.IBRARY HIVERSITT OP ^liFORNIA SAN DIEGO J DATE DUE MAR 24 1979 WN 1 . 1 accv« ! 1 .-9B >'i UNIVERSITY OF CAUFORN'A SAN DIEQC 3 18220182221 74 M $ ) ~S i < \, Fig. i. — Foot of Friedreich's disease. DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES BY EDWARD LIVINGSTON HUNT, M. D. INSTRUCTOR IN NEUROLOGY AND ASSISTANT CHIEF OP' CLINIC, COLLEGE OF PHYSICIANS AND SURGEONS, THE MEDICAL DEPARTMENT OF COLUMBIA UNIVERSITY, IN THE CITY OF NEW YORK J ASSOCIATE CONSULTING NEUROLOGIST TO ST. LUKE'S HOSPITAL; CON- SULTING NEUROLOGIST TO THE LINCOLN HOSPITAL, THE WORKHOUSE, AND PENITENTIARY J ATTENDING NEU- ROLOGIST TO THE CENTRAL AND NEUROLOGICAL HOSPITAL; MEMBER OF THE AMERICAN NEU- ROLOGICAL ASSOCIATION, AND OF THE NEW YORK NEUROLOGICAL SOCIETY. ILL USTR^UiED PHILADELPHIA AND LONDON W. B. SAUNDERS COMPANY 1914 Copyright, 1014, by W. B. Saunders Company PRINTED IN AMERICA PRESS OF W. B. 8AUNDERS COMPANY PHILADELPHIA To My Friend and Chief jft. alien &tanr, PROFESSOR OF NEUROLOGY, COLUMBIA UNIVERSITY, N. Y. PREFACE My students at Columbia University have asked me for several years to name a book in which they could hnd the salient points and leading symptoms of the principal nervous diseases -without the laborious search involved in consulting the larger text-books. This book, written to supply such a demand, is intended for the student, intern, and general practitioner, both as a reference and as an aid in diagnosis. I wish to express my thanks and sincere appreciation for the suggestions and valuable help given me by Dr. Thaddeus H. .Ames. He has many times improved, and on one or two occasions added to the manuscript. The illustrations, nearly all of winch are original, were taken from patients on my service in the Central and Neurological Hospital of Xew York City. For the help in obtaining them I am indebted to Dr. Thomas H. Price. It has not seemed advisable in a work of this sort to give credit on each page for each reference. A complete list of the books and authorities on which I have drawn is at the end of the volume. E. L. H. 54 We = 10 VD Fig. 10 — Fine vibratory tremor. The Various Tremors The following list of tremors will enable the student to understand them thoroughly: The Intention Tremor. — The distribution of the in- 62 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES tention tremor is not limited to the hands or arms, but extends to the muscles about the scapula and neck. It may even involve the legs or any other muscles. Its most common distribution is in the arms. The intention tremor is coarse, unusually jerky, and possesses considerable amplitude of excursion. Its name is derived from a distinctive trait. This trait is that the tremor is present only when the patient performs a 2^ -^v ^ 3 V J^^v-n^ gy^o 7 Fig. ii. — a, Handwriting of a patient suffering from multiple sclerosis. b, Normal handwriting of the same matter. voluntary action; in short, does something. The hands at rest evince no tremor. So soon as the patient attempts anything, to perform any act, the tremor appears. The best exhibition of the intention tremor is seen in the patient's attempt to drink a glass of water. As he sits at the table, with arms hanging loosely by the side, or resting, possibly on the table, no trembling is apparent. At the moment, however, that he raises his hand and TREMORS 63 carries the glass to the mouth, there appears in both arms and hands a tremor coarse and jerky in character, slow- in rate, and displaying considerable amplitude of excur- sion. These movements augment in both size and fre- quency the more prolonged is the effort which originates them. If the intention tremor is at all pronounced, the contents of the glass will be spilled. The handwriting is involved early. Wilkinson de- scribes it as being jerk}-, especially at the end of a word or sentence. The affection of straight lines is not so char- acteristic as is the occurrence of a sudden, jerky irregu- larity. The patient attempting to draw a straight line resorts to a series of disconnected blots and jerky, short lines. The walk of a patient suffering from an intention tremor of the legs displays much the same characteristic. It is unsteady and irregular. He stands well, but so soon as the legs begin to move there develops irregularity. The effect of external and emotional influences on the intention tremor is to increase it. This tremor is one of the cardinal signs of multiple sclerosis. The other three are nystagmus, scanning speech, and exaggerated knee-jerks. An excellent diagrammatic representation of the intention tremor is the one given by Charcot: B Fig. 12. — Diagram illustrating intention tremor. A is the point of rest. A-B is still the point at rest. B is the point where the patient begins to perform an action. C is the point where action ceases and the patient 64 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES again comes to a point of rest. During repose, line A-B, there is absolutely no tremor. When the patient begins to make a movement at B, tremor begins, continues, and increases during the continuance of the movement BC. List of diseases in which the intention tremor occurs: i. Multiple sclerosis. 2. Tumor of crura cerebri. 3. Tumor of the quadrate bodies. 4. Cerebellar tumors. The Tremor of Paralysis Agitans. — The distribution of the tremor is generally the same; it begins in the fingers and small muscles of the hands, then gradually extends up the arm, skips the trunk, and soon involves the leg and foot. The opposite side is not affected until much later in the disease. The result is that the patient presents a tremor in character hemiplegic. So distinctive is this characteristic that the condition often resembles a real hemiplegia, or a posthemiplegic tremor strongly suggests paralysis agitans. The main point to remember is that the posthemiplegic tremor is decidedly less coarse and faster. The tremor of paralysis agitans is the slowest of all. The oscillations do not exceed six a second. Their range of movement is very slight. According to Sir William Gowers, they average from one-eighth to three-quarters of an inch. This tremor is very regular and very coarse. The movements consist of flexion and extension, then in a most rhythmic manner come abduction and adduction. A very marked feature of this tremor is that it is most pronounced, most violent, during repose; any TREMOES 65 movement or any action on the part of the patient re- duces very greatly the trembling. Thus, it is not at all uncommon to see a patient, who has been trembling violently, raise a glass of water to his lips and drain the contents without spilling a drop. The handwriting of these patients is, strange to say, not affected till late in the disease. The formation of the letters is slow, but fairly good. The strokes of the pen display fine, wavy irregularities. There is nothing of the jerky appearance characteristic of the intention tremor. The walk of these patients is so characteristic that it has been given a special name. A full descrip- tion of this gait, known as " festination, " is to be found in the chapter on Gaits. Fig. 13. — Handwriting of a patient suffering from paralysis agitans. Still another characteristic of this tremor is the fact that it may often be checked for a few seconds by the patient's will, or by his putting the muscles of the hand under great tension. It diminishes in inverse propor- tion to the patient's attention. It ceases during sleep and is very considerably increased under emotion or excitement. Wilkinson says that it is diminished during a railway journey. As a result of this, one of the forms of treatment has been the ingenious suggestion of a vibrating chair. Weir Mitchell first called attention to the fact that by seizing the index-finger and over- extending it for a short time the tremor can be stopped. Great sorrow or great pleasure will equally augment the tremor. The attitude which the sufferer presents is s 66 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES unusual; the shoulders are rounded, the back is curved, he leans forward, and the legs are bowed at the knees, giving the appearance of advanced old age. There is marked rigidity, with slowness and deliberation in all movements. The hands, usually the most common seat of the tremor, present a characteristic appearance — one of flexion, immobility, and close approximation of index- finger to thumb. The presence of a regular, coarse tremor occurring in a hand held in a position of flexion corresponding to that of a penman gives rise to a peculiar motion. This motion has been compared to that of crumbling bread, and is designated as " pill-rolling. " This tremor is one of the cardinal signs of the disease, known as "paralysis agitans." The others are the attitude, the gait, the mask-like face, and the age. So prominent a position does the tremor occupy in the symptomatology of the disease that the laity have named the condition "the shaking palsy." It is a tremor which has many distinguishing characteristics. These two tremors in respect to each other stand in opposite extremes. Each is coarse; one is increased on movement, the other decreased. One, the intention tremor, is most common in the young; the other, the tremor of paralysis agitans, is an instance of beginning senility. The third place of importance can be assigned to the toxic tremors. These are tremors caused by poisons, the result of absorption of toxins. They are numerous and varied. The easiest classification is the one which groups them under two headings: i. Endogenous toxic tremors. 2. Exogenous toxic tremors. TREMORS 67 i. The endogenous tremors are those which result from poisons originating inside the body. These are the tremors of Graves's disease, general paralysis, and asthenia. 2. The exogenous tremors are those which result from poisons introduced into the body from without. These are: (a) Alcoholic tremors. (b) Metal tremors. (c) Drug tremors. The tremor of Graves's disease is distributed to the hands and arms. In aggravated cases it may rarely involve the other parts. It never involves the muscles of the face, trunk, or lips. It is fine and constant, num- bering about 8 to 10 oscillations per second. Rest has a beneficial and marked effect upon it. Voluntary movement does not necessarily increase it, although any action and movement on the part of the patient tends to increase it. The patient can raise a glass of water with only a slight change of level; it is never spilled. The handwriting in mild cases will show scarcely any abnormality; in the more advanced cases there is evident a slight, wavy irregularity. The walk shows nothing. It is the tremor which is greatly aggravated by mental exhilaration and excitement. It advances along with the disease. As the latter becomes more pronounced, the tremor becomes more aggravated. The cardinal signs of Graves's disease are exoph- thalmos, tachycardia, enlarged goiter, and a fine tremor. The distribution of the tremor in general paresis is variable; it may involve any muscle; it may involve any group of muscles; it usually involves the muscles of the 68 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES face, tongue, lips, and arms. The rate may be fast or slow; therefore, the tremor may be either coarse or fine; the most common type is coarse. The rhythm may be regular or irregular, constant or inconstant. Usually it is irregular and inconstant. The effect of rest is not to stop, only to modify. It should, however, not be for- gotten that the tremor of general paresis may assume the Fig. 14. — Exophthalmic goiter. form of an intention tremor. Voluntary movement serves to accentuate and aggravate the tremor. The patient raises a glass of water in either a tremulous or jerky man- ner; if the disease is far advanced he spills the water, but usually only shakes the glass. The ability to draw a straight line is invariably impaired; the paretic hand- writing is typical. The sentence begins with large letters TREMORS 69 and ends in very minute and indistinguishable hiero- glyphics. There is a distinct upward slant to the line, and a tremor is evident on the upstroke of each charac- ter. External and emotional causes exert a great influ- ence. In no tremor is this more evident than in that of general paresis. Any excitement, any stimulation, ag- gravates this tremor. The cardinal signs of general Fig. 15. — Exophthalmic goiter. paresis are of two kinds, physical and mental. On the physical side are the unequal, irregular, and immobile pupils; the abnormal reflexes, either absent, exaggerated, or unequal; the tremor, and the ataxia, both of speech and of movement. On the mental side are either the depression or exhilaration, the irritability, the lack of orientation, and the dementia. 70 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Alcoholic Tremor. — The tremor of alcoholism affects the lips, tongue, face, and hands. It may, in aggravated and long-standing cases, involve the rest of the body. It is fine, but slow. In rhythm it is regular and constant. Rest reduces it, while voluntary movement augments it. A marked feature is the fact that it is more in evi- dence early in the morning than at any other time of the day. Food and drink have a temporary effect of reduc- ing it. In aggravated cases the hands may be so severely affected as to interfere altogether with the patient's ability to raise a glass of water without spilling. The cJ&ffylfa Fig. 16. — Handwriting of an alcoholic. handwriting is tremulous and uncertain, but the patient never omits words or syllables and never adopts the slanting writing so characteristic of paresis. External influences aggravate it. The walk of the alcoholic is fully described in the chapter on Gaits. The cardinal signs of alcoholism are the tremor, the gait, the dilated pupil, the odor of alcohol, and the facies, bloated, cya- nosed, and pasty. Lead Tremor.— The distribution of the tremor in lead poisoning resembles somewhat that of the tremor in alcoholism ; it is more apt to affect the muscles of the hand and face. It may, however, invade the muscles TREMORS yi of the throat and tongue. It may be coarse or fine: usually it is fine, and occurs in the form of fibrillary twitchings. This tremor is exceedingly rare and has no other marked characteristic. The cardinal signs of lead poisoning are the colic, the blue line on the gums, the paralysis, and the presence of lead in the blood. The mercurial tremor is one of the exceptions to the general rule of toxic tremors. It is coarse and jerky. Fig. 17. — Handwriting of a patient suffering from lead tremor. In the beginning of the toxemia it is present on movement, ceasing during rest. Toward the end, how- ever, it is constantly present. The mercurial tremor is a rare condition, not necessarily because the symptom occurs rarely in the poisoning, but because poisoning by mercury, outside of two or three particular occupa- tions, is met with rarely. It occurs especially among mirror-makers, hat-makers, and those who are employed in working silver mines. The distribution, like that of most toxic tremors, is to the face and tongue, later to the extremities and entire body. It is supposed to 7 2 DIAGNOSTIC SYMPTOMS IX NERVOUS DISEASES resemble the intention tremor. It, however, does not, being coarser and more inconstant. Under the topic of toxic tremors mention should be made of the fine tremor which occurs in the later stages of morphinism, in the case of the habitual tea and coffee drinker, and lastly in the case of the cigarette smoker. !#£ Fig. 18. — a, Specimen of handwriting of a patient suffering from chloral and veronal poisoning ; b, specimen of same handwriting three weeks after stopping all drugs. These tremors are all distributed to the hands, especially to the fingers and small muscles of the hands. They are best illustrated by having the patient extend the fingers, or, in the more sensitive cases, by having the ex- aminer place his finger-tips extended and touching those of the patient. Chloral and cocain also present tremors. TREMORS 73 Asthenic tremor is the name applied to the trembling which accompanies prolonged illness in acute and wast- ing diseases. Its distribution may involve the entire body, usually, however, only the hands and the wrists. The rate is rapid and fine, the rhythm fairly regular. Rest modifies but does not stop it, while voluntary move- ment makes it more evident. The patient, as a rule, is too weak either to raise a glass of water, draw a straight line, or walk. If he is strong enough to write, the letters are faulty and very wavy. Any outside influence aggra- vates it. It is most apt to occur in phthisis, in heart disease, and following typhoid. Posthemiplegic Tremor. — The posthemiplegic tremor is distributed over one-half the body, is slow, regular, and coarse. It resembles in appearance the tremor found in paralysis agitans. Unlike that of paralysis agitans, it is diminished by rest and aggravated by voluntary movement. In the aggravated cases the patient is unable to hold a glass of water or to write. The gait is, of course, hemiplegic. Excitement or emotion greatly aggravates it. Tremors from Gross Brain Lesions. — The tremors from gross brain lesions are most apt to involve the arm and leg. They may be fine or coarse, and generally are regular. Rest diminishes but does not stop them, while voluntary movement increases them. The patient raises a glass of water, writes, or walks with great difficulty. The effect of external or emotional influence is slight, except in those cases in which the tremor is hemiplegic in character. The cardinal signs of the accompanying disease are headache, blindness, vertigo, and increasing paralysis. The tremor accompanying tumors of the crus 74 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES and pons is coarse and jerky, while that accompanying hemiplegia is usually fine. Cerebellar Tremor. — Cerebellar tremors generally affect the head and upper extremities. They are most apt to be slow and coarse, and sometimes of the inten- tion type. Neither rest nor voluntary movement seem to have any appreciable effect upon them. They are fairly frequent in occurrence. Wyllie says that a tremor is present in 50 per cent, of the cases. He also calls attention to the fact that the tremors are far more fre- quent when the lesion is on the left side. Fig. 19. — Handwriting of a patient suffering from tic. Hysteric Tremor. — There are hysteric tremors just as there are other hysteric signs. Their distribution may be general, but is most apt to affect the fingers and hands and particular groups rather than particular muscles. They may assume any one of the various types, fine, coarse, intention. Krafft-Ebing has called attention to some in which the tremor resembles that of paralysis agitans. In rhythm they may be regular or irregular. Rest .has a marked effect in quieting their motion, and under sleep they are apt to disappear. They are, as one would naturally suppose, much influenced by excitement, fatigue, and emotion. Voluntary movement aggravates TREMORS 75 them. The patient raises an object with a distinct tremor and writes in an irregular manner. The princi- pal characteristic of the hysteric tremors is the tendency to simulate or mimic some of the others. For that reason they are apt to present considerable difficulty in diagnosis, as only the absence of all organic signs and toxemia can make their presence even suspected. They are apt to appear early in life and as the result of some shock. Neurasthenic Tremor. — The tremor in neurasthenia involves the face and especially the eyelids, lips, and surrounding muscles, less often the hands. It is fine and rapid. The effect of voluntary movement is not considerable, as the patient can carry a glass of water with little disturbance, and the handwriting is not diagnostic. There is nothing unusual about the gait. The effect of an external or emotional influence upon this tremor is to increase it. This form is most apt to occur in one who is overworked or tired. Emotional Tremor. — The emotional tremor is most apt to involve the extremities, especially the legs and knees. It is slow— unusually so — and fine, but regular. Rest brings it to a standstill, while voluntary movement only serves to accentuate it. The patient evinces but slight trembling when he raises a glass or writes, but shows the greatest difficulty when he attempts to walk. This tremor is most often seen in after-dinner speakers, lecturers, and performers. Fear and emotion are its principal causes. Hereditary Tremor. — The hereditary tremor is most apt to affect the head and arms, especially the latter. It is rapid, fine, and regular. It is not affected by either 7 6 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES rest or voluntary movement. If the distribution in- volves the arms, the acts of raising a glass of water or of writing display only a slight irregularity. The gait is normal. External and emotional influences have little effect upon this condition. The hereditary tremor has no discoverable cause beyond the fact that it has Fig. 20. — Attempt on the part of a patient suffering from Friedreich's ataxia to write New York. been handed down through se\ T eral generations. It may appear at an early age — twenty. Graupner has re- ported the history of a family in which two brothers, a sister, and a niece were all afflicted with a tremor. In these people the distribution was chiefly restricted to the arms. The point to bear in mind in regard to the Fig. 21. — Specimen of handwriting of Friedreich's ataxia. so-called hereditary tremor is that it does exist, that it may assume different types in different families, and that, although it is most liable to affect the arms and head, that it may affect any part of the body, and that it may be transmitted through several generations. TREMORS 77 Senile Tremor. — In the early stage senile tremor is limited to the head; as it advances, the tremor in- volves the entire body. It is slow, fine, and regular. Rest does not affect it; voluntary movement always aggravates it, especially as it progresses. The handwrit- ing is irregular and small, and a glass of water is raised in a very slow and tremulous manner. External and emo- tional influences increase it. The senile tremor develops late in life, rarely making its appearance before the sixth decade. It differs very much from the tremor of paraly- Fig. 22. — Handwriting of a patient suffering from senile tremor. sis agitans, as in senility the hand moves separately and not with the forearm. Simple Tremor. — Apart from all the previous types of tremor there still exist isolated instances in which tremor is the only symptom. It may be fine or coarse, and its distribution is most apt to be in the hands. I have known of an instance where the patient was per- fectly well, and was a hard-working professional man in this city. His heredity was excellent. There was absolutely no history of any toxemia or infection. At about fifteen he developed a tremor coarse and dis- tributed to the right arm. He has now had this tremor for twenty-five years, and at no time in that long period has he had a sick day, or in any way developed any other physical sign or even indication of any nervous or de- 78 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES generative condition. There was no hereditary tremor in his family. The characteristic of the simple tremor seems to be that it neither advances nor gets better. Others have reported similar instances, so that there can be no question of the fact that a condition similar to the simple tremor does exist. The fibrillary twitchings which are seen in some of the wasting diseases are divisions of the fine tremors. These are very fine in character, rapid, and affect certain groups of muscles or certain portions of muscles. These twitchings are symptoms of wasting muscle tissue, and are directly traceable to those muscles whose centers in the anterior horns are degenerating. They therefore occur with great frequency in diseases of the lower motor neuron type. They can best be produced by tap- ping the muscles. Fibrillary tremors are fine twitchings which are dis- tributed to a particular portion of the body or td a particular muscle. They are usually devoid of rhythm and are irregular. They are inconstant and not affected by emotional or external influences. External stimula- tion, in the form of blows and cold, or, better still, slight tapping with the finger, will best produce them. They too indicate a disease in the motor cells which control the muscle. Fibrillary tremors occur in: i. Progressive muscular atrophy. 2. Syringomyelia. 3. Chronic poliomyelitis. 4. Tabes. 5. Sciatica. 6. Health following excesses. TREMORS 79 7. Emaciated persons under the influence of cold. 8. Neurasthenic persons. 9. Bulbar palsy. The classification of tremors into two divisions has still further advantages. It enables the student at once to arrange and to arrange systematically all those diseases in which tremor is a symptom. It is possible because the presence of either of these tremors conveys particular and especial information. The following table cites the num- Fig. 23. — Handwriting of a patient suffering from acute chorea. ber of variations per second of the different types of tremor^ as made by different observers : Paralysis agitans 3 to 7 per second Wilkinson Senile 4 to $yi per second Dana Hysteria 5K to 7^ per second Ma\-ie Graves's and alcoholic . . 8 to 9 per second Dana Neurasthenia 10 per second Dana A. A coarse tremor means only one thing — organic disease. There are one or two exceptions to this, as the tremor of mercurial poisoning is coarse, and the tremor of 8o DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES general paresis and hysteria may be coarse or fine. As a general rule, however, the presence of a coarse tremor indicates an organic disease. The organic diseases in which the coarse tremor appears are: paralysis agitans; general paralysis; multiple sclerosis; tumors of the brain. B. A fine tremor, on the other hand, means two things: i. Functional disease. 2. Toxic disease. The functional diseases in which the fine tremor occurs are neurasthenia and hysteria; and the toxic Fig. 24. — Handwriting of a patient suffering from Huntington's chorea. diseases are Graves's disease, alcoholism, metallic poison- ing (except mercury), drug poisoning. Division of Tremors as Regards Repose and Movement of the Limbs (Wilkinson) 1. Tremors present during repose ceasing during movement (tremor of paralysis agitans). 2. Tremors ceasing during repose present during movement (tremor of multiple sclerosis; brain lesion; others at a very early stage). 3. Tremors present during repose exaggerated dur- ing movement) senile; asthenic; hysteric; al- coholic). CHAPTER V TROPHIC DISORDERS The word trophic is from the Greek rpo^-f], and sig- nifies nourishment or nutrition. The trophic disorders are, therefore, disorders of nutrition. They are not diseases, but symptoms — symptoms which may affect any part of the body — the skin, the mucous membrane, the muscles, the joints, and the bones. The explanation of these disorders is somewhat obscure. They are closely related to the vasomotor apparatus, and no doubt some of them are connected with and modified by the mechanism of the latter. The most probable, as well as the most general, causes, however, lie in an interference with the nutrition of the centers. Starr explains it best when he says: "The central gray matter controls the nutrition of the muscles. Under certain conditions the ordinary sensory impulses are interfered with or perverted, and they, lacking their accustomed guide to repair, and misled by normal impulses, produce effects which are needless under the circumstances, or fail to produce those which ordinarily would be required." There are centers which preside over the nutrition of the various structures of the body. These are called trophic centers. They, together with the peripheral nerve and its termination, are responsible for the nutri- tion of the skin, muscle, nerve, joints, and bone. Any injury, therefore, which is inflicted upon the cells in the 6 81 82 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES anterior horn of the spinal cord and its efferent fiber will Fig. 25. — Charcot joint, showing retroflexion. be reflected in the nutrition of these various structures of the body. The distribution of the trophic disorders is of two TROPHIC DISORDERS 83 kinds. It may be general or local, that is, the disorder may be of such a type as to involve either the entire body or parts of it, or may be so localized as to follow the distribution of a given nerve or root, or some segment of the brain or spinal cord. I have arranged these trophic disorders under three headings — atrophy, hypertrophy, and dystrophy, and then I have placed in a list under each of these headings the various structures of the body from without inward, as skin, muscles, joints, bones. Atrophy The atrophies are as follows: 1. Of the skin: (a) Multiple neuritis. (b) Scleroderma. (c) Leprosy. 2. Of the muscles: (a) Progressive muscular atrophy Poliomyelitis. (b) Paralyses 2. Hemiplegia. 3. Facial palsy. 4. Birth paralysis. 5. Bulbar paralysis. (c) Syringomyelia. (d) Tumor of the cord. (e) Tabes. (/) Multiple neuritis. (g) Secondary to inflammatory joint disease. {h) Injury to nerves or joints. (i) Leprosy. (/) Hysteria. (k) Multiple sclerosis. (/) Myxedema. 84 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 3. Joints and bones: f 1 . Birth palsy. (a) Paralyses in children \ 2 . Cerebral palsy. (3. Poliomyelitis. (b) Cretinism. (c) Progressive muscular dystrophy. 4. Of the nervous system: (a) Optic nerve. (b) Simple atrophy of nerve-fibers after injury to peripheral nerves or tracts, or of tracts in pri- mary spinal cord diseases. Muscular Atrophy. — Under the heading muscular atrophy a few variations exist which are of sufficient importance to merit mention, and of sufficient value in differential diagnosis to warrant study. These are progressive muscular atrophy, poliomyelitis, and tumor of the cord. In progressive muscular atrophy the wasting begins in particular groups of muscles. It may be in the muscles of the shoulder, of the neck, or scapula, or those of the hips or legs, but usually it begins in the small muscles of the radial side of the hands. The characteristic of this type is to jump from one group to another — not to progress from one muscle to the next. Thus, the atrophy may begin in the small muscles of the hand, skip those of the forearm and upper arm, and then affect the neck or shoulder group. The condition continues to progress and eventually involves the entire muscular system; not only does it involve the entire muscular system, but also it involves the entire muscular system to a marked degree — to so great a degree that the muscles become mere strands. TROPHIC DISORDERS 85 1 \ The atrophy in poliomyelitis differs in many respects from that of progressive muscular atrophy. Its onset is rapid and sudden; it does not jump from one group to another. The most striking difference, however, is in distribution. This fol- lows the segmental in- volvement in the cord and therefore results in an atrophy involving groups of muscles. As the spinal cord involve- ment may be extensive or slight, so may the atrophy affect one or sev- eral groups of muscles. It may affect any group, but most com- monly those of the cer- vical or lumbar enlarge- ment. The atrophy in tumor of the spinal cord is wholly dependent upon the loca- tion and extent of the lesion. Inasmuch as all muscles receive nourish- ment and supply from more than one segment of the cord, the extent of atrophy depends upon the vertical extent of the tumor. The distribution usually involves an entire extremity. The atrophies in tabes are divided by Marie into two Fig. 26. — Late symmetric atrophies in tabes. 