Yjkii,,»-%, w^^m :^ N m^M.M^ .iT'J) m 'C .iiiCii^*^. i^% -vi;S'lSJ ,^^4#^^?^Ss?fPl|;^p^i: - \ ^^\^ ^;>-i// Sr^( lWA wvvtE.fv. V • ^ ■? " >:::r / Jt^r ^r y Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/practicaldiagnosOOhare PRACTICAL DIAGNOSIS: THE USE OF SYMPTOMS IN THE DIAGNOSIS OF DISEASE. BY HOBART AMOEY HARE, M.D., B.Sc, PROFESSOR OF THERAPEUTICS IN JEFFERSON MEDICAL COLLEGE OF PHILADELPHIA; PHYSICIAN TO THE JEFFERSON MEDICAL COLLEGE HOSPITAL ; LAUREATE OF THE MEDICAL SOCIETY OF LONDON, OK THE ROYAL ACADEMY IN BELGIUM ; CORRESPONDING FELLOW OF THE SOCIEDAD ESPANOL DE LA HIGIENE OF MADRID; MEMBER OF THE ASSOCIATION OF AMERICAN PHYSICIANS, ETC. ILLUSTRATED WITH 191 ENGRAVINGS AND 13 COLORED PLATES. r'lIILADELririA and new YORK: J. KA BK OTHERS ct CO. 1 8 ({. Entered according to the Act of Congress, in the year 1896, hy LEA BROTHERS & CO., In the Office of the Librarian of Congress. All rights reserved. nORNAN, PRINTER. M c"^ PREFACE, The object of this volume is to place before the physician and student the subject of medical diagnosis as it is met at the bed- side. To accomplish this the symptoms used in diagnosis are discussed first, and their application to determine the character of the disease follows. Thus, instead of describing locomotor ataxia or myelitis, there will be found in the chapter on the Feet and Legs a discussion of the various forms of and causes of paraplegia, so that a physician who is consulted by a paraplegic patient can in a few moments find the various causes of this condition and the differential diagnosis between each. So, in the chapter on the Tongue, its appearance in disease, both local and remote, is discussed. In other words, this book is written upon a plan quite the reverse of that commonly followed, for in the ordinary treatises on diagnosis the physician is forced to make a supposititious diag- nosis, and, having done this, turn to his reference book and read the article dealing with the disease supposed to be present, when if the description fails to coincide with the symptoms of his case he must make another guess and read another article. In this book, how- ever, the discovery of any marked .symptom will lead directly to the diagnosis. Tiius, if the patient is vomiting, in the chapter on Vomiting will be found its various causes and its diagnostic sig- nificance, and the differentiation of each form of this affection from another. iv PBEFA CE. The value of the book is increased by the preparation of two indexes: one of symptoms and the other of diseases. Basing his efforts upon the experience which lie has had in both didactic and clinical teaching of large classes of students during the last twelve years, the author hopes that the work may in some degree lighten the labors of the general practitioner and student, and relieve the all-important subject of diagnosis of some of the difficulties which surround it. He has also endeavored to make the text serve as an aid to the rational use of his Text-Book of Practical Therapeutics. Philadelphia, 222 South Fifteenth Street, August, 1896. CONTENTS. INTKODUCTIOX. GENERAL DIAGNOSTIC CONSIDERATIONS. PART I. THE MANIFESTATION OF DISEASE IN ORGANS. CHAPTER I. THE FACE AND HEAD. PAGE The expression and color of the face — Facial paralysis, unilateral and bilateral — Ptosis — Facial spasm — The shape of the head — The movements and position of the head ...... 25 CHAPTER II. THE HANI) AND ARM. The general appearance of the hands and arms — The shape of the hand in disease — Spasms of the fingers — Tremors of the hand — Paralysis of the hand and arms 48 CHAPTER III. THE FEET AND LEGS. The general appearance of the feet and legs when clothed — The gait — Spastic paraplegia -Paraplegia without spastic contraction — Crural monoplegia — Deformities of the feet — The joints — Alterations in the nutrition of the feet and legs aside from a change in the muscles ............ ~~ CHAl'TKR IV. HEMIPLEGIA 11 ronchitis," in all human probability the real cause of death was tubercidosis of the lungs. If the patient complains of pain, past or present, the best way in which to discover its true seat is to ask him to place his hand on the aflPected part, as in this way errors in his description of his anatomy will not be committed, and false impressions will not be conveyed to the physician's mind. Even this direct method of showing the area of pain is not to be absolutely relied upon, for often pains are referred to |)arts in which tiicrc is no disease. Thus, the pain of coxalgia is apt to be felt in the knee and ankle, and in children the pain of acute pulmonary disease is often described by the patient as felt in the abdomen. If the pain has been really abdominal, there will, in most cases, have been diarrlKca or free passage of llatus. It is not to bo forgotten, on the other hand, that aciuestion which discovers the fact of several movements of the bowels does not prove the pres- ence of true diarrluea, because a purgative may have been taken l>y the patient. In asking (|ucsti()ns as to constipation the physician must not for- get that the opinidu ol" the patient as to what constitutes regularity of buwcl-inovcincut is of very little value in manv instances. A 22 I^^'TB on UCTIOX. daily movement is not known to many patients, and a movement every few days may be quite sufficient to justify the statement, in their opinion, that no constipation is present. The young physician, in particular, in asking questions of women patients of the better class, should not hesitate to ask direct ques- tions as to the state of the bowels or of the menstrual function. To hesitate or ask indirect questions about such matters simply produces embarrassment, which otherwise would not exist, and intimates that the question is one of doubtful propriety, when in reality it is most important and proper. If the patient to be examined is a child, it is well for the physician to remember that his mere presence as a stranger may be a source of alarm, and that the association in the child's mind of sickness and the doctor, and badly tasting medicines, is sufficient to render him a much-to-be-dreaded individual. Generally it is best, on entering the room where the child is, to pretend to pay no attention to it what- ever, but to engage in conversation with the mother or other person, speaking of the case in a way which the child will not understand. Very often this very lack of attention will result in the child forcing the recognition of his presence upon the physician by making the first advances toward friendship, and this is particularly apt to be the case if the child is already spoiled by over-attention by the family and friends. Time should always be given the child to grow accustomed to the peculiarities of the visitor, and if any instrument for diagnosis is to be employed, it is best to hold it in the hand as if it were a plaything before attempting to put it into actual use. The tact which the physician must exercise in diverting a sick child is an essential to the successful treatment of children. Some physi- cians are welcomed to a house by the sick and well as a Santa Claus would be, and others, devoid of the trait of amusing children, are fled from as if they were dragons. During the time that the physician is allowing the child to ^et accustomed to his presence he should be gaining much useful infor- mation about the case by observing the movements and expression of the child; its color, size, nutrition, breathing; the shape and size of its head ; the condition of the lips, whether moist or dry; and, if the child is speaking, the tone of its voice, or, if crying, the character of its cry. It is needless to state that a child may cry from fright, from pain, anger, or hunger. Constant screaming crying is, how- ever, nearly always due to the pain of earache or hunger, for GENERAL DIAGXOSTIC CONSIDER ATIOXS. 23 abdominal colic is usually intermittent. If there be pain in the ear, the hand will often be rul)l)ed over the aflPected side of the head, and the child will not be pacified by the offer of the breast. If the child coughs, and then begins to cry, pneumonia or pleurisy may be pres- ent ; or in other cases the pain is so great that the child is cryless. A sharp, piercing shriek of crying indicates the pain of meningitis in many cases. If the crying child be placed at the breast, which it takes with avidity only to drop the nipple in a moment with a cry of pain or anger, one of two conditions is present : either the child has stoma- titis or the breast is empty ; or, again, if it seizes the breast and then lets go with a gasp, it probably has coryza, or syphilitic snuffles, which prevents it from breathing through the nose while sucking. Similar signs may be present in any other conditioB producing shortness of breath. If a child over four mouths of age cries and sheds no tears in the course of an illness, this is an unfavorable sign. It is important to notice whether there is languor or a tendency to play. A healthy infant, when awake and well-fed, is always kicking or cooing and moving its arms about, and has a happy expression on its face ; whereas if any cerebral trouble is ju'esent, it often has an anxious frown, or its hands are placed to the side of its head or rubbed over the vertex. In a perfectly healthy child which is sleeping the respiration should be practically inaudible, and it is a good practice to note the regularity of the breathing in all patients Avhile they are asleep, as it is then unatfectcd by voluntary effort. In children a sighing breathing, or one disturbed in rliythm, indicates a disturbed digestion or fever. The breath of the healthy chikl is invarial)ly odorless and sweet, but is apt to become heavy and sour in fever and gastric disorders, and in tonsillitis and diphtheria it is apt to have a peculiar sickening odor of a sweet character. In cases of empyema opening into a bronchus or in gangrenous stomatitis the breath is very offensive. The physician should also, by careful (juestioning of the nurse or mother, find out how long the illness has lasted, the manner in which it began, the fact as to whether a similar attack has occurretl l)efbre in this or otlier children of the family, and the state of the temper, appetite, bowels, and urine of the patient, for an irritable tenijwr in a child means ill-health, as does.also a poor appetite, con- stipation, diarrhica, or abnormal urine. 24 J^^TE OD UCTIOX. The expression ©f the face, shape of the head, and similar note- worthy points in the diagnosis of the case will be more thoroughly discussed in the chapter devoted to these parts. When it comes to a close examination of the child, great care must be exercised. The character and rapidity of the respirations are best studied at a distance before excitement has disturbed them, and the best way of listening to a young child's chest is when it is held over the shoulder of the mother as if she were carrying it for a walk, or, if the child can betaken in the physician's arras, its buttocks should rest on one hand, while its chest leans against the other. In this way the physician can listen to the back of the chest without diffi- culty, keeping the child amused by walking up and down the room while it is in his arms. If it is not possible by any bribe to cause the child to protrude the tongue for examination, the physician will often be able to see this organ when the mouth is widely opened in crying. In taking a child's pulse it is best to take it while it is asleep, if possible, as the excite- ment of the physician's visit or the crying on awakening will greatly increase the pulse- rate. PART I. THE MAXIFESTATIGX OF DISEASE IX ORGANS. CHAPTER I. THE FACE AXD HEAD. The expression and color of the face— Facial paralysis, unilateral and bilateral — Ptosis — Facial spasm — The shape of the head — The movements and position of the head. So much can ho learned by the physician from the expression and general ai)pearance of a patient's face and the carriai:;e and shape of his head, that a careful inspection of these parts should always be made. For this reason, in the consulting-room and at the bedside, the physician should always arrange his chair in such a way that the light falls upon the face of his patient, while his own is in the shadow, and this is of iiij])()rtance not only because the facial expres- sion of the patient can thus be well seen, but also because it prevents the patient from making a too clo.se scrutiny of the physician's face with the object of detecting encouragement, lack of sympathy, or alarm. The Pace. The Expression is produced by the formation of creases, or alter- ations in the contour of the skin and subcutaneous tissues by trophic and mu.scnlar action, and these changes are in time brought about by the mental tendencies and habits of the patient, his temperament, his intellectual development, his exposure to outdoor or indooi' inllu- ences, and finally, and these are very important, by pathological pro- cesses which may be going on somewhere in his body. The temper of the man also affects his expression, particularly as he approaches middle life, and he looks amiable, capable of sudden anger, or sullen, as the case mav be. 26 THE MANIFESTATION OF DISEASE IN ORGANS. The intellectual face is easily recognized. Sometimes it is deeply thoughtful and placid, at others eager or keenly alive to the sur- roundings or the conversation, and it separates the man descended from several generations of men who have lived as thinkers from him whose ancestors have been but recently wage-earners by physical labor, involving only ordinary human intelligence. Fulness of the lips, particularly of the lower lip, is supposed to be present in persons of strong sexual appetite, and often indicates a phlegmatic temperament, whereas the thin, mobile lip is typical of the high-strung, nervous individual. The expression of the lips as a whole is also to be regarded in connection with the expression of smiling. The risus sardonicus of strychnine-poisoning or tetanus is quite characteristic, and the simple smile of hysteria is equally notorious. The skin of the face and the expression about the eyes of one who has been exposed for years to the weather are so characteristic as to need no description, while the face of the clerk, whose life is almost entirely spent indoors, is pale and wan. Similarly, the face of a person who uses alcohol to excess is gener- ally flushed, heavy, and more or less expressionless. The eyelids are reddened more than normal, and the skin is apt to be puffy and unhealthy-looking. Women at the menstrual period, or when suffer- ing from menstrual disorders, often have dark areas under the eyes, and pigmentation of the eyelids is often seen in females very early in pregnancy. The color of the face is discussed in the chapter on the Skin, but it is not out of place to note at this point the pallor of the face in fright, faintness from hemorrhage, acute or chronic, that due to lack of proper food, and the peculiar pallor of chlorosis. In the latter disease the faint yellowish-green tinge of the skin in some parts of the face, which still retains its plumpness, is quite typical. A parch- ment-like skin stretched over the face so that it appears as if dried over the under-structures is seen in some young persons suffering from syphilis, and in some cases of alcoholic hepatic cirrhosis. The color of the face may be rendered gray or bluish by the in- gestion of overdoses of the coal-tar products, such as acetauilide, antipyrin, and phenacetin, and it is curious that this effect is best seen when the patient is viewed at a little distance. (For the indications of facial cyanosis, see chapter on the Skin.) In view of the extraordinary variations seen in the expression of THE FACE AND HEAD. '21 the face in the healthy it is not surprising that this part of the body should give the physician, when studying disease, so much useful information. It is an interesting fact, too, and one not unworthy of note, that the true facial ex])ression of a disease is rarely aped by a malingerer, and in all diseases is unrecognized by the patient even though he sees himself several times daily in the lonking-glass. Thus it is by no means uncommon to see a person, who is suffering from the onset of some sudden and grave disease, bearing upon his face what we call '' an expression of anxiety," when he himself as yet has no conception of the gravity of his illness. This expression is very characteristic of serious illness, and, though difficult to de- scribe, when recognized becomes quite valuable as a diagnostic factor, particularly as it rarely, if ever, is exaggerated by the })atient who bears it. It is seen most markedly in cases of sev^ore acute croupous pneumonia or peritonitis, or after severe injuries. When persons have had continuous pain for a lo^g time, as in patients who have growths of a malignant character or other organic disease, the expression of the face, naturally gentle, often becomes hard and stony, or, if the ])ain be in the head, the expression is not only that of pain, but of profound mental depression. In cases of carcinoma the face becomes thin, its skin yellow and straw-colored, and often- times greasy and thick, and there is often a marked look of anxiety. On the other hand, the patient sometimes has a dogged expression on his face as if he had been told of the true cause of his illness, and was rebelling against the inevitable progress of the disease. In the case of children, much information can be gained as to the state of the body by the facial expression, particularly while the child sleeps. If it is asleep and healthy and well, the eyelids are closed, the lips are ever so slightly parted, the nostrils are i)ractically immobile, and the general expression is very peaceful. If, on the other hand, the eyelids of a sleeping child are slightly parted so as to show the whites of the eyes, there is present some digestive or nervous disturbance, perhaps accompanied by moderate pain. If the disease is grave and the eyelids remain far enough apart to re- sult in glazing of the conjunctiva from dryness, this is a sign of grave import. Again, twitching of the eyelids often indicates nervous irri- tation or the early stages of the convulsive state, and it is not un- common for an expression to pass over the face.of a child wiio, while sleeping, issullcring from pain, which begins as a smile and ends with a drawing-in of the corners of the mouth, an expression somewhat 28 THE MASIFESTATIOX OF DISEASE IN OEGANS. like that seen ou the face of a waking child when it seems to be in doubt as to whether to laugh or cry. Whether asleep or awake a child in pain, if not crying, has a pinched look about its nose and mouth, and sometimes some idea of the seat of the pain may be gained by the part of the face which is drawn. AVhen pain is in the head, the forehead is apt to be wrinkled into a frown; if the nose is pinched and drawn, it is said to show that the pain is in the chest; and if the upper lip is raised, pain is probably felt in the belly. Aside from these symptomatic manifestations, however, we find in the face of a child several evidences of important diathetic tendencies, or even hereditary diseases. Thus we see the light flaxen-haired, slimly built child with a refined spirltueUe face and transparent skin, whose temporal veins can be easily traced and whose expression is often thoughtful and deep. Such a child often comes of tubercular parents, and is frequently a victim of tuberculosis, in one of its rapid forms, as it approaches puberty. Or, again, the child is heavy and cheesy-looking, apparently solid and sturdy, but its features are heavy or perhaps even coarse, while its neck is thick and short. Such a child is often a victim of tubercular bone disease. In other instances, a square projecting forehead with faulty bone-development elsewhere indicates rickets, or an immense bulging forehead with a wizened, puny face beneath shows hydrocephalic tendencies. Sometimes a broadness of the bridge of the nose or marked flatness of it indicates congenital syphilis. Such a child is often much wasted, its features pinched, and its lips thin, while the flattened nasal bridge is bluish and its face is often that of a little old man, shrivelled and wrinkled. Mucous patches at the corners of the mouth or around the anus are often found in such cases, and soon confirm the diagnosis of infantile syphilis. Finally, in respect to facial expression in childhood, atten- tion must be called to the " fish mouth," vacuous, and " nose- pinched " expression of those children who are " mouth-breathers " from nasal obstruction. (Fig. 1.) Great immobility of the lips and cheeks may be due to mucous patches or other ulcerations of the buccal mucous membrane, and if high fever is present tlie presence of herpetic blisters about the lips points to croupous pneumonia in the child or adult. In adults the facial expression of many diseases is even more characteristic than it is in children. Thus we see in acute pul- monary phthisis the widely opened eye, the hunted expression, the quivering nostrils, the red flush over the malar bones, the wasting THE FACE AND HEAD. 29 and dryness of the hair and skiu, and the eager, or apathetic, glance of the eye. In severe pneumonia the flushed face, with a deeper red on one cheek than the other, the auxious expression, and the dilated nostril are noteworthy ; and in the dyspncea of heart disease the dilated nostril and constant opening of the mouth as if seeking for air, with the facial pallor or cyanosis, are characteristic. Often, too, in chronic cardiac or pulmonary disease producing slight difficulty in respira- tion, the patient's lips are seen to be slightly parted and dry, and often appear somewhat cyanotic. In children suifering from lesions of the mitral valve of the heart it is very common for some blurring or indistinctness of the features to be present. Fig 1. Boy'agedlseven. Mouth-breaiher, from obstruction of the pharynx ; open mouth ; vacant expression; pinched nostrils; dull eyes; drooping eyelids ; sunken chest; round shoulders. e is dull and expressionless ; the teeth are covered by sordes, which become brown and blackish by exposure or by discoloration from medicines and foods; tiie lips are often moved in a low muttering delirium; and the whole appearance is that of apathy. pA'ea when spoken to, the face of a patient suffering from enteric fever rarely lights up in re- sponse to the greeting. Equally, if not more, characteristic is tlu' facial expression of acute peritonitis. The ui)p('r lip is drawn uj) in such a way as to show the teeth, and the e-xpivssion of anxiety and nervous unrest is well develoj)ed. Siinihirly in abdominal ]>ain due to .other cau.se8 than peritonitis there is often a twitching of the mascles of the lip and al)out the eye which is quite typical. This twitch is said by 30 THE MANIFESTATION OF DISEASE IN ORGANS. Fothei'gill to be peculiar to pain below the diaphiagm, and he is also responsible for the statement that it is best seen in the face of the parturient woman in the second stage of labor. The facial expression of hysteria may be apathetic, or it is that of devotion, rage, or grief, and these expressions are fixed if the patient be cataleptic. If she is not cataleptic, not infrequently one expression may succeed the other, or in their place there comes that curious smile or vacuous expression of the face which is so characteristic. It should be remembered, however, that this vacant, fatuous look may occur in women suffering from the early stages of disseminated scle- rosis and in children with chorea. Then we have the elated facial ex- pression of general paralysis of the insane, the excited look of acute mania, the beaten, Aveary, careworn look or apathetic glance of nervous exhaustion, and the hopeless expression of melancholia. The face of paralysis agitaus is sometimes called the " Parkin- sonian visage," is distressed and pathetic, and yet somewhat intense. (See chapter on Hand and Arm, part of on Tremor.) A pale, puffy face, generally looking worn and weary, may be seen in cases of chronic or subacute renal disease. In children there is often in this condition a peculiar transparent or pearly look in the lower eyelid, so that it seems somewhat pellucid. Great swelling or oedema of the face is seen in erysipelas, dropsy, and inflammatory swelling (see chapter on the Skin). In trichiniasis the eyelids are often swollen early in the disease, and then recover their normal ap- pearance only to become swollen again later in the malady. When the face bears a sleepy, listless expression, the forehead being devoid of wrinkles, and there are present faulty movements of the lips, which cannot be approximated, as in whistling, and at the same time the patient is unable to close the eyes entirely, although the lids droop, the physician should think of the possibility of these being the early symptoms of what has been called the " facio- humero-scapular " type of muscular atrophy (Landouzy and Dejeriue). This disease, as its name implies, speedily involves the scapulae and arms after affecting the face, and exophthalmos is often present. This form of muscular atrophy lacks the fibrillary twitch- ings seen in spinal progressive muscular atrophy; there are no changes in electrical excitability, except that owing to the loss of muscle-fibre the reaction is feeble. The fact that more than one member of the family is affected, and the long duration of the disease added to these signs, render the diagnosis easy. It is a rare disease. THE FACE AND HEAD. 31 An appearance of the face almost identical with that just described is seen in Friedreich's ataxia, and is often one of the earlier manifesta- tions of the disease; but the presence in Friedreich's ataxia of the ataxic gait, the jerky articulation, nystagmus, loss of knee-jerks, and absence of muscular atrophy separate it from the Landouzy-Dejerine type of muscular atrophy just described as facio-humero-scapular atrophy. Fig. 2. The facial expression of cretinism is exceedingly characteristic. The nose is broad and flat, the eyelids swollen, the lips are greatly thickened, and the enlarged tongue lolls out of the mouth, from wliich saliva constantly dribbles, while the waxy skin and sub- normal temperature of the body, with a poor circulation, slow respira- tion, and mental hebetude, complete the symptom-group. There is nearly always in well-developed cases marked lumbar lordosis. (Fig. 2.) In certain forms of leprosy the face ofteu becomes leontine or lion-like in ap})taranee. 32 THE MANIFEST ATIOX OF DISEASE IN ORGANS. The facies of exhausting disease about to produce death is very characteristic, and is seen frequently in cholera and in tuberculosis of the lungs. It is called the '' Hippocratic face/' and is peculiar in the sinking-in of the temples where the jaw-muscles are inserted; the eye is sunken, and around it are great hollows, so that the iufra- and supra-orbital ridges become greatly accentuated. The eyelids are slightly parted, the cornea somewhat glazed; the nose pinched, its skin drawn; and the lower jaw somewhat dropped. Such a face, if typical, is a sure forerunner of dissolution. Facial Asymmetry. Facial asymmetry is sometimes seen as a congenital defect, and curiously enough is often developed in children who suffer from congenital wry-neck. This is not to be confused with that extraordinary aiFection called facial hemiatrophy, which usually begins in childhood in one spot, and slowly proceeds until one side of the face, sharply outlined from the other, becomes wasted in its skin, muscles, bones, color, and hair. Even the eye may be sunken and shrunken. Rarely this wasting is bilateral. Sometimes in facial hemiatrophy the wasting is accompanied by painful twitchiugs, which increase with mental excitement. More rarely there is decrease in the acuity of taste and hearing on the affected side, while myosis, sweating, or excessive dryness of the skin may be found on this side. Such symptoms as the last show in- volvement of the sympathetic nerve-fibres. The changes are prob- ably due to disease of the fifth (trifacial) nerve. As to whether circumscribed scleroderma (morphoea) and facial hemiatrophy are identical, that is, whether the first is a well-devel- oped form of the latter, is not decided. Hyde apparently regards them as identical. (See chapter on Skin, Scleroderma.) Even more rare than facial hemiatrophy is facial hemihyper- trophy, one side remaining normal in size and the other becoming gigantic. The massive face of a person suffering from acromegaly is very characteristic (Fig. 3), and the face has a full-moon broadness in myxoedema. The face in osteitis deformans is shaped like a triangle with the base upward. The enlargement of the bony parts of the skeleton, the kyphosis, and the comparative muscular feebleness of acromegaly aid in the diagnosis of that disease, for in myxoedema there is no true bony enlargement. In osteitis deformans the shafts of the long bones become weakened, and their surfaces roughened from periosteal deposits. THE FACE A XL) HEAD. 33 Unilateral Facial Paralysis. Very notable changes in the face are produced by paralysis, the former being, as a rule, unilateral and depending upon central, peripheral or nerve lesions for its cause. Smiling, when unilateral paralysis is present, results in the drawing back of only one corner of the mouth (on the well side), and whistling or the pronunciation of labial sounds is difficult or impossible. The cheek of the paralyzed side is often jniffed out with each expiration. Fig. 3. k Acromegaly, showing the large face and hands. (Dercum.) but the wrinkling of the skin is on the side of the face which is not paralyzed, owing to contraction of the muscles which are unoj)posed. (For a description of the general anatomy and ])hysiology of the nervous tracts involved in paralysis of the face and elsewhere, see chapter on Arm and Hand.) Unilateral j)aralysis is the ft)rm of facial |)aralysis most com- monly seen, and it is generally due to injury of the facial nerve-trunk. The lesion producing the ])aralysis may be ])eri])heral — that is, in the 8 34 THE MAXIFESTATIOS OF DISEASE IN ORGANS. nerve itself, in the pons, or in the cerebral cortex. The former variety is the most common, provided the paralysis is purely facial, and it is usually due to inflammation of the nerve-sheath as it passes through the stylo-mastoid foramen, the loss of function being due to pressure on the axis-cylinders owing to the presence of swelling in so limited a canal. Such an attack will generally be found associ- ated with a history of exposure to cold or injury by a blow, or with that of middle-ear disease with caries of the petrous portion of the temporal bone following otitis, which inflammatory process causes pressure on the nerve. It is not necessary for the otitis to be sup- purative or for caries to exist in all cases, for it seems probable that by the extension of inflammation along the chorda tympani such a paralysis may result. Still more rarely facial paralysis results from swelling of the parotid gland, or tumor in its neighborhood, and it may occur as the result of pressure by growths at the base of the brain, syphilitic or otherwise, from fracture of the base of the skull involving the petrous portit^n of the temporal bone, and very rarely when the disease occurs in the newborn from hemorrhage, from the cerebellum during birth, or from the pressure of forceps. Finally, paralysis due to a peripheral lesion of the nerve may result from neu- ritis, and from primary hemorrhage into the nerve-sheath or stylo- mastoid canal. Facial paralysis may also arise from locomotor ataxia, the lesion being in the pons, and from hysteria. All these forms are very rare comparatively speaking. The cerebral or medullary lesions which produce unilateral facial paralysis usually consist in hemor- rhage and tumor. The determination that facial paralysis is due to a peripheral neu- ritis, or pressure, may be impossible at the first visit of the patient, if this visit is made, as it usually is, within a few hours of the onset of the malady; but it separates itself from facial paralysis of cerebral origin iu the course of ten days or two weeks, for, if the nerve is inflamed or pressed upon in the foramen, the muscles of the face speedily undergo degeneration, because they are cut off from their trophic centres. In the cerel»ral form, on the other hand, the trophic changes do not occur, and the reactions of degeneration fail to appear, because trophic impulses can still reach the facial nerve- trunk and the muscles. In other words, electrical response in the paralyzed side remains normal in centric lesions and is lost in periph- eral lesions. The only other condition in which there can be de- veloped the reaction of degeneration, and the lesion not be in the THE FACE A XI) HEAD. 35 nerve-trunk or foramen, is when there is a tumor at the base of the brain involving the facial fibres below the facial nucleus or destroy- ing the nucleus itself. Very rarely in cerebral facial paralysis is the loss of power as complete as it is in the peripheral form. Again, in cerebral facial paralysis the eye on the paralyzed side can usually be closed and the forehead wrinkled, whereas in the peripheral form it cannot. Why this should be so is not clear, unless it is that in the muscles used commonly in pairs, as in those of the forehead, there is an adequate nerve-supply through direct non -decussating tracts which innervate the muscles. When facial paralysis has associated with it none of the signs of peripheral wasting, and none of the remote causes of hemor- rhage, embolism or thrombosis, such as result from impaired blood- vessels or a diseased heart, and when the paralysis comes on gradu- ally (tiiough it may be sudden from surrounding inflammation), the condition is probably due to cerebral tumor. This diagnosis is con- firmed by the gradual spread of the paralysis to other parts, as the arm and then the leg on the same side of the body, and by the development, often before each spread of the paralysis, of a convul- sion. The facial paralysis resulting from tumor at the base of the brain differs from that due to cerebral tumor or hemorrhage by the fact, already stated, that the reaction of degeneration quickly develops in the paralyzed part; that the parts supplied by the frontal brancii of the facial are often quite as much paralyzed as are those supplied by the lower branch, which is rare in the cerebral lesion, and tiiere will com- monly be found other evidences of a growth which, in a region so densely filled with important centres, speedily affects other functions. Thus, there will nearly always be found in association with this form of facial paralysis paralysis of tlie oculo-motor and abducens, causing ptosis, a moderately dilated pupil, and internal or external squint. The optic nerve may show choked disk, and there may be disturbance of vision (see chapter on Eye). If the tumor grows large enough, or is so placed as to involve the facial fibres for both sides as well as those of the oculo-motor, abducens, and optic nerves on both sides, all these symptoms become, of course, bilateral. Facial palsy associated with deafness may indicate cerebellar tumor, tiie diagnosis of this cause being decided by the other cere- bellar symptoms, such as the peculiar gait. (See chapter on Feet and Legs.) Such growths are not uncommon in children. Sometimes very shortly after birth the child is seen to have a 36 THE MANIFESTATION OF DISEASE IN ORGANS. facial paralysis resulting from pressure by the forceps, which have slipped and injured the nerve, or have caused an extravasation of blood into the neighborhood of the parotid gland, thereby causing pressure on the nerve. The prognosis is usually favorable if due to such causes; but if the forceps have caused facial palsy by producing a cerebral hemorrhage, the outlook is bad. The possibility of facial paralysis being due to hysteria should not be forgotten. The loss of power under these conditions may be uni- lateral or bilateral, generally the former. Its association with the symptoms of hysteria described in the chapter on the skin, and else- where, in this l)Ook will aid in making the diagnosis. There yet remain to be considered several forms of facial paralysis unilateral in character yet associated with paralysis elsewhere. Unilateral facial paralysis very rarely occurs in association with monoplegia in acute anterior poliomyelitis. So seldom does it occur in this connection that it has been denied an existence. Often it is but temporary, while the monoplegia of the arm is permanent. It occurs more commonly in the disease in adults than in children. Facial paralysis with arm paralysis of the same side, followed in a short time by paralysis of the leg of the opposite side, is quite a characteristic symptom of syphilitic arteritis at the base of the brain. Crossed paralysis — that is, paralysis of the face on one side, and of the arm and leg on the other — is due to a lesion in the pons above the decussation of the pyramids and below that of the facial fibres. (Fig. 4.) Thus it is seen in this figure, on the left side, third in- scription, that the lesion in the pons cuts off the motor fibres in the place indicated, thereby causing the distribution of the paralysis just named. (See also chapters on Hemiplegia and on Arm and Hand.) Sometimes the muscles supplied by the facial nerve escape paralysis, but those of the jaw, namely, the masseters and temporals, become paralyzed either bilaterally or more commonly unilaterally. This is a rare affection, and depends upon paralysis of the inferior maxillary branch of the trifacial nerve. This may be due to pressure pro- duced by growths or inflammatory processes at the base of the skull. It may also occur as the result of hemorrhage into the raeduUa, or from progressive bulbar paralysis. Ptosis. In connection with the subject of facial paralysis that of ptosis or drooping of the upper eyelid must be considered. It de- pends upon loss of function of the oculo-motor nerve or its centre or nuclei. (Fig. 5.) It is a symptom of the greatest importance, THE FACE A XI) HEAD. 37 first, because it is so readily recognized ; second, because it is a source of great annoyance and alarm to the patient ; and, third, and more important, it often gives us very clear ideas of the condition of the patient. The presence of this symptom should call to the physician's mind the various causes which produce it. Fig. 4. Lesion of cerebral noplegia (brachial) Lesion of ordinary hemiplegia Lesion of cross paralysis (face of same side ivitk limbs of other side) A lesion causing xx^raplegia A lesion causing hemi- paraplegia Cortical centre for op- jyosite leg Cortical centre for op- posite arm Cortical centre for op- posite side of face Internal capsule (pos- terior limb) -Jlotor nerve to face Decussation of pyra- mids Crossed pyramidal tract Jlotor nerves to upper limb Crossed pyramidal tract Sensory nerves entering cord, and decussating soon after entry Motor nerves to lower limb Diagram to show the general tirrangement of the motor tract and the effect of lesions at various ix)ints. (OuMEiton.) In the first place, it sometimes occurs as a congential defect, and in such a case the history of the patient renders the diagnosis easy. Second, it depends upon a lesion of the oculo-motor nerve or its nucleus. If this nerve Ix' entirelv destroved so far as its function is 38 THE MANIFESTATION OF DISEASE IN ORGANS. concerned, there will be, in addition to ptosis, paralysis of all the external muscles of the eye except the superior oblique and external rectus, aud in addition there will be a moderately dilated pupil, which will not contract, and paralysis of the ciliary muscle — that is, loss of accommodation. The eye can be moved outward by the action of the external rectus, and a little downward and inward by the superior oblique. Diplopia is present, and a little exophthalmos Fig. 5. Ptosis in a case of alternate hemiplegia of syphilitic origin. (Philadelphia Hospital.) (Dercum.) may be present owing to the action of the superior oblique, which presses on the ball. If the lesion be in the oculo-motor nucleus, the near position of the nuclei of the fourth and sixth nerves will probably cause them to be affected also, thereby causing a general ophthalmoplegia. If the lesion is not nuclear, it may be due to disease in the nerve itself, as already pointed out. If this is the case, the lesion is probably due to pressure in the cavernous sinus or periostitis of the bones forming the sphenoidal fissure through which the nerve passes. Sometimes, however, the paralysis of the nerve may be only partial, so that the external muscles of the eyeball escape, and only ptosis and a dilated pupil are present. Very rarely ptosis results from a cerebral hemorrhage, without the other signs of oculo-motor paralysis being present. That is to say, the branch of the oculo-motor which supplies the levator palpebraris is affected, while the brandies supplying the evternal aud internal ocular muscles escape. If there is a history of a cerebral attack resembling a mild apoplexy, and a unilateral ptosis is present, the lesion is probably in the cortical centre for the oculo-motor nerve in the angular gyrus just below the THE FACE AM> HEAD. 39 inter-parietal fissure. The lesion is, of course, upon the opposite side of the cortex from the ptosis. Such a case is very rare. A fourth cause of ptosis is due to an affection of the sympathetic nerve, and is sometimes called p^eudo-ptosis. There are associated symptoms of vascular dilatation, with redness and swelling of the skin of the affected side, elevation of temperature in that part, contraction of the pupil on the affected side, and apparent shrinkage of the eye into the orbit. This form of ptosis results from the paralysis of the unstriped muscular fibres of Miiller which exist in the orbital fascia, for as these muscular fibres aid in holding open the lid their paral- ysis results in partial ptosis. Nothnagel asserts that such symp- toms occur with lesions in the corpus striatum. A fifth cause of ptosis is reflex irritation usually through the fifth nerve. This is probably due to an inhibition of the oculo-motor centre. It is usually only trausient. Sixthly, it is not uucommon in cases of nervous sy^ihilis for so- called alternate ptosis to develop. First, one eye is affected by ptosis, and then the other just as the first begins to improve or has re- covered. Ptosis has been known to complicate tetanus, probably as the result of reflex irritation of the fifth nerve. Ptosis, either unilateral or bilateral, may arise from hysteria and idiopathic muscular atrophy. If from hysteria, the diagnosis can be made from the age, sex, and history of the patient, from the presence of the hysterical sensory changes described in the cliapter on the skin, and from the fact that there is a tendency to spasm of the orbicularis muscle when the patient is made to look up. This contraction of the orbiculares ])rovcs that there is no true paralysis of the levators. If the ptosis is bilateral and hysterical, the head is tipped l)ack when the patient is told to look up. Single or doul)le ptosis is by no means a rare symptom of loco- motor ataxia, and is often associated with other evidences of oculo- motor palsy. Sometimes diplopia due to these changes are the first symptoms complained of, and the patient may state that the diplopia comes and goes. J^ilateral i)tosis may arise from tubercular or syphilitic changes about the base of the brain, or it may be congenital, or if transient be caused by poisoning by gelsemiiun or conium. It is also seen in feeble, overworked women, particularly in the early morning on awakening. 40 THE MAXIFESTATIOX OF DISEASE IN ORGANS. Again, it is not veiy rare to see sliglit drooping of both lids in all the members of a family, in which case the condition is usually most marked in the women, and is to some extent combated by the frontal muscles, which, in contracting, make the patient frown and draw up the eyebrows. Ptosis may also be due to tubercular or syphilitic disease of the corpora quadrigemina, and the reason for Flii. (i. Pulvinar Corpus f anticum. quadri- < geminum ( posticum. Locus acrukus. Eminentla tere.- middle ceirbellar peduncle. Ala cinerea Accessoriiis nuclcu Conarium, or pineal gland. Bradduin conjunctivum anticum. Bvachium conjunctivum posliciim. Corpus genicidatum mediate. Pcduncidus cerebri. ad corpiira qiindri- 1 01 niiixi. or ^uiii riiir II rrhiUar CrilS lirihiiirlr. > rere- ad iiiiiliil/oiii nhloH- belli. iiotaiii. or iiifrrior \ ccrdi'Jlar peduncle. J nb, .1 Clava Funiculus cuiieulu {I'urt of re.'ftij'orm body) Funiculus gi acdis i I'os'lfrior 1/1/ ram id Medulla oblongata with the corpora quadrigemina. The numbers IV-XII indicate the superficial origin of the cranial nerves, while those (3-12) indicate their deep origin— j. e., the position of their central nuclei ; 3 shows the deep origin of the oculo-motor nerve of one side. this will be clear when the deep origin of the oculo-motor nerves from their nuclei is renieml^ered. (Fig. 6.) Sometimes there will be associated with the ptosis internal squint due to paralysis of the abdiicens nerve (sixth), which arises from the nearby nucleus, and is connected with that of the oeulo-motor (Fig. 7). (See also chapter on the Eye.) If the condition is due to a serious congenital fault, we usually THE FACE AX I) HEAD. 41 find associated with it failure to elevate the eyeballs, and the failure is probably due to a unclear defect. If due to gelseraium or conium^ the symptoms of poisoning by those drugs will be present. Fig. Cochlea Semicircnlar Canals Diagram of the connections of the nucleus of the sixth nerve. (Bruce.) Ptosis, with hemiplegia of face and limbs on the opposite side of the body, associated it may be with hemianesthesia, is due to a lesion in the crus cerebri, provided the two sets of paraly.ses occur simul- taneously, otherwise they may be due to two separate lesions. (Hughlings Jackson.) A very rare condition, of which there are but twenty-seven cases on record according to Darquier, is recurrent paralysis of the oculo- motor nerve on one side. The attack begins with violent pain on one side of the head, nausea, and vomiting, and these symptoms are followed by ptosis, external strabismus, mydriasis, paralysis of ac- commodation, and cros.scd «li[)l<)pia. It is seen most ficcpicntly in women, but may date from as early a period of life as eleven months. The attacks may last for a few weeks, and tu'cur often or only after a lapse of many years. Bilateral Facial Paralysis is a rare condition, and when it vK'curs can only be due to a l)ilateral lesion in the cerebrum, to acute bulbar 42 THE MANIFESTATION OF DISEASE IN ORGANS. paralysis, to progressive bulbar paralysis, to a lesion in the pons just where the facial fibres decussate, to bilateral disease of the pons owing to disease of the basilar artery, syphilis at the base of the brain producing a tumor or inflammatory thickening, very rarely to bilateral inflammation of the mastoid foramina, resulting from cold or double otitis, from toxic multiple neuritis, but not from that toxic neuritis due to alcohol. Very rarely bilateral facial paralysis results from multiple neuritis in its diphtheritic form. The development of bilateral facial paralysis due to a double cere- bral cortical lesion never occurs without evidences of paralysis else- where in the body, such as monoplegia or hemiplegia. The bilateral paralysis of the facial nerve in acute bulbar paral- ysis is characterized by its limitation, as a rule, to the neighborhood of the lips, by dysphagia, lingual paralysis, affected speech, paral- ysis of the ocular muscles, and a rapid pulse. This disease is very rare and depends for its existence upon an acute inflammation or myelitis of the medulla oblongata. When due to progressive bulbar paralysis (glosso-labio-pharyngeal paralysis) the paralysis is confined chiefly to the lips, and is asso- ciated with alterations in the tongue (see chapter on the Tongue) and speech, with tremor of the tongue and stiffness of the lips. The mouth stands half-open, the lower lip is pendulous, and the patient's expression is tiiat of a person about to burst into tears. The symp- toms of glosso-labio-pharyngeal paralysis may, however, be exactly reproduced by diphtheritic paralysis, with this difference in prog- nosis: the first die and the second class get well. In making a diagnosis of bulbar paralysis it should be remem- bered that another condition exists in rare instances in which no definite pathological changes can be found in the nuclei in the medulla oblongata, and yet many of the symptoms manifested by the patient are identical with those of glosso-labio-pharyngeal paral- ysis (true bulbar paralysis). This condition has been called " asthenic bulbar paralysis," and in it we find, as early symptoms, that the muscles of swallowing and of speech become easily tired on exertion, showing failure of the nuclei of the fifth nerve; that de- fects in articulation and speech are developed, indicating disorder of the nuclei of the ninth and tenth nerves; and clumsy movements of the tongue are present, which are a sign that the nuclei of the hypo- glossal and twelfth pair are involved. These symptoms are j^racti- cally identical with those of true bulbar paralysis. What are the THE FACE AXD HEAD. 43 symptoms which bv their presence in the true disease and their al> sence in asthenic bulbar paralysis aid us in separating the two affec- tions ? The answer to this question is that the drooling of saliva, the atrophy of the tongue, lips, and extremities, the filirillary twitch- ing of the affected muscles, and the loss of electrical irritability in these muscles, all of which symptoms belong to true degenerative bulbar paralysis, are not to be found in the asthenic form. There is, however, in the latter disease a condition rarely f()wdered ehalU, The joint-surfaces them- 62 THE MANIFESTATION OF DISEASE IN ORGANS. selves are not primarily much altered, but secondarily grave changes occur in them. (Figs. 9 and 10.) Fig. 10. Same patient's hands as in Fig. 9. showing the appearance and explaining to some extent the supra-position of the bones, but from this picture alone one would hardly expect such serious bone lesions. Very commonly in gout the only joints of the hand which are in- volved are the first joints of the fingers, a knob developing on either Fig. 11. m Heherden's gouty nodes. Illustrating com- mon forms of terminal phalangeal deflection. Forefinger and little finger of a woman aged seventy years. "Crab's-eye" cysts over the joints are also depicted. (Duckworth.) Nodular swellings (Heherden's nodes) due to gouty arthritis on the forefinger and little linger of a woman aged fifty years. (Duck- WOETH.) side of the knuckle. (Fig. 11.) The little finger in gout is often bent at an acute angle at the middle knuckle so that it is held in an THE HAND AXI) ABM. 53 awkward hooked position. (Fig. 12.) This is most commonly sepn in women, while in men it is common to see forced flexion of the first phalanx of the middle finger into the palm of the hand even when very little if any deposit of urates has taken place. This drawing Fig. 12. Tophaceous gout ot right hand. Deflection of digits to ulnar aspect. On the wrist a scar of a large chalky deposit which had been treated by incision. (Duckworth.) down of the fingers is considered by Paget to be pathognomonic of gout, although the patient will claim that it is due to the use of a cane, a hammer, or other exlranet)us cause. (Fig. 13.) While the history of the patient, the localization of the manifestations of the disease, and its character render a differential diagnosis between tlie hand of gout and that of arthritis deformans a possibility, it should not be forgotten that the deformities of gout may take every position assumed by those of arthritis deformans. In arthritis deformans the distortion of the hand may be far more marked than in ^oiit, lor here there is not a sj)]int-like deposit about the joint, but in its stead (lie development of exostoses on the etlges of the articular surliu-es, which at t)iice lock and di.^joint the fingers, while at the same time the ojiposite side of the joint may l)e [)artially absorbed, so that dislocation is readily produced. As a result tliore is 54 THE MANIFESTATION OF DISEASE IN ORGANS. sometimes developed what is called the " seal-fin hand" (also seen in cases of gout), a hand in which the digits are deflected chiefly Fig. 13. Tophaceous gout of hands, illustrating deflection and torsion of digits and phalanges. The figure to left shows the " seal-fln " type. (Duckworth.) toward the ulna, through the action of the extensor muscles, which are supplied with nerves which are reflexly irritated by the condition of the joints, and thereby cause spasm (Charcot). (Fig. 14.) Chronic rheumatism may produce gradual changes in the shape of the hand chiefly through disuse, and the alterations which it causes in the capsules and ligaments. The chief alteration is immobility or stiffness. Some persons believe that when the hand wastes it does so not from disuse, but through reflex nervous influences. It rarely, if evei', occurs in the hands alone, but when it does the joints are often swollen and somewhat tender, but never hard as in gout. Distortion of the hand with drawing of the finger or fingers into the palm may be due to Diipuytren's contraction, which results from burns or other injury to the palmar fascia. The finger-joints are not commonly involved in acute articular rheumatism, certainly very rarely as the only manifestation of the disease. The inflammatory process is more apt to be about the ball of the thumb, or in the wrist and carpal joints. The hand is seen under these circumstances as a clumsy, swollen mass, puff^y, and ex- quisitely tender and hot. Sometimes it is quite red at the joints, THE HAXD A XI) ARJL &0 but often pallid, particularly in the'puffy, oedematons area on the back of the hand. The presence of intense local inflammation, the Fig. 14. |:K x\ A Riintgen ray picture slinuiiii,' ihu cuniUtidu ui tlic b.inesof the hand in a case of chronic rheumatoid arthritis. It will be seen that ihe peculiar outlines of the proximal phalanges are due to their positions— as lesions we may note anchylosis of the metacarpal of the middle and ring tjngers with the os magir.im and unciform deposits in the heads of the phalanges and dislocations. (From the Medical Chronicle, April, 1896.) Iiistory of sudden onset, and the intense pain on movement readily separate rheumatism from gout and arthritis deformans, and leave it to be separated from sprain, septic arthritis, and deei)-seated inflam- mation of the hand pro|)er. The first is excluded by the history, the second by the hi.story and general lack of evidence of gonorrhoja or sepsis or |)iirpiira, aud the third by the lack of accompanying general systemic disturljance and the aliscnce of a history of trau- matism or iulcction. The nervous disturhauccs which change tiie appearance of the hands are very numerous. Angioneurotic oedema is not peculiar to the haiul, although fre- 56 THE MANIFESTATION OF DISEASE IN ORGANS. quently involving this part of the body. It consists of a swelling varying in size from a dime to asilver dollar, which is not oedematous in the sense that it can be pitted on pressure. This swelling, which may be multiple, red in color, or pale and waxy in appearance, lasts but a few hours or days, disappears, and often speedily returns. Somewhat allied to angioneurotic oedema is that condition of the hand (or toes) characterized by a white and waxy or slate color of the fingers, associated with coldness, swelling and mottling of the skin, termed " Eaynaud's disease." Often this is a passing condition, but in its severe forms there is finally developed dry gangrene of the fingers involved. The conditions of the hand resembling it, from which it must be separated, are senile gangrene, in which the advanced age of the patient and the presence of diseased and thickened bloodvessels will enable us to decide on the latter as the cause; frost-bite, in which the history of exposure will be of value, although exposure to cold often precipitates an attack of Raynaud's disease; ergotism, which can be discovered by the history of the patient having taken food for a long time which may have contained bad rye; leprosy, which will probably be seen more marked in otlier parts, and in the patches of which can be found the leprous bacillus ; and alcoholic neuritis, of which we shall speak later (see chapter on the Skin). In that state known as Morvan's disease or " pain-ansesthesia with whitlow," there is a slowly progressive loss of power in the hand with atrophy and ulcers about the bases of the nails. Sometimes the terminal pha- langes undergo necrosis, and enlargement of the fingers, through swelling, may be very marked. It is probable that this condition represents two separate lesions, namely, neuritis and syringomyelia, and it is an exceedingly rare disease. In addition to these trophic changes in the hand we have the so- called " spade-like " hand seen in myxoederaa, acromegaly, and the pulmonary osteo-arthropathy of Marie. In rayxoedema the de- formity depends upon the alterations in the subcutaneous tissues? rather than on changes in the bones, so that the hand is swollen or boggy-looking, but does not pit on pressure as in true oedema. In acromegaly the enlargement is chiefly osseous, as it is also in pul- monary osteo-arthropathy, the formation being on a gigantic scale. In the latter disease, however, the hands and feet are alone affected, and the enlargement is not symmetrical. Further, this condition is nearly always associated with changes in the lungs, such as emphy- sema, tumors, and old bronchial troubles. The hands are not only THE HAND AND ARM. 57 greatly enlarged, but deformed, so that a side-view of the finger-tips reminds one of the shape of a parrot's beak, the nail being turned over the end of the fiuger. This is even more marked in the thumb. Alterations in the contour of the hand are, however, far more frequently produced by atrophic processes than by those which re- sult in hypertrophy. They arise in cases of paralysis not only from wasting of the muscular tissues, so that hollows or sunken places occur, but also from the distortions caused by the contractions of healthy muscles, which, having no opposition as in health, speedily draw the bones of the hand into abnormal positions. In other cases the diseased muscular fibres may be spasmodically contracted, over- coming the resistance of the healthy muscles. The wasting of the hand seen in old age, particularly in women, and in advanced phthisis, diabetes mellitus, and other gonditions in which the tissues of the body in general lose their plumpness, is so universally distributed that a diagnosis of wasting from old age is not difficult. On the other hand, the wasting due to nervous lesions is generally not universal, but limited to single muscles or groups of muscles, the remaining portion of the hand having its normal appearance, or being only indirectly influenced. Fig. 15. Claw-liiiml. ((_;itAV.) Under the name of ^' claw-hand," or " main-en-grlffe,^'' wc find a deformity of the hand which is in itself very characteristic, although indicative of .several causes which all operate in an identical maimer. The back of the iiand loses its normal convexity and becomes some- what concave, the tendons on the extensor surface stand out in ridges, the proximal phalanges are drawn backward toward the wrist, while the second and third phalanges are dmwu toward the 58 THE MANIFESTATION OF DISEASE IN ORGANS. palm of the hand (Fig. 15). Sometimes, however, the tips of the lingers are drawn toward the back of the hand. This deformity results from atrophy and paralyses of the interossei muscles and lumbricales, which are supplied by the median and ulnar nerves. The extensor communis digitorum and flexor digitorum produce a dorsal flexion of the first phalanges and a complete palmar flexion of the second and third phalanges. A certain amount of immobility is also caused by the fact that flexion of the hand is impossible in the fingers and almost lost at the wrist. The claw-hand having been recognized, it remains to be decided what are its causes. It may be due to disease of the peripheral nerves (the ulnar and median), of the cells in the spinal cord, and of the cells in cerebral cortex in the hand-area. Taking up for consideration paralysis of the median and ulnar nerve as a cause of claw-hand, we find that the most common cause is a neuritis produced by some mechanical injury resulting from an accident, or from the following of some occupation in which, for ex- ample, the artisan presses his elbow constantly on some hard surface. The deformity may be, therefore, either unilateral or bilateral (gen- erally the former), and there will be evidences of local injury, or a history which will indicate that the lesion is peripheral. Further than this, there will nearly always be found, in ulnar and median injury, sensory as well as motor paralysis; and Hirt asserts the re- markable fact that the claw-hand may develop in cases in which sen- sory disturbances are the only evidence of median and ulnar diffi- culty; in other words, before motility is lost through paralysis. (See chapter on the Skin, Anaesthesia of the Skin.) Toxic neuritis very rarely, if ever, causes claw-hand, as the musculo-spiral nerve is more commonly aflected in these cases and the extensors become paralyzed. There are several spinal causes of claw-hand, the most impor- tant of them being progressive muscular atrophy, that disease in which there are atrophy and abnormal change in the anterior horns of the gray matter of the spinal cord, particularly in the cervical region. (Fig. 16.) It will be remembered, too, that the anterior nerve-roots and motor nerves become involved in this process. As a result of these changes, we have developed loss of power in the hand and arm followed by the development of a claw-hand from wasting of the same muscles, as already described, the disease-pro- cess being generally bilateral, but affecting the right hand and arm more than the left as a rule. As progressive muscular atrophy often THE HAXD AND ARM. 59 makes its first manifestation in these muscles, tlie liand affords much diagnostic information in suspected cases, and if tlie patient -with Fig. 16. Areas of spinal cord involved in progressive muscular atrophy. The areas involved are the anterior horns of the gray matter chiefly (shading heavy) and the anterior lateral tracts and anterior root zones (shading light). Fig. 17. Fig. IS. Progressive muscular atrophy. Ape-hand. Progressive muscular atrophy. Sunken in EicHHORST.) interosseal spaces on the back of the band. (ElCHIIOILseudo-palsy, has been described |)articularly by Parrot. A child ai)p:ireiitly ])er- fectly well, and but a few weeks old, suddenly loses the power of its arm, so that the member hangs like a Hail. No wasting takes place, 76 THE MANIFESTATION OF DISEASE IN ORGANS. no degenerative reactions occur, there may be some pain, and crepi- tation on moving the arm. The cause of these symptoms lies in the fact that there has been a separation of the epiphyses from the shafts of the boues with consequent helplessness. Sometimes geueral par- alysis of the extremities arises from the extension of the disease to other limbs. The prognosis as to life is bad. It yet remains for us to discuss the paralysis of several important groups of the muscles of the arm. If the forearm cannot be flexed, there is loss of power in the biceps aud brachialis anticus, and to some extent in the supinator longus; and as the first two muscles are supplied by the musculo-cutaneous and the third by the musculo- spiral, such a failure iu flexion shows paralysis of these fibres. Paralysis of the extensors of the forearm, wrist, and hand, and of extension of the elbow with wrist-drop in consequence, and flexion of the tips of the fingers is due to disease affecting the inusculo- spiral nerve, but the fingers can still be partly extended through the action of the interossei and lumbricales, provided the tips are flexed. The back of the hand and wrist become unduly prominent after a short time because of the forced flexion of the hand and rapid wast- ing of the extensors. In most cases the supinator longus, which supinates the forearm after it is pronated, is paralyzed. When the ability to pronate the forearm is greatly impaired, and the thumb is extended and abducted, so that it cannot be brought in contact with the tips of the fingers, the trouble is probably paralysis of the median nerve, and this is confirmed if all the phalanges are paral- yzed except the first. If the arm cannot be moved outward, away from the body, there is paralysis of the deltoid supplied by the circumflex nerve. In this connection attention should be called to the loss of power with wasting of the muscles seen after direct blows on the muscle or after injuries to the joint, sometimes called '^ joint-palsies." Brachial Paraesthesia. Disturbances of sensation in the hand and arm consist in anaesthesia, analgesia and numbness, tingling, aud pain. The area of these sensations depends upon the nerve-trunks involved, and to some extent upon the degree of involvement. Thus, if the function of the nerve is merely impaired, the sensation may be that of tingling or pain; if still further impaired, the sensation may be that of numbness; and if the sensory fibres be totally destroyed or paralyzed, absolute ansesthesia and analgesia may be present (see chapter on Skin Ansesthesia). CHAPTER III. THE FEET AXD LEGS. The general appearance of tlie feet and legs when clothed — The gait — Spastic para- plegia — Paraplegia without spastic contraction — Crural monoplegia — Deformities of the feet — The joints — Alterations in the nutrition of the feet and legs aside from a change in the muscles. As the physician sees a patient approaching him, he can often gain information as to tiie aihiieut from which the mai). is suffering by noticing his gait and tlie appearance of the legs and leet, for, while the gait varies greatly in normal individuals, in some diseases it is so typical that he who runs may read the diagnosis. A glance at the feet revealing one foot more loosely covered than the other, or a slit in the shoe, or a very loose lacing, will point to the presence of some inflammatory or dropsical swelling, which forces the patient to give it room; and if the legs of a man of ordinary build look swollen and fill the trowsers tightly, while a glance at his face reveals that it is puffy, rather thau one which is obese, dropsy, still more widespread, is probably the cause. Gait. Aside from local injuries causing a lame gait, which will be found discussed in a book on surgical diagnosis by the writer's friend, Dr. Martin, we find that gout, rheumatism, and sciatica are the common causes of a limping gait, arising from trouble in one leg, and that in such cases there is a pained expression of the face at each movement, which shows the suffering that walking causes. The gait of such a patient is slow and cautious, and he is apt to rest every few steps, bearing his weight at such times chiefly on the well leg or, by means of his hands, upon chairs or tables that may be near. Aside from the alterations of gait produced by these causes, we see very typical gaits produced l)y locomotor ataxia, pseudo-locomotor ataxia (peripheral neuritis) due to alcoholic or lead-poisoning, syphilis, or peripheral neuritis arising from other causes, Friedreich's ataxia, general paresis, chronic myelitis, lateral sclerosis, acute poliomyelitis, pseudo-nuiscular hy{)ertrophy, cerebral infantile palsy, multiple sclerosis, paralysis agitans, cerebellar disease, 78 THE MANIFESTATION OF DISEASE IN ORGANS. organic and hysterical hemiplegia, and osteomalacia, and the gaits caused by rickets or other bony defects. In locomotor ataxia the gait is unsteady and waveringly uncertain, resembling that of a blindfolded person who is told that he is ap- proaching some inequality in the floor. The patient continually seems to be feeling for the ground with his feet, and carefully picks his way along a perfectly smooth surface in a labored fashion, using a cane to help him both in the way of support and of feeling the ground. If he looks up from the ground while walking, he sways suddenly and may fall, and if prevented from returning his eyes to the pavement almost surely falls if no aid is given him. (Fig. 26.) Fig. 26. r*. Gait in a dase of locomotor ataxia. From instantaneous .serial photographs of a patient of Dr. Dercum, made simultaneously from two different points of view by Muybridge. The gait of pseudo-tabes is sometimes identical with that just described, is usually associated with a history of alcoholic excess, and is due to multiple neuritis. In a majority of the cases, however, it is distinctive, and has been called the " steppage " gait. The foot is thrown forward and the toe is raised so that the heel first strikes the ground in much the manner adopted when one attempts to step over some obstacle. Sometimes this gait is found in cases of arsenical neu- ritis and that due to lead, but in alcoholic tabes there are generally THE FEET AND LEGS. 79 mental symptoms associated with this gait, while in lead-poisoning the pathognomonic signs of this condition, such as the blue line on the gums and -wrist-drop, when combined with the history, clear up the diagnosis. It must not be forgotten, however, that the diiferential diagnosis of tabes from pseudo-tabes is sometimes very difficult, and as Dana has well said : ''When D^jerine described as locomotor ataxia a case which now appears to have been one of alco- holic peripheral neurotabes, when Buzzard has diagnosticated as true spinal tabes a case of post-diphtheritic ataxia, when Seligmueller mistakes a case of wall-paper-poisoning for one of true spinal tabes, we may easily suppose that errors have been made by many others." The important symptoms which point to true locomotor ataxia are the swaying of the body when the eyes are closed (Romberg's symp- tom), the loss of knee-jerk (Westphal's sign), the history of gastric, laryngeal, or vesical crises, the presence of numbness in the feet, the slow onset of the disease, and the absence of any history of exposure to the causes of neuritis just named. If all these signs are present, and are combined with that most important symptom, the Argyll- Robertson pupil, the diagnosis is practically certain. The following table from Peterson's article in Dercum's Nervous Diseases shows very clearly and comparatively the symptoms of the first, second, and third stages of true locomotor ataxia. Initial Period. Second Stage. Final Stage. Inco-ordination,but no change of gait. Numbness of the feet. Shooting-pains in the legs. Diminished or lost knee-jerks, one or both. Sluggish or lost pupillary reflex to light. I Weakness of sexual function. Impotence. Greater inco-ordination, and marked ataxic gait. .More marked anaesthesias. Fains worse. Lost knee jerks. Lost pupillary reflex to light and myosis. Cannot walk because of ataxia. Extensive anaesthesia. P.ains less. Lost knee-jerks. Lost reflex to light, myosis, paralysis of acconimodation. Transient diplopia ; transient ptosis. Sluggish micturition. Optic atrophy. Trophic changes in the joints. Hemiatrophy of tongue. Ocular paLsies rare, or marked ophthalmoplegia. Impotence. Ophthalmoplegia. Increased vesical weakn&ss. Catheterization needed. Optic atrophy rarely develops. Blindness. Trophic changes not so com- mon. More marked if they Ijcgan in early stage. Deafness. Increased. I>aryngeal and visceral crises. Not so common. Girdle sensation. Unnoticed. 80 THE MANIFESTATION OF DISEASE IN ORGANS. In neuritis causing pseudo-tabes we have a history of rapid onset of the symptoms, paralysis and wasting of the muscles, and an absence of vesical symptoms and the Argyll-Rohertson pupils. Reflex action is decreased and the gait alteied in locomotor ataxia, because, though the inotor tracts are open, the sensory tracts in the nerves, the posterior nerve-roots, and the posterior columns of the cord are diseased. For these reasons the reflex arc is destroyed and the co-ordination of the muscles lost. The patient cannot tell how to use his muscles unless he can see them and co-ordinate them by the aid of the eye. The sensations of formication or numbness are also due to those sensory lesions. (Fig. 27.) (For description of motor and sensory tracts of the spinal cord, see early part of chapter on Hemiplegia, and chapter on the Skin.) Fig. 27. Cut showiug the areas of the cord involved in locomotor ataxia. The shading includes both the column of Goll, the inner, and that of Burdach, the outer. It is to be remembered that the lesions of locomotor ataxia are found in the peripheral nerves as well. Sometimes not only the gait, but the entire set of the ordinary symptoms of locomotor ataxia are aped by hysteria so closely that a diagnosis may be almost impossible, but the Argyll-Robertson pupil, the lost knee-jerks, and the optic atrophy will not be present if hysteria be the cause of the symptoms. On the other hand, Romberg's symptom may be marked to an extraordinary degree. The patient who is hysterical, in falling nearly always falls the same THE FEET AXD LEGS. 81 way, keeping her frame stiff like a board. (See chapter on Eye for differential ocular symptoms.) In Friedreich's ataxia the gait is peculiar. The legs are widely separated and moved in an uncertain, hesitating manner, and if the feet are placed close together and the patient told to stand still sway- ing at once develops. If the eyes be closed, the swaying may greatly increase, and the movements of the arms are inco-ordinated. These symptoms, which to a certain extent simulate true locomotor ataxia, are associated, as a rule, with others which separate the two affec- tions, for in this disease the symptoms often come on in very early life, there is sometimes nystagmus, usually a history of heredity, there is a slow and jerky articulation, scoliosis, talipes equino-varus, but there is no Argyll-Robertson pupil. (Fig. 28.) Fig. 28. 4 4 Cut showing the spinal areas chiefly involved In Friedreich's ataxia. The areas are the column of Burdach (1) ; the lateral pyramidal tracts (2) ; the columns of GoU (3) ; the posterior nerve-roots (4). Friedreich's ataxia mu.'^t l)o separated from another rare disease in which the gait is ataxic and the disease hereditary, namely, hereditary cerebellar ataxia, in which we have the following symp- toms not seen in Fricdrcicirs di.scn.sc, namely, nornuil or exaggerated kncc-jcrks, Argyll-lvobertson pupils, and a beginning of the malady after twenty year.? of age. The following table compiled by Collins, of New York, gives the differential points between these diseases: 6 82 THE MANIFESTATION OF DISEASE IN ORGANS. Hereditary Spinal Ataxia. Friedreich's disease. 1. Gradual impairment of co-ordination, first in legs, afterward in arms. Later in the disease the patient may reel as if under the influence of alcohol. A quick backward and forward balancing movement. 2. Station : Closure of eyes, as a rule, in- creases the unsteadiness ; this may be absent. 3. Titubation of upper extremities very un- common. Irregularity in voluntary move- ments of arms and fingers. 4. Frequently jerky, irregular movements of head and neck. Sometimes like an irregular tremor. •5. Mimetic muscles do not show ordinarily overcontraction. 6. Ataxia is not so great when the patient is lying. 7. Afiection of speech may be absent ; when it does occur is a late symptom, and consists of an eliding of syllables and an occasional hesitation. ! >*. Nystagmus is a very common symptom, but it may be lacking. 9. Myotatic irritability is lost. Knee-jerks maybe present in the beginning of the disease, but they soon disappear. Ankle-clonus is never present. 10. Mentally, normal. Very rarely any de- fect. 11. Deformities of the extremities such as pied boi and spinal curvature, very common. Hereditary Cerebellar Ataxia. 1. Gait : Uncertain, reeling ; gait of one in- ebriated. Patient frequently walks with body bent forward and head thrown backward, and the feet wide apart. Does not have to watch the feet. 2. Station : Romberg symptoms absent. 3. Titubation and inco-ordination and loss of dexterity in the upper extremities. Chorei- form movements exaggerated on voluntary effort; "intentional." 4. Not infrequently oscillations or jerky movements of the head, less often of the trunk. 5. Exaggerated contraction of the mimetic muscles on speaking. 6 Ataxia is very much less, or disappears when the patient is lying down, but the inco- ordination persists. 7. Speech : Hesitating, abrupt, explosive, ataxic, defective. S. Eyes : Twitching of the eyeballs very common, but not nystagmus. Optic atrophy, progressive choroiditis, paralysis or paresis of the external recti sometimes. 9. Myotatic irritability increased ; reflexes exaggerated, such as knee-jerks ; often ankle- clonus. 10. Mental shortcomings varying from slight psychical disturbances up to a considerable degree of dementia. 11. Deformities of the extremities and spine, such as pied bof or scoliosis, do not occur or are most rare. The feebleness of the limbs, the reflex iridoplegia (Argyll-Robert- sou pupil), aud the ataxic gait sometimes seen as the chief manifes- tations of general paresis may cause an error in diagnosis in favor of locomotor ataxia, but careful examination will reveal mental feebleness in the paretic case or at least evidences of delusions, and if the disease is at all advanced there will be a history of the patient having had convulsions or apoplectiform attacks. Sometimes there will be found present in paretic dementia increased knee-jerks and many of the symptoms of ataxic paraplegia, but the associated mental failure and fine intention-tremor of the hands decide the diagnosis in favor of paretic dementia. In chronic myelitis in the early stages, while motion is still pre- served the gait is typically that of feebleness, and the legs respond slowly to the cerebral desires, being dragged along after the patient, THE FEET AXI) LEGS. 83 ■\vho leaDS forward, supporting some of his weight on crutches or canes. If the lesions of the disease involve the lateral pyramidal tracts to a considerable extent, the gait is somewhat spastic, while if the sensory fibres are much involved it may be like that of ataxia. Under these circumstances the attitude and gait of a patient are some- times a combination of those of lateral spinal sclerosis (spastic para- plegia) and locomotor ataxia. In some instances the spastic symp- toms are more marked, in others the signs of locomotor ataxia are more prominent. This condition is called ataxic paraplegia, and in it we find the exaggerated knee-jerks of lateral sclerosis associated with the swaying of the body (Romberg's symptom) of ataxia. Ankle-cloous is also present. The crises of locomotor ataxia do not occur, and the Argyll-Robertson pupil is usually not present. (Fig. 29.) Fig. 29. Cut showing area.s of 87>inal cord involved in ataxic paraplegia, which is practically a com- bination of locomotor ataxia and lateral sclerosis. 1. Lateral or crossed pyramidal tracts. 2. Posterior columns of (joll and Burdach. 3. Direct pyramidal tracts or Tiirck's columns. In lateral sclerosis the gait is typically spastic, the legs being rigid from the hip-joint down, and the toe being dragged in a semicircle from behind forward. When the gait of a young child is stumbling, or the leg or legs arc dragged after it, or the ankles bend so that locomotion is impos- sible, the probable diagnosis is that the cause is acute poliomyelitis (see Paralysis of Log). In pseudo-muscular hypertrophy there is a peculiar waddling gait, 84 THE MANIFESTATION OF DISEASE IN ORGANS. a tendency to stumble, the body is usually bent backward, and there is difficulty in getting up from the floor and on going up and down stairs. The patient in all his movements shows a marked loss of Power in the legs with a great ap- parent increase in the size of the muscles in the legs. (Fig. 30.) The gait of pseudo-muscular hy- pertrophy is sometimes closely re- produced in children suffering from severe rickets, and the other fea- tures of the case which may mis- lead the physician are that the child, if fat, will have bulging legs, as if the muscles were hypertrophied, and lordosis due to spinal weakness. In the rickety case, however, the knee- jerk is preserved, and in the pseudo- muscular hypertrophy it is lost. The gait of a child suffering from infantile cerebral paralysis is quite characteristic. In the first place, it is spastic, and the patient walks on the toes or in some cases club- foot develops. The heels are everted and the toes turned inward, the knees being so closely approximated that the clothes may become worn between them from the rubbing. So great is the extension of the legs that the toes are very apt to drag, and, finally, the adduction spasm may be so great that the legs overlap each other as walking is attempted. (Fig. 31.) The gait in multiple sclerosis is often markedly spastic and paretic — that is, stiff atid feeble, and may in the early stages of the disease closely reseml)le that of spastic paraplegia due to lateral sclerosis. When the patient attempts to pick up a small object with his fingers- Typical pseudo-muscular hypertrophy. (Dekcum.) THE FEET AXD LEGS. 85 there are tremor and oscillation of the hand. There are also scan- ning speech and nystagmus. In paralysis agitaus the patient's gait is hurried because, from the bent-over position of his body, his centre of gravity is too far for- ward and he runs to keep up with it. This is called festination. The gait is also somewhat trotting or toddling. (Fig. 32.) (See chapter on Hand and Arm, part on Tremor.) Fig. 31. Fig. 32. '^ Spastic i>araplegia; crossed-legged pro- gression. (From a palient of Dercum's in the Jeflcrson Medical College Hospital.) Side view of a case of iiaralysis agitans show- ing lorward inclination of trunk. Tendency to propulsion. (Uerccm.) In cerebellar disease the gait may closely resemble that of a drunken man, and the })atient has the greatest difficulty in keeping from sheer- ing off to one side as ho walks, swaying, too, from side to side (oerc- bollar titubation). The middle lobe of the cerebellum is usually affected; but Nothnagel as.serts that, if these symptoms are associated 86 THE MASIFESTATION OF DISEASE IN ORGANS. with paralysis of the oculomotor nerves and other symptoms of brain-tumor, there is a growth in the corpora quadrigemina. In hemiplegia the gait is peculiar in the dragging along of the paralyzed limb by a peculiar outward swing, which soon wears away the sole of the shoe on the inuer side near the ball of the foot. It is sometimes called a mowing gait, because the leg sweeps around in a half-circle. Very often the shoulder opposite the paralyzed side is raised in order to tilt the pelvis on the paralyzed side, so as to make circumduction easy. This gait is to be clearly separated from that due to hysterical paralysis, for in this condition the leg is dragged after the body without this outward swing. It is dragged along like the broken hind limb of one of the lower animals or is shoved forward, and the well foot drawn after it, the reverse of what hap- pens in orgauic paralysis. The footsteps of the hysterical paraplegic are, moreover, apt to be careful and mincing. Further, the loss of power is usually left-sided, and associated with characteristic hyster- ical anaesthesia (see chapter on Skin), and often with areas of hyper- sesthesia. Again, in the gait of hysterical paralysis the patient is apt to be excessively laborious in her progress, and will exhaust her muscles in her strained movements. An altered gait due to irregularly distributed paralysis of groups of muscles is nearly always hysterical, and sometimes the patient who has hysterical loss of power will suddenly fall through giving away of her knees. A condition of the gait and station of the patient varying from normal, which occurs most commonly in hysteria, consists in an in- ability to co-ordinate the movements of the muscles of locomotion or those used in staudino;. This is called ^' astasia-abasia." It is in reality a form of ataxia often developing only when the patient attempts to walk. There is no loss of power in the legs, but an in- ability to use them regularly or with power while walking, although if the patient be made to lie down the movements of the limbs as made in walking can be performed perfectly. The knee-jerks are rarely lost, and in addition the general symptoms of hysteria can nearly always be found. The body often reels to and fro, and occa- sionally the muscles seem to be somewhat spastic. The symptom generally follows some severe shock, and is most commonly seen in young persons, usually female children. In osteomalacia there is increasing difficulty of walking, partly due to pain and partly to muscular weakness. The gait is hobbling, THE FEET AND LEGS. 87 totteriug, and is made up of short and evidently painful steps, '' the pelvis and leg being jerked forward as if in one piece." The kyphotic deformity of the spine, muscular tenderness, and lateral compression of the chest and pelvis, with distortions of the limbs, aid in making the diagnosis. Fir;. 33. Allison's case of osteomalacia. {Edinburgh Medical Journal. The gait of rickets is only peculiar wiicn curvature of the limbs or spine destroys the normal posture of the body or interferes with the movements of the limbs, but it is nearly always more or less waddling. Closely associated with alterations in power in the legs, producing 88 THE MANIFESTATION OF DISEASE IN ORGANS. changes in the gait, we have loss of power or paralysis aifecting the muscles of the lower extremities: either on both sides, in which case we have a condition called paraplegia; of one lower limb, a condition called crural monoplegia; and of groups of muscles, resulting in localized palsies. These paralyses often produce deformities, as will be shown shortly. Paraplegia. Given a case of paraplegia, what may be its cause ? It may arise from a cerebral lesion, which is very rare, except in children, when it is common,^ and it must depend upon a lesion on both sides of the cerebral cortex or in each capsule; that is to say, there must be present a lesion in the leg-centres on both sides of the cortex or in the fibres going to the legs through the internal capsules. Much more commonly the lesions causing paraplegia are in the spinal cord, very rarely ths symptom is due to involvement of the nerve- trunks on both sides after they have left the cord, and sometimes it is caused by hysteria and reflex irritation. Fig. 34. Spastic diplegia, congenital , presenting choreiform and athetoid movements. (Dercum.) (Philadelphia Hospital.) Spastic Paeaplegia. The paraplegia of cerebral infantile par- alysis is spastic, and follows difficult labors or injuries to the child before or after birth. Contractures nearly always ensue, and exist chiefly in the adductors of the thighs, so that the attitude is very characteristic. (Fig. 34.) Epileptic convulsions very often com- plicate these cases. Often these paraplegias are not manifested for some months, or even longer, after birth. In many cases they are 1 Such an occurrence in adults is very rare, but it is quite common in young children, as many as 14 per cent, of the cases of infantile cerebral palsy being paraplegias. (Sachs.) THE FEET AND LEGS. 89 first noticed when the child attempts to walk. Cerebral spastic para- plegia in infants also sometimes comes on in cases of so-called ar- rested development. Such cases present no abnormality for the first few months of life, then cease to develop in mental brightness, fail to recognize the nurse or mother, cease to play, gradually lose their vision, and develop nystagmus. Death usually takes place in one or two years at the latest. Convulsions do not occur in this state, but tremors are often present in the arms. There is no history in such cases of difficult labor or premature delivery. In both this and the infantile cerebral form of spastic paraplegia the pyramidal tracts are degenerated. It is important to remember that cerebral para- plegia is not associated with the development of the reactions of degeneration in the paralyzed part, and is associated with compar- atively little Avasting, thereby differing from the deformities of the lower extremities resulting from poliomyelitis or acute infantile palsy. Care should be taken that the spastic paraplegia of rickets is not mistaken for a birth-palsy. A cerebro-spinal cause of spastic paraplegia in adults is multiple cerebro-spinal sclerosis, in which condition the loss of power amounts to a paresis rather than an absolute paralysis. The presence of in- tention-tremors, exaggerated knee-jerks and ankle-clonus, nystagmus, and vertiginous, epileptiform, or apoplectiform seizures, with staccato speech, and local areas of loss of power elsewhere, associated with spastic paraplegia, renders the diagnosis easy. The spinal lesions giving rise to paraplegia of the lower extrem- ities are numerous, and are perhaps best grouped in the following table of Bramwell: 1. Organic disease f Inflammation of cord Softening " Hemorrhage " " Tumors " " Meningitis " " Meningeal hemorrhage Injuries Tumors Carles of bone Tumors of bone Medullary. Meningeal. I Osseous. J 2. Functional Hysterical. Reflex. Maliirial and anxmic. Dt'iHindenl on idea. The natural se({uence is to pass on to a consideration of the forms of spastic spinal paraplegia, and to take up first of all its manifesta- tion in children. This occurs in what is known as hereditary spastic 90 THE MANIFESTATION OF DISEASE IN ORGANS. paralysis, which is to be separated from infantile cerebral paralysis l)y the absence of a history of injury to the head at birth, and the absence of convulsions and defective mental development, all of which appear in the cerebral form, and this absence of convulsions and defective mental power in this form of spastic paraplegia almost certainly sep- arates it from the cerebral infantile type of paralysis. It is to be separated from the spastic paraplegia of lateral sclerosis by the fact that it occurs in early life, and that there is a history of heredity, or of several members of the family being affected by the disease. There are usually rigidities and contractures, but the bladder and rectum escape the paralysis, and there are no trophic changes. The reflexes are increased. This disease is rare. Fig. 35. Cut showing shaded areas involved in lateral sclerosis, viz., the crossed pyramidal tracts. In transverse myelitis there is often in the later stages of the malady spastic paraplegia as a result of the irritability of the spinal centres below the seat of the lesion, and this may cause a spastic gait. In distinction from lateral sclerosis, we find in myelitis that there are a girdle pain, involvement of the bladder and rectum, and sensory paralysis. In the adult, when there is loss of power in the lower limbs with spastic contraction of the muscles when the patient attempts to move them, so that they become rigid, or if before the stage of rigidity develops the gait is spastic and stiff and the reflexes are greatly ex- aggerated, the disease is generally lateral spinal sclerosis. (Fig. 35.) THE FEET AXD LEGS. 91 There is also in lateral spinal sclerosis absence of both sensory dis- orders and rectal and bladder troubles, l)ut sometimes there is pres- ent excessively hasty urination. The reason why the reflexes are increased in lateral sclerosis, and similar ailments associated with spastic paraplegia, is that the inhibitory fibres which descend from Setsch en ow's reflex inhibitory centre in the medulla oblongata are de- stroyed in the lateral pyramidal tracts. In amyotrophic lateral sclerosis similar symptoms associated with wasting of the muscles are present in the later stages, but in the early stages the arms are chiefly affected by the wasting and paralysis. (Fig. 36.) (See chapter on Hand and Arm.) Fig. 30. Cut showing area of spinal cord involved in amyotrophic lateral sclerosis. 1. Crossed pyramidal tracts. 2. Anterior horns of gray matter containing the trophic cells. Spastic paraplegia may also be due to spinal pachymeningitis, and the associated symptoms may so closely resemble those of myelitis that a diagnosis is impossible, but the spastic character of the ])ara- j)legia, the early appearance and severity of the ])ain, and the com- paratively slow development of the symptoms in pachymeningitis, will aid in separating the two affections, as will also the presence of persistently increased reflexes from tlie first. Sensory disturbances, aside from pain, are common in myelitis, but rare in this condition. If the inflammatory process becomes widesj)read, there may be sen- sory disorders and troj)hic sloughs owing to invasion of the por- 92 THE MANIFESTATION OF DISEASE IN ORGANS. lions of the cord connected with sensation and nntrition by a secon- dary myelitis. The development of signs of spinal caries in snch cases at once shows the condition to be raeuino;eal in orio-in, and the history of traumatism will point to meningitis rather than myelitis. Spastic paraplegia, greatly increased tendon-reflexes, low muscle- tension, vesical disorder, and slight sensory disturbances should make the physician think of spinal syphilis. NoN- SPASTIC Paraplegia. Passing from spastic paraplegia we come to those forms of paraplegia lacking this peculiarity. They are quite numerous and important. If the paraplegia comes on suddenly, the cause may be hemorrhage into the substance of the cord or into the spinal membranes, or be due to compression or de- struction of the cord by injuries to the back, whereby there is lacer- ation of the soft parts or fracture or dislocation of the vertebrse. When the paraplegia is slower in onset the spinal causes are acute ascending paralysis or Landry's paralysis, acute central myelitis, and acute transverse myelitis. On the other hand, the slowly oncoming paraplegias are due to chronic myelitis, to locomotor ataxia, amyotro- phic lateral sclerosis, lateral sclerosis, poliomyelitis, neuritis, and pressure due to disease of the vertebrae or to spinal tumors. Finally, we have what are called reflex and hysterical paraplegias. Hemorrhage into the spinal cord is an exceedingly rare condition unless preceded by grave disease of its tissues. Indeed, the exist- ence of such a condition in man has been denied. The patient pre- viously in good health is stricken suddenly to the ground, and there may be almost as much cerebral disturbance as in cerebral apoplexy, but consciousness is generally preserved. The total amount of para- plegia may be instant, or not be complete for twenty-four hours. Bedsores speedily develop, and death ensues from exhaustion or from extension of the hemorrhage upward to the vital centres. Practi- cally identical symptoms ensue when the hemorrhage takes place between the membranes covering the cord. In both instances the reflexes are lost if the hemorrhage be sufficient to produce total par- alysis. If, on the other hand, after a prodromal period of short duration, during which there is some fever, the patient is suddenly attacked with paraplegia, the cause may be the acute ascending myelitis of Landry, and the rapid extension to the trunk, the arms, and the res- piratory muscles, with the consequent early death of the patient, will confirm the diagnosis. There is usually no involvement of sensa- THE FEET AXD LEGS. 93 tion or trophic paralysis, and the sphincters of the bladder and rectum escape the paralysis. Similar sym])toms associated with sensory di."-- turbances are probably due to a polyneuritis. Dillor and Meyer state that the cardinal points for the differential diagnosis should be: 1. Flaccid paralysis of the muscles, spreading rapidly from one point over the rest of the body, generally beginning in tue legs, but sometimes following the reverse order, as in the French zoologist Cuvier. 2. Absence of muscular atrophy and of electrical reaction of de- generation. 3. Tendon and superficial reflexes absent. 4. Sensibility not, or only slightly, impaired. 5. Sphincters, as a rule, intact (exceptions rather freq^ient). By far the most common cause of paraplegia is myelitis in one of its forms, but, whether the onset be rapid or slow, it must be remem- bered that the symptoms of myelitis depend, first, upon the level at which the spinal cord is involved, and, second, as to whether the lesion involves the white matter or the gray. If the lesion is an acute central myelitis of the gray matter, it usually produces many of the symptoms about to be detailed under acute transverse myelitis, but tlie onset is malig-nant and the areas involved are usuallv wide- spread. It is attended by fever of a marked type, though the tem- perature of the paralyzed parts is below normal, and by early evi- dences of trophic lesions. Multiple arthritis may come on. The bladder and rectum are paralyzed, and, finally, delirium may develop. The prognosis is unfavorable. Acute central myelitis is to be sepa- rated from Landry's paralysis by the facts that in it sensation is lost, there are rectal and vesical paralysis, fever, and rapid tropiiic changes. From polyneuritis it is separated by the facts that there are no great trophic changes in this form of neuritis, and the rectum and bladder are rarely paralyzed. The symptoms of acute transverse myelitis are capable of being divided into three groups, in the first of which the onset is as sud- den as is that of an apoplexy, in the second the symptoms come on quickly, and in the third more subacutely. In the acute forms, however, the history will be that after a period of numbness, heavi- ness, and weakness of the legs, with more or less pain in the back, the patient has found it impossil)le to move iiis legs, has lost control of his bladder and rectum, or suffers from retention of the urine and 94 THE MANIFESTATIOy OF DISEASE IN ORGANS. feces instead, aud at the same time has developed anaesthesia of his lower extremities, and the girdle sensation, or, if the lesion be situ- ated high up in the cord, tingling in his arms (see chapter on Skin). The reflexes may be abolished at first, and then return in an exag- gerated form in the segments of the cord below the area affected. In other cases the reflexes do not return if the lesion is completely trans- verse. The patient is speedily bed-ridden, and to these symptoms just detailed are soon added the development of bedsores and sloughs on dependent parts of the legs or on the buttocks, followed, it may be, by death from exhaustion, although the case may survive for months and even become somewhat better. If improvement takes place, sensation returns in the course of from one to six months, some motion in from six to eighteen months, and, finally, spasms and con- tractures mav result from descending degeneration of the lateral tracts. The following diagram from Taylor's Index of Medicine shows the effect of a lesion in the spinal cord in transverse myelitis. Symptoms in Transverse Myelitis. The darkened portion represents the seat of lesion. Spinal cord. Reflexes normal Reflexes normal. Band of hyperaesthesia . f Muscles palsied, waste, and Lose their electrical reactions I Sensation lost ... Muscles palsied .... Do not waste .... No loss of electrical reactions . Reflexes increased Sensation lost . . . Bedsores Temperature above rest of body Band of hypertesthesia. Muscles palsied, waste, and Lose their electrical reactions. Reflexes lost. Sensation lost. Muscles palsied. Do not waste. No loss of electrical reactions. Reflexes increased. Sensation lost. Bedsores. Temperature above rest of body. T . THE FEET AND LEGS. 95 In cases in which paraplegia results from the more subacute form of transverse myelitis the symptoms are usually not quite so rapid in their onset as in the type just named. The patient first notices that his bladder and rectum are unduly irritable, and in his limbs there may be subjective sensory disturbances (see Paresthesia in chapter on the Skin). The motor symptoms begin by a feeling of heaviness or inability to move quickly the lower limbs, so that the pa- tient feels tired on slight exertion. Soon these symptoms deepen into absolute anaesthesia and motor paralysis, and the girdle sensation on the trunk becomes well developed (see chapter on Skin). The bladder, which at first was irritable, may now be toneless, paralyzed, and retentive or incontinent. Retentive, if the lesion is above the lumbar cord; incontinent, when the lower part of the lumbar en- largement is diseased. The reflexes may at first be abolished, but very soon some of them return, only those reflexes the centres for which are destroyed by the transverse lesion being abolished; that is, the reflexes recover after the first shock of the attack, aud those muscles and tendons having spinal centres below the lesion have their reflexes increased because they are cut off from the inhibiting centres higher up in the cord or medulla. The muscles of the legs, which at the first shock of the onset of the malady were all flaccid and j)aralyzc'd, now divide themselves into two classes, those that are con- nected with the diseased part of the cord, which remains i)aralyzed, and those which are connected with the lower centres, which recover some power; but as the lesion is so placed as to cut them all otf from cerebral influences, voluntiiry motion is lost as completely as if all were deprived of spinal influence. The truly paralyzed muscles waste, but the others which have unimpaired spinal centres do not, except very slowly from disuse. On the contrary, they often be- come spastically contracted. Other trophic changes, such as bedsores and bullae, develop in the skin connected with the diseased focus, but not in that connected witli centres below the lesion. Anaesthesia is present because the lesion prevents the sensory impulse from reach- ing the brain (see chaj)ter on Skin). When the entire cord is not evenly involved in the transverse lesion certain groups of muscles partly escape. It is asserted that the extensors escape oftener than the flexors. The height of the jiaralysis also dejx'uds upon the situ- ation of the lesion in the cord, and if high enough to involve the cervical region, and yet not high enough to paralyze the diaphragm and cause death (third or fourth cervical), there may be contraction 96 THE MANIFESTATION OF DISEASE IN ORGANS. of the pupil by involvement of the fibres from the nucleus of the third nerve, which runs down the cord to the last cervical vertebrae before joining the sympathetic. When the legs become spastic late in transverse myelitis the cause is supposed to be a descending de- generation in the pyramidal tracts. The symptoms of chronic transverse myelitis producing para- plegia are practically identical with the more acute form just de- scribed, except that they are very slow in their development. Having discussed the various forms of myelitis, we have still to study the question as to the seat of the lesion in each form. Let us suppose that a patient presents himself with the following condi- tion : There is complete paralysis of his arms and legs, with paral- ysis of the muscles of the trunk, and total anaesthesia of the same areas. The legs are in a state of spastic paralysis, their reflexes are increased and their nutrition is uuimpaired; while the arms are found relaxed and flaccid, devoid of reflex excitability, and under- goiug degenerative atrophy. The bladder and rectum are not reten- tive. All these symptoms point to a transverse lesion of the spinal cord in the cervical region, probably between the fifth cervical and first dorsal vertebrae. If, on the other hand, the upper extremities are not affected (ex- cept, perhaps, the small muscles of the hand), but there is the same loss of power in the legs, with spastic contraction of the muscles, and the other symptoms just named are preseut, combiued with de- generation of the muscles of the trunk, the lesion is probably some- where between the second and twelfth dorsal vertebrae. Again, if the paralysis of motion and sensation be only in the lower limbs, and there be flaccidity of the muscles (where before we discovered spastic contraction), with muscular degeneration, loss of reflexes, and paralysis of the bladder and rectum, the lesion is in the lumbar cord. Still further, if there be loss of power with degeneration of the small muscles of the feet, aud loss of sensation of the outside of the feet and toes, and of the skin about the anus, with preservation of power in the thighs and of the patellar reflex, the lesion is in the sacral cord. Finally, it is possible for disease of the cauda-equina to produce symptoms of a lumbar-sacral lesion owing to the fact that this part of the cord is composed of fibres derived from these two areas. The patellar reflex may be preserved as the lesion is below the reflex arc, and all the fibres may not be involved. THE FEET AXD LEGS. 97 Differential Diagnosis of Lumbar, Dorsal, and Cervical Myelitis.