces con- 
 
 and forearm, front 
 
 
 Supinator longus. 
 
 traction of the scapular 
 
 and back. 
 
 
 Supinator brevis. 
 
 muscles. 
 
 
 
 Rhomboid. 
 
 Supinator longus. 
 
 
 
 Teres minor. 
 
 Tapping its tendon in wrist 
 
 
 
 Pectoralis (clavicular part). 
 
 produces flexion of fore- 
 
 
 
 Serratus magnus. 
 
 arm. 
 
 
 VI. c. 
 
 Biceps. 
 
 Triceps. 
 
 Outer side of fore- 
 
 
 Brachialis anticus. 
 
 5th to 6th cervical. 
 
 arm, front and 
 
 
 Pectoralis (clavicular part). 
 
 Tapping elbow tendon 
 
 back. 
 
 
 Serratus magnus. 
 
 produces extension of 
 
 Outer half of hand. 
 
 
 Triceps. 
 
 forearm. 
 
 
 
 Extensors of wrist and 
 
 Posterior wrist. 
 
 
 
 fingers. 
 
 6th to 8th cervical. 
 
 
 
 Pronators. 
 
 Tapping tendons causes 
 
 
 
 
 extension of hand. 
 
 
 VII. c. 
 
 Triceps (long head). 
 
 Anterior wrist. 
 
 Inner side and back 
 
 
 Extensors of wrist and 
 
 7th to 8th cervical. 
 
 of arm and fore- 
 
 
 fingers. 
 
 Tapping anterior tendons 
 
 arm. 
 
 
 Pronators of wrist. 
 
 causes flexion of wrist. 
 
 Radial half of tho 
 
 
 Flexors of wrist. 
 
 Palmar. 7th cervical to 
 
 hand. 
 
 
 Subscapular. 
 
 ist dorsal. 
 
 
 
 Pectoralis (costal part). 
 
 Stroking palm causes 
 
 
 
 Latissimus dorsi. 
 
 closure of fingers. 
 
 
 
 Teres major. 
 
 
 
 VIII. c. 
 
 Flexors of wrist and 
 
 
 Forearm and hand, 
 
 
 fingers. 
 
 
 inner half. 
 
 
 Intrinsic muscles of hand. 
 
 
 
LOCALIZATION OF SPINAL COL/) DISEASES. 129 
 
 LOCALIZATION OF THE FUNCTIONS OF THE SEGMENTS OF 
 THE SPINAL CORD. 
 
 Segment. 
 
 Muscles. 
 
 Reflex. 
 
 Sensation. 
 
 I. D. 
 
 Extensors of thumb. 
 Intrinsic hand muscles. 
 Thenar and hypothenar 
 eminences. 
 
 
 Forearm, inner half. 
 Ulnar distribution to 
 hand. 
 
 II. to 
 XII. D. 
 
 Muscles of back and 
 
 abdomen. 
 Erectores spinae. 
 
 Epigastric. 4th to 7th 
 
 dorsal. 
 Tickling mammary region 
 
 causes retraction of the 
 
 epigastrium. 
 Abdominal. 7th to nth 
 
 dorsal. 
 Stroking side of abdomen 
 
 causes retraction of 
 
 belly. 
 
 Skin of chest and 
 abdomen, in bands 
 running around 
 and downward cor- 
 responding to 
 spinal nerves. 
 
 Upper gluteal 
 region. 
 
 I. L. 
 
 Ilio-psoas. 
 
 Sartorius. 
 
 Muscles of abdomen. 
 
 Cremasteric. 1st to 3d 
 
 lumbar. 
 Stroking inner thigh 
 
 causes retraction of 
 
 scrotum. 
 
 Skin over groin and 
 front of scrotum. 
 
 II. L. 
 
 Ilio-psoas. Sartorius. 1 Patella tendon. 
 Flexors of knee (Remak). Striking tendon causes ex- 
 Quadriceps femoris. tension of leg. 
 
 Outer side of thigh. 
 
 III. L. 
 
 Quadriceps femoris. 
 Inner rotators of thigh. 
 Abductors of thigh. 
 
 
 Front and inner side 
 of thigh. 
 
 IV. L. 
 
 Abductors of thigh. 
 Adductors of thigh. 
 Flexors of knee (Ferrier). 
 Tibialis anticus. 
 
 Gluteal. 
 
 4th to 5th lumbar. 
 
 Stroking buttock causes 
 dimpling in fold of but- 
 tock. 
 
 Inner side of thigh 
 
 and leg to ankle. 
 Inner side of foot. 
 
 V. L. 
 
 Outward rotators of thigh. 
 Flexors of knee (Ferrier). 
 Flexors of ankle. 
 Extensors of toes. 
 
 
 Back of thigh, back 
 of leg, and outer 
 part of foot. 
 
 I. to II. 
 
 S. 
 
 Flexors of ankle. 
 
 Long flexor of toes. 
 
 Peronei. 
 
 Intrinsic muscles of foot. 
 
 Plantar. 
 
 Tickling sole of foot 
 causes flexion of toes 
 and retraction of leg. 
 
 Back of thigh. 
 Leg and foot, outer 
 side. 
 
 III. to 
 V. S. 
 
 Perineal muscles. 
 
 Foot reflex. Achilles 
 
 tendon. 
 Overextension of foot 
 
 causes rapid flexion ; 
 
 ankle-clonus. 
 Bladder and rectal centres. 
 
 Skin over sacrum. 
 
 Anus. 
 Perineum. Genitals. 
 
130 
 
 FAMILIAR FORMS OF NERVOUS DISEASE, 
 
 SYMPTOMS OF SPINAL LESIONS. 
 
 In any case of spinal disease in which the location and 
 
 extent of the lesion are to 
 be determined, four sets of 
 symptoms are to be studied. 
 
 First, the extent of the 
 paralysis, and the exact mus- 
 cles which have atrophied 
 and have lost their faradic 
 reaction. Secondly, the con- 
 dition of the reflexes : those 
 which are lost; those which 
 are exaggerated ; those which 
 are normal. Thirdly, the ex- 
 act distribution of the region 
 of anaesthesia. Fourthly, 
 the position instinctively as- 
 sumed by the limbs. 
 
 I. In regard to the extent 
 and character of the paralysis, 
 it is always to be remem- 
 bered that a muscle may be 
 paralyzed from two separate 
 spinal lesions: first, because 
 voluntary impulses from the 
 brain to the spinal motor 
 centres are cut off; secondly, 
 because the spinal motor 
 centres are destroyed. In 
 the first case, when the dis- 
 ease is confined to the lateral 
 pyramidal columns of the 
 cord, and when impulses can- 
 not reach the healthy spinal 
 centres, the muscle, though 
 paralyzed, does not atrophy 
 to any marked degree, and 
 
 Fig. 35. —Diagram of a Spinal Segment as a 
 Spinal Centre and as a Conducting Medium 
 (Bramwell). B, Right; £', left hemisphere; .MO, 
 medulla oblongata; 1, motor tract from right 
 hemisphere; at M O it divides into a direct and a 
 crossed tract, the former passes down the right 
 ant. median column, the latter passes down the 
 left lateral column, giving off at 1' fibres to the 
 ant. gray horns of the cord, in which the motor 
 cells lie, from which nerves pass to muscles, M ; 
 3, motor tract from left hemisphere; .T, S', sensi- 
 tive areas on the left side side of the body; 3, 3' 
 the main sensory tract from the left side of the 
 body; it passes into the post, gray matter of the 
 segment, then decussates, and passes up the right 
 half of the cord in the post, columns, thence to 
 the right hemisphere of the brain; 4, 4', the main 
 sensory tract from the right side of the body; 5, 6, 
 the tracts of muscular sense from the legs, passing 
 up upon the same side of the spinal cord in which 
 it enters, in the column of Goll, decussating at the 
 medulla, above the motor decussation. The ar- 
 rows indicate the direction of nerve currents. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 
 
 131 
 
 preserves its power of normal response to the faradic and gal- 
 vanic currents. It has a firm consistence and may indeed be 
 quite rigid, and its contractility to percussion may be exag- 
 gerated. This is the first type of spinal paralysis. In the 
 second case, when the disease involves the gray matter and 
 destroys the group of cells which governs the muscle, the 
 muscle is not only paralyzed but also much atrophied, and 
 loses its power of contraction when the faradic current is ap- 
 plied, either entirely or in great part. Its power of contrac- 
 tion to galvanic stimulus may be changed, both diminished, 
 
 S.I. 
 
 Fig. 36. — Lateral Sclerosis (Gowers.) 
 The situation of the lesion producing the 
 first type of spinal paralysis. 
 
 Fig. 37. — Ant. Poliomyelitis. The atrophy of 
 the right anterior horn produced paralysis of the 
 second type in the peroneal and post, tibial 
 groups of muscles. Patient died at age of 28, 
 paralysis came on at age of 7. 
 
 so that the contractions obtained are slow and require a 
 stronger current to produce them, and also altered, so that the 
 muscle responds more actively to the positive than to the 
 negative pole (the so-called reaction of degeneration). The 
 muscle feels flabby and is relaxed, its muscular tone is dimin- 
 ished and it does not contract on percussion. This is the 
 second type of spinal paralysis. 
 
 The importance of the careful separation of these different 
 types of paralysis cannot be exaggerated, since the line of 
 treatment may be determined by the condition found. Thus 
 in one case studied at the clinic, it was found that all the 
 muscles below the waist were partially paralyzed ; but the 
 muscles of the abdomen and anterior surface of both thighs 
 
132 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 were atrophied, flabby, and failed to react to faradism, while 
 all the other muscles of the thighs and legs were of natural 
 size, were' rigid, their muscular contractility to percussion was 
 increased, and the electric contractility was normal. The 
 patient had fallen from a wagon and injured his dorsal 
 spine, there being a marked deformity from the ninth to the 
 twelfth dorsal vertebra,'. The question to be decided, nine 
 months after the injury, was the possibility of recovery from 
 the paralysis by a surgical operation on the spine which 
 should cprrect the deformity and remove pressure from the 
 spinal cord. This was decided in the negative, because the 
 atrophic paralysis of the quadriceps femoris indicated that 
 at the level of the second and third lumbar segments the cord 
 had been so completely crushed as to destroy the gray matter 
 of the anterior horns, and this fact being certain, it seemed 
 probable that the condition could not be benefited by the 
 removal of pressure. The rigid non-atrophic paralysis in the 
 other muscles indicated that the lateral pyramidal motor col- 
 umns were thrown out of function, a symptom possibly pro- 
 duced by pressure and not necessarily associated with their 
 destruction. Hence this symptom alone might have led to 
 an operation for the relief of the pressure, had not the other 
 shown that a part of the gray matter was destroyed, and hence 
 that the columns were in all probability destroyed as well and 
 not merely compressed. Thus the electrical condition of the 
 different paralyzed muscles may determine the question of 
 surgical treatment. 
 
 In another case, to be described more fully later, in which 
 there was no paralysis of voluntary motion, although there 
 was an area of total anaesthesia and a loss of bladder and rec- 
 tal control, the absence of electrical changes in the muscles in 
 connection with the other symptoms was sufficient to locate 
 the lesion in the lowest sacral segments and exclude one in 
 the cauda equina which had at first been suspected. And this 
 fact also determined the question of surgical interference. 
 Hence it is absolutely necessary in every case of supposed 
 spinal lesion to test both the power and the electric reaction 
 in each muscle separately. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 133 
 
 II. In regard to the tendon reflexes, it is to be remembered 
 that the normal or increased state of the reflex implies the 
 integrity of the segment of the spinal cord governing that 
 reflex. Thus if the knee-jerk is present the lumbar segment 
 is in a normal state, is not destroyed by the disease. If the 
 knee-jerk is exaggerated, it must be either because the control- 
 ling action of the brain is cut off, as by an injury to the cord 
 higher up than the second lumbar segment, or because the 
 second lumbar segment is irritated by contiguous inflamma- 
 tory disease. The former will be ascertained by the existence 
 of other motor and possibly of sensory symptoms. The latter 
 will be evident from the history of the progress of the disease, 
 which must show evidence of acute or chronic myelitis. In 
 the latter condition the exaggeration of the reflex will soon be 
 succeeded by its diminution and its loss. 
 
 When a reflex is lost it may imply destruction of the seg- 
 ment of the cord governing that reflex; but it does not neces- 
 sarily do so. For if impulses to or from that segment do not 
 pass along the nerves, the reflex act will not be performed. 
 Hence it is necessary to examine for an area of anaesthesia 
 corresponding to the sensory nerve along which the impulse 
 is carried to the segment ; or for a condition of paralysis with 
 atrophy and reaction of degeneraton in the muscles supplied 
 by the nerve which conveys the impulse from the segment. 
 If neither of these is found alone, the segment is probably 
 diseased. 1 The condition usually found in an injury at one 
 level of the spinal cord is a loss of reflex acts performed by 
 the injured segments, and an exaggeration of the reflex acts 
 governed by the segments below the level injured. Thus in 
 the case just mentioned of destruction of the second and third 
 lumbar segments the knee-jerks were lost, but ankle-clonus 
 was excessive on both sides. 
 
 What has been said regarding the knee-jerk is true of all 
 the tendon reflexes, and also of the automatic action of the 
 bladder and rectum. 
 
 1 For an interesting study of tendon reflexes the reader is referred to " Lectures 
 on Diseases of the Nervous System," by Dr. Thomas Buzzard. 
 
134 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 III. In regard to the exact extent of the anaesthesia in 
 lesions at various levels the following' diagrams will convey a 
 better Idea than any description. 
 
 The first diagram (Fig. 38) shows the area of anaesthesia 
 when the lowest extremity of the cord or the nerves to it are 
 involved, viz., the coccygeal and fifth and fourth sacral seg- 
 ments and nerves. This area includes the perimeum and gen- 
 ital organs. When these segments are involved the action of 
 
 Fig. 38.— Area of Anaes- 
 thesia in Lesion of V. and 
 IV. Sacral Segments. 
 
 Fig. 39. — Area of Anaes- 
 thesia in Lesion of V., IV., 
 and III. Sacral Segments. 
 
 Fig. 40.— Area of Anaesthe- 
 sia from Lesion at V. Lumbar 
 Segment. 
 
 the bladder and rectum is always imperfect, and if they are 
 destroyed all control is lost. 
 
 The second diagram (Fig. 39) shows the area of anaesthesia 
 when the lesion involves the third sacral segment as well as 
 those below it. 
 
 The third diagram (Fig. 40) shows the area of anaesthesia 
 when the last lumbar and all the sacral segments are destroyed. 
 It will be noticed that up to this level all anaesthesia is on the 
 back of the limbs. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 135 
 
 The fourth and fifth diagrams (Figs. 41 and 42) show the 
 area of anaesthesia when the lesion lies as high as the third 
 lumbar segment. The inner side of the leg and thigh as well 
 as the back are anaesthetic. 
 
 From this point upward to the second dorsal segment the 
 band of anaesthesia about the trunk will correspond to the 
 nerve arising from the highest segment invaded. Thus in 
 a lesion of the second lumbar segment, the level of anaesthesia 
 
 Fig. 41. — Area of Anaesthesia from Le- 
 sion at III. Lumbar Segment. Back. 
 
 Fig. 42. — Area of Anaesthesia from Le- 
 sion of III. Lumbar Segment. Front. 
 
 follows the ilio-inguinal nerve, and the entire front of the thigh 
 is included in the insensitive area. At the dorsal segments it 
 corresponds to the level of the intercostal nerves (Fig. 43). 
 
 The areas of anaesthesia produced by lesions of the cervical 
 portion of the cord are shown in Figs. 44, 45, and 46. 
 
 When the lower portion of the cervical enlargement is in- 
 volved the area of anaesthesia reaches the armpits on the trunk 
 at the sides, and follows the line of the second dorsal inter- 
 costal nerve around the back. In front it is lower than behind, 
 because the upper part of the chest is supplied by the supra- 
 
136 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 clavicular nerves from the upper cervical segments. The 
 inner side and back of the arm in its lower half is anaesthetic, 
 and the zone of anaesthesia extends down the inner side and 
 back of the forearm and over the back of the hand, and of the 
 little, ring, and one-half of the middle fingers. In Fig. 44, 
 which represents the area of anaesthesia in a case of lesion of 
 
 the seventh and eighth cervi- 
 cal segments and the first dor- 
 sal segment described by 
 Thornburn,' the anterior sur- 
 face of the arm and the radial 
 side of the forearm, the thumb 
 and index finger had not lost 
 sensation. A case recently re- 
 ported by Macewen 2 pre- 
 sented identical symptoms. 
 In Fig. 45 is represented the 
 
 Fig. 43--Transvers e .Myelitis at VI. Dorsal Seg- afea Q f anaes thesia ill a Case 
 ment; Area of Anesthesia. Case XXV. 
 
 of lesion of the same level 
 described by Herter. 3 In a 
 case of cervical pachymenin- 
 gitis reported by Ross {Brain, 
 Vol. VII., p. 68, 1884) without 
 autopsy, the same distribution 
 of sensory disturbance was 
 observed. 
 
 When the middle of the cer- 
 vical enlargement is invaded 
 and the sixth segment of the 
 cord is destroyed, the area of 
 fig. 44.-injury at vii. Cerv. segment; Area of anaesthesia is about the same 
 
 Anaesthesia. (Thorburn.) . . 
 
 upon the trunk,but invades the 
 entire arm below the insertion of the deltoid. This is shown 
 in Fig. 46. This case was one of Brown-Sequard paralysis 
 
 1 Thornburn : " A Contribution to the Surgery of the Spinal Cord," p. 39. 
 2 Macewen: Brit. Med. Jour., April 5th, 1890. 
 
 3 Herter : Jour, of Nerv. and Ment. Dis., January, 1890. These cases confirm 
 the theoretical statements of Ross, Brain, 18S7, p. 342. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 
 
 137 
 
 from caries of the fourth cervical vertebra with displacement 
 and pressure upon the left side of the spinal cord. It is fully 
 described in the next chapter (Case XXVI II), and the lesion was 
 as high as the sixth segment. The patient died of respiratory 
 paralysis, when the disease invaded the fourth and third seg- 
 ments of the cord, and as death 
 usually occurs from this cause 
 
 Fig. 45.— Injury at VII. Cerv. Segment; Fig. 46. — Injury at VI. Cerv. Segment, on 
 
 Area of anaesthesia in lines; of hyperaesthesia, one side only. Area of anaesthesia in lines; area 
 dotted. (Herter.) of hypersesthesia dotted. Case XXVII. 
 
 when the disease is situated at this level, no opportunity is 
 offered for the determination of sensory disturbances in such 
 cases. 
 
 It will be seen from a review of these diagrams that the 
 investigation of the exact area of anaesthesia is of great im- 
 portance in determining the level of the cord which is involved. 
 The tests are to be made by touching the surface simul- 
 
138 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 taneously on both sides at symmetrical spots with cotton 
 wool, by pricking it with a needle, and by touching it with a 
 test-tube Containing both cold and hot water. The great in- 
 dividual variations in the perceptions of the points of a com- 
 pass -distinguishing two points from one — and the careful 
 attention on the part of the patient necessary to make this 
 test, has led me to discard it as a test of sensation. The point 
 of chief importance in testing sensation is to find some part 
 of the patient's body which is unaffected {e.g., in spinal lesions 
 the neck, the face being too keenly sensitive), and to always 
 compare affected parts of the surface with this part as a 
 standard. 
 
 IV. In regard to the position of the patient when lying in 
 bed after an injury of the spinal cord at one level, the follow- 
 ing facts may be stated : 
 
 If the lesion is near to and below the third lumbar seg- 
 ment, and irritates it but does not destroy it, the patient is 
 likely to lie with the thighs drawn up and legs flexed. 
 
 If the lesion is above the third lumbar segment, he will lie 
 with the thighs and legs extended ; unless the lesion produces 
 great irritation, as in the last stages of lateral sclerosis, when 
 the thighs and legs are flexed and adducted. 
 
 If the lesion is about the two lower cervical segments and 
 irritates the fifth and sixth segments, he will lie with his arms 
 abducted about at a right angle, his forearms flexed on the 
 arms, and hands supinated or their position dependent on 
 gravitation, and fingers flexed. 1 
 
 If the lesion is about the middle cervical segment, as high 
 as the fourth, the arms will lie at the sides and cannot be 
 moved, as occurred in my second case of Brown-Sequard par- 
 alysis (Case XXVIII.). 
 
 A word of explanation will show the reason for these posi- 
 tions. Supposing two muscles of opposing action to be set in 
 action at one and the same time, the stronger will overcome 
 the weaker. Suppose one of these to be paralyzed, as soon 
 
 'Examples of this position are given by Thorburn, 1. c. ; Herter, 1. c. ; and 
 Macewen, 1. c. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 139 
 
 as the other acts once voluntarily or when by irritation of its 
 cells it is kept in action, the resulting position cannot be cor- 
 rected, for its opponent will never contract again voluntarily. 
 In either case the result is a fixed position not usually the 
 normal one. 
 
 In cerebral paralysis, when voluntary movements are cut 
 off from the arm, the arm is adducted, the forearm is held in 
 a flexed and supinated position, and the fingers are flexed; 
 because the balance of power between the abductors, exten- 
 sors, and pronators of the forearm and the adductors, flexors, 
 and supinators is in favor of the latter; all the impulses to 
 these muscles originating in the spinal cord. For the same 
 reason the leg is held rigid, somewhat adducted and extended, 
 in cerebral paralysis and in lateral sclerosis and in transverse 
 lesions of the cord when these are above the lower dorsal 
 region. Therefore the position of the affected limbs in cases 
 of hemiplegia, and of paraplegia from lateral sclerosis, is the 
 same and becomes a diagnostic symptom of an interference 
 of conduction of voluntary impulses from the brain to the 
 spinal cord — a symptom of cerebral paralysis, and of what has 
 been termed the first type of spinal paralysis. 
 
 In spinal paralysis from destruction of the gray matter, 
 that is, in the second type of spinal paralysis, the balance of 
 power between muscles holding the limb in position is in- 
 terfered with, because one or both sets of muscles have 
 entirely lost their tone. If one set alone is paralyzed the 
 other acts unopposed. Thus in a transverse lesion of the 
 lower half of the cervical enlargement, the arms are ab- 
 ducted, flexed, and supinated, because the muscles producing 
 these movements are not paralyzed, and contract voluntarily 
 and reflexly, while their opponents, the adductors, extensors, 
 and pronators, are totally paralyzed and do not act. Such 
 a condition in the leg leads to various forms of talipes. If 
 both sets of muscles are paralyzed together, as in many cases 
 of infantile spinal paralysis, or in general myelitis, the limb 
 hangs flaccid and not rigid, and falls into any position from 
 the action of gravitation. The ligaments in such a limb soon 
 become overstretched, and hence extraordinary positions can 
 
'4° 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 be given to a limb passively in such cases. Examples are 
 found in the partial dislocation of the head of the humerus in 
 infantile paralysis of the shoulder muscles; and in the abnor- 
 mally free motion of the hip and knee when the muscles mov- 
 ing them are paralyzed. When firm contractions with mal- 
 positions — such as occur in the forms of talipes — are produced 
 in infantile paralysis, it is because one of the muscles moving 
 the joint is not entirely paralyzed. A contracture does not 
 result when there is total paralysis of all the muscles moving 
 a joint. 
 
 ******* 
 In the majority of cases of spinal injury with crushing of 
 the cord or with acute transverse myelitis, and also in cases of 
 slow compression of the cord, the four classes of symptoms 
 here described are present together. It is thus possible to 
 confirm or to rectify a diagnosis formed from the study of one 
 class of symptoms by that of the others; and thus to reach a 
 certainty in the diagnosis of the location of the spinal lesion. 
 
 THE FUNCTIONS OF THE SPINAL SEGMENT. 
 
 Thus far the consideration of the localization of functions 
 in the spinal cord has been directed to the various segments 
 as they lie one beneath another throughout the length of the 
 organ. This study would be incomplete were the functions of 
 the various portions of each segment not mentioned briefly. 
 The appearance of a cross-section of the cord in the cervical 
 region is shown in Fig. 47, and the division of the white col- 
 umns into tracts and of the gray matter into anterior and 
 posterior horns and central or intermediate gray substance is 
 familiar. 
 
 In the gray matter the anterior horns contain the groups 
 of cells whose various functions in controlling both the action 
 and nutrition of different muscles has already been studied. 
 It is thought that the anterior and lateral groups of cells in 
 the horn preside over the muscles controlling " fundamental 
 motions" common to all vertebrates, such as flexion and ex- 
 tension of joints; while the median and central groups of cells 
 
LOCALIZATION OF SPINAL CORD DJSEASLS. 
 
 HI 
 
 preside over " accessory motions " peculiar to monkeys and to 
 man, such as the finer movements of the hand, fingers, and 
 thumb, the nice motions of the ankle and toes in walking. 1 
 In the .central and intermediate gray matter of the cord lie 
 the vaso-motor centres which control the circulation and 
 nutrition of the skin, nails, joints, bones, and viscera. The 
 separate existence of motor and trophic cells is still un- 
 proven, but disease in the anterior or posterior horns alone is 
 not followed by trophic or vaso-motor changes in the parts 
 
 Fig. 47. —Diagram 01 a acciion of the Spinal Cord in the Cervical Region. (Gowers.) A.C., 
 Ant. commissure ; P. C, post, commissure; I.g.s., intermediate gray substance ; P. Cor., post, cornu ; 
 c.c.p., caput cornu post.; L.L.L., lateral limiting layer; AL-A T, anterolateral ascending tract. 
 
 just named, while in disease limited to this intermediate gray 
 matter (syringo-myelitis) the vaso-motor and trophic changes 
 form a very important group of symptoms. And the definite 
 group of cells known as the vesicular column of Clarke, which 
 lies at the junction of the posterior horn with the intermedi- 
 ate gray matter, has been proven by Gaskell to have vaso- 
 motor functions. In the posterior grayhorns the cells do not 
 lie in groups, but are scattered through a dense felt-like struc- 
 ture of fine fibres in which the sensory nerve roots terminate. 
 The white columns of the cord have been separated into 
 
 This distinction is made by Ross and supported by the observations of Spitzka. 
 
142 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tracts by means of the embryonal studies of Flechsig, and of 
 the pathological studies of numerous investigators from Tiirck 
 to Gowers. 
 
 The anterior median column, which comes from the ante- 
 rior pyramid of the medulla of the same side on which it lies, 
 and the lateral pyramidal tract, which comes from the ante- 
 rior pyramid of the medulla of the opposite side, serve to 
 transmit voluntary impulses and inhibitory impulses from the 
 motor region of the brain to the motor cells of the cord. The 
 anterior ground fibres which surround the anterior horn and 
 form an extensive column are chiefly short fibres associating 
 the various levels of gray matter with one another and thus 
 bringing their action into harmony. The two remaining col- 
 umns of the lateral portion of white matter, the direct cere- 
 bellar column, and the antero-lateral ascending tract (Gowers) 
 transmit impulses upward to the brain ; but what kind of im- 
 pulse is still undetermined. The posterior columns are sen- 
 sory in function, transmitting tactile and muscular sense im- 
 pulses upward. The posterior external column (Burdach) is 
 chiefly made up of short nerve root fibres which pass upward 
 and downward in it for a shorter or longer distance after en- 
 tering the cord before terminating in the posterior gray horns. 
 The posterior internal column (Goll), on the contrary, is made 
 up of long fibres passing directly up to the medulla, and 
 thence to the brain by way of the lemniscus. In this column 
 the sensations from the legs go up in the fibres lying near the 
 periphery of the cord ; while those from the arms go up in 
 fibres lying near to the posterior gray commissure. 
 
 It is of course possible that each of these tracts may be 
 diseased alone. As a matter of fact, there are but two spinal 
 affections in which such a limitation of disease to the white 
 tracts is found, viz., lateral sclerosis and locomotor ataxia. 
 The symptoms of lateral sclerosis have been incidentally de- 
 scribed already under the title of spinal paralysis of the first 
 type (p. 130). Those of locomotor ataxia will receive atten- 
 tion in a subsequent chapter. 
 
 It is also evident that all these tracts will be diseased to- 
 gether in transverse lesions of the cord, whether due to hem- 
 
LOCALIZATION OF SPINAL COL' D DISEASES. I4i 
 
 orrhage or to slow compression or to any other cause. The 
 chief symptoms of such lesions have been already considered 
 and need not be restated. It is always to be remembered, 
 however, that in a transverse lesion of the cord at any level, 
 the paralysis and anaesthesia in the parts below the lesion are 
 due to the destruction of the white columns which should 
 transmit voluntary impulses and sensory impressions to and 
 from those parts, but which are cut off by the lesion. 
 
 In any case of spinal disease where it is desirable to local- 
 ize accurately the lesion, it is suggested that a written sum- 
 mary of the symptoms be compared with the table of localiza- 
 tion of the functions of the cord, when it will become evident, 
 by contrasting the normal with the abnormal conditions, what 
 part of the cord is affected. As Bramwell justly observes, 
 " the essence of the clinical examination of the spinal cord 
 consists in the systematic and separate examination of each 
 spinal segment, by observing the motor, sensory, reflex, vaso- 
 motor, and trophic conditions of its body area/' Such an ex- 
 amination will lead to accurate diagnosis of local lesions. 
 
 If that lesion is one which can be removed, such as com- 
 pression by a tumor, or by a displaced vertebra, it is impor- 
 tant to remove it as soon as possible. For experience has 
 shown that a long-continued compression is followed by as- 
 cending and descending degeneration of the white columns of 
 the cord ; and this condition is believed to be permanent, and 
 remains after the pressure is removed. Hence in spinal sur- 
 gery, prompt action is of great importance. The fact is illus- 
 trated by the history of the first case of Brown-Sequard 
 paralysis (Case XXVI.), in which an earlier operation might 
 have resulted in a greater degree of improvement than was 
 obtained. 
 
CHAPTER XI. 
 
 THE LOCALIZATION OF SPINAL CORD DISEASES 
 (CONTINUED). 
 
 Cases of lesions at various levels of the cord. — Lower sacral. — Sacral and 
 lower lumbar. — Upper lumbar. — Cases of lesion of the cauda equina 
 contrasted with those of the lower segments of the spinal cord. — 
 Case of Brown-Sequard paralysis at the ninth dorsal level. Opera- 
 tion. Improvement. — Cases of transverse lesion in the ninth and 
 sixth dorsal regions. — Cases of transverse and unilateral lesions at 
 the lower and upper cervical levels. 
 
 CASES OF TRANSVERSE LESIONS AT VARIOUS LEVELS OF 
 THE CORD. 
 
 In the last chapter the principal facts which enable one to 
 locate a spinal lesion have been stated. In this chapter a 
 • number of typical cases of spinal lesion at different levels, 
 from below upward, are described in order to illustrate the 
 possibility of locating a spinal lesion when the foregoing facts 
 are kept in mind. 
 
 CASE XIX.— HEMORRHAGE INTO THE SPINAL CORD INVOLV- 
 ING THE COCCYGEAL AND FIFTH AND FOURTH SACRAL 
 SEGMENTS— SECONDARY MYELITIS ADVANCING UPWARD 
 TO THE SECOND SACRAL SEGMENT. 
 
 A young woman, previously healthy, was suddenly seized, 
 after long standing and walking, on May ist, 1889, with severe 
 pain in the sacral region and down the back of the legs; with 
 retention of urine and faeces, so that catheterization was nec- 
 essary from the first, and the bowels only moved after ene- 
 mata; and with total anaesthesia of the vulva and vagina and 
 
LOCALIZATION OF SPINAL CORD DISEASES. 
 
 '45 
 
 perinaeum, and of the back over the area shown in Fig. 38. 
 For six months this condition remained. The pain became 
 dull and less severe in the back, but in an area on the back of 
 the left thigh, corresponding to the region shown in Fig. 39, it 
 was very intense. The urine was retained if not drawn, or 
 would dribble away when the bladder had become full. De- 
 fecation was always attended with pain. The anaesthesia was 
 permanent. She felt rather weak but was not paralyzed, and 
 could perform all the motions of the feet and walk well. 
 There was no atrophy of the limbs, no girdle sensation, and 
 no electrical changes. 
 
 I saw her, with Dr. F. J. Quinlan, in October, 1889, and in 
 addition to the symptoms mentioned, found the knee-jerks 
 exaggerated, the plantar and gluteal reflexes normal and no 
 ankle-clonus. A careful exploration of the pelvis failed to 
 reveal anything abnormal. The diagnosis was made of hem- 
 orrhage into the spinal cord, and its situation was evident 
 from the distribution of the anaesthesia. The pain in the left 
 thigh indicated that some inflammatory or sclerotic process 
 was advancing from the fourth into the third sacral segment 
 on the left side. 
 
 I saw her again, in February, 1890. Then the subjective 
 symptoms had increased. She had less pain but more numb- 
 ness, and the anaesthetic area was found to have extended 
 down both thighs and corresponded quite exactly to the area 
 shown in Fig. 39, being a little larger on the left side. In 
 addition, a slighter degree of anaesthesia was found on the 
 outer side of the left leg in the area shown in Fig. 40. In the 
 peroneal group of muscles on this leg, the faradic contrac- 
 tility had diminished from 45 to 60 . 1 It was therefore evi- 
 dent that the inflammatory changes had advanced upward in 
 the cord, had involved the entire third sacral segment and a 
 part of the second sacral segment on the left side. As the 
 area of the thigh had become insensitive, it had also become 
 less painful, showing that the irritative lesion had been fol- 
 
 1 An arbitrary scale. This fact would show that the peronei were the muscles 
 represented lowest down in the cord at the second sacral. 
 10 
 
I4 6 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 lowed by a destructive lesion in the third sacral .segment. 
 The same objective symptoms persisted. In spite of the an- 
 aesthesia over the sacrum, there was no tendency to bed-son. 
 and in spite of the paralysis of the bladder, there was no cys- 
 titis. She could walk well and there was no paralysis, but she 
 found her left ley grew weary more quickly than before, a 
 fact which corroborated the weakened state of the peroneal 
 muscles found by the electric examination. Counter-irritation 
 by cautery and cups, galvanism to the spine, iodide of potash, 
 and ergot had been faithfully employed but had not arrested 
 the progress of the disease. The possibility of a growing 
 tumor — which might have been removed — was ruled out on 
 account of the sudden onset and the absence of signs of pres- 
 sure upon the cauda equina, whose nerves lie all about the 
 sacral region of the cord. And the case was therefore thought 
 to be hopeless. 
 
 CASE XX.— COMPRESSION OF CAUDA EQUINA FROM POTT'S 
 DISEASE — SUBSEQUENT MYELITIS OF LUMBAR AND SAC- 
 RAL REGIONS. 
 
 The patient", a lady in middle life, was seen in June, 1887, 
 in consultation with Dr. V. P. Gibney, who was treating her 
 at that time for Pott's disease with marked deformity and 
 projection of the first lumbar vertebra. 2 Her legs were par- 
 alyzed, toe, ankle, and knee joints could not be moved volun- 
 tarily at all, and the motions of the hip joints, though possible 
 in all directions, were weak, especially upon the left side. 
 There was much atrophy and constant fibrillary twitchings of 
 the paralyzed muscles; and in all the muscles of the legs and 
 back of the thighs, including the glutei, there was a reaction 
 of degeneration. There was loss of tendon reflexes at the 
 knee and ankle, and of the abdominal and gluteal reflexes. 
 The area of anaesthesia was that shown in Figs. 41 and 42, 
 
 J Cases quite similar to this one have been recorded by KirchofT, Arch. f. Psych., 
 xv., p. 607; by Bernhardt, Berlin Klin. YVochen., Aug. Sth, iSSS; by Osier. Med- 
 ical News, Dec. 15th, iSSS; by Oppenheim, Arch. f. Psych., 18S9, xx., p. 298, with 
 autopsy; and by Mills. Medical News, March 1st, 1S00, Case II. 
 
 2 See Med. Record, Oct. 1st, 18S7; Dr. Gibney's report of this case. 
 
LOCALIZATION OF SPINAL CORD DISEASES 
 
 1 47 
 
 tactile sensations being lost and temperature and pain senses 
 being much impaired. On the front of the thighs, to the 
 knees and for a short distance below the knees on the front of 
 the leg, in the exact area which is not shaded in Fig. 42, she 
 was very hyperaesthetic, the least touch or cold application 
 giving her great pain. She had no girdle sensations and no 
 symptoms above the level of the hip joint in front. She lay 
 with legs extended, unable to move them. Her bladder and 
 rectum were under control for the first two months of her ill- 
 ness, during which time these symptoms had gradually devel- 
 oped, but then retention of urine and constipation set in, and 
 soon after a bed-sore developed over the sacrum. She grad- 
 ually grew worse during the summer and died of exhaustion 
 in February, 1888. The interesting feature in this case is the 
 existence of a hyperaesthetic area on the front of the thighs. 
 This is perfectly homologous to the band of hyperesthesia 
 found around the trunk above the anaesthetic band in cases of 
 dorsal myelitis, and is evidence of implication of the cord as 
 distinct from a lesion compressing the cauda equina. When 
 pain is present in cauda equina lesions, it is felt in the anaes- 
 thetic area, not in the area supplied by the nerves whose origin 
 is higher, as in myelitis. 
 
 Other points of differentiation manifest in this case were 
 the great atrophy, fibrillary twitchings, and reaction of degen- 
 eration in the muscles paralyzed, which indicate spinal cord 
 disease and are less marked in cauda equina compression. 
 Fibrillary twitching is not frequently seen in nerve injuries. 
 It is quite common when the gray matter of the cord is dis- 
 eased. The loss of bladder and rectal control is also very 
 common in spinal cord lesions and uncommon when the cauda 
 equina is compressed. 
 
 CASE XXI. — FRACTURE OF THE LOWER DORSAL SPINE— PAR- 
 APLEGIA FROM SPINAL INJURY AT THE SECOND LUMBAR 
 SEGMENT — THE QUESTION OF OPERATION. 
 
 The patient fell off a load of hay and broke his back in 
 November, 1888. For eight months he was confined to bed, 
 with total paralysis of motion and sensation below the waist 
 
i 4 S FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 and of bladder and rectal control. Then he gradually im- 
 proved, and in December, [889, was able to walk with help, 
 and came to the city to ascertain whether an operation upon 
 the spine would relieve his paralysis. The question was re- 
 ferred to me for decision by Dr. McBurney. 
 
 Though able to stand and to drag his feet along, his 
 powers of motion in the lower extremities were very bad. 
 The anterior thigh muscles were atrophied, relaxed, flabby, 
 and showed the reaction of degeneration. The other muscles 
 of the thighs and legs were rigid and moved with difficulty, 
 though their size and electric response were good. The legs 
 were cold and cyanotic. His abdominal and patella reflexes 
 were lost. Ankle-clonus was very active on both sides. 
 
 His urine dribbled away constantly, the sphincter being 
 paralyzed and his rectum could only be emptied by enemata. 
 His sensation was much impaired below the level of a band 
 passing around the trunk along the course of the ilio-hypo- 
 gastric nerves, above which a zone of hyperaesthesia one inch 
 wide was found. All sensations below this band were im- 
 paired, those of touch and pain to a considerable degree. He 
 was hypersensitive to cold, which was painful, but he did not 
 feel hot objects as hot. When any part of his leg was touched 
 he referred the sensation to some part of the thigh. His 
 knowledge of the position of his limbs was good. In walking, 
 his gait was spastic, the feet were dragged, the knees over- 
 lapped, and the trepidation from the feet would often become 
 so great as to necessitate his stopping for a moment. 
 
 There was a marked deformity with projection backward 
 of the spines of the ninth, ten, and eleventh dorsal vertebrae. 
 
 The symptoms pointed to a compression or a destruction 
 of the spinal cord at the second lumbar segment, which lies 
 opposite the eleventh dorsal vertebra, and their duration made 
 it probable that secondary degenerations had occurred. The 
 important question was whether there was a compression only 
 or also a destruction of the cord. The atrophy and reaction 
 of degeneration in the anterior thigh muscles, the loss of 
 knee-jerk and the zone of total anaesthesia in the region of the 
 iliohypogastric nerve, were thought to show the existence of 
 
LOCALIZATION OF SPINAL COLD DISEASES. 149 
 
 the destruction of the cord at that level. Hence the men 
 removal of compression was not thought advisable, since a 
 recovery from the paralysis was not possible, as the cord was 
 destroyed. 
 
 In contrast with these cases, in which the sacral and lum- 
 bar segments of the spinal cord were diseased, the following 
 cases are of interest. They are cases of injury of the cauda 
 equina, in which, however, the spinal cord was not affected. 
 Thorburn 1 and Mills 2 have directed attention to the possibil- 
 ity of differentiating spinal from caudal injuries. The chief 
 features of difference between the two classes of cases are 
 shown in the following cases. 
 
 CASE XXII. — HEMORRHAGE INTO THE SPINAL MEMBRANES 
 OF THE CAUDA EQUINA— NO LESION OF THE SPINAL 
 CORD. 
 
 A healthy man awoke, on November 10th, 1889, with ting- 
 ling and numbness in the back of both legs, especially in the 
 left one. The sensation was that of a foot asleep, and it ex- 
 tended up the back over the sacrum, down the back of the 
 thighs, and over the outer part as well as the back part of the 
 legs and soles of the feet. The perinseum and posterior part 
 of the scrotum were also numb and the rectum was partially 
 insensitive. This condition had remained about stationary, 
 when I saw him, in January, 1890, and was the only symptom 
 from which he had suffered. An examination showed an area 
 of hyperaesthesia corresponding to that shown in Fig. 41, 
 the anterior part of the thigh and the inner part of the leg 
 and foot having escaped. In the hyperaesthestic area, there 
 was much pain and tingling produced by the slightest touch, 
 and a very great hypersensitiveness to pain and to heat and 
 to electricity. He was not paralyzed, his motor power and 
 coordination were good, his muscles showed normal electrical 
 reaction, and had not atrophied. His reflexes were normal 
 and he had no loss of bladder or rectal control and no pain. 
 
 1 Thorburn: Brain, 1888. 
 
 2 Mills: Medical News, June 15th, iSSg, and March 1st, 1890. 
 
150 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 He had suffered from bleeding piles, which had been cured 
 just before the onset of these symptoms. 
 
 The tingling and hypersensitiveness certainly indicated an 
 irritation of all the sensor)- nerves of the sacral plexus. But 
 the absence of paralysis, atrophy, and bladder symptoms and 
 the preservation of normal reflexes negatived any spinal cord 
 disease. A careful pelvic examination by the rectum failed 
 to show anything abnormal there. And the sudden onset of 
 the symptoms and their stationary character ruled out the 
 possibility of either a pelvic or a spinal tumor. The posterior 
 roots of the sacral plexus must have been involved in a sud- 
 den pressure, and the only diagnosis remaining was a hemor- 
 rhage in the meninges about the Cauda equina, and chiefly on 
 its posterior surface; a diagnosis which was aided by the 
 probability of unusual venous congestion of the caudal veins 
 in consequence of the suppression of a customary hemorrhage 
 from the piles. 
 
 This case is interesting, since it serves to indicate the ne- 
 cessity of some care in diagnosis. The sensory symptoms alone- 
 might have been due to spinal cord disease and have led to 
 its diagnosis; but the absence of motor and reflex disturb- 
 ances and the integrity of the automatic action of the bladder 
 and rectum showed conclusively that the cord itself was not 
 the seat of disease. 
 
 CASE XXIII. — TUMOR (?) COMPRESSING THE CAUDA EQUINA. 
 
 The patient had strained his back in lifting a heavyweight 
 in August, 1889. He soon began to suffer from pain in the 
 sacral region, which has gradually increased to the present 
 time (April, 1890). This pain has been extending (always 
 being greater on the left side) at first into the area represented 
 in Fig. 39, then down the entire back of the thighs and legs ; 
 and now he has considerable pain over all the region indicated 
 in Fig. 41 ; a girdle sensation running along the ilio-inguinal 
 area and a moderate degree of anaesthesia in the region 
 represented in Fig. 40. During his illness he has become 
 progressively weaker and thinner in his lower limbs and now 
 
LOCALIZATION OF SPINAL CORD DISEASES. 151 
 
 ec 
 
 walks with a shuffling gait. 
 The muscles do not show 
 any change of electrical 
 reaction. His knee-jerks 
 are increased. His blad- 
 der and rectum act slowly, 
 but he has not lost control 
 over them. 
 
 The gradual onset in- 
 dicates either a tumor or 
 chronic meningitis or a 
 chronic myelitis. The po- r 
 sition of the girdle sensa- M 
 tion is such as to locate a 
 myelitis as high as the 
 second lumbar segment — 
 a point opposite the 
 eleventh dorsal vertebra 
 — a point much higher 
 than the seat of pain. The 
 hypothesis of a myelitis 
 here is negatived by the 
 preservation of the re- 
 flexes, by the preservation 
 of electrical reaction and 
 absence of much atrophy, 
 and by the absence of 
 pain and anaesthesia about 
 the front of the thigh and 
 leg, which are related to 
 the upper lumbar region, 
 and by the fact that the 
 symptoms are more on the 
 left side. Thorburn says 
 that if symptoms are asym- 
 metrical we have to do 
 with an affection of the 
 cauda rather than of the 
 cord. The slow progress 
 
 nAW 
 
 Fig. 48.— The Spinal Cord, the Spinal Nerves, the 
 Cervical, Lumbar, and Sacral Plexuses, and the Cauda 
 Equina. (Ferrier.) 
 
15- 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 of the case also negatives the hypothesis of a myelitis. In 
 myelitis of such duration bed-sores would be expected. The 
 hypothesis of a tumor is supported by the progress and by the 
 character and distribution of the- symptoms, especially by the 
 preservation of the reflexes and the control over the sphincters. 
 Thorburn' has shown that when the cauda equina is compressed 
 the symptoms appear in the nerves which lie within the cauda 
 and not on its surface— that is, in the sacral rather than in the 
 lumbar nerves. This statement is supported by the cases ob- 
 served by Osier-' and by Mills. 3 When, therefore, the area 
 of anaesthesia is as extensive as that shown in Figs. 40 and 41, 
 but the degree of paralysis is too slight and the preservation 
 of reflex and automatic activity too great to indicate a lesion 
 of the spinal cord in the third lumbar segment, the diagnosis 
 of compression of the cauda equina by tumor or by chronic 
 meningitis seems warranted. This will be confirmed if the 
 seat of pain is low down on the back, much lower than the 
 level of a spinal lesion would be. 
 
 The importance of differentiating tumors compressing the 
 cauda equina from myelitis of the spinal cord cannot be ex- 
 aggerated, since operations for the former condition are indi- 
 cated, while operations for the latter are impossible. 
 
 CASE XXIV. — ACUTE MYELITIS OF THE LUMBAR AND SACRAL 
 
 REGIONS. 
 
 Martin M., aged twenty-two, had been a perfectly healthy 
 man until the onset of his illness in April, 1881. While lifting 
 a heavy weight he suddenly felt a sharp pain in the lower part 
 of his spine, a numb sensation beginning at the hips and de- 
 scending to the feet, and a feeling of weakness in his legs so 
 that he fell to the ground and was unable to rise or move his 
 lower extremities. He was picked up and taken to a hospital, 
 where all the symptoms of complete paraplegia were found. 
 
 'Thorburn: Brain, 1887, vol. x., p. 381; see especially Cases II. and III., 
 which resemble this case in every particular. 
 
 a Osler: Medical News, 1888, vol. iii., p. 669. 
 3 Mills: Medical News, 1890, vol. vi., p. 217. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 153 
 
 For a week after the attack he had total loss of sensation and 
 of motion in the lower half of his body, and incontinence of 
 urine and faeces; and within three weeks large bed-sores had 
 developed over the sacrum and on both trochanters. There 
 was a slight return of sensation during the second week, but 
 no recovery of motor power; and within a month a constant 
 fibrillary tremor in the muscles of the legs was noticed, which 
 has continued. 
 
 He was transferred to Bellevue Hospital in November, 
 1881, seven months after the onset of the paraplegia, in a con- 
 dition in no way different, according to his own account, from 
 that present the day after the attack. 
 
 Examination revealed the following facts: 
 
 The patient is a large, fat man, well nourished, and shows 
 no traces of suffering. He is totally paralyzed in the lower 
 extremities and trunk below the middle of the spine. The 
 muscles are relaxed, there is no rigidity or contracture, there 
 is a marked fibrillary tremor, and the muscles are much atro- 
 phied, though the development of fat preserves the contour 
 of the limbs. All reflexes are abolished. There is a total 
 loss of faradic contractility, and reaction of degeneration in 
 all the muscles of both legs. 
 
 Sensations are almost wholly lost below the level of the 
 ninth dorsal nerve, although he is aware of deep pricking in 
 the right leg, feeling slightly the touch of the sharp instru- 
 ment, but no pain. Temperature and pain sensations are 
 wholly lost, but he is aware of the tremors in the muscles of 
 the legs, and can estimate imperfectly the position of the 
 limbs. A zone of hyperesthesia two inches wide extends 
 around the body above the ninth dorsal nerve. 
 
 There are no vaso-motor or trophic disturbances in the 
 legs, but the large bed-sores over the thighs and sacrum re- 
 main. These have exposed the bones, but the parts are in- 
 sensitive. There is incontinence of urine, and a chronic cys- 
 titis is present. The faeces are passed involuntarily. 
 
 The patient remained in a stationary condition for a 
 month. He then developed an acute purulent myocarditis — 
 described by Dr. Wm. H. Welch before the American Associ- 
 
154 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 ation of Physicians and Pathologists, [886 and died suddenly 
 
 of heart failure. 
 
 topsy. — There was considerable opposition to a post- 
 mortem examination by the friends, so that it was impossible 
 to obtain the entire spinal cord. The portions below the first 
 dorsal vertebra were, however, secured. The pia mater cover- 
 ing the cord was congested. At the level of the tenth dorsal 
 segment of the cord a region of marked softening was found 
 about half an inch in length. Section at this point showed 
 such a degree of disintegration that the gray matter was not 
 to be distinguished from the white columns. There was no 
 evidence of hemorrhage into the cord, and no deposit of pig- 
 ment. Microscopic examination of the fresh cord at the le- 
 sion showed the presence of Gluge corpuscles in large numbers. 
 An ascending degeneration was evident to the naked eye. No 
 descending degeneration was to be seen, but the entire cord 
 below the lesion was somewhat softened and the limitation of 
 the anterior cornua was indistinct. 
 
 The cord was hardened in Midler's fluid and preserved in 
 alcohol. Microscopic examination of sections made at various 
 levels revealed the characteristic lesions of an acute myelitis. 
 
 There was a great distention of all the intra-spinal vessels 
 and a marked thickening of their walls. No hemorrhages were 
 found. There was a total destruction of the gray matter of the 
 anterior cornua and central portion of the cord from the level 
 of the tenth dorsal segment downward. The posterior cornua 
 were destroyed at the tenth dorsal segment, but had escaped 
 in the parts below. The normal tissue was replaced by a dense 
 mass of connective-tissue in which numerous nucleated cells 
 were found. There was no trace of nerve cells. The columns of 
 the cord were sclerotic, and no trace of nerve fibres was to be 
 found at the level of the lesion. Below the lesion the poste- 
 rior columns and posterior nerve roots were normal, but all 
 other parts were sclerotic. Above the level of the lesion an 
 ascending degeneration was found in the column of Goll and in 
 the direct cerebellar column, and for a short distance in the 
 column of Burdach also. This also involved a zone of fibres 
 extending forward nearly to the anterior median fissure around 
 
LOCALIZATION OF SPINAL COA'f) DISEASES. 
 