86 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES classes: (i) The early and (2) the late. 1. The early forms present small localized and unilateral atrophies, in which there occur fibrillary twitchings and sometimes the reaction of degeneration. 2. The late atrophies are symmetric, appear late in the disease, and do not present the reaction of degeneration. Bones and Joints. — In both birth and cerebral palsies there is an atrophy of the bones and joints. The bones of the paralyzed limb are smaller and shorter, and, as is proved by the #-ray, the joints less well developed. In poliomyelitis the same atrophy has been shown. The Haversian system of the bones of the affected side is less well developed, the bones are smaller, and the joints contracted. The cretin displays diminished physical attributes as well as mental. The joints and bones are undersized. Hypertrophy Of the Skin: (a) In many skin diseases, as ichthyosis, etc. (b) Elephantiasis. (c) Myxedema. (d) Syringomyelia. (e) Brittle, ridged nails, as in syringomyelia and traumatic neuritis. Of the Muscles and Subcutaneous Tissue: (a) Adiposis dolorosa. (b) Elephantiasis. Of the Joints and Bones: Acromegaly and gigantism. Of the Nervous System: (a) Leprosy, in the ulnar nerve. (b) Elephantiasis. TROPHIC DISORDERS 87 Dystrophy or Mixed Atrophies and Hypertrophies and Vascular Lesions 1. In the Skin: (a) Bed-sores: 1. Multiple neuritis. 2. Tumors of the brain. 3. Tumors of cord. 4. Hemorrhage in brain or cord. 5. Syringomyelia. 6. Myelomalacia. 7. Meningitis of brain or cord. 8. Delirium tremens. 9. Any restless state where there is need of restraint. 10. Torticollis (on ear). 11. Fracture of the spinal column. (b) Raynaud's disease: 1. Anemias. 2. Hysteria. 3. Epilepsy. 4. Tabes. 5. Neurasthenia. 6. Myelitis. 7. Insanity, especially acute mania. 8. Urticaria. 9. Angioneurotic edema. 10. Scleroderma. 11. Trauma. 12. Influenza. 13. Grief. 14. Fatigue. 15. Fright. (c) Perforating ulcer of the foot: 1. Tabes. 2. General paresis. 3. Leprosy. 4. Paralysis of sciatic nerve. 88 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES (d) Gangrene in syringomyelia, neuritis of any form, hysteria. (e) Erythromelalgia. ) Pemphigus. ) Edema. i. Generalized. 2. Localized. (a) Angioneurotic edema. (b) Blue or white edema of hysteria. (c) Localized areas of hard edema. (//) Change in color of the hair: i. Generalized. 2. Localized, as in change in one eyebrow, or in beard following neuralgia. (J) Zoster. (/') Keratitis: i. Sciatica. 2. Spondylitis deformans. 3. In neuritis of ophthalmic branch of trifacial in trifacial neuritis. 4. Tumors of brain. (k) Whitlows — small abscesses in syringomyelia. (I) Ulcers in mucous membrane of mouth and nose, in trifacial paralysis. 2. In the Muscles: (a) Spinal form of progressive muscular atrophy (the Aran-Duchenne type). (b) Hereditary form (the Wernig-Hoffmann type) (c) Dystrophy. (d) Erb's juvenile form of dystrophy. (e) Facio-scapulo-humeral type of Landouzy-De- jerine. (/) Peroneal or leg variety of Charcot-Marie-Tooth. (g) Myotonia congenita — Thomsen's disease. 3. In the Joints and Bones: (a) Arthropathy or Charcot joint in tabes and syringomyelia. TROPHIC DISORDERS 8 9 (b) Spontaneous fractures and osteoporosis in tabes, syringomyelia, and progressive muscular dys- trophy. (c) Scoliosis in syringomyelia. (d) Gigantism in pituitary disease. Fig. 27. — Charcot knee, showing abduction at knee -joint. (e) Falling out of teeth in tabes, trifacial palsy. (/) Joint swelling in multiple neuritis, myxedema, and hemiplegia. 4. In the Nervous System: (a) Choked disc. (b) Myelitis, encephalitis, and compression myelitis. (c) Neuroretinitis. 90 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Perforating ulcer of the foot is one of the common trophic changes. It is one of the leading symptoms of tabes. Usually it is located in the plantar surface of the foot or the heel. It begins as a small corn. There is a slight discharge; a sinus is formed, and eventually a suppurating tract leads down to the bone of the joint. It is painless. The condition is almost impossible to heal. A perforating ulcer may also affect the mouth or the region of the buttocks. Diseases in Which Perforating Ulcer is Found i. Tabes. 2. Syringomyelia. 3. Leprous neuritis. 4. Injuries to posterior tibial nerve. 5. Traumatic neuritis of sciatica. 6. Tumor of the cord (sacral region). 7. Progressive muscular atrophy (Charcot-Marie- Tooth). Aran-Duchenne is the name applied to that particular group of cases of progressive muscular atrophy in which the small muscles of the hand are first affected. Later the condition spreads and finally involves the entire body. The affected muscles show the characteristic symptoms of fibrillary twitchings, wasting, and reaction of degeneration. Wernig-Hoffmann is the name applied to that type which begins in infancy and rapidly proves fatal. It involves first the muscles of the hip, then those of the back and abdomen, and finally those of the neck and shoulders. It is sometimes called the infantile type. TROPHIC DISORDERS 91 Erb's juvenile type is the name applied to that variety which appears in youth and tends to affect several mem- bers of one family. It first involves the arms and shoul- ders. Landouzy-Dejerine is the name applied to that variety Fig. 28. — Progressive muscular atrophy (Aran-Duchenne type). which affects the face as well as the arm and shoulder muscles. This is the one type in which the facies present a characteristic appearance. Charcot-Marie-Tooth is the name applied to that variety which affects the peroneal muscles. From the peroneal 92 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES group it advances upward, involving first the muscles of the calf, then of the thighs, and finally may extend to the trunk and arms. Myotonia congenita is the name applied to a rare condition first described by Dr. Thomsen. It is char- acterized by the development of tonic cramps when the patient attempts any voluntary movement. It is also a hereditary family condition. Trophic disorders of the joints may be of several types. The larger joints are those most apt to be affected, the knee and shoulder especially. These dis- orders may extend from a slight affection to the typical Charcot joint. They are found more often in female patients than in male. The most common and usual type is first a slight effusion without pain, from which the patient recovers, to be followed after a few weeks by another effusion, somewhat larger and more lasting, which then shows a weakness of the muscles and struc- tures, and then, with the aid of the #-ray, demonstrates a complete disintegration and destruction of the joint, surface lining, and structures. Charcot was the first to describe these joints. He divided them into two classes — the atrophic and the hypertrophic. In each the destruc- tion of the joint is complete. The fluid is, as a rule, serous, but in a few cases may be mixed with blood. The #-ray is of considerable value in diagnosing these arthropathies, and should always be used; it enables the examiner to differentiate between the simple effusion and a typical Charcot joint. In the latter the £-ray shows the destruction of all the tissues, including the bone, and admirably displays the condition which Church describes as a "bag of bones." These Charcot joints TROPHIC DISORDERS 93 Fig. 29. — Charcot wrist in tabes. Fig. 30. — Charcot wrist in tabes. 94 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES are typical of locomotor ataxia and syringomyelia. In the former disease they assume enormous proportions. Though the larger joints are those most commonly affected, those of the foot, the fingers, wrist, and elbow may be involved. The mobility of the joint approaches the type of pivot joint, and the swing is always pain- less. The starting-point of these Charcot joints is diffi- cult to indicate, although a careful examination often shows a slight traumatism near the joint involved. Therefore, always bear in mind that a sufferer from a spinal cord disease ought to take special care not to injure, even in the slightest way, an extremity or a joint. In hemiplegia, in addition to these Charcot joints, slight swellings appear. They differ from the typical Charcot joint in being painful and reddened. They neither appear with such rapidity nor reach such enor- mous dimensions. Finally, the hemiplegic joint changes are not destructive. Hysteria presents joint changes. These differ from the Charcot joints and the hemiplegic joints in that they are exceedingly painful. There is rarely any effusion. The Trophic Changes in Bones. — The trophic changes in bones can be classified under three headings : i. The tendency to interference with the growth of bones. 2. The hypertrophy of bones. 3. The tendency to fracture. The hypertrophy is especially illustrated in condi- tions of acromegaly; the tendency to fracture of the bone is seen in cases of tabes and syringomyelia. Here there is an unusual brittleness, so that a misstep or undue strain may often precede a fracture of one of the long bones. CHAPTER VI GAITS In neurology no subject is more interesting and none more brilliant in results than the study of gaits. The text-books ordinarily assign a very small space to the subject; most of them content themselves with saying that the gait is a leading symptom in diseases of the spinal cord. They then dismiss the subject with two or three paragraphs, or, at most, half a page. As a matter of fact, not only is the gait a leading symptom of diseases of the spinal cord, but it also occurs with affections of the brain, peripheral nerves, and even functional condi- tions. The student will find that he is amply repaid for the time he devotes to this subject. A man's gait is his manner of walking, together with his carriage. In studying the gait of a patient, there- fore, it is necessary to analyze two facts — his walk and his bearing. In analyzing a gait it is necessary first to decide whether the walk and carriage are normal or abnormal; second, if abnormal, in what respects; third, to what distribution the abnormality extends. For in- stance, a man may be lame in that he drags one foot and holds stiff one arm, whereas another man may be steady in both legs and lurch with his entire body. A gait, therefore, may be abnormal in respect to: i. The body. 2. The arms. 3. The legs. 95 96 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 4. The feet. 5. The steps. And in each instance so far as affects the — (a) Attitude. (b) Position. (c) Control. Before taking up the abnormal gaits, it is first neces- sary to understand what should be the gait of a normal individual. The normal gait attracts no attention: the body is erect, the head straight, the arms hang gracefully at the side, while the legs move regularly and evenly. The feet are slightly everted; the steps of even, moderate length. The shoes should wear out at the heel, showing that the heel tends to touch the ground first. The method to pursue in examining a patient's gait is, first, observe his entrance into the room — a patient will walk more naturally on his first introduction than a moment later, when he is conscious of being examined; second, have him walk forward and then backward; third, have him walk in these directions with his eyes shut; fourth, test his ability to stand erect with eyes closed — this is the test to which has been assigned the name Romberg; fifth, have him walk a straight line on the floor, or, in the event of its being a carpet, have him follow the pattern; in this effort one foot should be placed directly in front of the other, and so close that the heel and toe touch each other. This last test is, of all, the most important. A patient may be able to walk well, so well that even a very careful observer will fail to detect any abnormality. When, however, he essays the final and more delicate test of placing one GAITS 97 foot directly before the other so that heel and toe touch, the failure may be absolute. To execute this task suc- cessfully a man must be in every sense master of himself. Only the normally gaited man can correctly heel and toe a line. In observing the patient, carry out this test with great care: note carefully the particular crack or line on which the patient begins, as frequently he ends on one considerably to one side of this. In an ataxic gait often the first evidence is that, in attempting to heel and toe a line, the patient will succeed in carrying out the exercise, but will bring up at the end of the room on a line which is wholly different, and considerably removed from the one on which he started. Another practical way to test a man's gait is to ob- serve the wear of his shoes. One gait will wear down the toe, another the outer side, while the third, from the fact that it has so completely incapacitated the patient, will leave the shoes scarcely worn at all. Observe at which point occurs the greatest friction, and at which point the friction is least. There are eleven gaits which are important. A list of them follows: i. The ataxic. 2. The hemiplegic. 3. The steppage. 4. The spastic. 5. The clumsy. 6. The cerebellar. 7. Festination. 8. Staggering. 9. The gait of hysteric conditions. 10. The gait of arteriosclerosis. 11. The normal gait. 7 98 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES i. The ataxic gait is very common. It is character- ized by an attitude of uncertainty, with a lack of con- trol and a characteristic position of the body. The legs are uncertain. They are under poor control and are held far apart. This latter posture is followed in order to restore the disturbed equilibrium. The method of using the feet is unusual. They come down with a distinct stamp. The steps are uncertain, and of irregular length. The body sways and seems powerless to control the legs. The position of the head and eyes is unusual, as the patient follows the steps with great care. The legs, therefore, give the appearance of running away with the body. In the advanced cases the patient walks with a cane. In this gait the shoes, as a rule, show little wear. It is well to bear in mind that the lame man whose shoes appear in the best of condition and well kept is usually an ataxic. The attitude of the body is one in which the patient leans forward, usually resting on a stick, while at the same time the entire body sways. This uncer- tainty of carriage may extend to the upper parts of the body, or may involve only the legs. The principal features then of the ataxic gait are un- certainty, irregularity, and the stamping step. An ataxic can often be heard before he is seen. He is recognized by his stamp and his stick. The diseases in which the ataxic gait occur are: 1. Locomotor ataxia. 2. Combined posterolateral lesions. 3. Some forms of spinal syphilis. 4. The ataxic type of multiple neuritis. 5. Internal ear diseases. 6. Tumors of the frontal region of the brain. GAITS 7. Ataxic paraplegia. 8. General paresis. 9. Friedreich's ataxia. 99 Fig. 31. — A tabetic reeducating his gait. IOO DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 2. The hemiplegic gait is one of those in which but one leg is affected. The others are the steppage gait and the gait of hysteric hemiplegia. The hemiplegic gait is characterized by the very word to which it owes its name. Hemiplegia means the paralysis of one-half, and the hemiplegic gait is one in which is evident the symptoms, the physical signs, and the characteristics of a paralysis of one-half of the body. The affected leg is rigid. It moves wholly with the body, and not as an independent member. It rotates outward, swinging in a semicircle first from and then toward the trunk. The shoes are worn on the outer side. The affected half of the body is rigid, weak, and paralyzed, so that the patient leans toward the affected side. The arm is held in a characteristic position of semiflexion and rigidity. There is evident a slight asymmetry of the lower two- thirds of the face, with an expression of anxiety and dis- tress. This gait is best described by the word semicir- cular, or swinging. It is accompanied by exaggerated reflexes and steps which are regular and uncertain. The toe and whole side of the foot scrape along the floor. The patient often limps. At a distance he presents a twofold appearance of one who is lame and one who is walking in an uneven way, or, rather, in a one-sided way. The excursion of the affected foot is best illustrated by an inverted letter (Q). As in the ataxic gait, the sufferer from the hemiplegic walk can be heard before he is seen. The noise is regular, rhythmic, and grating. The principal features of the hemiplegic gait are rigidity and the side-wheel motion. Other names for the hemiplegic gait are the paralytic Fig. 32. — Diagram showing excursion of affected foot in hemiplegia. Case of hemiplegia of long duration. The right foot is turned out and drags distinctly (unfortunately the illustra- tion has been retouched and does not show this). The steps are uneven and there is occa- sional staggering. (From Posey and Spiller's "The Eye and Nervous System," J. B. Lip- pincott Co., Publishers.) :'; GAITS I OI and apoplectic. The conditions in which the hemiplegic gait occur are: 1. Apoplexy, embolus, thrombosis, or hemorrhage. 2. Tumor in the motor area. 3. General paralysis. 4. Paralysis agitans. 3. The Steppage Gait.— The step- page gait has many names. It is called the equine gait, the drop-foot gait, and, incorrectly, the alcoholic gait. It is sometimes called the high- step or horse-gait. The cause of the steppage gait is paralysis of the ante- rior tibial group of muscles; the feet are therefore dropped, the toes drag, and, in order successfully to clear the ground, the patient is of necessity obliged to raise the legs, and espe- cially the knees, sufficiently high to permit the overhanging or drop toes to clear the floor. The body is not affected. [The steps are regular and of normal length; the toes, even when the legs are raised, usually scrape along the floor, or, if j ■' 102 DIAGNOSTIC SYMPTOMS IX XERVOUS DISEASES the patient is unable to raise them sufficiently high, they come down with a rhythmic, flop-like noise. The two legs are. as a rule, equally affected. The wear of the shoes in this gait is unusually characteristic : as a result of the con- stant scraping and friction upon the toe-pieces, the two shoes are worn out equally at the toe. in a sharp, clean- cut manner, as though cut with a razor. The principal features, then, of the steppage gait are high knee action. Fig. 33. — Shoes of the steppage gait (worn at toes). sound of flopping, and characteristic wear of the shoes. The best description of the steppage gait is embodied in the description of the motion of a high-stepping horse. The diseases in which the steppage gait occur are : 1. Multiple neuritis. 2. Nerve lesions involving the nerves supplying the anterior tibial group of muscles. GAITS IO3 3. Poliomyelitis. 4. Progressive muscular atrophy. 4. The Spastic Gait. — The spastic gait is very diffi- cult for the student to recognize. He invariably con- fuses it with the ataxic. It is, however, quite different. The spastic gait rarely affects the legs alone. The attitude of the patient is equally involved. It is a general attitude of stiffness, with a tendency to lean forward. The legs are slightly bent at the knees and decidedly bowed forward. The legs are adducted, with the knees almost overlapping, and the feet inverted; the steps are regular, but very short. The feet can with great difficulty be raised from the floor; the patient hardly walks at all: he shuffles. The feet scrape along the floor, so that the shoes wear out on the front part of the soles, but not at the toe nor in so clean-cut a way as in the steppage gait. The patient is so stiff and incapacitated that he moves slowly, advances with difficulty, and presents the general picture of an old man creeping. This is the gait to which the layman has given the name " creeping palsy." The distinguishing features of the spastic gait are easy to remember. Each begins, like the word spastic, with the letter "s": stiffness, slowness, scraping, and shuffling. The diseases in which the spastic gait occur are: 1. Primary lateral sclerosis. 2. Disseminated sclerosis. 3. Combined sclerosis. 4. Amyotrophic lateral sclerosis. 5. Hereditary spastic paraplegia. 6. Spastic paraplegia. 104 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 7. Syringomyelia. 8. General paresis. 9. Compression myelitis. 10. Spinal meningitis. 5. The Clumsy Gait. — The clumsy gait is also known as the sailor gait. Oppenheim admirably describes it by the one word "waddle. " The clumsy gait is remark- able for the splendid appearance of the legs. To all out- ward appearance they possess enormous strength, and display unusual muscular development. Their manage- ment develops a very great degree of clumsiness. The attitude of the body is straight; in fact, unusually so. The patient tends to lean backward in order to retain his balance, and the back is hollowed out, with the abdomen unusually prominent; the general carriage is haughty. The muscles controlling the legs are weak and inefficient. As a result of this, those of the trunk are brought into play, and it is they which raise and propel the patient. The gait is, therefore, a rolling one; it reminds one strongly of the efforts made by a man to raise himself by his own boot-straps. The patient rolls from side to side in sailor-like fashion. The steps are a little uncertain, but regular; although in the clumsy gait it could almost be said, with much truth, that there are no steps at all, as the patient progresses entirely from the hips, and with the aid of the trunk muscles. The principal features of the clumsy gait are the splen- did appearance of the legs, together with the clumsy use made of them, and the added aid produced by the mus- cles of the trunk. The word to remember in connection with this gait is "waddling." The conditions in which the clumsy gait occurs are the muscular dystrophies. GAITS 105 In myxedema sometimes there occurs a slow, clumsy gait. 6. The Cerebellar Gait. — To the cerebellar gait is com- monly applied the word ataxic. It is a form of ataxia, however, which has distinct characteristics, and a form of ataxia which differs wholly from that seen in tabes and neuritis. The student, therefore, should consider this gait as one apart from, and in no way connected with, the ataxic gait. The cerebellar gait is characterized i by great unsteadiness, great irregularity, and a marked \ tendency to reel to one side. At rest or lying down, the patient does not suffer from ataxia. The moment, how- ever, that he raises himself, he becomes dizzy, and again, when he undertakes to make use of his legs, the infirmity is apparent. The stamping so characteristic of the gait in tabes is absent. The steps are less uncertain, but, if anything, more irregular. On the other hand, in walking, the sway of the body is greater. The best way to em- phasize the difference between these two forms of ataxia is by the following statement made by Wyllie: "In the tabetic type of ataxia the legs give the appearance of running away with the body; in the cerebellar type of ataxia the legs give the appearance of being run away with by the body." Finally, it should never be forgotten that in cerebellar ataxia the patient suddenly, unexpectedly, without any warning, will display the tendency to reel to one side. This is never present in the tabetic ataxia. This gait is sometimes spoken of as the cerebellar reel or stagger. The patient does reel, and the mode of walk- ing does suggest the stagger seen in the alcoholic more so than in any other gait. It is, however, only confusing to 106 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES the student to use the words reel and stagger in describ- ing the cerebellar gait. It is best to keep them for use in describing the gait of the drunkard. In the cerebellar gait the patient keeps his feet far apart, is very liable to stumble and to run amuck. It is not so much that the legs are uncertain, stiff or irregular, as that the body suddenly and persistently turns to one side, and tends to run away with the legs. The distribution of the ataxia is, neither in the cere- bellar nor in the tabetic type, limited to the legs. In the tabetic type it is, however, apt to involve only the legs; in the cerebellar type, it is more apt to extend to other parts. The attitude in the cerebellar ataxia is sufficiently marked to warrant studying, and to deserve a name of its own. It has been given the name of the "cerebellar attitude." The head is held high and retracted; there is marked rigidity of the cervical muscles, and one shoulder is higher than the other. If the patient is reclining, the attitude is even more characteristic. He is apt to lie on one side in an attitude of general flexion and rotation, with the head turned laterally, the chin elevated and pointed to one shoulder. The back of the head is, there- fore, somewhat lower than the chin.- Wyllie, in speaking of the cerebellar attitude, says that in most cases in the standing position there occurs a distinct lordosis; in the reclining position, a distinct tendency to work toward the edge of the bed. The principal features, then, in the cerebellar gait are the great irregularity, the lateral reeling, and the typical attitude. The diseases in which the cerebellar ataxic type of gait occurs are : GAITS 107 1. Diseases of the cerebellum. 2. Diphtheria. 3. Disseminated sclerosis. 4. Friedreich's ataxia. 5. Diseases of the frontal and quadrate lobes. 6. Diseases of the cerebral cortex. 7. Bulbar softening. 8. Diseases of the crus cerebelli. 9. Myelitis, early stages. 7. The Gait of Festination. — Festination is a good Eng- lish word, but one that is obsolete. It means hastening, hurry. It is derived from the Latin festinatio, which means a hastening, haste, or speed. In the description of gaits, it is applied to that particular gait in which the patient makes haste, the gait in which he hurries. In a word, it describes that gait in which the patient practises festination. In the gait known as festination the patient has one of several characteristic attitudes, in which he leans either forward, backward, or sideways. The legs move more and more rapidly, while the steps become shorter and faster. The general appearance is that of a prematurely old man, bent with age, who is trying, so to speak, to run after his own center of gravity, and is hurrying either forward or backward. Rigidity is the conspicuous char- acteristic. To so great a degree is the rigidity evident that the patient appears immobile, like one carved from stone and devoid of expression. The folds of the face are obliterated, the play of the muscles absent, the facies statuesque. The man with festination is said to have a mask-like countenance. The shoulders are stooped; the hand presents the appearance of one bent to write, while IOS DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Fig. 34. — Attitude of paralysis agitans. GAITS IO9 the whole body trembles violently in the advanced cases. The legs, stiff and bent at the knees, are also the seat of a constant and marked coarse tremor. The feet barely leave the ground, so that the steps are of necessity short and shuffling. The patient rises slowly and with great difficulty; he turns deliberately, and for a moment pauses, then he lurches forward, takes his short step slowly, and forthwith begins to hurry. He shuffles, at first slowly, then more rapidly, and at last he runs. This is the gait known as festination. The distinguishing features are rigidity, shuffling, and hurry. The disease in which festination occurs is paralysis agitans. 8. The Staggering Gait. — The staggering gait is pre- eminently the gait of the alcoholic. It is the gait which one sees in the drunkard on the street. The patient totters, he reels, he leans now forward, now backward, now to one side, and now to the other. He lurches in- discriminately. To the onlooker, at each movement he seems to be on the verge of losing his balance and falling, yet he just recovers himself and rarely, except in the most aggravated cases, does fall. There is almost no control over either body or legs. The feet are unsteady, the steps irregular and uncertain. The staggering gait invariably carries with it a physiog- nomy which portrays the drunkard and libertine. This type of gait differs from the cerebellar form of ataxia in that the patient may reel in any one of many directions. It differs from the spinal type of ataxia in that the patient neither follows his feet with the eyes nor presents the stamp which is so characteristic of the gait of locomotor ataxia; it differs from the gait of festination in not having IIO DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES the rigidity, the tremor, and the characteristic hurry; it differs from the spastic gait in that it lacks the stiffness, the scrape, and the shuffling movements; it differs from the clumsy gait in lacking the heaving or lifting motion, the sailor-like roll, and the marked use of the trunk muscles; it differs from the steppage gait in the absence of any paralysis, any high steppage, and any drop-foot. There is no characteristic wear to the shoes of the drunk- ard. The principal features, then, of the staggering gait are the wide diversity of excursions, the marked reeling, and the great degree of general ataxia which is evident in every position and motion. The diseases in which the staggering gait may occur are : i. Acute alcoholism. 2. Multiple sclerosis. 3. Cerebellar disease. 4. Brain tumors. 5. Multiple neuritis. 6. General paresis. 