^ Lumbar myelitis. Dorsal myelitis. Cervical myelitis. Paralysis. Paraplegia. 1. Dorsal, abdominal, and intercostal muscles, ac- cording to height of lesion. 2. Legs. Neck muscles, dia- phragm, arms, trunk, and legs. Sensation. Pains in legs, or girdle pains around loins ; hyperasthe- tic zone around loins ; an- aesthesia of legs, complete or uneven distribution. Girdle-pain and hyperaes- thetic zone between ensi- form cartilage and pubes. HynerBesthesia and pains in certain nerve- distributions of arms; below this ansesthesia of arms, body, and legs. Atrophiy. Of legs. Of dorsal and abdonainal (and intercostal muscles not subject to examina- tion ) corresponding to height of lesion; sometimes mild and slow of legs. Atrophy of neck mus- cles (rare) or more commonly of arms. Electrical reaction. R D. in atrophied muscles ; or in mild cases quantita- tive diminution. R. D. in dorsal and abdomi- nal muscles ; slight quanti- tative changes only in legs when wasted. R. D. jo atrophied muscles. Bladder. Incontinence from paralysis of sphincter. Retention, or intermittent incontinence from reflex action ; later from over- flow. Cystitis common. Same as in dorsal mye- litis. Bowels. Incontinence from paralysis of sphincter, disguised by constipation. Involuntary evacuation from reflex spasm or con- stipation. Same as in dorsal mye- litis. Reflexes superficial. Lost Temporary loss, then rapid increase. Same as in dorsal mve- litis. Reflexes superficial. Lost. Temporary loss, then slow increase. Same as in dorsal mye- litis. Priapism. Absent. Often present. Often present. In this connection the reader should compare that part of the chapter on the Skin which deals with ansesthesia. This subject is still further subdivided and elucidated by the following table and by the illustration on page 99. Localization of the Functions of the Segments of the Spinal Cord. (According to Starr.) Segment. Muscles. Reflex. Sensation. n. and III. C. Stern o-mas(oid. Trai)ezius. Scaleni and neck. Diaphragm. Hypochondrinm(?). Sudden inspiration produced by sudden pressure beneath tiae lower border of ribs. Back of head to vertex. Neck. IV. C. Diaphragm. Deltoid. Biceps. Coraco-brach ialis. Supinator longus. Rhonibfiid. Supra and infra spinalus. Pupil. 4th to 7th cervical. Dilatation of tl»e v>upil pro- duced by Irritation of the neck. Neck. Upper shoulder. Outer arm. ' From Prince's article in Dcrcum's' 7 Nervous Diseases." 98 THE MANIFESTATION OF DISEASE IN ORGANS. Segment. Muscles. Reflex. Sensation. V. C. VI. C. VII. C. VIII. C. I. D. II. to XII. D. I. L. II. L. III. L. IV. L. V. L. I. to II. S. III. to V. s. Deltoid. Biceps. Coraco-brachialis. Brachialis anticus. Supinator longus. Supinator brevis. Rhomboid. Teres minor. Pectoralis (clavicular part). Serratus maguus. Biceps. Brachialis anticus. Pectoralis (clavicular part). Serratus maguus. Triceps Extensors of wrist and fingers. Pronators. Triceps (longhead). Extensors of wrist and lingers. Pronators of wrist. Flexors of wrist. Subscapular. Pectoralis (costal part). Latissimus dorsi. Teres major. Flexors of wrist and fingers. Intrinsic muscles of hand. Extensors of thumb. Intrinsic hand muscles. Thenar and hypothenar eminences. Muscles of back and abdo- men. Erectores spinse. Ilio-psoas. Sartorius. Muscles of abdomen. Ilio-psoas. Sartorius. Flexors of knee (Remak). Quadriceps femoris. Quadriceps femoris. Inner rotators of thigh. Abductors of thigh. Abductors of thigh. Adductors of thigh. Flexors of knee (Ferrier). Tibialis anticus. Outward rotators of thigh. Flexors of knee (Ferrier). Flexors of ankle. Extensors of toes. Flexors of ankle. Long flexor of toes. Peronei. Intrinsic muscles of foot. Perineal muscles. Scapular. 5th cervical to 1st dorsal. Irritation of skin over the scapula produces contrac- tion of the scapular mus- cles. Supinator longus. Tapping its tendon in wrist produces flexion of fore- arm. Triceps. 5th to 6th cervical. Tapping elbow tendon pro- duces extension of forearm. Posterior wrist. 6th to 8th cervical. Tapping tendons causes ex- tension of hand. Anterior wrist. 7th to 8th cervical. Tapping anterior tendons causes flexion of wrist. Palmar. 7th cervical.to 1st dorsal. Stroking palm causes closure of fingers. Epigastric. 4th to 7th dorsal Tickling mammary region causes retraction of the epigastrium. Abdominal. 7th to 11th dor- sal. Stroking side of abdomen causes retraction of belly. Cremasteric. 1st to 3d lum- bar. Stroking inner thigh causes retraction of scrotum. Patella tendon. Striking tendon causes ex- tension of leg. Gluteal. 4th to 5th lumbar. Stroking buttock causes dimpling in fold of buttock. Plantar. Tickling sole of foot causes flexion of toes and retrac- tion of leg. Foot reflex. Achilles tendon. Overextension of foot causes rapid flexion; ankle-clonus. Bladder and rectal centres. Back of shoulder and arm Outer side of arm and forearm, front and back. Outer side of forearm, front and back. Outer half of hand. Inner side and back of arm and forearm. Radial half of the hand. Forearm and hand, inner half. Forearm, inner half. Ulnar distribution to hand. Ski n of chest and abdo- men, in bands run- ning around; and downward corre- sponding to spinal nerves. Upper gluteal region. Skin over groin and front of scrotum. Outer side of thigh. Front and inner side ol thigh. Inner side of thigh and leg to ankle. Inner side of foot. Back of thigh, back of leg, and outer part of foot. Back of thigh. Leg and loot, outer side. Skin over sacrum. Anus. Perineum. Genitals. THE FEET AND LEGS. 99 Paraplegia when due to locomotor ataxia is nearly always so sur- rounded by other typical symptoms of this disease as to render its separation from the paraplegia of myelitis easy, aud, further, it is rarely a true loss of power. The stabbing and darting pains of ataxia (see chapter on Pain), the presence of the Argyll-Robertson pupil, the absence of the patellar reflex, and the atrophy of the optic nerve are all characteristic of ataxia, and absent in myelitis (see also early part of this chapter on Gait). Fig. 37. 1st to 7th cervical segment. ■ 1st to 12th dorsal segment. 1st to 5th lumbar segment. 1st to 5th sacral segment. Diagram showing thu siirlace-ureas of the bacli corresponding approximately to the areas of the spinal cord supplying thu trunk and limbs. The symptoms of lateral sclerosis and amyotrophic lateral sclerosis have already been discus.sed under "Gait" and Spastic Paraplegia, but in the j)araplegia called " ata.xic paraplegia," also already discussed, there are in association lateral sclerosis and posterior sclerosis, and for this reason some of the symptoms of both are found to be present. Thu.s, in addition to loss of j)owcr there is a spastic condition of the legs with exaggerated refiexcs, absence of the Argyll-lvobertsou pupil, and of crises of pain, but the Romberg symptom, or swaying 100 THE MANIFESTATION OF DISEASE IN ORGANS. when the eyes are closed, is present. The condition which most closely resembles ataxic paraplegia is that of tumor of the middle lobe of the cerebellum, but in such cases we have, in addition, head- ache, vertigo, optic neuritis, titubation, and sometimes vomiting. The onset of paraplegia in a young child, preceded by an attack of fever, vomiting, restlessness, and general illness, lasting but a few hours or days, and which may be complicated by convulsions, all point to the cause being poliomyelitis of a severe type. The legs are, however, as a rule, completely paralyzed for but a brief period after the attack. Eventually the storm clears off and only the muscles directly connected with the diseased cells in the cord (anterior cornna) remain paralyzed. There is no loss of s^sation, but reflex action is abolished in the paralyzed parts. Far and away the most important point in the diagnosis is the symptom of rapid wasting of the muscles in the paralyzed parts and the rapid develop- ment of coldness in these areas, which is due to the destruction of the trophic centres in the spinal cord. Paraplegia resulting from tumor of the cord or its membranes only ensues when the growth is so placed as to cut off all the motor tracts supplying both limbs, which is rarely accomplished until after a long history of more or less well-developed motor and sensory fail- ure. The paralysis is developed in the areas supplied by the centres in the cord below or at the level of the growth, and the violent pain nearly always present in cases of tumor points to the diagnosis. Very painful paraplegia, therefore, indicates spinal tumor as its cause. The area of anaesthesia and the muscles involved may also give definite information as to the seat of the growth (see chapter on the Skin, and Starr's table just quoted.) If the paraplegia be due to compression from fracture or disloca- tion of the vertebrae or to other direct injury, the history of the patient and the evidences of external local mischief will decide the diagnosis. Sometimes during the course of severe disease, producing irrita- tion of the bladder, kidney, bowels, or rectum, as in violent cystitis, stone in the kidney, and dysentery, paraplegia comes on, due in some cases to an infectious myelitis, but in others to what is apparently only a reflex paralysis, as it often passes away with the removal of the source of irritation. Even worms in the intestine have produced such a paralysis, and their removal has been followed by cure. Gen- erally sensation in the limbs is unimpaired and the bladder and THE FEET AXD LEGS. 101 rectum act normally. Sometimes, however, in the presence of severe renal disease, as venal calculus, there may be all sorts of disturbance of sensation and pain, as well as great motor paralysis, with total loss of reflexes, following an exaggeration of the reflexes. Probably these severe cases are always due to a coincident myelitis rather than to reflex irritative cause. No form of paraplegia presents so many types or represents so many organic diseases as does that due to hysteria, for there may be not only great loss of motion but exaggerated or lost reflexes, relax- ation or spastic contraction of the muscles, anaesthesia and hyperses- thesia, pain or no pain. The very occurrence of such irregular manifestations in a young neurotic girl, the fact that the anaesthetic areas constantly tend to shift their position, and, finally, that the contractures, if present from hysteria, disappear on admiqistering an anaesthetic to a stage in which muscular relaxation is produced in the ordinary individual, aid us in making what is in some cases an almost impossible diagnosis (see that part of this chapter on Contractures). A pseudo-paralysis of the legs with immobility sometimes occurs as a symptom of scorbutus in infancy. The parents notice that the child flinches when picked up or handled, and seems as if tender from rheumatism. Often the gums are swollen and bleeding, and purpuric eruptions appear on the skin. The shafts of the bones of the legs or of the arms may be enlarged, and htematuria or bloody stools may appear. Pseudo-parai)]egia may occur in rickety children from faulty mus- cular and bony development. It is to be separated from the ordinary paraplegias of childhood by the state of the bones, the presence of knee-jerks, and the absence of local wasting or spasm, but general spasm, or carpo-i)edal s])asm, is often seen in rickety children. Not uncommonly a partial paraplegia occurs as a result or secpiel of diphtheria. The condition, however, is more ataxic than para- plegic, and Bourges asserts that there is no muscular atrophy such as occurs in true paraplegia due to neuritis, or in some spinal lesions. When neuritis produces paraplegia it may present symptoms verv closely allied to those of acute myelitis, if the symptoms come on suddenly, or of locomotor ataxia; that is, neuritis may cause pseudo- tabes if its onset be slow. The neuritis is always multiple and in- volves the arms and the body after affecting the legs ; there is well- developed auicsthesia (see chapter on Skin), preceded by sensory disturbances au. halt ci( l.mali/ntion of Cortical Centres (letrrniined on Medial Surface of Ccrehnmi i.iav HEMIPLEGIA. 117 function, and these fibres apprcxiraate one another more and more closely in the lower part of the brain until they form a bundle Fig. 50. ,_cwer limb DinRrnm showing the fibres from the cortex forming the coronji radiata, which after they are approximated pass into the internal capsule. It also shows the decussation of the pyramid of the left side, which passes to the right side of the spinal cord, and the direct or uncrossed tract. Finally it also shows secondary degeneration which occurs after cerebral hemorrhage or softening, and which follows the course of the motor tracts into the spinal cord. U. Site of lesion. The continuous lines are fibres going to the legs, the dotted are those going to the arms and motor cranial nerves. (Modified from V.^n fiEiii'cHTEN.) 118 THE 3IANIFESTATI0N OF DISEASE IN ORGANS. Fig. 51. Outline of horizontal section of brain, to sliow the internal capsule. Natural size. The gray matter of the cortex and claustrum is left unshaded, but that of the corpus striatum and optic thalamus is shaded ; OT, optic tlialamus, showing the median, lateral, and an- terior nuclei ; NL, nucleus lenticularis, showing the putamen large, and the inner division of the globus pallidus very small ; NO, nucleus caudatus, the large head in front of, and the diminishing tail near the thalamus; G, the knee of the internal capsule. From "Eye" to "Digits" marks the position of the pyramidal tract as a whole, and the several letters indicate broadly the relative positions of the several constituents of the tract, named according to the movements with which they are concerned : Thus Eye, movements of the eyes; Head, of the head; Tongue, of the tongue; Mouth, of the mouth; Shoul, of the shoulder ; Elbow, of the elbow ; Digits, of the hand ; Abdo, of the abdomen ; Hip, of the hip ; Knee, of the knee ; Toes, of the foot ; S, the temporo-occipital tract ; oc, fibres to the occipital lobe ; op, optic radiation. At this level the fibres of the frontal tract, in the fore limb of the capsule in front of the pyramidal tract, run almost horizontally, parallel with the plane of the section, cc, the rostrum of the corpus callosum, Spl, the splenium of the same, both cut across horizontally. The thick dark line indicates the boundary of the cavities of the anterior and descending horns of the lateral ventricle and of the third ventricle, the two ventricles being laid open into one by the removal of the velum and choroid plexus, etc. The oval outline in the fore part of this cavity indicates the fornix. Lateral to the nucleus lenticularis are seen in outline the claustrum, the cortex of the island of Reil, and the operculum or convolution overlapping the island of Reil. P is inserted to show which is the hind part of the section. PLATE II. Diagram showing Course of Motor Fibres from the Cerebrum and Cor<1 to the Periphery. (Flatau.) HEMIPLEGIA. 119 (corona radiata). Thus we see iu Plate II. how the fibres arising from the middle area of the cortex cerebri pass down through the lenticular nucleus into the knee or angle of what is called the internal capsule. This is a lateral view. In Fig. 50, which also shows the results of a lesion iu the capsule, we get an antero-pos- terior view. These fibres are arranged in such a way that those Fig. 52. — — Front nl lobe. Temporo- uphenoidal lohe. (ipital lohe. arising from the lower j)art ol the ('(irtcx', as in the face-centre, lie nearest the knee of the capsule, and those highest, furthest from this ])oint. (Fig. 51.) After the motor fibres have passed through the internal capsule, they pass into the crus cerebri of that side, 120 THE 2IANIFESTATI0y OF DISEASE IN ORGANS. which (the cms cerebri) connects the hemisphere of the same side with the cerebellum behind it, and the pons and medulla below it. The crura cerebri are two thick cylindrical bundles of white matter which emerge from the anterior border of the pons (Fig. 52), diverge as they pass upward and outward to enter the under part Fig. 53. Lesion of cerebral mo- noplegia (brachial) Lesion of ordinary hemiplegia Lesion of cross paralysi (face of same side witli limbs of otlier side) A lesion causing paraplegia- A lesion causing hemi paraplegia Cortical centre for op- posite leg Cortical ceyitrefor op- posite arm Cortical centre for op- posite side of face Internal capsule (pos- terior limb) Olotor nerve to face Decussation of pyra- m ids Crossed pyram idal tract 2Iotor nerves to upper limb Crossed pyramidal tract Sensory nerves entering cord, and decussating soon after entry Motor nerves to lower limb Diagram showing the general arrangement of the motor tract and the effect of lesions at various points. of each hemisphere, as if stretching out to receive the motor fibres from the internal capsule. From the crura cerebri the motor fibres pass downward into the pons Varolii. Here the fibres which have hitherto travelled together divide into two parts, namely, those from the face and tongue centre, which pass to the opposite side HEMIPLEGIA. 121 and become connected with the nuclei of the facial and hypoglossal nerves, which act as minor centres governing the face and tongue, and the fibres for the arm, leg, and trunk of the body which continue on down to the medulla oblongata, where thev form the so-called pyramids, and having done so most of the fibres cross to the oppo- site side of the spinal cord (the crossing of the pyramids), and so form the crossed or lateral pyramidal tracts. (Fig. 50.) A Fig. .54. Showing the mechaiii.-iin of diflerent hemiplegias. A lesion at A causes complete hemi- plegia by destroying the motor tract. One at M causes paralysis of third cranial nerve (motor oculi) by destroying its nucleus or root on same side, and paralysis of arm and leg on opposite side. A lesion at F causes facial palsy on same side, hemiplegia on opiKJsite side. In a lesion at II the hypoglossus would be aflected ou one side, with hemiplegia on the other. (Modifled from Edinoer.) smaller number of fibres, liowever, pass directly down to the s})inal cord from the nKnliilla oblongata, and from what is called the direct or anterior pyramidal tract. Direct, because it docs not cross; an- terioi-, becau.se it lies along tiio edge of the anterior fissure of the 122 THE MAXIFESTATIOX OF DISEASE IX OBGAXS. cord ; pyramidal, because it comes down from the pyramid. This is sometimes called Tiirck's column. (Fig. 50.) It is by means of these two tracts in the spinal cord that motor impulses pass down to the nerve-trunks and muscles. We can understand, therefore, that if a small lesion occurs at the peripheral endings of the corona radiata — that is, on the cerebral cortex — it will only produce a limited paralysis. Thus, as seen in Fig. 53, a clot at the arm-centre would only involve the arm-fibres. Fig. 55 Cut showing tracts in spinal cord. 1. Anterior horns of gray matter which contain the cells governing the nutrition of the muscles and give rise to the motor roots. 2. Posterior horns of gray matter which receive the sensory roots. 3. Crossed lateral pyramidal or chief motor tracts from cortex of brain. 4. Columns of Burdach or the outer sensory tracts carrying impulses upward. 5. Columns of Goll or inner sensory tracts carrying impulse upward. Tac- tile sensibility. 6. Direct cerebellar tract, which carries impulses of a sensory character up- ward. Tract of muscle-sense. 7. Antero-lateral tracts, which consist ot fibres conducting the gray matter of the cord into that of the medulla. They contain anterior nerve-roots and are the channels for reflex effects. There are also tracts in this root for pain and temperature sense. 8. Column of TUrck, or direct anterior pyramidal tract, which carries impulses of motion downward. 9. Lateral mixed tracts same as 7. If, however, the lesion be lower down where the fibres of the corona radiata are getting closer and closer, as, for example, in the internal capsule, then even a small lesion will produce widesj^read paralysis, since it will involve a large number of fibres running ultimately to widely separated areas in the body, and, if large enough, produce hemiplegia. (Figs. 53, and 54 lesion A.) If the lesion be situated in the pons on one side, it will cau.se facial paral- HEMirLEGIA. 123 ysis on that side aud hemiplegia ou the opposite side of the body, because, as shown in the diagram (Fig.s. 53, and 54 M), it will, uuder these circumstances, destroy the facial fibres after they have crossed, and the remaining motor fibres before they cross. The various tracts, motor and sensory, in the spinal cord are shown in Fig. 55. Hemiplegia from hemorrhage is characterized by sudden onset in most cases, by more or less mental disturbance and disorders of motion, sensation, and of the special senses according to the site of the leaking ve=sel. The skin-reflexes are a])t to be markedly de- creased and the deep reflexes increased, but the bladder and rectum are not usually paralyzed, although in the first shock of the acci- dent there may be vesical aud rectal incontinence. The mental dis- turbance usually amounts to a rapidly oncoming unconsciousness in hemorrhagic hemiplegia. ^ Fig. 56. Diagram of the arteries of the base of the brain, showing LO., the lenticular optic, and LS., lenticular striate set of arteries. One of the latter is called the artery of cerebral hemorrhage. V.A. Vertebralis. S.a. Spinalis anterior. S.p. Spinalis iHjs-terior. B. /I. Basilaris with median branches. C.b.s. A. Ccrebrahs sufierior. r i. Cerebelli inferior. C.p. A. C'erebralis posterior (profunda cerebri). Com. p. A. Comniunicantes i>f)steriores. C.a.f. Carotis interna, o. A. Oph- thalmica. Cm. A. Cerebralis media (A. fossii- Sylvii). t. A. Insularis. cft. A. Corp. striati. C.a. A. Cerebralis anterior. Com. A. C'ommunicans anterior. C.c.a.ll. A. Corp. cullosi. The question of the location of the lesion is very important. In tiie great majority of cases it is situated above the point at which the decussation of the motor fil)res takes place in the medulla, aud 124 THE MANIFESTATION OF DISEASE IN ORGANS. is, therefore, on the opposite side of the body from that on which the hemiplegia exists. If, however, the lesion be below the decus- sation, the paralysis and lesion are on the same side, as just described. The most common site for the lesion in hemiplegia is in the knee or posterior limb of the internal capsnle, owing to the fact that the middle cerebral artery in one of its lenticulo-striate branches perforates the internal capsule, and ends in the caudate nucleus, and this artery is so commonly ruptured that Charcot has called it the " artery of cere- bral hemorrhage." (Fig. 56.) If the hemorrhage does not involve the posterior third of the internal capsule, there are no sensory symp- toms associated with the motor loss, but the paralysis will be practi- cally universal on that side, involving the leg and arm, and the lower part of the face, so that the mouth is drawn toward the healthy side. (Explained by Fig. 51.) The symptoms associated with hemiplegia due to this cause often become very severe because the hemorrhage is 80 profuse that the lateral ventricles become filled with blood, and from them the blood passes to the third, and from there to the fourth ventricle, where, by pressure on the vital centres, it speedily produces death. In such cases deep unconsciousness, stertorous breathing, a slow, full pulse, and a flushed skin, becoming some- what cyanotic, may be present. Recovery never occurs, for the sec- ondary inflammation, or softening, following the outflow of blood produces fatal results, even if the patient survives for some days. In cases in which the hemorrhage is very limited consciousness may be lost for only a brief period, and at most there may be mental confusion. Often in mild cases there is a slight return of power in the affected side within a few days, and the temperature of the affected part, which has been raised, approaches the normal. Fi- nally, after six to eight weeks the dominant symptoms consist in partial loss of power of the arm and leg, and the facial paralysis has perhaps entirely disappeared, although the tongue when pro- truded may tend to go over to one side. If the case does not pass to such favorable results, instead of recovery of power at this time there are developed contractions and secondary rigidity from de- generative processes extending to the pyramidal tracts. (See Fig. 50.) Hitzig has shown that these conditions are apt to be least marked in the morning. Wasting of the paralyzed muscles only ensues from the disuse, and not from trophic change. When the case is not of the very severe type which causes death in a few hours, and yet the lesions are such that recovery is not going to HEMIPLEGIA. 125 take place, the patient at the third or fourth day becomes unconscious a second time, his temperature rises, he mutters, and grows restless, finally becomes comatose, then develops respiratory failure, or a hypostatic congestion of the lungs, and dies. When a patient is seized with headache, dizziness, vertigo, and vomiting, and rapidly oncoming hemiplegia and hemiantesthesia, at- tended at first with no loss of consciousness, but in a day by uncon- sciousness and coma, he is suffering from what has been called " in- gravescent apoplexy." The hemorrhage, under these circumstances, begins in the knee of the internal capsule, proceeds backward till it involves the sensory fibres in the internal capsule, and, finally, breaks into the lateral ventricle, soon after which death ensues. When a hemiplegia is followed by rigidity very early, with sensory involvement and convulsions, the lesion is proba^jly cortical, or, more correctly, is secondarily cortical to a deeper hemorrhage, and spreads over the centres for the face, arm, and leg. Most com- monly, however, cortical hemorrhages are due to injuries, or they may arise from unprovoked vascular rupture. In any case, they are usually ushered in by convulsions. Where, on the other hand, there is paralysis of the arm, trunk, and leg on one side, with facial paralysis and anaesthesia on the oppo- site side of a well-mari-ced type, associated with early rigidity of the paralyzed side, conjugate deviation of the eyeballs, very marked rise in bodily temperature, a contracted pupil, and convulsions, with difficulty in swallowing and in speech, the lesion is to be found in the pons Varolii on the side opposite the paralysis. This is due to the fact that the injury is below the decussation of the facial nerve. (Figs. 53 and 54.) If both sides of the face are paraly/ed with hemiplegia elsewhere, the lesion is in the puns where the facial fibres cross. Pons paralysis is nearly always associated with giddiness, vomiting, conjugate spasm with nystagmus, albuminuria, glycosuria, and marked disturbances in the respiration and heart. Pontile hem- orrhages are, however, very rare, and usually are rapidly fatal. Finally, if there is hemiplegia of the lower part of the face, arm, and leg, and in addition paralysis of the upper part of the face, and ptosis from paralysis of the facial and oculo-motor nerves on the opposite side, and in association impaired sensibility and vasomotor changes in the limbs, the lesion is probably in the crus cerebri on the side of the upper facial paralysis — that is, on the same side as the ptosis ; but this is only true if the two paralyses have been 126 THE MANIFESTATION OF DISEASE IN ORGANS. simultaneous in occurrence, as it is possible for one lesion in one place to produce paralysis of the face and another elsewhere to pro- duce the hemiplegia (see Ptosis in chapters on Face and on the Eye). If in the development of symptoms of cerebral hemorrhage there be little hemiplegia and temporary unconsciousness, followed in some hours by a sudden aggravation of the symptoms, it may be that in the beginning of the attack the lesion has been in the frontal lobes, but has gradually extended backward until it has ruptured into the lateral ventricle. So, too, a hemorrhage into the occipital lobe or the posterior part of the parietal lobe is rarely marked by much hemiplegia, and, if present, the leg is more paralyzed than the arm. The characteristic symptom, however, is well-marked hemian- sesthesia (see chapter on Skin), and hemianopsia (see chapter on Eye). Generally, however, such changes result from a thrombosis. AVhen there is developed, in cases of hemiplegia, aphasia or dis- ordered speech, there is probably a lesion in the neighborhood of the third frontal convolution, or the island of Reil (see chapter on Speech). Hemiplegia may be due to cerebellar hemorrhage, in which case there are loss of consciousness deepening into profound couia, con- tracted pupils, vomiting in many of the cases, and finally death when hemorrhao^e breaks into the lateral veutricb. The diagnosis of cere- bellar hemorrhage is very difficult. Of the irregular forms of hemiplegia there are several. Some- times the leg is from the beginning more affected than the arm, and remains paralyzed long after the face and arm have recovered. The leg may become rigid and distorted by contractures, and there will often be found present marked anaesthesia of the skin of the paral- yzed leg and arm, with hemianopsia and aphasia. Such symptoms indicate a lesion of comparatively small size involving the leg-fibres and some of the sensory fibres in the internal capsule, and results from rupture of the lenticulo-optic artery. When the arm suffers most the symptoms just described as in the leg are seen in it, and motor aphasia, if the lesion is on the right side, is often very marked, as is also facial paralysis. This is supposed to be due to the anterior frontal artery, a branch of the anterior cerebral artery, becoming diseased. When post-hemiplegic chorea attacks the paralyzed limbs there is often a focal lesion in the posterior extremity of the internal capsule. The symptoms we have just detailed may also arise, as we have HEMIPLEGIA. 127 already said, from embolism or thrombosis of the cerebral vessels as Avell as from hemorrhage from them. How are we to separate the hemiplegias of heinorrhage and occlusion ? In many cases this is im- possible, but there are some differential points which may aid us. In the first place, thrombosis is a condition of advanced age, while hemorrhage may occur at any time from thirty years of age on. The presence of hemiplegia in a young man, therefore, is probably not due to a thrombosis. Again, hemorrhage occurs often after exertion or the drinking of stimulants, and occurs rarely in sleep, whereas thrombosis not rarely comes on under these circumstances, and often develops during the night, so that the patient awakes paralyzed, and a patient may have both thrombosis and apoplexy. In hemorrhage, consciousness is generally lost, whereas in thrombosis it is often only dinuued. Vomiting and contracted pupils from pressure on the lower centres indicate hemorrhage, while their absence may point to thromljosis. Finally, the general systemic shock and febrile move- ment are apt to be greater in hemorrhage than in thrombosis. The history of syphilitic infection, ])roducing an endarteritis, also points to thrombosis, although hemorrhage may arise from this cause also. The diagnosis of embolism producing hemiplegia from the paral- ysis due to hemorrhage is always more or less difficult, but the pres- ence of chronic or ulcerative endocarditis or their results, or other cause for the formation of emboli, aid the diagnosis. AVhere the cause is embolism the onset is sudden, whereas in thrombosis it is sometimes more gradual. The paralysis from embolism is more conunonly on the right side of the body, owing to the fact that it is more easy for an embolus to pass into the left middle cerebral artery than into the right. Spastic hemiplegia may be due to cerebral tumor, and is often associated with convulsions, particularly if the growth be cortical. Very often the paralysis of cerebral tumor will be found, from the history, to have come on gradually. Thus, the history may be that at first the side of the fiice has been paralyzed, then the arm and then the leg, and that the complete loss of power has not been sudden l)ut gradual in the part affected, or that a convulsion has left that side, which was previously only impaired in strength, totally paralyzed. Hemiplegia also comes on as a result of cerebral syphilis, and, aside from a history of specific infection and response to specific medi- cation, presents few characteristic signs. The presence of intense 128 THE MAXIFESTATIOX OF DISEASE IN ORGANS. headache, convulsions of an epileptiform type, and the fact that the paralysis occurs in some cases in early youth, point to its origin. Another cause of hemiplegia is diffuse cerel^ral sclerosis of one hemisphere (not multiple sclerosis), in which the most constant symptoms are, in addition to the paralysis, evidences of motor irrita- tion, such as epileptoid convulsions of a bilateral or unilateral char- acter, rhythmical or arhythmical twitchiugs of the muscles like chorea, and dementia. Hemiplegia may also arise from hematoma of the dura mater. The symptoms, aside from the paralysis, are headache, stupor, irreg- ular pulse, vomiting, and contracted pupils, or, in other words, symptoms of cerebral compression. Sometimes twitchiugs of the paralyzed side occur, and if the clot be near the third frontal con- volution or the island of Reil, aphasia may be present. Sensation is usually not involved. The diagnosis of this form from that due to hemorrhage is often impossible. Hemiplegia arising from acute infantile cerebral paralysis has many of the distinctive features already described when discussing the paraplegia due to this diseased state. The age of the patient, the occurrence of epileptiform convulsions and of athetosis in the affected parts, and the patient's history are the important points to be recalled in making a diagnosis. The lesion is always due to a cerebral hemorrhage or to embolic softening. When hemiplegia occurs in locomotor ataxia, it depends not upon the disease, but upon a complicating hemorrhage, embolism, or thrombosis. A slowly developed hemiplegia sometimes results from multiple sclerosis, the pathological process involving the side of the pons and spinal cord, but the intention-tremor, the peculiar speech, the nys- tagmus, and the very excessive reflexes aid us in the diagnosis of this cause of the loss of power. A form of hemiplegia which is often very misleading is that oc- curring in general paralysis of the insane or paretic dementia. In this disease the patient often has attacks of vertigo, unconsciousness, and more or less marked hemiplegia or monoplegia, sometimes with aphasia if the right side is paralyzed. This form is also liable to be wrongly diagnosed by reason of the epileptiform convulsions, which frequently occur, and which in connection with the paralysis give the impression in the first attack that there is a hemorrhage of the cerebral cortex. The presence of the altered disposition of the HEMIPLEGIA . 129 patient, the loss of memory and intelligence, the peculiar stumbling speech, and the curious changes in the handwriting are some of the symptoms which complete the diagnostic picture. Hemiplegia sometimes comes on in purulent meningitis. The history of a head-injury or of a pyaemic or infective process, the cerebral symptoms, the stiffness of the back of the neck, the impair- ment of the normal movements of the eyeball, and the optic neuritis, associated with the convulsions, make the diagnosis possible. A very rare form of paralysis, in which the arm on one side and the leg on the other side are involved, is due to a bulbar lesion just where the decussation of the pyramids takes place. This is called crossed paralysis, and is due to cutting off of one set of fibres be- fore they cross, and the others after they have crossed. (See chap- ters on Hand and Arm, Feet and Legs, and Face and'' Head for further information as to crossed paralysis.) CHAPTER Y. THE TONGUE, MOUTH, AND PHARYNX. The general appearance of the tongue — Its coating — Its appearance in poisoning — Fissures and ulcers of the tongue — Eruptions on the tongue — Atrophy and hy- pertrophy of the tongue — Paralysis — Tremor and spasm of the tongue. The appearance of the tongue is recognized as indicative of the general condition of the patient, and is a valuable diagnostic aid in many diseases other than those associated with disorder of the gastro- intestinal mucous membrane. In examining this organ the physi- cian should take note of the condition of its surface, its shape as it lies in the mouth or is protruded, and the character of its move- ments. He should also see that it is well protruded, and examine the back of it more than the tip, as the latter is the part giving the least information. Before discussing the precise appearance of the tongue in the vari- ous disorders in which it becomes altered in appearance, it is well to remember that its surface is covered by mucous membrane, which differs in various parts. The epithelium is scaly and rests upon the corium or mucosa. The mucosa also supports many papillge which are thickly distributed over the anterior two-thirds of the tongue on its upper surface. These papillse give the peculiar roughness which is so characteristic of this surface, and occur in three forms, namely, the circumvallate or large papillse, the fungiform or mediate, and the filiform. The circumvallate are only eight or twelve in number, and are arranged at the back of the tongue in the shape of the letter V, with the point toward the root of the organ. The fungiform papillae are scattered freely over the tongue, mostly at the sides and tip, and appear as deep-red eminences, the bases of which are smaller than their free extremities. Their epithelial covering is very thin. The filiform papillse, which cover the anterior surface of the tongue, are very minute, and arranged in lines corresponding in direc- tion with the two rows of the circumvallate papillse. From their apices project many fine filiform processes, which are of a whitish THE TONGUE, MOUTH, AXD PHARYNX. 131 tint owiug to the density of tlie epithelium of which they are com- posed. There are, in addition, many simple papillae which cover the surface between the peculiar ones already described. It is the fungi- form papillae which are seen most commonly in cases of disease, for they become large and prominent, and because of their red color show throuo;h the coating as red dots. The appearance of the surface of the tongue varies greatly even in health according to the condition of its mucous membrane and the epithelium covering it. The most common alterations in its ap- pearance are due to mere superficial coatings or fur, which consist of dead epithelial cells, micro-organisms of many kinds, and abnor- mally shaped living epithelium. Small particles of food may also be present. Butlin believes that the coating is chiefly due to micro- organisms. The question as to how characteristic of a ''particular disease any one coating or fur may be has been warmly discussed. Some have gone so far as to assert that the coating of the tongue is not indicative of any state in particular, while others, of whom the author is one, are convinced that while an absolute diagnosis of dis- ease in other organs cannot be based upon the appearance of the tongue great aid can be gained by its study. There are, however, very few conditions of the coating of the tongue which are pathognomonic of any one disease, since tiie coat- ing is produced by the local conditions of the mouth rather than by the disease itself. Taking up for consideration the various forms of coating, we find that the area at the base between the circumvallate papillse is always somewhat coated even in the best of health, and that in disease the heaviest coating is generally found in this region, while the tip and sides, even in those diseases in which the coating is heaviest, are generally fairly clear. This is in part due to the ciiaracter of the epithelium in different parts, and to the fact that the tip and sides are generally scraped dean by the movements of the tongue. Further, it should be retnembcred that the development of coating, aside from digestive derangements, depends chiefly on three factors : first, imm()l)ility of the tongue, so that it is kept clean by rubbing; second, mouth-breathing, whereby the surface becomes dry and less easily cleansed; and, third, fever, which not only dries the surface of the tongue by mouth-breathing, but interferes with salivary secretion. Additional local causes are a decayed or raggwl tooth or follicular tonsillitis, which infects the lingual epithelium, lack of cleanliness, 132 THE MANIFESTATION OF DISEASE IN ORGANS. and habits, such as smoking. In the last class of patients a heavily coated tongue in the morning is veiy common. The tongue of the typhoid state, and of typhoid fever in particu- lar, is quite characteristic, because the prolonged illness, the great exhaustion, and the general apathy of the patient all conspire to produce a peculiar coating on this organ. Early in the disease the surface of the tongue may be more or less foul, resembling the tongue we shall describe in biliousness, in that the back part is coated evenly and with a paste, but very soon a characteristic sign appears, namely, that the tip of the tongue and its edges become red, and the coating becomes most marked on each side of the median fissure, which in- creases in depth from before backward. The tongue also becomes narrow instead of broad and flabby, as it is in biliousness, and is drier. If the attack be mild, this condition may remain till con- valescence is established; but if the disease runs a severe course, the coating becomes very heavy, more dry, rough and brown from ex- posure to air and medicine. The furred appearance becomes almost shaggy at the back portion, and the drying proceeds until the under- lying epithelial layer is cracked and fissured, so that tiny exudations of blood add to the lingual discoloration. The reddened edges be- come dusky in hue, and may be cracked and fissured also. (Fig. 1, Plate III.) The tongue is very slowly protruded on request, partly from mental apathy, partly from feebleness and because its surface is so stiffened that to move it is difficult. It is equally slowly withdrawn for similar reasons, and while protruded is often markedly tremulous. Toward the close of the attack the tongue cleans off through exfolia- tion of the dead epithelial accumulation, and this is a favorable or unfavorable sign according to whether the remaining surface is red and moist or dusky and dry. Sometimes these characteristic coat- ings do not appear, the tongue being brown and rough all through the disease. A small triangular patch devoid of coating is often seen at the tip of the tongue in relapsing fever. In biliousness the tongue is coated almost uniformly by a whitish- yellow, pasty coat, extending from back to tip and side to side. The tongue is broad and flabby, and sometimes indented by the teeth, while the breath is foul and heavy. (Fig. 2, Plate III.) A similar tongue is seen in severe tonsillitis, except that it seems even more foul and less yellow in tint. Similarly in jaundice of the acute catarrhal type we have a coating still more yellow in some cases, because, as FiCT- 1. PLATE III. Fig. 2. Tj'phoid Tongue. Kiliou.s Tongue, with Yellow Coating. Fic|. 3. Fig. 4. Tongue of Mucous Di.scase or Chronic Catarrh of Stomach. Tunguf of Chronic C.aslric Catarrh with Anivmia. THE TONGUE, MOUTH, AND PHARYNX. I33 Fothergill asserts, the coat has been stained by the tauro-cholic acid eliminated by the salivary glands. The circumvallate papilla? are often ])rominent and stand above the coating, which is easily removed on scraping. A broad, white, heavily coated moist tongue is often seen in acute articular rheumatism, becoming dry if the fever is high and the attack prolonged. The white tongue of persons who take large amounts of milk is generally not smooth and pasty, but rather rough in appearance. If the tongue be suffering from an attack of thrush (saccharomyces albicans), the white coating will consist of irregular white masses of the growth, which, if in great number, often coalesce and make a fairly even surface. The soreness of the mouth, the local heat, the salivation, and the age of the person — generally a young ohild, render the diagnosis easy. A grayish diphtheritic-looking coating of the tongue occurring in adults may be due to the growth of various forms of mycoses. Thus, a fine network of Icptothrix in threads and tufts often spreads over the tongue, particularly in the region of the circumvallate pa- pilhe. The growth may be quite dark in color, but it is separated from the exudate of diphtheria by microscopic study and the absence of systemic disturbance. Sometimes on examining tiio tongue of a child we find that it is broad and flabby and covered by a gray coating which is smooth and fairly moist. Scattered throughout this coating are patches in wliich the coating and epithelium have been shed, leaving red spots with sharply defined edges, which spots are said to be ''worm- eaten " in their appearance; that is, to have the irregular outline of the marks on a worm-eaten leaf. In these areas are to be seen enlarged and reddened fungiform papilla;. Such a tongue is typical of what has been called, by Eustace Smith, '' raucous disease," a condition in whicii there exists a more or less marked chronic catarrhal process in all the mucous membrane. (Fig. 3, Plate III.) If, on the other hand, there is a comparatively light coating dotted irregularly by bright-red spots, which are not raised above the sur- face, but are very numerous, and the patient is a ciiikl, the diagnosis may be made of acute or subacute gastric catarrh. (Fig. 4, Plate ni.) The so-called strawberry tongue is one in which the organ is covered by a thick whitish coat, thnuigh which project the fungiform 134 THE MANIFESTATION OF DISEASE IN ORGANS. papillae, which have been deprived of their epithelial covering, and being swollen or enlarged stand out prominently. This appearance of the tongue is seen commonly in scarlet fever, but is not, as has been thought, pathognomonic of that disease. The fungiform pa- pillae in the strawberry tongue of scarlet fever are, however, partic- ularly prominent and erect. When the tongue is excessively furred or rough in appearance, the coating is due to abnormally long and projecting papillae covered by an excess of living and dead epithelial cells; it may denote grave disease of the viscera, but in rare instances possesses no diagnostic importance, unless coupled with other symptoms. This tongue is sometimes seen in scrofulous children in whom strumous manifesta- tions are marked. Should the tongue be denuded not only of coating, but, in addi- tion, of its normal epithelium, so that it appears dry, hard and harsh to the touch, it denotes, as a rule, grave and advanced disease of an exhausting nature, such as renal, hepatic, or gastric disorder about to cause the death of the patient. Sometimes this condition is seen in advanced phthisis or gastric carcinoma, and is of evil omen. When it is bereft of epithelium, beefy and red-looking, elongated and narrowed, and shows a peculiar roundness when protruded, severe visceral disease of the abdominal organs, such as dysentery, or hepatic abscess, or carcinoma, will often be found, or, in some cases, this condition develops to add to the discomfort of cases of advanced pulmonary tuberculosis or acute peritonitis. This tongue is sometimes called the '^ parrot tongue." In this connection the point should be noted that dryness of the tongue in the presence of grave disease is always an evil omen, and returning moisture of the tongue a favorable one. Unilateral coating of the tongue may be due to a decayed or rag- ged tooth, or to hemiplegia, which prevents that side of the tongue from beiner cleaned through movement. Hillow and Fairlie Clark both assert that morbid conditions of the second division of the trifacial nerve cause unilateral coating, and that abnormalities of the third division do not produce these changes as we would expect. The coating of the tongue is often so stained by extraneous sub- stances as to be entirely changed in appearance. If the coating be black, the color may be due to the ingestion of iron, of bismuth, charcoal, ink, or blackberries, mulberries, cherries, or red wine. In very rare cases it is black, not from the growth of a fungus, as THE TONGUE, MOUTH, AND PHARYNX. 135 has been thought, but from overgrowth of the epithelium with the deposit of a black pigment of unknown origin. Usually this brown- ish-black discoloration is confined to the middle of the tongue. The affected surface is often rough, due to the enlarged papillae, and the edges of the spot are less black than the centre. In professional tea-tasters the tongue may be orange tinted. The coating may be stained brown from the chewing of tobacco, licorice, nuts, and prunes, or chocolate, and yellow from the ingestion of laudanum or rhubarb. The color of the tongue itself, aside from discoloration of its epi- thelium, isan important diagnostic aid. It is exceedingly pale in all forms of anaemia, particularly those due to lack of haemoglobin, such as chlorosis or acute anaemia from hemorrhage, and in pernicious anaemia, when well advanced, it has a remarkable pallor.^ It is livid and cyanotic in cases of pulmonary disease interfering with oxida- tion of the blood, or in cardiac disease with similar difficulty. Purple spots, which may be almost black, may be present in Addison's disease. Sometimes they are bluish-black, and always well defined and even with the surface. Very rarely the tongue is discolored by infarcts, blood-stains, and bruises. When the tongue has its edges dotted with yellowish patches of a slightly elevated character the condition is xanthelasma, and the liver will often be found to be disordered. In cases of poisoning by corrosive sublimate the tongue presents a most characteristic appearance, for it is white and shrivelled, and the papilke at the base are unusually large. When sulphuric acid has been swallowed the tongue has a parch- ment-like aj)pearance, is at first white and then gray or brownish- gray, and finally covered by a black slough, which as it separates leaves a swollen excoriated patch. In nitric- and chromic-acid-poison- ing the tongue is shrivelled and lemon-yellow in color, as it is when hydrochloric acid has been swallowed. The tongue of carbolic-acid- poisoning is very characteristic indeed, for it is shrivelled and puck- ered into folds. The spots where the acid has touched are brownish if impure acid has been swallowed, or white if the pure acid has been tiiken. In the course of a few hours this spot becomes surrounded by a red zone, and finally becomes dark brown or black in the centre. After oxali(;aci(l is tai<('n the tongue may be covered by a thick white coat and looks as if it had been scalded. Caustic potash and soda sol'ten the mucous membrane, so that it is pulpy and easily detached, and 136 THE MANIFESTATION OF DISEASE IN ORGANS. looks pearly red or yellow in hue. When ammonia is swallowed the color is white, but superficial oedema may make it pearly in appear- ance, and acid nitrate of mercury renders it very red. Cantharidal poisoning produces large lingual blisters and sores. Aside from the coating and the color of the tongue, its surface should be examined to discover fissures, cracks, ulcers, sloughs, and swellings. The tongue is often seen to be superficially and irregu- larly fissured in old persons, particularly in those who have used large quantities of strong alcoholic drinks or strong tea, or who have chewed tobacco incessantly for many years. The fissures cross each other in every direction, although the central fissure which runs longitudinally is generally deepest and longest. If the furrows are very deep, they may indicate the early stages of what Wunderlich has called dissecting-glossitis, which in turn may be due to syphilis,^ although, as a rule, the fissures of the tongue due to syphilis are deepest at the edges of the organ, and are due to pressure by and from irritation from the teeth or to ulceration, and subsequent cica- trization of small syphilitic nodules or gummata. The cervical glands are rarely involved in such cases. If only one ulcer is pres- ent, it may be chancre, which will have the peculiar Hunterian hard base, and, in such a case, the cervical glands will probably be en- larged. An epithelioma may also have an indurated base with secondary glandular enlargement. Lingual ulcers may also be pres- ent as the mucous patches of syphilis, or be due to wounds from the teeth, a broken pipe-stem, or a fi^rk. Wlien these become chronic their separation from those due to syphilis and tuberculosis is prac- tically impossible on superficial examination. Sometimes an ulcer of the tongue is due to epithelioma ; but if this is the case, the patient will probably be past thirty years of age. As deep syphilitic ulcers heal sclerosis of the tongue may develop. Multiple ulceration of the tongue may be due to tubercular dis- ease, which is very rarely primary, but rather secondary to its pres- ence elsewhere. The sores are often stellate in shape, and there is always swelling of the cervical lymphatics, whereas in multiple syphilitic ulceration of the tongue the glands generally escape. The diagnosis between tubercular ulcer and that due to epithelioma is more difficult, since in both diseases the cervical glands are in- volved. Both are more common in men than in women. The 1 This is denied by Demarquay and doubted by Butlin. THE TONGUE, MOUTH, AXD PHARYNX. 137 age of the patient, the presence of tubercular disease elsewhere, and the absence of induration point to tubercle. The tuberculous ulcer is not surrounded by much inflaaimation, is covered by grayish purulent mucus, and may contain bacilli of tubercle, and is often associated with tubercular nodules, which have not broken down. Ulcers of the tongue may also be due very, very rarely to lupus. A very similar tongue is seen in a tropical disease with intestinal disorder called by Thin " psilosis." An herpetic eruption appears on the tongue, which leaves large areas devoid of epithelium, while sinuous furrows or fissures develop. These fissures then heal, the patches become pallid, and recovery takes place. The various ulcerated surfaces so far described might be confused with ulcerative stomatitis, but their chronic character and insensi- tiveness as compared to acute ulcers of the tongue, asso<;iated with a specific history or manifestations of tuberculosis or syphilis else- where, render the diagnosis clear. An ulcer on the fraenum may be due to whooping-cough, in which disease the edge of the lower incisors may injure the tongue in the paroxysm of cough, or it may indicate the presence of a ragged tooth, which produces constant irritation, or, if the patient is advanced in years, represent the early stages of epithelioma, or that a broken pipe-stem has produced a wound. Very rarely the tongue partakes of the ulceration of the tonsils and roof of the mouth which is seen in cases of Schonlein's disease, accompanied by purjjuric eruptions on the skin and evidences of septicaemia. Should the tongue be marked by bites from the teeth the patient may be an epileptic. Even if he denies that he is affected by the disease, the attacks may be unknown to him, because they are noc- turnal. If the tongue is frequently bitten, the patient may be suf- fering from the early stages of glosso-labio-pharyngeal paralysis.^ The surface of the tongue may be attackwl by various eruptions, such as measles, variola, eczema, herpes, erysipelas, pemphigus, zoster, or hydroa, and from the rupture of the vesicles or bullse so formed ulcers may arise. If the sore is herpetic, de Mussy asserts that the eruption will be found in the distribution of the lingual branch of the chorda tym- j)ani along the under border at the sid(^ ' It may be pointed out in passing that if there be fits, and no biting of the tongue ever occurs, and the patient is a female, the attacks are probably hysterical. 138 THE MANIFESTATION OF DISEASE IN ORGANS. Sometimes the surface of the tongue is here and there devoid of epithelium, and in some of these patches excoriated. Pain may or may not be present. The condition is called chronic superficial glossitis by Hack, and is considered by some to be the same disease described by Kaposi as glossodynia exfoliativa. It is more common in men and lasts many years. Urticaria of the tongue has been reported by Laveran and xero- derma pigmentosum by Keating. The presence of a plaque on the anterior portion of the dorsum of the tongue to one side of the median line, which is raised, not ulcer- ated, but red and irritated-looking, may be due to excessive smoking, the smoke irritating the local epithelium. It is always very smooth, later covered by a yellowish-brown coat, and is sometimes called " smokers' patch." It may extend over the whole tongue and last for years. When the tongue has on its dorsum and edges dull-white or slate- colored dots, patches or lines, which are elevated, hard and horny to the touch, but not painful, the condition is known as leucokeratosis buccalis, or leucoraa or ichthyosis, and this may arise from smok- ing or glass-blowing. It rarely begins in persons under twenty or in those over sixty years. It is often a strong predisposing agent toward cancer of the tongue. These spots are arranged on the tongue in longitudinal lines. Hyde asserts that they are due to excessive keratinization of the epithelium covered by an adherent and dense pellicle. The history is chronic, and ultimately by the stiffness of the spots the tongue may become cracked, and this in turn, perhaps, give rise to carcinoma. When the tongue is covered by smooth, dense plaques and disks or rings, the condition may be lichen planus, but the diagnosis of lichen planus from leucokeratosis buc- calis is difficult, if not impossible. The plaques are most commonly seen in males bctvvcen twenty and forty years. Closely allied to this is the rare condition of hardening of the tongue due to sclero- derma, as described by Kaposi. A very rare condition of the tongue is one in which its surface is marked by rings or areas on the dorsum, which gradually enlarge until they reach the edge or coalesce. In appearance they are red and smooth, deprived of filiform papillae, but not of the fungiform variety. Often the border of the circle is more red than the centre, and the very edge is often yellowish. This condition is sometimes called wandering rash, geographical tongue, or annulus migrans. THE TONGUE, MOUTH, AND PHARYNX. 139 Little if anything is known of its cause, save that delicate children are most often affected. Feeble, sickly children sometimes develop upon the tongue, as well as on the lips and cheeks, a condition in which a tenacious exudation is thrown out, the mucous membrane becoming fissured and sore. Gaston and Sebestre have called this stomatitis impetiginosa. Qildema of the tongue, with the development upon it of vesicles, and, finally, sloughs, may occur, and is probably identical with the foot-and-mouth disease of domestic animals. Bilateral atrophy of the tongue is due to disease affecting the hypo- glossal nerves in some part of their existence in or below the nuclei (see Paralysis of the Tongue). It occurs as a symptom of glosso- labio-pharyngeal paralysis, in which case the tongue is shrivelled and atrophied in patches, and in the later stages of th(^ disease the organ has a crenated appearance. In other cases it is present in progressive muscular atrophy, and rarely in locomotor ataxia. It has also been seen in general paralysis of the insane. Unilateral atrophy may also occur from these causes, and Remak asserts that it sometimes arises from chronic lead-poisoning. Any disease involving the hypoglossal nerves may so result (see Paralysis of the Tongue). In cases where the tongue is much enlarged tiie increase in size may be due to malignant growth, to macroglossia, which is a form of congenital lymphangioma, inflammatory hypertrophy, and syphilis, or acute inflammation from irritant poisons or foods. It may also be due to dermoid cyst, fibroma, lipoma, papilloma, angioma, myx- oma, osteoma, and enchondroma. AVheu it is due to acute glossitis the organ is seen to be several times its normal size, is protruded from the mouth, and marked by the pressure of the teeth. The organ is also clumsy and stiff, and heavily coated on the back por- tion. There is a profuse flow of saliva, and swallowing and speech are almost impossible. Glossitis may also be due to mercurialism, to sej>tic infection, and may be either unilateral or bilateral. The tongue may b • greatly enlarged by actinomycosis, this condition in oldcu times being called angina Ludovici. Great enlargement of tlic tongue may also arise in acromegaly and in myxoedema. In the latter disease the organ is broad, flat, and soft. The movements of tiie tongue depend upon its innervation and its iuuscles, and afford valuable information in diagnosis. The rapidity of its jirotrusion in nervous and excitable persons when they are asked to show the tongue is noteworthv, and its constant rolling 140 THE MANIFESTATION OF DISEASE IN ORGANS. is often seen in persons who are feeble-minded. In all diseases associ- ated with mental hebetude its protrusion on request is very slow, al- though the patient will often do this act when all other orders fail to produce a response. In the various forms of coma due to apoplexy, diabetes, ursemia, aud cerebral cougestion, this coudition obtaius, and it is very characteristic of typhoid fever. Often the tongue which has been partially protruded is left so, even when the patient is told to draw it in. When the patient finds it difficult or impossible to remove food from between the teeth and cheek by means of his tongue, and complains that the power of speech is interfered with, because the tongue is clumsy in its movements, he may be suffering from the disease known as glosso-labio-pharnygeal paralysis or progressive bulbar paralysis. These lingual disorders are often the earliest signs of the disease. More rarely this disability of the tongue may arise from pseudo-bulbar paralysis, or what has been called glosso-labio-pharyngeal cerebral paralysis, a disease in which foci of softening occur in that portion of the cortico-muscular tract in which are the fibres which supply the muscles used in swallowing and speaking. This false type is separated from the true bulbar palsy by its sudden onset, an apoplectiform seizure, and other evidences of cortical disease. The tongue affords the most important points for differential diagnosis when a differential diagnosis is to be made under these circumstances, for in the false disease it does not waste or develop the reactions of degeneration, whereas in true bulbar paralysis these changes always speedily develop. Paralysis of the Tongue. In apoplexy the tongue is protruded toward the paralyzed side as it is also in the condition already described of hemiatrophy. The lesions of the hypoglossus which produce paralysis may be of cortical origin (unilateral), in which case the hemorrhage or other injury may be situated where the middle aud inferior frontal convolutions form the anterior central convolution,^ or in the supra-nuclear tract between the cortex and the medulla, or in the hypoglossal nucleus, or, again, in the infra-nuclear tract within the medulla. Insular sclerosis may very rapidly cause lingual paralysis. Paralysis of the tongue may also result from injury to the hypo- glossal fibres outside the medulla through meningitis or syphilitic or other growths. In still other cases pressure upon the nerve in its foramen may cause unilateral paralysis, or wounds of the neck, caries 1 This is probably a fact, but not yet confirmed by autopsy, unless we consider Edinger's case of softening under this area, which affected the tongue only, as a typical one. THE TOXGUE, MOUTH, AND PHARYNX. 141 of the first cervical vertebrte, or cervical tumors may so result. Often in such a case the spinal accessory nerve is also involved. Very rarely, indeed, the tongue may be paralyzed by a hypoglossal neuritis (Erb). In rare instances hemiatrophy of the tougue is associated with hemiatrophy of the face without hypoglossal injury (Gowers). Girard asserts that the sensory part of the trifacial contains trophic filaments for the tongue, and that unilateral wasting may be due to disease of this nerve. In paralysis of the facial nerve the tongue may be partially paralyzed through the fact that the lingualis muscle is supplied by means of the chorda tympani nerve. When a tongue which is paralyzed unilaterally is retained in the mouth, it is seen that its root on the paralyzed side is higher than the other, owing to the paralysis of the posterior fibres of the hypoglossus, but when it is protruded the tongue goes toward the paralyzed ^ide because it is pushed out by the fibres of the genio-glossus muscle on the well side. Finally, let us remember that if the tongue is paralyzed on one side the lesion is in the cortex or the ])ons on the opposite side of the body, or in the nucleus in the medulla on the same side of the body, or in the nerve after it has left the medulla. If it is bilateral paralysis the lesion is ])robably nuclear, because the nuclei are so closely situated that even a small lesion involves both of them, or it may be due to symmetrical disease of both sides of the cortex, the so-called pseudo-bulbar paralysis already spoken of. It should not be forgotten that paralysis of the tongue may occur as the result of diphtheria, Hirt asserts that the reaction of degeneration may be found in the tongue whether the lesion be cortical or in the nucleus. If the lesion is only cerebral this reaction will probably apjiear very late. A tremor seen in the tongue may indicate a variety of nervous ailments or severe acute disease, as in typhoid and other severe infectious diseases, but the freedom from excessive coating and the absence of the ordinary signs of acute illness will separate the case of tougue tremor of acute disease from the tremor representing nervous ailments. An important point to be regarded in noting lingual tremor is whether the tremor or fibrillary movement is constant, or whether it appears only when the tougue is moved to and fro or protruded. In tyj)hoid fever the tremor occurs on movement, whereas in glosso- Inbio-pharyngeal j)araly8is when the mouth is opened fibrillary movements of the organ are often marked, while the organ lies in 142 THE MANIFESTATION OF DISEASE IN ORGANS. the floor of the mouth powerless and beyond the control of the patient. Tremor of the tongue is also seen in a marked form in many cases of alcoholism, and associated with this tremor it will be noted that the protrusion of the organ is uncertain or in jerks. Spasm of the tongue may be unilateral or bilateral, most com- monly the latter. It is seen very commonly in cases of chorea, par- ticularly of the post-hemiplegic type, and in hysteria. In the first disease the movements are characteristically choreic. In the latter the spasm may be tonic or clonic or alternately tetanic and irregular. Often the spasm in hysteria is unilateral. Sometimes it is clonic in puerperal melancholia. Spasm of the tongue is a common symp- tom in association with the twitching of the lips of general paral- ysis of the insane. Jerky movements of the tongue may also occur in insular sclerosis, but this is not the cause of the peculiar speech of that affection. Very rarely the condition of lingual spasm is due to irritation of the hypoglossus by some cause as yet unknown. The tongue is darted in or out or thrown from side to side and often injured by the teeth. The spasms, as a rule, are not constant, but come on in attacks which closely resemble epilepsy, in that they are preceded by an aura (Remak and Berger). A very rare affection termed aphthongia (Fleury) is characterized by spasm of the tongue on attempting to speak. Romberg has recorded a case of lingual spasm due to irrita- tion of the fifth nerve from lingual neuralgia. In that very rare condition called '^ Thomsen's disease," " charac- terized by tonic spasms in the muscles during voluntary movements," the tongue may be involved, but in this case the other voluntary muscles will share in the affection. Having considered the diagnostic significance of changes in the appearance of the tongue in this chapter, and of the appearance of the lips in the chapter on the Face and Head, there is yet to be dis- cussed the condition of the buccal mucous membrane, the tonsils, the soft palate, the teeth, the upper part of the pharynx, and the post- nasal spaces. As almost all the conditions found in the latter regions are of interest to the rhinologist rather than the general practitioner, only one or two affections of these parts will be included in this work. Swelling and redness of the buccal mucous membrane occur in the various mild forms of stomatitis, and in the ulcerative type of this disease the more severe lesions are often found in this area. In the malignant ulcerative stomatitis called noma the slough which THE TONGUE, MOUTH, AXD PHARYNX. 143 separates from the inside of the cheek leaves a large excavation which may become so deep as finally to perforate the cheek. It is interesting to note that swelling of the cheek with great in- flammation of the buccal mucous membrane is sometimes seen as the result of the formation of a salivary calculus in the duct of Steno, and it is also stated that obstruction from inflammation of this duct often occurs as a result of poisoning by sulphuric acid. Again, in that rare disease called Schonlein's disease, or true peliosis rheumatica, the writer has seen a case, in which, in addition to the multiple arthritis, purpuric eruption, and great oedema, the formation of a large ulcer or slough threatened to perforate the cheek, and in healing produced a cicatrix which interfered with the patient's ability to open the mouth. This patient was an adult. If a patient presents himself to the physician with the statement that he is suffering from general pains all over the body, particu- larly in the srcall of the back, quite iiigh fever it may be, with much sore throat and difficulty in swallowing, the trouble in the majority of cases will be, in the adult, tonsillitis of the follicular form. If the symptoms are exceedingly severe, the inflammation may result in suppuration — suppurative tonsillitis. It is to be remembered in all cases that the systemic or constitutional disturbance is out of all proportion to the severity of the local lesions. If it is tonsillitis, the glands can be felt in the majority of cases a little beneath and for- ward of the angle of the jaw, and pressure upon them may produce considerable pain. If tl)e mouth is well opened and the tongue de- pressed, there will be found on each side of the throat a large pro- jecting and inflamed mass, in the depressions or follicular openings of which will be found a white or yellowish exudate, which in severe cases may spread over the surface of the gland till it slightly resem- bles the membrane of diphtheria. Pressure on the tonsil may cause the furt'icr |>r()JH;tion of these cheesy-looking masses. In the suj)purative form of the disease the surface of the gland may be smooth and reddened, and in a day or two become soft and fluctuating, and if lanced pus will escape. The severe constitutional disturbance, the soreness of the throat, difficulty in swallowing, and the Ibllicular exudate call to mind in all such cases the possibility of the disease being diphtheria; but in tonsillitis the exudate can be easily removed without leaving a bleed- ing surface i)ehind it, and it has not the dusky, dirty look of diph- theritic membrane. Again, in tonsillitis the exudate is seen on the 144 THE MANIFESTATION OF DISEASE IN ORGANS. tonsils only, whereas in diphtheria it spreads over the half-arches and uvula. The general symptoms may make one suspect the onset of scarlet fever, particularly if the patient be a child ; but the exam- ination of the throat in scarlet fever shows the intense redness of the pharyngeal mucous membrane with comparatively slight enlarge- ment of the tonsils. The lymphatic glands of the neck may be enlarged in scarlet fever, but are rarely so in tonsillitis. If the patient first complains of dysphagia, and, on examination, the pharynx is red, and the tonsils are covered with patches which speedily spread, as just described, so that by forty-eight or seventy- two hours the tonsils, pillars, and soft palate are covered by a gray membrane, the case should always be diagnosed as diphtheria, and treated as such unless a bacteriological examination of the exudate shows the infection to be due to a streptococcus aud not to the Klebs- Loeffler bacillus. Even if the patient has not true diphtheria he may be exceedingly ill. Again, it is to be remembered that while most of the cases of scarlet fever which present a membranous pharyngitis or tonsillitis are due to the streptococcus and not to the Loeffler bacillus, that in a certain proportion of these cases the two diseases, diphtheria and scarlet fever, exist simultaneously. Rarely a false membrane due to streptococcus infection, or still more rarely to the diphtheria bacillus, complicates the course of typhoid fever. If in any case of dipiitheria the false membrane extends to the nasal chambers, the prognosis is very unfavorable. Ordinary sore throat or acute pharyngitis is generally accompanied with little systemic disturbance, the local pain and soreness being the most characteristic symptoms. Inspection will show the pharyn- geal wall red and angry-looking and very likely unduly dry. Care should always be taken, in the case of children particularly, that the early sore throat of measles and scarlet fever is not taken for simple pharyngitis. Often the rash of measles can be seen on the pharyngeal wall some hours before the rash appears on the skin. Sometimes cases are seen in which there are tonsillar pain and irritation, in which careful examination proves the discomfort to be due to the presence of a small calculus in a follicle of the tonsil. When swelling of the tonsils is chronic the enlargement of these bodies may produce mouth-breathing, with the peculiar facies of that habit, deficient thoracic and general systemic development, and a peculiar cough, constant in character and worse at night. Often the THE TOXGUE, MOUTH, AXD PHARYXX. 145 swollen 01" enlarged glands extending across the pharynx actually touch one another (see illustration in chapter on Face). Finally, we can sometimes gain some information from the teeth as to the state of the patient. In children who are sufferers from rickets the teeth decay very early and rapidly, and if they be sufferers from inherited syphilis, the teeth are often cut in the early months of extrauterine life. Caries of the teeth to an undue extent is also seen in many preg- nant women and in cases of diabetes mellitus. If the permanent upper incisors are notched or pegged-shaped with notches in the free edge, as if cut out with a small gouge, they are a fairly sure indication of syphilis of a hereditary character (Hutchinson teeth), and if in association with this deformity of the teeth we find middle-ear catarrh and keratitis, we have the ''syph- ilitic triad," which is infallible as a sign of hereditary syphilis. These notches are not found in the so-called milk-teeth. Fig. 57. Hutchinsou teeth. The staining of teeth by tobacco or other materials held in the mouth may reveal certain habits of the patient, and a blue-line on the gums where they join the teeth will be an indication of the pres- ence of chronic lead-poisoning. Loosening of the teeth with bleed- ing, spongy gums should call to the physician's mind the possibility of scurvy or scorbutus, and the spongy gums are particularly indica- tive of this affection in bottle-fed babies. If it occurs in adults, it may be due to mercurial salivation. 10 CHAPTER YI. THE EYE. The general diagnostic indications atibrded by the eye — Diplopia and disorder of the external ocular muscles — Strabismus and squint — Disorder of the internal ocular muscles — The pupil — Hemianopsia — The visual fields — Color-vision — The optic nerve and its lesions — Eetinitis — Amblyopia and blindness. The eye affords more information for diagnostic purposes con- cerning the condition of other organs of the body than any single part which can be examined. We gather from it not only a clear idea as to its own state, and the state of the nervous centres more or less intimately connected with it, but in addition we often gain positive information as to the condition of organs more remotely situated, as, for example, the kidneys. The parts of the eye which give us the greatest amount of knowledge about changes in other tissues are the optic nerve and retina, and the ocular muscles. The crystalline lens, the conjunctiva, and cornea often give addi- tional evidence indicating the general systemic condition. Promi- nence of the eyeball or exophthalmos is seen as an almost constant symptom of true goitre, which for this reason is called exophthalmic goitre. Associated with the bulging eyeball we find more or less enlargement of the thyroid gland, an irritable heart, and a very rapid pulse, throbbing carotid arteries, marked general nervousness, often mental depression, and insomnia. In well-marked or ad- vanced cases of exophthalmic goitre we often have a condition in which the upper eyelid does not follow the eyeball in its downward movement. This is sometimes called ^' Graefe's symptom." Again, there may be almost total absence of winking as an involuntary act, " Stell wag's symptom." On examining the exterior of the eyeball we often notice a grayish ring along the junction of the cornea and sclera. It possesses when a complete ring but little significance, except age ; but if it is but the segment of a ring or in two segments, one above and the other be- low the cornea, it is a true arcus senilis, and indicates in some cases fatty degeneration of the tissues of the body. The one is an annulus THE EYE. 147 senilis, the other an arcus senilis, and the arcus is the change worthy of note, although clinicians deny that either has any significance. In addition to these objective symptoms wc have also a very im- portant set of signs connected with the ocular muscles, external and internal, as manifested by the various forms of strabismus or changes in the ])upil and accommodation of the eye, by the ptosis already discussed in the chapter on the Face, and in nystagmus and ocular spasm. Beyond this, too, we have two other ocular symptoms sub- jective in nature, namely, diplopia or double vision and partial or complete blindness. Diplopia depends upon the fact that in an eye in which the mus- cles are abnormal in their function the image which falls upon the fovea, or visual acuity spot of the retina, in the well eye fails to fall upon the same spot in the weak eye. To the well eye the object ap- pears to be in the direction in which the eye is turned, whereas to the weak eye it appears to be in another direction. As a result, the mind gets the impression of two objects instead of one. The im- pression made on the well eye is the '' true image" as it is called, and that in the diseased eye is called the ''false image." Any cause which interferes with the fixation of each eye on the same point pro- duces diplopia, and, as the eyes are normally directed to the object fixed by the ocular muscles, paralysis of any one of these muscles produces diplopia when the axis of one eye is deviated from the point of fixation, because the eye on one side is not properly moved by reason of the fact that one muscle has failed. Diplopia is ordi- narily a constant sign of ocular muscle paralysis ; but if only weak- ness or insufficiency of a muscle is present, diplopia may never be a symj)tom recognized by the patient. The forms of diplopia — that is, the position of the false images in res})ect to the true images — vary with the muscles afPected, and will be studied in a moment when paralysis of the muscles is tested for and their diagnosis discussed. It only remains at this j)lace, therefore, to point out the probable significance if a patient with diplopia is presented to a physician. Thus, a patient with diplopia may be sulTcring from a lesion in the cerebral cortex, such as hemorrhage, sclerosis, or softening ; or from a lesion in the cranial nerve nuclei, in the ])ons or corpora quadrigemina, or in the fascicular fibres. Again, dij)lopia may arise from lesions at the base of the brain, as meningitis, tul)orcular or syphilitic, or from injury to the nerves in the orbit or in their pcriph- ia in any disease wliicli 148 THE MANIFESTATION OF DISEASE IN ORGANS. may affect these parts, and it is quite a comraou symptom in loco- motor ataxia, in Friedreich's ataxia, and in paretic dementia. Probably it is seen most commonly in ataxia, and with it, as the oculomotor nerve in its branch supplying the levator palpebrse is particularly apt to be paralyzed in this disease, we may find ptosis. Diplopia is also found in cases of ptomaine-poisoning, and in poisoning by belladonna, spigelia, conium, and gelsemium, owing to their effects on the ocular nerves. The differential diagnosis between the various lesions producing diplopia is to be made by the other symptoms and the history of the case. Paralysis of Ocular Muscles, As something has already been said in the chapter on the Face and Head of the diagnostic import of paralysis of the ocular muscles in connection with the subject of ptosis, a further consideration of the abnormal changes in their func- tions will be discussed first in the preseut chapter.^ Before doing so, however, it is necessary to describe the methods resorted to for the purpose of demonstrating or determining departures from the normal in these muscles. In the first place, it must be clearly under- stood that the function of the extrinsic muscles of the eyeball is to direct the ball toward the object at which the patient desires to look, and they also evenly balance one another to keep the eye steady in its axis. Thus, the external and internal rectus muscles maintain the horizontal equilibrium of the eyeball. If the internal rectus is completely paralyzed in one eye, we have developed a unilateral external squint, the eye looking toward the outer side of the orbit ; and if the external rectus fails, the eyeball is turned toward the nose. If these muscles are affected in both eyes, we have a divergent squint in the first case and a convergent squint in the second. Not only do the muscles of each eyeball govern the eye- movements of that side, but by the nervous centres governing the eye-muscles the two sets of eye-muscles are co-ordinated, so that they move as one organ in health. Just here it is well for the reader to make a clear distinction between concomitant and paralytic squint, for they are two very different things in origin, symptoms, course, and prognosis. A con- comitant squint is a wrong relation of the visual axes, so that they do not intersect in the point looked at ; but there is no marked (.1 In the preparation of this chapter free use has been made of the article of my friend, Dr. de Schweinitz, on " Diseases of the Cranial Nerves," in Dercum's Nervous Diseases. THE EYE. 149 limitation of the movements of either eye iu any direction. Be the direction of the eyes what it may, the squiut remains practically un- changed. Further, if the fixing eye is covered, the other eye promptly fixes, and the covered eye deviates without the patient altering the position of the eye (Jackson). On the other hand, paralytic squint is the deviation which takes place when the attempt is made to turn the eyes in certain directions by means of the muscles which are paralyzed in whole or in part. When the attempt is made, the eye with the sound muscles turns as it should, while the eye with the paralyzed muscle hangs back, beginning to deviate as the eyes are turned, so that this muscle is required to perform its func- tion, and deviates more as greater effort is required. The degree of squitit and of separation of the double images it causes varies with the direction in which the eyes are turned, there bdng none at all in certain directions. We examine the functional activity of the ocular muscles by the following measures : The patient is told to look at the tip of a pencil or the tip of the finger of the physician, held about three feet from his face. This ol)ject is then gradually brought nearer and nearer to him, and the eyes of the patient necessarily converge more and more as it approaches the nose. Normally the eyes will be co-ordinately converged when the object is only three and a half inches from them; but if any weak- ness or insufficiency of one internus is present, the eye on that side will deviate or fail to converge before this point is readied. Again, a fine point like a pin-point is held about eight to ten inches from the eyes and below the horizontal, and one eye is cov- ered by a card or the hand. If the eye which is separated from the object by the card deviates inward, it indicates insufficiency of the external rectus. If, on the other hand, it deviates outward, it shows insufficiency of the internal rectus. On sudden removal of the card the eye at ouje sprinij;s back into place for the piu'pose of fixing upon the object, and " in general terms each millimetre of movement deviating from the fixation-point corresponds to what is called two degrees of insuffi('ien(;y, as measured by prisms" (iiandall). If the internus is insufficient, and the covered eye moves in to fix in several distinct impulses, each impulse should be multiplied into the foregoing result. A very useful, and the simj)lcst, apparatus for testing the func- tional l)alance of the ocular nniscles is the rod-test of Maddox. 150 THE MANIFESTATION OF DISEASE IN ORGANS. A cell in which is mounted a transparent glass rod is placed in a trial frame, which is then placed in front of the eyes. If the hori- zontal deviation is to be determined, the physician must '' seat the patient at six metres from a small flame, and place the rod hori- zontally before one eye, a colored glass before the other. If the line passes through the flame, there is orthophoria ("equipoise), as far as the horizontal movements of the eyes are concerned. Should the line lie to either side of the flame, as in most people it will, there is either latent convergence or latent divergence : the former, if the line is the same side as the rod (homonymous diplopia) ; the latter, if to the other side (crossed diplopia)." (Maddox.) (Fig. 58.) Fig. 58. A B C BM Maddox's rod-test for horizontal deviation. The rod is before the right eye. A. The line passes through the flame — orthophoria. B. The line passes to the right of the flame — latent convergence, or esophoria. C. The line passes to the left of the flame— latent divergence, or exophoria. (de Schweinitz.) When the vertical deviation is to be estimated the rod is placed vertically in the flame. If the patient states that the horizontal line of light passes directly through the flame, the vertical balance of the eyes is normal ; if, on the other hand, the Hue is above the flame, there is a tendency to upward deviation of the naked eye ; but if the line is below the flame, there is upward deviation of the eye covered by the rod-test. (Fig. 59.) Testing of this kind refers to the insufiiciencies and not to the palsies of the ocular muscles. The importance of being able to demonstrate these minor failures THE EYE. 151 in the ocular muscles by these meaus lies in the fact that in this manner headaches due to muscle eye-strain may be remedied by re- moving their cause by properly fitted glasses, or by gymnastic ex- ercises with prisms, or in some cases by tenotomy. Fig. 59. B Maddox's roil-test for vertical deviation. The rod is before the right eye. A. The line passes through the flame— orthophoria. B. The line passes below the flame. The upper image belongs to the left eye— right hyperphoria. C. The line passes above the flame. The upper image belongs to the right eye— left hyperphoria, (de Schwein'itz.) Where there are marked palsies of the ocular muscles there is usually some poison exercising its effects upon their nervous centres or the nerves themselves, or there is some central nervous lesion affecting the centres governing these muscles in the cortex, or there is a lesion in the nuclei or fasciculi, or, again, there may be lesions in the basal ganglia, or in the course of the fibres of the nerve be- tween the nucleus and the eye, or in the orbit or nerve-endings. The signs of paralysis of the ocular muscles consist in the follow- ing symptoms : Diplopia, which is due to the failure of the images to fall on the corresponding ]K)ints in each retina. This diplo]>ia i)ecoiiK'S more and more marked as the object i.s moved toward the side on which rhe paralyzed mu.scle lies. Strabismus, which may or may not be constant, u.siially develops when the j)atient en- deavors to turn his eyes in the direction of the paralyzed muscle. Vertigo, which is due to the diplopia, or, if the well eye is closed, to an erroneous localization of the objects in the field of vision. Altered carriage of the head, due to the fact that the patient tries to turn his head in the direction in whicli he is least troubled by double 152 THE MANIFESTATION OF DISEASE IN ORGANS. images ; that is, he obtains the natural fixation-point of the weak eye, and then adjusts the well eye accordingly. If the paralysis of the ocular muscle be complete, the squint and the loss of movement of the muscle which ia paralyzed will usually enable the physician to find out the paralyzed muscle ; but if there be only a partial paralysis or paresis of an ocular muscle, then squint is not necessarily present, and the diagnosis of the part affected must be made by a study of the double images. This is made by placing before the patient, at a distance of from three to five yards, a candle on the same level as his eyes. One eye is covered by a piece of red glass, so that the patient can readily dis- tinguish between the images. The lighted candle is then moved from the middle of the patient to the right and left, and the relative positions of the red and white images noted. Then the candle is moved up and down, and the results recorded. These operations having been recorded, it is to be remembered that diplopia is most marked and sometimes only appears when the patient turns his eyes in that direction which calls into play the aifected muscles, no Fig. 60. Paralysis of left abducens in a case of hemiplegia of syphilitic origin. (Dercum.) diplopia being present if other muscles are used. Again, the image which belongs to the affected eye is projected in the direction toward which the paralyzed muscle normally turns the eye, and, finally, the distance of the double image increases when the eyes are turned in the direction of the action of the paralyzed muscle, or, in other words, that image is false and belongs to the affected eye which in THE EYE. 153 the region of diplopia moves faster than the moving test-object — that is, the candle-flame. If we place a candle several yards (say three to five) in front of a patient suffering from paralysis of the external rectus (Fig. 60) and at the level of his eyes, the double images of two candles will appear as in Fig. 61, if he has complete paralysis of the external rectus or Fig. 61. Fig. 62. k The false image is in outline. internal squint of the left eye ; while if the right extertfal rectus is paralyzed, the images will appear as in Fig. 62. Further, if the ob- ject is moved to the right in the first condition, the false and true candle separate further and further ; whereas if the left externus is involved and the object is moved to the left, the same separation takes place. This condition is called homonymous diplopia, because the word homonymous indicates that the false image is seen on the same side as the eye affected. Fig. 63. Fig. 64. Fig. 65. Fig. 66. A The false image is in outline. If, on the other hand, the false image i.s found to the right of the true one, as in Fig. 63, the internal rectus of the left eye is paralyzed, and causes an external -S([uint if the paralysis is complete; and if this same muscle of the right eye is affected, the false image will also be to the left side of the true one. (Fig. 64.) Further, if the ol)ject is moved to the right in tlie first case, the two images separate more and more widely ; or if the right internus is involved, and the object is moved to the left, the same thing occurs. This is called crossed diplopia, because the image of the right eye appears on the left side, and the image of the left eye appears on the right side 154 THE MANIFESTATION OF DISEASE IN ORGANS. Supposing, again, that the images are seen as in Fig. 65, then the left superior rectus is involved (downward squint); Avhile if they appear as in Fig. Q^, the right superior rectus is affected. This diplopia occurs chiefly in the upper field, because, according to a rule already given, diplopia is most manifest in that portion of the field of fixation toward which the paralyzed muscle commonly rotates the eye. Fig. 67. Fig. 68. The false image is in outline. If the images appear as in Fig. 67, the left inferior rectus is affected; or if as in Fig. 68, the right inferior rectus muscle. This is also crossed diplopia, chiefly in the lower field, because the inferior rectus muscle rotates the eyeball downward. Again, if the images appear as in Fig. 69, the left inferior ob- lique muscle is paralyzed, and there will be inward and downward squint; if the right inferior oblique is affected, the images will be as in Fig. 70. There is a homonymous diplopia most marked in the upper field. Fig. 69. Fig. 70. Fig. 71. Fig. 72. The false image is iu outline. If due to paralysis of the left superior oblique, the images appear as in Fig. 71; and if, as in Fig. 72, the right is affected. There is an upward and inward squint, and there is a homonymous diplopia chiefly in the lower field. Finally, if there is divergent squint with failure of movement in all directions, except outward and slightly downward, and there are THE EYE. 155 ptosis, moderate mydriasis, and paralysis of accommodation, there are oculomotor paralysis and crossed diplopia. The followiug table of Hotz (Internalional Clinic, vol. iii., 4th series) summarizes the facts as to the diagnosis of the conditions producing strabismus : I. Lateral diplopia indicates paralysis of an internal or external rectus. 1. Homonymous diplopia indicates paralysis of an external rectus. a. Images separating to the right indicate paralysis of the ex- ternus of the right eye. b. Images separating to the left indicate paralysis of the externus of the left eye. 2. Crossed images indicate paralysis of an internus. «. Images separating to the right indicate paralysis of the internus of the left eye. b. Images separating to the left indicate paralysis of the internus of the right eye. II. Vertical diplopia in the upper field indicates paralysis of the superior rectus or inferior oblique. 1. Homonymous images indicate paralysis of the inferior oblique. a. Image of right eye higher means paralysis of the inferior ob- lique of the right eye. b. Image of right eye lo^ver means paralysis of the inferior ob- lique of the left eye. 2. Crossed images indicate paralysis of the superior rectus. a. Image of right eye means paralysis of the superior rectus of the right eye. b. Image of right eye lower means paralysis of the superior rectus of the left eye. III. Vertical diplopia in the lo\ver field indicates paralysis of the inferior rectus or superior oblique. 1. Homonymous images indicate paralysis of the superior ob- lique. (I. Image of the right eye higher means paralysis of the superior obi i( [lie of the left eye. 2. Crossed images indicate paralysis of the inferior rectus. (I. Image of the right eye lower means j)aralysis of the inferior rectus of the right eye. b. Image of the right eye higher means [):iralysis of the inferior rectus of the left eye. 156 THE MAXIFESTATION OF DISEASE IN ORGANS. o It is exceedingly difficult, however, always to localize exactly the affected muscle, a difficulty which is much increased when more than one is paretic, the paresis being of different degrees. Having now considered the means of determining that the mus- cles are defective, we must determine the diagnostic indications pre- sented by this examination. In other words, we must seek the cause of the paralysis or loss of power. Paralysis of the ocular muscles may be due to a lesion in oue of several places. Thus it may arise in hemorrhage, sclerosis, and soften- ing of the cerebral cortex, in which case the other symptoms of lesions iu those parts will be present as in apoplexy, disseminated sclerosis, or meningeal disease. Or it may depend upon lesions in the fasciculi between the cortex and the nuclear origin of the nerves, as in the crus. (This is rare.) Or, again, it may be due to lesions in the nuclei. If this be the case, we have developed ophthalmo- plegia,^ or paralysis of all the ocular muscles supplied by the third, fourth, and sixth nerves. This nuclear paralysis is divisible into two classes, the acute and chronic. Sometimes it is called acute and chronic nuclear palsy. The acute form is sudden in its onset, all the ocular muscles losing power. With the onset of the attack there may be fever, vomiting, and even convulsions. Such an attack results from minute hemorrhage among the nuclei, or from an acute hemorrhagic polioencephalitis in the fourth ventricle, aris- ing from syphilis, tuberculosis, ptomaine-poisoning, alcoholic and sulphuric-acid-poisoning. Such cases are usually rapidly fatal. A less fatal form follows injuries, and the effects of nicotine, lead, car- bonic acid, or such diseases as diabetes, syphilis, and epidemic influ- enza. Sometimes acute ophthalmoplegia comes on with acute polio- myelitis or acute bulbar paralysis. Chronic nuclear paralysis is gradual in its onset, muscle after muscle failing, and even ptosis coming on. Sometimes after a cer- tain degree of paralysis is reached the disease comes to a standstill. The trouble may be unilateral or bilateral, and is often unsymmetrical, and it results after acute ophthalmoplegia, as a congenital defect pro- ducing bilateral ptosis (see chapter on Face), as an acquired disease in childhood and adult life, and in conjunction with locomotor ataxia, paretic dementia, disseminated sclerosis, progressive muscular atro- 1 Ophthalmoplegia is here applied in its strict sense. The word is often used to signify loss of power in individual eye-muscles; and while its use in hoth ways is correct, it is better to confine its usage to nuclear and complete lesions. THE EYE. 157 phy, chronic bulbar paralysis, and in connection with paralysis of the frontalis and orbicularis palpebrarum, which are innervated by the facial nerve. The cause may be tuberculosis or syphilis, but in some cases no cause can be found. If the cause of the paralysis of one or two muscles be basilar lesions, these may arise from hemorrhage, pachymeningitis, menin- gitis, both simple and tubercular, chiefly the latter ; purulent men- ingitis, abscess as the result of middle-ear disease, and anaemia. It may also arise as the result of obliterating arthritis, particularly in syphilitics, and from tumors. In children sudden convergent stra- bismus and diplopia are often among the earliest symptoms of tuber- cular meningitis at the base. If the cause be in the nerve-trunks themselves, the lesion will probably be cellulitis, tenonitis, hemorrhages in the orbit, or fract- ures of the orbit ; or, again, there may be disease of the frontal sinus. If the lesion is distinctly peripheral, it may be due to rheumatism (when the external rectus is commonly affected), neurasthenia, or it may arise from uric-acid diathesis and gout. Further, such lesions may be due to influenza, diabetes, diphtheria, lead and alco- hol, or any one of the drugs which paralyze the ocular nerves. So much for general statements as to the common and possible sites of the lesions producing paralysis of the ocular muscles. We can now go further than this and locate the lesion more accurately from the knowledge we have gained as to the particular muscle affected and the other symptoms presented by the case. Let us suppose that a patient suffering from ])aralytic internal squint, or a diplopia which indicates paralysis of the external rectus, presents himself to the physician^ what diagnostic significance has this symptom ? ' In the first place, it is to be remembered that the external rectus receives its nerve-supply from the abdncens, or sixth nerve, which arises from the pyramidal body close to the pons. (Fig. 73.) Its deep origin is a nucleus under the floor of the fourth ventricle. The nerve pierces the dura mater on the basilar surface of the sphenoid bone, passes through the dinoid process, enters the cavernous sinus, and, finally, enters the orbit through the sphenoidal fissure between the heads of the external rectus. If this form of squint is :isso- ciated with honnplegia of the oj)|)nsite side of the body, the lesion > This refen to paralytic and not to concutnitant squint. 158 THE MANIFESTATION OF DISEASE IN ORGANS. is in the pons on the same side as the affected eye and the opposite from the hemiplegia, because the eye-fibres have crossed higher up, but the motor tracts for the limbs cross lower down. Fig. 73. d Co. The base of the brain and the cranial nerves, crura, pons, and medulla. (Allen Thompson.) I to XII. The cranial nerves, fh. Optic thalamus, h. Pituitary body. tc. Tuber cinereum. a. Corpora albicantia. P. Pes pedunculi. i. Interior e. Exterior geniculate body. Pc. Pons Varolii, pa. Anterior pyramid of medulla, o. Olive, d. Decussation of anterior pyramid. ca. Anterior column of spinal cord. cl. Lateral column of spinal cord. Ce. Cerebellum . fl. Flocculus of cerebellum. VI. The sixth or abducens nerve. On the other hand, if there is no monoplegia and abducens palsy (internal squint) on the same side of the body, the lesion is in their point of origin in the cortex, or, in other words, the lesion has taken foci above the point where the tracts cross. Such a paralysis is, therefore, cortical. THE EYE. 159 If, again, there is complete unilateral paralysis of the abducens (internal squint), with loss of the associated action of the iuternus, the lesion is in the nuclei under the floor of the fourth ventricle, be- cause the nuclei of the third and sixth cranial nerves are closely connected, so that a lesion involving the sixth nucleus weakens the nucleus of the third nerve. (Fig. 74.) Complete paralysis of the externus may, therefore, be due to a nuclear lesion; for if the lesion were above the nucleus, this nucleus might obtain collateral impulses, as seen iu this diagram, and, therefore, the paralysis would only be Fig. 74. "OfPW^ Cochlea Semiciicidar Canals Diagram of the couuectioiis ot the nucleus of the sixth nerve. (Bkuce.) partial. It may al.so be due to a peripheral lesion. Sometimes, however, an inHammatory process pressing upon the basilar surface of the sphenoid, and thereby involving the nerve, may cause a similar effect. Loss of power of the external rectus may also arise from neui'asthcnia, uric-acid diathesis, gout and rheumatism, and in tu- bercular or >yphilitic meningitis at the base, as already statctl. It also comes on in some cases of diabetes, la grippe, and in chronic poi-oniiig by lead and alcohol, or the acute poisoning of gelsemiura, ptomaine-poisoning, conium- and spigelia-poi.