PRACTICAL DIAGNOSIS: 
THE USE OF SYMPTOMS IN THE 
DIAGNOSIS OF DISEASE. 
SECOND EDITION, REVISED AND ENLARGED. 
BY 
HOBART AMORY M.H., B.Sc., 
PROFESSOR OF THERAPEUTICS IN THE JEFFERSON MEDIcYf. COLLEGE OF PHILADELPHIA ; PHYSICIAN 
TO THE JEFFERSON MEDICAL COLLEGE HOSPITAL; LAUREATE OF THE MEDICAL SOCIETY OF 
LONDON, OF THE ROYAL ACADEMY OF MEDICINE IN BELGIUM ; CORRESPONDING FELLOW 
OF THE SOCIEDAD ESPANOL DE LA HIGIENE OF MADRID ; MEMBER OF THE 
ASSOCIATION OF AMERICAN PHYSICIANS ; FELLOW OF THE COLLEGE 
OF PHYSICIANS OF PHILADELPHIA, ETC.; AUTHOR OF A 
TEXT-BOOK OF PRACTICAL THERAPEUTICS. 
ILLUSTRATED WITH 201 ENGRAVINGS AND 13 COLORED PLATES. 
LEA BROTHERS & CO., 
PHILADELPHIA AND NEW YORK. 
1897. Entered according to the Act of Congress in the year 1897, by 
LEA BROTHERS & CO., 
In the Office of the Librarian of Congress. All rights reserved. 
DORNAN,PRINTER PREFACE TO THE SECOND EDITION. 
The first edition of this book, which was published in August, 
1896, was so rapidly exhausted that the author has had an early 
opportunity to present a second edition, from which the unavoid- 
able faults of a first edition have been expunged and to which 
many new facts have been added. The author desires to reiterate 
the fact that the book was written with the hope that it would 
prove useful as a guide in bedside practice. That the profession 
needed a book dealing with diagnosis from the standpoint of the 
symptoms manifested by the patient seems to be evidenced by the 
rapid sale of the first edition. 
In this edition the two indexes of the first edition have been 
combined in one to avoid confusion and aid the reader. 
Philadelphia, 222 South Fifteenth Street, 
September, 1897. PREFACE TO THE FIRST EDITION. 
The object of this volume is to place before the physician and 
student the subject of medical diagnosis as it is met at the bedside. 
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 discus- 
sion 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 differen- 
tial 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 diagnosis, and, having 
done this, turn to his reference book and read the article dealing 
with tbe 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, however, the 
discovery of any marked symptom will lead directly to the diag- 
nosis. Thus, if the patient is vomiting, in the chapter on Vom- 
iting will be found its various causes and its diagnostic significance, 
and the differentiation of each form of this affection from another. 
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 he has had in both 
didactic and clinical teaching of large classes of students during VIII 
PREFACE TO THE FIRST EDITION. 
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 oj 
Practical Therapeutics. 
Philadelphia, 222 South Fifteenth Street, 
August, 1896. CONTENTS. 
INTRODUCTION. 
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 HANDS AND ARMS. 
The general appearance of the hands and arms—The shape of the 
hands in disease—Spasms of the fingers—Tremors of the hands— 
Paralysis of the hands and arms 54 
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 ............ 85 
CHAPTER IV. 
HEMIPLEGIA 127 CONTENTS. 
X 
CHAPTER Y. 
PAGE 
THE TONGUE, MOUTH, AND PHARYNX. 
The general appearance of the tongue—Its coating—Its appearance 
in poisoning—Fissures and ulcers of the tongue—Eruptions of the 
tongue—Atrophy and hypertrophy of the tongue—Paralysis— 
Tremor and spasm of the tongue 140 
CHAPTER VI. 
THE EYE. 
The general diagnostic indications afforded by the eye—Diplopia—Dis- 
order of the external ocular muscles—Disorder of the internal ocular 
muscles—Strabismus and squint—The pupil—Hemianopsia—The 
visual fields—Color-vision—The optic nerve and its lesions—Re- 
tinitis—Amblyopia and blindness 158 
CHAPTER VII. 
THE SKIN. 
The color of the skin—Eruptions of the skin—Gangrene, ulcers, and 
sloughs—Scars, sweating, dryness, oedema, hardness—Anaesthesia, 
and hemianaesthesia—Paraesthesia, liyperaesthesia, itching . . 195 
CHAPTER VIII. 
THE THORAX AND ITS VISCERA. 
The inspection of the normal and abnormal chest—Their topography— 
Alterations in the shape of the thorax—The rhythm of the respira- 
tions—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 . . 263 
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 320 
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 345 CONTENTS. 
XI 
CHAPTER XI. 
THE BLOOD. 
PAGE 
The various forms of red and white corpuscles—Their proportionate 
number in health and disease—Alterations in their form and 
character—The hsemoglobin of the blood in health and disease 
—The various forms of anaemia—Leucocythsemia and pseudo-leuco- 
cythsemia—Parasites of the blood 353 
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 abnor- 
mal urine—The normal and abnormal contents of the urine— 
Their significance—Tests for the contents of the urine . . .377 
CHAPTER XIII. 
THE BOWELS AND FECES. 
Constipation and diarrhoea—The causes of these two symptoms and 
their diagnosis—The diseases in which these symptoms occur— 
Choleraic diarrhoea—Dysentery—The color of the feces—Intestinal 
parasites 418 
PART II. 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
CHAPTER I. 
FEVER AND SUBNORMAL TEMPERATURES. 
The methods of taking the temperature—The significance of fever— 
The febrile movements of various diseases 433 
CHAPTER II. 
HEADACHE AND VERTIGO. 
The causes of headache—Digestive headache—Headaches due to the 
eyes—Headaches due to cerebral tumor and abscess—Headaches 
due to syphilis—Headaches complicating acute diseases . . . 456 XII 
CONTENTS. 
CHAPTER III. 
PAGE 
COMA OR UNCONSCIOUSNESS 472 
CHAPTER IV. 
CONVULSIONS OR GENERAL SPASMS. 
The convulsions of epilepsy in its various forms—Of infancy—Of hys- 
teria—Tetanic convulsions—Spasms—Chorea 480 
CHAPTER V. 
VOMITING, REGURGITATION, AND THE CHARACTER OF THE VOMIT. 
Due to uraemia—Cerebral lesions—Intestinal obstruction—Peritonitis 
—Cholera—Gastric disease—Hepatic disease—Poisons—The ap- 
pearance of vomit .......... 504 
CHAPTER VI. 
COUGH AND EXPECTORATION. 
The varieties of and indications of cough—The causes of cough—The 
sputum—Its pathological significance 522 
CHAPTER VII. 
PAIN. 
The kinds of pain—The significance of its locality—Colic . . . 535 
CHAPTER VIII. 
* 
TENDON-REFLEXES AND MUSCLE-TONE. 
The knee-jerk and ankle-clonus—The arm-jerk—The significance of 
decreased and increased reflexes ....... 547 
CHAPTER IX. 
SPEECH. 
The changes in the speech and voice—Their significance—Aphasia— 
Apraxia—Alexia—Paraphasia 552 PRACTICAL DIAGNOSIS. 
INTRODUCTION. 
GENERAL DIAGNOSTIC CONSIDERATIONS. 
A clear understanding by the physician of the value of the 
symptoms of disease which he sees and of those described by the 
patient is of vital importance for the purposes of diagnosis and 
treatment, and one of the advantages of older physicians over their 
younger brethren is the ability which they have gained through long 
training to grasp the essential details of a case almost at their first 
glance at the patient. Much of this ability is unconsciously pos- 
sessed because it is gained by a gradual process, yet it is none the 
less valuable, and its possession often impresses the patient with 
the insight which his physician has into his case. At first it is 
impossible for the novice to cast aside the minor symptoms, which 
the patient emphasizes as his major ones, and to perceive clearly 
that one or two facts that have been belittled in the narration of 
the story of the illness are in reality the stalk about which every- 
thing else in the case must be made to cluster. 
Let us suppose the patient before the physician is one who has 
been able to walk into the office or dispensary. The attentive 
physician can at once gather much information about the case from 
the clothing, the gait, the build, the voice, the expression, and the 
manner. The thin man, with a peaked face and provided with an 
unusually warm overcoat, and still further wrapped up with a 
muffler almost to his eyes, is in all probability a sufferer from some 
pulmonary or throat difficulty, while the heavily built, phlegmatic 
individual, with a large head and well-filled paunch, is much more 
apt to suffer from gastro-intestinal or biliary catarrhs. Such a per- 
son will probably be one who habitually wears his coat open on the 18 
IN TROD UCTION. 
coldest days. Again, chronic drunkards, or persons whose mental 
powers are failing, often are exceedingly careless about their cloth- 
ing, buttoning the coat or the trowsers with the wrong buttons, and 
keeping the clothing dirty and spotted. Some cases of diabetes 
have first been discovered by the white spots on the trowsers, as the 
result of having allowed a few drops of urine to fall on the cloth, 
where they have dried. Old men who have incontinence of urine 
often wear trowsers which are stained in front, and they often have 
an ammoniacal odor about them from this cause. 
The various forms of gait which indicate actual disease will be 
found discussed in the chapter on the legs and feet, but it may be 
mentioned in passing that in addition to these changes, which are 
dependent upon actual disease of the legs or the nervous system 
supplying them, that the general bearing and stride of a patient 
will often give us a clear idea of his general tone. The neuras- 
thenic patient walks feebly or with a step that might be called 
ataxic, while the strong, hearty man of good physique strides along 
with a gait quite different from this, or that of an individual who is 
delicate and feeble. 
Similarly, the patient’s build betokens disease or health. The 
thin, tall, and hollow-chested person is recognized as a fair mark 
for the tubercle-bacillus, and the heavy, closely knit, phlegmatic 
man as one who may suffer from hepatic disorders. Again, the 
bearing of a person possessing a highly organized nervous system 
shows itself in the constant activity of his mind and body. No 
part is quiet for more than a moment, and drugs are more apt to 
produce extraordinary symptoms as the result of idiosyncrasies in 
this type of patient than in any other. 
Alien the physician has gathered as much information as possible 
as to the age and general condition of his patient, by a careful scru- 
tiny of his face and extremities, of which scrutiny, however, the 
patient should be unconscious, he should ask him to tell what brings 
him for advice, and as a rule this will be the opportunity the suf- 
ferer seeks to pour out the story of his ailment as he sees or feels 
it. Often the story will seem wearisome, and, to the educated mind 
of the physician, wandering or unnecessary; but to the patient every 
word seems of the greatest importance, and to show any lack of in- 
terest may give the impression of carelessness, or it may interrupt 
the story just as a most important symptom is about to be described. 
Even if the patient is unable to convey a very clear idea of his con- GENERAL DIAGNOSTIC CONSIDERATIONS 
19 
dition, the manner in which his story is told, the character of his 
speech, and the expression of his face while speaking may give 
useful information as to his ailment or general state. 
If, instead of the patient being an office or dispensary case, he is 
one who is being visited at home, the fact that the patient meets 
the physician in one of the living rooms rather than in a bedroom 
indicates either that there is little immediate danger in the case, or, 
at least, that the difficulty is not acute, but chronic in type, as some 
slowly progressing form of pulmonary, cardiac, or renal disease. 
Of course, there are exceptions to this rule, as in the case of a 
patient who, having caught a heavy cold, is remaining indoors, but 
not in bed, for prudence’ sake. Or, again, if on seeing the patient 
we find him sitting in a chair only partly dressed and propped up 
with pillows, or instead leaning forward upon the back of a chair 
placed in front of him, we know that he is the subject most prob- 
ably of an acute or chronic heart disease, most likely an acute exac- 
erbation of the latter. A glance at the face of such a patient, reveal- 
ing a trembling nostril, blue lips, or an anxious facies, will aid still 
further in directing attention to the heart or lungs, and the hands 
if examined will appear relaxed and livid or darkened in hue, in- 
dicating capillary stasis and deficient oxidation. In other cases, 
however, the patient found sitting propped up with pillows may be 
a convalescent from some long illness; but if so, the general atmos- 
phere of the patient is better, and the surroundings are apt to be 
more tidy. 
If we find the patient in bed, he may be lying abnormally quiet 
as the result of faintness or acute nausea, or, perhaps, from partial 
or complete coma due to cerebral or renal disease, or from the effects 
of some drug; or, again, he may be rolling about the bed from the 
pain of acute belly-ache, or be keeping his legs and body very still 
while his hands and head are ever on the move to prevent anything 
from suddenly approaching or touching his abdominal wall, as in 
peritonitis. The striking difference between the activity of the 
head and the fixation of the lower part of the body, in peritonitis, 
is notable. Sometimes, however, anxious restlessness indicates acute 
internal or external hemorrhage; but here the movements are minute 
though active, and the patient does not expend much strength as he 
does when suffering from pain. Usually a patient who is lying on 
his side turns on his back as the physician or nurse approaches, in 
order to face his visitor; but if he persistently remains on the side 20 
INTROD UCTION. 
without moving except to partly turn his head, we may suspect 
that in that posture he is most comfortable, and that the position is 
assumed for its comfort or to relieve pain or dyspnoea. Tims, in 
acute pleurisy the patient lies with the affected side uppermost 
because it is too sore to permit him to touch it to the bed; whereas, 
if the stage of effusion has arrived, he lies on the affected side in 
order to give the side which is healthy free play in compensatory 
respiratory movements, and to remove the pressure of the effusion 
from the healthy lung. If the patient lying in this posture is not 
suffering from pleurisy, his position may be assumed to be due to 
an effort to relieve the discomfort caused by an enlarged liver. 
The fact that the patient lies constantly on the back is also a char- 
acteristic of grave and advanced disease in some instances. Very 
ill persons almost never lie on the side, and the fact that a desper- 
ately ill case of yesterday is found lying on the side to-day is an 
encouraging sign. Persons with severe heart disease are rarely, if 
ever, able to lie prone in bed, and have to be more or less propped 
up with bed-rests and pillows. Large growths in the abdominal 
cavity producing pressure on the diaphragm also necessitate this 
semi-prone posture, and double pleural effusions, or pulmonary con- 
solidation, or oedema, produce the upright or half-reclining attitude 
in order that the upper parts of the lung may be used to advantage. 
Again, if the patient wakes when spoken to, and then drops off 
to sleep at once, some form of poisoning may be present, as from 
opium, or the poison of advanced hepatic or renal cirrhosis may be 
present. (For the significance of picking at the bed-clothes, see 
chapter on the Hands and Arms.) 
We can next pass to a consideration of the objects to be sought 
in questioning a patient as to the illness from which he is suffering. 
Often much information can be gained by a well-directed question, 
and a favorable impression can be made upon the patient by the 
manner in which it is put and the bearing which it has on his case. 
Thus, if a man is evidently much emaciated, and his clothes fit him 
loosely, a question in regard to his loss of flesh is very appropriate; 
but if he is manifestly too stout for comfort such a question will be 
most unfortunate. Or, again, if a young married woman comes 
complaining of constant sickness of the stomach and a fanciful 
appetite, and the physician directs all his questions to the condition 
of the stomach without an eye to a slight increase in size about the 
waist or below it, his professional acumen is in grave danger of GENERAL DIAGNOSTIC CONSIDERATIONS. 
21 
being libelled by that same woman, who knows, or soon finds out, 
that her discomfort is due to pregnancy. 
If the woman is unmarried and there is no evidence of gastric 
disorder on her tongue, it is well to remember what Battey, of 
Georgia, said in regard to this condition : “ Always believe a young 
unmarried woman with abdominal tumor, of high social position 
and unimpeachable virtue, if she has been watched over by a 
platonic and abstemious young cousin of the male persuasion while 
the mother went out, to be pregnant.” 
Again, if a married woman of some years tells her physician that 
she has no children, the physician naturally asks some questions 
which elicit the fact that she has had frequent miscarriages. He 
in this way finds quite as much about probable syphilitic infection 
as if the question had been put: “ Have you ever had a sore on 
your privates,” which would embarrass the patient, produce 
domestic troubles, and probably be lied about if she was forced 
to answer the question. 
Again, when asking a woman about the health of the living 
parents, or the cause of death of the dead, care should be taken 
not to ask a direct question, as, for example, whether the mother 
has died of cancer, for the patient may be already greatly worried 
lest she has that disease. It is better to ask the cause of death, or 
of the illness she is suffering from. If the story is that the parents 
died of “ bronchitis,” in all human probability the real cause of 
death was tuberculosis 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 affected 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 parts in which there 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 de- 
scribed by the patient as felt in the abdomen. If the pain has been 
really abdominal, there will, in many cases, have been diarrhoea or 
free passage of flatus. It is not to be forgotten, on the other hand, 
that a question whicli discovers the fact of several movements of 
the bowels does not prove the presence of true diarrhoea, because 
a purgative may have been taken by the patient. 22 
INTRODUCTION. 
In asking questions as to constipation the physician must not 
forget that the opinion of the patient as to what constitutes regu- 
larity of bowel-movement is of very little value in many instances. 
A 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 pro- 
duces embarrassment, which otherwise would not exist, and inti- 
mates 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 physi- 
cian 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 atten- 
tion to it whatever, 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 physi- 
cian 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 vis- 
itor, aud 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 attempt- 
ing 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 physicians 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 get 
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 char- GENERAL DIAGNOSTIC CONSIDERATIONS. 
23 
acter of its cry. It is needless to state that a child may cry from 
fright, from pain, anger, or hunger. Constant screaming crying is, 
however, nearly always due to the pain of earache or hunger, for 
abdominal colic is usually intermittent. If there be pain in the 
ear, the hand will often be rubbed over the affected 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 present; or in other cases the pain is so great that the child 
is cryless. A sharp, piercing shriek of crying indicates the pain of 
earache or 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 several conditions is present: either the child has 
stomatitis 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 condition pro- 
ducing shortness of breath. 
If a child over four months 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 present, 
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 while they are asleep, 
as it is then unaffected by voluntary effort. In children a sighing 
breathing, or one disturbed in rhythm, often indicates a disturbed 
digestion or fever. 
The breath of the healthy child is invariably 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 sick- 
ening 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 always, by careful questioning of the nurse 
or mother, find out how long the illness has lasted, the manner in 24 
IN TROD UCTION. 
which it began, the fact as to whether a similar attack has occurred 
before in this or other children of the family, and the state of the 
temper, appetite, bowels, and urine of the patient, for an irritable 
temper ‘in a child means ill-health, as does also a poor appetite, 
constipation, diarrhoea, or abnormal urine. 
The expression of 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 time for 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 be taken in the physician’s arms, 
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 difficulty, 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 excitement of the physician’s visit or the crying on 
awakening will greatly increase the pulse-rate. PART I. 
THE MANIFESTATION OF DISEASE IN ORGANS. 
CHAPTER I. 
THE FACE AND 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 and neck. 
So much can be learned by the physician from the expression and 
general appearance of a patient’s face and the carriage 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 importance 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 close scrutiny of the physician’s face 
with the object of detecting encouragment, lack of sympathy, or 
alarm. 
The Face. 
The Expression is produced by the formation of creases, or 
alterations in the contour of the skin and subcutaneous tissues by 
trophic and muscular action, and these changes are in time brought 
about by the mental tendencies and habits of the patient, his tem- 
perament, his intellectual development, his exposure to outdoor or 
indoor influences, and Anally, and these are very important, by 
pathological processes which may be going on somewhere in his 
body. The temper of the man also affects his expression, particu- 
larly as he approaches middle life, and he looks amiable, capable of 
sudden anger, or sullen, as the case may be. 26 
THE MANIFEST A TION 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 surroundings 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 intelli- 
gence. 
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 gen- 
erally 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 suf- 
fering from menstrual disorders, often have dark areas under the 
eyes, and pigmentation of the eyelids is often seen very early in 
pregnancy. In women, and sometimes in men, excessive fatigue 
and loss of sleep cause marked infra-orbital discoloratious. A 
puffiness under the eyes, most noticeable in the morning', may indi- 
cate renal lesions or the excessive use of arsenic, and if it is unilat- 
eral it probably depends upon some local inflammation of the eye 
or rarely upon disease of one of the cerebral sinuses. So, too, an 
ecchymotic spot under the eye may be due to a bruise, to some one 
of the forms of purpura or to scurvy. 
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 THE FACE AND HEAD. 
27 
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 
ingestion of overdoses of the coal-tar products, such as acetanilide, 
antipvrin, 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 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 expression 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 looking-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 expres- 
sion is very characteristic of serious illness, and, though difficult to 
describe, when recognized becomes quite valuable as a diagnostic 
factor, particularly as it rarely, if ever, is exaggerated by the 
patient who bears it. It is seen most markedly in cases of severe 
acute croupous pneumonia or peritonitis, or after severe injuries. 
When persons have had continuous pain for a long 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 pain 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 oftentimes 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 practic- 
ally immobile, and the general expression is very peaceful. If, on 
the other hand, the eyelids of a sleeping child are slightly parted 28 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 result 
in glazing of the conjunctiva from dryness, this is a sign of grave 
import. Again, twitching of the eyelids often indicates nervous 
irritation or the early stages of the convulsive state, and it is not 
uncommon for an expression to pass over the face of a child who, 
while sleeping, is suffering from pain, which begins as a smile and 
ends with a drawing-in of the corners of the mouth, an expression 
somewhat like that seen on the face of a waking child when it 
seems to be in doubt as to whether to laugh or to 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. 
When 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, spirituelle 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 tuber- 
culosis, in one of its rapid forms, as it approaches puberty. Or, 
again, the child is “ stocky ” 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 tuber- 
cular 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, 
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, THE FACE AND HEAD. 
29 
attention 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 the 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 
and dryness of the hair and skin, and the eager, or apathetic, 
glance of the eye. 
Fig. 1. 
Boy, aged seven. Mouth-breather, from obstruction of the pharynx : open mouth ; vacant 
expression; pinched nostrils; dull eyes; drooping eyelids; sunken chest; round shoulders. 
(HOOPEil.) 
In severe pneumonia the flushed face, with a deeper red on one 
cheek than the other, the anxious expression, and the dilated nostril 
are noteworthy; and in the dyspnoea 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 respiration, the patient’s lips are seen to be slightly parted and 
dry, and often appear somewhat cyanotic. In children suffering 
from lesions of the mitral valve of the heart it is very common for 
some blurring or indistinctness of the features to be present. 
One of the most characteristic facial expressions that we meet 
with is that of typhoid fever or fevers of a typhoid type. The 
face is dull and expressionless; the teeth are covered by sordes, 30 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
which become brown and blackish by exposure or by discoloration 
from medicines and foods; the lips are often moved in a low mut- 
tering delirium; and the whole appearance is that of apathy. Even 
when spoken to, the face of a patient suffering from enteric fever 
rarely lights up in response to the greeting. 
Equally, if not more, characteristic is the facial expression of 
acute peritonitis. The upper lip is drawn up in such a way as to 
show the teeth, and the expression of anxiety and nervous unrest 
is well developed. Similarly in abdominal pain due to other 
causes than peritonitis there is often a twitching of the muscles of 
the lip and about the eye which is quite typical. This twitch is 
said by Fothergill to be peculiar to pain below the diaphragm, and 
lie 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 conies that 
curious smile or vacuous expression of the face which is so charac- 
teristic. It should be remembered, however, that this vacant, fat- 
uous look may occur in women suffering from the early stages of 
disseminated sclerosis and in children with chorea. Then we have 
the elated facial expression of general paralysis of the insane, the 
excited look of acute mania, the beaten, weary, careworn look or 
apathetic glance of nervous exhaustion, and the hopeless expression 
of melancholia. 
The face of paralysis agitans, sometimes called the “ Parkinso- 
nian visage/’ is distressed and pathetic, and yet somewhat intense. 
(See chapter on the Hands and Arms, and 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 swell- 
ing or oedema of the face is seen in erysipelas, dropsy (Fig. 2), 
and inflammatory swelling (see chapter on the Skin). In trichin- 
iasis the eyelids are often swollen early in the disease, and then 
recover their normal appearance 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 THE FACE AND HEAD. 
31 
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 possi- 
bility of these being the early symptoms of what has been called 
Fig. 2. 
Face of a patient with general anasarca doe to chronic parenchymatous nephritis. 
(From a patient in the author’s wards—Jefferson Medical College Hospital.) 
the u facio-humero-scapular ” type of muscular atrophy (Landouzy 
and Dejerine). The 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 
twitchings 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 facts that more than one 
member of the family is affected, and that the disease is of long 
duration, added to these signs, render the diagnosis easy. It is a 
rare disease. 
An appearance of the face almost identical with that just described 
is seen in Friedreich’s ataxia, and is often one of the earlier mani- 
festations of the disease; but the presence in Friedreich’s ataxia of 
the ataxic gait, the jerky articulation, nystagmus, loss of knee-jerks, 32 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
and absence of muscular atrophy separate it from the Landouzy- 
Dejerine type of muscular atrophy just described as facio-humero- 
scapular atrophy. (See Ataxia in chapter on Feet and Legs.) 
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 
which saliva constantly dribbles, while the waxy skin and subnor- 
mal temperature of the body, with a poor circulation, slow respira- 
tion, and mental hebetude, complete the symptom-group. There is 
Fig. 3. 
Cretin. (Dercum.) 
nearly always in well-developed cases marked lumbar lordosis. 
(Fig. 3.) The facial expression of myxoedema is heavy and list- 
less, as a rule. (See page 34 and chapter on Skin.) 
In certain forms of leprosy the face often becomes leontine, or 
lion-like in appearance. 
The facies of exhausting disease about to produce death is very 
characteristic, and is seen frequently in cholera and in tuberculosis THE FACE AND HEAD. 
33 
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 eyes are sunken, and around them are great hollows, so that the 
infra- 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 Deformity. Facial asymmetry is sometimes seen as a 
congenital defect, and curiously enough is often developed in cliil- 
Fig. 4. 
Acromegaly, showing the large lace and hands. (Dercum.) 
dren who suffer from congenital wry-neck. This is not to be con- 
fused with that extraordinary affection 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. 34 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
Sometimes in facial hemiatrophy the wasting is accompanied by 
painful twitchings, 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 involve- 
ment of the sympathetic nerve-fibres. The changes are probably 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 hemihypertrophy, 
one side remaining normal in size and the other becoming gigantic. 
Fig. 5. 
Myxoedema. (Meltzer.) 
The massive face of a person suffering from acromegaly is very 
characteristic. (Fig. 4.) The face has a full-moon broadness in 
myxoedema. (See Fig. 5.) The enlargement of the bony parts of 
the skeleton, the kyphosis, and the comparative muscular feeble- THE FACE AND HEAD. 
35 
ness of acromegaly aid in the diagnosis of that disease, for in 
myxcedema there is no true bony enlargement. The face in osteitis 
deformans is shaped like a triangle with the base upward. In 
osteitis deformans the shafts of the long bones become weakened, 
and their surfaces roughened from periosteal deposits. (See chapter 
on Hands and Arms.) 
Unilateral Facial Paralysis. Very notable changes in the face 
are produced by paralysis, the former being, as a rule, unilateral and 
depending upon central or peripheral 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 whist- 
ling or the pronunciation of labial sounds is difficult or impossible. 
The cheek of the paralyzed side is often puffed out with each expi- 
ration, 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 unopposed. 
(For a description of the general anatomy and physiology of the 
nervous tracts involved in paralysis of the face and elsewhere, see 
chapter on Hemiplegia.) 
Unilateral paralysis is the form of facial paralysis most commonly 
seen, and is generally due to injury of the facial nerve-trunk. The 
lesion producing the paralysis may be peripheral—that is, in the 
nerve itself—or central, as in the pons or 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 swell- 
ing in so limited a canal. Such an attack will generally be found 
associated 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 suppurative or for caries to exist in all cases, for it seems prob- 
able that by the extension of inflammation along the chorda tympani 
such a paralysis may result. Still more rarely facial paralysis re- 
sults from swelling of the parotid gland, or tumor in its neighbor- 
hood, 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 portion of the temporal bone, 
and very rarely, when the disease occurs in the newborn, from hem- 36 
THE MANIFESTATION OF DISEASE IN ORGANS. 
orrhage from the cerebellum during birth, or from pressure of 
forceps. Finally, paralysis due to a peripheral lesion of the nerve 
may result from neuritis, and from primary hemorrhage into the 
nerve-sheath or into the 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 speak- 
ing. The cerebral or medullary lesions which produce unilateral 
facial paralysis usually consist in hemorrhage and tumor. 
The determination that facial paralysis is due to a peripheral 
neuritis, 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 paral- 
ysis of cerebral origin in 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 cerebral 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 peripheral lesions. The only other condition in which there can 
be developed the reaction of degeneration, and the lesion not be in 
the 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 
destroying 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 hemorrhage, embolism or thrombosis, such as result from 
impaired bloodvessels or a diseased heart, and when the paralysis 
comes on gradually (though it may be sudden from surrounding 
inflammation), the condition is probably due to cerebral tumor. 
This diagnosis is confirmed by the gradual spread of the paralysis 
to other parts, as the arm and then the leg on the same side of the THE FACE AND HEAD. 
37 
body, and by the development, often before each spread of the paral- 
ysis, of a convulsion. The facial paralysis residting 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 degenera- 
tion quickly develops in the paralyzed part; that the parts supplied 
by the frontal branch of the facial are often quite as much paralyzed 
as are those supplied by the lower branch, which is rare in the cere- 
bral lesion, and there will commonly 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 
the oculo-motor and abdncens, 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, abclucens, and optic nerves on both sides, all these symptoms 
become, of course, bilateral. 
Facial palsy associated with deafness may indicate cerebellar 
tumor, the 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 
facial paralysis resulting from pressure by the forceps, which have 
slipped and injured the facial nerve, or have caused an extrava- 
sation 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 unilateral or bilateral, generally the former. Its association 
with the symptoms of hysteria described in the chapter on the skin, 
and elsewhere, in this book will aid in making the diagnosis. 
There yet remain to be considered several forms of facial paral- 
ysis unilateral in character yet associated with paralysis else- 
where. 
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 38 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
Fig. 6. 
Diagram to show the general arrangement of the motor tract and the effect 
of lesions at various points. (Ormerod.) 
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. 6.) Thus it is seen in this figure, on the left side, third THE FACE AND HEAD. 
39 
inscription, 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 Arms and 
Hands.) 
7 • • • 1 
Sometimes the muscles supplied by the facial nerve escape paral- 
ysis, 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 pres- 
sure produced by growths or inflammatory processes at the base of 
the skull. It may also occur as the result of hemorrhage into the 
medulla, 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 
depends upon loss of function of the oculo-motor nerve or its centre 
or nuclei. (Fig. 7.) It is a symptom of the greatest importance, 
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 physi- 
cian’s mind the various causes which produce it. 
Fig. 7. 
Ptosis in a case of alternate hemiplegia of syphilitic origin. (Dercum.) 
Iii the first place, it sometimes occurs as a congenital 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 be entirely destroyed so far as its function 40 
THE MANIFESTATION OF DISEASE IN ORGANS. 
is concerned, there will be, in addition to ptosis, paralysis of all the 
external muscles of the eye except the superior oblique and exter- 
nal rectus, and 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 
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 to 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 eye- 
ball 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 branches supplying the external and internal 
ocular muscles escape. 
If there is a history of a cerebral attack resembling a mild apo- 
plexy, 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 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 pseudo-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, con- 
traction 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 Muller which exist'in 
the orbital fascia, for as these muscular fibres aid in holding open 
the lid their paralysis results in partial ptosis. Nothnagel asserts 
that such symptoms occur with lesions in the corpus striatum. 
A fifth cause of ptosis is reflex irritation usually through the fifth THE FACE AND HEAD. 
41 
nerve. This is probably due to an inhibition of the oculo-motor 
centre. It is usually only transient. 
Sixthly, it is not uncommon in cases of nervous syphilis 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 
recover. 
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 llie 
presence of hysterical sensory changes described in the chapter 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 con- 
traction of the orbicularis proves that there is no true paralysis of 
the levators. If the ptosis is bilateral and hysterical, the head is 
tipped back when the patient is told to look up. 
Single or double 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 is the 
first symptom complained of, and the patient may state that the 
diplopia comes and goes. 
Bilateral ptosis 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 gelsemium or conium. It is also seen 
in slight degree in feeble, overworked women, particularly in the 
early morning on awakening. 
Again, it is not very rare to see slight 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 quadrigemiua, and the reason for 
this will be clear when the deep origin of the oculo-motor nerves 
from their nuclei is remembered. (Fig. 8.) Sometimes there will 
be associated with the ptosis internal squint due to paralysis of the 
abducens nerve (sixth), which arises from the nearby nucleus, and 
is connected with that of the oculo-motor. (Fig. 9.) (See also chap- 
ter on the Eye.) 
If the condition is due to a serious congenital fault, we usually 42 
THE MANIFESTATION OF DISEASE IN ORGANS. 
find associated with it failure to elevate the eyeballs, and the failure 
is probably due to a nuclear defect. If due to gelsemium or conium, 
the other symptoms of poisoning by those drugs will be present. 
Fig. 8. 
Medulla oblongata with the corpora quadrigemina The numbers IV-XII indicate the super- 
ficial origin of the cranial nerves, while those (3-12) indicate their deep origin— i. e., the position 
of their central nuclei; 3 shows the deep origin of the oculo-motor nerve of one side. (Gray.) 
Ptosis, with hemiplegia of face and limbs on the opposite side 
of the body, associated it may be with hemiansesthesia, is due to a 
lesion in the crus cerebri, provided the two sets of paralyses occur 
simultaneously, 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 accom- 
modation, and crossed diplopia. It is seen most frequently in women, THE FACE AND HEAD. 
43 
but may date from as early a period of life as eleven months. The 
attacks may last for a few weeks, and occur often or only after a 
lapse of many years. As already stated, alternate ptosis sometimes 
develops in syphilitic persons. 
Fig. 9. 
Diagram of the connections of the nucleus of the sixth nerve. (Bkuce.) 
Bilateral Facial Paralysis is a rare condition, and when it occurs 
can only be due to a bilateral lesion in the cerebrum, to acute bulbar 
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 
braiu 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 
cerebral cortical lesion never occurs without evidences of paralysis 
elsewhere 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 44 
THE MANIFESTATION OF DISEASE IN ORGANS. 
of the lips, by dysphagia, lingual paralysis, affected speech, paralysis 
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 associ- 
ated 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 that 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 
paralysis (true bulbar paralysis). This condition has been called 
u 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 
defects 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 is a sign that the nuclei of the 
hypo-glossal and twelfth pair are involved. These symptoms are 
practically identical with those of true bulbar paralysis. What 
are the symptoms which by their presence in the true disease and 
their absence in asthenic bulbar paralysis aid us in separating the 
two affections? The answer to this question is that the drooling of 
saliva, the atrophy of the tongue, lips, and extremities, the fibrillary 
twitching 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 so-called asthenic form. 
There is, however, in the latter disease a condition rarely found in 
the degenerative form, namely, paralysis of the oculo-motor, the 
lower facial, and the inferior division of the fifth or trifacial nerve, 
causing dilated pupils, diplopia (which, however, is not accompanied 
by strabismus), and ptosis (from the oculo-motor failure), facial 
paralysis about the mouth (from facial nerve failure), and loss of THE FACE AND HEAD. 
45 
expression about the eyebrows and forehead (due to facial and tri- 
facial failure). Whether the diagnosis be true degenerative bulbar 
paralysis or the asthenic form just discussed, in both the prognosis 
is most unfavorable. Indeed, the asthenic form is often the more 
rapidly fatal of the two. In the latter the nuclei in the pons are 
probably always involved, but, as already stated, no pathological 
changes have been demonstrated in any of these nervous centres. 
A very rare affection is oculo-facial paralysis, which is congen- 
ital or develops in childhood, and is chronic. There are present 
paralysis of the ocular muscles and ptosis. 
Facial Spasm. Spasm of the facial muscles may result from 
functional and organic disease, and occurs far more frequently in 
women than in men. The cause of the functional forms we do not 
understand, as they occur in neuropathic persons and about the 
climacteric period. Rarely the spasm arises from reflex irritation 
through the trifacial, resulting from a decayed tooth or a cause in 
the eye or in the skin. Habit-spasm arises from a trick learned by 
a child, or is acquired in taking snuff or in sniffling. The organic 
causes are many. Thus, there may be an irritative lesion of the 
facial nerve-trunk or one in the cortical centre for the face, a tumor 
pressing on the nerve at its point of origin, or an aneurism of the 
vertebral artery. The spasm may be confined to one side or dis- 
tributed over both sides, and may be clonic or tonic in type. Some- 
times it only occurs on attempted movement, in other cases it is 
constant. The clonic form is the more common. Spasm of the 
face is seen in chorea, convulsive tic, blepharo-facial spasm, in 
tetanus, meningitis, and epilepsy. When due to chorea it nearly 
always is clonic or twitching, as it is also in convulsive tic and 
habit-spasm, but in tetanus, meningitis, and epilepsy it is generally 
rigid or tonic. In blepharo-facial spasm the contractions may be 
tonic or clonic. In chorea the spasm is most marked about the 
corner of the mouth and the eyebrow or eyelids. The movements 
of convulsive tic are exceedingly sudden, darting across the face 
and involving all the muscles supplied by the facial nerve. As a 
rule, this affection is unilateral. These spasmodic movements of 
convulsive tic may be almost constant or appear in paroxysms, 
and rarely the muscles of the jaw, the neck, and the tongue are 
affected. The disease depends upon a disorder of the facial nerve, 
or its centres, which is not understood. The prognosis is bad so 
far as cure is concerned. Spasm of the levator palpebrse superioris 46 
T1IE MANIFESTATION OF DISEASE IN ORGANS. 
muscle is sometimes seen as a symptom of exophthalmic goitre. It 
is called “Abadie’s sign.” 
In blepharo-facial spasm there are paroxysmal spastic contrac- 
tions of the orbicularis palpebrarum and other facial muscles. The 
spasm often tightly closes the lids. Generally in children there is 
also photophobia with the spasm of the eyelids, which is often tonic 
in character and generally bilateral. This condition has associated 
with it what have been called “ Graefe’s spots,”1 namely, the pres- 
ence of spots near the supraorbital foramen or over the vertebrae, 
which when pressed on cause sudden relaxation of the spasm. 
These should always be sought for, as they aid us in giving relief 
to the patient. 
Spasmodic movements about the eyes such as have just been de- 
scribed are sometimes paralleled by what is called nictitating or clonic 
spasm, which is probably due to some uudiscovered cause of reflex 
irritation. 
The development of facial spasmodic twitching accompanied by 
a sudden burst of explosive speech, repeating the last word heard or 
said by the patient in conversation (called echolalia), or the sudden 
bursting out with some blasphemous or filthy word (called copro- 
lalia), sometimes is seen in neurotic adult females or children, and 
is often associated with perversion of moral sense. It is called by 
Gilles de la Tourette “ Maladies des tic convulsifs,” but this is 
an unfortunate term, because it is apt to be confused with ordinary 
convulsive tic of children or adults. (See Electric Chorea and 
Myoclonus Multiplex in the chapter on the Hands and Arms.) 
In tetanus the muscles of the jaw, the masseters, and temporals 
are first involved in the tonic contractions, and these are followed 
by rigidity of the muscles of the neck and body. Often the risus 
sardonicus is marked from the first, and the face soon looks like 
that of a very old man owing to the muscular contractions. 
In meningitis the characteristic symptoms which label the malady 
render facial spasm a comparatively unimportant symptom, and in 
epilepsy the convulsive seizure soon makes easy the diagnosis of the 
cause of the facial spasm unless the epilepsy is limited in its char- 
acter, when the history of the presence of an aura, or of uncon- 
sciousness, or biting of the tongue may be discovered. 
1 This is not to be confused with the more common use of the term “ Graefe’s sign ” to indi- 
cate the condition in exophthalmic goitre, in which the lids fail to follow the eyeballs when 
the patient looks down. THE FACE AND HEAD. 
47 
Spasm or contractures of the muscles of the face sometimes follow 
facial paralysis as recovery begins, and the contractures involve the 
formerly paralyzed muscles, whereas in paralysis in the limbs the 
contractures generally take place in the muscles which are not 
paralyzed. Sometimes these contractures in the face are permanent, 
and are due to incomplete restoration of the functions of the mus- 
cles affected. Care should be taken to remember that not very 
uncommonly contractures in the muscles of the face result from 
hysteria, and that they are often on the side opposite the facial 
paralysis if the latter exists. 
Active spasm of the muscles of the face may follow exposure to 
cold, and it sometimes follows the paralysis due to this cause, or, 
in other words, is a sequence of Bell’s palsy. 
The Head and Neck. 
In examining the head we look for variations from the normal 
in its shape, its fontanelles, the position in which it is held, and its 
movements as governed by the cervical muscles. Of the last we 
shall speak first, although it has been mentioned under the head- 
ing of wry-neck. We find that the head is moved abnormally in 
nodding spasm, chorea, and in tetanus and strychnine-poisoning. It 
is also thrown backward and forward or from side to side in epilepsy, 
and in hysteria or in the convulsive seizures occurring in young chil- 
dren. 
Nodding spasm of the head, depending upon somewhat rhyth- 
mical contractions of the sterno-mastoid and trapezius muscles, is 
sometimes seen in half-fed or rickety children. It also occurs in 
hysterical women, and in men who are not hysterical. The nod- 
ding may be slow and infrequent, only coming on with excitement, 
or it may be practically constant. It always becomes worse when 
the patient is examined, and may be so rapid and forcible as to 
seem almost severe enough to shake the head off the shoulders. 
Often the muscles involved will be found very rigid. 
If the spasmodic movement be not rhythmical, as it usually 
is in nodding spasm, and yet it is more or less constant and 
irregular, the cause is probably chorea minor if it is present in a 
child, or it may belong to the irregular movements of adults classed 
under the various forms of tic or choreiform spasm. (See chapters 
on Hands and Arms and on Convulsions and Spasms.) 48 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Wry-neck consists in a drawing of the head to one side by the 
sterno-mastoid muscle in a state of spasm, and at the same time the 
head may be tilted to the back or front according to the accessory 
muscles which are involved in the spasm. 
Sometimes a tonic spasm of the sterno-mastoid muscle, produced 
by exposure to cold or due to a distinct nervous lesion, causes the 
head to be drawn down over the shoulder, or bilateral spasm of this 
muscle causes fixation of the head. If the cause be exposure, with 
resulting myositis, the history of exposure, combined with that of 
a sudden onset, will permit a correct diagnosis and a favorable prog- 
nosis, it being remembered, however, if the patient is a female, that 
hysterical spasm may be the cause. If hysteria is the cause, the 
history of the patient and the presence of alteration in her color- 
fields and the other signs of hysteria can probably be elicited (see 
chapters on the Eye and on the Skin.) On the other hand, if the 
contraction lias come on gradually, after some injury or in associa- 
tion with some nervous affection elsewhere, it is evident that a true 
nervous lesion underlies the disorder. 
If it is a tonic spasm, the involved muscle is on the side toward 
which the head is drawn, whereas the muscle on the opposite side 
is seen to be prominent owing to its being stretched by its opponent. 
The chin is, however, directed upward and away from the affected 
side. Rarely the trapezius is the only muscle involved, in which case 
the head is drawn backward and toward the diseased side, or, if the 
sterno-mastoid and trapezius muscles are both involved, the head is 
tilted laterally and backward until the patient looks up in the air. 
Pain in the muscles only occurs from fatigue. This tonic spasm 
affecting the head can be separated from that occurring in tetanus 
by the fact that in tetanus there is a general diffusion of the spasm 
to other muscles, although in that form of tetanus called “ head 
or cephalic tetanus” the diagnosis is more difficult. This form 
of tetanus usually has with it the following diagnostic points: there 
is a history of infection, the character of the onset is sudden, there 
are trismus, difficult swallowing, respiratory disturbance, and facial 
paralysis with rare involvement of the ocular muscles. The spasm 
in cephalic tetanus is also often increased by movement or the at- 
tempt to take food. Strychnine-poisoning is also to be thought of. 
Should the muscles be affected by a clonic spasm, the head is 
jerked about instead of remaining fixed. 
Retraction of the head in children is an indication in many cases THE FACE AND HEAD. 
49 
of serious brain disease, and commonly arises from a basal menin- 
gitis, probably as the result of an effusion into the ventricles. It 
is to be remembered that some of these cases recover, though such 
a result is rare. Again, we should not forget that caries of the 
cervical vertebrae may cause this position, or that tender and enlarged 
glands in the neck may so result. Sometimes, too, it occurs after 
falls without there being any indication of meningeal irritation. 
Rarely in neurotic babies retraction of the head, as a temporary 
symptom, accompanies attacks of indigestion. 
Similarly, in adults suffering from cerebro-spinal fever the head 
is often held in a retracted posture. 
The posture of the head may also aid us in diagnosis when no 
spasm of its governing muscles exists. Thus, chronic deafness in 
one ear may cause the patient to hold one side of his head further 
forward than the other, in order to catch the sounds he seeks, and 
advanced strabismus may cause a child to so carry its head as to 
improve its sight and avoid diplopia. 
On the other hand, persons suffering from great mental depression 
with a tendency to melancholia often sit for hours with the head 
bowed forward with the chin resting on the chest. 
The changes from the normal in the shape of the head are to a cer- 
tain extent considered in that part of this chapter dealing with the 
symmetry and appearance of the face, but there still remain to be 
discussed the changes in the shape of the head as a whole. These 
occur in acromegaly, osteitis deformans, and in hydrocephalus, 
microcephalus, rickets, idiocy, myxoedema, and cretinism. The 
changes in several of these states have already been described in 
the part of this chapter devoted to the Face. 
The head of hydrocephalus is greatly enlarged above the level of 
the ears, and this causes the face, already having a tendency to 
faulty development, to look small and wizened. The eyes seem 
somewhat bulging, the orbital plates are oblique, and the back of 
the head flattened. Sometimes the fontanelle remains pulsating in 
true hydrocephalus for a long period. Again, in the true hydro- 
cephalus choked disk is sometimes manifested quite early. (See 
Chvostek’s and Trousseau’s signs.) In microcephalus, on the other 
hand, the head is small and often narrow. Technically, the term 
microcephalus is applied to idiots whose heads are less than seven- 
teen inches in circumference. Nearly always the head of an idiot 50 
THE MANIFESTATION OF DISEASE IN ORGANS. 
is abnormally formed. The cretinoid head is large, heavy, and 
massive. 
When a young child has unusually prominent parietal and frontal 
bones, which seem bulging, and there is a general resemblance in 
Fig. 10. 
Acromegaly with goitre (not exophthalmic). (G. R. Murray.) 
the shape of the skull to that of hydrocephalus, we suspect the pres- 
ence of rickets. As a rule, the forehead is broad and high, the top 
of the head flat, and the shape of the head more round than in the 
genuine disease. Sometimes in such a child we find, in addition to THE FACE AND HEAD. 
51 
these changes from the normal, spots of thinned bone in the occipital 
and parietal regions. These may be also somewhat softened, and this 
condition, called “ cranio-tabes,” is usually a sign of rickets which 
exists in association with infantile syphilis. Rickets is seen nearly 
twice as often in boys as in girls, and there is usually to be found 
deficient development of the bones everywhere, particularly in the 
ribs and legs. 
Fig. 11. 
Exophthalmic goitre. (Meltzer.) 
The condition of the fontanelles in young children is of impor- 
tance in diagnosis. In the healthy child all the fontanelles save 
the anterior fontanelle close during the early weeks of life, but the 
latter opening does not close entirely till the infant is about one 
year and a half old. During the first few months this fontanelle 
closes very slowly indeed, but after this time has elapsed its edges 
become rapidly approximated. The presence of other fontanelles 
in a child’s skull after it is several months old indicates rickets, 
syphilis, hydrocephalus, or some intracranial growth producing pres- 52 
THE MANIFESTATION OF DISEASE IN ORGANS. 
sure on the cranial bones, preventing their approximation. Gener- 
ally, however, these minor fontanelles are not found open, but 
closed, and the condition of the anterior fontanelle is the guide in 
diagnosis. In severe cases of rickets the anterior fontanelle remains 
open up till the third or fourth year, and should the rachitic ten- 
dency be developed early in life the edges of the fontanelle may not 
only fail to be approximated, but actually recede from one another. 
Sometimes if the edges of the fontanelle are found to be softer than 
usual the diagnosis of rickets can be so confirmed. If syphilis be 
the cause of the deficient bone development, evidences of this dis- 
ease in mucous patches about the mouth and anus may be found 
or a history of heredity adduced; while if the condition be hydro- 
cephalus the fontanelle will be markedly bulging. 
Fig. 12. 
Exophthalmic goitre in a male. The photograph does not clearly show the enlargement of 
the thyroid. (From a patient in the author’s wards.) 
If the skin over the fontanelle be found to be bulging tempora- 
rily to a slight extent, the cause probably lies in some acute disease 
with fever, producing cerebral congestion; whereas, if permanent, 
and the general dimensions of the skull are not increased, an intra- 
cranial growth may be the cause, or a cerebral hemorrhage, a puru- 
lent meningitis, or some cystic formation may be present, or THE FACE AND HEAD. 
53 
sometimes a thrombosis of a cerebral sinus produces hydrocephalus 
and bulging. This difference in the tension of skin over the fonta- 
nelle aids us in separating the meningeal symptoms of pneumonia 
from those of true meningitis, for in the true form the scalp is tense 
and in pneumonia it is often retracted. 
Marked sinking-in or collapse of the fontanelle always indicates a 
grave condition arising from some disease which seriously weakens 
the heart and general circulatory system, particularly marasmus and 
cholera infantum. Sometimes it appears as a result of thrombosis 
of the cerebral sinuses. Sometimes in rachitic babies auscultation 
of the fontanelle will reveal a murmur, haemic in origin. This is 
most frequently heard in this class of patients, but can occasionally 
be heard when no such disturbance of nutrition exists. 
Excessive sweating of the head, producing a wet pillow, is often 
an indication of rickets when it occurs in a child. 
A swelling in the neck in the median line, or on both sides of the 
median line, anteriorly, is probably due to goitre. (See Fig. 10.) 
If it is associated with cardiac palpitation and distress, exophthal- 
mos, tremor, nervousness, and depression of spirits, it is called ex- 
ophthalmic goitre. (See Figs. 11 and 12.) If these symptoms are 
absent, the condition is simply one of overgrowth of the thyroid 
gland. (For the movements of the head in epilepsy and hysteria, 
see the chapter on Convulsions.) CHAPTER II. 
THE HANDS AND ARMS. 
The general appearance of the hands and arms—The shape of the hands in dis- 
ease—Spasms of the fingers—Ti'emors of the hands—Paralysis of the hands 
and arms. 
The appearance of the hand and arm often gives us valuable 
hints in the diagnosis of disease, chiefly by reason of variation in 
their shape, manner of movement, and general consistency; but as 
all these conditions vary widely in normal individuals, we can only 
regard distinct and well-marked alterations from the normal type 
as indicative of a definite disease. We can, however, often gather 
general information as to the patient from the hands, particularly 
as to his occupation; thus we see the smooth, soft hand of the pro- 
fessional man or clerk, the horny hand of the laborer, the blackened 
nails and skin of the machinist, or the blue-back dottings of the 
hand of the miner; and Hirt asserts that atrophy of the antithenar 
eminence often ensues in cabinet-makers, perhaps from the exces- 
sive use of the plane. Even when no pathological condition exists 
we are wont to regard the heavy and somewhat thick and clumsy 
hand as an evidence of a phlegmatic temperament, and the thin, 
wiry, dexterous hand as indicative of the nervous temperament. 
Similarly, we recognize as the hand of the strumous that one in 
which the fingers are slender between the joints and the joints 
themselves thick and clumsy, or, again, in persons with tubercular 
tendencies, we see a slender, delicate hand, easily compressed and 
somewhat effeminate in type. A ery commonly, too, in children 
who have developed heart disease in early life the hand becomes 
square-looking, and the fingers are club-shaped through thickening 
at the tips. A similar clubbing also manifests itself in many cases 
of emphysema and chronic phthisis in adults. 
From the appearance of the nails we can often gain important 
information; thus, whenever the color of the blood in the capilla- 
ries under the nails is dusky we know that a deficient pulmonary 
function exists or that the circulation is impaired, it may be from 
feebleness or from cold. In anaemia the nails are often very pale, THE HANDS AND ARMS. 
55 
and Stephen Mackenzie has asserted that if pressure on the tip of 
the finger completely empties the capillaries under the nails so that 
the appearance is pale the red corpuscles are present in only half 
the usual number. 
White spots in the nail may be due to injury of the matrix by 
picking at the base of the nail, or be due to acute fevers producing 
trophic changes. 
When the nails are striated and in longitudinal ridges the patient 
is often of the gouty diathesis, while transverse ridges may indicate 
arrest of nail-growth through local injury to the matrix or the 
impairment of the general nutrition as the result of some severe 
systemic shock, such as a severe surgical operation or prolonged 
illness. Sometimes these marks result from a severe attack of gout, 
and Fothergill tells us that it took about seven months for such 
a mark to grow out of his nails. Ordinarily, this mark will be 
found about half-way up the nail three months after the attack. 
In hemiplegia or acute infantile palsy the growth of the nail of the 
paralyzed part is generally arrested, as can be determined by stain- 
ing it and watching it from day to day to see if the stained part 
gradually moves away from the base. When the nails are distorted 
and thickened the cause may be local injury or peripheral neuritis, 
or any condition of the nervous system resulting in decided trophic 
influences, as in that rare condition syringomyelia. 
Hypertrophy of the nails so that they are abnormally elongated 
is usually associated with thickening and the development of great 
fragility. The nail may even be spirally twisted (onychogyropho- 
sis), or, if very wide, may cut into the skin and produce paronychia. 
These conditions may result from skin lesions, such as eczema, or 
lichen ruber, at or near the matrix, or be due to syphilis, and Vogi 
asserts that mere thickening may arise from severe fevers. They 
may also be seen in cases of Raynaud’s disease, or in sclerodactyle, 
and in cases of pulmonary osteo-arthropathy. 
Atrophy of the nails may apparently arise from identical causes 
with those which produce hypertrophy, and Kaposi has seen the 
nails soft and membrane-like, with abscesses under them, from 
psoriasis of the fingers. 
A diagnostic indication given us by the fingers is seen in dactyl- 
itis due to syphilis (Fig. 13). Similar deformity, often multiple, 
also occurs in scrofulosis or tuberculosis. In other cases this is 
replaced by an eruption on the skin of the hand characteristic of 56 
THE MANIFESTATION OF DISEASE IN ORGANS. 
syphilis. Another indication is seen in the ulcers at the bases of 
the finger-nails, with ecchymotic spots on the skin, produced by the 
Fig. 13. 
Dactylitis syphilitica in the infant. (Taylor.) 
chloral-habit; and still another is the sores seen at the bases of the 
finger-nails in persons who handle irritating drugs, such as elate- 
rium. (See chapter on the Skin.) 
Congested veins on the hand may indicate obstruction to the 
venous circulation of the arm, or general lack of vascular tone and 
a feeble heart. 
When the hand is cold and clammy the condition may be due 
to bromidrosis, or a local disturbance in innervation of the sweat- 
glands. It is often seen in cases of so-called spinal irritation and 
nervous exhaustion. Excessive sweating of the hand is also often 
seen in cases of progressive muscular atrophy. 
There are two sets of movements associated with the muscles of 
the wrist and hand which possess grave prognostic and diagnostic 
importance. The first of these is twitching of the muscles of the 
forearm (subsultus teudinum). It indicates severe, exhausting dis- 
ease. The second is picking at the bedclothes. The description 
of the grave import of this dangerous symptom, “ picking at the 
bedclothes,” or carphologia, is given by Shakespeare in his descrip- 
tion of the death of Falstaff : “After I saw him fumble with the 
sheets, and play with flowers, and smile upon his fingers’ ends, I 
knew that there was but one way; for his nose was as sharp as a 
pen.” And again, Hippocrates has well emphasized the gravity of 
this symptom, for he says : “In acute fevers, in peripneumonias, THE HANDS AND ARMS. 
57 
iu pleuritis, and in headaches, the hands are moved to and fro about 
the face, seeking in the void, as if gathering bits of straw, picking 
at the coverings, or detaching objects from the walls of the room, 
constituting so many signs of a fatal termination.” 
Fig. 14. 
A Rontgen ray picture showing the condition of the hand in a case of chronic gout. It is 
seen that the tophi are comparatively transparent to the radiations. The changes to he seen 
in the hones are atrophy-erosion and dislocation ; the thumb has been completely dislocated, 
the phalanges being altogether displaced ; there has been anchylosis of the proximal phalanx 
of the first linger with its metacarpal, and a large erosion is shown on the ulnar side. Smaller 
erosions are shown on the metacarpal of the fifth finger at its bone, and also in the phalanges 
of the same finger. (From the Medical Chronicle for April, 1896.) 
The fingers are often distorted and twisted out of their normal 
position from the trophic changes which take place in gout and 
arthritis deformans (rheumatoid arthritis). In gout the deformity 
invades the small joints in particular, and in many instances appears 
most marked in the forefinger. Fixation and deformity of the 
fingers occur through the deposit of urate of sodium in large 
amounts about the joints in their tendons and sheaths, so that the 58 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Fig. 15. 
Radiograph of a case of gout in which the gouty deposits affected all the joints ot both 
hands, greatly deforming them. The outline of the hand shows the deformity, but in this 
case it is interesting to note that the gouty deposits do not prevent the passage of the rays. 
Marked gouty nodules were present in this case, from which chalky material was readily 
obtained. THE HANDS AND ARMS. 
59 
fingers are as in splints. The knobs of urate of sodium appear as 
hard, white masses, and, if very superficial, as glistening masses, 
the surfaces of which often break down and allow the escape of 
material looking like wet, powdered chalk. The joint-surfaces 
themselves are not primarily much altered, but secondarily grave 
changes occur in them. (Figs. 14, 15, and 16.) 
