m X 4-A- (Eiilumbia ImnFrBtUr ' Ut t\^t (Etty 0f 23^^«J fork H^f^r^tif^ ICthrara W4" :m:-^f'. i •■S Digitized by tine Internet Arciiive in 2010 witii funding from Open Knowledge Commons http://www.archive.org/details/diagnosisofdiseaOOhert SUGGESTIVE THERAPEUTICS. A Treatise on the Nature and Uses of Hypnotism. By 11. Bernheim, M.D., Professor in the Faculty of Medicine at Nancy. Translated from the second and revised French edition, by Christian A. Herter, M.D., of New York. 8vo, cloth $3 50 " Nowhere else will the reader find so complete an account of the manipulation of hypnotic suggestions used to cure disease ; and the pref- erences of the author do not lead him to lengths which are not fully to be accounted for by his natural enthusiasm and the seductive nature of his subject." — Medical and Surgical Reporter. " The book is both thoughtful and practical, and claims thorough read- ing and earnest consideration. It contains truths without some grasp of which no physician is tit for his charge." — N. E. Medical Gazette. G. P. PUTNAM'S SONS, NEW YORK AND LONDON. THE DIAGNOSIS OF DISEASES OF THE NERVOUS SYSTEM A MANUAL FOR STUDENTS AND PRACTITIONERS CHRISTIAN A. HERTER, M.D. PHYSICIAN TO THE CLASS OF NERVOUS DISEASES PRESBYTERIAN HOSPITAL DISPENSARY G. P. PUTNAM'S SONS RK HIRD STREET 24 EEDFO i^e Xmicktrbockcr l^rtss NEW YORK LONDON 27 WKST TWENTY-THIRD STREET 24 BEDFORD STREET, STRAND Copyright, 1892 BV CHRISTIAN A. HERTER Electrotyped, Printed, and Bound by Ubc IRnicfeerbocftcr Ipress, "fflevc Igorfc G. P. Putnam's SpN§ PREFACE. This volume is designed to aid the student and general practitioner in the recognition of the commoner forms of nervous disease. While the book is in every respect elementary in character, it is believed that the subject of which it t'^eats is presented with sufificient detail to make it serviceable. The arrangement that has been followed in the presen- tation of facts is somewhat unusual and requires notice. In the chapter on the structure and functions of the nervous system no effort has been made to give a sys- tematic outline of the anatomy of the brain and spinal cord. Indeed, little else has been attempted than the presentation of those facts regarding the motor and sen- sory paths that are of practical importance in diagnosis. The chapter on symptomatology contains a description of the most important symptoms of nervous disease, and, in most cases, the chief facts regarding their diagnostic significance and pathology. In the chapter on localiza- tion many of the facts given under symptomatology have been restated. The justification of this repetition is found in the belief that it is very desirable to emphasize the more important relations between symptoms and lesions by changing the point of view. In the fourth chapter, on the diagnosis of the nature of the lesion, an attempt is made, first, to give the main facts (from the standpoint of diagnosis) in the pathology IV PREFACE. of the different classes of lesions, and, secondly, to show the manner of employing the indications that are derived from the onset, from etiology, and from the position of the lesion. In discussing the indications derived from etiology (causal indications) considerable space has been devoted to the enumeration of the varieties of disease that may result from different causes, in the belief that a knowledge of these facts will frequently help in forming a conclusion as to the nature of the lesion. Next follows the chapter on clinical types, in which, while the types are necessarily somewhat rigidly drawn, an attempt is made to impress the fact that here, as in the classification of all natural phenomena, we must be prepared to recognize numerous variations in type and transitional forms. No subject is more important or more difificult to treat satisfactorily than the distinction of functional and organic disease. An endeavor is made, in the sixth chapter, to present the chief points of distinction between different forms of functional disease and the organic conditions with which they may be confounded. It was considered advisable, on the whole, to make a rather sharp separation between the traumatic neurosis and hysteria. The propriety of including in a work of so elementary a nature a short chapter on the examination of the patient will hardly be questioned. The illustrations of diagnosis which are given in the eighth chapter are designed to aid the student in the application of the methods of diagnosis to actual cases of disease. C. A. Herter. 839 Madison Avenue, March 7, 1892. CONTENTS. Spinal Chapter I. — Structure and Functions of the Nervous System ..... The Brain .... The Spinal Cord The Sympathetic Nervous System The Motor Tract . . The Sensory Tract . Reflex Paths .... The Spinal Nerves . The Cranial Nerves . . The Meninges of the Brain and Cord The Blood-Supply of the Spinal Cord and Brain Cranio-Cerebral Topography. Spinal and Topography ..... Chapter II. — The Symptomatology of Nervous eases ...... 1. Mechanical Injury 2. Loss of Blood Supply, Partial or Complete 3. Inflammation 4. Wasting of Nerve Elements Motor Paralysis Convulsions .... Tremor ..... Fibrillation .... Rigidity ..... Contracture and Contraction Catalepsy ..... Athetosis and Athetoid Movements .'\ssociated Movements Cord Dis- 16 22 24 30 35 39 41 59 61 65 70 70 71 71 72 80 87 90 92 95 97 99 102 VI CONTENTS. Inco-ordination ..... Conjugate Deviation of the Eyes and Head Strabismus Diplopia . Nystagmus Ptosis Pupillary Symptoms . Laryngeal Symptoms Abnormal Reflex Action Olfactory Symptoms . Visual Symptoms Ophthalmoscopic Changes Auditory Symptoms . Vertigo ... Gustatory Symptoms Trophic Symptoms . Vaso-Motor Symptoms Mental Symptoms Disturbances of Speech General Symptoms . Chapter III. — The Diagnosis of the Position of Lesion — Localization a. Cortex Cerebri b. White Substance and Centrum Ovale c. Corpus Callosum d. Corpus Striatum e. Optic Thalamus f. Internal Capsule g. External Capsule and Claustrum h. Corpora Quadrigemina i. Crus Cerebri j. Pons k. Medulla Oblongata /. Cerebellum . Base of the Brain Spinal Cord Nerve-Roots Cauda Equina . Peripheral Nerves CONTENTS. Vll PAGE Chapter IV. — The Diagnosis of the Nature of the Lesion 257 Hypersemia 258 Ansemia . 259 Hemorrhage 260 Softening . 264 Thrombosis of Sinuses 267 Inflammation . 268 Meningitis 269 Abscess . 276 Tumor 278 Degeneration . 283 I. The Onset of the Symptoms 288 II. The Causal Indications 289 III. The Position of the Morbid Process . 332 Chapter V. — The Diagnosis of Clinical Types 334 Meningitis ...... 336 Cerebral HemSrrhage 348 Acute Cerebral Softening . 353 Meningeal Hemorrhage 361 Sinus-Thrombosis 365 Infantile Cerebral Paralysis 367 Abscess of the Brain 373 Intracranial Tumor . 375 Intracranial Aneurism 382 Nuclear Ophthalmoplegia 384 Insular or Disseminated Sclerosis 390 Bulbar Paralysis 395 General Paralysis of the Insane 397 Hydrocephalus .... . 400 Spinal Meningitis 403 Intra-Spinal Hemorrhage 409 Myelitis . 412 Spastic Paraplegia . 429 Locomotor Ataxia 433 Ataxic Paraplegia 438 Friedreich's Disease . 441 Progressive Muscular Atrophy . 446 The Peroneal Form of Pre gress ive M uscular At roph) 452 Vlll CONTENTS. PAGE Pseudo- Hypertrophic Paralysis ...... 454 Erb's Type of Progressive Muscular Dystrophy . . -455 Intra-Spinal Tumor . . . . . . . -457 Syringomyelia . . . . . . . . .461 Neuritis .......... 465 Diseases of Special Nerves .....'. 468 Multiple Neuritis 509 Chapter VI. — The Distinction of Functional and Organic Disease 527 Hysteria .......... 528 The Traumatic Neurosis or Psycho-Neurosis . . . 538 Neurasthenia ......... 546 Epilepsy 547 Migraine 553 Chorea 555 Paralysis Agitans -558 Neuralgia . 560 Occupation Neuroses . . , . '. . . 5^4 Delirium Tremens ........ 566 Cerebral Concussion ........ 5^7 Malingering ......... 569 Chapter VII. — The Examination of the Patient . .572 Chapter VIII. — Illustrations of Diagnosis . . . 595 Index 617 DIAGNOSIS OF DISEASES OF THE NERVOUS SYSTEM. CHAPTER I. THE STRUCTURE AND FUNCTIONS OF THE NERVOUS SYSTEM, Introductory Remarks. — Simple dissection of the cerebro-spinal axis in the fresh state reveals little beyond the coarse arrangement of the gray and white masses. But in specimens that have been prepared by careful maceration in alcohol or a solution of bichromate of potash, it is possible to remove with a forceps bundle after bundle of fibres from without inward, and with such nicety that the general course and relative disposition of many such bundles or tracts may be readily demonstrated. Indeed, in the hands of Meynert, Burdach, Foville, and others, this method of cleavage or teasing has yielded results of the highest importance. Still, for the elucida- tion of the more minute relations of the gray matter and the complicated systems of fibres, it is not wholly ade- quate. Nor is it possible, with the microscope and modern methods of staining cells and fibres, to deter- mine precisely their connections or to unravel the net- 2 DISEASES OF THE NERVOUS SYSTEM. work of interlacing fibres, for at best only the structure of isolated elements is revealed by such means. Fortunately, there are other methods of research. Disease in man and physiological experiment in the lower animals aid us in the investigation and differentia- tion of the more intricate and finer relations of gray matter and fibre tracts, and of the latter to one another. For, when nerve-fibres are separated from their nutritiva centres (the ganglion-cells) either by some morbid pro- cess, as frequently occurs in man, or by actual section of a nerve in a lower animal, such fibres degenerate in the portion cut off from the ganglion-cells by the lesion, and hence definite bundles of fibres inay often be found altered in structure throughout their whole extent. On dissection the degenerated portion becomes visible to the naked eye by its change of color, and under the microscope the altered structure of the fibres is very marked. This process is known as secondary degenera- tion. The descending degeneration of the motor tract in the brain and in the lateral and anterior columns of the cord following coarse lesions in the cerebro-spinal axis, is an example of this process, the fibres of the motor tract being separated from their nutritive ganglion- cells in the cerebral cortex. Again, after tearing out accessible nerves and their end- organs, such as the optic nerve and the eye, in newly born animals, certain groups of ganglion-cells undergo a sort of retardation in development and an atrophy from non-use ; and when, in other living animals, such groups of cells are experimentally removed, the fibres leading thence to the end-organ degenerate. This method of investigation is known as Gudden's atrophy method. While extremely useful, it is as yet rather restricted in its application, since the lower animals only can be S'jkuciurf: and functions. 3 directly experimented upon, and the facts thus ascer- ^ tained cannot always be properly transferred to human physiological anatomy. Still another method of great value is one developed by Flechsig, and originally suggested by Meynert. Cer- tain tracts of nerve-fibres in the central nervous system have been found to develop their myeline sheaths at dif- ferent periods of time. For instance, the fibres of the posterior nerve-roots receive their myeline sheaths as early as the seventh month of foetal life, while those of the motor tract do not become perfected until birth. The microscope easily differentiates such bundles, and, even to the naked eye, the medullated fibres, by their white color, contrast strongly in transverse section with the gray non-medullated fibres. The functions of the central nervous system have been studied by the experimental stimulation and destruction of certain portions of the brain and cord in lower animals, but, the results of such experiments are not always applicable to man. Most of our knowledge of cerebral and spinal localization has been acquired by the careful observation of the symptoms of organic lesions in man, and their comparison with the pathological con- ditions observed at autopsies. While each of the methods mentioned is more or less limited in scope and application, and while the interpre- tation of morbid symptoms and processes in man has perhaps the highest value and significance, all these means of investigation have supplemented and corrob- orated one another so amply as to place beyond ques- tion most of the facts of cerebro-spinal anatomy and physiology, as employed to-day for purposes of clinical diagnosis. Before considering the chief facts in the functional 4 DISEASES OF THE NERVOUS SYSTEM. anatomy of the nervous system, certain general pre- liminary points should be reviewed. The chief elements of structure in the nervous system, those which underlie its physiological activity, are the nerve-cells and nerve-fibres. The cells originate or FIG. I. Diagram showing various forms of ganglion- or nerve-cells. A, pyramidal gan« glion-cells from the human motor cortex ; B, multipolar ganglion-cell from ante- rior horn of spinal cord ; C, axis-cylinder from B ; D, neuroglia cell ("'spider" cell) ; F-, spindle-cell from human cortex ; F, granule-cells from cortex ; G, Bipo- lar cell from spinal ganglion. receive impulses ; the fibres probably serve merely as conductors of impulses. There are wide variations in the shape and size of the nerve-cells, and a few illustrations are here given for STRUCTURE AND FUNCTIONS. 5 the purpose of making these differences apparent. Many quahfying names have been applied to them, such as angular, granular, pyramidal, ganglion, multipolar, globose, round, spindle-shaped, etc. The nerve-fibres also lack uniformity of structure. They occur as delicate threads, known as primitive FIG. 2. Diagram to illustrate the more important varieties of nerve-fibres. A and B, medullated nerve-fibres. S, sheath of Schwann. The myeline sheath lies be- tween the sheath of Schwann and the axis-cylinder. N, nucleus of the sheath of Schwann. IS, incisures of Schmidt. Node, constriction separating two seg- ments of a nerve-fibre. C, a nerve-fibre without a medullary sheath. D, fibre of Remak,from sympathetic. fibril!^, naked axis-cylinders, and axis-cylinders clothed in their myeline sheaths. Some of these forms of fibres are figured above, and the highest form of fibre is shown with its sheath of Schwann, myeline sheath, axis- cylinder, Ranvier's nodes, and Schmidt's incisions. 6 DISEASES OF THE NERVOUS SYSTEM. For the support and protection of these million of cells and fibres scattered throughout the labyrinth of blood- and lymph-vessels which go to make up the ner- vous system, there exists a tissue known as neuroglia, which is either homogeneous or finely granular in places where the most delicate imbedding material is required, or dense and fibrous where particularly strong support is needed. One particular form of cell, known as the neuroglia cell, is frequently met with in this supporting tissue. (See Fig. i.) The typical ganglion-cell is characterized by the pos- session of an axis-cylinder process, which is in all proba- bility continuous with the axis-cylinder of a nerve-fibre. Other prolongations are possessed by certain cells, and are protoplasmic in natuie. Whether these additional processes merely subserve nutrition, or afford means for direct or indirect communication from cell to cell by the interlacing of their fibrillary branches, is uncertain. Besides originating and receiving nervous impulses, the ganglion-cells exercise an influence over the nutri- tion of the nerve-fibres and other tissues with which these are in connection. Secondary degeneration of the distal portion of a nerve-fibre, on separation from the cell with which it is united, has already been mentioned. There is also in the course of time some trophic dis- turbance in the cell itself, and the portion of the fibre still connected with it, especially in very young animals. This trophic change is allied histologically to secondary degeneration, but is not precisely the same process. It is a species of dystrophy from non-use, and partakes also of the nature of arrest of development when it occurs in young animals. Nerve-fibres degenerate, as a rule, in the direction in which their nervous impulses travel. Thus, when a STRUCTURE AND FUNCTIONS. 7 cortical ganglion-cell is separated from the long motor fibre going down through the brain and spinal cord, the degeneration descends, following the path of former motor conduction. An important exception to this law is seen in the degeneration of sensory fibres in peripheral nerves. When separated from the ganglia of their roots such fibres degenerate downward, although con- duction takes place in the opposite direction. Clusters of the largest ganglion-cells, wherever met with in the nervous system, may be considered as sub- serving a motor function. Such aggregations of cells are commonly designated " centres." The word " centre " is employed correctly only in a physiological sense. We mean thereby any group of cells, not necessarily pos- sessing well-defined topographical limits, which act conjointly in some particular functional capacity. Some- times cell-groups are widely separated, although asso- ciated in the performance of some one function. They are nevertheless regarded as constituting a functional centre. There is nothing in the anatomical features of nerve- fibres to give us a clue to the nature of their functional activity. Their axis-cylinders, apparently insulated by myeline sheaths, seem to be conductors of nerve force. The axis-cylinders vary in size, but the significance of such variation has not yet been satisfactorily explained. Many of the largest certainly belong to fibre systems of great length, but we are not yet warranted in assuming any definite relation of the breadth to the length of these elements. The chief elements of nervous structure are so dis- tributed that it may be said, in general, that the cells constitute the gray, and the fibres the white matter of the nervous system. The gray matter completely envel- 8 DISEASES OF THE NERVOUS SYSTEM. opes the hemispheres of the brain, forming the layer known as the cortex, where most of the higher mental functions are supposed to reside. There are also large masses of gray matter at the base of the brain in the basal ganglia, and the nuclear cells of the cranial nerves are scattered through the interior of the crus, pons, and medulla. In the cerebellum the gray matter has a very complex arrangement, while in the cord, on transverse section, it is seen to have an H-like contour, as it lies imbedded in the midst of columns of white fibres. The Brain. — The accompanying illustrations offer a readier means of acquiring a knowledge of the topographi- FIG. 3. Diagram showing the division of the brain into lobes, outer surface, and of right hemisphere. cal distribution of the chief convolutions and fissures of the cerebrum than would a description in the text. The cortex varies in depth and structure in different regions, so that no less than eight distinct types of cortical lamination have been noted by some investigators. For STRUCTURE AND FUNCTIONS. FIG. 4. Diagram of the inner or medial surface of the brain showing the division into lobes. The parietal lobe does not extend so near the corpus callosum as here indicated. Par leto Occip FIG. 5. Diagram showing the chief convolutions and fissures on the outer surface of the right hemisphere. lO DISEASES OF THE NERVOUS SYSTEM. instance, in some regions there are but three layers in the cortex, in others seven. The largest ganglion- cells of the brain are found in the motor convolutions. These differences of structure condition differences in function, and modern research has localized, more or less perfectly, areas for voluntary motion, speech, cutane- ous sensation, visual, auditory, and olfactory impres- sions, and has outlined with some degree of certainty FIG. 6. Diagram showing the chief convolutions and fissures on the inner or medial surface of the right hemisphere. regions which subserve the higher intellectual opera- tions. The accompanying diagrams indicate with sufifi- cient clearness the relative positions of these regions. It is well to bear in mind that besides the fibres passing out from these cortical areas to the periphery of the body, there are numerous bundles of fibres which connect with one another different lobes and different convolutions, and join certain parts of the cortex with certain of the basal ganglia and the cerebellum. The STRUCTURE AND FUNCTIONS. II Diagram showing the position of the cortical motor area on the outer sur- face of the hemisphere. The vertical shading represents the position of the leg centre. The horizontal shading shows the position of the face centre. The dotted area shows the position of the arm centre. Diagram showing the position of the leg centre on the inner surface of the right hemisphere. R indicates the position of the fissure of Rolando on the outer surface. FIG. 9. Diagram showing the cortical visual centres on the outer surface of the right hemisphere. The horizontal lines show the approximate position of the half-vision centre. The dotted areas show the position of the supposed higher visual centre. ISU/V CeXTCR FIG. 10. Diagram showing the position of the visual (half-vision) centre and the probable position of the olfactory cen- tre on the inner surface of the right hemisphere. Diagram showing the position of the auditory centre in the first temporal convolution. Diagram showing the position of the motor speech centre in the left hemi- sphere. 12 DISEASES OF THE NERVOUS SYSTEM. former fibres, which in a manner project the organism upon the cortex, as the world is projected upon a map, are often termed "projection" fibres; while most of the latter, which undoubtedly serve to bring various parts of the brain into conjoint and harmonious action, are known as "association " fibres. The two cerebral hemi- spheres are associated in function by the large bun- dles of fibres passing from the cortex of one side to that of the other, and con- stituting the corpus cal- losum. In addition to this great commissure there are three small ribands, known as the anterior, middle, and posterior commissures, in the third ventricle, which are to a certain extent bonds of union between the two halves of the brain. Of these commissures, the anterior is the most im- portant, and is probably connected with the olfac- "^'■"^^^- tory nerves. Nothing definite of practical value is known concern- ing the functions of gray masses called the caudate and lenticular nuclei, composing the corpus striatum, and which are joined together by transverse fibres in the internal capsule. There are fibres passing from the outer surface of the nucleus caudatus and probably from the nucleus lenticularis to the cortex, and there are FIG. 13. The base of the brain and the cranial STRUCTURE AND FUNCTIONS. 13 bundles from both which descend through the crus into the pons. The optic thalamus is apparently connected with all parts of the cerebral cortex, and in particular with the visual area, and, furthermore, with the optic tracts. The anterior bodies of the corpora quadri- gemina are probably associated with the function of sight, but in precisely what manner is unknown. ^"J'^^'"" or FIG. 14. Diagram showing the nuclear origin of the cranial nerves ; the medulla, pons, and crus being seen from the side, and represented as transparent. The sensory- structures are in red. Ill, oculo-motor nucleus — i, fibres from the cells that sub- serve accommodation ; 2, fibres from cells subserving the reflex action of the iris ; 3, fibres from cells innervating the external muscles of the eye. P. L. B., poste- rior longitudinal bundle associating certain cells of the Hid nucleus with cells of the Vlth nucleus. The portion of this bundle which lies between the Vlth nucleus and the cord is not represented. Vm, motor nucleus of trigeminus. Vs, sensory nucleus. The ascending sensory root of the sth is reprinted as coming from the substantia gelatinosa of the cord. The descending or trophic root arises in the quadrigeminal region. VII, facial nucleus. VIII, auditory nuclei. IX, glosso-pharyngeal nucleus. X, vagus nucleus. The roots of the vagus receive filaments from the nucleus ambiguus. XI, spinal accessory nucleus. XII, hypo- glossal nucleus. The crus cerebri is the part through which all the nerve-fibres which connect the brain hemisphere with the rest of the body must pass, the olfactory and optic nerves being the only exceptions. In a transverse section through the crura the various tracts and nuclei lie as shown in diagram 29 The third nerve nucleus lies in the floor of the aqueduct of Sylvius, H DISEASES OF THE NERVOUS SYSTEM. PONS and the fibres of the nerve pass out through the crus on their way to the orbit. The practically useful facts in the anatomy of the pons and medulla relate especially to the disposition of the cranial nerve nuclei and certain bundles of fibres. The superficial origin of the cranial nerves is seen in Fig. 13. A knowledge of the relative positions of their nuclei is best gathered from the accom- panying diagrams. Some idea of the intri- cacy of the fibre-structure of the pons and medulla FIG. 15. may be obtained from the Diagram showing the nuclear origin of diagrams of tranSVCrSC SCC- tne cranial nerves (exc pt the auditorv). Thesensory structures are in ^i-^/ and the tlOnS Of thcSe tWO UartS, motor in black. '1 he flcjor of the 4th ven- _ ^ tricleis seen from above, and on the right givenonpagCS47, 5 I and "5 8. side the structures are represented as r o u u transparent. VI I, the facial nucleus. The fibres from this nucleus wind round the nucleus of the abdui ens n-rve (VI), and make their exit just l)elow the pons IX and X, common nucleus of the glosso- pharyngeal and vagus nerves. The roots of the vagus receive filaments from the nucleus ambiguus XI, spinal accessory nucleus. XII, hypoglossal nerve. V. the trigeminus nerve. Fibres pass to this nerve from above (descending or trophic root), from below (ascending sensory root), from the level of its exit from a sensory nucleus, and from a motor nucleus. P.I,.P>., posterior lonjitudinal bundle con- necting the Vlth nucleus below with the Hid nucleus above. VIII, the striae acousticae. The relations of certain of the cranial nerves to the motor tract will be treated in connection with the description of the latter. The superficial anatomy of the cerebellum is por- trayed in the two accom- panying, illustrations of its dorsal and ventral aspects. Each hemisphere of the cerebellum is joined to the corpora quadrigemina, to the pons, and to the medulla by three large diverging bundles of fibres, known respectively as the superior, middle, and inferior STRUCTURE AND FUNCTIONS. 15 FIG. 16. Diagram of dorsal surface of cerebellum, showing the position of the worm. (After Edinger.) tA>t)Oi.e FIG. 17. Diagram of ventral surface of cerehelluni. fAfter Edinger.) i6 DISEASES OF THE NERVOUS SYSTEM. cerebellar peduncles. The peduncles are shown in Fig. 1 8. We are still greatly in the dark as regards the physi- ology of the cerebellum. Disease here so easily produces indirect effects upon the pons and medulla that the actual focal symptoms are often obscured. But there is undoubted evidence of the relation of the organ to bodily equilibrium, for disease in a peduncle may produce forced movements to one side or the other, and the inco - ordination known as cerebellar staggering or titu- bation is due to disturbance of the middle portion of the cerebellum, the vermis, or worm. There is also some probability that this organ forms a sub-stratum for some of the intellectual processes, through its intimate connec- tion with the frontal lobes of the cerebrum by means of the fronto-cerebellar tract of fibres (sometimes called the "intellectual tract"). {Vide Fig. 29.) For further information as to the disposition of the various parts of the brain, the reader is referred to works on the descriptive anatomy of the brain. The Spinal Cord. — The spinal cord averages from seventeen to eighteen inches in length, and extends from the superior plane of the atlas to the second lumbar vertebra. The spinal canal is some nine or ten inches longer than the cord, reaching as it does through the remaining lumbar vertebrae and sacrum, to the coccyx. Diagram showing the three peduncles of the cerebellum — the superior pedun- cle going to the quadrigemin;il region, the middle peduncle going to ihe pons, and the inferior peduncle coming from the cord below. (After Edinger.) STRUCTURE AND FUNCTIONS. 1/ The segments of the cord are short, and each pair of spinal nerves takes a downward direction from the segment before it reaches the intervertebral foramen. The intraspinal course of the nerves is longer the lower we descend the cord, so that the lumbar and sacral pairs form the large bundle of nerves known as the cauda equina (horse-tail) occupying the lower end of the spinal canal. The cord is not of uniform diameter, for there is an intumescence in the cervical cord, called the cervical enlargement, due to the fact that it is the motor and sensory cord centre for the upper extremities ; and the lower extremity of the cord also presents an intumes- cence, known as the lumbar enlargement, containing the centres subserving motion and sensation in the lower extremities, together with the sexual, anal, and vesical centres. The term lumbar enlargement is a little mis- leading, and it must be remembered that though this enlargement gives rise to lumbar nerves, the greater portion of it is contained in the lowest part of the dorsal region of the spine. The spinal cord, taken as a whole, must be studied from two points of view : first, as a kind of cable through which nerve-impulses are transmitted to and fro between the peripheral portions of the body and the brain ; secondly, as a series of segments superimposed like blocks one upon the other, each giving rise to a pair of spinal nerves, and each serving as a centre for various reflexes, for trophic influences, and for vascular control. The long fibres necessary for the first purpose are dis- posed in columns running the whole length of the cord and surrounding the central gray matter. The H-shaped central gray matter consists of the anterior and posterior horns, which are connected with the anterior and posterior roots of the spinal nerves. i8 DISEASES OF THE NERVOUS SYSTEM. c FIG. 19. Diagrams of transverse sections of the cord (A, cervical, B, dorsal, C, lumbar cord) showing the position of the chief tracts. The cross- barred shading represents the crossed and direct pyramidal tracts. The dotted areas in the post, columns show the post. -median columns (Goll) which convey tactile sensibility. The postero- ext. columns (Burdach) lie just external to the post. -internal columns. The e.xternal portion of this postero-external column, marked off by a dotted line, is the posterior root-zone. The dotted area in the lateral column, just external to the crossed pj'ramidal tract, is the direct cerebellar tract, conveying muscular sensibility. It arises above the lumbar cord, and hence is not seen in the section of this part. Just antierior to the crossed pyramidal tracts and the direct cerebellar tract, is the antero-lateral ascending tract (Gower's traclj, seen in all three sections. It probably conveys sensations of pain and temperature. Just external to the posterior nerve-roots is the zone of T.issaiir ("border zone"). The lateral and ante- rior columns contain the motor fibres from the cortex, and the posterior columns cer.- tain sensory tracts. The anterior columns are often called the columns of Turck ; the posterior are composed of the columns of Goll and Burdach. Their exact positions, in dif- ferent regions of the cord, are indicated in the accompanying dia- grams of transverse sec- tions of the cord. Reflex, trophic, and vaso-motor centres are situated in the gray matter. The various reflexes will be con- sidered elsewhere. The trophic centres in the anterior horns regulate the nutrition of the motor nerves and muscles, and the des- truction of them is fol- lowed by degeneration of the motor nerves and atrophy of the muscles innervated by them. The ganglia STRUCTURE AND FUNCTIONS. 19 of the posterior roots are trophic centres for most of the fibres of the sensory nerves, but a few of the posterior root-fibres have trophic centres in the posterior horns. There are trophic centres, also, for viscera, bones, joints, and for the skin and nails, all along the cord, and these are probably situated in the gray matter about the cen- tral canal. There are communicating nerve filaments between them and the ganglia and fibres of the sym- pathetic nervous system. It must be borne in mind that the spinal cord, like the brain, is composed of two symmetrical halves, but more closely bound together. Throughout its whole extent fibres pass from one side to the other. There are, first, the sensory nerve-fibres which decussate along the whole of the cord, and besides these there are com- missural fibres between the anterior columns and anterior horns. The following is a table, slightly modified in the light of recent investigations from the excellent one first elaborated by Starr, which shows the relation between each segment of the spinal cord and the principal muscles or group of muscles, sensory areas, and reflexes in connection with it. Seg7neni 0/ cord Nerves Muscles Sensory areas Reflexes .Second and third cervical Occipitalis ma- jor and minor Auricularismag. Superficialis colli Supraclavicular Sterno-mastoid Trapezius Scaleni and neck muscles Diaphragju Neck and back of head Hypochon- drium (?) Fourth cervical Supraclavicular Circumflex Musculo-cuta- neous Musculo-spiral Diaphragm Supra- and infra- spinatus Deltoid Supinator longus Rhomboidei Neck Superior surface of shoulder Outer surface of arm Cilio - spinal ^4th cervic'l to 2d dor- sal) 20 DISEASES OF THE NERVOUS SYSTEM. Segment of cord Nerves Muscles Sensory areas Reflexes Fifth Supraclavicular Deltoid Back of shoul- Scapular cervical Circumflex Biceps and der and arm (5th cervic'l Externa] cuta- coraco-brachialis Outer side of to 1st dor- neous Supinator longus arm and fore- sal) Internal cuta- and brevis arm Biceps jerk neous Rhomboidei Supinator Posterior spinal Deep muscles of jerk branches shoulder-blade Pectoralis (clavic- ular part) Teres minor Serratus magnus Brachialis anticus Sixth External and Biceps Outer side and Elbow jerk cervical internal cuta- Brachialis ant. front of fore- (triceps) neous Pectoralis (clavic. arm. Wrist jerk Radial part) Subscapular Serratus mag. Triceps Extensors of wrist and fingers Pronators Back of hand (radial distri- bution) Seventh External and Triceps (long Radial and me- Palmar cervical internal cuta- head) dian distribu- (7 th cervi- neous Extensors of tion cal to 1st Radial wrist and fingers dorsal) Median Pronators Posterior spinal Flexors of wrist branches Subscapular Pectoralis (costal part) Serratus mag. Latissimus dorsi Teres major Eighth Internal cuta- Triceps(longhead) Inner side of cervical neous Flexors of wrist arm and fore- Ulnar and fingers arm Small muscles of Ulnar area of hand hand First dorsal Int. cutaneous Extensors of Inner side of nerve of Wris- thumb arm and fore- berg Small muscles of hand Thenar and hypo- thenar muscles arm STRUCTURE AND FUNCTIONS. 21 Segment of cord Nerves Muscles Sensory areas Reflexes Second Intercosto- Inner side of dorsal humeral arm near axilla Second to Intercostals and Muscles of back Skin of back and Epigastric twelfth dorsal posteriori and abdomen upper gluteal (4th to 7tli dorsal nerves Erectores spinas region, and of dorsal) breast and ab- Abdominal domen in bands (7th to nth running down- dorsal) ward & forward Skin over groin First Ilio-hypogastric Ilio-psoas Cremasteric lumbar Ilio-inguinal Sartorius and front of (ist to 3d Rectus scrotum Outer surface of lumbar) Second Genito-crural Ilio-psoas lumbar External cuta- Sartorius thigh neous Quadriceps fem'ris Quadriceps fem'ris Third Anterior Anterior surface Knee-jerk lumbar Crural Internal cuta- neous Long saphenous Anterior part of biceps Inner rotators of thigh of thigh Obturator Adductors of thigh Inner side of Fourth Internal cuta- 1 Adductors of thigh Gluteal (4th lumbar neous lAbductors of thigh thigh, leg, and to 5th lum- Tong saphenous Flexors of knee foot bar) Obturator Tibialis anticus Peroneus longus Fifth External popli-jOutward rotators Outer and back Ankle clonus lumbar teal of thigh side of leg and External saphe- Flexors of knee foot nous [neous Flexors of ankle Sole of foot Musculo-cuta- Extensors of toes Plantar Peronei First and Same as 5th Flexors and ex- Same as 5th Plantar (5th second lumbar tensors of ankle lumbar lumbar to sacral Small sciatic Long flexor of toes Small foot muscles 2d sacral) Third, Perineal Back of thigh. Vesical and fourth, Pudic Muscles of blad- anus, perineum. anal centres and fifth Inferior hemor- der, rectum, and genital organs sacral rhoidal Inferior puden- external genitals dal Coccygeal Fifth sacral Coccygeus Skin about anus & coccygeal and coccyx 22 DISEASES OF THE NERVOUS SYSTEM. In addition to the reflex centres indicated in the table, and which have great practical importance, there are others whose precise location has not yet been deter- mined (such as the parturition centre and the erectile and ejaculatory centres), although we know they are in the lumbar enlargement. The Sympathetic Nervous System. — This sys- tem consists of a series of ganglia lying above, between the cranial and facial bones, and running down each side of the vertebral column, from the skull to the coccyx, connected together by non-medullated nerve-fibres, send- ing branches to the smaller terminal ganglia of the tissues or viscera, and having communications with most of the cranial and spinal nerves, and through them with the central nervous system. Besides the pairs of lateral ganglia lying upon the sides of the vertebral bodies, there are prevertebral or collateral ganglia placed in the median line of the ventral spinal surface, such as the semilunar, inferior mesenteric, etc., all of which are likewise closely united to the double lateral series by conjugations. Fibres from both the anterior and posterior roots of the spinal nerves pass into the corresponding ganglia, and, in the cephalic region, there is a free exchange of fibres between the cranial nerves and the sympathetic. The largest gangliated plexuses are found in the thoracic and abdominal cavities. All the vaso-motor nerves originate in the cerebro-spinal axis, and leaving the spinal cord by the anterior roots, as fine medullated fibres, proceed to the lateral series of sympathetic ganglia, where they lose their myeline sheaths before being distributed to their vascular areas. The vaso-motor nerves appear chiefly in the roots of the dorsal spinal nerves. The vaso-dilator nerves, on the blRUCTURE AND FUNCTIONS. 23 Other hand, originate more particularly from the cranio- cervical and sacral regions. The viscero-motor nerves leave the cord in the upper cervical region and descend with the visceral branches of the accessory and vagus nerves to the ganglia of the vagus trunk, where they lose their myeline sheaths and are distributed to the alimentary canal, the peristaltic action of which they govern. The sympathetic system has certain independent func- tions which are performed even when all communication with the central nervous organs is cut off, such as the automatic movements of the heart, the intestines, ureters, blood- and lymph-vessels, Fallopian tubes, and uterus ; but these functions are more or less influenced in the way of inhibition and stimulation by fibres from the cerebro-spinal system. There are other functions, such as the sensory function of the splanchnic nerve, which are dependent upon the integrity and union of the two systems. Besides the vaso-motor and vaso-dilator nerves, supply- ing the vessels of the various tissues and viscera of the body, there are secretory nerves derived from the sympa- thetic system, governing such secretions as the tears, saliva, sweat, mucus, digestive juices, urine, etc., and there is in a measure a segmental representation of these functions in the ganglionic chain. One of the sympathetic functions which is of practical importance for diagnostic purposes is that of dilating the pupil. The cilio-spinal centre lies in the cord between the fourth cervical and second dorsal segments, and the pupil-dilating fibres pass from thence out by the rami communicantes into the cervical sympathetic, which con- veys them to the head. Section of these fibres causes contraction of the pupil, and stimulation dilatation. 24 DISEASES OF THE NERVOUS SYSTEM. The Motor Tract. — We may now pass to the con- sideration of the parts of the nervous system that are concerned in voluntary motion. Between the cortex of the brain of one side and the voluntary muscles of the opposite side of the body lies a system of fibres which we call the motor tract. It is convenient to regard this tract as composed of two portions or segments : one, the cerebro-spinal ; the other, the spino-muscular. Each of these segments is made up of a large number of elements. Each cerebro-spinal element consists of a cortical ganglion-cell with its connected nerve-fibre passing down through the brain and cord to a fibrillary termi- nation in the anterior horn. Each peripheral or spino-muscular element consists of a spinal ganglion-cell in the anterior horn and the fibre passing out from it to a fibrillary termination in the mus- cle. Each element, then, has a ganglion-cell at its upper end, and a long fibre dividing into fibrillse at its periphe- ral extremity. The branching cerebro-spinal nerve-fibre is in some manner connected with the processes of the ganglion-cell in the anterior horn, while the branching spino-muscular nerve-fibre is intimately connected with the muscular fibre through its complex motorial end-plate. Let us study the topography and relations of these segments, beginning with the part of the cortex especially connected with voluntary motion, the motor area. This area comprises the ascending frontal and ascending parietal convolutions bounding the Rolandic fissure (sometimes called from their position the " central " con- volutions), the superior parietal lobule, the paracentral lobule, and part of the precuneus. {Vt'de Figs. 7 and 8.) The leg muscles are mainly represented in the upper third of the central convolutions and in the paracentral lobule. STRUCTURE AND FUNCTIONS. 25 The arm muscles are governed from the middle third of these central con- volutions of the Rolandic region. The leg and arm areas probably overlap one another. The centre for the movements of the face is in the lower third of the ascend- ing frontal and possibly in a portion of the ascending parietal convolution. The tongue and lips are represented together in the lowest part of the ascending frontal convolution and in the inferior or third frontal convolution, and it . is not practicable to separate their regions, because of the habitual functional association of the orbicularis oris and transversus linguse. The motor area for speech occupies about the same position as the centre for the tongue and lips ; that is, the lower or third frontal convolution in its posterior part. These areas either immediately adjoin or over- lap each other, but the motor speech centre is usually located only in the left hemisphere. While there can be no doubt as to the relation existing between the parts described and voluntary motion, it must be remembered that sensation, also, is to a certain extent localized in the same regions, though probably in some special layer among the strata of cortical cells. The sensory areas and tracts will be discussed in a siibsequent paragraph. 2 6 26 DISEASES OF THE NERVOUS SYSTEM. The Rolandic region of the cortex contains the largest ganglion cells in the central nervous system, some of them being as much as 65 /i in diameter. They lie in what is known as the third of the five layers of the cor- Horizontal section through the brain showing the position of the optic thala- mus, the corpora striata (caudate and lenticular nuclei), and the internal capsvde. tex, and have a pyramidal shape, with their apices toward the periphery and their bases directed inward. From the bases of these pyramidal cells spring the fibres which carry motor impulses. As they descend toward STRUCTURE AND FUNCTIONS. 27 the lower part of the brain these fibres converge to form in the internal capsule the large compact bundle of the motor tract. The internal capsule is the name given to the knee- shaped mass of white substance seen upon making a horizontal section of the brain through the basal ganglia and lying between the nu- cleus lenticularis on the outside and the thalamus and nucleus caudatus on the inside. The motor tract occupies but a portion of the internal capsule, viz., the anterior two-thirds of the portion behind its angle or knee lying between the optic thalamus and the nu- cleus lenticularis. Before reaching the internal cap- sule the fibres for the leg, arm, and face hold the same relative position in the centrum ovale that they have upon the cortex — that is, from the median line outwards, leg, arm, face — L A F. As the bundles en- ter the internal capsule their relative positions change so that L A F is the formula to express their situation from behind forwards. Their positions are altered again as they enter the crus cerebri, the formula L A F showing their relative location from without inwards, for the kg bundle is outermost, the arm bundle next in order, and the face bundle nearest the FIG. 22. Diagram of horizontal section through the basal ganglia and internal capsule (left side), showing the position of the chief tracts in the internal capsule. The region of the capsule marked by the letters L A F is occupied by motor fibres : L corresponds to the leg fibres, A to the arm fibres, F to the face fibres (including fibres to face muscles, and tongue). The region F-(3 contains the fronto-cerebellar tr.ict (intellectual tract). The region marked S contains the general sensory tract from the opposite side and the fibres from the optic and olfactory nerves of the oppo- site side, sometimes called the " sen- sory crossway." 28 DISEASES OF THE NERVOUS SYSTEM. ■ERN AL CftPiULE. median line. Thus their situations with regard to the median line are completely reversed in their progress from the cortex to the pons. In the pons the same positions are maintained until the facial bundle crosses to its nucleus on the opposite side, and a little lower down the tongue fibres cross to the hypoglossal nucleus. The leg and arm bundles continue down together to form the remainder of the pyramidal tract. The motor tracts occupy the an- terior part of the pons and constitute the anterior pyramids of the medulla. Just as they pass from the medulla to the cord most of the fibres cross to the opposite side. The number of fibres which decussate to enter the opposite lateral column of the spinal cord is variously estimated by differ- ent authors at from seventy-five to ninety-seven per cent. The remain- der of the fibres of the motor tract continue down into the anterior col- umn of the same side, crossing to the opposite anterior horns at various FIG. 23. levels. The former bundle is desig- Diagram showing the nated the crosscd pyramidal tract, and position of the pyramidal _ -^ _ ' tract of the right side at the latter the direct pyramidal tract. different levels of the brain and in the spinal cord. There is good rcasou for believing (After Gowers.) ° . . that the crossed pyramidal tract is destined chiefly for the innervation of the trunk and lower extremity, and the direct pyramidal tract for that of the upper extremity ; for one continues to the lumbar enlargement, and the other generally disappears in the CORD STRUCTURE AND FUNCTIONS. 29 mid-dorsal region or the cervical enlargement. All of these fibres terminate in fibrillae probably connected with the branching processes of the ganglion-cells of the anterior horns. We have now traced the cerebro-spinal segment of the motor tract from its origin in the cortex to its termination in the anterior horns. Its course is uninterrupted throughout. Formerly it was supposed that the ganglion- cells of the corpus striatum were interposed in its path, but the study of secondary degeneration has proven that there is no connection between them. Passing to the consideration of the spino-muscular portion of the motor tract we have to examine the disposition of the ganglion-cells in the anterior horn. These cells are distributed in groups or clusters in the anterior horns, and their arrangement differ in the various levels of the spinal cord. We distinguish by their rela- tive position in transverse sections at certain levels the following five groups : a median, an anterior, an antero- lateral, a postero-lateral and a central. Often the second and third of these are not distin- guishable from one another by any well-marked line of separation. The aggregation of cells in clusters is most marked in the cervical and lumbar enlargements. In the dorsal region, where the anterior horns are small, the distinc- tion of isolated cell-groups is often difficult, but the an- terior and external clusters can usually be made out. A knowledge of this cell-grouping is not of much import- ance in diagnosis, for we have not yet learned of the exact relationship existing between particular aggrega- tions of cells and the muscles which they govern. We know much more of the relations of the masses of gan- glion-cells, taken as a whole, in the anterior horns of par- 30 DISEASES OF THE NERVOUS SYSTEM. ticular segments of the cord, and the muscles with which they are connected, although even here absolute pre- cision has not been attained. There are probably, also, frequent though inconsiderable variations in individuals, as regards the extent and complexity of the cell-repre- sentation of muscles at different levels of the cord. It should be noted that muscle-groups which have a higher position in the body are localized, as a rule, in higher levels of the cord. For example, the shoulder muscles have their spinal nuclei in the upper portion of the cer- vical enlargement, while the hand muscles, which occupy a lower position in the body, are represented in the lower portion of the enlargement. In the table of spinal localization already given, the relation of the different muscles to the various segments of the cord is presented. The ganglion-cells of the anterior horn are of large size, triangular in shape, and in general lie with their apices forward. Each cell originates a nerve-fibre. The fibres collect in bundles, and pass through the white substance to emerge as the anterior roots of spinal nerves from the cord. When joined by the posterior or sensory root at the intervertebral foramen it contributes to form a mixed nerve — that is, one having both motor and sen- sory fibres. There is no way of distinguishing the motor from the sensory fibres, since they have no characteristic arrangement in the spinal nerves and no known structural differences. As each nerve approaches muscles for which its motor fibres are destined, these latter leave the mixed nerve in bundles to enter the muscles and be distributed to their fibrillce. Each nerve fibril terminates in a muscular fibre as a motorial end-plate. The Sensory Tract.— We know far less of the ner- STRUCTURE AND FUNCTIONS. 3 1 vous structures that subserve ordinary sensibility than of those which underlie voluntary motion, and the difficul- ties of tracing the sensory paths are increased by the fact that, in certain parts at least, different forms of sensation are conducted by different structures. The skin is the seat of a variety of bodies related to sensory perception. Of these, some, like the corpuscles of Pacini and Meiss- ner, and the end-bulbs of Krause, are differentiated tactile organs, whose office it is to modify and possibly to mul- tiply the effects of stimuli upon the terminal nerve filaments, but we cannot as yet ascribe specific forms of sensory function to these different bodies. The simpler nervous structures in the skin are plexuses of non-medullated nerve-fibres terminating in free ex- tremities between the cells of the mucosa, and are more widely distributed than the end-organs just mentioned There is some reason for believing that these various terminal nerve-structures respond only to particular kinds of sensory stimuli. Sensory fibres also enter the muscles, and the impres- sions conveyed by them upon contraction of the muscle- fibres have much to do with the sense of posture and the nice control and proper co-ordination of muscular movements. There are good reasons for believing that the various sensations of touch, pain, heat, and cold, and the muscu- lar sense, have special terminal filaments for their appre- hension, and possibly for their conveyance from the periphery to the central nervous system ; but this is by no means definitely determined. Far from being able to distinguish by their appearance varieties of sensory nerve-fibres, we cannot even detect structural differences between the motor and sensory fibres of the peripheral nerves. DISEASES OF THE JSTERVOUS SYSTEM. In the intervertebral foramen all of the sensory fibres separate from the motor bundle to pass into the spinal cord as the posterior root. Upon entering the cord the sensory fibres take different directions. Opinions differ as to the course they pursue, but we may safely distin- guish the following sets of fibres : A. Fibres that pass through the gelatinous substance of the posterior horn, some ending there in small ganglion-cells, others proceeding at once to the anterior horns, but the larger number taking a vertical course, up or down, for a short distance FIG. 24. Diagram of transverse section of spinal cord, showing the course of the chief sets of fibres in the nerve-roots. (A. anterior horn ; V. posterior horn.) i and 2. Fibres which enter the postero-external column (Burdach) and take an ascending or de- scending course, many of them entering the postero-niedian column (column of beforC resuming theif for- (joII). 3. fibres which pass to the cells •-' of the column of Clarke, which in turn send fibres to the direct cerebellar tract. 4. Fibres passing to the proper sub- stance of the posterior horn. 5. Fibre coming through the anterior commissure from the direct pyramidal tract of the opposite side. 6. Fibre coming from a motor ganglion-cell of the opposite an- terior horn. 7. Fibre connected with motor ganglion-cell of the anterior horn of same side. This ganglion-ceil is proba- lily connected with a sensory fibre from , the opposite posterior horn 8. Fibres the pOStCHOr COmmiSSUre, from motor ganglion-cell of anterior horn of same side. This ganglion-cell is proba- bly connected with a sensory fibre from the posterior horn of the .same side. 9 and 10. Fibres from the crossed pyramidal tract of the same side. wards. ward direction in the gray matter. B. Fibres that traverse the column of Burdach. Many of these enter the posterior horn just behind taking either a horizontal course or proceeding ob- liquely upwards or down- Others pass inwards to the column of Goli. Many of the fibres of each set go forward to the pos- terior commissure, where it is probable that they are connected with nerve-cells. Others pass to a vertical series «f cells in the inner part of the neck of the pos- STRUCTURE AND FUNCTIONS. 33 terior horn, known as the vesicular column of Clarke. The cells constituting the column of Clarke are found mainly in the lower dorsal and upper lumbar region, although they are seen in much smaller numbers in other parts of the cord. They have an intimate ana- tomical connection with an important tract of the cord, the direct cerebellar tract, lying in the lateral region external to the crossed pyramidal tract. Thus, it is certain that two important white columns of the cord, the column of Goll and the direct cerebellar tract, have a direct communication with the posterior root. Both of these tracts degenerate upwards throughout the whole length of the cord, and as degeneration occurs in the direction of conduction, this is essentially a cor- roboration of the belief that they are sensory in function. But there is another tract of ascending fibres in the cord believed to be in communication with the posterior roots, although their anatomical connection has not been actually traced. It lies in the anterior part of the lateral column, and as it degenerates upwards must also con- duct in that direction. It is known as the antero-lateral ascending tract (Gowers' tract), and there is strong rea- son for supposing that its fibres come from the posterior root of the opposite side, by way of the posterior gray commissure of the cord. It is quite certain that these three tracts, the an- tero-lateral ascending, direct cerebellar, and column of Goll, convey different sensory impressions from the periphery to the brain, and the balance of evidence is in favor of the following conclusions : 1. That the antero-lateral ascending tract is the path for sensations of pain. 2. That the direct cerebellar tract conducts muscular sensations from the lower part of the trunk. 3 34 DISEASES OF THE NERVOUS SYSTEM, 3. That the column of Goll is the path for tactile sen- sibility, and probably also for the muscular sense of the limbs. The exact position of the path for temperature sensa- tions is unknown, but it is not improbable that it is contiguous to that for pain, since both forms of sensi- bility are frequently impaired together by limited lesions. All of the sensory paths, except that for muscular sense, cross to the opposite side of the cord, probably by the posterior commissure, at a level a little above the point of their entrance into the cord. They then con- tinue upwards to the cortex of the brain. Thus it is seen that Avhereas the motor tract decus- sates chiefly in the medulla the sensory tract decussates all along the cord. In the table of spinal localization already given, the sensory areas represented by each segment of the cord are noted. As regards the position of the sensory tract in the medulla, pons and brain, only general statements can be made, for our knowledge of this is not yet perfectly accurate. It is probable that the muscular impulses travel along the direct cerebellar tract into the middle lobe of the cerebellum, and that the other sensations are conveyed through the lemniscus or fillet and the net- work of fibres known as the formatio reticularis {vide Fig. 32) in the medulla and pons. The position of the sensory fibres in the crus is also shown {vide Fig. 29). We know their exact location when they reach the inter- nal capsule, for here they occupy the posterior third of the posterior limb {vide Fig. 22), a position immediately behind and contiguous to the motor tract. Hence both the motor and sensory fibres may be affected together, as they frequently are, by lesions in the internal capsule. In the upper part of the pons the sensory fibres from STRUCTURE AND FUNCTIONS. 35 the face (fifth nerve) join the general sensory tract, to pass with it into the internal capsule. In addition to the representation of the sensory areas of the opposite half of the body in the internal capsule, we have also in the same region fibres from the opposite special sensory organs, such as those of the auditory and optic nerves. From this spot, known as the " sensory crossway," the sensory impulses travel through the coro- na radiata to reach various parts of the cerebral cortex. The cortical area for ordinary sensation cannot be sharply defined, but includes the convolutions of the parietal lobe and the motor area, for there are clinical reasons for supposing the Rolandic region to also possess sensory functions. There is some ground for believing that the superior parietal lobule is the cortical substratum for muscular sense. Some of the fibres of the sensory tract are interrupted in the optic thalamus before reaching the cortex. Reflex Paths. — A reflex movement of the simplest kind may be imperfectly defined as one that results from the conversion or " reflexion " of a sensory stimulus into a motor excitation. A sensory or afferent impulse is conveyed centrally by a sensory nerve to motor gan- glion-cells, whence it is reflected outward along a motor nerve to a muscle or group of muscles. Thus the integrity of these three elements, the sensory fibre, the ganglion-cell and the motor fibre, is essential to the perfect performance of a reflex movement. Such a combination is called a " reflex arc," and this term is convenient, even though there may be more than three ele- ments underlying some of the more complex forms of reflexes. The motor cell or group of cells whence the reflex is discharged is known as the " reflex centre." These are 36 DISEASES OF THE NERVOUS SYSTEM. 1 NHIBI TORY PY|5^AMI DAL FIBER — the same cells that act as transmitters of the voluntary motor impulses descending from the cortex. The motor fibres connecting the cortical ganglion-cells with the ganglion-cells of the anterior horns do more than con- duct voluntary impulses, in that they exercise a restrain- ing or inhibitory influence upon their reflex function. They hold a rein, so to say, upon the movement, so that if these inhibitory fibres are injured in any part of their course, the activity of the reflex centre is uncon- trolled, and the motor phenomenon becomes ex- aggerated. The arcs of the deep or tendon re- flexes, more particularly, are constituted as just de- scribed, but the other re- flexes vary only in minor details. The gray substance of the spinal cord contains a series of reflex centres, cutaneous, muscular, and visceral. Some are com- plex and of considerable vertical extent. They consist of ganglion-cells of adjacent levels, which are har- moniously associated by means of fibres running short vertical courses between them. The following are the more important reflexes ; their relations to particular segments are given in the table of localization of the functions of the spinal cord. Cilio-Spinal. — The pupil dilates upon irritating the skill of the neck on the same side, by pinching or prick- ing, or by making use of the faradic brush. FIG. 25. Diagram illustrating the mechanism of a spinal reflex. Sensory impulses travel along sensory fibres from skin or muscle through the posterior horn of the cord to ganglion-cells in the anterior horn, where these impulses become converted into motor impulses, which descend motor nerve- fibres to muscles. Tlie mechanism is controlled by pyramidal fibres possess- ing an inhibitory function. STRUCTURE AND FUNCTIONS. 37 Scapular. — Upon tickling the skin over the scapula, or at its inner side, the scapular muscles contract. Biceps-yerk. — When the elbow is flexed at a right angle, and any part of the forearm is suddenly struck, especially the lower end of the radius, there is a contraction of the biceps. This is, as a rule, only obtained in morbid con- ditions affecting the reflex centre. Elbow-y erk (triceps-jerk). — Obtained by striking the tendon of the triceps when the forearm is hanging down- wards parallel with the body, the upper arm being ex- tended at a right angle from the trunk. This too is usually present only in morbid conditions (such as hemi- plegia). Wrist-'yerk. — Obtained by striking the long extensors of the thumb, or the tendon of the extensor carpi radi- alis, near their insertion, the hand being supported in that of the examiner, and not being allowed to hang down as is usually the practice. In this way these ten- dons are brought out more prominently, and the reflex is more readily elicited. Palmar Reflex. — The hand closes upon tickling the skin of the palm. Epigastric Reflex. — There is a contraction in the epi- gastric region upon tickling the skin in the neighborhood of the mamma. Abdominal Reflex. — Tickling the skin at the side of the abdomen causes contraction of the abdominal muscles. Cremasteric Reflex. — The scrotum is retracted upon one side when the inner surface of the thighs is irritated. Patellar Reflex (knee-jerk). — When the leg hangs at a right angle to the thigh, or when one leg is crossed over the other, so as to cause slight tension of the quad- riceps muscle, a sudden blow upon the ligamentum pa- tellae causes a contraction of the quadriceps femoris 38 DISEASES OF THE NERVOUS SYSTEM. muscle and extension of the leg. From a diagnostic point of view this is the most important of the reflexes. Gluteal Reflex. — A reflex of no great value, consisting of a contraction of the gluteal muscles upon stroking the buttock. Ankle Clonus (tendo Achillis reflex). — Sudden flex- ion of the foot upon the leg stretches the Achillis ten- don, and produces a series of rapid contractions of the muscles of the calf, occurring at the rate of about six per second. This reflex does not occur in normal individuals. Plantar Reflex. — Tickling of the sole of the foot causes flexion of the toes and withdrawal of the leg. In addition to these reflexes there are others, the cen- tres for which are situated in the spinal cord, but which have no diagnostic importance. There are, furthermore, certain cerebral reflexes, some of which are simple and familiar, and others highly- complex. Thus tickling of the lip causes contraction of the orbicularis oris, touching of the conjunctiva leads to closure of the eye, blowing into the ear produces a gen- eral excitement of the motor apparatus, irritation of the mucosa of the nose causes sneezing, etc. But by far the most striking and most important cerebral reflex is that of the iris. Iris Reflex. — The iris really presents three kinds of reflex. The dilatation of the pupil upon irritation of the skin of the neck has already been mentioned. Next, the pupil contracts in a bright light and dilates in the darkness ; the reflex arc in this case being composed of (i) the optic nerve, which conveys the sensory impres- sions, probably to (2) the ganglion habenulae,' whence ' This is a small mass of gray matter which projects into the third ventricle from the posterior and medial part of the optic thalamus. STRUCTURE AND FUNCTIONS. 39 the motor impulse is reflected outward along (3) the third nerve. What is known as the reflex of the iris during accommodation is an associated movement of the iris ; the pupil becoming larger when the eye is accommo- dated for distant, and smaller when accommodated for near, objects. The Spinal Nerves. — There are thirty-two pairs of spinal nerves. They arise at nearly equal intervals between the conus meduUaris and the medulla Each nerve is formed by the junction of an anterior (motor) and a posterior (sensory) root, and, leaving the spinal canal through the intervertebral foramen as a mixed nerve, soon divides into two branches, an anterior and a posterior. These branches either join with others in the formation of plexuses, from which arise new nerve- trunks, or pass directly to their cutaneous, muscular, or visceral distribution. The nerve-roots differ in size at various levels of the cord, those, for instance, of the dorsal region being smaller than those of the lower cervical and lumbar regions, and this leads to inequali- ties of size in the nerve-trunks formed by them. The spinal nerves give rise to three plexuses of cardi- nal importance, known as the brachial, lumbar and sacral. The brachial plexus is formed by the interlacing of the anterior branches of the spinal nerves arising from the four lower cervical and first dorsal segments of the cord. There is also a small communicating branch from the fourth cervical nerve. The manner of their union to form the outer, posterior, and inner cords of the plexus, and the subsequent division of these trunks into the great peripheral nerves of the upper extremity, are best seen in the accompanying illustration. (Fig. 26.) In the table of localization of the functions of the spinal 40 DISEASES OF THE NERVOUS SYSTEM. cord an attempt has been made to show the relations of the more important peripheral nerves to its segments. i3 FIG. 26. Diagram of brachial plexus. LV FIG. 27. Diagram of lumbar plexus. FIG. 28. Diagram of sacral plexus. The lumbar plexus is derived from the anterior branches of the last dorsal and first four lumbar nerves, and the STRUCTURE AND FUNCTIONS. 4 1 manner of their union and the chief nerve-trunks which arise from it are shown in the accompanying diagram. The sacral plexus, formed, as shown in the diagram, from the last lumbar and four sacral nerves, gives rise to the great trunk of the sciatic. The Cranial Nerves. — There are twelve pairs of cranial nerves which leave the base of the brain at un- equal intervals, thus contrasting with the regularity of arrangement of the spinal nerves. Like the spinal nerves, which arise from the gray matter around the central canal of the cord, the cranial nerves take their origin from clusters of ganglion-cells which occur in the gray matter irregularly disposed about the cavities in the medulla, pons, and crus, these cavities (the fourth ventricle and the aqueduct of Sylvius) being merely continuations upward of the central canal of the cord. Leaving their nuclei of origin, the fibres constituting the various cranial nerves pass, by more or less direct paths, to the base of the brain, to emerge at points known as their superficial origins. From here to their foramina of exit the nerve-trunks are of different lengths, and their relative disposition is such that pathological processes at the base of the brain produce very different and valuable localizing symptoms. Indeed a clear pic- ture of the position of the nuclei and of the arrangement of the intracranial courses of these nerves is of the greatest importance for diagnosis. For instance, in the diagram of the origins of the cranial nerves (Fig. 13), it will be seen that a lesion at the side and upper part of the medulla might involve six of the most important trunks ; that the long course of the sixth [)air over the pons renders them very susceptible to injury ; and again, that some pairs, like the optic nerves at the chiasm, the third nerves, and the sixth pair, 42 DISEASES OF THE NERVOUS SYSTEM. may be very readily affected together because of their nearness, or, on the other hand, seldom affected because of their wide separation at their superficial origin, as in the case both of the fourth and fifth pairs. We now pass to the discussion of the entire course of each of these nerves. The First or Olfactory Nerve. — Our knowledge of this nerve and its central connections is meagre. The peripheral filaments from the Schneiderian membrane pass through the numerous foramina of the ethmoid bone into the olfactory bulb lying along the under sur- face of the frontal bone. From this bulb the olfactory nerve passes backward, dividing into three roots. The fibres of the external root pass into the temporo-sphe- noidal lobe of the same side and disappear in the anterior part of the uncinate gyrus, which is probably the cortical area for the sense of smell. The fibres of the middle root disappear in the anterior perforated space, while those of the inner root are believed to go to the anterior cerebral commissure. There is good reason for believ- ing, that each olfactory nerve is connected with the corti- cal areas for smell of both hemispheres, but the exact paths of these connecting fibres are not yet known. The Second or Optic Nerve. — The nerve of sight is far more important in its diagnostic relations. Pass- ing backward from the retina, the optic nerve undergoes partial decussation, the fibres from the nasal half of the fundus crossing to the opposite side. The nasal half of the retina corresponds to the temporal half of the field of vision, and as it is larger than the temporal half of the retina, owing to the limitation of the nasal visual field by the projecting nose, a greater number of fibres decussate than follow the direct path. Although in dif- ferent animals the amount of decussation varies, and STRUCTURE AND FUNCTIONS. 43 although some investigators hold that the crossing at the chiasm is total in man, clinical and pathological evi- dence is strongly in favor of the partial decussation just described. After leaving the chiasm the nerve continues backward as the optic tract. In the optic tract the direct fibres from the temporal half of the retina occupy the upper side, and the crossed fibres the lower side, while certain inter-tractal fibres, uniting the two tracts through the posterior part of the chiasm, lie internally. Near the posterior part of the thalamus the tract divides into two unequal parts, an outer and an inner. The outer and larger division sends fibres to the corpus geniculatum externum, the pulvinar, and anterior corpus quadrigeminum, while the inner division, containing probably only the inter-tractal fibres, passes into the corpus geniculatum internum. The fibres of the outer root, after being interrupted by the masses of gray matter mentioned, continue backward through the sensory portion of the posterior limb of the internal capsule, constituting the " optic radiations," and, after traversing the white substance of the occipital lobe, are distributed to the visual area of the cortex. The cuneus is the chief cortical centre for sight, but other parts of the occipital cortex seem also to receive and store up visual impressions. If any part of the left optic path from the chiasm to the cortex be destroyed, blindness of the left half of each retina results, and this defect is termed homonymous hemianopsia or hemiopia. If it is the right optic path that is affected, the right retinal halves become blind. Hemianopsia has been caused by diseases of the apex, external surface, and internal surface of the occipital lobe, but is most com 44 DISEASES OF THE NERVOUS SYSTEM. mon when the cuneus is involved ; and it may be, when other occipital areas than the cuneus are invaded, with resulting hemianopsia, that the underlying fibres of the optic radiations are included in the lesion. Certain experiments made upon dogs render it proba- ble that, in these animals at least, there is a kind of serial representation of the quadrants of the visual half-field in the cortex, by which the anterior half of the occipital visual area corresponds to the upper quadrant, and the posterior half to the lower quadrant. Whether a similar arrangement exists in man has not been positively de- termined, but we do know that similar cortical lesions give rise to incomplete quadrantic visual defects. There are, furthermore, other features of the physiology of the cortical visual area not yet thoroughly understood, but which deserve some mention here. Thus it is held that, in addition to the half-vision centres of the cuneus, there exists a visual centre of a different character in the neighborhood of the angular convolution; one in which the entire retina of the opposite side is represented. The evidence of this is that disease in this region often gives rise to what is called crossed amblyopia — that is, diminution of visual acuteness in the opposite eye, usually associated with concentric limitation of the fields of vision. But it must be borne in mind that there are association fibres passing from the visual area of one hemisphere to that of the other, and it is possible that crossed amblyopia may be due to injury of such fibres, for in no case where this symptom was manifested has the lesion been confined absolutely to the cortex. The TJiird, Fourth, and Sixth Nerves. — These nerves are all closely associated in the innervation of the mus- cles which move the eyeball, and the third (or oculo- motorius) supplies; also the internal muscles of the eye — STRUCTURE A.ND FUNCTIONS. 45 namely, the sphincter iridis and ciliary. The muscles con- trolled by the third nerve are the sphincter iridis, superior rectus., inferior rectus, internal rectus\ levator palpebrce, and inferior obliqtie. The individual nerve-fibres from these muscles, after passing through the optic foramen and along the cavern- ous sinus, unite into a trunk of considerable size, which winds over the crus cerebri to dis- appear between the two crura, very close to its mate of the opposite side. The liability of the third pair to suffer together because of this nearness of their super- ficial origins has already been mentioned. En- tering the tegmentum, just internal to the crus, the fibres of the oculo- motorius pass through and by the cluster of cells known as the red nucleus (nucleus ruber), to some nests of gan- glion cells lying in the interior of the gray matter below the aqueduct of Syl- vius, at a point just under the region of the anterior corpora quadrigemina. The general nucleus of the oculo-motorius is known to consist of a series of nuclei, each of which represents some one of the muscles inner- vated by the nerve, and their relative arrangement, from FIG. 29. Diagram of section through crus at level of exit and origin of the third nerve. Subs. Nigra, substantia nigra, which separates the crus into two portions, an anterior (crusta of the crus) and a posterior (tegmentum of the crus). The crusta is divided into sev- eral important tracts of fibres — Pyr. Tract, the pyramidal or motor tract ; V. C, the fronto-cerebellar tract ("intellectual tract"); T. C, temporo-cerebellar tract (fibres which originate in the pons, but are connected with the cerebellum, and pass through the crus to the temporal and occipital lobes ; T, fibres to tegmentum ; Teg., fibres of un- known function connecting the corpus stria- tum with the pons (tegmental part). N III, nucleus of oculo-motor nerve; III, oculo-motor nerve ; R N, red nucleus ; fillet, upper fillet; U F, lower fillet; Aq, aqueduct; V D, descending root of the fifth nerve ; Corp. Quad., anterior corpora quad- rigemina ; C. G. I., internal geniculate body. 46 DISEASES OF THE NERVOUS SYSTEM. before backward, as determined by experiment in dogs and the selective nuclear paralyses recently studied in man, is probably very nearly as follows : Sphincter iridis Ciliary Levator palpebrse Internal rectus Superior rectus Inferior rectus Inferior oblique Certain ocular muscles act habitually in unison ; for example the rectus superior and levator palpebrse, and the nuclei of these muscles are observed to be con- tiguous. With the exception of one sub-nucleus, the cell-nests of the third nerve innervate muscles of the same side. Only the fibres from the nucleus of the internal rectus cross the median line, and the significance of this cross- ing will be seen later. The Fourth Nerve or Patheticus. — The fourth nerve, controlling the action of the superior oblique mus- cle, lies upon the outer side of the cavernous sinus in company with the branches of the third nerve, and is hence apt to suffer with it in lesions affecting this region. The superficial origin of this nerve is in the valve of Vieussens, in the roof of the fourth ventricle, the nerve appearing on the surface just external to the crus cere- bri and on a level with the upper border of the pons. Within the substance of the valve there is a decussa- tion of the fourth pair of nerves. It is probable that most, but not all of the fibres, take part in this decussa- tion. Then the fibre-bundles pass downwards and for- wards around the Sylvian aqueduct to the gray matter in its floor, just posterior to the nuclei of the third nerve. The Sixth Nerve or Abducens. — This nerve sup- plies the external rectus. In the cavernous sinus it STRUCTTTRK AND NC'l'K ).\S. 47 lies beside the flbre-bundles of the third and fourth nerves. From here it takes a long course over the prom- inent convex surface of the pons (thus rendering it very liable to suffer compression, especially from subtentorial growths) to its superficial origin between the lower pon- FiG. 30. Diagram of section through lower part of pons. This diagram is not quite accurate, as it represents, for convenience, certain structures which are not actually observed at exactly the same level. (Thus it shows the origin, course, and exit of the 7th nerve.) VI, abducens nerve and nucleus ; N Vll, nucleus of facial nerve ; VII, facial nerve; VIII ant. and VIII post., anterior and posterior or deep and superficial roots of the auditory nerve ; Corp. Rest., restiform body : Knee, knee of the facial nerve ; O. S., superior olive ; P.L.B., posterior longitudinal bundle ; S.T.F., superficial transverse fibres of the pons ; D.T.F., deep transverse fibres of pons; V. Asc, ascending root of trigeminus; Sub. Gel., substantia gelatinosa. The internal or " chief " auditory nucleus lies just internal to the nucleus of Deiter's. tine border and the pyramid of the medulla, not far from the median line. Both nerves often suffer together because of their nearness to each other in their origin and course, and lesions at the base of the brain some- times involve one of the sixth nerves together with the 48 DISEASES OF THE NERVOUS SYSTEM. fifth, for the abducens passes very close to the superficial origin of the latter in its course over the pons. The central origin of the sixth nerve is from a small nucleus immediately below the floor of the fourth ven- tricle, beneath the eminentia teres and in front of the strire acoustics. A transverse section of the pons at this level shows the seventh nerve curving about this nucleus of the sixth nerve, and these two nerves are sometimes affected together by a lesion. When they are thus involved, and without including the eighth nerve, disease .of the pons is indicated. The three ocular nerves, the third, fourth and sixth, have so close a physiological association that it would be natural to expect considerable proximity of their nuclei. But the whole length of the pons lies between the cell-nests of the third and fourth nerves, and the nucleus of the sixth. There is no doubt, however, that there are fibres passing between the two groups of cells, and it is probable that these association-fibres lie in the tract known as the posterior longitudinal bundle, which runs near the posterior surface of the pons adja- cent to the median line upward from the medulla to the gray matter of the third ventricle. These fibres sub- serve the conjugate movement of the eyes from side to side, for in such movements the external rectus of one eye (supplied by the sixth nerve) and the internal rectus of the other eye (supplied by the third nerve) must act simultaneously. The decussation of the fibres from the subnucleus of the internal rectus, which underlies this functional association, has already been mentioned. The oculo-motor nerves certainly possess a cortical representation, but we have as yet no exact knowl- edge as to its location, or the course of the fibres from the oculo-motor nuclei to the cerebral convolutions. STRUCTURE AND FUNCTIONS. 49 There is some probability that the oculo-motor area is contiguous to the facial centre, perhaps in the second frontal convolution. The Fifth Nerve or Trigeminies. — This nerve is both motor and sensory in function. Its motor fibres innervate the muscles which move the jaw. It gives sensory fibres to all parts of the face, conjunctiva, nasal, oral, pharyngeal and buccal cavities, to the tongue, and to the dura mater. In fact it is the sensory nerve for all of those parts whose movements are governed by the several motor cranial nerves from the hypoglossal to the oculo-motorius. Moreover, in a portion of its course, at least, it contains fibres which subserve the sense of taste. The three branches which have given it the name of trigeminus, viz., the ophthalmic, and superior and infe- rior maxillary nerves, unite into one great trunk, about an inch from the superficial origin of the nerve, upon meeting in the Gasserian ganglion. The inferior maxil- lary branch contains all the motor fibres. The sensory root enters the pons in close company with the motor root about the middle of the pons, but at some distance from the median line. The origins of this pair of nerves are the most widely separated of any of the cranial nerves, and to this is due the rarity of their involvement together in any one lesion. They are also quite remote from the roots of other nerves, the nearest being those of the fourth and sixth. The nuclear origin of the fifth nerve is very complex, particularly in its sensory portion. The sensory root passes backward and inward through the outer part of the pons to some small groups of cells lying beneath the floor of the fourth ventricle known as the middle nucleus. The majority of the fibres, however, turn downwards through the pons and medulla under the name of the 50 DISEASES OF THE NERVOUS SYSTEM. descending root. This root lies just internally to the restiform body, and, growing smaller as it passes down- wards, terminates in the upper part of the spinal cord in close connection with the upper expansion of the gelatinous substance of the posterior horn (the gray tubercle of Rolando). The descending root consists of several small bundles, which may be traced from the level of the middle nucleus in an upward direction as high as the upper part of the corpora quadrigemina, where they arise from large round nerve-cells. They lie external to the aqueduct of Syl- vius and are arranged in the form of a crescent. (See Fig- 3I-) The majority of the fibres of the motor root arise from a collection of large ganglion-cells of limited vertical extent, which lies just internal to the sensory root of the fifth nerve in the outer part of the tegmentum of the pons. (See Fig. 31.) There are many intricate arrangements of the sensory portion of this nerve, and they are not yet thoroughly understood. It receives fibres from the gray matter of the posterior horns of the cord and from the cerebellum ; and the great number of its reflex relations with the various motor cranial nerves is evidence of anatomical connection between them and this nerve. Nothing can be positively affirmed regarding structural connections between the fifth nerve and the opposite side, but fibres are described as passing inwards from the nerve to the raphe and to the opposite half of the pons. Most of the fibres of the nerve, both motor and sen- sory, decussate in the upper part of the pons in the for- matio reticularis, and pass through the tegmentum of the opposite side to follow the general sensory path, by way of the internal capsule. They eventually reach the sen- STRUCTURE AND FUNCTIONS. 51 sory area of the rortex already described. The centre for the masticatory muscles is contiguous and anterior to the facial centre in the cortex. The relation of the fifth nerve to the sense of taste is important, but our knowledge of the gustatory tract is very uncertain and incomplete, because of its compli- PLOOR OF FOURTH vawTRIGLft FIG. 31. Diagram of section through middle of pons, showing origin of the trigeminus. V Sens., sensory nucleus of the fifth ; V M, motor nucleus of fifth ; M Root, motor root of fifth; V, fifth nerve ; P.L.B., posterior longitudinal bundle. V D, Descending root of fifth nerve (" trophic " root). cated connection with two other cranial nerves, viz. : the seventh and the glosso-pharyngeal. Some idea of this complexity may be obtained from the diagram given in Fig. 54, which shows the probable course of the taste fibres in the fifth and facial nerves, as determined by pathological studies in man. From this arrangement we can see how section of the 52 DISEASES OF THE NERVOUS SYSTEM. lingual branch of the fifth in one part of its course will abolish taste in the anterior part of the tongue, on one side, and how disease in a certain part of the trunk of the facial nerve produces the same result. There are recorded cases of disease of the root of the fifth nerve in which taste was abolished, not alone in the anterior part of the tongue, but on one entire side. This would lead one to suppose that all of the taste fibres are to be found in the root of this nerve, and although we know there are taste fibres in the peripheral distribution of the glosso- pharyngeal, we have some evidence that there are none in its root. Hence there is a strong probability that the taste fibres of the glosso-pharyngeal- also take a devious course, through its connections with certain ganglia, and ultimately reach the brain by way of the root of the fifth nerve, together with all of the other taste fibres. The Seventh or Facial Nerve. — This nerve is sec- ond to none of the cranial nerves in the importance of its diagnostic relations, and hence deserves careful consideration. The muscles supplied by fibres from the facial nerve are as follows : Occipito-frontalis. Muscles of the external ear. Stylo-hyoid, Posterior belly of digastric. All of the facial muscles. Platysma. Stapedius. Tensor of palate and azygos uvulae (possibly). The nerve takes a winding course from its superficial origin at the lower margin of the pons, between the olivary and restiform bodies, to its point of exit from the stylo-mastoid foramen, passing through the Fallo- pian canal of the temporal bone. Within the Fallopian STRUCTURE AND FUNCTIONS. 53 canal the nerve is separated from the middle ear by only a thin lamina of bone pierced by foramina for a small artery, the chorda tympani and the nerve to the stape- dius. This fact is of importance, because it explains how inflammatory processes in the middle ear may ex- tend by contiguity to the facial nerve, with resulting paralysis. The angle or knee made by the seventh nerve at the hiatus of the bony canal is the site of the geniculate ganglion, from which passes the great superficial petrosal nerve to reach the spheno-palatine ganglion by way of the Vidian canal. The facial and auditory nerves are very close together at their superficial origins, and are in proximity at the internal auditory meatus. Hence their liability to suffer together in lesions in this position. The nucleus of the seventh nerve lies beneath the floor of the fourth ventricle a little external to the for- matio reticularis, just back of the fillet, and between this nucleus and the superficial origin the fibre-bundle of the nerve runs a very devious course, enclosing the nucleus of the sixth nerve in a sort of loop. There is good reason for believing that some of the muscles supplied by fibres from the facial nerve are not represented in the facial nucleus itself, but in the nuclei of other nerves. This statement refers to the orbicularis palpebrarum and orbicularis oris. With regard to the first-named muscle it is well known that it is not paralyzed in facial paralysis due to damage in the path between the cortex and the nucleus, but only in paralysis from involvement of the nucleus or the nerve- trunk itself. The orbicularis palpebrarum may be repre- sented in some cell-groups adjacent to the third-nerve nucleus, as has been experimentally observed in some of the lower animals. 54 DISEASES OF THE NERVOUS SYSTEM. The orbicularis oris is a muscle which probably has a representation in the h}qDoglossal nucleus, because of the intimate association of the movements of the lips and the transverse muscular fibres of the tongue. The fibres from the facial nucleus to the cortex decus- sate in the pons just above the nucleus. Hence, in facial paralysis from a one-sided lesion above the middle of the pons the paralysis of the face is on the side opposite to the lesion, whereas in lesions below this level the paralysis is on the sai?ie side. The course of the fibres through the crus and internal capsule, and the facial cortical area have already been described. The Eighth or Auditory Nerve. — The auditory nerve is formed by the union of two sets of fibres derived respectively from the cochlea and vestibule and from the semicircular canals. These sets of fibres differ in func- tion, the former conducting sotind-waves, and the latter apparently serving to carry from the semicircular canals impressions relative to the movements and position of the body. Changes in bodily position probably cause changes in the pressure of the endolymph within the canals, which are transferred to the nerve-fibres. There is at present no evidence that the semicircular canals are concerned in any way with hearing, but the possibility of some con- nection with that function cannot be positively excluded. Within the internal auditory meatus and at the base of the brain the auditory nerve lies side by side with the facial nerve, as already mentioned. Its surface origin at the junction of the pons and medulla is by two roots, a superficial and a deep root. The former winds around the inferior cerebellar peduncle and contains some gray matter among its fibres. Some of its fibres appear to be continuous with the striae acousticse, which run above the floor of the fourth ventricle, but by far the largest part of STRUCTURE AND FUNCTIONS. 55 them pass to a large nucleus, the internal auditory nucleus, lying just beneath the floor of the fourth ventricle near the median line. (See Fig. 30.) The vagus nucleus lies close by, but farther down in the medulla. Just external to this internal nucleus is a group of cells and longitudi- nal fibres known as the external auditory nucleus, or Deiter's nucleus, and with it some of the fibres of the superficial root seem to be connected, although it is very doubtful whether this nucleus is actually related to the auditory function. Fibres from the superficial root pass into the restiform body, some seeming to follow the direc- tion of the restiform fibres, others appearing to have a transverse course through the restiform body to the teg- mentum of the pons. The superficial root is believed to subserve the conduction of sound-waves. The deep root of the eighth nerve passes inwards and upwards to the restiform body, some of its fibres going to the middle lobe of the cerebellum, and others to both the internal and external auditory nuclei. The fibres of this root probably convey sensations of equilibrium from the semicircular canals to the middle lobe of the cere- bellum. Injury to these canals or to this part of the cerebellum produces the peculiar motor disturbances observed in Meniere's disease and in lesions of the cere- bellum affecting its middle lobe. It is probable that the auditory path to the cortex of the brain decussates a short distance above or between the auditory nuclei, and passing upward through' the teg- mentum of the pons and crus occupies the hindermost part of the internal capsule. In the internal capsule it is adjacent to all of the other sensory tracts of the sensory crossway. The first temporal convolution is the cortical area for hearing, and is connected with the auditory apparatus of the opposite side. The left auditory area is 56 DISEASES OF THE NERVOUS SYSTEM. regarded as being especially related to the memory of words, its destruction producing the form of aphasia known as word deafness. The Ninth or Glosso- Pharyngeal Nerve. — The ninth nerve is distributed to the back part of the tongue, the soft palate, the upper part of the pharynx, and the Eustachian tube. Besides supplying taste-fibres to the posterior part of the tongue and motor fibres to the other parts mentioned, it probably also furnishes fibres of common sensation to these parts and to the tympanic cavity. It has already been stated that although taste-fibres are found in the peripheral portion of this nerve, they doubtless ultimately enter the brain with the fifth nerve. Considerable uncertainty also exists as to the motor function of the ninth nerve. The motor fibres to the upper part of the pharynx come through the pharyngeal plexus, but whether from the ninth or tenth nerve cannot be positively stated. The digastric branch of the seventh communicates with the ninth, and it is not improbable that the stylo-pharyngeus derives its motor supply from the former. Whether the ninth sends any motor fibres to the palate has not been determined. This uncertainty regarding the exact function of the ninth nerve is due mainly to the fact that in man the nerve is seldom damaged by disease or injury apart from other adjacent cranial nerves, and experiments on animals have not been altogether satisfactory. Thus it happens that the functions of the nerve are inferred from a study of its anatomical distribution — a method which is apt to be misleading. The deep and superficial origins of the glosso-pharyn- geal will be considered in conjunction with those of the tenth and eleventh nerves. STRUCTURE AND FUNCTIONS. 5/ The Tenth or Vagus or Pneumogastric Nerve. — This nerve has the widest distribution of any cranial nerve, supplying as it does the vocal and respiratory organs, the heart, most of the alimentary canal, and some of the abdominal viscera. It has both sensory and motor fibres. It sends sensory branches to the meninges along the middle meningeal artery to the posterior part of the external auditory meatus, to the pharynx, larynx, trachea, bronchi, heart, oesophagus, stomach, and intestines. Its motor fibres go to the pharynx and larynx. The vagus is the inhibitory and accelerator nerve of respiration and the inhibitory nerve of the heart. It contains also motor fibres for the oesophagus and in part for the stomach and intestines. After receiving many fibres from the spinal accessory nerve, the pneumogastric trunk passes down the neck in the same sheath with the carotid artery. Its pharyngeal branches unite with those of the ninth to form the pharyngeal plexus. It gives off the superior and inferior (recurrent) laryngeal nerves, which supply all the muscles of the larynx. In the abdomen it enters into numerous conjugations with the splanchnic nerve. The tenth nerve emerges from the side of the medulla just anterior to the restiform body, as a series of rootlets, the filaments of the ninth lying immediately above, and the root of the eleventh immediately below. The line of separation between these three nerves at their superficial origin is not sharply defined, and hence it is rare for any lesion at this point, even though small, to affect one of these nerves alone. A part of the Eleventh or Spinal Accessory Nerve joins the pneumogastric, and receives its title because of being accessory to the vagus. The filaments which arise in this close relation to the tenth nerve constitute the accessory portion, the spinal portion arising at a wide interval, from 5! DISEASES OF THE NERVOUS SYSTEM. a lower level, in the anterior horn of the spinal cord. It is the accessory portion of the eleventh nerve which supplies the pneumogastric with its motor laryngeal fibres. The central origin of the ninth, tenth and eleventh nerves is from a continuous series of cell-nests forming a longitudinal, narrow, gray column, which lies just ex- ternal to the eminentia teres of the fourth ventricle, with its long axis running FLOOR or rouRTH FIG. 32. downward from the level of the auditory nucleus above. Some of the upper cells of this column give origin to the ninth, the middle cells to the tenth, and the lowest cells to the accessory por- tion of the eleventh nerve. From these Diagram of a transverse section through the grOUpS of CClls the medulla at the lower level of the fourth ventricle. Especially to be noted are the tenth and twelfth fibres TUn OUtward nerves and their nuclei of origin, the position of the olivary nucleus, the fillet, the anterior pyramids (the thrOUgh the formatlO motor path), the restiform body, and the ascending . . r i- root of the fifth nerve. Between the olive in front reticularis Of the and the tenth and twellth nuclei behind lies the j n l • substantia reticularis (the path of common sensi- meQUlla tO their bility). The posterior longitudinal bundles lie on - . . . . either side of the median line between the twelfth SUpertlCial OrigmS, "^'^^'" as described. In passing through the medulla these bundles of fibres traverse the ascending root of the fifth nerve, and this fact furnishes an anatomical explanation for some of the reflex relations of the fifth nerve. The spinal portion of the eleventh nerve rises from the upper cervical portion of the spinal cord, by a series of filaments from the anterior horn, and then takes £ STRUCTURE AND FUNCTIONS. $g unique course upwards into the cranial cavity, to tempo- rarily join the accessory portion before again passing out of the cranial cavity to supply the trapezius and sterno- cleido-mastoid with motor-fibres. It is in reality only a modified motor spinal nerve. It supplies these two mus- cles in conjunction with branches from some of the cervical nerves proper. T/ie Twelfth or Hypoglossal Nerve. — This is a purely motor nerve destined for the muscles of the tongue and for most of the muscles connected with the hyoid bone. It arises from the medulla between the anterior pyramid and olivary body, by a series of filaments which are in line with the motor roots of the spinal nerves and immediately adjacent to the rootlets of the eleventh. The twelfth pair are separated at their superficial origin by the prominent anterior pyramids, and are rarely involved together by disease external to the medulla. The eleventh and twelfth are so closely associated at their origin that they are frequently involved together, the result being paralysis of the tongue and vocal cord of the same side. The nucleus of the hypoglossal nerve is a long column of motor nerve-cells extending from the level of the lower angle of the fourth ventricle (calamus scriptorius) downward to the decussation of the pyramids. It lies close to the median line, and, in part of its course, just internal to the spinal-accessory nucleus. To reach the surface of the medulla, the fibres pass from the nucleus forward and outwards, through the formatio reticularis, and between the olivary nucleus and the anterior pyra- mid, some of the fibres generally traversing the former. The Meninges of the Brain and Cord. — There are three membranes which enclose the central nervous system. The outer or dura mater is the thickest. It is 6o DISEASES OF THE NERVOUS SYSTEM. formed of dense fibrous tissue, and in the vertebral canal is separated from the bony walls by a layer of fat and a plexus of large veins, while in the cranium it is closely approximated to the bones. The spinal dura is thus a loosely suspended long sac, attached only slightly to the spinal canal on its anterior surface. This outer space in the spine is called the epidural space, and is not con- nected with an analogous space in the skull. The dura has comparatively few blood-vessels, but is well supplied with lymphatics and with sensory nerves (in the skull by the fifth and ninth nerves, in the spine by filaments from the posterior roots). The inner surface is lined by endo- thelium and encloses the lymphatic subdural space, which contains a variable amount of serum. The middle mem- brane is the arachnoid, delicate and with few blood- vessels and no nerves, enclosing what is known as the lymphatic subarachnoid space. It is lined with endo- thelium on both surfaces. On the brain the arachnoid is separated from the innermost membrane, or pia mater, between the convolutions, where the latter dips down into the sulci ; but the separation between the two is com- plete in the spinal canal. There is no direct communi- cation between the subdural and subarachnoid lymph- spaces, but there is a free communication between the ventricles of the brain and the latter space by means of the foramen of Magendie and two smaller foramina in a part of the membrane projecting dorsally into the fourth ventricle. The base of the brain, therefore, lies upon a sort of water-bed, being separated from the base of the skull by an interval occupied by subarachnoid fluid and trabeculae. The nerve-roots and basal blood- vessels are thus carefully protected from certain forms of injury. The pia mater is a delicate membrane extremely rich in STRUCTURE AND FUNCTIONS. 6l blood-vessels, lymphatics and vaso-motor nerves. It dips down between the convolutions of the brain, and sends connective-tissue septa into the cord. The blood- vessels and nerves pass inwards from this membrane to the central nervous system, while the lymphatics com- municate externally with the subarachnoid space. The whitish granulations, known as Pacchionian bodies, which are seen upon the surface of the mem- branes on each side of the median line of the vertex of the brain, are connective-tissue villi which subserve the outflow of cerebro-spinal fluid from the subdural and subarachnoid spaces into the longitudinal and other dural sinuses. The Blood-Supply of the Spinal Cord and Brain. — Branches from the vertebral, intercostal, and other arteries enter the spinal canal with the spinal nerves. Anterior branches pass along the anterior nerve- roots to the anterior median fissure, where they join to form a continuous vertical vessel — the anterior spinal artery. Branches pass to the bottom of the fissure and enter the cord, dividing into lateral twigs at the anterior commissure, which are destined for the anterior horn and partly for the lateral column. Ramifications are made by both the anterior and posterior arteries in the pia mater, and twigs are given off everywhere to the white substance of the cord along the connective-tissue septa. The posterior arteries send branches into the caput cornu posterioris, where they take vertical courses. The veins have a very similar arrangement. Combin- ing to form anterior and posterior spinal veins, these empty their blood into the large venous plexuses of the epidural space. These plexuses receive blood also from the vertebrae and even from the skin and subcutaneous structures of the back, finally delivering it to the verte- 62 DISEASES OF THE NERVOUS SYSTEM. bral and intercostal veins. The tortuous course of the arteries destined for the spinal cord and the large size of the venous plexuses undoubtedly protect those por- tions of the central nervous system from the dangers of high pressure, over-distension, and rupture. The blood-supply of the brain is of far greater practi- cal importance to the physician than that of the spinal cord. It is derived from the carotid and vertebral arte- ries. The courses of the left carotid and of the left vertebral are much nearer a direct line from the heart than those of their companions of the opposite side, a fact which renders them more liable to receive embolic plugs washed away from the endocardium. On each side the internal carotid divides into the anterior and middle cerebral arteries, while the basilar artery, formed by the two vertebrals, redivides into the two posterior cei'ebral arteries. These three arteries, the anterior, middle, and posterior cerebral, supply each hemisphere in the regions designated by their name (page 63). Practically the middle cerebral or Sylvian artery is of especial importance, for, coursing through the fissure of Sylvius, it is distributed over the motor area of the cortex. Hence the hemiplegia so often produced by embolism and by thrombosis of this artery. Although it has anastomoses with branches from the other arteries on the surface of the brain, they are rarely sufficient for the establishment of a collateral circulation. The branches sent by these superficial vessels are short ones for the cortex, and long ones for the white matter. They enter straight into the cerebral substance from the pia and have very little communication with each other, and none with the vessels entering the base of the brain from the circle of Willis. The central arteries are those given off from the circle STRUCTURE AND FUNCTIONS. 63 FIG. 33. Area of cortex supplied by the branches of the middle cerebral artery. FIG. 34. Area of cortex on outer surface of hemisphere supplied by the anterior cerebral artery. FIG. 35. Area of cortex on inner surface of hemisphere supplied by the anterior cerebral artery. The dotted lines separate areas supplied by different branches of the artery. FIG. 36. Area of cortex on the outer surface of the hemisphere supplied by the posterior cerebral artery. FIG. 37. Area of cortex on the inner surface of the hemisphere supplied by the posterior cerebral artery. The dotted lines sepa- rate areas supplied by different branches of the artery 64 DISEASES OF THE NERVOUS SYSTEM. of Willis and from the first part of the trunks of the three cerebral arteries, and furnish the blood-supply for the basal ganglia and adjacent white substance. These ves- sels have no anastomoses within the brain. The most important of the central arteries is the group given off within the first inch of the trunk of the middle cerebral artery, and known as the " lateral group." They come off at a right angle from the main artery, and, entering the anterior perforated space, just in front of the optic tract and behind the roots of the olfactory nerve, are fk;. 38. Diagram of the blood supply ol the central ganglia and internal capsule. Mid. C, middle cerebral artery; E E, external, I, internal, lenticulo-striate arteries: III V, third ventricle. (After Buret.) distributed to part of the caudate nucleus, to the lenticu- lar nucleus, the internal capsule, and to part of the optic thalamus. The anterior vessels of this group ar.e sometimes called the lenticulo-striate and the posterior the lenticulo-thalamic arteries. It is one of these vessels which is so liable to rupture and produce serious symp- toms of cerebral hemorrhage. The pons, medulla and cerebellum derive their arteries from the vertebrals and basilar. The veins from the outer and median surfaces of the hemispheres course STRUCTURE AND FUNCTIONS. 65 upwards to enter the superior longitudinal sinus, while those from the base of the brain empty into the cavern- ous, petrosal and lateral sinuses. The veins of Galen, carrying blood from the choroid plexuses and walls of the ventricles, and from the upper surface of the cere- bellum, terminate in the straight sinus. There are free anastomoses between all of the sinuses, and there are also communications between them and veins outside the cranial cavity. Thus, the ophthalmic vein enters the cavernous sinus ; veins from the nose pass into the superior longitudinal ; veins from the diploe of the skull communicate freely with various sinuses ; some of the mastoid veins open into the lateral sinus ; veins from the internal ear reach the superior petrosal sinus ; and there are even numerous communications, some direct, others indirect, between veins of the face, scalp, and neck" and the cerebral sinuses. The spinal venous system is con- nected with that of the brain by six veins. The cerebral veins and sinuses have no valves. Cranio-Cerebral Topography, Spinal and Spinal-Cord Topography. — A knowledge of some of the relations of certain parts of the surface of the brain to the skull is of practical importance in diagnosis and for surgical purposes. The accompanying Siagram illustrates sufficiently well the general correspondence between the chief convolutions and fissures and the cranial bones. It will be noted that under the frontal bone lies three fourths of the first frontal convolution, about five sixths of the second, and nearly all of the third frontal convolution. Under the temporal bone lies all of the temporal lobe, except its most anterior and its most posterior portion. Under the occipital bone lies about one half (posterior) of the occipital lobe. The parietal bone covers what remains of the cortex. 66 DISEASES OF THE NERVOUS SYSTEM. The fissure of Rolando is the part of the brain which it is the most often necessary to locate. The upper end of the fissure is best found by measuring the distance from the root of the nose (glabella) to the external occipital protuberance (inion) along the middle line. A point one half inch posterior to the middle point of this dis- tance marks the upper extremity of the fissure. The fissure of Rolando in its upper two thirds makes an angle of 67° with the median line, in its lower one third the fissure is a little more vertical' The average length of the fissure is about three and a half inches. The central convolutions occu- py about an inch an- terior and posterior to the fissure, and the positions of the leg and face cen- tres may thus be ap- proximately located. What is known as the Sylvian line extends from the external angular process of the frontal bone to a point three quarters of an inch below the most prominent part of the parietal boss. The posterior limb of the fissure of Sylvius lies under the posterior three fifths of this line. The anterior limb of the fissure of Sylvius ascends almost vertically from the Sylvian line from the middle of the zygoma. A continuation of the Sylvian line back- ' The position of this fissure may be conveniently indicated on the skull by the use of a graduated steel tape, on which a piece of steel tape about four inches long slides at an angle of 67°. FIG. 39. Diagram showing the relation of the convolu- tions to the skull. STRUCTURE AND FUNCTIONS. 67 wards to the sagittal su- ture marks the position of the parieto-occipital fissure. A knowledge of the re- lations of the various seg- ments of the spinal cord to the spines of the verte- brae is essential both for the diagnosis and success- ful treatment of certain spinal cord affections. These relations vary somewhat in different individuals, but one de- scription is sufficiently accurate for practical purposes. The chief facts may be deduced from the accompanying drawing. These facts are as follows : 1. The spinal cord in the adult terminates about the lower border of the first lumbar vertebra (in children one to two years of age the cord extends as low as the third or fourth lumbar vertebra). 2. The different pairs of nerves, excepting the upper cervical nerves, leave the vertebrae from which they are named at The mutual relations of the vertebral bodies and spines to the segments of the cord and to the exit of the nerves (Gowers). 68 DISEASES OF THE NERVOUS SYSTEM. a lower level than that at which they are given off from the corresponding segments of the cord. This difference in the level of exit and origin of the nerve- roots increases from above downwards.' The first, second, and third cervical spines correspond in level to the origins from the cord of the third, fourth, and fifth cervical nerves. Between the fourth and fifth spines arises the sixth pair ; between the fifth and sixth, the seventh cervical pair. The seventh cervical spine is opposite the first dorsal segment. The fifth, sixth, seventh, eighth, ninth, and tenth spines correspond, nearly, to the seventh, eighth, ninth, tenth, eleventh, and twelfth nerve-roots and spinal segments. The first lum- bar nerve arises opposite the eleventh dorsal spine. The first sacral nerve arises just above the first lumbar spine. 