COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDAR|D HX641 23472 RC348 . H44 1 907 Diagnosis of organic RECAP t- s: ^ rK<.*^^jrjxmoom€K^.^i^^ Columbia ® nibersitp \^ oi in tfje dtp of ^eto gork COLLEGE OF PHYSICIANS AND SURGEONS jFrom tfje Hibrarp of 3Br. CJjrigtian ^. ^erter Honateb bp 1920 Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/diagnosisoforganOOhert DIAGNOSIS OF ORGANIC NERVOUS DISEASES BY CHRISTIAN A. HERTER, M.D. PROFESSOR OF PHARMACOLOGY AND THERAPEUTICS AT COLUMBIA UNIVERSITY VISITING PHYSICIAN TO THE CITY HOSPITAL REVISED AND ENLARGED BY L PIERCE CLARK, M. D. VISITING NEUROLOGIST TO THE RANDALl's ISLAND HOSPITALS AND SCHOOLS CONSULTING NEUROLOGIST AT THE MANHATTAN STATE HOSPITAL, N. Y. CONSULTING NEUROLOGIST AT THE CRAIG COLONY FOR EPILEPTICS SONYEA, N. Y. ; ASSISTANT NEUROLOGIST AT VANDERBILT CLINIC (COLUMBIA college) NEW YORK WITH 109 ILLUSTRATIONS G. P. PUTNAM'S SONS NEW YORK AND LONDON ^be 1knickert)oc??er press 1907 Copyright, 1892 BY CHRISTIAN A. HERTER Copyright, 1907 BV CHRISTIAN A. HERTER For Revised Edition Ube 1Rnicl?crbocF?cr prces, IRew Jljorft PREFACE TO THE SECOND EDITION. The uninterrupted demand for the first edition of this little manual as a guide in the teaching of the diagnosis of nervous diseases has led me to believe that a revised and modernized edition would prove welcome. As my interest in medicine has gradually become concentrated on other fields than those of neurology, it has seemed wise to entrust the work of revision to one identified with the teaching and practice of neurology. Dr. L. Pierce Clark, who has undertaken the revision, has con- tributed much that is new to the edition now offered to the profession, without, however, altering or extending the scope of the earlier publication. Dr. Clark has re- written in greater part the chapter on the anatomy and physiology of the nervous system, and has modernized the section dealing with the symptomatology of nervous diseases. The chapter on the examination of the patient has been wholly rewritten. These and the new illustra- tions added will be found, it is believed, to contribute a revision that is thorough without being destructive of the original plan of the book. It has been thought de- sirable to alter the title of the volume in order to express more plainly its preponderant relation to organic nervous diseases. C. A. Herter. New York, Jan. 1907. Ill PREFACE. This volume is designed to ai.d 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 treats 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 vi 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 difficult 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 Avenuk, March 7, 1892. CONTENTS. System Chapter I. — The Structure and Functions of the Nervous System Introductory Remarks The Brain . The Spinal Cord . The Sympathetic Nervous 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 Spinal Cord Topography Chapter II. — The Symptomatology of Nervous Dis EASES 1. Mechanical Injury . 2. Loss of Blood-Supply, Partial or 3. Inflammation .... 4. Wasting of Xerve Elements . Motor Paralysis .... Convulsions Tremor ...... Fibrillation Rigidity Contracture and Contraction Catalepsy Athetosis and Athetoid Movements vii Complete I 10 19 27 29 38 43 44 47 74 75 80 84 85 85 86 86 87 95 103 106 108 III 113 115 Vlll CONTENTS Eyes and Head Associated Movements Inco-ordination Conjugate Deviation of the Strabismus Diplopia Nystagmus . Ptosis .... Pupillary Symptoms . - - Laryngeal Symptoms . Abnormal Reflex Action Sensory Symptoms Headache . . , . ^ Olfactory Symptom?. . Visual Symptoms Ophthalmoscopic Changes Auditory Symptoms . Vertigo .... Gustatory Symptoms . Trophic Symptoms , . . Vaso-Motor Symptorns Mental Symptoms Disturbances of Speech General Symptoms Chapter III. — The Diagnosis of the Position of the Lesion — Localization .... a. Cortex Cerebri ..... b. White Substance and Centrum Ovale c. Corpus Callosum .... d. Corpus Striatum .... e. Optic Thalamus .... /. Internal Capsule .... g. External Capsule and Claustrum h. Corpora Quadrigemina . , . i.. Crus Cerebri . ...... y. Pons . . .......... k. Medulla Oblongata I.. Cerebellum Base of the Brain .... CONTENTS IX Spinal Cord . Nerve- Roots Cauda Equina Peripheral Xerves Chapter IV. — The Diagnosis of the Nature of the Lesion Hyperaemia Anaemia Hemorrhage Softening Thrombosis of Sinuses Inflammation Meningitis Abscess . . . Tumor Degeneration I. The Onset of the Symptoms II. The Causal Indications III. The Position of the Morbid Process Chapter V. — The Diagnosis of Clinical Types Meningitis Lumbar Puncture in the Diagnosis of Meningitis Cerebral Hemorrhage . Acute Cerebral Softening . Meningeal Hemorrhage Sinus-Thrombosis Infantile Cerebral Paralysis Abscess of the Brain . Intracranial Tumor Intracranial Aneurism Nuclear Ophthalmoplegia . Multiple of Disseminated Sclerosis Bulbar Paralysis .... General Paralysis of the Insane . Hydrocephalus .... Spinal Meningitis Intra-Spinal Hemorrhage . Myelitis 253 267 268 273 274 275 276 277 281 284 285 286 293 295 301 305 306 350 352 355 360 367 371 379 3^4 386 394 397 403 406 411 416 419 422 426 432 435 CONTENTS Spastic Paraplegia Locomotor Ataxia Ataxic Paraplegia Friedreich's Disease Progressive Muscular Atrophy The Peroneal Form of Progressive Muscular Atrophy Pseudo-Hypertrophic Paralysis Erb's Type of Progressive Muscular Dystrophy Intra-Spinal Tumor Syringomyelia Neuritis Diseases of Special Nerves Tumors of Peripheral Nerves .... Lesions of the Cauda Equina .... Multiple Neuritis Chapter VL — The Distinction of Functional and Organic Disease Hysteria The Traumatic Neurosis or Psycho-Neurosis . Neurasthenia Epilepsy Migraine Chorea Paralysis Agitans Neuralgia Occupation Neuroses Delirium Tremens Cerebral Concussion Malingering Chapter VIL — The Examination of the Patient Chapter VIIL — Illustrations of Diagnosis Index DIAGNOSIS OF ORGANIC NERVOUS DISEASES DIAGNOSIS OF ORGANIC NERVOUS DISEASES 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 disposi- tion of many such bundles or tracts may be readily demonstrated. Indeed, in the hands of Meynert, Bur- dach, Foville, and others, this method of cleavage or teasing has yielded results of the highest importance. Still, for the elucidation of the more minute relations of the gray matter and the complicated systems of fibres, it is not wholly adequate. Nor is it possible, with the microscope and modern methods of staining cells and fibres, to determine precisely their connections or to 2 DISEASES OF THE NERVOUS SYSTEM. unravel the network 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 nutritive 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 may 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 micro- scope the altered structure of the fibres is very marked. This process is known as secondary degeneration. The descending degeneration of the motor tract in the brain and in the lateral and anterior columns of the cord fol- lowing 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 THE NERVOUS SYSTEM. 3 its application, since the lower animals only can be 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 different 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 after 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 experimental stimulation and destruction of certain portions of the brain and cord in lower animals, but the results of such experiments are not always ap- plicable 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 conditions observed at autopsies. Investigations in the realm of histology have, in recent years, added much to our knowledge of the finer nervous anatomy. In this field Golgi and Ramon y Cajal have rendered inestimable service and have made possible a fuller conception of the anatomical structure of the central nervous system embodied in the neuron theory suggested by Waldeyer. This theory pictures the central nervous system as composed of various systems of units, the cell and fibre of the older parlance being combined in the Nerve-cell ,^ Dendrites ■" Nerve process Collateral Medullary sheath Axis-cylinder Neurilemna Terminal ramification FIG. I. Diagram of a neuron. (Stohr.) THE NERVOUS SYSTEM. 5 neuron of the new. In the neuron therefore are combined (a) the cell body containing various anatomical struc- tures including the nucleus and nucleolus, (b) the axis- cylinder process which is the means of transmitting impulses from one set of neurons to another and the band by which the neurons are chained together into systems, and (c) the dendrites which are the other processes from the cell body whose function it probably is to perceive or apprehend impulses and carry them over from other neurons. The dendrites thus serve for the reception and diffusion of sensations while their combination and ex- tension may be conceived as taking place in the cell body and their ultimate transmission from higher to lower groups of neurons is accomplished through the axis-cylinder process. This conception of the nerve-cell and -fibre as consti- tuting a single organ, the neuron, and of the central nervous system as being made up of groups of these organs which are in themselves separate and distinct, has not met with entire acceptance and corroboration, although its main features are well founded. Bethe and Apathy claim to have demonstrated histologically a fibre continuity between two separate neurons, which they think sufficiently demonstrates the non-existence of the neuron as an independent unit; while Held and more recently Nissl have put forward the theory of the great functional importance of the intercellular substance and have observed its minute fibrillary structure. Whether or not these views shall, in the future, be proven correct is immaterial for the present purpose. If established they may be accepted as corollaries to the neuron conception, while its principle will remain. For the purposes of this book, therefore, we shall accept the conceptions of the neuron theory. 6 DISEASES OF THE NERVOUS SYSTEM. Before considering the chief facts in the functional anatomy of the nervous system, certain general prelim- inary points should be reviewed. The chief structural element underlying the physio- logical activity of the central nervous system is the ^Sf FIG. 2. 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); E, spindle-cell from human cortex; F, granule-cells from cortex; G, bipo- lar cells from spinal ganglion. neuron consisting of a nerve - cell and its processes. The reception, perception, combination, correlation, and transmission of the impulse have been referred to. The great variations of the neuron in size and THE NERVOUS SYSTEM. 7 shape are illustrated herewith. Many qualifying names have been applied to them, such as angular, granular, pyramidal, ganglion, multipolar, globose, round, spindle- shaped, etc., all of which are being superseded by terms applying more directly to a given neuron system. The nerve-fibre or axis-cylinder process of the neuron lacks FIG. 3. 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. uniformity of structure. It occurs either as a naked axis-cylinder, or an axis-cylinder clothed with a myeline sheath. Some of these forms of fibres are figured above, and the highest form of fibre is shown with its sheath of 8 DISEASES OF THE NERVOUS SYSTEM. Schwann, myeline sheath, axis-cylinder, Ranvier's nodes, and Schmidt's incisions (Fig. 3). For the purposes of support and protection of the '■'•st^- FIG. 4. Normal Betz cell from the human paracentral lobule. (Meyer.) neurons of varying types and their delicate appendages, there exists a tissue known as the neuroglia which is composed of branching cells and fibres derived from THE NERVOUS SYSTEM. 9 these cells, whose function is probably a purely supportive one (see Fig 2). In addition to these there are other non-branching cells existing chiefly in the cerebral cortex and whose function is probably that of a support to the more delicate nervous structures. Besides originating and receiving nervous impulses the neuron exercises a nutritional influence over every por- tion of its structure. In consequence of this, when an axis-cylinder process or a dendrite is severed from the body of the neuron, the distal portion degenerates. It will be perceived, therefore, that the direction of degen- eration in a nerve-fibre does not necessarily follow the course and direction of the impulse. 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. Groups of neurons of the larger type, such as are shown in Fig. 4, may be considered as subsetving a motor function wherever met with. The figure repre- sents one of the so-called Betz cells found in and char- acteristic of certain portions of the motor cortex, but similar neurons occur in the anterior horns of the spinal cord, here constituting the lower or second set of neurons in the motor system. Groups of neurons such, for ex- ample, as those above designated are commonly called ''centres." This term is employed correctly only in a physiological sense. We mean thereby any group of neurons, not necessarily possessing well-defined topo- graphical limits, which act conjointly in a functional lO DISEASES OF THE NERVOUS SYSTEM. capacity. Sometimes such groups are widely separated, although functionally associated. They are therefore 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 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 body of the neuron and its axis-cylinder process contribute respectively the gray and white matter of the cerebro-spinal axis. The gray matter completely en- velops the hemispheres of the brain, forming a layer known as the cortex, the seat of the higher mental func- tions. 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 in- terior of the crura, pons, and medulla. In the cerebel- lum 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 topo- graphical 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 differ- ent regions, so that no less than eight distinct types of cortical lamination have been noted by some investiga- tor« For instance, in some regions there are but three THE NERVOUS SYSTEM. II layers in the cortex, in others seven. The neurons vary greatly in type and size in the various layers and re- gions of the cortex. The largest are found in the motor convolutions. These differences of structure subserve differences in function, and modern research has localized, more or less perfectly, areas for voluntary motion, speech, cutaneous FIG. 5. Diagram showing the division of the brain into lobes, outer surface, and of right hemisphere. sensation, visual, auditory, and olfactory impressions, and has outlined with some degree of certainty regions which subserve the higher intellectual operations. The accompanying diagrams indicate with sufficient 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 con- nect with one another different lobes and different con- volutions^ and join certain parts of the cortex with certain 12 DISEASES OF THE NERVOUS SYSTEM. FIG. 6. 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 I eto bccipita FIG. 7. Diagram showing the chief convolutions and fissures on the outer surface of the right hemisphere. THE NERVOUS SYSTEM. 13 of the basal ganglia and the cerebellum. The 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 (see Fig 15). The two cerebral hemispheres are associated in func- FIG. 8. Diagram showing the chief convolutions and fissures on the inner or medial surface of the right hemisphere. . tion by the large bundles of fibres passing from the cortex of one side to that of the other, and constituting the corpus callosum. In addition to this great commis- sure there are three small ribands, known as the anterior, middle, and posterior commissures, in the third ven- tricle, which are to a certain extent bonds of union between the two halves of the brain. Of these commis- sures, the anterior is the most important, and is largely connected with the olfactory system, while the middle is of little or no importance. 14 DISEASES OF THE NERVOUS SYSTEM. FIG. FIG. lO. 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. Ol tacto VltWAk CtHTtn FIG, II. FIG. 12. 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. 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. FIG. 13. Diagram showing the position of the auditory centre in the first temporal convolution. FIG. 14. Diagram showing the position of the motor speech centre in the left hemi- sphere. THE NERVOUS SYSTEM. 15 Very little is known concerning the functions of the caudate nuclei. The lenticular nucleus and the optic thalamus are of great importance as primary terminals of the great sensory systems from the periphery. The optic thalamus is of especial importance in this particu- lar. Moreover, this mass forms a primary termination FIG. 15. The association fibres. A, between adjacent convolutions ; B, between frontal and occipital areas ; C, between frontal and temporal areas, cin^- lum ; D, between frontal and temporal areas, fasciculus uncinatus ; E, between occipital and temporal areas, fasciculus longitudinalis inferior ; C N, caudate nucleus ; O T, optic thalamus. (Starr.) for ocular and auditory fibres from the periphery and is connected with the visual and auditory areas of the cerebral cortex. It may, therefore, be regarded as the great way station for the entire sensory system. The anterior bodies of the corpora quadrigemina are asso- ciated with the function of sight, while the posterior are associated with the function of hearing. These bodies also have other functions not well known. All the fibres connecting the periphery with the brain hemispheres pass through the crura cerebri (the olfactory i6 DISEASES OF THE NERVOUS SYSTEM. and optic tracts excepted). There are in addition special bundles of fibres connecting the cerebrum and cerebel- FIG. i6. The projection tracts joining the cortex with lower nerve centres. Sagittal sec- tion showing the arrangements of tracts in the internal capsule. A, tract from the frontal lobe to the anterior half of the capsule, thence in part to the optic thalamus, A^, and in part to the pons, and thus to the cerebellar hemisphere of the opposite side; B, motor tract from the central convolutions to the facial nucleus in the pons and to the spinal cord ; C, sensory tract from posterior columns of the cord, through the posterior part of the medulla, pons, crus, and capsule to the pari- etal lobe; D, visual tract from the optic thalamus (O T) to the occipital lobe; E, auditory tract from the int. geniculate body (to which a tract passes from the VIII. n. nucleus) to the temporal lobe; F, superior cerebellar peduncle; G, mid- dle cerebellar peduncle; H, inferior cerebellar peduncle; C N. caudate nucleus; C Q, corpora quadrigemina. The numerals refer to the cranial nerves. (Starr.) lum, the fronto-, occipito-, and temporo-pontine tracts, which ultimately terminate in the cortex of the great THE NERVOUS SYSTEM. 17 lobes of the cerebellumby means of ponto-cerebellar fibres which pass out through the middle cerebellar peduncles. In a transverse section through the crura the various tracts and nuclei lie as shown in diagram 19. The third nerve nucleus lies in the floor of the aqueduct of Sylvius, and the fibres of the nerve pass out through the crus on their way to the orbit. The practical and use- ful 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. 17. A knowledge of the relative positions of their nuclei is best gath- ered from the accompany- ing diagrams (18 and 19). The relations of certain of the cranial nerves to the motor tract will be treated of in connection "•^'"^es. with the description of the latter. The superficial anatomy of the cerebellum is portrayed in the two accompanying illustrations (Figs. 20, 21) of its dorsal and ventral aspects. Each hemisphere of the cerebellum is joined to the mid-brain, to the pons, and to the medulla by three large diverging bundles of fibres, known respectively as the superior, middle, and inferior cerebellar peduncles. The peduncles are shown in Fig. 22. FIG. 17, The base of the brain and the cranial i8 DISEASES OF THE NERVOUS SYSTEM. We are still greatly in the dark as regards the physiol- ogy 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 titubation CORP. QUAD. "^""SSAT, FIG. l8. 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 Illd 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 5th 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. is due to disturbance of the middle portion of the cere- bellum, the vermis, or worm. There is some evidence that it influences the power of muscular movements, and there is also some probability that this organ forms a sub- stratum for some of the intellectual processes, through its intimate connection with the frontal lobes of the cere- brum by means of the fronto-cerebellar tract of fibres THE NERVOUS SYSTEM. 19 SUP. PONS INf. (sometimes called "intellectual tract"). {Vide Fig. 22.) For further information as to the disposition of the various parts of the brain, the reader is referred to works on the descriptive anat- omy of the brain. The Spinal Cord. — The spinal cord averages from seventeen to eigh- teen 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 re- maining lumbar vertebras and sacrum to the coccyx. 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 de- scend 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 Diagram showing the nuclear origin of the cranial nerves (except the auditorv). The sensory structures are in red and the motor in black. The floor of the 4th ven- tricle is seen from above, and on the right side the structures are represented as transparent. VII, the facial nucleus. The fibres from this nucleus wind round the nucleus of the abducens nerve (VI), and make their exit just below 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.L.B., posterior longitudinal bundle con- necting the Vlth nucleus below with the Illd nucleus above. VIII, the striae acoustics. 20 DISEASES OF THE NERVOUS SYSTEM. FIG. 20. Diagram of dorsal surface of cerebellum, showing the position of the worm, [After Edinger.) rA\0Oue FIG. 21. Diagram of ventral surface of cerebellum. (After Edinger.) THE NERVOUS SYSTEM. 21 Sup Pttt. 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 intumescence 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 misleading, and it must be rem.embered that though this enlargement gives rise to lumbar nerves, the greater portion of it is con- tained 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-im- pulses are transmitted to and fro between the periph- eral portions of the body and the brain; secondly, as a series of segments super- imposed 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 vas- cular control. The long fibres necessary for the first purpose are disposed 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. The lateral and anterior columns contain the motor-fibres from the cortex, and the posterior columns certain Diagram showing the three peduncles of the cerebellum — the superior pedun- cle going to the quadrigeminal region, the middle peduncle going to the pons, and the inferior peduncle coming from the cord below, (After Edinger.) 22 DISEASES OF THE NERVOUS SYSTEM. sensory tracts. The anterior columns are often called the columns of Tiirck; the posterior are composed of the columns of GoU and Burdach. Their exact positions are indicated in the accompanying diagram of a trans- verse section of the cord. Reflex, trophic, and vaso-motor centres are situated ioo«s FIG. 23. Diagram of a section of the spinal cord in the cervical region. A. C, anterior commissure; P. C, posterior commissure; I. g. s., intermediate gray substance ; P. Cor., posterior cornu ; c. c p., caput cornu posterioris ; 1. 1. 1., lateral limiting layer; a.-l. a. t.. antero-lateral ascending tract, which extends along the periphery of the cord. (Gowers.) 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 destruction of them is followed by de- generation of the motor nerves and atrophy of the muscles innervated by them. The ganglia of the pos- THE NERVOUS SYSTEM. 23 terior 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 central canal. There are communicating nerve-filaments between them and the ganglia and fibres of the sympa- thetic 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 commissural 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 groups of muscles, sensory areas, and reflexes in connection with it. Segment 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 Diaphragm 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 cer\'ic'l to 2d dor- sal) 24 DISEASES OF THE NERVOUS SYSTEM. Segment of cord Nerves Muscles Sensory areas Reflexes Fifth Supraclav cular Deltoid Back of shoul- Scapular cervical Circumfl ex Biceps and der and arm (5th cervic'l External 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- (7th 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(long head) Inner side of cervical neous Flexors of wrist arm and fore- Ulnar and fingers Small muscles of hand arm Ulnar area of 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 THE NERVOUS SYSTEM. 