Fig. 16. 
Same patient’s hands as in Fig. 14, 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 
involved are the first joints of the fingers, a knob developing on 
either side of the knuckle. (Fig. 17.) The little finger in gout is 
often bent at an acute angle at the middle knuckle, so that it is held 
in an awkward hooked position. (Fig. 18.) This is most com- 
monly seen 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 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 extraneous cause. 
(Fig. 19.) 
Distortion of the hand with drawing of the finger or fingers into 
the palm may be due to Dupuytren’s contraction, which results 
from burns or other injury to the palmar fascia. 
While the history of the patient, the localization of the mani- 
festations of the disease, and its character render a differential diag- 
nosis between the 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 maybe far more 60 
THE manifestation of disease in organs. 
Fig. 17. 
Nodular swellings (Heberden’s nodes) due 
to gouty arthritis on the forefinger and little 
finger of a woman aged fifty years. (Duck- 
worth.) 
Heberden’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.) 
Fig. 18. 
Tophaceous gout of 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.) THE HANDS AND ARMS. 
61 
marked than in gout, for here there is not a splint-like deposit about 
the joint, but in its stead the development of exostoses on the edges 
of the articular surfaces, which at once lock and disjoint the fingers, 
while at the same time the opposite side of the joint may be par- 
tially absorbed, so that dislocation is readily produced. (Fig. 20.) 
As a result there is sometimes developed what is called the “ seal-fin 
hand” (also seen in cases of gout), a hand in which the digits are 
deflected chiefly 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. 19.) 
Fig. 19. 
Tophaceous gout of hands, illustrating deflection and torsion ot digits and phalanges. 
The figure to the left shows the “ seal-fin ” type. (Duckworth.) 
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 ever, occurs in the hands alone, but when it does the joints 
are often swollen and somewhat tender, but never hard as in gout. 
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 62 
THE MANIFESTATION OF DISEASE IN ORGANS. 
seen under these circumstances as a clumsy, swollen mass, puffy, and 
exquisitely tender and hot. Sometimes it is quite red at the joints, 
but otherwise quite pallid, particularly in the puffy, oedematous area 
on the back of the hand. The presence of intense local inflamma- 
tion, the history 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 deep-seated 
Fig. 20. 
A Rontgen ray picture showing the condition or the bones of the hand in a case of chronic 
rheumatoid arthritis. It will be seen that the 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 fingers with the os magnum and unciform deposits in the heads of the phalanges and 
dislocations. (From the Medical Chronicle, April, 1896.) 
inflammation of the hand proper. The first is excluded by the 
history, the second by the history and general lack of evidence of 
gonorrhoea or sepsis or purpura, and the third by the lack of accom- 
panying general systemic disturbance and the absence of a history 
of traumatism or infection. In this connection it should not be 
forgotten that synovitis of the joints of the hands, wrists, and elbows THE HANES AND ARMS. 
63 
sometimes occurs during the fall of temperature in scarlet fever and 
is often not associated with any rise of temperature as a result of its 
development. The condition is sudden in onset and usually rapid 
in its course. The same state may exist in the joints of the lower 
limbs, but Marsden found it in the hands and wrists in seventy-two 
out of one hundred cases and twenty-five times out of a hundred in 
the larger joints. The condition usually appears, however, in 
rheumatic children and those with a rheumatic heredity, and is 
generally relieved by salicylates, so it is not a pure septic arthritis. 
The nervous disturbances which change the appearance of the 
hands are very numerous. 
Angioneurotic oedema is not peculiar to the hand, although fre- 
quently involving this part of the body. It consists of a swelling 
varying in size from a dime to a silver 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 “ Raynaud’s disease.” Often this is a passing condi- 
tion, 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 thick- 
ened 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 other 
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 phalanges undergo necrosis, and en 
largement 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. 64 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Swelling of the hand, followed in some months by rupture of the 
skin, may, in a person from the tropics, mean mycetoma, which is,how- 
ever, seen more commonly in the lower extremity as “Madura foot/’ 
In addition to these trophic changes in the hand we have the 
so-called “spade-like” hand seen in myxcedema, acromegaly, and 
the pulmonary osteo-arthropathy of Marie. In myxcedema the 
deformity 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 cBdema. 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 
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 finger. This is even more marked in the thumb. 
The differentiation of pulmonary osteo-arthropathy from acro- 
megaly is to be found in the fact that in the first-named disease there 
are no changes in the face, the skin, lips or orbital ridges. Neither 
is there spinal kyphosis in the cervical region, although it may be 
present lower down. Again, in pulmonary osteo-arthropathy the 
long bones of the upper extremities are greatly enlarged in their 
epiphyses, while in acromegaly they are not so enlarged. 
Alterations in the contour of the hand are, however, far more 
frequently produced by atrophic processes than by those which result 
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 conditions 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 THE HANDS AND ARMS. 
65 
muscles, the remaining portion of the hand having its normal 
appearance or being only indirectly influenced. 
Fig. 21. 
Under the name of claw-hand,” or u main-en-grijfe,” we find 
a deformity of the hand which is in itself very characteristic, 
although indicative of several causes which all operate in an iden- 
tical manner. The back of the hand loses its normal convexity 
and becomes somewhat 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 drawn 
toward the palm of the hand (Fig. 21). Sometimes, however, the 
tips of* the fingers are drawn toward the back of the hand. This 
deformity results from atrophy and paralysis of the interossei 
muscles and lumbricales, which are supplied by the median and 
ulnar nerves. The extensor communis digitorum and flexor digi- 
torum 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 the cerebral cortex in the hand-area. 
Taking up for consideration paralysis of the median and ulnar 
nerves 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 
example, the artisan presses his elbow constantly on some hard sur- 
face. The deformity may be, therefore, either unilateral or bilateral 
Claw-hand. (Gray.) 66 
THE MANIFESTATION OF DISEASE IN ORGANS. 
(generally the former), and there will be evidences of local injury, 
or a history which will indicate that the lesion is peripheral. Fur- 
ther than this, there will nearly always be found, in ulnar and 
median injury, sensory as well as motor paralysis; and Hirt asserts 
the remarkable fact that the claw-hand may develop in cases in 
which sensory disturbances are the only evidence of median and 
ulnar difficulty; 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 affected in this condition and the 
extensors become paralyzed. 
There are several spinal causes of claw-hand, the most important 
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. 22.) 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-process being 
generally bilateral, but affecting the right hand and arm more than 
the left as a rule. As progressive muscular atrophy often makes its 
first manifestation in these muscles, the hand affords much diag- 
nostic information in suspected cases, and if the patient with this 
disease be watched as he unbottons his coat, it will be found that 
he does not use his thumb and first finger, but pushes the buttons 
or the edge of the buttonholes with the back of his fingers. (Figs. 
23, 24, and 25.) The additional symptoms are some pain or par- 
sesthesia in the affected parts prior to the wasting, and that the 
paralysis spreads, as its name indicates, from muscle to muscle. 
Thus, beginning in the ball of the thumb it passes to the interossei, 
and thence up the forearm and arm. Sometimes, however, the fore- 
arm muscles escape, and the shoulder muscles are attacked secon- 
darily. Very rarely are the shoulder muscles first affected. Soon 
after this the dorsal muscles fail and lordosis begins, or the head 
falls forward on the chest. Finally, the respiratory muscles are 
attacked. The irritability of the muscles is increased, so that they 
contract if tapped, and fibrillary tremors constantly affect them in 
many instances. No vasomotor changes take place in the affected 
part, but. finally, the reactions of degeneration develop. The dis- 
ease may last for many years. THE HANDS AND ARMS. 
67 
Sometimes in chronic poliomyelitis in the adult a deformity some- 
what like that of claw-hand may exist, but this is a very rare con- 
dition, comparatively speaking, and is separated with difficulty from 
Fig. 22. 
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. 23. 
Fig. 24. 
Progressive muscular atrophy. Ape-hand 
(Eichhorst.) 
Progressive muscular atrophy. Sunken-in 
interosseal spaces on the back of the hand. 
(Eichhorst.) 
the claw-hand of peripheral neuritis of a general and severe type. 
As the result of the acute poliomyelitis of infancy, we may also 68 
THE MANIFESTATION OF DISEASE IN ORGANS. 
have the hand distorted by contractures, such as forced extension 
in paralysis of the flexors, forced flexion in paralysis of the ex- 
tensors, and claw-hand in paralysis of the interossei, but in most 
cases of this disease the foot is the part involved in the disorder. 
In progressive muscular atrophy the atrophy often precedes the 
paralysis, whereas in poliomyelitis the paralysis precedes the atrophy, 
so that in the former the reaction of degeneration develops late, and 
in the latter develops early. A somewhat claw-shaped hand is also 
sometimes seen in that very rare condition called Morvan’s disease, 
but it has not the characteristic appearance of viain-en-grijfe, there 
being a slow symmetrical wasting of the muscles with a drawing of 
the fingers into flexion. There are also analgesia and painless whit- 
lows. It usually occurs in young or middle-aged males. Morvan’s 
disease of the fingers, as already stated, may arise from a syringo- 
myelia and neuritis, or neuritis alone. 
Fig. 25. 
Hand and forearm in chronic spinal muscular atrophy, showing especially wasting of thenar 
and hypothenar eminences. (Dercum.) 
Another spinal lesion producing great alterations in the appear- 
ance of the hand and arm, through wasting of the thenar and anti- 
thenar and interossei and the muscles of the arm, is amyotrophic 
lateral sclerosis. Here again the hand often shows the first mani- 
festations of the disease in the loss of power of which the patient 
complains. The early symptoms of amyotrophic lateral sclerosis 
may closely resemble those of progressive muscular atrophy in the 
loss of power in the thumb muscles, but in this disease the reflexes 
are markedly increased in the affected muscles, whereas in pro- 
gressive muscular atrophy they are lost, although fibrillary muscular 
twitchings may be caused by tapping. Again, the patient is usually 
manifesting some of the symptoms of lateral sclerosis when he comes THE HANDS AND ARMS. 
69 
before the physician, such as weariness, stiffness, and loss of power 
in the legs. (See chapter on Legs, Paraplegia.) There are also 
exaggerated knee-jerks and ankle-clonus, and wrist-jerk is marked. 
Wasting of the muscles of the hand, causing distortion, may also 
be due to syringomyelia, but generally there will be with this loss 
of power and disturbance of sensation, such as anaesthesia. Often 
in syringomyelia there will be developed an arthropathy of the arms 
such as is seen in the legs in tabes. 
Wasting of the hand, with flexion and rigidity and sometimes 
contractures, is seen rarely in advanced paralysis agitans in place of 
the characteristic tremor. 
In the “ cerebral palsy of children,” sometimes called “ spastic 
infantile hemiplegia,” the hand may be flexed on the forearm, and 
the forearm on the arm, the thumb 
drawn into the palm of the hand 
and the fingers flexed as in Fig. 26. 
These deformities are not necessarily 
confined to one arm alone, but are 
sometimes bilateral. A peculiarity 
of these cases is that the muscles 
waste very slightly, and do not de- 
velop the reactions of degeneration, 
so that the case separates itself from 
poliomyelitis. The fingers in the 
cerebral palsy of children can often 
be placed in curious positions with 
ease, and, if the limb be suddenly 
flexed, a lock-like sensation will be 
imparted to the physician’s hand. 
Convulsive seizures of an epilepti- 
form type are very frequent in cases 
of cerebral palsy in children. Cohn 
asserts that there are on record eight 
cases in which intention-tremor has 
taken the place of the spastic rigidity just described, and he reports 
a ninth. Similar lesions may follow infantile cerebral hemorrhage, 
thrombosis, or embolism. 
Again, in persons who have had apoplexy it is not uncommon as 
time goes on for the temporary spasm seen in the muscles of the 
hand and arm to be replaced by permanent contractions resulting 
Fig. 26. 
Right hemiplegia, with contractures 
and retarded growth of arm Onset of 
disease at eight years of age, following 
typho-malarial fever. (Sachs.) 70 
THE MANIFESTATION OF DISEASE IN ORGANS. 
in deformity. These contractions, if they occur early, are an evi- 
dence of irritation of the pyramidal tract or the fibres just behind 
the knee of the internal capsule, and are of serious import, as they 
indicate the extension of marked inflammatory processes. When 
they come on later they show that a degenerative process is de- 
scending the pyramidal tracts. Wasting finally comes on. (For 
further discussion of the significance of paralysis in the arm and 
hand, see succeeding pages and chapter on Hemiplegia.) 
A very important point always to be remembered in examining 
contractures of the hand and arm, or of the lower limbs, is the fact 
that they often are due to hysteria, in which case the history is that 
they set in suddenly, and they are generally accompanied by other 
hysterical manifestations, which can be discovered if sought for. 
As a rule, the muscles do not waste or develop degenerative reac- 
tions, but rarely such wasting may occur. (Figs. 27 and 28.) Care 
Fig. 27. 
Fig. 28. 
Hysterical atrophy of the hand with flexion oi 
the last two phalanges into the palm, particu- 
larly the last phalanges of the index and middle 
fingers. (Gilles de la Tourette.) 
Same hand in another view. 
must be taken in giving a prognosis for cases of hysterical contrac- 
ture, since organic lesions sometimes supervene. Charcot states 
that if the contractures persist when the patient is under anaesthesia, 
and the muscles are atrophied, organic disease exists. It is impor- 
tant to remember this, for these contractions may be practically 
permanent when once induced, and as injuries may produce a true 
organic or a false hysterical contracture, much medico-legal interest 
centres about this differential diagnosis. Closely allied to these 
cases are those of hysterical contracture, in which after grasping 
an object the patient cannot let go until the muscles are stroked. 
Putting an Esmarch bandage on such a forearm will usually pro- 
duce the spasm. 
When in the course of an acute illness in a child the fingers are THE HANDS AND ARMS. 
71 
drawn down into the palm of the hand, with the tips touching the 
palm and the thumb turned in beneath them with its tip pressing 
the palm, the patient may have meningeal congestion or inflamma- 
tion, or hydrocephalus, and a general convulsion may be imminent. 
When the fingers are bent toward the palm, but the tips extended 
and the thumb turned in (“ the accoucheur’s hand”), the position 
is typical of tetany, but in this condition the rest of the body will 
give evidence of involvement. The nervous irritability in this 
condition is greatly increased, and pressure on a large bloodvessel 
or nerve-trunk will often produce the spasm. Curiously enough, 
gastric dilatation or thyroid wasting will often be found with tetany. 
In other cases it appears to be due to profound debility, as after 
prolonged nursing. (See Tetany in chapter on Convulsions and 
General Spasms.) Care must be taken to separate the so-called 
carpopedal spasm of rickety, hydrocephaloid children from true 
tetany, in which the body is usually involved, and from spastic 
paralysis due to infantile cerebral palsy. 
Spastic rigidity of the arms is often one of the earliest signs of 
chronic hydrocephalus, even before the skull begins to enlarge, and 
convulsions may be present from time to time. In congenital 
spastic rigidity due to sclerosis or defective development of the 
cortex cerebri the spastic condition is usually confined to the legs. 
(See chapter on Legs and Feet.) 
Spasm of the fingers of a rigid type on attempting to make cer- 
tain movements is also seen as the result of excessive use of the 
part involved, and occurs in seamstresses, cigarette-rollers, cigar- 
rollers, typewriters (rarely), telegraphers, milkers (rarely), persons 
who use a pen to excess, and in piano, flute, clarionet, and violin 
players, or in persons engaged in any occupation requiring constant 
and comparatively minute and well co-ordinated effort. It seems 
to be more common in men than women by a large proportion (39 
to 4). 
Sometimes paralysis, tremor, or vasomotor disturbances take the 
place of occupation-spasm. 
The spasm resulting from occupation must be separated from that 
sometimes seen in the hand in post-hemiplegic chorea, progressive 
muscular atrophy, the various forms of toxic peripheral neuritis, 
and that due to irritative cerebral foci, such as tumors of the brain. 
The history nearly always clears up the diagnosis. Spasm of the 
muscles of the hand and arm, rhythmical or otherwise, may also 72 
THE MANIFESTATION OF DISEASE IN ORGANS. 
be due to hysteria, and may resemble, when due to this cause, true 
tetany (not tetanus). 
Choreic movements are seen chiefly in children as a manifestation 
of chorea minor. They are usually seen in rheumatic and neurotic 
children, and heart-murmurs are generally to be heard in these cases. 
The first evidence of spasm may be developed in the hand, and be 
limited to that member in rare cases, and the hand often drops things 
that are placed in it. The hand itself is rarely involved alone, and 
the muscles of the arm toss the entire arm and hand from spot to spot 
with a fidgety, jerking movement which is very characteristic. A 
form of chorea minor, usually limited to the arm, is called paralytic 
chorea. It comes on suddenly, and is characterized by loss of power 
with a few feeble twitches. It affects only children. 
Sometimes choreic movements come on in the latter half of life, 
often preceded bv emotional disturbances. These movements are 
not true chorea. They are often called senile chorea. 
In some cases of adult chorea the patient tends to become maniacal, 
particularly toward night. Such cases usually occur in women, and 
the prognosis as to life is bad. There is often in these cases great 
mental heaviness. 
Several other affections which somewhat resemble true chorea are 
sometimes met with, but all of them lack, with one exception, the 
peculiarity of its movements. One of these is what has been called 
habit-chorea, or, more correctly, habit-spasm, in which condition 
the patient acquires a nervous trick of jerking a muscle or a set of 
muscles. Unlike true chorea, it is more frequently seen in adults 
than children. Its limitation, as a rule, to a single set of muscles 
and the history of the case usually separate it from chorea minor, 
and the muscular movements consist in sudden twitchings rather 
than jerking, irregular muscular movements. 
In paramyoclonus multiplex the disease, as the name implies, 
usually involves symmetrical parts, the contractions of the muscles 
appear in paroxysms, and the muscles involved are usually the 
biceps, deltoid, and triceps in the arms, and the quadriceps femoris 
and calf muscles of the lower limbs. Myoclonus multiplex is a 
disease of adult life, and chorea is usually seen in childhood. Some- 
times the muscles in myoclonus are exceedingly irritable. 
Under the name of electric chorea, or “ Dubinins disease,” Dubini 
described a disease, affecting both sexes and all ages, in which sudden 
shock-like contractions of the muscles take place, as if they were THE HANDS AND ARMS. 
73 
being stimulated by a slowing interrupted faradic current. The 
disease usually begins in the upper extremities and gradually in- 
volves the rest of the body, and progressively passes to a fatal issue. 
This is a very rare disease, and the sudden contraction of the muscles 
in tonic spasm separates it from chorea. 
Still another form of electric chorea is that of Bergeron, which is 
probably identical with what has been called hysterical chorea. 
Here, again, the shock-like muscular contractions are manifested 
chiefly about the shoulders. The patient is usually a female, and 
has the stigmata, sensory and otherwise, of hysteria. (See chapters 
on Skin, Eye, and Feet and Legs.) 
Again, the physician may meet, exceedingly rarely (almost never, 
in the United States or England), with a condition called convulsive 
tic or palmus, which has also been called “ the jumpers,” in which 
the movements are not in the slightest like true chorea, but are 
sudden muscular movements, usually imitative of the act of some 
other person or animal. This is often associated with echolalia— 
that is, repeated or echoed speech—or coprolalia or filthy speech. 
Finally, another very rare disease is that known as Huntington’s 
or hereditary chorea, a condition in which the twitching usually 
begins in the face and extends to the arms and legs. This ailment 
is hereditary, rarely begins before thirty years of age, is accompanied 
by progressive mental deteriorations, a tendency to melancholia, and 
may last ten or twenty years. 
Mercurial poisoning producing tremor may cause so coarse a 
movement in advanced cases that the case may be thought choreic. 
(For a description of tremors, see latter part of this chapter.) 
In “Thomsen’s disease” the hand is placed in tonic spasm as 
soon as voluntary movement is attempted. Closely resembling 
Thomsen’s disease, or myotonia congenita, is what is called para- 
myotonia, which exists in three forms : first, a patient suffering 
from paralysis agitans on attempting to move is seized with rigidity 
of the muscles, which holds him fixed; second, a patient is suffering 
from ataxia and muscular weakness, and is seized with an attack of 
muscular rigidity; and, third, a patient may have the muscular 
fixation occurring just as it does in Thomsen’s disease, save that it 
is produced by cold or exposure, and not by intention-movement, 
and may last for hours. This is called paramyotonia congenita. 
(See also Athetosis.) 
The position of the hand may be very various. Thus the hand 74 
THE MANIFESTATION OF DISEASE IN ORGANS. 
may drop edgewise from the radius toward the ulna from paralysis 
of the extensors on the radial side of the forearm resulting from 
neuritis or acute infantile poliomyelitis, while marked drop-wrist 
may occur from paralysis of the extensors in chronic lead-poisoning, 
or in any form of neuritis, toxic or otherwise, involving the nerve- 
supply of these muscles (musculo-spiral nerve). (Fig. 29.) Wrist- 
drop may also be’developed by pressure upon the musculo-spiral 
Fig. 29. 
Boy with multiple neuritis, with double wrist-drop and slight foot-drop. (Sachs.) 
nerve, as in crutch-palsy. If the wrist-drop is bilateral, it may be 
due to toxic neuritis; but if unilateral, it is probably but not posi- 
tively due to pressure-paralysis from sleeping with the head resting 
on that arm, or from pressure by a crutch, or some similar pressure 
capable of injuring _the nerve. Very rarely unilateral wrist-drop 
is seen in lead-poisoning. When lead is the cause the supinator 
longus usually escapes, as does also the short extensor of the thumb, 
so that the forearm can be'flexed and the thumb extended. Pain THE HANDS AND ARMS. 
75 
is rarely present in pressure or lead wrist-drop, but is present in 
wrist-drop due to alcoholic and other forms of toxic neuritis. 
Often, too, in these cases the flexors are considerably involved (see 
part of this chapter on Brachial Monoplegia). 
Tremors of the Hand and Arm. The movements of the hand 
should always be carefully watched in cases of suspected nervous 
disease. The most common alteration will be found to be tremor, 
which may indicate paralysis agitans, general paresis, chronic mer- 
curial, plumbic, or alcoholic poisoning, hysteria, senility, Graves’s 
disease, and disseminated sclerosis. Sometimes a tremor may be 
found in naturally nervous women who are drinkers of tea to excess. 
In paralysis agitans the whole hand is involved, and generally 
both hands are equally affected. The tremor is rhythmical and 
fine or minute in character at first, but later may be quite coarse. 
It is a slow tremor of about five vibrations per second, which is 
more or less constant, and worse when attention is called to it, but 
it is not greatly increased, and, perhaps, is even decreased, by a 
voluntary act, such as an attempt to raise a glass of water. Very 
rarely, however, the reverse holds true, and the tremor is increased 
by voluntary effort. The fingers are generally semi-extended and 
the thumb is adducted, so that it constantly rubs the index finger 
with its pulp, as if it were attempting to rub off the skin of that 
member. Frequently there are pain and aching of the extensor 
muscles of the forearm and wrist from the constant exertion. (See 
chapter on Feet and Legs, part on Gait.) 
The tremors of disseminated sclerosis are also slow, but coarse in 
character. They are not constant, but are developed upon inten- 
tional movement, and have a greater amplitude than those of Park- 
inson’s disease (paralysis agitans). Often threading a needle will 
be possible for a person with this disease, because it is a short act, 
while lifting a glass of water will be impossible. The other symp- 
toms of disseminated sclerosis beside intention-tremor are staccato 
or scanning speech, exaggerated knee-jerks, ankle-clonus, jaw-jerk, 
and wrist-jerk, disordered speech, nystagmus, muscular weakness, 
with rigidity and paralysis of groups of muscles, causing mono- 
plegia, paraplegia, or paralysis of the cranial muscles. 
The tremor of mercurial, plumbic, and alcoholic poisoning re- 
sembles that of paralysis agitans, save that it is more rapid, reaching 
nine or ten vibrations per second, and in the case of alcoholic tremor 
is decreased by a large drink of liquor, while those due to lead and 76 
THE MANIFESTATION OF DISEASE IN ORGANS. 
mercury may be rapidly relieved by potassium iodide. Further 
than this, the tremor of alcoholism is generally worse in the morning. 
A point of some importance in plumbic neuritis producing tremor 
and wrist-drop is the fact that painful sensations are rarely present; 
in arsenical neuritis, on the other hand, they are often the most 
prominent symptom, even preceding the motor disturbance. In 
mercurial neuritis, on the other hand, tremor precedes all evidence 
of loss of power, and, finally, may become so coarse as to resemble 
chorea. The tremor of general paresis is also rapid, eight or nine 
per second, and is a very fine tremor, which may be felt only when 
the arm is extended and the finger rested on the hand of the physi- 
cian. In other words, the tremor of the hand in general paresis is 
generally not a predominant symptom, but is elicited when the 
muscles are put upon a strain. In regard to the fineness of the 
tremor of general paresis, it should be remembered that it closely 
resembles that of Basedow’s or Graves’s disease (exophthalmic 
goitre) (eight or nine per second), since the tremor of this condition 
is not only equally fine, but generally unseen except when the arm 
is extended and tips of the fingers rested upon the fingers of the 
doctor. This tremor has been called the “ railroad bridge tremor,” 
because of its fineness and vibratory character. The individual 
fingers do not separately tremble in Graves’s disease. 
In post-hemiplegic tremor the trouble is unilateral, there is a 
history of cerebral injury, and paralysis is present. 
Tremor of a very marked character may be due to hysteria, and 
arises most frequently in those who have been exposed to shocks or 
accidents. The tremors may occur constantly or only with inten- 
tion-movements, or be increased in amplitude but not in rhythm on 
movement. The latter form is known as the “type Rendu,” and 
has a rhythm of seven to nine per second, while the slower hysteri- 
cal tremor may be four or five per second. 
Beyond the state of tremor should be recalled the movements of 
chorea, which may be limited to one arm or hand, and which in 
their milder forms may be confused with the pronounced movements 
produced by effort in disseminated sclerosis. The latter are often 
very arhythmical, and so the choreic movement the more closely 
resembles them ; but those of sclerosis are purposive, while those 
of chorea are not, since the movement contemplated in chorea is 
opposed by a contradictory contraction. 
Movements of the Hand and Arm. Aside from the movements THE HANDS AND ARMS. 
77 
of tremor, careful notes should be made of the movements of the 
hand as a whole, and of the co-ordination of its lingers and of the 
arm governing it. Thus, trembling contractions of the extensor 
tendons (subsultus tendinum) are a sign of grave and advanced forms 
of typhoid fever, and picking at the bedclothes (carphologia) is of 
still graver import (see beginning of this chapter). Inability to 
write, to play musical instruments requiring the use of the lingers, 
or to sew, may indicate the rare form of locomotor ataxia involving 
the upper extremities, so that if the patient is asked to close his 
eyes and feed himself the fork or spoon misses his mouth through 
lack of co-ordination, although loss of power may not be present. 
Sometimes in locomotor ataxia as the disease becomes advanced 
paroxysmal twitching of the lingers may come on, or involuntary 
movements of the lingers occur in association with voluntary move- 
ments elsewhere. 
In locomotor and Friedreich’s ataxia also the movements of the 
hand are often lacking in co-ordination. The hand may be ad- 
vanced past the object which the patient desires to grasp, or else 
falls short of it. On endeavoring to pick up an object the lingers 
are spread over it like a widespread claw. Generally these ataxic 
symptoms will be more marked in the other parts of the body and 
be bilateral, but Ormerod has reported an instance in which only 
one hand (the left) was involved. This faulty movement of the 
hand may, however, be due to the fact that the ocular muscles are 
affected, and the “erroneous projection” due to this cause leads 
the patient to pass the hand beyond the object reached for. 
When fibrillary twitchings of the muscles are present and tapping 
the muscles produces idiopathic muscular contraction progressive 
muscular atrophy may be present. 
Sometimes, as the result of infantile cerebral paralysis or from 
lesions developing in later life, the muscles of the hand are affected 
by a slow, constant movement, so that the fingers assume curious 
constrained and unusual postures, being moved into extreme or 
forced extension, flexion or pronation, or supination. (Fig. 30.) 
This condition is called athetosis, and is separable from chorea in 
that the movements are slower and limited to the fingers and wrists, 
the arm escaping. 
In this connection mention should be made of “ mirror-writing,” 
a curious condition in which the patient writes from right to left 
instead of left to right. It occurs in some cases of mental feeble- 78 
THE MANIFESTATION OF DISEASE IN ORGANS. 
ness, hereditary or acquired, and rarely in hysteria. u Mirror- 
writing ” may also be present in cases of cerebral paralysis. The 
Fig. 30. 
Examples of the position ot the fingers in the movements ot athetosis. (StrOmpell.) 
above example of this, taken from the case reported by Clapham, 
illustrates the character of the handwriting. The patient, a girl of THE HANDS AND ARMS. 
79 
twenty-four years, could write all three ways, but mirror-writing 
was easiest to her. (Fig. 31.) 
Very rarely athetoid movements of the hugers occur in advanced 
spinal tabes, probably as the result of a related lesion, and not from 
tabes itself. 
Fig. 31. 
Paralysis of One Arm, or Brachial Monoplegia. Absolute loss 
of power in one hand and arm without the necessary development of 
subsequent deformity results from cerebral or peripheral lesions, as a 
rule, being rarely spinal in origin, and is called brachial monoplegia. 
The causes of this loss of power when its origin is cerebral may be 
various. Thus, the lesion may be cortical or subcortical; that is, in 
the surface of the brain or in the internal capsule, or between the cor- 
tex and the capsule in the corona radiata. As a rule, however, mono- 80 
THE MANIFESTATION OF DISEASE IN ORGANS. 
plegia is cortical in origin, for below the cortex the motor fibres run 
so closely together that only a very small lesion can involve one with- 
out involving all, and so producing a hemiplegia. These cortical 
lesions when they do occur are generally, but not always, associated 
with a convulsive seizure in the paralyzed limb, and Seguin has called 
this convulsion the “ signal-symptom ” indicating a cortical lesion. 
Brachial monoplegia not due to hysteria or neuritis, preceded and 
accompanied by a convulsion and loss of consciousness, and lacking 
in signs of involvement of lower nervous centres, is, therefore, cor- 
tical, and is generally due to the formation of a clot in the hand 
and arm centre resulting from injury or from the ordinary vascular 
causes of apoplexy. In other cases it is due to cerebral embolism 
or thrombosis, or to the growth of some neoplasm, specific or other- 
wise, or to a localized meningitis. 
The probability of the lesion being an embolism or thrombosis is 
decreased by the recollection of the fact that the cortex is so well 
supplied by vessels from the pia mater that paralysis of a centre 
from lack of blood-supply from such a cause is rare, unless the 
lesion is subcortical, or, in other words, not deep enough to involve 
fibres from other centres as they approach each other, and vet suffi- 
ciently deep to prevent the tissues from partaking of the nutrient 
blood-supply from the pia mater as just mentioned. Aside from 
the discovery of a condition of the internal organs, such as cardiac 
valvular disease or sepsis, which might cause embolism, the diag- 
nosis between paralysis from hemorrhage and embolism is prac- 
tically impossible, and this is also true of the paralysis due to 
thrombosis, except that in cases of thrombosis we often find the 
presence of general endarteritis, and the paralysis of thrombosis 
may be slow and gradual in its onset. If the paralysis rapidly 
spreads, the lesion is probably due to a hemorrhage. 
The history of there having been some sudden cause for an in- 
crease in arterial tension, as by muscular effort, and the presence of 
atheromatous vessels aid us in deciding as to the probability of the 
lesion being due to a hemorrhage, and the sudden onset, coupled 
with the symptoms named, makes the diagnosis clear in a certain 
proportion of cases. 
• Neoplasms or tumors of the brain producing monoplegia are 
gradual in their development, accompanied generally by headache, 
by changes in the optic disks, and sometimes by mental disturbances 
or pressure-symptoms. A specific history pointing to the formation THE HANDS AND ARMS. 
81 
of a syphilitic tumor is of value in the diagnosis. (See chapter on 
Headache.) 
If brachial monoplegia results from a lesion in the internal cap- 
sule, the lesion must be very limited, or, in other words, only large 
enough to cut off the hand and arm fibres. Tumors and lesions 
from traumatisms in this area are very rare, and hemorrhages, which 
frequently cause paralysis by affecting this area, are generally pro- 
fuse enough to cause hemiplegia—that is, injury of the motor fibres 
supplying the leg muscles as well. Sometimes, however, sudden 
inflammatory processes are set up in the tissues surrounding a tumor 
which may precipitate sudden paralysis. 
Although the onset of a monoplegia due to cortical, subcortical, 
or capsular causes is sudden, the reactions of degeneration do not 
come on for a long period of time in such cases, because the muscles 
in the paralyzed area are still connected with the trophic centres in 
the cord, and this affords us a valuable point in differential diagnosis. 
Sometimes a suddenly developed monoplegia affecting the arm 
comes on as a manifestation of hysteria, and follows the type of 
true cerebral hemorrhage so closely as almost to defy diagnosis. 
This condition may be accompanied by hysterical oedema, the hand 
becoming puffy and swolleu. The presence of a neurotic tempera- 
ment and other hysterical signs, coupled with the prompt develop- 
ment of contractures, and the fact that the muscles do not rapidly 
waste, point to the cause of the loss of power in some cases, and this 
is emphasized if the presence of hysterical anaesthesia of the skin 
can be discovered. Further, if the hand is affected, Patrick asserts 
that in making an attempt to grasp an object the thumb and fore- 
finger are chiefly used; but if the object is placed suddenly in the 
ulnar part of the hand, the remaining fingers can grasp it easily. 
(See chapter on the Skin for additional hysterical symptoms.) 
In all cases of brachial monoplegia due to peripheral lesions we 
find that atrophy of the muscles comes on very rapidly from cutting 
off of the muscles from their trophic centres in the spinal cord. 
Brachial monoplegia is very often the result of injury to the 
brachial plexus or to some of its important branches. The symp- 
toms consist in heaviness or numbness of the arm with more or less 
loss of power. The motions of the arm which are particularly 
affected are usually abduction and elevation, which movements 
depend upon the circumflex nerve. If the power of extending the 
arm is lost, the loss depends upon paralysis of the musculo-spiral, 82 
THE MANIFESTATION OF DISEASE IN ORGANS. 
which supplies the triceps ; whereas if the power to hex the fore- 
arm is lost, there is paralysis of the musculo-cutaneous, which is 
the supply of the brachialis anticus and biceps. If the supinator 
longus is involved, the musculo-spiral is also affected. 
When brachial monoplegia depends for its existence upon primary 
brachial neuritis there is pain in the wrist and hand at first, or on 
the scapula and in the axilla, thence radiating down the arm. This 
pain is constant and dull, and now and then excruciating, and is 
made worse by movement, even when the loss of power is compara- 
tively slight. Sometimes, on the other hand, when the neuritis is 
septic in origin, it may start in the ulnar nerve and gradually 
extend up to the plexus. In still other cases brachial mono- 
plegia may depend upon fracture or dislocation of the head of the 
humerus, aud in such a case the paralytic symptoms are apt to be 
very well developed. The musculo-spiral nerve is often paralyzed 
by fracture of the humerus, and this results in paralysis of the 
muscles of the back of the arm and forearm and back of the hand, 
and of the skin covering these parts. Sometimes in locomotor ataxia 
the peripheral nerves seem quite as much involved as the spinal 
cord, and symptoms precisely like the paralysis of a toxic neuritis 
develop. Thus, Strumpell has reported cases of musculo-spiral 
paralysis from this cause, and Remak aud Hirt record cases in 
which the median nerve has been affected, so that not only loss of 
power but wasting of the muscles has resulted. This is particularly 
the case if the muscles are much used in the daily pursuits. The 
ulnar nerve may also be affected. Such cases are separated from 
pseudo-tabes by the pupillary reflexes and other pathognomonic 
ataxic symptoms. (See chapter on the Feet and Legs and that 
on the Fye.) Widespread muscular atrophy of the arm some- 
times takes place in locomotor ataxia as a result of a coincident 
neuritis. There are still two comparatively rare forms of brachial 
monoplegia of the plexus type, namely, that due to pressure of 
growths in the neck, or axilla, and brachial paralysis of the upper 
arm type, sometimes called Erb’s paralysis. This latter form occurs 
from paralysis of the fifth and sixth cervical nerves or their roots. 
In adults this commonly results from blows or heavy weights 
striking on the shoulder, and in infants from pulling on the neck 
in difficult labor. As already said, it is an upper arm palsy, and is 
due to the loss of nerve-supply to the deltoid, biceps, brachialis 
anticus, and supinator longus and brevis, and the supra- and infra- THE HANDS AND ARMS. 
83 
spinatus muscles. The adult form is often associated with anaesthe- 
sia and is persistent. In infants it is often temporary and sensory 
symptoms are commonly absent. 
When the lower arm is paralyzed as the result of trouble in the 
brachial plexus the lesion is in the nerves arising from the seventh 
and eighth cervical and first dorsal roots, and the muscles affected 
are the triceps, the flexors of the wrist and fingers, the pronators of 
the hand, the extensors of the fingers, and the muscles of the hand. 
The arm can still be raised by the deltoid and the forearm flexed 
on the arm. 
When there is wasting with paralysis of the thenar, hypothenar, 
and interossei muscles, not due to progressive muscular atrophy, 
with antesthesia in the arm and forearm in the part supplied by the 
ulnar nerve, and in addition myosis on the side of the lesion, with 
sluggish pupil, retraction of the eyeball, and partial closure of the 
lids, there is probably a lesion of the first dorsal root of the brachial 
plexus and the communicating branch of the second dorsal. The 
cause may be neuritis or pressure by a tumor. This form is some- 
times called “ Klumpke’s paralysis.” 
The presence of bilateral brachial monoplegia should always 
make the physician suspicious of lead-poisoning or crutch-paralysis. 
(For a description of the areas involved in the spinal cord, which 
cause loss of power in the arms and legs, see chapter on Feet and 
Legs, part on Paraplegia, and tables of localization in that chapter, 
also plates in chapter on Skin.) 
Apparent brachial monoplegia, in reality a syphilitic pseudo-palsy, 
has been described particularly by Parrot. A child apparently per- 
fectly well, and but a few weeks old, suddenly loses the power of its 
arm, so that the member hangs like a flail. No wasting takes 
place, no degenerative reactions occur, there may be some pain, and 
crepitation 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 bones with consequent helplessness. Sometimes gen- 
eral paralysis 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 and brachialis anticus, and to 
some extent in the supinator longus; and as the first two muscles 84 
THE MANIFESTATION OF DISEASE IN ORGANS 
are supplied by the musculocutaneous and the third by the musc.ulo- 
spiral, such a failure in 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 musculo- 
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 wasting 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, 
and 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 sensa- 
tion may be that of numbness; and if the sensory fibres be totally 
destroyed or paralyzed, absolute anaesthesia and analgesia may be 
present. (See Anaesthesia, chapter on Skiu.) CHAPTER III. 
TJIE FEET AND LEGS. 
The general appearance of the feet and legs when clothed—The gait—Spastic para- 
plegia—Paraplegia without spastic contraction—Crural monoplegia—Deformi- 
ties 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 the ailment from which the man is suffering 
by noticing his gait and the appearance of the legs and feet, 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 pres- 
ence 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 than 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 by locomotor ataxia, pseudo- 
locomotor ataxia (peripheral neuritis) due to alcoholic or lead-pois- 
oning, syphilis, or peripheral neuritis arising from other causes, 
Friedreich’s ataxia, general paresis, chronic myelitis, lateral scle- 
rosis, acute poliomyelitis, pseudo-muscular hypertrophy, cerebral 
infantile palsy, multiple sclerosis, paralysis agitans, cerebellar dis- 
ease, 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 uncer- 
tain, resembling that of a blindfolded person who is told that he is 86 
THE MANIFESTATION OF DISEASE IN ORGANS. 
approaching 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. 32.) 
Fig. 32. 
Gait in a case of locomotor ataxia. From instantaneous serial photographs of a patient or 
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, how- 
ever, 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 neuritis and that due to lead, but in alcoholic 
tabes there are generally 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 differential diagnosis of tabes from pseudo-tabes THE FEET AND LEGS. 
87 
is sometimes very difficult, and as Dana has well said: “ When 
Dejerine described as locomotor ataxia a case which now appears to 
have been one of alcoholic 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 
symptom), 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 witli that most important symptom, 
the Argyll-Robertson pupil, the diagnosis is practically certain. 
Grube has, however, reported recently three cases of diabetes 
mellitus producing a pseudo-tabes due to neuritis who had the 
Argyll-Robertson pupil, and in addition attacks of abdominal pain 
like the crises of true ataxia. 
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. 
Greater inco-ordination, and 
marked ataxic gait. 
Cannot walk because of ataxia. 
Numbness of the feet. 
More marked anaesthesias. 
Extensive anaesthesia. 
Shooting-pains in the legs. 
Pains worse. 
Pains less. 
Diminished or lost knee-jerks, 
one or both. 
Lost knee-jerks. 
Lost knee-jerks. 
Sluggish or lost pupillary reflex 
to light. 
Lost pupillary reflex to light 
and myosis. 
Lost reflex to light, myosis, 
paralysis of accommodation. 
Weakness of sexual function. 
Impotence. 
Impotence. 
Transient diplopia; transient 
ptosis. 
Ocular palsies rare, or marked 
ophthalmoplegia. 
Ophthalmoplegia. 
Sluggish micturition. 
Increased vesical weakness. 
Catheterization needed. 
Optic atrophy. 
Optic atrophy rarely develops. 
Blindness. 
Trophic changes in the joints. 
Trophic changes not so com- 
mon. 
More marked if they began in 
early stage. 
Hemiatrophy of tongue. 
Deafness. 
Increased. 
Laryngeal and visceral crises. 
Not so common. 
Girdle sensation. 
Unnoticed. 88 
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-Robertson pupils. 
From a prognostic and therapeutic standpoint it is interesting to 
note that about 80 per cent, of all cases of tabes dorsalis are syph- 
ilitic. (Duckworth.) 
Reflex action is decreased and the gait altered in locomotor ataxia, 
because, though the motor 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. Tiie sensations of formication or numbness are 
also due to these sensory lesions. (Fig. 33.) (For description of 
motor and sensory tracts of the spinal cord, see early part of chapter 
on Hemiplegia, and chapter on the Skin.) 
Fig. 33. 
Showing 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 he 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, Rom- THE FEET AND LEGS. 
89 
berg’s symptom may be marked to an extraordinary degree. The 
patient who is hysterical, in falling nearly always falls the same 
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, 
swaying 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 
affections, 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. 34.) 
FfG. 34. 
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 Goll (3); the posterior nerve- 
roots (4). 
Friedreich’s ataxia must be 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 Friedreich’s disease, namely, normal or exaggerated 
knee-jerks, Argyll-Robertson pupils, and a beginning of the malady 90 
THE MANIFESTATION OF DISEASE IN ORGANS. 
after twenty years of age. The following table compiled by Collins, 
of New York, gives the differential points between these diseases : 
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 down. 
7. Affection of speech may be absent; when 
it does occur is a late symptom, and consists of 
an eliding of syllables and an occasional hesi- 
tation. 
8. Nystagmus is a very common symptom, 
but it may be lacking. 
9. Myotatic irritability is lost. Knee-jerks 
may be 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 hot 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. 
8. 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 hot or scoliosis, do not occur or 
are most rare. 
The feebleness of the limbs, the reflex iridoplegia (Argyll-Robert- 
son pupil), and 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 feeble- 
ness 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- THE FEET AND LEGS. 
91 
served the gait is typically that of feebleness, and the legs respond 
slowly to the cerebral desires, being dragged along after the patient, 
who leans 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 
sometimes a combination of those of lateral spinal sclerosis (spastic 
paraplegia) and locomotor ataxia. In some instances the spastic 
symptoms 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-clonus is also present. The crises of locomotor 
ataxia do not occur, and the Argyll-Robertson pupil is usually not 
present. (Fig. 35.) 
Fig. 35. 
Showing areas of spinal cord involved in ataxic paraplegia, which is practically a combina- 
tion of locomotor ataxia and lateral sclerosis 1. Lateral or crossed pyramidal tracts. 2. 
Posterior columns of Goll 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 semi- 
circle from behind forward. 
When the gait of a young child is stumbling, or the leg or legs 
are 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 Leg.) 92 
THE MANIFESTATION OF DISEASE IN ORGANS. 
In pseudo-muscular hypertrophy there is a peculiar waddling gait, 
a tendency to stumble, the body is usually bent forward, and there 
is difficulty in getting up from the door 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. 36.) 
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 
iufantile 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. 37.) 
The gait in multiple sclerosis is 
often markedly spastic and paretic 
—that is, stiff and feeble, and may 
in the early stages of the disease 
closely resemble that of spastic paraplegia due to lateral sclerosis. 
When the patient attempts to pick up a small object with his 
Fig. 36. 
Typical pseudo-muscular hypertrophy. 
(Dercum.) THE FEET AND LEGS. 
93 
fingers there are tremor and oscillation of the hand. There are 
also scanning speech and nystagmus. 
In paralysis agitans the patient’s gait is hurried because, from 
the bent-over position of his body, his centre of gravity is too far 
forward and he runs to keep up with it. This is called festinatiou. 
The gait is also somewhat trotting or toddling. (Fig. 38.) (See 
chapter on Hands and Arms, part of on Tremor.) 
Fig. 37. 
Fig. 38. 
Spastic paraplegia; crossed-legged pro- 
gression. (From a patient of Dercum’s in 
the Jefferson Medical College Hospital.) 
Side view of a case of paralysis agitans show- 
ing forward inclination of trunk. Tendency to 
propulsion. (Derctjm.) 
In cerebellar disease the gait may closely resemble that of a 
drunken man, and the patient has the greatest difficulty in keeping 
from sheering oft' to one side as he walks, swaying, too, from side 
to side (cerebellar titubation). The middle lobe of the cerebellum 
is usually affected; but Nothnagel asserts that, if these symptoms- 94 
THE MANIFESTATION OF DISEASE IN ORGANS. 
are associated with paralysis of the oculomotor nerves and other 
symptoms of brain-tumor, there is a growth in the corpora quadri- 
gernina. 
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 inner 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, the 
reverse of what happens in organic 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 hysterical anaesthesia (see chapter on Skin), and often 
with areas of hyperaesthesia. Again, in the gait of hysterical paral- 
ysis 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 way 
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 
inability to co-ordinate the movements of the muscles of locomotion 
or those used in standing. 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 
inability 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 hys- 
teria can nearly always be found. The body often reels to and fro, 
and occasionally the muscles seem to be somewhat spastic. The 
symptom generally follows some severe shock, and is most com- 
monly seen in young persons, usually female children. 
In osteomalacia there is increasing difficulty of walking, partly THE FEET AND LEGS. 
95 
due to pain and partly to muscular weakness. The gait is hobbling, 
tottering, 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. 
Fig. 39. 
Allison’s case of osteomalacia. (Edinburgh Medical Journal.) 
The gait of rickets is only peculiar when 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 96 
THE MANIFESTATION OF DISEASE IN ORGANS. 
changes in the gait, we have loss of power or paralysis affecting 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, re- 
sulting in localized palsies. These paralyses often produce deform- 
ities, 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,1 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 this 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. 
When paraplegia occurs in a young child it is due in a great 
majority of the cases to caries of the vertebrae, and the pressure so 
produced does not necessarily depend upon compression by the 
bones, but by the inflammatory exudate. 
The spinal lesions giving rise to paraplegia of the lower extremi- 
ties are numerous, and are perhaps best grouped in the following 
table of Bramwell: 
Inflammation of cord 
Softening “ “ 
Hemorrhage “ “ 
Tumors “ “ 
Meningitis “ “ 
Meningeal hemorrhage 
Injuries 
Tumors 
Medullary. 
1. Organic disease 
Meningeal. 
Caries of bone 
Tumors of bone 
Osseous. 
2. Functional 
Hysterical. 
Reflex. 
Malarial and ansemic 
Dependent on idea. 
Spastic Paraplegia. The paraplegia of cerebral infantih 
paralysis is spastic, and follows difficult labors or injuries to tin 
child before or after birth. Contractures nearly always ensue, anc 
exist chiefly in the adductors of the thighs, so that the attitude ii 
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. 
97 
very characteristic. (Fig. 40.) Epileptic convulsions very often 
complicate these cases. Often these paraplegias are not manifested 
for some months, or even longer, after birth. In many cases they are 
first noticed when the child attempts to walk. Cerebral spastic 
paraplegia in infants also sometimes comes on in cases of so-called 
arrested 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 his- 
tory in such cases of difficult labor or premature delivery. In both 
Fig. 40. 
Spastic diplegia, congenital, presenting choreiform and athetoid movements. (Dekcum.) 
(Philadelphia Hospital.) 
this and the infantile cerebral form of spastic paraplegia the py- 
ramidal tracts are degenerated. It is important to remember that 
cerebral paraplegia is not associated with the development of the 
reactions of degeneration in the paralyzed part, and is associated 
with comparatively little wasting, thereby differing from the de- 
formities 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 
intention-tremors, exaggerated knee-jerks and ankle-clonus, nystag- 98 
THE MANIFESTATION OF DISEASE IN ORGANS. 
mus, and vertiginous, epileptiform, or apoplectiform seizures, with 
staccato speech, and local areas of loss of power elsewhere, associ- 
ated with spastic paraplegia, renders the diagnosis easy. 
The natural sequence is to pass on to a consideration of the other 
forms of spastic spinal paraplegia, and to take up first of all its mani- 
festation in children. This occurs in what is known as hereditary 
spastic paralysis, which is to be separated from infantile cerebral 
paralysis by 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 separates it from the cerebral infantile type of paralysis. 
It is to be separated from the spastic paraplegia of lateral sclerosis 
by the facts 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. 41. 
Showing shaded areas involved in lateral sclerosis, viz., the crossed pyramidal tracts. 
Iii 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 THE FEET AND LEGS. 
99 
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 
exaggerated, the disease is generally lateral spinal sclerosis. (Fig- 
41.) There is also in lateral spinal sclerosis absence of both sensory 
disorders and rectal and bladder troubles, but sometimes there is 
present 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 Setschenow’s reflex inhibitory centre in the medulla oblongata 
are destroyed in the lateral pyramidal tracts. In amyotrophic lat- 
eral 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. 42.) (See 
chapter on Hands and Arms.) 
Fig. 42. 
Showing area of spinal cord involved in amyotrophic lateral sclerosis. 1. Crossed pvramida 
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 para- 
plegia, the early appearance and severity of the pain, and the com- 100 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 the first. Sensory disturbances, 
aside from pain, are common in myelitis, but rare in this condi- 
tion. If the inflammatory process becomes widespread, there may 
be sensory disorders and trophic sloughs owing to invasion of the 
portions of the cord connected with the sensation and nutrition by 
a secondary myelitis. The development of signs of spinal caries in 
such cases at once shows the condition to be meningeal in origin, 
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 in an 
adult, should make the physician think of spinal syphilis. 
Spastic paraplegia in early childhood, when not due to cerebral 
lesions, as already discussed, is usually due to Pott’s disease. The 
reflexes are exaggerated, the hands are drawn up, and the feet 
are extended. If the lumbar cord is diseased, the reflexes are lost. 
Inquiry will perhaps reveal a history that the child has been easily 
tired before the paralysis came on, and has complained of belly-ache, 
which has really been due to pain along the intercostal nerves from 
the irritation at their roots. Thus, pain in the region of the navel 
suggests inflammation at the eighth dorsal vertebra, or at the ensi- 
form cartilage at the fourth or fifth dorsal vertebra. Early in the 
disease pressure on the spinal column may increase the reflexes. 
The area of the cord involved can be determined by the symptoms 
as detailed on pp. 106 and 107. The prognosis is not always un- 
favorable, as extraordinary recoveries take place. 
Xon-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 
destruction of the cord by injuries of the back, whereby there is 
laceration of the soft parts or fracture or dislocation of the vertebrae. 
When the paraplegia is slower in onset the spinal causes are 
acute ascending paralysis or Landry’s paralysis, acute central mye- 
litis, and acute transverse myelitis. On the other hand, the slowly 
oncoming paraplegias are due to chronic myelitis, to locomotor 
ataxia, amyotrophic lateral sclerosis, lateral sclerosis, poliomyelitis, THE FEET AND LEGS. 
101 
neuritis, and pressure due to disease of the vertebrse 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, 
previously 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 paraplegia 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. Practically 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 suffi- 
cient to produce total paralysis. 
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 trunks, the arms, and the 
respiratory muscles, with the consequent early death of the patient, 
will confirm the diagnosis. There is usually no involvement of 
sensation or trophic paralysis, and the sphincters of the bladder 
and rectum escape the paralysis. Similar symptoms associated with 
sensory disturbances are probably due to a polyneuritis. 
Filler and Meyer state that the cardinal points for the differential 
diagnosis are : 
1. Flaccid paralysis of the muscles, spreading rapidly from one 
point over the rest of the body, generally beginning in the legs, but 
sometimes following the reverse order, as in the French zoblogist 
Cuvier. 
2. Absence of muscular atrophy and of electrical reaction of 
degeneration. 
3. Tendon and superficial reflexes absent. 
4. Sensibility not, or only slightly, impaired. 
5. Sphincters, as a rule, intact (exceptions rather frequent). 
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 
remembered that the symptoms of myelitis depend, first, upon the 
level at which the spinal cord is involved, and, second, as to 102 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 the onset is malignant and the areas in- 
volved are usually widespread. It is attended by fever of a marked 
type, though the temperature of the paralyzed parts is below normal, 
and by early evidences of trophic lesions. Multiple arthritis may 
come on. The bladder and rectum are paralyzed, and, finally, deli- 
rium may develop. The prognosis is unfavorable. Acute central 
myelitis is to be separated from Landry’s paralysis by the facts that 
in it sensation is lost, and there are rectal and vesical paralysis, fever, 
and rapid trophic 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 sudden 
as is that of 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, heaviness, and 
weakness of the legs, with more or less pain in the back, the patient 
has found it impossible to move his legs, has lost control of his 
bladder and rectum, or suffers from retention of the urine and feces 
instead, and at the same time has developed anaesthesia of his lower 
extremities and the girdle-sensation, or, if the lesion be situated 
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 eases the reflexes do not return if the lesion is completely 
transverse. The patient is speedily bed-ridden, and to these symp- 
toms just detailed is 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 
contractures may 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. THE FEET AND LEGS. 
103 
The darkened portion represents the seat of lesion. 
Symptoms in Transverse Myelitis. 
Spinal cord. 
Reflexes normal 
Band of hypersesthesia .... 
Reflexes normal. 
Band of hypersesthesia. 
Muscles palsied, waste, and lose 
their electrical reactions. 
Reflexes lost. 
Tender spines. 
Tender spines. 
Muscles palsied, waste, and lose 
their electrical reactions . . 
Reflexes lost 
Sensation lost 
Sensation lost. 
Muscles palsied. 
Do not waste. 
No loss of electrical reactions. 
Reflexes increased. 
Sensation lost. 
Bedsores. 
Temperature above rest of body. 
Muscles palsied 
Do not waste 
No loss of electrical reactions . 
Reflexes increased 
Sensation lost 
Bedsores 
Temperature above rest of body 
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 Paraesthesia in 
chapter on the Skin). The motor symptoms begin by a feeling of 
heaviness or inability to quickly move the lower limbs, so that 
the patient 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, paral- 
yzed, and retentive or incontinent. Retentive, if the lesion is above 
the lumbar cord; incontinent, when the lower part of the lumbar 
enlargement 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, and 104 
THE MANIFESTATION OF DISEASE IN ORGANS. 
those muscles and tendons having spinal centres below the lesion 
have their reflexes increased because they are cut off from the in- 
hibiting 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 paralyzed, now divide themselves into two classes, those 
that are connected with the diseased part of the cord, which remains 
paralyzed, 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 off from cerebral influences, voluntary 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 become spastically contracted. Other trophic 
changes, such as bedsores and bullse, develop in the skin connected 
with the diseased focus, but not in that connected with centres below 
the lesion. Anaesthesia is present because the lesion prevents the 
sensory impulse from reaching the brain (see chapter 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 ex- 
tensors escape oftener than the flexors. The height of the paralysis 
also depends upon the situation 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 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 sup- 
posed to be a descending degeneration in the pyramidal tracts. 
The symptoms of chronic transverse myelitis producing paraplegia 
are practically identical with the more acute form just described, 
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 con- 
dition: there is complete paralysis of his arms and legs, with par- 
alysis 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 unimpaired; while the arms are 
found relaxed and flaccid, devoid of reflex excitability, and under- 
going degenerative atrophy. The bladder and rectum are not THE FEET AND LEGS 
105 
retentive. All these symptoms point to a transverse lesion of the 
spinal cord in the cervical region, probably between the fifth cer- 
vical and first dorsal vertebrae. 
If, on the other hand, the upper extremities are not affected 
(except, 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 present, combined 
with degeneration of the muscles of the trunk, the lesion is prob- 
ably somewhere 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 retlexes, and paralysis of the bladder and rectum, the lesion 
is in the lumbar cord. 
Differential Diagnosis of Lumbar, Dorsal, and Cervical 
Myelitis.1 
Lumbar myelitis. 
Dorsal myelitis. 
Cervical myelitis. 
Paralysis. 
Paraplegia. 
1. Dorsal, abdominal, and 
intercostal muscles, ac- 
cording to heigh t of lesion. 
2. Legs. 
Neck-muscles, dia- 
phragm, arms, trunk, 
and legs. 
Sensation. 
Painsinlegs, or girdle-pains 
around loins: hypersesthe- 
tic zone around loins; an- 
esthesia of legs, complete 
or uneven distribution. 
Girdle-pain and hyperaes- 
thetic zone between ensi- 
form cartilage and pubes. 