^oning. Again, let us suppose that the internal rectus is paralyzed, causing 160 THE MANIFESTATION OF DISEASE IN ORGANS. external squint. We remember that it is supplied by the oculomotor nerve, which arises from a nucleus in front of the corpora quadri- gemina, which extends from the level of the posterior commissure to a point near the nucleus of the fourth nerve or patheticus. (Fig. 73.) Landois states that these two nuclei (the third and fourth) are united. The nucleus of the oculomotor nerve has been divided into several groups, as shown in Fig. 75, after Bruce, where, however, it is seen Fig. 75. Scheme of the segments of the nucleus of the third nerve and their relations to each other and to the nucleus of the fourth nerve, in. R. Third nerve, m. Median nucleus, a. Anterior nucleus, interior part. Aj. Anterior nucleus, lower part of main nucleus. Ao. Anterior nucleus, intermediate portion. A3. Anterior nucleus, upper portion, p.i. Postero-internal nucleus, p.e. Postero-exterual nucleus, e. External nucleus, s. Superior nucleus. Some of the root-fibres from the lower and intermediate parts of the anterior nucleus are repre- sented by dotted lines as crossing to the opposite side. iv. The nucleus of the fourth nerve. iv.R.i, iv.R.o, IV. R. 3. The first, second, and third portions of the root respectively. (Bruce.) that the third and fourth nuclei are not united. The nerve itself pierces the dura mater below the posterior clinoid process, passes along the outer wall of the cavernous sinus, and after dividing into two branches enters the orbit through the sphenoidal fissure. The upper branch supplies the superior rectus and the levator palpebral, and the lower one after dividing into three branches supplies the internal rectus, the inferior rectus, and the inferior oblique muscles. THE EYE. 161 The oculomotor nerve receives filaments from the cavernous plexus of the sympathetic, and from the first division of the fifth nerve. In addition to divergent squint there is, as already pointed out in the last few pages, in oculomotor paralysis, as additional symptoms, ptosis, mydriasis, and paralysis of accommodation. The lesion pro- ducing unilateral ptosis may be found in the cerebral cortex on the opposite side from the affected eye in the angular gyrus just below the interparietal fissure. Again, tubercular or other degenerative disease of the corpora quadrigemina may cause double ptosis. If the patient has ptosis with preservation of the function of the intraocular muscles (that is, partial oculomotor paralysis), with hemiplegia of the opposite side of the body, the lesion, according to Mauthner, probably affects the fascicular fibres — that is, those between the cortex and the nuclei. There may be associated with this form of oculomotor paralysis loss of power in the hypoglossal and facial nerves. On the other hand, if the oculomotor paralysis is complete, the lesion is almost certainly at the base of the brain, and this diagnosis becomes practically certain if there is associated with it paralysis of other cranial nerves. Paralysis of the oculomotor nerve on one side with hemiplegia on the opposite side of the body is not positively a crus or fascicular lesion unless the paralysis occurs simultaneously. (Hughlings Jackson.) If, however, there be double oculomotor paralysis, the lesion is bilateral and probably due to a lesion at the base, as meningitis or arteritis; or to an infiammatory exudate involving both nuclei ; or, again, to diphtheritic poison or the lesions of tabes dorsalis. If that very rare form of ocular muscle paralysis, namely, iso- lated palsy of the fourth trochlear nerve, is present, we will probably iind that the j)aralysis is due to a lesion at the base of the brain, due to meningitis, or the pressure of a growth. Supposing, however, that a patient j)resents himself with swelling of the eyelids, exophthalmos, a contracted, followed by a dilated, pupil, aniesthesia of the skin of the upper eyelid and of the temple, or the area su|)plied by the first division (ophthalmic) of the fifth nerve, and ophthalmoplegia — that is, paralysis of the extrinsic ocular mus(,'leson one side — where will be the lesion productive of" this train of interesting symptoms? It will be seen at once that such ai'ondition is the restdt of paralysis of the oculomotor (third), pathetic (fourth), and ai)ilucens (sixth) nerves, and that as in all probability only one lesion has produced these symptoms it must exist at some point 11 162 THE MANIFESTATION OF DISEASE IN ORGANS. where all these iierve-fibres are so closely approximated that they are readily involved together. It will be recalled that the course of these nerves is as follows : The oculomotor nerve having arisen from the nucleus in the corpora quadrigemina pierces the dura mater below the posterior clinoid process, passes along the outer wall of the cavernous sinus and there divides into two branches. The pa- thetic nerve passes near the clinoid process along the outer wall of the cavernous sinus and with the oculomotor nerve enters the orbit through the sphenoidal fissure. The sixth nerve pierces the dura mater on the basilar surface of the sphenoid bone, passes through the clinoid process, and enters the cavernous sinus, finally reaching the orbit through the sphenoidal fissure. It is thus seen that a lesion at the sphenoid fissure and pressure in the cavernous sinus would cause all the symptoms described above. This occurs in cases of thrombosis of the cavernous sinus. Where there is an arterio-venous aneurism of this sinus there will be pulsating exophthalmos. Injury or inflammation may also produce a series of symptoms if in this area. The significance of conjugate lateral paralysis producing a deviation of both eyes to the right or left, as, the case may be, is that some lesion exists in the cerebral cortex, the corona radiata, or the internal capsule, or in the pons before the fibres have crossed. The lesion, if in the cortex, however, does not have to be localized in one spot, for any source of irritation in the cortex may apparently cause conjugate deviation. If the lesion is the result of an apoplexy, the eyes are turned toward the side opposite to the paralysis (Pre- vost's symptom) — that is, the ''patient looks at his lesion." The rea- son that a unilateral lesion can cause a bilateral deviation is that the lateral movements of the eye are governed by an impulse which passes down from the cortex to the sixth-nerve nucleus and thence across the posterior longitudinal fasciculus to the opposite side, where it passes to the nucleus of the third nerve. As conjugate lateral devia- tion is caused by contraction of the internal rectus on one side (third nerve) and the external rectus on the other (sixth nerve), the mechan- ism of the deviation is clear. Thus if the lesion be a distinctive one on the left side of the brain, causing right hemiplegia, the eyes will be turned to the left by the action of the unaffected left external rectus and the right internal rectus ; while if the lesion be on the right side of the brain, the reverse will occur. If, however, the lesion be irritative (as a tuqaor), this deviation is reversed, because in this case THE EYE. 163 the centres are irritated and cause spasm of the muscles receiving their nerve-supply from the affected side of the cerebrum. In other words, the eyes are turned toward the side of the body which is convulsed. In the first instance the eyes are turned away from the affected side because the muscles of the eyes on that side are also paralyzed, and the eyes are therefore turned by the muscles which remain intact. In the second instance the eyes are turned toward the convulsed side because the internal aud external rectus are spasmodically contracted and so overcome the healthy muscles. We find, however, that, if the lesion be in the pons rather than in the cortex, these conditions are reversed, for now a destructive lesion causes the eyes to be turned to the paralyzed side, and an irritative lesion directs them away from the paralyzed side. This is best explained by the following diagram anc? description from Swanzy's well-known booU. (Fig. 76.) Fig. 1. Left est. rectus ; 2. I^ft Int. rectus ; 3. Right int. rectus ; 4. Right ext. rectus ; 5. Nucleus left third nerve ; 6. Nucleus right third ner\-e ; 7 and 8. Post, longitudinal bands from sixth nerve to opposite third nerve ; 9. Nucleus left sixth nerve; 10. Nucleus right sixth nerve; 11 and 12. Left and right cortical centreii. An impulse starting from 12 would travel down to 9, and produce an associated movement of the eyes to the left. A destructive lesion at 12, the right cortical centre, involving also motor centres of the body, would cause left hemi[)lcgia; and, Bince the external rectus of the left eye and internal rectus of the right eye would be paralyzed, the antagonists would turn the eyes- to the right; i.e., away from the paralyzed side. A destructive lesion of the right side of the pons, also producing left hemiplegia, if it involves the sixth nucleus, will produce paralysis of the external rectus of the right eye and of the internal rectus of the left eye, and then the antagonists would turn the eyes to the left; i.e., toward the paralyzed side. It is easy to see how irritative lesions would produce exactly the opposite effects. S(piint which is due to hysteria is always caused by sj)asmodic contraction of the eye-muscle and is never due to paralysis, as it 164 THE MANIFESTATION OF DISEASE IN ORGANS. ofteu is in organic disease. Very often there is a spasm of the eyelid or eyebrow associated with it. The administration of a relaxant, such as chloroform, will at once overcome such a squint. Nystagmus, or the rapid oscillation of the eyes from side to side or in a vertical or rotary movement, is usually bilateral.^ When not congenital it is a frequent symptom of disseminated sclerosis, Fried- reich's ataxia, and advanced locomotor ataxia, and while it does not localize the lesion it indicates very positively that one is present and that the case is not one of hysteria or functional disease. Nys- tagmus occurring in children is very often associated with imperfect vision of great degree or with blindness as a result of opacity of the cornea, congenital cataract, or atrophy of the nerve. In other instances, however, it arises from growths in the cerebellum or pons, and it is sometimes seen in hydrocephalus and very rarely in acute meningitis and in epilepsy. Very rarely lateral nystagmus is seen in children who seem otherwise normal, and it then possesses no particular diagnostic importance. Paralysis or Disorder of the Intraocular Muscles. Hav- ing discussed the diagnostic indications of changes in the function of the extraocular muscles, we next proceed to a consideration of these facts in connection with the intraocular muscles. These consist, it will be remembered, in the muscular fibres of the iris, cir- cular and radiating, and the ciliary muscle. The nerve-supply of tlie iris consists in fibres from the oculomotor or third nerve, the upper or ophthalmic division of the fifth, and the sympathetic. It will be remembered that in the posterior part of the orbit there is situated a ganglion called the ciliary or ophthalmic ganglion. By its short or motor root this ganglion is connected with the third nerve, by its sympathetic root with the cavernous sympathetic plexus and the cervical sympathetic plexns, while by its long or sensory root it is connected with the nasal branch of the ophthalmic or upper branch of the fifth nerve. From this ganglion extend forward two sets of nerves, one short (the short ciliary nerve), which supplies the iris and the ciliary muscle, and one set long (long ciliary nerves), which also go to the iris. The filaments which go to the ganglion by means of its short or motor root (from the oculomotor nerve) pass forward to the circular fibres of the iris, while those which have arisen in the sympathetic plexus pass forward to the radiating fibres. These last 1 The physician should remember that some occupations, such as mining, produce in some persons nystagmus without the presence of the disease about to be named. THE EYE. 165 fibres are in part derived from the cervical sympathetic ganglion, run through the carotid plexus, and are controlled to some extent by the cilio-spinal centre of Buuge in the spinal cord at about the seventh cervical or first dorsal vertebra. The ciliary muscle is supplied by the fibres of the short ciliary nerves, which have arisen in the floor of the third ventricle and which is connected with the nucleus of the third nerve. The size of tlie normal pupil is about 4 millimetres in diameter, but this varies according to the degree of light to which the patient is exposed. It ought always to be measured by a millimetre meas- ure which gives its approximate diameter. The pupil to be tested must be free from any abnormal conditions produced by new or old inflammation of the iris, and the light used should not be excessively bright, but about that usual to the eye. Testing the Pupil. The patient is to be placed facing the light and told to look at some distant object. The bauds of the physician are then placed one over each eye, the patient being told to keep his eyes open and to endeavor to see tiie object seen before the eyes were covered. One hand is now quickly removed from one eye and the pupil observed. This observation must be acute or the pupillary contraction will occur before it is seen. This reflex is due to the fact that we have an irritation of the optic nerve by light, and this sends a reflex wave to the centres governing the pupil and causes it to con- tract. Not only does the uncovered pupil react in this manner, but the covered one does the same thing. The first is called a direct reflex, the second is called the indirect or consensual reflex. The exact pathway of this reflex is unknown, but we know that the light- impulse passes along the optic nerve, aud, arriving at its semi-decus- sation in the chiasm, passes along each of the tracts to the corpora quadrigemina, and thence by the communicating fibres (Meynert's fibres) between these bodies and the oculomotor centres to the centre for the sphincter pupilloe or circular muscle-centre, and from there to the ciliary ganglion, the ciliary nerves, and the muscles of the iris. (Fig. 77.) ' Not only does the pupil change its size by reason of the ordinary light-reflex, but it also contracts or dilates in association with the other muscles governing accommodation and convergence, namely, the ciliary muscle and internal recti. This is the associated reaction of the pupils and is tested by causing the patient to direct his eyes to a near object — for example, the point of a pencil. If the sight is intact, contraction <»f the piij)il will occur. 166 THE MANIFESTATION OF DISEASE IN ORGANS. The pupil-dilating centre is in the medulla and is very sensitive to reflex irritation. Supposing that the pupillary movement is abnormal, we should recollect before studying the case further what the causes of its perversion may be. Thus its size is altered by drugs, by local dis- ease of the iris, by spinal disease and disease of the sympathetic, by localized cerebral lesions, by abeyance of the cerebral functions, and by irritation of the brain. Let us suppose, however, that on test- FlG. 77. 3n, centre of third nerve ; 1, connection between nuclei of third nerves ; 2, Meynert's fibres ; Q, corpora quadrigemina ; c, chiasma ; o, optic nerve ; p, myotic fibres of tliird nerve ; l, seat of lesion ; arrows show path of impulse in lesion of right tract at l. (Swanzy.) ing the ocular reflexes in the manner already described, we find that the pupil of one eye when uncovered does not contract, but imme- diately does so as soon as the other eye is uncovered, what is the indication ? It indicates that there is disease of the optic nerve of that eye which does not convey the impulse of light from the retina ; whereas if it contracts when the other eye is uncovered, it shows that the rest of the mechanism involved in the reflex is intact. Ac- commodative reaction of the })upil is iutaet also. Again, supposing that irides fail to react to light, but do to accommodation and con- vergence, we have the ''Argyll-Robertson pupil," so-called, which indicates that a lesion exists in the communicating fibres (Meynert's fibres) which convey the impulses from the corpora quadrigemina to the oculomotor nuclei. (See Fig. 77.) riiE EYE. 167 This condition is seen in locomotor ataxia, fjeneral paralysis of the insane, sometimes in cerebral syphilis and as the result of poison- ing by the bisulj)hide of carbon. It is worthy of note, however, that late in all these affections the reaction to accommodation may also be lost. Rarely the reverse of the Argyll-Robertson pupil occurs as the result of a lesion in the second and third parts of the oculomotor nucleus. If the eyes fail to react to light and to accom- modation, there is probably blindness due to optic-nerve disease. If on throwing light into the right eye there is no reaction of the pupil of that eye, and on throwing it into the left eye there is still no reaction in the pupil of the right eye, there must be a lesion of the nucleus of the right oculomotor nerve or palsy of the conducting fibres of each optic nerve. Dilatation of the pupil occurs in cases of glaucoma^ optic-nerve atrophy, in disease of the orbit, and under the effect of drugs possess- ing a mydriatic action, as, for example, atropine. It also occurs in persons suffering from fright, neurasthenia, aortic regurgitation, and irritation of the cervical sympathetic, as by aneurism. A dilated pupil is also often seen in idiotic children. Dilatation of the pupil results from two causes, opposite in character: the first is irritation due to tumor, meningitis, or other irritating lesion of the upper part of the spinal cord; the second to paralysis of the cerebral centre of the oculomotor nerve, resulting from cerebral hemorrhage, thrombosis, tumors, or abscess of the brain. Contraction of the pupil is also due to lesion similarly situated and results from sources of irritation in the cerebrum, resulting from meningitis and cerebral tumor, and Berthold asserts that a contracted pupil shows that a sudden attack of paralysis is due to embolism and a dilated pupil shows hemorrhage. Myosis (contraction of the pupil) results from paralyzing lesions of the spinal cord situated in the region of the cervical ventebne, and occurs notably in locomotor ataxia. It is also seen in general paralysis of the insane (paretic dementia), the false paretic dementia of syphilis, and in bulbar pa- ralysis with progressive muscular atrophy. It is also one of the most notable signs of <)|)iuni-j)()is()ning. Under tiie name of " hemiopic pupillary inaction " or "Wernicke's pupil " we sometimes, though rarely, meet with a condition associatevi with hetnianopsia or blindness in one-half of the eye, which is dem- onstrated in the following manner : The patient is seated in a dark room and one eye is covered. Tiie other eye is now illuminatetl by 168 THE MANIFESTATION OF DISEASE IN ORGANS. just sufficient light from a flat mirror to enable the physician to see the eye. By means of the concave mirror of an ophthalmoscope the physician now directs into the uncovered eye a bright beam of light, taking care that it falls upon one side of the retina, or, in other words, enters the eyes obliquely aud strikes on the side of the retina which is blind. If when the light falls on the blind side of the retina there is no pupillary reaction, it is considered that the lesion exists in the right arc between the optic chiasm and the corpora quadrigemina; but if there is a pupillary reaction, the lesion must be further back in the visual centres, back of the reflex arc. When the lesion is found back of the reflex arc it may indicate a lesion of the optic tract, the posterior segment of the thalamus, the posterior part of the chiasm, or rarely it may be caused by a lesion of the optic nerve if the hemianopsia be monocular, which is rarely the case. Finally a rhythmical contraction and dilatation of the pnpil, called "hipjms,'' are seen in health for a moment on sudden exposure to light ; but when constant is a sign of disseminated sclerosis, epi- lepsy, or the early stages of acute meningitis. It is sometimes seen in hysteria. The presence of a recurrent, unequal dilatation of the pupils of a transitory character is said to be by Rampoldi an early and almost constant sign of pulmonary tuberculosis. He claims that this is due to a reflex irritation of the nerves governing the pupil through the sympathetic system. Probably in these cases enlarged glands in the chest are the cause of the pupillary phenomenon, just as an aneurism may be. Destree claims that 97 per cent, of his cases of phthisis present this pupillary symptom. Knies points out that pupillary contraction and dilatation take place in association with Cheyne-Stokes breathing. Dilatation usually exists with the inspiratory movements, and myosis occurs during the interval of apncea. Chang-es in the Acuity of Vision. Having discussed the diagnostic value of alterations from the normal in the function of the extra- and intraocular muscles of the eye, we can proceed to a consideration of the value in changes in the acuity of vision. The questions of the acuity of vision in relation to errors in the refrac- tive media of the eye will not, of course, be included in this book. Failure of vision in part or in toto depends upon a lesion which destroys the peripheral ocular sense-organ (the eye), the optic nerves, the optic tracts, or the receptive and perceptive centres of sight. It THE EYE. 169 also is dependent upon bilateral lesions in the crystalline lens, as in cataract, or in the cornea, as in severe keratitis. Fig. 78. Heft Eye VisuaUjeld The visual tract. The result of a lesion anywhere between the chiasm and the cuneus Is to produce homonymous hemianoiwia. n. I.^sion at chiasm causing bilateral temjwral hemi- anopsia. N. Ix!8ioti at chiasm causing unilateral na.sal hemiamipsla. t. Lesion at chiasm causing unilateral temjKmil hemianopsia, sn. Substantial nigra of cms. l. Lemniscus in crus. i;.N. Ueil nucleus, ill. Thinl nerves, p, y. it, s, f. Lesions in the occipital lobe and In front of it producing left homouynmus lateral hemianopsia. 170 THE MANIFESTATION OF DISEASE IN ORGANS. Before we discuss these various causes of blindness it is necessary that we recall the nervous anatomy of the organs of sight. These nerve-fibres starting with the rods and cones of the retina and the fibres from the macula pass back along the optic nerve until they come to what is known as the chiasm, where the various fibres from the eye decussate, in that the fibres from the inner half of each eye cross to the opposite side, whereas those of the outer half of each eye pass to the same side, as is shown in Fig. 78. After the optic tracts have been formed by this (partial) decussation each one winds around the corresponding crus cerebri, and terminates in two roots upon the corpora geniculata externa and interna and upon the poste- rior part of the optic thalamus. The pupillary fibres also branch here to the corpora quadrigemina. These parts are known as the primary optic centres. After leaving them the fibres pass backward into the posterior part of the posterior limb of the internal capsule and thence to the cortex, rise in a fan-shape, pass outside the tip of the lateral ventricle, and reach the secondary or true optical centre in the lower part of the median aspect of the occipital lobe. (See Fig. 78.) Hemianopsia. As lesions of the nervous centres frequently pro- duce partial or complete blindness, it is of importance, first, that the presence of partial blindness should be discovered, and, second, that the lesion causing it should be located. Aside from general failure of vision due to changes in the retina or optic nerve we have in many cases of nervous disease a condition called hemianopsia or partial or complete blindness of one-half of the retina. Usually hemianopsia is bilateral — that is, in both eyes ; and it is usually homonymous — that is, on the same side of each eye; or, in other words, if it is the outer half of the left eye, it will be in the inner half of the right eye. If this is the case, it is called left bilateral homonymous hemianopsia. If, on the other hand, the outer half of each eye is blind, this is called bi- temporal hemianopsia; or if the blindness is found in the nasal side of both eyes, it is called binasal hemianopsia. It must be remem- bered, however, that the apparent blindness of the outer side of the eye is really due to disease of the fibres supplying the opposite side of the retina, as is shown in Fig. 79. The presence of hemianopsia in any form is determined by the following method of examination : The patient is placed with the back to the light and one eye is cov- ered, while the other is fixed upon the centre of the physician's face, which should be two feet away. The finger of the physician is now THE EYE. 171 moved to the left aud right as far as the patient can see it, the head and the eyeball of the patient remaining fixed. If the eye fails to see the finger when but a little distance to one side or the other of the fixation-point, hemianopsia is present. Fig. 79. LEFT VISUAL FIELD. RIGHTVISL^ALFIELD. Fixafinn Poinf. Fixation Poutf. We measure the field of vision more accuratel}' by means of what is known as a perimeter, which is a semicircular metal band which revolves upon its middle point, being capable therefore of describ- ing a hemisphere in space. This arc is divided into degrees marked on it from 0° to 90°, and at the centre of it is placed the eye which is to be examined, which eye finds its fixation-point in the centre of the semicircle. A small piece of white paper is now moved along the metal arc on its inner surface, from the extremity and toward the centre, until it comes into view, when the physician notes the number of degrees at which the object is seen and notes it on a chart (see Fig. 80). The area of the normal field is well seen in this figure. Let us suppose that on using the tests just described we find lelt 172 THE 2IAyiFESTATI0N OF DISEASE IX OBGANS. lateral homonymous hemianopsia — that is, blindness in the visual field, as shown in Fig. 81. This signifies that the patient has a lesion somewhere in the visual tract back of the chiasm, either Chart of F. V. of right eye. Fig. 81. Left homonymous hemianopsia from a case of gunshot-wound, with suspected lesion of the right cuneus, from a case under the care of S. Weir Mitchell, at the Infirmary for Nervous Diseases, (de Schweinitz.) THE EYE. 173 in the cuncus, iu the occipital lobe, in the optic radiations, in the internal capsule, iu the primary optic centres, or in the optic tract. Fig. 78 shows the sites of these lesions and why they cause left homonymous hemianopsia. Supposing, on the otiier hand, that in place of left homonymous hemianopsia we tiud bitemporal iiemi- anopsia (Fig. 82), this indicates that the patient has a lesion of the optic tracts in the crossing fibres in the middle of the chiasm (see " H " in Fig. 78); or if binasal hemianopsia, that he has a lesion on both sides of the chiasm or one on the outer side of each optic nerve. This is a very rare lesion. Fig. 82. 270 270 Bitemporal hemianopsia from a case of akromegaly originally under the care of Dr. LI.C. Wood and later studied by Dr. Packard. Eyes examined in 1885 by Dr. G. E. de Scfiweinitz. and above fields found, (de Schweinitz.) Hemianopsia of the homonymous form is very rarely iound in hysteria, generally in a.ssociation with hysterical hemiana^sthcsia, iu which condition the conjunctiva is usually anesthetic, thereby differ- ing from the condition of the conjunctiva of persons suffering from hemian;estlicsia of an organic origin. In some cases in place of hemianopsia we have simply an altera- tion in the visual fields for color. It will be remembered that the boundaries of the power of the clear perception of colors are not identical with the boundary for white light nor they are identical with one another. Passing from the periphery toward the centre of the visual field in ordinary daylight we find that 1)1 ue is the color first seen, its boundary being almost as great as that of white. After 174 THE MANIFESTATION OF DISEASE IN ORGANS. blue comes yellow, orange, red, and finally green. The blue, red, and green being the most important colors, their boundaries are shown in Fig. 83. These fields are determined by means of small pieces of colored paper passed around the perimeter in the manner already described. Fig. 83. WHITE BLUE — — - RED GREEN Chart of F. V. of left eye. (Landolt.) The alteration of the visual field for colors is called, if so situated, homonymous hemidyschromatopsia, and the lesions producing it is situated in the cortex of the occipital lobe; while if the colors are indistinguishable, it is called hemiachromatopsia. This, however, has recently been denied. The transposition of the visual fields for color is usually a symptom of hysteria, and as a rule the red field takes the place of the blue, and vice versa. The fields for all the colors are also markedly narrowed in hysteria. This transposition, rather than loss of color-sense, helps us sometimes to a distinction between the ocular symptoms of hysteria and of true tabes dorsalis, a distinc- tion which is of great importance, yet one which is often exceedingly difficult, save for these and two other symptoms, namely, that in hysteria the knee-jerks are usually preserved and the Argyll-Rob- THE EYE. 175 ertson pupil is not seen. The following table from Charcot's lectures for 1888-89 summarizes these differential points : Tabes. Hysteria. Motor apparatus of the Paralysis from lesion of a motor 1. Sometimes associated paralysis, eye. nerve of the eye (bulbar or peri- 2. Blepharospasm. pheral ; consequent diplopia. 3. Monocular diplopia ; micropsia and macropsia. Pupillary disturbances. Argyll-Robertson pupil. Optic disk. Atrophy. Symptoms due to aftec- 1. Irregulai concentric contrac- 1. Regular concentric contraction tions of the optic nerve tion of the visual fields. of the visual fields. or visual centres. ' 2. Tabetic achromatopsia or dys- 2. Dyschromatopsia from simple chromatopsia, affecting first contraction of the visual fields green and red, yellow and blue for colors. Frequently perception being preserved to the lasi. of red alone persists. 3. Progres.sive blindness. 3. Transitory a&blyopia or ama- urosis. The Optic Nerve, and the Ophthalmoscope. There still remain to be considered the diagnostic indications afforded us by the optic nerve. Before taking up tiiis subject mention must be made of the manner of using the ophthalmoscope. The patient is to be seated in a darkened room, and by his side, at the level of the eye to be examined and far enough back of him for his face to be in shadow, should be placed a lamp, or, if gas can be had, an Argand burner. The physician now seats himself, if the right eye is to be ol)serve(l, at the right side of his patient, and takes a chair slightly higher than that of the patient. The o|)hthalnu)- scope is now taken in the right hand and held in such a positii)n that the concavity of the physician's l)r()\v fits over the convexity of the instrument. The eye of the physician is so placed that he can readily see through the aperture in the centre of the ophthalmoscope, and by means of the concave mirror on the face of the instrument he reflects the light into the eye through the pupil. The patient must not look directly into tite ophthalmoscope, but to one side, and his vision should Ik; distant and accommodation as far as possible relaxed. If the examiner is not skilled in the use of the ophthalmo- scope and the result of the examination is of great importance in the diagnosis of the case, it is justifiable to use homatropine to dilate the pupil and prevent the alleiations of accommodation by paralyzing this function. The ophtlialmoscope and the head of the physician are now approached as closely as possible to the eye of the patient, the 176 THE MANIFESTATION OF DISEASE IN ORGANS. angle of the two heads being as nearly as possible identical as shown in Fig. 84. If the light be now directed slightly toward the nasal side of the eye, the optic nerve will be seen, or in its stead a retinal bloodvessel will be seen across the field of vision, and this should be traced along its course to its origin in the papilla. If the patient or the physician is short-sighted (myopic), the ophthalmoscope must Relative position of physician and patient whilst employing the direct method. (NoRRis and Oliver.) be adjusted to correct this error by placing over the aperture a concave lens; but if ordinary degrees of far-sightedness (hyper- metropia) are present, the use of a convex lens is not necessary, be- cause the accommodation of the eye makes up for the error in refrac- tion. If the hypermetropia is so great that accommodation cannot overcome it, then a convex lens must be used. The view of the eye which is obtained ordinarily by a beginner is clouded, not because of myopia or hypermetropia, hut because the physician has not as yet learned to relax his accommodation in making the examination. A concave glass usually remedies this. PLATE IV. Normal Kye-Cround (average tiiitl. (Norris & Oliver.) FIG. 2. Primary Atrophy of Optic Nerve i Spinal Atrophy). Modified from Ilaal). ide Scliweinitz.l I'oiit-rapillitic or Consecutive Atrophy of the optic Nerve. Modified from Jiiler. (deSchweiiiit/.) TH?: EYE. 177 In health the optic nerve appears as a nearly round or slightly oval disk, situated somewhat to the nasal side of the eye, and varying in color from grayish-pink to red, the centre being whiter and the nasal half the darkest part. Around the papilla are seen two rings, the outer one darker and generally incomplete or absent, while the inner one is a faint white stripe, which becomes more marked as the patient grows older. The first is called the choroidal ring, and repre- sents the edge of the choroidal coat of the eye where it is pierced by the nerve. The second is the scleral ring, which is the edge of the sclerotic coat. The centre of the optic papilla may be even with the surface or cupped and may be stippled or dotted in appearance. The retinal arteries emerge from this central spot and the chiet venous trunks empty into it. Generally one arterial and one ven- ous stream pass up and a similar one downward, and ^oth soon bifurcate, afterward still further dividing. The arteries are dis- tinguished from the veins by their bright-red hue, while the veins are darker in color. The veins are about one-third larger than the arteries. A bright stripe due to an optical delusion seems to divide each vessel longitudinally into two parts. The arteries of the nor- mal eye do not pulsate, but pulsation of the veins is quite common. It must be remembered that the appearance of the papilla and of the i)loodvessels as they leave it varies very greatly within perfectly physiological limits. As already stated, the cupping of the papilla may be quite deep or quite shallow, and the bloodvessels may divide as already described, or divide in the papilla into four branches. The veins are usually more tortuous than the arteries. (Plate IV., Fig. 1.) The retina is practically transparent so that the underlying choroid is seen. In })ersons with a dark skin the retina has a gray- ish hue in the neighborhood ot the papilla, which is most marked on its nasal side and is slightly streaked. To the outer side of the })apilla, slightly below the horizontal merid- ian, is the macula lutea or yellow spot, which is about the size of the end of the optic nerve, but darker in color, somewhat granular, and /\ \ / \ \ / \ \ / / \ \ / ^ A ) \ A / /\ , \ /\ \ / \ V \ 15 / N. // / \ \\ / ^ ^ // / \ \\ 1 l\ V // / ^ A\ / / \ v\// J / / VV / \ \ \ 10 / / /\. N/ / \ \ V / r / > / \ \ \ / y / ^ / \ \ \ / / / M \ N , v / /y \ V V / • // \ \ ^ ^>v^ b / y^ / <\ / f '^ / \\— —^"^■~> .^ ^~- l~.«^ ^ ^ X ^ \ . /^ """-^^ ^~~ -.^ y ^ ^ \y ^"■^^^ ^ "•-^ 16-20 21-25 28-30 31-35 30 ■ 40 41-46 46 - 50 51 - 55 66-60 61-65 66-70 71-75 Upper curve, frcfiuency of tabes. Middle curve, frequency of severe ocular symptoms. Lower curve, freijuency of atrophy of the optic nerve. (Bekgek.) sutler from this change. Again, it is seen in cases of paretic dc- nieutia .somewhat less frequently. Optic atrophy is often .seen in cases of disseminated sclerosis. Because of the fact that gray atrophy of the nerve is one of tiie earliest signs of locomotor ataxia, in some cases it is a valuable one in the diagnosis of this grave disorder, sepa- 180 THE MANIFESTATION OF DISEASE IN OBGANS. rating it from pseudo-tabes due to ordinary peripheral neuritis. The following table, also taken from de Schweinitz's article on this sub- ject, shows the relation between age, severe ocular symptoms, and atrophy of the optic nerve, (Fig. 85,) The more advanced forms of optic atrophy with a hazy outline of the disk usually result from diseases in the optic centres or in the nerve itself. Thus there may be present a tumor pressing on the chiasm or optic tracts. Again, if on the use of the ophthalmoscope we find that there is a faint haziness of the retina, that whitish streaks are found in it which may be bluish-gray or yellowish in hue, that the bloodvessels are tortuous and minute vessels are easily seen because of their en- largement, that hemorrhagic exudations of a flame-like chaiacter are present, and that dark pigmented spots represent where previous hemorrhages have been, and, finally, that the head of the optic nerve is not clearly outlined, we have the pictuie of retinitis. Generally, in association with these signs, we find as subjective symptoms changes in the visual field, a distorted vision, so that straight lines appear bent inward or outward, and there are pain and fear of light. If the vitreous humor is opaque, in addition to these symptoms, •syphilis may be present, and the iris may give evidence of iritis. Where the hemorrhages are very manifest and profuse (hemorrhagic retinitis) the cause may be disease of the heart and bloodvessels. By far the most important of these forms of retinitis from a diag- nostic standpoint is what is known as albuminuric retinitis or that due to Brigiit's disease. Here, in addition to the flame-like hem- orrhagic areas, we find irregular spatterings of white which may be star-sha[)ed. The importance of the discovery of such changes is that by it is the first suspicion of renal trouble discovered. This is of the greatest value in pregnancy. Retinitis also sometimes re- sults from diabetes. Hemorrhages into the retina without retinitis usually are the re- •sult of septicaemia, ulcerative endocarditis, hemophilia, diabetes, gout, and malarial fever of a severe type. It is also seen in cases of great cardiac hypertrophy with stenosis, and after suffocation. The iris indicates disease in other organs more rarely than the retina and optic nerve and the muscles, but an irregular pupil indi- cating an old iritis should raise a question as to a history of injury, syphilis, or rheumatism. Finally, it should not be forgotten that cataract sometimes occurs THE EYE. 181 as the result of diabetes mellitus and that corneal ulceration is often an evidence of scrofulous tendencies, while a distorted pupil due to an old iritis should raise a suspicion of syphilis. It must not be forgotten that patients often have, in distinction from distorted images, visions or flames of light or bright sparks l)efore the eyes, or in their place dark dots called muscaj volitantes. Often the visions are the prodromes of an attack of migraine or of an epileptic seizure. In the case of spots of light or stars we usually find them as a result of severe indigestion, and the dark spots may arise from the same causes. Muscte volitantes may also be due to small particles of mucus floating over the cornea or to small floating bodies in the vitreous. Partial or complete blindness is sometimes seen in cases which are under the influence of a drug, as, for example, quinine or other drugs; and sometimes partial or complete blindness results from unemia (urtemic amaurosis). As a rule, it does not occur as a single symp- tom, but follows an attack of acute ursemic manifestations ; that is, it is found after a convulsion or period of coma has passed by. As a rule, nothing abnormal is found in the eye to account for it, and the pupillary reflexes are intact. The efi'ect of the poison in the blood is therefore exercised upon the optical centres, probably in the occipital lobe. Sight is usually regained in these cases in a few days. CHAPTER VII. THE SKIN. The color of the skin — Eruptions on the skin — Gangrene, ulcers, and sloughs — Scars, sweating, dryness, oedema, hardness— Anpesthesia, and hemianfesthesia — Parsesthesia, hyperfesthesia, itching. Much information can be obtained by careful examination of the skin in many cases of disease. The examiner should make a note of the color of the integument, of its general nutrition, of its pliabil- ity and its sensibility. Naturally the eye at once takes in any erup- tion or scars which may mar its naturally smooth surface, and, as eruptions and scars are often the manifestations of more or less active systemic disorders, an insight into the presence of internal disease may be obtained from them. The color of the skin in health in the white race depends upon the presence of pigment in the cells of the raucous layer of the epi- dermis, and in the corium in those parts of the body where pigmen- tation is marked, or to the condition of the subcutaneous circulation or of the blood in the subcutaneous vessels. Thus we often find the skin of the perineum, scrotum, axillae, and of the lower abdomen much darker tnan elsewhere in persons in perfect health. Similarly we see a marked reddish or yellowish-brown hue in those parts of the skin which have been exposed to sun and weather, as a result of a deposition of pigment and an increased capillary circulation. With these normal alterations in color, however, we have little to do, for it is the abnormal colorations which interest us from a diag- nostic standpoint. The most common of these changes in color due to pigment is jaundice; the next the chloasma of pregnancy or uterine disease, a condition usually limited to the face. Abdom- inal growths due to tuberculosis, cancer or lymphoma, and tubercu- losis of the peritoneum also cause pigmentation of the skin, and in melanotic cancer there is often very dark discoloration, so marked as to be confused with that of Addison's disease. Again, it is not un- common for persons who have hepatic torpor with constipation to develop what are called liver-spots, in which the skin has rather THE SKIN. 183 a dirty hue. Under the name of vagabond's ''pigmentation, " we sometimes see discoloration induced by the irritation of the skin produced by lice and exposure to dirt and weather, and this is capa- ble of being mistaken for the pigmentation of Addison's disease. Finally, we see the yellowish-brown hue of the skin due to tinea versicolor, the bronzing of the skin in Addison's disease, and the slate-blue hue of argyria or chronic silver-poisoning. (See further on in this chapter.) The changes in color depending upon disturb- ance of the subcutaneous circulation or on alterations in the blood are either local or general. In extreme nervousness, flushing or blushing, due to a local vasomotor relaxation with increased blood- supply, may redden the face and neck, or in hectic fever a hyperemia of the skin over the malar bones may give rise to an increase in color, which may be dusky red, due to imperfect oxidation of the blood. Considerable cyanosis of the face and hands in a case of tuberculosis of the lungs is a very grave symptom. Again, we see in pneumonia a peculiar dusky red flushing of one cheek or of the entire face, and in erysipelas the zone of hypertemic redness is characterized by its sharp line of demarcation and its raised edge. In the altera- tions in color due to changes in the quality of the blood we have, as causes, anaemia due to lack of corpuscles or of hfemoglobin, arising from the various etiological factors producing such states. Jaundice. Taking up the color-changes due to pigment, we find that in jaundice the deposition of the biliary coloring-matter varies in degree from a slight tinge or almost imperceptible yellowing to a dark citron or olive-green hue. In examining the skin for jaundice care should be taken not to do so l)y gas or candle-light, for the yellow flame masks the biliary color; and if the tinge is very slight, it may be made more marked by stretching the skin on the palm of the hand or by pressing upon the skin a glass slide so that the yellow hue .shows through it. Having discovered that biliary coloring-matter has been deposited in the rete mucosum, it remains for the piiysician to decide what the cause of the jaundice may be. In the first place, it nnist bo remem- Ix-roil that jaundice may be hepatogenous — that is, arise from disorder in the liver, ov i)e hematogenous from disorders of the blood with the setting free of blood-jiigmcnt. The hepatogenous jaundice is by far the more common of the two conditions, and the most common cause of this form of jaundice is catarrhal inflammation of the smaller 184 THE MANIFESTATION OF DISEASE IN ORGANS. ducts and common bile-duct which generally occurs in association with gastro-duodenal catarrh. The following table from Taylor's Index of lledicine summ&rlzes the causes of hepatogenous jaundice : Tabular View of the Causes of Hepatogenous Jaundice. Obstructive (feces clay- colored) , „ ,, . , . .,,,.,(■ in common duct. 1. Gall-stones and inspissated bile - . , . , „ , ^ (in radicles of ducts. 2. New growth Jlalisrnant f of liver itself I secondary infiltration of glands I in transverse fissure. I of stomach, j of pylorus. I of duodenum. I of pancreas, of kidney. Non-malignant -j syphilis. lymphadenoma. 3. Catarrh of stomach and duodenum. 4. Abdominal aneurism. 5. Hydatid cysts. 6. Accumulation of feces. 7. Ovarian or uterine tumors. |_ S. Perihepatitis. As a result of this catarrhal process the bile-duct becomes blocked by the swollen mucous membrane and the mucus which is secreted; the biliary coloring-matter is absorbed into the hepatic, circulation and general circulation, and is by this means distributed over the body. Another common cause of hepatogenous jaundice is the ob- struction offered to the flow of bile by the presence of a gall-stone or gall-stones in the ducts; and a third cause of obstructive jaundice so-called is pressure on the ducts by growths or inflammatory prod- ucts in the immediately adjacent organs, or of adherent inflammation in the ducts themselves, or by the presence of a round worm in the duct. Very rarely the jaundice may arise from pressure on the common duct produced by floating kidney. Catarrhal jaundice of the acute type is generally produced by in- discretions in diet associated with exposure. The patient after more or less marked symptoms of gastric and intestinal disturbance and indigestion feels wretchedly. There is a premonitory mental heavi- ness, with languor and malaise, and within forty-eight hours or less the yellowing of the conjunctiva and skin appears. The tempera- ture is generally subnormal to a slight degree. The tongue is heav- ily coated and often somewhat dry. There are marked loss of appe- tite, great distress, headache, and depression of spirits. Examination THE SKIN. 185 of the hypochondrium may reveal some local tenderness and slight hepatic enlargement, while the abdomen will be in some instances markedly tympanitic as a result of intestinal fermentative processes in the absence of antiseptic bile. The bowels are constipated, often refusing to move except with powerful purgatives. There is little pain, except headache. This condition lasts for a few days or a week, when the color of the skin and conjunctiva usually begins to fade and the normal hue is reached in the course of a week or more. The presence of persistent jaundice should raise the suspicion that it is due to more serious disorder than simple catarrhal inflammation. The jaundice due to obstruction by stone may be due to blocking of the biliary duct, w'hereby there is a stagnation of the flow with reabsorption of the bile, or to stoppage of the flow by the presence of a stone in the common duct just as it enters the bowel. iV differen- tial diagnosis as to whether the stone is in one or the other of these })laces is often impossible, but in the variety in which the obstruc- tion is below the opening of the cystic duct it may be possible some- times to discover by abdominal palpation a pear-like swelling due to a distended gall-bladder. The jaundice of gall-stone obstruction may be sudden or gradual in onset. If sudden, it is often, but not always, preceded by a vio- lent attack of pain in the hypochondrium, or, in other w'ords, hepatic colic, in which the agony is excruciating and is accompanied by nausea and vomiting. The area of the pain is, however, distinctly hepatic, and it does not radiate dow^n the inside of the thigh and into the testicle or penis as does that due to renal calculus. In place of the subnormal temperature so often seen in catarrhal jaundice we find in obstructive jaundice that the temperature is often considerably raised, and this is particularly apt to be the case in those instances in which the onset is gradual and the jaundice persistent, being due to reflex irritation, or septic absorption, produced by the impacted stone, which may be scratching or ulcerating the lining membrane of the duct. The history of repeated attacks of gall-stone colic, the presence of gall-stones now and then in the stools, the swollen gall- bladder in which, in very thin persons, the stones may sometimes be felt, the age of the patient, who is generally in or past middle life, and the fact that tiie patient is a female, all point to gall-stone as a cause of the jaundice. As a rule, there is great loss of flesh in all forms of jaundice; but if the local damage done by the stone is great and septic absorption is marked and the fever high, the failure in 186 THE MAXIFESTATIOX OF DISEASE IX OEGAXS. strength may be most alarming, while the repeated rigors and sweats increase the distress of the patient. Jaundice very rarely arises from pressure on the ducts by an areurism of the abdominal aorta, or more commonly from disease involving the hepatic artery. Three such cases are recorded by Frerichs. Jaundice has also been seen in aneurisms of the supe- rior mesenteric artery as the result of pressure and in cases in M'hich there has been, or is, perihepatitis, with displacement of the liver in such a way that the adhesions cause twisting or dragging on the ducts. The jaundice of malignant disease pressing upon the gall-ducts is usually not intense, and is characterized by the physical signs of a tumor, by the marked wasting of the patient, and, as a rule, by the very gradual onset of the pigmentation of the skin. Generally the lesion in such cases is carcinoma of the head of the pancreas. Jaundice is also seen in hepatic hypeftrophic cirrhosis to a slight extent in a small proportion of cases, and it is to be remembered that in those cases of this disease in which delirium and muscular twitching occur that the symptoms may resemble acute yellow atrophy of the liver, and all forms of jaundice produce headache and may cause de- lirium. In acute yellow atrophy of the liver (see below) the liver is greatly reduced in size, whereas in hypertrophy it is greatly in- creased in size; and in atrophy the temperature is subnormal, whereas in the jaundice due to hypertrophic cirrhosis it is apt to be above normal. Jaundice also may be a manifestation of acute poisoning by phosphorus, which condition is generally accompanied by hepatic swelling and tenderness and with coifee-ground vomiting. Jaundice is present in all fatal cases of yellow fever and often in cases which ultimately recover. It also is a constant symptom in Weil's disease, which is probably in reality a septic icterus, but it is very rarely seen in suppurative hepatitis. A fleeting and light hue of jaundice is sometimes seen in cases of chronic valvular cardiac disease in which compensation is gradually failing. Rarely this hue becomes deeper as the heart-failure increases. This jaundice is due to engorgement of the liver (nutmeg-liver) which in time re- sults in catarrh of the bile-duets, with consequent obstruction to the flow of bile. In amyloid disease of the liver Bartholow states that jaundice occurs in about one-tenth of the cases as a result of enlargement of the lymphatics in the hilus with pressure on the hepatic duct. In THE SKIS. 187 jaundice resulting from cancer of the liver the growth must be so situated as to compress the ducts, consequently jaundice only occurs in about one-third of the cases. Similarly jaundice may result frum the presence of echinococci, but this is not a common symptom of the growth of these parasites and the disease is very rare in the United States. Jaundice sometimes complicates diabetes. Under these circum- stances it may be regarded as a coincidence or a valuable diagnostic aid, for, as we have already stated, tumors of the pancreas by pressing on the common duct may cause jaundice, and, as is now well known, widespread disease of the pancreas may cause diabetes. Jaundice in a case of diabetes should therefore direct attention to the pancrea-. In this connection it is well to rememVjer that Hauot, under the name of diabSte bronz^, has described one other pigtuentation of the skin which contains iron (that of Addison's disease and melan- semia do not), and which is associated with diabetes and hypertrophic cirrhosis of the liver. The coloration occurs most markedly upon the face, limbs, and genital organs; the glycosuria is abundant and slight ascites may be present. Other noteworthy symptoms of hepatogenous jaundice are intense itching of the skin; a very slow pulse when the patient is at rest, due to stimulation of the vagus by the bile in the blood; and staining of the sweat due to the bile-pigment may also be present. Should the jaundice be due to gall-stones impacted in the ducts, and producing irritation or ulceration of their lining so that septic absorption or *' Charcot's fever" develops, the pulse may become more rapid and running, from the general feebleness which rapidly asserts itself, liigorsof extreme severity, followed by sweatings and marked febrile movement, develop in such cases, the chills occurring daily or periodi- cally in a manner closely resembling those of intermittent fever. As these symptoms sometimes develop iu cases in which the po-t- raortem discovers no sign of pus, it has been thought that the dis- turbances were due to reflex causes, but the opinion of Charcot that there is present in all sucli cases a true infection seems the most l)robable. When the gall-stone produces active suppuration the fever becomes more like remittent fever and the patient rapidly eraacMates and presents all the signs of active suppuration. The urine in all cases of hepatogenous jaundice is heavily bile- stained (see Urine), and tiie stools generally clay-colore:e of a fly-blister, a mustard plaster, or other counter-irritants, and a brown discoloration of the skin, which might possibly be confused with that of Addi- son's disease, is produced by the free use externally of oil of cade. Sometimes these spots are produced by the prolonged use of arsenic, aud the writer has reported a case in which the coalescence of the spots produced a curious grayish-brown hue of the entire l)odv, so that the man looked somewhat like a mulatto. Sometimes brown pigmentation of the skin of the neck and face appears as a symptom in exophthalmic goitre, and this disease may also produce similar lesions on the chest and wrists. Very closely resembling these spots is tlie bronzing of the skin in patches whicli is seen in persons suffering from Addison's disease; but although bronzing of the skin is a somewhat constant symptom of Addison's disease, its presence is neither a positive nor negative sign in diag- nosis, for l)ronzing is sometimes seen in cases in which the supra- renal capsules are normal. In some instances the bronze color deepens into a dark gray or even a black line, and although the discoloration is generally in patches, it may extend over the entire surface of the skin, even to the edges of the finger-nails. The nails, however, escape, as does also the mucous membrane of the lips, aUhmigh the lining of the mouth itself may be dotted with pigmenta- tion. The color is due to pigmentation of the rete Malpighii, and j)ressure has no effect on it. The symj)toms of Addison's disease to be found associated with these skin-changes are " ana?mia, gen- 192 THE MAXIFESTATIOy OF DISEASE IX OBGAXS. eral languor or debility, remarkable feebleness of the heart's action, and irritability of the stomach." (Addison.) The slate-colored skin of argyria or chronic silver-poisoning can be readily distinguished from the bronze color of Addison's disease ; but if a further test is needed, it will be found that washing the skin of argyria with a solution of iodine changes its color, while that of Addison's disease remains unaltered. White patches, or leucoderma, are also sometimes seen iu some cases of true goitre, and bro^yn ones in tuberculosis. In carcinoma of one of the internal organs, or of the breast, ol an advanced form, the appearance of the skin is drawn and unusually smooth, often shiny or greasy-loooking, somewhat gummy and leathery to the touch, particularly where the integment is naturally dense. Although it is difficult to describe, this skin is almost pathog- nomonic of carcinoma, although it may also be present to some extent in far-advanced cases of pernicious ansemia or sarcoma. Pallor of the skin is due to absence of the normal pigment, to deficient blood, to central or local vasomotor disturbance as is typified by fainting, and far more rarely by Raynaud's disease. As a type of the pallor due to lack of pigment in the skin we see viti- ligo, while the pallor due to pernicious auEemia or pseudo-leukaemia and malaria is due to lack of red corpuscles. Similarly, a pallor due to lack of haemoglobin is typified by chlorosis. (See Blood.) In all of these diseases the pallor of the skin may be of ghastly whiteness or tinged with yellow. The skin is apt also to be very white, and even chalky in appearance, iu chronic contracted kidney and chronic parenchymatous nephritis. In chlorosis the entire surface of the body is exceedingly pale, and the skin of the face, particularly about the mouth and nose and eyes, is somewhat greenish in hue. Avery important diagnostic point to be remembered is that red cheeks often cause the physician to overlook well-advanced anaemia in young women. (See chapter on the Blocd.) In those cases in which the skin is pale from alteration of the subcutaneous circulation there is usually incompetence of the heart or vasomotor disturbance, but the most marked form of general pallor is that due to myxoedema. Cyanosis or blueuess of the skin depends upon the circulation in the subcutaneous vessels of imperfectly oxidized blood The small veins are often seen to be swollen, particularly those of the face and THE SKIX. 193 the bauds and feet. The most marked form of cyanosis with which we meet is the cyanosis of the newborn child, suflPering from a patulous foramen ovale, and in this condition the color may vary from slate-colored blue to an almost black hue. The lobes of the ears, the tongue, the scrotum, and the toes show the color most deeply. It is important to remember that this form of cyanosis is greatly decreased as a rule by placing the child on its right side. Anything which produces excitement increases the cyanosis greatly, whereas cyanosis due to other causes is not subject to great variations. In the cyanosis of the newly born, males are far more frequently affected than females, in the proportion of about 2 to 1 or 3 to 1, and it is a noteworthy fact that even when the cyanosis is due to a mal- formation of the heart it may not l)e present from the time of birth, but may develop several days afterward. J. Lewis Smitli records forty-one cases in which the cyanosis due to a congenital heart-lesion came on at periods ranging from two wrecks to forty years after birth. About 35 per cent, of the cases of cyanosis due to congenital defects die in the first year. The following table from Lewis Smith shows the character and relative frequency of these lesions : Cases. 1. Pulmonary artery absent, rudimentary, impervious, or partially obstructed 97 2. Right auriculo-ventricular orifice impervious or contracted .... 5 3. Orifice of the pulmonary artery and the right auriculo-ventricular aperture imj>ervious or coutracted 6 4. Right ventricle divided into two cavities by a supernumerary septum . U 5. One auricle and one ventricle 12 6. Two auricles and one ventricle 4 7. A single auriculo ventricular opening; iuterauricular and intraventricu- lar septum incomjdete 1 8. Mitral orifice closed or contracted 3 9. Aorta absent, rudimentary, impervious, or partially obstructed ... 3 10. Aortic and the left auriculo-ventricular orifice impervious or contracted . 1 11. Aorta and pulmonary artery transposed 14 12. The cavae entering the left auricle - . . 1 13. Pulmonary veins opening into the right auricle or into the cavae or azygos veins 2 14. Aorta impervious or contracted above its point of union with the ductus arteriosus; pulmonary artery wholly or in part supi)lying blood to the descending aorta through the ductus arteriosus 2 Total 162 The ciiances are ai)out ton to one that in cyanosis of the newborn the lesion is al>sence of a properly developed interauricular or inter- ventricular wall. In the adult or child cyanosis may be produced by serious cardiac disease, by pulmonary disease, such as pneumonia, pul- 13 194 THE MANIFESTATION OF DISEASE IN ORGANS. mouary congebtiou, and bronchiectasis with emphysema and asso- ciated cardiac dilatation. It also occurs iu laryngeal obstruction arising from external pressure or intralaryngeal difficulty, and in cases of asthma of a severe form. (See chapter on the Thorax and its Viscera.) In some cases of paretic dementia the skin of the forehead is dull and dusky-looking. In other instances a grayish-blue or cyanotic appearance may arise from the ingestion of drugs, which reduce the haemoglobin of the blood, sucii as antipyrine or acetanilid, and in such instances the discoloration is first seen about the base of the thumb-nail or in the skin of the face, particularly if the patient be examined from a little distance. The condition of the skin, so far as its nutrition is concerned, is of great importance in diagnosis. In profound failure of the vital forces continuing over a great length of time it becomes abnormally dry and scaly, the hair becomes straggliug and lustreless and frequently falls. In young persons suffering from grave disease of the lungs or heart of a chronic type there is often not only an undue dryness of the cuticle, but an abnormal growth of downy hair all over the body and limbs, and more particularly down the spine and over the breast-bone. Eruptions on the Skin. The influence of age upon the development of skin lesions is very great, and Stephen Mackenzie has summed up the relationship of skin disease to age in the fol- lowing amusing manner: "The seven stages of man could be well illustrated by diseases of the skin, though we lack a Shake- speare to do justice to the theme. In the ' mewling and puking ' infant we meet with sclerema and oedema neonatorum, the ' red gum ' or strophulus of the older writers, intertrigo, eczema, urticaria papillosa (lichen urticatus), urticaria pigmentosa, xeroderma pig- mentosum, and impetigo ; the ' schoolboy,' with his chilblains and ringworm, alopecia areata, pityriasis rosea, ecthyma, and ' foot- ball disease ; ' and then the ' lover,' with his acne and sycosis, and, as a result of irregular sexual excursions, his syphilides ; ' and then the justice, in fair round belly' with acne rosacea, diabetic boils, and pruritus ani ; the sixth stage shifts into the ' lean and slippered pantaloon,' with rodent ulcer and ' gouty ' eczema ; ' last scene of all, sans teeth, sans eyes, sans taste, sans everything ' — except an incessant and intolerable itching of the skin which we call senile prurigo." THE SKIN. 195 There are two conditions of the skin in which valuable evidence is given that the patient is suffering from rheumatism. One is the pres- ence of erythema in one of its many forms, the other is the appearance of purpura, or, as it has been called, peliosis rheumatica. That the presence of erythema points in many cases to rheumatic trouble is proved beyond all doubt, either erythema papulatum, amiulaire, marginatum, or nodosum being indicative of the systemic taint, but it is worthy of note that the erythema marginatum is most diagnostic and erythema nodosum the least diagnostic of rheumatic poisoning. Sometimes this eruption may be the only manifestation other than cardiac involvement, and when the marginate eruption is present severe cardiac involvement is commonly seen. The papulate erup- tion is most commonly found on the back of the wrists, the hands, and the feet when it occurs as a rheumatic sign, while the nodose variety is generally confined to the front aspect of the legs or the extensor surfaces of the arms. It must be remembered that these forms of erythema may be distributed anywhere over the body in rheumatism, but that they become especially diagnostic if limited to the areas named. Purpuric discolorations of the skin, somewhat resembling multi- ple bruises in appearance, are due to a number of causes and possess a varied significance. In the first place, they are due to the disease known as purpura hjemorrhagica, which may be divided intothe acute and subacute forms, and that which is secondary as the result of severe infections and certain poisonings. The acute form of pur- })ura runs a rapid course and reaches a fatal result in most cases in a short time. It is a comparatively rare disease and usually attacks young adults, chiefly males, up to twenty-eight years of age. It is sometimes seen in young girls and more rarely in young pregnant women. The chief symptoms consist in hemorrhages from the ujucous membranes, purpuric spots, high fever, and a general class of symptoms resembling those of sepsis, as chills, pyrexia, and exhaustion. In other instances active hemorrhages take place into the viscera, and if into the meninges of the brain cause cerebral symptoms at once. The liver and spleen are nearly always en- larged. The subacute type, while severe, runs a far more favorable course as to its manifestations and results. It usually attacks children or young adult males from twenty to thirty years of age. The patient after a feeling of wretchedness, and perhaps a chill, followed by the 196 THE MAXIFESTATIOX OF DISEASE IX ORGANS. purpuric eruption, is attacked by swelling of the joints and perhaps hemorrhages from the kidneys, bowels, and mucous membranes. If the hemorrhage be from the gums, the teeth are not loosened, as in scurvy. Prostration may be great and the patient appear as if suffering from typhoid fever. The prognosis is good for ultimate recovery. It is sometimes called peliosis rheumatica or Schon- lein's disease. This subacute form, however, occurs in a more severe manner, as " Henoch's disease," in the persons of children be- tween nine and twelve years, and is much more common in males than females (five to one). In this form we have as additional symptoms marked pain and tenderness in the belly and bloody stools, with tenesmus and active vomiting. The illness may last a long time, but recovery often occurs, about 25 per cent, dying. The joint- symptoms of the other forms of purpura may be slight or absent. Often, too, the purpura is accompanied or replaced by erythema. Subcutaneous fibroid nodules sometimes occur in cases of rheuma- tism and vary in size from a hemp-seed to a walnut. They are usually situated in the subcutaneous connective tissue, but may be attached to the deep fascia or muscular sheaths. The question as to whether purpuric eruptions are ever truly indicative of rheumatism has been much discussed and their diag- nostic value deuied, but the author believes that in some cases of rheu- matism purpura is a symptom, appearing often in the neighborhood of the involved joints, nearly always on the lower limbs, and often breaking out before any evidence of articular trouble exists. In other instances the development of the purpura is simultaneous with the disappearance of joint-trouble. The eruption usually fades in a few days, but frequent relapses or new crops of it often occur. Purpuric eruptions may be produced by quinine in persons who have an idiosyncrasy to this drug and by iodide of potassium, chloral, and salicylic acid. They may also accompany any severe infec- tious disease and follow the entrance into the body of any poison which destroys the blood, such as the poison of snake-bite. They also result from severe jaundice, from profound anaemia, from congenital syphilis with vascular changes, from endocarditis (a form of sepsis), and in eases of multiple sarcomata. Rarely purpura has followed fright and severe grief. Urticaria may occur as a manifestation of rheumatism, but it has no diagnostic value. Sometimes it ensues upon the use of salicylic acid, turpentine, and quite commonly follows the ingestion of iodide THE SKI X. 197 of potassiuai. The wheals produced by the latter drug differ from those of urticaria by being unduly red. The development of polymorphic skin lesions, consisting of hyperemia, cederaa, and hemorrhage, with arthritis occasionally and visceral disturbances, consisting in attacks of vomiting or diarrhcea, endocarditis, pericarditis, acute nephritis, and hemorrhages from the mucous membranes, indicates the j)reseuce of a condition called ery- thema exudativum multiforme. The attacks are apt to be recurrent. Sometimes the skin-manifestations are absent. Hemorrhages of tlie skin occur spontaneously in some cases of hysteria and paretic dementia and after epileptic attacks, particularly about the ey&s, and often from injuries received in other parts of the body during the convulsion. Minute hemorrhages may also occur in the course of severe whooping-cough, and, in the form of pete- chite, result from snake-poisoning, septicaemia, cerebro-spinal menin- gitis, iodism, ergotism, and after inhaling the vapor of benzine. They are also seen in scurvy and in some cases of profound wasting, as in the course of phthisis and carcinoma. Petechial rashes closely resembling those of malignant smallpox, typhoid fever, or cerebro-spinal fever may be due to the presence of acute ulcerative endocarditis. Hemorrhages into the skin sometimes also appear in the skin cov- ering a part affected by a severe pain in the crisis of locomotor ataxia. A very extraordinary manifestation of spontaneous subcutaneous hemorrhage is seen in wiiat is known as hsematoraa auris, a condi- tion in which a free extravasation of blood takes place into and beneath the skin of the ear. The color of the swollen ear is quite red in color if the hemorrhage has been recent, or dark blue if it is an old occurrence. The left ear is more commonly affected than the right and it is seen more commonly in males than females. Excessive redness of the skin is seen in acute inflammations of the skin or the subcutaneous tissues, and as the result of hot applica- tions, the redness being more and more marked as the heat is prolonged and is groat. Often the prolongal use of great heat will produce a peculiar mottling of the skin like that of an old bruise. Aside from the redness of th»' cheeks and forehead from blushing we should rememi)er the general flusliing seen so commonly in per- sons suffering from phthisis, particularly when they are excitid, which differs from the more dusky redness seen over the malar bones in hectic fever. 198 THE MANIFESTATION OF DISEASE IN OEGANS. Another interesting diagnostic sign in the skin is what is known as the " tache cerehrale,''^ a condition of vasomotor disorder in which wheu the finger is gently drawn over the skin of the fore- head a red patch speedily develops. It is seen in meningeal irrita- tion, brain abscess, epilepsy, in some cases of exophthalmic goitre, and in paretic dementia. Sometimes it is called " tache meningealeJ' Erythema or rose-rash, sometimes called roseola, is a redness of the skin and occurs in many pathological conditions. It may be localized or diffused. In a number of diseases it aids us v^ery greatly in reaching a diagnosis, but the physician should always be cautious in depending much upon it, since it may mislead, owing to the fact that it often appears when dev^oid of diagnostic importance. The development of a diffuse, punctuated rose-rash on the skin of a person who is suffering from malaise, fever, nervous disturbance, and sore throat should direct the physician's attention to the possible presence of two infectious diseases, namely, scarlet fever, which is more common in childhood, and syphilis, which is more frequent in adults. The rash of scarlet fever is of a very bright-red color and shows itself at the end of the first, or on the second day of the dis- ease, first appears on the chest and neck and then speedily in- volves nearly the whole surface of the body, although the fore- head often escapes and the skin about the corners of the mouth remains nearly always white and free from eruption. On the other hand, the soles of the feet and palms of the hands are very markedly affected. So intensely reddened is the patient's surface that it may have the color of a boiled lobster. This redness depends upon an acute hypersemia of the skin, which though removed by pressure in- stantly returns when the finger is withdrawn. A noteworthy point is its punctate and mottled appearance, for, while the entire skin may be red, there are points which are more red than the rest of the skin and also certain areas which are particularly so. The skin is often slightly swollen and feels teuse, and itching is commonly present. The rash usually lasts three or four days and then fades, desquama- tion of the cuticle speedily setting in, which is completed in al)out two weeks. Sometimes, however, it remains for ten days to three weeks. Often when the rash can scarcely be seen on the skin its full development will be found on the pharyngeal wall. In the malignant types of scarlet fever petechise and subdermal hemorrhages occur. An erythema'reserabling scarlet fever, not only in its appearance, THE SKIN. 199 but also by its association with swelling of the lymphatic glands and reddening of the mucous membranes of the mouth, sometimes de- velops about the second or third day in cases of dengue or break- bone fever. In children there are several other conditions than scarlet fever which are associated with rose-rash, and these are more apt to lead to errors in diagnosis tlian is the rash of syphilis. The most frequent of these is erythema roseola, or roseola of acute indigestion, or that following the use of a food to which the patient has an idiosyncrasy. It is generally, but not always, widely diffused and is often asso- ciated with acute and severe febrile movement and vomiting, but it can be separated from scarlet fever by the facts that there is an absence of severe constitutional and nervous symptoms (except in neurotic children), there is no sore throat nor enlarged cervical glands, and the rash does not come out on the clavicles and grad- ually trav^el down the body. Another condition closely resembling scarlet fever is rarely seen, namely, acute exfoliating dermatitis, called, in its mild form, erylhema scarlatiniform, which has a sudden onset with febrile movement and a rash which rapidly spreads over the entire body and lasts four or five days, finally ending in desquamation. So closely may this dis- ease resemble scarlet fevei that a diagnosis during the first attack may be impossible for the first few days, but the condition of the throat and tongue does not resemble the condition seen in scarlatina. Dosqiramation is often even more complete than in scarlatina, and the hair and nails are frequently shed, lielapses are very common and give rise to the reported cases of repeated attacks of scarlet fever. The rash of rubella or rotheln (Gorman measles) is a roseola and more closely r-esembles that of scarlet fever in some cases than it does that of measles, but it is never as scarlet, is distinctly macu- lated, and only at a distance looks homogeneous. Close examination always r-cveals the rash in oval patches, and it lacks the diffused char-actor of the rash, the jjunctation of the skin, the gr-avo systemic disturbance, an:, if it be variola, it per- sists. This is called the " grisolle sign." Among other diseases in which rose-rash appears we find diph- theria, septicferaia, cholera, typhoid fever, malarial poisoning, and Bright's disease. In diphtheria it may lead the physician to a diagnosis of scarlet fever with severe faucial manifestations, and only a careful examination of the throat, the rapid subsidence of the rash, and the bacteriological examination of the false membrane will settle the diagnosis. Sometimes, however, a roseola appears late in the course of diphtheria, probably as a result of septic absorption. The presence of a very high temperature, of nervous irritability, and the predominance of the throat-lesions of scarlet fever ought to decide the diagnosis in favor of scarlet fever. The roseola of early syphilis resembles that of scarlet fever, in that it first appears on the trunk, but it is not bright scarlet, but rather dusky red. It appears in patches and is not diffuse, and it ensues about six weeks or three months after the appearance of an initial lesion, occurs in an adult as a rule, is not associated with high fever, and soon involves the face and forehead. These symp- toms aid us in separating it from scarlet fever, although it often ap- pears in full blast in the palms of the hands and soles of the feet, but a roseolous rash in these areas in an adult is always suspicious of specific trouble. These patches speedily change from rose-rash to other more marked lesions in cases of syphilis, and one of the first changes that they undergo is to become circinate. They fade and reappear, last an indefinite time, fade in the centre, and so change into marginate or circinate erythema. When roseola develops after a surgical operation or after deliv- ery in a j)U('rn('ral female, it is not scarlet fever, but is due to sepsis, although it is of course possil)le for scarlet fever to attack such cases at any time. The rash is usually found over the abdo- men and inner sides of the thigh. The absence of sore throat, the possible presence of aseptic process, and the absence of a strawberry- tongue all help to exclude scarlatina. Sometimes, late in an attack of cholera, a rash like surgical roseola appears in the same areas, or in the period of reaction, comes out on the forearms, backs of the hands, and rarely on the back. The roseolous rash of typhoid is sometimes widely distributed and 202 THE MANIFESTATIOy OF DISEASE IN ORGANS. almost like measles in appearance, but, as a rule, it is limited to a few or many rose-spots on the abdomen, chest, or back. These rose- spots disappear on light pressure, but immediately return when the pressure is removed, and are most marked in typhoid fever about the seventh to the tenth day of the disease. They may be- come slightly papular. In the relapse of typhoid fever the rose- spots often appear as early as tjie third or fourth day. In typhus fever they are much more plentiful and often form petechise. In Bright's disease a roseola often appears over the feet and ankles, wrists, and hands, and sometimes spreads to the skin of the chest and abdomen. Desquamation may take place, but absence of febrile move- ment and the presence of renal trouble render the diagnosis easy. This manifestation has not a dangerous import. A dusky red rash rapidly spreading over the neighboring skin, above the level of which the affected area is raised, and which is separated from the sound skin by a sharp line of demarcation which can be both seen and felt, is characteristic of erysipelas. The skin soon becomes brawny to the sight and touch, and the line of demarc- ation feels particularly indurated. Most commonly the disease appears on the face, starting from the inner canthus of the eye, the nostril, or the corner of the mouth. Very rarely does erysipelas affect the skin of the trunk. The fever may be quite marked, even in mild cases, and usually falls by crisis on the sixth day. In severe cases with fatal tendencies there may develop in place of crisis a typhoid state with low fever and delirium. If the disease be severe, blebs and bullpe form, and oedema of the skin becomes very profound, and finally suppuration may occur, forming what is known as phlegmonous erysipelas (see also Glanders). Erysipelatous inflammation of the skin without systemic disturb- ance may follow the application of arnica. A condition also closely resembling erysipelas in its raised surface is urticaria, which, how- ever, differs so materially in other respects that a diagnosis is readily made. Aside from the absence of systemic disturbance in urticaria the swelling of the skin is not red, but pale and pearly in hue, although it may be surrounded by an erythematous blush ; the onset is extraordinarily sudden, so that a skin seemingly normal at one moment after a slight bruising by the finger or rubbing by the clothes develops the complete eruption in a moment. A marked roseola or dermatitis involving the inside of the thighs or the scrotum or vulva should give rise to the belief that the patient THE SKIX. 203 is suffering from some failure properly to pass or retain the urine, which, on escapini;, irritates the skin. This is particularly apt to result if the urine is that rcs from Periphery to Cord. Cerebrum and Cerebellum, il-'lntnii.i THE SKTX. 225 ratus. In other words, auything which interferes with the trans- mission of an impulse to the perceptive centres in the brain may be its cause. Of the functional causes, the most frequent is hysteria, and the presence of ausesthesia in a female should always arouse a suspicion of its being due to this cause. Earely it is seen in hysteri- cal males. The organic causes of anaesthesia of the skin are cerebral hemorrhage, cerebral tumor, hemorrhage of the pons or tumor of the pons, hemorrhage of the cord, tumor of the cord, myelitis (trans- verse), locomotor ataxia, cerebro-spinal meningitis, spinal meningitis, compression of the cord by vertebral caries, by fractures, by dis- locations, and hemorrhage into its membranes. Additional causes are pressure on the posterior nerve-roots, by reason of caries and growths, inflammation of the nerves (neuritis), injuries to the nerves by blows, pressure, or cutting, and, finally, by paralysis of the nerve- endings by cold or the action of drugs. Anaesthesia, because of its area of distribution, may be divided into hemiansesthesia, crossed ansesthosia, bilateral anfesthesia, irregu- lar but complete anaesthesia, and partial anaesthesia. Hemiansesthesia occurs most frequently as a result of hysteria, next most commonly from lesion of the posterior part of the internal capsule, and more rarely from spiual injuries or growths in the cord of a unilateral character. The hemiansesthesia of hysteria involves, as its name implies, one side of the body, and is usually universal on that side, except that here and there there may be patches of hyperesthesia or tenderness, dotted like oases in the midst of the absence of sensation. This antesthesia is often unaccompanied by motor jiaralysis, and its area is separated from the opposite side of the body by a sharp line of demarcation, which runs along the middle of the trunk and face. The presence of such a well-defined line of separation in a young woman is of great significance of hysteria. The anaesthesia is generally absolute, and severe injury may be done to the skin in some cases without the patient feeling it; but, notwithstanding its intensity, it is a noteworthy fact that the ana3sthesia may transfer itself to the opposite side of the body with great suddenness, and equally suddenly return to its cai'ly site. In a great majority of cases, for some unexplained reason, the left side is the one affected by auiesthesia, and hyperiesthesia of the opposite side increases the contrast which exists between it and that in which sensation is lost. (See Hyperresthesia.) In some cases of iiysterical hemiana>stliesia 15 226 THE ^IANIFESTATIO^' OF DISEASE IN ORGANS. the paralysis of sensation involves the nerves of special sense, and loss of smell, taste, hearing, and impairment of sight may ensue on the same side. The peculiarity of the visual changes are so char- acteristic that they practically decide the character of the case when they are discovered in any instance of doubtful diagnosis, and consist in a loss of the color- vision (first, violet is lost, then blue, and then red) and a great limitation of the visual field, whereas in the heraianses- thesia due to an organic lesion in the internal capsule, so situated as to involve the nerve-fibres connected with vision, there is hemiopia. Hemianopsia, due to hysteria, is so rare as to be denied by most authorities, but Lloyd and de Schweinitz have seen a case. Gen- erally the loss of vision on the aufssthetic side is a total one for both sides of the eye in hysterical blindness. (See chapter on Eye.) Nearly always in hysterical hemianaesthesia a spot can be found over the shoulder which is not ansesthetic. The age of the patient, her sex, the general expression of the face, and the history of her illness, associated, as is frequently the case, with some, or all, of the hysterical symptoms detailed further on in this chapter, will generally decide the diagnosis in favor of hysteria. A form of hysterical hemianaesthesia very apt to lead to an error in diagnosis is that seen in persons who have suffered from infantile cerebral paralysis with the resulting deformity (a disease not char- acterized with sensory disturbances), but who have in later life super- imposed upon the old picture of disease that of hysteria with this sensory manifestation. Anaesthesia, irregular in its distribution, or absolute hemianaesthesia, may occur in the course of chorea. The presence of chorea in its motor manifestations clears up the diagnosis as to the cause of the loss of sensation. Hemianaesthesia when not hysterical is nearly always due to an organic lesion in the posterior part of the hinder limb of the internal capsule on the opposite side of the brain from the anaesthesia, and the additional symptoms which sometimes accompany it depend for their existence upon whether the lesion is large enough to involve, not only the fibres from the cutaneous areas, but also those of special sense, such as sight, hearing, or taste. Nearly always the area destroyed is sufficiently large to result not only in hemianaesthesia, but also loss of motion on the same side. The loss of sensation in such a case is rarely as complete as in hysteria, and the sole of the foot and palm of the hand are often not affected. In rare instances, THE SKIX. 227 however, the hemiansesthesia of capsular disease may be absolute and universal, or, more rarely still, occur in patches, thereby closely resembling the aujesthetic patches seen iu hysteria. Hemiansesthesia may also be produced by a large lesion of the cortex in the occipital, temporal, and parietal lobes, in which case it will involve the side of the head as well as the trunk, aud will be associated with such definite evidences of apoplexy or injury that the diagnosis will be readily made. If it is widespread, all the special senses will be involved. Sensory disturbances of the skin are more frequent in softeniug of the brain than iu hemorrhage into the brain, and most commonly are associated with subcortical, rather than cortical lesions. In this connection it should be remembered that the irregularity of distribution of the lesions in disseminated sclerosis may cause a hemiansesthesia, partial or complete. Anaesthesia resulting from tumor of the brain occurs iu about 20 per cent, of the cases of brain-tumor, aud may be unilateral and confined to the paralyzed side, or appear as an isolated symptom without motor paralysis. When of the latter form it is often asso- ciated with lesions iu the neighborhood of the fissure of Rolando, and iu tumors involving the posterior parietal region and the pos- terior part of the internal capsule. Autopsies aud experiments show that hemianiesthesia may arise from a lesion in the optic thalamus, but such an occurrence is very rare. A very important and essential factor in making the diagnosis that the anresthesia is cerebral in origin is the history of the begin- ning of the attack, which has been sudden if due to hemorrhage, embolus, or thrombus (see Hemiplegia), and characteristic of the con- dition which we call apoplexy. Unilateral an:c.sthesia associated with motor paralysis, l^oth being somewiiat irregular in their distribution, may be due to a lesion, such as a tumor in the pons or medulla ol)longata, but death so com- monly ensues soon after the apoplexy that the symptom is often overlooked or cannot be developed. Further, the discovery of such antcsthesia does not positively localize the lesion in the pons, for we do not know much al)out the course of the sensory fibres in this part. If, however, the area supplied by the trifacial nerve, namely, tile face, is anajsthetic, and these symptoms are associated with it, then it is fair to assume that the trouble lies in the pons aud 228 THE MANIFESTATION OF DISEASE IN ORGANS. has involved the nucleus of the fifth nerve. (See Anaesthesia of Face.) Anaesthesia of irregular distribution or confined to one limb may result from cerebral or spinal lesions, or be due to a neuritis, of which form we shall speak further on. If it is a monoansesthesia from cerebral disease, which is very rare, the ausesthesia is most marked at the distal part, and gradually fades off as the trunk is approached. It is evenly distributed, so far as circumference is concerned, and has no sharp line of demarcation. When such an anaesthesia is due to spinal disease the cause may be tumor of the spinal cord, the symptoms depending in their char- acter on the area involved; but in any event the upper border of the area involved is sharply outlined and a constriction-band sensation is often present. The irregular form, due to hysteria, has the same general pecu- liarities of migration as are seen in hemianesthesia from this cause, and in its symmetrical form it closely resembles the anaesthesia due to multiple neuritis. Thus, in the hand the area of anaesthesia may be that covered by a gauntlet glove, in the foot that covered by a sock, the line of normal sensation being present just above the place to which these protections usually extend. Crossed Ax.esthesia. When sensory paralysis of one side, asso- ciated with partial paralysis of motion or paresis on the same side, comes on, and with it there is hyperaeraia of the skin on that side from vasomotor paralysis, there is a strong probability that there is a lesion in the cerebral peduncle of the opposite side. If there is at the same time paralysis of the muscles supplied by the oculomotor nerve on the opposite side from the anaesthesia — that is, on the same side as the lesion, this diagnosis is still further confirmed ; and if the tongue and half of the face of the paralyzed side of the body are paralyzed, still further confirmatory evidence of a peduncular lesion is obtained. Thus there might be hemianaesthesia and paralysis of the right side of the body, including the face and right half of tongue, and ptosis, from oculomotor palsy, on the left side of the face. The paralysis o5 the body, face, and tongue would be on the side opposite to the lesion, but the oculomotor paralysis would be on the same side as the lesion. Crossed anaesthesia of the limbs and face — that is, anaesthesia of one side of the body with antesthesia of the opposite side of the face — can only occur in lesions involving the upper part of the pons in ' THE SKIX. 229 such a way that the fibres of the trifacial are diseased on one side, and the path for sensory impulses of the other side of the body is also destroyed. (See chapter on Face, Head, and Hemiplegia.) An important point to be noted in the diagnosis of cerebral anaes- thesia is the fact that the reflexes are preserved, though the patient may not feel the touch or painful impression ; that is to say, irrita- tion of the skin causes movement in the arm or leg, not by any intention of the patient, but owing to the fact that the sensory cen- tres in the cord receiving an impulse cause the corresponding motor centres to send out impulses which contract the muscles. Partial hemiantesthesia, with partial hemiplegia on the opposite side in crossed paralysis, may occur from lesions on one side of the spinal cord, and, if high up, involve a large part of the trunk and lower limbs. (See chapter on Feet and Legs, part on ^Myelitis. ) These cases have been explained by a theory of Brown-Sequard, which has recently been doubted owing to the studies of Mott and others. Thus, until recently, it has been considered as proved that sensory impulses entering the cord crossed to the opposite side almost at once, at least in greater part, passing to the lateral columns in front of the pyramidal tract, and that a very small num- ber entered the posterior columns, while a few ascended in the gray matter. The recent studies of Mott, in confirmation and criticism of still other investigators, seem to prove that the reverse is the case and that the greater part of tiie sensory impulses do not cross the cord, only a few fibres passing to the opposite side on entrance. He be- lieves that the main pathway for heat and cold sensations is in the gray matter, while the tactile pathways are in the posterior columns, although it is possible that some few isolated fibres may exist in the lateral columns and that these cross in the cord about the level of entrance. Bilateral An.ksthesia. Anaesthesia of hysterical origin in- volving both legs, and sometimes the lower part of tlie trunk on both sides, may occur, and, aside from the tyj)ical signs of hysteria in general which distinguish it, may be discovered by the fact that in hysteria the failure of sensatiDU does not involve the skin of the genitals, as it does in organic lesions producing somewhat similar symptoms. In addition it will be found that in hysteria a V-shaped piece of skin over the sacrum is not aujosthetic. Ansesthesia of this variety, corre- sponding in the sensory organs to what we call jviraplegia in the motor aj)paratu-*, is practically never produced by a cerebral lesion, 230 THE 3IANIFESTATI0N OF DISEASE IN ORGANS. and, if not hysterical in cause, must be spinal ; but it is much more rare than is motor paralysis in these parts from lesions in the spine. When it does ensue from spinal causes motor paralysis will in the great majority of cases be found associated with it at least to some extent. To express it concisely, the characteristic of a typical spinal anaesthesia is that it is bilateral and usually involves both sides quite symmetrically ; that motor paralysis is generally associated with it ; that the reflexes are greatly perverted ; and that trophic changes may be present as a result of an involvement of the trophic cells in the anterior cornua coincidently with the disease of the sensory parts of the cord. The diseased conditions of the cord which result in symmetrical anaesthesia of the skin of the legs and trunk are, first and most prominent, locomotor ataxia ; second, myelitis ; and, finally, hemor- rhages, tumor of the cord or its membranes, meningitis, or injuries which cause pressure on the sensory tracts by producing fracture of the vertebrae or dislocation. Very rarely, however, a lesion of the pons may so result. Anaesthesia of the lower portions of the body and legs occurs in the later stages of locomotor ataxia, and is usually preceded by forms of paraesthesia. (See Paraesthesia.) The anaesthetic areas are most marked in the soles of the feet and about the malleoli, according to Belmont. In other words, blunting of sensibility is seen in nearly all cases of tabes dorsalis late in the disease. In some cases the sense of touch is preserved and the sense of pain lost (analgesia), while in others the opposite condition is present. Again, we find loss of tactile sense and of pain-sense without loss of heat and cold sense and vice versa. A very characteristic sensory symptom of tabes is the delay in the recognition of an irritation of the sensory nerves, so that if the patient be blindfolded and then pricked with a pin he will not make an exclamation or draw his foot away for several seconds. In other instances the patient com- plains of repeated pricks when only one has been given, or, when asked the number of points pricking him, states that there are four or five instead of the one really present. If, in addition to these sensory disturbances, we rind Romberg's symptom (see Legs), Argyll- Robertson pupils (see Eye), and loss of patellar reflex (see Reflexes), and a number of the other diagnostic peculiarities of tabes, the deci- sion as to the cause of the anaesthesia is easily made. Slight anaesthesia, retardation of the transmission of sensory im- THE SKIX. 231 pulses from the skin, and perversions of temperatiire-sense may be rarely developed late in the course of Friedreich's ataxia: Bilateral anaesthesia of the character just discussed, as caused by locomotor ataxia, may also occur as a result of acute or chronic myelitis. The first change under these circumstances is a mere obtiuuling of sensitiveness, which gradually deepens till loss of pain-sense, pressure-sense, and, lastly, complete anaesthesia is de- veloped. The development of these symptoms indicates involve- ment of the posterior columns. Loss of reflex activity in the legs is developed in direct proportion to the destruction of the motor and sensory nerve-tracts in the cord. The predominance of motor paralysis, the fact that the lower limbs are both involved, and the absence of the characteristic symptoms of locomotor ataxia all tend to make the diagnosis certain, while the absence of the'^painsof tabes and the other signs of that disease still furtlier exclude its presence from the case. Furtlier thau this, the myelitis creeps up the cord, involving new areas, aud new parts of the skin become auEesthetic. An important point, too, in regard to the anaesthesia of acute myelitis is this, namely, that while in the upper extremities the loss of sensation and motion is associated, so that both functions are lost in the same area, in the lower extremities these two functions are not lost in the same areas. Thus myelitis of the lumbar enlarge- ment in its lower part is accompanied by anaesthesia of the gluteal area and motor paralysis of the anal muscles ; and, again, anaesthesia of the gluteal region, the back of the thigh, and the back of the calf is associated with loss of power in the muscles that move the foot, while in lesions of the upper part of the lumbar segment the anaes- thesia involves the thigh, the inner side of the leg and the foot, in association with paralysis in the quadriceps extensor and deeper muscles of the thigh. (See chapter on Feet and Legs, part on Mye- litis.) The development of sudden bilateral anaesthesia, which is accom- panied by severe pains of a tearing or burning character, creeping rapidly up the body, is indicative of acute hemorrhage into the spinal membranes, or it may be due to that very rare lesion, hemorrhage into the cord. In either case motor paralysis is present. Anaes- thesia, or the milder perversions of normal sensibility of the skin, may be present in cases of compression of the cord by caries, and by curvature, tumors, or aneurisms producing erosion. Sometimes, while tactile anscsthesia is complete in these cases, severe pain is con- 232 THE MANIFESTATIOy OF DISEASE IX ORGANS. stantly suffered (autesthesia dolorosa), aud this is often the case, according to Wood, in cancer of the spine. Partial anaesthesia of the skin of the trunk and arms of a bilateral character, associated with progressive muscular atrophy, scoliosis, aud trophic lesions in the skiu, points strongly to syringomyelia. The loss of pain and temperature-sense is usually the first symptom. The areas of anaesthesia are best shown in Fio;. 93. Fig. 93. Sensorv chart, .showing j 1 areas of [ yj^ermo- Anaesthesia, :iJii 1 Analgesia_ n^S^-iS''^'"' Tactile Anaesthesia and areas in which the patients answer to tests of temperature showed reversal O O o o c o o o Cold-Hot; (Dercum.) Hot-Cold. Having considered the general spinal causes of anaesthesia of the skiu, it yet remains to determine what part of the cord is involved by the pathological process ; and this is fortunately possible, chiefly through the very accurate and noteworthy studies of M. Allen Starr, Thorburn, and Head, not to mention collateral ones of great value by Horsley and many others; but the field is only partly covered, and some of our uncertainties depend upon lack of knowledge as to the course of the sensory fibres in the cord. Roughly, we may state that disease of the cervical cord generally produces disturbances of sensation in the arms, hands, and fingers ; THE SKIN. 233 disease of the dorsal cord, disturbances in the sensation of the back and trunk, which may radiate into the thighs ; and disease of the lumbar cord gives rise to these symptoms in legs and feet. Fig. 94. 1st to 7th cervical segment. 1st to 12th dorsal segment. I- 1st to 5th lumbar segment. 1st to 5th sacral segment. Diagram showing the surface-ureas of the back corresponding approximately to the areas of the spinal cord supplying the trunk and limbs. Again, it is to be remembered that, as a rule, in a transverse lesion of the spinal cord the ana?sthesia begins at a les'el which is three or four inches below the lesion in the cord (Horsley and Gowers) ; this being due, as proved by Sherrington, to the fact that each area of skin is supi)lie(l by three nerve-roots whose peripheral filaments overlap one anotiier. For the ready study of the subj'^ct the cord has been separated into segments corresponding with the vertebric covering it. The areas of ansestlicsia produced by .spinal injury or disease are best described in Starr's well-known article and diagrams, from which we quote. In this connection the reader should refer to the tabic on pages 97 and 98, showing the localization of the functions of the segments of the spinal c^ord. (Sec chapter on Legs and Feet.) The anrcsthetic areas included in zones I. and II. in Fig. 95 are 234 THE MANIFESTATION OF DISEASE IN ORGANS. due to a lesion involving the conus raedullaris and the fourth and fifth sacral segments of the cord. These zones include the perineum, the posterior part of the scrotum in males, the vagina in females, and the mucous membrane of the rectum. Anaesthesia in zone III. is due to lesion of the third, fourth, and fifth sacral segments, and includes a large part of the buttock and the upper part of the thigh, posteriorly, in a triangular space. Zone IV. is practically an enlargement of zone III. in every direction, particularly toward the popliteal spaces, and is probably due to a lesion in the first and second sacral seg- FiG. 95. VII WW Areas of ansesthesia iu lesions at various levels of the spinal cord from sacral v. to lumbar ir. (After Starr.) I. Sacral v. IV. Sacral i. II. Sacral iv. V. Lumbar v. III. Sacral in. VI. Lumbar iii. VII. Lumbar ii. ments ; but this needs confirmation, as Starr points out, by autopsy. Zone V. includes all the first four zones just named, and extends down through the popliteal space in a band-like shape ; after it passes this space it descends the outer side of the leg and foot, sometimes ending at the ankle, sometimes at the sole or the three outer toes and half the next toe. Such an area indicates a lesion involving all the segments of the sacral cord, and extending into the lumbar cord to the fifth lumbar segment. Zone VI. is caused by a lesion extending THE SKIX. 235 to the third lumbar segment, and when it is present the anesthesia covers the back of the thighs and legs and also the front of the thighs, except in an area which extends from above downward along the shin, sometimes to the foot, as in Fig. 95. If the foot is in- volved, the lesion in the lumbar cord is probably above the third lumbar segment. Zone VII. , which is larger than all, follows a lesion in of the four lumbar segments — that is, all but the first. The line of anaesthesia, Starr tells us, is lower in front than behind. When the abdominal wall is involved in the anaesthesia the first lumbar segment is probably diseased. The ascent of anaesthesia from the abdomen up corresponds very closely to the levels in the cord if we allow for the space already mentioned, of two to three inches for the interlacing anastomosis of the nerve-fibres of the posterior roots. They are about as follows, according to Thorburn : AVhen the anaesthesia is as high as the anterior inferior spine of the ilium, the lesion is at the twelfth dorsal vertebra ; if at the umbilicus, at the eleventh and twelfth dorsal vertebra ; if up to the lowest floating rib, the whole eleventh dorsal vertebra ; if to one to "four inches above the umbilicus, the ninth and tenth dorsal, and perhaps part of the eighth dorsal vertebra ; if as high as the nipples, the fourth dorsal vertebra ; and if to the third rib, the lesion is as high as the second dorsal verterba. Starr has also given us in another paper than that already quoted equally good ideas of the areas of anaesthesia occurring above those just described. (Fig. 96.) When the anaesthesia extends to the arras and is found upon the inner side of the arm and the forearm, reach- ing to the wrist, but not to the hand, and also involves a small zone on the extensor and flexor surface of the arm and forearm, the second dorsal region is the site of the lesion. If the anaesthetic area includes the ulnar side of the hand, the palmar and dorsal surfaces of the same, and the little ring-finger, and extends in a narrow strij) up to the axilla on i)oth the anterior and i)osterior surfaces of the arm and forearm, the lesion is probably at the level of the eighth cervical vertebra. When the zone involved extends to the middle of the central finger on the palmar and dorsal aspect, and runs "up the cen- tre of the forearm and arm, the seventh cervical area is diseased. Again, when the remaining skin of the hand up to the wrist and a narrow strip of skin up the forearm and arm on both surfaces to the axilla is affected, the lesion is at the sixth cervical vertebra, while 236 THE MANIFESTATION OF DISEASE IN ORGANS. ansesthesia of the forearm and arm on the outer surface as high as the deltoid insertion indicates that the fifth cervical vertebral area is in trouble. Lesions higher than this usually produce death before it is possible to test sensibility. Fig. 96. VII VII Areas of antesthesia from lesions and various levels of the spinal cord from the second dorsal to the fifth cervical. (After Starr.) Tn order that the reader may gain a still better idea of the prob- able, or rather approximate, area of distribution of the spinal nerves, the three charts of Thorburn, Starr, and Head are here reproduced, as prepared in colors, with significant lettering by Thorburn, for the International Medical Annual for 1896. (Plates VI., VII., and VIII.) Anaesthesia of the skin in any part of the body may not only be due to cerebral or spinal lesions, but also to neuritis or inflam- mation of a nerve-trunk, or to some injury which prevents its functional activity by pressure, bruising, or cutting. As a rule, loss of sensation from neuritis occurs late in the disease, hyper- sesthesia or parsesthesias being the earlier manifestations ; but in some cases these are absent and anaesthesia begins at once. The PLATE VII. (.