25 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 posterior and abdomen upper gluteal (4th to 7th dorsal nerves Erectores spinae region, and of breast and ab- domen in bands dorsal) Abdominal (7th to nth running down- ward & forward Skin over groin dorsal) 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- neous Sartorius Quadriceps fem'ris Quadriceps fem'ris thigh Third Anterior Anterior surface Knee-jerk lumbar Crural Internal cuta- neous Long saphenous Anterior part of biceps Inner rotators of thigh of thigh Obturator Internal cuta- Adductors of thigh Adductors of thigh Abductors of thigh Inner side of Fourth Gluteal (4th lumbar neous thigh, leg, and to 5th lum- Long saphenous Flexors of knee foot bar) Obturator Tibialis anticus External popli- Peroneus longus Fifth Outward 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 Same as 5th Peronei First and Flexors and ex- Same as 5 th 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- dal Coccygeal external genitals Fifth sacral Coccygeus Skin about anus & coccygeal 1 and coccyx 26 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 determined (such as the parturition centre and the erectile and ejac- ulatory centres), although we know they are in the lumbar enlargement. The reflexes here given vary somewhat in importance. The knee jerk and the character of the plantar response are of greatest importance. The latter is known as the Babinski sign and will be further dealt with in the chap- ter on diagnosis. It is always to be borne in mind that changes in the character of a given reflex mean primarily the involve- ment of the cord segment in which it is represented. For example, in spinal-cord tumor we shall have an absence of or a change in the character of all the reflexes, super- ficial and deep, up to the segment involved. The sympathetic nervous system was originally so called because of its supposed relationship to emotional states. The name is obviously bad and should be dropped, more especially since this system subserves no such purpose. It is composed of the afferent and effer- ent nerve-fibres distributed to the various viscera and the vascular apparatus, the ultimate centres for which are within the cerebro-spinal axis. The so-called sym- pathetic system pet- se 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, sending 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 sys- tem (see Fig. 24). Besides the pairs of lateral ganglia THE NERVOUS SYSTEM. 27 raG. or HOOT opPneumog.^ T» PETROSAL e. 0, Glosso-p// fkOM 1^ CER vicalN^ 2*. iGAHOllON or niB£S \CAROriD PLtiUS ' '"^NTf 0. TO 5\''N. a 0. liJ a. 1- 1 .'2 2 A s^ )5 10 b M-a 1 J?\ )7 ). —< z < 2 r3 t^i rt U3 u bJ3^ " In rt-O _ D 4) &>>« per Dorsal IGd-Lombar. FIG. 29. Diagrams of the groups of nerve-cells in the anterior cornu. Groups : I, inner or medial; A, anterior; A.-L., antero-lateral ; P.-L., postero-lateral ; I. L. P., inter- mediate lateral process; P. V, C, posterior vesicular column or tract. The two mid-cervical sections are only a few millimetres apart, and show how the anterior group, separate in the one, may be blended with the antero-lateral group in a neighboring part of the cord. (Gowers.) A knowledge of this grouping is not of much importance in diagnosis, for we have not yet learned of the exact re- lationship existing between particular neuron aggrega- tions and the muscles which they govern. We know 36 DISEASES OF THE NERVOUS SYSTEM. much more of the relations of the masses of neurons taken as a whole in the anterior horns of particular Columns of gray matter and motor nuclei of the cervical enlargement (After F. Sane). Columna medialis — i, a, short rotators of head; M. subhyoid muscles; i, c, d^ e^ f^ extensors and rotators of the vertebral column. 2, nucleus diaphragmatis (the series of sympathetic nuclei composed of small cells have not been drawn in), they are situated behind the column medialis near the columna canalis centralis. Columna intermedio-lateralis — 8, «, accessorius M. trapezius and M. sterno-cleido mastoideus; b, c, plexus cervicalis; Mm. trapezius sterno-cleido-mastoideus ; f fViA rliffp'r motor ganglion-cell of the opposite an- tne relation ot tne amer- ^^^^^^ g^^^ ^ ^.^^^ connected with ent muscles to the various motor ganglion-cell of the anterior horn of same side. 1 his gangliori-ceil is proba- SegmentS of the cord is bly connected with a sensory fibre from ° the opposite posterior horn. 8. r ibres Dresented. from motor ganglion-cell of anterior horn ^ ' of same side. Ihis ganglion-cell is proba- The neurons of the an- tly connected with a sensoryfibre from the posterior horn of the same side. 9 and terior horn are of large lo. Fibres from the crossed pyramidal tract of the same side. Size, the axis - cylinder processes of which 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 pos- terior or sensory root at the intervertebral foramen it contributes to form a mixed nerve — that is, one having enlargement. The spinal representation of many of the larger muscles ex- tends through several seg- ments. In the table of spinal 38 DISEASES OF THE NERVOUS SYSTEM. both motor and sensory fibres. There is no way of dis- tinguishing 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 the muscles for which its motor fibres are destined, these latter leave the mixed nerve in bundles to enter the muscles and be distributed FIG. 32, Motor nerve-ending of intercostal muscle-fibres of a rabbit, (Stohr.) to their fibrillae. Each nerve fibril terminates in a mus- cular fibre as a motorial end-plate. The Sensory Tract. — We know far less of the ner- 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 THE NERVOUS SYSTEM. 39 skin is the seat of a variety of bodies related to sensory perception. Of these some, like corpuscles of Pacini and Meissner, and the end-bulbs of Krause, are differen- tiated tactile organs whose office it is to modify and possibly to multiply the effects of stimuli upon the ter- minal 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 move- ments. There are good reasons for believing that the various sensations of touch, pain, temperature, and the muscular sense, have special terminal filaments for their appre- hension, and possibly for their conveyance from the periphery to the central nervous 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. The fibres composing a sensory nerve are to be looked upon as the dendrites of the neuron, the body of which is in the ganglion of the sensory root with its axis- cylinder process in the spinal cord. The first neuron in the sensory system is, therefore, composed of a single dendrite which extends into the periphery and 40 DISEASES OF THE NERVOUS SYSTEM. appreciates the sensation, a body which is located in the posterior-root ganglion and an axis-cylinder process which transmits the sensation for a longer or shorter distance in the spinal cord. This anatomical arrange- ment applies to all sensory nerves. The destination of the various axis-cylinder processes entering the cord varies considerably. The following are generally distin- guished (see Fig. ^;^) : A. Fibres ending by communication with the various types of cells found in the posterior horn. B. Fibres that enter the posterior columns and terminate by communication with the cells of the nucleus gracilis and nucleus cuneatus. C. Fibres which pass to the anterior-horn cells of the same side constituting the direct reflex path and fibres which pass to the opposite side forming a bundle which transmits the sensations of temperature and pain. Among the first group of fibres we recognize, besides those terminating in the cells composing the gelatinous substance, others which terminate by communication with neurons situated at the base of the posterior horn. These bodies constitute Clarke's vesicular column and are found especially well marked in the dorsal and upper lumbar regions of the spinal cord. They exist less pronounced in the cervical and lower lumbar regions, where they are known as Stilling's column. These groups of cells are of great importance because of their relation- ship to the direct cerebellar tract which lies just to the outer side of the crossed pyramidal tract. A further tract to the cerebellum is derived from neurons lying at the base and at the junction of the anterior and posterior horns (Gowers' bundle). The second (B) group of fibres mentioned above do not terminate till they reach the nucleus gracilis and nucleus cuneatus of the medulla. THE NERVOUS SYSTEM. 4I From these nuclei the sensory system is continued to the brain cortex, on the one hand, by the formation of the lemniscus, which is made up of crossed fibres from these nuclei, and to the cerebellum, on the other, by fibres passing by way of the restiform body to the cortex of the vermis. Some of these fibres pass direct, without interruption in these nuclei. Among the third (C) group of fibres are those which pass to the antero-lateral cord region of the opposite side and which transmit pain and temperature sensations. These fibres form a distinct bundle in that region known as the fasciculus-spino-tectalis et thalamicum (Horsley) fibres, which ultimately find their way into the lemniscus and end in the thalamus opticus. We see that the path and distribution of a sensory nerve is extremely complex; fibres being distributed to and ultimate terminations being found in the posterior horns of the same and the opposite side and the anterior horns of the same side in the cord; fibres to the cerebel- lum which are interrupted in the cord (Clarke's column) and ftbres to the cerebellum which are interrupted in the medulla (nuclei gracilis and cuneatus), fibres which reach the basal ganglia, and other fibres which are ulti- mately distributed to the cerebral cortex. All sensory nerves are thus complex and in addition contain also elements belonging to the so-called sympathetic system. Like the motor tract the decussation of the sensory tract is an incomplete one. Much of this decussation takes place in the spinal cord, but rather more occurs in the medulla. As regards the position of the sensory tract in the medulla, pons, and brain only general statements can be made. In the upper portion of the medulla the cerebellar 42 DISEASES OF THE NERVOUS SYSTEM. FIG. 33. Schematic diagram of the more important tracts of the posterior columns of the cord. Gsp, spinal ganglion (1, lumbar, d, dorsal, c, cervical) ; CCl, Clarke's col- umn ; Ks, cerebellar tract ; G, Coil's column ; B, Burdach's column ; Ng, nucleus gracilis; Nc, nucleus cuneatus ; DLm, decussation of the lemniscus; Crst, resti- torni body ; Narc, nucleus arcuatus ; Oi, inferior olive ; Os, superior olive ; Lnim, medial lemniscus ; Lml, lateral lemniscus ; Nil, nucleus of the lateral lemniscus ; Qp, Qa, anterior and posterior corpora quadrigemina ; Tho, optic thalamus ; Cc, ci rebral cortex. (Obersteiner.) THE NERVOUS SYSTEM. 43 fibres have already passed to their destination, and the crossed sensory fibres which here constitute the lemniscus or fillet are only to be considered. They end in nuclei belonging to the optic thalamus and ultimately reach the cortex in all probability through various groups of fibres known as the inferior, an- terior, posterior, and external radiators of the thala- mus. Another group of sensory fibres occupies the posterior third of the posterior limb of the internal cap- sule, a position immediately behind and contiguous to the motor tract. The cortical termination is probably in the ascending frontal and ascending parietal convolu- tions and contiguous areas of the parietal lobe. From what has gone before it will be seen that certain of the sensory fibres cross to the opposite side in the cord (temperature and pain), while certain others (tactile and muscle sense) remain uncrossed till they reach the medulla. From this circumstance is made possible the symptom-complex of Brown-Sequard's paralysis. It is probable that the fibres making up the posterior columns transmit certain muscular impulses, as well as tactile sense and muscle pain sense. 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 neuron to a motor neuron, whence it is reflected outward along a motor nerve to a muscle or group of muscles. Thus the integrity of two neurons is necessary in order to make possible reflex action, a sensory neuron on the one hand and a motor neuron on the other, and such a combination constitutes a "reflex arc." The motor element in this" arc" is known as the "reflex centre," and these are the same neurons as those constituting the 44 DISEASES OF THE NERVOUS SYSTEM. final link in the cerebro-spinal motor system, under which circumstances they act as transmitters of voluntary motor impulses descending from the cortex. The upper neuron elements in the motor system do more than conduct voluntary impulses from the brain to the lower neuron group, in that they exercise a re- straining or inhibitory influence upon the elements of the reflex arc, more particularly its motor element. If, therefore, the upper neuron is injured or destroyed, as occurs, for example, in lesions of the internal capsule or disease of the motor cortex or the crossed pyramidal tracts, this inhibitory influence is removed, the activity of the reflex centre is uncontrolled, and the motor phenomenon becomes exaggerated. This applies par- ticularly to the deep tendon reflexes. The gray substance of the spinal cord contains a series of reflex centres, cutaneous, muscular, and visceral. Some are complex and of considerable vertical extent. The relations of the more important reflexes to particu- lar segments are given in the table of localization of the functions of the spinal cord. The technique of their examination will be dwelt upon in another chapter. The Spinal Nerves. — There are thirty-two pairs of spinal nerves. They arise at nearly equal intervals be- tween the conus medullaris 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 of the dorsal region, for instance, being smaller than those of the lower cervi- THE NERVOUS SYSTEM. 45 FIG. 34- 46 DISEASES OF THE NERVOUS SYSTEM. til snx3id iJVQi^ni snx3id ivyovs FIG. 35. THE NERVOUS SYSTEM. 47 cal and lumbar regions, and this leads to inequalities of size in the nerve-trunks formed by them. The spinal nerves give rise to three plexuses of cardinal 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. 34). In the table. of localization of the functions of the spinal cord an attempt has been made to show the relations of the more important peripheral nerves to their segments. The lumbar plexus is derived from the anterior branches of the last dorsal and first four lumbar nerves, and the manner of their union and the chief nerve-trunks which arise from it are shown in the accompanying diagram (Fig. 35). The sacral plexus^ formed, as shown in the diagram (Fig. 35), 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 ot 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. 48 DISEASES OF THE NERVOUS SYSTEM. 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 picture of the position of the nuclei and of the arrange- ment 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. 17) 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 pair 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, may be very readily affected together because of their nearness, or, on the other hand, that others may be 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 per- ipheral filaments from the Schneiderian membrane pass through the numerous foramina of the ethmoid bone into the olfactory bulb lying along the under surface 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-sphenoidal 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 dis- THE NERVOUS SYSTEM. 49 appear in the anterior perforated space, while those of the inner root pass to the anterior cerebral commissure. There is good reason for believing that each olfactory nerve is connected with the cortical areas for smell of FIG. 36. The olfactory bulb and tract. A, Schneiderian membrane in nose in which lies peripheral olfactory neuron ; B, glomerulus of olfactory bulb ; C, mitral cells with dendrites in B, and axones in D, olfactory lobe ; E, granule cells ; F, cells in olfactory lobe; H, G, fibres of olfactory tract. (Ramon y Cajal.) both hemispheres, but the exact paths of these connect- ing fibres are not yet known. The Second or Optic Nerve. — The nerve of sight is far more important in its diagnostic relations. Passing back- ward 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. The amount of decussation varies somewhat in differ- ent animals and in individuals. In the chiasm we recog- nize three groups of fibres : (i) The decussating fibres 50 DISEASES OF THE NERVOUS SYSTEM. mentioned above (from the nasal side of the retina); (2) non-decussating fibres from the temporal side of the ret- ina ; (3) fibres passing between the two optic tracts and which have no connection with the retina. (See Fig. 37 ) After leaving the chiasm these varied fibres form what is known as the optic tract. The crossed fibres occupy the lower portion of the tract, the non-decussating fibres the upper portion, while the intertractal fibres lie pos- teriorly. Near the posterior part of the thalamus the tract divides into two unequal parts, the outer being the larger and being distributed chiefly to the external geniculate body and the pulvinar of the thalamus. About seventy per cent, of the tract fibres end thus. The fibres of the inner division end in the anterior corpora quadrigemina and constitute about twenty to thirty per cent, of the tract fibres. These endings are to be looked upon as the points of termiijation of the second neuron in this particular sensory system. The first neuron lies entirely within the retina. From these various points the second neuron completes the system to the cortex, the fibres being gathered into a considerable bundle, the anterior arm of the corpora quadrigemina. These fibres pass to the most posterior portion of the internal capsule and finally reach the cor- tex through the optic radiation. A few fibres probably reach the cortex without inter- ruption in the basal ganglia. The cortical areas in which the optic radiation termi- nates are certain portions of the occipital lobe, outer aspect, the cuneus, and certain areas about the calcarine fissure. If it is the right optic path that is affected, the right retinal halves become blind. Hemianopsia has been THE NERVOUS SYSTEM. 51 caused by diseases of the apex, external surface, and internal surface of the occipital lobe, but is most com- Schematic diagram of the central origin of the optic nerve. R, retina— dark portion derives its nerve supply from the left, while the light portion is supplied from the right hemisphere; No, optic nerve; Tro, optic tract ; CM, Meynent s commissure : Cg, Gudden's commissure ; 1, lateral root tract ; m, medial root tract; Tho, optic thalamus ; Cgl, lateral geniculate body ; Qa, anterior corpora quad- rigemina; Rd, direct root tract to the cortex ; Sm, optic radiation to the occipital lobes ; Co, posterior occipital cortex. (Obersteiner.) mon when the cuneus is involved ; and it may be, when other occipital areas than the cuneus are invaded with 52 DISEASES OF THE NERVOUS SYSTEM. resulting hemianopsia, that the underlying fibres of the optic radiations are included in the lesion. The Third^ Fourth^ and Sixth Nerves. — These nerves are all closely associated in the innervation of the muscles which move the eyeball, and the third (or oculo- motorius) supplies also the internal muscles of the eye, namely, the sphincter iridis and ciliarius. The muscles controlled by the third nerve are the sphincter iridis, superior rectus, inferior rectus, internal rectus, levator palpebrae, and inferior oblique. 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 disappear 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 superficial origins has already been mentioned. Entering 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 ganglion-cells lying in the in- terior of the gray matter below the aqueduct of Sylvius, 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 innervated by the nerve, and their relative arrangement from before backward is probably very nearly as follows: Rectus in- ferior, obliqus inferior, rectus internus, rectus superior, levator palpebrae. (See Fig. 38.) The cell group bear- ing relationship to the ciliary muscles of the iris is prob- ably separate from the others and is constituted in a group known as the Edinger-Westphal nucleus, the two halves of which are situated near the median line. THE NERVOUS SYSTEM. 53 The arrangement of the muscle representation in the nucleus from without inward is also shown in the dia- gram of the accompanying sagittal projection. The Fourth Nerve or Patheticus. — The fourth nerve, controlling the action of the superior oblique muscle, lies upon the outer side of the cavernous sinus in com- pany with the branches of the third nerve, and is hence apt to suffer with it in lesions affecting this region. The FIG. 38. Scheme of the oculo-motor nucleus (modified after Bemheimer"), sagittal projec- tion. M, median nucleus ; EW, Edinger-Westphal's nucleus. (Obersteiner.) superficial origin of this nerve is in the valve of Vieus- sens, in the roof of the fourth ventricle, the nerve ap- pearing on the surface just external to the crus cerebri, 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 all of the fibres take part in this decussation. Then the fibre-bundles pass downwards and forwards around the 54 DISEASES OF THE NERVOUS SYSTEM. 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 supplies the external rectus and probably gives some fibres also to the internal rectus. In the cavernous sinus it lies beside the fibre-bundles of the third and fourth nerves. FIG. 39. Scheme of the oculomotor nucleus (modified after Bernheimer"), basal projec- tion. M, median nucleus ; EW, Edinger-Westphal's nucleus. (Obersteiner.) From here it takes a long course over the prominent convex surface of the pons (thus rendering it very liable to suffer compression, especially from sub-tentorial growths) to its superficial origin between the lower pon- tine border and the pyramid of the medulla, not far from the median line. Both nerves often suffer together THE NERVOUS SYSTEM. 55 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 fifth, for the abducens passes very close to the superficial origin of the latter in its course over the pons. RetT. eoPY FIG. 40. 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 VII, 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. The central origin of the si'xth nerve is from a small nucleus immediately below the floor of the fourth ven- tricle, beneath the eminentia teres and in front of the striae acusticae. A transverse section of the pons at this level shows the seventh nerve curving about this 56 DISEASES OF THE NERVOUS SYSTEM. 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. There is no direct anatomical connection between the nuclei of the sixth and seventh nerve as formerly supposed. 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. These various nuclei are, however, associated together by means of association-fibres lying in the tract known as the posterior longitudinal bundle which runs near the posterior surface of the pons adjacent to the median line upward from the medulla to the gray matter of the third ventricle. These fibres Pj^ subserve the conjugate movement Diagram of the mechanism of the CyCS from side tO side, for in for the associated lateral guch movemcuts the external rectus movement of the eye. (Gow- ^"■^•^ of one eye (supplied by the sixth nerve) and the internal rectus of the other eye (supplied by the third nerve) must act simultaneously, as shown in Fig. 43- It is highly probable that these muscle groups have a bilateral cortical representation. That is, each muscle is represented on both sides in the cerebral cortex. This is true of some other muscle groups as well, such as the upper facial and the back muscles. In fact, the law of bilateral representation seems to apply to certain muscle THE NERVOUS SYSTEM. 57 groups capable of being used voluntarily, but under con- stant usage having passed from under the immediate control of the will. We are thus enabled to understand why complete paralysis of these muscles of cortical origin is never seen. No definite cortical area for this group of muscles is positively known. Paresis of the levator palpebrae fol- lowing lesions of the angular gyrus of the opposite side has led to the association of this area with this muscle. The Fifth Nerve or Trigeminus. — This nerve is both motor and sensory in function. Its motor fibres inner- vate 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, it contains fibres which sub- serve the sense of taste. The three branches which have given it the name of trigeminus, viz., the ophthalmic and superior and in- ferior 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 (see Fig. 44). 