Hyperaesthesia and 
pains in certain 
nerve-distributions 
of arms; below this 
anaesthesia of arms, 
body, and legs. 
Atrophy. 
Of legs. 
Of dorsal and abdominal 
(and intercostal muscles 
not subject to examination) 
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. in 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 mye- 
litis. 
Reflexes 
superficial. 
Lost. 
Temporary loss, then slow 
increase. 
Same as in dorsal mye- 
litis. 
Priapism. 
Absent. 
Often present. 
Often present. 
1 From Prince’s article in Dercum’s Nervous Diseases. 106 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Still further, if there be loss of power with degeneration of the 
small muscles of the feet, and 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. 
In this connection the reader should study that part of the 
chapter on the skin which deals with anaesthesia. 
This subject is still further subdivided and elucidated by the 
following table and by the illustration (Fig. 43). 
Localization of the Functions of the Segments of the Spinal 
Cord. (According to Starr.) 
Segment. 
Muscles. 
Reflex. 
Sensation. 
II. and II. 
C. 
Sterno-mastoid. 
Trapezius. 
Scaleni and neck. 
Diaphragm. 
Hypochondrium. (?) 
Sudden inspiration produced 
by sudden pressure beneath 
the lower border of ribs. 
Back of head to vertex. 
Neck. 
IV. C. 
Diaphragm. 
Deltoid. 
Biceps. 
Coraco-brachialis. 
Supinator longus. 
Rhomboid. 
Supra- and infra-spinatus. 
Pupil. 4th to 7th cervical. 
Dilatation of the pupil pro- 
duced by irritation of the 
neck. 
Neck. 
Upper shoulder. 
Outer arm. 
V. C. 
Deltoid. 
Biceps. 
Coraco-brachialis. 
Brachialis anticus. 
Supinator longus. 
Supinator brevis. 
Rhomboid. 
Teres minor. 
Pectoralis (clavicular part). 
Serratus magnus. 
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. 
Back of shoulder and 
arm. 
Outer side of arm and 
forearm, front and 
back. 
VI. C. 
Biceps. 
Brachialis anticus. 
Pectoralis (clavicular part). 
Serratus magnus. 
Triceps. 
Extensors of wrist and 
fingers. 
Pronators. 
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. 
Outer side of forearm, 
front and back. 
Outer half of hand. 
VII. C. 
Triceps (long head). 
Extensors of wrist and 
fingers. 
Pronators of wrist. 
Plexors of wrist. 
Subscapular. 
Pectoralis (costal part). 
Latissimus dorsi. 
Teres major. 
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. 
Inner side and back of 
arm and forearm. 
Radial half of the 
hand. THE FEET AND LEGS. 
107 
Segment 
Muscles. 
Reflex. 
Sensation. 
VIII. C. 
Flexors of wrist and fingers. 
Intrinsic muscles of hand. 
Forearm and hand, 
inner half. 
I. D. 
Extensors of thumb. 
Intrinsic hand muscles. 
Thenar and hypothenar 
eminences. 
Foream, inner half. 
Ulnar distribution to 
hand. 
II. to XII. 
D. 
Muscles of hack and abdo- 
men. 
Erectores spina}. 
Epigastric. 4th to7th dorsal. 
Tickling mammary region 
causes retraction of the 
epigastrium. 
Abdominal 7th to 11th dor- 
sal. 
Stroking side of abdomen 
causes retraction of belly. 
Skin of chest and 
abdomen, in bands 
running around and 
downward corre- 
sponding to spinal 
nerves. 
Upper gluteal region. 
I. L. 
Ilio-psoas. 
Sartorius. 
Muscles of abdomen. 
Cremasteric. 1st to 3d lum- 
bar. 
Stroking inner thigh causes 
retraction of scrotum. 
Skin over groin and 
front of scrotum. 
II. L. 
Ilio-psoas (Sartorius). 
Flexors of knee (Remak). 
Quadriceps femoris. 
Patellar tendon. 
Striking tendon causes ex- 
tension of leg. 
Outer side of thigh. 
III. L. 
Quadriceps femoris. 
Inner rotators of thigh. 
Abductors of thigh. 
Front and inner side 
of thigh. 
IV. L. 
Abductors of thigh. 
Adductors of thigh. 
Flexors of knee (Ferrier). 
Tibialis anticus. 
Gluteal. 
4th to 5th lumbar. 
Stroking buttock causes 
dimpling in fold of buttock. 
Inner side of thigh and 
leg to ankle. 
Inner side of foot. 
V. L. 
Outward rotators of thigh. 
Flexors of knee (Ferrier). 
Flexors of ankle. 
Extensors of toes. 
Back of thigh, back of 
leg, and outer part of 
foot. 
I. to II. 
S. 
Flexors of ankle. 
Long flexor of toes. 
Peronei. 
Intrinsic muscles of foot. 
Plantar. 
Tickling sole of foot causes 
flexion of toes and retrac- 
tion of leg. 
Back of thigh. 
Leg and foot, outer 
side. 
III. to V. 
s. 
Perineal muscles. 
Foot-reflex. Achilles tendon. 
Overextension of foot causes 
rapid flexion; ankle-clonus. 
Bladder and rectal centres. 
Skin over sacrum. 
Anus. 
Perineum. Genitals. 
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, and, 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). 
The symptoms of lateral sclerosis and amyotrophic lateral scle- 
rosis have already been discussed under Gait and Spastic Para- 
plegia, but in the paraplegia called “ ataxic paraplegia,” also 
already discussed, there are in association lateral sclerosis and pos- 
terior sclerosis, and for this reason some of the symptoms of both 108 
THE MANIFESTATION OF DISEASE IN ORGANS. 
are found to be present. Thus, in addition to loss of power there 
is a spastic condition of the legs with exaggerated reflexes, absence 
of the Argyll-Robertson pupil and of crises of pain, but the 
Romberg, symptom, or swaying 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, headache, vertigo, optic neuritis, titu- 
bation, and sometimes vomiting. 
Fig. 43 
1st to 7th cervical segment 
}■ 1 st to 12th dorsal segment. 
1st to 5th lumhar segment. 
1st to 5th sacral segment. 
Showing the surface-areas of the back corresponding approximately to the areas of the 
spinal cord supplying the trunk and limbs. 
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 cornua) remain paralyzed. There is no loss of sensation, THE FEET AND LEGS. 
109 
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 
development of coldness in these areas, which is due to the destruc- 
tion 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 
failure. 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 appar- 
ently only a reflex paralysis, as it often passes away with the re- 
moval of the source of irritation. Even worms in the intestine 
have produced such a paralysis, and their removal has been fol- 
lowed by cure. Generally sensation in the limbs is unimpaired 
and the bladder and rectum act normally. Sometimes, however, 
in the presence of severe renal disease, as renal 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 exaggera- 
tion of the reflexes. Probably these severe cases are always due 
to a coincident myelitis rather than to reflex irritative cause. 
Vo 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, 
relaxation or spastic contraction of the muscles, anaesthesia and 
hyperaesthesia, pain or no pain. The very occurrence of such 
irregular manifestations in a young, neurotic girl, the facts that the 110 
THE MANIFESTATION OF DISEASE IN ORGANS. 
anaesthetic areas constantly tend to shift their position, and, finally, 
that the contractures, if present from hysteria, disappear on admin- 
istering 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 haematuria or 
bloody stools may appear. 
Pseudo-paraplegia may occur in rickety children from faulty 
muscular 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-pedal spasm, is often seen in rickety 
children. 
Not uncommonly a partial paraplegia occurs as a result or sequel 
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 very 
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 
involves the arms and the body after affecting the legs; there is 
well-developed anaesthesia (see chapter on Skin), preceded by sensory 
disturbances and marked muscular and nerve-trunk tenderness; but 
there is no girdle-sensation, as there is in myelitis and tabes. There 
are often trophic changes in the skin in neuritis (see chapter on Skin), 
but no bedsores as in myelitis. Toxic agents producing a neuritis 
may sometimes cause a paraplegia of the lower extremities. Da Costa 
states that malarial neuritis may cause such a symptom, but, as a 
rule, a toxic neuritis produces loss of power in the arms. Very 
rarely paraplegia of the lower extremities results from diabetes 
mellitus, the lesion being in all probability a multiple neuritis. 
Monoplegia of a lower extremity may be due to cerebral THE FEET AND LEGS. 
111 
lesions or to spinal or nerve-trunk lesions. The cerebral lesion 
producing monoplegia in one leg is very rare, and if it occurs, at 
any age, indicates a lesion in the convolutions at the upper end of 
the fissure of Rolando, and the continuation of this area in the para- 
central lobule of the marginal convolution. Unlike the paraplegias 
of infantile cerebral paralysis, monoplegia of the leg very rarely 
arises from this cause. If there are no signs of cerebral trouble, 
the presence of a complete leg monoplegia can mean one of several 
things, namely, a lesion limited to one side of the cord, as, for 
example, a hemilateral myelitis, hysterical paralysis, in which 
there will be irregular anaesthesia (see Skin), and the other hys- 
terical signs, or a tumor pressing on the crural nerve in the pelvis, 
or section of the nerve by injury. Apparent monoplegia may, 
however, be due to muscular pain or a painful phlebitis producing 
muscular fixation. 
Diagram showing Symptoms in Hemilateral Myelitis. 
(The dark mass represents the site of the lesion.) 
Spinal cord. 
Reflexes normal 
Band of hyperesthesia . . 
Band of anesthesia . . . 
Reflexes lost 
Motor palsy 
Hyperesthesia 
Reflexes increased .... 
Temperature above the rest 
of the body 
Reflexes normal. 
Band of hyperesthesia. 
Band of anesthesia. 
Motor power unaffected. 
Anesthesia. 
Reflexes unaffected. 
Temperature same as the rest 
of the body. 
If the condition is due to a lesion on one side of the cord, the 
symptoms are quite characteristic. There is paralysis of all the 
muscles of the leg which are supplied by the part of the cord 
affected or below it. The muscles, the nerve-supply of which 
comes directly from the affected part, eventually waste and undergo 
degenerative changes. The most typical symptom of this lesion is, 
however, the crossed character of the sensory paralysis. That is to 
say, there is loss of sensation in the opposite limb from that in which 
motion is lost, and in the limb in which motion is lost there is hyper- 
aesthesia, so that the lightest touch may be very painful. The cause of 112 
THE MANIFESTATION OF DISEASE IN ORGANS. 
this is obscure, for the studies of Mott have proved that the sensory 
tracts in the cord do not decussate on entering it, as has been sup- 
posed heretofore. There is, however, a symmetrical band of ames- 
thesia round the body at the level of the lesions, and a similar band 
of hypersesthesia above the lesious. The reflexes of the parts sup- 
plied by the diseased area are lost, but those supplied by the area 
below the lesions are increased as in ordinary myelitis. Very com- 
monly the paralyzed limb is over-warm from vasomotor palsy. 
Fig. 44. 
Areas involved in acute and chronic poliomyelitis. In children it is sometimes called acute 
infantile paralysis. Shading shows area of cells in anterior cornua of gray matter which are 
involved. 
Paralysis of certain groups of muscles or a single muscle in the 
legs is most commonly due to anterior poliomyelitis or neuritis. 
(Fig. 44.) In poliomyelitis the child will be found to have loss of 
power in certain muscles in one or both legs (see also Paraplegia), 
so that there is a dragging of the toe or “ foot-drop,” the shoe 
becomes irregularly worn through, being dragged on one edge along 
the ground, the involved muscles being peculiarly relaxed and 
flaccid, so that the leg may wobble, to use a crude term. This is 
sometimes called a “ Punchinello leg.” There is no tendency to 
spastic contraction, the reflexes are rapidly lost in the affected part, 
and the muscles speedily waste and develop the reaction of degen- 
eration. (Fig. 46.) When contractures take place they are not 
spastic, and are due to healthy muscles being unopposed by the THE FEET AND LEGS. 
113 
diseased ones. The temperature of the paralyzed part is lower than 
normal. The history in poliomyelitis is that of sudden onset with 
fever, vomiting, and restlessness. The two conditions of acute 
cerebral paralysis and anterior poliomyelitis are so clearly separated 
in well-marked cases that no error can be made, particularly if the 
Fig. 45. 
Fig. 46. 
Case of acute infantile cerebral palsy for 
comparison with Fig. 46. (Sachs.) 
Case of infantile spinal palsy: paralysis and 
atrophy of left leg chiefly. (Sachs.) 
history of the attack be borne in mind, unless it be in the obscure 
forms of cerebral infantile palsy in the early stages. The above 
figures show the two different types of paralysis resulting from these 
cerebral and spinal diseases in the child. (Figs. 45 and 46.) In 
acute infantile paralysis of spinal origin the right lower extremity 
is most frequently affected, after this, a close second, the left leg. 
Sometimes muscular atrophy may be masked in young children by 
the abundance of subcutaneous fat. A point of some importance 
in examining the reflexes is that presence of knee-jerk should not 114 
THE MANIFEST A TIO N OF DISEASE IN ORGANS. 
exclude the diagnosis of poliomyelitis, because the reflex act is only 
destroyed if the centres which cause this jerk are diseased ; that is, 
if the disease has only affected that part of the cord supplying the 
foot, a tap on the knee may readily produce a response, whereas if 
the disease be higher up in the cord the reflex will be lost. The 
chronic anterior poliomyelitis of adult life presents very similar 
symptoms to the acute form of infancy, but is a very rare disease. 
Care must be taken that paralysis of the leg resulting from an 
injury to the peroneal nerve with resulting neuritis is not mistaken 
for acute poliomyelitis. The history of an accident, of pain, swell- 
ing, and the presence of a bruise aid us in making a diagnosis. If 
these symptoms occur in an adult, a possible cause is paralysis of 
the peroneal nerve occurring in the course of tabes. (In connection 
with this chapter see that on the significance of anaesthesia of the 
skin.) 
Deformities of the Feet and Legs. Much of what has been 
said in the preceding chapter as to the diseases which produce altera- 
tions in the shape of the hand and arm applies equally to the changes 
from the normal seen in the appearance and movements of the feet 
and legs. The feet are greatly enlarged symmetrically in acro- 
megaly and in Marie’s pulmonary osteo-arthropathy. In the latter 
disease the enlargement is particularly noticeable because it is the 
extremities which are chiefly hypertrophied, whereas in acromegaly 
there is simultaneous enlargement of the shafts of the long bones. 
(See chapter on Hands and Arms.) It is to be remembered that in 
both acromegaly and pulmonary osteo-arthropathy the enlargement 
seems to be due to hypertrophy of all the tissues composing the foot, 
whereas, on the other hand, in myxoedema the foot, though enlarged, 
is puffed and swollen in appearance through hypertrophy of the 
subcutaneous tissues alone. Often the foot appears to be a good 
deal enlarged as the result of deformity, particularly that which 
consists in partial displacement of the articular surfaces of the meta- 
tarsal and phalangeal bones through the wearing of badly fitting 
shoes, or joint-troubles, of which we shall speak later. 
Under the name of “sciopedy” Power has reported a case of 
congenital symmetrical enlargement of the anterior part of the foot 
not involving the heel. Any enlargement of the legs associated 
with this condition, he states, only results from hypertrophy of the 
muscles’resulting from the effort to lift the feet. 
The claw-hand spoken of in the chapter on that part of the body THE FEET AND LEGS. 
115 
is represented by a similar deformity in the foot which may arise 
from the same causes, in regard to the nervous lesions, and depend 
upon atrophy of the interossei and other intrinsic muscles of the 
foot (Fig. 47); but progressive muscular atrophy rarely involves 
the foot, although it may begin there. When progressive muscular 
atrophy does begin in the lower extremities, it may fall into the 
class called progressive neural muscular atrophy, or the peroneal 
or leg-form of progressive muscular atrophy, affects the leg chiefly, 
and rarely involves the foot proper first. The extensor muscles of 
Fig. 47. 
Fig. 48. 
“Claw-foot” from atrophy of interossei 
and other intrinsic muscles of foot. (Du- 
CHENNE.) 
Pes equinus in a boy five years of age, from 
atrophy of tibialis anticus. (Sachs.) 
the toes lose their power, the interossei waste, the foot may be flat- 
tened or claw-shaped, or, in other instances, any one of the forms 
of club-foot may develop. If the deformity is bilateral, it is a 
strong evidence of its being the leg-type of progressive muscular 
atrophy, and not due to infantile paralysis. There will probably 
be a history of heredity in such cases. It must be carefully sepa- 
rated from the pes equinus seen as a result of progressive and acute 
infantile spinal paralysis involving the tibialis anticus as seen in 
Fig. 48. The toes are hyper-extended, and the foot is very broad 
when viewed from side to side at the metatarsal joints. It is stated 116 
THE MANIFESTATION OF DISEASE IN ORGANS. 
that this sign is considered characteristic of the early development 
of the disease in families with the heredity. Sometimes in place 
of this deformity the foot becomes almost parallel with the tibia in 
excessive extension, with eversion as the result of shortening of 
the peroneus longus. (Fig. 49.) In other instances the deformities 
undergo marked changes as the disease progresses, so that they not 
Fi<;. 49. 
FlO. 50. 
Plantar surface exhibiting changes due to contracture of peroneus longus, shortening ol 
transverse diameter, A C, and torsion of foot, D. (Sachs.) 
only grow worse, but are altered in type. (Figs. 49, 50, 51, and 
52.) In distinction from ordinary progressive muscular atrophy 
this leg-type often has marked disturbance of sensation associated 
with it. (Dana.) It generally occurs in males. According to 
Marie, another form of claw-foot is seen in Friedreich’s ataxia, 
there being associated with it club-foot. 
Progressive neural muscular atrophy is a rare disease which must 
be separated from multiple neuritis by the pain of the latter affec- 
tion and the fact that neuritis rarely produces double club-foot, and, 
further, that in neuritis there is no history of heredity. From polio- 
myelitis we separate it by the fact that in this peroneal type of par- 
alysis the onset is more slow and by the fact that there is a loss of THE FEET AND LEGS. 
117 
the reflexes in severe poliomyelitis, though they are preserved for 
a long time in the peroneal type. From Friedreich’s ataxia it is 
separated by the fact that in that disease the reflexes are lost, there 
is a peculiar unsteadiness in walking, and an absence of electrical 
changes in the muscles. 
In some cases of locomotor ataxia flat-foot from loss of the plantar 
arch is seen, and various dystrophies of the joints take place as the 
disease progresses. 
Fig. 51. 
Fig. 52. 
Case of progressive muscular atrophy in a child with a spinal lesion. The four figures (49, 50, 
51, and 52) illustrate the progressive wasting of the muscles and the deformities resulting there- 
from. In Fig. 52 hyperextension of the fingers and of the big toe is very striking. (Thomson 
and Bruce.) 
The peroneal leg-type of progressive muscular atrophy may so 
closely resemble the so-called Aran-Duchenne type of progressive 
muscular atrophy as to defy diagnosis, but as a rule the latter dis- 
ease affects the arms first, and sensation is not involved. (See 
chapter on Hands and Arms.) 
Wasting of the muscles of the inner surface of the foot affecting 118 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the big toe, and those on the outer side involving the movements 
of the little toe, the interossei and the flexor brevis communis, may 
occur from the neuritis due to locomotor ataxia, and as the plantar 
aponeurosis retreats the toes are rendered immovably flexed; in 
other cases in place of flexion we get strong extension, as in this 
figure. (Fig. 53.) 
Fig. 53. 
Tabetic foot. (Shingleton Smith.) 
A shrivelled, undeveloped foot and leg with drawing up and 
deformity are seen most commonly as the ultimate result of the 
acute cerebral paralysis of infancy. (Fig- 54.) 
Acute cerebral paralysis of infancy is to be separated from spinal 
paralysis of acute or subacute poliomyelitis anterior of infancy, or 
the rare polioymelitis of later life. In these there may be bilateral 
paralysis, although only one leg and foot are more often involved. 
Like the paralysis from cerebral disease, spinal paralysis comes on 
suddenly, but there is this marked difference, viz., that in old cere- 
bral paralysis there are spastic rigidity and spastic contractures, no 
atrophy of the muscles, until by disuse or secondary changes in the 
cord the muscles lose their nutrition, there is marked increase of 
the reflexes, and the electrical reactions remain normal for a long 
period of time; whereas in the early stages of acute spinal paralysis 
there is an entire absence of spastic contraction, the muscles being THE FEET AND LEGS. 
119 
peculiarly lax, flabby, and lifeless; contractions with resulting de- 
formity only arising from the action of healthy muscles robbed of 
their natural antagonists. The contractures 
of the leg which occur in acute infantile par- 
alysis of spinal origin are not spastic, and are 
often only developed upon intention-move- 
ments or by the unopposed healthy muscles. 
A very important form of contracture fol- 
lowing paralysis or occurring without it, 
which is apt to lead to a mistake in diagnosis, 
is that seen in hysteria (Figs. 55 and 56). 
As a rule, the contractures come on in asso- 
ciation with paraplegia. Sometimes, how- 
ever, they affect the arms or an arm. It is a 
characteristic of these contractures due to 
hysteria that they set in suddenly, and are 
always accompanied by such hysterical 
symptoms as borborygmi, ovarian tender- 
ness, and often areas of anaesthesia. Weir 
Mitchell has divided these cases into two 
forms. The first only involves single parts 
or limited muscle-groups, and, though the 
contractures may last for years, joint- or 
muscle-changes do not occur. In the sec- 
ond class, one limb after another is at- 
tacked until all means of locomotion, or 
even moving the trunk, are lost, and the 
muscles, joints, and areolar tissue undergo 
organic changes. The reflexes are lost in 
such cases in the late stages, and the elec- 
trical reaction of the muscles is impaired. The diagnosis is to be 
reached by the sex, the personal history, the history of the illness, 
the presence of anaesthesia (see chapter on Skin), and hyperaesthe- 
sias. Usually the contracture comes on suddenly; it is very rigid, 
and the muscles on both sides of the limb are fixed; that is, the 
contracture involves antagonistic muscles. Sleep does not always 
cause a relaxation of hysterical contraction, but ether or chloroform 
usually does so. (See chapter on Hands and Arms.) 
Deformity or distortion of the legs may result from the secondary 
muscular atrophy following upon chronic inflammation in a joint or 
Fig. 54. 
Shrivelled foot of infantile 
cerebral paralysis. (Hiet.) 120 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Hysterical spasm and contracture, sbowingthe condition of the affected leg in the recumbent position. (Bbamwei.i,, 
Fig. 55. THE FEET AND LEGS. 
121 
joints. The muscular wasting under these circumstances arises from 
neuritis, which is associated with the arthritis. 
The Joints. The joints of the lower limbs may be swollen from 
an arthritis arising from many 
causes, such as locomotor ataxia, 
hemiplegia, rheumatoid arthri- 
tis (arthritis deformans), acute 
myelitis, cerebro-spinal menin- 
gitis, Morvan’s disease, septicae- 
mia, or the infectious processes, 
such as acute articular rheuma- 
tism and typhoid fever. 
The most marked alterations 
in the joints are those produced 
by advanced locomotor ataxia, 
and are called arthropathies. 
Often they are associated with 
spontaneous fractures of the 
bones. The knees are most 
commonly involved, then the 
ankles and hips. A joint or 
several joints may become sud- 
denly swollen with or without 
pain, and without apparent 
cause until the swelling becomes 
quite massive. There are then 
developed osseous hyperplasia 
and a tendency to dislocation 
with crepitation on movement, 
and the ends of the bone be- 
come worn away and absorbed. 
Dislocation and fractures are 
common, and the bones are 
atrophied. 
In rheumatoid arthritis there 
is a gradual enlargement of the 
joints from accumulation of 
fluid, which in turn is absorbed, 
leaving the articulating surfaces roughened, uneven, and deformed, 
but there are no deposits of urate of sodium as in gout, the deform- 
Fig. 56. 
Hysterical spasm and contracture, showing 
the attitude in the erect position. (Bramwell.) 122 
THE MANIFESTATION OF DISEASE IN ORGANS. 
ities being due to alterations in the articulating surfaces themselves, 
and the periarticular development of bone. The disease always re- 
mains in the joint originally attacked, although new joints are in- 
volved. Pain is often severe, dislocations and fractures are rare, 
and the small joints are often involved. (See chapter on Hands and 
Arms.) 
Rheumatoid arthritis when it progresses to an advanced stage 
causes great deformity by the locking of the joints through the 
development of osteophytes. By the destruction of the cartilages, 
wasting of the muscles, and thickening or contraction of the liga- 
ments, it may cause dislocation of all sorts, and false positions. In 
the great majority of cases it occurs in women between twenty and 
thirty years of age, but it may develop in early childhood. Pain is 
severe in some cases, absent in others. The thighs become flexed 
upon the abdomen, and the leg on the thigh. The number of joints in- 
volved varies greatly, but the involvement is generally symmetrical. 
Sometimes this disease, which is generally gradual in its onset, 
becomes very acute, speedily involving many joints, causing swelling 
of the synovial sheaths and bursae, and being accompanied by some 
febrile movement. The suddenness of its onset, the febrile move- 
ment when the onset is sudden, and the pain may cause it to 
resemble acute articular rheumatism, but the absence of redness 
in the joints and of the migration of the swelling from one joint to 
another aids in the differentiation. The arthritis of acute central 
myelitis is sudden in its onset, generally multiple, and accompanied 
by the other symptoms of that disease (see Paraplegia and Anaes- 
thesia of the Skin). 
The arthritis of cerebro-spinal meningitis is really to be classed 
as an infectious arthritis, and the presence of the characteristic sigus 
of the disease renders its cause evident. The joints are many of 
them affected simultaneously with swelling, pain, and serous or 
puruleut effusions. In cases of septic arthritis the joints become 
swollen and often suppurate, so that the articular surfaces become 
more or less destroyed. This may occur after infection during the 
puerperium or in any case of pyaemia. In Morvan’s disease or 
syringomyelia the small joints are usually affected. 
The onset of an inflammation in the lower end of the femur or in 
the upper end of the tibia, producing what, at first glance, seems to 
be an arthritis and sometimes simultaneously involving other areas 
near joints, should raise a suspicion of acute osteomyelitis, which is THE FEET AND LEGS. 
123 
a fatal disease in many cases unless surgical aid comes to the patient. 
The symptoms consist of boring pain in the part, great tenderness 
and swelling, and the skin soon breaks down as a purulent and offen- 
sive discharge makes its way to the surface. 
Closely allied to this is the acute epiphysitis of infancy, in which 
there is suddenly developed a chill followed by great pain and swell- 
ing of the joints or their neighborhood. The skin becomes engorged 
with blood and the joint fills with pus. Care must be taken to sepa- 
rate this condition from rheumatism and the joint-swelling some- 
times seen after typhoid fever. This state is practically identical 
with the acute arthritis of childhood. 
When arthritis is due to gonorrhoeal infection it is generally seen 
in the knees or ankles, and occurs in men, as a rule. It is an infec- 
tious arthritis and lasts very persistently, often attacking at the same 
time joints so rarely involved by rheumatism as the jaw, the verte- 
bral joints, and the sterno-clavicular articulation. According to 
the late Dr. Howard, of Montreal, it occurs in five forms: 
а. Arthralgic, in which there are wandering pains about the joints, 
without redness or swelling. These persist for a long time.. 
б. Rheumatic, in which several joints become affected, just as in 
subacute articular rheumatism. The fever is slight; the local 
inflammation may fix itself in one joint, but more commonly 
several become swollen and tender. In this form cerebral and 
cardial complications may occur. 
c. Acute gonorrhoeal arthritis, in which a single articulation be- 
comes suddenly involved. The pain is severe, the swelling exten- 
sive and due chiefly to periarticular oedema. The general fever is not 
at all proportionate to the intensity of the local signs. The affection 
usually resolves, though suppuration occasionally supervenes. 
d. Chronic hydrarthrosis. This is usually monoarticular, and is 
particularly apt to involve the knee. It comes on often without 
pain, redness, or swelling. Formation of pus is rare. It occurred 
only twice in ninety-six cases tabulated by Nolen. 
e. Bursal and synovial form. This attacks chiefly the tendons 
and their sheaths., and the bursse and the periosteum. The articula- 
tions may not be affected. The bursse of the patella, the olecranon, 
and the tendo Achillis are most apt to be involved. 
Acute articular rheumatism in the knee or ankle produces swell- 
ing of the joint, redness, heat, exquisite tenderness, immobility from 
pain, swelling of the surrounding tissues. It does not remain for a 124 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
long period unchanged in one joint, and is a process accompanied 
by fever. 
Although gout is capable of causing deformity in the lower ex- 
tremities, it has one fact about it which is of practical importance, 
namely, that it involves the small joints of the foot, while rheuma- 
tism attacks the large joints, such as the knee, by preference. Gout 
involves the feet most commonly, while rheumatism is more fre- 
quently seen in the hand, if small joints are affected, and the big 
toe is the favorite place for gouty manifestation. Aside from the 
swelling, redness, and exquisite tenderness of gouty joints, all of 
which symptoms exceed in acuteness similar manifestations in acute 
rheumatism, there is often an additional and permanent cause of 
deformity in the chalk-stones which are deposited about the joints, 
and which are never seen in rheumatism. The history of frequently 
recurring attacks lasting but a few days, accompanied by enlarge- 
ment of the veins about the joint and shedding of the skin locally, 
points, when added to the symptoms named, to a typical case of 
gout. It may be almost impossible to determine whether a case be 
one of chronic rheumatism or gout unless chalk-deposits can be found. 
Sometimes in chronic lead-poisoning we have developed what is 
known as plumbic gout, owing to the deposition of urate of lead and 
sodium. 
Acute synovitis is generally the result of an injury, is confined 
to one joint, is often accompanied by a far greater effusion into the 
joint than is seen in rheumatism, and there is no systemic disturb- 
ance. Should a single joint be apparently effaced by an aberrant 
attack of acute rheumatism or synovitis, the physician should never 
forget the possibility of its being a gonorrhoeal arthritis. 
The onset of a multiple arthritis, with which there are headache, 
chills, intense aching in the bones, joints, and muscles, and a fever 
rising as high as 106° or 107°, and rarely an erythematous rash, 
may indicate the presence of dengue. The joints are swollen and 
painful, and often both the large and small ones are involved. 
Another arthritis, probably infectious, is sometimes seen in epidemic 
dysentery and in scarlet fever. Rarely immediately after or some 
months after typhoid fever a hypertrophic osteoarthritis comes on 
as a result of a local difficulty produced by the bacillus of Eberth. 
This is to be separated from ordinary septic arthritis following 
typhoid fever. 
In Schonlein’s disease, which is a form of very severe purpura, THE FEET AND LEGS. 
125 
multiple arthritis, with great pain, and purpuric eruptions occur, and 
the presence of the subcutaneous exudate with oedema and sloughing 
of the mucous membrane of the mouth adds to the picture. The 
patient seems very ill, but death rarely follows. Such cases are 
rare, but the writer saw one in consultation with Dr. Wilson, of 
Woodbury, New Jersey, in which alarming sloughs of the tonsils 
and buccal mucous membrane occurred. (See chapter on Skin.) 
Very nearly allied to this are the joint-involvements of hemo- 
philia, which in their sudden onset and pain closely resemble rheu- 
matism, particularly as the large joints are commonly involved. 
The history of the patient being a bleeder, or of his being related 
to one, may clear up the diagnosis. 
Intense swelling of the leg, aside from that due to ordinary 
oedema, may be due to milk-leg, which is a condition of swelling 
of the entire limb, generally limited to one side, and seen during 
the puerperium or after any one of the infectious fevers, such as 
typhoid. The joints are not particularly affected. On the con- 
trary, the calf of the leg is the part most affected, it being white, 
firm, hot, but slightly, if at all, oedematous. Pain is excessive, 
there is entire loss of power in the affected limb, and its tempera- 
ture is much higher than normal. 
If the swelling of the leg is bilateral and pits on pressure, it is 
practically always the result of anasarca from renal or cardiac dis- 
ease; but if unilateral, it may be, as just stated, due to thrombosis 
of the femoral vein (see chapter on the Skin; (Edema.) 
Three very important serious alterations in the nutrition of the 
foot remain to be noted, namely, perforating ulcer due to tabes 
dorsalis, diabetic gangrene, and senile gangrene. Perforating ulcer 
usually appears in one foot, beginning with the formation of a bleb, 
which changes to an abscess, which in turn is followed by necrosis of 
all the tissues of the foot immediately underlying the destroyed skin. 
With it are associated the signs of ataxia. Sometimes perforating 
ulcer of the foot occurs during the course of diabetes mellitus, but 
it is probable in many such cases that locomotor ataxia is associated 
with diabetes. (Fig- 57.) In diabetic gangrene the toes are 
nearly always affected in preference to other parts of the body. 
An analysis of the urine will aid the diagnosis (see chapter on 
Skin). In senile gangrene the age of the patient, bad bloodvessels, 
and the absence of a sufficient cause for gangrene, as from trauma, 
separate the case from any other condition, while the fact that senile 126 
THE MANIFESTATION OF DISEASE IN ORGANS. 
gangrene generally affects the inner side of the foot, especially the 
big toe, and is a dry gangrene, renders the diagnosis easy. 
Gangrene of the extremi- 
ties sometimes follows the 
infectious diseases, such as 
scarlet and typhoid fevers, 
from thrombosis of the fem- 
oral artery. It may also 
occur in the course of ex- 
ophthalmic goitre. 
More rarely gangrene of 
the feet and hands follows 
embolism due to valvular 
cardiac disease. It is usu- 
ally a moist gangrene, ex- 
tremely painful, and septic 
fever may ensue. 
In this connection men- 
tion may be made of ‘ ‘ Ma- 
dura Foot/7 or mycetoma, 
a chronic local disease of 
tropical climates and called 
“fungus foot disease” in 
India. A small tumor de- 
velops ou the foot or hand, which, after the lapse of twelve to twenty- 
four months, bursts and leaves several sinuses from which escape 
black particles or whitish-red bodies like fish-roe. The disease may 
spread all the way up the leg. The pale particles in the discharge 
look like actinomyces. 
Alterations in the appearance of the tibiae or shins often give us 
a clear idea of the presence of late syphilis, either because of gum- 
matous swellings in this neighborhood or owing to the development 
of periosteal thickening and exostoses. 
Fig. 57. 
Tabetic ulcer. (Shingj.eton Smith.) PLATE I. 
FIG. I, 
Chart of Localization of Cortical Centres determined on External Surface of Cerebrurn. (Gray.) 
FIG. 2. 
Chart of Localization of Cortical Centres determined or> Medial Surface of Cerebrum. (Gray.) CHAPTER I V. 
HEMIPLEGIA. 
Having considered the manifestations of disease as seen in the 
arms and legs in connection with monoplegia and paraplegia, 
spasm and contracture, we must now study the diagnostic meaning 
of hemiplegia, or that form of paralysis which involves the arm and 
leg and head on one side of the body. This form of paralysis, 
when complete, is always due to a lesion arising above the spinal 
cord—that is, it is cortical or due to lesions in the lower tracts of 
the brain; and the character of the paralysis, the association of 
other symptoms with it, and the history of the patient and his ill- 
ness, will render a diagnosis easy as to the approximate site of the 
lesion in most cases. The most common causes are hemorrhage 
into the cerebral tissues from a ruptured bloodvessel, or embolism 
or thrombosis of some vessel supplying important areas. Still 
other causes of hemiplegia are brain-tumors, meningeal hemorrhage, 
degenerative processes, and hysteria. 
Before we enter into consideration of the various symptoms re- 
sulting from central nervous lesions it is well to stop for a moment 
for the purpose of clearly understanding the anatomy and physi- 
ology of the parts involved, in order that we can properly study the 
results of lesions in the nerve-centres or nervous tracts. 
It is not necessary to remind the reader that the brain is divided 
into three areas, the frontal area being concerned with intellection, 
the middle area with motion, and the posterior area with sensation 
and special sense. These areas are again divided into subareas, 
each of which governs or is connected with several functions, and 
still further subdivisions exist, in which reside the centres govern- 
ing small areas, as, for example, a single muscle or group of muscles. 
(Figs. 1 and 2, Plate I.) Disease of any part of the brain surface, 
therefore, modifies more or less the function of that part and the 
part of the body tributary to it. Beneath the surface, through the 
so-called white matter, various fibres pass, which carry to or from 
the centres in the cerebral cortex the impulses connected with their 128 
THE MANIFESTATION OF DISEASE IN ORGANS. 
function, and these fibres approximate one another more and more 
closely in the lower part of the brain until they form a bundle 
Fig. 58. 
Diagram showing the fibres from the cortex forming the corona 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 spi nal cord, and the direct or uncrossed tract. 
Finally it also shows the secondary degeneration which occurs after cerebral hemorrhage or 
softening, and which follows the course of the motor tracts into the spinal cord. H. Site of 
lesion. The continuous lines are fibres going to the legs, the dotted are those going to the 
arms and motor cranial nerves. (Modied from Van Gehuchten.) HEMIPLEGIA. 
129 
Fig. 59. 
Outline of horizontal section of hrain, to show 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. 0 T, optic thalamus, showing the median, lateral, and anterior 
nuclei; N L, nucleus lenticularis, showing the putamen large, and the inner division of the 
globus pallidus very small; N C, nucleus caudatus, the large head in front of, and the dimin- 
ishing tail near the thalamus; G the kuee 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 move- 
ments with which they are concerned : thus Eye, movements of the eyes; Head, of the head ; 
Tongue, of the tongue ; Mouth, of the mouth; Shout, 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 pyram- 
idal 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 claus- 
trum, the cortex of the island of Beil, and the operculum or convolution overlapping the 
island of Reil. P is inserted to show which is the hind part of the section. 130 
THE MANIFESTATION OF DISEASE IN ORGANS. 
(corona radiata). Thus we see in 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 inter- 
nal capsule. This is a lateral view. In Fig. 58, which also shows 
Fig. 60. 
(After Gray.) 
the results of a lesion in the capsule, we get an antero-posterior view. 
These fibres are arranged in sucli a way that those arising from the 
lower part of the cortex, as in the face-centre, lie nearest the knee 
of the capsule, and those highest, furthest from this point. (Fig. 
59.) After the motor fibres have passed through the internal cap- PLATE II. 
Diagram showing Course of Motor Fibres from the Cerebrum and Cord 
to the Periphery. (Flatau.) HEMIPLEGIA. 
131 
side they pass into the crus cerebri of that side, which (the crus 
cerebri) connects the hemisphere of the same side with the cere- 
bellum 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. 60), diverge as 
they pass upward and outward to enter the under part of each hemi- 
Fig. 61. 
Diagram showing the general arrangement of the motor tract and the effect of lesions at 
various points. (Ormerod.) 
sphere, 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 132 
THE MANIFESTATION OF DISEASE IN ORGANS. 
from the face and tongue centre, which pass to the opposite side 
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 con- 
tinue on down to the medulla oblongata, where they form the so- 
called pyramids, and having done so most of the fibres cross to the 
Fig. 62. 
Showing the mechanism of different 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 opposite side. In a lesion 
at H the hypoglossus would be affected on one side, with hemiplegia on the other. (Modified 
from Edinger.) 
opposite side of the spinal cord (the crossing of the pyramids), and 
so form the crossed or lateral pyramidal tracts. (Fig- 58.) A 
smaller number of fibres, however, pass directly down to the spinal 
cord from the medulla oblongata, and form what is called the direct 
or anterior pyramidal tract. Direct, because it does not cross; ante- HEMIPLEGIA. 
133 
rior, because it lies along the edge of the anterior fissure of the cord; 
pyramidal, because it comes down from the pyramid. This is some- 
times called Turck’s column. (Fig. 58.) 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. 61, a clot at the arm-centre would only involve the arm-fibres. 
Fig. 63. 
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 ot 
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 impulses 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 of 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 Tfirck, or direct anterior pyramidal tract, which carries impulses ot 
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 widespread 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. 61 and 62 lesion A.) If the lesion be situated 134 
THE MANIFESTATION OF DISEASE IN ORGANS. 
in the pons on one side, it will cause facial paralysis on that side 
and hemiplegia on the opposite side of the body, because, as shown 
in the diagram (Figs. 61 and 62 M), it will, under these circum- 
stances, 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. 63. 
Fig. 64. 
Diagram oi the arteries of the base of the brain, showing L.O., the lenticular optic, and L.S. 
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 posterior. B.A. Basilaris with median 
branches. (7.6.s. A. Cerebralis superior, c.i. Cerebelli inferior. C.p. A. Cerebralis posterior 
(profunda cerebri). Com. p. A. Communicantes posteriores. C.a.i. Carotis interna, o. A. Oph- 
thalmica. C.m. A. Cerebralis media (A. fossse Sylvii). i. A. Insularis. cst. A. Corp. striati. 
C.a. A. Cerebralis anterior. Com. A. Communicans anterior. C.c.a.ll. A. Corp. callosi. 
(Dercum.) 
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 vessel. The skin-reflexes are apt 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 accident 
there may be vesical and rectal incontinence. The mental disturb- 
ance usually amounts to a rapidly oncoming unconsciousness in 
hemorrhagic hemiplegia. HEMIPLEGIA. 
135 
The question of the location of the lesion is very important. In 
the great majority of cases it is situated above the point at which 
the decussation of the motor fibres takes place in the medulla, and 
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 capsule, owing to the fact that the 
middle cerebral artery in one of its lenticulo-striate branches per- 
forates the internal capsule, and ends in the caudate nucleus, and 
this artery is so commonly ruptured that Charcot has called it the 
“artery of cerebral hemorrhage.” (Fig. 64.) If the hemorrhage 
does not involve the posterior third of the internal capsule, there 
are no sensory symptoms associated with the motor loss, but the par- 
alysis will be practically 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. 59.) The symptoms 
associated with hemiplegia due to this cause often become very 
severe because the hemorrhage is so profuse that the lateral ven- 
tricles 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 somewhat cyanotic, may be present. Recovery never 
occurs, for the secondary 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 only 
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. 
Finally, 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 protruded 
may tend to go over to one side. If the case does not pass to such 
favorable results, iustead of recovery of power at this time there are 
developed contractions and secondary rigidity from degenerative pro- 
cesses extending to the pyramidal tracts. (See Fig. 58.) Hitzig has 
shown that these conditions are apt to be least marked in the morn- 136 
THE MANIFESTATION OF DISEASE IN ORGANS. 
mg. 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 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 hemianaesthesia, 
attended at first with no loss of consciousness, but in a day by 
unconsciousness and coma, he is suffering from what has been called 
“ ingravescent apoplexy.” The hemorrhage, under these circum- 
stances, begins in the knee of the internal capsule, proceeds back- 
ward 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 probably 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 
opposite side of a well-marked type, associated with early rigidity 
of the paralyzed side, conjugate deviation of the eyeballs, very 
marked rise in bodily temperature, a contracted pupil, and convul- 
sions, 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. 61 and 62.) If both sides of the face are 
paralyzed with hemiplegia elsewhere, the lesion is in the pons where 
the facial fibres cross. Pons paralysis is nearly always associated 
with giddiness, vomiting, conjugate spasm with nystagmus, albu- 
minuria, glycosuria, and marked disturbances in the respiration and 
heart. Pontile hemorrhages are, however, very rare, and usually 
are rapidly fatal. 
Finally, if there is hemiplegia involving the lower part of the HEMIPLEGIA. 
137 
face, the arm, and the 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 sensi- 
bility 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 par- 
alyses have been simultaneous in occurrence, as it is possible for 
one lesion in one place to produce paralysis of the face and another 
elsewhere to produce 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 hemianaes- 
tliesia (see chapter on Skin), and hemianopsia (see chapter on Eye). 
Generally, however, such changes result from a thrombosis. 
When 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 coma, con- 
tracted pupils, vomiting in many of the cases, and finally death 
when hemorrhage breaks into the lateral ventricle. The diagnosis 
of cerebellar hemorrhage is very difficult. 
Of the irregular forms of hemiplegia there are several. Sometimes 
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 
paralyzed leg and arm, with hemianopsia and aphasia. Such symp- 
toms 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. WThen the arm 
suffers most the symptoms just described as in the leg are seen in 138 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 inferior 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 
already said, from embolism or thrombosis of the cerebral vessels 
as well as from hemorrhage from them. How are we to separate 
the hemiplegias of hemorrhage and occlusion ? In many cases this 
is impossible, 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 prob- 
ably 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, but a patient may have both thrombosis and apoplexy. 
In hemorrhage, consciousness is generally lost, whereas in throm- 
bosis it is often only dimmed. Vomiting and contracted pupils 
from pressure on the lower centres indicate hemorrhage, while their 
absence may point to thrombosis. Finally, the general systemic 
shock and febrile movement are apt to be greater in hemorrhage 
than in thrombosis. The history of syphilitic infection, producing 
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 
presence of chronic or ulcerative endocarditis or their results, or 
other cause for the formation of emboli, aids the diagnosis. AVliere 
the cause is embolism the onset is sudden, whereas in thrombosis it 
is sometimes more gradual. The paralysis from embolism is more 
commonly 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 HEMIPLEGIA. 
139 
at first the side of the face has been paralyzed, then the arm and 
then the leg, and that the complete loss of power has not been 
sudden but 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 
medication, presents few characteristic signs. The presence of in- 
tense 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 cerebral sclerosis of one 
hemisphere (not multiple sclerosis), in which the most constant 
symptoms are, in addition to the paralysis, evidences of motor irri- 
tation, such as epileptoid convulsions of a bilateral or unilateral 
character, rhythmical or arhythmical twitchings of the muscles like 
chorea, and dementia. 
Hemiplegia may also arise from hsematoma of the dura mater. 
The symptoms, aside from the paralysis, are headache, stupor, 
irregular pulse, vomiting, and contracted pupils, or, in other words, 
symptoms of cerebral compression. Sometimes twitchings 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. Similar symptoms, too, may 
arise in the course of Raynaud’s disease. 
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 
nystagmus, and the very excessive reflexes aid us in the diagnosis 
of this cause of the loss of power. 140 
THE MANIFESTATION OF DISEASE IN ORGANS. 
A form of hemiplegia which is often very misleading is that 
occurring in general paralysis of the insane or paretic dementia. 
In this disease the patient often has attacks of vertigo, unconscious- 
ness, 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 
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. 
In this condition we should not forget the possibility of hemi- 
plegia or monoplegia occurring with suddenness in the course of 
renal disease with uraemia. The paralysis may be permanent or 
only transient, but the urine will be found to be albuminous, and 
the other signs of renal disorder may be manifest. 
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 before 
they cross, and the others after they have crossed. (See chapters 
on Hands and Arms, 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 
hypertrophy 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 
various 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 
papillae, which are thickly distributed over the anterior two-thirds 
of the tongue on its upper surface. These papillae give the peculiar 
roughness which is so characteristic of this surface, and occur in 
three forms, namely, the circumvallate or large papillae, the fungi- 
form 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 papillae, which cover 
the anterior surface of the tongue, are very minute, and arranged in 
lines corresponding in direction with the two rows of the circum- 
vallate papillae. From their apices project many fine, filiform pro- 
cesses, which are of a whitish tint owing to the density of the epi- 142 
THE MANIFESTATION OF DISEASE IN ORGANS. 
theliiun of which they are composed. There are, in addition, many 
simple papillae which cover the surface between the peculiar ones 
already described. It is the fungiform papillae which are seen most 
commonly in cases of disease, for they become large and promi- 
nent, and because of their red color show through 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 
appearance are due to mere superficial coatings or fur, which con- 
sist of dead epithelial cells, micro-organisms of many kinds, and 
abnormally 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 par- 
ticular disease any one coating or fur may be has been warmly dis- 
cussed. 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 diag- 
nosis of disease in other organs cannot be based upon the appear- 
ance 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 the 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 circum vallate papillae 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 character of the 
epithelium in different parts, and to the fact that the tip and sides 
are generally scraped clean by the movements of the tongue. Fur- 
ther, it should be remembered that the development of coating, aside 
from digestive arrangements, depends chiefly on three factors : first, 
immobility of the tongue, so that it is not 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 secre- 
tion. Additional local causes are a decayed or ragged tooth or follic- 
ular tonsillitis, which infects the lingual epithelium, lack of clean- PLATE HI. 
Fig. 1. 
Fig. 2. 
Typhoid Tongue. 
Bilious Tongue, with Yellow Coating. 
Fig. 3. 
Fig. 4. 
Tongue of Mucous Disease or Chronic 
Catarrh of Stomach. 
Tongue of Chronic Gastric Catarrh 
with Anemia. THE TONGUE, MOUTH, AND PHARYNX. 
143 
liness, and habits, such as smoking. In the last class of patients, 
the smokers, a heavily coated tongue in the morning is very 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 coating associated with 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, Avliich increases 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 convalescence is established; but if the disease runs 
a severe course, the coating becomes very heavy, more dry, rough 
and brown from exposure to air and medicine. The furred appear- 
ance becomes almost shaggy at the back portion, and the drying 
proceeds until the underlying epithelial layer is cracked and fissured, 
so that tiny exudations of blood add to the lingual discoloration. 
The reddened edges become dusky in hue, and may be cracked and 
fissured also. (Eig. 1, Plate III.) The tongue is very slowly pro- 
truded 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 pro- 
truded is often markedly tremulous. Toward the close of the attack 
the tongue cleans off through exfoliation of the dead epithelial accu- 
mulation, 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 coatings 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 144 
THE MANIFESTATION OF DISEASE IN ORGANS. 
cases, because, as Fothergill asserts, the coat has been stained by the 
tauro-cholic acid eliminated by the salivary glands. The circum- 
vallate papillae are often prominent 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 child 
—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 leptothrix in threads and tufts often spreads 
over the tongue, particularly in the region of the circumvallate 
papillae. The growth may be quite dark in color, but it is sepa- 
rated from the exudate of diphtheria by microscopic study and the 
absence of systemic disturbance. 
Sometimes on examining the 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 
which 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 papillae. Such a tongue is typical of what 
has been called, by Eustace Smith, “ mucous disease,” a condition 
in which 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 surface, but are 
very numerous, and the patient is a child, the diagnosis may be 
made of acute or subacute gastric catarrh. (Fig. 4, Plate III.) 
The so-called strawberry tongue is one in which the organ is at 
first covered by a thick whitish coat, through which project the 
fungiform papillae, which have been deprived of their epithelial THE TONGUE, MOUTH, AND PHARYNX. 
145 
covering, and being swollen or enlarged stand out prominently. 
The edges of the tongue are usually red and bare of coating, and 
in these edges the fungiform papillae are also enlarged. As the 
disease progresses the coating is lost from all over the entire organ. 
This appearance of the tongue is seen commonly in scarlet fever, 
but is not, as has been thought, pathognomonic of that disease. 
The fungiform papillae in the strawberry tongue of scarlet fever 
are, however, particularly prominent and erect. 
When the tongue is excessively furred or rough in appearance, 
the coating is due to abnormally long and projecting papillae cov- 
ered by an excess of living and dead epithelial cells; it may denote 
grave disease of the viscera, but in rare instances possesses no diag- 
nostic importance, unless coupled with other symptoms. This 
tongue is sometimes seen in scrofulous children in whom strumous 
manifestations 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 the tongue 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 
ragged tooth, or to hemiplegia, which prevents that side of the 
tongue from being 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 146 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
has been thought, but from overgrowth of the epithelium with the 
deposit of a black pigment of unknown origin. Usually this 
brownish-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 inges- 
tion of laudanum or rhubarb. 
The color of the tongue itself, aside from discoloration of its 
epithelium, is an important diagnostic aid. It is exceedingly pale 
in all forms of anaemia, particularly those due to lack of haemo- 
globin, 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 oxidation of the blood, or in cardiac disease with similar diffi- 
culty. 
Purple spots, which may be almost black, may be present on the 
tongue 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 papillse at the base are unusually large. 
When sulphuric acid has been swallowed the tongue has a parcli- 
ment-like appearance, is at first white and then gray or brownish- 
gray, and finally is covered by a black slough, which as it separates 
leaves a swollen, excoriated patch. In nitric- and chromic-acid- 
poisoning 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 the mucous 
membrane is shrivelled and puckered into folds. The spots where 
the acid has touched are brownish if impure acid has been swal- 
lowed, or white if the pure acid has been taken. In the course of THE TONGUE, MOUTH, AND PHARYNX. 
147 
a few hours this spot becomes surrounded by a red zone, and finally 
becomes dark brown or black in the centre. After oxalic acid is 
taken the tongue may be covered by a thick white coat and looks 
as if it had been scalded. Caustic potash and soda soften the 
mucous membrane, so that it is pulpy and easily detached, and looks 
pearly red or yellow in hue. When ammonia.is swallowed the color 
is white, but superficial oedema may make it pearly in appearance, 
and acid nitrate of mercury renders it very red. Cantharidal poison- 
ing produces large lingual blisters and sores. 
Aside from the coating and color of the tongue, its surface should 
be examined to discover fissures, cracks, ulcers, sloughs, and swell- 
ings. The tongue is often seen to be superficially and irregularly 
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 fur- 
rows are very deep, they may indicate the early stages of what Wun- 
derlich has called dissecting-glossitis, which in turn may be due to 
syphilis,1 although, as a rule, the fissures of the tongue due to syph- 
ilis are deepest at the edges of the organ, and are due to pressure 
by and from irritation from the teeth or to ulceration, and subse- 
quent cicatrization of small syphilitic nodules or gummata. The 
cervical glands are rarely involved in such cases. If only one ulcer 
is present, it may be chancre, which will have the peculiar Hunterian 
hard base, and, in such a case, the cervical glands will probably be 
enlarged. An epithelioma may also have an indurated base with 
secondary glandular enlargement. Lingual ulcers may also be 
present as the mucous patches of syphilis, or be due to wounds 
from the teeth, a broken pipe-stem, or a fork. When these become 
chronic their separation from those due to syphilis and tuberculosis 
is practically 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 syph- 
ilitic 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 
1 This is denied by Demarquay and doubted by Butlin. 148 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 involved. 
Both are more common in men than in women. The age of the 
patient, the presence of tubercular disease elsewhere, and the absence 
of induration point to tubercle. The tuberculous ulcer is not sur- 
rounded by much inflammation, 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, associated 
a specific history or manifestations of tuberculosis or syphilis else- 
where, render the diagnosis clear. 
An ulcer on the frsenum 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 ad- 
vanced 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 purpuric 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 
suffering from the early stages of glossodabio-pharyngeal paralysis.1 
The surface of the tongue may be attacked by various eruptions, 
such as measles, variola, eczema, herpes, erysipelas, pemphigus, 
1 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. THE TONGUE, MOUTH, AND PHARYNX. 
149 
zoster, or hydroa, and from the rupture of the vesicles or bulhe 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 
tympani along the under border at the side. 
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 
ulcerated, 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 u 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 leucoma or ichthyosis, and this may arise from smoking 
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 
buccalis is difficult, if not impossible. The plaques are most com- 
monly seen in males between twenty and forty years. Closely 
allied to this is the rare condition of hardening of the tongue due 
to scleroderma, 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 150 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
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 impeti- 
ginosa. 
GSdema of the tongue, with the development upon it of vesicles, 
and, finally, sloughs, may occur, aud is probably identical with the 
foot-and-mouth disease of domestic animals. 
Bilateral atrophy of the tongue is due to disease affecting the 
hypoglossal nerves in some part of their course 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 shriv- 
elled aud atrophied in patches, and in the later stages of the 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 in- 
volving the hypoglossal nerves may so result (see Paralysis of the 
Tongue). 
In cases where the tongue is much enlarged the increase in size 
may be due to malignant growth, to macroglossia, which is a form 
of congenital lymphangioma, inflammatory hypertrophy, and syph- 
ilis, or acute inflammation from irritant poisons or foods. It mky 
also be due to dermoid cysts, fibroma, lipoma, papilloma, angioma, 
myxoma, osteoma, and enchondroma. When it is due to acute glos- 
sitis the organ is seen to be several times its normal size, is pro- 
truded from the mouth, and marked by the pressure of the teeth. 
The organ is also clumsy and stiff, and heavily coated on the back 
portion. There is a profuse flow of saliva, and swallowing and 
speech are almost impossible. Glossitis may also be due to mercu- 
rialism, to septic infection, and may be either unilateral or bilateral. 
The tongue maybe greatly enlarged by actinomycosis, this condition THE TONGUE, MOUTH, AND PHARYNX. 
151 
in olden times being called angina Ludovici. Great enlargement 
of the tongue may also arise in acromegaly and in myxoedema. In 
the latter disease the organ is broad, flat, and soft. 
The movements of the tongue depend upon its innervation and 
its muscles, and afford valuable information in diagnosis. The 
rapidity of its protrusion in nervous and excitable persons when 
they are asked to show the tongue is noteworthy, and its constant 
rolling is often seen in persons who are feeble-minded. In all dis- 
eases associated with mental hebetude its protrusion on request is 
very slow, although 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, uraemia, and cerebral congestion, 
this condition obtains, 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 move- 
ments, he may be suffering from the disease known as glosso-labio- 
pharyngeal 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 diag- 
nosis is to be made under these circumstances, for in the false 
disease it does not waste or develop the reactions of degeneration, 
wdiereas 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 de- 
scribed of hemiatrophy. The lesions of the hypoglossus which pro- 
duce paralysis may be of cortical origin (unilateral), in which case 
the hemorrhage or other injury may be situated where the middle 
and inferior frontal convolutions form the anterior central convo- 152 
THE MANIFESTATION OF DISEASE IN ORGANS. 
lution,1 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 hypoglossal fibres outside the medulla through men- 
ingitis 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 of the first cervical vertebrae, 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 hemi- 
atrophy of the tongue 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 the 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 side 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 pons 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 probably nuclear, because the nuclei are so closely situ- 
ated 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 appear very late. 
A tremor seen in the tongue may indicate a variety of nervous 
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 TONGUE, MOUTH, AND PHARYNX. 