•i-rvical Knots nrf rtpitsciitid by tlic letter C, Dorsal Roots by tin- litUi I),:iii:ir Koots liy ll-.e letter I,. (Chart after Tliorbiirn.) PLATE VIII. Cervical Konis are represented by the letter C, Dorsal Roots by the letter I), and Lumbar Roots by the letter I,. (Cliart after Head.) PLATE IX. Cervical Roots are represeutid by the letter C, Dorsal Roots by the ktltr I), atul Lumbar Roots by the letter L. (Chart after Starr.) THE SKIN. 237 characteristic of such an anaesthesia is that it is confined to the area supplied by the affected nerve, although the presence of a multiple neuritis may produce such a universal anaesthesia by involving all the nerves that this sign is masked. While a mono-anaesthesia might be due to other causes, it is in the great majority of cases due to neu- ritis. The signs of an anaesthesia due to neuritis are loss of motion and sensation, tenderness on pressure over the nerve-trunks supply- ing the affected area, trophic changes in the tissues of the part, with the development of reactions of degeneration and pain in the involved nerves or parts supplied by them. Somewhat similar symptoms occur in anterior poliomyelitis, but pain is not commonly present in this disease, and there is no anaesthesia, either in children or adults. (See chapters on Hand and Arm, Feet and Legs.) Toxic peripheral neuritis producing anaesthesia ma/ arise from poisoning by arsenic, lead, alcohol, and mercury, from infectious diseases, and from se[)tic states of the body. That due to the mineral poisons has in each case certain differen- tial points of importance. The anaesthesia of arsenical poisoning is more marked than in lead- poisoning, in which condition it is often almost absent, and the lower extremities are very apt to be involved, whereas in lead-poisoning, as is well-known, the nerves of the arm are peculiarly susceptible. (See Arm and Hand.) Arsenical neu- ritis may also produce pigmentation of the skin. In alcoholic neuritis the temperature of the anaesthetic areas is often subnormal and there are nearly always mental disturbances represented by delusions. In mercurial poisoning, shaking like paralysis agitans may be present. An analysis of the motor symptoms in all these cases is important, and the discovery of any one of these poisons in the urine, with the history of the patient, generally makes the diagnosis possible. Diphtheritic neuritis is quite common, and in 50 per cent, of the cases in which it occurs sensil)ility is lost or disturbed in the areas supplied by the involved nerves. (Ireatcare is needed in all cases of neuritis, lest the mistake be made of diagnosing the condition as one of locomotor ataxia, when in reality it is pseudo-tabes. It has already been stated that in neuritis the area of aiuesthesia is that supplied by the affected nerve. For this reason we can the area of one nerve, as the ulnar, or involve all the skin of the hands, or more rarely of the feet. General nervous excila- bility is generally associated with the local manifestations. Some- times the scalp may be the area involved. 244 THE MANIFESTATION OF DISEASE IN ORGANS. -Acroparaesthesia is to be separated from the sensory disturbances of hysteria by its irregular outline, for generally in the latter disease the areas are distinctly outlined, by the fact that the hysteri- cal condition is usually unilateral and by the absence of the char- acteristic general hysterical symptoms. From organic disease it is separated by the absence of the signs of neuritis about to be described, by the absence of tenderness, pain, and loss of power. From cere- bral or spinal disease it is separated by the absence of symptoms produced by lesions in these parts, aud by the fact that in both these instances there is paralysis of motion in association with the sensory disturbance, and in the case of spinal lesions the symptoms are usually in the legs, while acroparaesthesia generally manifests itself in the hands. Closely associated with pargesthesia, if not an actual form of it, is the *' girdle sensation ; " that is, the patient feels as if a tight belt was strapped around a limb on the trunk. This is seen as a prominent symptom in locomotor ataxia, myelitis, and tumors of the cord or its envelopes. When the lesion is in the lower cervical or dorsal region the sensation is in the chest or abdomen ; but this relation- ship between the growth and the sensation of constriction is not always constant. (See chapter on the Feet and Legs.) Hyper.esthesia of the skin is an important symptom of both hysteria and neurasthenia, and its discovery in association with the peculiar symptoms which occur in the former morbid state confirms a diagnosis most positively. The most important and curious of these hypersesthesias are the so-called hysterogenous zones, or, in other words, areas involving the skin and subcutaneous parts, which possess great sensitiveness and which, when pressed upon, cause in many cases convulsive seizures of the hysterical type. Not only is this true, but in addition it is a noteworthy fact that after the ner- vous disturbance produced by this means is set in motion, a second pressure on the hysterogenous zone may arrest the seizure. These zones commonly exist over the ovaries, in the groin, somewhere about the periphery of the mammary glands, or upon the spine in the lum- bar or dorsal region. (See chapter on Pain.) The hyperaesthesia due to neurasthenia is to a great extent spinal in character, but the skin of the rest of the back, particularly over the great muscles on each side of the spine, may also be involved. Often the neurasthenic patient will complain that in brushing or combing his hair pain or extreme sensitiveness is developed upon THE SKIN. 245 the scalp, and there may be tender areas on the chest. These areas in neurasthenics can hardly be confused, even by the careless, with the hyperaesthetic zones of hysteria, and the personal history and characteristics of the individual aid still further in separating the two conditions. Hyperesthesia of the skin, aside from that seen in hysteria and neurasthenia, occurs in peripheral neuritis and locomotor ataxia, the skin of the back being particularly tender in this disease, and is fre- quently seen in a zone extending a little above the anaesthetic areas of transverse myelitis, this hyperaesthetic area being soon rendered anaesthetic by the progress of the disease. Hyperaesthesia in the skin of the limbs is also rarely seen in myelitis, and when there is motor paralysis of one side and sensory paralysis of the other it is commonly found on the side on which motion is lost. A condition of excessive dermal hypenesthesia is also present in cerebro-spinal meningitis, in which disease it is often a very early symptom. It usually ajipears first in the legs, then in the hands and arms, and, finally, the skin of the face and head become involved. Hypenesthesia of the skin occurs, often associated with skin erup- tions, in that very rare condition called chronic leptomeningitis. Motor symptoms are nearly always present if the cord become involved. Hyperaesthesia of the skin is considered by some authors to be, when found in association with other characteristic symptoms, almost pathognomonic of brain-tumor. It may be found on the scalp, over a large part of the body, or in the part which is paralyzec?. It is also found during the convalescence of typhoid fever, and in re- lapsing fever. It also appears in the paralyzed side of persons suffering from hemiplegia, in the area supplied by a nerve suffering from neuralgia, particularly that of a migraine type, in the scalp of ])ersons suffering from gout, and in the same area in women about the time of the menopause. General tenderness of the skin or deeper tissues is quite frequently seen in cases of rickets, the child crying whenever it is moved, as if sore and tender, and tender spots often appear over the ribs in cases of pleurisy. Sometimes in a neurotic girl ai)iMit'the time of pul)erty, or in a woman, one breast becomes exceedingly painful and tender and the skin of the breast becomes so hyperajsthetic that the slightest touch causes pain. The whole breast is, moreover, tender, and the move- 246 THE MANIFESTATION OF DISEASE IN ORGANS. ment of the arm may be impossible, owiag to paiu thereby caused in the gland. This hysterical breast can be separated from the painful breast due to a tumor by the general diffuse character of the swelling, the failure to outline any distinct mass, the neurotic char- acter of the patient, and the age of the individual. The hypersesthesia of chronic alcoholism may be both dermal and deep, and is well marked along the course of the peripheral nerves, particularly where they emerge from deeper stuctures. It is also seen in the neuritis of lead and arsenical poisoning. Increased sensibility of the skin may follow the use of opium or ergot, and is met with in the course of, or as a sequel of, influenza, and in some cases of profound amemia. In some cases hypergesthesia is an early sign of the onset of non- tuberculated leprosy, and will generally be found in the course of the ulnar or sciatic nerves in such cases. A very interesting fact from a physiological and diagnostic point of view is that disease of the internal organs or viscera often pro- duces areas of hyperaesthesia or tenderness upon the skin, which, may in future be used to aid in the localization of the lesions. This sub- ject has been well studied by Head {Brain, 1893 and 1894), from whose researches much information may be derived, but the results of which will have to be confirmed in many cases before they can be used as diagnostic guides. (See article on Pain.) Pain in the skin is very various in its manifestations, and nearly always is due to functional nervous troubles. Duhring has noted a boring sensation in some cases. It should direct the physician's attention to the possibility of hysteria or tabes dorsalis. Pruritus or intense itching of the skin may be due to contact with some irritant, but its presence, if persistent, particularly if wide- spread or near the genitals, should always raise a suspicion of diabetes mellitus, or chronic lead-poisoning, or gout, or chronic con- tracted kidney. Very rarely opium may produce a pruritus, and jaundice is nearly always accompanied by some itching. Pruritus about the anus is often due to piles. Finally, one important point is to be remembered, viz., we can- not attempt to make a general diagnosis merely from a study of the areas of anaesthesia or other perverted sensibility of the skin in any case. The results obtained from studies of the sensation of the skin are only to be used as additions to the motor and other symp- toms which will be found discussed under the chapters on the Limbs. CHAPTER YIII. THE THORAX AND ITS VISCERA. The inspection of the normal and abnormal chest — Their topography — Altera- tions in the shape of the thorax^The rhythm of the respirations — The results of using inspection, palpation, percussion,, and auscultation in health and disease — The characteristic signs and symptoms of the various diseases of the thoracic organs. The chief coutents of the thoracic cavity consist of vital organs, which are unfortunately only too often subject to disease. A careful study of the signs associated with the normal functions of these parts is, therefore, of importance, as i^ also that of the symptoms indicating pathological changes. AVhile it is true that in many instances patients present themselves to the physician with well- marked objective and subjective symptoms pointing to abnormali- ties in the organs of the chest, it is also a fact that in many others none of these signs exist, or at least in such an indefinite manner that the physician's attention is not attracted to them, and as a result important thoracic changes from the normal are overlooked or made light of. AVe base our diagnosis of the character of a case by the changes which we find in the surface of the thorax as to its contour and as to its movements, by the respiratory and cardiac sounds and the other physical signs about to be described. Before we attempt to study the alterations produced by disease in this portion of the body we must, however, have a clear conception of the normal appearance of the chest and of the normal sounds which are produced within it. Inspection of the Normal Chest when free from clothing will reveal the fact that it is conical in form, tlie broader part of the cone being in the upper portion. Above tiie clavicles there is usually a slight depression (the supra-clavicular fossa), and below the clavicles, which may be somewhat prominent, there is also a slight convexity, which extends as far down as the fourth rib. This convexity varies considerably according to the muscular dcvelojimcnt of the individual, the f(ji-mation of the bony portion of the chest- wall, and the deposit of fat in the subcutaneous tissues of the chest. The nipple is by no means as definite a landmark as is sometimes thougiit, as its position. 248 THE MAXIFESTATIOX OF DISEASE IN ORGANS. in respect to the ribs under it, varies greatly in different individuals; and it is still further altered in its position by the presence of much fat under it, or, again, in multiparous women owing to the relaxa- tion of the breast. In the average adult male or virgin female the nipple is on a level with the fourth rib or fourth interspace. The ribs in a well-developed person are not prominent in the upper two- thirds of the chest, but in the lower third are more readily seen, particularly at the sides, because of their thin covering by muscles aud the other subcutaneous tissues and the skin. The sternum in front and the spine behind are normally in the middle line. Over the top of the sternum is a depression called the episternal notch. Fig. 103. The regions of the anterior aspect of the chest. The Roman numerals indicate the ribs. Lateral examination of the normal chest when compared to the front view will show that the autero-posterior diameter is less than the lateral diameter. The surface of the chest anteriorly, posteriorly, and laterally, has been arbitrarily divided by imaginary lines into spaces, as shown in the accompanying figure. The lines running from the middle of the clavicles downward through the nipple are called the mammillary lines. (Fig. 103.) The parasternal line, not shown in the figure. THE THORAX AND ITS VISCERA. 249 is a vertical line half-way between the middle of the sternum and the mammillary line ; and a line running down the side from the axilla is called the mid-axillary line. These artificial divisions enable us to describe the locality of symptoms. If we could see through the chest-wall, we would find that the lungs extend above the clavicks. Immediately back of the inner end of the clavicle is the beginuino; of the innominate vein, and back of this again the common carotid artery on the left side. On the right side the innominate artery bifurcates just behind the junction of the sternum and clavicle. The figure given below shows the relation of the cavities of the heart and its great vessels to the chest- wall. (Fig. 104.) Fig. 104. Position of heart in relation to ribs and sternum. Anteriorly the lung extends as far as the sixth rib on the right, but the dome of the liver reaches to the level of the fourth inter- space. On the left side the lung extends a little lower than on the right side. liaterally the lung on Ixtth sides extends to the ninth rib in the mid-axillary line. Posteriorly on the right side the lung 250 THE MANIFESTATION OF DISEASE IN ORGANS. extends as low as the tenth rib and on the left side as low as the ninth. Marked variations in the shape of the chest occur in healthy individ- uals without possessing any direct pathological significance. Thus, it is very common to see one shoulder slightly higher than the other, and, in the case of clerks or persons who work much at a desk, the left shoulder is very apt to be somewhat elevated. Occupations which cause the individual to assume certain positions, or to use cer- tain muscles continually, also cause variations in the contour of the thorax. Inspectiox of the Abnormal Chest. The configurations of the chest which show a tendency to disease or the results of attacks of disease are numerous. Fig. 105. Fig. 106. The alar chest of phthisis. Side view of same patient. The most familiar of these is the so-called phthisical chest, which has been called the '^ alar chest, " because the scapulae stand out from the back like wings. (Fig. 105.) The antero-posterior diameter, particularly in the upper two-thirds, is very slight, and instead of convexity in this part there may be flattening or hollowness. (Fig. THE THORAX AXD ITS VISCERA. 251 106.) This area scarcely moves on inspiration, but the lower thirds, which are bulging, move markedly with the respiratory efforts, as does also the epigastrium. The shoulders are very sloping, the neck, anteriorly, is receding at the episternal notch, but springs for- ward toward the Adam's apple and the chin. The ribs in the alar chest fall downward toward the belly from their points of origin, instead of coming forward in a normal curve. (Fig. 107.) Fig. 107 Phthisical chest. If, on the other hand, the chest bulges anteriorly and posteriorly to such an extent that the antero-postorior diameter is greater than, or equal to, the lateral diameter, and if this bulging is fairly uniform, the sliDuldcrs being elevated, the bai'k rounded, and the neck short in appearance from the raised shoulders, the patient is probably a sufferer from emphysema of the lungs. This chest is often called the ^' barrel-shaped chest." The chest-wall moves very little or not at all with the respiratory movements, which are chiefly diaphrag- matic. (Fig. 108.) Localized bulging of the See " Mediastinal Disease," by the autlior, Fothergllliuii Prize Kssay of Medical Society of London for 1888. 254 THE MANIFESTATION OF DISEASE IN ORGANS. apparently taking the pulse. In the newly born child in perfect health the respirations are often as high as forty-four, but in the adult male at rest they are usually about fourteen to sixteen per minute. During sleep the number may fall to eight or ten. The ratio of pulse to respiration is usually four to oue, but in disease it may be one to one. Rapid respirations not due to any recent sudden exertion are always indicative of respiratory trouble, primary or secondary. If the primary trouble be in the lung, it will probably be due to croupous pneumonia, catarrhal pneumonia, severe bronchitis, asthma, tubercu- losis, pulmonary abscess, or tumors of the luugs. If it be due to secondary lesions in the lung, it may arise from pulmonary oedema due to nephritis, from congestion or hypostatic exudation as the result of a weak heart, from pulmonary embolism, from a pleural effusion which seriously interferes with the action of the lung or lungs, from growths in the mediastinum pressing upon bloodvessels and so caus- ing exudation into the lungs or pieura, and from ascites or abdomi- nal growths pressing upon the diaphragm. If the lungs be clear of trouble, then the difficulty may be present in the trachea or larynx, either as the result of spasmodic contraction of these passages or because they are occluded by growths, such as papilloma or malig- nant growth, inside or outside, which may act by pressure, thereby narrowing the tube. Any cause which interferes with the patient receiving the full amount of air usually inhaled causes rapid breath- ing in order that the loss of air may be compensated for by increased frequency of respiration. There are, moreover, several other causes which affect the char- acter of the respiration without affecting the larynx or lung-tissue directly or indirectly. These are fever, which acts as a respiratory stimulant, and excitement, nervous or mental, particularly that of hysterical patients. Again, apoplectic seizures, ursemia, and diabetic coma may be accompanied by rapid breathing. The respirations are slowed or decreased in number by great obstruction to the entrance of air into the luugs from any cause ; by the action of poisons made in the body, as the poison of urnemia or diabetes ; by the effect of poisons swallowed or absorbed in other ways, notably opium, chloral, aconite, chloroform, or antimony. The rhythm or relative time of inspiration, expiration, and the pause is in health in the mouth and trachea as follows : If 10 repre- sents a complete respiratory cycle, inspiration is represented by 5,, THE THORAX AXD ITS VISCERA. 255 expiration by 4, and the pause by 1. If there is difficulty in the entrance of air into the chest, as in spasmodic croup, the inspiration is much prolonged. This prolongation is also sometimes very marked in cases of paralysis of the posterior crico-aryteuoid muscles. If there is difficulty in expelling the air, the expiration is prolonged, as in asthma or in emphysema. Sometimes Avhen the chest is flexible, as is that of a child, the in- spiration is jerking when there is obstruction to breathing. This is due to the fact that the chest is forced into expansion by muscular effort, and at the same time is subjected to the external atmospheric pressure, while the air slowly enters the lung owing to the obstruction. The most remarkable change in rhythm is the so-called Cheyne- Stokes breathing, iu which the patient after a pause of several sec- onds begins to breathe with gradually increasing rapidity^nd depth, and then after reaching an acme of hurried respirations gradually decreases their rapidity and depth till they fade to nothing, when, after a pause, the same process is repeated. This breathing is seen commonly in apoplexy, in uraemia, in braiu-tumor, in cerebro-spinal fever, in meningeal tuberculosis, in some rare cases of cardiac valvu- lar disease, probably as the result of embolism, and in haematuric malarial fever. Rarely it occurs in cases of acute febrile disease, as typhoid fever, scarlet fever, pneumonia, whooping-cough, and puer- peral septicaemia. It also may be met with in the course of diabetes. Its presence is an exceedingly bad prognostic sign, but cases of recovery after its onset have been observed, and Murri has reported a case in which Cheyne-Stokes breathiug lasted forty days, and Sansom one in which it lasted one hundred and eight days. If the cause be an acute disease, recovery is more common after this symp- tom than if it be due to some chronic process with an acute exacer- bation. The fuuttion of breathing and the movements of the chest are closely associated. In men the respiratory movements chiefly affect the lower ribs and the abdominal walls, owing to the fact that as the diaphragm descends it pushes the abdominal contents downward, so causing abdominal bulging. In women, however, this is not so marked, and the breathing is chiefly costal, the upper part of the chest moving more than the lower (costal breathing). If abdominal breathing is absent in a man and is replaced by breathing of the costal type, we can be assured that the movements of his diaphragm are impaired by the pressure of fluid in the al)d()mi'U (ascites) ; by 256 THE MANIFESTATIOX OF DISEASE IN ORGANS. peritonitis, causing fixation of the diaphragm, owing to pain ; by the presence of large growths in the abdomen or by great enlargement of the liver and spleen. Other possible causes would be a sub- phrenic abscess or a greatly enlarged cystic kidney, or hydronephrosis. If the costal breathing of a woman is absent, there is nearly always some pulmonary cause for it, such as faulty development, or, if due to disease, its absence arises most commonly from tuberculosis or pleurisy, or old pleural adhesions which bind down the chest-wall. Labored breathing (dyspnoea) is seen in all cases in which the blood cannot be provided with sufficient oxygen owing to obstruction to the entrance of air into the chest, to spasm of the bronchioles, or to the occluding of the air- vesicles by any form of exudate, croup- ous, catarrhal, or serous. These conditions may be primary or sec- ondary to disease elsewhere, as in ursemia or cardiac disease. Inspec- tion of the chest in such a case shows great activity of the accessory respiratory muscles, such as the sterno-mastoids, the scaleni, the pec- torals, and the abdominal recti. The nostrils are dilated and the face anxious. The posture of the patient is that of sitting up in bed. Finally, we have to notice the extent of the chest-movements. These are very slight in the characteristic chest of a person having a tendency to tuberculosis, and ia the barrel-shaped and rigid chest of emphysema of the lungs. Deficient expansion on inspiration is not only a predisposing cause for lung disease, but an important diagnostic sign. When one side of the chest moves more than the other to a considerable extent, we suspect, in the side which moves slightly, a pneumauia, a pleuritis, a pleuritic effusion or adhesion, or tubercular consolidation, provided that the patient has not naturally a greater development on one side than the other, or has not pursued a trade or occupation causing unilateral hypertrophy. In this connection should be mentioned the '^ wavy breathing," seen most commonly in pneumonia, a condition in which inspiration and expiration do not seem to occur regularly or evenly all over the chest, one part filling or emptying a moment before the other. This usually indicates a grave pulmonary condition. Palpation of the chest reveals alterations in its contour and in its elasticity. It will also reveal the ability of the thoracic viscera and the chest-wall to transmit vibrations produced by the voice (vocal fremitus). This so-called vocal fremitus depends upon the fact that below the vocal bauds lies a column of air which reaches to the vesic- ular portions of the lung, so that when an individual speaks this THE THORAX AND ITS VISCERA. 257 column of air is set into vibration and these vibrations are in turn transmitted to the chest-wall. Of course, a chest-wall greatly thickened by fat or by highly developed muscles will not transmit these vibrations as readily as a thin chest-wall ; but aside from these causes of variations in fremitus in health we have a number of causes in disease Avhich greatly modify vocal fremitus. It must be remembered, too, that this vibration is more marked in men than in women and children, because the voice of a man is so much louder and has greater volume. Vocal fremitus is also greater on the right side than the left, because the principal bronchus supplying this lung is larger than that of the left side, is joiued to the trachea at a less acute angle, and is nearer the vertebral column; and, again, as recently emphasized by Gary, the bronchus going to the right upper lobe is given off at a point very near the origin of the right bronchus, and in many cases '' fully two and a half inches above the corresponding left bronchial tube." Sometimes this upper tube comes off the trachea directly. The conditions of disease which cause a decrease in vocal fremitus are pleural effusions of any kind, which not only cut off the trans- mission of sound, but by their contact prevent vibration of the chest- wall ; pneumothorax, which causes collapse of the transmitting med- ium, the lung ; any condition which causes occlusion of a large bron- chus, such as tumor or a large mass of mucus, and great pleural thickening. When the vocal fremitus is increased it is an indica- tion of pneumonia, of tubercular thickening or consolidation of the lung, of the presence of cavities or of tumor in the thorax touching the chest-wall. Fremitus is increased in these conditions because the consolidated lung transmits the vibrations of the air in the bronchial tubes to the chest-wall, or, in the case of a cavity, the sound is trans- mitted directly to it, and it there causes so great a vibration of the air in tile hollow space that the vibration of the chest-wall is marked. (In this connection, see part of this chapter on Auscultation.) ral|)ation of the chest-wall will also give information as to the position and character of the cardiac pulsations. Thus, the apex- beat of the heart in persons standing erect will usually be felt, in persons not inordinately fat and who are healthy, between the fifth and sixth ribs, about two inches to the left of the sternum. (See Fig. 126.) If the apex-beat is below this level, its depression may be due to enlargement of the heart (hypertrophy or dilatation), to efTusion in the j)oricardial sac or pleural cavity on the left side, to 17 258 THE MANIFESTATION OF DISEASE IN ORGANS. pulmonary emphysema causing abnormal descent of the diaphragm, and with it cardiac hypertrophy. Sometimes tumors in the chest produce a similar depression. On the other hand, if the apex-beat of the heart is felt above the fifth interspace, the heart may be raised by pericardial adhesions following inflammation, by pleural adhesions or effusions, by abdominal effusion (ascites), by tumors, distention of the colon by gas, and by great enlargement of the spleen. Displace- ment of the apex-beat to the left is generally associated with down- ward displacement, and is generally due to hypertrophy of the left ventricle, to pleural adhesions, and particularly to pleural effusion on the right side. Displacements to the right are due to hypertrophy and dilatation of the right ventricle, so that the apex-beat is felt in the epigastrium or against the edge of the sternum. Pleural effusion on the left side may also cause this displacement. (See figures show- ing changes in cardiac area on pages 267 and 268.) The area of the normal apex-beat is about one square inch. In dis- ease this area often extends over several square inches, generally as the result of hypertrophy and dilatation of the ventricles. The strength of the beat in health depends largely upon the depth of the chest and the thickness of its walls. In disease it is increased in hypertrophy of the heart and decreased in cases of feebleness of the heart-muscle, by effusious into the pericardium and the pres- ence of pulmonary emphysema, which cause the projection of a part of the enlarged lung between the heart and the chest-wall. Thrills felt in the chest-wall over the heart may be due to abnor- malities in the blood-current when valvular disease or aneurism is present. We find thrills in the prsecordium, or the neighborhood of the apex, in disease of the mitral valve, both regurgitant and ob- structive ; and thrills in the neighborhood of the second right costal cartilage indicate an aortic lesion, generally that of aortic stenosis, of aortitis, or of aortic aneurism. When thrills are felt in the tricuspid area, namely, in the midsternal region or a little to the right of it, the lesion is probably tricuspid regurgitation, as tricuspid obstruction is quite rare, or to aneurism of the descending part of the aorta. In this connection we should remember the pulsation felt in the chest-wall in some cases of empyema. In nearly every instance this pulsation, wlien it occurs, is found on the left side. It is produced by the impulse of the heart against the effusion, and occurs in two forms : the internal, in which the effusion transmits a heaving im- pulse to the chest; and the external, in which there is a pulsating THE THORAX AND ITS VISCERA. 259 tumor external to the chest- wall. Sometimes this is called " pulsating pleurisy." Percussion of the chest is commonly performed by placing one finger, generally the middle one of the left hand, on the chest-wall and tapping it on the back with the tip of tlie bent finger of the right hand, the movement of the striking hand being entirely a wrist- movement. Sometimes percussion is made by directly striking the chest with the fingers or palm of the hand (direct percussion). Many physicians also employ a percussion-hammer with a rubber head and a ])lexiraeter, or chest-piece, of ivory, celluloid, or glass. Glass is by far the best material for the chest-piece, as it does not produce a note of its own when struck by the hammer, as do the other materials. The disadvantage of this means of percussion is that the^ physician cannot determine the degree of resistance offered by the surface per- cussed, which is of the greatest service in many cases of doubtful character, as, for example, in a case in which pneumonia is suspected, and the results of the percussion will decide the diagnosis. Care should be taken in performing percussion : first, that similar points on the chest-w^all on each side are carefully compared ; second, that the finger which is applied to the chest is placed iu the same relation to the ribs, or intersj)aces, on each side when it is struck ; and, finally, in studying the effects of percussion the physician should always employ it both during forced inspiration and forced expiration, in order to determine the resonance of the chest with its full quota of air and when it has only residual air. The resonance produced on percussion is due to three things : first, to the vibrations of the air in the lungs ; second, to the vibrations of the chest-wall when it is struck ; thinl, to the vibrations in the plex- i meter placed on the chest. The last need only be considered as a factor when a piece of celluloid or ivory takes the place of the finger, for the finger itself does not vibrate enough to alter the note de- veloped. The note produced by vibration of the chest-wall can also be excluded as of little importance unless the chest is very pliable and resilient, as in a thin child, and the blow be delivered very hard. The most important factor in the [)roduction of the percussion-note is that first named, viz., the vibration of the air in the chest caused by the i)l()w delivered on the chest-wall. A large part of the percussion-note depends therefore upon the amount of air in the chest ; the tension of the chest-wall ; and the condition of the pulmonary tissues. The 260 THE MANIFESTATION OF DISEASE IN ORGANS. sound produced when the liealthy chest is percussed is called normal pulmonary resonance. On percussing the right side of the chest anteriorly in the mammil- lary line we fuid in health normal pulmonary resonance as low as the fourth interspace or fifth rib, at which point the resonance begins to be impaired, so that at the sixth interspace or seventh rib we find the dulness. The area of partial and absolute hepatic dulness is shown in Fig. 140, in the chapter on the Abdomen. Posteriorly we find on percussion that the normal pulmonary resonance begins as high as the suprascapular area, and ends as low as the tenth or eleventh rib. It is much less resonant as compared with the percussion-notes obtained from the anterior aspect of the Fig. 110. Skodaic resonance on percussion. Compressed lung. Tympany and dollar resonance. Air. Succussion on shaking. Fluid. Flat on percussion. Loss of vocal resonance and fremitus. The condition ol parts in hydro-pneumothorax from a perforation in the pleura. Metallic tinkling is represented by drops falling on the surface of the fluid. (Gibson and Russell.) chest by reason of the thickness of the chest-wall and the presence of the scapuhe. For this reason pulmonary resonance is best de- veloped posteriorly at the bases of the lungs below the scapulae. Before percussing the back the patient should be made to lean for- ward and fold the arras in order to stretch the tissues and make them tense and as thin as possible. We can divide the abnormal sounds produced by percussion into the tympanitic, the dull, and the flat. We can also develop by per- cussion of the chest in disease what is known as a '' cracked-pot sound." A tympanitic sound is best produced in its most typical form by percussing the epigastrium when the stomach and colon contain some THE THORAX AXB ITS VISCERA. 261 gas. We obtain this sound when the chest is percussed if there is present in the lung a large cavity, and also in pneumothorax (see Fig. 111. Pectoriloquy. Consolidated area. . Fremitas increased. Vocal resonance increased. Dulness on percussion. Increased vocal resonance and fremitus. Cavity with cavernous breathing and gurgling rales. Hyper- resonance on per- cussion. Consolidation— bronchial breathing. Increased fremitus and resonance. Dulness on percussion. Tubercular infiltration. Impaired resonance on percussion. Congestion — crepitant and subcrepitant riiles. Phthisis at various stages in one lung, the physical signs depending on the stage. (Gibson and Russell.) Fig. 110), in consolidation of the lung in some cases, and in some instances of adhesions or collapse of the lung-tissue. If the cavity be in the lung itself, it must be of some size and be near the surface, and, if it communicates with a bronchus, the char- FiG. 112. Diagram showing at x moderate dulness over tubercular infiltration. (GtasoN and Russell.) actcr of the note will change when the inoutli is closed or opened. (Fig. 111.) If the ca.se be one of pneumothorax, with fluid in the chest, changes in the posture of the patient will greatly alter the char- 262 THE MANIFESTATION OF DISEASE IN ORGANS. acter of the note. Consolidation of the lung, as in pneumonia and tuberculosis (Figs. 112 and 113), generally gives a dull rather than a tympanitic note, but if the consolidated area surrounds a very super- ficially placed bronchus, the percussion-stroke may produce vibra- tion in the air in this tube, and this will cause a note, tympauitic in character, which varies as the mouth is closed or opened. Collapse of the lung causes a tympauitic note because the comparatively little air in the lung vibrates as a whole, its vibrations not being stopped as in Fig. 113. Diagram showing heightening of pitch anteriorly from consolidation posteriorly. The shaded part is the consolidated part ; x indicates the position where the percussion-sound is raised in pitch. (Gibson and Russell.) health by the tense septa and vesicular walls. It is best heard in cases of pleural effusion over the apex of the chest, into which the collapsed lung has been pushed by the effusion. This is sometimes called '^ skodaic resonance.'' If the compression is sufficient to consolidate the lung, the tympanitic note is lost. This note is not altered by opening and closing the mouth. The '' cracked-pot sound" is produced by the sudden expulsion of the air from a cavity through a small opening by the force of the per- cussion-stroke. It occurs on percussing a healthy child when its mouth is open, the air being forced by the blow from the lung through the glottis. In disease the cracked-pot sound most commonly results from the presence of a cavity in the lung. It may also be heard in cases of pneumothorax with a fistulous tract opening externally or into a bronchus ; in a few cases of pleural effusion in thin-chested persons ; and in rare instances before consolidation has occurred in pneumonia. In cases of pleural effusion a flat note on percussion is heard over THE THORAX AND ITS VISCERA. 263 the effusion, and it is of very mucli"~the same character as the sound elicited by percussion of the soUd tissues of the thigh. (Fig. 110.) Cardiac dulness. On percussing the chest anteriorly on the left side it will be found that the normal resonance is decreased by the presence of the heart. At the apex of the chest on this side percussion develops normal resonance, but as we descend in the line situated half-way between the mammary line and the midsterual line we find an impairment of resonance at the third rib, which becomes, in the next inch of descent, a very marked dulness, which is produced Portion of heart uncovered by lungs. A shows the area of superficial cardiac dulness. (AlTKEN.) by the presence of a solid organ, the heart. The impairment of resonance is not complete at the upper border of the heart because of the fact that the edge of the lung intervenes between the heart and the che.st-wall, and so the note which results on percussion is neither the normal resonance of the lung nor the dulness produced by the pres- ence of the heart. (Fig. 114.) The outlines of the normal cardiac dulness on percussion are shown by the diagram which is appended, and they form what have been called tiie " cardiac triangles." (Fig. 115.) 264 THE MAXIFESTATIOX OF DISEASE IX ORGAXS. The large triangle begins at the level of the second left costal cartilage and extends down the midsternal line to the level of the sixth costal cartilage. The base then extends to the apex-beat, normally situated in the fifth interspace just inside of the cla- vicular line. The hypothenuse of the triangle joins these points. In this area we have included the partial and total cardiac dulness. Fig. 115. Diagram showing cardiac triangles. Compare this figure with Fig. 114. The small cardiac triangle, which includes the absolute cardiac dul- ness, begins at the third costal cartilage and extends to the sixth. The base-line extends to within one and one-half inches of the nip- ple, and the hypothenuse joins this point with the third costal car- tilage at the midsternal line. As will be seen from the diagram the borders of the heart really extend further than this, but are not near the chest- wall and are partly covered by lung-tissue. (Compare Fig. 114.) The greater part of the cardiac dulness on percussion is due in health to the presence of the right ventricle, which is nearest the chest-wall. The right auricle also is well forward, while the left ventricle only fringes the edge of dulness to the left. This is well shown in the accompanying diagram. (Fig. 116.) THE THORAX AXD ITS VISCERA. Fic. 116. ■2Qo Position of heart in relation to ribs and sternum. Fig. 117 ^ Outline of percussion-dulnes.-; in a case of extensive pericardial etflision. (Byram-Bramwell, after Sibson.) 266 THE MANIFESTATION OF DISEASE IN ORGANS. When hypertrophy or dilatation of the heart occurs it will be found that the area of cardiac dulness extends to the right of the sternal line and to the left of the long side of the triangle, while the apex-beat is apt to be displaced downward and to the left. Great distortion of the triangles occurs as the result of pericardial effusion (Fig. 117), but in this case the heart-sounds will be distant on auscultation and the apex-beat very feeble or lost, whereas in hypertrophy they are exaggerated and the apex-beat forcible. The diagnosis of pericarditis, after the stage of dryness and friction-sound has passed by, is by no means as easily made as some of the text-bopks would make it appear. One of the most reliable signs of pericardial effusion is that of Rotch, namely, that any considerable dulness in the fifth right intercostal space means pericardial eff'usion, pro- vided pulmonary consolidation and pleural effusions or adhesions are excluded. In dilatation of the heart the area of the apex-beat is usually diffuse, and the heart-sounds, while feeble, are clearly heard. In this connection the following summary, prepared by Sansom, of the differential diagnosis between dulness due to pericarditis and that due to dilatation of heart may be of interest: Outline of dulness . Rate of development of dulness .... Impulse and apex- beat Pericarditis with Effusion. J Dulness pear-shaped, and en ' largement chiefly upward. f Often rapid, and then charac- 1 teristic. (The impulse, when present, is in the third or fourth inter- space ; apex-beat tilted up- ward and outward, or effaced. Dilatation of the Heart. ! Dulness not pear-shaped, and en- largement chiefly downward. Usually very slow, though a rapid dilatation of the heart sometimes occurs. Impulse can usually be felt to the left of the lower end of the ster- num or in the epigastrium. Relation of dulness r to left apex-beat . | Pain over praecordia and tenderness in the epigastrium Pulsation in the veins of the neck' . . . Etiology Dulness may extend to the left f Dulness does not extend to the left I Usually absent. Often present. May be present if endocarditis / 0"en present when right heart I dilated. complicates. Usually acute, in course of acute rheumatism, cirrhotic Bright's di-sease, etc. Fever J Often present, Usually chronic ; often associated with chronic valvular lesions, fatty and fibroid degeneration. f Absent unless from some compli- (^ cation. The same author also tabulates the facts in the differential diag- nosis between increased dulness due to pericarditis and hypertrophy of the heart as follows: THE THORAX AND ITS VISCERA. 267 Pericarditis with Effiision. Rate of development Usually rapid. Hypertrophy. Usually slow. r [ Impulse powerful; if left ventricle ] Impulse, when present, is in | hypertrophied, apex displaced Impulse ; apex-beat the third or fourth lefl inter- space, and is feeble ; apex i tilted upward and outward, I or beat effaced. downward and outward ; if right ventricle hypertrophied, apex displaced downward and inward; beat may be in the epigastrium. Pulse Weak and quick ; may be ir- regular. r Character of the pulse depends on the side of the heart which is hypertrophied and the cause of J the hypertrophy. When left ven- I tricle hypertrophied, and no I aortic obstruction or mitral re- I gurgitation, the pulse is large [ and powerful. In emphysema of the luugs the cardiac triangles may be obliterated by the extension of the lung between the chest-wall and heart. They may also be distorted by reason of pleural effusions pressing the heart upward and to the right, or in the case of right-sided pleural effusion the heart may be pushed unduly to the left. Pneumothorax may cause similar results, or, again, old pleural adhesions and con- ditions may so displace the lungs or heart that the triangles cannot be found. Fig. 118. Fig. 119. Dlagramof the normal heart, the continuous Diagram of the heart in aortic obstruction line indicating the outline of the right, and and regurgitation. The dotted lines indicate the incomplete of the left cavities. (San.som.) enlargement of the left cavities, especially the ventricle. The liver-area only slightly in- creased. (Sansom.) The various valvular and other lesions of the heart result in alteration in the si/c of the various cavities without the entire viscus i)eing ('(puilly affected. Thus aortic regurgitation causes enormous enlargement of the left ventricle (dilatation and hypertrophy), and aortic stenosis also causes the same enlarjiement as a rule in less 268 THE MANIFESTATION OF DISEASE IN ORGANS. degree. Mitral regurgitation causes hypertrophy and dilatation of the left ventricle and some enlargement of the left auricle, as does also mitral stenosis. Tricuspid regurgitation causes hypertrophy and dilatation of the right auricle and hypertrophy of the right ventricle, and mitral stenosis often has a similar influence over the right side of the heart by damming back the blood into the lungs and right side of the heart. The following figures from Sansom will illustrate the deformity of the cardiac triangles under these various conditions. (See Figs. 118, 119, 120, and 121.) Fig. 120. Fig. 121. Diagram of the heart in regurgitation at the mitral orifice. The dotted lines indicate en- largement of the left auricle and the left ven- tricle, the continuous lines enlargement of the right ventricle and right auricle. The liver-area is much enlarged. (Sansom.) Diagram of the heart in obstruction at the mitral orifice. The dotted line indicates en- largement of the left auricle. The continuous lines show enlargement of the right cavities. The liver-area is much enlarged. (Sansom.) Finally, it is to be remembered that much information as to the thoracic organs maybe gained by the sensation of resistance offered to the fingers on percussion. It is slight over cavities, greater over healthy lung-tissue, still greater over consolidations, and very great over effusions. AuscuLTATiox of the chest reveals in health two chief varieties of breath-sounds, namely, vesicular breathing and bronchial breathing. The first type is heard in its most typical form over the apices of the lungs anteriorly, the latter at the angles of the scapulae posteriorly. We may listen to these sounds by placing the ear directly against the chest, or by the use of a single or a binaural stethoscope. The patient must be in an unconstrained position, as should be that of the physician, and if the ear is placed against the chest, or a single stethoscope is used, the face of the physician should always be turned THE THORAX AND ITS VISCERA. 269 away from that of the patient, because the breath of a sick person is often very disagreeable and the breath of the doctor may be equally annoying to the patient. Care should be taken in the use of the stethoscope to see that the edge of the bell is in close contact with the chest-wall on its entire circumference. The sounds which are heard in health in the chest on auscultation are respiratory and cardiac. The respiratory sounds consist, as already stated, in the vesicular murmur and the bronchial or blow- ing sounds, which are sometimes called tubular breathing. In the vesicles the air is subdivided into many minute parts, whereas in the bronchial tubes it moves along in a column. Whatever may be the actual cause of the production of normal vesicular breathing, we know that when it is present it signifies a healthy pulmonary paren- chyma, and when absent one more or less diseased. Bronchial breathing, normal in the bronchial tubes, becomes an abnormal sign when it is heard in an area in which vesicular breath- ing should be present, as will be shown shortly. After determining the fact that the sounds of normal vesicular breathing are present in the anterior parts of the chest, or that those of bronchial breathing can be heard between the shoulders, we next take note as to the relative duration of the inspiratory and expiratory sounds. Normally in the perfectly healthy chest the ratio of the expiratory sound to the inspiratory sound is as one to three, although if the volume of air itself be measured the duration of expiration is six to five. In other words, so far as auscultation of the vesicular portion of the lung is concerned, inspiration is far longer than expi- ration. Just at this point we learn one of the most important points in the physical examination of the chest, namely, that while the expiratory sound may be entirely absent in health, any marked increase in its length anil loudness, so that it equals or exceeds the inspiratory sound, is a sign indicative of some diseased state which impairs the elasticity of the lung, such as early tuberculosis, pneu- monia, and' emphysema. The other variations in the vesicular respiratory sounds differing from those of health are harsh, or, as it is sometimes calletl, puerile breathing, and irregular breathing. In children, as the term " puerile l)r('athing " indicates, the normal vesicular breathing is loud, clear, and iiarsh, because of the great elasticity of the lung and the thin- ness of the chest-wall. If it is exaggerated in a child or present in the area of normal vesicular l)reathing in adults, it usually indicates 270 THE MANIFESTATION OF DISEASE IN ORGANS. some irritation of the bronchial mucous membrane. If it is found in the apices of the lungs in a marked degree and expiration is prolonged, it is an important and fairly sure sign of early pulmonary tuberculosis. Sometimes physicians speak of '^ broncho-vesicular breathing," meaning a breath-sound consistiug of both bronchial and vesicular sounds. It is sometimes heard in a healthy person when he breathes superficially, aud in disease usually indicates early pneumonic changes or early tuberculosis of the lung. It is ouly of value as a diagnostic sign if localized in one part of the lung. This harsh breathing of exudation and thickening differs from normal puerile breathing in this important particular, namely, that in the former expiration holds its normal ratio to inspiration, whereas in the latter it is greatly prolonged. Irregular breathing occurs in the chest of a healthy sobbing child and in that of an hysterical woman, but it possesses pathological significance if it occurs when a full breath is taken, as it is often present as an early sign of incipient pulmonary phthisis. Bronchial breathing in health is best heard in the posterior part of the chest, as already stated, between the scapulae and the seventh cervical to the fourth dorsal vertebra. When this bronchial or tubular breathing is heard in other parts of the chest it is a sign of disease, for while the bronchial tubes are distributed to all parts of the lung, the breath-sound which is in them is masked by the sounds of vesicular breathing and muffled by the lung-tissue surrounding them. If this vesicular tissue becomes consolidated by disease, the vesicular murmur is lost and the solid lung transmits the bronchial sounds directly to the ear of the examiner. Bronchial or tubular breathing, or, as it is sometimes called, " blowing breathing," heard in the part of the lung in which vesicular breathing is normally heard, is therefore a sign of tubercular or pneumonic consolidation (Fig. 122) or of compression or collapse of the lung above a pleural effusion. Bronchial breathing is also heard in the area of the chest, in which vesicular sounds normally predominate, and in cases of cavity of the lung, because in such a lung the bronchial sound is trans- mitted directly to the cavity, and thence to the ear without being inflamed by the intervention of healthy lung-tissue. In other words, consolidated tissues and cavities transmit sound better than the normal vesicular portion of the lung, which is a combination of air and vesicular wall. If the cavity be large, we have a loud THE THORAX AXD ITS VISCERA. 271 sound developed by the^trausmisslou of the brouchial sound into its open space and by the passage of air through it. This is called cavernous breathing. If the cavity is not very large, or is pecu- liarly situated iu relation to the supplying bronchus, we have wliat is called " araplioric breathing " — that is, a sound like that produced by blowing over the mouth of an empty bottle. This sound is also rarely heard in cases of pneumothorax in which the bronchial tubes, running near to the pleural cavity, transmit their sound to the air in the pleural space. Fig. 122. Increased vocal resonance and fre- mitus on auscultation and pal- pation. Dulness on percussion. Bronchial breathing. Pneumonia of the inferior lobe with the physical signs characteristic of consolidation. (Gibson and Rossell.) It is never to be forgotten that in examining the chest the two sides must be compared, since the well side often gives a standard for that affected by di.sease, and in doing so it must be remembered that disease not only modifies the signs in the lung in which the morbid process is situatescess. 3. From pleural effusion. And 4. 286 THE MANIFESTATION OF DISEASE IN ORGANS. From chronic pueamonia. There are several subdivisions of these diseases that might be made, but to all iuteuts and purposes these are sufficient. Pericarditis may perhaps be named as the fifth lesion to be thought of. Aneurism in the thorax is sometimes so extremely difficult of absolute diagnosis that but few rules can be laid down for its differ- ential diagnosis from growths in the mediastinum, for deeply seated aneurism in this region cannot be said to possess any pathognomonic symptoms. The various portions of the aorta in which aneurism occurs make its symptoms different in almost every case, and we are forced to rely more upon general conditions than absolute signs. Thus, if a patient has no direct symptoms of aneurism, and none of those conditions present which we know predispose to such a lesion, such as atheroma of the bloodvessels, due to Bright's disease or any other similar cause, or syphilis, rheumatism, or a history of violent exertion or severe toil, we may with a certain degree of assurance look further for symptoms of mediastinal trouble of another sort. (See ''Aneurism" in this chapter.) Unfortunately, the most common age for aneurism is much the same as that for mediastinal disease, although mediastinal disease seems to occur more frequently in youths than does aneurism, or, in other words, is scattered over a wider range of years. The pain of aneurism is generally considered to be more violent than that of any other thoracic lesion, but there exists reasonable doubt whether the lancinating pain of a growth in this position does not exceed it. This doubt rests on sufficient basis to prevent one using this symptom as an aid in any way to diagnosis. If the aneurismal sac be large enough to give us a wide area of dulness on percussion, as Dr. Graves has stated, there ought to be an expansile movement. Haemop- tysis is not in any way a differential sign, since in the one case it may be due to aneurismal leakage, and in another to ulceration of small bloodvessels by pressure exercised by a tumor, be it aneurismal or malignant, or even benign. From abscess the diagnosis of mediastinal tumors is much more readily made. In the first place, in abscess we generally have a history of traumatism, or, if the case be one of cold abscess, it is commonly associated with a history of struma. If the abscess be acute, there is generally the history of pain, followed by a chill more or less severe, and fever ; or, if cold, then we frequently have irregular febrile movements, with long-continued anorexia and loss THE THORAX AXD ITS VISCERA. 287 of flesh. Cold abscess, too, is generally in the posterior mediasti- num, while acute abscess generally occurs in the anterior space. Pulsation may frequently occur, owing to the transmission of the aortic or cardiac impulses, and affords no better diagnostic point here than elsewhere. In some cases, where the theory of aneurism is extremely doubtful and the likelihood of abscess extremely prob- able, an exploratory needle may be used, either through a hole drilled in the sternum or passed between the ribs ; but a careful review of the history of the case should certainly always be made and used as a basis from which to draw conclusions. By far the greatest difficulty may be experienced when we attempt to diagnosticate between pleural effusion produced by pleurisy and pleural effusion produced by mediastinal disease, provided the case be not seen from the first and the history be obscure. If^the effu- sion be not great, we may be able to discern friction-sounds produced by the rubbing of the tumor against the chest-walls ; but if the effu- sion be large, this sign may not be recognizable. All other methods failing, it would be advisable to tap the chest, and, if the fluid drawn be fibrinous, we know it to be inflammatory ; while if it be clear and limpid, or at least thin and not viscid, it is probably due to pressure. This is not, however, a positive sign, since very fre- quently in cases of asthenic inflammation we have an exudate lack- ing entirely in the fibrinous constituents. Tumors of the mediastinum invading the lungs have frequently been mistaken for chronic and even acute pneumonia, passing, as they do, along the larger bronchial tubes and bUxxlvessels. Without doubt, in a certain number of cases, either hypostatic pneumonia, or pneumonia due to pressure on the bronchial vessels, develops as the tumor invades the lung, and in such cases it is abso- lutely impossible to make any diagnosis unless by symptoms of pressure in the mediastinum, or some history pointing to such a result. AValsh has stated that if the lesion be due to a tumor, the affected side will increase in bulk rather than diminish, and that dyspnoja out of proportion to tiie degree of consolidation points to a mediastinal disorder rather than one confined to the lungs. If the heart be dis[)laced in eitlier direction, the odds point to mediastinal tumor, l)ut the presence or absence of a luemoptysis, as has just been stated, induences the diagnosis not at all. The diagnosis of pericarditis from metliastinal lesions is much more readily made. The history of sudden prascordial pain and the 288 THE MANIFESTATION OF DISEASE IN ORGANS. limited area of duluess on percussiou aid us very materially iu decid- ing as to what the disorder is, while the description of the onset of the attack, with a few pointed questions as to systemic taints, etc, may do much to unravel the mystery. The distention of the peri- cardial sac from effusion may give us a regular outline on percus- sion, while the dulness of mediastinal disease may be irregular and varying. Heart-sounds and Signs, On attempting to study the heart-sounds we usually auscult the neighborhood of the apex-beat and expect to find, if the heart be healthy, two sounds, occurring one immediately after the other, which resemble the sounds of the words " lub dup ;" the^'lub" being the so-called first sound of the heart produced by the contrac- tion of the heart muscle and the tense valves, and the '^ dup " being caused by the slapping to of the aortic valves. After listening in this region we next place the ear over the second right costal cartilage in order to come as near as possible to the point of origin of the second sound produced by the aortic valves. If the heart is normal, we find only these sounds, " lub dnp," and nothing else. If it is feeble from exhausting disease, from fainting, or by reason of fatty degeneration, we find that the sound " lub " is feeble, and the " dup " sound is also feeble, because the valves do not slap back into place with as much force as is normal. If, on the other hand, the heart is hypertrophied or stimulated, we find these sounds accentuated, and it is of impor- tance to remember that marked accentuation of the aortic second sound, showing forcible closure of the aortic valves, indicates a condi- tion of high arterial pressure, often the result of vascular spasm aris- ing from chronic contracted kidney. On the other hand, if the pulmonary second sound at the second left intercostal space is accent- uated, it indicates an increase in pulmonary pressure due to impedi- ment to the flow of blood in the lungs. It is markedly accentuated in both mitral obstruction and regurgitation and in some cases of pneumonia. The sounds produced at the various orifices of the heart are heard best at the following points (Fig. 125) : The mitral valve is heard best at the apex-beat ; the aortic valve at the second right costal cartilage, the tricuspid valve over the sternum on a line drawn from the third left intercostal space to the fifth right costal cartilage. THE THORAX AND ITS VISCERA. 289 Fig. 125. and the pulmonary vals'e at the second left intercostal space. All the heart-sounds may be reduplicated in health and in disease as the result of contraction in an un- equal manner of the papillary mu.scles. If di.sease of the valves be present, ^ve are apt to find re- duplication of the second sound in cases of mitral stenosis and lung disease producing an ab- normally high tension in the pulmonary circulation. Such re- duplication is also seen in some individuals suffering from aortic stenosis. ' Supposing that on listening to the heart in the mitral area there is heard in place of the normal sounds ('Mub dup "), or with them, a murmur, what docs it mean ? It means that, friction- j , . Ill • 1 Sbowing the areas in which the various heart- sounds being excluded, cither sounds are best heard in health. A is the area valvular disease of the heart for the aortic valve ; P, that for the pulmonary ' valve , T, for the tricuspid valve ; and M, for the aneurism of the aorta, or marked mitral valve. anaemia is present. Particularly is the ana?raic murmur apt to be heard in case of feeble children suffering from chorea, and it will generally be found most marked at the left margin of the sternum.^ Having found that there is a murmur, and, from the absence of an.'cniia, that it is due to organic cardiac disease, it is now necessary t(» determine at what orifice of the heart it is j)roduced, and the rule is to be remembered that a murmur is always heard loudest at about its point of origin. We therefore place the ear over the aortic car- tilage (second right). If the murmur be mitral in origin, it will not be heard at this place, unless it be so loud as to be trausmitted. If it is aortic in origin, it will be louder here than at the apex. If it is tricuspid, it will be loudest in the tricuspid area; if pulmonary, loudest at the pulmonary area. As murmurs at the tricus])id and pulmonary valve are rare, we nearly always have to deal with aortic 1 It must not be forgotteu that murmurs due to endocarditis also arc fre. Mitral stenosis and regurgitation ; tricuspid regurgitation. 10. Aortic stenosis ; mitral stenosis and regurgitiition. 296 TIIE MANIFESTATION OF DISEASE IN ORGANS. 11. Aortic regurgitation ; mitral stenosis and regurgitation. 12. Aortic stenosis ; mitral regurgitation ; tricuspid regurgitation. 13. Aortic regurgitation and stenosis ; mitral regurgitation; pul- monary regurgitation. 14. Aortic stenosis and regurgitation ; mitral stenosis. 15. Aortic regurgitation ; mitral stenosis. 16. Aortic regurgitation ; mitral regurgitation ; tricuspid regurgi- tation. 17. Mitral stenosis ; tricuspid regurgitation. 18. Aortic stenosis ; mitral stenosis and regurgitation ; tricuspid regurgitation. 19. Aortic stenosis ; mitral stenosis. 20. Aortic regurgitation and stenosis ; mitral stenosis and tricus- pid regurgitation. , 21. Aortic regurgitation ; mitral stenosis and regurgitation ; tri- cuspid regurgitation. 22. Aortic regurgitation and stenosis ; mitral stenosis and regurgi- tation ; tricuspid regurgitation. 23. Aortic regurgitation and stenosis ; mitral stenosis and regurgi- tation ; tricuspid stenosis and regurgitation. 24. Aortic stenosis ; pulmonary stenosis. 25. Aortic stenosis ; mitral stenosis and regurgitation ; tricuspid stenosis and regurgitation. 26. Mitral stenosis and tricuspid stenosis. The relative gravity of heart-lesions is, according to Walsh, as follows, the least dangerous being placed last and the most dangerous first : Tricuspid regurgitation. Mitral obstruction and regurgitation. Aortic regurgitation. Pulmonary obstruction. Aortic obstruction. The general symptoms, subjective or objective, which a patient suffering from the various forms of valvular lesion presents, in some instances, have not been spoken of up to this point, because it is to be distinctly uuderstoo:! that murmurs produced by any form of val- vular lesion may exist with great intensity without there being any systemic disturbance or the patient being conscious of their presence. On the other hand, the murmur may be so faint as to be almost indistinguishable, and yet the general symptoms of heart disease be THE THORAX AND ITS VISCERA. 297 very marked. This is because the development of general symptoms depends entirely upon the question of compensation by hypertrophy. If there is a leak in a valve or a constriction of an orifice, this leak or obstruction must be overcome by compensatory hypertrophy of the heart-mnscle. If the heart-muscle can make up for the regurgi- tation or obstruction by increased effort, the circulation is unimpaired ; but if it cannot do so, we have developed more or less rapidly, accord- ing to the lesion present and the condition of the heart-muscle, char- acteristic symptoms. Let us suppose that the valvular lesion is that of mitral regurgitation with failure of compensation. The first and one of the most prominent symptoms, is shortness of breath on exertion ; the lips and ears do not possess their normal red hue, but are a little bluish ; and if the congestion of the auricle and pul- monary veins is great, bronchitis may be constant or attacks of haemoptysis may develop Palpitation of the heart will also be com- plained of ; and if the patient has developed the le.sion in early life, the finger-tips are apt to Ije clubbed. If the rupture or failure of com- pensation is more complete, all these symptoms become more marked, and the shortness of breath, even when lying down, becomes most distressing ; indeed, the patient may be comfortable only when sitting up. Dropsy of the lower extremities now comes on and the liver becomes enlarged from portal congestion, while the urine becomes albuminous, not from any true renal lesion, but as the result of its engorgement with blood. The general symptoms of mitral obstruction are identical with those just described. The general symptoms of aortic obstruction are also much like those described as resulting from mitral regurgitation, but in addi- tion there are apt to be present, early in the process of failing com- pensation, some lightness of the head, dizziness or vertigo, or faint- ness, owing to a deficient blood-supply to the brain. Very com- monly, too, it will be found that in association with the aortic stenosis there also exists mitral regurgitation, which speedily produces in its turn well-marked pulmonary symptoms. Dropsy is very rarely seen in patients with aortic stenosis. On the contrary, they present, as a rule, tiie lean and poorly nourished appearance so often found in the adult, well-advanced in years, with atheromatous tendencies in his vessels. The association of ruptured compensation with aortic regurgita- tion presents more typiciil general systemic symptoms than any of 298 THE MANIFESTATION OF DISEASE IN ORGANS. tlie ordinary valvular lesious of the heart. lu addition to headache, vertigo, and a tendency to syncope, associated with palpitation and a sense of cardiac oi)pression, we often have a great deal of cardiac pain, of a dull, aching character in rare instances, but more often intensely sharp and lancinating, often darting down the left arm, particularly at night. The dyspucea is often extreme, the patient suffering^ from terrible attacks of shortness of breath and often sit- ting day and night in a chair with his head resting on the back of a chair placed in front of him. As time goes on the constant strug- gling for breath exhausts him and he falls asleep, only to awake in a few moments gasping to get air. Long before any of these grave symptoms arise we may, however, find a number of interest- ing signs of this heart-lesion, chief among which is the '^water- hammer" or ''trip-hammer " or '' Corrigan pulse," the throbbing carotid arteries, and capillary pulsation in the skin and mucous mem- brane is to be seen. This is best developed by drawing the thumb- nail sharply across the forehead, thereby causing a red mark which can be seen paling and flushing with each beat of the heart, or by pressing a glass slide on the inner part of the lower lip, when the same capillary pulsation will be found. Ophthalmoscopic examina- tion will often reveal pulsation of the retinal arteries. Beyond valvular lesions, producing heart-symptoms, we have a number of other causes which seriously disturb the action of the heart and the general circulatory condition. The first of these is dilatation of the heart. Let us suppose that a man presents himself with a history of shortness of breath on exertion so great that his activities are greatly reduced and his usefulness impaired. He gives a history that he has been well until he had made some extraordi- nary exertion, generally of a prolonged character, rather than a brief and sudden effort, which would perhaps cause aneurism. Since that time his symptoms of heart-failure have been marked. He may perhaps have attacks of syncope. Examination of his heart reveals on inspection a diffuse thrill in the region of the apex, but this thrill is too feeble to be felt, though well marked to the eye if his chest is thin. Percussion shows that the area of cardiac dulness is increased vertically and laterally, and auscultation will discover feeble heart- sounds ; and if the dilatation of the muscular portion of the heart is associated with dilatation of the orifices, a murmur may be present, most commonly that of mitral regurgitation. Sometimes tricuspid regurgitation is also found. The first sound before it becomes very THE THORAX AND ITS VISCERA. 299 feeble may be short and flapping like the ordinary second sound. Marked arhythmia of the heart is often present. Again, we have hypertrophy of the heart occurring in persons without valvular lesions, sometimes as the result of excessive and severe toil. It is seen most commonly by the author in the chests of medical students, who, during tiieir holidays, devote their time to severe athletic sports, or to too much manual labor, and who, on leading sedentary lives in the winter, develop irregular cardiac action, palpitation, and some shortness of breath. Examination of the prajcordium in such cases shows a forcible impulse of the apex of the heart against the chest-wall, some bulging of the chest-wall if the hypertrophy be very great, and no murmurs, l)ut in their place heart-sounds very much louder than normal. Palpation shows the apex-beat to be lower than normal, and on percussion an increase in the area of cardiac dulness is also found. Again, let us suppose that a patient presents himself with a very rapidly l)eating heart, he tells us that his skin is alternately red and ])ale, and a careful examination of the heart fails to reveal any murmurs or organic abnormality. There are consider- able shortness of breath on exertion and marked j)alpitation and arhythmia. Such a case may be suffering from a condition in which there is some deficient action of the pneumogastric nerve, whereby the heart is not pro])erly controlled, or the irregular cardiac action may be due to sudden vasomotor relaxations and spasms, which by dilating or closing the blood-paths remove the normal arterial resistance or make it excessive. This is a condition seen in associa- tion with some neuroses and very commonly seen in persons who use tobacco to excess. The physical signs of the so-called ''tobacco- heart " are indeed chiefly those of arhythmia due to pneumogastric disorder. Rarely l)ecause of irritation of the vagus nerves or centres a state of bradycardia develops, in which the heart beats very slowly, ]M>rhaps only thirty or even as slowly as twelve times a minute, liradycardia or great slowness of the heart may not only be due to a neurosis of the vagi, but to typhoid fever or otiier infectious diseases. It is also seen in jaundice. One of the most common causes of tachycardia, or rapid heart, is exoj)hthalmic goitre, in which condition Ave have not only exoph- thalmus and <>nlargemeut of the thyroid gland, l)ut, in addition to the tachycardia, a marked thrill over the carotid arteries, in which 300 THE MANIFESTATION OF DISEASE IN ORGANS. vessels a purring murmur of considerable intensity can also be heard. The patient often suffers from considerable nervous excitement or mental depression. It is an interesting fact that in this disease the electrical resistance of the body is often diminished. An exceedingly irregular arhythmical action of the heart coming on in the course of acute infectious disease, or in any state produc- tive of sepsis, points to the possibility of the patient having an embolism or thrombus of one of the coronary arteries. If the ves- sel is suddenly plugged, death speedily occurs ; but if the process is gradual, an anaemic necrosis or white infarct is produced. Sudden attacks of cardiac feebleness sometimes come on as cardiac crises in glosso-labio-pharyngeal paralysis and in locomotor ataxia. Before discussing the signs of so-called fatty heart we must decide what is meant by this term. True fatty heart — that is, the con- dition of the heart in which this organ has undergone true fatty degeneration — has no pathognomonic signs, so far as the heart itself is concerned. In these instances we base our diagnosis upon the presence of fatty degeneration of the more superficial organs, such as the arcus senilis in the eye, the presence of atheromatous blood- vessels, the feeble heart-sounds at all times, and the evident feeble- ness of the heart on exertion. The history of poisoning by any one of the poisons causing fatty degeneration is also to be sought after in some cases. Marked fatty degeneration is often present in cases of pernicious anaemia. It is not possible to make a differen- tial diagnosis from the physical signs between fatty and fibroid heart. Another state quite distinct from true fatty heart, but with some- what similar symptoms, is seen in cases in which an excessive amount of fat has been deposited around the heart as well as in or around the other organs of the body. Here there is little or nothing the matter with the heart-muscle, except that it is overloaded with a weight of fat. Where a man shows signs of general degenerative changes, has a feeble heart, some dyspnoea, and perhaps some cedema of the lower extremities, we may conclude that he has, unless valvular disease is discovered, degenerative myocarditis. Such cases make up the greater number of sudden deaths, called popularly " death by sudden car- diac failure." Finally, let us suppose that a young child is seen who is, and has been since birth, more or less cyanotic, according as to whether it is quiet or moving and varying its posture. In all probability THE THORAX AND ITS VISCERA. 301 such a child is the subject of cougenital raalforrnation of the heart. The following rules, laid down by Hochsinger, may be used for their diagnosis : 1. In childhood loud, rough, musical heart-murmurs, with nor- mal or only slight increase in the heart-dulness, occur only in con- genital heart-disease. The acquired defects with loud heart-murmurs in vouno; children are almost alwavs associated with o-reat increase in the heart-dulness. 2. In young children heart-murmurs, with great increase in tiie cardiac dulness and feeble apex-beat, suggest congenital chauges. The increased dulness is chiefly of the right heart, whereas the left is only slightly altered. On the other hand, in the acquired endo- carditis in children, the left heart is chiefy affected and the apex- beat is visible ; the dilatation of the right heart comes late and does not materially change the increased strength of the apex-beat. 8. Tiie entire absence of murmurs at the apex, with their evident presence in the region of the auricles aud over the pulmonary ori- fice, is always an important element in differential diagnosis, and points rather to septum defect or pulmonary stenosis than to endo- carditis. 4. An abnormally weak second pulmonic sound associated with a distinct systolic murmur is a symptom which, in early childhood, is only to be explained by the assumption of a congenital pulmonary stenosis, and possesses, therefore, an importance from a point of differential diagnosis which is not to be underestimated. 5. Absence of a palpable thrill, despite loud murmurs which are heard over the whole pricciordial region, is rare, except with cogeni- tal defects in the septum, and it speaks therefore against an acquired cardiac affection. 6. Loud, especially vibratory, systolic murmurs, with the point of maximum intensity over the uppar third of the sternum, associated witli a lack of marked symptoms of i)ypertrophy of the left ventricle, are very important, for the diagnosis of a ])ersisteuce of the ductus Botalli, and cannot be ex];)laiued by the assum[)tion of an endocar- ditis of tlie aortic valve. CHAPTER IX. THE ABDOMEN AND THE ABDOMINAL VISCERA. The surface of the abdomen — Changes in the appearance and shape of the abdominal wall — The signs and symptoms of disease of the abdominal organs. The condition of the abdominal surface and abdominal contents is best studied by means of inspection, palpation, percussion, and Fig. 131. The regions of the abdomen and their contents. (Edge of costal cartilages in dotted outline.) auscultation. For the purposes of inspection the surface of the abdomen has been arbitrarily divided by diagnosticians into a uum- THE ABDOMEN AND THE ABDOMINAL VISCERA. 303 ber of spaces, which are best shown in the accompanying figure (Fig. 131), and which get their names from the regions in which they are located, or from the organ immediately underneath the abdominal wall. By means of these arbitrary outlines we can read- ily describe the exact spot in which a physical sign or symptom is found. The table which is appended, from Gray's Anatomy, clearly shows the viscera to be found under each of the areas named : Right Hypoeliondriac. The right lobe of the liver and the gall-bladder, hepatic Epigastric Region. The pyloric end of the stomach, left lobe of the liver, flexure of the colon, and part and lobulus Spigelii, the pan- of the right kidney. Right Lumbar. Ascending colon, part of the right kidney, and some con- volutions of the small intes- tine. Right Inguinal (Iliac). The caecum, appendix caeci. Left Hypochondriac. The splenic end of the stom- ach, the spleen and extremity of the pancreas, the splenic flexure of the colon, and part of the left kidney. Left Lumbar. Descending colon, part of the omentum, part of the left kid- ney, and some convolutions of the small intestine. Left Inguinal (Iliac). Sigmoid flexure of the colon. creas, the duodenum, parts of the kidneys and the supra- renal capsules. Umbilical Region. The transverse colon, part of the great omentum and mes- entery, transverse part of the duodenum, and some convo- lutions of the jejunum and ileum, part of both kidneys. Hijpogadric Region. Convolutions of the small in- testine, the bladder in chil- dren, and in adults if dis- tended, and the uterus during I pregnancy. I Inspection. The general abdominal wall is pushed outward or protruded by many perfectly normal causes, such as an unusual amount of fat in the omentum, pregnancy, and an accumulation of liquid and food in the stomach after a heavy meal. It is also convex to an abnormal degree in cases in which ascites is present, when the stomach and bowels are over-distended with gas (tympanites), and when any of the organs found in the ])eritoiu'al cavity are the seat of swellings or tumors of large size. In children a protruding pot- belly, '* the frog-belly " of the French, is seen in cases of scrofula or tuberculosis of the mesenteric glands, and in tho.se cases which suffer from chronic gastro-intestinal catarrh. It is claimed in a recently published paper by a French clinician that the intestinal canal is not oidy dilated but of greater length than is normal in these ca.ses. If, on the other hand, the belly-wall is retracted, con- cave, or '* scaphoid " as it is sometimes called, we look for the cause in abstinence from food, or remember the possibility that excessive vomiting or purging may have em[)li('d the gastro-intestinal tract of 304 THE MANIFESTATION OF DISEASE IN ORGANS. its usual contents. Thus excessive summer diarrhoea may produce such a result. We also find a retracted belly-wall in nearly all cases of advanced wasting diseases, such as carcinoma or tuberculosis of the lungs; and if the retraction is associated with muscular rigid- ity of the bslly-vvall and pain, we suspect the early stages of peri- tonitis or the presence of some acutely painful afPection, such as renal or hepatic colic or lead colic. Marked concavity and retraction of the belly-wall are also seen sometimes in cases of tubercular men- ingitis. The abdomen is distended very greatly by gas in many cases of peritonitis, typhoid fever, aud flatulent colic, and the anterior sur- face of the belly will be found to give a high-pitched tympanitic note on percussion. We separate, diagnostically, the swollen abdo- men due to wind from that due to ascites by the fact that in the latter condition the epigastrium is moderately flat, while in the case of tympanites it is more protruding. Again, in ascites the greatest bulging is often seen in the flanks, or, if the patient sits or stands erect, the hypogastric region bulges from the change in the position of the fluid. If the fluid be due to a mo:lerate-sized ovarian cyst, this variation will not occur, as the cyst is not readily movable. If the ovarian tumor be large, the differential diagnosis may be most difficult and almost impossible, except by the history or by examining the liquid withdrawn by tapping. The following table from Brown's Diagnosis aids in this diagnosis: Ascites. I. History. No history of lateral development. II. Inspection. When patient lies on the baclj there is bulg- ing at the flanks. If the ascites is consider- able, the umbilicus is pressed outward. III. Percussion. On percussion there is dulness in the flanks, and a clear note over the centre of the abdo- men. Changes of position alter the lines of dul- ness in the manner already described. IV. Aspiration. Ascitic fluid presents the following charac- ters : 1. Specific gravity 1.010 to 1.015. 2. Light straw color. 3. Coagulates spontaneously when exposed to the air. 4. Does not contain paralbumin. Ocanan Cyst. I. History. Tumor develops from one iliac fossa. II. Inspection. 'i he greatest swelling is anterior, not in the flanks. Sometimes one side of the abdomen is more prominent than the other. III. Percussion. The dulness is central, the intestines^giving a clear note at the sides. Change of position does not alter the lines of dulness. IV. Aspiration. Ovarian fluid has the following characters : 1. Specific gravity 1.018 to 1.024. 2. Amber colored ; often syrupy. 3. Seldom or never coagulates spontane- ously. 4. Contains paralbumin. THE ABDOMEN AND THE ABDOMINAL VISCERA. 305 In cases of ascites due to free li<[uid in the abdominal cavity percussion will elicit flatness over the flanks and resonance only when the intestines containing gas are floated up against the anterior belly-wall in front of the effusion. Palpation will also reveal fluctua- tion in ascites, but none in tympanitic distention. As the result of gradually increasing intra abdominal pressure the floating ribs be- come pressed outward, the apex-beat of the heart is often displaced Fig. 132. Dotted line shows area of cancerous liver extending far beyond its normal area. Over the entire surface of this mass could be felt hard iioilular masses. (From the author's wards, JelVerson Medical College Hospital.) upward and outward, and the umbilicus becomes protruded instead of retracted. The skin of the belly-wall becomes thin and shining, and the recti muscles becoming separated render the peristaltic movements of the bowels readily felt through the intervening skin. Very often there is developed in cases of ascites, particularly when that condition arises from hepatic ciirhosis, a more or less well- defined bunch of veins on the anterior belly-wall, which is some- times called the Caput J[e(Ias(c, as the result of an attempt at 20 306 THE MANIFESTATION OF DISEASE IN ORGANS. collateral circulation to compensate for the obstructed flow caused by the changes in the liver. Sometimes a mediastinal growth will cause a somewhat similar development. When the pressure is lower down than the liver the veins of the lower part of the abdomen (hy- pogastrium) will be found distended. Fig. 133. "'^^fT A case of chronic enlargement of the spleen following typhoid fever. The darli line shows the margin of the organ on palpation, while the retraction in the line and the dotted line indicate the position of the splenic notch. (From the author's wards in the Jefferson Medical College Hospital.) Localized bulging of tiie abdominal walls, chiefly on the right side, is found in cases in which the liver is enlarged by hypertrophic cirrhosis, or by cancer or other morbid growth, such as gumma or sarcoma, and by abscess. The swelling, if its origin be in the liver, will arise under the floating ribs on the right side, and will extend downward and forward toward the umbilical area. If the enlarge- ment be great, it will extend far below the umbilicus and across the umbilical area to the opposite side of the abdomen. (Fig. 132.) In THE ABDOMEN AXD THE ABDOMiyAL VISCERA. 307 enlargement of the spleen similar signs, springing from the floating rihs well over to the left side, may be developed (see Fig^. ] 33 and 134), and large cystic kidney on either side may cause abdominal bulging, particularly if it be floating. Marked swelling of the epigastrium indicates distention of the stomach by gas, by food, or that this organ is the seat of morbid growth. Sometimes a similar distention results from enlargement of the posterior mediastinal and retro-peritoneal glands. Again, Fig. 134. A case of profound anaraia with great enlargement of the spleen, as shown in the large out- lined area. The smaller outlines indicate the areas of ana-mic murmurs near the base of the heart and in the carotid artery. distention of the epiga>triiini i.s apt to be caused by enlargement of the left lobe of the liver. In ovarian tumors the growth often gradually distends the entire belly equally ; but, as already stated, the hi.story is usually that of swelling, low down, and of its being chiefly unilateral at first. It should be remenil)ered that the discovery of a pyriform swelling in the hypogastrium in a female may po.ssibly be due to a i)r(iinant uterus, or in a man to r. teution of urine, with consecjuent distention of the bladder. Cases of dilatation of the stomacii often show verv 308 THE MANIFESTATION OF DISEASE IN ORGANS. great bulging of the umbilical area of the abdominal wall when that viscus is distended by food and gas, (See Percussion in this chapter.) We discover the condition of the stomach as to its size and shape by means of washing it clean with the stomach-tube and then filling it with a known quantity of water, which can be siphoned out and measured. Or we can use the so-called gastrodiaphane of Ein- horn, which consists of a small electric lamp, protected by strong glass, and attached to a rubber tube which contains the necessary wiring for the electric current, and which is swallowed just as is the ordinary stomach-tube. The stomach having been thoroughly cleansed by lavage is then filled with pure water and the lamp swallowed. If the patient be moderately thin and the inspection is made in a dark room, the outline of the lighted stomach can be seen through the abdominal wall, and some idea of its dimensions obtained. Normally, the greater part of the stomach will be found to the right of the middle line and only about one to two inches above the umbilicus. (See Percussion.) Fig. 135. TUrck's gyroaiele. a represents a thin metal wheel, covered on one side by soft, unpolished rubber, which rotates on a smaller wheel by friction. 2 is the stationary outer tube held by the button or spool b. At the end of the tube, which reaches to the cardia only, is a bearing within the tube to make the cable run more smoothly. 3 is the cable, which is fastened to the revolving apparatus by the screw c. 4 is the sponge, which fits into a socket of the cable at d, and may be removed at will. Another useful means of diagnosing dilatation of the stomach is by means of the ^'gyromele" of Tiirck, which in its improved form consists of four parts, namely : A revolving apparatus ; a station- ary outer tube ; a cable covered with tight-fitting rubber tube ; and a sponge-spiral attached to the cable. Tiirck says : '' To show the outline of the greater curvature, a tube containing a cable with a sponge at its extremity is iutro- THE ABDOMEN AND THE ABDOMINAL VISCERA. 309 duced iuto the stomach. An apparatus for prodiicing revolutions is attached to the outer end of the cable. The cable is passed on- ward and it glides along the great curvature, plainly showing the outline of the stomach. Moving onward, the cable passes upward toward the pylorus, and then turns and passes along the lesser cur- vature. When rapid revolutions are produced the sponge and cable can be felt in their respective situations. To determine the disten- sibility of the stomach, cables of different degrees of flexibility are used. A very flexible cable (No. 1) is used first. It is introduced until it meets with resistance at the lesser curvature, and its length is noted. At the same time the revolving sponge is examined by palpation through the abdominal wall. A stiffer cable (No. 2) is then used, and pushed onward until it meets with resistan^-e at the lesser curvature, and its length is noted. The lengths are compared, and their difference shows the degree of distensibility. The degree of distention also is found by palpation through the abdominal wall." (For the symptoms of gastric dilatation, see the chapter on Vomit- ing, and that part of this chapter on the Diagnosis of Gastric Car- cinoma with Dilatation.) In inspecting abdominal swellings the physician should watch to see if they move up and down with respiration. If they do, they are probably connected with the diaphragm and depend upon disease of the liver and spleen, as tumors of the pancreas, stomach, and kidney are usually not attached to the diaphragm, and therefore generally do not move. Inspection of the abdominal wall will also show pos- sible venereal infection if the glands in the groin are enlarged, or if in suppurating they have left puckered scars. If silvery lines extend across the belly, they may indicate pregnancy past or present, or any state of the abdominal cavity causing great stretching of the skin. Great bulging in the neighborhood of the umbilicus will naturally suggest umbilical hernia, and swelling in the groin, not due to pus, inguinal hernia, or perhaps an appendicular abscess. Pai>i»ath).v and Pkkcussion. Alore important than any other external method of studying the condition of the abdominal contents is the use of gentle palpation, the fingers being gradually worked down into the abdominal cavity in such a way as not to cause pain or excite the muscles of the abdominal wall to resistance. The hand should always be carefully warmed before palpation is attempted, and the object of the examiner is to discover, first, the hardness or resistance to pressure ; second, the consistency and form of the organs 310 THE MANIFESTATION OF DISEASE IN ORGANS. which he can touch ; aud, thirdly, whether auy swellings which he feels are movable, bound down and immovable, pulsating, soft or hard, nodular or smooth. The patient whose abdomen is to be palpated must be placed flat on his back with the knees drawn up to relax the abdominal muscles, the head and neck should be raised, and, if possible, the attention of the patient should be diverted by conversation about some symptom which exists elsewhere than in the belly while the examiuation is made, as iu this way voluntary muscular resistance is removed to some extent. He should be made to breathe easily through his opened mouth ; and if the belly-wall remains so rigid that a perfect examination is impossible, and yet the results of such an examination are very important, ether or chloroform should be given to relax the muscles. Great resistance of the rigid abdominal muscles is found whenever peritonitis is present in an acute form, in some cases of renal and hepatic colic, and more commonly in lead colic and in hysteria. In peritonitis great tenderness to the slightest touch is also present. Another symptom of acute peritonitis, aside from the exquisite tender- ness of the abdomen, the drawn lip, the thirst, and the distention or rigidity of the belly-wall, is pain of a severe character ; unless it be septic peritonitis, when pain may be absent. There are also the drawing up of the limbs to relieve abdominal tension ; obsti- nate constipation, moderate fever, aud a very rapid, quick pulse. The tongue speedily becomes dry and parched, and collapse may speedily ensue in severe cases. It is not to be forgotten that localized peri- tonitis may result from many causes, usually from disease of the appendix vermiformis or the genito-urinary tract in women, and that the local symptoms and lesions may be limited by a wall of lymph to a very small area of the abdominal cavity. It must be remembered, however, that the anterior abdominal wall, particularly that of nervous persons, is often very sensitive or '^ ticklish," and the mere exposure of the skin to the air of the room, coupled with the fear of the examination, may cause great rigidity of the belly-wall without there being any abnormal condi- tion present. This can generally be overcome by gentleness in palpation and by resting the palm of the hand on the belly and partly flexing the fingers, rather than by attempting to insert the finger-tips between the abdominal muscles. The writer has recently seen a case of rhythmical hysterical spasm of the recti muscles in a THE ABDOMEX AXD THE ABDOMINAL VISCERA. 311 male, which at first gave the sensation of an enormous diffuse pul- sating aneurism of the abdominal aorta. Let us suppose that on placing the hand upon the epigastrium and the upper part of the umbilical area that we find a swelling. In the first place, we must decide as to whether it is in the abdominal wall or in the abdominal cavity. If it is in the wall, it will be mov- able with the tissues of the wall and readily grasped by deep palpa- tion ; but if in the abdominal cavity, the abdominal wall may be made to move over it, unless it be attached to the parietal peritoneum. Let us suppose it is in the wall of the abdomen, what can the swell- ing be ? It may be a fatty tumor ; in which case its surface will be dimpled and resistant, probably not painful, unless the part has been inflamed by rubbing or an injury, and it will not fluctuate. There will generally be a history that the person has exercised constant pressure on the part, as in leaning against a bench or table. Again, it may be an abscess ; but aside from the rarity of this condition, we can exclude such a possibility by the absence of pain, fluctuation, and the history of a severe injury. Very much more commonly a swelling in the epigastrium, or upper unibilical area, is due to an intra-abdominal cause. In adults the most common cause is probably a growth (generally a carcinoma) of the pyloric end of the stomach. In other instances it is due, par- ticularly in children, to enlarged lymphatic glands, as in tubercular disease of the mesentery. This is also sometimes seen in adults. Sometimes by reason of tubercular peritonitis a nodular mass is not only felt in this area, but an abscess containing tubercular pus may be formed and become surrounded by walls formed by the gluing together of the organs by lymph. Carcinoma of the pancreas may also cause a swelling in this neighborhood, or a cyst of the pancreas may be i)rcsent. Aneurism of the abdominal aorta is also not to be forgotten. Sometimes, too, a distended or carcinomatous gall- bladder may project into this area. If the growth be gastric carcinoma, the patient will be in or past middle life (probably between the fortieth and seventieth year) ; will have a iiistory of constantly increasing pain and discomfort in the stomach ; there will have been much sour bL'lching, and perhaps vomiting of colTec-ground-looking material ; marked loss of flesh and some cachexia will be present. According to Welch's statistics, out of I'WO cases of gastric; cancer, 701 were in the pylorus, 148 in the lesser curvature, 104 in tiic cardia, 08 in the posterior wall, 312 THE MANIFESTATION OF DISEASE IN ORGANS. and 61 involved the whole stomach. The remainder were in the fundus, the greater curvature, or the anterior wall. The growth, if in the pylorus, is usually freely movable, and for this reason can be readily felt, and then is often momentarily lost to palpation. Its position is apt to change with the posture of the patient and the presence or absence of food in the stomach. Pain is usually elicited on deep pressure, and, if the growth be large and at the pylorus, the symptoms of dilatation of the stomach will be present, because that viscus is dilated through the obstruction of the pyloric opening, which results in retention of the gastric contents. Under these circumstances, whatever the cause of the obstruction may be, or if the gastric dilatation simply results from inherent feebleness of the stomach-walls, the entire upper part of the abdomen will be found distended, tense, but yielding, and the history will show that the patient is attacked now and again by vomiting, during which the most extraordinary quantity of food and liquid, which has gradu- ally accumulated, will be expelled. The probable diagnosis of gas- tric cancer and of gastric dilatation can be usually confirmed by percussion, after distention of the stomach, and by the use of the gastrodiaphane. (See early part of this chapter.) Ev^eu before the stomach is artificially distended with gas percus- sion will give us valuable information in this connection, for, if obstruction of the pylorus exists, there will be found either a large area of gastric tympany through the accumulation of gas from fer- mentation, or, if no vomiting has taken place for some time, an equally great area of gastric dulness due to an accumulation of food and liquid. If in such a case we first wash out the stomach by means of a stomach-tube and then fill it with gas by giving the patient to drink, first, a half-glass of water with sodium bicarbonate in it, and then another half-glass with tartaric acid dissolved in it, so that gas will distend the viscus, we shall be able by means of per- cussion to outline the stomach with ease. It is best to mark the edge of gastric resonance by means of a blue pencil and thus to map out the gastric area. If there is a growth at the pylorus, causing obstruction, there will be impairment of resonance wherever the pylorus may be situated. While this is a somewhat indefinite state- ment, it is to be remembered that a more definite one is liable to mislead the student, for even in health the position of the pylorus changes greatly when the stomach is empty or filled with food. Thus when empty the viscus hangs with the pylorus very low, but THE ABDOMEN AXD THE ABDOMINAL VISCERA. 313 when it is filled the pylorus is raised. Fig. 136 shows the normal gastric area when the stomach is distended with gas. Fig. 187, taken from Osier's Lectures on Abdominal Tumors, illustrates the Fig. 136. Outline of normal position and size of stomacli in an adult when distended with gas. (After Meinert.) Fig. 137. Profile view of the abdomen of a woman aged sixty-live years, showing the tumor formed by the dilated stomach. (Oslek.) 314 THE MANIFESTATION OF DISEASE IN ORGANS. extraordinary descent of the stomach made in some cases of gastric dilatation in the adult. (Figs. 137, 138, and 139.) Fig. 138. Showing the position and size of the stomach. (Osler.) Fig. 139. Tumor of tlie abdomen caused by a dilated stomach. (Osi.er.) THE ABDOMEX AXI) THE ABDOMINAL VISCERA. 