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 com- 58 DISEASES OF THE NERVOUS SYSTEM. plex as shown in Fig. 43, particularly in its sensory portion. The sensory root passes backward and in- ward through the outer part of the pons to some small groups of cells lying beneath the floor of the fourth FIG. 42, Fifth nerve or trigeminus. ventricle known as the middle nucleus. The majority of the fibres, however, turn downwards through the pons and medulla under the name of the descending root. This root lies just internally to the restiform body, and, growing smaller as it passes downwards, term- THE NERVOUS SYSTEM. 59 mates in the upper part of the spinal cord in close con- nection with the upper expansion of the gelatinous FIG. 43- Scheme of the central course of the trigeminal nerve. Rs, sensory root ; Rm, motor root ; Rsp, spinal root ; Re, cerebral root ; Ns, sensory nucleus ; Sg, sub- stantia gelatinosa ; Nm, motor nucleus ; Sf , substantia ferruginea ; Ra, raphe. (Obersteiner.) substance of the posterior horn (the gray tubercle of Rolando). 6o DISEASES OF THE NERVOUS SYSTEM. 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. These lie external to the aqueduct of Sylvius and are arranged in the form of a crescent. FIG. 44. 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). The majority of the fibres of the motor root arise from a collection of large ganglion-cells of limited vertical ex- tent which lies just internal to the sensory root of the fifth nerve in the lateral part of the tegmentum of the pons. There are many intricate arrangements of the sensory portion of this nerve. Its so-called descending root THE NERVOUS SYSTEM. 6l corresponds to the Rolandic substance of the posterior horns of the spinal cord and really consists of small cells from which the sensory fibres destined ultimately to join the great sensory tract, the lemniscus, take their origin. G.S.P. lC- \ ~^s!s^ €^ Aud, Post A u. FIG. 45. Diagram of facial nerve and its connections (modified from Leube), showing course of taste fibres. V, trigeminal nerve; i, 2, 3, first, second, and third divisions of trigeminus; F, facial nerve ; Aud, auditory nerve; G. S. P., great superficial petrosal; S. S. P., small superficial petrosal; Gen, geniculate ganglion; Ot, otic ganglion; M, Meckel's ganglion ; Uv, uvula; L, lingual nerve; C. T., chorda tympani ; Stap, nerve to stapedius; St. M., stylo-mastoid foramen ; Post. A.U., posterior auricular nerve; G. P., glosso-pharyngeal nerve; P_, petrous ganglion of glosso-pharyngeal; Jac, Jacobson's nerve; Car, tympanic plexus near carotid artery. , N. B.— Dotted line = taste fibres from anterior two thirds of tongue ; dash line = taste fibres from posterior third of tongue. (AUchin.) The distribution of the sensory fibres so originating forms no exception to the disposition of the sensory system generally, as already described. There is a partial de- 62 DISEASES OF THE NERVOUS SYSTEM. cussation of the tract so formed, a considerable portion passing to the opposite side, the fibres ultimately joining the lemniscus in the region of the red nucleus. Fibres from the same side also pass to the cerebellum. Those which join the lemniscus terminate, first, in the optic thalamus, and, secondly, in the cortex as mentioned above for the sensory system in general. The centre for the masticatory muscles is contiguous and anterior to the facial centre in the cortex. The relationship of the fifth nerve to the sense of taste is important and quite complex as shown in the accom- panying diagram. (Fig. 45.) A correct understanding of this arrangement is of great importance clinically, since it enables us to under- stand the reason for the disturbances and occasional examples of loss of taste in a portion of one side of the tongue following middle-ear disease through the exten- sion of such disease process to the Fallopian canal trav- ersed by the chorda tympani. The Seventh or Facial Nerve. — This nerve is second to none of the cranial nerves in the importance of its diagnostic relations, and hence deserves careful con- sideration. The muscles supplied by fibres from the facial nerve are as follows: Occipito-frontalis, muscles of the external ear, stylo-hyoid, posterior belly of di- gastric, 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 Fallopian canal of the temporal bone. Within the Fallopian canal the nerve is separated from the middle ear by only a thin lamina of bone pierced by foramina for a small artery. THE NERVOUS SYSTEM. 63 the chorda tympani nerve, and the nerve to the stapedius. This fact is of importance, because it explains how in- flammatory processes in the middle ear may extend 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 geniculate ganglion is really not a ganglion in the ordinary sense, but merely an enlarge- ment in the curve of the nerve-trunk due to the junction of it at that point with several other nerves. 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. (See Fig. 46.) The nucleus of the seventh nerve lies beneath the floor of the fourth ventricle at a point ventral to the striae medullaris. It lies immediately dorsal to the medial lemniscus (the great sensory tract) with the superior olive to its inner side and the nucleus of the fifth lying a little dorsal and to the outer side. From this nucleus of origin the fibres take a devious course, passing first to a point dorsal to the nucleus of the sixth nerve, where they ascend for a short distance, finally making their exit from the medulla at the point above mentioned. (See 50-) There is good reason for believing that some of the muscles supplied by fibres from the facial are not repre- sented in the facial nucleus, but in the nuclei of other nerves. This applies especially to the fibres composing the superior branch of the facial and which are dis- tributed to the occipito-frontalis, the corrugator supercilii, and the orbicularis palpebrarum. This group of muscles 64 DISEASES OF THE NERVOUS SYSTEM. is not paralyzed in palsies of cerebral origin, but only in palsies involving the trunk. This can also be explained on the theory of the bilateral cortical representation of these muscles, in favor of which there is some evidence. \ INfRAOfiB.S''* ORBITAL f. / /AJ f^J^sf^^ 5W- MCNTAU 5^ FIG. 46. Seventh nerve, facial, diagrammatic. I. Great petrosal, to form vidian with No. 5. Small petrosal, to otic ganglion. External petrosal, to plexus on mid. meningeal artery. 4. Tympanic br. to stapedius, etc. 5. Br. from carotid plexus, making vidian with No. i. 6. 7. Brs. to auriculo-temporal of 5th. 8. Br. to auricular of vagus. M. The ganglion of Meckel. O. A. F. Orifice of aqueductus Fallopii. The fibres to the orbicularis palpebrarum originate in the nucleus of the third nerve, but course in the seventh. The orbicularis oris probably has a certain representa- THE NERVOUS SYSTEM. 65 tion in the hypoglossal nucleus, because of the intimate association of the movements of the lips and 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 same 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 respec- tively from the cochlea and vestibule and from the semi- circular canals. (See Figs. 47 and 48.) These sets of fibres differ in function, the former conducting sound-waves, and the latter serving to carry from the semicircular canals impressions relative to the movements and position of the body. Changes in bodily position probably cause irritation of the mucosa of the semicircular canals by means of solid bodies contained in the endolymph. Thus we are to conceive of the vestibular portion of this nerve as conducting impressions relative to the posi- tion of the body in space and are to consider the semi- circular canals of the vestibule as the point from which these special sensations depart. This sensory nerve follows the same arrangement as obtains for sensory nerves in general. The fibres are first interrupted in the vestibular ganglion and from this point pass to enter the medulla together with the cochlear fibres at a point ven- tral to the corpus restiformis, and to end finally in the vestibular nucleus lying immediately beneath the striae medullaris of the floor of the fourth ventricle. There is also a group of larger cells lying to the outer side of this nucleus, which is commonly known as Deiter's 66 DISEASES OF THE NERVOUS SYSTEM. nucleus, and these two cell groups form the chief end- ings in the medulla of the vestibular fibres. There are two other nuclei which belong properly to the cerebellum which are a part of the vestibular system and in which e. eU. ! // 9p. Ci. Eighth or auditory nerve, diagrammatic. Thin black lines, vestibular division of eighth nerve; dotted lines, cochlear division of eighth nerve; v., vestibule t V.O., vestibular ganglion; cbl., superior vermis of cerebellum ; B., nucleus of Becterew ; d., nucleus of Deiter ; D.Rt, descending root of eighth nerve; t.n., triangular nucleus ; v.s.t., vestibulo-spinal tract ; v. ex., vestibulo-cerebellar tract; o.c, organ of Corti ; G c, ganglion cochleare ; t.ac, tubercular acusticum ; st.M , striae medullares ; ac.n., accessory nucleus: o s., superior olive ; l.m., lateral lemniscus ; p.q b., posterior quadrigeminal body ; m.g.b., median geniculate body c.cbi., cortex cerebri, third temporal convolution ; C.R., corpus restiforme. THE NERVOUS SYSTEM. 67 vestibular fibres terminate, viz., the nucleus angularis and the nucleus tecti. The association of these various nuclei with the spinal cord is brought about by means of two systems of fibres which extend the vestibular ap- paratus to the lower levels of the cord. A portion of these fibres course in the fasciculus longitudinalis pos- terior and another in the so-called descending acoustic root. It is to be noted that the latter really contains no acoustic fibres whatever. The cortical termination of this system is in the vermis of the cerebellum. We are thus enabled to understand the occurrence of motor dis- turbance in diseased conditions involving the middle lobe of the cerebellum on the one hand or the semi- circular canals on the other (Meniere's disease). The cochlear fibres of the eighth nerve are those im- mediately concerned with the sense of hearing. Begin- ning in the mucous membrane of the cochlea the fibres are first interrupted in the cochlear ganglion lying in the whorl of the cochlea. The fibres proceed, together with those from vestibular portion above described, to a point below the pons and ventral to the corpus restiformis to enter the medulla. The primary distribution of these fibres is twofold; one portion passing to the ventral acoustic nucleus which lies immediately ventral to the corpus restiformis and the other portion passing to the tuberculum acusticum (accessory nucleus) lying dorsal to the corpus restiformis. These two nuclei are the primary medullary nuclei of the cochlearis. From these two nuclei the acoustic tract is continued by means of fibres from the accessory nucleus which form the striae acusticae on the floor of the fourth ventricle and cross the middle line to the opposite side, and fibres from the chief nucleus (ventral), some of which pass by means of the corpus trapezoides to cross the median line and join 6S DISEASES OF THE NERVOUS SYSTEM. I'^^r The auditory tract. Th, optic thalamus; Int, int. capsule; Ci, corp. genicu- latum int.; Tem, temporal lobe ; L, lemniscus ; Cqa, corp. quadrigeminum ant.; L-qp, corp. quad, post.; R, red nucleus of tegmentum ; Sn, substantia nigra ; Ce, cochlea ; T, dorsal nucleus of auditory nerve. (Starr.) THE NERVOUS SYSTEM. 69 the fibres from the striae acusticse and end in the superior oHve of the opposite side. From the superior olive the acoustic tract is continued cerebral-wards by means of the lateral lemniscus which forms to the outer side of the superior olive to end in the posterior quadrigeminal body and to be further continued cerebral- wards as the brachium of the posterior quadrigeminal body. These fibres terminate in the middle geniculate body of the thalamus opticus and are finally distributed to the cortex of the first temporal convolution. The course of the auditory fibres is thus seen to be quite complex. The wide difference in function between the cochlear and the vestibular fibres of the eighth nerve should always be borne in mind. The left cortical auditory area is especially related to the memory of words, its destruction producing the form of aphasia known as word deafness. The fact that the eighth nerve at the base of the brain and at the internal auditory meatus lies side by side with the facial is an anatomical point of some importance. 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 JO DISEASES OF THE NERVOUS SYSTEM. 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. The Tenth, 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 NERVOUS SYSTEM. 71 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 acces- sory portion, the spinal portion arising at a wide interval from a lower level, in the anterior horn of the spinal cord. 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 lateral to the eminentia teres of the fourth ventricle, with its long axis running 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 portion of the eleventh nerve. Motor fibres are derived from a special group of cells known as the nucleus ambiguous. From these groups of cells the fibres run outward through the formatio reticularis of the medulla to their superficial origins as described. In passing through the medulla these bundles of fibres traverse the ascending root of the fifth nerve. T^ DISEASES OF THE NERVOUS SYSTEM. ru)OR or rouRTH vcnthicle 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 a unique course upwards into the cranial cavity to join tempo- rarily the accessory portion before again passing out of the cranial cavity to supply the trapezius and sterno - cleido- mastoid with motor fibres. It supplies these two muscles in conjunction with branches from some of the cervical nerves proper. The Twelfth or Hypoglossal Nerve. — This is a purely motor nerve des- tined for the mus- cles 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 sepa- rated at their superficial origin by the prominent an- terior pyramids, and are rarely involved together by disease external to the medulla. The eleventh and FIG. 49. Diagram of a transverse section through ^ the medulla at the lower level of the fourth ventricle. Especially to be noted are the tenth and twelfth nerves and their nuclei of origin, the position of the olivary nucleus, the fillet, the anterior pyramids (the motor path), the restiform body, and the ascending root of the fifth nerve. Between the olive in front and the tenth and twellth nuclei behind lies the substantia reticularis (the path of common sensi- bility). The posterior longitudinal bundles lie on either side of the median line between the twelfth nerves. THE NERVOUS SYSTEM. n 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 FIG. 50. Schematic basal section of the medulla oblongata, Po, pons; Brcj, Brachium conjunctivum ; Va, spinal, Vd, cerebral, Vm, motor, Vs, sensory root of the trigeminal nerve ; NVm, motor, NVs, sensory root of the trigeminal nucleus ; NVII, nucleus of the facial nerve ; VII, a, b, c, root of the facial nerve ; VII, exit of the facial nerve; NVI, abducens nucleus; NXII, hypoglossal nucleus; IXa, spinal root of the glosso-pharyngeal nerve (X) ; IX, its exit ; No, olivary nucleus; X, vagus nerve ^or glosso-pharyngeal) showing its part origin from the nucleus ambiguous ; Na, nucleus ambiguous ; Ca, anterior horn of the spinal cord; Ca, Na, NVII, NVm, column of origin of motor nuclei. of motor nerve-cells extending from the level of the lower angle of the fourth ventricle (calamus scriptorius) down- ward to the decussation of the pyramids. It lies close to the median line, and in part of its course just medial 74 DISEASES OF THE NERVOUS SYSTEM. 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 be- tween the olivary nucleus and the anterior pyramid, some of the fibres generally traversing the former. The rela- tive origin and course of the ninth, tenth, and twelfth nerves in the medulla are shown in the schematic dia- gram of Fig. 50. 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 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 approximate 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 endothelium and encloses the lymphatic subdural space, which contains a variable amount of serum. The middle membrane 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 endothe- lium 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 complete in the spinal canal. There is no direct com- munication between the subdural and subarachnoid THE NERVOUS SYSTEM. 75 lymph-spaces, but there is a free communication be- tween 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, there- fore, lies upon a sort of water-bed, being separated from the base of the skull by an interval occupied by sub- arachnoid 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 blood-vessels, lymphatics, and vasomotor nerves. It dips down between the convolutions of the brain, and sends connective-tissue septa into the cord. The blood- vessels and nerves pass inward 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 ']6 DISEASES OF THE NERVOUS SYSTEM. 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- 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 practical importance to the physician than that of the spinal cord. It is derived from the carotid and vertebral arteries. 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 an- terior and middle cerebral arteries, while the basilar artery, formed by the two vertebrals, redivides into the two posterior cerebral arteries. These three arteries, the anterior, middle, and posterior cerebral, supply each hemisphere in the region designated by their name. Practically the middle cerebral or Sylvian artery is of especial importance, for, coursing through the fis- sure of Sylvius, it is distributed over the motor area of the cortex. Hence the hemiplegia so often pro* THE NERVOUS SYSTEM. 17 duced by embolism and by thrombosis of this artery. Although it has anastomoses with branches from the FIG. 51. Arteries at the base of the brain. (Oppenheim.) other arteries on the surface of the brain, they are rarely sufficient for the establishment of a collateral circulation. 78 DISEASES OF THE NERVOUS SYSTEM. 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 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 distributed to part of the caudate nucleus, to the lentic- ular nucleus, the internal capsule, and to part of the optic thalamus. The anterior vessels of this group are 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 the serious symptoms accompanying 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 upwards to enter the superior longitudinal sinus, while those from the base of the brajn 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 cerebel- lum, terminate in the straight sinus. There are free anastomoses between all of the sinuses, and there are THE NERVOUS SYSTEM. 79 FIG. 52. Area of cortex supplied by the branches of the middle cerebral artery. FIG. 53. Area of cortex on outer surface of hemisphere supplied by the anterior cerebral artery. FIG. 54. 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. 55. Area of cortex on the outer surface of the hemisphere supplied by the posterior cerebral artery. FIG. 56. 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 So DISEASES OF THE NERVOUS SYSTEM. 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 sys- FiG. 57. Diagram of the blood supply of the central ganglia and internal capsu! C, middle cerebral artery; E E, external, I, internal, lenticulo-striate III V, third ventricle. (After Duret.) e. Mid. arteries : tern is connected 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 diagram on page 83 illustrates sufficiently well the general correspondence be- tween the chief convolutions and fissures and the cranial bones. It will be noted that under the frontal bone lie THE NERVOUS SYSTEM. 8l 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 pos- terior portion. Under the occipital bone lies about one half (posterior) of the occipital lobe. The parietal bone covers what remains of the cortex. 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 ex- ternal occipital pro- tuberance (i n i o n) along the middle line. A point one half inch posterior to the middle point of this distance marks the upper ex- tremity of the fis- sure. The fissure of Rolando in its upper two thirds makes an angle of sixty-seven degrees with the median line, in its lower one third the fissure is a little more ver- tical. The average length of the fissure is about three and a half inches. The central convolutions occupy about an inch anterior and posterior to the fissure, and the positions of the leg and face centres may thus be approximately 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 FIG. 58. Diagram showing the relation of the convolutions to the skull. 82 DISEASES OF THE NERVOUS SYSTEM. The mutual relations of the vertebral bodies and spines to the segments of the cord and to the exit of the nerves (Gowers). of the parietal boss. The posterior limb of the fis- sure of Sylvius lies under the posterior three fifths of this line. The anterior limb of the fissure of Sylvius ascends almost vertically from the syl- vian line at the middle of the zygoma. A continu- ation of the Sylvian line backwards to the sagittal suture 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 ver- tebrae is essential both for the diagnosis and success- ful treatment of certain spinal-cord a ff ec t i o n s. Theserelations varysome- what in different individ- uals, but one description is sufficiently accurate for practical purposes. The chief facts may be de- duced from the accom- panying drawing. These facts are as follows: (i) The spinal cord in the adult terminates at THE NERVOUS SYSTEM. 83 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 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 lumbar 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 exact 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- b4 SYMPTOMATOLOGY OF NERVOUS DISEASES. 85 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- so DISEASES OF THE NERVOUS SYSTEM. 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 hyperaesthesia. 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 87 is temporary, the latter permanent. It is important to remember that the effects of destruction and those ot 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 segriient or its lower 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 88 DISEASES OF THE NERVOUS SYSTEM. x-'^C 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 l\\&same side, and of the face. arm. 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 same 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 XI 1th 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 89 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 more common form there is a more or less marked loss of voluntary motion involving face, tongue, arm, and leg on the same side — complete hemiplegia. Such hemiplegia may result from a lesion anywhere in the motor tract between the cortex and the pons. 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 hemiplegia results. In the inter- nal 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. While this is theoretically possible it is practically of rare occurrence, and a more or less complete hemiplegia in range is the rule. The motor fibres are more and more widely sepa- rated in their course through the corona radiata of the cortex. Hence, in these situations even a lesion of con- siderable 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 more or less completely, the arm being paralyzed alone. Such a paralysis is called brachial monoplegia. Other monoplegias, as face and arm, arm and leg, but not face and leg, may occur from single lesions. The expression "complete hemiplegia" implies that the paralysis affects all of one side, but this is not strictly true. Thus the upper facial muscles (orbicularis pal- pebrarum and occipito-frontalis) move almost or quite as well as on the non-paralyzed side, and the muscles of the eyeball and the muscles of mastication are unaffected. The tongue as a whole deviates towards the paralyzed 90 DISEASES OF THE NERVOUS SYSTEM. side when protruded because the projecting apparatus on that side is weakened and does not oppose the genio- hyo-glossus. Inasmuch as this muscle also retracts as well as protrudes the tongue, the organ is not so high on the paralyzed side when in repose. The muscles of respiration and the muscles of the face and trunk are not involved in ordinary action. The movements of the superior intercostal muscles are greater on the paralyzed side, though if the patient take a deep respira- tion there is defective chest expansion of the affected side. In general it may be said that in hemiplegia the extent FIG. 6l. Respiratory movements in a case of right hemiplegia. R, right side ; L, left ie ; A B and a' b', normal respiration ; b c and b' c', forced respiration. sid of the paralysis in the part is proportional to the degree in which the 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 innervated from both hemispheres, although not quite equally. The leg, which, though generally used with its fellow, is capa- ble of some unilateral use and is also represented to some extent in both hemispheres, suffers less, and usually recovers more power than the arm. This re- covery is through compensation by the normal hemi- SYMPTOMATOLOGY OF NERVOUS DISEASES. 