153 
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 tongue 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 tongue is moved to and fro or protruded. 
In typhoid fever the tremor occurs on movement, whereas in 
glosso-labio-pharyngeal paralysis when the mouth is open fibrillary 
movements of the organ are often marked, while the organ lies in 
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 associatd 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, 
particularly 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 paralysis 
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, and in that they are pre- 
ceded 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 irritation of the fifth nerve from lingual neuralgia. 
In that very rare condition called “ Thomsen’s disease,” “ char- 
acterized by tonic spasms in the muscles during voluntary move- 
ments,” the tongue may be involved, but in this case the other 
voluntary muscles will share in the affection. 154 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
discussed 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 
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 
inflammation 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, particularly 
in the small of the back, quite high 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 
forward of the angle of the jaw, and pressure upon them may pro- 
duce considerable pain. If the mouth is well opened and the tongue 
depressed, there will be found on each side of the throat a more or 
less projecting and inflamed mass, in the depressions or follicular THE TONGUE, MOUTH, AND PHARYNX. 
155 
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 
resembles the membrane of diphtheria. Pressure on the tonsil may 
cause the further projection of these cheesy-looking masses. 
In the suppurative 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 follicular 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 behind it, and it has not the dusky, dirty look of diph- 
theritic membrane. Again, in tonsillitis the exudate is seen on the 
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 ex- 
amination of the throat in scarlet fever shows the intense redness of 
the pharyngeal mucous membrane with comparatively slight enlarge- 
ment of the tonsils. The intense redness of the throat in scarlatina 
and the development of the rash on the skin aid in making a differ- 
ential diagnosis. 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 pharnyx 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 and 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 
many of the cases of scarlet fever which in their early stages present 
a membranous pharyngitis or tonsillitis are due to the streptococcus 
and not to the Loeffler bacillus, in the later stages of the disease 
the Loeffler bacillus is the cause of the local lesion.' The differ- 
entiation is to be made chiefly by bacteriological tests, but it is worthy 
of note that the early formed streptococcic membrane does not 
spread as does the diphtheritic membrane, and does not return so 
rapidly when removed. The two diseases, diphtheria and scarlet 
fever, exist simultaneously. Rarely a false membrane due to strep- 156 
THE MANIFESTATION OF DISEASE IN ORGANS. 
tococcus infection, or still more rarely to the diphtheria bacillus, 
complicates the course of typhoid fever, and also occurs as a grave 
complication of measles. 
If in any case of diphtheria the false membrane extends to the 
nasal chambers, the prognosis is very unfavorable. 
Ordinary sore throat or acute pharyngitis is generally accompa- 
nied with little systemic disturbance, the local pain and soreness 
being the most characteristic symptoms. Inspection will show the 
pharyngeal 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. 
Koplik asserts that this eruption on the pharyngeal mucous mem- 
brane is not characteristic. With this we cannot agree. He also 
asserts that an eruption appears on the buccal mucous membrane 
which precedes the eruption on the skin, and is characteristic before 
the skin eruption appears. It loses its peculiarities as the skin be- 
comes involved and merges into a more diffuse redness, which entirely 
disappears before the skin has returned to its normal state. The 
buccal eruption consists in small, irregular red spots with a bluish- 
white centre, and should be looked for in a good light. Koplik 
believes that these spots are absolutely characteristic. They are to 
be separated from the reddened mucous membrane of scarlet fever, 
the large, white spots of thrush, and the sore mouth of stomatitis. 
They do not appear in rotheln. 
Pigmentation of the buccal mucous membrane often occurs in 
Addison’s disease. 
Sometimes cases are seen in which there are tonsillar pain and 
irritation, and 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 swollen or 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 suf- THE TONGUE, MOUTH, AND PHARYNX. 
157 
ferers 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. 65. 
The staining of teeth by tobacco or other materials held in the 
month may reveal certain habits of the patient, and a blue-line 
on the gums where they join the teeth is an indication of the 
presence of chronic lead-poisoning. Loosening of the teeth with 
bleeding, spongy gums should call to the physician’s mind the pos- 
sibility of scurvy or scorbutus, and the spongy gums are particularly 
indicative of this affection in bottle-fed babies. If loosening of the 
teeth occurs in adults, it may be due to mercurial salivation. 
Hutchinson teeth. CHAPTER VI. 
THE EYE. 
The general diagnostic indications afforded 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 intimaitely connected with the government of its movements 
and its special functions, but in addition we often gain positive in- 
formation as to the condition of organs more remotely situated, as, 
for example, the kidneys. The very fact that so many different 
tissues are found in this organ renders it susceptible to the many 
diseases affecting similar tissues elsewhere in the body. 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 additional evidence indicating the general systemic con- 
dition. Cataract should make the physician suspect diabetes, even 
if it appear in persons advanced in years. The eyelids, if puffy in 
appearance, may indicate renal disease, cardiac lesions, or the over- 
use of arsenic (see chapter on the Face). An examination of the 
inner side of the lids may reveal a pallor due to anaemia. Slight 
conjunctival hemorrhage may result from violent coughing. In old 
persons such a hemorrhage, if not due to injury, may indicate degen- 
erative vascular changes. 
Prominence of the eyeball or exophthalmos is seen as an almost 
constant symptom of true goitre, which for this reason is called 
exophthalmic goitre. (See Figs. 11 and 12.) Associated with the 
bulging eyeball we fiud 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 THE EYE 
159 
insomnia. In well-marked or advanced 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, “ Stellwag’s symptom.” 
Or, again, there is insufficiency of convergence, so that a near point 
cannot be seen with both eves at once (Moebius’s sign). 
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 
below the cornea, it is a true arcus senilis, and is said to indicate in 
some cases fatty degeneration of the tissues of the body. The one is 
an annulus senilis, the other an arcus senilis, and the arcus is the 
change worthy of note, although many clinicians, including the 
author, deny that either has any significance. 
An examination of the pupil may reveal that it is immobile from 
an old plastic iritis, due to syphilis or rheumatism, but it is not to 
be forgotten that this condition may arise from iritis due to purely 
local causes. A widely dilated pupil may indicate the use of some 
mydriatic or the ingestion of atropine. It is also seen in fright, in 
some hysterical seizures, and in glaucoma and whenever the vision 
is lost, unless it be contracted by disease of the iris. A contracted 
pupil indicates the use of a myotic or the existence of central nerv- 
ous disease, such as ataxia, which causes the Argyll-Robertson pupil 
as well. Sometimes corneal inflammation by causing photophobia 
may cause excessive myosis. Pin-point pupils may also result from 
the use of opium or its alkaloids, and serve to differentiate the condi- 
tion from true coma, in which the pupils are usually dilated. If, how- 
ever, the coma be due to cerebral inflammation or meningitis, the 
pupils may be contracted; or if it be due to intracranial pressure, 
they are usually dilated. (See Paralysis of the Intraocular Muscles.) 
In addition to these objective symptoms we 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 pupil and in the 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 
subjective in nature, namely, diplopia or double vision and partial 
or complete blindness. 160 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Diplopia depends upon the fact that in an eye in which the 
muscles 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 appears 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 impression made on the well eye is the “ true image,” as it is 
called, and that in the diseased eye is called the u false image.” 
Any cause which interferes with the fixation of each eye on the 
same point produces 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 ordinarily a constant sign of ocular muscular paralysis; but if 
only weakness or insufficiency of a muscle is present, diplopia may 
never be a symptom recognized by the patient. The forms of dip- 
lopia—that is, the position of the false images in respect to the true 
images—vary with the muscles affected, and will be studied in a 
moment when paralysis of the muscles is tested for and their diag- 
nosis discussed. It only remains at this place, therefore, to point 
out the probable significance if a patient with diplopia presents 
himself to a physician. 
Thus, a patient with diplopia may be suffering from a lesion in 
the cerebral cortex, such as hemorrhage, sclerosis, or softening; or 
from a lesion in the cranial nerve nuclei, in the pons or corpora 
quadrigemina, or in the fascicular fibres. Again, diplopia may arise 
from lesions at the base of the brain, as meningitis, tubercular or 
syphilitic, or from injury to the nerves in the orbit or in their 
peripheral endings. As a result, we find diplopia as a symptom of 
any disease which may affect these parts, and it is quite a common 
symptom in locomotor 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, coniurn, and gelsemium, owing 
to their effects on the ocular nerves. THE EYE. 
161 
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 
functions will be discussed first in the present chapter.1 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 
understood 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 main- 
tain 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 tilings in origin, symptoms, course, and prognosis. A 
concomitant squint is a wrong relation in the visual axes, so that 
they do not intersect in the point looked at; but there is no marked 
limitation of the movements of either eye in any direction. Be the 
direction of the eyes what it may, the squint remains practically 
unchanged. 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 
1 la 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. 162 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
function, and deviates more as greater effort is required. The de- 
gree of squint and of separation of the double images it causes varies 
with the direction in which the eyes are turned, there being 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 
object is then gradually brought nearer and nearer to him, and the 
eyes of the patient necessarily converge more and more as it ap- 
proaches the nose. Normally the eyes will be co-ordinately con- 
verged when the object is only three and a half inches from them; 
but if any weakness or insufficiency of one interims is present, the 
eye on that side will deviate or fail to converge before this point is 
reached. 
Again, a fine point like a pin-point is held at 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 once springs back into place for the purpose 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 insufficiency, as measured by prisms” (Ran- 
dall). If the interims 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 simplest, apparatus for testing the func- 
tional balauce of the ocular muscles is the rod-test of Maddox. 
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 horizon- 
tally 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 THE EYE. 
163 
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. 66.) 
Fig. 66. 
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 line 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. 67.) 
Testing of this kind refers to the insufficiencies and not to the 
palsies of the ocular muscles. 
The importance of being able to demonstrate these minor failures 
in the ocular muscles by these means lies in the fact that in this 
manner headaches due to muscle eye-strain may be remedied by 
removing their cause by properly fitted glasses, or by gymnastic 
exercises with prisms, or in some cases by tenotomy. 
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  THE MANIFESTATION OF DISEASE IN ORGANS. 
164 
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 
between the nucleus and the eye, or in the orbit or nerve-endings. 
Fig. 67. 
Maddox’s rod-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 be- 
longs to the left eye—right hyperphoria. C. The line passes above the flame. The upper 
image belongs to the right eye—left hyperphoria, (de Schweinitz.) 
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 points in each retina. This diplopia 
becomes more and more marked as the object is moved toward the 
side on which the paralyzed muscle lies. Strabismus, which may 
•or may not be constant, usually develops when the patient endeavors 
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 erro- 
neous localization of the objects in the field of vision. Altered car- 
riage of the head, due to the fact that the patient tries to turn his 
head in the direction in which he is least troubled by double 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 is 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 THE EYE. 
165 
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 distinguish 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 affected muscles, no diplopia being present if 
Fig. 68. 
Paralysis of left aMucens in a case of hemiplegia of syphilitic origin. (Dercum,) 
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 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 and 
at the level of his eyes, the double images of two candles will 
appear as in Fig. 69, if he has complete paralysis of the external 
rectus or internal squint of the left eye; while if the right external 
rectus is paralyzed, the images will appear as in Fig. 70. Further, 
if the object is moved to the right in the first condition, the false 166 
THE MANIFESTATION OF DISEASE IN ORGANS. 
and the 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 diplo- 
pia, because the word homonymous indicates that the false image 
is seen on the same side as the eye affected. 
Fig. 69. 
Fig. 70. 
The false image is in outline, (de Schweinitz.) 
If, on the other hand, the false image is found to the right of the 
true one, as in Fig. 71, the internal rectus of the left eye is paral- 
yzed, and causes an external squint if the paralysis is complete; 
and if the same muscle of the right eye is affected, the false image 
will also be to the left side of the true one. (Fig. 72.) Further, 
if the object is moved to the right in the 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 ou the right 
side. 
Fig. 71. 
Fig. 72. 
Fig. 73. 
Fig. 74. 
The false image is in outline, (de Schweinitz.) 
Supposing, again, that the images are seen as in Fig. 73, then the 
left superior rectus is involved (downward squint); while if they 
appear as in Fig. 74, 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. 
If the images appear as in Fig. 75, the left inferior rectus is THE EYE. 
167 
affected ; or if as in Fig. 76, the right inferior rectus muscle. This 
is also crossed diplopia, chiefly in the lower field, because the inferior 
rectus muscle rotates the eyeball downward. 
Fig. 75. 
Fig. 76. 
The false image is in outline, (de Schweinitz.) 
Again, if the images appear as in Fig. 77, the left inferior oblique 
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. 
78. There is a homonymous diplopia most marked in the upper 
field. 
If due to paralysis of the left superior oblique, the images appear 
as in Fig. 79; and if, as in Fig. 80, the right is affected. There is 
an upward and inward squint, and there is a homonymous diplopia 
chiefly in the lower field. 
Fig. 77. 
Fig. 78. 
Fig. 79. 
Fig. 80. 
The false image is in outline, (de Schweinitz.) 
Finally, if there is divergent squint with failure of movement in 
all directions, except outward and slightly downward, and there are 
ptosis, moderate mydriasis, and paralysis of accommodation, there 
are oculomotor paralysis and crossed diplopia. 
The following table of Hotz (.International Clinics, 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. 168 
THE MANIFESTATION OF DISEASE IN ORGANS. 
a. Images separating to the right indicate paralysis of the extern us 
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 intern us. 
a. 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 lower means paralysis of the inferior oblique 
of the left eye. 
2. Crossed images indicate paralysis of the superior rectus. 
a. Image of right eye higher 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 lower field indicates paralysis of the 
inferior rectus or superior oblique. 
1. Homonymous images indicate paralysis of the superior ob- 
lique. 
a. Image of the right eye higher means paralysis of the superior 
oblique of the left eye. 
2. Crossed images indicate paralysis of the inferior rectus. 
а. Image of the right eye lower means paralysis of the inferior 
rectus of the right eye. 
б. Image of the right eye higher means paralysis of the inferior 
rectus of the left eye. 
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 muscles 
are defective, we must determine the diagnostic indications presented 
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 one of THE EYE. 
169 
several places. Thus it may arise in hemorrhage, sclerosis, and 
softening of the cerebral cortex, in which case the other symptoms 
of lesions in 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,1 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 hemorrhages among the nuclei, or from an acute 
hemorrhagic polioencephalitis in the fourth ventricle, arising 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, carbonic acid, 
or such diseases as diabetes, syphilis, and epidemic influenza. Some- 
times acute ophthalmoplegia comes on with acute poliomyelitis 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 unsymmet- 
rical, and it occurs after acute ophthalmoplegia, as a congenital 
defect producing bilateral ptosis (see chapter on Face), as an acquired 
disease in childhood and adult life, and in conjunction with loco- 
motor ataxia, paretic dementia, disseminated sclerosis, progressive 
muscular atrophy, 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 resnlt of middle-ear disease, and anaemia. It 
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 both ways is correct, it is better to 
confine its usage to nuclear and complete lesions. 170 
the manifestation of disease in organs. 
may also arise as the result of obliterating arteritis, 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 frac- 
tures of the orbit; or, again, there may be disease of the frontal 
sinus. If the lesion is distinctly peripheral, it may be due to rheu- 
matism (when the external rectus is commonly affected), neurasthe- 
nia, or it may arise from uric-acid diathesis and gout. Further, 
such lesions may be due to influenza, diabetes, diphtheria, lead and 
alcohol, 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 paralytic 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 abducens, or sixth nerve, which 
arises from the pyramidal body close to the pons. (Fig. 81.) 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 clinoid process, enters the cav- 
ernous sinus, and, finally, enters the orbit through the sphenoidal 
fissure between the heads of the external rectus. If this form of 
squint is associated with hemiplegia of the opposite side of the body, 
the lesion 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. 
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 
place above the point where the tracts cross. Such a paralysis is, 
therefore, cortical. 
1 This refers to paralytic and not to concomitant squint. THE EYE. 
171 
If, again, there is complete unilateral paralysis of the abducens 
(internal squint), with loss of the associated action of the interims, 
the lesion is in the nuclei under the floor of the fourth ventricle, 
Fig. 81. 
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. Pv. 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. 
because 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. 82.) Complete paralysis of the 
externus may, therefore, be due to a nuclear lesion; for if the lesion 172 
THE MANIFESTATION OF DISEASE IN ORGANS. 
were above the nucleus, this nucleus might obtain collateral impulses, 
as seen in this diagram, and, therefore, the paralysis would be only 
partial. It may also be due to a peripheral lesion. Sometimes, 
however, an inflammatory 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 
Fig. 82. 
Diagram of the connections of the nucleus of the sixth nerve. (Brock.) 
from neurasthenia, uric-acid diathesis, gout and rheumatism, and 
in tubercular or syphilitic meningitis at the base, as already stated. 
It also comes on in some cases of diabetes, la grippe, and in chronic 
poisoning by lead and alcohol, or the acute poisoning of gelsemium, 
ptomaine-poisoning, conium- and spigelia-poisoning. 
Again, let us suppose that the internal rectus is paralyzed, causing 
external squint. We remember that it is supplied by the oculo- 
motor nerve, which arises from a nucleus in front of the corpora 
quadrigemina, which extends from the level of the posterior com- 
missure to a point near the nucleus of the fourth nerve or patheticus. 
(Fig. 81.) Landois states that the two nuclei (the third and fourth) 
are united. The nucleus of the oculomotor nerve has been divided 
into several groups, as shown in Fig. 83, after Bruce, where, how- THE EYE. 
173 
ever, it is seen that the third and fourth nuclei are not united. The 
nerve itself pierces the dura mater below the posterior clinoid pro- 
cess, 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 oculomotor nerve receives filaments 
Fig. 83. 
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, hi. r. Third nerve, m. Median nucleus, a. Anterior 
nucleus, interior part. Ai. Anterior nucleus, lower part of main nucleus. A2. Anterior 
nucleus, intermediate portion. a3. Anterior nucleus, upper portion, p.i. Postero-internal 
nucleus, p. e. Postero-external 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.1; iv.r.9, iv.R.3. The first, second, and third portions of the root respectively. (Bruce.) 
from the cavernous plexus of the sympathetic, and from the first 
division of the fifth nerve. In addition to divergent squint there 
are, as already pointed out in the last few pages, in oculomotor paral- 
ysis, as additional symptoms, ptosis, mydriasis, and paralysis of 
accommodation. The lesion producing unilateral ptosis may be 
found in the cerebral cortex on the opposite side from the affected 174 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 be- 
tween the cortex and the nuclei. There may be associated with 
this form of oculomotor paralysis loss of power in the hypoglossal 
and facial nerves. Ou 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 oculo- 
motor 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 inflammatory 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, isolated 
palsy of the fourth trochlear nerve, is present, we will probably find 
that the paralysis 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 presents himself with swelling 
of the eyelids, exophthalmos, a contracted, followed by a dilated, 
pupil, anaesthesia of the skin of the upper eyelid and of the temple, 
or the area supplied by the first division (ophthalmic) of the fifth 
nerve, and ophthalmoplegia—that is, paralysis of the extrinsic ocular 
muscles on one side—where will be the lesion productive of this 
train of interesting symptoms? It will be seen at once that such a 
condition is the result of paralysis of the oculomotor (third), pathetic 
(fourth), and abducens (sixth) nerves, and that as in all probability 
only one lesion has produced these symptoms it must exist at some 
point where all these nerve-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 THE EYE. 
175 
branches. The pathetic 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 cav- 
ernous 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, if in this area, may also 
produce a series of symptoms. 
The significance of conjugate lateral paralysis producing a devia- 
tion 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 (Prevost’s 
symptom)—that is, the “ patient looks at his lesion.’’ The reason 
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 deviation is caused by contraction of the internal rectus on 
one side (third nerve) and the external rectus on the other (sixth 
nerve), the mechanism of the deviation is clear. Thus if the lesion 
be a distinctive one on the left side of the brain, causing right hemi- 
plegia, the eyes will be turned to the left by the action of the unaf- 
fected 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 tumor), this deviation is 
reversed, because in this case 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, 176 
THE MANIFESTATION OF DISEASE IN ORGANS. 
and the eyes are therefore turned by the muscles which remain in- 
tact. In the second instance the eyes are turned toward the con- 
vulsed side because the internal and external rectus are spasmodic- 
ally 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 and description 
from Swanzy’s well-known book. (Fig. 84.) 
Fig. 84. 
1. Left ext. rectus. 2. Left int. rectus. 3. Right int. rectus. 
4. Right ext. rectus. 5. Nucleus left third nerve. 6. Nucleus 
right third nerve. 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 centres. 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 hemiplegia; and, 
since 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 pro- 
duce exactly the opposite effects. 
Squint which is due to hysteria is always caused by spasmodic 
contraction of the eye-muscle and is never due to paralysis, as 
it often 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 THE EYE. 
177 
or in a vertical or rotary movement, is usually bilateral.1 When 
not congenital it is a frequent symptom of disseminated sclerosis, 
Friedreich’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 dis- 
ease. Nystagmus 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. Having 
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 libres of the iris, circular and 
radiating, and the ciliary muscle. The nerve-supply of the 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 plexus, 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 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 Bunge in the spinal cord at about 
the seventh cervical or first dorsal vertebra. 
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. 178 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
Testing the Pupil. The size of the 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 measure, 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. 
The patient is to be placed facing the light and told to look 
at some distant object. The hands of the physician are then 
placed one over each eye, the patient being told to keep his eyes 
open and to endeavor to see the 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 contract. 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 consen- 
sual reflex. The exact pathway of this reflex is unknown, but we 
know that the light-impulse passes along the optic nerve, and, 
arriving at its semi-decussation in the chiasm, passes along each of 
the tracts to the corpora quadrigemina, and thence by the commu- 
nicating fibres (Meynert’s fibres) between these bodies and the oculo- 
motor centres to the centre for the sphincter pupillse or circular 
muscle-centre, and from there to the ciliary ganglion, the ciliary 
nerves, and the muscles of the iris. (Fig- 85.) 
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 reac- 
tion 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 of the pupil will occur. 
The pupil-dilating centre is in the medulla and is very sensitive 
to reflex irritation. 
Supposing that the pupillary movement is abnormal, we should THE EYE. 
179 
recollect before studying the case further what the causes of its per- 
version may be. Thus its size is altered by drugs, by local disease 
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 
testing the ocular reflexes in the manner already described we find 
that the pupil of one eye when uncovered does not contract, and 
immediately 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 
Fig. 85. 
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 third nerve; l, seat 
of lesion; arrows show path of impulse in lesion of right tract at l. (Swanzy.) 
retina; whereas if it contracts when the other eye is uncovered, it 
shows that the rest of the mechanism involved in the reflex is in- 
tact. Accommodative reaction of the pupil is intact also. Again, 
supposing that irides fail to react to light, but do to accommodation 
and convergence, 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. 85.) 
This condition is seen in locomotor ataxia, general paralysis of the 
insane, sometimes in cerebral syphilis and aS the result of poisoning 180 
THE MANIFESTATION OF DISEASE IN ORGANS. 
by the bisulphide of carbon. Recently Grube has reported three 
cases in which the A rgyll-Robertson pupil developed in the course 
of diabetes mellitus. 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 accommodation, 
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 pos- 
sessing a mydriatic action, as, for example, atropine. It also 
occurs in persons suffering from fright, neurasthenia, aortic regurgi- 
tation, 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 char- 
acter: the first is irritation due to tumor, meningitis, or other irri- 
tating 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 (contrac- 
tion of the pupil) results from paralyzing lesions of the spinal cord 
situated in the region of the cervical vertebrae, 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 paralysis with progressive muscular atrophy. It is also 
one of the most notable signs of opium-poisoning. 
Under the name of “ hemiopic pupillary inaction ” or “ Wernicke’s 
pupil” we sometimes, though rarely, meet with a condition associ- 
ated with hemianopsia or blindness in one-half of the eye, which is 
demonstrated in the following manner: the patient is seated in a THE EYE. 
181 
dark room and one eye is covered. The other eye is now illumi- 
nated by just sufficient light from a flat mirror to enable the physi- 
cian to see the eye. By means of the concave mirror of an ophthal- 
moscope 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 eye obliquely and 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 arc between the optic chiasm and the 
corpora quadrigemiua; 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 indi- 
cate 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 pupil, 
called “ hippus,” are seen in health for a moment on sudden expo- 
sure to light; but when constant is a sign of disseminated sclerosis, 
epilepsy, 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 apnoea. 
Changes in the Acuity of Vision. Having discussed the diag- 
nostic value of alterations from the normal in the function of the 
extra- and intraocular muscles of the eye, we can proceed to a con- 
sideration of the value of 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 182 
THE MANIFESTATION OF DISEASE IN ORGANS. 
destroys the peripheral ocular sense-organ (the eye), the optic nerves, 
the optic tracts, or the receptive and perceptive centres of sight. It 
Fig. 86. 
The visual tract. The result of a lesion anywhere between the chiasm and the cuneus is to 
produce homonymous hemianopsia, h. Lesion at chiasm causing bilateral temporal hemi- 
anopsia. N. Lesion at chiasm causing unilateral nasal hemianopsia, t. Lesion at chiasm 
causing unilateral temporal hemianopsia, sn. Substantial nigra of crus. L. Lemniscus in 
crus. rn. Red nucleus, hi. Third nerves, p, q, r, s, u. Lesions in the occipital lobe and 
1 n front of it producing left homonymous lateral hemianopsia. THE EYE. 
183 
also is dependent upon bilateral lesions in the crystalline lens, as in 
cataract, or in the cornea, as in severe keratitis. 
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. 86. 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 pos- 
terior 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. 86.) 
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 bitemporal hemianopsia; or if 
the blindness is found in the nasal side of both eyes, it is called 
bing,sal hemianopsia. It must be remembered, however, that the 
apparent blindness of the outer side of the eye is really due to dis- 
ease of the fibres supplying the opposite side of the retina, as is 
shown in Fig. 87. The presence of hemianopsia in any form is 
determined by the following method of examination: the patient 184 
THE MANIFESTATION OF DISEASE IN ORGANS. 
is placed with the back to the light and one eye is covered, 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 moved 
to the left and 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. 
LEFT VISUAL FIELD. RIGHT VISUAL FIELD. 
Fig. 87. 
(Oliver.) 
We measure the field of vision more accurately 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 describing 
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. THE EYE. 
185 
(See Fig. 88.) The area of the normal field is well seen in this 
figure. 
Let us suppose that on using the tests just described we find left 
lateral homonymous hemianopsia—that is, blindness in the visual 
Fig. 88. 
Chart of F. Y. of right eye 
Fig. 89. 
Left homonymous hemianopsia from a ease of gunshot-wound, with suspected lesion of the 
right cuneus. (de Schweinitz.) 186 
THE MANIFESTATION OF DISEASE IN ORGANS. 
field, as shown in Fig. 89. This signifies that the patient has a 
lesion somewhere in the visual tract back of the chiasm, either in 
the cuneus, in the occipital lobe, in the optic radiations, in the 
internal capsule, in the primary optic centres, or in the optic tract. 
Fig. 86 shows the sites of these lesions and why they cause left 
homonymous hemianopsia. Supposing, on the other hand, that in 
place of left homonymous hemianopsia we find bitemporal hemian- 
opsia (Fig. 90), 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. 86); 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. 90. 
Bitemporal hemianopsia from a case oi akromegaly originally under the care of Dr. H. C. 
Wood and later studied by Dr. Packard. Eyes examined in 1885 by Dr. G. E. de Schweinitz, 
and above fields found, (de Schweinitz.) 
Hemianopsia of the homonymous form is very rarely found in 
hysteria, generally in association with hysterical hemianaesthesia, in 
which condition the conj unctiva is usually anaesthetic, thereby differ- 
ing from the condition of the conjunctiva of persons suffering from 
hemianaesthesia of an organic origin. 
In some cases in place of hemianopsia we have simply au 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 are they identical 
with one another. Passing from the periphery toward the centre THE EYE. 
187 
of the visual field in ordinary daylight we find that blue is the 
color first seen, its boundary beiug almost as great as that of white. 
After blue come yellow, orange, red, and finally green. The blue, 
red, and green being the most important colors, their boundaries are 
shown in Fig. 91. These fields are determined by means of small 
pieces of colored paper passed around the perimeter in the manner 
already described. 
Fig. 91. 
WHITE - 
Blue - 
RED — 
GREEN - 
Chart of F. V. of left eye. iLandolt.) 
The alteration of the visual field for colors is called, if so changed, 
homonymous hemidyschromatopsia, and the lesion producing it is 
situated in the cortex of the occipital lobe; while if the colors are 
indistinguishable, it is called hemiachromatopsia. This site of the 
lesion 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 vei'sa. 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 be- 
tween the ocular symptoms of hysteria and those of true tabes dorsalis, 188 
THE manifestation of disease in organs. 
a distinction 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- 
Robertson pupil is not seen. The following table from Charcot’s 
lectures for 1888-’89 summarizes these differential points: 
Tabes. 
Hysteria. 
Motor apparatus of the 
eye. 
Paralysis from lesion of a motor 
nerve of the eye (bulbar or per- 
ipheral) ; consequent diplopia. 
1. Sometimes associated paralysis. 
2. Blepharospasm. 
3. Monocular diplopia; micropsia 
and macropsia. 
Pupillary disturbances. 
Argyll-Robertson pupil. 
Optic disk. 
Atrophy. 
Symptoms due to affec- 
tions of the optic nerve 
or visual centres 
1 Irregular concentric contrac- 
tion of the visual fields. 
2. Tabetic achromatopsia or dys- 
chromatopsia, affecting first 
green and red, yellow and blue 
being preserved to the last. 
3. Progressive blindness. 
1. Regular concentric contraction 
of the visual fields. 
2. Dyschromatopsia from simple 
contraction of the visual fields 
for colors. Frequently perception 
of red alone persists. 
3. Transitory amblyopia or amau- 
rosis. 
The Optic Nerve and the Ophthalmoscope. There still remain 
to be considered the diagnostic indications afforded us by the optic 
nerve. Before taking up this 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 observed, at the right side of his patient, and 
takes a chair slightly higher than that of the patient. The ophthal- 
moscope is now taken in the right hand and held in such a position 
that the concavity of the physician’s brow 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 ophthal- 
moscope, 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 the ophthalmoscope, but to one 
side, and his vision should be distant and accommodation as far as 
possible relaxed. If the examiner is not skilled in the use of the 
ophthalmoscope and the result of the examination is of great im- 
portance in the diagnosis of the case, it is justifiable to use homatro- THE EYE. 
189 
pine to dilate the pupil and prevent the alterations of accommodation 
by paralyzing this function. The ophthalmoscope and the head of 
the physician are now approached as closely as possible to the eye 
of the patient, the angle of the two heads being as nearly as possible 
identical as shown in Fig. 92. 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. 
Fig. 92. 
Relative position of physician and patient whilst employing the direct method. 
(Norris and Oliver.) 
If the patient or the physician is short-sighted (myopic), the ophthal- 
moscope must be adjusted to correct this error by placing over the 
aperture a concave lens; but if ordinary degrees of far-sightedness 
(hypermetropia) are present, the use of a convex lens is not neces- 
sary, because the accommodation of the eye makes up for the error 
in refraction. 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, 190 
THE MANIFESTATION OF DISEASE IN ORGANS. 
not because of myopia or hypermetropia, but because the physician 
has not as yet learned to relax his accommodation in making the 
examination. A concave glass usually remedies this. 
In health the optic nerve appears as a nearly round or slightly 
oval disk, situated somewhat to the nasal side of the eye, and vary- 
ing 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 represents 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 chief venous trunks empty into it. Generally one arterial 
and one venous stream pass up and a similar one downward, and 
both soon bifurcate, afterward still further dividing. The arteries 
are distinguished 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 normal 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 bloodvessels 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 persons with a dark skin the 
retina has a grayish hue in the neighborhood of the papilla, which 
is most marked on its nasal side and is slightly streaked. 
To the outer side of the papilla, slightly below the horizontal 
meridian, 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 devoid of any retinal vessel. It is the point of the 
eye-ground in which direct vision is best developed. In its centre 
is a bright spot, the fovea centralis. As a person grows older these 
clear distinctions vanish and the macula lutea is to be distinguished PLATE IV. 
FIG. I. 
Normal Eye-Ground (average tint), (Norris & Oliver.) 
FIG. 2. 
Primary Atrophy of Optic Nerve (Spinal 
Atrophy). Modified from Haab. 
(de Schweinitz.) 
Post-Papillitic or Consecutive Atrophy of 
the Optic Nerve. Modified from Juler. 
(de Schweinitz.) THE EYE. 
191 
from the surrounding eye-ground only by its darker hue and the 
absence of vessels. The macula is difficult to see, because as the 
light falls on it the pupil at once contracts. If the eye is dilated 
by a mydriatic, however, and the patient looks directly into the 
ophthalmoscope, the macula is readily seen. 
The red glare produced by throwing the light into the eye by the 
ophthalmoscope is due to reflection from the bloodvessels of the 
choroid coat. 
The pathological significance of alterations in these normal appear- 
ances is very great. Let us suppose that on examining the eye- 
ground we find the end of the optic nerve red and its edges irregular 
and obscure, or, if the morbid condition is further advanced, that the 
nerve-head looks protruding or mound-like and the arteries going to 
it are smaller than normal and partly concealed, while the veins 
are enlarged and tortuous. Hemorrhages may be seen in the papil- 
lary region or near it, occurring in flame-like shapes. These are the 
signs of optic neuritis, and optic neuritis depends upon intraorbital 
or intracranial disease, although, if the process is not marked, it may 
be due to hypermetropic astigmatism. Vision is often unaffected, 
but if the lesion be in the cerebellum sudden blindness may come on. 
As some differences of opinion exist as to the various forms of 
neuritis of the optic nerve the term papillitis is often used to signify 
all the forms of optic neuritis which we meet with, or in other cases 
is spoken of as choked disk. Papillitis is more commonly the result 
of brain-tumor than of any other intracranial lesion, and, again, it 
is much more common in lesions of the cerebellum than in tumors 
elsewhere in the brain. Another fairly common cause of papillitis 
is meningeal inflammation, particularly about the base of the brain, 
and tubercular meningitis is very prone to produce it. Cerebral 
abscess may also cause this change in the optic nerve. 
In addition to the cranial causes of papillitis we have acute febrile 
disorders, syphilis, toxaemias from lead and alcohol, rheumatism 
and anaemia. Sometimes, however, they produce an acute or chronic 
retrobulbar neuritis. There is nearly always in such cases a large 
central scotoma, which causes a failure to recognize color, as, for 
example, green or red. Sometimes the patient realizes the failure 
of his vision, which may be impaired otherwise than by disorder of 
the color-sense. In other cases he fails to do so until his eyes are 
examined. The chronic form of retrobulbar neuritis is generally 
the result of the excessive use of tobacco and alcohol, and produces 192 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
what is called tobacco-amblyopia or toxic amblyopia, with failure of 
vision from these causes. In such cases there is a central scotoma 
between the macula and the optic nerve where the senses of red and 
green are lost. The ophthalmoscope may reveal in such cases discol- 
oration of the disk and a triangular spot of atrophy in the outer and 
lower part of it. Supposing, however, on using the ophthalmoscope 
we find in place of a papillitis an atrophied state of the nerve, in 
which, if the disease be young, the nerve-ending looks gray and 
the outline of the disk is sharp (Plate IV., Fig. 2), or if it be well 
Fig. 93. 
Upper curve, frequency of tabes. Middle curve, frequency of severe ocular symptoms. 
Lower curve, frequency of atrophy of the optic nerve. (Berger.) 
advanced the edges appear hazy, the arteries contracted, and the 
veins large and tortuous, while the disk is quite white. (Plate V.) 
This primary or gray form of atrophy is most typically seen in 
the optic-nerve lesion of locomotor ataxia, and so is often called 
tabetic atrophy. About 34 per cent, of all tabetics suffer from 
this change. Again, it is seen in cases of paretic dementia 
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 the earliest signs of locomotor ataxia, in some cases PLATE V. 
Embolic Atrophy of the Optic Nerve. From a case in the Jefferson Medical College Hospital. 
(de Schweinitz.) THE EYE. 
193 
it is a valuable one in the diagnosis of this grave disorder, separating 
it from pseudo-tabes due to ordinary peripheral neuritis. The dia- 
gram (Fig. 93) on page 192, taken from de Schweinitz’s article on 
this subject, shows the relation between age, severe ocular symp- 
toms, and atrophy of the optic nerve. 
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 
enlargement, that hemorrhagic exudations of a flame-like character 
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 picture 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 Bright’s disease. Here, in addition to the flame-like hemor- 
rhagic areas, we find irregular spatterings of white which may be 
star-shaped. The importance of the discovery of such changes is 
that by it is the first suspicion of renal trouble aroused. This sign is 
of the greatest value in pregnancy. Retinitis also sometimes results 
from diabetes. 
Hemorrhages into the retina without retinitis usually are the result 
of septicaemia, ulcerative endocarditis, haemophilia, diabetes, gout, 
and malarial fever of a severe type. They are 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 
or rheumatism. 194 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Finally, it should not be forgotten that cataract sometimes occurs 
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 
before the eyes, or in their place dark spots called muscae 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 usu- 
ally And them as a result of severe indigestion, and the dark spots 
may arise from the same causes. Muscae 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 
uraemia (uraemic amaurosis). As a rule, it does not occur as a 
single symptom, but follows an attack of acute uraemic manifesta- 
tions; 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 effect 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—Anaesthesia and hemianeesthesia— 
Pallesthesia, hypersesthesia, 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 pliability 
and its sensibility. Naturally the eye at once takes in any eruption 
or scars which may mar its naturally smooth surface, and, as erup- 
tions 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 mucous layer of the 
epidermis, and in the corium in those parts of the body where pig- 
mentation is marked, or to the condition of the subcutaneous circu- 
lation 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 than 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 circula- 
tion. With these normal alterations in color, however, we have little 
to do, for it is the abnormal colorations which interest us from a 
diagnostic 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. Abdominal 
growths due to tuberculosis, cancer or lymphoma, and tuberculosis 
of the peritoneum also cause pigmentation of the skin, and in melan- 
otic cancer there is often very dark discoloration, so marked as to be 
confused with that of Addison’s disease. Again, it is not uncom- 
mon for persons who have hepatic torpor with constipation to develop 
what are called liver-spots, in which the skin has rather a dirty hue. 
Under the name of vagabond’s e< pigmentation ” we sometimes see 196 
THE MANIFESTATION OF DISEASE IN ORGANS. 
discoloration induced by the irritation of the skin produced by lice 
and exposure to dirt and weather, and this is capable of being mis- 
taken 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 chap- 
ter.) The changes in color depending upon disturbance 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 hypersemia 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 
iu erysipelas the zone of hyperaemic redness is characterized by its 
sharp line of demarcation and its raised edge. In the alterations in 
color due to changes in the quality of the blood we have, as causes, 
anaemia due to lack of corpuscles or of haemoglobin, 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 by gas or candle-light, for the yellow flame masks the biliary 
color. 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 physician to decide what 
the cause of the jaundice may be. In the first place, it must be 
remembered that jaundice may be hepatogenous—that is, arise from 
disorder in the liver, or be hematogenous from disorders of the 
blood with the setting free of blood-pigment. 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 inflamma- 
tion of the smaller ducts and common bile-duct which generally 
occurs in association with gastro-duodenal catarrh. THE SKiN. 
197 
As a result of this catarrhal process the bile-duct becomes blocked 
bv 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 
obstruction 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 pro- 
ducts in the immediately adjacent organs, or of adherent inflamma- 
tion in the ducts themselves, or by the presence of a round worm in 
the duct. Very rarely the jaundice may arise from the pressure on 
the common duct produced by floating kidney. 
The following table from Taylor’s Index of Medicine summarizes 
the causes of hepatogenous jaundice : 
Tabular View of the Causes of Hepatogenous Jaundice. 
in common duct, 
in radicles of duct. 
1. Gall-stones and inspissated bile 
of liver itself. 
secondary infiltration of glands 
in transverse fissure, 
of stomach, 
of pylorus, 
of duodenum, 
of pancreas, 
of kidney. 
Malignant . . 
Obstructive 
(feces clay- 
colored) 
2. New growth 
Non-malignant 
syphilis. 
lymphadenoma. 
3. Catarrh of stomach and duodenum. 
4. Abdominal aneurism. 
5. Hydatid cysts. 
6. Accumulation of feces. 
7. Ovarian or uterine tumors. 
8. Perihepatitis. 
Catarrhal jaundice of the acute type is generally produced by 
indiscretions 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 
heaviness, with languor and malaise, and within forty-eight hours 
or less the yellowing of the conjunctiva and skin appears. The 
temperature is generally subnormal to a slight degree. The tongue 
is heavily coated and often somewhat dry. There are marked loss 
of appetite, great distress, headache, and depression of spirits. Ex- 
amination of the hypochondrium may reveal some local tenderness 198 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 consti- 
pated, 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, whereby 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. A differ- 
ential diagnosis as to whether the stone is in one or the other of 
these places is often impossible, but in the variety in which the 
obstruction is below the opening of the cystic duct it may be pos- 
sible sometimes 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 
violent attack of pain in the hypocliondrium, or, in other words, 
hepatic colic, in which the agony is excruciating and is accompanied 
by nausea and vomiting. The area of the pain is, however, dis- 
tinctly hepatic, and it does not radiate down 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 jaun- 
dice 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 per- 
sistent, 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 gener- 
ally in or past middle life, and the fact that the 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 THE SKIN. 
199 
fever high, the failure iu strengtli 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 
aneurism of the abdominal aorta, or from aneurism involving the 
hepatic artery. Three such cases are recorded by Frerichs. Jaun- 
dice has also been seen in aneurisms of the superior mesenteric 
artery as the result of pressure and in cases in which there has 
been, or is, perihepatitis, witli 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 hypertrophic 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 that all forms of jaundice produce headache 
and may cause delirium. In acute yellow atrophy of the liver (see 
below) the liver is greatly reduced in size, whereas in hypertrophy 
it is greatly increased 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 coffee- 
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 car- 
diac disease in which compensation is gradually failing. Rarely 
this hue becomes deeper as the heart-failure increases. This jaun- 
dice is due to engorgement of the liver (nutmeg-liver), which in 
time results in catarrh of the bile-ducts, with consequent obstruc- 
tion 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 200 
THE manifestation of disease in organs. 
jaundice resulting from cancer of the liver the growth must be so 
situated as to compress the ducts, consequently jaundice occurs in 
about only one-tliird of the cases. Similarly jaundice may result 
from 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 press- 
ing 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 pancreas. 
In this connection it is well to remember that Hanot, under the 
name of diabete bronze, has described a pigmentation of the skin 
which contains iron (that of Addison’s disease and melansemia do 
not), and which is associated with diabetes, hypertrophic cirrhosis 
of the liver, and enlargement of the spleen. The coloration occurs 
most markedly upon the face, limbs, and genital organs; the gly- 
cosuria is abundant and slight ascites may be present, the lower 
limbs may be oedematous, the loss of weight and strength is rapid, 
and death soon ensues from pneumonia or coma. Hanot and Marie 
both regard it as a distinct disease from ordinary diabetes mellitus. 
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 stain- 
ing 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. Rigors of extreme severity, followed by sweatings 
and marked febrile movement, develop in such cases, the chills 
occurring daily or periodically in a manner closely resembling 
those of intermittent fever. As these symptoms sometimes de- 
velop in cases in which the post-mortem discovers no sign of pus, 
it has been thought that the disturbances were due to reflex causes; 
but the opinion of Charcot that there is present in all such cases a 
true infection seems the more probable. When the gall-stone pro- 
duces active suppuration the fever becomes more like remittent THE SKIN. 
201 
fever and the patient rapidly emaciates and presents all the signs 
of active suppuration. 
The urine in all cases of hepatogenous jaundice is heavily bile- 
stained (see Urine), and the stools generally clay-colored owing to 
absence of bile in the feces. 
A very rare cause of jaundice is acute yellow atrophy of the liver, 
a disease which is seen somewhat more frequently in women than 
in men, and particularly in association with pregnancy. The age 
of occurrence is usually between the twentieth and thirtieth years. 
The symptoms begin with gastro-intestinal disorder, followed by 
headache, delirium, muscular twitching, and perhaps convulsions. 
Simultaneously with the onset of the headache the jaundice appears, 
the patient becomes typhoidal and dies from exhaustion, although 
recovery has been known to occur. The stools during the attack 
are clay-colored and the urine contains leucin in discs and tyrosin 
in needle-like crystals. 
Hematogenous jaundice is due, as its name implies, to breaking 
down of the blood to so great an extent that the liver cannot deal 
with the waste material with sufficient rapidity, and.as a result 
altered haemoglobin is deposited in the tissues. Any poison which 
produces excessive hemolysis, such as picric acid and the coal-tar 
products, chlorate of potassium, glycerine, and poisonous mushrooms, 
may cause this condition to develop, and in extreme malarial disease 
(remittent and pernicious malarial fever), dengue, relapsing fever, 
pernicious anaemia, pneumonia, and in other infectious maladies 
jaundice may be produced in this manner. It is particularly apt 
to occur in cases of marked sepsis. 
Its causes are shown in the following table from Taylor’s Index : 
Causes of Hematogenous Jaundice. 
f Fevers 
Yellow fever. 
Typhus fever. 
Scarlet fever. 
Kelapsing fever. 
Animal 
Snake-bite. 
Pyaemia. 
Non-ohstructive 
(feces normal 
in color) 
Poisons 
Chemical 
Phosphorus, copper, 
mercury, antimony, 
chloroform, ether. 
Acute atrophy of liver. 
Neurosis: joy, grief, fear, passion. 
Cirrhosis of liver in its later stages. 202 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Jaundice sometimes occurs after severe hemorrhage of a prolonged 
character and in prolonged exhausting fevers, and is then due not 
to any local hepatic trouble, but to blood-changes, with the produc- 
tion of urobilin in excessive amounts. The urine fails to carry off 
all the urobilin which is produced from haematoidin or bilirubin. 
This condition is called “ urobilin icterus.” 
In nearly all cases of hematogenous jaundice the discoloration of 
the skin is very slight, and the important fact is to be remembered 
that the stools are not light or clay-colored as in hepatic jaundice, 
but contain a normal or excessive amount of pigment. Again, the 
systemic symptoms of catarrhal or obstructive hepatic jaundice are 
practically absent in the hematogenous variety, and the jaundice is 
simply a minor symptom associated with more grave manifestations 
which characterize the individual infectious process. If the poison- 
ing is very marked, convulsions, coma, or active delirium may come 
on, but it is probable that these symptoms are due more to the 
poison of the disease than to the broken-down blood. 
Vierordt states that a very small amount of biliary coloring-matter 
is often found in the urine of patients suffering from pyaemic jaun- 
dice, and regards this as an important sign that the discoloration of 
the skin is due in a given case to blood-changes and not to biliary 
obstruction, whereas an excessive amount of biliary matter in the 
urine indicates hepatic trouble. 
There remains to be considered the jaundice seen in the new- 
born, usually within the first or second day of life (icterus neona- 
torum), which some believe to be due to a decrease in the blood- 
pressure in the portal vessels subsequent to the arrest of the placental 
circulation, with consequent absorption of bile into the blood, owing 
to the comparatively high tension of this fluid in the bile capillaries. 
Others think this jaundice is due to breaking down of the blood- 
corpuscles shortly after birth as the result of some mild infection. 
Probably both causes act in some cases. If the cause be altered 
blood-pressure, the prognosis is favorable, and recovery takes place 
in about ten days or two weeks; but if the cause be an infection, 
the condition often proves rapidly fatal. Should this jaundice of 
the newborn be very marked the patient may be suffering from 
congenital stenosis, or absence of the common or hepatic duct (which 
cause is rare); from septicaemia, through infection by way of the 
umbilicus; from phlebitis of the umbilical vein, or from a hepatitis 
due to hereditary syphilis. In any of these latter causes death THE SKIN. 
203 
will probably occur, whereas in the mild form of icterus neona- 
torum the prognosis is very favorable, even though the discolora- 
tion lasts for weeks. The mild form of icterus neonatorum, if due 
to blood-changes, is rarely accompanied by great discoloration of the 
urine, and the feces are usually no lighter than normal in color; 
but if hepatic disease be present, the urine is bile-stained and the 
feces are light in hue. 
Jaundice sometimes comes on in the course of acute ulcerative 
endocarditis, and has been mistaken for that of acute yellow atrophy 
of the liver, and it often appears as a symptom of pernicious mala- 
rial fever, with vomiting, diarrhoea, and grave nervous symptoms. 
Rarely jaundice follows severe fright or extreme anger, and 
Da Costa states that it sometimes ensues after concussion of the 
brain. 
Other Changes in the Color of the Skin. A condition of 
the skin characterized by yellow, more or less elevated patches is 
xanthoma, which Murchison states often complicates hepatic trouble, 
and which in its nodular form may possibly attack the liver and so 
produce jaundice. Its favorite distribution is about the eyelids, 
but it may appear elsewhere. Lesions similar to xanthoma some- 
times appear in the course of diabetes (Hutchinson, Besnier), and 
under these circumstances generally develop suddenly, and spon- 
taneously disappear after some weeks or months. 
When the skin of the entire body, the face being particularly 
affected, is of a livid or bluish-slate color, resembling somewhat the 
appearance of a person exposed to rays of light passing through blue 
glass, the condition is that of argyria or chronic silver-poisoning. This 
discoloration is so characteristic as to admit of no difficulty in diag- 
nosis, since the absence of any circulatory or respiratory embarrass- 
ment excludes the possibility of its being due to cyanosis. Owing 
to the decrease in the amount of silver given internally by physi- 
cians chronic argyria is becoming more and more rare. The 
discoloration is due to a deposit of oxide of silver in the rete 
Malpighii. 
Discoloration of the skin of the entire body of a sallow, lemon- 
yellow tint, sometimes called a “muddy-yellow” hue, is seen in 
persons who are sufferers from prolonged malarial poisoning, and 
in some cases the subjects of prolonged suppurative processes not 
tubercular in character. A greasy, yellowish skin does, however, 
occur as an accompaniment of some cases of pulmonary phthisis 204 
THE MANIFESTATION OF DISEASE IN ORGANS. 
and these cases have as a rule a gloomy prognosis. Often chronic 
hepatic disease, such as cirrhosis, produces this sallow appearance. 
Other changes in the color of the skin, which cannot be said to 
be due to deposition of pigment, although they seem to be caused 
by this, are seen most markedly in the peculiar yellowish, cheesy 
pallor of carcinoma, the greenish-yellow tinge of true chlorosis, the 
curious cadaveric hue of advanced pyaemia, and the yellow skin 
with a greasy feeling in some cases of paretic dementia. 
Local pigmentations of the skin result from many causes, both 
local and systemic, direct and indirect. When brownish-yellow 
spots or streaks appear on the face, so thqit chloasma is developed, 
we should look for uterine or hepatic disturbance or pregnancy; 
they are practically large freckles of a more or less distinct brown 
hue. In other instances chloasmic spots or localized discoloration 
of the skin results from injury to the skin, as pressure by clothes, 
chafing, or after constant severe scratching in the course of eczema 
or pediculosis or scabies. If the pigment is found in the nuchal 
and sacral regions, it is probably from the scratching caused by 
pediculi; if on the body in irregular distribution, it may have been 
caused by prurigo. Again, the presence of a brown pigmentation 
of the skin in clearly outlined patches may indicate the earlier use 
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 Addison’s disease, is produced by the free use exter- 
nally of oil of cade. Sometimes these spots are produced by the 
prolonged use of arsenic, and the writer has reported a case in which 
the coalescence of the spots produced a curious grayish-brown hue 
of the entire body, 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 the bronzing of the skin 
in patches which is seen in persons suffering from Addison’s dis- 
ease; 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 diagnosis, for bronzing is sometimes seen in cases 
in which the suprarenal capsules are normal. In some instances 
the bronze color deepens into a dark gray or even a black hue, 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- THE SKIN. 
205 
nails. The nails, however, escape, as does also the mucous mem- 
brane of the lips, although the lining of the mouth itself may be 
dotted with pigmentation. The color is due to pigmentation of the 
rete Malpighii, and pressure has no effect on it. The symptoms of 
Addison’s disease to be found associated with these skin-changes 
are u ansemia, general 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 in cases 
of true goitre, and brown ones in tuberculosis. 
In carcinoma of one of the internal organs, or of the breast, of an 
advanced stage, the appearance of the skin is drawn and unusually 
smooth, often shiny or greasy-looking, somewhat gummy and leathery 
to the touch, particularly where the integument is naturally dense. 
Although it is difficult to describe, this skin is almost pathognomonic 
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 typi- 
fied 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 vitiligo, 
while the pallor due to pernicious anaemia or pseudo-leukaemia and 
malaria is owing 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 skin may be of ghastly whiteness or tinged 
with yellow. The skin is apt also to be very white, and even 
chalky in appearance, in 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. 
A very important diagnostic point to be remembered is that red 
cheeks often cause the physician to overlook well-advanced amen] ia 
in young women. (See chapter on the Blood.) 
In those cases in which the skin is pale from alteration of the 
subcutaneous circulation there is usually incompetence of the heart 206 
THE MANIFESTATION OF DISEASE IN ORGANS. 
or vasomotor disturbance, but the most marked form of general 
pallor is that due to myxoedema. 
Cyanosis or blueness 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 hands and feet. The most marked form of cyanosis with which 
we meet is the cyanosis of the newborn child, suffering from a patu- 
lous foramen ovale, and in this condition the color may vary from 
a slate-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. Any- 
thing which produces excitement increases the cyanosis greatly, 
whereas cyanosis due to other causes is not subject to great varia- 
tions. In the cyanosis of the newly born, males are far more fre- 
quently 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 malformation of the heart it may not be present from the 
time of birth, but may develop several days afterward. J. Lewis 
Smith records forty-one cases in which the cyanosis due to a con- 
genital heart-lesion came on at periods ranging from two weeks 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 J. 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 
impervious or contracted 6 
4. Right ventricle divided into two cavities by a supernumerary septum . . 11 
5. One auricle and one ventricle 12 
6. Two auricles and one ventricle 4 
7. A single auriculo-ventricular opening; interauricular and intraventricular 
septum incomplete 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 cavse entering the left auricle 1 
13. Pulmonary veins opening into the right auricle or into the cavse or azygos 
veins 2 
14. Aorta impervious or contracted above its point of union with the ductus 
arteriosus; pulmonary artery wholly or in part supplying blood to the 
descending aorta through the ductus arteriosus 2 
Total 162 THE SKIN. 
207 
The chances are about ten to one that in cyanosis of the newborn 
the lesion is absence 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, pulmonary con- 
gestion, and bronchiectasis with emphysema and associated cardiac 
dilatation. It also occurs in 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, such 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 straggling and lustreless and fre- 
quently 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 devel- 
opment of skin lesions is very great, and Stephen Mackenzie has 
summed up the relationship of skin disease to age in the following 
amusing manner: “ The seven stages of man could be well illus- 
trated by disease of the skin, though we lack a Shakespeare to do 
justice to the theme. In the 1 mewling and puking’ infant we 
meet with sclerema and oedema neonatorum, the ‘ red gum ’ or 
strophulus of the older writers, intertrigo, eczema, urticaria papil- 
losa (lichen urticatus), urticaria pigmentosa, xeroderma pigmen- 
tosum, 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 208 
THE MANIFESTATION OF DISEASE IN ORGANS. 
slippered pantaloon,’ with rodent idcer and ‘ gouty’ eczema; Mast 
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.” 
There are two conditions of the skin in which valuable evidence 
is given that tiie patient is suffering from rheumatism. One is the 
presence 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, 
annulaire, 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 papu- 
late eruption 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 multiple 
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 hsemorrhagica, which may be divided into the 
acute and subacute forms, and that which is secondary as the result 
of severe infections and certain poisonings. The acute form of pur- 
pura 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 
mucous membranes, purpuric spots, high fever, and a general class 
of symptoms resembling those of sepsis, as chills, pyrexia, and ex- 
haustion. 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 enlarged. 
The subacute type, while severe, runs a far more favorable course THE SKIN. 
209 
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 
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 may appear as if 
suffering from typhoid fever. The prognosis is good for ultimate 
recovery. It is sometimes called peliosis rheumatica or Schonlein’s 
disease. This subacute form, however, occurs in a more severe man- 
ner, as “ Henoch’s disease,” in the persons of children between 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. 
The development of polymorphic skin lesions, consisting of liyper- 
semia, oedema, and hemorrhage, with arthritis occasionally and vis- 
ceral disturbances, consisting 'in attacks of vomiting or diarrhoea, 
endocarditis, pericarditis, acute nephritis, and hemorrhages from the 
mucous membranes, indicates the presence of a condition called ery- 
thema exudativum multiforme. The attacks are apt to be recurrent. 
Sometimes the skin-manifestations are absent. 
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 denied, but the author believes that in some cases of 
rheumatism purpura is a symptom, appearing often in the neighbor- 
hood 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; cMorai 210 
THE MANIFESTATION OF DISEASE IN ORGANS. 
and salicylic acid. They may also accompany any severe infectious 
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 cases 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, or turpentine, and quite commonly follows the ingestion of 
iodide of potassium. The wheals produced by the latter drug differ 
from those of urticaria in being unduly red. 
Hemorrhages of the skin occur spontaneously in some cases of 
hysteria and paretic dementia and after epileptic attacks, particu- 
larly about the eyes, 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 
petechiae, result from snake-poisoning, septicaemia, cerebro-spinal 
meningitis, iodism, ergotism, and after inhaling the vapor of ben- 
zine. They are also seen iu scurvy and in some cases of profound 
wasting, as in the course of phthisis and carcinoma. 
Petechial rashes closely resembliug those of malignant smallpox, 
typhoid fever, or cerebro-spinal fever may be due to the presence 
of acute ulcerative endocarditis. 