3. The cervical enlargement of the cord corresponds very closely to the cervical spines. The lumbar enlarge- ment corresponds to the tenth, eleventh and twelfth dorsal and to the first lumbar spines. ' It is convenient at times to know the e.\:act lengths of certain of these nerves (especially the lower ones) between their origin and their exit from the spinal canal. It is easy to remember that the course of the third lumbar is about three inches, and that of the fifth lumbar about five inches. CHAPTER II. THE SYMPTOMATOLOGY OF NERVOUS DISEASES. The symptoms of organic disease of the nervous sys- tem, though exceedingly varied, can for the most part be referred to the operation of a small number of funda- mental mechanisms. In the first place an important class of symptoms result from the destruction, complete or in- complete, of nervous structures. Complete destruction of a portion of the nervous sys- tem always results in complete loss of function of the part involved. This loss of function is permanent except in cases where neighboring parts of the nervous system make up the loss, to some extent, by compensation. In adults extensive compensation can occur only in the brain, some functions of which are diffuse — that is, dependent on the activity of a large number of cells scattered over a wide area. Thus a destructive lesion in the frontal lobe of the brain, which is chiefly concerned with higher intel- lectual processes, does not cause any special loss of func- tion, but simply a general lowering of its functional activity as a whole. The restoration of speech which occurs in children in whom the motor speech centre of the left side has been destroyed, is a good example of compensation, which, in this instance, occurs in corre- sponding structures of the opposite hemisphere. Com- pensation is limited, where, as in the cord and the medulla, and some parts of the brain, a particular function is per- 69 70 DISEASES OF THE NERVOUS SYSTEM. formed only by certain sharply limited structures, and these are destroyed. Partial damage of nerve elements also gives rise to loss of function, which may be of any degree of severity. The following are the chief causes of structural damage to nerve elements : 1. Mechanical Injury. — Mechanical damage may cause destruction of cells and fibres, or interruptions in their continuity. Hemorrhage or trauma are the chief causes of such mechanical lesions. There is absolute loss of function of the parts thus injured. An important form of mechanical injury to nervous structures is pressure. The severity of the effects of pressure depend largely on the rapidity of its production. A considerable degree of pressure, if of very gradual development, may give rise to little functional disturb- ance. Thus the entire motor area of the brain may be gently compressed by slow subdural or subarachnoid hemorrhage without giving rise to motor paralysis. Again, the spinal cord may be slowly compressed by Pott's disease to a surprising degree with little or no interference with the functions of the cord. A slight grade of pressure, on the contrary, if rapidly brought about, does far more damage to the nerve elements, and may cause immediate loss of function. 2. Loss of Blood Supply, Partial or Complete. — The loss of function is complete, if the blood supply is arrested ; partial, if there is merely diminution in blood supply. In both cases the effect comes on very rapidly if the interference with the circulation be sudden. Where the interference is gradual, the effects are of more gradual onset and of less severity, probably because there is time for the establishment of a collateral circulation. Both cells and fibres suffer from diminished blood sup- SYMPTOMATOLOGY OF NERVOUS DISEASES. 7 1 ply, but not equally. The nerve-cells are in general far more sensitive to the effects of deficient blood supply. For example, if the blood supply to the spinal cord of the rabbit be cut off by compression of the abdomi- nal aorta, the motor ganglion-cells cease to functionate at once, but the white matter shows no reaction at first. If the circulation is restored after half an hour, the cells recover function : if not, necrotic changes begin, first in the cells, later in the white matter. 3. Inflammation, which involves the nerve and fibres (parenchyma), the blood-vessels, and usually the intersti- tial tissue. The process may be acute or chronic ; in the latter case the changes begin in interstitial structures, and secondarily damage the nervous elements. 4. Wasting of Nerve Elements. — A very frequent cause of the destruction of nervous tissues is the degen- eration which affects cells and fibres. Often degenerative changes occur in these structures as a consequence of inflammation of interstitial tissues, but in a large and im- portant class of cases the changes in the cells and fibres are primary. Many symptoms however of nervous disease, result not from destruction of nerve elements but from their irritation. This irritation usually expresses itself by an increase of action, or functional overaction, as, for example, in convulsive movements, or hypersesthesia. But irritation does not always result in overaction ; it may lessen function by the process termed inhibition. A good example of this effect of irritative inhibition is the loss of the knee-jerk which follows immediately on a severe mechanical injury to the spinal cord above the lumbar enlargement, say in the cervical region. The important difference between the diminution or loss of function which results from irritative inhibition and that which results from a destructive lesion, is that the former 72 DISEASES OF THE NERVOUS SYSTEM. is temporary, the latter permanent. It is important to remember that the effects of destruction and those ol irritation are often met with in combination, as for ex- ample when a tumor causes both paralysis and spasm. The mechanisms which have been mentioned as pro- ductive of symptoms relate mainly to organic diseases. There is a large and important class of symptoms which cannot be referred to structural changes in the nervous elements but which probably depend upon changes in their nutrition, changes of whose nature we at present know little. Motor Paralysis. — Loss of voluntary muscular power (paralysis) may result from disease involving any part of the motor path — its upper segment or its lowei segment (p. 24). Thus, paralysis may arise from dis- ease of the motor cortex, of the motor path in the cen- trum semiovale, internal capsule, crus, pons, medulla, or cord (upper segment), or from disease of the anterior cornual cells, anterior nerve-roots, motor nerves, or mus- cle plates (lower segment). Disease in other parts of the nervous system than those enumerated does not cause motor paralysis, unless it does so by giving rise to pressure on these structures. Paralysis may or may not be associated with wasting or atrophy of the muscles paralyzed, according to the position of the lesion. In general it may be said that paralysis and marked atrophy are rarely associated in disease involving the cerebro-spinal or upper segment of the motor path (p. 24), and that they are nearly always associated in disease of any part of the lower segment (ganglion-cells, nerve-roots, or nerves). The varieties of paralysis according to distribution are without number, but certain typical forms are of SYMPTOMATOLOGY OF NERVOUS DISEASES. 73 FIG. 41. Diagram showing the effect of lesions at different levels of the motor path. A small lesion at some point, A, between the cortex aud the internal capsule, will cause a local paralysis — a lesion at A would cause a brachial monoplegia; a lesion at B will produce hemiplegia (complete) on the side opposite the lesion; a lesion at C would cause paralysis of the Hid nerve on the sa7>ie side, and of the face. .irm. and leg on the opposite side ; a lesion at D would cause hemiplegia on the opposite side ; a lesion at E would cause paralysis of the face on the satne side, of the arm and leg on the opposite side; a lesion at F, paralysis of arm and leg on the opposite side (and perhaps of the Xllth nerve on the same side — Xllth nerve not represented) ; a lesion at G would cause paralysis of the arm and leg on the same side. 74 DISEASES OF THE NERVOUS SYSTEM. practical importance from their diagnostic significance and frequent occurrence. Hemiplegia. — Hemiplegia is the paralysis of several groups of muscles of one lateral half of the body. In its most common form there is loss of voluntary motion involving face, tongue, arm, and leg on the same side — complete hemiplegia. Such hemiplegia may result from a lesion a?iyzuhere in the motor tract bctiveen the cortex and the po?is. In the pons and crus the fibres of the motor tract are so close together that a lesion practically always involves all the fibres of the tract, and complete hemi- plegia results. In the internal capsule the fibres begin to spread out, and a lesion here, if very small, may fail to involve all its fibres, thus giving rise to an incomplete hemiplegia, but this is of rare occurrence, and complete hemiplegia is the rule. The motor fibres are more and more widely separated in their course through the corona radiata to the cortex. Hence in these situations, even a lesion of considerable size may fail to affect all the parts of one side, — face, tongue, arm, and leg. Thus it is not rare for the face and leg to escape entirely, the arm being paralyzed alone. Such a paralysis is called a brachial ''monoplegia." Other monoplegias, — -face and arm, arm and leg, but not face and leg, occur from single lesions. In complete hemiplegia the paralysis is said to affect all of one side, but this is not strictly true, for the whole of one side is not involved. Thus the upper facial mus- cles, orbicularis palpebrarum and occipito-frontalis, move almost or quite as well as on the paralyzed side, and the muscles of the eyeball and the muscles of mastication are unaffected. The tongue deviates as a whole towards the paralyzed side, when protruded, because the pro- jecting apparatus of that side is weakened and does not SYMPTOMATOLOGY OF NERVOUS DISEASES. 75 oppose the genio-hypoglossus of the opposite side ; but the tongue itself is rarely paralyzed. The muscles of respiration and the muscles of the face and trunk are unaffected in ordinary action, though if the patient take a deep respiration, there is defective chest expansion on the paralyzed side. In general it may be said that in hemiplegia the extent of the paralysis in a part is proportioned to the degree in which that part is capable of unilateral use. Thus the muscles of one hand are habitually employed alone, are chiefly innervated from one side of the brain, and suffer severely ; while the intercostals of one side are never used by themselves, are enervated from both hemispheres, and escape in hemiplegia. The leg, which though generally used with its fellow, is capable of some unilateral use, and is represented to some extent in both hemispheres, suffers less, and usually recovers more power than the arm. This recovery is through compensation (p. 69) by the normal hemisphere, and in early life is usually extensive. Recovery is more rapid in the arms and thighs than in the hands and feet. The hemiplegia is always on the side opposite the lesion. This is explained by the cross- ing of the pyramids in the medulla. A few exceptions to this rule have been recorded, but it is probable that these exceptions were apparent rather than real. Double hemiplegia, paralysis is of all four extremities and the face (this is really a paraplegia), may result from two extensive lesions, or a single diffuse lesion covering both hemispheres. In the inconsistent nomenclature of the day a double hemiplegia is called a "diplegia." Common hemiplegia, such as has been described, is not usually accompanied with hemianaesthesia, but is com- monly associated with partial loss of tactile sensibility in the extremities. ']6 DISEASES OF THE NERVOUS SYSTEAf. The processes which most frequently give rise to hemiplegia are cerebral hemorrhage, acute softening, tumor and abscess. Instead of the face, arm and leg being paralyzed on the same side of the body, it is not very rare for the face to be paralyzed on one side and the limbs on the other. This condition is known as crossed hemiplegia (also im- properly termed " alternate " hemiplegia). It occurs when a lesion is so placed that it interrupts the motor path to the limbs above its decussation in the medulla, and the downward facial path of the same side after it has crossed the median line from the opposite facial tract. As this crossing of the facial path occurs about the level of the middle of the pons, the interruption can happen only when the lesion is in the lower half of the pons. (See Fig. 41.) This form of paralysis is crossed hemiplegia in the restricted sense of that term. Taken in a wider sense, the term refers also to the paralysis of one or more of the other cranial nerves on one side, with paralysis of the extremities of the opposite side. The nerves most frequently involved in this way are the third, sixth, and seventh. If the third nerve is paralyzed on one side, and the face and limbs on the other, the lesion is in the crus on the side of the nerve, and this is the only situation in which a lesion can cause such a paralysis. In such cases the face paralysis has the usual characters of a peripheral facial palsy ; involvement of both upper and lower muscles of the face, RD, etc. It sometimes happens that a lesion at a level which makes crossed hemiplegia possible is so small, or is so placed, that it simply involves the motor tract to the limbs, and the cranial nerves or nerve tracts escape. In other words, hemiplegia from disease in such a region is by no means always crossed hemiplegia. SYMPTOMATOLOGY OF NERVOUS DISEASES. 7/ Spinal Hemiplegia is a type of hemiplegia that results from lesions interrupting the motor path of one half the cord. Both arm and leg are involved when the lesion is high in the cord. When the lesion is below the brachial enlargement one leg only, that on the side of the lesion, is involved. The palsy is then termed a "hemiparaplegia," and may be classed either as a hemi- plegia or as a paraplegia. Strictly speaking, it is a crural monoplegia. The unilateral lesion which causes spinal hemiplegia is seldom confined to the motor tract. Hence there is commonly anaesthesia below the level of the dis- ease, and this always on the side opposite the lesion and the motor palsy. In the cases where there is no anaesthesia, this condi- tion of spinal hemiplegia must be carefully distinguished from the combined arm and leg paralysis which results from cerebral disease. Spinal hemiparaplegia is also termed Brown-Sequard's paralysis. Paraplegia in its widest sense signifies a symmetri- cally bilateral paralysis, but the term is generally used to designate a particular form — paralysis of both lower extremities. When all parts below the head are paralyzed the con- dition is termed cervical paraplegia. In this state the intercostal muscles are involved and respiration is dia- phragmatic. Anaesthesia may or may not accompany paraplegia, and there may or may not be involvement of the bladder and rectum. The conditions which determine the presence . or absence of these symptoms will be discussed elsewhere. Paraplegia is most frequently a symptom of spinal cord disease (usually myelitis) but may result from disease else- where. In the pons and medulla the motor tracts are 78 DISEASES OF THE NERVOUS SYSTEM. close together, and it sometimes happens that a lesion there has sufhcient transverse extent to involve the fibres of both sides. Then paraplegia results. More rarely bi- lateral involvement of the crura leads to a similar result. Occasionally paraplegia results from bilateral disease of the motor area of the cerebral cortex. It has been al- ready alluded to as double hemiplegia. Ordinary para- plegia involving both lower extremities only, may result from a localized process of disease, such as a tumor, located in the great longitudinal fissure so as to damage the paracentral lobule of either side. Paraplegia is not an uncommon occurrence in periph- eral nerve affections. Lesions of the cauda equina and multiple neuritis ordinarily give rise to it. But paraplegia is not always referable to organic dis- ease. There is a form known as hysterical paraplegia which is a functional affection. Paraplegia dependent upon idea is closely allied to hysterical paraplegia but may occur independently of hysteria, and is apt to be associated with general debility and mental anxiety. Reflex Paraplegia, also called " urinary paraplegia," is a transient variety supposed by some to be due to anaemia of the cord, caused by reflex irritation from the genito-urinary tract. While the possibility of such a form cannot be denied, it must be admitted that instances of it are extremely rare. Slight organic lesions may readily have been the actual basis for the symptoms in many of these cases. Ischaemia of the lumbar region of the cord is certainly competent to cause paraplegia, and this is probably the mechanism of those temporary paralyses which follow excessive muscular exertion in walking. It is certainly the mechanism of those very rare paraplegias which follow compression of the abdomi- nal aorta. SYMPTOMATOLOGY OF NERVOUS DISEASES. 79 Monoplegia signifies paralysis of one limb, or of one side of the face, and according to the part involved the paralysis is termed a brachial monoplegia, a crural mono- plegia, or a facial monoplegia. A monoplegia may arise from a cerebral, spinal, or peripheral lesion. A localized paralysis is a palsy confined to a particular muscle, or to one or more groups of muscles. When all the important muscle groups of an extremity are involved, the palsy is a monoplegia, though no sharp line can be drawn between the two forms of paralysis. There are certain general facts about the distribution of paralysis which aid one in determining whether a palsy be of peripheral, spinal, or cerebral origin. If the paral- ysis be confined to a muscle or set of muscles known to be innervated by a single nerve trunk or branch, the paralysis is unquestionably peripheral. If groups of muscles having a certain function in common are in- volved, as, for example, the flexors or extensors of the wrist, the lesion is probably in the anterior cornua of the spinal cord or in the anterior nerve-roots, because in these situations we have represented muscular groups related to particular functions rather than particular nerves. But this rule is not universally applicable. When paralysis involves all the muscles of an arm or leg— that is, of a segment of the body, the seat of the lesion is probably in the upper portion of the motor path, for here we have represented segments of extremities rather than individual muscles or particular groups of muscles. While these indications of the general position of the lesion derived from the distribution of the paralysis are often insuffi- cient, they should always be taken into consideration. It is to be noted that paralysis when due to lesions of the central nervous system is usually referable to disease of a definite region. This is especially true of localized So DISEASES OF THE NERVOUS SYSTEM. paralysis, which is consequently often spoken of as a focal symptom, in distinction to symptoms which, like general convulsions, point to an extensive disturbance of function, and are hence called diffuse. This distinction between focal and diffuse symptoms is useful, but cannot always be made in practice. For example, some symptoms may be at one time focal, at another diffuse. This is the case with headache and with optic neuritis. The term paralysis is correctly applied to all grades of motor loss, from slight weakness to complete abolition of function. Sometimes, however, the word is used only to designate the severest forms of loss, the term " paresis " being applied to slight grades of weakness. There is no difference of quality or character between paresis and paralysis ; the difference is purely one of degree. It is of course necessary to distinguish between the loss of voluntary motion due to defective innervation — paralysis — and that referable to injuries, muscle disease, joint disease, etc. — pseudo-paralysis, as it is sometimes called. Convulsions. — By this term is generally understood involuntary paroxysmal, purposeless, muscular contrac- tions, of variable intensity and duration, and of extensive or limited distribution. Convulsions may occur in consequence of disease situated in the cerebrum, pons, medulla, or spinal cord, but they are particularly frequent in cerebral disease, and their relation to such disease is of especial importance. They may arise (i) as the result of active irritation of brain tissue, such as occurs in meningitis, encephalitis, and active brain tumors ; (2) in consequence of station- ary, non-active lesions, in which some nerve-cells are still able to generate nerve force, but do not possess the power of perfectly controlling its discharge ; (3) from spon- SYMPTOMATOLOGY OF NERVOUS DISEASES. 8 1 taneous discharge of nerve force, without determinable irritation in the cortex, as in epilepsy ; (4) from discharge of vaso-motor centres of the medulla, causing cortical anaemia (some cases of epilepsy). Convulsions may be local in their commencement — that is, confined to particular groups of muscles, and subse- quently become general, or they may remain localized, or they may be general from the beginning. General convulsions occur in organic disease of the brain, and from a large number of conditions external to and within the nervous system, which, when the ganglion- cells of the cerebral cortex are in a state of unstable equilibrium from defective nutrition or other cause, seem capable of determining a discharge of nerve force from them, though they are the seat of no structural changes. Thus, general convulsions are very commonly observed in idiopathic epilepsy, in uraemia, and especially in chil- dren at the commencement of febrile diseases, during teething, from gastro-intestinal disturbances, worms, etc. It is an important fact that a very large majority of all the cases in which general convulsions occur are tiot examples of organic disease of the brain. In organic disease of the brain convulsions are usually general in distribution when the lesion is not situated in the motor area of the cortex or the subjacent white mat- ter, and when the lesion is a diffuse process, such as meningitis or hydrocephalus. On the other hand, con- vulsions that are local in their commencement or remain limited in extent always indicate disease in or adjacent to the motor tract, and particularly disease in or very near the motor area of the cortex. The disease is usually structural in character, but in some instances no structural change can be detected to account for the local beginning, and here there are probably nutritional changes that give 6 82 DISEASES OF THE NERVOUS SYSTEM. rise to the local instability. In other words, localized convulsions constitute a focal symptom ; general con- vulsions a diffuse symptom. The general convulsions which are the result of organic disease of the brain bear a close resemblance to the con- vulsions of idiopathic epilepsy — that is to say, there is usually a period of tonic spasm, followed by a period of clonic spasm, during which the patient becomes suddenly unconscious. In local or partial convulsions the local onset is refera- ble to the nervous discharge commencing at the seat of irritation. Thus the spasm begins in one side of the face from irritation of the facial centre, and in the arm or leg from the irritation of their respective centres. When a convulsion is very slight it may be limited to the muscles in which it begins, and there is no loss of consciousness. If of greater severity, the spasm may extend gradually or rapidly to other parts of the side of the body on which it begins. In such cases consciousness may be lost. If the discharge of nerve force is of still greater severity the convulsions may involve both sides of the body, and in such cases there is generally loss of consciousness. Strictly speaking, it is probable that no convulsions are general from the very commencement. For example, even in infantile eclampsia and ursemic convulsions it is very common for the spasm to begin in one extremity a few seconds before it passes to the remaining half of the body or becomes general. True local convulsions (" Jacksonian epilepsy") repeatedly commence in one extremity, and, if they do not remain local, at least continue so for an appreciable time. It is not uncommon for a warning or aura to imme- diately precede a convulsive attack. The aura is usually sensory in character, and begins in the part which is SYMPTOMATOLOGY OF NERVOUS DISEASES. 83 afterwards the seat of convulsion. The sensation may ascend the limb first involved, and even pass to the second extremity affected before the convulsion comes on. Such sensory aurae undoubtedly result from a nervous discharge from sensory cells, analogous to that which occurs from motor nerve-cells. But we know that the motor area of the cortex contains sensory as well as motor cells and that disease situated in the motor area may give rise to convulsions which are ushered in with a sensor)^ aura — both aura and convulsions being doubtless due to discharge in adjacent cells. Hence it is probably correct to look upon all sensory aurae beginning in the face, leg, or arm as equivalent in diagnostic signifi- cance to a motor spasm having the same commencement. Aurs of the special senses — as a flash of light, a certain odor, or a sound — are not very uncommon in idiopathic epilepsy, but they are of relatively rare occurrence in organic disease of the brain. AVhen they do occur they indicate that the lesion is near or in the special sense centre of the cortex corresponding to the aura — in the occipital lobe when there is a visual aura, etc. Slight weakness in the part or parts involved is usual after a convulsion. If the convulsions recur frequently, at short intervals, the weakness ma^/ be very decided, but in any case it soon wears away. If the con' ulsion hap- pens to involve the extremities of one side cf the body, the paresis is, as might be expected, hemiplegic, but is readily distinguishable from hemiplegia by wearing off within twenty-four hours or earlier. The weakness fol- lowing convulsion is called " post convulsive paralysis." It is explained on the supposition that a severe convulsive seizure exhausts the ner\-e-cells related to the part. As to the diagnostic significance of local convulsions, it may be said that this is the same whether the convul- 84 DISEASES OF THE NERVOUS SYSTEM. sions remain localized or subsequently become unilateral or general. In either case they are strongly suggestive of organic disease. They do not quite prove the presence of structural disease, because, in rare instances, idiopathic epilepsy, ursemic convulsions, and diabetic convulsions may begin looally. But every case where convulsions be- gin locally should excite a suspicion of organic disease, and should lead to a minute and careful search for it. It is also to be noted that the significance of repeated local convulsions is not diminished by the occurrence of gen- eral convulsions at other times. Convulsions which are general from the commencement, on the contrary, point to idiopathic epilepsy. But they do not exclude the possibility of structural disease, be- cause general convulsions are not uncommonly symp- toms of organic diseases of the brain. In such cases the distinction must be made by establishing the presence or absence of other symptoms of organic disease ; it cannot be made from the character of the convulsions alone. Convulsions are occasionally met with in diseases of the spinal cord — generally at the outset of acute processes, especially myelitis, and polio-myelitis. They occur both in children and adults, and are more frequently the result of lesions in the cervical enlargement than in the lumbar enlargement or dorsal cord. The convulsions are general from the beginning, and are associated with pyrexia and other constitutional symptoms. Nothing definite is known of the pathology of these convulsions. General convulsions, besides being met with in organic diseases of the brain and spinal cord,. are observed in idio- pathic epilepsy, tetanus, uraemia, and hysteria. It is not very uncommon for hysterical convulsions to occur in the course of organic disease of the brain, and this sometimes leads to errors in diagnosis. Such convulsions not rarely SYMPTOMATOLOGY OF NERVOUS DISEASES. 85 result in the course of intracranial tumors ; occasionally they are seen in meningitis. Localized convulsions (monospasm, hemispasm) are much more frequently met with in intracranial tumor than in any other form of disease. The neoplasm causing them is usually situated very near the motor cortex. When the tumor is situated at a considerable distance from the motor area, the local convulsions are probably the result of meningitis over the cortex. Local convul- sions sometimes occur in cerebral abscess, when the tumor is beneath or near the motor cortex. They also oc- cur in infantile hemiplegia (hemorrhage and thrombosis). Convulsions are frequently classified on a purely me- chanical basis, according as they are tojiic or clonic in character. Such a distinction is useful clinically, for purposes of description, but does not as yet rest on any reliable pathological basis. A tonic or tetanic convulsion is one in which the mus- cular contraction continues for an appreciable but short period of time. Such spasm is met with in many condi- tions — for example, at the onset of an epileptic paroxysm, in some cases of petit mal, in hysteria and hystero- epilepsy, and in tetanus. Tetanic seizures, lasting for hours, or even days, sometimes result from disease involv- ing the gray matter in the floor of the fourth ventricle, and perhaps from cerebellar disease. The condition may closely resemble tetanus. Purely tonic spasm is observed in tetany, in which the flexors of the arms and legs are chiefly affected. The paroxysms usually occur several times daily and last min- utes or hours. They may be excited by pressure on the larger nerves or arteries (Treasseau's symptom). The mechanical and electrical irritability of the peripheral nerves is increased during the intervals. 86 DISEASES OF THE NERVOUS SYSTEM. Localized tonic spasm is sometimes a symptom of con- siderable importance. It is seen as trismus (spasm of the muscles of mastication), in tetanus (early symptom), in some cases of hysteria, and sometimes in meningitis. Tonic spasm of the calf muscles (cramp) is observed in hysterical, neurasthenic, and alcoholic subjects as a con- sequence of over-use of these muscles. Another form of tonic spasm is that of the sterno-cleido-mastoid, causing "wry-neck." When tonic spasm is of considerable duration or of gradual onset, it is perhaps more properly spoken of as rigidity, and will be considered under this title (p. 92), although it must be understood that a sharp distinction cannot always be made. Clonic convulsions are characterized by the rapidly in- termittent character of the muscular contractions which produce them. They are distinguished from tremor by being usually wider in range, less rhythmical in character, and of shorter duration ; but here again the distinction between the two kinds of spasm is not always absolute. Clonic convulsions occur in various forms in a great variety of morbid conditions of the nervous system, alone, or with those that are tonic. In the condition known as paramyoclonus multiplex we sometimes have examples of purely clonic convulsions. In this disease there is rapidly repeated clonic spasm occurring at varying intervals. The spasms vary from 50 to 180 per minute, and involve several muscles of a physiological group at once, thus giving the appearance of purposive action. The term "internal convulsions " has been applied, not inaptly, to conditions of muscular spasm in internal organs. Thus, the laryngeal spasm of rickety children, known as laryngismus stridulus, may be regarded as analogous to the general convulsions which sometimes occur in these SYMPTOMATOLOGY OF NERVOUS DISEASES. 87 same subjects. The spasm is thought to result from dis- charges from lower nervous centres in the medulla. Tremor. — Tremor or trembling may be defined as a rapid involuntary to-and-fro movement of a part, result- ing from the alternate and usually rhythmical contraction of antagonistic muscles. Tremor, in the strict sense of the word, is always an oscillation of narrow range. It may or may not be present when the part in which it oc- curs is at rest — most tremors are not then present. The tremor of paralysis agitans usually continues during rest, and the tremor which results from cold and from emotion originates when the body is at rest. The majority of tremors continue during voluntary motion and are in- creased by it. The tremor of paralysis agitans, however, may be inhibited by voluntary effort for a few and some- times for many seconds, but it recommences, notwith- standing continued effort of the will. The term "intention-tremor," borrowed from the Ger- man, is used to designate tremors which occur only during voluntary movement. Almost every form of tremor, excepting that of paraly- sis agitans and the tremor of fright and cold, begins when the extremity in which it occurs is extended and without support. Such extension of a limb requires voluntary effort, and, on this ground, the term intention-tremor may be made to include the majority of tremors, though it is generally restricted to those forms in which the tremor is originated by a voluntary movement. Such forms of tremor are seen in insular sclerosis and in mercurial poisoning. They are frequently wide in range and irregular in rhythm, and are then to be regarded as ataxic in character. Roughly speaking, the extent of a tremor is inversely proportional to its rapidity, but the same tremor may vary somewhat in range at different times. 88 DISEASES OF THE NERVOUS SYSTEM. There is considerable difference in the rapidity of dif- ferent kinds of tremor, and these differences are suffi- ciently constant to be of some diagnostic value. For instance, the tremor of alcoholism is rapid and varies from S to 1 1 per second, while in hysteria it usually varies from 7 to 8, and in paralysis agitans from 4 to 7 per second. Tremor is a symptom in a variety of diseases of the nervous system. It is sometimes the result of organic disease, but is commonly met with in diseases of a nutri- tional character, in which no structural changes in the nerve elements have been detected. Thus, it is seen on the one hand, in multiple sclerosis, after hemiplegia, in dementia senilis, and some forms of neuritis, and, on the other, after exhausting diseases, in neurasthenia, paralysis agitans, hysteria, and Basedow's disease. Very frequently it is a toxic symptom. As such it is seen in alcoholism, in poisoning from lead, mercury, opium, cocaine, and after the excessive use of tea, coffee, tobacco, and qui- nine. But tremor is also encountered in cases where no assignable exciting cause can be detected and in which there is no associated abnormal state. It is sometimes he- reditary, and may be present from early life. It may affect several members of a family, and it has been known to affect many members of a family through several genera- tions. Sometimes this simple tremor, as it is called, seems to be related to emotion or to prolonged anxiety, and not infrequently a neuropathic heredity can be traced. Sim- ple tremor has no tendency to shorten life or to influence the general health. The term senile tremor is applied to a fine tremor which occurs in extreme old age, but does not exhibit the rigidity and muscular weakness observed in paralysis agitans. It is doubtful whether this form of tremor is not really related to paralysis agitans, but it is SYMPTOMATOLOGY OF NERVOUS DISEASES. 89 sometimes classed as a simple tremor. Most tremors cease during sleep ; rarely a tremor is diminished or not stopped. The upper extremity is most frequently the seat of tremor, and the head is more frequently involved than the legs. With regard to the pathology of tremor nothing definite can be said. We know that when a voluntary movement is made, every contraction of one set of muscles is accompanied by a corresponding contraction of antago- nistic muscles. This arrangement serves to make motion even and regular, and is doubtless subserved by a close anatomical association in corresponding motor centres. A continuous voluntary muscle contraction probably consists of a series of single contractions following each other at very short intervals — due to innervation im- pulses from the central nervous system (cortex), which are liberated at the rate of about 10 or 12 per second, according to the position in which they are generated. So long as these impulses follow one another rhythmi- cally, and simultaneously reach the antagonistic mus- cles involved in a voluntary movement, the motion is a^ continuous one. But it is conceivable that the nice mechanism in which these simultaneous liberations of nerve force occur, may readily be slightly deranged by nutritional disease, which is far short of being structural, and that the parallelism of the innervating rhythm in opposed muscles would suffer slight derangement. The opposing muscles would then contract, not simulta- neously but alternately, and the expression of such alternation is tremor. But the disturbance of the gray matter in which motor impulses are generated is prob- ably not the only manner in which tremor may arise. Structural changes in the nerve fibres which conduct voluntary impulses, may damage the axis-cylinders 90 DISEASES OF THE NERVOUS SYSTEM. enough to modify without destroying their conductivity, and it is probable that some forms of tremor, as that of multiple sclerosis, and that of neuritis, depend on such interference with conduction. The majority of tremors, however, undoubtedly depend on nutritional, and, more rarely, on structural changes in motor ganglion-cells, and it is to the motor cells of the cerebral cortex that these tremors are most often referable. There is good reason to believe, though there is no positive evidence, that in paralysis agitans, dementia paralytica, in hysteria, fear, and in alcoholism, the tremor is of cortical origin. The physiological pathology of tremor being thus obscure, it is not strange that its diagnostic significance should be somewhat vague. Roughly speaking, tremor is to be regarded as one evidence (there are usually others) of functional derangement of motor cells, generally of the cortex, due usually to nutritional disease, sometimes to that which is structural. More cannot be said. In order to determine the location of the disease, and whether it is functional or structural, it is necessary to interrogate the conditions associated with the tremor. Not infrequently these points cannot be decided. Fibrillation. — Fibrillary contractions are involuntary contractions of small numbers of muscle-fibres. They give rise to no movements of the parts in which they occur, and are recognizable only when they occur in muscle-fibres which lie just beneath the skin. A fibrillary contraction appears as a small wave-like elevation run- ning rapidly along the muscle in which it occurs. When very extensive a considerable area may be the seat of successive small undulations. Fibrillary contractions are chiefly met with in the extremities, but are also seen in the muscles of the tongue and face. They may be of very frequent occur- SYMPTOMATOLOGY OF NERVOUS DISEASES. 9I rence, or may take place at considerable intervals of time, especially after muscular exertion. It is often easy to demonstrate them at a time when they are not occur- ring spontaneously, by cooling the skin or by gently tap- ping the muscle in which they occur. The mechanical irritability of the muscle-fibres is increased by most of the conditions which cause fibrillation. Fibrillation occurs under two distinctly different clini- cal conditions, — as the expression of general, slight, functional derangement of the nervous system, and as the result of a degenerative process in the muscle-fibres. Thus it is met with in neurasthenic persons who are free from organic disease, and after excessive exercise, or excessive venery. Under these circumstances the con- tractions are usually infrequent and not confined to any particular group of muscles ; but they are sometimes very persistent and frequent, with a tendency to involve particular muscle groups. On the other hand, almost any lesion which gives rise to degenerative muscular atrophy is capable of causing fibrillation in the atrophied- muscles. For example, poliomyelitis, chronic muscular atrophy, and degenera- tive neuritis are common causes of fibrillation. The fibrillation is usually frequent and persistent,' and is always localized in the wasted muscles. In progressive muscular atrophy it is apt to be especially frequent, and persists through a long period of time, as the atrophic process is a slow one. Fibrillation is of course not pathognomonic of chronic muscular atrophy, as has been held, nor is it an absolutely constant accompaniment of this disease. Fibrillation ' It ceases when the atrophic muscle-fibres are extensively atrophied, and therefore does not last long in acute lesions which cause rapid and extensive destruction of fibres. 92 DISEASES OF THE NERVOUS SYSTEM. may occur in atrophic diseases before the muscles give any evidence of wasting. Certain drugs, as aconitia, physostigmine, and pilocar- pine, may cause fibrillation, probably by irritating the motor nerve-endings. Whether fibrillation is generally due to irritation from nutritive changes in the motor nerve-endings, or whether it may be caused by slight pri- mary changes in the muscle-fibres themselves, cannot be stated. It is an important clinical fact, however, that fibrillation seldom or never occurs in muscular atro- phies of idiopathic type (muscular dystrophies). Rigidity. — The tonic muscular spasm which shows itself as rigidity in one or more extremities, or in the muscles of the trunk, is met with in both nutritional and structural diseases of the nervous system. It occurs in the tonic convulsive seizures of epilepsy and hysteria, and is seen widely distributed in tetanus. These particu- lar forms have been considered under convulsions. Here will be considered especially the rigidity of organic disease of the nervous system and the somewhat rare condition of catalepsy. Rigidity occurs as a symptom of so many widely dif- ferent diseases of the nervous system that some explan- ation of the general pathological processes which may give rise to it will facilitate an understanding of its occurrence. Rigidity may result from an active irritative process anywhere in the motor path — in its upper or its lovver segment. The rigidity of meningitis is an example of its occurrence from irritation of the cortex. The stiff- ness of the muscles varies in degree and distribution from time to time, often rapidly, probably in consequence of changes in the degree and position of the irritation. Meningeal irritation is, however, capable of diminishing SYMPTOMATOLOGY OF NERVOUS DISEASES. 93 the tonus of the muscles instead of increasing it. Rigidity is then absent, and the muscles may be quite relaxed. Why irritation should sometimes cause overaction of the motor nerve-cells of the cord, and at others should inhibit their activity, is unknown. The rigidity which occurs so frequently after lesions of the internal capsule (commonly hemorrhage or soften- ing) is also the result of the irritation which attends them, and involves the extremities which are the seat of the hemiplegia. This is true also of disease of the pyramidal tract in the crus, pons, and medulla. When rigidity comes on immediately after the onset of the hemiplegia, and lasts only a few or several hours, it is called " initial " rigidity. When it comes within a few days of the onset and lasts two or three weeks, it is spoken of as " early " rigidity. Usually, early rigidity is slight in degree ; occasionally it is very marked. Neither early nor initial rigidity is a constant accompaniment of hemiplegia. Both forms are certainly the result of irri- tation — initial rigidity resulting probably from the me- chanical irritation of motor fibres by the lesion which interrupts their continuity, early rigidity from the in- flammation which often follows. Rigidity from irrita- tion of the pyramidal tracts in the cord is uncommon, but is a very frequent symptom of conditions which irritate the anterior nerve-roots. Thus it is a usual ac- companiment of spinal meningitis, and of tumors external to the cord, and is sometimes seen in processes which cause slow compression of the cord, as in Pott's disease. But there is a mechanism other than irritation which is a common cause of rigidity. The normal tone of muscles depends on the integrity of the ganglion-cells of the anterior horns with which they are connected. De- struction of these cells results not only in paralysis of the 94 DISEASES OF THE NERVOUS SYSTEM. muscles, but in a loss of tone, as evidenced by their relaxation. Now these ganglion-cells are capable, under normal circumstances, of liberating more nervous energy than is required to give the muscles their normal tonicity, and are continually held in check, or inhibited, to pre- vent such overaction, by stimuli descending the pyramidal tracts from the cortex of the brain. If these inhibitory stimuli are cut off by the processes of disease, overaction of the spinal centres is the necessary result. There is hypertonicity or rigidity of the muscles. This rigidity may be constant, or it may diminish considerably during rest. Degeneration of the pyramidal tracts effectually interrupts the inhibition from the higher centres, and hence it is that we find rigidity in the many types of dis- ease in which such degeneration occurs. After hemi- plegia, for example, there occurs a secondary degenera- tion of the pyramidal tract in which the lesion lies. In the course of a few weeks the rigidity appears, — late rigidity it is termed, — and remains for months or years. If the degeneration be great in degree the rigidity may be permanent. A similar secondary degeneration may result from interruption of the fibres in the pons, medulla, or cord, from hemorrhage, softening, or inflam- mation. The primary degeneration of the pyramidal tracts in the cord, as seen in lateral sclerosis, also gives rise to rigidity in paralyzed muscles. In the case of amyotrophic lateral sclerosis, the presence of rigidity depends on the condition of the ganglion-cells of the anterior cornua. If these are only slightly injured and can still maintain the muscle tonus, this is increased by the degeneration in the lateral tract. If they are so ex- tensively altered as to lose their control of the muscle tonus, no degree of degenerative change in the lateral tracts is capable of restoring or increasing the muscular SYMPTOMATOLOGY OF NERVOUS DISEASES. 95 tone. Hence it is that we have a tonic and an atonic type of chronic muscular atrophy. (See p. 450.) In general, we may say that rigidity is due to irrita- tion to motor structures in acute processes, and to de- ficient control of the reflex machanism which subserves muscular tone, in chronic forms of disease. The motor overaction is seldom equal in degree in antagonistic muscle groups. Either the flexors or the extensors predominate and determine the position of the limb. If the spasm causes persistent shortening of a certain set of muscles the resulting condition is a con- tracture. Contracture and Contraction. — These words are used in different senses by different authors, and this has given rise to considerable confusion. According to the best English usage the word co7itractu7-e is applied to the shortening of a muscle or group of muscles from active contraction of the muscular fibres, and not from structural changes in these fibres. The contracture may last for a few minutes or for years. Good examples of contracture are seen in cerebral tumor involving the motor tract, in the late rigidity of hemiplegia, and in hysteria. The contracture of hysteria may persist many years. A contracture can always be overcome tempo- rarily by gentle, firm extension of the muscle, A contraction is the shortening of a muscle or group of muscles from structural changes in the muscle-fibres — structural contracture it is sometimes called. A contrac- tion cannot be reduced by extension. Contraction of a muscle from structural changes is always preceded by a period of active contracture in which connective tissue alterations have not yet occurred. The causes of con- traction are : a. The unequal paralysis of antagonistic muscles. 96 DISEASES OF THE NERVOUS SYSTEM. The stronger muscles assert themselves and give rise to serious deformity of the limb, though there is no spasm. This is often seen in polio-myelitis. b. From long-continued spasmodic contracture from any cause whatever. The structural changes in such cases develop very slowly — often not until many years have passed. Such structural changes occur even from hysterical contracture in some of the rare instances in which such contracture has existed unaltered for years. Since contractures are generally associated with some degree of motor weakness, even when they result from spasm, they are often regarded as late conditions of paralysis, though it is to be remembered that they some- times occur independently of motor loss. Contractures may result from paralysis of cerebral, spinal, or peripheral origin. By far the most common cerebral cause of con- tracture is hemiplegia. The contracture is produced by the late rigidity already spoken of. In the upper extremity the position which results from the contracture is one in which there is flexion of the elbow and pronation of the wrist, and flexion, often great, of the fingers, especially of the second and third phalanges. By passively flexing the wrist these phalanges can be readily extended, be- cause such flexion lengthens the course of the flexor tendons, but, if the wrist is extended somewhat, the fingers return to their original state of flexion. The contracture thus preponderates in the flexors, but there is usually some rigidity in the extensors. In the leg there is usually extensor contracture, the antagonistic muscles being much more equally balanced, and the leg is straight. In the foot there is a tendency, often marked, to take the position of talipes equinus or equino-varus. The great cause of contracture from spinal-cord dis- ease is poliomyelitis, and especially the infantile form. SYMPTOMATOLOGY OF NERVOUS DISEASES. 97 It is unusual for all the muscles of an extremity to be involved, or to be involved equally. In the lower ex- tremity the tibialis aiiticus and personei suffer most fre- quently, and there is a resulting contracture of the calf muscles, which are either intact or only slightly involved. Hence talipes equinus results ; and it is equino-varus or equino-valgus according as the peroneal group or the tibialis anticus is most involved. When the calf muscles suffer most, as they occasionally do, talipes calcaneus results. In the arm contractures are much less apt to result than in the leg, and, when they do occur, give rise to less deformity. The contracture of poliomyelitis early becomes struc- tural contracture. Contracture from disease of the peripheral nerves is not common. It occurs chiefly as the result of long- continued irritation, especially of the anterior nerve- roots, or as the result of injury to motor nerves. Catalepsy. — This is a condition of infrequent occur- rence in disease of the nervous system, but it requires brief mention. Catalepsy may be defined as a state of general or localized muscular rigidity, associated with and perhaps dependent upon a condition of perverted consciousness. The rigidity may be tetanic in charac- ter, opposing considerable resistance to passive motion, or it may exhibit the more striking characteristic known as waxen flexibility (catalepsia cerea). In this state of catalepsia cerea the slight resistance of the muscles is easily overcome by passive motion, and the limb or part retains the position imposed upon it, much as it would do if made of soft wax. When the tetanic form of rigidity is present the condition is sometimes called false catalepsy in distinction to the form in which cata- lepsia cerea is met, and which is known as true cata- 98 DISEASES OF THE NERVOUS SYSTEM. lepsy. The propriety of these designations is doubtful, as we know of no pathological reason for such a distinc- tion, and it is at least probable that both forms are closely allied in significance and genesis. In considering the occurrence of catalepsy, we have to distinguish between those cases in which it originates spontaneously, and the instances in which it is induced experimentally as one of the phenomena of hypnotism. Spontaneous catalepsy has been met with at almost all ages above three years. Usually it is seen in the female sex in early adult life. Frequently there is evidence of hysteria in the patient, or there is a history of emotional excitement or depression. Sometimes there is no ascertainable cause for the attack, and then the catalepsy is looked upon as a disease by itself, and not a symptom. Nervous or physical exhaustion is a predisposing cause. Catalepsy is an episode in some forms of mental disease, particularly melancholia, and it is a most important feature of the affection called katatonia. Catalepsy has occasionally been observed as a tran- sient symptom in the course of organic disease of the brain. Thus it has been an accompaniment of cerebral abscess, tumor, hemorrhage, softening, and meningitis, — always at a time when consciousness has been dis- tinctly impaired. The onset of spontaneous catalepsy is commonly rapid, with partial or complete loss of consciousness, if this be not already present. The features grow expres- sionless, the respiratory movements and heart's action are depressed, and there is a variable degree of general anjesthesia and analgesia, with diminished reflex activity. The cataleptic seizure wears away gradually or rapidly. Sometimes the attacks recur with inexplicable regularity. SYMPTOMATOLOGY OF NERVOUS DISEASES. 99 During the interval of the seizures the general health may appear to be excellent, or there may be evidences of a neurotic state. A cataleptic condition, apparently differing in no way from that which occurs spontaneously, can be induced in a state of hypnotism. It can often be brought on in an extremity simply by lifting it, or it may be necessary to make use of spoken words — verbal suggestion — to induce the rigidity. The catalepsy usually endures a short time only, and the rigidity yields slowly to gravita- tion, but in persons who have been frequently hypnotized it may last several hours. The so-called cataleptic stage of hypnotism, which is induced by staring at a bright light, or by a sudden loud noise, and in which the cata- lepsy is unilateral, is the result of repeated hypnotic influence, and is to be regarded as an unusual and highly artificial hypnotic phenomenon. It is probable that in many cases which have been described as spontaneous catdepsy, the catalepsy has been an epiphenomenon in the course of spontaneous hypnotism or somnambulism. At present, the diagnostic significance of catalepsy is small, but its recognition as a symptom is of some importance. Athetosis and Athetoid Movements. — The word athetosis was introduced to designate a peculiar form of chronic spasm, — "mobile spasm" it has been aptly called, — which gives rise to slow, irregular, inco-ordinated movements. The movements usually involve the hand and foot, sometimes also the face, but they are always most marked in the hand. In distribution the move- ments may be either strictly confined to one side of the body, or they may be bilateral. This condition of athetosis has been looked upon as a primary type of disease, since it is said to occur occa- lOO DISEASES OF THE NERVOUS SYSTEM. sionally in persons apparently healthy, unassociated with any other abnormal state. Movements of essentially the same character as those of athetosis are not infrequently seen as a post-hemi- plegic condition. They are often met with in children, and sometimes in adults. As in athetosis, they affect the hand more often, and in greater degree, than the foot. Usually the lesion which causes them is unilateral, and hence the movements are generally one-sided. When the lesion is bilateral, the movements may involve both sides of the body. These " athetoid movements," as they are called, never occur while the hemiplegia remains absolute, but develop with the return of volun- tary power, usually some months after the onset of the paralysis. There is usually associated with these spasmodic movements a certain amount of muscular rigidity, which tends to give to the part some particular attitude, and this rigidity is related to the degree of paralysis, being slight when the weakness is inconsider- able. The recognition of the dependence of this symptomatic form of athetosis, as it may be termed, upon a cerebral lesion is usually not difficult. The history of a hemiplegic attack, the loss of power and rigidity in the extremity which is the seat of the athetoid movements, and in children the arrest of development in bone and muscle, all point clearly to an organic cerebral process. But it is well known that a slight lesion, especially during childhood, may be so far re- covered from, in the course of time, that there remain only slight objective evidences of a cerebral process. Under these circumstances, the distinction between a symptomatic athetosis and a primary athetosis may be exceedingly difficult or impossible. Hence it is not difficult to understand that from time to time, cases of SYMPTOMATOLOGY OF NERVOUS DISEASES. lOI what are evidently symptomatic athetosis (athetoid movements) should be described as cases of primary athetosis. This circumstance, and the fact that a careful examination of a supposed case of primary athetosis, in the light of our present knowledge of infantile hemi- plegia, often reveals traces of an old hemiplegia which, ten ybars ago, might have been overlooked, has led some observers to deny the existence of a primary athetosis. But while we have reason to think that many so- called cases of athetosis are of post-hemiplegic origin, we are not at present justified in maintaining that this is true of every case which has been described as athetosis. The athetoid movements are usually slow, and always independent of voluntary motion, though they may be increased by it. Sometimes the movements are not slow but quick, and they may then bear some re- semblance to chorea. On the strength of this occasional resemblance these athetoid movements have been de- scribed as post-hemiplegic chorea, — ati objectionable term, because the condition has nothing to do with true chorea. As already mentioned, athetoid movements are a sequel to hemiplegia, particularly of that which occurs in childhood. The lesion is usually meningeal hemor- rhage or venous thrombosis ; sometimes it is embolism, sometimes hemorrhage. In adults the disease may succeed cerebral hemorrhage, or softening from any cause. In general, the movements are more likely to follow cere- bral softening than hemorrhage. As regards the position of the lesion which underlies these athetoid movements, no accurate generalization can yet be made. Frequently the motor cortex has been the seat of disease, and it has been shown that disease in this situation is by itself com- I02 DISEASES OF THE NERVOUS SYSTEM. petent to occasion the symptom. Disease of the internal capsule may cause the symptom, and involvement of the adjacent gray matter (optic thalamus and caudate nucleus) is probably not an essential condition for its production. Associated Movements. — When a voluntary movement of one group of muscles is accompanied by an involuntary contraction of muscles in another part of the body, this is termed an associated movement. Asso- ciated movements are met with generally as the result of hemiplegia, particularly the hemiplegia of infancy. Usually the movements are confined to the upper ex- tremity, the fingers of the paralyzed side undergoing involuntary movement, of limited range, during the voluntary activity of the other arm. Sometimes these movements are associated only with extensive move- ments of the normal limb, and are then themselves extensive in range, as when the paralyzed arm is lifted above the head, when the other is employed in an action which, like pullihg the strap in a car, requires the eleva- tion of the arm above the head. More commonly the associated movements are narrow in range, and are best seen when the hand of the unparalyzed side is employed in fine co-ordinated movements, as in the buttoning or unbuttoning of the coat, or in the fingering of any small object. Associated movements have a significance similar to that of athetoid movements. They cannot be said to possess much diagnostic importance. Inco-ordination. — During an ordinary muscular movement there occurs not only an accurately pro- portioned contraction of the various muscles which produce the movement, but a less powerful contraction of antagonistic muscles. This adjustment of opposed muscles makes the movement which results from their SYMPTOMATOLOGY OF NERVOUS DISEASES. 103 activity regular and continuous. If the contraction of muscles in either group is excessive, or less than normal, the movement which results is not that intended, but is irregular and broken, and efforts to remedy it are often excessive in degree and increase the difficulty. The condition of irregular, inco-ordinated voluntary move- ment is termed ataxia. It is difficult to say just what de- fects of co-ordination the term ataxia should include ; whether it should be applied to all forms of inco-ordina- tioD, or whether it should be strictly limited to that form of inco-ordination in which there is loss of harmony in the various muscle-groups used in the purely voluntary exe- cution of particular acts and in which an effort to correct the defect only serves to increase it. We shall employ the term in this more restricted sense.' According to the position of the lesion in the nervous system it is customary to distinguish several varieties of ataxia. Thus there is described a cortical ataxia, a cerebellar ataxia, a bulbar ataxia, a spinal ataxia, and an ataxia from peripheral nerve disease. • Some of these regional forms, however, are not ataxias, strictly speak- ing, and we shall therefore speak of them all as varieties of inco-ordination, specifying which are true ataxias. Cortical Inco-ordination. — Inco-ordination of movement from cortical lesions is usually associated with paral- ysis of the same distribution. The inco-ordination which is observed in athetoid movements (so-called post-hemiplegic chorea) has been mentioned. In cases of infantile hemiplegia, however, inco-ordination may be developed only during voluntary movement and be ' Under this definition ataxia does not include jerky inco-ordination or ataxic tremor such as is seen in multiple sclerosis and general paralysis, nor mere uncertainty in voluntary movements, nor the staggering which results from defective equilibration. 104 DISEASES OF THE NERVOUS SYSTEM. of a jerky oscillatory character, deserving the name of ataxia (hemiataxia it is called, when due to a unilateral lesion). Sometimes it is difficult to say whether we should class a given form of post-hemiplegic inco-ordina- tion as an intention-tremor or as true ataxia. The same difficulty is met in the inco-ordination of dementia para- lytica, which is sometimes truly ataxic, but more gener- ally consists of movements of narrow range which are more properly designated tremor. The disturbances of co-ordination which occur in hys- teria are probably of cortical origin. They may exist alone or be accompanied with loss of power or anses- thesia. It is doubtful whether the movements are ever those of true ataxia. In on^ form movements are well controlled and regular while the eyes are directing them, but when the visual control is withdrawn they be- come grossly irregular. In other cases there is good" co-ordination while the patient lies in the horizontal position, but in standing she begins to sway from side to side. Again hysterical patients in whom there is no loss of cutaneous or muscular sensibility, though quite steady with the eyes open, may oscillate from side to side, or even fall when the eyes are closed.' The effect of withdrawing the visual guidance in these cases is greater than it ever is in true ataxia without de- fective sensibility. This latter form of inco-ordination may be of considerable diagnostic value, since it may exist when other marked evidences of hysteria are absent. ' The term " astasia " is sometimes used to designate the unsteadi- ness in standing, with or without visual guidance, that is seen in some cases of hysteria. The word " abasia " is used to designate the un- steadiness in walking, which often does not amount to inco-ordination, seen in the same class of cases. SYMPTOMATOLOGY OF NERVOUS DISEASES. I05 Why ataxia sometimes occurs in cortical disease, but more frequently does not occur, it is impossible at pres- ent to say. Sometimes it seems to be due to damage of the cortical centre for the muscular sense (superior parietal lobule), sometimes to the disturbance of cuta- neous sensibility which the lesion produces. The inco- ordination seen in alcoliolic and other forms of intoxica- tioruis probably in part cortical. Cerebellar Inco-ordinatlon (cerebellar titubation). — This form of motor disturbance consists in an inability to maintain the erect position or to walk straight, in consequence of deficient equilibrium. The patient, in order to increase his base of support, stands with the feet apart. The body is bent forward and the arms are used to help in the maintenance of the equilibrium, but there is no true ataxia, although the condition is often called cerebellar ataxia. The forefinger can be placed on the nose without difficulty and, if the patient is supine, there is no diflficulty in moving the lower extremities as de- sired. The disorder is chiefly one of defective equi- libration, and the gait frequently is much like that seen in intoxication from alcohol. Rarely the upper extremities present marked jerky inco-ordination. This symptom is generally due to damage of the middle lobe of the cere- bellum, sometimes to disease in it, sometimes to pressure upon it from disease of one of the cerebellar hemispheres. Disease of the cerebellar hemispheres is per se not pro- ductive of cerebellar inco-ordination ; but wild inco- ordinated movements, resembling those of cerebellar titubation, may result from pontine and medullary dis- ease, probably from damage to the sensory tract (fillet). A peculiar difficulty in maintaining the equilibrium in the act of walking is sometimes seen in paralysis agitans, and may bear some resemblance to cerebellar Io6 DISEASES OF THE NERVOUS SYSTEM. titubation. As the patient tries to walk the first steps may be taken with difficulty and slowly, but they grad- ually increase in rapidity, and soon the patient may appear about to run in a staggering way. This tendency to run is termed festination. The body often inclines forward, and the patient may seem to be about to fall as he staggers forward, — " propulsion " the tendency is called when marked. More rarely it is easier for the patient to walk backwards than forwards, and there then exists an unavoidable inclination to fall backwards ; this is termed " retropulsion." The occurrence of festination has been accounted for on the supposition th \t the forward incli- nation of the body and head makes the patient run after his centre of gravity, but this is certainly not the entire explanation, for retropulsion, which doubtless has a similar mechanism, may occur though the head and body still incline forward. Bulbar Inco-07'dinatio7i. — Occasionally inco-ordination is met with as a result of disease of the medulla involv- ing the fillet (see page 34) which is probably one path for sensory impressions from the muscles. This is an unusual cause of inco-ordination. The characters of bulbar inco-ordination appear to be largely those of the inco-ordination of spinal cord disease. Inco-ordination from Spinal-Cord Disease. — The mus- cular inco-ordination which constitutes so important a symptom in certain forms of spinal-cord disease, is probably of sensory origin, though it is usually classed with motor symptoms. The underlying cause of the symptom, which in chronic disease of the cord usually amounts to ataxia, is, in the majority of instances, dis- ease of the posterior columns of the cord, especially the posterior median column, occurring alone or in combina- tion with disease of the posterior nerve-roots. Disease SYMPTOMATOLOGY OF NERVOUS DISEASES. lO/ of the posterior median columns, containing, as we have seen (page 34), one of the paths for muscular sensibility, is probably operative in the production of inco-ordination, by the arrest of the upward conduction of impressions from the muscles to the cerebellum. The impressions thus carried are probably an important factor in cerebel- lar co-ordination, and it is not difficult to conceive how interruption of this path may bring about disturbance of co-ordination. In the condition known as ataxic para- plegia this is the probable mechanism of the ataxia that is observed. In cases of unilateral lesion of the cord, also, loss of the sense of posture, followed by ataxia, has been observed. This ataxia is referable to arrest of sensory conduction from the muscles, and not to anaes- thesia, for the ataxia is on the same side as the lesion, while the cutaneous anaesthesia is on the opposite side, and the ataxic muscles have been known to lose their sensitiveness to pressure. The injury to the direct cere- bellar tract, one of the paths of muscular sensibility, which occurs in these cases of unilateral lesion, may also be a factor in the production of the ataxia. But the mechanism of inco-ordination in spinal-cord disease is not always so simple as in ataxic paraplegia. In locomotor ataxia, for example, in which we meet with ataxia in its most typical form, there occurs, .is an almost constant process, disease of the posterior nerve-roots, and often there is also disease of the sensory peripheral nerve-fibres. Among other effects resulting from the involvement of these structures is cutaneous anaesthesia, which, though not an absolutely constant condition, is rarely entirely absent. This cutaneous anaesthesia has been regarded by some as a very important factor in the production of ataxia. But it is highly probable that while cutaneous anaesthesia may be an accessory cause I08 DISEASES .OF THE NERVOUS SYSTEM. of ataxia, it cannot operate as a primary cause. It has been shown that there is no definite relation between the degree of inco-ordination and the degree or extent of the anaesthesia in conditions where both are present, and it is not rare to meet with absolute and extensive anaesthesia without the least ataxia, while, on the other hand, there are cases in which there is marked ataxia without anaes- thesia. Yet there is good reason to believe that anaes- thesia may increase pre-existing ataxia, and it probably does so by withdrawing the guidance to the motor cere- bral centres, which the ordinary cutaneous impressions continually furnish. It is interesting to note in this connection that visual impressions give similar guidance, and that the withdrawal of this aid, by closure of the eyes, always increases pre-existing inco-ordination. We may, therefore, regard anaesthesia as an element in the production of inco-ordination of locomotor ataxia. As in ataxic paraplegia, the primary factor is usually the inter- ruption of impressions from the muscles to the cerebellum consequent upon sclerosis of the postero-median columns. But, as we shall presently see, disease of the sensory peripheral nerves is competent to give rise to inco-ordi- nation, and such disease is frequently encountered in locomotor ataxia. We must therefore admit this addi- tional factor in the production of the ataxia of tabes. Inco-orditiation frojti Disease of Peripheral Nerves. — Inco-ordination of movement may occur from disease involving exclusively the peripheral nerves. It may be dependent, in part, upon the resulting anaesthesia, as just explained, but the important factor is probably the interruption of impressions from the muscles to the cerebellum, the result of disease of the sensory muscle- nerves. The process may involve the sensory nerves throughout their extent from the muscles to the cord or SYMPTOMATOLOGY OF NERVOUS DISEASES. lOQ may involve them in a limited part only of their extent, for example at the posterior nerve-roots, as in locomotor ataxia, Inco-ordination of similar origin is seen in alcoholic, diphtheritic, and some rarer forms of multiple neuritis. In the alcoholic form the inco-ordination is sometimes indistinguishable from that of tabes. The sense of posture is undoubtedly derived in great part from the stimulation of the sensory muscle-nerves by muscular contraction and tension, but it is probable that nerve-filaments supplying adjacent joint-surfaces play a role in the recognition of posture, by the centripe- tal transmission of impressions from the apposition of joint-surfaces at different parts, according to the position of the segments above and below the joint. These sen- sory impressions probably help in the co-ordination of muscular movements, and their interruption may lead to some disturbance of co-ordination, but how far this mechanism may be effective we do not yet know. Certain symptoms referable directly or indirectly to the ocular muscles may be conveniently considered here. These are conjugate deviation, strabismus, diplopia, nystagmus, and ptosis. Conjugate Deviation of the Eyes and Head. — In many cases of brain disease there is a lateral move- ment of the eyes (by the external rectus of one side and the internal rectus of the other), and often a rotation of the head (chiefly by the opposite sterno-mastoid) toward one or other side. This is known as conjugate devia- tion. The axes of the eyes are always parallel in conju- gate deviation, whatever may be their direction. Conjugate deviation occurs most often as an accompa- niment of hemiplegia, whatever may be its cause, and may occur when the lesion is in the cortex (probably the pos- terior part of the second frontal convolution), in the sub- no DISEASES OF THE NERVOUS SYSTEM. cortical white substance, in the internal capsule, or in the pons. The symptom may depend on a destructive pro- cess (paralytic conjugate deviation) or on an irritative process (spasmodic conjugate deviation). In the former case the deviation is to the side of the lesion ; the pa- tient is said to "look at his lesion." In the latter case the deviation is to the side opposite the lesion — that is, to the paralyzed side. Spasmodic conjugate deviation is generally transient. It is often present for a short time after acute hemiplegias, and is not rarely seen in acute meningitis. The spasmodic form also occurs in some cases of uraemia, generally associated with convulsions. It then depends on cortical irritation by morbid blood products. In cases where conjugate deviation occurs the associ- ated condition of the limbs show whether the symptom is paralytic or spasmodic in origin. In some cases of disease of the pons there occurs a peculiar form of associated paralysis of the external rectus of one side with the internal rectus of the other, in which the eyes can be turned towards the lesion to the middle line, but not beyond it. Strabismus. — Strabismus is loss of parallelism in the visual axes of the two eyes. This loss of parallelism is a conspicuous symptom of many cases of paralysis of the ocular muscles. But strabismus is not always of para- lytic origin ; it may depend on spasm of ocular muscles. Spasmodic strabismus is usually transient, with one ex- ception — the ordinary form of squint (due most often to myopia), in which it is persistent. In cases of strabismus dependent on paralysis there occurs what is known as " secondary deviation." Pri- mary deviation is the deviation of the axis of the eye paralyzed, from parallelism with that of the normal eye. SYMPTOMATOLOGY OF NERVOUS DISEASES. Ill Secondary deviation is something quite different. It is an excessive movement on the part of the sound eye, which increases the deviation from parallelism when the sound eye is prevented (as by interposing the hand or a piece of ground glass) from seeing an object looked at with the eye paralyzed. By means of this secondary deviation it is possible to distinguish between paralytic and spasmodic strabismus, for secondary deviation always occurs in paralytic, never in spasmodic strabismus. Spasmodic strabismus is the same in all positions of the eyes ; paralytic strabismus occurs only in those positions of the eyes that necessitate the use of the muscle or muscles affected. Strabismus may be divergent (external strabismus) or convergent (internal strabismus), or may cause a differ- ence in the level of the two eyes. Transient spasmodic strabismus is not rarely seen in irritative brain diseases, as meningitis, tumor, abscess, hemorrhage, or softening, and occasionally occurs in hysteria. Diplopia. — Double vision is present in all recent cases of strabismus, and is due to the erroneous projection of the field of vision of the affected eye. When the stra- bismus is of long duration (whatever may be the cause) the patient learns to disregard the image formed on the retina of the affected eye (" false image "), and he then becomes aware only of those things that are seen with the normal eye. In such chronic cases the false image may be brought out by placing a bit of colored glass before one eye (preferably the sound eye), in order to color either the true or false image (the true image in the case of the normal eye). Double vision is often an early symptom of brain dis- ease, as meningitis, tumor, abscess, multiple sclerosis. ri2 DISEASES OF THE NERVOUS SYSTEM. In many cases it accompanies the onset of sudden lesions, especial!}^ those in or near the pons. It depends here on spasmodic strabismus, but this is of such short duration- as to be unrecognized. The occurrence of diplopia in children who are free from eye disease (errors of refrac- tion) is suggestive of meningitis. When not dependent on eye disease diplopia is usually a sign of serious ner- vous disease, but this is not always the case. It occurs, for example, as a transient symptom in many cases of acute alcoholic intoxication and in some cases of cerebral concussion. Nystagmus is the term applied to rapid involuntary and rhythmical movements of the eyes. The movements are usually bilateral and similar in character in both eyes. Most often the movements are horizontal ; sometimes they are rotary ; rarely they are vertical. They vary in frequency from 60 to 200 movements per minute in the same direction. Usually the rhythm of movement is regular. Nystagmus is usually constant. Occasionally it occurs only when the eyes are moved in certain directions. During sleep the movements cease. In cases that date from early life, the patients are not conscious of the movement of their eyes ; but in some cases that begin in adult life there is apparent movement of objects. Nystagmus is observed in a number of different condi- tions. It occurs {a) from conditions external to the nervous system, and (^) in many different diseases of the nervous system. Of the conditions external to the ner- vous system that cause nystagmus, the following are the chief : albinism, a very common cause, and local eye affections causing defective sight, as opacities of the cor- nea or lens and diseases of the choroid or retina (effective chiefly in childhood). It is also of frequent occurrence in miners who work in coal mines in a dim light. ^SYMPTOMATOLOGY OF NERVOUS DISEASES. II3 Of the diseases of the nervous system in which nystag- mus occurs, the most important are these : multiple scler- osis, hereditary ataxia, meningitis, meningeal hemorrhage and cases of tumor, and hemorrhage and softening in almost any situation. Cerebellar disease (especially tumor) is often associated with nystagmus, and pontine disease is occasionally the apparent cause of nystagmus. In chronic ear disease and in mastoid disease, nystagmus is sometimes developed, in association usually with symp- toms indicating irritation of the adjacent membranes. Severe cerebral concussion is sometimes followed im- mediately by nystagmus (the oscillations may be very rapid) of temporary duration, and may depend in these cases on minute hemorrhages into the brain substance. Nystagmus is occasionally observed in the course of urasmic convulsions. The mechanism and significance of nystagmus is but imperfectly understood. The symptom certainly has little or no localizing value, for it arises from disease in a great variety of positions in the brain. It is, however, an important symptom, for it probably always indicates more than purely functional disease. When it develops gradually in adults, as the result of nervous disease, this is most often degenerative in nature. Ptosis, or drooping of the eyelid, is a symptom of several distinct conditions. Most often it is the result of disease of the third nerve (generally syphilitic disease), and is then associated with other symptoms. But it may result from disease of the third nerve nucleus, or of the tract of the third nerve anywhere between the nucleus and the cortical centre. (The position of the cortical centre is uncertain ; perhaps it is in the lower parietal lobule.) Generally, ptosis from disease o^ the third nerve 114 DISEASES OF THE NERVOUS SYSTEM. tract is unilateral, but in some cases of nuclear disease and disease of the nerve itself the symptom is bilateral. Ptosis from paralysis of the sympathetic is occasionally seen, and is distinguished by other evidences of sympa- thetic involvement, especially contraction of the pupil on the same side. In these cases the drooping of the lid probably depends on paralysis of the smooth muscular fibres of the facia of the orbit (fibres of Miiller), which are supplied by the sympathetic, and normally act on the tarsal cartilages. Some cases (usually bilateral and partial) of ptosis are congenital, and ignorance of this fact may lead to errors in diagnosis. Hysterical ptosis is sometimes seen, and may be bilateral or single. It is generally associated with spasm of the orbicularis. Reflex ptosis, a rare form, generally depends on some morbid state (irritative usually) of the fifth nerve, as extraction of a tooth, or injury of the nerve. In some neurasthenics ptosis develops in middle life. It is always double. " Morning ptosis " is a form in which the patient, on waking, is temporarily unable to lift the lid. Some other forms of ptosis are associated with over-action of the occipito-frontalis. Pupillary Symptoms. — Deviations from the normal reaction and size of the pupils are of frequent occurrence in disease of the nervous system, and possess considerable diagnostic importance. The most important of these deviations are the following : (i) Dilatation of the Pupils with normal reactions to light and during accommodation. Such dilatation is often observed in children and in nervous and irritable adults in apparently good health. It is frequently seen in neurasthenic, hysterical, and maniacal persons, and SYMPTOMATOLOGY OF NERVOUS DISEASES. II5 also occurs as a result of irritation of the cervical sympa- thetic, either direct or through the irritation produced by certain lesions of the cervical spinal cord. Stimulation of the skin of the neck normally causes temporary dilata- tion of the pupils. (2) Contraction of the Pupils is observed in senility, in locomotor ataxia, in dementia paralytica, in acute lesions of the pons and medulla (hemorrhage and soften- ing), in many irritative diseases of the brain (meningitis, tumor, abscess), in irritative conditions of the eye (iritis, cilliary neuralgia), and in some forms of poisoning, especially opium and chloral poisoning. In locomotor ataxia and dementia paralytica the myosis is associated with loss of light reflex and preserved accommodation reflex, or with total immobility. A high grade of myosis in persons in the first half of life, who are free from refractive errors, is always pathological and suggests organic disease of the nervous system. Dilatation of the pupil in the second half of life, in those without eye- disease, has the same significance. (3) Dilatation of the Pupils with Immobility is observed in almost all forms of coma, in cases of advanced glaucoma, and in lesions of the third nerve. The pupil is contracted in coma only when the condition results from poisoning, or occurs in a person who has myosis from an organic degenerative disease of the nervous system. Dilatation of the pupil, with paralysis of accommodation and slug- gish but preserved contraction to light, is often seen in diphtheritic paralysis. In these cases there is usually contraction on an endeavor to accommodate. (4) Loss of Reaction to Light with Preservation of Reac- tion during Accommodation (Argyll-Robertson pupil) is the most significant of all pupillary symptoms. It probably always indicates organic disease (especially degenerative Il6 DISEASES OF THE NERVOUS SYSTEM. disease) of the brain, which interrupts the reflex path between the optic nerve and the nucleus of the third nerve. The Argyll-Robertson pupil is a characteristic symptom of locomotor ataxia and of dementia paralytica, and is an occasional symptom of multiple sclerosis. In rare cases it is observed in persons who have syphilis but have no signs of organic brain disease. The Argyll- Robertson pupil is usually associated with contraction of the pupil ; occasionally with dilatation, or with pupils of normal size. (5) Mere Difference in the Size of the Pupils has no single significance. Such difference is common in cases where the two eyes refract differently. A high grade of inequality is sometimes seen when there is little defect in vision. Inequality is often observed in irritative dis- eases of the brain — meningitis, abscess, tumor, extra- dural hemorrhage, etc., and in degenerative diseases, such as locomotor ataxia and dementia paralytica — but is seldom of more than secondary importance in diagnosis. Changes in the size and reaction of the pupils from nervous diseases are readily distinguishable from the changes in size and immobility that depend on iritic adhesions. The immobile pupils of iritis are almost always irregular in form, and proper illumination will reveal the presence of synechiae. (6) Hemianopic Pupillary Inaction. — This term is ap- plied to the imperfect reaction which occurs when light is thrown on the blind half of the retina in certain cases of hemianopsia. The cases of hemianopsia in which pupillary reaction is diminished or lost when the blind half-field is stimulated, are those in which the lesion is in the optic tract ; the cause of the phenomena being the interruption of the path to the corpora quadrigemina (or ganglion habenulse). In cases of hemianopsia due to SYMPTOMATOLOGY OF NERVOUS DISEASES. II/ lesions of the hemisphere the hemianopic pupillary inac- tion does not occur. Hence the symptom, if carefully determined, is of value in distinguishing between lesions of the tract and those of the intra-cerebral optic path and centres. Laryngeal Symptoms. — Disordered action of the larynx, the organ of voice, may give rise to important symptoms and signs. Of these symptoms the chief are : (i) altered phonation, or entire loss of voice : (2) res- piratory symptoms, as stridor and dyspnoea, from imper- fect regulation of entrance of air in breathing, or cough from imperfect closure of the glottis. The signs of laryngeal disorder consist chiefly of defective movement of the vocal cords, which may be observed by means of the laryngoscope. It is convenient to consider the grouping of these symptoms and signs in the various forms of laryngeal disorder (especially paralysis) that are met witli as the result of nervous disease. (i) In Total Bilateral Paralysis of the larynx (or what is more common, paralysis of all the laryngeal muscles except the crico-thyroid) the vocal cords are in the "cadaveric position" — that is, in a state of slight ab- duction from the median line, and cannot be moved. When an attempt at phonation is made the cords can- not be approximated ; hence there is loss of voice. There is also inability to make a natural explosive cough — a symptom of much importance and one which always indicates laryngeal paralysis, usually organic in character. There may be stridor during deep in- spiration. (2) In Total Unilateral Paralysis of the Larynx the para- lyzed cord lies motionless in the "cadaveric position." The unparalyzed cord moves freely and may even pass Il8 DISEASES OF THE NERVOUS SYSTEM. beyond the median line of the glottis during phonation. In consequence of this compensating action phonation is possible, but the voice is hoarse and low in pitch. There is no stridor, and an explosive cough is impossible. Total unilateral paralysis of the larynx may result from disease of the spinal accessory nucleus or its nerve-roots by the side of the medulla, or from disease of the root of the pneumogastric. But the most common cause of uni- lateral paralysis, and indeed of all laryngeal paralyses, is disease of the recurrent laryngeal nerve. Aneurism of the vessels round which the nerve passes, thoracic tumor, enlarged bronchial lymph-nodes, and enlargements of the thyroid are all causes of pressure upon the nerve. The crico-thyroid muscle is of course exempt in these cases, but the symptoms are practically the same as when all the muscles are involved. The causes of total bilateral palsy are the same as those of the unilateral form, acting on both sides. (3) In Total Abductor Paralysis of the Larynx (paralysis of the posterior crico-arytenoids) the cords lie close together (much nearer than in the position of cadaveric rigidity), and are not abducted during inspiration. The effect upon respiration is that inspiration is difficult and accompanied with stridor. There may even be alarming dyspnoea, with lividity of the face, etc. Expiration is unembarrassed, cough is normal, and the voice is little changed. (4) In Unilateral Abductor Paralysis the recession of the unparalyzed cord prevents both stridor and the dyspnoea which characterizes the bilateral palsy. Neither cough nor voice are distinctly affected. The symptoms are therefore chiefly negative. Abductor paralysis of the larynx may be due to local palsy, as laryngeal catarrh, or to central disease. Some- SYMPTOMATOLOGY OF NERVOUS DISEASES. I I9 times it appears to be due to disease of the recurrent laryngeal nerve. Occasionally it occurs as an hysterical paralysis, and is then double. (5) In Adductor Paralysis the vocal cords are separated and cannot be brought together nearer than the cadaveric position, but abduction is possible during deep inspira- tion. The voice is lost, but cough is usually perfect, because the paralysis is generally partial and the cords can be approximated during the attempt to cough, though not for phonation. There is no stridor and no dyspnoea. Adductor paralysis is only rarely due to organic disease. It is most often of hysterical origin, and gives rise to the aphonia of hysteria. Occasionally it results from simple catarrhal laryngitis. (6) Adductor Spasm of the Larynx is a common occur- rence in many laryngeal diseases. It always depends on a state of abnormal central excitability. Under favorable conditions of excitability in the laryngeal mechanism (such as are frequently present in children) almost any nerve irritation, whether direct, reflex, or central, may determine a paroxysm of adductor spasm. The parox- ysms consist of sudden and intense difficulty in breathing and loud stridor, lasting only a few minutes. In children very slight nerve irritation often suffices to determine the paroxysm. In children with rickets laryngeal paroxysms of peculiar type, associated with cardiac and vaso-motor disturbance and known as " laryn- gismus stridulus," are not uncommon. These paroxysms are related in their pathology to the general convulsions which may occur in rickets. Any irritative lesion of the superior or inferior laryngeal nerve may cause adductor spasm, which may be bilateral or unilateral. Adductor spasm occurs also at the onset of attacks of grand mal, I20 DISEASES OF THE NERVOUS SYSTEM. causing the "epileptic cry," during hydrophobia, and occasionally in hysteria and tetany. Abnormal Reflex Action. — The modifications of reflex action which possess diagnostic value may con- veniently be considered here. Loss of Reflex Action occurs whenever the reflex arc which subserves the reflex in question, is interrupted.' As every reflex arc consists of a centripetal portion (sen- sory nerve), a centrifugal portion (motor nerve), and a central portion (motor ganglion-cell of cord), the disease abolishing reflex action may be in any one of these three positions. In which particular one it lies in a given case is to be determined by the associated conditions. If the disease is in the sensory path, there is loss of sensibility as well as reflex ; if in the peripheral motor path, or in the motor centre, there is corresponding loss of motion, with nerve degeneration and atrophy. This is true both of the superficial and of the deep reflexes, but in the case of the former, it has little diagnostic value, while as regards the latter (especially the knee-jerk), it is of diag- nostic importance, for the degenerative atrophy which results from implication of the motor elements is readily appreciated in the latter but not in the former instance. Disease within the reflex arc is not the only cause of arrested reflex action, for both superficial and deep reflexes may be temporarily arrested by irritative inhibi- tion from above — that is, from irritative disease at any level higher than the motor ganglion-cells on which the reflex depends. This is the explanation of the unilateral reflex loss which is frequently encountered immediately after hemiplegia, and of the bilateral reflex loss which is seen below the lesion for a variable time after sudden ' The different levels of the spinal cord upon which the more important reflexes depend, are given on pages 20 and 21. SYMPTOMATOLOGY OF NERVOUS DISEASES. 121 damage to the cord — as from fracture or dislocation of the cervical vertebrse. Persistent loss of cutaneous reflex (unilateral or bilateral) occasionally occurs as a result of disease of the hemispheres. Persistent loss of tendon reflex probably never occurs from brain disease, but temporary loss of knee-jerk occurs sometimes in irritative disease (tumor) of the cerebellum, and is not uncommon in lesions which irritate the cortex of the convexity (con- vexity meningitis, subarachnoid hemorrhage). Probably this is due to irritative inhibition. Loss of Patellar Tendon Reflex (knee-jerk) is of much diagnostic significance. The more important conditions in which it occurs may be tabulated as follows : (A.) Diseases of the brain : Almost any irritative brain disease involving motor structures (tumor, meningitis, abscess, hemorrhage, acute softening) ; loss usually unilateral, always temporary (hours, days or weeks) ; in convexity meningitis and subarachnoid hemorrhage (bilateral) the loss may be bilateral. (B.) Diseases of the spinal cord : 1. Locomotor ataxia. Very early and constant symp- tom ; bilateral (in very early stage may be present on one side) ; due to destruction of reflex arc by disease of posterior nerve-roots ; persistent. 2. Poliomyelitis of lumbar cord. Immediate onset ; generally unilateral, sometimes bilateral ; due to inter- ruption of reflex arc by disease of ganglion-cells of ante- rior horns. 3. Any diffuse destructive process in lumbar cord, as transverse myelitis. 4. Spinal meningitis. After stage of irritation ; due to compression of anterior or posterior nerve-roots by exudation. 122 DISEASES OF THE NERVOUS SYSTEM. (C.) Diseases of the peripheral nerves : 1. Alcoholic neuritis. Loss usually occurs early ; not absolutely constant, for knee-jerk may be present throughout the disease when muscle-nerves for ex- tensors of knee are not involved ; due to interruption of reflex arc by disease of sensory muscle-nerves. 2. Diphtheritic neuritis. Frequent loss when there is no subsequent paralysis ; almost constant loss when there is post-diphtheritic paralysis ; comes on about one month after onset of disease ; usually bilateral, rarely unilateral ; return of knee-jerk after variable period. 3. Acute ascending paralysis. Bilateral and early loss very constant ; usually persistent, but knee-jerk may return. 4. Any severe lesion of anterior crural nerve, sensory or motor fibres, or both. Immediate unilateral loss of knee-jerk. Besides the conditions that have been given as causes of loss of knee-jerk, there are others whose mechanism is at present obscure. Thus, the knee-jerks may be lost during the febrile stage of secondary syphilis and in severe forms of malarial fever, — possibly in both instances from slight neuritis of the sensory muscle-nerves on which the knee-jerk depends ; for it is certain that very slight disease of these nerves may cause temporary loss of myotatic irritability. The knee-jerk may be perma- nently lost in diabetes mellitus. It should be remembered that in very rare instances persistent absence of knee-jerk is observed in persons in good- heal, h. It is claimed by some that this is not such an uncommon occurrence, but we believe that if the precautions recommended on page 589 are observed in testing the knee-jerk such cases will be found to be very rare. SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 23 Thus it is seen that loss of knee-jerk is by no means a pathognomonic symptom. Its chief general significance is interruption of the reflex arc on which it depends. The exact character and seat of the disease which is thus operative must be determined by the study of other symptoms. But it should not be forgotten that interrup- tion of the reflex arc is not the only significance of the symptom. Excess of Reflex Action is of frequent occurrence in disease of the nervous system, and is evidence for each reflex that its arc is intact. Increase in cutaneous reflex action is of little diagnostic significance, partly because of the variable character of the different skin reflexes in different normal individuals, and the consequent difficulty in determining what constitutes a pathological change. An increase is, however, seen in conditions which, like strychnia poisoning and tetanus, are characterized by an increased irritability of reflex centres generally, and is an inconstant effect of lesions, which, like certain cerebral and spinal diseases involving the pyramidal tract, diminish spinal inhibition. In locomotor ataxia the superficial reflexes are sometimes much increased early in the disease, the plantar increase being particularly notice- able. As the disease progresses upwards, the increase may be seen in the abdominal reflex. Probably this increase is the effect of irritation in the -reflex arc. Increase in the activity of the deep reflexes, particu- larly the knee-jerk, is a sign of considerable diagnostic importance. It is sometimes due to primary over-action of the reflex centres, as in tetanus and strychnia poison- ing. Usually it depends on defective inhibition from higher (cerebral) centres, and this defective inhibition may be brought about by organic or functional disease. Permanent exaggeration of the knee-jerk is almost always 124 DISEASES OF THE NERVOUS SYSTEM. consequent on degeneration of the pyramidal tracts. The excess is at first slight in degree and increases gradually. Since the conditions that lead to degeneration of the pyramidal tracts are numerous, it is not singular that exaggerated tendon-reflex is seen in a variety of organic processes. The following are the main conditions in which it is observed : 1 . Hemiplegia from any cause ; tumor, hemorrhage, softening ; increase comes on in about a week ; especially noticeable on side opposite lesion ; may be bilateral ; regular symptom, except in slight cases. 2. Dementia paralytica ; common and early symptom ; excess bilateral. 3. Transverse myelitis above lumbar enlargement ; bi- lateral excess usually great. 4. Slow compression of the cord above lumbar enlarge- ment, as from caries, tumor, etc. Early and great excess always present ; may occur when there is no secondary degeneration, and may disappear when compression is removed. 5. Primary degenerative diseases of the cord ; primary lateral sclerosis ; spastic paraplegia ; amyotrophic lateral sclerosis. 6. Injuries of spinal cord ; hemisection, complete transverse section ; sudden destruction at one level above lumbar enlargement from fracture or dislocation of verte- brae. When injury is one-sided, excess is unilateral and on same side ; excess following fracture or dislocation is preceded by complete loss of reflex if transverse de- struction is extensive. Bilateral increase of the knee-jerks is seen in func- tional (nutritional) diseases ; in hysteria, hypochondri- asis, neurasthenia, and in certain neuroses that follow traumatism (traumatic neuroses). SYMPTOMATOLOGY OF NERVOUS DISEASES 1 25 Increase of other tendon reflexes, triceps, radial, has the same general significance as increase of patellar tendon reflex, but is of less practical diagnostic value. Very active knee-jerks are frequently seen in perfectly healthy persons. Ankle Clorms (" foot-clonus," foot-phenomenon," im- properly designated " spinal epilepsy ") consists of a series of to-and-fro movements (flexion and extension) of the foot at the ankle joint, which may sometimes be induced by suddenly flexing the foot (dorsal flexion) on the extended and relaxed leg. It may also occur spon- taneously when the patient sits with the tips of the toes on the ground and the heel raised. The movements are highly rhythmical, and number from six to ten per second. The general significance of ankle clonus is that of exaggerated tendon reflexes, but the phenomenon usually occurs only in conditions where the knee-jerk is very much exaggerated, and is only rarely a symptom in functional affections. Ankle clonus is usually evidence of organic disease, especially of degeneration of the pyramidal tract, but it is frequently very marked in cases of compression of the cord in which secondary degeneration has not occurred. It is also seen in hysteria, but not frequently, and in the "traumatic neurosis." Ankle clonus may be obtained in some normal individuals after they have stood on tip- toe for some time. It is very exceptional to meet with ankle-clonus without exaggeration of the knee-jerks. Temporary loss of knee-jerk with ankle-clonus on the same side has been met with in purulent meningitis. Clonus of the rectus muscle (rectus clonus) is some- times obtained by striking the tendon just above the patella. This condition is usually present when there is ankle clonus, but may occur unassociated with it. 126 DISEASES OF THE NERVOUS SYSTEM. Sensory Symptoms are of frequent occurrence in both organic and functional disease of the nervous sys- tem, and of the various forms that are encountered loss of sensibility is the most important. Certain forms of sensory loss possess important localizing significance, but many forms are at present of little value, owing to our imperfect knowledge of the sensory paths. It is important to remember that sensory structures (especially fibres) often preserve their functional activity entirely or in part, when damaged to a degree (for ex- ample by pressure) that in motor elements would pro- duce complete loss of function. Hence it is that lesions involving both motor and sensory structures frequently either give rise to no sensory loss, or are soon followed by partial or complete recovery of sensibility. Different forms of sensory loss (anaesthesia, analgesia) often coexist, but not infrequently certain forms are present while others are lost. It is convenient to con- sider separately the different forms of sensory loss. AncBstkesia (the word anaesthesia is also used in a general sense to include loss of pain sense), loss of tactile sensibility, is met with in diseases of the brain, spinal cord, and peripheral nerves, and in some nutritional affections (hysteria, traumatic neuroses). Certain types of sensory loss, based on distribution, may be distinguished. ffejfiiancesthesia, or loss of tactile sensibility involving one lateral half of the body — face, trunk, and extremities of one side, — is invariably of central origin. The hemi- anassthesia may be complete or partial, and may or may not be associated with hemiplegia, which may be of any degree. When of organic origin, complete hemianaes- thesia is rarely associated with a high grade of motor paralysis (unilateral). Loss of pain and temperature senses may be associated with hemianaesthesia, but the three forms of sensibility seldom suffer equally. The SYMPTOMATOLOGY OF NERVOUS DISEASES. \2J anaesthesia usually does not extend quite to the median line (within one or two centimetres), but occasionally it may extend a few cm. on the other side. It involves not only the skin but the mucous membranes as well (lips, conjunctivia, rectum, urethra). Hemianaesthesia of organic origin is always due to interruption of the sensory tract between the junction of the ascending and descending roots of the fifth in the pons (upper extremity of the pons) and the cortex of the opposite side or to disease of the cortex itself. Its exact position must be determined by other symptoms. If the disease is in the pons, the region supplied by the fifth nerve (face) escapes (because the path from the fifth crosses to the opposite side high in the pons), unless the lesion be one involving the entire formatio reticularis in the upper part of the pons. The most common seat of the lesion causing hemianaesthesia is the posterior third of the hinder limb of the in- ternal capsule (see Fig. 22) between the lenticular nu- cleus of the corpus striatum and the optic thalamus. The sensory tract is here contiguous to the motor path, but owing to the arrangement of the vascular supply of the region it is common for a lesion to injure the former without the latter, or the latter without the former, though an extensive lesion may damage both, and cause both motor and sensory symptoms. The sensory path in the capsule also lies close to the path for the special senses, which may be involved on the same side as tactile sensibility, with the exception of vision, the defect of which is hemianopsia (see page 147) Hemianaesthesia may occur from disease of the cortex itself, or of the subjacent white substance, but com- plete hemianaesthesia from this cause is vety rare. This is because the fibres of the sensory tract are here greatly spread out, to cover a large area, and only a very ex- 128 DISEASES OF THE NERVOUS SYSTEM. tensive lesion can involve them all. Hemianaesthesia is not infrequently of hysterical origin, and it may be one manifestation of cer- tain traumatic neuroses. In both these cases it is probably of cortical origin (nutritional disease). The points of distinction be- tween functional and organic disease are con- sidered in chapter VI. A partial form of hemi- anassthesiawhich is of con- siderable importance from its frequent occurrence is that which accompanies ordinary hemiplegia. The loss of sensibility does not extend to the median line. It exists chiefly or exclu- sively in the limbs, the loss being most distinct in the hands and feet. The sen- sibility to pain is usually diminished in these cases, but not in the same degree as the loss of tactile sen- sibility. Crossed Hemianesthesia — (alternate hemianaes- thesia). — Loss of tactile sensibility of one side of the face and of the opposite limbs is of rare occurrence. The sensory loss in the face is due to damage of the ascending root of the fifth FIG. 42. Diagram illustrating the distribution of the sensory line in a case of crossed hemi- anesthesia. The horizontal lines show the distribution of the analgesia, which was complete above, partial below. The vertical lines show the area of hyper- algesia. In this area, contact with cotton caused a peculiar prickly sensation. SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 29 LfH Crus Xi.V Nerve nerve of the sa7ne side in some part of its course ; the loss on the trunk and limbs to damage of the sensory tract from these parts of the opposite side. In the pons (below the up- per third), and in the medulla, these tracts lie close together, hence a lesion in the pons or upper part of the medulla involv- ing the entire lateral extent of the f ormatio reticularis and the fifth nerve-root gives rise to crossed hemi- ansesthesia. (See figs. 43 and 47). Crossed hemianesthesia is never of functional origin. Bilateral Ana;sthe- sia, involving the limbs on both sides, may occur as a con- sequence of disease of the pons damaging the sensory tract on both sides. The anaesthesia is seldom complete. Para-AncEsthesia. — Anaesthesia involving both extrem- ities (" anaesthesia of paraplegic distribution " it is some- times called) is generally dependent upon disease of the spinal cord (but not infrequently on peripheral neuritis), sometimes upon disease of the cauda equina, FIG. 43. Diagram illustrating the mechanism of crossed aiicESthesia. (After Starr.) Any lesion inter- rupting the general sensory tract from the lines above the crossing of this tract in the medulla and the ascending root of the fifth nerve on the same side will produce crossed ansesthesia. The conditions will vary, however, with the level of the lesion. Thus, a lesion at A will cause typical crossed anaesthesia and rotation of the body to the side of the lesion from involvement of the middle peduncle of the cerebellum ; a lesion at B will cause complete anesthesia of the opposite limbs and trunk, but the anassthesia of the face on the same side as the lesion will not involve the entire face, sensation remaining normal in its upper portion ; a lesion at C will cause anaesthesia of entire opposite half of the body, but probably only partial and greatly limited anaesthesia of the face on the same side as the lesion. 