315 Many of these cases of gastric dilatation are also associated with atrophy of the gastric tubules, or at least au absence of any secretion of normal gastric juice. The matters vomited, or washed out of the stomach, are often devoid of hydrochloric acid, but loaded witii an excess of lactic acid. Lactic acid is tested for as follows, the hydro- chloric-acid test being given below : A few drops of neutral ferric chloride solution are mixed with one or two drops of pure carbolic acid, or 10 c.c. of a 5 per cent, solution of carbolic acid, and water added until an amethyst hue develops. A few drops of the filtrate derived from the stomach-contents are now added, and if lactic acid or lactates are present the amethyst-blue will become yellow in color. This is a very delicate test for lactic acid. Sometimes in cases of chronic gastric ulcer the area involved becomes so indurated as to be felt as a hard mass in the ''stomach- wall. In such instances the points which aid us in separating the condition from gastric cancer are the facts that the patient is young and usually a woman ; that the vomiting occurs immediately after taking food, for in gastric cancer it is only seen in most cases several hours after food has been taken ; that there is no sign of gastric obstruction ; that there is an excess of hydrochloric acid in the gastric contents in cases of ulcer, and an absence of HCl in cases of can- cer ; and, finally, that there is no cachexia in cases of gastric ulcer, though there may be anicniia. There is usually in cases of ulcer no great loss of weight, unless the symptoms have been present a long time. In cases of gastric ulcer great pain is often produced by deep or even superficial pressure over the epigastrium and a painful spot can generally be found on the back, about the angle of the right scapula. There is no better place than the present to speak of the manner of testing the stomach-contents for hydrochloric acid. The patient is directed to take no food for at least twelve hours before presenting himself to the physician. On his arrival for examination he is given what is known as " Kwald's test-breakfast," which consists of an ordinary dry roll and a little over half a pint of water which has been warmed, and lie is directed, after swallowing tluse materials, to wait for an hour. The stomach is now emptied by the introduction of the bulbed stomach-tube, and the gastric contents filtered. A few drops of a solution of phloroglucin and vanillin are next placed in a porcelain dish and a few droj)S of the gastric liquid are allowed to trickle down to the edge of the solution. The porcelain dish is 316 THE MANIFESTATION OF DISEASE IN ORGANS. gently heated over a spirit-lamp or Bunsen burner, and if hydro- chloric acid is present there will appear a red tinge, which is an absolute proof of the presence of hydrochloric acid. The solution of phloroglucin and vanillin is made as follows : Phloroglucin gr. xxx. Vanillin gr. xv. Absolute alcohol fSj. This solution is pale yellow in hue. It must be kept in dark bottles, as on exposure to the air and light it becomes brown and worthless. If the cause of the swelling of the abdominal wall be tubercular glands, they will be found, in all probability, on deeper and more general palpation, to be scattered all through the abdominal cavity ; there will be a history of alternate constipation and diarrhoea, of fever, of general loss of strength, of loss of appetite, and examination of other parts of the body may reveal the signs of tuberculosis else- where. The presence of a resisting mass, deeply situated in the epigas- trium, or the upper part of the umbilical area, and felt only on deep palpation, and then often indistinctly, should bring before the mind the possibility of the presence of carcinoma of the pancreas, a diag- nosis which will be largely confirmed if cachexia be asserting itself, if there be great pain in this neighborhood, and if there are oily stools after fats are taken, as a result of the absence of pancreatic juice. Still further confirmation of this diagnosis will be present if diabetes mellitus be developed by the patient (pancreatic diabetes). Such a growth in the pancreas is usually scirrhus cancer and may be primary or secondary. Segre found that of 627 cases of carcinoma of the upper abdominal organs cancer of the pancreas occurred in 127, but only in 12 of these primarily. Stiller asserts that the following symp- toms are fairly sure signs of pancreatic cancer, namely, marked dys- pepsia, rapid emaciation and cachexia, subnormal temperature, per- sistent and progressive jaundice without hepatic enlargement, but often with swelling of the gall-bladder from obstruction to its duct. These signs are, of course, only of value if the evidence of malignant growth elsewhere can be excluded. Very rarely swelling of this region, either rapid or slow in onset, follows upon the forma- tion of cysts in the pancreas, as a result of obstruction of the duct of the gland. When they occur these cysts may quite fill the ab- dominal cavity, although, as a rule, they are quite small. As THE A B DOMEX AXD THE ABDOMIXAL VISCERA. 317 pointed out, however, by Jordan, the real cause of swelling in the pancreatic region may ba hemorrhage into the lesser peritoneal cav- ity. He summarizes some of his views in regard to this matter as follows : '' Contusious of the upper part of the abdomen may be followed by the development of a tumor in the epigastric, umbilical, and left hypochondriac regions. Such tumors may be due to fluid accumu- lations in the lesser peritoneal cavity, and when the contents are found (on aspiration) to have the power of converting starch into sugar we may assume that the pancreas has been injured." Finally, Jordan states that " many such tumors have been regarded as true retention-cysts of the pancreas." In other instances a swelling in this neighborhood may be due to what is called pyo-pneumothorax subphrenicus, a condition cJf abscess in the peritoneal cavity below the diaphragm, produced by perfora- tion of the stomach or transverse colon. The abscess so produced may contain gas, and for this reason the swelling may be quite resonant on percussion. Abscess in this region also follows abscess of the pancreas, or fat-necrosis of this organ in rare instances. Sometimes, too, we have marked enlargement of the head of the pancreas, due to a malignant pancreatitis. This is particularly apt to be associated with cholelithiasis. The appearance of sudden swelling in the neighborhood of the pancreas, associated with intense pain, nausea, and vomiting, may be due either to acute hemorrhagic pancreatitis, to intestinal obstruction, or to acute peritonitis, resulting from perforation. The last two are the more common. An exploratory operation is the only way of deciding the diagnosis jjositively. (See chapter on Vomiting for symi)toms of intestinal obstruction.) Aortic ])ulsation is often transmitted to the hand by enlarged abdominal glands or tumor-masses. If the pulsation of the aorta is not transmitted by glands or tumors, it may be due to aneurism of the abdominal aorta, the diagnosis of which is established, if, in addition to a pulsating sensation, we also find on palpation a marked thrill, an expansile movement of the tinnor, and on auscultation we hear a bruit. Pain due to the pressure of the aneurismal sac upon some of the nerves of the abdominal cavity may also be a prominent symptom. Localized swellings due to other causes than those already dis- cussed are due to impaction of feces, volvulus, and intestinal obstruc- 318 ^HE MANIFESTATION OF DISEASE IN ORGANS. tion from other causes, as, for example, cancer of the bowel, which occurs most frequently in the csecura, when the growth will be found in the right groin, or in the sigmoid flexure, when it will be found in the left groin. Tumors or foreign bodies in the bowel can nearly always be moved about, unless bound down by inflammatory adhesions, so differing from growths which involve the immovable parts, such as the retroperitoneal glands. Very rarely we find cancerous tumor of the omentum, which usually becomes retracted and indurated so that its hardened edges can be felt extending across the abdominal cavity. More commonly multiple nodules in the omentum, or studded over the surface of the bowels, are due to peritoneal tuber- culosis. Not rarely these nodular masses are studded over the mesentery. Floating kidney may also cause a marked movable swelling or tumor-like mass in the upper zone of the abdomen. If the belly- walls are thin, the kidney-shape can sometimes be outlined by palpa- tion and even the pulsation of the renal artery can be felt ; but, as a rule, this cannot be done, and the dilatation of the pelvis of the kidney by the obstruction of the ureter, which has become twisted, may distort the shape of the organ. Deep palpation of the flank, if the kidney has floated away from its normal seat, may reveal lessened resistance in this area, and bimanual palpation, one hand being placed at the back and the other in front, may reveal the shape of the organ elsewhere. Further, if the patient be made to lie on the side the dislocated kidney may sometimes be clearly outlined by bimanual palpation. When the kidney is enlarged from cystic degeneration, from ordinary hydronephrosis, and from echinococeus cysts, it may be readily felt in the umbilical area in many instances. Hydronephro- sis has been mistaken, in children particularly, for sarcoma of the kidney, and in adult females for ovarian tumor. The diagnosis can only be made in some of these cases by tapping. The fluid obtained in hydronephrosis will usually be somewhat turbid and contain epithelial cells. It should not be forgotten that the condition of hydronephrosis may be intermittent, for, if this is not remem- bered, the physician may be misled into thinking that the disappear- ance of the swelling is due to a floating kidney slipping back into its place. Bulging of the flank, with pain, fever, and perhaps fluctuation. THE ABDOMEN AXD THE ABDOMIXAL VISCERA. 319 indicates perinephritic abscess or caries of the spine with cold abscess. Peristaltic movements of the intestines can soQietimes be felt through the belly-walls, and, if the contraction of the muscular fibres is excessive, nodular masses of momentary existence may be caused. Closely associated with this sensation on palpation is what is called '' phantom tumor." Such a formation is generally found in hysterical women and often leads to ludicrous errors in diagnosis. It is due to persistent dilatation of a knuckle of intestine by gas, thereby forming a moderately hard, and more or less constant, mass which may resemble a real tumor. Examination of the patient under ether will usually reveal its true character. Localized super- ficial and inconstant tumors may arise through spasmodic but local- ized contractions of the recti muscles. '' Finally, a swelling in the neighborhood of the umbilicus should always arouse the suspicion of an umbilical iieruia, and the situation of the swelling at the umbilicus, the fact that percussion over it gives a highly tympanitic note, owing to the gas in the prolapsed gut, and the possibility of reducing its size by taxis, will render a diagnosis of umbilical hernia possible. If on palpating the epigastrium and umbilical area nothing abnor- mal has been found, we next seek to discover if there is anything ab- normal in the right hypochondrium, or, in other words, whether there is any disease of the liver. Normally, in the adult, this gland cannot be felt below the ribs, except part of the left lol)e in the epigastrium occasionally. Some- times, on deep inspiration, the diaphragm pushes the liver low enough for it to be felt. In children the liver is naturally large enough to be felt below the ribs. AVheu the normal liver is percussed we finti that it lies in the area shown in Fig. 140, and that as we percuss above it on the ribs in the mammary line we first get ])ulmonary resonance, then a little Ix'low this impaired resonance, due to the fact that the lower edge of the lung is interposed between the chest-wall and the liver; and still lower we find absolute dulness or flatness due to the solid liver itself. Helow this area, which ceases just i>elow the lowest rib, we usually find tympany on percuasion, due to the gas-distended bowel. If we percuss in the midsternal linn, we get the same signs, but they begin as high as the nip|)le, or above it, and then cease on a line drawn across the abdomen about midway between the ensiforni 320 THE MANIFESTATION OF DISEASE IN ORGANS. cartilage and umbilicus. To the left of the middle line of the sternum the liver-dulness merges into the cardiac duluess. (See Fig. 140.) In the mammary line liver-dulness begins at the fifth rib, laterally it begins at the seventh and eighth, posteriorly at the tenth, owing to the sloping ])osition of the diaphragm. Fig. 140. Showing absolute and relative percussion-dulness of liver and heart. 1. Relative dulness of liver. 2. Absolute dulness. 3. Relative dulness of heart. 4. Absolute dulness. When a hard and firm mass, with a smooth surface, can be felt in the right hypochondrium or right umbilical area, which is mov- able, and which has an edge which can be readily felt on deep pal- pation, the mass is probably an enlarged liver or one pushed down into the abdominal cavity by a large pleural effusion or a subphrenic abscess, or sometimes by an emphysematous lung. The causes of en- largement are amyloid degeneration, congestion, hypertrophic cir- rhosis and abscess, carcinoma, sarcoma, and lymphadenoma. When the surface is found to be smooth the condition is probably amyloid THE ABDOMEX AND THE ABDOJIIXAL VISCERA. 321 or fatty degeneration, or congestion. If the surface is rough, it will probably be clue to cirrhosis, which gives a granular sensation to the hand when the abdominal wall is moved over the organ. In malisf- nant growth large and small nodules may often be found, and depressions or umbilications of its surface may be marked. When, on palpating the liver, we find marked tenderness and some swelling, and, associated with these symptoms, fever, rigors, sweats, and some- times vomiting, and, in addition, a history that the patient has had dysentery or has had exposure to tropical heat or has swallowed much bad water, we are forced to the belief that an abscess of the liver exists. This may be single or multiple. If the latter, it is probably due to pyiemia, and no spot of fluctuation will be found as a rule ; whereas, if it is large and single, fluctuation is sometimes felt. Further, the enlargement of the liver in the pyaemic form is uniform, whereas in the single abscess there is often one spot which is swollen or enlarged. If a single large pyriform swelling, which is yielding and somewhat painful on palpation, be found, and there is some fluctuation present, abscess must be thought of, or in its place impaction of the gall-bladder with gall-stones or its dis- tention by obstruction to its duct. The history of the case will usually separate the conditions, one from the other, for diagnostic purposes, for in the case of abscess the history will probably be that of a person exposed to tropical heat or one who has had an injury, an acute infection, or an amoebic dysentery, while if gall-stones be the cause of the swelling there will be a history of gall-stone colic, of jaundice, or of hepatic fever. More rarely a single hepatic swelling may be due to hydatid cyst, but the history and presence of fluctua- tion, coml)ined with the result of examining the fluid aspirated from the swelling, will decide the diagnosis. The consistency of the liver is usually very hard in cases of cirrhosis, carfMnoma, ami amyloid degeneration. In cirrhosis there will be some ascites in many cases, some swelling of the legs perhaps, and dull pain in the hc|)atic region. The digestion will be disordered, there will 1)0 marked loss of flesh and often hj^raatemesis. Sometimes coma comes on. In the malignant disease there will l)e pain, marked emaciation, and cachexia; nodules will be felt in the liver-substance, and the (trgan be foutid much enlarged. Tenderness on pressure will be marked. Soiuctitiies ascites will be present and a growth may be found, usually as the |)rimary lesion, in the stomach or bowel. In the case of amyloid liver there will be a history of prolonged sup- 21 322 THE MAXIFESTATIOX OF DISEASE IN ORGANS. puration elsewhere, and there will be present disordered digestion, irregular bowel -movements, and little pain. Marked tenderness of the hypochoudrium is usually found in con- gestion of the liver, in inflammation of its tissues, such as that caused by an infection or by gall-stones in its substance, and in malignant growth. Tenderness is practically absent in waxy liver and in fatty degeneration. In cases of cirrhosis of the liver, whether it be in the hypertrophic or atrophic form, the organ presents no symptoms in itself save that in the liy})ertrophic state its size is increased so that it can be felt below the ribs, whereas in the atrophic state it cannot be felt except Fig. 141. Morning Sickne Hoematemesis Dynpepsia iPaUor,Pain Spleen-i and jEnlargement Hcemorrhoids To illustrate symptoms of cirrhosis of liver. by pushing the fingers well up under the ribs. The symptoms accompanying cirrhosis are chiefly connected with disorders of the alimentary canal, either through direct failiire in the digestion and assimilation of food, or from clianges in the blood-supply of the abdominal contents. The following excellent diagram from Taylor's Index of Medicine sliows what these symptoms are, and discerns their cause at the glance, the cirrhotic process, of course, obstructing the flow of blood in the liver. (Fig. 141.) Finally, the physician who finds the lower margin of the liver abnormally low down in the abdominal cavity should not make a diagnosis of enlargement of this organ until he has assured himself that the extension of the mari^iu of the liver is not due to an effusion THE ABDOMEN AND THE ABDOMINAL VISCERA. 323 Fig. 142. iu the right pleural cavity which presses upon this orgau. So, too, if the patieut is a 'woman, the lower border of the liver may have been pushed down by tight lacing, and careful palpation may reveal a furrow across its surface produced by the corset. A small pear-shaped mass protruding from under the liver is usually due to an enlarged gall-bladder, distended by bile or calculi, If the former, pressure may cause it to disappear owing to the bile being pressed out into the intestine. In the left hypochondrium the spleen can be very readily outlined by percussion, in persons not inordi- nately fat. Its normal position is best shown in theaccompauying figure, 142. The upper border of the spleen is on a level with the tenth dorsal vertebrae and the lower border on a level with end of the eleventh rib. Its upper edge or limit is on a level with the ninth rib. In percussing the spleen heavy percus- sion is to be avoided, since this may develop the resonance of the stomach or bowels. The spleen cannot be pal- pated unless greatly enlarged, but it may be found i)ulging from beneath the lowest rib in typhoid fever ; in scarlet fever ; as the result of acute or chronic malarial fever ; iu leucocy- tluemia f)f the spleno-medullary variety; in atnyloid disease, as that after long suppuration ; in early syphilitic infec- tion ; and in any disease which causes venous engorgement of the abdominal viscera, such as cardiac disease or hepatic cirrhosis. Sometimes dis- placement of the spleen downward arises from emphysema t)f the lungs or left-sided pleural effusion. Acute splenic swelling sometimes comes on in cases of general septicsenu'a. Nearly always the splenic surface is smooth, except for the notch in its surface (see Fig. 133, p. 306), unless the disease be the rare condition of hydatid disease or carcinoma. There yet remains for discussion the significance of increased Normal position of the spleen. 324 THE MANIFESTATIOy OF DISEASE IN ORGANS. resistance ou palpation, and percussiou-dulness, in the groins. In the right iliac region the presence of swelling, increased resistance, impaired resonance, or tympanites, particularly if pain and tender- ness are present, point strongly to appendicitis or to inflammation about the caput coli. Sometimes, however, the presence of a dis- tinct lump in this region in a person advanced in life may mean a malignant growth, for carcinoma of the caput coli is not rare. If the left groin is affected in a person well advanced in years, carcinoma is also to be regarded as possible, for the sigmoid flexure is a frequent seat of such growths. In a young person, or a child, impaction of feces, a foreign body, or intestinal obstruction is to be considered. (See chapters on Vomiting and on the Bowels.) For the diagnosis of renal diseases reference is to be made to the chapters on the Bladder and Urine, on the Blood, on the Bloodvessels and the Pulse, and that upon the Thorax, that part on the heart ; the chapters on Vomiting and on Headache, and to those on Coma and Unconsciousness, and Convulsions and Sj^asms. For further information in regard to the diagnosis of diseases of the abdominal viscera, the reader is referred to the chapters ou the Skin, that part on jaundice ; the chapter on Vomiting, part on intes- tinal obstuction ; that in the Bladder and Urine ; and that upon the Bowels and Feces. CHAPTER X. THE BLOODVESSELS AND PULSE. The condition of the bloodvessels on palpation — Feeling and counting the pulse — The quality, force, and volume of the pulse in health and disease One of the first things that tlie physician does when he is study- ing the condition of a patient is to feel the pulse, even if the symp- toms which are present do not indicate circulatory disturbance, because the pulse is an index of the condition of the heart as to its power, its valvular action, and its nervous state. The pulse very often gives us information of the presence of renal disease, and it will frequently give us a. general idea of the tone or degree of debility of the patient. By feeling the pulse we also gather valuable information as to the condition of the arteries, and this is a very important part of the diagnosis, for, to use an old saying, " a man is only as old as his arteries," and if he is sixty years of age and has good vessels he is, as a rule, as young in health as another man of thirty with bad vessels, because it is by the blood- vessels that the tissues of the body are nourished, and, as life depends upon this process of nutrition, the better the vessels the l)etter the vitality. When examining the pulse of a patient who is well enough to be iij) and about the physician should wait until sufficient time has elapsed after exercise for the pulse to Ijecome steady, and the patient shoidd be in a sitting or reclining posture in order to prevent over- action of the lieart. Particularly is it important in the case of ner- vous individuals to wait for sedation to follow the excitement of meeting the physician. Often when called to see a sick child or a nervous woman, who may be sleeping at the moment of the physician's arrival, a true estimate of the pidse can be made without disturbing the patient by gently putting the tip of the finger on the temporal artery where it passes over the zygomatic process. This artery may also be used for this purpose in cases of tremor, chorea, delirium, or mania, where the hand is constantly moved about so that the radial artery cannot be felt. 326 THE MANIFESTATION OF DISEASE IN ORGANS. In counting the pulse it is best to count it for the entire minute, or to count it for fifteen seconds and then multiply the result by four. If the pulse is irregular, it is always best to count it for a minute. If the pulse l>e very irregular and running, and so difficult of counting, the count should be made by listening at the praicor- dium for the apex-beat. Before considering the qualities of the pulse in health or disease, it is well to understand what it is due to and the manner in which the circulation is carried on. The bloodvessels consist of the arteries, arterioles, capillaries, venules, and veins. These vessels always contain blood during life, and the function of the heart is to propel the blood through them. The flow of blood is maintained, first, by the force expended by the heart, and, second, by the tonicity of the bloodvessels. If the bloodvessels of the body become relaxed, as in death, all the blood is readily held by the ones most relaxed, namely, the abdominal, thoracic, and other veins. We find therefore that the vessels are only filled with blood when their walls are to a certain extent constricted by the contraction of their muscular fibres ; and that this contraction is maintained by the action of the vasomotor centre in the medulla oblongata, which also controls many minor centres governing small areas of vessels. The arteries are very elastic in health, and when filled with blood are slightly distended. Behind the column of blood, which being a fluid confined laterally is practically a solid, for fluids are incompressible, is the heart, and in the arterioles are muscular fibres, which by their contraction regu- late the flow of blood into the capillaries, from which the nutritional processes are carried on. The blood in the arteries is, therefore, subjected to three chief pressures, namely, that of the heart behind the column, that of the elastic and distended arterial walls on the sides of the column, and the resistance of the contracted arterioles in front of the column. By these means blood-pressure or tension is maintained. If the heart beats more strongly or the arterioles con- tract more tightly than normal, the blood-stream is under a greater pressure than before. If the heart is feeble or the arterioles lax, the pressure falls, because the blood is not pressed upon behind or ob- structed in its flow in front. If the tension is above or below normal, the interchange of food and oxygen and carbonic acid between the tis- sues and the blood in the capillaries is perverted, for the rate of flow in the capillaries depends largely upon the blood-pressure in the arte- ries. Now the capacity of the capillary system of vessels is many THE BLOODVESSELS AXD PULSE. 327 times greater than that of the arteries, and, if the arterioles relax, the capillaries and veins will retain all the blood, and in thera it will stagnate and become useless. The manner in which arterial tension is chiefly maintained hav- ing been described, we can now consider the pulse-oeat itself. The individnal pulse-beat is not a wave of blood sent out by the heart, but it is the transmission of the force of the heart-beat sent along the blood-column, and the character of the beat gives us, therefore, an idea of how forcibly the heart is driving another quantity of blood into the aorta, and also how much blood is being sent out at each beat. Supposing, therefore, that on feeling the radial pulse we find that the artery is tense and hard, and that the individual beat is strong and its volume great, this signifies that there is an excited vasomotor centre, causing contraction of the vessels, and that an excited, over- actinsc heart is forcingr the blood into the already tense vessels. If this condition increases, one of three things can happen, either the heart will be unable to pump the blood out into the arteries against the pressure and consequently become distended and paralyzed, or the bloodvessels will burst in the weakest spot, or the spasm of the arterioles will have to give was'. It is the first result which we meet in cases of true angina pectoris, for in this state we find great arterial tension, with distention and engorgement of the left side of the heart, and the moment nitroglycerin or nitrite of amyl relaxes the spasm of the arterioles the symptoms are relieved. It is the second result which often produces apoplexy by rupture of the weakest vessel, usually the middle cerebral artery. It is the third result which we try to bring about for the relief of the j)aticnt, either by ^appears with each deep ins|)iration. It is usiuilly due to indurative mediastino-perii-arditis, whereby iuHammatory l>ands press on tlie bloodvessels or the heart. If the beats of the heart are irregular in force, but regular in rhythm, we have developed a pulsus allernans. 330 THE MAXIFESTATION OF DISEASE IN ORGANS. A dicrotic pulse is oue -which is characterized by a reduplication, which feels like a secoud beat following the first before the latter is over. It is found in many cases of exhausting fever, and depends upon an undue elasticity of the bloodvessels, with relaxation of the arterioles, so that the blood first unduly distends the arteries, which then contract upon it, and thus produce the second wave or apex to the pulse-curve. We can study the pulse either by the touch or by the sphygmo- sraph. If by the latter meaus, the instrument of Dudgeon is the best. (Fig. 143.) The normal pulse-wave is shown in Fig. 144. Fig. 144. ab. Percussion upstroke, abc. Percussion-wave. cde. Tidal wave. ejg. Dicrotic wave. def. Aortic notch, fg Diastolic period. It will be seen that there is a distinct upstroke produced, which is called the line of ascent. This is due to the distentiou of the artery produced by the ventricle forcing blood out into tlie aorta. There is after this a line of descent interrupted by two separate secondary waves, which are called catacrotic waves. The second or lower of these is called the dicrotic wave, and is the one which becomes marked enough to be felt in some cases of disease. The duration of the period of descent corresponds to the time the blood is flowing out of the arteries into the capillaries, and, if this flow is rendered difficult by vascular spasm, the line of descent will be gradual. If easy from vascular relaxation, it will be short. If the drop is very sudden, it is pulse of '' empty arteries," so-called, as after severe hemorrhage in cases of acute regurgitation. Very small irregularities of the line of descent are due to the elastic bloodvessel being thrown into vibrations by a forcible pulse- wave. In Fig. 145 is shown the typical pulse-wave of aortic regurgita- tion ; and in Fig. 146 that of mitral stenosis, which is irregular in time and volume. The rapidity and force also depend largely on the condition of THE BLOODVESSELS ASD PULSE. 331 the bloodvessel-walls, particularly the rapidity. The latter also depends upon the activity of the pneumogastric nerves in regulating the beat of the heart. Thus, if the arterial pressure be very high, through spasm of the arterioles, the difficulty experienced by the heart in forcing blood into the arteries will be so great that pulsa- FlG. 145. Tracing from a case of aortic regurgitation. (Mcsser.) Fig. 14G. Tracing from a case of mitral stenosis, sliowing increased tension and some irregularity. (MUSSER.) tion will be very slow ; whereas, if the normal resistance to the action of the heart be removed by vasomotor relaxation, the beat will be rapid, just as the wheels of a locomotive fly around on a slippery track when the friction or the resistance is removed. If the vessels are relaxed, the impetus communicated to the column of blood in the vessels by the heart is lost, and so the pulse is not forcible ; or if the resistance is excessive, the force is dissipated. The vagus or pneumogastric nerves are continually holding the heart in check, and by causing full diastole enable it to send out a large wave of blood at each contraction. If they are greatly stimu- lated, we have a very slow pulse and a full wave of blood with each lu'art-i)eat ; but as the heart now beats very slowly the blood- ])ressure may fall for lack of blood in the vessels, unless there is an increased force of the heart at each contraction to make uj) for the number of l)eats in the minute which have been lost, or unless there is also a great increase in arterial tension by contraction of the ves.sels. A very slow j»ulse de])ends in the great majority of cases u[)i)n a high arterial tension from vascular spasm — /. e., resistance to the flow of blood ; more rarely it is due tion lens for use with a condenser. The eye-pieces used are usually Xos. 2 and 4. The finger-tip of the patient having been waslunl clean, a sharp needle or the tip (tf a tenotome is used to puncture the skin and the drop of blood which escapes is placed upon a tj;lass slide and covered with a cover-glass, so that the film of blood is very thin indeed. 336 THE MAXIFESTATION OF DISEASE IN ORGANS. Examined under the microscope this will give a crude idea of the proportion of white to red corpuscles, and of their color and shape ; but more accurate methods are advisable, and for their use we resort to what is called a hsematocy to meter, of which the best is the Thoma- Zeiss apparatus, which consists in part of a glass capillary tube. Fig. 147 0.100 mm. 4-^0 sq- mm. Thoma-Zeiss blood-counting apparatus. A heavy glass slip (a), in the middle of which is a cell {B) exactly l/lo millimetre iti depth. The cell is limited at the periphery by a circular gutter to prevent fluid placed upon the cell from flowing beyond it between the slip and cover- glass. The floor of the cell is ruled into squares whose sides are 1/20 m.m. Dark lines mark out large squares containing twenty-five small squares. Thick, carefully ground cover-glasses (D) are provided in the case. The ordinary Potain Melangeur {Sj is used to measure and mix the blood. It consists of a capillary tube the upper portion of which is blown into a chamber {E) holding 100 c.m.m. The stem of the tube is graduated at 0.5 and at 1 c. m.m. Fig. 148 ::} ; > :''" ' C % 'ol" ', " •> c ■• '■.'■" n ' -' o ; ' ,'•. ° = ■'0 ' ;• lv° "0*^0 V/ t'° ' ,°, 'j: „° °c };» ° y^ ::"-> °: .' ^v. ' ^ „ \ ■' ',°° i-^: :"■' "o'o } 1° °\° ,e „ °'l o° \i •y° [o\ v; y 0^' \'^ ', °. , OO '= V o"" °o° ,« ,' ' „' "T' % a %\ S" ° »■',"» %°,° ,' / "0°. c'o } \ °i~. h h 1 inometer. u-scd. Flci.sclil's apparatus consists in a small table, in the centre of which is a hole into which fits a round cylinder with a glass bottom, divided perpendicularly in the middle by a metal diaphragm, and both sides of which are filled with pure water. Under the stand is a fratne in which is set a piece of colored glass as near the hue of diluted blood as possible, and this glass is tapered off gradually, so as to give a lighter .shade of red at one end than the other. The frame carrying the glass is marked by a graduated scale and is moved 342 THE MANIFESTATION OF DISEASE IN ORGANS. from side to side in a track under the half of the cylinder, which is to contain only pure water, by a thumb-screw. Under the glass and cylinder is a white reflector to direct the rays of light through them. (Fig. 152.) The rest of the apparatus consists iu a little capillary tube attached to a tiny wire handle. This tube will hold just enough jjure and healthy blood to color the water on one side of the cylinder to the hue shown iu the colored glass wheu it is opposite the normal mark ''100." The finger being punctured, the end of the capillary tube is lightly touched to the drop of blood which runs up the capil- lary tube, and the tube is then immersed in the water on one side of the cylinder, and stirred about till all the blood is washed out of it. The apparatus is then exposed to gas or lamplight, because with day- light the hue of the glass does not match blood-color, and the frame is moved backward and forward until the color of the glass, under the side of the cylinder which contains only pure water, seems to the eye to match the fluid containing the blood on the side through which the pure light streams. If the glass matches the blood-color when the mark on the frame is at 50, it shows that the haemoglobin equals only 50 per cent, of normal, or if it is at 85, it signifies 85 per cent. As a matter of fact, an examination of perfectly healthy blood will often give not more than 85 to 90 per cent, of haemo- globin with this apparatus. Care should be taken in regard to three points : first, to be sure that all the blood is washed out of the capillary tube into the water ; second, to be sure that the two halves of the cylinder are filled to the brim with water so that there is neither a positive nor a negative meniscus ; and, third, to be careful to cleanse the entire apparatus thoroughly after each use of it before putting it away. Anaemia. Having studied the methods of examining the blood we come next to the consideration of the diagnostic value of the con- ditions which we find in it. We find, first, that ansemia, or blood- deficiency, is represented by two conditions, in one of which the pallor and other symptoms are due to a diminution in the number of red blood-corpuscles, while in the other there is a decrease in the amount of hemoglobin in each corpuscle. In regard to the white corpuscles we find even more valuable diagnostic data, since their variation in number, form, and character is marked in some diseases. Practically all conditions of the blood which are pathological represent diseases in organs connected with the blood directly or indirectly, and do not depend upon primary changes in this liquid, except in rare instances. THE BLOOD. 343 A patient's 1)1oik1 having been found lacking in the proper num- ber of red blood-corpuscles, the question naturally arises as to what conditions underlie this variation from the normal. The most com- mon causes of this decrease are the infectious diseases, which all result in producing a degree of anaemia most marked during early conva- lescence, and the history of such an attack should always be sought for, and, if found, regarded as an important point for consideration in reaching a diagnosis. If there be no history of acute illness, the most natural condition to be thought of is that known as simple ansemia, produced by no apparent disease of the organs of the body, but due to lack of good food, pure air, proper hygienic surroundings, and exercise. If this is excluded from the diagnosis, w^e must not forget that if food is taken and not absorbed properly the corpus- cular richness of the blood is decreased, and therefor^ chronic indigestion, notal)ly that condition called atrophy of the gastric tubules, may be the cause of the difficulty. Again, the presence of profound anaemia, as to the number of the red blood-corpuscles, may be present and seem inexplicable, until it is discovered that the patient suffers from bleeding hemorrhoids, and the daily loss of blood, even though it be small, is sufficient to produce anaemia. Similarly r^^peated attacks of nose-bleed or of excessive menstruation may so result. Naturally the physician will have excluded the possibility of the anaemia being due to a profuse hemorrhage from any cause before searching as far as this for a diagnosis. There still remains to be considered the aiuemia which is called "■ pernicious," in that it progre.ssively gets worse till death occurs, in the majority of eases, although a few may recover. There is every reason to believe that in the near future we will understand its pathology, but at present we do not. It is characterized by marked pallor without loss of flesh, or, to speak more correctly, the subcutaneous tissues are added to rather than robbwl of fat. There is gradual increasing dyspn(ea, failure of strength, cardiac palpitation, venous murmurs, some vertigo, and roaring in the ears. The blood shows a most extraordinary and continually diminishing numi)er of red blood-corpuscles, until the numl)er may amount to only 143,000 to the cubic millimetre. In addition, the following points of great diagnostic importance are to be noted. First, the individual red corpuscles are richer than normal in hicmoglobin ; second, many of them arc larger than normal (megalocytes) ; tliinl, the red corpuscles arc deformed, .some being 344 THE MAXIFESTATIOy OF DISEASE IX OBGANS. ovoid, others irregular in shape from projections and constrictions on their surfaces (poikilocytes) ; fourth, there are present mi- crocytes or red blood-cells, which are smaller than normal ; fifth, nucleated red blood-cells (normoblasts) ; and fifth, and quite con- stantly, there are other large cells like the megalocytes, named mega- loblasts, which have a pale staining nucleus. These last are often larger than the megalocytes, and are sometimes called the " corpuscles of Ehrlich,"^ since he regards them as pathoguomonic of pernicious anseraia. The white blood-corpuscles are normal in number, or slightly decreased, although the great diminution in the red cells renders the proportion of white to red greater than normal. Ansemia depending upon lack of haemoglobin in the corpuscles, rather than a decrease in their actual number, is seen most typically in that condition called chlorosis. In this state the corpuscular dimi- nution is so slight that it may be ignored ; but the decrease in haemo- globin is extraordinary, sometimes falling as low as 20 per cent, of the normal or below it. The red corpuscles are, however, very commonly irregular in form; that is, there is more or less poikilocytosis, but the white corpuscles remain normal in number or slightly increase. The diagnostic points, in addition to those of chlorosis just named, are the fact that the patient is generally a young girl of from fourteen to twenty-five years, that the skin is peculiar in its pallor (see chap- ter on Skin), and there is often little if any menstrual flow, which is usually only faintly pink in hue. Dyspnoea, cardiac irregularity, constipation, and a wayward appetite are often present. Ausculta- tion of the neck on the right side over the jugular vein will reveal a peculiar murmur called a" humming-top " murmur. Febrile move- ment of slight degree may also be present. In addition to these causes of ansemia we find anaemia due to a decrease in both the corpuscles and haemoglobin. A large proportion of these cases have already been mentioned when speaking of the anae- mias of convalescence and hemorrhage, but a far more important cause of this condition, yet one often overlooked, to the great regret of the physician in later years, is the possibility of the cause being tubercu- losis. Still other causes of such anaemia are cancer, sarcoma, and renal disease, particularly gastric cancer, in which condition the blood may resemble that of pernicious anaemia, and gastric ulcer, in which the loss of corpuscles may also be extraordinary, even if no 1 These are not to be confused with the myelocytes of Ehrlich. THE BLOOD. 345 hemorrhage occurs. Chronic lead-poisoning, arsenical poisoning, and urtemic poisoning may cause it, and it arises from the presence of numerous forms of parasites in the bowels, such as tapeworm, anchylostomum duodenale, and last, and by no means least, malarial infection, either as manifested l)y acute attacks, frequently repeated, or by slow poisoning with the development of cachexia. (See further on in this chapter.) Leukaemia. There yet remain to be considered those conditions in which we find not only those states already described, but, in addition? marked alterations in the white blood-corpuscles as well as the red? alterations of such moment that they become the salient features of the blood when it is examined, and they are of great diagnostic impor- tance. The points of importance in examining blood in regard to the white corpuscles are their number and their peculiarities and kinds. The discovery that the proportion of white to red corpuscles is far too great, varying from the normal (1 to 450, approximately), should cause the physician, first, to exclude all possibility of transient causes of variation by making an examination at various times of day, or by *»xcluding the presence of acute infectious disease characterized by leucocytosis — that is, the presence of an unusually large number of white corpuscles. This can be done, not only by excluding the presence of an infection, but also by the fact that in leucocytosis in infectious diseases the increase is solely in the polynuclear neutro- phile corpuscles. Thus it is well known that the taking of meals increases the white corpuscles during digestion, and that exercise and massage do the same thing, at least so far as the proportion in the peripheral vessels from which we draw the blood is concerned. If, however, these causes are excluded, and we find a patient of from twenty-five to forty years of age and a male (in the proportion of 2 to 1) pallid and pufFy-looking, dyspncjeic, and feeble, with a marked and constant increase in the proportion of his white corpuscles, what does it mean ? It probably means that the patient is suffering from leukjcmia (leucocythuMuia) in one of its two forms, namely, spleno-% medullary leukaMuia or lymphatic icukuMuia, of which the former is by far the most common. When the disease leukaemia is present in its splcno-iiu'dullary form, the typical change, aside from the great increase in the num- ber of the granular neutroj)hiIe white cells already described, is the presence of an additional cell, which is supposed to be derived from marrow, and is called a myelocyte, sometimes called the " myelocyte of 346 THE MANIFESTATION OF DISEASE IN ORGANS. Elirlich." They are large mononuclear cells with their protoplasm filled with fine neutrophile granular masses. We have already described the white corpuscles of healthy blood in the beginning of this chapter. We can, therefore, pass directly to a discussion of the means to which we resort when we desire not only to examine the blood for the number of these cells, but also for the abnormal myelocyte just named. The best solution for staining purposes is that of Ehrlieh, which is called a triple stain. It is composed as follows : Saturated watery solution of orange " g," 125 cc ; saturated hydro-alcoholic (20 per cent, of alcohol) solution of acid fuchsine, 125 cc. These ingredients having been mixed gradually and thoroughly shaken, the following constituents are added, the shaking being continued : Saturated watery solution of methyl-green, 125 cc ; absolute alcohol, 75 cc. This solution should stand for several weeks to allow of sedimenta- tion ; it improves with age ; and when it is used the supernatant liquid is to be drawn off by a pipette in order to avoid the sediment, This stain acts in a few minutes. Some cover-glasses having first been well cleansed by alcohol and water, the surface of one is touched to a drop of freshly drawn blood, and then another cover-glass pressed on its surface until the blood is evenly distributed. The glasses are then separated and allowed to dry. After they have dried they are still further hardened over an alcohol flame or on a hot stage made of sheet copper, and kept at 212° F. for fifteen minutes to two hours. After this they are placed in the staining-fluid for from one to four minutes, then washed in pure water, dried, and mounted in Canada balsam or cedar oil. The Canada balsam should not be prepared with chloroform, as it will decolorize the specimen. The glass is then ready for microscopic examination with yV oil-immersion lens. The nuclei of the eosino- phile corpuscles will be stained a reddish hue, the neutrophile granules in the granular leucocytes will be stained purple, and the nuclei of the ordinary leucocytes bluish-green or blue. (Plate X.) The other changes found in leukoemia are an increase of the eosino- phile cells, but the polynuclear cells with fine dust-like neutrophile granules are about the normal number. The red blood-cells are greatly decreased in number, and a large number of nucleated red cells may be seen. The haemoglobin is decreased. Cavafy states that the amoeboid movements of the white cells are impaired. The proportion of one to three red cells is often seen. The additional PLATE X. FIG. 2. /^ii"^ ^r^ o •I-^ ^a- Severe Ansemia with Leucocytosis. Dry preparation. Ki.\ed with picric acid. Stained with hicniato.xlin IJohmer, -x 300. Red corpuscles few, almost colorless, varying in size, show poikilocytosis ; two nucleated reds (normoblasts). The increa.se in the white cells seen to be in the polynuclear elements. (Rieder's " .-///((.v (ft> h'litiisiht)! Mikniskopie dfs Hluti-s."\ Splenic-Myelogenic lyeukfemia. Eosin-haematoxylin, x 300. Red corpuscles rosy- red, of nearly uniform size, round. To the left a normoblast with eccentrically placed nucleus. Many large mononuclear leucocytes (myelocytes) and three eosinophiles seen. (Rieder ) FIG. 3. ^ C Si)lenic-Myel()genic I.eukiemia. Same case. Kosin-hiumatoxylin, x iioo one normoblast, one polynuclear leucocvte. one mye- locyte, two eosinophiles. The neutrophilic gran- ules of the ])olynuclear leucocyte and of the mve- locylc do not show with this stain. The large mononuclear eosiiiophile above is believed to be also a myelocyte iMarkzelle), the smaller one below, an eosinoi)hile such as can be found in normal blood, ikiedor.) Myelocyte, Normoblast, Megaloblast. Triple stain, (i. myelocyte showing neutrophilic grnnules; II, normoblast, both from a case of s|)lenic myelogenic leukicmia : I, large nucleated red corpu.scle (megaloblast) from a case of pernic- ious aniemia. (Osier.) PLATE XI. 'he FaraSitfc of Tertian Fever 9 ® 1^ •A, >^ *"■»'* -1 :0'- :if^^ The Parasite of Quartan Fever. • 9 O t 'tAt /^^j^ THE BLOOD. 347 symptoms of this form of leuksemia are great and gradual enlarge- ment of the spleen, with marked splenic tenderness. Auscultation over this organ may reveal a murmur and palpation a crepitus. Hemorrhage, generally from the nose, is common, and dyspnoea and diarrhtca are often present. Often retinitis develops, and slight fever may occur. Ly.mphatic Leukj:mia. When the proportion of white to red cells is one to ten, the white corpuscles all remaining normal in number, except the lymphocytes (that is, the mononuclear, deeply staining cells, with a rim of non-granular protoplasm), which are greatly increased in number, we suspect lymphatic leukaemia. Mye- locytes, so typical of the spleno-medullary form, do not appear in this condition and splenic enlargement is absent, but in ifs place there is often enlargement of the superficial lymph-glands, but these never grow so large as in Ilodgkin's disease or pseudo-leukiemia. Parasites of the Blood. We still have for consideration the parasitic diseases of the blood. These consist in the malarial germ of Laveran, or, as it is more properly called, the " htematozoon malarife " of Marchiafava and Celli, and the filaria sanguinis hominis. Malarial Organisms. Xo more important addition to the study of disease, from a diagnostic standpoint, has been made than the dis- covery of the presence of a parasite in the blood of persons suffering from malarial fever, which is always present under these circum- stances, and in all probability acts as the cause of all malarial mani- festations. These parasites are varieties of sporozoa, whicii live inside the red blood-corpuscles of the individual attacked.' The parasite of nruilarial fever occurs in three forms, namely, as that (»f tertian fever, that of (puirtan fever, and as the parasite of the so-called aestivo-autumnal fever. The tertian parasite is a small hyaline, colorless body, which occupies but a slight extent of the interior of the red blood-corpuscle. (Plate XI., Figs. 2, 3, 4.^) When quiet they are round like the corpuscle in which they lie ; but if the specimen examined be fresh, they may be seen to j)ossess active amnc!)()id movements, thereby changing their shaj)e. Soon this aina'boid botly grows in size and begins to develop red- 1 In this country the chid invcstlRfttora into the lifc-liistory of the mnliiriiil i>"riisite have been Osier, Councilman, uml. more recently, Thayer ami llewetson, from wliose exiinnstive ami able nionoKraph on " Tlie Malarial Fevers of Hallimore" mueli of the information in tlie text of this book is derived. - No. I. is normal red corpuscle. This plato is taken from Thayer and Hewetson's Nonograph. 348 THE MAXIFESTA TTOX OF DISEASE IX ORGANS. dish-brown pigment-grauules (Plate XI., Figs. 6, 6, 7) in itself. These pigment-granules are rapidly moving bodies, and as they are often found in the projections of the parasite, it may look, until this fact is corrected by fine focussing, as if several parasites were in one corpuscle. As the pigment-masses increase, the corpuscle which con- tains the parasite becomes more and more pale, and at the same time swells up or expands and the amoeboid movements grow less and less, while the pigment tends to arrange itself toward the periphery. (See Plate XI., Figs. 7 and 8.) Finally, only a shell of corpuscle is left (Plate XL, Fig. 9), the pigment after collecting in the centre becomes motionless, and then the parasite undergoes segmentation ; and, finally, we have developed 10 to 20 segments, arranged about the central clump of pigment like a rosette. Each segment has a spot looking like a nucleus, and soon the mature bodies so formed break out of their host and attack new and previously healthy blood- cells. Sometimes the parasite becomes so large that it entirely de- stroys the corpuscle and floats free in the blood, in which case the pigment-granules quiet down and the mass becomes misshapen and apparently dead, breaking up into smaller masses, and gives rise to several smaller bodies, which, however, soon seem to lose life (Plate XI., Fig. 21), or it becomes filled with vacuoles (Plate XI., Figs. 23, 24), or, finally, we have springing from these extra- cellular bodies flagella or waving arms, extending from the margin of the parasite. (Plate XI., Fig. 33.) These flagella break off now and again and keep waving through the blood, looking like spirilla. The entire process just described seems to consume about forty-eight hours, and it is of interest to note that the acme of the paroxysm of the disease occurs with the segmentation of the full- grown parasite, so that the presence of segmenting bodies indicates the near approach of an attack. If, on the other hand, we have a double tertian infection — that is, an attack daily, or a quotidian form, we have two sets of parasites, each one of which reaches its period of segmentation on alternate days, and so a daily attack is caused. In such blood during a paroxysm will be found two sets of parasites : one set segmenting or causing the paroxysm, and the other set half-developed, which produce the attack of the morrow. The quartan parasite, or the one causing an attack every third day in its earlier stages of development, looks very much like that of the tertian form, for it occurs as small hyaline amoeboid bodies filling a fraction of the corpuscle. They soon, however, develop PLATE XII. The Parasite of Aestivo Autumnal fe\^er # :^'^ \ • • & r^ «• " ."^-.■".*v*";"2f. -;" - ^\ V %,/ ^aU' # THE BLOOD. 349 the following differences : first, they develop a sharper outline ; sec- ond, they are more refractive; third, the amoeboid movements are slower (Plate XI., Fig. 26) ; fourth, the pigment-granules are coarser and darker (Plate XI., Fig. 27), and, more important still, they lie very quietly around the edge of the parasite ; fifth, the corpuscle acting aH host does not increase in size, and finally disappear as it does when affected by the tertian type, but grows smaller and darker, more refractive and metallic-looking (Plate XI., Figs. 28 to 34). Reaching their complete development at about 64 to 72 hours, they appear as small, round bodies, taking up nearly all the space in the corpuscles in which they live, or they appear free in the blood- serum (Plate XL, Fig. 35). As the time for the paroxysm approaches the pigment-grauules which have been scattered begin Ao collect at the centre (Plate XI., Figs. 36 to 39) in a stellate form, and the pro- toplasm of the mass then divides by segmentation into from six to twelve small pear-like bodies, each of which has a refractive centre. These bodies become more and more separated from one another, and simultaneously we find new corpuscles infected by the orig- inal small round bodies which we first saw. Sometimes these parasites expand, become very transparent, and their pigment-granules become very active, but finally become quiet, and the body of the parasite grows more and more indistinct. They become dead parasites. (Plate XI., Fig. 40.) Again, the })arasite may undergo a breaking up into smaller bodies, which are badly formed and indistinct ; also a degenerative form and vacuoles may develr)p. (Plate XT., Fig. 42.) Finally, flagolla may develop, as in the tertian organism (Plate XI., Fig. 41), and they differ from the tertian form in being smaller, and their granules are coarser. In the third form of infection (jestivo-autunnial fever) we find at first the small hyaline bodies, but they have a ringed appear- ance, and are sometimes very small. (Plate XII., Figs. 3 to 6.) Suddenly this body becomes larger and the ring is lost, the edge becoming wavy, and amoeboid movemenis occur, the pseudopodia often joining to form a true ring. Pigment-gramiles finally develop after a variable length of time, hut they are few, rarely more than two in a parasite, near the edge (Plate XII., Figs. 7 to 12), and (piitc still. The corpuscles are not decolorized, but often are shrivelled and very brassy-looking. The peripheral circulation during the paroxysm of lestivo-au- 350 THE MANIFESTATION OF DISEASE IN ORGANS. tumnal fever contaius very few, if any, parasites, but blood drawn from the spleen may show intracorpuscular parasites, with blocks of pigment and some free parasites. As segmentation goes on, the parasite may look like the tertian form, but it is far smaller. (Plate XII., Figs. 21 to 28.) After this parasite has been present for some days we find in the blood larger parasites, of an egg-shape, or crescent shape, the remains of the blood-cell, looking like a small quarter of an apple glued to the side of the crescent. (Plate XII., Fig. 29.) Vacuolization and flagellation may develop in this form as in the others, and the use of quinine in the first week may prevent the development of the crescents. The following table separates each of these malarial forms from the others : Tertian Parasite. Develops in 48 hours. Pale and indistinct. Actively am(jeboid. Pigment fine. Pigment active in movement. Pigment light. Full size of the corpuscle. Degenerative forms twice as large as corpuscle. Segments 16 to 20 Irregular segments often. Corpuscle becomes colorless and swollen. Quartan Parasite. Develops in 72 hours. Sharply outlined and refrac- tive. Slightly amoeboid and later motionless. Pigment coarse. Pigment slow in movement. Pigment dark. Smaller than the corpuscle. Degenerative forms very much smaller than in ter- tian. Segments equal 6 to 12. Beautiful rosettes. Corpuscle becomes brassy- looking and shrunken. JEslivo-aulumnal. Develops in 24 to 48 hours. Have a winged appearance. Actively amoeboid. Pigment-granules are very few. Pigment-granules quite still. Very much smaller than a corpuscle. The process of segmentation goes on in the internal or- gans, so segmenting form is not found in the blood. Forms crescents. Corpuscle is shrivelled and very brassy, but not de- colorized. The blood is usually examined for the malarial parasite by what is called the direct or '' without staining" method. The cover- glasses which are to be employed are cleansed very carefully by washing in alcohol and ether. The lobe of the ear, after being care fully cleansed, is then stabbed with a needle or small tenotome, and the first few drops of blood wiped away. A perfectly clean cover- glass is now picked up by means of a pair of forceps and touched to the tip of the drop of blood and then placed blood-side down upon a clean glass slide. The blood is equally distributed between the glasses, and only the merest touch of the cover-glass should be made to the drop of blood, as otherwise too much blood will be taken up. THE BLOOD. 351 The microscope should be fitted with a yV oil-immersion lens and a No. 4 eye-piece. When it is desired to keep the specimen and to stain it, the best stain is that of methyleue-blue and cosine, which is prepared as fol- lows : A concentrated watery solution of raethylene-blue is diluted one-half with water and mixed with an equal volume of a | per cent, solution of cosine, in 60 per cent, of alcohol. The blood is then obtained in the manner described above, but, instead of puttiug the cover-glass on a slide, two cover-glasses are placed face to face, aud then after the blood is evenly distributed on each the preparation is fixed by immersing it for half an hour in abso- lute alcohol and allowing it to dry. This fixed cover-glass may now be dipped into the stain giveu for from half to one minutCj-'and having been washed free from an excess of stain is ready for examination. We can use another method, in which we stain by placing the dried cover-glass in Chcnzynski's solution and gently heating it for fifteen minutes. This solution is made as follows : Methylene- blue in saturated watery solution, 40 c.c; cosine in ^ per cent, solution in 60 per cent, alcohol, 40 c.c; distilled water, 40 c.c. The hnematozoa are stained blue, the red cells and leucocytes light blue, their nuclei a deep blue, and the eosinophile granules of the cells deep red. We have already stated that the paroxysm of the malarial disease takes place at the time when the parasite is breaking up into seg- ments. In other words, the attacks occur whenever the cycle of growth of a set of parasites is completed, whic^h in tertian fever is every forty-eight hours, and in quartan fever every seventy-two hours. If there be two sets of parasites in the l)lood, however, of the tertian type, the attacks may be daily, or (piotidian, since each set mature on alternate days. This is often called double tertian. This is the most common form of the disease in the United States. If there be a double cjuartan infection, the attacks come on two successive days, then a day of intermission ensues. If three sets of parasites of this type are present, the attacks may be daily for three days, triple quartan infection. (See ciiapter on Fever.) The pnrasite of a'stivo-autmnnal fever is irregular in its develoj)- ment, and is often the cause of the irregular malarial fever seen in the fall of the year. It yields less readily to quinine than the others. Fir.AUiA. The (ilaria sanguinis hominis a|)p('ars in the blood in three forms and has been well described by F. \*. Henry, of Philadel- 352 THE MANIFESTATION OF DISEASE IN ORGANS. phia, ina rocent paper. These three forms are : 1. Filaria diwna ; 2. Filaria noctunia ; 3. Filaria perstans. These names are indicative of the habits of the aiiiranl, the filaria diurna being found in the super- FlG. 153. m ■ '; €■-'" ffi'Ate* L^SHUm Filaria alive i;i the blood. Instantaneous pbotomicrograph. Four hundred diameters magnification. Four millimetres Zeiss apochromatic. (Henry's case.) ficial vessels solely or chiefly daring the day ; the filaria nodurna solely or chiefly daring the night ; while the filaria perstans is con- FlG. 154. Filaria in the blood. Eight hundred diameters. (Henry's case.) stantly present in the capillaries of the integument. The filaria diurna and the filaria perstans are confined, thus far, to the west THE BLOOD. 353 coast of Africa and adjoining districts ; while the Jilaria nocturna is pandemic in the tropics and endemic in certain sections of the United States. The adults of jilaria nocturna have been frequently found ; that of jilaria perstans never, so far as Henry has been able to ascer- tain. In the opinion of ISIanson, the jilaria loa of the eye of the negro of Old Calabar is probably the adult form of the jilaria diurna. If it is not, he argues, then there must be another blood- worm yet to be discovered, for the embryos of the loa must escape from the body of their host through the medium of the circulation. The Maria perstans has been practically proved by Manson to be tlie cause of the fatal " sleeping-sickness" of the Congo region. The second is the one ordinarily seen in blood obtained from the peripheral circulation during sleep or at night. (Figs. 153" and 154.) The male filaria measures 83 millimetres long by 0.407 millimetre broad, and the tail is twisted into a spiral form. The female mea- sures 155 millimetres long by 0.715 millimetre wide, and the vulva is 2.56 micromillimetres from the anterior extremity. The em- bryo measures 270 to 340 micromillimetres long by 7 to 11 micro- millimetres wide, and has a pointed tail. This embryo is in an ahiKiSt imperceptible shell which does not impede its movements, and as it is about the size of a red blood-corpuscle it passes through the capillaries in extraordinary numbers. Its active move- ments and typical apjjearance render it readily seen in the blood. Tiie discovery of this parasite in the blood renders a diagnosis certain, and it should always be sought for if chyluria or elephan- tiasis is j)resent. If the patient remains awake at night and sleeps during the daytime, the organism will be found in the blood during the sleeping-period. The filaria diurna is found in the blood during waking-hours, and the embryos of the filaria perstans are the only form of this parasite known. 23 CHAPTER XII. THE URINARY BLADDER AND THE URINE. Disorders and diseases of the urinary bladder — Retention of urine — Incontinence of urine — The characteristics of normal and abnormal urine— The normal and abnormal contents of the urine — Their significance — Tests for the contents of the urine. The urinary secretion is one which is too frequently ignored by the student and physician in studying the diagnosis of disease. In many instances it will, if properly tested, give such positive evi- dence in regard to obscure affections that a correct diagnosis is at once possible, and in other cases its examination, as a matter of routine, will discover important facts the existence of which has been unsuspected. Again and again will a diagnosis prove erroneous if the importance of urinary examinations is ignored, and costly errors for the patient and the reputation of the physician ensue. In asking questions about the character of the urine passed and its quantity, the physician should be sure that the patient clearly understands his questions. Often we will be told that much urine is passed, when, in reality, it is only in small amount, but passed often ; or that it is blood-red, when simply red from urates and uric acid. In inquiring about its color, wo should remember that if large amounts of liquid have been swallowed it will probably be light in hue, or, if small amounts of drink taken, dark in hue. Anomalies connected with the urine may be divided into those which involve the organs which secrete, retain, and expel the fluid, and those which are manifested in the urine itself by alterations in its quantity, odor, specific gravity, and in its naked-eye appearance, its microscopical appearance, and, finally, by those changes which are discovered by means of tests which possess no influence of note on the urine of the healthy. The objective symptoms of many cases of disease of the kidneys have already been discussed. (See chapter on the Skin, such as oedema and color of the skin, and chapter on Face, expression.) Aside from these evidences of renal disease no alteration can usually be noted unless it be loss of weight. The subjective symptoms of THE URiyARY BLADDER AXB THE URIXE. 355 the patient commonly consist in loss of ambition, malaise, disturbed digestion, and shortness of breath. Rarely is there pain in the lumbar region, unless pyelitis, stone in the kidney or ureter, or peri- nephritic troubles are present, when pain becomes an important sign. Fig. 155. 1st to 7th cen'ical segment. - 1st to 12th dorsal segment. 1st to 5th lumbar segment. 1st to 5th sacral segment. Diagram showing the surfacr n. ,i i,, i.ick corresponding approximately to the areas of the spinal cord supplying the trunk and limbs. The Bladder. The objective symptoms of bladder-difficulties- are generally local, unless they are very chronic, when the face may appear worn and weary, and, if a purulent cystitis be present, septic fever may occur. The subjective .symptoms arc tenderness, tenesmus^ and pain (see chapter on Pain and ciiapter on Abdomen), and reten- tion or incontinence of urine. Retention of urine, .so far as the bladder itself is concerned, is rare, the cause of the retention generally being outside this viscus. It may, however, arise from disease or injury which destroys or temporarily impairs the function of the cells in the spinal cord which govern the contraction of the inusclcs involved ii> expelling urine from the bhidder. These centres are situated at or about the level at which are given olT the .second, third, and fonrth sacral nerves. (Fig. 155.) 356 THE MANIFESTATION OF DISEASE IN ORGANS. Paralysis of the bladder with retention may, therefore, follow severe injuries to the spinal cord produced by falls, blows, or other traumatisms, or be due to a myelitis which destroys such centres. (See chapter on Legs and Feet, part on Paraplegia.) Again, reten- tion of urine may arise from paralysis of the muscular part of the vesical walls by pressure produced in severe labor (childbirth). Retention sometimes comes on in locomotor ataxia, in which disease the impulses from the bladder are not recognized, or are perverted so that the sphincter which closes the bladder does not relax to permit the escape of urine, or the cord or brain fails to rec- ognize that the bladder is full, and so sends no impulse for its relief. Finally, we see cases in which the bladder cannot be emptied, because the walls of the bladder have been paralyzed by overdistentiem with urine. On the other hand, incontinence results from loss of power in the sphincter, due to injury or disease in the cord at the level of the second, third, and fourth sacral nerves ; and this, by the way, is a far more frequent occurrence than is absolute retention. The real condition under these circumstances is that the expel ling-muscles and retention-muscles are both paralyzed, so that the urine accumu- lates in the bladder and then dribbles through the unguarded neck into the urethra. Sometimes, too, this incontinence is caused by the urethra being so insensitive that it fails to recognize the presence of tlie urine, and so does not send an impulse to the sphincter to tighten its hold. Incontinence also results from excessive reflex irritability of the walls of the bladder, so that the urine no sooner trickles into this viscus than an impulse is sent to the spinal centres which send a motor impulse to the muscles of expulsion. This is often the condi- tion in the nocturnal incontinence of children, for as soon as the child sleeps its will-power over the bladder ceases, and reflex activity is alone in control. Irritating, concentrated urine may pervert the reflexes of the bladder and so cause incontinence. The bladder-symptoms seen in myelitis — transverse, traumatic, or otherwise — usually come on in the acute form within a few hours after the sensory and motor disturbances have been noticed by the patient, and either incontinence or retention, or both, may occur. If, however, the myelitis is not complete the bladder may escape. On the other hand, if the portion of the cord which is involved hap- pens to be that part governing the bladder, vesical symptoms may develop before the motor symptoms are clearly marked. Again, THE URINARY BLADDER AND THE URINE. 357 it is a noteworthy fact that when recovery takes place vesical con- trol may be regained before any marked improvement can be found elsewhere. Often the loss of coutrol over the bladder is such that the patient cannot voluntarily expel the urine and cannot retain it, and it dribbles away without his knowledge. Under such cir- cumstances there is probably a myelitis involving the lower part of the dorsal cord and the upper and lower part of the lumbar cord ; in other words, all that portion in which the vesical centres are situ- ated. If the dribbling of urine takes place wiihout distention of the bladder, the fluid passing directly from the ureters through the urethra, the lower part of the lumbar enlargement of the cord is affected, owing to the paralysis of the sphincter. On the other hand, distention of the bladder, due to retention of iifine, occurs when the myelitis is in the lower dorsal and upper lumbar cord, and is due to paralysis of the detrusor muscles, which make no effort to expel the urine, while the sphincter, the centres of which are intact, maintains a tightly closed orifice. Such cases may empty the blad- der spasmodically at long intervals (overflow-incontinence) — that is, sphincter-paralysis from distention may ensue. In such a condi- tion the bladder should be emptied by the catheter to avoid paralysis and vesical disease. To put the case in another way, we can say that the spinal centre for the control of the walls of the bladder is situ- ated at a higher point in the cord than is that for control of the sphincter, and, therefore, retention of urine indicates a lesion higher up in the coi-d than does incontinence without retention. Precisely similar vesical symptoms occur in cases of spinal tumor producing transverse lesions of the cord (see chapter on Feet and Legs, para- plegia), or may arise from spinal apoplexy. The bladder-symptoms of locomotor ataxia are often quite char- acteristic:, and are to be sejiaratcd from those of myelitis, spinal tu- mor, and the vesical troubles due to traumatisms of the cord. The disorder depends entirely upon interference with the reflexes of the viscns, and so presents varying symptoms which are motor and sensory. The patient sometimes complains of the fact that he has to strain for a long time before he can start a stream which, even after it is started, is often jerking or interrupted ; or, again, he must sit down and bend over in order to have the aid of his abdominal nuiscles before he can evacuate the bladder. As a result of this, residual urine in excess is always present, and cystitis or milder degrees of vesical irrital)ility develop. In other instances, the 358 THE MANIFESTATION OF DISEASE IN ORGANS. desire to urinate comes upon the patient so suddenly and forcibly that the urine is voided before he can, with iiis impaired gait, reach a place where he can pass it in a proper manner ; or, on the other hand, it may be retained and can only be removed by a catheter. Still others find that urine escapes on langhino;, coughing, or sneez- ing, owing to lack of complete control of the bladder and its sphincter ; or, again, after many attempts to urinate, the patient gives up the effort, only to be humiliated by an involuntary passage of urine immediately upon his penis being withdrawn into his clothes. These symptoms differ so materially from myelitis as to make a diagnosis as to their cause nearly always possible. In obscure cases of ataxia the vesical symptoms may aid the diag- nosis quite markedly ; thus the presence of bladder-symptoms would confirm a diagnosis of ataxia as against pseudo-tabes, due to peripheral neuritis. Again, in myelitis the presence of vesical symp- toms points to that disease, and excludes from the diagnosis such affec- tions as poliomyelitis and lateral sclerosis, affections in which vesical paralysis rarely, if ever, occurs. Precisely similar vesical symptoms are sometimes seen in cases of general paralysis of the insane, but the delusions of grandeur or melancholia and other characteristic signs of this disease separate it at once from ataxia. The sensory disturbance of the bladder will be found discussed in the chapter on Pain, but it is worth noting here that accompanying the symptoms already named as characteristic of locomotor ataxia vesical crises of spasm and pain frequently occur. When there is pain in the bladder, made worse by the attempted act of micturition, and tenesmus, with darting pain into the urethra, there is probably present a cystitis; but the physician should remem- ber that cystitis may be present with almost no painful manifesta- tions, even when in its acute form. In other cases this condition arises from concentration of urine, which produces irritation of the viscus, such as is seen in cases of acute nephritis or renal congestion. In children this concentration of the urine is the most common cause of nocturnal urinary incontinence. Involuntary passage of the urine sometimes occurs in idiots, in some cases of insanity, in attacks of apoplexy or any condition of abnormal unconsciousness, and sometimes in very severe infectious diseases, such, for example, as diphtheria. Oftentimes it results in children from irritation of the foreskin or vag-iua, or from rectal THE URIXARY BLADDER AND THE URIXE. 359 irritation produced by seat-worms, since all these causes disturb the reflex activity of the spinal centres. Interference with the passage of urine may also arise from two causes, which are surgical in character, namely, stoue in the bladder and tumors of the bladder, which are often situated near its neck, and so produce obstruction. Finally, that most commonly met with cause of difficult micturition, enlargement of the prostate, is to be remembered. Aside from these causes of interference with the passage of urine, we must not forget the possibility of its obstruction by stricture of the urethra, nor should the physician ignore the fact that some per- sons have " nervous bladders," which will not respond to an effort of the will if any person is near by, although the urine^is instantly passed as soon as the patient is alone. The Condition of the Urine itself is determined, first, by its general appearance, quantity, odor, specific gravity; second, by its microscopical appearance ; and, third, by its chemical reactions and response to tests. Any changes in this fluid of an abnormal char- acter are solely symptomatic, and point with more or less distinct- ness to disorders of bodily metabolism, disease or disorder of the kidneys, ureters, bladder, or urethra, and sometimes of the prostate, testicles, vagina, or uterus. The urine which is to be tested should always be passed directly into the vessel in which it is brought to the physician, and this bottle should be scrupulously clean ; or, if the urine is passed into any other vessel, care must be taken that it is perfectly clean. When it is thought that urethral disease may obscure the investiga- tion, a catheter should be passed, all urine in the bladder drawn off, and then the catheter allowed to remain in place, so that the urine will trickle directly from the ureters to the catheter, and so to a receiving vessel. This is very important when the urine is voided involuntarily. If the condition of the bladder is bad, this viscus should be washed out l)y boric-acid injections, in order to prevent it from contaminating the urine which is to be tested. The quantity of urine passed by a healthy adult varies from two to four pints in the twenty-four hours, according to the amount of liquid ingested, the freedom of perspiration, and the amount of exerci.-^e. The significance of any great and constant increase in the amount of urin(> passe«l in a given case is multiple. Thus, we find it greatly increased in any disease of the tliabetic centre, or of the liver, or 360 THE MANIFESTATION OF DISEASE IN ORGANS. pancreas, which results in diabetes mellitus ; in diabetes insipidus, in some cases of neurasthenia, and in some cases of hysteria. It is also increased in many cerebral lesions. Hypertrophy of the heart, par- ticularly if associated vnili chronic contracted kidney, causes an increase in the urine ; and, therefore, if a patient has to urinate fre- quently or has to arise at night to empty the bladder, we suspect this trouble if diabetes is excluded. The same result ensues if the heart ana kidney are stimulated to increased effort by the action of drugs, such as digitalis, caft'ein, or alcohol. We also find an increase in urinary secretion, without its possessing any grave significance, in convalescence from such diseases as typhoid fever and pneumonia. The quantity of the urine is diminished in cases in which the heart fails to doits ])roper amount of work, with resulting stasis of the blood in the kidney, and whenever any large amount of liquid is taken away from the body, as in diarrhoea. It is also decreased by fevers and by the sweats following febrile movement. Persistent vomiting also has a similar effect. Parenchymatous nephritis, both acute and chronic, greatly diminishes the urine, and in grave, fatal illnesses urinary suppression also takes place. The odor of freshly passed urine is faint, but characteristic. What is often called a " urine odor" is really due to the develop- ment of ammonia in urine which has decomposed. The odor is altered by many drugs and foods, notably by copaiba, turpentine, eucalyptus, valerian, musk, asafoetida, and by asparagus, and diabetic urine possesses a heavy, sweet odor. The specific gravity of the urine varies from 1005 to 1040 at 60° Fahr. ; but a persistently low specific gravity indicates chronic contracted kidney if no dietetic cause can be found, while a persis- tently high specific gravity either shows concentration of the urine as the result of fever, or, if the urine is light in color, the cause is probably diabetes mellitus, the high specific gravity being due to the sugar which it contains. The naked-eye appearance of the urine often gives very impor- tant information, if its clearness, opacity, and color are studied. Its clearness and color are modified by the presence of blood or other pigments derived from outside sources, such as the educts of carbolic acid or salicylic acid, of senna or hsemataxylon, and bile, urobilin, and many other substances coming from inside sources. Many of these causes may render it opaque, but there is one condition, above all others, which renders the urine cloudy even when freshly THE URINARY BLADDER AXD THE URINE. 361 passed, namely, cystitis with phosphaturia. After urine has stood for some hours and undergone chemical changes, it often becomes opaque. When urine is dark red in color and somewhat opaque this dis- coloration may be due to blood, htemoglobin, santonin, rhubarb, senna, logwood, and the presence of an excess of urates. Again, it may be rendered almost black, instead of red, by an excess of biliary coloring-matter, and a black urine is often seen in cases of melanotic cancer, the color being due to melanin. If the color be due to blood or hcematitria, the urine will be of a more or less bright red, according to the freshness of the sample brought to the physician and the seat of the hemorrhage. If the urine has been voided several hours, it will be of a dingy red or smoky iiue, and on standing will cause a coffee-ground "br reddish sediment of a somewhat flocculent appearauce. If, on the other hand, the urine is seen as soon as passed, it may be a bright red or a dingy red, according to the seat of the hemorrhage and the time which has elapsed since the bleeding began ; if it has arisen in the kidney or ureter or bladder, and has been gradual, the mixture of blood and urine will have been so intimate that chano;es in the blood will have taken place, whereas if the hemorrhage has occurred, simultaneously with urination, from the neck of the bladder or the urethra, the blood will be almost unchanged when it escapes from the urethra. The presence of clots in recently ])as»ed urine indicates a not very recent hemorrhage, and yet one of such size that the urine could not l)y dilution completely prevent clotting. Blood from the kidney usually possesses the following character- istics : It is well mixed with the urine, and is generally altered in appearance to the naked eye and under the microscope, both as to color and the shape of the corpuscles. The cells and casts which may be present are changed in color by the hjumoglobin which is free in the urine. Again, blood-casts or red blood-corpuscles clinging to casts indicate renal hemorrhage. When the blood comes from the kidney pelvis it may appear in the urine iu long, worm-like clots (moulds of the ureter), and their extrusion from the ureter produces symptoms of colic. Under such circumstances ther(> may be alter- nations of hiomaturia and normal urine, due to the blocking of the ureter on the diseased .side by a clot, so that all the urine comes from the healthy kidney. A sudden profuse hemorrhage in the urine, sullleiently large to endanger liCi', may come from cystic tumor of the kidney. 362 THE MANIFESTATION OF DISEASE IN ORGANS. When the blood comes from the bladder it is generally due to some capillary growth or to injury. Rarely in certain cases of locomotor ataxia, haematuria develops after the vesical crises which we have already described (see Bladder in this chapter). The origin is capillary hemorrhage from the bladder-walls. When the blood comes in the first part of the urine passed and not in the last part, it almost certainly comes from the urethra. The urine, when not discolored by blood, may be discolored by the pres- ence of the coloring-matter of the blood. This is called haemo- globin uria. Microscopical examination of the urine in such cases will show no corpuscles, although the urine will be coagulated by the acid test ; but this coagulation does not settle in flakes as it usually does in albuminous urine, but floats on the surface in a brownish mass. The naked-eye appearance of the nrine is that of clear port wine. If a few drops of urine be placed on a watch-glass, and a drop of strong acetic acid be added, the blood-crystals of Teich- mann will be found, showing that the coloring-matter is hsemoglobin. If the discoloration of the urine be due to blood, a microscopical examination will reveal red blood-corpuscles, white blood-corpuscles, and perhaps fine filaments of clots ; but the corpuscles will not be found in rouleaux, as in ordinary blood outside the body, and they may be crenated and distorted in shape, particularly if the urine is alkaline. The test which can be most easily applied to determine the pres- ence of blood, if the microscope cannot be used, is Heller's test, which consists in adding to a few c.c. of urine a little caustic soda, so as to render the liquid strongly alkaline. The urine is now heated to boiling, and if blood is present a bottle-green color is produced, and the phosphates fall to the bottom of the test-tube in fine flakes, tinged brownish-red by the coloring-matter of the blood. The significance of haematuria is various, since any solution of continuity in the bloodvessels of the genito-urinary tract may pro- duce it. When the blood comes from the kidney some of the pos- sible causes are acute parenchymatous nephritis, resulting from any one of the severe infectious diseases, such as scarlet fever or malarial fever; from embolism, resulting from ulcerative or other forms of endocarditis; renal infarction, from sepsis of the kidney; from the ingestion of irritating drugs, such as cantharides or turpentine; and from strains or blows of the back, producing rupture or other dis- organization of the kidney. All these conditions produce what may THE URIXARY BLADDER AXD THE URIXE. 363 be called acute hsematuria. If the cause l)e acute nepliritis from the presence of an infectious malady, such as scarlet fever, the pain in the loins, the presence of albumin in the urine, and the eruption will render the diagnosis easy. Hsematuria due to malarial poisoning may appear with the first malarial paroxysm, of the intermittent type, which the patient has ever had, and at a time when the history of the case renders it cer- tain that a hidden malarial condition could not have previously damaged the renal tissues or those of other organs in the body. In other words, there are cases in which a free hemorrhage from the kidney takes place, by reason of the chill, in much the same manner in which hemorrhage takes place in an acute nephritis due to expos- ure to cold or to irritants. Under these circumstances there may or may not be developed a true organic lesion of the kidney in the sense of permanent disease. Secondly, we have cases in which bloody urine appears, not in the first malarial paroxysm of the intermittent type, but in association with the later attacks, which may have followed the first either rapidly or slowly. In these ^ases there may be no further cause for the hemorrhage than excessive congestion, but in all probability the vast majority of such patients present distinct renal changes, which permit such a symptom to develop when the paroxysm asserts itself. Thirdly, we j)ass from those cases of bloody urine due to inter- mittent forms to those due to remittent attacks, which, in many cases, have gradually merged from the first into the remittent. In these patients the process by which a bloody-colored urine is de- veloped may be very complicated, since it may be due to renal incontinence, functional or organic, or to a true Imemoglobinuria, arising from dissolution of the rod blood-cells in the bloodvessels or blood-making organs. Finally, there is a type of malarial lijeraaturia which is only pro- duced by the administration of quinine (Karamitsas el al). All these forms of Inematuria can be diagnosed by the presence of the malarial germ in the blood (see Blood) and the characteristic malarial symptoms, cxce|)t that which occurs in jjorsons who have a dyscrasia from old malarial poisoning. If the hematuria be due to embolic infarction of the kidney, an examination of the heart will j)rol)al)ly reveal signs of valvular disease, from which source the embolism will have resulted, or, in 364 THE MANIFESTATION OF DISEASE IN ORGANS. other cases, the physical signs, combined with the history, will show malignant eudocarditis with renal sepsis therefrom. If such disease is not present, the history of the ingestion of an irritating drug will be the diagnostic guide, or, if injuries be the cause, a history of traumatism is all that is needed to elucidate the case. The cau3es of chronic or persistent hemorrhage from the kidney are chronic hemorrhagic nephritis, cancer of the kidney, calculus in the pelvis of the kidney producing ulceration, injury of the kidney by jarring of a stone, tuberculosis of the kidneys, and cystic degeneration. If the chronic hsematuria arise from chronic hemorrhagic nephritis, the diagnosis is made by the pallor of the skin, anorexia, nausea, headache, oedema, decreased amount of urine, and albuminuria. If the cause be renal cancer, the cachexia, pain, and the mixture of pus, blood, and disorganized renal tissue in the urine will render the diagnosis possible. If due to calculus, there may be a previous his- tory of attacks of renal colic or of violent pain in the kidney ; and if ulceration of the renal pelvis has occurred, there will be disturb- ances of tlie body-temperature, pain in the lumbar area, and pus in the urine. The presence of tubercle bacilli in the urine decides the presence of renal tuberculosis. If cystic degeneration is present, it can only be determined if the cyst is large enough to be felt. Fig. 156. Distoma hEematobiurn male and female. The two small bodies (10 diameters) are the eggs (150 diameters). There are other forms of hsematuria which must not be forgotten, although comparatively rare, namely, tliat due to the presence in the blood of the filaria .sanguinis horaini.s, which is a condition in which the presence of chylous urine so overshadows that of blood that the appearance is that of pinkish cream or milk, and microscopi- cal examination will show blood-corpuscles and fat-globules, as well as the embyros of the filaria. (See Chyluria in this chapter.) The second still more rare cause of hfematuria is the distoma haema- tobium of Egypt and Abyssinia. (F'g- 156.) The.se produce what has been called tropical haematuria. The third cause is even THE URiyARY BLADDER AXD THE URIXE. 365 more rare in man, namely, the strougylus gigas, which also causes pyelitis and renal colic. A fourth form of haeraaturia is that seen in some cases of scurvy, and, lastly, hfematuria may also appear as a symptom of purpura hemorrhagica, hemophilia, and very rarely in leukgemia. Hcernof/lohinuria arises from a number of cases, such as in- fectious disease, poisoning by mushrooms and certain coal-tar deriva- tives, chlorate of potassium, and glycerin. ISIalarial poisoning some- times causes it instead of hematuria. One form of malarial hsemo- globinuria is intermittent, the urine being at one hour limpid, the next hour bloody, and the third hour clear again. The possibility of confusing the htemoglobinuria of idiosyncrasy about to be described, when in a severe form, with trnc^and severe malarial poisoning is very great. The entire history of paroxysmal hsemoglobinuria teems with reports of cases in which the chief mani- festations of a malarial attack were present, such as chills, fever, and sweats. Lichtheim and Ponfick have shown that the injection of lamb's blood into the vessels of man results in violent shivering, fever, sweats, and pain in the lumbar region over the kidneys. This condition also follows severe burns and the transfusion of blood, and occurs in paroxysmal haimoglobinuria, a condition which seems to be produced by mere chilling of the surface of the body or to immersing the hands of a susceptible ])erson in iced water. It may also be produced either by exposure to cold and damp, which are generally present in malarial localities, or to the chill of the milder forms of malarial paroxysm. If the urine be red from other caues than blood, it may be due to the ingestion of logwood. The history of the ingestion of this sub- stance will clear up the diagnosis. If it be due to senna, it will be carmine, due to the chrysophan in this drug ; but this only appears if the urine is alkaline. Precisely similar changes are due to the taking of rhubarb. So in santonin-poisoning a blood-red urine is sometimes seen, but it usually attains this aj)pearance after being at first yellow, then saffron, and then i)urple-red. One of the con- ditions of the urine, due to a j)oison which can be readily confused with h:em()glol)inuria or ha'inaturia, is that produced by carbolic acid. This color is not due to l)looil, but to oxidized ediicts of the acid. The same educts produce a simihir discoloration after naph- thalin, creosote, and uva ursi have been taken in overdosi". I'iually, the urine is often dark rcdtlish-brown or porter-colored 366 THE MANIFESTATION OF DISEASE IN ORGANS. in jaimdice, owing to the presence in it of biliary coloring-matters. Under these circumstances it may be clear or opaque, and the fluid is apt to be frothy on shaking and to have au increased surface-tension, so that powdered sulphur does not sink to the bottom of the vessel when the sulphur is dropped on the urine. These biliary colors are at once recognized by the reaction with nitric acid in Gmelin's test, for, if a little of the urine be placed on a white plate and nitric acid be allowed to touch the margin of the wet place, the play of colors from green to blue, blue to violet, and violet to red occurs. The green color is the only one characteristic of the biliary reaction, for indican will give with nitric acid the other colors. The same test can be used by wetting bibulous paper with urine, and the acid, if brought to the edge, will stain the paper in the colors named. (For the symptoms of jaundice, see the chapter on the Skin.) A greenish-colored urine is seen in cases of poisoning by salicylic acid, due to the indican and pyrocatechin ; and from the use of saffron. The urine is yellow in santonin-poisoning, and when rhu- barb has been taken, if it is alkaline. When through diseased processes indican is formed and excreted in the urine, it may be by oxidation transformed into a blue color (iudigolin),or into a red hue (iudirubin). If chromogen is present in large amount, shaking the urine with air will develop a violet-blue color, or this change may take place in the bladder. If urine cou- tainino^ indican be treated with two or three times its volume of hydrochloric acid, it will turn a violet hue. Indicanuria is present in intestinal obstruction, general peritonitis, cholera, cancer of the liver or stomach, and pernicious anaemia. It may, however, be present in health as a result of constipation. Blue urine is also caused l)y the ingestion of methyl-violet as a drug. A black urine is sometimes seen in a case of melanotic cancer, or after the brownish urine produced by carl)olic acid or uva ursi has been exposed to the air. Red urine, due to none of the causes which have been enumerated, may be due to an excess of urates (except urate of sodium, which is usually white). If the urine becomes brown on the addition of nitric acid when the fluids join, it is due to urates ; but if all the fluid is brown, the patient has probably been taking iodine or iodine com- pounds freely. White or milkv-lookin^ nrine is seen in that condition called THE URIXARY BLADDER AXD THE URINE. 367 chyluria, clue to the presence of filaria sanguinis hominis in the blood. Tliis urine on standing forms a creamy layer on its surface, and, if it is shaken with ether, some of the fat can be removed, ren- dering the urine clear. The diagnosis can only be confused by urine becoming mixed with milk or cream, and can always be made if the embryos of the filaria can be found in the urine. They lie in very delicate sheaths, and show a constant vibratory movement. The diagnosis is still further confirmed if they are found in the blood, where they are present in large numbers at night. (See chapter on the Blood.) Urine may have a somewhat milky-white appearance from an excess of phosphates, mixed more or less with mucus, as in catarrh of the bladder. • When the urine is passed in large quantities, and is of a very pale straw-color or has a slightly greenish tinge, it will often con- tain sugar ; or, in other words, be the urine of diabetes mellitus, or of glycosuria from other causes. The fact, that it remains markedly acid for a long time after it is passed, and that it has a high specific gravity, point still more to its being diabetic, and the diagnosis is confirmed if the characteristic reaction with Haines's, Whitney's, or Fehling's solution is obtained. (See Tests in this chapter.) Microscopic Appearances of the Urine and its Contents, Having considered the macroscopical appearance of the urine, we may turn to its microscopical appearance, and this part of the subject is of even greater importance than the study of the gross appearance of this secretion, for, very commonly, a sample of urine which looks quite normal to the naked eye is loaded with microscopic objects of the greatest pathological significance. The most important of these objects are what are called " casts" — that is, moulds of the uriniferous tubules, formed as a result of the disease-process present in the kidney. These casts consist of epithelial cells, blood- and pus-corpuscles, masses of micro-organisms, or of broken-down organic matter, as in fatty casts, and in hyaline or transparent bodies, or moulds which are made up of unknown material, but often covered by corpuscles, pus-corpuscles, or epithelial cells. In addition to these bodies we find a large numl)er of organic bodies or derivatives of organic mat- ter, and inorganic substances derived from the tissues or from food. The reader who desires to examine urine successfully i)y the aid of the microscope must bear in mind that it can only i)e examined 368 THE MANIFESTATION OF DISEASE IN ORGANS. satisfactorily after it has stood still in a glass or other vessel for a loug enough time to allow sedimentation to take place — that is, until the objects floating in the fluid have had time to settle. iflG. 157. Holder for urine-tube. By far the best method of obtaining the sediment, however, is by the use of the centrifuge, an apparatus by means of which the solids in a fluid are separated by centrifugal force. In this apparatus a Fig. l.nS. Casts containing epithelial cells. (Peyer.) sediment can be obtained in a few minutes after urine is passed. (Fig. 157 and chapter on Blood.) This sediment is to be drawn up into a pipette which has been introduced into the urine and a few drops placed upon a glass-slide, THE URIXARY BLADDER AXD THE URIXE. 369 after which the drops are to be covered by a cover-glass and the slide placed under the microscope. Casts composed of epithelial cells present an appearance similar to that seen in Fig. 159, and are due to proliferation or exfoliation of the epithelium lining the uriniferous tubules. The cells look swollen and granular and may contain globules of fat. These epi- thelial casts occur in three forms : first, they may appear as hollow casts of the tubule when the epithelium has exfoliated en masse (that is, the lining of the tube is cast off in one piece) ; second, they appear as casts made up of epithelial cells glued to one another ; and, tliird, the cells are attached to the surface of a clear transparent basis, looking like a hyaline cast. All these varieties are highly refractive of light and are not altered by chemical substances as easily as are the other casts about to be described. Having found bodies of this sort in the urinary sediment, what is their significance ? They are a positive sign of an inflammatory process in the parenchyma of the kidney, or, in other Avords, of parenchymatous nephritis. Blood-casts consist of more or less well-preserved blood-cor])uscles, attached to one another in a mould of the tube in which they have escaped. They are rarely seen and are masked by freely floating cells. The significance of these blood-casts is great, as they indicate an acute inflammation of the kidney, acute congestion of this organ, or a renal infarction. They are of importance, too, in separating hajmaturia arising from other sources than the kidney from hemor- rhage of tiiis organ, because they are not found unless the escape of blood has been in the uriniferous tubules. Casts composed of pus-corpuscles are still more rarely seen, but, if constantly present, may indicate multiple abscess of the kidneys. When masses of micrococci become grouped together in the tubules they nuiy be expelled in casts, and under a low power look some- what like granular casts (see below). They can be seen to consist of micrococci if a high power is used, and they are not quickly changed by acids, as are casts composed of other materials. Tiie .significance of their discovery is that septic infection of the kidney is i)resent, as the result, it may be, of septic embolus brouglit from a distant infected part. They are seen in SMpi)urativc renal inflammation and in cases of pyelunephritis in which the true renal tissues are being involved by an extension of the disease. Casts, composed of broken-down oi-ganic matter, are found as 370 THE MANIFESTATION OF DISEASE IN ORGANS. granular and fatty bodies ; that is, they represent broken-down blood-corpuscles and epithelial cells, and their appearance varies greatly according to the stage of the process and the origin of the materials composing them. Thus, the granular appearance may be very fine, as shown in Fig. 159, or light and refractive, dark or opaque. Very often the edges of these casts are irregular and the ends frayed aud uneven. The color of these bodies may be yellow^ brown, or grayish. Fig. 159. a a. Epithelial casts, b b. Opaque granular casts, from a case of acute Bright's disease. (Roberts.) The significance of granular casts is not as positive as those named so far, but they often indicate a slow degenerative process in the renal parenchyma. Fatty casts, composed of minute globules of oil, cohering to one another or attached to a central core of epithelium or fat-crystals, are found in cases of widespread fatty degeneration, as the result of disease or poisoning, as in the case of large white kidney on the one hand, or phosphorus, arsenical, antimonial, or iodoform-poisoning on the other. They show the presence of a very slow process if due to disease, but have not the same significance if caused by poison. (Plate XIII., Fig. 1.) Hyaline casts are lung, worm-like, tran.sparent bodies, with very fine granulation, particularly along the edges, and because they are transparent they are often hard to find. These bodies are supposed to PLATE Xni FIG. 1. Casts, Fatty, Waxy, Hyaline ami Cranular. Crystals of Uric Acid. FIG. 3. Ammonium Urate Crystals. Epithelial Cells. A, squamous epithelium ; B, bladder epithel- ium ; C, kidney epithelium ; D, kidney epithelium I fatty). THE URINARY BLADDER AND THE URISE. 