 '55 
 
 the periphery of the cord. And inasmuch as there was no 
 evidence of meningitis, it must be concluded that the ascend- 
 ing degeneration had involved a portion of the cord not in- 
 cluded in the direct cerebellar column but lying anterior to it, 
 viz., the .anterolateral ascending tract of Gowers. 
 
 The history of the case shows the difficulty in distinguish- 
 
 D vil 
 
 Fig. 49. — Ascending Degeneration in Case 
 XXIV. Col. of Goll, direct cerebellar col., and . 
 col. of Gowers were degenerated on both sides. 
 
 Fig. 50. — Ascending Degeneration in 
 Gowers' Case, c, Col. of Goll; d, col. 
 of Eurdach; e, antero-lateral ascending 
 tract or col. of Gowers. (Gowers.) 
 
 ing clinically between an acute myelitis and aspinal hem- 
 orrhage. 
 
 The total paralysis with atrophy, the reaction of degener- 
 ation, and the fibrillary tremors in all the muscles of the legs 
 were sufficient proof during life of an extension of the lesion 
 to the anterior cornua of the cord in their entire longitudinal 
 extent below the level of the lesion — thus distinguishing the 
 case from simple transverse myelitis; and the zone of hyper- 
 aesthesia showed the exact level of the upper limit of the 
 disease. 
 
 CASE XXV. — HEMORRHAGE IN THE SPINAL CORD AT SIXTH 
 DORSAL SEGMENT — LOCALIZED TRANSVERSE MYELITIS 
 AT THIS REGION. 
 
 The patient, a male, forty-six, was seen in October, 1! 
 with Dr. L. A. Sayre. On December 4th, 1886, he was sud- 
 denly seized with a very severe pain in the middle of the back 
 
156 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 and became absolutely paralyzed from the waist down, both 
 motion and sensation being" entirely abolished below the sixth 
 intercostal nerve, and the bladder and rectum being beyond 
 control. He has remained in this condition ever since, suffer- 
 ing greatly from pain in the spine between the shoulders, and 
 being incapable of moving a muscle or of feeling any sensa- 
 tion whatever below the level of the sixth rib. His reflexes 
 are all preserved and are exaggerated below the lesion, the 
 only reflex lost being the epigastric skin reflex. The muscles, 
 though paralyzed as far as volitional motions go, contract on 
 percussion and on irritation of the skin; they have atrophied 
 to some degree from disuse, but their electrical contractility 
 is perfect except in the intercostal muscles of the sixth inter- 
 space, where reaction is lost. His bladder empties itself as 
 soon as a couple of ounces of urine have collected. The rec- 
 tum has to be cleared out by enemata or by digital explora- 
 tion. When any part of his body below the lesion is touched, 
 he says he feels it at the level of the sixth vertebra in the 
 back, but the strongest faradic current causes no pain. The 
 vaso-motor condition is interesting; stroking the skin, or 
 touching it with a hot or cold object or with a faradic brush, 
 causes, immediately, intense redness; so does pressure of any 
 kind, so that he lies naked on a sheet and is turned over every 
 half-hour by two attendants in order to prevent the formation 
 of bed-sores, which the pressure of his limbs have frequently 
 produced and which have been healed with difficulty. Around 
 his body from the sixth to the fourth intercostal space, over a 
 band two inches wide, there is extreme hyperesthesia (Fig. 
 43). The absence of any tendency to contractions or to rigid- 
 ity in the muscles is remarkable. The position of his limbs is 
 governed wholly by gravitation. 
 
 The diagnosis in this case was that of a hemorrhage divid- 
 ing completely the spinal cord and distending the membranes 
 at the level of the sixth dorsal segment." 
 
 •Bastian has stated that in complete division of the spinal cord there is no in- 
 crease of tendon reflexes and no rigidity. This case contradicts the first statement 
 and confirms the second. See Med. Chir. Soc. Rep., Lancet, March 1st. 1890. 
 
LOCALIZATION OF SPINAL CO 'A'/ J DISEASES. 
 
 157 
 
 BROWN-SKQUARD PARALYSIS. 
 
 The term Brown-Sequard paralysis is given to a condition 
 in which one-half only of the spinal cord is affected at one 
 level. This lesion gives rise to a very characteristic set of 
 symptoms below its level. These are paralysis of motion on 
 one side with preservation or exaltation of sensation, and par- 
 alysis of sensation on the 
 
 LEFT 
 
 right: 
 
 opposite side, with preser- 
 vation of motion. The 
 explanation of these symp- 
 toms is evident from Fig. 
 51. A lesion on the left 
 side of the cord (as in 
 Case XXVI.) cuts off, 
 from the parts below it, all 
 voluntary impulses which 
 come from the right half 
 of the brain and pass down 
 the left lateral column ; 
 hence it causes paralysis 
 of motion in the left leg. 
 The same lesion cuts off 
 from the left half of the 
 cord below it, all sensory 
 impulses going up to the 
 brain. But these sensory 
 impulses have crossed 
 
 QYpr- trip- COrd 3.S SOOn a.S P ara 'y s > s - L, Lesion in left naif of cord cuts off motor 
 
 impulses to left leg, sensory impulses from right leg, 
 they have entered it be- and sensory impulses from XD nerve. It irritates IXD, 
 IOW. The Sensations from musing hyperesthesia. CaseXXVI. 
 
 the left (paralyzed) leg ascend in the right half of the cord 
 and are, therefore, not cut off by the left-sided lesion ; while 
 those from the right (unparalyzed) leg ascending on the left 
 side of the cord are arrested at the point of the lesion. At 
 the level of the lesion, all sensations coming in by the pos- 
 terior nerve roots will be arrested, and this gives rise to a 
 band of anaesthesia around the body; the band being, how- 
 
 Diagram of Lesion causing Brown-Sequard 
 
158 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 over, one segment higher on the side of the lesion than upon 
 the other side, as shown in the diagram. The two following 
 cases illustrate this condition. The rapid course and fatal 
 termination of the second case make it remarkable. The neg- 
 ative result from an operation for the relief of pressure in the 
 fust case — the first case of this kind on which an operation 
 has been performed — makes it interesting and shows the limits 
 of spinal surgery. 
 
 CASE XXVI.— FRACTURE OF NINTH DORSAL VERTEBRA 
 
 BROWN-SEQUARD PARALYSIS — OPERATION, WITH PAR- 
 TIAL RECOVERY. 
 
 A teacher, twenty-lour years old, had a fall upon his back, 
 in February, 1887, which resulted in fracture of his dorsal spine 
 and total paraplegia with loss of sphincter contol, which re- 
 mained for some months and then gradually diminished to 
 some extent. From the very first he noticed that power was 
 diminished to a greater extent in the left leg than in the right ; 
 while sensation was affected more in the right leg than in the 
 left. He had a bed-sore over the right buttock. When seen, 
 October, 1888, he had a typical spastic paraplegia: the legs 
 were rigid, the voluntary power much impaired, so that he 
 could hardly walk with help, and the tendon reflexes much 
 exaggerated. The motor symptoms were much more marked 
 on the left side than on the right. The differences between 
 the two sides in regard to sensation was very great. While 
 on the right side he was quite insensitive to cold, heat, pain, 
 and touch, on the left side he was extremely sensitive to 
 these impressions, the slightest contact giving rise to pain. 
 Any irritation of the surface on the left side left a broad red 
 streak on the skin, an indication of vaso-motor paralysis, 
 which was confirmed by the fact that the surface temperature 
 was perceptibly lower on this side. The disturbances of sen- 
 sation ceased at the mid-dorsal region, where a zone of partial 
 anaesthesia existed around the body, and above this a zone of 
 hyperesthesia was found about two inches wide on both sides. 
 The anaesthetic zone followed the line of the ninth dorsal 
 
LOCALIZATION OF SPINAL CORD I) IS LASTS. 
 
 ■59 
 
 nerve on the left side and the tenth dorsal nerve on the right 
 side (see Figs. 51 and 52). The skin reflexes were increased 
 upon both sides, but more so on the right side. He could 
 control his sphincters. Motions of the trunk were painful 
 and limited; the pain being felt in the spine at the region 
 from the sixth to the tenth dorsal vertebrae, which were very 
 tender to pressure. A deflection of the ninth dorsal spine to 
 the right was quite evident. There were 
 no symptoms in the arms. 
 
 Diagnosis. — The questions of inter- 
 est in diagnosis were, first, as to the ex- 
 act nature of the lesion, and, secondly, 
 as to the possibility of operative inter- 
 ference. 
 
 The nature of the lesion might have 
 been either a mere compression of the 
 cord by the displaced and fractured ver- 
 tebras, or a serious injury to the cord 
 at the time of fracture with myelitis, or 
 a hemorrhage into the cord, or a hemor- 
 rhage outside of the cord in the mem- 
 branes. 
 
 A hemorrhage into the membranes 
 usually infiltrates them and extends 
 downward, filling the spinal canal if 
 severe, and forming a local clot if slight. 
 Such a clot usually extends around the 
 
 COrd, producing general pressure of and Hyperesthesia in Case of 
 
 Brown-Sequard Paralysis. Case 
 
 slight degree. If severe enough at the xxvi. Lines indicate anssthe- 
 outset to produce a total temporary sia; dots indic3te hyperaesthes,a - 
 paraplegia, it would hardly have been so strictly localized 
 upon one side as to have caused the Brown-Sequard paralysis 
 which remained. A unilateral clot within a membrane whose 
 structure is not such as to limit the extent of a bloody effu- 
 sion, seemed improbable. A hemorrhage in the cord itself is 
 often produced by injury and is not infrequently unilateral. 
 At its occurrence the initial pressure might have produced 
 the temporary paraplegia, and after the contraction of the 
 
160 FAMILIAR FORMS OF NERVOUS PIS EASE. 
 
 clot the unilateral destruction of the canal would give rise to 
 Brown-Sequaial paralysis. The clot, however, must inevitably 
 have caused an actual destruction of spinal tissue. In this case, 
 however, there was no evidence of a destruction of the cord, 
 to an)' extent, upon the side of the lesion; for the abdominal, 
 epigastric, scapular, and dorsal reflexes were not lost and the 
 zone of anaesthesia about the left side was not total, as is 
 usual when a part of the cord, and consequently its sensory gray 
 matter, is destroyed. The reaction of the abdominal and in- 
 tercostal muscles to faradism was also perfect, which indicated 
 an integrity of the anterior gray matter at the dorsal segments 
 opposite the site of injur)-. If the hemorrhage were not in 
 the gray matter it might certainly be within the white col- 
 umns; but in that case the motor symptoms should predomi- 
 nate if the clot were in the lateral column, or the sensory 
 symptoms should predominate if the clot were in the posterior 
 column. As a matter of fact, neither of these symptoms was 
 specially predominant ; hence it was concluded that an intra- 
 spinal hemorrhage was impossible. 
 
 An extensive myelitis subsequent to injury was also im- 
 probable, since the permanent symptoms indicated a unilateral 
 lesion without any great destruction of gray matter. 
 
 The diagnosis by exclusion was therefore a compression 
 of one-half of the spinal cord by displaced bone, a diagnosis 
 warranted by the existence of deformity and tenderness with 
 restricted movement of the vertebrae. The possibility of some 
 movement in all directions and the character of the deform- 
 ity, a slight displacement of the spinous process to one side, 
 made it improbable that any dislocation of the vertebrae had 
 occurred. Pressure of the bone on the cord would surely sus- 
 pend its functions at the point of pressure and might give rise 
 to degenerations upward and downward. The pressure sud- 
 denly produced would at first cause a general bruising of the 
 entire segment affected, with total paraplegia, and later these 
 symptoms would give place to those of local pressure only, 
 viz., Brown-Sequard paralysis. The pressure, though sufficient 
 to suspend the transmission of impulses through the white 
 matter, might not be sufficient to destroy the gray matter or 
 
LOCALIZATION OF SPINAL CO RD DISEASES. 161 
 
 to arrest its reflex action. And the fact that some transmis- 
 sion of impulses was still possible through the compressed 
 part, was shown by the performance of slight voluntary mo- 
 tions in the left leg and the perception of strong irritations in 
 the right leg. Hence it was thought that no part of the cord 
 Was absolutely destroyed. Thus the symptoms corresponded 
 with considerable accuracy to the hypothesis of unilateral 
 pressure with secondary degenerations, and negatived other 
 hypotheses. 
 
 The question of operation next presented itself. The 
 time which had elapsed since the injury was eighteen months, 
 and the symptoms indicated a probability of a descending de- 
 generation below the level of the lesion. It is still a matter 
 of uncertainty whether regeneration occurs in the spinal cord. 
 Experimentally after section in animals it does not. But 
 many cases of paraplegia from Pott's disease, in which rigidity 
 and increased reflexes are present, recover to a considerable 
 degree when the spine is straightened and the pressure on the 
 cord removed. It seemed, therefore, that an operation in this 
 case would offer the only possible relief and might be followed 
 by improvement. It was accordingly undertaken by Dr. 
 McBurney. 
 
 The details of the operation will be published by him else- 
 where. When the spine was exposed and the spinous process 
 of the ninth dorsal vertebra removed, it was found that a bony 
 deposit, probably callous, on the inner surface of the left 
 lamina of the vertebra had made lateral pressure upon the left 
 side of the cord, which appeared to be pressed over toward the 
 right side in the spinal canal. This lamina was, therefore, 
 removed. A probe passed upward and downward outside of 
 the dura failed to encounter any obstacle. The dura did not 
 pulsate. Its resistance at all points seemed equal. It was 
 not opened. 
 
 The patient made a satisfactory recovery from the opera- 
 tion, though for a few days after it all his spinal symptoms 
 were increased, the bladder being irritable and much pain 
 being felt in the umbilical region and around the body. After 
 the eighth week the improvement in his spinal symptoms 
 
162 FAMIIJAR FORMS OF NERVOUS DISEASE. 
 
 began to appear. Six months after the operation an exami- 
 nation showed that the actual voluntary power in the left leg 
 was greater than prior to the operation, but it was still rigid, 
 spastic, and its reflexes much exaggerated. The vaso-motor 
 paralysis had ceased, the temperature of the leg was the same 
 as on the other side, and irritation did not leave as marked a 
 line. All hyperaesthesia and anaesthesia of this side of the body 
 had ceased. He could walk with aid and balanced himself 
 better than before the operation. There was, therefore, a 
 slight improvement in the motor symptoms, and a relief of the 
 vaso-motor and sensory symptoms on the side of the lesion. 
 In the right side there was also a change. He perceived sen- 
 sation of touch, temperature, and pain more acutely and 
 more quickly than before the operation, but was still unable 
 to locate them correctly, occasionally referring touch to his 
 groin when it was made below the knee, a symptom which 
 had been present from the beginning. The result of the ope- 
 ration was, therefore, some relief of the symptoms, but not a 
 great degree of improvement. The pressure of the bone had 
 probably caused degenerations in the cord, which were not 
 affected by the removal of their cause. 
 
 The question of the possibility of regeneration has been 
 decided negatively; for at the end of eighteen months after 
 the operation the condition remains about the same. He 
 walks better than before the operation, but the spastic rigidity 
 of the left leg remains, and it is slightly cooler to the touch 
 than the right one. The sensation in the right leg is better 
 than before the operation. He can feel all sensations on the 
 outside of the leg normally, but on the inside of the leg and 
 upon the foot warmth is not felt at all, and touch and pain 
 are not accurately located. There is no girdle sensation and 
 no area of absolute anaesthesia anywhere. 
 
 This case therefore appears to corroborate the statement 
 made by Thornburn ' that "a certain amount of improvement 
 may follow a crushing lesion, due probably to the recovery of 
 those portions of the cord structure that have only been com. 
 pressed and not destroyed." 
 
 1 " Surgery of the Spinal Cord," p. 159. 
 
LOCALIZATION OF SPINAL CORD DISEASES. 1^3 
 
 Thornburn's conclusion, from a study of sixty-one cases, 
 is that "the operation of trephining the spine for traumatic 
 lesions as compared with the condition which it is intended to 
 relieve does not present any very great dangers, and appears 
 unlikely to increase the gravity of the prognosis, but as 
 both a priori argument and the results of published cases 
 show that it is unlikely to be of service, it should be aban- 
 doned, except in cases of injury to the cauda equina, and in 
 the latter, on the other hand, it will probably prove to be an 
 eminently practicable and serviceable procedure." 
 
 This case indicates that the removal of pressure from a 
 degenerated cord is not followed by complete recovery. 
 This patient, however, is so much improved that he declares 
 that he is very glad that the operation was performed. 
 
 With these facts in mind, I have refused to recommend an 
 operation in three cases, one of Brown-Sequard paralysis and 
 two of traumatic transverse myelitis, which were seen at the 
 clinic within a year, although in two of these manifest defor- 
 mity was present. I do not think, however, that when there is 
 evident pressure upon the cord without absolute signs of a 
 destruction of tissue in it, it is right to refuse the patient the 
 benefit of the operation. 
 
 The record of cases successfully treated by Macewen, 1 
 Horsley, 2 Abbe, 3 and others where pressure has been removed 
 and a considerable degree of recovery has ensued, seems to 
 warrant this conclusion. 
 
 CASE XXVII. — CASE OF CERVICAL PARAPLEGIA. — AUTOPSY. 
 
 The following case, reported by Dr. Christian A. Herter 4 
 and kindly placed at my disposal by him, is here inserted as a 
 typical illustration of a transverse lesion of the lower cervical 
 segments: 
 
 1 Macewen : Brit. Med. Jour., 1888, vol. ii., p. 308. 
 
 2 Horsley : Med. Chir. Trans., 1888, vol. lxxi., p. 402. 
 
 3 Abbe : N. Y. Med. Jour., Nov. 24th, 1888 ; and N. Y. Med. Rec, Feb. 
 9th, 1889. 
 
 4 Jour. Nerv. and Merit. Dis., January, 1890. 
 
164 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 The patient fell and broke his back on October gth, 1889. 
 He was taken to the Presbyterian Hospital, in this city, and 
 there found to have a tender spot without deformity over the 
 sixth and seventh cervical vertebra;. His respiration was 
 purely diaphragmatic. There was complete paralysis of mo- 
 tion and of sensation below the arm-pits. In the upper ex- 
 tremities there was complete loss of power in the intrinsic 
 muscles of the hands and interossei, in the flexors and exten- 
 sors of the wrist, and in the triceps. There was slight loss of 
 power in the pronators and supinators and in the biceps and 
 pectorals. The deltoids, trapezii, and muscles of the neck 
 and head were normal. All reflexes except the left plantar 
 were lost, and there was retention of urine. The area of an- 
 aesthesia is shown in the diagram (Fig. 45, page 137) and in- 
 volved the corresponding regions upon the back of the arms 
 as well as upon the front. The dotted area around the neck 
 was hyperaesthetic, and here a girdle sensation was felt. The 
 posture assumed was that described by Thorburn in his cases: 
 arms abducted, forearms flexed and supinated. The patient 
 died in forty-eight hours. The autopsy showed the cord to 
 be crushed, by a dislocation of the sixth cervical vertebra, at 
 the eighth and seventh cervical segments. 
 
 CASE XXVIII. — CARIES OF CERVICAL VERTEBRA— BROWN- 
 SEQUARD PARALYSIS — DEATH. 
 
 A girl of fifteen, previously in good health, noticed in 
 August, 1887, that her neck was becoming stiff and painful on 
 motion. The pain was in the course of the great occipital 
 nerves, and by October her head had become so rigid that no 
 active or passive motion was possible. During October weak- 
 ness in the arms, especially in the left arm, began, and soon 
 the left leg also became weak. She was sent to me on the 
 22d of October by Dr. G. A. Kretchmar, and then presented 
 the following symptoms. The head was held rigid, turned 
 slightly to the right, the chin slightly elevated, and passive 
 motion was prevented by the rigidity of the deep muscles of 
 the neck as well as by a deformity of the spioe, which was 
 
LOCALIZATION OF SPINAL CORD DISEASES. 16$ 
 
 evident both by a deep hollow in the neck at the fourth and 
 fifth cervical vertebrae and by a projection at the back of the 
 pharynx. Pain in the neck and over the back of the head 
 was a prominent symptom, but was not associated with anaes- 
 thesia (Fig. 46, page 137). The left upper extremity was par- 
 tially paralyzed, all movements being very much impaired ; 
 those at the shoulder and elbow joints more than those at the 
 wrist and fingers. No motion of the arm was possible, it 
 hanging helpless. Motions of the forearm were very weak, 
 extension being impossible ; the forearm was semi-flexed upon 
 the arm. While all the fingers could be moved, she had no 
 grip. The triceps and wrist tendon reflexes were greatly ex- 
 aggerated, a triceps clonus being obtained. All sensations 
 were perceived equally in the left side and in the face ; and 
 the muscular sense was keen and quick. 
 
 The left lower extremity was weak, both at hip, knee, and 
 ankle joints, and the tendon reflexes were much exaggerated. 
 The sensation was normal — that is, the same as in the face. 
 
 The right upper extremity was freely moved, but was mark- 
 edly anaesthetic up to the shoulder. Tactile sensations, sensa- 
 tions of pain, heat, and cold were not perceived by any means 
 as promptly, as accurately, or as intensely as in the correspond- 
 ing part of the opposite limb. There was marked ataxia of 
 movement in the right hand when her eyes were closed ; and 
 the perception of its position was less rapid and accurate than 
 on the left side. There was no motor paralysis and no in- 
 crease of tendon reflexes. 
 
 The right lozver extremity was not paralyzed, the knee-jerk 
 was normal, no ankle-clonus was obtained. The same kinds 
 of anaesthesia were found as on the right arm, though sensa- 
 tions were rather better in the lower than in the upper ex- 
 tremity. The area of anaesthesia is shown in Fig. 46, page 
 
 137- 
 
 The gait was much impaired. She staggered in standing 
 
 and walking, with a tendency to fall toward the right when 
 
 her eyes were closed, and her gait was decidedly ataxic. 
 
 The control of the sphincters was somewhat impaired. She 
 
 had to strain a long time before her water would pass, and a 
 
1 66 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 loss of voluntary control of the bladder soon ensued, so that 
 a catheter had to be vised. 
 
 There was no hyperesthesia of the paralyzed side and no 
 hand of anaesthesia about the trunk on that side. 
 
 By the end of November, 1887, all of the symptoms had 
 increased in intensity, the paralysis of motion of the left side 
 being complete and the anaesthesia on the right side being 
 increased; she was unable to sit up or to control her sphinc- 
 ters. She had distressing attacks of dyspneea. 
 
 The condition finally became one of total paraplegia, and 
 in January, 1S88, she died. 
 
 Diagnosis. — It was evident from the first that a caries of 
 the fourth and fifth cervical vertebrae had resulted in a dis- 
 placement of these bones, which had produced pressure upon 
 the left half of the spinal cord at the level of the fifth and 
 sixth cervical segments That these segments or their nerves 
 were seriously implicated was evident from the fact that a 
 marked atrophy, as well as paralysis and a reaction of degen- 
 eration, was found to exist in the deltoid, biceps, triceps, 
 supinator longus, supra and infra spinatus, and pectoral mus- 
 cles of the left arm, while no such atrophy or reaction was 
 found in the other muscles in spite of their paralysis. In the 
 right arm the anaesthesia was more marked over the back of 
 the shoulder and arm and on the outer side of the arm and 
 forearm than elsewhere. The pressure was sufficient to cut 
 off to some extent motor impulses downward to the left leg 
 on the side diseased, and sensory impressions of all kinds from 
 the right side of the body below the level of the lesion. 
 
 Operative interference appeared to be impossible, and the 
 disease made rapid progress, producing finally total paraplegia 
 and death from respiratory paralysis. An autopsy was not 
 made. 
 
 ******* 
 
 The cases brought together in this chapter demonstrate 
 the differences in the symptoms produced by lesions at vari- 
 ous levels of the spinal cord. They also show that a study of 
 local symptoms in spinal lesions results in exactness of diag- 
 nosis and may lead the way to successful surgical treatment. 
 
CHAPTER XII. 
 LOCOMOTOR ATAXIA. 
 
 WITH SOME REMARKS ON THE TREATMENT BY SUSPENSION. 
 By WINSLOW W. SKINNER, M.D., 
 
 Second Assistant in the Nervous Clinic. 
 
 LOCOMOTOR ataxia, or posterior sclerosis, or tabes dorsalis, 
 as it has been variously named, is a chronic disease of certain 
 limited regions of the spinal cord characterized anatomically 
 by'a typical sclerotic degeneration of the posterior external 
 columns and adjacent parts, and clinically by motor disturb- 
 ances, chiefly incoordination, and by remarkably diverse de- 
 rangements of the various forms of sensibility. 
 
 The principal symptoms of the disease found in the patients 
 applying for treatment at the clinic were as follows : 
 
 (i) A feeling of weakness, often strangely in contrast with 
 the actual power of the muscles when the latter was measured. 
 
 (2) A hesitation or feeling of insecurity and unsteadiness 
 when standing or walking in the dark, or with closed eyes. 
 
 (3) A sensation as of walking on springs, on a cushion, or 
 on velvet, confined to the soles of the feet and due to anaesthe- 
 sia of those parts. 
 
 (4) Fulgurating or lightning pains, often described as stab- 
 bing, darting, or tearing pains, which were said to shoot 
 through the limbs, generally the lower extremities, causing 
 excruciating suffering during a few seconds or minutes, then 
 disappearing, only to return after a short time. 
 
 (5) A feeling of constriction, generally about the trunk, 
 called the girdle sensation. 
 
 (6) The so-called crises which occur suddenly in attacks 
 and are infrequent. They may be manifested as spasmodic 
 
i6S FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 pains in the viscera, or as exaggeration of the function of a 
 viscus. Crises may take the form of severe griping pains in 
 the region of the stomach, accompanied by flatulence, gener- 
 ally by vomiting, rarely by nausea (gastric crises); they may 
 resemble attacks of renal colic (nephralgic crises), or consist 
 of pain in the bladder, urethra, or rectum (vesical, urethral, 
 rectal crises); or paroxysms of coughing or of dyspnoea (bron- 
 chial and laryngeal crises). Crises connected with the sexual 
 organs have not been observed. 
 
 (7) Various disturbances of cutaneous and muscular sen- 
 sibility of all degrees of intensity and of very various forms. 
 These merit a partial enumeration. They consist of insen- 
 sibility of the skin to simple touch or contact {anesthesia)', 
 abnormally increased sensibility to touch {hyperesthesia); 
 sensations referred to the skin and not corresponding to the 
 causes producing them, as formication, a velvety or furry feel- 
 ing, crawling, tingling, etc. {paresthesia?) an exaggerated and 
 abnormal sensibility to cold felt all over the whole body, 
 obliging patients to dress unusually warmly and to live in super- 
 heated rooms for comfort {eryesthesia 1 ); insensibility to pain 
 from pricking, pinching, etc. {analgesia) ; abnormally increased 
 sensibility to pain — e.g., great pain felt from a slight prick or 
 even from the touch of a soft object {hyperalgesia) ; two new 
 symptoms which will be explained further on {hyper thermal- 
 gesia and hypercry algesia) ; loss of the sense of the position of 
 the members (disturbance of muscular sense); and retarda- 
 tion of pain — e.g., the pain of the prick of a needle may not be 
 felt until several seconds after the contact of the needle has 
 been received (Remak's sign). 
 
 The above-named symptoms, however, most of which are 
 dependent upon an alteration of the various forms of sensibil- 
 ity, while very numerous, varied, and exceedingly interesting 
 from a clinical and even from a pathological point of view, are 
 subjective, are not uniformly present, and are not essential to 
 the diagnosis of the disease. 
 
 The diagnosis is based upon three objective signs, the pres- 
 
 ' Cryresthesia, from Kf)iog, icy cold. Dieulafoy, Gaz. hebdomadaire de Med. et 
 de Chir., June 25th, 1S86, p. 426. 
 
LOCOMOTOR ATAXIA. 169 
 
 ence of which together may be considered quite pathogno- 
 monic of locomotor ataxia, viz. : Westphal's symptom — that is, 
 loss of patellar reflex; Romberg's symptom — that is, swaying 
 widely and falling on standing with eyes shut; and Argyll- 
 Robertson's symptom — that is, a loss of the pupil reflex to 
 light, the reaction in accommodation being present. With 
 these data, a diagnosis of tabes dorsalis may unhesitatingly be 
 made, even in the absence of any or all of the others. On 
 the other hand, the absence of any' one of these three signs 
 throws a doubt upon the accuracy of the diagnosis unless the 
 latter be confirmed by a number of other symptoms; while 
 the absence of Westphal's symptom alone is a quasi-proof 
 that the disease is not pure tabes. 1 
 
 In addition to these diagnostic signs, the following objective 
 phenomena are found in the fully developed disease : 
 
 (1) Incoordination or ataxia in standing (static ataxia), 
 which is more marked when the eyes are closed and the base 
 of support is diminished in area, as when the feet are placed 
 as closely together as possible. 
 
 (2) Ataxia in movement of any of the extremities; as in 
 walking (locomotor ataxia, ataxic gait), when the patient may 
 not be able to control the movements of the feet properly, 
 or to put them down naturally even after repeated efforts, so 
 that the gait is uncertain and staggering, the feet being placed 
 wide apart and often being lifted too high and coming down 
 to the floor with a noise; or ataxia in fine movements, such as 
 seizing an object, placing the fingers on the ear and nose with 
 the eyes closed, buttoning the clothing, writing, etc., in which 
 the irregular jerky, swaying motions, quite unintentional, are 
 very characteristic. 
 
 (3) Temporary or permanent paralysis of one or more of 
 the muscles of the eyeball ; paralytic strabismus or ptosis. 
 
 (4) Atrophy of the optic nerve, causing diminution of the 
 visual field to colors and then to light, followed by blindness, 
 which may become total. 
 
 (5) Disturbance of the action of the bladder, either incon- 
 
 1 In a few cases when the disease begins in the cervical region the knee-jerk 
 persists for some months after the onset. — M. A. S. 
 
 if 
 
I70 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tinence or difficulty in beginning the act of urination; consti- 
 pation; temporary increase followed by loss of sexual power. 
 (6) Trophic disturbances, such as painless swelling and dis- 
 
 L I 
 
 Fig. 53. — Area of Sclerosis in the First Stage of Locomotor Ataxia. Patient died one year 
 after the onset of the first symptoms. The knee-jerk was lost on the left side where the sclerosis (S) 
 was found to be much more intense than on the right side. The sclerosis extended as high as the 
 IX. dorsal segment. No secondary sclerosis was found. — M. A. S. 
 
 integration of joints (Charcot's joint, ataxic or tabetic arthro- 
 pathy), deformities of the feet, perforating ulcers, loosening 
 and falling out of the hair, teeth, and nails. 
 
 Without entering more fully 
 into the general description of this 
 disease, it may here be mentioned 
 that the seat of the lesion charac- 
 teristic of tabes dorsalis is not ex- 
 clusively in the posterior columns 
 of the spinal cord, as was once be- 
 lieved, but has been shown to in- 
 
 F,c. 5 4.-Area of Sclerosis in Last Vade ° ther regions of the COrd, 
 
 stage of Locomotor Ataxia (Gowers). either primarily or secondarily. 
 
 Both of the posterior columns are com- ,-_. , . e / - l ,, . ,. 
 
 pletely sclerotic, the lesion being more TllUS the Column of Goll, the direct 
 
 intense in the coi. of Burdach (<i) than cerebellar tract of Flechsig, and the 
 
 in the col. of Goll (c). . _, 
 
 antcro-lateral tract of Growers are 
 usually affected secondarily ; and the analgesia tract of Spitzka 
 and the border-zone (Randzone) of the posterior horn (the tract 
 of Lissauer)' are sometimes primarily affected by sclerosis. 
 
 1 " Beitrage zum Faserverlauf im Ilinterhorn des menschlichen Rtickenmarks." 
 Arch, fur Psychiatrie, 1886, p. 377. 
 
LOCOMOTOR ATAXIA. \ji 
 
 Symptoms closely resembling those of the disease in ques- 
 tion, if not identical with them, have been described in cases 
 in which the posterior columns were healthy and only peri- 
 pheral neuritis was found at the necropsy. 1 
 
 From the date of the establishment of the Vanderbilt 
 Clinic in February, 1888, to January 1st, 1890, there have been 
 24 cases of tabes dorsalis treated at the institution. Of this 
 number 2 were women, a proof of the greater frequency of 
 the disease in males. Of this number 6 denied syphilis and 
 presented no evidences of that disease. 
 
 An endeavor has been made to ascertain the first symptom 
 manifested by the patient in these cases. In 17 this was de- 
 termined. It was pain in 6 cases; a feeling of general weak- 
 ness and fatigue in 2 cases; ataxia in 4 cases, chiefly locomo- 
 tor; paresthesia in 2 cases; numbness in both hands in 1 case; 
 enuresis in 1 case; and swelling of the great toe in 1 case. 
 
 In the 24 cases, on examination the following symptoms 
 were found : Incoordination (other than static) was recorded 
 in 13 and was absent in 7 cases. An ataxic gait was observed 
 in over one-half of the patients. Romberg's sign was present 
 
 1 Dejerine : "Alterations des Nerfs cutanes chez les Ataxiques," Arch, de 
 Physiol., 1883, vol. ii., p. 72. The first case was reported at a meeting of the 
 Societe de Biologie, Feb. 18th, 1882. Dejerine et Sollier : " Nouvelles recherches 
 sur le tabes peripheriques (Ataxie locomotrice par nevrites peripheriques)," Arch, 
 de Me'd. experimentale, 1889, vol. i., p. 251. 
 
 The differential diagnosis between locomotor ataxia and peripheral neuritis 
 is thus described by Prof. Starr in his lectures on multiple neuritis : " Ataxia, 
 loss of knee-jerk, pain, and sensory disturbances, including loss of muscular 
 sense, Romberg's symptom, and optic neuritis, are common to the two diseases. 
 In multiple neuritis the relatively rapid onset of the ataxia, which follows closely 
 upon the sensory symptoms ; the prominence of numbness and anaesthesia rather 
 than of lightning pains ; the extreme degree of anaesthesia and analgesia ; the 
 tenderness of the muscles and nerves ; the usual occurrence of some degree of 
 actual paresis with atrophy and the reaction of degeneration ; and absence of 
 bladder and sexual symptoms will point inevitably to the diagnosis. Furthermore, 
 the ataxic form of neuritis only occurs after poisoning with alcohol or arsenic, or as 
 a sequel of diphtheria, and the establishment of the causation will aid the diagno- 
 sis. Here, too, the course of the case toward recovery with return of the knee-jerk 
 will decide in favor of neuritis, if the diagnosis has not been reached in the early 
 stage." — " The Middleton Goldsmith Lectures for 1887," Med. Record, Feb. 
 5th, 1887. 
 
*7- 
 
 FAMIUAR FORMS OF XERVOUS DISEASE. 
 
 in 22 cases, including both women, or ninety-two per cent. 
 In 4 cases there was or had been some paralysis of the intra- 
 orbital muscles. No monoplegias, hemiplegias, or paraplegias 
 were noted. 
 
 Symptoms involving reflex activity were, or course, found 
 in every case. The knee-jerk was invariably absent. The 
 Argyll-Robertson pupil was noted seventeen times. In 2 cases 
 there was complete immobility of the pupil both to light and 
 to accommodation. In 2 cases the reaction to light was slow 
 and slight. 
 
 The sexual power was recorded as good in 6 cases, as lost 
 in 3, as diminished or incomplete in 2. 
 
 Sensory symptoms, those apparently spontaneous as well 
 as those elicited by methodical examination, were found in 
 their usual variety and abundance. Fulgurating pains were 
 complained of in 19 cases (seventy-nine per cent), eighteen 
 times in the lower extremities, three times in the upper, and 
 once in both lower and upper extremities. Girdle sensation 
 was present in 9 cases. In one of these the "girdle" had 
 moved upward, during the progress of the disease, from the 
 abdomen to the level of the nipple. Paresthesias were com- 
 plained of by the majority of the patients. Pricking, tingling, 
 or numbness in the hands and feet, especially the latter, with 
 a sensation in the soles of the feet as if the patient were walk- 
 ing on a cushion or velvet, was present in 13 cases, and cryces- 
 thesia was quite marked in eight per cent of the cases. One 
 of these patients felt continually cold, could not dress warmly 
 enough for comfort, and kept his room at the temperature of 
 32 C. (90 F.) and still felt chilly all the time. Another had 
 felt continual chilliness during five years. This symptom, as 
 well as hyperthermalgesia and hypercryalgesia, soon to be de- 
 scribed, has not been mentioned, at least to my knowledge, as 
 one of the morbid sensory phenomena due to tabes dorsalis. 
 It has been noted especially in chronic parenchymatous nephri- 
 tis and also in chronic alcoholism, and it is interesting to note 
 in this connection that in both of these diseases peripheral 
 neuritis is not infrequently present. It is possible, therefore, 
 that in all three of these affections this symptom is clue to 
 
LOCOMOTOR ATAXIA. 1 73 
 
 chronic inflammation or degeneration of the cutaneous nerves. 
 Complete anaesthesia of the feet was found in 1 case. Anal- 
 gesia was observed in 4 cases, in 3 of which the insensibility 
 to pricking and pinching was limited to the lower extremities. 
 In 1 case it extended as high as the umbilicus. 
 
 Alterations in the muscular sense were not often noted. 
 In one patient this sense was lost in the left leg and dimin- 
 ished in the right arm. 
 
 Remak's sign was present in 3 cases (twelve per cent), two 
 of the patients having had this disease four years, the other, a 
 woman, two years. The retardation of sensory conduction 
 was noted as being of ten seconds' duration in one case and 
 twenty seconds in another, which is not far from that of fifteen 
 seconds, as in one of Dr. Remak's patients. 
 
 Hyperthermalgesia and hypercryalgesia, which are here put 
 forward as new symptoms of tabes dorsalis, are two painful 
 subjective phenomena due to hyperesthesia of the sense of 
 temperature. They represent sensations that are quite out of 
 proportion to the degree of heat or of cold that is applied to the 
 surface of the skin. Hyperthermalgesia (Oep/j-y} heat) means 
 hyperalgesia produced by the application of heat to the cutane- 
 ous surface, hypercryalgesia (xpuo$, great cold) signifies hyperal- 
 gesia to cold applied in the same manner. The former is present 
 when the patient feels pain and starts as though hurt upon 
 brief contact with a body having a temperature of + 50 C. 
 (about 120 F.) or a few degrees less, a temperature which to 
 a normal nervous system is quite supportable; the latter 
 when the patient is similarly affected by contact with a tem- 
 perature of + io° C. (50 F.) or a few degrees higher. 1 The 
 tests are made by heating or cooling water in a test-tube and 
 holding the tube against the skin. Hyperthermalgesia was 
 
 1 The terms thermalgesia and cryalgesia would be properly used to express 
 normal sensations, the first meaning a painful sensation of heat, the second of cold, 
 which can be elicited from any normal organism by the application of a certain 
 temperature which would correspond to the sensations felt. It is only when the 
 senisation is not proportional to the exciting cause, thus becoming a hypersensation 
 — if we may be allowed the expression — that it becomes pathological, as in the 
 cases here reported. 
 
174 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 present in four cases, hypercryalgesia in three. All the latter 
 cases were also hyperthermalgesic, and these two symptoms 
 were manifest in the same regions of the body in the three 
 cases (abdomen, thighs, and legs). In one case they were 
 very marked, the patient starting and uttering an exclamation 
 of pain whenever the warm or cool body (a test-tube filled 
 with water) was applied to the bare skin of the above-men- 
 tioned regions. The following is a brief history of this case: 
 
 Case XXIX. — J. E., hair-dresser, French, thirty-seven 
 years of age, of medium height, strongly built and muscular, 
 had a hard chancre at the age of nineteen, which was treated 
 in France by mercury in large doses during a long period of 
 time. Six years ago he began to have fulgurating pains of 
 great intensity in the calves of the legs and in different regions 
 of thighs both in front and behind. These pains were so 
 severe that they forced him to cry out. They came and went 
 suddenly and were not of the nature of muscular cramps. 
 He has followed treatment for these pains during several 
 years without relief. 
 
 At present, the knee-jerks are lost ; he has moderate myo- 
 sis with Argyll-Robertson pupils; no ataxia, either static or 
 locomotor, but constipation and various disturbances of 
 sensibility. The latter consist of analgesia of both lower 
 extremities and an abnormally painful sensibility to moderate 
 heat or cold when applied to the surface of the legs. The 
 hyperthermalgesia and hypercryalgesia are observed in the 
 regions of analgesia (absence of pain from the prick of a pin, 
 from pinching, etc.), and only in these regions. There is no 
 false perception of the quality of the temperature, as heat is 
 aways recognized as heat and cold as cold, but there is false 
 perception of its quantity. Remak's sign is absent. 
 
 These observations bring additional evidence of the inde- 
 pendence of the different forms of cutaneous sensibility, and 
 show that one form (as tactile sensibility) may remain normal, 
 while another (the thermic in the last case) may be impaired. 
 They also demonstrate that the rapidity of conduction of sen- 
 sation may still remain intact when the sensation itself is im- 
 paired. The two subjective phenomena of hyperthermalgesia 
 
LOCOMOTOR ATAXIA. 175 
 
 and hypercryalgesia have not, so far as the writer has been 
 able to discover, been mentioned before in the symptomato- 
 logy of spinal diseases. In the remarkable article of Dr. 
 Remak, 1 of Berlin, upon the disturbances of sensibility in tabes 
 dorsalis there is no reference to them, although certain elec- 
 tric phenomena and the extraordinary retardation of painful 
 sensations are there described. In one of our patients hyper- 
 algesia to temperature was felt in the analgesic regions ; in 
 another there was no disturbance of cutaneous sensibility ex- 
 cept hyperalgesia to temperature, and the sensitiveness to cold 
 (which was the greater) was so painful that he begged that 
 the tube be removed at once, although the temperature of the 
 water in it was but + 15 C. (58 F.). 
 
 In regard to ocular symptoms, there was diplopia in 2 
 cases, polyopia in 1, optic atrophy in 3, and unilateral mydri- 
 asis due to paralysis of the ciliary muscle in I case (a wo- 
 man). In 4 cases the color-field was diminished and in an- 
 other case there was right nasal hemiopia. 
 
 Enuresis was present in 1 1 cases (forty-six per cent). 
 
 Tabes was, in one instance, associated with general paresis 
 of the insane, which manifested itself by the patient's general 
 optimism, by marked tremor of lips and tongue, and by hesi- 
 tation in speech. His memory was preserved to a certain ex- 
 tent, for he remembered (or at least gave immediately, as if 
 he remembered) various dates, as that of his birth, of his mar- 
 riage, of his children's birth, etc. He could also calculate 
 fairly, although he was said to have been losing this faculty of 
 late. 
 
 In 2 cases the disease has lasted thirteen years, which is 
 the maximum duration of the disease observed thus far in our 
 patients ; in 3 it was only of two years' duration. The two 
 patients who have had it the longest do not show so many 
 troublesome symptoms as many who have acquired the disease 
 more recently. Sexual power is still good in one of them. 
 
 1 " Sensibilitatsstorungen der Tabes dorsalis," Arch. f. Psychiatrie, 1877, vii. , 
 496. In one patient he found hyperalgesia (to touch) on the right thigh with 
 anaesthesia of opposite thigh to all kinds of excitation — i. e., analgesia, thermo- 
 analgesia, electro-analgesia. 
 
1-6 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 The treatment of these 24 eases was varied and was gener 
 ally constitutional as well as symptomatic. Mercurial inunc- 
 tions followed by potassium iodide were prescribed in most of 
 the eases which presented a syphilitic history, but rarely with 
 any marked effect. One patient before coming to the clinic 
 had been taking nitrate of silver and reported unfavorable 
 effects from it. It was not continued. Fowler's solution was 
 ordered in a number of cases, and is in Dr. Starr's opinion of 
 as much service as any medicinal remedy. Tonic remedies, 
 as iron and strychnia, were administered to several patients as 
 needed. As an anodyne to the fulgurating pains, antipyrine 
 and antifebrine were commonly employed and usually with 
 success. Occasionally the faradic brush relieved an attack of 
 pain. In one case the pains were relieved by a teaspoonful of 
 the following mixture, taken every four hours: 
 
 I£ Potass, iodidi, ...... 2.0 
 
 Tinct. opii, ....... 2.0 
 
 Ext. gelsemii fl., . . . . . . 2.5 
 
 Ext. cimicifug. fl., 5.0 
 
 Syr. sarsap. co., 
 
 Aq., ...... aa. ad 60.0 
 
 Treatment by Suspension. — As soon as this method of treat- 
 ment was put forward by Charcot, it was applied to nearly all 
 of the patients systematically, the number then treated being 
 ten. The disuse into which it has fallen after three months' 
 trial is proof of its inability to relieve the symptoms. It is 
 now rarely employed. Notwithstanding its discomfort to the 
 patient and its occasional dangers, to one of which I had oc- 
 casion last year to call attention,' and notwithstanding the 
 disappointment in the method after so much benefit had been 
 hoped for, there was still a certain small amount of good done 
 by it in a few cases. One patient, tabetic during nine years, 
 averred that suspension "took all his pains out." Another, a 
 woman, showed much improvement in walking after submit- 
 ting to suspension frequently during several weeks. A third 
 
 1 " A Danger to be Avoided in the Treatment of Nervous Affections by Suspen- 
 sion," N. Y. Med. Jour., June 29th, 1889, p. 715. 
 
LOCOMOTOR ATAXIA. 177 
 
 obtained an apparatus and suspended himself daily for six 
 months, thinking that it helped him in walking: he has re- 
 cently given it up. The two symptoms, pain and ataxic gait, 
 are the only ones we have seen ameliorated by this mode of 
 treatment. The conclusions derived from our experience 
 harmonize with those on the subject expressed at a recent dis- 
 cussion in the Neurological Society of London,' that suspen- 
 sion fails to benefit patients in the large majority of cases. 
 On the other hand, one patient thought that suspension did 
 him harm, and the majority to whom it was applied found 
 that they derived no permanent benefit from it. The method 
 has been faithfully tried by Prof. Starr upon six private 
 patients without any favorable result. 
 
 One patient, a healthy-looking married man of thirty years 
 of age, who has had tabes for the past four years, gave up all 
 medicinal treatment about one year ago, and has sought gay 
 society and amusements and now reports himself improved. 
 There can be no doubt of the exactness of the diagnosis in his 
 case for he shows Romberg's, Westphal's, Argyll-Robertson's, 
 and Remak's signs. He suffers from fulgurating pains, cryaes- 
 thesia, and hyperthermalgesia. 
 
 As regards cures, there can, of course, be none reported. 
 Four cases have improved, three appear stationary; in the 
 remainder the disease is progressing. One patient has died. 
 
 1 Reported in La Semaine Medicale, Feb. 26th, 1890. 
 12 
 
CHAPTER XIII. 
 THE PARALYSES OF INFANCY. 
 
 I. Traumatic paralysis of the brachial plexus, Erb's paralysis. — II. Infan- 
 tile spinal paralysis, atrophic paralysis (anterior poliomyelitis). — III. 
 Infantile cerebral paralysis. 
 
 THERE are three forms of paralysis commonly seen in in- 
 fants; and since each of these is dependent upon a different 
 lesion and each has a very different prognosis and requires a 
 different manner of treatment, they are grouped together in 
 order that the contrast may be evident. These various forms 
 are (i) Erb 's paralysis of the arm, or obstetrical paralysis* due 
 to an injury during delivery of the fifth and sixth cervical 
 nerves at their junction in the brachial plexus; (2) Infantile 
 spinal paralysis, due to an acute inflammation of the groups 
 of cells in the anterior gray horns of the spinal cord ; and (3) 
 Infantile cerebral paralysis, due to hemorrhage or embolism 
 with subsequent sclerosis and atrophy, or possibly to an acute 
 inflammatory process in the motor area of the brain cortex. 
 
 (i) ERB'S PARALYSIS — OBSTETRICAL PARALYSIS — BIRTH- 
 PALSY. 
 
 This foim of paralysis is noticed within a few hours or 
 days of the birth of the infant. It is usually limited to the 
 deltoid, biceps, brachialis-anticus, infra-spinatus, and supina- 
 tor longus muscles, but occasionally involves the extensor 
 muscles of the hand. The arm hangs loosely at the side of 
 the body, its position as a whole being governed by gravita- 
 
 'Described by Duchenne as " paralysie obstetricale infantile du membre 
 superieur," and by Erb as " Entbindungslahmung." Ziemssen's Cyclo. , 
 Amer. Ed., vol. xi., p. 562. 
 
THE PARALYSES OF INFANCY. 179 
 
 tion only, with the forearm extended and pronated and the 
 wrist and fingers flexed. If the arm be lifted and then let go 
 it falls at once into this position. The muscles which are par- 
 alyzed are relaxed and their opponents are not rigid, so that 
 the joints are all freely movable and motion does not give 
 the child pain. In response to surface irritation the un- 
 affected arm is seen to move freely, while in the paralyzed arm 
 the only movements made are those of extension of the fore- 
 arm upon the arm, of flexion and extension of the wrist and 
 of the fingers. Sometimes when the extensors of the wrist 
 are involved, there is slight extension of the two distal pha- 
 langes of the fingers only. A few days after birth, if the par- 
 alyzed muscles are examined electrically, it will be found that 
 they have lost their contractility to the faradic current, and 
 that on applying the galvanic interrupted current contractions 
 occur more forcibly under the positive than under the nega- 
 tive pole (the reaction of degeneration). In these tests the 
 unaffected arm should be taken as a standard for comparison 
 with the other. If sensibility is tested by a needle, it will usu- 
 ally be found to be very much impaired over the area of the 
 arm corresponding to the distribution of the cutaneous 
 branches of the circumflex nerve, an oval area whose centre 
 is the insertion of the deltoid muscle. It is best to test the 
 sensibility of an infant by pricking the surface of this area on 
 the unaffected side and noticing how promptly reflex acts of 
 movement and of crying are produced by slight irritation. 
 Then, when the babe has become quiet, the affected side may 
 be tested with the same amount of irritation, when the reflex 
 acts will not be produced so promptly or in some cases at all. 
 After the condition has remained for several weeks or 
 months without much change, as it often does, the muscles 
 which are paralyzed become considerably atrophied, and feel 
 unduly soft and yielding. The actual size of the limb, how- 
 ever, may not be very perceptibly reduced, for the deposit of 
 fat in a fairly healthy baby is much greater than the sub- 
 stance of muscular tissue, and therefore there is not the rapid 
 wasting of the arm and forearm which is noticed in adults 
 suffering from paralysis of the brachial plexus. When the 
 
FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 condition has lasted for three or four months there sometimes 
 appears a slight stiffness of the unparalyzed muscles, so that 
 bending the forearm at the elbow or opening the little closed 
 hand is not as easy as at the beginning. A permanent 
 rigidity, however, rarely if ever develops. 
 