9. Hysteric Gaits. — The hysteric gait may be of three types, according as to what part is involved in the func- tional paralysis. There may be a monoplegia, a hemi- plegia, or a paraplegia; the gait will of necessity vary in each instance. If a monoplegia, as a rule the foot will be more affected than the leg; if a hemiplegia, the facial mus- cles and those of the trunk usually escape; if a paraplegia, there are almost invariably contractures and marked incapacity. The characteristics of the hysteric gaits are sudden development, complete paralysis, and preserva- tion of automatic movements. There may be contrac- tures or the paralysis may be flaccid. There is no marked rigidity, and under sudden stress the patient may invol- GAITS III untarily use the paralyzed limb. In the monoplegic the foot does not leave the ground : it is dragged ; in the hemi- plegic the leg is dragged, the sole again not leaving the ground; in the paraplegic, it being manifestly impossible for the patient to drag both legs successfully, resort is had to a crutch. The type which is most apt to develop contractures is the paraplegic. Oppenheim describes the gait as that of a child walking on stilts. In the hysteric paralyses there are apt to be, associated with the paralysis, stigmata and marks of degeneration. The gait of hysteric hemiplegia differs from that of organic hemiplegia in that it lacks the characteristic de- formity, the typical side-wheel motion, and in that it presents a more completely paralyzed limb. Usually the leg hangs like a flail, and either is completely raised from the ground or else the sole never leaves the floor. If the latter, the patient drags the leg behind as though held by ball and chain. The unaffected leg is perfectly normal. In this gait therefore there can hardly be said to exist an abnormality of step. The body as a rule leans toward the affected side. The principal characteristics of the hysteric gaits are: i. Complete palsy. 2. Drag-foot. 3. Ability to use the limb in emergency. These gaits occur only in hysteric paralyses. Astasia-abasia is really one of the forms of hysteria. The leading characteristic in this condition is inability of the patient to stand or walk, while yet possessing in every other movement perfect control of the legs. In bed, in the sitting posture, even in the position of crawling, the patient is able to make perfect use of the legs. When, 112 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES however, he begins to walk, there results complete failure. The first few steps may be taken in the normal way, then they become slower, and in a very few moments cease altogether. The patient's expression is one of anxious distress and fear. He looks about for help, rubs his legs, tries to lift them, and finally in sheer desperation and discouragement gives up and drops to the floor. The condition is rare. 10. The Gait of Arteriosclerosis. — There is still one more gait different from all the others, yet not particu- larly distinctive in character. This is the gait of arterio- sclerosis, sometimes called the senile gait. The patient complains of difficulty in walking, yet without being able to define exactly what is the obstacle. The legs are weak, the steps irregular, but not necessarily ataxic. There is unexpectedly a halting. The patient feels unable to ad- vance. Each step appears to increase the difficulty. Or, again, the halting may be absent and the patient may be able to advance, yet the legs simulate a scissors-like movement, or the feet so interfere one with the other as to render progress practically impossible. There is no gait in which the patient is more conscious of his infirmity and more sensible of his disability than in the gait of ar- teriosclerosis. The attitude which accompanies this gait is one of old age, with its attendant slowness and rigidity. The blood- pressure is high, the circulation weak, and there is every evidence of beginning senility. It is always well to re- member that this gait is rarely seen in a man under fifty; in other words, the gait of arteriosclerosis, like the gait of festination, is generally an accompaniment of gray hairs. The reverse is true of the ataxic gait. GAITS 113 11. The Normal Gait. — The normal gait has been suffi- ciently described at the beginning of the chapter. In addition to these gaits, typical and classic as they are, there are others that, although not particularly individ- ual, and not specially diagnostic in any condition, are yet distinct enough to warrant a description. There is the gait which occurs in the varied and pro- gressive stages of paresis. Frequently in some of the protean diseases it is not possible to apply to it any par- ticular train of symptoms. In paresis there may be an ataxic, a steppage, a spastic, or a hemiplegic gait. Yet it should be borne in mind that in paresis there is an attitude and manner of walking which occurs with suffi- cient frequency in the incipient and more advanced cases to warrant at least our describing it and putting it under the head of the paretic gait. In the beginning of paresis, while there is no charac- teristic movement of the legs, there is evidence of a gen- eral weakness. This results in an incomplete adjustment of the muscular movements, together with a marked slow- ness and shortened step. As a result of the weakness of the legs, there is a corresponding bending at the knees, which gives to the attitude that of a beginning senility. The effort to progress is great, and the patient evidently labors. Together with this is a loss of tone of the facial muscles, a lack of expression, and an appearance of be- ginning dementia. As the disease advances the gait becomes more pronounced. The patient requires greater efforts to progress. The speed is much slower, the general weakness more apparent, and the evidences of dementia more pronounced. It should never be forgotten that in paresis the dis- 8 114 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES ease may affect only certain groups of muscles, so that in this way a parotic may present a drag-toot or a hemi- plegic gait. He may also show a typical ataxic or a typi- cal spastic gait. Hereditary chorea is a condition which presents a gait apart. The peculiarity varies with the progress oi the disease. When the condition is well pronounced, the entire body is constantly in motion. The legs, feet, and body move from side to side and place to place. Oppen- heim describes it by sayine that the movement is rocking, with flinging movements oi the arms and scraping move- ments of the legs. Again, the patient may suddenly come to a momentary standstill. The word which best de- scribes the situation is the word clam-like. Sciatica may at times be diagnosed from its gait. In this condition the lameness is limited to one leg. The muscles supplied by the sciatic nerve are idle. The lower part oi the leg is kept in a position oi slight flexion; the hip is abducted. Any effort to extend the leg is avoided. The patient gives the impression that the disabled leg is painful, and uses it as little as possible. The foot is raised at the heel, and the patient, if he progresses at all, does so on the ball of the big toe. There may be a slight bending of the body toward the affected side. There are always great deliberation ami caution attendant on every effort to progress. The facies are those of a patient in pain. Mixed gaits often occur. These are the result oi the sit- uation of the pathologic lesion. There may be a spastic- ataxic, or elumsy-steppage gait, or, in fact, any combina- tion may exist. It is also possible to have two diseases occur in the same individual, so that a mixture of Tost i- GAITS 115 nation and hemiplegia, or steppage and festination, may be present. Again, certain factors may be present which serve either to modify or confuse the gait. Tremor is very marked and, as sometimes happens in hemiplegia or par- alysis agitans, will completely alter the appearance of the picture. Pain, resulting either from trauma, neo- plasm, or hysteria, will also behave in the same way. Finally, it should always be borne in mind that it is possible for a patient to have one type of gait occurring in one leg, with a wholly different one in the other; thus, a patient may have a hemiplegia on the right side, and at the same time a drop- foot on the left. This would, of course, produce a most confusing situation. CHAPTER VII ATAXIA Ataxia, derived from a Greek word meaning disorder, is the name applied to a condition that occurs in many diseases, and that may result from a lesion in various parts of the nervous system. Man executes muscular movements by bringing into play varied groups of muscles. These he controls and moves in a definite, regular, systematic manner. These movements emanate from centers, situated in various parts of the central nervous system. A disturbance of these centers, therefore, will cause these muscular move- ments to be indefinite, irregular, and lacking in system. Such a disturbance we call ataxia. Again, the centers which control these movements, themselves normal, may yet fail to receive the necessary stimulation from the ex- tremities, and in this way the resulting movements may be irregular and ataxic, or finally, as Leyden has pointed out, the joints may be so anesthetic as to preclude the sending of the proper impulse to the center, and in this way the resulting movements may be ataxic. It is, there- fore, evident that not only may a lesion in the brain cen- ters disturb this coordination, but also one that may be situated in the afferent tracts running to the brain cen- ters. Thus, the lesion may be in the cerebrum, in the cerebellum, or in any part of the afferent tracts, either in the posterior nerve-roots themselves or in the posterior columns. 116 ATAXIA 117 Ataxia must not be confused with paralysis. It does not necessarily mean loss of power, but rather misapplied power. Ataxia must not be confused with anesthesia; it may be present with or without anesthesia. In one in- stance it may occur as the result of an anesthetic joint, because in this case the impulse to the center is trans- mitted either erroneously or not at all; it may, on the other hand, occur as the result of a central lesion with no anesthesia or with anesthesia which is secondary to some wholly different condition. Ataxia must not be confused with tremor. In tremor the disorder of motion is regular, persistent, and more or less constant; it is a change in the number of oscillations which pass down the muscle. In ataxia the disorder of motion is more irregular, more jerky, and less persistent. It is due to faulty management and control of muscles. In tremor the muscle trembles, but the patient can con- trol it; in ataxia there is no trembling, but the patient fails to gage his movements. Either he falls short or overshoots the goal. Ataxia and incoordination differ only in degree. In other words, ataxia is advanced incoordination; inco- ordination is mild ataxia. The varieties and causes of ataxia are: I. As to nature: 1. Motor. 2. Static. 3. Cerebellar. II. As to distribution: 1. Hemi-ataxia. 2. Both arms or both legs. 3. All extremities. Il8 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES III. Causes of ataxia : i. Lesions affecting deep sensibility, as in tabes. 2. Toxic lesions of peripheral nerves, as in per- ipheral neuritis. 3. Lesions in higher centers. Brain — tumors in frontal or parietal lobe, inner capsule, and corpus quadrigeminus. Cerebellum — hem- orrhage, softening, and abscess. 4. Lesions of pons, medulla, and cord, as hem- orrhage, sclerosis, etc. 5. Congenital defects. IV. The important ataxias: 1. Locomotor ataxia. 2. Cerebellar ataxia. 3. Disseminated sclerosis. 4. Acute disseminated myelitis. 5. Friedreich's ataxia. 6. Ataxic paraplegia. 7. Hysteric ataxia. 8. Miscellaneous. As to Nature 1. Motor Ataxia. — The word motor when applied to ataxia occupies the position of a qualifying adjective. It is the form of ataxia which appears upon motion; at rest it is absent. The distribution may be local or general. Distribution in no way affects it. 2. Static ataxia is failure to coordinate while at rest. It includes the inability to hold the outstretched arm still and the inability to stand upright without swaying. Static ataxia occurs with aggravated forms of motor ataxia. A patient who suffers from ataxia when standing ATAXIA 119 is almost sure to suffer from it while in motion, whereas, on the other hand, a patient who suffers from motor ataxia does not necessarily suffer from static ataxia. 3. Cerebellar ataxia is the type which results from disease of the cerebellum. Another name for it is the Fig. 35. — Charcot ankle in tabes. term applied to it by Babinski, "cerebellar asynergia." It is one of the most important forms and one that the student would do well to familiarize himself with thor- oughly. It is preeminently a disturbance in motion, and 120 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES differs from any other type of ataxia. It lacks disturb- ance of sensation. The resulting incoordination is due to three factors: first, the presence of vertigo; second, the existence of hypotonia; third, the lack of coordination between cerebellum and cortex. Cerebellar ataxia may affect all four extremities; its most common distribution, however, is the legs. There- fore, the best illustration of this form of ataxia is seen in the gait, which has been described elsewhere. The difference between this form of ataxia and that which occurs in tabes is that, in the latter, there is some tendency to ex- cessive movement, as the result of interference with the sensory impulses, while in the former there is a tendency to uncertain movement, as a result of a lesion in the coordinat- ing center. In one the movement is excessive; in the other it is uncertain. The particular lesions of the cerebellum which cause cerebellar ataxia are: i. Tumor. 2. Abscess. 3. Maldevelopment. 4. Sclerosis. Fig. 36. — Charcot knee. ATAXIA 121 5. Inflammation of the cerebellum. 6. Softening of the cerebellum. *o Diseases in which the Gait of Cerebellar Ataxia Occurs Early stages of myelitis. Diphtheritic paralysis. Disseminated sclerosis. Friedreich's ataxia. Diseases of the quadrate bodies and frontal lobes. Diseases of the cerebellar cortex, crura cerebri. Bulbar softening. Romberg's sign is the name which is given to the test for ataxia. It derived its name from the man who first introduced it. To elicit the Romberg sign have the pa- tient stand in soldier fashion, that is, with the hands to the side and the feet so close together that both toes and heels touch and with the eyes closed. Then stand some little distance in front of him. Observe carefully whether he stands straight or whether he sways. The normal man should and can stand thus in a steady manner without swaying. If he sways, the Romberg symptom is present. In other words, the presence of the Romberg sign is an indication of some disturbance in equilibrium. Diseases in which the Romberg Symptom Occurs Locomotor ataxia. General paresis. Multiple sclerosis. Multiple neuritis. Brain tumor. Cerebrospinal syphilis. 122 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES As to Distribution The distribution of ataxia may be general or local; it may involve the upper or lower extremities, or all four. It may or may not involve the head. Hemi-ataxia describes a condition in which one-half of the body is ataxic. The occurrence of this condition is unusual; its principal importance lies in the fact that it is found with lesions of the optic thalamus. Causes The causes of ataxia are numerous. i . It may result from lesions affecting deep sensibility. Any interference with the deep sensations, those of weight, movement, position, etc., will result in faulty transmis- sion of the impulses running to the center. In other words, there will be an interference with the afferent tracts. The inevitable result of such a state of affairs will be defective coordination or ataxia. This is best illustrated in the ataxia of tabes. 2. It may result from toxic lesions of peripheral nerves, as in peripheral neuritis. Here there is a disturbance of the more superficial sensibility. Anesthesia of the legs, feet, arms, and hands takes place; there is the same in- terference with the transmission of afferent impulses, and again ataxia results. 3. It may result from lesions in the higher centers. The center of equilibrium is situated in the brain. Any lesion in either the cerebellum or in certain portions of the cere- brum will interfere with the centers of coordination and ataxia will result. Such lesions may be tumors in the frontal or parietal lobe, the inner capsule, or corpus quad- rigeminus. The lesions in the pons, medulla, and cord ATAXIA 1 23 which may result in ataxia are sclerosis, abscess, hemor- rhage, etc. To summarize then: The causes of ataxia can really be placed under two headings — one an interference with the afferent tracts running to the centers of equilibrium, the other a lesion affecting the centers themselves. The two types of ataxia vary somewhat — the best illustration of the first is that seen in tabes, of the second that seen in lesions of the cerebellum. To examine for ataxia it is best to adopt the following systematic method. Examine: 1. The arms. 2. The legs. 3. The trunk and head muscles. 4. Speech, tongue, and handwriting. To examine for ataxia in the arms have the patient hold the arms at right angles, with all the fingers flexed except the index; then, while the eyes are shut, tell him to touch the tip of the nose with each index-finger in turn. The normal man can do this without tremor. A slight degree of ataxia will cause a blunder; a marked degree of ataxia will result in absolute failure. After this test make the patient try to approximate the finger-tips of the two index-fingers, first with the eyes open, and then with them shut. Next have him touch the finger of the examiner as the latter approaches with extended hand. Finally, have him try to pick up objects, and button and unbutton his clothes. Ataxia will render his efforts ungainly and vain; a very ataxic patient cannot button and unbutton his clothes. To examine for ataxia in the legs make the patient walk, follow a pattern in the carpet, and heel and toe a 124 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES line. Have him try this latter motion with eyes shut. Next essay the Romberg test. Have him stand with both feet together, heel and toe touching, eyes shut, and arms to the side. This will test the sense of equilibrium. The normal man is able to stand for a few seconds in this position without swaying. The significance of the Romberg test is a disturbance of coordination; it occurs in locomotor ataxia, general paresis, and multiple scler- osis, some forms of multiple neuritis, and brain tumor. Another method of testing for ataxia of the legs is as follows: Have the patient in bed. Ask him to try to touch the foot, the ankle, and the knee of one leg with the heel of the other. The importance of this is twofold. It elicits slight degrees of ataxia, and it also enables us to differentiate between static ataxia and that of the cerebellar type. To test for ataxia of the head and trunk muscles tell the patient to approximate the head to certain fixed objects. Varieties of Ataxia The important ataxias are : i. Locomotor Ataxia, or Tabes. — Here there is an in- terference with deep sensibility. The defect lies in the transmission of the afferent impulse to the center. The center itself is intact. The type of ataxia resulting may be motor or static according as the condition is advanced or not. It can never be cerebellar. The cardinal signs of tabes are the Argyll-Robertson pupils, the lightning pains, the absent knee-jerks, the ataxic gait, and the crises. Tabes in women is unusual, but does occur. Its one peculiar characteristic is that female tabetics are less apt ATAXIA 125 to be ataxic than males. This is probably due to the fact that the skirts of women prevent their looking at the ataxic movements of the feet. There is no doubt that a tabetic walks better and is less ataxic when he dispenses with the use of his eyes ; one of the first lessons in Fraenk- el's movements is for the patient to avert the eyes from the legs. It is a fact that a blind tabetic is rarely ataxic, and that an ataxic tabetic usually has the use of his eyes. A student will often notice in the wards of a neurologic hospital that the tabetic with the use of his eyes will have much more occasion to use a stick than the tabetic who has lost the use of his eyes. Those tabetics who are free from crises of pain are apt to be afflicted with gastric crises, and vice versa. Juvenile tabes is a term applied to tabes occurring in the very young. Though unusual, there are instances on record in which it has developed in the teens. 2. Cerebellar Ataxia. — Here the interference is in the center of equilibrium. There _is__nq_defect in the trans- mission of jthe a fferent impulse. The type of ataxia is somewhat different. In walking, the body appears to run away from the legs. Again, in this form the patient is very apt to lean or walk to one particular side. This is due to the fact that the lesion may be situated in var- ious parts of the cerebellum. Usually the leaning is to the side of the lesion. Not only does he walk and lean to the side of the lesion, but he turns persistently toward that side. In cerebellar ataxia there is little control. 3. Disseminated Sclerosis. — Here the interference may be of either type, according to where the patch of sclerotic tissue lies. The very meaning of the word disseminate intimates that the lesion may be scattered. A 126 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 4. Acute disseminated myelitis occupies very much the same position. 5. Friedreich's ataxia, or hereditary ataxia, is a congen- ital condition, developing early in life, and is due to a maldevelopment of certain portions of the spinal cord, particularly the posterior and lateral columns. Remem- ber that in this condition the center of coordination is itself spared, whereas the pathologic lesion lies in the tract running to the center — the afferent tract. There are no sensory disturbances, and the ataxia is increased by closing tne eyes. The principal symptoms of Friedreich's ataxia are: 1. Incoordination. 2. Loss of knee-jerks. 3. Nystagmus. 4. Thickened speech. 5. Lateral curvature of the spine. 6. Deformity of the feet. A practical point to remember is that in Friedreich's ataxia the plantar reflex is of the extensor type, whereas in locomotor ataxia the plantar reflex is of the flexor type. Marie's hereditary cerebellar ataxia is due to a lesion of the cerebellum itself. It is difficult to differentiate it from Friedreich's ataxia, as the two are much alike. It is perhaps better to say that the two conditions belong to the same disease. In one the cerebellar type predom- inates; in the other, the spinal. In Marie's ataxia the reflexes are not lost. o. Ataxic Paraplegia. — Here the disturbance is purely one of the afferent tracts. The cardinal signs of this disease are ataxia, exaggerated knee-jerks, and a steadily increasing paralysis of the lower extremities. ATAXIA 127 7. Hysteria. Hysteric Ataxia. — A form of ataxia may occur in hys- teria, which, like all hysteric conditions, is more apt to resemble the same condition in other diseases. In this particular instance it resembles the ataxia that is found in multiple sclerosis. It is a form of ataxia which is not difficult to recognize, because it is performed in a more purposeless way, and displays movements which are de- Fig. 37. — Atrophy of arm. cidedly excessive. This latter point is best brought out by Oppenheim, who speaks of a patient that, when told to touch his nose with his finger, not only failed to come near his nose, but went to so great a distance as to touch his eye. Another, when diverted and made to look at the examiner, was able to dispense with the ataxic movements, and appear quiet and normal. 8. Miscellaneous Ataxias. — In many instances the use 128 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES of the word ataxia is arbitrary; in others it describes a particular condition. The following list includes some of the miscellaneous types of ataxia : bulbar, diphtheritic, drunkard's, heredi- tary, hereditary cerebellar, locomotor, hysteric, spinal, Briquet's, hemi- and posthemi-plegic, toxic, fatigue. Bulbar Ataxia. — Of this form Oppenheim says: "Bul- bar ataxia has the character of so-called sensory, cere- bellar, and motor ataxia, or may show a combination of these types." This form of ataxia is really a difficulty in articulation — a difficulty in performing the necessary muscular move- ments to express language. It may be a nuclear lesion, or may be due to a paralysis of the organs of speech. Diphtheric Ataxia. — This is general in character, and is a form which follows an attack of diphtheria and ac- companies the paralysis. It involves the hands and legs, and is very rapid in onset. Drunkard 's or toxic ataxia is the result of acute alco- holism. It is due to an affection of the higher centers, and shows both in the patient's gait and speech. It is, therefore, both cerebellar and cerebral. Fatigue Ataxia. — Fatigue ataxia is best elicited in the incoordination, trembling, and uncertainty that accom- pany some of the occupation neuroses. In the ataxic type of multiple neuritis Dresgfeld distin- guishes two varieties — the paralytic and the ataxic. In the ataxic he groups those cases in which the muscular sense was so greatly impaired as to bring about a con- dition of ataxia. This is the type which is so easily con- fused with tabes: the type to which the name of pseudotabes has been given. Starr calls attention to ATAXIA 1 29 this fact, that ataxia is so exclusively limited to this type that it may occur coincident with paralysis. The same division can be made of arsenical neuritis. Toxic paraplegia is the name given to a disease the symptoms of which are weakness and rigidity of the lower limbs, together with exaggerated reflexes and ataxia. Spinal Diseases m which Ataxia Occurs 1. Locomotor ataxia (tabes dorsalis). 2. Friedreich's disease (hereditary ataxia). 3. Ataxic paraplegia. 4. Combined posterolateral degeneration associated with anemia and various toxic conditions. 5. Some form of spinal syphilis (Erb's spinal syphilitic paraplegia) . 6. Occasionally disseminated sclerosis. 7. Myelitis— disseminated, acute, and of infectious origin. Other diseases causing ataxia in which the primary lesion is not in the spinal cord : 1. Tumors and other lesions of the cerebellum. 2. Hereditary cerebellar ataxia (of Marie). 3. The acute ataxia of Leyden (due to disseminated inflammatory patches in medulla, pons, and crura) . 4. Occasionally tumors of the prefrontal region. * 5. Internal ear disease. 6. Rare forms of peripheral neuritis (ataxic forms). 7. Occasionally hysteria. CHAPTER VIII CONVULSIONS A convulsion is an unnatural, violent, irregular con- traction of the muscular parts. In studying convulsions inspection will yield the great- est rewards. The student must observe with great care and intelligence the premonitory signs, the presence or absence of an aura, the onset, the course of the convul- sion, the duration, and distribution. He must note whether or not an outcry is present, the condition and position of the eyes, tongue, mouth, and sphincters. He should take the pulse and respiration, observe whether or not the patient passes water during or after the convulsive stage, and, finally, take into account the postparoxysmal condition and the temperature. Convulsive movements are so frequent and so similar in appearance that a differential diagnosis can be made only after collecting and weighing much data. The epilepti- form is the most usual and therefore the one with which the student must be most familiar. It is the one to suspect in every case of convulsion. The best* arrangement and classification of convulsions is the following: Classification of Convulsions I. Epilepsy: (a) Grand mal. (b) Petit mal. (c) General. id) Jacksonian. 130 CONVULSIONS 131 II. Convulsions due to Pressure: (a) Brain tumor — general or localized. (b) Brain abscess — general or localized. , s j 1. Tumor. (c) Bony pressure j 2 Depresse d fracture. (d) Hydrocephalus — general. III. Vascular Diseases: (a) Hemorrhage during apoplexy. m , . / 1. Cerebral. (b) Thrombosis j 2 Sinus 1. Thrombosis. (c) Syphilitic arteritis ■ 2. Hemorrhage. ( 3. Aneurysm. (d) Meningeal hemorrhage. (e) Anemia of brain. (/) Hyperemia of brain. IV. Toxic Action: (a) Drugs, as strychnin, lead, alcohol, ar- senic, morphin, prussic acid, atropin, aconite. (b) Uremia. (c) Eclampsia. (d) Tetany. V. Infection: , . f 1. Diffuse. (a) Syphilis 1 2 Gummatous . f 1. Cerebrospinal. (b) Meningitis - 2. Tuberculous. 3. Serous. 4. Pachymeningitis. (c) General paresis. ' (d) Tetanus. (e) Parasitic invasion of Cysticercus celluloses. VI. Functional: Hysteria. 