Hemorrhages sometimes appear in the skin covering a part which 
has been affected by a severe pain in a crisis of locomotor ataxia. 
A very extraordinary manifestation of spontaneous subcutaneous 
hemorrhage is seen in what is known as hrematoma auris, a condition 
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 iu males than females. 
Intense redness of the skin is seen in acute inflammations of 
the skin or the subcutaneous tissues, and as the result of hot appli- 
cations, the redness being more and more marked as the heat is 
prolonged and is great. Often the prolonged use of high heat 
will produce a peculiar mottling of the skin like that of an old 
bruise. 
Aside from the redness of the cheeks and forehead from blushing, THE SKIN. 
211 
we should remember the general flushing seen so commonly in per- 
sons suffering from phthisis, particularly when they are excited, 
which differs from the more dusky redness seen over the malar 
bones in hectic fever. 
Another interesting diagnostic sign in the skin is what is known 
as the “tache cerebrate,’’ a condition of vasomotor disorder in which 
when the finger is gently drawn over the skin of the forehead a red 
patch speedily develops. It is seen in meningeal irritation, brain 
abscess, epilepsy, in some cases of exophthalmic goitre, and in paretic 
dementia. Sometimes it is called “ tache meningeale.” 
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 very 
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 devoid of diagnostic impor- 
tance. 
The development of a diffuse, punctated rose-rash on the skin 
of a person who is suffering from malaise, fever, nervous disturb- 
ance, 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 disease, first appears on the chest and neck, and then 
speedily involves nearly the whole surface of the body, although 
the forehead 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 red- 
ness depends upon an acute hypersemia of the skin, which though 
removed by pressure instantly returns when the finger is with- 
drawn. A noteworthy point is its punctate and mottled appear- 
ance, 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 
tense, and itching is commonly present. The rash usually lasts 
three or four days and then fades, desquamation of the cuticle 
speedily setting in, which is complete in about two weeks. Some- 212 
THE MANIFESTATION OF DISEASE IN ORGANS. 
times, 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 petechiae and subdermal hemorrhages occur. 
Sometimes, too, in those cases of scarlet fever which have severe 
symptoms of ulcerating sore throat with ear or nose complications 
there develops, about the third week of the disease, a dark-red pap- 
ular or macular erythema on the extensor aspects of the large joints. 
It is a grave symptom. 
An erythema resembling scarlet fever, not only in its appearance, 
but also by its association with swelling of the lymphatic glands 
and reddening of the mucous membranes of the mouth, sometimes 
develops 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 than is the rash of syphilis. The most fre- 
quent of these is erythema roseola, or roseola of acute indigestion, 
or that following the use of a food to which the patient has an idio- 
syncrasy. It is generally, but not always, widely diffused and is 
often associated with acute and severe febrile movement and vomit- 
ing, 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 or enlarged cervical 
glands, and the rash does not come out on the clavicles and gradually 
travel down the body. Roseolous eruptions also appear in persons 
with delicate skins after coming in contact with irritant plants, and 
Dukes asserts that it may develop from handling caterpillars. 
Another condition closely resembling scarlet fever is rarely seen, 
namely, acute exfoliating dermatitis, called, in its mild form, ery- 
thema scarlatinifarm, which has a sudden onset with febrile move- 
ment and a rash which rapidly spreads over the entire body and 
lasts four or five days, finally ending in desquamation. So closely 
may this disease resemble scarlet fever that a diagnosis during the 
first attack may be impossible for the first few days, but the condi- 
tion of the throat and tongue does not resemble the condition seen 
in scarlatina. Desquamation is often even more complete than in 
scarlatina, and the hair and nails are frequently shed. Relapses 
are very common and give rise to the reported cases of repeated 
attacks of scarlet fever. THE SKIN. 
213 
The rash of rubella or rubeola or rotheln (German measles) is a 
roseola, and more closely resembles that of scarlet fever in some 
cases than it does that of measles, but it is never as scarlet, is dis- 
tinctly maculated, and only at a distance looks homogeneous. Close 
examination always reveals the rash in oval patches, and it lacks 
the diffused character of the rash, the punctation of the skin, the 
grave systemic disturbance, and the throat-symptoms of scarlet 
fever. Further, the febrile movement is comparatively slight, and 
the rash lasts only two or three days. Slight desquamation may, 
however, occur. 
German measles is separated from true measles in many cases by 
the marked glandular enlargements, chiefly the posterior, cervical, 
axillary, and inguinal. 
The eruption of measles (morbilli) is very characteristic, aud can 
be in most cases easily separated from the other exanthemata by 
close examination. It is a roseola in character, but more dusky 
than that of scarlet fever. It appears about the fourth day of the 
illness in association with catarrh of the mucous membrane of the 
eyes and respiratory tract. Unlike scarlet fever it appears iu 
macules first upon the forehead or face, then on the neck, trunk, 
and limbs. The macules, which often coalesce, are arranged in 
crescents which are red, but become somewhat yellowish on pres- 
sure. They are slightly raised. There is nearly always to be seen 
some uninvolved skin, the entire surface not being covered as in 
scarlet fever. In some instances in which the eruption is aberrant 
a diagnosis of measles from scarlet fever is admittedly impossible 
until the case has been watched for some days; but the slow onset 
of measles, in which the eruption appears on the fourth day as 
against the first day in scarlet fever, the swollen eyes and nose, the 
pufliness of the face, the catarrhal condition of the mucous mem- 
branes, the curious fall of temperature after the preliminary rise on 
the first day, the short duration of the rash, all aid in the diagnosis 
of measles. The dusky eruption of measles can nearly always be 
found on the pharyngeal mucous membrane. (For the mouth and 
throat symptoms of scarlet fever and measles, see chapter on the 
Mouth and Tongue.) 
An erythema or roseola sometimes appears over the skin of chil- 
dren who have been vaccinated, generally about eight to ten days 
after the operation. It rarely lasts more than two days, and on its 
disappearance there is slight desquamation. 214 
THE MANIFESTATION OF DISEASE IN ORGANS. 
It also appears sometimes in cases of smallpox previous to the 
outbreak of the true eruption. Under the latter circumstances it 
is found most commonly about the groin and inner surface of the 
thighs and on the hypogastrium, loins, clavicles, and the extensor 
surfaces. So closely may the early rash of smallpox simulate the 
aberrant type of measles as to lead to grave mistakes in diagnosis. 
Sometimes an immediate diagnosis is impossible, even by the most 
experienced, but the rash of measles commonly appears on the face, 
therefore this difference, coupled with a history of exposure, the 
gradual development of the peculiar “ shot under the skin” sensa- 
tion of variola, and the ultimate distinct papulation, vesiculation, 
and pustulation of smallpox soon remove the doubt from the physi- 
cian’s mind. 
Day of Eruption of the Various Exanthemata. 
Day. 
Disease. 
Area. 
First to second day 
Rotheln or German measles. 
Varicella or chicken pox. 
Face first. 
Face or trunk. 
Second day 
Scarlet fever. 
Neck and chest. 
Third to fourth day 
Measles or morbilli or rubeola. 
Variola or smallpox. 
Face. 
Forehead, face, and wrists. 
Fourth to fifth day 
Typhus or ship fever. 
Trunk. 
Seventh to ninth day .... 
Typhoid or enteric fever. 
Abdomen. 
The remembrance that the incubation period of variola is twelve 
days, that of varicella seventeen days, of measles ten days, of rubella 
twenty-one days, and scarlet fever four days, will aid the diagnosis 
if a history of exposure cau be obtained. 
A diagnosis between the eruption of measles and variola often can 
be made by stretching the skin between the fingers, when, if it be 
measles, the papule cannot be felt, whereas, 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, septicaemia, 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 ab- THE SKIN. 
215 
sorption. 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 the rash often 
appears 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 delivery 
in a puerperal female, it is not a manifestation of scarlet fever, but 
is due to sepsis, although it is of course possible for scarlet fever to 
attack such cases at any time. The rash is usually found over the 
abdomen and inner sides of the thighs. The absence of sore throat, 
the presence of a septic 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 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 this connection it should not be forgotten 
that the rose-rash of typhoid fever may be so profuse, particularly 
in persons with a delicate skin, as to resemble scarlet fever; and, 
further, it is to be borne in mind that very rarely scarlet fever and 
typhoid may complicate one another. The abdominal symptoms 
of typhoid fever and the throat symptoms of scarlet fever aid in 
the differential diagnosis. It should be remembered, however, 216 
THE MANIFESTATION OF DISEASE IN ORGANS. 
that the exhaustion following an attack of scarlet fever may render 
the general appearance extremely like typhoid. In the relapse of 
typhoid fever the rose-spots often appear as early as the third or 
fourth day. In typhus fever they are much more plentiful and 
often form petechiae. 
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 ab- 
sence of febrile movement 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 
demarcation feels markedly 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 bailee form, the 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 insides of the thighs 
or the scrotum or vulva should give rise to the belief that the patient 
is suffering from a failure to properly pass or retain the urine, 
which, on escaping, irritates the skin. This is particularly apt to 
result if the urine is that of a diabetic. Again, it is an interesting THE SKIN. 
217 
fact that in some cases of tubercular peritonitis an erythematous rash 
appears on the abdominal wall around the navel. 
The presence of a roseola or erythematous rash often indicates the 
untoward influence of some drug, following its external or internal 
use. We find that it very commonly follows the ingestion of 
copaiba, and, as many persons suffering from venereal disease take 
this drug, the physician must use care not to be led into a diag- 
nosis of syphilitic roseola. It also follows the use of quinine, 
opium, antipyrine, and many other drugs, such as digitalis and 
chloral. 
The roseola caused by the use of copaiba appears by preference 
on the upper and lower extremities, and particularly on the backs 
of the hands, about the knees, the ankles, and on the chest, and it 
is often accompanied by fever. Indeed, the eruption caused by 
copaiba may closely resemble a papular syphilide; but its sudden 
onset, itching, and disappearance when the drug is stopped separate 
it diagnostically from the specific disease. 
The roseola following the use of bromide of potassium is, accord- 
ing to Veiel, very rare, and is distributed over the lower limbs. In 
children it may closely resemble measles. 
The roseola or erythema caused by quinine is to be separated from 
that of scarlet fever by the absence of fever, of the scarlet tongue 
and sore throat, and by the fact that there are no prodromes or cir- 
culatory disturbance except the characteristic evidence of cinchonism. 
In doubtful cases this is still further confirmed by analysis of the 
urine or by the use of the following simple test. Observe the dis- 
appearance of the fluorescence of the urine caused by quinine, after 
the sodium chloride has been removed by precipitation by nitrate of 
mercury, or after separating the quinine as an iodide by the addition 
to the urine of a solution of two parts iodine, one part of iodide of 
potassium, and forty parts of water. The iodide of quinine can be 
again dissolved by the application of heat. 
A distinct diffuse roseola sometimes follows the use of arsenic. 
Roseola may be caused by the use of salicylic acid and strych- 
nine, and a scarlatiniform rash sometimes appears in blotches over 
the face and body in persons who are taking turpentine. 
Roseola also ensues in some persons after the application of sur- 
gical dressings containing iodoform,corrosive sublimate, and carbolic 
acid, being due either to a local effect of these drugs or to their 
absorption from the dressings. Arnica tincture applied for sprains 218 
THE MANIFESTATION OF DISEASE IN ORGANS. 
or bruises may produce marked roseola, or even erythematous and 
erysipelatous swelling of the skin, as already stated. 
By far the most important drug-exanthem is that caused by atro- 
pine, the rash produced by it being very like that of scarlet fever, 
except that it lacks the red punctations of that disease. This rash 
may be associated with a slight rise in temperature and be followed, 
rarely, by desquamation. The face of a child suffering from an 
overdose of atropine is very characteristic. The eyes are bright, 
the pupils widely dilated, and the skin over the malar bones is red, 
but striking lines of pallor reach from the corners of the mouth to 
the nose. There may be active, talkative delirium and very mild 
convulsions from overdoses of atropine, thus making the resem- 
blance to the onset of scarlet fever very striking. The brief dura- 
tion of the rash, its lack of punctation, the absence of high fever, 
and the history of the patient having taken atropine or belladonna, 
all help to make the differential diagnosis. 
Roseola, followed by desquamation, has been known to follow the 
hypodermic injection of mercury. Sometimes the use of blue oint- 
ment produces a widespread rash resembling measles, and this resem- 
blance may be increased by the development of a febrile movement. 
A similar eruption may ensue from the ingestion of opium. 
Erythematous rashes, too, frequently follow slight irritation of 
the skin in persons who use chloral. 
Acne of the skin, particularly on the face, is often produced by 
the use of bromide or iodide of potassium, or of any preparation 
containing bromine or iodine. That produced by iodine is gener- 
ally sudden in its onset and profuse in its distribution. The base 
of the pimple is bright red, the top speedily becomes pustular, and 
Fournier states that it may be hemorrhagic. Stopping the inges- 
tion of the drug speedily relieves, or at least decreases, the eruption. 
The acne due to bromine is often very profuse, and the pimples in 
severe cases may coalesce, making sloughs of considerable size with 
an indurated base. 
In some persons, generally females, there is developed an acne on 
the face, breast, and back, as the result of taking iron as a tonic. 
In addition to the acne caused by drugs, or their compounds, we 
should also mention the acne and furuncles appearing in persons 
working in paraffin, which is due to blocking of the sebaceous glands. 
Closely associated with this form of eruption is that which is 
characteristic of smallpox and chickenpox. The eruption of small- THE SKIN. 
219 
pox appears on the second or third day in the form of tiny specks, 
resembling flea-bites. These rapidly become papules, which have 
Fig. 94. 
Smallpox eruption on the seventh day. 
an indurated base, so that they feel as if shot were under the skin. 
(Fig. 94.) After about thirty-six hours these papules become vesi- 
cles, containing a turbid fluid, which speedily becomes purulent, 
Fig. 95. 
Smallpox eruption on the eighth day. 
forming; a pustule. (Figs. 95 and 96.) Generally this process of 
maturation takes three days and, with the development of the pus, 220 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
the so-called secondary fever, which may be even higher than the 
primary fever of invasion, sets in. After a period of eighteen to 
twenty-one days the pustules drop off, having become dried up, 
leaving, if the attack has been severe, or the skin delicate, deeply 
pitted scars. Although the eruption of smallpox appears on the 
Fig. 96. 
Smallpox eruption on the eleventh day. The pock is seen to he umbilicated. 
forehead, which is the favorite seat of acne in many cases, a differ- 
ential diagnosis is not difficult, since the grave systemic disturbance, 
febrile movement, and rapid involvement of the whole surface of 
the body speedily indicate the true nature of the disease. The 
early appearance of the rash on the hands in variola is also a diag- 
nostic sign, as acne in this part of the skin is practically unknown. 
Then the sudden development of the eruption in smallpox is entirely 
different from the gradual onset even of the most intense acne. THE SKIN. 
221 
In some cases a purulent acne of the forehead develops in syphilis. 
The separation of variola from measles has already been discussed, 
and it is only in the papular stage that the former disease can be 
confused with the latter, while the reddened mucous membranes and 
swollen face of the case of measles soon determine the diagnosis. 
The rapid formation of vesicles and the shot-like sensation of the 
eruption show that the eruption is not measles. 
Fig. 97. 
Typical vaccine vesicles. Tenth day. 
The appearance of the eruption of vaccinia following vaccination 
must be next described. Three or four days after the vaccination 
a single or several papules arise on the scarified surface, which by 
the sixth day are changed into umbilicated vesicles, which soon 
unite and form one vesicle the size of a five-cent piece. This vesicle 
finally forms a scab which falls off after the expiration of about 
three weeks from the inoculation. A “ good take” is always sur- 222 
THE MANIFESTATION OF DISEASE IN ORGANS. 
rounded by au areola of rosy red of several inches in width. Rarely 
severe inflammation and sloughing ensue. (Fig. 97.) 
In chickenpox the eruption appears on the first or second day 
and keeps coming out for several days. It is rose-colored and occurs 
as papules, which immediately become vesicles. They last but four 
or five days, and are usually associated with very mild febrile dis- 
turbance, the child remaining but little indisposed if well cared for 
and nursed. Unlike smallpox, varicella does not become umbilicated, 
and rarely leaves pits in the skin unless the vesicles are picked at 
by the finger-nails. Neither do the vesicles become pustules unless 
infected by picking or the child is in a condition of debility or suffers 
from struma. YTaricella is separated from variola by the absence of 
severe systemic disturbance, by the rash first appearing on the chest 
and neck instead of the forehead and hands, by the presence of 
other cases of the disease in an epidemic, and, finally, by the fact that 
it attacks children who have been well vaccinated, whereas small- 
pox does not. The history of exposure is, of course, an important 
point to be investigated. 
An eruption closely resembling chickenpox or smallpox is that 
called impetigo contagiosa, in which there are found multiple, flat- 
tened or slightly umbilicated roundish or oval vesicles, pustules, or 
blebs, which form after some days dry yellowish crusts. It occurs 
in childhood, or early adult life, and is often associated with some 
degree of fever. The areas involved are the face, neck, buttocks, 
hands, and feet. The lesions of the skin are larger than in chicken- 
pox, but often follow this disease. As its name indicates, the 
disease is contagious, and the occurrence of a series of cases in close 
proximity to one another should not mislead the physician into a 
diagnosis of variola or varicella. The eruption lasts about two 
weeks, and Kaposi asserts that swelling of the submaxillary glands 
is always present. We can further separate impetigo contagiosa 
from varicella by the localization of its eruption to one area, as a 
rule, by the faet that the eruption becomes bullous or purulent, and 
by the larger size of the vesicle. From smallpox we can separate 
it by the absence of severe pain in the back, the grave systemic dis- 
turbance, and the secondary fever of that disease, accompanied as 
they are by the smallness of the pox, the peculiar odor of the 
patient, and the history of exposure to variola. 
In the presence of a papular, pustular, or vesicular eruption of 
the skin it must be remembered that quinine sometimes develops THE SKIN. 
223 
these lesions in susceptible persons. In some instances where it 
involves the hands it may indicate that a local effect has been pro- 
duced by working with the drug. 
Eczema in its various forms may appear as the result of the use 
of quinine internally or locally, or of the employment of mercury 
internally or externally. When it arises from the use of iodide of 
potassium, which is very rare, it chiefly affects the scalp and scro- 
tum. The development of an eczematous irritation of the skin 
sometimes follows the use of chloral. 
Herpes labialis is a very constant lesion associated with croupous 
pneumonia, and its development is said to be a favorable sign. It 
is also an important sign for the separation of epidemic cerebro- 
spinal meningitis from meningitis due to other causes, as it is not 
commonly present in the non-epidemic form. It sometimes arises 
as a result of using salicylic acid. 
The development of recurring crops of boils in persons not ex- 
posed to paraffin or tar should cause the physician to suspect the 
presence of diabetes mellitus, or at least that there is general de- 
bility, and particularly an absence of lime salts from the system in 
the proper quantity. When the ordinary boil passes into a condition 
of marked induration about its base, with sloughing of the sub- 
cutaneous tissue and necrosis of the skin, which becomes perforated 
by the openings of several sinuses, we have to deal with a carbuncle 
or anthrax simplex. The disease usually appears on the back of 
the neck, on the back, or the lip. The systemic disturbance is very 
great and the exhaustion profound. The skin covering the area 
involved becomes grayish or bluish-black, and then separates as a 
large mass, while the subcutaneous tissue comes away in shreds. It 
is a dangerous disease in all persons, but particularly so in those who 
are already weakened by other diseases or excess. 
The development of a painless macule on the skin of the hand 
or foot, followed by an acutely inflamed papule which itches and is 
soon changed into a relaxed vesicle containing bloody serum, in 
which there is a hard nucleus which rests upon an indurated base, 
is the initial manifestation of anthrax maligna or malignant pustule. 
The lymphatics soon become swollen, and metastatic abscesses 
speedily form elsewhere, as in the axillary glands. The systemic 
symptoms are severe, sometimes being manifested in high fever, in 
other cases by a typhoid state. Death is very commonly the sequel 
(65 per cent.), even if prompt surgical interference takes place. 224 
THE MANIFESTATION OF DISEASE IN ORGANS. 
There is generally a history of exposure to infected animals or their 
hides. Malignant pustule is to be separated from carbuncle by its 
fulminating character and peculiar appearance. 
When an erysipelatoid rash with swelling of the skin and the 
development of papules, vesicles, pustules, and bullae appears in 
association with induration of the skin, with sloughing eventually 
taking place, the disease may possibly not be erysipelas of a phleg- 
monous form, but glanders or equina. Numerous inflammatory 
foci appear in the skin in glanders which end in local abscesses and 
hemorrhagic nodules, and profound systemic infection is always 
present. The presence of a sanious discharge from the nose aids in 
confirming the diagnosis. Death usually comes in a few days in 
this acute form. Should the course of glanders be chronic, pustules 
somewhat like those of smallpox, except that they are not umbili- 
cated, lie on an indurated base, and in them is formed a viscid or 
sanious pus of offensive odor. This disease is rare. Both forms 
arise from infection from a horse suffering from the malady. Glan- 
ders may be confused with variola or the pustular and gummatous 
stages of syphilis. 
The development of pea-sized or larger bullae upon the skin may 
indicate the presence of pemphigus, or if there is central nervous 
disease involving the spinal cord and resulting in trophic lesions 
similar bullous eruptions may take place. The bullae, if they con- 
tain a dark bloody fluid and are situated upon a limb in which there 
is an abnormally high temperature, are peculiarly indicative of cen- 
tral nervous lesions, particularly if there is a tendency to dilatation 
of the capillaries of the skin on slight irritation; but if the tem- 
perature of the entire body be raised, the physician should remem- 
ber that pemphigus is a disease in which there is often marked 
febrile movement. Sometimes these bullous manifestations are fol- 
lowed by gangrene in cases of neuritis or other disease causing 
trophic lesions, such as myelitis and paretic dementia. 
Bullae on the face may follow the ingestion of antipyrine or iodine 
compounds. 
The development of a pemphigus-like eruption in the skin may 
follow the use of salicylic acid or copaiba. 
In the cases of herpes zoster the skin lesion often has its origin in 
compression of the spinal cord, or in such diseases as tabes, spinal 
meningeal irritation, and peripheral neuritis. 
Glossiness of the skin, in which its minute creases become THE SKIN. 
225 
smoothed out and it appears unduly shiny, often results from chronic 
disease involving some portion of the nervous system connected with 
the government of nutrition. Very commonly it results from 
peripheral neuritis. In addition to glossiness there are often red- 
ness and marked thinning or thickening of the cuticle and subcuta- 
neous tissues. 
Gangrene of the skin may follow nerve injuries or central ner- 
vous lesions. Thus it may follow upon division of a nerve-trunk, 
or be due to cerebral abscess, in which case the gangrene will be 
with the other localizing symptoms on the opposite side of the body. 
The cerebral form develops suddenly and without the prodromal 
redness of bed-sores as seen in prolonged illnesses. Similar rapidly 
developing sloughs and ulcerations of the skin are seen in cases of 
acute myelitis and in the second and third stages of paretic dementia. 
A very interesting condition is the so-called spontaneous gangrene 
of hysteria. On the skin, generally of the breast of a young girl, 
a spot develops which feels to her to be hot and burning. The skin 
soon becomes very white, then in a few hours very red and forms a 
wheal. This rapidly becomes dark and bluish-black, looking like 
a burn of sulphuric acid, and a slough finally comes away, leaving 
a permanent cicatrix. 
Gangrene of the skin follows upon diabetes mellitus, and may 
involve the scrotum or vulva if the irritation of these parts by the 
urine is constant. More commonly the toes are affected, and there 
is this important differential point that in the gangrene of old 
age with bad vessels the lesion is usually at the tip of the toe, 
whereas in diabetic gangrene it is frequently about the ball of the 
biff toe or on the sole or dorsum of the foot. Previous to the devel- 
oprnent of gangrene there are developed bullae and other inflamma- 
tory changes in the skin which is about to be affected. Kaposi 
describes a serpiginous form of gangrene affecting the leg in diabetics 
and a variety of tissue break down, in which a dermatitis, followed 
by ulcers and a lupus-like formation, also occurs in diabetes. 
Perforating ulcer of the foot occurs in locomotor ataxia and in 
paretic dementia. 
Closely related, yet quite distinct from angioneurotic oedema, is 
that condition called Raynaud’s disease, symmetrical gangrene, or 
local asphyxia, according to its severity. The fingers and toes or 
the nose, with or without exposure to cold, are found to be pale 
and livid, looking like a hand from which all the blood has been 226 
THE MANIFESTATION OF DISEASE IN ORGANS. 
removed by the use of au Esmarch baudage. The part often feels 
as if “ asleep,” and is more or less numb and without sensation. 
To the touch the part is cold and waxy, and it does not bleed when 
pricked. With the onset of these signs there are often general 
chilliness and malaise. Often this manifestation speedily disap- 
pears, leaving the skin apparently normal; but if it persists, the 
skin becomes glossy, shrivelled, and looks as if it had been soaked 
in hot water for hours. When the disease is more severe the pale 
waxiness is supplanted by cyanosis till the finger-tips, for example, 
look as if dipped in blue ink; there is often local swelling; the skin 
is frequently found to be sweating freely and is distended with blood. 
The skin may rapidly separate from the deeper tissues and become 
necrotic in patches or en masse, and the entire tip of the finger, after 
becoming black, shrivels up into a condition resembling dry gan- 
grene, which is separated from the sound skin by a sharp line of 
demarcation. Sometimes small necrotic patches slough out, which 
leave cicatrices telling of the attack. The prognosis is not bad. 
The most interesting complication of the disease is paroxysmal 
hsemoglobinuria. 
The development of gangrene of the fingers and toes sometimes 
follows the prolonged use of bread made from rye which is iufected 
by ergot. 
Sometimes gangrene of the skin follows severe attacks of the 
exanthemata in children who are strumous or very feeble, or who 
are syphilitic. 
Ulcers about the base of the finger-nails should rouse the suspi- 
cion of the excessive use of chloral. 
Bedsores may develop whenever by long-continued pressure upon 
any part of the body the local circulation is disturbed, particularly 
if in addition there is general systemic debility from some exhaust- 
ing disease, such as typhoid fever. They also develop very speedily, 
and apparently almost spontaneously, in the course of acute trans- 
verse myelitis. Under these circumstances the sacrum is the area 
most severely affected. Sometimes these sloughs have been known 
to develop as early as six hours after the beginning of the attack. 
Associated with the involvement of the soft tissues the bones may 
break down, and cellulitis about the rectum and bladder place the 
patient’s life in immediate jeopardy. In hemiplegia, particularly in 
that which is due to cerebellar hemorrhage, bedsores often form on 
the buttocks, and in paraplegia, from other causes than transverse THE SKIN. 
227 
myelitis, upon the sacrum. They also appear on the heels, inside 
of the knees, and about the hips in some cases of paraplegia. 
Sudden sloughing of the skin of the nates sometimes occurs in 
cases of intracranial hemorrhage, and is said by Joffroy to be con- 
nected with lesion of the occipital lobes. 
The value of roseola and rupial eruptions in the diagnosis of 
syphilis has already been dwelt upon. When the roseola becomes 
transformed into slightly elevated or bean-shaped spots, irregularly 
scattered, but sometimes forming groups which are apt to be circu- 
lar, and these circles become marginated and then scaly on the 
edges, resembling lepra or psoriasis, or even go further than this and 
develop bullse and blebs, and when the sores which form are filled 
with a clear liquid which may become sanious or turbid and on 
drying leave crusts, the removal of which reveals deeply excavated 
sloughs, the area of the slough often being as large as a silver dollar, 
but often irregular in outline, syphilitic rupia is probably the lesion. 
There is, however, this important differential point, namely, that 
in specific rupia there is an essential feature, a peripheral ring of 
induration, whereas in the non-specific form this induration is 
absent. 
If, in addition to these variations, the eruptions are dusky red 
and leave behind them on healing copperish-looking discoloration 
of the skin, and appear on areas, such as the flexor surfaces, where 
ordinary skin eruptions are rarely seen, the diagnosis of syphilis is 
highly probable. If the eruption is chiefly tuberculated and the 
tubercles are large and more marked than usual, and if they ulcer- 
ate and become deep sores, and finally form on healing well-marked 
cicatrices, tertiary syphilis is to be considered the probable cause. 
If, agaiD, we find small nodules under dusky red skin, which 
finally breaks down and discharges bloody serum, or pus which in 
burrowing forms discharging sinuses, syphilis of the third stage 
may be regarded as a likely cause. 
The appearance of hard, dark-brown infiltrated areas in the skin 
may be due to the excessive use of bromine, and as they gradually 
become depressed in the centre closely resemble in some cases the 
nodules of syphilis. 
The skin of the abdominal walls in cases of ascites is apt to be 
not only thinner than normal, but tense and slightly shiny, while its 
appearance when viewed in a good light may be slightly blue like 
the iridescence of certain kinds of glassware. 228 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Scars of the skin often give us much useful information. 
Early tendencies to struma or tuberculosis may be found in the scars 
resulting from suppurating cervical glands. In the groin such 
scars may be an evidence of venereal infection, although it should 
be remembered that suppuration of these glands usually takes place 
as a result of chancroids and not from true chancre. It has already 
been shown that syphilitic skin lesions often leave scars to mark 
their site. Scars upon the head tell us of possible injuries to the 
brain in suspected traumatic epilepsy, or of falls in epileptics. 
Similarly, other traumatisms in the history of the patient may be 
discovered by scars elsewhere. 
The presence of numerous regularly arranged fine scars on the 
chest or elsewhere may develop the fact that the patient has at some 
time been wet-cupped for some pulmonary or other disease; or if the 
peculiar three-pointed scar of the leech is seen, another good evi- 
dence of a bleeding is presented. 
When the skin of the abdominal wall exhibits striae or scars 
arranged in parallel series, it indicates that it has been stretched 
very considerably by pregnancy, ascites, or, more rarely, by exces- 
sive corpulence. Sometimes these striae appear on the lower limbs 
in pregnant women or in persons with dropsy. Very rarely they 
may develop on the arms or legs or elsewhere during convales- 
cence from some grave disease, such as typhoid fever. 
Sweating of the skin, aside from the normal and almost im- 
perceptible exhalation of moisture, takes place in health as a result 
of severe muscular exertion, whereby the peripheral circulation is 
increased and the bodily temperature raised, or when the body is 
very heavily clad or exposed to external heat in excess. In all 
these cases the sweating is to be regarded as a physiological effort 
on the part of the body to reduce its temperature by increased evap- 
oration from the surface. In disease sweating provides us with very 
important information in many conditions. 
During the course of fevers, which naturally end by crisis, the 
occurrence of a profuse sweat (generally associated with a fall of 
temperature) gives us the first sign of beginning convalescence, and 
in irritative fevers, or those due to cold and congestion, the artificial 
production of a sweat is decidedly a good omen. The sweat of 
crisis is perhaps most marked in croupous pneumonia. Profuse 
sweating is also a characteristic symptom of relapsing fever, pyae- 
mia, acute ulcerative endocarditis, phthisis, malarial fever of the THE SKIN. 
229 
distinctly periodic type, and of typhoid fever and collapse. Con- 
stant profuse sweating is marked in some cases of acute articular 
rheumatism, and it is worthy of note that while sweating generally 
occurs in febrile diseases at a time when the temperature is falling, 
in rheumatism the febrile movement may even increase during the 
sweat rather than decrease. 
Profuse so-called colliquative sweats often occur at night in debil- 
itated persons without the presence of any febrile movement, and 
are an evidence of profound nervous and vasomotor relaxation. 
Moderate sweating sometimes is seen from similar causes in feeble 
persons after taking anything in the food or drink which produces 
circulatory or nervous excitement. Localized sweatings occur 
almost solely in subjects of nervous disease, which is often organic, 
as in paretic dementia, and sometimes functional, as in hysteria 
or Raynaud’s disease. They depend upon perverted vasomotor 
influences sent to the glands and their supplying vessels in partic- 
ular areas. Localized sweating of one side of the face or neck or 
chest is often a most important sign of a thoracic aneurism pressing 
on the cervical sympathetic. Bromidrosis may occur in hysteria, 
or the head may be the only part affected in Graves’s disease and 
in migraine. Profuse sweating of the head of an infant when 
sleeping may be indicative of rickets. 
In cases of the uraemia of cholera or of renal disease there may 
be profuse sweating, which takes the place of the dry and hot skin 
seen more commonly in this condition. The surface of the entire 
body is usually involved in the sweat. 
The quality of the sweat varies greatly in many persons. In 
cases of deficient renal activity it often contains urinary elements, 
smells uriniferous, and may even deposit particles on the skin in 
small white scales, particularly on the forehead and nose. This is 
called uridrosis. In jaundice the sweat may be bile-stained. 
Excessive dryness of the skin is seen in grave forms of renal 
disease, in nearly all acute fevers with a high temperature, and in 
cholera and diabetes, in which diseases the dryness is largely the 
result of the drainage of liquids from the body. 
Sometimes after a prolonged dryness of the skin during high 
fever, as soon as sweating begins hundreds of little blisters develop, 
due to retained sweat under the epiderm. These are called miliaria 
or sudamina. 
When the skin is dry and harsh, and the naturally thickened por- 230 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
tions have in their folds a peculiar white appearance as if filled with 
meal, diabetes should be sought for. Rarely the physician may be 
deceived by profuse sweating in diabetes. 
Dropsy and Swelling- of the Skin. Swelling of the skin and 
subcutaneous tissues occurs most frequently as a result of dropsy, in 
which condition the lymph-spaces become filled by liquid. The skin 
in the area involved is not only swollen but doughy, or if the effu- 
sion is very great the skin may be of almost board-like hardness, 
so tensely is it distended. Pressure with the tip of the finger upon 
such an area will result in pitting, and this is one of the more im- 
portant signs separating dropsy or true oedema from the swelling of 
acute inflammation, which, while it may be very tense, does not pit. 
Further, the swelling of inflammation is usually localized, reddened, 
and feels hot to the touch, whereas the dropsical swelling is more 
diffuse, is pale, and the temperature of the part is lower than 
normal. 
When the effusion of liquid is limited to one portion of the body 
it is usually called oedema or localized dropsy, whereas if the entire 
body is boggy it is designated general anasarca. Dropsy is to be differ- 
entiated from myxoedema by the facts that in the latter disease the 
onset is very slow, the swelling does not pit on pressure and is univer- 
sal and fairly equally distributed over the body, the thyroid gland 
will often be found diseased, the subcutaneous tissues are not boggy 
but resistant, and there is ansesthesia of the skin. When the sub- 
cutaneous tissues are distended by air, instead of liquid, they are 
even less resistant than in dropsy, the swelling is usually very local- 
ized and does not pit, and the part crackles or crepitates on gentle 
pressure. 
The presence of dropsy is indicative of many widely separated 
diseases. In the first place, it may indicate a deficient circulation 
of blood, either by reason of a feeble or diseased heart or because 
of obstruction by the pressure of growths, thrombi or emboli. 
It may be due to disease of the walls of bloodvessels and lym- 
phatics, as is generally the case in renal disease, or it may arise from 
disease of the blood itself. Again, in some cases it is due to dis- 
ordered nervous control of the vessels, by reason of centric or 
peripheral changes which may be organic or functional. 
The significance of a widely diffused general dropsy or anasarca 
is generally that there is well-marked renal disease, and this proba- 
bility is greatly strengthened if the oedema of the face be well THE SKIN. 
231 
marked, particularly in the morning on arising, disappearing as the 
day goes on. The skin in such cases will usually be quite pale, 
and an examination of the urine will reveal the presence of the 
signs of nephritis. The next most common cause of general ana- 
sarca after renal disease is heart disease. When due to this cause 
it willjbe found that the ghastly pallor of renal anasarca is replaced 
by cyanosis, and often by engorgement of some of the superficial 
veins, while the physical signs of cardiac disease will confirm the 
diagnosis. General anasarca may rarely arise as a result of a mul- 
tiple peripheral neuritis, and it also occurs as a symptom of beri- 
beri and from the excessive nse of large amounts of arsenic. This 
arsenical anasarca may be due to the neuritis produced by the drug, 
although Wood thinks it is due to a cellulitis. Rarely we find gen- 
eral anasarca in cases of advanced cancerous cachexia, and care 
must be exercised that the hsemic murmur due to anaemia does not 
mislead the physician into a diagnosis of heart disease. 
Dropsy widely diffused or localized in the feet and legs also occurs 
in scurvy. 
The most common seat of localized dropsy or oedema is the feet 
and legs, particularly about the instep, the ankles, and the tibiae. 
When it is bilateral it is generally indicative of cardiac failure or 
more rarely of renal disease. Nearly always, if it be renal, a care- 
ful examination will discover the oedema in other parts of the body, 
although it may be most marked in the feet and legs. In many 
cases the various serous sacs, such as the pericardium, peritoneum, 
and pleurae, will be found to contain more liquid than normal, and 
the tissues generally will be found infiltrated. 
Other causes of oedema of the feet and legs are anaemia, and 
obstruction to the return of blood from the lower limbs by reason of 
growths in the abdomen pressing upon the iliac veins or inferior 
vena cava. Thus cancer of the pancreas sometimes causes oedema 
of the feet and legs in this manner. Very rarely oedema of the 
lower extremities follows hepatitis or cirrhosis of the liver as a 
primary symptom. Usually such lesions produce ascites alone, or 
if the legs are involved they become so by reason of the pressure of 
the fluid in the pelvis during the time that the patient is sitting up 
or standing. This latter cause of bilateral oedema of the lower 
limbs is, however, rare. Sometimes oedema of both legs and feet 
comes on in persons who, though feeble and relaxed, remain stand- 
ing with little muscular movement during many hours in the pur- 232 
THE MANIFESTATION OF DISEASE IN ORGANS. 
suit of their occupation, as in typesetters and salesmen. In other 
instances, very much more frequently, oedema of the feet and legs 
comes on in the course of profound anaemia resulting from slow 
hemorrhages or other causes. It is also seen in the cachectic stage 
of gastric cancer, owing to the anaemia which is present. General 
swelling of a leg in a puerperal woman is probably due to phleg- 
masia alba dolens, and this affection may also be bilateral. Both 
Herman and Cameron Kidd have each reported a case of bilateral 
phlegmasia alba dolens occurring in a virgin with anaemia. When 
it occurs in males it is most commonly unilateral and a complication 
of convalescence in typhoid fever. It is due to thrombosis of the 
left femoral vein, as a rule. 
When the face is oedematous the swelling is most marked under 
the eyes, the lower lids of which are particularly puffy in the morn- 
ing and nearly normal in appearance at night. This form of oedema 
is most marked in, and is almost pathognomonic of, renal disease. 
Its only other causes are the excessive taking of arsenic and angio- 
neurotic oedema. More alarm should be felt at a slight swelling of 
the face of this character than if the feet are markedly puffed. 
Sometimes oedematous swelling of the side of the face and scalp 
which has been involved in a severe attack of neuralgia takes 
place. 
When oedema of one or both eyelids occurs, with protrusion of 
the eyeball, the swelling extending to the rest of the face as time 
goes on, it forms an important symptom in obscure cases of sus- 
pected cerebral thrombosis, and is caused by the intimate association 
between the intracranial vessels and those of the face. 
Sometimes oedema of the eyelids comes on in neurotic subjects 
and may extend to the forehead. This may be seen in children, 
most commonly about puberty, and is probably the result of a 
neurosis. 
(Edema of the upper extremities alone only results from causes 
interfering with the flow of blood, such as are produced by morbid 
growths in the chest, as mediastinal growths, and in cases of aneu- 
rism. When the swelling is limited to one arm or leg it is a sign 
that there is interference with the local circulation, as, for example, 
the obstruction of the femoral vein by thrombus, as in phlegmasia 
alba dolens following labor or enteric fever, or, when the oedema is 
in the left leg, by cancer of the sigmoid flexure. If the swelling 
of the arms and head is manifested suddenly, it may be due to THE SKIN. 
233 
that rare condition in which an aortic aneurism ruptures into the 
vena cava; whereas if it develops slowly, it is due to pressure by 
a growth. 
There remain three forms of local oedema of some diagnostic sig- 
nificance, namely, that occurring in a limited area over some deep- 
seated suppurative process, as in the skin back of the ear in cases 
of mastoid abscess or thrombosis of the lateral sinuses, that over 
the ribs in cases of purulent exudation into the pleura, and that 
on the thigh in the deep muscular abscesses which sometimes follow 
typhoid fever. 
(Edema of the legs and wrists sometimes complicates relapsing 
fever, and is evidence of profound feebleness, without necessarily 
indicating renal or cardiac disease. Such a limited oedema, or even 
general anasarca, may occur during convalescence from typhoid 
fever from similar causes. Unless this effusion is associated with 
signs of grave renal or cardiac mischief the prognosis, according to 
Lendel, is favorable. 
When the, skin is pale and affected by an oedematoid swelling, 
with thickening, hardening, and loss of elasticity, particularly about 
the face, and also in the trunk and extremities, and if this swelling, 
which resembles oedema, fails to pit on pressure, the physician should 
remember that myxoedema, or the cretinoid oedema of Gull, may be 
present. If in addition to these signs there is a half-idiotic or 
heavy expression of the face, a slow and labored manner of speech, 
with thickened, clumsy fingers, the diagnosis is made practically 
certain. The brain in this disease perceives or grasps ideas very 
slowly, and all the functions of the body seem torpid. 
There are several other diseases in which great thickening of the 
skin takes place, which cannot, however, be confounded with myx- 
oedema. In elephantiasis there is a hypertrophy of skin and subcu- 
taneous tissues which is confined to some particular region of the 
body and arises from local circulatory disturbance in the blood and 
lymph-vessels. The skin is very hard, so that the leg, if affected, 
feels like a solid mass of wood. The disease most commonly affects 
one of the legs, rarely both, and the scrotum. In both myxoedema 
and elephantiasis the process develops very slowly. 
When the skin is dotted with irregular patches or streaks, which 
may be depressed, elevated, or tightly stretched, or if the entire 
skin is thickened, covered with thin scales, or possesses a plaster- 
like appearance, the physician should recognize these symptoms as 234 
THE MANIFESTATION OF DISEASE IN ORGANS. 
indicative of scleroderma. If in addition to these signs there is a 
fleeting pitting of the skin on pressure, and it cannot be pinched 
into a fold, the diagnosis is confirmed. Sometimes the skin in 
scleroderma seems bound down by tense cords or bands of retracted 
connective tissue. 
If during the first months of life the skin of an infant becomes 
oedematous, hard, tense, and glossy, varying in color from a white 
to a reddish or dirty yellowish-brown, and if this rapidly involves 
the entire surface so that the integument becomes cool, immovable, 
and resistant, the child appearing as if frozen into stiffness, it is 
probably suffering from sclerema neonatorum, a disease entirely 
different from the scleroderma of the adult. As a rule, death 
speedily ensues; but before this take place the parts first affected 
become thin and lose their swelling and may develop cyanosis and 
gangrene. 
The affection just described is to be separated from oedema neona- 
torum, a condition arising in prematurely born children. Within 
a few days after birth there is discovered a pallid, cold condition of 
the buttocks, thighs, legs, and arms. The parts speedily become 
oedematous and livid blue. Finally the oedema may become very 
marked and the skin tense in consequence. Intense drowsiness is a 
characteristic of the disease. Death commonly ensues, but recovery 
may occur. While the color of the skin may be identical in oedema 
neonatorum and sclerema neonatorum, the former affection lacks the 
stiffness of the jaws and other joints, and the pitting on pressure is 
marked. As scleroderma does not occur before the first year it can 
be excluded from the diagnosis. 
Very qlosely allied in its causes and appearance with urticaria of 
the severe type is angioneurotic oedema. In this condition there 
appear upon the skin numerous patches or plaques of circumscribed 
puffy swellings, which have a red appearance and vary from the size 
of a nickel to a silver dollar or larger. There is an absence of itch- 
ing, an important difference from true urticaria, but the part affected 
may be tense or hot to the patient. These attacks are generally 
recurrent, and take place in neurotic persons. They may cause loss 
of sight through swelling of the eyelids and, where the mucous 
membranes of the pharynx and larynx are involved, serious inter- 
ference with breathing. The swelling of angioneurotic oedema 
does not pit, and it is to be separated from the blue oedema and 
white oedema of hysteria. True angioneurotic oedema is rare in THE SKIN. 
235 
hysteria, and if localized swellings do result from this condition the 
physician will generally find marked hysterical signs manifested, 
such as disorders of sensation or tenderness over the ovaries. 
The ocular appearance and touch of the skin having been 
studied in so far as its surface affords evidence of more deeply 
seated disease or functional disturbance, we next pass to a 
study of its sensibility, having the same diagnostic objects in 
view. 
Sensation in the Skin. Before considering the various perver- 
sions of its sense it is important to remember that the sensibility of 
the skin may be divided into four parts, namely, its tactile sense, 
its pain sense, its thermic sense, and its sense of pressure. Any 
one of these senses may be perverted or in abeyance without the 
others being affected in a similar manner, and it is noteworthy that 
while corresponding areas of the skin in all individuals have prac- 
tically identical sensibilities, each part of the skin has a sensitiveness 
of its own, so that while in some parts the slightest touch is felt, in 
others severe irritation must be produced to cause much of a result. 
These differences have been carefully studied by many observers, 
the most thorough being Weber, who has found that the average 
ability to separate points brought in contact with the skin is about 
as follows: at the finger-tips points can be separated at from 2 
to 3 millimetres, on the lips 4 to 5 millimetres, on the tip of the 
nose 6 millimetres, on the cheeks and backs of fingers 12 millimetres, 
and on the forehead 22 millimetres. The skin on the neck separates 
points at 34 millimetres; that on the forearm, on the lower leg, and 
back of foot at 40 millimetres; on the chest at 45 millimetres, on the 
back at 60 millimetres, and on the arm and thigh at 75 millimetres. 
If tests be frequently repeated in a single individual, the ability to 
separate the points increases with training. Care should always be 
taken that the pressure on both points is equal, applied simulta- 
neously, and that the points are equally sharp. 
In testing tactile sensibility, not only should points be used, but 
also objects. Often single points may be applied without any 
abnormal manifestation, and, in some cases of disease, the skin, 
which seems devoid of sense on ordinary touch, is found to be exces- 
sively hypersesthetic if the hand is drawn lightly over it. 
The best apparatus for testing tactile sensibility is the aesthesi- 
ometer of Carroll, which is a pair of double-pointed compasses con- 
nected by a graduated scale. (Fig. 98.) 236 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The ability to distinguish pain-giving and thermal applications 
is most acute in the normal skin of the hands, in which tactile sense 
is also most acute. 
Fig. 98. 
Carroll’s aestheslometer. 
The methods by which we test the pain sense are several, but 
chiefly by pricking the skin, more or less deeply, with some sharp- 
pointed instrument, such as a pin, or by pinching the integu- 
ment. The thermal sense is studied by applying bodies which are 
hot or cold against the skin, such as a cold knife, a small piece 
of ice, or a test-tube which contains very cold or hot water. In 
all such tests the physician should use both hands simultaneously. 
With one he should apply his instrument to the suspected area, 
and with the other a similar instrument to an area known to be 
healthy, in order that an actual comparison as to the sensations 
may be noted by the patient. Thus the face may be used as the 
normal area in a spinal lesion, and the skin of the arms as a control- 
surface in a lesion involving the legs. The eyes of the patient 
should be blindfolded, and if tactile sense is being tested the instru- 
ment must be of the same temperature as the body. 
Disturbances in the sensation of the skin may arise from func- 
tional or organic disease involving the peripheral nerves, the sen- 
sory tracts in the spinal cord, similar tracts in the lower part of the 
brain, and, finally, the subcortical or cortical parts of the cerebrum 
itself. 
The sensory pathway or the afferent fibres pass upward, starting 
with the peripheral sense-organ in the skin, or elsewhere, and after 
forming part of the nerve-trunk and entering the ganglion on the 
posterior root, enter the spinal cord by what is called the posterior PLATE VI. 
Diagrarn showing Course of Sensory Fibres frorri Periphery to Cord, 
Cerebrurp and Cerebeilurp. (Flatau.) THE SKIN. 
237 
root, which is shown in the figure near the words “Lissauer’s 
zone.” (See Figs. 99 and 100.) 
The posterior root enters the cord in three sets of fibres; one of 
these, the one lying nearest the posterior median fissure, is composed 
of coarse fibres and is called the median bundle, and'passes obliquely 
into the lateral part of the column of Burdach. 
Fig. 99. 
Diagram of the relations of the nerve-roots to the spinal cord. A, Anterior root; B, posterior 
root; D, motor part; E, sensory part; F, mixed nerve. (Edinger.) 
Some of these fibres also enter the column of Goll. As soon as 
they have entered this column they turn at right angles and run 
upward for some distance, thereby helping to form the column of 
Burdach. Some of them also run downward a short distance. 
The second set, near the side of the cord, goes directly into the 
gray matter of the posterior horn through the substance of Bolando, 
and the third set, nearest the side of the cord, enters the cord very 
superficially, and, turning at once at a right angle, goes upward to 
form Lissauer’s zone. The longitudinal course of these fibres is 
shown in Plate VI. Here it is seen that they pass upward chiefly 
in the column of Goll (posterior median) to the medulla oblongata. 
Before reaching the medulla, however, the column of Goll ends in 
the gracile nucleus and the column of Burdach in the cuneate 
nucleus. 
These nuclei which have received the fibres of the two sensory 
columns give origin to fibres which pass to the brain. They sweep 
forward to the front of the central canal of the medulla and decus- 238 
THE MANIFESTATION OF DISEASE IN ORGANS. 
sate at a higher level than the motor tracts. A great majority of 
these fibres pass upward to the brain, but some pass forward, and 
Fig. 100. 
Chart showing the sensory tracts in the spinal cord with entrance of the sensory nerve-roots. THE SKIN. 
239 
finally join the restiform body on the posterior aspect of the medulla. 
Those which pass upward from the so-called fillet pass into the crus 
cerebri, in that part of it called the tegmentum, and thence into 
the posterior part of the posterior limb of the internal capsule, 
whence they spread out in the corona radiata to the occipital lobe 
and temporo-sphenoidal lobes. 
The duty of the physician in all cases is to determine first whether 
the disease is functional or organic, and then where the lesion pro- 
ducing the symptoms is situated. 
The two chief manifestations of perverted sensibility in the skin 
are anaesthesia and hyperaesthesia, and the minor ones are paraes- 
thesia or numbness, tingling and formication, and analgesia, or the 
failure to feel pain. Whatever the cause of these symptoms may 
be, the history of the patient and his general symptoms should be 
carefully studied when examining these signs, as frequently a diag- 
nosis is impossible with them alone as guides. 
Anaesthesia. Anaesthesia of the skin is indicative of a very 
large number of conditions arising anywhere in the sensory appa- 
ratus. In other words, anything 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 cutaneous anaesthesia in a female should 
always arouse a suspicion of its being due to this cause. Rarely 
it is seen in hysterical males. The organic causes of anaesthesia 
of the skin are cerebral hemorrhage, cerebral tumor, hemorrhage 
in the pons or tumor of the pons, hemorrhage in the cord, tumor of 
the cord, myelitis (transverse), locomotor ataxia, cerebro-spinal men- 
ingitis, spinal meningitis; compression of the cord by vertebral 
caries, by fractures, by dislocations; and hemorrhage into its mem- 
branes. 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 from cold or the 
action of drugs. 
Anaesthesia, according to its area of distribution, may be divided 
into hemianaesthesia, crossed anaesthesia, bilateral anaesthesia, irreg- 
ular but complete anaesthesia, and partial anaesthesia. 
Hemianesthesia occurs most frequently as a result of hysteria, 
next commonly from lesion of the posterior part of the internal 240 
THE MANIFESTATION OF DISEASE IN ORGANS. 
capsule, and more rarely from spinal injuries or growths in the cord 
of a unilateral character. 
The hemianaesthesia of hysteria involves, as its name implies, 
one side of the body, and is usually universal on that side, except 
that here and there may be patches of hvperaesthesia or tenderness, 
dotted like oases in the midst of the absence of sensation. This 
anaesthesia is often unaccompanied by motor paralysis, 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. 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 anaesthesia may transfer itself to the 
opposite side of the body with great suddenness, and equally sud- 
denly return to its former site. In a great majority of cases, for some 
unexplained reason, the left side is the one affected by anaesthesia, 
and hyperaesthesia of the opposite side increases the contrast which 
exists between it and that in which sensation is lost. (See Hyperaes- 
thesia.) In some cases of hysterical hemianaesthesia the paralysis 
of sensation involves the nerves of special sense, and loss of smell, 
taste, and hearing, and impairment of sight may ensue on the same 
side. The visual changes are so characteristic that they practically 
decide the character of the case when they are discovered in any 
instance of doubtful diagnosis; they consist in a loss of the color- 
vision (first, violet is lost, then blue, and then red), and there is a 
great limitation of the visual field, whereas in the hemianaesthesia 
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 an exist- 
ence by most authorities, but Lloyd and de Schweinitz have seen 
a case. Generally the loss of vision on the anaesthetic 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 anaesthetic. 
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. THE. SKIN. 
241 
A form of hysterical hemianesthesia 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, 
superimposed upon the old picture of disease, that of hysteria with 
this sensory manifestation. 
Anaesthesia irregular in its distribution, or absolute hemianaes- 
thesia, may occur in the course of chorea. The presence of chorea 
in its motor manifestations clears np 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, 
however, the hemianaesthesia of capsular disease may be absolute 
and universal, or, more rarely still, occur in patches, thereby closely 
resembling the anaesthetic areas seen in hysteria. 
Hemianaesthesia 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, and 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 softening 
of the brain than in 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 
hemianaesthesia, partial or complete. 
Anaesthesia resulting from tumor of the brain occurs in about 20 
per cent, of the cases, and 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 associated with 242 
THE MANIFESTATION OF DISEASE IN ORGANS. 
lesions in the neighborhood of the fissure of Rolando, and in 
tumors involving the posterior parietal region and the posterior 
part of the internal capsule. 
Autopsies and experiments show that hemianesthesia 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 anesthesia 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 
condition which we call apoplexy. 
Unilateral anesthesia associated with motor paralysis, both being 
somewhat irregular in their distribution, may be due to a lesion, 
such as a tumor in the pons or medulla oblongata, 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 
anaesthesia does not positively localize the lesion in the pons, for we 
do not know much about the course of the sensory fibres in this 
part. If, however, the area supplied by the trifacial nerve, namely, 
the face, is anaesthetic, and these symptoms are associated with it, 
then it is fair to assume that the trouble lies in the pons and lias 
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 we shall speak further on. If it is a mono-anaesthesia from 
cerebral disease, which is very rare, the anaesthesia 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 sensa- 
tion is often present. 
The irregularly distributed form of anaesthesia due to hysteria 
has the same general peculiarities of migration as are seen in hemi- 
anaesthesia 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 ordinarily by a sock, the line of THE SKIN. 
243 
normal sensation being present just above the place to which these 
protections usually extend. 
Crossed Anaesthesia. When sensory paralysis of one side, 
associated with partial paralysis of motion or paresis on the same 
side, comes on, and with it there is hypersemia 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 on the anaesthetic side of the 
body are paralyzed, still further confirmatory evidence of a pedun- 
cular 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 of 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 anaesthesia of the opposite side of the 
face—cau only occur in lesions involving the upper part of the pons 
in 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 chapters on Face and Head, and on Hemi- 
plegia.) 
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 hemianaesthesia, 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 was considered as proved that 
sensory impulses entering the cord crossed to the opposite side 244 
THE MANIFESTATION OF DISEASE IN ORGANS. 
almost at once, at least in greater part, passing to the lateral col- 
umns in front of the pyramidal tract, and that a very small number 
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 the sensory impulses do not cross the 
cord, only a few fibres passing to the opposite side on entrance. 
He believes 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 Anaesthesia. Anaesthesia of hysterical origin in- 
volving both legs, and sometimes the lower part of the trunk on 
both sides, may occur, and, aside from the typical signs of hysteria 
in general which distinguish it, may be discovered by the fact that 
in hysteria the failure of sensation 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 angesthetic. Anaesthesia of this 
variety, corresponding in the sensory organs to what we call para- 
plegia in the motor apparatus, is practically never produced by a 
cerebral lesion, 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 involve- 
ment 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 
amesthesia 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. THE SKIN. 
245 
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 complains of re- 
peated 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 find Romberg’s symptom (see Legs), Argyll-Rob- 
ertson pupils (see Eye), and loss of patellar reflex (see Reflexes), and 
a number of other diagnostic peculiarities of tabes, the decision as 
to the cause of the amesthesia is easily made. 
Slight anaesthesia, retardation of the transmission of sensory im- 
pulses from the skin, and perversion of temperature-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 
obtunding of sensitiveness, which gradually deepens till loss of pain- 
sense, pressure-sense, and, lastly, complete anaesthesia is developed. 
The development of these symptoms indicates involvement 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 pains of tabes and of the 
other signs of that disease still further excludes its presence from the 
case. Further than this, the myelitis creeps up the cord, involving 
new areas, and new parts of the skin become anaesthetic. An im- 
portant point, too, in regard to the anaesthesia of acute myelitis is 246 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 enlargement 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 anaesthesia involves the 
thigh, the inner side of the leg, and the foot, in association with 
paralysis of the quadriceps extensor and deeper m uscles of the thigh. 
(See chapter on Feet and Legs, part on Myelitis.) 
Fig. 101. 
Sensory chart, showing 
areas of 
Thermo-A naesthesia 
Analgesia 
1 Thermo-Anaesthesia 
J and Analgesia 
Tactile Anaesthesia, and areas in which the patient’s answer to tests of temperature 
showed reversal 
Cold-Hot; (Dercum.) 
Hot-Cold. 
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, hemor- 
rhage in the cord. In either case motor paralysis is present. Ames- THE SKIN. 