 Some of these cases go on to spontaneous recovery. Thus 
 in two cases seen at the Polyclinic, this occurred within six 
 months. Many of them may be benefited by treatment, and 
 recover within a year. This has been the case in three patients 
 under my observation. Others, however, do not recover 
 rapidly: the condition remains for three or four years, and 
 only recovers when the child is old enough to be taught sys- 
 tematic gymnastic exercises. Several such cases have been 
 observed, and I have seen a girl of fourteen who still had some 
 disability of movement at the shoulder-joint due to the occur- 
 rence of birth-palsy. Erb gives a rather unfavorable progno- 
 sis in such cases. 
 
 The varying course of the disease, from complete recovery 
 within four months to partial recovery after several years, 
 depends upon the severity of the lesion and upon the line of 
 treatment pursued — as in all cases of traumatic neuritis. 
 
 The lesion in cases of birth-palsy is a traumatic neuritis 
 of the upper two nerves of the brachial plexus. Erb has 
 shown that it is possible by careful faradic examination to find 
 a spot which corresponds to the point of emergence of the 
 sixth cervical nerve between the scaleni at which the irritation 
 of the faradic current will produce a contraction in the del- 
 toid, biceps, brachialis anticus, and supinator longus muscles. 
 Stronger irritation will also cause the extensors of the wrist 
 to contract. It is here, therefore, that the brachial nerves 
 pass. Any pressure at this spot will easily injure them on 
 their way to the muscles named. Such pressure is often made 
 during delivery. This is particularly the case when the child 
 presents by the breech and when it is necessary to extract 
 the head. The common method of delivery in such cases is 
 to put two fingers of the right hand upon the maxillary bones 
 of the child's face and to place the index arid middle fingers 
 of the left hand, opened like a fork, upon the shoulders of the 
 
THE PARALYSES OF INFANCY. 181 
 
 child and thus make traction. In the so-called Prague method 
 the same position of the left hand is employed. The left hand 
 is at the same time used as a fulcrum around which the head 
 is rotated, so that pressure over the shoulders is made forcibly 
 and for some time. It is the pressure of the obstetrician's 
 fingers which causes the injury of the brachial plexus in the 
 majority of cases ; and I have noticed that in over seventy- 
 five per cent of the cases seen the paralysis was in the left 
 arm, which finds its explanation in the greater length of the 
 middle finger of the hand which is doing the damage. In 
 the act of traction there is a tendency for the obstetrician to 
 flex the fingers, and thus the tip of the" finger is pressed deeply 
 into the side of the child's neck. The cause being thus evident, 
 this complicating affection may be avoided by a little care. 
 In some cases injury of the brachial plexus is produced in 
 other ways. Thus when it is necessary in a hand or arm pre- 
 sentation to replace the limb and bring down the head ; or 
 when it is necessary to bring down a misplaced arm ; or when 
 in version traction is made on the arm it is very easy to injure 
 the brachial plexus. The application of forceps in an awk- 
 ward manner to the head may also produce pressure on the 
 neck and thus injure the plexus. Thus this form of paralysis 
 is rightly termed obstetrical. 
 
 Children do not appear to be at all liable to injuries to the 
 nerves, in spite of the many accidents which befall them. I 
 have not seen a case of traumatic neuritis of the extremities 
 in a child below the age of fourteen excepting of the form just 
 described. 
 
 The treatment of Erb's paralysis is of much importance, as 
 recovery can undoubtedly be hastened if proper means are 
 employed. The arm should be kept as far as possible with 
 the elbow flexed and not allowed to hang down, since its 
 weight often suffices to over-stretch the ligaments of the 
 shoulder, which are no longer assisted by the action of the 
 deltoid. The arm should be rubbed daily, the mother being 
 taught the kneading process of massage. Unintelligent peo- 
 ple will be more likely to keep up the necessary rubbing if 
 some simple lotion or ointment be ordered. The circulation 
 
[82 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 and nutrition of the limb will also be aided by sponging alter- 
 nately with hot and cold water followed by brisk friction. 
 And as soon as any voluntary motion can be made the child 
 should be encouraged to make it, even if it be necessary to tie 
 the unaffected limb to the side of the body. As the child 
 grows older, systematic exercises of a gymnastic kind should 
 be insisted upon daily. 
 
 The application of electricity probably aids the process of 
 regeneration in the nerves and certainly helps to keep up the 
 proper nutrition of the paralyzed muscles. For both pur- 
 poses galvanism is required ; for the faradic current has no 
 catalytic action and fails to produce any contraction in the 
 paralyzed muscles in these cases." Galvanism is to be used in 
 two ways: first, it is to be applied as a continuous current; 
 secondly, it is to be applied as an interrupted current. In the 
 first method a flat electrode is placed over the back of the neck 
 or between the shoulders and the other electrode is stroked 
 gently along the shoulder and down the arm, not being lifted 
 from the skin. The current employed should not exceed six 
 or eight milliamperes,* and the duration of the application 
 should not exceed five minutes daily or every second day. 
 The poles may be used alternately. The object sought by 
 this method is to promote the chemical processes which lie at 
 the basis of all nutrition and regeneration in both muscles 
 and nerves. The second method has another object. It is to 
 strengthen the muscles by inciting them to action. A muscle 
 which acts improves in nutrition, as the blacksmith's arm is 
 usually cited to prove. When voluntary action is impossible, 
 artificial action must be substituted. When an electric cur- 
 rent is suddenly sent through or is interrupted in its passage 
 through a muscle, a sudden change of electrical state is pro- 
 duced in the muscle, irritating it and making it contract. 
 Such a contraction is called the closure contraction or the 
 opening contraction, according as the current is suddenly sent 
 
 1 See Chapter on Electricity as a Therapeutic Agent. 
 
 a Batteries differ so much in power and the skin of patients differs so much in 
 resistance that no number of cells can be specified to be used. It is absolutely 
 necessary to control the amount of galvanism given by means of a galvanometer. 
 
THE PARALYSES OF INFANCY. 183 
 
 through or is suddenly stopped while passing. The muscle 
 does not contract during the passage of the continuous cur- 
 rent. It only contracts when it receives a shock— that is, when 
 the current is interrupted. To secure the desired end, there- 
 fore, in the second method, one of the poles used should have 
 a key by means of which the finger by pressure can make or 
 break the circuit, and during the application the circuit should 
 constantly be closed and broken. A current should be used 
 just strong enough to cause a contraction in the paralyzed 
 muscles, and since in cases where the reaction of degeneration 
 is present, as in birth-palsy, the muscle reacts more promptly 
 to the positive than to the negative pole, it is the positive 
 which should be placed upon the muscle. 1 The daily use of 
 this artificial exercise is recommended, and after a little in- 
 struction the parents will easily learn how it should be done. 
 The only dangers to be avoided are the application of too 
 strong a current and too long an application. The mildest 
 current which will cause contractions is to be used, and each 
 muscle should not be exercised more than half a minute at a 
 time, and not .more than three times at one application. Let 
 any one try to keep up rapid voluntary movement of any 
 muscle — for example, the index finger — for more than a half a 
 minute, and he will realize that further motion results in undue 
 fatigue rather than in stimulation. Hence electric fatigue 
 should be avoided in the application when electric exercise is 
 the object. 
 
 When the child grows to an age when gymnastic exer- 
 cises can be taught it, these should be systematically employed 
 to exercise the muscles which are weak. 
 
 (2) INFANTILE SPINAL PARALYSIS— ANTERIOR POLIOMYELITIS. 
 
 Etiology. — This form of paralysis occurs with greatest fre- 
 quency between the ages of one and four years. Thus of 31 
 
 1 In order to be sure which pole is negative, dip the wires in water and let a 
 current pass ; notice from which wire bubbles begin to come off : that is the 
 negative pole. The negative pole is also the most painful one when applied to 
 
 the skin. 
 
[84 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 cases seen at the Polyclinic and Vanderbilt Clinic, in 20 the 
 age. of onset was between these limits. Four cases began be- 
 fore the age of one year; others as late as the age of thir- 
 teen. I believe there is no case on record of a child born 
 with anterior poliomyelitis, though in some cases of spina 
 bifida a total destruction of the lower lumbar cord has been 
 observed, and subsequently paralysis with talipes has been 
 present. But in such cases sensory symptoms as well as 
 motor paralysis are to be found, and therefore they need 
 not be mistaken for infantile paralysis. The age of onset 
 will, therefore, prove of value in differentiating infantile spinal 
 paralysis, on the one hand from Erb's paralysis, which is 
 always congenital, and on the other from cerebral paralysis, 
 which ma)- occur at birth. 
 
 The onset of the disease in infantile paralysis is usually 
 sudden, with febrile symptoms, and not infrequently with con- 
 vulsions and delirium. The fever leads to vomiting, diarrhoea, 
 and general prostration, and as the age of onset coincides with 
 the age of teething, the parents usually suppose that the dis- 
 ease is due to this physiological process. 
 
 One case was brought to the clinic on the day after the 
 onset and was found to have a temperature of 103 . Anti- 
 pyrine was given, and also ergot ; the spine was blistered over 
 the lumbar region, and subsequently the child entirely recov- 
 ered the use of its legs, though for six weeks it could not walk. 
 Since acute congestion of the spinal cord is known to be 
 present at the onset, too much importance cannot be paid to 
 counter-irritation early. In 13 of these cases such a febrile 
 onset was known to have occurred. In some of them it had 
 no known cause; in others it followed the occurrence of mea- 
 sles, scarlet and typhoid fevers, and severe malarial poisoning. 
 
 One child tumbled into a pail of ice-water on the morning 
 of the onset. Another noticed the paralysis soon after a vio- 
 lent exertion in lifting a heavy load, and it appeared in the 
 right arm, on which the chief weight had rested. The effort of 
 learning to walk has been supposed to be an occasional cause 
 of paralysis in the legs, and though no cases can be cited to 
 support this theory, the last case mentioned lends probability 
 
THE PARALYSES OF INFANCY. 
 
 18; 
 
 to it. The cases at the clinic did not show any uniform rela- 
 tion between the season of the year and the onset. 
 
 Tabic Shozving Age at Onset. 
 
 Between 2 and 3 years, 10 cases. 
 
 5 
 
 mon 
 
 ths 1 
 
 n 2 
 
 cases. 
 
 7 
 
 " 
 
 
 ' i 
 
 case. 
 
 8 
 
 a 
 
 
 ' r 
 
 case. 
 
 12 
 
 a 
 
 
 ' -> 
 
 cases. 
 
 14 
 
 a 
 
 
 ' 1 
 
 case. 
 
 16 
 
 a 
 
 
 ' 1 
 
 case. 
 
 18 
 
 tt 
 
 
 ' 1 
 
 case. 
 
 20 
 
 K 
 
 
 ' 2 
 
 cases. 
 
 22 
 
 it 
 
 
 ' 1 
 
 case. 
 
 " 3 " 4 
 
 
 
 2 " 
 
 " 4 " 5 
 
 " 
 
 
 2 " 
 
 At age of 5 
 
 " 
 
 
 i case 
 
 " " 7 
 
 a 
 
 
 1 " 
 
 "11 
 
 " 
 
 
 1 " 
 
 " " 13 
 
 it 
 
 
 1 " 
 
 Males, 15. Femal 
 
 ss, 
 
 16. 
 
 
 The Character of the Paralysis. — The onset of infantile par- 
 alysis is not only sudden, but the distribution of the paralysis 
 is extensive and its character severe ; far more so than it is 
 ever destined to remain permanently. Thus it is not uncom- 
 mon for both legs to be totally paralyzed at the onset, but 
 after a few months to find the paralysis limited to a few mus- 
 cles of one leg. This occurred in four of the cases observed. 
 Again, where the arms are paralyzed it is usual to find both 
 arms affected seriously for several days, so that none of the 
 joints can be voluntarily bent ; and then finally the paralysis 
 passes off, excepting in three or four muscles of one arm. 
 This was the history in three cases. Or the extent of the 
 paralysis is very alarming, all the extremities being involved 
 and the little patient being utterly helpless. In one case both 
 legs were at first affected, and six months later both arms 
 were invaded. In such a case — of which I have seen two 
 other examples — the final extent of the paralysis is usually in 
 one arm and one leg. 
 
 In the terminal stage of the disease it is very uncommon 
 to find any limb totally paralyzed or to find both arms or 
 both legs equally affected, though at the onset both of these 
 conditions may have beert present. This feature in the course 
 of the disease has given origin to the name " regressive para- 
 lysis," an unfortunate name, since there is rarely if ever a 
 total disappearance of all symptoms. 
 
1 86 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 The usual form of the paralysis is flaccid atrophic paraly- 
 sis. Each muscle affected is seriously paralyzed ; is soft and 
 yielding, never rigid ; it has lost all mechanical irritability and 
 its tendon reflex is never preserved; it soon suffers in its 
 nutrition, so that a rapid diminution in the size of the limb is 
 noticeable within two weeks; and it presents a reaction of 
 defeneration. The entire limb at the outset and for some 
 weeks thereafter is relaxed, and its position depends entirely 
 on the force of gravitation. It falls into any position which 
 the posture of the child allows. In these respects the symp- 
 toms in individual muscles are identical with those of Erb's 
 paralysis, but present a very marked contrast to the symp- 
 toms of cerebral palsy. 
 
 The extensive distribution of the initial paralysis has al- 
 ready been mentioned. After a month, when the effects of 
 the severe spinal congestion have passed off, it is possible to 
 ascertain just what muscles are to be affected for some time. 
 The distribution of the permanent paralysis in the 31 cases is 
 shown in the following table : 
 
 Both legs in 9 cases. 
 Right leg " 6 " 
 Left leg " 6 " 
 Right arm " 3 " 
 Left arm " 1 case. 
 
 Both arms in 1 case. 
 
 Arm and leg " 2 cases. 
 
 Trunk with both legs " 1 case. 
 Trunk with left leg " I " 
 
 Both letjs and both arms " I 
 
 The records of the muscles affected in each case are too 
 extensive to warrant their reproduction. It is sufficient to 
 say that in the large majority of the cases in which one or both 
 legs were affected (26 cases) the paralysis was finally limited 
 to the muscles below the knee; the anterior tibial group, the 
 posterior tibial group, and the peroneal group being affected 
 in the order of frequency named. In but 4 cases were the 
 muscles above the knee paralyzed. In no case were all the 
 muscles of the limb equally affected. When the anterior 
 tibial group was totally paralyzed, the posterior tibial group, 
 though often partially paralyzed and somewhat atrophic, usu- 
 ally preserved some power and pulled the foot downward 
 into a position of talipes equino-varus. When the peroneal 
 
THE PARALYSES OF INFANCY. 
 
 187 
 
 group was paralyzed, the persistence of power in the others 
 favored the development of deformities. It is the unequal 
 distribution of the paralysis which leads to the conditions of 
 late rigidity and malpositions which are so often seen. For 
 it is found that the flaccid paralysis in these cases is frequently 
 followed after a year or more by a condition of rigidity and 
 contractures with resulting de- 
 formities. Such contracture has 
 this characteristic, that it de- 
 velops in the muscles which are 
 not the ones most paralyzed; 
 thus contrasting sharply with 
 the rigidity found in cerebral 
 paralysis. For example, in the 
 patient whose picture is pre- 
 sented (Fig. 55) the inability to 
 flex the first phalanges or to ex- 
 tend the second and third pha- 
 langes in the hand on account of 
 paralysis of the interossei and 
 lumbricales, while the long flex- 
 ors and extensors are not para- 
 lyzed excepting the extensors of 
 the radial side of the wrist, has 
 resulted in a permanent state of 
 deformity in the hand as shown 
 in Fig. 55. But the contracture 
 is easily overcome by passive mo- 
 tion. In another patient Suf- FlG - 5.5-— Infantile Spinal Paralysis of 
 ... , . , Left Upper Extremity. The deformity of 
 
 fermg from Cerebral paralysis, the hand and the inequality in the size of the 
 
 whose picture is given in the next scapula are noticeable. 
 section (Fig. 60), the flexion of the elbow and of the wrist are 
 due to the fact that all the muscles of the arm are suffering 
 equally from voluntary paralysis, but the balance of reflex 
 spinal action being in favor of the flexors, these predominate 
 over the extensors. Here it is difficult to overcome the 
 spastic rigidity. If any doubt should arise as to the nature 
 of the paralysis in a case of secondary rigidity, the spinal form 
 
iSS 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 can always be diagnosticated from the cerebral form, by the 
 
 presence in the latter of mechanical and reflex activity, which 
 in the former is always lost. 
 
 When the arms are affected by paralysis the entire arm is 
 rarely involved, though many of the muscles may be affected, 
 as is seen in the patient, whose picture is given (Fig. 56). 
 Usually the paralysis is limited in extent and the cases here 
 collected bear out the observation of Remak that it is easily 
 
 possible to separate an upper- 
 arm type from a lower-arm 
 type. In the former the mus- 
 cles affected are the deltoid, bi- 
 ceps, brachialis anticus, and su- 
 pinator longus. In the latter 
 the muscles affected are the ex- 
 tensors or the flexors of the 
 wrist and fingers — rarely both 
 together. Cases have also been 
 recorded in which the only mus- 
 cles affected were the intrinsic 
 muscles of the hand. Remak 
 calls attention to the fact that 
 the supinator longus and the 
 long extensors of the fingers, 
 
 Fig. 56.— Infantile Spinal Paralysis of the tllOUgll lying side by side, are 
 Left Upper Extremity. The atrophy of the , , , , . , 
 
 entire extremity, including the bones of the very rarely paralyzed together. 
 
 shoulder, is evident. The girl is now 13; the TliereaSOll for the peculiar 
 
 onset occurred at the age of 3. ,. ., . , . ... 
 
 distribution of the paralysis in 
 cases of spinal paralysis will be seen at once if reference is 
 made to the facts embodied in the table of localization of 
 spinal functions.' It is there made evident that the groups of 
 cells which govern the motion and nutrition of the different 
 muscles lie in various segments of the spinal cord, and that 
 an acute inflammation limited to one or at most two segments 
 (as the lesion in anterior poliomyelitis usually is) will affect 
 certain groups of cells only, while other groups lying above or 
 below the affected segments will escape. Thus when a lesion 
 
 1 Chapter X., pages 126 and 140. 
 
THE PARALYSES OF INFANCY. 
 
 189 
 
 u 
 
 lies in the upper cervical region it will naturally produce the 
 upper-arm type of paralysis, and the supinator longus will be 
 necessarily involved because its group of cells lies side by 
 side with those of the biceps and brachialis anticus, whose 
 function of flexion it materially assists; while if the lesion is 
 situated low down in the cervical cord in such a place as to 
 affect the group of cells related to the extensor muscles on 
 the forearm, the supinator longus necessarily escapes, since its 
 group is far above the lesion. 
 
 In any case of infantile spinal paralysis, if the exact mus- 
 cles paralyzed are determined, a reference to the table will in- 
 dicate at once the extent 
 of the lesion in the cord 
 (see Fig. 37, page 131). 
 
 Another fact is brought 
 out by reference to the 
 table which explains the 
 varying degree of the pa- 
 ralysis in many cases, and 
 its great extent at first 
 and subsequent regres- 
 sion. Each group of cells 
 in the cord has a consid- 
 erable longitudinal ex- 
 
 & Fig. 57.— Diagram of the Arrangement and Extent of 
 
 tent, 1 and may be Seen tO Groups of Cells in the Spinal Cord. Some groups are 
 1- . 1 • _ much longer than others, and lie in several segments. 
 
 he not merely in one seg- 
 ment, but often to form a part of two or three segments. 2 And 
 such groups are not of equal length nor arranged side by side at 
 all levels, but one may overlap, as it were, another, as is seen in 
 the diagram (Fig. 57). The consequence is that if one segment 
 only of the spinal cord is destroyed, one entire group may be 
 destroyed if it is a short one, but others are only partly de- 
 stroyed, the parts of the group which extend into adjacent 
 
 r 
 
 1 For an exact description of these groups and their extent, the reader is referred 
 to my article on the localization of spinal functions, Amer. Jour, of Neurology and 
 Psychiatry. Aug., 1884. 
 
 2 This fact seems to be overlooked by Thorburn in his remarks on localization 
 of motor groups. 
 
190 
 
 FAMILIAR FORMS OF XFR VOL'S DISEASE. 
 
 uninjured segments escaping. Hence the symptomatic result 
 of the lesion will be a total paralysis of the muscle correspond- 
 ing to the short group, and only a partial paralysis of the 
 muscles corresponding to the long groups. The latter may 
 be at first entirely put out of action by the shock or intense 
 collateral congestion, but subsequently, since a half or even 
 more of their spinal cells remain intact, the function is grad- 
 ually resumed, and, parallel with this, there is some recovery 
 
 Fig. 53. — Infantile Paralysis of the Left Hand and Forearm. The position is due to paralysis of 
 the extensors on the radial side of the forearm. 
 
 of power in the muscles. In some cases of anterior poliomy- 
 elitis the lesion found after death has been limited exclusively 
 to a single group of cells in one segment, the groups lying 
 about it being unaffected. This was the case in a patient, ob- 
 served by Prevost, who had a paralysis of the muscles of the 
 thenar eminence only. In such a case the recovery of the 
 majority of the muscles after the acute onset is due to the 
 fact that as the congestion attendant upon that onset sub- 
 sides, the groups which arc uninjured resume their function. 
 
THE PARALYSES OF INFANCY. 
 
 I 9 I 
 
 This pathological explanation of the symptoms in infantile- 
 spinal paralysis applies, of course, to all cases, both those of 
 paralysis of the arm which have been cited as examples and 
 also those of paralysis of the trunk and of the leg. The rarity 
 with which the trunk and abdominal muscles are found to be 
 paralyzed is due to the fact that 
 the groups of cells governing 
 them are very long and very nar- 
 row and extend through sev- 
 eral segments of the dorsal re- 
 gion of the cord. A lesion which 
 is usually of short extent will, 
 therefore, not involve the long 
 groups seriously. That the 
 trunk does not, however, always 
 escape is shown by the picture 
 of one of the cases (Fig. 59), 
 and by the case that Birdsall 
 has reported in which the ab- 
 dominal muscles of one side 
 were involved alone. In such 
 a case the longitudinal extent 
 of the lesion in the cord must 
 be considerable. 
 
 The atrophy in infantile spi- 
 nal paralysis is a very marked 
 feature. It has led to the nam 
 atrophic paralysis, which has 
 
 been adopted by GowerS. It Fig. 59.— Infantile Spinal Paralysis. The 
 
 develops rapidly, and it is USU- ^ophyof the left side of the trunk and of the 
 
 1 * J entire left lower extremity is evident. The 
 
 ally permanent in SOme Of the child is now 3 years old; the onset occurred at 
 
 muscles. In none of the 31 the age of J year - 
 cases did the corresponding limbs on the two sides present the 
 same measurements in circumference. In several cases of 
 such paralysis which have recovered the power of motion to 
 a very great degree, the difference in size remains. The atro- 
 phy may be less evident in fat children, especially before the 
 age of four. In many cases there is also a decided difference 
 
[ 9 2 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 in the length of the limbs. The lesion affects the rapidity of 
 growth in the paralyzed limb, so that the unaffected one soon 
 outstrips it. Tims in the case shown in Fig. 59, the left leg 
 is half an inch shorter than the right one, two years after the 
 onset of the disease. This difference gives rise to much de- 
 formity in some cases, marked scoliosis resulting from the 
 shortening of one leg. This has been observed in two cases. 
 It is therefore important to bear this in mind in ordering ap- 
 pliances for support of the limb. In cases in which the 
 growth of the bone is affected, the lesion lies deep in the gray 
 matter nearer to the central canal than in other cases; see 
 page 141. 
 
 A secondary effect of the atrophy and paralysis is to 
 weaken the support given by the muscles to the ligaments of 
 the joints; hence the joints become abnormally movable and 
 subluxation may occur. This is shown in Fig. 56. 
 
 The change in the response of the muscles to electrical 
 irritation is of importance in regard to prognosis as well as to 
 diagnosis. Duchenne was the first to observe that those mus- 
 cles recovered in which the faradic reaction persists. It may 
 also be said that those muscles will recover in which the fara- 
 dic reaction returns, though lost, within six weeks. The test 
 for the reaction of degeneration therefore affords the informa- 
 tion which the parents chiefly desire as to the prospect of re- 
 covery. In one private case under my care the left leg was 
 at first totally paralyzed, but the faradic reaction did not dis- 
 appear in any muscle except the tibialis anticus. After four 
 weeks it returned in that muscle, and at the end of one year 
 all muscles, except the tibialis anticus, had regained their nat- 
 ural size and power, and after two years the recovery was per- 
 fect in the entire limb. In the muscles which present at the end 
 of six weeks the reaction of degeneration, I have never seen 
 a perfect recovery, although I have seen a great progressive 
 improvement. Thus in all the cases of which pictures have 
 been given, the persistent use of galvanism (applied in the same 
 manner as has been described in the treatment of Erb's par- 
 alysis), in the one case for two years, in the other case for 
 one year, has been followed by a steady improvement in both 
 
THE PARALYSES OF INFANCY. 
 
 '93 
 
 power and nutrition. Yet I am convinced that the degree of 
 improvement possible in any case is dependent entirely upon 
 the extent of the lesion. If the entire group of cells govern- 
 ing a muscle is destroyed, no treatment will avail to restore 
 the muscle. If, however, some part of the group remains, a 
 part of the muscle is capable of recovery, and this part may 
 be so developed by exercise, voluntary or electrical, as to in 
 the end nearly do the work of the normal muscle. The elec- 
 trical application does not affect the lesion, but it counteracts 
 its effects. 
 
 The total absence of sensory symptoms is characteristic of 
 infantile spinal paralysis, and in the absence of a history of 
 the onset might be the only means of differentiating it from 
 Erb's paralysis. In the majority of cases, however, the man- 
 ner and time of the beginning of the two diseases present such 
 strong contrasts that they cannot be confounded. And the 
 distribution of the paralysis in anterior poliomyelitis rarely 
 resembles exactly that in Erb's paralysis. 
 
 This is the only form of spinal paralysis observed with any 
 frequency in childhood; hence it is not necessary to consider 
 its differential diagnosis from other varieties of myelitis, a 
 diagnosis not always easy in adults. 
 
 In the treatment of infantile spinal paralysis, the chief 
 object is to increase the nutrition of the limb and to protect 
 it from injury. It is always cold, hence it should be well 
 wrapped up in winter. It is always heavy and in the way, 
 hence it should be carried in a sling or aided by a brace, a 
 measure which also counteracts the tendency of gravitation to 
 stretch the ligaments. The means of aiding nutrition are 
 rubbing, massage, hot and cold douches, and electricity ap- 
 plied in the same manner as in Erb's paralysis. Such treat- 
 ment must be kept up faithfully for several months, or even 
 for years, and therefore may be intrusted to intelligent parents, 
 and regular attendance enforced upon unintelligent clinic 
 patients. Great aid is afforded by the application of proper 
 braces, and the ingenuity of the physician must be exerted to 
 devise the exact form of apparatus which shall supply the 
 lacking muscular strength without overloading the weak limb. 
 13 
 
194 FAMILIAR FORMS OF NERVOUS FISFASF. 
 
 A great aid to recovery is the constant practice of systematic, 
 well-planned gymnastic exercise, so adapted to each case as to 
 bring out all latent power in weakened muscles. 
 
 (3) INFANTILE CEREBRAL PARALYSIS WITH RETARDED DE- 
 VELOPMENT. 
 
 By DR. EDWIN E. SWIFT, 
 
 Third Assistant at the Nervous Clinic. 
 
 Under this title are included all those cases resulting from 
 lesions situated above the level of the pons Varolii. Such 
 lesions may exist in the cerebral meninges, cortical motor 
 centres, or pyramidal tracts of either hemisphere as the)' 
 traverse the internal capsule, crus, or pons (Fig. 26, p. 94). But 
 in the majority of the cases the lesion is cortical in location. 
 
 Cerebral paralyses are easily differentiated from those of 
 poliomyelitis, inasmuch as in the latter there are found, con- 
 comitant with the flaccid paresis, a loss or diminution of the 
 reflexes, rapid atrophy, no rigidity, and a degenerative electri- 
 cal reaction. Cerebral paralyses, on the other hand, usually 
 begin in children suddenly, with convulsions or spasms and 
 with fever and delirium ; there is manifested more or less brain 
 disturbance; the paralysis is of the hemiplegic type; there is 
 much tendency to rigidity in the paralyzed limb; the reflexes 
 are exaggerated; there is neither rapid nor extreme wasting, 
 and the electrical reactions are normal. 
 
 Of the 36 cases of infantile cerebral disease examined at 
 this clinic from February, 1888, to January, 1890, 20 were males 
 and 16 females; 11 were left hemiplegias, 9 were right, 4 were 
 paraplegias, 1 was a monoplegia, 1 a diplegia, and there were 
 IO cases of maldeveloped brain without paralysis. 
 
 Etiology. — In nearly all of these cases, the onset could be 
 dated before the age of four years. Seven date from birth, in 2 
 of which a distinct history of injury was obtained; these were 
 delivered with instruments; one was a complete hemiplegia 
 and the other a monoplegia. The latter presents not only a 
 brachial palsy but a pear-shaped skull. The child's intellect 
 is, however, bright. 
 
THE PARALYSES OF INFANCY. \g$ 
 
 In none of these cases could a syphilitic history be ob- 
 tained and in none could maternal impressions be proven. 
 
 Among the cases which dated from birth, it is probable 
 that meningeal injury was the cause of paralysis. Dr. McNutt, 
 in her complete monograph on this subject,' has shown how 
 this can occur. When labor is protracted and the head pre- 
 sents, the mechanical compression congests the basal meninges 
 and rupture of the vessels often ensues. In breech presenta- 
 tions the parietal meninges are also congested and suffer a 
 like injury. Such a rupture is predisposed to by the existence 
 of fatty degeneration in the vessels, a condition which Hubner 
 has found not infrequently in childhood. 
 
 The accompanying damage to the brain is the cause of the 
 convulsions, of the paralysis of the limbs, and of the perma- 
 nent symptoms. These cases vary much in degree, and it is 
 only in the more severe forms that all of these symptoms are 
 present. 
 
 One of the patients with hemiplegia dating from birth was 
 a twin, the other child being asphyxiated during delivery, 
 thus showing the greater danger of paralysis in double births. 
 
 Cerebral tumors were diagnosticated in 2 cases, but these 
 were not detected until a few months after birth. 
 
 Eight hemiplegic cases dated from convulsions, and four 
 from teething. One case of paraplegia followed a fright which 
 occurred at the age of four years, when the child was left 
 alone at night. 
 
 Four dated from scarlet fever and cerebro-spinal menin- 
 gitis and two from diphtheria. Striimpell and Bernhardt 
 have noted the relations of these palsies to acute diseases. 
 
 In the remaining cases no direct causes could be ascer- 
 tained. 
 
 Symptomatology — Paralysis. — Among those cases with no 
 pronounced onset it was noticed, first, that one arm or one 
 leg did not move; sometimes none of the limbs were under 
 the full command of the will. These latter cases, if slight, are 
 apt to receive less attention than the one-sided cases, because 
 
 1 Amer. Jour, of Med. Sci., Jan.. 1SS5. 
 
196 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 no comparison can be made between the two sides. A sud- 
 den onset with convulsions had occurred in the majority of 
 the cases. The convulsions were usually confined to one side ; 
 in a few cases they were general. The head was turned back- 
 ward, the thumb was in a position of inversion, and there was 
 persistent rigidity of the part convulsed. In many cases the 
 convulsions were followed by loss of consciousness, which lasted 
 from a few hours to many days. In some there was present a 
 rise of temperature which was only transient, but this was often 
 quite high when the convulsion ceased. Delirium occurred in 
 about half of the convulsive cases. 
 
 The paralysis which was discovered when the child recov- 
 ered consciousness was generally a complete hemiplegia; less 
 frequently it was incomplete, the paresis being more marked 
 in the arm and resulting gradually in total loss of power; and 
 in some instances the entire loss of power was established 
 only after repeated convulsions. 
 
 Among the facial muscles the frontalis and orbicularis 
 palpebrarum usually escaped, and the inferior muscles which 
 were paretic made a rapid recovery as a rule. If the para- 
 lysis is in the right side — as it was in 3 cases — it may be 
 accompanied by distinct motor aphasia in children who have 
 already acquired the power of speech. Aphasia does occur 
 rarely with left-sided paralysis in children. 
 
 The residual paralysis resembles the hemiplegia of adults, 
 being most marked in the arm and next in the leg (Fig. 60). 
 It differs, however, in the more rapid recovery of the leg. In 
 all infantile cases the leg improves much more speedily than 
 the arm and the paralysis may completely disappear, an event 
 which rarely happens in the upper extremity. The atrophy 
 in the leg is not so marked and the growth is not frequently 
 seriously arrested. When the leg is of fair size and the mus- 
 cular development is good, there may be only a slight drag- 
 ging of the limb perceptible upon rapid walking, instead of the 
 hemiplegic curve so noticeable in an undeveloped limb and 
 in extreme paralysis. The arm manifests much atrophy and 
 weakness. The power sometimes returns partly in the shoul- 
 der and elbow and to a less extent in the hand. 
 
THE PARALYSES OF INFANCY. 
 
 I 9 7 
 
 In the four cases of paraplegia the atrophy and arrested 
 development were manifested alike in each leg. 
 
 Reflexes. — The reflexes at the knee were exaggerated in 1 1 
 of the cases. Ankle-clonus was obtained in four instances. 
 The wrist reflex was also exaggerated. In the diplegia both 
 reflexes were absent. In paraplegia the rigidity of the muscles 
 sometimes prevents the examiner from obtaining a knee-jerk. 
 
 FlG. 60.— Infantile Cerebral Paralysis of the Right Arm with Athetoid Motions. Girl Of 8; 
 hemiplegia at age of 2. Face and leg have recovered; arm still paralyzed. 
 
 Rigidity and Contracture. — In 14 cases the rigidity was well 
 marked. In the extreme cases where this rigidity had lasted 
 for years, contractures had resulted in which condition re- 
 laxation was no longer possible on account of the structural 
 changes which had taken place in the muscles. Unless con- 
 tractures have set in, the rigidity disappears during sleep, and is 
 increased by emotion and aggravated by any forcible attempt 
 to overcome the spasm. The face never participates in any 
 form of late rigidity. The position which the upper limb as- 
 
198 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 sumes is that of adduction of the shoulder, flexion of the 
 elbow, flexion and pronation of the wrist, and marked flexion 
 of the fingers. The leg assumes the position in which the 
 extensors and flexors are each rigid, the heel is elevated, foot 
 inverted, producing a talipes equino-varus. 
 
 Athetosis. — Athetoid movements were present in four ol 
 the cases. The character of the movements was very slow 
 
 Fig, 61. — Infantile Cerebral Paralysis of the Right Arm with Athetoid Motions. 
 
 (Figs. 60, 61, and 62). They were usually limited to the arm 
 or hand. It was adducted, the elbow was flexed, and occa- 
 sionally the arm was carried backward by the spasm and rotated 
 inward, so that the hand was held against the lumbar region 
 with the palm turned outward; usually the hand was carried 
 forward against the chest with the palm turned downward. 
 Three successive positions are shown in Figs. 60, 61, and 62. 
 The girl was eight years old, and her hemiplegia had occurred 
 at the age of two. The motions were constant during her 
 
THE PARALYSES OF INFANCY. 
 
 199 
 
 waking hours, and were increased by any attempt at volun- 
 tary motion. 
 
 In an athetoid hand the interossei and lumbricales which 
 flex the metacarpophalangeal and extend the phalangeal 
 joints are affected ; rarely are the long extensors and the 
 long flexors affected. Therefore the hand is usually in the 
 so-called interosseal position, with flexion of the proximal 
 and extension of the middle and distal phalanges. The illus- 
 tration shows these athetoid movements of the hand (Fig. 63). 
 
 The athetoid movements of the toes correspond to those 
 of the fingers in point of 
 action. In severe cases 
 the movements continue 
 during rest and may per- 
 sist during sleep. 
 
 Post-Hemiplegic Cho- 
 rea. — This was present in 
 three cases. It occurs 
 in partially but never in 
 completely paralyzed 
 limbs, and usually ap- 
 pears simultaneously 
 with a marked diminu- 
 tion of the paralyzed 
 symptoms. The spasms 
 as a rule become grad- 
 ually established as mo- 
 tor power returns, although they may appear suddenly or seem 
 to be induced by an effort to move the paralyzed limb. The 
 movements affected by choreiform spasm are greater in the 
 fingers and toes and are less as the shoulder and hip are 
 reached. These movements are of a wider range than those of 
 hemiplegic tremor; they cease during sleep and are aggravated 
 by voluntary effort. The tremor which succeeds hemiplegia is 
 fine and is limited to the seat of paralysis. In one case of 
 right hemiplegia and in the case of diplegia, which was of the 
 flaccid variety, there were choreiform movements of the head 
 alone. The latter case was one of typical chorea nutans. 
 
 Fig. 62. 
 
 -Infantile Cerebral Paralysis of the Right Arm 
 with Athetoid Motions. 
 
200 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 One interesting- case, from a diagnostic point of view, was 
 that of a right hemiplegia and a left hemichorea in a boy of 
 nine years of age. On examination it was ascertained, how- 
 
 Fig. 63.— Athetoid Motions of the Hand. (Strumpell.) 
 
THE PARALYSES OF INFANCY. 201 
 
 ever, that the hemiplegia was of four years' duration, while the 
 hemichorea had lasted but a week and was idiopathic. 
 
 Associated Movements.— The face, while presenting no ap- 
 parent rigidity, will often, during a smile, overact on the side 
 which was paralyzed, and this is a most valuable diagnostic 
 indication in cases of old infantile hemiplegia, of which little 
 trace may remain elsewhere. 
 
 A strong effort to grasp with the unaffected hand will 
 sometimes cause a similar movement in the paralyzed hand, 
 and vice versa. This was present in 3 cases. 
 
 More frequently the paralyzed part is affected during the 
 act of yawning and stretching. 
 
 Epilepsy. — This was present in 5 cases. The epileptiform 
 attacks commenced simultaneously with the hemiplegia in 3 
 cases, and occurred subsequently in 2. They are far more 
 frequent after infantile than after adult hemiplegia. They 
 were as a rule confined to the paralyzed side. In one case 
 they were general. Aura was present in the majority of the 
 cases, and in four of them it began deliberately in some por- 
 tion of the paralyzed side. 
 
 In hemiplegia of sudden onset due to vascular obstruc- 
 tions, softening or sclerosis follows, the brain tissue adjacent 
 is usually damaged by collateral changes, and the nerve cells 
 suffer a change in the nutrition and function, causing insta- 
 bility which is continued by their repeated discharge. It is 
 probable that in idiopathic epilepsy a sudden discharge of 
 nerve cells or the violent liberation of nerve energy occurs 
 in the cortex, a theory to which this class of cases lends 
 support. 
 
 Metital Defects. — These were very common and presented 
 every conceivable degree, from a mere tendency to some func- 
 tional disturbance up to pronounced idiocy. The cranium 
 was misshapen. The palate was arched high and the teeth 
 were in many cases defective. 
 
 Pathology. — The pathological conditions which produce 
 infantile cerebral hemiplegias may be assumed to be of two 
 kinds: one is vascular occlusion, or rupture, and the other, as 
 maintained by Strumpell, is inflammation of the gray mat- 
 
202 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 ter of the cortex — a polioencephalitis analogous to polio 
 myelitis.' 
 
 The vascular theory has much to support it. It is the 
 common cause of cerebral cavities known as porencephalia. 
 
 Vascular rupture is a known complication of such general dis- 
 eases as frequently precede the cerebral palsies. 
 
 Whether the lesion is a result of embolism or of throm- 
 bosis is uncertain ; the former has generally been assumed, and 
 in support of this Hiibner reports a case of bilateral palsy 
 with rigidity and trismus developed during bronchitis in a 
 child one year old. Cavities were found in both hemispheres 
 and in the pons with clots in the middle cerebral arteries; but 
 these clots were canalized and the arteries beyond were per- 
 vious. In the majority of cases of proven embolism there 
 has been an obvious source for the occluding plug — usually 
 
 endocarditis. 
 
 It is known that primary thrombosis occurs in the sinuses 
 of children, and infantile hemiplegia may be the result of it. 
 
 In cases with no evident softening in which there is no 
 cavity, but only shrinking and induration of a part of the 
 cortex, Gowers suggests that the lesion is probably throm- 
 bosis in a surface vein, and that the reason why the lesion is not 
 found more frequently at autopsies is because in fatal cases the 
 clot usually spreads into a sinus before death, and so the case 
 is regarded as one of sinus thrombosis. The closure of a vein 
 does not cause softening of the entire cerebral tissue from 
 which the blood should pass into the vein, but merely venous 
 congestion, minute extravasation, and punctiform softening — 
 a condition that may well leave the state of atrophy and indu- 
 ration met with in some cases. Lastly, in many cases, a large 
 clot due to the rupture of a vein in the pia compresses the 
 brain cortex and prevents its development. This is probably 
 the most common cause of infantile hemiplegia. The theory 
 of Strumpell, that an acute inflammation limited to the motor 
 
 1 For a complete discussion of this subject, the reader is referred to an excellent 
 little book on "Cerebral Palsies of Children " by Prof. William Osier, and to a 
 monograph, with bibliography, by Drs. Sachs and Peterson; Jour, of Nerv. and. 
 Ment. Dis., May, 1890. 
 
THE PARALYSES OF INFANCY. 
 
 203 
 
 area of the cortex may occur, has no pathological basis as 
 yet ; though the analogies observed between the course of the 
 disease in brain and cord cases offers some ground for its 
 acceptance. 
 
 Whatever the original lesion in cerebral palsies may have 
 been, the final result in more than one-half of the cases 
 is a condition of atrophy and sclerosis of the convolu- 
 tions. The most common seat of this atrophy is the motor 
 area of the brain, and hence the frequency with which paral- 
 ysis is found in such cases; but other areas may be involved, 
 and many cases of imbecility from sclerosis of the frontal 
 region, or of blindness from atrophy of the visual region, or 
 of deafness and consequent dumbness from atrophy of the 
 convolutions about the Sylvian fissure are on record. Such 
 atrophy may be of sufficient extent and depth to produce a 
 cavity in the brain substance. In addition to atrophy and 
 sclerosis it is common to find cysts, and the remains of old 
 clots in the cortex. In but a few of the recorded cases could 
 embolism or thrombosis be actually proven. If the condition 
 described by Striimpell occurs — a true inflammation of the 
 cortical gray substance limited to the motor zone — it is a rare 
 affection. 
 
 Prognosis. — The recovery of the face is usually assured. 
 The leg is nearly always greatly improved and often recovery 
 is complete. There is generally a permanent disability of the 
 arm, including atrophy and slight contracture. 
 
 Treatment. — This at the onset during the active symptoms 
 demands the use of sedatives, cathartics, cold to the head and 
 leeches to the temples, or counter-irritation to the neck. 
 
 Subsequently, as the temperature of the paralyzed parts is 
 usually lowered and the circulation is sluggish, the limbs should 
 be wrapped in wool. Massage should be practised daily for 
 half an hour, with the use of olive oil or other unguenta. 
 Faradic electricity should be resorted to and persevered in, 
 with more frequent applications than are wont to be em- 
 ployed. It should be applied especially to the extensors to 
 overcome flexion. 
 
 When the rigidity and contractures are marked, warm 
 
204 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 baths with massage and with passive flexion and extension 
 are of service. 
 
 The palsied arm of hemiplegia cannot be much benefited, 
 but in cases of spastic diplegia and paraplegia, manipulations 
 and orthopaedic measures may enable a crippled child to walk. 
 
 The following cases illustrate the disease and demonstrate 
 the most common forms observed. 
 
 CASE XXX. — INFANTILE CEREBRAL PARALYSIS — ONSET AND 
 
 PROGRESS. 
 
 J. C, aged six, was seen by Dr. Starr in consultation with 
 Dr. Gibney February nth, 1886. ' He had been feverish and 
 restless for two weeks, and on the 4th of February had been 
 seized with a severe convulsion attended by high fever (106 ), 
 which had yielded to baths after lasting all night. During 
 the following four days a condition of right hemiplegia with 
 hyperesthesia and with aphasia developed, the arm being 
 affected first and most seriously, and occasional spasmodic 
 twitching being observed during this time in the affected limbs 
 without loss of consciousness. During these days the temper- 
 ature varied from ioo° to 104 . 
 
 When examined a typical condition of right hemiplegia 
 was found with slight hemianaesthesia and motor aphasia, but 
 no disturbance of consciousness or of understanding. His 
 pupils were normal. The face, tongue, arm, and leg were all 
 involved, the paralyzed parts being relaxed, not hot, not cya- 
 notic or oedematous, and reflexes being increased on the 
 paralyzed side. The evacuations occurred involuntarily. 
 
 During the following month a gradual improvement oc- 
 curred, and by the end of three months the aphasia was pass- 
 ing off so that he said a number of words; the face and tongue 
 no longer showed evidence of paralysis; the arm was seriously 
 affected, but he could raise it slightly and move the fingers, 
 Avhich showed some tendency to contracture in a flexed posi- 
 tion; the leg had so far recovered that he could walk. Reflexes 
 were still exaggerated on the paralyzed side and slightly 
 •Reported by Dr. Gibney, X. Y. Med. Record, 1886. 
 
THE PARALYSES OF INFANCY. 205 
 
 so on the other. Hemispasms continued at intervals. During 
 the past four years growth and improvement have been 
 steady, but the paralysis in the arm remains and he has not 
 entirely recovered his speech. 
 
 CASE XXXI.— INFANTILE CEREBRAL PARALYSIS — TERMINAL 
 
 CONDITION. 
 
 Mary C, aged nine, came to the Vanderbilt Clinic Feb- 
 ruary 18th, 1889. She was found to be a healthy child, ex- 
 cepting for the presence of a weakness of the left arm and 
 leg, the arm being chiefly affected. There was a decided in- 
 ability to use the hand; only the large motions of the joints 
 could be performed, fine adaptations being impossible; there 
 was a general imperfect development of the limb, the arm and 
 forearm being three-quarters of an inch in circumference less 
 than those of the right side, but the atrophy was not limited 
 to any one muscle or group of muscles. The affected limb 
 was cooler, bluer, and the skin rougher. It was very stiff to 
 passive motion. Sensation was equal on both sides. The 
 length of the arm was one and one-half inches less than that 
 of the right one, and the size of the hand was less. The same 
 differences were noted in the leg to a less 'degree. The face 
 was not affected, nor was speech involved. The parents stated 
 that this condition had been present from birth. 
 
CHAPTER XIV. 
 MULTIPLE NEURITIS. 
 
 The discover}- of the disease. — Pathology. — Etiology. — Symptoms: sen- 
 sory, motor, electric changes, deformities, vaso-motor, trophic, men- 
 tal. — Course and duration. — Diagnosis. — Types of the disease. — 
 Beri-beri. — Prognosis. — Treatment. 
 
 MULTIPLE neuritis is a disease of the peripheral nervous 
 system, consisting of a more or less widespread, symmetric- 
 ally distributed degeneration in the nerves. 
 
 This disease has only recently been generally recognized 
 and diagnosticated. The symptoms which it presents had 
 been for man)- years known and classified under the terms 
 "alcoholic paralysis," "general spinal paralysis," " acute as- 
 cending myelitis," and had been erroneously referred to dis- 
 ease of the spinal cord. In 1864, Dumenil," of Rouen, re- 
 corded a case of paralysis in which lesions of the nerves were 
 found after death, and two years later he published another 
 similar case. 2 But no notice was taken of these cases until 
 1876, when Eichhorst, of Berlin, recorded a case 3 of wide- 
 spread disease of the peripheral nerves. This article of Eich- 
 horst, and those of Joffroy, 4 in 1879, Leydcn, 5 1880, Lance- 
 reaux, 6 1881, and Grainger Stewart, 7 1881, attracted attention 
 to the new disease, and many observations followed : so that 
 in 1884 Buzzard 8 was able, in the Harveian lectures, to pre- 
 sent a clinical picture of the affection, and the writer in 1887,'' 
 in the Middleton Goldsmith lectures, was able to collect a 
 large number of facts bearing upon the pathology, etiology, 
 and diagnosis of this disease. Ross has published 5 a series of 
 articles on the disease recently (1890) which sum up concisely 
 our present knowledge of the affection. 
 
 Pathology. — The lesions in multiple neuritis are limited to 
 the peripheral nerves, and are found to be more intense in 
 
M UL TIP J. E NE UNI TIS. 
 
 207 
 
 the peripheral branches of those nerves than in the nerve- 
 trunks. The condition found is one of degeneration, similar 
 in all respects to the degeneration present after injury of a 
 nerve. The medullary sheath of the nerve-fibre is swollen, is 
 divided into segments of semi-fluid consistency and fatty ap- 
 pearance, its continuity is broken, and its insulating function 
 suspended. This may be the only lesion in a very mild case, 
 and regeneration may follow the degeneration (Fig. 64). In 
 more severe cases the degeneration proceeds, the medullary 
 sheath is broken up into fine granules of fat or into a molecular 
 debris and is absorbed, and the axis cylinder is not only 
 swollen, degenerated, and divided, but may also be changed 
 into a granular mass and completely absorbed, so that an empty 
 sheath of Schwann alone remains as a trace of the former 
 
 0^~^> 
 
 Fig. 64.— Multiple Neuritis. Lesion in the medullary sheath in a mild case. (Mayer.) 
 
 nerve-fibre. In all the process the sheath of Schwann parti- 
 cipates, its connective-tissue nuclei being swollen and seg- 
 mented, and new nuclei appearing inside and outside of it. 
 All these processes may be present simultaneously in various 
 fibres of a nerve (Fig. 65). 
 
 After the degeneration has proceded for a time, regeneration 
 begins. This takes place either by a development of new axis 
 cylinders and medullary sheaths from nuclei in the old sheath 
 of Schwann, as Neumann 10 holds, or by the growth of new 
 axis cylinders outward from the undegenerated part of the 
 old fibre into the old sheath, as Ranvier teaches." This form 
 of neuritis, in which the changes are especially marked in the 
 nerve-fibres, is termed parenchymatous neuritis, in distinction 
 from the second form, in which the connective-tissue elements 
 take a more active part in the inflammation. Interstitial neu- 
 ritis appears to have the same origin, and to occur under the 
 
208 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 same circumstances, as parenchymatous neuritis, but in it the 
 endoneurium and perineurium take part in the process, and 
 the increase of connective-tissue elements in the affected 
 
 1 2 3 4 
 
 Fig. 65. — Multiple Neuritis (Mayer). 1, Swelling and granular appearance of axis cylinder; 2 and 
 
 3, absorption of debris leaving empty sheath ; 4, regeneration beginning. 
 
 nerves is very noticeable.' 4 As far as is known, the process of 
 regeneration does not differ in the two varieties. Lastly, a 
 diffuse neuritis may occur in which both parenchyma and in- 
 terstitial tissue are affected together (Fig. 66). 
 