9I sphere, whose nerve impulses probably travel over other than pyramidal tracts. In early life the amount of recovery 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 to the lesion. This is explained by the crossing of the pyra- mids in the medulla. A few exceptions to this rule are met with, and often the parts on the same side of the lesion are slightly weakened, due to an incomplete cross- ing of the pyramids and the persistence of a larger bundle in the direct pyramidal tracts. Double hemiplegia or diplegia is a paralysis of all four extremities, and may result from two extensive lesions or a single diffuse lesion covering both hemispheres, as from meningeal hemorrhage in birth palsy. Common hemiplegia, such as has been described, is not often accompanied with hemianaesthesia, but it may be associated with partial loss of tactile sensibility in the extremities for a time, if the lesion involve the sensory tracts lying far back in the capsule, or when the optic thalamus is injured. The processes which most frequently give rise to hemiplegia are cerebral hemorrhage from arterial rup- ture, thrombosis, acute softening, embolism, 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. The condition is known as crossed hemiplegia. It occurs when the 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 in the pons from the opposite facial tract. The lesions must be below the 92 DISEASES OF THE NERVOUS SYSTEM. middle of the pons, as the crossing of the facial path occurs just above. (See Fig. 62.) 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 onone side with paralysis of the ex- tremities of the opposite side. The nerves most fre- quently involved in such a lesion 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 or presses on it 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 character of a complete peripheral facial palsy; involvement of upper as well as lower muscles of the face, R. D., etc. (See Fig. 62 for explanation of these anatomic facts in paralysis.) Hemiplegia from a disease in such region is by no means always of the crossed type, since there may be only a slight weakening of some one or more cranial nerves, the lesion being so small or situated in the motor tract only. Spinal Hemiplegia or Browh-Sequard' s Paralysis is a type of hemiplegia that results from lesions interrupting the motor path of one half of the cord. Both arm and leg are involved when the lesion is high in the cord; the paralysis of the leg may be incomplete, while that of the arm is complete, as fibres for the leg cross lower down in the cord. The lesion which causes spinal hemiplegia is seldom confined to the motor tract or even to one side of the cord. Hence there is not only anaesthesia on the side opposite the lesion, but there is commonly some weakening of that side also. The anaesthesia never ex- tends quite to the level of the lesion, as the sensory SYMPTOMATOLOGY OF NERVOUS DISEASES. 93 fibres cross in the cord a little above their level of en- trance. The symptoms on the side of the lesion are: Motor palsy, slight hypersesthesia of skin, impairment of muscular sense, reflex action at first lessened and then increased, and the temperature slightly raised. The symptoms on the side opposite the lesion are: Muscular power nearly or quite normal, loss of skin sensibility, temperature same as that above the lesion. The typical symptoms are less definite as the lesion approximates the lumbar enlargement. A lesion on one side of the lumbar enlargement often affects sensation on the same side as motion because it damages the sensory path before it has crossed. In all cases of crossed motor and sensory paralysis the sensibility of the muscles differs from the other forms of sensibility. And if muscular sensibility is affected on one side this is the side of the motor palsy and not of the cutaneous anaesthesia. Paraplegia is a term used generally to designate a paralysis of both lower extremities. When all parts below the head are paralyzed the condition is termed cervical paraplegia. The intercostal muscles are in- volved and respiration is diaphragmatic. 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 absence or presence of these symptoms will be discussed elsewhere. Paraplegia is most frequently a symptom of spinal- cord disease, but may result from disease elsewhere. In the pons and medulla the motor tracts are close together, and it sometimes happens that a lesion there has suffi- cient transverse extent to involve the fibres of both sides (such as tumors), when paraplegia results. More rarely bilateral involvement of the crura leads to a similar re- sult. Occasionally paraplegia results from bilateral 94 DISEASES OF THE NERVOUS SYSTEM- disease of the motor area of the cortex, as that seen in spastic paraplegia of infants. It has been already- alluded to as double hemiplegia. Paraplegia is a rather common occurrence in peripheral nerve affections, as in alcoholic multiple neuritis. Com- pression of the Cauda equina by tumor or fracture ordinarily gives 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. A functional paraplegia from premature senile changes in the arteries to the lower part of the cord and paraplegia in chlorotic women some- times develops independently of hysteria. 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 monoplegia, or a facial monoplegia. The lesion may be cerebral, spinal, or peripheral. 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 paralysis be confined to a single muscle or group of muscles known to be innervated by a single peripheral nerve branch the paralysis is unquestionably peripheral. If groups of muscles having a certain function in com- mon are involved, as for example the dorsal flexors or adductors of the foot, the lesion is probably in the anterior horn of the spinal cord, as muscle groups re- lated to particular functions are represented in the cord. 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 the upper portion of the motor path of the brain, for here movements of entire segments of an extremity are represented rather than of individual SYMPTOMATOLOGY OF NERVOUS DISEASES. 95 muscles or groups of muscles. While these general rules are often insufficient in themselves to establish the loca- tion of the lesion 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 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. While this distinction between focal and diffuse symptoms is useful it cannot always be made in practice. For example, some symptoms may be signs of focal disease at one time and at another of diffuse disease. This is the case with headache and with optic neuritis. The designation paralysis is correctly applied to all grades of motor loss from slight weakness to more or less complete abolition of function. Sometimes the term " paresis " is applied to slight grades of weakness. The difference is purely one of degree, and the latter term should not be used, as it is often employed in another sense to designate a form of mental disease. The terms complete and incomplete are much the better expressions -to qualify the degree of paralysis present in any given case under description. Convulsions. — By this term is generally understood involuntary, paroxysmal, purposeless, muscular contrac- tion, of variable intensity and duration and of extensive or limited distribution. Convulsions may occur in consequence of disease situ- ated in the cerebrum, basal ganglia, pons, medulla, or spinal cord, but are most often seen in cerebral dis- ease, and their relation to such disease is of especial 9^ DISEASES OF THE NERVOUS SYSTEM. importance. Convulsions may occur from disease of any part of the nervous system where there is an aggre- gation of motor cells forming part of a reflex arc. They may arise (i) as a result of active irritation of brain tissue, particularly of the cortex, such as occurs in meningitis or meningo-encephalitis and active brain tumors; (2) in consequence of more or less stationary, non-active lesions, in which some nerve-cells are still able to generate nerve force, but do not possess the power of perfectly controlling their discharge, as in epileptic convulsions following infantile cerebral hemi- plegia; (3) from spontaneous discharge of nerve force without a demonstrable gross lesion or irritation in the cortex, as in idiopathic epilepsy; (4) from discharge of ponto-bulbar centres or from centres in the cord itself, as in myelitis and polio-myelitis resulting from an acute morbid blood state. Convulsions may be local or partial in their commence- ment, that is confined to particular groups of muscles or to one muscle of an extremity, and subsequently become general; or they may remain localized or 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 from other causes such as toxic and autoxic agents, seem capable of deter- mining a discharge of nerve force from them, though they may be the seat of no gross structural change. Thus general convulsions are very commonly observed in idiopathic epilepsy, in uraemia, and especially in chil- dren at dentition, and at the commencement of febrile diseases, from gastro-intestinal disturbances, etc. It is SYMPTOMATOLOGY OF NERVOUS DISEASES. 97 an important fact that a very large majority of all the cases in which general convulsions occur are not examples of gross organic disease of the brain. In organic disease of the brain convulsions are usually- general when the lesion is a diffuse one such as meningo- encephalitis and not circumscribed in the motor area of the cortex or the subjacent white matter. On the other hand, convulsions that are local in their commencement or remain limited in extent always indicate disease in or adjacent to the motor area of the cortex. The disease is usually structural in character, but in a few instances no structural change can be detected to account for the local beginning, and here there are probably nutritional changes that give rise to a pathological local instability. In other words, localized convulsions constitute a focal symptom, general convulsions a diffuse symptom. The general convulsions from organic disease of the brain bear a close resemblance to the convulsions of idiopathic epilepsy, that is to say, there is usually a. period of tonic followed by clonic spasm, during which the patient becomes rapidly or suddenly unconscious. A focal beginning in a general convulsion, however short, probably indicates an organic disease of the brain, if uraemia can be excluded. In local or partial convulsions the local onset is refer- able 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. If a convulsion is very slight it may be limited to the muscles in which it begins, and there may be no per- ceptible 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 7 98 DISEASES OF THE NERVOUS SYSTEM. it begins. The order of its extension is usually from the free end of an extremity toward the trunk, involving an entire segment or extremity before extending to other parts of the same side. In such cases consciousness is usually lost as soon as the convulsion is well advanced. The degree of loss of consciousness and the length of time consciousness re- mains absent is proportional to the rapidity and com- pleteness of nerve discharge from the cortical centre. If the discharge of nerve force is of the highest grade of intensity the convulsions may involve both sides of the body at the same time and in such cases loss of consciousness is usually complete from the start. Strictly speaking it is prob- able that no convulsions are • general from the very com- i mencement. For example, even in infantile eclampsia and uraemic convulsions it is very common for the spasm to begin Localized spasm of the left side of . • r j the face in a patient suffering from lU OUC extremity a ICW SCCOndS Jacksonian epilepsy. (Starr.) , . . . before it passes to the remam- ing half of the body or becomes general. True local convulsions, however, repeatedly commence in one ex- tremity, and if they do not remain local at least con- tinue so for an appreciable time. It is not uncommon for a warning or aura to immedi- ately precede a convulsive attack. The aura is always sensory in character and often begins in the part which is afterwards the seat of convulsion, and this is particu- larly true if there be a general convulsion with a local onset. The sensation may ascend the limb first in- FIG. 02. SYMPTOMATOLOGY OF NERVOUS DISEASES. 99 volved, and even pass to the second extremity affected, before the convulsion comes on. Such sensory aurae undoubtedly result from a nervous discharge from sen- sory cells which precedes that which occurs from motor nerve-cells, the functional control of which is one of their chief functions. The motor area of the cortex contains sensory as well as motor cells, and the presence of a sensory aura before the spasm indicates that the convulsion has its initiative in sensory elements, that is; cerebral convulsions are a sensory-motor reflex and are largely sensory in origin with a resultant motor expression. Aurae of the special senses, as a flash of light, an odor, or a sound, are not uncommon in idiopathic epilepsy, but they are of relatively rare occurrence in organic dis- ease of the brain. When they do occur they indicate that the lesion has its maximum intensity at or near the special sense centre 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 local or partial convulsion. If the convulsions recur frequently at short intervals the weakness may be very decided. In most cases it soon passes away, but in rare instances permanent paralysis may result. In such cases the convulsions have probably given rise to a destructive lesion by hemorrhage. If the convulsions happen to involve the extremities of one side of the body the weakness is, as might be expected, hemiplegic, but it is readily distinguished from hemiplegia by wearing off in two or three days or earlier. The weakness fol- lowing convulsions is called post-convulsive or exhaus- tion paralysis. It is explained on the supposition that a severe convulsive seizure exhausts the motor nerve-cells related to the part. The resultant paralysis is greatest lOO DISEASES OF THE NERVOUS SYSTEM. in those particular parts which are most actively engaged in the preceding convulsions. Exhaustion paralysis occurs most frequently in those cases suffering from a previous incomplete organic hemiplegia of children in which epileptic convulsions have been superinduced in later life. The general exhaustion seen after general convulsions is probably analogous in cause and effect to the weakness which occurs in certain parts following local convulsion. As to the diagnostic significance of local convulsions it may be said that this is the same whether the convul- sions remain localized or subsequently become unilateral or general. They do not quite prove the presence of structural disease because in rare instances idiopathic epilepsy, ursemic convulsions, and diabetic convulsions may begin locally. But every case where convulsions begin locally should excite 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 convulsion is not diminished by the occurrence of general convulsions at other times. Convulsions which are general from the commence- ment, on the contrary, point to idiopathic epilepsy. But they do not exclude the possibility of structural disease, because 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 convulsions alone. General convulsions, besides being met with in organic diseases of the brain and spinal cord, are observed in idiopathic epilepsy, tetanus, uraemia, diabetes, and hysteria. It is not very uncommon for hysterical con- vulsions to occur in the course of organic disease of the SYMPTOMATOLOGY OF NERVOUS DISEASES. lOI brain, and this sometimes leads to errors in diagnosis. Such convulsions not rarely result in the course of intra- cranial 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 and usually quite superficially. 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. Convulsions are frequently classified on a purely mechanical basis according as the tonic or clonic ele- ment predominates. Clonic spasm does not necessarily differ from tonic convulsion in its origin or essential character, but the impulses in the nerve discharge are infrequent enough to permit the muscular apparatus a temporary intermittent relaxation. A tonic or tetanic convulsion is one in which the muscular contraction continues for an appreciable but short period of time. Such spasm is met with in many conditions, for example at the onset of a grand mal epileptic paroxysm, in some cases of petit mal, in major hysteria, and in tetanus. Tetanic seizures lasting for hours or even days some- times result from disease involving the gray matter in the floor of the fourth ventricle and perhaps from cere- bellar disease and secondary pressure on the cruri. From their resemblance to tetanus the convulsions are often designated tetanoid. Purely tonic spasm (Trousseau's symptom) may be excited by pressure on the larger nerves and arteries, as in laryngismus stridulus. The mechanical and elec- trical irritability of the peripheral nerves is increased during the intervals. I02 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 tjtle (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. I03 same subjects. The spasm is thought to result from discharges 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 resulting 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 occurs 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 the extra muscular tension. The tremor of paralysis agitans may be inhibited at will by voluntary effort for a short time, but it soon recommences. The term ** intention tremor," borrowed from the Germans, is used to designate tremors which occur only during voluntary movement causing increased muscle tension. It is more accurately named action tremor. It is frequently seen in disseminated sclerosis and in mercurial poisoning. It is often wide in range, irregular in rhythm, and ataxic in character. Roughly speaking, the extent of a tremor is inversely proportionate to its rapidity, but the same tremor may vary somewhat in range at different times. There is considerable difference in the rapidity of different kinds of tremor, and these differences are sufficiently constant to be of some diagnostic value. For instance, the tremor of alcoholism is rapid and varies from seven to eight, and that of paralysis agitans from four to seven 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 I04 DISEASES OF THE NERVOUS SYSTEM. a nutritional character in which no gross structural changes in the nervous elements have been detected. Thus it is seen on the one hand in disseminated sclerosis after hemiplegia, in senile dementia, and certain forms of toxic neuritis; and, on the other hand, after exhaust- ing diseases, in neurasthenia, paralysis agitans, hysteria, and Basedow's disease. Very frequently tremor is a toxic symptom, and as such it is seen in alcoholism, in poisoning from lead, mercury, opium, cocaine, and after the excessive use of tea, coffee, tobacco, and quinine. But tremor is also encountered in cases where no as- signable exciting cause can be detected and in which there is no associated abnormal state. It is sometimes not only congenital but also hereditary, and may be present throughout a lifetime without any other nervous affection being present. It may affect several members in a family through several generations. 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. Simple tremor neither shortens life nor influences the general health. Senile tremor occurs in extreme old age or in early senility, and while it does not exhibit the same rigidity and muscular weakness observed in paralysis agitans it is doubtless closely associated and probably dependent upon an allied structural change in the nerve elements. Most tremors cease during sleep; rarely a tremor is di- minished or unaffected. The upper extremities are most frequently the seat of tremor, and the head is more involved than the leg. With regard to the pathology of tremor nothing defi- nite can be said. We know that when a voluntary movement is made every contraction of one set of muscles is accompanied by a corresponding relaxation of SYMPTOMATOLOGY OF NERVOUS DISEASES. IO5 antagonistic 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 con- traction probably consists of a series of single contractions following each other at very short intervals, due to inner- vating impulses from the cerebral cortex, which are liberated at the rate of about ten or twelve 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 muscles involved in a voluntary movement, the motion is a con- tinuous one. It is conceivable that the nice mechanism in which these simultaneous liberations of nerve force occur may be readily deranged to a slight degree by nutritional disease which is far short of being a gross structural change and that the parallelism of the inner- vating rhythm in opposed muscles would suffer slight derangement. The opposing muscles would then act, not simultaneously, but alternately, and the expres- sion of such alternation would be tremor. But the disturbance of the cortical gray matter in the brain in which motor impulses are controlled and generated is probably not the only manner in which tremor may arise. Structural changes in the nerves which con- duct voluntary impulses may damage the axis-cylinders enough to modify without destroying their conductivity and it is probable that some forms of tremor, as that of disseminated sclerosis and of neuritis, depend on such interference with conduction. The majority of tremors, however, undoubtedly depend on nutritional alterations and less commonly on structural changes in sensory in- hibiting cells in the cerebral cortex. There is good rea- son to believe — although the evidence is not conclusive I06 DISEASES OF THE NERVOUS SYSTEM. — that in paralysis agitans, dementia paralytica, hys- teria, fear, and in alcoholism the tremor is of cortical origin. Inasmuch as the pathology of tremor is still obscure its diagnostic significance is somewhat vague. Roughly speaking tremor is to be regarded as one evi- dence of nutritional derangement of functions of the sensory-motor cortex, which may or may not present gross structural changes. More cannot be said. In order to determine the location of the lesion and whether the change is simply one of nutrition and not one of gross structural change, the conditions associated with the tremor must be interrogated. Not infrequently these points cannot be decided. Myographic tracings of vari- ous forms of tremors are shown in Fig. 63. Fibrillation. — Fibrillary twitchings or fibrillations are involuntary contractions of small numbers of muscle- fibres. As they give rise to no movements of the parts in which they occur, they are recognized only when occurring in muscle-fibres which lie just beneath the skin. The contraction appears as a small wave-like elevation running rapidly along the muscle in which it occurs. It may be confined to a part of one muscle or may be seen in all the muscles of an extremity. It is chiefly met with in the extremities, face, and tongue. The contractions may be almost constant or may be separated by considerable intervals. It is often easy to produce them at will by cooling or tapping the skin over the muscles. In those conditions giving rise to fibrilla- tion the mechanical irritability of the muscle-fibres is increased. Fibrillary tremors occur under two dis- tinctly different clinical 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. lO/ FIG. 63. Myographic tracing of various forms of tremor taken directly from the moving parts. Reduced to one half, i, tremor after hemiplegia, very fine, rather irreg- ular ; 2-6, paralysis agitans — 2 and 3, very fine tremor, 4, 5, 6, coarse tremor ; 7, insular sclerosis, very irregular in range, although in time ; 8, general paralysis of the insane ; 9, hysterical tremor. (Gowers. ) lo8 DISEASES OF THE NERVOUS SYSTEM. persons who are free from organic disease and after excessive exercise or excessive venery. Under these circumstances the contractions 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 fibril- lary twitchings in the atrophied muscles. For example, primary muscular atrophy and degenerative neuritis are common causes of fibrillation. It ceases in polio-myelitis when the atrophic muscle-fibres are extensively atro- phied; it therefore does not last long in acute lesions. In progressive muscular atrophy it is especially frequent and persists through a long period of time as the process of atrophy is a slow one. The fibrillation is usually fre- quent and persistent and is always localized in the wasted muscle. Fibrillary twitchings are of course not pathognomic of chronic muscular atrophy, as has been held, nor are they an absolutely constant accompaniment of this disease. Fibrillation may occur in atrophic diseases before the muscles give any appreciable evidence of wasting. Certain drugs, as aconitia, physostigmine, and pilo- carpine, may cause fibrillary twitchings, probably by irritating the motor-end plates in the muscles. Fibrillation is generally due to irritation or destruction of nerve-endings or of the trophic centres of the cord in the anterior-horn cells. Fibrillary twitchings seldom or never occur in the pure types in muscular distrophies. 