247 
tliesia, or the milder perversions of normal sensibility of the skin, 
may be present in cases of compression of the cord by caries, and 
by spinal curvature, tumors, or aneurisms producing erosion. Some- 
times, while tactile amesthesia is complete in these cases, severe 
pain is constantly suffered (anaesthesia dolorosa), and 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 bilat- 
eral character, associated with progressive muscular atrophy, scolio- 
sis, and trophic lesions in the skin, points strongly to syringomyelia. 
The loss of pain and temperature sense is usually the first symptom. 
The areas of anaesthesia are best shown in Fig. 101. 
Fig. 102. 
Fig. 102. 
1st to 12th dorsal segment. 
Showing the surface-areas of the hack corresponding approximately to the areas of the 
spinal cord supplying the trunk and limbs. 
Having considered the general spinal causes of anaesthesia of the 
skin, 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 248 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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; 
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 the legs and feet. 
Again, it is to be remembered that, as a rule, in a transverse lesion 
of the spinal cord the anaesthesia begins at a level 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 supplied by three nerve-roots whose peripheral filaments 
overlap one another. 
Fig. 103. 
Areas of anaesthesia in lesions at various levels of the spinal cord from sacral v. to lumbar n. 
(After Starr.) 
I. Sacral v. 
II. Sacral iv. 
III. Sacral m. 
IV. Sacral i. 
V. Lumbar v. 
VI. Lumbar nr. 
VII. Lumbar u. 
For the ready study of the subject the cord has been separated 
into segments corresponding with the vertebrae covering it. The 
areas of anaesthesia produced by spina] injury or disease are THE SKIN. 
249 
best described in Starr’s well-known article and diagrams, from 
which we quote. In this connection the reader should refer to the 
tables on pages 106 and 107, showing the localization of the func- 
tions of the segments of the spinal cord. (See chapter on Legs 
and Feet.) 
The anaesthetic areas included in zones I. and II. in Fig. 103 are 
due to a lesion involving the conus medullaris and the fourth and 
fifth sacral segments of the cord. These zones include the peri- 
neum, 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 seg- 
ments, and includes a large part of the buttock and the upper part 
of the thigh, posteriorly, in a triangular space. Zone IV. is prac- 
tically 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 segments; but this needs confirmation by 
autopsy, as Starr points out. 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 to the third lumbar seg- 
ment, and when it is present the anaesthesia 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. 103. If the foot is involved, the lesion in the 
lumbar cord is probably above the third lumbar segment. Zone 
VII., which is larger than all, follows a lesion in one 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 prob- 
ably diseased. 
The area of the anaesthesia from the level of the abdomen corre- 
sponds very closely to the levels in the cord if we allow for the space 
already mentioned, of two to three inches for the interlacing anasto- 
mosis of the nerve-fibres of the posterior roots. 
They are about as follows, according to Thorburn: when the 
anaesthesia is as high as the anterior inferior spine of the ilium, the 250 
THE MANIFESTATION OF DISEASE IN ORGANS. 
lesion is at the twelfth dorsal vertebra; if at the umbilicus, at the 
eleventh and twelfth dorsal vertebrae; if hip 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 vertebra. 
Fig. 104. 
Areas of anaesthesia from lesions aud various levels of the spinal cord from the 
second dorsal to the fifth cervical. (After Starr.) 
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. 104.) When the anaesthesia extends to the 
arms and is found upon the inner side of the arm and forearm, reach- 
ing to the wrist, but not to the hand, and also involves a small zone 
on the extensor and flexor surfaces of the arm and forearm, the sec- 
ond 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 finger, and extends in a narrow strip PLATE VII. 
Cervical Roots are represented by the letter C, Dorsal Roots by the letter D, and 
Lumbar Roots by the letter L. (Chart after Thorburn.) PLATE VIII. 
Cervical Roots are represented by the letter C, Dorsal Roots by the letter D, and 
Lumbar Roots by the Letter L. (Chart afterStarr. PLATE IX. 
Cervical Roots are represented by the letter C, Dorsal Roots by the letter D, and 
Lumbar Roots by the letter L. (Chart after StarJL) Head.) THE SKIN. 
251 
up to the axilla on both the anterior and posterior 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 aspects, and runs up 
the centre of the forearm and arm, the seventh cervical area is dis- 
eased. 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 sur- 
faces to the axilla is affected, the lesion is at the sixth cervical ver- 
tebra, while anaesthesia of the forearm and arm on the outer surface 
as high as the deltoid insertion indicates that the fifth cervical ver- 
tebral area is in trouble. Lesions higher than this usually produce 
death before it is possible to test sensibility. 
In 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 VII., VIII., and 
IX.) 
Neuritis as a Cause of Anaesthesia. 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 inflammation of the nerve-trunk, or 
to some injury which impairs its functional activity by pressure, 
bruising, or cutting. As a rule, loss of sensation from neuritis 
occurs late in the disease, hyperaesthesia or paraesthesia being the 
earlier manifestations; but in some cases these are absent, and anaes- 
thesia begins at once. The 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 may be due to other causes, it is in the 
great majority of cases due to neuritis. The signs of an anaesthesia 
due to neuritis are loss of motion and sensation, tenderness on pres- 
sure over the nerve-trunks supplying 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 poliomye- 
litis, but pain is not commonly present in this disease, and there is 
no anaesthesia, either in children or adults. (See chapters on Hands 
and Arms, and on Feet and Legs.) 
Toxic peripheral neuritis producing anaesthesia may arise from 252 
THE MANIFESTATION OF DISEASE IN ORGANS. 
poisoning by arsenic, lead, alcohol, or mercury, from septic states 
of the body, and from infectious diseases, particularly diphtheria, 
influenza, and typhoid fever. 
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 particularly susceptible. (See Arms and Hands.) Arsenical 
neuritis 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 sensibility is lost or disturbed in the areas 
supplied by the involved nerves. 
Great care 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 anaesthesia 
is that supplied by the affected nerve. For this reason we can 
determine what nerve-trunk is affected by studying the area of 
anaesthesia, always remembering, however, that the sensory fibres of 
the nerves, particularly in the hands and feet, anastomose so freely 
with those of adjacent nerves that the area of the anaesthesia may 
not be exactly that supplied by the nerve involved; or, in other 
words, the presence of loss of power in a region supplied in health 
by a nerve which has been divided is constant, but very often sensa- 
tion is not disturbed, even though the divided nerve be the sensory 
as well as the motor supply to the part. 
It is well to remember also that sensory disturbances of the skin 
following injuries of nerves are often not nearly so great as the 
motor disturbance, even where there is no sensory transmission by 
anastomosis, and where they are present they usually disappear, 
more rapidly than the motor loss, as recovery takes place. 
The following facts are, therefore, of diagnostic interest. If the THE SKIN. 
253 
anaesthesia is found to be due to a neuritis and to involve the palmar 
surface of the thumb, fore and middle fingers, tlie median nerve is 
Fig. 105. 
Fig. 106. 
Showing areas of sensory loss in injuries of the median nerve. (Bowlby.) 
Fig. 107. 
Fig. 108. 
Showing areas of sensory loss in injuries of the ulnar nerve. (Bowlby.) 
probably the one at fault (Figs. 105 and 106), and the area may 
even include in rare instances the backs of these fingers at their 254 
THE MANIFESTATION OF DISEASE IN ORGANS. 
bases and the half of the third finger nearest the thumb. When 
there is disturbance of sensation in the ulnar side of the ring-finger 
and in the skin of the little finger there may be, ulnar neuritis 
(Figs. 107 and 108). (See also chapter on Hands.) The nerve- 
supply of the skin of the entire upper extremity is well seen in 
Fig. 109. 
Fig. 109. 
Cutaneous nerve-supply of the trunk and upper extremity. (Fowler.) sa. Supraclavicular 
nerve, iid. Second dorsal, ps. Posterior branches of the spinal nerves. LI. Lateral branches 
of the intercostal nerves, ai. Anterior branches of the intercostal nerves, c. Circumflex nerve. 
ih. Intercostal humeral, w. Nerve of Wrisberg. i'cb. Internal cutaneous branch of musculo- 
spiral nerve, ecb. External cutaneous branch of musculo-spiral nerve, icb. Internal cuta- 
neous nerve, mc. Musculo-cutaneous nerve, r. Radial nerve, u. Ulnar nerve, m. Median 
nerve. 
The development of sensory disturbances in the feet, resulting 
from neuritis, are as follows: When there is perverted sensation of 
the inner side of the foot from the tip of the big toe to the heel, and 
thence up the inside of the calf to the knee, the nerve involved is 
the long or internal saphenous. When the dorsal surface of the THE SKIN. 
255 
foot has its cutaneous sense disturbed the nerve involved is the 
musculo-cutaneous, a branch of the external popliteal. Disturbance 
of sensation on the outer side of the foot and calf indicates failure 
of function in the external saphenous, which is composed of the 
cutaneous branches of the external and internal popliteal nerves. 
Fig. 110. 
Cutaneous nerve-supply of the lower extremity. (Fowler.) Lumbar plexus, ih. Ilio-hypo* 
gastric nerve, n. Ilio-inguinal. iil. Second lumbar nerve, gc. Genito-crural. ec. External 
cutaneous, mc. Middle cutaneous, ic. Internal cutaneous, is. Internal saphenous, pp. 
Plexus patellae. Sacral plexus, dp. Dorsalis penis of pudic. ip. Inferior hemorrhoidal of 
pudic. p. Superficial perineal of pudic and inferior pudendal of small sciatic, ig. Inferior 
gluteal of small sciatic, ss. Small sciatic, ep. Branches from external popliteal, es. Ex- 
ternal saphenous, mgs. Musculo-cutaneous. at. Branches of anterior tibial. pt. Branches 
of posterior tibial. 
Disturbed sensation on the posterior surface of the calf also indi- 
cates trouble in the external saphenous nerve and communicans per- 
onei, while when the sensation of the skin of the heel is disturbed 256 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the plantar cutaneous nerve, a branch of the posterior tibial, is 
involved. 
In the skin of the thigh the anterior surface is supplied by the 
middle cutaneous nerve, which is a branch of the anterior crural; 
on the inner side by the internal cutaneous, also a branch of the 
anterior crural; and on the outer side by the external cutaneous, 
which arises from the second and third lumbar nerves. Laterally 
the external cutaneous gives the supply. Posteriorly the small 
sciatic gives the nerve-supply to the skin. 
Anaesthesia of the greater portion of the skin of the thigh, except 
in a narrow strip on the back part and in the area supplied by the 
internal saphenous nerve, often occurs as the result of paralysis of 
the anterior crural nerve, arising from pelvic tumors, psoas abscess, 
and vertebral disease. 
Facial anaesthesia and its diagnostic meaning are still to be 
considered. When it occurs it indicates that the fifth nerve, or 
its nucleus, is involved. 
If the area be that of the forehead, upper eyelid, the conjunctiva 
and the nostril, the ophthalmic branch of the fifth nerve is at fault, 
and the lesion is probably at the sphenoidal fissure or within the 
orbit, and reflex winking of the eye no longer takes place because 
the conjunctiva is anaesthetic. 
If the skin of the upper part of the face is anaesthetic, the supe- 
rior maxillary branch is involved; and if the skin of the temporal 
region and that of the jaw and the under lip is anaesthetic, the in- 
ferior maxillary branch is diseased. When both of these branches 
are paralyzed there is probably a tumor of the superior maxillary 
bone; and if the entire area of the three branches is anaesthetic, 
the Gasserian ganglion may be the part affected, and this will be 
accompanied by trophic changes in the anaesthetic parts. The 
most common cause of anaesthesia of the trifacial is, however, 
neuritis. 
Lomberg makes the following differential statements: 
a. The more the anaesthesia is confined to single filaments of the 
trigeminus, the more peripheral the seat of the cause will be found 
to be. 
b. If the loss of sensation affects a portion of the facial surface, 
together with the corresponding faucial membrane, the disease may 
be assumed to involve the sensory fibres of the fifth pair before they 
separate to be distributed to their respective destinations; in other THE SKIN. 
257 
words, a main division must be affected before or after its passage 
through the cranium. 
c. When the entire sensory tract of the fifth nerve has lost its 
power, and there are at the same time derangements of the nutritive 
functions in the affected parts, the Gasserian ganglion, or the nerve 
in its immediate vicinity, is the seat of the disease. 
d. If the anaesthesia of the fifth nerve is complicated with dis- 
turbed functions of adjacent cerebral nerves, it may be assumed 
that the cause is seated at the base of the brain. 
Anaesthetic patches on the skin may be due to leprosy or syrin- 
gomyelia, but in the former disease the macular patches are present, 
or there may be found evidences of their previous existence in 
areas of skin, especially on the back, thighs, and calves, which 
are paler than normal and in which the sensation is partially 
blunted. 
Rarely the anaesthesia of leprosy may be confused with that of 
Morvan’s disease, and it may require a search for the lepra bacillus 
to separate them. 
Other Disturbances of Sensation than Anaesthesia. The 
other disturbances of sensation of the skin than anaesthesia, which 
are usually subjective rather than objective, are parsesthesia, hyper- 
aesthesia, and analgesia. 
Paraesthesia, or numbness, tingling, and burning, is seen in nearly 
all cases in which anaesthesia ultimately develops as a result of 
organic lesions. When a patient complains that he cannot feel the 
contact of clothing about his feet and legs, or that the feet when he 
walks feel as if wrapped in some thick material, or as if he were 
walking on moss, or that the soles of his feet feel as if they were 
numb and at the same time tickled by ants walking over them, the 
characteristic sensory disturbance of the skin seen in locomotor 
ataxia is present. 
Often there is tingling or numbness of the fingers, particularly of 
the ring and little fingers, and a sensation as if a girdle is about the 
patient is common. These are the subjective disturbances of sensa- 
tion in tabes dorsalis, and, as they are often the earliest manifestations 
of the disease, possess great diagnostic importance. The objective 
sensory perversions consist in the discovery by the physician, when 
studying the sensibility of the skin, of areas of anaesthesia, anal- 
gesia, and hyperaesthesia, which are usually bilateral. Belmont 
has stated that we also find these areas in spinal syphilis, either on 258 
THE MANIFESTATION OF DISEASE IN ORGANS. 
one or both sides. Numbness, tingling, and formications affecting 
the skin are also often early symptoms of brain-tumor in the area 
supplying the affected part, and this possibility is increased if there 
is associated spasm. The actual objective sensibility of the skin 
may be preserved for some time after these symptoms appear, or it 
may be impaired almost at the outset, owing to the involvement of 
all or part of the sensory tracts in the cord. Similar symptoms are 
often seen in the early stages of myelitis. They are very frequently 
seen after injuries to nerves, and severe tingling in its acute variety 
occurs when the “ funny bone” of the elbow is knocked against an 
object, owing to bruising the nerve. It is also seen in cases of 
aconite-poisoning, and when the hands have been exposed to carbolic 
acid. Paresthesias are also frequently seen in cases of neurasthenia. 
Perversions of sensation in the skin sometimes take a curious 
form, as, for example, that known as allochiria, in which a sensory 
impulse in one hand is referred by the patient to the opposite hand. 
This is seen in tabes dorsalis, myelitis, multiple sclerosis, and hys- 
teria. In other cases, as in paralysis agitans, this perversion takes 
place in the form of failure to distinguish heat and cold, and sub- 
jective sensations of extreme heat are felt. The part affected may 
actually have its temperature raised several degrees. 
Magnan asserts that a sensation as if a worm or bug were crawl- 
ing under the skin is indicative of cocaine-intoxication. 
Very closely associated with the numbness of hysteria or neuras- 
thenia, and lying between functional and organic disease of the nerves, 
is that condition called acroparesthesia or waking numbness. This 
state is usually seen in women past middle life, but may occur in 
men. On waking in the morning marked formication and numb- 
ness of the fingers are present, which usually pass off as the day 
progresses, but as the condition becomes more marked they may last 
all day. While there is no anesthesia, strictly speaking, the dis- 
turbed sense of touch renders sewing or performing any small act 
with the fingers almost impossible. These sensations may be con- 
fined to the area of one nerve, as the ulnar, or involve all the skin 
of the hands, or more rarely of the feet. General nervous excita- 
bility is usually associated with the local manifestations. Some- 
times the scalp may be the area involved. 
Acroparesthesia is to be separated from the sensory disturbances 
of hysteria by its irregular outline, for generally in the latter dis- 
ease the areas are distinctly outlined, by the fact that the hysterical THE SKIN. 
259 
condition is usually unilateral, and by the absence of the character- 
istic general hysterical symptoms. From organic disease it is sepa- 
rated by the absence of the signs of neuritis about to be described, and 
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, and by the facts that in both 
these lesions 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 acroparsesthesia generally manifests 
itself in the hands. 
Closely associated with parsesthesia, 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 or the trunk. This is seen as a prom- 
inent 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.) 
Hypercestliesia 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, about the 
periphery of the mammary glands, or upon the spine in the lumbar 
or dorsal region. (See chapter on Pain.) 
The hypersesthesia 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 or one who has phosphaturia will 
complain that in brushing or combing her hair pain or extreme 
sensitiveness is developed upon 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 hypersesthetic zones of 260 
TITE MANIFESTATION OF DISEASE IN ORGANS. 
hysteria, and the personal history and characteristics of the indi- 
vidual aid still further in separating the two conditions. 
Hypergesthesia 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 the latter disease, and 
the excessive sensitiveness is frequently seen in a zone extending a 
little above the anaesthetic areas of transverse myelitis, this hyper- 
aesthetic 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 sen- 
sory paralysis of the other it is commonly found on the side on 
which motion is lost. A condition of excessive dermal hyperaes- 
thesia is also present in cerebro-spinal meningitis, in which disease 
it is often a very early symptom. It usually appears first in the 
legs, then in the hands and arms, and, finally, the skin of the face 
and head become involved. 
Hyperaesthesia 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 paralyzed. It 
is also found during the convalescence of typhoid fever, and in 
relapsing 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 
persons 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 about the time of puberty, or in a 
woman, one breast becomes exceedingly painful and tender, and the 
skin of the breast becomes so hypertesthetic that the slightest touch 
causes pain. The whole breast is, moreover, tender, and move- 
ment of the arm may be impossible, owing to pain thereby caused 
in the gland. This hysterical breast can be separated from the THE SKIN. 
261 
painful breast due to a tumor by the general diffuse character of 
the swelling, the failure to outline any distinct mass, the neurotic 
character of the patient and her age. 
The hypenesthesia 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 structures. 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 anaemia. 
In some cases hyperaesthesia 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 subject 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 physi- 
cian’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 
widespread 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 cannot 
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 VIII. 
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 re- 
sults 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 contents of the thoracic cavity consist of vital organs, 
which are unfortunately only too often subject to disease. A care- 
ful study of the signs associated with the normal functions of these 
parts is, therefore, of importance, as is also that of the symptoms 
indicating pathological changes. While it is true that in many 
instances patients present themselves to the physician with well- 
marked objective and subjective symptoms pointing to abnormalities 
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. We 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 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, the broader part of the 
cone being in the upper portion. Above the clavicles there is 
usually a slight depression (the supra-clavicular fossa), and below 
the clavicles, which may be somewhat prominent, there is a slight 
convexity which extends as far down as the fourth rib. This 
convexity varies considerably according to the muscular develop- 
ment of the individual, the formation of the bony portion of the 
chest-wall, and the deposit of fat in the subcutaneous tissues of the THE THORAX AND ITS VISCERA. 
263 
chest. The nipple is by no means as definite a landmark as is some- 
times thought, as its position, 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 multi- 
parous women owing to the relaxation of the breast. In the aver- 
age adult male or virgin female the nipple is on a level with the 
fourth rib or fourth interspace. The ribs in a well-developed per- 
son 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 and the 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. 111. 
The regions of the anterior aspect of the chest. The Roman numerals indicate the ribs. (Tyson.) 
The result of lateral examination of the normal chest when com- 
pared with the front view will show that the antero-posterior diam- 
eter 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 264 
THE MANIFESTATION OF DISEASE IN ORGANS. 
clavicles downward through the nipple are called the mammillary 
lines. (Fig. 111.) The parasternal line, not shown in the figure, 
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 tire locality of symptoms. 
If we could see through the chest-wall, we would find that the 
lungs extend above the clavicle. Immediately back of the inner 
end of the clavicle is the beginning of the innominate vein, and 
Fig. 112. 
Position of heart in relation to ribs and sternum. (Tyson.) 
back of this again the common carotid artery on the left side. On 
the right side the innominate artery bifurcates just behind the junc- 
tion of the sternum and clavicle. The figure given above shows 
the relation of the cavities of the heart and its great vessels to the 
chest-wall. (Fig. 112.) 
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 THE THORAX AXD ITS VISCERA. 
265 
right side. Laterally the lung on both sides extends to the ninth 
rib in the mid-axillary line. Posteriorly on the right side the lung 
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 
individuals 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. Occu- 
pations which cause the individual to assume certain positions, or 
to use certain muscles continually, also cause variations in the 
contour of the thorax. 
Inspection 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. 113. 
Fig. 114. 
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. 113.) The antero-posterior diam- 
The alar chest of phthisis. 
Side view of same patient. 266 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
eter, particularly in the upper two-thirds, is very slight, and instead 
of convexity in this part there may be flattening or hollowness. 
(Fig. 114.) This area scarcely moves on inspiration, but the lower 
third, which is bulging, moves markedly with the respiratory 
efforts, as does also the epigastrium. The shoulders are very sloping, 
the neck, anteriorly, recedes at the episternal notch, but springs 
forward 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. 115.) 
Fig. 115. 
Phthisical chest. 
If, on the other hand, the chest bulges anteriorly and posteriorly 
to such an extent that the antero-posterior diameter is greater than, 
or equal to, the lateral diameter, and if this bnlging is fairly uni- 
form, the shoulders being elevated, the back 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.” (Fig. 116.) The chest- THE THORAX AND ITS VISCERA. 
267 
wall moves very little or not at all with the respiratory movements, 
which are chiefly diaphragmatic. 
Localized bulging of the chest results, in its most diffused type, 
from the presence of chronic pleural effusion; bulging of a limited 
area also arises from cardiac hypertrophy, particularly that occur- 
ring in childhood; from aortic aneurism, causing bulging by pres- 
sure (Fig. 117); from pericardial effusion; and, finally from medias- 
tinal growths. Marked bulging over the lower part of the chest 
on the right side should cause us to look for some hepatic affection 
as well as to examine the lung, and, if the bulging is low down on 
the left side, to examine the spleen. 
Fig. 116. 
Fig. 117. 
Boy fourteen years old with emphysema ot 
lungs. Shows barrel-shaped chest. 
Bulging of the chest-wall, with erosion of ribs 
from aortic and innominate aneurism. 
Bulging or protrusion of the sternum, and the cartilaginous por- 
tions of the ribs attached to it, is called “ pigeon breast,” and is 
due either to rickets or to the presence of some obstruction to 
respiration of a more or less chronic character during the time 
the chest-wall was soft and capable of being moulded. Some- 
times on each side of the sternum, over the costal cartilages, there 
is seen a groove or depression as the result of rickets. In other 268 
THE MANIFESTATION OF DISEASE IN ORGANS. 
cases a depression or groove extends from the ensiform cartilage 
back on either side toward the spine. This is called “ Harrison’s 
groove,” and is developed in children with poor bony systems, as 
the result of repeated attacks of asthma or other obstructive 
respiratory difficulty. 
When examining the chests of children the physician will often 
notice swellings of the tissues at the costo-cartilaginous junctions, 
which look and feel to the touch like large beads under the skin. 
These beaded ribs are indicative of rickets, and are a manifestation 
of the general tendency to epiphyseal enlargement. This beading 
is usually most marked on the lower ribs. 
Fig. 118. 
Fig. 119. 
Showing shrinkage and partial collapse of left side of chest and distortion of spinal column 
due to chronic tubercular pleurisy in a boy of fifteen years. (From the author’s wards in the 
Jefferson Medical College Hospital.) 
Finally, unilateral bulging of the chest may be due to curvature 
of the spine, which part of the body 'should always be examined 
before a diagnosis as to deformity of the chest is attempted. 
Shrinkage of the chest in one part may be due to the contraction 
of old pleural adhesions (Figs. 118 and 119). It is sometimes seen THE THORAX AND ITS VISCERA. 
269 
over the diseased area in pulmonary tuberculosis, and may be appar- 
ently present, but in reality due to wasting of the tissues covering 
the part. 
While inspecting the surface of the chest the physician should 
also note the presence or absence of enlarged or pulsating blood- 
vessels on its surface or about the base of the neck. The cervical 
vessels are commonly seen to be distended in cases of advanced 
emphysema of the lungs and in chronic bronchitis, and systolic pul- 
sation of the jugular veins indicates tricuspid regurgitation. Again, 
in cases of thoracic aneurism pressing upon the superior vena cava 
and innominate veins we find spongy venous masses above the 
clavicles, and the veins of the trunk and arms are apt to be en- 
gorged. Intrathoracic growths produce similar symptoms.1 Pul- 
sation in the cervical vessels is also sometimes seen in cases of severe 
anaemia. 
The shape and surface of the chest having been studied, we can 
go further and learn much from its movements in respiration : first, 
from the rapidity of respiration; second, from the respiratory 
rhythm; third, from the character of the breathing; and, fourth, 
from the movements of the ribs. 
When counting the respirations the physician should always 
endeavor to do so without letting the patient know what he is doing, 
since it is difficult for many persons not to control their breath- 
ing when their attention is called to it. Generally the eye can 
detect the frequency of the breathing by simply watching the move- 
ment of the chest, or the information can be gained by resting the 
hand on the abdomen or thorax, while the wrist is also held and 
the doctor is 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 one, but in disease 
it may be one to one. 
Rapid respirations not due to any recent sudden exertion arc 
always indicative of respiratory trouble, primary or secondary. If 
the primary trouble be in the lung, it will probably be due to crou- 
pous pneumonia, catarrhal pneumonia, severe bronchitis, asthma, 
tuberculosis, pulmonary abscess, or tumors of the lungs. If it be 
1 See “ Mediastinal Disease,” by the author. Fothergillian Prize Essay of Medical Society of 
London for 1888. 270 
THE MANIFESTATION OF DISEASE IN ORGANS. 
due to secondary lesions in the lung, it may rise 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 causing exudation into the lungs or pleura, and from ascites 
or abdominal 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 malignant growth, inside or outside, which may act by pressure, 
thereby narrowing the tube. Any agency which interferes with the 
patient receiving the full amount of air usually inhaled causes rapid 
breathing 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, uraemia, 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 lungs from any cause; 
by the action of poisons made in the body, as the poison of uraemia 
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 rep- 
resents a complete respiratory cycle, inspiration is represented by 5, 
expiration by 4, and the pause by 1. If it is difficult for air to 
enter 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-arytenoid muscles. If 
there is difficulty in expelling the air, the expiration is prolonged, 
as in asthma and in emphysema. 
Sometimes when the chest is flexible, as is that of a child, the 
inspiration 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 enters the lung slowly owing to the obstruction. THE THORAX AND ITS VISCERA. 
271 
The most remarkable change in rhythm is the so-called Cheyne- 
Stokes breathing, in which the patient after a pause of several sec- 
onds begins to breathe with gradually increasing rapidity and 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 brain-tumor, in cerebro-spinal 
fever, in meningeal tuberculosis, in some rare cases of cardiac val- 
vular disease, probably as the result of embolism, and in hsematuric 
malarial fever. Rarely it occurs in cases of acute febrile disease, 
as typhoid fever, scarlet fever, pneumonia, whooping-cough, and 
puerperal 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 breathing 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 
symptom than if it be due to some chronic process with an acute 
exacerbation. 
The function 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 abdom- 
inal breathing is absent in a man and is replaced by breathing of 
the costal type, we can be assured that the movements of his dia- 
phragm are impaired by the pressure of fluid in the abdomen 
(ascites) ; by 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 subphrenic 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 272 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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, crou- 
pous, catarrhal, or serous. These conditions may be primary or 
secondary to disease elsewhere, as in uraemia or cardiac disease. 
Inspection of the chest in such a case shows great activity of the 
accessory respiratory muscles, such as the sterno-mastoid, the scaleni, 
the pectorals, 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 in 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 pneumonia, 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 is usually performed by placing the 
finger-tips or the whole hand, palm downward, on the chest. This 
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 
bands lies a column of air which reaches to the vesicular portions 
of the lung, and when an individual speaks this column of air is 
put 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 which greatly modify vocal fremitus. It must be remem- 
bered, too, that this vibration is more marked in men than in THE THORAX AND ITS VISCERA. 
273 
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 on the left because the principal bronchus supply- 
ing this lung is larger than that of the left side, is joined to the 
trachea at a less acute angle, and is nearer the vertebral column; 
and, again, as recently emphasized by Cary, 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 conies 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 
medium, the lung; any condition which causes occlusion of a large 
bronchus, 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 bron- 
chial tubes to the chest-wall, or, in the case of a cavity, the sound 
is transmitted directly to it, and it there causes so great a vibration 
of the air in the hollow space that the vibration of the chest-wall 
is marked. (In this connection, see part of this chapter on Auscul- 
tation.) 
Palpation 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 
effusion in the pericardial sac or pleural cavity on the left side, to 
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 adhe- 
sions or effusions, by abdominal effusion (ascites), by tumors, disten- 274 
THE MANIFESTATION OF E IS EASE IN ORGANS. 
tion of the colon by gas, and by great enlargement of the spleen. 
Displacement of the apex-beat to the left is generally associated 
with downward 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 showing changes in cardiac area on pages 283 and 284.) 
The area of the normal apex-beat is about one square inch. In 
disease 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 fee- 
bleness of the heart-muscle, by effusions into the pericardium and 
the presence 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 
obstructive; 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, when it occurs, is found on the left side. It is pro- 
duced by the impulse of the heart against the effusion, and occurs in 
two forms: the internal, in which the effusion transmits a heaving 
impulse to the chest; and the external, in which there is a pulsating 
tumor external to the chest-wall. Sometimes this is called “ pul- 
sating 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 the bent finger of the THE THORAX AND ITS VISCERA. 
275 
right hand, the movement of the striking hand being entirely a 
wrist-movement. Sometimes percussion is made by directly strik- 
ing the chest with the lingers or palm of the hand (direct percus- 
sion). Many physicians also employ a percussion-hammer with a 
rubber head and a pleximeter, 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 percus- 
sion is that the physician cannot determine the degree of resistance 
offered by the surface percussed, 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-wall on each side are carefully 
compared; second, that the finger which is applied to the chest is 
placed in the same relation to the ribs, or interspaces, 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 vibra- 
tions of the chest-wall when it is struck; third, to the vibrations in 
the pleximeter placed on the chest. The last need only be consid- 
ered 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 developed. The note produced by vibration of the chest- 
wall can also be excluded as of little importance unless tihe chest is 
very pliable and resilient, as in a thin child, and the blow be deliv- 
ered very hard. The most important factor in the production of 
the percussion-note is that first named, viz., the vibration of the air 
in the chest caused by the blow 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 sound produced when the healthy 
chest is percussed is called the normal pulmonary resonance. 
On percussing the right side of the chest anteriorly in the mam- 
millary line we find 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 276 
THE MANIFEST A1 ION OF DISEASE IN ORGANS. 
we find the dulness. The area of partial and absolute hepatic dul- 
ness is shown in Fig. 150, 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 
chest by reason of the thickness of the chest-wall and the presence 
of the scapula?. For this reason pulmonary resonance is best devel- 
oped 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 arms in order to stretch the tissues and make 
them tense and as thin as possible. 
Fig. 120. 
The condition of 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.) 
We can divide the abnormal sounds produced by percussion into 
the tympanitic, the dull, and the flat. We can also develop by 
percussion of the chest in disease what is known asa “ 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 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. 120), 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- THE THORAX AND ITS VISCERA. 
277 
acter of the note will change when the mouth is closed or opened. 
(Fig. 121.) If;jthe case be one of pneumothorax, with fluid in the 
Fig. 121. 
Pectoriloquy. 
Consolidated area. 
Fremitus increased. 
Vocal resonance increased. 
Dulness on percussion. 
Phthisis at various stages in one lung, the physical signs depending on the stage. 
(Gibson and Russell.) 
chest, changes in the posture of the patient will greatly alter the 
character of the note. Consolidation of the lung, as in pneumonia 
Fig. 122. 
Showing at x moderate dulness over tubercular infiltration. (Gibson and Russell.) 
and tuberculosis (Figs. 122 and 123), generally gives a dull rather 
than a tympanitic note, but if the consolidated area surrounds a 
very superficially placed bronchus, the percussion-stroke may pro- 
duce vibration in the air in this tube, and this will cause a note, 278 
THE MANIFEST A TIDE OF DISEASE IN ORGANS. 
tympanitic in character, which varies as the mouth is closed or 
opened. Collapse of the lung causes a tympanitic note because the 
comparatively little air in the lung vibrates as a whole, its vibra- 
tions not being stopped as in health by the tense septa and vesicular 
Fig. 123. 
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. ) 
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 u 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 
percussion-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 com- 
monly results from the presence of a cavity in the lung. It may 
also be heard in cases of pneumothorax with a fistulous tract open- 
ing 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 effusion, and it is of very much the same character as the sound 
elicited by percussion of the solid tissues of the thigh. (Fig. 120.) 
Cardiac dulness. On percussing the chest anteriorly on the left 
side it will be found that the normal resonance is decreased by the THE THORAX AND ITS VISCERA. 
279 
presence of the heart. At the apex of the chest on this side per- 
cussion develops normal resonance, but as we descend in the line 
situated half-way between the mammary line and the midsternal 
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 by the presence of a solid organ, the heart. The im- 
pairment of resonance is not complete at the upper border of the 
heart because of the fact that the edge of the lung intervenes 
Fig. 124. 
Position of heart uncovered by lungs. A shows the area of superficial cardiac dulness. 
(AITKEN.) 
between the heart and the chest-wall, and so the note which results 
on percussion is neither the normal resonance of the lung nor the 
dullness produced by the presence of the heart. (Fig. 124.) The 
outlines of the normal cardiac dulness on percussion are shown by 
the diagram which is appended, and they form what have been 
called the u cardiac triangles.’7 (Fig. 125.) 
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, 280 
THE MANIFESTATION OF DISEASE IN ORGANS. 
normally situated in the fifth interspace just inside of the clavicular 
line. The hypothenuse of the triangle joins these points. In this 
area we have included the partial and total cardiac dulness. The 
small cardiac triangle, which includes the absolute cardiac dulness, 
begins at the third costal cartilage and extends to the sixth. The 
base-line extends to within one and one-half inches of the nipple, 
and the hypothenuse joins this point witli the third costal cartilage 
Fig. 125. 
Diagram showing cardiac triangles. Compare this figure with Fig. 124. 
at the midsternal line. As will be seen from the diagram the bor- 
ders of the heart really extend further than this, but are not near 
the chest-wall and are partly covered by lung-tissue. (Compare 
Fig. 124.) 
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. 126.) 
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 THORAX AND ITS VISCERA. 
281 
Fig. 126. 
Position of heart in relation to ribs and sternum. 
Fig. 127. 
Outline of percussion-dulness in a case of extensive pericardial effusion, 
(Byram-Bramwell, after Sibson.) 282 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 127), 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-books would make it appear. One of the most reliable signs 
of pericardial effusion is that of Rotch, namely, that any consider- 
able dulness in the fifth right intercostal space means pericardial 
effusion, provided 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 the heart may be of interest : 
Pericarditis with Effusion 
Dilatation of the Heart. 
Outline of dulness 
Dulness pear-shaped, and en- 
largement chiefly upward. 
Dulness not pear-shaped, and en- 
largement chiefly downward. 
Rate of development 
of dulness. . . . 
Often rapid, and then charac- 
teristic. 
' Usually very slow, though a rapid 
dilatation of the heart sometimes 
occurs. 
Impulse and apex- 
heat 
The impulse, when present, is 
in the third or fourth inter- 
space ; apex-beat tilted up- 
ward and outward,or effaced. 
Impulse can usually be felt to the 
left of the lower end of the ster- 
num or in the epigastrium. 
Relation of dulness 
to left apex-beat . 
Dulness may extend to the left 
of the apex-beat. 
Dulness does not extend to the left 
of the left apex-beat. 
Pain over prsecordia 
and tenderness in 
the epigastrium. . 
Often present. 
Usually absent. 
Pulsation in the veins 
of the neck . . . 
May be present if endocarditis 
complicates. 
Often present when right heart 
dilated. 
Usually chronic; often associated 
with chronic valvular lesions, 
fatty and fibroid degeneration. 
Etiology 
Usually acute, in course of 
acute rheumatism, cirrhotic 
Bright’s disease, etc. 
Fever 
Often present. 
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. 
283 
Pericarditis with Effusion, 
Hypertrophy. 
Rate of development 
Usually rapid. 
Usually slow. 
Impulse powerful; if left ventricle 
hypertrophied, apex displaced 
downward and outward ; if right 
ventricle hypertrophied, apex 
displaced downward and inward; 
beat may he in the epigastrium. 
Impulse; apex-beat. 
Impulse, when present, is in 
the third or fourth left inter- 
space, and is feeble; apex 
tilted upward and outward, 
or beat effaced. 
Character of the pulse depends on 
the side of the heart which is 
hypertrophied and the cause of 
the hypertrophy. When left 
ventricle hypertrophied, and no 
aortic obstruction or mitral re- 
gurgitation, the pulse is large 
and powerful. 
Pulse . . . 
f• Weak and quick; may be ir- 
t regular. 
In emphysema of the lungs the cardiac triangles may be obliter- 
ated 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. Pneu- 
mothorax may cause similar results, or, again, old pleural adhesions 
and conditions may so displace the lungs or heart that the triangles 
cannot be found. 
Fig. 128. 
Fig. 129. 
Diagram of the normal heart, the continuous 
line indicating the outline of the right, and 
the incomplete of the left cavities. (Sansom.) 
Diagram of the heart in aortic obstruction 
and regurgitation. The dotted lines indicate 
enlargement of the left cavities, especially 
the ventricle. The liver-area only slightly 
increased. (Sansoji.) 
The various valvular and other lesions of the heart result in alter- 
ation in the size of the various cavities without the entire viscus 
being equally affected. Thus aortic regurgitation causes enormous 
enlargement of the left ventricle (dilatation and hypertrophy), and 284 
THE MANIFESTATION OF DISEASE IN ORGANS. 
aortic stenosis also causes the same enlargement as a rule in less 
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. 128, 129, 130, and 131.) 
Fig. 130. 
Fig. 131. 
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 may be gained by the sensation of resistance offered 
to the lingers on percussion. It is slight over cavities, greater over 
healthy lung-tissue, still greater over consolidations, and very great 
over effusions. 
Auscultation of the chest reveals in health two chief varieties 
of breath-sounds, namely, vesicular breathing and bronchial breath- 
ing. 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 pos- 
teriorly. 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 THE THORAX AND ITS VISCERA. 
285 
single stethoscope is used, the face of the physician should always 
be turned 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 
parenchyma, 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 expira- 
tory 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 expiration. 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 and 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, pneumonia, and emphysema. 
The other variations in the vesicular respiratory sounds differing 
from those of health are harsh, or, as it is sometimes called, puerile 
breathing, and irregular breathing. In children, as the term “ puerile 
breathing” indicates, the normal vesicular breathing is loud, clear, 
and harsh, 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 286 
THE MANIFESTATION OF DISEASE IN ORGANS. 
in the area of normal vesicular breathing in adults, it usually indi- 
cates 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 pul- 
monary tuberculosis. 
Sometimes physicians speak of “ broncho-vesicular breathing,” 
meaning a breath-sound consisting of both bronchial and vesicular 
sounds. It is sometimes heard in a healthy person when lie breathes 
superficially, and in disease usually indicates early pneumonic 
changes or early tuberculosis of the lung. It is only 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. 132) or of compression or collapse of the luug 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 
transmitted directly to the cavity, and thence to the ear without 
being impaired 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 combina- THE THORAX AND ITS VISCERA. 
287 
tion of air and vesicular Avail. If the cavity be large, Ave have a 
loud sound developed by the transmission of the bronchial 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 
peculiarly situated in relation to the supplying bronchus, we have 
Avhat is called “ amphoric breathing”—that is, a sound like that 
produced by bloAving over the mouth of an empty bottle. This 
sound is also rarely heard in cases of pneumothorax iu Avhich the 
bronchial tubes, running near to the pleural cavity, transmit their 
sound to the air in the pleural space. 
Fig. 132. 
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 Russell.) 
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 disease, and in doing so it must be remembered 
that disease not only modifies the signs in the lung in which the 
morbid process is situated, but also changes the normal signs. Thus 
pneumonia, or pleurisy or pleural effusion, causes a louder vesicular 
and bronchial breathing on the healthy side than is normal because 
this lung has to take in more air to make up for the loss of activity 
on the diseased side. Great care should, therefore, be exercised that 
the loud harsh breathing of the healthy part in such a condition is 
not mistaken for the harsh breathing of disease. 
Thera arc a number of other sounds heard in the chest in cases 288 
THE MANIFESTATION OF DISEASE IN ORGANS. 
of disease of the air-passages. These consist in rfiles of various 
kinds, voice-sounds (vocal resonance), friction-sounds, and succus- 
sion notes or sounds. 
Rales are divided into two chief classes, moist and dry. The moist 
are subdivided into the crepitant, or crackling, the fine bubbling, and 
the coarse bubbling. The dry are called sonorous, or sibilant and 
hissing. Sometimes the sonorous rales are called rhonchi. The 
fine crepitant rale is best imitated by pressing the thumb and finger- 
tip tightly together and then separating them while they are held 
near the ear. This rale is due to the separation of the vesicular 
walls, which have become adherent because of exudate. It occurs, 
of course, during the latter part of inspiration, and is an impor- 
tant sign of croupous pneumonia in its early stages before con- 
solidation has occurred. It also is heard in cases of pulmonary 
collapse and oedema, but not always in any of these diseased condi- 
tions. Care should be taken that the fine rales sometimes heard in 
the chest at the bases, posteriorly, in a person who has been long in 
one position in bed, are not thought to be indicative of pneumonia. 
Fine bubbling rales occur chiefly in the smaller bronchioles and 
the coarse bubbling rales in the larger bronchioles, and they are 
caused by the passage of air through liquid or mucus. These are 
commonly heard in bronchitis and in pulmonary oedema in the lower 
parts of the chest, chiefly posteriorly. If such rales are heard ante- 
riorly or in the area for vesicular breathing, they indicate the stage 
of resolution of a pneumonia, or if this disease has not been present, 
or is long gone by, they possess the serious import of breaking down 
of tissue from tuberculosis in the lung. Sometimes these rales are 
limited to inspiration or expiration. In convalescence from an 
attack of asthma they occur with a to-and-fro character, and are 
often musical or tinkling in character. 
If a cavity has formed and liquid is in it, we may hear in the 
chest a peculiar hollow tinkling, called by Laennec “ metallic tink- 
ling.” These sounds are sometimes heard over the stomach when 
this viscus is in motion and contains a little liquid and air. 
There is another condition in which metallic tinkling is heard 
very clearly, and that is in hydro-pneumothorax. In this condition 
there is a continual dropping of liquid from the apex of the chest, 
or, more correctly, from the compressed lung in the apex of the 
chest, and as the drops fall through the air in the chest they strike 
the surface of the watery effusion with a tinkling sound. (Fig. 120.) THE THORAX AND ITS VISCERA. 
289 
Rales are often removed or altered in character, if not crepitant, 
by coughing. 
It has already been pointed out that dry rales may be divided 
into the coarse and sonorous and the small or tine sibilant rales. 
They are produced by the passage of the air, in the large or smaller 
bronchial tubes, through partly inspissated and sticky mucus. If 
they are sonorous, the larger tubes are the part involved; if sibi- 
lant, the small bronchioles are affected. 
It should not be forgotten that harsh breath-sounds made in the 
mouth or in the nose may cause the transmission of rough sounds or 
rales into the lungs, which will mislead the physician in his diag- 
nosis if he thinks they arise in the pulmonary tissues. 
Friction-sounds in the chest depend upon disease of the pleura 
or of the pericardium, generally the former. Normally the visceral 
and parietal layers of the serous membranes, which form the peri- 
cardium and pleurae, present smooth surfaces which glide over one 
another noiselessly, but when they become roughened by disease a 
sound of friction is developed. Sometimes the friction-sound is so 
slight as to be almost inaudible, and again so harsh as to sound like 
a loud creaking, which can be not only heard, but will convey a 
sensation to the hand when it is placed on the chest. As a rule, 
friction-sounds due to pleuritis are best heard toward the close of 
inspiration and occur only in the early stages of the disease, ceasing 
with the development of the effusion and perhaps reappearing as 
the effusion is absorbed. The place where the sound is most audi- 
ble is the axilla. If a friction-sound is heard at the apex of the 
chest, tuberculosis will often be the cause of its existence in this 
locality. Care should always be taken that fine rales are not mis- 
taken for friction-sounds. They can be separated one from the 
other by the recollection of the facts that rales are modified by 
coughing, not affected by deep pressure on the chest-wall, and are 
usually well diffused, while the friction-sound is not modified by 
coughing, is intensified by pressure on the chest-wall, and is usually 
limited to a narrow area. 
Pericardial friction-sound is, of course, heard best in the praecor- 
dium at the base of the heart—that is, at about the third rib. It 
is separated from pleural friction by the fact that it continues when 
the patient holds his breath. 
Laennec likened this friction-sound to the noise made by the 
leather of a new saddle when ridden for the first time. Sometimes 290 
THE MANIFESTATION OF DISEASE IN ORGANS. 
it sounds like the crunching of snow under the shoe. It is usually 
a to-and-fro sound. 
Vocal resonance is closely allied to the sensation called vocal fre- 
mitus which is felt on palpation, as already described in this chapter. 
It is due to the transmission of the voice-sounds down the trachea into 
the bronchial tubes and bronchioles, and thence through the various 
portions of the lungs. If a stethoscope is placed in the episternal 
notch while the patient speaks, and the ear of the examiner which 
is not closed by the instrument is closed by the pressure of his 
finger, the voice of the patient will be very clearly heard. If the 
stethoscope be placed between the vertebral column and the scapula 
posteriorly—in other words, over the bronchial tubes—the voice 
also will be clearly heard, but not as clearly as over the trachea, for 
two reasons : first, because the sound has already been divided into 
the different bronchial tubes, and, second, because the thickness of 
the chest-wall muffles it. If the stethoscope be placed over the 
anterior part of the chest toward the sides in the area of typical 
vesicular breathing, the sound of the voice will be still more mod- 
ified, because the sound, like the air that conveys it, is now minutely 
subdivided, and the vibrations are decreased by the multitude of 
vesicular walls. Of course, the degree of transmission of vocal 
resonance is governed largely by the character of the voice, and for 
this reason it is more distinct in men than in women. 
If the patient being examined is a man and has a well-developed 
voice, it is usually best to have him speak in a whisper, because the 
full volume of his voice is so great that it will be heard all over 
the chest and the nice differences between the transmission of the 
sound in the healthy lung and the diseased area cannot be distin- 
guished. Usually we get the patient to speak by asking him to 
repeat his name or to count “ one, two, three.” The unemployed 
ear of the physician should always be closed, and the counting or 
speaking only be continued while the physician is actually listening 
to the chest. 
In diseased states of the lung we find the resonance is increased 
by those changes which aid in the transmission of the sound and 
decreased by those changes which obstruct its transmission. As- 
pointed out when speaking of vocal fremitus, a solidified lung and 
the opposite state, namely, a cavity, transmit sound better than 
healthy tissue, which is partly air and partly lung-tissue. We find, 
therefore, that the vocal resonance, or the sound of the voice of tho THE THORAX AND ITS VISCERA. 
291 
patient when he speaks, is increased in pneumonia, in tubercular 
consolidation, and in cavity, and decreased in cases of emphysema, 
or in cases in which a pleural effusion separates the lung from the 
chest and deadens sound. (Fig. 115.) Vocal resonance, however, 
may be increased over pleural effusions, particularly the resonance 
of the whispered voice. This is called “ Baccellbs sign,” and 
Baccelli claims that it serves to separate serous effusions from puru- 
lent effusions, because in his experience it is absent in the latter 
class of cases and present in the former.1 
When a cavity is situated near the surface of the lung so that the 
sound of the voice is transmitted to it and from it through the 
chest-wall with unusual clearness, the sound so clearly heard is 
called 11 pectoriloquy.” It is usually very marked over a cavity 
connected with a bronchial tube. 
Sometimes, when the voice sounds through the chest-wall as if it 
were of a bleating character it is called “ segophony.” It is usually 
heard at the angle of the scapula, near the margin of a pleural 
effusion, and is supposed to be caused bv compression and partial 
occlusion of a bronchus. 
Finally, in pyo- or hydro-pneumothorax, if the ear be placed 
against the chest and the patient is shaken, we have developed a 
splashing or slopping sound, called “ Hippocratic succussion.” It 
is not always heard in these cases, and may be developed when a 
large cavity in the lung is partly filled with liquid. 
The healthy physical signs, and the variations from the normal 
signs met with in diseased conditions of the lungs, have now been 
discussed. The next step is to group these various signs with other 
characteristic symptoms in order that we may obtain a complete 
picture in the diagnosis of a given disease. 
Let us suppose that a patient, previously in health or without any 
serious pulmonary complaint, is found, after a physical examination 
of his chest, to have rapid breathing, a somewhat anxious expres- 
sion, a bright eye, and a dusky flush on one or both cheeks. Pal- 
pation discovers a hot, fevered skin, which is dry or more rarely 
moist, and increased vocal fremitus over both sides of the chest, 
more marked on one side than the other. Percussion reveals im- 
pairment of resonance over the area where fremitus was found most 
1 This sign is mentioned here for what it is worth. The writer has never been able to use it 
with success. 292 
THE MANIFESTATION OF DISEASE IN ORGANS. 
increased, and auscultation in this area shows bronchial breathing, 
fine crepitant rales, and increased vocal resonance. Under these 
circumstances we have before us the physical signs of acute croupous 
pneumonia. The pulse is apt to be rapid, but not as fast as the 
respiration would lead us to expect, for it is a characteristic of 
this disease that the respirations are out of proportion to the pulse. 
The diagnosis is confirmed by the presence of pain in the side 
affected, by the cough, the rusty, sticky sputum, and the history 
that the illness was sudden in onset and was initiated by a chill 
which may or may not have followed exposure. After a few days 
the rales disappear as consolidation becomes complete in the affected 
part, and the area which gave impaired resonance on percussion now 
gives a dull note, while the bronchial breathing in the affected part 
becomes more marked. The lips are apt to be attacked by herpes. 
With the fall of temperature, or crisis, which may be reached by the 
third to the ninth day, the rales return {rales redux) and become 
more and more loose, coarse, and moist as resolution progresses, 
until the lung becomes entirely clear, and only a slight roughening 
of the breath-sounds is to be heard. Bad symptoms in such a case 
are delirium, a feeble pulse, a feeble heart with distant heart-sounds, 
or one in which the action is labored and irregular. Prune-juice 
sputum, or, as the disease progresses, purulent sputum, are bad signs 
also. If the temperature falls to normal about the fifth day, and 
then rises again, forming a pseudo-crisis, the attack will probably be 
prolonged. When a child is affected by croupous pneumonia it is 
very common for us to find all the ordinary objective symptoms 
without any of the physical signs just named. The dulness on 
percussion is difficult of development because the chest is so resil- 
ient, that the percussion blow makes the whole chest resound, and 
it is noteworthy that percussion of the chest on the diseased side 
quite commonly develops a high-pitched tympanitic note such as we 
often find above a pleural effusion. 
The condition of croupous pneumonia cannot readily be confused 
with any other disease because of its characteristic symptoms, but 
catarrhal pneumonia and tuberculosis of the lung often are con- 
fused. In catarrhal pneumonia the patient usually presents a history 
of some previous illness. The disease rarely begins with the marked 
and startling symptoms of the croupous form, but is insidious and 
accompanied by a milder but more prolonged and constant fever. 
Percussion often will not give the positively dull note which can be THE THORAX AND ITS VISCERA. 
293 
elicited in croupous pneumonia, and only impairment of resonance 
may be developed. There is increased vocal fremitus on palpation 
and increased vocal resonance on auscultation; there are also 
increased bronchial breathing and more bronchial rales than in the 
croupous form, for the disease is a broncho-pneumonia involving 
the bronchial tubes and vesicles. The signs are generally diffuse, 
very often heard best at the bases posteriorly, and clear tubular 
breathing, such as is heard in the croupous form, is rarely to be 
found. The sputum is not sticky or rusty; the fever does not end 
by crisis, but rather by lysis; and the lung returns to its normal 
state very slowly, its progress toward health often remaining almost 
stationary for weeks at a time. 
The separation of these symptoms of catarrhal pneumonia from 
those of early pulmonary tuberculosis is practically impossible by 
the physical signs until the case has progressed to a well-advanced 
position. Often catarrhal pneumonia merges into the tubercular 
condition, and very often the diagnosis of catarrhal pneumonia 
proves to have been made in a case in which the disease is really 
tuberculosis. We have to rest the diagnosis of tuberculosis chiefly 
on the family history, the personal history, the fact that recovery 
does not take place, and, more important than all, the presence of 
tubercle bacilli in the sputum, or yellow elastic fibres which indicate 
a breaking down of the lung-tissues. 
If the malady be tubercular and progressive, we soon find in the 
chest and sputum signs which make the diagnosis clear. The chest 
on inspection does not move with costal breathing as much as is 
normal; the hand placed upon it feels, when the patient speaks, that 
there is not only increased fremitus but a bubbling feeling from 
coarse rales, and auscultation also reveals the signs of the breaking 
down of lung-tissue. Finally, when a cavity is developed the per- 
cussion-sound over it becomes high-pitched, and, if the cavity be 
large, almost tympanitic, although all around it dulness may be 
present. The breathing now becomes more tubular or amphoric, 
and vocal resonance may be increased to such an extent that bron- 
chophony or pectoriloquy becomes marked even in that part of the 
lung in which in health the vesicular sounds are heard most typic- 
ally. (Fig. 133.) Prolongation of expiration is also present, and 
sweats, irregular hectic fever, and great loss of flesh ensue. 
The history of the case and its symptoms are our chief means of 
separating pulmonary abscess from pulmonary tuberculosis with the 294 
THE MANIFESTATION OF DISEASE IN ORGANS. 
development of cavity, for the physical signs are about the same. 
In cases of abscess we find that the patient lias suffered from pneu- 
monia or from pyaemia, with embolic infarction. In other cases 
discharges from the nose and throat entering the lungs produce such 
lesions. The symptoms of abscess, which separate it from cavity 
due to tuberculosis, are as follows: in abscess the lesion exists in 
the lower lobe as a rule, while the tubercular cavity is usually 
Fig. 133. 
Case of pulmonary cavity due to tuberculosis. The central ring is the area giving the physi- 
cal signs of cavity, with cavernous breathing and whispering pectoriloquy, and the outer ring 
that of consolidation (dulness), with rapid breaking down of the lung-tissue (moist rales). 
found at the apex or in the upper lobe. The constitutional disturb- 
ance in abscess is often very slight, whereas in tuberculosis it is 
usually severe. In abscess the sputum is copious and purulent, 
and often coughed up in gushes, whereas in tuberculosis it is often 
scanty, and not markedly purulent, as a rule. Again, in the last- 
named disease tubercle bacilli may be found, but they are absent in 
abscess. 
If the patient has the signs of cavity of the lung, and in addition 
an exceedingly fetid breath, with great wasting, the case is probably 
one of pulmonary gangrene. Gangrene is usually found at the 
base of one lung, as is abscess. The sputum is usually brownish. THE THORAX AND ITS VISCERA. 
295 
Bronchiectasis with fetid breath is occasionally met with, but the 
fetor after coughing is never so horribly strong as it is in cases of 
gangrene. 
There are two areas in the lung often affected very early in pneu- 
monia, particularly of the croupous type, and in pulmonary tuber- 
culosis, which are apt to be overlooked, namely, the axilla and the 
septum between the upper and middle lobe on the right side, an 
Fig. 134. 
Area of dulness found in many cases of obscure pulmonary tuberculosis, when the arm is 
raised so that the scapula no longer covers the septum. 
area only exposed to percussion and auscultation when the right 
hand of the patient is placed on top of his head in such a way that 
the angle of the scapula is drawn away from the vertebral line. 
(Fig. 184.) If this is done, the inner border of the scapula will 
approximate the line of the septum, and along this line there will 
often be found in tuberculosis of this portion of the lung marked 296 
THE manifestation of disease in organs. 
(lulness on percussion or, on auscultation, rales, and the other phys- 
ical signs of consolidation, even though the physician is unable to 
find elsewhere any evidence of local disease to account for the gen- 
eral systemic symptoms. Very often careful auscultation of the 
axillary area will also reveal signs not to be found elsewhere which 
account for the illness, such as those of pneumonia or pleurisy, for 
here, as a rule, the friction-sounds of the latter affection are best 
heard. 
The physical signs of pulmonary oedema may develop suddenly 
as a result of an injury to the vagus, or in acute disease of the 
lungs. Generally, however, their onset is slow and insidious, but the 
rapid breathing, crepitant rales, the limitations of these signs to the 
lower part of the chest, combined with duluess on percussion, the 
absence of fever, the frothy sputum, and, it may be, the history of 
renal disease all point to the true state of affairs. 
There is another state that gives dillness on percussion, crepitant 
rales, and the other physical signs of pneumonia, namely, pulmon- 
ary congestion dependent upon the action of a feeble heart in the 
course of prolonged exhausting fevers; but the history of the ill- 
ness, the feeble heart, and the development of these sigus in the 
dependent parts of the chest effectually preclude the idea of any 
acute inflammatory process in the lung. 