132 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES I. Epilepsy. —(a) The Grand Mal. — The grand mal is a general convulsion which is severe and violent. It is preceded by an aura, accompanied by an outcry, and followed by a complete loss of consciousness. The aura may assume one of many types. It is immediately followed by a twitching, which quickly becomes general and violent. The patient is cyanosed, froths at the mouth, rolls the head to one side, and cries out. He falls to the floor, bites his tongue, passes his water, breathes in a stertorous way, and after two or three minutes lapses into a deep sleep. (b) The Petit Mal of Epilepsy. — The petit mal is really no convulsion at all. It may or may not be preceded by an aura, is not always accompanied by a loss of conscious- ness, and never by an outcry. It may simply take the form of dizziness, loss of memory, or absent-mindedness. (c) General. — The general convulsion is so called to distinguish it from the Jacksonian, and is in reality grand mal. (d) Jacksonian Convulsion. — The Jacksonian convul- sion is localized epilepsy. In this form the convulsion begins in a particular muscle or group of muscles, and may or may not extend to a general involvement. If it does extend, it is in a definite and systematic manner. The cause of the Jacksonian convulsion is a focus of irri- tation in that particular part of the cortex of the brain which controls the particular group of muscles. II. Convulsions Due to Pressure. — (a) The general convulsion occurring in tumors of the brain is violent and apoplectiform. It is the result of intracranial irritation or pressure. The second, or localized, type is really a Jacksonian CONVULSIONS 133 convulsion, that is to say, it involves one group of muscles or one extremity. Like the Jacksonian convulsion, it may begin locally, then spread and become general. This type should be observed with care and precision; it is of importance in aiding the diagnosis, as it serves to localize the cause of irritation. It should be kept in mind that some parts of the cortex are more sensitive than others, and therefore much more apt to discharge. In tumors of the cerebellum convulsions do occur, but with less frequency. (b) In abscess convulsions are rare; they are most apt to appear just before death or when the encephalitis begins to break down. (c) Bony pressure, either from a spicula of bone, new- growth, or depressed fracture, behaves in the same manner as does a neoplasm and causes the same kind of convulsion. (d) In hydrocephalus the convulsion is a late manifes- tation. III. Vascular Diseases. — Hemorrhage during an apo- plectic stroke may be initiated, accompanied, or followed by convulsions. They are, however, unusual and, unless the hemorrhage is severe, do not occur. Their presence indicates that the bleeding has become extensive and probably has invaded the ventricles. These convul- sions may be general, local, or unilateral. If unilateral, Starr says they are an infallible sign of a lesion of the cortex in the central region. In the case of children suffering from cerebral hemorrhage convulsions are still more usual and frequent. The type of convulsion oc- curring in cerebral hemorrhage is, of course, apoplecti- form. V 134 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES In sinus thrombosis convulsions occur. They are either general or unilateral, and are more frequent in children than in adults. In meningitis, especially in the meningitis of child- hood, convulsions are frequent. They occur early, are violent, and persist. They may be general, unilateral, or they may assume the form of a localized spasmodic twitching. They are most frequent in tubercular men- ingitis, in which disease they are general in character; in the epidemic tvpe of meningitis they occur with almost equal frequency. In syphilis of the brain the type of convulsion is epi- leptiform and general. In cerebral anemia general convulsions occur, provided the loss of blood is severe. They are by no means in- frequent, and are general in character. In cerebral hyperemia convulsions are fairly frequent. They occur in the advanced stage, are preceded by men- tal irritability, confusion, vertigo, apathy, and flashes of light, and accompanied by a rise in the blood-pressure. They are general in character, violent, and usually sev- eral closely follow one another. IV. Toxic convulsions follow overdoses of strychnin, alcohol, lead, aconite, atropin, arsenic, morphin, and prussic acid. They are most frequent in strychnin poisoning, less so in alcohol, and rather unusual in lead. They are general, violent, and epileptiform. In strych- nin poisoning the convulsions present both clonic and tonic spasms, follow each other frequently, and finally attain the stage of opisthotonos. In this condition the patient may reach so great a state of susceptibility that the slightest irritation, such as the presence of a light CONVULSIONS 135 or the rustling of a newspaper, may induce a series of these convulsions.. V. Infection. — Convulsions in general paresis, as a rule, usher in and accompany the third stage, although they may occur early in the disease. They assume varied forms: from the simple congestive attack, which oc- curs in incipient paresis, to the violent general convul- sion of the terminal stages. These latter may be apo- plectiform, epileptiform, or general. In tetanus convulsions begin as spasms in the fingers and toes and gradually extend toward the trunk until eventually they involve the entire body. Simultaneously with this progressive involvement the spasm becomes a convulsion, which steadily increases, in severity until there results a general opisthotonos. VI. The hysteric convulsion is one which occurs in all the different types of hysteria, in the minor, the major, and in catalepsy. Pitres says that in hysteria 82 per cent, of the women develop the convulsive type, whereas only 22 per cent, of the men. The principal feature of this type of convulsion is that the period of motor activity is preceded by a period of preparation, and followed by one of mental excitement or delirium. The convulsion itself may be one of two kinds, that is, either clownish or emotional. The at- tack, if of the latter type, may assume tremendous dimen- sions and cause the onlookers the greatest discomfort and even fear. The patient may assume the opisthotonos position. The preparatory period is one in which the patient may be depressed or irritable and may display a good deal of dissatisfaction with surroundings. There is also much motor activity. CHAPTER IX SENSATION The best, the most comprehensive, and the one plan most widely adopted for explaining the sensory disturb- ances is that suggested by Drs. Henry Head and James Sherren. Their theory is that afferent impulses coming from the periphery are conducted along distinct classes of nerve- fibers. These three classes are named deep, interme- diate, and superficial sensibility. This plan extends to the spinal roots. So soon as these impulses enter the spinal posterior roots nature's arrangement is changed. There is a complete rearrangement. There is no longer any deep, intermediate, or superficial sensibility. There are tracts; in each tract are gathered together, so to speak, all the fibers of sensation of that particular type, regardless of whether they are superficial, deep, or intermediate. In the spinal cord there are the tracts of pain, temperature, and touch. The Head plan divides the sensory mechanism into two parts: I. The sensory peripheral mechanism. II. The sensory spinal mechanism. In the sensory peripheral mechanism are three sets of impulses, which travel by different paths. i. Those Which A feet Deep Sensibility. — In this type the impulses are produced by pressure. Thus is 136 SENSATION 137 recognized the sensation of muscular and articular movement. 2. Those Which A feet Intermediate Sensibility. — In this type the impulses are produced by painful cutaneous stimuli and the extremes of temperature. This type Fig. 38. — Syringomyelia, showing the winged or angel scapula, the scoliosis, and the atrophy of the arm. has been named by Head the protopathic. This in- termediate type is more wide-spread in its distribution than the others and is accompanied by tingling. 3. Those Which Affect Superficial Sensibility. — In this 138 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES type the impulses are produced by touch in its restricted meaning, that is, the impulses are produced by gentle touches, minor degrees of temperature, and the recog- nition of two points of a compass as two points. This type has been named the epicritic. The unit of the proto- pathic supply is the pos- terior root. The unit of the epicritic supply is the peripheral nerve. Sherren says division of posterior roots produces an area of loss of protopathic greater than the area of loss of light touch. Division of peripheral nerves produces an area of loss of protopathic either smaller or almost as extensive as the area of loss of light touch. Sensory Spinal Mech- anism. — In the spinal cord there is an entirely different mechanism. Here we have groups of sensations of: Pain. Temperature. Touch. Fig. 39. — Syringomyelia, showing atrophy of the hands and arms, right claw-hand, lateral scoliosis, and sym- pathetic paralysis on the left. SENSATION 139 Passive position and movement, together with dis- crimination of adjacent points. The Method of Examination for Sensation Many instruments and many methods have been de- vised to test sensation. The student will do best to dis- card all of the complicated ones, and rely on the simplest. The only instruments needed are a small camel's-hair brush, a pin, a compass, two test-tubes, one contain- ing hot water, the other cold, and the examiner's fingers. The room should be quiet, the patient stripped and blind- folded. The student should then proceed in a systematic manner. Tell the patient to say "Yes" whenever he feels any sensation of touch, and then to qualify his state- ment by telling the location and nature of the sensation. Never say to a patient, "Do you feel that?" or "What was that?" as in some cases these questions give a clue as to the sensation. Do not forget to make the tests at ir- regular intervals and of a nature varying enough so that the patient will not know what test to expect. (a) Epicritic. — First test for light sensibility; that is epicritic. Test for light touch, light pain, light dif- ferences in degrees of temperature, and the discrimina- tion of distance between two points. The test for touch is made by touching, in the gentlest possible way, the skin with a camel's-hair brush, a piece of cotton-wool, or even with the fingers of the examiner. The test for pain is made by touching the skin with the point of a pin, the requirement of the patient being to tell whether it is the head or the point of the pin. The test of the de- gree of temperature is made by touching the skin with the two test-tubes, one of which contains water only a 14-0 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES trifle warmer than the body, and the other of which con- tains water only a trifle colder than the body. The dis- crimination test is made by a compass, or roughly by the two ringers of the examiner, the object being to de- termine the distance of the points at which the patient fails to appreciate the two points and feels the sensation of one point only. In this connection it is well to men- tion another delicate test. Move the camel's-hair brush or the pinpoint very lightly in either vertical or horizontal streaks on the skin, asking the patient to de- termine both the direction and distance traversed. This distance traversed includes really the compass test be- sides the sense of direction. (b) Protopathic. — The protopathic sensibility is the name applied to more strenuous applications of the touch of the camel's-hair brush or finger, a rather quick jab of the pinpoint, and the difference between the test-tubes that are quite hot and those that are ice cold. There- fore, following the epicritic test, carry out the one for protopathic sensibility as described above. (c) Deep Sensibility. — Finally examine for deep sen- sibility. This test involves the knowledge of the vari- ous positions of the arms, fingers, legs, and toes when the eyes are closed. This is tested in several ways: i. By asking the patient to bring his finger-tip to within an inch of his nose, and then stop without touching the nose. (This test will also demonstrate any tremors or inco- ordination, although not its primary object.) 2. Similarly, hold one hand or foot of the patient, asking him to touch it quickly with the other hand. When the deep sense is lost, the patient may reach in the wrong direction with the second hand. 3. Hold one extremity in an SENSATION 141 awkward or unusual position, asking the patient to duplicate or imitate the position with the opposite imb. Sometimes it is of value to ask the patient to open the eyes and tell if the limb is where he thought it was. 4. Grasp the little finger or big toe between the thumb and forefinger. Move it up, down, and sideways, at the same time asking the patient to describe the direction of each movement. Bear in mind that it is necessary to grasp the lateral sides rather than the dorsal and palmar as- pects, as the patient might tell from superficial sensation that the finger of the examiner touching the dorsal sur- face of the toe could do nothing else than flex. This is the most delicate of any of the tests for joint sense. It can be made even more delicate by moving the toe only slightly up or down instead of alternating between extreme flexion and extension. This sense as to passive motion is kinesthesia; its absence is called akines- thesia. 5. Test the recognition of weight by placing in the patient's hands coins or metallic articles of varying weights. 6. Test the stereognosis sense. This test in- volves size, shape, character of surface, and weight. It is the most complex and one of the most important of all the tests. To carry it out successfully the patient must have in his hands several articles of varying char- acter, weight, and size. Without seeing them he must try to describe and distinguish them and their charac- teristics. The absence of this sense is called astereognosis and is described later on. Sensory Disturbances (a) Varieties as to distribution. (b) Varieties as to nature. 142 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES (a) Varieties as to Distribution: i. Over several muscle segments or several spinal nerve segments, as in tract disease of the cord. 2. Over individual segments, following trauma. As definite segments, as in ulnar nerve injury. 3. One-half the body, as in hysteria. 4. Both lower extremities, as in tumor of cord. 5. Generalized over the body, as in tabes. 6. Irregular distribution over various segments, not following the course of nerves, as in hysteria. (b) Varieties as to Nature: 1. Touch. (a) Hyperesthesia, excessive sensibility to touch and other stimuli. (b) Hypesthesia, diminished sensibility to touch. (c) Anesthesia, loss of tactile sensibility. 2. Pain. (a) Hyperalgesia, excessive sensibility to pain. (b) Hypalgesia, reduced sensibility to pain. (c) Analgesia, loss of sensibility to pain. 3. Thermal. (a) Increased. (b) Decreased. (c) Absent. 4. Dissociated anesthesia, in which tactile and pain sensibility is preserved, sensibility to heat and cold is diminished or lost. 5. Varieties of deep sensation. (a) Kinesthesia, loss of sensation as to position of joints. (b) Pallanesthesia, loss or diminution of the vibration sense. (c) Astereognosis, loss of the power of recog- nition of objects by sense of touch. SENSATION 143 U5 C c o o 144 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Varieties of Disturbed Sensation i. Thermal Anesthesia: Syringomyelia. Hysteria. Tumor of com. 2. Analgesia-hypalgesia : Tabes. Hysteria. Tumor of cord. 3. Anesthesia-hypesthesia: Tabes. Trauma. Myxedema. Hysteria. 4. Dissociated Anesthesia: Syringomyelia. Hematomyelia. Hysteria. 5. Kinesthesia: Tabes. 6. Pallanesthesia: Tabes. 7. Hyperalgesia: Tumor of cord. Hysteria. Zoster. 8. Hyperesthesia: Alcoholic multiple neuritis. Hysteria. Zoster. 9. Brown-Sequard Type: Tumor of cord. CHAPTER X REFLEXES Knowledge of reflexes is essential to a knowledge of neurology. The student must know how to obtain reflexes, their relationship to symptoms, their significance, and the pathologic conditions which they foreshadow and declare. There are many reflexes, some of which are irrelevant to neurology. The student should learn to give close attention to the most important, and not to waste time over those of little value. First, it is best to understand just what a reflex is and what is reflex action. A reflex action, according to Webster, is ''any action per- formed involuntarily, in consequence of an impulse or impression transmitted along afferent nerves to a nerve- center, from which it is reflected to an efferent nerve, and so calls into action certain muscles, organs, or cells." In other words, a reflex action is the performance of a given action which results from a sensory impulse pro- duced on the spinal cord, regardless of the patient's aid or knowledge. It is constantly seen in the acts of the lower animals. To accomplish a reflex act it is necessary to have a complete and unimpaired mechanism. This mechan- ism consists of three parts: the sensory nerve running to the center, the center itself in the cord, and the motor nerve running from the center. These three parts to- gether make up what is known as the reflex arc. Any IO 145 146 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES injury or interference with any portion of this arc will result in destroying the transmission of impulse and so bring about a loss of reflex. Thus, a stab wound, a patch of sclerotic tissue, or inflammation will break the arc, destroy the transmission of the impulse, and result in an absent reflex. A certain degree of mental control is transmitted over all reflex acts through the spinal cord from the brain. If some injury or pathologic change takes place in the columns of the spinal cord, this cerebral control will be interfered with, the reflex will cease to be controlled, and there will result an exaggeration of the reflex. Again, if certain poisons are administered they will act as stimulants to the spinal cord, will irritate the centers, and so bring about an exaggeration of the reflex. Thus there is one cause for a lost reflex act : a break in the reflex arc. There are two causes for an exaggerated reflex act : re- moval of cerebral inhibition and overstimulation of the spinal centers. In order to perform a reflex act properly, it is necessary that each of the three parts of the reflex arc should be intact. When they are intact, an impulse or stimulus given to the external skin or tendon is conveyed by the afferent fiber to the center, and by the center trans- mitted to the efferent fiber, which in turn stimulates the muscle or skin, and so produces the motor action. The integrity of the reflex, then, is wholly dependent upon the integrity of the reflex arc. A break in the reflex arc will result in a lost reflex. Such a break may result from trauma, inflammation, EEFLEXES I 47 hemorrhage, a patch of sclerotic tissue, poison, degenera- tion, and new-growths. A reflex arc, therefore, consists of three distinct parts: 1. The afferent fiber running to the center. 2. The efferent fiber running from the center. 3. The center, together with its connecting fibers, which serve as a link between the two. Special Reflexes There are four groups of reflexes : I. Pupillary. II. Superficial (skin and mucous membrane). III. Deep (tendon). IV. Organic. I. Pupillary Reflexes The pupillary reflexes consist of: (a) The light reflex. (b) The accommodation reflex. (c) The ciliospinal reflex. To test for the light reflex, examine each eye separately. The best way is to shade one eye and at the same time alternately admit light and darkness to the other. \ Normally, from the admission of light there should re- sult a contraction of the pupil, and, from shading, a dilatation. Pathologically, the pupil may be either sluggish or absolutely immobile. The first condition is suggestive of a beginning immobile pupil. The sec- ond is a pupil which has become immobile. To obtain the accommodation reflex, have the patient look first at a near and then at a distant object. Normally there should result a contraction and dilata- T48 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES tion. The loss of the power of accommodation is un- usual; it may occur in certain lesions of the sympathetic system. To obtain the ciliospinal reflex, pinch the skin of the neck. The result will be a dilatation of the pupil of the corresponding side. The spinal center? which contain the ciliospinal center are situated in the lowest cervical and highest dorsal regions. II. The Superficial Reflexes The superficial reflexes are not so important as the deep. They involve both the skin and mucous mem- brane. The method of obtaining them is by irritating the skin or mucous membrane, either by scratching or pinching. As a result of this stimulus, there follows a certain definite contraction. While it is admitted that the skin reflexes are controlled by certain centers in the cord, yet it is not admitted that the control is as thorough or as important as in the case of either the pupillary or the deep reflexes. There are many superficial reflexes. A list of the principal ones follows: i. The corneal. 9. The plantar. 2. The conjunctival. 10. The Babinski. 3. The pharyngeal. 11. The Oppenheim. 4. The palatal. 12. The Gordon. 5. The scapulohumeral. 13 The Bechterew-Mendel. 6. The epigastric. 14. The palmar. 7. The abdominal. 15. The sphincter. 8. The cremasteric. The corneal reflex is produced by taking a very small piece of absorbent cotton, rolling it tightly, and carry- ing it over the conjunctiva to the cornea. Normally REFLEXES 149 the eye should wink. In the pathologic condition the patient will allow the examiner to place the cotton on the cornea without any movement on the part of the eyelid. At the same time the conjunctival reflex can be obtained. The centers which control these two reflexes Fig. 41. are not well defined. These reflexes are often absent in functional conditions. While their absence is very frequently an indication of hysteria, it should never be forgotten that they may be present even in mild cases of neurasthenia. To obtain the pharyngeal or palatal reflex stroke the back of the throat with a spatula or some small wooden 150 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES object. The importance of these reflexes is on a par with the two preceding. To obtain the scapulohumeral reflex stroke the skin over the scapula. There should result a contraction of the scapular muscles. In pyramidal tract lesions this reflex is exaggerated. To obtain the epigastric reflex stroke the skin of the epigastrium. Normally there would result a contraction of the upper fibers of the recti muscles of the epigastric region. This reflex should be obtained on both sides. The segment of the spinal cord in which it is located is the seventh to the ninth dorsal. The abdominal reflex is illustrated by irritation, in a similar manner, of the lower part of the abdomen. Normally there should result a retraction of the ab- dominal muscles. The segment which controls this re- flex is situated in the ninth to the twelfth dorsal. The absence of this reflex is not at all unusual in the crises of tabes. Following apoplexy the lost abdominal reflex indicates the paralyzed side. Diseases in which the Abdominal Reflex is Lost Hemiplegia. Multiple sclerosis. Brain tumor. Tabes (crises of). Epidemic cerebrospinal meningitis. The cremasteric reflex is obtained by stroking or pinching the inner side of the thigh. There results a retraction of the testicle of the same side. The seg- ments in the spinal cord which control this reflex are the first and second lumbar. REFLEXES 151 The plantar reflex is, of all the cutaneous reflexes, the most important. To obtain it stimulate with some blunt object the sole of the foot. Have the patient elevate the leg, while the examiner supports the calf, to place it in a passive" position. Use either a blunt ob- ject or the thumb-nail of the examiner, slowly rubbed along the inner side of the sole of the foot toward the toe or from side to side. In the normal individual, as a result of such stimulation there would result a plantar flexion of the toes. This, of course, is best illustrated in the phenomena of tickling the sole of the foot. If, however, the reflex is abnormal, then there results a phenomenon which is known as the Babinski. This consists of a flexion of the smaller toes, a marked extension v of the large toe, and sometimes a. spreading in fan-like manner of the four smaller toes. This characteristic spreading of the toes has given to the reflex the name of the signe de Veventail. The name of Babinski, by which it is commonly known, was given to it as a result of its first description by this French authority. The \ significance and importance of the Babinski reflex lies in the fact that its presence is indicative of an involve- ment of the pyramidal tracts. It is, therefore, a posi- | tive indication of paralysis of the upper motor neuron type. It should never be forgotten that in infancy, up to the age of eighteen months, the pyramidal tracts remain undeveloped, and that, therefore, at that age , the Babinski sign will be found, not pathologically, but physiologically. The Babinski reflex is a very important sign in the differential diagnosis between organic and functional conditions. It is well to remember that in hysteria the pure Babinski reflex is not present. 152 diagnostic symptoms in nervous diseases Diseases in which the Babinski Reflex Occurs i. Multiple sclerosis. 2. Tumors of cord and brain. 3. Hemiplegia. 4. Spastic spinal paralysis. 5. Congenital spastic paralysis. 6. Friedreich's disease. 7. Meningitis. 8. Amyotrophic lateral sclerosis. 9. Fracture of spinal column. 10. Spinal caries. 11. Myelitis. 12. Poliomyelitis (occasionally). Conditions in which the Plantar Reflex is of the Flexion Type 1. Tabes. 2. Peripheral neuritis. 3. Paralysis agitans. 4. Poliomyelitis. 5. Neurasthenia. 6. Chorea. The Oppenheim reflex consists of a contraction of the extensor muscles of the big toe and of the anterior tibial muscles. To obtain it, stroke from above downward just behind the inner border of the tibia. It is local- ized in the first three sacral segments of the spinal cord. To obtain Gordon's reflex make deep pressure on the muscles of the calf of the leg. The result should be ex- tension of the toes. The centers which control this reflex are located in the first three sacral segments of the spinal \ . cord. REFLEXES I 53 To obtain the Bechterew-Mendel reflex tap the toe tendons. There should result either a flexion or exten- sion of the toes. The centers which control this reflex are located in the first three sacral segments of the spinal cord. The last three reflexes occur only in pyramidal lesions. The palmar reflex is illustrated by stroking the palm of the hand, with the resultant flexion of the fingers and slight retraction of the hand. The normal thickness of the skin in this region will often make it impossible to illustrate this reflex. Too great importance, therefore, is not to be attributed to it. It is localized in the eighth cervical to the first dorsal. The sphincter reflex is twofold — bladder and rectum. To obtain the sphincter reflex of the bladder introduce a sound. If present, the instrument will be gripped. To obtain the sphincter reflex of the rectum introduce a finger. Normally the sphincter contracts tightly over the finger. Abnormalities of Sphincter Control: i. Incontinence. 2. Retention. (a) Tabes. (b) Tetany (sphincters may be tonically con- tracted). Varieties of Incontinence : (a) Continuously, as fast as any excretion is pro- duced. (b) At intervals — whenever there is accumulation. (c) As result of distended bladder; as overflow. (d) Nocturnal enuresis. (e) Accidental, under emotions, or haste, or acute alcoholism. (/) Epileptic convulsion. 154 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 3. Occurrence of Incontinence: (a) Tabes. (b) Brain tumor. (c) Tumor of the spinal cord. (d) Multiple sclerosis. (e) Idiocy. (/) Epileptic convulsions. (g) Senile dementia. (//) Hysteria. (1) Myelitis. (J) Landry's paralysis. (k) Cerebrospinal meningitis. (I) Multiple neuritis (occasionally). Deep Reflexes The deep reflexes are many. The important ones are: 1. The jaw jerk. 2. The elbow, or triceps, jerk. 3. The wrist jerk. 4. The knee jerk. 5. The Achilles jerk. 6. Clonus — ankle, patella, leg, wrist, elbow. V To get the jaw jerk have the patient extend the chin, while at the same time the examiner places a flat substance, preferably an ivory paper-cutter, over the lower teeth. As a result of repeated tapping there oc- curs a contraction of the muscles which elevate the jaw. This is not a reflex of any very great importance, but, according to Beevor, it is frequent in amyotrophic lateral sclerosis. To obtain the triceps reflex have the patient rest the arm on the examiner's hand with the forearm hanging REFLEXES 1 55 loosely. A slight tap, just above the elbow, at the insertion of the triceps muscle, ought then to cause an extension of the forearm. The segment of the spinal cord which controls the triceps jerk is the sixth cervical. To obtain the wrist jerk support the extended arm while the hand of the patient is allowed to hang down- ward. A tap, either with a percussion hammer or with the fingers. will then bring forth a contraction of the hand. The blow should not be severe, and should be applied above the dorsal surface of the forearm in the radial end. The spinal segments which control the wrist jerk are the sixth to eighth cervical. Diseases in which the Wrist Jerk hay be Absent 1. Progressive muscular atrophy. 2. Erb's arm paralysis. 3. Any neuritis affecting the arms. 4. Poliomyelitis affecting the arms. 5. Tabes if the cervical cord is affected. 6. Syringomyelia if the cervical cord is affected. Diseases in which the Wrist Jerk may be Exag- gerated Diseases affecting the upper motor neurons. Amyotrophic lateral sclerosis. The knee jerk is the most important of all reflexes. Unusual care and tact must be exercised to test for its presence. First have the patient cross one leg over the other. In this position feel for the lower end of the patella, and, with a percussion hammer, a book, or the fingers, strike the quadriceps tendon just below its in- sertion into the patella. Normally, there should occur an extension of the leg. Pathologically, there may occur 156 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES either an exaggeration of this phenomenon or a complete absence of movement of the part of the leg. If the patient happens to be confined to his bed, each knee can be supported in the hand of the examiner. Neither of these methods, however, should be deemed satisfactory or final. The only proper way to test for the knee jerk is to have the patient sit on a table, with the legs hanging loosely, very much as though he were sitting on a country stile. If this method should fail the examiner ought not to be satisfied until he has tried additional methods, known as reinforcements. The Jendrassik method consists in having the patient clench his two hands, and, at the moment at which the exam- iner tests the knee jerk, pull the clenched hands in op- posite directions. If this method should fail, the exam- iner should then try the method which goes by the name of Lauferauer's. This consists in having the patient sit with his soles flat on the floor, while he squeezes to- gether his two hands. Just at this moment the patella tendon is tapped. If there is the slightest response, it will be evident to the examiner's hand, which should be grasping the patient's quadriceps muscle. Still an- other method is to have the patient, while sitting on a table, read aloud rapidly, with a newspaper between him and his knees, the object being to convey to him the im- pression that his vision and speech are being tested. This method is probably the surest of all, and if under these conditions no reflex is obtained, it is safe to feel that the reflex is absent. In every instance where the presence of a knee jerk is in question, the student must try each one of these methods. This holds true even in the case of bed patients. A bed patient can always be supported on REFLEXES 157 a table and induced either to clasp his hands or to read. It is surprising how many functional and hysteric cases that have been bedridden for years will under these Fig. 42. Atrophy resulting from alcoholic neuritis in a man formerly weighing over two hundred pounds. conditions and none other present a reflex, thus enabling the examiner to clear up a doubtful case. Another name for the knee jerk is the patellar reflex. Its absence is known as Westphal's sign. The spinal centers which 158 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES control it are situated in the second, third, and fourth lumbar nerve roots. The knee jerk is absent in the following conditions: 1. In lesions of the afferent limb of the reflex arc. 2. In lesions of the efferent limb of the reflex arc. 3. In lesions of the gray matter at the level of the re- flex arc. 4. In coma, exhaustion, narcosis, and spinal anesthesia. 