130 DISEASES OF THE NERVOUS SYSTEM. . though in this case the anaesthesia usually involves the skin on the lower extremities irregularl3^ Anaesthesia of the lower extremities may be due to a transverse lesion (myelitis, tumor) or to a systematic lesion involving only the sensory tract of the cord, the posterior median columns. The upper level of the anaesthesia affords an important indication of the upper level of the lesion, sometimes a more accurate one than the motor palsy, which generally coexists, but whose exact distribution and degree it is often difficult to determine. The exact upper limit of the anesthesia in lesions of different levels in the cord is given on page 248. Anaesthesia may be limited to one extremity, and such localized anaesthesia may be of cerebral, spinal, or peri- pheral origin. When due to organic disease of the brain (hemiplegia), as it occasionally is, the anaesthesia is most marked at the extremity of the limb, and grows gradually less marked as the trunk is reached — that is, it has the characters of the common form of anaesthesia that is met in hemiplegia. If the anaesthesia corresponds closely to the area supi>lied by one or more nerve-trunks and there is no cincture pain, it is probable that the lesion is in one or more nerve trunks, or the plexus above them. When there is evidence of a segmental loss of sensibility (inner border of arm, forearm, and hand, for example) and there is a girdle-pain or sensation, the lesion may be referred to a corresponding segment or nerve-root of the spinal cord (especially the arm). It is very important to know that anaesthesia of one extremity, with a sharply limited upper border, is frequently of hysterical origin. Anaesthesia limited to well defined areas of the extrem- ities or trunk, and which corresponds to the distribution of SYMPTOMATOLOGY OF NERVOUS DISEASES. I31 one or more nerves or nerve branches, generally indicates disease of the nerve itself, — more rarely disease of the nerve-roots. In studying the distribution of the sensory loss from lesions of mixed nerves, it is helpful to bear in mind Schroeder Vander Kolk's law, that the sensory fibres of a mixed nerve supply, generally speaking, the integument over the muscles innervated by the motor fibres of the same nerve. Irregular areas of anaesthesia, of indeterminate nerve supply, are not infrequently met with in the trunk or limbs. Such patches may be due to disease of the sen- sory nerve-endings in the skin, to the irregular incidence of disease in the peripheral nerves, to disease of the nerve-roots, to systematic disease of the cord (posterior sclerosis), or to the occurrence of irregular islets of sclerosis in the cord (multiple sclerosis), and pos- sibly also in the brain. Perhaps the most frequent structural cause of anaesthetic patches is disease in- volving several nerve-roots, as spinal meningitis. Usually the localization of the process causing the anaesthesia is easily accomplished with the help of other symptoms. It is to be remembered that irregular areas of anaesthesia are not infrequently met with in hysteria, and are sometimes seen in neurasthenia and alcoholism. Very rarely cases are observed in which there is general loss of tactile and pain sense, associated with tremor, increased reflexes and mental depression, and in which the autopsy gives no explanation of the phenomena. Analgesia. — Loss of sensibility to pain may occur with or without loss of tactile sensibility. In the spinal cord and medulla we know the paths for these two forms of sensibility to be distinct, and this explains 132 DISEASES OF THE NERVOUS SYSTEM. the frequency with which one form of sensibihty suffers without, or in less degree than, the other, from disease in these situations. In the brain we know little as regards these paths. They probably lie close together, and both forms of sensibility usually suffer together, though one, usually tactile sense, is generally more affected than the other. In disease of the peripheral nerves and nerve- roots, also, both forms generally suffer, though not necessarily in equal degree. Where the two paths lie adjacent, as in the nerves and nerve-roots, a slight grade of damage frequently arrests the conduction of tactile sensation, while painful impressions continue to be transmitted. This probably depends on the greater molecular disturbance created in the nerve path by painful stimuli. What was said of the varieties of anaesthesia in their bearing on the position of the lesion applies in general to analgesia. As regards the spinal cord the indications of the level of the lesion are the same in disturbances of tactile and pain sense, though the indications as to the horizontal position of the lesion are different. Anal- gesia may be of functional origin. In this connection may be mentioned the delay in the transmission of sen- sory impulses (as pain), which is seen in some forms of spinal-cord disease (notably in tabes, amd in compres- sion of the cord). The delay may amount to five, ten, twenty, or even sixty seconds. When marked, such delay is evidence of organic disease (usually of the cord). It must be carefully distinguished from the apparent delay which is seen in psychic conditions (dementia, delusional states). Loss of Temperature Sense is generally observed to be associated with loss of sensibility to pain, but fre- quently both forms of sensibility do not suffer in equal SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 33 degree, and one may be involved without the other. The character of the loss varies in different instances. Sometimes there is absolute inability to recognize either heat or cold. In other cases considerable degrees of heat and cold are recognized, while slighter degrees are not perceived. The sensibility to heat and to cold is not always affected in the same degree (this being due in all probability to the fact that the conduc- tion of heat and cold are subserved by different nerve- fibres). As regards the topographical distribution of loss of sensibility to pain in disease, the same may be said, in general, that was stated in regard to anaes- thesia. In the brain, nerve-roots, and peripheral nerves — that is, wherever the sensory paths for touch, pain, and tem- perature lie close together, all three forms of sensibility are apt to suffer together in disease, and have the same general distribution. But in the spinal cord and me- dulla the tracts for' touch are separated from those for pain and temperature (which probably lie close together) by such an interval (p. ^^^), that the former is readily affected without the latter, and m'ce versa. Some ob- servers place the paths for pain and temperature in the antero-lateral ascending tracts of the cord. Others be- lieve that the central gray matter of the cord is concerned, at least in part, with the upward transmission of these forms of sensibility. In the peculiar condition of the cord, known as syringomyelia, there is observed loss of pain and temperature sense, of one extremity or of one side of the body, with little or no disturbance of tactile sensibility. Focal processes and injury of the cord may produce the same effect. Loss of Muscular Sensibility is observed when the path which conducts impressions from the muscles be- 134 DISEASES OF THE NERVOUS SYSTEM. comes the seat of disease. As already stated (p. 34), this path, after reaching the posterior nerve-roots, Avith other sensory fibres, probably passes up the cord in the poste- rior median column and direct cerebellar tract, without undergoing decussation. After reaching the post-pyra- midal nuclei, the tract decussates in the interolivary tract, and passes by the fillet to the level of the posterior corpora quadrigemina, whence fibres probably pass to the superior parietal lobule of the cortex. The direct cerebellar tract goes to the cerebellum. Practically loss of muscular sense is more frequently observed in disease affecting the peripheral nerves (multiple neuritis) and the posterior nerve-roots (tabes) than in disease nearer the brain. Yet it is met with in marked degree in unilateral and transverse lesions of the cord. In unilat- eral disease of the cord the loss of muscular sense exists only on the side of the lesion, that is, on the side of the motor loss, and opposite the general sensory loss. The muscular sense may also be lost in consequence of disease confined to the interolivary tract in the medulla, and the sense of posture of a limb during active and passive movement, which is dependent in part on the muscular sense (cutaneous and joint sensations being the other factors), may be much impaired or lost from disease of the cortex, and probably also of the central ganglia. There is some reason to believe that the sense of posture is regularly impaired in the limbs of the opposite side whenever there is destructive. disease of the superior parietal lobule. Hypercesthesia and Hyperalgesia. — Increased sensibility to pain is designated hyperalgesia, or, less correctly, hypersesthesia. Probably there is no cutaneous hyper- sesthesia in the sense of increased tactile sensibility, with recognition of two points of the sesthesiometer SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 35 at smaller distances than normal. Sometimes a light touch on the skin causes pain, or an unpleasant sensation, but this is probably due to irritation of over sensitive end-organs which subserve common sensibility (pain), and not to increased tactile acuteness. This increased sensitiveness is frequently due to irritation of sensory fibres in some part of their course — peripheral, spinal, or cerebral. Probably the irritation is operative by exalting the sensory impression as it passes, but it may also act by increasing the irritability of the cortical sensory centres. The distribution of the sensory disturbance is sometimes of service in localizing the position of the lesion, and the same general statements are applicable that have been mentioned in connection with anaes- thesia. Increased cutaneous sensibility is observed in a variety of processes — as meningitis, cerebral and spinal tetanus, hydrophobia, hysteria, traumatic neuroses, etc. It is a common and important symptom of neuritis and multiple neuritis. When tactile or painful stimuli give rise to perverted forms of sensation, as numbness, tin- gling, or formication, these are designated parsesthesi^, Paraesthesiae may have a purely subjective origin, or they may be of cerebral, spinal, or peripheral origin. Pain, another expression of sensory irritation, is an important symptom of organic disease of the nervous system. It is, however, so common in functional affec- tions, that many varieties of pain are in themselves of little diagnostic importance. Severe recurrent limb pains may arise from any form of nervous disease which involves the sensory tract and partially, but only par- tially, destroys it. As examples, may be mentioned the pains of multiple neuritis from neural irritation, of spinal meningitis, spinal tumor, spinal compression, and locomotor ataxia, from irritation of the posterior nerve- 136 DISEASES OF THE NERVOUS SYSTEM. roots, of myelitis from irritation of sensory structures within the cord, of cerebral hemorrhage, softening, or tumor involving the sensory tract in the internal capsule, and of irritative processes in the motor cortex. Pain in the distribution of the fifth nerve is an important and early symptom of disease of the nucleus or trunk of the nerve. The pains that result from irritation of the nerve- roots by vertebral disease are generally increased by movement. This is often marked in vertebral cancer and caries. Pai7i Referred to the Spinal Column is not infrequently observed in disease involving the vertebrce and the dura mater. Occasionally it is met with in spinal-cord disease of long standing, as myelitis. It is then often referred to the parts in the vicinity of the spine, as the sacrum and loins, as well as to the spine itself. Its mechanism and exact significance are not known. Where there is organic disease of the bones, pain, often severe, is a persistent symptom, and is usually associated with local tenderness, but the same association of spontaneous pain and tenderness to ]jressure is seen in the purely neuralgic affection of the spine known as " rachialgia." Sometimes the pains of chronic spinal-cord disease, and of acute processes, are not acute, but dull and per- sistent. These pains are often regarded as rheumatic, particularly when exacerbations occur, as they frequently do in chronic disease, during wet or cold weather. Per- sistent or rheumatoid pains in the limbs should always lead to a search for more unequivocal evidences of spinal-cord disease — such as slight localized loss of power, anaesthesia, or altered reflex action. Cincture Pain (girdle-pain) is a persistent sense of painful constriction, as of a band encircling the body, the limbs, or the neck. It is most frequently observed SYMPTOiMATOLOGY OF NERVOUS DISEASES. 1 37 in cases where the cord is damaged transversely, as in myelitis, and fracture or dislocation of the vertebrae. The pain is due to the irritation of sensory structures just above the seat of the lesion — that is, in the lowest part of the healthy cord, and is referred, as is the rule, to the peripheral sensory nerve-endings. It possesses considerable diagnostic significance, for it is not only evidence of organic disease, but indicates the upper level of the lesion in the cord. A cincture-pain also occurs in locomotor ataxia, but is far less frequently observed than in myelitis. Muscular Tenderness is a symptom which, from its con- stancy in some diseases of the peripheral nerves (mul- tiple neuritis) and muscles (polymyositis), is of diagnostic importance. In polymyositis the muscles are exceed- ingly painful on pressure, though there may be little spontaneous pain except on movement. In multiple neuritis there are neuritic pains and tenderness of the nerve trunks, but the sensitiveness of the muscles to pressure is even more constant. The occurrence of muscular tenderness in trichiniasis must be remembered in this connection. It is usually associated with con- siderable spontaneous pain. Headache. — The head is very frequently the seat of pain. In a large majority of cases this pain is the ex- pression of functional derangement, which is of widely different character in different cases. The headaches which result from gastric disturbance, anaemia, febrile conditions, renal disease, various forms of toxemia and errors of refraction, probably constitute more than ninety-five per cent, of all the headaches met with in general practice. But organic disease within the cranial cavity is also a frequent cause of headache, and the importance of distinguishing between functional dis- 138 DISEASES OF THE NERVOUS SYSTEM. turbance and organic intracranial processes makes it necessary to study carefully the character of every case of headache. The pain of organic disease is usually constant. It varies in degree from time to time, but the patient is seldom entirely free from it. The severity of the pain is also a suggestive feature. In a considerable proportion of cases the pain is at times intensely severe. It persists through the night, and either prevents the patient from sleeping or awakens him from his sleep. This is an im- portant diagnostic point, for the headache of functional disease rarely prevents sleep. Whenever, therefore, a patient complains that his headache frequently keeps him awake during the night, the possibility of organic brain disease should be thought of, and other evidences of such disease should be sought. But it must not be forgotten that in point of severity alone some functional headaches, as neuralgia and migraine, resemble closely the pain of organic diseases. Their paroxysmal char- acter and short duration make an error in diagnosis impossible. The pain of organic disease is increased by anything that leads to increased vascular tension within the cranium, as stooping or coughing, but this is not a distinctive feature of such disease. The headache of organic disease is some- times diffuse, sometimes frontal or occipital, or both ; sometimes it is distinctly one-sided, and occasionally it is sharply localized. Pain which is very limited in extent is more apt to be functional than organic in origin. Pain that is one-sided is seldom due to disease of an opposite region of the brain, but it is never possible to say, from the headache alone, whether there is a close correspond- ence between the seat of pain and the seat of the lesion. If the disease is at the surface of the brain, or in the SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 39 meninges, or very near the surface, there is probably a close correspondence between the two. When the dis- ease is thus superficial there is often local tenderness on light percussion over the seat of the lesion. Sometimes no correspondence exists between the seat of the head- ache and the lesion — for example, the headache is some- times frontal when the lesion is in the cerebellum. The intracranial processes which give rise to head- ache are generally irritative and progressive in character, as, for example, tumor, abscess, and the different varie- ties of meningitis. Nevertheless, little or nothing is known as to the mechanism by which these processes give rise to pain ; even the structures which are the seat of pain cannot be positively designated. The dura mater receives sensory nerve filaments and may unquestiona- bly be the seat of pain when the membrane is the seat of disease, and probably also when it is not the seat of appreciable structural change. The brain of a highly organized animal may be mutilated without giving rise to evidences of pain, but neither this fact nor the cir- cumstance that sensory fibres have not yet been dis- covered in the pia-mater or the cerebral substance can be regarded as showing that those structures are insensi- ble to pain under conditions of disease. It has been supposed that increased intracranial pressure is operative in the production of headache in certain diseases, but while this may be a factor in some cases, it has been shown that processes which, like internal hydrocephalus, increase the intracranial pressure as much as it is ever increased, but cause no tissue irritation, often run their course without causing headache. We have seen that the constancy and severity of a headache may be suggestive, perhaps highly suggestive, of intracranial disease. Yet these characteristics of a 140 DISEASES OF THE NERVOUS SYSTEM. headache never prove the existence of organic disease. Actual proof can be supplied only by the association with headache of other evidences of disease. Of these optic neuritis is the most significant. But double optic neuritis and headache occur as symptoms of certain con- stitutional states, notably lead poisoning, chronic diffuse nephritis, and a high grade of anaemia. If we can ex- clude these conditions, we may regard the occurrence of marked double optic neuritis with headache as evidence of some form of organic intracranial disease. It is hardly necessary to say that neither the absence of headache nor its slight character in any particular case renders it possible to exclude organic disease. In the presence of symptoms of doubtful character, the absence of headache is of some significance in lessening the probability of the existence of organic disease, but in the presence of unequivocal symptoms, such as local paralysis or convulsions, its absence does not materially modify the diagnosis. Cephalic Sensations Other than Pain are frequently complained of by patients who are hypochondriacal or neurasthenic, or whose brains are overworked. The sensations are variously described. Very frequently there is a sense of pressure, slight or great, as if the top of the skull were being forced in. Sometimes the pa- tient feels as if the sides of the head were being forced in, but generally the sensation is referred to the vertex. A feeling of expansion, as if the top of the skull were being lifted, is often complained of. Another and more common sensation, described chiefly by neurasthenics, is a crackling feeling within the skull as if something had broken, followed often by a curious sense of empti- ness or lightness of the head. Sometimes there is sim- ply a sense of fulness of the head or a sense of throb- SYMPTOMATOLOGY OF NERVOUS DISEASES. 14I bing. These sensations and many more are very often described in extravagant language. They are seldom constant, and are always functional. They are generally aggravated by attention. We are in ignorance as to how these sensations are produced, but there is no reason for attributing them to cerebral congestion, or to con- gestion at the base of the brain. Symptoms Referable to the Special Senses. Olfactory Symptoms. — Anosmia, loss of smell, is much more frequently the result of disease of the olfac- tory mucous membrane (chronic inflammation, polypi), than of intracranial disease, and such local disease must be excluded before the symptom can be considered sig- nificant of brain disease. Blows on the head have been known to cause anosmia by mechanically tearing the olfactory filaments from the bulb, but this is an infre- quent occurrence. Another rather infrequent cause of anosmia is pressure on the nerve or bulb by tumor in the anterior fossa of the skull, or by bone disease. Meningitis may also involve the nerve, and it has been compressed in internal hydrocephalus. Rarely anosmia occurs in degenerative diseases of the nervous system, as locomotor ataxia, and dementia paralytica. Disease in the sensory part of the internal capsule (posterior limb) has caused anosmia on the side opposite the lesion. An extensive cortical or subcortical lesion occasionally produces -the same effect. Disease of the tip of the temporo-sphenoidal lobe, involving the olfactory centre, may unquestionably give rise to anosmia on the same side as the lesion. Functional loss of smell may occur in hysteria. It is always associated with other forms of sensory loss, hemiansesthesia, crossed amblyopia, loss of taste, etc. In attaching significance to the presence 142 DISEASES OF THE NERVOUS SYSTEM. of anosmia, it must be remembered that it is sometimes congenital (due to congenital absence of the bulbs), and that it may result indirectly from disease of the trigem- inus, through trophic changes in the olfactory mucous membrane, or from defective local secretion. Hyperosmia or Olfactoiy Hypet'cesthesia is occasionally observed in hysteria. It consists in the development of great acuteness in the sense of smell, so that odors are perceived which are ordinarily not recognized. The symptom has little diagnostic significance. Olfactory Halbici nations. — Subjective sensations of smell may be of functional or organic origin. In in- sanity they are not very uncommon. The epileptic par- oxysm is sometimes ushered in with an olfactory aura, usually unpleasant in character. In several instances the development of gross organic disease (tumor) of the anterior part of the temporo-sphenoidal lobe has been accompanied by olfactory aurae. An aura may also result from disease involving the olfactory tract. The repeated occurrence of such an aura is of great diagnostic signifi- cance in the presence of evidence of organic disease, for it gives a clue to the position of the lesion, sometimes when other indications are wanting. Visual Symptoms. — Amblyopia and Amaurosis are terms used to designate different degrees of visual defect, the form'er meaning a partial loss or blurring of sight, the latter complete blindness. Complete blindness (of nervous origin) of one eye, indicates that the optic nerve is dam- aged between that eye and the chiasma — that is, in the orbit, at the optic foramen, or within the skull between the foramen and the chiasm. Such damage may result from pressure by tumors, from basal disease, from inflammation, and from embolism of the central artery of the retina, etc., but in these cases the blindness is not always absolute. SYMPTOMATOI^OGY OF NERVOUS DISEASES. . I43 Frequently there is concentric limitation of the field, and sometimes there are regular defects. Amblyopia of one eye may also result from disease of considerable extent in the cortex of the opposite hemisphere, involv- tng the lower and posterior part of the parietal lobe (angular and supra-marginal convolutions). There is usually considerable limitation of the visual field in such cases, and though the patient does not notice any defect in the vision of the other eye, examination usually reveals a slight concentric restriction of the field of that side. HemianfEsthesia is also frequently observed in these cases, and its occurrence helps in the distinction of crossed amblyopia from the amblyopia of optic-nerve disease. Other points of distinction are as follows : (i.) the pupillary reaction is diminished in disease of the optic nerve, but is normal in cortical disease ; (2.) The motor nerves of the eyeball are frequently involved in optic- nerve disease, never in disease of the parietal cortex. Functional loss of vision of one eye only is exceedingly rare, but may result in a reflex manner from irritation of the fifth nerve, and, rarely, from hysteria. A functional amblyopia aff'ecting both eyes, as in organic crossed amblyopia, and associated with hemianaesthesia, is some- times observed in hysteria. This functional form is much more frequent than the organic form, though it is probably not as common as has been supposed. Bilateral loss of vision, partial or complete, is infre- quently observed in the course of organic disease of the nervous system, as the result of optic neuritis or optic atrophy, primary or post-neuritic. The relation of these processes to intracranial disease will be discussed else- where. It is important to bear in mind the fact that a considerable error in refraction often gives rise to am- blyopia, and that such an affection must be excluded 144 DISEASES OF THE NERVOUS SYSTEM. before we can attribute the visual defect to disease of the optic nerve. Defective Central Vision sometimes results from ir- regular patches (scotomata) of retinal ansesthesia in- volving the fixing point (macula lutea), and extending a very little distance about it. Such central scotomata tend to be symmetrical in situation, though the vision of one eye may be more impaired than that of the other. The visual loss is seldom absolute, even in the portion of the field where it is most decided, and the loss for colors is usually more extensive than that for white light. This form of amblyopia is met with in those who use tobacco to excess (" tobacco amblyopia "), and occa- sionally occurs from the excessive use of alcohol. It is generally a transient affection, and for this reason is often classed with functional amblyopia, but it is really due to an inflammation of the central fibres of the optic nerve (axial neuritis). Temporary amblyopia, involving both eyes, occurs in certain functional diseases of the brain, notably epilepsy and migraine, but there is little danger of confounding this with amblyopia of organic origin, as the loss of vision is not only transient but distinctly paroxysmal in character. In epilepsy the loss of sight usually just precedes loss of consciousness. In migraine the defect of vision is always partial, and may consist in general blurring of sight, or in unilateral defect in each eye — hemianopsia. Functional amblyopia of one eye from irritation of the fifth nerve has been alluded to. But such reflex am- blyopia is more often bilateral than one-sided, though the loss of sight is frequently most marked on the side of the nerve which is the seat of irritation. The pain of neuralgia may be effective in producing reflex ambly- SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 45 opia ; sometimes the cause is the irritation of a carious tooth, generally a molar. How such causes are effective is not definitely known. Probably the arrest of visual func- tion is the result of inhibition exerted on the nervous ele- ments of the retina, or on the visual centres of the cortex. Bilateral loss of sight, usually of short duration, but often complete in degree, is sometimes met with as a consequence of toxic blood-states— " toxic amblyopia " it is called. Uraemic poisoning is the most frequent cause of such blindness (which is frequently of sudden onset), but poisoning by lead and quinine occasionally produce a similar result. There are usually no ophthal- moscopic changes to which the blindness in these cases can be ascribed. Concentric Limitation of the Visual Field^ both for white light and for colors, is observed in many of the affec- tions that have been mentioned as causes of ambly- opia. If we exclude those cases in which the limitation is the result of structural change in the optic nerve (neuritis, atrophy) there remain a number of conditions of the nervous system, both functional and organic, in which this limitation is of frequent occurrence. , Of these conditions the following are of especial importance : crossed amblyopia of organic origin, crossed amblyopia of hysterical origin, crossed amblyopia occurring in the course of the traumatic neuroses, the amblyopia of epi- lepsy and of neurasthenia, and the amblyopia of multiple sclerosis. The acuity of central vision may be impaired in any of these conditions, but in some of them {e. g., the traumatic neuroses) it is frequently normal. He77iianopsia.^ — Hemianopsia is loss of vision in one lateral or vertical half of the visual field. It almost ' The word hemiopia is properly used to designate loss of sight in one half of the retina. A left hemiopia is therefore equivalent to a 146 DISEASES OF THE NERVOUS SYSTEM. always involves both visual fields, but partial damage to one optic nerve occasionally gives rise to a unilateral hemianopsia. In bilateral hemianopsia either one hori- zontal or vertical half of each field may be obscured. A horizontal defect is, however, exceedingly rare. Ver- tical hemianopsia, on the contrary, is not very infrequent, and constitutes a symptom of the greatest importance for the localization of cerebral lesions. Several varieties of bilateral vertical hemianopsia (which is always due to an intracranial lesion) must be distinguished. A. — Temporal or Bi- Temporal Hejiiianopsia, is that variety in which the temporal half of each field is obscured. It therefore represents a defect of the nasal half of each retina, which can result only from disease of the central portion of the optic chiasm, involving the decussating fibres of each retina. Often the process (tumor or inflammation) which gives rise to temporal hemianopsia extends laterally, and involves the non-de- cussating fibres of one side of the chiasma, thus causing total blindness of the corresponding eye, or, if both sides of the tract are involved, of both eyes. In some cases of temporal hemianopsia from syphilis at the base, a rapid and frequent variation of the dark half-fields has been noted (so called " oscillating bi-temporal hemian- opsia "). It is probably of some diagnostic importance, as evidence of basal syphilis (gumma, chronic menin- gitis), but cannot be regarded as pathognomonic. B, — JVasal Hemianopsia. — Obscuration of the nasal half of each field from anaesthesia of the temporal half of each retina is not only the rarest form of hemianopsia right hemianopsia, and, conversely, a right hemiopia to a left hemi- anopsia. The word hemianopia is used synonymously with hemian- opsia. Lateral hemianopsia is also known as homonymous, hemianopsia. SYMPTOMATOLOGY OF NERVOUS DISEASES. I47. but is the rarest of all visual defects, since it can result only from a lesion which involves each side of the optic chiasm without damaging the central part. In one case, such hemianopsia was produced by the pressure of cal- cified and enlarged carotid arteries on the sides of the chiasm. C. — Lateral, or Homonymous Hemianopsia, is that form of hemianopsia in which corresponding visual fields are obscured. Thus, in right lateral hemianopsia both right half-fields are blind. In all cases of lateral hemianopsia the lesion is posterior to the optic chiasm. It may be in one optic tract, in one of the primary optic centres (corpora geniculata externa), in the pulvinar of the thalamus, in the sensory tract of the internal capsule, in the optic radiation, in the occipital lobe, or in the half- field centre of the cortex (cuneus). In whichever one of the enumerated positions the lesion lies, it is on the side opposite the half-fields obscured. A lesion of the an- gular gyrus may also cause lateral hemianopsia, but probably it can do so only by injuring the immediately underlying optic radiation. The determination of the position of the lesion in the optic apparatus is based on the associations of the hemianopsia. The extent of the half loss of the visual fields varies in different instances. The line of division between the obscured and seeing halves may pass through the fixing point (corresponding to the macula lutea), or may pass just to one side of it, leaving it within the region of sight. These are the typical forms of hemianopsia. In other instances the line of division is irregular, or inclines obliquely to one side or the other above and below the fixing point. These variations do not depend on the position of the lesion causing the hemianopsia, but on individual pecul- iarities in the decussation in tlie optic nerves. Certain 148 DISEASES OF THE NERVOUS SYSTEM. Other variations, however, are related to the situation of the lesion. In the first place, hemianopsia may be incom- plete, a portion only of the half-fields being obscured. The area of defective vision is in these cases sector-like, being frequently irregularly quadrantic in outline. This incomplete loss is probably dependent on partial destruc- tion of the visual path, or half-vision centre, most fre- quently the latter. Secondly, lateral hemianopsia may be associated with concentric limitation of the half-fields of vision that remain. This limitation of the remaining fields is always greatest in the eye of the side opposite the lesion. It probably indicates that the lesion involves not only the half-vision centre of the cortex, or the optic fasciculus in the occipital lobe, but also the higher visual apparatus (see page 42), which is supposed to lie in and beneath the inferior parietal lobe. In about one half of the cases of hemianopsia the symptom is associ- ated with transient or permanent hemiplegia of organic origin, both symptoms being effects of the same lesion. The hemiplegia is on the side of the loss of vision ; the patient "cannot see his paralyzed side." Complete loss of sight in both eyes occasionally results from double lateral hemianopsia. It depends on the occurrence of two lesions, one in each hemisphere, involving the visual path posterior to the chiasm. Lateral hemianopsia which has been complete for several months, seldom passes away entirely. It may remain, with little change, during many years ; in one case it is known to have endured twenty-three years. It is important to know that hemianopsia may exist for a considerable time without being noticed by the patient. Lateral hemianopsia is not a very uncommon symptom of migraine. It is of short duration, and often the loss involves the right-half fields in one attack, and the left- SYMPTOMATOLOGY OF NERVOUS DISEASES. 149 FIG. 44. Diagram illustrating the course of the optic and visual tracts. (AfterStarr.) A, lesion of left optic nerve, causing total blindness in left eye ; B, lesion causing bilateral temporal hemianopsia ; C, C, lesions in the optic or visual path posterior to the chiasm. All such lesions cause bilateral homonymous hemianopsia, but give riseto different associated symptoms according to the position of the lesion. Thus, a lesion in the int. capsule, as at C, causes also hemiplegia of the opposite side of the body. The rest of the diagram requires no explanation. I50 DISEASES OF THE NERVOUS SYSTEM. half fields in another. Not infrequently other forms of visual disturbance occur during other attacks. It is well to bear in mind the fact that the hemianopsia of migraine may occur as an isolated symptom, though it is usually associated with some degree of headache and gastric disturbance. It is probable that migraine is the chief functional affection in which hemianopsia occurs. It is exceedingly probable that the symptom is only rarely of hysterical origin. Transient hemianopsia is frequently observed during the onset of cerebral hemorrhage, but in this case it is probably an indirect symptom, due to inhibition of the cortical centre by irritation. In almost all cases of hemianopsia the loss of vision for white light is associated with a corresponding loss for colors. It occasionally happens, however, that there is hemianopsia for colors — " hemi-achromatopsia," it is called — when there is no loss whatever for white. In these cases an object, when moved across the field, is seen in all positions, but becomes uniformly gray when moved beyond the vertical line of separation between the half- fields. The explanation of this remarkable phenomenon must lie in the existence of a distinct centre for color vision, adjacent, in all probability, to the half-vision centre in the cuneus. Symptoms referable to irritation of the optic apparatus occasionally appear in the course of organic processes which eventually give rise to atrophy or inflammation of the optic nerve, but such phenomena are of much more frequent occurrence in functional and nutritional disturbances of the nervous system. Muscas volantes, sparks, etc., not infrequently appear to pass before the eyes of neurasthenic and hysterical patients. A zigzag appearance, described as the ''fortification spectrum," is often seen in migraine, but is not met with in any SYMPTOMATOLOGY OF NERVOUS DISEASES. 151 Other neurosis. It usually lasts many minutes. Sparks, flashes of light, colors before the eyes, and other irrita- tive symptoms related to the visual apparatus occur in migraine, and also in epilepsy. In epilepsy a visual aura is not uncommon ; indeed, such an aura is more frequent in epilepsy than all other warnings of the special senses combined. Sometimes these impressions are very elabo- rate, and may represent a complex perception, as of a human face ; sometimes they consist of crude sensations, such as luminous flashes, etc. Rarely a visual aura is a precursor of convulsions due to organic cerebral disease. In most cases of this kind the lesion has been located in the cortex or white substance of the occipital lobe. Ophthalmoscopic Changes. — Pathological changes in the fundus of the eye, and particularly in the optic nerve, are of frequent occurrence in the history of structural disease of the nervous system. Many of these alterations in the optic nerve may be carefully studied during life with the aid of the ophthalmoscope, for in the optic disc we have presented to direct view the termination of the optic nerve. The information thus obtained is of the highest importance in diagnosis, and renders a knowledge of ophthalmoscopic technique in- dispensable to the student of nervous diseases. Of the changes which are observed, some are the direct conse- quence of the cerebral or spinal cord lesion — that is, they are consecutive to the process in the nervous system ; others are not related directly to the morbid process in the nervous system, but to the ultimate cause of this pro- cess — that is, they stand in the same relation to this cause as does the process within the nervous system, and are hence denominated associated changes. The consecutive changes are optic neuritis (or inflammation of the optic nerve) and some forms of atrophy of the optic nerve. 152 DISEASES OF THE NERVOUS SYSTEM. In Optic Neuritis the optic nerve may be inflamed threughout its entire extent, or the inflammatory pro- cess may be most marked in one particular part of its course. When the inflammation is most intense behind the eyeball (retro-ocular neuritis), the visible signs of neuritis may be slight or absent, though there is con- siderable loss of vision. When the inflammation is most marked, as it generally is, at the optic papilla within the globe, there are always distinctive ophthalmoscopic signs (papillitis). At first the disc becomes slightly swollen, and its edge, which is normally sharply defined, grows less distinct. This loss of distinctness or '' softening " of the edge of the disc is the important characteristic of beginning papillitis, the swelling of the disc being at first only very slight and causing little appreciable pro- jection of the papilla. The nasal side of the disc (which possesses more nerve-fibres than the temporal side) is generally the first to grow indistinct ; later the blurring involves the entire circumference of the papilla. The normal white central depression (physiological cup) is soon obliterated, and the whole disc, which at first shows only slightly increased vascularity, assumes a full red tint, or a grayish opalescence. On direct examination (p. 584) the disc has a distinctly striated appearance, the strice radiating from the centre of the disc and corre- sponding to the course of the nerve-fibres. Early in the process the vessels show little change ; when the swelling is marked the veins become wider and tortuous, and may be lost as they pass over the edge of the disc. The arteries may remain normal in size ; frequently they are contracted. They may be partially hidden from view by the opacity. As the papilla grows more and more promi- nent the breadth increases, until it may attain twice the diameter of a normal papilla. The prominence of the SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 53 disc is so great in some cases that it can be distinctly seen with a 7 D convex lens. A gradual subsidence of these changes takes place after a few weeks or months. The opacity of the disc slowly disappears and the out- lines of the papilla again become recognizable, although the disc may continue for some time to look hazy ("woolly disc "). In slight degrees of neuritis the disc may regain its normal appearance. In more severe cases the papilla grows white or pale, and the arteries continue narrow or grow even more contracted ; "consecutive" or " post neuritic " atrophy sets in. The inflammatory changes which are seen with the aid of the microscope in the papilla can often be observed, though in less degree, throughout the course of the optic nerve, and may be traced through the chiasma. Imme- diately behind the eyeball the space between the inner and outer sheath of the nerve is generally distended with fluid inflammatory products. An intense grade of optic neuritis (papillitis) always gives rise to impaired vision. The acuity of sight is diminished and the field of vision becomes restricted both for white and for colors. Sometimes the impair- ment of vision is very great, particularly for green and red, but not infrequently it is inconsiderable, even with a high grade of neuritis. The grade of visual disturbance is often greater during the subsidence of the neuritis than during the period of most intense congestion. In optic neuritis of slight or moderate intensity there may be a corresponding degree of visual defect, but it is an important fact that even a considerable grade of neuritis frequently causes no appreciable disturbance of sight. We can never exclude optic neuritis because a patient has a high grade of visual acuity. Optic neuritis may occur in consequence of several 154 DISEASES OF THE NERVOUS SYSTEM. different intracranial processes. Of these causes tumor is by far the most frequent. The nature, size, and seat of the tumor appear to exert little influence in the pro- duction of the neuritis. The neuritis of tumor is often in- tense, and it is of diagnostic importance that an intense degree of neuritis is not often the result of any other process. Optic neuritis occurs in about nine tenths of all intracranial tumors. Meningitis is the next most frequent cause, and the neuritis is somewhat more fre- quent in meningitis of the base than of the convexity. Cerebral abscess (though less frequently a cause than meningitis) is certainly not an infrequent cause of optic neuritis. About six per cent, of all cases of multiple sclerosis are accompanied with optic neuritis, which is frequently slight and of short duration. In these cases there are inflammatory or sclerotic patches in the optic nerve. In thrombotic softening and hemorrhage, optic neuritis is of rare occurence, but in embolic softening it is less uncommon. Occasionally optic neuritis is met with in diffuse cerebritis. It is also seen after sunstroke and in idiopathic hydrocephalus. The optic neuritis of brain disease is almost always double, but the process is often more advanced in one eye. In multiple sclerosis the neuritis is very often one-sided, in consequence of unilateral involvement of the nerve by a sclerotic patch, and it is occasionally one-sided in other forms of brain disease, but, in general, unilateral neuritis is much more often due to disease within the orbit or at the optic foramen than to cerebral processes. In rare instances optic neuritis has been developed in the course of acute or subacute disease of the spinal cord — transverse and disseminated myelitis, for example. It is probable that in most of these cases the neuritis is to be re- garded as an associated and not as a consecutive process. SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 55 Not infrequently optic neuritis occurs in consequence of disease outside of the nervous system. It is often seen in the course of chronic diffuse nephritis, and oc- casionally occurs in chlorosis, marked ansemia, diabetes, lead poisoning, scarlet fever, typhoid fever, and erysipe- las. In some of these conditions, notably in anaemia, lead poisoning, and nephritis, there may be considerable headache, and the association of this with optic neuritis may give rise to a suspicion of intracranial disease, if the occurrence of papillitis under these circumstances is not borne in mind. Degenerative changes are often seen in the retina in cases of nephritic optic neuritis (neuro-retinitis). These changes consist of small white patches of fatty degeneration, often characteristically grouped about the macula lutea. When these changes are present they show the neuritic process to be depend- ent on kidney disease. Their absence, however, does not by any means exclude the possibility of the nephritic origin of the neuritis. As regards the mechanism by which optic neuritis is produced, there is still considerable difference of opin- ion, but it is probable that the most important single factor is a descending inflammation along the optic nerve, or along the sheath by which it is invested. This view is supported by the pathological findings in a large num- ber of cases of optic neuritis, and it is the only mechanism which will explain the occasional occurrence of unilateral opiic neuritis on the side opposite a cerebral tumor. Dis- tension of the optic sheath immediately behind the globe with serous fluid is of frequent occurrence in optic neu- ritis, and may be a factor in heightening the inflamma- tion of the papilla, by preventing the escape and absorp- tion of products of inflammation. It is also possible that this fluid may at times contain irritating pathogenic 156 DISEASES OF THE NERVOUS SYSTEM. material which is capable of inducing a certain degree of neuritis. There can be no doubt, however, that the first- mentioned mechanism is frequently alone effective. The theory that increased intracranial pressure is opera- tive in causing optic neuritis by causing pressure on the cavernous sinus is now untenable : (i) Because a free anastomosis has been shown to exist between the orbital and facial veins ; (2) because large tumors of the brain and great hydrocephalus may exist with little or no neu- ritis ; (3) because tumors so small as to cause no appre- ciable change in intracranial pressure often produce a high grade of optic neuritis. It is to be regretted that this theory once gained so firm a hold that many still cling to it in the face of the objections mentioned. In the minds of many there is even at the present day a belief that optic neuritis is a symptom which is of use in the localization of cerebral lesions. This is an error. Optic neuritis is usually a diffuse and not a focal symp- tom, and while it is a little more common with lesions in certain locations in the brain than in others, the symp- tom possesses pratically no localizing value. Atrophy of the Optic Nerve. — Several clinical varieties of atrophy of the optic nerve, of importance in their bearing on the diagnosis of disease of the central nervous system, must be distinguished. Primary or simple atrophy, that is, atrophy which is not preceded by any recognizable inflammatory change in the papilla or surrounding structures, occurs in the degenerative diseases of the brain and spinal cord. It is probably of more frequent occurrence in multiple sclerosis and loco- motor ataxia than in any other forms of disease. In multiple sclerosis it is much more common, in some degree, than is generally supposed. In a small propor- *-ion of these cases the atrophy is complete ; in a consid- SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 57 arable proportion (about 20 per cent.) the atrophy is partial, but involves the whole papilla, and in nearly the same number of cases the atrophic change is partial and involves only the temporal half of the disc. In loco- motor ataxia, optic atrophy is present in about 15 per cent, of all cases, and is frequently an early symptom. The form of atrophy is rather characteristic, the disc being usually gray, as seen by the ophthalmoscope, with little or no diminution in the size of the vessels, — " gray atrophy." In a closely allied disease, dementia paralyt- ica, optic atrophy occurs in a small proportion of cases (5 per cent.), but here, as in multiple sclerosis, the atrophy is probably to be regarded as an associated and not as a consecutive change. Primary atrophy also occurs unassociated with central disease. Such atrophy has been attributed to cold, menstrual disturbance, migraine, exhausting diarrhoeas, and, very rarely, to diabetes, syphilis, and various spe- cific diseases. Tobacco, alcohol, and lead may lead to partial atrophy, but this is frequently preceded, in the case of tobacco and alcohol, by an axial neuritis. Primary atrophy generally involves both eyes, but one is often involved much earlier than the other. Not very rarely one eye alone is affected. Disease of the optic nerve behind the eye or at the chiasm may cause atrophy (usually gray) of the optic nerve. Occasionally such atrophy is preceded by slight neuritis ; usually it is not. This form is denominated " secondary atrophy." Loss of sight generally precedes visible signs of atrophy by a considerable period. Neuritic or papillitic atrophy is that variety which follows optic neuritis. Frequently, but by no means always, the neuritis leaves changes in the choroid and in the vessels which make it possible to distinguish neuritic 158 DISEASES OF THE NERVOUS SYSTEM. atrophy from the simple form. Another variety of atrophy is that which occurs after disease of the choroid and retina. The ophthalmoscopic appearances of atrophy vary somewhat in different cases. In all cases the disc is whiter than normal, but the degree and character of the pallor presents differences. The pallor may affect the whole disc or its temporal side only. But the temporal side of the disc is normally somewhat pale, because the nerve-fibres are there least numerous, and this may give rise to some difficulty in diagnosis when the pallor of atrophy is confined to the temporal side of the papilla. The pallor of atrophy is due to ihe wasting of the capil- laries of the disc which accompanies the degeneration of the nerve-fibres. The tint of the disc varies, being in some cases milk-white, in others grayish, and in others bluish or yellowish. There is no diminution in the size of the optic disc in atrophy, because, although the nerve usually shrinks, the size of the papilla is dependent on the size of the sclerotic opening. Frequently the edge of the disc becomes very sharp and distinct. Sometimes the ves- sels are diminished in size, but this is not a constant change. When optic atrophy is pronounced there is some diminution in the acuity of vision. In general, the degree of visual loss is related to the degree of visible change (pallor) in the optic nerve, but to this rule there are important exceptions. In some cases there is a high degree of visual defect with little or no pallor. When it is remembered that the whiteness of the disc depends on wasting of the capillaries, while the visual loss depends directly on the degree of change on the nerve-fibres of the optic nerve, it is not surprising to find that there is not infrequently a want of correspondence between visual acuity and the tint of the papilla. SYMPTOMATOLOGY OF NERVOUS DISEASES. I 59 The visual field, both for colors and for white, shows some degree of peripheral limitation in almost all cases of atrophy. In some cases this limitation is concentric, in others sector-like. Impaired color-vision is another accompaniment of optic atrophy, which, in some degree, is present in a large proportion of cases. Green is usually the color first lost ; red the next Of the Associated Ophthabnoscopic Changes of importance in relation to nervous disease, the following are the prin- cipal : 1. Primary atrophy of the optic nerve, occurring for the most part in association Avith degenerative diseases of the brain and spinal cord. 2. Albuminuric retinitis is of importance, because it is so frequently associated with atheromatous change in the arteries, and such degeneration may lead either to cerebral hemorrhage or to thrombotic softening. 3. Syphilitic choroiditis and the atrophy which follows it are frequently seen in brain disease from acquired and sometimes from congenital syphilis. Certain forms of atrophy of the choroid, however, result from other conditions than syphilis (posterior staphyloma, hemor- rhage, senile change). 4. Tubercles of the choroid are in rare cases met with in tubercular meningitis. They are much less frequently observed when there is tubercular meningitis only than when such meningitis is associated with general tuber- culosis. When they develop early in the disease they may be of the greatest assistance in diagnosis. 5. Embolism of the central artery of the retina very rarely occurs in cases of cerebral embolism. 6. Retinal hemorrhages occur under a variety of con- ditions — in albuminura, leucocythaemia, purpura, etc. Occasionally small hemorrhages are found in the l6o DISEASES OF THE NERVOUS SYSTEM. meninges, particularly the pia-mater, in these conditions, but they generally give rise to no symptoms. The routine use of the ophthalmoscope in all cases of nervous disease in which there is even a possibility of discovering changes in the fundus cannot be too strongly urged. It is, however, important to remember that the condition of the circulation within the eye is not in any sense an index of the condition of the circulation within the cranial cavity. Auditory Symptoms. — Deafness of nervous origin, that is, due to disease of the terminal auditory filaments in the labyrinth, or to disease of the auditory nerve or its central connections (p. 55), is of relatively uncommon occurrence as compared with deafness from middle- and external-ear disease. The character of such " nervous deafness " is the same, whether the disease causing it be central or peripheral ; there is defective conduction of soufid through the cranial bones as well as through the air. This constitutes a sharp distinction from the deafness dependent on disease of the middle and external ear, which impairs the perception of sounds conducted through the air, while it does not destroy the ability to perceive sounds conducted through the cranial bones. In making use of this method of distinguishing between deafness due to disease of nervous structures and that dependent on middle- or external-ear disease, either a vibrating tuning-fork or a watch may be employed. In persons more than fifty years of age it is not rare to find some diminution in the perception of vibrations trans- mitted through the bones of the skull, owing to changes in the labyrinth incidental to the degenerative period of life. This diminution is bilateral and never amounts to complete loss, though frequently the ticking of a watch is no longer perceived when the latter is in contact with the zygoma. SYMPTOMATOLOGY OF NERVOUS DISEASES. l6l Since the character of the deafness is the same, whether it be due to labyrinthine, nerve, or central disease, the localization of the situation of the disease depends on associated symptoms. If there is paralysis of the facial nerve on the same side as the deafness, and there is no middle-ear or bone disease, the lesion is certainly in the auditory nerve, either within the auditory canal or be- tween this and the superficial origin of the nerve from the upper part of the medulla. If deafness of rapid or sudden onset is associated with symptoms of medullary or pontine disease, especially with hemiplegia on the side opposite the loss of hearing, the lesion probably involves the auditory nucleus (p. 55). Deafness associated with hemiansesthesia or hemiplegia on the same side probably indicates disease of the internal capsule or extensive cortical disease involving the auditory centre in the first temporo-sphenoidal convolution. Deafness from disease involving this centre is exceedingly rare. Much the most frequent cause of nervous deafness, both unilateral and bilateral, is labyrinthine disease. Such disease also gives rise to tinnitus and frequently to vertigo, and the association of one or both of these con- ditions with nervous deafness suggests, but does not prove, the existence of disease of the labyrinth. It does noi prove its existence because disease of the nerve may have the same association, but in this case there is usually evidence of other nerve disease (facial paralysis). The nature of the labyrinthine disease varies in different cases. Acute and chronic inflammation, syphilitic dis- ease, and degenerative processes occur. The deafness produced by certain drugs (quinine, etc.) is probably of labyrinthine origin. The auditory nerve suffers chiefly from processes originating in neighboring structures — meningitis, simple and syphilitic, new growths, etc. l62 DISEASES OF THE NERVOUS SYSTEM. Disease involving the auditory nuclei is generally softening or hemorrhage, sometimes tumor. Disease of the auditory path above the nuclei, in the tegmentum of the crus, in the internal capsule, or in the white substance of the temporo-sphenoidal lobe, is rare. Occasionally deafness is of functional origin. It is not uncommon in hysteria in association with hemian- aesthesia, etc. Tinnitus Aiirium is a term used to designate all sounds which are referred to the ear, and have no objective cause external to the body. These subjective sounds, as described by patients, are exceedingly varied in charac- ter. Generally they are simple in nature — that is, of a low degree of elaboration, and are spoken of as ** sing- ing," "ringing," ''hissing," "buzzing," " whistling," etc. Sometimes they are more elaborate in character, and are compared to the ringing of bells, the rustling of wind in the trees, etc. The simpler sounds may be either aural or central in origin, but those of greater elabora- tion are almost always of central (cortical) origin. The sound may be constant or intermittent, continuous or pulsatory. In intracranial aneurism (carotid or verte- bral) a pulsating sound has in very rare instances been produced, which could be heard by another person, and such a sound, if audible on auscultation, makes the exist- ence of aneurism highly probable, and practically certain if there are at the same time evidences of a tumor at the base of the brain. But though the diagnostic significance of this sign is great, its extreme rarity makes it of little practical use. In the great majority of cases tinnitus is of aural origin, for nearly all diseases of the ear, inner, middle, or outer, may be accompanied by it. Much less fre- quently the cause is organic irritative disease of the SYMPTOMATOLOGY OF NERVOUS DISEASES. 163 auditory nerve or centre. Functional derangement of the cortical auditory centres occasionally gives rise to tinnitus. Thus, an epileptic attack may be preceded by a paroxysmal sound, due no doubt to nervous discharge from the nerve-cells constituting the auditory centre, and very rarely such sounds occur in migraine. Occa- sionally a continuous tinnitus occurs in cases of neuras- thenia, mental depression, etc. Intense habitual stimu- lation of the auditory nerve, as by the sound of cannon, musical instruments, etc., may cause tinnitus. Usually some degree of deafness coexists with tin- nitus. When this is the case both deafness and tinnitus are dependent on the same cause, and what this cause is must be determined by a study of the associated symp- toms, as already mentioned in speaking of deafness. Vertigo. — This word has been loosely used to desig- nate almost any subjective sensation that is associated with a feeling of imperfect equilibrium, or of transient mental confusion. When correctly used, the term is applied only to sensations in which there is experienced a feeling of movement, often of turning, or in which surrounding objects, which are really at rest, have the appearance of moving in a definite direction. These subjective sensations are often accompanied by a com- pensatory movement of the body of the patient, which may result in a fall. Some impairment of conscious- ness, never amounting to actual loss, always exists in vertigo. Vertigo is a frequent symptom of organic brain dis- ease, but it is a much more common symptom of periph- eral disturbance. Occasionally it occurs where there is no discoverable cause for it, and then it is sometimes termed " essential " vertigo. It is, however, never to be regarded as a definite disease, but always as a symptom, 164 DISEASES OF THE NERVOUS SYSTEM. although in many caSes it is the most obtrusive symptom of the condition on which it depends. Before mentioning the varieties of vertigo, it is desira- ble to consider briefly the manner in which the equi- librium of the body is maintained. When the body is in any position requiring the active contraction of muscles for the maintenance of its balance, the centrifugal motor impulses which leave the brain for the establishment of this balance are influenced through the mediation of cerebral centres by certain sensory impressions which serve for the guidance of these centres in adapting the position of the body to its environment. The most important of these sensory impressions are those derived from the semicircular canals and from the motor nerves of the eyeball. Other impressions that furnish the brain with guiding information as to the relation of the body with surrounding objects are derived from the skin of those parts which are in contact with external things, and from the muscles whose activity determines posture. If any one of these different kinds of guiding sensory impressions becomes imperfect or deranged its expression in consciousness is felt as a derangement of the cerebral centre — that is, as vertigo. Derangement of the aural impressions gives rise to aural vertigo, derangement of the guiding impressions of the muscles of the eyeball results in ocular vertigo. Aural Vertigo — that is, vertigo dependent on disease of the semicircular canals — is by far the commonest and most important variety of vertigo, constituting at least nine tenths of all cases of true vertigo. The disease of the semicircular canals is usually evidenced by tinnitus aurium and by nervous deafness. Often the latter is slight. Sudden lesions of the labyrinth generally give rise to violent attacks of vertigo and marked audi- SYMPTOMATOLOGY OF NERVOUS DISEASES. 165 tory disturbance, and this variety of aural vertigo is properly known as Meniere's disease, although this name is sometimes made to include slighter forms of the affec- tion. It is common for aural vertigo to be mistaken for evidence of organic disease of the brain, particu- larly for hemorrhage and softening. Ocular Vertigo is a rare and usually slight form of vertigo which is due to paresis of an ocular muscle. The vertigo depends on the erroneous projection of objects caused by the diplopia resulting from the pare- sis. The occurrence of diplopia makes the diagnosis of the trouble easy. Vertigo is not infrequently associated with dyspepsia, and the occurrence of vertigo in connection with gastric symptoms has led to the description of what is called gasti'ic vertigo. It is doubtful whether vertigo is ever really referable entirely to gastric disorder. The ma- jority of the cases described as gastric vertigo are due to labyrinthine disturbance and are really varieties of aural vertigo. But frequently the evidences of labyrinthine trouble are slight, and the true character of the disorder is readily overlooked. It must not be supposed, how- ever, that gastric disorder has no influence in bringing about vertiginous attacks. It is easy to understand how a disordered stomach may act, through the central con- nections of the vagus, as an important exciting cause of vertigo, by disturbing the balance of an already unstable cerebral centre. Vertigo sometimes constitutes an aura of the seizures of petit mal, and, at times, of grand mal. The distinction of this form from aural vertigo is described on page 552. The convulsions of organic disease of the brain are also at times preceded by vertigo. As a symptom of organic brain disease, vertigo has little diagnostic significance, l66 DISEASES OF THE NERVOUS SYSTEM. for it may occur in connection with a variety of lesions. It is especially frequent in lesions of the cerebellum and pons, and disease of the middle peduncle of the cerebel- lum gives rise not only to vertigo, but to an actual forced rotation in the long axis of the body towards the side of the lesion. The mere occurrence of vertigo, however, is of no localizing value, as it may be produced by disease in almost any part of the brain. It may occur in the course of cerebral tumor, abscess, chronic meningitis, general paralysis, multiple sclerosis, and at the onset of cerebral hemorrhage, embolism, or thrombosis. When vertigo is severe it is apt to be accompanied by vomiting, which seems to be entirely dependent on the severity of the vertigo and not upon its cause. Slight vertiginous attacks, consisting merely in a sense of defective equilibrium, may occur in the course of hys- teria, neurasthenia, anaemia, etc. Gustatory Symptoms. — The more important facts relating to loss of taste have already been sufficiently con- sidered in connection with the anatomy of the fifth nerve (p. 51). There remain to be mentioned only the per- version of the sense of taste (parageusia) which is occasionally observed in hysteria, insanity, and other neuroses : the increased sensitiveness of taste, which is of occasional occurrence, under the same conditions ; and the various subjective sensations of taste, usually un- pleasant in character, that occur in insanity, and, rarely, as the aura of an epileptic paroxysm. With the possible exception of aurse of taste these disturbances are of slight diagnostic importance. Trophic Symptoms. — The nutrition of the various tissues of the body is to a considerable extent under the domination of nervous structures, but we know little of the exact character of this influence and of the conditions SYMPTOMATOLOGY OF NERVOUS DISEASES. 167 on which it depends. In the case of certain tissue ele- ments the changes in nutrition that result from morbid conditions of the nervous system, in consequence of this dependence, are very striking and possess considerable diagnostic significance. The principal structures in which such alterations occur are the skin, the bones and joints, and the muscles. Trophic Changes in the Skin may result from peripheral, spinal, or cerebral lesions. They vary considerably in character according to the acuteness of the lesion which gives rise to them, and are much more marked and frequent in peripheral and spinal than in cerebral disease. When the changes are rapid and intense, as they are in acute disease of the nerves (for example, acute neuritis), or spinal cord (acute myelitis), the skin becomes hot and red, bullae form, and slight pressure may give rise to slough- ing. In chronic lesions of the nerves and cord (chronic myelitis, syringomyelia) there is a gradual change in the nutrition of the skin, which grows thin, red, and glossy, and the nails become retarded in growth, brittle, and thick. In chronic cerebral disease (hemorrhage, softening, etc.) the skin sometimes becomes rough, dry, and thick, and the nails occasionally grow curved and brittle. In general, it may be said that the most serious trophic changes in the skin take place when the gray substance of the cord or posterior nerve-roots are involved in irritative processes, and there can be little doubt that the nutrition of the skin is dependent on fibres which pass through the posterior nerve-roots. Whether there are special trophic nerve- fibres is not known. The situation of the trophic centres is also obscure, but it is probable that both the gray sub- stance of the cord and the posterior root-ganglia are in some way related to the nutrition of the skin. One form of eruption is unquestionably dependent on l68 DISEASES OF THE NERVOUS SYSTEM. a nervous lesion : the eruption of herpes zoster. There is some reason to believe this affection to be dependent on an inflammatory process involving a nerve-trunk or its terminal nerve-filaments, and sometimes one or more intervertebral ganglia. It is very possible that other forms of eruption (psoria- sis, scleroderma) are dependent on nervous lesions, and several varieties of cutaneous ulceration (bed-sores of myelitis, perforating ulcer of foot) have long been re- garded as true trophic lesions. But it is probable that in the case of these ulcerations the death of tissue is caused by external agencies, such as injuries and micro-organic infection, which is rendered possible by the ansesthesia that exists in these cases. Probably in addition to the ansesthesia, the nervous lesion causes, in these cases, some modification of the nutrition of the parts, which predisposes them to necrosis from trivial injuries. The trophic changes that occur in the eyeball in con- sequence of disease of the trigeminus may be mentioned in this connection. Lesions of the trigeminus, partic- ularly irritative lesions involving the first division (oph- thalmic) of the nerve, are frequently followed by ulceration of the cornea and subsequent perforation. This is espe- cially apt to occur when the lesion involves the Gasserian ganglion, or the nerve in front of it. Whether these alterations in the nutrition of the eyeball are to be regarded as true trophic changes, or simply as conse- quences of injuries which the accompanying ansesthesia makes it difficult to guard against, cannot be positively stated. It is certainly true that under strict antiseptic care, ulcers of the cornea can be made to heal rapidly and perfectly, while the nerve-lesion continues in progress. Trophic changes in the Bones and joints are observed in the course of spinal cord and cerebral disease. Retar- . SYMPTOMATOLOGY OF NERVOUS DISEASES. 169 dation in the growth of the bones, without pathological changes in their histology, occurs in children when the ganglion-cells of the anterior horns are the seat of acute inflammation, and in most cases of hemiplegia coming on in the course of childhood. In rare instances similar changes occur after peripheral nerve-lesions. Extreme atrophy of the bones, together with atrophy of the skin and subcutaneous tissue, occurs in the rare condition known as progressive facial atrophy (facial hemiatrophy). The affection is strictly unilateral, and probably depends on some derangement in the trophic function of the fifth nerve, possibly on disease of its trophic root (see Fig. 31). Brittleness of the bones {f?-agilitas ossium) lead- ing to fracture from slight injuries, so-called "spon- taneous " fracture, is occasionally observed in dementia paralytica, amotrophic lateral sclerosis, and locomotor ataxia. It is a question whether the fragility in these cases is due directly to the nervous lesion, or is merely one consequence of defective general nutrition. Inflammation in the larger joints is occasionally met with in acute cerebral and spinal-cord diseases. The cer- ebral affection with which this change is associated is usually hemorrhage or softening (the latter more fre- quently), and the joint changes are limited to the hemi- plegic side. The synovitis comes on in the course of a few weeks after the onset of the hemiplegia. Bilateral effusion into the knee-joints is occasionally observed in the course of acute myelitis. Extensive changes in the larger joints (knee, shoulder, elbow) are sometimes ob- served in the course of locomotor ataxia (" spinal arthro- pathies," Charcot's joint disease). These changes consist of rather sudden and painless swelling of the affected joint, followed by destructive disease ot the articulation itself, — erosion of the cartilage, atrophy of the heads I/O DISEASES OF THE NERVOUS SYSTEM. of the bones, and relaxation of the ligaments. Some- times there are irregular osteophytic growths external to the articulation. At times these changes appear to be related to slight injury. Their painless character is an important diagnostic feature of these arthropathies. When these changes involve the tarsal articulation, the foot may become fiat (" tabetic foot "). Trophic Changes in the Muscles. The trophic changes that occur in muscles exceed in diagnostic importance all other nutritive changes dependent on nervous disease. The diagnostic indications are derived, first, from changes in the bulk and consistence of the muscles, and, secondly, from alterations in their electrical excitability. Muscular Atrophy is a frequent consequence of organic disease of the brain, spinal cord, and peripheral nerves, but a high degree of wasting is seen only in disease in- volving the lower segment of the motor path — that is, in disease of the motor ganglion-cells of the anterior horns, the anterior nerve-roots, or the motor nerves. Such a degree of wasting may follow acute lesions, or may occur in the course of those that are chronic in their progress. In the former case the atrophy is preceded by motor par- alysis of sudden or rapid onset (acute poliomyelitis, acute myelitis, acute neuritis, injuries to motor nerves) ; in the latter, the paralysis progresses pari passu with the weak- ness, being due to the gradual Avasting of muscular tissue (progressive muscular atrophy). In an important group of cases of muscular atrophy of gradual development, in which no changes in the spinal-cord or peripheral nerves have yet been detected, and which are looked upon as myopathic in origin (progressive muscular dystrophies — idiopathic muscular atrophy) a high degree of muscular wasting is frequently observed. These cases constitute the only exception to the rule that a high grade of mus- ■ SYMPTOMATOLOGY OF NERVOUS DISEASES. I/f cular atrophy is due to anterior cornual or peripheral nerve disease. Their distinction from forms of atrophy dependent on nervous lesions is considered elsewhere. It must not be supposed that all cases of disease of the anterior cornua, or motor nerves, are productive of a high degree of muscular wasting. In lesions of moderate severity or of gradual onset the wasting may be moderate or -slight in degree, and, unless the distribution be dis- tinctive, may resemble that which occurs after cerebral lesions. The atrophy which follows disease of the upper segment of the motor path (cerebral disease, many forms of spinal-cord disease not involving the anterior cornua) is usually slight in degree ; occasionally it is considerable, but it never reaches the grade commonly observed in dis- ease of the lower segment (myelitis, progressive muscular atrophy, multiple neuritis). The rapidity with which muscular atrophy develops ^varies greatly under different circumstances. In disease of the lower segment of the motor path the rapidity of wasting depends chiefly on the acuteness or chronicity of the lesion to Avhich it is due. In acute processes the wasting progresses with rapidity, often reaching a high degree in the course of a month, and often being readily appreciable after the lapse of ten days (acute myelitis, acute poliomyelitis). In gradually progressive lesions the atrophy is proportionately slow. Disease involving the upper segment of the motor path is generally followed by some muscular atrophy, but this is almost invariably late in its development. This atrophy is particularly noticeable in young subjects and is frequently a result of irritative lesions. In a very small proportion of cases, cerebral lesions, especially disease of the corte:: and subjacent white substance, are followed not by late but by early atrophy — atrophy which reaches its height 1/2 DISEASES OF THE NERVOUS SYSTEM. in from three to six weeks after the onset of the lesion, which is generally irritative in character. These early cerebral atrophies are mainly observed during adoles- cence and during early adult life, and the motor paralysis (hemiplegia) is apt to be associated with sensory phenom- ena. Usually the degree of wasting is inconsiderable. Both late and early atrophies are probably dependent, in a measure, on secondary degeneration of the pyramidal tracts, which, when due to irritative processes, seems to exert a detrimental influence on the nutrition of the gan- glion-cells of the anterior horns and through these on the muscles. In disease or the lower segment of the motor path the muscles usually become flabby and lose their tone ; they un- dergo " atonic atrophy." In disease of the upper segment the muscles may retain their tone, or, if there be well-devel- oped secondary degeneration of the pyramidal tracts and increased reflex action, may grow hypertonic and exhibit muscular rigidity. When there is secondary degeneration of the pyramidal tracts, muscular rigidity may be pre- served in cases of atrophy from disease of the ganglion- cells of the anterior horns, provided some of the ganglion- cells of the anterior cornua are only partially damaged, and still exert enough control over the muscular tone to cause that over-action which develops under the influence of degeneration in the upper segment of the motor path. If, however, the ganglion-cells of the anterior cornua are so extensively diseased as to abolish the muscular tonus, the degeneration of the upper segment is incapable of causing rigidity. The distribution of the atrophy corresponds closely with the distribution of the motor paralysis in cases where the wasting follows such paralysis. In cases where the wasting is not secondary in time or causation to motor SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 73 paralysis, the distribution of atrophy presents considerable variety and forms a basis for the distinction of clinical types. True Muscular Hypertrophy rarely occurs as a phenome- non of disease, but an increase in the bulk of certain muscles, associated with a change in their consistence and diminution of power, and due to an overgrowth of the interstitial connective tissue, and subsequent deposition of fat, is observed in one variety of the progressive mus- cular dystrophies (pseudo-hypertrophic muscular paraly- sis). Muscular hypertrophy occurs in Thomsen's disease, and in the healthy leg, in some old cases of poliomyelitis, as a result of increased activity. Altered Electrical Irritability of Nerves and Muscles — Reaction of Degeneration. — In health the muscles and motor nerves are excitable by galvanism and faradism. Either current, when applied to a motor nerve ' (indirect stimulation), is capable of producing a contraction in the muscle or muscles supplied by this nerve. The faradic current causes a contraction which continues during its application, but, if the distinct shocks of which it con- sists are passed through the nerve at short intervals, each stimulus gives rise to a contraction of momentary duration. A galvanic current of moderate intensity applied to the nerve gives rise to a muscular contraction only when the circuit is made or broken — that is, when the current is passed or stopped — or when a sudden change is made in the current strength. A slight diminution in the irrita- bility of the nerve to both faradic and galvanic currents is observed in diseases of the nervous system which im- ' The point on the surface at which a motor nerve passes to its muscle is called a " motor-point." It is customary, in electro-diag- nosis to obtain contractions by stimulating motor-points. These points are given in most text-books on general medicine. 174 DISEASES OF THE NERVOUS SYSTEM. pair the nutrition of either the upper or the lower motor segment ; considerable diminution or complete loss of irritability to the strongest currents is observed only in disease of the lower segment (degeneration of the nerve- fibres from any cause). Either faradic or galvanic current, when applied to a mitscle without the intervention of a motor nerve (direct stimulation), can be made to produce a contraction of this muscle. The muscle possesses two irritable structures, which it is convenient to think of as being physiologically distinct : (i) the intra-muscular termination of the motor nerve-fibres with their motorial end-plates, and (2) the muscular fibres themselves. In health both these struc- tures may be excited by either current, but it is probable that it is mainly by the action of these currents on the motorial end-plates that the contractions are produced. When these end-plates undergo degeneration, as they do in consequence of degeneration of the motor nerve-fibres or spinal ganglion- cells with which they are connected, and the motor nerve is no longer excitable by faradism (vide supra), the muscle also loses its faradic irritability, because faradism is incapable of stimulating the muscular fibres themselves when these have suffered in their nu- trition. But the galvanic current, notwithstanding the ex- istence of nutritive changes in the muscle-fibres and from degeneration of the nerve-fibres and motor nerve-endings, is still capable of exciting a muscular contraction, by directly stimulating the muscular fibres. The contraction, however, which is obtained under these circumstances differs from that which is obtained in health in several respects. First, it occurs more readily for a time than the contraction of health — that is, the muscle responds to a feebler galvanic current. Secondly, the contraction is not the quick, sharp, and complete contraction of SYMPTOMATOLOGY OF NERVOUS DISEASES. 1/5 health, but is tardy, wave-like, and often imperfect. Thirdly, there is a change in the readiness of response at the two poles. Under normal conditions a contraction occurs more readily at the negative pole when the circuit is closed (kathodal closure contraction, KCC), than at the positive pole when the circuit is closed (anodal closure contraction, ACC), — that is, KCC > ACC, and with a current of sufficient strength to produce both ACC and KCC the latter is always more vigorous than the farmer. Under the conditions of disease of which we are speaking (complete degeneration of the lower motor segment), the anodal closure contraction either occurs with a weaker current than the kathodal closure contraction, or both contractions occur with equal readi- ness — that is, ACC > KCC, or ACC = KCC. These different changes in the contractility of the muscles — loss of faradic irritability, temporary increase of galvanic irri- tability, with changed polar reactions and sluggish re- sponses — constitute what is known as the reaction of degeneration, which may be conveniently expressed by the symbol RD. The RD is so called because it is evi- dence of a degenerative change in the motor nerve-fibres, which, when stimulated, no longer react to either current (vide supra). We have here described what may be called the com- plete or typical form of RD — the form which is observed in the severer varieties of lesions in the lower segment of the motor path, acute degenerative or inflammatory pro- cesses in the nuclei of the motor nerve-cells anywhere in the spinal cord, medulla, pons, or crura cerebri, or in the motor nerves which spring from these cells. Other forms of RD exist, however, presenting innumerable differences in the degree and character of the changes in electrical excitability. Of these, there are two forms or types of 176 DISEASES OF THE NERVOUS SYSTEM, RD that require mention. The first of these is observed in chronic forms of degenerative disease of the lower segment of the motor path, in which the nutrition of the nerve-fibres and muscle-fibres is gradually more and more impaired. The nerve-fibres and their motorial end-plates suffer slowly in nearly equal degree, and there is conse- quently a gradual loss to faradism and to galvanism in both nerve and muscle. This form of RD differs from the complete form, in that at no period of the degenera- tive process is the irritability of the nerve-fibres lost while that of the muscle-fibres is preserved. There is conse- quently no time when the muscles show an increased irritability to galvanism and loss of irritability to faradism. The other phenomena of the complete form are, however, present ; there is the characteristic sluggish response to galvanism, and, generally, the alteration in polar reaction. The other variety of degenerative reaction that remains to be mentioned is termed the " mixed form." It is characterized by the presence of slight or marked changes in the irritability of the muscles, while the nerve either reacts normally or shows only slight diminution in irrita- bility to both currents. The changes in the muscle vary considerably in different cases. Usually there is increased or diminished galvanic excitability, changed polar reaction, and sluggish contraction. The galvanic irritability may be nearly normal, however, and the altered polar reactions and tardy contraction may not be very pronounced. The mixed form of RD is observed in cases where some mus- cle-fibres are degenerated and others in the same muscle are normal or nearly normal, this condition of the muscle- fibres being dependent on a corresponding mixture of normal and degenerated nerve-fibres in the nerve. Clini- cally it is observed in peripheral paralyses, in progressive muscular atrophy, acute and subacute poliomyelitis, etc. SYMPTOMATOLOGY OF NERVOUS DISEASES. I ;/ It is important to note the fact that the slow, sluggish contractions which are observed in RD constitute its most important and characteristic feature. They are present even in the slightest grades of RD, in cases where the irritability of the nerves to both currents is retained, where the faradic irritability of the muscles is only slightly diminished, and where the polar reactions are normal or only slightly modified. The development and course of the electrical changes which constitute the RD vary according to the severity and chronicity of the morbid processes on which they depend. In cases where the lesion is very severe and acute in its development (acute neuritis, acute poliomye- litis, severe nerve injuries), there is an early ^ and rapid fall in the irritability of the nerve, both to faradism and galvanism ; in the course of two or three weeks the irri- tability of the nerve becomes extinct. In the muscle i;here is a fall in faradic irritability which corresponds in time and extent (being due to the nerve-endings) with that observed in the nerve. The galvanic irritability of the muscles may remain unchanged for several days after the onset of the lesion, or may fall slightly. Then occurs a considerable increase in irritability, which reaches its height in about a month, and is followed by a gradual decline, until, after the lapse of a year, or, in some in- stances, two years, no reaction can be obtained with a current that can be borne." In such a case there is no recovery of electrical irritability or of power of voluntary contraction. In somewhat less severe cases of acute ' This fall usually begins about the middle of the first week, some- times not until its end. ^ When galvanic irritability of the muscle is extinct to ordinary modes of stimulation, the insertion of a needle into the muscle as one pole of the battery may elicit a local contraction. 1/8 DISEASES OF THE NERVOUS SYSTEM. onset the condition of electrical irritability may be the same as that just described during the early months. Then, after a period varying from six months to a year, there is a gradual return of faradic irritability in the mus- cle and afterwards in the nerve. In chronic lesions of great severity (progressive muscular atrophy) the loss of irritability to both currents in muscle and nerve is very gradually lost,' the galvanic irritability of the muscle en- during the longest, but becoming extinct after the lapse of a few or several years. In lesions of acute and subacute development, but of moderate severity, the fall in nerve irritability does not differ greatly in rapidity of progress or degree from that observed in the severest forms. Muscle irritability to faradism begins to sink in the course of a week, and is lost in from three to five weeks. For a week or ten days there may also be a fall in galvanic excitability corre- sponding to that for faradism. Then occurs a rise in galvanic irritability which reaches its maximum in a month or six weeks. Very soon (six weeks to three months) there is a reappearance of irritability in the nerve, and in consequence of this (the intramuscular nerve-endings sharing in the nutritive changes in the nerve trunk) a reappearance, in slight degree, of the faradic irritability of the muscle. About the same time there is a slight recovery of power. The excessive galvanic irritability may continue a considerable length of time (three or five months) before returning to the normal, which it does gradually. In lesions of slight severity there is frequently a slight rise in nerve irritability. This may last several weeks, and be followed by an inconsiderable fall in irritability, ' lasting a few weeks or months. Pov\'er of voluntary con- traction is never entirely lost, and the loss which occurs SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 79 WEEKS 1 3 10 «30 50 100 _i '•^^^»»Mtr,: — ■ .^rr: — JTr-r*^.^.. <•*< \, ^"^-^. Z \ \ « 'o- Li > a: •*\ lUiie lit **<^s 2 POWER NO ^l E JMO N£ N0N£ A DAYS 30 ro "*•... '--..., ■^^N '*^.:iN .i'^' t:.^^* POWER EKABUE FIG. 45. Fig. A shows type of electrical reactions in a case of severe and permanent damage to a nerve. The broken lines a™™i™^»™ in this and the follow- ing chart show the state of galvanic irritability. The broken lines ==«■■»•■■""■ show the state of faradic irritability. The broken curves in the upper half of each chart show the state of electrical irritability in the muscle ; the dotted lines in the lower half of each chart show the state of electrical irritability in the nerve. The horizontal dotted line represents the normal degree of irritability. Fig. B shows type of electrical reaction in a case of slight damage to a nerve. l8o DISEASES OF THE NERVOUS SYSTEM. is recovered from in from three to six weeks. The irrita- bility of the muscle to faradism corresponds, in general, to that of the nerve, but there is seldom increased faradic irritability even when this occurs in the nerve. The gal- vanic excitability has the same character as in lesions of moderate severity, but the increase is less and of shorter duration. Since the extent of the changes in nerve and muscle irritability varies, in general, with the severity of the degenerative process in the nerve, we have in the RD a valuable aid in prognosis, for the severity of the case and its duration (in the case of acute lesions) are proportional to the loss of nerve irritability. If there is complete loss of nerve irritability, and greatly increased galvano- muscular excitability, with sluggish contractions, etc., the degenerative process is one of severity. The question then arises whether or not regeneration can take place within the nerve — that is, whether or not there will be recovery of trophic innervation, return of power, etc. The possibility of some recovery is not gone until there is complete loss of irritability to both currents in the muscle, but if there is no return of faradic irritability in the muscles at the end of a year, and their atrophy has been rapid and great, only slight improvement, at best, will occur. If the lesion is an acute one, and the muscles have lost their faradic irritability after the lapse of a week or ten days, considerable atrophy will certainly follow, and the loss of motor power will be of long duration. If the faradic loss does not occur until two or three weeks have passed, there will be less atrophy and earlier recovery, but the paralysis will last many months. If there is only slight loss of faradic irritability, or no loss whatever, recovery will begin in the course of a few weeks or months. SYMPTOMATOLOGY OF NERVOUS DISEASES. l8l The presence of RD, as already stated, indicates dis- ease of the lower segment of the motor path. The more important clinical conditions in which it is observed are poliomyelitis, progressive (spinal) muscular atrophy, amyo- trophic lateral sclerosis, lesions of the ganglion-cells of the anterior horns from hemorrhage, tumor, syringo- myelia, etc., bulbar paralysis, injuries of the peripheral nerves, neuritis of all kinds (rheumatic neuritis, multiple neuritis, toxic paralyses, and paralyses after infectious dis- eases). The absence of RD does not exclude the possi- bility of a slight affection of the anterior horns or motor nerves. It may be absent in very slight peripheral par- alyses from injury. On the other hand, RD may be present, in slight degree, in cases of lead poisoning and slight injury to a nerve in muscles that show no appreci- able loss of power. Diminished Irritability of nerve and muscle to both currents, without RD, is due to slight changes in the peripheral nerves, which may or may not depend on cor- responding changes in the motor ganglion-cells. In the case of lesions in the upper segment of the motor path (cerebral paralysis — pyramidal tract lesions) the electrical changes are due to the nutritive alterations produced in the motor nerve-cells by the irritative influence of de- scending degeneration in the pyramidal tract. The clinical conditions in which simple diminution of irritability without qualitative change is observed, are as follows : (i) Cerebral paralyses; diminished irritability in par- alyzed muscles in the course of three or four months, usually preceded by a rise in irritability. (2) Spinal-cord diseases ; bulbar paralysis, amyotrophic lateral sclerosis ; sometimes difficult to distinguish from the slighter RD which occurs in some of these conditions. 1 82 DISEASES OF THE NERVOUS SYSTEM. (3) Peripheral nerve disease ; after slight injuries, after recovery from RD, in multiple neuritis and in arsenical paralysis. (4) Muscular conditions ; atrophy from disuse, arthri- tic atrophy, progressive myopathic atrophies (muscular dystrophies). 3. Increased Irritability of nerve and muscle to both currents, without qualitative changes, is frequently observed in the early period of hemiplegia when irritative phenomena are present, in the early stage of acute and subacute myelitis, in the early stage of progressive mus- cular atrophy (the increase in irritability in these cases is usually very great), and in the first days of slight neuritis. An increase has also been observed in some cases of hemichorea, tetany, locomotor ataxia (pre-ataxic stage), and dementia paralytica. A peculiar variety of increased muscular irritability to both currents is that which occurs in myotonia congenita (Thomsen's disease), and is hence called the myotonic reaction. The myotonic reaction consists in increased faradic contractility, with prolonged contraction after the current ceases, and in excessive galvanic irritability when the circuit is closed (ACC and KCC), with exceedingly sluggish, lasting, and wavy con- tractions. The nerve excitability is normal. Vaso-Motor Symptoms are of frequent occurrence in the course of both organic and nutritional disease of the nervous system, but the diagnostic indications fur- nished by them are of comparatively little importance and will be only briefly mentioned here. The disturbances which are the expression of disor- dered vaso-motor function manifest themselves clinically as local or general changes in color and temperature, or by alterations in secretion, or by the presence of oedema. In general, all these changes are most marked in acute SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 83 lesions of an irritative character. Local changes in color and temperature are observed in many cases of cerebral, spinal, and peripheral disease. In hemiplegia there is often an increase of -|- degree F. in the temperature of the paralyzed limb, and this may be accompanied by dis- tinct redness of the skin. In other cases there is a fall in the surface temperature of the limbs ; they become pale and livid. A slight degree of oedema is frequently ob- served in the paralyzed extremity, and occasionally there is a marked local increase in perspiration. Any or all of these changes may be produced by disease of the cortex or of the vaso-motor path from it to the posterior limb of the internal capsule. In spinal-cord disease slight vaso-motor disturbances are very common, and more marked changes-are always present in inflammatory processes, whatever may be the position of the disease. At first the changes are those produced by vaso-motor dilatation (redness, increase of temperature, sometimes sweating) ; later, there is depression in the temperature of the limbs involved, which become livid, often extremely so, at the ex- tremities. CEdema is not uncommon in the early stages of acute processes, but may also accompany disease of exceedingly sIoav development (for example, syringomyelia). In diseases of the peripheral nerves vaso-motor dis- turbance is of frequent occurrence and has the same character as spinal-cord disease. Very slight neuritis is capable of producing very marked changes in the tem- perature of a part for a considerable period of time. It is thus seen that no deductions as to the position of the lesion can be made from the existence of vaso- motor symptoms ; these must be made from the associat- ed conditions (motor paralysis, sensory symptoms, muscu- 184 DISEASES OF THE NERVOUS SYSTEM. lar atrophy, etc) which are commonly present, and from the general distribution of the phenomena. Peripheral vaso-motor disturbance is not at all infre- quent in hysteria and allied conditions, and is often most marked in its manifestations. The distinction of vaso- motor symptoms of functional origin from those that de- pend on organic disease, is usually simple, and is based on the mutability, temporary duration, and dependence on emotional disturbance, which is observed in the for- mer. The extent to which the vaso-motor apparatus is under the influence of psychical processes is illustrated by the fact that, in rare instances, local hyperaemia and even vesication have been produced by verbal suggestion in subjects, usually hysterical, in the hypnotic state. The ^^ tache cercbrale," in which slight cutaneous irri- tation is followed by distinct local congestion of the skin of considerable duration, is a vaso-motor disturbance dependent on loss of tone in the smaller vessels from de- fective innervation of the local ganglia in their walls. It is not diagnostic of meningitis, as has been supposed, but is observed in many different conditions in which the general nervous system suffers in its nutrition. Mental Symptoms. — Loss of Consciousiiess is one of the most significant and frequent symptoms of orgsinic disease of the brain, but since it is also a symptom of many conditions that depend not on structural disease, but on nutritional disturbance of the cortex (functional disease), its exact significance depends largely on its associations. The expression " loss of consciousness," as employed in medicine, refers to loss of the external mani- festations of mental activity, not to the loss on the part of the patient of purely subjective consciousness, though the two may coincide. Considerable variations in the degree of unconsciousness occur. In cases where it is possible SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 85 to temporarily rouse the patient from his sleep, the loss of consciousness is regarded as partial, and is termed "stupor." When the loss is complete and the patient cannot be roused by any ordinary stimulus (voice, rub- bing, slapping), the condition is termed " coma " if it endures longer than a few minutes. In coma there is partial or complete loss of control over the sphincters, superficial reflex action is generally lessened or lost, the muscles are relaxed, and there may be loss of the deep reflexes. The pupils are usually dilated and immobile ; sometimes they are contracted (generally in toxic states). The pulse is often slow and irregular in force and fre- quency ; sometimes it is rapid and feeble. Respiration is diminished in frequency and force. The relaxation of the palate permits it to vibrate with the air-current and gives rise to stertorous breathing. Frequently the res- piration is irregular, and sometimes it presents the rhythmical changes in depth known as " Cheyne-Stokes respiration." In stupor, on the other hand, the reflexes, both super- ficial and deep, are retained, the pharyngeal reflex may be excited, and the pupils react to light, but there is usually some loss of sphincteric control. Loss of consciousness may be produced by almost any- one of the pathological processes to which the brain is subject. In every case the impairment of conscious- ness probably depends on interference with the highest functions of the cortex, and such interference may be due either to disease of the cortex itself, or to the inhibitory action of lesions elsewhere in the brain. Chronic processes impair consciousness either through the involvement of a considerable area of the brain cortex, or by increasing greatly or rapidly the intracranial pres- sure. Lesions of sudden onset (hemorrhage or soften- r86 DISEASES OF THE NERVOUS SYSTEM. ing) on the contrary, may cause loss of consciousness in whatever region of the brain they may be situated, probably by their irritative inhibitory effect on the cortex. When the loss of consciousness is suddenly produced, as it usually is in sudden lesions, it is termed " apoplexy." Cerebral hemorrhage ' is by far the most frequent cause of apoplexy, and on this account the word is frequently used synonymously with " hemorrhage into the brain " Apoplexy may also result from the arrest of blood supply which leads to cerebral softening, and may be caused by embolism or thrombosis of a cerebral artery. Sometimes it results from simple concussion (often slight) of the brain, and in rare cases it can be ascribed, on reasonable grounds, to congestion. In old persons apoplexy occa- sionally occurs without the existence of any cerebral changes to which it can be attributed. In dementia paralytica also, apoplectic attacks occur which cannot be satisfactorily accounted for. Temporary loss of con- sciousness, of sudden onset, occurs in epilepsy and con- stitutes an important feature of the paroxysms. Of the causes outside the nervous system that may give rise to loss of consciousness those that depend, like uraemia, diabetes, and cholaemia, on the production of toxic sub- stances in the organism (auto-intoxication), and those that depend on the introduction of poisons from without (alcohol, opium, chloral), are the most important. The loss of consciousness of cardiac syncope in anaemia depends on a temporary deficiency in the cerebral cir- culation, and should be classed with the functional varieties of such loss. The diagnosis of the cause of coma is often a matter of the greatest moment on account of its bearing on prog- ' Depressed fracture of the skull is also a frequent cause of loss of consciousness, but only pathological causes are considered here. SYMPTOMATOLOGY OF NERVOUS DISEASES. 187 nosis and treatment, but is often attended with considera- ble difficulty. It frequently happens that a patient is brought to a hospital in coma, and that the medical attendant is, for the time at least, without any knowledge of the previous history of the case. The correct diagno- sis in such a case rests on its objective features, and every case of coma requires an exceedingly careful examination. Even then it is frequently impossible. The points of distinction between the different organic diseases (hemorrhage, thrombosis, embolism,) which may give rise to coma are described in Chapter V., but the main differences between coma of organic cerebral origin and the loss of consciousness that is due to functional disease of the brain, or to toxic influences, will be briefly mentioned. In every instance focal symptoms of brain disease are to be looked for. Hemiplegia may be detect- ed during coma, if there is some restlessness, as the move- ments are most marked or confined to one side, but if the coma be very deep, evidence of paralysis may be entirely wanting. The presence of hemiplegia must then be infer- red from other indications, and of these the most important is the condition of the reflexes. The unilateral loss of the abdominal, plantar, or tendon reflex (knee-jerk) makes the existence of a one-sided cerebral lesion probable, and this probability is considerably increased if two or more of these reflexes are absent. On the other hand, if no distinct abnormality in the skin or deep reflexes can be detected, and there are no decided indications of hemi- plegia or other focal symptom, it is improbable that there is a cerebral lesion. Conjugate deviation of the eyes is usually evidence of a unilateral organic cerebral lesion, the deviation being usually to the side of the lesion. If there is no evidence of an organic lesion the loss of con- sciousness is probably due to functional disease of the 1 88 DISEASES OF THE NERVOUS SYSTEM. brain, or to some toxic condition, — as alcoholic, diabetic, or uraemic intoxication. Of the functional states that cause coma the chief are epilepsy and hysteria. Post-Epileptic Stupor is usually of short duration (one to two hours) ; the patient can be easily roused ; one-sided symptoms are absent ; the temperature is normal or slightly elevated, and the loss of consciousness is fol- lowed by temporary headache and often by a confused state of mind. Hysterical Coma occurs in patients of the sex and age that suggest hysteria, is generally preceded by other symp- toms of hysteria (especially convulsion or headache), and is characterized, even in cases of apparently profound unconsciousness, by the preservation of the power of swallowing. There are no distinctive objective symptoms, but varying rigidity of the muscles and twitching of the eyelids are very frequently observed. If headache has been present it ceases when the coma comes on. Urcemic Coma may closely resemble apoplexy from an acute cerebral lesion. In both conditions there may be albuminuria and convulsions. The absence of albumen in the urine is strongly against uraemia, but not absolutely ; its presence has not much significance, except in persons under thirty-five years of age. Repeated convulsions oc- curring at short intervals favor uraemia ; single or few convulsive seizures make it improbable. The convulsions of uraemia may have a local commencement, and may remain local (unilateral) ; usually they are general. The presence of neuro-retinitis of the albuminuric type strongly suggests, but does not prove, that the coma depends on uraemia, and its absence does not exclude the uraemic origin of the coma. Continuous subnormal tem- perature favors uraemia. If there is a history of sudden complete blindness before the coma this makes its uraemic , SYMPTOMATOLOGY Uf NERVOUS DISEASES. 1 89 origin practically certain. The pupils are usually dilated in uraemia coma. Alcoholic Coma may be exceedingly difficult to distin- guish from the coma of hemorrhage or softening. Its duration is short, there are no unilateral symptoms, and there is usually evidence of drinking. The presence of alcohol in the breath is of course no proof that the coma is due to alcohol. It may be necessary to wait a few hours before coming to a positive conclusion. Diabetic Coma may be preceded by other cerebral symp- toms, especially headache, and sometimes convulsions. The diagnosis is based on the detection of glucose and acetone in the urine, both of which are probably present in all cases of diabetic coma. Acetone is, however, present in many conditions, especially gastro-intestinal disorders, other than diabetes. The breath in diabetic coma often smells of acetone. Delirium. — The word delirium is employed to ex- press very different ideas. As used here it is intended to designate illogical and incoherent mental processes, as expressed in word or act. The perversion of mental ac- tivity that occurs in delirium is distinguished from the similar alteration that constitutes insanity by its acute course and temporary duration, and by its dependence on pyrexia, toxaemia, or organic disease of the brain. In what is termed " quiet " delirium there are sensory images without corresponding sensory impressions — " hallucina- tions," — or actual peripheral impressions give rise to false sensory images — "illusions." There are false ideas or delusions, the nature of which is frequently determined by the character of the hallucinations or illusions. The patient generally talks incoherently in a low tone, and often this muttering speech is almost continuous. He lies quietly in bed or exhibits only slight restlessness. In IQO DISEASES OF THE NERVOUS SYSTEM. " active " delirium, on the contrary, the patient is restless and may attempt to leave his bed. He attempts to act according to his delusions, and in these attempts he may commit acts which threaten his life or that of his attend- ant. The delusions of delirium change rapidly in char- acter and never present the systemized and elaborate character of those observed in some forms of insanity. There is rarely much emotional depression. Delirium is much more often dependent on pyrexia, toxaemia, etc., than upon organic disease of the nervous system. The cerebral processes on which it depends most often are meningitis, tumor, extensive softening, and cerebritis. The occurrence of delirium in the course of spinal-cord and peripheral-nerve disease (myelitis, multi- ple neuritis) depends on the pyrexia which accompanies these processes, and not on their situation or nature. The character of the delirium gives no clue in determin- ing whether it is due to pyrexia, its most frequent cause, or to organic disease of the brain. If, in a given case, delirium is the only symptom referable to the nervous system, it can be attributed to organic disease of the brain only if the body temperature is below loi ° F., be- cause the existence of a temperature greater than this makes it probable that the delirium is referable to the pyrexia. In persons who habitually use alcohol in excess, in those who are in debilitated health, and in the aged, a slighter degree of fever may give rise to delirium, and this must be borne in mind in forming an opinion of its significance. But the coexistence of delirium and a temperature above loi ° is indicative of the non-organic origin of the delirium only in cases where there are no symptoms suggestive of encephalic disease, and such symptoms should be sought for with the greatest care before a conclusion is reached. The occurrence of SYMPTOMATOLOGY OF NERVOUS DISEASES. I9I muscular rigidity, convulsions, diplopia, or strabismus, or of repeated vomiting, should excite grave suspicion of organic mischief. The coexistence of optic neuritis makes organic disease practically certain, for, although optic neuritis sometimes occurs after acute infectious dis- eases, it does not in these cases make its appearance until after the height of the disease has been passed. The association of delirium and headache is exceedingly important. If the headache is severe it should excite suspicion of organic disease. The headache of fever usually lessens or ceases when delirium is developed. Hence the persistence of slight headache is an equivocal symptom. Simple Mental Deterioration is of frequent occurrence both in cases of nutritional and organic brain disease. It is manifested chiefly by defective memory — amnesia. Memory is subserved, in all probability, by the same physical elements that subserve intellectual processes generally, and of these the structures that make up the cerebral cortex and bring into association its constituent cell-elements are the most important. Loss of memory may result from any condition of disease which impairs the nutrition of the brain generally or that of the cortex. It is observed after acute infectious diseases, after severe mental shock (often such as occurs from the fright experienced when an injury is received), in hysteria, in epilepsy, and in neurasthenia. It results also from vari- ous organic processes, particularly from those that involve the cortex or the subjacent white matter — meningitis, hemorrhage, softening, new growths, and degenerative processes (dementia paralytica, dementia senilis). In- ability to concentrate the attention is often associated with amnesia, and may be its cause, the loss of memory being a[jparent rather than real. 192 DISEASES OF THE NERVOUS SYSTEM. Defects in the Moral Sense are very apt to be associ- ated with mental failure. Often the change is slight and difficult of estimation by the physician. In given cases the degree of defect can be measured only by comparison with the previous moral status of the individual. It is exceedingly important to take into account the signifi- cance of slight defects in the moral sense of which the patient is unconscious, and which contrast with the patient's previous sense of propriety. Such defects are always of serious import. They are often the first indi- cations of dementia paralytica, making their appearance before the unsystematized and characteristic delusions of this disease. A rude disregard of the comfort or interests of others in one who has been habitually thoughtful in these respects, or the telling of unnecessary and usually blundering falsehoods by one who has always been strictly truthful, should in adults always excite some suspicion of degenerative brain disease. This is par- ticularly true if the moral defects are associated with conspicuous loss of memory or defective power of atten- tion. The refusal to swallow food when there is no pharyngeal paralysis is usually an indication of a consid- erable degree of mental failure. Indecent exposure of the body, or the passage of urine and faeces in the bed when there is no sphincteric paralysis, are evidences, except in children, of considerable mental or moral change. The passage of urine and faeces in the bed, under these conditions, is frequent in some forms of or- ganic cerebral disease — softening, dementia paralytica, etc. Disturbances of Speech. — Disturbances of speech ' ' The word speech is here used in its broadest sense — that is, to denote the ability of one individual to communicate thought to another by means of symbols, and to recognize such symbols when made by others. SYMPTOMATOLOGY OF NERVOUS DISEASES. 