M UL TITLE NE URI TIS. 
 
 209 
 
 Etiology. — There are many causes which produce multiple 
 neuritis, and the cases may be classified according to the 
 etiology. 
 
 There are. first, cases due to toxic agents; of which alcohol, 
 lead, arsenic, bisulphide of carbon, and illuminating gas are 
 the most active. All these agents produce widespread and 
 serious effects upon the nervous system, but in many cases 
 those effects are chiefly manifested in life and at the post- 
 mortem table in changes in the peripheral nerves. The ma- 
 
 Fig. 66. — 1, Cross Section, Normal Nerve ; 2, Cross Section, Diffuse Neuritis. (Joffroy ) 
 
 jority of cases of "alcoholic paralysis," "lead palsy," and 
 " arsenical pseudo-tabes " are due to multiple neuritis. 
 
 There are, secondly, cases due to infectious agents, of which 
 those producing diphtheria, variola, typhus, typhoid, malaria, 
 and tuberculosis have been hitherto recognized. In the course 
 of all these diseases, or as a sequel to them, multiple neuritis 
 may develop, and its occurrence is too frequent to be acci- 
 dental. 
 
 There are, thirdly, cases occurring in epidemics in many 
 tropical countries, notably Brazil, India, Japan, Africa, and in 
 the East and West Indies. Sporadic cases of this description 
 developing among sailors on shipboard occasionally find their 
 way to our seaports. The disease is called kakke in Japan: 
 14 
 
2io FA MILIAR FORMS OF NERVOUS DISEASE. 
 
 beriberi In India and Brazil. It presents certain features 
 which differ from those of the ordinary form. It has been 
 ascribed to dampness, to a diet of rice or of fish, and to an 
 infectious micro-organism. 
 
 There are, fourthly, cases supposed to be due to exposure to 
 eold and dampness and to over-exertion^ or in which no cause 
 is known. 
 
 In all these forms the clinical features of the disease are 
 essentially the same, although different cases present a variety 
 of combinations of symptoms. 
 
 Males are more liable than females. All ages after puberty 
 are equally represented, excepting in diphtheritic cases, which 
 occur chiefly in childhood. 
 
 Symptoms. — The individual symptoms of multiple neuritis 
 are very numerous. 
 
 The sensory symptoms are the earliest to appear and the 
 last to pass away. In the majority of the cases on record, 
 from whatever cause, numbness, tingling, or formication 
 ushers in the disease. These forms of paraesthesiae begin in 
 the feet and hands, and extend to the knees and elbows. They 
 may be associated with burning, stretching, boring, or tearing 
 sensations, which distress the patient especially during the 
 onset. But all such sensations usually subside as the affection 
 reaches its height. Their recurrence, as the case goes on, may 
 be regarded as a favorable symptom, however annoying, for 
 they frequently precede recovery, and are among the last evi- 
 dences of the disease to disappear. Pain is usually present as 
 well as paraesthesiae. It may occasionally be sharp in charac- 
 ter, but is usually moderate and not continuous. At times it 
 may be lancinating, and so severe as to necessitate the use of 
 morphine. But it is rarely as distressing as in cases of locomo- 
 tor ataxia. Tenderness in the nerves and muscles is a con- 
 stant symptom. It may be so marked that the limbs cannot 
 be moved or handled, and thus it may interfere with the ap- 
 plication of electricity and massage. When the tenderness 
 and pain are referred to the joints, as not infrequently occurs 
 in the early stage of the disease, the case may be mistaken for 
 one of acute articular rheumatism, and if the joints are swollen 
 
MUL TIPLE NKURI TIS. 2 1 1 
 
 or the limbs oedematous, the difficulty of diagnosis is greatly 
 increased. 
 
 In addition to these subjective feelings, some demonstrable 
 disturbance of the various sensations is usually present. Hy- 
 peresthesia to touch, and also to electricity, is not infre- 
 quently observed during the first few weeks. It is usually 
 followed by some anaesthesia, although this rarely becomes 
 complete. In some cases the loss of tactile sense is quite evi- 
 dent from the onset, either limited to the cutaneous distribu- 
 tion of some special nerve, in which case oddly shaped areas 
 of insensibility will be found; or, as is most often the case, 
 about uniformly distributed over the distal parts of the ex- 
 tremities. When the anaesthesia is at its height the patient 
 has difficulty in locating a touch upon the limb, even though 
 he feels it. The transmission of pain and temperature sen- 
 sations may then be delayed, but the impressions are usually 
 felt quite acutely. The sense of pressure has been tested in 
 only a few cases, and in those it was decidedly impaired. The 
 muscular sense escapes being involved in some cases, but in 
 others it is the most profoundly disturbed of all the senses. 
 When it is involved, the incoordination and ataxia are well- 
 marked symptoms, and, as already stated, some of the cases 
 have been mistaken for locomotor ataxia, because of the pre- 
 dominance of the disturbance of muscular sense. 
 
 These sensory symptoms are usually limited to the fore- 
 arms and hands and to the legs and feet. In a few cases they 
 have involved the entire extremities, and even the trunk; and 
 one case of facial tingling,with anaesthesia, has been recorded. 12 
 The skin reflexes are usually preserved. In a very few cases 
 the sensory symptoms have been entirely wanting. 
 
 The special senses are rarely affected in multiple neuritis. 
 It is true that optic neuritis has occurred in a few cases, and 
 in two cases hearing as well as sight has been affected. These 
 cases prove that no nerve can be said to be exempt from im- 
 plication in this disease, but the liability to affection seems to 
 be slight in the case of the nerves of special sense. 
 
 The motor symptoms are as marked and as important as the 
 sensory. Paralysis, beginning as simple weakness, with a 
 
212 FAMILIAR FORMS OF NERVOUS PIS EASE. 
 
 feeling of Fatigue on any exertion, gradually increases in sever- 
 ity, until at the height of the disease it becomes complete. It 
 usually comes on rapidly, so that within two weeks the patient 
 is helpless; but it may be less sudden, and not deprive him of 
 the power of walking and of using his hands for two or three 
 months. In a few cases a very acute onset is recorded, all the 
 symptoms developing within three or four days. The distribu- 
 tion of the paralysis is not uniform at the outset. It may de- 
 velop in the muscles supplied by a single nerve, and advance 
 to others; it may begin in all the muscles of the legs, and then 
 involve those of the forearms; it may commence in all four 
 extremities at once. It is always more severe in the muscles 
 which move the joints of the feet and hands and the ankles 
 and wrists. It rarely invades those which move the knees and 
 elbows. When the disease is fully developed, all the muscles 
 below the knees and elbows are much weakened or totally 
 paralyzed. In a few cases those of the thighs and arms are 
 also involved, and occasionally the muscles of the trunk and 
 those of respiration become affected and the patient dies. In 
 some cases of multiple neuritis the motor cranial nerves be- 
 come involved; those of the eye and of the face being most 
 liable to invasion. It is only in fatal cases that the action of 
 deglutition has been affected ; and when the pneumogastric is 
 invaded and the heart becomes rapid and irregular, the prog- 
 nosis is always grave. Spasms rarely occur. 
 
 The paralyzed muscles are relaxed, flabby, and atrophied; 
 they may or may not lose their mechanical irritability, but 
 their normal tone is always lost, and hence the so-called ten- 
 don reflexes are abolished. To the electric current their ex- 
 citability is very rapidly and markedly changed; but the 
 conditions which have been observed are quite various. Some- 
 times there is a simple diminution of excitability, and then a 
 very strong faradic or galvanic current is needed to produce 
 contractions. Frequently all faradic excitability is lost, and 
 then the muscles react to a galvanic current only. In this 
 condition it may require a very strong galvanic current to pro- 
 duce contraction, and this fact is quite pathognomonic of 
 neuritis. For in anterior poliomyelitis, where the muscles re- 
 
MUL TITLE NEURITIS. 2 I 3 
 
 spond to galvanism only, it docs not require a strong current 
 to cause a motion until some months after the invasion. The 
 action of the different poles is not uniform. In many cases 
 the contraction of the muscle when stimulated with the pos- 
 itive pole is greater than when stimulated with the negative 
 pole, and the contractions may be sluggish. Then the reac- 
 tion of degeneration is present. But in some cases the normal 
 condition is found, and the negative pole produces stronger 
 contractions than the positive pole. If the muscles that are 
 not paralyzed be tested, the same electrical changes may often 
 be discovered in them. A loss of faradic irritability and a 
 marked decrease in the galvanic irritability of the muscle and 
 nerve are, therefore, important symptoms of multiple neuritis. 
 And as the disease goes on to recovery a gradual increase in 
 the galvanic irritability occurs, a fact which is often of much 
 aid in prognosis, if careful measurements of the strength of 
 current used be made by the galvanometer. 
 
 As a result and accompaniment of the paralysis, abnormal 
 positions are assumed by the limbs. The dropped wrist and 
 dropped foot are quite characteristic of multiple neuritis. But 
 other deformities may be present. In a few cases there have 
 been extreme contractures of all the extremities in flexed 
 position. And not infrequently the appearance of the claw- 
 shaped hand and some one of the various forms of talipes 
 indicates a serious shortening of one set of muscles and cor- 
 responding weakness of its opponents. These deformities 
 usually subside as the power returns, or if they do not, they 
 can be corrected by proper manipulation and by apparatus. 
 In a few cases it has been necessary to resort to tenotomy, 
 but a permanent deformity has not been recorded. 
 
 The vaso-motor and trophic symptoms are less constant than 
 those already described. They are present in the epidemic 
 form in all cases, and are especially severe. In some cases 
 marked oedema has been an early and a permanent symptom. 
 This may develop in the feet and hands, or may appear about 
 the joints. It usually is temporary. The circulation is not 
 impaired any more than is customary in a limb whose muscles 
 are inactive, and coldness and cyanosis are rarely sufficient 
 
214 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 to attract attention. Sometimes profuse perspiration is a 
 noticeable symptom, being limited to the paralyzed parts. It 
 may be offensive, and by its evaporation always causes a 
 complaint of coldness. In other cases glossy skin makes its 
 appearance early, and remains until regeneration of the nerves 
 begins. Its disappearance in one of my own cases was the first 
 sign of recovery in the lower extremities. Other forms of 
 trophic disturbance are rarely met with in multiple neuritis. 
 And this is quite remarkable in view of the fact that it has 
 been the tendency of late to refer such trophic affections as 
 ulcerations, bed-sores, gangrene, pemphigus, and various erup- 
 tions to lesions of the nerves. It is true that inflammations 
 of the joints, resembling those appearing in acute rheumatism, 
 sometimes occur at the onset of neuritis; but as they disap- 
 pear quickly, while other symptoms remain, it is improbable 
 that they are to be traced to the changes in the nerves. They 
 may be due to the infectious agent, or to the same obscure 
 cause which sets up the neuritis, or they may be evidence of 
 an attack of acute articular rheumatism, which is in turn fol- 
 lowed by neuritis; but they cannot be described as trophic 
 symptoms of the disease, otherwise they would be more con- 
 stant in their occurrence and more permanent in their duration. 
 One feature of alcoholic paralysis remains to be noticed, 
 viz., the cerebral symptoms. These are hardly ever wanting. 
 There is at first excitement rising to the degree of active 
 delirium, with illusions and hallucinations of the various 
 senses; there is insomnia, which so soon exhausts the pa- 
 tient if it is not remedied ; there is the loss of memory, es- 
 pecially of recent occurrences; and the lack of power of atten- 
 tion or concentration, which prevents intelligent conversation. 
 The indifference to bodily wants may be so great as to lead to 
 uncleanliness, and since paralysis of the sphincter is the rare 
 exception, incontinence is usually to be ascribed to the mental 
 state. It is useless to attempt to get any reliable history of 
 their illness from these patients. Their statements are unin- 
 telligible" or unreliable. And here it may be well to notice a 
 symptom first remarked by Strumpell. These patients will 
 relate occurrences as having happened recently, with much 
 
MULTIPLE NEURITIS. 2 l$ 
 
 elaboration of detail, when, as a fact, the story is entirely a 
 product of their imagination. Thus one patient of my own, 
 who had been confined to bed for many days, told me one 
 afternoon that she had been out to see an eminent gynecolo- 
 gist during the morning; had gone to his office and waited 
 for him several hours; had seen other patients there; and 
 finally had been told by the doctor's brother that he would 
 not return in time to see her, so she had come home again. 
 And this was all related in apparent good faith, so that I have 
 no doubt that she believed that what she said had occurred. 
 With the possibility of such delusions in view, it is evident 
 that the statements of these patients cannot be accepted re- 
 garding anything, especially as to their own history. 
 
 One patient, who was admitted to Bellevue Hospital dur- 
 ing my service there, told me a different history of her case 
 every day for a week, and it was only by interviewing her 
 friends that the correct account was obtained. 
 
 A negative symptom of some importance is the absence of 
 any interference with the automatic acts controlled by the 
 sphincters, in the majority of cases. 
 
 The onset is usually sudden, and is sometimes, in toxic 
 and spontaneous cases, accompanied by a marked febrile 
 movement, with chill, and temperature of 103 to 104.5 F. 
 The fever may persist for several days, but usually subsides 
 spontaneously, and does not recur. In a few cases there has 
 been a constant elevation of temperature from one-half a de- 
 gree to one degree and a half above the normal ; and an in- 
 crease in the rapidity of the pulse throughout the disease has 
 been noticed. A pulse of ninety need give no alarm, but if it 
 runs up to one hundred and forty and becomes irregular, 
 there is reason to believe that the disease has attacked the 
 vagus nerve, and then the prognosis becomes serious, though 
 not by any means hopeless. 
 
 The duration of the disease varies considerably in different 
 cases. An average of 25 cases gives seven months as the prob- 
 able time required for complete recovery. But in these cases 
 the duration varied from two months, in the most favorable, 
 to sixteen months, in the most refractory. 
 
2l6 
 
 FAMILIAR FORMS OF XFRVOUS DISEASE. 
 
 Diagnosis. — It is by reference to the etiology and to the 
 course of the case, as well as to the combination of symptoms 
 present, that the diagnosis of multiple neuritis must be 
 reached. The most important diagnostic symptom is tender- 
 ness along the course of the peripheral branches of the nerves 
 and in the muscles. The cases most liable to be mistaken for 
 multiple neuritis are anterior poliomyelitis, locomotor ataxia, 
 and diffuse central myelitis. The following tables present the 
 differences usually found : 
 
 Anterior Poliomyeli i is. 
 
 Sudden onset with fever and devel- 
 opment of paralysis in all limbs, fol- 
 lowed in from three to five days by 
 subsidence of paralysis, which remains 
 in a few muscles of one limb ; or, if 
 two are affected, the paralysis is very 
 rarely symmetrical. If onset is sub- 
 acute, four weeks is the duration of 
 onset. Muscles not tender. 
 
 Sensory symptoms are rare, and when 
 present soon subside. 
 
 Multiple Neuritis. 
 
 Fatigue for some weeks, then sud- 
 den onset and progress for two weeks 
 with or without fever. Legs first 
 affected, then arms, then body, and 
 paralysis has no tendency to subside 
 for a month ; the limbs are affected 
 symmetrically, and the muscles affected 
 are very tender. 
 
 Sensory symptoms are constant and 
 severe, and increase ; anaesthesia be- 
 coming well developed. 
 
 Paralysis, atrophy, reaction of degeneration, coldness of 
 the limbs, loss of tendon reflexes, and preservation of bladder 
 control, are common to both diseases. 
 
 Locomotor Ataxia. 
 Pains are lightning-like in character. 
 
 Nerves are not tender. 
 
 Ataxia developes slowly and after a 
 period of pain. 
 
 Anaesthesia and analgesia slight. 
 No actual paralysis, no atrophy. 
 No change in electric reactions. 
 Argyll-Robertson pupil present. 
 
 Multiple Neuritis. 
 
 Paresthesia is more marked than 
 pain. 
 
 Pain is produced by pressure on 
 nerves. 
 
 Ataxia is an early symptom, develops 
 rapidly, and may exist without pain. 
 
 Anaesthesia in patches total. 
 
 Paralysis with atrophy. 
 
 Change in electric reactions. 
 
 Pupils react normally. 
 
 There are very few symptoms of diffuse myelitis which 
 are not found in cases of neuritis. But cases of diffuse mye- 
 litis of the type of Duchenne — paralysie generale spinale sub- 
 aigue ascendante — are very rare, and, indeed, by Leyden it 
 
MULTIPLE NEURITIS. 2 ly 
 
 has been affirmed that all such cases arc multiple neuritis. 
 Other authorities dispute this assertion and leave us to estab- 
 lish points of difference. These are as follows: In neuritis 
 affections of the functions of micturition and defecation do 
 not occur. Girdle sensation is very rarely mentioned as a 
 symptom ; bed-sores and cystitis have not been observed. 
 The advance of the paralysis is rarely from the legs to the 
 thighs and trunk, and then to the arms ; it is usually from the 
 legs to the forearms, the trunk and thighs escaping, and, as a 
 rule, the distal portions only of the extremities are paralyzed. 
 If the muscles of the abdomen and respiration are involved, it 
 is only in rapidly fatal cases. In neuritis there is usually 
 some ataxia, and loss of muscular sense is quite evident ; while 
 in some, at least, of the cases of myelitis of Duchenne, there 
 were no sensory symptoms at all. Finally, the tenderness of 
 muscles and nerves, and the absence of tenderness to pressure 
 ■or to heat in the spine, would decide in favor of neuritis. The 
 diagnosis from meningitis of the cord, from tumors or hemor- 
 rhages into the cord, or from general paralysis of the insane, 
 would rarely present any difficulty to one who was familiar 
 with the symptoms in those affections and who knew the 
 prominent features of multiple neuritis. 
 
 There are certain common types of the disease, a familiar 
 ity with which may aid in the diagnosis. If a patient, known 
 to be alcoholic, complains for a time of tremor and muscular 
 weakness, and then is suddenly paralyzed in the legs and 
 arms, develops fever, becomes delirious, and shows great ten- 
 derness of the limbs and rapid loss of faradic electric reaction 
 in the muscles, the diagnosis of multiple neuritis can be made. 
 If a patient, who has been taking arsenic medicinally for some 
 time, begins to complain of paraesthesiae, clumsiness, and 
 fatigue, and soon shows a marked ataxia in hands and feet, 
 with tenderness along the nerves, some atrophy in the weak 
 muscles, and a change in their electric reactions, the diagnosis 
 of multiple neuritis can be made. Lead-palsy is easily recog- 
 nized. Diphtheritic paralysis is usually limited to the muscles 
 of the pharynx, or of the eyeballs; but the sudden onset of 
 marked ataxia without a preceding stage of pain after diph- 
 
218 familiar forms of nervous disease. 
 
 theria, warrants the diagnosis ot neuritis. If a tuberculous 
 individual suddenly develops pain and tenderness and weak- 
 ness in both arms or both legs, and this is followed by paraly- 
 sis and atrophy in a few symmetrically situated muscles, the 
 diagnosis of multiple neuritis can be made. And lastly, if any 
 one of these clinical pictures is presented by a patient who 
 has been exposed to cold or to wet, or has overstrained him- 
 self severely, and a careful examination fails to reveal the 
 characteristic symptoms of general diffuse myelitis, while the 
 limbs are very tender to pressure, multiple neuritis may be 
 suspected. 
 
 Cases of beriberi may be slight or severe. 
 
 There are, first, slight cases, in which the onset is gradual, 
 being usually preceded by a little fever, coryza, and conjunc- 
 tivitis, which cease when the actual symptoms commence. 
 The patient first notices a weak and heavy feeling in his legs, 
 and finds that he tires so easily that he cannot walk as much 
 as usual. The tired feeling is soon associated with numbness 
 and pain in the legs, and with a slight cedematous swelling. 
 Then, if not before, palpitation of the heart, oppression and 
 weight in the epigastrium, loss of appetite, and general malaise 
 are felt, and the patient finds it necessary to apply for treat- 
 ment. An examination then shows some diminution of power 
 in the feet and legs, and also in the hands, with loss of tendon 
 reflexes, and much tenderness in the muscles, which show a 
 diminished electric excitability. There is never any ataxia, 
 though the patient sways when his eyes are closed. There is 
 discovered a slight degree of anaesthesia, of irregular distribu- 
 tion, chiefly in the legs and in the radial-nerve region on the 
 forearms. Though the patients look pale, it is usually impos- 
 sible to find anaemia by examination of the blood. The circu- 
 lation in the extremities is sluggish. The heart is irregular 
 and rather rapid, and the oedema of the extremities indicates 
 a failure of its power. Dr. Wallace Taylor' 3 finds that a 
 sphygmographic tracing is characterized by a sudden high up- 
 stroke in ventricular systole, by a precipitous descent from the 
 apex of the percussion-wave, and by dicrotism. Beyond this 
 point these cases, which make up the majority, do not ad- 
 
MUL TITLE NE UNI TIS. 
 
 219 
 
 vance. They usually recover in a few days, or at most a 
 month; although a few become chronic and require several 
 months before the cure is complete. 
 
 There are, secondly, severe cases. These may present 
 three different types. There is the atrophic or dry type, in 
 which, after an onset similar in nature to that in the slight 
 cases, but much more rapid, the weakness develops into a true 
 paralysis, associated with marked wasting of the muscles and 
 reaction of degeneration, with great diminution of galvanic 
 excitability. Within a week the patient has to go to bed, and 
 then the paralysis soon spreads from the legs to the arms, 
 and may involve the trunk and even the face. The entire 
 muscular system wastes away till the patient is a mere skele- 
 ton. In addition to the motor symptoms there is great sen. 
 sory disturbance. The suffering from pafn, paraesthesiae, and 
 general muscular tenderness is extreme, and the patient lies 
 totally helpless, and unable to tolerate the lightest touch. 
 The skin may be glossy. There is usually some anaesthesia, 
 but it is never complete, although it may involve the entire 
 body. The temperature sense is seldom affected. Pain may 
 be delayed in transmission. There are no gastric symptoms, 
 and no oedema. Some cases prove fatal from general ex- 
 haustion, or intercurrent disease, but the majority recover 
 after a convalescence which lasts a year or more, during which 
 the muscular system is rebuilt. 
 
 There is, secondly, the hydropic or wet type. In these cases 
 heart-failure appears early, and is associated with a marked 
 decrease of arterial tension and much oedema of the entire 
 body, effusion into the cavities being added to that beneath 
 the integument. The swelling of the oedematous parts con- 
 ceals the atrophy which is going on in the muscles, but this is 
 indicated by the paralysis, which is as severe as in the preced- 
 ing form, and it becomes evident during recovery when the 
 oedema has subsided. I have seen an example of this in the 
 captain of a vessel who came to this city from the Philippine 
 Islands. The disease developed during the voyage. 
 
 There is, thirdly, the acute pernicious type. In this all 
 the symptoms of the two former types appear in rapid succes- 
 
220 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 sion, and, in addition, gastrointestinal symptoms and a sup- 
 pression of urine combine to make the condition an alarming 
 one. Effusions into the pleura and pericardium appear early. 
 The pulse becomes small and irregular, and cyanosis indicates 
 the heart-failure which precedes death. 
 
 Prognosis. — The prognosis of multiple neuritis is good, ex- 
 cepting in severe alcoholic cases, and in the very severe forms 
 of beriberi just described. The progress of the recovery may 
 be slow ; in some cases two years may elapse before it is com- 
 plete, but seven months may be considered the average dura- 
 tion, and slight cases may get well in three months. 
 
 Treatment. — The majority of the cases being toxic in origin, 
 the most important indication is to remove the cause. Total 
 abstinence from alcohol is necessary for at least two years 
 after recovery to prevent a relapse. Lead and other poisons 
 must be eliminated from the system. Such hygienic measures 
 as may be used to counteract influences of an infectious kind 
 must be employed. The direct treatment of the disease is 
 aided by the spontaneous tendency to recover in a person 
 whose constitution is sound, and whose strength is maintained 
 by general tonic treatment. It is possible to hasten the pro- 
 cess of regeneration by the use of full, nutritious, and espe- 
 cially fatty diet, including cream and cod-liver oil ; and by the 
 administration of strychnine, phosphorus, iron, and arsenic, 
 no one remedy being continued for more than three weeks at 
 a time. The use of warm and cold douches to the paralyzed 
 limbs, of skillful massage when the tenderness has sufficiently 
 subsided, and of mild (io ma.) constant stabile galvanic cur- 
 rents along the limbs (see page 182), probably aids the regen- 
 eration by stimulating the circulation and increasing metamor- 
 phosis of tissue. The daily use of the interrupted galvanic 
 current to the muscles, of sufficient strength to produce con- 
 traction in them, gives them proper exercise to maintain their 
 tone (see page 183). Rest is enforced by nature for some time, 
 but moderate exercise is indicated during recovery, but should 
 not be carried to the point of fatigue. 
 
MULTIPLE NEURITIS. 2 2I 
 
 BIBLIOGRAPHY. 
 
 1. Dumenil : Gaz. Hebdom., 1864, p. 203. 
 
 2. Ibid., 1866, No. 4. 
 
 3. Eichhorst : Virchow's Archiv, Bd. 69, p. 265. 
 
 4. Joffroy : Arch, de Phys. Norm, et Pathol., 1879, p. 172. 
 
 5. Leyden : Charite Annalen, 1880, and Zeitsch. f. klin. Med., 1880. 
 
 6. Lancereaux : Gaz. Hebdom. de Med., 1881, p. 120. 
 
 7. Grainger Stewart : Edinburgh Med. Jour., April, 1881. 
 
 8. Buzzard : Harveian Lectures, Lancet, November and December, 1885. 
 
 9. Starr : Middleton Goldsmith Lectures for 1887. Med. Record, February, 
 
 1887, where a complete bibliography to date is to be found. 
 
 10. Neumann : Arch. f. Mikro. Anat., xviii. 
 
 11. Ranvier : Lecons sur THistologie du Syst. Nerv., tome ii., p. 42. 
 
 12. Lowenfeld : Neurol. Centralblatt, 1885, No. 7. 
 
 13. Wallace Taylor : Kakke. Tokio, Japan, 1887. 
 
 14. Byrom Bramwell : Amer. Jour, of the Med. Sci., June, 1888. 
 
 15. Ross: Med. Chron., October, 1889-April, 1890. 
 
CHAPTER XV. 
 PARALYSIS AGITANS. 
 
 Analysis of twenty-three cases. — Etiology. — Symptoms. — The varieties 
 of tremor. — Rigidity and contractures. — Gait and its peculiarities. — 
 Treatment. 
 
 By FREDERICK TETERSON, M.D., 
 
 Chief of the Nervous Clinic. 
 
 TWENTY-THREE cases of Parkinson's disease have been 
 under treatment in the Nervous Department up to January 
 ist, 1890. Of these 10 were females and 13 were males. This 
 is over one per cent of the whole number of nervous cases 
 recorded (2,070). Ordenstein (" Sur la Paralysie agitante et la 
 Sclerose en plaques generalisee," Paris, 1868) places this dis- 
 ease fifth in order of frequency among nervous disorders, 
 stating also that it is more common than locomotor ataxia — 
 facts which are not borne out by our statistics. Berger noted 
 37 cases of paralysis agitans among 6,000 patients suffering 
 from diseases of the nervous system, a little over one-half of 
 one per cent. 
 
 ETIOLOGY. 
 
 Age at Onset. — In the majority of our cases the disorder 
 developed between the ages of fifty and sixty years, next in 
 order between forty and fifty, and in all between thirty and 
 seventy years. Eighteen patients were between forty and 
 sixty years of age at the time of onset, agreeing in this re- 
 spect with the statistics of all other observers. The periods 
 of life in which the tremor began in this series of cases are 
 classified in the following table: 
 
J' A RA L YSIS A GI TA NS. 
 
 223 
 
 Age at Onset. 
 
 30 to 40 years. . . . 
 
 40 to 50 " 
 
 50 to 60 " 
 
 60 to 70 " .... 
 
 Total 
 
 Male. 
 
 Female. 
 
 Total. 
 
 2 
 3 
 
 I 
 
 I 
 I 
 
 7 
 1 
 
 3 
 
 4 
 
 14 
 
 2 
 
 .3 
 
 10 
 
 23 
 
 Sex. — The fact that men are more frequently affected by 
 this disease than women is borne out by our own figures. 
 
 Heredity. — It is a moot question whether heredity plays 
 any particularly important role in its development or not. In 
 only two of our own cases could any such factor be suspected. 
 These two cases were brother and sister. In the former it is 
 still mild in its manifestations, while in the sister the disorder 
 has led to irremediable contractures in both hands and both 
 feet and to such general rigidity that locomotion is almost 
 impossible and even speech difficult. 
 
 Occupation. — All of the patients were from the common 
 walks of life, but a few of them followed pursuits in which 
 they were especially subjected to exposure to extremes of 
 heat or cold. Thus one was a night-watchman, one a coach- 
 man, one a messenger, one an engineer, one an out-of-door 
 laborer, and one had worked as a tobacconist in a damp base- 
 ment for thirty years. 
 
 Exposure to Cold and Wet as a Cause. — In five cases the im- 
 mediate cause given for the tremor was working in the wet 
 and cold. Two cases, both men, date the onset of the disease 
 from the famous "blizzard" of March 14th, 1888, when New 
 York City was snowed in to such an extent that all travel 
 was suspended, and several people were lost and frozen to 
 death in the streets. These two men were both out in the 
 storm, and the tremor appeared almost immediately after the 
 exposure to the cold and the exertion required to reach their 
 homes. 
 
 Worry and Anxiety as Causes. — One of our cases was an 
 illicit distiller of whiskey, and the disease appeared soon after 
 his discovery and trial and the confiscation of all his property. 
 
224 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 In 2 cases domestic infelicity was an etiological clement. One 
 woman developed it dining an anxious period of nursing her 
 dying mother; and another woman during a period of worry 
 over her drunken son. 
 
 Traumatic Causes. — In one woman the tremor besian in the 
 right arm soon after a fall from a step-ladder. (This patient is 
 the one whose brother is also afflicted with the disease; and 
 the brother has been made much worse by his constant fear 
 and worry, lest he should some time become as helpless as the 
 sister.) 
 
 An excellent example of trauma as an exciting cause was 
 that of one man who, at the age of fifty-two, was driving a 
 refractory horse. The horse ran away and threw him out of 
 the vehicle upon his left shoulder. No immediate harm was 
 done, but paralysis agitans soon became manifest, the tremor 
 beginning in the left arm. In such a case as this fright may 
 have also had a share in its production. 
 
 Miscellaneous Causes. — In one case fever and ague of three 
 months' duration immediately preceded the development of 
 Parkinson's disease. In another articular rheumatism in the 
 left foot was antecedent to the appearance of tremor in the 
 same extremity. 
 
 Among causes given by other authors in their collections 
 of cases are to be mentioned gout, by L'Hirondel (These de 
 Paris, 1883) and typhoid fever, by Berger. 
 
 SYMPTOMATOLOGY. 
 
 Tremor. — This is one of the cardinal symptoms of paraly- 
 sis agitans, although, paradoxical as it may seem, quite a num- 
 ber of cases have been recorded of true Parkinson's disease 
 without tremor. Thus Charcot observed 2 such cases, Berger 
 and Wienskowitz 2, Buzzard 1, Hardy I, Amidon 1 (A^. Y. 
 Med. Record, November 24th, 1883), and Beevor has very re- 
 cently descibed 4 (Med. Chir. Soc. Proceed., 1889, Vol. VIII., 
 page 8). The other chief symptom, rigidity, is always present 
 when the tremor is wanting. 
 
 Tremor was noted as present in every one of our 23 cases. 
 
PARALYSIS AGITANS. 22£ 
 
 The extremities in which it made its first appearance, as re- 
 lated by the patients, are tabulated as follows: 
 
 In the right hand 
 
 in 
 
 10 cases 
 
 " left 
 
 a 
 
 6 " 
 
 left foot 
 
 a 
 
 3 " 
 
 In both hands 
 
 a 
 
 3 " 
 
 " both feet 
 
 it 
 
 i case. 
 
 Total 23 
 
 The extent of the tremor at the time of examination may- 
 be gathered from the following table : 
 
 Table Showing Extent of Tremor. 
 
 In one extremity, 
 
 3 cases 
 
 In two extremities, 
 
 .11 " 
 
 In three extremities, . 
 
 • 3 " 
 
 In four extremities, 
 
 . 6 " 
 
 In head as well as limb, 
 
 • 5 " 
 
 Charcot's statement that the head never takes part in the 
 tremor, but is only moved by the contiguous shaking of the 
 upper extremities, has been proven to be unfounded in fact. 1 
 
 It will be observed that there was tremor of the head in 5 
 of our 23 cases, and in all of these it was possible to determine 
 the participation of the cervical musculature in the tremor. 
 
 With the exception of the shivering from cold or terror, 
 the tremor of paralysis agitans is almost the only one devel- 
 oped when the body is in a condition of rest. Almost all 
 
 1 The following are some of the authorities who have disproved Charcot's 
 assumption : 
 
 Oppolzer : Spital Zeitung, No. 17, 18, 1861. 
 Clement : Lyon Medical, No. 26, 1869. 
 Jones : Brit. Med. Jour., 1873. 
 Westphal : Charite Annalen, iii. u. iv. Jahrg. 
 Demange : Revue d. Med., ii., 1882. 
 
 Buzzard : Clinical Lectures on Dis. of the Nerv. Syst., 1882. 
 Huber : Virchow's Arch., vol. cviii., p. 45. 
 Gowers (8 out of 37 cases) : Dis. of Nerv. Syst., 1888. 
 15 
 
226 FAMILIAR FORMS OF NERVOUS DISEASE 
 
 W^§^^ 
 
 1 1 * 
 1 •, \\ n 
 
 '•-.: i" v v 
 
 - \tiit* • jM 
 
 Ik* 
 
 
 i 
 
 IVU, ; 
 
 Fig. 67. — Tracing of Tremor of Paralysis Agitans. 1, Tremor of extensors of carpus, right 
 hand, 5.3 per second ; 2, tremor of extensors of carpus, right hand, 5.1 per second ; 3, Tremor 
 of head while hands held chair, 4.4 per second ; 4, Tremor of head while hands held chair, 4.6 per 
 second ; 5. tremor of head, no effort with hands, 4.8 per second ; 6, Tremor of single fingers, 4.5 
 per second. 
 
PARALYSIS AGITANS. 
 
 227 
 
 others belong to the class of intention tremors, or to such as 
 are originated by the extension of limbs without support. 
 Furthermore, the tremor varies greatly in extent and rate of 
 rhythm at different times, and even in different parts of the 
 body of the same individual. We noticed in some cases that 
 there was a cessation of the tremor completely for an hour 
 or two daily, or in others great diminution or increase for an 
 indefinite period. 
 
 By means of an Edwards sphygmograph, numerous trac- 
 ings of tremors in various diseases have been taken at the 
 clinic, some of which were made the subject of a short con- 
 tribution on muscular tremor by myself at the meeting of the 
 American Neurological Association in Washington, September 
 20th, 1888. 1 I determined the average rate of vibration of this 
 tremor to be from 2-7 to 5.6 per second, thus agreeing with 
 all other investigators (excepting Gowers), as will be noted by 
 glancing at the following table: 
 
 Au 
 
 thor. 
 
 Publication. 
 
 Rate per Second. 
 
 Marie 
 
 
 5 
 
 4-5 
 
 5 
 
 4-14-5-34 
 
 3-43-5-57 
 
 4.8-7 
 
 5-i 
 '3-7-5-6 
 
 
 Mai. du Systeme Nerv 
 
 Ewald 
 
 Berl. klin. Woch., 1883, No. 32 
 
 Arch, fur Psych., 1885 
 
 Grashey 
 
 Huber 
 
 Virchow's Arch., Vol. 108, p. 45 
 
 Dis. of the Nerv. Syst., 1888, p. iooi t 
 Brit. Med. Journ., May 19th, 1S88... 
 Journ. Nerv. & Ment. Dis., Feb., 1889. 
 
 Gowers . . . 
 Wolfenden 
 
 & Williams 
 
 
 It is probable that all tremors are a modification of the 
 rhythmic discharges of energy from the motor ganglion cells, 
 which as is well known occur at the rate of ten per second. 
 Consequently when we have fewer per second, it is because of 
 the fusion of two or three impulses. The dicrotic character 
 of the oscillations in paralysis agitans has been demonstrated 
 by Wolfenden and Williams by means of specially-constructed 
 myographic apparatus. 
 
 Illustrations of the tremor of paralysis agitans taken from 
 various portions of the body, and also a series of myograms 
 from different diseases for comparison, are here inserted. 
 
 1 See Journal of Nerv. and Ment. Dis., Feb., 1889. 
 
228 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Ten Seconds. 
 
 
 
 
 
 
 
 
 
 
 
 ,..,. c- 
 
 ff— V 
 
 - 
 
 
 
 
 
 atf* 
 
 
 
 ^ 
 
 ^ 
 
 
 ^/^ 
 
 Ar. 
 
 fa 
 
 / 
 
 '""/•v. 
 
 
 /■■' 
 
 "\ 
 
 ^Tv"\,v . 
 
 
 \. » 
 
 
 
 •1' 
 
 i 
 
 v» A Avvvwyv^faA 
 
 Fig. 68.— A Comparative Series of Myograms of Tremor, i, Paralysis agitans ; 2, Basedow 
 disease . 3, multiple sclerosis ; 4, hysterical tremor ; 5, neurasthenic tremor ; 6, delirium tremens. 
 
PARALYSIS AGITANS. 229 
 
 Rigidity. — This cardinal symptom was present in every one 
 of the 23 cases studied, although more marked in some than 
 in others. As is well known, rigor musculorum manifests 
 itself in the extremities, trunk, neck, and face. The muscles 
 of the eyes are extraordinarily seldom affected. Debove has 
 reported cases where there was rigidity of the ocular muscles 
 {Le Progrcs Medical, 1878). In one of our cases the orbicu- 
 laris oris was so inflexible that the patient had no control 
 over it and driveled constantly. Rigidity of the lingual mus- 
 culature was observed in a few cases; and probably a certain 
 amount of stiffness of the muscles concerned in articulation 
 and phonation accounts for peculiarities of speech noted in 
 some. 
 
 In one case, a woman aged sixty-five, with a " hemi- 
 plegic type " of paralysis agitans affecting only the left side 
 of the body, the rigidity was limited with remarkable precision 
 to the muscles of the left side of the face and neck, left arm 
 and left leg, and even to the left sides of the tongue and 
 orbicularis oris. There was no history or symptom of hemi- 
 plegia. 
 
 Contractures. — Over eighty per cent of the cases presented 
 the typical position of Parkinson's disease as figured in the 
 text-books. The bowed head, flexed elbows and knees and 
 flexed metacarpo-phalangeal joints are to be looked upon as 
 a species of contracture. The flexors of the elbow were often 
 so contracted that complete extension could not be made, and 
 almost always an attempt to stretch the biceps proved painful. 
 
 One case, a woman, aged fifty-seven, was completely help- 
 less with the most advanced degree of contracture that I 
 have ever seen in this disease, with one exception. There was 
 a double talipes-equino-varus and absolute anchylosis of the 
 joints of the ankles and feet, and of all the joints of the hands, 
 of the fingers, and of the wrists, in the characteristic position, 
 but of an extremely exaggerated type. This patient could 
 move her thighs when placed in a standing position, so that 
 she could walk when supported by another ; but it was im- 
 possible for her to turn in bed, or to rise up from a chair or 
 from a recumbent position. 
 
230 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Propulsion, Retropulsion, Lateropulsion, — Eleven cases pre- 
 sented no peculiarity of gait as evidenced by " running after 
 the centre of gravity." Festination, or propulsion, alone was 
 observed in 6 cases. Both propulsion and retropulsion were 
 of frequent occurrence in 5 cases, and lateropulsion was noted 
 in but 1. Anton Heimann, who reports in detail 19 cases of 
 Parkinson's disease in his exhaustive monograph ("Ueber Para- 
 lysis Agitans," Berlin, 1888), noticed also the presence of latero- 
 pulsion in but 1 case. A tabular view of these phenomena o 
 locomotion in our 23 cases is here appended: 
 
 Form of Movement. 
 
 Propulsion only 
 
 Both pro- and retro-pulsion. 
 
 Lateropulsion 
 
 No peculiarity of gait 
 
 Total. 
 
 Males. 
 
 13 
 
 Females. 
 
 Total. 
 
 6 
 
 5 
 
 1 
 
 11 
 
 23 
 
 Tendon Reflexes. — In only 5 cases were the knee, wrist, and 
 elbow jerks exaggerated. In 2 they were hypertypical and 
 in all the rest normal. The exaggeration was not so marked 
 as in cases of organic disease of the cerebro-spinal segment of 
 the motor tract, and indeed no more than is commonly ob- 
 served in people of advanced age, in whom we ordinarily ex- 
 pect an increase of the deep reflexes. Ankle-clonus was not 
 elicited in any case. 
 
 Electrical Changes. — In one case of eight years' standing, in 
 which the disease was limited wholly to the left side, I was 
 enabled to conclusively demonstrate diminished neuro-muscu- 
 lar contractility to faradism upon the affected side. This cor- 
 roborates Benedikt's statement, who many years ago noted 
 diminution of electrical irritability in the affected extremities 
 of old cases. His further statement that neuro-muscular con- 
 tractility is markedly increased in such parts in recent cases I 
 had no opportunity to confirm. 
 
 The Voice and Speech. — Buzzard in a clinical lecture on 
 shaking palsy (Brain, January, 1880) called attention to the 
 
PARALYSIS AGITANS. 
 
 231 
 
 high pitch and piping quality of voice in some cases of the 
 disease, and other authors have mentioned the occasional 
 peculiarity of a sort of halting ejaculation of words. 
 
 There were distinctive characteristics of articulation and 
 phonation in no less than 9 of the 23 cases. There is proba- 
 bly no question that these changes depend almost wholly 
 upon a certain amount of rigidity in the muscles concerned in 
 speech and vocalization. The particular features I have 
 noted in the 9 cases are, firstly, a condition of monotonia, as 
 though there were difficulty in adjusting the vocal cords for 
 the purpose of varying the pitch; secondly, a high pitch and 
 piping quality of tone, which may possibly depend upon a 
 certain minute degree of contracture in the crico-thyroid, 
 posterior crico-arytenoid, and internal thyro-arytenoid muscles 
 (a laryngologist might make an interesting study of vocaliza- 
 tion in this disease) ; thirdly, there is often what has been well 
 termed a species of festination in speech. There will be some 
 difficulty in beginning a sentence, a hesitation upon the first 
 word, but that word having been articulated, the patient rap- 
 idly repeats the whole sentence if a short one; if it be long he 
 pronounces quickly five or six words, and then stops, appar- 
 ently to readjust his muscles previous to the ejaculation of 
 another series of words. 
 
 Thermal ParcestJiesia. — A feeling of excessive heat over 
 the whole body usually, sometimes over limited areas, has 
 been mentioned by various writers as frequent in Parkinson's 
 disease. Charcot found no alteration in temperature in such 
 cases, while a later observer, Berger, claims that there may be 
 marked peripheral increase although the general temperature 
 is normal. This subjective sensation of heat was noted in 5 
 of our cases, in 4 general, over the whole bodily surface, in 
 1 limited to the abdominal surface. This last case, a man 
 aged sixty, had such a continual feeling of intense heat over 
 his abdomen that he was constrained to keep constantly 
 lifting his clothing from that surface. I placed an Immisch 
 surface thermometer, carefully covered, upon his abdomen 
 for seven minutes, and an ordinary clinical thermometer under 
 his tongue simultaneously for the same interval of time. 
 
232 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Temperature in the mouth was 9S 1 ..', upon the abdominal 
 surface 97 . 
 
 At the summer meeting of the French Society for the Pro- 
 gress of Sciences {Centr alb. fur Nervenheilk.\ November 15th, 
 1 8891, Mosse, of Montpellier, reported his observations upon 
 this condition in 2 cases of the disease. He discovered no 
 actual increase of peripheral temperature. In 1 case the ther- 
 mal paresthesia was coincident with broad patches of super- 
 ficial redness on the back of the hands and inner surfaces of 
 the forearms. He regards the sensation of heat, as well as 
 the exanthema and oedema sometimes observed in shaking 
 palsy, as phenomena due to disturbance in vaso-motor centres. 
 
 Paresthesia of Cold. — This symptom was present in but 2 
 of the 23 cases. One woman, aged sixty-five, whose tremor 
 began in the left arm, has always had a subjective sensation 
 of cold in that arm A man, aged sixty-eight, who has the 
 disease confined to both arms, complains of a feeling of great 
 cold in these extremities. But in neither case was any par- 
 ticular coldness discoverable upon examination. 
 
 Miscellaneous Parcesthcsice. — Patients often complain of 
 numbness and prickling, sometimes of pains, in the affected 
 extremities. They often speak of the pains as rheumatism. 
 One man had shooting pains in his legs; another a dull aching 
 pain in the three members involved ; another numbness in the 
 hands and soles of the feet ; another much rheumatoid pain 
 in his two arms, which were the seat of the disease. Two wo- 
 men also suffered from pain in the limbs affected. 
 
 Restlessness. — Very many patients have a feeling of general 
 discomfort, making them exceedingly restless, especially at 
 night. It is a species of anxietas tibiarum, only it affects the 
 whole organism. Five of the 23 cases made particular men- 
 tion of this trying symptom. 
 
 Hyperidrosis. — If it is present, this symptom is, as a rule, 
 associated with thermal paraesthesia, and in. all likelihood de- 
 pends upon similar vaso-motor disturbances. Hyperidrosis 
 existed in but one of the series of cases here cited, and in him 
 the perspiration was very profuse and the sensation of heat 
 extreme. 
 
PARALYSIS AGITANS. 233 
 
 Tachycardia. — Although Marie and Azonlay (Progres Me"d., 
 1885, No. 49) mention the frequency of this symptom in cases 
 of paralysis agitans, it did not exist in any one of the cases 
 here collected. 
 
 Mental State. — Although in many cases diminished intelli- 
 gence or veritable psychoses have been described in connec- 
 tion with Parkinson's disease, there was no affection of this 
 character in any of our patients. 
 
 TREATMENT. 
 
 The exact pathology of shaking palsy not yet having been 
 determined, all treatment has thus far been more or less em- 
 pirical, or symptomatic. Treatment has been particularly 
 directed toward diminishing the tremor and lessening the 
 bodily discomfort. The following list of some of the more 
 important therapeutic agents that have been employed in the 
 disorder has a historic interest as well as pessimistic signifi- 
 cance : 
 
 Potassium bromide and iodide. 
 
 Tincture of veratrum — veratrin (Feris). 
 
 Chloride of barium (Brown-Sequard). 
 
 Carbonate of Iron (Elliotson). 
 
 Strychnine (Trousseau). 
 
 Ergotine. 
 
 Calabar bean (Ogle). 
 
 Chloral hydrate. 
 
 Opium. 
 
 Morphine (Heimann). 
 
 Atropine. 
 
 Gelsemium. 
 
 Curare. 
 
 Hyoscyamine (Charcot). 
 
 Hydrobromate of Hyoscine (Peterson and Langdon, N.Y. 
 Med. Rec, September 19th, 1885). 
 
 Fowler's solution (Eulenburg). 
 
 Arsenite of potash, subcutaneously (Eulenburg). 
 
 Coniine (Berger) 
 
 Eserine (Riess). 
 
-34 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Hcimann is an enthusiast as regards the use of morphine 
 in these cases. He says (Joe. cit.) : "It is the only remedy 
 which can for at least a short time make the patient comfort- 
 able." 
 
 Probably hyoscyamia has been employed more than any 
 other drug in the treatment of these cases at the Vanderbilt 
 Clinic. In at least two patients it has had a decidedly bene- 
 ficial effect, almost causing the tremor and restlessness to dis- 
 appear. In one or two patients the results were so bad after 
 its exhibition for a considerable time that the remedy had to 
 be discontinued. We are accustomed to prescribe one ^^ 
 grain tablet morning and evening, increasing to thrice daily 
 if desirable, but only in very rare instances giving as much as 
 -$$ grain at a dose. 
 
 Recognizing the value of opiates as a remedy or antidote 
 for the discomfort, restlessness, anxietas tibiarum, etc., from 
 which these patients so often suffer and by which they are so 
 often made continually miserable, I have lately employed 
 codeia with considerable benefit, especially when combined in 
 the form of a pill with hydrobromate of hyoscine (codeia gr. i. 
 - ij., hyos. hydrobrom. gr. yfo-) and administered twice or 
 thrice daily; while codeia possesses many of the useful attri- 
 butes of morphia, it is less deleterious in its influence upon 
 the system. 
 
 The use of warm baths of half-hour duration deserves men- 
 tion, as the best means of allaying the muscular discomfort,, 
 weariness and restlessness, of which these patients complain. 
 
CHAPTER XVI. 
 CHOREA. 
 
 Analysis of One Hundred and Twenty-four Cases. — Etiology. — Month of 
 Onset. — Relapses. — Relation to Rheumatism, Endocarditis, and Ma- 
 laria. — Duration of Attacks. — Treatment. 
 
 By WALTER VOUGHT, M.D., 
 
 First Assistant to the Nervous Clinic. 
 
 The data for this chapter have been obtained from 75 
 cases of chorea seeking treatment at the Vanderbilt Clinic 
 from the time of its opening in February, 1888, to January 1st, 
 1890, together with the records of 49 additional cases which 
 Professor Starr has kindly placed at my disposal. 
 
 The whole number of cases of nervous diseases under ob- 
 servation during this time was 2,070, so that the proportion of 
 cases of chorea to all nervous diseases would be as I to 28. 
 
 Sex. — Of the 124 cases 36 were males and 88 females; the' 
 proportion being as I to 2.16. 
 
 Age 
 
 Age 
 
 Age 
 
 Five years 3 
 
 Six 
 
 Eight 
 
 Nine 
 
 Ten 
 
 Eleven 
 
 Twelve 
 
 Thirteen years 14 
 
 Fourteen 
 
 Fifteen 
 
 Sixteen 
 
 Seventeen 
 
 Eighteen 
 
 Nineteen 
 
 Twenty years. 
 
 Twenty-eight years. 
 
 Thirty-two 
 
 Thirty-five 
 
 Thirty-seven 
 
 Forty-nine 
 
 Fifty-four 
 
 Age not stated 2 
 
 From the above table it is seen that the greatest number 
 of cases occurred between the ages of eight and fourteen 
 years, and that after fourteen years of age there is a gradual 
 decrease until twenty, after which but few cases are found and 
 these are apt to be chronic cases. 
 
 Extent. — In 76 cases, more than fifty per cent, the disease 
 
236 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 was general, and of these the right side was more affected 
 than the left in 5, and in 3 cases the opposite of this obtained. 
 Twenty cases, or sixteen and one-eighth per cent, were limited 
 to the left side alone and thirteen, or ten and two-fifths per 
 cent, to the right side. Four cases were of the " habit chorea," 
 I of them limited to the shoulders, 1 to the shoulders and head, 
 1 to the head, and 1 to the face. In 11 cases the extent is not 
 stated. 
 