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. IO9 the tonic convulsive seizures of epilepsy and hysteria, and is seen widely distributed in tetanus. These par- ticular 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 differ- ent diseases of the nervous system that some explanation 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 lower segment. The increased muscle tone giving rise to rigidity is called hypertonicity. The rigidity of menin- gitis is an example of its occurrence from irritation of the upper part of the motor path in the cortex. Menin- geal irritation is, however, capable of diminishing the tonus of muscles (hypotonus) instead of increasing it. Rigidity is then, of course, absent; the muscles may, indeed, be quite flaccid. The rigidity which occurs subsequent to lesions of the internal capsule (commonly hemorrhage or secondary softening) 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 in any part of the pyramidal tract below the capsule. 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 appears within a few days of the onset and lasts two or three weeks it is spoken of as early rigidity. Usually the 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 irritation — initial rigidity no DISEASES OF THE NERVOUS SYSTEM. resulting from the mechanical irritation and shock of motor fibres by the lesion that interrupts their conti- nuity, early rigidity from the inflammation which often follows. Lesions which may produce irritation and therefore rigidity in the pyramidal tracts of the cord are rather uncommon. External cord lesions however are common (meningitis, compression paraplegia from tumors) and rigidity is a frequent accompaniment of such affections. But there is an influence other than irritation which is a common cause of rigidity. The normal lone of muscles depends on the integrity of the ganglion-cells of the anterior horns with which they are connected. Destruction of these cells results not only in paralysis of the 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 prevent 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 effectu- ally interrupts the inhibition from the higher centres, and hence it is that we find rigidity in the many types of disease 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. Ill permanent. A similar secondary degeneration may re- sult from interruption of the fibres in the pons, medulla, or cord, from hemorrhage, softening, or inflammation. 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 condi- tion 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 extensively altered as to lose their control of the muscle tonus, no degree of de- generative change in the lateral tracts is capable of re- storing or increasing the muscular tone. Hence it is that we have a tonic type of chronic muscular atrophy. (See p. 450.) In general, we may say that rigidity is due to irritation of motor structures in acute processes, and to deficient control of the reflex mechanism which subserves muscu- lar 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 contracture. 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 co7itracture is applied to the shortening of a muscle or group of muscles from active contraction of the muscular fibres, and not from struc- tural changes in these fibres. The contracture may last for a few minutes or for years. Good examples of 112 DISEASES OF THE NERVOUS SYSTEM. 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 temporarily 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 con- traction cannot be reduced by extension. Contraction of a muscle from structural changes is always preceded by a period o. active contracture in which connective- tissue alterations have not yet occurred. The causes of contraction are: a. The unequal paralysis of antagonistic muscles. The stronger muscles assert themselves and give rise to serious deformity of the limb, though there is no spasm. This is often seen in poliomyelitis. 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 periph- eral origin. By far the most common cerebral cause of contracture is hemiplegia. The contracture is pro- duced by the late rigidity already mentioned. In the upper extremity the position which results from the con- tracture is one in which there is flexion of the elbow and SYMPTOMATOLOGY OF NERVOUS DISEASES. II3 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 because 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 an- tagonistic 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. 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 anticus and peronei suffer most fre- quently and there is a resulting contracture of the calf muscles, which are either unparalyzed 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- 114 DISEASES OF THE NERVOUS SYSTEM. rence in organic disease of the nervous system. It is practically confined to major hysteria and to the kata- tonic stupor of dementia precox. Trance, lethargy, tetanic rigidity, and cerea flexibilitas are all states of the same general condition. Catalepsy may be defined as a state of general or local muscular rigidity as- sociated with a state of perverted consciousness. It may occur spontaneously in disease or it may be in- FIG. 64. A case of catalepsy (Dana), duced in a state of hypnotism. It has been noted in brain abscess, tumor, hemorrhage, softening, and men- ingitis, but only when consciousness has been much im- paired. Its practical diagnostic significance at present is confined to hysteria and the adolescent insanities. In the absence of hysterical stigma and the presence or a history of stupor, negativism, automatism, excitement alternating with depression, stereotypy, verbigeration, etc., it points to pronounced mental disease. In the latter SYMPTOMATOLOGY OF NERVOUS DISEASES. II5 disease the origin of the katatonic stupor is commonly rapid with partial or complete obscuration of conscious- ness. The features grow expressionless, the respiratory- movements and heart action are depressed. The volun- tary impulses seem to be overcome by counter impulses. An act may be begun but almost immediately is checked by a counter impulse which produces an act contrary to the one desired. Athetosis and Athetoid Movements. — The word athetosis (meaning,- "without form") 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 move- ments usually involve the hand and foot, sometimes also the face, but they are always most marked in the hand. In distribution the movements may be either strictly confined to one side of the body, or rarely 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- 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-hemiplegic 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 re- mains absolute, but develop with the return of volun- tary power, usually some months after the onset of the Examples of the position of the fingers in the movements of athetosis (personal observation). (Strumpell.) SYMPTOMATOLOGY OF NERVOUS DISEASES. II7 paralysis. There is commonly associated with these spas- modic 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 inconsiderable. 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 at- tack, 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 recovered 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 pri- mary athetosis may be exceedingly difficult or impossible. Hence it is not difficult to understand that from time to time cases of 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 infan- tile hemiplegia often reveals traces of an old hemiplegia which ten years 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 Il8 DISEASES OF THE NERVOUS SYSTEM. but quick, and they may then bear some resemblance to chorea. On the strength of this occasional resemblance these athetoid movements have been described as post- hemiplegic chorea, or choreatic paresis — an objectionable term, because the condition has nothing to do with the 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 suc- ceed cerebral hemorrhage or softening from any cause. In general, the movements are more likely to follow cerebral softening than hemorrhage. As regards the position of the lesion which underlies these athetoid movements or choreatic paresis, no accurate generaliza- tion can yet be made. Frequently the motor cortex has been the seat of disease, and it has been shown that dis- ease in this situation is by itself competent 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. Any slight diffuse lesion of the motor path of the brain during development may give origin to the symptom. Associated Movements. — When a voluntary move- ment of one group of muscles is accompanied by an in- voluntary contraction of muscles in another part of the body this is termed an associated movement. Associated movements are met with generally as the result of hemi- plegia, particularly the hemiplegia of infancy. Usually the movements are confined to the upper extremity, the fingers of the paralyzed side undergoing involuntary movement, of limited range, during the voluntary activ- SYMPTOMATOLOGY OF NERVOUS DISEASES, II9 • ity of the other arm. Sometimes these movemerrts are associated only with extensive movements 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 pulling the strap in a car, requires the elevation of the arm above the head. More commonly the associated move- ments 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. As- sociated movements have a significance similar to that of athetoid movements. Their explanation is doubtless to be found in the connection of the subsidiary centres through which they are produced. They possess little diagnostic importance. Inco-ordination. — During an ordinary muscular movement there occurs not only an accurately propor- tioned contraction of the various muscles which produce the movement, but a less powerful contraction of an- tagonistic muscles. This adjustment of opposed muscles makes the movement which results from their 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 defects of co-ordination the term ataxia should include; whether it should be applied to all forms of inco-ordina- tion, 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 I20 DISEASES OF THE NERVOUS SYSTEM. execution of particular acts and in which an effort to correct the defect only serves to increase it. We shall employ the term in this restricted sense. 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 de- fective equilibration. According to the position of the lesion in the nervous system it is customary to distinguish several varieties of ataxia. Thus there are described a cortical ataxia, a cere- bellar ataxia, a bulbar ataxia, a spinal ataxia, and an ataxia from peripheral nerve disease. Probably all are cortical in their primary origin. Some of these regional forms, however, are not ataxias, strictly speaking, and we shall therefore speak of them as varieties of inco- ordination, specifying which are true ataxias. Cortical Inco-ordination. — Inco-ordination of movement from cortical lesions is usually associated with paralysis of the same distribution. The inco-ordination which is observed in athetoid movements (so-called post-hemi- plegic chorea) has been mentioned. In cases of infantile hemiplegia, however, inco-ordination may be developed only during voluntary movement and be of a jerky, oscil- latory 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-ordination as an active tremor or as a true ataxia. The same difficulty is met in the inco- ordination of dementia paralytica, which is sometimes truly ataxic, but more generally consists of movements of narrow range which are more properly designated tremor. The disturbances of co-ordination which occur in SYMPTOxMATOLOGY OF NERVOUS DISEASES. 121 hysteria are probably of cortical origin. They may exist alone or be accompanied with loss of power or anaesthe- sia. It is doubtful whether the movements are ever those of true ataxia. In one form movements are well controlled and regular while the eyes are directing them, but when the visual control is withdrawn they become grossly irregular. In other cases there is good co- ordination while the patient lies in the horizontal posi- tion, 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 term " astasia " is sometimes used to designate the unsteadiness in stand- ing, with or without visual guidance, that is seen in some cases of hysteria. The word " abasia " is used to designate the unsteadiness in walking, which often does not amount to inco-ordination, seen in the same class of cases. 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. Why ataxia sometimes occurs in cortical disease but more frequently does not occur, it is impossible at pre- sent 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 cu- taneous sensibility which the lesion produces. The inco-ordination seen in alcoholic and other forms of intoxication is probably in part cortical. Cerebellar Inco-ordination {^cerebellar titubatiori) . — This form of motor disturbance consists in an inability to 122 , DISEASES OF THE NERVOUS SYSTEM. maintain the erect position or to walk straight, in conse- quence 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 aie 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 difficulty in moving the lower extremities as desired. The disorder is chiefly one of defective equilibration 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 gener- ally due to damage of the middle lobe of the cerebellum, sometimes to disease in it, sometimes to pressure upon it from disease of one of the cerebellar hemispheres. Dis- ease of the cerebellar hemispheres is/ 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 156 DISEASES OF THE NERVOUS SYSTEM. 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 157 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- 158 DISEASES OF THE NERVOUS SYSTEM. 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, hemianaesthesia, crossed amblyopia, loss of taste, etc. In attaching significance to the presence SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 59 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 Olfactory Hyperesthesia 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 Hallucinations. — 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 aurse. 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, theformer 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. l6o DISEASES OF THE NERVOUS SYSTEM. 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. Hemiansesthesia 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. In hysterical amblyopia, which is almost always unilateral, vision may amount to complete blindness. The fields are contracted concentrically, and since the retina exhausts rapidly, the limitation may be more marked with each succeeding test at the one examination. A functional - amblyopia affecting both eyes, as in organic crossed amblyopia, and associated with hemianaesthesia, is sometimes 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. l6l 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 ambly- opia, and that such an affection must be excluded before we can attribute the visual defect to disease of the optic nerve. Defective Central Vision sometim'es results from ir- regular patches (scotomata) of retinal anaesthesia 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 l62 DISEASES OF THE NERVOUS SYSTEM. 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- 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). It may also occur in malaria, which disappears on exhibiting full doses of quinine. Oddly enough, a similar defect also occurs in poisoning by quinine. Lead occasionally produces similar results. There are usually no ophthalmoscopic 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 163 Hemianopsia.^ — Hemianopsia is loss of vision in one lateral or vertical half of the visual field. It almost 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 Hemianopsia^ 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. ' 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 right hemianopsia, and, conversely, a right hemiopia to a left hemianopsia. The word hemianopia is used synonymously with hemi- anopsia. Lateral hemianopsia is also known as homonymous hemianopsia. 164 DISEASES OF THE NERVOUS SYSTEM. B. — Nasal Hemianopsia. — Obscuration 01 the nasal half of each field from anaesthesia of the temporal half of each retina is not only the rarest form of hemianopsia 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 y or Ho7no7iymous 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 165 lesion causing the hemianopsia, but on individual pecu- liarities in the decussation in the optic nerves. Certain 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 50), which is supposed to lie in and beneath the inferior parietal lobe. In about one ha-lf 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 ; m 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 l66 DISEASES OF THE NERVOUS SYSTEM. FIG. 68. 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 rise to 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 167 involves the right-half fields in one attack, and the left- 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 — w^hen 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. Muscse volitantes, 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 l68 DISEASES OF THE NERVOUS SYSTEM. Other neurosis, except in rare cases of epilepsy. It usually lasts many minutes. Sparks, flashes of light, colors before the eyes, and other irritative symptoms related to the visual apparatus occur in migraine, and also in epilepsy. In epilepsy a visual aura is not un- common ; 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 ; usually 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 iji 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 169 In optic Neuritis the optic nerve may be inflamed throughout 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-bulbar 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. 605^) the disc has a distinctly striated appearance, the striae 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 maybe 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 170 DISEASES OF THE NERVOUS SYSTEM. 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. I/I different intracranial processes. Of these causes tumoi 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 neu ritis 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 1/2 DISEASES OF THE NERVOUS SYSTEM. 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 anaemia, 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 optic 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 173 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- tion of these cases the atrophy is complete ; in a consid- 174 DISEASES OF THE NERVOUS SYSTEM. erable 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 papillilic 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 175 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 the 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. 176 DISEASES OF THE NERVOUS SYSTEM. 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 Ophthalmoscopic 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 with 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 albuminuria, leucocythaemia, purpura, etc. Occasionally small hemorrhages are found in the SYMPTOMATOLOGY OF NERVOUS DISEASES. J// 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. 67), 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 sound through the cranial bones d.^ 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. 1/8 DISEASES OF THE NERVOUS SYSTEM. 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 Tio\. 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 1/9 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 Aurium 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 wand 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 l8o DISEASES OF THE NERVOUS SYSTEM. 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, SYMPTOMATOLOGY OF NERVOUS DISEASES. l8l 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- l82 DISEASES OF THE NERVOUS SYSTEM. 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 gastric 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 582. 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, SYMPTOMATOLOGY OF NERVOUS DISEASES. 183 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. 61). 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 aurae 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 oi the exact character of this influence and of the conditions l84 DISEASES OF THE NERVOUS SYSTEM. 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. There are no special trophic nerve-fibres. The situation of the trophic centres is also obscure, but it is probable that the posterior root-ganglia are in some way related to the nutrition of the skin. One form of eruption is unquestionably dependent on SYMPTOMATOLOGY OF NERVOUS DISEASES. 185 a nervous lesion : the eruption of herpes zoster. There is reason to believe this affection to be dependent on an inflammatory process involving one or more in- tervertebral ganglia, a nerve-trunk or its terminal nerve- filaments. 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- organismic infection, which is rendered possible by the anaesthesia that exists in these cases. Probably in ad- dition to the anaesthesia, 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 anaesthesia 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- I86 DISEASES OF THE NERVOUS SYSTEM. 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. 44). Brittleness of the bones {fragilitas ossium) lead- ing to fracture from slight injuries, so-called "spon- taneous " fracture, is occasionally observed in dementia paralytica, amyotrophic 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, loUowed by destructive disease ot the articulation itself, — erosion of the cartilage, atrophy of the heads SYxMPTOMATOLOGY OF NERVOUS DISEASES. 187 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 flat {" 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 wasting of muscular tissue (progressive muscular atrophy). In an important group of cases of muscular atrophy of gradual development, in which no constant changes in the spinal-cord or periph- eral nerves have yet been detected, and which are looked upon as myopathic in origin (progressive muscu- lar dystrophies — idiopathic muscular atrophy), a high de- gree of muscular wasting is frequently observed. These cases constitute the only exception to the rule that a high l88 DISEASES OF THE NERVOUS SYSTEM. grade of muscular 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 considerabl'^, 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 which 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 cortex and subjacent white substance, are followed not by late but by early atrophy — atrophy which reaches its height SYMPTOMATOLOGY OF NERVOUS DISEASES. 189 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. Usually the degree of wasting is inconsiderable. Both late and early atrophies are probably dependent, in a measure, on secondary de- generation of the pyramidal tracts, which, when due to irritative processes, seems to exert a detrimental influ- ence on the nutrition of the ganglion-cells of the anterior horns and through these on the muscles. In rare in- stances hypertrophy of paralyzed parts may occur, which is, as yet, without satisfactory explanation. In disease of 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 190 DISEASES OF THE NERVOUS SYSTEM. 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, both the true and false type, occurs in Thomsen's disease, and in .the healthy leg, in some old cases of poliomyelitis, as a result of in- creased activity, and in rare cases of infantile cerebral hemiplegia with athetosis and without. 