5. In cerebral conditions in which there is increased pressure of the cerebrospinal fluid. 6. Congenital (rarely, but it does occur). 7. In pyrexial states. 8. In certain conditions of diseases of the cord above the reflex arc. 9. In clear transverse lesions of the cord. \f Diseases in Which the Knee Jerk may be Absent 1. Tabes. 2. Neuritis (alcohol, diphtheria, diabetes, arsenic, grip). 3. Poliomyelitis. 4. Progressive muscular atrophy (Charcot-Marie Tooth type). 5. Coma preceding death. 6. Diabetes. • 7. Syringomyelia. 8. Injuries to the crural nerve. 9. General paresis. 10. Beriberi. 11. Tumors of the pons. 12. Friedreich's disease. ■ 13. Combined posterior and lateral column disease. REFLEXES I 59 14. Muscular dystrophy. 15. Spinal meningitis. 16. Landry's paralysis. 17. Increased pressure of spinal fluid. [8. Cerebral meningitis. 19. Epidemic cerebrospinal meningitis. 20. Exophthalmic goiter (rarely). 21. Postepileptic conditions. The knee jerk is exaggerated in the following condi- tions : 1. Any lesion of the pyramidal tracts. 2. Brain tumors. 3. Functional neuroses. Diseases in Which the Knee Jerk may be Exag- gerated 1. Hemiplegia. 2. Multiple sclerosis. 3. Spastic paraplegia. 4. General paresis. 5. Brain tumor. 6. Tumor of the spinal cord. 7. Multiple neuritis in early stage. 8. Hysteria. 9. Spinal meningitis. 10. Myelitis. Such a condition as inequality or irregularity of the knee jerks may occur, so that the knee jerk on one side may be present while the corresponding one is absent. Or, it may be exaggerated, with the other either absent or normal. This state of affairs may follow apoplexy, where the reflex on the hemiplegic side is exaggerated, l6o DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES whereas the opposite one is normal. Or, again, it may oc- cur in a beginning toxic neuritis or in a unilateral neu- ritis. It is, however, most commonly seen in cases of general paresis. So frequently does the condition occur in this disease that the student should never dismiss a case of unequal or irregular knee jerks without first eliminating a diagnosis of general paresis. This ine- quality of the knee jerks occurs with almost as much fre- quency as inequality and irregularity of the pupils, and is certainly as. important. There is no question but that in a few isolated cases the knee jerks are congenitally absent. I personally have known of two cases in which no knee jerk ever showed itself. The ankle reflex, or Achilles jerk, is almost invariably present. E. Bramwell has advanced the theory that in persons over fifty years of age this reflex is often absent. Other observers, however, have not confirmed his view. To obtain the Achilles jerk have the patient kneel on a chair, with legs well separated. A slight tap just above the heel in a normal individual elicits an extension of the foot. The segments of the spinal cord which control the Achilles jerk are the first and second sacral. The main importance of the Achilles jerk lies in the fact that it of all reflexes is apt to be the earliest to dis- appear. Usually it is absent in those cases in which there is loss of the knee jerk, and sometimes several months in advance of the latter. This is especially so in tabes, alcoholic cases, and in general paresis. Thus, it will be seen that it is of value in foretelling conditions rather than in actually diagnosing them. REFLEXES l6l THE ACHILLES JERK MAY BE ABSENT EN i. Early tabes. 2. Peripheral neuritis. 3. Syphilis of the nervous system. 4. Sciatica. 5. Lesions of the lumbar and sacral regions. 6. Lesions of the caucla equina. 7. Infantile paralysis. 8. Diphtheria. 9. Diabetes. Clonus is derived from the Greek word, kXovos, meaning commotion. It is an involuntary, reflex, irregular con- traction of the muscles when suddenly put upon the stretch. It is a to-and-fro vibratory movement, and is never present in normal conditions. It is named, accord- ing to the part stimulated, ankle, knee, or foot clonus. Functional conditions present a movement akin to it which is called spurious clonus. Of all the varieties, the most common is the ankle clonus. This phenomenon is due, as Weir Mitchell pointed out, to a contraction of the soleus muscle. To obtain the ankle clonus have the patient either lie in bed or sit in a chair, while the examiner supports the flexed leg in a position of slight external rotation; with one hand under the calf, the other should grasp the distal part of the foot, and with the leg in a com- plete state of passiveness the foot should be suddenly flexed directly in a line with the leg. If under these conditions there should result a constant and regular series of to-and-fro movements, which continue as long as pressure on the foot is kept up, a true clonus is present. To obtain patellar clonus have the patient relax 11 1 62 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES the extended leg when lying down, and then bring sudden and continued pressure on the patella downward. The spurious ankle clonus met with in hysteria is not so regular, nor can it be maintained so long. The char- acter of the contractions is also less pronounced; they lack an absolute simulation. The cord segments which control clonus are the first three sacral. The significance of the ankle clonus lies in the fact that its presence indicates abnormal excitability of the reflex arc. It indicates that the cerebral inhibition has been withdrawn, and it is, therefore, one of the lead- ing signs of paralysis of the upper motor neuron type. DISEASES IN WHICH ANKLE CLONUS OCCURS i. Spastic paralysis. 2. Hemiplegia. 3. Multiple sclerosis. 4. Brain tumor. 5. Cord tumor. The absence of a deep reflex conveys to the examiner the information that in that particular reflex there has been an interruption; in short, a lost reflex means a break in the reflex arc. If the break is in the afferent fiber, there is, in addition to the loss of the reflex, a loss of sensation; if in the efferent fiber or in the anterior horns, there are muscular paralysis and atrophy. The site of the lesions, therefore, in the loss of the deep reflexes may be: 1. Peripheral sensory nerves. 2. Reflex centers of the cord. 3. Anterior horns of the cord. REFLEXES I 63 4. Peripheral motor nerves. The examination of the deep reflexes conveys to the examiner the information that either there has been (i) loss of the cerebral inhibition, that is to say, conveyance of the impulse from the brain to the cord has been inter- fered with, or (2) overstimulation of the spinal cord. The conditions in which an exaggeration of the deep reflexes occur are: 1. Lesions of the pyramidal tract. 2. Poisons, as alcohol and arsenic. The actual diseases are: 1. Cerebral thrombus and hemorrhage. 2. Lateral sclerosis. 3. Ataxic paraplegia. 4. General paresis. 5. Myelitis. Oppenheim says that diseases of the pyramidal tracts are the most common cause of exaggerated reflexes. Diseases in which the Knee Jerk may be Retained and the Achilles Reflex Lost 1. Amyotrophic lateral sclerosis. 2. Paralysis of the posterior tibial nerve. 3. Sciatica. Finally, the student should bear in mind the two fol- lowing rules: 1. Exaggeration of the deep reflexes means a lesion of the corticospinal or upper motor neuron tract. 2. Loss of the deep reflexes means a lesion of the spinomuscular or lower motor neuron tract. It is almost a rule that in disease the superficial and deep reflexes are rarely of the same character, that is, when the deep reflex is exaggerated the skin reflex is lost. CHAPTER XI THE EYE Examination of the eye affords threefold information : First, it gives an insight into the condition of certain of the cranial nerves; second, information as regards certain reflexes, and, third, information as to the ingestion effects of certain toxins and drugs. Here, as well as in gaits, in- spection will greatly reward the student and afford wide information. It will be very advantageous to acquire the habit of observing a patient's pupils. This can be done when the patient first presents himself. By standing directly in front of the subject and then moving a little to one side, it is possible to throw upon the pupil first dark- ness and then light. In this way it is possible to diag- nose Argyll-Robertson pupils, irregular pupils, unequal and very much dilated pupils. A practical point worth remembering, though not one of universal application, is that a markedly dilated pupil is frequently sympto- matic of functional disease, whereas a markedly con- tracted pupil is symptomatic of organic disease. Another point to remember is that a large number of organic affections, both of pupils and of muscles that control the eye, are the result of syphilis. It is best to consider the relation of the eye to nervous diseases under three headings: i. The physical signs of the pupil. 164 THE EYE 165 2. The physical signs aside from the pupil. 3. The eye reflexes. The physical signs of the pupil: 1. Miosis. 2. Mydriasis. 3. Inequality or anisocoria. 4. Irregularity. 5. Immobility. 6. Hippus. The physical signs aside from the pupil: 1. Ophthalmoplegia. 2. Optic neuritis. 3. Choked disc. 4. Optic nerve atrophy. 5. Ptosis. 6. Diplopia. 7. Nystagmus. 8. Conjugate motion of the eyes. 9. Hemianopsia. 10. Achromatopsia. 11. Dyschromatopsia. 12. Scotoma. 13. Hemeralopia. 14. Interstitial keratitis. 15. Graefe's sign. 16. Stellwag's sign. . The eye reflexes: 1. The Argyll-Robertson pupil. 2. The consensual reflex. 3. Wernicke's hemiopic pupillary reaction. 4. Ciliospinal reflex. 5. Associated movement of iris in accommodation. » 1 66 diagnostic symptoms in nervous diseases Physical Signs of the Pupil Miosis is contraction of the pupil. It is one of the two forms of pathologic alteration in the diameter of the pupil. Another name for it and one by which it is often known is that of "pinpoint" pupil. The lesion in miosis is situated in the sphincter inhibi- tory center, or in the fibers coming from it. There are two types: spastic miosis and paralytic miosis. In the spastic form there is contraction of the sphincter iridis by stimulation; in the paralytic form there is paralysis of the dilator pupillae. Miosis is a physical sign in these conditions: Spastic or Irritative Miosis Paralytic Miosis Cerebral tumor (early stages). Tabes. Meningitis. General paresis. Cerebral abscess. Cerebral syphilis. Apoplexy. Certain drugs. Mydriasis is dilatation of the pupil. It, with miosis, comprises the only forms of pathologic alteration in the diameter of the pupil. Mydriasis may result from several causes, such as: i. Impulses to the ciliospinal center in the cord, com- ing either from the brain or from any region of the body. 2. A rundown physical condition. 3. Any irritation of the medulla exciting the respira- tory centers. 4. Emotional causes. 5. Stimulation of the sympathetic fibers in the neck. Mydriasis, like miosis, should be regarded as irritative or paralytic: THE EYE 167 Irritative : An irritative lesion in the upper part of the spinal cord. An irritative lesion of the sympathetic dilating fiber in the neck. Paralytic : Intracranial pressure. Lesions of part of third-nerve nucleus. Anisocoria is a synonym for inequality. It is a condi- tion in which the pupils are of different sizes, without regard to regularity of outline or mobility. It may occur in diseases of the stomach, lungs, kidneys, liver, and arteries, such as inflammation of the pleura, apical tuberculosis, pneumonia, and aneurysm. It is especially common in neurologic conditions. Conditions in which Anisocoria may Occur Congenital affections of the sympathetic. Different refractions of the two eyes. Unequal illumination of the two eyes. A lesion in only one centripetal light-reflex tract. A lesion in only one centrifugal light-reflex tract. Aneurysm. Inequality of the pupils may occur in several or- ganic and toxic nervous conditions; it is especially common in — Locomotor ataxia. General paresis. Cerebral syphilis. Alcoholism. The unequal pupil should, therefore, be regarded as strongly indicative of the presence of syphilis. Irregularity is a condition in which the contour of the 1 68 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES pupil is not uniform; it is often confused with inequality, but is entirely different. Pupils may be both irregular and unequal. Unequal pupils appear: O Q Irreg- ular pupils: Q M Irregularity is one of the physical signs of a syphilitic pupil. Immobility is a condition in which the pupil fails to respond to the light reflex and remains immobile. It is a loss of the light reflex, and is called the Argyll-Robertson pupil. This condition is caused by a break in the reflex arc of the pupil. A pupil which responds to light slower than the normal, and yet is not absolutely immobile, is called "sluggish." These three conditions of inequality, irregularity, and immobility are particularly characteristic of a pupil resulting from syphilis. The combination of the three, then, is especially to be found in general paresis, tabes, and cerebral syphilis. As all three begin with I, and all relate to the symptoms of the eye, to remember them is easy Irregularity, nequality. mmobility Hippus is a condition in which there is an alternate contraction and dilatation of the pupil. As one observes the pupil he sees it change constantly from contraction to dilatation and vice versa. The condition is especially seen in mania, anemia, and some of the functional conditions. Physical Signs Aside from the Pupil Ophthalmoplegia is a syndrome; it is the name given to a paralysis of certain ocular muscles. When the ex- ternal muscles of the eyeball, i. e., those supplied by the Ii Fig. 43. — Double ophthalmoplegia. Fig. 44. — Double ophthalmoplegia. 169 170 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES third, fourth, and sixth nerves, are paralyzed, an ophthal- moplegia externa occurs. When the muscles of the iris and pupil are paralyzed, an ophthalmoplegia interna occurs. Ophthalmoplegia externa means that the action of the eyeball is involved; ophthalmoplegia interna means that the action of the pupil is involved, that is, the iris and ciliary muscle. Either type may be acute or chronic, single or double; there may even be a mixed type. The latter is a very rare condition. Causes of Ophthalmoplegia Externa 1. Chronic alcoholism. 2. Hemorrhage. 3. Embolus and thrombosis. 4. Tumors. 5. Multiple sclerosis. 6. Tabes, general paresis, and syphilitic exudations. 7. Toxemia. 8. Poisoning (lead and mcotin). 9. Exophthalmic goiter. 10. Diseases of the medulla. n. Traumatism. 12. Diabetes. 13. Tubercular meningitis. Causes of Ophthalmoplegia Interna 1. Infection: (a) Syphilis (most frequent cause). (b) Influenza. (c) Acute rheumatism (rare). (d) Scarlet fever (rare). (e) Measles (rare). (/) Erysipelas (rare). THE EYE 171 (g) Pneumonia (rare). {h) Mumps (rare). (i) Typhoid (rare). (j) Zoster. (k) Postdiphtheritic. (/) Tuberculosis. 2. Exostoses and syphilitic periostitis. 3. Thrombosis of sinus cavernosus. 4. Toxic origin: (a) Alcoholism (chronic). (b) Diabetes. (c) Acute nephritis. (d) Saturnine poisoning. (e) Fish, meat, and oyster poisoning. (/) Aconite, atropin poisoning. (g) Mushroom poisoning. Optic Neuritis. — The condition known as optic neuritis consists of a swelling of the optic disc, which is of grayish color, striated, with a blurring of the margin; a swollen, tortuous condition of the veins, with a constriction of the arteries. It begins as a papillitis, and, when it has pro- gressed a few degrees, becomes a choked disc. Dana defines the choked disc as a papillitis with much serous infiltration. Remember, optic neuritis and choked disc differ in degree only. Therefore, cases will occur in which what to one man is an optic neuritis to another is a choked disc. In optic neuritis there are less swelling and less pro- jection of the disc. There is, however, more exudation, and this extends more beyond the disc into the retina. In choked disc the swelling is limited to the disc; the predominant characteristics are the engorgement and 172 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES the edema. Of the two, inflammation is more pro- nounced in neuritis. In either form sight may or may not be impaired. The more advanced the neuritis, the greater is the likelihood of a defect in the vision. The most frequent and most Fig. 45. — Sixth nerve palsy. important cause of these two conditions — conditions which are really the same but different in degree — is tumor of the brain. Sir William Cowers says that in four out of five cases of brain tumor optic neuritis is present. Wyllie says in cerebellar tumors the propor- tion is fifteen in sixteen. THE EYE 173 Optic neuritis may affect one or both eyes; it may develop early or late; it may advance rapidly or slowly. The type which accompanies the cerebral tumor and tumors of the cerebellum is the same. Optic neuritis, or, to use the better term, papillitis, occurs in the following conditions: 1. Heredity. 2. Orbital and peri-orbital affections. 3. Brain tumors and abscess. 4. Hydrocephalus. 5. Meningitis. 6. Infectious fevers. 7. Nephritis. 8. Toxic neuritis. 9. Alcohol. 10. Lead poisoning, n. Severe hemorrhage. o 12. Diseases of menstruation, pregnancy, and lacta- tion. 13. Idiopathic. The most frequent cause is tumor of the brain. Next to this comes meningitis. The form of papillitis most common in brain tumors begins as an optic neuritis, later becoming a choked disc. These conditions of papillitis, optic neuritis, and choked disc can be observed and diagnosed only by the ophthal- moscope. The skilled user of this instrument can with a little practice measure the amount of swelling of the disc. The diameter of the disc may be even two or three times its normal size. Choked Disc. — Von Graefe first gave us the term " choked disc." Its origin has never been made clear. 174 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Two theories have been suggested to explain it: one is pressure, edema, and inflammation; the other is toxemia. i Fig. 46. — Hernia cerebri following decompression. The final stage that choked disc attains is optic nerve atrophy. Therefore, a patient suffering from a choked disc or optic neuritis requires constant observation; if THE EYE 175 the condition advances, surgical interference may be necessary to relieve pressure on the optic nerve and thus save the sight. Optic Nerve Atrophy. — In this condition there is degeneration of the optic nerve, with resulting atrophy and loss of vision. There are two types: 1. Primary optic nerve atrophy, or simple. 2. Secondary optic nerve atrophy, or inflammatory. 1. Primary optic nerve atrophy is sometimes called simple atrophy. In this form the disc is white, with sharply defined edges and a saucer-shaped excavation. The size is somewhat diminished. The lamina cribrosa is often seen very plainly; the minute vessels have dis- appeared; the arteries of the retina are diminished in caliber. Simple atrophy is due to: 1. Syphilis, general paresis, and tabes. 2. Tumors. 3. Multiple sclerosis. 4. Malaria. 5. Diabetes. 6. Certain poisons, i. c., wood alcohol, lead. 7. Myxedema. 8. Hemorrhage. 9. Idiopathic. 2. Secondary atrophy is also called postneuritic atrophy. In this form the disc is white, but the edges are irregular. There is no saucer-like depression, and the disc is covered with new connective tissue from the previous neuritis, which hides the lamina cribrosa. Secondary atrophy is due to: 176 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES i. Papillitis. 2. Retrobulbar neuritis. 3. Retinitis. Fig. 47. — Ptosis. 4. Embolism of the central artery. 5. Glaucoma. 6. Pigmentary degeneration of the retina. 7. Fracture of the orbital canal, causing wounds to nerve. THE EYE 177 Ptosis. — The term ptosis means drooping of the eyelid. It results from paralysis of the third nerve. In addition to drooping of the lid there occurs double vision, diver- gent strabismus, dilatation of the pupil, loss of the light reflex, and loss of the power of accommodation. All muscles supplied by the third nerve are usually not attacked simultaneously. It may occur in all degrees and may be single or double. Unilateral ptosis is most frequently syphilitic in origin. The causes are: 1. Syphilis. 2. Congenital. 3. Traumatism. 4. Non-development of the nucleus of the third nerve. 5. Postdiphtheritic. 6. Epidemic cerebrospinal meningitis. 7. Polio-encephalitis hemorrhagica superior. 8. Chronic progressive ophthalmoplegia. 9. Intoxications. 10. Multiple sclerosis, n. Tabes. 12. General paresis. 13. Functional disturbances. 14. Syringomyelia. 15. Brain tumor. 16. Neurasthenia. 17. Myasthenia gravis. Diplopia means double vision. It is due to the fact that the images of the object fall on non-corresponding fields of the retina. Diplopia occurs in the following conditions: 1. Tabes. 2. General paresis. 12 178 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 3. Cerebrospinal syphilis. 4. Alcoholism. 5. Brain tumor. 6. Myxedema. 7. Hysteria. The cause of diplopia is a paralysis of certain eye- muscles. Diplopia may be of two kinds: homonymous, when the false image is on the same side as the sound eye; heter- onymous, when the false image is on the opposite side. Diplopia is a symptom of: 1. Oculomotor, or third nerve, palsy. 2. Abducens, or sixth nerve, palsy. 3. Pathetic, or fourth nerve, palsy. Nystagmus is an oscillation of the eyeball. The best illustration is the eye of a person observing passing objects from a rapidly moving train. The oscillations are rapid and the extent of their excursions is short. The direction of these oscillations may be any one of several. Therefore, nystagmus may be lateral, vertical, mixed, or rotatory. The condition is nearly always bilateral. Nystagmus may be physiologic or pathologic, and occurs in the following conditions: 1. Physiologic nystagmus. (a) Person riding in a train. (b) Person suddenly whirled around. (c) Galvanism. (d) Irritations of the inner ear by alternate hot and cold irrigations. 2. Pathologic nystagmus. (a) Congenital amblyopia; error of refraction. THE EYE 179 (b) Sudden anemia or disorders of the cerebral circulation. (c) Certain conditions of intoxication. (d) Certain brain lesions: affections of the cerebellum; affections of the cerebellar peduncle, the nuclei of the oblongata, the posterior longitudinal bundle, the vestibular nerve. (e) Certain occupations: miners. (/) Disseminated sclerosis. ■ (g) Meningitis. (h) Hereditary ataxia. (i) Reflex symptom. (j) Reflex symptom from remote irritation. Diseases in which Nystagmus Occurs 1. Multiple sclerosis. 2. Friedreich's ataxia 3. Alcoholism. 4. Syringomyelia. 5. Brain tumor. 6. Heredity. 7. Meningitis. 8. Cerebral hemorrhage and softening. 9. Cerebral and lenticular opacities (choroiditis and retinitis). 10. Albinism. Nystagmus may be elicited by having the patient's eye follow the examiner's ringer as he holds it well out to one side. Pathologic nystagmus is not present unless apparent during the movement of the eye, as the oscil- lations which appear after the eye is at rest in the l8o DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES extreme position may be physiologic and the result of fatigue. The occurrence of nystagmus in diseases of the spinal cord is without doubt an indication of the involvement of the cerebrospinal nervous system or the cerebellum or the parts adjoining it. Conjugate Motion of the Eye. — The two eyes move together. They may converge to observe a near object; they may diverge to observe a distant one; they may turn up or down. In any event in the normal individual they move together. The mechanism necessary to bring about this condition is complex. Some clinicians maintain that : Destructive lesions of the brain cause the patient to look toward the lesion. Irritative lesions of the brain cause the patient to look away from the lesion. Hemianopsia means absence of half the field of vision of each eye. There are two varieties: (a) homonymous, when it affects the corresponding halves of the eyes; (b) heteronymous, when it affects the opposing halves of the eyes. Heteronymous is of two kinds: bitemporal and binasal. Thus, a blindness of the two outer halves of the eyes would be bitemporal hemianopsia, whereas a blindness of the outer half of the right and the inner half of the left retina would be a left homonymous hemia- nopsia. These various forms depend upon the location of the lesion. The causes of bitemporal heteronymous hemianopsia are tumors at the base, tumors of the hypophysis, and syphilis at the base. THE EYE l8l The three rules to remember in regard to hemianopsia are as follows: i. If the blindness is restricted to one eye or affects both eyes, but is not symmetric, then the lesion must be in the optic nerve itself. 2. In homonymous hemianopsia the lesion is above the chiasm. 3. In bitemporal hemianopsia the lesion is in the chiasm itself, located anteroposteriorly. This is seen in acromegaly. Hemianopsia is almost invariably a symptom of an organic disease. It may, however, rarely be found in certain functional conditions and in migraine and gout. The organic conditions in which hemianopsia occurs are as follows: 1. Hemorrhage. 2. Inflammation. 3. Tumors. 4. Softening. The test for it is to have the patient look steadily and straight at the examiner; meanwhile the latter brings some small object from the extreme right and left into the field of vision. The patient, if suffering from hemian- opsia, will not be aware of its presence until it has traversed one-half of the visual field. A second test is that the eyelid will not wink at the close proximity of the finger to the blind half of the eye. Achromatopsia means loss of color vision. Dyschromatopsia means imperfect color sense. Scotoma is a blind spot. It may be on the periphery of the visual field or in the center, and, in accordance with its location, is known as peripheral or central sco- 182 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES toma. It should be tested for by moving a small piece of paper while the patient looks straight ahead at a fixed point, one eye being closed until the test paper reaches a point in the field of vision at which it appears dull, colorless, or is invisible. Pathologically patients notice the defects in the field of vision. There may be central scotomata only in respect to cer- tain colors — a common symptom in tobacco poisoning. Diseases in which a Central Scotoma Occurs i. Organic diseases of the optic nerve \ TT ," { Hemorrhage. 2. Organic diseases of the retina. 3. Central opacities in lens or cornea. 4. Multiple neuritis. 5. Migraine. 6. Partial destruction of peripheral optic tract. 7. Tobacco and alcohol poisoning. 8. Multiple sclerosis. Hemeralopia is day-blindness. This is a condition in in which the patient is able to see better in a dim light. It is a symptom which occurs along with amblyopia and is common in nicotin poisoning. Stewart says that " it is probably due to the fact that the bright light rapidly fatigues the retina, and by producing pupillary contrac- tion causes the peripheral part of the retina to be less in use than the central, whereas in the dim light the pupil dilates and the unaffected peripheral portion of the retina comes into play." Von Graefe's Sign. — The upper eyelid does not smoothly accompany the eyeball when the patient's eye follows the finger from above downward : it lags. THE EYE 183 Stellwag's Sign.— A widening of the palpebral fissure, together with a decrease in the frequency of winking, is known as Stellwag's sign. THE EYE REFLEXES In the Argyll-Robertson pupil the reflex to light is lost, though the reflex to accommodation is preserved. The condition is usually bilateral; it may be unilateral. It is caused by a break in the reflex arc. To impress this remember the two last letters of the word Argyll — L. L. means loss of light. The way to test for the symptom is to have the patient look at a distant object, shade the eye to be examined, and then suddenly admit light to the pupil. In health the pupil should at once contract. A good light should always be used; at times an electric light is best. Most of the internes in the hospitals carry small pocket elec- tric light lamps. With this method a good light can be quickly admitted to or removed from the pupil. An- other method of examining the pupil is to throw a light into the eye by means of an ophthalmoscopic mirror; still another, by means of a lens. Judgment should never be pronounced on a pupil until it has been tested by a good light. It should always be borne in mind that no hard and fast rule can be laid down. There is, in the case of the reflexes of the pupil, as in every other instance, every degree of gradation from the normal to the pathologic. Previous to the pupil becoming rigid, there is a stage in which the reaction is slow or, as it is technically called, "sluggish." The sluggish type of pupil is an incipient 184 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Argyll-Robertson pupil, and one which becomes so after a time. The sluggish pupil may precede the Argyll- Robertson by months or even years. The Argyll-Robertson pupil is a symptom of: 1. Tabes. 2. General paralysis. 3 . Progressive muscular atrophy (Charcot-Marie-Tooth type). 4. Disseminated sclerosis. 5. Cerebral softening or atrophy. 6. Cerebral syphilis. 7. Hydrocephalus. 8. Tumors of third ventricle. 9. Congenital syphilis. Sluggish pupils occur in — 1 . Filix-mas poisoning. 2. Chloroform narcosis. 3. Acute alcoholism. 4. Acute morphinism. It is, however, most common as a symptom of: 1. Tabes. 2. General paresis. 