 Number of tJie attack. — Of the 124 cases, 46, i.e., thirty- 
 seven per cent, were first attacks and 54, i.e., forty-three and 
 five-tenths per cent, were relapses ; of these 54, 30, i.e., twenty- 
 four and one-fifth per cent of the whole number of cases, were 
 second attacks; 6 were third, 5 were fourth, 4 were fifth at- 
 tacks, 1 was the sixth, 1 the seventh attack and 4 patients are 
 recorded as having had several preceding attacks, 1 was the 
 eighth, 1 the ninth attack, 2 cases were chronic, and in 24 cases 
 the number of the attack is not stated. 
 
 Frequency of Relapses. — Examination regarding the fre- 
 quency shows that 1 case had nine attacks, 1 case seven at- 
 tacks, 2 cases four attacks and 2 cases three attacks in a cor- 
 responding number of years. One case had five attacks in 
 fifteen years and on each occasion the affection was limited to 
 one side of the body; in 1 case there were four attacks in 
 fourteen years, and in I case exacerbations occurred twice 
 yearly for five years. 
 
 Month of Onset. — In 74 cases where it was possible to ac- 
 curately determine the month of onset, it was found that 11 
 each began in September and October, or nearly thirty per 
 cent, and in the months of April, May, and June, 21 cases, or 
 more than twenty-eight per cent. By reference to the chart 
 it will be seen that, beginning with February, the frequency 
 rises steadily to May, then falls to July, and again steadily 
 rises to September, remaining up through October, when it 
 suddenly drops to remain down through December, rising 
 slightly to January when it again falls to February. The 
 curve of the months of applying for treatment will be found 
 on the same chart and undergoes almost the same variations 
 as the months of onset (See Fig. 69). 
 
CHOREA. 
 
 237 
 
 An interesting fact was presented by 3 cases; 1 of them 
 had had nine attacks in as many years and each attack began 
 in September, 1 had 3 attacks in as many years, each begin- 
 ning in February, and the third had 4 attacks in as many years, 
 each beginning in the spring of the year. Dana's ' observa- 
 tions correspond closely to these, he finding, from 130 cases, 
 that the disease was most frequent in the spring months, next 
 to these in the fall months, then in the winter and least frequent 
 in summer. When the different statements of different authors 
 on this point are examined, it seems probable that the disease 
 
 No. Cases. | Jan. Feb. Mch. Apr. May. June. July. Aug. Sept. Oct. Nov. Dec. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 V 
 
 
 
 
 
 
 
 
 
 
 
 
 
 V 
 
 
 
 
 
 *.. 
 
 . 
 
 
 ,< 
 
 
 \ 
 
 
 \ 
 
 
 . 
 
 
 .m' 
 
 
 
 
 4 
 
 
 
 \ 
 
 
 
 '#•' 
 
 
 
 
 
 V 
 
 
 
 
 ( _« 
 
 .» 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 69. — Diagram to show Relation of the Development of Chorea to Months. Line = applied 
 for treatment; clotted line = disease began. 
 
 does not occur everywhere with equal frequency during the 
 same seasons of the year. Thus Lewis, 2 of Philadelphia, found 
 that March had the highest number and October and Novem- 
 ber the lowest. Koch 3 found that most of his cases occurred 
 in December. Gowers 4 says, "in this country (England) the 
 influence of season does not seem to be great." Meigs and 
 Pepper, 5 quoting Gerhardt and Weir Mitchell, say that they have 
 observed that chorea occurs more frequently and in a more 
 severe form in the spring than at any other season and that 
 relapses of the disease are most apt to take place at that time. 
 
 1 N. Y. Med. Jour., Apr. ist, 1889. 2 Polyclinic, Jan., 1S87. 
 
 3 Deut. Arch. Klin. Med., Bd. xl., Heft 5-6. 
 
 * Dis. of the Nerv. Syst., vol. ii., p. 549. 5 Dis. of Children, 7th Ed., p. 611. 
 
238 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 From the above we may conclude that there exists a 
 marked tendency for the disease to relapse; that this is 
 more marked during the first year after the first attack, and 
 that with* each following year the liability to a return dimin- 
 ishes progressively. In addition to the tendency to relapse, 
 there is also shown a tendency to relapse at certain times of 
 the year. 
 
 Etiology.— Rheumatism was present or had previously ex- 
 isted in 21 cases, being assigned as the direct cause in 10. 
 Fright was the cause in 14 cases, overstudy at school in 2, 
 over-excitement, overwork, measles, and pregnancy each in i # 
 In 2 cases the disease followed a fall. The combination of 
 rheumatism and scarlet fever is said to have been the cause 
 in 1 case. No cause was found in 81 cases and in 6 cases it is 
 distinctly stated that there was no fright. Malarial poisoning 
 was the cause in 3 cases. 
 
 The Relation between Malarial Poisoning and Chorea. — As 
 above stated, in three cases this was the cause, and inas- 
 much as the proofs in 2 of these cases were positive and in the 
 third a strong probability existed, it has been thought worth 
 while to cfive the histories of these cases. The first of these 
 patients was a girl ret. nine years, who applied for treatment 
 October 12th, 1889, giving the following history. During two 
 weeks in August preceding she had been at College Point, 
 Long Island ; while there she was in her usual health ; soon after 
 she began to complain of general pains, headache, poor appe- 
 tite and to have some fever in the afternoons, and she lost her 
 previous good color. Two weeks before applying for treat- 
 ment she had been much frightened by burglars in the house, 
 and the muscular twitchings began a few days afterward. She 
 had never had chorea or rheumatism. Examination showed 
 a well-marked chorea, the spleen enlarged, and an anaemic 
 bruit at the base of the heart, and examination of the blood 
 showed the presence of the crescentic and pigmented intra- 
 cellular bodies characteristic of malarial poisoning. She was 
 put upon arsenic and quinine and on January 20th, nine 
 weeks after, was completely well. 
 
 The second patient was a lad a.-t. ten, who had had an attack 
 
CHOREA. 
 
 239 
 
 five years previously. He had never had rheumatism. His 
 trouble began three weeks before application for treatment. 
 Examination showed marked chorea. The patient was unable 
 to feed himself. There was heard over the cardiac apex a soft 
 blowing systolic murmur, no cardiac hypertrophy. Examina- 
 tion of the blood showed the presence of a few pigmented in- 
 tracellular bodies. The patient was treated with Fowler's 
 solution, and was completely well in four weeks. 
 
 The third patient was a lad set. eleven, who four years previ- 
 ously had had a similar attack lasting three weeks. Present 
 attack began one week ago. No fright; never had rheuma- 
 tism. Physical examination was negative. Put on Fowler's 
 solution for two weeks; at the end of that time, the patient 
 being no better, sulphate of quinine three grains, three times a 
 day were given. He was completely well at the end of three 
 weeks, improvement being marked at the end of one week. 
 
 The attention of the writer was called to the possibility of 
 a relation existing between malarial poisoning and chorea, by 
 Dr. A. B. Pope of the Children's Department of the Clinic, - 
 in the summer of 1889, he having observed that some patients 
 would recover in a short time when treated with quinine, 
 other lines of treatment having been tried in vain. The 
 blood from six different patients was examined with negative 
 result, but in all of these treatment had been begun before 
 the examination. The seventh patient examined was the first 
 above cited; she was examined at the time of first application 
 for treatment, as were the second and third patients. Since this 
 time other patients have been similarly examined but with neg- 
 ative results, examination being made at the time of applica- 
 tion for treatment. It would be desirable to continue the 
 examination of the blood from cases of chorea to see what 
 connection, if any, exists between malarial poisoning and it, 
 it being the writer's belief that some relation exists between 
 the two diseases in this city ; whether it be any more than that 
 malarial poisoning acts as a predisposing cause is at present 
 difficult to say. It is the hope of the writer that others may 
 follow out this line of observation. 
 
240 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Eichhorst ' says that the disease may follow intermittent 
 fever. 
 
 Weir Mitchell says: "There is, however, no evidence to 
 favor the view that chorea can have a malarial origin except 
 that it arises in spring with as much certainty as ague." 
 
 That malarial poisoning gives rise to neuralgias and head- 
 aches is acknowledged. In the blood from a case of beriberi 
 where well-marked neuritis was present the writer found the 
 malarial organism, and in a case of multiple neuritis with dis- 
 tinct history of chronic malarial exposure the examination of 
 the blood showed the presence of the malarial organism. 
 
 The depreciated physical condition which patients are 
 often brought to from prolonged malarial poisoning certainly 
 predisposes to the development of chorea. Chorea is not as 
 common in the negro as in the white. Mitchell says that the 
 weight of evidence is in favor of the opinion that the black is 
 less liable to chorea than the white, and the infrequency of 
 malarial poisoning in the negro is well known. It is in the 
 spring and fall that we see the most manifestations of malarial 
 poisoning, and in the fall months especially do we find most 
 of the cases of chronic malarial poisoning. Of 74 cases of 
 chorea, where the beginning of the disease could be accurately 
 determined, 8 began in May and 1 1 each in September and 
 October. We know that one attack of malarial fever predis- 
 poses to other attacks; the liability of chorea to relapse at 
 certain times of the year has been spoken of. 
 
 The treatment of malarial poisoning by the administration 
 of arsenic is the one that meets with the most success, likewise 
 this is the standard treatment of chorea. 
 
 Relation to Rheumatism. — The possibility of chorea being 
 the result of some infectious material in the system has been 
 put forward by the following authors, Joffroy, 3 Leube, 4 Eulen- 
 burg, 5 Prior, 6 Strumpell. 7 One writer, Koch (1. c), considers 
 
 1 Pathologie und Therapie, Aufl. 3, Bd. 3. 
 
 3 Dis. of Nerv. Syst., 1881, p. 141. 3 \ jf > Progrcs Medical, 1885, No. 22. 
 
 4 Deutsches Archiv fur klin. Med., Bd. xxv., S. 242. 
 
 s Real Encyc, iv., 269. 6 Berl. klin. Woch., 1S86, No. 2. 
 
 7 Lehrb. d. Inn. Krankh., I5d. ii., S. 441. 
 
CHOREA. 24 1 
 
 that "a definite cause is demanded for chorea with its charac- 
 teristic and constant train of symptoms, its typical course, and 
 necessarily well-defined localized anatomical seat." That a 
 relation exists between rheumatism and chorea and between 
 endocarditis and chorea writers on this subject are at present 
 generally in accord, and the most convincing proofs of this 
 are given by Osier, 1 who found that of no cas-es of chorea 
 re-examined at periods varying from two years to sixteen 
 years after the attack for which they had sought treatment, 54 
 cases presented signs of valvular disease ; that in 22 cases, forty 
 and seven-tenths per cent, there was a distinct history of artic- 
 ular trouble sometimes with the chorea, but in 6 cases, from 
 one to five years after the attacks. The larger proportion, 
 fifty-nine and three-tenths per cent, of the cases were without 
 any history of rheumatic trouble. Of the 21 cases which had 
 had three or more attacks of chorea, only 7 had had rheuma* 
 tism. 
 
 In the author's cases endocarditis was present in 12 and 
 existed without rheumatism in 6, and dependent on it or at 
 least coexisting with a distinct history of it in 5. In 1 case, ex- 
 amined one year after an attack, endocarditis had developed. 
 
 Koch having previously considered the relation existing 
 between chorea, polyarthritis, and endocarditis says: "Thus 
 we see how chorea, polyarthritis, and endocarditis may occur 
 in varying order. The primary affection has in the vast ma. 
 jority of the cases its seat in the nervous system, less often in 
 the joints, and least of all in the endocardium. It is caused 
 by the characteristic choreaic virus, but often indeed by that 
 of polyarthritis closely allied to it, and perhaps in isolated 
 cases other infectious germs may give rise to a like train of 
 symptoms." 
 
 When we consider that an injury may give rise to tuber- 
 culosis, exposure to cold and wet to rheumatism, and to a new 
 attack of intermittent fever (in one predisposed to it), as the 
 writer himself has not infrequently seen, why is it not in per- 
 fect accord with the theory of an infectious disease that the 
 nervous system being a locus minoris resistentiae may, by a 
 
 1 Am. Jour. Med. Sci., vol. xciv., p. 372. 
 16 
 
242 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 sudden psychic effect, as fright or a fall, or by more gradual 
 ones as over-study, over-work, or systemic weakening from 
 pregnancy, become the seat of invasion of an infectious mate- 
 rial or predisposed to its development ? 
 
 Complications. — Acute articular rheumatism developed in 4 
 cases during the existence of the attack of chorea. 
 
 Endocarditis existed in 12 cases and in 6 of these it was 
 independent of rheumatism, in 5 cases a rheumatic history 
 was found, and in the other case no mention was made either 
 of the presence or absence of this disease. The mitral valve 
 was affected in 6 cases, and in the other 6 no mention is made 
 on this point. In 93 cases the positive 1 absence of endocar- 
 ditis is noted and in the remaining 19 no mention is made. 
 
 Hajmic or functional murmurs were present in 10 cases. 
 
 One case examined one year after the cure of a first attack 
 had in the interval developed chronic endocarditis. 
 
 Melancholia coexisted in 1 case, speech was markedly 
 affected in 2 cases, and 2 patients were feeble minded; night 
 terrors were present in 2 cases, irritability of temper was pres- 
 ent in several, and 1 case was of such severity that there was 
 complete inability to perform any voluntary motion, the pa- 
 tient being confined to bed unable to move or to speak. 
 
 Electrical Reaction. — In 5 cases of hemi-chorea examined, 
 there was an increased irritability of the muscles of the af- 
 fected side in response to the faradic current. In another 
 case no difference could be detected. 
 
 THE DURATION OF THE DISEASE AND ITS TERMINATION. 
 The Duration of the Disease in Cases Cured. 
 
 2 weeks, .... 
 
 4 "... . 
 
 6 "... 
 
 8 "... . 
 12 "... 
 16 "... 
 20 "... 
 Unknown, 
 
 1 This is, of course, as far as diagnostic means will permit. 
 
 in 
 
 I 
 
 case. 
 
 << 
 
 13 
 
 cases. 
 
 (< 
 
 4 
 
 << 
 
 a 
 
 4 
 
 « 
 
 a 
 
 4 
 
 it 
 
 (t 
 
 4 
 
 a 
 
 it 
 
 1 
 
 case. 
 
 a 
 
 2 
 
 cases. 
 
CHOREA. 243 
 
 Cases Improved. 
 
 in 3 weeks, ..... 2 cases. 
 
 in 4 " 11 
 
 in 6 " . . . . .1 case, 
 in 12 " . . . .2 cases. 
 
 Three cases were unimproved after one, five, and twenty- 
 one months respectively. 
 
 In 1 case where the disease had lasted for one year, cure 
 was affected in two months. 
 
 Four cases of adult chorea occurring in patients of thirty- 
 two, thirty-seven, forty-nine, and fifty-four years of age re- 
 spectively, and lasting from five months to four years before 
 application for treatment was made, were not materially 
 benefited. 
 
 Three cases of chronic chorea occurring in patients of thir- 
 teen, fourteen, and seventeen years of age and existing four, 
 five, and two years respectively, were also not benefited by 
 treatment, but it seems probable that the inability to attend 
 regularly, bad hygienic surroundings, and the early discour- 
 agement which dispensary patients show if they do not im- 
 prove rapidly, was a large factor in the failure of a cure or im- 
 provement. 
 
 TREATMENT. 
 
 In all cases the patient's general health has been attended 
 to, the withdrawal of all bad influences and surroundings 
 secured, and the correction of any errors of refraction in the 
 eye made. Rest of body and mind as far as possible, and the 
 administration of baths and good food ; the administration of 
 arsenic and chloral ; and the use of quinine and iron for the 
 anaemia are the therapeutic measures employed in all the 
 cases. Arsenic is given in as large doses as the patients can 
 bear, beginning with a small dose and increasing gradually. 
 When symptoms arise from its administration, cessation for a 
 few days and beginning at the dose left off has been the rou- 
 tine treatment. One of the greatest difficulties to contend 
 against in dispensary practice is the withdrawal of the patient 
 from school. This is in many cases a very difficult thing to 
 
244 FAMILIAR FORMS OF NERVOUS DISEAES. 
 
 accomplish, parents not appreciating the value of this as a 
 therapeutic measure. Parents are in all cases warned of the 
 liability to relapse and are requested to bring their children 
 for examination at the slightest symptoms of any return of 
 the disease. 
 
 PARAMYOCLONUS MULTIPLEX, AND ITS DIAGNOSIS FROM 
 CHOREA. WITH A REPORT OF A CASE. 
 
 By DR. STARR. 
 
 Paramyoclonus multiplex is a spasmodic affection of the 
 muscular system of peculiar character, distribution, and course, 
 dependent upon irritation of the nervous motor mechanisms, 
 and somewhat resembling chorea, hence it is appended to this 
 chapter. 
 
 The chief features of this disease are illustrated by the fol- 
 lowing case : 
 
 John D., aged thirty-three, of Kingston, Canada, a grocer, 
 of good family history, but of nervous temperament, was in 
 his usual health until September 15th, 1886, when he strained 
 his back and right shoulder by lifting a box, sixty pounds in 
 weight, while in an awkward position. The pain, below the 
 right shoulder blade, resulting from this strain was so severe 
 that he went at once to his physician, Dr. H. J. Saunders, in 
 whose office he had a peculiar attack. He began to cry and 
 scream with pain and soon felt a choking sensation and was 
 unable to get his breath; then followed convulsive movements 
 of the body and legs, the latter being drawn up and thrust out 
 forcibly. These lasted an hour, after which he was taken 
 home. They returned at short intervals, for three days, being 
 attended by pain in the back ; and then they began to involve 
 the muscles of the upper extremities and neck; and a few 
 twitching movements of the face also occurred. The spasms 
 were always very rapid, but were chiefly confined to muscles 
 attached to the trunk, it being noticed from the first that the 
 muscles of the forearms and hands and of the legs and feet 
 did not take part in the spasms. The diaphragm was affected 
 
PARAMYOCLONUS MULTIPLEX. 245 
 
 usually, so that dyspnoea and exhaustion attended the attack, 
 and it was occasionally followed by vomiting, when occurring 
 after a meal. He had at first ten or twelve such attacks in 
 twenty-four hours, each lasting nearly an hour. After two or 
 three weeks, the attacks became less severe, the legs being less 
 violently moved, and their duration decreased. But they had 
 continued until May 2d, 1887, when I saw him, varying in 
 severity and duration, but constantly diminishing, so that then 
 he was having but three or four a day, though sometimes they 
 were more frequent. He had several attacks in my presence, 
 each lasting from one to five minutes, and leaving him much 
 exhausted. The muscles first affected were those of the back 
 and abdomen, a series of quick, alternate contractions of the 
 dorsal muscles and of the recti abdominis, resulting in a rapid 
 protrusion and retraction of the abdomen. As this became 
 more rapid and forcible, the body and head were thrown back- 
 ward and forward, without any spasm of the muscles of the 
 neck, and in one attack which occurred while he was standing, 
 similar complementary movements to preserve his balance 
 produced alternate slight flexion and extension of the hips. 
 In a much more severe attack which was observed when he 
 was stripped, the muscles involved were first those of the back 
 and abdomen already mentioned ; then the neck muscles, so 
 that the head was not only nodded, but was turned from side 
 to side; then the muscles of the upper arm, the pectorals, 
 deltoid, biceps, and triceps, being all in action, and lastly, the 
 muscles of the thigh, the quadriceps femoris, biceps, and semi- 
 tendinosus and semi-membranosus, with the glutei, acting with 
 such force as to cause movements of both hip and knee-joints. 
 The contractions of these muscles were rapid, the rate rising 
 to ninety per minute. The spasm in the arms was not severe 
 enough to move the shoulder or elbow joints, but the muscles 
 named were seen to contract and raise the skin. He said that 
 the wrist and fingers, ankles and toes, had never participated 
 in the spasm. He had noticed that formerly there was some 
 movement in the forearms, probably of the supinator longus 
 muscles, but this I did not see. There was also, in a severe 
 attack, a spasm of the diaphragm resulting in a long inspira- 
 
246 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tion, accompanied by a sound, and while this was tonic, rapid 
 movements of the intercostal and accessory respiratory mus- 
 cles to supply the lack of inspiratory action of the diaphragm 
 were made. Only at the very first had there been seen any 
 spasm of the facial muscles, and for some months these had 
 not been affected. 
 
 The spasms were so severe as to make me fear that he 
 would fall while standing, as he said he had done several times, 
 and would nearly throw him out of an arm chair when sitting. 
 They came on suddenly, but were usually preceded by a pecu- 
 liar sensation which ascended from the legs to the head, and 
 ceased as suddenly, leaving him in a state of considerable ex- 
 haustion, panting and perspiring, and looking badly as if about 
 to faint. During the interval between the spasms an occa- 
 sional fibrillary twitching in the muscles of the back and pec- 
 torals was observed, but not elsewhere. He could not stop 
 the spasm voluntarily or in any way limit its course. Nor 
 could he start it voluntarily. But any exposure of the skin to 
 cold, any irritation of the skin by electricity, any tapping of 
 the tendons at the knee or attempt to elicit ankle clonus was 
 sufficient to start a spasm at once. He said it often came on 
 after muscular effort, such as a long walk. It was also more 
 likely to occur after mental excitement, and it usually came 
 on when he began to talk about his condition or went to see 
 a stranger. From the beginning of the affection, pressure on 
 the right shoulder blade, where he had the pain, produced a 
 spasm at once. It ceased during his sleep and never woke 
 him by occurring at night. He thought that a drink of 
 whiskey arrested it sometimes. 
 
 His motor power, sensory perception, and voluntary co- 
 ordination were not in anyway impaired. His skin and tendon 
 reflexes were exaggerated, a marked ankle clonus being pres- 
 ent on both sides. His muscles responded normally to both 
 electrical currents. Mentally, he was perfectly clear, but 
 somewhat excitable, and after each attack in his exhausted 
 condition, tears came to his eyes as he spoke of his trouble. 
 He did not appear, however, to be of an hysterical tempera- 
 ment. Treatment had been somewhat successful, as he con- 
 
PARAMYOCLONUS MULTIPLEX. 247 
 
 sidered his condition much better than it had been six months 
 ago, for he said that the attacks were less severe, shorter, and 
 less frequent. Dr. Saunders reported his cure four months 
 after I saw him. 
 
 This spasmodic affection, limited to the muscles of the 
 body and proximal portion of the limbs and only occasionally 
 affecting the neck and face, has been termed by Friedreich, 
 who described it first, as paramyoclonus multiplex. Since 
 its first description, a number of cases have been reported 
 by Lowenfeld, Marie, Silvestrini, Bechterew, Seeligmiiller, 
 Homen, Remak, Fry, and Vanlair. It must be regarded as 
 a distinct disease, since it is different from chorea, from hys- 
 terical spasms, from epileptiform convulsions, from convulsive 
 tremor or tetanilla, and from tic convulsif. 
 
 Its causation is uncertain. In 3 cases fright, in 1 case 
 severe hemorrhage, which may have caused fright, in 1 case the 
 shock of a cold bath, and in my own case an overstrain causing 
 pain have preceded the development of the spasm. In Fry's 
 case over-exertion was the cause. Vanlair thinks it may be 
 due to severe peripheral irritation. In 2 of the cases, a chronic 
 spasmodic affection had been present for several years. It 
 has been observed twice in a female, the remaining cases being 
 males. The age of the individual has little to do with its 
 development, for persons of all ages from ten to fifty-two have 
 been affected. Its symptoms are quite characteristic. The 
 spasms are bilateral and symmetrical. They are limited to 
 certain muscles. In 8 cases, the quadriceps femoris and flexors 
 of the leg, and the so-called " upper arm group of muscles," 
 the deltoid, biceps, and supinator longus, were affected. In 
 7 cases, the muscles of the back were involved. In 6 cases, 
 the muscles of the neck contracted; in 5 cases, the glutei. 
 In 4 cases, the face and the diaphragm were involved. In no 
 case have the muscles of the hands or forearms, of the feet or 
 legs been affected. The usual limitation of the spasm to the 
 body muscles with those of the thighs and arms is very 
 noticeable. 
 
 The character of the spasm is also characteristic. It is a 
 rapidly repeated clonic spasm occurring at intervals. In 6 
 
248 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 cases, the rate of contraction has been counted. It has varied 
 from 50 per minute to 180 per minute. In my own case, it 
 was about 90. It is not a sudden, single, irregular muscular 
 contraction, like that of chorea, but appears to be always 
 bilateral and to involve several muscles of a physiological 
 group at once, thus resulting in a series of movements, any 
 one of which can be voluntarily made. In several cases, a 
 tonic contraction has occurred in one or more of the muscles 
 affected, before or during the clonic seizure. In my own case, 
 the spasm of the diaphragm was tonic for one-eighth to one- 
 quarter of a minute during each attack, and in the early at- 
 tacks, the spasms of the back were tonic for some seconds. 
 The clonic contractions continue, when once set up, for a 
 varying time, from half a minute to ten minutes, and are 
 succeeded by a complete interval of freedom from spasm. In 
 my own case, this interval had varied from half an hour to 
 about one week. And the fact that the free quiet intervals 
 were getting longer had encouraged him to hope for a recov- 
 ery. During the spasm itself, the resulting movements were 
 of a very violent nature. The head was thrown about by the 
 movements of the body, rendering the patient dizzy. The 
 body was tossed about in the chair, so that there seemed to 
 be danger of his being thrown out upon the floor. If the 
 spasm occurred while he was walking, he was quite liable to 
 be thrown down, and had hurt himself several times. But this 
 violence is not always present — for in two cases, the spasms 
 were never severe enough to cause a movement of the joints, 
 and were only observed when the patient was stripped — being 
 then of the nature of a fascicular twitching. In my own case^ 
 such a fascicular muscular twitching was occasionally seen 
 during the intervals in the muscles of the back and the 
 pectorals. 
 
 In the majority of the cases, any tapping of the tendons or 
 any irritation of the skin was sufficient to produce a spasm. 
 This seems to be an important point, for I am not aware that 
 it has been observed in hysterical or choreic spasms. It is 
 true that, in hysterical cases, certain zones or areas can occa- 
 sionally be found on the body, irritation of which may cause 
 
PARAMYOCLONUS MULTIPLEX. 
 
 249 
 
 or may arrest the attack. But in this condition the spasm is 
 produced by irritation anywhere on the skin — or by tapping 
 the tendons at the knee and ankle — and was not associated 
 with disturbances of sensation, which are characteristic of 
 hysterical zones. The knee-jerk has been increased in 4 cases, 
 was less in 1 case, and was not tested in the remainder. The 
 skin reflexes were also increased in 4 cases, and are mentioned 
 as normal in but one of the remainder. Mental excitement 
 seems to have predisposed to the onset of the spasm in 3 
 cases. Had the disease been hysterical in nature, this would 
 probably have been observed in a larger proportion. Volun- 
 tary effort stopped the spasm in 4 cases and made it worse in 
 3 cases. Had the disease been hysterical, volition would 
 probably not have influenced it favorably in the majority of 
 cases. The spasm has ceased during sleep in 4 cases, but has 
 continued in 1 case. 
 
 In none of the cases have consciousness, motion, sensation, 
 co-ordination, or. electric excitability been in any way affected 
 — an important negative fact, since it proves at once that the 
 condition is a functional neurosis, and makes it very unlikely 
 that it is of an epileptic or an hysterical nature. In one case, 
 which died of phthisis, a careful exmination by Prof. Schultze, 
 of Heidelberg, failed to reveal any lesion of the nervous system. 
 
 It is evident from this review of the symptomatology that 
 the characteristics of the disease are quite distinct ; that it 
 can be differentiated from chorea, from hysteria, and from 
 epilepsy. 
 
 These characteristics may be summed up as follows : Par- 
 amyoclonus multiplex is a spasmodic affection of the muscular 
 system, occurring bilaterally in symmetrically situated mus- 
 cles attached at one or both ends to the trunk, and in muscles 
 whose function is associated with these, consisting of a series 
 of violent clonic spasms of considerable rapidity and severity, 
 occurring only at intervals; and associated with fascicular 
 tremors of the affected muscles, persisting during the interval 
 between the spasms. It occurs after some mental or physical 
 strain, and is not accompanied by any disturbance of sensory 
 or motor functions, excepting by an increase of the superficial 
 
250 FAIUMAR FORMS OF NERVOUS DISEASE. 
 
 and deep reflexes. It can be excited by irritation of the skin 
 or tendons. 
 
 In regard to the prognosis, it may be said that this is fa- 
 vorable. The majority of the cases have recovered quite rap- 
 idly under treatment. In 2 cases, however, relapses have 
 occurred. 
 
 The treatment which has been of most service has been 
 the application of strong galvanic currents to the spine and 
 neck, and the application of the anode to sensitive points in 
 case these exist. Under this treatment Fry's case recovered 
 in three weeks. Many nerve sedatives have been used, and 
 also nerve tonics. The exact effect of these seems to be 
 doubtful. In my own case, sedatives, tonics, and electrical 
 applications had all been equally futile to arrest the attacks, 
 but the patient had improved to a considerable degree under 
 the varied treatment. I prescribed galvanism to the spine, 
 arsenic and chloral with some beneficial effect. Hammond 
 has advised the hypodermatic use of arsenic. 
 
 It is useless to discuss the nature of the disease from so 
 few cases as are at our disposal. It has been regarded as a 
 functional neurosis, and to this all must agree, both on ac- 
 count of the absence of any lesion, in one case examined by 
 the most competent neuro-pathologist in Germany, and on ac- 
 count of the absence of symptoms of organic disease and the 
 recovery of the cases. Whether it has a central origin and is 
 produced by a hyper-excitability of the brain or spinal cord, 
 induced by the sudden vaso-motor spasm accompanying fright 
 or mental or physical strain, as Friedreich believed, or whether 
 it may be a reflex spasm due to some peripheral irritation 
 which, being conveyed to the spinal and medullary centres, 
 produces the spasm reflexly, as another author has suggested, 
 remains for the future to decide. The case here reported 
 would seem to favor the latter view. 
 
 BIBLIOGRAPHY. 
 
 1. Friedreich : Virchow's Archiv, Bd. 86, S. 421. See also Schultze, Neurol. 
 
 Centralbl., 1886, 363. 
 
 2. LoWENFELD : Neurol. Centralbl.. 1884, p. 395. 
 
PAR AM YOCLONUS MUL TIP LEX. 
 
 2 5 I 
 
 3. Marie: Progres Medical, 1886, Nos. 8 et 12. 
 
 4. Silvestrini, quoted by Marie, 1. c. Medicinia Contemporanea, May, 1886. 
 
 5. Bechterew: Neurol. Centralbl., 1887, p. 181. 
 
 6. Seeugmuller : Dent. Med. Wochen., 1886, No. 24. 
 
 7. Homen : Archives de Neurologie, 1887, p. 200. 
 
 8. Remak : Arch. f. Psych., xv., 8, 853. 
 
 9. " Convulsive Tremor," Hammond, N. Y. Med. Jour., 1867. 
 ro. Hammond: " Nervous Diseases," 1886. 
 
 11. Hammond : " Report of a Case of Convulsive Tremor," Post-Graduate Quar- 
 
 terly Bulletin, vol. i., p. 246. 
 
 12. Brown : Ditto, p. 263. 
 
 13. Henoch ; " Diseases of Children," Wood's Library, p. 81. 
 
 14. Fry : Jour. Nerv. and Ment. Dis. , 1888, p. 397. 
 
 15. Zichen : Arch, fur Psych., 1888, xix., 465. 
 
 16. Marina: Arch, fur Psych., xix., p. 684. 
 
 17. Vanlair : Rev. de Med., 1889. 
 
 18. Faldella : Revis. Sper. de Fren., xiv., p. 193. 
 
 19. Bechterew : Arch, fiir Psych., xix. 
 
CHAPTER XVII. 
 EPILEPSY. 
 
 A classification of epileptics. — The causes of the disease. — The frequency 
 of attacks. — The aura. — Psychical epileptic equivalents. — Reflex 
 neuroses of an epileptiform type and their diagnosis. — The treat- 
 ment of epilepsy. 
 
 EPILEPSY is such a common disease, two persons in every 
 thousand being epileptics, that every fact which can be estab- 
 lished regarding its causation, its phenomena, its nature, or its 
 treatment is of importance. The study of a large number of 
 cases enables the physician to divide epileptics into certain 
 groups — such as those suffering from convulsive attacks (grand 
 mal), and those, suffering from slight attacks without move- 
 ments (petit mal) ; or, those in whom the attack is preceded 
 by an aura, and those in whom no aura occurs; or those in 
 whom an organic nervous lesion, or a source of peripheral 
 irritation, or no ascertainable cause can be found. Such at- 
 tempts at classification are found to lead to the conclusion 
 that epilepsy is a protean affection, presenting very different 
 features in different groups of cases. The study of these 
 groups results in a division of all epileptics into three classes 
 — the first, in which the disease is distinctly cortical in origin ; 
 the second, in which the disease is medullary in origin; the 
 third in which it is reflex in origin. 
 
 In the first class of cases the epileptic attack presents many 
 features which resemble those found in one or other of the 
 forms of Jacksonian epilepsy already studied (Chapter IV.). 
 The attack begins with a conscious sensation, either a sensa- 
 tion of motion, or of tingling and numbness, or of light or 
 color, or of sound or smell or taste, or some visceral feeling 
 such as nausea, suffocation, palpitation, etc., etc. Such spon- 
 taneous conscious s-ensations imply necessarily, as we have 
 
EPILEPSY. 253 
 
 already seen, cortical irritation. Or the attack begins with 
 peculiar abnormal states of consciousness which will be de- 
 scribed further on as the psychical epileptic equivalent. The 
 attack goes on to a more or less general series of move- 
 ments. These may be merely a twitching of the eyes, smack- 
 ing the lips, irregular balancing motions of the body to prevent 
 a fall, or awkward movements of the hands; such as occur in 
 many light attacks. They may on the other hand present all 
 the features of a severe general convulsion, with a cry, a biting 
 of the tongue, and enormous and powerful motions in every 
 muscle of the body. In Jacksonian epilepsy, as we have seen, 
 the spasm may be limited to one limb, or may invade an adja- 
 cent part, or may become unilateral, or may finally become 
 general. In Jacksonian epilepsy the rate of extension is slow. 
 In this first class of epileptics the extension of the movements 
 is very much more rapid, but it is found that there is such an 
 extension and that the attack, as a rule, does not begin, as in 
 the second class of cases, at once in all the parts. The attack 
 is succeeded by a condition of deep sleep or of great mental 
 confusion. All the functions of the cortex appear to be for a 
 time suspended. The patient is unable to think clearly, to 
 give any account of himself, or to realize what has occurred. 
 In Jacksonian epilepsy the spasm is succeeded by paralysis, 
 the hallucinations of vision by blindness, the tingling by anaes- 
 thesia, the movement by ataxia. Thus in both Jacksonian 
 epilepsy and in this first class of epileptic cases there is evi- 
 dence of severe involuntary cortical irritation, beginning in 
 one region and extending to others, and followed by a suspen- 
 sion of cortical activity for a time. The analogy between the 
 phenomena is very striking. It seems reasonable to conclude 
 that since Jacksonian epilepsy is known to be due to irritation 
 in the cortex, in the first class of epileptic cases the seat of 
 the disease is in the cortex of the brain. In this first class of 
 epileptics are included, therefore, all cases of petit-mal and of 
 grand-mal with an aura, and all cases of so-called psychical 
 epileptic equivalent, soon to be considered, as well as all cases 
 of epilepsy from traumatic affections of the cortex and from 
 organic cortical disease. 
 
254 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 In the second class of cases the epileptic attack presents a 
 different series of phenomena. There is no conscious warning. 
 There is a sudden loss of consciousness only (petit-mal) or a 
 sudden general convulsion with loss of consciousness. Fol- 
 lowing the attack there is, in some cases, the same condition 
 of confusion and coma which occurs in the first class, but in 
 other cases this is absent. Such attacks resemble the attack 
 with which a gross lesion in the pons Varolii and medulla 
 oblongata usually begins. Furthermore, such attacks can be 
 experimentally produced by irritation of these parts of the 
 brain in animals, as Nothnagel showed in 1872. Epileptic at- 
 tacks have been long ascribed to a discharge of nervous energy 
 from the medulla, or to vaso-motor spasm whose starting- 
 point is supposed to be from the medulla. The arguments 
 urged by Nothnagel ' and recently restated by Ziehen 2 in 
 support of this view have much strength and afford a satis- 
 factory explanation for this second class of epileptic cases. 
 They do not explain the first or third classes of cases at all. 
 In this class are included all cases without aura, commonly 
 called genuine idiopathic epilepsy. 
 
 In the third class of cases, which is very small in compari- 
 son with either of the other two classes, the origin of the epi- 
 leptic attack is found in a source of peripheral irritation. It 
 has long been known that an injury to any part, especially if 
 that injury causes a division or compression of a nerve trunk, 
 may be followed by epileptic attacks, in a person previously 
 free from epilepsy. It is sometimes noticed in these cases, 
 that a sensation in the scar precedes the attack, or that pres- 
 sure on the scar will bring an attack on. It has long been 
 known that, in nervous little children, persistent irritation of 
 the genital organs, such as may be due to phimosis, to concre- 
 tions beneath the prepuce, or to foreign bodies in the vagina, 
 or such as may be produced by masturbation, gives rise to 
 attacks of an epileptiform kind. It has long been known 
 that in some women the function of menstruation is uniformly 
 attended by seizures of a nervous character resembling epi- 
 
 1 Nothnagel : Ziemssen's Cyclo. of Med., Amer. Edit., vol. xvi., pp. 185 to 221. 
 'Ziehen: Arch. f. Psych., 1890, vol. xxi., p. 863. 
 
El'l LEI'S Y. 
 
 255 
 
 lepsy. It has long been known that, in nervous children, 
 gastro-intestinal irritation may bring on convulsions. It has 
 recently been argued that irritation arising from the eye, 
 chiefly from imperfect muscular action and consequent un- 
 conscious ocular effort, 1 and also that irritation produced in 
 the naso-pharyngeal cavity may cause nervous attacks of an 
 epileptiform nature. The attacks occurring in this class of 
 cases differ from the attacks in the other two classes in the 
 fact of the great frequency of their occurrence from the out- 
 set, in the fact that between the attacks more or less subjec- 
 tive discomfort or pain, or objective signs, attract attention to 
 the irritated part, and in the fact that removal of the source 
 of irritation is followed by very prompt cessation of the at- 
 tacks. In all such cases the attack may be explained by sup- 
 posing that a long-continued irritation of moderate degree 
 has a cumulative effect upon the gray matter constituting 
 primary sensory centres in the spinal cord or brain axis, that 
 this state of irritation extends to the medulla oblongata, 
 which finally takes on a condition of unstable equilibrium, 
 such as is present in the second class of epileptic cases. The 
 medulla is then ready to set free a sudden nervous discharge 
 upon any sudden peripheral irritation. This relieves its strain. 
 After the discharge, the cumulative action again begins. The 
 continued peripheral irritation thus produces occasional epi- 
 leptiform attacks. In the third class of cases, therefore, are 
 included all the cases in which a source of peripheral irritation 
 can be found whose removal is followed by cure. 
 
 It will be observed that in discussing these classes of cases 
 the character of the convulsion and the condition of con- 
 sciousness during it have not been particularly emphasized. 
 This is because, in all three classes, the various phenomena 
 characterizing epileptic attacks may present themselves, so 
 that, from a consideration of the attack at its maximum of in- 
 tensity, no distinction between these classes of cases can be 
 reached. When, however, single cases are carefully studied 
 in all their details, it is found that characteristic symptoms, 
 
 1 G. T. Stephens, M.D. : " Functional Nervous Diseases," 18SS. Wigglesworth, 
 Brain, No. xlv. 
 
-5° 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 additional to the mere fit, enable the observer to assign the 
 case to its proper category. And the importance of such a 
 classification of cases will be appreciated when the subject of 
 treatment is discussed. 
 
 The statements in this chapter are based upon the records 
 of 167 cases of epilepsy, of which 94 were observed at the 
 Vanderbilt Clinic from February, 1888, to January, 1890; 32 at 
 the Polyclinic between 1885 and 1888; and the remainder in 
 m_\- private practice. 
 
 ETIOLOGY. 
 
 There were 84 males and 83 females. The following table 
 shows the age of the patient at the onset of the attacks. 
 
 Age of Onset. 
 
 Birth to age of 5 years, 
 Age of 5 to age of 10 years, 
 
 " 10 " 
 
 a I5 „ 
 
 " 20 " 
 
 " 30 " 
 
 " 4O " 
 
 " 50 " 
 
 Age unknown, 
 
 15 
 20 
 
 30 
 40 
 50 
 65 
 
 29 cases. 
 22 
 
 30 
 16 
 
 30 
 
 9 
 8 
 
 3 
 18 
 
 It thus appears, that nearly sixty per cent began before the 
 age of twenty, and that the development of the disease after 
 the age of thirty is rare — thirteen per cent. 
 
 Convulsions had occurred in infancy in 30 cases in addition 
 to the 29 in which the disease began before the age of 5 ; a 
 fact which demonstrates that infantile convulsions are the 
 most common of all the predisposing causes of this disease — 
 or, to state it in a different way, that a congenital irritable 
 nervous system predisposes the child to the occurrence of 
 convulsions from any slight cause and may be the underlying 
 foundation for the development of the disease. This is true 
 in one-third of the cases. Convulsions had occurred in some 
 very near ancestor in 16 cases. An injury to the head by a 
 
EPILEPSY. 257 
 
 blow or a fall had occurred in 1 1 cases. Among other causes 
 assigned by the patients were fright, worry, great anxiety, 
 sunstroke, alcoholism, scarlet-fever, measles, " brain-fever," 
 masturbation, poisoning by copper, uterine and ovarian dis- 
 ease, and syphilis. When convulsions occurred as a symptom 
 of syphilitic disease of the brain or its membranes, the case 
 was not classed among the epileptics in the table of cases, and 
 in the few cases in which syphilis was ascribed as a cause, no 
 other symptoms of syphilis were present. In 7 of the female 
 patients the attacks were distinctly menstrual in their oc- 
 currence, and had been so from their beginning. In 4 cases 
 a source of peripheral irritation was found, once in the eye, 
 once in the nose, twice in the genital organs. 
 
 In the large majority of the cases, careful questioning 
 failed to elicit any ascertainable cause for the disease. 
 
 CHARACTER AND FREQUENCY OF ATTACKS. 
 
 In a large majority of the cases the interval between the 
 first and second attacks was a long one, from two years to 
 four months; the interval between the second and third at- 
 tacks was shorter, from one year to three months, and the 
 greatest frequency of attacks was only attained after the dis- 
 ease had been established for several years. 
 
 In a few cases epileptiform convulsions began with great 
 frequency, several occurring in a day and a number within 
 the first two weeks. In all of these cases some distinct cause 
 was ascertained. This was either irritation of the brain by 
 hemorrhage, meningitis, or from an injury to the skull ; or irri- 
 tation' of some internal organ, as constipation, chronic gastro- 
 intestinal irritation, genital irritation, nasal irritation, or de- 
 fects of vision. Nine of the patients had attacks of petit-mal 
 only. Forty had both petit-mal and grand-mal. One hun- 
 dred and nine had grand-mal only. In the large majority of 
 the cases the disease had been in existence several years at 
 the time the patients were seen. The greatest frequency with 
 which attacks of grand-mal occurred is shown in the following 
 table. 
 
 *7 
 
j 5 S FAMILIAR FORMS OF NERVOUS DISEASF. 
 
 Table Showing Greatest Frequency Of Epileptic Attacks. 
 
 I in i year or over, . 
 
 9 cas 
 
 I " 6 months, .... 
 
 2 
 
 1 3 • 
 
 6 ' 
 
 T " <? " 
 
 10 ' 
 
 I " I month, .... 
 
 25 ' 
 
 I " 2 weeks, . 
 
 22 ' 
 
 I " I week, .... 
 
 7 ' 
 
 I per week, less than I per day, , 
 
 28 ' 
 
 Over one attack daily, 
 
 28 ' 
 
 Frequency not recorded, 
 
 30 ' 
 
 It becomes evident that in less than twenty per cent of 
 the recorded cases did the attacks exceed one a day. In 
 these cases such frequency was by no means permanent. It 
 had occurred at some time in the course of the disease and 
 therefore was recorded. But it may be said to be unusual in 
 epileptics under treatment — for in but 6 of these cases did 
 the attacks fail to be reduced by treatment to less than one a 
 day — a nd in many they were reduced to one a week or less. 
 Thus in numerous cases the record shows a reduction of daily 
 attacks to one in two or three weeks ; of weekly attacks to 
 one in three months ; of monthly attacks to one in six months. 
 From a study of these cases it would seem that about two 
 per cent of epileptics continue to have very frequent fits in 
 spite of medicinal treatment. In these cases evidences of 
 marked cerebral disease — shown by mental deterioration — 
 was usually found. And it may be noted incidentally that in 
 the cases classed under mal-development of the brain, in 
 many of which epilepsy was present (but which are not in- 
 cluded in this list), the attacks were very frequent in their 
 occurrence. It would, therefore, appear that very great fre- 
 quency of attacks in epilepsy, persisting permanently, may be- 
 taken as evidence of organic cerebral changes. 
 
 In all the cases in which attacks of petit-mal were present 
 the number of these attacks was much greater than those of 
 grand-mal. Usually several such attacks were occurring daily 
 when the patients applied. 
 
EPILEPS Y. 
 
 259 
 
 The patients were always questioned regarding the possi- 
 bility of attacks occurring during the night. The result was 
 
 Nocturnal attacks only in, 22 cases. 
 
 Nocturnal attacks as well as diurnal in, 17 
 
 It is evident, therefore, that nocturnal attacks are compar- 
 atively rare, being present in but twenty-five per cent of the 
 cases — a fact which may be explained by the exemption of 
 the nervous system from external sources of irritation during 
 sleep. 
 
 Procursive attacks, that is, an attack which consists of or 
 begins with rapid running either forward or in a circle, 
 avoiding obstacles, and not falling, occurred in 2 cases only 
 — one of these a case already recorded (p. 124) as an illustra- 
 tion of a tendency to turn to one side in walking. 
 
 THE AURA IN EPILEPSY. 
 
 In 65 cases the attack was preceded by a conscious sen- 
 sation which was so constant in its occurrence and was so 
 definitely remembered, as to be considered by the patient a 
 positive warning of the recurrence of an attack. 
 
 In each patient the aura was always the same — a variety 
 of auras in the same patient not having been observed. 
 
 The character and relative frequency of the aurae were as 
 follows : 
 
 1. Epigastric sensations, which the patients likened to the 
 feeling produced by a voluntary forcible contraction of the 
 abdominal muscles, or to a ball rising from the stomach, 
 occurred in 19 cases. This was the aura most frequently 
 observed. 
 
 2. Visual sensations, of light, or sparks, or a blue color, or 
 a red color, or a purple color, occurred in 14 cases. One 
 patient saw a coffin before her as the attack began, another 
 saw a face, another several faces advancing toward her. 
 
 3. Tactile sensations, in the form of tingling or numbness 
 in the body or limbs occurred in 10 cases. One patient com- 
 plained of a sudden sense of cold or chilliness all over her 
 
260 FAMILIAR FORMS OF NERVOUS JUS EASE. 
 
 prior to the attack. Another of a coldness in the feet, which 
 ascended to the trunk before she lost consciousness. Three 
 patients could not describe the sensation felt, but were con- 
 scious of an indefinite sensation coining over the entire body. 
 Several perceived the convulsive movements of the head or 
 arms before losing consciousness. 
 
 4. Vertigo was complained of as an aura in 7 cases. 
 
 5. A sensation of fear without known cause occurred in 8 
 cases. 
 
 6. Palpitation of the heart, a sensation of suffocation, a 
 drowsiness, heaviness of the eyelids, a sudden inability to 
 speak, were mentioned by different individuals as aurae. And 
 in other cases the psychical aurae soon to be discussed were 
 present. 
 
 In 47 cases the existence of an aura was distinctly denied. 
 In the remainder, 55 cases, no record of an aura was made, 
 but as the aura was inquired into as a matter of routine, it is 
 probable that in these cases none was felt. It may be stated 
 that in the majority of epileptics there occurs no warning 
 whatever of the occurrence of the attack. 
 
 In view of the recently developed theory 1 that the begin- 
 ning of the nervous " discharge " in an epileptic attack is fre- 
 quently in the cerebral cortex, the study of the aura becomes 
 interesting. It resembles in an epileptic fit the " signal symp- 
 tom " occurring in Jacksonian epilepsy as the beginning of a 
 local spasm. And since the " signal symptom " is of great 
 value in determining the point of beginning cortical irritation, 
 it is not unlikely that the aura in epilepsy may have a similar 
 significance. A visual aura might indicate that the nervous 
 discharge began in the occipital lobes; a theory supported by 
 the fact that in three patients the aura of light was always 
 seen to one side of the middle line (compare also p. 52) ; a 
 vertigo might indicate that it began in the cerebellum; a sen- 
 sation of numbness or of movement that it began in the sen- 
 sory-motor area of the cortex. And in view of the fact that 
 in localized spasm excision of the cortex at the seat of irrita- 
 tion has, in a few cases, resulted in recovery, the practical value 
 
 1 Gowers : " Diseases of the Nervous System," vol. ii., p. 697. 
 
EPILEPSY. 261 
 
 of the study of the aura becomes evident. It is not impossi- 
 ble that patients may appreciate a previously unnoticed aura 
 if their attention be directed to it. I have found this to be 
 so in a few cases. And it is evident that the existence of 
 such varieties of aurae is in itself an argument of no little- 
 strength, that the nervous discharge in an epileptic attack is 
 not of uniform nature nor of uniform situation. 
 
 It is well known that " intellectual aurce" have been de- 
 scribed by Hughlings Jackson/ and attacks which he has 
 called a " dreamy state." He thinks that they afford evidence 
 of the origin of a nervous discharge from the highest cerebral 
 centres. In one of the cases at the Polyclinic, the patient 
 told of certain " queer thoughts " which he refused to disclose, 
 always coming into his mind before an attack. A private 
 patient of my own, a professor of mathematics, has as an in- 
 variable aura, the sudden coming into consciousness of an 
 algebraic formula which arrests his attention no matter what 
 he is thinking of. 
 
 THE PSYCHICAL EPILEPTIC EQUIVALENT. 
 
 In some cases of epilepsy, there is evidence of the exist- 
 ence of a state of consciousness, not only differing from the 
 normal consciousness, but also differing from the state of un- 
 consciousness usually occurring in an epileptic attack. These 
 attacks are termed psychical epileptic equivalents. Those 
 who find the essence of an epileptic attack in the loss of con- 
 sciousness, find difficulty in assigning such attacks to a proper 
 place in their definition of the disease. Those who regard the 
 whole epileptic phenomena as evidence of sudden involuntary 
 nervous discharge from the cortex, see in these cases exam- 
 ples of discharge from the highest cerebral centres. To ex- 
 plain a psychical epileptic equivalent it is necessary to sup- 
 pose a discharge in the areas which preside over the higher 
 conscious actions of the mind. This may give rise to invol- 
 untary mental processes sufficiently distinct to arrest and 
 
 1 Hughlings Jackson : On a particular variety -of Epilepsy, "Intellectual 
 Aurse." Brain, 1888, vol. xi., p. 179. See also Chas. Mercier: "The Nervous 
 System and the Mind," 1888, chap, i., "The Nervous Discharge." 
 