193 are of frequent occurrence in brain disease, and often give indications as to the position of the disease which gives rise to them. Hence they are of considerable diagnostic importance and deserve careful study. The symptoms of speech affection are, however, numerous and highly intricate in their relations, and their study is rendered difficult by the circumstance that accurate information as to the effects of local lesions in producing these symptoms is still scanty. Often, too, the same facts are susceptible of different interpretations. Two distinct mechanisms exist for the expression of articulate speech. One of these, situated in the cortex of the brain, subserves the arrangement of the various elements which enter into speech. This may be termed the higher speech mechanism. The other, consisting of nerve-cells in the medulla and pons, is related to the form and not to the arrangement of the speech elements — that is, it is simply concerned with the articulation of words. This is the lower speech mechanism. It is brought into use by stimuli which descend to it from the higher mechanism. Disease of the lower speech mechanism gives rise to defects or loss of articulation. Disease of the higher speech mechanism gives rise to defects in the use and arrangement of words. Defects of Articulation (dysarthria, anarthria) may result from any lesion involving the lower speech mechanism (nuclei of hypoglossal and facial nerves) or the peripheral paths from it (that is, the lower segment of the motor path to the muscles concerned in speech). Whenever there is considerable defect in articulation there is appre- ciable paralysis of the muscles concerned in articulate speech. The defect may be due to unilateral or bilateral palsy. Defective articulation may arise also from disease in the upper segment of the motor path, either in the 194 DISEASES OF THE NERVOUS SYSTEM. cortex or in the path from it. When the disease is unila- teral, the speech defect is usually transient, because com- pensation takes place from the other hemisphere ; but if the disease is bilateral — that is, involves the structures concerned in articulation in both hemispheres, — the defect is permanent. The changes in articulation that depend on disease of the lower segment of the motor path vary according to the muscles that are involved in the palsy. Palsy of the tongue causes imperfect articulation of the Unguals / and /. Paralysis of the lips causes their imperfect ap- proximation and consequent defect in the pronunciation of labial consonants. P, b, and n are replaced by / and V. Paralysis of the palate gives the voice a nasal and monotonous quality. It also causes imperfect pronuncia- tion of the consonants / and b (" explosive " labials), because non-closure of the nares hinders the compression of air within the mouth necessary for their production. Separation of syllables, changes in rhythm, and sudden explosive utterance of words in what is termed " scanning speech " (also "staccato" speech), is a form of disturb- ance frequently observed in multiple sclerosis, of which it is rather characteristic, and occasionally in chorea and in affections causing imperfect transmission of impulses from partial damage to nerve-roots. " Confluent " artic- ulatioii is one of the manifestations of slighter disease of the bulbar mechanism, and consists in the running together of terminal consonants and syllables with those that follow. Speech Defects Dependent on Disease of the Cerebral Hemi- sphere and expressed, not as defects in articulation, but as errors in the arrangement or nature of the speech ele- ments, are designated by the word aphasia. Cerebral processes of speech are either motor or sensory in char- SYMPTOMATOLOGY OF NERVOUS DISEASES. 195 acter, and the leading forms of speech defects, 77iotor aphasia and sensory aphasia, are due to derangement of the corresponding processes of speech. The motor speech processes are those by which language is uttered. They are effected in the posterior part of the third frontal convolution, and possibly also in the neighboring part of the anterior central convolution. In the lower part of the anterior central convolution of either side is the centre for the muscles concerned in articulation, which is interfered with by the bilateral involvement of these cortical centres, as already mentioned, and to some extent by their uni- lateral involvement. The motor speech centre (Broca's centre), in which the arrangements for the expression of word processes is effected, must be carefully dis- tinguished from the articulatory centre just mentioned. The two are adjacent and perhaps some structures are common to both, but articulation may be impaired with- out impairment of the higher motor processes, and the latter may be impaired without any defect in the power of articulation, though frequently both are impaired together. From the centre for the movement of the lips and tongue, fibres pass through the internal capsule to the lower mechanism of articulation. A lesion destroying the left motor speech centre usually gives rise to total loss of voluntary speech (motor aphasia). The loss is of voluntary speech only, because emotional and automatic speech is subserved by both hemispheres, and is continued by the speech centres of the right hemispheres when those of the left are damaged. In persons who are right-handed the speech centre for voluntary speech is in the left hemisphere, the corre- sponding centre on the right side being related only to involuntary and automatic utterance, although it is capable of being educated to supplement the action of the struc- 196 DISEASES OF THE NERVOUS SYSTEM. tures on the left side. In those who are left-handed, although they may use the right hand for writing, vol- untary speech is subserved by the centre in the right hemisphere. Not only may voluntary speech be lost in consequence of extensive destruction of the motor speech centre, but there may be impairment of expression by means of gestures. The patient may for a time make with his head the sign of negation when he wishes to express assent. Very soon there is some recovery of the ability to say simple words like "yes" and "no." These words may be employed in two ways — as propositions, to express the ideas of assent and dissent (propositional use), and as interjections, for the expression of emotion, and they may be regained and employed as interjections before they are again acquired as propositions. Many other words possess these two forms of use, and the proposi- tional use is always regained the later. Thus many patients can swear or sing songs who could not deliber- ately and propositionally make use of the words of an oath or of a song. In some cases a considerable degree of speech loss persists for a long period of time. In the majority of cases there is slow recovery of speech after the lapse of a few months, so that eventually recovery of language occurs. When the lesion in the speech region is destructive in character, this ultimate recovery of language is unquestionably due to compensation through education of the right hemisphere (speech centre) for higher processes than it originally subserved (voluntary speech). The extent to which this supplemental action of the undamaged speech area is possible varies greatly even in adults. In children it occurs to an astonishing extent. It is exceedingly rare to see motor aphasia in a child in consequence of disease in the left hemisphere. SYMPTOMATOLOGY OF NERVOUS DISEASES. 197 That this is because of extensive compensation by the right speech region is shown by the fact that a second lesion in this situation has been known to cause permanent loss of speech. In non-destructive lesions of the left centre, or in lesions of limited extent, some recovery of function is possible in the nerve-elements of this side, and it is often difficult to distinguish between the recovery which is due to compensation in the opposite hemisphere, and that due to recovery on the side of the lesion. In the speech that remains after an attack of aphasia, or in that which is regained, there is frequently error either in form or in use. The error in form is in the elements of the word. Thus, one patient said *'tinors" for scissors; another, " lant " for lance; and another, " trayling to dool " for trying to do. In these cases the error lies in the elements of the word used ; there is not usually any defect in articulation associated with the error in form. This erroneous formation of words, which often results from disease of the motor speech region, has / heen termed ataxic ap/iasia, but as a very similar condition^ may occur from disease elsewhere in the brain (see word- deafness) the term motor aphasia is the preferable desig- nation for all effects of disease of the motor speech area. Frequently there is an erroneous use of words without error in form. At first even the simplest words, as " yes," " no," may be erroneously employed. Where there remains considerable speech, wrong words, which may or may not resemble the ones intended, may be used repeatedly. Agraphia, or loss of power of writing, is practically always the consequence of motor aphasia. In order that a word may be written, the motor speech processes corre- sponding to it must be correctly arranged in the motor speech area, from which they pass from a subcortical tract of fibres to the motor centre for the hand in the 198 DISEASES OF THE NERVOUS SYSTEM. middle of the ascending frontal convolution of either side. From these centres the motor impulses are con- ducted by the pyramidal tracts to the cord, and, through it and the peripheral path to the writing hand. It is important to note that the ability to write does not depend on paralysis of the movements of the arm and hand, for, even when these movements are perfect, a lesion in the motor speech centre causes agraphia. Agraphia is also caused by a small lesion involving the subcortical tract from the speech centre to the hand centre. The loss of the power of writing, like motor aphasia, may be complete or partial. When the loss is partial, the errors in writing are similar in character to those which occur in speaking, and frequently they are greater. In these cases the power of copying is pre- served. Motor aphasia is not always the consequence of disease of the cortex. It may follow interruption of the conduct- ing tract to the hand centre of the same side, which lies just beneath the cortex, or a lesion in the internal capsule. If the lesion is in the internal capsule the loss of speech is transient ; if beneath the cortex it may be permanent. No disturbance of intellect is necessarily associated with motor aphasia. Motor aphasia may be produced by any pathological process which involves the speech region or the subjacent white matter. It is most frequently produced by cerebral softening. The motor speech area lies within the province of the first branch of the middle cerebral artery (see Fig- 33), and hence must suffer if this is occluded by embolism or thrombosis. Aphasia from hemorrhage, though less frequent than that from softening, is also fre- quent. Tumor is not an infrequent cause. In children tubercular meningitis is frequently operative in producing SYMPTOMATOLOGY OF NERVOUS DISEASES. I99 motor aphasia, for the irritation of meningitis seems com- petent to inhibit the speech centre as it does the motor centres. Sensory speech processes subserve the reception and revival of language. It is chiefly through the senses of hearing and sight that these processes are brought into activity, and there is consequently a close connection between these senses and the disturbances of speech which depend on the arrangement of the sensory pro- cesses, auditory and visual, of speech. Such disturbances of speech are designated sensory aphasia, the leading varieties of which are word-deafness and word-blindness. In Word- Deafness words that are spoken by another are not understood. This does not depend on deafness in the ordinary sense ; the patient hears the spoken words, but they are meaningless to him. Words of his own language sound strange ; there is failure to associate these words with the ideas they represent. Word-deafness depends on disease of the posterior half of the first tem- poral convolution, usually of the left side. This is, there- fore, the situation of the structures that subserve the auditory perception of words, but it is also the situation of the auditory centre itself. Whether the two centres, the auditory perceptive centre and the auditory centre, are identical it is impossible to say. They are at present indistinguishable. When this region of the cortex is dis- eased there is usually, in addition to word-deafness, transient deafness in the ear opposite the lesion. When word-deafness exists there is always distinct de- rangement of speech. This is because the revival of the memory of words in the mind, before their arrangement in the motor speech centre, previous to utterance, occurs mainly in the auditory perceptive centre of the cortex. Without this ability to revive past auditory impressions 200 DISEASES OF THE NERVOUS SYSTEM. the patient's memory for words depends on his faculty for reviving the motor processes for words which have left behind changes in the cortical cells (residual states) which facilitate this revival — that is, he has to fall back on what may be called his motor memory. This is im- perfect, and errors in the form and use of words occur even when the word-deafness is only partial. Word-deafness is rarely absolute, because the auditory perceptive centre is habitually aided in the automatic revival of words by corresponding centres in the right hemisphere. Considerable recovery of the ability to under- stand spoken words and of the voluntary revival of words usually occurs in the course of time, and this is due to the education of the latent powers of the right-sided centre. In word-deafness the patient is not conscious of the errors of speech which he makes. In this respect there is a striking contrast with motor aphasia, in which the patient not only appreciates his errors but tries to correct them. Word- Blindness is the inability to comprehend the written symbols of language. There is usually no loss of sight ; the patient sees letters and words, but he fails to recall to mind the ideas they represent. The position of the lesion that gives rise to word-blindness cannot at present be definitely located. The symptom may be produced by a lesion in the inferior parietal lobule, and perhaps also by lesions involving the angular gyrus or the occipital lobe of the left side. In word-blindness there is usually some error in the use and form of words, but in some cases this is very slight. Word-blindness and word-deafness often coexist. Usually the power of speaking is retained. Mind-Blindness (" soul-blindness ") is a rare condition in which, without mental defect, there is entire loss of visual memory of every kind The patient no longer SYMPTOMATOLOGY OF NERVOUS DISEASES. 20I recognizes familiar faces or objects. There is also loss of recognition of visual word symbols^ — that is, the loss includes word-blindness, which may be regarded as par- tial mind-blindness. The lesion in cases of mind-blind- ness is probably in the posterior part of the parietal lobes and in the occipital lobes, anterior to the half vision centres (p. 43). Probably permanent mind-blindness is due to bilateral involvement of these areas. Some- times hemianopsia is associated with mind-blindness. Mind- Deaf ness is a rare condition in which, without mental defect, there is loss of auditory memory. This symptom is especially striking in musicians, who may lose the faculty of appreciating music or following melodies, or of playing or following notes. The word Apraxia is used as a general term to desig- nate an inability to recognize the meaning or use of an object. Hence there are as many varieties of apraxia as there are modes of special sensation. Both mind-blind- ness and mind-deafness are varieties of apraxia. Alexia^ or inability to read understanding ly, is of course an essential feature of word-blindness. It is important, however, to recognize the fact that alexia may result from a pure motor aphasia. In many persons, particularly those who are imperfectly educated, motor speech processes are essential to the comprehension of written speech symbols ; a kind of internal speech goes on while these persons are reading, the external evidence of which is the movement of the lips which is often seen in these persons. When these persons are deprived of their motor word-processes by disease, alexia results. The alexia gradually lessens, however, because some motor word processes are regained, and serve to rein- force the visual centre. When the alexia is due to word- blindness the inability to comprehend visual word 202 DISEASES OF THE NERVOUS SYSTEM. symbols is absolute, and the motor speech processes art; generally unimpaired. Dyslexia is a term applied to a rare symptom consist- ing in a peculiar condition of mental fatigue from read- ing, which makes its appearance a few minutes after the patient begins to read, and makes it impossible to read more than a few words consecutively. There is no motor speech disturbance. This condition is not asso- ciated with any visual defect, and is unaccompanied by ocular pain. It is thought to depend on a subcortical lesion beneath the angular gyrus. Amnesic Aphasia, or difficulty in voluntarily recalling words, particularly those which, like nouns, are special in character, may result either from partial word-deafness or from pure motor aphasia. It is claimed that in cases where amnesic aphasia is the only form of speech defect from the beginning it constitutes a distinct variety of aphasia, and depends on a distinct pathological condi- tion. This condition is supposed to be a lesion which interrupts the conducting path between the motor and auditory centres, and thus prevents that action of the auditory on the motor speech centre which is essential to the perfect revival of motor word-processes. For this reason it has been termed, somewhat unfortunately, " conduction aphasia " (" Leitungs Aphasie "). It can- not be said that the evidence on the strength of which amnesic aphasia is considered a distinct variety of aphasia is as satisfactory as could be desired. Speech disturbances are not always due to organic disease of the brain. They occur not infrequently as an expression of functional derangement of the cerebral centres. Thus, transient motor aphasia often occurs after right-sided convulsions from any cause, probably from the exhaustion of the motor speech centre which results SYMPTOMATOLOGY OF NERVOUS DISEASES. 203 from the discharge of nerve force. In migraine slight motor or sensory aphasia is not very uncommon during the attacks, especially in right-handed persons, when there is some sensory disturbance (tingling, numbness) in the right limbs, particularly the arm. Partial motor aphasia occasionally occurs during emotion or excite- ment, in persons (women) of hysterical character. In severe cases of typhoid fever motor aphasia, usually transient, has many times been noted. In some of these cases it was unquestionably of organic origin ; in others it has occurred under conditions which make probable its dependence on defective cortical nutrition from the morbid blood state. Congenital aphasia, motor or sensory, is exceedingly rare, and when it exists probably depends on traumatic meningeal hemorrhage during labor. The ability of an aphasic patient to make a will may constitute an important practical question. In order that a valid will may be made, it is necessary that the testator should be able (i) to understand the proposition that is put before him, and (2) that he should be able to ex- press assent or dissent in an unmistakable manner. If there is word-deafness it is impossible to say with cer- tainty that the patient understands what is said to him, and hence a valid will cannot be made if what is put before the testator is spoken. If, however, the patient understands written words, and propositions are com- municated in writing only, word-deafness is no obstacle to the making of a will. The coexistence of word-deaf- ness and word-blindness of course destroys all testament- ary capacity. Motor aphasia, even absolute in degree, does not destroy testamentary capacity if spoken words are understood and if the testator can indicate assent and dissent by means of signs. 204 DISEASES OF THE NERVOUS SYSTEM. General Symptoms. — Temperature. — Elevation of temperature is of frequent occurrence in nervous disease. The fever may be simply an associated condition — that is, the morbid process in the nervous system and the eleva- tion of temperature are referable to a common cause. This is particularly the case with processes that are due to infection — for example, some forms of multiple neuri- tis, poliomyelitis, cerebral embolism, etc. In some con- ditions it is difficult to say to what extent the fever is due to the general condition or the morbid process in the nervous system. This doubt arises, for instance, when tubercular meningitis and general tuberculosis occur together. The fever may be dependent chiefly on the character of the process without particular reference to its situation in the nervous system. Acute inflamma- tory processes in any position are attended with fever, which is generally to be regarded as consecutive to the inflammation. In the case of intracranial disease an important peculiarity is frequently observed : There may be only slight rise of temperature or even no rise of temperature in the course of inflammatory processes of considerable or great severity. This is true, for exam- ple, in some cases of meningitis. This peculiarity prob- ably depends on the inhibitory influence of irritative processes on the heat centres within the brain. It is important to remember that the absence of fever or its slight degree does not indicate the absence of inflamma- tion within the cranium. Sometimes the pyrexia that results from central nervous disease depends, not on the nature of the pathological process, but upon its direct action on the heat centres, or the apparatus which controls them. This is particularly the case with acute lesions (hemorrhage, softening) in the upper part of the cervical cord, medulla, pons, or optic SYMPTOMATOLOGY OF NERVOUS DISEASES. 205 thalami. In these cases there is often a rapid and great rise in temperature — the fever may rise to 103° or to 105°, and in the case of medullary and pontine lesions even higher (io6°-io8°). Death usually follows such an elevation of temperature within a short time. In some cases of sunstroke very high temperatures are seen (io8°-iio°), and there is often a great premortal rise in cases of meningitis. In the case of sunstroke the hy- perpyrexia does not necessarily foreshadow a fatal termination. Sometimes the rise of temperature is the secondary effect of nervous disease, particularly disease of the brain. Any condition — for example, tetanus, epilepsy — which gives rise to many successive attacks of convul- sions is followed by a rise, often considerable, in tempera- ture. This is due apparently to the excessive muscular action. During the " status epilepticus " ' (p. 547) the temperature may rise to io6°-io9.° A subnormal temperature sometimes occurs in brain disease, rarely in disease of other parts ot the nervous system. The process which gives rise to it is generally hemorrhage, the depression of temperature occurring usually at its onset. If the extravasation of blood be great, the temperature may fall to 95°, 93°, or even 90° (rectal). In such cases there are the usual signs of col- lapse. A slight initial fall may be succeeded by a rise in temperature. Pulse. — Most forms of organic nervous disease have no special effect on the rapidity, force, or rhythm of the pulse. Inflammatory intracranial disease may inhibit the pulse rate even when there is a considerable elevation of temperature, and it is not uncommon in meningitis to ' In this state the paroxysms recur at short intervals for a con- siderable time (often many hours). 2o6 DISEASES OF THE NERVOUS SYSTEM. meet with a temperature of 103° or 104° and a pulse rate which is normal or even less than normal. A higher tem- perature from intracranial disease is generally associated with a soft and rapid pulse. Infrequency of the pulse rate (50-40-30 per minute) is sometimes observed at the onset of acute lesions (hemorrhage, softening). A habit- ually rapid pulse rate (90-120 per minute), without fever, is not uncommon in neurasthenia and some forms of hys- teria. Marked irregularity of pulse is often an important early sign of irritative intracranial disease. Respiration is markedly influenced by organic disease of the nervous system chiefly Avhen this is extensive (hemorrhage, softening), or when it involves the parts in the neighborhood of the respiratory centre in the medulla. In such cases respiration is often exceedingly irregular, both as regards rhythm and rate, and may eventually cease from exhaustion of the respiratory centre. Sud- den cessation of respiration occurs from a sudden lesion (hemorrhage, thrombosis, embolism) in the respiratory centre of one side or both sides, and may occur from in- hibition of this centre from acute lesions adjacent to the centre. When the lesion is external to but near the re- spiratory centre, the depression of respiration may con- tinue many hours, and then disappear spontaneously. Irregularity in the rhythm and force of the respiratory movements is often observed in inflammatory cerebral lesions. It is especially frequent in acute meningitis, and is so common and so decided in most cases of tuber- cular meningitis as to be rather characteristic of this dis- ease. Cheyne-Stokes respiration (peculiar rhythmical changes in breathing, characterized chiefly by the alternation of periods during which there is a gradual and extreme dim- inution in the force and frequency of the respiration, with SYMPTOMATOLOGY OF NERVOUS DISEASES. 20/ periods of increasing depth of breathing, these periods being separated by a variable interval of time — 5-40 sec- onds) is sometimes observed toward the close of cerebral diseases (hemorrhage, meningitis, tumor). The patient is usually comatose and rarely recovers when this form of breathing has begun. Cheyne-Stokes breathing occurs in many diseases external to the nervous system (heart disease, pneumonia, nephritis, diphtheria, etc.), and under these circumstances is of less grave significance than when due to brain disease. Mucus accumulates in the bronchi and trachea in states in which the cerebral functions are in abeyance, for example, in the course of prolonged coma. The bronchial and tracheal rales which result must not be mistaken for bronchitis. Passive congestion of the lungs and hypostatic pneumonia are of common occurrence under the same circumstances, and constitute a frequent cause of death in central nervous disease. Of the symptoms referable to the Digestive Organs^ Vomiting is by far the most important. As an effect of organic nervous disease vomiting is chiefly observed in intracranial disease, although it is not uncommon as an effect of acute processes in the upper cervical cord, and occurs paroxysmally in some chronic general diseases of the spinal cord (locomotor ataxia). Vomiting occurs as a symptom of organic disease of the brain in many different conditions — in meningitis, tumor, abscess, and not infrequently in cerebral hemorrhage — that is, in irritative conditions. Sometimes it occurs re- peatedly in the course of endarteritis of vessels of the base, before complete obstruction takes place. Generally speaking, any condition giving rise to considerable in- crease in intracranial pressure inay occasion vomiting. The situation of the lesion does not seem to exert any 208 DISEASES OF THE NERVOUS SYSTEM. . important influence in determining the symptom, except- ing in the case of cerebellar lesions, which are particularly apt to give rise to it. Vomiting of cerebral origin cannot be said to possess any features that are to be regarded as highly distinctive. Still, certain characters, chiefly negative, of such vomit- ing are sufficiently frequent to be suggestive. These are : (i) The rejection of food soon after its ingestion; (2) the absence of discomfort after eating ; (3) the absence of nausea ; and (4) the absence of other gastric symptoms. In general the vomiting of functional nervous disease (hysteria) possesses the same negative characteristics. Hence it is that the diagnostic significance of vomiting depends mainly on its associations. The organic processes which give rise to vomiting are exceedingly apt to cause persistent headache, or optic neuritis, or both. The as- sociation, therefore, of either of these symptoms and, a fortiori, of both of them, with frequent vomiting, makes intracranial disease probable. The vomiting of intracranial disease depends on an in- creased excitability of the gastric centre in the medulla. When this exaltation of excitability is great, vomiting may occur spontaneously — that is, without any trace- able gastric cause. Before this high degree of irritability is reached, slight peripheral causes, such as dietetic indis- cretion, may cause vomiting more readily than would be the case in the absence of this increased irritability. Hence it is easy to understand the vomiting which may be the first indication of organic disease. Every patient, and particularly every child, who vomits without experi- encing the indisposition that generally attends vomiting from gastric cause, should be carefully watched. The vomiting which is associated with vertigo has already been mentioned. SYMPTOMATOLOGY OF NERVOUS DISEASES. 209 Constipation usually accompanies cerebral and spinal- cord diseases which are attended with elevation of tem- perature, but has little diagnostic significance. Obstinate constipation is almost a constant symptom of destructive disease of the cord above the lumbar enlargement. The pathological changes that occur in The Urine as the result of nervous disease are few, and, generally speaking, of little help in diagnosis. Transient albumi- nuria and glycosuria are occasionally observed in disease of various parts of the brain, and particularly in lesions of the medulla and pons. Much more frequently albumi- nuria is associated with diseases of the cerebral vessels (endarteritis, hemorrhage, atheroma, miliary aneurisms) which result in cerebral hemorrhage or softening. Other urinary changes (oxaluria, excessive or insufficient excre- tion of uric acid, increase in indican, etc.) are common in nutritional diseases of the nervous system, as neuras- thenia, some forms of headache, etc. These changes are, as yet, not sufficiently understood to be of material aid in diagnosis, but it is likely that in the future they will prove of considerable help in the diagnosis of the nature of nutritional diseases of the nervous system. Affections of the Sphincters of the Bladder and Anus are of frequent occurrence in organic disease of the nervous system, but are exceedingly rare from disease of the pe- ripheral nerves external to the spinal column. Interrup- tion of the voluntary path (probably the pyramidal tract) from the brain cortex to the reflex centres for the bladder and rectum in the lumbar enlargement of the cord (lowest lumbar and sacral segments) results in the loss of volun- tary control of the functions of these viscera. Their action becomes purely reflex. As soon as a sufficient amount of urine accumulates in the bladder, the viscus is emptied by the reflex contraction of the detrusor urinae 2IO DISEASES OF THE NERVOUS SYSTEM. FIG. 46. Diagram illustrating the innervation of the bladder and the effect of lesions in various parts of the spinal cord upon the function of micturition. A lesion, A, which interrupts the voluntary path to the bladder centre in the sacral cord, causes incontinence of urine; when a sufficient quantity of urine accumulates in the bladder there occurs a reflex con- traction of the detrusor and relaxation of the sphincter. The sensory path from the cord to the brain being unin- volved, the patient is conscious of the prcccss, but cannot exercise voluntary control over it. With a lesion, B, which involves also the sensory path, the patient is unconscious of the filling and reflex emptying of the bladder. A lesion, C, which causes destruction of the sacral reflex centre for the bladder causes continuous dribbling of urine, and not its automatic expulsion at in- tervals. and synchronous relaxation, also reflex, of the sphincter ; when fseces accumulate in the rectum and irritate its mucous membrane, they are expelled by an analogous mechanism. The inconti- nence of urine is called " intermittent " or " reflex incontinence." It is impor- tant to understand that there is no paralysis of the sphinc- ters in this form of inconti- nence. The proof of this is (in the case of the rectum) that the introduction of the finger into the rectum is followed, after slight relaxa- tion, by firm and tonic con- traction of the sphincter. The interruption of the vol- untary path which results in this loss of cerebral control may result from different conditions ; generally from spinal-cord disease (mye- litis or injury above the lumbar enlargement, lateral sclerosis, etc.). In reflex incontinence there is usually some weakness of the detru- sor urince after a time. Then retention occurs, and the dis- tension of the bladder leads SYMPTOMATOLOGY OF NERVOUS DISEASES. 211 to relaxation of the sphincter and incontinence — " over- flow incontinence." When the functions of the brain are in abeyance (stupor, coma) from any cause, there may be retention of urine and incontinence, but the incontinence consists in these cases of the dribbling of urine from a full bladder, " overflow incontinence," and there is no actual weakness of the sphincter. There is also involun- tary passage of faeces in these cases. The reflex apparatus for expelling the contents of the bladder and rectum, and for preventing their continuous evacuation may be disordered in its function by disease involving the rectal and vesical centres in the lumbar en- largement, or the efferent and afferent nerves connected with these centres. Most frequently the disturbance of function depends on destructive disease of the lumbar centres. In this condition fseces or urine are passed as soon as they enter the rectum or bladder. The urine dribbles away continuously ; the condition of the rectal sphincter can be determined by the introduction of the finger, which shows it to be persistently relaxed. When there is partial damage to the lumbar centres, of gradual development, there is often difficulty in exciting the action of the detrusor (patient " cannot start his urine "), and this may result in retention. Damage to the cauda equina sometimes produces disturbances like those that result from partial disease of the lumbar centres for the bladder and rectum. Disorde7's of the Sexual Functio7is are of frequent occurrence in nervous diseases, but do not possess much diagnostic importance, and will be only briefly touched upon. They are more common as the result of functional than of organic disease. The sexual act is largely a reflex act, and its perfect performance depends on the integrity of a reflex arc whose centre lies in the sacral cord near 212 TDISEASES OF THE NERVOUS SYSTEM. that for the bladder and rectum. The action of this centre is, however, to some extent under cerebral control, and in this, as in other respects, the sexual reflex re- sembles closely the skin reflexes. Disease of the sexual centre in the sacral cord, or of the nerves leading to or from it, causes Joss of sexual power, as shown in the male by loss of erectile and ejac- ulatory power. Thus the sexual reflex is lost with loss of control over the anal and vesical sphincters, when the lumbo-sacral cord is destroyed, as in myelitis. In loco- motor ataxia it is lost from disease of the sensory portion of the arc. When the damage is partial in the reflex arc the corresponding loss of function is partial only. Disease which cuts off the controlling path from the brain to the reflex sexual centre causes over-action of this centre with resulting priapism. This is seen in dorsal myelitis, compression and crush of the cord, etc. In women various menstrual disorders may accompany or- ganic disease, especially cord disease. Periods of great sexual excitement occur in some women with locomotor ataxia (so-called " clitoris crises "). A great variety of sexual disturbances, including increased and diminished sexual desire, spermatorrhoea, and priapism, are observed in functional disorders (hysteria, neurasthenia, traumatic neuroses). In some cases of hysteria deep pressure over the ovarian region, especially the left, causes severe and characteristic pain, often with nausea and vomiting, and perhaps excites an hysterical paroxysm. CHAPTER III. THE DIAGNOSIS OF THE POSITION OF THE LESION LOCALIZATION. It is convenient to think of all morbid processes affect- ing the nervous system as divisible into two great groups — those which consist of changes in the cell-elements, that are demonstrable by present methods of investigation (organic diseases), and those that consist of alterations of variable degree in the nutrition of these elements, but are unassociated with demonstrable structural changes (nutritional or "functional" diseases). These two groups merge into one another insensibly, both in their pathological and clinical characters, but for practical purposes their separation is desirable, and the general principles on which the clinical distinction of organic and functional disease is based are elsewhere presented (P- 527)- This distinction, which occasionally constitutes a problem of the greatest difficulty, ordinarily is made with ease, and having been made, at least provisionally, should be followed by a systematic endeavor to obtain more accurate knowledge of the morbid process. In general, an effort should be made — first, to locate as accurately as possible the seat of the morbid process within the nervous system (local diagnosis) ; and, secondly, to determine the pathological nature of this process (patho- logical diagnosis). 213 214 DISEASES OF THE NERVOUS SYSTEM. In the case of organic disease on the nervous system it is of great practical importance to locate accurately, i.e.^ to " localize " the lesion (which includes an estimate of its extent), because this information not only is an important guide to prognosis, but may furnish the most important indications for treatment.' Fortunately the data now at command enable a local diagnosis to be made with precision in a large majority of all cases of organic nervous disease. In the case of functional disease of the nervous system, the localization of the morbid process (nutritional), though desirable, is much less important, since the prog- nosis and treatment depend on other indications. It is also much less practicable, and is at best uncertain, since the localization depends on inferences based on what is known of the effects of organic lesions. It is inferred, for example, that certain hysterical paralyses depend on disease (nutritional) of the motor cortex, because it is known that organic disease of the motor cortex gives rise to symptoms which present a close resemblance (segmental distribution of palsy, con- tractures, normal electrical reaction) to the characters observed in functional palsy. The following review of the chief manifestations produced by disease in various parts of the nervous system relates exclusively to the effects of organic processes. The chief symptoms of nervous disease, and the parts concerned in their produc- tion, have already been considered, and it is necessary now to look at these facts from another point of view — to consider the symptoms from a regional standpoint. It is convenient to consider, first, the chief symptoms that result from lesions in various parts of the brain ; secondly, the symptoms produced by disease in differ- ^ This relates especially to operative treatment. DIAGNOSIS OF THE POSITION OF THE LESION. 2 1 5 ent regions of the spinal cord, and in the peripheral nerves. a. Cortex Cerebri. — i. Destructive disease of the Central and Motor Area of the brain (anterior and posterior central convolutions and paracentral lobule, anterior half of superior parietal lobule) gives rise to hemiplegia on the opposite side of the body. The hemiplegia is usually partial, because the lesion more often involves a small than a large part of the central area. This partial hemiplegia (monoplegia) occurs much more commonly from disease of the cortex than from disease more deeply seated in the motor path. Hence, a partial paralysis, if due to brain disease, points to the existence of a cortical lesion. The parts that suffer from the palsy vary according to the position of the lesion. The leg suffers alone chiefly when the lesion involves the paracentral lobule, or the central convolutions close to the longitudinal fissure. If the lesion is confined to that part of the leg centre which lies in the upper part of the anterior central convolution, the paralysis probably affects mainly the foot. If the lesion lies between the longitudinal fissure and the junc- tion of the middle with the lower third of the central convolutions, there is paralysis of the arm, and if the lesion involves the middle third only of these convolu- tions, paralysis of the arm alone. A lesion in the upper part of the arm centre paralyzes the shoulder more than the rest of the arm. A lesion in the very lowest part of the anterior central convolution gives rise to paralysis of the tongue and lips. Any slight defect in articulation that may result from a unilateral lesion in this situation is transient, being soon compensated by the correspond- ing centre in the opposite hemisphere. In cortical disease the lesion is not usually confined to 2l6 DISEASES OF THE NERVOUS SYSTEM. one of the functional areas mentioned (area for the arm, or leg, or face), but involves adjacent areas. Hence it is that paralysis of the arm and leg, or of the face and arm, is more often encountered as a result of cortical disease than paralysis of one of these parts alone. If a destruc- tive lesion is not confined strictly to the cortex (and it usually is not), it may involve subjacent white tracts from other regions of the cortex which are not the seat of dis- ease, and thus give rise to symptoms not referable to the area which is the seat of the cortical lesion. In addition to motor paralysis, lesions of the cortex give rise very often to convulsions. This is the case with lesions that are purely irritative in character and with those that are destructive and stationary but in which the destruction is partial only. The convulsion begins locally in the leg, arm, or face, according to the position of the disease which causes it, in or adjacent to the area whose destruction gives rise to motor paralysis. Such local commencement is highly suggestive of cortical dis- ease. If there is reason to regard the lesion as stationary — that is, no longer active and incapable of further struc- tural recovery, the recurrence of local convulsions makes the existence of cortical disease certain. Their recur- rence under these conditions, however, does not neces- sarily mean that the region of the cortex corresponding to the locality of the initial spasm is the part most dis- eased. A lesion, for example, situated on the leg centre may give rise to convulsions beginning in the face or arm centre, because the disease is capable of starting dis- charges from adjoining areas which are less diseased but more excitable. Localized convulsion, therefore, is to be regarded as a less accurate indication of the exact seat of the lesion than localized motor paralysis. This an important point. DIAGNOSIS OF THE POSITION OF THE LESION. 2 1/ Disease of the central area of the brain very often gives rise to loss of sensation in the extremity of the part (or parts) paralyzed. The loss of sensibility is generally slight in degree. It involves chiefly tactile sensibility, but there may be some loss of pain and temperature sense. Complete hemianassthesia probably never results frorn lesions confined to the motor area. The sense of posture of the limbs paralyzed is sometimes impaired in some degree by lesions of the motor cortex (especially its posterior part), but there is sometimes a similar loss from disease of the motor path between the cortex and the lower part of the internal capsule. Lesions of the supe- rior parietal lobule also cause impairment of the sense of posture. 2. Lesions of the Frontal Lobe of the brain, anterior to the motor area, give rise, with one exception, to no dis- tinctive focal symptoms. When there is disease of the pos- terior part of the left third frontal convolution in right- handed persons there is motor aphasia. A lesion in the corresponding position in the right frontal lobe produces the same effect in left-handed persons. Extensive disease of the cortex usually, but not invariably, causes consid- erable mental impairment, as shown by loss of memory and attention, and sometimes by emotional disturbance. Similar mental defect may result from extensive cortical disease in other parts of the brain, but a lesion of equal extent probably causes less impairment than is produced by disease of the frontal lobe. Disease in the posterior part of the second frontal convolution perhaps gives rise to conjugate deviation of the eyes and head (page 109). Disease involving the frontal lobes in such a way as to damage the olfactory bulb or tract causes anosmia on the side of the lesion. 3. The precise effects of lesions of the Parietal Lobe 2l8 DISEASES OF THE NERVOUS SYSTEM. posterior to the motor area are still undetermined. Le- sions of the superior parietal lobule give rise to loss of the sense of posture in the limbs of the opposite side. Disease of the inferior parietal lobule probably causes ptosis on the opposite side, but the exact area on which this depends is not known. It is questionable whether lesions of the angular gyrus which are limited to the cor- tex are competent to cause crossed amblyopia, but it is probable that the destruction of this region on the left side causes word-blindness (p. 200). Destructive disease of the entire parietal lobe generally impairs, though it does not abolish, sensibility of the opposite side" of the body (trunk and limbs). Lesions involving both the parietal lobe and the motor area give rise to more complete hemianaesthesia than is produced by a lesion limited to either region. 4. Lesions of the cuneus of the Occipital Lobe cause homonymous hemianopsia. Lesions involving the upper and lower half of the cuneus, respectively, are probably capable of producing partial hemianopsia — that is, qua- drantic homonymous defects (p. 147). It is possible that disease just anterior to the half-vision centre (cuneus) or in its anterior part may give rise to color hemianopsia. Disease of the external surface of the occipital lobe seems capable of causing mind-blindness, which is often associated with hemianopsia from involvement of the sub- jacent visual tract. 5. Lesions involving the first and second temporal convolutions of the Temporo- Sphenoidal Lobe of the left side give rise to word-deafness. Disease of the posterior part of the first temporal convolution probably gives rise to transient deafness in the opposite ear, and an irritative lesion in this situation may give rise to an auditory aura. DIAGNOSIS OF THE POSITION OF THE LESION. 219 The auditory centre in man cannot at present be very accurately located. A lesion in the uncinate convolution, or involving the apex of the temporo-sphenoidal lobe may cause marked disturbance of the sense of smell. Irritative disease in this situation may determine an olfactory aura. 6. Disease of the Island of Reil has many times been associated with hemiplegia, and disease extending through the insula of the left side has been considered effective in producing aphasia by interruption of the path between the motor and auditory speech centres. It is doubtful whether hemiplegia is ever the effect of a lesion limited to the cortex of the insula, although disease of the branches of the middle cerebral artery, as they pass over the insula, may undoubtedly lead to lesions elsewhere (motor cortex and subjacent white substance) that pro- duce motor paralysis. It also remains to be shown that simple interruption of the path beneath the insula, above mentioned, is competent by itself to produce amnesic aphasia. b. White Substance and Centrum Ovale. — Disease of the white substance of the hemisphere and centrum ovale gives rise to symptoms referable, on the one hand, to the interruption of the various association tracts which connect different gyri and functional areas of the cortex with one another, and, on the other, to in- terruption of tracts which have a peripheral destination (projection tracts). Lesions of the association tracts, if extensive, probably cause mental symptoms chiefly, loss of memory and attention, defective will-control, etc. It is doubtful whether any lesions of this kind give rise to symptoms that possess localizing value. Lesions of the tracts which connect the cortex with peripheral nervous mechanisms (retina, motor apparatus, etc.) produce symp- 220 DISEASES OF THE NERVOUS SYSTEM. toms which resemble those that result from disease of the region of the cortex with which the particular tracts are connected. Thus, a lesion of the white substance of the occipital lobe, involving the visual path to the cuneus, gives rise to lateral hemianopsia ; a lesion interrupting the fibres that converge from the central area of the cortex to the internal capsule gives rise to hemiplegia. The various tracts mentioned all converge from different areas of the cortex, widely separated, to the internal capsule. Hence, generally speaking, lesions yz/j-/ beneath the cortex produce symptoms like those dependent on disease of the over- lying cortical region, while those that approach the in- ternal capsule produce effects like those of capsular disease. General convulsions are not common in disease of the white substance of the hemisphere, even when such disease is irritative in character, unless it be placed just beneath the cortex. When in this position (particularly when the lesion is beneath the motor cortex) an irritative lesion (as tumor) often gives rise to the local spasm (Jacksonian spasm) which is so characteristic of cortical disease. The motor aphasia which follows interruption of the path from the motor speech region (third frontal gyrus) to the internal capsule is temporary, except when the interruption is just beneath the cortical centre. Con- jugate deviation of the eyes is common from subcortical lesions. c. Corpus Callosum. — Lesions are so rarely limited to the corpus callosum that the diagnostic indications of its damage cannot as yet be formulated. Bilateral paresis of the extremities has been noted in many cases where the callosum was damaged, but this is doubtless referable to pressure upon or extension into the motor tract in the cerebral hemispheres. There is some reason to believe that destruction of the anterior extremity of the callosum DIAGNOSIS OF THE POSITION OF THE LESION. 221 gives rise to mental dulness, loss of memory, and other evidences of impaired mental power. d. Corpus Striatum. — Disease of the corpus striatum (caudate or lenticular nucleus) causes no symptoms that can be referred to damage of its gray substance. Acute lesions limited to either nucleus may produce transient hemiplegia, but this symptom is doubtless due to irritation of the adjacent fibres of the internal capsule. Chronic dis- ease of the nuclei produces no symptoms, unless the motor or sensory fibres of the internal capsule be damaged also. e. Optic Thalamus. — Most of the symptoms ob- served in lesions of the optic thalamus are referable to involvement of the contiguous internal capsule and not to the direct effect of the thalamic disease. Thus, the hemi- plegia which often follows disease of the middle third of the thalamus is due to implication, often slight, of the motor iibres of the capsule, which lie just external to this part of the ganglion. Similarly, the hemianaesthesia which is observed to accompany disease of the posterior extremity of the thalamus (pulvinar) depends not on the thalamic lesion, but on damage to the sensory part of the capsule. Disease of the middle and posterior thirds of the thalamus seems to be directly effective in producing inco-ordination and hemiathetosis of the opposite ex- tremities, but it cannot be denied that these symptoms may be due, at least in part, to irritation of the neighbor- ing motor tract. It is highly probable that lateral hemi- anopsia may be produced by a destructive lesion limited to the pulvinar of the thalamus, and that the symptom is then to be regarded as the direct result of this destruc- tion. The association of hemianopsia with hemianaes- thesia indicates a lesion of the posterior part of the thalamus and the adjacent sensory fibres of the internal capsule. 222 DISEASES OF THE NERVOUS SYSTEM. /. Internal Capsule. — Lesions of the internal cap- sule give rise to symptoms which vary much according to the part of the capsule involved. Disease limited to the anterior division of the internal capsule, anterior to the knee (between the caudate and lenticular nuclei), is rare, and does not give rise to characteristic symptoms. Some- limes mental symptoms, similar to those referable to dis- ease of the frontal lobe, are produced by disease of the anterior part of the capsule, but usually it seems to cause no definite effects. Disease involving the angle (knee) and the anterior two thirds of the posterior division of the capsule causes hemiplegia of the ordinary variety — that is, paralysis of the opposite leg, arm, and face (lower part). If the lesion is on the left side there is frequently motor aphasia, but this is always transient. If the lesion be of acute onset there is often at first conjugate deviation of the eyes, to the hemiplegic side where the symptom is due to irritation. Sometimes there is permanent conjugate deviation. This is usually due to destruction, and the deviation is then to the side of the lesion {:vide p. 109). Convulsions occasionally attend the onset of hemiplegia from disease in this region. They seldom recur after the onset. Hemiathetosis often follows incomplete hemiplegia, but it is not certain whether the symptom is referable to the capsular disease or to adjacent disease of the thalamus. The hemiplegia of disease of the internal capsule is usually complete. A very small lesion, limited to the angle of the capsule, may give rise to facial paralysis only, and, similarly, minute lesions in the anterior and middle thirds respectively of the posterior division of the capsule, may produce a brachial monoplegia and a crural monoplegia. It is exceedingly rare, however, for a paraly- sis from such lesions to involve exclusively face, arm, or leg, although one of these parts may be chiefly affected DIAGNOSIS OF THE POSITION OF THE LESION. 223 Probably three fourths of all cases of hemiplegia result from disease of the internal capsule ; hence, in the ab- sence of symptoms pointing to another locality as the seat of the lesion, there is always a strong presumption that a hemiplegia depends on damage to the internal capsule. Disease of the posterior third of the posterior division of the internal capsule, in which lies the sensory tract, gives rise to hemianaesthesia. Taste, hearing, and smell may be lost on the anaesthetic side, as the paths for the special senses are contiguous to the path for common sensibility. The visual path is also involved in such cases and the resulting symptom is lateral hemianopsia. g. External Capsule and Claustrunio — Lesions of the external capsule and claustrum do not give rise to distinctive symptoms and cannot therefore be localized. /i. Corpora Quadrigemina.— Lesions limited to the corpora quadrigemina are of exceedingly rare occurrence. Hence there is still considerable doubt as to the precise effect of disease in this situation. Disease of the ante- rior pair has been thought to produce blindness, loss of pupillary reflex and nystagmus. It is certain that there is no adequate reason to suppose that blindness is ever directly referable to disease of the corpora quadrigemina. Irritative disease (tumor) of the quadrigeminal region, like such disease elsewhere, may give rise to optic .neu- ritis and secondary optic atrophy, and by this mechanism to amblyopia, but, except in this manner, visual acuity is not impaired. There has been no impairment of vision even in cases where the corpora quadrigemina were wholly destroyed. The condition of the pupillary reflexes varies so much in different cases of quadrigeminal disease that no general statement can be made regarding it. It is probable that in some cases of such disease the reaction to light is lost. Nystagmus may occur from irri- 224 DISEASES OF THE NERVOUS SYSTEM. tative disease of the quadrigeminal region as from irri- tative disease in other regions. It probably bears no particular relation to the anterior pair, and, as elsewhere stated (p. 112), has no localizing value. Disease of the posterior pair has many times been associated with inco- ordination of movement (unsteadiness in walking and standing, reeling or staggering gait), and is probably, in some degree, a highly constant symptom of such disease. It must be owned that there is still some doubt as to whether the symptom is really due to the quadrigeminal disease and not to implication of the middle lobe of the cerebellum, but the balance of evidence is much in favor of the former view. Paralysis of the muscles supplied by the oculomotorius nerve is a frequent and important symptom of disease of the quadrigeminal region. It doubtless depends on implication of the subjacent nuclei of the third nerve and not on the quadrigeminal disease itself. Usually the muscles are neither symmetrically nor equally involved in the paraly- sis, nor are they all implicated. While it is impossible, therefore, to localize a lesion of one or other pair of corpora quadrigemina, disease of the quadrigeminal region may frequently be diagnosed with accuracy. The symptoms on which such a diagnosis can be made are the coexistence of inco-ordination of move- ment (of early development usually) and unsymmetrical and incomplete ophthalmoplegia referable to the oculo- motor nucleus. i. Crus Cerebri. — Lesions of the crus cerebri (pes) frequently cause a characteristic combination of symp- toms — hemiplegia, involving the lower half of the face and the limbs, and paralysis of the third nerve on the side of the lesion — that is to say, on the side opposite the hemi- plegia (crossed or " alternate " heminlegiaV Usually th'^ DIAGNOSIS OF THE POSITION OF THE LESION. 22$ paralysis of the third nerve is complete ; occasionally it is partial. It is important to bear in mind that if the process which results in this form of crossed hemiplegia is of acute onset^the lesion cannot be referred to the crus unless both hemiplegia and ocular palsy are of simul- taneous occurrence. In the case of chronic processes the separate development of the two symptoms leaves a doubt as to whether or not they depend on the same lesion. Convulsions are rarely observed in cases of disease of the crus. Irritative disease, however, may give rise to rigidity. If the lesion involves the sensory path in the tegmentum of the crus, anaesthesia may be associated with the motor paralysis. Occasionally (chiefly in irri- tative disease) there is lateral hemianopsia, from implica- tion of the contiguous optic tract. Occasionally, also, there is unilateral inco-ordination. j. Pons. — Lesions of the pons Varolii generally give rise to distinctive symptoms. Unilateral disease commonly involves the motor path to one side of the body and cer- tain of the cranial nerves (fifth, sixth, or seventh) of the other side. Several different varieties of crossed hemi- plegia may thus arise from unilateral pontine disease, according to the size and level of the lesion. Thus, the limbs may be paralyzed on one side and the face on the other — that is, on the side of the lesion — by a lesion which involves the facial path before it crosses and the motor path on the same side. In this case the entire half of the face is paralyzed and the muscles give the R D. If the lesion is near the median line and near the middle of the pons, it may be so placed as to involve the facial paths of both sides with the motor path of one side. Both the sensory and motor part of the fifth nerve, or either alone, may be involved. If the sensory part of the fifth is dam- aged by an irritative lesion there is severe pain on one 220 DISEASES OF THE NERVOUS SYSTEM. side of the face. If the nucleus of the sixth nerve of one side is involved in a destructive lesion there is conjugate deviation of both eyes to the side opposite to the lesion. This implies loss of function of the internal rectus muscle which habitually acts with the external rectus muscle (that is, the internal rectus of the opposite eye) which has been paralyzed by destruction of the nucleus of the sixth nerve. In conjugate movements of the eyes this loss of function in the internal rectus exists, although for other purposes (convergence) there may be no loss of power. Where the lesion is in the motor path of the pons at the level at which the sixth nerve traverses the pons in passing from its nucleus to the surface, the nerve-trunk is apt to be involved. Then there is hemiplegia with paraly- sis of the external rectus on the side of the lesion. The associated internal rectus of the other eye acts normally, and hence there is no conjugate deviation of the eyes. A lesion may be so placed in the motor path of the pons that there is no coincident affection of any of the cranial nerves. In such cases the lesion is usually above the middle of the pons — that is, in a part of the pons in Avhich the upward paths from the nuclei of the nerves in question have already crossed to the opposite side. The resulting hemiplegia cannot of course be distinguished from that which depends on capsular disease. Bilateral disease of the pons is not rare and may give rise to a variety of symptomatic combinations. A lesion implicating the motor path of both sides may cause com- plete paraplegia. The cranial nerves escape or are bi- laterally involved according to the size and level of the lesion. Bilateral disease of acute onset usually gives rise to apoplexy and often to rapid death. Convulsions are uncommon in pontine lesions unless they are of acute onset. Sometimes the convulsions are DIAGNOSIS OF THE POSITION OF THE LESION. 22/ peculiar in distribution ; they affect chiefly both arms or both legs. Irritative processes involving both pyramidal tracts may give rise to rigidity of all the extremities. Tonic spasm is very often met with in partial disease of the motor path within the pons, and may correspond in distribution to the motor paralysis. Other motor symp- toms referable to irritation (trismus and facial spasm, choreic movements) are rare. Lesions involving the tegmental region of the pons, especially the formatio reticularis and root of the fifth nerve, give rise to loss of sensibility in the limbs, trunk, and face. A unilateral lesion thus placed in the sensory path in the upper third of the pons may cause complete hemianaesthesia on the side opposite the lesion. If the lesion is below the upper third of the pons and damages the sensory path from the face and limbs, there is " crossed " ansesthesia — that is, anaesthesia of the face on the side of the lesion and of the limbs on the opposite side (see page 128). There may be considerable pain in the anaesthetic side of the face in these cases. Conjunc- tivitis sometimes exists on the side of the lesion^ and there may be unilateral rhinitis. These symptoms are apt to be present in acute processes which give rise to considerable irritation. Crossed anaesthesia is sometimes associated with inco-ordination of one or both lower ex- tremities. Disease involving the sensory tract of both sides gives rise to bilateral anaesthesia, but this is seldom complete. Unilateral disease limited to the formatio reticularis may cause only anaesthesia of the opposite limbs and trunk. Disease of the posterior part of the pons may involve several of the cranial nerve nuclei and give rise to symp- toms referable chiefly to their implication. A combina- 228 DISEASES OF THE NERVOUS SYSTEM. tion which is not very rare is paralysis of the sixth and seventh without the auditory. This is highly character- istic of pontine disease. Both the motor and sensory path from the limbs may be involved by a large unilateral pontine lesion, but the degree and extent of the anaesthesia and motor palsy are seldom proportioned. This depends on the fact that the two paths are separated from one another by the considerable interval occupied by the deep transverse fibres of the pons (see Fig. 30). Acute irritating processes (especially hemorrhage)) particularly in the upper part of the pons, often cause contraction of the pupils by their indirect effect on the oculomotorius nuclei. Disturbance of respiration, tem- porary but often grave, may result from acute lesions of the pons in almost any situation. Cardiac disturbance is less frequent. Deafness is uncommon in pontine lesions, and taste is not often affected. Sight may be impaired as a result of optic neuritis, never as a direct consequence of pontine disease. If the lesion encroaches on the mid- dle peduncle of the cerebellum there may be a tendency to rotation to the side of the lesion in walking and severe giddiness at the onset of an acute process. Hyperpyrexia not infrequently follows acute lesions of the pons, and in itself suggests pontine or medullary disease. Lesions of considerable size in the pons sometimes cause much psychical disturbance. The most frequent characteristic symptoms of pontine disease are the crossed motor paralyses already described. When such a paralysis occurs suddenly it is practically pathognomonic of a lesion of the pons. Crossed anaesthesia is much less frequent than the crossed motor palsies, and may result from disease of the upper part of the medulla, but its occurrence makes a pontine lesion practically cer- tain. In the absence of any of these characteristic DIAGNOSIS OF THE POSITION OF THE LESION. 229 ! paralyses the diagnosis may be difficult or even impossi- ble. When possible, the diagnosis must be based on the peculiar symptomatic combinations that result from the involvement of neighboring structures which take their origin in the pons. k. Medulla Oblongata. — Lesions of the medulla oblongata, like those of the pons, may give rise to a con- siderable variety of symptoms, according to the region involved. The most characteristic of these symptoms are those that depend on damage of the cranial nerve nuclei lying beneath the floor of the fourth ventricle. These nuclei are the ninth, tenth, eleventh, and twelfth. The ascending root of the fifth also arises in part from the medulla. Disease of the bulbar nuclei frequently gives rise to a characteristic group of symptoms — paralysis of the tongue, palate, pharynx, and often of the larynx — constituting glosso-labio-laryngeal or bulbar paralysis. The paralysis is commonly bilateral, because it depends usually on a degenerative process in the nuclei ; when it depends on acute disease (hemorrhage or softening) the paralysis is generally bilateral (acute bulbar paralysis), be- cause the nuclei in question lie very near the median line, and are damaged on both sides. The orbicularis oris is generally involved in the bulbar palsy. Acute lesions (es- pecially hemorrhage) of the medulla, unless exceedingly small, lead almost invariably to death, which may occur in- stantaneously or after the lapse of a few hours. The cause of death is interference with the functions of the cardiac and respiratory nuclei. Small hemorrhages (bilateral) into the vagi nuclei have been known to cause sudden death. Motor paralysis from acute bulbar disease is sometimes slight and limited in distribution, since a lesion suffi- ciently large to interrupt the entire motor path is usually quickly fatal. Motor symtoms (paralysis and spasm) may 230 DISEASES OF THE NERVOUS SYSTEM. be either bilateral or unilateral. When bilateral, either the upper or lower extremities may be chiefly involved in the paralysis and spasm. A small chronic lesion (tumor) may damage the pyramidal tract above the decussation and the hypoglossal nerve of the same side. The result- ing variety of crossed hemiplegia (paralysis of the tongue and limbs on opposite sides) is distinctive of disease of the medulla. The tongue in such a case deviates to the side opposite the limbs palsied. This form of crossed paralysis is much less frequent than the crossed seventh and limb palsy that occurs from pontine disease. The face is never implicated in a lesion of the medulla, but the orbicularis oris may be involved, since it is innervated, not by the seventh nerve, but by the hypoglossal nucleus or cells connected with it. Lesions of the medulla in some cases cause paralysis of motion, or paralysis of sensation, or both, according to the situation of the lesion in the motor or sensory tract, without giving rise to symptoms that are characteristic of or even suggest medullary disease. Glycosuria and poly- uria are occasionally observed in the course of chronic lesions (tumor) involving the flioor of the fourth ventricle, but the causation of these symptoms is too obscure and their occurrence too inconstant to make them of diag- nostic value. /. Cerebellum. — A destructive lesion of consider- able size involving the Aliddle Lobe of the cerebellum gives rise to unsteadiness in standing and walking. In walking the patient may grope about with the feet widely sepa- rated, the hands extended, and the body inclined forward. The tendency to oscillation may make progress so irregu- lar that the gait resembles that of a drunken man. This titubation is sufficiently characteristic and frequent to make it suggestive of cerebellar disease. Occasionally DIAGNOSIS OF THE POSITION OF THE LESION. 23 1 the gait of tabes resembles cerebellar titubation, but in disease of the middle lobe there is not the ataxia that characterizes locomotor ataxia. There is also usually no inco-ordination in the upper extremities, closure of the eyes may not increase the unsteadiness, and there may be no ataxia whatever in the upper or lower extremities when the patient lies supine. Occasionally disease of the middle lobe causes a tendency to fall backwards when the patient attempts to stand. In irritative disease of the middle lobe of the cerebel- lum (tumor, hemorrhage, softening), giddiness and vertigo are of frequent occurrence. The giddiness may or may not be associated with titubation or staggering. Vomit- ing is also a frequent symptom of active cerebellar dis- ease, but both vomiting and giddinesss are often caused by disease in other parts of the brain. Hence, although these symptoms are distinctly more constant in cerebellar disease than in disease elsewhere, they possess only a slight degree of localizing value. Optic neuritis is per- haps somewhat more constant in cerebellar disease than in similar disease elsewhere, and is often an early symptom. Disease of the lateral lobes or hemispheres of the cere- bellum probably gives rise to no symptoms of localizing significance, unless it involves the middle peduncles or exerts pressure on the middle lobe of the cerebellum. In the latter case the symptoms are those referable to disease of the middle lobe. Irritative lesions of the cerebellum ( especially tumor ) sometimes inhibit temporarily the spinal reflex centres on which the knee-jerk depends, so that the knee-jerk may be lost or very much diminished. In some instances the knee-jerk is lost for days or weeks and then reappears, to be lost again after a variable period of time. The knee- jerks may be unequal in activity on the two sides. 232 DISEASES OF THE NERVOUS SYSTEM. Sometimes the knee-jerks are diminished for a long period of time. It is not known whether this unique symptom is related to disease of any particular region of the cere- bellum. In cases of chronic organic intracranial disease, in which indications of the position of the lesion are absent, the occurrence of this symptom suggests a cer- ebellar process. Disease ( tumor ) of the middle or lateral lobes of the cerebellum may exert pressure on surrounding parts, particularly on the pons. The symptoms referable to such pressure are mainly the symptoms of pressure on one or both pyramidal tracts — slight or considerable weakness of the extremities, increased knee-jerk, etc. Usually the symptoms are most marked on the side opposite the cerebellar lesion ; sometimes they are con- fined to the same side. Sometimes there is also evidence of nuplication in the sensory paths in the pons, slight anaesthesia parsesthesia, etc. There is seldom sufficient pressure to cause more than slight and transient sensory disturbance. Sometimes the cranial nerves arising from the pons suffer from the pressure. The sixth nerve is particularly apt, on account of its passage under the prominence of the pons, to be involved. Convulsion is of rare occurrence in cerebellar disease. Rigidity of the limbs and muscles of the back of the neck may occur, as a temporary or as a constant phenomenon. It is prob- ably dependent on pressure exerted upon the pons. It is important to remember that even extensive lesions of the cerebellar hemisphere may produce no symptoms that suggest intracranial disease, but this is probably the case only in very chronic processes which cause little irri- tation (for example, osteoma and some cases of massive tubercle). Active disease of the Middle Peduncle of the Cerebellum DIAGNOSIS OF THE POSITION OF THE LESION. 233 (processus ad pontem) almost invariably gives rise to distinctive symptoms. The most important of these is vertigo, which is often intense, and a tendency to rotation of the body on its long axis (forced or compulsory move- ments), to or from the sides of the lesion, or simply a tendency to lie on one side, or rotate to one side in walking. A lesion seldom involves exclusively the middle cere- bellar peduncle ; it usually encroaches on the side of the pons or on the corresponding hemisphere of the cerebel- lum. In the former case there may be paralysis of the fifth nerve, and, if the motor tract is compressed, uni- lateral weakness of the limbs. Stationary disease of the middle peduncle, and lesions which simply exert pressure on it, may cause no characteristic symptoms. Disease at the Base of the Brain (tumor, meningitis) often produces symptoms which are highly characteristic. This depends chiefly on the circumstance that in most instances basal disease damages two or more of the cranial nerves between their superficial origin from the brain and their exit from the skull, thus giving rise to symptom-groups which possess localizing value. It is convenient to consider separately the symptoms of basal disease in the anterior, middle, and posterior fossse of the skull. Disease may be limited to the Anterior Fossa of the skull, in which case it may produce symptoms referable to damage of the olfactory nerves, or, if the process compresses or invades the frontal lobes, there may be mental symptoms. Frequently morbid processes origi- nating in the anterior fossa extend backwards and involve the optic nerve or chiasm. Implication of the optic nerve is usually unilateral, and causes unilateral ambly- opia or amaurosis. Damage to the chiasma may affect 234 DISEASES OF THE NERVOUS SYSTEM. chiefly the decussating fibres, with resulting temporal hemianopsia. Disease in the Middle Fossa causes symptoms referable chiefly to the fifth nerve. The Gasserian ganglion is usually involved, and all three divisions of the nerve are apt to be damaged, though they may suffer singly or unequally. The symptoms may be those of irritation or of paralysis (pain or anaesthesia) of the nerve. When the Gasserian ganglion is damaged there is neuro- paralytic ophthalmia, and the association of this symptom with symptoms of irritation and paralysis of the fifth is highly distinctive of disease of the middle fossa. The symptoms are, of course, unilateral. Sometimes the crus is involved by extension ; there may then be hemiplegic weakness. Occasionally the third, fourth, and sixth nerves of one side suffer damage from disease near the sphenoidal fissure. Disease in the Posterior Fossa of the skull causes com^ binations of symptoms that resemble those produced by disease within the pons and medulla, with similar varia- tions according to the position at which the process is effective. There are two facts, however, which generally serve to distinguish disease originating in the posterior fossa from that which involves the pons and medulla primarily. First, the combinations of the cranial nerves that can be damaged by disease are different in the two cases; and secondly, when there is disease in the fossa the cranial nerves are prone to suffer before there is evidence of damage to the motor path in the pons and medulla. In basal disease the fifth and sixth nerves readily suf- fer together, since the sixth in its course passes close to the former. This combination is exceedingly rare in pontine disease. The seventh and eighth readily become DIAGNOSIS OF THE POSITION OF THE LESION. 235 involved together in disease at the base, while the same combination is possible only in very extensive disease of the pons. Similarly, but more rarely, the sixth, seventh and eighth are damaged together. The eleventh and twelfth or the ninth, eleventh, and twelfth may be injured together. In the latter case there is unilateral paralysis of the tongue, palate, and vocal cord — a combination dis- tinctive of disease at the side of the medulla. Disease of the same parts from a central lesion is generally bi- lateral, and is associated with palsy of the lips. Occa- sionally, many cranial nerves are damaged by a process (chronic meningitis) in the posterior fossa. Thus, the fifth, sixth, seventh, eighth, ninth, tenth, eleventh, and twelfth have been known to be involved on one side. The number of nerves involved in a basal lesion, and the order and degree of their implication, are subject to great variations. The cranial nerve paralyses from disease of the posterior fossa are rarely strictly unilateral through- out the disease. When the fifth is involved there may be ophthalmitis, but this is less frequent than in disease of the middle fossa. The motor path is often involved unilaterally, with the usual results. Occasionally the middle cerebellar peduncle suffers from pressure. Con- vulsions may result from pressure on the pons, but these possess no distinctive character from those which result from disease in its substance. Having passed in review the chief symptoms of brain disease in their relation to the position of the lesion, it becomes necessary to mention certain general facts of diagnosis which are of importance in forming correct conclusions in localization. In any case of brain disease in which the symptoms are of acute onset it is necessary to distinguish the indirect from the direct effects of the lesion. This can be done surely only by waiting until 2X6 DISEASES OF THE NERVOUS SYSTEM. the indirect symptoms have disappeared or diminished greatly, and this usually occurs in the course of ten days or two weeks. In this way the symptoms that de- pend on actual destruction of tissue may be certainly distinguished from those that result from irritation, and the distinction is important, not only for accurate local- ization, but for prognosis. Of course, a prediction can be made soon after the development of the symptoms, as to which symptoms are direct, but at best the truth can only be approximated. In the case of chronic lesions (tumor) which both irritate and destroy, the distinction is often difficult and may make a nice localization im- possible. A second point of importance relates to the order of appearance of the different symptoms. It is es- pecially desirable to note this in the case of acute lesions, since ojily such symptoms as make their appearance together are to be referred to the same focus of disease. When all the symptoms are of gradual onset it may be difficult to determine whether they are to be referred to the same or to different lesions. Multiple lesions of the brain are usually difficult to localize accurately, since they are apt to produce combinations of symptoms that are of doubt- ful significance. If, however, there are two lesions in op- posite halves of the brain, it is frequently an easy matter to localize them, especially if they are not simultaneous in their development. In any case it is exceedingly import- ant to determine accurately the mode (whether sudden or gradual) and order of development of the symptoms, before formulating a conclusion as to the locality of the lesion. Spinal Cord. — The localization of lesions of the spinal cord is in many respects less difficult than the localization of lesions of the brain. This depends chiefly on the fact that even a small focus of disease in the sub- DIAGNOSIS OF THE POSITION OF THE LESION. 237 stance of the cord almost invariably interrupts structures that have important motor or sensory functions, the dis- turbance of which indicates approximately or accurately the position of the morbid process. Most diseases of the spinal cord involve a part only of its substance. Some lesions damage a considerable ex- tent of certain structures, white or gray, without invading adjacent structures. The term "system-diseases" has been applied to such lesions. Other lesions are of small vertical extent, and may be confined to particular struc- tures, as the ganglion-cells of the anterior horns or the pyramidal tracts, or may damage all the structures of the cord at a particular level. Lesions which are limited both in vertical and horizontal extent are called " focal " lesions. The problem of localization includes the deter- mination of both the vertical and horizontal extent of the lesion. The indications of the horizontal extent of the lesion depend on the fact that different areas of the white and gray substance at the same level have widely different functions. I. Lesions involving the Gi'ay Substance of the spinal cord produce different symptoms according as the morbid process involves («) the anterior horns, {J)) the posterior horns, or (<:) both anterior and posterior horns. Disease of the Anterior Horns g\\t% rise to three distinct results. There is, first, motor paralysis. This depends on the fact that destruction of the ganglion-cells of the anterior horns constitutes an interruption of the motor path from the cerebral cortex to the muscles. In addition to motor paralysis there is degenerative atrophy of the paralyzed muscles with R D. The combination of par- alysis with degenerative atrophy always localizes the lesion to some part of the lower segment of the motor path. The third result of disease of the anterior horn 238 DISEASES OF THE NERVOUS SYSTEM. is loss or impairment of reflexes in which the muscles paralyzed are concerned. The clinical type of paralysis resulting from disease of the anterior horns may be termed atrophic spinal paralysis. The distribution of these symptoms depends on the level of the spinal cord at which the ganglion-cells are involved, and on the extent of the damage in a vertical direction. The special symptoms of anterior cornual disease at various levels will be considered later. If the lesion of the anterior horn is of acute onset (for example, poliomyelitis) the loss of voluntary power is also of rapid development. Degenerative atrophy fol- lows, and the atrophy and altered electrical reactions become apparent in the course of one or two weeks. When the lesion is of gradual development (progressive muscular atrophy) the paralysis and atrophy develop pari passu. Disease limited strictly to the anterior horn does not give rise to sensory symptoms, and the absence of such symptoms seems to distinguish disease of the anterior horns from disease of other parts of the lower segment of the motor path. Paralysis, wasting, and loss of reflex action are symptoms common to disease in any part of the lower segment of the motor path, but disease of the periph- eral part of the path is usually (not always) associated with sensory symptoms — numbness, tingling, anaesthesia, etc. — because the motor fibres are mixed with sensory fibres, and the former seldom suffer alone. When an acute lesion of the anterior horns is accom- panied with sensory symptoms, these are due to damage, often slight, to adjacent sensory structures. At the onset of an acute lesion of the anterior comua spasm may be a prominent symptom. Disease limited to the structures of the Posterior Horn niAGNOSIS OF THE POSITION OF THE LESION. 239 is exceedingly rare, and there is some uncertainty as to the exact character of the symptoms that result from such dis- ease. Irritative disease probably gives rise to pain, and perhaps to hyperalgesia, in a corresponding skin area. Destructive disease probably causes loss of certain forms of sensibility, especially the sensibility to pain and tem- perature. It is very doubtful whether tactile sensibility or the muscular sense are ever disturbed. Chronic lesions (chiefly gliomatous infiltration and cavity formation) involving both Anterior and Posterior horns of gray matter are occasionally observed. They are characterized by the development of muscular atro- phy with R D, gradual loss of voluntary power, and dis- turbances of sensibility, not for touch, but for pain and temperature. Since these sensory disturbances are not obtrusive they may be overlooked unless they are especially sought for, and the symptoms (atrophy and wasting, etc.) may be referred to the anterior horns (progressive muscular atrophy). The chief condition that gives rise to this characteristic combination of motor and sensory symptoms mentioned is syringomyelia (p. 461). 2. White Matter. — Disease of the Anterior and Lateral White Columns of the cord gives rise to a characteristic group of symptoms. There is, first, loss of voluntary power below the level of the lesion. This loss of power is not associated with degenerative atroj^hy of the mus- cles. Secondly, there is excessive action of the spinal centres (ganglion-cells of anterior gray cornua) below the lesion. This is manifested, by the presence of two symptoms, {a) excessive reflex action, shown especially by increase in the knee-jerk, and often by the presence of an ankle clonus, and {h) spasm or rigidity of the mus- cles below the seat of the disease. The former symptom 240 DISEASES OF THE NERVOUS SYSTEM. may be present without the latter where the excess is not great, but in many cases both expressions of the over- action of the spinal centres are present. The clinical type of paralysis that results from disease of the lateral columns is called spastic spinal pai-alysis. When only the anterior and lateral columns are involved in disease there is, as stated above, no degenerative atrophy. If, how- ever, the ganglion-cells of the anterior horns suffer also, as they may, degenerative atrophy occurs in the muscles connected with them, and with this there is diminution or loss of reflex action, notwithstanding the fact that reflex action may previously have been increased. The symptoms described as evidence of disease of the anterior and lateral columns depend on the involvement of the pyramidal tracts. We cannot yet say precisely what symptoms are produced by lesions involving the other important conducting tracts of these columns, (direct cerebellar tract, antero-lateral tract). It is evident from what has gone before that two dis- tinct clinical types of paralysis (atrophic spinal paralysis, spastic spinal paralysis) may result from spinal-cord lesions, according as the morbid process involves the anterior horns or the pyramidal tracts of the anterior and lateral columns. The clinical features of these forms, which are sometimes blended, are elsewhere enumerated (see Chap. V.). Disease confined to the Postero- External Column of the posterior column of the cord gives rise to distinctive symp- toms. These are ( i ) inco-ordination in the extremities below the level of the lesion ; (2) loss of tactile sensibility, varying in distribution (usually chiefly in the legs) accord- ing to the vertical extent and position of the lesion ; and (3) diminution or loss of reflex action (loss of knee-jerk if the lesion is in the lumbar cord). These symptoms DIAGNOSIS OF THE POSITION OF THE LESION. 24 1 depend on the fact that the postero-external columns con- tain many of the fibres of the posterior nerve-roots which are necessarily interrupted by a morbid process in the former situation. The posterior nerve-roots are often diseased by degenerative processes that involve the postero-external columns, and give rise to similar and sometimes identical symptoms — with the exception that pain is often a prominent feature in nerve-root disease (the path for painful stimuli being contained in these roots), while it is open to question whether disease limited to the postero-external columns causes pain. Disease limited to the Postero-Internal Columns of the cord (columns of Goll) is exceedingly rare, but disease of these columns secondary to disease (usually degenera- tive) of the postero-external columns is not of infrequent occurrence. There is little clinico-pathological evidence to show what symptoms result from disease in this posi- tion, but it is on the whole probable that it gives rise to disturbance of co-ordination or of equilibrium. Ordi- narily any disturbance of this nature must be masked by the inco-ordination that results from the disease of the postero-external columns, to which lesions of the posterior median columns are secondary. A Unilateral Lesion of the spinal cord gives rise to a highly characteristic group of symptoms. First, there is motor paralysis on the side of the lesion and below its level. This depends on the interruption of the fibres of the pyramidal tracts. Often there is slight weakness on the opposite side, usually of the leg. Secondly, there is loss of sensibility on the side opposite the lesion. The loss of sensibility does not extend quite as high as the level of the lesion. This is because the sensory path does not decussate immediately at the level of the entrance of the sensory nerves, but a short distance above this. There is 16 24: DISEASES OF THE NERVOUS SYSTEM. ffioroR TRACT 8ENS.n-(S.AtT TRACT FoSL ttusci-e $e,NS£ SENSORY FIG. 47. Diagfratn showing the arrangement of the sensory and motor tracts in the cord and medulla and the effects of a unilateral lesion. R, R, R, nerve-roots. The sensory paths are represented in red, the motor paths in black. It is to be noted that the tracts conveying- general sensibility cross to the opposite side of the cord soon after entering it, while the tracts conveying muscular sensi- bility cross in the medulla just above themotdr decussation. The nerve-roots are to be considered in the dorsal cord, the cervical cord being left out. A unilateral lesion in the dorsal region of th§ cord would produce the following effects : Paralysis of motion on the same side (leg), loss of muscular sense in the same side in the parts below, loss of sensation on the opposite side (leg) below the lesion. DIAGNOSIS OF THE POSITION OF THE LESION. 243 one exception to the rule that sensation is affected on the side opposite a unilateral lesion of the cord. This relates to one-sided lesions of the lumbar enlargement, in which the sensory loss is frequently on the same side as the lesion. The explanation of this is that in such cases the sensory path is involved (in its ascent) before it crosses to the opposite side. FIG. 48. Areas of aneesthesia and hyperaesthesia in case of Brown-S6quard paralysis. Lines indi- cate anaesthesia ; dots indicate hyperaesthe- sia. (Starr.) FIG. 49. Diagram of area of sensory loss in case of crush of first lumbar segment of cord. In unilateral cord lesions the muscular sense may be impaired or lost in the muscles below the level of the lesion, but it is impaired on the satne side as the lesion, since, as already stated (p. 134), the path for the muscular sense does not cross in the cord. Of the other forms of sensibiHty those for pain and temperature are almost constantly impaired, and in the majority of cases tactile 244 DISEASES OF THE NERVOUS SYSTEM. sensibility is also affected. There is often an area of hyperalgesia on the side of the lesion which corresponds in position with the anaesthesia of the opposite side. The reflexes, superficial and deep, are increased below the lesion on the same side, except at the onset of acute lesions, when there is sometimes loss of knee-jerk on the same side. Besides these motor and sensory phenomena below the level of the lesion there are others at the same level and on the same side. There are {a) a zone of hyperalgesia due to irritation of sensory nerve-roots at the upper level of the lesion ; {^) a narrow zone of anaesthesia just below {a), from injury to the sensory roots before they cross ; and {c) localized unilateral degenerative muscular atrophy in cases where a considerable number of motor cells are damaged. The effects of this damage are best observed in lesions of the cervical or lumbar enlargement. The typical results of a unilateral lesion ' of the cord may conveniently be tabulated as follows : A. At or near the level of the lesion and on the same side of the body — A band of hyperalgesia. A band of anaesthesia. B. Below the level of the lesion and on the sa7ne side — Motor paralysis. Hyperalgesia. Impairment or loss of muscular sense (sometimes with ataxia). Early loss of reflexes, including knee-jerk (in acute cases). Subsequent increase of knee-jerk and frequently ankle-clonus. ' This characteristic group of motor and sensory symptoms is some- times denominated Brown-Sequard's paralysis. DIAGNOSIS OF THE POSITION OF THE LESION. 245 C. Below the level of the lesion and on the opposite side — Loss of sensation (pain, temperature, touch). A Complete Transverse Lesioft of the cord gives rise to loss of motor power and loss of all varieties of sensibility below the level of the lesion. The motor and sensory loss is as complete (so far as voluntary motion and sensation are concerned) as though the entire cord below the lesion were destroyed, since motor and sensory conduction are abolished. In other words, the functions of the cord as a conductor to and from the brain are destroyed as re- gards parts below the level of the disease. It is otherwise with the functions of the cord as a centre — that is, as a trophic and reflex centre. The ganglion- cells of the anterior horns, being intact below the lower level of the morbid process, still continue to subserve their trophic and reflex functions. Hence^ there is fio degenerative atrophy in the muscles supplied by nerves derived from the part of the cord below the lesion. The ganglion- cells that subserve the various reflexes, being no longer under cerebral control, overact, and this overaction is shown by increased knee-jerks and often by the existence of ankle-clonus. It must be remembered, however, that the knee-jerks may be abolished for days or weeks in consequence of inhibition from the irritation of the lesion. In such cases overaction eventually sets in, if the patient survives the damage to the cord sufficiently long. In addition to these phenomena dependent on a com- plete transverse lesion of the cord, there may be after a time degenerative atrophy in certain groups of muscles corresponding to the level of the lesion. This atrophy de- pends on the destruction of ganglion-cells of the anterior cornua at the level of the lesion ; hence when the lesion 246 DISEASES OF THE NERVOUS SYSTEM. is of slight vertical extent the atrophy may be impercep- tible, but when the lesion is of considerable vertical extent the atrophy has a correspondingly wide distribu- tion. The atrophy is of course chiefly noticeable when the disease is in the cervical and lumbar enlargements. Just above the level of the anaesthesia there is usually a girdle pain or a band of hyperalgesia. This depends on sensory irritation in the lower end of the upper portion of the normal cord. We may tabulate the results of a complete transverse lesion as follows : A. At the level of the lesion — A zone of hyperaesthesia. Muscular atrophy of limited distribution. B. Below the level of the lesion — Complete motor paralysis. Complete sensory paralysis (all forms). Initial loss of knee-jerk (in acute lesions). Eventual excess of knee-jerk and ankle clonus. The distribution of these symptoms vertically depends on the level of the cord at which the lesion is situated, and this is true also of unilateral lesions of the cord. In every case it is necessary to determine as accurately as possible the upper and lower limits of the lesion. The upper limit of the lesion is indicated by the upper limit of the anaesthesia and motor paralysis. More than this cannot be learned from the distribution of the motor and sensory paralysis, since this is the same whatever may be the downward extent of the lesion. In order to determine the lower level of the lesion it is necessary to study the condition of the reflexes and the trophic state of the muscles — that is, to interrogate the cord as a cen- tral organ. If reflex action is retained, this shows that DIAGNOSIS OF THE POSITION OF THE LESION. 247 the reflex or loops on which the reflexes depends are not included in the lesion. On the other hand, loss of reflex action indicates that the lesion has destroyed the integrity of the reflex loops, and presumably that of the ganglion-cells, or nerve-roots, or both, on which the reflex depends. Both the deep and superficial reflexes should be studied with care. The table on page 19 shows the regions of the cord with which the different reflexes are in relation, and with this knowledge it is easy to infer from the state of the reflexes whether particular regions of the cord have retained or lost their integrity. The extent downwards of the lesion is indicated also by the state of muscular nutrition and the elec- trical reactions. The presence of atrophy and of R D shows that the anterior cornua or the corre- sponding motor roots have been damaged, and the extent of these , • T 1 -11 Diagram showing area of changes indicates the precise levels sensory loss in case of crush of , „ . _ , , ,. Vllth cervical segment of cord. thus affected. In order to localize The distribution of analgesia , 1,1 1 -I 1 /• , 1 and anaesthesia in the arms is accurately the lower level of the characteristicof a lesion at this 1 • T_ • /• r ii . 1 • level. Area of hyperalgesia lesion by inference from the trophic dotted. state, it is necessary to bear in mind the relations of the various muscles and muscle- groups to the cord. These relations are given in the table. The indications of the extent of the lesion afforded by the trophic state of the muscles are espe- cially valuable when the disease is in the lumbar and cer- 248 DISEASES OF THE NERVOUS SYSTEM. vical .enlargements. When the destructive process is in the dorsal region the effect on muscular nutrition is less noticeable and less valuable as an aid in localizing the lesion, but it is just in this region that the indications ob- tained from the state of the reflexes are of the greatest aid. With the help of these facts, and the tables showing the representations of the motor, sensory, and reflex functions of the cord, it is possible, in most cases, to make an accurate diagnosis of the position and extent of the lesion. It may be well, however, to outline briefly the distribution of the motor and sensory loss that results from a complete transverse lesion of the cord at the most important levels of the cord. Individual differences exist in the distribution of symptoms from disease at the same levels, but these differences are sel- dom considerable, and do not seriously invalidate the following types. A lesion which destroys only the extremity of the cord (conus medullaris) as high as the fifth sacral nerves, causes paralysis of the bladder and rectum, and a small area of anaesthesia near the tip of the coccyx. Such lesions are very rare. If the lesion destroys the cord at the level of the fourth and fifth sacral segments there is, besides paralysis of bladder and rectum, loss of power in the perineal muscles (erector penis, transversus peri- nei, accelerator urinas), with loss of ejaculatory and erec- tile power. There is also a characteristic anaesthetic area, which probably depends on injury of the fourth sacral segments or roots. There is a saddle-shaped region of anaesthesia on the back of the thighs and sacrum. The internal surfaces of the thighs high up are also anaes- thetic, and the anaesthesia usually extends to the exter- nal genitals and perineum. Figure 51 represents the saddle-shaped area in such a case. DIAGNOSIS OF THE POSITION OF THE LESION. 249 In lesions involving the upper sacral segments there is paralysis of the muscles of the leg and foot, and a strip of anaesthesia on the back of the thigh, which extends to the back of the leg and ankle and to the sole and dorsum of the foot. The skin of the inner side of the leg usually escapes. Damage to the cord as high as the lumbar region causes paralysis of the flexors of the knee and abductors of the thigh. There is also anaesthesia of the anterior and inner aspect of the leg and of the inner and posterior part of the thigh. When the middle of the lumbar region is destroyed, the motor paralysis includes the extensors of the knee and the abductors of the thigh, and the loss of sensation extends as high as the anterior aspect of the thigh (lower part at least). When the disease affects the upper part of the lumbar enlargement the loss of sensibility includes the upper and outer aspect of the thigh and the skin of the groin and part of the scrotum. The flexors of the thigh and the sartorius are then paralyzed. As the level of the lesion ascends in the dorsal region the level of the anaesthesia and motor paralysis extends to a correspondingly higher level on the trunk. The ab- dominal muscles are first paralyzed, then the intercostals. The umbilicus corresponds to the eleventh dorsal seg- ment. When the anaesthesia reaches one inch above the umbilicus the lesion is as high as the tenth dorsal segment. The epigastrium corresponds to the sixth and seventh dorsal segments, the nipples to the fourth dorsal, and the third rib to the third dorsal segment. When a lesion is placed as high as the first dorsal segment (that is, the lower part of the cervical enlarge- ment) the first impairment of sensibility and loss of power in the upper extremity are observed. There is loss of 250 DISEASES OF THE NERVOUS SYSTEM. power in the intrinsic muscles of the hand and loss of sensibility in part or all of the area of the hand supplied by the ulnar nerve. When the lesion invades the cord at the level of the seventh cervical segment the anaesthesia usually reaches as high as the median line, anteriorly and posteriorly, of the arm, forearm, and hand. Figure 50 shows this characteristic distribution of anaesthesia in a case of total transverse lesion at this level of the cord. The motor loss in such cases is sufficiently indicated by the table. A lesion destroying the middle of the cervical enlarge- ment (fifth, sixth, seventh) causes loss of sensation in the entire arm and part of the shoulder. The motor paralysis extends to the shoulder muscles and the serratus magnus. There is also sometimes some loss of power in the tra- pezius and sterno-mastoid when the lesion is placed as high as the fifth cervical segment. When the fourth cervical segment is destroyed the anaesthesia extends to the entire shoulder and lower part of the neck. The action of the diaphragm is impaired and the motor paral- ysis extends to the few remaining muscles of the shoulder (supra- and infra-spinati). A complete transverse lesion at this level is usually quickly fatal. The accessory mus- cles of respiration (scaleni, sterno-mastoids) may give the patient enough air to maintain life a few days, but not longer. In the lower part of the cervical cord an acute lesion may inhibit respiration so as to cause death in the course of a few days. Nerve-Roots. — Lesions of the Anterior Nerve-Roots give rise to motor over-action or motor paralysis accord- ing as they are irritative or destructive in character. The distribution of the spasm and paralysis depends on the number and locality of the roots involved. The table (on page 19) shows. -the representation of the different DIAGNOSIS OF THE POSITION OF THE LESION. 25 1 muscles in the anterior roots, this being practically the same as in the corresponding segments of the cord. In chronic irritative disease long-continued and persistent spasm (from tumor) may produce loss of voluntary power, and in acute irritative lesions (meningitis) irri- tation symptoms far exceed paralytic phenomena and may even exist alone. Irritative lesions of the Posterior Nerve- Roots cdM'iQ pain and hyperalgesic skin areas corresponding to the irritated roots. The pain is often severe and persistent. Destruc- tive lesions cause loss of sensibility. When the destruc- tion is partial, tactile sensibility may be chiefly impaired ; when it is complete, all forms of sensibility are abolished in the corresponding skin area. Cauda Equina. — The cauda equina not very in- frequently suffers from the effects of pressure. This pressure is exerted most often in consequence of injury to the lumbar spine, especially dislocation. Less fre- quently the pressure results from tumor or from spina bifida. The resulting symptoms vary considerably ac- cording to the position and extent of the lesion. In a lesion which involves the entire cauda equina, or the larger number of its constituent roots, the nerve-roots which take their origin from the lowest part of the cord (that is, lie nearest the median line) are more seriously injured than those abjve them. If all the roots are origi- nally involved the upper ones may soon recover entirely, while the lower ones continue to suffer seriously. This is a fact of some diagnostic importance. While there is nothing absolutely distinctive about the distribution of the motor and sensory symptoms in cases of injury to the cauda equina, there is considerable uniformity in the phenomena, and many of the cases conform more or less closely to a certain type. The motor paralysis is espe- 252 DISEASES OF THE NERVOUS SYSTEM. cially apt to affect the branches of the sciatic and pudic nerves, and particularly the lower branches of the former. The anterior crural and obturator distribution are also frequently involved, but the paralysis is apt to be less in degree. The R D may or may not be present, according to the severity of the damage. The anaesthesia com- monly involves especially the distribution of the great and small sciatic and pudic nerves. When the fourth and fifth sacral roots suffer chiefly, as they sometimes do, the anaesthesia is limited to the perineum, external genitals, and a saddle-shaped area on the buttocks and thighs. Sometimes the anaesthesia is limited to the perineum and genitals and upper part of the inner surfaces of the thighs, even though there is considerable loss of power in the lower extremities. The condition of the reflexes is different in different cases. The knee-jerk is usually absent, as is also the plantar reflex. Retention of urine, with overflow incon- tinence, is not common. Such incontinence may exist for several months in consequence of a cauda injury, and yet terminate in recovery of function when the pressure ceases or diminishes. As a rule, the sphincters are only slightly or not at all affected in pure cauda lesions. Trophic disturbances (bed-sores, perforating ulcer) occur in a considerable proportion of cases. The distinction of cauda equina disease from lesions of the lower part of the spinal cord may be exceedingly difficult. If the damage is of traumatic origin the position of the local symptoms (fracture, displacement of vertebrae, etc.) is of much assistance, since the cord itself does not extend below the lower border of the first lumbar vertebra, and any displacement below this level would injure the cauda and not the cord. In the absence of distinct local indica- tions, the distribution of the motor and sensory phe- DIAGNOSIS OK THE POSITION OF THE LESION. 253 nomena and their mode of development may be of aid. Anaesthesia limited to the buttocks (saddle-shaped areas) or to the buttock and backs of the thighs, or to the but- tocks and thighs and the legs (posterior aspect), suggests a dependence on a cauda lesion and not on a cord lesion, but it is not certain that ansesthesia of similar distribu- tion may not result from partial destruction of the conus FIG. 51. Area of ansesthesia in a lesion of the Cauda equina, depen- dent probably on damage to the fourth and fifth sacral roots. (Starr.) FIG. 52. Diagram showing the area of ansesthe- sia in a woma.n with a lesion of the cauda equina. meduUaris and lumbar cord in cases where there is little or no involvement of the nerve-roots. Considerable sen- sory loss (as that shown in diagram 51), with slight loss of motor power and slight involvement of the sphincters, also suggests a cauda and not a cord lesion. Pain in the area of anaesthesia points to a cauda-equina lesion, pain above the area of anaesthesia to a cord lesion. The pain of 254 DISEASES OF THE NERVOUS SYSTEM. Cauda lesions is referred to the sacrum rather than the lumbar spine, which is generally the seat of pain in spinal-cord disease. With the aid of these points of dis- tinction a diagnosis can generally be made between damage of the lumbar, or lumbar and sacral cord, and damage of the cauda equina. But when, as is probably not rarely the case, the conus medullaris is involved with the Cauda equina, the recognition of this involve- ment may be impossible. As already stated, it is not certain that damage of the conus and lower end of the cord may not be competent to cause some of the pecul- iarly disposed anaesthesias which are thought to be characteristic of a cauda lesion.' It may be that the involvement of the conus simply intensifies the symptoms of cauda disease. Destruction of the conus medullaris causes complete paralysis of the bladder and rectal sphincters and loss of sexual power. It is not yet known whether such complete paralysis is ever the result of pure lesions of the cauda. There is some reason to think it is not. When, therefore, the symptoms suggest a cauda lesion, but the sphincters are completely paralyzed, there is reason to think that the conus medullaris is also im- plicated. Further investigation is needed to clear up these points. Asymmetry of the motor and sensory loss suggests a lesion of the cauda rather than of the cord, and extreme chronicity of development (years) has the same significance. ' Thus in one case of dislocation of the first lumbar vertebra there was complete paralysis of motion below the knee and anaesthesia of the buttock, back of thigh, leg, and sole of foot, but the autopsy failed to show any damage to the cauda equina. The autopsy did show, however, crushing of the sacral and lowest lumbar segments of the cord and slight damage of the nerve-roots as they lie on the cord at this level. DIAGNOSIS OF THE POSITION OF THE LESION. 255 The distinction of disease or injury of the Cauda equina from lesions of the peripheral nerves is usually not difficult. Multiple neuritis is the only disease of the peripheral nerves that can be mistaken for a Cauda lesion. The diag- nostic points are else- where presented (p. 509). Occasionally an injury of the nerves in their extra-spinal course, par- ticularly one involving the lumbo-sacral plexus, gives rise to considerable diagnostic difficulty. Tht points to be borne in mind in making the dis- tinction are the bilateral symmetry (not always perfect) of the symptoms from Cauda injury, and the usual occurrence of local evidences of injury. In rare instances injuries of the Cauda have pro- duced chiefly unilateral motor and sensory Symp- . Diagram showing the area of sensory loss ■' ■' i in a case of crush of the cauda equina and toms, but even in these «""^ "'f^"."^""-, «■';.> tT °f=^"^J'h^^'^ ' and analgesia, ihe lightly shaded areas cases there are USUallv °" the buttocks and legs represent a slight- •^ er degree of sensory loss. some symptoms that suggest an intra-spinal nerve lesion (disturbances of bladder and rectum, peculiar distribution of ansesthesia, etc.). FIG. 53. 256 DISEASES OF THE NERVOUS SYSTEM. Peripheral Nerves. — The localization of lesions in- volving the nerves in their extra-cranial and extra-spinal course is, generally speaking, less difficult than the locali- zation of lesions of the brain and spinal cord. The data for an accurate local diagnosis are easier to obtain and are less equivocal in significance than in the case of cen- tral lesions ; local signs play a more important role and the diagnosis is less distinctly inferential in character. An accurate knowledge of the course and distribution of the nerves and of the anomalies that occur, must be the foundation on which every diagnosis rests. The pos- sibilities of collateral innervation must also be borne in mind in determining the effect of a lesion in a given situation. The general symptomatic characters of peripheral- nerve lesions may conveniently be considered in the chap- ter on clinical types. The special symptomatic charac- ters of such lesions vary with the special functions and distributions of the nerve or nerves implicated. Certain symptomatic combinations are sufficiently frequent and important to require special notice, and are mentioned as clinical types of disease. CHAPTER IV. THE DIAGNOSIS OF THE NATURE OF THE LESION. Having established the situation of the lesion in a given case of organic disease of the nervous system, there remains for determination the nature of the morbid pro- cess which constitutes the lesion. Generally speaking, this problem presents greater difficulties than the local diagnosis. In many instances, it is true, an exact diag- nosis of the nature of the lesion is readily reached, but the cases are quite as numerous in which an approximate diagnosis only can be made. Sometimes the best that can be done is to narrow the diagnosis to one of two possibilities, and occasionally it is impossible to do better than to make a guess. Notwithstanding the obstacles to an exact diagnosis of the character of the pathological process, the problem is one of the highest practical importance, and demands for its solution the most painstaking care in balancing the available diagnostic indications. In the case of lesions of the central nervous system the pathological diagnosis is usually of distinctly greater importance to the patient than the exact local diagnosis, for on it depends, in great degree, both the prognosis and the treatment. Before studying the more important indications that guide us in determining the nature of the lesion it is use- ful to consider briefly the various morbid processes which are encountered in practice and constitute the great '7 257 258 DISEASES OF THE NERVOUS SYSTEM. majority of the cases of nervous disease. These processes are few if we consider only the ultimate processes to which the symptoms of disease are due. They are hem- orrhage, necrotic softening, inflammation, abscess, tumor, and degeneration. To this list may conveniently be added congestion and anaemia, although these are not, strictly speaking, organic conditions. Hyperaemia. — The subject of Congestion of the Brain is one of considerable obscurity. It cannot be said that we possess any exact knowledge in regard to it. The results of post-mortem examination are to a con- siderable extent negative — that is, there are no constant or characteristic changes in cases which, from their symp- toms, seem referable to cerebral congestion. This fact, however, does not in itself make the possibility of the oc- currence of congestion impossible, since general pathology teaches that distinct active congestion of other parts may leave no trace after death. Indeed cases occasionally occur in which the symptoms can reasonably be referred to cerebral congestion alone. The hyperaemia may be active or passsive. In the former case there is an excess of blood in the arteries, in the latter an excess in the veins. In both instances the capillaries are over-distended, and it is to this over-distension that the symptoms of con- gestion are due. In both instances the brain suffers from a deficiency of oxygen, in consequence of the stasis, but in passive congestion there is also an excessive accumula- tion of carbonic acid in the capillaries. It is probable that prolonged passive congestion during life may cause a permanent increase in the size of the capillaries. Me- chanical venous congestion may result a short time after death from gravitation of blood to dependent portions of the brain. When ante-mortem passive congestion has ex- isted in such cases, its effects cannot be distinguished in DIAGNOSIS OF THE NATURE OF THE LESION. 