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 ^ 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. I9I is observed in diseases of the nervous system which im- 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 muscle 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 192 DISEASES OF THE NERVOUS SYSTEM. health, but is ' tardy, wave-like, and often imperfect. Thirdly, theref 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 former. 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. I93 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. 13 194 DISEASES OF THE NERVOUS SYSTEM. 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 there 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 ot the muscles may remain unchanged for several days after the onset of the lesion, or may fall slightly. Then oceans 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 195 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. Power of voluntary con- traction is -^iever entirely lost, and the loss which occurs 196 DISEASES OF THE NERVOUS SYSTEM. WEEKS 1 3 •0 do JO /oo ! —1 /" "^»^_ -Jbi? »" 'Hal *"'*"*^'»^ • "■--, iL.W Li > OH UJ -z. ■^^ -— --UfiTibiA,.., Line POWER NO ^E IN NT ^0N£ DAYS \S 30 ro too -I o 3 Si nVSinK •■««;, '••^..- X .^' ...-• UJ > Of ^•X ..•bAtiupi. POWER NONE NONE SklC-tiT KiDKMkBas FMi^ fONSi £:f\ABl-£ B FIG. 69. Fig. A shows type of electrical reactions in a case of severe and permanent damage to a nerve. The broken lines cf — 1^ 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 o' each chart show the state of electrical irritability in the ?nuscle : 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 197 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. 198 DISEASES OF THE NERVOUS SYSTEM. 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. Dmiinished 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 1 99 (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 200 DISEASES OF THE NERVOUS SYSTEM. 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 J 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. OEdema is not uncommon in the early- stages of acute processes, but may also accompany disease of exceedingly slow 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- SYMPTOMATOLOGY OF NERVOUS DISEASES. 201 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 " iache chebrale^'' or better, dermographism, in which slight cutaneous irritation 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 defective innervation of the local ganglia in their walls. It is not diagnostic of men- ingitis, 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 Consciousness is one of the most significant and frequent symptoms of organic disease of the brain, but since it is also a symptom of many conditions that do not depend 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 202 DISEASES OF THE NERVOUS SYSTEM. to rouse temporarily 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 sphincter 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- SYMPTOMATOLOGY OF NERVOUS DISEASES. 203 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 acute 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. 204 DISEASES OF THE NERVOUS SYSTEM. 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, arid 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 are the condition of the reflexes, the unequal move- ments of the superior intercostals on the two sides, and the presence of Babinski's sign. 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- SYMPTOMATOLOGY OF NERVOUS DISEASES, 205 sciousness is probably due to functional disease of the 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 at most, even after a series of seizures); the patient can be easily roused ; one-sided symptoms are absent, except in hemiplegic (old) epilepsy ; the temper- ature is normal or slightly elevated, and the loss of consciousness is followed by temporary headache and often by a confused state of mind. An epileptic also usually bears physical stigma of his disease — bromic acne, bruises, etc. 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 so; its presence has not much significance, except in per- sons under thirty-five years of age. Repeated convulsions occurring 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 206 DISEASES OF THE NERVOUS SYSTEM. ursemic oriofin of the coma. Continuous subnormal tem- perature favors uraemia. If there is a history of sudden complete blindness before the coma this makes its uraemia 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 20/ often this muttering speech is almost continuous. He lies quietly in bed or exhibits only slight restlessness. In " 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 208 DISEASES OF THE NERVOUS SYSTEM. before a conclusion is reached. The occurrence of 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 apparent rather than real. ,SYMPTOMATOLOGY OF NERVOUS DISEASES. 209 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. 14 2IO DISEASES OF THE NERVOUS SYSTEM. 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 211 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 t. 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 f 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- ulation 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- 212 DISEASES OF THE NERVOUS SYSTEM. acter, and the leading forms of speech defects, motor 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- SYMPTOMATOLOGY OF NERVOUS DISEASES. 213 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. 2 14 DISEASES OF THE NERVOUS SYSTEM. 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 been termed ataxic aphasia^ 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 21 5 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. 57), 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 2l6 DISEASES OF THE NERVOUS SYSTEM. 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- Deaf 7iess 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 217 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 2l8 DISEASES OF THE NERVOUS SYSTEM. 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. 50). Probably permanent mind-blindness is due to bilateral involvement of these areas. Some- times hemianopsia is associated with mind-blindness. Mind- Deaf tiess 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 unde r standingly ^ 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 SYMPTOMATOLOGY OF NERVOUS DISEASES. 219 symbols is absolute, and the motor speech processes are 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 220 DISEASES OF THE NERVOUS SYSTEM. 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, m 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. SYMPTOMATOLOGY OF NERVOUS DISEASES. 221 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 cau^. 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 of the medulla. 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 222 DISEASES OF THE NERVOUS SYSTEM. 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 ah 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, aided possibly by the accumulated and retained products of extraordinary tissue destruction, caused by the convulsions. During the " status epilepticus " ' (p. 576) the temperature may rise to io6°-io9°. There is not uncommonly a post-mortem rise in temperature in status of epilepsy, general paresis, uraemia, and in many other states terminated by a series of convulsions. 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 ^ 111 this state the paroxysms recur at short intervals for a consider- able time (often many hours or days). SYMPTOMATOLOGY OF NERVOUS DISEASES. 223 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 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, such as tumor. Respiration is markedly influenced by organic disease of the nervous system chiefly when 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 hourSj 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 tubercular meningitis as to be rather characteristic of this disease. The paradoxical respiratory sign (page 90) is to be found in all capsular lesions of hemiplegia. 224 DISEASES OF THE NERVOUS SYSTEM. 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 periods of increasing depth of breathing, these periods being separated by a variable interval of time — 5-40 seconds) is sometimes observed toward the close of cerebral diseases (hemorrhage, meningitis, tumor, and status epilepticus). The patient is usually comatose and rarely recovers when this form of breathing has begun. Cheyne-Stokes breathing occurs in many diseases ex- ternal to the nervous system (heart disease, pneumonia, nephritis, diphtheria, etc.), and under these circum- stances is of less grave significance than when due to brain disease. Its explanation may rest upon the bi- lateral withdrawal of cerebral inhibitory influence- upon the medullary centres. 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 — SYMPTOMATOLOGY OF NERVOUS DISEASES. 22$ 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 may occasion vomiting. The situation of the lesion does not seem to exert any 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, »5 226 DISEASES OF THE NERVOUS SYSTEM. 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. 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 not common 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- SYMPTOMATOLOGY OF NERVOUS DISEASES. 22/ tary control of the functions of these viscera. Their ac- tion becomes purely reflex. As soon as a sufficient amount of urine accumu- lates in the bladder, the vis- cus is emptied by the reflex contraction of the detrusor urinae and synchronous re- laxation, also reflex, of the sphincter ; when faeces ac- cumulate in the rectum and irritate its mucous mem- brane, they are expelled by an analogous mechan- ism. The incontinence of urine is called '' intermit- tent " or "reflex inconti- nence." It is important 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 FIG. 70. 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 process, 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. 228 DISEASES OF THE NERVOUS SYSTEM. spinal-cord disease (myelitis or injury above the lumbar enlargement, lateral sclerosis, etc.). In reflex inconti- nence there is usually some weakness of the detrusor urinae after a time. Then retention occurs, and the dis- tension of the bladder leads to relaxation of the sphinc- ter and incontinence — " overflow incontinence." When the functions of the brain are in abeyance (stupor, coma) from any cause, there may be retention of urine and in- continence, 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 involuntary 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 faeces 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. Disorders of the Sexual Functions are of frequent occurrence in nervous diseases, but do not possess much diagnostic importance, and will be only briefly touched SYMPTOMATOLOGY OF NERVOUS DISEASES. 229 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 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 loss 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- 556). 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). 230 DIAGNOSIS OF THE POSITION OF THE LESION. 23I In the case of organic disease on the nervous system it is of great practical importance to locate accurately, /.y (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- 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 of 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 THE DIAGNOSIS OF CLINICAL TYPES. 387 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 monoplegic. 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. b. The knee-jerks and reflexes generally are much ex- aggerated. Usually this increase of reflex is most marked on the side paralyzed if the case be one of diplegia. 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 and perfectly than is the case when hemiplegia occurs in the adult, and the ultimate paralysis may be chiefly in the arm. /. There are no disturbances of sensibility. 2. In the cases of infantile cerebral paralysis that de- velop in children who have acquired language, transient 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 nearly all cases of infantile cerebral paralysis there is arrest or retardation of development in the limbs 388 DISEASES OF THE NERVOUS SYSTEM. paralyzed. 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 usually present.^ 4. Nearly all cases of infantile cerebral paralysis are ac- companied with some degree 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 par- alysis are followed by epilepsy. In most cases the form is that of general epilepsy (grand mal),with a local onset, but in a considerable number the attacks are partial, in- complete, or Jacksonian in type. The convulsions persist and sometimes survive all traces of the original paralysis. For clinical purposes it is desirable to distinguish three types of infantile cerebral palsy : (I.) Paralysis of intra-uterine onset ; (II.) palsy at birth ; (III.) the acquired form. (/.) hi Paralysis of hiira-uterine Onset. In paralysis of intra-uterine onset, which is of comparatively rare occurrence, the morbid lesion usually is parencephaly with large areas of cortical destruction, defective devel- opment of the pyramidal tract, and imperfect develop- ment of those parts of the brain subserving the higher mental processes. 1 In rare instances hypertrophy of paralyzed parts occurs owing to athetosis and other morbid movements. THE DIAGNOSIS OF CLINICAL TYPES. 389 (//.) The Congenital Form of Infantile Cerebral Palsy {Cerebral Birth-Palsy^ Infantile Meningeal Hemorrhage). — The congenital form of infantile cerebral palsy FIG. 78. Cerebral diplegia (" crossed-leg progression"). (cerebral birth-palsy, infantile meningeal hemorrhage). This form of infantile cerebral palsy depends on menin- geal hemorrhage over one or both sides of the convexity 390 DISEASES OF THE NERVOUS SYSTEM. of the brain or on its base, the result of injury during birth. This acute lesion is followed by chronic inflam- Fio. 79. Infantile cerebral hemiplegia. mation of the cerebral cortex and its membranes, finally ending in diffuse or lobar sclerosis, cystic degeneration. THE DIAGNOSIS OF CLINICAL TYPES. 39I and partial atrophy of the affected parts. In about two thirds of the cases the paralysis is of the hemiplegic form ; in one third it is diplegic. The facts that indicate the existence of the congenital form of palsy are: (i) A history of hemiplegia or diplegia only exception- ally without convulsions dating 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 distinct onset after birth. (2) There is a history of some distinct difficulty in birth, either an unnatural presentation or more fre- quently prolonged and difficult labor with head presenta- tion in primipara. Comparatively few instances can be attributed to forceps delivery alone. Precipitate de- livery produces compression of the head similar to that occurring in prolonged labor. The symptoms in these cases are those already enumerated : Partial paralysis, hemiplegia or diplegia with rigidity and contractures, arrested development, increased reflexes, post-hemiplegic movements, mental impairment, and frequently epileptic seizures. There is nothing distinctive about these symptoms or their combi- nations, 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 after birth The deep reflexes on the paralyzed side, which are all abolished for a time after the stroke, are regained in a day or two and remain permanently exaggerated. The skin reflexes, on the other hand, are always abolished on the hemiplegic side. Dorsi flexion of the great toe always occurs on the paralyzed side when the sole of 392 DISEASES OF THE NERVOUS SYSTEM. the foot is stroked. The temperature of the hemiplegic parts is about a degree less than on the sound side. More or less marked aphasia occurs in lesions of the left hemisphere in right-handed individuals and in the right hemisphere in the left-handed. {III.) The Acquired Form of Infantile Cerebral Palsy (Acute Cerebral Infantile Palsy, Infantile Hemiplegia). There is considerable difference of opinion as to the pathological process which underlies the acquired form of infantile cerebral palsy and it is certain that this is not the same in all cases. The following morbid pro- cesses have been found to underlie the condition : Meningeal hemorrhage (most frequent); thrombosis of superficial cortical veins from syphilitic endarteritis and from atheroma; hemorrhage, especially into the cortex, or pia, or subarachnoid space ; cerebral embolism. ; and last but not least, an inflammatory process known as pol- ioencephalitis, involving the motor cortical ganglion cells and supposed to be analogous to the process in the spinal cord known as poliomyelitis. There are good reasons to think that each of these processes may at times be effective in causing infantile hemiplegia, but in the case of thrombosis of cortical veins and particularly of polio- encephalitis this supposition is as yet based chiefly on theoretical considerations. The terminal states of the processes just enumerated are the same as those in the congenital form. Aside from a slight temporary awk- wardness in its use the tongue itself is rarely paralyzed. 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 DIAGNOSIS OF CLINICAL TYPES. 393 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, 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 ^ Very extensive subarachnoid hemorrhage is sometimes seen in the cases that develop during pneumonia. * 394 DISEASES OF THE NERVOUS SYSTEM. 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 so-called paraplegia form of infantile cerebral paralysis the palsy may possibly be confounded with that from disease of the spinal cord. Close examination, however, shows, that there is usually some motor de- rangement in the upper extremites in the former cases. It is important also to note that the chronic spastic paraplegia that results from spinal-cord disease is ex- ceedingly rare in young children. If vertebral caries be excluded, such paraplegia 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 fourth^ of all the cases there is present a THE DIAGNOSIS OF CLINICAL TYPES. 395 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^ and Babinski's sign. 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 ^ 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 where there is very slight motor paralysis. 396 DISEASES OF THE NERVOUS SYSTEM. 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 {vide ante) 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). THE DIAGNOSIS OF CLINICAL TYPES. 397 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 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 progressive 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- 398 DISEASES OF THE NERVOUS SYSTEM. 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 ante), 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 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). ' 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 with syphilis. THE DIAGNOSIS OF CLINICAL TYPES. 399 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 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. 400 DISEASES OF THE NERVOUS SYSTEM. A carcinoma 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 ante) of acute cerebral soften- ing. Cerebral tumor is distinguished from the members of this group of vascular lesions, by the simple but im- 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. THE DIAGNOSIS OF CLINICAL TYPES. 40I Diagnosis behveen 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 points 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 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 402 DISEASES OF THE NERVOUS SYSTEM. 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 anaesthesia or hemian- aesthesia. 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 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 THE DIAGNOSIS OF CLINICAL TYPES. 403 general convulsions constitute a conspicuous symptom. The convulsions of tumor usually have a local com- mencement 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- 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 404 DISEASES OF THE NERVOUS SYSTEM. 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 justified, 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 : 1. 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 (d) 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 embolism. 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 THE DIAGNOSIS OF CLINICAL TYPES. 405 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 as they comprise two-thirds of all cases of intracranial aneurism: 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 and usually in the frequency of the order named, only rarely the 3d or 12th. There may be severe occipital headache. There may be crossed paralysis. There are no symptoms in about one-third of all cases. Con- vulsions 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, which usually happens in one-half the cases. Such a rupture gives rise to the symptoms of severe apoplexy. If there have been no symptoms to suggest aneurism 406 DISEASES OF THE NERVOUS SYSTEM. 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 endocarditis 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 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. THE DIAGNOSIS OF CLINICAL TYPES. 407 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 the 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 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- ^ Chronic progressive ophthalmoplegia is so commonly caused by nuclear disease that the term is used synonymously with nuclear disease. 408 DISEASES OF THE NERVOUS SYSTEM. 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 association 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 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 THE DIAGNOSIS OF CLINICAL TYPES. 409 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. 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 (. Erb's Form of Pro- gressive Muscular Dystrophy. )- E. The Landouzy-Deje- rine Type of Pro- gressive Muscular Dystrophy. Progressive Muscular Atrophy (Chronic Spinal Muscular Atrophy, Wasting Palsy, Amyotrophic Lateral Sclerosis, Chronic Poliomyelitis). — The distinctive clin- ical feature of progressive muscular atrophy is the slow and usually extreme wasting of certain groups of muscles. The pathological basis of the disease consists of a grad- ual degeneration of the ganglion-cells of the anterior horns of the cord, at a level of the cord corresponding to the muscles wasted, and of a like degenerative process in the anterior root-fibres with which these cells are con- nected. In association with these lesions in the ganglion- cells and their prolongations the root-fibres, there is usually a degeneration of the direct and crossed pyra- midal tracts of the cord — a degeneration which may be traceable a considerable distance along the motor path in the brain. Like the other degenerative diseases of the spinal cord that have been described, progressive muscular atrophy fails to conform to any rigid type in its symptoms. On THE DIAGNOSIS OF CLINICAL TYPES. 471 the otber hand, it resembles these diseases in having a symptomatology that varies within considerable limits. Now in order to comprehend the meaning of these variations in type it is essential to bear in mind certain variations in the lesions which will be mentioned in the description of the symptomatology of the disease. As already stated, the striking clinical feature of pro- gressive muscular atrophy is slow muscular atrophy. This FIG; 50. Atrophy and paralysis with main en griffe in chronic anterior poliomyelitis. (Starrs.) muscular atrophy commences in the arms in about nine tenths of all the cases (Aran-Duchenne type). In the majority of the cases beginning in the arm the atrophy commences in the muscles of the hand, but a considerable number commence in the muscles of the shoulder. Of the hand muscles those of the thenar and hypothenar eminences (thumb and little finger) are usually the first to suffer, but the interossei and especially \.h.Q first dorsal 472 DISEASES OF THE NERVOUS SYSTEM. interosseus (abductor indicis) usually suffer very early. This commencement of the atrophy in the small muscles of the hand and interossei is so common as to be a charac- teristic feature of the disease. The atrophy generally begins on one side and does FIG. 51. Atrophy of the muscles about the shoulder-blades and arms in a case of chronic anterior poliomyelitis. The triceps and latissimus dorsi have escaped. (Starrs.) not appear on the other until some time (often a year) -has passed. When the atrophy commences in the shoul- der the deltoid generally suffers first, but whether hand or shoulder first shows the wasting it soon extends to other parts of the limb. Thus both the flexors and ex- tensors of the wrist, the supinators, the biceps, and triceps THE DIAGNOSIS OF CLINICAL TYPES. 