2b2 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 hold the attention of the individual. An)' of these discharges 
 ina\' be so light as not to extend to adjacent brain areas, in 
 which case it is a single idea which comes to mind. But if 
 the\' are severe ami the irritation extends to neighboring 
 areas, the mental impression may rise to such a height that 
 maniacal acts are performed ; the thought goes on to a con- 
 fusion of man)' ideas and a loss of consciousness. The anal- 
 og)- between the cases of cortical disease already considered 
 and some of these cases of epilepsy is evident. The follow- 
 ing cases illustrate these phenomena. 
 
 CASE XXXII. — PSYCHICAL EPILEPTIC PHENOMENA. 
 
 A gentleman in middle life, of rather nervous disposition, 
 and mentally an active man, was attacked at the age of forty- 
 two with grand-mal; and during the past three years since 
 the first attack has had four severe nocturnal general convul- 
 sions at intervals of fourteen months, ten months, two months, 
 and eight months. After each convulsion he is acutely mani- 
 acal for about three hours, during which time he has to be 
 restrained from injuring himself and others, and from doing 
 much damage. The mania is succeeded by a deep sleep from 
 which he wakes without any memory of what has occurred 
 since the onset of unconsciousness with which the convulsion 
 begins. (Such maniacal attacks are not very uncommon, and 
 occasionally it is the case that the attack of mania occurs in 
 place of a convulsion rather than succeeding it. It is then 
 termed the psychical equivalent of a convulsion.) The inter- 
 esting feature of this case is, however, the development dur- 
 ing the past year of peculiar attacks, which occur almost daily, 
 of the following kind. While the patient is talking, reading, 
 walking, or at his professional work, he will suddenly cease 
 what he is about, and his face will assume a broad grin for 
 about ten seconds, then he looks about in an absent-minded 
 way, and immediately resumes his occupation. At these 
 times there is no apparent loss of consciousness; he never 
 staggers if standing, nor lets anything drop which he is hold- 
 ing, but when questioned as to what has amused him he has 
 
EPILEPSY. 263 
 
 no recollection of having been amused, or any notion that 
 anything unusual has occurred. These attacks are undoubt- 
 edly of the nature of petit-mal, but the fact of the change of 
 mental expression seems to indicate that, when they occur 
 there is present a second state of consciousness, in which the 
 patient perceives something funny, just as in the maniacal 
 condition there is a second state of consciousness in which 
 the mind is excited by frightful perceptions or notions. The 
 recollection of neither of these second states remains. While 
 the severe attacks are now under control by the bromides, 
 the minor attacks are not at all affected by treatment. 
 
 CASE XXXIII. — PSYCHICAL EPILEPTIC EQUIVALENT. DOUBLE 
 CONSCIOUSNESS. 
 
 A young man of fair intelligence and good physique was 
 first seized with an epileptic convulsion after a severe fall, in 
 which he hit his head, five years ago. Since that time he 
 has had numerous attacks of grand-mal at irregular intervals. 
 
 He was put under treatment by bromides in July, 1884, and 
 up to January 10th, 1885, had had no return of the convul- 
 sions. On January 10th he came home from work as usual, 
 ate his supper, and went to bed. He slept with his brother, 
 who is sure that during the night he had no convulsion. The 
 patient says that when he woke up on the nth of January, 
 he found himself in Bellevue hospital and learned to his sur- 
 prise that it was evening. He has no recollection of anything 
 which occurred between going to bed on Friday night and 
 waking in the hospital on Saturday night. From his family, 
 however, it was ascertained that he got up as usual on Satur- 
 day morning, and while it was noticed that he acted a little 
 strangely at breakfast nothing was said to him and he went 
 as usual to work. His employer thought that his eyes looked 
 brighter (possibly his pupils were dilated) and that he did not 
 appear natural, but he took no special notice of this and soon 
 after his arrival at the shop in 24th St. he sent him up to a 
 house in 46th Street (about a mile) on an errand, to obtain a 
 carpenter's bit and brace. He went up to 46th St., did the 
 
264 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 errand, and evidently explained himself intelligibly for he was 
 given the bit and brace. The next trace he has of his move- 
 ments was at 8th Avenue near Bleecker St. (about two miles 
 away), though how he got there he does not know. He there 
 went into a plumber's shop, and asked to be allowed to sit 
 down and rest. Me had nothing in his hands, so must have 
 lost the bit and brace on the way. He soon got into a lively 
 talk with the plumber, and became quarrelsome, so that he 
 was told to go out. He went away, but in an hour came 
 back, entered the shop, and tried to strike the plumber. This 
 was for him an unusual proceeding, as he is of a mild and 
 gentle disposition. An officer was summoned, who took him 
 to the police station, where it was evident that he was out of 
 his head; so they sent him to St. Vincent's Hospital, whence 
 he was at once transferred to Bellevue. He fell asleep soon 
 after admission to Bellevue, and on waking in an hour or so 
 was surprised to find where he was. His manner of talking 
 made it at once evident that nothing was the matter with him, 
 and he was discharged at once and went home, rather indig- 
 nant at having been sent to a hospital and anxious to find out 
 the reason. Being a very intelligent lad he became interested 
 in his own case at once, on learning a few of the facts, and 
 ascertained by inquiry the various occurrences which have just 
 been described. Soon after this I lost track of him and do 
 not know whether any similar attacks have since occurred. 
 
 The case must be classified among cases of double conscious- 
 ness, or psychical epileptic equivalent. The development of 
 this state is known to be most frequent among epileptics. It 
 is of interest to notice that three states of consciousness fol- 
 lowed one another in this patient; first the normal state, sec- 
 ond, the abnormal state, third, the normal state. In the 
 second abnormal state he had a memory of things which 
 occurred in the first state, for he went to work as usual; and 
 must have had a recollection of his usual habits, of his place 
 of business, etc. In the third state he had a recollection of 
 what had occurred in the first state, but not of the events of 
 the second or abnormal state. A certain degree of conscious- 
 ness and continuity of recollection were, therefore, continu- 
 
EPILEPS Y. 265 
 
 ous from the first state into the second, and from the first 
 state into the third. The absolute break lay between the 
 second state of abnormal consciousness and the third state 
 of normal consciousness. I have called it a state of abnormal 
 consciousness, and there is evidence that he acted during it in 
 a rather unnatural manner. That the entire abnormal state- 
 was an epileptoid phenomenon is only an assumption based 
 on the lack of memory of its occurrences, and the existence 
 of epilepsy in the patient. It gives no explanation of the 
 peculiar occurrence at all, unless the theory of a discharge 
 and subsequent period of feeble activity in the higher cere- 
 bral centres be accepted. 
 
 CASE XXXIV. — PSYCHICAL EPILEPTIC EQUIVALENT. 
 
 A small messenger boy came to my dispensary class one 
 day in considerable genuine distress. He said that on two 
 occasions while out on errands in the city, he had suddenly 
 lost his way, and had become so completely bewildered that 
 he had to get a policeman to take him home. He was per- 
 fectly familiar with' New York, had always lived here, knew 
 the streets and buildings well, and never, except on these two 
 occasions had had the slightest difficulty in finding his way 
 about. But at both these times it seemed to him as if he 
 were in a perfectly strange city, and he had no idea in which 
 direction, to turn. There was no loss of consciousness, and 
 he had never had a convulsion. He was such an honest-look- 
 ing little fellow that I could not doubt his story, and further 
 inquiry proved it to be true. Similar cases have been re- 
 corded by a French authority which had occurred in epilep- 
 tics, and I suppose that this boy had on each of these occa- 
 sions a peculiar attack of a psychical character — an epileptic 
 equivalent with subsequent loss of memory. 
 
 CASE XXXV. — PSYCHICAL EPILEPTIC EQUIVALENT. 
 
 A teacher of considerable eminence consulted me some 
 time ago about a peculiar phenomenon which troubled him 
 greatly. On several occasions, which had recently been in- 
 
266 FAMILIAR FORMS OF NERVOUS DISEASF. 
 
 creasing in frequency, he found his attention arrested, no 
 matter what he was doing, by a strange and unfamiliar set of 
 ideas which suddenly came up to his mind. He was obliged 
 to think of these at once, and to keep his attention upon 
 them about as long as it took him to walk 20O feet, when 
 they would as suddenly fade out of consciousness, leaving no 
 memory of their contents. He was sure that there was no 
 cessation of consciousness at any time, though he admitted 
 that he could not go on talking, or notice a question, or do 
 anything during the attack, but follow the idea presented to 
 the mind. And though he has no recollection of the idea 
 after it is gone, he recognizes the same idea as occurring again 
 in the next attack. So that now, as soon as this peculiar 
 notion of which he is unable to give an account comes into 
 his thought, he fumbles in his pockets for his bottle of amyl 
 nitrite and usually succeeds in uncorking it and inhaling the 
 drug, thus arresting the attack. Frequently the attacks are 
 succeeded by a headache which lasts a day. Bromides de- 
 crease the frequency of their occurrence. Mental work in- 
 creases their frequency markedly. The sudden occurrence of 
 an attack of a definite character, the inability to carry on a 
 normal mental process during the attack, and the total lack of 
 memory of the forcible idea which presents itself in the at- 
 tack, seem to indicate a powerful involuntary cerebral action, 
 of such intensity as to command attention, and so completely 
 unrelated to the normal train of thought as to leave behind 
 it no associations in memory by means of which it can be 
 reached by consciousness. I should consider this a nervous 
 discharge in the higher cerebral centres presiding over men- 
 tal action, corresponding in kind to the nervous discharge in 
 the motor centres which give rise to monospasm. It is a 
 sort of psychical epileptic phenomenon, and the irritation 
 probably has its location in the frontal lobes, since speech is 
 suspended during its progress. 
 
 Such cases, then, offer a strong argument for the possibility 
 of " nervous discharges " from those parts of the cortex whose 
 activity is synchronous with mental processes. Cases with 
 an aura of sensation indicate a discharge from the sensory 
 
EPILEPSY. 267 
 
 areas of the cortex. Cases with a conscious spasm of limited 
 extent, indicate a discharge from the motor areas of the cor- 
 tex. Cases with conscious visceral sensations indicate a dis- 
 charge from those parts of the cortex presiding over the in- 
 ternal organs, the location of which is not yet known. It thus 
 becomes evident that the study of the aura in every epileptic 
 case is of the greatest importance, for it may indicate the 
 exact seat of the disease, organic, functional, or nutritive, 
 not only in the cortex but in some definite cortical area. It 
 also will enable cases of epilepsy of cortical origin to be dif- 
 ferentiated from so-called genuine idiopathic epilepsy. 
 
 THE DIFFERENTIAL DIAGNOSIS BETWEEN EPILEPSY AND EPI- 
 LEPTIFORM ATTACKS DUE TO PERIPHERAL IRRITATION. 
 
 In some cases of supposed epilepsy the removal of some 
 source of peripheral irritation is followed by complete recov- 
 ery. The assertion has, therefore, been made that peripheral 
 irritation may produce true epilepsy. This I believe to be 
 erroneous, since the careful study of the two classes of cases 
 shows that a differential diagnosis between epilepsy and con- 
 vulsive attacks of reflex origin is possible. This diagnosis 
 can in some cases be made by a study of the attack. In a 
 reflex case, the attack is often attended by an incomplete dis- 
 turbance of consciousness, the patient knowing what is going 
 on during the attack and being able to tell, when the attack 
 is over, what has been said or done to him during its pro- 
 gress. This is illustrated in the second case here appended. 
 In epilepsy, as a rule, the loss of consciousness is complete and 
 the patient has no memory of anything between the onset and 
 his recovery. 
 
 There are some cases of reflex neurosis, however, in which 
 the diagnosis cannot be made from the nature of the attack. 
 It is truly epileptiform in character. In these cases much 
 may be learned if the mode of onset of the disease, the fre- 
 quency of attacks at the outset, and the concomitant symp- 
 toms are studied. In a reflex case- the onset usually occurs 
 at a time when, from some general constitutional disease, the 
 nervous system is in a state of irritable weakness. Girls who 
 
268 FAMILIAR FORMS. OF NERVOUS DISEASE. 
 
 are anaemic, or are just developing, and boys who arc suffering 
 from the exhaustion of sexual abuse or from malarial poison- 
 ing, are particularly susceptible. The frequency of the attacks 
 of whatever kind is very great from the very beginning. Thus 
 in a case of reflex neurosis from genital irritation, seen with 
 Dr. G'Dwyer in a boy of three, within a week of the onset, 
 the attacks had reached the number of eight or ten daily, 
 and within three weeks the number had risen to sixty a day. 
 The attacks were of a petit-mal type. He would stop play- 
 ing, turn pale, stand with eyes fixed and pupils dilated, un- 
 conscious but not falling, for about thirty seconds, and then 
 recover consciousness and look about in a frightened manner 
 and cry a little, and then go on playing. This case was cured 
 by circumcision. In another case, due to irritation in the 
 pharynx, the attacks of great mental irritation, almost mani- 
 acal, occurred several times daily from the outset. This case 
 was cured by excision of the pharyngeal tonsil. And in the 
 first case here appended, due to eye strain, the attacks oc- 
 curred daily from the outset. This great frequency of attacks 
 at the onset does not occur in idiopathic epilepsy. The in- 
 terval between the first and second fits is often one or two 
 years, usually over three months, rarely a month. The in- 
 tervals then become shorter, but I have never known a patient 
 with genuine idiopathic epilepsy ' to have a fit daily within a 
 year of the onset. In the 167 cases of epilepsy, less than 
 twenty per cent had attacks daily, and these were all cases in 
 which the disease had been present for several years. In none 
 had the interval between the first and second fit been less than 
 a month. 
 
 Lastly, in reflex neuroses, there are usually other symptoms 
 which indicate the seat of the peripheral irritation. If that 
 irritation is in a scar, there is pain or numbness in it, and 
 pressure on it may cause an attack. If the irritation arises 
 from the genitals, there is evident irritability and undue red- 
 ness of the organs, tendency to handle them, especially during 
 an attack, difficulty of micturition, and evident phimosis, as 
 in the second case appended, or vaginal irritation. If the 
 
 1 l'y this term I mean to include the second class of cases. 
 
EPI LEI'S Y. 269 
 
 irritation is from the uterus or ovaries, symptoms of disease 
 of these organs other than the attacks will be discovered and 
 tenderness in the region will be found. In this list of cases 
 are two of genuine epilepsy, from whom the ovaries had been 
 removed without any effect on the frequency of attacks. If 
 the irritation be from the digestive tract, indigestion, consti- 
 pation, and flatulence will be complained of. If the irritation 
 arises from the respiratory tract, a careful examination will 
 probably be made because the imperfect nasal breathing or 
 nasal voice, or the existence of catarrh, will call attention to 
 these parts. And if the irritation is from eye strain the pa- 
 tient will complain of headache, frontal or occipital, aching in 
 the nape of the neck, or discomfort about the eyes after using 
 them for near or far objects as the case may be. Impacted 
 wax will cause a coufjh, or tinnitus or deafness. Thus, in any 
 case of peripheral irritation of sufficient severity to produce 
 a reflex neurosis, nature will indicate the source of the trouble 
 by discomfort or abnormal sensations in the part which is the 
 seat of irritation. 
 
 In genuine epilepsy, on the other hand, the patient usually 
 feels perfectly well between the attacks and presents no 
 symptoms of nervous irritation. 
 
 Since, in every patient suffering from epilepsy, the nervous 
 centres are always ready to discharge their reserve energy 
 upon slight external excitement, it is a matter of common 
 necessity to remove all possible causes of serious peripheral 
 irritation. Such causes must necessarily be looked for and 
 prevented. In a true epilepsy, this may decrease the fre- 
 quency of the attacks to some extent. In a reflex neurosis, re- 
 covery immediately follows the removal of the exciting cause. 
 
 The following cases which were seen at the Clinic are good 
 examples of reflex neuroses. I may add that, in my experi- 
 ence, reflex neuroses of an epileptiform type are exceedingly 
 rare. 1 I have records of 6 cases only in a series of 3,500 cases 
 of nervous diseases. 
 
 1 For a confirmation of the statement that reflex neuroses from eye strain are 
 infrequent, the reader is referred to an exhaustive article on this subject by 
 D. B. St. John Roosa, Med. Record, April 19th, 1890. 
 
2JO 
 
 FAMILIAR FORMS OF XER VOL'S DISEASE. 
 
 CASE XXXVI. — REFLEX NEUROSIS FROM EYE STRAIN. EPI- 
 LEPTIFORM ATTACK. 
 
 A boy of twelve began to have attacks in September, 1888, 
 of the following kind, without known cause. He feels a numb- 
 ness and tingling in the right hand which ascends the arm, 
 then he clasps his hands, utters a cry, and loses consciousness, 
 has a general convulsion of moderate intensity and short 
 duration " two to three minutes " (?) without biting his tongue 
 or frothing at the mouth, after which he is sleepy for an hour. 
 From the beginning he had had at least one attack daily, 
 usually at night, and within two months of the onset he was 
 having several daily as well as several at night. No intestinal 
 or genital irritation was discovered, but his eyes troubled 
 him after reading, and an ocular examination showed marked 
 hypermetropia and astigmatism, and hyperemia of the left 
 optic disc. His attacks had been in no way influenced by 
 the use of nitroglycerine or by moderate doses of bromides; 
 but after proper glasses were given, the attacks ceased at 
 once, and a year subsequently he reported that they had 
 not returned. 
 
 CASE XXXVII. — REFLEX EPILEPTIFORM ATTACKS FROM GEN- 
 ITAL IRRITATION. 
 
 The boy, now aged nine, has had attacks since the age of 
 five. He has no aura, but while at play suddenly straightens 
 his body, becomes rigid, does not fall, twitches in all his mus- 
 cles slightly, laughs in a silly manner, seems dazed, but will 
 make a random reply to questions at any time during an at- 
 tack, and when it passes off he goes to sleep at once and 
 sleeps for several hours. These attacks have been very fre- 
 quent from the outset ; he had several in the first week, and 
 had six attacks the day before I saw him. He always has an 
 attack soon after getting into bed at night, which attracts 
 attention because he laughs aloud. The attacks have dimin- 
 ished slightly under bromides. An examination led to the 
 suspicion of masturbation, which he freely admitted, having 
 
EPILEPSY. 271 
 
 discovered the possibility of orgasm and never having spoken 
 of it to any one. His penis was large, the prepuce tight so 
 that it could not be retracted, the meatus was quite red, and 
 the examination produced erection at once. He was told to 
 stop the habit and was referred to his physician, with a recom- 
 mendation that circumcision be done ; this was followed by 
 complete cessation- of the attacks at once. 
 
 THE TREATMENT OF EPILEPSY. 
 
 In regard to the treatment of epilepsy, it may be stated 
 at once that when causal factors are removed so far as pos- 
 sible, and all sources of irritation in the various organs are 
 eliminated, the chief reliance in the treatment must be in 
 the use of the bromides. A combination of the bromides of 
 potash, soda, and ammonia, to which an alkaline potash salt is 
 added, with a small amount of arsenic, is the form used at 
 the Clinic. This is given largely diluted in a tumbler full of 
 water, either before meals or two hours after eating. In 
 cases of nocturnal epilepsy, it is given at bed time only and 
 in these cases belladonna (Tincture ttj v.-x.) or sulphate of 
 atropia in full dose ( T £o gr.) is added. In each case the 
 amount of medicine given is regulated wholly by its effect 
 upon the attacks, each patient keeping a register, and his 
 daily or weekly amount being varied in accordance with his 
 condition. The daily amount given at the outset is one 
 drachm of the mixed bromides and this is increased or de- 
 creased as the case goes on. If proper attention is paid 
 to the condition of the bowels and of the skin and of the kid- 
 neys, there appears to be little danger of the occurrence of 
 objectionable symptoms of brominism. 
 
 The effect of bromide upon the occurrence of attacks is 
 in many cases very marked. This is true of the first and sec- 
 ond classes of epileptics, but less of the third class. In several 
 cases the number of attacks was reduced from one in a month 
 to two in a year. In one case monthly attacks ceased and 
 the patient has been nine months without an attack. In sev- 
 eral cases weekly attacks have been reduced to one in two 
 
FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 months. In one case weekly attacks were reduced to one at- 
 tack in six months. The addition of chloral to the bromide 
 mixture was found very serviceable in main- cases. The most 
 favorable result was in a boy aged 16, who had had convul- 
 sions since infancy and who was having three or four fits daily 
 when put upon treatment. There was a progressive diminu- 
 tion in the attacks upon the use of one drachm daily of brom- 
 ides, so that at the end of ten months his record showed that 
 he had been ten weeks for several periods without an attack. 
 In this case twenty grains of chloral was given daily in addi- 
 tion to the drachm of bromide. There was little or no men- 
 tal depression produced, and for the past six months he had 
 been able to work in a store, and his improvement has been 
 maintained for two years.' 
 
 There are some cases in which bromides do not appear to 
 have any marked effect. This is often true of those cases in 
 which it produces severe gastro-intestinal catarrh This was 
 observed in five per cent of the cases. In these cases it ap- 
 pears to be useless to continue it if its combination with other 
 remedies has no effect. Other remedies, such as borax, iodide 
 of zinc, valerianate of zinc, antifebrine, sulphonal, and nitrogly- 
 cerine have been tried in these cases without any success, and 
 the conclusion is reached that they are incurable. One patient, 
 in whom a history of a fall was obtained and a scar on the 
 scalp and a groove in the bone over the parietal region were 
 found, was trephined by Dr. McBurney without any perma- 
 nent result, although for two weeks after the operation his fits 
 ceased; they then returned with the former frequency, four 
 daily. It is to be noticed that in this case there was no aura. 
 The addition of digitalis or strophanthus to the bromide is 
 made when there is a weakened heart or when the use of 
 bromide produces an indefinite sensation of fear, a symptom 
 not infrequently observed. 
 
 During the past two years a number of new remedies have 
 been tested with some care at the Clinic, and in private prac- 
 
 1 The lectures of Seguin on the Treatment of Epilepsy (N. Y. Med. Jour., 
 March and April, 1890) contain most complete and valuable suggestions on this 
 subject. 
 
EPILEPS Y. 
 
 273 
 
 tice. Tincture of simulo was tried in 14 cases during three- 
 months, severe cases being selected in which daily or weekly 
 attacks were present. The remedy showed some tendency to 
 reduce the number of attacks of grand-mal, but had no effect 
 whatever upon petit-mal. Thus in one case daily attacks of 
 grand-mal were reduced to two per week ; in another case at- 
 tacks occurring every two weeks were reduced to one in two 
 months; in another, monthly attacks were reduced to one in 
 three months; thus the effect of the remedy was shown to be 
 a decided one. In two cases, in which the attacks always 
 occurred at the menses only, simulo had no effect, though 
 used in daily half-ounce dose for two weeks at a time, before 
 the attacks were due. In four cases it failed to have any 
 perceptible effect. 
 
 The combination of simulo with the bromides was found 
 to be more efficacious than either drug alone in four cases — 
 but it failed in one. Its high price prevents its routine use in 
 dispensary practice. Antifebrine has been tried in a number 
 of cases without any favorable result. It does not seem to 
 have any power of influencing the frequency of attacks. 
 
 Every patient who has an aura is furnished with a small 
 bottle containing cotton wool saturated with amyl nitrite, and 
 is instructed to inhale the remedy as soon as the aura is per- 
 ceived. In about one-quarter of the cases it aborts the at- 
 tack; such cases are also often improved by the use of nitro- 
 glycerine y-J-Q- gr. t. i. d., or of codeine \ gr., t. i. d. given in ad- 
 dition to the bromide and chloral mixture. 
 
 The treatment of petit-mal is less satisfactory than that 
 of grand-mal. The only remedy of any service is nitroglyce- 
 rine. In one case, a male, the success of the drug has been 
 so marked as to warrant mention. Daily attacks have ceased 
 and for six months he has had no attacks at all. In a number 
 of cases it has produced about the same relative diminution 
 in the number of attacks which has been produceo by bro- 
 mides in the attacks of grand-mal. In many cases, however, 
 it fails to affect the disease, and as no rule can yet be laid 
 down as to the character of the cases in which it is successful, 
 
 a trial is always made of it in every new case 
 18 
 
2- 4 FAMILIAR FORMS 0/ NERVOUS DISEASE. 
 
 Should the further study of epileptic cases establish the 
 classification here proposed, and should further experience in 
 the surgfeal treatment of Jacksonian epilepsy show it to be 
 efficient, it is not impossible that surgical treatment of the 
 first class of cases of epilepsy may become possible. It is, 
 however, not yet time to urge its trial. 
 
CHAPTER XVIII. 
 
 SOME PAINFUL FUNCTIONAL AFFECTIONS AND 
 THEIR TREATMENT. 
 
 Trigeminal Neuralgia. — Tic Convulsif. — Reflex or transferred pains. — 
 Headaches, their varieties and treatment. 
 
 I. TRIGEMINAL NEURALGIA. 
 
 Of the 151 cases of trigeminal neuralgia seen in two 
 years at the Vanderbilt Clinic, the large majority were of 
 malarial origin and yielded to treatment by a single mercurial 
 purgative, followed by Warburg's tincture or quinine, the lat- 
 ter drugs being given in three full doses at intervals of an 
 hour, beginning six hours before the attack was due. Others 
 due to chronic malarial poisoning were found to yield to 
 arsenic, with tonics and cod-liver oil. A considerable number 
 not malarial have been successfully treated by aconitia, begin- 
 ning with -g^o gr. twice daily and increasing daily one -^ gr. 
 until the physiological effect of tingling of the extremities, 
 face, and tongue and a chilly feeling in the back was reached. 
 This dose was then reduced slightly and kept up for some 
 days, usually with favorable results, the condition of the 
 heart being watched. The combination of drugs included in 
 the neuralgic tablet (page 326) has also been of great service. 
 In three cases, one of infra-orbital and two of dental neuralgia, 
 surgical interference was found necessary. These were referred 
 to Dr. Hartley and were operated upon by him in Roosevelt 
 Hospital. In the first case the infra-orbital nerve was reached 
 by a curved incision following the natural line in the face 
 below the eye; a portion, a centimetre in length, was exsected, 
 with immediate relief which has continued for over two years. 
 In the second case the inferior dental nerve was reached by 
 trephining the ramus of the lower jaw, the superficial inci- 
 
2j6 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 sion being along its posterior border. In this case also the 
 relief of the neuralgia has been permanent for two years. 
 
 In the third case the inferior dental nerve was reached 
 through the mouth, the mucous membrane being anaesthetized 
 with cocaine and the operation being done without ether, as 
 the patient was an old man with feeble heart and atheroma- 
 tous arteries. In this case the relief from pain has been con- 
 tinued for three months, and at present he has no return of 
 the symptoms. 
 
 It is interesting to find that, although all the patients com- 
 plain of tingling and numbness in the area of distribution of 
 the divided nerve, and all have a considerable degree of an- 
 aesthesia in this area, this anaesthesia is not total in any case 
 — a fact which demonstrates that the anastomosing network 
 of nerve fibres under the skin suffices to convey impressions 
 from the domain of one nerve trunk into that of another. 
 This fact has been utilized in the treatment of several cases 
 of traumatic neuritis in the arm. For it has been found that 
 by stroking the surface with a fine faradic brush from the 
 anaesthetic area over into the sensitive area, sensation grad- 
 ually returns in the borders of the anaesthetic area, so that by 
 the application the area of anaesthesia may be decidedly di- 
 minished before the union and regeneration of the divided or 
 injured nerve in the arm has been complete. 
 
 II. TIC CONVULSIF. 
 
 A spasmodic twitching of the facial muscles has been ob- 
 served in several cases. In one case ocular defect was the cause 
 and the correction of it by glasses brought relief. In two cases 
 the tic had been of long duration and had given the patient 
 much discomfort. In both of these cases all medicinal reme- 
 dies had been tried in vain. In tic convulsif the spasm is 
 usually a reflex motor act in consequence of sensory irritation. 
 Sometimes the seat of the irritation is evident because a local 
 pain is present, and then division of the painful nerve will give 
 relief. In neither of the cases mentioned was there any defi- 
 nitely localizable pain. It became necessary, therefore, to 
 
SOME PAINFUL FUNCTIONAL AFFECTIONS. 
 
 277 
 
 determine (1) whether the spasm were reflex; (2) if so, in 
 which branch of the trigeminal nerve the irritation began. 
 This was arrived at by injecting cocaine beneath the skin of 
 the face successively at the point of emergence of the supra- 
 orbital, infra-orbital, and dental branches of the trigeminal 
 nerve. In the first case the injections had no effect on the 
 spasm when the upper two branches were anaesthetized, but 
 the injection at the mental foramen in the lower jaw was suc- 
 ceeded by immediate stoppage of the spasm, which cessation 
 lasted half an hour, until the local effect of the cocaine had 
 subsided. This was interpreted to mean that the spasm was 
 reflex, and that the irritation began in the lower branch of the 
 trigeminal nerve. The patient was then operated upon by 
 Dr. Hartley, who exsected this branch at its exit from the 
 jaw with the effect of permanent cure of the tic. In the sec- 
 ond case, referred to me by Dr. R. H. Derby, injection into 
 the infra-orbital branch of the nerve stopped the spasm, and 
 division of this branch was followed by permanent cure of 
 the tic. In a few cases when no cause was found a labile gal- 
 vanic current, 2 to 4 ma. applied for ten minutes daily, has 
 given relief. 
 
 III. REFLEX OR TRANSFERRED PAINS. 
 
 There are many nervous individuals who complain of either 
 sharp neuralgic pains or dull aching pains in various regions 
 of the body for which no cause can be found on examining 
 the painful region. Much light has been thrown upon these 
 forms of pains by Dr. C. L. Dana. His observations are prac- 
 tical and of much value, and with his permission the following 
 diagrams and table are introduced. 
 
 So called reflex pains are really transferred pains. For 
 example, an irritation in the stomach may cause a pain and 
 tenderness between the shoulders, particularly from the fifth 
 to the eighth dorsal vertebrae. The explanation is as follows : 
 the branches of splanchnic nerves from the stomach enter the 
 spinal cord at the level of the fifth to the eighth dorsal seg- 
 ments ; irritation along these nerves excites sensory impulses 
 in these segments ; those impulses are sent to the brain, and 
 
Ana-mia 
 Endometritis. 
 
 BhidiU r 1 
 
 _,Eye. 
 J . , Decayed tcctit 
 
 
 Fig. 7c 
 
 . 
 
 
 Fig. 71. 
 
 Area. 
 
 Strands of cerebrospinal 
 nerves. 
 
 Distribution. 
 
 Associated ganglia of 
 sympathetic. 
 
 Main distribution. 
 
 [.. . 
 
 Trigeminus, facial, etc. 
 
 Face and anterior scalp. 
 
 4 cerebral. 
 
 Head. 
 
 II... 
 
 1 pper 4 > ervical. 
 
 Occipital region, neck. 
 
 1st icrvical. 
 
 Head (slightly to ear). 
 
 Ill 
 
 Lower 4Cerv. and istdor. 
 
 I'pper extremities. 
 
 2d and ^d cerv., 1st dor. 
 
 Hea-t. 
 
 [V. ... 
 
 dorsal. 
 
 Thoracic wall. 
 
 1st to 6th dorsal. 
 
 Lungs, 
 
 V 
 
 Lower 6 dorsal except 
 
 abdominal wall, upper lumbar. 
 
 5th to 12th dorsal. 
 
 Abdominal viscera, ti stes, 
 
 
 last. 
 
 upper lateral thigh surface. 
 
 
 ovary, fundus uteri via- 
 
 VI 
 
 12th dorsal, 4 lumbar. 
 
 Lumbar region, upper gluteal, 
 
 
 renal plexus. 
 
 
 
 ant. and inner thigh and knee 
 
 1st to 4th lumbar. 
 
 Pelvic organs. 
 
 VII.. .. 
 
 5th lumbar and 5 sacral. 
 
 Lower gluteal, posterior thieh.ist to 5th sacral. 
 
 To pelvic onri'-i, svmpa- 
 
 
 
 lesf. 
 
 iheticsupply 1 eing small. 
 
 Table showing distribution of the seven cerebro-spinu! s.rjnJs of nerves, and location of re.lex pains. 
 
SOME PAINFUL FUNCTIONAL AFFECTIONS. 
 
 279 
 
 are there referred by consciousness to the dorsal segments of 
 the spinal cord. But since, in general experience, sensations 
 and pain coming from those segments have been due to irri- 
 tation in the surface of the body corresponding to them, these 
 splanchnic sensations are referred to this surface. Hence the 
 discomfort which should be referred to the stomach is referred 
 to the back. The mistake is perfectly comparable to that 
 which often occurs after an amputation when irritation in the 
 stump leads the patient to refer sensations to the amputated 
 hand or foot. Dana has studied the location of these reflex 
 or referred pains very carefully and his figures demonstrate, 
 more concisely than description, the area of pain in the dis- 
 eases of the various viscera of sympathetic origin 1 (Figs. 70 
 and 71). 
 
 It will be seen, from their inspection, that there is hardly 
 any viscus in which disease may not give rise to some referred 
 pain. It is also evident that without some knowledge of the 
 localities of these referred pains, the presence of such pains 
 might easily mislead the physician. I have had several pa- 
 tients brought to me for supposed spinal disease in the dorsal 
 region; the symptoms being pain in the back and sometimes 
 in the epigastrium, tenderness of the dorsal spine, general 
 weakness and neurasthenic complaints; in which the correc- 
 tion of a chronic gastric dyspepsia, a condition which had 
 been supposed to be secondary to the more serious spinal 
 affection, has been followed by permanent relief of the symp- 
 toms. It is not necessary to enumerate cases illustrative of 
 these reflex painful affections. They are familiar to every 
 practitioner. A study of the diagrams may, however, throw 
 much light upon some hitherto obscure cases. 
 
 In reflex pains, treatment must be directed to the relief of 
 the functional or organic disease in the viscus affected. It 
 may be added that not infrequently sharp counter-irritation 
 over the seat of the pain is followed by relief not only of the 
 pain, but also of the disturbance of function in the viscus, 
 which is the seat of disease. 
 
 1 N. Y. Med. Jour., July 23d and 30th, 18S7. 
 
280 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 IV. HEADACHES. 
 
 The More Common Forms am> Their Treatment. 
 By DR. M. L. GOODKIND, 
 
 Fourth Assistant at the Nervous Clinic. 
 
 Headache is a symptom for whose relief, during the past 
 year, at the nervous department of the Vanderbilt Clinic, 287 
 patients applied, and in presenting a brief description of the 
 different varieties, I shall classify them in accordance with 
 their frequency, avoiding all superfluous considerations, and 
 confining myself strictly to the essential and inherent charac- 
 ters of each. 
 
 I. Anccmic. 
 
 118 Females ; i Male. 
 
 The first class in number and importance constitutes that 
 variety of headache found almost exclusively in women, and 
 which, from its etiological factor, it is usual to call ancemic 
 headache. 
 
 This condition was found, as a rule, in women of middle 
 age, who had become enervated by multiple cares of mater- 
 nity ; and in young women living and working in a vitiated 
 atmosphere and unable through poverty to regard proper 
 hygienic rules. In both of these classes, poor living and a 
 bad selection of food and drink (diet of cakes and pies, exces- 
 sive tea drinking, etc.) were potent causative agents in the 
 production of this form of cephalalgia. 
 
 The majority of these patients complained of a boring, 
 frontal, or vertex pain, accompanied by ringing in the ears, 
 palpitation and constipation; and presented usually a pale ap- 
 pearance. In more severe cases, there were amenorrhcea, 
 vertigo, dyspnoea, oedema of the feet, and cardiac oppression 
 causing fear and causeless apprehension. The violence of 
 these various symptoms was so marked, in some cases, as to 
 simulate organic disease; and especially prominent was the 
 disposition of these patients to refer their symptoms to the 
 
SOME PAINFUL FUNCTIONAL AFFECTIONS. 2 <Sl 
 
 heart. Upon auscultation of this organ it was often possible 
 to detect a functional, systolic murmur at the base, with ac- 
 centuation of the pulmonary second sound ; and a venous 
 hum in the large veins of the neck. 
 
 All these patients, ranging in age from fourteen to seventy 
 years, received treatment, which consisted in correcting their 
 dietary (excluding cakes, candy, pies, tea, etc.) and directing 
 sanitary regimen, with proper exercise in the open air; and in 
 the administration of iron, arsenic, strychnine, cod-liver oil, 
 and other tonics. The persistent use of aloin, in accordance 
 with the suggestion in a valuable paper by Sir Andrew Clark,' 
 was found to be of the greatest service in the treatment of 
 these cases. 
 
 II. Gastric. 
 
 29 Females ; 18 Males. 
 
 This class, like the preceding, presented many phases, but 
 the following were very constant symptoms. 
 
 The patient complained of a headache, referring the pain 
 to the occipital region, or to the forehead, or less often to 
 the vertex, and gave a history of constipation, with flatulence, 
 eructations, vertigo, nausea, and occasionally vomiting; and 
 more rarely, in severe cases, cough, dyspnoea, hypochondriasis, 
 and a feeling as though there were a weight in the orbit press- 
 ing upon the eyeball. They often complained of pain in the 
 back. 
 
 These symptoms were present in various degrees of sever- 
 ity and duration — from hours to weeks. 
 
 Our first object in the treatment of these patients was to 
 relieve them of the accumulation of faeces and products of 
 decomposition, which generated noxious gases in their alimen- 
 tary tract, causing a sort of individual sewer gas poisoning, 
 and from which they were only relieved by emptying the in- 
 testines promptly and efficiently and several times. If ene- 
 meta were of no avail, resort was had to calomel or to the 
 compound aloin tablet of the dispensary, followed by artifi- 
 
 1 Lancet, Jan. 1st, 1887. 
 
282 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 cial Carlsbad salts or a rhubarb and soda mixture, together 
 with carminatives. Alkaline drinks were prescribed and in 
 some cases charcoal, as they were indicated. These had, as 
 a rule, the desired effect. As a prophylaxis against recur- 
 rence, we enforced upon our patients the necessity of regular 
 habits, the avoidance of overfeeding, and the need of the con- 
 stant use of large draughts of water. Much gastric headache 
 with constipation may be relieved by enforcing the use, 
 especially upon females, of a sufficient amount of water daily. 
 Hot water before each meal was found of great service. 
 
 III. Malarial. 
 19 Females ; 10 Males. 
 
 Under this heading we include those headaches, charac- 
 terized by a train of periodically recurring symptoms, which 
 are sufficiently distinctive to warrant the diagnosis of malarial 
 origin, and which differed in form and location from the pain 
 of trigeminal neuralgia. 
 
 The pain was usually supra-orbital in location, though it 
 was sometimes occipital and not infrequently involved the 
 entire side of the head. 
 
 It was variously described as a dull, heavy, or sharp, shoot- 
 ing pain. The time of its greatest severity was usually midday 
 or in the afternoon. At the time of the severe paroxysms, 
 the patient usually suffered from a feeling of chilliness, flashes 
 of heat and cold, sometimes profuse sweating, malaise, and 
 languor. Anorexia and constipation were frequent accom- 
 panying symptoms. Unless subjected to treatment, the head- 
 aches recurred day after day, or every third day or once a 
 week. This tendency to periodicity was very marked in this 
 form of headache. 
 
 The treatment pursued in these cases was the administra- 
 tion of a mercurial purgative, followed by 20 grains of quinine 
 three hours before the attack was expected, or three doses of 
 ten grains at intervals of an hour, beginning five hours before 
 the onset. In many cases Warburg's tincture or extract was 
 found to have a more prompt effect than quinine. This course 
 
SOME PAINFUL FUNCTIONAL AFFECTIONS 283 
 
 of treatment was usually of avail in the management of these 
 cases, but in a few intractable cases, quinine failed to have the 
 desired effect, when arsenic was used with satisfactory results. 
 In a single case both arsenic and quinine failed, when given 
 separately, while their combination was followed by subsid- 
 ence of the headache, and other symptoms, which were very 
 severe in this instance. 
 
 IV. Syphilitic. 
 6 Females ; 14 Males. 
 
 In cases of this form of headache, a history of syphilitic 
 disease could often be obtained by direct admission of the 
 patient, but when this was denied, either designedly or from 
 ignorance, the concomitant symptoms (periostitis of tibia and 
 frontal bone, enlarged glands, loss of hair, eruptions, scars on 
 skin and mucous membranes, complaint of sore throat and 
 rheumatic pains, etc.) generally elucidated the nature of the 
 headache. 
 
 The symptoms, which this type of headache presented, 
 were quite characteristic. The pain was usually most severe 
 at night. Even though the patient had continuous pain, he 
 would suffer an exacerbation as night approached. The pain 
 was frontal or occipital, or diffused over the whole scalp, or 
 the scalp would present small areas exquisitively sensitive 
 and painful, so that a person ordinarily of good temper and 
 equable disposition would become peevish and ill-tempered, 
 and some deteriorated rapidly in health from the insomnia 
 which ensued. 
 
 This class of headache is very persistent, unless subjected 
 to treatment, to which it is ordinarily very amenable. The 
 treatment consisted in the administration of the saturated 
 solution of iodide of potash, beginning with ten drops t. i. d., 
 well diluted with water or milk, and increasing one drop a 
 dose until they took 3 ss. to 3 i. t. i. d. If this treatment proved 
 inefficient, after two weeks' trial, inunctions of mercurial oint- 
 ment, used in addititon to the potassic iodide, generally secured 
 a favorable result. 
 
2 $4 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 This treatment was resorted to not only in the well-identi- 
 fied cases of syphilis, but also in those obscure cases giving a 
 history of. headache, only present in the evening or worse at 
 nierht, and with no other evident cause, and the results in a 
 few such cases, where every other form of treatment failed to 
 relieve, justified this suspicion. 
 
 V. Eye Strain. 
 
 7 Cases. 
 
 In 7 of the patients treated, no other cause of headache 
 could be discovered than an error in refraction of the eyes. 
 In nearly all these cases hypermetropia with astigmatism ex- 
 isted, and from the strain imposed on the ciliary muscles, in 
 increasing the convexity of the lens, to counteract the effects 
 of this error of refraction a more or less severe headache — 
 usually frontal in location — ensued. Until the proper methods 
 for the rectification of the eye trouble were made use of, viz., 
 the fitting of proper glasses, these cases were not relieved. 
 
 VI. Traumatic. 
 
 8 Cases. 
 
 In 8 cases, histories of blows or falls on the head were ob- 
 tained with no evidences of fracture of the cranial bones. 
 
 These were treated by applications of cold cloths to the 
 head, and by the bromides and iodide of potash. They were 
 usually intractable cases. 
 
 VII. Plethoric. 
 
 12 Cases. 
 
 In 12 cases, all males, no other etiological factor could be 
 acsertained than general plethora. These were men, for the 
 most part, of short stature and florid habit, indulgent to 
 themselves in the way of rich living, addicted to alcoholic 
 excesses and of indolent disposition. They were very prone 
 to sudden alterations in the cerebral circulation, following 
 emotions of any kind, and this they manifested by outbursts 
 
SOME PAINFUL FUNCTIONAL AFFECTIONS. 285 
 
 of violent temper and irascibility, or at times by becoming 
 very despondent and melancholy. 
 
 During the attacks they described themselves as being sub- 
 ject to sensations of vertigo, with spots before the eyes, tinni- 
 tus aurium, feeling of suffocation, and intense frontal headache. 
 
 The treatment to be followed in these cases is sufficiently 
 evident; changing the mode of life, sedatives to allay the 
 vascular and cerebral excitement, aconite, chloral, bromides, 
 etc., depletion of the overburdened vessels by active saline 
 catharsis, and the use of ergot. 
 
 VIII. Miscellaneous Cases. 
 40 Cases. 
 
 .In 40 cases the following causes were detected: nephritis; 
 headaches, frontal and worse in the early morning, high ten- 
 sion pulse: carious teeth; headache temporal, and unilateral: 
 gout; headaches usually relieved by a full meal: rheumatism 
 and lithaemia; dull general headaches: arterio-sclerosis; head- 
 ache severe, dull pain, worse about 4 A.M., when the patient 
 was awakened by pain. 
 
 No causative factor could be found to which the headache 
 might be attributed in 17 of the patients. 
 
 The treatment in these cases of headache was causal, while 
 in the last class of cases, to which no cause could be assigned, 
 treatment was conducted empirically, and the drugs which 
 were of the greatest utility were antipyrine, antefebrine, and 
 phenacetine. Exalgine was tried for a time, but was given up 
 as inferior to the former drugs in these cases as well as in those 
 of neuralgia. 
 
 Almost every form of headache, even including headache 
 from cerebral tumor, was found to yield promptly to antipyrine 
 in 15-grain doses or to phenacetine in 10-grain doses. The 
 dose rarely had to be repeated, once after an hour. No un- 
 toward symptoms have been observed from the use of these 
 drugs. The only form of headache which they usually failed 
 to relieve was that due to general neurasthenia. They are 
 invaluable for the relief of pain during the slow removal of 
 the cause by other measures. 
 
CHAPTER XIX. 
 THE TREATMENT OF NEURASTHENIA. 
 
 The vasomotor origin of neurasthenic symptoms. — Mental recreation. — 
 Overfeeding. — Baths. — Vascular stimulation. — Exercise. — Tonics vs. 
 Sedatives. — Alkalies. 
 
 THE symptoms of neurasthenia are so well known as to 
 require no comment. The causes of the disease are very 
 numerous, but by far the most frequent one is a strain of an 
 emotional kind, some worry, anxiety, grief, fright, or mental 
 depression involving a constant irritation of the feelings, and 
 a consequent excitement of the vaso-motor portion of the 
 nervous system. Instability of vascular tone, irregularity in 
 the circulation of the blood in one or more of the organs of 
 the body and in the brain, seems to be the most constant 
 element in the production of the symptoms of neurasthenia. 
 This has been so fully demonstrated by the experiments of 
 Mosso and of Angel, and so clearly shown by the pulse trac- 
 ings of Webber, as to need no additional proof. In a large 
 majority of the cases observed at the clinic this element has 
 been clearly recognized. Without dwelling upon it full)', I 
 desire to note that it is this instability of vascular tone which 
 in neurasthenics prevents the maintenance of functional hy- 
 peremia of the brain during work, thus preventing a concen- 
 tration of attention during mental labor and hence producing 
 the impairment of memory, the incapacity for continued read- 
 ing, or study, or writing, or listening or conversation so often 
 complained of. It is also manifested in other organs and 
 causes the undue muscular fatigue, the imperfect gastro- 
 intestinal digestion, the imperfect hepatic action, and possibly 
 the imperfect assimilation of food and excessive excretion of 
 uric acid so often observed. For while the coincidence of 
 
THE TREATMENT OE NEURASTHENIA. 287 
 
 neurasthenia and lithaemia cannot be denied, their mutual 
 etiological relation is by no means finally determined. It is 
 not a constant cerebral hyperaemia or a continuous cerebral 
 anaemia from which neurasthenics suffer, but from an unstable- 
 vascular tone. The necessary sequel of such irregularity of 
 circulation is an impairment of nutrition in the nervous sys- 
 tem. 
 
 In the treatment of neurasthenia, the removal of the 
 cause of mental distress is a sine qua non, and if this cannot 
 be accomplished treatment can only be palliative. Time is 
 the healer of much anxiety, grief, and worry, but while it is 
 slowly soothing the cares away, mental occupation of suffi- 
 cient variety and novelty to divert and amuse is a great aid. 
 Mental rest is not secured by an absence of mental activity. 
 but by directing the mind into new channels, and calling into 
 play new departments of the organism, thus incidentally leav- 
 ing those previously acting and now exhausted to recuperate. 
 This is the secret of the success of travel, diversion, and novel 
 employment in the treatment of neurasthenia. And these 
 are therapeutic agents not to be despised. 
 
 In neurasthenic persons there appears to be an entire lack 
 of surplus energy available for special efforts. They live on 
 what they make. They are always on the verge of nervous 
 bankruptcy. It is necessary for their recovery, therefore, to 
 secure a supply of nerve force sufficient not only to carry 
 them along from day to day, but to accumulate a credit on 
 account for extra demands. Hence the need of what appears 
 to be overfeeding in such persons. Three good generous 
 meals, including all varieties of food, supplemented by three 
 light lunches of easily digested fluids, such as milk, kumyss, 
 weak punches, bouillon, chocolate with whipped cream, cocoa, 
 egg-nog, or wine whey, are needed. And if artificial digestives 
 are given, they should be given generously after each repast. 
 Each person is capable of ascertaining the diet best suited to 
 his needs, for what is one man's food is another man's poison, 
 and the object is rather to feed the patient than to pursue any 
 special theoretical scheme of dietetics. Hot water may or 
 may not aid his digestion. Vichy, lithia, and seltzers waters 
 
288 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 may or may not increase his powers of assimilation. As a 
 rule an excess of fluid as well as of food seems to be of ser- 
 vice, helping in the rapidity and completeness of the assimila- 
 tive process throughout the body. Stimulants are, as a rule, 
 to be avoided, but in a few cases, especially where heart stim- 
 ulants are indicated, they may be allowed. 
 
 Next to mental diversion and overfeeding, come those 
 means which aid the building up of new nerve tissue by secur- 
 ing a rapid circulation of the blood in all the organs. Mate- 
 rial of repair must be carried to the seat of damage. To 
 secure a sudden flushing of the neurasthenic brain and spinal 
 cord with blood, is like bringing water to a thirsty man, or 
 giving air to one nearly suffocated. Experimentally it can be 
 shown that peripheral irritation produces vaso-motor reflex 
 effects. This is the fact which hydrotherapeutic measures are 
 based upon. It is of less importance what kind of water is 
 used or at what temperature it is used, than that it should be 
 so used as to produce a sudden change of state on the surface 
 of the body. It is the shock which stimulates, not the contin- 
 uous application. Therefore, whether hot or cold packs or 
 baths or douches are employed, let either be followed by the 
 other. My favorite methods are a warm spinal douche ap- 
 plied from the back of the head clown to the coccyx for three 
 minutes, followed by a cold application, by douche or sponge 
 or damp towel for a half minute; or a warm pack in sheet 
 and blankets for twenty minutes, followed by cool sponging 
 for a minute; both being followed by brisk rubbing, or, if 
 needed, by massage, and both being used at night as they 
 prove most efficient hypnotics. 
 