Finally, we frequently have after a pulmonary apoplexy an area 
of consolidation in the lung; but if this be the case, we also have, 
as a rule, a history of haemoptysis. This condition is, however, 
comparatively rare. 
To cite another form of thoracic disease, let us suppose that a 
healthy man is seized with pain in the thorax and a chill followed 
by fever. An examination of his thorax will reveal on inspection 
deficient breathing on the affected side, which is fixed because of 
pain produced by the inflamed pleural surfaces moving over one 
another on inspiration. Exaggerated breathing will be found on 
the opposite side to compensate for this fixation, and auscultation 
on the painful side will reveal a friction-sound, probably best heard 
in the axilla. After these signs have existed some hours the second 
stage develops, and as effusion takes place we find that the friction- 
sound disappears and that the affected side, previously almost nor- 
mally resonant, is beginning to become dull, and, finally, is flat on 
percussion at the most dependent part of the pleural sac, namely, 
at the base of the lungs posteriorly. This area of flatness on per- THE THORAX AND ITS VISCERA. 
297 
cushion gradually rises higher and higher until the effusion is com- 
pleted. It extends anteriorly, and may be demonstrated as well 
here as it can be posteriorly and laterally, although, if the patient 
lies on his back or is partly recumbent, the entire anterior surface 
of the chest may be resonant, owing to the fluid leaving the front 
of the chest and going to the more dependent parts. In other 
words, in cases of non-sacculated serous pleural effusion changes in 
the position of the patient cause alterations in the area of flatness 
on percussion, unless the effusion is large enough to fill the chest 
entirely, when, of course, it is immovable. Inspection will show 
an increase in the size of the chest on the diseased side, with bulg- 
ing of the intercostal spaces. 
A curious yet important point in this connection is the fact that 
the line where flatness on percussion ceases at the top of the effusion 
posteriorly is wavy or sigmoid (S-sliaped). Above the level of the 
effusion percussion over the compressed lung gives a somewhat hol- 
low note or hyper-resonance, called “ skodaic resonance,” and the 
sense of resistance to the percussed finger is less at this point than 
over the effusion, where the resistance is great. In ausculting the 
chest in the area in which flatness has been developed by percussion 
very distant breath-sounds are audible, except in the back near the 
vertebral column, where there may be marked blowing breathing. 
If the patient speaks, there will be found loss of vocal resonance 
and of fremitus over the effusion, but along the margin of the spine 
on the diseased side there may be heard in some cases bron- 
chophony, or even the bleating voice-sound called segophony. In- 
spection and palpation will show the apex-beat of the heart displaced 
to the right and downward in cases of effusion into the left pleura, 
and to the left in cases of right-sided effusion. Again, if the effu- 
sion be on the left side, it will be found on percussing “ Traube’s 
semilunar space,” a space directly in the nipple-line and a little 
below the nipple, that the usual tympanitic resonance normally 
found in this area is extinguished through the downward pressure 
of the fluid. 
If the effusion be accompanied by pneumothorax, we will find 
three sets of physical signs, namely, those of effusion, which will 
be at the lowest part of the chest; next above this an area in which 
percussion gives a clear tympanitic note due to the air in the pleural 
cavity; and above this the physical signs of the compressed lung in 
the apex of the chest cavity. In this condition we may also hear 298 
THE MANIFESTATION OF DISEASE IN ORGANS. 
suCcnssion or splashing sounds, if' the patient is shaken while the 
physician’s ear is against the chest-wall, and the metallic tinkling, 
or dropping sounds, as the fluid falls from the top of the chest- 
cavity into the effusion. Again, we may use what has been called 
“ dollar percussion.” This consists in having an assistant place 
a silver dollar against the chest-wall on the diseased side anteriorly, 
and then the physician listens at the posterior aspect of the chest, 
his unused ear being closed by his finger. The assistant now strikes 
the silver dollar with the edge of another silver dollar. If the 
dollars be struck together below the surface of the effusion, very 
little of the metallic sound will be transmitted through the chest. 
If the dollars are struck together at the level of the layer of air, 
the sounds come through the chest-cavity with startling clearness; 
but if at the level of the lung, they are less clearly heard than at 
the level of the air, but more so than at the level of the effusion. 
The reasons for this are obvious, for the liquid prevents the trans- 
mission of the metallic sounds, as does also to some extent the com- 
pressed lung at the apex of the chest, whereas the space filled with 
air conveys the sounds directly to the ear. 
Finally, if the effusion is absorbed by unaided nature, the area of 
flatness on percussion becomes less and less great from above down- 
ward, the expansion of the chest on inspiration increases, the inter- 
spaces cease to bulge, and the friction-sounds may return for a brief 
period. 
If the effusion does not disappear, the physical signs of its exist- 
ence persist; and if it becomes purulent, the patient is apt to lose 
flesh and strength, to have chills, fevers, and sweats, and to present 
all the evidences of an accumulation of pus in some part of the 
body. Particularly is this result apt to follow a pleurisy compli- 
cating one of the acute infectious diseases, such as scarlet fever, 
typhoid fever, some instances of pneumonia, and in many cases in 
which tuberculosis is responsible for the illness. 
Particular attention should be called to the possibility of pleural 
effusions coming on insidiously. There is probably no other mas- 
sive pathological change anywhere in the body so often unsuspected 
or overlooked, and it is noteworthy that when pleural effusion is insid- 
ious in its onset and devoid of prodromes, that it is often due to an 
undiscovered tuberculosis, whether the exudate be found to be serous 
or purulent. Again, the fact that tubercle bacilli cannot be found 
in the effusion when it is aspirated in no way proves that the effu- THE THORAX AND ITS VISCERA. 
299 
sion is not tubercular in origin, since they are rarely found in the 
fluid even when tubercular pleurisy is most active. 
Serous pleural effusion single or double may result from throm- 
bosis of the vena azygos. It is particularly apt to come on in 
patients suffering from typhoid fever or other exhausting diseases. 
Such a transudation can be separated from the effusion due to in- 
flammation by the method of Pohl and Rosenbach. This consists 
in withdrawing some of the fluid by an aspirating-needle after the 
patient lias received a dose of iodide of potassium. A few drops 
of fuming nitric acid are added to the fluid, and it is then agitated 
with chloroform, when, if the effusion be a transudation, the iodine 
will be seen of a red color sinking to the bottom of the test-tube 
with the chloroform. If it be an inflammatory exudate, the iodine 
will be passed into the effusion. 
If on aspirating the fluid in the chest it is found to be hemor- 
rhagic in character, the cause may be one of the diseases which pro- 
duce marked asthenia, notably carcinoma, nephritis, one of the 
acute infectious diseases in a malignant form, or tuberculosis. 
The cancer may or may not be in the chest. Rarely such an effu- 
sion occurs in otherwise healthy men without these causes. The 
possibility of the hemorrhagic effusion being due to a leaking aneu- 
rism, or to leakage from an ulcerated bloodvessel in tubercular dis- 
ease of the lung, is to be remembered. 
If after exposure to cold there is a sense of soreness in the chest, 
with more or less oppression and a hard cough, which seems to tear 
the bronchial tubes, the cough being without associated expectora- 
tion and the febrile movement but moderate, we suspect the presence 
of an acute bronchitis, a diagnosis which will be confirmed if we 
find the following physical signs : 
There is marked roughening of the breath-sounds all over the 
chest, particularly over the bronchial tubes at the back, between the 
scapubn, without any increase in vocal resonance and fremitus, or 
any impairment of resonance on percussion. As the disease pro- 
gresses these rough sounds of harsh breathing give way to rides, 
which are at first fine and moist, then coarse and sonorous, as the 
second stage, or stage of secretion, develops; and, finally, they 
decrease little by little, as health is approached and the mucus is 
expelled by coughing. Care should always be taken to determine in 
examining a case of suspected bronchitis that the symptoms are not 
due to a broncho-pneumonia. 300 
THE manifest a tion of disease in organs. 
Should the case become chronic the sounds of coarse, and more 
or less sonorous, rales will persist and will become constant. Such 
cases usually become worse in winter, and the sputum is sometimes 
very profuse (bronchorrhoea). The physician should always be 
careful in these cases to see to it that renal disease or a feeble heart 
is not the cause of the bronchial disorder. The health suffers but 
little in simple chronic bronchitis; but if‘bronchiectasis develops, it 
may be much impaired. 
Under the name u putrid bronchitis” we have a state in which 
the sputum is foul and expelled in a liquid form, in which float 
little yellow plugs (Dittrich’s plugs). This condition may end in 
pulmonary gangrene or cause metastatic abscess. 
The presence of a barrel-shaped chest, with almost immovable 
walls and marked abdominal breathing, points to the presence of 
emphysema of the lungs, and this opinion is confirmed if on auscul- 
tation of the chest we find marked prolongation of expiration, dimin- 
ished vocal resonance and fremitus, and increased resonance on 
percussion. The face is often quite cyanotic, the superficial veins 
of the neck turgescent, the abdominal respiratory movements abnor- 
mally great, and the superficial veins in the epigastrium enlarged. 
If bronchitis or bronchiectasis is associated with the emphysema, as 
is frequently the case, we find more or less marked rales all over 
the chest, particularly posteriorly. Sometimes a systolic murmur 
can be heard over the tricuspid area, due to regurgitation on the 
right side of the heart. Cardiac dulness is generally obliterated 
by the enlarged lung, and the apex-beat cannot be felt except in the 
neighborhood of the ensiform cartilage or in the epigastrium. Both 
the hepatic and splenic dulness are found to begin and extend lower 
than normal, owing to the expansion of the lung. We may also 
find accentuation of the second sound in the pulmonary artery. 
The tricuspid regurgitation usually develops from a damming up 
of the blood in the right ventricle. 
When a patient is seized with a violent attack of dyspnoea its 
cause may be asthma, a foreign body in the air-passages, or laryn- 
geal spasm. 
If it is asthma, there will be labored breathing in which all the 
accessory muscles of respiration in the neck and trunk aid the ordi- 
nary respiratory muscles. The posture of the patient will usually 
be that of sitting up in bed and somewhat leaning forward. The 
face will be flushed, the vessels of the face and neck turgid, and the THE THORAX AXI) ITS VISCERA. 
301 
lips may be cyanotic. Often the patient, while sitting up, supports 
himself by resting on his hands, which are placed at his side in 
order to raise his shoulders and fix the chest-walls for contraction 
of the muscles which are endeavoring to drive out the air, for it is 
to be remembered that the respiratory difficulty in asthma depends 
more upon the fact that the patient cannot empty the lungs than 
upon the fact that lie cannot fill them. As a matter of fact, they 
are too full of air which has been used. 
Inspection not only shows these signs in asthma, but also reveals, 
in cases in which emphysema has not developed to such an extent 
as to cover the heart with the lung, that the apex-beat is diffused 
and the heart laboring. Palpation reveals little, except when coarse 
rfiles are present in large numbers, when some bubbling may be felt. 
Percussion usually gives an increased resonance because the chest is 
inordinately full of air, and auscultation reveals very loud blowing 
breathing, musical notes, or squeaking or creaking noises, both on 
inspiration and expiration. Finally, as secretion begins to be estab- 
lished musical and cooing rales may be heard in well-marked cases 
all over the chest before the ear is placed against the patient. At 
first these rales are heard chiefly on expiration, but very shortly 
they occur equally loudly on both inspiration and expiration. 
Toward the end of the attack coughing brings up a limited amount 
of sputum, which contains Curschmann’s spirals and Charcot- 
Leyden crystals. (See chapter on Cough and Expectoration.) 
As asthma is a symptom, not a disease in itself, the physician 
should always examine the nose, with the object of discovering some 
source of reflex irritation in the nasal mucous membrane, or the 
urine to discover whether renal disease is present, or the heart to 
discover if a cardiac lesion accounts for the symptoms. Sometimes 
gastric disorder is responsible for the attack. 
Care should be taken that a catarrhal pneumonia developing after 
an attack of asthma is not overlooked until the patient is danger- 
ously ill. 
If on ausculting the chest we find it filled with musical and cooing 
rales heard in every part, though most marked in the bronchial tubes, 
we can be fairly sure that an attack of asthma is about passing away; 
but if, on the other hand, the attack is beginning, the prolonged ex- 
piration, with comparatively few rales, the harsh bronchial breath- 
ing, and the general objective symptoms of the case will explain 
the cause of the pulmonary condition. 302 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
The dyspnoea due to a foreign body in the air-passages, whether 
it be a piece of meat or a false membrane, is quite different from 
that of asthma, for in this case the difficulty is commonly in the 
entrance of air. The onset of the attack is usually sudden, but 
inspection will show that on inspiration the costal interspaces are 
greatly drawn in, as is also the epigastrium. There will be prac- 
tically no signs in the chest which are not evidently due to the 
efforts at forced breathing, and a history of having had a foreign 
body in the mouth or of some laryngeal disease will usually be 
obtainable. Obstruction may, however, be present and this history 
be absent, in cases in which an abscess has burst into the air-passages 
from the mediastinum or through the posterior pharyngeal wall. 
In such a case, however, there would be, in all probability purulent 
expectoration. 
Laryngeal spasm, producing difficult breathing, causes symptoms 
precisely like those of foreign body in the larynx, except that in 
spasm the cough is often constant and is very brassy or ringing. The 
patient will show by a gesture with his hand that the obstruction is 
in the larynx, if unable to speak. Such obstruction when seen in 
children is due to spasmodic croup, as a rule, and, if so, probably 
depends upon one of three causes, namely, laryngeal catarrh, rickets, 
or digestive disturbance. If in an older person, it is probably due 
to aneurism pressing on the recurrent laryngeal nerve, to locomotor 
ataxia, or growths in the mediastinum producing pressure on the 
nerve-trunks going to the laryngeal muscles. Sometimes great 
enlargement of the retro-bronchial glands will cause laryngeal 
spasm, or obstruction by pressure. 
Tumors occur in the chest generally as mediastinal growths, and 
are most commonly sarcomata or lymphadenomata. There will be 
found, if the growth be large, evidences of its pressure upon the 
chest-wall such as bulging and dulness on percussion over the swell- 
ing. This level of dulness is unaltered by changing the posture, 
as it would be in pleural effusion. Generally there will be evidence 
of pressure on the bronchial tubes, which causes dyspnoea, and of 
pressure on the thoracic vessels, which produces signs of impaired 
circulation as shown by cyanosis, venous engorgement, and flushing 
of the skin of the face and neck. Often such growths cause pleural 
effusions by pressure on the bloodvessels, or produce pulmonary 
consolidation by causing an exudation into the lung-tissue. 
The diseased conditions from which it is necessary we should dis- THE THORAX AND ITS VISCERA. 
303 
tinguish mediastinal growths during life are as follows: 1. From 
aneurism. 2. From abscess. 3. From pleural effusion. And 4. 
From chronic pneumonia. There are several subdivisions of these 
diseases that might be made, but to all intents 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 
than aneurism. (See Aneurism in this chapter.) 
Unfortunately, the most common age of 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 symp- 
tom as an aid of any value in 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. 
Haemoptysis is not in any way a differential sign, since in the one 
case it may be due to aneurismal leakage, and in another to ulcera- 
tion 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 304 
THE MANIFESTATION OF DISEASE IN ORGANS. 
or less severe, and fever; or, if cold, then we frequently have irreg- 
ular febrile movements, with long-continued anorexia and loss of 
flesh. Cold abscess, too, is generally in the posterior mediastinum, 
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 
effusion 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 
frequently in cases of asthenic inflammation we have an exudate 
lacking 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 bloodvessels. 
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 
absolutely impossible to make any diagnosis unless by symptoms of 
pressure in the mediastinum, or some history pointing to such a 
result. Walsh has stated that if the lesion be due to a tumor, the 
affected side will increase in bulk rather than diminish, and that 
dyspnoea out of proportion to the degree of consolidation points to 
a mediastinal disorder rather than one confined to the lungs. If 
the heart be displaced in either direction, the odds point to medias- 
tinal tumor; but the presence or absence of a haemoptysis, as has 
just been stated, influences the diagnosis not at all. THE THORAX AND ITS VISCERA. 
305 
The diagnosis of pericarditis from mediastinal lesions is much 
more readily made. The history of sudden prsecordial pain and 
the limited area of dulness on percussion aid us very materially in 
deciding 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 pericardial sac from effusion may give us a regular outline 
on percussion, while the dulness of mediastinal disease may be irreg- 
ular 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 listen- 
ing 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 dup,” 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 accent- 
uated, and it is of importance to remember that marked accentuation 
of the aortic second sound, showing forcible closure of the aortic 
valves, indicates a condition of high arterial pressure, often the 
result of vascular spasm arising from chronic contracted kidney. 
On the other hand, if the pulmonary second sound at the second 
left intercostal space is accentuated, it indicates an increase in pul- 
monary pressure due to impediment 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. 135): 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 306 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the third left intercostal space to the fifth right costal cartilage, and 
the pulmonary valve 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 unequal manner of the papillary muscles. 
Fig. 185. 
Showing the areas in which the various heart-sounds are best heard in health. A is the 
area for the aortic valve; P, that for the pulmonary valve ; T, for the tricuspid valve; and M, 
for the mitral valve. 
If disease of the valves be present, we are apt to find reduplication 
of the second sound in cases of mitral stenosis and lung disease 
producing an abnormally high tension in the pulmonary circulation. 
Such reduplication 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 (“ lub dup”), or with them, 
a murmur, what does it mean? It means that, friction-sounds 
being excluded, either valvular disease of the heart, aneurism of 
the aorta, or marked anaemia is present. Particularly is the anaemic 
murmur apt to be heard in the case of feeble children suffering from 
chorea, and it will generally be found most marked at the left 
margin of the sternum.1 
1 It must not be forgotten that murmurs due to endocarditis also are frequently found in 
choreic children. THE THORAX AND ITS VISCERA. 
307 
Having found that there is a murmur, and, from the absence of 
anaemia, that it is due to organic cardiac disease, it is now necessary 
to determine at what orifice of the heart it is produced, 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 cartilage (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 trans- 
mitted. 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 
Fig. 136. 
Showing at x the apex-beat where the murmurs of mitral regurgitation and obstruction can 
he best heard. The arrow pointing to the axilla indicates the direction in which the regurgi- 
tant murmur is transmitted, and the arrow pointing to the sternum the direction of transmis- 
sion of the obstructive murmur. 
pulmonary, loudest at the pulmonary area. As murmurs at the 
tricuspid and pulmonary valves are rare, we nearly always have to 
deal with aortic or mitral murmurs, or both. In this way, there- 
fore, we can determine the origin of the murmur, and that it is a 
mitral or an aortic murmur. Let us suppose that it is mitral. We 
must determine whether it is that of mitral regurgitation or ob- 
struction, or, as they are also called, incompetence and stenosis. The 
probabilities are that it is the regurgitant murmur, because this 
lesion is by far the most common murmur heard in the heart; and if 308 
THE MANIFESTATION OF DISEASE IN ORGANS. 
to this probability we add the fact that it is transmitted well into 
the axilla, and even heard at the angle of the scapula, our diagnosis 
is greatly aided, for this is the area of transmission of the murmur 
of mitral regurgitation. The most important diagnostic point, 
however, is the discovery that the murmur occurs simultaneously 
with the first sound of the heart, or with systole—that is, with the 
apex-beat or the carotid pulse. If it does, and the other signs of 
mitral disease are present, it is almost certainly one of mitral regur- 
gitation. This murmur occurs with the first sound, or systole, 
because the ventricle in contracting drives most of the blood in the 
normal direction into the aorta, and also forces some of it back 
through the auriculo-ventricular orifice into the auricle, causing a 
regurgitant murmur. There will be found very often in such cases 
a very marked accentuation of the second sound at the pulmonary 
orifice. The area of greatest intensity of the mitral regurgitant 
murmur is shown in Fig. 136. 
In adults inspection and palpation will rarely reveal much of a 
thrill over the praecordium in mitral regurgitation, but in children 
this thrill is rarely absent and is usually well marked. Percussion 
will show that the area of cardiac dulness (see earlier part of this 
chapter) is broadened, extending beyond the right edge of the ster- 
num and to the left of the mammillary line. 
If, on the other hand, it is found that the murmur does not occur 
with systole, but just before it, and is not transmitted into the axilla, 
but to the right, over to the midsternal line, it is probably that of 
mitral stenosis—that is, the presystolic mitral murmur (see Figs. 136 
and 137). This murmur can often be exaggerated by placing the 
patient in a prone position, and occurs before systole, or the first 
sound, because it is made by the blood passing through an obstructed 
auriculo-ventricular orifice, and, as the ventricle does not contract 
(systole) till it is filled, the murmur must be made while it is filling, 
and so is presystolic in time. Palpation of the praecordium in 
such a case will usually reveal a marked thrill in the fourth or 
fifth interspace. If the compensation of the heart in a case of 
mitral stenosis is broken, these signs are accompanied bv a very 
irregular action of the heart, the first sound becoming accentuated 
and the murmur disappearing. In some cases what is called a 
“ gallop rhythm” develops, the heart-sounds being reduplicated in 
such a manner as to make a galloping sound. 
If, however, we have found the murmur to be aortic, we must THE THORAX AND ITS VISCERA. 
309 
exclude aneurism and then determine whether it is that of aortic 
regurgitation or obstruction. The characteristic symptoms of 
aortic aneurism are a “ bruit’'* or angry murmur, systolic in 
point of time, and heard best in the area between the third rib and 
the clavicle on the right side, accompanied by pulsation, which is 
Fig. 137. 
mo shows area of greatest intensity ot a mitral obstructive murmur, tk shows area of 
greatest intensity of a tricuspid regurgitant murmur. 
often expansile; by an angry thrill; by bulging of the chest-wall 
(Figs. 117 and 188) if the disease is advanced and presses forward; 
by glossiness of the skin over the bulging; by unilateral sweating 
of the face and neck from pressure on the cervical sympathetic; by 
inequality of the pupils from the same cause; and by inequality of 
the radial pulses, owing to the arrest of the blood in the sac, so that 
it does not enter the vessels on both sides synchronously. Again, 
we usually have a very considerable degree of dyspnoea, and some- 
times dysphagia from pressure on the oesophagus. There may also 
be history of syphilis and of severe strain or injury in many cases. 
Although these are the general symptoms of aortic aneurism, 310 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
there are others which depend upon the seat of the aneurism and 
which materially modify the points so far named in diagnosis. Let 
us suppose that a patient presents himself with great engorgement 
of the vessels of the head and neck and arm of the right side, with 
perhaps oedema of the arm. The heart may be pushed downward 
and to the left, and the voice may be lost or partially impaired by 
Fig. 138. 
Case of aortic and innominate aneurism, with erosion of the clavicle and ribs, from the 
author’s wards in the Jefferson Medical College Hospital. This case is of extraordinary in- 
terest because this picture was taken thirty-five months after Dr. D. D. Stewart had caused 
an arrest of the growth of the aneurism by electrolysis. 
pressure on the recurrent laryngeal nerve of the right side. Gen- 
erally such symptoms will be due to an aneurism of the greater 
curvature of the ascending aorta, although they may be due to a 
tumor in the anterior or middle mediastinum; but the expansile 
pulsation, the bruit, and the history of the case will often make the 
differentiation possible. Such a growth will probably cause bulg- 
ing of the second or third interspace on the right side. Again, let 
us suppose that the chief symptoms manifested by the patient are 
a brassy, ringing, and constant cough, with difficulty in swallowing, 
and an examination of the vocal cords shows that the left cord is 
paralyzed rather than the right, thereby causing hoarseness, and THE THORAX AND ITS VISCERA. 
311 
there is more or less bulging and distention of the innominate or 
left carotid arteries, while the radial pulse is delayed, then we may 
consider that the aneurism is probably of the transverse portion of 
the arch. Still farther, if an irregular action of the heart, with 
great pain in the back, is found, in addition to the ordinary signs of 
aneurism, it is possible that the aneurism may be in the descending 
aorta and be eroding the vertebra. If the aneurism be of the first 
two forms named, there may be found, on percussion, dulness over 
the swelling or over the area of expansile thrill and bruit. Thus 
the aneurisms of the ascending part of the arch which project for- 
ward and to the right cause dulness on the right side of the sternum, 
while those of the transverse part of the arch cause dulness on per- 
cussion on the left side or in the middle line. On the other hand, 
the lesion of the descending aorta often causes dulness and bulging 
between the vertebral column and the scapula on the left side. 
There are other symptoms connected with aneurism which should 
not be overlooked. The first of these is “ tracheal tugging,” a 
sign which is found in some cases of aneurism. The patient being 
in the erect position the fingers of the physician grasp the cricoid 
cartilage and gentle upward traction is produced. If aneurism is 
present, a distinct tug will be felt with each beat of the heart. 
Another sign mentioned by Osier is the loss of pulsation in the 
peripheral vessels, the result of the loss of the heart’s impulse in 
the aneurismal sac. 
If the symptoms of aortic aneurism are excluded, we proceed to 
determine the question as to whether the murmur is that of aortic 
stenosis or obstruction or incompetence or regurgitation. Aortic 
obstruction is the more common lesion of the two. This murmur 
occurs with the systole of the ventricles, or the carotid pulse or 
apex-beat; it is harsh as a rule, and is transmitted up into the car- 
otid and it may be into other arteries of less importance. (See Fig. 
139.) It is produced by the contraction of the ventricle driving 
the blood through a narrowed or roughened aortic orifice. Consid- 
erable hypertrophy of the left ventricle is usually present, and the 
apex-beat is strong and forcible. 
If, on the other hand, the murmur occurs after the systole or 
apex-beat, and is aortic, the murmur is that of aortic regurgitation, 
and is called the diastolic aortic murmur. It is heard loudest at 
the aortic cartilage, but is transmitted down along the sternum very 
clearly and into the left ventricle, so that it is heard at the apex. 312 
THE MANIFESTATION OF DISEASE IN ORGANS. 
(See Fig. 140.) In this condition we have usually marked dilata- 
tion of the heart with hypertrophy (the so-called “ ox-heart”), and 
a peculiar trip-hammer pulse (see chapter on Pulse), sometimes 
called the “ water-hammer ” or Corrigan pulse. This murmur is 
due to incompetence of the aortic valve, which allows the blood to 
regurgitate into the heart after it is driven out into the aorta. 
Fig. 139. 
Fig. 140. 
Showing the area of greatest intensity and the 
direction of transmission into subclavian and 
carotid arteries of the aortic obstructive murmur. 
Showing the area in which the murmur 
of aortic regurgitation can be most clearly 
heard. 
If the examination has shown that the tricuspid valve is diseased, 
it is] to be remembered that in the vast majority of cases the mur- 
mur is due to tricuspid regurgitation, for tricuspid stenosis is an 
exceedingly rare condition. The time of the murmur of the tri- 
cuspid lesion is identical with that of the mitral regurgitant (sys- 
tolic), because this valve is the counterpart in the right side of the 
heart of the mitral valve. Actual disease of the pulmonary valves 
is exceedingly rare, and the regurgitant form of lesion is almost 
never met with. The murmurs sometimes heard, ami the thrills 
sometimes felt, in this area are generally due to anaemia, the puer- 
peral state, or some neurosis; or to congenital narrowing of the 
pulmonary artery; or to compression of the vessel by the heart. If TEE THORAX AND ITS VISCERA. 
313 
the last two causes are present, the ventricular septum is usually 
deficient and cyanosis is noticeable. 
In the diagnosis of all murmurs in the heart we must remember 
that several valves may be diseased, producing associated murmurs. 
Some discussion as to the relative frequency of these associations 
has arisen, but the results of H. J. Smith in the London hospitals 
are usually accepted as correct. His results are as follows, in the 
order of frequency and association : 
1. Aortic regurgitation and stenosis and mitral regurgitation. 
2. Mitral stenosis and regurgitation. 
3. Aortic stenosis and mitral regurgitation. 
4. Aortic regurgitation and mitral stenosis. 
5. Aortic regurgitation and stenosis. 
6. Aortic regurgitation and stenosis: mitral stenosis and regur- 
gitation. 
7. Mitral regurgitation and tricuspid regurgitation. 
8. Aortic regurgitation and stenosis; mitral regurgitation; tricus- 
pid regurgitation. 
9. Mitral stenosis and regurgitation; tricuspid regurgitation. 
10. Aortic stenosis; mitral stenosis and regurgitation. 
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 regur- 
gitation; tricuspid regurgitation. 
23. Aortic regurgitation and stenosis; mitral stenosis and regur- 
gitation; tricuspid stenosis and regurgitation. 314 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
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 danger- 
ous 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 understood that murmurs produced by any form of 
valvular 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 very marked. This is because the development of gen- 
eral 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 compensa- 
tory hypertrophy of the heart-muscle. If the heart-muscle can 
make up for the regurgitation or obstruction by increased effort, the 
circulation is unimpaired; but if it cannot do so, we have developed 
more or less rapidly, according to the lesion present and the condi- 
tion of the heart-muscle, characteristic 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 symp- 
toms 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 con- 
gestion of the auricle and pulmonary veins is great, bronchitis may 
be constant or attacks of haemoptysis may develop. Palpitation of 
the heart will also be complained of; and if the patient has devel- 
oped the lesion in early life, the finger-tips are apt to be clubbed. 
If the rupture or failure of compensation 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 THE THORAX AND ITS VISCERA. 
315 
be comfortable only when sitting np. 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 engorgement of the 
kidneys 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 
addition there are apt to be present, early in the process of failing 
compensation, some lightness of the head, dizziness or vertigo, or 
faintness, owing to a deficient blood-supply to the brain. A7ery 
commonly, too, it will be found that in association with the aortic 
stenosis there also exists mitral regurgitation, which speedily pro- 
duces 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, the 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 typical general systemic symptoms than any of 
the ordinary valvular lesions of the heart. In addition to head- 
ache, vertigo, and a tendency to syncope, associated witli palpitation 
and a sense of cardiac oppression, 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 dyspnoea is often extreme, the 
patient suffering from terrible attacks of shortness of breath and 
often sitting 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 con- 
stant struggling for breath exhausts him and he falls asleep, only 
to wake in a few moments gasping for air. Long before any of 
these grave symptoms arise we may, however, find a number of inter- 
esting signs of this heart-lesion, chief among which is the “ water- 
hammer” or u trip-hammer” or 11 Corrigan pulse,” the throbbing 
carotid arteries, and capillary pulsation in the skin and mucous 
membranes is to be seen. The last 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 316 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the same capillary pulsation will be found. Ophthalmoscopic exam- 
ination 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 was well until he 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 dul- 
ness is increased vertically and laterally, and auscultation will dis- 
cover 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 regurgita- 
tion. Sometimes tricuspid regurgitation is also found. The first 
sound before it becomes very 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 bv the author in medical 
students, who, during their holidays, devote their time to severe 
athletic sports, or to much manual labor, and who, on leading seden- 
tary lives in the winter, develop irregular cardiac action, palpitation, 
and some shortness of breath. Examination of the praecordium 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, but 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 the 
statement that be has attacks in which he suffers from a very rapidly 
beating heart. His skin is alternately red and pale, and sweats with- THE THORAX AND ITS VISCERA. 
317 
out cause, but a careful examination of the heart fails to reveal any 
murmurs or organic abnormality. There are considerable shortness 
of breath on exertion and marked palpitation 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 properly controlled, or the irregular cardiac action may be due 
to sudden vasomotor relaxations, which by dilating the blood-paths 
reduce the normal arterial resistance. This is a condition seen in 
association with some neuroses and very commonly seen in persons 
who use tobacco to excess. The symptoms of the so-called “ tobacco- 
heart” are indeed chiefly those of arhythmia due to pneumogastric 
disorder. 
Rarely because of irritation of the vagus nerves or centres a state 
of bradycardia develops, in which the heart beats very slowly, per- 
haps only thirty or even as slowly as twelve times a minute. 
Bradycardia or great slowness of the heart may not only be due to 
a neurosis of the vagi, but to typhoid fever or other infectious dis- 
eases. It is also seen in jaundice. 
One of the most common causes of tachycardia, or rapid heart, 
is exophthalmic goitre, in which condition we have not only exoph- 
thalmus and enlargement of the thyroid gland, but, in addition to 
the tachycardia, a marked thrill over the carotid arteries, in which 
vessels a purring murmur of considerable intensity can also be 
heard. The patient often suffers from considerable nervous excite- 
ment 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 an acute infectious disease, or in any state pro- 
ductive of sepsis, points to the possibility of the patient having an 
embolism or thrombus of one of the coronary arteries. If the 
vessel is suddenly plugged, death speedily occurs; but if the pro- 
cess is gradual, an ansemic necrosis or white infarct is produced. 
Sudden attacks of cardiac feebleness sometimes come on as car- 
diac 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 condi- 
tion 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 318 
THE MANIFESTATION OF DISEASE IN ORGANS. 
presence of fatty degeneration of the more superficial organs, such 
as the arcus senilis in the eye,1 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 round the heart as well as in or 
around the other organs of the body. Here there is little or noth- 
ing 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 oedema 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 cardiac failure.” 
Great feebleness of the heart and general system, loss of flesh (or 
sometimes maintenance of weight), pigmentation of the skin and 
buccal mucous membranes point strongly to Addison’s disease (see 
chapter on Skin). 
Finally, let us suppose that a young child is seen who is, and has 
been since birth, more or less cyanotic. In all probability such a 
child is the subject of congenital malformation of the heart. The 
following rules, laid down by Hochsiuger, may be used for their 
diagnosis: 
1. In childhood loud, rough, musical heart-murmurs, with normal 
or slight increase in the heart-dulness, occur only in congenital 
heart-disease. The acquired defects with loud heart-murmurs in 
young children are almost always associated with great increase in 
the heart-dulness. 
2. In young children heart-murmurs, with great increase in the 
cardiac dulness and feeble apex-beat, suggest congenital changes. 
The increased dulness is chiefly of the right heart, whereas the left 
is only slightly altered. On the other hand, in the acquired endo- 
1 Ophthalmologists and many clinicians deny that arcus senilis has any significance of this 
character. THE THORAX AND ITS VISCERA. 
319 
carditis iu children, the left heart is chiefly 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. 
3. The entire absence of murmurs at the apex, with their evident 
presence in the region of the auricles and over the pulmonary orifice, 
is always an important element in differential diagnosis, and points 
rather to septum defect or pulmonary stenosis than to endocarditis. 
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 dif- 
ferential diagnosis which is not to be underestimated. 
5. Absence of a palpable thrill, despite loud murmurs which 
are heard over the whole prsecordial region, is rare, except with 
congenital defects in the septum, and it speaks therefore against an 
accpiired cardiac affection. 
6. Loud, especially vibratory, systolic murmurs, with the point 
of maximum intensity over the upper third of the sternum, associ- 
ated with a lack of marked symptoms of hypertrophy of the left 
ventricle, are very important, for the diagnosis of a persistence of 
the ductus Botalli, and cannot be explained by the assumption of 
an endocarditis of the 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. 141. 
The regions of the abdomen and their contents (Gray.) (Edge of costal cartilages in 
dotted outline.) THE ABDOMEN AND THE ABDOMINAL VISCERA. 
321 
auscultation. For the purposes of inspection the surface of the 
abdomen has been arbitrarily divided by diagnosticians into a num- 
ber of spaces, which are best shown in the accompanying figure 
(Fig. 141), 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 
readily describe the exact spot in which a physical sign or symptom 
is found. 
The following table, from Gray’s Anatomy, clearly shows the 
viscera to be found under each of the areas named : 
Right Hypochondriac. 
The right lobe of the liver 
and the gall-bladder, hepatic 
flexure of the colon, and part 
of the right kidney. 
Epigastric Region. 
The pyloric end of the 
stomach, left lobe of the liver, 
and lobulus Spigelii, the pan- 
creas, the duodenum, parts of 
the kidneys and the supra- 
renal capsules. 
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. 
Right Lumbar. 
Ascending colon, part of the 
right kidney, and some con- 
volutions of the small intes- 
tine. 
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. 
Left Lumbar. 
Descending colon, part of the 
omentum, part of the left kid- 
ney, and some convolutions of 
the small intestine. 
Right Inguinal (Iliac). 
The caecum, appendix cseci. 
Hypogastric Region. 
Convolutions of the small 
intestine, the bladder in chil- 
dren, and in adults if dis- 
tended, and the uterus during 
pregnancy. 
Left Inguinal (Iliac). 
Sigmoid flexure of the colon. 
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 con- 
vex 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 peritoneal 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 scrof- 
ula or tuberculosis of the mesenteric glands, and in those 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 only dilated, but of greater length than is normal in 
these cases. If, on the other hand, the belly-wall is retracted, con- 322 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 emptied the gastro-intestinal tract of 
its usual contents. Tims 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 tubercu- 
losis of the lungs; and if the retraction is associated with muscular 
rigidity of the belly-wall and pain, we suspect the early stages of 
peritonitis or the presence of some acutely painful affection, such as 
renal or hepatic colic or lead colic. Marked concavity and retrac- 
tion of the belly-wall are also seen sometimes in cases of tubercular 
meningitis. 
The abdomen is distended very greatly by gas in many cases of 
peritonitis, typhoid fever, and in persons suffering from flatulent 
colic. If this be the cause of the distention, percussion of the 
anterior belly-wall when the patient is lying on the back will give 
a tympanitic note. 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 when the patient 
is lying down, while when tympanites is present it is more protrud- 
ing. Again, in ascites the greatest bulging is generally to be found 
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 
swelling be due to a moderate-sized ovarian cyst, this variation in 
form will not occur, as the cyst is not readily movable. If the 
ovarian tumor be large, the differential diagnosis may be most diffi- 
cult and almost impossible, except by the history or by examining 
the liquid withdrawn by tapping. 
In cases of ascites due to free liquid in the abdominal cavity per- 
cussion will elicit flatness over the flanks and resonance only where 
the intestines containing gas are floated up against the anterior 
belly-wall above the effusion. Palpation will also reveal fluctua- 
tion in ascites, but none in tympanitic distention. To develop this 
fluctuation the patient is placed on his back and the finger-tips of 
the left hand of the physician are placed against the skin of the 
flank. By means of the finger-tips of the right hand the opposite 
flank of the patient is struck a blow as in performing ordinary per- 
cussion, when the impulse if fluid is present will be transmitted to 
the fingers of the left hand. As the result of gradually increasing 
intra-abdominal pressure the floating ribs become pressed outward, THE ABDOMEN AND THE ABDOMINAL VISCERA. 
323 
the apex-beat of the heart is often displaced upward and outward, 
and the umbilicus becomes protruded instead of retracted. The 
skin of the belly-wall becomes thin and shining, and the recti mus- 
cles becoming separated enables the peristaltic movements of the 
bowels to be readily felt through the intervening skin. 
Fig. 142. 
Dotted line shows area of cancerous liver extending far heyond its normal area. Over the 
entire surface of this mass could be felt hard nodular masses. (From the author’s wards, 
Jefferson Medical College Hospital.) 
Having decided that the distention is due to an accumulation of 
free fluid in the abdomen, it remains for the physician to determine 
what the cause of the ascites may be. Its most frequent cause is 
cirrhosis of the liver, which results in engorgement of the abdom- 
inal vessels with secondary transudation of fluid (Fig. 151). If 
it be not due to cirrhosis, it may arise from an abdominal tumor, 
which by pressing on large vessels results in an effusion of liquid 
through their walls, or to tubercular peritonitis, to obstruction of 
the thoracic duct, valvular disease of the heart causing an obstruc- 
tion to the flow of blood in the vena cava, and, finally, to acute 324 
THE MANIFESTATION OF DISEASE IN ORGANS. 
diffuse or chronic parenchymatous nephritis. If the last two 
causes be present, there will usually be some oedema of the lower 
extremities or general anaemia with dyspnoea and albuminuria. 
For the typical symptoms and physical signs of these various 
affections the reader is referred to those parts of this book in which 
they are discussed (see Index); but there is an additional source 
of information as to the cause of the ascites to be utilized, namely, 
the character of the effusion. 
If the fluid withdrawn on aspiration has a specific gravity of 1.008 
and contains but a trace of albumin (about 0.97 per cent.), it is prob- 
ably due to hepatic cirrhosis, whereas if due to the pressure of a 
tumor the specific gravity is usually about 1.012 and the albumin 
nearly 2 per cent. Such a specific gravity and proportion of albu- 
min also result when the ascites is due to heart disease or pressure 
on the thoracic duct. When the effusion is the result of Bright’s dis- 
ease the specific gravity is apt to be only 1.006 and the proportion 
of albumin only a trace. In cases in which the ascites arises from 
some disease directly affecting the cells lining the peritoneal cavity, 
as carcinoma of the peritoneum or of the abdominal viscera, or tuber- 
cular peritonitis with or without pus, the specific gravity is much 
higher than just stated, namely, from 1.018 to 1.027 as a rule, and 
the proportion of albumin ranges from 3.80 in the case of growths 
to 5.76 in the case of tubercle, and 7.10 when there is pus. Further 
than this, it is asserted by Fold and Rosenbach that the effusions due 
to venous engorgement, heart disease, and renal lesions can be sep- 
arated from those due to disease in the peritoneum affecting this 
membrane directly by a test following the administration of iodide 
of potassium. When this drug is given to the first class of cases it 
speedily appears in the effused fluid; but should effusion be due to 
the organic diseases of the peritoneum which have been named, it 
will not appear. The fluid to be tested is placed in a test-tube 
and some nitric acid and chloroform added, when if iodine is 
present its characteristic color will appear. Should the cause of 
the ascites be a ruptured ovarian cyst the diagnosis of its cause 
except from the history of a previous localized swelling is exceed- 
ingly difficult. The fluid under these circumstances is usually of 
a specific gravity of 1.026, but its specific gravity may be much 
lower. It is asserted that the instances in which the specific 
gravity of the fluid is very low are due to a cyst of the broad 
ligament. THE ABDOMEN AND THE ABDOMINAL VISCERA. 
325 
Very often there is developed in cases of ascites, particularly 
when that condition arises from hepatic cirrhosis, a more or less 
well-defined bunch of veins on the anterior belly-wall, which is 
sometimes called the Caput Medusae, as the result of au attempt at 
collateral circulation to compensate for the obstructed How caused 
by the changes in the liver. Sometimes a mediastinal growth will 
cause a somewhat similar development. When the obstruction is 
lower down than the liver the veins of the lower part of the abdo- 
men (hypogastrium) will be found distended. 
Fig. 143. 
A case of chronic enlargement of the spleen following typhoid fever. The dark 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 the 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, 326 
THE manifestation of disease in organs. 
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 as in Fig. 142. 
In enlargement of the spleen similar signs, springing from the 
floating ribs well over to the left side, may be developed (see Figs. 
143 and 144), and large cystic kidney on either side may cause 
abdominal bulging, particularly if it be floating. (See Floating 
Kidney and Spleen.) 
Fig. 144 
A case of profound anaemia with great enlargement of the spleen, as shown in the large out- 
lined area. The smaller outlines indicate the areas of anaemic murmurs near the base of the 
heart and in the carotid artery. (From the author’s wards in the Jefferson Medical College 
Hospital.) 
Marked swelling of the epigastrium indicates distention of the 
stomach by gas or food, or that this organ is the seat of morbid 
growth. Sometimes a similar distention results from enlargement 
of the posterior mediastiual and retro-peritoneal glands. Again, 
distention of the epigastrium is apt to be caused by enlargement of 
the left lobe of the liver. In ovariau tumors the growth often 
gradually distends the entire belly equally; but, as already stated, THE ABDOMEN AND THE ABDOMINAL VISCERA. 
327 
the history is usually that of swelling, low down, and of its being 
chiefly unilateral at first. 
It should be remembered that the discovery of a pyriform swell- 
ing in the hypogastrium may possibly be due to a pregnant uterus, 
or to retention of urine, with consequent distention of the bladder. 
Cases of dilatation of the stomach often show very great bulging of 
the umbilical area of the abdominal wall when that viscus is dis- 
tended by liquid 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 Einhorn, 
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 ordi- 
nary 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 about one to two inches above the 
umbilicus. (See Percussion.) 
Fig. 145. 
Turck’s gyromele. 
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 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 sta- 328 
THE MANIFESTATION OF DISEASE IN ORGANS. 
tionary outer tube; a cable covered with tight-fitting rubber tube; 
and a spouge-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 introduced 
into the stomach. An apparatus for producing revolutions is 
attached to the outer end of the cable. The cable is passed onward 
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 curvature. 
When rapid revolutions are produced the sponge and cable can 
be felt in their respective situations. To determine the distensibility 
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 resistance at the lesser cur- 
vature, 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 A"om- 
iting, and that part of this chapter on the Diagnosis of Gastric 
Carcinoma 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 there- 
fore generally do not move. Inspection of the abdominal wall will 
also show possible 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 appen- 
dicular abscess. 
Palpation and Percussion. More 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 THE ABDOMEN AND THE ABDOMINAL VISCERA. 
329 
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; secondly, the consistency and form 
of the organs which he can touch; and, thirdly, whether any swell- 
ings which he feels are movable, bound down and immovable, pul- 
sating, 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 examination is made, as in this way volun- 
tary 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 ten- 
derness 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; obstinate 
constipation, moderate fever, and 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 pal- 330 
THE MANIFESTATION OF DISEASE IN ORGANS. 
pation 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 lias recently seen 
a case of rhythmical hysterical spasm of the recti muscles in a male, 
which at first gave the sensation of an enormous diffuse pulsating 
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 
movable with the tissues of the wall and readily grasped bv deep 
palpation; but if in the abdominal cavity, the abdominal wall may 
be made to move over it unless it be attached to the parietal perito- 
neum. Let us suppose it is in the wall of the abdomen, what can 
the swelling be? It may be a fatty tumor; in which case its sur- 
face 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 and fluctuation, and the history of a severe injury. 
Very much more commonly a swelling in the epigastrium, or 
upper umbilical 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, 
particularly in children, to enlarged lymphatic glands, as in tuber- 
cular 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 tubercu- 
lar 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 present. Aneurism of the abdominal aorta 
is also not to be forgotten. Sometimes, too, a distended or carcino- 
matous 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 history of constantly increasing pain and discomfort in 
the stomach; there will have been much sour belching, and perhaps THE ABDOMEN AND THE ABDOMINAL VISCERA. 
331 
vomiting of coffee-ground-looking material; marked loss of flesh 
and some cachexia will be present. According to Welch’s statistics, 
out of 1300 cases of gastric cancer, 791 were in the pylorus, 148 in 
the lesser curvature, 104 in the cardia, 68 in the posterior wall, 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 symp- 
toms 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 a 
most extraordinary quantity of food and liquid, which has gradually 
accumulated, will be expelled. The probable diagnosis of gastric 
cancer and of gastric dilatation can usually be confirmed by percus- 
sion, after distention of the stomach, and sometimes by the use of 
the gastro-diaphane. (See early part of this chapter.) 
Even 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 
percussion to outline the stomach with ease. It is best to mark the 
edge of gastric resonance by means of a blue pencil, and thus 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- 332 
THE MANIFESTATION OF DISEASE IN ORGANS 
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 is filled with food. 
Thus when empty the viscus hangs with the pylorus very low, but 
when it is filled the pylorus is raised. Fig. 146 shows the normal 
Fig. 146. 
Outline of normal position and size of stomach in an adult when distended with gas. 
(After Meinert.) 
gastric area when the stomach is distended with gas. The fol- 
lowing figures, taken from Osier’s Lectures on Abdominal Tumors, 
illustrate the extraordinary descent of the stomach made in some 
cases of gastric dilatation in the adult. (Figs. 147, 148, and 149.) 
Many of these cases of gastric dilatation are also associated with 
atrophy of the gastric tubules, or at least an 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 with 
an excess of lactic acid. Lactic acid is tested for as follows, the 
hydrochloric-acid test being given below: a few drops of neutral ferric THE ABDOMEN AND THE ABDOMINAL VISCERA. 
333 
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 through the 
Fig. 147. 
Profile view of the abdomen of a woman aged sixty-five years, showing the tumor 
formed hy the dilated stomach. (Oslek.) 
abdominal wall. In such instances the points which aid us in sep- 
arating 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 gas- 
tric obstruction; that there is an excess of hydrochloric acid in the 
gastric contents in cases of ulcer, and an absence of this acid in cases 
of cancer; and, finally, that there is no cachexia in cases of gastric 334 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Fig. 148. 
Showing the position and size of the stomach. (Osler.) 
Fig. 149. 
Tumor of the abdomen caused by a dilated stomach. (Osler.) THE ABDOMEN AND THE ABDOMINAL VISCERA. 
335 
ulcer, though there may be anaemia. 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 “ Ewald’s test-breakfast,” which consists 
of an ordinary dry roll and a little over half a pint of water which 
has been warmed, and he is directed, after swallowing these mate- 
rials, 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 minims of a solution of phloroglucin and vanillin 
are next placed in a porcelain dish and a few drops of the gastric 
liquid are allowed to trickle down to the edge of the solution. The 
dish is gently heated over a spirit-lamp or Bunsen burner, and if 
hydrochloric acid is present there will appear a red tinge. This 
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 ftj. 
This solution is pale yellow in hue. It must he 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 abdomen be tubercular glands, 
they will be found, in all probability, on deep and general palpa- 
tion, 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 an examination 
of other parts of the body may reveal the signs of a widely dis- 
tributed tuberculosis. 
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 336 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
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. Segr6 found that of 627 cases of carci- 
noma of the upper abdominal organs cancer of the pancreas occurred 
in 127, but only in 12 of these primarily. Stiller asserts that the 
following symptoms are fairly sure signs of pancreatic cancer, 
namely, marked dyspepsia, rapid emaciation and cachexia, subnor- 
mal temperature, persistent 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 formation 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 abdominal cavity, although, as a rule, they are 
quite small. As pointed out, however, by Jordan, the real cause of 
swelling in the pancreatic region may be hemorrhage into the lesser 
peritoneal cavity. He summarizes some of his views in regard to 
this matter as follows : 
“ Contusions 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- 
lating 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 of 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 THE ABDOMEN AND THE ABDOMINAL VISCERA. 
337 
pancreas, associated with intense pain, nausea, and vomiting, may 
be due either to acute hemorrhagic pancreatitis, to intestinal obstruc- 
tion, 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 positively. (See chapter on Vomit- 
ing for symptoms of intestinal obstruction.) 
Aortic pulsation 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 tumor, and on auscultation we 
hear a bruit. Pain due to pressure of the aneurismal sac upon 
some of the nerves of the abdominal cavity may also be a promi- 
nent symptom. 
Localized swellings due to other causes than those already dis- 
cussed are due to impaction of feces, volvulus, and intestinal obstruc- 
tion from other causes, as, for example, cancer of the bowel, which 
occurs most frequently in the caecum, 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 retroperitonal 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 tuberculosis. 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 338 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
We should not forget the possibility of a floating spleen, a rare 
condition, but one more common than is generally thought. The 
shape of the organ, if it can be palpated, will aid the diagnosis, and 
the presence of resonance on percussion over the area of normal 
splenic dulness will confirm the diagnosis that the spleen has be- 
come displaced. As the spleen in this condition may fall as low 
as the virgin uterus, it may simulate any growth from a uterine 
myoma to a tumor of the bowel or pancreas. By reason of twist- 
ing of its pedicle and secondary engorgement its size may be enor- 
mous; but if this continues, atrophy finally takes place. As such 
a dislocated spleen drags on the stomach and pancreas, it may cause 
a long train of curious symptoms, and even intestinal obstruction. 
Sutton asserts that by pressure it may cause displacements of the 
uterus. 
When the kidney is enlarged from cystic degeneration, from ordi- 
nary hydronephrosis, and from echinococcus cysts, it may be readily 
felt in the umbilical area in many instances. Hydronephrosis 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 epi- 
thelial cells. It should not be forgotten that the condition of 
hydronephrosis may be intermittent, for, if this is not remembered, 
the physician may be misled into thinking that the disappearance 
of the swelling is due to a floating kidney slipping back into its 
place. 
Bulging of the flank, with pain, fever, and perhaps fluctuation, 
indicates peri nephritic abscess or caries of the spine with cold abscess. 
Peristaltic movements of the intestines can sometimes 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 diag- 
nosis. It is due to persistent dilatation of a knuckle of intestine 
by gas, thereby forming a moderately hard and more or less con- 
stant mass, which may resemble a real tumor. Examination of the THE ABDOMEN AND THE ABDOMINAL VISCERA. 
339 
patient under ether will usually reveal its true character. Local- 
ized superficial and inconstant tumors may arise through spasmodic 
but localized contractions of the recti muscles. 
Finally, a swelling in the neighborhood of the umbilicus should 
always arouse the suspicion of an umbilical hernia, and the situa- 
tion 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 
abnormal 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 lobe in the epigastrium occasionally. Some- 
times, on deep inspiration, the diaphragm pushes the liver low 
enough to be felt. In children the liver is naturally large enough 
to be felt below the ribs. 
When the normal liver is percussed we find that it lies in the 
area shown in Fig. 150, and that as we percuss above it on the 
ribs in the mammary line we first get pulmonary resonance, then a 
little below 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. Below this area, which ceases just below the lowest 
rib, we usually find tympany on percussion, due to the gas-distended 
bowel. If we percuss in the midsternal line, we get the same signs; 
but they begin as high as the nipple, or above it, and then cease at 
a line drawn across the abdomen about midway between the ensi- 
form cartilage and umbilicus. To the left of the middle line of the 
sternum the liver-dulness merges into the cardiac dulness. (See 
Fig. 150.) 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 position of the diaphragm. 
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 340 
THE MANIFESTATION OF DISEASE IN ORGANS. 
enlargement are amyloid degeneration, congestion, hypertrophic 
cirrhosis and abscess, carcinoma, sarcoma, and lymphadenoma. 
When the surface is found to be smooth the condition is probably 
amyloid or fatty degeneration, or congestion. If the surface is 
rough, it will probably be due to cirrhosis, which gives a granular 
Fig. 150. 
Showing absolute and relative percussion-dulness of liver and heart. 1. Relative dulness ol 
liver. 2. Absolute dulness. 3. Relative dulness of heart. 4. Absolute dulness. 
sensation to the hand when the abdominal wall is moved over the 
organ. In malignant growth large and small nodules may often 
be found, and depressions or umbilications of its surface may be 
marked. (Fig. 142.) 
When, on palpating the liver, we find marked tenderness and 
some swelling, and, associated with these symptoms, fever, rigors, 
sweats, and sometimes 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 THE ABDOMEN AND THE ABDOMINAL VISCERA. 
341 
an abscess of the liver exists. This may be single or multiple. 
If the latter, it is probably due to pyaemia, and no spot of fluctua- 
tion 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 pysemic 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 distention 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 fluctuation, combined 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, carcinoma, and amyloid degeneration. In cirrhosis there 
will be some ascites in many cases, some swelling of the legs perhaps, 
aud dull pain in the hepatic region. The digestion will be disor- 
dered, there will be marked loss of flesh and often haematemesis. 
Sometimes coma comes on. In malignant disease of the liver there 
will be pain, marked emaciation, and cachexia; nodules will be felt in 
the liver-substance, and the organ be found much enlarged. Tender- 
ness on pressure will be marked. Sometimes ascites will be present 
and a growth may be found, usually as the primary lesion, in the 
stomach or bowel. In the case of amyloid liver there will be a 
history of prolonged suppuration elsewhere, and there will be present 
disordered digestion, irregular bowel-movements, and little pain. 
Marked tenderness of the hypochondrium is usually found in 
congestion 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 342 
THE MANIFESTATION OF DISEASE IN ORGANS. 
that in the hypertrophic state its size is increased so that it can be 
felt below the ribs, whereas in the atrophic state it cannot be felt 
except by pushing the fingers well up under the ribs. The symp- 
toms accompanying cirrhosis are chiefly connected with disorders 
of the alimentary canal, either through direct failure in the diges- 
tion and assimilation of food, or from changes in the blood-supply 
of the abdominal contents. The following excellent diagram from 
Taylor’s Index of Medicine shows what these symptoms are, and 
discovers their cause at a glance, the cirrhotic process, of course, 
obstructing the flow of blood in the liver. (Fig. 151.) 
Fig. 151. 
To illustrate symptoms of cirrhosis of liver. 
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 margin of the liver is not due to an effu- 
sion in the right pleural cavity which presses upon this organ. So, 
too, if the patient 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 it is 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 THE ABDOMEN AND THE ABDOMINAL VISCERA. 
343 
by percussion in persons not inordinately fat. Its normal position 
is best shown in the accompanying figure (152). 
The upper border of the spleen is on a level with the tenth dorsal 
vertebra and the lower border on a level with the end of the eleventh 
rib. Its upper edge or limit is on a level with the ninth rib. In 
percussing the spleen heavy percussion is to be avoided, since this 
may develop the resonance of the stom- 
ach or bowels. The spleen cannot be 
palpated unless greatly enlarged, but 
it may be found bulging from beneath 
the lowest rib in typhoid fever; in 
scarlet fever; as the result of acute or 
chronic malarial fever; in leucocythse- 
mia of the spleno-medullary variety; 
in amyloid 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 he- 
patic cirrhosis. Sometimes displace- 
ment of the spleen downward arises 
from emphysema of the lungs or left- 
sided pleural effusion. 
Acute splenic swelling sometimes 
comes on in cases of general septicae- 
mia. 
Nearly always the splenic surface is 
smooth, except for the notch in its sur- 
face (see Fig. 143), unless the disease be the rare condition of 
hydatid disease or carcinoma. (For Floating Spleen, see p. 338.) 
There yet remains for discussion the significance of increased 
resistance on palpation, and percussion-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 
Fig. 152. 
Normal position of the spleen. 344 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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, the Blood, the Bloodvessels 
and the Pulse, and upon the Thorax (that part on the Heart), to 
the chapters on Vomiting and on Headache, and to those on Coma 
and Unconsciousness, and Convulsions and Spasms. 