473 may In time become one or all involved. Often the various muscle groups are unequally atrophied. Usually after a time the muscles of the back, especially the trapezii, suffer. A peculiarity of the trapezius atrophy is that its upper part {ultimum moriens) often remains intact when the rest is much wasted. The sterno-mastoid also is often involved. The respiratory muscles may suffer early or late, and thus threaten life. Both inter- costals and diaphragm may be affected. In exceptional cases the atrophy commences, not in the upper extremity, but in the legs. There is good reason to think that the lesion that underlies these cases that com?ncnce in the leg is of the same nature as that which underlies the cases that begin in the upper extremity, but as there is no direct proof of this, this class of cases is considered elsewhere {vide Peroneal Type). Although it is exceptional to meet with cases in which the atrophy commences in the leg, it is not very unusual for cases commencing in the arm to show slight wasting of the legs after a long lapse of time. The face is rarely involved in the atrophy, but the lips may be wasted owing to the not infrequent complication of progressive muscular atrophy with bulbar paralysis. The muscles that undergo atrophy gradually fail in power. This loss of power is in a general way proportioned to the degree of the wasting^ to which it is usually due. There is an important exception to this general rule. It is that the legs may gradually lose power where there is no wasting, or such slight wasting that the loss cannot be due to this. The paralysis that accompanies wasting depends, like the wasting, on dis- ease of the ganglion-cells of the anterior horns ; the paralysis that occurs without wasting, or is greatly in excess of it, depends on degeneration of the pyramidal tracts of the cord. In addition to the atrophy and weakness that 474 DISEASES OF THE NERVOUS SYSTEM. occur in progressive muscular atrophy there are the fol- lowing important conditions: a. Fibrillary Contractions of the atrophied muscles. This is so frequent a symptom in progressive muscular atrophy as to be characteristic when present, but it is not of invariable occurrence. There is also increased mechanical irritability. b. Changed Electrical reactions. When the w^asting is slow there is usually simple diminution of irritability to faradism and galvanism. When the wasting is rapid the faradic loss may be out of proportion to the galvanic loss, and there may even be partial or complete RD in certain muscles. c. Changes in Reflex Action. As a rule, there is loss of myotatic irritability in the atrophied muscles. The knee- jerk is lost as soon as there is even slight wasting of the anterior thigh group, in those cases where the leg is affected. When the legs are paralyzed without wasting (that is, from degeneration of the pyramidal tracts), the knee-jerks are exaggerated and there is clonus. There may, indeed, be true rigidity, and the leg symptoms may thus resemble closely those of spastic paraplegia. d. Changes in the Tone of the Muscles. The atrophied muscles are ordinarily flaccid and without tone ; they are in a state of " atonic atrophy." Occasionally the muscles are in a state of rigidity from the first, /. ^., they are in a state of " tonic atrophy." Beside the symptoms of progressive muscular atrophy that have been enumerated there may occur others of minor importance. Thus, an early symptom is aching pain in the parts that become atrophied, and later there may be numbness in the parts, but there is never any true anaesthesia. The unequal paralysis of antagonistic muscles may lead to various deformities ; in the hand the bird- THE DIAGNOSIS OF CLINICAL TYPES. 475 claw hand {vide ulnar paralysis) is apt to occur. Sexual power is frequently lost. The sphincters are unaffected. Some of the variations in the symptomatology of progres- sive muscular atrophy have been briefly stated (variations in reflex state, m.uscle tonus, and degree of wasting). It remains to be indicated how these variations form the basis of certain clinical types. We may regard as typical forms of progressive mus- cular atrophy those cases in which there is considerable atrophy of the atonic sort in the upper extremity and upper part of the trunk, combined with weakness and rigidity, without atrophy or with very slight atrophy^ in the legs. The atonic atrophy in the upper part of the body depends on the degenerative changes, already mentioned, in the ganglion-cells of the anterior horns. The weakness and spasm in the legs (with increased knee-jerk and clo- nus ) depend, on the other hand, upon degeneration of the pyramidal tract i^vide symptoms, Rigidity or Spasm), and on those fibres of the tract that pass to the leg centres. For, although the pyramidal tract may be degenerated throughout its entire extent, the degeneration of those fibres that go to the arm-centres of the cord does not cause overaction in the arm muscles. This is because the ganglion-cells of the anterior cornua of the cervical cord are so extensively degenerated that no degree of degeneration of the pyramidal tract can cause the arm muscles they innervate to overact. Were these ganglion- cells less degenerated, or were some of them intact and others degenerated, the case would be different. The degenerated pyramidal tract would in this case cause overaction in the cervical ganglion-cells, with resulting rigidity of the upper arm and upper trunk muscles. This is precisely what happens in some cases— namely, the cases of progressive muscular atrophy in which there is 476 DISEASES OF THE NERVOUS SYSTEM. tonic atrophy (often slight) in the arms, and simply weakness and spasm, or spasm and weakness with mod- erate atrophy, in the legs. It is instructive to picture still another pathological variation in the same direction. Cases occur in which the degeneration of the pyramidal tracts forms the chief lesion, and in which the degeneration of the cervical ganglion-cells is very slight indeed. These cases are closely allied to a condition that has been already de- scribed, viz., spastic paraplegia — in fact, they differ from it clinically merely in the slight atrophy of certain mus- cles of the upper extremity. Finally, another variation, opposed in character to the last, must be noted. Cases occur in which the ganglion- cells of the cervical and lumbar cord are all so exten- sively degenerated that notwithstanding the presence of degeneration of the pyramidal tracts, there is no rigidity or spasm in the lower extremities. There is, in such cases, what may be called universal atonic atrophy — the arms and legs are atrophied (often extensively), flaccid, and have lost their myotatic irritability. Enough has been said to show that in progressive muscular atrophy there are extensive variations in type, based on corresponding variations in pathological anat- omy. There is, indeed, every conceivable gradation in the combination of spasm, atrophy, weakness, and myo- tatic increase, between widespread tonic atrophy, verging on pure spastic paraplegia, on the one hand, and on uni- versal atonic atrophy on the other. The forms of progressive muscular atrophy in which spasm is marked have been designated amyotrophic lateral sclerosis, and have been considered pathologi- cally distinct from the atonic forms. This view is untenable, since lateral sclerosis is present, as we have THE DIAGNOSIS OF CLINICAL TYPES. 477 seen, even in cases that present no spasm or myotatic excess; the effect of the laterg,! sclerosis, in producing overaction in the anterior cornual cells, being rendered inoperative by the degeneration of those cells. It is, therefore, more in accord with the facts of pathology to regard all cases coming under the designation amy- otrophic lateral sclerosis as varieties of one varying pathological state, than to attempt their establishment as a distinct condition. Progressive muscular atrophy has been attributed to a large variety of different conditions, but none of these bear a sufficiently distinctive relation to the disease to aid us materially in diagnosis [^vide p. 289). Two etiological facts, however, it is well to bear in mind : first, that the disease is essentially one of adult life, though it may commence in adolescence or in advanced life ; and second, that when hereditary influences can be traced they are only rarely direct. The Peroneal Form of Progressive Muscular Atrophy ( Leg Type, Primary Neuritic Atrophy ). — The peroneal form of progressive muscular atrophy has many features that ally it with the typical progressive muscular atrophy that has just been described. It is, moreover, probable, upon the whole, that it depends on changes in the spinal cord similar to those that cause the atrophy of the typical form, though some authors consider it a peripheral affection. The feature of this disease is slowly progressive mus- cular atrophy of peculiar distribution. The atrophy begins in the lower extremities. Very often the begin- ning is in the extensor hallucis longus or the common extensor of the toes, from which it extends to the peronei muscles. The small muscles of the foot may or may not be affected. The calf muscles atrophy after the 478 DISEASES OF THE NERVOUS SYSTEM. peronei, and, last of all and often at a late date, the thigh muscles are involved. After a long time the atrophy- extends to the small muscles of the hand. The atrophy is always atonic, and usually symmetrical. The knee-jerks are lost when the thigh muscles waste— that is, late. The electrical changes present the same variations as in typical progressive muscular atrophy. Fibrillation occurs in the wasted muscles not infrequently, but not with the con- stancy that it occurs in progressive muscular atrophy. Vaso-motor disturbances are common, and slight sensory disturbance may occur. This form of progressive mus- cular atrophy is sometimes known as the "leg type," to distinguish it from the usual form, which may be called the "arm type." The leg type generally develops during early youth. There may be direct hereditary influence and several cases may occur in the children of the same parents. The distinction between the two described forms of muscular atrophy is of course most simple as a rule. As the arm type may involve the leg, and as the leg type may eventually involve the arm, an error might occur if we failed to discern the order of spreading of the atrophy. Without this knowledge, a diagnosis might be difficult ; but the known difference in the influence of heredity, and the fact that the arm type causes oiften unilateral atrophy in the leg, while the atrophy is symmetrical in the cases of the leg type, might be of service in diagnosis. Both types are distinguished from poliomyelitis by their gradual development and progressive course. The leg type cannot be confused with congenital club-foot if due care is taken in bringing out the history of the case. The further distinction of these types from other conditions may be conveniently postponed. THE DIAGNOSIS OF CLINICAL TYPES. 479 Progressive Muscular Dystrophies. — The progressive muscular dystrophies are those forms of muscular atro- phy that depend, not on disease of the central nervous system, but on primary lesions of the muscles. The progressive muscular dystrophies have several general characters in common, which serve to separate them clinically from the typical form of progressive muscular atrophy. These characters are as follows : (i) develop- ment in early youth ; (2) the occurrence of true or false hypertrophy of the muscles ; (3) the absence of degenerative electrical reactions ; (4) the absence of fibrillary contractions. The forms of progressive muscular dystrophies to be discussed are as follows : 1. Pseudo-hypertrophic paralysis. 2. Erb's form of progressive muscular dystrophy. 3. The Landouzy-Dejerine type of progressive muscular dystrophy. Of these three forms, the first may be separated in classification from the second and third without hesita- tion. The second and third forms, however, have so many features in common, that we are scarcely justified in making a sharp line between them. They are here considered separately for the sake of convenience. Pseudo-Hypertrophic Paralysis (Pseudo-Muscular Hypertrophy). — The chief characters of this disease are as follows : (a) Weakness in the muscles of the leg, and a waddling gait, associated with {b) Apparent increase in the size of certain leg muscles, especially the muscles of the calf, or the calves and thighs. There may be also considerable enlargement of some of the muscles of the shoulder, especially the infra- 480 DISEASES OF THE NERVOUS SYSTEM. spinati and deltoids. Eventually many of the hyper- trophic muscles may undergo atrophy, as shown in the FIG. 52. Pseudo-hypcrtrophic paralysis. muscles of the shoulder girdle in Fig. 52. In rare in- stances the muscles are at no time larger than normal. THE DIAGNOSIS OF CLINICAL TYPES. 48 1 U) A peculiar difficulty in rising from the ground, due to weakness of the extensors of the knee and hip. The hands are placed upon the knees in rising, to transfer part of the weight of the body from the upper to the lower part of the femur, — thus giving the extensors of the knee a distinct mechanical advantage. This and other peculiarities in rising have justified the saying, " the patient climbs up on himself." The difficulty is highly characteristic of pseudo-hypertrophic paralysis, but is not quite pathognomonic. (d) After the disease has lasted for a variable period (several years), contractions occur in the affected muscles (this contraction in the calf muscles causes talipes equinus). Often lumbar lordosis is a late symptom. {e) The knee-jerk is usually lost when the extensors of the knee are involved. The electrical reactions are normal, except in a late stage of the disease, when there is often diminished electrical irritability to both currents. There is no disturbance of sensibility and there are no fibrillary contractions. (/) The disease is slowly progressive. (g) The disease is one of early youth, and is generally inherited through the mother, though the mother may not herself be a subject of the disease. Pseudo-hypertrophic paralysis is sometimes confounded with cases of spastic paraplegia {v/de p. 429). The two conditions resemble one another in that there are weak- ness in the lower extremities and contraction of the calf muscles, in that the calf muscles may be large in each, and in the fact that both occur in children. In spastic paraplegia, however, there is active contracture of the calf muscles, which can be overcome by pressure, the ■ gait is spastic, the knee-jerks are increased, there is ankle clonus, and there is no difficulty in rising from the ground. 482 DISEASES OF THE NERVOUS SYSTEM. Erb's Type of Progressive Muscular Dystrophy (so-called "juvenile form " of progressive muscular dys- trophy). — This is an exceed- ingly rare form of muscular atrophy possessing the follow- ing characters: (a) There is progressive atrophy and weakness in many groups of muscles, especially the muscles of the shoulder, the upper part of the arm, the pelvic girdle, the thigh, and the back. Most often the atrophy begins in the arm. The fore-arm and leg muscles suffer very late, or not at all. (d) The atrophy of the muscle fibres may or may not be associated with pseudo-hyper- trophy of some of the muscles — usually there is no pseudo-hy- pertrophy. (., 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 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. 5l6 DISEASES OF THE NERVOUS SYSTEM. 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 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 plirenic nerve is derived from the third, fourth, and fifth cervical nerves. THE DIAGNOSIS OF CLINICAL TYPES. 517 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 violent muscular effort as in lifting a heavy hammer. Some- times 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 gener- ally on the right side, as seen in Fig. 57? 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. ^ This nerve is derived from the fifth and sixth cervical nerves. 5l8 DISEASES OF THE NERVOUS SYSTEM. Paralysis of the Supra- Scapular Nerve.^ — Damage tc the supra-scapular nerve causes paralysis of the supra- FIG. 57. Position of shoulder-blades in paralysis of the right serratus magnus during abduction of the arms. spinatus and infra-spinatus muscles. The paralysis of the former gives rise to no obtrusive symptoms, but ' This nerve is derived from the fourth and fifth cervical nerves. THE DIAGNOSIS OF CLINICAL TYPES. 519 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 often affected together with the cir- cumflex in consequence of dislocation of the head of the humerus, and in obstetrical paralysis. 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 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- Cutaneous 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- ' This nerve is derived from the fifth, sixth, seventh, and eighth cervical nerves. 520 DISEASES OF THE NERVOUS SYSTEM. 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, FIG. 58. Paralysis of the musculo-spiral nerve ; maximum extension of wrist and fingers. The extension of the fingers progressively diminishes from the first to the fourth. From a photograph. (Gowers.) 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. THE DIAGNOSIS OF CLINICAL TYPES. 521 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 paralysis 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. 522 DISEASES OF THE NERVOUS SYSTEM. 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 pollicis 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 Ijrachial plexus. THE DIAGNOSIS OF CLINICAL TYPES. 523 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 FIG. 55. Diagram illustrating the area of anaesthesia 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 anaesthesia which is observed in cases of injury to the median nerve is sufliciently well shown in the accompanying diagrams. The degree and extent of the anaesthesia vary much in 524 DISEASES OF THE NERVOUS SYSTEM. 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 THE DIAGNOSIS OF CLINICAL TYPES. 525 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 paralysis of the interossei leads to a deformity which is almost distinctive of ulnar paralysis. The fin- gers cannot be flexed at the first, or extended 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. 526 DISEASES OF THE NERVOUS SYSTEM. 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 FIG. 57. 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 way 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. 32 THE DIAGNOSIS OF CLINICAL TYPES. 527 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 difiicult 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 528 DISEASES OF THE NERVOUS SYSTEM. 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. FIG. 60. Diagram illustrating the area of anaes- Diagram illustrating the area of an- thesia in a case of injury to the ulnar sesthesia in a case of injury to the ulnar and median nerves. (Palmar surface.) and median nerves. (Dorsal surfa«e.) 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 THE DIAGNOSIS OF CLINICAL TYPES. 529 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. ErFs Paralysis (obstetrical palsy). — These names are given to a peculiar form of paralysis dependent on damage principally 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 brevis, and supra- and infra-spinati. There is often anaesthesia on the outer side of the arm in the distribution of the cir- cumflex and external cutaneous nerve; there is usually considerable muscular atrophy. The characters of Erb's paralysis differ considerably in adults and young chil- dren. 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 undue stretching of the nerve trunks, during delivery, thus causing stretching and rupture of the nerve sheaths and trunk. Hence it is commonly termed "obstetrical paral- ysis." ^ 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 " brachial birth palsy." 530 DISEASES OF THE NERVOUS SYSTEM much in different cases. In the slighter cases of injury tht 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 detected with difficulty. The paralysis in mild cases usually wears away in the course of a few months, some- times in a few weeks, but in all severe cases some pa- ralysis, atrophy, and deformity usually remain. The peculiar distribution of the paralysis and detection of the lesion of connective tissue overgrowth at Erb's point by means of palpation, and its occurrence during de- livery, if this can be established, make the diagnosis clear. Some care must be taken not to confound this condition with some forms of poliomyelitis {vide p. 452), or with injuries to the shoulder-joint or muscles. The characteristic electrical reactions in the paralyzed muscles serve to distinguish Erb's paralysis from all conditions 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 ^ Derived from the third and ft^urth lumbar nerves. THE DIAGNOSIS OF CLINICAL TYPES, 53 1 lumbar plexus. Occasionally, however, the nerve itself is damaged by pressure against the pelvis during delivery. 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 ^ Flexion is merely impaired because the psoas is supplied by other lumbar nerves. ^ This nerve is derived from the lumbo-sacra] cord. 532 DISEASES OF THE NERVOUS SYSTEM. extensors of the hip are included in the paralysis. The sciatic nerve external to the pelvis may be damaged in 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 outer 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 I?iternal 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?tal Plantar Nerve causes loss of THE DIAGNOSIS OF CLINICAL TYPES. 533 power in the muscles of the little toe, the flexor acces- 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 534 DISEASES OF THE NERVOUS SYSTEM. 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 obturatoi 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, parsesthesia, 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 unilateral, 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 THE DIAGNOSIS OF CLINICAL TYPES. 535 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, paraesthesia, 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 Equina 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 53^ DISEASES OF THE NERVOUS SYSTEM. causes fracture - 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. THE DIAGNOSIS OF CLINICAL TYPES. 537 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, paraesthesia, 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. Anaesthesia, if present, is of irregular distribution. Tumor of the cauda equina, however, generally causes bilateral symptoms and the peculiar areas of anaesthesia 538 DISEASES OF THE NERVOUS SYSTEM. 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. THE DIAGNOSIS OF CLINICAL TYPES. 539 neuritis may be added a condition whose pathology is as yet unsettled, but which probably depends on multiple neuritis — acute ascending paralysis. Alcoholic Neuritis. — 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) Hyperaesthesia (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. 540 DISEASES OF THE NERVOUS SYSTEM. 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 FIG. 65. Multiple alcoholic neuritis ; palsy of extensors of the wrist and flexors of ankle. (Gowers.) 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 : THE DIAGNOSIS OF CLINICAL TYPES. 541 ( 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. (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, fabrica- tions, and general mental failure constituting a distinct psychosis, which may accompany polyneuritis (Korssa- kow's disease). These symptoms are not usually present until the disease is well established. They may, how- ever, 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 (/. O -M ^ Oh 1^ ^ B o -S a § ^ f ^ f^ :^ K^ ^ ^ ^ u Id O o ex, to S Co s ^ a to s» to S pq 0) CO ctS O o lO i o -Si ^ S O .^ -^ --^ ^ <^ -^ '^ '^ C) PL, a PQ en a O o (^ "-I Co c< to -Si «o CM f^ w-i 00 Ov O o o ^ s to H ^ •Si . ^ ^ r^ ^ •♦-4 § 1 ^C> ^ 'tf -^^ «^ i»*i •^ r-^ ^ V. o^ lo O to ^ ^ S • ^^ -^ Co ^-,cqcq(/)OQCi,k^[jqkHtq s. ^ o 5» to -^ Q ^ ■ ^ ^ V ^ ^ ^ S g Q to to s '^ « io 1 1 "^^i S Q $>** ^ ?s v . 4:^ ?^ g ^ to o •^ s to K^ O <^ H^« wHi HfN whs VO cvj 04 o O l>^ N N H ^ H->. H-^ ^ S § -^ .^ -^ f^ »-] ^ O ^ Co to --Si Co to -^ ta «o ^ to -§ ^ to to b^ t^ tii ^ O fe ^-I ^4 ^ "^ Q g to a o U Q "tn O '^ H M-l O • r-l be •T-t a (D P^ CD O OJ O u CO oooooodo o o o to (^ 2^ -O ^ ^ S '-3 2 00 '^ ooooooooo 6 «o <0 CD * - ^ ^ rs ^ "Jo - -"^ to ^ ^ Q <^ ■^ a,hiCqco^k!