 Such measures increase the force and frequency of the 
 heart, dilate the vessels of the central nervous system, increase 
 the strength and depth of respiratory efforts, and move the 
 venous blood along the limbs — all important factors in the 
 acceleration of the flow of blood. Massage aids the flow by 
 promoting venous return, and, if combined with movements 
 involving effort against resistance, by stimulating functional 
 hyperaemia of muscles. General faradism does the same in 
 less degree. Central galvanization may have the same effect 
 
THE TREATMENT OF NEURASTHENIA. 289 
 
 and possibly an additional effect in increasing chemical change. 
 In a Turkish bath the douche, massage, and electrical appli- 
 cations may be combined, provided their duration be not so 
 long as to weary the patient. In every case such measures 
 should be succeeded by a period of rest, the patient being in- 
 structed how to relax his muscles and being advised to lie in 
 any other than the dorsal position. 
 
 Regular exercise both in-doors with Indian clubs or a house 
 gymnasium, and out-of-doors by walking, driving, riding, or 
 bicycling, are essential, and even if this exercise has to be 
 begun when it can only be pursued for a very short time, five 
 or ten minutes, it must be enforced and the time gradually 
 lengthened. 
 
 In all these measures the ability of the patient is to be 
 considered, and the rule followed never to pursue any means 
 of occupation, of exercise, of diversion, or of treatment, long 
 enough to produce weariness. Nature furnishes a time limit 
 by the sense of fatigue. 
 
 It having been for so long the custom to order sedative 
 mixtures — such as bromides — in cases of nervous excitement, 
 it may awaken surprise when the medicinal means employed 
 at the clinic are reviewed. Bromides, chloral, hyoscyamus, 
 antipyrine, phenacetine, and sulphonal will produce a tempo- 
 rary relief in many cases of neurasthenia. But while this fact 
 is admitted, I do not hesitate to say that I discountenance 
 their use. It is like quieting the fear and hallucinations of 
 one in delirium tremens by giving him more alcohol, to give 
 bromides to a neurasthenic. The last state of the man is 
 worse than the first. There are cases of delirium tremens 
 where heart failure threatens life, and whiskey must be used 
 with the food which combats the state of starvation present. 
 So there are cases of extreme nervous irritation and anxiety 
 with sleeplessness in which phenacetine, sulphonal, and the 
 other drugs mentioned are necessary while other means are 
 being employed. Such cases are the exception. The best 
 medicinal treatment in neurasthenia is one directed to building 
 up the nervous system and to combating the irritable ner- 
 vous weakness by giving strength rather than by suppressing 
 T 9 
 
2QO FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 irritation. Iron, strychnia, arsenic, phosphorus, quinine, the 
 alkaline hypophosphites, and cod-liver oil are the drugs most 
 frequently prescribed in these cases.' No one remedy is to be 
 used more than ten days. A succession of different tonics 
 acts better than a combination of all or than any one used 
 continuously. And an occasional intermission in the medi- 
 cinal treatment serves to enforce the idea that the general 
 measures are of far greater importance than drugs. The reg- 
 ulation of gastro-intestinal digestion may be borne in mind 
 when the nerve tonics are administered ; the strychnine may 
 be given as Tr. nucis vomicae before meals as a stimulant to 
 the appetite, or the iron as the albuminate with some form of 
 pepsin after meals. Phosphoric acid will aid the gastric juices, 
 or the alkaline hypophosphites will counteract gastric acidity, 
 as well as other acids or alkalies. Thus one means may ac- 
 complish two results. I regard arsenic as one of the best 
 nerve tonics, especially in those forms of neurasthenia which 
 are characterized by a loss of vascular tone. 
 
 The lithaemic state is one which so often coincides with 
 neurasthenia that it requires notice. An occasional dose of 
 calomel, the use of salicylate of soda, phosphate of soda, and 
 carbonate of lithia, with or without small doses of opium, is 
 not to be neglected when the two conditions are combined, 
 and in such conditions a non-starchy diet is employed. 
 
 1 The formulae used at the clinic are given in the last chapter. 
 
CHAPTER XX. 
 
 THE ORDINARY FORMS OF INSANITY. 
 
 Analysis of seventy-one cases of insanity. — A practical grouping of cases 
 of insanity. — I. Defective brains. — II. Diseased brains. — Varieties of 
 each group. — Home vs. asylum care. 
 
 By FREDERICK PETERSON, M.D., 
 
 Chief of the Nervous Clinic. 
 
 PHYSICIANS in general practice are continually brought 
 into contact with the same classes of mental infirmity or dis- 
 ease as those which frequent the Vanderbilt Clinic. They are 
 as a rule cases of congenital brain defect, or of the quieter 
 psychoses, or incipient forms of brain disease; such as the 
 various degrees of feeble-mindedness, imbecility, idiocy; and 
 hypochondriasis, melancholia, paranoia, general paresis, and, 
 more rarely, some of the maniacal conditions, and terminal 
 dementia. 
 
 Certain points of interest may, therefore, be of value in 
 connection with the diagnosis and treatment of these cases, 
 and it is the object of this study to call attention to these 
 practical features. 
 
 CASES AT THE VANDERBILT CLINIC. 
 
 There have been received and treated in the Nervous De- 
 partment of the Vanderbilt Clinic, up to January 1st, 1890, 71 
 cases of insanity, 41 males and 30 females, which may be sim- 
 ply classified, according to the diagnoses entered in the clinic 
 records, as follows: 
 
»9- 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Form. 
 
 Hypochondriasis 
 
 Melancholia , 
 
 Paranoia 
 
 Imbecility 
 
 Idiocy 
 
 General Paresis 
 
 Hallucinatory Mania 
 
 Senile Dementia 
 
 Secondary Dementia 
 
 1 1 ysterical Mania 
 
 Acute Masturbational Insanity. 
 Heboidophrenia 
 
 Total 41 
 
 Mali v. 
 
 17 
 I 
 
 4 
 5 
 4 
 7 
 
 Females. 
 
 1 
 10 
 
 5 
 4 
 
 4 
 
 30 
 
 Total. 
 
 IS 
 II 
 
 9 
 9 
 8 
 8 
 2 
 2 
 1 
 1 
 1 
 1 
 
 17 
 
 7i 
 
 The relatively large number of hypochondriacs in propor- 
 tion to other cases is of course due to the fact that it is in the 
 nature of the patient afflicted with this disorder to consult 
 numerous doctors and to frequent successively most of the 
 dispensaries of the city. Of the 17 males, the majority were 
 suffering from this psychosis as a result of various abuses or 
 maladies of the sexual apparatus. Some of the cases improved 
 under treatment directed both to their general nervous con- 
 dition and to the local etiological element; one or two recov- 
 ered ; but the majority disappeared from the clinic without 
 much change in their mental state. 
 
 The cases of melancholia were mostly recent and simple, 
 and owed the origin of their disorder to the usual dual cause, 
 viz., physical ill health and mental strain. Two cases were puer- 
 peral and one was brought on by religious excitement. One 
 of the puerperal cases was suffering from her second attack. 
 In only one case was heredity ascertained. Two recovered 
 under the opium treatment, which in my experience is the 
 most advantageous, and the rest either were ordered to be 
 sent to institutions or were lost sight of. 
 
 In most of the cases of paranoia a hereditary history was 
 readily elicited. All had either fixed systematized persecu- 
 tory delusions alone, or these in combination with delusions of 
 a grandiose character. Two of the women were sisters, and 
 presented an excellent example of folic siniultanc'e (in their case 
 folie a dat.v). Their mother was a paranoiac with the fixed 
 
THE ORDINARY FORMS OF INSANITY. 293 
 
 delusion that she was the Virgin Mary. One of the young 
 women wrote for me an autobiographical sketch and the other 
 a series of letters which were used as a basis for a study of 
 their cases in the Alienist and Neurologist, January, 1890. The 
 two sisters were brought before the students with other cases in 
 a clinical lecture on paranoia, and naively exhibited their men- 
 tal infirmities very clearly and perfectly, describing their con- 
 tinual persecution by an organized band of conspirators; their 
 hallucinations of sight, hearing, smell, taste, and feeling; their 
 delusions of poisoning by the introduction of deleterious sub- 
 stances into their food and water, and of noxious vapors into 
 their rooms; and their continual moving from one house to 
 another, and their applications to the police for assistance, in 
 order to escape the machinations of their persecutors. Both 
 sisters were eager to narrate their story, and what one failed 
 to include the other supplied, until the mosaic of their psy- 
 chosis was perfected. 
 
 Another paranoiac presented himself at the clinic with a 
 large broad strip of thin sheet lead rolled up in his pocket, 
 and an electro-telephonic instrument of his own invention 
 which he called a " stethoscope." He was persecuted by a 
 " gang " which made use of telephony and electric apparatus 
 to annoy him. At night he wrapped the lead sheet about 
 him for protection from currents. Each member of the 
 "gang "had a " stethoscope," and he also had made one in 
 order to ascertain the schemes of his enemies, and thus be 
 better able to escape them. He explained the derivation of 
 the word " stethoscope " as from " stetho," stealthy, and 
 " scope," to scoop, for by its use the " gang " expected to 
 "stealthily scoop him into their clutches! " 
 
 There was nothing especially noteworthy in the 17 cases 
 of idiocy and imbecility received. We made an effort to secure 
 the proper treatment for hopeful cases, and by this is meant of 
 course mental and industrial training. One or two we were en- 
 abled to send to the State Asylum for Idiots at Syracuse. 
 Several cases of partial or complete mutism were sent to in- 
 stitutions in the city for the education of the speech faculty. 
 
 The 8 cases of general paresis seen by us were mostly in 
 
? 9 4 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 the early stages of the disease. Two remained under our ob- 
 servation until their death by convulsions, without exhibiting 
 further mental changes than a progressive dementia, present- 
 ing none of the characteristic grandiose delusions or condi- 
 tions of melancholy, or outbursts of maniacal excitement not 
 uncommonly met with. Three were sent to asylums for the 
 insane and the rest are still under treatment. One case was 
 unusual on account of the youth of the patient. He was 
 twenty-one years of age and had the typical somatic and 
 psychic symptoms of the disease. (A number of younger 
 cases have been recorded in literature.) One case developed 
 rather suddenly after a fall upon the head, and at first pre- 
 sented symptoms which led us to consider his malady a 
 pachymeningitis hemorrhagica. Later developments proved 
 it to be unmistakable paretic dementia of traumatic origin. 
 
 One case was a fine example of heboidephrenia recently de- 
 scribed by Kahlbaum {Allg. ZcitscJir. fiir Psych., 1889, part 
 iv.). The rest of the insane patients presented no unusual 
 features. 
 
 A PRACTICAL GROUPING OF CASES OF INSANITY. 
 
 A student or a general practitioner unfamiliar with the 
 various phases of insanity, if brought into contact for a time 
 with a large number of insane people, for instance, by a week's 
 visit to a public asylum, would, in a short time, unconsciously 
 arrive at a simple grouping of the insane into classes. 
 
 In a walkthrough the wards he would probably be at first 
 struck by a diversity of shape in the heads of patients, for in 
 every public asylum a certain number of cranial malforma- 
 tions are to be encountered. He would thus be able to clas- 
 sify the insane there met with into those with normally-shaped 
 heads and those with heads abnormally formed — or, in other 
 words, into such as had brains properly developed but fallen 
 a prey to disease in adult life, and such as had brains defective 
 from birth. Thus the first distinction he would make would 
 be between the following two groups: 
 
 I. Defective Brains. 
 
THE ORDINARY FORMS OF INS AN J TV. 
 
 2Q5 
 
 II. Diseased Brains. 
 
 Upon further examination of the first class he would dis- 
 tinguish certain degrees of defect, and would divide this class 
 into such as were most infirm — idiots; such as were only mod- 
 erately defective — imbeciles; and such as were manifestly only 
 congenitally weak in mental capacity — the feeble-minded. 
 
 In the second class he would be able to distinguish greater 
 diversity. From mere observation of physiognomy he would 
 select the gloomy visages of the melancJioliacs, establishing at 
 once a distinct class of patients in a condition of mental de- 
 pression (Fig. 72). The opposite extreme of great mental and 
 motor excitement — an exalted or maniacal state — would be 
 quickly noted. 
 
 He would furthermore see large numbers of patients who, 
 though apparently idiotic, imbecile, or feeble-minded in their 
 speech and demeanor, were yet distinguishable from such 
 cases by the possession of normally-shaped heads, and in 
 these he would soon 
 learn, by inquiry into 
 their histories, to rec- 
 ognize a class whose 
 brains had once en- 
 joyed normal faculties 
 and ordinary activity, 
 but had been weak- 
 ened intellectually by < 
 some acute antece- 
 dent brain-storm, usu- 
 ally either mania or 
 melancholia — a condi- 
 tion of mental enfee- 
 blement, or dementia as 
 it is generally termed. 
 It is a dementia conse- 
 quent upon a prior at- 
 tack of insanity, and 
 hence, as a rule, is called secondary or terminal dementia. 
 
 It would not be long before a certain number of the pa- 
 
 Fig. 72. — Composite Photograph of Six Patientssuffer- 
 ing from Melancholia. (.Noyes.) 
 
296 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tients would appear to possess a positive symptom-complex, 
 identifying them as a class by themselves— a clinical entity 
 
 Fig. 73.— Composite Photograph of Eight Patients suffering from Dementia Paralytica. (Noyes.) 
 
 consisting of a progressively increasing paresis or paralysis of 
 the body together with a progressive enfeeblement of the 
 mind, and therefore correctly termed dementia paralytica, or 
 general paralysis of the insane (Fig. 73). 
 
 Still another class would now appeal to the systematic 
 observer — patients with fixed delusions, generally of persecu- 
 tion, often of personal aggrandizement, and in whom by 
 careful inquiry and examination a hereditary taint was to be 
 ascertained and some degenerative stigma (such as cranial 
 malformation) detected. They have congenital instability of 
 the intellectual centres, and at the same time their actual in- 
 sanity may not have developed until the attainment of adult 
 life; therefore it is difficult to determine whether they belong 
 in the first or second great categories into which the novice 
 
THE ORDINARY FORMS OF INSANITY. 
 
 2<j 7 
 
 has attempted to classify the insane. He may decide, like 
 Magnan, to consider them as congenitally deficient, yet prone 
 to degenerate, a higher class than the idiots or imbeciles, and 
 higher even than the feeble-minded — a sort of superior de- 
 generate class. He will learn to call them cases of psychical 
 degeneration or paranoia, which is the name now generally 
 adopted. 
 
 This is my own early experience of the crystallization of 
 insanity groups in the mind; I will not dignify it by the title 
 of a classification, but I will call it a grouping of the various 
 forms of insanity, which is so simple and natural as to better 
 serve the requirements of the student and general practitioner 
 than the studiously-elaborate classifications of the text-books, 
 which are more adapted to the needs of the specialist. 
 
 The grouping arrived at, then, is as follows: 
 
 I. Defect of Brain. 
 
 (a) Idiocy. 
 (p) Imbecility. 
 
 (c) Feeble-mindedness. 
 
 (d) Psychical degeneracy (paranoia). 
 
 II. Diseases of Brain. 
 
 (a) Mental depression (melancholia). 
 
 (b) Mental exaltation (mania). 
 
 (c) Mental enfeeblement (dementia). 
 
 (d) General paresis (dementia paralytica). 
 
 The student or general practitioner needs no further clas- 
 sification. As his experience ripens, he will of course learn to 
 recognize associated conditions or causes — hysterical, toxic, 
 pubescent, puerperal, lactational, climateric, senile, hypochon- 
 driacal, epileptic, organic, cerebral — and to distinguish acute, 
 subacute, chronic stages and primary, secondary, periodical, 
 recurrent, circular, stuporous, or frenzied forms. 
 
 Paranoia. 
 
 A typical case of paranoia exhibits certain positive features 
 which make this form of insanity a clinical syndrome. There 
 are hereditary taints; some eccentricities in childhood ; more 
 
298 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 marked peculiarities during youth, often associated with a 
 degree of hypochondriasis; and at about the age of thirty, 
 sometimes earlier, sometimes later, the growth and systemati- 
 zation of delusions of persecution, which may in turn be com- 
 bined with or give place to systematized delusions of an 
 exalted character (either religious, philosophic, patriotic, or 
 erotic). Such delusions completely dominate their entire 
 mental action without impairing every faculty. 
 
 This is the typical form as exemplified in the case so well 
 described by Dr. William Noyes {Am. Jour, of Psychology, 
 
 May, 1888) of the brilliant 
 but " unfinished " artist 
 whose delusions of an ex- 
 alted religious nature were 
 wonderfully expressed in 
 his own drawings and paint- 
 ings reproduced to illus- 
 trate Dr. Noyes' papers. 
 
 Another perfectly typi- 
 cal case, a man of unusual 
 intellectual culture and lit- 
 erary ability, was he who,, 
 under the title of " The Pil- 
 ing of Tophet " wrote an 
 autobiography, now in my 
 possession, extracts from 
 which, with his history, will 
 be found in my paper in the Am. Journ. of Psychology, January, 
 1889. He was a religious paranoiac, and had a paranoiac uncle. 
 The two sisters already referred to are excellent examples 
 of cases with systematized delusions of persecution. 
 
 Some time ago, through the courtesy of Dr. M. D. Field, of 
 this city, I had the opportunity of seeing and examining an 
 erotic paranoiac, viz., the man who followed the actress, Miss 
 Mary Anderson, over this country and Europe, for several 
 years, never gaining an audience with her, but always deluded 
 with the idea that she loved him, as he did her, with a pure, 
 Platonic affection. He had hallucinations of hearing her 
 
 Fig. 74. — Photograph ota Paranoiac. (Field.) 
 
THE ORDINARY FORMS OF INSANITY. 
 
 2 99 
 
 make love to him. Besides this 
 purely mental love for her, he had 
 expansive delusions of personal i 
 grandeur, claiming to be a great as- 
 trologer and the writer of a book 
 explaining the cosmogony of the 
 universe. I reproduce here his pho- 
 tograph (Fig. 74), together with the 
 cranial measurements and drawings 
 I made at the time of my exami- 
 nation (Figs. 75 and j6). There was 
 an abnormal increase of height of 
 the skull. A complete description 
 of the case, together with transcripts 
 from his own writings, will be found 
 in Dr. Field's paper in the Journ. of 
 Nerv. and Ment. Dis., for September, 
 1889 (Cf. also N. Y. Med. Journ., 
 December 7th, 1889). 
 
 To illustrate the dangers to which 
 
 Fig. 75. — Measurements of the Cra- 
 nium in Jas. D. The pathological 
 variation is in 3 X and B, and hence, 
 although below the average in most of 
 its measurements, the head of this para- 
 noiac is above the average in the naso- 
 occipital arc and binauricular arc, 
 owing to the pathological height of 
 the skull. 
 
 Fig. 76.— Measurements and Shape of 
 Cranium in Jas. D. 
 Cephaloscopic Drawings of the Head 
 of an Erotic Paranoiac. Fig. 1. — Depart- 
 ure from the normal proportion in the 
 naso-occipital arc, owing to great vertical 
 height of skull. Fig. 2. — Vertical mea- 
 surement £ x i s excessive, and a patho- 
 logical variation from the normal. Fig. 
 3. — Shows asymmetry of the skull in 
 horizontal circumference, the right fron- 
 tal segment being greater than the left, 
 and the left parietal segment greater than 
 the right. 
 
 society is sometimes exposed by the presence among us of 
 paranoiacs with persecutory delusions I need but refer to the 
 case of Ernst Duborgue, who some years ago ran though 
 
?oo 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Fourteenth Street in this city stabbing right and left with 
 steel compasses. Upon examination the diagnosis of para- 
 noia was made, and he was sent to the Hudson River State 
 Hospital for the Insane. He died there of pulmonary and in- 
 testinal tuberculosis, July 28th, 1886. I made an autopsy upon 
 him. There was very marked asymmetry of his skull, sclerosis 
 of the cranial bones, increase of cerebro-spinal fluid, and con- 
 volutional asymmetry. His brain weighed forty-three and 
 one-quarter ounces avoirdupois. 
 
 Table of Cranial Measurements. 
 
 Circumference 
 
 Volume (rough approxi- 
 mation) 
 
 Naso-occipital arc 
 
 Naso-bregmatic arc 
 
 Bregmato-lambdoid arc. . 
 
 Binauricular arc 
 
 Antero-posterior diameter 
 
 Greatest transverse diam- 
 eter 
 
 Length-breadth index . . . 
 
 ]'>inauricular diameter.. . . 
 
 /3 X (Bregma to X) 
 
 Facial length 
 
 Empirical greatest height 
 (/3B) 
 
 Average 
 Hi normal 
 male skull. 
 
 52 
 
 I500 
 
 32 
 
 12.5 
 12.5 
 32 
 
 17-7 
 
 14.6 
 82.2 
 Brachy- 
 cephalic 
 12.4 
 11. 7 
 12.37 
 
 Limits of 
 physiological 
 
 I20I — I75I 
 
 28—38 
 IO.9 — I4.g 
 9.1— 14.4 
 28.4—35 
 16.5— 19 
 
 13-16. 5 
 76.1—87 
 
 10.9— 13.9 
 
 10-12.65 
 
 10.5— 14.4 
 
 13.3 11. 5— 15 
 
 Jas. 
 
 D. 
 
 Head. 
 
 Skull. 
 
 54-7 
 
 51.5 
 
 
 1390 
 
 36-5 
 
 34-3 
 
 12.5 
 
 12.5 
 
 12 
 
 12 
 
 37 
 
 34-7 
 
 1S.8 
 
 17. s 
 
 14.8 
 
 13.8 
 
 78.7 
 
 77-4 
 
 Mesali- 
 
 Dolico- 
 
 cephalic 
 
 cephalic 
 
 T3.2 
 
 12.5 
 
 13.4 
 
 12.9 
 
 12.5 
 
 12.5 
 
 15-5 
 
 15.5 
 
 Below average. 
 
 Below average. 
 Above average. 
 
 Average. 
 Below average. 
 Above average. 
 About average. 
 
 Below average. 
 
 Below average. 
 
 About average. 
 
 Pathological. 
 Above average. 
 
 Tathological. 
 
 The best historical and critical survey of the subject of 
 paranoia has been written by J. Seglas. It has been trans- 
 lated into English by Dr. William Noyes and published in the 
 Journ. of Ncrv. and Ment. Dis. of March, April, May, June, 
 1 888. For studies of paranoiacs, famed in national annals and 
 in bcllestristic and aesthetic domains, such as the rulers of 
 Russia, Austria, Bavaria, Spain, the cases of Louis Riel, Gui- 
 tcau, Swedenborg, William Blake, etc., the interested reader 
 is referred to Dr. W. W. Ireland's " The Blot upon the Brain " 
 and " Through the Ivory Gate." 
 
 Although it would be well to restrict the term paranoia as 
 much as is possible to the class of cases I have cited, which 
 were formerly called " monomania " by Americans, primare 
 
THE ORDINARY FORMS OF INS AN FT V. 
 
 30 r 
 
 Verrilcktheit by the Germans, and even still by the all-too-con- 
 servative English "monomania" or "delusional insanity " (see 
 Bevan Lewis' "Text-book of Mental Disease," 1890, page 
 192), yet there are undoubtedly cases not so typical as those 
 I have described to which the term paranoia often appears to 
 be equally applicable. These are what may be considered 
 formesfmstes of paranoia ; some for instance which break down 
 altogether at puberty, some which pause at one of the stages 
 of evolution to progress no farther, and some again which 
 may be conjoined with other varieties of insanity. The ec- 
 centric individuals popularly known as " cranks " are without 
 doubt imperfectly developed cases of paranoia. 
 
 As regards the treatment of these patients, little can be 
 done except perhaps in the way of moral methods, and these 
 are of most value in the earliest stages. They may abort the 
 psychosis. The asylums are the destination of most para- 
 noiacs, and in the best of these institutions the discipline, em- 
 ployment, recreations, and regularity of eating and sleeping, 
 exercise a beneficial influence upon the course of the disease. 
 Paranoiacs should be very carefully examined, especially 
 those with persecutory delusions, as to the presence of ideas of 
 retaliation and vengeance upon their persecutors. If there is 
 any suspicion of their possessing dangerous tendencies they 
 should of course be deprived of their liberty as soon as pos- 
 sible. 
 
 Melancholia. 
 
 This form of insanity is so well-known, that a definition is 
 unnecessary here. But I would call attention to the necessity 
 of early isolation of melancholic patients from their relatives 
 and friends, and to the particularly careful examination re- 
 quisite to determine the existence of suicidal inclinations. 
 Suicide is more frequent among the quiet cases of mild melan- 
 cholia who seem not to need asylum care than among those 
 actually sent to asylums; and I am sure I am correct in say- 
 ing that many cases go unrecognized as real insanity by the 
 family physician, until suicide, or possibly both homicide and 
 suicide, suddenly awaken him to his irremediable error. 
 
302 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Thorough investigation, unceasing vigilance, speedy separation 
 from friends, and early commitment to an institution, should 
 be the physician's rule in all of these cases. 
 
 With regard to medicinal treatment, the use of opium in 
 the form of tincture or extract, in gradually increasing doses, 
 I have found, in common with many other asylum physicians 
 who have carefully tried its utility upon large numbers of 
 patients, to be productive of the best results; morphia is not 
 so efficacious, but I have at times employed successfully *he 
 
 Fig. 77. — Photograph of Patient suffering from Melancholia. (Peterson.) 
 
 bromide of morphia. Opium should be administered without 
 the knowledge of the patient (indeed it is safest that no one 
 but the physician himself should know what is prescribed) 
 and carried to the extent of forming a habit, if need be, later 
 gradually diminished until it can finally be withdrawn alto- 
 gether. 
 
 A valuable feature of the opium treatment is, that instead 
 of increasing the constipation coincident with this disease, I 
 have found it to counteract this condition. After a short 
 time the bowels move with regularity every day. 
 
 I have much faith in the use of the prolonged warm bath 
 (one-half to two hours) as a hypnotic agent in melancholia. 
 
THE ORDINARY FORMS OF INS AN FRY. 
 
 303 
 
 Frequent feeding, even forcible feeding if necessary, is of 
 the greatest importance in the treatment. It combats the 
 condition of anaemia and physical prostration which is often 
 the cause of the disease. 
 
 The excellent composite photograph of six cases of melan- 
 cholia made by Dr. William Noyes is, with his kind permission, 
 reproduced (Fig. 72) ; and also a photograph of one of my own 
 patients (Fig. 77). 
 
 Mania. 
 
 Maniacal conditions are so familiar and so readily recog- 
 nized that they need not be described here. Most cases of 
 this kind are preferably treated in hospitals or asylums, rather 
 than at home. But when for some reason immediate removal 
 is impossible, the motor and mental excitement are tempora- 
 rily allayed best by the hypodermic injection of hyoscyamia 
 or hydrobromate of hyoscine (doses of from t~o to eV at first), 
 and exhaustion prevented by the wet pack and overfeeding. 
 In feeding maniacal patients, liquid food only can as a rule 
 be used, whether by ordinary forcible methods, or by the 
 nasal or stomach tube. This liquid food should consist of 
 milk, raw eggs, Valentine's meat juice, sugar, and, where indi- 
 cated, whiskey. I think the employment of the tube only 
 rarely necessary; in fact I finally abandoned it in my asylum 
 practice, because I found few patients to resist more peace- 
 ful methods for any dangerous length of time, and in the 
 worst cases I was able to feed without the tube on making 
 the attempt just as they were passing under the influence of 
 the- hypodermic injections. While non-restraint is the rule 
 of asylum practice, the long-sleeved camisole is often abso- 
 lutely necessary in cases treated at home. 
 
 General Paresis. 
 
 Dementia paralytica in its earliest stages first comes into 
 the hands of the general practitioner, and is usually treated 
 by him for months before pronounced insanity develops. I 
 
304 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 need not dwell upon the importance o{ earl) - recognition of 
 this disease, not indeed for purposes of treatment, which is 
 rafely if ever of any avail to stay its fatal progress, but on 
 account of the gravity of the prognosis which is to be made. 
 The onset of this disorder is protean in its manifestations. 
 The earliest symptoms may be either physical or mental or 
 both. Tremor of the fingers and of the hand in writing; 
 fibrillar}- tremor of the tongue and lips; slight difficult}- in 
 the pronunciation of certain words such as occur in the phrase 
 "Grief brings frightful dreams " ; overaction of the occipito- 
 frontal muscle; slight irregularity or inequality of pupils, 
 myosis, or loss of the pupillary reflexes; exaggeration of the 
 wrist, elbow, and knee-jerks (rarely diminution); all these are 
 among the earliest somatic characteristics. Later these be- 
 come more and more pronounced until diagnosis is inevitable. 
 
 The mental symptoms are particularly variable. There 
 may be at first but a melancholy or a hypochondriacal condi- 
 tion. This is more common as an early symptom than that 
 feeling of well-being and personal aggrandizement which al- 
 most always makes its appearance at some epoch in the dis- 
 ease. Loss of memory, temporary amnesia, and, as a result 
 of these, a certain amount of incongruity of action ; emotional 
 susceptibilities; the inappropriate or misplaced use of words; 
 these are among the most frequent of the psychic prodromi. 
 Sometimes unexpected maniacal outbreaks occur. 
 
 Convulsions, epileptiform or apoplectiform, generally usher 
 in the later stages of general paresis, but these may also make 
 their appearance very earl}' and very unexpectedly. 
 
 A limited number of cases will progress to a fatal termin- 
 ation without manifesting symptoms necessitating their re- 
 moval from home, but the great majority ultimately require 
 the special supervision and care of the infirmary ward of an 
 institution. 
 
 Where syphilis has a share in the etiology, treatment 
 should of course be directed to this factor, but it will seldom 
 alter the fatal course of cortical dissolution. Physostigmine 
 and ergot in small doses may be administered. These drugs 
 occasionally modify some of the symptoms, but no agent as 
 
THE ORDINARY FORMS OF INSANITY. 305 
 
 yet known will do more than slightly postpone the lethal ter- 
 mination. 
 
 On two occasions of late, trephining seems to have caused a 
 temporary remission in general paresis, possibly, as claimed, 
 by lessening intracranial pressure {Brit. Med. Jour., Nov. 
 16th, 1889). If surgical interference could be depended upon 
 to produce even a remission, it would certainly be justifiable. 
 
 Remissions, with considerable improvement at times, and 
 lasting for months, rarely for a year or more, may be antici- 
 pated in a restricted number of cases; but such episodes have 
 no influence upon the unfavorable prognosis. 
 
 HOME AND ASYLUM TREATMENT. 
 
 While it is apparent from the foregoing that I believe in 
 the early removal of most cases of insanity from the environ- 
 ment in which the psychosis has developed, I am by no means 
 an admirer of asylums in general as now conducted. The 
 large public institutions are hampered in their treatment by 
 the enormous number of patients and by the lack of a corre- 
 sponding number of physicians and attendants. The superin- 
 tendent is seldom a thoroughly trained alienist, and in some 
 States these charities of the people are unfortunately made 
 to subserve the interests of the great political machine. Pa- 
 tients cannot derive that benefit which they should from the 
 medical superintendent's long experience, because their indi- 
 vidual requirements must be sacrificed to the many demands 
 upon his time in the general management. His assistants are 
 too few and too pre-occupied with their clerical and office 
 duties to carefully individualize and treat the patients. Fi- 
 nally there are too many patients. A State asylum contain- 
 ing but two hundred patients has but an indifferent public 
 standing. It must have a thousand or two thousand patients 
 in order to satisfy the ambition of the community and of the 
 managers. Small wonder, then, that the actual object of the 
 institution should so often be lost to sight! 
 
 Until therefore these great charities, now little more than 
 
 warehouses for the storage of articles unnecessary or in 
 
 20 
 
306 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 society's way, conform more to the character of a hospital, 
 with its modern equipment, its attending physicians, and its 
 consulting specialists, the higher classes of private asylums in 
 the hands of men who are known for their professional attain- 
 ments and probity of character will always be more desirable 
 as places for the reception and treatment of such insane 
 patients as are so fortunate as to be able to enjoy their ad- 
 vantages. 
 
 It is to be hoped, however, that at some future day our 
 general hospitals will provide special wards or pavilions for 
 this particular class of cases, so that in every city one or sev- 
 eral places will be at all times ready to receive the acute in- 
 sane and care for their sick brains in the highest scientific 
 manner. 
 
CHAPTER XXI. 
 ELECTRICITY AS A THERAPEUTIC AGENT. 
 
 Elementary physics. — I. Static electricity. — II. Voltaic electricity or gal- 
 vanism. — Catalytic effects. — Cataphoric effects. — Electro-tonic ef- 
 fects. — III. Faradism or the induced current. — Summary. 
 
 The modern view of electricity differs widely from the 
 older views often reproduced in medical literature. To follow 
 them closely would lead one to consider electricity as an 
 entity, possibly a fluid, which can be administered like a drug. 
 The term " current " is partly responsible for this fallacy, it 
 being difficult to deal with this term without imagining a flow 
 of something in a definite direction. Yet just as the older 
 term caloric is now discarded, and the old notion that " heat 
 is the result of caloric being poured into a body " raises a 
 smile, so similar fallacious notions regarding electricity should 
 at present meet with disapproval. 
 
 The sooner it is realized that electricity, like heat and 
 light, is merely a form of activity in matter, or, to be some- 
 what more precise, in the imponderable ether surrounding 
 each molecule of matter, and the sooner the term " electrical 
 current " gives place to the more accurate phrase state of elec- 
 trification, the sooner will the mystery surrounding this agent 
 be cleared away. 
 
 When electricity is applied to the body a change is pro- 
 duced in the normal condition of the molecules making up 
 the body, a new molecular condition is produced, but nothing 
 is added to or subtracted from the body itself. 
 
 Between the two poles of the battery this molecular state 
 is more intense than elsewhere, and under one pole it is some- 
 what different from that under the other. The intensity of 
 the change is measured roughly in terms of the strength of 
 
j08 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 its pull upon a balanced needle — but this should not lead to 
 the adoption of such terms as a dosage of electricity, which, 
 like the term current, is sure to mislead. 
 
 When electricity is thus regarded as a mode of energy 
 capable of estimation, like other modes, in terms of work, it 
 becomes evident that a valuation of the various forms under 
 which this energy appears is possible. 
 
 In common usage these forms are static or fractional elec- 
 tricity, voltaic electricity or galvanism, and induced electricity 
 or faradism. It should be distinctly understood that all these 
 forms are really the same mode of energy displayed under 
 varying conditions. An illustration may make this plain. 
 Suppose that you have a dry sponge and a tumbler of water. 
 If you throw the water over the sponge the greater part of it 
 will run off, leaving only the surface of the sponge wet. You 
 have applied a quantity at once, and your effect is short and 
 soon over. Suppose, on the other hand, you let the water 
 fall on the sponge drop by drop. It will soak in and wet it 
 thoroughly but gradually, until in the end all the water will 
 remain in the sponge, which is now soaking. The effect is 
 slow but intense. Water and sponge are the same in both 
 cases. The conditions vary under which they have been 
 brought together. 
 
 This illustration, which is not to be taken literally, may 
 convey some notion of the difference between static and vol- 
 taic electricity. By the former sudden transient effects are 
 produced very limited in intensity. By the latter, slow, per- 
 manent effects are produced of much intensity. 
 
 I. STATIC ELECTRICITY. 
 
 It seems strange, when the history of the uses of electricity 
 is reviewed, to find how much credence is still placed in the 
 effects of frictional electricity. In the first place, the change 
 of electrical state produced by it is limited exclusively to the 
 surface of bodies charged. Take a metal ball insulated by a 
 glass stand over which two hemispheres are fitted, and charge 
 this with static electricity. If the hemispheres be now re- 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 
 
 309 
 
 moved from the surface, they are found to carry all the elec- 
 trical charge, and no change of electrical state has been pro 
 duced in the metal ball beneath them. There is absolutely 
 no proof that the human body acts in any way differently 
 from the metal ball. Any effects obtained by static electric- 
 ity must, therefore, be from surface stimulation; and, hence, 
 wholly reflex and indirect in character. 
 
 When the surface of a body is charged with static electric- 
 ity, it discharges itself gradually into the air by diffusion, or 
 directly into the ground if the body be not insulated. The 
 human body cannot be permanently charged with electricity. 
 
 The state of electrification on the surface of the body is 
 communicated to the air about, which is thus put in a similar 
 electrical state. But bodies in a like state of electrification 
 repel one another. Hence the hair, when charged, is repelled 
 from the body, and stands on end ; air, when charged by dif- 
 fusion, moves away from the body, and the air in motion may 
 be felt as a breeze ; hence, when a person is charged with 
 static electricity this breeze is perceived. 
 
 If all effects of static electricity are reflex in their nature,, 
 due to irritation of the skin, then the agent differs in no re- 
 spect from any mild form of counter-irritation — such as whip- 
 ping with twigs, lomi lomi of the Sandwich Islanders, the 
 needle douche of a Turkish bath — excepting, possibly, in the 
 convenience of application. Stimulation of the circulation, 
 contraction of muscles as from a blow, agreeable sensations, 
 or sharp pain, may all be produced in such a reflex manner, 
 if they are considered desirable. But no further distinctly 
 curative effects can be produced. And, as we shall see later, 
 the same effects can be secured by faradism. 
 
 It is possible to produce muscular contractions by the use 
 of static electricity through the clothing, and therefore the 
 necessity of undressing a patient is obviated by the use of this 
 form of electricity, which is, therefore, convenient in large 
 clinics. But it is not easy to limit its action to definite mus- 
 cles, and as in the majority of cases of paralysis it is desired 
 to obtain a tonic nutritive action as well as mere exercise, the 
 other forms of electrical application are preferable. Another 
 
3io FAMILIAR FORMS OF XFRl OFS DISEASE. 
 
 objection to the use of static electricity is the fact that an 
 efficient apparatus is cumbersome, takes up a large amount 
 of space, cannot be transported, and requires an assistant to 
 revolve the wheels. 
 
 There is something so startling in the application of elec- 
 tric sparks to the body that static electricity has been em- 
 ployed for producing sudden mental impressions. 
 
 The elements of mystery and of expectant attention doubt- 
 less play a part in the treatment of some functional nervous 
 affections. It is an open question how far they may be le. 
 gitimately employed. When static electricity relieves hysteri- 
 cal affections, it must be admitted that it is largely by means 
 of the mental effect produced. 
 
 II. VOLTAIC ELECTRICITY OR GALVANISM. 
 
 A frictional machine does all its work suddenly, in a frac- 
 tion of a second. It is not capable of producing a constant 
 electro-motive force. This can, however, be obtained froirl a 
 galvanic battery; and very soon after the discovery by Volta, 
 the use of static electricity was largely superseded in medicine 
 by that of galvanism. The fact that a voltaic battery fur- 
 nishes a definite amount of electro-motive force capable of 
 doing a measurable amount of work and producing definite 
 effects on the body suffices to explain its continued use. Yet, 
 when definite effects from galvanism are considered, there are 
 few physicians to be found who will contend for a moment 
 that there is any such certainty regarding the therapeutic 
 effects on the body as there is regarding the use of drugs. 
 Opium will quiet pain; aconite will depress the heart. But 
 there is no statement which can be made with equal definite- 
 ness regarding electricity. 
 
 As far as the effects of galvanism are now known, they 
 may be classified under three distinct heads, viz., catalytic, 
 cataphoric, and electro-tonic effects. 
 
 a. Catalytic Effects. — The splitting up of a compound ele- 
 ment into its constituent parts is one of the ways in which 
 the work done by electricity is measured. The compound 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 311 
 
 body is put into a state of electrification which makes the 
 condition of its molecules so unstable that they fly apart, and 
 as they burst asunder those which have taken on a state like 
 that of one pole of the battery are repelled from it and ap- 
 pear at the opposite pole. A strong current passing through 
 the body produces intense catalytic effects, disintegrating and 
 destroying the tissues, and raising blisters under each pole, 
 the one (negative) containing acid, and the other (positive^ an 
 alkaline fluid. Even with a weak current, the taste produced 
 in the mouth differs at the different poles, one being sour, the 
 other salty. There is no doubt, then, that marked chemical 
 changes may be produced by the galvanic current. 
 
 This power, then, may be used like that of any other de- 
 structive agent, to dissolve body tissues. For some purposes 
 — such as elimination of hairs from the face — it is convenient. 
 How successful it may prove in the destruction of tumors — ■ 
 especially of the internal organs — it is hardly time to judge. 
 In the resolution of strictures its use is strongly combated by 
 eminent authorities after thorough trial. In any case the dif- 
 ficulty of limiting its action, the serious nature of the wound 
 which is left, the slow healing and deep scars which remain, 
 combine to make it less certain, less definite, less satisfactory, 
 than ordinary surgical procedures — and, consequently, it is 
 not indorsed by surgeons generally. 
 
 The use of mild, non-destructive currents has been urged 
 by some, and it has been claimed that a catalytic effect of a 
 moderate kind may aid nutrition. Nutritive processes are de- 
 pendent upon chemical and molecular changes. Is it possible 
 to stimulate these by a constant galvanic current? Theory 
 here is aside from the point. Experience must furnish facts. 
 The only scientific observation which I have been able to find 
 is furnished by Prof. James K. Thacher, of Yale College, and it 
 is certainly extremely valuable and interesting. In a case of 
 bilateral paralysis of all the extremities, due to diphtheritic 
 multiple neuritis, Dr. Thacher made a series of therapeutic 
 experiments upon the arms, each arm being treated alone for 
 a week at a time, and its relative gain under treatment being 
 compared with that of the opposite untreated arm. The re- 
 
312 
 
 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 Galvanized 
 
 Untreated 
 
 arm. 
 
 arm. 
 
 1 7° gain 
 
 12° gain. 
 
 15 " 
 
 IO° " 
 
 7-4° " 
 
 O.9 " 
 
 suits were measured in degrees of strength of grip as deter- 
 mined by a dynamometer. 
 
 It was found that the arm to which a labile constant gal- 
 vanic current was applied daily for ten minutes, gained in 
 strength in a degree far greater than that of the untreated 
 arm. So that the gain under galvanism could be exhibited as 
 follows : 
 
 1. Ten days' treatment to left arm, 
 
 2. Seven " " to right " 
 
 3. Seven " " to left " 
 
 The galvanized arm made almost double the progress of 
 the other (1 : 1.72). 
 
 The gain under faradism was much less perceptible. 1 
 
 I know of no other accurately measured, scientific test 
 under proper conditions which demonstrates so perfectly the 
 power of the constant galvanic current to promote nutrition. 
 It would add greatly to our knowledge if similar observations 
 were made. And it is undoubtedly the catalytic effect of the 
 electricity which is responsible for the nutritive changes. 
 
 It is very important to produce nutritive changes in man)' 
 nervous cases, especially in all forms of paralysis, where it is 
 necessary to keep the muscles strong, until the lesion is re- 
 paired by nature. It is undoubtedly through its catalytic 
 action that galvanism produces many of its most beneficial 
 effects in nervous diseases. 
 
 This is particularly true of its effects in neurasthenic con- 
 ditions due to imperfect nutrition of the general nervous sys- 
 tem. A neurasthenic person usually feels refreshed and in- 
 vigorated by an application of galvanism to the spine or to 
 the body generally. This should be made by means of large 
 sponge electrodes applied to different parts of the spine and 
 moved up and down during the application ; or by means of 
 central galvanization, first described by Beard, one pole being 
 placed on the epigastrium and the other moved about over 
 
 1 Medical News, April 18th, 1885. 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 313 
 
 the entire body; or, by another method of Beard in which 
 the patient's feet are placed on one electrode and the other 
 is placed upon the spine. In such treatment the strength of 
 the current must depend somewhat upon the sensations of 
 the patient. A daily application for ten minutes of a current 
 of twenty milliamperes (ma.) is to be employed. Twenty 
 milliamperes is usually as strong a current as can be borne 
 when sponges six inches in diameter are used. If the size of 
 the sponge is increased, the current, being spread over a larger 
 area, must be increased in strength to produce the same effect 
 at any part of this large area as it produced in any part of 
 the smaller area. Thus the strength of current has to be reg- 
 ulated by the size of electrode as well as by the varying resist- 
 ance of the patient's skin, which latter factor is extremely 
 variable. Hence the absolute necessity of using a galvano- 
 meter in all galvanic applications. 
 
 In diseases of the brain, such as cerebral hemorrhage, 
 sclerosis, abscess, tumor, or embolic softening, as well as in 
 all forms of insanity, electrical treatment is useless. It can- 
 not affect the pathological process which causes the symp- 
 toms. In diseases of the spinal cord it is usually recommended 
 and often applied. Roughly, we may divide these diseases 
 into (1) inflammatory destructive lesions of the gray matter, 
 and (2) sclerotic- processes. In the first class, of which dis- 
 seminated myelitis and infantile paralysis may be taken as 
 types, there may be an object in reducing congestion ; but it is 
 not certain that this can be accomplished for any length of time 
 by electricity, as it can by counter-irritation or by cupping. 
 After the acute stage is over, spontaneous recovery will occur 
 in greater or less degree in many cases. It is possible that 
 this may be aided by the application of electricity to the spinal 
 cord. In the second class, of which locomotor ataxia is a 
 type, it is theoretically difficult to assign any effect upon the 
 sclerotic process of a change of molecular state. And, prac- 
 tically, few definite results can be affirmed regarding the ef- 
 fects of its application. Ataxia and spastic rigidity do not 
 appear to be removed either temporarily or permanently, and 
 the analgesic effects of electricity are very often disappoint- 
 
314 
 
 FAMILIAR FORMS OF NERVOUS DIS EASE. 
 
 ing. In spinal affections, therefore, it seems to me that ex- 
 perience does not confirm the statements of some text-books 
 and of those whose interests lie in the direction of its use. 
 
 This experience conforms to that of such a careful ob- 
 server as Gowers, who, in his recent text-book, states that 
 electrical treatment fails in his experience to affect the pro- 
 gress of organic nervous diseases. 1 
 
 Another question of importance is, to what degree the 
 electrical state is induced in deep-lying tissues such as the 
 brain and spinal cord. The body is not homogeneous and 
 the power of conduction of different tissues varies greatly. 
 If two pipes lead out of a reservoir, one free, the other plugged 
 with rubbish, the water will seek the easy outlet to the exclu- 
 sion of the other. To rely upon the older diagrams of the 
 diffusion of electric currents in the body is to be misled. 
 
 1 The following quotations from Gowers are cited in support of the statement 
 in the text. 
 
 " There is no evidence that'the application of electricity to the spinal column 
 has any influence on the process of recovery in acute myelitis. Its chief value is 
 to maintain, as far as possible, the nutrition of any muscles of which the nerves 
 have undergone degeneration." — Vol. i., p. 235. 
 
 No mention of electricity is made by Gowers in dealing with the treatment of 
 chronic myelitis. — Pp. 245-6. 
 
 " Electricity has been strongly advocated and largely used in the treatment of 
 infantile paralysis, and there is reason to believe that it is useful, although its influ- 
 ence has been much exaggerated. In no sense is it a curative agent, and there is 
 no evidence that its application to the spine is capable of increasing the degree or 
 accelerating the course of the recovery of the nerve elements. Nor is it easy to 
 obtain evidence of its influence over the muscles. If the wasting is rapid, this 
 progresses in spite of daily and sedulous applications. Nevertheless, its de- 
 monstrable effect on the muscles in causing their contraction must have an influence 
 in the right direction upon their nutrition. This is of no avail if no recovery 
 takes place in the spinal cord, but in most cases some recovery in the cord does 
 occur." — P. 270. 
 
 " Electricity has little influence on the chief symptoms of tabes. The voltaic 
 current is powerless over either the pains or the ataxy, whether it be applied to the 
 spine or to the limbs." 
 
 After alluding to faradization of the skin in pain, and in incontinence of 
 urine, Gowers adds : 
 
 " The central cause usually renders local treatment ineffective." — P. 326. 
 
 " Electricity is useless in spastic paraplegia." — P. 340. 
 
 "The most sedulous and skilful use of electricity, voltaic or faradic, fails, as 
 a rule, to produce any effect on the course of progressive muscular atrophy." — P.3S0. 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 315 
 
 Muscle conducts easily, bone less so, least of all the nervous 
 tissue, which is peculiarly insulated by its fluid surroundings. 
 The result must be that but a small fraction of the current 
 reaches the nervous organs in comparison with the amount 
 applied. Just how much does reach them has never yet been 
 accurately determined, and cannot be from the nature of the 
 case in a state of health. 
 
 It is, therefore, necessary to be guided still in the use of 
 electricity in central nervous diseases by the teachings of ex- 
 perience and to use it in a somewhat empirical manner if at 
 all. 
 
 In peripheral nerve lesions many of the objections urged 
 against the use of electricity in affections of the central organs 
 are obviated. It is possible to localize the application and to 
 determine by the sensations and motions produced just what 
 nerves are affected. It is certain that favorable nutritive 
 effects are produced by the increased circulation and more 
 rapid chemical changes induced by the agent. It would be 
 interesting to ascertain definite time results in the treatment 
 of these diseases, but facts are still to be collected. Is the 
 duration of a lead palsy shortened by the application of a 
 constant current ? Is the course of a facial paralysis in any 
 way affected by its use? I have been much disappointed by 
 the lack of rapid results in the former. I have seen the latter 
 go on to the most severe form, with a permanent paralysis, in 
 spite of the most careful applications of electricity. Many 
 cases of both diseases get well. It is still impossible to esti- 
 mate the exact value of electrical applications in such affec- 
 tions, but that they are of great use both in aiding nutrition 
 in the muscles paralyzed and by giving those muscles proper 
 exercise is certain. 
 
 In neuralgia the galvanic current is also of service, the 
 palliative effects of the positive pole being proven. The rule 
 proposed by Dr. Gibney, of placing one pole over the nerve 
 trunk and increasing the current until the patient has peri- 
 pheral sensations in the area of distribution of the nerve 
 treated, seems to me of great value, for unless such sensations 
 are perceived it is unlikely that the nerve is really brought 
 
316 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 into a state of electrification. If the spinal cord is really ex- 
 cited by the current, why should not general peripheral sen- 
 sations be produced ? It is rarely that I have succeeded in 
 causing them, and I do not think they are elicited in the usual 
 method of application. 
 
 b. Cataphoric Effects. — The power of electricity to promote 
 osmosis is well proven. A transfer of substances from the 
 positive to the negative pole through intervening organic 
 tissue can be made. This is termed a cataphoric action. It 
 has been used of late ' in the production of local anaesthesia, 
 and for the quieting of neuralgic pain ; cocaine, morphia, and 
 aconitia having been brought into direct contact with painful 
 nerves in this manner. As a method of treating neuralgia 
 this is of distinct service, and it may also be used in painful 
 affections of the muscles. 
 
 The method of the application is simple. A short glass 
 cylinder is covered at one end with parchment securely tied 
 and sealed with collodion. Into this tube, filled with the solu- 
 tion of the drug to be used, the positive pole is introduced 
 through a cork which serves to retain the fluid. The parch- 
 ment surface is then applied over the painful spot and the 
 current allowed to pass, the negative pole being placed at any 
 part of the body desired. The strength of current used 
 should be from eight to twelve milliamperes, and the duration 
 of the application from four to ten minutes. The drug is 
 carried by osmosis through the parchment and through the 
 skin. 
 