371 be composed of albumin which has been exuded into the tubules. Their significance is exceedingly grave, as they point very strongly to that incurable malady, chronic interstitial nephritis. If the casts are very large, they may show amyloid degeneration of the kidney. They have often been wrongly called " waxy " casts. (Plate XIII., Fig. 1.) Casts are not to be coufused with cylindroids or streamers. These cylindroids appear in several forms. Most commonly they look like threads or filaments which are transparent and often some- what striated or hyaliue in appearance. They are often long enough Albuminous urine, a, 6, and c. Ribbon-like forms, d. Cast-like form, with cells upon surface. e. Filamentous forms in a clump. to extend completely across the microscopic field, and if followed out to the end will l)e found to taj)er off or gradually become more and more transparent until they cannot be outlined. For this reason too much light should not Ix' used in searching for them, nor should too high a power lens be used. These cylindroids often are grouped In bunches. In other instances we find cylindroids in the form of ribbons, or, in other words, they are wider than the thread-like masses just described. In still otiier instances the resemblances to true tube- casts are so marked that a differentiation is scarcely i)ossible, except that thev are sometimes fonnd to have a filiform tail-like endiiiir. 372 THE MANIFESTATION OF DISEASE IX ORGANS. (See Figs. 160, 161, 162, and 163.) The siguilicance of cylindroids is uot defiuitely knowu, but they may be taken as an indication of irritation of the kidneys, even if albumin and true casts cannot be found in the urine. They are often seen in the renal irritation following or, rather, accompanying the conditions called lithamia Fig. 1G1. Fig. 162. Xon-albuminous urine. Cast-iike forms, with deposit of urates. Non-albuminous urine. a and b. Cast-like forms, c. Filamentous. or urictemia, and in that condition in which we find oxaluria. (For further information concerning cylindroids, see Stengel's paper in The Medical Xeics of July 15, 1893.) Fig. 163. Filamentous and ribbon-like cylindroids. According to Bramwell, the following is the best method of stain- ing and mounting tuljc-casts and other urinary deposits. He u.ses picrocarmine : " 1. An ordinary conical urine glass is filled with equal parts of THE URIXARY BLADDER AND THE URINE. 373 urine and an aqueous solution of boric acid, and set aside until the deposit settles. '^ 2. The deposit is then drawn off by means of a pipette, and transferred to an ordinary test-tube, in which a small quantity (half a drachm is quite sufficient) of picrocarmine solution has been pre- viously placed. '' 3. The urine and staining-fluids are then thoroughly mixed by inverting the test-tube two or three times, the end being closed, of course, by the thumb. " 4. The test-tulie containing; the urine and stainino^-fluid is then set aside to stand for twenty-four hours. ^' 5. The deposit, which has by that time settled at the bottom of the test-tube, is then drawn off by a fine-mouthed pipette, placed on a slide, covered, and examined under a low power. " If any tube-casts are present, they are very easily detected by this method. "' When a cast is detected, it should be carefidly brought to the centre of the field and exan:ined with a higher power. If amyloid degeneration is suspected, methyl-violet may be used, for in some cases of waxy disease of the kidney the tube-casts give the character- istic rose-pink reaction with methyl-violet. For permanent prepara- tion the deposit is drawn c»ff as in No. 5, above, and transferred to a small tube of Farrant's medium,' in which it remains until the organic deposit has settled, when it is again drawn oft' and trans- ferred to clear Farrant's solution, whence it is mounted in the usual manner. All organic deposits are thus stained and mounted in a perfectly clear medium. Their minute characters can be studied with the highest powers ftf the microscope." The most important sedimentary substances for diagnostic pur- poses, other than casts, are the products of tissue-changes, or are derived from articles of food. These substances are chiefly the acid urate of sodium and potassium and alkaline urate of ammonium and potassium, uric acid, oxalate of lime, the phosphate, carbonate and sulphate of lime, and the so-called triple phosphates (ammonio- magnesic-phos])hate). Tiie discovery in a urinary sediment of fine shapeless granules, ' Fftrmnl's solution is niaile (is follows : Dissolve 1 grni. of arsenious acid in 2<)0 c.c. of dis- tilled water. In ;this dissolve 130 grras. of gum acacia with frequent stirring, and add 100 c.c. of glycerin. Filter the solution through fine Swedish j)aper ujkju which has been deposited a thin layer of talc. 374 THE MANIFESTATION OF DISEASE IN ORGANS. which may be crystalline and shaped like a fan, which are generally brown or pinkish in hne, indicates acid sodium urate. Urine con- taining such deposits is found to be acid on standing, and will form a brick-dust deposit as soon as the urine is cooled. Acid potassium urate and acid calcium urate, which occur in an amorphous form, are mixed with it in smaller quantities. The urates themseh-es have no particular importance except that they are often present in excess in fever, wasting diseases, in gastric disorders, and in attacks of gout. When in a highly acid urine the student finds rhombic or dia- mond-shaped plates (Plate XIII., Fig. 2), or plates of a similar shape with the lateral angles rounded off, or quadrate crystals or square plates, or plates like double-headed arrows, or rosettes of crystals, or bundles of crystals like bundles of kindling-wood, these forms are uric acid. Any urine will deposit such crystals if it stands for many hours (say ten hours), as its acidity increases, and therefore the discovery of these crystals only possesses significance if they are found in from four to six hours, as this shows an excess of uric acid, which in turn is found in gouty, rheumatic persons or those who eat to excess and take no exercise. Often an excess of uric acid in the urine antedates the development of chronic contracted kidney. Uric acid also appears in excess in cases suffering from fever and acute inflammations. It is also eliminated in excess in leukaemia, splenic enlargement, hepatic cirrhosis, and gastro-intestinal catarrh. The rosette crystals just named are often found in diabetic urine. Small square, brilliant, octahedral crystals which are perfectly transparent refract light strongly, and look somewhat like the back of a square envelope at times, are those of oxalate of lime. (See Fig. 164.) The significance of oxaluria is quite important, for it is often a concomitant symptom of melancholia, dependent upon im- proper metabolism producing such symptoms, and so if present separates this class of cases from those of the true disease melan- cholia and indicates the use of nitrohydrochloric acid. It is found in the urine of persons who have eaten of peas, cabbage, and toma- toes, and in that of persons suffering from spermatorrhoea. If not due to the ino;estion of these foods, oxaluria indicates deficient oxida- tion of nitrogenous tissues. Creatin in the urine occurs in very brilliant prisms of a rhomboid THE UEIXAEY BLADDER AND THE UEIXE. 6i0 form, the end of which is ofteu split into a fraved end. (See Fig. 165, a.) It is not present in normal urine. Frn. 1f)4. Oxalate of lime crystals. Creatinin also exists in normal urine in small amounts in pris- matic, colorless, brilliant crystals of the shape shown in Fig. 165, h. Fig. 1G5. Crystals of crcatin and creiitinin. (Charles.) a. Crystals of creatin. b. Crystals of crealiniii. c. Crystals of chloride of zinc and creatinin. When tlariv-brown spherical masses covered with thorn-like crystals or .sharp spicules arc formed in alkaline urine they are composed of ammonium urate (Plate XIII., I'ig. 3), and they will he found a.sso- 376 THE MANIFESTATION OF DISEASE IN ORGANS. ciated with crystals which are flat or shaped like coffin-lids, or more rarely are feathery, star-shaped masses which are large in size. These are the crystals of the triple phosphates. (See Fig.' 166.) In addi- tion, such urine will contain amorphous calcic phosphate. The crystals of the triple phosphates are of some diagnostic im- portance, as they do not exist naturally in the normal urine, but are formed when the ammonia is set free by the decomposition of the If such crj'stals are found in freshly passed urine, they indi- urea. cate that ammoniacal fermentation is taking place in the bladder, a condition often seen in chronic cystitis and in some cases of paraplegia Fig. 166. Triple phosphate crystals. arising from injury to the cord or myelitis. A deposit of the triple phosphates and amorphous calcium phosphate, making a sediment like that of purulent urine, is sometimes seen in overwork of the nervous system and in cases of general debility. In addition to these amorphous and crystalline bodies found in the urine there are a number of others derived from the body, or due to extraneous contamination. These are epithelial cells derived from the kidneys, ureters, bladder, or urethra (Plate XIII., Fig. 4). Eggs or bodies of several parasites, tubercle bacilli, gonococci and streptococci, or staphylococci, are also sometimes seen under the micro- scope. In addition, we find spermatozoa in certain cases. (See Fig. 169.) THE URINARY BLADDER AXD THE URIXE. 377 Thus we may find the embryos of filaria, echinococcus hooklets (Fig. 167), and the eggs of distoma haematobium, which are very rarely seen. Fig. 167. Echinococcus, with two hooklets, aud section of cystic membrane, greatly magnified. (Peyer.) Tubercle bacilli are to be found by the same stainiog-processes as when they are sought for in the sputum (see chapter on Cough and Expectoration), and, if found in the urine, indicate renal or vesical tuberculous infection, provided that the patient has not contaminated the vessel holding the urine by sputum infected with the organism. They are not to be confused with the bacilli found in preputial smegma, which look ^'"- ^^^• like tubercle bacilli and take the same stains. ''v Gonococci indicate the presence of a specific * • \ "-v.... urethritis or vaginitis, and are found by staining _ •. /'„.:;;•. ■■• '"• and usint:: a tV homoo;eneous immersion lens with ■••;•. ••■'.••. ■-■•. a No. 2 eye-piece. The process of staining is the ••; ;•••• i eosin and methylene-blue stain. The material on ,_.' :"■..•• \ the cover-p-la.ss is stained for a few seconds in an ''<■■. .. .V'' alcoholic solution of eosin, then the excess of stain streptococci. (Abbott.) is washed off and the slide is then stained for ten minutes in an aqueous .solution of methylene-blue. Streptococci appear in chains and are stained by the same proces,s. They show infection from pus or are found in cases of erysipelas. (See Fig. 108.) Staphylococci also represent pus in the urinary tract. 378 THE MANIFESTATION OF DISEASE IN ORGANS. The presence of spermatozoa is more rare thau is generally thought. They may be iu the urine either as the result of a true spermator- rhcea, which is rare, or from some of the semen remaining in the urethra after an ejaculation iu coitus, or from an emission at night without intercourse. They appear as small transparent bodies having a head and tail and, if alive, possessing very active movements. (Fig. 169.) Fig. 169. Spermatozoa, with casts of seminal tubules and spermine crystals. Fermentation resulting from the presence of a number of special fungi takes place both in healthy and diseased urine after it is passed. In normal urine the acidity, w^hich is generally present to a slight degree, becomes still more acid through the growth of a special fungus. This process is accompanied by the deposition of uric acid, acid sodium urate and calcium oxalate, and also amorphous urates. After the urine is exposed still longer it undergoes an alkaline fer- mentation, and there develop in the fluid the micrococcus urese and bacterium ure?e. As a result the urea takes up water and decomposes with the development of CO2 and ammonia. No sooner is a positive alkaline reaction established than tho.se ingredients of the urine which are insoluble in an alkaline solution are precipitated, namely, amor- phous calcic phosphate, ammonium urate, and ammonio-magnesic phosphate. The first is amorphous, but the ammonium urate appears under the microscope in the form of small granules of a dark color THE URIXAEY BLADDER AXD THE UBTXE. 379 which are covered with spines. The crystals of aninionio-magnesic phosphate arc shaped like a coffiu-lid, and are large. The third form of fermentation taking place in the urine is that which occurs in diabetic urine, and is due to the saccharoniyces albicans, the micro-organism which produces fermentation in ordinary solutions of glucose. Chemical Tests. The chemical tests of the urine give us much important information. We commonly test it for albumin and for sugar, and, if we wish still further information, we examine it for its percentage of urea, uric acid, and for its peptones, or, to use a better term, its albumoses. Albuminuria. There are a great number of tests for albumin and sugar. Many of them are open to fallacies, and they^are there- fore to be avoided i)y the busy practitioner, who can rest assured that if he finds no albumin by the heat and nitric-acid test, if properly carried out, that he can put albuminuria out of the possibilities of the case, provided he tests samples taken at different times and on several different days, for sometimes albuminuria is intermittent. The best test consists in taking filtered urine and pouring enough of it into a perfectly clear test-tube to fill it about two-thirds. To this are now added a few drops of acetic acid to render it acid ; for, if neutral, the albumin will not be coagulated by heat. The upper ])art of this urine is now boiled by holding it over an alcohol lamp, and if albumin is present a fine cloud will appear in the boiled part of the urine, while the lower part remains clear. This cloud may be due t(» albumin or earthy phosphates. If a drop or two of nitric acid is allowed to trickle down the side of the tube, the cloud is dissipated if due to phosphates, but not changed if due to albumin. If the urine l)e tui'bid before the test by reason of an excess of urates, the fluid can be rendered clear by gently heating all of it. Heller's test of adding a few drops of urine to IIXO3 in a test-tube is too fallacious to be used. The quantitative tests for albumin are many of them impractical for the busy doctor. The best method is by means of j)ercentage- tulxs ])I;ic('(l in a centrifuge-machine. By this means all the albumin is thrown down. The lubes are filled to the 10 c.c. mark with urine and '21 c.c. of potassium ferrocyauidc solution (one part to ten) are added. Xext we add 1} c.c. acetic acid and thoroughly mix all these rK|uids, and the tube being placed in the centrifuge the matjhine is worked till all the albumin litis si'ttled. K:ich j^j c.c. mark on 380 THE MANIFESTATION OF DISEASE IN ORGANS. the tube represents 1 per cent, by bulk of albumin ; that is, if the albumin extends up to the 3| cubic centimetre mark the albumin amounts to 35 per cent. The significance of albumin is not as grave in all cases as it was considered at one time, nor is its quantity of great import necessarily, for in some of the gravest cases of renal disease, as chronic contracted kidney, it is excreted in very small amount, and it occurs in the urine sometimes in large quantities without any kidney lesion being present. As a rule, however, it indicates renal disease in one of its inflamma- tory forms, provided it is associated with other renal symptoms. It may depend on changes in the blood in which the diffusibility of its albumin is increased (Semmola), and we see albuminuria in cases of anaemia and in convalescence from long disease or from the effects of poisons. Again, circulatory changes may cause albuminuria by causing congestion of the kidney, as in cases of failing heart from its various causes. There is an intermittent, little understood, form of albuminuria, called cyclic albuminuria, or the albuminuria of adolescence, in which the albuminuria is absent on rising from bed in the morning, but appears if exercise is taken. An excess of albumin in the diet may cause albuminuria. Sugar ix the Urixe. The presence of sugar is determined by a large number of tests, of which the simplest and most reliable are Haines's test and the test of Whitney. Haines's test consists in making a solution as follows : Pure copper sulphate, thirty grains ; distilled water, half an ounce ; and thoroughly dissolve the copper in this water ; then add pure glycerin, one-half an ounce, which is to be thoroughly mixed ; and then add liquor potassa, five ounces. One drachm of this is to be placed in a test-tube and gently boiled, and to this are now added six to eight drops of the urine, and the liquid again gently boiled. If sugar is present, a copious yellow precipitate is formed. This is better than Fehling's test, because it is a perma- nent fluid. AVhitney's test is a solution of amraonio-cupric sulphate, of which one drachm is decolorized by ^\j- grain of glucose. The solution to the amount of one drachm is placed in a test-tube and heated to the boiling-point. The urine is now added drop by drop. If no sugar is present, no change Avill occur ; but if it is, the blue color will begin to fade, and finally the liquid will become perfectly colorless. As the fading process begins ihe uriue should be added more slowly, three to five seconds of boiling intervening between each drop. If THE URIXARY BLADDER AND THE URIXE. 381 there is any shade of blue or green left in the solution, reduction has not taken place. The following table shows how this test may l)e used for the quantitative estimation of sugar : If reduced by It contains to the ounce. Percentage. 1 drop 16 or more grains. 3.33 2 drops 8 1.67 3 " . 5.33 1.11 4 •• 4 0.83 5 •• 3.20 0.67 6 '• 2.67 0.56 7 " 2.29 0.48 8 '• 2 0.32 9 •' 1.78 0.37 10 '• 1.60 0.33 If the urine contains more than 3.33 per cent, of sugar, it is to be diluted by from one to ten parts of water, and the amount found in the table multiplied by the amount of dilution.' As Fehling's test is so widely used it must be described. AVickham Legge thus de.scribes it : This solution maybe prepared in the following way : 665J grains of crystallized potassio-tartrate of sodium are dissolved in five fluid- ounces of a solution of cau.stic potash, sp. gr. 1.120. Into this alka- line sohition is poured a fluid pre})ared by dissolving 133} grains of sulpiiate of copper in ten fluidrachms of water. The solution is exceedingly apt to decompose, and must always be kept in stop- pered iiottles and in a cool place. It is usually, therefore, more convenient not to mix the alkali and copper until tiie solution be wanted for use. In this case, a fluidrachm of the sulphate of cop- per solution may be added to half a fluid-ounce of the alkaline solu- tion prepared as above. About a couple of drachms of this test-solution arc })oure(l into an ordinary test-tube and the fluid boiled over a lamp, and set aside for twelve hours. If no deposit forms, the solution may be used for analysis ; but if a red precipitate be thrown down, the liquid has decomposed, and a fresh supply must be had. While the solution is boiling in the test-tul)e the urine must be added to it, drop by droj), and the effect watcheil. A few drops of a sample of urine which contains a large })ercentage of sugar will at once give a precipitate of yellow or red suboxide of copper; but if no preci[)itat(' occur, the urine should be added to the fluid, drop by dro]), any dejxjsit being carefully looked for, until a quantity ccpial ' This test, iiiuler the iiniue of Aciiue Sapphlriim, ciin be h(i;s, the symptoms just de- scribed come on gradually and insidiously and the tendency to ana- sarca is- marked and persistent, we have before us a case of chronic pnrenchi/mafojis nephritis, in which the prognosis is most grave. Urjomic vomiting and coma may occur in tliis class of patients (see chapter on Vomiting). Blood-cells are also found in the setliraeut of tlic urine in tliese cases, but are not so numerous as in acute diffu.se nephritis. 392 THE MANIFESTATION OF DISEASE IN ORGANS. A set of symptoms which differ very markedly from those just described occur in cases of chronic contracted kidney (chronic inter- stitial nephritis). The following description of the symptoms may be taken as representing a typical case : The patient, who is usually past middle life, finds that he or she urinates more frequently and passes a greater amount of urine than heretofore. Often the sleep is disturbed by the necessity of arising to urinate. Instead of the urine being heavy and clouded, it is unusually clear and limpid ; and in place of the high specific gravity of diff'use parenchymatous nephritis, we find it unusually low (only 1.010 to 1.015). Albumin is only found inconstantly and in traces, and is generally to be sought for in the urine passed by the patient when first arising from bed. The pulse is usually much increased in tension, and atheroma of the bloodvessels is more or less marked. This high-tension pulse is a valuable diagnostic sign. The heart, which in acute diffuse nephritis may be slightly dilated, or in chronic parenchymatous nephritis somewhat hypertrophied, is in this disease usually markedly hypertrophied, and the second sound at the second right costal car- tilage is accentuated. In addition to these symptoms we find that chronic bronchitis is not rare, and that pulmonary oedema and attacks of shortness of breath are often present, the latter being most marked at night. Ursemic symptoms are more commonly seen in this class of cases than in any other, and violent vomiting difficult of control should always make the physician test the urine to discern renal mischief. Unlike parenchymatous nephritis, dropsy is a rare complication of chronic contracted kidney. Microscopic examination of the urine will only reveal a few hyaline and granular casts. The prognosis as to cure is bad, but life may be prolonged indefinitely. A copious flow of urine of a low specific gravity and of a pale, clear appearance, containing fatty, hyaline, and finely granular casts, is often seen in cases of amyloid disease of the kidney, and the pres- ence of syphilis, of prolonged suppuration, or extensive bone disease, due, it may be, to tuberculosis, with concomitant enlargement of the liver and spleen, separates it from any other ailment. Albuminuria may be a marked or an absent symptom. Let us suppose, however, that a patient comes to us with a his- tory of exceedingly copious urination, of great thirst, of loss of flesh, and has a dry, harsh skin, we immediately recognize that a test THE URINARY BLADDER AND THE URINE. 393 of the urine will probably reveal the case to be one of diabetes mel- litus. This will be poiatetl to if a high specific gravity is found present in a clear limpid urine, and confirmed if the tests for sugar already given produce a reaction. If the urine has a constant low specific gravity and contains no albumin or sugar, the case is probably one of diabetes insipidus. The other prominent symptoms of diabetes raellitus are furuuculosis, intense itching and erythema (see chapter on the Skin), an excessive appetite, and, in severe cases, gangrene of the extremities or diabetic coma (see chapter on Coma and Uncon- sciousness), Should much pus be present in the urine it is probably derived from a pyelitis or a suppurative inflammatiou of the pelvis of the kidney. The symptoms of this state are, briefly, a constant or inter- mittent pyuria, usually an acid reaction of the urine, chills and fever, which may mislead the physician into a diagnosis of malarial poisoning, or, in other cases, if the pyelitis be tubercular, hectic fever may be present. Sometimes violent attacks of pain resem- bling renal colic are passing symptoms, and not uncommonly an anfemia and loss of strength are notable. There is often pain in the back, which is made worse by pressure with the hand, and, rarely, if the suppurative process be marked, typhoid symptoms may be present. If the pyelitis be tubercular, tubercle bacilli may be found in the urine. If due to a calculus, there may be a history of gravel and renal colic. Pyelitis is to be separated from cystitis by the fact that in it the mine is acid, in cystitis it is ammonical ; by the pain in the rei)al region, often unilateral; and l)y theuseof the cystoscopc. The prognosis varies. If dne to an infectious fever, recovery usually occurs. Tuberculous pyelitis may also recover. CHAPTER XIII. THE BOWELS AXD FECES. Constipation and diarrhcea — The causes of these two symptoms and their diagnosis — The diseases in which these symptoms occur — Choleraic diarrhceas — Dysentery — The color of the feces — Intestinal parasites. The consideration of the condition of the bowels and feces as indic- ative of disease affecting the intestines themselves and other organs closely associated with their functions, can be best divided into sev- eral jaarts, namely, the functional disorders of the intestines and the organic diseases from which they may suifer, on the one hand, and the appearance of the feces in both functional and organic diseases of the abdominal viscera in general, on the other. The most com- mon forms of intestinal disturbance are constipation and diarrhoea. Constipation may be due to mere sluggishness of bowel-move- ment because of both nervous and muscular atony, or to deficient secretion of the intestinal juices, or, again, to the too rapid absorption of the liquids from the fecal matter while it is passing through the colon. It is also associated with all those conditions which prevent the proper secretion of bile, which liquid very materially increases peristalsis. Thus, we see obstinate constipation in most cases of jaundice, catarrhal or obstructive ; in cases of hepatic disease, produc- ing a deficient biliary flow ; and in phosphorus-poisoning, in which the fatty degeneration and hepatitis prevent biliary secretion. Further than this, the constant ingestion of foods which are absorbed nearly in toto, or, in other words, leave little residue, particularly raw or boiled milk, produces constipation. Again, the use of wines con- taining large amounts of tannic acid may produce similar results be- cause of the astringency of this substance, and chronic constipation from the use of large quantities of badly infused or boiled tea made with hard water is frequently met with. When too rapid absorption of the liquids takes place from the feces the cause may be lack of liquid ingested, and the remedy be full draughts of pure water ; or, again, constipation occurs as a manifestation of diabetes insipidus or diabetes mellitus, because the polyuria of these affections drains the body of THE BOWELS AXD FECES. 395 liquid. Obstinate constipation should therefore always call the phy- sician's attention to these affections and to two other possibilities, namely, that the condition depends upon wilful disregard by the pa- tient of the calls of nature, so that the bowel is forced to retain fecal matter until it becomes hard and dry; or, quite as important, that the consti})ation may be due to some reflex cause, which, as the result of irritation, results in an arrest of peristaltic movement. Thus, a woman with ovarian and other pelvic trouble may have obstinate constipation which yields little, if at all, to purgatives, but readily to nervous sedatives or even to an opiate. Or, again, in chronic lead-poisoning the inhibitory fibres of the splanchnic nerves may be so irritated that peristalsis is impossible. Here a hypodermic injec- tion of morphine may make a movement possible. y The organic diseases of the bowel producing constipation are many and of great importance. They consist in intestinal obstruc- tion in all its forms, as by bands, by growths, by the process of intussusception, by volvulus, by cicatricial contractions, and by im- pacted foreign l)odies or fecal matter. The presence of a sudden attack of constipation, or the presence of this condition in a degree which fails to yield to mild laxatives, should ulways put the physi- cian on his guard lest some such grave condition is present. As severe and, finally, stercoraceous vomiting is a fairly constant and more marked symptom of intestinal obstruction than is constipa- tion, a discussion of the various symptoms of intestinal obstruction will be found under the chapter on Vomiting, and the diagnosis of growths of the intestine will be found in the chapter on the Abdomen. Aside from these causes, it is manifestly impossible to discuss all the conditions of the system in which constipation may be present. The })hysician must always bear in mind that constipation often results in the absorption of all sorts of poisonous materials from the bowels, which in turn may produce all sorts of symptoms, nervous or otherwise, from epileptiform attacks, in rare cases, to severe headache and vertigo, with vomiting, in others. DiARKiKKA of an acute type depends, as a rule, upon one of four causes, namely, the presence of irritant material in the bowel, which the intestines attempt to get rid of by increased secretion and exces- sive peristalsis ; to relaxation of the bloodvessels of the intestine, with profuse serous leakage and consequent wateiy purging ; to acute inflammation, with excessive secretion of mucus ; and to the endeavor of the system to eliminate poisons in tiiis manner, as in 396 THE MAXIFESTATION OF DISEASE IN ORGANS. cases of sudden profuse diarrhoea, in cases of chronic reual disease, in which the purj^ing is an effort at elimination. Such forms of diarrhoea as these are usually sudden in onset and speedily get well of themselves, and it is a mistake to check them too suddenly. It is impossible to speak of all the possible causes of diarrhoea, or of all the diseases in which it is met with. Only those in whicti it is a prominent symptom, or one of importance, can be discussed. One of these is cholera morbus, a disease which manifests itself in profuse watery purging, accompanied by violent pain in the belly, and, after several stools have passed, in a considerable amount of tenesmus. Mucus is almost entirely absent from the dejecta, but particles of undigested food may be found in them. Vomiting is often a severe and simultaneous manifestation of the gastro-intestinal disorder which results in these symptoms, and, if the attack be very severe, it is practically impossible to separate it from true cholera Asiatica if an epidemic of that disease is present. The patient speed- ily becomes cold and pinched-looking, exceedingly weak, and finally passes into collapse. The pulse becomes feeble, rapid, and running; the face livid, and finally the patient may develop the fades Hippocratica. The urine is greatly decreased or entirely sup- pressed, because of the watery purging and possibly by reason of the effects of certain poisons upon the kidneys. In the great major- ity of cases the symptoms are not so severe as this, and complete recovery ensues as soon as the offending materials are passed out of the bowels and the patient has time to convalesce. When an attack of diarrhoea, such as has just been described, comes on in a young child it is usually called cholera infantum, or summer complaint, and it is nearly always due to improper feeding or to the unintentional use of bad food or bad milk. The stools of the child are usually at first filled M'ith curds of milk and green masses, look- ing as if the curds had been stained with grass-juice or spinach. The child often passes with extraordinary rapidity into a state of collapse, and may die in a few hours or days. The tenesmus often becomes constant and is a distressing symptom, and the tissues become shrunken to a marked degree. The child manifests not only the evidences of the results of profuse purgation, but, in addition, is evidently intoxicated by the toxins absorbed from the bowels, so that it lies on the lap of the nurse in a relaxed and torpid state. The surface of its body is often al)norraally cold, and its extremities THE BOWELS AND FECES. 397 may be pinclied and blue, but the temperature of the internal organs is generally abnormally high, so that while the axillary temperature may be below normal, the thermometer will reveal a temperature of from 102° to 103° in the rectum. Sometimes the head becomes retracted, as if meningitis was present. The respirations may be sighing or of the Cheyue-Stokes type. If the child or adult is seized with symptoms such as those described under cholera morbus or cholera infantum, and a suspicion of the presence of true cholera is raised, are there any facts which will point to the correct decision in a case, even if, as already stated, a positive differential diagnosis cannot be made? In the first place, a train of symptoms of a malignant type point to the true cholera, rather than cholera morbus or cholera nostras, as it is sometimes call(. Sometimes a diphtheritic or false membranous dysentery is de- veloped in persons having chronic heart disease, and it has been seen as a result of acute croupous pneumonia. This is called secondary diphtheritic dysentery, and death generally results from exhaustion, only a suspicion of the intestinal condition having existed during life. Such a state is sometimes a complication of Bright's disease, probably owing to the irritation of the intestinal mucous membrane produced by the urea decomposing into carbonate of ammonium. In acute primary dysentery of a diphtheritic character the patient may rai)idly pass into a typhoid state, and the case be diagnosed as one of typhoid fever with profuse diarrhoea. The discharges are the only means of separating the two conditions (enteric fever and diph- theritic dysentery), as they often are filled with blood and mucus in iaie. segmented globule.-:. If the stools containing the eggs be set aside in a warm place, the embryos can be .seen to develop in the eggs, liloody .stools may be due to the presence of this parasite. The so-called whip-worm, or trichocephalus dispar, is a fine thread- worm without aiiv medical interest. PART II. THE MANIFESTATION OF DISEASE BY SYMPTOMS. CHAPTER I. FEVER AND SUBNOKMAL TEMPERATURE^ The methods of taking the temperature — The significance of fever — The febrile movements of various diseases. Fever is that state of the human body in wliidi its temperature is raised above the normal limit, or 98.8° F. Hyperpyrexia is a term applied to a febrile movement in which the temperature rises as high as 106° F., and cases are on record of a temperature of 115° or even more. The method of taking the temperature consists in placing a self- registering clinical thermometer in the mouth under the side of the tongue, the lips being then closed tightly about its stem ; or of insert- ing it in the axilla, the hand and arm being then placed across the patient's chest, or epigastrium, so as to cause the axillary tissues to be in close contact with the bidb of the thermometer. Before the thermometer is placed in the axilla this space should be carefully wiped dry, since if perspiration is present its evaporation will so chill the thermometer that a false record will be made by the index. Sometimes the temperature of the patient is taken by inserting the thermometer into the rectum, and, if this is done, the bulb should be passed well inside the external sphincter. Rarely the teiuperature is taken in the vagina. The precautions to be taken in all (Mscs in which a thermometer is used, in addition to those named, is to have a thermometer which is accurate, and to be sure that there is no acute or chronic iuHam- matory process present which will produce local heat, and so give an erroneous impression as to the actual temperature of the entire body. This is particidarly apt to be the case iu diseases of the 410 THE MANIFESTATION OF DISEASE BY SYMPTOMS. mouth in children , thus stomatitis may raise the local temperature from one to two degrees. Hot liquids, if taken into the mouth just previous to or during the time at which the thermometer is inserted, will so raise the temperature of the local tissues as to make the ther- mometer register several degrees above normal, and a similar effect may be produced by cold liquids or ice held in the mouth. This subject has recently been studied by Lazarus- Barlow, who asserts that the effects of hot objects taken into the mouth last much longer than do those produced by cold, and that a mouth-temperature should never be taken within one hour of the time that any hot food is ingested. He even shows that holding the mouth open for some time renders a true estimate of the body-heat impossible, and advises that the temperature shall never be taken in the mouth if it is pos- sible to take it elsewhere. The significance of fever is great. It always shows the presence of an ailment sufficiently severe to make it wise for the physician to order the patient to bed till the fever abates or until he can surely determine its cause. The significance of a raised bodily temperature from a physiological point of view is that the nervous centres gov- erning heat-production and heat-dissipation are disturbed by some substance circulating in the blood or by reflex irritation, or perhaps by both. The danger of high fever is that it may cause coagulation of the protoplasm of the heart or vital centres in the base of the brain, but the danger of ordinary febrile temperatures has been greatly exaggerated. Indeed, in some cases moderate fever prob- ably aids the body in throwing off' or, rather, conquering the dis- ease which has attacked it, in three ways, namely, by producing a temperature less favorable to the grovvth of certain disease-germs than is the bodily temperature in health ; by increasing cellular activity it may increase phagocytosis and the development of antitoxic materials ; and, finally, by virtue of the .increased temperature the effects of poisons may be rendered nil. This is the case, for exan:iple, in regard to digitalis, which will rarely produce its ordinary effects on the heart when well-marked fever is present. Another point of importance in this connection is this, namely, that the duration of fever has more to do with its importance as a symptom than has its degree, for a temperature of 105° for a few hours may be borne with immunity, whereas one of 103° for many days cannot fail to produce evil effects. Febrile movements are generally associated with a dry, hot skin. FEVER A XI) SVEXORMAL TEMPERATURES. 411 but sometimes with u cold, wet skin. The latter couditiou is of evil significance as a rule, and must be overcome if possible. Fever in children does not possess nearly as much significance as it does iu adults, for children often develop high temperatures from slight causes and have s]>eedy recoveries. The balance of their heat- mechanism is easily upset. The older the patient the greater the significance of fever, and a rise of two or three degrees in a man of sixty years is more alarming than one of four or five degrees in a child of five or six years. When fever is not due to some distinct pathological change iu some part of the body, generally of an inflammatory kind, it may arise from mild irritation of a mucous membrane so that a catarrhal condition is set up. Such fevers are seen in cases of mild gastro- intestinal catarrh in children after the ingestion of bad food or exposure to cold, and apparently arise as the result of the reflex irritation produced by difficult teething. (See chapter on the Tongue.) In many instances, however, the fever of dentition depends upon a more or less closely related, but overlooked, gastric catarrh. Sometimes after a urethral sound or catheter has been passed in a man, in the course of a few minutes or hours he develops a severe chill, followed by a fever which may be quite high, but does not last long. Feveu IX Infectious Diseases. Nearly all infectious diseases are ushered in by tlie development of fever of greater or less degree, and this is particularly ti-ue of the exanthemata. In typhoid fever the febrile movement is very characteristic in some cases, althougli in many instances it does not follow the description laid down iu text-books. After several days of general wretchedness the patient develops a slight fever of from 100° in the morning to 101° at night, and this temperature progressively rises so that the next morning it may be 101° and that night 102°, the next morning 102°, that nigiit 103°, and so on until the morning temperature may be 103° and the evening temjx'iature 104° or rarely 10o°. The fever usually reaches its acme by the end of the first week or ten days, and then lor another wci'k remains almost unchanged, there being a morning fall and evening rise of an almost e(pial extent. Toward the end of the third week, or sometimes earlier or later, according to the severity of the attack, the morning remissions become more marked and then the evening rises fail to reach their former height. Often these marked morning remissions 412 THE MANIFESTATION OF DISEASE BY SYMPTOMS. are the first indication of the tendency to recovery. Very high even- ing temperatures are indicative of a severe attack, but are not so indicative of serious ilhiess as are high temperatures in the raorniug. After the third week, in a moderately severe case, the temperature falls gradually till by the twenty-eighth day it usually reaches the normal. In very rare cases the temperature speedily reaches its acme at the very beginning of the disease and then passes through the course already described. Such cases are generally prolonged, but may in some instances end by the fourteenth day. Sudden falls of temperature during the course of typhoid fever are nearly always of grave import. The most common cause of such a sudden fall is an intestinal hemorrhage, and the fall may occur sometimes before the blood appears in the stools. In other cases it is an evidence of intestinal perforation. The other causes of a sudden fall are severe nose-bleed, or hemorrhage of any form ; as, for example, that o^'curring iu connection with abortion in a female patient. Sometimes, too, vvithout any of these causes, the temperature falls very rapidly, and the patient goes into colhipse. Such cases are very grave and the prognosis unfavorable. Fig. 175. lU^ 1 IftQ ^ ^ -J i V J \\ 1 1 1 ■rlfiO ■A Z a / LU r 1 / f 1 \ f / \ \ ' V 1 £ on i / ■j \ ll 1 _ G ^ V, \. . _ V ^ _ ,1 1 ' ^^ V^- _ RMAL4 — ^ — — — r~ n^ r -H — _i "v ^ L^ — -^ r — Sifc kirH u^ -;•- t- \ J \ 1 1 *N 1 i 1 1 j ^ j 1 1 1 1 1 1 Chart showing recrudescence of fever in a case of typhoid fever. A recrudescence or return of the fever, in which it rises quite rapidly to a point as high or higher than at any time during the attack, occurs in some persons who, during the stage of convalescence from typhoid fever, take solid food too soon, or are excited by the visit of a friend. Such rises are but temporary. (Fig. 175.) More rarely, as a result of getting out of bed, or bad feeding, or other causes, a true relapse takes place, and the disease runs a second course, which is FEVER AND SUBNORMAL TEMPERATURES. 413 usually, but not always, of a shorter and milder character than the first attack. (Fig. 176.) Sometimes a mild, irritative fev^er, perhaps due to anaemia, persists for some weeks, but the physician should not rest content with a belief that anjemia is the cause until he has excluded all pos- sibility of there being pul- monary, pleural, or bone dis- ease, as these conditions very commonly ensue as sequels of typhoid. In other instances, after the morning tempera- ture has reached normal, the evening temperature remains pyretic for a number of days, and it may persist for some time. If the fever of typhoid ever rises as high as 107° or 108°, the prognosis at once becomes very grave. Very rarely enteric fever, so-called, runs its entire course without any fever. Fisk, of Denver, has seen such cases, and the author had five such cases at St. Agnes's Hosi)ital in one term of service. Sti'iimpell asserts as a rare occurrence that the fever may become intermittent, being normal in the morning and as high as 104° at night dur- ing almost the entire illness. The association of such a temperature-iurveas just de- Flfl. 176. FAHRENHEIT SCALE C'linrt sliowiiig a rclniise in typhoid fever. 414 THE MANIFESTATION OF DISEASE BY SYMPTOMS. scribed v;ith the other characteristic signs of typhoid fever, as, for example, the development of the rose-rash on the chest and abdomen, on or about the seventh day (chapter on the Skin), the ochre-colored, loose stools, the peculiar stupid, drowsy appearance of the face, and in some cases the peculiar typhoid odor about the patient, all make the diagnosis certain. The differential diagnosis of acute tuberculosis from typhoid fever may be quite difficult in certain cases. When the symptoms of the two conditions are compared this is not difficult to believe, for we often have in both diseases headache, epistaxis, a very similar tem- perature-chart, and a feeble pulse, while there may be in both con- ditions an eruption on the skin, which rather tends to confuse the physician than to aid him. Again, the delirium in each case is very similar, and the facial expression of the patient in both diseases is apathetic. Even the respiratory sounds in both diseases in their early stages may be apparently only those of a moderate bronchitis ; and, finally, abdominal swelling, tympanites, and meteorism may occur in both maladies. Under these circumstances the hereditary and recent history of the patient may be of much value, as showing a tendency to tuberculosis on the one hand, or exposure to typhoid infection on the other. Again, if it be typhoid fever, the spleen is nearly always found to be enlarged on percussion. Then, too, the lesions in the lungs of a typhoid-fever patient are generally at the bases, while in tuberculosis they are oftoner at the apices. The stools may be loose in both diseases, but in tuberculosis they are not apt to be ochre-colored ; and, again, in tuberculosis the loss of flesh is often exceedingly rapid and profuse sweats and high fever are not rarely seen. The discovery of the bacillus of Eberth in the feces and the presence of the diazo-reaction in the urine would, of course, indicate typhoid fever. (See chapter on Urine.) Finally, careful and repeated examinations of the chest will usually, in the course of the disease, demonstrate the presence of tuberculosis of the lungs or bowels if this be the cause of the illness. It seems hardly necessary to state that if any expectoration exists the sputum is to be carefully ex- amined for tubercle bacilli in all doul)tful cases. The febrile movement and other symptoms of enteric fever are often imitated very closely by those of ulcerative endocarditis of a typhoid type. In addition to an irregular fever, there may be diar- rhoea, parotitis, stupor, and progressive feebleness in both diseases. An examination of the heart may reveal the presence of endocar- FEVER Ay I) SUBNORMAL TEMPERATURES. 415 ditis, or the existence of some focus of infection, such as a wound, a septic process, or the fact that the patient is in the puerperium will, in combination with the sudden development of endocarditis, render a diagnosis possible. An irregular fever with muscular pains and a great deal of dis- comfort in the belly, the case simulating typhoid fever, may occur in cases of trichinosis. A febrile movement closely resembling that of typhoid fever, a resemblance which is increased by the association with it of head- ache, insomnia, and anorexia, may be Malta fever, a disease which can be excluded in the vast majority of cases if there is no history of exposure to the exciting cause in the island of Malta. Sometimes it might be confused with relapsing fever, except for the longer febrile movement in this disease. Thus after three or four weeks of illness convalescence seems to be established, and the temperature falls, but in a few days all the symptoms return with even greater vehemeuce than before. Such relapses may occur again and again. Violent pain in the joints on moving the body are often present. The temperature-chart of typhus fever is so different from that of typhoid fever that it gives us a valuable differential point at the very beginning of the disease, for, after several days of languor, headache, and pain in the limbs, the fever suddenly springs on the patient, so that on the first night it may reach 105° F. Often it reaches 106° in a day or two, and while present is constant, the morning fall being very slight indeed. The development of the spots in a copious eruption on the third to the seventh day, which spots may develop into petechiie before fading or remain unchan>2;ed in appearance, the great exhaustion, the severity of the illness, and the sudden rise of temperature, followed i)y a constant fever point to typhus fever. Finally, the conclusion of the febrile movement in favorable cases l)y the end of the second week by crisis or by a more rapid fall of temperature than we are accustomed to see in typhoid, all help to make the differential diagnosis, which is, how- ever, in many eases very difficult or impossible at first. The temperature of rdap^yiiif/ fcrcr nearly always rises suddenly at the beginning of the attack to from 103° to 10")°, aud remains high with slight morning remissions from three to seven days, when it suddenly falls as ijy crisis to the normal or below it, after being on the ])receding afternoon or evening unusually high. Sometimes it falls as low as 92° or !)3° V. Tiie patient now remains free from fevei- 416 THE MANIFESTATION OF DISEASE BY SYMPT03IS. for from several days to two weeks, wheu with a sudden leap the fever and other symptoms of the first attack recur. A temperature of 105° to 106° in relapsing fever rarely indicates a grave outlook as it does in typhoid. The only condition which resembles this temperature- range of relapsing fever is intermittent malarial fever; but the rarity of relapsing fever in America, the frequency of mala- rial fever in certain parts, the presence of the spirillum of Obermeier in the blood in relapsing fever, and the malarial germ in the blood of intermittent fever, all make the diagnosis possible. In scarlet fever the temperature suddenly rises on the first day to 104° or 105° F., and still higher the next day, and then remains con- stant as loug as the eruption is on the skin in full development. Just so soon as the eruption begins to fade the temperature also falls, not by crisis, but by a lysis, not so slowiy as in typhoid fever, but far more slowly than in pneumonia. This arrest of the fever usually takes place in simple cases by the end of seven days; and if it per- sists louger, is proliably due to some complications, such as otitis or the " collar of brawn," due to enlarged cervical glands. (Fig. 177.) Fig. 177. DAY OF, DISEASE] 1 2 ■i \ 4 3 1 G < s 3 j 10 11 12 1 13 " 1.', 105' 104' 103- 102° lor 100- 99 M E M E M E M E M E M E M E M E M eIm E M E M E M E M E M E A A /l J \/\ /\ / / \ /{ / V / / i/ A / / / [A / A / v V \/v .^1 .... TEMP v-T V r / 1 I- 98 Chart of scarlet fever. The characteristic strawberry punctated rash and scarlet hue appear- ing on the first or second day, the ultimate dermal desquamation, the violence of the onset of the symptoms, the sore throat, and the peculiar appearance of the skin, all complete the clinical picture, particularly if the symptoms be in a child. (See chapter on Skin.) In rare cases the fever in scarlatina is remarkably mild or almost absent, and these cases, as a rule, have a favorable prognosis. If the temperature be very high and persistent, on the other hand, the case is usually to be regarded as most grave. In measles the fever at first rises sharply to 103° or thereabout, FEVER AXD SUBNORMAL TEMPERATURES. 417 then falls to a little above normal, is slight for several days, and then markedly increases with the development of the eruption on the fourth day, often ranging as high as 104° or 105°, at which point, with little variation, it remains for the two days during which the rash is well developed. (Fig. 178.) With the fading of the rash the temperature also falls by crisis. If fever persists to any extent, it is always due to some complicating cause other than the original disease ; such a complication, for example, as a bronchial or gastro-duodenal catarrh. Fig. 178. B 1 ] i —r \ j 1 1 * 1 1 1 ', 1 ! 1 ' j / 2 T ' 104 \—z =if :W: _!_ < G — f— -\ / — T— — t— 2 1 4- _L 103 1 j— — "— _i_ — |— 1 1 i / : . \/ to. ^n >1 1 T 1 ' 1 ^' \ 1 A /\ . 1 ^ ' / 1 / 1 1 U 4 ^j .-^ /\ !/ / ' 1 I i "/ —i— ~l — [— q: 6 I C — - i d- A- v~ \~ lA 1 1 £ 2 100 8 c — H- fe t :^^ id ]- z:z 1^ . — - 1 2 99 -k-j — t— 1 -r- —^— V ^ -A vn _■ _ , v^ _ N0RM1L4 98 — 1 — t^ ' Chart of a case of measles showing initial fever with the subsequent fall and then a rise when the rash is well developed. Also shows an ending of the fever by crisis. Tiie fever of rnOirln, if any occurs, is very seldom more than 102°, and has no typical preliminary rise as has measles, so that the temperature-chart of the disease may aid materially in a differential diagnosis. (See chapter on the Skin.) The febrile movement of smallpox is, with the exception of that of typhoid, the most characteristic of all the eruptive diseases. With a sudden onset of iever, pain in the back, severe headache, and malaise, the patient takes to his bed if possible, and his temperature if taken will be found speedily to rise even to 105° or more in some cases, and then falls back to almost normal for two or three days, during which time the eruption appears. In ihis way, therefore, the temperatm-e-chart of variola ditTers diametrieally from that of the eruptive fevers so far discussed, Ibr in these cases the lever rises 9.7 418 THE MANIFESTATION OF DISEASE BY SYMPTOMS. with the appearance of the eruption, whereas in this instance the tem- perature falls with the appearance of the eruption. This lower temperature persists for several days, from half to one degree above normal, till the ninth day of the disease or the sixth of the eruption, when with the change of the pocks from vesicles to pustules the temperature rises again in what is called the fever of suppuration, which lasts with greater or less persistence for at least a week, when it ends by lysis or a gradual fall. Excessively high fever of 108° "is a sign of approaching death or of very grave import. The febrile movement of varicella, or chickenpox, is usually of very short duration and of little severity ; but it may reach proportions entirely out of consonance with the general systemic disturbance, which is usually very slight in previously healthy children. Thus it may rise in children who are prone to active febrile movements to as high a point as 105° for a very brief period, and yet may not seem to render the child ill. The temperature-range seen in cases of erysipelas is quite typical. At the beginning of the attack the rise is quite prompt and sharp to 105^ or 106° or even above this, and, instead of remaining constantly high through the course of the inflammatory process in the skin, goes through marked intermissions or remissions, which frequently occur and are followed by rises in temperature as high as that which occurred with the first onset. The fever ends in some cases by crisis and in others by lysis, the latter mode of ending usually taking place in those cases which have had a very severe attack prolonged in character, or which have been in an asthenic state prior to the disease. The diagnosis of erysipelas is easily made by the brawny, swollen, and red skin, with the peculiar line of demarcation at the edge of the swelling. (See chapter on Skin.) A fever which rises sharply from normal to 103° or 104°, being preceded by a chill and followed in a very few hours by a sweat, the whole term of acute illness, if we exclude general physical discom- fort, lasting but eight to twelve hours, is in the majority of cases that of intermittent malarial fever. The peculiarities of intermittent malarial fever, aside from those just named, are that the febrile movement begins to decline before the stage of sweating begins, and in some cases it begins to rise before the sensation of chilliness of the first stage leaves the patient. (Fig. 179.) The fall of temperature is usually less abrupt than the rise, and is sometimes delayed by slight temporary rises or arrests in its down- FEVER ASD SUBSORMAL TEMPERATURES. 419 ward course. The febrile movement is repeated at intervals, raugiug from one to seven days or even at longer intervals than this. If the attacks occur daily, they are called quotidian, and this is due to infection by two sets of tertian parasites which segment on alternate Fig. 179. Chart showing daily paroxysm duo to double tertian infection. One set of parasites seg- mented at 4 P.M. and the second set at 8 p..m. Paroxysm stopped by quinine on fourth day. days, or it may be due to infection with three sets of quartan para- sites. If the attacks occur every other day, they are called tertian (Fig. 180) ; if on the third day, quartan ; if on the fourth, quintan. If two attacks come on the same day, it is called double quotidian. Fig. 180. Chart showing paroxysms of iciliiui fuvcr, tlic scguifiiuiiion of the urgmii.sin occurring at aboiil twelve o'clock each day. Another point of importance in connection witli malarial attacks is that they often occur earlier each day by anhoiir or more. Karelv, they are delayed. Intermittent malarial fever is to be separated from other intermit- ting fevers by a number of facts. First, the presence of the mala- 420 THE MANIFESTATION OF DISEASE BY SYMPTOMS. rial organism in the blood at the time of the attack, or evideuces of its presence at other times. (See chapter on Blood.) Second, by the history of exposure to malarial influences. Third, by the marked effect for good ou malarial fever produced by the administration of quinine. Care must always be taken that the intermitting fever of the various forms of sepsis are not diagnosed as malarial intermittent fever. The most common error of this character is the making of a diagnosis of irregular malarial intermittent, because chills, fever, and sweat appear every ev^ening, when, in reality, the real cause is an un- discovered pulmonary or abdominal tuberculosis. Again, acute ulcer- ative endocarditis and purulent phlebitis may cause similar symptoms, as may also hepatic abscess, inpaction of gallstones, with suppurative cholangitis, causing the so-called Charcot's fever (see below). The absence of a history of malarial exposure, the possible presence of a cough, and the discovery of a tubercular lesion in the chest or abdo- men by careful physical examination will aid in deciding that the fever is tubercular and not malarial in origin. (See chapter on Chest and on Abdomen.) In ulcerative endocarditis the temperature-curve may exactly re- semble intermittent malarial fever, but in many instances the presence of an external wound, acute sepsis in some part of the body, or the presence of the puerperiura will reveal the source of an infection. (Fig. 181.) In the typhoid type of ulcerative endocarditis the profound asthenia and general prostration will separate the diseases even if the temperature-chart be unequal. In this form the febrile movement is rarely typically intermittent. The crucial test of the differential diagnosis lies in an examination of the heart, in which a murmur may be heard in some but not in all cases, unless there has already been some grave valvular mischief. The cardiac feeble- ness and asthenia, on the one hand, and the result of the blood- examination, on the other, aid the diagnosis. The duration of the case is not of much value in making a diagnosis, for cases of ulcera- tive endocarditis have lasted from two days to more than a year. Rarely it lasts more than six weeks. Death usually occurs in ulcera- tive endocarditis, unless there has been previously present chronic endocarditis, in which case recovery may rarely occur. The discovery of some spot showing a 'phlebitis may jjoint to this cause for intermittent fever. The fever of catarrhal or suppurative cholangitis often closely resembles intermittent fever, but the presence of hepatic symptoms, FEVER AND SVByoRMAL TEMPERATURES. 421 422 THE MAXIFESTATWX OF DISEASE BY SYMPTOMS. of marked jaundice, of a history of gallstone colic, and of exceed- ingly severe rigors, enables us to separate them. When fever of an intermittent type has been observed, and inter- mittent malarial fever, tuberculosis, and cholangitis cannot be dis- covered as a cause, search should be made for tenderness and swelling of the liver, due to hepatic abscess. Profuse sweats also wall be found in such cases, as in most instances of septic fever. The diag- nosis of hepatic abscess will be strengthened by the history of the patient having suffered from dysentery, as hepatic abscess is fre- quently caused by amoebic dysentery. The presence of fever preceded by chills, the temperature rising to 104° or even 105°, and followed by excessive sweats, in a person who is profoundly cachectic, may be due to i^ernicious anoemia or to septic poisoning, as already pointed out; but it should be recol- lected that such a temperature-chart is often seen in cases of gastric cancer. Similar symptoms as to fever in association with enlarge- ment of the lymphatic glands, particularly those of the neck, indi- cate Hodgkin's disease. An intermittent fever may also be seen in suppurative pyelitis, in association Avith pyuria. This pyelitis may or may not be tubercular. Remittent fever rising and falling every few days for two or three weeks, rarely rising abov^e 103° to 104°, and even falling to the normal line, associated with enlargement of the spleen and liver, yel- lowing of the skin or jaundice, bilious vomiting, and a history of exposure to malarial poisoning, indicates remittent malarial fever, a form more chronic and very much more grave than the intermittent form just described, because it responds less readily to treatment, and, second, because it is accompanied by more marked changes in the viscera. It depends upon infection with what is known as the festivo-autumnal form of the malarial parasite, which has an irregu- lar or variable period of growth. The conditions produced by this parasite are collectively grouped under the names remittent, continued, bilious remittent, and typho-malarial fever. In some cases the temperature and other symptoms will so closely resemble those of typhoid fever that nothing short of an examination of the blood can decide the diagnosis. If small ovoid, moving parasites are fcfund in the first week, or crescentic parasites after that time, this will decide that the case is malarial. (See chapter on the Blood.) A febrile process somewhat closely resembling remittent malarial fever, yet so rare, comparatively, as never to be confused with it, FEVER AXD SUBXORMAL TEMPERATURES. 423 is Weil's disease. In this condition the fever runs a remitting course, is associated with jaundice and swelling of the liver and spleen, and the stools may be clay-colored. There is one important point of difference between malarial remittent fever and Weil's dis- ease, namely, that in the latter gastro- intestinal symptoms are nearly always wanting or are mild, whereas in the former they are apt to be very severe. Usually the fever of Weil's disease ceases by the end of two weeks or earlier. It is probably an infectious jaundice. In dengue, a disease seen most commonly in epidemics in certain parts of the Southern United States, the patient, after suffering from violent aching pains in the body and limbs, swelling of the joints, and the development of a variable rash on the chest, develops an active fever, which lasts with the pain till the fifth day, when both the pain and fever decrease or cease, and then often return with equal force. These facts, combined w'ith the fact that it is an epi- demic disease, separate it from malarial fever. The fever of yellow fever is rarely over 103° or 104°, and is one of the milder symptoms of the disease, but it possesses this peculi- arity, namely, that after the lapse of from twelve hours to several days there is a marked remission of the fever and all the other symptoms, and from this time on the patient may get well, or after a few hours this calm stage is followed by the true violent symptoms of the dis- ease, such as black vomit, tarry stools, jaundice, and hemorrhages from the mucous membranes. Generally the full course of disease to convalescence or death is run in about one week. There is only one other disease which can be readily confused with yellow fever, namely, l)ilious remittent fever, and a case of the latter disease occurring during an epidemic of yellow fever can hardly fail to be incorrectly diagnosed. In the absence of an epidemic, however, the probabilities of the case being bilious remittent fever are very great, and tlie presence of bilious vomiting rather than that of blood, the characteristic temperature-chart, and, above all, the presence of a history of malarial exposure and of the signs of malarial infection in the blor)d, with tiio partial control of the symp- toms l)y (juinine in certain stages of remittent fever, ])oint to the malarial disease ratiier than to yellow fever. Just as in yellow fever, so in spotted fever or crrrhro-spitud meninf/ifis of an epidemic form, the fever itself is one of the ler.st imi>ortant symptoms, for, aside from the fact that it is apt to be irregular and intermitting, it is rarely very higii, as compared with 424 THE MANIFESTATION OF DISEASE BY SY2IPT0MS. the violent cerebro-spinal symptoms, the rigidity of the back of the neck, the headache, convulsions, and vomiting. The presence of these symptoms in an epidemic does more to confirm a diagnosis than the febrile movement. In some cases of spotted fever, how- ev^er, of a very grave type, the fever becomes a hyperpyrexia, but in cases tending toward recovery the temperature usually begins to fall by lysis before any moderation in the other symptoms is manifested. Even in the presence of an epidemic it should never be forgotten that middle-ear disease often causes marked meningeal symptoms, and that croupous pneumonia often produces a similar train of manifesta- tions, probably by infection with its particular micro-organism. The possibility of tubercular infection should cause the physician to examine the patient carefully for signs of tubercular disease in other parts of the body from which infection might arise, as, for example, the lungs. Fever due to septiccemia may produce a temperature-chart which closely resembles that of enteric fever, but it generally possesses one characteristic which, in the face of other symptoms suggesting sepsis, is of great importance, namely, the extraordinary rises and falls from normal to 105° or 106°, and from that i)oint even to a subnormal degree within a very few hours, so that the lines on the chart pass up and down in long sweeps. These sweeps are even more sharp and sudden than in an intermittent malarial fever, and their cause is determined by the discovery of some septic process in some part of the body. The presence of such a chart, in association with dull or violent headache, delirium, vertigo, and vomiting inde- jiendent of taking food, would point to cerebral abscess, particularly if a history of injury could be obtained. A somewhat similar chart to this may occur in connection with cases of active p)ulmonary tuhercidosis, when the lesions are well developed and septic absorption is active ; but usually in the hectic fever of phthisis we have a normal morning temperature, with a rise from two to three degrees, or even more, toward night. (Fig. 182.) This symptom of fever in any form occurring in a person with sus- piciously " weak lungs " should cause the physician to be confident that he has overlooked some focus which another careful examina- tion may discover, and it possesses another important diagnostic sig- nificance, namely, that the more active the febrile movement in phthisis pulmonalis the more active the disease process, and less active the fever the less active the process. Fever may, however, FEVER AND SUBNORMAL TEMPERATURES. 425 be almost eutirely absent in some tubercular cases with diseased lungs. Tiie febrile mov^ement of acute miliary tuberculosis has nothing characteristic about it, except that in some cases it may closely resemble that of typhoid fever, and if the physician does not care- fully examine the case an erroneous diagnosis may be reached. If, however, the disease involve the meninges of the brain, a hyper- pyrexia may be developed, and death speedily occurs in sucii cases, either in the fever or in a sudden collapse. The peculiar dyspnoea, the cyanosis, the profuse sweats, and the diffuse pulmonary signs render a diagnosis of acute miliary tuberculosis possible in some cases. Fig. 182. y Chart of a case of pulmonary tuberculosis, showing rising and falling of the temperature morning and night. When fever is associated with marked catarrhal symptoms, chiclly of the bronchial tubes and upper respiratory tract, with sneezing, lassitude, pains in the back and limbs, and excessive cough, the fever rising as high as 104° or 105° in severe cases and then falling almost to normal, we may have before us injiuenza or catarrhal fever, either of the sporadic or epidemic form. In this condition there maybe in severe cases great prostration and cardiac failure or vomit- ing and diarrhoea. The febrile movement is of the most irregular tyjx', even when some grave comi)licati()n, such as severe bron- chitis or pneumonia, comes on, although croupous j)netMnonia ran-lv occurs as a complication of " la gripi)e." The respiratory symiitonis just dcscrihcd are also seen fre(|uenlly, in as.sociation with moderate fever, in "//«// 7'V/vr," that condition seen in susceptible persrjiis during haying-season or late in the summer. Fig. 183. 426 THE MANIFESTATION OF DISEASE BY SYMPTOMS. The fever of pneumonia of the croupous type runs a very typical course in uncomplicated cases. Following a more or less severe chill, the fever quickly mounts to the high point of 103° or 104°, or even more than this. (Fig. 183.) For the next few days, if not modified by antipyretics and the u.se of cold, the fever remains high ; but there may be temporary remissions which look as if crisis was about to be established, when in reality they are followed at once by a return of the fever (pseudo-crises). Finally, in the majority of cases of croupous pneumonia the temperature Chart of a case of croupous pneu- Suddenly falls by crisis on the seventh monia, showing primary rise of tem- to ninth day (Fig. 184) and COUVa- perature to 105.4° aud crisis occurring , . i i • i i i i as early as the third day. lesceuce IS cstabUshed, although the sudden fall of fever may throw the patient into dangerous collapse. Sometimes this convalescence is broken by brief and slight febrile movements. If the case has been prolonged, or of the typhoid type, the fever may end by lysis. Fig. 184. 1 1 ~ - ' — ^ ^7^ ~-H o \ Ifl^ , -^ - ' 1 1 *l ; * f in^ » ( I 1 R { A Y 1 Z. \ '\ Y o 1 . j \ 1 y ° •" 4 U t \ ^^lOO- \ ^s j 1 t S e 1 \ A ^ 4 /\ V ' » if 90. \ 1 \ ~ ■ 1 1 ^ \ ^ f(ORMAL4 \ ./ \ , \ If *>, 1 ^ ""^S- i ^ * 5 -''* ' ^ « r V ? Chart of a case of croupous pneumonia, with crisis on the seventh day ; admitted to author's wards on second day of illness. It is to be remembered that the fever of catarrhal 'pneumonia is rarely as high as in the croupous form, 101°-103°, and ends by lysis, not by crisis. (See chapter on the Chest.) FEVER AXD SUByORMAL TEMPERATURES. 427 The fever of acute bronchitis possesses uo peculiarities over that of other acute inflammations. It is not proper to leave the subject of fever due to the various infectious diseases without calling attention to that due to syphilis in the secondary period of its course. With the onset of the roseola or other skin-lesion a fever, more or less marked, is nearly always present and is often preceded by chilly sensations and general malaise. This febrile movement may then follow one of three courses : it may never rise above 101°, and proceed as does a sim- ple continued fev^er, with slight morning remissions and evening exacerbations ; or it may be as remittent as is a malarial remittent fever ; or, again, it may resemble a malarial intermittent, rising to a high point and then falling almost to the normal. Phillips, of London, has reported a case of syphilitic fever in which this febrile movement lasted for weeks, and, after being treated by quinine as a supposed tertian ague, ended at once under antisyphilitic medication. (See chapter on Skin Eruptions.) In anthrax (splenic fever) the temperature rises rapidly and becomes very high, and in the course of from three to fiv^e days becomes subnormal, when death occurs. The history of exposure to possibly infected hides or hair, the early development of a papule, vesicle, and pustule, surrounded by brawny swelling and enlargement of the neighboring lym]ili-glands, renders the dia'j:;nosis easy; but if any doubt exists, it can be promptly dispelled by a microscopical examination of the fluid from the pustule, when, if the disease be anthrax, the anthrax bacilli will be found. (See chapter on Skin.) Fever with a vesicular eruption about the lips and on the mucous membrane of the mouth accompanied by disorder of the stomach and bowels may l)e due, particularly in children, to infection by the milk of cows suffering from foot-and-mouth disease or epidemic stomatitis. The j)r()gnosis is generally exceedingly unfavorable. In r/io/era Asiaticadnviwr the stage of collapse the surface is very cold, but the rectal temperature may be found as high as 103° or 104^ In cholera infantum, which is a form of gastro-intestinal irritation often produced by infected milk, there may be fever amounting to 102° or 103°, and not uiu^onunonly much higher, even to 107° or 108° in fatal cases. The diarrhd'a and obstinate vomiting, the age of the patient, the season of the year (usually hot weather), and the profound wasting, all complete the array of facts necessary for diag- 428 THE MANIFESTATION OF DISEASE BY SYMPTOMS. uosis. It is important to remember in these cases that the skin may feel cold and clammy e^^eu when tlie rectal temperature is very high. The febrile movement associated with the progress of acute paren- chymatous nephritis may or may not be preceded by a chill. The temperature may rise to from 100° to 104°, but the course of the fever itself is of no diagnostic import. The pulse, pain in the back, headache, perhaps drowsiness and coma, and the diminished urinary secretion, bloody urine, and albuminuria, render the diagnosis easy and the cause of the fever evident. Very marked fever up to 104° or 105° may dev'elop in the early course of acute infections tonsil- litis or in suppurative tonsillitis. The fever seen in most cases of tetanus is very moderate, but it is subject to excessive fluctuations, and in cases approaching a fatal ending may reach 110°. The fever occurring in acute appendicitis is a very unreliable symptom, notwithstanding assertions to the contrary. It rarely rises above 101° or 103° and sometimes not above 100°. Even in those cases in which the peritoneum has become involved by the inflammation the fever may not be marked, particularly if the peri- tonitis is septic. In other words, the presence of fever in association with pain in the right iliac region is a positive sign of some irritative or inflammatory process ; but if the physician excludes appendicitis on the ground that fever is not present, he may make a serious mistake. The fever of ordinary cases of acute articular rheumatism is usually moderate, rarely exceeds 103°, and possesses no typical characteris- tics ; but in very severe forms of the disease with cerebral manifesta- tions, a rheumatic hyperpyrexia may be developed, when, with delir- ium, convulsions, and cyanosis, the fever rises to 106° and even to 108°, after which death often ensues. The history of previous attacks of articular rheumatism, the hot, swollen joint or joints (usually the large ones), and the successive invasion of other joints as the ones first affected get well, point to the correct diagnosis. It must not be forgotten, however, that gonorrhoeal and other forms of septic arthritis occur with febrile movement. Pysemia, osteomyelitis, and purpura also may produce a fever with swelling of the joints. (See chapter on Legs and Feet.) When a person, previously afebrile, during hot weather or when exposed to artificial heat in excess, is attacked by unconsciousness, convulsions, and very high fever, he is probably suffering from FEVER AXD SUBNORMAL TEMPERATURES. 429 thermic fever or heat-stroke. Theoretically similar symptoms might be caused by a lesion due to embolism or hemorrhage in the neigh- borhood of the pons Varolii, but this is very rare. (See chapter on Monoplegia aud Face and Head.) The fever in sunstroke may rise as high as 110° to 112° or even more; the skin is hot and dry, or more rarely cold and moist with sweat, but, even if this is the case, the rectal temperature will be found hyperpyretic. A great rise of temperature (110° to 112°) often occurs after injuries to the cervical region of the spinal cord. Fever of considerable degree may be met with in cases suffering from hysteria, acute febrile neuritis, infantile spinal paralysis, apo- plexy, and acute myelitis. Temperatures as high as 106° have often been reported as occur- ring in hysteria, but in a certain number of cases these records are really fictitious and produced by some trick with the thermometer. Only the rectal temperature, taken while the physician is present, should be relied U})on in such cases. The rapid development of fever, pain in the back and limbs, and particularly in the nerve-trunks, the temperature soon reaching 103° or 104°, may be due to an attack of acute multiple neuritis, and the history that the illness has followed exposure to cold and wet may, on the one hand, make the physician believe that his case is suffering from rheumatism or influenza, or on the other, in the absence of such a history, from the early stages of one of the infectious diseases. The early appearance of tingling, numbness, loss of power, and wast- ing of the muscles soon decides the diagnosis in favor of neuritis. The nervous disease which most closely resembles acute febrile neu- ritis is Landry's paralysis, and a differential diagnosis may be diffi- cult ; but in neuritis there are loss of sensation, muscular wasting, sigus of degeneration, ami fever, whereas in Landry's paralysis all these are wanting, excepting the sensory symptoms, which in both diseases may be similar. The predominant symptoms of Landry's ])aralysis are paralysis and loss of reflexes. (See chapter on tiie Legs and Feet.) The prognosis of the severe form of febrile neuritis is grave, as death may ensue from respiratory ])aralysis. The fever of infandlc .spiual iHtralij.sis (anterior poliomyelitis) often is the chief symptom usiiering in the disease, and rises to 104° or even 10")° in some cases. There may be convulsions, headache, and twitching of the muscles, and, after the acute attack has j)assed off, 430 THE MANIFESTATION OF DISEASE BY SYMPTOMS. loss of power is speedily discovered in several muscles of one limb as a rule. (See chapter on Legs and Feet.) Fever at first amounting to only one or two degrees, but after- ward rising as high as 104°, associated with numbness and weak- ness of the legs and loss of reflexes, followed by paraplegia, may be present as a symptom of acute myelitis, traumatic or otherwise. (See chapter on Legs and Feet, part on Paraplegia.) A rise of several degrees of fever may come on after an epileptic convulsion. A febrile attack not rarely seen in children, yet not readily placed under the heading of any given disease, has been described by Donkiu and Goodhart, and the writer has also met with it quite frequently. This condition has been called gastro-pulmouary fever ; but as either pulmonary or gastric signs may be absent, this term does not apply to all cases. A previously healthy child is suddenly seized with marked fever, rapid respirations, and rales may be heard in its chest. There are often vomiting, headache, and drowsiness, with recovery taking place in several days. Often these attacks are associated with gastric catarrh, but sometimes this state is not present. Donkin states, and it is the writer's own experience, that they are apt to be produced by fright or excitement. In a case of the writer's the sight of an angry skunk attacking a pet dog produced a violent attack. Subnormal temperature of the body is seen as the result of any profound nervous shock, as after an accident or surgical opera- tion, or prolonged aniesthetization. It occurs, too, at the ending of the fever of croupous pneumonia and other febrile movements ending by crisis. It is also seen in severe cholera morbus and cholera Asiatica and sometimes in cholera infantum, and often is present either in the early part of the cold stage of intermittent malarial attacks or more commonly after the fever of the attack has fallen. Subnormal temperatures are also seen in some cases of con- fnsioual insanity, and of tubercular meningitis and hysteria. An important variety of subnormal temperature is that seen in the form of heat-stroke called heat-exhaustion, when, in place of fever, a condition of collapse is induced. Severe injury to the dorsal region of the spinal cord often produces a great fall of temperature. CHAPTER II. HEADACHE AND VERTIGO. The causes of headache — Digestive headache — Headaches due to the eyes — Head- aches due to cerebral gi'owths and abscess — Headaches due to syphilis — Head- aches complicating acute diseases. Headache is, of course, always a symptom and never a disease, and it arises from such widely different causes that it is impossible in this book to discuss all of them. Only the more common condi- tions resulting in its development can be considered, more particu- larly in relation to its diagnostic significance in serious pathological states. The most common cause of headache is probably disorder in the function of the digestive apparatus, the next most common cause is eye-strain in its various forms, and the third is nervous ex- haustion or neurasthenia with or without associated aujemia. These may be all considered as perversions of function causing headache — that is, the pain in the head may be termed a functional headache. Less frequently, but far more important from a diagnostic standpoint, is the headache seen in persons suffering from renal disease, brain- tumor, and meningitis in its various forms. The remaining causes of jjeadache in both of these classes are numerous, and some of them will be considered later; but the most important of the first class are the headaches of the gouty or rheumatic, and of the second class those of cranial periostitis, middle-ear disease, and acute inflamma- tions of the eye or in the jaw. Headaches depending upon disturbance of the digestive system are nearly always accompanied by evidences of such disorder, consist- ing in gastric or intestinal distress, belching, hiccoughing or vomiting, or even by diarrluen. Often there is a distinct history of the inges- tion of indigestible food or digestion-disturbing drink, but in other cases exposure to coM so congests the abdominal viscera that catarrh of the stomach and bowels is induced, and with it congestion of tlie liver followed by jaundice. The headache of disturbed digestion is nearly always frontal, and in many cases congestive to such an extent that the face may be flushed, or at least the intracranial circu- 432 THE MANIFESTATION OF DISEASE BY SYMPTOMS. latiou is so disdirbed that the patient is unable to lower the head, because such a posture increases the pain. Sucli eases are relieved by hot foot-baths, which relieve the congestion of the head ; nearly always by the act of vomiting, which should be iuduced if need be by an emetic or by putting the iiuger in the back of the throat. Vomiting makes such headaches very much worse for a time, owing to the congestion of the head in the efforts at vomiting, and this is an important point in diagnosis, for in renal disease or some other states the vomiting is sometimes so easily performed that no straining ensues. That disturbances of the digestive tube are capable of altering the intracranial circulation is proved by numerous facts. Thus Brunton quotes the experiments of Ludwig and Dogiel, who showed that moving the intestines by the finger introduced through an abdominal incision caused a great increase in the flow of blood through the car- otid arteries. Headache due to disorder of the digestion rarely ensues imme- diately after food is taken, since some time must elapse before the ingested material becomes changed into an irritating or toxic mass by fermentation or putrefactive processes. As a consequence several hours or even a day may pass without any discomfort in the head, after which time the full force of the headache develops. The head- aches of indigestion are, however, characterized by two important facts, viz., that they are not constant, and, second, that they are often relieved or prevented by the use of a purgative, even if constipation has not been present. Such headaches are very apt to be pulsating and accompanied by great nausea. Sometimes such a headache takes a form called migraine or hemicrania, a condition in which the pain is chiefly, if not entirely, unilateral, and there is associated with the pain early and more or less persistent hemianopsia. It is to be remembered, however, that in some cases of hemicrania of nervous origin the sickness at the stomach seems to be secondary to the severe pain in the head. Headaches resulting from digestive disturbance do not always de- pend entirely upon irritation of the stomach and bowel with reflex dis- turbance of the circulation and sensory nerves of the head, but upon the absorption of poisonous substances formed in the digestive tube. These poisons are usually formed only to be destroyed by the liver, or are developed in too small quantities to have any effect ; but no sooner do congestion of the liver and deficient biliary secretion HEADACHE AND VERTIGO. 433 ensue tbaQ they are formed in large amounts, and enter the general blood-stream, owing to the absence of antiseptic bile and the coin- cident or consequent constipation. As a result, we see very violent headache in jaundice due to catarrhal changes, particularly if the kidneys are not active in the elimination of toxic substances. Similar symptoms to those just described may occur in cases suf- fering from paroxysmal h^emoglobinuria, for in this state severe headache, nausea, vomiting, and persistent yawning are often present, with an icteroid discoloration of the skin. The reddish urine, pain in the liver, and sometimes an urticarial eruption will aid the diagnosis of this primary hsemoglobinuria. In other cases in which no jaundice is present violent headaches, which utterly incapacitate the patient, come on from autbiutoxica- tion. Thus a man apparently perfectly well goes to bed on a cer- tain night and wakes in the morning feeling a little more drowsy than usual. On rising he may feel a little stupid, and perhaps be slightly vertiginous, but is able to eat his breakfast as heartily as usual. In the course of a few hours the mental heaviness becomes more marked and a pain in the brow develops, which gradually gets worse and worse till it is unbearable. The ordinary remedies for neuralgic headache are futile, and he finds no relief until by the use of a purgative he removes the source of his intoxication, and his kidneys have time to eliminate the toxins already absorbed. Some- times vomiting comes to his relief, and the emptying of the stomach, produced by the efforts of vomiting, so stimulates his liver and intestines that the process of autointoxication ceases. Some of the intestinal poisons have been isolated by Brieger, Harnack, and others, and have a physiological action like many well-known drugs. Thus one produces effects like those of digitalis, another like those of helladonna, and a third like those of aconite. Pulsating pain and a slow, full pulse may indicate the absorption of the digitalis- like toxin ; a flushed face and hot, dry skin, the belladonna-like toxin ; and pallor, faintness, and a feei)le }>ulso, if no nausea is present, the presence of the aconite-like toxin. Persons suffering from headache of this type are nearly always much freer from discomfort in the head after such attacks than they have been for some time before. lirunton has also pointed out that digestive headaches are often associated with an objective and subjective sensation of increased intraocular tension and tenderness on the upper surface of the eye- ball, and the author has frequently confirmed this ol)servation. 434 THE MANIFESTATION OF DISEASE BY SYMPTOMS. The headache of eye-drain is usually due to insufficiency of the ocular muscles. Most commonly, according to Noyes, the externi (abductors) are the muscles which are the seat of the difficulty. Such headaches may be felt in any part of the head, but are most com- monly said to be in the occipital region. If, in association with such headache, immediately after or long after reading, there is blurred vision, pain in the muscles of the eye on suddenly moving the eye- ball, any tendency to congestion of the lids or hyperemia in the conjunctiva over the insertion of the muscle, the diagnosis of head- ache from eye-strain is practically certain. (See chapter on Eye.) Violent pain in the head may also be due to irritable retina and to astigmatism and spasm of tlie ciliary muscle. Acute inflammatory processes in any part of the eye may produce severe headache, par- ticularly iritis, the pain of which is very apt to be worse at night. Whether insufficiency of the ocular muscles or eye-strain can cause "sick headache" by reflex irritation is still undecided, but those oph- thalmologists who are inclined to carry the theory of refractive errors in the production of morbid symptoms to excess believe that it can. Violent headache is often produced by acute or chronic glaucoma, and is usually felt about the eyes or orbit. Often it is of a unilateral character, and the sharp, shooting pain causes a false diagnosis of neu- ralgia to be made, or in some cases the patient is thought to be suf- fering from migraine, because in addition to unilateral pain there are often nausea, vomiting, and pallor of the face. The examination of the eye will show glaucoma to be present. Quite similar symptoms may appear as the result of a foreign body lodged in the cornea. The headache associated with nervous exhaustion or neurasthenia may be superficial or deep ; that is to say, neuralgic or apparently within the skull. It is often associated with some dizziness and vertigo, and is nearly always occipital in character, more rarely ap- pearing over the brows. In addition to the pain, which is generally not very severe, there is often a sense of constriction about the head. Such a headache persists as long as a person who is overworked per- sists in fatiguing himself, and rapidly disappears when rest is taken. More rarely tlie pain in the head in neurasthenia is that of migraine, and is complicated by hemianopsia and hemicrania, often by a dilated pupil on the affected side, and flushing and pallor of one side of the iace. Headaches due to rheumatism are often quite severe, and are asso- ciated with much tenderness of the scalp or muscles covering the HE A DA CHE A XD VER TIG 0. 435 skull. Similar headaches, but more dull in character, are also seen iu persons suffering from phosphaturia, and are relieved by beuzoate of ammonium. A headache is a symptom very commonly seen in persons who are subject to the chloral-habit, and it may be general or limited to the forehead. It is commonly associated with vertigo, flushing of the face, and intense heaviness and drowsiness. Headache of a violent, bursting character may be produced by full doses of nitroglycerin, the salicylates, and quinine, and by the use of large quantities of tobacco. Leaving the headaches due to functional disturbances not asso- ciated with organic change, we pass to those due to organic disease. Headaches due to renal disease are of two classes, namely, they are an evidence of ursemia, or they are congestive and due to the high arterial tension so often seen as the result of chronic contracted kid- ney with its associated conditions of cardiac hypertrophy. Uraemic headache, as pointed out in the chapter on Vomiting, is often asso- ciated with nausea or vomiting of a persistent type, and sometimes with diarrhoea, for purging is an effort at elimination. The pain is not of the shooting, darting, or neuralgic type, but dull even if severe, and is often associated with a sensation of fulness in the head. Some- times the tendency to drowsiness is very marked, and, even if the patient does not sleep, he may seem on the verge of sleep all the time. These uneraic headaches may occur in any form of renal dis- ease, acute or chronic, which results in uraemia ; but, if the cause be chronic contracted kidney, there will be a high arterial pressure, and often a strongly beating iieart with an accentuated second sound. This form, with high arterial pressure, will often be relieved by full doses of nitroglycerin, which not only relieves the tension, but also produces an increased renal activity. Tlie urinary examination is of the utmost importance, and no surely correct diagnosis can be made in any case of suspected kidney trouble till this secretion has beeii examined and found abnormal. (See cliapter on Urine.) While headache is far less common as a symptom of diafufrs than of nephritis, it occurs in tiie former disease eitiier as a iluli pain with lassitude and depression of spirits or as violent neuralgia. ncadaciie which is constant, although it usually varies in degree, may be due to hrdin-iumor, and is one of the most important symj)- toms to be noted in the diagnosis of a case in which such a lesion is suspected. The pain is oflen worse at night, and is usually more 436 THE MANIFESTATION OF DISEASE BY SYMPTOMS. severe in persons suffering from tumor of the cerebellum than in cases in which the growth is in the cerebrum, probably because cere- bellar growths often cause effusion which produces pressure inside the skull. A tumor of the cerebral cortex, as a rule, produces more pain than one in the white matter deeper down. Meningeal growths are also apt to produce severe headache, but bony tumors of the skull often press upon the brain to an extraordinary degree without causing any symptoms. Headaches due to brain-tumor often have exacerbations with a regularity suggesting malarial disease, and, conversely, care should be taken not to mistake malarial headache for brain-tumor. After constant headache, the most valuable confirmatory evidence of brain-tumor is papillitis of the optic nerve, which is present in about 80 per cent, of the cases. There may also be vomiting, and convulsions if the growth be in the motor cortex. Local paralysis, indicating the position of the growth, may be entirely absent, or it may exist and yet utterly mislead the physiciau as to the focal area which is diseased, since cases are on record in which, for example, a hemiplegia has existed and at the post-mortem examination the growth has been found in the frontal lobes. Tumors of the base of the brain cause focal symptoms most commonly, and in addition to unilateral choked disk we find in many such cases ptosis from paralysis of the oculomotor nerve, disturbances in the functions of the trifacial nerve in its sensory filaments, so that painful tic (see chapter on Face and Head) or anaesthesia of the face may be present aud complete facial (Bell's) palsy may occur. If the hypoglossal nerve is affected by the pressure, the tongue is protruded to one side, it develops hemiatrophy, and disorders of speech result. Hirt points out that a tumor in the anterior fossa is apt to produce paralysis of the olfactory and oculo- motor nerves and the upper branch of the trifacial. A tumor in the pituitary body causes pressure on the chiasm with resulting amaurosis, ptosis from oculomotor palsy, and internal squint from paralysis of the abducens (sixth), anesthesia of the skin and muscles of the eye- brow, forehead, nose and eye, from involvement of the first division of the trifacial. A tumor of the middle fossa above the dura causes oculomotor palsy (ptosis), patheticus paralysis (downward deviation of the eyeball from paralysis of the superior oblique), amaurosis from pressure on the chiasm. On the other hand, if it is below the dura, the oculomotor, the pathetic, the abducens, and the fifth nerve are paralyzed. When tumors occur in the posterior fossa they cause HEADACHE AXD VERTIGO. 437 paralysis of the trifacial, facial, auditory, glosso-pharyngeal, vagus, spinal accessory, aud abducens, or, in other words, cause anaesthesia of the upper part of the face, facial paralysis, deafness, loss of taste, irregular cardiac action, loss of power in sterno-mastoid and trapezius muscles, and internal squint. Tumors of the lenticular and caudate nucleus, the interior portion of the thalamus, the corpus callosum, the fornix, choroid plexus, and of any part of the cerebellum except the vermiform process, may be present without any localizing signs. Still more localizing symptoms are early paralysis of the oculo- motor nerve from a lesion in the crus, hemianopsia in tumor of the occipital lobe, and tonic convulsions with preservation of conscious- ness and a staggering gait in tumor of the vermis of the cerebellum. Should amaurosis be present, very valuable data as to tlie position of the growth is to be had from a study of the functions of the eye. If the pupils react properly to light, this shows that the optic nerve and tract are intact, or, in other words, that the ocular reflex arc is perfect, and that the lesion must be in the ocular centres further back. On the other hand, if the reflex is absent, the growth is prob. ably in the nerve or tract. (See chapter on the Eye.) The failure of a pupillary reaction may, however, depend upon amaurosis from lateral hemianopsia, in which case we examine the patient for what is known as " Wernicke's sign of hemiopic pupil- lary inaction." This is done by throwing the light by the ophthal- moscope so that it falls upon the blind half of the retina. If the pupil does not react, we have in all probability a lesion of the optic tract of that side ; whereas, if the pupil does react, we have evidence that the tract is intact and there must l)e a bilateral lesion of the optic radiations of the occipital lobes, or in the centre of vision in the cortex. (Sec chapter on Kye.) Other general symptoms of brain-tumor are slow breathing, par- ticularly when the patient sleeps ; a slow pulse, and, as the growth increases, symptoms of cerebral compression. Care should be taken in cases of constant severe headache that it be not thought due to brain-tumor until the possibility of its being due to syphilitic arteritis is excluded, for the same mental depression, sharp exacer!)ations of pain, and an increase of pain at night, also occur in this state. There is often nocturnal delirium in these cases. In arteritis due to syphilis the jKiin is usually diffuse, whereas in tumor or syphilitic gumma it may l)e localized. Optic neuritis, if present, makes the diagnosis of tumor certain. The chief symptoms 438 THE MANIFESTATION OF DISEASE BY SYMPTOMS. of syphilitic arteritis are headaclie, giddiness, weakness of groups of muscles, difficulty of speech so that words are dropped out, and very commonly symptoms of general paresis develop. It is, however, often impossible to separate headache due to cerebral syphilis from that due to chrouic meningitis or cerebral tumor due to other causes, except by the history of specific infection or manifestations of this disorder in scars or other external signs of syphilis. Violent headache is the most marked symptom of brain-abscess ; but focal symptoms — that is, localized palsy pointing to the area of the abscess — are very often absent, although the localizing symp- toms which have just been described as due to tumor may, of course, be due to abscess if it is so placed as to press on nerve-tracts or centres. The rises of temperature which frequently occur in cerebral ab- scess are also indicative of the presence of pus, while the more rapid course of the disease, often only one or two weeks, points to abscess rather than tumor. Further than this, choked disk is rare in abscess and common in cases of tumor. The difficulty of separating the headache of brain-tumor from that due to brain-abscess is very great, for the symptoms with the head- ache are almost if not quite identical in both cases. One of the most important of the differential points is the history of an injury to the head or of the presence of an infecting focus, which could have caused cerebral abscess. In some cases of acute cerebral abscess, particularly in children, there is a curious tendency to bore the head into the pillow, or, if the child is still about, the head is rubbed or butted into the wall or against tlie body of the nurse. These symptoms are, however, absent in the slow, insidious forms. When the physician has made a diagnosis of cerebral abscess from the headache and associated symptoms, he must not be misled into a reversal of his diagnosis by marked improvement in the patient, who may so far recover as to go back to his occupation, for it some- times happens that a remission or latent period develops in the sub- acute forms of abscess. During this apparent remission, however, the temperature is rarely constantly normal, and the patient is any- thing but well, and chilly sensations may be present. Severe headache well diffused over the skull, coming on rather rapidly and associated with fever, stiffness of the back of the neck, vomiting, photophobia, delirium, and, finally, stupor and paralysis, HEADACHE AXD VERTIGO. 439 is probably clue to meningitis or to tubercular meningitis, effusion at the base of the brain, or, more rarely, to the onset of a severe attack of one of the acute infectious diseases. If the disease be tubercular meningitis, the head-pains will often be paroxysmal in character, so that the patient will at intervals of varying length give vent to sharp cries, evidently due to a sudden dart of j)ain. Vomiting may also be present and ocular symptoms develop, such as ptosis, strabismus, and unequal pupils, with a slug- gish reaction. The febrile movement will be irregular, now high, Fig. 185 Comniunicafion through- parietal foramen ivith externalveins of skiUl. Ext. jugular vein Int. jugular vein Diagram showing the comtnuaications existing between the superior longitudinal and lateral sinuses and the external veins, indicated in the figure by *. (Leube.) then very low ; the temper peevish, if consciousness is present ; and the skin pale and transparent. In the severe and rapid cases of tubercular meningitis marked delirium comes on, the patient picks the bedclothes, and there are tenderness and stiffness of the nape of the neck. Puhnonary signs of tubi-rculous disease are often present. Care must be taken that the case is not mistaken for and thought to be typhoid fever, which it may closely resemble in its early stages when iieadache, malaise, languor, and remitting delirium are present. 440 THE MANIFESTATION OF DISEASE BY SYMPTOMS. The symptoms of meuingitis are, however, closely followed by those due to thrombosis of the cerebral sinuses, so closely, indeed, that only the presence of the typical signs of such occlusions can determine the diagnosis. Thus, if the superior longitudiual sinus is affected by thrombosis, there may be epistaxis from distention of the nasal veins, and the temporal veins will be swollen and the near-by tissues oedema- tous through their close connections with the sinus through the emis- sary veins of Santorini, which escape from the skull by way of the parietal foramina. (Fig. 185.) In children there is usually in such cases bulging of the fontanelles and heaviness. Somnolence or deli- rium may be present with many of the characteristic symptoms of meningitis. This condition usually arises in connection with chronic exhausting diseases, such as long-continued diarrhoea and the con- tinued fevers. Thrombosis of the cavernous sinus is usually accompanied by quite typical symptoms. There is oedema of the eyelids and finally of the entire side of the face on the side of the affected sinus, but this facial symptom may be absent or very fleeting in its duration. Sometimes there is exophthalraia, and if the thrombus is septic a phlegmonous inflammation of the orbital connective tissue may occur. These symptoms are due to the communication between the sinus and the ophthalmic veins. Finally, as pointed out in the chapter on the Face and Head and on the Eye, paralysis of the oculo- motor nerve, the ophthalmic branch of the fifth nerve and of the adducens and patheticus may occur, as these nerves pass through the cavernous sinus or in its walls. Nearly always thrombosis of the cav- ernous sinus results from some diseased processes near-by, as in disease of the middle ear and mastoid. Sometimes the affection is bilateral- If the lateral sinus is affected by thrombosis, there is usually marked oedema back of the ear, owing to the clot extending to the small veins of the scalp, which pass through the mastoid and pos- terior condyloid foramina. The external jugular vein on the affected side is partly collapsed particularly on full inspiration (Gerhardt's symptom). Rarely this vein may be unduly distended (Fig. 186). Thrombosis of the lateral sinus occurs far more frequently than that of the other sinuses. Suppurative otitis is its most common cause, and agonizing earache is therefore a symptom often associated with it. Not only may cerebral thrombosis present symptoms resembling those of meniuffitis, but in addition those of cerebral abscess. Violent headache with vertigo, staggering, and confusion of thought, HEADACHE AXD VERTIGO. 