3. Cerebral syphilis. The Argyll-Robertson pupil is a most valuable sign in the diagnosis of tabes, in which it occurs in 90 to 95 per cent, of the cases and in general paresis. Another name for it is reflex iridoplegia. The Consensual Reflex. — The consensual reaction is the reaction to light, which occurs in one pupil as the result of the admission of light to the other. To test for this reflex, shade and then illuminate the eye to be ex- amined while at the same time we note the light reaction THE EYE 185 in the other. Immobility in either eye proves a deficient light conduction, and therefore an absence of the con- sensual reflex. This is directly opposed to the direct reflex, which simply means that the pupil examined is susceptible to light and darkness. Wernicke's Hemiopic Pupillary Reaction. — A ray of light thrown on the blinded halves of the retinas (in ho- monymous lateral hemianopsia) causes no contraction of the pupil if the lesion is peripheral to the point at which the reflex fibers to the Edinger-Westphal pupillary nu- cleus are given off. Illumination of the sensitive halves of the retinas does, on the contrary, cause contraction of the pupil if the lesion is central to the point at which the above reflex fibers are given off. The ciliospinal reflex consists of the dilatation of the pupil caused by stimulation of the skin of the neck on the same side. CHAPTER XII DISTURBANCES OF SPEECH Just as certain neurologic conditions have gaits and tremors that are characteristic and diagnostic, so others exhibit peculiar forms of speech and expression in which not only expression, but also tone of voice, is altered. To examine the patient's speech it is necessary first to have him speak, next to have him read aloud, and lastly to have him repeat some test phrase. It is best to ex- amine his speaking ability while he is telling the his- tory of the case, so that his attention will be distracted from what the examiner is trying to discover. In read- ing aloud the patient should be given some simple mat- ter, preferably the daily paper. In repeating the catch phrases he should be given ample opportunity to hear and comprehend the significance of the words, and then be asked to repeat after the examiner. There are many phrases which are used. It is best to have two or three and always to make use of the same ones. In this way the examiner gets accustomed to the various pronuncia- tions of set phrases: " Third riding artillery brigade," "Methodist Episcopal," and " Hippopotamus hurrying home." These phrases should always be repeated three times in succession. The normal speech is free from any idiosyncrasy. There is no blurring or elision of syllables. It is note- worthy neither for slowness nor for rapidity. The words 186 DISTURBANCES OF SPEECH 1 87 are expressed in a clear, straightforward manner. The tongue and lips are free from any tremor. In testing speech it is important to observe the manner of expression, the speed with which the patient talks, the clearness with which he pronounces the different words, and the absence of any elision or slurring. It should be noted, whether the pitch of the voice is high or low. I. Dysarthria, or disturbances in articulation. A. Varieties: 1. Disturbances in phonation: vowels and consonants indistinct. 2. Disturbances due to paralysis of lips, tongue, or palate muscles; nasal voice and as if patient had pudding in mouth. 3. Bulbar speech. 4. Anarthria. 5. Bradylalia and scanning speech. 6. Stuttering. 7. Lisping: negligent, organic, neurotic. 8. Stumbling speech. 9. Slurring speech. B. Causes: Due to toxic action of alcohol; early stage of ether anesthesia. Due to lack of development and infan- tile disease: Idiocy and cretinism. Diplegia. Hereditary ataxia. Due to local disturbances: Cleft-palate. Hare-lip. Absence of teeth. Perforated nasal septum. Stomatitis. 1 88 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES 4. Due to disease: Multiple sclerosis. General paresis. Brain tumor. Hemiplegia. Myasthenia gravis. Chorea. Epilepsy. Bulbar palsy. Paralysis agitans. Insanity (senile and manic) . Meningitis. Progressive lenticular degeneration (Wilson's disease). Myxedema. Friedreich's disease. Diplegia. II. Aphonia. A. Due to hysteria. B. Due to paralysis of vocal cords. C. Due to paralysis of muscles of larynx. D. Due to tumor of larynx. III. Aphasia. A. Motor. B. Sensory. Varieties of Dysarthria There are many kinds of disturbances in articulation. A list of the principal ones stands at the head of this chapter. Here I shall say only a word or two in describ- ing the most important. The simplest form of all is that which results from an indistinct manner of pronouncing the various letters, both vowels and consonants. The second type is the one resulting from a paralysis .DISTURBANCES OF SPEECH 1 89 of the several muscles concerned in the act of speaking. This type varies according to which muscles are involved : if the lip muscles alone are involved, the defect is evident in the labials and in the labiodentals. If the tongue only is involved the defect is evident in the Unguals and in the appearance of the tongue itself, which is shriveled, tremulous, and protruded with difficulty. If the palate alone is involved, it is evident in the palatals and in the nasal twang. There may exist any combination of these conditions. Bulbar speech is the name given to that type of speech which accompanies lesions of the bulb, that is, lesions of the pons and medulla. This is fully described elsewhere. Anarthria is the term applied to that form of speech which is absolutely unintelligible. It is neither aphasia nor aphonia. In anarthria the patient can emit sounds, but they convey no sense. Bradylalia is slowness of speech. It is characteristic of some imbeciles, of the child learning to speak, and even of some normal people, who cerebrate with great slowness. Scanning speech is placed under this heading because of its slowness; however, its most marked char- acteristic is the great deliberation and clearness with which each syllable is enunciated. The sound conveyed to the listener is that of a person scanning a line of Virgil. This scanning speech is described later on. It occurs most commonly in multiple sclerosis; it may, however, accompany general paresis and some forms of aphasia. Stuttering is a spasmodic form of speech disorder. The muscles of speech are affected with cramps or spasms. Lisping, according to Scripture, may be of three kinds. The negligent type is due to defective perception and 190 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES execution of sounds; the organic type is due to abnormal condition of the speech organs ; the neurotic type is due to functional disturbances and the temperament of the patient. Slurring speech is synonymous with thickness of speech. It is especially evident following protracted and severe illness, such as typhoid. Causes of Dysarthria The speech of the alcoholic varies from simple garru- lousness to complete paralysis. The release of motor impulses is greatly accelerated, with the result that the patient repeats those phrases which are most familiar and which he has long since learned by heart. He is apt to make use of compound words and rhymes. In the lowest forms of idiocy, babbling, grunting, and echolalia are the characteristics, and also the use of words of the patient's invention. Lalling and stammer- ing are of frequent occurrence, but are more likely to be met with as we ascend the scale. The speech of the cretin has neither characteristic difficulty nor unusual tone. It is slow, labored, and develops late. The vocabulary is limited. The speech of diplegia is slow and stammering. If the condition appears in the very young, speech may never develop; if in older children, the result is usually a gradual loss of. speech. The speech of Friedreich's disease, or hereditary ataxia, is slow, ataxic, and scanning. It resembles neither the pure type of multiple sclerosis nor that of paresis; it is rather a combination of the two; some words come quickly, others slowly. The pitch of the voice is apt to DISTURBANCES OF SPEECH 191 change suddenly and in the midst of a sentence. As the disease advances, a mental enfeeblement becomes evi- dent, which further serves to modify the articulation. This speech is clumsy, and conveys the impression to the listener that the patient has a mouthful of something very hot. The most common defects of speech due to local disturbances are those resulting from hare-lip and cleft- palate. In the former there is an interference with the proper pronunciation of the labials, while in the latter there is an interference of the palatals, accompanied by a nasal twang. The speech of multiple sclerosis is peculiarly diagnostic. While the tone is monotonous, the enunciation of the words is clear and measured. It can best be designated by the word "scanning," as its tones recall the scanning of a line of Virgil. Scripture describes it as bringing out each syllable with a distinct effort, but without the char- acteristic anxiety of the stutterer. Oppenheim says that the patient speaks like a child spelling out letters. An- other word that has been used in connection with it is "staccato." The Speech of General Paresis. — The words which best describe the speech of the paretic are ataxic, stumbling, and alliterative. There is a marked tendency to slight words, and even syllables. The speech is slow, halting, and at times stops altogether. It can be compared to the patient's gait. It is irregular, stumbling, and un- certain. Accompanying the mechanical defect in speech is a loss of memory, together with a progressive enfeeble- ment of mind and a tremor of the muscles about the mouth. These factors complicate the picture and pre- 192 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES sent a form of speech which is both cortical and peripheral. This is the one form of speech which is most clearly illustrated by use of the test phrases. In brain tumors the speech may or may not be affected, according to the location of the growth. If it is in the third left frontal convolution so as to affect the speech center, all varieties of disturbances will arise. At first there may be only a slight disinclination to speak; later on mild aphasia will develop, and eventually complete loss of speech. The prevailing hebetude, which is so diagnostic of these patients, becomes evident in the speech. The patient is slow to think, slow to talk, and does so with difficulty. If the lesion is in other parts of the frontal convolution, there may be no disturbance. If the lesion is in the left temporal lobe, there will be word-deafness, amnesic aphasia, and paraphasia. If the lesion is in the left inferior parietal lobe, there will be alexia and agraphia. It must always be borne in mind that if the patient is left-handed a tumor situated in the right hemisphere will give all the symptoms of one in the left hemisphere of a right-handed man. The speech of hemiplegia is often involved. The char- acter of the defects differs according to the location of the lesion. If the paralysis is on the right side, the le- sion on the left, the speech center is involved, and there may result one of the many forms of aphasia, apraxia, or alexia. If, on the other hand, the paralysis is on the left, the lesion on the right, there is no involvement of the speech center. The difficulty is one of articulation rather than of speech. In this instance the voice is thick and indistinct; the Unguals are improperly pronounced, and, DISTURBANCES OF SPEECH 193 from the physical interference which the paralyzed half of the tongue, lips, and cheek muscles causes, the enun- ciation is slurring, indistinct, and thick. It should al- Fig. 48. — A case of tabes showing double ptosis and nodule deformities at the costochondro articulations (Charcot ribs). ways be borne in mind that this condition of affairs may be completely reversed, as in left-handed persons the speech center is on the right side of the brain. 13 194 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES The speech of myasthenia gravis is variable. It may remain normal. It may, as a result of the weakening of the muscles, slowly and gradually become more and more indistinct, until it is lost altogether; it may simulate that of bulbar palsy. The principal feature is a pro- gressive tendency to grow fainter, feebler, and more in- distinct, until following a period of rest it again becomes normal. The speech of the choreas is jerky and irregular. The words are broken, and, being affected by the breathing movements, come forth in a violent and aggressive man- ner. They are hurled forth. This defect of speech is more evident in the chronic forms, but to a slight degree does exist in the acute types. In the advanced and ag- gravated cases the patient may be unable to speak at all. The speech of epilepsy is neither characteristic nor dis- tinctive, although in some cases monotonous. In many instances the enunciation is thick and indistinct; this is due to the fact that the patient is suffering more from overdoses of bromid than from epilepsy. As a postepi- leptic manifestation there often develop disturbances which are ( central in origin and accompany mental de- terioration. The speech of bulbar palsy is nasal. It becomes gradu- ally indistinct, more labored, and finally unintelligible. The principal mechanical difficulty is inability on the part of the patient to pronounce the dentals and Unguals. Added to this is an inability to express the words. The paralysis of the throat, tongue, and lips renders it ex- ceedingly difficult for the patient to get the words out of his mouth. He is, therefore, forced to make extra- ordinary efforts, and so conveys the impression of one DISTURBANCES OF SPEECH 1 95 1 who makes an effort beyond his powers, and who raises his voice to an unnecessarily high pitch. The voice is usually nasal; it may be hoarse, and in the aggravated cases is explosive. Added to all these difficulties are a dribbling of saliva, a tremor of the lips, a nasal regurgi- tation of fluids, and a difficulty in swallowing and cough- ing. The speech of paralysis agitans can best be compared with the gait of paralysis agitans. As the patient festin- ates in his walk, so does he festinate in his talk. He is slow to begin, the lips are opened, great deliberation is displayed, there is hesitancy, and at last, slowly and deliberately, the first few words make their appearance. Then he speaks faster and faster until finally the words seem to tumble out after each other, so rapid and explo- sive is the utterance. Another feature of this condition is the change of voice. It becomes shrill, high-pitched, and piping. In myxedema the speech becomes slow, rough, and monotonous. Besides this list there are also the different brain con- ditions which produce the aphasias. I have not included them in this category, as I regard them as being of suf- ficient importance to occupy a place of their own. Apha- sia, alexia, apraxia, etc., have always been confusing to students, and ought, therefore, to be in a class by them- selves. CHAPTER XIII APHASIA The word aphasia is derived from the Greek a, priv- ative, and 4>r]ni, which means to speak. The technical meaning of the word, therefore, is absence of speak- ing. Webster gives an excellent explanation of the term when he defines it as "loss of the power of speech or of the appropriate use of words, the vocal organs remain- ing intact, and the intelligence being preserved." In other words, the aphasic is one who is afflicted with a lesion in one of his speech centers, and yet, at the same time, is perfectly conscious of his infirmity. These speech centers are situated in the cortex of the brain. The fibers that connect them are subcortical. The subject of aphasia has always been exceedingly confusing and difficult to every student. This has, to a great extent, been the fault of the text-books and the teachers. There has never been any definite agreement among authors as to the proper and uniform division of the subject. The only way to understand the subject of aphasia is to look at it from the simplest point of view, to apply to it as few and as simple terms as possible, and to divide and subdivide it in a systematic, common-sense way. Looked at and studied under these conditions, it ceases to be the bugbear which students always picture it; there emerges from a mass of unintelligent words a clear, comprehensible system. 196 APHASIA IQ7 To accomplish the act of speaking correctly the brain must do two things: First, receive an impression, and second, express the idea. In other words, the function, of the brain is that of an organ which first is being actec upon, and then, in response to the external stimulus, itself acts. To each function is given a special name. Motor is the name given to the function of expressing impres- sions; sensory is the name given to the function of receiving impressions. There are, therefore, two types of aphasia, motor and sensory. Motor aphasia means faulty expression. Sensory aphasia means faulty per- ception. Fix these two divisions clearly in mind. All other types of aphasia and all other words relating to aphasia may be classified under these two headings. The next division of aphasia is a subdivision of these types, motor and sensory. To make this division in- telligible, one must bear in mind that there are two main ways in which impressions may be conveyed to the brain, and that there are two ways in which the brain can express these impressions. These two chief ways of conveying an impression to the brain are by means of the two senses of seeing and hearing. The two ways in which the brain may express an impression are by the acts of speaking and writing. You will readily see, therefore, that there are two types of motor aphasia and two types of sensory aphasia. The important point at this stage is to have in mind what are these two kinds of motor aphasia and what are these two kinds of sensory aphasia. Inasmuch as the brain has two ways of receiving an im- pression, through hearing and seeing, an interference with either one of these two methods will cause sensory apha- sia. The memories of words which are heard and of 198 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES words which are seen are stored up in certain parts of the brain, from which, later on, they can be drafted for use. These parts of the brain are called centers. In the case of words heard the center is called the auditory word center; in the case of words seen the center is called the visual word center. A lesion affecting either of these centers or a lesion affecting the fibers which connect these centers, either with themselves or with the two motor centers, will produce aphasia. The character of the aphasia will depend wholly upon whether the individual center is affected, whether the individual center plus the fiber leading to another center is affected, or whether more than one center is affected. The absolute location of these centers must be learned. The auditory word center lies at the upper surface of the left temporal lobe, in the near-lying posterior end of the first temporal con- volution. The visual word center is situated in the angu- lar gyrus. The same principle holds true concerning the two motor centers. Here there are also centers in which the same process of storing-up is carried on. These, too, are called the centers of speaking and writing. They are situated in Broca's convolution, that is, the third left frontal, in the near-lying part of the precentral convolu- tion. A patient, therefore, is suffering from sensory aphasia who hears, but not understandingly, and who sees, but not understandingly. That is to say, he may hear perfectly, but the sounds conveyed to him are un- intelligible ; the speaker appears to him to be talking in a foreign language. He sees, but the object as conveyed to him is not as it appears to the normal man. He expresses his ideas intelligibly. He cannot, however, converse, APHASIA 199 nor answer written or spoken questions. A patient is suffering from motor aphasia who understands what is spoken and what he reads, but at the same time is unable to express his ideas in intelligible language, or to express them in intelligible written form. He is conscious of his defects; he is able to utter sounds. These may be the constant repetition of some particular word or small sentence, or they may be simply a jargon. The writing Sensory Fig. 49.— Parallelogram for examining an aphasic. is of the same character. It may be one or two letters, parts of words, or simply strokes of the pen. Causes.— The type of lesion which may cause an apha- sia is usually circulatory, and, therefore, apoplectic. Rarely it is due to the presence of a new-growth, to ab- scess or softening. In the first instance it may be an embolus, a thrombus, or a hemorrhage. It is very dif- ficult to differentiate among the three. Stewart, how- 20O DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES ever, puts it quite aptly when he says: "Embolism pro- duces the symptoms suddenly; hemorrhage takes sev- eral minutes; thrombus perhaps hours; abscess and tumors are still more gradual." I have appended a diagram which is a combination of one from B ram well and one from Stewart. Turn to it, and, with it before you, carefully follow these directions: The base of the picture is an outline of the brain. There are four shadows on it — two in the fore part, two in the lower and posterior part. These four shadows repre- sent the four centers; the two front ones are the centers for speaking and writing. They are the ones which are involved in motor aphasia. The two lower and posterior ones are the centers for seeing and hearing — the visual word center and the auditory word center. These are the two centers which are involved in sensory aphasia. Draw a line connecting the two sensory centers with the two motor centers, that is to say, the visual word center with the writing, and the auditory word center with the speaking. Then connect the two sensory cen- ters with each other, that is to say, the auditory word center with the visual word center. There is now practi- cally a parallelogram. With this picture in mind, plan now the form of examination which you are going to follow. EXAMINING AN APHASIC In order to examine an aphasic, it is necessary to ask him questions which will prove or disprove the integrity of each center; secondly, questions which will establish the broken or unbroken connection from the one center to the other, and, thirdly, questions which APHASIA 20 1 will prove or disprove the connection between three of those centers. Therefore, first ascertain if the center for speaking is intact. Then if the center for writing is in- tact. Then if the auditory word center is intact and the visual word center. Secondly, ascertain if the patient can receive an impression in either of the sensory cen- ters and express it in the motor. Thirdly, if he can re- ceive an impression in either sensory center, convey it to its fellow, and then transmit it to the corresponding motor center. In examining an aphasic it is necessary to have two lists — one of articles and one of questions; also paper and pencil. The articles should be such as are in daily use, as: pencil, knife, scissors, coins, match-box, watch, keys, etc. The questions should be of the simplest and couched in plain language. The best are: "How are you?" "Where do you live?" "What day is this?" The examination will take time and ought to be con- ducted in a systematic and regular way: 1. Test for the Integrity of the Motor Speaking Cen- ter. — In the examination of this center the point to as- certain is whether the patient can speak intelligibly. Note his ability to talk, to pronounce, his choice of words, and his method of talking spontaneously. 2. Test for the Integrity of the Writing Center. — The same questions should be asked and the same method of examination carried on in this as in the test of the speak- ing center, that is to say, have the patient write, and note the character of his writing, his method of writing, and his penmanship. 3. Test for the Auditory Word Center. — Here the questions should be directed to ascertaining whether he 202 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES comprehends what he hears. .Direct him to perform certain simple acts, to point out the watch, the pencil, etc., and ask him questions the answers to which will convey information as to whether he comprehends what is being said. 4. Test for the Visual Word Center. — The point to as- certain in this test is whether the patient can comprehend written language. Write down a series of easy questions, such as the following, and ask the patient to answer them: "How old are you?" "Where do you live?" "What is your wife's name?" 5. Test for the integrity of one sensory and one motor center, together with the fibers connecting them, as, for instance, the visual center and the writing center. The object here is to ascertain the patient's ability to com- prehend something which he sees, to store up that im- pression, and then to convey it in practical form. Have the patient copy a simple sentence, such as: "This is a fine day." "I have been very sick." 6. The test for the integrity of the corresponding sen- sory and motor centers, together with the fibers con- necting them, namely, the auditory word center and the speaking. Ascertain if he can copy what he hears, if he can copy words and sentences which he has heard. Direct the patient to write from dictation simple sen- tences, such as, "This is a fine day"; also to repeat aloud after the examiner. 7. Test for the integrity of the two sensory centers, together with one motor, namely, the auditory word center, the visual word center, and the writing center. Can he comprehend what he hears, convey it to the visual word center, store it up, and then transmit it to the APHASIA 203 writing center; in other words, can he write from dicta- tion? Have the patient write a line from dictation. 8. Test for the integrity of the two sensory centers, together with the other motor center, that is to say, can he perceive something, transmit it to his hearing center, store it up, and express it through the speech center; in other words, can he read aloud, and by his hearing know he has read correctly? Have the patient read aloud. In addition to these tests, finally he should be directed without speaking to him to imitate you. This is to es- tablish his ability to perform gestures and pantomime movements. These two acts occur more or less invari- ably in aphasia. These tests are quite sufficient to conduct a satisfactory examination of an aphasic. They represent, as you will see by looking at the diagram, every possible combina- tion of centers, except putting together the two motor, which manifestly is impossible, and the very unusual routes of transmission from the auditory word center direct to the writing, and from the visual word center direct to the speaking. These are so unusual as not to be necessary for the student to concern himself. Varieties of Aphasia There are certain terms which you ought to know. These are: Auditory aphasia. Visual aphasia. Motor aphasia. Apraxia. Alexia. Agraphia. 204 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES Auditory aphasia is simply, as you have seen, beginning word-deafness. It may be of two types. This is de- pendent upon whether the lesion is cortical or subcortical. The latter type is exceedingly rare and need not concern you. In cortical word-deafness, or cortical auditory aphasia, the lesion is in the cortex itself; the patient not only suffers from word-deafness, but he has additional symptoms, due to the fact that the motor speech center is no longer controlled by the auditory center. The pa- tient makes mistakes both in speaking and reading. He makes mistakes in spelling. He is able to talk, but his language is an absolute jargon because he is suffering from word-deafness and is unaware of his own errors. This is distinct from pure motor aphasia, where the pa- tient recognizes his own mistakes as soon as he has ut- tered them. Visual aphasia is another term for word-blindness, or alexia. Here the patient can see, but cannot compre- hend. The letters are to him like those of a foreign language. Here, too, he may suffer from a cortical or subcortical lesion; the symptoms vary in accordance with it. In the subcortical type the incoming fibers are affected, though the visual word center itself remains intact. He knows what he wishes to write, and is able to write it, but once having accomplished this, he is unable to read it. In the cortical type, in addition to the symp- toms described in the subcortical, the patient suffers from agraphia. In motor aphasia the patient cannot express what he wishes in spoken words. I Iughlings Jackson describes it very well when he says: "The patient is speechless, but not wordless." As a rule, he repeats certain phrases, APHASIA 205 being at the same time conscious of his error. This variety is also either cortical or subcortical. In treating the subject of aphasia, do not forget that I have described only the chief types, which are the dis- tinct types. It is necessary to do this to render the sub- ject intelligible and clear. Bear in mind always that the purely classic case is rarely the one which pre- sents itself; that you are most apt to sec not the pure type of aphasia, but combinations of these, irregular, unusual types, or even a complete destruction of all the centers, resulting in total aphasia. The cerebral artery is the one which supplies the speech centers. It is also the vessel which supplies the motor areas of the cortex and the corpus striatum; therefore, total aphasia and right hemiplegia often go together. Always bear in mind that the examination of a left-handed person must be exactly reversed, because in him the speech center is on the right. About nine-tenths of the people are right- handed, and it is therefore in very rare instances that this rule must be applied. There is a form of aphasia which is not organic, and to which has been given the name of hysteric aphasia. It is fairly common, and one which you must be on the lookout for. Like most hysteric conditions, it is accompanied by other symptoms, including stigmata of degeneracy and peculiar psychic and motor symptoms. Apraxia signifies the inability of a patient to perform certain regular, definite, muscular movements when he is suffering neither from physical nor mental impairment. Thus, a patient may be given a pencil, and may use it as he would a cigar, or when given a pair of scissors may use it as a button-hook. 206 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES The final division of aphasia is into cortical and sub- cortical. If the lesion is in any one of the centers, that is, the auditory, visual, speaking, or writing, the lesion is said to be cortical. If, on the other hand, the lesion is in the fibers running to the center, connecting the centers with each other, or leading from the centers, it is said to be subcortical. The symptoms of the two conditions will differ materially. It is evident that if the lesion is in the center itself, the damage will be greater, more ex- tensive, and more pronounced. It is, therefore, necessary to fix clearly in your mind the symptoms which occur in both the cortical and sub- cortical types of each one of these centers. Symptoms of Motor Aphasia Patient cannot express himself by spoken language. He is speechless, but not wordless (Hughlings Jackson). (a) Symptoms of cortical motor aphasia : Voluntary speech . . . J Repetition Reading aloud • Lost or impaired. Voluntary writing. . Writing to dictation. Copying Comprehension of spoken language [ Retained. Comprehension of written language (The latter impaired, according to Dejerine.) (b) Subcortical motor aphasia: Voluntary speech . . Repetition * Lost or impaired. Reading aloud Reading ] Writing [ Retained. Comprehension of spoken language APHASIA 207 Lost or impaired. (c) Cortical sensory aphasia: Voluntary speech conserved, but verbal para- phasia. Copying retained Repetition Reading aloud Voluntary writing Writing to dictation Comprehension of spoken speech . Comprehension of written speech . (d) Subcortical sensory aphasia: Voluntary speech Voluntary writing -Retained. Copying. . . . Comprehension of written speech. . Comprehension of spoken speech . T Repetition f j^° j ^ Writing to dictation J P CHAPTER XIV ELECTRIC REACTIONS In health electric stimulation of a muscle causes a contraction which follows certain definite laws and affects the different poles in a definite manner. The character of this contraction is sharp and jerky. The polar reaction is considerable, but unequal, and the re- sponse made to the negative pole is greater than that made to the positive. To examine a patient electrically requires either a portable or a wall battery. It must supply both the galvanic and faradic currents. Two connecting wires and two sponge electrodes are indispensable. One elec- trode must have an interrupter, that is, a key which will make it possible to make or break the current. In this way it is possible to interrupt the current and so study the muscular contractions. Immerse the sponges in warm water to which has been added a little salt. Warm water is more agreeable to the patient, and the saltiness causes a stronger reaction. Before applying, squeeze the sponge electrodes, to re- move the surplus water and avoid wetting the patient. Place one electrode on some definite, fixed part of the patient, preferably the sternum or the back of the neck. Place the other electrode on the part to be examined. This latter should be the smaller of the two, so as to make possible the selection of particular muscles and motor points. On this electrode place the interrupter. 