 Medicated electric baths, which might be arranged on this 
 principle, cannot be at present commended, since the dosage 
 of the drug thus employed is wholly uncertain. 
 
 c. Elcctrotonic Effects. — It has already been stated that the 
 application of electricity produces a state of electrification in 
 the molecules of the body. This state varies under the differ- 
 ent poles of the battery, and each pole is supposed to produce 
 an effect the exact reverse in kind from that under the other 
 pole. These opposite states are known as anelectrotonus and 
 
 1 "Electric Cataphoresis as a Therapeutic Measure." F. Peterson, M.D., N. 
 Y. Med. Jour., April 27th, 1889. 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 317 
 
 .katelectrotor.us. It is not necssary for us to determine 
 whether the state produced is due to a parallelism of molecu- 
 lar vibration, comparable to that occurring in polarized light, 
 or whether it is a state induced in the dielectric, the impalpa- 
 ble ether surrounding the molecules. Suffice it to say that 
 two electrotonic states exist, one at each pole, and that the 
 tissues between the poles share in these states in the direct 
 ratio of their nearness to the poles. 
 
 The sudden production of either state excites violent 
 molecular movements in the tissues, and these become doubly 
 violent if either state is suddenly replaced by its opposite. 
 
 Each tissue manifests its irritation in its own manner, the 
 muscle by contraction, the motor nerve by sending a motor 
 impulse to the muscle, the sensory nerve by transmitting a 
 sensory impulse to the brain. Hence to excite tissues to 
 functional activity sudden changes in their electrotonic state 
 are produced by suddenly closing or opening or reversing the 
 constant galvanic current. The last-named procedure, re- 
 versing the current, or using voltaic alternatives, is necessarily 
 the most active excitant of all. No one can deny the bene- 
 ficial effects produced by exciting the functional activity of 
 the various organs, especially when, as in paralysis, the organs 
 cannot be voluntarily set to work; for exercise aids nutrition, 
 promotes the circulation, assists metabolism. It is probable 
 that no other method equals this in these respects, although 
 massage has a parallel effect. The electrotonic effect upon 
 the vessel walls is also proven, for a decided dilatation of the 
 smaller arteries can be seen after an application ; and when 
 this condition has passed off, if the part be immersed in warm 
 water, the local redness becomes again manifest. This has 
 been ascribed to the chemical changes set up by the catalytic 
 action of the current, but the fact that it is more intense at 
 the negative pole demonstrates that the result is due, in part 
 at least, to the electrotonic state produced; and the fact that 
 it is caused by a faradic current, which has no catalytic effect, 
 confirms this statement. 
 
 Galvanism or voltaic electricity properly administered with 
 accurate measurements is undoubtedly of great service in 
 
jl8 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 the treatment of nervous diseases. For it produces chemical 
 changes which aid nutrition ; it transfers substances from 
 place to place in the body, thus possibly stimulating the natu- 
 ral movement of fluids in vessels and lymphatics; and it ex- 
 cites organs whose function is suspended by disease to func- 
 tional activity. It thus meets many of the needs which the 
 physician appreciates in the treatment of nervous affections. 
 As has been shown, however, it is of much greater service 
 in functional disorders of nutrition and in peripheral nervous 
 diseases, such as neuritis and neuralgia, than in grave lesions 
 of the central nervous system. When used in the latter it is 
 merely to combat individual symptoms, such as paralysis, and 
 not to affect the process of disease to which the symptoms 
 are due. 
 
 III. FARADISM, OR THE INDUCED CURRENT. 
 
 It has been stated that when the galvanic current is closed 
 or opened, a sudden change of state is produced in the body. 
 The same change of state is produced in an independent wire 
 which lies at the side of the wire conducting the galvanic cur- 
 rent. The current in the independent wire is said to be in- 
 duced by magnetism. If such a wire be wound in a coil, each 
 layer of the coil reinforces every other by magnetism, and 
 when the coil is large the induced current produced is very 
 strong. The strength of a faradic current can be increased 
 by increasing the number of layers in a coil; or more conven- 
 iently by using coils of different thickness, or by pushing a single 
 large coil further and further over the original galvanic coil, 
 thus bringing more and more of the secondary coil over the 
 primary one. While a galvanic current is passing contin- 
 uously the induction of electricity does not occur in the sec- 
 ondary coil; hence the presence in every faradic battery of a 
 vibrating rod which constantly interrupts the passage of the 
 primary weak galvanic current, making and breaking the cir- 
 cuit and inducing the secondary current. 
 
 If electrodes are attached to the ends of the secondary coil 
 of wire and the electricity is applied to the body, it is evident 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 31^ 
 
 that a series of rapidly recurring shocks will be given. The 
 physical effect is so far exactly the same as in the application 
 of a galvanic interrupted current. But a very strong effect of 
 an electrotonic kind is produced by such a faradic application 
 and a very weak or hardly perceptible catalytic and cata- 
 phoric effect. 
 
 The effects of faradism are, therefore, wholly electrotonic 
 effects, never catalytic or cataphoric. Its convenience in 
 being produced in a portable apparatus is its only advantage 
 over voltaic alternatives. The difference of reponse to the 
 faradic current from that to voltaic alternatives in conditions 
 known as the reaction of degeneration, is not to be ascribed to 
 any difference in the nature of the current, but only to the fact 
 that the degenerated muscle will not respond to changes of 
 state rapidly produced in it. This has been proven by in- 
 creasing by a mechanical device the rapidity of voltaic inter- 
 ruptions, when the degenerated muscle finally ceases to re- 
 spond to them, while the healthy muscle on the contrary 
 becomes tetanized. 
 
 Tetanic contraction is produced in a healthy muscle by 
 voltaic alternatives, whose rapidity is over twenty to the 
 second. In a degenerated muscle, as the rapidity of the alter- 
 natives rises from five per second, the degree of contraction 
 becomes progressively less, and when a rate of twenty per 
 second is reached the muscle no longer contracts. 1 The rap- 
 idity of faradic interruptions is usually above twenty per sec- 
 ond. Since muscular contractions are desired in the treat- 
 ment of paralysis, it follows that faradism is useless unless 
 the muscles act to it. In any case of paralysis, therefore, in 
 which faradism produces contractions, viz., in all forms of 
 paralysis from brain lesion, and in many very mild cases of 
 spinal and peripheral paralysis, faradism may be used. If, 
 however, as in the last named diseases, a nutritive and stimu- 
 lant to chemical action is desired as well as mere muscular 
 exercise, the galvanic current must be employed. 
 
 Admitting the great use of interrupted currents in exciting 
 
 1 I am indebted to Mr. Charles Young, of Princeton College, for these facts and 
 for a demonstration of them. 
 
J20 FAMILIAR FORMS OF NERVOUS DISEASE. 
 
 tissues to activity by producing changes of electrotonic state, 
 
 can further claims be allowed ? There is one which has al- 
 ready been alluded to in dealing with static electricity, namely, 
 the reflex effect of surface irritation. It is not unlikely that 
 changes of circulation or of molecular state — very beneficial 
 in character — may be exited in central organs by such reflex 
 irritation. It is evident, then, that the only effect which oc- 
 curs from an application of static electricity can be produced 
 equally well by interrupted currents. 
 
 Faradic electricity has one other use. In cases of anaes- 
 thesia from any cause, the faradic current applied by means 
 of a wire brush over the anaesthetic surface is sometimes fol- 
 lowed by a decrease in the degree of anaesthesia. And it has 
 had also a reputation for quieting pain if applied in the same 
 manner. Its limits, however, as is evident, are many; and for 
 general use the galvanic current is of far greater service when 
 properly applied. 
 
 To sum up the facts here presented, we may say that : 
 
 1. Static electricity offers nothing beyond an interrupted 
 galvanic current, and fails to furnish those effects which are 
 most desirable in the treatment of disease. 
 
 2. A constant galvanic current can produce chemical 
 changes which aid nutrition, or destroy tissue according to 
 the strength employed. 
 
 3. A constant galvanic current can transfer medicines into 
 the body from without. 
 
 4. An interrupted galvanic current, or a faradic current, 
 can excite various organs to functional activity, thereby aid- 
 ing their nutrition. 
 
 5. It is questionable whether the pathological state caus- 
 ing organic diseases can be in any way influenced by elec- 
 tricity. 
 
 6. If functional diseases are benefited, it is in an uncertain 
 manner; it being undecided whether it is by influencing the 
 molecular condition, the chemical changes, the circulation, or 
 the electrical state of the organ affected; or by the state of 
 mental expectation induced. The agent is, therefore, used 
 empirically, and the physiological indications for it are as yet 
 
ELECTRICITY AS A THERAPEUTIC AGENT. 
 
 321 
 
 uncertain. As a therapeutic agent its use is very limited, and 
 carefully balanced scientific observations are still needed to 
 establish its proper sphere. 
 
 I cannot, however, close this chapter without stating that 
 after the constant use of electrical treatment for the past six 
 years in dispensary and in private practice, I have been dis- 
 appointed in the results obtained. And I cannot ascribe this 
 lack of result to any defect in the applications, for they have 
 been made with care, with the best of apparatus, and with 
 exact galvanometric measurements, according to the methods 
 described by such authorities as Erb, De Watteville, Bene- 
 dickt, and Beard. My experience coincides with that of Gowers, 
 that the therapeutic effects of electrical applications have 
 been much exaggerated and are really quite limited. 
 21 
 
CHAPTER XXII. 
 
 PRESCRIPTIONS IN USE IN THE NERVOUS DEPART- 
 MENT OF THE VANDERBILT CLINIC. 
 
 Mist. Ac. Nitro-Muriat. 
 
 $ Ac. nitro-mur. dil ill iiss. 
 
 Tinct. nuc. vomic ill i. 
 
 Tinct. calumbae ill x. 
 
 Syr. limon ill x.\. 
 
 Aquae q. s. ad ll. Z i. 
 
 M. Dose 5 ss. 
 
 Mist. Acid. Tonic. 
 
 1 1 Tinct. nuc. vomic TH, v. 
 
 Ac. nitro-mur. dil TTJ, x. 
 
 Tinct. cinchon. comp q. s. ad fl. Z i. 
 
 M. Dose 3 i. 
 
 Mist. Alkalina. 
 
 B, Magnes. sulph gr. viiss. 
 
 Magnes. carb gr. iv. 
 
 Spir. amnion, arom ii[ iv. 
 
 Aquae q. s. ad fl. 3 i. 
 
 M. Dose 3 i. 
 
 Tablet A loin, Belladon. et Strych. 
 
 B, Aloin gr. 4 
 
 Ext. belladon gr. J 
 
 Strych. sulph gr. T fa 
 
 M. One tablet. 
 
 Tablet Bromide Comp. 
 
 Morphia brom gr. J 
 
 Hyoscin. hydrobrom gr. , ,', „ 
 
 Camph. monobrom gr. i. 
 
PR INSCRIPTIONS. 
 
 323 
 
 Tablet Bromide Comp. No. 2. 
 
 Morphia brom : gr. ,',. 
 
 Hyoscin. hydrobrom gr. .,,',„ 
 
 Camph. monobr gr. ! 
 
 Mist. " Brown-Sequard." 
 
 B; Pot. iod a . .. gr. vi. 
 
 Pot. brom., 
 
 Ammon. bromid aa gr. xv. 
 
 Sod. bicarb gr. iv. 
 
 Tinct. nuc. vomic il[ vi. 
 
 Tinct. gentian, co v\ viij. 
 
 Aquse q. s. ad fl. 3 i. 
 
 M. Dose 3 i. 
 
 Mist. Capsici. 
 
 B: Tinct. capsic, 
 
 Tinct. zingib aa, 1U v. 
 
 Tinct. cinchon. comp q. s. ad fl. 3 i. 
 
 M. Dose 3 i. 
 
 Mist. Cascar^e Comp. 
 B Ext. cascar. fl., 
 
 Tinct. nuc. vomic, 
 
 Tinct. belladon ■ . . . aa TT[ iv. 
 
 Glycerin q. s. ad fl. 3 i. 
 
 M. Dose 3 i. 
 
 Mist. Cephalalgiaca. 
 
 B; Ammon. chloridi gr. iss. 
 
 Morph. acetat gr. \ 
 
 Caffein. citrat g r - 2V 
 
 Spir. ammon. aromat TTj, \ 
 
 Aq. menth. pip fl. 3 ss. 
 
 Elix. guaran q. s. ad fl. 3 i. 
 
 M. Dose 3 i. 
 
 Mist. Chorea. 
 
 B; Liq. pot. arsenit TT[ iij. 
 
 Aq. menth. pip q. s. ad fl. 3 i. 
 
 M. Dose 3 i- 
 
3^4 
 
 PRESCKir TIONS. 
 
 Mist. Chorea Comp. 
 
 \[ Liq. pot. arsenit v\ iij. 
 
 Chloral, hydrat gr. v. 
 
 Aq. month, pip q. s. ad fl. 3 i. 
 
 M. Dose 5 i- 
 
 Pil. Colitis. 
 
 IJ Strych. sulph gr. fa 
 
 ThIy. ipecac, 
 Ext. belladon., 
 
 Ext. colocynth. comp aa gr. \ 
 
 Ext. gentian q. s. 
 
 M. One pill. 
 
 Pulv. " Digestive." 
 
 # Pepsin gr. v. 
 
 Bismuth subnit gr. x. 
 
 Strych. sulph gr. -j-^j- 
 
 Carb. ligni gr. v. 
 
 Thymol gr. \ 
 
 M. Dose gr. xx. 
 
 Mist. " D. T." 
 ]$ Pot. bromid., 
 
 Sod. bromid aa gr. xv. 
 
 Chloral, hydrat gr. x. 
 
 Tinct. zingib HI x. 
 
 Tinct. capsic iT[ v. 
 
 Spir. amnion, aromat fl. ~ i. 
 
 Aquae q. s. ad fl. 3 ij. 
 
 M. Dose ~ ij- 
 
 Mist. Epileptica. 
 $ Pot. bromid., 
 
 Sod. bromid aa gr. x. 
 
 Ammon. bromid gr. v. 
 
 Sod. bicarb gr. ij. 
 
 Liq. pot. arsenit HI i. 
 
 Aquae q. s. ad fl. 3 i. 
 
 M. Dose 3 i. 
 
PRESCRIP T10NS. 325 
 
 Mist. Epileptica Comp. 
 
 F> Tinct. belladon TTj, ij. 
 
 Pot. bromid gr. xv. 
 
 Chloral, hydrat gr. v. 
 
 Aquae q. s. ad 11. 3 i- 
 
 M. Dose .3 i. 
 Tablet Euonymin Co. 
 
 I£ Euonymin gr. J 
 
 Podophyllin, 
 
 Aloin aa gr. J- 
 
 M. One tablet. 
 Pil. Ferri Carb. 
 
 " Blaud's Pill." 
 IJ Pot. carb gr. liss. 
 
 Fer. sulph. exsic gr. iss. 
 
 M. One pill. 
 Mist. Ferri Chloridi. 
 
 rj Tinct. ferri chlor V\ xv. 
 
 Glycerin TT[ xx. 
 
 Aquae q. s. ad fi. 3 i- 
 
 M. Dose 3 i. 
 Tablet Iron, Arsenic, and Strych. 
 
 5 Ferri redact gr. i. 
 
 Acid, arsenios gr. T £g- 
 
 Strych gr. fa. 
 
 M. One tablet. 
 Mist. Ferri et Strych. 
 
 IJ Strych. sulph g r - "3V 
 
 Ferri pyrophosph gr. x. 
 
 Tinct. zingib Tf[ i. 
 
 Glycerin TT| v. 
 
 Aquae q. s. ad ft 3 i. 
 
 M. Dose 3 i. 
 Mist. Ferri Salicylatis. 
 
 IJ Acid, salicylic gr. xx. 
 
 Fer. pyrophosph gr. iv. 
 
 Sod. phosph gr. 1. 
 
 Aquae q. s. ad fl. 3 ss. 
 
 M. Dose 3 ss. 
 
PRESCRIPTIONS. 
 
 Vinum FerRi Amar. 
 
 i; Fer. et quin. cit gr. ij. 
 
 Tinct. aurant. amar ni iv. 
 
 Klixir. simp] H| xv. 
 
 Vin. xeric fl. 7 ss. 
 
 Aquce q. s. ad fl. 3 i. 
 
 M. Dose 3 i- 
 Pulv. Laxans. 
 
 1> Sod. chlor gr. vi. 
 
 Sod. bicarb gr. xxiv. 
 
 Sod. sulph. exsic 3 i- 
 
 Magnes. sulph 3 ss. 
 
 M. Dose 3 ij. 
 Pil. Laxativa. 
 
 IJ Pulv. aloes gr. iss. 
 
 Ext. nuc. vomic gr. \ 
 
 Ext. belladon gr. -J- 
 
 Ext. colocynth. comp gr. ij. 
 
 M. One pill. 
 Mist. Magnes. et Ferri Sulph. 
 
 IJ, Magnes. sulph gr. xv. 
 
 Ferri sulph gr. i. 
 
 Acid, sulph. dil 1U xv. 
 
 Aquae q. s. ad rl. 3 i. 
 
 M. Dose 3 i. 
 Tablet "Neuralgic." 
 
 IJ Quin. sulphat gr. \ 
 
 Morph. sulphat g r - tV 
 
 Strych. sulphat gr. T £-g- 
 
 Acid, arsen gr. -fa 
 
 Ext. aconit gr. -J 
 
 Sig. One tablet repeated in i hour. 
 Mist. Pot. Iodid. et Colchici. 
 
 IJ Pot. iodid gr. vi. 
 
 Tinct. cimicif Tq iv. 
 
 Tinct. opii camph., 
 
 Vin. colch. rad aa ill v. 
 
 Aq. cinnam q. s. ad fl. 3 i. 
 
 M. Dose 3 i- 
 
PRESCRIPTIONS. 327 
 
 Sol. Phosphori, Thompson. 
 
 fy Phosphori gr. i. 
 
 Alcohol, absolut fl. 3 v. 
 
 Dissolve with the aid of gentle heat and add, pre- 
 viously heated: 
 
 Glycerin fl. 3 iss. 
 
 Alcohol fl- 3 ij. 
 
 Spir. menth. pip fl- 3 i- 
 
 M. Dose iTL xij. 3 i- contains gr. -fa phosphorus. 
 
 Pil. Qtjin., Fer. et Strych. 
 
 1^ Strych. sulph g r - -gV 
 
 Quin. sulph., 
 
 Fer. redact aa gr. i. 
 
 M. One pill. 
 
 Mist. Rhei et Sod^e, I. 
 
 I£ Pulv. rhei gr. ij. 
 
 Sod. bicarb gr. v. 
 
 Pulv. ipecac gr. £ 
 
 Aq. menth. pip q. s. ad fl. 3 ij. 
 
 M. Dose 3 ij. 
 
 Mist. Rhei et Some, II. 
 
 3 Pulv. rhei gr. i. 
 
 Sod. bicarb gr. x. 
 
 Aq. menth. pip q. s. ad fl. 3 ss. 
 
 M. Dose § ss. 
 
 Mist. Rhei et Sod^e Comp. 
 
 I£ Pulv. rhei gr. Ij. 
 
 Sod. bicarb gr. x. 
 
 Pulv. ipecac gr. ^ 
 
 Tinct. nuc. vomic TT| v. 
 
 Aq. menth. pip q. s. ad fl. " ij. 
 
 M. Dose 3 ij- 
 
 Mist. Salina. 
 
 t>. Sod. et pot. tart 3 i- 
 
 Sod. bicarb 3 ss. 
 
 Pot. acetat gr. xv. 
 
 Aquae q. s. ad fl. 3 ss. 
 
 M. Dose 3 ss. 
 
3 2 s PRESCRH ' TJONS. 
 
 Tablet "Sciatic." 
 1| Tinct. colchici, 
 Tinct. cimicifug., 
 Tinct. aconit., 
 
 Tinct. belladon aa tti f 
 
 M. One tablet. 
 
 Mist. Sedativa. 
 
 # Morph. sulph g r - tV 
 
 Acid, hydrobrom. dil HL viiss. 
 
 Spts. chloroform Tl[ v. 
 
 Syr. scillce ill xv. 
 
 Syr. tolutan q. s. ad fl. 3 i- 
 
 M. Dose I i. 
 
 Mist. Sod. Salicylat. 
 
 1J Acid, salicylic gr. x. 
 
 Sod. bicarb q. s. 
 
 Ext. glycyrrhiz gr. iij. 
 
 Glycerin fl. 3 ss. 
 
 AquK q. s. ad fl. 3 ij- 
 
 M. Dose 3 ij- 
 
 Mist. Tonic. 
 
 1;£ Tinct. nuc. vomic TT[ iv. 
 
 Ac. phosph. dil TU viij. 
 
 Syr. hypophoph. cal. et sod q. s. ad fl. 3 i- 
 
 M. Dose 3 i- 
 
REGISTER OF CASES TREATED AT THE NERVOUS 
 DEPARTMENT OF THE VANDERBILT CLINIC FROM 
 FEBRUARY, 1888, TO JANUARY, 1890. 
 
 Diseases. No. of Cases. 
 
 Acroneuroses 19 
 
 Alcoholism 72 
 
 Anaemia 25 
 
 Anterior Poliomyelitis 22 
 
 Aphasia 6 
 
 Aphonia hysterica 2 
 
 Athetosis, functional 2 
 
 Ataxic paraplegia 3 
 
 Atrophy of shoulder muscles 3 
 
 Atrophy of arm and leg from joint 
 
 disease 1 
 
 Arteritis chronica 10 
 
 Brachial Spasm 6 
 
 Brown-Sequard paralysis 2 
 
 Bulbar paralysis 2 
 
 Cerebral hyperemia 2 
 
 Cerebral tumor 3 
 
 Chorea 75 
 
 Coccygodynia 1 
 
 Concussion of spine 1 
 
 Crutch paralysis 1 
 
 Congenital contraction of muscles. 1 
 
 Defect of speech 2 
 
 Debility 3 
 
 Dementia senilis 2 
 
 Dementia, terminal 1 
 
 Dyspepsia 17 
 
 Endarteritis deformans 3 
 
 Epilepsy 94 
 
 Epilepsy, cortical 7 
 
 Erb's paralysis 3 
 
 Exophthalmic goitre 9 
 
 Facialparalysis (Bell's palsy) 12 
 
 General paresis 8 
 
 Headache 298 
 
 Hemiplegia 46 
 
 Hydrocephalus. 2 
 
 Diseases. No. of Cases. 
 
 Hysteria 39 
 
 Hystero-epilepsy 5 
 
 Hypochondriasis. . . 18 
 
 Hydrosis of extremities 1 
 
 Idiocy 8 
 
 Imbecility g 
 
 Insomnia 20 
 
 Lateral sclerosis 5 
 
 Lead palsy 14 
 
 Lithsemia 4 
 
 Locomotor ataxia 26 
 
 Lumbago 3 
 
 Malaria 8 
 
 Mal-development of brain 29 
 
 Mania 5 
 
 Melancholia 11 
 
 Meniere's disease 5 
 
 Meningitis, basilar syphilitic 2 
 
 " tubercular. ... 3 
 
 Migraine 22 
 
 Monoplegia, brachial 5 
 
 crural 2 
 
 Multiple sclerosis 15 
 
 Myalgia 9 
 
 Myelitis, transverse n 
 
 " general 11 
 
 Neuralgia, trigeminal 151 
 
 occipital 10 
 
 brachial 12 
 
 crural 6 
 
 Neurasthenia 209 
 
 Neuritis of circumflex n 7 
 
 " " brachial plexus 32 
 
 " " median n 3 
 
 " " musculo-spiral n 34 
 
 " " peroneal n 2 
 
 " " radial n 2 
 
 " " ant. tibial n 4 
 
 " " ulnar n 1 
 
33° 
 
 REGISTER OF CASES TREATED. 
 
 No. of Cases, 
 
 Neuritis multiple, alcoholic 6 
 
 arsenical i 
 
 '• diputheritic • ■ . • 2 
 
 scarlatinal 1 
 
 Neuroses, traumatic (> 
 
 toxic, from tobacco 5 
 
 vesical 2 
 
 climacteric 6 
 
 Nocturnal terrors 2 
 
 Occupation neuroses 9 
 
 1 cigarmaker's, 1 plasterer's, 
 
 1 pianist's, 3 telegraphers', 
 
 2 writers', 1 sewing. 
 Ophthalmoplegia externa 1 
 
 Pachymeningitis, cerebralis 3 
 
 cervicalis I 
 
 Paralysis, of third n 3 
 
 Paralysis agitans 23 
 
 Paranoia 9 
 
 Paraplegia 1 
 
 Pons lesion (alternating paralysis). 1 
 
 Pseudo-musc. hypertrophy I 
 
 Psychoneuroses from sexual excess. 8 
 
 Diseas No. of Cases. 
 
 Progressive muscular atrophy .... 4 
 
 Rheumatism 28 
 
 Sciatica 42 
 
 Senility 12 
 
 Somnambulism 3 
 
 Somnolence 1 
 
 Spasm of head (rotary) I 
 
 Spasm (habit) 2 
 
 Spinal irritation 2 
 
 Syphilis of the brain and mem 
 
 branes 36 
 
 Tic convulsif 2 
 
 Tic douloureux 5 
 
 Tinnitus aurium 4 
 
 Torticollis 2 
 
 Tremor post-hemiplegic 3 
 
 " senile 4 
 
 Unclassified 82 
 
 Vaso-motor neuroses 2 
 
 Vertigo 23 
 
I N DEX. 
 
 Abscess of the brain, 56 
 Abstract ideas, 103 
 Action a cortical function, 13 
 Age of onset of chorea, 235 
 of epilepsy, 256. 
 of infantile cerebral par- 
 alysis, 194 
 of infantile spinal paraly- 
 sis, 1S5 
 of paralysis agitans, 222 
 of paranoia, 298 
 Agraphia, 69 
 
 Alcoholic paralysis, 206, 214, 217 
 Amnesia, 70 
 
 Amyl nitrite in epilepsy, 273 
 Anatomical proofs of localization, 6 
 Anaemic headaches, 280 
 Anaesthesia in locomotor ataxia, 
 168 
 in multiple neuritis, 210 
 in spinal cord disease, 134 
 Analgesia, 168 
 Anelectrotonus, 316 
 Anterior horns of spinal cord, 140, 
 189 
 poliomyelitis, 131, 139, 1S3 
 Antifebrine in epilepsy, 273 
 
 in headaches, 2S5 
 Antipyrine in headaches, 2S5 
 Aphasia, 57 
 
 cases of motor, 42 
 cases of sensory, 73 
 lesions producing, 2, 5, 64, 69 
 operation for relief of, 43, 73 
 
 Aphasia, temporary, after local 
 spasm, 29, 31 
 
 tests for, 72 
 
 varieties of, 65 
 Apraxia, 59 
 
 cases of, 64-77 
 
 definition of, 60 
 
 lesions producing, 63 
 
 operation for relief of, 60 
 
 tests for, 60, 62 
 
 varieties of, 59 
 Areas of anaesthesia in birth palsy, 
 179 
 in spinal lesions, 134-139 
 Argyll-Robertson pupil, no, 169, 
 
 172, 174 
 Arsenic in chorea, 243 
 
 in epilepsy, 271 
 
 in locomotor ataxia, 176 
 
 in neurasthenia, 289 
 
 in paramyoclonus, 250 
 Arsenical paralysis, 209 
 Association of ideas, 58 
 
 of memories, 100 
 
 of mental images, 58 
 
 of perceptions, 12 
 Association tracts in the brain, 98 
 
 in the spinal cord, 142 
 Ataxia in neuritis, 217 
 
 locomotor, 169 
 
 static, 169 
 Athetosis, 198 
 Atrophy of the brain cortex, 203 
 
 of the brain tracts, 6 
 
INDEX. 
 
 Atrophy of the muscles in paraly- 
 sis, 131 
 
 of the optic nerve, 169, 175 
 Atrophic paralysis. 131, 1S6, 191 
 Atropia in epilepsy 271 
 Auditory centres in cortex, 87 
 
 tract, 91 
 Aura in epilepsy, 252, 259 
 
 arrest of, by amyl nitrite, 273 
 
 varieties of, 259 
 
 Ballet, 61 
 Bamberger, 116 
 
 Rase of brain, 105 
 Baths in neurasthenia. 288 
 Beevor, 8, 23, 96 
 Benedikt, 230 
 Beriberi, 21S 
 
 slight cases, 218 
 
 severe cases, atrophic type, 219 
 hydropic type, 219 
 pernicious type, 219 
 Bibliography of localization, 9 
 
 of multiple neuritis, 221 
 
 of paramyoclonus multiplex, 
 250 
 Birdsall, 56 
 Birth-palsy, 178 
 Bladder centre, 129 
 Blindness from cortical disease, 
 
 5i. 54 
 
 of mind, 60 
 Brachial paralysis, 178, 186, 198 
 
 spasm, 29, 31, 32 
 Brain, appearance of, 16 
 
 convolutions of, 18 
 
 fissures of, 17 
 
 surgery, 38, 40, 41, 43, 60, 73 
 Bramwell, 130, 143 
 Brtgon, 1 19 
 Br fere, 1 1 7 
 Brissaud, 6 
 Br oca, 2, 5 
 
 Broca's convolution or centre, 68 
 Bromides in epilepsy, 271 
 
 Bromides in neurasthenia, 2S9 
 Brominism, 271 
 
 Brown-Sequard paralysis, 157 
 
 cases of, 158, 164 
 Burdach, column of, 142 
 Buzzard, 122, 133, 206, 224, 230 
 
 Catalytic effects of electri- 
 city, 310 
 Cataphoric effects of electricity,3i6 
 Cauda equina, compression of, 146 
 lesions of, 149 
 tremor of, 1 50 
 Centrum ovale, lesions of, 89 
 
 tracts in, 90 
 Cerebellum, connection with cere- 
 brum, 91 
 lesion of, in procursive epi- 
 lepsy, 1 19 
 middle peduncle of, 122 
 Cerebral convolutions, see Brain, 16 
 hemorrhage, 41, 201 
 localization, 1 
 
 facts established, 4 
 history of discovery, 2 
 proofs of theory, 3-7 
 ■ surgery, 19, 37, 40, 41, 43, 56, 
 60, 73 
 Character, changes of, in frontal 
 lesions, 84 
 of attacks in epilepsy, 257 
 Charcot, 4, 170, 224, 227, 231 
 Chloral in chorea, 243 
 in epilepsy, 272 
 in neurasthenia, 289 
 Chorea, 235 
 
 age of onset, 235 
 complications, 242 
 duration of attacks, 242 
 electric reaction of muscles,242 
 extent of spasm, 236 
 month of onset, 237 
 number of attacks, 236 
 post-hemiplegic, 199 
 relapses, 236 
 
INDEX. 
 
 333 
 
 Chorea, relation to endocarditis, 
 
 241 
 
 relation to malaria, 238 
 relation to rheumatism, 240 
 treatment, 243 
 Classification of epileptics, 252 
 
 of insanity, 297 
 Clinical evidence of localization, 4 
 Columns of the spinal cord, 142 
 Commissural tracts in the brain, 96 
 Comparative anatomy of the brain,7 
 Compression of the cauda equina, 
 
 146, 150 
 Concepts, 58 
 
 physical basis of, 58 
 Concrete memories, 99 
 Consciousness in epilepsy, 261 
 in Jacksonian epilepsy, 28 
 Contractures in hemiplegia, 197 
 
 in infantile paralysis, 187 
 Convolutions of the brain, 18 
 Convulsions in epilepsy, 256 
 
 in infantile paralysis, 184, 196 
 Corpus callosum, 96 
 Cortical areas, limits of, 19 
 
 areas of unknown function, 
 
 85 
 clot removed successfully, 42 
 hemorrhage, 39 
 paralysis, 39 
 spasms, 27 
 Counter-irritation in infantile par- 
 alysis, 184 
 in reflex pain, 279 
 Cranial measurements in paranoia, 
 298 
 nerve paralysis, 115 
 Cranio-cerebral topography, 19 
 Crises in locomotor ataxia, 167 
 Criteria of evidence for localiza- 
 tion, 14 
 Crural monospasm, 33, 35 
 Crus cerebri, lesions in, no, 113 
 Cryaesthesia, 173 
 Cryalgesia, 173 
 
 Dana, 86, 237, 277 
 
 Dax, Marc, 2 
 
 Deafness, 87 
 of mind, 69 
 
 Debove, 229 
 
 Deformities in cerebral disease, 139 
 in multiple neuritis, .213 
 in spinal cord diseases, 139 
 
 Degeneration of columns of cord, 
 
 143 
 of nerves, 207 
 
 of tracts in nervous system, 6 
 Dejerine, 171 
 
 Destruction of tissues by electric- 
 ity, 311 
 Diagnosis of epilepsy from reflex 
 neurosis, 267 
 of forms of spinal paralysis, 1 31 
 of locomotor ataxia, 168 
 of multiple neuritis from spinal 
 
 paralysis, 216 
 of multiple neuritis from loco- 
 motor ataxia, 216 
 of multiple neuritis from mye- 
 litis, 217 
 of neuritis from spinal paral- 
 ysis, 194 
 of spinal from cerebral paral- 
 ysis, 194 
 of syphilitic endarteritis from 
 meningitis, 36 
 Digitalis in epilepsy, 272 
 Diphtheritic paralysis, 217 
 Disturbances of consciousness, 261 
 Double consciousness, 263 
 Dropped foot, 213 
 
 wrist, 213 
 Dumenil, 206 
 
 Edinger, 7, 95 
 
 Electricity, 307 
 
 catalytic effects of, 310 
 cataphoric effects of, 316 
 chemical changes produced 
 by, s 1 1 
 
134 
 
 INDEX. 
 
 Electricity, electrotonic effects of, 
 316 
 farad ic, 318 
 galvanic, 310 
 in diagnosis, see Reaction of 
 
 Degeneration, 
 in treatment of anaesthesia, 276, 
 320 
 of brain diseases, 313 
 of infantile spinal paral- 
 ysis, 193 
 of locomotor ataxia, 313 
 of neuralgia, 315 
 of neurasthenia, 312 
 of neuritis, 182, 220, 315 
 of paralysis, 182, 319 
 of paramyoclonus multi- 
 plex, 250 
 of spinal diseases, 313 
 reflex effects of, 309 
 static or frictional, 308 
 voltaic, 310 
 Electrical changes in birth palsy, 
 179 
 in chorea, 24.2 
 in infantile spinal paral- 
 ysis, 131 
 in multiple neuritis, 212 
 in paralysis agitans, 230 
 measurements in physiology, 8 
 in treatment, 182 
 Embryology of brain, 6 
 Endarteritis syphilitica, 36 
 Epigastric aura in epilepsy, 259 
 Epilepsy, 252 
 
 classes of cases, 252 
 diagnosis of, 267 
 etiology of, 256 
 reflex origin of, 267 
 symptoms, 257 
 treatment, 271 
 with hemiplegia, 201 
 Erb's paralysis, 178 
 Exner, 14 
 Experimental atrophy, 6 
 
 Expression a cortical function, 13 
 External geniculate body, 49 
 
 Facial spasm in Jacksonian epi- 
 lepsy, 29 
 in tic convulsif, 276 
 Facts of localization established, 4 
 Farad ism, 318 
 Farjes, 62 
 Fear as an aura in epilepsy, 259 
 
 as a symptom of brominism, 
 272 
 Ferrier, 3, 9, 47, 1 26 
 Fissures of the brain. 17 
 
 relation to lines of skull, 20 
 Flatten, 122 
 Flecksig, 6, 93 
 Flour ens, 2 
 Food in insanity, 302, 303 
 
 in neurasthenia, 287 
 Fore/, 7 
 Forms of epileptic seizure, 252 
 
 of insanity, 292 
 Fracture of spine, 147 
 Frequency of fits in epilepsy, 257 
 Frit sch and Hitzig, 3 
 Frontal lobes, 17 
 
 areas and functions, 84 
 Functions of cortex, general, 1 1 
 special, 14 
 
 of spinal segment, 141 
 
 of spinal segments, 128 
 
 Gait in lateral sclerosis, 1 39 
 in locomotor ataxia, 169 
 in paralysis agitans, 230 
 Galvanism, 310 
 Gastric crises, 168 
 headaches, 281 
 General paresis, 303 
 
 prognosis, 304 
 remissions, 304 
 symptoms, 304 
 treatment, 304 
 
INDEX. 
 
 335 
 
 General symptoms vs. local symp- 
 toms, 15 
 
 Geniculate bodies, 91 
 
 Genital irritation in children, 255 
 
 Gibney, 315 
 
 Girdle sensation, 148, 150, 153, 156, 
 164, 167, 217 
 
 Goll, column of, 142 
 
 Gouty headaches, 285 
 
 Gowers, 126, 127, 131, 142, 155, 202, 
 237 
 
 Granet, 61 
 
 Groups of cases of insanity, 294 
 of cells governing ocular mus- 
 cles, 108 
 in spinal cord, 140, 189 
 
 v. Gudden, 6 
 
 Hallucinations, 5, 293 
 
 auditory, 87, 293 
 
 olfactory, 87 
 
 visual, 53 
 Hamilton, A. McL., 87 
 Hamilton, D., 96 
 Headaches, 280 
 
 anaemic, 280 
 
 from eye strain, 284 
 
 from gout, 285 
 
 from lithaemia, 285 
 
 from nephritis, 285 
 
 gastric, 281 
 
 malarial, 282 
 
 plethoric, 284 
 
 syphilitic, 29, 119, 283 
 
 traumatic, 284 
 Hearing, function of, 88 
 Heimann, 230, 234 
 Hemianopsia, 49 
 
 permanent, 54 
 
 temporary after hallucinations, 
 52 
 
 varieties of, 50 
 Hemiplegia, adult, 39, 93, 101 
 
 infantile, 194, 196 
 Hemorrhage in the brain. 41 
 
 Hemorrhage in the spinal < ord, 144 
 
 in the spinal membranes, [49 
 H crier, 136,138, 163 
 Hervi, 7 
 
 Horsley, 8, 23, 26, 163 
 Htm, 34 
 
 Hyperesthesia, 168 
 Hyperalgesia, 168 
 Hypercryaesthesia, 173 
 Hyperthermalgesia, 173 
 Hypochondriasis, 292 
 
 Idiocy, 85, 295 
 Imbecility, 85, 295 
 Impressions, motor, 12 
 
 sensory, 12 / / 
 
 Incontinence of urine, 169, 173 
 Infantile brachial paralysis, see 
 
 Birth palsy, 178 
 Infantile cerebral paralysis, 194 
 
 athetosis in, 198 
 
 cases illustrative of, 204 
 
 contractures in, 197 
 
 epilepsy with, 201 
 
 etiology, 194 
 
 lesions, 202 
 
 paralysis, character of, 195 
 
 pathology, 201 
 
 prognosis, 203 
 
 reflexes in, 197 
 
 rigidity in, 197 
 
 symptoms, 195 
 
 treatment, 203 
 Infantile spinal paralysis, 183 
 
 age of onset, 184 
 
 atrophy in, 191 
 
 character of paralysis, 1S4 
 
 distribution of paralvsis, 
 186 
 
 etiology, 183 
 
 lesion, 131, 189, 190 
 
 manner of onset, 1S4 
 
 treatment, 193 
 Inhibition, 13 
 Insanity. 291 
 
336 
 
 INDEX. 
 
 Insanity, dementia, 295 
 
 general paresis, 296, 303 
 groups of cases, 294 
 hypochondriasis, 292 
 
 idiocy. 295 
 
 imbecility, 295 
 
 mania, 295, 303 
 
 melancholia, 295, 301 
 
 ordinary forms of, 292 
 
 paranoia, 292, 296, 297 
 
 treatment in asylums, 305 
 Intellectual acts, 13 
 
 aura in epilepsy, 261 
 Internal geniculate body, 91 
 Interparietal fissure, 17 
 Intracerebral tracts, 89 
 
 Jackson. Hughli)igs, 3, 13, 26, 27, 52, 
 
 87, 117, 261 
 Jacksonian epilepsy, 26-39 
 
 surgical treatment of, 37 
 
 symptoms, 27 
 
 Kakkk, 218 
 Kast, 61 
 
 Katelectrotonus, 317 
 Keen, 33, 38, 40 
 Knee-jerk, 133 
 Koch, 239, 241 
 
 Language, physical basis of, 5, 57 
 
 Lead palsy, 209 
 
 Lithaemia, 287, 290 
 
 Localization of cerebral functions, 1 
 
 of spinal functions, 126 
 Localized spasms, 26 
 Local symptoms, 15 
 Locomotor ataxia, 167 
 
 arthropathy, 170 
 
 ataxia, 169 
 
 crises, 168 
 
 lesion, 170 
 
 objective signs, 168 
 
 ocular paralysis, 169, 175 
 
 Locomotor ataxia, optic n. atrophy, 
 169 
 
 sensory symptoms, 168, 172 
 suspension in, 176 
 treatment, 176 
 
 Macewen, 60, 136 
 Mader, 117 
 
 Mai ret, 1 19 
 Mania, 303 
 
 Manual delivery as cause of par- 
 alysis, 180 
 Mc Bunny, 43, 46, 161, 272 
 McNutt, 195 
 
 Median surface of hemisphere, 87 
 Melancholia, 295, 301 
 Memories, association of, 99 
 localization of, 13 
 physical basis of, 13 
 varieties of, 58 
 Meningitis, syphilitic, 36, 115 
 Mental defects in children, 201 
 diversion in neurasthenia, 287 
 diseases, see Insanity, 291 
 images, 12, 58 
 
 symptoms in alcoholic par- 
 alysis, 214 
 in frontal lesions, 84 
 Mirror writing, 96 
 Mobius, 1 1 7 
 ?'. Monakow, 7 
 Monoplegia, 39, 101 
 Mosse, 232 
 Mosso, 286 
 Motor aphasia, 68 
 area, 22 
 
 divisions of, in monkeys, 26 
 for head and eyes, 25 
 for lower extremity, 25 
 for upper extremity, 23 
 how determined, 3,8 
 lesions of, 40 
 limits of, 22 
 operations upon, 42 
 tract, 93 
 
INDEX. 
 
 337 
 
 Movements, how learned, 5, 12 
 
 voluntary, 23 
 Multiple neuritis, 206 
 
 bibliography, 221 
 diagnosis, 216 
 etiology, 209 
 pathology, 206 
 symptoms, 210 
 treatment, 216 
 Muscular sense, 46, 86 
 Musical sense, 61 
 Myelitis, acute, 152 
 
 anterior polio-, 184 
 
 chronic, 146 
 
 lesion of, 154 
 
 transverse, 152 
 
 unilateral, see Brown-Sequard 
 
 Neumann, 207 
 Neurasthenia, 286 
 
 theory of origin, 286 
 treatment by baths, 288 
 by drugs, 289 
 by electricity, 288, 312 
 by mental diversion, 287 
 by overfeeding, 287 
 by tonics, 289 
 by vascular stimulants, 288 
 Neuralgia, trigeminal, 275 
 Neuritis, multiple, see Multiple 
 neuritis, 206 
 traumatic, of brachial plexus, 
 179 
 Nitrite of amyl in epilepsy, 273 
 Nitro-glycerine in epilepsy, 273 
 Nocturnal attacks in epilepsy, 259 
 Nothnagel, 14, 103, 116, 125 
 Noyes, 295, 296, 298, 300 
 Nutritive changes produced by 
 electricity, 311 
 
 Obstetrical paralysis, 178 
 Occipital lobe, lesions of, 55 
 Ocular irritation as cause of reflex 
 neurosis, 267 
 22 
 
 Oculo-motor centres, 138 
 Ocular muscles, paralysis of, 105 
 
 nerves, paralysis of, 105 
 Ophthalmoplegia externa, 109, 113 
 
 interna, no 
 Oppenheim, 61 
 Optic thalamus, 49, 91 
 
 tract, 50 
 Osier, 201, 241 
 
 Pain of locomotor ataxia, 167 
 
 reflex or transferred, 277 
 Palpitation as aura in epilepsy, 252 
 Paracentral lobule, 18, 35 
 Paralysis agitans, 222 
 
 age of onset, 223 
 diagnosis of tremor, 227 
 etiology, 222 
 gait in, 230 
 symptoms, 224 
 treatment, 235 
 tremor in, 225 
 from cortical disease, 39 
 in infancy, 178 
 in spinal cord disease, 130 
 of cranial nerves, 116 
 of conjugate motion of eyes, 
 
 108 
 of fourth nerve, 105 
 of ocular muscles, 108 
 of oculo-motor nerve, 105 
 of seventh nerve, 95, 116 
 of sixth nerve, 105 
 of third nerve, 105 
 temporary, after local spasms, 
 
 28 
 types of spinal, 131 
 Paramyoclonus multiplex, 244 
 cases, 244, 247 
 diagnosis from chorea, 248 
 etiology, 247 
 symptoms, 249 
 treatment, 250 
 Paranoia, 292, 296, 297 
 Paraphasia, 71, 80 
 
m 
 
 INDEX. 
 
 Paretic dementia, 296, 303 
 Parietal lobe, 86 
 Parieto-occipital fissure, 17, 21 
 Parkinson's Disease, see Paralysis 
 
 agitans, 222 
 Perceptions, 11,12 
 Peterson, 109 
 Phenacetine in headache, 285 
 
 in neurasthenia, 287 
 Physiology of brain cortex, 3 
 Polioencephalitis of Striimpell, 202 
 
 of Wernicke, 108 
 Poliomyelitis anterior, 131, 139, 183 
 Pons lesions, 118, 122 
 Position of limbs in cerebral dis- 
 ease, 139 
 in multiple neuritis, 213 
 in paralysis agitans, 230 
 in spinal disease, 138 
 Posthemiplegic chorea, 199 
 Prescriptions, 322 
 Prevost, 190 
 
 Procursive epilepsy, 124, 259 
 Projection tracts, 91 
 Proofs of cerebral localization, 5 
 Propulsion in paralysis agitans, 230 
 Psychical blindness, 59 
 
 deafness, 60 
 
 defects, see Idiocy, 85, 295 
 
 epileptic equivalent, 261-265 
 Pupil, Argyll-Robertson, no 
 
 paralysis of, no 
 
 Ramskell, 117 
 
 Panvzer, 207 
 
 Reaction of degeneration, 131, 148, 
 
 179, 192, 212, 319 
 Reading, defects of, see Word- 
 blindness, 67 
 Reflex irritation, 267 
 
 neuroses, 270 
 
 pains, 277 
 Register of cases, 329 
 Reid's guiding lines, 21 
 Pemak, 126, 188 
 
 Remak's sign in locomotor ataxia, 
 
 168 
 Romberg's sign in locomotor 
 
 ataxia, 169 
 Poss, 126, 136 
 
 SCHAFER, 23, 26 
 Scguin, 27, 35, 40, 48, 272 
 Self-control, 13 
 Sensations, 4, 12 
 Sensory aphasia, 57 
 
 epileptic seizures, 52 
 Signal symptom in Jacksonian 
 
 epilepsy, 27 
 Simulo in epilepsy, 273 
 Smell, hallucinations of, 87 
 localization of sense, 87 
 Spasm, localized, 27 
 
 in paramyoclonus, 246 
 Spastic paralysis, 131, 197 
 Spinal cord, disease of, 126 
 
 in anterior horns, 140, 189, 
 in central gray, 141 
 in cervical region, 136 
 in dorsal region, 155, 159 
 in lateral column, 131 
 in lumbar region, 146, 153 
 in posterior column, 170 
 in sacral region, 144, 147 
 localization of functions in, 
 
 126, 141 
 relation to vertebrae, 127 
 surgery of, 161 
 
 symptoms of disease, 130-137 
 table of functions, 128 
 transverse lesions, 144 
 Spit ska, 7, 91, 96 
 Staggering to one side, 118 
 Striimpell, 195, 201, 214, 240 
 Subcortical lesions, 89, 101 
 Surgery of the brain, 37, 41, 43 
 
 of the spinal cord, 161 
 Surgical treatment of neuralgia, 
 275 
 treatment of tic, 277 
 
INDEX. 
 
 339 
 
 Suspension in locomotor ataxia, 176 
 Syphilis, treatment of, 283 
 Syphilitic basilar meningitis, 119 
 
 headaches, 283 
 
 meningitis of convexity, 36 
 Syringo-myelitis, 141 
 
 Tactile sense, localization of, 46 
 Taste, localization of, 88 
 Taylor, Wallace, 218 
 Temporal convolutions, 18 
 Temporo-sphenoidal lobe, 86 
 Tendon reflex in cerebral diseases, 
 42, 197 
 in general paresis, 304 
 in locomotor ataxia, 170 
 in paralysis agitans, 230 
 in paramyoclonus multi- 
 plex, 249 
 in spinal lesions, 133 
 Thacher, 311 
 
 Theory of cerebral localization, 1 
 of origin of neurasthenia., 286 
 Thorburn, 136, 138, 149, 1.51, 162 
 Tic convulsif, 277 
 Tonics in headache, 281 
 in neurasthenia, 290 
 Tracts within the brain, 89 
 association, 97 
 auditory, 91 
 commissural, 96 
 motor, 93 
 projection, 91 
 sensory, 95 
 visual, 91 
 Transferred pains, 277 
 Treatment of cerebral paralysis, 
 203 
 of chorea, 243 
 of epilepsy, 271 
 of headaches, 280 
 of locomotor ataxia, 176 
 
 Treatment of neuralgia, 275 
 of neuritis, multiple, 220 
 of neuritis, traumatic, 181 
 of paralysis agitans, 233 
 of paramyoclonus, 250 
 of reflex pains, 279 
 of spinal paralysis, 193 
 of tic convulsif, 276 
 
 Tremor, varieties of, 227 
 
 Trephining, 42, 272 
 
 Trigeminal neuralgia, 275 
 
 Trophic symptoms, 141, 170 
 
 Trunk, spasm of, 35 
 
 Tumors of brain, 29, 39 
 
 Tilrck, 6 
 
 Uncinate convolution, 17, 89 
 Unilateral cranial nerve palsy, 115, 
 122 
 spasm, see Jacksonian epi- 
 lepsy, 27 
 Unknown regions of cortex, 84 
 
 Vasomotor cells in spinal cord, 141 
 
 centre in medulla, 125 
 
 symptoms, 213 
 Vertigo in epilepsy, 252 
 Visual area of cortex, 48 
 
 destruction of, 49 
 irritation of, 52 
 
 aura in epilepsy, 252 
 
 hallucinations, 52 
 
 tract in brain, 49-51 
 Voltaic alternatives, 317 
 
 electricity, 310 
 
 Weir, 35, 38, 40, 56 
 Wernicke, 4, 56, 66, 71, 108 
 Westphal's sign in locomotor 
 
 ataxia, 169 
 Word- blindness, 67, 73, jy 
 Word-deafness, 65, 73, jy 
 
 ZUCKERKANDL, 7 
 
APR 24I97-J1 
 
 tf* 
 
 «wi4 
 
A 
 
 1892 
 
■ : V. 
 
 warn 
 
 '<*.;, ■■BBS 
 
 I ^H 
 
 
 ■HA 
 
 f*K«E 
 
 ■MBS- 
 
 iJi 
 
 H