259 the presence of the more obtrusive results of gravitation. It is important to note that even the most intense passive congestion, such as occurs in asphyxia, may leave no trace after death. What has been said of our imperfect knowledge of cer- ebral congestion may be said with equal truth of congestion of the cord. It is probable that active primary congestion of the cord occurring independently of the initial stage of myelitis is an exceedingly rare condition. A so-called secondary congestion of the cord is not an infrequent consequence of excessive physiological activity of the nerve elements of the cord, especially of the motor elements. Passive congestion of the cord is of exceed- ingly rare occurrence. The influence of gravitation in producing mechanical congestion of the cord after death is probably as great as in the case of the brain. The same influence is operative in the cord during life, but to a far slighter degree. Of congestion of the membranes of the brain and spinal cord, as conditions distinct from the first stage of inflam- mation, nothing is known. Likewise nothing is known of simple congestion of the peripheral nerves. Anaemia. — Ancemia of the Brain may result from gen- eral anaemia, in which the quantity or quality of the entire amount of blood is defective. This is seen in cases of simple ansemia, hemorrhage, chlorosis, etc. The blood supplied to the brain may also be diminished in the absence of any systemic causes for such diminution, as from cardiac weakness. Localized cerebral ansmia may result from obstruction to the flow of blood through the cerebral vessels. Permanent obstruction of this kind often leads to another pathological process — that is, softening. The various causes of ansemia of the brain may be suddenly or gradually operative, and the symp- 26o DISEASES OF THE NERVOUS SYSTEM, toms vary accordingly. There is some reason for be- lieving that angiospasm (arterial spasm) is capable of causing anemia of greater or less areas of brain sub- stance, sometimes with resulting temporary hemiplegic symptoms. AiKzmia of the Spinal Cord, as a persistent condition, dependent on arterial obstruction, is unknown, but it is certain that such mechanical obstruction to the blood- supply of the cord may result in local anaemic necrosis and subsequent inflammation. It is uncertain whether the symptoms that suggest transient anemia of the cord depend primarily on arterial spasm, or are due to primary functional derangement of the nerve elements, causing arterio-spasm. In certain blood states, as simple ansemia, chlorosis, and anasmia from blood loss, the nutrition of the entire body suffers, and with this the nutrition and functional activity of the spinal cord. Here, as in the brain, the essential pathological factor is the defective quantity or quality of the blood. Concerning anaemia of the peripheral nerves nothing is known. Hemorrhage. — Hemorrhage within the Cranial Cavity may invade the brain substance itself or the meninges. In either case the hemorrhage is due to rupture of a ves- sel. Meningeal hemorrhage is almost invariably ' due to injury ; hemorrhage into the substance of the brain (in- cluding pons, medulla, and cerebellum) generally occurs spontaneously— that is, as the result exclusively of in- ternal pathological conditions. The hemorrhage is usu- ally from an artery. But occasionally it is from a vein or from capillaries. Excepting from traumatic influences, an artery ruptures only when its walls are the seat of disease. The local factor in producing hemorrhage may ' In children extensive subarachnoid hemorrhage sometimes occurs in the course of acute infectious diseases. DIAGNOSIS OF THE NATURE OF THE LESION. 261 be the sole appreciable cause of the rupture. Frequently, however, there is a local increase in blood pressure, and such an increase causes the diseased and weakened arterial wall to give way more readily than it would otherwise do. When the walls of an artery become weakened by dis- ease they gradually yield before the blood pressure. This gradual yielding leads to local thinning of the coats of the vessel, which eventually become so thin and weak that they may rupture. As the walls yield before the pressure of blood, a bulging occurs, and this bulging constitutes an aneurism. Aneurisms occur in two different situations — in the larger arteries at the base of the brain and over the convexity, and in the small arteries that lie imbedded within the brain substance. Aneurisms of the former class are of uncommon occurrence. They usually attain considerable size and are few in number or single. They may give rise to symptoms due to pressure, and thi« is especially liable to occur when they are situated on ves- sels at the base of the brair. These aneurisms (intra- cranial aneurism proper) may eventually rupture, but, until they do so, their symptoms, if symptoms exist, are those of intracranial tumor. The aneurisms within the substance of the brain, which form on the small arterial branches, are of small size d^ to ^V inch) and are hence termed miliary aneurisms. These miliary aneu- risms are always numerous. They are found most fre- quently on the vessels to the central ganglia, probably because these small vessels are given off directly from a vessel (middle cerebral) of much greater calibre, in con- sequence of which the arterial pressure is considerably higher in them than in vessels of the same size which branch more gradually. The fact that the internal cap- sule (motor part) is supplied by vessels that are often the 262 DISEASES OF THE NERVOUS SYSTEM. seat of miliary aneurisms is of great practical importance, since hemorrhage in this situation is a frequent cause of hemiplegia. The bursting of miliary aneurisms is the predominant cause of spontaneous cerebral hemorrhage, but it is cer- tainly not the sole cause. Inflammation and degeneration (chronic endarteritis, obliterating endarteritis, atheroma, hyaline degeneration) may weaken the coats of the arteries in which they occur to such a degree that these vessels rupture without the previous development of miliary aneurisms. Miliary aneurisms seem to depend mainly on a primary degenerative process in the arterial wall, affecting chiefly the contractile and elastic elements. The muscular coat of the vessel disappears and the intima and adventitia come in con- tact. The most important known factors in the production of this degeneration are the blood pressure to which the arteries are subjected, and the degenerative tendency that exists in the second half of life and that is associated with atheroma. Cerebral hemorrhage may occur without pre- existing changes, as atheroma, in the vessel walls visible to the naked eye, but it is an important fact that atheroma of the larger vessels is present in a large proportion of cases of cerebral hemorrhage, even when the hemorrhage is due to bursting of miliary aneurisms. Certain blood states, notably purpura, scurvy, pernicious anaemia, and leuco- cythemia, may lead to cerebral hemorrhage, or rather to cerebral hemorrhages, since the extravasations are gener- ally multiple. In many of these cases it is impossible to demonstrate pathological changes in the vessels. Cerebral hemorrhage may occur in any region of the brain, but is especially frequent in and about the basal ganglia and in the internal capsule. Hemorrhage into the cortex is of rare occurrence. DIAGNOSIS OF THE NATURE OF THE LESION. 263 Hemorrhage gives rise to symptoms by destroying nerve elements, and by compressing neighboring struc- tures and irritating them. This irritation of the adjacent tissue elements is chiefly operative during and imme- diately after the onset, and, in conjunction with pressure, is responsible for many indirect symptoms. Hemorrhage into the Spinal Cord, from any cause what- ever, is an exceedingly rare occurrence, and its rarity con- trasts strikingly with the frequency of cerebral hemorrhage. Primary hemorrhage into the cord is so uncommon that its occurrence has been doubted, and it is certainly true that the conditions which, in the brain, further its production seem to be absent in the cord. The vessels to the cord are long and tortuous and the pressure within them is never high. Miliary aneurisms probably do not occur. Secondary hemorrhage into the cord, during inflamma- tion of the cord, occasionally occurs and may readily be mistaken for primary hemorrhage. Secondary hemor- rhage may also occur from certain highly vascular tumors of the cord, especially certain gliomata. Traumatic hemorrhage is more common than secondary hemorrhage and is especially apt to follow falls which severely concuss the spine. Not infrequently there is hemorrhage into the central canal of the cord. Minute hemorrhages into the substance of the cord often occur .in the course of asphyxial and convulsive diseases (tetanus, Hydrophobia, etc.), but they cause no symptoms. In all forms of hemorrhage into the spinal cord the gray matter is particularly apt to be involved. Hemorrhage into the Membrajies of the Cord is rare; The hemorrhage may be extra-meningeal or intra-me- ningeal. The chief cause of either form is injury. The minute secondary extravasations which occasionally occur in the peripheral nerves cause no symptoms. 264 DISEASES OF THE NERVOUS SYSTEM. Softening. — The expression " softening of the brain, ' when correctly used, relates to an actual diminution of consistence of the brain substance, due to the disintegra- tion of tissue elements. The term is, however, frequently employed by the laity in an entirely different sense — that is, to designate almost any variety of chronic mental fail- ure, but especially dementia paralytica. Literal cerebral softening may be the result of several distinct processes. Of these processes the chief are in- flammation and arrest of blood supply. We shall con- sider here the latter only. Arrest of blood supply depends on the occlusion of an artery. This occlusion deprives a certain area of the brain of its nutrition, because, in many regions of the brain, the terminal arterioles do not anastomose suf- ficiently to permit a re-establishment through the col- lateral circulation of the nutritive processes in the dependent part. The tissue elements, thus deprived of nutrition, lose their vitality and their function, and undergo disintegration— that is, softening, — necrotic soft- ening it is termed. The process is also termed acute softening, owing to the rapidity with which the necrosis occurs. Two distinct pathological processes may cause obstruc- tion of an artery. These are thrombosis and embolism. Thrombosis is the formation of a blood clot within a vessel at the point of obstruction of the vessel. Obstruc- tion from embolism depends on the lodgment of a plug — usually derived from a distant part of the vascular system — in an artery which is too small to permit its further passage. Thrombosis is sometimes secondary to embolism from coagulation in the distal end of an obstructed artery, and embolism is occasionally secondary to thrombosis, from detachment and subsequent advance of a thrombus, DIAGNOSIS OF THE NATURE OF THE LESION. 265 but the two processes are usually quite distinct and separate. Thrombosis of an artery generally results from local disease of the arterial walls, but occasionally it is due to morbid blood states in the absence of any changes in the artery. The predominant forms of arterial change are atheroma and syphilitic endarteritis. Both atheroma and syphilitic disease cause changes in the arterial walls, which usually narrow the lumen and roughen the inner surface of the thickened intima. The alteration of the inner surface of the vessel disposes to the formation upon it of a clot. Any morbid blood state, or any condition which weakens the action of the heart, or otherwise leads to the slowing of the blood current through the diseased vessels may facilitate the occurrence of thrombosis. Atheroma involves chiefly the arteries at the base of the brain, especially the internal carotid, middle cerebral, basilar, and vertebral. Obliteration of the lumen of the middle cerebral or of its branches causes softening in or near the central ganglia or internal capsule. Occlusion of the pontine branches of the basilar causes softening of the pons. It is important to note that the atheroma is often symmetrically distributed. Atheroma is of frequent occurrence during the second half of life. Occasionally it occurs earlier — at thirty-five or forty years of age. Its early occurrence is facilitated by the existence of chronic diffuse nephritis, an impor-' tant clinical fact. Atheroma increases in frequency as age advances. Syphilitic endarteritis leads to a greater narrowing of the calibre of the affected vessel than do other forms of arterial disease, and sometimes the thickened tissue for- mation may in itself obliterate the lumen. Generally a thrombus forms when the vessel is considerably narrowed. 266 DISEASES OF THE NERVOUS SYSTEM. The vessels involved in the process are chiefly those of the base, but the small arteries are often diseased, and may be diseased when the changes in the basal vessels are slight or wanting. The distribution of the change may be symmetrical, but it is usually irregular. Syphilitic arterial disease is usually a result of acquired syphilis, and as the arterial changes are commonly devel- oped in the course of four or five years after infection, they are generally operative in producing softening during adult life and especially during early adult life. In Embolism the plug takes its source from some point between the lungs and the artery which is obstructed. In a large majority of cases the obstructing embolus comes from the heart, being derived either from vegetations on the valves or from a coagulum in the left auricle. The embolus may come either from the mitral or the aortic valve. Generally it comes from the mitral valve, and mitral stenosis is the most frequent valvular cause of em- bolism. Embolism occurs somewhat less frequently in the course of chronic endocarditis than in recent cases of endocarditis or in the course of fresh exacerbations of endocardial inflammation. And embolus sometimes takes its origin from the aorta, when this is the seat of atheromatous change. There is some reason to believe that minute emboli of septic ma- terial may pass through the pulmonary capillaries and find lodgment in the brain. Only capillary cerebral vessels can be obstructed by emboli so minute that they do not lodge in the lung capillaries. If localized cerebral softening results from the lodgment of septic material this is purulent. There may be multiple foci of septic soft- ening in the brain, and these may coalesce to form ab- scesses. Whenever the embolus contains septic material derived from any part of the vascular system (usually from DIAGNOSIS OF THE NATURE OF THE LESION. 267 ulcerative endocarditis), there may be septic inflammation about the obstructed vessels, with clinical evidences of septic infection. Embolism occurs at all periods of life. It is particu- larly frequent between adolescence and middle life. Its occurrence is usually associated with conditions which are attended with endocarditis — especially with acute articular rheumatism, chorea, and scarlet fever — and occasionally it results from the endocarditis which some- times develops in the course of acute specific diseases. Conditions which increase the coagulability of the blood may favor the occurrence of embolism by the formation of a clot on diseased valves or in a feebly acting heart, with subsequent detachment. Embolism from this cause is not very uncommon in the puerperal state. The same blood-state may lead to the occurrence ot thrombosis under similar circumstances. Acute Softening of the spinal cord, from loss of blood supply, is unknown as a distinct condition. The possi- bility of the occurrence of necrotic softening from vascu- lar obstruction as the first stage of inflammation is mentioned elsewhere. Thrombosis of Sinuses. — Thrombosis of sinuses of the brain may result (i) from any blood state or con- dition of the circulation that favors coagulation (primary thrombosis), or (2) from disease adjacent to the sinuses (secondary thrombosis). Primary Thrombosis is usually associated with pro- tracted and exhausting disease — for example, acute specific fevers, tuberculosis, carcinoma, chronic sup- puration, and very frequently, in infants, prolonged and exhausting diarrhoea. These difl^erent causes are operative in two ways — by weakening the action of the heart, and by increasing the coagulability of 268 DISEASES OF THE NERVOUS SYSTEM. the blood. The superior longitudinal sinus is by far the most frequent seat of sinus thrombosis, probably because the blood current through it is exceedingly slow and feeble. It has been supposed that primary thrombosis occurs in cerebral veins, as distinguished from sinuses, and that a lesion of this nature, in the veins of the con- vexity, may underlie many cases of infantile hemiplegia. There is at present little evidence that such a process is ever thus operative, but with the present state of our knowledge the possibility that venous thrombosis con- stitutes the pathological basis of some cases of infantile hemiplegia cannot be denied. Secondary Sinus Thro7nbosis is most often due to caries of cranial bones, particularly of the bones of the ear. Occasionally it results from disease external to the cranium, as erysipelas, or carbuncle of the face or neck. Almost any cerebral sinus may be the seat of secondary throm- bosis, but the sinus affected is usually the one nearest the local disease. The local process is generally ear disease ; hence the superior petrosal or lateral sinus is the usual seat of the thrombosis. Local disease usually causes thrombosis in one of two ways. The inflammation either passes directly to the wall of the sinus, causing a phlebitis, which results in throm- bosis, or a clot passes by extension to the sinus through a vein leading from the seat of the local disease to the sinus. In the former case the wall of the sinus is inflamed (phlebitic thrombosis) ; in the latter the wall of the sinus is healthy. Inflammation. — Inflammation of the Subsiatice of the Brain, as distinguished from inflammation of the mem- branes of the brain, is of rare occurrence, and when it occurs is usually secondary in origin and restricted in its limits. Acute cerebritis may follow injury to the head, DIAGNOSIS OF THE NATURE OE THE LESION. 269 or bone disease, but constitutes a condition of little medi- cal interest, unless it is accompanied with meningitis. The cerebritis of injury usually goes on to the formation of abscess. Tumors are often surrounded by a zone of inflammatory softening, and there is usually a zone of in- flammation about foci of acute softening. Acute specific diseases, and septic conditions generally, may lead to the formation of small foci of encephalitis containing many micrococci. An acute idiopathic cerebritis (polio-enceph- alitis) has been considered the probable cause of many cases of infantile hemiplegia. There is as yet no direct evidence that this is the case, but there is some reason to believe that such a process may be effective in a small pro- portion of cases of sudden cerebral palsy in children. Meningitis. — Inflammation of the Membranes of the Brain is from a medical standpoint by far the most im- portant form of intracranial inflammation. Inflammation of the dura mater (pachymeningitis) is of rare occurrence except after injury. A peculiar form of pachymeningitis is that known as pachymeningitis interna hemorrhagica or haematoma of the dura mater. The lesion in these cases consists of delicate newly formed connective tissue, rich in small blood-vessels, and containing in its meshes, or on its surface, the remains of extravasations of blood. Inflammation of the Fia Mater, or pia-arachnoid (lepto- meningitis), is of very frequent occurrence. The inflam- matory process may be diffuse, and affect chiefly the base or the convexity, or it may be localized within nar- row limits. Certain forms of meningitis, dependent on the grade or nature of the inflammatory process, may be distinguished. These are simple, purulent, tubercular, and syphilitic meningitis. It is impossible to draw a sharp line between all cases of simple and purulent men- ingitis. The cases to be classed as purulent meningitis are 270 DISEASES OF THE NERVOUS SYSTEM. those in which a layer of purulent exudate over the mem- branes inflamed is distinctly visible to the naked eye. All cases of inflammation (except specific forms) in which the amount of exudation or infiltration falls short of produ- cing a distinct purulent layer are to be classed as simple meningitis. In many of these cases of simple meningitis there is merely a slight or considerable opacity and thick- ening of the pia in certain parts, though the microscope shows the presence of distinct and often considerable in- filtration of the membrane with small spheroidal cells. It is difficult to say to which class some cases of menin- gitis belong. The difference between the two varieties of inflammatory change is probably merely one of degree and not of kind. Simple or Noji-P iiriilcnt Menmgitis'x^ considerably more common than the purulent form. It is sometimes met with after insolation and, more frequently, in the course of acute specific diseases, or without apparent cause. Focal lesions of the brain, such as tumor, abscess, and occasion- ally softening or hemorrhage, may excite a localized simple meningitis in their vicinity. Inflammatory ad- hesions between the dura and pia mater frequently occur in the neighborhood of new growths. Purulent Meningitis most commonly results from ad- jacent suppuration. A frequent cause is disease of the middle ear. Another common cause of purulent menin- gitis is suppuration in distant parts. Thus it is observed in various forms of pyaemia and septicaemia. It also oc- curs at times in the course of acute infectious diseases. The pathological changes in purulent meningitis may involve the entire extent of the membranes or chiefly the convexity or base. Usually the changes are ex- tensive, and occasionally they extend to the spinal meninges. Purulent meningitis is, of course, always of DIAGNOSIS OF THE NATURE OF THE LESION. 271 bacterial origin. Several different forms of micrococci may give rise to it. Tubercular Meningitis is much the most common variety of meningitis. Its distinctive character is the occurrence of miliary tubercles in the pia in associa- tion with meningitis which generally possesses the appear- ances of simple meningeal inflammation and is rarely purulent. The membranes at the, base are usually chiefly involved in the inflammatory exudation, and the distinc- tive S3'mptoms of the process are those of unequal damage to the cranial nerve-roots. The products of inflammation are especially abundant about the chiasma, in the inter- peduncular space, and on the inferior surface of the cere- bellum. The tubercles themselves are usually seen as minute translucent grayish-white granulations, which are most numerous about the smaller arteries of the pia. They are apt to be especially numerous about the vessels at the commencement of the fissure of Sylvius. Tubercles of the pia may exist without the gross appearances of meningitis, and the development of actual meningitis is probably always preceded by the deposition of miliary tubercles in the pia. There seems to be little relation between the number of the tubercles and the extent or degree of the inflammatory process. Clinically it is impossible to distinguish between cases of miliary tuber- culosis of the membranes without inflammation, and tubercular meningitis, since the symptoms of the former condition cannot be distinctly separated from those of the latter. Massive, or solitary tubercle, however, not rarely gives rise to the symptoms of tumor before the develop- ment of tubercular meningitis. When such a meningitis is grafted on a pre-existing tuberculous growth the symptoms of the two conditions are complex in char- acter. 2/2 DISEASES OF THE NERVOUS SYSTEM. Tubercular meningitis probably depends on the depo- sition of tubercle bacilli in the vessels of the pia. In a very large proportion of cases the tubercular process in the meninges is secondary to a similar process elsewhere. In children it is almost invariably associated with general tuberculosis. Cases occur, however, in which there are no indications of tuberculosis and in which the menin- gitis appears to be primary. These cases usually occur in young adults. The primary focus of tuberculosis may be in almost any part of the body that is the seat of such disease. In adults the primary process is usually in the lungs. In children it is often in the bronchial, cervical, or mesen- teric glands. Tubercular meningitis is particularly a disease of childhood, but may occur at any period of life. Syphilitic Meningitis is usually a chronic process of limited extent. Occasionally the inflammatory products involve the meninges of the base or of the convexity ; generally they are limited chiefly or entirely to a small region of the base, especially of the posterior fossa of the skull. The pia is usually much thickened with the inflam- matory exudation, and may be glued to the dura. In a later stage of the process the inflammatory material un- dergoes organization, and thick layers of fibrous tissue may surround and compress the nerves at the base. When the meninges of the medulla are the seat of such a chronic inflammatory process, the openings of the fourth ventricle may be obliterated, with consequent internal hydrocephalus. Frequently syphilitic meningitis occurs about a syphilitic new growth (gumma). Inflammation of the Spinal Cord is a condition of fre- quent occurrence. The morbid process may begin in the nerve elements themselves, or in the neurogliar elements, and may involve the gray substance or both gray and DIAGNOSIS OF THE NATURE OF THE LESION. 273 white substance. Inflammation causes disintegration of the fibres and cells involved, and the first gross alteration that results is a diminution in consistence — that is, soften- ing. In the course of time the inflammatory products may undergo organization into new connective tissue, with perhaps an ultimate increase in the consistence of the cord. When the morbid process runs a chronic course, the cells and fibres undergo slower disintegration, and are gradually replaced by the products of cell pro- liferation in the non-nervous elements. If the changes are very chronic, the cord may be little or not at all softened in consistence. It may be difficult in such a case to decide whether the process in question is really inflam- matory and not degenerative in character, and the decision in a doubtful case will depend much on our conception of inflammation. The mechanism by which myelitis is produced is ex- ceedingly obscure. In many acute cases the inflammation is probably due to the invasion of the vessels of the cord by micro-organisms. It is certain that an ansemic necro- sis or softening of the cord (especially the gray sub- stance), from arrest of blood supply, may go on to inflammation, and it is not improbable that vascular obstruction by thrombosis or embolism is a more import- ant factor in causing myelitis than has been supposed. The elements of the cord, especially of the gray substance, have very little or no power of repair. Inflammation of the Spinal Meninges may involve chiefly the dura (pachymeningitis), or the pia (leptomeningitis). The process may run an acute or chronic course. Acute inflammation rarely remains limited to the membrane in which it begins ; it extends to the other. Chronic inflam- mation, on the other hand, may remain limited to the membrane (dura or pia) in which it commences. Hence 274 DISEASES OF THE NERVOUS SYSTEM. it is only in chronic cases that the symptoms of men- ingitis can be referred to one or the other membrane, according to their character, Avith any degree of certainty. For practical purposes it is convenient to divide menin- gitis into two forms — external meningitis, and internal meningitis. External Meningitis is that form which begins outside the dura mater. It is probably always secondary to ad- jacent disease, and of such disease the most frequent cause, by far, is bone disease — caries. The inflammation is usually purulent in character or semi-purulent. Fre- quently the dura is covered by a thick layer of soft or hard cheesy matter containing tubercle bacilli. These inflammatory materials, if abundant, may seriously com- press the cord, and then the symptoms of compression are combined with those of inflammation. The nerve-roots, as they pass through the dura, are either irritated and in- flamed or compressed and atrophied. The vertical extent of the inflammation is usually limited. Internal Meningitis, or inflammation inside the sheath of the dura, usually commences in the pia, but may extend to it from the inner surface of the dura. The inflammatory process may be simple (very rarely), puru- lent, or tubercular, or, in chronic cases, syphilitic. The causes of acute internal meningitis are often obscure. The disease may follow exposure to cold, trauma, surgical procedures, etc. Sometimes it occurs in the course of acute febrile diseases or septicaemia. Not rarely it results from extension, either from the mem- branes of the brain or from external meningitis. The symptoms in acute cases are : first, those of irritation of the nerve-roots, later those of pressure. The inflamma- tion is generally of wide extent when it is acute. In both acute and chronic meningitis, it must be noted, the sub- DIAGNOSIS OF THE NATURE OF THE LESION. 275 Stance of the cord may suffer from the inflammation (meningo-myelitis), and the symptoms of the two condi- tions are then mixed. Probably all cases of acute internal meningitis are of bacterial origin. Injlammation of Nerves — Neuritis — may be acute or chronic, primary or secondary, interstitial or parenchy- matous. The interstitial form is that in which the con- nective tissue which separates the fibres is chiefly involved. In the parenchymatous or degenerative variety the fibres suffer chiefly and primarily. Secondary neuritis may be syphilitic, tubercular, cancerous, or leprous, according to the character of the process to which the inflammation is secondary. Syphilitic and tubercular neuritis affect chiefly the central ends of nerves, which become involved, either from the direct extension of corresponding inflam- matory processes in the meninges, or from similar inflam- mations in adjacent tissues. Syphilitic neuritis frequently involves the cranial nerves. The term neuritis is ordinarily used to include two dif- ferent processes. First, it is applied to those changes in nerves which are unquestionably inflammatory in origin, including increased vascularity, small spheroidal-celled infiltration, and the formation of new connective tissue, with increase in the size and consistence of the nerve. Secondly, the word is employed to include destructive changes in the nerve-fibres, that extend down the nerve, beyond the seat of the original inflammation, to the periphery. These changes are, histologically, essentially those that occur in nerve-fibres which have been sepa- rated partially or entirely from their ganglion-cells ; they are the changes of secondary or Wallerian degener- ation (pp. 2 and 6). In many instances these degenerative alterations are not so severe in degree as those which occur, for example, after nerve-section, but they are the 2"]^ DISEASES OF THE NERVOUS SYSTEM. same in kind. Slight evidences of inflammation may extend a short distance down a nerve after a traumatism, but the changes soon become purely degenerative in character (p. 2S3). Occasionally a neuritis passes up a nerve (neuritis migrans, ascending neuritis), and the changes are then purely inflammatory in nature. Generally one nerve trunk only is involved in neuritis, but many nerves may suffer at the same time in the con- dition called multiple neuritis. Multiple neuritis is most commonly a result of alcoholism, but it occurs not very rarely in a variety of constitutional conditions, of which diphtheria, lead poisoning, and typhoid fever are the principal (toxic degenerations). Injury, both slight and severe, is a very common cause of neuritis. Extension from adjacent inflammation is also a frequent mode of origin. When the cranial nerve-roots or the spinal nerve-roots become the seat of inflammation, it is usually by extension. Abscess. — Abscess of the Brain is usually the result of chronic suppurative inflammation of the middle ear, of traumatism with or without injury to the skull, or of sup- purative processes at a distance, — as, for example, empy- sema, suppurating cavities in the lungs, etc. In rare instances it results from caries of the nasal or orbital bones. Chronic otitis is the most common cause (about 42 ^), and traumatism stands next in frequency (about 24 ^). Chronic otitis is often associated with caries of the temporal bone or of the mastoid cells. The abscess is usually in the cerebral or cerebellar hemisphere of the side of the otitis,^nearly four times as frequently in the former as in the latter. When the abscess follows dis- ease of the mastoid cells it is apt to be in the cerebellum. As a result of pyaemia cerebral abscess is rare, and when it occurs the collections of pus are multiple and usually DIAGNOSIS OF THE NATURE OF THE LESION. 277 small. In a considerable proportion of cases of abscess (about one sixth) there has been no discoverable cause. Abscess may occur in any region of the brain. It is, however, most frequent in the cerebrum or cerebellum, and only occurs rarely in the pons, medulla, or central ganglia. The collection of pus is generally within the substance of the brain, but sometimes it is on the surface, and in this case the meninges, which are locally inflamed and thickened, form the outer wall of the abscess. As a rule there is one abscess only (about four fifths of all cases). When there are two or more abscesses, they are generally the result of a septic process at a distance. When abscess is due to ear disease, or follows traumatism, it is single in about nine tenths of the cases. In size, abscesses vary between that of a hen's egg and a walnut. Symptoms of cerebral abscess may be few or absent, in chronic cases, for a considerable period of time, some- times for years, notwithstanding the lesion is^ large and in a situation from which focal symptoms might be ex- pected. When acute symptoms eventually commence, they are often dependent on rupture, either into the lat- eral ventricles, or into the membranes, with subsequent ependymitis in the former case, with meningitis in the latter, if the patient lives long enough. More frequently, acute cerebral symptoms are due to enlargement of the abscess without rupture. All cases of cerebral abscess depend on micro-organic infection. Several different varieties of pyogenic bacteria appear competent to cause cerebral abscess. Abscess of the Spinal Cord is a condition of extremely rare occurrence. Acute inflammatory affections of the cord seldom go on to abscess formation. Small accumu- lations of leucocytes sometimes occur in the gray sub- stance of the cord (^.^.,in poliomyelitis), but these col- 2/8 DISEASES OF THE NERVOUS SYSTEM. lections are seldom visible to the naked eye, and can never be said to constitute abscess. In cases of purulent internal meningitis, however, pus may form in large quantity in the substance of the cord, and this probably constitutes the only mode of abscess formation in the spinal cord- The purulent meningitis in these instances is always of septic origin. Thus, in one case, it followed a fetid bronchitis ; in another it was secondary to gonor- rhoea. Occasionally abscess is secondary to traumatism (especially fracture of vertebras). The practical importance of abscess of the spinal cord is not great, as its distinction from myelitis is usually im- possible. Occasionally acute irritative spinal symptoms, associated with a cause of septic suppuration, may point to abscess rather than myelitis. In many instances the acute spinal symptoms of abscess are obscured by the symptoms of the pre-existing purulent meningitis. Tumor. — Tumor of the Brain may be of almost any variety, but certain kinds are much more common than others. Syphilitic and tubercular intracranial growths (so-called diathetic tumors) are more common than other varieties. For clinical and other reasons it is convenient to speak of syphilitic and tubercular growths as tumors. They are not, however, tumors in the strict sense, and it is preferable to regard them as the results of specific forms of inflammation. Next in the order of frequency come the sarcomatous tumors, sarcoma and glioma. Then comes carcinoma, which is always of the soft variety. Other kinds of cerebral tumor (fibroma, osteoma, lipoma, neuroma, echinococcus and cysticercus cysts) are rare, but are occasionally encountered. Intracranial aneurism (of the larger vessels), though it does not constitute a new growth, may be classed clinically with tumors because of its pressure symptoms. DIAGNOSIS OF THE NATURE OF THE LESION. 279 The cause of most intracranial tumors is obscure. Generally speaking they are twice as common in males as in females. During the first six months of life, and in old age, they are rare. The majority of cases occur in childhood and in early adult life. Syphilitic tumors occur chiefly between the twenty-fifth and fiftieth years, and in consequence of acquired syphilis. The time of their development after the initial lesion is commonly between five and ten years, but may be considerably earlier or later. Three quarters of all tubercular tumors of the brain occur before the twentieth year, usually in subjects who have a family history of phthisis or who have signs of pulmonary tuberculosis. Glioma and sarcoma are most frequent during adult life. Carcinoma is exceedingly rare before fifty. Local injury occasionally operates as an immediate excitant of a new growth, and such an influence has been traced not only in tumors which, like glioma, are supposed to be of purely local origin, but in the case of the diathetic tumors (syphilitic and tubercular). Tumors may either compress or infiltrate the substance of the brain ; some do both. Growths that spring from the dura or from the bones of the skull usually compress but do not invade the brain tissue. Growths that origi- nate in the brain substance or in the pia may either com- press or infiltrate it. The brain tissue is gradually de- stroyed, in either case, before the advance of the tumor, and there is usually a corresponding loss of function, though it is important to note that the degree of functional loss (expressed as symptoms) may be much less than our knowledge of the functions of the parts and the size of the tumor would lead us to expect. This probably de- pends on the fact that many of the nerve elements which are compressed by, or included in, the advancing tumor 280 DISEASES OF THE NERVOUS SYSTEM. are not deprived of all functional power. We have al- ready noted the tolerance of nerve elements, especially fibres, to gradual pressure. The development of a tumor generally gives rise to irritation, irritation which results partly from the pressure exerted by the growth, partly from the vascular derangement that is associated with it. This irritation may be considerable in degree, and, in the immediate vicinity of the advancing tumor, may be in- flammatory in character. This is the cause of the zone of softening which often surrounds a tumor. The men- inges, and particularly the pia, are apt to be inflamed in the neighborhood of the new growth, and some meningeal inflammation may occur even at a distance from a rapidly growing tumor. Many of the most important and dis- tinctive symptoms of tumor are referable to this irritation incidental to their growth, and it is an important fact that the degree and range of these symptoms are often dispro- portioned to the size of the tumor. There remain to be mentioned certain individual forms of tumor that possess some diagnostic importance. Tubercular tumors of the brain are usually in the cerebral substance, unconnected with the membranes ; occasionally they spring from the dura. Their most fre- quent seat is the cerebellum, but they occur almost as frequently in the cerebrum. They are more apt to be two or more in number than to be single. They com- press the brain tissue, and do not usually invade it. Sometimes they grow rapidly, sometimes slowly ; often they develop rapidly and then become stationary. A tubercular growth may cause very little irritation. Syphilomata are usually superficial and connected with the pia ; occasionally they spring from the dura. , They compress but usually do not infiltrate the brain. Their chief seat is the cerebrum (hemisphere) and somewhat less DIAGNOSIS OF THE NATURE OF THE LESION. 28l frequently they occur in the pons. A syphiloma usually grows rather rapidly and causes considerable and often great irritation. Gliomata are single nine times out of ten. They de- velop in the brain substance, usually in that of the cere- brum (one half of the cases) often in the cerebellum (one quarter of the cases). They invade the brain substance without displacing it. They include rather than destroy the nerve elements, though there is often considerable destruction. The growth of a glioma is usually slow, sometimes very slow. The tumor is often highly vascular, and is sometimes the seat of sudden hemorrhage, which may be indicated by an apoplectic seizure. Sarcomata may grow from the brain substance, from either membrane, or from bone (especially of the base). Usually they do not infiltrate like gliomata, but possess distinct limits, though the softer varieties may have the in- vasive tendency of glioma. Their growth is usually slow, and they are generally single. Carcinoma may originate from the dura or the brain substance. It may occur in any part of the brain, but is most often observed in the cerebral hemisphere. It is usually single, and generally both invades and compresses the brain substance. Tumors of the Spinal Cord. — New growths within the spinal canal may originate external to the dura, or inter- nal to the dura. The tumors that arise outside the dura may take their origin from the membrane itself, from the extra-dural tissue (fat) or from the adjacent bones. Sar- comata, carcinomata, and enchondromata occasionally spring from the bones or intervertebral substance. Lipo- mata may originate in the fat between the dura and the bone, but are very rare. Extra-dural growths produce symptoms by compressing the spinal cord, and irritating or compressing the nerve-roots with which they are in 282 DISEASES OF THE NERVOUS SYSTEM. contact. Accumulations outside the dura, of inflammatory- nature from tubercular bone disease (caries), give rise to effects similar to extra-dural new growths. The former condition is of very frequent occurrence, while all forms of new growth are rare. Of the tumors that originate inside the dura, the ma- jority begin in the membrane, inside the substance of the cord itself. Such tumors are most often syphilitic ; less frequently they are sarcomatous or myxomatous. They compress the cord and its nerve-roots, and are apt to damage the former more seriously than do extra-dural tumors, but they do not often invade the substance of the cord, even if they spring from the pia. Of the new growths which occur within the substance of the cord itself, syphiloma and glioma are the most common, or, more accurately, the least infrequent. Sar- comata, myxomata, and tubercular tumors are rare. Syphilomata usually spring from the pia, gliomata from the peri-ependymal tissue immediately about the central canal of the cord. Gliomata often have a considerable vertical extent, and, when vascular, are sometimes the seat of hemorrhage, as in the brain. Sometimes, also, an extensive infiltration of the spinal cord with gliomatous tissue breaks down spontaneously, and leads to the for- mation of cavities in the cord, which usually connect with the central canal of the cord, — a condition known as syringomyelia. Tumors growing within the substance of the cord com- press and destroy the nerve elements. They are less apt than extra-spinal tumors to compress and irritate the nerve-roots. What has been said of the progress of the different varieties of intracranial tumors applies in gen- eral to tumors of the cord. Tumors of the spinal cord are usually single and small or moderate in size. Sarco- . DIAGNOSIS OF THE NATURE OF THE LESION. 283 mata are sometimes multiple and very numerous. When they invade the substance of the cord, its tracts are fre- quently the seat of secondary degeneration, ascending and descending. The Cauda Equina is occasionally the seat of a sarcoma, or fibro-sarcoma. A tumor in this region may attain con- siderable size without producing pressure symptoms, because of the large size of the vertebral canal. Tumors of the Peripheral Nerves are occasionally observed. Any morbid growth on a nerve is called a neuroma, but a distinction is made between true neuromata, which consist of nervous tissue, and false neuromata, which contain no nervous elements. False neuromata are most often hard fibromata, occasionally sarcomata, myxomata, or gliomata. Neuromata gener- ally lie between the nerve bundles, which they push aside, but do not usually involve. They are usually single, but may be very numerous. The nerves of the extremities are most often affected. Degeneration. — The tissue elements of the brain, and of the spinal cord, frequently undergo a gradual change in structure known as degeneration. This change consists of two distinct pathological processes. One of these is the slow wasting of the nerve elements — the gradual atrophy of the ganglion-cells, or nerve fibres, or both. 'The other is an overgrowth of the interstitial or connective-tissue (neurogliar) elements. It is customary to distinguish two forms of the degenerative process — that which is confined to structures which possess the same or similar functions, and that which is apparently random in its distribution, and is not limited to structures having the same function. The former type of the de- generative process is well exemplified by the so-called " system diseases " of the spinal cord, in which particular 284 DISEASES OF THE NERVOUS SYSTEM. (functional) tracts of fibres are the exclusive seat of the morbid process. Locomotor ataxia, in which the poste- rior median columns of the cord are degenerated, and primary lateral sclerosis, in which the crossed pyramidal tracts are similarly involved, are illustrations of system- diseases. Other examples are secondary degenerations — that is,, degenerations which occur in the brain and in the spinal cord, when certain tracts of nerve-fibres have been separated, from any cause, from the ganglion-cells that constitute their trophic centres. When the fibres have been thus separated from their nutritive centres for a period of two, three, or four weeks, the medullary sheath and the axis-cylinder undergo disintegration, and the tract or tracts in which this change occurs becomes gradually gray in color, somewhat shrunken, and perhaps somewhat harder than normal. In certain tracts these secondary degenerative changes progress in an upward di- rection (ascending degeneration), in others in a downward direction (descending degeneration) ; in general, the de- generation progresses in the direction in which the tracts involved habitually conduct nervous impulses. Thus the motor tracts, the direct pyramidal tract and the crossed pyramidal tract, undergo descending degeneration, whilst the sensory tracts, the posterior median columns, the direct cerebellar tracts, and the antero-lateral ascending tracts (p. ^^) degenerate in an upward direction. A transverse lesion of the cord is often the cause of second- ary degenerations, both of an ascending and descending character. This is well seen in transverse myelitis and in certain tumors of the cord. After hemiplegia from any organic disease of the brain there is a descending degeneration of the direct pyrami- dal tract on the same side and of the crossed pyramidal tract of the opposite side, the degenerative process be- DIAGNOSIS OF THE NATURE OF THE LESION. 285 ginning in the motor path just below the lesion in the brain, whatever may be its position. In the primary de- generative disease of the cortex known as dementia paralytica, there are usually extensive secondary degen- erations of the pyramidal tracts of either side, consequent on the changes in the ganglion-cells of the cortex. It is highly probable that, in all the system degenera- tions, the changes in the nerve elements are primary and that the interstitial overgrowth is a secondary change. In the second type of degenerative changes, on the other hand, this is not the case. Here the alterations begin, in all probability, in the interstitial elements external to the nervous elements, which are involved secondarily. A good example of this type of degeneration is insular sclerosis, in which patches of degenerative change are irregularly scattered through the central nervous system. Irregular areas of degeneration in the brain and spinal cord are also observed in some cases of the so-called traumatic neuroses, and such changes are probably more frequent after traumatism than has been supposed. These changes are sometimes associated with extensive hyaline and fatty degeneration of the cerebro-spinal arteries. Some instances of this second type of degeneration are probably intermediate in their pathological characters between true degeneration and chronic inflammation. The etiology of the primary degenerations of the brain and spinal cord, affecting nerve-fibres or nerve-cells or both, is obscure. What is known concerning it will be alluded to elsewhere in this chapter. The structural changes which the nerve-fibres of a peripheral nerve undergo after their separation from the cells to which they belong, differ somewhat in character from the changes of secondary degeneration in the cen- tral nervous system. The medullary sheaths of the 286 DISEASES OF THE NERVOUS SYSTEM. nerve-fibres break up into segments, and these in turn break up into droplets of various size and shape. When these alterations have progressed to a certain point the axis-cylinders usually break up and may be more or less completely destroyed. The nerve-fibre sheaths (sheaths of Schwann) and their nuclei do not usually degenerate. The products which they contain of the disintegration of the medullary sheaths may be eventually absorbed. In a case of complete degeneration of a nerve from injury, the complete segmentation of the myeline sheaths and axis- cylinders is evidenced clinically by a loss of nerve irrita- bility to electrical stimulation. Such a loss of irritability usually occurs at the end of two weeks, but it is not a sudden loss, and is preceded by a fall in irritability which probably corresponds to the partial segmentation of the fibres and nutritional changes in the axis-cylinders. In some cases a slow process of regeneration occurs during the second, third, and fourth month of the injury. This regenerative process consists of a development of new axis-cylinders, which in time develop myeline sheaths, from the central end of the nerve. The causes of nerve degeneration, which is often a partial process not progressing beyond a moderate degree of structural change, are numerous. We may group them under three heads : first, mechanical injuries, such as incision, over-extension, crushing, or compression ; sec- ondly, disease of the special nerve centres (ganglion-cells of anterior horns and the motor cranial nerve nuclei) with which the peripheral nerves are in communication, as poliomyelitis ; third, disease of the peripheral nerves themselves, as inflammation. The process which has been here described as degen- eration is regarded by some as inflammatory and not degenerative in character, and the condition has been DIAGNOSIS OF THE NATURE OF THE LESION. 28/ described as one of parenchymatous inflammation. The ordinary evidences of inflammation are often marked in the neighborhood of the primary lesion, but seldom extend far below the lesion, where the pathological changes may be with propriety considered degenerative. When a motor nerve undergoes degeneration, changes soon occur in the nutrition of the muscles. After a lapse of ten days or two weeks the muscle fibres become nar- rower and undergo distinct changes in their histology. If regeneration eventually occurs in the nerve, the muscles are gradually restored to their normal structure and func- . tion. If no regeneration takes place, the atrophy of the individual fibres, and of the muscles as a whole, progresses, but the decrease in size from muscular wasting is partially compensated by the growth of connective tissue between the muscular fibres. This new connective tissue gradu- ally contracts, and this contraction may result in perma- nent shortening of the muscles involved. Having reviewed the general pathology and etiology of the various morbid processes which occur in the brain, spinal cord, and peripheral nerves, we may pass to the consideration of the indications that serve to distinguish the several lesions. These indications are of especial im- portance in establishing the pathological diagnosis in cases of disease of the brain and of the spinal cord, the diagnosis of the nature of peripheral affections being in general much simpler. The following considerations are therefore mainly applicable to disease of the central nervous system. The indications above referred to as essential to the determination of the pathological diagnosis, are the fol- lowing : first, the manner of onset of the symptoms, which usually makes it easy to distinguish between certain 288 DISEASES OF THE NERVOUS SYSTEM. general classes of morbid processes to be hereafter men- tioned ; secondly, the causal indications, which comprise the various causes of disease that can be traced or excluded ; thirdly, the position of the morbid process, taken in con- junction with the special and known liability of certain parts of the brain and cord to particular forms of disease. I. The Onset of the Symptoms. — The time oc- cupied by the onset of the symptoms — that is^ the time that intervenes between the first symptoms of the lesion and their development to a considerable degree of in- tensity — is an important guide to the nature of the lesion. If the onset occupies only a few minutes or less, it is designated sudden, and the lesion which produces the sudden onset is almost always avascular lesion (provided, of course, that the disease is organic). A vascular lesion in the brain may be either hemorrhage or softening from vascular obstruction ; in the spinal cord such a lesion is practically always hemorrhage. If the onset, instead of being sudden, occupies from an hour or two to a week, it is described as acute. An acute onset is usually indica- tive of an inflammatory process, but vascular lesions are not always sudden in their development, which may occupy a few hours or days. When, therefore, the lesion develops in a few hours, it may be either vascular or inflammatory in nature. Which it is must be determined by the study of other indications. When the symptoms attain a considerable degree of intensity only after the lapse of several weeks, the onset is said to be subacute j and such an onset usually charac- terizes the development of the subacute inflammatory processes, some forms of tumor, and in the spinal cord also some pressure lesions not dependent on tumor. In cases where the development of the symptoms takes a chronic course — that is, occupies more than a DIAGNOSIS OF THE NATURE OF THE LESION. 289 month — the morbid process is usually a new growth or a degeneration. Thus a knowledge of the mode of development of the symptoms may enable us at once to roughly classify the lesion in question. For instance, if the lesion is sud- den, it must be vascular in character ; if it is chronic, it is probably a degeneration or a new growth. As a rule, however, the time of the onset simply enables us to limit the process to one of two lesions. For example, a case which is intermediate between a sudden lesion and an acute lesion, and occupies several hours, may be either vascular or inflammatory in nature. Beyond this point the study of the onset cannot take us ; the decision de- pends on other indications. II. The Causal Indications. — The^causal indica- tions that bear on the diagnosis of the nature, of the lesions of the nervous system are numerous and import- ant. There is, however, a wide difference in their rela- tive significance, some having, like age and sex, only a low value ; others, like certain kinds of injury and cer- tain forms of infection (syphilis, tuberculosis), possessing a value, under some circumstances, that is highly signifi- cant. While the causes which are to be reviewed will of course be those that bear especially on the organic dis- eases of the nervous system, it will be well to touch on some of the relations of these causes to the functional forms of nervous disease. The relations of each etiological condition will be given to each class of lesion (hemorrhage, degeneration, tumor, etc.) in so far as is practicable or desirable, and when profitable the more important relations between these conditions and particular clinical types of disease will be briefly stated. It is convenient to group the etiological factors to be 290 DISEASES OF THE NERVOUS SYSTEM. reviewed, as follows : age, sex, habits, infection, toxic influences, trauma, state of general health, psychic influ- ence, heredity, influence of treatment. Age. — A knowledge of the age at which the various morbid processes occur is sometimes of considerable value in determining the nature of a lesion. With most processes, however, the occurrence extends over so wide a period, with so nearly equal incidence in several dec- ades, as to deprive the age factor of decided significance. The vascular lesions of the nervous system are met almost exclusively in the brain. Regarded as a group, these vascular lesions (including hemorrhage, embolism, thrombosis) occur at all times of life, but the various members of the group are especially frequent at particu- lar periods. Thus, embolism is rare after fifty and be- fore puberty ; syphilitic thrombosis occurs chiefly in the third, fourth, and fifth decades, and both hemorrhage and thrombosis from atheroma are diseases practically limited to the second half of life. The vascular lesions which depend, like extra-dural hemorrhage and spinal meningeal hemorrhage, on injury, occur especially during early adult life (twenty to forty). The inflammatory pro- cesses, like the vascular lesions, occur at every period of life, but are on the whole most common in early adult life and infancy. This is especially true of the acute inflammations. Thus, acute cerebral meningitis and cerebro-spinal meningitis are relatively most common before the twentieth year, and although purulent menin- gitis is a disease of adult life especially, this is due mainly to the usual traumatic origin of the disease. Acute poliomyelitis, by far the most common inflamma- tory affection of the substance of the central nervous system, is essentially a disease of infancy and childhood. An acute spinal lesion occurring in infancy or child- DIACiNOSIS OF THE NATURE OF THE LESION. 29 1 hood is almost certainly poliomyelitis. Acute myelitis occurs particularly between ten and forty. The various forms of inflammation of the peripheral nerves (multiple neuritis, neuritis), acute and sub-acute, are particularly common in early adult life. More than one half the cases of cerebral abscess occur between ten and thirty (partly due to the influence of trauma). The more chronic inflammatory processes, both of the central nerv- ous system and of the peripheral nerves, probably occur, as a rule, later in life than the acute lesions (for example, chronic pachymeningitis, chronic myelitis, chronic sciatic neuritis). The best example of the influence of age is found in the case of the degenerative affections, of which proba- bly more than two thirds of the cases commence between the thirtieth and fiftieth years. This group includes loco- motor ataxia, primary spastic paraplegia, ataxic paraple- gia, general paralysis, progressive muscular atrophy, etc. There are, however, some exceptions to the rule of com- mencement between the ages of thirty and fifty. Bulbar paralysis often begins after fifty, insular sclerosis most often begins between twenty and thirty-five, and Fried- reich's ataxia most often between seven and twenty. But these cases form a very small proportion of all the cases of degenerative disease. As a class the new growths show no striking features in relation to age. They are rare in infancy and after sixty. The most frequent forms (tubercle, glioma, syphiloma) belong particularly to the first half of life, the tubercular and gliomatous forms being most often observed between five and thirty, and the syphilomata between twenty and forty. Carcinomata belong to the second half of life. The group of so-called functional nervous diseases be- longs largely to the adolescent period and early adult life 292 DISEASES OF THE NERVOUS SYSTEM. (fifteen to thirty-five). This is conspicuously the case with the most common forms, chorea, epilepsy, hysteria, neural- gia and migraine. Paralysis agitans is, however, a marked exception, in that it rarely begins before fifty. Wry- neck and neuralgia also occur very frequently between thirty-five and fifty, but these cases do not in any way in- validate the truth of the general statement made above. Sex. — Looking at nervous diseases, in so far as we can, as a class, it is difficult to say in which sex they prepon- derate. Certain it is, however, that to the male sex be- longs considerably more than half of all the cases of organic disease. This special liability on the part of the male appears to depend mainly on the effects of injury, alcohol, and syphilis, to all of which he is more exposed than the female. The functional forms of nervous disease are more frequent, as a class, in females, owing mainly to the preponderance of two common diseases, hysteria and chorea. In paralysis agitans, migraine, and tetanus, the greater number of cases occur in males — in the case of tetanus the large preponderance depending, no doubt, on the greater exposure of the male to injuries favoring the necessary infection. The greater prevalence of organic disease in males is particularly noticeable in the group of degenerative affec- tions. In the case of locomotor ataxia the unequal incidence in the sexes is very striking, — being probably at least ten to one in favor of males. An even greater inequality is noticeable in an allied degenerative disease — dementia paralytica. A less striking inequality obtains in ataxic paraplegia and progressive muscular atrophy. Among the inflammatory processes there is a marked preponder- ance in males of those conditions that depend to a con- siderable extent, or mainly, on injury, — as acute myelitis, DIAGNOSIS OF THE NATURE OF THE LESION. 293 meningitis of the convexity, and abscess of the brain (two to one), on alcohol (multiple neuritis, pachymenin- gitis), or on syphilis (as syphilitic endarteritis, chronic meningitis, etc.). With the possible exception of embolic softening, the vascular lesions preponderate slightly, and in the case of cerebral hemorrhage, largely, in males. The indications of the nature of the lesion which are derived from the consideration of age and sex, are, of course, to be regarded as quite subsidiary to the indica- tions obtained from other causal factors. Some of the factors which have been mentioned may, however, be allowed weight when the more important indications, in a given case, appear evenly balanced, and occasionally the facts noted will prove of real service in diagnosis. Habits. — A variety of influences in the production of nervous disease, which might properly be classed as habits, could be enumerated, but of these there is only a small number that deserve special attention. The excessive use of alcohol and tobacco, and sexual excess, including mas- turbation, belong to this class. Of these influences, al- coholic excess is by far the most important as regards the causation of organic disease. Excessive Use of Alcohol. — A history of the exces- sive use of alcoholic drink serves to clear up the nature of a variety of aff^ections of the nervous system. It is im- portant, however, to distinguish between the acute dis- turbances from alcoholic intoxication and the different morbid states of the nervous system that develop grad- ually as a consequence of habitual excess. The most im- portant form of acute disturbance from alcohol is de- lirium tremens (p. 566) or acute alcoholic delirium ; other forms of pathological interest are the various manifesta- tions of alcoholic insanity — maniacal, melancholic, etc. These acute alcoholic insanities are commonly associated 294 DISEASES OF THE NERVOUS SYSTEM. with hereditary predispositions to mental derangement. The common variety of ,acute alcoholic intoxication, known as "intoxication" pa?- excellence, does not con- cern us. A feature of practical importance in the causation of various forms of nervous disturbances that are slowly induced by habitual excess is that they may occur in persons whose excess has always fallen short of actual intoxication. It may thus become difficult, in a given case, to say what constitutes excess. The daily quantity of alcohol that is borne without detriment varies much with different individuals, and with the same in- dividual at different times and in different conditions of health. Sedentary occupations are particularly unfavor- able to the perfect assimilation of considerable quantities of alcohol. Probably most adult males can safely dispose of the equivalent of two ounces of absolute alcohol in a day — many of much more, and some undoubtedly develop disease from the habitual use of smaller quantities. The form in which it is used, whether spirits, wine, or beer, seems to make little difference, but the excessive use of beer seems particularly apt to lead to multiple neuritis. The organic diseases that might be accounted for by a history of alcoholic excess are chiefly subacute or chronic in course, and inflammatory in character. To these in- flammatory lesions the peripheral nerves appear especially prone. Thus, by far the most frequent organic affection from alcohol is multiple alcoholic neuritis. Neuralgic pains in the limbs, without atrophy or weakness, are com- mon as a result of alcoholic excess. They depend some- times on slight acute neuritis, sometimes on functional (nutritional) changes. Subacute and chronic myelitis with or without neuritis, are occasional results. Of the cerebral affections that may depend on alcohol. DIAGNOSIS OF THE NATURE OP^ THE LESION. 295 slight chronic meningitis (with slight optic neuritis, head- ache, and mental failure) is the most common, but habit- ual alcoholic excess favors atheroma of the walls of the cerebral arteries and is then a factor in producing cere- bral hemorrhage. Two closely allied degenerative affec- tions of the central nervous system — general paralysis and locomotor ataxia — occur frequently in alcoholics, but it is doubtful whether alcohol is ever the sole cause of either disease. Some cases of chronic alcoholic men- ingitis closely resemble general paralysis (pseudo general paralysis). Atrophy of the optic nerve probably never re- sults from alcoholic excess alone. Epilepsy is apparently an occasional consequence. Hemianaesthesia (of uncer- tain nature) is said to depend at times on alcoholism. By far the most common nervous affection that results from the habitual abuse of alcohol is a fine irregular tremor involving the lips, tongue, and hands, and often the legs — alcoholic tremor. Such habitual abuse also strongly favors the development of professional neuroses and the muscular atrophies from over-use. The Excessive Use of Tobacco (by smoking or chewing), appears to give rise to but few organic diseases of the nervous system. The principal condition consequent upon such excess is a peculiar form of amblyopia characterized by the existence of central scotomata, especially for the colors green and red. A variety of functional disturb- ances may be accounted for by the habitual excessive use of tobacco — headache, tremulousness, insomnia, ir- ritability, palpitation, tachycardia, blephorospasm and various digestive disorders. Sexual Excess is an exceedingly rare cause of organic disease of the nervous system, but a common cause of functional derangements. Repeated sexual acts have been the cause, in males, of hemorrhage into the lumbar 296 DISEASES OF THE NERVOUS SYSTEM. enlargement of the cord, followed in some cases by mye- litis. In some cases these conditions have resulted in males from coition (not necessarily repeated) in the erect position. A much less unusual effect of repeated sexual intercourse is transient weakness, slight or consider- able, of the lower extremities. This depends probably on temporary nutritional derangement of the anterior cornual cells of the lumbar cord ; perhaps in some instances on minute extravasations. The sexual act several times repeated has in rare in- stances been the exciting cause of hemiplegic attacks in persons with atheromatous cerebral arteries. Similarly, persons with syphilitic arterial disease have been known to become hemiplegic after one or more sexual acts.' The functional nervous derangements which are the remote consequence of sexual excess are numerous and varied. They include the protean manifestations of neurasthenia and hysteria. Especially common, how- ever, are irritability, slight mental failure, headache and other cephalic sensations than pain, dilated pupils, amblyopia, palpitation, various vasomotor symptoms (flushing, etc.), fibrillary twitchings, mental depression, undue fatigue, oxaluria, phosphaturia, and digestive dis- orders. These symptoms are of far more frequent occurrence in men than in women. In those who are subject to epilepsy, sexual indulgence occasionally deter- mines the occurrence of paroxysms. Wry-neck sometimes appears to be due solely to sexual excess. ' In one case of this kind the autopsy showed the presence of acute softening. The patient was a woman, and the paralysis came within a few minutes after the sexual act. It is probable that the circulatory changes in the brain which follow and accompany violent sexual ex- citement may determine the occurrence of vascular lesions in such cases as that mentioned. DIAGNOSIS OF THE NATURE OF THE LESION. 297 Masturbatio?i. — It is exceedingly doubtful whether masturbation is ever a cause of organic nervous disease, though it may very remotely influence the course and development of such disease. The functional derange- ments consequent on this habit are, however, numerous, and of frequent occurrence. The derangements resemble in character the neurasthenic symptoms mentioned as dependent on sexual excess, with the general difference that they frequently attain a greater degree of severity.^ A mental symptom which is some- what characteristic of masturbational excess, though it sometimes occurs in cases of ordinary sexual excess, is a peculiar disposition to ramble from one topic of con- versation to another in a superficial or incoherent manner. Sometimes, again, there is a morbid tendency to drowsi- ness during the day, and, in rare cases, young subjects have been in stupor for many days as a consequence of repeated acts of masturbation. The evil results of masturbation are more equally distri- buted between the sexes than are those of sexual excess. Though most common among individuals between the age of puberty and the twentieth year, masturbation is often practised by much younger subjects. The habit is not rarely begun in young children by the teaching of lascivious nursery-maids. Not infrequently it originates in young children from genital irritation due to the passage of the ' Sexual excitement is probably always followed by an increase of indican in the urine. Normally this substance is present in the urine in very small quantities or is entirely absent. The presence of more than .020 gm. of indican in the twenty-four hours' urine is to be regarded as pathological. Although other causes than sexual excitement may cause an increase of indican in the urine, such increase is sometimes a valuable aid in the detection of the habit of masturbation. 298 DISEASES OF THE NERVOUS SYSTEM. irritating urine that commonly results from digestive derangements. The proportion of persons (of each sex) who practise masturbation at some period of life is probably very large. In the majority of instances the habit is not continued sufficiently long or with sufficient perseverance to give rise to serious functional disturbances. Infectio7i. — The introduction of pathogenic micro- organisms into the body is the essential condition of infection. After these have obtained mechanical lodg- ment in some part, local and general conditions, but im- perfectly understood, determine their pathogenic influence. An extension (direct or through the blood or lymph channels) of infection from the parts first involved may lead to the implication of the nervous system, and such infection constitutes, perhaps, the most important class of influences in the production of organic disease of the nervous system. Two specific forms of infection, the tubercular and the syphilitic, concern us especially, since they play a most conspicuous part in the causation of organic disease. The infection which results in suppura- tive processes in the nervous system (abscess, suppurative meningitis, etc.) is considered, for clinical reasons, under other headings. Tubercular Infection. — The organic conditions of the nervous system which result from the invasion of tubercle bacilli from primary foci of infection are chiefly inflam- matory in character. By far the most frequent of these inflammatory conditions is tubercular meningitis. In infancy and childhood this is much the most common form of cerebral disease. In connection with tubercular meningitis, or occurring quite independently, there may be an agglomeration of tubercles in the substance of the brain, constituting one or more massive or conglomerate DIAGNOSIS OF THE NATURE OF THE LESION. 299 tubercles (so-called " solitary " tubercle or " tubercular tumor "). Much less frequently the spinal cord is the seat of solitary tubercle, which produces the symptoms of tumor. The peripheral nerves are involved in a neuritic affection in some cases of advanced tubercular cachexia, and this affection has been regarded as a multiple neuritis of tubercular origin. The correctness of this view is rendered somewhat questionable by the fact that the class of patients in whom the affection occurs (advanced con- sumptives), is a class in whom alcoholic stimulants are extensively employed in treatment. Conditions are pres- ent, therefore, which favor the occurrence of alcoholic neuritis, and it is possible that many of the cases which pass for tubercular multiple neuritis are, in reality, in- stances of alcoholic neuritis. The forms of tubercular disease of the nervous system above enumerated, depend, with the exception of the neuritis above mentioned, on the presence of tubercle bacilli in the tissues of the parts affected. Such local deposition is not usually the case with one of the most frequent consequences of tubercular disease, the so-called compression myelitis. Here, the lesion is a tuberculosis of the vertebrae, which leads to the accumulation of tubercular material outside a thickened dura, and conse- quent compression of the cord. The compression of the cord causes a diminution in its size, and sometimes an actual- myelitis. But the myelitis which results from compression is , only rarely tubercular in character, and when this is the case the inflammation is derived from a direct extension from the outer surface of the dura to the pia, and from the pia to the substance of the cord. In these cases there is probably always the formation of tubercles in the cord before the actual myelitis develops. 300 DISEASES OF THE NERVOUS SYSTEM. The tubercular affections of the nervous system maj*' be secondary to tubercular processes in a variety of sit- uations. In adults, the primary lesion is usually pulmonary tuberculosis ; in children, there is commonly general miliary tuberculosis, and the primary focua may be tubercular bronchial nodes, interstitial tuberculo- sis, tubercular bone disease (especially knee and hip), or tubercular teno-synovitis. In adults, the genito-urinary system- is sometimes the seat of the lesion. In the male, the testicle, prostate, and seminal vesicles may be affected ; in the female, the uterus and Fallopian tubes. Thus the infection which terminates in tubercular disease of the nervous system, may make its entrance by way of the respiratory tract, the digestive tract, the genito-urinary tract, or through slight injury to the skin at any point. In some cases the evidences of local tuberculosis are dis- tinct (as in chronic pulmonary tuberculosis, or hip disease), and give most important indications for diagnosis, but it is essential to note that in many cases the original lesion is so obscure in its symptomatology as to afford no indi- cations whatever of the character of the lesion within the nervous system. Hence it is that the nervous lesions often have the aspect of primary affections. While, therefore, the presence of tuberculosis in some part of the body other than the nervous system may be of the highest aid in determining the nature of the nervous lesion, the absence of indications of such disease should carry very little weight if the symptoms themselves sug- gest a tubercular process. Syphilitic Infection. — No form of infection gives rise with such frequency to organic disease of the nervous system as syphilis. Of the organic conditions that arise from syphilitic infection, some, like gummatous growths, are processes which are distinctive of syphilis and never DIAGNOSIS OF THE NATURE OF THE LESION. 301 occur as the result of any other cause than syphilis. Others, like certain degenerative processes of the brain and cord (locomotor ataxia, progressive muscular atrophy, etc.), though commonly dependent on syphilis, may arise from other causes, and possess no pathological features that are distinctive of syphilis. It is important, in think- ing of the consequences of syphilitic infection, to bear in mind these differences in the relations of its effects. Both the brain and spinal cord are very frequently the seat of organic disease which is the consequence of syphilitic infection. Of the specific syphilitic processes (gumma, endarteritis), the brain is a much more common seat than the cord. The chief vascular lesion of the nervous system, of syphilitic origin, is acute softening of the brain from the thrombosis of cerebral vessels that results from syphilitic endarteritis. This is a very important and frequent clinical condition (p. 353). Whether syphilitic endarter- itis of the vessels of the cord is a cause of focal softening and inflammation of the cord cannot be positively stated, but there is some reason to believe that it may not rarely give rise to these conditions. A much more rare effect of syphilitic vascular disease is intracranial aneurism. An important class of syphilitic lesions is inflamma- tory in character. The clinical conditions which belong to this group are characterized by their subacute or sub- chronic course. This group includes pachymeningitis, cerebral and spinal, and leptomeningitis. Cerebral syphi- litic meningitis is usually local. In the cord, inflamma- tion of the pia is seldom local, and is usually associated with pachymeningitis. Inflammation of the substance of the brain and cord, possessing the pathological characters of a syphilitic process, probably does not occur. Whether acute myelitis is ever due to syphilis 302 DISEx\SES OF THE NERVOUS SYSTEM. it is as yet impossible to say. Subacute disseminated myelitis probably depends in some cases on syphilis, but its precise relations to the disease are not fully under- stood. Whether syphilitic infection ever leads to multiple neuritis must be regarded as uncertain. If it does ever cause multiple neuritis, it must be in very rare instances. It is possible that some of the cases of Landry's paralysis which have been shown to be due to peripheral neuritis, were the result of syphilitic infection. Syphilitic meningitis, either of the brain or of the cord, is not rarely associated with the formation of gummata. In such cases the symptoms of tumor are added to those of meningitis. Gummata may occur with very little meningitis, and the symptoms of tumor then prepon- derate. They are much more frequent in the brain than in the cord. The degenerative diseases of the nervous system stand in an important relation to syphilis. None of them appear to be invariably due to syphilis, and some of them probably never are due to it, but a considerable number are commonly a late sequel of syphilitic infec- tion. In two important and closely allied conditions, locomotor ataxia and general paralysis, a history of syphilis can be traced in seventy-five or eighty per cent, of the cases, and probably exists in even a larger pro- portion. The various forms of ophthalmoplegia that ai-e observed in tabes may occur as isolated conditions and depend usually on syphilis. The same may be said of cases of simple atrophy of the optic nerve, and of the rare cases of isolated Argyll- Robertson pupil. Progres- sive muscular atrophy and primary spastic paraplegia are probably occasional consequences of syphilis. In the case of ataxic paraplegia and insular sclerosis, it is very doubt- ful whether there is ever any dependence on syphilis. DIAGNOSIS OF THE NATURE OF THE LESION. 303 A recognition of the various possible consequences to the nervous system of syphilitic infection is often of con- siderable aid in practical diagnosis. Having first deter- mined from the character of the symptoms the location of the lesion, and from their course its probable nature (vascular, inflammatory, degenerative, etc.), we may ask ourselves, in any given case, whether the process that has thus been provisionally diagnosticated is one of those that may be the result of syphilis. If the process in question may be due to syphilis, it becomes very im- portant to know whether the patient has a history of syphilis. In a considerable number of cases there has been syphilitic infection without the knowledge of the patient, and this is especially common in women, in whom the primary lesion is apt to be overlooked, and in whom secondary symptoms are often slight or absent. As a rule, in an intelligent person, who has been infected, it is not difficult to elicit a reasonably straightforward history, but, even in such cases, slight symptoms may have passed entirely unnoticed and left no objective traces. It is important, therefore, to realize the fact that we can never positively exclude syphilis, unless we can exclude the possibility of infection from impure sexual congress. There are, however, many cases where the possibility of such infection cannot be excluded, in which the proba- bility of infection having ever occurred is exceedingly slight. When, in a given case, there is uncertainty as to past syphilitic infection, to what extent should this fact be permitted to influence the diagnosis ? It is probable that too much weight is allowed to this uncertainty. The important principle to bear in mind is that any decided indications, positive or negative, regarding the nature of the lesion, that may be gathered from the nature and course of the symptoms, must be allowed full weight 304 DISEASES OF THE NERVOUS SYSTEM. even if they are not supported by what is known or believed regarding a history of syphilis. Thus, if the symptoms justify the belief that we have to deal with a syphilitic process, a process such as rarely depends on any other cause than syphilis, this belief should be maintained, even if no history of syphilis can be elicited, — unless, of course, the possibility of infection can be quite excluded, which is not commonly the case in adults. On the contrary, if the case is one in which the sj^mptoms make a syphilitic lesion unlikely, this likeli- hood is not distinctly lessened even if it can be shown that the patient has been infected. But if the indications of the nature of the process as regards syphilis are equivocal, we must be guided largely by the facts regard- ing the history of syphilis, and even if these are clear there may remain a considerable chance for error. There is no satisfactory proof that syphilis can ever be looked upon as the special cause of any functional diseases of the nervous system. Even its influence as an indirect factor must be considered uncertain. It is possible, however, that many morbid conditions, both organic and nutritional, may be remotely related to the disease. The manner in which organic changes in the nervous system result from syphilis is not fully under- stood ; in all probability many of them depend on the action of a toxalbumin, the result of the life processes of micro-organisms, which are with reason considered the agents of infection but about whose characters there is still no positive information. Diphtheritic Infection. — By far the most frequent and important organic disease of the nervous system which depends on the action of the diphtheritic poison is the so-called diphtheritic paralysis. This paralysis, which is peculiar in distribution (p. 520), depends on a lesion in- DIAGNOSIS OF THE NATURE OF THE LESION. 305 flammatory in character and limited mainly to the lower or spino-muscular segment of the motor path. In some cases both the gray matter of the cord and the peripheral nerves are involved, but in many instances it is probable that the lesion is confined to the peripheral nerves. It is certain that the peripheral nerves are especially liable to suffer from the effects of the diphtheritic poison. An important peculiarity of the diphtheritic affection is the liability of the vagus nerve to be affected. The relation between the local affection in the naso-pharynx and the paralysis i) In extra-dural hemorrhage there is usually an interval of lucidity, and the injury causing the condition may be slight ; in laceration of the brain there is no interval of lucidity, and the injury is always severe, (c) Severe and persistent convulsions on one side of the body suggest laceration of the brain, especially if this con- dition be unassociated with hemiplegia. In cases of hemorrhage from a sinus the position of the wound is a sufficient indication of the nature of the condition. It is practically impossible to make a diagnosis be- tween extra-dural hemorrhage and hemorrhage into the arachnoid. The former is much the more frequent and important condition, and fortunately the treat- ment for it — trephining — is also the proper treatment for the latter condition. Which condition we have to deal with is perfectly evident when the button of bone is removed from the temporal region. In the case of extra-dural hemorrhage the clot lies next the bone ; in the case of arachnoid hemorrhage, if this is considerable and has caused symptoms closely resemb- ling a typical extra-dural hemorrhage, the dura will probably be found to bulge from the pressure of the clot beneath it. THE DIAGNOSIS OF CLINICAL TYPES. 365 In some cases of extensive Subarachnoid Hemorrhage'^ the symptoms are highly equivocal. There may be no symptoms for four or five days after the injury except slight headache. Then there may be repeated general convulsions during several days, with fever (ioi°-io3^), delirium and somnolence. These symptoms may pass away entirely for several days, and the patient may ap- pear about to recover, when stupor reappears, deepens into coma, the temperature rises and the case terminates in death. The presence of convulsions, headache, fever and delirium in such a case may lead to a suspicion of meningitis, but the only form of meningitis that is likely to follow immediately on a severe injury to the head is suppurative in character and is distinguished by higher fever and a more rapid and progressive course. It is important to note the fact that a slowly developing sub- arachnoid hemorrhage (with a long lucid interval) may cause no hemiplegia, although the motor area of the brain is much compressed. Sinus-Thrombosis. — The principal facts relating to the pathology of sinus-thrombosis have been already ' Sub-pi al hemorrhage often occurs in association with subdural or subarachnoid hemorrhage. Its symptoms, if there are any, are then usually lost in the more obtrusive symptoms of the condition with which the sub-pial hemorrhage is associated. But sub-pial hemorrhage may occur unassociated with hemorrhage elsewhere. It depends in such cases on injury to the head which causes severe concussion but no fracture. The hemorrhage is usually single, is located over the convexity (especially of the frontal or parietal region), and varies in size from half an inch to two inches in diameter. The layer of extravasated blood is usually thin. If located over the m.otor area the hemorrhage may cause repeated convulsions and slight hemiplegic weakness. A hemorrhage not over the motor region may cause no symptom except stupor, but on the other liand may cause repeated general convulsions. It may be difficult to distinguish between the effects of the hemorrhage and those of concussion. 366 DISEASES OF THE NERVOUS SYSTEM. considered (p. 267). Clinically it is necessary to keep distinct the two forms of sinus-thrombosis — primary or marantic thrombosis and secondary thrombosis. a. Primary or Marantic Thrombosis. — The symptoms that indicate this condition are : (i) stupor gradually deepening into coma, (2) general convulsions frequently repeated with or without focal paralysis, associated with (3) an exhausting disease — as phthisis or cancer in its last stages, long-continued suppuration, acute specific disease or, most frequently of all, prolonged diarrhoea during infancy, and (4), in some instances, distension of external veins connected with the sinus thrombosed. In young children (especially infants), in whom a very large percentage of the cases of marantic sinus-throm- bosis occur, the general cerebral symptoms that result from the thrombosis are often obscured by the general cerebral symptoms that accompany an exhausting diar- rhoea, for stupor, coma and general convulsions may result from the cerebral anaemia which an exhausting diarrhoea frequently induces. The diagnosis of sinus- thrombosis should be suspected in young children only when there are present, in addition to the general cerebral symptoms, symptoms of a focal character (local paraly- sis, local convulsions, local rigidity) or external tume- faction " developing after the other symptoms. The diagnosis is to be considered certain only in the rare cases in which the latter is present. In adults in whom there is a cause for thrombosis (exhausting disease — phthisis, cancer, in terminal ' The positions in which the external distension of veins or oedema occurs are : oedema and distension of the veins on the forehead and sides of the head in thrombosis of the superior longitudinal ; oedema of the eyelids and temples in thrombosis of the cavernous sinus ; oedema over the mastoid process in thrombosis of the lateral sinus. THE DIAGNOSIS OF CLINICAL TYPES. 367 stage), marantic sinus-thrombosis may be suspected if there are the acute cerebral symptoms already men- tioned, provided there can be excluded all causes of arterial thrombosis (especially atheroma, heart disease, degenerative time of life). But here, as in children, a positive diagnosis can be made only in the presence of external distension of veins or oedema. It is important to note that in persons over fifty the cerebral symptoms referred to are far more apt to be due to arterial throm- bosis than to sinus-thrombosis. b. Secondary Thrombosis. — There is nothing character- istic about the symptoms of secondary sinus-thrombosis. The sinus-thrombosis results in most cases from caries of bone, especially from disease of the internal ear, more rarely from meningitis (especially tubercular) and suppuration external to the skull, and such symptoms as are due to the thrombosis are obscured by the more obtrusive evidences of the primary trouble. Speaking generally, the symptoms that attend secondary sinus- thrombosis closely resemble those of meningitis running an acute or subacute course, and they are, indeed, usually due to meningitis. In many cases the breaking down of the clot, which is septic, leads to symptoms of septicae- mia. The conditions, therefore, that suggest secondary sinus-thrombosis are : (i) the presence of a cause of secondary thrombosis ; (2) symptoms resembling acute or subacute meningitis, associated with or succeeded by (3) symptoms of septicaemia. But it is only when these symptoms are associated with external oedema or venous distension that a diagnosis of secondary sinus-thrombosis can be made with a high degree of probability. Infantile Cerebral Paralysis. — The paralyses of cerebral origin that are frequently observed during in- 368 DISEASES OF THE NERVOUS SYSTEM. fancy and childhood are not all dependent upon one path- ological state, but may probably result from any one of several distinct conditions — from hemorrhage, arterial or venous thrombosis, embolism, etc. Notwithstanding these different modes ol origin of the infantile cerebral paraly- ses, their symptoms resemble one another so closely, what- ever may be their origin, and their pathology is in some instances so obscure, that it is not at present feasible or desirable to classify them according to the nature of the lesions to which they are due. It is preferable to group them all under the clinical designation above adopted — infantile cerebral paralysis. The clinical characters of infantile cerebral paralyses, though differing widely in some cases, have enough points of resemblance to constitute a very distinct clini- cal type. These characters are as follows : 1 . Motor paralysis, usually hemiplegic in form, occa- sionally diplegic and rarely paraplegic. The paralysis, whatever may be its form, has the following features : a. There is marked rigidity in the muscles paralyzed, and in most cases contractures, which may be extreme. In very rare instances the paralysis is flaccid and not spastic. b. The knee-jerks and reflexes generally are much exaggerated. Usually this increase of reflex is most marked on the side paralyzed. c. The paralysis is frequently followed after a time by athetoid, associated, choreiform or other movements. d. The muscles paralyzed do not present the RD, and electrical changes, when present, are quantitative or slight in degree. e. The paralysis is usually partial. If considerable at first it rapidly lessens. In hemiplegic cases the face often escapes entirely. The leg recovers more rapidly THE DIAGNOSIS OF CLINICAL TYPES. 369 and perfectly than is the case when hemiplegia occurs in the adult, and the ultimate paralysis may be chiefly or exclusively in the arm. f. There are no disturbances of sensibility. ' 2. In the cases of infantile cerebral paralysis that de- velop! in children who have acquired language, motor aphasia is often developed. In cases of hemiplegia in children aphasia is almost as common when the lesion is on the right side of the brain as when it is on the left side. 3. In all cases of infantile cerebral paralysis there is arrest or retardation of development in the limbs para- lyzed. The paralyzed extremities become shorter and smaller than those not paralyzed. The arrest may be noticeable in the shape of the cranium, and in a diminu- tion in most of the cranial diameters. There are well- marked vaso-motor changes in the paralyzed extremities, and atrophy of the muscles, slight or considerable in degree, is present. 4. About two thirds of the cases of infantile cerebral paralysis are accompanied with some form of mental impairment. In a small proportion there is idiocy (most often in diplegic and paraplegic cases), in others there is imbecility, and most frequently there is simple feeble- mindedness (most common form in hemiplegia). 5. Nearly one half the cases of infantile cerebral paralysis are followed by epilepsy. In most cases the form is that of general epilepsy (grand mal), but in a considerable number there is Jacksonian epilepsy. The convulsions persist for years and sometimes survive all traces of the original paralysis. For clinical purposes it is desirable to distinguish two types of infantile cerebral paralysis : (I.) the congenital, and (II.) the acquired form. 370 DISEASES OF THE NERVOUS SYSTEM. I. The Co7igenital Form of Infantile Cerebral Paralysis (Cerebral Birth-Palsy, Infantile Meningeal Hemorrhage). This form of infantile cerebral paralysis depends on meningeal hemorrhage over one or both sides of the convexity of the brain, the result of injury during birth. In about two thirds of the cases the paralysis is of the hemiplegic form ; in one third it is diplegic or para- plegic. The facts that indicate the existence* of the congenital form of palsy are : 1. There is a history of hemiplegia or diplegia, usually with but sometimes without convulsions, dating either from birth or from a few days subsequent to birth, though the paralysis may not have been observed for some time after parturition. There is never a history of a distinct onset after birth. 2. There is a history of some distinct difficulty in birth, either an unnatural presentation, or, more frequently, prolonged and difficult labor with a head presentation. The symptoms in these cases are those already enu- merated : partial paralysis, hemiplegic or diplegic, with rigidity and contractures, arrested development, increased reflexes, post-hemiplegic movements, mental impair- ment and frequently epilepsy. There is nothing distinc- tive about these symptoms or their combinations, and the diagnosis of this form of cerebral palsy depends on the etiological facts above stated and on the absence of a distinct onset of the symptoms. II. The Acquired Form of Infantile Cerebral Paralysis (Acute Cerebral Infantile Palsy, Infantile Hemiplegia). There is still considerable difference of opinion as to the pathological process which underlies the acquired form of infantile cerebral paralysis, and it is certain that this is not the same in all cases. The following pro- cesses have each been claimed as the cause of a certain THE DIAGNOSIS OF CLINICAL TYPES. 37 1 proportion of the cases : arterial thrombosis, from syphi- litic endarteritis and from atheroma ; thrombosis of a superficial cortical vein; hemorrhage, especially into the cortex, or pia, or subarachnoid space ; cerebral embolism; and last, but not least, an inflammatory process known as polioencephalitis, involving the motor cortical ganglion- cells and supposed to be analogous to the process in the spinal cord known as poliomyelitis. There is reason to suppose that each of these processes may at times be effective in causing infantile hemiplegia, but in the case of polioencephalitis and thrombosis of cortical veins this supposition is based chiefly on theoretical considerations. In the acquired form of infantile cerebral paralysis the form of the paralysis is hemiplegic in fully nine tenths of all the cases ; diplegias and paraplegias are rare as compared with their occurrence in the con- genital form. The recognition of this form (acquired) of cerebral paralysis depends on the following facts : 1. The onset of the paralysis is acute or sudden, and occurs during infancy or early childhood. In about one half the cases the onset is attended with convulsions, usually one-sided, sometimes general. There may or may not be loss of consciousness lasting hours or days, and there may or may not be fever and vomiting at the onset. 2. In nearly half the cases the disease is distinctly secondary to some other condition. In these cases the exact period of onset of the paralysis may be obscured by the symptoms of the primary disease. The conditions to which the acquired form are most often secondary are as follows : pneumonia/ scarlet fever, measles, whooping-cough and injury to the head, ' Very extensive subarachnoid hemorrhage is sometimes seen in the cases that develop during pneumonia. 372 DISEASES OF THE NERVOUS SYSTEM. but it occasionally follows almost every acute specific or, general disease. The distinction between the two above-described forms of infantile cerebral paralysis is usually easy, and may be made from the facts already given relating to their etiology and mode of development. The diagnosis between infantile cerebral palsy and other forms of brain disease is also easy as a rule. The hemiplegia that occurs in tumor is distinguished from that of acute infantile cerebral palsies by the gradual onset and progressive development of the symptoms of the former as distinguished from the acute onset and stationary or retrogressive character of the symptoms in the latter. Typical cases of infantile cerebral paralysis cannot be confounded with typical cases of poliomyelitis — infan- tile spinal paralysis — but both are large groups, the variations within which are such that cases are met with in each that bear a considerable though superficial re- semblance to one another. A case of infantile cerebral paralysis in which there is considerable paralysis and atrophy in one arm (the leg having recovered partially or entirely), may closely resemble a case of poliomyelitis involving one arm, and the resemblance may be height- ened by the history, in both cases, of an acute onset with fever and convulsions. In such an instance the diagnosis would depend (chiefly) on the electrical reactions, which would be normal, or nearly so, in the cerebral case, but would present some form of RD in the spinal case. In the paraplegic form of infantile cerebral paralysis the palsy may possibly be confounded with that from dis- ease of the spinal cord. Close examination, however, shows, that there is usually some motor derangement in the upper extremities in the former cases. It is import- THE DIAGNOSIS OF CLINICAL TYPES. 373 •ant also to note that the chronic spastic paraplegia that results from spinal cord disease is exceedingly rare in young children. If vertebral caries be excluded, such spastic ] araplegia is almost invariably due to a cerebral lesion. (See Primary Spastic Paraplegia.) Abscess of the Brain. — The symptoms of abscess of the brain are exceedingly variable and often equiv- ocal. They consist, first, of diffuse symptoms, which are much like those of tumor (see p. 375) — headache, vomit- ing, optic neuritis and mental apathy ; and, secondly, oi focal symptoms, which depend entirely on the situation of the abscess and are even more variable than the dif- fuse symptoms. In some cases the focal symptoms are entirely wanting. In many instances there are in addition to the diffuse and focal symptoms the general symptoms due to suppuration — fever and repeated rigors. In about three fourths of all the cases there is present a distinct and recognizable cause of cerebral abscess, such as trauma, caries of cranial bones, chronic ear disease, or suppuration elsewhere, as in the lung. Of the focal symptoms, hemiplegia, often incomplete, is the most constant, occurring as it does in about half of all cases of cerebral abscess Local convulsions are less common. They are usually associated with hemiplegia, and both symptoms depend on the location of the lesion near or in the motor path. When there is a considerable degree of paralysis of one side there is almost always a great exaggeration of the knee-jerk on this side usually with very pronounced ankle clonus.' ' Ankle clonus, we believe, is a very regular symptom in cases of cerebral abscess involving the motor path, and is often seen in cases of abscess of the frontal lobe reaching back and slightly encroaching upon the motor path. Violent clonus may be obtainable vi'here there is very slight motor paralysis. 374 DISEASES OF THE NERVOUS SYSTEM. The course of abscess of the brain is exceedingly varia^ ble and necessitates the recognition of two groups of cases : first, cases which run an acute course, and, secondly, cases which run a chronic course. 1. The acute cases are those that commence with well marked cerebral symptoms — headache, vomiting, etc., — which progress rapidly, and without distinct diminution, into a stage characterized by severe general cerebral symptoms — headache, vomiting, optic neuritis, general convulsions, and mental apathy, delirium and coma ; per- haps also by focal symptoms — hemiplegia and local con- vulsions. This is the terminal stage. The entire course of the disease varies in these acute cases from a week to a month. 2. The chronic cases are those in which there is a long period of latency between the initial and terminal cerebral symptoms, the former being often so slight as to be entirely overlooked. This period of latency may last weeks, months, or years, and may be complete or incomplete. If incom- plete, there may be present some equivocal cerebral symptoms, as headache, occasional vomiting, convulsions, slight mental failure, apathy, etc. Then, after a variable time, all these symptoms increase, and pass, gradually or rapidly, into a terminal stage like that above described, characterized by headache, convulsions, optic neuritis, delirium and stupor deepening into coma. If the latency is complete there are no recognizable evidences of brain disease until the terminal stage of grave cerebral symptoms is suddenly or rapidly reached. In those cases of abscess in which there are well- marked general and local cerebral symptoms and symp- toms indicative of a suppurative process — fever and repeated rigors, in the presence of a cause [iiide ante) THE DIAGNOSIS OF CLINICAL TYPES. 375 that is adequate to account for a cerebral abscess — the diagnosis is not difficult. In those cases, however, in which the period of latency is complete, or nearly so, and the terminal symptoms come on suddenly or rapidly, a diagnosis of apoplexy from cerebral hemorrhage or acute cerebral softening may be erroneously made. Such an error may be avoided if a recognizable cause for abscess exists and leads to a suspicion of abscess. Hemorrhage and softening could be positively excluded if examination revealed the existence of optic neuritis in the absence of chronic diffuse nephritis. The two diseases with which abscess is most often con- founded are tumor and meningitis. The points of dis- tinction from the former are given on page 379. The diagnosis between abscess and meningitis has been given elsewhere (see p. 343). Intracranial Tumor.— The symptoms that point to the existence of a tumor within the cranial cavity are of two kinds — diffuse or general and focal. The most significant and frequent diffuse symptoms are : (i) head- ache — severe and persistent ; (2) vomiting — especially without gastric cause and (3) double optic neuritis. Other diffuse symptoms of importance are : (i) general convulsions ; (2) attacks of petit mal ; (3) giddiness ; (4) slowness of speech ; (5) simple mental failure ; and as terminal symptoms, (6) stupor and coma. The focal symptoms, unlike the diffuse symptoms, depend on the situation of the tumor and afford an indication of its position. Some of the focal symptoms are irritative in character, others destructive. The symptoms and their combinations that depend on the position of the tumor within the cranium maybe inferred from the facts of localization already presented (see Chap. III). The focal symptoms of tumor that are of most frequent 1^6 DISEASES OF THE NERVOUS SYSTEM. occurrence are : (i) motor paralysis, usually of local commencement (monoplegia) with subsequent extension (hemiplegia or partial hemiplegia) ; (2) local spasm — corresponding to the seat of the motor paralysis ; (3) aphasia— usually motor, sometimes sensory ; (4) dis- turbances of sensibility ; (5) paralyses of cranial nerves. An exceedingly important general characteristic of all these symptoms of tumor is that they are oi gradual onset and run a gradually p7-ogressive course. The gradual onset is as distinctive of tumor as is the sudden onset of vascular disease — cerebral hemorrhage and acute cere- bral softening. It is important to note, however, (i) that the course of the tumor is not usually uniformly progressive — periods of intermission often alternating with periods of progress ; and (2) that sometimes symp- toms increase rapidly in intensity by causing inflamma- tion in neighboring structures ; and (3) that some forms of tumor (glioma) may cause symptoms of sudden onset from rupture of vessels within their substance. When the diagnosis of tumor has been made and the position of the growth determined by the rules of local- ization already given {vide a?tte), it remains to fix upon the nature of the growth. Sometimes this can be done with a high degree of probability, or even with certainty ; more often the diagnosis of the nature of the tumor can be narrowed down to one of two possibilities ; and more often still the data afford a basis for nothing more than a guess. Syphilomata, tubercular growths, sarcomata (including gliomata), and carcinomata probably make up at least nine tenths of all intra-cranial growths. In other forms of tumor it is impossible in a very large majority of cases to make a pathological diagnosis. The diagnostic effort is therefore practically limited to the cases included in the first group. THE DIAGNOSIS OF CLINICAL TYPES. 377 The indications that suggest that the tumor is a syphilitic growth are as follows : 1. A distinct history or symptoms of constitutional syphilis.' 2. Symptoms indicating that the tumor is in the cor- tex of the brain (see Localization), and is producing irritative rather than destructive phenomena. 3. Evidences of rapid growth at the onset, followed by a period of slow growth or a stationary condition. 4. Retrogression and gradual arrest of the symptoms of a tumor under antisyphilitic treatment (iodide and mercury). 5. The development of the tumor during early or middle adult life (twenty to forty-five years). This is, of course, of little value, as most forms of tumor are most common at this period. The indications that suggest a tubercular growth are : 1. The presence of tubercular disease in some other organ than the brain, or a family history of tubercular disease. 2. A rapid development of the symptoms, which after a time become stationary. 3. Symptoms indicating that the tumor is in the cere- bellum or in the pons. 4. The development of the symptoms before the twentieth, and especially before the tenth year. This indication refers also to glioma. 5. A history of injury to the head. 6. Improvement under tonic treatment. The indications that suggest the existence of a sarcoma ' A history of a chancre without secondaries has a similar significance. A syphiloma cannot, of course, be excluded, unless the possibility of syphilitic infection can be also excluded. It must be remembered that a growth of another nature may coexist v/ith syphilis. 378 DISEASES OF THE NERVOUS SYSTEM. are : (i) the presence of a sarcomatous tumor else- where (this makes the probability very high) ; evidence that the tumor is not in the brain substance itself, as when it is in the bones (rarely available). The following indications suggest a glioma : 1. The occurrence of sudden loss of consciousness, with exacerbation of all symptoms, in the course of a tumor. This is practically confined to glioma. 2. The situation of the tumor in the cortex, with pre- dominance of irritative symptoms. This character is shared with syphiloma. 3. The absence of all evidence of tubercular and syphilitic disease and of sarcoma or carcinoma in other parts of the body. 4. The age of the patient is under fifty. If over fifty, glioma is improbable. A carchioma is suggested by : 1. The presence of carcinoma elsewhere. This makes the diagnosis highly probable. 