441 followed by uucousclousness, may follow meningeal hemorrhage due to disease of the bloodvessel.*, which are ruptured by some strain or by increased blood-pressure under the influence of stimulants. Hemi- plegia or localized spasms may be present. The patient may survive several days in severe case?, or may recover if the hemorrhage is small ; but usually a hemorrhage large enough to cause marked symptoms is large enough to cause death. Fig. 1S6. Communiaition with veins at hack of neck Diagram showing the communication existing Ixitween the lateral and cavernous sinuses and the external veins, indicatelf larks danger, vertigo always produces great discomfort, if not fear. Vertigo arises from the patient being subjeoted to a whirling motion, from rough sea-voy- ages, and from indigestion, deficient circulation, or excessive cerebral 444 THE MANIFESTATION OF DISEASE BY SYMPTOMS. congestion. Often it is due to the cerebral anreraia arising from ex- cessive hemorrhage. When it arises from indigestion it is probably due to reflex irritation, and perhaps to the absorption of toxic materials. Vertigo as a symptom has a far more serious significance when it arises from organic disease. The most common lesions which cause it are middle-ear disease, Meniere's disease, tumors of the cerebellum, of the pons, of the crura cerebri, and the corpora quadrigemina. Vertigo also is not only a premonitory sign of an epileptic attack, but in the epileptic state called petit mal or minor epilepsy it is often the only symptom. In persons with atheromatous arteries it is very common, and sometimes it is a persistent symptom for some days before an apoplectic seizure. It is also present in disseminated sclerosis. Finally, many drugs, su'ch as quinine and the salicylates, may produce it. As the diagnostic points connected with most of the lesions here named are discussed elsewhere in this book, only Meniere's disease will be mentioned at this place. In addition to vertigo the charac- teristic symptoms of Meniere's disease are vomiting, noises in the ears, and, finally, deafness. The vertigo may be so severe that the patient falls to the ground. Aural examinations are usually futile in dis- covering any cause. Some authorities believe the disease to be due to a neurosis of the vasomotor nerves supplying the semicircular canals. An unknown form of vertigo in America, the paralyzing vertigo of Switzerland, described by Gerlic, is a paroxysmal vertigo with great loss of power in the limbs, partial ptosis, and preserved con- sciousness. CHAPTER III. COMA OR UXCOXSCIOUSXESS. Coma is a condition of unconsciousness or insensibility from which the patient can be roused but partially or not at all, and it may arise from injuries to the head, while the patient is in other- wise perfect health, which injuries produce laceration of the brain- substance, cerebral dr meningeal hemorrhage, or concussion. Again, it may be due to the influence of certain poisons, as alcohol, opium, chloral, cannabis indica, very large amounts of the bromides, or poi- sonous doses of other narcotics. Thirdly, it may arise from auto- intoxication, as in uraemia resulting from renal disease ; in cases of profound exhausting disease, like typhoid fever or ulcerative endo- carditis; in cases of diabetes, or from acute yellow atrophy of the liver and pernicious malarial fever. Fourth, as a coincident symp- tom or sequel of hemorrhage into the brain (apoplexy), as the result of an epileptic attack, (jf a cerebral embolism or thrombosis, of throm- bosis of the cerebral sinuses, of cerebral abscess, of pachymeningitis, leptomeningitis, or cerebro-spinal meningitis, of cerebral syphilis, of general paralysis, multiple sclerosis, and heat-stroke. The various points in connection with the diagnosis of coma from head-injuries are to be found in surgical treatises, and the history of a head-injury or the very presence of any injuries to the head is an important point to be sought after in the diagnosis. Care should be taken, however, that any head-injuries found to be present are not the result of a fall due to the onset of sudden unconsciousness, rather than that thev are the cause of the coma. The coma of «CMlegia; one side tossed, the other re- maining motionless. 6. Respiration stertorous, the lips being in- flated on one side on expiration. 7. Facial fMlsy. 8. UnconsciovLsness complete. The smell of alcohol in the breath is no guide, as acute alcoholism may have caused the rupture of a cerebral bloodvessel. 29 450 THE MANIFESTATION OF DISEASE BY SYMPTOMS. Coma due to cerebral softening, following embolism or thrombosis, has no signs other than those discussed iu the diagnosis of these lesions in connection with hemiplegia (which see). Coma due to thrombosis of the sinuses of the brain is accompanied by the follow- ing diagnostic symptoms, namely, irritation or paralysis of the cranial nerves resulting in strabismus, nystagmus, and lockjaw, stiffness of the neck, and clonic spasms. If the cavernous sinus is thrombo.'^ed, there will generally be found stasis of the veins in the eye, which means retinal congestion. The eyeball may be protruded, the eye- lids swollen, and perhaps loss of function in the oculomotor nerve may be present, causing ptosis, and, if the abducens is affected, caus- ing internal strabismus from paralysis of tiie external rectus. If the transverse sinus is involved, there will probably be oedema behind the ear, and, if the petrosal sinus or internal jugular be obstructed, the proximal part of the vein collapses. Thrombosis of the superior longitudinal sinus causes epistaxis and engorgement of the temporal veins. Thrombosis of any of these sinuses, however, may be present without these signs. Coma due to subdural hemorrhage (pachymen- ingitis interna hemorrhagica) is peculiar in the fact that its onset is usually very slow, and the signs of nervous irritation last a long time and are quite violent, often amounting to epileptic paroxysms. Commonly, too, there will be rigidity of one limb, but the cranial nerves usually escape. The coma usually follows these signs, and the condition is peculiarly common in the chronic insane and in paretic dements. Coma from cerebral abscess is accompanied by symptoms closely resembling those of acute meningitis. The patient is dull and delir- ious ; has headache, fever, and often has a hyperpyrexia. The sen- sibility becomes less and less, and deepens into the coma which ends in death if relief is not given. The localizing symptoms of paral- ysis may indicate that a lesion is in a certain part of the brain; but generally these signs are absent, because cerebral abscess is usually in the frontal lobes. If there is a history of injury, purulent otitis, infectious disease involving other parts, such as septicaemia from wounds or empyema, and if there are vertigo, vomiting and headache, fever, and an absence of choked disk of the optic nerve, the diagnosis is probably cerebral abscess; but a long duration of months is no sign that it is not abscess, as these cases often run a very prolonged course. COMA OR UNCONSCIOUSNESS. 451 The coma of purulent lepto-meningitis resembles that of abscess in many of its associated symptoms, bnt the intense headache, the rapid development of delirium and unconsciousness, the stiffness of the neck, the optic neuritis and disturbed movements of the ocular muscles, combiued with the absence of a history of septic absorption, may make a differential diagnosis possible. Purulent lepto-menin- gitis is rare, but it sometimes occurs in association with croupous pneumonia, and the presence of this disease will point to the cause of the coma. The coma due to epidemic cerebrospinal meningitis is diagnosed by the characteristic rigidity of the neck, excessive headache preceding the unconsciousness, the disturbances of the cranial nerves producing strabismus, unilateral or bilateral ptosis, nystagmus, impaired pupillary reaction, mydriasis and myosis. The face is often painfully distorted. The presence of an epidemic, of course, makes the diagnosis clear. Cerebral syphilis may result in the production of coma by pro- ducing hemorrhage, embolism, arteritis, tumor of the brain, or ahnost any other lesion, and its diagnosis as the cause of an attack of coma is not easy. Of course, a history of syphilitic infection and the presence of symptoms of this condition in a patient who is too young to have secondary arterial changes from age render the probability of syphilis as a cause very great. Scars on the skin (see chapter on Skin) may show specific taint. When coma results from general parali/sis it usually succeeds the peculiar epileptic attacks which come on late in that disease, and the history of delusions, tremor of the hands, peculiar speech, loss of the reflexes, with earlier milder attacks, like the one before us, com- bined witli the age of the patient, render a diagnosis possible. Practically identical symptoms may attend the development of coma from multiple sclerosis, and without the history of the latter affection the diagnosis may be impossible. If this history shows a spastic gait and intention-tremor, nystagmus, mental weakness, and heightened reflexes, the probability of the attack being due to mul- tiple sclerosis is increased. Coma is sometimes seen as a later manifestation of Addison^s disease, and it often develops very suddenly. Heat-stroke produces coma as one of its almost constant symp- toms. The history of exposure to lieat and the hyperpyrexia are the two diagnostic points of importance. (See Fever.) 452 THE MANIFESTATION OF DISEASE BY SYMPTOMS. Sudden uucousciousness may arise from heart-failure due to dis- ease or fright ; we call this fainting. Frequent attacks of this char- acter should cause the physician to listen to the heart to discover if there is valvular disease, particularly aortic stenosis and fatty heart, and he should be on the outlook for reual difficulty. Sometimes sudden uucousciousness will be due to petil mal or miuor epilepsy. CHAPTER IV.^ CONVULSIONS OR GENERAL SPASMS. The convulsions of epilepsy in its various forms — Of infancy — Of hysteria — Tetanic convulsions — Spasms — Chorea. A CONVULSION is a condition in which by reason of sudden tonic or clonic contractions of groups of muscles the body in whole or in part is thrown into spasmodic movements. Convulsions can be divided into those which are clonic or epileptiform and ihose which are tonic or tetanic. Further, it is a general rule that convulsions which are epileptiform or clonic in character have their origin in the cerebral cortex, while those of tetanic or rigid type arise from excita- tion of the motor tracts in the spinal cord. The clonic variety of convulsions are represented by idiopathic, traumatic, reflex, and syphi- litic epilepsy, hysterical convulsions of an epileptic type, ursemic convulsions, and those convulsions which arise from the presence of growths or other sources of irritation in the cerebral cortex. Certain poisons may also rarely produce such attacks, notably lead and alcohol, and sometimes malingerers imitate very successfully the epi- leptic paroxysm. The convulsion in epilepsy is characterized in some cases by the primary appearance of an aura — that is, a sensation in some part of the body, which the patient discovers comes on before each convul- sion. This aura may be of any character and appear in any part. Most commonly it is sensory, and is as if a cloud or wave was pass- ing up the body to the head. As the sensation reaches the head, the patient may utter the peculiar epileptic cry or sigh, and with this sound the patient becomes rigid from momentary tonic sjva-^in of the muscles. This spasm now relaxes for an instant, and then the patient's muscles pass into a state of alternate relaxation and contrac- tion which throws the patient's body from one place to another. The primary tonic spasm of the face produces risus sardonicus in some cases; the head is often drawn to one side, the eyes commonly turned to the same side, and the lower jaw locked tightly against the upper jaw. The arms arc strongly flexed at the elbows, the hands ' For local spasms, see chapters dealing with face and head, hand and nriu, and feet and legs. 454 THE MANIFESTATION OF DISEASE BY SYMPTOMS. flexed at the wrist, and the fingers bent into the palm of the hand with great force. As a rule, the evidences of the powerful flexors over- coming the extensor muscles predominate; but sometimes the reverse is the case, and forcible, rigid extension of the parts affected takes place. The duration of these tonic contractions rarely exceeds two minutes, and in most cases is limited to but a few seconds. It is followed by the clonic spasms, already described, which are ushered in by more or less violent tossiugs, but whose onset is fore- warned by peculiar vibratory thrills, which run through all the affected muscles. The eyelids tremble, the body changes its position ever so slightly, and then, as if the vibrations gained greater and greater power with each moment, the fibrillary tremors give way to muscular con- traction. The expression of the face, which in the preceding stage was set and firm, is now constantly changed by the movements of the facial muscles ; the jaws, no longer locked together, are gnashed and crunched one upon the other ; the tongue is alternately pro- truded and drawn back, and, as a consequence, is often caught between the teeth and lacerated. The excessive movements of the muscles of mastication force the increased quantities of liquid secreted by the salivary glands from the mouth in the form of froth, which is often stained with blood by reason of the injuries to the tongue. The constancy of the convulsive movements now becomes less and less marked ; well-developed remissions occur between each toss of the body, until the movements cease entirely; but it should be con- stantly borne in mind that the prolongation of the remissions does not produce any decrease in the severity of the intervening spasm, the final spasm often being even more violent than the first. The intense discoloration of the face begins to pass away as soon as the remissions, by their length, permit the blood to be oxygen- ated, its disappearance being temporarily arrested by each paroxysm. Finally, the spasms having ceased, the patient lies before us relaxed, unconscious, and exhausted, and passes into a deep sleep or coma, which lasts a variable length of time, and from which he cannot be aroused, except very rarely, and then with great difficulty. When one part of the body is involved in an epileptic paroxysm, the rest of it escaping, the condition is one of Jacksonian epilepsy. By far the most important of its peculiar signs is the character of the onset, which always begins, in the typical Jacksonian form, in some peripheral portion of the body, and most frequently in the muscles of the thumb or hand, so that for the moment the convul- CONVULSIONS OR GENERAL SPASMS. 455 sive movements are localized. They may remain localized at the point of origin, or immediately diffuse themselves over muscle after muscle until all the arm, leg, or other groups of muscles are in- volved. It is of the greatest importance, however, that the reader should keep the aura of an attack separated in his mind from the onset, remembering that the term onset is here used by the writer to designate the beginning of the period following the aura, if there be one. Jacksooiau epilepsy may be of almost any severity. In rare cases only one muscle may suffer throughout an entire attack, but in others the entire body may be at last convulsed. There may or may not be loss of consciousness, its presence or absence being dependent upon the seat of the lesion in the brain and the severity of the attack. In those instances in which only a few localized muscles are involved consciousness is more commonly preserved than lost. Typical Jacksonian epilepsy may develop in the course of general paresis. Epileptiform convulsions may be divided into two classes, in one of which the patient suffers from a single convulsion, the result of a cerebral hemorrhage, and in the other the changes produced by the hemorrhage result in epileptic attacks. When the con- vulsion occurs at the time of an apoplectic effusion it is generally Jacksonian in character ; that is to say, one muscle or a group of muscles is involved, or, if nf)t this, the attack is, at most, only uni- lateral. Further than this, it is always associated with the symp- toms of apoplexy as generally seen, for there are inequality of the pupils, drawing of the face to one side, and a consequent hemiplegia which lasts indefinitely. Of the attack itself it may be said that, so far as the movements are concerned, they differ in no way from those of the true epileptic seizure; but it sliould be remembered that hemiplegia often follows ordinary idio])athic e|)ilepsies ; so that the fact that hemiplegia is permanent, and is not temporary, is more of a sign that the attack is due to hemorrhage than the actual paralysis is. It should also be remembered that apoplexy may complicate epilepsy, being produced by the convulsion. In a considerable num- ber of cases of epilepsy it will be found that the convulsions succeeded an attack of paralysis, which was sudden in onset and possessed the charadcristics of vascular rupture. In some persons the history of this attack is very indistinct, owing to its occurrence in early life; while in others the paralysis has been so slight or temporary as not to bear any relation in the mind of the j)ati('nt with the convulsive 456 THE MANIFESTATION OF DISEASE BY SYMPTOMS. seizures following, which, in many cases, do not occur for some time after. The attack may not leave a trace of loss of power behind it, but the convulsions continue, and closely resemble the so-cal'ed idio- pathic form of the disease. The writer also wishes to call attention to the fact that the palsy and convulsions are not always due to hemorrhage, but to any pathological cerebral change. Heart disease, by causing embolism, may bring them on, and rheumatism, syphilis, and puerperal sepsis may all produce a softening of the cortex, with an epileptic state following the paralysis. We cau very readily divide post-hemiplegic epilepsy into two classes, for we find that in about one-half of the cases the convul- sion occurs along with the paralysis, and then follows at intervals, while in the other half the paralysis is not followed by convulsive seizures for weeks, months, or years. Post-hemiplegic epilepsy may occur at any age, but there can be no doubt that it far more commonly occurs in children than in adults. In at least two-thirds of the cases the onset is before five years of age, aud in nearly one-half it is during the first two years of life. Very curious results are reached if the statistics of the affection are analyzed — results which are quite unexplainable unless by hypothe- sis. Indeed, they tend to overturn many of our preconceived ideas. Thus, it will be found that in the cases which date from infancy females are twice as numerous as males, but in cases after five years of age there is no difference between the frequency in the two sexes. One of the theories of these infantile cases has been that they were produced by the use of instruments during labor, aud repeated post- mortem examinations have confirmed the possibility of this occur- rence. On the other hand, every obstetrician knows that the birth of a boy generally means a more difficult labor than that of a girl, owing to the greater size of the head in the male child. A priori reasoning Avould seem to show, therefore, that the heads of male children would, accordingly, have instruments applied most fre- quently, and consequently that infantile cerebral trouble would be the result more commonly in males than in females ; but, as has been said, this conclusion is contradicted by the facts. Another symptom of great interest is that the paralysis in tlie infantile cases is more frequently on the left side than the right, but after the fifth year it is equally common on both sides. The writer has already spoken of the fact that the convulsions may occur along with the first attack of paralysis, and continue, or that CONVULSIONS OR GENERAL SPASMS. 457 an interval may occur between the attack and the subsequent par- oxysm. The chronic recurrent fits date from the onset in about one- third of the cases, but it is not uncommon for the paralysis to occur in infancy and the epilepsy to begin at puberty. It would seem that cells injured in early life may lay undisturbed till the increased de- mands of maturity call them out into diseased action. This prolonged interval occurring so commonly in children separates them from adults in this disease, for in the latter class it is very rare for the epilepsy to be delayed for more than one year. A distinct aura is present in about five-sixths of the cases, and is consequently far more frequent than in the ordinary idiopathic dis- order. When the reader considers the etiology of this affection it will be clear to him that these conditions are virtually forms of 'Jacksouian epilepsy so called, at least so far as the causative lesions are concerned. The frequency with which post-hemiplegic epilepsy comes on in the hemiplegia of childhood has been very recently studied, and the conclusion reached that its occurrence is quite common. Thus in Osier's cases twenty children out of ninety-seven suffered from it. In the eighty cases collected by Gaudard eleven children had hcmi- plegic epilepsy, and sixty-six children out of one hundred cases col- lected by Wallenburg were epileptic after hemiplegia. In another series of cases collected by Osier fifteen children out of twenty- three were thus affected. Syphilitic epilepsy is only one of the many nervous aff'ections which afflict those who may be so unfortunate as to contract this disease. There can be no doubt that syphilis produces an enormous amount of epilepsy, and the presence of ej)ilepsy in a person in whom the slightest suspicion of a specific taint exists should cause him to be instantly placed under antisyphilitic treatment. That this is true is evidenced by the statements of the foremost neurologists the world has ever known, for we find no less noted a writer than Charcot stating that epilepsy is the most frequent manifestation of cerebral syphilis, and the equally eminent syphilograi)her, Fouruier, has insisted most strongly on this point, as have also Bravais and M. Lagneau. In England, Hughlings-Jackson, Broadbet, Todd, and Buzzard have promulgated this doctrine, and in America AVeir Mitciiell, Sj)it/ka, Wood, and Carter Gray have recorded their belief in it, as have also Nothnagel and many equally eminent Germans. Indeed, it would be difficult to name any one statement in medicine which receives more widespread assent on all sides than does this. 458 THE MANIFESTATION OF DISEASE BY SYMPTOMS. The symptoms of syphilitic epilepsy really differ in no way from those of the simple idiopathic variety, but some points peculiar to this form of the affection are well worthy of attention. In 118 cases of syphilitic epilepsy Echeverria found the symptoms of headache in forty-five males aud thirty-eight females, or 70.30 per cent, of them all. In fifty-nine patients praecordial pain was found in twenty-seven males and thirty-two females, or 50 per cent, of the whole number of cases. Of the eighty-three patients with cephalalgia ten males and sixteen females had parietal pain, and eleven males aud eight females suffered from pain in the temples, while nine males aud seven females suf- fered from occipital pain. In the remaining twenty-two cases the headache was felt all over the head. The peculiarity of the cephalalgia of syphilis, when complicated with epilepsy, is the constancy with which it annoys or agonizes the patient, always being present to some extent, and frequently exacerbated toward nightfall or during the night, generally getting worse until the con- vulsion breaks forth, or it may in some instances abate as the storm approaches. Indeed, many syphilographers believe this to be the rule rather than the exception. There is certainly something very typical about the syphilitic headache which, nevertheless, baffles the descriptions that one would like to give of it. Ouce seen it can rarely be mistaken for anything else, and even the first view of such a case must impress the careful observer with several salient points. The face, one notices, expresses constant suffering, or at least distress and weariness, and the unrelenting character of the pain seems to crush the patient's vitality and liveliness with an iron heel. If spoken to, the man, who has been resting his head on the hands, will either answer slowly and painfully in monosyllables, or, gradually raising the face to that of the questioner, give an answer, and ouce more return to his former position. These symptoms are not, of course, pathognomonic, but they are certainly characteristic. The pain, too, is in other ways peculiar, and Charcot has expressed the opinion that the crossed character of the pain in this disease is of value, as it points to the motor zone. Indeed, he regards this headache as typical of the disease, particularly when it is, as it gen- erally is, bilateral ; that is, in both temples or both occipital regions at the same time. In the place of the headache we may have, as prodromal symp- CONVULSIONS OB GENERAL SPASMS. 459 toms, slight loss of memory, unwonted slowness of speech, general lassitude, and especially a lack of willingness to make niental exer- tion. Somnolence may be excessive, and, if any of these symptoms are seen in a person whose history is syphilitic, they should be re- garded as warnings of an approaching crisis of epilepsy or of some other cerebral disorder. The optic disks should be carefully exam- ined, for in many, but not all, cases evidence of brain disease may be noted in the eye. This is particularly true of syphilitic epilepsy as contrasted with its other forms. There is also one symptom which may occur early in syphilitic epilepsy, or sometimes only late in the disease, namely, repeated partial, passing palsies, which, while they may be in some cases hys- terical, are in the syphilitic almost pathognomonic of brarfi-involve- ment — a momentary weakness of one arm ; a slight drawing of the face to one side, which disappears in a few hours ; a temporary drag- ging of the toe ; a partial aphasia W'hich appears and disappears ; a squint which to-morrow leaves no trace behind it. A symptom whicii has been asserted as being frequent in this disease is the com- mon occurrence of nocturnal attacks; indeed, cases have been reported by Charcot and Lagneau in which this was the case, but there are similar instances, by the score, in ordinary idiopathic cases. In syphilitic epilepsy there are often well-marked psychical dis- tur!)ances with incomplete palsies, which, curiously enough, rarely involve the cranial nerves, as has been particularly noted by lieub- ner; or there may be an excess of psychical disturbance with a minor epileptic convulsion, and with involvement of the basal cranial nerves. It is important to determine whether idiopathic epilepsy can be separated from that due to syphilis simply by the symptoms. Of course, this is a very difficult question to decide ; but the answer to a question of this character ought to be that, so far as the convulsion itself is concerned, it is not possible to separate them. If, however, we can obtain any history, the matter becomes nuich more simple. It is characteristi(.' of syphilis to have severe darting or aching pains in the tibite, particularly at night ; and it is also char;;icteristic of syi)h- ilitic epilepsy to have severe frontal headache before the attack, while in idiopathic epilepsy this pain generally follows j;he seizure. Fournier, in his lectures on epilepsy, in the Loiivain, in Paris, in 1875, gave a summary of his views as follows : 1. In syphilitic epilepsy there is nearly always absence of tiie shrill cry at the onset, so characteristic of the idiopathic variety. 460 THE MANIFESTATION OF DISEASE BY SYMPTOMS. 2. There is frequently paralysis immediately after the attacks. 3. The seizure is incomplete or unilateral in character. 4. Attacks constantly increase in severity. A therapeutic point, which may be used with the greatest suc- cess, is the administration of iodide of potassium in large doses. If the epilepsy be syphilitic, it will rapidly become less severe, and enormous amounts of the drug will be borne with impunity. As much as 450 grains in twenty-four hours will often do good. It has been thought by some that the mental hebetude between the attacks is greater in syphilitics than in others. This depends very largely on the area of the cerebrum iuv^olved, and not upon the disease itself. Of course, if there is a history of a chancre or any syphilitic scars or erosions are to be seen, the diagnosis is manifest. It is very common in syphilitic epilepsy to find that the attacks are followed by prolonged attacks of paralysis, not due so much to the exhaustion of the centres as to the irritation produced by the gumma or the inflammation which sometimes springs up around it. It is also a noteworthy fact that the paralysis most commonly seen involves the oculomotor, abducens, and patheticns, nerves. The diagnosis of syphilitic epilepsy from the idiopathic form is of the utmost importance, since the ultimate result must be largely gov- erned by the cause. Dowes has analyzed no less than 274 cases in order to discover any useful points in this respect. He insists, as the writer has already done, that epileptic attacks beginning after thirty years of age are almost surely syphilitic, particularly if no history of traumatism or heredity is present. It is also found that, if some degree of mental alienation is present between the parox- ysms, it will generally yield to specific remedies. Cyanosis is less frequent, and pallor is more common in syphilitic epilepsy than in the ordinary disease. The convulsions of an eruptive fever differ from the true epileptic attack very slightly indeed. It is only by the history of the patient and by waiting for developments that we can determine which is which, for as soon as the eruption or high temperature of an exanthem occurs the character of the attack is evident. Epileptic convulsive disorders may arise owing to the action of a very large number of toxic substances, of which the writer shall here consider only a few, as an enumeration of all of them is mani- festly impossible. CONVULSIONS OR GENERAL SPASMS. 461 Alcoholic epilepsy consists of two distinct varieties produced by overindulgence in intoxicating drinks. In one of these the convul- sions are symptomatic of acute poisoning, and come on during a drunken orgy, or immediately after a single large draught of liquor. In the second variety the convulsion does not origcinate while there is alcohol in the blood, but in the intervals between the attacks of delirium tremens resulting from chronic excessive alcoholic indul- gence. Under these circumstances the paroxysms are generally accompanied by hallucinations or by dementia or imbecility. In the alcoholic convulsion the symptoms may closely resemble those of true epilepsy, and not rarely the attack is ushered in by headache, gastric embarrassment, disorders of vision, and excessive tremors, or some similar prodrome which may be looked upon as partaking of the nature of an aura. As a general rule, these alcoholic convulsions occur in paroxysms — two, three, four, or more, one after the other, at intervals of a few minutes. Not only may grand mal be closely simulated by alcoholic epilepsy, but simple vertigo or true petit mal may exist, either alone or associated with major convulsions. Alcoholic epilepsy is often associated with hallucinations, especially of terror, and not rarely is followed for days by a certain degree of mental disturbance. Rather curiously these cerebral disturbance, result rather in suicidal than homicidal tendencies, which is just the reverse of the insanity following simi)le epilepsy. It is very impor- tant that the reader remember that alcoholism in producing epilepsy very frequently produces a permanent nervous disorder which the withdrawal of the poison will not remove. The symptoms of an urfemic convulsion will be spoken of further when studying its differential diagnosis in connection with epilepsy. As some cases of sudden epileptiform convulsions are apt to result in an official investigation as to their cause, and as the character of the treatment of the case before death may influence the question of life and death for the accused very greatly, it is well for the physician to bear in mind that certain drugs when taken in poisonous doses produce well-developed epileptic convulsions. This is particularly true of the so-called cardiac sedatives or depressants, such as aconite, veratruni viride, sabadilla, hydrocyanic acid, and one or two similar substances. Suffice it to say that experimental researches have proved that they act by disordering the cerebral circulation. The symptoms of epilepsy due to chronic poisoning by lead are chiefly as follows : The man, apparently in his usual health, or 462 THE MANIFESTATION OF DISEASE BY SYMPTOMS. who has had for a few days a feeling of weight in the head, or lieadache, is suddenly seized with most violent convulsions, which are often fatal, and which during their presence resemble ordinary epilepsy so closely as not to be separated from it. They end in coma, and are separated from each other by intervals of nervousness and disquiet. In some cases one convulsion follows the other so rapidly that death ensues from exhaustion, but in much more rare instances the attacks may resemble Jacksonian epilepsy very closely, and there may be no loss of consciousness. If such a condition occur, it is almost sure to be followed by a more violent fit. The attacks are not preceded by any aura whatever, but previous to the head- ache, already mentioned, the patient may have had amaurosis, and ophthalmoscopic examination of the eyes may show choked disk and neuritis of the optic nerve. As a general rule, such cases are fatal, but they may recover under careful treatment. Malarial epilepsy is an uncommon disorder, even in countries and regions which are notoriously malarial, but it has undoubtedly occurred, particularly in the southern part of the United States and in Brazil. The only cases which the writer can find recorded are by American or English observers, namely, Jacobi, Payne, and Hamil- ton. The latter gives but a passing glance at the subject, and the articles of the others the author has not been able to obtain ; so that he knows them solely by reputation. In Hamilton's case, a young man, who had lived for many years in an exceedingly malarious re- gion, had more or less periodic epileptic attacks, attended by great preliminary rise of temperature and intense congestion of the face and head. He was unusually somnolent, and in the intervals fre- quently suffered from facial neuralgia. Change of the place of habitation and the use of quinine removed the disease entirely. The differential diagnosis between idiopathic epilepsy, that which is due to demonstrable cause, and the diseases which resemble it, is quite possible in many cases. Undoubtedly the most similar convulsive condition that we have is that known as hysteria, and the diagnosis of one from the other is as difficult in some cases as it is essential and necessary for treat- ment and cure. The other conditions with which it might be con- fused are uraemia, alcoholic epilepsy, tetanus, and syncope. On the following page are arranged all these disorders in a table, which briefly and succinctly shows the different points between them, al- though, of necessity, it is somewhat arbitrary on account of the lack of CONVULSIOyS OB GENERAL SPASMS. 463 space. Nevertheless, it is hoped that it will be clear enough to be of service, particularly in connection with what the author is about to say. Table of Differential Diagnosis of Epilepsy from Hysteria, etc. Signs. 1 Epilepsy. None. Generally present, but short. Apparent cause, Aura or prodro- mata, Onset, Sudden. Scream, Convul- sion, At onset and sud- den. First tonic, then clonic. Biting, Tongue. Micturi- tion, Frequent. Defecation. Talking. Occasion- ally. Never. Duration, A few minutes. Conscious- Lost. ness, Termina- tion, Spontane- ous. Hysteria. Emotion. Globus hystericus; palpitation; choking. Often gra- dual. I During attack. Rigidity more pro- nounced, with more aching. [ People, tongue, lips, and j hands. Never. 1 Never. Frequent. Generally many minutes. Generally preserved. May be in- duced by shock. Ureemia. Petit mal. Alcoholic epilepsy. None. None. Headache, Faintness vomiting, and dim- and dys- ness of pepsia. vision. Often gra- Sudden, dual. Frequently Frequently none. none. Rigidity No rigidity, generally absent. Tongue. Never. Never. Muttering. From a minute to hours. Lost. Spontane- ous. None. None. Tremors. Sudden or gradual. May or may not be present. Movements more clonic than tonic. Rarelv. Rarely, ex- Rarely, cept when bladder is affected. Never. Rarely. Never. ! Momen- tary. Not lost always, but clouded. Spontane- ous. Never. May be prolonged. Lost. Spontane- ous. Tetanus. ' Syncope. None. Nervous- ness. Gradual begins in jaw. None. Always tonic. Some- times. Rarely. Never, Hours. Pre- served. Mental shock. Not so well de- fined as in epilepsy. Sudden or gradual. None. None. None. Never. Never. None. Indefinite time. Lost. Spontan- Gradual, eous. with no . somno- leQce. The very irregularity of true epilepsy makes it extremely difficult to give clear and well-defined outlines of it against another disease, particularly when we remember that epilepsy and hysteria often go hand in hand. By far the most important differential point between the two di.s- orders just named, when not complicated with .still another disease, is the character of the movements. As already pointed out, in ej)i- lepsy they are typically at variance with those of daily life, while in hysteria they are almost equally typical of ordinary muscular con- tractions, or, in other words, are more purposive in character ; and frcHjuently there is prolonged tonic contraction of the mu.scle.'^, giving ' This table is taken from the author's essay on Epilepsy, the jirize essay of the Royal Acad- emy of Medicine in Belgium, January, 1889. 464 THE MANIFESTATION OF DISEASE BY SYMPTOMS. rise to the assumption of positions which bear more or less resem- blance to normal attitudes. In hysteria, also, consciousness is im- paired sometimes, but never so completely as in true epilepsy. In- deed, most commonly the individual knows all that goes on around her, for, while she may give no sign of consciousness by \vords or looks during the attack, she may afterward be able to narrate all that has occurred. Less commonly, however, a condition known as automatic consciousness exists, in which, during the paroxysm, the patient understands all that is said, but forgets everything on the return to quietnes.«. The fact that the patient is a female cannot be regarded as affirma- tive evidence of hysteria in the least, but the condition occurring in a male may be taken as fairly positive evidence of its being epilepsy ; and yet it should always be remembered that males may suffer from hysterical attacks. The movements of the hysterical patient after the tonic condition has passed away are as clonic as those of the epileptic, but still pos- sess some purposive characteristics, and are not so bizarre as are those of the true disease. Thus the head, arms, and legs are struck with evident endeavor against the floor or suri-ounding furnituie. An- other point, which, when it occurs, is very distinctive, is the onset, toward the close of a hysterical convulsion, of a second stage of tonic spasm, such as occurred at the beginning. It will be remembered that this does not occur in epilepsy, although it must be borne in mind that in cases of the '' status epilepticus" the rapid onset of another attack may show a second tonic stage. This can be sepa- rated, however, by the fact that it is followed by clonic movements, whereas the secondary tonic stage of hysteria is usually followed by relaxation and temporary recovery. In the secondary hysterical tonic contractions emprosthotonos and opisthotonos may occur, and are even more rigid in their character than they are in the first attack, in some cases. Finally, too, in hysteria, some peculiar emotional position is often assumed, as of the crucifix or of intense grief, or, perhaps, immoderate laughter is indulged in, with corresponding movements of the trunk. If the patient is quiet at this time a smile may float across the face, while the eyes, with a look of pleasure, jjain, or entreaty, may seem to be gazing at some object very far off. In some very well-developed oases the expression of pleasure is followed by a look of pain, with painful movements, or an appearance of intense voluptuous entreaty,. CONVULSIONS OR GENERAL SPASMS. 465 with sensual venereal desire evidenced by gestures. Great terror may be present, and, as the scene constantly changes, the woman is now joyous, now mournful, now scolding, now praising her attendants or herself. Such is the history of a fully developed attack of hysteria. Hysterical convulsions in their fully developed form are rarely seen among Americans, Germans, Belgians, or corresponding races, but are very frequently observed by French practitioners of medicine. In France there can be no doubt that the tongue is commonly bitten in hysterical convulsions, and that frothing of the mouth is frequently present ; but in other countries this symptom may be regarded as indicative of epilepsy rather than hysteria. Doubtless the inexperienced reader will say, upon comparing these^ symptoms with those which were given as occurring in epilepsy proper, that the two disorders are easily separated from one another ; but the author would insist most strenuously upon the fact that in both cases he has given only the most typical characteristics of the diseases, and he repeats that all cases are not by any means so well defined. He would also remind the reader that the chief difficulty in making a diagnosis lies in the fact that frequently it must be made without any previous history of the case, as when a patient is brought into a hospital, in a fit, for treatment. Where the history is obtainable or where the diagnosis can be put off until the case may be studied,, the question becomes more easily solved. If a large number of patients suffering from these hysterical at- tacks be questioned between times, it will be found that the so- called globus hystericus becomes an almost constant precursory symptom of an attack ; and if the relatives be questioned, it will often appear that they have noticed that the fall to the floor is more gentle than in true epilepsy; but this is not always so by any means. Again, the expression of the face in hysteria is, between the attacks, often very characteristic, and the surrounding atmos- phere of the patient seems, even to the inexperienced, to breathe hysteria. Very commonly areas of anaesthesia and hypera?sthesia occur in these patients, and are of all degrees of intensity and limi- tation. Search for them generally shows their presence after attacks of convulsions, but they may exist from one attack to the other, or develop spontaneously. In nearly all cases these areas are unilat- eral, and may extend entirely over one-half of the body, the line of demarcation of the ansesthesia or hyperiesthesia from the sound area 30 466 THE MANIFESTATION OF DISEASE BY SYMPTOMS. being clearly and abruptly defined, generally at the median Hue of the front and back of the trunk. (See chapter on the Skin ; that part dealing with autesthesia.) It will be called to mind that such conditions are very rare in true epilepsy. Hallucinations are far more common after the fit in hysteria than in epilepsy, and some- times they even occur during the attacks. They are always asso- ciated with the mental state ; if terror is present, rats or disgusting objects are seen, aiid, according to Charcot, are generally seen on the side which, during the intermissions, is anaesthetic. The pupil is more mobile in hysteria than in epilepsy, but may be contracted, normal, or widely dilated. The following table gives, in as brief a manner as possible, the differential diagnosis between epilepsy and hystero-epilepsy, and is founded on a lecture by Professor Charcot, delivered at the Salpe- triere. True Epilepsy. Aura short. Cry is violent. Spasms first tonic, then clonic, then followed by stertor. Sometimes after fit delirium or violent impulse or mania. Mental power is lost. No emotional attitudes. Hystero-epilepsy. Aura extremely prolonged. Cry is more moderate and prolonged. Ataxic contractions, extension of limbs, turn- ing of head, clonic movements, slight stertor. Bizarre contractions, no delirfum, may be hallucinations. Mental power preserved. Emotional attitudes. A very useful differential point, strongly insisted upon by Char- cot and Bourneville, is that in true epilepsy there is generally a very considerable rise of temperature during an attack, while in hystero- epilepsy the temperature remains normal or only slightly raised. In the diagnosis of true epilepsy from convulsions of a hysteroid character it is well for the physician to remember that the propor- tion of the two conditions in frequency of occurrence is, according to Gowers, 815 to 185 in every 1000 cases. The differentiation of epilepsy from urcemia is much more readily carried out, for there is usually a previous history of symptoms pointing to renal trouble, as, for example, some cedema, or somno- lence, or mental apathy, for some days or hours before the attack. Of -course, in such cases recourse may be had to the ordinary tests for such conditions of the urinary organs as are generally found where urjemia exists ; but it is to be remembered that epilepsy and kidney disease may exist hand in hand, and that for this reason the prognosis and diagnosis are to be carefully formed and given. If in a given case a prolonged history of dyspepsia, of frequent vomiting, CONVULSIONS OR GENERAL SPAS3fS. 467 occasional attacks of asthma, and failure of general health is found to be present, the correct diagnosis probably will be unemia. The pres- ervation or loss of consciousness in uraemic convulsions is variable. Generally, if the convulsion is widespread and severe, the intellection is lost ; but if it be only a slight attack, consciousness may be preserved. So long ago as 1840 Dr. Bright described cases of uraemia, on the other hand, in which furious convulsions occurred without loss of consciousness, and Roberts has reported similar instances. Just here the author may remind tiie reader that not more than thirty years ago some physicians of very high standing believed epilepsy to be due entirely to uraemia. Thus Sieveking firmly be- lieved in this theory, and reported a case in support of his views. Fatal uraemia may also occur in a patient whose urine is apparently normal ; aud, in a large number of cases of chronic contracted kid- ney, albumin may be absent from the urine for long periods of time. The specific gravity of the urine should be carefully noted, and in very doubtful cases careful estimations of the urea be made. If the specific gravity is constantly below 1.010, the kidney will nearly always be found contracted unless diabetes insipidus exists. Tests of the urine passed at different times of the day should always be made. Another means of testing the integrity of the kidney is to admin- ister iodide of potassium and study its elimination. It is affirmed that, after a full dose, this drug can in an hour be readily recog- nized in the urine by adding nitric acid and then starch; bufc when contracted kidney exists the iodide fails to appear or is excreted only in very small quantities. The temperature of the body may also be used to differentiate between unemia and epilepsy. In 1865 Kien called attention to the fact that even when uriemic convulsions are most violent they are accompanied by a fall of temperature of as marked a character as the rise noted in respect to epilepsy. Since then this has been confirmed by Roberts, Hirtz, Hutchinson, Char- cot, Bourneville, and Teinurier. The diagnosis l)etween puerperal eclampsia and epilepsy consists chiefly in the acuteness of. the attack, and the fact that with no pre- vious convulsive history a woman becomes suddenly convulsed dur- ing the puerperal state. This is not a place for the discussion of the identity of uncmia and pucrjx'ral eclampsia, although we believe tiiat unemia is generally responsible i'or the nervous disturbance. If the convulsions are urteraic, the temperature, according to the investi- gators just quoted, should fall ; and according to Bourneville, puer- 468 THE MANIFESTATION OF DISEASE BY SYMPTOMS. peral convulsions are distinctly separated from those of uraemia by reason of the fact that the temperature rises with great rapidity in the very beginning of the convulsions and there remains with great steadiness. The condition of bodily temperature can, therefore, be used to differentiate puerperal eclampsia and urtemia. It is unnecessary to state once more that ^3c^i7 mal is but a variety or modification of haul mal. ^Nevertheless, it is useful to be able to separate it somewhat from the more severe form of the disease in the attempt to form a prognosis. Some suppose that petit mal may be designated as consisting of one or two of the chief symptoms of epilepsy proper, and others have thought that the preservation of consciousness was the chief dividing-line between it and fully developed epilepsy. The last idea is certainly incorrect, but it is impossible to give any outline which will absolutely separate the two conditions, so far as symptoms go. An important and useful point first discovered by the celebrated neurologist, Weir Mitchell, is that, whereas the inhalation of amyl nitrite stops true epilepsy, the use of this drug increases the severity of an attack of petit mal. Alcoholic epilepsy occurring during an attack of mania a potu is, of course, easily diagnosed, and the general appearance of the patient, combined with his history, suffices to make the physician's decision. The movements are more clonic than tonic, and often are lacking in force. There is, however, no constant distinction between the symp- toms applicable to all cases. Generally one seizure of alcoholic epi- lepsy follows the other every few minutes until three or four have taken place, when the paroxysms cease. It is not to be forgotten that alcohol may produce all degrees of epilepsy, from the mildest petit mal to the most severe paroxysms, and it is also to be remem- bered that hallucinations of terror are very commonly present. There may be an aura in alcoholic epilepsy quite as marked as in the true disease. The separation of syncope from epilepsy is one of the easiest tasks imposed upon us. The color of the face, the weakened heart-beat, sudden loss of consciousness, and the general appearance aid us here very much. The separation of epilepsy from hemicrania has been very well written of by Silva. He thinks that epilepsy begins in childhood before puberty, most commonly, while hemicrania comes on after puberty; and that the attacks of hemicrania decrease in violence and CONVULSIONS OR GENERAL SPASMS. 469 frequency as age increases, while the contrary rule applies to epilepsy. These views are in accord with those of Striimpell and Wagner. The diagnosis of lead epilepsy from the idiopathic varieties is somewhat difficult, if the patient is seen for the first time during an attack; but the ordinary methods of determiuing chronic lead- poisoning are, of course, of equal value here. The blue line on the gums may be present, and, if so, the diagnosis is almost certainly lead-poisoning ; but its absence is no proof that lead is not present. The administration of iodide of potassium also will so increase the elimination of the poison as to benefit the case and render it more easy to recover lead from the urine. The history of exposure to lead in any form is, of course, exceed- ingly valuable evidence, but it should not be forgotten tliat in many cases this histoiy is wanting. Thus, the poison may be derived from a hair-dye, or cosmetic, or from water which contains lead from pipes, or from an endless line of similar hidden and obscure sources. Amaurosis may be present in some cases, or optic neuritis with atrophy may occur. Where double wrist-drop is present the diag- nosis is much more easy. It is exceedingly important to differentiate between those convul- sions which arise from the uremia brought on secondarily by an action of lead on the kidneys and those which are due to a direct action on the brain. This may be difficult from the mere symptoms presented, Ijut there are some points of difference. In the first place, the convulsion of urtemia is, as a general rule, not so violent in its movements nor so sudden in its onset. It is generally preceded by a few days of somnolence, or weeks of gastric disorder and head- ache, while lead epilepsy is generally sudden or preceded by cepha- lalgia by only a few days or hours. Again, examination of the urino in uncniic convulsions will show a decreased amount of urates in proportion to the quantity of urine passed, while in plumbic epi- lepsy just the reverse will be true, unless the kidneys are affected pari pnasu with the cerebrum. If albumin be present, uritMuia is pointed to ; but if the urine has a low specific gravity and is passed in large amounts, the indications are that there is chronic contracted kidney, wliicli may or may not be the cause of tlic nervous disturb- ance. Before closing this portion of this chapter the writer must bring forward the points to be used in differentiating epilepsy from those attacks simulated by malingerers. Often this is most difficult ; and 470 THE MANIFESTATION OF DISEASE BY SYMPTOMS. it is related of Fournier that, after his expressing au opinion that a man could always tell them apart, one of his assistants threw himself to the floor on his next visit in a pretended attack, whereupon Four- nier, completely misled, exclaimed, " Poor M — ; he is epileptic!" upon which the assistant, smiling, arose to his feet and confuted the statement. Very serious injuries are sometimes submitted to by these per- sons to carry out their designs. The points to be looked into are : The condition of the pupils, which, in the simulated attack, always react normally ; nor can the corneal reflexes be held back ; the color of the face is rarely changed; and the thumbs are rarely flexed as they should be. Marc has pointed out that in malingerers the by- stander can readily straighten the thumbs out, and that they remain so; whereas in epilepsy they instantly l:>ecome flexed again. Suggestions, as to movements, are sometimes followed by malin- gerers, and the movements generally lack the bizarre character so typical of epilepsy. If tobacco or ammonia be held to the nose of the fraud, he gener- ally is forced to disclose his true nature. The fact that in malingerers there is no rise of temperature may also serve as a differential point. Convalsions appearing in infants or young children may result from injuries to the brain in birth, to the presence of growths, or to other distinct cerebral causes and irritation of the alimentary canal. In these cases they may be reflexly produced. Certainly they often arise from the reflex irritation produced by teething in children en- tirely free from rickets and from gastro-intestinal irritation due to the ingestion of improper foods. Whether adherent prepuce and other causes of peripheral irritation ever result in convulsive seizures is a matter of doubt, some authorities believing that such causes are frequently present, while others deny their existence. The author believes that given a child with a distinctly neurotic temperament and a marked source of peripheral irritation, convulsions are pro- duced. Stevens asserts that insufficiency of the ocular muscles very frequently causes epilepsy, and he is not alone in this belief. Cer- tainly in cases in which such possible causes of nervous excitation exist the physician should remove them as his first attempt at treatment. There is one variety of infantile convulsive seizure due to menin- gitis which is in itself often tubercular and associated with retrac- tion of the head and squint ; and another variety in which the CONVULSIONS OB GENERAL SPASMS. 471 symptoms very closely resemble those clue to actual meningeal lesions, but in reality are quite independent of them. This con- dition has been called "pseudo-meningitis" or " hydrocephaloid disease," and is seen in young infants generally after attacks of severe diarrhoea. The fontanelle is depressed, the child is somno- lent or comatose, and fever may or may not be present. The prog- nosis in the first class of cases is very bad. In the second class it is bad enough, liut recovery quite often occurs if the treatment gen- erally employed in the first class is set aside and a highly nutritious and supporting treatment is instituted. If a <;hild suddenly develops symptoms of acute meningitis and has delirium, rigidity of the neck, and the major manifestations of the disease, the lungs should be carefully examined for croupous pneumonia, as this disease in children very often causes these cere- bral or meningeal symptoms. Even in the adult maniacal delirium and rigidity of the neck may be present in croupous pneumonia. Convulsions, which are epileptiform, sometimes occur in the latter stages of Addison's disease. Tetanic Convulsions. The convulsions which are of spinal origin, namely, those that are tetanic, are the result of tetanus or the ingestion of strychnine in poisonous dose, or its fellow ignatia, and sometimes are due to hysteria. The diagnosis is aided by what has been said in respect to the symptoms of hysterical convulsions in the last few pages, and finally by the discovery of the hysterical stig- mata, or the signs manifested by the skin, and when examination can be made between attacks, of the eyes (see chapters on Skin and Eyes). Tetanus convulsions and strychnine-poisoning are to be separated from one another by the fact that in tetanus the locking of the jaws comes first, while in strychnine-poisoning it comes last. The con- vulsions of tetanus rarely, if ever, completely relax, while those of strychnine do have periods of relaxation. There is a different his- tory in each case. In one. perhaps, of an injury, as of a nail run into the foot ; in the other, of a dose of poison having been swal- lowed. The differential diagnosis between strychnine-poisoning and hys- terical convulsions is more difficult. The convulsions are rarely so persistently tonic in hysteria as in strychnine-poisoning, and the peculiar expression of the hysterical face is often seen in this dis- ease. The history of the patient, if obtainable, will throw much 472 THE MANIFESTATION OF DISEASE BY SYMPTOMS. light on the case aud aid very materially in the separation of the two conditions. When a patient is seized with sudden and symmetrical tonic spasms of the hands, extending to the upper arms and shoulders, so that the fingers are flexed at the metacarpo-phalangeal joints and extended in the phalangeal joints, while the lower arm is flexed and the legs extended, while the toes are flexed, the condition is one of tetany. It is most commonly seen in hysterical cases and has no relation to true tetanus. Pressure on a nerve-trunk or bloodvessel will often produce an attack in such persons. This is sometimes called " Trous- seau's symptom." The pressure must be applied for several min- utes in some cases, and the best place to apply it is the bicipital sulcus or the crural sulcus. It is not a constant symptom, but pathognomonic if found. Another equally useful diagnostic sign is called Chevostek's symptom. This consists in the fact that the muscles are irritable, so that when they are tapped by the finger-tip, or hammer, contraction results. The prognosis is favorable, but recur- rences are frequent. It occurs most commonly in males up to twenty years, and may occur as early in life as two to four years of age. Convulsions limited to a few muscles or more widespread in char- acter may appear as symptoms in acute yellow atrophy of the liver ; but the peculiar symptoms of this disease render easy the diagnosis of their cause. Typical epileptiform convulsions are the most constant symptoms of liydatid cyst in the cerebral cortex, but the diagnosis of this con- dition is impossible unless from a history of probable infection. Convulsions may also arise from hcematoma of the dura mater (internal hemorrhagic pachymeningitis), but the diagnosis from those due to cerebral hemorrhage is practically impossible. General violent convulsions have also been seen quite frequently in nervous patients during the paroxysmal pain of gall-stone colic, and they also sometimes usher in the acute poliomyelitis of child- hood and the infectious diseases. Epileptiform convulsions may come on in adults as the result of multiple sclerosis, and they are very commonly seen in sunstroke when the patient is first attacked. Curiously enough, severe convulsions have been known to follow irrigation of the pleural cavity after aspiration, and they may also be seen in young children suffering from whoojjing-cough at the time of the paroxysm. CONVULSIONS OR GENERAL SPASMS. 473 Spasms. General spasms, in distinction from convulsions, are represented by chorea in its various forms, and by saltatoric and palmic spasm, paramyoclonus multiplex, and the occupation-neuroses. There are other localized spasms from nervous disease, such as facial spasm and wry-neck, athetosis, and post-hemiplegic chorea. Some of these conditions will be found discussed in the chapter on the Hand and Arm and that on the Face and Head. When a patient is afflicted more or less constantly and more or less universally by disordered, irregular, jerking movements which throw the part or parts affected into unusual positions, which are not, however, maintained even for a moment, the condftion is prob- ably chorea minor. Often the speech is seriously disturbed by rea- son of the choreic movements of the lips and tongue or jaws, and some loss of power may be manifest in certain muscles. This true chorea or St, Vitus's dance may affect the whole body or only one arm or leg, but generally it is diffused. Commonly it ceases at night when the child sleeps, but it often persists day and night, and then becomes a serious malady, because of the exhaustion produced. It often follows fright, prolonged bad weather, and other causes which may upset the nervous balance of the child. Chorea is so characteristic in its manifestations that it can lie readily recognized in most cases; but it sometimes has to be separated from disseminated sclerosis, progressive muscular atrophy, hysteria, and Friedreich's ataxia. The movements in disseminated sclerosis are, however, fine muscular tremors, instead of minor jerking movements; and there are present nystagmus and scanning speech in sclerosis, l)ut not in chorea. Again, in progressive muscular atrophy there is fibrillary muscular tremor, but not twitching of a marked form, and ti)e muscles are wasted. In hysteria the muscular movements are rarely choreic, and the presence of changes in the color-fields and the other stigmata of iiysteria (see chapter on Skin and Eyes) renders a diag- nosis of the latter condition easy. Friedreicli's ataxia is to be separated from chorea by the scanning speech, scoliosis, slow iuco-ordinate movements, and the family his- tory of the disease. Rarely, when there is some paresis witli ciiorea, tlie patient may present symptoms of acute poliomyelitis; but the paralysis in the 474 THE MANIFESTATION OF DISEASE BY SYMPTOMS. latter affection is more marked, and there are no movements in the affected muscles, such as occur in chorea. Chorea insanieus is a violent form of ordinary chorea associated with mania, which is not to be confused with choreic movements occurring in the choreic insane. Choreic movements sometimes come on in the aged, and must be separated from paralysis agitans and senile trembling. This is pos- sible by the fact that in paralysis agitans the movements are tremors, and there is loss of power with the peculiar facial expression ("Par- kinsonian visage"). Senile trembling is usually an affection limited to the head, and consists in a tremor and not in marked twitching. (See chapter on Hand and Arm ; part on Tremor.) A rare form of chorea has been called Huntington^ s chorea. It occurs iu adults about the age of thirty to forty years. It is hered- itary ; that is, there is generally a history of the same trouble in the ancestors of the patient, and finally as it progresses psychical disturb- ances ensue. Irregular movements first appear in the hands, which movements become markedly inco-ordinated, the arms are thrown about in excessive and rapid jerkings, and when the infection involves the legs a characteristic gait is developed of a dancing or " hop, skip, and jump " character. Sometimes, early in the malady, the movements can be controlled by the will. The face passes through slowly formed grimaces, and the gait may be staggering. The speech becomes indistinct, and enunciation is not clear. Finally, dementia closes the scene. The movements of Huntington's chorea are not sudden as in true chorea ; it is a disease of adult life, and mental disturbance is a prominent symptom. These facts separate it from ordinary chorea. When the patient involuntarily bends over in a profound bow the cause of his movements may be rhythmical contraction of his abdom- inal muscles, producing the so-called salaam convulsions or chorea major. A still more rare malady is electric chorea or " Dubini's disease," in which the muscles of the arm and then the leg on the same side are affected with a sudden muscular spasm or shock, such as is pro- duced by the electrical current. Wasting of the affected muscles, loss of faradic irritability, occasional epileptic convulsions, and rarely elevation of temperature come on. The disease is a fatal one, and generally occurs in Italy in malarial regions. Under the same name CONVULSIONS OR GENERAL SPASMS. 475 of electric chorea Bergeron has described a state of rhythmical mus- cular spasm which usually ends in recovery. When a condition of clonic muscular spasm affecting the trunk, limbs, and perhaps the neck, is present, the hands and toes being uninvolved, as a rule, the possibility of the presence of 'paramyo- clonus multiplex is to be considered. The spasms in this rare disease are bilateral and occur at intervals, often only on an attempted move- ment or speech. So violent are the muscular contractions in some cases that the patient may be thrown to the ground or, if in bed, to the floor. These movements may vary from three or four to 120 per minute, but are generally about fifty per minute. The sym- metrical bilateral involvement, the fact that the movements are not choreic in character, and that the patient is a male,^are to be remembered in making the diagnosis. The ultimate prognosis is favorable unless the movements are so constant as to cause exhaus- tion. Care must be taken not to confuse hysterical movements with this condition. The bilateral movements which affect only the larger muscles, and the fact that paramyoclonus multiplex is nearly always seen in the male, separate it in part from hysteria, while the hysterical stigmata when they are present will point to hysteria as the cause of the disorder. Sometimes a patient will be met with in whom, when he attempts to stand, the leg muscles first become rigid and then are thrown into violent contractions, which cause him to jump up and down, or he may be thrown to the floor. This condition is called saltatoric spasm or " jumpers." It is to be separated from the condition of the legs seen in lateral sclerosis of the cord by the fact that in the latter disease the legs become spastically stiff on attempting to use them, from Huntington's chorea in that voluntary movements with the hands] may be performed perfectly, and from chorea minor by the absence of small inco-ordinated twitchiugs. Such a patient will often act on suggestions or in imitation of the acts of other persons or of animals. Some writers confine the term " saltatoric spasm " to those cases which possess no imitative features. In such cases the disease is far more moderate in its manifestations. (^uite distinct from these clonic spasms of the muscles brought on by attempted movement is that in which the muscles become tonic on attempted movements. At first they are stiff and slow in their movemeuts, but ultimately develop a tonic spasm, so that 476 THE MANIFESTATION OF DISEASE BY SYMPTOMS. walking is at first almost impossible, but the limbs limber up on exercise. This is a rare affection, called Thoinsen's disease, or one of the forms of myotonia congenita. (See chapter on Feet and Legs.) Forced gyratory movements of the body are sometimes seen as the result of a lesion of the middle peduncle of the cerebellum. CHAPTER Y. VOMITING, REGURGITATION, AND THE CHARACTER OF THE VOMIT. Due to ursemia — Cerebral lesions — Intestinal obstruction — Peritonitis — Cholera — Gastric disease — Hepatic disease — Poisons — The appearance of vomit. Vomiting is the act by which the contents of the stomach are forcibly expelled from this viscus through the cardiac orifice, the oesophagus, the pharynx, and mouth. The vomiting-centre in the medulla oblongata gives rise to the necessary nervous impulses and is provoked to this by direct stimulation or by reflex irritation. Thus, in ursemia the vomiting sometimes encountered is the result of irritation of the centre by some unknown poison, and when apomor- phine is given the centre is also stimulated. Centric vomiting is also caused by the administration of anaesthetics, notably ether and chloroform. On the other hand, gastric, intestinal, or other abdom- inal disorder may reflexly produce very persistent emesis, and for these reasons vomiting is of considerable diagnostic importance. Vomiting being produced by many maladies is a symptom fre- quently met with. It occurs with a certain degree of constancy as a complication or symptom of unemia, diabetes, apoplexy, brain- tumor, brain-abscess, Meniere's disease, tubercular meningitis, hys- teria, intestinal obstruction from all its various causes, gastric and intestinal indigestion, gastritis, gastric ulcer, gastric cancer, perito- nitis, nephritic colic, hepatic jaundice, hepatic colic, in cholera, yel- low fever, and a host of other ailments. The vomiting of unemia may be one of the earliest manifestations of renal disease, and its presence, when persistent in the absence of local gastric or other causes, should always lead to an examination of the urine, since valuable time may be lost if the patient is considered to be suffering from some slight indiscretion in diet. Its association either as a preceding, concomitant, or consequent symptom of con- vulsions renders a diagnosis of ursemia probable, while a history of uraemic amaurosis, colHf[uativc diarrhoea, and failure of the general health will be very im[)ortaiit points in reaching a (kx'ision. No pathognomonic symptom of urtcmic vomiting exists unless we con- sider the urinary evidence a symptom, but in some cases the vomited 478 THE MANIFESTATION OF DISEASE BY SYMPTOMS. matters smell strongly of carbonate of ammonium, resulting from the decomposition of the urea, which has been eliminated from the blood into the stomach by the gastric mucous membrane. Ursemic vomit- ing is, therefore, not only due to centric irritation by a poison in the blood, but to irritation of the stomach by the urea which is excreted into it. Diabetes comparatively rarely produces vomiting by the toxaemia which it causes, but in any case the urinary examination and polyuria decide the diagnosis. When vomiting results from cerebral hemorrhage^ embolism, or thrombosis, the focal or hemiplegic symptoms characteristic of apo- plexy are present. Possibly the vomiting is more indicative of hemorrhage than of plugging of the vessel. A sudden attack of vomiting in a previously healthy man of advanced years or in one who is young, but has a specific history, should raise the question as to the possible presence of one of these lesions ; provided, of course, that ordinary gastric disorder is not present as a cause. The vom- iting due to cerebral tumor is generally preceded by the characteristic severe and constant headache, vertigo, a slow pulse, impaired memory, and sometimes by epileptiform convulsions. Further than this, the important diagnostic ocular symptom "called choked disk" of the optic nerve is to be sought for, and if found is of great positive value. Tumor of the brain, if near the base, often causes, too, involvement of the various cranial nerves. The vomiting of cerebral tumor is in- dependent of taking food, and commonly comes on early in the morn- ing, thereby differing from some of the forms of vomiting due to gastric disorder. The vomiting arising from cerebral abscess has symptoms precisely like those just named, so that a differential diag- nosis is almost impossible. The history of injury or of an infectious process producing a secondary brain-abscess may point to this cause of the vomiting ; the real points of difference are that in abscess choked disk is rarely seen, fever is commonly present, and the cra- nial nerves generally escape. When purulent meningitis produces vomiting it may be impossible to tell whether this symptom is due to it or to an abscess, as the purulent collection may be localized. Vomiting sometimes results from profound cerebral ancemia of an acute type due to hemorrhage, in fainting or in chronic aneemia, as in clilorosis. Generally, however, the symptom is only a constant nausea. The presence of great pallor and other evidences of anaemia aids in the diagnosis, but it must not be forgotten that some severe anaemias are accompanied by febrile movement and by marked VOMITING. 479 choked disk, which should not mislead the physician into a diag- nosis of cerebral tumor. "When vomiting is due to cerebellar tumor the diagnosis is aided by the presence of vertigo, the peculiar staggering gait, and finally by evidences of choked disk, on ophthalmoscopic examination, with disordered vision. The vomiting of meningitis is ([uite frequently an early symptom, but it also often occurs later in the disease, and is caused by the meningeal irritation, and not by any condition of the stomach, unless that viscus has been disordered by the unwise use of drugs. This form of vomiting can nearly always be separated from that due to other causes by the excessively severe headache, chiefly of an oc- cipital type; by the pain in the nape of the neck and in tli^ spine; by the rigidity of the dorsal muscles, so that opisthotonos may be caused in severe cases ; and, finally, by the disordered functions of the cranial nerves, as a result of which there are found trouble in the oculomotor nerve, strabismus, double or single ptosis, slovvly reacting pupils, which may be unequal, nystagmufc', and sometimes facial contractions due to involvement of the facial nerve. Vomiting due to acute miliary tuberculosis often comes on at the very onset of the malady, and is associated with obstinate constipa- tion, or, on the other hand, active diarrhoea ; but the fever, the very rapid pulse, the wasting of the patient, the possibly present physi- cal signs of tuberculosis of the lungs, and, very important, the pecu- liarly severe dyspnoea, for which no adequate cause can be discovered on piiysical examination, all point to the general infection. If a skilful examination of the eye can be made with the ophthalmoscope, the choroid may be found to be studded with tubercles. The reflex forms of vomiting are very numerous, and depend chiefly upon organic and functional disorders of the abdominal viscera. In some of these conditions vomiting is of little importance, except for its gravity if the patient is exhausted ; in other words, it is simply a disagreeable symptom. In others the symptom vomiting is of con- siderable diagnostic value as indicating the grave mischief wiiich pro- duces it. One of the most important of the latter conditions is intes- tinaf obstruction, whether it arises from intussusception, constrictions by bands, volvulus, or impactions. In intussusception vomiting is practically a constant symptom, occurring witli the sudden pain, or, at times, even preceding it. In children it continues till shortly before death, and is rarely feculent. 480 THE MANIFESTATION OF DISEASE BY SYMPTOMS. In the adult, and in the chronic form, there may be complete ab- sence of vomiting, though this is certainly exceedingly rare. Leich- tenstern takes exception to the statement that the seat of obstruction is indicated by the period at which vomiting is developed. The ileum-invagination is most frequently accompanied by early vomiting, not because of its seat, which is usually but little removed from the ileo-csecal valve, but because it is commonly obstructive. The vomiting, both in time of development and in nature, will de- pend, not upon the seat of the trouble, but upon tlie presence or completeness of obstruction, and may be early if the obstruction is absolute in the sigmoid flexure, and feculent if the bowel is occluded in the upper part of the ileum. The pain is usually sudden, violent, diffuse, or, if localized, usu- ally placed in the ileo-csecal or umbilical region. After a few hours in children, a much longer interval in the adult, the pain ceases, often as suddenly as it commenced, and there is an interval in which there is little to suggest that the pathological condition still continues. This is followed by a return of the pain, the paroxysms becoming more violent and prolonged, the intervals less marked as the disease progresses, or in the adult, if it passes into the chronic form, and in- tervals even of days may elapse between the paroxysms. The pain is frequently accompanied by tenderness, but this is an exceedingly variable symptom, and at times pressure seems to relieve the pain. Blood-stained mucous evacuations are a symptom of intestinal ob- struction which, in children, is rarely wauting. Of 108 cases of invagination in the first year of life this symptom was absent in but four. It occurs within a few hours of the first attack. At the first the discharge is of blood-stained feces ; later, if obstruction is devel- oped, of blood and mucus, and is usually exceedingly offensive. In children diarrhoea is common throughout the whole course of the case. At times, following complete constipation and feculent vomit- ing, there will suddenly appear copious evacuations from the bowel, mingled with blood, and in which may be found evidences of the necrosed intussusception. Where this slough is extensive it may be lodged in a lower portion of the bowel and cause fatal obstruc- tion.^ In connection with the muco-sanguinolent evacuations the tenes- mus or straining is a symptom so common that it is of some diag- 1 For much information on the subject of intestinal obstruction see the Fiske Fund Prize Essay of the Rhode Island Medical Society for 1890, by Martin and Hare. rOMITIXG. 481 nostic import. That it is not dependent upon the character of the evacuation is shown by the fact that it is present in cases of complete obstruction. Brinton has shown that this symptom is seldom de- veloped except in the ileo-ctecal and colon invaginations. A much rarer condition, and one which Leichteustern ascribes to the secondary effect of intense tenesmus, is a patulous condition of the anus due to paralysis and dependent upon invagination of the descending colon and rectum. This is never produced by invagina- tion of the ileum. Leichtenstern's statistics show that a tumor can be felt either through the parietcs or by rectal examination in 52 per cent, of all cases. In the first year of life this most important diagnostic sign was present in 63 per cent. The tumor is usually felt' in the loft iliac region, or by the finger passed into the anus. The ileo-cjccal invagination is most frequently accompanied by demonstrable tumor; the ileum-invagination exhibits this symptom with less frequency. Many authors have noted that the tumor varies in size and con- sistency from time to time, now, during an acute paroxysm of pain, being hard, knotty/and plainly perceptible, shortly afterward eluding the most carefnl search. Ducliaussoy has described two distinct movements which can often be perceived in the tumor, namely, the erectile and the vermicular motion. Distention of the abdomen is not of great significance, because it is often absent. In children especially it may not appear at all, or only just before death. In adults, in whom obstruction is more common, it may l>ecome as well marked as in obstruction from any other cause. Dance calls attention to an inequality in the shape of the abdomen dependent upon the meteorism, and in view of which he states that the seat of obstruction can often be inferred. But few authors, however, have been able to profit by his ol)S('rvation. In the chronic form of invagination the syniptoms arc less violent in onset ; there may be nothing more characteristic of the attack than recurring ])aroxysms of pain, meteorism, and obstruction, with symptoms of intestinal stricture constantly manifesting themselves. These cases terminate either in cure by reduction or by extrusion of a slough, or perish from exhaustion, inanition, or in the course of an acute attack. In over one-half of the recorded cases a correct diagnosis was not made. The additional symptoms nj)()n wliirh a diagnosis of vomiting from intussusception is to be based arc the acute onset of colicky 482 THE MANIFESTATION OF DISEASE BY SYMPTOMS. pain, and its intermittent character : passages from the bowels con- taining blood and mncus ; the presence of a tumor, commonly in the left iliac region, or felt through the anus, varying in size and con- sistency from time to time, with an erectile or vermiform motion ; and the ordinary obstruction-symptoms. The diagnosis is further confirmed if there are violent peristalsis and tenesmus, and if these symptoms occur in an infant. According to Leichtenstern, Bryant, and others, 40 per cent, of all cases of intestinal obstruction are due to intussusception, and this condition is most common in the first year of life, after which it becomes more and more rare until the fortieth or fiftieth year, when it increases in frequency. The prognosis is bad, the mortality varying from 73 to 90 per cent, unless early surgical relief is given. Internal strangulation by bands occurs in from 25 to 30 per cent, of the cases of obstruction of the intestine, and affects males most commonly between twenty and forty years of age. In 133 out of 151 cases the small intestine was involved. The typical symptoms are as follows : 1. Sudden, agonizing pain, constant, and located about the umbili- cus, with paroxysmal increments. 2. A rapid, weak pulse and subnormal temperature. This is nearly constant in the early stages of the attack ; later on, when local or general peritonitis develops, the temperature and pulse may assume the features characteristic of inflammation. 3. Vomiting. First of the contents of the stomach, then of bile, and, finally, in a large percentage of cases, of feculent matter. The feculent vomiting rarely appears before the third day, and in cases running a very acute course death may ensue before this symptom has time to develop. The vomiting is constant and gives no relief to the patient. 4. Constipation. Exceptionally there may be one or two pas- sao"es representing the contents of the bowel below the seat of obstruction ; after that the constipation is absolute, not even flatus passing by the anus. Treves has suggested that the evacuations sometimes observed toward the termination of the case, and not due to the relief of obstruction, may be dependent upon the beginning of peritonitis. 5. Tympanitic distention. Where there is a large segment of gut involved in the strangulation its early distention may give rise to a localized abdominal enlargement, which is exceedingly suggestive as VOMITING. 483 to the cause of the attack. In general, the meteorism is not marked except when peritonitis supervenes. Since in the large majority of cases the obstruction is localized in the lower portion of the small intestine, the primary distention will be observed in the middle abdominal region — i. e., the epigastric, umbilical, and hypogastric areas. Laugier claims by this symptom to locate the obstruction with some certainty. The violent peristalsis and repeated vomiting prevent the extreme meteorism characteristic of intestinal paralysis. 6. Localized tenderness and percussion-dulness. When present these signs are of exceeding great importance, since they denote the position of the strangulated bowel. Exceptionally a tumor may be felt formed by the congested gut or the matting together of the intestinal coils. The urine is diminished in quantity and may be suppressed. In acute strangulation it commonly contains albumin, and it is stated that this is of diagnostic value. In this connection the history is of great importance. Other congenital deformities would suggest the possibility of Meckel's diverticulum as a cause. A preceding typhlitis, pelvic peritonitis, or severe abdominal trau- matism would respectively assign an adherent vermiform appendix, peritoneal bunds, or rents in the omentum or mesentery as the causa- tive agents in the production of the symptoms. The age of the patient should also be considered, since this form of obstruction usually occurs between the twentieth and fortieth year. The sudden onset of violent, persistent pain, subnormal tempera- ture and frequent pulse, the obstinate, absolute constipation, the per- sistent, repi'ated vomiting, becoming fecal, and the rapid course of the disease, all point to internal strangulation. Auscultation of the abdomen is at times of value, a sound com- pared to the click of the water-hammer being heard most distinctly at the point of obstruction. Palpation and percussion should not be omitted, as thereby the seat of obstruction has been distinctly located. VoIvhIks is the most frequent form of intestinal obstruction after intussusception and that due to strangulation. N'omiting occurs, but is not so constant a symptom as in those forms first named. Thus it occurred in from od, mucus, water, and sometimes bile. The vomit may be tasteless or sour from fermentation, and may have an offensive odor from similar causes. Often it contains blood either in bright-red streaks or as a brownish-red fluid, or in similarly colored clots, which may be brown when they have been in the stomach for some time. Often the exuded blood, changed by mixture with the stomach-contents, looks like cofEee-grouuds, producing " coffee-ground vomit." This coffee-ground vomit is not ])athognomonic of gastric cancer, but is very characteristic of this disease. Microscopically the vomited ma- terials are seen to consist of particles of food, yeast-cells, cocci, and broken-down blood-corpuscles. (For the other symptoms of gastric cancer, see chapter on the Abdomen.) Coffee-ground vomit is also sometimes seen in cases of locomotor ataxia following a gastric crisis. Vomiting due to gastric ulcer is preceded by pain, and is gener- ally brought on by taking food, and so occurs soon after eating. The food is, therefore, only slightly digested, and evidences of fer- mentation are absent to a great extent. If blood is present, it is nearly always bright red and in considerable quantity, and indi- cates that a hemorrhage has recently taken place from the surface of an ulcer. Very large hemorrhages into the stomach may cause vomiting by irritating and distending this viscus. The history of vomiting after eating, the presence of blood in the vomit, the pain in the stomach, the age of the patient (generally twenty to thirty years), the sex (generally female), and the hyperchloric acidity, com- bined with the other symptoms (see chapter on Abdomen), complete the diagnostic array of facts. There are, however, other causes of vomiting of blood or hfema- temesis than gastric ulcer and cancer. Thus it occurs from obstruction to the portal circulation from hepatic cirrhosis, and from growths and splenic affections which result in varicosity of the bloodvessels of the stomach. Haematemesis also follows severe blows, kicks, and other injuries to the epigastrium. Sometimes it takes place in cases of heart disease in which there has resulted hepatic engorgement with secondary gastric congestion, and it may be developed in small degree by any form of violent vomiting which strains the stomach, VOMITIXG. 487 particularly if an irritant substance has already destroyed the mucous membraue. Again, hsematemesis is seen in scurvy, typhus, yellow fever, and acute yellow atrophy of the liver, as a result of breaking down or destruction of the coats of the vessels. Sometimes it is seen in cases of dengue, in influeuza of the epidemic type, and in relapsing fever. Hsematemesis may also occur in purpura hemorrhagica, in haemophilia, and as a result of vicarious menstruation. In malarial fever of a severe character the dark-colored vomit is generally due to bile, but it may be due to exuded blood. Such a case is reported by Boon as occurring in a child. Care should always be taken that the physician is not misled by the vomiting; of swallowed blood into a diagnosis of gastric hemor- rhage from any of the causes just named. It may enter into the stomach from the pharynx, as after epistaxis, or blood may be swal- lowed by a malingerer. Hamatemesis is to be separated from haemoptysis by the fact that in the latter there are physical signs in the lungs, the sputum is frothy and bloody, there is absence of retching or vomiting-movements, and the blood is bright red in haemoiitysis ofteuer than in hsematemesis. In order to determine that the discolored vomit of any case is due to blood a microscopical examination for the corpuscles must be made, and if these are greatly altered a chemical test may be used. (See further in this chapter.) The development of vomiting with suflden pain in the abdomen, resembling colic, which fails to yield to ordinary remedies, and is associated with sources for an embolism, should lead the physician to a consideration of possible embolism in the superior mesenteric artery. This condition must not be confounded with the vomiting of acute pancreatitis, in which colicky pain in the epigastrium, deeply seated and extending to the right shoulder and ba(!k (see Hepatitis, in this chapter), and great restlessness, pncconlial distress, dyspnoea, and faintness are present. The matters vomited are greenish, clear, and viscid, and the efforts at vomiting increase the pain. There is no jaundice, and death soon comes to the relief of the patient. As an early diagnosis of acute pancreatitis may permit surgical interference with possible recovery of the patient, the diagnosis is important. The mistake commonly made is to consider the case one of intestinal obstruction. Under the name of meltena neonatorum there is a condition of hsematemesis occurring in children within the first few days or weeks of life. This condition has been thoutjht bv Leul)e to be due to gastric 488 THE MANIFESTATION OF DISEASE BY SYMPTOMS. and duodenal ulcers, and his views are indorsed by Buhl and Iluhn, Spiegelberg, Biuz, and Landau. In one of the latter's cases throm- bosis of the umbilical vein was present, and it has been thought that when expansion of the chest takes place in the newborn child small clots may escape from this vessel through the ductus arteriosus into the descending aorta and gastric arteries, and thus cause an ulcer of the stomach by embolism. Vomiting of a peculiar character is always present in phosphorus- poisoning. The symptoms associated with ingestion of the poison may not come on for some hours. At the end of that time the pecu- liai taste of phosphorus may be noticed in the mouth, the breath is heavily laden with its odor, and burning pain in the oesophagus, stomach, and abdomen ensues. Vomiting and purging now assert themselves, and both the matters vomited and passed from the bowels may be luminous in the dark, owing to the presence of phosphorus. The vomiting is at first made up of food, then mucus, then bile, then perhaps blood. AW the symptoms of a mild gastro-enteritis may develop, but it is to be noted that constipation of an obstinate type may replace the purging. Very soon the liver increases in size, and gives rise to general hypochondriac pain and tenderness, as well as local swelling. At the end of twenty-four hours, or perhaps after the second day, a cessation in the symptoms occurs, and, if the physician be not on his guard, this will lead him to a hopeful prog- nosis. In the course of a few hours jaundice begins in the conjunctiva, and then extends over the entire body. With the onset of jaundice the vomiting and pain return with renewed vigor. The matters vom- ited are often the color of " coffee-grounds," due to exuded and altered blood. The bowels are absolutely confined, or the few hard masses passed are white and clay-like, because of the absence of bili- ary coloring-matter. There is no bile in the vomit in this stage, because the hepatic ducts have been closed by the inflammation set up in the liver. After this nervous symptoms ensue. Muscular twitchings, headache, vertigo, wild delirium, erotic convulsions, and finally unconsciousness and death occur. Sometimes the convul- sions occur just before dissolution. Even if the patient survive the acute stage, he generally dies of the changes produced in his vital organs, which consist in widespread fatty degeneration, even in the acute stages, i^ trophy of the liver, destruction of the gastric tubules, pancreatic involvement, and kidney degenerations aid in producing the ultimately fatal result. VOMITING. 489 During the course of poisoning by phosphorus the urine is scanty and perhaps albuminous, and is peculiar because of the unusual sub- stances found in it. The most unusual of these is sarco-lactic acid, which results from the breakiug-down of muscular tissues. Leucin and tyrosiu are also found, and tube-casts, with fatty globules in them, are seen. Free fat-globules may also occur. Bile acids and bile coloring-matter arc found in large amount, and the urine is generally dark colored for this reason. As phosphorus is eliminated as hypophosphoric acid, this substance is also present. The symptoms may so closely resemble those of acute yellow atrophy of the liver as to make a differential diagnosis impossible, unless some evidence of the presence of phosphorus is obtainable. The vomiting of acute gastric catarrh is generally seen in chil- dren, and is often preceded by great nausea. The contents of the stomach are first gotten rid of, then mucus, water, and bile may be ejected, and finally exhausting retching ensues if the attack is severe. The tongue in such cases is coated and dotted with red spots from the enlarged fungiform papillae, and the epigastrium is tender on pressure. There may or may not be fever and looseness of the bowels. The attack usually follows indiscretions in diet or exposure to cold. Vomiting from chronic gastric catarrh is usually a condition met with in adults, and when seen in the male is most frequently the result of a frequent use of alcoholic beverages to excess. In women it often develops from excessive tea-drinking associated with errors in diet. When due to alcoholism, the vomiting is often present only in the morning before or after taking food, and tiien is called the '' morning vomiting of drunkards." (See chapter on the Tongue.) Vomiting due to true gastnlis or inflammation of the stomach in its deeper layers is very rare, except as a result of the ingestion of an irritant ])oison or hot liquid. Perhaps the vomiting occurring in id until the chest is emptied of air. In the early stages of the disease this is all that occiu's, and unimpevith a rather forcible push, which will stretch the muscles of the calf of the leg. The biceps tendon is tested by placing the arm in semi-extension and tapping the tendon, when the forearm is still further flexed. In this connection mention should also be made of the cremasteric re- flex, which is developed when the skin of the inside of the thigh is tickled, the cremaster muscle drawing up the testicle on that side. It is most marked in boys. Having learned how to test for these muscle-jerks, we now turn to a consideration of what they mean when abnormally increased or absent. A loss of knee-jerk is not characteristic of any disease unless this loss is associated with other symptoms, which only need the dis- covery of this symptom to confirm the diagnosis. The nervous con- ditions in wiiich we find the reflexes decreased or lost, taking the patellar reflex as a type, are locomotor ataxia ; peripheral neuritis ; poliomyelitis, acute or chronic ; transverse myelitis, if the disease involves the reflex arc ; Friedreich's ataxia ; diphtheritic paralysis ; apoplexy, immediately after the shock ; Landry's paralysis ; spinal meningitis; spinal injnries, immediately after accident; epilepsy, immediately after an atta(;k ; and chorea. AVe also find a total loss of reflexes in advanced diabetes mellitus and sometimes in diabetes insi|)idus. By far tlu^ most common cause of the loss of knee-jerk is loco- motor ataxia, but any lesion involving the posterior cohuuns of the cord or the jiosterior nerve-roots in the second, third, or fourth liitubar segment will produce the same results. Therefore, loss of knee-jerk is symptoni:iti<' of transverse myelitis of this region as well as of ataxia. .Viiain, if the motor tract of the cord at these levels 520 THE MANIFESTATION OF DISEASE BY SYMPTOMS. are diseased, the kuee-jerk is lost, as, for example, iu acute and chronic poliomyelitis or myelitis involving the motor part of the reflex arc ; and, fiually, peripheral neuritis, which blocks the path- way from the periphery to the cord, and from the cord to the muscles, also causes loss of knee-jerk. If the cause of loss of knee-jerk be locomotor ataxia, we will prob- ably find in addition to this symptom some difficulty in walking, particularly if the eyes are shut ; a lack of steadiness if the feet are placed together when the patient stands with his eyes shut ; Argyll- Robertson pupils or a reaction to accommodation, but not to light; attacks of severe pain in the body or limbs ; and, it may be, laryn- geal crises or spasms and atrophy of the optic nerve. If the cause of loss of knee-jerk be neuritis, we will find tender- ness on pressure along the nerve-trunks, diminished muscular tone and some wasting ; an absence of any disturbance of the bladder and no Argyll-Robertson pupil, laryngeal or other crises, nor optic atrophy. Again, if the cause be acute poliomyelitis, there will be a history of sudden onset with fever, the limbs will be relaxed and flabby, the muscles will rapidly waste and become very feeble or paralyzed, and there will be no sensory symptoms whatever. The patient will usu- ally be a child if the disease is acute. If the loss be due to a trans- verse myelitis of the second, third, and fourth lumbar segments, the symptoms of paraplegia, parsesthesia, and anaesthesia, with atrophy of the muscles and loss of control of the bladder and rectum, will be present, and a girdle-sensation may be marked. In Friedreich's ataxia the history of heredity, the nystagmus, the early age of the patient, the absence of pupillary symptoms, the ataxic gait, and the loss of reflexes, are the facts which go to form our basis for a diagnosis. In the remaining diseases named the his- tory of the case points to the cause of the loss of the knee-jerk very clearly. The conditions in which we find the knee-jerk increased are apo- plexy soon after tlie attack ; disseminated sclerosis ; cerebral palsy of childhood ; paretic dementia (not constant); primary lateral sclerosis ; amyotrophic lateral sclerosis ; ataxic paraplegia ; hysterical para- plegia ; transverse myelitis if the lesion is above the reflex arc ; epilepsy some minutes after the attack ; unilateral lesions of the cord on the paralyzed side; injuries to the spinal cord, after recovery from first shock ; pressure on spinal cord above the reflex arc ; heredi- TEXDOX-REFLEXE.S AXD MUSCLE-TONE. 521 tary cerebellar ataxia ; sciatica ; tetanus ; rheumatoid arthritis ; and neurasthenia. The history of sudden paralysis and unconsciousness in a case of apoplexy with stertorous breathing, followed by loss of the knee-jerk, and then its return in an exaggerated manner, make the diagnosis clear unless the attack be one of the apoplectiform attacks of dissem- inated sclerosis, in which case there will be present a history of the intention-tremor, nystagmus, and the syllabic speech, so that though the knee-jerk is exaggerated in both diseases the diagnosis can be readily made. In the cerebral palsy of childhood, the age of the patient, the contractures and gait, with the history, decide the diagnosis. In lateral sclerosis the spastic rigidity, excessive exaggeration of the knee-jerks, absence of sensory disturbances, and ocular symptoms, all render the diagnosis possible. Similar exaggeration is also seen in amyotrophic lateral sclerosis, in which disease there is wasting of the muscles, particularly of the hand. In both these ailments the exaggeration of the knee-jerk is due to disease of the lateral pyramidal tracts, which block the inhibitory fibres from the higher centres. For similar reasons we find exaggerated knee-jerk in ataxic paraplegia. In hysterical paraplegia the age and sex of the patient, the pecu- liar facies, the areas of anaesthesia and hyperaesthesia, and the pecu- liar gait ])oint to the diagnosis. The increased knee-jerk in cases of transverse myelitis occurs when the lesion is situated at such a point in the cord that the lateral tracts are cut off and the reflex arc is preserved. In neurasthenia the knee-jerks are exaggerated, but are easily ex- hausted. Leaving the knee-jerk as a ty|)e of a reflex, we find that the skin- reflexes are often lost in cases of apoplexy when the deep reflexes are exaggerated. The table on following page from Taylor's Index of Medicine shows the area of skin reflexes very well. In glosso-labio-pharyngeal paralysis the reflexes of the tongue and throat are lost and those of the face sometimes increased ; in progressive muscular atrophy the reflexes of the arms are lost, while those of the legs are preserved, and in tul)ercular meningitis the reflexes arc apt to be more marked on one side than on the other: In athetosis the reflexes are increased in the affected part. Ankle-clonus is found most marked in hiteral sclerosis, in dis- sennnated sclerosis, and in amyotrophic lateral selerosis. A false clonus is sometimes seen in hysteria. 522 THE MANIFESTATION OF DISEASE BY SY3IPT0MS. Reflex. Point of stimulation. Situation of centre. Significance. 1. Plantar, Irritating skin of soles. Extreme end of cord. Usual in health. 2. Gluteal, Irritating skin of but- tocks. Origin of 4th and 5th lumbar nerves. Rare in health. 3. Cremasteric, Irritating skin of inner side of thighs. Origin of 1st and 2d lumbar nerves. Usual in health ; best marked in boys on account of the newly formed cremaster. 4. Abdominal, Irritating skin of abdo- men in line of nipples. Origin of 8th to 12th dorsal nerves. Frequently absent. 