208 ELECTRIC REACTIONS 209 It is necessary to place the smaller, or examining electrode over certain fixed points of the muscles. This is essential, because at these points the stimulation of the current is at its maximum, and, therefore, a stronger, more obvious contraction results. These points are called the motor points. They can be learned only by M. frontalis Upper branch of facial M. comig. superciL M. orbic. palpebr. Muscles of the / M. rvgomatiei M orbicuL oris * Middle branch of facial M. 111 asset er M. levator menti M. quadr. menti M. triang. menti N. hypogloss. JJouer branch of facial M. ptatrsma myoides Muscles 'of the f root of tongue \ M. omohyoideas JV. thoracic, anter. (M. pector.j Al phrenicia Suprascapular point, (Erb's point M. deltoid., biceps, brachial, intern, and Bupinat. long.) Plcxttt brachial is Region of centra! convolutions Region of the third frontal convolution M. temporalis Upper branch of facial in front of ear N. facialis y. auriculo. past. Middle branch of facial Lower br. of facial M. flplenins M- sternocleido- mastoideus N. accessories M. levator angnll sen pu lie M. cucullaris N. dors, scapulas fr thoracic, long. (M. serratua &atic. maj 1 Fig. 50. — Nerves and motor points in face and neck (Erb). reference to the tables on the following pages. They are called motor points because they are the points at which the motor nerves emerge from the muscle or those at which the nerves are nearest the skin. Therefore, being nearest the electrode, stimulation at these points gives the best results. Place the limb or part to be examined so as to afford 14 2IO DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES the best results. In the case of the hand, flex the fingers and avoid any active resistance. In the case of the arm avoid rigidity and let it hang loosely. In examining with the galvanic current, if it is difficult and troublesome to decide which pole is positive and M. delLoidoua A' radiatii M. bracblaL intern. M. supinator long. M. radial, ext. long. M. radial, ext. brev. M. extensor digit, communis M. extensor indicia M. abductor pollic. long. M. extensor pollic. breT. M. loterou. dorsal. I M. tneepa (caput longiim) 1 M. triceps (caput ex- i tern.) <— M. ulnar, extern. M. supiuat. brev. M. extent, digit! minim, M. extens. indicia exteus. poll. long. M. abduct, digit, min. M. Inieross. dorsaL III etIV Fig. 51. — Nerves and motor points in upper extremity (Erb). which negative ascertain definitely in this way: remove the electrodes, put the ends of the wires in a glass of water, turn on the galvanic current. A steady column of bubbles will rise from the negative pole. Always test the muscle of the healthy side first, as ELECTRIC REACTIONS 211 this will enable one to establish a standard. Always test each current on yourself before applying it to the patient, thus avoiding a shock to him. Always begin with a cur- rent weaker than is necessary, gradually increasing to a point where the required strength is reached. This should be sufficient to bring about a strong contraction. It is necessary to have connected with the instrument a galvanometer, which will measure the amount of current used. It is the nerve which responds to faradic current, and. although the muscle responds by a contraction, it in all probability receives the stimulus only through the nerve. The galvanic current causes a contraction through direct stimulation of the muscles themselves, the nerve exer- cising only a controlling influence. KCOACOAOOKOC When there is a lesion in the lower motor neuron the order of susceptibility becomes ACC KCC KOC>AOC. In practical testing it is the closing contraction on which the attention is usually centered, for, if ACC is greater than KCC, that in conjunction with the other evidence is sufficient to indicate abnormal reaction with- out troubling about the opening contractions. Practical Considerations. — i. If at first too strong a current is used, the resulting contraction is too wide- spread to give any reliable information. In the general effect the reaction of any particular muscle or group of muscles is lost. The unpleasant sensation causes the patient to lose confidence, making further testing diffi- cult, beside causing pain to the patient. 2. The farther away the muscle under observation is from the central axis of the body, the greater, even under 212 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES normal conditions, is the strength of the current required to produce a contraction. 3. The resistance of the skin to the passage of the elec- tric current is very great, and time, patience, and con- stant wetting of the skin are necessary to overcome the resistance. 4. In fat people patience is required to give the elec- tricity time to get through the skin and fat to the muscle. M. adductor magnus M. adduct. longus M. TMtUS If, I'M I1U3 ■' M. tensor fasciae laic; M. Karlorius M. quadriceps feiuoris M. rectus femoris M. vastus externua Fig. 52. — Nerves and motor points in lower extremity (Erb). Careful differentiation is sometimes necessary to dis- tinguish between a normal fat limb and a pseudohyper- trophic dystrophy. Abnormal Reactions. — In addition to the reactions which I have already described, there occur in medicine, and especially in neurology, several reactions which are unusual and, therefore, abnormal. I have classified these under six headings. The first comprises the increase of ELECTRIC REACTIONS 213 both the faradic and the galvanic currents. The second heading is the reverse of the former, and comprises those conditions in which there is either a diminution or an absence of both the faradic and galvanic currents. A list of these follows: A. Increased to both faradic and galvanic currents: > M gluteus ma-imiis JV#f-i\ Uchiadicua M. biceps fern. (cap. long.) M biceps fem. (cap breT.) M gastrocoem. (cap. extern.) M. sulcus M flexor balluols loagus M. adductor roijnin M. seiuitcndinosus M. semiiuembrsnoaus M. fastrocDem. (cap. lot.) M eoleus M. flexor dlgilor comm, longus Fig. 53. — Nerves and motor points in lower extremity (Erb). i. Undue irritability, such as in chorea and early spastic paralysis. 2. Diseases characterized by profuse sweating (which diminishes the resistance of the skin to the electric current), as in Graves' disease. 3. Hysteria, in which there is sometimes an increased susceptibility to faradism. 214 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES B. The reaction of degeneration (R. D.) indicates, as a rule, a lesion of the lower motor neuron type; in the upper motor neuron type there is no such reaction. The following table gives the diseases in which the reaction of degeneration occurs: i. Diseases of the anterior horns: (a) Poliomyelitis. (b) Amyotrophic lateral sclerosis. (c) Spinal gliosis. (d) Diffuse cervical and lumbosacral myelitis (with in- volvement of the gray matter). 2. Diseases of the nuclei of the bulbar nerves corre- sponding to those of the anterior horns (progressive bul- bar paralysis, acute inferior polioencephalitis, etc.). 3. Diseases of the anterior roots: (a) Compression from tumors and thickening of the meninges, as in syphilis, cervical hypertrophic pachymen- ingitis. (b) Compression in the intervertebral foramina in diseases of the spinal column (caries, tumor, fracture, dislocation). 4. Severe affections of the peripheral nerves: (a) Traumatic (section, severe bruising, pressure by tumor) . (b) Rheumatic (facial paralysis). (c) Toxic and infectious: Lead paralysis. Alcoholic paralysis. Arsenical paralysis. Infective forms of multiple neuritis, etc. In addition to those two headings there occur three other abnormal reactions. These are called (C) myas- ELECTRIC REACTIONS 215 thenic reaction, (D) tetanic reaction, and (E) myotonic reaction. Each reaction has characteristics of its own, and each is diagnostic of the particular condition in which it occurs. Each will, therefore, merit a short descrip- tion, and the student should be made familiar with each. The myasthenic reaction occurs in the condition known as myasthenia gravis. The main characteristic of this abnormal condition consists of the gradual exhaustion M. tibial, antic. M. extena. digit. comnL long. >L peroneus brevia M. extensor hallucis long. Mi. interossei dorsales I »n\ peroneus M. gastrocnem. extern. M. peroneus longus SL sole t3 M. flexor hallucia long. M. extens. digit, conim. bmni M. abductor digit! rain. Fig. 54. — Nerves and motor points in lower extremity (Erb) of the muscular responses. There is no reaction of de- generation. There is neither irritability nor marked susceptibility. There simply occurs, following rapid stimulation, a gradual exhaustion of the muscular re- sponses, both of the faradic and galvanic currents. The second characteristic of this reaction is that, after the tired muscles are given a short period of rest, they again respond to both currents. The myasthenic reaction, 2l6 DIAGNOSTIC SYMPTOMS IN NERVOUS DISEASES therefore, is one in which the response of the muscles to both the electric currents becomes weaker and weaker until it finally ceases. The myotonic reaction occurs in myotonia, or Thorn- sen's disease. Its main characteristic is an abnormal susceptibility on the part of all the muscles to the electric current. The response of the two poles is about equal, but all responses are prolonged and tonic. The muscles display an unusual degree of mechanical excitability, even to blows, especially, however, to the electric stimulation. The myotonic reaction is, in some respects, a counter- part of the myasthenic. The tetanic reaction occurs in tetanus. In this re- action there is a marked increase of the electric excit- ability of the sensory as well as of the motor nerves. The increased excitability of the motor nerves is far more constant than that of the sensory. In fact, it is found in every instance, even in those in which the current is weak. REFERENCES Bixg, Robert: Compendium of Regional Diagnosis (translation by F. S. Arnold). Collie, Sir John: " Malingering and Feigned Sickness." Church and Peterson: "Nervous and Mental Diseases." Cushing, Harvey: "The Pituitary Body." Dana, Charles L.: "Text-book of Nervous Diseases." Kraepelin, Emil: "Psychiatrie. " Liepmann: "Drei Aufsatze aus dem Apraxiegebietel. " Obersteiner, H.: "Anatomic." Oppexheim: "Text-book of Nervous Diseases." Posey and Spiller: "The Eye and Nervous System." Scripture, E. W.: "Stuttering and Lisping." Starr. M. A.: "Nervous Diseases, Organic and Functional." Sherren: "Injuries of Nerves." Stewart: "Diseases of the Nervous System." Williamson-, R. T.: "Diseases of the Spinal Cord." Wyllie, John: "Tumors of the Cerebellum." INDEX Abdominal reflex, 150 diseases in which lost, 150 Abscess of brain, convulsions in, 133 Accommodation reflex, 147 Achilles jerk, 160 diseases in which absent, 161, 163 Achromatopsia, 181 Acromegaly, 26 Acute ascending paralysis, 52 disseminated myelitis, ataxia of, 126 Agraphia, 204 Alcoholic gait, 101, 109 neuritis, atrophy in, 159 paralysis in, 31 speech, 190 tremor, 67, 70 Alexia, 204 Alternating hemiplegia, 44 Analgesia-hypalgesia, 144 Anarthria, 189 Anemia, cerebral convulsions in, Anesthesia, ataxia and, differen- tiation, 117 dissociated, 144 thermal, 144 Anesthesia-hypesthesia, 144 Angel scapula, 34 Anisocoria, 167 conditions in which occurs, 167 Ankle, Charcot, in tabes, 119 clonus, 161 diseases in which occurs, 162 reflex, 160 Anterotibial paralysis, 49 Aphasia, 196 auditory, 204 causes, 199 cortical, 206 definition of, 196 Aphasia, examination in, 200 hysteric, 205 motor, 197, 199, 204 symptoms of, 206 parallelogram for examination in, 199 sensory, 197, 198 subcortical, 206 test for auditory word center in, 201 for integrity of corresponding sensory and motor centers in, 202 of motor speaking center in, 201 of one sensory and one motor center in, 202 of two sensory centers, to- gether with one motor in, 202 of two sensory centers, to- gether with other motor center in, 203 of writing center in, 201 for visual word center in, 202 varieties of, 203 visual, 204 Aphonia, 188 Apoplectic stroke, hemorrhage dur- ing, convulsions after, 133 Apraxia, 205 Aran-Duchenne type of muscular atrophy, 90 Arc, reflex, 145-147 Argyll-Robertson pupil, 168, 183 Arm paralysis, 48 Arms and legs, examination of, 21 ataxia in, examination for, 123 Arsenical neuritis, ataxia of, 129 paralysis, S3, 54. Arteriosclerosis, gait of, 112 Articulation, disturbances in, 187, 188 217 2l8 INDEX Astasia-abasia, in Asthenic tremor, 73 Asynergia, cerebellar, 119 Ataxia, 116 anesthesia and, differentiation, 117 bulbar, 128 causes, 118, 122 cerebellar, 119, 125 gait of, diseases in which oc- curs, 121 hereditary, 126 lesions of cerebellum causing, 120, 121 diphtheric, 128 distribution of, 122 drunkard's, 128 examination for, 22, 123 fatigue, 128 Friedreich's, 126 handwriting in, 76 hemi-, 122 hereditary, 126 speech of, 190 hysteric, 127 in arms, examination for, 124 in head and trunk muscles, ex- amination for, 123 in legs, examination for, 123 locomotor, 124 Marie's, 126 miscellaneous, 127 motor, 118 of acute disseminated myelitis, 126 of arsenical neuritis, 129 of disseminated sclerosis, 125 of multiple neuritis, 128 of spinal diseases, 129 paralysis and, differentiation,! 17 Romberg's sign in, 121 static, 118 toxic, 128 tremor and, differentiation, 117 varieties, 117, 118, 124 Ataxic gait, 98, 105 diseases in which occurs, 98, 99 paraplegia, 126 Athetosis duplex, 149 Atrophied tongue, 30 Atrophy, 83 Atrophy in alcoholic neuritis, 157 in poliomyelitis, 85, 86 in tabes, 85 in tumor of spinal cord, 85 mixed, 87 muscular, 84 Aran-Duchenne type, 90 Charcot-Marie-Tooth type, Erb's juvenile type, 91 infantile type, 90 Landouzy-Dejerine type, 91 progressive, 84 Wernig-Hoffmann type, 90 of bones, 86 of face, 30 of joints, 86 of nervous system, 84 of optic nerve, 174, 175 postneuritic, 175 primary, 175 secondary, 175 simple, 175 of skin, 83 Attitude, cerebellar, 106 of paralysis agitans, 108 Attitudes, unusual, 25 Auditory aphasia, 204 word center, 198 in aphasia, test for, 201 Babinski reflex, 151 v diseases in which occurs, 153Q Bag of bones, 92 Bechterew-Mendel reflex, 153 Bell's paralysis, 50 Belly, pot-, 34 Bends, 52 Benediction hand, 33, 48 Bernhardt's paralysis, 53 Birth paralysis, $$, 48 atrophy of bones and joints in, 86 Blind spot, 181 Blindness, day-, 182 word-, 204 Blue foot, 34 Bones, atrophy of, 86 dystrophy of, 88 hypertrophy of, 86 trophic changes in, 94 f INDEX 219 Bradylalia, 189 Brain, abscess of, convulsions in, 133 bony pressure on, convulsions from, 133 lesions, gross, tremors from, 73 syphilis of, convulsions in, 134 tumors of, convulsions in, 232 speech in, 192 Brown-Sequard's paralysis, 54 Bulbar ataxia, 128 paralysis, 53 speech of, 194 speech, 189 Bulging eyes, 30 Caisson disease, 52 Central scotoma, 181, 182 Cerebellar asynergia, 119 ataxia, 119, 125 gait of, diseases in which oc- curs, 121 hereditary, 126 lesions of cerebellum causing, 120, 121 attitude, 106 gait, 105 diseases in which occurs, 107 reel gait, 105 tremors, 74 Cerebral anemia, convulsions in, 134 hernia after decompression oper- ation, 174 hyperemia, convulsions in, 134 paralysis, atrophy of bones and joints in, 86 Charcot ankle in tabes, 119 joint, 92, 93 ribs, 193 Charcot-Marie-Tooth type of muscular atrophy, 91 Chloral tremor, 72 Choked disc, 171, 173 Chorea, acute, handwriting in, 79 hereditary, gait in, 114 Huntington's, handwriting in, 80 speech of, 194 Cigarette smoker, tremor of, 72 Ciliospinal reflex, 148, 185 Circumflex paralysis, 48 Clasp-knife rigidity of legs, 34 Claw-hand, S3 Cleft-palate, speech of, 191 Clonus, 161 ankle, 161 diseases in which occurs, 162 foot, 161 knee, 161 patellar, 161 spurious, 161 Club-foot, 34, 35 Clumsy gait, 104 Coarse tremor, 57, 61 Cocain tremor, 72 Coffee drinker, tremor of, 72 Color sense, imperfect, 181 vision, loss of, 181 Compression myelitis, 56 Conjugate motion of eye, 180 Conjunctival reflex, 149 Consensual reflex, 184 Contraction of pupil, 166 Contracture of tendo Achillis, 50 Convulsions, 19, 130 . after hemorrhage during apo- plectic stroke, 133 classification of, 130 due to pressure, 132 examination for, 22 from bony pressure on brain, 133 hysteric, 135 in abscess of brain, 133 in cerebral anemia, 134 hyperemia, 134 in general paresis, 135 in hydrocephalus, 133 in infection, 135 in meningitis, 134 in sinus thrombosis, 134 in syphilis of brain, 134 in tetanus, 135 in tumors of brain, 132 in vascular diseases, 133 toxic, 134 Corneal reflex, 148 Cortical aphasia, 206 Corticospinal paralysis, 38 Creeping palsy, 103 Cremasteric reflex, 150 Cretin, atrophy of bones and joints in, 86 220 INDEX Cretin, speech of, 190 Cretinism, 26, 27 Crossed hemiplegia, 44 Crutch paralysis, 54 Curled-up attitude, 35 Curvature of spine, 31, 35 Day-blindness, 182 Decompression operation, hernia cerebri after, 1 74 Deformities, 18, 25 characteristic of spinal cord diseases, 35 miscellaneous, 34 of body as whole, 26 of extremities, 31 of hand, 33 of head, 28 position, 29 shape, 28 size, 28 of spinal column, 31 of upper extremities, 31 Dilatation of pupil, 166 Diphtheria, paralysis in, 31 Diphtheric ataxia, 128 paralysis, 53 Diplegia, 45 speech of, 190 Diplopia, 177 conditions in which occurs, 177 heteronymous, 178 homonymous, 178 Disc, choked, 171, 173 Disseminated sclerosis, ataxia of, 125 Dissociated anesthesia, 144 Divers' paralysis, 52 Double hemiplegia, 45 vision, 177 wrist-drop, 31 Dragged leg, 49 Drooping of eyelid, 177 Drop-foot gait, 10 1 Dropped foot, 34, 35, 49 scapula, 34 wrist, 48, 55 Drug tremors, 67 Drunkard's ataxia, 128 Duchenne-Aran type of muscular atrophy, 90 Duchenne's paralysis, 54 Dwarfism, 26, 27 Dysarthria, 187 causes of, 190 from paralysis of lips, tongue or palate muscles, 188, 189 varieties of, 188 Dyschromatopsia, 181 Dystrophy, 87 of bones, 88 of joints, 88 of muscles, 88 of nervous system, 89 of skin, 87 Elbow reflex, 154 Electric examination, 23, 24 reactions, 208-216 abnormal, 212 Electricity, examination by, 208 Emotional tremor, 75 Enophthalmos, 30 Epicritic sensation, 138, 139 Epigastric reflex, 150 Epilepsy, 132 grand mal of, 132 Jacksonian, 132 petit mal of, 132 speech of, 194 Equine gait, 101 Erb's juvenile type of muscular atrophy, 91 paralysis, 53 Examination, electric, 24 for ataxia, 22 for convulsions, 22 for trophic changes, 21 laboratory, 23 mental, 24 of arms and legs, 21 of eyes, 20, 21, 23 of gait, 22 of grip, 21 of hearing, 21 of legs and arms, 21 of nervous case, 17, 20 of pupils of eyes, 23 of reflexes, 23 of sensory impulses, 22 of skin, 20 of smell, 20 INDEX 221 Examination of speech, 23 of sphincter control, 23 of taste, 21 of tongue, 21 .r-ray, 24 Exophthalmic goiter, 68, 69 External influences, effect of, on tremors, 60 Extremities, deformities of, 31 Eye, 164 bulging, 30 conjugate motion of, 180 examination of, 20, 21, 23 paralysis of, 28 pop-, 30 pupil of, 28 contraction, 166 dilatation, 166 immobility, 168 inequality, 167 irregularity, 167 physical signs, 166 reflexes, 183 Eyelid, drooping of, 177 Face and neck, motor points, 209 nerves of, 209 atrophy of, 30 congested, 30 mask-like, 30 myopathic, 31 pallid, wax-like, 30 purple, 30 Facial muscles, tremor of, 30 paralysis, 50 Fatigue ataxia, 128 Festinating gait, 65, 107 Fibrillary twitchings, 78 Fingers, tapering, 33 Foot, blue, 34 clonus, 161 club-, 34, 35 dropped, 34, 35, 49 horse-, 50 perforating ulcer of, 90 diseases in which occurs, 90 red, 34 turned-out, 49 Fourth-nerve paralysis, 56 Friedreich's ataxia, 126 handwriting in, 76 speech of, 190 Gait, 95 abnormal, 95 alcoholic, 101, 109 ataxic, 98, 105 diseases in which occurs, 98, 99 cerebellar, 105 diseases in which occurs, 107 reel, 105 clumsy, 104 drop-foot, 10 1 equine, 10 1 examination of, 22, 96 festinating, 65, 107 hemiplegic, 100, no, in diseases in which occurs, 101 high-step, 10 1 horse-, 10 1 hysteric, no mixed, 114 monoplegic, no, in normal, 96, 113 of arteriosclerosis, 1 1 2 of cerebellar ataxia, diseases in which occurs, 121 of hereditary chorea, 114 of paresis, 113 Oppenheim's, 104 paraplegic, no, in sailor, 104 sciatic, 114 senile, 112 spastic, 103 diseases in which occurs, 103, 104 staggering, 105, 109 diseases in which occurs, no steppage, 101 diseases in which occurs, 102, 103 waddling, 104 ( las paralysis, 54 General paresis, convulsions in, 135 tremor in, 67 Geographic tongue, 30 Giantism, 26 Gigantism, 26 Gli i-so-labio-laryngcal paralysis, 53 , . ( ilove and stocking paralysis, 53 Goiter, exophthalmic, 68, 69 Gordon's reflex, 152 222 INDEX Grand mal of epilepsy, 132 Graves's disease, tremor of, 67 Grip, examination of, 21 paralysis after, 33 Hammer-toe, 50 Hand, benediction, ^^, 48 claw-, ^3 deformities of, ^t, Klumpke's, S3 monkey-, S3 preachers', ^3 skeleton-, ^^ Handwriting in acute chorea, 79 in alcoholic, 70 in chloral poisoning, 72 in Friedreich's ataxia, 76 in Huntington's chorea, 80 in lead tremor, 71 in multiple sclerosis, 62 in paralysis agitans, 65 in senile tremor, 77 in tic, 74 in veronal poisoning, 72 Hare-lip, speech of, 191 Head and Sherren's theory of sensory disturbances, 136 deformities of, 28 position, 29 shape, 28 size, 28 hydrocephalic, 28 microcephalic, 28 Hearing, examination of, 21 Heel, retracted, 34 Hemeralopia, 182 Hemianopsia, 180 binasal, 180 bitemporal, 180 heteronymous, 180 homonymous, 180 organic conditions in which oc- curs, 181 Ilemi-ataxia, 122 Hemiplegia, 42 alternating, 44 crossed, 44 double, 45 hysteric, 45 infantile, 45 sequels of, 44 Hemiplegia, speech of, 192 varieties of, 44 Hemiplegic gait, 100, no, in diseases in which occurs, 101 Hemorrhage during apoplectic - stroke, convulsions after, 133 Hereditary ataxia, 1 26 speech of, 190 cerebellar ataxia, 126 chorea, gafl in, 114 tremor, 75 Hernia cerebri after decompression operation, 174 High-step gait, 101 Hippus, 168 History, 17 Horse-foot, 50 Horse-gait, 101 Huntington's chorea, handwriting in, 80 Hutchinson teeth, 28, 29 Hydrocephalus, 28 convulsions in, 133 Hyperalgesia, 144 Hyperemia, cerebral, convulsions in, 134 Hyperesthesia, 144 Hypertrophy, 86 mixed, 87 of bones, 86 of joints, 86 of muscles, 86 of nervous system, 86 of skin, 86 of subcutaneous tissue, 86 Hysteria, ataxia in, 127 changes in joints in, 94 Hysteric aphasia, 205 ataxia, 127 convulsions, 135 gaits, 1 10 hemiplegia, 45 paralyses, 37 tremor, 74 Idiocy, speech of, tqo Immobility of pupil of eye, 168 Incontinence, occurrence of, 154 varieties of, 153 Incoordination, 117 Infantile hemiplegia, 45 INDEX 223 Infantile paralysis, 52 type of muscular atrophy, 90 Infection, convulsions in, 135 Insomnia, 20 Intention tremor, 60, 61 diseases in which occurs, 64 Iridoplegia, reflex, 183, 184 Jacksonian epilepsy, 132 Jaw jerk, 154 Jendrassik's test for knee reflex, 156 Joint, Charcot, 02, 93 Joints, atrophy of, 86 changes in, in hysteria, 94 dystrophy of, 88 hypertrophy of, 86 trophic disorders of, 92 Juvenile tabes, 125 Kinesthesia, 144 Klumpke's paralysis, S3, 54 Knee clonus, 161 jerk, 155 diseases in which absent, 158 in which exaggerated, 159 in which retained, 163 Jendrassik's test for, 156 Lauferauer's test for, 156 Westphal's sign in, 157 Laboratory examination, 23 Landouzy-Dejerine type of mus- cular atrophy, 91 Landry's paralysis, 52 Lauferauer's test for knee jerk, 156 Lead neuritis, paralysis in, 31 paralysis, 54 tremor, 70 Leg, dragged, 49 paralysis, 49 Legs and arms, examination of, 21 ataxia in, examination for, 123 clasp-knife rigidity of, 34 Light reflex, 147 Lisping, 189 Little's disease, 45 Locomotor ataxia, 124 Lower extremity, motor points, 212, 213, 215 nerves, 212, 213, 215 Lumbar puncture, 23 Main de singe, ^^ de squelette, 34 Marie's ataxia, 126 Mask-like face, 30 Median paralysis, 49 Meningitis, convulsions in, 134 Mental examination, 24 Mercurial tremor, 71 Metal tremors, 67 Microcephalic head, 28 Miosis, 166 paralytic, 166 spastic, 166 Monkey-hand, t,^ Monoplegia, 41 Monoplegic gait, no, in Morphinism, tremors of, 72 Motor aphasia, 197, 199, 204 symptoms, 206 disturbance, 19 points in face and neck, 209 in lower extremity, 212, 213, 215 in upper extremity, 210 Mouth, tapir, 30 Multiple neuritis, ataxic type, 128 sclerosis, speech of, 191 Muscles, dystrophy of, 88 facial, tremor of, 30 hypertrophy of, 86 Muscular atrophy, 84 Aran-Duchenne type, 90 Charcot-Marie-Tooth type, 91 Erb's juvenile type, 91 infantile type, 90 Landouzy-Dejerine type, 91 progressive, 84 Wernig-Hoffmann type, 90 Musculospiral paralysis, 48, 50 Myasthenia gravis, reaction in, 215 speech of, 194 Myasthenic reaction, 215 Mydriasis, 166 Myelitis, acute disseminated, ataxia of, 126 compression, 56 224 INDEX Myopathic facies, 31 Myotonia congenita, 92 reaction in, 216 Myotonic reaction, 216 Myxedema, speech of, 195 Neck and face, motor points, 209 nerves of, 209 Nerve, optic, atrophy of, 174, 175 postneuritic, 175 primary, 175 secondary, 175 simple, 175 sixth, paralysis of, 172 Nerves of face and neck, 209 of lower extremity, 212, 213, 215 of upper extremity, 210 peripheral, division of, effect pro- duced by, 138 Nervous case, examination of, 17, 20 system, atrophy of, 84 dystrophy of, 89 hypertrophy of, 86 Neurasthenic tremor, 75 Neuritis, alcoholic, atrophy in, 159 paralysis in, 31 arsenical, ataxia of, 129 lead, paralysis in, 31 multiple, ataxic type, 128 optic, 171 conditions in which occurs, 173 Numb sensations, 19 Nystagmus, 178 diseases in which occurs, 179 pathologic, 178 physiologic, 178 Obstetric paralysis, 33, 48, 54 Ophthalmoplegia, 168 double, 169 external, 170 causes, 170 internal, 170 causes, 170 Oppenheim's gait, 104 reflex, 152 Optic nerve, atrophy of, 174, 175 postneuritic, 175 Optic nerve, atrophy of, primary, 175 secondary, 175 simple, 175 neuritis, 171 conditions in which occurs, 173 Pain, 18 Palatal reflex, 149 Palate, cleft-, speech of, 191 Pallanesthesia, 144 Palmar reflex, 153 Palsy, 36. Paralysis. Papillitis, 171 Parallelogram for examining an aphasic, 199 Paralysis, 36 acute ascending, 52 after grip, 33 agitans, 53 attitude of, 108 speech of, 195 tremor of, 64 anterotibial, 49 arm, 48 arsenical, 33, 54 ataxia and, differentiation, 117 Bell's, 50 Bernhardt's, 53 birth, 33, 48 atrophy of bones and joints in, 86 Brown-Sequard's, 54 bulbar, 53 speech of, 194 cerebral, atrophy of bones and joints in, 86 character of, 36 circumflex, 48 classification of, 37 corticospinal, 38 creeping, 103 crutch, 54 definition of, 36 degree of, 37 diphtheric, 53 distribution of, 36 divers', 52 Duchenne's, 54 Erb's, 53 facial, 50 INDEX 225 Paralysis, fourth-nerve, 56 functional, 37 gas, 54 general, tremor in, 67 glosso-labio-laryngeal, 53 glove and stocking, 53 hysteric, 37 in alcoholic neuritis, 31 in diphtheria, 31 in lead neuritis, 31 infantile, 52 Klumpke's, 33, 54 Landry's, 52 lead, 54 leg, 49 lower motor neuron type, 37. 38 diseases which occur in, 47 symptoms, 39 median, 49 miscellaneous, 30 musculospinal, 50 musculospiral, 48 obstetric, 33, 48, 54 of eye, 28 organic, 37 patheticus, 56 peripheral, 38, 48 peroneal, 49 plantar-nerve, 50 Saturday-night, 50 sciatic, 49 shaking, 53, 66 sixth-nerve, 172 spinomuscular, 38 stocking and glove, 53 sympathetic, 53 symptoms of, 39 ulnar, 48 upper motor neuron type, 37, 38 diseases following le- sion of, 41 symptoms, 39 Paralytic disturbance, 19 miosis, 166 Paraplegia, 45 ataxic, 126 spastic, 45 affections of nervous system causing, 46 toxic, 129 Paraplegic gait, no, 111 15 Paresis, 36 gait in, 113 general, convulsions in, 135 speech of, 191 Patellar clonus, 161 reflex, 155, 157 Patheticus paralysis, 56 Perforating ulcer of foot, 90 diseases in which occurs, 90 Peripheral nerves, division of, effect produced by, 138 paralysis, 38, 48 Peroneal paralysis, 49 Petit mal of epilepsy, 132 Pharyngeal reflex, 149 Phonation, disturbances in, 187, 188 Pill-rolling, 66 Pinpoint pupil, 166 Plantar reflex, 151 conditions in which of flexion type, 152 Plantar-nerve paralysis, 50 Plegia, 36. See also Paralysis. Plegias, 41 Poliomyelitis, 52 atrophy in, 85, 86 Pop-eyes, 30 Posterior roots, division of, effect produced by, 138 Posthemiplegic tremor, 73 Pot-belly, 34 Preacher's hand, 33 Pressure, convulsions due to, 132 Priapism, persistent, 34 Progressive muscular atrophy, 84 Pronunciation, disturbances in. 188 Protopathic sensation, 137, 140 Ptosis, 1 70. 