^[5cQ o O o ^ ^- ^ in '^ t3 o >- 5^ g» Co «o to o u Co to to u rs *^ «0 c:i ^ ■^ to ►^ ^ "^ ^ ii: r^ ^ il" ^ <<; K< si •»* to O *o to •^ - ^ ;::d § 1^ b Co to ■4J CO 2 o o S a) O Pi 307 Agraphia, 214 Alcohol, abuse of, 311 Alcoholic coma, 206 Alcoholic delirium, 596 Alcoholic meningitis, 365 Alcoholic neuritis, 539-544 Alcoholism, acute, 596 Alexia, 218 Amaurosis, 159 Amblyopia, varieties of, 159- 162 Amnesic aphasia, 219 Amyotrophic lateral sclerosis, 470 iVnsemia of brain, 276 Ansemia of spinal cord, 277 Anesthesia, 143-148 Anaesthesia dolorosa, 441 Analgesia, 148 Anarthria, 210 Aneurism, intracranial, 278, 403-406 Aneurism of basilar artery, 405 Aneurism of internal carotid, 405 Aneurism of middle cerebral artery, 405 Angiospasm, 277 Ankle clonus, 142, 631 Anosmia, 158 iVnterior crural nerve paraly- sis, 531 Anterior fossa of skull, le- sions of, 250 Anterior horns of cord, le- sions of, 254 Anterior nerve-roots, lesions of, 267 Aphasia, 211 Aphasia, amnesic, 219 Aphasia, ataxic, 214 Aphasia, conduction, 219 Aphasia, examination for, 644 Aphasia, motor, 212 Aphasia, sensory, 212 Aphonia, hysterical, 564 Apoplectic softening, 379 Apoplexy, 203 Apoplexy without hemor- rhage, 371 Apraxia, 218 Arachnoid membrane, 74 Aran-Duchenne type of mus- cular atrophy, 471 677 678 DISEASES OF THE NERVOUS SYSTEM. Argyll-Robinson pupil, 132, 458, 627 Arm-type of progressive mus- cular atrophy, 478 Arsenical neuritis, 547 Articulation, defects of, 210 Associated movements, 118 Association fibres, 13 Association-tracts, lesions of, 236 Astasia, 121 Astasia-abasia, 565 Ataxia, 119 Ataxia, determination of, 624 Ataxia, hereditary, 465 Ataxia of tabes dorsalis, 459 Ataxic paraplegia, 472 Atheroma, acute cerebral softening from, 374 Atheroma of cerebral arteries, 282 Athetoid movements, 115 Athetoid movements, post- hemiplegic, 115 Athetosis, 115 Athetosis, primary, 115 Athetosis, symptomatic, 117 Atonic atrophy, 474 Atrophy, muscular, 187, 469 Atrophy of optic nerve, 173- 176 Auditory nerve, 65 Auditory symptoms, 177 Auditory tract, 67-69 Auras, 98 Aurae, sensory, 98 Aurae of special senses, 99 Aural vertigo, 181 Axis-cylinders, 5 B Babinski's reflex, 631 Base of brain, lesions of, 250 Basilar artery aneurism, 405 Basilar ineningitis, 356 Beri-beri, 551 Biceps jerk, 627 Bird-claw hand, 525 Birth-palsy, brachial, 529 Birth-palsy, cerebral, 389 Blood supply, loss of, 85 Blood supply of brain and cord, 75-80 Bones and joints, trophic changes in, 185 Brachial birth-palsy, 529 Brachial neuritis, 528 Brachial plexus, 47 Brain, 10 Brain, abscess of, 363, 394- 396 Brain, anaemia of, 276 Brain, congestion of, 275 Brain, dropsy of, 422 Brain, embolic softening of, 372 Brain, inflammation of, 285 Brain, tumor of, 363 Broca's centre, 212 Brown-Sequard's paralysis, 92-93. Bulbar inco-ordination, 123 Bulbar paralysis, 416-418 Burdach, columns of, 22 Cadaveric position of vocal cords, 134 Caisson paralysis, 441 Capsular hemorrhage, 369 Capsule, internal, 31 Capsule, internal, lesions of. 239 Carbonic oxide neuritis, 548 Cardiac disease, influence of, 343 Caries .of vertebrse, as a cause of cord disease, 427, 443 Catalepsy, 113-115 Cauda equina, 19 Cauda equina, lesions of, 268 Caudate nuclei. 15 Causal indications, 306 Cell, nerve, 5 Central convolutions, 30 INDEX. 679 "Centres," 9 Centrum ovale, disease of, 236 Centrum ovale, hemorrhage of, 369 Cephalic sensations, 157 Cerebellar hemorrhage, 369 Cerebellar in co-ordination, 121 Cerebellar titubation, 121 Cerebellum, 17 Cerebellum, lesions of, 247 Cerebral abscess, 363 Cerebral, arteries, atheroma of, 282 Cerebral birth-palsy, 389 Cerebral commissures, 13 Cerebral concussion, 597-599 Cerebral cortex, 10 Cerebral embolism, 281 Cerebral hemorrhage, 203, 367-371 ^ ., Cerebral paralvsis, mfantile, 386 • ' Cerebral sinuses, thrombosis of, 284 Cerebral softening, acute, 371 Cerebral softening, embolic, 372 Charcot s joint disease, 186 Cheyne-Stokes respiration, 202, 224 Choked disk, 169 Chvostek's reflex, 614 Chorea, 584-587 Chorea, hereditary, 586 Chorea, Huntington's, 586 Chorea, post-hemiplegic, 118, 586 Choreatic paresis, 118 Choroiditis, 176 Chronic meningitis in infants, 366 Ciliary muscle, paralysis of, 496 Cilio-spinal centre, 29 Cilio-spinal reflex, 626 Cincture-pain, 153 Circumflex ner\'e paralysis, 519 ! Clarke, column of, 40 Claustrum, lesions of, 240 Cleavage method, i Clitoris crises, 229 Clonic convulsions, 102 Cochlea, 65 Cold, exposure to, 340 Columns of Goll. disease of, 258 Coma, 202 Coma, alcoholic, 206 Coma, diabetic, 206 Coma, hysterical, 205 Coma, uraemic, 205 Compression of spinal cord, 443-445 Concentric limitation of visual field, 162 Concussion, cerebral, 597-599 Conduction aphasia, 219 Confluent articulation, 211 Congestion of brain, 275 Congestion of cord, 276 Conjugate deviation, 126 Conjugate deviation, para- lytic, 126 Conjugate deviation, spas- modic, 126 Conjunctival reflex, 626 Consciousness, loss of, 201 Consciousness, loss of, in convulsions, 98 Contraction, 111-113 Contracture, 111-113 Convulsions, 95-103 Convulsions, general, 96 Convulsions, internal. 102 Convulsions, localized, 97, O o n •^^ Convulsions, partial, 97 Cord, congestion of, 276 Cord, transverse lesions of, 262 Cord, unilateral lesion of, 258 Corneal reflex. 626 Corpora quadrigemina. 15 Corpora quadrigemina, le- sions of, 240 Corpus callosum, 13 68o DISEASES OF THE NERVOUS SYSTEM. Corpus callosum, lesions of, 237 Corpus restifonnis, 65 Corpus striatum, lesions of, 238 Cortical hemorrhage, 369 Cortical inco-ordination, i2q Cramp of calf muscles, 102 Cranial nerve-nuclei, 17 Cranial nerves, 47 Cranio-cerebral topography, 80 Cremasteric reflex, 626 Crises, clitoridal, 229 Crises of locomotor ataxia, 459 Crossed anaesthesia, 244 Crossed pyramidal tract, 34 Cross-legged progression, 455 Crura cerebri, 15 Crura cerebri, lesions of, 241 Crush of spinal cord, 445-448 D Deafness, nervous, 177 Defective central vision, 161 Defects of articulation, 210 Defects of muscular power, determination of, 622 Degeneration, 301 Degeneration, reaction of, 190 Deglutition in bulbar paraly- sis, 417 Deiter'r, nucleus, 65 Delirium, 206 Delirium, alcoholic, 596 Delirium tremens, 596 Delusions of general paresis, 420 Dementia paralytica, 419 Dendrites, 5 Dermographism, 201 Deviation of eyes, 127 Diabetes, 345 Dialectic coma, 206 Diabetic convulsions, 206 Diabetic neuritis, 345 Diagnosis of clinical types, 352 Diagnosis of nature of lesion, 274 Diaphragm, paralysis of, 516 Diphtheritic infection, 322 Diphtheritic neuritis, 549 Diphtheritic paralysis, 322 Diplegia, 91 Diplopia, 128, 610 Diseases of brain, 352 Diseases of peripheral nerves, 354 Diseases of special nerves, 495 Diseases of spinal cord, 354, 426 Diver's paralysis, 441 Double vision, 128 Drug-treatment, influence on nervous diseases, 346 Dura, haematoma of, 367 Dura mater, 74 Dysarthria, 210 Dyslexia, 219 Dystrophies, muscular, 472 Dystrophies, progressive muscular, 474 E Electrical examination, 631- 637 Embolic softening of brain, 372 Embolism of cerebral ar- teries, 281 Embolism of spinal cord, 441 Encephalomalacia, 371 Endarteritis, syphilitic, 378 Endolymph, 65 Epidemic cerebro-spinal meningitis, 357 Epigastric reflex, 626 Epilepsy, 576-582 Epilepsy, nocturnal, 577 Epilepsy, psychical, 577 Erb's paralysis, 529 INDEX. 68 I Erb's type of progressive muscular dystrophy, 482 Erroneous projection, 609 Erysipelas and nervous affec- tions, 326 Examination of the patient, 602 Exhaustion paralysis, 99 Exposure to cold, 340 Exposure to heat, 341 External capsule, lesions of, 240 External plantar nerve, par- alysis of, 532 External popliteal nerve, paralysis of, 532 Extradural hemorrhage, 380- 385 Eyeball, trophic changes in, 185 Facial nerve, 62 Facial i;erve, examination of, 613 Facial nerve, superior branch of, 63, 64 Facial paralysis, 502-506 Facial paralysis, double, 505 Facial spasm, 506 False wryneck, 513 Festination, 122 Fibrillation, 106 Fifth nerve, 57 Fifth nerve, paralysis of, 498 Fissure of Rolando, 81 Fissure of Sylvius, 82 Focal symptoms, 204 Foot clonus, 142, 630 Foot phenomenon, 630 Foramen of Monro, 75 Fortification spectrum, 167 Fourth nerve, 53 Fourth nerve paralysis, 496 Fragilitas ossium, 186 Friedrich's disease, 349, 465- 469 Frontal lobe, lesions of, 234 Galton's whistle, 615 General paralysis of insane, 419 General paresis, 419 General paresis, course of, 421 General paresis, delusions of, 420 General paresis, differential diagnosis of, 421—422 General paresis, pupillary changes in, 421 General paresis, speech in, 420 General paresis, symptoma- tology of, 419-421 General paresis, tremor in, 420 Geniculate ganglion, 63 Girdle pain, 153 Glioma, 298 Glossopharyngeal nerve, 69 Glossopharyngeal nerve, ex- amination of, 616 Glossopharyngeal nerve, mo- tor fibres of, 69 Glossopharyngeal nerve par- alysis, 507 Glossopharyngeal nerve, taste fibres of, 69 Glossy skin, 494 Gluteal reflex, 626 Grandmal epilepsy, 577 Gray cord substance, lesions of, 254 Gray tubercle of Rolando, 59 Gudden's atrophy method, 2 Gustatory symptoms, 183 H Habits, influence of, 310 Haematoma of dura mater, 367 Hallucinations, olfactory, 159 Headache, 154 682 DISEASES OF THE NERVOUS SYSTEM. Heat, exposure to, influence of, 341 Hemianaesthesia, 144 HemiancBSthesia, crossed, 145 Hemianesthesia, hysterical. Hemianopsia, 163 Hemianopsia, homonymous, 164 Hemianopsia, lateral, 164 Hemianopsia, nasal, 164 Hemianopsia, temporal, 163 Hemianoptic pupillary inac- tion, 133 Hemiataxia, 120 Hemichorea, 586 Hemicrania, 582 Hemiopia, 163 Hemiplegia, 89, 204, 232 Hemiplegia, "complete," 86 Hemiplegia, crossed, 91-93 Hemiplegia, double, 91 Hemiplegia, hysterical, 563 Hemiplegia, infantile, 392 Hemiplegia from lesion of internal capsule, 239 Hemiplegia, recovery from, 91 Hemiplegia, sensory disturb- ances of, 91 Hemiplegia, spinal, 92 Hemorrhage, capsular, 369 Hemorrhage, cerebellar, 369 Hemorrhage,cerebral,367-3 7i Hemorrhage, cortical, 369 Hemorrhage .extradural, 380- 385 Hemorrhage in centrum ovale, 369 Hemorrhage, infantile menin- geal, 367, 380 Hemorrhage into cord, 280 Hemorrhage into cord-mem- branes, 280 Hemorrhage into cord-sub- stance, 434 Hemorrhage, intracrainal, 277. 367-371 Hemorrhage, intraspinal, 432 Hemorrhage, meningeal, 277 Hemorrhage, meningeal spinal, 432-433 Hemorrhage, pontal, 369 Hemorrhage, retinal, 176 Hemorrhage, subarachnoid. Hemorrhage, ventricular, 369 Hemorrhagic myelitis, 435, 438 Hereditary ataxia, 465 Hereditary chorea, 586 Heredity, 347 Huntington's chorea, 586 Hydrocephalus, 422 Hydrocephalus, diagnosis of, 425-426 Hydrocephalus, types of, 423-425 _ Hyperacusis, 616 Hyperaemia of brain, 275 Hyperassthesia, 151 Hyperalgesia, 151 Hyperosmia, 159 Hypertonicity, 109 Hypertrophy, muscular, 190 Hypertrophy, pseudo-mus- cular, 479-480 Hypoglossal nerve, 72 Hypoglossal nerve, exam- ination of, 619 Hypoglossal nerve paralysis, 514 Hypotonus, 109 Hysteria, 364, 533-567 Hysterical aphonia, 564 Hysterical coma, 205 Hysterical hemianaesthesia, 564 Hysterical hemiplegia, 563 Hysterical monoplegias, 559- 561 Hysterical paraplegia, 561- 563 Hysterical ptosis, 565 Hysterical strabismus, 565 Illustrations of diagnosis, 656-676 INDEX. 683 Incontinence of feces, 228 Incontinence of urine, 227 Inco-ordination, 119 Inco-ordination, bulbar, 123 Inco-ordination, cerebellar, 121 Inco-ordination, cortical, 120 Inco-ordination, peripheric, 125 Inco-ordination, spinal, 123 Inequality of pupils, 133 Infantile cerebral paralysis , 386 Infantile hemiplegia, 392 Infantile meningeal hem- orrhage, 367, 380, 389 Infantile paralysis, 449 Infectious diseases, influence of, 315 Inflammation of bram, 285 Inflammation of nerve -sub- stance, 86 Influenza and nervous affec- tions, 327 Inhibition, irritative, 86 "Intellectual tract," 19 Intention tremor, 103 Intercellular substance, 5 Internal capsule, hemorrhage into, 367-369 Internal capsule, lesions of, 239 Internal carotid aneurism, 405 Internal popliteal nerve par- alysis, 532 Intracranial abscess, 363 Intracranial aneurism, 278, 403-406 Intracranial hemorrhage, 367-371 Intracranial tumor, 397-403 Iris, paralysis of, 496 Irritability of nerve, dimin- ished, 198 Irritability of nerve, in- creased, 199 Irritation of optic apparatus,- 167 Island of Reil, lesions of, 236 J Jacksonian epilepsy, 98 Jaw-jerk, 627 Juvenile type, progressive dystrophy, 482 K Kidney disease, influence on nervous system, 344 Knee-jerk, 628 Knee-jerk, loss of, 138, 458 Knee-jerks, exaggeration of (in general paresis), 421 L Landouzy-Dejerine type of progressive muscular dys- trophy, 483 Landry's paralysis, 553-556 Laryngeal nerves, 71 Laryngeal symptoms, 134 Laryngismus stridulus, 136 Larynx, adductor paralysis of, 136 Larynx, total abductor par- alysis of, 135 Larynx, total bilateral par- alysis of, 134 Larynx, total unilateral par- alysis of, 134 Larynx, unilateral abductor, paralysis of, 135 Lead neuritis, 545-547 Lead-poisoning, 329 "Leg-type," progressive mus- cular atrophy, 477 Lemniscus, 41 Lenticular nucleus, 15 Leprosy, anaesthetic, 552 Leprous neuritis, 552 Leptomeningitis, 286 Light action of pupil, 627 Light inaction of pupil, 627 Lightning pains of locomotor ataxia, 457 Localization, rules of, 230 684 DISEASES OF THE NERVOUS SYSTEM. Locomotoir ataxia, 457-462 Locomotor ataxia, ataxic phenomena of, 458 Locomotor ataxia, crises of, 459 Locomotor ataxia, differ- ential diagnosis of, 460-461 Locomotor ataxia, lightning pains of, 457 Locomotor ataxia, neuralgic stage of, 459 Locomotor ataxia, pre-ataxia stage of, 458 Lumbar enlargement, 21 Lumbar plexus, 47 Lumbar plexus, lesions of, 533 Lumbar puncture, 360 M Malingering, 599-601 Masturbation, 314 Measles and nervous affec- tions, 325 Mechanical injury of nerve- substance, 85 Median-nerve paralysis, 522 Median-ulnar nerve paralysis, 527 Medulla oblongata, lesions of, 246 Meningeal hemorrhage, 379- 384 Meningeal hemorrhage, m- fantile, 379-384, 389 Meninges of brain and cord, 74 Meningitis, 286 Meningitis, acute internal, 428 Meningitis, alcoholic, 365 Meningitis, basilar, 356 Meningitis, cerebral, 355-360 Meningitis, cerebro-spinal, 357 Meningitis, chronic, 365 Meningitis, chronic, in infants, 366 Meningitis, chronic internal, 430 . , Meningitis, diseases simulat- ing, 361-367 Meningitis, external, 291 Meningitis, internal, 291, 428 Meningitis of convexity, 356 Meningitis, purulent, 287, 356 Meningitis, simple, 287, 359 Meningitis, spinal, 290, 426 Meningitis, syphilitic, 289, 319, 366 Meningitis, tubercular, 288, 316, 358 Mental deterioration, simple, 208 Mental shock, 343 Mental symptoms, 201 Mercurial poisoning, 332 Middle cerebral artery aneur- ism, 405 Middle fossa of skull, disease in, 251 Middle peduncle of cerebel- lum, lesions of, 249 Migraine, 582-584 Migraine, ophthalmic, 583 Mind-blindness, 217 Mind-deafness, 218 Mixed nerve, 37 Mobile spasm, 115 Monoplegia, hysterical, 559- 561 Monoplegias, 89, 94, 232 Monospasm, 101 Moral sense, defects of, 209 Morbid blood-states, 345 Morvan's disease, 492 Motor oculi, examination of, 607 Motor paralysis, 87 Motor points, 190 Motor tract, 29 Multiple neuritis, 538 Multiple sclerosis, 41 1-4 16 Muscle pain sense, 643 Muscles, excessive use of, 341 Muscles, trophic changes in, 187 INDEX. 685 Muscular atrophy, 187, 469 Muscular atrophy, progres- sive, 472 Muscular dystrophies, 472 Muscular hypertrophy, 190 Muscular sense, 643 Muscular sensibility, loss of, 150 Muscular tenderness, 154 Musculocutaneous nerve par- alysis, 519 Musculospiral nerve paraly- sis, 520 Myelitis, acute, 435-440 Myelitis, chronic, 442 Myelitis, diffuse, 438 Myelitis, hemorrhagic, 435, 438 Myelitis, transverse, 436, 438 Myelitis, types of, 435-436 N Nasal hemianopsia, 164 Nerve-elements, wasting of, 86 Nerve-substance, inflamma- tion of, 86 Nerve-substance, mechanical injury of, 85 Nerves, tumors of, 300 Nervous deafness, 177 Neuralgia, 590-594 Neuralgic stage of tabes dor- salis, 458 Neuralgiform pains, 592-594 Neurasthenia, 575-576 Neuritis, 292, 493-495 Neuritis, alcoholic, 539-544 Neuritis, carbonic oxide, 548 Neuritis, diphtheritic, 549 Neuritis, disseminated, 538 Neuritis, leprous, 552 Neuritis, migrans, 494 Neuritis, multiple, 538 Neuritis, optic, 169 Neuritis, primary brachial, 528 Neuritis, rheumatic, 498 Neuritis, tuberculous, 316 Neurons, 3 Neuroses of occupation, 594- 596 Neuroses, traumatic, 567 Nocturnal epilepsy, 581 Nuclear ophthalmoplegia, 409 Nucleus ambiguus, 71 Nucleus angularis, 67 Nucleus tecti, 67 Nystagmus, 129 O Obstetrical paralysis, 529 Obturator nerve paralysis, 530. Occipital lobe, lesions of, 235 Occupation neuroses, 594- 596 Ocular muscles, paralysis of, 495 Ocular nerves, 56 Ocular paralyses, types of, 497-498 Ocular vertigo, 182 Oculomotor paralysis, 495 Olfactory hallucinations, 159 Olfactory nerve, 48 Olfactory nerve, examination of, 604 Olfactory symptoms, 158 Ophthalmic migraine, 583 Ophthalmoplegia, nuclear, 406-411 Ophthalmoplegia, periodical, 411 Ophthalmoplegia, recurrent, 411 Ophthalmoscopic changes, 168 Optic apparatus, irritation of, 167 Optic nerve, 49 Optic nerve, atrophy of, 173 Optic nerve, examination of, Optic neuritis, 169 686 DISEASES OF THE NERVOUS SYSTEM. Optic thalamus, 15 Optic thalamus, lesions of, 238 Optic tra^ct, 50 Over-fatigue, 341 Pachymeningitis interna hemorrhagica, 367 Pachymeningitis, spinal, 427 Pain, 152 Pain, neuralgiform, 592-594 Pain referred to spine 153 Pain, reflected, 592 Pain, sensibility to, 639 Papillitis, 170 Para-anaesthesia, 146 Paracentral lobule, 30 Paraesthesiae, 152 Paralysis, acute anaesthetic, 553-556 Paralysis agitans, 588-590 Paralysis, bulbar, 416-418 Paralysis, determination of, 623 Paralysis, infantile, 448 Paralysis of ciliary muscle, 496 Paralysis of sphincter iridis, 496 Paraplegia, 93 Paraplegia, ataxic, 462 Paraplegia, hysterical, 458, 561-563 Paraplegia, primary spastic, 454-457 Paraplegia, spastic, 453 Paresis, 95 Paresis, general, 419 Parietal lobe, lesions of, 234 Parkinson's disease, 587 Pars accessorius of vagus, ex- amination of, 616 Patellar reflex, 130 Patellar reflex, loss of, 138 Patheticus, 53 Patheticus, examination of, 607 Patient, examination of, 602 Periodical ophthalmoplegia, 411 Peripheral nerves, lesions of, 273 Peripheral nerves, tumors of, 534 Peroneal form of progressive muscular atrophy, 477 Peroneal nerve paralysis, 532 Petit mal epilepsy, 577 Pharyngeal nerves and plex- us, 70, 71 Pharyngeal paralysis, 508 Pharyngeal spasm, 508 Phrenic nerve paralysis, 520 Pia mater, 75 Plantar nerve paralyses, 532 Plantar reflex, 626 Pneumogastric nerve, 70 Pneumogastric nerve paraly- sis, 507 Pneumonia and nervous af- fections, 326 Poliomyelitis, 448 Poliomyelitis, acute anterior, 449 Poliomyelitis, chronic, 452, 472 Poliomyelitis, subacute, 452 Polyneuritis, 538 Pons Varolii, lesions of, 242 Pontal hemorrhage, 369 Position of morbid process, 350 Post-epileptic stupor, 205 Posterior fossa of skull, dis- ease in, 251 Posterior horn of cord, dis- ease of, 255 Posterior nerve-roots, lesions of, 268 Posterior thoracic nerve par- alysis, 517 Postero-extemal column of cord, disease of, 257 Post-hemiplegic a t h e t o i d movements, 115 INDEX. 687 Post-hemiplegic chorea, 118, 586 Postero-internal column of cord, disease of, 258 Pre-ataxic stage of tabes dor- salis, 458 Precuneus, 30 Pregnancy, 346 Pressure lesions, 85 Progressive muscular atro- phy, 472-477 Projection fibres, 13 Propulsion, 122 Pseudo-hypertrophic paraly- sis, 479 Pseudo-muscular hypertro- pV. 479 Pseudo-paralytic (terminal) stage of ataxia, 459 Pseudo tabes, 541 Psychical epilepsy, 577 Psychoneurosis, traumatic, 568-574 Ptosis, 130, 496 Ptosis, hysterical, 565 Pulse, 222 P upil, Argyll- Robertson ,132, 627 Pupil, contraction of, 132 Pupil, dilatation of, 131 Pupil, dilatation of, with immobility, 132 Pupil, light action of, 627 Pupil, light inaction of, 657 Pupillary accommodation, loss of, 496 Pupillary changes in general paresis, 421 Pupillary inaction, hemian- opic, 133 Pupillary reaction to light, loss of, 496 Pupillary reflex, 626 Pupillary symptoms, 131 Pupils, inequality of, 133 Purulent meningitis, 356 R Rachialgia, 153 Reaction of degeneration, 190 Reflected pains, 592 Reflex action, abnormal, 2)1 Reflex action, excess of, 140 Reflex action, loss of, 137 Reflex arc, 43 Reflex, Babinski's, 631 Reflex centre, 43 Reflex, Chvostek's, 614 Reflex, cilio-spinal, 626 Reflex, conjunctival, 626 Reflex, corneal, 626 Reflex, epigastric, 626 Reflex, gluteal, 626 Reflex influences, 339 Reflex, patellar, 130 Reflex paths, 43 Reflex, plantar,, 626 Reflex, pupillary, 626 Reflexes, deep, 44 Reflexes, examination of, 625-631 Respiration, 223 Respiration, Cheyne-Stokes, 202 Retinal hemorrhages, 176 Retinitis, albuminuric, 176 Retropulsion, 123 Retrocollic spasm, 513 Rheumatic neuritis, 498 Rheumatism (acute) and nervous affections, 326 Rickets, 345 Rigidity, 1 08-1 11 Rigidity, tonic, 102 Rolandic region, 30 Romberg symptom, 408 Sacral plexus, 47 Scanning speech, 211 Sciatic nerve paralysis, 531 Sciatica, 593 Sclerosis, disseminated, 416 Sclerosis, insular, 416 Secondary degeneration, 2 Secondary deviation, 608 Semicircular canals, 65 688 DISEASES OF THE NERVOUS SYSTEM. Senile tremor, 589 Sense, muscle-pain, 643 Sense, muscular, 643 Sense, temperature, 640 Sensibility to pain, 639 Sensibility to touch, 637 Sensory examination, 637 Sensory paralyses of fifth nerve, 498-499 Sensory symptoms, 143 Sensory tract, 38 Serratus magnus paralysis, 517 Sex, 309 Sexual excess, 313 Sexual functions, disorders of, 228 "Shaking palsy," 587 "Sick headache," 582 Sieveking'sassthesiometer,638 Silver poisoning, 7,7,7, Sinus-thrombosis, 384 Skin, trophic changes in, 184 Small sciatic nerve paralysis, 533 Small-pox and nervous aiiec- tions, 325 Softening of brain, 281 Solitary tubercle, 316 Soul-blindness, 217 Spasm, determination of, 624 Spasmodic wryneck, 512 Speech disturbances, 209 Speech in general paresis, 420 Sphincters, affections of, 226 Spinal accessory nerve, 71 Spinal accessory nerve, ex- amination of, 618 Spinal accessory nerve par- alysis, 509 Spinal cord, 19 Spinal cord, abscess of, 441 Spinal cord, anaemia of, 277 Spinal cord, compression of, 443-445 Spinal cord, crush of , 445-448 Spinal cord, degeneration dis- eases of, 453 Spinal cord, diseases of, 426 Spinal cord, embolism of, 441 Spinal cord, hemorrhage into, 280 Spinal cord, localization of lesions in, 253 Spinal-cord topography, 80 Spinal inco-ordination, 123 Spinal meningitis, 426 Spinal nerves, 44 Spinal paralysis, atrophic, 255 Spinal paralyses, spastic, 257 Spinal topography, 80 Sterno-mastoid paralysis, 510 Stilling's column, 40 Strabismus, 127 Strabismus, convergent, 128 Strabismus, divergent, 128 Strabismus, external, 128 Strabismus, hysterical, 565 Strabismus, internal, 128 Stupor, 202 Stupor, post-epileptic, 205 Subarachnoid hemorrhage, 383 Subarachnoid space, 74 Subcortical lesions, 237 Subdural space, 74 Superior gluteal nerve par- alysis, 531 Superior parietal lobule, 30 Supinator jeik, 627 Supra-scapular nerve par- alysis, 518 Sylvian fissure, 82 Sylvian line, 81 Sympathetic nervous system, 26 Symptomatology of nervous diseases, 84 Symptoms, onset of, 305 Syphilis as a factor in degen- erative diseases, 320 Syphilitic endarteritis, 318 Svphi'litic endarteritis and hemorrhage, 378 Syphilitic infection, 318 Syphilitic meningitis, 366 Syphilitic thrombosis, 373 INDEX. 689 Syringomyelia, 488-493, System-diseases of cord, 254 Tabes dorsalis, 457 Tache cerebrale, 201 Temperature, 221 Temperature sense, 640 Temperature sense, loss of, 149 Temporal lobe, lesions of, 235 Tetanoid spasms, loi Tetanus, 338 Thomsen's disease, 349 Thrombosis of cerebral ar- teries, 281 Thrombosis of c e re b r a 1 sinuses, 284 Thrombosis of sinus, primary, 384 Thrombosis of sinus, secon- dary, 386 Thrombosis, simple arterial, 375 Tic convulsif, 506 Tinnitus aurium, 179 Titubation, cerebellar, 121 Tobacco, excessive use of, Tongue, paralysis of, 514 Tongue, spasm of, 515 Tonic atrophy, 474 Tonic spasms, loi Torticollis, 511 Touch, sensibility to, 637 Transverse lesion of cord, 262 Trapezius paralysis, 509 Trauma and nervous affec- tions, 334 Traumatic hysteria, 567 Traumatic neurosis, 567 Traumatic psychoneurosis, 568-574 Tremor, 103-106 Tremor, action, 103 Tremors, determination of, 624 Tremor, intention, 103 Tremor, senile, 104, 589 Tremor, simple, 104 Triceps jerk, 627 Trifacial nerve, 57 Trifacial nerve, examination of, 611 Trophic symptoms, 183 Trousseau's symptom, loi Tubercles of choroid, 176 Tubercle, solitary, 316 Tubercular meningitis, 358 Tuberculosis of vertebrae, 317 Tuberculous infection, 316 Tumor, intracranial, 295, 397-403 Tumor, intraspinal, 485-488 Tumor of brain, 7,63 Tumor of nerves, 300 Tumors of peripheral nerves, 534 Tumors of spinal cord, 298 Typhoid fever and nervous affections, 323 U Ulnar nerve paralysis, 524 Unilateral lesions of cord, 258 Urcemic coma, 205 Urine, 226 Urine, incontinence of, 227 V Vagus, examination of, 616- 618 Vagus nerve, 70 Vascular disease, 344 Vasomotor symptoms, 199 Ventricular hemorrhage, 369 Vertigo, 180 Vertigo, aural, 181 Vertigo, essential, 180 Vertigo, gastric, 182 Vertigo, ocular, 182 Vestibule, 65 Vision, defective central, 161 -i- MEDICAL PUBLICATIONS. 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