2. By the patient's being over fifty years of age. Tumor of the brain may be confounded with other organic diseases of the brain, with functional diseases of the nervous system and with diseases outside the nervous system. Diagnosis from Other Organic Diseases of the Brain. — All organic diseases of the brain may be roughly but conveniently divided into two great groups ; — that in which the symptoms are of sudden onset, and that in which the onset of the symptoms is more or less gradual. The first group comprises a large and very important part of all organic brain diseases— cerebral hemorrhage, and the various forms {vide a7tte) of acute cerebral soften- ing. Cerebral tumor is distinguished from the members of this group of vascular lesions, by the simple but im- THE DIAGNOSIS OF CLINICAL TYPES. 379 portant fact that its symptoms are never of sudden onset and never reach a considerable degree of development in the course of a few hours. In rare cases of tumor (especially cases of glioma), sudden symptoms sug- gesting a vascular lesion occur, but these symptoms (which are, indeed, due to hemorrhage from rupture of vessels in the tumor) always follow symptoms of more gradual onset. It is therefore necessary to consider only the dis- tinction of tumor from the diseases that comprise the second group above mentioned — in which the develop- ment of the symptoms is more or less gradual. This group includes the following conditions : meningitis, acute and chronic, abscess, aneurism, general paralysis, insular sclerosis and bulbar paralysis. For the diagnosis between tumor and meningitis, see page 342. Diagnosis between Tumor and Abscess. — Cases of ab- scess occur that bear a close resemblance to tumor. The diffuse symptoms, especially, are often those of tumor — there is headache, vomiting, double optic neuritis and mental failure. If there are well marked and progressive focal symptoms — as monoplegia, hemiplegia, paralysis of cranial nerves, etc., this is in favor of tumor. The absence of focal symptoms j)oints to abscess. If there is a considerable grade of optic neuritis, this is some- what in favor of tumor, and if the optic neuritis is intense (six dioptrics or more), the diagnosis of tumor is practically certain. On the other hand, a period of con- siderable duration in which the symptoms are slight and stationary, followed by a period of rapid increase in the severity of the symptoms, is in favor of abscess. The occurrence of fever and rigors, especially if associated with exacerbation of the symptoms, points to abscess. If severe symptoms of rapid onset gradually lessen, this 380 DISEASES OF THE NERVOUS SYSTEM. is in favor of tumor. The etiology may give important aid in the distinction. The absence of any traceable cause for the disease is distinctly in favor of tumor if the symptoms are equivocal. If there is ear disease, or dis- ease of the cranial bones, or a distant focus of suppura- tion, this makes abscess more than probable. If, how- ever, there has been an injury to the head, this gives no help, for although injury is more commonly a cause of abscess than of tumor this is compensated by the fact that tumor is a more common condition than abscess. The diagnosis between tumor and the cases of hysteria that resemble it is ordinarily very simple ; yet such cases are not rarely mistaken for tumor, and even more often cases of tumor are regarded as instances of hysteria. These errors would seldom or never be made were the facts relating to the distinction of functional and organic disease elsewhere considered (see Chapter VI.) borne in mind. Only the main points of distinction will be con- sidered here. The cases of hysteria that are mistaken for tumor are usually those in which there are well marked unilateral manifestations, — local paralysis, monoplegia, or hemi- plegia, contractures, spasm, local anggsthesia or hemian- sesthesia. There may be in these cases a considerable de- -gree of headache, there may be repeated vomiting, and there may be general convulsions — each of which increases the resemblance to tumor. The peculiar distribution of the hysterical paralyses and anaesthesias, their rapid onset after some emotional disturbance, the absence of local convulsions and of unilateral changes in the reflexes, the absence of optic neuritis and the variations that oc- cur in the hysterical symptoms make the distinction easy, especially in patients showing the mental characteristics of hysteria. The error of ascribing the symptoms of THE DIAGNOSIS OF CLINICAL TYPES. 38 1 tumor to hysteria is generally made in young women who have an inclination to emotional disturbance, which, in the presence of organic disease has led to the develop- ment of distinct hysterical symptoms. In other words, in such a case the symptoms of tumor are associated with and perhaps, somewhat obscured by the existence of true manifestations of hysteria. Error can always be avoided by remembering that no symptom or symptoms should be attributed to hysteria until the various evidences of or- ganic disease have been eliminated by a careful search. In tumor of the brain there are always some distinct indications of organic disease — as optic neuritis, focal paralysis, local convulsions, etc., which it is inexcusable to overlook. Cerebral tumor may be confounded with idiopathic epilepsy in cases where the tumor runs a slow course and general convulsions constitute a conspicuous symptom. The convulsions of tumor usually have a local com- ipencement and this is an important point of difference from those of epilepsy, but does not constitute an abso- lute criterion, since the local commencement may be absent in tumor and is in rare cases present in epilepsy. An aura, particularly a special sense aura, preceding the attacks is rather in favor of tumor. But it is rarely necessary to base the distinction on these features ; other evidences of organic disease are usually present, — e. g., there is optic neuritis, or there is organic headache, or local paralysis. In the absence of more unequivocal indications, a neurotic heredity, as of epilepsy, chorea, or hysteria, may be allowed some weight as increasing the probabilities of functional disease. The error of ascribing a combination of optic neuritis and headache in cases of extreme anaemia, Bright's dis- ease or lead poisoning, to an organic cause (and espe- 382 DISEASES OF THE NERVOUS SYSTEM. cially to tumor), has already been mentioned (see optic neuritis), and does not require further consideration here. Intracranial Aneurism. — The term intracranial aneurism as here employed relates only to aneurisms of the main cerebral arteries, and not to the miliary aneu- risms that occur on their branches within the brain sub- stance. Miliary aneurisms give rise to no symptoms until rupture occurs, and then the symptoms are those of cerebral hemorrhage. Intracranial aneurisms, when they attain a considerable size and press upon important structures, give rise to symptoms, — differing in this re- spect from miliary aneurisms. But it is important to note that, in many instances, intracranial aneurisms, like miliary aneurisms, cause no symptoms until they rupture. The symptoms of aneurism, when they occur, are those of a small tumor at the base of the brain, pressing usually either upon the motor tract or upon the cranial nerves, or upon both. A certain diagnosis of the presence of aneu- rism can be made only in cases where there is an aneuris- mal murmur that is distinguishable on auscultation of the skull. Such a murmur is heard only in rare cases of intra- cranial aneursim, and probably only in cases where the aneurism is situated either on the internal carotid or the vertebral artery. Hence a positive diagnosis of aneurism can be made only in very exceptional instances. The cases are, however, much more numerous where a suspi- cion of aneurism is justiiied, or where even a probable diagnosis can be made. The indications that make the diagnosis of aneurism more or less probable in the pres- ence of symptoms of a basal tumor are as follows : I. The history or presence of a cause of aneurism which is not also a cause of new growths within the cranium. Such causes are {a) arterial degeneration and {i>) THE DIAGNOSIS OF CLINICAL TYPES. 383 endocarditis. Arterial degeneration, fibroid or atheroma- tous, is sometimes a cause of aneurism in persons over forty. In many cases of aneurism occurring in persons under forty years of age there are indications of past or present endocarditis. The significance of this circum- stance depends on the fact that many cases of aneurism depend on emboHsm. Syphilis, by causing endarteritis, is a cause of aneurism, but a history of syphilis has no diagnostic value, as specific disease is more frequently a cause of syphiloma or chronic syphilitic meningitis than of aneurism. A history of injury (which is frequent in aneurism) is likewise of no value, because injury is a cause both of aneurism and tumor. 2. Indications that the tumor (lesion) is in the position of a large artery. The most common positions for aneu- rism are, first, on the middle cerebral artery, next on the basilar and internal carotid arteries. Much less often aneurisms are situated on the anterior cerebral, posterior communicating, anterior communicating, vertebral, or posterior cerebral arteries. The focal pressure symptoms that result from an aneurism in these different positions may be inferred from the relations of the vessels to sur- rounding parts, but the symptoms that result from aneu- rism on the middle cerebral, basilar and internal carotid arteries may be briefly summarized : a. Middle Cerebral. — Hemiplegia and convulsions are common — paralysis of cranial nerves rare. When on the left side there may be motor aphasia. b. Basilar. — The symptoms are those due to pressure, unilateral or bilateral, on the pons and on the cranial nerves. The nerves affected are generally several and vary according to the position of the aneurism on the artery. The 5th, 6th, 7th, 8th, 9th, loth and nth may be affected ; only rarely the 3d or 1 2th. There may be severe occipi- 384 DISEASES OF THE NERVOUS SYSTEM. tal headache. The fifth nerve suffers most often. There may be crossed paralysis. Convulsions are uncommon. c. Internal Carotid. — The chief pressure symptoms are blindness of one eye from pressure on the optic nerve, combined with paralysis of one or more ocular nerves — especially ptosis — from pressure on the nerves in the cavernous sinus. Smell may be lost and occasionally there may be symptoms of pressure on one crus. In any case where an intracranial aneurism is suspected the diagnosis is much strengthened if rupture occurs. Such a rupture gives rise to the symptoms of severe apo- plexy. If there have been no symptoms to suggest aneu- rism before rupture occurs, the cause of the apoplexy would be suspected only in case it occurred in a person under forty years of age who had suffered from endo- carditis or syphilis, or who gave a history of trauma to the head. The chief conditions from which aneurism has to be dis- tinguished are intracranial tumor and chronic syphilitic basilar meningitis. The points on which the distinction from tumor is made, when this is practicable, have been mentioned above. The question of a diagnosis from chronic syphilitic meningitis arises in cases where there is pressure only upon cranial nerves. The distinction is frequently impossible, especially if there is a distinct history of syphilis. The chief criterion in such instances is that afforded by the effect of antisyphilitic treatment : in chronic meningitis there is regularly improvement under treatment ; in aneurism there is none. But this indication, while valuable, is far from absolute. Nuclear Ophthalmoplegia (Nuclear Ocular Paraly- sis). — Disease of the nuclei of the motor nerves of the eye (third, fourth, and sixth) is often the cause of paraly- sis of the ocular muscles — both the external muscles of THE DIAGNOSIS OF CLINICAL TYPES. 385 the eyeball (extrinsic muscles of the eye) and the mus- cles within the globe (internal or intrinsic muscles). In some cases the paralysis is the result of involvement of an isolated nucleus ; in others, several or all of the nuclei are affected. Some of the lesions that cause nuclear paralysis are acute in their development ; others are chronic. Thus it is that the symptoms of nuclear ophthalmoplegia vary widely in different cases, according to the position and nature of the morbid process. It is desirable to distinguish clinically two different forms of ophthalmoplegia — an acute form and a chronic form. Owing to its far greater importance the chronic form will be first considered. Chronic Nuclear Ophthalmoplegia (Chronic Progressive Ophthalmoplegia,' Chronic Nuclear Paralysis, Chronic Ophthalmoplegia). — The symptoms of chronic nuclear ophthalmoplegia vary so widely in different cases that it is difficult to say what constitutes the most typical form of the disease. The following are the chief characteristics of the disease : I . The gradual and successive paralysis of many or all of ike ocular muscles. At first only a small number of muscles (or one only) is affected. One of the first indications of this involvement is often double vision (usually transient). The loss of power is at first slight, but gradually increases and extends to other muscles than those first affected. After the lapse of years most of the muscles of both eyes become involved, and even all of them may be in- cluded in the paralysis (total ophthalmoplegia). The isolated loss of reflex action of the iris and the isolated ' Chronic progressive ophthalmoplegia is so commonly caused by nuclear disease that the term is used synonymously with nuclear disease. 386 DISEASES OF THE NERVOUS SYSTEM. paralysis of the ciliary muscle are to be regarded as varieties of chronic progressive ophthalmoplegia. Usu- ally the muscles are involved in a random irregular man- ner without reference to their function (this is somewhat characteristic of nuclear disease), but not rarely the muscles first affected are associated in action (as the external rectus of one side and the internal rectus of the other, or both internal recti, or the superior recti and levators). Ptosis is usually absent, and when present is rarely complete. Nystagmus and slight exophthalmos are occasional symptoms. The process is sometimes much more advanced in one eye than in the other, and occasionally the paralyses are all unilateral. The intrin- sic muscles of the eye, though commonly affected in some degree, may escape entirely. Most cases of chronic ophthalmoplegia are slowly progressive, though in some cases there is little prog- ress for many years. Occasionally cases which are unquestionably of nuclear origin, after reaching an ad- vanced stage of paralysis in both eyes, regain perfectly the power of movement in both eyes. Such cases cannot at present be satisfactorily explained. 2. The associatio7i of these ocular paralyses with evi- dences of other diseases of the nervous syste?n. Sometimes chronic ophthalmoplegia exists by itself, but more often it is associated with other forms of nervous disease. Of these other forms the most com- mon are locomotor ataxia, general paralysis of the insane, multiple sclerosis and optic-nerve atrophy. Psychical disturbance is a common association ; sometimes this is the precursor of the symptoms of general paralysis. In other cases the mental disturbance is apparently func- tional (hypochondriasis, hallucinatory insanity). The relation of chronic ophthalmoplegia to the associated THE DIAGNOSIS OF CLINICAL TYPES. 387 condition varies in different cases. Either the nervous disease or the associated state may give rise to the first symptoms, and in some cases both sets of symptoms appear and develop almost simultaneously. The lesion on which chronic nuclear ophthalmoplegia depends is a slow degenerative process in the nuclei corresponding to the muscles paralyzed. In a consid- erable proportion of these cases a syphilitic history can be traced, and is probable in many cases where it cannot be traced, but there are many cases in which no cause whatever can be found. Sometimes ophthalmoplegia is a congenital and perhaps an hereditary condition. The diagnosis of chronic nuclear ophthalmoplegia will be touched upon after briefly alluding to the acute form of the disease. Acute Nuclear Ophthalmoplegia. — In rare instances many or all of the ocular muscles are suddenly or rapidly para- lyzed from disease of their nuclei, and this condition is called acute nuclear ophthalmoplegia. In some cases the condition has been due to hemorrhage, in others to acute softening, in the region of the third nerve nuclei. Whether it is ever really due to acute inflammation of the nuclei (so-called acute polioencephalitis superior) is doubtful. Perhaps some cases of diphtheritic ocular paralysis (in- cluding the common form of paralysis of the ciliary muscle-cycloplegia) are examples of nuclear disease. Having established the existence of paralysis of ocular muscles, an effort must be made to determine whether the lesion is of nuclear origin or of peripheral origin. In some cases a conclusion can be reached which is almost positive ; in other cases it is impossible to reach a conclu- sion. The indications upon which the diagnosis is based differ somewhat in acute and chronic cases of ocular paralysis, and it is convenient to consider them separately. 388 DISEASES OF THE NERVOUS SYSTEM. In cases of acute development a nuclear lesion is proba- ble if the muscles paralyzed correspond to an irregular involvement of the functions of the nerve structures, or if the muscles paralyzed are very unequally involved. Thus, if several of the muscles innervated by the third nerve are paralyzed without reference to function {e. g., the internal and inferior recti), it is highly improbable that the lesion is peripheral Again, if all or nearly all the external muscles of the eyeball are involved, but some (as the levator) are much less paralyzed than the others, this suggests a nuclear lesion. If the intrinsic muscles of the eye escape entirely, while the external muscles are extensively involved, a nuclear lesion is almost certain. All these indications except the last are greatly strength- ened in significance if the palsy of the ocular muscles is bilatei'al. In acute or subacute palsies the associated symptoms may throw light on the position of the lesion. Thus, if the symptoms are such as to suggest a quadri- gemifial lesion (see Localization), it is certain that the ocular palsy is nuclear. The probable nature of the lesion may aid in the diagnosis. Vascular lesions, for example (hemorrhage, acute softening), can give rise only to nuclear paralysis, or to fascicular paralysis, /. e., para- lysis involving the various bundles of the third nerve between the nucleus and the surface origin of the nerve. A distinction between a nuclear paralysis and a fascicular paralysis cannot at present be made, either in the case of acute or of chronic lesions. A chronic palsy is almost always nuclear and almost never fascicular, but an acute or subacute palsy is probably as often fascicular as nuclear. The involvement of all the functions of a nerve in almost equal degree indicates a peripheral lesion. In cases of ocular paralysis of chronic development, the distinction of a nuclear (or fascicular) from a periph- eral palsy is based on the following indications : THE DIAGNOSIS OF CLINICAL TYPES. 389 1. The exemption of the intrinsic muscles of the eye. This is a very valuable indication, but is not absolutely distinctive of nuclear disease. 2. The absence or slight development of ptosis. 3. Bilateral distribution of the symptoms. 4. Irregular, apparently random distribution of the paralysis. 5. The association of chronic ocular palsy with cere- bral or spinal symptoms, especially symptoms that suggest a lesion of a degenerative character. In cases where both the internal and external muscles of both eyes are paralyzed the diagnosis of a nuclear lesion can be made only after excluding the presence of disease at the base of the brain {j)ide Localization). Recurrent Ophthalmoplegia (Periodical Ophthalmo- plegia). — In rare cases there is observed a transient paralysis of ocular muscles (chiefly those supplied by the third nerve of one side), which makes its appearance at long or short intervals during a long period of time. The character of the attacks varies somewhat in different cases. The onset is rapid and is usually attended with pain, generally severe, in the eye affected, and often there is unilateral headache and vomiting. The paroxysms thus closely resemble attacks of migraine with ophthalmoplegia super- added [vide Migraine). The paralysis is sometimes com- plete, sometimes incomplete. Ptosis is generally present, and the intrinsic muscles of the eye are often involved with the extrinsic muscles. The duration of the attacks varies much in different cases, and even in the same case at different times. Usually the paralysis lasts from two to six weeks, its duration being longest when the intervals are long. The frequency of the attacks also varies greatly in different cases — in most cases the interval between the paroxysms varies from one month to one year. 390 DISEASES OF THE NERVOUS SYSTEM. It is important to note that in some cases slight loss of power persists during the intervals. The nature of these cases of recurrent ophthahnoplegia is obscure, but there is good reason to believe that the condition is closely related, both clinically and pathologically, to migraine (ophthalmic migraine). The palsy probably depends not on organic changes, but on vascular and perhaps in some cases on nutritional changes in the nuclei. Insular or Disseminated Sclerosis. — Insular sclerosis is a degenerative disease of the central nervous system — of the cord as well as of the brain, — in which patches of sclerosis occur irregularly scattered through- out its white substance. The favorite seats for the islets of sclerosis are the centrum ovale, crus, pons, medulla and cord, but they may occur in almost any part and entail a corresponding multiplicity in the characters of the symptoms. The characteristic and almost distinctive feature of in- sular sclerosis is a coarse jerky inco-ordination {vide p. 87) of the limbs and especially of the arms. This inco- ordination is present only during voluntary effort (" inten- tion tremor "). It is associated usually from the beginning with some loss of power in the limbs affected, and this loss progresses gradually as the disease advances. The reason why this combination of jerky inco-ordination and weakness in the limbs is so constantly observed in cases of insular sclerosis is that the pons and cord are very regularly the seat of patches of sclerosis, some of which almost necessarily involve some part of the motor path. Associated with the jerky inco-ordination and weakness are usually a variety of other symptoms of less constant occurrence. Of these the following are the most im- portant : THE DIAGNOSIS OF CLINICAL TYPES. 39 1 1. Nystagmus. This is an early and frequent symptom (present in three fourths of all cases). 2. A peculiar defect in articulation, consisting usually of an undue separation and accentuation of the syllables of words (known as " scanning " speech), or of the words of a sentence. 3. A slight and variable degree of mental defect. This consists generally of loss of memory and an unnatural con- tentment with the patient's surroundings and condition. 4. Atrophy of the optic nerve with gradual loss of sight. Advanced atrophy of the optic nerve is met with in only a small proportion of the cases, but a slight degree of change is present in a very large number of cases {m'de page 156). 5. Increase of knee-jerks and of muscle reflexes generally is observed in most of the cases in which there is jerky inco-ordination. In addition to (or in place of) these cardinal symptoms of insular sclerosis, others of less frequent occurrence are observed, among them loss of knee-jerk, sensory dis- turbances, paralysis of cranial nerves — especially the fifth, seventh, and twelfth nerves — headache, vertigo, giddiness and double vision. Like other degenerative diseases, insular sclerosis is slowly progressive in its course, but it is not generally unifonnly progressive, for periods of progress alternate with periods during which the disease appears stationary. Sometimes in the course of the disease there are acute attacks of vertigo and giddiness, associated occasionally with vomiting and accompanied at times with diplopia. After such an attack the symptoms of the disease are aggravated. These attacks usually occur early in the dis- ease, and they may be the first symptoms observed. Insular sclerosis may be confounded with paralysis 392 DISEASES OF THE NERVOUS SYSTEM. agitans, locomotor ataxia, intracranial tumor, general paralysis, primary lateral sclerosis, infantile cerebral paralysis, and with some manifestations of hysteria. The distinction from paralysis agitans is seldom diffi- cult. The tremor of insular sclerosis is coarse, irregular, and jerky, and is present only during voluntary effort ; that of paralysis agitans is usually regular, rhythmical, and relatively narrow in range and is continued during rest, except in rare instances in the beginning of the disease. In paralysis agitans the parts that are the seat of tremor are early rigid and the hand assumes a distinctive atti- tude of flexion which is absent in insular sclerosis. In the cases where the tremor of paralysis agitans stops during rest, the carriage of the patient, the fixed gaze and the rigidity are sufficiently distinctive. The head frequently shares in the tremor of insular sclerosis ; it is rarely affected in paralysis agitans. Nystagmus is com- mon in insular sclerosis, unknown in paralysis agitans. In insular sclerosis the speech is usually " scanning " in character ; in paralysis agitans it may be normal or un- duly rapid, with a tendency to confluence of syllables, and a decided monotony of voice. It is rare for insular sclerosis to commence after the fortieth year, and it is equally rare for paralysis agitans to begin before the fortieth year. In cases in which tremor is the only marked symptom and the diagnosis seems doubtful, the presence of optic atrophy (usually slight in degree) points to insular sclerosis, and in less doubtful cases strengthens the diagnosis. The distinction from locomotor ataxia is considered under the latter disease, and from general paralysis of the insane under that title. A superficial resemblance exists between cases of tumor and insular sclerosis in the cases where tumor of the THE DIAGNOSIS OF CLINICAL TYPES. 393 pons or crus (see Localization) is accompanied with wild jerky inco-ordination almost identical with that of insular sclerosis. There the resemblance stops, and it is hardly possible to confound the other characters of tumor (headache, optic neuritis, local spasm, local paralysis), with the picture of insular sclerosis that has been pre- sented above (combination of tremor and weakness, with nystagmus, mental failure, defective articulation, and optic nerve atrophy). The diagnosis between insular sclerosis and primary lateral sclerosis is considered under lateral sclerosis. Infantile cerebral paralysis (diplegic form) occasionally presents symptoms that resemble closely those of insular sclerosis. There may be the wild jerky inco-ordination of the arms upon voluntary movement that is so sugges- tive of insular sclerosis. If the patient is between ten and twenty years of age, shows little evidence of paraly- sis, and only slight mental failure and slight speech de- fect, the distinction from insular sclerosis may not be easy. The most important help in making the diagnosis in such a case is the fact that in infantile cerebral paraly- sis there is usually a history of trauma during birth, or a history of a distinct acute onset, with or without trauma, or an acute specific fever as a factor after birth, while in insular sclerosis there is the history of a, gradual develop- ment of the disease. In infantile cerebral paralysis there is further a history of distinct paralysis which has gradually disappeared. If no history of the mode of development of the disease can be obtained the distinction rests on the objective features of the case. In infantile cerebral paralysis (diplegic form) some of the evidences of the former paralysis are usually present (slight weakness, difficulty in performing fine acts with fingers, atrophy, arrest of development, contractures, etc.). There may be 394 DISEASES OF THE NERVOUS SYSTEM. some cranial deformity, with a high arched palate. The mental defect of infantile cerebral paralysis is some grade of dementia ; that of insular sclerosis is a slighter grade of simple mental failure combined with a state of undue complacency. The presence of nystagmus would make the diagnosis of insular sclerosis certain. It is more common for insular sclerosis to be mistaken for hysteria than for the opposite error to be made, but each mistake is occasionally made. Insular sclerosis may be mistaken for hysteria when the former disease occurs, as it frequently does, in young women who present some actual symptoms of hysteria.' Generally this error is avoidable. The mere fact of the existence of nystagmus indicates that the condition is not purely hysterical and strongly suggests organic disease. Sometimes there occurs in hysteria an intention tremor, irregular in character, and thus resembling that of insular sclerosis, but differing from it in being much narrower in range and more rapid, and in being associated with distinct voluntary rigidity of the antagonistic muscles involved. It is usually easy to recognize the combination of the symptoms of the two diseases when this exists, but it may be impossible to say whether certain symptoms belong to the account of the insular sclerosis or to that of the hysteria. Thus, in a case presenting spastic paralysis of the lower extremities, un- certain gait, nystagmus, scanning speech and partial atrophy of the optic nerve, all these symptoms would be explicable by the supposition of an insular sclerosis, but if there existed a persistent rhythmical tremor of one upper extremity combined with these symptoms it would be plain that this was not dependent on the organic dis- ease but on an associated functional disturbance — /. e., 'Probably no organic disease of the brain is so apt to have asso- ciated with it some manifestations, slight or considerable, of hysteria. THE DIAGNOSIS OF CLINICAL TYPES. 395 that it was of hysterical origin. If, however, there also existed in this instance concentric limitation of the visual fields and loss of sensibility of the extremities it would be difficult or impossible to fix on the correct interpre- tation of these symptoms, since they might be referable either to the organic or to the functional disturbance. Bulbar Paralysis. — Progressive bulbar or glosso- labio-laryngeal paralysis is a chronic degenerative disease of certain nuclei of the medulla oblongata. Its symp- toms depend on the locality of the lesion and as this is usually the same, the manifestations of the disease are reasonably constant. The great characteristic of the con- dition is a slowly progj'essive and strictly bilateral paralysis of the tongue, lips, palate, pharynx, and frequently of the larynx, often associated with visible wasting of the tongue and lips. The effect of this paralysis is to cause : (i) im- perfect articulation of sounds in which the tongue plays an important role — especially lingual consonants,_ /, n^ r, and/y and (2) difficulty in swallowing, from weakness of the pharynx and palate. After a period which varies in different cases from one to several years from the commencement of the disease, the patient falls into a characteristic condition of partial helplessness, from the progress of the above mentioned paralysis. In this terminal state the tongue lies motion- less, the saliva dribbles from the open mouth, the lower part of the face is without expression and articulate speech is impossible. The intellect remains perfectly clear. Not uncommonly chronic bulbar paralysis is associated with chronic degenerative processes in other parts. Of these associations the most common is progressive muscu- lar atrophy (see p. 446). In some cases the bulbar symptoms, in others the spinal symptoms, make their appearance first and are chiefly conspicuous. 396 DISEASES OF THE NERVOUS SYSTEM. Besides this chronic progressive type of bulbar paralysis there are two other clinical forms of bulbar paralysis. These forms resemble the chronic form in presenting the same combination of glosso-labio-laryngeal paralysis of symmetrical distribution, but differ from it in being of sudden or rapid onset. The similarity in distribution of symptoms depends on a similarity in the position of the lesion ; the difference in the onset depends on a difference in the nature of the lesion. In both the forms mentioned the lesion is a vascular lesion ; in one it is hemorrhage, in the other inflammation. In the first form (hemor- rhagic)' the symptoms come on suddenly, often with vomiting and giddiness, but usually without loss of con- sciousness. At first there may be some loss of power in the limbs and perhaps some sensory disturbance, but this wears rapidly away, leaving behind a stationary con- dition of glosso-labio-laryngeal paralysis. In the second form (inflammatory)," which is much more rare than the first, the symptoms come on rapidly (acutely) but not suddenly, and are accompanied with fever, vomiting, etc." The diagnosis of chronic bulbar paralysis is usually not difficult, for the distribution of the paralysis, with its bilateral symmetry and slowly progressive course, is highly distinctive. A tumor outside the medulla, dama- ging the nerve-roots, or in the substance of the medulla, may cause bulbar symptoms of slow onset resembling those of the degenerative disease. The diagnosis is based ' These are simply cases of hemorrhage into the medulla, which are symmetrical and occupy the same nuclei as are affected in the degen- erative process. Much more often hemorrhage into the medulla is a random process. - These cases are allied to cases of acute poliomyelitis. ^ Neither form is of course to be regarded as a distinct disease, for the same processes that cause them are much more common in other regions. THE DIAGNOSIS OF CLINICAL TYPES. 397 on the fact that tumors in either of these situations usually produce unilateral symptoms, or if they produce bilateral symptoms these have not the highly symmetrical distribution that distinguishes chronic bulbar paralysis. In tumor, again, there is usually headache, and often con- vulsions, and sometimes optic neuritis, all of which are absent in chronic bulbar paralysis. The age at which chronic bulbar paralysis occurs may help in the diagnosis, for tumors are not frequent after the fiftieth year, while chronic bulbar paralysis seldom commences before this time. Symmetrical lesions in the motor paths of both hemi- spheres may give rise to symptoms resembling those of bulbar paralysis, bilateral paralysis of tongue, lips and pharynx — " pseudo-bulbar paralysis " it is called. When such symptoms depend on acute lesions (hemorrhage, softening), as they usually do, the diagnosis is easy. When they depend on chronic lesions (tumor, chronic meningitis), the distinction may be more difficult, and is then based chiefly on the fact that in these cases there are usually evidences of involvement of other parts than the tongue, lips and pharynx, (face, arm, leg) — that there is in fact, or has been, a double hemiplegia. Another point of distinction is that in these cases there is no atrophy of the lips and tongue, and that reflex action of the pharynx is never impaired. But these are not absolute criteria. General Paralysis of the Insane (Paretic or Paralytic Dementia). — The symptoms of general paralysis of the insane are exceedingly varied, but in all cases there are present evidences of both mental and physical de- rangement. Sometimes the mental symptoms, sometimes the physical symjjtoms, are the first to appear. Either set of symptoms may be especially obtrusive during the 398 DISEASES OF THE NERVOUS SYSTEM. course of the disease, or both sets may be equally conspicuous. The mental symptoms that are most characteristic are as follows : 1. Loss of mental power, as shown by defective attention, defective memory and early mental fatigue in the performance of ordinary duties. 2. Change in character, as shown by irritability, in- difference to the wants or sufferings of others as well as to personal interests, defective will power, with partial or entire loss of moral sense. 3. Unsystematized and varying delusions, especially delusions of grandeur, in which the patient believes him- self to be some celebrated personage (^.^., Napoleon, Cassar, Christ), or to be possessed of enormous wealth, or of great personal strength, etc., etc. These exaggerated and vari- able personal delusions are not usually present during the earliest periods of the disease, but are rarely absent after it has become established. They are always associ- ated with, and generally preceded by, a period in which the patient has an exalted sense of well-being, which, when present, is highly characteristic. Side by side with these mental changes are developed a series of physi- cal phenomena of which the most distinctive are as fol- lows : 1. Hesitating and monotonous speech with a tend- ency to slur the endings of words. 2. Tremor on voluntary movement, especially marked in the upper extremities and in the lips during articula- tion ; fibrillary tremor in the tongue when protruded, and in the muscles of the face during speech or during excitement. 3. Pupillary changes, especially marked inequality, myosis and loss of light reaction. THE DIAGNOSIS OF CLINICAL TYPES. 399 4. Exaggeration of the wrist-, elbow-, and knee-jerks. The symptoms above enumerated are very constant, the majority of them making their appearance in all cases of general paralysis. In addition to these there are others of considerable importance that are much less constant, but are liable to make their appearance at almost any period of the disease. These symptoms are both menta,l and physical, and comprise the following phenomena : 1. Melancholia or hypochondriasis. These are usu- ally early symptoms. 2. Maniacal outbreaks. 3. Sudden epileptiform attacks. 4. Apoplectiform seizures characterized by sudden loss of consciousness and hemiplegic symptoms. In a small proportion of cases the symptoms of posterior sclerosis are combined with the symptoms of general paralysis {vide p. 433). In such cases the knee-jerks are lost instead of being exaggerated, there are lightning pains, and ataxia is a prominent symptom. General paralysis, like other progressive degenerative diseases, is not uniformly progressive. Periods of remis- sion, often of considerable duration, alternate with periods of progress, but there are great differences in the duration of the disease (one to five years). In all cases where death does not occur from the acute episodes of the disease (apoplectic attacks), or from intercurrent disease, their termination is in complete dementia and physical help- lessness. In a fully developed case of general paralysis there are practically no difficulties in diagnosis ; the con- spicuous mental failure and characteristic expansive delu- sions, in combination with tremor, speech disturbance, etc., make the nature of the disease only too evident. In the early stages of the affection the case is very differ- ent ; the symptoms may be so equivocal that a positive 400 DISEASES OF THE NERVOUS SYSTEM. diagnosis is not possible. The conditions with which general paralysis may be confounded are : (i) neurasthe- nia, (2) chronic alcoholism, (3) chronic meningitis, (4) tremor, (5) senile dementia, and (6) the sequelae of sun- stroke. The diagnosis from neurasthenia may be impos- sible at an early period, but a diagnosis can generally be made when the patient is first seen by the physician. In neurasthenia there may be some mental failure — loss of memory, defective attention, etc., and there may be tremor in the upper extremities, but the mental failure is never so considerable in degree as in general paralysis, and the patient is not only conscious of its existence but exaggerates its importance, while in general paralysis he is only rarely cognizant of the existence of any mental weakness. The neurasthenic is able to concentrate his attention sufficiently to write correctly at dictation. The general paralytic is frequently unable to do this ; he omits letters or transposes them in a way that indicates defective attention, although he may be making a pronounced effort to write correctly. If in addition to mental weakness and irritability there is speech disturbance and tremor on movement of hand and lips, there is a strong presumption that the condition is general paralysis and not neurasthe- nia, and this is true a fortiori, if there is evidence of delusions or if there are immobile pupils. Hydrocephalus (Dropsy of the Brain). — The word hydrocephalus is employed to designate an accumulation of serous fluid within the skull. When the accumulation is in the arachnoid space the condition is termed external hydrocephalus ; when within the ventricles, internal hy- drocephalus. Hydrocephalus may run an acute or chronic course, may be congenital or acquired, and may be ap- parently primary or distinctly dependent on some other morbid process. THE DIAGNOSIS OF CLINICAL TYPES. 40I Acute Hydrocephalus is usually dependent on meningitis, and owing to the frequency with which some degree of serous accumulation accompanies cases of meningitis the terms acute hydrocephalus and meningitis have been used synonymously. Clinically acute hydrocephalus is of secondary importance to the meningitis on which it depends and of which it is merely one symptom. The serous effusion depends, in acute hydrocephalus, on in- flammation of the pia, ependyma and choroid plexuses. Chronic External Hydrocephalus is a condition of little clinical interest and may be passed by. Chronic Intei'nal Hydrocephalus, on the other hand, is a condition of fre- quent occurrence and considerable importance. It occurs as a congenital and as an acquired condition. Congenital internal hydrocephalus develops during intra-uterine life. After birth the cranium enlarges rapidly, the face remain- ing of normal size. The fontanelles become large and prominent, the sutures separate widely and the cranium attains a characteristic globular form. There is usually much mental defect. Death usually occurs after a few- months, but in some instances the process becomes sta- tionary and the patient reaches adult life, though with considerable mental weakness and perhaps disorders of motion. The acquired form of chronic internal hydrocephalus usually occurs without known cause. Sometimes, how- ever, it is apparently secondary to a morbid process which causes effusion mechanically by the obliteration of the openings ' through which the ventricular fluid ordinarily passes. Tumors, chronic syphilitic meningitis and acute ' It is thought that closure of the openings in the membrane closing the fourth ventricle from the subarachnoid space is the most import- ant mechanical cause of hydrocephalus, Ijut the entire subject of causa- tion is involved in obscurity. 26 402 DISEASES OF THE NERVOUS SYSTEM. meningitis are the chief conditions by which this result may be brought about. Both primary and secondary forms of acquired chronic internal hydrocephalus occur in chil- dren and in adults. In children the symptoms are much the same as in the congenital form. In adults there are no distinctive symptoms. A positive diagnosis of hydrocephalus can be made only in cases where there is decided and progressive en- largement of the cranium, and in such cases there is rarely any diagnostic difficulty. When the enlargement of the cranium is not considerable hydrocephalus may be con- founded with the enlargement of the head that occurs in rickets. The head in hydrocephalus has a globular form, and the fontanelles are always tense. In the typical rachitic head the cranium has a pyramidal shape, there is no bulging of the fontanelles and other evidences of rickets are plain enough. It must not be forgotten, however, that many cases of rickets are associated with hydrocephalus,— the nature of the relation between the rachitic and the hydrocephalic process being but imper- fectly understood,— and cases occur in which it is difificult to determine the true character of the head enlargement. The most important indication of a hydrocephalic process is the rapidity of the cranial enlargement and the existence of a bulging fontanelle. When the bones are firmly united, as in adults, the diagnosis of hydrocephalus is extremely difficult and usually impossible. A positive diagnosis is possible only in the rare cases in which there is distinct enlargement of the head and separation of the sutures. But in the absence of such enlargement hydrocephalus may perhaps be suspected if mental weakness, somnolence, coma, convulsions, loss of power, etc., follow very slowly on one or more attacks of acute meningitis. In very rare instances general thickening of the cranial bones may be THE DIAGNOSIS OF CLINICAL TYPES. 403 confounded with the enlargement of the head that occurs in hydrocephalus. External and internal hydrocephalus may sometimes be distinguished by the introduction of an exploring syringe and the withdrawal of fluid in the former case from the arachnoid space, in the latter from the ventricles, but even this method is not infallible. Diseases of the Spinal Cord. Spinal Meningitis. — The individual symptoms of spinal meningitis vary considerably in distribution, ac- cording to the position of the disease, and in their char- acter, according to the acuteness of the process. In most cases there are present certain local symptoms, as pain, spasm, rigidity, hypersesthesia, anaesthesia, motor paraly- sis, etc., and it is convenient to think of these symptoms according as they are due (i) to irritation of the mem- branes, (2) to irritation of the nerve-roots, (3) to com- pression of the nerve-roots, or (4) to compression of the cord. The chief symptom of irritation of the inflamed membranes is pain in the back, usually constant and in- creased by movement. The chief indication of irritation of the nerve-roots are radiating pains and hypersesthesia from irritation of sensory (posterior) roots, and rigidity and spasm or contractures from irritation of the motor (anterior) roots. When the nerve-roots are compressed instead of irritated, there are analgesia and ansesthesia instead of pain and hyperaesthesia, and muscular paralysis and relaxation in place of rigidity and spasm. If the compression of the nerve-roots is considerable there are trophic changes (atrophy) in the muscles paralyzed, with loss of reflex action. The symptoms of involvement of the cord by pressure resemble those of a transverse lesion of the cord {vide page 245) : paralysis of motion and 404 DISEASES OF THE NERVOUS SYSTEM. sensation below the level of the lesion, increased reflex action, etc. It is convenient to distinguish the following clinical forms of spinal meningitis : (i) External meningitis, (2) Internal meningitis, (a) Acute, [d) Chronic. External Meningitis i^^xttmaX Spinal Pachymeningitis). — External meningitis is probably secondary, in all cases, to adjacent disease, and the particular form of disease to which it is almost invariably secondary is caries of the spine (Pott's disease). The symptoms of the disease vary considerably, ac- cording as the process runs an acute or chronic course, and also according as the symptoms of caries (its usual cause) are obtrusive or inconspicuous. In acute cases the symptoms of external pachymenin- gitis closely resemble those of internal meningitis {vide internal meningitis). In such cases the following are the chief indications of the disease : 1. Pain in the back, increased by movement. 2. Rigidity of the muscles of the spine. 3. Radiating pains in the extremities, with or without spasm. 4. Hypersesthesia of the skin. 5. Fever, often considerable in degree. These symptoms may exist alone, or may be combined with symptoms of pressure or inflammation of the cord itself, especially paraplegia or paraplegic weakness, and excessive reflex action in the lower extremities when the pressure is above the lumbar enlargement. The symptoms indicating a more chronic process dif- fer from those above enumerated chiefly in the absence of considerable fever and in the less obtrusive character of the irritative symptoms, especially muscular rigidity THE DIAGNOSIS OF CLINICAL TYPES. 405 and spasm. In very chronic cases there are no distinc- tively meningitic symptoms. The symptoms are those of the bone disease. The distinction of external menin- gitis from internal meningitis is impracticable from the symptoms alone. In order to establish the diagnosis it is necessary to consider the etiology of the affection with much care, with a view to discovering evidence of a condition to which the meningitis may be secondary. The presence of caries of the spine makes the diagnosis certain ; but as it is easy to overlook the slighter evi- dences of such disease (local tenderness, irregularity of the spines), caries cannot be positively excluded unless the spine has been repeatedly and carefully examined. In the majority of cases of external meningitis the evi- dences of caries are sufficiently distinct to enable the diagnosis of the character of the meningeal affection to be made ; in a few cases only is the diagnosis impos- sible. Acute Internal Meningitis. — The symptoms that point to the existence of acute internal meningitis are essen- tially those of the acute form of external meningitis already described (p. 403) : pain in the back, rigidity of the muscles of the spine, radiating pains in the extrem- ities, with hypersesthesia, and spasm brought on espe- cially by movement. The onset of these symptoms is acute, and is generally attended with fever, sometimes by rigors. The grouping of the symptoms enumerated varies with the situation of the disease. When the meninges of the lumbar region are chiefly involved, the pain and spasm and hypersesthesia are confined to the lower extremities. When the dorsal meninges are chiefly affected, the symptoms extend to the muscles and skin of the trunk. When the cervical meninges are the seat of the disease the symptoms affect the arms, and there 406 DISEASES OF THE NERVOUS SYSTEM. may be bulbar symptoms, as dyspnoea and difficult swallowing. Acute internal spinal meningitis may be complicated by cerebral meningitis, or the symptoms of cerebral meningitis may precede those of the spinal disease. The symptoms indicating extension to the cerebral meninges are vomiting, headache, delirium and paralysis of cranial nerves {vide acute meningitis). The character of the inflammation, whether purulent or tubercular, does not entail any distinctive difference in the character of the symptoms. The duration of the acute symptoms varies from a few days (severe cases) to several weeks. In cases that recover, or in which death does not occur early, the symptoms grow gradually less acute. This subacute stage may endure for months, and may pass into a chronic stage. The etiology of acute internal spinal meningitis does not usually give much help in the diagnosis of the affec- tion. The disease may follow exposure to cold, over- exertion, trauma, sunstroke, acute febrile diseases, septi- caemia, etc., but the influence of some of these factors is uncertain, and all of them are related to many other con- ditions of the nervous system besides meningitis. The principal affections of the nervous system from which acute internal spinal meningitis must be distinguished are acute myelitis, cerebro-spinal meningitis, meningeal hemorrhage and tetanus. In acute myelitis paraplegia occurs early ; in meningitis it is absent, and there is at first little or no motor weakness of any kind. Moreover, the spasm of the limbs and pain in the back, which occur in meningitis, are not present, although there is often rigid- ity of the limbs in the later stages of myelitis if the lesion is above the lumbar enlargement. When meningitis and myelitis coexist, the decision into which category the THE DIAGNOSIS OF CLINICAL TYPES. 407 condition belongs must depend on the greater obtrusive- ness of the cord symptoms on the one hand, or of the meningeal symptoms on the other, and upon the order in which these symptoms have made their appearance. The distinction from meningeal hemorrhage is given under this disease (p. 409). The diagnosis from tetanus depends on the occurrence in meningitis of fever at the onset, and of marked sensory symptoms, and on the occurrence in tetanus of trismus and the ready excitation of spasms by peripheral impressions. Chro7iic I?iternal Meningitis. — The symptoms of chronic internal meningitis, like those of acute internal meningitis, depend on meningeal irritation, on irritation and pressure of the nerve-roots, and on damage to the cord itself. The character of the symptoms varies much in different cases, according as one or other of these mechanisms in the production of the symptoms is pre- dominant. In the majority of cases the following are the symp- toms observed in chronic internal meningitis : At first — I. Pain or discomfort in the back. 2. Stiffness of the muscles of the back (retraction of the head when the meningitis is cervical). 3. Radiating pains in the arms, legs, or trunk, accord- ing to the position of the disease. 4. Hyperaesthesia. Followed by — 5. Loss of sensation in the regions for- merly hyperassthetic. 6. Weakness in the muscles formerly rigid, with atrophy. 7. Diminished pain. 8. Symptoms of compression of the cord {vide p. 420). In cases where the process of disease affects mainly the pia mater (chronic leptomeningitis), the symptoms that 408 DISEASES OF THE NERVOUS SYSTEM. are due to meningeal irritation are especially conspicu- ous, /. only, the disease is probably cortical. Cortical disease may, however, cause partial and strictly uni- lateral facial paralysis. If the spasm appears due to cold or to neuralgia, there is probably functional derangement of the nucleus. If there is no apparent cause for the 480 DISEASES OF THE NERVOUS SYSTEM. spasm, or if it appears related to mental influences (emo- tion, etc.), the disease (nutritional) is probably in the cortical cells or perhaps in the cells of the facial nucleus. Paralysis of the Glosso-Pharyngeal Nerve. — The ninth nerve seldom suffers alone and the symptoms of its iso- lated paralysis are not definitely known. Probably it causes loss of sensibility and partial loss of power in the upper part of the pharynx. The nerve is not rarely dis- eased in company with other cranial nerves, and is espe- cially apt to suffer in disease of the nerve-roots of the medulla (tumor, meningitis). Paralysis of the Pnemnogastric Nerve. — Owing to the varied distribution of the tenth nerve disease involving it may give rise to many different symptoms, according to the position and nature of the morbid process. Generally speaking, the chief symptoms of paralysis of the nerve are (i) paralysis of the larynx, (2) increased frequency of the pulse, and (3) retardation of respiration. With these symptoms of paralysis may be associated the symp- toms of irritation of the tenth, of which the chief are (i) laryngeal spasm, and (2) vomiting. Some of these symptoms have been sufficiently described elsewhere (see Laryngeal Paralysis, Laryngeal Spasm, Cheyne-Stokes' Respiration.) It is necessary to mention here only two other results of pneumogastric derangement, paralysis of the pharynx and spasm of the pharynx. Paralysis of the pharynx is shown by the inability of the patient to swal- low food, which, when placed in the pharynx remains there. Pharyngeal paralysis may result from disease of the nuclei of the tenth, or from disease at the base (menin- gitis, tumor), involving the roots at the side of the medulla, and sometimes from diphtheric neuritis. Unless the pha- ryngeal nerves are involved on both sides the difficulty in swallowing is slight. THE DIAGNOSIS OF CLINICAL TYPES. 48 1 Spasm of the pharynx never results from organic disease. In some cases of hysteria it is associated with a sensation as of a large mass in the pharynx, known as the " globus hystericus." Its nature is readily recognized by the existence of other hysterical symptoms. The spasm is of short duration in these cases. Pharyngeal spasm is also seen in some cases of hydrophobia. The diagnosis of the exact position of the lesion which causes vagus paralysis depends largely, as in many other cranial nerve paralyses, on the associated conditions. The roots of the nerve at the side of the medulla and the branches of the nerve are much more often the seat of disease than the trunk of the nerve. If the lesion involves the roots at the side of the medulla, there are the signs of implication of other nerves, especially the hypoglossal. The recurrent laryngeal nerves are the branches of the vagus most often involved, and the symp- toms attending their disease have been already described (see p. 117). The causes of damage to the vagus are nu- merous. Disease of the nucleus, which is usually bilateral, may be either softening, hemorrhage, or degeneration, and in most cases is associated with the signs of involvement of adjacent nuclei in the medulla. When the nerve is injured at the side of the medulla the lesion is com- monly meningitis or tumor, sometimes vertebral aneurism. The trunk of the nerve is damaged occasionally by wounds of the neck, sometimes inflicted during surgical operations ; sometimes the trunk is compressed by new growths of the neck, enlarged nodes, etc. The recurrent laryngeal is often compressed by aneurism (especially on the right side) within the thorax, and sometimes by cheesy nodes or new growths in the chest. The diagnosis in such cases is greatly aided by the presence of physical signs of thoracic disease, but sometimes such signs are absent 482 DISEASES of' the NERVOUS SYSTEM. and the diagnosis is difficult. Neuritis of the vagus is the lesion in some cases of diphtheritic paralysis (which is very apt to involve the vagus) and in the cases of loco- motor ataxia in which laryngeal " crises " occur. It is said that in rare instances exposure to cold may cause symptoms of vagus derangement from neuritis of the trunk. Paralysis of the Spinal Accessory Nerve. — Paralysis of the " accessory " portion of the eleventh nerve (see Anat- omy) gives rise to paralysis of the larynx, (see p. 117) and need not be considered here. Paralysis of the " spinal " portion of the nerve, which supplies the sterno-mastoid and trapezius muscles, causes characteristic symptoms dependent on the loss of function of these muscles. Each sterno-mastoid muscle by its contraction rotates the face towards the opposite side, while it draws down the head to the side on which it contracts. If one sterno-mastoid muscle is paralyzed it produces little or no effect on the position of the head or in its movements, as the loss is compensated by other muscles. The de- fective rotation to the opposite side may, however, be easily determined. The unparalyzed muscle may incline the head to the side opposite the paralyzed muscle, by its contracture. The fact that mere paralysis of the sterno-mastoid causes no deformity when the head is at rest is of some practical importance. When both sterno- mastoids act they support the head in the anatomical position, and when the head is put back they together draw it forward. Paralysis, therefore, of both sterno- mastoids makes it very difficult for the patient to bring forward the head when it falls back. The sterno-mastoid atrophies when it is paralyzed. The trapezius consists of three portions, an upper, a middle, and a lower portion. Disease of the eleventh THE DIAGNOSIS OF CLINICAL TYPES. 483 causes paralysis of the upper part and partial paralysis of the middle part. The upper part is used mainly dur- ing respiration, and its paralysis is shown chiefly by a sinking in of the muscle which causes a change in the contour of the neck, especially marked during deep respiration. Paralysis of the middle portion of the trapezius (which elevates the scapula and the shoulder, and rotates the scapula with the lower angle out), causes a dropping of the scapula and shoulder and a rotation in of the lower angle of the scapula, with defective elevation of the arm. This middle part of the trapezius is, how- ever, only partially paralyzed in spinal-accessory disease. The parts affected waste and show altered electrical reactions, which vary with the character of the disease causing the paralysis. Bilateral trapezius paralysis causes a falling forward and sinking of the head, the chin resting on the sternum. The precise distribution of the paralysis of spinal accessory disease varies with the position of the lesion. When disease (usually degenerative) involves gray matter from which the spinal accessory arises, the paralysis is never confined to the sterno-mastoid and trapezius, and the affection is bilateral (see Bulbar Paralysis). The entire trapezius is usually involved in degenerative disease of the gray substance. When the nerve-trunk is the seat of the lesion, the paralysis involves the sterno-mastoid and the upper part of the trapezius. If the spinal accessory nerve is damaged in its course within the skull, both portions of the nerve (spinal and accessory) may be involved. There is then paralysis of the larynx on the side of the lesion, in addition to the muscular paralyses that characterize spinal accessory disease. With these symptoms there may be associated paralysis of one half of the tongue, owing to the proximity of the eleventh and 484 DISEASES OF THE NERVOUS SYSTEM. twelfth nerves. Paralysis of the palate (levator palati) on the side of the lesion is sometimes seen in these cases, and may depend on disease of the eleventh or perhaps on disease of the twelfth nerve. When the eleventh nerve is damaged, as is sometimes the case, after it has passed through the sterno-mastoid, the paralysis is confined to the trapezius. Spasm of the Muscles Supplied by the Spinal Accessory Net-ve (" Wry-Neck," " Torticollis ").— The term " wry- neck " is applied to several different affections in which muscular contraction produces an abnormal position of the head. In some cases the unnatural position of the head depends on persistent shortening of a muscle (usu- ally the sterno-mastoid). Such cases are usually con- genital, and this form of wry-neck is known as congenital or fixed wry-neck. In other cases, which are of much greater importance from a diagnostic point of view than the congenital cases, the unnatural position of the head depends, not on muscular contraction, but on some quite different condition — usually on caries of the upper cer- vical spine. Such cases are sometimes spoken of as cases of " false wry-neck." In a third class of cases the devia- tion of the head is due to muscular rheumatism (acute myositis), and the tender muscles are the most important cause of the unnatural fixation of the head. In other cases still wry-neck is produced by hysterical spasm. None of these cases will be considered here except in so far as they are liable to be confounded with true wry-neck. Spasmodic or True Wry-Neck depends on active spasm, usually of the muscles supplied by the spinal accessory nerve. The cause of this spasm appears to be a peculiar instability in the nerve-cells (cortical or spinal) that con- trol the muscles involved. In no case has an organic lesion been detected as the cause of the condition. THE DIAGNOSIS OF CLINICAL TYPES. 485 The distribution and character of the spasm vary in different cases. Several muscles are usually affected, most often the sterno-mastoid and trapezius (upper part) of the same side. Not rarely the spasm involves also the splenius, and occasionally the scaleni and platysma myo- ides are included. Sometimes the spasm, which has a ten- dency to extend, includes other muscles than those of the neck, as the muscles of the face, jaw, or arm. Occasionally the spasm is limited to one muscle of the neck, which is almost invariably the sterno-mastoid, and in rare cases all the neck muscles participate in the spasm. Generally the spasm involves chiefly or exclusively the muscles of one side ; occasionally the muscles of both sides are about equally affected. Owing to such wide differences as these in the distri- bution of the spasm, and to similar differences in its degree, the resulting change in the position of the head varies much in different cases. The chief positions ob- served are as follows : {a) rotation of face to side oppo- site spasm and slight inclination of head to side of spasm, — dependent on spasm of one sterno-mastoid ; (3) rotation of face to side opposite spasm and great inclina- tion of head to side of spasm — dependent on spasm of sterno-mastoid and trapezius of one side ; (<:) extreme rotation of head to one side, dependent on spasm of sterno-mastoid of one side and of the splenius of the other — /. ^., the side to which the face turns ; (^) retro- flexion of head (" retrocollic " spasm), due usually to bilateral spasm of trapezii, splenii, and sterno-mastoid. Sometimes the spasm of torticollis is tonic, at others clonic, and sometimes clonic and tonic spasms occur together. The spasm varies in degree and character from time to time, and at times there may be short or long in- termissions, or the spasm may be continuous. The onset 486 DISEASES OF THE NERVOUS SYSTEM. of the spasm is usually gradual, rarely acute, and is often attended or preceded by pain. The muscles involved never waste, but may hypertrophy in time. Spasmodic torticollis is usually a disease of long duration and in severe cases persists during life with little change. . The diagnosis of spasmodic wry-neck is rarely difificult. Sometimes it is confounded with the false wry-neck already mentioned, when, as not rarely happens, the latter is among the earliest evidences of caries of the cervical spine. There are several points of distinction between wry-neck of functional origin and that which depends on vertebral disease, and error may always be avoided by bearing them in mind. In spasmodic wry-neck the face is turned to the side opposite the contracting sterno-mastoid muscle. In false wry-neck the sterno-mastoid is rigid on the side to which the face is turned. The former condi- tion is painless, except at the onset ; in the latter there is often pain, neuralgic in character, in the distribution of the sensory branches of the first and second cervical nerves over the occiput. Moreover, in the latter condi- tion this pain is greatly aggravated or induced by sudden pressure on the top of the head. Hysterical wry-neck differs from the true form in that the spasm rarely remains limited to the muscles of the neck, in its dependence on emotion, in its rapid onset, and in its occurrence in women under thirty years of age, before which time true wry-neck is very uncommon in females. Paralysis of the Hypoglossal Nerve. — The chief effect of disease of one hypoglossal nerve is loss of power in the tongue. When the tongue is at rest in the mouth, its base is a little higher on the paralyzed than on the un- paralyzed side. When the tongue is moved withiji the mouth, there is imperfect power of motion to the paralyzed THE DIAGNOSIS OF CLINICAL TYPES. 487 side ; but when the tongue xi, protruded, the tongue deviates to the paralyzed side, because it is pushed to that side by the fibres of the genio-hyo-glossus on the normal side In disease of both hypoglossal nerves the tongue cannot be moved in the mouth and cannot be protruded. In such cases there is very defective articulation. Paralysis of the tongue may result from disease any- where in the motor path to the tongue, disease between the cortex and the hypoglossal nucleus, disease of the nucleus, or disease of the nerve, in or out of the medulla. The associations of the paralysis give the data for the localization of the lesion which causes loss of power in the tongue. When the disease is in the upper segment of the motor tract to the tongue, — i.e., is supra-nuclear, the tongue paralysis is associated with hemiplegic weakness on the side of the paralysis. Whether this disease is situated in the hemisphere (including disease of lowest part of the third frontal convolution), in the crus, or in the pons, must be determined by other indications (see Localization, also Hemiplegia). When disease involves the nucleus, the paralysis is bilateral, owing to the close- ness of the nuclei to one another (see p. 59). There is also atrophy of the tongue in such cases, and generally paralysis of the lips. Nuclear disease is almost always degenerative (bulbar paralysis, rarely locomotor ataxia) in character, but may result from vascular lesions (hemorrhage, softening). If the hypoglossal fibres are involved within the medulla, there is usually, but not necessarily, paralysis of the limbs on the opposite side (crossed paralysis), owing to the contiguity of the nerve and the motor path. Both hypoglossals may be involved by a bilateral lesion. Vascular lesions or tumors may cause paralysis from disease of the fibres within the medulla. Disease of the hypoglossal at the side of the 488 DISEASES OF THE NERVOUS SYSTEM. ^ medulla is one-sided, and is accompanied by damage to the roots of the spinal accessory, which causes paralysis of the larynx and palate on the same side. Chronic syphilitic meningitis and new growths are the chief causes of such paralysis. The tongue wastes to some extent in disease of any part of the lower segment of the path to the tongue-nucleus, nerve, or path in the medulla between nucleus and nerve. Spasm of the tongue, causing its deviation to one side on protrusion is occasionally met with as a symptom of hysteria. It then is usually associated with other more distinctive signs of this disease, especially convulsion, but may occur apart from any other spasmodic symptoms. Paralysis of the Phrenic Nerve} — The consequence of paralysis of the functions of the phrenic nerve is in- action of the diaphragm. If the paralysis is unilateral the diaphragm does not descend on that side during inspiration, but the loss of movement is not considerable, as the other side of the diaphragm continues to act. When both phrenics are paralyzed the inaction of the diaphragm produces a decided effect upon respiration. The movement of the thorax is increased, but if the hand is placed on the abdomen below the ribs, the advance of the abdominal wall and the descent of the viscera which occurs during normal inspiration can no longer be felt. The phrenic nerve may be paralyzed from disease or injury of the spinal cord (most common cause), from damage to the roots of the nerve, and from disease or injury to the nerve trunk, either in the neck or thorax. When the paralysis depends on cord disease, it is bilateral, and other paralyses are associated with that of the dia- phragm. Compression and crush of the cord are the ' The phrenic nerve is derived from the third, fourth, and fifth cervical nerves. THE DIAGNOSIS OF CLINICAL TYPES. 489 most frequent causes of such paralysis. When the nerve trunk is the seat of the lesion only the diaphragm suffers and the paralysis is generally unilateral. The nerve may suffer in the neck from deep wounds, or in the thorax from tumors or aneurisms. Sometimes it is the seat of neuritis from cold or from diphtheria, and the paralysis may then be bilateral. In some cases of hysteria the diaphragm may be little used for a considerable period of time, the upper part of the thorax acting as when the diaphragm is paralyzed. Knowledge of this fact and the detection of activity of the diaphragm will avoid an error, but it may be necessary to observe for some time before forming an opinion. The movements of the diaphragm are arrested or diminished in some cases of diaphragmatic pleurisy, but the pain which accompanies this condition will serve to prevent an error in diagnosis. Paralysis of the Posterior Thoracic Nerve} — Damage to the posterior thoracic nerve results in paralysis of the serratus magnus muscle. The chief effects of this paralysis are : (i) rotation of the scapula on its vertical axis when the arm is put forward, with recession of the edge of the scapula from the thorax — so-called " winged scapula " (this is characteristic of serratus paralysis) ; (2) the lower angle of the scapula is rotated inward and upward when the arm is carried forward ; (3) the power of elevat- ing the arm above the level of the shoulder is greatly weakened. There is usually severe pain in the neck and shoulder during the development of the paralysis. The evidences of isolated serratus paralysis are so char- acteristic that an error in diagnosis is scarcely possible. The nerve is usually damaged in the neck, either by direct pressure of heavy angular objects on the shoulder or by ' This nerve is derived from the fifth and sixth cervical nerves. 490 DISEASES OF THE NERVOUS SYSTEM. violent muscular effort as in lifting a heavy hammer. Sometimes it is injured by a wound or contusion. In rare cases the paralysis follows exposure to cold. Isolated serratus paralysis is usually one-sided ; rarely it is bilateral. It is much more common in men than in women, and is generally on the right side. Sometimes the posterior thoracic nerve is paralyzed from disease of its cells of origin in the cord, as in progressive muscular atrophy and infantile paralysis, or crush of the cord. Other muscles than the serratus are then paralyzed and the nature of the affection is plain. Paralysis of the Supra- Scapular Nerve? — Damage to the supra-scapular nerve causes paralysis of the supra- spinatus and infra-spinatus muscles. The paralysis of the former gives rise to no obtrusive symptoms, but paralysis of the infra-spinatus causes a loss of outward rotation of the humerus. An important effect of this loss is the inability to carry the hand from left to right as in writing. There is seldom isolated paralysis of the supra-scapu- lar nerve, but it is not rarely affected together with the circumflex in consequence of dislocation of the head of the humerus. Paralysis of the Circumflex Nerve ' causes loss of power in the deltoid and teres minor muscles. The paralysis of the former is by far the more important. Its chief sign is inability to raise the arm. In some cases there is loss of sensation on the outside of the upper part of the arm over the muscles. The deltoid wastes, and this alters the contour of the shoulder. After a time trophic changes occur in the shoulder joint (the circumflex sends filaments to the joint), and adhesions may form. Paralysis of the circumflex nerve is easily recognized. It is impossible to ' This nerve is derived from the fourth and fifth cervical nerves THE DIAGNOSIS OF CLINICAL TYPES. 49 1 confound it with the loss of motion that is seen in anchylosis of the shoulder joint, if it is remembered that in the latter state passive motion of the arm moves the scapula as well as the arm. The circumflex nerve is often injured by falls on the shoulder and by dislocations of the head of the humerus. Rarely it is the seat of " spontaneous " neuritis. It is sometimes paralyzed with other nerves belonging to the brachial plexus (see Brachial Plexus, Diseases of) in a highly characteristic manner. Paralysis of the Musculo- Cutaneoits Nerve (External Cutaneous, Perforans Casserii) causes loss of power in the biceps and brachialis anticus muscles, the effects of which are unmistakable (loss of flexion of elbow — espe- cially marked when the forearm is supinated and the supi- nator longus cannot act as a flexor). There may or may not be anaesthesia on the outer half of the forearm in front and behind, and over the arm in its lower part and outer side. The musculo-cutaneous is rarely paralyzed by itself. Paralysis of the Musculo- Spiral Nerve^ in the vicinity of the brachial plexus causes loss of power in all the ex- tensors of the forearm and wrist and the supinators. Extension of the elbow is impossible, the wrist drops, and the fingers are flexed at their distal joints. The fingers can, however, be extended by the interossei and lumbricales if the first phalanges are flexed. Supination, though not entirely lost (the biceps being active), is greatly weakened. After a time the excessive flexion of the carpus leads to undue prominence of the carpal bones and the synovial sacs at the back of the wrist. When the damage to the nerve is serious there is in a few weeks a perceptible diminution in the size of the fore- ' This nerve comes from the fifth, sixth, seventh, and eighth cer- vical nerves. 49- DISEASES OF THE NERVOUS SYSTEM. arm, due to the atrophy of the paralyzed extensors, and the muscles present the RD in various degrees. If the damage to the nerve is in the middle of the arm the biceps is generally involved. The supinator longus escapes only in rare cases of musculo-spiral paralysis. The loss of sensation in the parts supplied by the mus- culo-spiral varies considerably in different cases. In actual division of the nerve above its cutaneous branches there is usually loss of sensation in the outer part of the arm (about one quarter its circumference) from the level of insertion of the deltoid to the external condyle of the humerus, and on the back of the forearm on the outer side above, fading into normal sensation in the lower third of the forearm. The skin on the dorsal surface of the hand is anaesthetic over the thumb and metacarpal bones of the thumb, index, and middle fingers. In many cases of musculo-spiral paralysis there is no anaes- thesia either in the hand or arm. Musculo-spiral jDaralysis is of frequent occurrence, the course of the nerve exposing it to various kinds of injury. High up the nerve may be damaged by the pressure of a crutch. Indeed, crutch-paralysis is usually due to mus- culo-spiral injury. The nerve is apt to be torn in cases of fracture of the humerus, and may be pressed upon by callus. The most common cause of the paralysis, however, is pressure on the nerve during sleep. The patient lies on a hard bed or on the floor with the arm under him and receiving his weight. The nerve suffers as it passes around the humerus about the middle of the arm. So often does this occur in patients who have fallen asleep after excess in alcohol that it is known as "Saturday-night paralysis," or " Sunday-morning paraly- sis," from the times at which the paralytic effects are usually detected. THE DIAGNOSIS OF CLINICAL TYPES. 493 It is necessary to distinguish musculo-spiral paralysis from some forms of multiple neuritis — notably from lead paralysis and alcoholic neuritis. In lead paralysis the mus- cles supplied by the musculo-spiral nerve are involved {vide Lead Paralysis), but the affection is almost invariably bi- lateral (though the two sides may suffer very unequally), and the supinator longus muscle is almost always ex- empted from the palsy. In musculo-spiral paralysis, on the contrary, the paralysis involves only one nerve (in rare cases a cause of musculo-spiral paralysis operates bilaterally), and the supinator longus is almost invariably included in the palsy. Moreover, the onset of lead palsy is gradual and the development of musculo-spiral paralysis is rapid or sudden. The cause of musculo-spiral paralysis is usually readily elicited. The distinction from alcoholic neuritis is usually extremely easy (see Alcoholic Neuritis). The bilateral character of the paralysis, its extensive distribution, and the alcoholic history will prevent error even when the paralysis affects chiefly the upper extremities. Paralysis of the Median Nerve? — Severe damage to the median nerve above its muscular branches causes loss of power in the flexors of the fingers (excepting the ulnar Half of the flexor profundus), in the pronators, in the flexor carpi radialis, in the two outer lumbricales, and in all the muscles of the ball of the thumb except the ab- ductor poUicis and the ulnar half of the flexor brevis pollicis. In consequence of this loss of power the ability to flex and pronate the forearm is greatly diminished but not abolished. Flexion at the wrist to the ulnar side is still possible by the action of the flexor carpi ulnaris ; pro- nation is feebly performed by permitting the weight of the hand to rotate the forearm after it has been supi- ' This nerve arises from all the roots of the brachial plexus. 494 DISEASES OF THE NERVOUS SYSTEM. nated, the supinator longus being capable only of pronating the arm to a position midway between supination and pro- nation. The thumb is extended and abducted in a char- acteristic manner, and cannot be brought in contact with the tips of the fingers. The second phalanges can no longer be flexed on the first, and in the first and second Diagram illustrating the area of ansesthesia in a case of injury to the median nerve. (Palmar surface.) FIG. 56. Diagram illustrating the area of anaesthesia in a case of injury to the median nerve. (Dorsal surface.) fingers there is also loss of flexion of the third phalanges. The first phalanges are flexed by the interossei. The characteristic distribution of ansesthesia which is observed in cases of injury to the median nerve is sufficiently well shown in the accompanying diagrams. The degree and extent of the ansesthesia vary much in THE DIAGNOSIS OF CLINICAL TYPES. 495 different cases. Sometimes there is no affection of sensa- tion whatever. In a case of severe damage to the median the appearance of the hand and forearm soon becomes highly characteristic. The forearm is much atrophied on the radial side in front, the wrist is inclined to the . ulnar side and perhaps hyper-extended, the ball of the thumb is greatly wasted, the head of the metacarpal bone is prominent, and the thumb is usually rotated out, so that its palmar surface is on a plane with that of the hand, as is the case in apes. The median nerve is often injured. It suffers most frequently just above the wrist-joint, where it is more superficial than in the rest of its course, and is readily divided. It may, however, be damaged in almost any part of its course. In the forearm it is not rarely injured in fractures of the ulna and radius. In the upper arm it is most often invaded just above the bend of the forearm. It is said to be in some cases the seat of primary neuritis. Very rarely it is injured by violent contraction of the pro- nator radii teres. Paralysis of the Ulnar Nerve. — When the ulnar nerve is divided or severely damaged above the origin of all its branches, there is loss of power in the ulnar half of the flexor profundus digitorum, in the flexor carpi ulnaris, in all the muscles of the little finger, in all the interossei, in the two ulnar lumbricales, in the abductor pollicis and in the inner head of the flexor brevis pollicis. When this paralysis has lasted some time (three or four weeks or longer), the action of the unparalyzed opposing muscles brings the hand into a very characteristic posi- tion. The wrist is slightly bent backwards and to the radial side of the forearm, by the action of the extensor carpi radialis, extensor carpi ulnaris and flexor carpi radialis. The hand is considerably thinner than normal 496 DISEASES OF THE NERVOUS SYSTEM. owing to the wasting of the interossei and the muscles of the little finger, which leave the metacarpal bone of that finger very prominent. There are depressions be- tween the metacarpal bones, but there is a particularly- marked depression on the radial side of the metacarpal bone of the index finger on the back of the hand, owing to the wasting of the first dorsal interosseus. The jDaralysis of the interossei leads to a deformity which is almost distinctive of ulnar paralysis. The fin- gers cannot be flexed at the first, or ex-tended at the second and third phalanges, and, in consequence of this, the opponents of the interossei (extensor communis digitorum) by their contracture over-extend the first pha- langes and flex the second and third. This deformity of the hand is known as the " bird-claw hand," or the "claw-like hand."' The deformity is especially marked in the third and fourth fingers ; the first and second are less affected because their lumbri- cales escape paralysis. This deformity occurs not only when the ulnar nerve is damaged high up above its mus- cular branches, but also in injuries at the wrist, though it is perhaps less extreme in the latter class of cases. The state of sensation in ulnar paralysis varies consid- erably ; in some cases there is no anaesthesia, in others, of severe damage to the nerve, the loss may be that in- dicated in figures 57 and 58 — a typical distribution of anaesthesia. The ulnar nerve is probably more often damaged than any other spinal nerve. It is frequently injured in wounds of the forearm, especially in wounds at the wrist, where the nerve is superficial. When the nerve is in- ' It is seen also in progressive muscular atrophy, where disease affects the cells of origin of the ulnar nerve before those of the mus- culo-spiral. THE DIAGNOSIS OF CLINICAL TYPES. 497 jured at the wrist it is generally above the origin of the dorsal cutaneous branch. Higher up in the forearm the nerve may be hurt by fractures of the ulna and radius. At the back of the elbow, just external to the olecranon, the nerve is very liable to suffer from wounds, and is occasion- ally injured by pressure or contusion. Long-continued Diagram illustrating area of anaes- thesia and position of fingers in a case of injury to the ulnar nerve. (Dorsal surface.) After Bowlby. Diagram illustrating area of anaes- thesia and position of fingers in a case of injury of the ulnar nerve. (Palmar surface.) flexion at the elbow sometimes suffices to cause ulnar paral- ysis. Sometimes paralysis arises in this vv^ay during sleep. The nerve is very rarely injured in the arm above the elbow. Sometimes the symptoms of an apparently spon- taneous ulnar neuritis are observed in persons in reduced health. 498 DISEASES OF THE NERVOUS SYSTEM. The diagnosis of ulnar paralysis is simple. Error may possibly arise in rare cases of disease of the cervical enlargement, in which the ulnar nerve distribution is chiefly affected. Other evidences of spinal cord disease are never wanting in these cases. Paralysis in the Distribution of Two or More Nerves of the Arm, and due to disease outside the spinal canal, is not very uncommon. Thus, the median and ulnar nerves not rarely suffer together in fractures of the ulna and radius, and in wounds at the wrist ; the musculo-spiral and ulnar, sometimes the musculo-spiral, ulnar and median, in fractures of the humerus ; and any or all of the nerves of the brachial plexus (usually including the circumflex) may be compressed or lacerated by dislocation of the humerus (especially sub-coracoid dislocation). Inflammation may ascend one nerve and, reaching the brachial plexus, spread to others ("ascending neuritis," "neuritis mi- grans"). Thus the ulnar may be implicated by an as- cending median neuritis ; and conversely, the median may be involved by an ascending ulnar neuritis. The original wounds are usually infected in such cases. In cases where nerves of the arm, and especially of the forearm, have been injured, and tendons and muscles have been injured with the nerves, it may be difficult to distinguish the effects of the nerve injury and the effects of injury to the tendons and muscles. This is because there is often considerable cicatricial change in muscles and tendons, leading to deformity, which may simulate closely that of nerve injury, and because certain of the most important signs of nerve injury, namely, changes in the irritability of muscles and nerves, may be obscured by the contraction that sets in. Even the most careful attention to every detail in the history and examination THE DIAGNOSIS OF CLINICAL TYPES. 499 of such cases may not enable the observer to arrive at a correct conclusion as to the extent and situation of the nerve damage. Non- Traumatic or Primary Brachial Neuritis is an uncommon condition in which the cords of the brachial plexus become the seat of an unevenly distributed inflam- matory process. The symptoms vary much in different FIG. 59. Diagram illustrating the area of anaes- thesia in a case of injury to the ulnar and median nerves. (Palmar surface.) FIG. 60. Diagram illustrating the area of an- aesthesia in a case of injury to the ulnar and median nerves. (Dorsal surface.) cases, according to the distribution of the neuritis and its intensity. The earliest symptoms are sensory in character, and include pain, parsesthesia and anaesthesia of irregu- lar distribution. The pain is usually referred to the shoulder ; sometimes also to the hand and fingers. These sensory symptoms may be followed by gradual 500 DISEASES OF THE NERVOUS SYSTEM. loss of power in certain muscles and muscular atrophy. The muscles suffer unequally and present various grades of RD, but rarely the complete form. Vaso-motor and trophic symptoms may occur but are only rarely very decided. This form of brachial neuritis appears to de- pend, in some cases, on exposure to cold or over-exertion. Its diagnosis is simple if its occurrence is borne in mind. ErUs Paralysis ( " Upper-Arm Type of Paralysis " ). — These names are given to a peculiar form of paralysis dependent on damage to the fifth and sixth cervical nerves at one point in the neck, just in front of the edge of the trapezius. The paralysis involves regularly the deltoid, biceps, brachialis anticus, and supinator longus, and sometimes the supra- and infra-spinati. There is often anesthesia on the outer side of the arm in the distribution of the circumflex and external cutaneous nerve ; there is usually considerable muscular atrophy. The characters of Erb's paralysis differ considerably in adults and young children. In adults the paralysis is often complete, sensory symptoms are marked, and the affection is frequently of long duration. The cause of the paralysis in adults is usually a trauma, but sometimes the condition depends on the presence of a cervical tumor, and occasionally the paralysis develops without known cause. Erb's paralysis is probably much more often -seen in infants than in adults, but even in them it is an uncom- mon form of paralysis. It always depends, in infants, on pressure upon the neck, usually by the finger or hook, dur- ing delivery. Hence it is commonly termed " obstetrical paralysis. " " The severity of the damage to the nerves varies ' This term is sometimes applied to the facial paralysis that arises from the pressure of forceps, and to some forms of infantile cerebral palsy. A better name is " peripheral birth-palsy." THE DIAGNOSIS OF CLINICAL TYPES. 501 much in different cases. In the slighter cases of injury the paralysis may be unnoticed for some time after the birth of the child. In a well developed case the paralysis can hardly escape detection, and is so peculiar in distribution as- to assert its nature. The arm hangs by the side with the forearm in extreme pronation, or some power of elbow flexion may remain. Atrophy of the paralyzed muscles can- not be distinguished until several months after the dam- age, and may appear very slight even then, as it is masked by the large amount of fat over the muscles. Sensation is rarely impaired, and when it is the impairment may be with difficulty detected. The paralysis usually wears away in the course of a few months, sometimes in a few weeks. The peculiar distribution of the paralysis, and its occur- rence during delivery, if this can be established, make the diagnosis clear. Some care must be taken not to confound this condition with poliomyelitis ( vide p. 426), or with injuries to the shoulder-joint or muscles. The characteristic electrical reactions in the paralyzed mus- cles serve to distinguish Erb's paralysis from all con- ditions outside the nervous system. The nerves of the lower extremity are, on the whole, less frequently the seat of injury and disease than those of the upper extremity. Paralysis of the Obturator Nerve ' gives rise to loss of power in the adductors of the thigh, and to defective outward rotation of the thigh. The defective power of adduction renders the patient unable to cross the leg of the paralyzed side over the other leg. The obturator nerve is seldom paralyzed except from damage to the lumbar plexus. Occasionally, however, the nerve itself is damaged by pressure against the pelvis during delivery. ' Derived from the third and fourth lumbar nerves. 502 DISEASES OF THE NERVOUS SYSTEM. Paralysis of the Anterior Crural Nerve causes loss of power and atrophy in the extensors of the knee, and loss of knee-jerk from damage to the reflex arc. When the nerve is damaged within the pelvis the branch to the iliacus muscle is involved and there is impaired ' power of flexing the hip, as well as loss of extension of the knee. Paralysis of the anterior crural nerve causes also anaesthesia, which involves the entire thigh, with the exception of a strip of variable width along the back of the thigh (supplied by the sacral nerves) and the inner side of the leg and foot. The anterior crural nerve may be damaged in the thigh or groin, may suffer from pres- sure during parturition, or from dislocation of the hip, or may be involved by disease affecting the lumbar plexus. Paralysis of the Superior Gluteal Nerve ° causes loss of abduction and circumduction of the thigh, from paralysis of the gluteus minimus and medius. As an isolated paralysis, apart from affections of the plexuses, it is a very rare condition. Paralysis of the Sciatic Nerve causes symptoms which vary considerably with the seat of the lesion. Damage to the nerve is usually below the upper third of the thigh, and, if severe, gives rise to paralysis of all the muscles below the knee and anaesthesia of the sole and outer side of the foot and the outer side of the leg. The gait in such cases is much like that observed in many cases of poliomyelitis in children. If the lesion is above the middle third of the thigh the flexors of the knee and extensors of the hip are included in the paralysis. The sciatic nerve external to the pelvis may be damaged in ' Flexion is merely impai>-ed because the psoas is supplied by other lumbar nerves. " This nerve is derived from the lumbo-sacral cord. THE DIAGNOSIS OF CLINICAL TYPES. 503 wounds of the thigh, by disease of the femur, by adjacent tumors, and occasionally by dislocation of the hip. The nerve is often the seat of primary neuritis. Paralysis of the External Popliteal (Peroneal) Nerve causes loss of power in the tibialis anticus, extensor longus digitorum, extensor brevis digitorum and peronei, in consequence of which there is loss of flexion of the ankle and of extension in the first phalanges of the toes. The patient in such cases has " drop-foot," and in the course of time talipes equinus develops. In cases of severe damage to the nerve there is anaesthesia on the outei: half of the front of the leg, and on the greater part of the back of the foot. The external popliteal nerve is very superficial in its course, and passes over the fibula. It is consequently exposed to all kinds of injury — from wounds, from fracture of the fibula, from pressure, etc. It is also sometimes the seat of primary neuritis. Paralysis of the Internal Popliteal Nerve causes loss of power in the posterior tibial group of muscles (includ- ing the tibialis posticus and popliteus) and the long flexors of the toes, and in the muscles of the sole of the foot. Extension of the ankle-joint is impossible, and if the branch to the popliteus is involved there is loss of inward rotation of the leg when it is flexed. When the damage to the nerve is sufficiently severe to cause anaes- thesia there is loss of sensation over the outer part and posterior aspect of the lower part of the leg and on the sole of the foot. The posterior tibial nerve is rarely injured except in fractures of both bones of the leg. The branches of the internal popliteal nerve, the ex- ternal and internal plantar nerves, are rarely involved alone. Paralysis of the Exter^ial Plantar Nerve causes loss of power in the muscles of the little toe, the flexor acces- 504 DISEASES OF THE NERVOUS SYSTEM. sorius, the interossei, the two outer lumbricales, and the adductor of the big toe. Certain of these muscles (lum- bricales and interossei, abductor and flexor minimi digiti) flex the first phalanges, and extend the second and third, an action of much importance in walking, in the propul- sion of the body forward just before the foot leaves the ground. The loss of this action is a hindrance in walk- ing, as is the later contracture of the opponents of the interossei, which leads to flexion of the second and third phalanges. The sensory loss in cases of external plantar paralysis includes the skin of the outer half of the sole of the foot and of the little toe, and that of the adjacent half of the fourth toe. Paralysis of the Internal Plantar Nerve causes loss of power in the short flexor of the toes, the intrinsic muscles of the big toe (with the exception of the adduc- tor), and of the inner lumbricales. It gives rise also to anaesthesia on the inner part of the sole of the foot and the plantar surface of the three inner toes and the adjacent half of the fourth toe. Paralysis of the Small Sciatic Nerve causes paralysis of the gluteus maximus, with consequent interference with the power of rising from a seat and loss of sensibility in an area of variable size on the posterior surface of the thigh. The small sciatic nerve is damaged only in disease of the sacral plexus, and is seldom the only nerve involved. The Lumbar Plexus itself may be involved by abdom- inal tumors, enlarged nodes, or psoas abscess ; and caries of the lumbar spine may cause compression of the nerve- roots that make up the plexus. The plexus is usually irregularly invaded, some nerves suffering more than others. Sensory symptoms of an irritative character are often among the first symptoms of disease of the plexus. There is frequently severe pain in the course of the THE DIAGNOSIS OF CLINICAL TYPES. 505 genito-crural, ilio-inguinal, and ilio-hypogastric nerves. Later there may be anaesthesia of irregular distribution and loss of power in the distribution of the obturator and anterior crural nerves. The Sacral Plexus is liable to suffer from various forms of pelvic disease, especially pelvic tumors and pelvic inflammation. Occasionally it is compressed during delivery. Sometimes, also, it is the seat of primary neuritis. In other cases it is the seat of neuritis consequent upon extension of inflammation from the sciatic nerve. The symptoms of disease of the sacral plexus are usually at first irritative in character (pain, paraesthesia, etc.); later they are indicative of a destruc- tive process (anaesthesia, paralysis, atrophy, etc.). The precise distribution of these symptoms varies in different cases, and the various muscular and sensory dis- tributions of the different nerves arising from the plexus may be variously and unequally affected. The manifes- tations of disease of the plexuses are rarely confined to the distribution of any single nerve arising from them, although a single nerve (as the anterior crural) may for a time be the chief or exclusive seat of the symptoms. Plexus disease is almost invariably imilateral^ but in rare cases of pressure paralysis and spontaneous neuritis it is bilateral. The distinction of lesions of the lumbar and sacral plexuses from other forms of disease, especially cauda-equina lesions and certain forms of non-symp- tomatic neuralgia, is considered elsewhere. In all cases where plexus disease is suspected a careful rectal explo- ration is of the utmost importance and may reveal the presence of a pelvic tumor, an aneurism, or an abscess which exerts pressure upon the lumbar or sacral plexus. Tumors of Peripheral Nerves. — The chief forms of tumors of peripheral nerves have been already 5o6 DISEASES OF THE NERVOUS SYSTEM. mentioned (see 278). The diagnosis of a neuroma can be made with certainty only when the tumor can be felt. The presence of such a tumor may, however, be suspected in cases where pain, parsesthesia, anaesthesia, and loss of power come on slowly and grow progres- sively worse, and are limited to the distribution of one nerve-trunk. But there is no way of distinguishing, purely by the symptoms, the effects of damage by a neu- roma from the effects of pressure from an adjacent nerve, or even from the effects of neuritis. When the neuroma can be felt there arises the question whether it is a " false " or a " true " neuroma. If there are multiple tumors they are probably of the " true " form. False neuromata are, however, sometimes multiple, but in such cases they are generally of rapid growth. If the tumor appears to grow from the side of the nerve it is probably a " false " neuroma. The symptoms that characterize Lesions of the Cauda Kquina in general have been elsewhere touched upon (p. 251). There remain for consideration here certain clinical forms of Cauda disease dependent on the nature of the lesion — namely, compression and crush. Little need be said here regarding crush "of the cauda equina. It de- pends on injury from fracture and dislocation, usually of the upper lumbar vertebrae. The symptoms, which vary in severity in different cases, are of immediate on- set, and the nature and position of the surgical affection renders the localization of the damage perfectly evident. The question which arises in some of these cases as to the implication of the conus medullaris has already been discussed. Compression of the cauda may be of rapid or slow development. When of rapid development it always depends on injury — usually an injury which THE DIAGNOSIS OF CLINICAL TYPES. 507 causes fractirre - dislocation of lumbar vertebrae. In such cases there may be both crush and compression of the Cauda, and it is impossible to distinguish between these conditions. It is probable that in rare cases the Cauda is rapidly compressed by hemorrhage in the ab- sence of fracture-dislocation. When the compression of the cauda is slow, the diagnosis of the condition causing it is more difficult than in surgical cases, as all external indications are wanting. The only exception to this is where the compression depends on the pressure of a meningocele in spina bifida, the nature of the case being here sufficiently obtrusive. Slow compression of the Cauda usually depends on tumor within the spine. The symptoms differ considerably in different cases of tumor, and the number of cases that have been carefully studied is not yet sufficient to enable us to draw conclusions which fit all cases. The following may be regarded as the chief clinical characters of tumor of the cauda equina : 1. Severe pain in the region of the sacrum, persistent and increasing in intensity. Often the pain radiates down the back of the legs. The sacrum may be tender to pressure in the median line, and the spontaneous pain may be greatly increased during movement. This sacral pain is usually the first symptom of a cauda tumor. It may continue or pass away when anaesthesia is de- veloped. 2. The gradual development of anaesthesia of the peculiar distribution already described (p. 253), loss of control over the bladder (often very early) and rectum, gradual development of paralysis and atrophy in the legs, especially below the knee, and gradual but early loss of knee-jerks, perhaps first on one side. Some- times there are attacks of clonic spasm in the muscles of the legs. 508 DISEASES OF THE NERVOUS SYSTEM. 3. The symptoms are always bilateral and are gen- erally highly symmetrical. The accurate localization of the lesion in the cauda depends on a knowledge of the representation of various sensory and motor structures in the cauda, but an accu- rate diagnosis is sometimes impossible. The diagnosis of the nature of the tumor is usually impossible. When it is made it is upon general principles. Syphiloma, sar- coma, and cavernous angioma have been met with. Most cases of tumor of the cauda equina are progressive (one to three years), but in rare cases, apparently belong- ing to this category, they have retrogressed, or remained for a long time stationary. The points of distinction between tumor of the cauda equina and tumor of the spinal cord do not require special mention. They are sufficiently covered by the points of difference between cauda and cord lesions that have been touched on elsewhere (see Localization). There is,however, one disease of the cord which is liable to be confounded with a tumor of the cauda equina, namely, locomotor ataxia. Sharp radiating pains, parassthesia, involvement of the bladder, loss of knee-jerks, and impaired gait are com- mon to both. But in locomotor ataxia the pains are incon- stant, there is distinct ataxia, and pupillary symptoms are usually present early. The absence of ataxia and pupillary symptoms, and the presence of marked atrophy and dis- tinctive anaesthesia, are sufficient to prevent error if the possibility of confounding the conditions is remembered. There is usually no difficulty in distinguishing a tumor of the cauda from disease of the limb plexuses. In disease of the plexuses the symptoms are generally one-sided. Anesthesia, if present, is of irregular distribution. Tumor of the cauda equina, however, generally causes bilateral symptoms and the peculiar areas of anaesthesia THE DIAGNOSIS OF CLINICAL TYPES. 509 SO often mentioned. A rectal examination will sometimes clear up the diagnosis. Bilateral lumbo-sacral neuritis of primary origin may for some time cause symptoms that cannot be distinguished from a commencing cauda lesion. On the other hand, the symptoms of tumor may be for a time unilateral. In such cases it is necessary to wait for unequivocal symptoms to appear. Multiple Neuritis (Polyneuritis — Disseminated Neu- ritis). — The term "multiple neuritis" is used to designate a large and important class of cases in which several nerves become inflamed either at the same time or in quick succession. Broadly speaking, these cases resemble one another in the occurrence of motor, sensory, and trophic disturbances, but they differ so much in the degree, distribution, and course of their symptoms that it would not be profitable to study them as a single group. All the plans yet proposed for classifying cases of multiple neuritis are imperfect. Perhaps the least objection- able classification is that based on etiology (toxic form, infectious form, spontaneous form, etc.). For the present purpose, however, it is impracticable to adhere to any one classification ; it is preferable to study separately in their diagnostic relations the chief clinical types of multiple neuritis as they occur in practice. We may thus dis- tinguish the following forms of neuritis : (i) alcoholic neuritis, (2) diphtheritic neuritis, (3) neuritis from lead poisoning, (4) neuritis from carbonic oxide poisoning, (5) Beriberi, and (6) leprous neuritis.' To these varieties of ' This list comprises the most important forms of multiple neuritis. Many other kinds of neuritis (dependent on different causes) might be described, but most of these are not sufficiently distinctive or com- mon to require separate discussion. Some of them will, however, be touched on in connection with the diagnosis of the forms above enumerated. 5IO DISEASES OF THE NERVQUS SYSTEM. neuritis may be added a condition whose pathology is as yet unsettled, but which probably depends on multiple neuritis — acute ascending paralysis. Alcoholic Neui'itis. — The diagnosis of alcoholic multiple neuritis is based chiefly on a combination of motor symptoms of paraplegic type with obtrusive and rather characteristic sensory symptoms, the onset of the process being subacute, or, as is less often the case, acute. I. Sensory Symptoms. The sensory symptoms of alco- holic neuritis, though they usually develop hand in hand with motor paralysis, are often the earliest indication of the disease. They are chiefly irritative in character and consist at first of paraesthesias — as tingling, sensations of "pins and needles," rheumatoid pains, etc., in the ex- tremities — usually the lower extremities, sometimes the arms. These symptoms are soon succeeded by the fol- lowing manifestations : (i) Pain, sharp or burning, rarely dull, in the nerve- trunks of the affected extremities and often in the areas supplied by these nerves. The pain may be very severe. Occasionally it is slight. (2) Hypergesthesia (hyperalgesia) of the extremities. (3) Muscular tenderness. The muscles when pressed are very sensitive. This is a highly characteristic and common symptom of alcoholic neuritis. (4) Anaesthesia, partial loss of muscular sense and par- tial loss of pain and temperature sense. The anaesthesia may be confined to irregular areas of skin, or even to the distribution of a single nerve (as the ulnar). Generally it implicates a considerable part of the distal portion of the extremity. The sensory symptoms of multiple neuritis are sym- metrically distributed, the degree of symmetry being often very striking. THE DIAGNOSIS OF CLINICAL TYPES. 5 II II. Motor Symptoms. — Sensory symptoms are not long present before loss of power becomes associated with them. The paralysis usually commences in the legs but may begin in and be limited to the arms. Both legs are involved together or in rapid succession. The weakness is especially marked below the knees but usually extends to the thigh muscles. Often the paralysis extends to the upper extremities — first to the muscles of the hand, then to the forearm. The extensor groups of muscles are especially affected in both extremities, but often both flexors and extensors suffer in high degree. In the leg there is " drop-foot," in the upper extremity " wrist-drop." The bilateral drop-foot is as suggestive of alcoholic neu- ritis as is wrist-drop of lead neuritis. The paralyzed muscles are flaccid, become much atrophied, and show the RD. In rare cases there is double facial paralysis. Par- alysis of the sphincters is very rare, unless there is also myelitis. Associated with these motor and sensory phenomena are often the following conditions : ( i) Inco-ordination, usually slight in degree and con- fined to the lower extremities. Occasionally the inco- ordination is the most obtrusive symptom of the disease, being greatly out of proportion to the sensory and para- lytic phenomena. Such cases may closely resemble loco- motor ataxia, and are hence termed "pseudo-tabes." ( 2 ) Loss of myotatic irritability in the paralytic muscles. In the cases where the lower extremities are affected, the knee-jerk is lost early, even when there is only slight loss of power in the extensors of the knee. Cases occasionally occur, however, in which the knee- jerk is not lost at any time in the disease, probably because in these cases the extensors of the knee are not involved. 512 DISEASES OF THE NERVOUS SYSTEM. ( 3 ) Cerebral symptoms are seldom wanting in severe cases of multiple neuritis, and are especially constant in women. They comprise active delirium, with illusions and hallucinations, insomnia, loss of memory and gen- eral mental failure. These symptoms are not usually present until the disease is well established. They may, however, be present from the first, as when multiple neuritis develops during delirium tremens. ( 4 ) Trophic symptoms in the skin and nails of the paralyzed extremities are common, and resemble those observed in simple neuritis. When the onset of the disease is acute, there may be considerable elevation of temperature during the first weeks of the disease. The duration of the disease varies with the acuteness and severity of the process. In a moderately severe case of subacute development ( /. ^., a typical case as regards course ) the severity of the symptoms increases during a month or six weeks, and improvement in power does not begin until a month or six weeks more have elapsed. Some chronic cases run a very long and tedious course ( one to two years ). Ex- cept in mild cases, contractures are apt to remain over. The etiology of cases of alcoholic neuritis is an aid in the diagnosis of the condition, since a history of alco- holic excess is seldom wanting ( vide p. 293). Such a history is, however, not often necessary for a diagnosis ; the distribution of the palsy, the obtrusive and suggestive sensory symptoms and the escape of the sphincters suffice to indicate the nature of the case. But the diagnosis of the condition is not always so simple. There are three con- ditions with which the disease is readily confounded. These are poliomyelitis, transverse myelitis, and locomotor ataxia. Paralysis, muscular atrophy, RD, and loss of tendon THE DIAGNOSIS OF CLINICAL TYPES. 513 reflex occur both in alcoholic neuritis and in poliomyelitis. In the latter condition, however, sensory symptoms are absent ( except, perhaps, during the onset of the symp- toms ), the paralysis is unsymmetrical, if not unilateral ; there is some retrogression of the paralysis after the onset, especially if this be acute, and the development of the symptoms is fairly rapid if not acute. In alcoholic neuritis, on the other hand, sensory symptoms are obtru- sive, the paralysis is usually symmetrical and always progressive, and the onset is usually ( though not always ) gradual. The resemblance between some cases of alcoholic neuritis and locomotor ataxia is close. In both condi- tions there may be inco-ordination, loss of knee-jerks, sharp pains in the lower extremities, defective muscular sense, and great unsteadiness when the eyes are closed and the feet are close together ( Romberg's symptom). The chief diagnostic points are the following : In alco- holic neuritis there are no true lightning pains, the mus- cles are tender to pressure, there is distinct loss of power, atrophy and some degree of RD, bladder symptoms are absent, and the inco-ordination, if sufficiently marked to be confounded with that of locomotor ataxia, is distinguished by its rapid development in the early course of the disease. An occasional source of difficulty in diagnosis arises from the circumstance that locomotor ataxia may be complicated with severe neuritis. Whenever unequivocal symptoms of locomotor ataxia are associated with paral- ysis and muscular atrophy of limited extent, or with limited patches of anaesthesia and analgesia, it is safe to conclude that those symptoms depend on neuritis.' But ' The gastric and laryngeal crises of tabes probably depend on neuritis, but, of course, their occurrence gives rise to no question as to diagnosis. 