1 77 Puncture, lumbar. Pupil, Argyll-Robertson, 168, 183 of eye, 28 contraction, [66 dilatation, 166 examination of, 23 immobility, 168 inequality, [67 irregularity, 1(17 physical signs, 166 pinpoint, 1 sluggish, 168, 183 226 INDEX Pupillary reaction, Wernicke's, hemiopic, 185 reflexes, 147 Reactions, electric, 208-216 abnormal, 212 myasthenic, 215 myotonic, 216 tetanic, 216 Red foot, 34 . Reel gait, cerebellar, 105 Reflex, 145 abdominal, 150 diseases in which lost, 150 accommodation, 147 Achilles, 160 diseases in which absent, 161 _ 163 action, 145 ankle, 160 arc, 145-147 Babinski, 151 diseases in which occurs, 152 Bechterew-Mendel, 153 ciliospinal, 148, 185 conjunctival, 149 consensual, 184 corneal, 148 cremasteric, 150 deep, 154 absence of, 162 elbow, 154 epigastric, 150 examination of, 23 eye, 183 Gordon's, 152 iridoplegia, 183, 184 knee, 155 diseases in which absent, 158 in which exaggerated, 159 in which retained, 163 Jendrassik's test for, 156 Lauferauer's test for, 156 Westphal's sign in, 157 light, 147 ( )ppenheim, 152 palatal, 149 palmar, 153 patellar, 155, 157 pharyngeal, 149 plantar, 151 :o Reflex, plantar, conditions in which of flexion type, 152 scapulohumeral, 150 special, 147 sphincter, 153 superficial, 148 triceps, 154 wrist, 155 diseases in which absent, 155 in which exaggerated, 155 Rest, effect of, on tremor, 59 Retracted heel, 34 Rhythm of tremor, 59 Ribs, Charcot, 193 Romberg's sign, 96, 121 diseases in which occurs, 121 Sailor gait, 104 Saturday-night paralysis, 50 Scanning speech, 189, 191 Scapula, angel, 34 dropped, 34 wing, 34 Scapulohumeral reflex, 150 Sciatic gait, 114 paralysis, 49 Sclerosis, disseminated, ataxia of, 125 multiple, speech of, 191 Scoliosis, 32, 35 Scotoma, 181 central, 181, 182 diseases in which occurs, 182 peripheral, 181 Senile gait, 112 tremor, 77 Sensation, 136 deep, 136, 140 disturbed, varieties of, 144 epicritic, 138, 139 intermediate, 136 method of examination for, 139 protopathic, 137, 140 superficial, 136 testing, 139 Sensory aphasia, 197, 198 disturbances, 19, 141 impulses, examination of, 22 peripheral mechanism, 136 spinal mechanism, 138 Shaking paralysis, 53, 66 INDEX 227 Sherren and Head's theory of sen- sory disturbances, 136 Sign, Romberg's, 96, 121 diseases in which occurs, 121 Stellwag's, 183 von Graefe's, 182 Westphal's, 157 Signe de l'eventail, 151 Sinus thrombosis, convulsions in, .134 Sixth nerve paralysis, 172 Skeleton-hand, ^^ Skin, atrophy of, 83 dystrophy of, 87 examination of, 20 hypertrophy of, 86 Sleeplessness, 20 Sluggish pupil, 168, 183 Slurring speech, 190 Smell, examination of, 20 Spastic gait, 103 diseases in which occurs, 103, 104 miosis, 166 paraplegia, 45 affections of nervous system causing, 46 Speech, bulbar, 189 disturbances of, 19, 186 examination of, 23, 186 normal, 186 of alcoholics, 190 of brain tumors, 192 of bulbar palsy, 194 of chorea, 194 of cleft-palate, 191 of cretin, 190 of diplegia, 190 of epilepsy, 195 of Friedreich's disease, 190 of general paresis, 191 of hare-lip, 191 of hemiplegia, 192 of hereditary ataxia, 190 of idiocy, 190 of multiple sclerosis, 191 of myasthenia gravis, 194 of myxedema, 195 of paralysis agitans, 195 scanning, 189, 191 slowness of, 189 slurring, 190 Speech, staccato, 191 thickness of, 190 Sphincter control, 20 abnormalities of, 153 examination of, 23 reflex, 153 Spina bifida, 31 Spinal column, curvature of, 31 deformities of, 31 cord diseases, deformities char- acteristic of, 35 tumor of, atrophy in, 85 diseases, ataxia in, 129 mechanism, sensory, 138 Spine, curvature of, 35 Spinomuscular paralysis, 38 Spondylitis deformans, 31 Spurious clonus, 161 Staccato, 191 Staggering gait, 105, 109 diseases in which occurs, no Static ataxia, 118 Stellwag's sign, 183 Steppage gait, 101 diseases in which occurs, 102, Stocking and glove paralysis, 53 Stuttering, 189 Subcortical aphasia. 206 Subcutaneous tissue, hypertrophy of, 86 Sympathetic paralysis, 53 Syphilis of brain, convulsions in, 134 Syringomyelia, 137, 138 Tabes, 124 atrophy in, 85 Charcot ankle in, 119 juvenile, 124 Tapering fingers, 55 Tapir mouth, 30 Taste, examination of, 21 Tea drinker, tremor of, 72 Teeth, Hutchinson, 28, 29 Tendo Achillis, contracture of, 50 Test, Jendrassik's, for knee- jerk, 156 Lauferauer's, for knee-jerk, 156 Romberg's, 96, 1 2 1 Wassermann, 23 228 INDEX Testing sensation, 139 Tetanic reaction, 216 Tetanus, convulsions in, 135 reaction in, 216 Thermal anesthesia, 144 Thomsen's disease, 92 reaction in, 216 Thrombosis, sinus, convulsions in, .134 Tic, handwriting in, 74 Toe, hammer-, 50 Toeing-in, 35 Tongue, atrophied, 30 examination of, 21 geographic, 30 tremor of, 30 Toxic ataxia, 128 convulsions, 134 paraplegia, 129 tremors, 66, 72 endogenous, 66, 67 exogenous, 66, 67 Tremors, 57 alcoholic, 67, 70 asthenic, 73 ataxia and, differentiation, 117 cerebellar, 74 chloral, 72 classification of, 57, 61 coarse, 57, 61 cocain, 72 distribution of, 58 division of, 57, 61 drug, 67 effect of external influences on, 60 of rest on, 59 of voluntary movements on, 60 emotional, 75 fibrillary, 78 fine, 57, 61 from gross brain lesions, 73 hereditary, 75 hysteric, 74 in general paralysis, 67 intention, 60, 61 diseases in which occurs, 64 lead, 70 mercurial, 71 metal, 67 morphin, 72 Tremors, neurasthenic, 75 of cigarette smoker, 72 of coffee drinker, 72 of facial muscles, 30 of Graves's disease, 67 of morphinism, 72 of paralysis agitans, 64 of tea drinker, 72 of tongue, 30 posthemiplegic, 73 rate of, 59 rhythm of, 59 senile, 77 simple, 77 toxic, 66, 72 endogenous, 66, 67 exogenous, 66, 67 varieties, 61 Triceps reflex, 154 Triplegia, 45 Trophic centers, 81 changes, examination for, 21 in bones, 94 disorders, 81 distribution, 82, 83 of joints, 92 Tumors of brain, convulsions in, 132 speech in, 192 of spinal cord, atrophy in, 85 Turned-out foot, 49 Twitchings, fibrillary, 78 Ulcer, perforating, of foot, 90 diseases in which occurs, 90 Ulnar paralysis, 48 Upper extremity, motor points. 210 nerves, 210 Vascular diseases, convulsion? in, 133 Vision, color, loss of, 181 double, 177 Visual aphasia, 204 word center, 198 in aphasia, test for, 202 Voluntary movements, effect of, on tremor, 60 von Graefe's sign, 182 INDEX 229 Waddling gait, 104 Word-blindness, 204 Walking, 19 Wrist, Charcot, 93 Wassermann test, 23 jerk, 155 Wernicke's hemiopic pupillary re- diseases in which absent, 155 action, 185 in which exaggerated, 155 Wernig-Hoffmann type of muscu- Wrist-drop, 48, 55 lar atrophy, go bilateral, 31 Westphal's sign, 157 double, 31 Wing scapula, 34 single, 31 Word center, auditory, 198 in aphasia, test for, 201 visual, 198 in aphasia, test for, 202 X-ray examination, 24 SAUNDERS* BOOKS on Pathology, Physiology Histology, Embryology and Bacteriology W. B. SAUNDERS COMPANY West Washington Square Philadelphia 9, Henrietta Street Covent Garden, London Our Handsome Complete Catalogue will be Sent You on Request Mallory's Pathologic Histology Pathologic Histology. By Frank B. Mallory, M. D., Associate Professor of Pathology, Harvard University Medical School. Octavo of 500 pages, with 375 original illustrations. READY IN NOVEMBER This new work by Dr. Mallory is destined to take a place of first rank. It is complete and thorough, written in a most clear and definite style. All through the entire work I >r. Mallory has emphasized the practical side of the subject. His reputation as a careful worker give^ the book the stamp of authority. The illustrations are all original and stand out as a striking feature. They are magnificent. As a thoroughly reliable and up-to-date work on pathologic histology this new book from the pen of Dr. Mallory is bound to take the lead. SAUNDERS' BOOK'S ON Jordan's General Bacteriology A Text=Book of General Bacteriology. By Edwin 0. Jordan, Ph.D., Professor of Bacteriology in the University of Chicago and in Rush Medical College. Octavo of 623 pages, illustrated. Cloth, $3.00 net. THE NEW (3d) EDITION Professor Jordan's work embraces the entire field of bacteriology, the non- pathogenic as well as the pathogenic bacteria being considered, giving greater emphasis, of course, to the latter. There are extensive chapters on methods of studying bacteria, their development and composition ; on enzymes and fermentation -products ; on the bacterial production of pigment, acid and alkali ; and on ptomains and toxins. Especially complete is the presentation of serum treatment. This work will also appeal to academic and scientific students. It con- tains chapters on the bacteriology of plants, milk and milk-products, air, agriculture, water, food preservatives, the processes of leather tanning, tobacco curing, and vinegar making ; the relation of bacteriology to house- hold administration and to sanitary engineering, etc. Prof. Severance Burrage, Associate Prof, of Sanitary Science, Purdue University. " I am much impressed with the completeness and accuracy of the book. It certainly covers the ground more completely than any other American book that I have seen." Buchanan's Veterinary Bacteriology Veterinary Bacteriology. By Robert E. Buchanan, Ph.D., Professor of Bacteriology in the Iowa State College of Agriculture and Mechanic Arts. Octavo of 516 pages, with 214 illustrations. Cloth, $3.00 net. THE BEST PUBLISHED Professor Buchanan"s new work is a comprehensive one. The author has gone minutely into the consideration of immunity, opsonic index, reproduc- tion, sterilization, antiseptics, biochemic tests, culture media, isolation of cul- tures, the manufacture of the various toxins, antitoxins, tuberculins, and vac- cines that have proved of diagnostic or therapeutic value. Then, in addition to bacteria and protozoa proper, he considers molds, mildews, smuts, rusts, toadstools, puff-balls, and the other fungi pathogenic for animals. B. ¥\ Katipp, D. V. S., State Agricultural College, Fort Collins. " It is the best in print on the subject. What pleases me most is that it contains all the late results of research. It fills a long felt want." HISTOLOGY AND PHYSIOLOGY. Eyre's Bacteriologic Technic Bacteriologic Technic. A Laboratory Guide for the Medi- cal, Dental, and Technical Student. By J. W. H. Eyre, M. D., F. R. S. Edin., Director of the Bacteriologic Department of Guy's Hospital, London. Octavo of 520 pages, 219 illustrations. Cloth, $3.00 net. JUST READY— NEW (2d) EDITION, REWRITTEN Dr. Eyre has subjected his work to a most searching revision. Indeed, so thorough was his revision that the entire book, enlarged by some 150 pages and 50 illustrations, had to be reset from cover to cover. He has in- cluded aW the latest technic in every division of the subject. His thorough- ness, his accuracy, his attention to detail make his work an important one. He gives clearly the technic for the bacteriologic examination of water, sew- age, air, soil, milk and its products, meats, etc. Howell's Physiology A Text=Book of Physiology. By William H. Howell, Ph. D., M. D., Professor of Physiology in the Johns Hopkins University, Baltimore, Md. Octavo of 1018 pages, with 306 illustrations. Cloth, #4.00 net. FOURTH EDITION Dr. Howell has had many years of experience as a teacher of physiology in several of the leading medical schools, and is therefore exceedingly well fitted to write a text-book on this subject. Main emphasis has been laid upon those facts and views which will be directly helpful in the practical branches of medicine. At the same time, however, sufficient consideration has been given to the experimental side of the science. The London Lancet '• This is one of the best recent books on physiology, and we warmly commend It to the attention of those who desire to obtain by reading a general all-round, yet concise survey of the scope, facts, theories, and speculations that make up its subject matter." SAUNDERS* /:P(>A'S C.Y McFarl&nd's Pathology A Text-Book of Pathology. By Jos: ph McP vrland, M. I )., Professor of Pathology and Bacteriology in the Medico-Chirui ical College of Philadelphia. Octavo of 856 pages, with 137 illustrations, many in ( olor>. Cloth, s5.cc net; Hall Moid. 50 net. SECOND EDITION Dr. McFarland's work was written to furnish a ready means of acj- •. i daily help in your ; For this edition evi e has been gone over most eare- fiilU. ting, omitting the obsolete, and adding the new. Some sections have been entirely rewritten. St. Paul Medical Journal •• I: . who are better qualified I ■ lime" of the un this subject than McFarland. 'the subject-matter is thoroughly up to date.'' Boston Medical and Surgical Journal " It contains a great m ( >ne of the best sections is that on the special pathology ..1 the blood." McFarland's Medical Biology Biology: Medical and General. By Joseph McFarland, M. D., Professor of Pathology and Bacteriology in the Medico- Chirurgical College of Philadelphia. Octavo of 440 pages, with 160 illustrations. Cloth, Si- 75 net. ILLUSTRATED All of the problems of medical science are in a sense biologic, and many of the problems of biology medical. This work is both a general and medical biology. The former because it discusses the peculiar nature and reactions of Living Substance generally; the latter because particular emphasis is laid on those subjects of special interest and value in the study and practice of medi- cine. Prof. W. R. McConnell, Pennsylvania Stale College. " It has some admirable features, the most valuable of which, it seems to me, is the careful resume of the subjects of heredity and evolution." BA C 1 EKIOL OGY A ND HIS TOL OGY, McFarland's Pathogenic Bac- teria and Protozoa Pathogenic Bacteria and Protozoa. By Joseph McFar- land, M. I)., Professor of Pathology and Bacteriology in the Medico-Chirurgical College of Philadelphia. Octavo of 878 pages, finely illustrated, (loth, S3. 50 net. NEW (7th) EDITION, ENLARGED Dr. McFarland has subjected his book to a most vigorous revision, bring- ing this edition right down to the minute. Important new additions have increased it in size some 180 pages. By far the most important addition is the inclusion of an entirely new section on Pathogenic Protozoa. This sec- tion considers every protozoan pathogenic to man ; and in that same clean-cut, definite way that won for McFarland's work a place in the very front of medical bacteriologies. The illustrations are the best and are beautifully executed. Hill's Histology and Organography A Manual of Histology and Organography. By Charles Hill, M. D., formed v Assistant Professor of Histology and Em- bryologv. Northwestern University, Chicago. 121110 of 468 pages, with 337 illustrations. Flexible leather, 52.00 net. THE NEW (2d) EDITION Pennsylvania Medical Journal •' It is arranged in such a manner as to be easy of access and comprehension. To any contemplating the study of histology and organography we would commend this work." SATXItEfiS' BOOKS OX Mallory and Wright's Pathologic Technique Filth Edition Pathologic Technique. A Practical Manual for Workers in Pathologic Histology, including Directions for the Performance of Autopsies and for Clinical Diagnosis by Laboratory Methods By Frank B. Mallory, M. D., Associate Professor of Pathology, Harvard University ; and James H. Wright, M. D.. Director of the Clinico-Pathologic Laboratories, Massachusetts General Hos- pital. Octavo of 500 pages, with 152 illustrations. Cloth, §3. 00 net. WITH CHAPTERS ON POST-MORTEM TECHNIQUE AND AUTOPSIES In revising the book for the new edition the authors have kept in view the needs of the laboratory worker, whether student, practitioner, or pathologist, for a practical manual of histologic and bacteriologic methods in the study of pathologic material. Many parts have been rewritten, many new methods have been added, and the number of illustrations has been considerably increased. Among the new matter are the following: Smith's staining method tor encapsulated bacteria, the antiforahn method for detection and cultivation of tubercle bacilli, Musgrave's and Clegg's method for the culti- vation of amebae, Wright's method for staining myelin sheaths in frozen sec- tions, Ghoreyeb's method for spirochetes, Alzheimer's method for the cvto- logic examination of cerebrospinal fluid, Giemsa's new method for protozoa and bacteria in sections, and the WassermannXoguchi tests for syphilis. PERSONAL AND PRESS OPINIONS William H. Welch. M.D., Professor of Pathology, Johns Hopkins University, Baltimore, Md. "I have been looking forward to the publication of this book, and I am glad to say that 1 find it a most useful laboratory and post-mortem guide, fall of practical information and well up to date." Boston Medical and Surgical Journal " This manual, since its first appearance, has been recognized as the standard guide in pathological technique, and has become well-nigh indispensable to the laboratory worker." LM BRYOLOGY Heisler's Embryology A Text=Book of Embryology. By John C. Heisler, M.D., Professor of Anatomy in the Medico-Chirurgical College, Phila- delphia. Octavo volume of 435 pages, with 212 illustrations, 32 of them in colors. Cloth, $3.00 net. THIRD EDITION The fact of embryology having acquired in recent years such great interest in connection with the teaching and with the proper comprehension of human anatomy, it is of first importance to the student of medicine that a concise and yet sufficiently full text-book upon the subject be available. Heisler' s Em- bryology has become a standard work. G. Carl Huber, M.D., Professor of Embryology , Wistar Institute ; University of Penn. " I find the second edition of 'A Text-Book of Embryology ' by Dr. Heisler an improve- ment on the first. The figures added increase greatly the value of the work. I am again recommending it to our students." Bohm, Davidoff, and Huber's Histology A Text=Book of Human Histology. Including Microscopic Technic. By Dr. A. A. Bohm and Dr. M. Vox Davidoff, of Munich, and G. Carl Huber, M. D.. Professor of Embryology at the Wistar Institute, University of Pennsylvania. Octavo of 528 pages, with 361 beautiful original illustrations. Flexible cloth, S3. 50 net. SECOND EDITION, ENLARGED The work of Drs. Bohm and Davidoff is well known in the German edition, and has been considered one of the most practically useful books on the subject of Human Histology. This second edition has been in «reat part rewritten and very much enlarged by Dr. Huber, who has also added over one hundred original illustrations. 3 )r. Huber's extensive additions have made the work the most complete students' text-book on Histology in existence. Boston Medical and Surgical Journal " Is unquestionably a text-book of the first rank, having been carefully written by thorough masters of the subject, and in certain directions it is much superior to any other histological manual.'' to S A CYDERS' BOOKS OX Wells' Chemical Pathology Chemical Pathology. — Being a Discussion of General Path- ology from the Standpoint of the Chemical Processes Involved. By H. Gideon Wells. Ph. D., M. L>.. Assistant Professor of Pathology in the University of Chicago. Octavo of 549 pages. Cloth. SZ- 2 S net - A PRACTICAL BOOK Dr. Wells* work is written for the physician, for those engaged in research in athology an : ; hysiologic chemistry, and for the medical student. In the introductory chapter are discussed the chemistry and physics of the animal cell, giving the essential facts of ionization, diffusion, osmotic pressure, etc., and the relation of these facts to cellular activities. Wm. H. Welch, M.D., P-r^ssor of Pathology, Johns Hopkins University. " The work fills a real need in the English literature of a very important subject, and I shall be glad to recommend it to my students." Lusk on Nutrition Elements of the Science of Nutrition. By Graham Lusk, Ph. D., Professor of Physiology at Cornell Medical School. Octavo volume of 402 pages. Cloth, $3.00 net. THE NEW 2d EDITION Prof. Lusk presents the scientific foundations upon which rests our knowledge of nutrition and metabolism, both in health and in disease. There are special chapters on the metabolism of diabetes and fever and on purin metabolism. The work will also prove valuable to students of animal dietetics at agricultural stations. Lewellys F. Barker, M. D. Professor of the Principles and Practice of Medicine, Johns Hopkins University " I shall recommend it highly to my students. It is a comfort to have such a dis- cussion of the subject in English." ZOOLOGY. ii Daugherty's Economic Zoology Economic Zoology. By L. S. Daugherty, M.S., Ph. D., Professor of Zoology, State Normal School, Kirksville, Mo., and M. C. Daugherty, author with Jackson of " Agriculture Through the Laboratory and School Garden ' ' : Part I — Field and Laboratory Guide. nmo of 275 pages, interleaved. Cloth, Si 25 net. Part II — Principles. i2ino of 406 pages, illustrated. Cloth, 52.00 net. ILLUSTRATED There is no other book just like this. Not only does it give the salient facts of structural zoology and the development of the various branches of ani- mals, but also the natural history — the life and habits — thus showing the inter- relations of structure, habit, and environment. In a word, it gives the princi- ples of zoology and their actual application, emphaizng the economic phase in every branch. The work is the direct result of some fourteen years' experience in class-room and laboratory work. Every statement has been carefully weighed and tested as to its correctness. There is a profusion of illustrations, all extremely instructive. Drew's Invertebrate Zoology A Laboratory Manual of Invertebrate Zoology. By Gilman A. Drew, Ph. D., Assistant Director of the Marine Biological Laboratory. With the aid of former and present Mem- bers of the Zoological Staff of Instructors at the Marine Biolo_ Laboratory, Woods Hole. Mass. 121110 of 213 pages. Cloth, Si. 25 net. JUST ISSUED— NEW 2d EDITION Prof. Ellison A. Smyth, Jr., Virginia Polyi " I think it is the best laboratorv manual on zoology I have yet seen. The lair' number of forms dealt with makes the work applicable to almost any locality." *2 SAUNDERS' BOOKS ON Norris* Cardiac Pathology Studies in Cardiac Pathology. By George W. Norris, M.U., Associate in Medicine at the University of Pennsylvania. Large octavo of 235 pages, with 85 superb illustrations. Cloth, $5.00 net. SUPERB ILLUSTRATIONS Boston Medical and Surgical Journal "The illustrations are arranged in such a way as to illustrate all the common and many of the rare cardiac lesions, and the accompanying descriptive text constitutes a fairly continuous didactic treatise." McConnell's Pathology A Manual of Pathology. By Guthrie McConnell, M. D., Professor of Bacteriology and Pathology at Temple Uni- versity, Philadelphia. i2mo of 523 pages, with 170 illustrations. Flexible leather, $2.50 net. SECOND EDITION Dr. McConnell has discussed his subject with a clearness and precision of style that make the work of great assistance to both studtnt and practitioner. The illustrations have been introduced for their practical value. New York State Journal of Medicine " The bosk treats the subject of pathology with a thoroughness lacking in many works of greater pretension. The illustrations — many of them original — are profuse and of ex- ceptional excellence." Hektoen and Riesman's Pathology American Text-Book of Pathology. Edited by Ludvig Hek- toen, M. D., Professor of Pathology, Rush Medical College, Chicago; and David Riesman, M. D., Professor of Clinical Medicine, Philadel- phia Polyclinic. Octavo of 1245 pages, 443 illustrations, 66 in colors. Cloth, #7.50 net ; Half Morocco, $9.00 net. HISTOLOGY, Dtirck arid Hektoen's Special Pathologic Histology Atlas and Epitome of Special Pathologic Histology. By. Dr. H. Durck, of Munich. Edited, with additions, by Ludvig Hektoen, M. D., Professor of Pathology, Rush Medical College, Chicago. In two parts. Part I. — Circulatory, Respira- tory, and Gastro-intestinal Tracts. 120 colored figures on 62 plates, and 158 pages of text. Part II. — Liver, Urinary and Sexual Organs, Nervous System, Skin, Muscles, and Bones. 123 colored figures on 60 plates, and 192 pages of text. Per part : Cloth, $3.00 net. /// Saunders" Hand-Atlas Scries. The great value of these plates is that they represent in the exact colors the effect of the stains, which is of such great importance for the differentia- tion of tissue. The text portion of the book is admirable. William H. Welch, M. D., Professor of Pathology , Johns Hopkins University, Baltimore. " I consider Diirck's 'Atlas of Special Pathologic Histology,' edited by Hektoen, a very- useful book for students and others. The plates are admirable." Sobotta and Hubert Human Histology Atlas and Epitome of Human Histology and Microscopic Anatomy. By Privatdocext Dr. J. Sobotta, of Wurzburg. Edited, with additions, by G. Carl Huber, M. D., Professor of Histology and Embryology, and Director of the Histological Laboratory, University of Michigan, Ann Arbor. With 214 colored figures on 80 plates, 6S text-illustrations, and 248 pages of text. Cloth, $4.50 net. In Saunders Hand- At las Series. Lewellys F. Barker, M. D., Professor of the Principles and Practice of Medicine. Johns Hopkins University. " I congratulate ycu upon the appearance of this volume. The illustrations are certainly very fine, and Dr. Huber has made important contributions to the text. The book should have a large sale." I 4 " SAUNDERS' BOOKS ON Bosanquet on Spirochaetes Spirochaetes. By W. Cecil Bosanquet, M. D., Fellow Royal College of Physicians, London. Octavo, 152 pages, illus- trated. $2.50 net. ILLUSTRATED This is a complete and authoritative monograph on the spirochetes, giving morphology, pathogenesis, classification, staining, etc. Pseudospirochietes are also considered, and the entire text well illustrated. The high standing of Dr. Bosanquet in this field of study makes this new work particularly valuable. Levy and Klemperer's Clinical Bacteriology The Elements of Clinical Bacteriology. By Drs. Ernst Levy and Felix Klemperer, of the University of Strasburg Translated and edited by Augustus A. Eshner, M. D., Pro- fessor of Clinical Medicine, Philadelphia Polyclinic. Octavo volume of 440 pages, fully illustrated. Cloth, $2.50 net. Lehmann, Neumann, and Weaver's Bacteriology Atlas and Epitome of Bacteriology : including a Text- Book of Special Bacteriologic Diagnosis. By Prof. Dr. K. B. Lehmann and Dr. R. O. Neumann, of Wurzburg. From the Second Revised and Enlarged German Edition. Edited, with additions, by G. H. Weaver, M. D., Assistant Professor of Pathology and Bacteriology, Rush Medical College, Chicago. In two parts. Part I. — 632 colored figures on 69 lithographic- plates. Part II.— 511 pages of text, illustrated. Per part: Cloth, $2.50 net. In Saunders Hand-Atlas Series. PATHOLOGY, BACTERIOLOGY, AND PHYSIOLOGY. 15 Durck and Hektoen's General Pathologic Histology Atlas and Epitome of General Pathologic Histology. By Pr. Dr. H. Durck, of Munich. Edited, with additions, by Ludvig Hektoen, M. D., Professor of Pathology in Rush Medical College, Chicago. 172 colored figures on 77 lithographic plates, 36 text-cuts, many in colors, and 353 pages. Cloth, $5.00 net. In Saunders 1 Hand- Atlas Series. American Text- Book of Physiology Second Edition American Text-Book ok Physiology. In two volumes. Edited by William H. Howell, Ph. D., M. D., Professor of Physiology in the Johns Hopkins University, Baltimore, Md. Two royal octavos of about 600 pages each, illustrated. Per volume : Cloth, $3.00 net ; Half Morocco, #54.25 net. " The work will stand as a work of reference on physiology. To him who desires to know the status of modern physiology, who expects to obtain suggestions as to further physiologic inquiry, we know of none in English which so eminently meets such a demand " — The Medical News. Warren's Pathology and Therapeutics Edition Surgical Pathology and Therapeutics. By John Collins Warren, M. D., LL. D., F. R. C. S. (Hon.), Professor of Surgery, Harvard Medical School. Octavo, 873 pages, 136 half-tone and litho- graphic illustrations, ^ in colors. Cloth, $5.00 net; Half Morocco, $6.50 net. Gorham's Bacteriology A Laboratory Course in Bacteriology. For the Use of Medical, Agricultural, and Industrial Students. By Frederic P. Gorham, A. M., Associate Professor of Biology in Brown University, Providence, R. I., etc. l2mo of 192 pages, with 97 illustrations. Cloth, $1.25 net. "One of the best students' laboratory guides to the study of bacteriology on the market. . . . The technic is thoroughly modern and amply sufficient for all practical purposes." — American Journal of the Medical Sciences. Raymond's Physiology Third Edition Human Physiology. By Joseph H. Raymond. A. M.. M. D., Pro- fessor of Physiology and Hygiene, Long Island College Hospital, New York. Octavo of 685 pages, with 444 illustrations. Cloth, $3.50 net. "The book is well gotten up and well printed and may be regarded as a trust- worthy guide for the student and a useful work of «^« %*« J^^^EEE" The illustrations are numerous and are well executed. - Die Lancet, London. tioner 1 6 BACTERIOLOGY, PHYSIOLOGY, AND HISTOLOGY. Ball's Bacteriology Seventh Edition, Revised Essentials of Bacteriology : being a concise and systematic intro- duction to the Study of Micro-organisms. By M. V. Ball, M. D., late Bacteriologist to St. Agnes' Hospital, Philadelphia. l2mo of 289 pages, with 135 illustrations, some in colors. Cloth, $1.00 net. In Saunders 1 Question- Compend Series. " The technic with regard to media, staining, mounting, and the like is culled from the latest authoritative works." — The Medical Tunes, New York. Budgett's Physiology Third Edition Essentials of Physiology. Prepared especially for Students of Medicine, and arranged with questions following each chapter. By Sidney P. Budgett, M. D., formerly Professor of Physiology, Washing- ton University, St. Louis. Revised by Hayan Emerson, M. D., Demon- strator of Physiology, Columbia University. l2mo volume of 250 pages, illustrated. Cloth, $1.00 net. Saunders' 1 Question- Compend Series. " He has an excellent conception of his subject ... It is one of the most satisfac- tory books of this class. — University 0/ Pennsylvania Medical Bulletin. Leroy's Histology Fourth Edition Essentials of Histology. By Louis Leroy, M. D. , Professor of Histology and Pathology, Vanderbilt University, Nashville, Tennessee. i2mo, 263 pages, with 92 original illustrations. Cloth. $i.co net. In Saunders" 1 Question- Compend Series. " The work in its present form stands as a model of what a student's aid should be ; and we unhesitatingly say that the practitioner as well would find a glance through the book of lasting benefit "—The Medical World, Philadelphia. Barton and Wells' Medical Thesaurus A Thesaurus of Medical Words and Phrases. By Wilfred M. Barton, M. D., Assistant Professor of Materia Medica and Therapeu- tics ; and Walter A. Wells, M. D., Demonstrator of Laryngology, Georgetown University, Washington, D. C. l2mo, 534 pages. Flexible leather, $2.50 net. American Pocket Dictionary New (8th) Edition American Pocket Medical Dictionary. Edited by W. A. New- man Dorland, M. D. Containing the pronunciation and definition of the principal words used in medicine and kindred sciences, with 64 extensive tables. Containing 677 pages, flexible leather, with gold edges, $1.00 net ; with patent thumb index, $1.25 net. " I can recommend it to our students without reserve." — J. H. Holland, M.D., of the Jefferson Medical College, Philadelphia. A A 000 221529