5. Epigastric, Irritating skin of chest in 5th and 6th spaces. Origin of 4th to 6th dor- sal nerves. May be absent in health. 6. Erector spinse, Irritating skin from sca- pula to crest of ilium. Origin of all the dorsal nerves. Rare in health ; frequent in wasting disease. 7. Interscapular, Irritating skin between scapulae. Origin of 6th cervical to 3d dorsal. Rare in health. 8. Palmar, Palms of hands. Cervical bulb. Only in infants. 9. Cranial: Conjunctival, Sclerotic, or inner sur- face of eyelid. Medulla. Absent in disease of 5th nerve only. Iris (to light), Pupil. Anterior portion of ocu- lomotor nucleus. Absent in disease only. Palate, Soft palate and uvula. Medulla. Absent in disease only. Nasal (sneez- ing), Naso-respiratory pas- sages. Medulla. 1 Absent in disease only. CHAPTEE IX. SPEECH. The changes in the speech and voice — Their significance — Aphasia — Apraxia — Alexia — Paraphasia. The character of the speech and the tones of the voice often con- vey a considerable amonut of diagnostic information to^ the jihysi- cian. While in many diseases no marked alterations from the nor- mal manner of speech are present, in others marked changes take place. Thus, in acute laryngitis due to exposure to cold or irritant vapors the patient has a whinpering voice. In persons sufPering from pulmonary tuberculosis the development of hoarseness and whisper- ing, or labored speech tells ns only too well of the fact that the grave and distressing complication called laryngeal tubercidosis has arisen, and that the progress of the case will be more rapid toward the fatal result. Again, the sudden onset of whispering voice or complete aphonia, occurring in a young girl whose facies is hysterical, should always arouse a suspicion of liysteria, while if the signs of this con- dition are absent and the patient has none of the signs of tubercu- losis, we should examine the larynx for a papillomatous growth. Again, if hoarsenesH or a whispering voice is manifested by a male of adult years, who is also suffering from dyspnoea, unilateral flush- ing or sweating of the face and neck, and unequal radial pulses, we should suspect aortic aneurism or a mediastinal tumor which is pressing on iiis recurrent laryngeal nerve. When a child speaks with a nasal twang or indistinctly we suspect the presence of adenoid vegetations, and will probably find that he or she suffers from mouth- breathing; and stuttering or stammering may also be due to this cause. A feeble^ hesUallng speech is often a sign of exhausting disease, and a short and quick but feebly spoken sentence generally indicates that the patient is suffering from some cardiac or pulmonary com- plaint, which renders his breath short, so that he hurries through his sentence in order to be able to breathe freely again. Thus, in cases of pneumonia or of pultnonary oedema this hurricil speech is a very constant siurn. 524 THE MANIFESTATION OF DISEASE BY SYMPTOMS. Again, in cases of typhoid fever, when the tongue is dry and im- mobile from accumulated sordes, a mumbling character of the speech is present, even if the brain is entirely clear, and in severe stoma- titis the same quality of the voice may be present. It is in connection with the disorders of the nervous system, how- ever, that the most typical alterations of the voice occur. Let us suppose that a patient in middle life or in more advanced years de- velops a slow, scanning speech, with intention-tremors (see chapter on Hand), nystagmus, and more or less muscular weakness. In all probability he is a sufferer from insular, or, as it is otherwise called, disseminated sclerosis. When he speaks each syllable is sharply accentuated and slowly pronounced. The only other conditions in which a slow, scanning speech is of great diagnostic importance is in that rare disease, Freidreich's ataxia ; but the fact that this disease begins in childhood, that several members of the family are apt to be affected, that there are ataxic symptoms and early talipes equinus, renders it easy to separate this affection from insular sclerosis. (See Paraplegia, in chapter on Feet and Legs.) A hesitating, halting speech associated with Argyll-Robertson pupils, unequal pupils, delusions of grandeur, and tremor of the tongue, which last symptom may be so marked as to cause the speech to be indistinct and blurred, is indicative of paretic de- mentia. If an incoherent speech develops in a child who is not suffering from an acute illness causing delirium, there will usually be found in association with this symptom the nervous twitchings of chorea, for speech- disturbances occur in about one-third of the patients suf- fering from this disease. A very indistinct speech of a mumbling character, great difficulty being experienced in the pronouncing of dental and lingual sounds, and perhaps associated with feebleness of the voice, if the larynx is involved, is seen in cases of glosso-labio-pharyngeal paralysis. If the cause of the defective speech be this disease, there will be found, as associated symptoms, wasting of the tongue, lingual tremors, some dribbling of saliva from the mouth, and immobility of the lips, the face about the mouth being expressionless. Somewhat similar symptoms due to paralysis of the lips, with escape of the tongue and pharynx, at least for a long time after labial paralysis develops, is sometimes seen in advanced cases of amyotrophic lateral sclerosis ; and a still more close resemblance SPEECH. 525 raay be produced by the so-called '' pseudo-bulbar paralysis," the lesion of which is in the motor cortex of the brain on both sides, in the lower part of the ascending frontal convolution. Rarely the latter is only a unilateral disease. A rather shrill, j)iping voice, the sentence being begun with hesi- tation and then hurried to an end in rapid volley of words, is some- times seen in paralysis agitans. By far the most interesting speech-defect is that called aphasia. It is divided into motor aphasia and sensory aphasia. Before studying these conditions we must discuss the nervous mechanism of speech. When a child learns to talk it performs a purely imitative act. Its auditory nerve conveys the>«ound to its perceptive centres, and from here an impulse is sent to its motor speech-centres, and these again send impulses to the inferior speech- nuclei in the medulla oblongata, which in turn move the muscles of speech. Simultaneously the child learns the words and stores them in memory-centres for sounds, and also stores in memory -centres " motor memories," which tell him how to repeat the muscular movements a second time. Again, when he learns to recognize objects and call them by name he must use "visual memory" centres. These centres are all best develo[)ed in the left hemisphere of the brain in right-handed persons and in the right half of the brain in left-handed persons. If a person suffers from pure aphasia, he simply loses the memory of how to say certain words, and the lesion is in the third left frontal (Broca's) conv^olution. He can read to himself, because he has not forgotten the meaning of the words, and for this reason he under- stands what is said to him, and may be able to rej)eat a word imme- diately after you have said it by a purely imitative process. Gener- ally we find with aphasia a condition called agraphia in which the patient cannot write volimtarily, but can copy perfectly. In the great majority of cases of apiiasia, however, tlie patient is paralyzed in his rigiit hand, so that the symptoms of agraphia cannot be demon- strated. Under the name oi paraphasia we sometimes meet with a cx)n(lition in which the i)ationt can speak quite freely, but transposes words or interpolates useless words to such an extent that what he says is unintelligible. In another condition closely connected with aphasia we have a state in whicli the j)atient can spell out words from a page set before him, but he cannot read, because the words convey no idea to him. 526 THE MANIFESTATION OF DISEASE BY SYMPTOMS. This is called alexia or '' word-blindness." Again, he may forget the use or significance of certain objects, such as a knife or fork ; this is called apraxia. Still further, words when spoken to the patient in his native language may be heard perfectly, and yet understood no more than if in some unheard-of language. This is called " word- deaf uess." If the patient has simple aphasia, he has a lesion in the third frontal convolution in its posterior part. If he has word-blindness or alexia, the lesion is in the angular gyrus, extending back into the occipital convolution. If he has apraxia or the loss of memory of objects, the lesion is in the same area as in alexia ; and if '^ word- deafness " is present, the lesion is in the posterior part of the first temporal and upper part of the second temporal convolution. As the various symptoms of aphasia in all its forms are closely associ- ated with those of focal lesions of the brain, resulting, for example, from hemorrhage or embolism, the reader should read the chapter on Hemiplegia in this connection. The following plan of testing a patient, devised by Eskridge from a shorter one of M. Allen Starr, may be followed with advantage : 1. The power to recognize objects seen, heard, felt, tasted, smelt, and their uses. 2. The power to recall the spoken names of objects seen, heard, felt, tasted, and smelt. 3. The power to understand sounds other than speech. 4. The power to understand speech and music. 5. The power to call to mind objects named and point them out at request. 6. If word-deaf, can he recognize his own name when it is spoken ? 7. The power to recognize a word spelled aloud. 8. The power to call up mentally the sound of a note, figure, letter, or word. The examination thus far will test the various sensory areas, but more especially the auditory and the association tracts between the different sensory areas connected with speech. 9. The power to recognize letters, figures, notes, and colors seen. 10. The power to understand printed and written words seen. 11. The power to read printing, writing, and music aloud and inaudibly, and to understand what he reads. 12. The power to recall objects, the names of which are seen. SPEECH. 527 13. The power to write voluntarily. 14. Tiie power to write at dictation. 15. The power to copy, and the manner of copying, printing, and writing. 16. The power to write the name of objects seen, heard, felt, tasted, and smelt. 17. The power to read aloud and inaudibly, and to understand what has been written. 18. The power to write his name and the ability to read it when written by himself and by another person, or when it is printed. 19. The power to recognize a letter by tracing it with the index- finger or with a pencil, the movements beiug guided by pnother. 20. The power to call up mentally the appearance of an object, a figure, a note, letter, or word, when word-blind. These additional tests will aid in determining the condition of the visual word-memories in the angular gyrus, and the connection between this area and the surrounding sensory and motor areas : 21. The power to speak voluntarily, and, if impaired or lost, the character of the defect. 22. The power to repeat words after another. 2.3. Does the patient recognize his mistakes iu speaking and writing, and can he correct them ? 24. Can the patient think in speech (proposition ize) ? 25. Is there any special difficulty in the use of nouns, verbs, or other parts of speech ? 26. The power to understand pantomime or gesture expression. 27. The power to employ intelligently gesture in expression. 28. The power to read figures and to calculate. 29. The power to count both money and in numbers. 30. The power to play a game of cards or other games. INDEX OF DISEASES. ABSCESS, cerebral, choked disk not generally present in, 178,478 character of pain in, 509 coma of, 450 diagnosis of, 424 fever in, 478 symptoms of, 438 tarltf rerchrale, a sign of, 198 vomiting in, 470 hepatic, brick-dust sputum in, if communicating with lung, 500 character of pain in, 517 symptoms and signs of pysemlc, 321,401 svmptoms and signs of tropical, " 321 vomiting in, 492 lumbar, sciatic pain in, 512 mastoid, u-dema i)ack of ear in, 218 mediastinal, purulent sputum in, 501 multiple, of kidnev, casts of pus-cells in, 309 perinephritic, bulging in (lank in, 318 pulmonary, anchf)vysauce sputum in auKchic dysentery, 500^ chronic morning cough in, 49(5 copious and purulent sputum in, 278, 501 diagnosis between mediastinal growths and, 28(5 elastic (ibres in sputum of, 503 history, symptoms, and physical signs of, 277 usually in lower lobe, 278 pyoi)ni'urnotliora.x subphrenicus,317 suliphrcnic, purulent sputinu in, 501 Acromegaly, enlargement of ("eet in, 105 enlargement of tongue in, 139 face of, 32 spade-like hanalior of, 26 poiUilocyosis in, 344 sliglit fever in, 344 wiiyward appetite in, 344 Cholangitis, catarrbal or suppurative, character of ftver in, 422 gall-stone colic in. 422 marked jaundice in, 422 Cholera Asiatica, comma bacillis in, 397 diagnosis of, 397 llippocratic face in impending death of, .32 indicanuria in, 36t) sulinornia! tempcratiu'c in, 430 532 INDEX OF DISEASES. Cholera Asiatica, systemic infection in,397 temperature in, 427 vomiting in, 485 infantum, character of fever in, 427 Chevne-Stokes respiration in, 397 cold skin and high rectal tem- perature in, 428 diarrho?a in, 427 disparity between axillarj' and rectal temperature in, 397 mousv, musty odor of stools in, 403 obstinate vomiting in, 427 subnormal temperature in se- vere, 430 symptoms of, 396 morbus, subnormal temperature in severe, 430 symptoms of, 396 nostras. See Cholera Morbus. Chorea, antemic murmur in children in, 289 character of spasms in, 473 diagnosis of, 473 electric, 65, 474 expression in, 30 facial spasm in, 43 Huntington's, 65, 474 hysterical, 65 incoherent speecli in, 524 insaniens, 474 loss of knee-jerk in, 519 paralytic, 64 senile, 64 spasm of head in, 46 of tongue in, 142 Chronic poliomyelitis, claw-hand in, 60 Continued fever. See Malaria, Eemittent. Coryza, action of child toward breast in, 23 in influenza 423 Cretinism, facial expression in, 31 Croup, spasmodic, character of cough in, 495, 497 inspirations pi-olonged in, 255 laryngeal spasm in, 285 Croupous pneumonia. See Pneumonia, Croupous. Cyst, echinococcus, of liver, 321 hematuria in renal, 364 of kidney, 318 of pancreas, 317 ovarian, diagnosis of, 304 Cystitis, character of pain in, 516 chronic, triple phosphates in urine in. 376 darting pain in urethra in, 358 phosphaturia, cloudiness of urine in, 361 purulent, septic fever in, symptoms of, 355 tenesmus in 355 DEMENTIA, paretic, delusions of grandeur in, 524 hemiplegia in, 128 hesitating, halting speech in, 524 knee-jerk in, 520 localized sweating in, 215 tremor of tongue in, 524 Dengue, an epidemic disease, 423 character of fever in, 423 erythema in, 199 hfematemesis in, 487 jaundice in, 188 joint-involvements in, 114 pain involving entire body, 517 Diabete bronze, 187 Diabetes insipidus, constipation in, 394 great increase of urine in, 360 loss of knee-jerk in some cases, 519 urine in, 393 mellitus, boils occurring in, 209 caries of teeth in, 145 cataract in, 181 color of urine in, 367 coma in, 393 constipation in, 394 development in carcinoma of pancreas in, 316 diagnosis of coma in, 448 dry, harsh skin in, 392 fermentation of urine is due to sacchai'omyces albicans in, 379 gangrene in, 211 great increase of urine in, 360 headache rarely in, 435 heavy, sweet odor of urine in, 360 high specific gravity of urine in, 360 jaundice occurring in, 187 knee-jerk lost in advanced, 519 ocular palsy in, 156 paraplegia rarely occurring in, 102 polydipsia in, 383 polyphagia in, 383 prognosis in, 383 prognosis of, if associated with obesity, 383 influenced by age, 383 pruritus in, 246 retinitis in, 180 roseola occurring in, caused by urine, 202 rosette crystals of uric acid in urine of, 374 wasting in, 383 white spots on trousers in, 18 urine in, 393 vomiting a rare symptom, 478 Diphtheria, antesthesia in 50 per cent, of, due to neuritis, 237 IXDEX OF DISEASES. 533 Diphtheria, casts of larynx and upper bronchial tubes at times coughed up in, 502 double oculomotor paralysis in, 161 paralysis of tongue following, 141 paraplegia as a sequel in, 101 rose-rash in, -01 sickening, sweet odor of breath in, 23 symptoms of, 144 Dubini's disease, 65, 174. See Electric Chorea. Hh'sentery, acute primary, of a diph- theritic character, 401 amcebic, amreba coli the cause of, 401 liver-abscess in, 401 symptoms of, 400 character of stools in, 400 fever of 1° or 2° in, 400 secondary diphtheritic, a complica- tion of Bright's disease, 401 due to acute croupous pneu- monia, 401 in chronic heart disease, 401 slight chill in, 400 thirst in, 400 ECLAMPSIA, puerperal. .SV.- Puer- peral Eclampsia Eczema, appearance of nails in, 50 due to mercury, 209 due to quinine, 209 Electric chorea, 65 Elephantijisis, sometimes caused by filaria sanguinis hominis, 353 symptoms of, 219 Embolism, cerebral, vomiting in, 478 in kidney, casts of micrococci in, 369 haematuria in, 368 of coronary arteries, 300 of pons Varolii, 429 of superior mesenteric artery, symp- toms of. 487 Emphysema, appearance of hands in, 48 ''barrel-shaped" chest of, 251 expiration prolonged in, 255, 283 lessening area i)f cardiac dnlness, 267 pulmonary and cardiac hypertrophy causing depression of apex-beat in, 258 spleen displaced downward in, 373 vocal fremitus of intestinal tract, diarrhani due to, 401 pain due to periostitis of skull, 509 papillitis in, 178 panesthesia in spinal, 243 parchnieut-like skin of, 26 pseudo-palsy in, 76 ptosis in changes due to, about base of brain, 39 retinitis in, 180 rose-rash in, 201 spa-stic i)araplegia in, 92 symptoms of arteritis due to, 437 sy{>hilitic triad, 145 Syringomyelia appearance of nails in, 49 loss of i)ain and temperature-sense in, 2:)2 partial anii'sthesia in, 232 patches of ana'sthesia, 232 symptoms of, 2152 wa.sting of hands with ansestbesia in, 61 S<- Locomotor TABES doi-salis. Ataxia. Tetanus, character of convulsions in, 471 of fever in, 428 facial spasm in, 43 head or ceplialic, 45 increased knee-jerk in, 521 ptosis in, 39 Tetany, accoucheur's hand in, 63 character of convulsions in, 472 Chevostek's symptom in, 472 Trousseau's symptom in, 472 Thermic fever. /SVc Sunstroke Thomsen's disease, diagnosis of, 476 spasm of hand in, 66 of tongue in, 142 Thorax, aneurism of, diagnosis between mediastinal growths and, 286 localized sweating in, 215 spongy ^enous masses above clavicle due to, 253 Thrombosis, cerebral, 218 of cavernous sinus, 161 of cerebral sinuses, symptoms of, 440 coma of 450 of umbilical vein in malsena neona- torum, 488 y. symptoms of, 218 vomiting in, 478 Thrusii, appearance of tongue in, 133 Tonsillitis, chronic iiight cough in, 498 crvstals of margaric acid in follicu- lar, 504 difl'erentiation between diphtheria, scarlet fever and, 143 sickening sweet odor of breath in, 23 symptoms of follicular, 143 symptoms of suppurative, 143 Tiichinosis. See Trichniasis. Trichniasis, diagnosis of, 415 pufiy eyelids in. 30 Tuberculosis, anremia in, 344 albumosuria in, 385 bronchial breatliing and consolida- tion in. 270 bronchitis ?) as cause of death, 20 bronchophony, 677 Charcot-Levden crvstals in sputum of, 502 Cheyne-Stokes breathing in menin- geal, 255 chronic loose morning cough in cavity of, 496 crej)itant rales and breaking down of lung-tissue duo to, 272 diagnosis between catarrhal pneu- monia and pulmonary, 277 between typiioid fever and, 414 of acute miliary, 425, 479 diarrim-a of, 39-I dia/.o reaction in severe pulmonarv, 390 elastic libres in sputum of, 503 frog-belly in children with, of en- larged mesenteric glands, .303 iiii-moptysi:, in, 500 heavy face of tubercular bone dis- ease, 28 hemorrhagic pleurisy in, 282 iiollow-olu'sted build' in, 18 544 INDEX OF DISEASES. Tuberculosis, multiple ulceration of tongue in, 136 necessity of examining axilla and septum of upper and middle lobe of right lung in, 278 ocular palsy due to, 156 of bones in amyloid disease of kid- ney. 392 of kidney, luematuria in, 364 pain of pleuritis due to, 516 percussion-note dull in consolidation due to, 262 pleurisy complicating, apt to become purulent, 2S2 with etihsion coming on insidi- ously in undiscovered, 282 ptosis in changes about base of brain due to, 39 puerile breathing an earlv sign of, 270 rapidity of respiration in, 254 retraction of abdominal wall in, 304 scars on neck resulting from suppu- rating glands in, 214 spiritueile face of children with diathesis of, 28 sputum, Curschraann's spirals rarely seen in, 501 transitory unequal dilatation of pupil sign of, 168 vocal resonance increased and con- solidation due to, 374 vomiting of acute miliary. 492 Tumor, abdominal, character of pain in, 516 brain, Cheyne-Stokes breathing in, 255 hyperaesthesia in, 245 parsesthesia in, 243 symptoms of, 436 unilateral anaesthesia in, 237 vertigo in, 444 cerebellar, choked disk in, 479 peculiar staggering gait of, 479 vomiting in, 479 cerebral, character of pain in, 436, 509 choked disk in, 48 impaired memory in, 478 severe headache in, 435, 478 slow pulse in, 478 vertigo in, 478 vomiting independent of taking food, 478 detection of, in intussusception, 431 diagnosis of fattv, of abdominal wall, 311 girdle-.sensation in cord or meningeal, 244 of abdomen, 317 of bladder, interference with passage of urine in, 359 Tumor of cord, bladder symptoms of, 357 of mediastinum, 285 of nerves, pain in, 515 phantom, 319 pontine, anaesthesia in, 227 rapidity of respiration in lung, 254 Typhoid fever, albumosuria in, 385 appearance of eruption in, 201 bacillus of Ebertli the cause of, 414 bloody stools, 404 bradycardia in, 299 causes of mumbling speech in, 633 of recrudescence of fever in, 412 of vomiting in, 485 character of coma in, 448 of fever in, 411 date of eruption in, 200 delirium in, 414 diagnosis of, 414 between acute miliary tu- berculosis and, 425 acute tuberculosis and, 414 tricliinosis and, 415 ulcerative endocarditis and, 414 Ehrlich's diazo reaction in, 390 enlargement of spleen in, 323 face in, 29 fever may be intermittent in, 413 persisting due to ansemia, 413 due to pulmonary,pleu- ral, or bone disease, 413 headache in. 442 hypercesthesia in convalescence from, 245 increase of urine in convales- cence from, 360 lesion of lungs generally at bases, 414 meteorism in, 414 moderate bronchitis early in, 414 mushy stool, 403 oedema of thigh over deep mus- cular abscess following, 218 parotitis in, 414 pleurisy with eftusion compli- cating, apt to become puru- lent, 281 relapse in, 412 sudden fall in temperature due to hemorrhage of any sort, 412 due to intestinal hemorrhage, 412 INDEX OF DISEASES. 545 Typhoid fever, stupor in, 414 sudden fall in temperature due to intestinal perforation, 412 tongue of, 132 tympanites in, 414 without fever, 413 Typho-malarial fever. See Malarial Re- mittent Typhus fever, character of fever in, 415 eruption in, 415 crisis in, 415 date of eruption in, 200 great exhaustion in, 415 hfcmatemesis in. 487 headache in, 415 ypETHRIITlS, specific, gonococci in, Uricjemia, 372. See Lithtemia VAGINITIS, specific, gonococci in, 377 Valvular heart disease. See Heart in Symptom Index. Varicella. See Chickenpox. Variola. See Smallpox. WEIL'S disease, almost total absence of gastro-intestinal symptoms in, 423 character of fever in, 423 clay-colored stools in, 423 jaundice in, 423 swelling of liver and spleen in, 423 Whooping-cough, character of, cough in, 495 ulcer of frsenum due to, 137 vomiting in, 493 ^ELLOW atrophy of liver, acute, con- 1 vulsions in, 472 diagnosis of coma in, 448 hfematemesis in, 487 jaundice in. 188 symptoms off* 188, 488, 492 fever, black vomit in, 423 character of fever in, 423 diagnosis of, 492 between bilious remitent fever and, 423 hsematemesis, 487 hemorrhage from mucous mem- branes in, 423 jaundice in, 423 tarrv stools in, 423 35 INDEX OF SYMPTOMS, ORGANS, AND TERMS. ABADIE'S sign," 44 Abdomen, 302 causes of distention of, 3(t4 of localized bulging of wall of, 306 of pain in, 513, 516 of protrusion of wall of, 303 of retraction of wall of, 303 of swelling in epigastrium, 311 inequality of shape, due to me- teorism in intussusception,481 palpation of, 309 tumors of, 317 Accoucheur's hand in tetany, 63 Acne due to bromine or iodine, 204 due to iron, 204 due to workiug in paraffin, 204 Acroparaesthesia, 243 diagnosis of, 244 ^gophony over pleural effusions, 275 iEsthesiometer, 221 Agrapliia, 525 location of lesion in, 526 Albuminuria, boiling-test in, 379 in antemia, 381 cyclic. 381 due to congestion of kidney, 381 Heller's test in, 379 indicative of renal disease, 381 marked or absent in amvloid disease of kidney, 392 quantitative tost by centrifuge, 379 transient, in chronic interstitial ne- pliritis, 392 Albumosuria, Harris's test for, 383 in normal puerperium, 385 said to be due to action of micro- organisms, 385 significance of, 3S5 test for, 383 Alexia, 525 location of lesion of, 526 Allochiria in hysteria, 243 multiple sclerosis, 243 myelitis, 243 tabes dorsalis, 243 Alpiia cori)Uscles, 335 Amaurosis, IHl significance in brain-tumor, 437 Amblyopia, 178 Amceba coli, 401 Amphoric breathing, rarely heard in pneumothorax, 271 in small cavity, 271 Anaesthesia, 224 y bilateral, peculiarities of, in hysteria, 221 never in cerebral lesions, 230 due to spinal lesions, 230 of body and legs due to locomotor ataxia, 230 causes of, 225 crossed, in lesion of peduncle, 228 differential diagnosis in facial, 242 distribution in special nerve involve- ment, 240 dolorosa in cancer of spine, 232 of face due to involvement of fifth nerve and its nucleus, 241 gauntlet or stocking form of, in hys- teria, 228 location of lesion of, in the spinal cord, 323 in 50 per cent, of neuritis due to diphtheria, 237 of Friedreich's ataxia, 231 of myelitis, 231 other causes of, 231 patches of, in leprosy, 242 in syringomyelia, 242 reflexes preserved in cerebral, 229 signs of, due to neuritis, 236 in toxic peri|thcral neuritis, 237 zones of, 2-'>4 Analgesia in locomotor ataxia, 230 Anasarca, general. «S'(«' General Anasarca. Anatomy of brain. 117 of optic nerve, 170 of sensory tracts, 224, 229 of tongue, 130 Anchylostomum duodenale, aniemia due to, 346, 407 Ankle-clonus, false, in amyotrophic late- ral sclerosis, 521 in hysteria, 521 how best devebiped, 519 in lateral sclerosis, 521 most marked in disseminated sclerosis, 521 548 INDEX OF SYMPTOMS, ORGANS, AND TEBMS. Aphasia due to hemorrhage into the island of Reil, 126 due to haematoma near island of Eeil, 128 Aphonia in hysteria, 523 Apoplexy, albumosuria in, 385 Cheyne-Stokes breathing in, 255 coma of, 449 conjugate lateral laralysis of ocular muscles in, 162 contractions following, 62 diagnosis between coma of, and alco- holism, 449 ingravescent, 125 involuntary passage of urine in, 359 knee-jerk decreased immediately after shock, 519 exaggerated some time after shock, 521 skin-reflexes lost when deep reflexes exaggerated, 521 vertigo before, 44 Appetite, wayward in chlorosis, 344 Apraxia, 526 location of lesion in, 526 Arcus annulus, 146 senilis, 146 Argyll-Robertson pupil, 166 not present in ataxic paraplegia, 83 not present in Friedreich's ataxia, 81 Argyria, 190 Arms, movements of, 59 spastic rigidity an early sign of chronic hydrocephalus, 63 tremors of, 67 Arterial tension, 327 causes of high, 328 of low, 328 high in acute diffuse nephritis, 391 Ascaris lumbricoides, 407 Ascites, cardiac apex raised in, 258 caput Medusie in hepatic cirrhosis causing, 305 diagnosis of, 304 Asthma, character of rales in, 283 due to cardiac lesions, 284 expiration prolonged in, 254 due to gastric disorder, 284 physical signs and symptoms of, 283 rapidity of respiration in, 254 due to reflex nasal irritation, 284 due to renal disease, 284 sputum of, Charcot Leyden crystals in, 283, 501 Curschmann's spirals in, 283, 501 pearls of Laennec in, 501 Asymmetry, facial, 33 Atheroma of bloodvessels, headache in, 444 Atheroma, in chronic interstitial nephri- tis, 392 in old age, 327 symptoms of, 327 in syphilis, 327 Atrophy, bilateral, of tongue, diseases in which it occurs, 139 BACCELLI'S sign, 274 Bacilli, anthrax, in lesions of, 427 of Eberth in stools of typhoid fever, 414 found in preputial smegma, 377 in stools of cholera, 397 of tuberculosis in urine, 397 methods of examining for, 504 in tubercular pyelitis, 39H Bedsores, in acute transverse myelitis. 212 in hemiplegia, 212 Behavior, in advanced hepatic and renal cirrhosis, 20 of children with cerebral trouble, 23 of healthy child, 23 in poisoning due to opium, 20 Biceps tendon reflex, how developed, 519 Bladder, character of blood in urine from, 362 causes of retention of urine in, 356 nervous, 359 stone in, interference with passage of urine, 359 symptoms of disease of, 355 of inflammation of, 358 Blood, character of, in haemoptysis, 500 estimation of haemoglobin by hsemo- globinometer of v. Fleischl, 341 Heller's test for, in the urine, 362 method of staining with Ehrlich's triple stain, 347 normal constitution of, 333 parasites of, 347 red corpuscles in, estimation of, by hsematocytometer, 336 with hrematocrit, 338 character of change in anaemia, 343 coloring-matter decreased in oligochromaemia, 334 decreased in myelogenous leu- kaemia, 347 in oligocythaemia, 333 extraordinary decrease of, in pernicious anaemia, 343 increased in polycythtemia, 333 megaloblasts, 341 microblasts, 344 normoblasts, 344 nucleated, 340 poikilocytes, 340 varieties of, 333 INDEX OF SYMPTOMS, ORGANS, AND TERMS. 549 Blood in stools, 361 character and significance of, 402, 404 in dysentery, 400 in entero colitis, 399 tests for, 494 in the urine, 361 in vomitus, 486 white corpuscles, amceboid move- ment impaired in leuksemia, 347 estimation of, with hsemato- cytometer, 338 eosinophiles, 335 increase of, 335 lympliocytes alone increased in lymphatic leuk;emia, 347 mononuclear lymphocytes, 334 multinuclear lymphocytes, 334 neutrophiles, 335 proportion of, to red, 335 altered by taking food, 335 by pregnancy, 335 Toison's solution for counting, 338 Blowing breathing. See Bronchial Breathing. Boils in diabetes mellitus, 209 Bothriocephalus latus, 405 Bowels, constipated in jaundice, 185 patient's idea as to regularity, 21 Brachial monoplegia, apparent, 75 causes of cortical lesions in, 73 due to cortical lesions, 72 due to crutch-paralysis, 75 Erb's paralysis, 75 due to fracture or dislocation of the head of the humerus, 74 in hysteria, 73 due to injury of brachial plexus or important branches of, 74 Klumpke's paralysis, 75 due to lead-poisoning, 75 due to locomotor ataxia, 74 paralysis of special muscles in, 36 ' panesthesia, 76 Bradycardia, 299, 331 in jaimdice, 299 ty])boid fever. 299 Bramwell's method of staining and mounting casts in urine, 372 Breath, ciiaracter of, in diphtheria, 23 in empyema opening into bron- chus, 23 fetid, in bronchiectasis, 278 in fever, 23 in gastric disorders, 23 in healthy child, 23 in tonsillitis, 23 Bromidrosis, cold clammy hands in, 511 in hysteria, 215 Bronchial breathing, due to compression of lungs over pleural effusion, 370 _ in cavity, 270 in catarrhal pneumonia, 270 in consolidation due to pneu- monia or tuberculosis, 370 Bronchiectasis, fetid breath of, 278 purulent sputum in, 501 sacculated, loose morning cough in, 496 _ Broncho-vesicular breathing, 270 Bronchophonv in tuberculosis of lungs, 277 Brow ague, due to malaria, 508 Bullse, on face, due to antipyrine or iodine, 211 in pemphigus, 210 trophic lesions of disease of central nervous system, 210 CACHEXIA, general anasarca in can- cerous, 217 Calculus s, 478 Chyluria caused by filaria sanguinis hominis. 363 test for, 367 Cirrhosis, hepatic, ascites in, 321 caput MedusEe in ascites caused by, 305 disorders of digestion in, 321 enlargement of spleen in, 323 hfematemesis in, 321 symptoms due to, 322 Cirrhosis, hepatic, uric acid in excess in urine of, 374 Cofiee-ground vomit in gastric ulcer, 486 in locomotor ataxia, 486 in phosphorus-poisoning, 488 Colic, causes of abdominal, 513 character of crying in children caused by abdominal, 23 convulsions in, 472 gallstone, in catarrhal cholangitis, 422 hepatic, 185, 514 lead, pain in, 514 renal, character of pain in, 514 diagnosis of, 514 retraction of abdominal wall in renal hepatic, and lead, 304 sometimes due to strongylus gigas, 365 ureteral, 361 Coma, ability to protrude tongue in, when otiier orders fail to gain response, 140 of acute alcoholic poisoning, 445 of acute vellow atrophy of liver, 448 of Addison's disease, 451 of apoplexy, 449 causes of, 445 due to cerebral disease, 19 due to cerebral softening, 450 of cerebral syphilis, 151 of chloral-poisoning, 447 of diabetes, 393, 448 due to epidemic cerebro-spinal men- ingitis, 451 of general paralysis, 451 may occur in chronic parenchyma- tous nephritis, 391 of multiple sclerosis, 451 of opium-poisoning, 446 due to purulent leptomeningitis, 451 rapidity of respiration in diabetic or ursemic, -^54 due to renal disease, 19 slowness of breathing in uraemic or diabetic, 254 due to subdural hemorrhage, 450 of sunstroke, 451 of typhoid fever, 448 Congestion, pulmonary, 278 physical signs and history of, 278 renal, albuminuria in, 381 blood-casts in, 369 irritation of bladder in, 358 Constipation, causes of, 394 in chlorosis, 344 in chronic lead-poisoning, 395 in diabetes mellitus, 394 insipidus, 394 indicanuria in, 366 INDEX OF SYMPTOMS, ORGANS, AND TERMS. 551 Constipation, due to intestinal obstruc- Cough, chronic, loose, morning, in tiiber- tion, 395, 482 in jaundice, 394 due lo reflex irritation, 395 Convulsions in acute articular rheuma- tism with hyperpyrexia, 428 in Addison's disease, later stages, 471 in anterior poliomyelitis, 429 in cerebro-spinal meningitis, 424 clonic and tonic, 433 clonic, of acute alcoholism, 461, 468 due to cardiac sedatives, 461 due to chronic lead-poisoning, 461 diagnosis of, 463 of epilepsy, 453 due to eruptive fever, 460 of hemicrania, 469 due to hysteria, 462 of Jacksonian epilepsy, 454 due to malaria, 462 in malingerers, 469 of post-hemiplegic epilepsy, 456 of puerperal eclampsia, 467 of syphilitic epilepsy, 456 of syncope, 468 erotic, in phosphorus-poisoning, 488 of infants, due to meningitis, 471 due to pseudo-meningitis, 471 due to reflex irritation, 470 tetanic, due to acute yellow atrophy of liver, 472 in gallstone colic, 472 due to hiematoma of dura mater, 472 culosis with cavity, 496 during aspiration of fluid in pleu- risy, 497 followed by cry, suspect pneumonia or pleurisy in children, 23 hard and dry, in bronchitis, acute,282 in hysteria, 498 laryngeal, due to pressure by aneur- ism, 497 due to pressure by carcinoma of the cesophagus, 497 due to irritant dusts or vapors, 497 due to mediastinal tumors, 497 nervous, or due to reflex irritation, 498 obstinate, in Bright's^isease, 497 in paraly,sis of diaphragm, 498 significance of cessation of, in ad- vanced plitliisis, 499 smothered, or suppressed in pleuro- pulmonary inflammation, 496 value of loose, 496 varieties of, 495 in whooping-cough, 495 Cranio-tabes, 46 Crisis, apparent, in relap.sing fever, 415 in croupous pneumonia, 426 with fading of eruptions in measles, 417 fever in erysipelas ending by either lysis or, 418 gastric, in locomotor ataxia, 486 subnormal temperature in many dis- eases at, 430 in typhus fever, 415 due to hydatid cyst of cerebral ' Crying in children, absence of, in pneu- cortex, 472 I during irrigation of pleural cavity, 472 in multiple cirrhosis, 473 in strychnine-poisoning, 471 in tetanus, 471 in tetany, 472 in unemia, 477 Coprolalia, 44 Cough, causes of night, 498 due to change of position in pleu- risy with efl^usion, 497 character of, in acute laryngitis, 497 | monia, 23 causes of, 23 constant, due to earache or hun- ger, 22 of earache not pacified by offer of breast, 23 of four months old without shed- ding tears an unfavorable sign, 23 intermittent, due to abdominal colic, 22 sharp, piercing shriek in menin- gitis, 23 brassy, in aneurism of transverse ] Crystals, ammouinm urates '^"'^ arch of aorta, 293 in false croup, 497 ■ in laryngeal phtliisis, 497 chronic, loose, moriiing, in empyema rupturing into bron- clius, 496 in pulmonary abscess, 496 in sacculated bronchi- ectasis, 490 amor[)li()us pliospliates, 376 Charcot- 1 ieydoii, 501 creatin, 374 creatinin, 375 hsemin, 494 of leucin and tyrosin in phosphorus- poisoning, 489 margaric acid, 504 oxaialo of lime, 374 of triple uliospluites, 376 552 IXDEX OF SYJ\IPT03IS, ORGANS, AND TEEMS. Crystals of urates, 374 uric acid, 374 Curschmann's spirals in asthmatic at- tacks, 501 rarely in croupous pneumonia, 501 in pulmonary tuberculosis, 501 Cyanosis in acute miliary tuberculosis, 425 articular rheumatism with hy- perpyrexia, 42S causes of, 193 due to drugs as antipyrine or acet- anilid, 194 in dyspnoea due to heart disease, 29 in laryngeal obstruction, 194 in newborn, 193 in pulmonary diseases, 194 relative frequency of causal lesions in newborn, 193 from serious cardiac disease, 193 Cyclical vomiting, other symptoms de- pendent upon, 491 Cylindroids, significance of, 372 varieties of, 371 DEFOKMITY of feet and legs, 105 due to acute cerebral paraly- sis of infancy, 109 Delirium, a bad omen in croupous pneu- monia, 276 in acute articular rheumatism with hyperpyrexia, 428 in acute yellow atrophy of liver, 448 incoherent speech in, 524 mild, in mitral regurgitation, 443 in thrombosis of cerebral sinus, 440 wild, in phosphorus-poisoning, 448 Dentition, fever in difficult, 411 Diarrhiea, accompanying abdominal pain, 21 causes of, 395 in cholera morbus, 396 infantum, 396, 427 colliquative, in unemia, 477 decrease of urine due to, 360 of dissecting room, 401 in entero-colitis, 398 fatty, due to cod-liver oil, 402 due to disease of pancreas, 402 in jaundice, 402 in fissure of the anus, 398 in hysteria, 40'^ in influenza, 425 in leukajmia, 347 lienteric 399 in locomotor ataxia, 398 due to malignant ulceration, 401 may be caused by purgatives, 21 nervous, 398 Diarrhoea, paroxysmal, sero-mucous, or bloody, in exophthalmic goitre, 402, 491 in pulmonary gangrene or tubercu- losis, 401 due to renal disease, 398 a symptom of septicaemia, 401 due to syphilitic ulceration, 401 Dilatation of heart, symptoms and physi- cal signs of, 298 of stomach, atrophy of gastric tubules in, 315 character of vomiting in, 490 constitution of vomitus in, 490 methods of examining, 308, 312 in pyloric cancer, 311 due to pressure by pancreatic growths, 490 sarcinffi ventriculi found in vom- itus in, 490 total absence of hydrochloric acid in, 490 torula cerevisife causing fermen- tation in, 311, 489 Diplopia, crossed, 150, 155 explanation of, 147 homonymous, 150, 153, 155 in poisoning, 147 sign of ocular muscle paralysis in, 147, 151 a symptom in ataxia, 147 of lesion at base of brain, 147 of nerve nuclei, 147 of cerebral cortex, 147 of nerve in its course, 147 vertical, 155 Distoma haMnatobium, eggs of, in urine, 377 hematuria due to, 364 pulmonum, 504 Dropsy. See (Edema and General Ana- sarca, causes of, 216 differential diagnosis between myx- cedema and, 216 of eyelids in renal disease, 218 in other affections, 218 feet and legs in antemia, 217 due to abdominal growth causing pressure, 317 in renal disease, 217 rare in chronic interstitial nephritis, 392 in scurvy, 217 widespread, usually indicative bf renal disease, 217 Dupuytren's contraction, 54 Dysmenorrhoea, character of pain in, 516 Dyspnoea due to asthma, 283 INDEX OF SYMPTOMS, ORGANS, AND TEEMS. 553 Dyspnwa, associated with aortic insuffi- ciency, 298 in chlorosis, 344 due to foreign body in air-passages, 283 gradual and increasing, in anfemia, 343 of heart disease, 29 due to laryngeal spasm, 284 in leukfemia 347 peculiarly severe in miliary tuber- culosis, 479 position due to, 19 worse at night in chronic interstitial nephritis, 392 EARACHE, character of crying in children with, 23 rubbing of hand over affected side of head, 23 Echolalia, 44 Ehrlich's corpuscles, 344 diazo reaction in urine myelo- cyte of, 345, 390 triple blood-stain of. 346 Emprosthotonos, in hysteria, 464 Enteroliths, 484 Eosinophile corpuscles, 315 numerous, in myelogenous leu- kaemia, 335 Eruptions, of anthrax maligna, 210 appearance of, in erysipelas, 202 in impetigo contagiosa, 208 in Smallpox, 205 in vaccinia, 208 character of, in typhus, 415 date of, in various dise:ises, 200 of glanders, 210 herpetic, along nerve-trunks in sci- atic neuritis. 512 macular, of measles, 200 pemphigus-like, due to salicylic acid or copaiba, 211 purpuric, caused by drugs, 196 caused by diseitse, 196 due to quinine. 209 of r'.thcln, 199 of syphilis, 243 vesicular, about mouth in foot-and- mouth disease in man, 427 Erythema. S'-t> Roseola, in dengue, 199 in (liplitiieria, 201 following surgicul operation or par- turition, 201 indicative of rheumati.sm, 195 in scarlet fever, 198 in syphilis. 201 in typhoid fever, 201 Esophoria, 150 Ewald's test-breakfast, 215 Examination, of abdomen. 309 of blood by hiematocytometer, 336 by hematocrit, 338 by hwmoglobinometer, 341 in leukiemia, 346 for micro-organisms of malaria, 350 of children, 22 of eye by ophthalmoscope, 146, 175 of field of vision, 171 of functional activity of ocular mus- cles, 149 for hemianopsia, 170 method of, in consulting-room, 25 of pulse, 325 of pupillary reflex, 165 of skin for jaundice, 183 of sputum, 502 of stomach, 308 ^ of tongue, 130 Exophoria, 150 Expectoration. See Sputum. Expression, of acute peritonitis, 229 beaten, weary, and careworn, of nerv- ous exhaustion, 30 of cretinism, 31 of face, how formed, 25 as early symptom of facio- humero-scapular type of mus- cular atrophy, 30 elated, of general paralysis of insane, 30 in epileptic seizures, 454 excited, of acute mania, 30 fatuous, of hysteria, 30 fixed, of catalepsy, 30 in Friedreich's ataxia, 30 how modified, 25 hard and stony, due to long-con- tinued malignant disea,se 27 hopeless, of melancholia. 30 of moderate jiain in children, 27 peaceful, of healthy sleeping child, 27 in typhoid fever, 29 Eye, amaurosis, 181 alterations of color-field, 174 anatomy of optic nerve. 170 appearance of healthv eye-ground, 177 causes of ocular paralysis, 151, 156 dark areas under, during menstrua- tion, 8fi diderential diagnosis between ocular symptoms of tabes and hysteria, l"75 diplopia, 147 examination of, bv ophthalmoscope, 175 exophthalmos in goitre, 146 (Jraefe's symptom. 146 hemianopsia, 170 554 IXDEX OF SYMPTOMS, ORGANS, AND TERMS. Eye, homonymous and crossed diplopia, 160 iritis, 180 lesion of optic nerve in locomotor ataxia, 179 method of determining ocular par. esis, 152 of examining functional activity of muscles. 149 muscie volitantes, 181 nerve-supply to interocular muscles, 164 orthophoria, 150 papillitis, 178 puffiness about, in acute diffuse ne- phritis, 391 retinitis, 179 retrobulbar neuritis, 178 rod-test of Maddox for functional balance of muscles, 150 significance of arcus senilis, 146 of annulus senilis, 146 of conjugate lateral paralysis, 162 of external squint, 157 of internal squint, 157 strain, cause of headache, 434 of symptoms of thrombosis of cavernous sinns, 162 associated with congestive head- ache, 433 signs of ocular paralysis, 151 squin t, con comi tant and paralytic, 1 48 varieties of ocular muscular pa- ralysis, 161 Eyelids, closed in healthv sleeping child, 27 oederaatous, in angioneuritic oedema, 219 due to arsenic, 218 indicative of cerebral thrombo- sis, 218 of neurotic subjects, 218 pigmentation of, early in pregnancy, 26 puffy, in trichinosis, 27 of renal disease, 218 showing glazed conjunctivfe, 27 slightly parted in sleeping child showing congestive or nervous pain, 27 twitching, in nervous irritation, 27 FACE, anesthesia of, due to involve- ment of the fifth nerve or its nu- cleus, 241 anxious and covered with cold sweat in angina pectoris, 511 asymmetry congenital, 32 developed in the case of congeni- tal wry-neck, 32 Face of acute peritonitis, 29 pulmonary phthisis, 28 blurring of features in children suf- fering from lesions of mitral valve, 29 of carcinoma, 27 of catalepsy, 30 of chorea in children, 30 of chronic or subacute renal disease, 30 of cretinism, 31 diagnosis of ancesthesia of, 342 of early stages of disseminated scler- osis, 30 expression, of anxiety in acute croup- ous pneumonia, peritonitis, and severe injury, 27 in epileptic seizure, 454 in syphilitic epilepsy, 458 while telling symptoms, 18 facio-humero-scapular type of mus- cular atrophy, 30 of Friedreich's ataxia, 31 full moon, of myxoedema, 32 gray or bluish, by overdose of coal- tar product, 26 heavy cheesy-looking, in child, 28 hemiatrophy of, 32 hemihypertrophy of, 32 Hippocratic, of impending death, 32 of hysteria, 30 intellectual, 26 leonine, of leprosy, 31 massive, of acromegaly, 32 pallor of, in fright, 26 in hemorrhage, 26 of paralysis agitans, 30 paralysis of, bilateral, 41 unilateral, 33 peculiar pallor of, in chlorosis, 36 of severe pneumonia, 99 spasm of, 43 spirituelle, of child, 28 of those exposed to weather, 26 of those living indoors, 26 of those using alcohol to excess, 26 of typhoid fever, 29 triangular, of osteitis deformans, 32 Farrant's solution, 373 Fatty degeneration of phosphorus poison- ing, 488 Feces. See Stools- causes of variation in quantity of, 402 color of, 403 consistency of, 403 odor of, 403 Feet, claw-foot, 106 contractures of, in diphtheria, 110 deformity of, due to poliomyelitis, 109 due to progressive neural or muscular atrophy, 106 INDEX OF SYMPTOMS, ORG ASS, AX J) TERMS. ooo Feet, deformity of. due to acute cerebral paralysis of infancy, 109 distribution of aniesthesia of, in neu- ritis, 240 enlarged, due to deformity, 105 in myx'tdema, 105 flat-, in locomotor ataxia, 115 in Marie's pulmonary osteo-arthro- pathy, 105 perforating ulcer of, due to diabetic gangrene, 115 due to senile gangrene, 115 due to tabes dorsalis, 115 "sciopedy," 106 symmetricallv enlarged in acromeg- aly, 105 tabetic, 109 Fehling's test for sugar in urine, 381 Fever, absence of, in pulmonary cedema, 278 appearance of nails in, 49 causes of tertian, quartan, and sestivo- autumnal, 348, 350 cold, wet skin of evil import in, 411 character of, in acute appendicitis, 428 in acute articular rheumatism, 428 in acute miliary tuberculosis, 425 in acute multiple neuritis, 429 in acute myelitis, 430 in acute pulmonarv tubercu- losis, 424 of anthrax, 427 in catarrhal pneumonia, 426 in catarrhal or suppurative cho- lansfitis, 420 in cerebral abscess, 424 in cerebro-spinal meningitis, 424 in chickenpox, 4 IS in cholera Asiatica. 427 in cholera infantum, 427 in croupous pneumonia, 426 in dengue, 114, 423 after epileptic attack, 430 in erysipelas, 418 in foot-and-mouth disease, 427 in gtustro ])ulmonary fever, 430 in hjemoglobina'mia, 492 in hay fever. 425 in hepatic abscess, 442 in Ilodgkin's disease, 422 in hysteria. 429 in infantile spinal paralvsis, 429 in iufhien/.a, 425 in injuries to cervical portion of spinal cord, 429 in intermittent malarial fever, 418 in Malta fever, 415 in mexsles, 200, 417 in obstruction of rectum, 484 Fever, character, in parenchymatous ne- phritis, 428 in pernicious ansemia, 422 in pyelitis, 393, 422 in relapsing fever, 415 in remittent malarial fever, 422 re.spirations of ciiild with, 23 in rotheln, 418 in scarlet fever, 416 in septic poisoning, 422 in septicemia, 424 in smallpox, 417 in syphilis. 427 in tetanus, 428 in thermic fever, 429 in tonsillitis, 428 in typhoid fever, 411 in typhus fever, 415 in ulcerative endocarditis, 420 in Weil's di.sea.«e. 423 in yellow fever, 423 Charcot's, 187 chlorides decreased in some, 390 increased during convalescence from, 390 of difficult dentition, 411 dry, hot skin in, 410 dryness of skin in, 215 of dysentery, 400 face of typhoid, 29 high specific gravity of urine in. 360 of mild gastro intestinal catarrh in children, 411 in pemphigus, 210 in pyelitis, 393 rapid pulse in, 332 rapidity of res|)iration in, 354 septic, in purulent cystitis, 355 significance of, 410 in children, 41 1 .slight, in chlorosis, 344 in leiika'mia, 347 sour breath in. 23 irregular in trichinosis, 415 rarely intermittent, 413 typhoid, recrudescence of, 412 fever alxent in .some ca.ses of, 41 3 urates in excess in urine of, 374 quantitv of urea excreted increased in, 3S9 uric acid in excess in urine of, 374 urine decresLsed by, 36(1 Filaria sanguinis hominis, chyluria and elephantiasis caused bv, 353 description of, 353 embryos found in urine, 377 diurna, 3'>2 ha»maturia in, 364 loa, 353 nocturna, 352 porstan.s, 352 556 INDEX OF SYMPTOMS, ORGANS, AND TERMS. Fingers, appearance of, diagnostic of chloral-habit 50 of irritating drugs, 50 distorted and twisted in gout and arthritis deformans, 51 in syphilitic dactylitis, 50 first joints involved in gout, 51 fixaiion of joints by deposit of urate of sodium, 5i spasm of, due to occupation, 64 Foot-drop, 103 Forehead, square and projecting, indic- ative of hydrocephalic tendency, 28 wrinkled, showing pain in the head. 28 Fremitus, vocal, decrease of, by pleural effusion, 357 by occlusion of large bron- chus, 357 by pneumothorax, 257 increase of, in cavities or tumors touching chest-wall, 257 mode of production of, 357 Friction-sounds, 273 as a rule, due to pleuritis, 273 at apex of chest usually due to tuber- culosis, 273 best heard in axilla, 273, 278 pericardial, 273 nABBETTS method of staining for U tubercle bacilli, 506 Gait, 77 " in acute poliomyelitis, 83 " astasia abasia," S6 cause of, in locomotor ataxia, 80 in cerebellar disease 85 in Friedreich's ataxia, 81 in general paresis, 82 of health, 18 in hemiplegia, 86 in hereditary cerebellar ataxia, 81 in hysteria, 80 in infantile cerebral paralysis, 84 in lateral sclerosis 83 limping in gout, 77 in rheumatism, 77 in sciatica, 77 in multiple sclerosis 84 of neurasthenia, 18 in osteomalacia, 86 in paralysis agitans, 85 peculiar staggering, in cerebellar tumor, 47y in pseudo-muscular hypertrophy, 83 in rickets, 84, 87 -steppage of pseudo-tabes, 78 Gall-bladder, diagnosis of obstruction of, 321, 323 -stones in stools, 404 (iallop rhythm in mitral stenosis, 291 Gangrene due to central nervous lesion, 211 in diabetes, 211 in ergotism, 56, 212 in exophthalmic goitre, 115 of extremities following infectious fevers, 115, 212 in frost-bite, 58 of intestines, fetid odor of stools, 403 in leprosy, 56 due to nerve-injury, 211 pulmonary, blood-streaked sputum in children, 500 character of sputum in, 501 crystals of margaric acid in sputum of, 504 elastic fibres in sputum of, 503 fetid breath in, 278 muco-purulent bowel move- ments in, 401 vomiting in, 493 in Raynaud's disease, 56, 212 spontaneous, of hysteria. 211 Gastralgia, character of pain in, 513 diagnosis of, 513 neuralgic spots in, 513 Gastric dilatation. See Dilatation of Stomach. Gastro-diaphane of Einhorn, 302 General anasarca, in advanced cancerous cachexia, 217 in children with acute diffuse nephritis, 391 due to arsenic, 217 in beri-beri, 217 in marked tendency to, in chronic parenchymatous nephritis, 391 multiple peripheral neuritis, 217 in renal or heart disease, 217 j Girdle sensation, 243 in locomotor ataxia, 244 in myelitis, 244 in tumors of cord and meninges, 244 Glycosuria, Fehling's test for, 381 Haines's test for, 380 quantitative yeast test of Roberts, 382 significance of, 383 Whitney's test in, 380 Gmelin's test for bile in urine, 366 Gonococci, indicative of specific ureth- ritis or vaginitis, 377 method of staining, 377 Graefe's signs, 44 symptoms, 146 Gums, blue-line on, in lead -poisoning, 145 spongy, in scurvy, 145 in mercurial salivation, 145 Gyromele of Tiirck, 308 INDEX OF SYMPTOMS, ORGANS, AND TERMS. 557 HABIT-SPASM, 43, 65 Hsematemesis due to blood from epistaxis being swallowed, 487 in cirrhosis of the liver, 321, 486 diagnosis between h?emoptysis and, 487 disea-ses in which it occurs, 487 in gastric cancer. 486 in gastric ulcer, 486 due to injury of the stomach, 486 in locomotor ataxia, 486 in malingerers, 487 in mehcna neonatorum, 488 as vicarious menstruation, 487 Hsematocrit, 338 Hsematocytoraeter of Thoma-Zeiss. 336 Hfematoma auris, 197 Hreraatozoa malariie. 347 Haematuria, acute, due to embolism, 363 due to irritating drugs, 362 due to malaria, 363 due to scarlet fever, 363 blood-casts in, 369 character of blood from bladder in, 362 from kidney in, 361 from urethra in, 362 chronic, due to chronic liemorrhagic nephritis, 364 due to cyst of kidney, 364 due to distoma hiematobium, 364 due to tilaria sanguinis hominis, 364 due to renal cancer, 364 due to stone in kidney, 364 due to tuberculosis of kidney, 364 general character of color of urine in, 361 other causes for, 365 Hiemoglobin, greatly decreased in chlo- rosis, 344 in leukemia, 347 of individual red corpuscles greater than normal in pernicious antemia, 843 Hffimoglobinipmia accompanied by vom- iting, 492 symptoms of, 492 urine in, 492 Hsemoglobinometer of von FleischI, 341 Hsemoglobinuria, causes of, 365 headaclie in, 433 signs of, 362 symptoms associated witli, 4!!3 Hsemometer. See Iliemoglobinometer. Hsemoptysis, at times caused by distoma ]>ulmonum, 504 causes of, 500 diagnosis of, 500 Haemoptysis, diagnosis between hr^mate- mesis and, 487 significance of occurrence of "cur- rant-jelly" clots in, oOO Haines's modification of Haeser's method for computing total quantity of solids in urine, 390 test for sugar in the urine, 308 Hands, accoucheur's, in tetany. 63 of acute articular rheumatism, 55 of angio-neurotic a'deraa, 56 appearance of, 48 in heart-disease, 19 changes of shape of, in chronic rheumatism, 54 of child with cerebral trouble, 23 in children with heart-disease, 58 choreic movements of, and in arms in children with cljorea minor, 64 claw-, due to diseases of median and ulnar nerves, 58 of cells of si)inal cord, 58 of cerebral cortex in hand-area, 58 cold and clammy, due to bromi- drosis, 50 due to local innervation of sweat-glands, 50 contractures of, due to hysteria, 62 following apoplexy, 62 distribution of anaesthesia of, in neu- ritis, 239 Dupuytren's contraction of, 54 in emphv.sema and chronic phthisis, 48 excessive sweating of, due to pro- gressive muscular atrophy, 50 flexion of, in cerebral palsy of chil- dren, 61 gangrene of, in ergotism, 56 in leprosy, 56 in Morvan's disease, 56 in Raynaud's disease, 56 movement of, ()9 position of, in meningeal congestion or hydrocephalus in children, 63 seal-fin. of arthritis deformans, 54 spade-like, in acromegaly, o^ in myxu'dema, 56 in pulmonary osleo-arthropathv, 56 tremors of, 67 wasting, with ana^thesia in syringo- myelia, 61 witli flexion and rigidity rarely seen in paralysis agitans, 61 due to nervous lesion, 57 due to old age, 57 Harris's test for albimio.se in urine, 383 Harrison's grooves, in rickets, 252 Head, activity of and tixation of body in peritonitis, 19 558 INDEX OF SYMPTOMS, ORGANS, AND TERMS. Head, chauges of shape of, in cretinism, 46 in cholera infantum, 397 excessive sweating of, 47 in hydrocephalus, 46 in idiocy, 46 in microcephalus, 46 retraction of, in attack of indigestion in neurotic babies, 47 may be due to caries of cervical vertebrae, 47 to fall. 47 to tender and enlarged glands of, 47 generally due to basal menin- gitis, 47 in rickets, 46 Headache, 431 in acute parenchymatous nephritis, 41^8 in Addison's disease, 492 of anfemia, 442 in anterior poliomyelitis, 429 associated with phosphaturia, 435 due to autointoxication, 433 of brain-abscess, 438 causes of, 439 in cerebral tumors, 478 cerebro-spinal meningitis, 424 constant, of brain tumor, 435 character of, in diabetes, 435 character of, due to digestive disturb- ance, 431 character of, in uraemia, 435 due to disease of cranial bones, 443 in early stages of croupous pneu- monia, 432 in early stages of smallpox, 432 due to eye -strain, 434 due to exposue to cold, 443 of gastro-pulmonary fever, 430 of glaucoma, 434 in hsemoglobina^mia, 492 due to intracranial aneurism, 443 in jaundice, 433 of malaria, 442, 446 in Malta fever, 415 of measles, 442 of meningitis, 438 in migraine, 434 of nasal catarrh, 442 due to neurasthenia, 434 occipital, in meningitis, 479 ocular symptoms in, due to digestive disturbance, 433 in paroxysmal hremoglobinuria, 433 in phosphorus-poisoning, 488 due to rheumatism, 434 in sunstroke, 442 of syphilitic arteritis, 437 of syphilitic epilepsy, 458 Headache of tubercular meningitis, 439 in typhoid fever, 442 in typhus fever, 415 due to use of drugs, 435 of valvular heart-disease, 443 vertical, in ha?matoma of dura, 442 Heart, alterations in area of dulness. 267 apex-beat, area of, 258 depression of, due to pul- monary emphysema and cardiac hypertrophy, 258 displaced to left by hyper- trophy of left ven- tricle, 259 bv pleural adhesions, '258 by pleural effusions, 258 displaced to right by hy- pertrophy or dilatation of right ventricle, 258 normal position of, 257 raised by ascites, 258 b}' intra-abdominal growths, 258 strengtli of, 258 asthma due to lesion of, 284 blood-streaked sputum in valvular disease of, 500 cause of pain in neighborhood of, 510 causes of thrills of, 258 cough in valvular disease of, 498 dilatation of, 266, 298 failure, in influenza, 425 failure, unconsciousness in, 452 fatty degeneration of, 300 deposition on, 300 general malformation of, 301 greatly hypertrophied in chronic interstitial nephritis. 392 headache in valvular disease of, 443 hypertrophy of, 209, 267 irregular, in children, 344 location of murmur of, 289 neuroses of. 299 secondary diphtheritic dysentery in chronic disease of, 401 slightly dilated, in acute diffuse ne- phritis, 392 somewhat hypertrophied, in chronic parenchymatous nephritis, 392 accentuation of, 288 reduplication of, 289 where best heard, 288 sounds, 288 symptoms associated with murmurs of, 297 Heller's test for albumin in urine, 308 for blood in urine, 362 Hemiachromatopsia, 174 ISBJJX OF SYMPTOMS, ORGANS, AND TERMS. 559 Hemiansesthesia due to capsular disease, 226 due to cortical lesion, 227 in disseminated sclerosis, 227 of hysteria, 225 partial, with partial hemiplegia on opposite side may be due to lesions of one side of cord, 229 unilateral, due to tumor of brain, 297 Hemianopsia, 170 in brain-tumor, 43G honionyniou.s, 173 in migraine, 433 rarely found in hysteria, 173 significance of, 173 Hemiatrophy, facial, 32 Hemidyschromatopsia, 174 Hemiiiypertropiiy, facial, 32 Hemiplegia from acute infantile paral- ysis, 128 anatomy of brain -areas involved in, 117 appearance of nails in, 49 of tongue in, 134 bedsores in, 213 in cerebellar hemorrhage, 126 crossed, due to Ijulbar lesions, 129 diflerential diagnosis between, due to hemorrhage, embolism, or throm- bosis, 126 due to ditluse cerebral sclerosis of one hemisphere, 128 gait in, 86 arising from ha?matoma of dura mater, 128 from hemorrhage, 123 in hemorrhage in pons Varolii, 125 in cms cerebri, 12') into frontal lobe. 126 hy perns! liesia in, 245 in ingravescent apoplexy, 125 irregular forms of, 126 location of hemorrhage in, 123 most common site for a hemorrhage, 124 occurring in locomotor ataxia, 128 occurring in paretic dementia, 128 in pundent menin<^itis, 129 as a nj'iult of ccrdirid syphilis, 127 resulting from multiple sclerosis, 128 symptoms associated with, due to cerebral tumor, 127 symptoms associated witir, in cortical hemorrhage, 125 symptoms iissociated with, when due to iifinorrhage in the internal cap- sule. 124 Hemorrhage, anii-mia in. 343 into brain cortex, diplopia a .symp- totn of, 147 causing hemiplegia, 123 Hemorrhage into brain causing ocular paralysis, 156 cerebral, vomiting in, 478 indicated by anxious restlessness, 19 jaundice after severe prolonged, 188 into membranes or cord, 331 meningeal, symptoms of, 441 movements minu e, although active in, 19 from mucous membranes, in yellow fever, 423 from nose in leukaemia, 247 pallor of face in, 26 pulmonary diseases in which it oc- curs, 500 pulse of emplv arteries in severe, 330 into retina, 180 into .skin, 197 subdural, cause of. 4^0 in typhoid lever, 412 Herpes labiali.s, in croupous pneumonia, 209 in epidemic spinal meningitis, 209 due to salicylic acid, 209 Hippocratic face, 32 Hippus, 168 Hunger, character of crying in children caused by, 2-5 Hutchinson teeth, 145 Hydroce|ihalus. sliape of head in, 46 Hydrochloric acid, test for, in stomach- contents, 315 llypertesthesia, in brain-tumor, 245 in cerebro-spinal meningitis, 245 in chronic alcoholism, 246 in ciironic leptomeningitis, 245 early sign of non-tuberculated lep- rosy, 246 in hemiplegia, 245 hvsterogenous zones of, in hysteria, "244 in locomotor ataxia, 245 in neuralgia, 245 in neurasthenia, 244 in peripiicral neuritis, 245 in relapsing fever, 245 in transverse myelitis, 245 Hyperpyrexia, 409 in acute articular rheumatism, 428 in injuries to cervical portions of spinal cord, 429 in tetanus, 428 Hypertrophy, cardiac, a.s.sociated with chronic contracted kidney, great increase of urine in, 360 diagnosis of, 267 great forie of pulse in, 332 great in ciironic interstitial nephriti.s, 392 limited bulging of chest in, 252 560 INDEX OF SYMPTOMS, ORGANS, AND TERMS. Hypertrophy, to a limited degree in chronic parenchymatous nephritis, 392 symptoms and physical signs of, 399 ICTERUS. See Jaundice. 1 Idiosyncrasy, to drugs. 18, 196 hiemoglobinuria of, 365 Incontinence of urine, ammoniacal odor in, 419 due to concentrated urine, 356 due to excessive reflex irrita- bility of walls of bladder, 356 due to insensitive urethra, 356 due to loss of power of sphincter, 356 nocturnal, in children, 358 trousers stained in, 18 Indicanuria, diseases in which it occurs, 366 in intestinal obstruction due to im- paction, 484 test for, 366 Indigestion, antemia in chronic, 343 character of respiration of child with, 22 erythema in, 199 headache associated with, 421 muscse volitantes in severe, 181 sour breath in, 123 vertigo in. 494 Insomnia, in Malta fever, 415 Iritis, headache due to, 483 due to injury, 180 due to rheumatism, ISO due to syphilis, 180 JAUNDICE, in acute phosphorus-pois- oning, 186 in acute yellow atrophy of liver, 186, 188 albumosuria in, 385 in amyloid disease of liver, 187 bradycardia in, 299 causes of, J 89 of hematogenous, 188 of hepatogenous, 184 of, complicating diabetes, 187 of constipation occurring in, 394 color of urine in, 366 in chronic valvular heart disease, 186 diabete bronze, 187 fatty diarrhea occurring in, 402 headache due to, 433 in hypertrophic cirrhosis of liver, 186 of malignant disease, 186 method of examining for, 183 of newborn, 189 Jaundice, persistent and progressive, in carcinoma of pancreas, 316 due to pressure by aneurism, 186 pruritus in, 246 purpuric eruptions in severe, 196 in remittent malarial fever, 422 stools, light colored, in, 403 symptoms of catarrhal, 185 symptoms of hepatogenous, 187 symptoms of obstructive, 185 test of urine in, 366 vomiting in, 492 Joints, in acute epiphysitis of infancy, 112 articular rheumatism, 113, 428 central myelitis 112 cerebro-spinal meningitis, 112 • osteomyelitis, 112 alterations of, in locomotor ataxia, 111 in chronic lead-poisoning, 114 different modes of infection in gon- orrhceal arthritis, 112 enlargement of, in rheumatoid ar- thritis, 111 in gout, 113 in hfemophilia, 114 involvement with fever in pyaemia, 428 in osteomyelitis, 428 in purpura, 428 involvements of, in dengue, 114 of, in epidemic dysentery and scarlet fever, 114 in milk-leg, 114 in Schonlein's disease, 114 small, aflfected, in Morvan's disease, 112 in septic arthritis, 112 violent pain in, on motion, in Malta fever, 415 KIDNEY, blood-casts in acute inflam- mation of, 369 character of blood in urine from, 361 fatty degeneration of, fatty casts in, 370 hsematuria due to stone in, 364 hydronephrosis, 318 irritation of, cylindroids found in urine, 372 septic infection of, casts of micro- cocci in, 369 slow degeneration of parenchyma of, granular casts in, 370 symptoms of floating, 318 Knee-jerk, diseases in which, decreased, 519 increased, 520 how best developed, 518 peculiarity of, in poliomyelitis, 105 reinforced, 518 INDEX OF SYMPTOMS, ORGANS, AND TERMS. 561 LACTIC acid, test for, in stomach-con- tents, 215 Laveran, malarial germ of, 347 Leucocytosis, 3-lo in pneumonia, 335 Lips, fulness of, in persons of strong sex- ual appetite. 26 indicating plilegmatic tempera- ment, 2(5 greatly thickened in cretinism, 31 immobility of, due to mucous patches or ulceration of buccal mucous membrane, 28 thin and mobile, in nervous indi- viduals, 26 twitcliingof raised upper lip, in peri- tonitis or pain below diaphragm, 29 Liver, causes of tenderness of, 322 enlarged and smootli, in amyloid disease, 320 enlargement of, in amyloid disease of kidney, 392 headache in congestion of, 432 indicanuria in cancer of, 366 nodules and umbilication of, in ma- lignant disease, 221 percussion-note over, 319 pushed down by right pleural effu- sion, 322 rough, due to cirrhosis, 321 swelling of, in Weil's disease, 423 symptoms of tropical abscess of, 321 of cirrhosis of, 321 of malignant disease of, 321 Localization of functions of segments of spinal cord, 97 Lordosis, in cretinism, 31 Lyons's method of estimating urea, 385 Lysis, fever in erysipelas ending by either crisis or, 418 in scarlet fever ending by, 416 in smallpox ending by. 418 in typhoid ending by, 425 in catarriia! |)neutnulbar paral- ysis. 41 564 IXDEX OF SYMPTOMS, OBGANS, AND TERMS. Paralysis, bilateral facial, due to bilateral inflammation of mastoid foramen, 42 due to bilateral lesion of cerebrum, 41 due to cold or double otitis, 42 due to lesion of pons, 42 due to progressive bulbar paralysis, 42 due to syphilis at base of brain, 42 due to toxic peripheral neuritis, 42 of bladder with retention, due to pressure during childbirth, 356 of diaphragm, causes of, 498 cough in, 498 of intraocular muscles, 164 of ocular muscles, 48 due to acute or chronic lesions of nuclei. 156 due to basilar lesions, 157 causes of conjugate lateral, 162 due to hemorrhage of cer- ebral cortex, 156 due to lesion of nerve- trunks, 157 between cortex and nuclear origin of nerve, 156 method of determining partial, 152 varieties of, location of lesion in, 161 due to sclerosis of cerebral cortex, 156 significance of conjugate lateral, 162 signs of, 151 symptoms of thrombosis of cavernous sinus causing, 162 oculo-facial, 42 progressive bulbar, 42 differential diagnosis be- tween asthenic bulbar paralysis and, 42 recurrent, of oculomotor nerve on one side, 41 due to traumatic myelitis, 356 unilateral facial, 33 absence of trophic changes in cerebral, 34 caused by exposure to cold, 34 arising in locomotor ataxia, 34 associated with monoplegia in acute anterior polio- myelitis, 36 Paralysis, unilateral facial, caused by fracture at the base of the skull, 34 by hysteria, 36 by injuries, 34 by otitis media, 34 by pressure of forceps, 34 by pressure of growths at the base of the skull, 34 by primary hemor- rhage into the nerve- sheath, 34 by swelling of parotid glands, 34 in crossed paralysis, 36 location of cause of, 34 nerve-degeneration in per- ipheral, 34 peculiar distribution in some cases, 36 prognosis of, in pressure by forceps, 36 reaction of degeneration in, caused by tumor in- volving facial fibres be- low, or facial nucleus, 34 in syphilitic arteritis caus- ing other paralyses, 36 Paraphasia, 525 Paraplegia, 88 of arrested development, 89 ataxic, exaggerated knee-jerk in, 521 causes of, 88 of cerebral infantile paralysis, 88 hysterical, knee-jerk increased in, 521 in lateral spinal sclerosis, 90 multiple cerebral spinal sclerosis a cause of, 89 non-spastic, in acute transverse my- elitis, 93 in chronic transverse myelitis, 96 due to compression from frac- ture or dislocation of vertebra, 100 due to hemorrhage into the spinal cord or its membrane, 92 due to hysteria, 101 due to injury of cord or myelitis, triple phosphates in urine of, 376 in locomotor ataxia, 99 due to neuritis, 101 occurring in hereditary spastic paralysis, 90 in Landry's paralysis, 92 INDEX OF SYMPTOMS, ORGANS, AND TERMS. 565 Paraplegia, non-spastic, partial, as a sequel of diphtheria, 101 in poliomyelitis. 100 due to polyneuritis, 92 pseudo-, in rickets, 101 in scorbutus in infancy, 101 rarely in diabetes mellitus, 102 subacute transv^erse myelitis, 95 due to tumor of cord or mem- branes, 100 of rickets, 89 spastic, 88 due to spinal pachymeningitis, 91 in spinal lesions causing it in the lower extremities, 89 in spinal syphilis, 92 Parasites, anteniia due lo ankylostomum duodenale, 340 due to tapeworm, 346 of lung, distorau j)ulmonum, 504 ecchinococcus of lung, 504 intestinal, ankvlostomum duodenale, 407 ascaris lumbricoides. 407 bothriocephalus latus, 405 oxyuris vermicularis, 407 taenia cucumerina, 407 mediocanellata, 405 solium, 405 trichocephalus dispar, 407 of malaria, aestivo-autumnal, 349, 350 quartan, 348, 350 tertian, 348, 350 of urine, distoma haematobium, 364 filaria sanguinis hominis, 352 Parkinsonian visage, 30 Paronychia, 50 Percussion-note, in ascites, 305 cracked-pot sound, 262 in tul)erc'ulosis, 262 dollar-test in hvdropneumothorax, dull, due to consolidation of lung in pneumonia, 2(i2 dulness of, in pulmonary rcdema, 278 in congestion, 278 flat, over pleural elliision, 280 over liver, 319 tympanitic in lung, due to large cavities, 261 due to pneumothorax, 261 Phosphaturia, iieadache associated with, 435 PoikiIf)cytosis in chlorosis, 344 in pernicious auiomia, 344 Polycylhiemia, due to congenital cardiac disease in children. 333 Polydipsia, a svmi)tnm of dialietcs mel- litus, 3S3 Polvpliagia, a symptom of diabetes mel- li'tus, 383 Position, due to action of drugs, 19 due to acute bellyache, 19 in acute nausea, 19 pleurisy, 320 in coma, partial or complete, 19 in dyspnoea due to asthma, 283 as an encouraging sign. 20 due to enlarged liver, 20 in grave or advanced disease, 20 indicative of convalescence, 19 due to large growths in abdominal cavity, 20 in oedema of lungs, 20 in peritonitis, 19 persistently on side, 19 in pleurisy with effusion, 20 in pulmonary con.solid'ation, 20 result of faintnee destroyed, 38 as a congenital dtfect, 37 delinitioii and causes of, 36 in feeble, overworked women in the morning, 39 566 INDEX OF SYMPTOMS, ORGANS, AND TERMS. Ptosis, witli hemiplegia- of face and limbs on opposite sides of body, 41 in idiopathic muscular atrophy, 39 in locomotor ataxia, 39 in meningitis, 479 in recurrent paralysis of oculomotor nerve on one side, 431 transient, from poisoning by gel- semium or conium, 39 in tubercular or syphilitic changes about the base of the brain, 39 Puerile breathing, 269 Pulse, best taken in children asleep, 24 cause of slow, 331 character of, 329 dicrotic, 330 of empty arteries in severe hemor- rhage, 330 examination of, 325 feeble, rapid, and running, in cholera morbus, 396 force of, 332 hard and tense, in acute diffuse ne- phritis, 391 high tension of, in chronic intersti- tial nephritis, 392 method of production of, 326 normal wave of, 330 pulsus alterans, 329 paradoxus, 329 rapid, due to stimulation of heart, 332 and weak in intestinal obstruc- tion, 482 rate of, 328 slow in cerebral tumor, 478 of digitalis, 331 volume of, 328 Punchinello leg, 104 Pupil, in acute alcohol-poisoning, 145 Argyll-Robertson, 166 causes of altered size of, 166 contraction of, 167 dilatation of, 167 hippus, 168 method of testing, 165 in opium-poisoning, 446 reaction of, to accommodation, 165 to light, 165 size of normal, 165 transitory unequal dilatation of, in tuberculosis, 168 Wernicke's sign of hemiopic inac- tion of, 167, 437 RALES, 272 altered by coughing if not crepi- tant. 272 bubbling in bronchitis, 272 in oedema, 272 Kales, bubbling, in resolution in pneu- monia, 272 character of, in asthma, 284 crepitant, in early stages of croup- ous pneumonia, 272 in pulmonary collapse or oede- ma, 272 congestion, 278 in tubercular breaking down, 272 redux in pneumonia, 276 Eeflexes, 518 ankle-clonus, how developed, 519 biceps tendon, how tested, 519 diseases in which decreased, 519 in which increased, 520 knee-jerk, how best developed, 518 loss of patellar, in locomotor ataxia, 230 preserved in cerebral anaesthesia, 229 of skin, table of, 522 Relapse, frequency of, in Malta fever, 515 in typhoid fever, 412 Resonance, vocal, 274 Baccelli's sign, 274 decreased, in emphj'sema, 274 over pleural effusion, 274 increased, in cavity, 274 above pleural effusion, 274 in pneumonia, 274 in tubercular consolidation, 274 Respiration, causes of labored, 256 of rapidity of, 254 slowing of, 254 character of, in peritonitis, 256 Cheyne-Stokes, 255 of disturbed digestion or fever in children, 23 of healthy child, 23 inspiration prolonged in spasmodic croup, 255 method of studying in children, 24 prolonged expiration, in asthma and emphysema, 254, 283 wavy breathing, of pneumonia, 256 Retention of urine, in locomotor ataxia, 356 due to overdistention, 356 due to pressure during child- birth, 356 due to traumatic myelitis, 356 Retinitis, albuminuric, 180 in diabetes, ISO in leukfemia. 347 in syphilis, 108 Retro-bulbar neuritis, 178 Robert's yeast-test for sugar in the urine, 382 Roseola. See also Erythema. IXDEX OF SYMPTOMS, ORGANS, AND TERMS. 567 Roseola due to arsenic, 203 due to atropine, 204 due to bromide of potassium, 203 due to copaiba. 203 due to quinine, 208 due to salicylic acid, -03 due to surgical dressings containing drugs, 203 due to syphilis, 213 due to turpentine, 203 following vaccination, 200 Kose-rash. See Erythema. Kupia, in syphilis, 13 SACCHAROMYCES albicans, causing fermentation in diabetic urine, 379 Sarcinie ventriculi, test for, 390 in vomitus, from chronic gastric catarrh, 490 from gastric cancer, 490 dilatation, 490 Sciopedy, 106 Scotoma; 178 Skin, in acute alcohol-poisoning, 445 in Addison's disease, 191 anaesthesia of, 224 appearance of, in angioneurotic (edema, 220 in chloasma of pregnancy, 191 in elephantiasis, 219 in redema neonatorum, 220 in sclerema neonatorum, 220 in scleroderma, 219 in carcinoma of internal organs, 191 cold and moist, with high rectal teuiperature in sunstroke, 429 and wet, in fever, a bad symp- tom, 31 1 color of, in health and disease, 182 condition of, as regards nutrition, 194 cyanosis of, 192 dropsy and swelling of, 216 dry :md hot, in fever, 410 eruptions of, in disease, 199 excess of dryness of, 21o gangrene of, 21 1 glossiness of, 21 1 harsli anddrv, in acute ditl'use neph- ritis. .391 ■ hemorrhages into, 197 hot and dry, in sunstroke, 429 hypersesthesia of, 244 increased .sensibilitv of, due to ergot, 24(; in inlluenza, 24(5 in jaundice, 1S3 muddy-yellow, in chronic malarial poisoning, 190 due to opium, 246 pain of, 246 i Skin, pallor of, 192 I parsesthesia of. 246 parchment-like, in syphilis, 26 j due to profound anrd(lcafne.s.s, 526 feeble, iiesilating, in pneumonia or pulmonary n-doma, 523 lialling, Iiesilating, in paretic de- mentia, 524 incolierent, due to ciiorea in ciiildren, 524 due to delirium, 524 568 INDEX OF SYMPTOMS, ORGANS, AND TERMS. Speech, indistinct mumbling due to amyo- trophic lateral sclerosis, 524 due to bulbar paralysis, 524' due to glosso-labio-pharyn- geal paralysis, 524 due to stomatitis, 523 due to typhoid fever, 523 nervous mechanism of, 525 slow scanning, in disseminated scle- rosis, 524 in Friedreich's ataxia, 524 in syphilitic arteritis, 438 tests for defects, 526 Spermatozoa, significance of, in urine, 378 Sphygmograph , 330 Spinal cord, great rise in temperature due to injuries to cervical, 429 localization of function of seg- ments of 97 location of lesions in anaesthesia, 233 Spirillum of Obermeier, in blood of re- lapsing fever, 416 Spleen, causes of enlargement of, 323 of distention of, downward, 323 enlarged, in typhoid fever, 414 enlargement of, in amvloid disease of kidney, 392 great enlargement of, in leukaemia, 347 method of examination of, 323 normal position of, 323 swelling of, in Weil's disease, 423 uric acid in excess in enlargement of, 374 Sputum, actinomyces in, 504 " anchovy sauce " in amebic abscess, 500 in an asthmatic attack, 501 blood-streaked, due to leakage from aortic aneurism, 500 due to pulmonary gangrene in children, 500 due to valvular heart disease, 500 bloody, in hiiemoptysis, 499 due to ruptured bloodvessel in posterior pharyngeal walls, 500 brick-dust, in hepatic abscess com- municating with lung. 500 in chronic bronchitis, 283 in laier stages of bronchitis, 499 brownish, in gangrene of lung, 278 casts of bronchioles found in fibrinous bronchitis, 502 of smaller bronchial tubes found occasionally in croupous pneu- monia 502 Sputum, causes of purulent, 501 character of, in pulmonary gangrene, 501 Charcot-Leyden crystals and Cursch- mann's spirals in asthmatic, 284 copious and purulent, in pulmonary abscess. 278 crystals of margaric acid in, due to pulmonary gangrene, to purulent bronchitis, and follicular tonsil- litis, 500 Dittricb's plugs in purulent bron- chitis, 283 elastic fibres in, due to abscess of lung, 503 due to gangrene of lung, 503 due to tuberculosis of lung, 503 eggs of distoma pulmonum in, 504 examination of, with centrifuge, 502 of, for elastic fibres, 503 frothy, in pulmonary oedema, 278 hooks of echinococcus in, 504 liquid and watery, in pulmonary (jederaa, 501 in epidemic influenza, 501 method of staining for tubercle bacilli in, 505 microscopical examination of, 503 rusty, stickv of croupous pneumonia, 275, 499' Squint, diagnosis between concomitant and paralytic, 149 due to hysteria, 163 in meningitis, 479 in ocular palsy, 151 significance of external, 160 Stelwag's symptom, 146 Stomach, character of vomiting in dila- tation of, 489 cough due to reflex irritation from, 498 distention of. by gas, 312 indicanuria in cancer of, 366 method of examination of, by gastro- diaphane, 308 by gyromele, 308 test for liydrochloric acid in con- tents of, 215 for lactic acid in contents ofj 315 for urates in urine in disorders of, 374 Stone in bladder, interference with pas- sage of urine due to, 3'J9 Stools. Stx also Feces almost devoid of mucus in cholera morbus, 396 bilious, 404 bloody, 404 in poisoning by arsenic, 397 INDEX OF SYMPTOMS, ORGANS, AND TERMS. 569 Stools, character of, in dysentery, 400 in intussusception of children, 480 in phosphorus-poisoning, 488 of cholera, comma Ijacilli in, 397 in cholera infantum, 390 clay-colored, in hepatogenous jaun- dice, 187 in Weil's disease, 423 gall-stones in, 404 intestinal parasites in, 405 mixed with mucus, 404 oilv, in carcinoma of pancreas, 316 of "proctitis, 399 ribbon-shaped, in follicular entero- colitis, 399 rice-water, in poisoning bv antimony, 397 significance and character of blood in, 402 tarry, in yellow fever, 423 Strabismus. SV Squint. Strongylus gigas, hiepiaturia due to, 365 Stupor, in typhoid fever, 414 in ulcerative endocarditis, 414 Subsultus tendinum, 50 Sudamina, 215 Sugar in urine See Glycosuria and Urine. Sweating of skin, 214 in acute miliary tuberculosis, 425 in antimonial poisoning, 397 in hepatic abscess, 422 in intermittent malarial fever, 418 localized, 215 in obstruction of rectum, 484 uriniferous, in deficient renal activity, 215 TACHE cerebrale, 197 meningeale, 197 Tachycardia. 332 in exophthalmic goitre, 299 Taenia cucumerina, 407 mediocaneli.ita, 405 solium, 405 Tapeworm. Ser Parasites. Teeth, caries of, in diabetes mellitus, 145 in pregnanciy, 145 cut early in inherited syphilis, 145 early decay of, in rickets, 145 Hutchinson, 145 loosening of, with spongy gums in scurvy, 145 Teichmann's crystals in hiemoglobinuria, 362 Temperature in acute alcohol-poisoning, 446. See, also, Fever. Temperature, causes of fall of, in typhoid fever, 412 of diabetic coma, 448 great rise of, in injuries to cervical region of spinal cord, 429 high, in rectum though surface cold in cholera Asiatica, 427 even though skin feels cold in cholera infantum, 428 with cold, moist skin in some cases of sunstroke, 429 in intestinal obstruction, 482 methods of taking, 409 precautions in taking, in mouth, 409 subnormal, conditions in which it occurs, 430 in heat-exhaustion, 430 in injuries to dorsal region of spinal cord. 4^0 Tenesmus, in bladder-trouble, 355 in cholera infantum, 396 in dysentery, 400 in intussusception, 480 proctitis, 399 due to stricture of rectum, 398 Tests, for albumin in urine, boiling test, 3'<0 Heller's test, 380 quantitative, by centrifuge, 380 for albumo.se, 383 Harris's, 3.S3 for chlorides, 390 chromogen, in urine, 366 chyle in urine. 367 for defects in intellectuality, 526 Ehrlich's diazo reaction, 390 for elastic fibres in lungs, 503 Gmelin's, for bile in urine, 366 for hiemin crystals, 494 Haine-i's modification of IT:eser's method for total quantity of solids in urine, 390 Heller's test for blood in urine, 362 for hydrochloric acid in stomach contents, 315 for indicanuria, 36(5 for lactic acid in stomach-contents, 315 for sarcinie vt-ntriculi, 490 for sugar in urine, Fehling's, 381 Haines's, 380 Roberts's veast, 38*J Whitney's, 380 for urates, 366 Thirst, in lrations. Cloth, $6.50; leather, .$7.50. BUMSTEAD (F. J.) AND TAYLOR (R. W.). THE PATHOLOGY AND TllKATMENT OF VEXEREAL DfS EASES. See Taybr on Venereal Diseases, pilL'!' I'>. .fil.tt rrailii. BURNETT CHARLES H. i. THE EAR: FTS ANATOMY, PHYSIOLOGY ANJ) JUSEASES. A Practical Treatise for the U.se of Students and Practitioners. Second edition. In one 8vo. volume of 580 pages, with 107 illustration.''. Cloth, $4; leather, $5. BUTLIN (HENRY T. . IHSEASES OF THE TONGUE. In one pocket-size IJnin. voluiiH- (>( l")t'. pages, with S colored plates aiul 3 engravings. Limp cloth, $3,50. See .SVri'. Limited edition, de luxe binding, .$4. (Net.) DRAPER JOHN C). MEDICAL PHYSICS. A Text-book for Students and Prac- titioners of Medicine. In one handsome octavo volume of 734 pages, with 376 engrav- ings. Cloth, .'?4. DRUITT (ROBERT). THE PRINCIPLES AND PRACTICE OF MODERN S URGERY. A new American, from the twelfth London edition, edited by Stanley Boyd, F.R.C.S. In one large octavo volume of 965 pages, with 373 engravings. Cloth, $4 ; leather, $5. DUANE ^ALEXANDER). THE STUDENT'S DICTION AR Y OF MEDICINE ANI) THE ALLIED SCIENCES. Comprising the Pronunciation, Derivation and Full Explanation of Medical Terms. Together with much Collateral Descriptive Matter, Numerous Tables, etc. New edition. With Appendix. In one square octavo volume of t)90 pages. Cloth, $3; half leather, $3.25; full sheep, $3.75. Thumb-letter Index for ijuick use, 50 cents extra. Just ready. DUNCAN (J. MATTHEWS). CLINICAL LECTURES ON THE DISEASES OF WOMEN, delivered in St. Bartliolomew's Hospital. In one octavo volume of 17") i)agcs. Ciotli, .^1.50. DUNGLISON iROBLEY). .1 DICTIONARY OF MEDICAL SCIENCE. Con- taining a full P>xpianation of the Various Subjects and Terms of Anatomy, Physiology, Medical Chemistry, Pharmacy, Pharmacology, Therapeutics, Medicine, Hygiene, Dietetics, Pathology, Surgery, Ophtlialiiiology, Otology, Laryngology, Dermatology, Gynecology, Obstetric«, Pediatrics, Medical .Juris])rudence, Dentistry, etc., etc. By R<»hlky Dinoli- SON, M.D., LL.D., late Profe^^or of Institutes of Medicine in tiie .lellerson Medical Col- lege of Philadelphia. Edited by Riciiaki) J. I)rN<;Lis(iN, A.M., M.D. Twenty-first edition, thoroughly revised and greatly enlarged and improved, with the Pronunciation, Accentuation and Derivation of the Terms. NVitli Appendix. In one magnificent im|)erial octavo volume of 1225 page*. Cloth, $7 ; leather, $S. Thumb-letter Index for (piiik Msf. 75 cents extra. Just ready. EDES (ROBERT T.\ TEXT-BOOK OF THERAPEUTICS AND MATERIA MFDK ■. I . In one Svo. volume of 544 pages. ( 'loth, $3.50 ; leather, $4.50. EDIS (ARTHUR W.). DISEASES OF WOMEN. A Manual for Student-* and Practitioners. In one handsome 8vo. volume of 576 pages, with 148 engravings. (lotli. ••<:;; lc:itlicr, >;4. ELLIS GEORGE VINER). DEMONSTRATIONS IN ANATOMY. Being a Guide to tiie Knowledge of the Human Body by Dis-section. From the eighth and revised English edition. In one octavo volume of 716 pages, with 249 engravings. Cloth, $4.25 ; leather, $5.25. Philadelphia, 706. 708 and 710 Sansom St.— Mew York, 111 Fifth Ave. {cor. 18th St.). LEA BROTHERS & CO.'S PUBLICATIONS. EMMET (THOMAS ADDIS). THE PRINCIPLES AND PRACTICE OF G YNJECOLOGY. For the use of Students and Practitioners. Third edition, enlarged and revised. In one large 8vo. volume of 880 pages, with 150 original engravings. Cloth, %b ; leather, $6. ERICHSEN (JOHN E.). THE SCIENCE AND ART OF SURGERY. A new American from the eighth enlarged and revised London edition. In two large octavo volumes containing 2.316 pages, with 984 engravings. Cloth, $9; leather, $11. ESSIG (CHARLES J.). PROSTHETIC DENTISTRY. See American Text-books of Dentistry, page 2. FARQUHARSON (ROBERT). A GUIDE TO THERAPEUTICS. Fourth American from fourth English edition, revised bv Frank Woodbury, M.D. In one 12mo. volume of 581 pages. Cloth, $2.50. FIELD (GEORGE P.). A MANUAL OF DISEASES OF THE EAR. Fourth edition. In one octavo volume of 391 pages, with 73 engravings and 21 colored plates. Cloth, $3.75. FLINT (AUSTIN). A TREATISE ON THE PRINCIPLES AND PRACTICE OF MEDICINE. jVew (7th) edition, thoroughly revised by Frederick P. Henry, M.D. In one large 8vo. volume of 1143 pages, with engravings. Cloth, $5; leather, $6. A MANUAL OF AUSCULTATION AND PERCUSSION; of the Physi- cal Diagnosis of Diseases of the Lungs and Heart, and of Thoracic Aneurism. Fifth ' edition, revised by James C. Wilson, M.D. In one handsome 12mo. volume of 274 pages, with 12 engravings. A PRACTICAL TREATISE ON THE DIAGNOSIS AND TREAT- MENT OF DISEASES OF THE HEART. Second edition, enlarged. In one octavo volume of 550 pages. Cloth, $4. A PRACTICAL TREATISE ON THE PHYSICAL EXPLORATION OF THE CHEST, AND THE DIAGNOSIS OF DISEASES AFFECTING THE RESPIRATORY ORGANS. Second and revised edition. In one octavo vol- ume of 591 p^ges. Cloth, $4.50. MEDICAL ESSA YS. In one 12mo. volume of 210 pages. Cloth, $1.38. ON PHTHISIS : ITS MORBID ANA TOMY, ETIOL OGY, ETC. A Series of Clinical Lectures. In one 8vo. volume of 442 pages. Cloth, $3.50. FOLSOM (C. F.). AN ABSTRACT OF STATUTES OF U. S. ON CUSTODY OF THE INSANE. In one 8vo. volume of 108 pages. Cloth, $1.50. FORMULARY, THE NATIONAL. See Stille, Maisch & Caspari's National Dispensa- tor\j, page 14. FOSTER (MICHAEL). A TEXT-BOOK OF PHYSIOLOGY. New (6th) and revised American from the sixth English edition. In one large octavo volume of 923 pages, with 257 illustrations. Cloth, $4.50 ; leather, $5.50. FOTHERGILL (J. MILNER). THE PRACTITIONER'S HAND-BOOK OF TREATMENT. Third edition. In one handsome octavo volume of 664 pages. Cloth, $3.75 ; leather, $4.75. FOWNES (GEORGE). A MANUAL OF ELEMENTARY CHEMISTRY {IN- ORGANIC AND ORGANIC). Twelfth edition. Embodying Watts' P%sica« and Inorganic Chemistry. In one royal 12mo. volume of 1061 pages, with 168 engravings, and 1 colored plate. Cloth, $2.75 ; leather, $3.25. FRANKLAND (E.) AND JAPP (F. R.). INORGANIC CHEMISTRY. In one handsome octavo volume of 677 pages, with 51 engravings and 2 plates. Cloth, $3.75 ; leather, $4.75. FULLER (EUGENE). DISORDERS OF THE SEXUAL ORGANS IN THE MALE. In one very handsome octavo volume of 238 pages, with 25 engi-avings and 8 full-page plates. Cloth, $2. Just ready. FULLER (HENRY). ON DISEASES OF THE L UNGS AND AIR-PASSAGES. Their Pathology, Physical Diagnosis, Symptoms and Treatment. From second English edition. In one 8vo. volume of 475 pages. Cloth, $3.50. Philadelphia, 706, 708 and 710 Sansom St— New York, 111 Fifth Ave. [cor. 18th St.). LEA BROTHERS & CO.'S PUBLICATIONS. 7 GANT (FREDERICK JAMES). THE STUDENT'S SUBGEBY. A Multum in Parvo. In one sfjuare octavo volume of 845 pages, with 159 engi-avings. Cloth, $3.75. GIBBES (HENEAGE). PBACTICAL PATHOLOGY AND MOBBID HIS- TOLOGY. In one very handsome octavo volume of 314 pages, with 60 illustrations, mostly photographic. Cloth, ?2.75. GIBNEY (V. P.). OBTHOPEDIC SUBGEBY. For the use of Practitioners and Students. In one 8vo. volume profusely illastrated. Preparing. GOULD (A. PEARCE). SUBGICAL DIAGNOSIS. In one 12mo. volume of 589 pages. Cloth, -$2. See Students' Series of 3Ianuals, page 14. GRAY^ (HENRY). ANATOMY, DESCBIPTIVE AND SUBGICAL. A new- American edition, thoroughly revised. In one imperial octavo volume of 1239 pages, mth 772 large and elaborate engravings. Price with illustrations in colors, cloth, $7 ; leather, $8. Price, with illustrations in black, cloth, >>& ; leather, $7. Just ready. GRAY (LANDON CARTER). A TBEATISE ON NEBVOUS AND MENTAL DISEASES. For Students and Practitioners of Medicine. New (2d) edition. In one handsome octavo volume of 728 pages, with 172 engravings and 3 colored plates. Cloth, $4.75; leather, $5 75. Just ready. ^ GREEN (T. HENRY). ^.V INTBODUCTION TO PATHOLOGY AND MOB- BID ANATOMY. New (7th) American from the eighth London edition. In one handsome octavo volume of 595 pages, with 224 engravings and a colored plate. Cloth, $2.75. GREENE (WILLIAM H.). A MANUAL OF MEDICAL CHEMISTBY. For the Use of Students. Based upon Bowma:m's Medical Chemistry. In one 12mo. volume of 310 pages, with 74 illustrations. Cloth, $1.75. GROSS (SAMUEL D.). A PBACTICAL TBEATISE ON THE DISEASES, INJUBIES AND MALFOBMATIONS OF THE UBINABY BLADDEB, THE PBOSTATE GLAND AND THE UBETHBA. Third edition, thoroughly revised and edited by Samuel W. Gross, M. D. In one octavo volume of 574 pages, with 170 illastrations. Cloth, §4.50. HABERSHON (S. 0.). ON THE DISEASES OF THE ABDOMEN, comprising those of the Stomach, (Esophagus, Caecum, Intestines and Peritoneum. Second Amer- ican from the third English edition. In one octavo volume of 554 pages, with 11 engrav- ings. Cloth, $3.50. HAMILTON (ALLAN McLANE ) . NEB VO US DISEASES, THEIB DESCBIP- TION AND TBKA TMENT. Second and revised edition. In one octavo volume of 598 pages, with 72 engravings. Cloth, $4. HAMILTON (FRANK H.). .4 PBACTICAL TBEATISE ON FBACTUBES AN I) DISLOCATIONS. Eighth edition, revised and edited by Stephen Smith, A.M., M.D. In one handsome octavo volume of 832 pages, with 507 engravings. Cloth, $.5.50; leather, $0.50. HARDAWAY i W. A.). MANUAL OF SKIN DISEASES. In one 12mo. volume of 41(t pages. Clotli, .$.3. HARE fHOBART AMORYi. A TEXT-BOOK OF PBACTICAL THERA- PKUTKJS, with Special Kelerence to the Application of Remedial Measures to Disease and their Emi)loyment upon a Rational Bii-^is. With articles on various subjects by well- known specialists. New (5th) and revi-sed edition. In one octavo volume of 740 pages. Cloth, $3.76; leather, $4.75. Just ready. PRACTICAL DIAGNOSIS. The L'sc of Symptoms in the Diagnasis of IHsease. In one octavo volume of 5ti() pages, with 191 engravings, ami 13 full-page plates in colors and nionochroine. Cloth, $4.75. Just ready. HARE (HOBART AMORY), Editor. A SYSTEM OF PRACTICAL THERA- PEUTICS. By American and Foreign Authors. In a series of contributions by emi- nent practitioners. In four large octavo volumes comprising about 45(il) pages, with about 5.50 engravings. Vol. IV., in /»/»w. Price per volume, cloth, $5 ; leather, $(5 ; half Kiissia. $7. For nfde by subscription only. Full prospectus free <. A TREATISE ON THE FUNCTION OF DIGESTION, ITS J US ORDERS AND THEIR TREATMENT. From the second London edition. In one Svo. volume of 238 pages. Cloth, $2. PAYNE (JOSEPH FRAITK). A MANUAL OF GENERAL PATHOLOGY. I)i'signed a.s an Intnjduction to the Practice of Medicine. In one octavo volume of 524 payes, with 153 engravings and 1 colored plate. Cloth, $3.50. PEPPERS SYSTEM OF MEDICINE. See page 2. PEPPER (A. J.). SURGICAL PATHOLOGY. In one 12mo volume of 511 pages, with s] engravings. <'loth, $2. See Students' Series of Manuals, page 14. PICK (T. PICKERING). FRACTURES AND DISLOCATIONS. In one 12mo. volume of ')',H) ii;ii,'t>, with 93 engravings. Cloth, $2. See Series of Clinical Manuals, p. 13. PIRRIE I WILLIAM ) . TITE PRLXCIPLES A ND PR A CTICE OF S URGER Y. In one octavo volume of 7S0 pages, with 316 engravings. Cloth, $3.75. PLAYFAIR (W. S.^ A TREATISE ON THE SCIENCE AND PRACTICE OF MIDWIFERY. Sixth American from the eighth English edition. Edited, with additions, by R. P. Hakuis, M.D. In one octava volume of 697 pages, with 217 engrav- ings and 5 plates. Cloth, $4; leather, $5. THE SYSTEMATIC TREATMENT OF NERVE PROSTRATIoy AND HYSTERIA. In one 12mo. volume of 97 pagis. Cloth, $1. Philadelphia, 706, 708 and 710 Sansom St.— New York, 111 Fifth A^e. (cor. 18th St ). 12 LEA BROTHERS & CO.'S PUBLICATIONS. POLITZER (ADAM). A TEXT-BOOK OF THE DISEASES OF THE EAR AND ADJACENT ORGANS. Second American from the third German edition. Translated by Oscar Dodd, M.D , and edited by Sir William Dalby, F.K..C.S. In one octavo volume of 748 pages, with 330 original engravings. Cloth, $5.50. POWER (HENRY). HUMAN PHYSIOLOGY. Second edition. In one 12mo. volume of 396 pages, with 47 engravings. Cloth, $1.50. See Student^ s Series of Manuals, page 14. PURDY (CHARLES W.). BRIGHT'S DISEASE AND ALLIED AFFEC- TIONS OF THE KIDNEY. In one octavo volume of 288 pages, with 18 engrav- ings. Cloth, $2 PYE-SMITH (PHILIP H.). DISEASES OF THE SKIN. In one 12mo. volume of 407 pages, with 28 illustrations, 18 of which are colored. Cloth, $2. QUIZ SERIES. See Students' Quiz Series, page 14. RALFE (CHARLES H.). CLINICAL CHEMISTRY. In one 12mo. volume of 314 pages, with 16 engravings. Cloth, $1.50. See Students' Series of Manuals, page 14. RAMSBOTHAM (FRANCIS H.). THE PRINCIPLES AND PRACTICE OF OBSTETRIC MEDICINE AND SURGERY. In one imperial octavo volume of 640 pages, with 64 plates and numerous engravings in the text. Strongly bound in leather, $7. REICHERT (EDWARD T.). A TEXT-BOOK ON PHYSIOLOGY. In one handsome octavo volume of about 800 pages, richly illustrated. Preparing. REMSEN (IRA). THE PRINCIPLES OF THEORETICAL CHEMISTRY. New (5th) edition, thoroughly revised. In one 12mo. volume of 326 pages. T'loth, $2. Just ready. REYNOLDS (J. RUSSELL). A SYSTE3I OF MEDICINE. Edited, with notes and additions, by Henry Hartshorne, M.D. In three large 8vo. volumes, containing 3056 closely printed double-columned pages, with 317 engravings. Per volume, cloth, |5 ; leather, $6. For sale by subscription only. RICHARDSON (BENJAMIN WARD). PREVENTIVE MEDKJINE. In one octavo volume of 729 pages. ( !loth, $4 ; leather, $5. ROBERTS (JOHN B.). THE PRINCIPLES AND PRACTICE OF MODERN SURGERY. In one octavo volume of 780 pages, with 501 engravings. Cloth, $4.50; leather, $5.50. THE COMPEND OF ANATOMY. For use in the Dissecting Koom and in preparing for Examinations. In one 16mo. volume of 196 pages. Limp cloth, 75 cents. ROBERTS (SIR WILLIAM). A PRACTICAL TREATISE ON URINARY AND RENAL DISEASES, INCLUDING URINARY DEPOSITS. Fourth American from the fourth London edition. In one very handsome 8vo. volume of 609 pages, with 81 illustrations. Cloth, $3.50. ROBERTSON (J. McGREGOR). PHYSIOLOGICAL PHYSICS. In one 12mo. volume of 537 pages, with 219 engravings. Cloth, $2. See Students' Series of Manuals, page 14. ROSS (JAMES). A HANDBOOK OF THE DISEASES OF THE NERVOUS SYSTEM. In one handsome octavo volume of 726 pages, with 184 engravings. Cloth, $4.50; leather, $5.50. SAVAGE (GEORGE H.). INSANITY AND ALLIED NEUROSES, PRACTI- CAL AND CLINICAL. In one 12mo. volume of 551 pages, with 18 typical engrav- ings. Cloth, $2. See Series of Clinical Manuals, page 13. SCHAFER (EDWARD A. ) . THE ESSENTIA LS OF HISTOL OGY, DESCRIP- TIVE AND PRACTICAL. For the use of Students. New (4th) edition. In one liandsome octavo volume of 311 pages, with 288 illustrations. Cloth, $3. Philadelphia, 706, 708 and 710 Sansom St—New York, 111 Fifth Ave. {cor. 18th St.). LEA BROTHERS & CO.S PUBLICATIONS. 13 SCHMITZ AND ZUMPTS CLASSICAL SERIES. ADVANCED LATIN EXERCISES (loth, 60 cents; half bound, 70 cent-. SCHMITZ 'S ELEMENT A R Y LA TIN EXER CISES. Cloth, 50 cents. SALLUST. Cloth, 60 cents; half bound, 70 cents. NEPOS. Cloth, 60 cents ; half bound, 70 cents. VIRGIL. Cloth, 85 cents; half bound, §1. CURTIUS. Cloth, 80 cents; half bound, 90 cents. SCHOFIELD (ALFRED T.). ELEMENTARY PHYSIOLOGY FOR STU- DENTS. In one 12mo. volume of 380 pages, with 227 engravings and 2 colored plates. Cloth, S2. SCHREIBER (JOSEPH). A .MANUAL OF TREATMENT BY MASSAGE AND METHODICAL MUSCLE EXERCISE. Translated by Walter Z^Iexdel- SON, M. D , of New York. In one handsome octavo volume of 274 pages, with 117 fine engravings. SEILER (CARL . A HANDBOOK OF DIAGNOSIS AND TREATMENT OF DISEASES OF THE THROAT AND NASAL CAVITIES. New (5th) edition. In one 12mo. vol. of about 425 pages, with about 120 engravings and 2 colored plates. //, !„■>.<.<. SENN I NICHOLAS). SURGICAL BACTERIOLOGY. Second edition. In one octavo volume of 268 pages, with 13 plates, 10 of which are colored, and 9 engravings. Cloth, $2. SERIES OF CLINICAL MANUALS. A Series of Authoritative Monographs on Important < linical Subjects, in 12mo. volumes of about 550 pages, well illustrated. The following volumes are now ready: Broadbent on the Pulse, $1.75; Yeo on Food in Health and Disease, new (2d) edition, $2.50; Carter and Frost's Ophthalmic Surgerv, $2.25; HuTcnixsoN on Syphilis, $2.25; Marsh on Wseases of the Joints, $2; Morris on Surgical Diseases of the Kidney. $2.25; Owen on Surgical Diseases of Children, $2; Pick on Fractures and Dislocations, $2; Bi'tlin on the Tongue, $3.50; Sav.vge on Insanity and Allied Neuroses, $2 ; and Treves on Intestinal Obstruction, $2. For separate notices, see under various authors' names. SERIES OF STUDENTS' MANUALS. See next page. SIMON (CHARLES E.). CLINICAL DIAGNOSIS; BY MICROSCOPICAL AN J) CHEMICAL METHODS. In one handsome octavo volume of 504 pages, with 132 engravings an- svo. volume of 253 pages. Cloth, $2.25. SMITH I J. LEWIS). A TREATISE ON THE DISEASES OF INFANCY AND CHILDHOOD. New (8th) edition, thoroughly revised and rewritten and greatly enlarged. In one large 8vo. volume of 9S3 pages, with 273 illustrations and 4 fnli-pag( plates. ( loth, $1..")0 ; leather, $5. .50. J mt ready- SMITH (STEPHEN). OPERATIVE SURGERY. Second and thoroughly revi.sed fiiitioii. Ill OIK' iHtavo vol. of 892 pages, with 1005 engravings. Cloth, $4; leather, $5. SOLLY (S. EDWIN). A HANDBOOK OF MEDICAL CLIMATOLOGY. Ill niic liaiidsoiiii' octavo volume of about 450 pages. Slmrlly. STILLE (ALFREDS. CHOLERA; ITS ORIGIN, HISTORY, CAUSATION, SYMrTO.MS, LESIONS, PREVENTION AND TREATMENT. In one 12mo. volume of Ki:} pages, with a chart showing roulcft of previous epidemic."*. ( loth, $1.25. THERAPEUTICS AND MATERIA MEDIC A. Fourth and nvis...l ..,li,i,,„ In two octavo volumes, containing 1936 pages. Cloth, $10; leather, $12. Philadelphia, 706, 708 and 710 Sansom St.— New fork III Fifth A^e. (cor. 18th St.). 14 LEA BROTHERS & CO.'S PUBLICATIONS. STILLE (ALFRED), MAISCH (JOHN M.) AND CASPARI (CHAS. JR.). THE NATIONAL DISPENSATORY: Containing the Natural History, Chemistry, Pharmacy, Actions and Uses of Medicines, including those recognized in the latest Phar- macopoeias of the United States, Great Britian and Germany, with numerous references to the French Codex. Fifth edition, revised and enlarged in accordance with and em- bracing the new U. S. Pharmacopoeia, Seventh Decennial Kevision. With Supplement containing the new edition of the National Formulary. In one magnificent imperial octavo volume of 2025 pages, with 320 engravings Cloth, $7.25; leather, |8. With ready reference Thumb-letter Index. Cloth, $7.75; leather, $8.50. STIMSON (LEWIS A.). A MANUAL OF OPERATIVE SURGERY. New (3d) edition. In one royal 12mo. volume of 614 pages, with 306 engravings. Just ready. Cloth, $3.75. A TREATISE ON FRACTURES AND DISLOCATIONS. In two hand- some octavo volumes. Vol. I., Fractures, 582 pages. 360 engravings. Vol 11., Dislo- cations, 540 pages, 163 engravings. Complete work, cloth, $5.50 ; leather, $7.50. Either volume separately, cloth, $3 ; leather, $4. STUDENTS' QUIZ SERIES. A New Series of Manuals in question and answer for Students and Practitioners, covering the essentials of medical science. Thirteen volumes, pocket size, convenient, authoritative, well illustrated, handsomely bound in limp cloth, and issued at a low price 1. Anatomy (double number); l!. Physiology; 3. Chemistry and Physics ; 4. Histology, Pathology and Bacteriology ; 5. Materia Medica and Thera- peutics ; 6. Practice of Medicine ; 7. Surgery (double number) ; 8. Genito-Urinary and \^enereal Diseases ; 9. Diseases of the Skin ; 10. Diseases of the Eye, Ear, Throat and Nose; 11. Obstetrics; 12. Gynecology; 13. Diseases of Children. Price, $1 each, except Nos. 1 and 7, Anatomy and Surgery, which being double numbers are priced at $1.75 each. Full specimen circular on application to publishers. STUDENTS' SERIES OF MANUALS. A Series of Fifteen Manuals by Eminent Teachers or Examiners. The volumes are pocket-size 12mos. of from 300-540 pages, pro- fusely illustrated, and bound in red limp cloth. The following volumes may now be announced: Herman's First Lines in Midwifery, $1.25; Luff's Manual of Chemistry, $2; Bruce's Materia Medica and Therapeutics (fifth edition), $1.50; Treves' Manual of Surgery (monographs by 33 leading surgeons), 3 volumes, per set, $6 ; Bell's Compara- tive Anatomy and Physiology, $2; Robertson's Physiological Physics, $2; Gould's Surgical Diagnosis, $2; Klein's Elements of Histology (4th edition), $1.75; Pepper's Surgical Pathology, $2 ; Treves' Surgical Applied Anatomy, $2 ; Power's Human Physiology (2d edition), $1.50; Ealpe's Clinical Chemistry, $1.50; and Clarke and Lockvtood's Dissector's Manual, $1.50 For separate notices, see under various authors' names. STURGES (OCTAVIUS). AN INTRODUCTION TO THE STUDY OF CLIN- ICAL MEDICINE, in one ]2mo volume. Cloth, $1.25. SUTTON (JOHN BLAND). SURGICAL DISEASES OF THE OVARIES AND FALLOPIAN TUBES. Including Abdominal Pregnancy. In one 12mo. vol- ume of 513 pages, with 119 engravings and 5 colored plates. Cloth, $3. TUMORS, INNOCENT AND MALIGNANT. Their Clinical Features and Appropriate Treatment. In one 8vo. volume of 526 pages, with 250 engravings and 9 full-page plates. Cloth, $4.50. TAIT (LAWSON). DISEASES OF WOMEN AND ABDOMINAL SURGERY. In two handsome octavo volumes. Vol. I. contains 554 pages, 62 engravings, and 3 plates. Cloth, $3. Vol. II., preparing. TANNER (THOMAS HAWKES). ON THE SIGNS AND DISEASES OF PREGNANCY. From the second English edition. In one octavo volume of 490 pages, with 4 colored plates and 16 engravings. Cloth, $4.25. TAYLOR (ALFRED S.). MEDICAL JURISPRUDENCE. Eleventh American from the twelfth English edition, specially revised by Clark Bell, E^q., of the N. Y. Bar. In one octavo vol. of 787 pages, with 56 engravings. Cloth, $1.50; leather, $5.50. Philadelphia 706, 708 and 710 Sanson) St.~New York, III Fifth Ave. (cor. 18th St.). LEA BROTHERS & CO.'S PUBLICATIONS. 15 TAYLOR (ALFRED S.). ON POISONS IN RELATION TO MEDICINE AND MEDICAL JURISPRUDENCE. Third American from the third London edition. In one Svo. volume of 788 pages, with 104 illustrations, ('loth, $5.50; leather, 556.50. TAYLOR (ROBERT W.). THE PATHOLOGY AND TREATMENT OF VENEREAL DISEASES. In one very handsome octavo volume of J 002 pages, with 230 engravings and 7 colored plates. Cloth, §5 ; leather, $6. Net. A CLINICAL ATLAS OF VENEREAL AND SKIN DISEASES. Including Diagnosis, Prognosis and Treatment. In eight large folio parts, measuring 14 X 18 inches, and comprising 213 beautiful figures on 58 full-page chromo-lithographic plates, 85 fine engravings, and 425 pages of text. Complete work now ready. Price per part, sewed in heavy embossed paper, $2.50. Bound in one volume, half Russia, $27 ; half Turkey Morocco, $28. For sale by subscription only. Address the publishers. Spec- imen plates by mail on receipt of 10 cents. SEXUAL DISORDERS IN THE MALE AND FEMALE. In one octavo volume. In active preparation. TAYLOR ( SEYMOUR). INDEX OF MEDICINE. A Manual for the use of Senior Students and others, in one large 12mo. volume of 802 pages. Clpth, $3 75. THOMAS (T. GAILLARD) AND MUNDE PAUL F.). A PRACTICAL TREATISE ON THE DISEASES OF WOMEN Sixth edition, thoroughly revised by Paul F. Muxde, M. D. In one large and handsome octavo volume of 824 pages, witli 347 engravings. Cloth, $5; leather, $6. THOMPSON (SIR HENRY). CLINICAL LECTURES ON DISEASES OF THE URINARY ORGANS. Second and revised edition. In one octavo volume of 203 pages, with 25 engravings. Cloth, §2.25. THE PATHOLOGY AND TREATMENT OF STRICTURE OF THE URETHRA AND URINARY FISTULJE. From the third English edition In one octavo volume of 359 pages, with 47 engravings and 3 lithographic plates. Cloth, .$3.50. TODD (ROBERT BENTLEY). CLINICAL LECTURES ON CERTAIN ACUTE DISEASES. In one 8vo. volume of 320 pages. Cloth, $2.50. TREVES (FREDERICK). OPERATIVE SURGERY. In two 8vo. volumes con- taining 1550 pages, with 422 illustrations. Cloth, $9; leather, $11. A SYSTEM OF SURGERY. In Contributions by Twenty-five English Sur- geons. In two large octavo volumes, containing 2298 pages, with 950 engravings and 4 full -page plates. Per volume, cloth, $8. Jmi ready. A MANUAL OF SURGERY. In Treatises by 33 leaiUng surgeons. Three 12mo. volumes, containing 1806 pages, with 213 engravings. Price per set, $6. See Shi- dent.i' Series of Manuals, page 14. THE STUDENTS' HANDBOOK OF SURGICAL OPERATIONS. In one 12mo. volume of 508 pages, with 94 illustrations. Cloth, $2.50. SURGICAL APPLIED ANATOMY. In one 12mo. volume of 540 pages with 61 engravings. Cloth, $2. See Students' Series of Mnmtals, page 14 INTESTINAL OBSTRUCTION. In one 12mo. volume of 522 pages, with 60 illustrations. Cloth, $2. See Series of Clinical Manuals, page 13 TUKE (DANIEL HACK). THE INFLUENCE OF THE MIND UPON THE BODY IS IIKM/ni AND DISEASE. Set-end edition. In one Hvo. volume of 4<>7 paires, witli 2 coiori'ij pl.-itos. ( lotli, .*3. VAUGHAN (VICTOR C.i AND NOVY (FREDERICK Q.). DTO MAINS, LEUCOMAINS, TOXINS AM> AyTITtJX r.\S, or the ( homical Factor* in the Causation of Disease. New (3d) edition. In one 12mo. volume of 603 pages. Cloth, $3. Ju.<'i^--"