33 514 DISEASES OF THE NERVOUS SYSTEM. cases occur in which localized sensory and motor dis- turbances are associated with symptoms that strongly suggest locomotor ataxia, but are nevertheless equivocal. The question arises in such instances : have we to deal with a case of alcoholic multiple neuritis, or with a case of locomotor ataxia, associated with severe neuritis ? If this question cannot be decided by means of the indi- cations that have been already mentioned, it may be necessary to wait an.d watch the course of the symptoms before reaching a conclusion. There is seldom any reason for confounding alcoholic neuritis and transverse myelitis. In myelitis involving the lumbar enlargement there is paralysis of motion and sensation in the lower extremities and loss of knee- jerks. But the motor paralysis in such cases shows no tendency to remain confined to the distal portion of the extremities ; the sensory symptoms differ from those of alcoholic neuritis in that they are largely indicative of destruction of nerve elements rather than irritation ; the sphincters are affected, and often there is a girdle- pain. In myelitis above the lumbar enlargement the knee-jerks are not lost, but are increased,' and this fea- ture alone serves to distinguish it from a neuritis involv- ing exclusively the lower extremities. In rare instances alcoholic neuritis is complicated by myelitis, and the bearing of such an occurrence upon prognosis renders its recognition exceedingly important. The following facts are to be borne in mind in consid- ering the possible existence of a complicating myelitis. During the time when a case of alcoholic neuritis is increasing in severity we cannot say positively that the lesion will not extend to the cord, and the question of ' In rare cases of acute myelitis above the lumbar enlargement the knee-jerks are temporarily lost. THE DIAGNOSIS OF CLINICAL TYPES. 515 exact localization can hardly be said to have arisen. When, however, the symptoms become stationary, the question may come up. If there is no improvement in the symptoms after they have remained stationary for a period of four months, it is highly probable that the cord is involved, or that the patient is still taking alcohol. Again, if additional symptoms make their appearance after the neuritic process has been stationary for a time, such a progression probably depends on myelitis, pro- vided the continued use of alcohol can be excluded. The symptoms which under these circumstances are par- ticularly significant are an increase of paralysis, rapid muscular atrophy, the replacement of parsesthesia by ansesthesia, loss of control over the sphincters, and the appearance of bedsores. The relation of alcoholic neuritis to the condition known as acute ascending paralysis is discussed in con- nection with the latter disease. Cases are not rarely met with in which there are numb- ness, tingling, pain, and slight ansesthesia in irregular areas of the hands. These cases occur usually in women about the time of the climacteric, especially in those whose general health is for some reason depressed, and whose hands are much exposed to the action of water. The patients are very commonly persons who do not use alcohol to excess. It is only necessary to be aware of the occurrence of this affection, which depends probably on a palmar neuritis, to avoid confusing it with the early stage of alcoholic neuritis. Lead- Neuritis. — The chief symptoms of neuritis from lead are localized muscular paralysis and atrophy and pains in the limbs. These conditions may be associated, or may occur separately. The most important and char- acteristic result of lead neuritis is the local paralysis. 5l6 DISEASES OF THE NERVOUS SYSTEM. Generally the paralysis affects the extensor muscles of the wrist and fingers and causes bilateral wrist-drop, a condition highly suggestive of lead neuritis. Usually the paralysis remains confined to the upper extremities, but it sometimes involves the muscles of the legs, espe- cially the long extensors of the toes and peronei. In the arm the deltoid not rarely suffers, and may suffer early. The biceps is also occasionally involved. A peculiarity of considerable diagnostic importance relates to the distribution of the palsy in the forearm muscles. In a very large proportion of cases of lead palsy two muscles of the forearm are exempt from the loss of power ; these are the supinator longus and the extensor ossis metacarpi pollicis. In the majority of cases of lead palsy from neuritis, the loss of power precedes the wasting of the muscles, and the muscles present the RD. In other words, the character of the palsy closely resembles that observed when a motor nerve has been involved in a traumatic lesion. But the type of lead paralysis is not always of this kind. Cases occur in which paralysis and atrophy of the muscles develop together, pai-i passu, and in which there is simply a gradual and proportional diminution of the irritability of the muscles to the faradic and galvanic currents. In these cases the paralysis may begin in almost any part of the extremities, but it is especially apt to begin in the small muscles of the hand. This form of local muscu- lar atrophy may be likened to that which is so character- istic of progressive muscular atrophy. It is important to recognize clearly the existence of these two types of paralysis from lead, for, though inter- mediate forms occur, the large majority of cases conform to one or other type. Moreover, it is probable that the two types of paralysis are referable to a difference in THE DIAGNOSIS OF CLINICAL TYPES. 517 the seat of the lesion. In the type which resembles the paralysis resulting from an injury of a peripheral nerve, the lesion is almost always confined to the peripheral nerves ; in the type which resembles progressive muscu- lar atrophy, there is often, and perhaps always, involve- ment of the ganglion-cells of the anterior horns of the spinal cord as well. Sensory symptoms in lead paralysis are usually slight, and may be entirely absent. Sometimes there is consid- erable pain in the limbs affected at the time of the onset of the symptoms. Muscular tenderness may be found also. Sometimes there is slight anaesthesia of the skin over the affected muscles. In cases of lead poisoning without paralysis there are often dull or sharp limb pains, dependent on slight neuritis, but not distinctive in character. The reflexes are lost in lead neuritis under the same conditions that cause their loss in alcoholic neuritis. The diagnosis of lead neuritis is usually easy. From alcoholic neuritis it is distinguished by the localization of the paralysis to the upper extremities, by the absence or trifling character of sensory symptoms, and by the pres- ence of other indications of lead poisoning, such as colic, the lead line on the gums, and ancemia. Cases of alcoholic neuritis occur, however, in which the paralysis is limited to the upper extremity, and in which the sen- sory symptoms are slight. In such a case the chief points of distinction from lead neuritis are the involve- ment of the supinator longus and extensor ossis meta- carpi pollicis and a distinct history of alcoholic excess. Sometimes an old-standing case of lead neuritis comes under observation in which there are contractures in the arms and legs, which have developed after slowly pro- gressive paralyses (including wrist-drop and drop-foot), and in which there is no history of lead poisoning. 5l8 DISEASES or THE NERVOUS SYSTEM. Unless some source of lead poisoning can be traced, the nature of such a case may not be recognized. The diagnosis from progressive muscular atrophy may be difficult in the cases already mentioned, which resem- ble this disease in the nature and distribution of the palsy. A history of lead poisoning or the detection of lead in the urine may be necessary before a positive diagnosis is made. The distinction between lead neuritis and musculo- spiral paralysis has been already considered (see p. 490). Arsenical Neuritis. — The symptoms that characterize arsenical neuritis resemble both thoee of alcoholic neu- ritis and those of lead neuritis. These symptoms are paralysis of the muscles of the limbs, especially of the extensors of the hand and feet, and inco-ordination, especially in the lower extremities. With these symp- toms there are usually marked sensory disturbances, in- cluding severe darting pains in the arms and legs and anaesthesia of the skin over the affected muscles. The knee-jerks are generally lost. The chief points of distinction between arsenical and lead neuritis are the usual onset of the former after acute arsenical poisoning, the greater severity of the sensory symptoms, and the involvement of the anterior tibial and peroneal groups of muscles in the leg in addition to the extensor paralysis in the upper extremities. In the cases that depend on chronic arsenic poisoning (as from the careless use of medicinal preparations of arsenic), the cause of the neuritis is usually sufiiciently evident. Where there is some doubt as to the nature of the case the presence of arsenic in the urine may deter- mine the diagnosis. The distinction of arsenical from alcoholic neuritis may be very difficult in the absence of a history of alcoholic excess. Here, again, the finding THE DIAGNOSIS OF CLINICAL TYPES. 519 of arsenic in the urine may clear up the nature of the case. Neuritis from Carbonic Oxide Poisoning. — This is a rare affection, the symptoms of which vary widely in different cases. In most cases there are obtrusive sen- sory and motor symptoms, and in many cases vaso- motor and trophic symptoms are also present. The sensory symptoms of carbonic oxide neuritis are numb- ness, partial loss of tactile sensibility and sometimes pain in the extremities — usually over the muscles that are the seat of paralysis. The motor symptoms consist of local paralyses of irregular and variable dis- tribution. In some cases the paralysis has the distribu- tion so often observed in alcoholic neuritis, causing double wrist-drop and drop-foot. Sometimes the paraly- sis is confined to a single nerve territory (ulnar, radial or peroneal paralysis).' The paralysis has been known to be hemiplegic in distribution. In other cases only the lower extremities have been involved. In one case all the muscles of the eyeball, intrinsic and extrinsic, were paralyzed. The vaso-motor and trophic symptoms of carbonic oxide neuritis include redness of the skin, oedema, changes in surface temperature and herpetic eruptions along the course of nerve-trunks. The recognition of carbonic oxide neuritis is usually easy, because there is generally a distinct history of exposure to the gas, which is developed in considerable quantities whenever coal or charcoal is burned in a space to which oxygen has imperfect access. In cities a common mode of poisoning by carbonic oxide gas is the inhalation of illuminating gas which has escaped ' There is some reason to think that the paralysis in some of these cases was due to pressure on a nerve-trunk during the period of un- consciousness which usually preceded the development of the neuritis. 520 DISEASES OF THE NERVOUS SYSTEM. into a closed room. A period of unconsciousness usually precedes by a few hours or days the symptoms of neu- ritis, but the loss of consciousness may be partial, and is sometimes entirely absent. The neuritic symptoms are often preceded or accompanied with pain in the hypocondriac region, shortness of breath, and dyspnoea on exertion. Transient mental symptoms, such as de- pression of spirits and loss of memory, are of common occurrence in the early stage of the neuritic affection, and are rather characteristic. These symptoms may persist for many months. Diphtheritic Neuritis. — The symptoms that indicate the presence of diphtheritic neuritis are usually highly char- acteristic. They consist chiefly of motor phenomena of peculiar distribution. The paralysis is of gradual onset and development in each part and usually involves in succession different and widely separated regions, so that recovery of power often goes on in the parts originally affected while the paralysis is invading other regions. The order in which the paralysis involves the affected parts varies in different cases. The paralysis usually be- gins in the palate, the loss of power being shown by the nasal tone of the voice and the partial regurgitation of food. The paralysis may not spread to other parts, but usually it soon involves the ciliary muscle of the eye and gives rise to loss of power of accommodation, with impaired vision for near objects. Very often at the time when accommodation is first impaired the loss of power extends to the limbs. The legs are usually involved be- fore and in greater degree than the arm. The paralysis is generally slight in degree and always bilateral. It is always of the atonic kind, the muscles being flabby and relaxed. With these characteristic symptoms there is associated THE DIAGNOSIS OF CLINICAL TYPES. $21 a symptom which is so constant as to be of much diag- nostic value. This is loss of knee-jerk. The loss occurs early in the disease, and is generally present even when the legs are not paralyzed. In severe cases of diphtheritic neuritis there are evi- dences of implication of the vagus — initial retardation of the pulse followed by irregular and rapid heart action. These symptoms have little diagnostic value, as more characteristic evidences of the disease usually precede them by a considerable time. The sensory symptoms of diphtheritic neuritis are gen- erally slight. Sometimes there are numbness, tingling, hyperaesthesia, and anaesthesia of the skin, usually at the extremities of the limbs that are the seat of paralysis. The development of paralysis of the palate and later of paralysis of accommodation and progressive weakness of muscles of the lower extremities constitute so distinctive a group of symptoms that their nature is always clear. There is, moreover, almost invariably the history of a throat affection not longer than a month before the onset of neuritic symptoms, and such a history removes any doubt as to the character of the affection. The diagnosis may be more difficult when the local evidences of diph- theria have been slight and the palate and eye symptoms have been slight and of transient duration. Any leg symptoms which exist in such a case may then appear to indicate disease of the spinal cord. The presence of ataxia and loss of knee-jerk may suggest locomotor ataxia, but the development of these symptoms is too rapid, and there is too little pain and too much weakness in the legs to permit an error to be made. From acute poliomyelitis diphtheritic neuritis is distinguished by the slower onset, the marked symmetry and slighter degree of the paralysis and atrophy, the slighter changes in the 522 DISEASES OF THE NERVOUS SYSTEM. electrical irritability of the muscles, and the presence of sensory symptoms. Bert-beri, Kak-ke} — These names are applied to cases, apparently of multiple neuritis, of widely varying severity and type, which occur in endemic or epidemic form along the coasts of Japan, Borneo, Ceylon, India, on the coast of Brazil, and along the Red Sea. Cases of the disease are occasionally seen in the United States, chiefly in Malayan and Chinese sailors or in travellers. The condition requires only brief notice here. The chief nervous symptoms of beri-beri are pains in the extremities, numbness, tingling, hyperaesthesia, and anaesthesia, associated with paralysis and muscular atrophy, chiefly of the lower extremities, but sometimes of the extensors of the forearm as well. In mild cases the development of these symptoms is gradual, and re- covery occurs usually in less than a month. In severe cases the symptoms are of rapid onset and soon reach a high degree of development. In some cases the nervous symptoms are most conspicuous, but in the majority of cases the disease is of the " hydropic " or " wet " type, in which the nervous symptoms are inconspicuous and a high degree of general oedema, serous effusion into the pleural and peritoneal cavities, and heart failure are the chief manifestations. In other cases still, also of the severe type, very marked nervous symptoms are associ- ated with the symptoms which characterize the hydropic ' There is still considerable question as to the cause of beri-beri. At present the most generally accepted view is that it is a contagious disease dependent on the entrance into the body, probably by the lungs, of a specific micro-organism. This view must, however, be accepted with caution. There are many facts which suggest that the disease may arise from an animal poison, which occurs in decomposed tunny-fish. THE DIAGNOSIS OF CLINICAL TYPES. 523 type and suggest a morbid blood-state, Paralysis of the diaphragm, probably from phrenic neuritis, is an early symptom in many of the severe cases of beri-beri. The distinction of this disease from other forms of mul- tiple neuritis is usually not difficult if the conditions under which it occurs are known, as it is only observed in the United States in persons who have recently been in the countries where the disease is epidemic' Leprous Neuritis (Anaesthetic Leprosy). — This condi- tion, which was formerly observed only in the countries where leprosy prevails (Sandwich Islands, India, Nor- way), is now occasionally met with in the United States. The chief manifestations of leprous neuritis are anaes- thesia, muscular atrophy and trophic changes, especially marked in the most distal parts of the extremities and of very gradual development. The anaesthesia is pre- ceded almost invariably by the appearance of a patch of hyperassthesia, commonly on the hand or foot. In these hyperaesthetic areas there is usually more or less spon- taneous pain of a burning character. Very gradually, usually after the lapse of many months, the hyperaes- thesia is replaced by ansesthesia. In some cases the loss of sensibility corresponds closely to the distribution of one or more nerve trunks ; more often the loss does not correspond accurately to nerve distribution. When anaesthesia is established there is usually some weakness and atrophy in the muscles of the part involved, the flexors of the hands and feet become the seat of con- tractions, and in consequence of the resulting deform- ities the patient becomes unable to use his hands or to walk. Both hands and both feet are usually thus in- ' A disease resembling closely some forms of beri-beri has been ob- served in Massachusetts fishermen who have returned from fishing trips, during which they have been on a diet chiefly of fish. 524 DISEASES OF THE NERVOUS SYSTEM. volved in from four to six years after the first symptoms of the disease. When the muscular atrophy is advanced other trophic changes make their apearance. An ulcer appears usually near the base of the big toe. This ulcer remains small, but after a time involves the joint of the toe. Then the bones of the toe become necrosed and the part eventually separates. In a similar manner the fingers and the remaining toes are gradually involved. The symptoms that have been described characterize the anaesthetic form of leprosy. Very often these symp- toms are associated with the appearance of small hard nodules on various parts of the body, and especially the face, and with fever (so-called " tubercular " form of lep- rosy) a combination of symptoms known as the " mixed " form of leprosy. The distinction of anaesthetic leprosy from syringo- myelia has been already touched upon (p. 464). Acuie Ascending Paralysis (Landry's Paralysis). — The designation acute ascending paralysis is employed both in a restricted sense and in a more general sense. In consequence of this difference in usage some confusion has arisen. Acute ascending paralysis, in the restricted sense, is a disease characterized by : (i) the rapid development of ascending paralysis (legs, then arms, diaphragm, neck, and sometimes palate) with fiaccidity of the muscles in- volved ; (2) loss of reflex action (including knee-jerks) in the muscles paralyzed ; (3) the absence of fever ; (4) the absence of a considerable degree of pain or sen- sory loss ; and by (5) the absence of muscular atrophy and RD in the cases which live long enough to have made the development of these conditions possible. As to the character of the lesion which gives rise to these symptoms, it is sufficient to say that nothing whatever is THE DIAGNOSIS OF CLINICAL TYPES. 525 at present known, and that there is as yet no sufficient reason for regarding any of the cases of this type as dependent on multiple neuritis.' In the wider sense of the designation, acute ascending paralysis includes, in addition to the well defined group of cases just mentioned, cases in which the loss of motor power has the same rapid development and ascending course as in those cases, but in which there are marked sensory symptoms (pain, paraesthesia, ansesthesia), RD, muscular atrophy, and, in some cases, affections of the sphincters, and fever. '^ There is good reason to believe that many of the cases which belong in this second group are instances of multiple neuritis,^ and it is certainly true that there occur undoubted cases of alcoholic neu- ritis, diphtheritic neuritis, and beri-beri, in which the symptoms are rapidly ascending in progress and run a quickly fatal course. It is sometimes very difficult to say whether a case is one of Landry's paralysis in the strict sense, or one of the cases that depend on a multi- ple neuritis. The points to be especially studied in such a case are the sensory symptoms, the state of nutrition of the muscles, and the electrical reactions. Another point of some importance is the fact that in multiple neuritis ' There is some reason to think that these cases may depend on the action of a toxic substance in the blood upon the fibrillary termina- tions of the upper segment of the motor tract, and upon the motor ganglion-cells of the cord with which these are connected. The rela- tion of some cases to acute specific diseases, and the enlargement of the spleen and lymph nodes sometimes observed, suggest the agency of a toxic substance. ^ The propriety of including these cases under Landry's paralysis is rather doubtful, but has been unquestioned by some writers of excel- lent repute. ' It has been thought that some of these cases are instances of mye- litis of a peculiar type, but there is little to support the view. 526 DISEASES OF THE NERVOUS SYSTEM. bulbar symptoms are usually slight or absent, while in acute ascending paralysis they are almost constant. Ex- tensive poliomyelitis, involving the lumbar, cervical, and bulbar centres may simulate acute ascending paralysis, but the early appearance of muscular atrophy and RD, and the absence of sensory symptoms sufficiently indi- cate the nature of the condition in such cases. Cases of acute ascending paralysis differ considerably in the rate of their progress. In many cases they end fatally within a week. Sometimes they run their course and terminate fatally within two days. In other in- stances the disease runs a course of two, three, or four weeks. Most cases that have been reported as instances of recovery from acute ascending paralysis have prob- ably been cases of multiple neuritis or myelitis. CHAPTER VI. THE DISTINCTION OF FUNCTIONAL AND ORGANIC DISEASE. The distinction of functional and organic disease of the nervous system constitutes a general diagnostic prob- lem of the highest importance. The object of correct diagnosis being accurate prognosis and rational treat- ment, it needs no argument to show how necessary is the clear separation of processes that involve actual de- struction or alteration of tissue, and limited power of repair, from those which consist in disorders of function .and nutrition with practically unlimited possibilities of recovery. The terms "functional disease" and "organic dis- ease " are commonly employed in the case of the nervous system, as with other parts, in an antithetical sense. We picture to ourselves, on the one hand, a class of morbid conditions in which the symptoms depend on demonstrable structural changes in nerve-elements, or their vascular and connective-tissue belongings, and, on the other, a category of cases in which the symptoms are due to disorders of function alone, without correlative changes in structure. But such separation of categories is, in part at least, erroneous. . A functional disease is strictly speaking a derangement of function without a pre-existing alteration in nutrition. The cases that actually belong in this class are probably very few, and 527 528 DISEASES OF THE NERVOUS SYSTEM. are separated by a wide gap from the class of undoubted organic disease. In this gap lies a large class of cases in which alteration in the nutrition of nerve-elements may be assumed to underlie disordered function. In some cases these nutritional changes are slight, in others they are profound, and it is readily to be con- ceived that a state is often reached in which the nutri- tional alterations reach a point where slight alterations in structure make their appearance. There is every conceivable gradation, it should seem, between the disease that is purely functional and the marked changes of organic disease, and experience teaches that many of the functional disorders of one generation are classed with organic diseases in the next, under the influence of im- proved microscopical technique. The antithetical terms " organic disease " and " functional disease " may desig- nate with sufficient accuracy the extreme types of disease, but do not cover satisfactorily the transitional territory between, and their inadequacy must be borne in mind when they are employed in the wide and rather loose sense which convenience and custom sanction. It is designed in this chapter to touch upon the salient features of the various forms of functional (and nutritional) disease of the nervous system in their relation to diagnosis, special stress being laid on the distinction of forms which simulate organic disease. The great type of functional disease of the nervous system is hysteria, and we may well commence with a consideration of its characteristics. Hysteria, — The word hysteria is employed to desig- nate a morbid state of the nervous system which is especially common in the female sex during the period of adolescence and early adult life, and which consists, broadly speaking, in a primary derangement of the FUNCTIONAL AND ORGANIC DISEASE. 529 highest cerebral centres, through which lower centres, both in the brain and in the cord, may become more or less extensively involved in a secondary manner. The variety of these secondary derangements of lower cen- tres give to hysterical disorders a latitude of range which constitutes one of the most striking features of a remark- able malady. In the category of the symptoms of hysteria is included almost every symptom known to organic disease. Here are found paralyses, spasm and contracture, convulsive seizures, states of disordered consciousness, as stupor and coma, mental disorders, dis- turbances in gait without paralysis, headache and pain of almost every kind and distribution, speech disorders, and the most varied disturbances of general and special sensibility. These varied forms of hysterical manifestation may, in their various clinical combinations, present a close resemblance to certain forms of organic disease. There are, however, certain broad characters that are com- monly possessed by the hysterical conditions, which often serve in making the distinction from organic disease. First, there is the circumstance that hysterical dis- orders very commonly develop after emotional disturb- ance, as after fright, grief, or anger. Often, also, the onset of the symptoms follows immediately on an injury which is slight in degree and out of all proportion to the extent and apparent gravity of the consecutive symp- toms. A careful inquiry in such cases will generally show that with this slight trauma was associated a considerable degree of emotional disturbance. In some cases the hysterical symptoms come on after the patient has witnessed similar or remotely analogous symptoms in another person — as, for example, where hysterical 530 DISEASES OF THE NERVOUS SYSTEM. tremor develops in a patient who has lived with a case of chorea. Secondly, there is the fact that hysterical symptoms often increase distinctly on attention. During examina- tion many symptoms may become aggravated. When such increase under attention occurs it is a highly significant sign ; but it is frequently absent, and hence its absence has little negative significance. Thirdly, the symptoms of hysteria are frequently unsettled. They may vary, not only under attention, but without apparent cause. Symptoms of one kind may disappear suddenly or rapidly, to be followed by others of a different character, — in fact, of a character so different that they could not be referred to the same organic process. Thus the hemi-anaesthesia which is right-sided one day is left-sided the next ; or, to take a less uncommon instance, a paralysis which is complete, becomes within a few hours partial in degree. Again, anaesthesia and hyperalgesia may rapidly alternate with one another. This mutability in the character of the symptoms is highly distinctive of hysteria. But the most important element in the diagnosis between hysteria and organic disease is the fact that differences actually exist, in the majority of instances, between symptoms that are hysterical and the corre- sponding and similar symptoms of organic origin. As examples of these differences, we may take different types of paralysis : the monoplegic type, the paraplegic type, and the hemiplegic type, and compare the func- tional (hysterical) form with the organic. An hysterical monoplegia may involve either arm or leg — more frequently the former, — and may be of sud- den or gradual onset. The paralysis may be complete or partial ; it is rarely complete from the onset. The P^UNCTIONAL AND ORGANIC DISEASE. 53 1 paralysis has a segmental distribution, — i.e., the distribu- tion characteristic of paralysis of cerebral origin ; the muscles of the hand are involved, or the muscles of the hand and forearm, or of the hand, forearm, and arm. This segmental character of the paralysis distinguishes it (generally speaking) from nerve-palsies, where the paralysis corresponds to definite nerve distribution, and from spinal paralysis, in which functionally related groups of muscles are involved. If the paralyzed muscles are contractured, this con- tracture presents a characteristic which is distinctive of all hysterical contractures, namely, that when an effort is made to reduce the contracture, the resistance ex- perienced is not uniform, but varies from instant to instant and gives the impression of spasmodic voluntary resistance. This is a very important point of distinction between hysterical and cerebral (organic) paralyses. In an hysterical monoplegia the paralyzed muscles never undergo any considerable degree of atrophy. The limb may, indeed, grow flabby, and in time undergo such slight diminution in bulk as occurs from disuse ; but there is no such wasting as is regularly seen in the paralyses of spinal and neural origin. The electrical reactions are at first normal, and may be normal through- out, but in many instances the slight wasting from disease is associated with slight alterations in the irritability of the muscles {vide page 173). The RD is never observed even in its partial forms. Hysterical monoplegias may be unassociated with any alteration in the sensibility of the skin overlying the paralyzed muscles ; but often there are sensory changes. When present, these sensory changes are often distinctive in character. 532 DISEASES OF THE NERVOUS SYSTEM. The most important general characteristic of the ancesthesias and analgesias of hysterical monoplegias is their segmental distribution Instead of corresponding to the distribution of one or more nerve trunks, as is the case with the anaesthesias and analgesias of peripheral and spinal origin, they correspond in general to the seg- ments of the limb affected — hand, hand and forearm, or hand, forearm, and arm — if it be the upper extremity. In respect to this segmental distribution the hysterical anaesthesias resemble the anaesthesias that result from organic cerebral disease. There is, however, one impor- tant poiiit of difference which is, as a rule, available. In the anaesthesia that accompanies an hysterical monoplegia the loss of sensibility extends to a certain level on the limb, and then ends abruptly, but in the loss of sensibility that accompanies a monoplegia due to a cerebral lesion, the sensory loss (which is commonly slight in degree and limited in extent) fades gradually from the periphery towards the central end of the limb. These points of distinction will serve to distinguish even the cases of hysterical monoplegia in which the general indications of hysteria are equivocal. Under the designation " hysterical paraplegia " are included several conditions, which, though closely allied, should be clearly distinguished. The first class of cases comprises those in which there is a purely cerebral derangement of control over the lower extremities — a paralysis of volition, without even secondary functional derangement of the spinal cord. The central functions of the cord are preserved ; the reflexes, superficial and deep, are normal ; there is no affection of the sphincters, and the muscles show little or no wasting. But the patient cannot move her legs, or can move them only slightly ; only rarely is the loss absolute. When the FUNCTIONAL AND ORGANIC DISEASE. 533 patient makes an effort to overcome resistance, the group of muscles chiefly concerned in the act is antagonized in a hesitating or jerky manner by the opposing muscles, and the resulting movement is irregular and jerky. Sometimes when an attempt is made to obtain the knee- jerk, a contraction of the extensors of the knee is pre- vented by a semi-voluntary contraction of the antago- nistic flexors. This may create the erroneous impression that no knee-jerk is present. In some of these cases of hysterical paraplegia there is some loss of sensibility of the legs, but it is usually slight in degree. It is scarcely conceivable that such a case should be confounded with an organic affection of the cord, but with cases of the second class of "hysteri- cal paraplegias " such an error may be more readily made. The important characteristic of the cases of the second class is that they present distinct evidence of disordered function of the spinal cord. In addition to considerable or slight loss of power in the lower extremities, there is an increase in the myotatic irrita- bility of the leg muscles. The knee-jerks are increased, and may be obtained by striking the quadriceps tendon above the patella. In rare cases there may be obtained a true ankle clonus, but more often there is merely a semi-voluntary jerky spasm, known as the "spurious clonus." There may be retention of urine, but never incontinence, either of urine or fseces. There is often some spinal pain and tenderness in the lumbar region, but never a cincture pain. The legs may be flabby, but never waste, and never present the RD. Sensibility is only slightly or not at all affected. Attention to these points of distinction from paraplegia of organic origin will prevent an error of diagnosis. 534 DISEASES OF THE NERVOUS SYSTEM. The last variety of hysterical paraplegia to be men- tioned differs little in its symptoms from that just described. But it differs in its history in this important respect, that the symptoms of disordered function of the cord are merely aggravated by the development of the hysterical state, and are preceded by a considerable period in which the patients have had slight symptoms of spinal cord disturbance, which are not due to hysteria. These symptoms are slight weakness in the legs, fatigue on slight exertion, spinal pain, and flabby muscles, occurring usually in women in depressed health from any cause (but especially prolonged anaemia and debili- tating febrile diseases). When hysterical symptoms develop in such women, the existent spinal symptoms ("spinal weakness") determine the direction of de- velopment of the hysterical symptoms, and hysterical paraplegia results. Hysterical hemiplegia may be readily distinguished from hemiplegia of organic origin by the following char- acters : In hysterical hemiplegia the face is never involved ; in organic hemiplegia the face rarely escapes, unless the arm and leg are very slightly involved or the lesion is in the pons or medulla. The contractures of hysterical hemiplegia have the characters noted in connection with hysterical monoplegias (p. 531). The skin reflexes are generally normal, never lessened, as at the onset of organic hemiplegia. The knee-jerks are usually equal, not increased on the paralyzed side. There is never an ankle clonus on the paralyzed side unless there is great contracture of the posterior tibial group, but a " spurious clonus" is sometimes obtained when there is no contracture. In hysterical hemiplegia the loss of power is never absolute, as it so often is in the organic paralysis, and FUNCTIONAL AND OROANIC DISEASE. 535 the leg is not rarely more affected than the arm. When progression is possible, it is different in hysterical and organic hemiplegia. In the former, the affected leg is brought nearly straight forward from behind, the toes trailing on the ground ; in the organic paralysis the palsied leg is advanced with a marked lateral movement, the foot being thrown out in such a way as to describe the arc of a circle. In most cases of hysterical hemi- plegia there is anaesthesia of the paralyzed side. It may involve the whole of one side, including the face (hemianaesthesia ), or may affect chiefly the arm or the leg. In cases of hemianaesthesia the special senses are implicated in the peculiar manner described elsewhere (p. 127). The onset of hysterical hemiplegia is often rapid, but is never sudden, as is the case with vascular lesions that cause hemiplegia. It is, moreover, never accompanied with loss of consciousness. The occasional cases of bilateral hysterical hemiplegia, with bilateral or one-sided anaesthesia, cannot be con- founded with bilateral organic hemiplegia if the facts relating to the distinction of hysterical hemiplegia are borne in mind. The most common form of hysterical paralysis is adductor palsy of the larynx, with resulting aphonia. It is important and easy to distinguish this form of palsy from organic laryngeal palsies. Its characters are highly distinctive : there is loss of voice, but, notwithstanding this, the cough is in most instances perfect. In all other laryngeal palsies loss of phonation is associated with loss of cough. In local affections of the larynx, such as laryngitis, there is always an effort to phonate, with resulting hoarseness. Inspection of the larynx in a case of hysterical aphonia shows that the cords move normally during respiration, but that they are not 536 DISEASES OF THE NERVOUS SYSTK>(. approximated when the patient attempts to speak. Very rarely abductor paralysis of the vocal cords occurs as an hysterical affection, with laryngeal symptoms like those of the organic form of the same paralysis. The diag- nosis here depends on evidence of an associated hys- terical affection. A form of hysterical disturbance known as astasia- abasia is liable to be confounded with inco-ordination due to organic disease. This condition, when typically developed, consists of an inability to stand without swaying violently from side to side, and of an inability to walk without a side-to-side staggering motion, due to the alternate and violent contraction of antagonistic muscles. There is no ataxia, strictly speaking. If the patient be steadied in the erect position the toes are readily guided into contact with neighboring objects. The upper extremities are entirely free from irregularity of movement, and when the patient lies, control over the lower extremities is perfect. Sometimes the defect is hemiplegic in distribution. The knee-jerks are often increased, and the condition is often associated with unmistakable signs of hysteria. These characters serve to separate the condition from the inco-ordination of spinal and cerebellar disease. In its fully developed form and as the dominant symptom of hysteria, this condition is rare. A slighter grade of the disturbance with other hysterical manifestations is common. It appears not to depend on cutaneous anaesthesia. Hysterical internal strabismus may be confounded with organic paralysis pf ocular muscles, unless it is remem- bered that it is due to spasm, and that the absence of paralysis may be demonstrated by testing the muscles of each eye with the other closed. Hysterical ptosis, when single, is easily detected by asking the patient to look up, FUNCTIONAL AND ORGANIC DISEASE. 53/ when the orbicularis spasm on which it depends becomes exaggerated in order to prevent the lid from moving up. When double, the head is thrown back when the patient is requested to look up. The convulsive paroxysms of hysteria are distinguished by their associations from the convulsions of acute organic disease and by their general distribution, irregular charac- ter, and tendency to extensor spasm, from the locally com- mencing seizures that characterize chronic focal lesions of the brain. There are other hysterical conditions besides those mentioned here that have been confounded with organic disease of the nervous system, but it is believed that the points of distinction given here and in the chapter on symptomatology will sufifice in the great majority of in- stances for the separation of the hysterical from the organic conditions. But certain general facts regarding conditions that appear to be of hysterical origin remain to be emphasized. The first step in the diagnosis of any condition in which there is a suspicion or distinct evi- dence of hysteria is to look most carefully for symptoms that indicate the presence of organic disease, and not until such disease has been excluded is it safe to assume that the hysterical manifestations present constitute the primary disease. Many women who are the subjects of organic disease of the nervous system (as multiple sclero- sis and certain other organic brain diseases) suffer also from hysteria, the occurrence of which is determined by the presence of the organic disease. It is therefore evident that until the possibility of a primary organic condition has been eliminated, even the most pronounced signs of hysteria in a woman of the age at which hysteria prevails should not be allowed weight as to the nature of the primary disease. Close attention to this rule will prevent 538 DISEASES OF THE NERVOUS SYSTEM. many errors in diagnosis. When, as occasionally occurs, the symptoms appear distinctive of neither hysteria nor organic disease, and are to all appearances quite inde- cisive, a diagnosis, if possible, must be based on a knowl- edge of the differences (which almost always exist) in the minute characters and associations of the symptoms com- mon to the two different states. The Traumatic Neurosis or Psycho-Neurosis. — It is generally acknowledged that many forms of injury that are accompanied, at the time of their infliction, with a considerable degree of mental shock (railroad injuries especially), are followed, after a variable period, by ner- vous symptoms varying widely in character in different cases, but agreeing in this, that they indicate a more or less general disturbance of cerebral function. The symp- toms in many of these cases suggest cerebral disturbance of the most purely functional type. In fact, these cases possess the characters that have been described as dis- tinctive of hysteria, and they have been very appropri- ately designated " traumatic hysteria." Often the subjects are males who have some neurotic predispositions. In some cases the symptoms are such as indicate purely general cerebral disturbance ; in others local symptoms, as monoplegic or local sensory disturbance, are especially obtrusive. But even in these cases the cerebral and functional nature of the symptoms is plainly shown by the nature of the local symptoms and by their associa- tion with more general hysterical manifestations. The criteria of distinction from organic disease are, of course, the same in these cases as those that have been described in the preceding section {vide Hysteria). But there remains a large and important class of cases in which the symptoms following injury and mental fright (shock) are such as to suggest, by their character and FUNCTIONAL AND ORGANIC DISEASE. 539 permanency, a graver condition than can properly be in- cluded even under the broad term hysteria. There is good reason to believe that the symptoms in these cases cannot be referred to a mere disturbance of function, but depend on nutritional alterations in nervous elements, which vary in degree in different cases, and which may even consist, in some instances, in fine structural changes at present beyond the cognizance of histology. The cases belonging to this class present important differences in the severity of their symptoms, and fade imperceptibly, on the one hand, into the severer forms of traumatic hysteria, and, on the other, into the milder forms of diffuse and focal organic disease of the brain. The term " traumatic neurosis " has been and is still used to designate this class of cases, but its use is open to the objection that it implies a distinct and specific fon:^ of cerebral disturbance, whereas it must be owned that the cases included in the term may and probably do differ considerably in their pathology. But the name is con- venient, and the objection to its use is much reduced if it be borne in mind that it probably does not designate a pathological entity. Those who wish to emphasize the characteristic and obtrusive psychical element, use the term " traumatic psycho-neurosis." There are those who see no justification for excluding the traumatic neurosis from the long chapter of hysterical affections. They hold that the points of distinction which have been brought forward are not sufficiently great to justify a separation and a new designation. There may be cases, they say, which are not typical of hysteria, but this fact does not call for the creation of a new type. It must be admitted that there is a great opportunity for malingering, and if this malingering were excluded, to- gether with the untypical forms of hysteria, a large part 540 DISEASES OF THE NERVOUS SYSTEM. of the remaining cases would be unquestionable cases of hysteria.' It is believed that such reasoning as this is incorrect. The traumatic neurosis regularly presents symptoms which cannot be purely functional in character, and it appears an unwarrantable extension of the term hysteria to make it include forms of disease that are so stable in symptoma- tology that they must depend on decided nutritional alterations in nervous tissues. The " traumatic neurosis " is as much entitled to a separation from hysteria as are the numerous cases of chorea that follow fright. But it must be owned, even by the most zealous advocates of the traumatic neurosis, that there are cases on the border- land between hysteria and the traumatic neurosis, which it is difficult to classify, and about whose classification there is room for a just difference of opinion. There are also cases in which hysterical symptoms are mixed with symptoms of the traumatic neurosis, which cause great difficulties in diagnosis. It must be owned, furthermore, that the entire subject of traumatic hysteria and the trau- matic neurosis is beset with difficulties and is likely for a long time to come to afford opportunity for the expres- sion of widely different views. After a brief description of the main clinical features of the traumatic neurosis will be presented the main points of distinction from hysteria. ' Some writers contend that the traumatic neurosis is merely a com- bination of hysteria and neurasthenia. They hold that trauma acts in these cases by causing a kind of mental over-strain, the short duration of the influence being compensated by its intensity. There can be little doubt that trauma may lead to the development of combined hysterical and neurasthenic symptoms, but this, we take it, does not constitute the traumatic neurosis. The severity of the symptoms in most cases of the traumatic neurosis, and their rapid onset in many instances, would serve, it should seem, to completely separate at least these cases from any that may reasonably be termed neurasthenia. FUNCTIONAL AND ORGANIC DISEASE. 54I The symptoms of the traumatic neurosis come on within a short time of the injury and fright, or, as happens with equal frequency, they do not appear for weeks or months afterwards. In a considerable proportion of cases the patient be- comes unconscious for a short period (few minutes) after the injury, or passes temporarily into a state of mental confusion. Much more rarely the period of shock lasts many hours or even days. Sometimes acute insanity (hallucinatory type) follows immediately on the injury. In most cases there are no immediate symptoms. The patient seems perfectly well for several days — is able to work as usual, etc. Then symptoms, at first slight and perhaps overlooked, make their appearance, and with the lapse of time (weeks or months) become gradually more obtrusive. Sometimes the original surgical injury occu- pies the sole attention of the patient and his physician for weeks or months, the symptoms of the neurosis meanwhile developing insidiously. The first distinct symptoms are usually purely subjec- tive in character, and include the following : Pain, especially at or near the seat of injury, and when there is no local injury, but only general concussion, espe- cially in the lower dorsal, lumbar, and sacral regions. The pain is increased by movement in the part affected, and leads to some limitation of motion. In addition to pain, which is almost always observed, there are usually restlessness, general irritability, and very often an expression of anxiety. The mental changes grow rapidly or slowly more marked, until they develop into a state of hypochondriacal depression, associated commonly with considerable irritability. Insomnia is a frequent and early symptom. It is rarely absolute, but the patient has an nncjuiet sleep, broken by frequent cries due to bad dreams. General tremor, attacks c)f syncope^ and occa- 542 DISEASES OF THE NERVOUS SYSTEM. sional convulsions may be among the earlier manifesta- tions of the disease. The intellectual faculties remain unaltered or only slightly changed. Some form of motor defect is of almost constant occurrence. The loss of power is usually partial and often very slight. The distri- bution of the palsy is determined partly by the seat of the injury, partly by other circumstances. All four extremi- ties may be slightly paretic, or there may be more marked paralysis of hemi-,para- or monoplegic distribution. These paretic conditions have many of the characters of the paralyses of hysteria which have been already mentioned — there is little or no atrophy, and the electrical reac- tions are normal or show only slight quantitative changes. When the paralyses are monoplegic they show a distinct tendency to segmental distribution, never the distribution which corresponds to peripheral nerves or spinal segments. Occasionally a considerable degree of atrophy is observed in the paralyzed muscles, with distinct histological changes in the muscle-fibres. Sensory symptoms are common and highly character- istic. Very often there is partial or complete hemianses- thesia, like that observed in hysteria, with alterations in the special senses on the same side, especially concentric limitation of the field of vision, for colors and for white. A variety of disturbances of speech are observed, but there is never aphasia. Most often there is simple slow- ing of speech ; not rarely the patient brings out his words in an irregular and uncertain manner, apparently owing to mental excitement. The knee-jerks are very often in- creased, never lost. Occasionally a true ankle clonus is obtained. The pupillary reflex is usually normal, but is sometimes lost. The functions of the bladder and rec- tum are not commonly involved, but there is sometimes retention of urine, as in hysteria. Loss of sexual desire FUNCTIONAL AND ORGANIC DISEASE. 543 is very common. (Edema and cyanosis of the paralyzed extremities are not rarely observed. One of the most important of the objective symptoms of the traumatic neurosis is tachycardia. In most patients the heart's action is habitually more rapid than normal (90-130), and on excitement may reach 130-140-150 or 160 beats per minute. Sometimes this condition leads to actual cardiac hypertrophy and dilatation. As a rule, the patients who suffer from the condition described grow progressively worse, by the addition of one symptom to another, and by the gradual or rapid advance of those that first appear. After a variable period the condition either slowly im- proves or settles into a chronic state, with slight alterations for the better or worse. The prognosis as regards life is good ; as regards recovery it is bad. Among the most per- sistent and unchanging symptoms are the mental alterations. The injury that gives rise to the traumatic neurosis varies much. There may be a slight or considerable local inju- ry, or there may be merely a general concussion. The gravity of the disease appears to bear no fixed relation to the severity of the injury. It is, however, greatly influ- enced by the mental shock that constantly accompanies these cases. Indeed, it is to this regular accompaniment of the trauma that the peculiar character of the disease ap- pears to be due. That severe mental shock is the essen- tial element in the causation of the neurosis is shown by the occasional occurrence of cases of typical character in which the mental shock has been profound but physical injury could not be detected. Among the criteria that serve for the distinction of the traumatic neurosis from traumatic hysteria are the following : I. The Greater' Fixity of the Symptoms which the two 544 DISEASES OF THE NERVOUS SYSTEM. conditions have in common This is especially notice- able in the sensory symptoms. The hemianaesthesia of the traumatic neurosis is subject to relatively slight vari- ations in distribution and intensity ; there is never a transfer or a rapid change in the degree of anaesthesia. This greater fixity is also very striking in the case of the mental symptoms. There are, indeed, changes, but these are not considerable within short periods of time, and the general nature of the mental disturbance remains the same, whilst in hysteria it may vary much. A similar but less striking difference in the permanence of symptoms is noted in the motor and vaso-motor disturbances. II. The traumatic neurosis generally occurs in per- sons who have no recognizable neurotic predisposition, and who have been otherwise healthy. It is very rare, on the contrary, to find cases of hysteria of equal gravity, in which a neurotic predisposition is not traceable or even obtrusive. This is an exceedingly important etiological point of distinction. III. Differences in the Symptoms Themselves. — While there is a strong general resemblance between many of the symptoms of the two conditions, there are important differences in the grouping, detail, frequency of occur- rence and character of certain symptoms. Thus in the traumatic neurosis the mental change is a state of hypochondriacal depression, a dominant and charac- teristic condition. In hysteria a continuous change of this nature is very rare. In the traumatic neurosis, insomnia, in some degree, is an important symptom, and one of whose existence there are objective proofs. If present in traumatic hysteria, it is rarely a prominent symptom. Distinct muscular atrophy, histological altera- tions in the muscle-fibres, and oedema of the paralyzed extremities are more often observed in the traumatic FUNCTIONAL AND ORGANIC DISEASE. 545 neurosis than in traumatic hysteria. True ankle clonus is not uncommon in the traumatic neurosis ; in hysteria it is rare. An important and common objective condition in the traumatic neurosis is tachy- cardia. It is highly characteristic of the condition, and is not a continuous symptom in cases of pure hysteria. Generally speaking the symptoms of the traumatic neu- rosis are symptoms of a graver character than those of hysteria, and suggest more distinct nutritional changes in the nerve elements. Indeed some cases of the trau- matic neurosis show conditions that can be referred only to anatomical alterations within the nervous system (optic neuritis, optic atrophy). The recognition of gross organic lesions, which may be combined with the symptoms of the traumatic neurosis, is of course a sim- ple matter. But it is no easy task, indeed it is often impossible, to state whether a given symptom or combi- nation of symptoms is due to advanced nutritional changes or to slight organic changes. It is important, however, to try to form some conception in each case of traumatic neurosis of the degree of the nutritional changes in the nervous system. The great point to remember is that we have to deal with a nutritional dis- ease of the nervous system, which in its graver forms imperceptibly shades into slight organic conditions (optic neuritis, optic atrophy, central degenerative changes, as shown by loss of pupillary reaction, etc.), which for pur- poses of prognosis it is extremely important to detect. The detection of such conditions can be accomplished only by making a systematic search for the slightest un- equivocal sign of organic disease. It is unnecessary to repeat here what these signs are (see Paralysis, Atrophy, Electrical Reactions, Ophthalmoscopic Changes, Convul- sions, Abnormal Reflex Action, etc.). 546 DISEASES OF THE NERVOUS SYSTEM. Neurasthenia ' is a nutritional disease of the brain due to disturbance of the general nutrition of the body, resulting especially from defective assimilation of food. One of the most important immediate elements in the production of the nervous symptoms is a vaso-motor instability which leads to continual alterations in the blood-supply of the brain. Associated with this condi- tion of vaso-motor instability is probably an alteration in the quality of the cerebral blood-supply, but of this there is no actual knowledge. The indirect causes of the disease are numerous, but the most important are anxiety, grief, fright, prolonged emotional excitement, and sexual excesses and mastur- bation. Not rarely neurasthenia is associated with hys- teria and with the traumatic neurosis. The chief symptoms and signs of neurasthenia are gen- eral debility, defective memory, slight diminution in will power, abnormal irritability, mental depression, incapacity for prolonged mental or physical exertion, insomnia or ab- normal somnolence, headache (often occipital),^ peculiar cephalic sensations (p. 140), asthenopia, palpitation, tachycardia, fibrillary contractions, blepharospasm, vari- ous dyspeptic troubles, night sweats, and concentrated urine.' While many of these symptoms are of cerebral ' No form of nervous disease is of such common occurrence as some degree of neurasthenia. * The headache of neurasthenia is never severe, and is exceedingly apt to be temporarily diminished after the ingestion of food. ' There are few cases of neurasthenia which do not show in the urine or faeces some indication of defective metabolism. The condi- tions found vary considerably. The fseces often contain excessive amounts of urobilin or some related substance. The urine is usually concentrated and of small volume (600-1000 c.c. in 24 hours). Fre- quently there is an excessive excretion of phosphoric acid (P2^6)' ^^^ an alteration in the quantitative relation of urea and uric acid. In FUNCTIONAL AND ORGANIC DISEASE. 547 origin, many others are due to visceral disturbances, but the latter may be entirely absent. Not rarely there is associated with neurasthenic symptoms that form of mental depression which is due to false ideas of bodily ailments such as might conceivably exist, viz., hypo- chondriasis. The distinction of neurasthenia from other forms of functional disease gives rise to no difficulties, but it is important to remember how often it occurs with such diseases. Only occasionally is there difficulty in dis- tinguishing between neurasthenia and organic disease. The cases that resemble general paralysis of the insane are elsewhere considered {jide p. 400). Fibrillary contrac- tions may be very persistent, and may be localized for days to special groups of muscles. There is no danger in confounding such cases with progressive muscular atrophy if the associations of neurasthenia are borne in mind. Careful inquiry will usually show that the fibrillary contractions have at some previous time been general in distribution. Persistent headache may be associated with local spasm, such as might suggest a focal brain lesion, but any error may be avoided by remem- bering that the local spasm of neurasthenia does not recur for more than a few days in the same place, and that the associations of neurasthenia and those of a focal lesion are quite different. Epilepsy. — Epilepsy is a chronic functional (nutri- tional) disease of the central nervous system (brain), characterized by the recurrence at irregular intervals of health the relation of the uric acid to the urea excreted varies between I to 45 and I to 60 in adults. In neurasthenia (as well as some other conditions) the relation is often i to 40, i to 35, or i to 30. Indican is often present in pathological quantities, especially in cases of sexual jieurasthenia. Oxalate of lime is often present in excess in the urine. 548 DISEASES OF THE NERVOUS SYSTEM. convulsive seizures of a certain type, or by the sudden loss or impairment of consciousness, or by a combination of these conditions. For clinical purposes it is convenient to classify the different forms of epilepsy under the following heads : 1. Common spasmodic epilepsy ("grand mal," "major seizures "). 2. Attacks consisting of brief loss of consciousness, with or without slight muscular spasm, or (rarely) of slight muscular spasm, or a sudden sensation without actual loss of consciousness ("petit mal," "minor seiz- ures," improperly called " epileptic vertigo " ). 3. Attacks consisting of apparently volitional and co- ordinated motor or mental actions during a state of modified consciousness. The mental state during these attacks differs both from normal consciousness and from the unconsciousness that usually occurs in epileptic attacks (" psychical epilepsy," " psychical epileptic equiv- alent " — so-called because the paroxysms may take the place of typical minor seizures). 4. Hystero-epilepsy, a combination of the symptoms of epilepsy -with the motor symptoms of hysteria. These different forms of epilepsy may be variously combined in the same individual. The most frequent combination is that of grand mal and petit mal. The diagnosis of " grand mal," from organic disease of the brain is always a most important problem, and some- times an exceedingly difficult one. A diagnosis has to be made from cases of acute cerebral disease (vascular lesions) and from cases of chronic cerebral disease. In epilepsy the convulsions are general, tonic spasm is succeeded by clonic spasm, the duration of the attack is short (less than five minutes), the attack is succeeded by a period of sleep in which the patient may be partially FUNCTIONAL AND ORGANIC DISEASE. 549 aroused, there is no local paralysis (except in rare cases of unilateral spasm where the weakness is transient), there is often a history of repeated attacks of a similar character, and there is often an aura. In vascular lesions of the brain, on the contrary, there may be no convulsions, and, if present, they are chiefly unilateral and clonic ; loss of consciousness is usually prolonged, there is hemiplegic weakness with changes in reflex action on the same side, there-is no aura, and if the attack is not a first one the number of preceding attacks is small (one or two). In the diagnosis of epilepsy and chronic brain disease a distinction must be made between active brain disease and old retrogressive lesions. The convulsions of chronic active brain disease (tumor, abscess, chronic meningitis) usually have a local commencement, and are often partial in their extension {vide p. 82). This is a most important point of distinction from idiopathic epilepsy ; but it must be remembered that it is not an absolute distinction, for the convulsions of epilepsy sometimes have a local commencement, and the convul- sions of organic brain disease may have a general and not a local commencement. Other features than the convulsions themselves have therefore to be considered. It is essential to make a careful inquiry for and to ex- clude all evidences of organic disease, especially severe and persistent headache, persistent hemiplegic or mono- plegic weakness, vomiting without gastric cause, optic neuritis, and paralysis of cranial nerves. Certain forms of retrogressive, non-active brain disease, as atrophic tumors (tubercular), old cases of so-called polioencephalitis and meningeal hemorrhage in infancy, and old patches of softening, may give rise to convulsive seizures closely resembling attacks of grand mal. Often 550 DISEASES OF THE NERVOUS SYSTEM. these forms of disease cause permanent hemiplegia, and when this is the case the diagnosis is simple. But many of the cases of hemiplegia of infancy recover largely from the paralysis. In any case, therefore, in which convulsions date from infancy, and especially if they are unilateral, careful search must be made for signs of an old hemiplegia. The most important of these signs are slight hemiplegic weakness, hemiplegic rigidity, increased myotatic irritability, and slight retardation of growth on the weaker side. The diagnosis, in many instances, de- pends on these objective features of the case, as the original hemiplegia, if slight, is often overlooked. It is important to note that the first recurrence of convulsions may occur a long time (years) after the convulsions that attended the onset. In seeking to discover the cause of the paroxysms in any case of grand mal, it is important to study the pos- sible influence of injury to the head. A not inconsider- able number of cases of grand mal follow closely, in their development, upon blows or falls on the head. Many of these cases are indistinguishable by their symp- toms from the so-called idiopathic cases of epilepsy. Their recognition is especially important, because in some instances it is possible to relieve them by operation. In many cases local changes are found in the meninges. It is important, also, to recognize the influence which dis- ordered nutrition exerts in some cases of apparently idiopathic epilepsy in determining the occurrence of paroxysms. ' . ' The most important evidence of such nutritional disorder is ob- tained by a study of the urine. In some cases of idiopathic epilepsy (perhaps a considerable proportion) there are distinct evidences of abnormal putrefactive processes in the small intestine. The occur- rence of such processes is shown, in a general way, by a disturbance FUNCTIONAL AND ORGANIC DISEASE. 55 1 The distinction of grand mal and the convulsions of hysteria is usually easy. In typical epileptic seizures there is no apparent cause for the seizure, there is often an epigastric or one-sided aura, the onset is abrupt and is often accompanied with a cry, the seizure itself con- sists of tonic spasm followed rapidly by clonic spasm, frequently the tongue is bitten, the pupils are widely dilated, and the face is pallid or livid at the onset (an important sign), micturition is common, the patient never talks during the seizure, and the duration of the entire attack is never more than a few minutes. These features contrast sharply with hysteroid convulsive seizures, in of the relation which normally exists between the preformed and the combined or ethereal sulphates in the urine (lo-i). In the cases to which reference is made, this relation is habitually changed, so that there is present an excessive proportion of the ethereal sulphates (7-1, 5-1, or even 3-1). The form in which the ethereal sulphates occur in the urine of such cases appears to vary in different instances. Usually they consist in large part of indoxyl sulphate, which is esti- mated as indigo blue. In other cases they may be represented chiefly by phenol (carbolic acid). It is not, of course, claimed that the pres- ence of these substances is pathognomonic of epilepsy. They are known to occur in excess in most cases of chronic Bright's disease, and probably occur in many other states associated with derangement of intestinal function. This circumstance does not, however, dimin- ish the significance of their presence in excess in certain cases of epi- lepsy, for it is a striking fact that when these substances are present they bear a direct relation to the occurre^ice of the paroxysms ; i.e., though habitually present in excess they become greatly increased just before the occurrence of the paroxysms, and diminish immedi- ately thereafter. Moreover, in some instances these substances have been diminished by means of intestinal antiseptics, and so long as these have been thus effective, paroxysms have been staved off. It has been claimed that the occurrence of epileptic paroxysms is related to the defective elimination of uric acid. In a large series of unpub- lished observations which bear upon this question, we have found no support for this hypothesis. 552 DISEASES OF THE NERVOUS SYSTEM. which emotion commonly determmes the attack, there is no true aura, the onset is not rarely gradual, there is no cry at the onset, the attack itself consists of periods of prolonged rigidity, and wild, apparently purposive, move- ments with or without opisthotonos, the pupils never dilate, micturition never occurs, if there is biting it is indiscriminate (hands, lips, tongue, people, and things), talking and groaning are common, and the duration of the attack is much longer than in epilepsy. In epilepsy the attack is followed by stupor ; in hysteria the mental state is clear immediately after the attack ceases. Nocturnal attacks of grand mal may go long unrecog- nized. The most trustworthy signs of such attacks are a feeling of soreness in the limbs, general headache, and a sense of exhaustion, minute hemorrhages under the skin of the face and neck and in the conjunctivae (almost pathognomonic), and, in adults, the occasional wetting of the bed. The distinction of grand mal from the con- vulsions of uraemia and lead poisoning depends on the recognition of the causes of the latter. There is no organic disease of the nervous system which is likely to be confounded with petit mal. The minor attacks may generally be distinguished from attacks of syncope by their sudden onset and termination, and their occurrence without evident exciting cause (such as usually exists in syncope). Faintness, dizziness, or pal- pitation may occur in either condition before the attack, but the occurrence of a true aura (visual, olfactory, audi- tory, visceral, motor) shows the attack to be epileptic. Similarly, slight mental confusion after the attack, mic- turition and slight rigidity or tremor during the attack, strongly suggest the epileptic nature of the seizure. A small number of cases of petit mal are distinguished by the occurrence of a vertiginous sensation, and must FUNCTIONAL AND ORGANIC DISEASE. 553 not be confounded with true vertigo. In true vertigo there is rarely loss of consciousness, and the dizziness persists, while in petit mal consciousness is generally lost or clouded, and the vertiginous sensation passes quickly away. Aural vertigo (due to labyrinthine disease) {vide p. 164.) can hardly be confounded with petit mal, if it is re- membered that aural vertigo is characterized by persist- ent dizziness after the attacks, tinnitus aurium, and often by persistent and defective hearing, none of which condi- tions occur in epilepsy. Migraine (Hemicrania — "Sick Headache," "Bilious Headache," " Blind Headache "). — Migraine is a paroxys- mal nervous disorder of which the most characteristic feature is headache (often one-sided). Nausea and vom- iting frequently accompany the pain in the head. In a large number of cases sensory disturbances of one kind or another are associated with the headache, and in ex- ceptional instances these sensory symptoms are the chief elements in the paroxysm, the headache being slight or even entirely absent. Rarely there are motor disturb- ances in the limbs at the time of the paroxysms. Of the sensory accompaniments of migraine the most important are the disturbances of vision,'which are pre- sent in some form in more than half the cases. These manifestations are usually unilateral, and consist in some cases of amblyopia, in others of hemianopsia, and in others of a bright moving spot on one side of the visual field (scintillating scotoma, an early symptom of an attack). The disturbances of speech which not rarely accompany paroxysms of migraine are usually of the nature of sen- sory aphasia (especially partial word-deafness). When sensory phenomena involve the limbs, they consist, like the visual symptoms, of manifestations of combined sen- sory irritation and sensory loss : there is tingling sue- 554 DISEASES OF THE NERVOUS SYSTEM. ceeded by numbness and perhaps anaesthesia (fingers most often involved, leg rarely, always unilaterally). When motor symptoms occur, they consist of transient unilateral weakness (arm, especially fingers), and very rarely of slight spasm. Muscles supplied by the third nerve are sometimes paralyzed for a considerable period (weeks — see p. 389). It occasionally happens that migraine is confounded with organic brain disease. The cases in which this is most likely to happen are those in which migraine is as- sociated with ophthalmoplegia ("ophthalmic migraine"). In these cases the palsy (always one-sided, ptosis, strabismus) comes on acutely with the pain of migraine, but persists for days or weeks with gradual improve- ment and ultimate recovery, to recur at some future paroxysm of migraine. In acute ophthalmoplegia from nuclear hemorrhage, the symptoms of hemorrhage (apoplexy, etc.) are so obtrusive that no confusion can occur, but from syphilitic ophthalmoplegia the distinction is not always so easy, for the onset of the palsy may be rapid and attended with headache, and there may be spontaneous recovery with subsequent recurrence of the symptoms. The diagnosis is to be made by close attention to the symptoms and character of the onset. In migraine the palsy coincides with a paroxysm which is usually distinctive in character, and the pain ceases or diminishes when the ophthalmoplegia comes on. In syphilitic ophthalmoplegia the palsy is never sudden, and headache (if present) precedes and follows the ocular symptoms. Cases of migraine of the ophthalmic variety appear to be not rarely followed by general paralysis of the insane. The recognition of the latter disease is sufficiently simple if its connection with these cases of migraine be FUNCTIONAL AND ORGANIC DISEASE. 555 known. The symptoms of ordinary migraine recurring after the onset of general paralysis may give rise to error, in that they may be confounded with the paroxysmal attacks of that disease. Mental symptoms resembling superficially the symptoms of general paralysis (defec- tive memory, confusion of thought^ hesitation in speech) may occur after severe paroxysms of migraine, but are distinguished from them by their transient duration and non-progressive course. In most cases of migraine an exciting cause can be traced for each paroxysm (over- fatigue, dietetic indiscretion, ocular fatigue, sexual ex- cess, or several of these factors combined), and this is sometimes an aid in determining the nature of a par- oxysm (as in the diagnosis between migraine and petit mal).' Chorea. — Chorea is a disease especially of childhood and the adolescent period of life, characterized by spon- taneous spasmodic and irregular movement (especially ' There are probably few typical paroxysms of migraine which are not associated for the time being with evidences of disordered metabo- lism. The nature of the disturbance seems to be different in different cases. The urine excreted just previous to the paroxysm is usually highly concentrated and may contain a large excess of phosphoric acid. Whether there is any abnormality in the excretion of uric acid in migraine, as some have claimed, is as yet unsettled. It is improbable that there is any constant relation between uric acid excretion and migraine. In one case of recurrent paroxysmal vomiting, perhaps allied to mi- graine, there was a striking diminution in the excretion of uric acid during a two days' period of persistent and uncontrollable vomiting. In the long intervals (several months) between the attacks, the patient, a boy of eight, enjoyed excellent health, and the relation be- tween the uric acid and urea excreted was normal (about 1-60) ; during the attack it was as follows: first day, 1-159; second day, 1-135. Immediately after the attack the relation again became normal. 556 DISEASES OF THE NERVOUS SYSTEM. of face and arm) and by inco-ordination of voluntary movement. With these symptoms are associated very fre- quently slight loss of power in the parts affected by spasm, and slight, sometimes considerable, mental change. We have observed that an excessive excretion of uric acid is a highly constant condition in cases of pronounced chorea. In the cases that have been studied in relation to this point it has been observed that the excretion of uric acid has reverted to normal in proportion as the symptoms have been controlled by treatment. In many cases of chorea the urine has a peculiar and rather characteristic red (somewhat eosine-like) color, probably not due to urobilin. Another rather common feature of chorea urines is a diminution of the chlorides in rela- tion to the urea. Almost all chorea urines are of high specific gravity (1024-1030) and of very small volume in the twenty-four hours. The disease is usually of limited duration (six weeks to six months), but occasionally lasts (usually in slight degree) for years. The chief immediate cause of chorea is emotion, especially fright.' The diagnosis in the large majority of cases of chorea can hardly be said to present any difficulties. In atypi- cal cases there is sometimes the possibility of confusion with organic disease. Thus, in those cases in which ' The frequent association of endocarditis or rheumatism, or both, with chorea, must be borne in mind. The relation between these conditions is not understood, but it is certain that this association is too frequent to be explained by coincidence. It seems probable, upon the whole, that both the chorea and the endocarditis which pre- cedes or accompanies it are dependent upon a blood-state identical with or allied to that of rheumatism. The excessive excretion of uric acid in chorea, which we have noted, is of interest in this con- nection. The theory that chorea is due to the obstruction (by emboli washed from cardiac valves) of the small vessels supplying the motor structures of the brain has little to commend it. FUNCTIONAL AND ORGANIC DISEASE. 557 there is considerable weakness and very little spasm an organic cerebral paralysis may be thought of. But the associated symptoms of a chronic focal lesion (headache, optic neuritis) are absent, the paralysis is limited to one arm, and close attention will show slight choreic spasm and inco-ordination in the affected limb and perhaps in other parts. When the legs are chiefly affected in chorea, there may be difficulty in walking and standing, but confusion with spastic paraplegia need not arise, for in this disease spasmodic movements are conspicuous only on voluntary motion, and an ankle clonus is always obtainable. Not very rarely the movements of chorea are unilateral (hemi-chorea), and such cases may be confounded with so-called " post-hemiplegic chorea " (mobile spasm, athetoid movements). These movements, however, are usually slow (occasionally they are rapid) and rhythmical, persist during sleep, and contrast with the quick irregular movements of chorea, which cease during sleep. There is also usually more or less rigidity in the parts that are the seat of the post-hemiplegic movements. The history or evidence of preceding hemiplegia of course fixes the diagnosis. Hysterical patients sometimes develop true chorea ; in otiier cases they develop symptoms which while resembling chorea must be distinguished from it (hysterical chorea). In order to justify a diagnosis of hysterical chorea there must be distinct evidence that the attack arose from imitation. The spasmodic move- ments of hysterical chorea may be indistinguishable from those of chorea, but sometimes they have a rhyth- mical character, and often they are more violent and abrupt than those of chorea. Hereditary Chorea (Huntington's Chorea) is an ob- scure form of disease characterized by spontaneous ir- 558 DISEASES OF THE NERVOUS SYSTEM. regular spasmodic movements resembling closely those of ordinary chorea. In other respects it differs greatly from typical chorea, for it is a disease especially of adult life, is distinctly hereditary (often through several generations), and affects many members of a family, runs a progressive course, shows no special re- lation to cardiac disease or to rheumatism, never develops from chorea, and is generally characterized by mental failure and eventually by dementia. The disease is to be distinguished from general paralysis, which it may re- semble in its mental symptoms, and from bilateral post- hemiplegic athetoid movements. From post-hemiplegic disorders of movement, the absence of rigidity and the irregular and wild character of the movements, together with the history, serve for a distinction. There are, how- ever, cases of bilateral athetosis without any history of pre- ceding acute cerebral disease which it may be difficult to distinguish from hereditary chorea, and which are regarded by some as possibly atypical forms of the latter disease. Paralysis Agitans (Parkinson's Disease — Shak- ing Palsy). — Paralysis agitans is a nutritional disease ' of the central nervous system in the second half of life, and is distinguished by the presence of three cardinal symptoms — tremor, muscular weakness, and rigidity. The disease is chronic and in most instances progressive. The tremor, which is characterized by the fact that it continues during rest, usually precedes the weakness and rigidity, which come on together. Usually the symptoms begin in the upper extremity (hand), ex- ' Recent extended observations on the urine in paralysis agitans have shown it to be normal as regards chlorides, sulphates, urea, and uric acid. In many cases the phosphates have been observed to be present in small amount, but it is doubtful whether this diminution was sufficiently marked to be considered pathological. FUNCTIONAL AND ORGANIC DISEASE. 559 tend to the leg of the same side, and if the extension continues, to the arm and then to the leg of the opposite side. The extension of the disease is thus hemiplegia. Typical, well-marked cases of paralysis agitans present no difficulty in diagnosis. Cases occur, however, in which weakness and rigidity of the limbs come on with- out tremor and without the characteristic attitude and facial expression of paralysis agitans, namely, a bending forward of the head and tqjper part of the spine and a fixed anxious expression. If in such cases there is con- siderable mental weakness, the diagnosis from organic brain disease may be difficult until the appearance of tremor. An important point of distinction from slight hemiplegia is that the knee-jerks are not increased on one side as in hemiplegia. The legs are sometimes chiefly affected in paralysis agitans, and in such cases the suspicion of spinal cord disease may arise, but will be dispelled by the detection of slight tremor in the arms and by the fixity of gaze. The diagnosis from insular sclerosis is always easy if the following facts be remembered : In insular sclerosis the tremor occurs only on movement (intention tremor), and is wider in range and more irregular than that of paralysis agitans. Insular sclerosis rarely commences after forty, paralysis agitans rarely before forty. The head is regularly involved in the tremor of insular sclero- sis ; in paralysis agitans it is only occasionally affected. Nystagmus is usually present in insular sclerosis ; in paralysis agitans it never occurs. The speech disturb- ances of the two diseases are different. In paralysis agi- tans the voice is monotonous and without emotion and expression, and the words are often run together ; in in- sular sclerosis the syllables are unduly separated as a rule. The fundus is normal in paralysis agitans ; in insular scle- 560 DISEASES OF THE NERVOUS SYSTEM. rosis there is commonly slight ophthalmoscopic change (slight optic nerve atrophy). Furthermore, the peculiar attitude, fixity of facial expression, and muscular rigidity of paralysis agitans are all absent in insular sclerosis. Post-hemiplegic tremor is fine, while the tremor of paralysis agitans is coarse. In post-hemiplegic tremor the carriage and facial expression are normal and a his- tory of hemiplegia is usually available. These points serve to prevent error in diagnosis. Paralysis agitans is to be distinguished from " senile tremor," a fine tremor of the limbs which is seen in many aged persons. The tremor is finer than that of paralysis agitans, affects the head early, involves both upper ex- tremities about the same time and is unassociated with the rigidity which is so characteristic a feature of paraly- sis agitans. These features serve for a distinction from paralysis agitans, but there are cases intermediate in character between the two conditions which it is impossi- ble to classify. Neuralgia. — The word neuralgia is merely a euphe- mism for nerve-pain, and nerve-pain may occur under two very different conditions, namely, as the result of struc- tural irritative disease of a nerve, and as the result of purely nutritional changes in a nerve without any demon- strable alterations in its structure. It is eminently de- sirable that the word neuralgia should be restricted to that form of nerve-pain in which there is no structural disease of the affected nerve or nerves — "idiopathic" neuralgia. The form of nerve-pain that depends on structural disease (" symptomatic neuralgia ") should be referred to the process which is its usual cause, namely, neuritis. While the distinction of these two forms of nerve-pain is thus clear in theory, it is by no means always easy in FUNCTIONAL AND ORGANIC DISEASE. 561 practice. They possess many features in common, and their successful separation involves an accurate knowl- edge of the diagnostic characters of each form. The chief diagnostic features of typical neuralgia are as follows : (i) the unilateral distribution of the pain ; (2) its distinctly paroxysmal character ; (3) changes in the position of the pain ; (4) the absence of all evidences of organic disease of the nerve involved (absence of local tenderness and swelling of nerve where the nerve is ac- cessible). In some cases of neuralgia the pain is not migratory, but fixed. Such neuralgia must be distinguished both from the fixed pain of pressure neuritis and from that of slight spontaneous neuritis. Where the nerve-pain depends on pressure (bone disease, tumor), there are almost certainly other symptoms of such pressure, and the pain steadily progresses in intensity and suggests its dependence on a progressive cause. The pain of neuralgia is sometimes indistinguishable from that of slight neuritis. Usually, however, a dis^ tinction can be made and is based on the following facts : (i) the pain of neuritis is continuous or nearly so ; (2) changes in the sensibility of the skin supplied by the nerve are apt to be present and are persistent in charac- ter (hyperaesthesia, anaesthesia); (3) if the affected nerve is a "mixed " nerve, the mu-scles which it supplies become flabby, and their irritability to galvanism and faradism is at first slightly increased; (4) there are often slight trophic changes in the skin ; (5) if the nerve is accessible it is usually tender to pressure and often swollen. Of course the mere absence of nerve tenderness and swelling does not exclude neuritis. On the other hand the presence of transient tenderness at the time of the pain paroxysm does not mean neuritis, for such tenderness is common in 3^ 562 DISEASES OF THE NERVOUS SYSTEM. neuralgia. It is only where local tenderness exists both at the time of the paroxysm and in the intervals, and is present eai-ly in the affection (within the first few weeks), that it can be regarded as a certain indication of neuritis. When the indications as to the nature of the nerve pain are equivocal the history of the case may be allowed weight. Thus the fact that the patient has been a sufferer from nerve pains in other parts makes the neu- ralgic nature of the affection probable. The etiological factors may also be given some importance. Thus, a family history of neuralgia or of functional nervous disease, a history of a period of general debility before the development of the pain, or a knowledge of the fact that the nerve pains are often related to mental influences, would each of them increase the probability that the trouble was functional and not organic. Various organic affections of the nervous system are apt to be confounded with neuralgia. We may touch briefly upon some of the errors in diagnosis that are especially liable to arise. In caries of the upper cervical vertebrae, there are often severe neuralgiform pains in the region of the greater and lesser occipital nerves during the early stage of the disease. Usually the pain is one-sided. The distinction of these cases from cervico-occipital neuralgia may cause some difficulty unless it be barne in mind that the pain of caries is aggravated by motion or jarring and that such pain is associated with spasm in the deep cervical muscles on the side of the pain. Neuralgiform pains are common in disease of the ab- dominal and thoracic viscera. Whenever, therefore, there is unilateral neuralgic pain in the trunk, a careful physical examination must be made of the organs near the seat of pain. In some cases of thoracic disease the pain does FUNCTIOiVAL AND ORGANIC DISEASE. 563 not correspond to the seat of the disease, but is " reflected " to distant parts. Thus an aneurism of the aorta may cause little local pain, but may give rise to severe neuralgiform pain in the arm. In ordinary intercostal neuralgia there are tender points at certain characteristic situations in the course of the nerve — at a point corresponding to the emergence of the nerve from the intervertebral foramen, at a point near the middle line in front, and at a point in the axillary region about midway between these. These points of tenderness are seldom found in the neuralgias from disease of internal organs. The " hghtning pains " of tabes are sometimes experienced in the trunk, especially in its lower part. These pains are, however, of such short duration and so shifting in seat that they are not likely to be confounded with neuralgia. Moreover, they are associated usually with pains in the legs, with disturbances of sensibility, and, usually, with loss of knee-jerk or loss of the light-reflex of the iris. The trunk may be the seat of severe neuralgiform pains in the early stage _ of a tumor of the spinal cord. The severity and constancy of these pains are their character- istic features, and should always excite suspicion of organic disease. Moreover, the pain is usually increased by a lateral or rotary movement of the spine, a feature most suggestive of organic disease. In the cases where there is evidence of pressure upon the cord, there is, of course, no diagnostic difficulty, but it often happens that the neuralgiform pains precede the development of such symptoms by a considerable period. In disease of the ver- tebral column there is often intense unilateral pain, but this pain is usually much increased by any movement of the trunk. The diagnosis of sciatica may conveniently be con- sidered here. The term sciatica is applied to any con- 564 DISEASES OF THE NERVOUS SYSTEM. dition characterized by pain in the region of the sciatic nerve, whether the pain be due to a primary affection of the nerve, or whether it depends on damage to the nerve from causes outside it. It is well to restrict the word to the primary affections of the nerve, sciatic neuralgia and sciatic neuritis. The chief point of distinction between sciatic neuralgia and sciatic neuritis is that in the latter condition there is persistent tenderness of the sciatic nerve. The pain of sciatica is sometimes felt near the hip- joint, but it is almost impossible to confound the pains of hip-disease with those of sciatica. In sciatica the pain extends far down the thigh in the line of the sciatic nerve, and is increased in this distribution when the nerve is put on the stretch, and there is usually some tenderness (at least at times) in the nerve. When sciatic pain is secondary to pressure on the sacral plexus by pelvic or abdominal tumors there is usually little tenderness of the nerve in proportion to the degree of pain referred to it. This condition should excite suspicion of organic pelvic disease and lead to a rectal examination. It is important to remember that primary sciatica is practically never bilateral. Primary neuralgia in the distribution of the anterior crural nerve is rare. Neuralgiform pain in this situation is likely to depend on pressure upon the lumbar plexus, or upon neuritis of this plexus secondary to a sciatic neuritis. In either case there is some wasting of the anterior thigh muscles and slight or considerable changes in their elec- trical irritability. In many cases there is, moreover, loss of knee-jerk. None of these conditions are ever present in neuralgia. Occupation Neuroses. — It is here convenient to touch very briefly on the diagnosis of that class of affec- FUNCTIONAL AND ORGANIC DISEASE. 565 tions which is characterized by the occurrence of certain motor and sensory symptoms (especially spasm and pain) as the consequence of frequently repeated muscular acts appertaining usually to the occupation of the patient. The mDst important general characters of these " occu- pation neuroses," as they are called, are as follows : (i) The symptoms above referred to occur in the part which is concerned in the habitual muscular action. (2) This habitual muscular action is interfered with and perhaps effectually prevented by the symptoms. (3) The most common symptom is spasm in the parts affected (" cramp " ; hence " writer's cramp," " telegraphist's cramp," etc.). (4) With this spasm, or unassociated with it, occurs pain, referred to the muscles, bones, joints, or nerves, and excited, at first, only by the special muscular action. The chief forms of occupation neuroses are the follow- ing : Writer's cramp, piano-forte player's cramp, teleg- raphist's cramp, needle-women's cjamp, and violin play- er's neurosis. But almost any occupation that involves often repeated special muscular acts occasionally makes a victim of an occupation neurosis. In most cases of oc- cupation neurosis there is a combination of spasm and pain ; but very often one of these symptoms predomi- nates, and it is accordingly convenient to distinguish a motor or spasmodic form and a sensory or neuralgic form of occupation neurosis. The occupation neuroses seldom occur in persons in perfect health. They develop usually in persons who have become debilitated from some cause, and are dis- tinctly neurasthenic. Often a neuropathic heredity can be traced. A period of anxiety not rarely precedes the development of the neurosis, and sometimes its develop- ment is related to a local disease or injury. It seems 566 DISEASES OF THE NERVOUS SYSTEM. probable that these varied influences operate by produ- cing a functional derangement in the nervous centres (especially the cerebral centres) concerned in the par- ticular act whose frequent repetition has excited the local affection. The diagnosis of the occupation neurosis is not usually difficult. The relation between a given affection and the action on which it depends is generally sufficiently obtru- sive. In the case of the most common of these neuroses — writer's cramp — confusion may at times arise with paralytic affections (chiefly hemiplegia of gradual onset) in which the interference with writing is thought to de- pend on the neurosis. Knowledge of one fact suffices to make the distinction of writer's cramp from all other forms of disease. It is this : In writer's cramp the symp- toms are at first brought on only by the act of writing. In all other affections (paralysis, paralysis agitans, tremors, etc.), the symptoms are not limited to the act of writing, but may be observed in all other acts that require the use of the affected parts. This diagnostic feature applies, mutatis mutandis, to the diagnosis of the less common forms of occupation neuroses. Delirium Tremens (Acute AlcohoHsm, Alcoholic De- lirium). — Delirium tremens is an acute nutritional affec- tion of the brain, involving especially the nerve-elements of the cortex. The disease runs a definite course, and has a strong tendency to subside spontaneously. It is practically confined to drunkards, and usually follows a prolonged " spree." The symptoms of delirium tremens are of rather rapid development and usually attain their full development in the course of a few days. The early symptoms are par- tial insomnia, bad dreams, restlessness, mental depression, and loss of appetite. When the symptoms are fully de- FUNCTIONAL AND ORGANIC DISEASE. 567 veloped, there are distressing and rather characteristic hallucinations and illusions, especially of sight, both at night and during the day. Very often the patient sees snakes or spiders crawling on his bed or on the walls, or sees grinning faces of men or devils. The false sense impressions give rise to delusions of a fearful character. Associated with this mental condition is a characteristic irregular tremor of rather wide range, which occurs on movement. The temperature is almost always elevated, the degree of fever being proportioned to the severity of the disease. The diagnosis of delirium tremens seldom presents any difficulty. From acute meningitis it is distinguished by the absence of headache, spasm, and paralysis. From ordinary symptomatic delirium it is readily distinguished by the great prominence of the terrifying visual halluci- nations and by the presence of tremor. Sometimes de- lirium tremens is confounded with general paralysis of the insane or with acute mania. The horrifying halluci- nations of delirium tremens cannot be mistaken for the exalted mental and physical activity of acute mania. The characteristic irregular tremor of delirium tremens is absent in acute mania. Considerable irregular tremor may, however, occur in general paralysis ; but the busy anxiety and visual hallucinations of alcoholic delirium make a strong contrast with the unnatural complacency and delusions of grandeur that characterize the organic cerebral affection. Cerebral Concussion. — A certain degree of cerebral concussion is an accompaniment of many forms of injury to the head, and its symptoms are then lost in those of the trauma. Numerous cases occur, however, in which the only symptoms are such as must be referred to violent concussion of the brain. It is probable that in some of 568 DISEASES OF THE NERVOUS SYSTEM. these cases of violent concussion the symptoms depend, in part at least, on the occurrence of minute foci of hemorrhage into the substance of the brain (sub-cortical white substance, sometimes mid-brain and pons). This fact removes these cases from the category of strictly functional disease, but the character of the symptoms is such as suggests functional rather than organic disease, and justifies their consideration here. The symptoms of cerebral concussion vary much. The blow or fall which causes the concussion gives rise almost immediately to loss of consciousness, or to a confused mental state. In some cases the loss of consciousness is associated almost immediately with irritative phenomena of a cortical nature — unilateral and bilateral clonic spasm, increased reflex irritability, increase in myotic irritability, and often ankle clonus. The pupils are often contracted, the pulse is slowed, and there may be repeated vomiting. Nystagmus is a common symptom. It is often very rapid, and the oscillations may be vertical as well as horizontal. Rapidly changing strabismus often occurs ; internal stra- bismus alternates with external strabismus. In young children nystagmus, rotary spasm of the muscles of the neck, and strabismus often follow relatively slight con- cussions (falls from chairs or cribs) without loss of consciousness. These irritative symptoms are usually of short duration (few hours or days), and gradually wear away. In adults cerebral symptoms may persist for several weeks (headache, mental confusion, slight spasm, slow pulse). A slight elevation of temperature occurs in some cases and lasts several days. The diagnosis from organic disease is not always easy if the history of a concussion is not known. The irri- tative symptoms (unilateral and general spasm, strabis- mus, vomiting, slow pulse,) and slight fever may suggest FUNCTIONAL AND ORGANIC DISEAS?:. 569 meningitis. The spasm in concussion is often more violent than that of meningitis, and more continuous. The symptoms are also more rapidly changeable. In short, the irritative symptoms are more intensely acute. In concussion the symptoms come on immediately after the injury and reach their maximum in a short time. They also rapidly subside. In meningitis the symptoms more slowly reach their maximum, there is more fever, and de- lirium precedes stupor. When the irritative symptoms are not so marked, there may be a just suspicion of com- mencing meningitis for several days. Thus headache, som- nolence, mental confusion, slight fever, a slow pulse, and slight spasm may last many days after a concussion, and then gradually clear up. It is exceedingly important to distinguish between cerebral concussion and extradural hemorrhage. The two conditions may co-exist. The distinction rests chiefly on the fact that in extradural hemorrhage there are distinct evidences of hemiplegia with or without spasm, while in concussion, paralysis, if present, is slight, and on the fact that the symptoms of extradurul hemorrhage are preceded by a lucid interval, and do not come on sud- denly. In extradural hemorrhage, again, there is usually evidence of fracture. In young children, the significance of nystagmus, or rotary spasm and nystagmus, following immediately on an injury is sufficiently plain. Malingering. — Malingering is the simulation of a morbid condition which has no basis whatever in fact, and in the case of nervous diseases is not very un- common. Malingering must be carefully distinguished from the mere exaggeration of a morbid condition, which is very common indeed, especially in hysterical con- ditions. 570 DISEASES OF THE NERVOUS SYSTEM. Many cases of malingering are so patent that they would not impose on a novice, others require much patience and knowledge for their detection, and others still may deceive the best educated physician. The at- tempt to feign organic disease, or diseases with decidedly objective signs, is not very common, and need never be successful. But functional diseases, of which the symp- toms are chiefly subjective, are often successfully simu- lated. Thus pain of every variety and distribution may be successfully feigned, but it is more difficult to feign convulsive seizures or paralysis. There is good reason to think that loss of sensibility to pain may be so suc- cessfully simulated, even under the severest tests by the faradic brush, the needle, etc. In any case where malingering is suspected, especial attention should be given the objective signs that may exist, for the purpose of comparing these, as regards de- tail and grouping, with forms of actual disease which they resemble. Close attention will always reveal im- portant though perhaps slight differences. Thus while a malingerer may imitate closely the character of seizures of grand mal, examination at the beginning of the paroxysm will show that the vaso-motor symptoms — facial pallor and dilatation of the pupil — do not occur. An almost universal tendency is for malingerers to overdo their part — both in the feigning of objective symptoms and in complaints about subjective states. But while a diagnosis may often be made from the symptoms themselves, it is commonly desirable or neces- sary to obtain information from other sources. The history of the patient should be obtained with regard especially to his character, his social and his financial condition, It is especially important to know what incentive there may be for malingering, whether, for FUNCTIONAL AND ORGANIC DISEASE. 571 example, in alleged traumatic cases, the patient expects to recover damages (as in railroad cases), whether the patient is poor and shiftless or independent and thrifty. An exceedingly important thing, where elaborate ma- lingering is suspected, is to find out whether the patient has had opportunities for the observation of the symptoms of nervous diseases, whether he has lived in hospitals, or has been about from dispensary to dispensary, and has been repeatedly examined for nervous symptoms. Thus some symptoms, as hemiangesthesia, hemianopsia, re- striction of the visual field, etc., are not likely to be feigned, but may, nevertheless, be successfully feigned by an intelligent patient who has discovered, by experience at hospitals and dispensaries, the significance attached to these signs. A single unequivocal symptom or sign of organic disease should be allowed great weight if found. Of such symptoms and signs the most im- portant are local muscular atrophy, changes in electrical reaction (RD), ankle clonus, increase or loss of knee- jerk on one side, slight optic neuritis or atrophy, incon- tinence of urine or fseces, and paralysis of cranial nerves. Insomnia is a symptom which cannot long be successfully feigned. Its persistence when the patient believes him- self to be free from observation is significant of at least functional disturbance. When the symptoms of actual disease, functional or organic, are exaggerated by a patient, it is exceedingly difficult to estimate the degree of exaggeration, unless this be very extreme. A close watch for feigned symptoms for a considerable period of time may furnish data for the estimation of the degree of exaggeration, but there are many cases in which the best observers would differ in their judgment on this point. CHAPTER VII. THE EXAMINATION OF THE PATIENT. In the clinical study of nervous diseases it is essential for accuracy and rapidity in diagnosis to employ a systematic method of examining j^atients. The forms of nervous disease vary so much in charac- ter that no one method of examination can always be adhered to rigidly, but this does not destroy the feasibil- ity of using system in the study of cases. In the follow- ing pages are indicated a general method of procedure which must be modified (or curtailed) to suit individual instances of disease. When a patient is first seen by the physician it is eminently desirable that a preliminary rapid survey of the case should be made. Such a survey sometimes enables the examiner to make a provisional diagnosis, which has the great value of giving intelligent direction to his subsequent more elaborate and special examina- tion. The points to which the preliminary observation should be directed are the mental state of the patient, the speech, the expression, the general attitude, the gait, and the presence of any morbid movement or deformity. We may review the chief facts that are to be learned by such observation. The Mental State. — The patient may be conscious, or may be delirious, comatose, or in a state of stupor. A certain dull, heavy expression is often seen in epileptics, 572 THE EXAMINATION OF THE PATIENT. 573 and is rather suggestive. Mental hebetude is observed in many functional and organic diseases — chorea, hys- teria, paralysis agitans, and extensive cerebral lesions, especially those of the frontal lobes. Emotional excite- ment or depression is seen especially in paralysis agitans, chorea, recent hemiplegias, insular sclerosis, hemorrhage and softening, general paralysis and other forms of insanity. In children, feeble-mindedness, imbecility and idiocy are suggestive of infantile cerebral palsy. An undue mental complacency is often seen in insular sclerosis and general paralysis. Deficient attention oc- curs in neurasthenia and organic diseases (general paralysis, insular sclerosis, tumors, etc.). Delirium sug- gests a toxsemic state (fever or lead poisoning, alcohol- ism, narcotic poisoning, uraemia), or meningitis. Facial Exp7-ession. — Certain expressions of the face at once put the observer on the proper line of inquiry. For example, a rigid face and fixed expression of the eyes suggests paralysis agitans ; an expressionless, mask-like face or overaction of the occipito-frontalis points to general paralysis ; a drooping of one side of the mouth indicates a hemiplegia or Bell's paralysis and very prominent eyes suggest Basedow's disease. Posture. — Flexion of the elbow, wrist, and fingers on one side indicates a hemiplegia of considerable duration ; a stooping posture, with flexion at the elbow and knee, strongly suggests paralysis agitans ; an unnatural dis- placement of the head to one side or backwards probably means wry-neck ; unilateral wrist-drop generally means musculo-spiral paralysis ; bilateral wrist-drop, lead paralysis or alcoholic neuritis. Retraction of the head is a strong indication of meningitis in a patient sick enough to be confined to bed. Deformity. — The deformities that are dependent on 574 DISEASES OF THE NERVOUS SYSTEM. nervous disease are frequently very marked and highly characteristic. Particularly noticeable are the following conditions : the large globular head of hydrocephalus, the microcephalic head, prognathism, and highly arched palate observed in infantile cerebral palsies and in cases of defective cerebral development generally ; the claw- hand of ulnar paralysis ; the flexed fingers and hollow palm of Dupuytren's contraction ; the winged scapula observed in paralysis of the serratus magnus muscle ; the various forms of club-foot that suggest cerebral palsy (equino-varus) or poliomyelitis (equinus, varus, valgus, calcaneus, cavus) ; the strabismus and ptosis of cerebral disease. Some of the conditions mentioned under posture and expression might be included here. Morbid Movements. — Among the most important move- ments that are immediately recognizable are the follow- ing : the irregular jerky inco-ordination of chorea ; the coarse and continuous tremor of paralysis agitans ; the intention tremor of multiple sclerosis ; the mobile spasm of athetosis ; the spasmodic movements of the head in spasmodic torticollis and retrocollis ; the twitching of the eyelids in blepharospasm ; the spasm of the face and sometimes neck and shoulder in tic convulsif. Gait. — The mode of locomotion of the patient is often highly suggestive of the nature of the disease from which he suffers. Thus, in the "tabetic gait" of loco- motor ataxia each leg is thrown outwards and forwards in a peculiar manner, and the foot is brought to the ground with a slap. In the " hoppmg gait of spastic para- plegia the legs are so rigid that they are advanced only with much effort, and the reflexes are often so exaggerated that as the foot is dragged along the floor and stepped upon there is set up a clonic spasm of the calf muscles. Sometimes in these cases there is considerable spasm THE EXAMINATION OF THE PATIENT. 575 in the adductors of the thighs, and this leads to com- plete crossing of the legs during progression — the so-called "cross-legged " progression. This gait is char- acteristic of the cerebral paraplegias of children. What is known as the " frog-walk " is seen in this same class of cases : there is double talipes equino-varus and con- tracture of the flexors of the knees and adductors of the thighs. In the "equine" or "high-action " gait the foot is lifted high in walking, in order to prevent the toes from catching on the floor. This gait depends on drop- foot from paralysis of the anterior tibial group of mus- cles, and is especially suggestive of poliomyelitis and of alcoholic multiple neuritis. In paralysis agitans the patient sometimes loses his balance, and owing to the rigidity of his muscles cannot control his locomotion. Instead of falling he " runs after his centre of gravity," either in a forward direction (festination or propulsion), backward (retropulsion), or move rarely, sidewise (lateropulsion). A " waddling gait," in which the body oscillates from side to side and the legs are held wide apart to preserve the equilibrium, is seen in pseudo-hypertrophic paralysis. This gait cannot be confounded with the waddling gait of rickets, in which disease the legs are bowed and other rachitic deformities are conspicuous. In the hemiplegic gait one leg is dragged heavily along after the other, but with a characteristic semi-cir- cular swing outwards, which serves to distinguish the true hemiplegic gait from that of an hysterical hemiplegia, in which the weak leg is dragged directly forwards. A staggering gait, not necessarily associated with par- alysis, anaesthesia, inco-ordination or tremor, is strongly suggestive of cerebellar disease (cerebellar titubation). A similar gait is seen in acute alcoholic intoxication. 576 DISEASES OF THE NERVOUS SYSTEM. Speech. — Most speech disorders require considerable study before their diagnostic significance is fully deter- mined. Some conditions, however, are so characteristic 'that they immediately suggest the state on which they depend. Slow, monotonous, staccato speech (" scan- ning" utterance) suggests multiple sclerosis. Slurring speech, due to imperfect co-ordination of the muscles necessary for the perfect enunciation of syllables, is seen in general paralysis of the insane. A high-pitched monotonous voice with rapid utterance ("festination ") and some confluence of syllables is highly distinctive of paralysis agitans. The cephalic cry, a sudden loud scream recurring in a child without apparent cause (but due probably to headache), is highly suggestive of tubercular meningitis. Systematic Examination of the Functions of the Nervous System. The systematic examination of the functions of the nervous system should include an investigation of all the motor, sensory, trophic, and reflex functions, with a view to the discovery or exclusion of the symptoms that have been described under corresponding headings in Chapter II. Only those conditions which require more or less special examination are referred to in the present chapter ; conditions which are recognizable by simple inspection are not considered, as they have been suffi- ciently treated elsewhere. Examination of Motor Functions. — If the preliminary examination of the patient reveals loss of power in a particular part, as for example in the arm, it is desirable that the examination of the motor power should be com- menced in this part. If, however, no loss of power has been noted, or such loss as has been observed is hemi- THE EXAMINATION OF THE PATIENT. 577 plegic in distribution, it is convenient to commence the examination with the study of voluntary power in the face and to pass subsequently to the arm and leg. The pa- tient is requested to perform in succession the following acts : to close his eyes, first together, then one at a time ; to show his teeth ; to snarl up the nose ; to wrinkle the forehead ; to whistle or blow ; to depress the angles of the mouth ; to smile. In the course of these various movements it is easy to recognize the presence of any insufficiency of the facial muscles. It is important to remember in this connection that the naso-labial folds are often unsymmetrical in normal individuals. The state of the ocular muscles is determined with sufficient accuracy for most purposes by making the patient fol- low the finger, first to one side of the head, then to the other, then up and down. A considerable degree of insufficiency of the internal recti is easily recognized by making the patient follow the examiner's index-finger as it is moved gradually toward the nose. The condition of the muscles moving the tongue is ascertained by causing the patient to protrude the tongue, which deviates to the paralyzed side in hemiplegia. The muscles of the jaw are not usually tested in routine examinations, unless there is some reason to believe that the motor portion of the fifth nerve is the seat of disease. The masseters and temporals may be tested by placing the fingers on the muscles of opposite sides and causing the patient to bring the teeth forcibly together, as in the act of biting, when the feebleness of the affected muscle is readily apparent. The external pterygoids are tested by making the patient move the jaw laterally and by de- pressing the jaw. In studying the degree of voluntary power in the extremities we may begin at the distal portion of the 578 DISEASES OF THE NERVOUS SYSTEM. limb and work up, or at the upper part and work down, as happens to be most convenient. In all examinations it is important to compare homologous muscles of oppo- site sides. Weakness of the elevators of the shoulders (upper part of trapezius — levator anguli scapulae) may- be determined by pressing down on the shoulder, first upon one side, then on the other, while the patient makes an effort to lift it. The power of the infraspinatus and of the teres minor muscles may be tested by causing the patient to move the hand along a line as in writing. The motion is im- paired by the paralysis of either of these muscles. The deltoid is tested by requiring the patient to raise the arm out from the body, the examiner meanwhile resisting this ef¥ort. By resisting, in turn, the action of the extensors and flexors of the forearm, of the extensors and flexors of the wrist, of the pronators and supinators, of the ex- tensors and flexors of the fingers, of the flexors and extensors of the thighs, of the flexors and extensors of the leg, and of the flexors and extensors of the ankle, it is possible to obtain a good idea of the power of these muscles and to detect even a slight grade of paralysis. It is sometimes important (as in lead paralysis) to test the power of the supinator longus. This is done by causing the patient to flex the elbow with the forearm midway between pronation and supination, the move- ment being meanwhile resisted by the examiner. If the supinator be of normal strength it stands out promi- nently ; if involved in paralysis, it is relaxed. The power of the interossei may be tested by making the patient separate the fingers of the extended hand. In connec- tion with examinations of the flexors and extensors ot the wrist, it is important to bear in mind the fact that in paralysis of the extensors of the wrist there is always THE EXAMINATION OF THE PATIENT. 579 some apparent loss of grasping power in the hand. The power of the legs may be studied by requiring the pa- tient to stand upon one foot and flex his knee and thigh as if to sit down. The extensors and flexors of the ankles maybe tested by causing the patient to stand first on his toes, then on his heels. Instruments known as dynamometers have been de- vised for the purpose of measuring accurately the power of certain groups of muscles. Most of these instruments are exclusively adapted to the determination of the grasping power of the hand, and few of them can be relied upon as accurate. When it is desired to compare carefully the grasping power of the two hands in an indi- vidual or to record it, a Collin dynamometer may be employed. Ordinarily such an instrument is quite unnecessary ; the power of the patient's grasp may be determined with sufficient accuracy by causing the ex- aminer's two hands to be squeezed with the full force of the patient's corresponding hands (right in right, left in left). The presence of rigidity of slight degree may be detected by causing the patient to make very rapid move- ments of flexion and extension with the suspected mus- cles, the muscles of opposite sides being carefully com- pared. A slight degree of rigidity of the fingers may be detected if the fingers are caused to glide rapidly, one after another, over the thumb, or if the patient be caused to beat a tattoo upon the table. The presence of tremor in the upper extremity may be detected, even where it is slight, by causing the patient to extend his arms and hands before him and separate his fingers widely. Protrusion of the tongue reveals any tremor in this organ. Tremor of the lips is detected by getting the 58o DISEASES OF THE NERVOUS SYSTEM. patient to show his teeth, tremor of the eyelids by getting him to partially close the eyes. The state of equilibrium may be tested by getting the patient to stand with his eyes closed and his feet close together, so as to reduce the base of support. A great many apparently normal persons show considerable sway, lateral and antero-posterior, under this test, and all show some. Neurasthenics are apt to show wide oscillations. If the patient falls, or tends to fall, under the test, this manifestation is known as the Romberg symptom. The equilibrium of a patient may also be tested by making him walk away from the examiner, and then turn quickly to retrace his steps. If there is defec- tive equilibrium, it is shown in the act of turning. Inco- ordination is usually revealed by the patient's walk. When present, it is increased if the patient walks with eyes closed. Its presence in the upper extremities may require more careful examination. The patient should be made to stand erect, with the feet close together. The arms are then extended horizontally to the side, and the tip of each index finger in turn is brought quickly in contact with the tip of the nose. If co- ordination is imperfect, this act cannot be rapidly and well performed. The test is made more difficult if the eyes are closed. It may be varied by making the patient bring the tips of the index fingers together before the face, instead of alternately to the end of the nose. Slight inco-ordination of movement in the fingers, un- associated with appreciable loss of power, may be de- tected if the patient is caused to use the fingers of one hand in such acts as the buttoning and unbuttoning of the vest. Even slight inco-ordination in the legs maybe detected by causing the patient while sitting to approxi- mate the toes of each foot in turn to the finger of the THE EXAMINATION OF THE PATIENT. 581 examiner held some distance above. The test is im- proved by putting a pin into the front of the patient's shoe and causing the extremity of the pin to be brought into contact with the finger held above it. Examination of the Sensory Functions. — It is usually desirable to determine in turn the state of tactile sensibility in the skin, the pain sense, the sensibility of the skin to heat and to cold, and the state of the muscular sense. There are many sources of error in forming conclusions about the state of the sensory func- tions, and it is desirable to repeat frequently at short intervals the tests that have been employed. In many cases the mental state of the patient is such that any results regarding sensibility are imperfect or quite use- less. In testing tactile sensibility a piece of cotton is lightly stroked over or laid upon the surface of the area to be tested. The tip of the finger or a feather may be employed in place of cotton, but neither is so satisfactory. It is frequently useful to place two pieces of cotton simultaneously upon corresponding regions of opposite sides, when, if even slight anaesthesia be present, the cotton will be perceived only, or more distinctly, on the normal side. The eyes of the patient must be closed while the test is being carried on, and the test must be very carefully made in order to insure accuracy. Especial care and considerable patience are often necessary in defining accurately the limits of an anaes- thetic area. Many physicians employ an instrument known as an sesthesiometer in determining the state of tactile sensi- bility. Most sesthesiometers are constructed on the principle of a pair of compasses, and the object of the physician is to determine what is the least distance upon the skin at which the two points of the instrument are 582 DISEASES OF THE NERVOUS SYSTEM. felt as two. The area to be tested is compared with the corresponding area of the normal opposite side, or the results obtained for a given area are compared with the known and tabulated results obtained from many observations. ' This is an unreliable and unsatisfactory way of studying tactile sensibility for clinical purposes, and has no real advantage over the method above given. AVhen studying the tactile sense it is well to test the ability of the patient to localize sensations by making him touch certain points tested. The sense of pain is tested by pricking the skin with a point that is not too fine, as the point of a quill pen or a toothpick. A pin or needle may be employed, if not too sharp. If convenient, the faradic brush may be used. The temperature sense may be tested by blowing alternately hot and cold upon the skin, or by using two test-tubes, one filled with warm and the other with cold water, or, what is sometimes more convenient than the latter method, by using a hot and a cold spoon. Nor- mally differences of about 1° Fahr. are readily recognized by the skin within the range of 80° and 100° Fahr. On the finger-tips a variation of about ^° is recognizable ; on the back, a variation of 2° should be perceived. In clinical work, however, it is only rarely necessary to test the temperature sense with such precision. The muscular sense may be tested by examining the ability of the patient to judge of differences in weights, to recognize the postures of the extremities when the ' The following are said to be the smallest distances (in milli- metres) at which the two points of a compass are distinguishable in various parts of the body : tip of tongue 1-2, finger-tip 2-3, lips 4-5, tip of nose 6, cheeks and back of fingers 11 -16, forehead 22, back of hands 31, forearm, leg, and instep 40, chest 45, thigh and arm 77. THE EXAMINATION OF THE PATIENT. 583 eyes are closed, and to appreciate the peculiar and somewhat painful sensation that accompanies the con- traction of a muscle, say to the faradic current. The eyes should be closed in testing the muscular sense. Four small rubber balls of the same size, but unequally loaded with shot, or wooden balls plugged with lead, so as to make weights of one half, one, two, and four ounces, are convenient in testing the sense of weight. Normally differences of about one fortieth of the total weight are perceived. An excellent test for sense of posture is to place the fingers, or one hand, or the leg, in a certain position, the patient's eyes being closed, and then cause him to imitate this posture on the opposite side. In moving the fingers or limbs of the patient they should be lightly held at the side by the examiner, in order that the tactile sense may interfere as little as possible with the test. In examining the sense of smell it is important to bear in mind that this sense is frequently much impaired by changes in the mucous membrane of the nose. Each nostril should be separately tested. It is customary to use a variety of stimuli. The tinctures of musk, pepper- mint, cinnamon, and asafoetida may be conveniently em- ployed. These substances may be kept in small glass bottles, well stoppered, containing absorbent cotton or sponge. The olfactory sense may be greatly reduced temporarily by over-stimulation with any of these sub- stances. The examination of the sense of sight belongs largely to the domain of ophthalmology, but it is important for the physician to be able to make an estimate of the visual acuteness, to map out roughly the visual fields, and to observe the optic disk both by the indirect and the direct method of ophthalmoscopic examination. The 584 DISEASES OF THE NERVOUS SYSTEM. method of estimating visual acuity by means of test- types is so simple and well known as to require no de- scription. The extent of the visual field is best measured by means of the perimeter, the use of which is described in text-books on ophthalmology, but considerable defects may be satisfactorily detected without its help. Asking the patient to cover one eye and keep the other fixed upon the examiner's face, an object, such as a card, a knife, or a pen, is brought gradually into his visual field, first from one side, then from the other, then from above and from below, the patient immediately informing the examiner when the object comes into view. A small white card fixed to the end of a pencil is an excellent object to introduce into the field. Colored cards may be used in determining the limits of the visual field for dif- ferent colors. A convenient and accurate method of measuring the field is to place the patient, with one eye open, in front of a blackboard and about a foot away, the eye being fixed on a chalk mark and the periphery of the field being gradually outlined by introducing an object within it, as above described. The different points obtained by introducing the object to the edge of the field from different directions are joined by a line, and the resulting figure is a rough outline of the visual field of the eye examined. An ophthalmoscopic examination of the fundus should be made in all cases where organic disease of the central nervous system is suspected, especially where the symp- toms point to a cerebral lesion. The indirect method of examination is most generally useful, but should be supplemented when practicable by the direct method. The technique of such examinations is described in all text-books on ophthalmology. It is desirable that the examiner should be able not only to observe the fundus THE EXAMINATION OF THE PATIENT. 5S5 of the eye, but also to estimate with reasonable precision, by means of the ophthalmoscope, the condition of the refraction of the eye. In examining the sense of hearing, it is well to com- mence by testing its acuity. A watch may be con- veniently employed for this purpose. Normally a watch which ticks with average loudness can be heard about twenty inches from the ear tested. The ear not tested should be closed during the test. If"there is deafness, it is important to determine whether it depends on disease of the external ear or tympanic cavity, or on disease of the internal ear (labyrinth) or nerve. If a watch is heard better through the bone than through the air, it is highly probable that the labyrinth and nerve are normal. The tuning-fork is an important aid in examining a case of deafness. If the patient cannot hear the vibrating tuning-fork held close to the ear, but hears it distinctly when placed in contact with the bones of the skull, the cause of the deafness lies in the middle or external ear, and the labyrinth and nerve are normal. Under normal circumstances, as the vibrations of a tuning-fork grow less distinct, they can be heard for a longer period through the air than through the bone. If the tuning- fork is heard for a longer time through the air than through the bone, notwithstanding the fact that there is some deafness to sounds conducted through the air, the deafness depends on disease of the nerve or labyrinth, or possibly on disease of the central mechanism of hearing. The sense of taste is readily tested by means of sapid substances, such as the following, in solution : sodium chloride (ten-per-cent. solution), tartaric acid (ten-per- cent, solution), strychnia sulphate (i-iooo), saccharine (1-250). These solutions may be conveniently kept in 586 DISEASES OF THE NERVOUS SYSTEM. long stoppered acid-test bottles, the long stoppers being useful in dropping the liquid on any particular part of the tongue. Narrow strips of filter paper, saturated with these solutions and then dried, may be carried in a pocket-case and dipped in water when used. Care must be taken that the action of the test solution is confined to the part of the tongue examined ; the patient must not be permitted to move his tongue about while the test is in operation. A weak galvanic current is a very convenient means of testing the taste sense. It may be applied by means of two insulated wires whose exposed ends are about two millimetres apart. Even a very weak current (as from one Leclanche cell) gives rise to a metallic taste whenever the gustatory sense is unimpaired. A strong current should not be used, as the pain it causes obscures the gustatory sensations. In the study of the trophic state of the muscles it is well to employ a graduated tape for the measurement of muscular atrophy. To insure accuracy a steel tape should be applied to the corresponding limbs of opposite sides, at exactly the same distances above and below the olecranon process for the upper extremity, and at exactly the same distances above and below the patella for the lower extremities. Two measurements should be made at each circumference of the limb examined — one with the tape applied loosely to the limb, the other with the tape drawn down tightly. In acute and severe spinal cord or peripheral nerve disease, it is sometimes well to make limb measurements every other day for a time. In unilateral atrophies the wasted limbs are to be carefully compared with the normal ones. In all cases where examination detects the presence of muscular atrophy, it is desirable to further interrogate the state of nutrition THE EXAMINATION OF THE PATIENT. 587 of the muscles by means of an electrical examination. The examination should always be commenced with a study of the faradic ^ irritability of the muscles, the reac- tions of the atrophied muscles being compared with those of the opposite side, if these are normal ; or, if they are not normal, with muscles that are ; or, better still, with the corresponding muscles of a normal person, if there is any doubt about the reactions obtained. One of the electrodes should have an interrupting handle and should be placed on the motor point of the muscle to be tested ; the other may be placed at any convenient spot, not necessarily in the median line of the body. It is important that the sponges of the electrodes be well satu- rated with water, preferably with water containing a small amount of common salt or bicarbonate of soda. It is also very important that the skin of the patient be thor- oughly moistened to reduce its resistance, before the examination is begun. The neglect of these very simple precautions has led to many mistakes on the part of be- ginners, who are apt to find a loss of faradic irritability where there is little or no loss. Before passing the cur- rent through the patient the examiner should take it for an instant himself. If the muscles under examination react well to the faradic current, it is unnecessary to further examine them with the galvanic current. If, however, they fail to re- act, or react only imperfectly, to the faradic current, it is desirable, though not necessary, to complete the electri- cal examination with the use of the galvanic current. This has the advantage of confirming any results obtained with the faradic current, and furthermore may give cer- ' A very reliable and convenient portable faradic battery is that known as the Barrett chloride-of-silver battery. The only objection to it is its expense ($25). 588 DISEASES OF THE NERVOUS SYSTEM. tain indications as to prognosis which the faradic current does not give. The precautions above mentioned in connection with the faradic examination apply to the examination with galvanism. In addition it is important to bear in mind that, in order to obtain the polar reactions satisfactorily, one electrode should be placed over an indifferent point, say over the sternum, or abdomen, or over some part of the spine. The galvanic battery should be provided with a current changer, and, if possible, with a milliam- peremeter and a rheostat. In studying the quantitative relation between the KCC and the ACC (see p. 175) in a muscle, it is well to use the weakest current that will give these contractions, as any difference, normal or patho- logical, in the irritability of the muscle to these two polar excitations is then more apparent than when a strong current is used. In a systematic examination of a case of nervous disease it is important to take note of the state of certain superficial and deep reflexes. Of the superficial reflexes, three are of especial importance — the plantar, cremasteric, and abdominal reflexes. The manner of obtaining these reflexes has already been sufficiently described. Of the deep reflexes the one which it is inost important to investigate is the knee-jerk. The knee-jerk may be con- veniently obtained when one leg is crossed over the other, by striking a sharp blow with the edge of the hand upon the patellar tendon, just below the patella. If the patient is in bed, the knee-jerk may be obtained by lifting the relaxed and extended leg a few inches from the bed with one hand, so as to put the quadriceps slightly upon the stretch, while the patellar tendon is struck with the edge of the palm, or the tips of the fingers of the other hand. An effort should be made to obtain the knee-jerk by THE EXAMINATION OF THE PATIENT. 589 Striking the quadriceps tendon at its junction with the patella, the quadriceps muscle being slightly on the stretch. If a distinct knee-jerk can be obtained in this way, as well as by striking the patellar tendon, the knee- jerk is said to be exaggerated. If, however, the knee-jerk is very active when the patellar tendon is struck, but can- not be obtained by striking above the patella, the knee- jerk is not exaggerated, but merely hypertypical, and is not to be considered abnormal. In testing the knee-jerk it is important that the extremity should be quite relaxed, and that the quadriceps muscle be put slightly on the stretch by the examiner, as above described. Neglect of the latter precaution causes frequent errors. If it is im- possible to obtain the knee-jerk in a given case, or if the knee-jerk is feeble, the effect upon it of " reinforcement " should be tried, — that is, a strong muscular effort should be made in some part an instant before the blow is struck upon the patellar tendon. Such a muscular effort has the effect, under normal conditions, of increasing the knee-jerk, and makes a feeble or doubtful knee-jerk appreciable. If, however, the knee-jerk is absent from disease, reinforcement has no effect upon it. A con- venient way of obtaining reinforcement is to cause the patient to hook together the semiflexed fingers of the two hands, and pull th-e arms vigorously in opposite directions. This is known as Jendrassik's method. If the knee-jerk is increased it is necessary to examine for the presence of ankle clonus. This is done by sup- porting the extended leg by one hand placed under the calf and sharply flexing the foot with the other. If there is ankle clonus, this is shown as a series of contractions, about six to the second, in the muscles of the calf. It is sometimes necessary to perform repeated dorsiflexions of the foot before obtaining the ankle clonus. Ankle clonus 590 DISEASES OF THE NERVOUS SYSTEM. is never present in health. It must not be confounded with the irregular semi-voluntary contractions, termed spurious clonus, that are observed in some hysterical persons. The wrist-jerk is elicited by a blow upon the tendon of the extensor indicis or extensor ossis metacarpi pollicis when they are made prominent by passive extension of the hand of the patient in that of the examiner. If much exaggerated, the wrist-jerk is easily obtained by striking any flexor or extensor tendons at the wrist. The wrist- jerk is frequently absent in normal individuals. The triceps or elbow jerk is obtained by raising the arm until the forearm hangs loosely downward parallel with the body, and then striking with the finger-tips or a percussor the tendon of the triceps above the olecranon. An active triceps-jerk is to be considered pathological. This reflex is very frequently absent in normal persons. The periosteal biceps-and-supinator-jerk is obtained when the periosteum of the lower end of the radius is struck a smart blow, the examiner taking care to have the elbow partly flexed at the time. This reflex is usually obtainable in health. To obtain what is known as the jaw-jerk, the patient's mouth should be partly open, and the examiner, placing one finger transversely across the middle of the chin, so as to depress the lip until the lower teeth show, strikes the finger thus held a sharp downward blow. The lower teeth should be watched for the jaw-jerk. The presence of a very well marked jaw- jerk usually indicates an extensive degenerative brain lesion, such as multiple sclerosis or general paralysis. In less degree it is often obtainable in health. In every systematic examination of a patient who is supposed to be suffering from organic disease of the central nervous system, it is important to investigate the THE EXAMINATION OF THE PATIENT. 59I ocular reflexes. The reflex to light may be tested by the use of a match or candle in a dimly lighted room, or by causing the patient to face a window, while the examiner alternately exposes the eyes and screens them with his hands. The associated movement of the pupil during accommodation (incorrectly called the reflex to accom- modation) may be tested by placing the patient with his side to the window and asking him to look first at the wall or ceiling and then at the tip of the examiner's finger held near his eyes. In such an examination the light reflex does not interfere with the accommodative move- ments. In degenerative brain and spinal cord diseases, it is important to look with especial care for the condition known as the Argyll-Robertson pupil, in which there is loss of reflex to light and preservation of the associated movement of the pupil during accommodation. In all lesions involving the cervical portion of the spinal cord, the cilio-spinal reflex, in which there is dilatation of the pupil on one side from painful irritation of the skin of the neck, should be tested. The hemiopic pupillary reaction need be looked for only in cases of brain disease in which there is hemiopia (see p. 116). In all cases of disease in which the sphincters of the rectum and bladder are affected, it is well to make a rectal examination with a view to ascertaining whether the nor- mal tone of the rectal sphincter is preserved or lost. When the finger is introduced into a normal sphincter there is slight relaxation followed by firm tonic contrac- tion. If the sphincteric centre in the cord is destroyed the sphincter is quite relaxed. The condition of the bladder sphincter may be inferred from that of the rectal sphincter. In every case of nervous disease in which there is dis- order of speech, it is necessary to investigate with much 592 DISEASES OF THE NERVOUS SYSTEM. care the character of this disorder. It is necessary to determine, first, whether the defect is a cerebral speech defect or merely a defect in articulation. If the defect is a cerebral defect, this constitutes an aphasia, and it is necessary to apply certain tests for the determination of the exact nature of the difficulty. As a routine practice an effort is made to test in turn the integrity of the motor memory, visual memory, and auditory memory areas. To appreciate the condition of the motor speech centre (Broca's centre) and its association-tracts, the examiner must note the ability of the patient (i) to speak volun- tarily and (2) his ability to repeat words spoken by the examiner. To test the integrity of the visual speech centre in the angular gyrus, the patient must be studied with regard to the following things : (i) his ability to understand written or printed words ; (2) his ability to write spontaneously ; (3) his ability to write the names of common things which he sees (as knife, button, etc.), which he hears, or which he touches ; (4) his ability to copy writing ; (5) his ability to understand written directions, as shown by his execut- ing them. To test the integrity of the auditory speech centre (and its association-tracts with other sensory areas), the following things are to be noted : (i) the power of the patient to recall the names of familiar objects seen, heard,^ touched, etc.; (2) his ability to understand ordinary speech ; and (3) his ability to recognize musical airs (whistling of "Yankee-Doodle," for example). There are certain facts of general application which bear on the examination of the patient and which it is well to keep constantly in mind. In most cases it is on the careful examination of the patient for the detection of the signs and symptoms of disease that the diagnosis THE EXAMINATION OF THE PATIENT. 593 largely rests. The history of the patient and of the de- velopment of his disease as gathered from the patient or his friends is, of course, of great inportance, but the diagnostic indications that are obtained in this way are to be used, in general, in subordination to the objective signs of disease. Where the indications derived from the two sources conflict, preference is always to be given to conclusions that are derived from an examination of the patient. In short, an effort should always be made to make the diagnosis as purely objective as possible, the history being used chiefly in subordination to the physical signs, for the confirmation and correction of the diagnosis based upon them. Where a clear history is obtainable from intelligent persons, it is of the highest value, and may lead to con- clusions which could never have been reached but for the history. In many cases, however, no history what- ever can be obtained, and in a considerable proportion of the cases that come under observation both in hospital and private practice the history that is obtained is unre- liable in some degree. There is no better opportunity for the use of good judgment on the part of the physician than in determining what part he may safely believe of a history that is thought to be in some degree uncertain, either from the ignorance or insincerity of his informants. It is always important for the physician to interrogate patients very closely as to the exact symptoms they have had during previous illnesses ; it is seldom safe to trust the names they give to their previous diseases. Thus one patient of considerable intelligence insisted that he had recently had acute articular rheumatism in his knees, but a careful inquiry showed that he had had paralysis and atrophy in the lower extremities, and the disease proved to have been alcoholic neuritis. Another patient insisted 594 DISEASES OF THE NERVOUS SYSTEM. that he had had severe " sciatica " in one leg, but close questioning showed that the pain was not in the back but in Xhe. front of the thigh, and the condition proved to be an anterior crural neuritis. It is a common error on the part of students to pass too quickly to the special examination of their patients. Thus the tyro in neurological diagnosis is apt to test the knee- jerks in a case of paralysis in a very early stage of the examination, in much the same way that the beginner in physical diagnosis rushes with his stethoscope at every patient who has a cough. A very careful general survey of the case, including not only the subjects mentioned in the first part of this chapter, but also in many instances the condition of the pulse, respiration, and temperature, should precede the investigation of the special manifes- tations of nervous disease. If this has been done, the physician will have often gathered enough facts concern- ing the nature of his case to enable him to predict with some degree of accuracy the results of his special exami- nation, which he interprets, at least provisionally, as he proceeds. If, on the other hand, he begins with his special investigation, the results obtained can mean little or nothing to him until a more general inquiry has been made, and will obscure rather than clear his way. CHAPTER VIII. ILLUSTRATIONS OF DIAGNOSIS. The following illustrative cases are placed here with a view to showing how the methods of diagnosis are em- ployed in actual practice. The cases are for the most part typical, and present few diagnostic difficulties but some of them deviate considerably from the common types of disease, and illustrate some of the difficulties in diagnosis that so frequently arise. I. A man fell headlong from a scaffold, a distance of twelve feet, and at once became paraplegic. Examination showed the sixth cer- vical vertebra to be somewhat displaced. Below the arms there was complete motor paralysis ; in the arms there was complete paralysis of the intrinsic muscles of the hands, flexors and extensors of the wrists, and triceps, and partial paralysis of the biceps, supinators, and pronators. There was loss of sensation to pain or touch below a V-shaped line across the upper part of the chest, and, roughly speak- ing, in the inner half of the arms, forearms, and hands. It was in- ferred from the distribution both of the motor and the sensory loss, that there was a destructive lesion of the seventh and eighth cervical segments of the spinal cord (see pp. 20 and 249). Above the line of sensory loss was an area of hyperalgesia, which extended to the lower part of the neck. This indicated that the fifth and .sixth segments of the cord were partially dawiaged. From the completeness of the motor and sensory loss in the parts below the level of the lesion, it was inferred that the cord was destroyed in a large part of its trans- verse extent at the level of damage. The examination of the reflexes confirmed this opinion, for the knee-jerks, cremasteric, abdominal, and plantar reflexes were abolished, the knee-jerks being thus lost in cervical injuries only in cases of severe damage to the cord. The 595 596 DISEASES OF THE NERVOUS SYSTEM. bladder and rectum were emptied automatically, which showed that the reflex centres of the cord for the bladder and rectum were no longer under cerebral control. The diagnosis of the nature of the lesion in this case presented no difficulties. The damage to the cord was plainly such as could be produced only by the crushing effect of displacement of bone. The fact that there was only slight external evidence cf displacement did not render this view any less probable, because it is common in cases of fracture-dislocation of the cervical spine for the displaced vertebra to spring back at least partially into place. The patient died in less than two days after the accident, and the autopsy confirmed the diagnosis. There was a dislocation forward of the sixth upon the seventh cervical vertebra, the seventh and eighth cervical segments of the cord were severely crushed, and there were indications of slighter damage (chiefly hemorrhage into the central canal) to the sixth and fifth segments. 2. A young man, aged twenty-three, and of unusually strong build, was suffering from a considerable degree of paralysis in the legs and slighter paralysis in the arms when he first came under observation. Examination showed that the loss of power in the legs involved chiefly the anterior and posterior tibial groups of muscles and the extensors of the knee, the adductors and abductors of the thigh and the flexors of the knee being involved in less degree. In the upper extremity the loss of power was almost confined to the muscles of the forearm and hand, the extensors of the wrist being especially weak. The paralyzed muscles, both in the upper and lower extremities, were flabby and wasted, and showed the RD, the wasting and the changes in irritability being most pronounced in the muscles that were weakest. Sensi- bility to touch and pain was slightly diminished below the knees. Elsewhere in the legs there was a marked degree of hyperalgesia. The anterior crural nerves were exceedingly sensitive to pressure. The muscles of the legs were very tender to firm pressure. From lime to time there was considerable spontaneous pain of a shooting character in the legs. In the upper extremities there were no dis- turbances of cutaneous sensibility, but the forearm muscles were ten- der to pressure, and there was some spontaneous pain in the arms. The knee-jerks were abolished. The bladder and rectum were under per- fect control. The patient's mind was clear. The temperature was normal. The paraplegic distribution of the symptoms in this case immediately suggested disease of the spinal cord or peripheral nerves. ILLUSTRATIONS OF DIAGNOSIS. 59/ Spinal cord disease was, however, quickly excluded. Slow compres- sion of the cervical cord might cause partial loss of power in the upper and lower extremities, and disturbances of sensibility, but could not be held responsible for the muscular atrophy, tenderness of the mus- cles, and loss of knee-jerk observed in this case. A lesion in the lumbar cord might account for the loss of power, sensory disturb- ances, wasting, and loss of knee-jerk, but such a lesion would prob- ably involve the functions of the bladder and rectum, and would cer- tainly not explain the symptoms in the upper extremities. In short, no single lesion of the spinal cord would be adequate to explain all the symptoms here present, and the supposition of multiple lesions of the cord was not t® be seriously considered until more likely ex- planations had been sought. On the other hand, the assumption that the symptoms were due to a multiple affection of the peripheral nerves, afforded an explanation of the phenomena present that was thoroughly satisfactory. The paralysis, atrophy, RD, sen- sory disturbances, loss of knee-jerk, and preservation of the functions of the bladder and rectum could be thus explained. That the process in the nerves was a neuritis, was shown by the tenderness of nerve- trunks, the pain, the hyperalgesia, and the tenderness of the muscles. The diagnosis, then, as based on the objective features of the case, was multiple neuritis involving mixed nerves of both upper and both lower extremities. Certain features of the case, namely the slight degree of anesthesia, the prominence of irritative sensory symptoms, as pain and hyperalgesia, and the tenderness of the muscles, sug- gested the dependence of the multiple neuritis on alcohol. This inference was borne out by the history. It was learned that for sev- eral years the patient had been in the habit of using alcoholic drinks very freely, though never to the extent of producing intoxication. He drank chiefly beer, the quantity averaging from fifteen to twenty glasses a day. Until eight weeks before he came under our obser- vation he was in good health. Then he began to suffer from numb- ness and pains in the legs, to which was soon added a gradual but rather rapidly progressive paralysis, first of the lower then of the upper extremities. Thus the history confirmed the diagnosis of alcoholic multiple neuritis. The ultimate recovery of the patient was another evidence of the correctness of the diagnosis. 3. A boy, aged eighteen, complained of weakness in both lower extremities. It was immediately observed that his gait was peculiar. Each leg was brought forward in turn with considerable effort, and 598 DISEASES OF THE NERVOUS SYSTEM.' was observed to be rigid and extended. Examination showed that the loss of power in the legs was nowhere considerable ; the weakness was most marked in the flexors of the thighs, knees, and ankles. The extensors of the knees showed no appreciable loss of power. In the upper extremities power was normal. The muscles of the legs were the seat of extensor spasm, which was especially marked during move- ment. The muscles showed no atrophy or loss of tone but were, on the contrary, well developed and firm. The electrical reactions were normal. The knee-jerks were greatly exaggerated on either side and an ankle clonus was readily obtainable. The functions of the bladder and rectum were normally discharged. It was inferred from this combination of weakness and spasm in the legs that the case was one of involvement of the pyramidal tracts of the cord. That the lesion was confined to these tracts was made probable by the entire absence of sensory and trophic symptoms. It was learned from the patient that the spasm and weakness had come on gradually during the two preceding years, the symptoms having been at first more marked in the right than in the left leg. The apparent limita- tion of the process to the pyramidal tracts and the gradual and slow development of the symptoms left little doubt that the morbid process was degenerative in nature. The case was, therefore, to be regarded as one of spastic paraplegia from sclerosis of the lateral pyramidal tracts. But there remained the question, is this lateral sclerosis pri- mary or secondary ? Usually cases of lateral sclerosis are secondary to disease of the brain or spinal cord. There were no evidences whatever of a cord lesion to which a lateral sclerosis might be second- ary — no symptoms suggesting myelitis, or tumor or compression of the cord from any cause. There were no signs of vertebral disease. An endeavor was next made to discover signs of brain disease, old or recent. It was observed that the patient was mentally dull, and had some hesitation in speech, but there were no other cerebral symptoms. The skull was well developed and symmetrical. There was no stra- bismus or nystagmus. The patient was free from headache. Inquiry into the history of the case likewise failed to give evidence of cerebral disease. There was no history of traumatism during birth or of con- vulsive seizures during infancy or childhood, and, as already stated, the symptoms of spinal cord disease did not begin until two years before the patient came under observation. As no evidences could be obtained of brain or cord disease to which degeneration of the lateral tracts might be secondary, the case was regarded as one of primary ILLUSTRATIONS OF DIAGNOSIS. 599 lateral sclerosis. It must be admitted, however, that this diagnosis was not perfectly satisfactory. The mental retardation and speech disturbance remained unaccounted for ; and as cases of unquestionable primary lateral sclerosis are of very rare occurrence as compared with cases of secondary lateral sclerosis, the possibility that the process was in this case secondary to an old and obscure cerebral lesion could not be entirely excluded. 4. A boy, aged ten, slipped upon the ice and fell to the ground in the sitting posture. He walked to his home, which was some distance away, and after several hours began to complain of weakness, numb- ness and pain in his legs. Examination about twenty-four hours after the fall showed complete loss of power below the knees and consid- erable weakness of the thigh and hip muscles. Sensation was un- impaired but for numbness and tingling in the legs. The knee-jerks were abolished, and there was incontinence of urine and faeces. There was a slight elevation in temperature. In the course of a few days the muscles of the thighs and hips lost all power, and the tactile and pain senses were abolished below a transverse line a short distance above the pubes. The plantar and cremasteric reflexes were lost at this time, but the abdominal reflex was preserved. There was still a slight rise in temperature. The diagnosis of the position of the lesion in this case presented no difficulties. The initial loss of power in the legs, the abolition of the knee-jerks, and the paralysis of the sphincters indicated clearly that the structures in the lower part of the luinbar enlargement which subserve motion and the visceral and tendon reflexes were the seat of disease. The initial preservation of sensibility in the legs made it probable that the damage was limited chiefly, if not entirely, to the motor structures of the cord. The subsequent loss of sensibility in the legs and the ascent of the motor paralysis to the flexors and exten- sors of the thigh led to the inference that there had been an increase both in the transverse and vertical extent of the lesion. The com- pleteness of the motor and sensory loss made it probable that the lesion involved the greater part of the transverse extent of the cord. The vertical extent of the lesion was inferred from the distribution of the paralysis and the state of the various reflexes. The paralysis of the rectal sphincter, the loss of sensibility over the perineum, and the loss of plantar reflex showed that the cord was involved as low as its sacral segments. The loss of cremasteric reflex showed that the cord was involved as high at least as the first or second lumbar segments. 6oo DISEASES OF THE NERVOUS SYSTEM. That the lesion did not extend much higher than this was inferred from the preservation of the abdominal reflex, which depends on the integrity of the dorsal ners'es from the seventh to the twelfth, and also from the transition to normal sensibility a short distance above the pubes. The diagnosis of the nature of the lesion was less simple. The extension and progress of the motor and sensory symptoms and the presence of fever made it certain that the lesion soon became inflam- matory in character, whatever may have been its original character. It was believed by some that the initial lesion was hemorrhage into the gray matter of the cord, but the facts that the symptoms did not come on for several hours after the fall, and that they developed rap- idly but not suddenly, made it more probable that the lesion was from the first an inflammation. The diagnosis of lumbar myelitis was confirmed, if such confirmation was needed, by the subsequent course of the case. The paralyzed muscles atrophied greatly, and showed the RD, bed-sores formed, and the patient at length died of exhaustion. 5. A man, aged thirty-two, presented himself with inco-ordination and weakness in the lower extremities. Both these symptoms were apparent in his gait. As the patient progressed unsteadily across the floor, his feet were lifted high and brought to the ground with an irregular flap. A slight degree of dropping of the feet from weak- ness of the anterior tibial groups of muscles was also observable. Examination showed slight inco-ordination of the upper extremities, but no weakness. In the legs there was a high degree of inco- ordination, and the patient was unable to stand with his eyes closed. The loss of power in the legs appeared to be confined to the anterior tibial and peroneal groups of muscles, but the patient said he felt weak also in the knees. The anterior tibial and peroneal muscles showed a slight degree of atrophy and a partial form of RD. The posterior tibial group showed partial RD, but no appreciable weak- ness or wasting. Sensibility was normal except on the soles and backs of the feet, where' there was slight anaesthesia and analgesia. There were panesthesise in other parts of the legs, and from time to time considerable sharp pain. The knee-jerks were abolished on both sides. By far the most obtrusive symptom in this case was the inco- ordination. A high degree of inco-ordination may be of cerebral, spinal, or peripheral origin. In this case there was nothing to suggest ILLUSTRATIONS OF DIAGNOSIS. 6oi brain disease. The associated loss of power in the legs, the atrophy, the RD, the disturbances of sensibility, and the loss of knee-jerks, all indicated that the lesion was one of the cord or peripheral nerves. A lesion of the posterior columns of the cord and posterior root-zones would explain the presence of inco-ordination, pains in the legs, slight antesthesia, and loss of knee-jerks. A lesion of these structures almost invariably depends on a degenerative process, and then gives rise to the clinical picture of locomotor ataxia. But the diagnosis of locomotor ataxia did not afford a full explanation of the symptoms, in this case ; it did not explain the presence ot weakness, wasting, and altered electrical reactions. These symptoms might depend either on a limited lesion of the ganglion cells of the anterior horns in the middle of the lumbar enlargement, or on disease of the motor fibres originating in these structures and forming part of the pe- ripheral nerves. The former condition is not an associated lesion of locomotor ataxia ; the latter frequently is. All the symptoms, then, might be explained on the supposition that we had to deal with a case of locomotor ataxia with associated changes (neuritis) in certain peripheral nerves. But this is not the only condition that would account for the symptoms. As intimated above, the inco-ordination present might depend on a lesion limited exclusively to the peripheral nerves. Such a lesion, involving both the motor and sensory fibres of mixed nerves, would explain satisfactorily not only the inco- ordination but also the weakness, atrophy, RD, loss of knee-jerks, and sensory symptoms. In short, the symptoms of the case might be satisfactorily explained either by a locomotor ataxia with associ- ated neuritis or by a multiple neuritis alone. The distinction between these conditions could not be made from the facts gathered by the examination of the patient. It therefore became necessary to see what bearing the history of the case might have upon the diagnosis. It was learned that six months before the date of examination the patient was in fair general health. He then began to lose flesh and suffered from numbness, tingling, and sharp pains (never very severe) in the legs. In a few months he grew unsteady in walking and developed some weakness in the legs. Both these symptoms increased rather rapidly. Ten years ago the patient had a hard chancre and during the two years previous to examination had used alcohol in great excess. The history of excessive use of alcohol before the onset of the symptoms rendered an alcoholic neuritis a jDrobable condition ; the clear history of a hard chancre would explain the presence of loco- 6o2 DISEASES OF THE NERVOUS SYSTEM. motor ataxia. The facts of etiology, therefore, did not aid in solving the diagnostic problem. But the following facts all pointed to the presence of alcoholic neuritis rather than locomotor ataxia : the relative youth of the patient (thirty-two years), the development of all the symptoms within so short a time as six months, the absence of ver}' severe fulgurating pains, and the absence of all ocular symptoms — especially the absence of the Argyll-Robertson pupil. This diagnosis was made with some caution, but was considered highly probable by several skilled physicians. It has not been borne out by time. A year has elapsed since the patient first came under notice, but there has been little or no improvement in the symptoms and the pains have been more severe than before. The diagnosis,' therefore, still remains uncertain. 6. A man, aged thirty-three, complained of pain in his right arm. Inspection showed that the extensors of the wrist were paralyzed and gave rise to pronounced wrist-drop. The ilexors of the wrist showed some apparent loss of power owing to the dropping of the wrist, but there was no actual paralysis. The muscles on the back of the forearm were considerably atrophied and showed the RD. Sensibility was unimpaired. The limitation of paralysis and degenerative atrophy to the extensors of the wrist on one side immediately suggested the dependence of these symptoms on a lesion of the musculo-spiral nerve. The power of the supinator longus muscle was then tested, and it was found to be somewhat diminished. It also showed a diminution in faradic irritability, and equal and somewhat sluggish polar reactions to the galvanic current. These observations tended to confirm the diagnosis of musculo-spiral paralysis. The history of the case was next considered with a view to its bearing on this diagnosis. Careful inquiry was made for some cause of pressure on the musculo-spiral nerve, but none could be found. It was learned that the paralysis had come on in the course of a few days, and that it had now lasted several weeks. It was also learned that for some weeks before the paralysis appeared there had been pains in both forearms. The patient was a painter and had recently been much exposed to lead in "flatting." These facts strongly suggested the dependence of the paralysis on lead, but the apparently unilateral distribution of the palsy, together with the absence of a lead line ^ This case illustrates well the difficulties of diagnosis. The correct diagnosis was of much importance in this case, as the prognosis is very different in the two forms of disease. ILLUSTRATIONS OF DIAGNOSIS. 603 or a history of colic, rendered lead palsy improbable. A more care- ful examination was now made of the left arm. Slight weakness was soon detected in the extensors of the wrist and an electrical examination showed a decided diminution of faradic irritability in these muscles. The discovery of involvement of the extensors of the left arm, slight though it was, entirely altered the aspect of the case. The bilateral extensor paralysis, preceded by slight sensory symptoms and occurring in a painter, made it evident that the case was one of lead neuritis. The unequal involvement of the muscles of the two sides is an unusual feature of lead paralysis. The slight loss of power in the supinator longus of the right side did not militate against the diagnosis, for such partial involvement of the supinator is not rare in lead palsy. 7. A boy, aged ten years, came under my observation on account of the frequently repeated epileptiform seizures to which he was sub- ject. Inspection showed the patient to be much below the average size of boys of his own age — his twin brother was about four inches taller and correspondingly larger. The walk of the patient was exceedingly unsteady, and showed considerable weakness in the lower extremities ; there was a high grade of mental weakness (imbecility), and only monosyllabic speech. Examination showed all four extremi- ties to be small and imperfectly developed. The weakness in the legs was not confined to a particular group of muscles, but involved the leg as a whole. The extensors, however, were very slightly affected. The muscles, though small, showed no indication of atrophy. Their tone was normal or even greater than normal, there being slight ex- tensor spasm at times. The electrical reactions were normal. Both knee-jerks were much exaggerated. The skin reflexes were all active. Ankle clonus could not be obtained. In the upper extremity there was a well marked intention tremor. Sensibility was everywhere normal. The head was abnormally small and the palate was high- arched. The prominent features of this case were the mental weak- ness, the evidences of arrest of development in the extremities and in the cranium, the occurrence of epileptiform attacks, and the weakness and spasm in the legs. All of these conditions indicated the pres- ence of a cerebral lesion. Certain of the symptoms, as weakness and spasm in the legs, occurring by themselves would suggest spinal cord disease rather than a cerebral process, but with the associations above mentioned these symptoms indicate a cerebral and not a spinal cord lesion. The bilateral distribution of the symptoms and their involve- 604 DISEASES OF THE NERVOUS SYSTEM. ment of the arms as well as the legs, indicated that the motor path was implicated in a considerable part of its extent in bot'^ hemi- spheres of the brain. The signs of retarded development, both mental and physical, made it plain that the morbid process was one of long duration, in fact that it must have commenced in infancy or early childhood. Cerebral palsies at this time of life are either congenital or acquired, the congenital form being generally dependent upon injury during birth, the acquired form depending on a variety of dif- ferent conditions in different cases (see p. 367). It was impossible to say with certainty in which of these catagories the case belonged, with- out taking into consideration the history of the case. But the pres- ence of a high grade of mental defect, the physical evidences of con- siderable retardation of growth, and the bilateral and symmetrical distribution of the symptoms suggested that the condition was a birth palsy. This view was corroborated by the history of the case. It was learned that the patient was the first child born in a twin labor, that the mother was at that time a primipara, that the second stage of labor lasted nearly twenty hours, and that the child had several general convulsions during the hour following delivery. These con- vulsions were frequently repeated during the first months of life and had continued, with decreasing frequency, ever since. These facts were a perfect confirmation of the diagnosis, and removed any doubts as to the nature of the lesion, which could have been nothing else than a meningeal hemorrhage, extending over both convexities, result- ing eventually in a sclerosis and atrophy of the parts of the cortex and subcortical substance involved and secondary degeneration of the pyramidal tracts. 8. A child, three years of age, came under observation suffering from paralysis in both lower extremities and partial loss of power in the right arm. There were typical athetoid movements in the fingers of the right hand, with temporary flexor spasm, moderate atrophy of the forearm muscles, and slight loss of power. The faradic irritability of the forearm muscles was slightly diminished, but there was no RD in any muscles of the upper extremity. Sensibility was nowhere affected. These conditions in the upper extremity at once suggested a cerebral palsy, and this idea was strengthened by observa- tion that the patient was backward in intelligence and speech. The lower extremities were next examined to see whether their condition corroborated the diagnosis of a cerebral palsy. There was a high grade of paralysis of all the muscles of the legs except the flexors of ILLUSTRATIONS OF DIAGNOSIS. 605 the hips, the paralyzed muscles were greatly atrophied and flabby, and showed the RD. Below the knees the paralysis was absolute and the feet were in equinus. The knee-jerks were lost. The sphincters were unaffected. Sensibility was everywhere normal in the lower extremities. The extremities were cold and the color of the skin showed defective circulation. The presence of a high grade of paralysis and atrophy in the legs, the reaction of degeneration in the paralyzed muscles, and the loss of knee-jerks all pointed to the existence of a lesion of the lumbar en- largement, involving the ganglion-cells of the anterior horns. That the lesion was confined to these motor structures was shown by the fact that only the trophic, motor, and reflex functions of the cord were impaired, the various forms of sensibility being intact. The same case therefore presented unmistakable evidences of two quite distinct lesions, one involving the motor path in the brain, probably in the cortex or subcortical region, the other involving motor ganglion- cells in the lumbar enlargement of the cord. The cord symptoms were of the kind observed in an advanced stage of acute poliomyelitis. Further indications as to the nature of the lesions in the brain and cord were derived from a consideration of the onset of the symptoms. It was learned from the mother of the patient that, one 3'ear before the child came under observation, it became restless and feverish for sev- eral days, and at the end of this became delirious, had high fever, and vomited repeatedly. During this latter period of acute illness there were repeated clonic spasms in the right arm and leg, strabismus, and ptosis. The one-sided convulsions lasted about two days and then the rigid arm was noticed to be without power. The mother was uncertain as to the state of the right leg at this time, but believes it was little or not at all weak. Five days after the onset of the convul- sions it was observed that there was complete loss of power in both legs. There was gradual recovery of power in the right arm, but little or no improvement in power in the legs, which soon wasted. With this history there could be little doubt that both the cerebral and the spinal cord lesion were dependent on similar morbid processes, infectious in origin, and giving rise in the one case to an acute corti- cal lesion in the left motor region (polio-encephalitis, thrombosis of cerebral veins?), in the other to an acute anterior poliomyelitis. Cases similar to this one are very rare, but are instructive as illustrating the relationship in etiology between some cases of acquired infantile cerebral palsy and anterior poliomyelitis. 6o6 DISEASES OF THE NERVOUS SYSTEM. Q. A girl, aged nine, was suffering from partial paralysis of the right arm and right leg when she first came under observation. In the leg the paralysis was of slight degree and involved about equally all the muscles of the limb. In the arm the degree of weakness was greater, and there was a well marked contracture of the flexors of the forearm. The face was uninvolved. There was no atrophy of the affected muscles, and sensibility was everywhere normal. The hemiplegic distribution of the weakness in this case suggested the dependence of the paralysis on a cerebral lesion. Some support was lent this view by the fact that there was internal strabismus of the left eye, such as often remains after an infantile cerebral palsy. Moreover, the knee-jerk was greatly exaggerated on the paralytic side and unchanged on the normal side, and this indicated a secon- dary degeneration of the pyramidal tracts on the paralytic side, such as usually follows a cerebral palsy. But, on the other hand, certain facts about the case failed to confirm the diagnosis of a cerebral palsy, and even tended to disprove it. First there was no loss whatever in mental power. The patient was, on the contrary, highly intelligent and well developed mentally. Such entire immu- nity from mental defect is unusual in infantile cerebral palsies which give rise to a considerable degree of permanent paralysis. Sec- ondly, there were no evidences of arrest of development in the affected limbs, and such evidences are almost always present in cerebral palsies of children if the paralysis has endured a consid- erable length of time. An inquiry into the history of the case soon did away with any doubts as to the position and nature of the lesion. It was learned that the child had been perfectly well until she was seven years of age (or two years before), and that she then developed weakness in both legs. This weakness slowly increased in the legs and extended to the arms, so that at the end of six months there was complete paralysis of motion below the neck. There was also entire loss of sensation below the neck. The muscles of the neck had meanwhile grown weak, and the patient was unable to keep the chin from resting on the neck. She was kept quiet in the recumbent position for many months, and gradually the anaesthesia wore away. Then there was a gradual return of power in the legs and left arm, but the right arm continued weak. In course of time the muscles of the neck regained full power. The paraplegia could have been due only to disease of the upper cervical region of the cord, and the gradual onset of the ILLUSTRATIONS OF DIAGNOSIS. 607 symptoms and recovery after a period of recumbency left no doubt that the lesion was a compression of the cord from caries of the upper cervical vertebrae. At the time vs^hen the patient came under observation there were no evidences whatever of disease of the cer- vical vertebras, and the conditions bore no little resemblance to those observed in cerebral palsies. The strabismus, it was learned, was present many years before the development of nervous symptoms and therefore had nothing to do with these symptoms. It is doubt- ful whether a correct diagnosis could have been made in this case without some knowledge of the previous history. 10. A man, aged fifty-four, complained for several days of head- ache and slight numbness in the left extremities, and soon after arising one morning became rapidly hemiplegic. The loss of power involved the left leg, left arm, and left side of the face in its lower part. There was no loss of consciousness at the time of the onset, but the patient felt giddy and had considerable headache. When examined, about twenty-four hours after the onset of the hemiplegia, the patient was in a state of stupor from which he could be partially aroused. Temperature, 100 ° Fah. ; pulse, 80 ; radial arteries, atheromatous ; respiration, 20, regular. There was complete left hemiplegia, and the arm and leg muscles were quite relaxed. Sensi- bility was diminished in the extremities in their distal portions. The knee-jerfe was greatly diminished on the left side, normal on the right. The pupils were equal and moderately large. There was no spasm or other irritative symptoms. The diagnosis of the position of the lesion was not difficult. Complete left-sided hemiplegia might result from a lesion in the right motor path anywhere between the motor cortex and the upper half of the pons. The absence of spasm made it exceedingly im- probable that the lesion was cortical or subcortical, and there was nothing to indicate a lesion of the crus. It was therefore highly probable that the lesion was in the right internal capsule — the seat of damage in most cases of sudden hemiplegia. The diagnosis of the nature of the lesion was less easy. A sudden hemiplegia usually depends on hemorrhage or acute softening. Acute softening is gen- erally due to thrombosis from atheroma or from syphilitic endarte- ritis, or to embolism. Embolism was excluded because there were no evidences of heart disease, and because there were distinct pre- monitory symptoms before the onset of the hemiplegia. Thrombo- sis from atheroma was considered /,.;probal)le on account of the 6o8 DISEASES OF THE NERVOUS SYSTEM. age of the patient. Either cerebral hemorrhage or thrombosis from syphilitic endarteritis would explain the symptoms, and between these two conditions it was difhcult to decide. The facts which favored the supposition of hemorrhage were the age of the patient and the presence of atheroma of the accessible arteries. The facts favoring syphilitic endarteritis were the presence of distinct pre- monitory symptoms (headache, numbness, slight weakness) for several days before the onset, and the absence of loss of con- sciousness. These facts also weighed against the diagnosis of hemorrhage, for in hemorrhage true premonitory symptoms are rare, and a capsular hemorrhage sufficiently large to produce com- plete hemiplegia would almost certainly have given rise to loss of consciousness. Although no history of syphilis could be obtained, several tubercles were observed on the upper part of the chest, which had the appearance of gummata. On the whole, therefore, the facts of the case pointed to acute softening from syphilitic endar- teritis rather than to hemorrhage. The patient was put on large doses of iodide of potassium, and in time made a good recovery. In about two weeks from the time of the onset he had largely recov- ered power in thehemiplegic parts and the headache had grown much less severe. Eventually gross power was entirely regained, but there remained some awkwardness in executing the finer movements of the fingers. Slight attacks of giddiness occurred from time to time after recovery of power, and the knee-jerk became greatly exaggerated on the left side. There also developed an ankle clonus on this side. It was learned many months after the attack that the patient had had a chancre several years before. About eighteen months after the hemiplegia the wife of the patient came under observation for an abundant syphilitic eruption over both legs. These facts all con- firmed the diagnosis of the nature of the lesion underlying the hemiplegia. II. A woman, aged thirty-four, was admitted to the hospital in a condition of stupor and with slight elevation of temperature. About two inches above the root of the nose and just a little to the left of the median line was a suppurating incised wound. Examination showed that the frontal bone was fractured just beneath the wound. The patient could be roused for a moment from her stupor, and at times uttered partially intelligible monosyllables when so aroused. The eyes had a fixed, staring expression. At times the left hand was placed on the head while the patient groaned with pain. The ILLUSTRATIONS OF DIAGNOSIS. 609 temperature was loi °. There was nothing noteworthy about the pujse or respiration. The pupils were equal, of moderate size, and reacted tO' light. There was incomplete ptosis of the left lid. The right arm was almost completely paralyzed ; the right leg was less completely paralyzed. The right arm was constantly rigid ; no spasm elsewhere. There was general hypersesthesia. On the right side there was great exaggeration of the knee-jerk and violent and prolonged ankle clonus. On the left side the knee-jerk was in- creased, but ankle clonus could be obtained only with difficulty. There was entire loss of control over the sphincters. The presence of loss of power in the right arm and partial loss of power in the right leg, with exception of the face, made it certain that there was a lesion in the left motor path. A lesion involving the cortex might give rise to such a partial hemiplegia but would produce more decided irritative symptoms than were here present. A lesion in the internal capsule or in the motor path below the internal capsule would not be apt to exempt the face unless the lesion were vei7 small. But a lesion between the cortex and the internal capsule might be of considerable size and nevertheless involve chiefly the path to the arm of the opposite side, and such a lesion would not be apt to cause clonic spasm. It was upon the whole probable, therefore, that the lesion was one of the subcortical white substance of the left motor path. The diagnosis of the nature of the lesion could be de- termined with less certainty. The limitation of the paralysis to the parts above-mentioned and the completeness of the motor loss made it probable that the lesion was destructive in character. Such a ' lesion might be a vascular lesion, or an inflammatory lesion, or a new growth. But it was known that the symptoms were not of sudden onset, and hence a vascular lesion was out of the question. The presence of fever made it likely that the lesion was inflammatory in nature. It could scarcely be meningitis, for mere meningitis would not give rise to such complete and definitely limited paralysis, and would cause more decided irritative symptoms than were here present. An abscess, however, would be competent to cause a local paraly- sis, would not necessarily be accompanied with irritative symptoms and would almost certainly be attended with fever. The presence of a neglected compound fracture of the frontal bone offered a sufficient explanation for the occurrence of abscess. The patient died in a few days without developing any new symp- toms of importance. The autopsy showed the presence of an abscess 39 6lO DISEASES OF THE NERVOUS SYSTEM. of the left frontal lobe, which contained from two to three ounces of pus. The abscess extended back to and somewhat into the white substance beneath the motor area. 12. A boy, aged ten, much emaciated and anaemic, was in a state of deepening coma when examined for the first time. He lay upon his back picking alternately at the bedclothes and at his lips. The pulse was 130, small, feeble, and irregular. Respiration was irregu- lar (20-30 per minute). Temperature, i03|-° Fah. There was con- jugate deviation of the eyes to the left. The pupils were of moderate size, equal, and reacted to light. There was some rigidity of the muscles of the back and sides of the neck. The right arm and leg and the left arm were the seat of rigidity, which varied somewhat in degree from hour to hour. No distinct loss of power could be made out. The knee-jerk of the right side was exaggerated. The left knee-jerk could not be tested as the leg and hip-joint were immo- bilized on account of an exacerbation of the hip-joint disease from which the patient had suffered several years. Examination revealed the presence of a considerable grade of optic neuritis. The most important localizing symptoms in this case were symp- toms of an irritative nature — rigidity in the extremities, conjugate deviation of the eyes and rigidity of the muscles at the back and sides of the neck. The presence of these conditions indicated a diffuse meningeal process. The rigidity of the right limbs and the conju- gate deviation of the eyes to the left were referred to irritation of different portions of the left and right motor regions respectively. The rigidity of the neck muscles was referred to irritation of struc- tures at the base of the brain. It was inferred from the presence of the irritative symptoms just mentioned, from the presence of double optic neuritis and the considerable elevation in temperature, that the morbid process was inflammatory ; in other words, a meningitis afTecting both the base and convexity of the brain. The presence of hip-disease made it exceedingly probable that the process was tuber- cular in nature. No physical signs of lung disease could be detected. The presence of optic neuritis and of irregular respiration suggested that the process was tubercular, although both these conditions may be and are met with in other forms of meningitis. The diagnosis of meningitis was confirmed by the history of the case. The patient had had hip-disease for several years. About ten days before the examination above recorded he had an exacerbation of pain in the hip, with increase of rigidity of the muscles about the ILLUSTRATIONS OF DIAGNOSIS. 6l I joint. During this the temperature rose to 105° and he complained of general headache. The temperature fell to normal and the head- ache stopped. About this time he vomited once without known gastric cause. Four days before the examination the temperature rose to 103° and the patient complained of intense headache. The temperature continued, ranging between 101^ and 104°; there was re- peated vomiting, and delirium developed. Two days before, there was widespread rigidity and temporary paralysis of the left arm and leg. On the ninth day after the examination the patient died. At the autopsy was found tubercular meningitis of the base and convexity of the brain. Fresh miliary tubercles were present in both lungs. 13. A boy, aged twenty, complained for several months (probably five or six) of headache and of numbness and occasional ' ' twitching " in the right leg. In time the right leg became weak and occasional twitchings occurred in the right arm, the fingers of which some- times became numb. When examined for the first time the patient was in fair general health bvit suffered from severe and almost con- tinuous headache, which was sometimes general, sometimes limited to the left side of the head. The right leg showed some loss of power, which was most marked in the muscles below the knee. There was no wasting of the muscles, and the electrical reactions were normal. The right knee-jerk was exaggerated, and an ankle clonus could beobtained on this side. Tactile sensibility was dimin- ished on the foot and lower part of the leg. In the arm there was slight loss of power in the flexors of the wrist and fingers, as shown by diminution of the grasping power. From time to time, usually several times a day, there occurred convulsive twitchings in the right leg. At times these spasms were confined to the anterior and poste- rior tibial groups of muscles, at other times they extended to the muscles of the right hand and forearm and, more rarely, to the right side of the face. In some of these seizures in which the spasm was not limited to the leg the patient became unconscious for a few min- utes. There was a temporary increase in weakness in the extremities after they had been the seat of spasm. Intellect was unimpaired, but speech was somewhat disordered. There was usually a decided slowness in speech and an undue sepa- ration of syllables. At times the patient was unable to think of the names of familiar objects as paper, ink, knife, etc. Spoken and written words were perfectly understood. The use of objects was perfectly understood, and the patient was distressed at his inability 6l2 DISEASES OF THE NERVOUS SYSTEM. to recall and utter familiar words. The motor speech defect was regularly worse after spasm, whether this was or was not accom- panied by loss of consciousness. At times the motor speech defect was very slight. Examination of the fundus of either side showed a high grade of optic neuritis. The temperature, pulse, and respiration of the patient were normal. It was inferred from the hemiplegic distribution of the paralysis and spasm, from the disturbance of speech, and from the severity of the headache, that the patient was suffering from an intracranial process. The initial involvement of the right leg, and the gradual extension of the symptoms (weakness and spasm) to the right arm, made it exceedingly probable that the lesion involved the left motor tract where the paths for the leg and arm are farther separated than in the internal capsule or the parts below ; in other words, that the lesion involved the motor tract somewhere above the internal capsule — in the motor cortex or the corona radiata. From the frequently repeated clonic spasm it was inferred that the lesion invaded the motor cortex or the white substance immediately be- neath it. The extension of the paralysis and spasm made it proba- ble that the morbid process began in the motor structures related to the leg and had subsequently extended to the arm. It was learned that the involvement of the face in spasm was a recent development, and this indicated that the morbid process was gradually invading the path for the face. As to the nature of the lesion there could be little doubt. The gradual development of the symptoms during a period of several months made it certain that the morbid process was either a new growth or an inflammation. The inflammations which it was neces- sary to consider were chronic meningitis and abscess. Only a chronic syphilitic meningitis could give rise to well marked focal symptoms, and it was doubtful whether such decided focal symp- toms as existed in this case could be explained by a purely menin- gitic process. No history of syphilis could, however, be obtained, and while syphilitic infection could not be positively excluded, there was reason to believe such infection very unlikely. An abscess occu- pying the subcortical motor region would account for all the focal symptoms present, and perhaps for the headache. But there were no causal indications of abscess — no ear or bone disease, no evi- dences of suppuration elsewhere, not even a history of injury to the head. Moreover, the absence of fever made abscess improbable. ILLUSTRATIONS OF DIAGNOSIS. 613 On the other hand, everything learned from the examination and history of the case pointed to the presence of tumor. The gradual but distinct progress of well marked focal symptoms, especially paralysis and spasm, the severe and constant headache, the presence of a high grade of optic neuritis, the absence of fever — all these conditions favored the diagnosis of tumor. The diagnosis of the nature of the tumor vi^as difficult ; could not, in fact, be made. The absence of a history of syphilis made a syphi- loma unlikely. Thegood general condition of the patient, the ab- sence of fever during several weeks' observation, and the absence of physical signs of tubercular lung disease made a solitary tubercle un- likely, but did not justify its positive exclusion. Of the remaining forms of tumors, glioma and sarcoma were the ones to be most seri- ously considered ; but between these it was impossible to decide. The diagnosis of cerebral tumor was confirmed by autopsy. During the remaining six weeks of the patient's life the paralysis extended to the face and tongue, and a high grade of motor aphasia was devel- oped. The number, intensity, and extent of the unilateral spasms in- creased, and the patient one day had an apoplectic seizure, with re- peated general convulsions, in which he died. The autopsy revealed a large glioma involving the white matter, and, to a less extent, the cortex of the left hemisphere, in the motor region, and the adjacent portion of the frontal lobe. The tumor was highly vascular. In the middle of the mass was a recent hemorrhage of considerable size, which was undoubtedly the direct cause of the apoplectic seizure im- mediately preceding death. 14. A woman, aged forty-five, presented herself with weakness and loss of sensation iu her right arm. Examination showed that there was some loss of power in all the muscles of the arm, but no movements were entirely lost. There was no wasting of the limb, and all the muscles reacted normally to faradic and galvanic stimulation. There was loss of sensibility to pain and diminution in tactile sensibility over the entire arm as high as a sharply defined line over the acromion to the axilla. There were no trophic or vaso- motor changes in the limb. The knee-jerks were active, but not exaggerated. The patient was well nourished and in good general health, barring irregular menstruation incidental to the climacteric. The presence of weakness in the right arm without muscular atro- phy and changes in the electrical irritability of the muscles made it at once evident that the monoplegia was of cerebral origin. The seg- 6^14 DISEASES OF THE NERVOUS SYSTEM. mental distribution of the motor and sensory loss, and the sharp limi- tation of the latter, made it exceedingly probable that these symptoms were dependent on disturbance of the functions of the cortex, and were due to functional and not to organic disease. The functional nature of the disturbance was furthermore indicated by the entire ab- sence of all indications of organic cerebral disease. Interrogation of the patient elicited the fact that the arm trouble had developed a few weeks before, within a few minutes after the announcement of the sudden death of her brother. The dependence of the monoplegia upon emotional disturbance left no doubt that it was of purely func- tional (hysterical) nature. Applications of the faradic current to the weak arm caused an immediate improvement in grasping power and in tactile sensibility. It gave rise also to partial return of sensibility to pain in irregular areas over the arm. These facts were additional confirmation of the hysterical nature of the case. 15. A boy, aged ten, was picked up in the street in an unconscious condition and brought to the hospital. When seen a few minutes after he was having irregular movements of nystagmus and clonic spasms in the lower extremities. The seizures began regularly in the left leg and extended to the right leg, recurred every few minutes, and lasted from ten to sixty seconds. The spasm involved chiefly the an- terior and posterior tibial groups of muscles. The limbs were quite relaxed after each paroxysm. A convulsive seizure could readily be excited by dorsal flexion of the right foot, or by an a.ttempt to test the knee-jerk. On the right side no knee-jerk could be obtained ; on the left side the knee-jerk was exaggerated. No true ankle clonus could be obtained, but dorsal flexion of the left foot gave rise to irregular semi-voluntary contractions of the calf-muscles, which in a few sec- onds passed into spasm of the same distribution as the spontaneous seizures. The patient could with difficulty be partially roused for a few seconds. The rectal temperature was ioo|°, the pulse 100, weak, and irregular. In the absence of any knowledge of the history of this case it was impossible to come to a final conclusion as to the diagnosis. The most conspicuous symptom, clonic spasm in the lower extremities, in- dicated the presence of an irritative process in some part of the motor path. That this irritation was of cerebral origin was rendered prac- tically certain by the presence of stupor and nystagmus. The com- bination of clonic spasm, stupor, and elevation of temperature might have suggested meningitis, but the slight degree of the fever, the ILLUSTRATIONS OF DIAGNOSIS. 615 rapid recurrence of the clonic spasms, the absence of rigidity, and presence of nystagmus would not have lent much support to this view. The presence of nystagmus suggested the dependence of most of the symptoms upon a general disturbance of cerebral functions. No diagnosis was made, and it was decided to watch the further develop- ment of the symptoms before attempting to come to a definite con- clusion. The next morning all the symptoms had passed away. It was learned that the patient had slipped upon the sidewalk and had fallen, striking his head against the stone, just before being brought into the hospital. The symptoms that have been described were therefore due, in all probability, to a severe concussion of the brain. INDEX. Abducens nerve, 46 Abductor paralysis of vocal cords, 118 ; hysterical, 536 Abscess of the brain, 276, 373 ; acute, 374 ; chronic, 374 ; dis- tinction of, 375 Abscess of the spinal cord, 277, 418 Accessory portion, 57 Active delirium, 190 Acute alcoholism, 566 Acute anterior poliomyelitis, 426 Acute ascending paralysis, 524 Acute atrophic paralysis, 426 ' , Acute cerebral softening, 264 ; diagnosis of, 354 ; from embo- lism, 354 ; from syphilitic thrombosis, 355 ; from athero- ma, 356 ; from blood-states, 357 ; distinction from cerebral hemorrhage, 358 ; case of, 607 Acute lesions, 288 Acute rheumatism as a cause of nervous disease, 308 Adductor paralysis of vocal cords, 119 ^sthesiometers, uses of, 581 Age, influence of, in diagnosis, 290 Agraphia, 197 Albuminuria, transient, 209 Albuminuric retinitis, 159 Alcohol, excessive use of, 293 Alcoholic delirium, 293, 566 Alcoholic intoxication, 294 Alcoholic neuritis, 510 ; case of, 596 Alcoholic pseudo-tabes, probable case of, 600 Alexia, 201 Alternate hemiansesthesia, 128 Alternate hemiplegia, 76 Amaurosis, 142 Amblyopia, r42 ; temporary, 144 ; functional, 144 ; tobacco, 144 ; toxic, 145 ; ursemic, 145, crossed, 145 Amnesic aphasia, 202 Amyotrophic lateral sclerosis, 446 Ansemia, of the brain, 259 ; of the spinal cord, 260 Anaesthesia, 126 Anaesthesia dolorosa, 421 Anaesthetic leprosy, 523 Analgesia, 131 Anarthria, 193 Aneurism, intracranial, 382 Angle of facial nerve, 53 Ankle clonus, 125 ; examination for, 589 Anosmia, 141 Anterior crural nerve, paralysis of, 502 Antero-lateral ascending tract, 33 Antisyphilitic treatment, in- fluence of, in diagnosis, 328 Aphasia, ataxic, 197 ; conduction, 202 ; congenital, 203 ; motor, 195; sensory, 195; transient, 202 Apoplexy, 186 Apraxia, 201 Arachnoid, anatomy of, 60 617 6i8 INDEX. Aran-Duchenne type, 447 Argyll-Robertson pupil, 115, 591 Arsenic as a cause of nervous disease, 314 Arsenical neuritis, 314, 518 Articulation, defects of, 193 Associated movements, 102 Association fibres, 12 Astasia-abasia, 536 Ataxia, 103 Ataxic aphasia, 197 Ataxic paraplegia, 438 Atheroma of cerebral vessels, 265 Atheroma, influence of, 326 Athetoid movements, 99 Athetosis, 99 Atonic type of muscular atrophy, 95 Auditory nerve, 54 Auditory perceptive centre, 199 Aura, visual, 151 Aural, deafness, i6(?; vertigo, 164 Axial optic neuritis, 144 Axis-cylinders, 5 B Base of brain, lesions in, 233 Beri-beri, 522 Bilateral anaesthesia, 129 Bilious headache, 553 Bird-claw hand, 496 Blepharospasm, 479 Blind headache, 553 Blood supply, of brain, 62 ; of spinal cord, 61 Brachial neuritis, 499 Brachial plexus, 39 Brain, arteries of , 63 ; circulation in, 62 Brain disease, general characters of, 334 . Bright's disease, diagnostic sig- nificance of, 326 Broca's centre, 195 Brown-Sequard's paralysis, 77 Bulbar inco-ordination, 106 Bulbar paralysis, 395 ; chronic, 395 ; acute, 396 Burdach, columns of, 18 Cadaveric position of vocal cords, 117 Caisson paralysis, 418 Capsule, internal, 27 ; anterior portion of, 27 ; posterior por- tion of, 34 ; symptoms of disease of, 222 Carcinoma, of cord, 281 ; of brain, 278 Cardiac centre, 57, 58 Cardiac disease, influence of, 325 Caries of spine, 404, 422, 440 Catalepsia cerea, 97 Catalepsy, 97 Cauda equina, 17 ; lesions of, 506 ; compression of, 506 ; crush of, 506 ; localization of lesions in, 251 ; tumors of, 283 Caudate nucleus, 12 Causal indications in diagnosis, 288 Cavities in cord, 461 Cells, nerve, varieties, 4 ; func- tions, 4 ; of anterior horn, 29 Central arteries, 62 Central convolutions, 24 Central ganglia, 12 ; arteries of, 64 Central region of cortex, 24 Centres, 7 Centrum ovale, symptoms of disease of, 219 Cephalic cry, 576 Cephalic sensations, 140 Cerebellar, inco-ordination, 105 ; peduncles, 14 ; tract, direct, 18 ; titubation, 105, 575 Cerebellum, 16 ; functions, 16 ; hemisphere, 16 ; middle lobe, r6, 55 ; disease of, 230 ; middle peduncle, disease of, 232 Cerebral abscess, 276, 373 ; case of, 608 Cerebral birth-palsy, 370 ; case of, 603 Cerebral commissures, 12 Cerebral concussion, 567 ; case of, 614 INDEX. 619 Cerebral cortex, 8 Cerebral embolism, 266 Cerebral hemorrhage, 348 ; di- agnosis of, 351 Cerebral, tumor, 278 ; syphilitic, 278, 280 ; tubercular, 278, 280 ; sarcoma, 278, 279 ; glioma, 278, 279 ; aneurism, 278 ; case of, 611 Cerebro-spinal segment, 24 Cervical hypertrophic pachymen- ingitis, 408 Cheyne-Stokes respiration, 206 Chiasma, optic (see optic nerve), 43 Choked disc, 152 Chorea, 555 ; hereditary, 557 ; post-hemiplegic, 557; uric acid in, 556 Chronic meningitis, 344 ; alco- holic, 345 ; syphilitic, 345 ; infantile, 346 Chronic nuclear paralysis, 385 Chronic ophthalmoplegia, 385 Chronic poliomyelitis, 428, 446 Chronic progressive ophthalmo- plegia, 385 Chronic spinal musciilar atrophy, 446 Cilio-spinal centre, 23 Cincture pain, 136 Circulation in brain, 61 Circumflex nerve, paralysis of, 495 Clarke, column of, 33 Claw-like hand, 496 Cleavage method, i Clitoris crises, 212 Clonic convulsion, 85 Cochlea, function of, 54 Collateral heredity, 330 Collin dynamometer, 579 Column, of Burdach, 32 ; of Clarke, 33 ; of Goll, 32 ; of Cowers, 33 ; of Tiirck, 18 ; posterior, 32 ; postero-external. 32 ; postero-internal, 32 Coma, hysterical, 188 ; uremic, 188 ; alcoholic, i8g ; diabetic, Combined cerebral and spinal infantile paralysis, case of, 604 Compensation of function, 69 Compression of the spinal cord simulating cerebral hemiplegia, case of, 606 Compression of the spinal cord, 420 ; rapid, 420 ; slow, 420 Concentric limitation of visual fields, 145 Conduction aphasia, 202 Confluent "articulation, 194 Congenital anosmia, 142 Congenital aphasia, 203 Congestion, of brain, 258 ; of spinal cord, 259 Conjugate deviation, 109 ; para- lytic, no ; spasmodic, no Consciousness, loss of, 184 Constipation, 209 Contraction, 95 ; fibrillary, 90 ; of the pupils, 115 Contracture, 95 Convergent strabismus, no Convulsions, 216 ; definition of, 80 ; significance of, 84 ; of spinal cord disease, 84 Co-ordination, investigation of the power of, 580 Cord, abscess of, 418 ; blood supply of, 61 ; crush of, 422 ; degeneration of, 284 ; embolism of, 418 ; inflammation of, 272 ; symptoms in compression, 420 Corpora quadrigemina, 13 ; symp- toms of lesions of, 223 Corpus callosum, 12 Corpus striatum, 12 ; symptoms of disease of, 221 Cortex, cerebral, 8 ; lamination of, 8 Cortical centre for hearing, 55 Cortical inco-ordination, 103 Cranial nerve nuclei, 14 Cranial nerves, 41 Cranio-cerebral topography, 65 Cremasteric reflex, 37 Crises in tabes, 435 Crossed amblyopia, 143 Crossed hemiansesthesia, 128 620 INDEX. Crossed hemiplegia, 76, 224 Crossed pyramidal tract, 28 Cross-legged progression, 431 Crus cerebri, 13 ; symptoms of lesions of, 224 Crush of the spinal cord, 422 ; case of, 595 Crutch paralysis, 492 Cuneus, 43 Cutaneous aneesthesia, influence of, in causing inco-ordination, 107 D Deafness, 160 Decussation of optic nerves, 42 ; pyramids, 28 Deep retlexes, 123 Deep root of auditory nerve, 55 Defects in moral sense, 192 Deformities in infantile paralysis, 427 Deformity, significance of, 573 Degeneration, 283 ; ascending, 284 ; causes of, 284 ; descend- ing, 284 ; of nerve-fibres, 6 ; secondary, 284 Degenerative reaction, 173 Deglutition in bulbar paralysis, 396 Deiter's nucleus, 55 Delayed sensation, 132 Delirium, 189 Delirium tremens, 566 Deltoid muscle, paralysis of, 490, 500 Descending degeneration, 284 Descending root of fifth nerve, 50 Destruction of nerve-elements, 71 Deviation of eyes, conjugate, 109 ; primary, ITO ; secondary, no Diabetes, diagnostic significance of, 327 Diabetic coma, 189 ; convulsions, 189 ; neuritis, 327 Diagnosis of, clinical types, 334 ; nature of lesion, 257 ; seat of lesion, 213 Diaphragm, paralysis of, 488 Diffuse myelitis, 413 Diffuse symptoms, 80 Dilatation of the pupils, 114 Diphtheria and, brain disease, 305 ; cord disease, 305 ; periph- eral disease, 305 Diphtheritic, infection, 304 ; neuritis, 520 Diplegia, 75 Diplopia, III Direct cerebellar tract, 33 Direct heredity, 330 Direct pyramidal tract, 28 Direct symptoms, 236 Disarthria, 193 Dislexia, 202 Disorders of digestion, influence of, 327 Disseminated myelitis, 413 Disseminated neuritis, 509 Disseminated sclerosis, 390 Distinction of hysteria and in- sular sclerosis, 394 Disturbances of speech, 192 Divergent strabismus, in Divers' paralysis, 418 Double hemiglegia, 75 Double vision, in Dropsy of the brain, 400 Dura mater, anatomy of, 60 ; hematoma of, 346 Dynamometer, 579 Dystrophies, muscular, 453 Early rigidity, 93 Electrical examination of mus- cles, 587 Embolism, cerebral, 266 ; of the spinal cord, 418 Encephalomalacia, 353 Endarteritis, syphilitic, 265 Epidural space, 60 Epilepsy, 547 ; diagnosis of, 548 ; diagnosis from organic disease, 549 ; influence of disordered nutrition in the causation of, 550 ; varieties of, 548 Epileptic cry, cause of, 120 INDEX. 621 Epileptic vertigo, 548 Equilibrium, investigation of,. 580 Erb's paralysis, 500 Erb's type of progressive mus- cular dystrophy, 455 Erysipelas as a cause of nervous disease, 308 Etiology of nervous diseases, 289 Exanaination, of motor functions, 576 ; of sensory functions, 581 Excessive use, of alcohol, 293 ; of tobacco, 295 Exposure, to cold, influence of, 322 ; to heat, 323 External plantar nerve, paralysis of, 503 External popliteal nerve, paraly- sis of, 503 Extra -dural hemorrhage, 317, 361 ; distinction from cerebral hemorrhage, 363 ; distinction from laceration of the brain, 363 ; distinction from sub- arachnoid hemorrhage, 364 Facial expression, significance of, 573 Facial hemiatrophy, i6g Facial nerve, 52 ; paralysis of, 474 Facial spasm, 478 False catalepsy, 97 False image, iii Faradic irritability of muscles, examination of, 587 Festination, 106 Fibres, length of, 7 Fibrillary contractions, 90 Fibrillation, 90 ; from drugs,' 92 Fifth nerve, paralysis of, 471 Fissure of Rolando, location of, 66 Flechsig's method, 3 Focal symptoms, 80 Foot-clonus, 125 Foot-phenomenon, 125 Fortification spectrum, 150 Fourth nerve, paralysis of, 469 Fragilitas ossium, 169 Friedreich's disease, 441 Fright, influence of, 325 Fronto-cerebellar tract, 16 Functional paralysis, 317 Gait, cross-legged progression, 575 ; disturbances of, 574 ; equine, 575 ; festination, 575 ; frog walk, 575 ; hemiplegic, 575 ; high-action, 575 ; hop- ping. 574 ; significance of, in diagnosis,574 ; staggering, 575 ; tabetic, 574 ; waddling, 575 Galvanic irritability of muscles, examination of, 587 Ganglia of posterior roots, ig General characters of brain disease, 334 ; of peripheral nerve disease, 336 ; of spinal- cord disease, 335 General convulsions, 81 General paralysis of the insane, 397 Girdle-pain, 136 Glioma of the brain, case of, 611 Glosso-labio-laryngeal paralysis, 395 Glosso-pharyngeal nerve, 56 ; paralysis of, 480 Glycosuria, transient, 209 Goll, columns of, 18, 34 Grand mal, 548 Gray optic atrophy, 157 Gray substance, 7 Grippe as a cause of nervous disease, 309 Gudden's atrophy method, 2 H Habits, influence of, in diagnosis, 293 Hsematoma of dura mater, 346 Hallucinations, 189 Headache, 137 ; causes of, 137 ; of organic disease, 137 Heart disease, influence of, 325 622 INDEX. Hemi-achromatopsia, 150 Hemiansesthesia, 126 Hemianopic pupillary inaction, 116 Hemianopsia, 145 ; bilateral, 146 ; nasal, 146 ; oscillating bitemporal, 146 ; temporal, 146 ; vertical, 146 ; homony- mous, 147 ; lateral, 147 Hemiataxia, 104 Hemicrania, 553 Hemiopia, 145 Hemiparaplegia, 77 Hemiplegia, 74, 222 Hemorrhage, into the brain, 260 ; into the membranes of the brain, 260 ; into the mem- branes of the cord, 263 ; into the spinal cord, 263, 411 ; in- traspinal, 40Q Hereditary ataxia, 441 Hereditary mental taint, 329 Heredity, dissimilar, 329 ; hete- rologous, 329 ; influence of, in diagnosis, 329 ; collateral, 330 ; direct, 330 ; similar, 330 Herpes zoster, 168, 314 History of syphilis, bearing of, on diagnosis, 303 Huntington's chorea, 557 Hydrocephalus, 400 ; acute, 401 ; chronic external, 401 ; chronic internal, 401 Hypersemia, of brain, 258 ; of spinal cord, 259 Hypertesthesia, 134 Hyperalgesia, 134 Hyperosmia, 142 Hyperpyrexia, 228 Hypoglossal nerve, 59 ; paralysis of, 4S6 Hysteria, 529 Hysterical aphonia, 535 Hysterical convulsions, 537 Hysterical hemiplegia, 534 Hysterical monoplegia, 530 ; case of, 613 Hysterical paraplegia, 78, 532 Hysterical ptosis, 114 Hystero-epilepsy, 548 Illusions, i8g Illustrations of diagnosis, 595 Immediate effects of injury, 317 Incisions, Schmidt's, 5 Incontinence, intermittent, 210 ; reflex, 210 ; of urine, 210 ; of faeces, 211 ; overflow, 211 Inco-ordination, 102; from periph- eral disease, 108 Inequality of the pupils, 116 Infantile cerebral paralysis, 367 ; congenital form, 370 ; acquired form, 370 Infantile hemiplegia, 370 Infantile meningeal hemorrhage, 370 ; case of, 603 Infantile paralysis, 426 Infection as a cause of nervous disease, tubercular, 298 ; syphi- litic, 300 ; diphtheritic, 304 Infection, influence of, in causing disease, 298 Inflammation, of substance of brain, 268 ; of membranes of brain, 269 ; of membranes of spinal cord, 273 ; of spinal cord, 272 ; of nerves, 275 Influence of alcohol in causing disease, 294 Influenza as a cause of nervous disease, 309 Inhibition, 71 Initial rigidity, 93 Injury as a cause of nervous disease, 316 Insular sclerosis, 390 ; distinction of, 391 Intellectual tract, 16 Intention-tremor, 87 Internal capsule, 27 Internal convulsions, 86 Internal plantar nerve, paralysis of, 504 Internal popliteal nerve, paralysis of, 503 _ Intracranial aneurism, 382 Intracranial hemorrhage, 260 INDEX. 623 Intracranial tumor, 375 ; diagno- sis of, 377 ; distinction from abscess, 379 ; distinction from hysteria, 380 ; distinction from epilepsy, 381 Intraspinal hemorrhage, 409 Intraspinal tumor, 457 Irritation of nerve-elements, 71 J Jacksonian epilepsy, 82 Jaw-jerk, examination of, 590 Jendrassik's method of testing knee-jerks, 589 Juvenile form of progressive muscular dystrophy, 455 K Kak-ke, 522 Kidney disease, influence of, 326 Knee-jerk, examination of the, 588 _ Krause's end-bulbs, 31 L Laceration of the brain, 317 Lamination of cortex, 8 Landouzy-Deje'rine type of pro- gressive muscular dystrophy, 456 Landry's paralysis, 524 Laryngeal paralysis, 117 Laryngismus stridulus, 86, 119 Late rigidity, 94 Lead as a cause of nervous disease, 311 Lead colic, 312 Lead neuritis, 515 Lead paralysis, 311 ; case of, 602 Lead poisoning, headache of, 140 Leg type of progressive muscular atrophy, 452 Length of fibres, 7 Lenticulo-striate arteries, 64 Lenticulo-thalamic arteries, 64 I-«prous neuritis, 523 Limb measurements, how to take, 586 Lingual branch of the fifth, 52 Local convulsions, 81, 82 Local saturnism, 314 Localization of lesions in cortex cerebri, 215 ; central area, 215 ; frontal lobe, 217 ; parietal lobe, 217 ; occipital lobe, 218 ; tem- poro- sphenoidal lobe, 218; island of Reil, 219 ; centrum ovale, 219 ; corpus callosum, 220 ; corpus striatum, 221 ; optic thalamus, 222 ; internal capsule, 222 ; external capsule, 223 ; corpora quadrigemina, 223 ; crus cerebri, 224 ; pons Varolii, 225 ; medulla oblon- gata, 229 ; cerebellum, 230 ; middle peduncle, 232 ; anterior fossa of skull, 233 Localized convulsions, 216 Locomotor ataxia, 433 ; symp- toms of, 433 ; neuralgic stage, 434 ; ataxic stage, 435 ; pseudo- paralytic stage, 435 ; diagnosis of, 436 Loss of blood-supply, effect of, 70 Loss of consciousness, 184 Loss of knee-jerk, 121 Lumbar myelitis, case of, 599 Lumbar plexus, 40 ; affections of, 504 M Magendie, foramen of, 60 Major seizures, 548 Malingering, 569 Measles as a cause of nervous disease, 307 Mechanical injury to nerve- elements, 70. Median nerve, paralysis of, 493 Meissner's corpuscles, 31 Meningeal hemorrhage, 361, ' 409 ; case of, 603 Meningitis, diagnosis of, 336 ; of the base, 337 ; purulent, 338 ; epidemic cerebro-spinal, 624 INDEX. 338 ; lepto-meningitis, 269 ; simple meningitis, 270 ; tuber- cular, 339 ; localized tuber- cular, 340 ; simple non-puru- lent, 341 ; distinction from acute general diseases, 341 ; distinction from intestinal dis- • ease in children, 342 ; dis- tinction from tumor of brain, 342 ; distinction from abscess, 343 ; distinction from hysteria, 344 ; chronic, 344 Mental shock, influence of, 325 Mental state, significance of, 572 Mercurial tremor, 315 Mercury as a cause of nervous disease, 314 Middle cerebral artery, 62 Middle fossa of skull, 234 Migraine, 553 ; ophthalmic mi- graine, 554 ; diagnosis of, 554 Miliary aneurisms, 261 Mimic spasm, 478 Mind-blindness, 200 Mind-deafness, 201 Minor seizures, 548 Mixed form of reaction of de- generation, 176 Mixed nerves, 30 Mobile spasm, gg Monoplegia, 79 Morbid blood-states, 328 Morbid movements, significance of, 57A Morning ptosis, 114 Morvan's disease, 465 Motor area, 24 Motor paralysis, 72 Motor point, 173 Motor power, investigation of, 5 76 Motor root of fifth nerve, 50 Motor tract, 24 Multiple neuritis, 5og ; alcoholic, 510 ; lead, 515 ; arsenical, 518 ; carbonic oxide, 519 ; diph- theritic, 520 ; Beri-Beri, 522 ; leprous, 523 ; acute ascending paralysis, 524 Muscular atrophy, causes of, 170 ; from disease of lower segment of motor path, 1 71 ; from disease of upper segment of motor path, 171 ; atonic atrophy, 172 Muscular hypertrophy, 173 Muscular sense, investigation of, 582 ; loss of, 133 Muscular tenderness, 137 Musculo-cutaneous nerve, paral- ysis of, 491 Musculo-spiral nerve, paralysis of, 491 Musculo-spiral paralysis, 328 Myelitis, 412 ; acute, 413 ; chronic, 419 ; hemorrhagic, 416 ; transverse, 415 ; diffuse, 415 ; disseminated, 413 ; polio- myelitis, 413 ; focal myelitis, 413 Myopathic facies, 456 N Needle-women's cramp, 565 Nerve-cells, 4 Nerve-fibres, 4 Nerve supply of orbicularis pal- pebrarum, 53 Neuralgia, 560 ; symptomatic, 560 ; idiopathic, 560 ; diagnosis of, 562 Neurasthenia, 546 Neuritic atrophy, 157 Neuritis, 275, 465 ; optic, 152, 154. 155 ; -migrans, 276, 467 ; ascending, 276 ; from carbonic oxide poisoning, 519 Neuroglia, 6 Neurotic heredity, 329 Nuclear ocular paralysis, 384 Nuclear ophthalmoplegia, 384 ; chronic, 385 ; acute, 387 ; diagnosis of, 3S6, 387 Nystagmjjs, 112, 391 O Obstetrical paralysis, 500 Obturator nerve, paralysis of, 501 Occupation neuroses, 564 INDEX. 625 Ocular reflexes, examination of, 591 Ocular strain, influence of, 321 Oculo-motorius, 44 Olfactory aurce, 142 Olfactory hallucinations, 142 Olfactory hypersesthesia, 142 Olfactory nerve, 42 Ophthalmoscopic examinations, indications for, 584 Optic nerve, 42 Optic nerve atrophy, 156 Optic neuritis, appearances in, 152 ; causes of, 154 ; pathology of, 155 Optic radiations, 43 Optic thalamus, 13 Origin of vaso-dilator nerves, 22 Origin of vaso-motor nerves, 22 Over-fatigue as cause of nervous disease, 323 Pacchionian bodies, 64 Pachymeningitis interna hsem- orrhagica, 346 Pacinian corpuscles, 31 Pain, 135 Pain sense, investigation of, 582 Papillitic atrophy, 157 Papillitis, 152 Para-ansesthesia, i2g Parageusia, 166 Paralysis, 72 Paralysis agitans, 558 Paralysis from lessened atmos- pheric pressure, 418 Paralysis of the fourth nerve, 469 Paralysis of the third nerve, 468 Paralysis without wasting, 72 Paralysis with wasting,»72 Paralytic dementia, 397 I Paramyoclonus multiplex, 86' Paraplegia, 77 ; spastic, 429 Paresis, 80 Paretic dementia, 397 Patheticus, 46 Pathology of tremor, 89 Peduncles of cerebellum, 14 Perimeter, uses of, 584 Periodical opththalmoplegia, 389 Peripheral birth-palsy, 500 Peripheral nerve disease, general characters of, 336 Peripheral nerves, tumors of, 283, 505 Peroneal form of progressive muscular atrophy, 452 Peroneal nerve, paralysis of, 503 Petit mal, 548 Pharynx, paralysis of, 480 ; spasm of, 481 Phimosis, influence of, in causing nervous disease, 321 Phrenic nerve, paralysis of, 488 Physiological centres, 7 Pia mater, anatomy of, 60 Pianists' cramp, 565 Pneumogastric nerve, 57 ; paraly- sis of, 480 Pneumonia as a cause of nervous disease, 308 Poliomyelitis, 425 ; acute, 425 ; chronic, 425 Polyneuritis, 509 Post-convulsive paralysis, 83 Posterior longitudinal bundle, 48 Posterior sclerosis, 433 Posterior thoracic nerve, 489 Post-hemiplegic chorea, loi Post-hemiplegic tremor, 560 Posture, significance of, 573 Pregnancy, influence of, 328 Pressure on nerve-elements, 70 Primary deviation, no Primary lateral sclerosis, case of, 597 Primary neuritic atrophy, 452 Primary optic atrophy, 156 Primary sinus thrombosis, 267 Primary spastic paraplegia, 430 Progressive bulbar paralysis, 395 Progressive muscular atrophy, 446 ; symptoms of, 447 ; diag- nosis of, 451 ; different types of, 449 Progressive muscular dystrophies, 453 626 INDEX. Projection fibres, 12 Propositional use of words, 196 Propulsion, 106 Pseudo-bulbar paralysis, 397 Pseudo - hypertrophic paralysis, 454 Pseudo - muscular hypertrophy, 454 Pseudo-paralysis, 80 Psychical epilepsy, 548 Psychical epileptic equivalent, 548 Ptosis, 113 Punctate hemorrhages into the brain, 317 Pupils, contraction of, 115 ; dila- tation of, 115 ; inequality of, 116 Pyramids, decussation of, 28 Pyrexia, 204 Quiet delirium, iJ R Rachialgia, 136 Reaction of degeneration, 173 Recurrent ophthalmoplegia, 389 Reflex action, loss of, 120 ; ex- cess of, 123 Reflex are, 35 Reflex centre, 35 Reflexes, cilio-spinal, 36 ; scap- ular, 37 ; biceps-jerk, 37 ; el- bow-jerk, 37 ; wrist-jerk, 37 ; palmar, 37 ; epigastric, 37 ; abdominal, 37 ; cremasteric, 37 ; patellar, 37 ; gluteal, 38 ; ankle clonus, 38 ; plantar, 38 ; iris, 38 Reflexes, examination of the, 588 Reflex influences as causes of nervous disease, 321 Reflex paraplegia, 78 Reflex paths, 35 Reflex ptosis, 114 Reinforcement of reflexes, 589 Rheumatic ophthalmoplegia, 322 ! Rheumatism as a cause of nervous disease, 308 Remote effects of injury, 318 Residual states, 200 Retrocollic spasm, 485 Retropulsion, 106 Rickets, influence of, 327 Rigidity, 92 ; detection of, 579 Rules of localization, 235 S Sacral plexus, 41 ; affections uf, 505 Saturday-night paralysis, 492 Scanning speech, 194, 391 Scanning utterance, 576 Scarlet fever as a cause of nervous disease, 307 Schmidt's incisions, 5 Schroeder VanderKolk'slaw, 131 Schwann, sheath of, 5 Sciatica, 563 Sciatic nerve, paralysis of, 502 Sciatic neuralgia, 564 Sciatic neuritis, 564 Secondary degeneration, 2 Secondary deviation, no Secondary optic atrophy, 157 Secondary sinus thrombosis, 267, 268. Secondary spastic paraplegia, 430 Senile tremor, 88, 560 Sense of hearing, examination of, 585 Sense of sight, examination of, 583 Sense of smell, investigation of, 583 Sense of taste, examination of, 585 Sensory crossway, 35 Sensory tract, 30 Sex, influence of, in diagnosis, 292 Sexual act, mechanism of, 2H Sexual excess, 295 ; influence of, in causing nervous disease, 296 Sexual reflex, 212 Sheath of Schwann, 5 Sick headache, 553 INDEX. 627 Silver as a cause of nervous dis- ease, 315 Simple optic atrophy, 156 Simple tremor, 88 Sinus thrombosis, 267, 365 ; primary or marantic, 366 ; sec- ondary, 367 Sixth nerve, 46 ; liability to pressure, 47 ; nucleus of, 48 ; paralysis of, 469 Slow pressure, effect of, 70 Small-pox as a cause of nervous disease, 308 Small sciatic nerve, paralysis of, 504 Softening from arterial occlusion, 353 Softening of the brain, 264 Solitary tubercle, 299 ; of brain, 271 5oul-blindness, 200 Spasm of the larynx, 119 Spastic paraplegia, 429 Spastic spinal paralysis, 230 Speech disturbances, 192, 576 ; examination for, 591 Speech mechanisms, 193 Spinal accessory nerve, 57 ; paral- ysis of, 482 Spinal arthropathies, 169 Spinal cord, acute softening, 267; length of, 16 ; localization of . lesions in, 236 ; segments of, 17 ; transverse lesions of , 245 ; tumors of, 281 ; unilateral lesions of, 241 Spinal cord disease, general char- acters of, 335 Spinal epilepsy, 125 Spinal hemiplegia, 77 Spinal meningitis, 403 ; external, 404 ; internal, 405 ; acute in- ternal, 405 ; chronic internal, 407 Spinal nerves, 39 Spinal pain, 136 Spinal portion, 57, 58 Spino-muscular segment, 24 Spontaneous catalepsy, 98 Spurious clonus, 534, 590 Staccato speech, 194 Starr, table of, 19 Strabismus, no Striae acousticee, 54 Stupor, 185 Subacute poliomyelitis, 428 Subarachnoid space, 60 Subdural space, 60 Sudden lesions, 288 Sunday-morning paralysis, 492 Sunstroke as cause of nervous disease, 323 Superficial root of auditory nerve, 55 Superior gluteal nerve, paralysis of, 502 Suprascapular nerve, paralysis of, 490 Sylvian line, 66 Sympathetic nervous system, 22 Syphilitic infection, 300 Syringomyelia, 461 ; symptoms, 462 ; diagnosis, 464 ; peculiar sensory symptoms of, 463 ; distinction from Morvan's disease, 465 System diseases, 283 Systematic examination of the functions of the nervous sys- tem, 576 Tabes dorsalis, 433 Tabetic foot, 170 Table of localization, 19 Tache cerebrale, 184 Tactile sensibility, investigation of, 581 Taste aurfe, 166 Taste-fibres of the fifth, 52 Telegraphist's cramp, 565 Temperature sense, investigation of, 582 ; loss of, 132 Testimentary capacity, 203 Tetanic convulsion, 85 Tetany, 85 Third nerve, paralysis of, 468 Thrombosis oi cerebral arteries, 265 ; of sinuses, 267 628 INDEX. Tic convulsive, 478 Tinnitus aurium, 162 Tobacco amblyopia, 144 Tobacco, excessive use of, 295 Tonic convulsion, 85 Tonic type of muscular atrophy, 95 Torticollis, 484 ; false, 484 ; spasmodic, 484 ; congenital, 484 _ Toxic influences in the causation of nervous disease, 310 Trauma as a cause of nervous disease, 316 Traumatic hysteria, 538 Traumatic neurosis, 325, 538 Traumatic psycho-neurosis, 538 Transient albuminuria, 209 Transient aphasia, 202 Transient glycosuria, 209 Treatment by drugs, diagnostic value of, 328 Tremor, definition of, 87 ; detec- tion of, 579 Triceps-jerk, examination of, 590 Trigeminus nerve, 49 Trismus, 86 Trophic state of the muscles, examination of, 586 Trophic symptoms, 166 Trousseau's symptom, 85 Tubercular infection, 298 Tubercular meningitis, 339; case of, 610 Tiirck, columns of, 18 Tumor of the spinal cord, 281 Tuning-fork, uses of, 585 Typhoid fever as a cause of nervous disease, 306 Typhus fever as a cause of nervous disease, 307 U Ulnar nerve, paralysis of, 495 Unsystematized delusions, 398 Upper-arm type of paralysis, 500 Urinary paraplegia, 78 Van der Kolk, law of, 131 Vascular disease, influence of, 326 Vaso-dilator nerves, origin of, 22 Vaso-motor nerves, origin of, 22 Vaso-motor symptoms, 182 Veins of Galen, 65 Vertigo, causes of, 163 ; essential, 163 ; aural, 164 ; ocular, 165 ; gastric, 165 Vesicular column, 33 Vestibule, function of, 54 Violinist's neurosis, 565 Visual aura, 151 Visual field, measurement of, 584 Visual half-fields, 44 Voluntary power, investigation of, 576 Vomiting, causes of, 207 ; from intracranial disease, 208 W Wasting palsy, 446 White substance, 7 Word-blindness, 200 Word-deafness, 199 Wrist-drop, 519 Wrist-jerk, examination of, 590 Writer's cramp, 565 Wry-neck, 484 '^y^jd^^',}', ■'-. > s .'' 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