For further information in regard to the diagnosis of diseases of 
the abdominal viscera, the reader is referred to the chapter on the 
Skin (that part on Jaundice), the chapter on Vomiting (part on 
Intestinal Obstruction), that on the Bladder and Urine, and that 
on 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 tilings that the 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 de- 
bility 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 bloodvessels that the 
tissues of the body are nourished, and, as life depends upon this 
process of nutrition, the better the vessels the better the vitality. 
When examining the pulse of a patient who is well enough to be 
up and about the physician should wait until sufficient time has 
elapsed after exercise for the pulse to become steady, and the patient 
should be in a sitting or reclining posture in order to prevent over- 
action of the heart. Particularly is it important in the case of 
nervous 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 pulse 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. 346 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Ill 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 be very irregular and running, and so diffi- 
cult of counting, the count should be made by listening at the prae- 
cordium for the apex-beat. 
Before considering the qualities of the pulse in health or disease, 
it is well to understand wliat it is due to and the manner in which 
the circulation is carried on. The bloodvessels consist of the arte- 
ries, 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 there- 
fore 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 con- 
fined laterally is practically a solid, for fluids are incompressible, is 
the heart, and in the arterioles are muscular fibres, which by their 
contraction regulate the flow of blood into the capillaries, from 
which the nutritional processes are carried on. The blood in the 
arteries is, therefore, subject 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 contract 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 obstructed in its flow in front. If the tension is 
above or below normal, the interchange of food and oxygen and 
carbonic acid between the tissues and the blood in the capillaries is 
perverted, for the rate of flow in the capillaries depends largely 
upon the blood-pressure in the arteries. As the capacity of the THE BLOODVESSELS AND PULSE. 
347 
capillary system of vessels is many times greater than that of the 
arteries, so, if the arterioles relax, the capillaries and veins will 
retain all the blood, and in them it will stagnate and become useless. 
The manner in which arterial tension is chiefly maintained having 
been described, we can now consider the pulse-beat itself. The in- 
dividual 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 auother 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- 
acting heart is forcing 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 wav. 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 patient, 
either by drugs or by bleeding. Where we have atheroma or hard- 
ening of the bloodvessels as the result of old age, syphilis, or chronic 
vessel-changes the very inelasticity of the vessel, associated, per- 
haps, in some cases, with some irritability of the vasomotor centre, 
causes a high arterial tension, with a laboring heart, a congested 
head, and a feeling of fulness of the head, of which the patient will 
seriously complain. The second sound of the heart will also be 
much accentuated. 
The discovery of a high arterial tension in a young person, or in 
an older one who has not atheromatous vessels, will generally mean 
the presence of an excited circulation, in connection with some acute 
inflammatory disease in its early stages, and, if high fever is present 348 
THE MANIFESTATION OF DISEASE IN ORGANS. 
in a previously healthy person, the pulse will be found to be quick 
and hard. 
A condition of intense vascular relaxation, due to failure of the 
heart or the arterioles to maintain blood-pressure, is seen in cases 
of fainting and syncope on the one hand, or of collapse and shock 
on the other. Here we find a soft, easily extinguished blood-stream, 
which can, by pressure on the artery, be readily cut off from the 
distal vessels. The artery feels relaxed to the physician’s finger 
and the skin may be bedewed with sweat. 
We can conclude, therefore, that high arterial tension indicates 
in the young, as a rule, an excited circulation, due to some acute 
ailment in its early stages, or, if in an older person not suffering from 
an acute malady, it is due to atheroma of the bloodvessels, renal 
disease of a chronic interstitial type, or hypertrophy of the heart: 
provided, of course, in all cases that there is no history of the recent 
ingestion of powerful stimulants to the circulation. 
A very low arterial tension indicates a feeble condition of the 
system, such as is seen in all exhausting diseases, acute or chronic, 
or, if no disease be present, in the sense of an acute malady, it indi- 
cates general nervous debility, with or without the presence of a 
feeble and dilated heart. 
The pulse itself varies as to volume, character, rapidity, and 
force, and does so within normal limits, and still more so under the 
effects of disease. It varies greatly according to age. Thus, the 
pulse of the newborn child is usually about 135 to 140, at one year 
120 to 130, at two years 105, at four years 97, at ten years about 
90, at fifteen years 78, and from twenty to fifty years at 70 per 
minute. At eighty years of age it is usually about 80 beats per 
minute. The rate is also increased by taking food, by exercise, 
nervousness, and by pain and fever, as will be stated again in a 
moment. 
The volume of the pulse-wave depends chiefly upon the quantity 
of blood expelled from the heart at each systole, and also upon the 
condition of the aortic valves of the heart, in so far as their ability 
to prevent regurgitation is concerned. Stimulation of the vagus 
nerves usually results in a large pulse-wave, as already pointed out, 
as does also cardiac hypertrophy with dilatation. If, on the other 
hand, part of the blood thrown out of the heart into the aorta falls 
back into the ventricle, we have a pulse of small actual volume, 
and this is called, because of the peculiar sensation which it gives THE BLOODVESSELS AND PULSE. 
349 
to the finger, the 11 trip-hammer,” “ water-hammer,” or u Corri- 
gan’s pulse.” In such a case, because of the power of the ventricle, 
the blood is forced out into the aorta with great force, but as the 
last part of the wave regurgitates the pulse is found to be short 
and sharp. In mitral regurgitation or in mitral stenosis the pulse 
is usually small in volume, because the left ventricle has not, or 
cannot get, enough blood at each beat to send out a voluminous 
wave. 
So far as the character of the pulse is concerned, we recognize one 
which is slow and full, as that seen after digitalis is used; that 
which is short and sharp, as in aortic regurgitation; that which is 
small and hard, as is often seen in aortic obstruction; and the small, 
wiry pulse of acute peritonitis. 
Fig. 153. 
A sphygmograph. (Dudgeon’s.) Certain supporting parts are omitted so that the multiply- 
ing levers may be displayed, a is a small metal plate which is kept pressed on the artery by 
the spring b. The vertical movements of a cause to-and-fro movements of the lever c about 
the fixed point d. These are communicated to and magnified by the lever e, which moves 
round the fixed point f. The free end of this lever carries a light steel marker which rests 
on a strip of smoked paper, g. The paper is placed beneath two small wheels and rests on a 
roller which can be rotated by means of clock-work contained in tbe box h. The paper is 
th us caused to travel at a uniform rate. The screw graduated in ounces (Troy) is brought 
to bear on the spring b by means of a cam, and by this the pressure put on the artery can be 
regulated. The levers magnify the pulse-movements fifty times. 
Various names are applied to a pulse possessing certain peculiari- 
ties. Thus, we have under the name pulsus paradoxus a pulse which 
disappears with each deep inspiration. It is usually due to indura- 
tive mediastino-pericarditis, whereby inflammatory bands press on 
the bloodvessels or the heart. If the beats of the heart are irregular 350 
THE MANIFESTATION OF DISEASE IN ORGANS. 
in force, but regular in rhythm, we have developed what is called a 
pulsus alterans. 
A dicrotic pulse is one which is characterized by a reduplication, 
which feels like a second 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- 
graph. If by the latter means, the instrument of Dudgeon is the 
best. (Fig. 153.) 
The normal pulse-wave is shown in Fig. 154. 
Fig. 154. 
a b. Percussion up-stroke, ab c. Percussion-wave, c d e. Tidal wave. efg. Dicrotic 
wave, d ef. Aortic notch, f g. 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 distention of the 
artery produced by the ventricle forcing blood out into the 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. 155 is shown the typical pulse-wave of aortic regurgita- THE BLOODVESSELS AND PULSE. 
351 
tion; and in Fig. 156 that of mitral stenosis, which is irregular in 
time and volume. 
The rapidity and force of the pulse also depend largely on the con- 
dition of the blood vessel-walls, particularly the rapidity. The latter 
also is influenced by the activity of the pneumogastric nerves in regu- 
lating 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 pulsation 
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 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. 
Fig. 155. 
Tracing from a case of aortic regurgitation. (Mosser.) 
Fig. 156. 
Tracing from a case of mitral stenosis, showing increased tension and some irregularity. 
(Musser.) 
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 
heart-beat; but as the heart now beats very slowly the blood-pressure 
may fall for lack of blood in the vessels, unless there is an increased 
force of the heart at each contraction to make up for the number of 
beats in the minute which have been lost, or unless there is also a 
great increase in arterial tension by contraction of the vessels. A 
very slow pulse depends in the great majority of cases upon a high 
arterial tension from vascular spasm—i.e., resistance to the flow of 
blood; more rarely it is due to irritability of the vagus nerves, pro- 
duced by pressure or disease, or by drugs, such as digitalis. 352 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The term bradycardia is applied to a very slow pulse. The pulse 
may be as slow as twelve a minute. 
A rapid pulse is seen most commonly as the result of stimulation 
of the heart by drugs, by fever, or by fear. Fear causes the vagus 
to lose control of the heart, and fever acts by reason of the stimulant 
effect of heat upon this viscus. In other words, the quick pulse of 
fever is not a mere coincident symptom of fever, but the result of 
it. When the heart’s action becomes exceedingly rapid it is called 
tachycardia. It is due in the majority of instances to relaxation 
of the bloodvessels, or more rarely to depression of the pneumogas- 
tric nerves. Often in this condition the pulse becomes so fast that 
it cannot be counted. 
Great force of the pulse is due to hypertrophy, or over-action of 
the heart because of stimulation; and great feebleness generally is 
caused by marked dilatation not associated with hypertrophy, or in 
acute disease to exhaustion of the heart-muscle. CHAPTER XI. 
THE BLOOD. 
The various forms of red and white corpuscles—Their proportionate number in 
health and disease—Alterations in their form and character—The haemoglobin 
of the blood in health and disease—The various forms of anaemia—Leucocy- 
thaemia and pseudo-leucocythaemia—Parasites of the blood. 
As already pointed out iu the chapter devoted to the skin, 
marked changes in the blood speedily produce manifest alterations 
iu the appearance of the patient. The present chapter will be 
devoted to a consideration of the changes in the blood when we 
examine it by means of the naked eye or by means of various forms 
of delicate apparatus designed to give us accurate results. Before 
studying the conditions of the blood which are found in disease, it 
is well to briefly rehearse the characteristics of normal blood when 
it is examined outside the body. 
The blood consists of a liquid basis or plasma, in which are found 
two great varieties of cells—the red blood-cells and the white blood- 
cells. The red cells are called erythrocytes, the white cells leuco- 
cytes. The red cells are biconcave disks, dark at the edges and 
with a clear or bright spot in the centre, due to their biconcavity. 
They do not contain a nucleus. The red color of the blood is due 
to the aggregation of immense numbers of these bodies, the coloring- 
matter of which is called haemoglobin; but if a few corpuscles be 
placed in a bright light on the stage of the microscope, they look 
bright and yellow. The number of red blood-cells is about 5,000,000 
to the cubic millimetre of blood in a healthy adult male, and about 
4,500,000 in the healthy female. If this number is exceeded, which 
is very rare, the condition is called polycythemia; if decreased, the 
condition is called oligocythoemia. One of the most marked in- 
stances of polycythaemia which occurs is the very extraordinary 
increase of red blood-cells which is often met with in cases of congen- 
ital cardiac disease in children, amounting to as many as 8,000,000 
to the cubic millimetre. Beside the ordinary red blood-cells we 
find in health small red cells supposed to be immature red cells and 354 
THE MANIFESTATION OF DISEASE IN ORGANS. 
called microcytes, and sometimes, though rarely, megalocytes or very 
large red cells. Not only may the red blood-cells change in num- 
ber, but the quantity of their haemoglobin may also vary. Normal 
blood should contain 100 per cent. of haemoglobin, but often we find 
perfect health when the haemoglobin is only estimated at 85 per cent. 
If the proportion of haemoglobin is decreased, we call this condition 
one of oligochromaemia. 
In disease we find more or less marked alterations in the red cells 
themselves and in their coloring-matter. The microcytes and mega- 
locytes already named may become abnormally great in number. 
Red cells which are deformed are found in great number and are 
called poikilocytes. Other red cells which, unlike ordinary healthy 
cells, possess a nucleus and are capable of amoeboid movement, are 
found and are called by the unfortunate and confusing name of 
11 normoblasts/’ and finally we find other red cells pigmented or 
vacnolized; or, again, so dim in appearance as to be called u shadow 
corpuscles.” The disease in which these changes are found will 
be discussed further on. 
The proportion of the white to the red cells in health is about 
1 to 500, but very great variations occur. Thus, after meals the 
white corpuscles are always increased, so that the proportion may 
be 1 to 150 of the red cells. On the other hand, after this primary 
increase, they may be decreased, and the proportion may be 1 to 
800. Time of day is also a factor in producing a variation. Hirt 
found before breakfast the proportion to be 1 to 716; one hour 
after breakfast, 1 to 347; three hours after breakfast, 1 to 1514; 
ten minutes after dinner, 1 to 1592; half an hour after dinner, 1 
to 429; two and a half hours after, 1 to 1481; half an hour after, 
before supper, 1 to 544; and two hours after supper, 1 to 1227. 
In frequency, the proportion is about 1 in 280. 
The white cells appear in the blood of healthy individuals in five 
forms: 
1. They occur as white cells as small as, or smaller than, the ordi- 
nary red cells. This small white cell contains a nucleus so large 
that it almost completely fills its body and prevents us from seeing 
any surrounding protoplasm. It is called a lymphocyte. It forms 
about 20 per cent, of the total number of white cells in health. 
2. They occur as what are called large mononuclear leucocytes 
cells, much larger than the red cells, possessing a moderately large 
single nucleus, which is surrounded by a zone of pale, non-granular THE BLOOD. 
355 
protoplasm. Sometimes these cells show a change in the shape of 
the nucleus, and are then called transitional leucocytes. These 
mononuclear cells make about 10 per cent, of the white blood-cells. 
3. They occur as large, white cells with a nucleus of irregular 
shape (polymorphous nucleus), or a nucleus split up into several 
smaller nuclei (polynuclear). They are often called for this reason 
polymorphous or polynuclear leucocytes. Their protoplasm con- 
tains fine granules, which stain when brought in contact with neutral 
dyes, and for this reason these cells are often called neutrophiles. 
A neutrophile, a polymorphous leucocyte or polynuclear leucocyte, 
are therefore one and the same thing. They equal about 60 per 
cent, of the white blood-cells. 
4. We find very large polymorphous leucocytes containing very 
coarse granules, which stain when brought in contact with acid 
dyes, of which the chief is eosin. They are called oesinophilic, and 
are very limited in number or entirely absent in many cases. In 
disease we find variations from these types as to proportional and 
actual number, and in addition other white cells are present. 
In nearly all infectious diseases of moderate severity we find an 
increase in the number of white cells. This condition is called 
leucocytosis. The particular form of white cell which is increased 
in number in these states is the polymorphous or polynuclear cells. 
On the other hand, the eosinophiles are almost never found. Per- 
haps the acute infectious disease which illustrates leucocytosis most 
typically is croupous pneumonia. 
In leukaemia of the spleno-medullary type, which is by far the 
most common form, we find that an entirely different white blood-cell 
from those already described is present, namely, a large white cell, 
several times larger than the ordinary cells, with a single large 
nucleus, usually situated to one side, and the protoplasm of which 
contains granules which stain with neutral dyes. In so far as the 
granules are concerned, this cell resembles, then, the ordinary poly- 
morphous leucocyte, but it is separated from it by its large size and 
by the fact that the nucleus is single. Ilarely these granules take acid 
(eosinophiles) or basic stains (basophiles). The large mononuclear 
leucocytes are also slightly increased in leukaemia as to number, as 
may be the transitional forms. Eosinophiles, as described above, 
are often present in considerable number, and though at one time 
thought to be pathognomonic of leukaemia, are not so considered at 
this time. 356 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Iii leukaemia of the lymphatic type the lymphocytes are the cells 
greatly increased. 
In order that the various forms of white cells that we have named 
may be readily separated from one another we have to resort to cer- 
tain stains, it having been shown by Ehrlich and many others that 
the nuclei of these cells are susceptible to different stains, as are also 
the granules found in their protoplasm. These stains differ as to 
their color and reaction. We have basic stains, acid stains, and 
neutral stains. If the white cell is readily stained by an acid stain, 
it is called an eosinophile; if by a basic stain, a basophile; if by a 
neutral stain, a neutrophile. Further, these stains render the nucleus 
one color and the granules another, as in Plate X., in several of the 
figures of which will be found cells with red granules and blue nuclei. 
The best solution for staining-purposes is that of Ehrlich, which 
is called a triple stain. It is composed as follows: saturated watery 
solution of orange “ g,” 125 c.c.; saturated hydro-alcoholic (20 per 
cent, of alcohol) solution of acid fuschin, 125 c.c. 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 c.c.; absolute alcohol, 75 c.c. 
Within the last year Ehrlich has suggested the following in place 
of this formula, viz.: saturated watery solution of orange “ g,” 
135 parts; saturated watery solution of methyl-green, 110 parts; 
saturated watery solution of acid fuchsin, 100 parts. 
To these are added glycerin, 100 parts; absolute alcohol, 200 
parts; and water, 800 parts. 
This solution should stand for several weeks to allow of sedimen- 
tation; 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 with 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 hard- 
ened 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 chlo- THE BLOOD. 
357 
roform, as it will decolorize the specimen. The glass is then ready 
for microscopic examination with one-twelfth oil-immersion lens. 
The eosinophile granules in the corpuscles will be stained a reddish 
hue, the neutrophile granules purple, and the nuclei bluish-green or 
blue. (Plate X.) 
We examine the blood not only by the microscope, but by color- 
tests. The object of the microscopic examination is both to deter- 
mine the quality and character of the red and white corpuscles, their 
number and the presence of parasites. The color-tests are for the 
purpose of determining the proportions of haemoglobin, or, in other 
words, the ability of the corpuscles to carry oxygen to the tissues. 
To study the blood microscopically we need a quarter-inch objective 
for ordinary corpuscular work, or, as they say on the Continent of 
Europe, a Number 7 Hartnack or a D. Zeiss; and for examinations 
for parasites a 1-12 oil-immersion lens for use with a condenser. 
The eye-pieces used are usually Nos. 2 and 4. 
Fig. 157. 
Thoma-Zeiss blood-counting apparatus. A heavy glass slip (a), in the middle of which is a 
cell (B) exactly 1/10 millimetre in 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 mm. 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 (,S) 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.mm. The stem of the tube is graduated at 0.5 and at 1 c.mm. 
The finger-tip or the lobe of the ear of the patient having been 
washed clean, a sharp needle or the tip of a tenotome is used to 
puncture the skin, and the drop of blood which escapes is placed 
upon a glass slide and covered with a cover-glass, so that the film 
of blood is very thin indeed. Examined under the microscope this 358 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
will give a crude idea of the proportion of white to red corpuscles, 
and of their color and shape; but more accurate methods are advis- 
able, and for their use we resort to what is called a haematocytom- 
eter, of which the best is the Thoma-Zeiss apparatus, which consists 
in part of a glass capillary tube, about 10 cm. long, with an expan- 
sion near the middle, which expansion contains a small glass ball, 
which is movable. On the tube are three marks. Part way up it 
is marked 0.5, below the expansion 1, and above the expansion 101. 
Fig. 158. 
Appearance of blood in the Thoma-Zeiss cell, 
The second piece of apparatus is a small cell 1-10 millimetre in 
depth, and the floor of the cell is divided by finely drawn lines into 
squares. Each square equals 1-4000 cubic mm., and these squares 
are separated into groups of 16 by plainer lines. (Figs. 157 and 
158.) 
The finger having been freshly pricked, the blood is drawn up 
to the mark 0.5 in the capillary tube, and the tip of the tube is then 
wiped clean. A three per cent, solution of common salt is drawn 
up after it, until the tube and bulb are filled to the point marked 
101. The tip of the tube is now wiped dry by means of a clean 
cloth. By shaking the glass ball in the tube the blood and salt 
solution become well mixed in the proportion of 1 to 200. After 
the salt solution in the lower part of the capillary tube has been 
forced out by gently blowing into the upper end of the pipette 
and the blood-mixture has reached its tip, a drop of this homogeneous 
fluid is forced out into the cell just described and a cover-glass 
gently placed over it, all air being excluded. The cell should now 
be allowed to stand for several minutes to allow the corpuscles to 
settle and become stationary. The corpuscles in each of the sixteen THE BLOOD. 
359 
squares in the cell are now counted, added together, and the 
average number in a cell obtained by dividing the number of 
corpuscles by the number of squares. This number in turn is mul- 
tiplied by 800,000, and this result is the number of corpuscles in a 
cubic millimetre of blood; or multiply the number of corpuscles 
counted in all the squares by 4000 (4000 being the cubic contents 
overlying a square), and the result by 200 or 100, according to the 
dilution; after this divide the product by the number of squares, 
and the result will equal the number of cells in a cubic millimetre 
of blood. 
If the blood is drawn up to the point marked 1 in the pipette 
before the saline solution is added, we multiply by 400,000 instead 
of 800,000, since the blood solution is twice as strong. In making 
the count it will be found that some of the corpuscles overlap the 
line of a given square, and may therefore be counted twice or left 
out altogether. For this reason it is customary to include these 
corpuscles which overlap the upper and left-hand borders. Fur- 
ther, it is best to put down the number of cells found in each square 
as they are counted, and not to attempt to carry the addition in the 
memory, since the loss of one corpuscle makes a great difference in 
the ultimate result, and for this reason the more squares included in 
the original count the more accurate the result. For careful study 
of the blood several counts of several different fillings of the glass 
cell should be made and the result obtained by taking the average 
of these. 
In making the count of the red blood-corpuscles care should 
also be taken to estimate the white corpuscles, since the proportion 
of white to red often gives us very valuable information in disease. 
This may be done by using as a diluent for the blood in the pipette 
what is called Toison’s solution, instead of the solution of salt already 
named. This has the advantage that it stains the white cells blue, 
and so renders them more readily counted. Toison’s solution is 
composed of: 
Methyl-violet 0.03 {% grain) 
Neutral glycerin 30.0 (1 ounce) 
Distilled water 80.0 (2K ounces) 
Mix thoroughly and add 
Chloride of sodium 1.0 (15 grains) 
Sulphate of sodium ........ 8.0 (2 drachms) 
Distilled water 80.0 (21/, ounces) 
This is then filtered; it requires about eleven minutes for the white corpuscles to he stainad 
by it. 360 
THE manifestation of disease in organs. 
When we desire to count the white corpuscles alone we employ a 
pipette, which makes the dilution of the blood in the proportion of 
1 to 10, and we use in place of salt solution as a diluent a 0.3 per 
cent, solution of glacial acetic acid in water. This acid solution 
dissolves the red corpuscles, but makes the white ones more readily 
seen. The method of calculating the number of white corpuscles 
in a cubic millimetre is the same as that given for the red corpuscles, 
except that as the dilution is 1 to 10, instead of 1 to 100, we multiply 
by 40,000 instead of 400,000. 
Fig. 159. 
Centrifuge. 
Another very useful and rapid method of obtaining an approxi- 
mate estimate of the number of the red and white blood-cells is by 
the use of the centrifuge, with the haematocrit attachment (Fig. 160), 
which takes the place of the test-tube holders shown in Fig. 159. THE BLOOD. 
361 
This instrument is an improvement upon the Blitz-Hedin hfema- 
tocrit, and is used for the volumetric estimation of the red and 
white blood-corpuscles without previous dilution of the blood. One 
turn of the handle of the centrifuge will rotate the upright shaft 65 
times, and 77 rotations of the handle will cause the haematocrit to 
make 5000 revolutions per minute. This enormous speed is attained 
with only moderate exertion on the part of the operator. The 
hfematocrit attachment consists of a metallic frame, carrying two 
graduated capillary glass tubes, 50 mm. long, J mm. bore, in which 
is placed the freshly drawn blood. These accurately graduated 
glass tubes, seated in rubber-cushioned cups at 1 and 2, are held in 
position securely by spring cups, AA, so that there is no possible 
danger of losing the tubes during rotation. By drawing back the 
milled heads BB the tubes are instantly released and as quickly 
clamped again into position. (Fig. 160.) This apparatus should 
Fig. 160. 
Haematocrit attachment for centrifuge. 
be made of aluminum, in order that it may be strong and light. 
The advantage gained by the use of this metal is that it is possible 
to greatly increase the length of the arms of the hsematocrit; thereby 
taking advantage of the well-known law of mechanics that u the 
centrifugal forces of two equal bodies, moving with equal velocity 
at different distances from centre, are inversely as their distance 
from the centre.’’ In order, therefore, to obtain any desired amount 
of centrifugal force it is not necessary to increase the speed of the 
machine, but simply to increase the distance from the centre, or, in 
the case of the centrifuge, the length of the hsematocrit. 
The finger of the patient is thoroughly cleansed with water, and 
then punctured by means of a spear-pointed needle. The first 
drop of blood is rejected, and a second drop is secured by very 
slight pressure. The blood is then drawn, by suction, by means 
of a constricted dropper (Fig. 161) with rubber-bulb connection, 
and by this means placed in the hsematocrit, which is rapidly 
revolved for at least one minute. 362 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The rapidity and simplicity of this process are apparent at once. 
The blood does not have time to coagulate, and by the centrifugal 
force the red corpuscles, having the greatest specific gravity, are 
thrown to the distal extremity of the tube, and will occupy about 
one-half of the tube, or to about the mark 50. 
Fig. 161. 
The white corpuscles, next in specific gravity, will occupy a posi- 
tion between the red corpuscles and the liquor sanguinis, which is 
found in the proximal end of the tube, quite clear and free from 
corpuscles. 
Fig. 162. 
Von Fleischl’s haemometer. 
When the column of red blood-corpuscles extends to mark 50 we 
have, as a rnle, about five million red corpuscles per cubic milli- 
metre; but if the precipitated corpuscles reach only mark 30, there THE BLOOD. 
363 
are only about three million per cubic millimetre, or sixty volume 
per cent. If they reach only mark 20, there are about two million 
per cubic millimetre, or forty volume per cent. 
Having discovered the number and the quality of the corpuscles, 
an equally important measure is to discover the quantity of haemo- 
globin which they contain. We do this best by the use of the 
haemoglobi nometer of v. Fleischl, although that of Gowers is some- 
times used. Fleischl’s apparatus consists of 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 frame 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 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. 162.) The rest of 
the apparatus consists in a little capillary tube attached to a tiny 
wire handle. This tube will hold just enough pure and healthy 
blood to color the water on one side of the cylinder to the hue shown 
in the colored glass when 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 capillary tube. 
The blood is now washed from the capillary tube into one of the 
sections of the hsemometer container, by directing through the tube 
a stream of distilled water from a fine-pointed pipette. Both com- 
partments are then filled to the brim with distilled water. The 
inside of the capillary tube should be perfectly dry before filling it 
with blood, and, when filled, no blood must be allowed to cling to 
the outside. Neglect of these precautions invites serious inaccura- 
cies in the results obtained. The apparatus is then exposed to gas- 
light or lamplight, because with daylight 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 con- 
taining 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 364 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 haemoglobin with this appa- 
ratus. ; * 
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 nega- 
tive meniscus; and, third, to be careful to cleanse the entire appa- 
ratus 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 
conditions which we find in it. We find, first, that anaemia, 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 haemoglobin 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 dis- 
eases. 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. 
A patient’s blood 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 angemia most marked during early 
convalescence, and the history of such an attack should always be 
sought for, and, if found, regarded as an important point for con- 
sideration 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 anaemia, 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, 
we must not forget that if food is taken and not absorbed properly 
the corpuscular richness of the blood is decreased, and therefore 
chronic indigestion, notably that condition called atrophy of the 
gastric tubules, may be the cause of the difficulty. Again, profound 
anaemia, as to the number of the red blood-corpuscles, may be THE BLOOD. 
365 
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 re- 
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 anaemia which is called 
pernicious, in that it progressively gets worse until death occurs in 
the majority of cases, although a few may recover. At present we 
do not understand the pathology of this disease. It is characterized 
by marked pallor without loss of flesh; or, to speak more correctly, 
the subcutaneous tissues are added to rather than robbed of fat. 
There is gradual increasing dyspnoea, failure of strength, cardiac pal- 
pitation, venous murmurs, some vertigo, and roaring in the ears. The 
blood shows a most extraordinary and continually diminishing num- 
ber of red blood-corpuscles, until the number 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 haemoglobin; second, many of 
them are larger than normal (megalocytes); third, the red corpuscles 
are deformed, some being ovoid, others irregular in shape from pro- 
jections and constrictions on their surfaces (poikilocytes); fourth, 
there are present microcytes or red blood-cells, which are smaller 
than normal; fifth, nucleated red blood-cells (normoblasts); and 
sixth, and quite constantly, there are other large cells like the mega- 
locytes, named megaloblasts, which have a plain staining nucleus. 
These last are often larger than the megalocytes, and are sometimes 
called the u corpuscles of Ehrlich/’1 since he regards them as path- 
ognomonic of pernicious anaemia. The white blood-corpuscles are 
normal in number, or slightly decreased, although the great diminu- 
tion in the red cells renders the proportion of white to red greater 
than normal. 
Anaemia 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 
diminution is so slight that it may be ignored; but the decrease in 
haemoglobin is extraordinary, sometimes falling as low as 20 per 
1 These are not to he confused with the myelocytes of Ehrlich, which are large white cells. 366 
THE manifestation of disease in organs. 
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. Normoblasts are quite constantly found in 
chloroses of a severe type, but the larger varieties of nucleated 
erythrocytes are not seen. 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 chapter 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. Auscultation of the neck on the right side over 
the jugular vein will reveal a peculiar murmur called a “ humming- 
top” murmur. Febrile movement 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 propor- 
tion of these cases have already been mentioned when speaking of 
the anaemias of convalescence and hemorrhage, but a far more im- 
portant 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 tuberculosis. 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 extra- 
ordinary, even if no hemorrhage occurs. Chronic lead-poisoning, 
arsenical poisoning, and uraemic 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, but by no 
means least, from malarial infection, either as manifested by acute 
attacks, frequently repeated, or by slow poisoning with the develop- 
ment of cachexia. (See further on in this chapter.) 
Leukaemia. Th6re 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 importance. 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 PLATE X, 
FIG, I. 
FIG. 2, 
Severe Anemia with Leucocytosis. 
Dry preparation. Fixed with picric acid. 
Stained with heematoxlin Bohmer, x 300. 
Red corpuscles few, almost colorless, varying in 
size, show poikilocytosis; two nucleated reds 
(normoblasts). The increase in the white cells 
seen to be in the polynuclear elements. (Rieder’s 
“ Atlas der Klinischen Mikrosknpie des Blutes.”) 
Splenic-Myelogenic Leukaemia. 
Eosiu-hsematoxylin, 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, 
FIG, 4, 
Splenic-Myelogenic Leukaemia. 
Same case. IJosin-haematoylin, x noo. One 
normoblast, one polynuclear leucocyte, one mye- 
locyte, two eosiuophiles. The neutrophilic gran- 
ules of the polynuclear leucocyte and of the mye- 
locyte do not show with this stain. The large 
mononuclear eosiuophile above is believed to be 
also a myelocyte (Markzelle), the smaller one 
below, an eosinophile such as can be found in 
normal blood. (Rieder.) 
Myelocyte, Normoblast, Megaloblast. 
Triple stain. G,myelocyte showing neutrophilic 
granules; H, normoblast, both from a case of 
splenic myelogenic leukaemia; I, large nucleated 
red corpuscle (megaloblast) from a case of pernic- 
ious anemia. (Osier.) THE BLOOD. 
367 
to red corpuscles is far too great, varying from the normal (1 to 450, 
approximately), should cause the physician, first, to exclude all pos- 
sibility of transient causes of variation by making an examination at 
various times of day, or by excluding the presence of acute infectious 
disease characterized by leucocytosis—that is, the presence of an 
unusually large number of white corpuscles of the polymorphonu- 
clear variety. This can be done, not only by excluding the pres- 
ence of infection, but also by the fact that in leucocytosis in 
infectious diseases the increase is solely in the polynuclear neutro- 
phile corpuscles. Again, 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, dyspnceic, and feeble, with a 
marked and constant increase in the proportion of his white cor- 
puscles, what does it mean ? It probably means that the patient 
is suffering from leukaemia (leucocythaemia) in one of its two forms, 
namely, spleno-medullary leukaemia or lymphatic leukaemia, of 
which the former is by far the most common. 
When the disease leukaemia is present in its spleno-medullary 
form the typical change in the blood is the increase in large mono- 
nuclear leucocytes and in the presence of the so-called myelocyte 
of Ehrlich, a large white corpuscle with a pale-staining nucleus of 
even outline, and neutrophilic fine granules. The myelocyte is 
frequently of the same size as the large mononuclear leucocyte, and 
can be distinguished from this cell only by the fact that it contains 
neutrophilic granules, while the protoplasm of the mononuclear 
leucocyte is clear. The ordinary large mononuclear cells are not 
greatly increased, and the polymorphous or polynuclear cells are 
rather decreased. Eosinophile cells may or may not be present. 
The myelocyte of Ehrlich is a giant-cell, without amoeboid move- 
ment. When stained with Ehrlich’s tri-acid stain the granules of 
the eosinophilic leucocyte appear as coarse reddish-bronze granules 
scattered through the protoplasm of the cell, and often superim- 
posed upon the nucleus. 
The other changes found in leukaemia are that the red blood-cells 
are greatly decreased in number, and a large number of nucleated 
red cells may be seen. The haemoglobin is decreased. The pro- 368 
THE MANIFEST a tion OF DISEASE IN ORGANS. 
portion of one to three red cells is often met with. The additional 
symptom of this form of leukemia is 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 diarrhoea are often present. Often retinitis develops, and slight 
fever may occur. 
In advanced anaemia 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, deeper staining 
cells, with a rim of non-granular protoplasm), which are greatly 
increased in number, we suspect lymphatic leukaemia. Myelocytes, 
so typical of the spleno-medullary form, do not appear in this con- 
dition, and splenic enlargement is absent, but in its place there is 
often enlargement of the superficial lymph-glands, but these never 
grow so large as in Hodgkin’s disease, or pseudo-leukaemia. 
Pseudo-leukaemia, or Hodgkin’s disease, is supposed to be differ- 
entiated from true leukaemia by the blood examination, it being 
stated that in this malady there is usually only a slight decrease in 
the red cells and no other marked changes. Recently, however, 
Martin and Matthewson have emphasized the fact that in some 
cases of pseudo-leukaemia the lymphocytes have increased as greatly 
as in many instances of true leukaemia. As a general rule, how- 
ever, the blood condition separates the affections. (See chapter on 
Fevers.) 
Parasites of the Blood. We still have for consideration the 
parasitic diseases of the blood. These consist in the malarial germs 
of Laveran, or, as it is more properly called, the “ haematozoon 
malariae ” of Marchiafava and Celli, and the filaria sanguinis 
hominis. 
Malarial Organisms. No more important addition to the 
study of disease, from a diagnostic standpoint, has been made than 
the discovery of the presence of a parasite in the blood of persons 
suffering from malarial fever, which is always present under these 
circumstances, and in all probability acts as the cause of all mala- 
rial manifestations. These parasites are varieties of sporozoa, which 
live inside the red blood-corpuscles of the individual attacked.1 
1 111 this country the chief investigators into the life-history of the malarial parasite have 
been Osier, Councilman, and, more recently, Thayer and Hewetson, from whose exhaustive 
and able monograph on “The Malarial Fevers of Baltimore ” much of the information in the 
text of this book is derived. PLATE XI. 
The Parasite of Tertian Fever. 
The Parasite of Quartan Fever. THE BLOOD. 
369 
The parasite of malarial fever occurs in three forms, namely, as 
that of tertian fever, that of quartan fever, and as the parasite of 
the so-called sestivo-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., Pigs. 2, 3, and 4.)1 
When quiet they are round like the corpuscle in which they lie; 
but if the specimen examined be fresh, they may be seen to possess 
active amoeboid movements, thereby changing their shape. 
Soon this amoeboid body grows in size and begins to develop red- 
dish-brown pigment-granules (Plate XI., Figs. 5, 6, and 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 
contains 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 XI., 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 pre- 
viously healthy blood-cells. Sometimes the parasite becomes so large 
that it entirely destroys the corpuscle and floats free in the blood, 
in which case the pigment-granules quiet down and the mass be- 
comes misshapen and apparently dead, breaking up into smaller 
masses, and gives rise to several small 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 
1 No. I. is a normal red corpuscle. Plates XI. and XII. are taken from Thayer and Hewet- 
son’s monograph. 370 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 a small hyaline amoeboid body 
filling a fraction of the corpuscle. They soon, however, develop 
the following differences : first, they develop a sharper outline; 
second, 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 cor- 
puscle acting as 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). Peaching their complete development in about sixty-four 
to seventy-two hours, they appear as small, round bodies, faking up 
nearly all the space in the corpuscles in which they live, or they 
appear free in the blood-serum (Plate XI., Fig. 35). As the time 
for the paroxysm approaches the pigment-granules which have 
been scattered begin to collect at the centre (Plate XI., Figs. 36 
to 39) in a stellate form, and the protoplasm 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 be- 
come more and more separated from one another, and simultane- 
ously we find new corpuscles infected by the original small round 
bodies which we first saw. 
Sometimes these parasites expand and become very transparent, 
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 parasite may undergo a breaking up into smaller 
bodies, which are badly formed and indistinct; also a degenerative 
form, and vacuoles may develop. (Plate XI., Fig. 42.) Finally, 
flagella may develop, as in the tertian organism (Plate XI., Fig. PLATE XII. 
The Parasite of Aestivo- Autumnal Fever THE BLOOD. 
371 
41), and they differ from the tertian form in being smaller, and 
their granules are coarser. 
In the third form of iufection (sestivo-autumnal fever) we find at 
first the small hyaline bodies, but they have a ringed appearance, 
and are sometimes very small. (Plate XII., Figs. 3 to 6.) Sud- 
denly this body becomes larger and the ring is lost, the edge becom- 
ing wavy, and amoeboid movements occur, the pseudopodia often 
joining to form a true ring. Pigment-granules finally develop after 
a variable length of time, but they are few, rarely more than two in 
a parasite, near the edge (Plate XII., Figs. 7 to 12), and quite still. 
The corpuscles are not decolorized, but often are shrivelled and very 
brassy-looking. 
The peripheral circulation during the paroxysm of sestivo-autumnal 
fever contains 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 
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 amoeboid. 
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 tertian. 
Segments equal 6 to 12. 
Beautiful rosettes. 
Corpuscle becomes brassy- 
looking and shrunken. 
jEslivo-autumnal. 
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 cor- 
puscle. 
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, hut not decolor- 
ized, 372 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
carefully 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 microscope should be fitted with a 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 methylene-blue and eosine, which is prepared as fol- 
lows : a concentrated watery solution of methylene-blue is diluted 
one-half with water and mixed with an equal volume of a \ per 
cent, solution of eosine in 60 per cent, alcohol 
In order to prepare blood-specimens for staining, two cover-glasses 
are required. After a small drop of blood has been allowed to 
fall on the centre of one cover-glass the second cover-glass is 
placed upon it, and as soon as the blood has spread out between 
the two in a thin film the glasses are drawn apart, the surface of 
each bearing a thin, even layer of corpuscles. The cover-glasses 
are now rapidly dried in the air, and immersed in a mixture of 
equal parts of absolute alcohol and ether for half an hour, to “fix” 
the preparations. The specimens are then dried and stained. 
We can use another method, in which we stain by placing the 
dried cover-glass in Chenzynski’s solution and gently heating it 
for fifteen minutes. This solution is made as follows : methylene- 
blue in saturated watery solution, 40 c.c ; eosine in J per cent, solu- 
tion in 70 per cent, alcohol, 70 c.c.; distilled water, 40 c.c. The 
luematozoa are stained blue, the red cells take the color of eosine, 
the nuclei of the leucocytes are stained blue, and the eosinophile 
granules of the cells bright 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, which in tertian fever is THE BLOOD. 
373 
every forty-eight hours, and in quartan fever every seventy-two 
hours. If there be two sets of parasites in the blood, however, of 
the tertian type, the attacks may be daily, or quotidian, 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 quartan infection, the attacks come on two suc- 
cessive 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 chapter on Fever.) 
The parasite of sestivo-autumual fever is irregnlar in its develop- 
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 others. 
Widal’s test for typhoid or enteric fever depends upon the fact 
that the blood-serum of a patient suffering from typhoid fever exer- 
cises an antagonistic effect upon the typhoid bacillus. The method 
of Widal, as modified by Johnston, of Montreal, is as follows : the 
lobe of the patient’s ear having been pricked, the drop of blood is 
placed on a clean glass slide and allowed to dry. A loop of bouillon 
culture of the typhoid bacillus is now placed on an absolutely clean 
cover-glass, and to this is added a large loopful of a watery solution 
of the dried blood. From the mixture of blood and typhoid 
bouillon a “ hanging-drop ” preparation is made, and examined 
with a or dry objective, when it will be noticed, if the patient 
is suffering from typhoid fever, that the typhoid bacilli rapidly form 
clumps. If the patient has not typhoid fever, this clumping and 
entanglement of the bacilli with arrest of their movements do not 
take place, unless he has had the disease within several months, 
when the reaction may occur without signifying the onset of a new 
attack. 
Filaria. The filaria sanguinis hominis appears in the blood in 
its embryonal form, and is found fully developed only in the lym- 
phatics. It occurs in three forms, and has been well described by F. 
P. Henry, of Philadelphia, in a recent paper. These forms are: 
1. Filaria diurna ; 2. Filaria nocturna ; 3. Filaria perstans. These 
names are indicative of the habits of the animal, the filaria diurna 
being found in the superficial vessels solely or chiefly during the 
day; the filaria nocturna solely or chiefly during the night; while 
the filaria perstans is constantly present in the capillaries of the 
integument. The filaria diurna and the filaria perstans are con- 
fined, thus far, to the west coast of Africa and adjoining districts; 374 
THE MANIFESTATION OF DISEASE IN ORGANS. 
while the filaria nocturna is pandemic in the tropics and endemic in 
certain sections of the United States. The adults of filaria nocturna 
Fig. 163. 
Filaria alive in the blood. Instantaneous photomicrograph. Four hundred diameters 
magnification. Four millimetres Zeiss apochromatic. (Henry’s case.) 
have been frequently found; that of filaria per.dans never, so far as 
Henry has been able to ascertain. In the opinion of Manson, the 
Fig. 164 
Filaria in the blood. Eight hundred diameters. (Henry’s case.) 
filaria loa of the eye of the negro of Old Calabar is probably the 
adult form of the filaria diurna. If it is not, he argues, then there 
must be another bloodworm yet to be discovered, for the embryos THE BLOOD. 
375 
of the loa must escape from the body of their host through the 
medium of the circulation. Thq filaria perstans has been practi- 
cally proved by Manson to be the cause of the fatal u sleeping-sick- 
ness ” of the Congo region. 
The second is the one ordinarily seen in blood obtained from the 
peripheral circulation during sleep or at night. (Figs. 163 and 164.) 
The male filaria measures 83 millimetres long by 0.407 millimetre 
broad, and the tail is twisted into a spiral form. The female meas- 
ures 155 millimetres long by 0.715 millimetre wide, and the vulva 
is 2.56 micromillimetres from the anterior extremity. The embryo 
measures 270 to 340 micromillimetres long by 7 to 11 micromilli- 
metres wide, and has a pointed tail. This embryo is in an almost 
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 movements and 
typical appearance render it readily seen in the blood. The dis- 
covery of this parasite in the blood renders a diagnosis certain, and 
it should always be sought for if chyluria or elephantiasis is present. 
If the patient remains awake at nights and sleeps during the day- 
time, 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. 
Sugar in the Blood. The blood in persons suffering from 
diabetes contains sugar in excess, and R. T. Williamson has sug- 
gested its discovery by the following process. The normal blood 
will not give this reaction. A small, narrow test-tube is well 
cleaned, and at the bottom of the tube are placed 40 c.mm. of 
water. To measure this the capillary tube of a Gower’s Inemo- 
globinometer is used, which is graduated for 20 c.mm. The tip of 
one of the patient’s fingers is cleaned and dried, then pricked, and 
when a large drop of blood has escaped it is sucked up into the 
small capillary heemoglobinometer tube. Twenty c.mm. of blood 
are taken up from the finger. The blood is then blown gently into 
the water at the bottom of the small test-tube. If it should adhere 
to the side of the tube, it must be carefully shaken to the bottom. 
Then 1 c.cm. of a 1 in 6000 watery solution of methyl-blue is 
added. Finally, to the mixture 40 c.mm. of liquor potassa are 
added. The contents of the tube are then well mixed by shaking. 376 
THE MANIFESTATION OF DISEASE IN ORGANS. 
As a control-experiment a second test-tube of similar size is taken, 
and into this is placed the same quantity of non-diabetic blood, with 
the same proportion of water, methyl-blue, and liquor potassa. 
The fluid in each tube has a fairly deep-blue color. Both tubes 
are then placed in a beaker or capsule containing water. This is 
heated over a spirit lamp until the water boils; it is allowed to con- 
tinue boiling for about four minutes. By the end of this time the 
fluid in the tube containing the diabetic blood has changed its color 
from fairly deep blue to a dirty pale yellow (almost the color of 
normal urine). While the fluid in the tube containing the non- 
diabetic blood remains blue, occasionally it becomes bluish-green, 
sometimes pale violet, but it is never decolorized—that is, it never 
loses its blue color. The tubes should be kept quite still while in 
the water-bath, as by shaking the decolorized methyl-blue is oxidized 
by the oxygen of the atmosphere, and a blue tint may then return 
to the fluid. This is the reason why it is necessary to use a water- 
bath, since if the test-tubes be heated directly over the spirit lamp 
it is difficult to avoid shaking the fluid. 
If the assertions of Freund are correct, the testing for sugar in 
the blood is of value as a means of separating carcinoma and sar- 
coma in diagnosis. Thus he asserts that in carcinoma there is an 
increase in the sugar in the blood, whereas in sarcoma no such 
increase takes place. 
For this purpose the test just named is scarcely delicate enough, 
and it is wise to remove the proteids by boiling with sodium sul- 
phate, and then after filtering to apply the ordinary urinary tests 
for sugar. 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 evidence 
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 unsus- 
pected. 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, we 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 378 
THE MANIFESTATION OF DISEASE IN ORGANS. 
be noted unless it be loss of weight. The subjective symptoms of 
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. 165. 
1st to 7th cervical segments. 
1st to 12th dorsal segments. 
• 1st to 5th lumbar segments. 
► 1st to 5th sacral segments. 
Showing the surface-areas of the back 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 arc very chronic, when the face may 
appear worn and weary, and, if a purulent cystitis be present, septic 
fever may occur. The subjective symptoms are tenderness, tenes- 
mus, and pain (see chapter on Pain and chapter on Abdomen), and 
retention 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 func- 
tion of the cells in the spinal cord which govern the contraction of 
the muscles involved in expelling urine from the bladder. These THE URINARY BLADDER AND THE URINE. 
379 
centres are situated at or about the level at which are given off the 
second, third, and fourth sacral nerves. (Fig. 165.) 
Paralysis of the bladder with retention may, therefore, follow 
severe injuries to the spinal cord produced by a fall, blows, or other 
traumatisms, or be due to a myelitis which destroys such centres. 
(See chapter on Legs and Feet, part on Paraplegia.) Again, re- 
tention 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 dis- 
ease the impulses from the bladder are not recognized, or are per- 
verted, so that the sphincter which closes the bladder does not relax 
to permit the escape of urine, or the cord or brain fails to recognize 
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 over- 
distention 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 expelling-muscles 
and retention-muscles are both paralyzed, so that the urine accumu- 
lates in the bladder and then dribbles through the unguarded neck 
of the bladder. Sometimes, too, this incontinence is caused by the 
urethra being so insensitive that it fails to recognize the presence 
of the 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 condition 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. 380 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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, it 
is a noteworthy fact that when recovery takes place vesical control 
may be regained before any marked improvement can be found else- 
where. Often the loss of control of 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 circumstances 
there is probably a myelitis involving the lower part of the dorsal 
cord and the upper and lower parts of the lumbar cord; in other 
words, all that portion in which the vesical centres are situated. If 
the dribbling of urine takes place without 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 urine, 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 bladder spasmod- 
ically at long intervals (overflow incontinence)—that is, sphincter- 
paralysis from distention may ensue. In such a condition 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 spiual 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 cord 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 separated from those of myelitis, spinal 
tumor, and the vesical troubles due to traumatisms of the cord. 
The disorder depends entirely upon interference with the reflexes 
of the viscus, 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 THE URINARY BLADDER AND THE URINE. 
381 
abdominal muscles 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 irritability develop. In other instances 
the desire to urinate comes upon the patient so suddenly and forci- 
bly that the urine is voided before he can, with his impaired gait, 
reach a place to pass it in a proper manner; on the other hand, 
it may be retained and can only be removed by a catheter. Still 
others find that urine escapes on laughing, coughing, or sueezing, 
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 
diagnosis quite markedly; thus the presence of bladder-symptoms 
would confirm a diagnosis of ataxia as against pseucio-tabes due to 
peripheral neuritis. Again, in myelitis the presence of vesical 
symptoms points to that disease, and excludes from the diagnosis 
such affections 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 disturbances 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- 
tious, even when in its acute form. In other cases this condition 
arises from concentration of urine, whcli 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 382 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 vagina, or from rectal 
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, stone 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 
persons 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 
responses 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 investigation 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 receiv- 
ing vessel. This is very important when the urine is voided invol- 
untarily. If the condition of the bladder is bad, this viscus should 
be washed out by 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 exercise. THE URINARY BLADDER AND THE URINE. 
383 
The significance of any great and constant increase in the amount 
of urine passed in a given case is multiple. Thus, we find it greatly 
increased in any disease of the diabetic centre, or of the liver, or 
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, 
particularly if associated icith chronic contracted kidney, causes an 
increase in the urine; and, therefore, if a patient has to urinate 
frequently 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 and kidney are stimulated to increased effort by the actiou of 
drugs, such as digitalis, caffein, or alcohol. We also find an in- 
crease in urinary secretion, without its possessing any grave signifi- 
cance, 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 do its proper amount of work, with resulting stasis of 
the blood in the kidneys, 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. Per- 
sistent vomiting also has a similar effect. Parenchymatous neph- 
ritis, 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 dia- 
betic 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 persist- 
ently 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 important 
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 car- 384 
THE MANIFEST A IT ON OF DISEASE IN ORGANS. 
bolic acid or salicylic acid, of senna or haematoxylon, and bile, uro- 
bilin, 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 
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 the dis- 
coloration may be due to blood, haemoglobin, 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 hcematurici, 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 hue, and on standing will cause a coffee-ground or reddish 
sediment of a somewhat flocculent appearance. 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 changes 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 passed urine in- 
dicates a not very recent hemorrhage, and yet one of such size that 
the urine could not by 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 haemoglobin which is 
free in the urine. Again, blood-casts or red blood-corpuscles cling- 
ing to casts indicate renal hemorrhage. When the blood comes 
from the kidney pelvis it may appear in the urine in long, worm- 
like clots (moulds of the ureter), and their extrusion from the ureter 
produces symptoms of colic. Under such circumstances there may THE URINARY BLADDER AND THE URINE. 
385 
be alternations of hsematuria 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, sufficiently large to endanger life, may come from cystic 
tumor of the kidney. 
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, hsematuria 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 
presence of the coloring-matter of the blood. This is called hsemo- 
globinuria. 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 urine 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 Teichmann will be found, showing that the coloring-matter is 
haemoglobin. 
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 pro- 
duced, 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 hsematuria 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 386 
THE MANIFESTATION OF DISEASE IN ORGANS. 
one of the severe infectious diseases, such as scarlet fever or mala- 
rial 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 on the back, producing rupture or other 
disorganization of the kidney. All these conditions produce what 
may be called acute hsematuria. If the cause be acute nephritis 
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 erup- 
tion 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 acute nephritis due to exposure 
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 associa- 
tion with the later attacks, which may have followed the first either 
rapidly or slowly. In these cases 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 pass 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 devel- 
oped may be very complicated, since it may be due to renal incon- 
tinence, functional or organic, or to a true luemoglobinuria, arising 
from dissolution of the red blood-cells in the bloodvessels or blood- 
making organs. 
Finally, there is a type of malarial hsematuria which is only pro- 
duced by the administration of quinine (Karamitsas et al.). 
All these forms of hsematuria can be diagnosed by the presence THE URINARY BLADDER AND THE URINE. 
387 
of the malarial germ in the blood (see Blood) and the characteristic 
malarial symptoms, except that which occurs in persons who have 
a dyscrasia from old malarial poisoning. 
If the haematuria be due to embolic infarction of the kidney, an 
examination of the heart will probably reveal signs of valvular dis- 
ease, from which source the embolism will have resulted, or, in 
other cases, the physical signs, combined with the history, will 
show malignant endocarditis with renal sepsis therefrom. Some- 
times thrombosis of a renal vein occurs in feeble, wasted infants, 
and so causes haematuria. If heart-disease is not present, the his- 
tory 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 causes 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 degen- 
eration. 
If the chronic haematuria arise from chronic hemorrhagic neph- 
ritis, the diagnosis is made by the pallor of the skin, anorexia, 
nausea, headache, oedema, decreased amount of urine, and albumin- 
uria. 
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 
history of attacks of renal colic or of violent pain in the kidney; 
and if ulceration of the renal pelvis has occurred, there will be dis- 
turbances of the 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. 
There are other varieties of haematuria which must not be for- 
gotten, although comparatively rare, namely, that due to the pres- 
ence in the blood of the filaria sanguinis hominis, which is a 
condition in which the presence of chyle in the urine so masks that 
of the blood that the urine has the appearance of pinkish cream or 
milk, but microscopical examination will show blood-corpuscles and 
fat-globules, as well as the embryos of the filaria. (See Chyluria 
in this chapter.) Another still more rare cause of haematuria is the 388 
THE MANIFESTATION OF DISEASE IN ORGANS. 
distoma haematobium of Egypt and Abyssinia. (Fig. 166.) These 
produce what has been called tropical haematuria. The third cause 
is even more rare in man, namely, the strongylus gigas, which also 
causes pyelitis and renal colic. A fourth form of haematuria is that 
seen in some cases of scurvy, particularly of the infantile type, and, 
lastly, haematuria may also appear as a symptom of purpura hemor- 
rhagica, hemophilia, and very rarely in leukaemia. 
Fig. 166. 
Distoma haematobium, male and female. The two small bodies are the eggs. 
Hcemoglobinuria arises from a number of causes, such as infectious 
disease, poisoning by mushrooms and certain coal-tar derivatives, 
chlorate of potassium, and glycerin. Malarial poisoning sometimes 
causes it instead of haem atari a. One form of malarial 1 Hemoglo- 
binuria is intermittent, the urine being at one hour limpid, the next 
hour bloody, and the third hour clear again. 
The possibility of confusing the lisemoglobinuria of idiosyncrasy 
about to be described, when in a severe form, with true and severe 
malarial poisoning, is very great. The entire history of paroxysmal 
hemoglobinuria 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 hemoglobinuria, a condition which 
seems to be produced by mere chilling of the surface of the body or 
by immersing the hands of a susceptible person in iced water. It 
may also be produced either by exposure to the cold and damp, 
which are generally present in malarial localities, or to the chill of 
the milder forms of malarial paroxysm. It may also be a symptom 
of Raynaud’s disease. 
If the urine be red from other causes than blood, this may be due 
to the ingestion of logwood. The history of the ingestion of this 
substance will clear up the diagnosis. If it be due to senna, it will THE UBINAR Y BLADDER AND THE URINE. 
389 
be carmine, due to the chrysophan in this drug; but this discoloration 
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 appearance after 
being at first yellow, then saffron, and then purple-red. One of the 
conditions of the urine, due to a poison, which can be readily con- 
fused with hsemoglobinuria or hsematuria, is that produced by car- 
bolic acid. This color is not due to blood, but to oxidized educts 
of the acid. The same educts produce a similar discoloration after 
naphthalin, creosote, and uva ursi have been taken in overdose. 
Red urine, due to none of the causes which have been enumer- 
ated, may be owing to an excess of urates (except urate of sodium, 
which is usually white). If the urine becomes brown on the addi- 
tion of nitric acid where the fluids join, it is due to urates; but if 
all the fluid is brown, the patient has probably been taking iodine 
or iodine compounds freely. 
Finally, the urine is often dark reddish-brown or porter-colored 
in jaundice, 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 an 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, a 
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 gives 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 
rhubarb has been taken, if it is alkaline. 
When through disease-processes indican is formed and excreted 
in the urine, it may be by oxidation transformed into a blue color 
(indigolin), or into a red hue (indirubin). If chromogen is present 
in large amount, shaking the urine with air will develop a violet- 390 
THE MANIFESTATION OF DISEASE IN ORGANS. 
blue color, or this change may take place in the bladder. If urine 
containing 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 perito- 
nitis, 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 by 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 carbolic acid or uva ursi has 
been exposed to the air. 
White or milky-looking urine is seen in that condition called 
chyluria, due to the presence of the filaria sanguinis hominis in the 
blood. This urine on standing forms a creamy layer on its sur- 
face, and, if it is shaken with ether, some of the fat can be removed, 
rendering 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 milkv-white appearance from an 
excess of phosphates, mixed with more or less 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 mark- 
edly acid for a long time after it is passed, and that it lias a high 
specific gravity, point still more to its being diabetic, and the diag- 
nosis is confirmed if the characteristic reaction with Haines’s, Whit- 
ney’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 sub- 
ject 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 micro- 
scopic objects of the greatest pathological significance. The most 
important of these objects are what are called “ casts ”—that is, THE URINAR Y BLADDER AND THE URINE. 
391 
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 mate- 
rial, but often covered by corpuscles, pus-corpuscles, or epithelial 
cells. In addition to these bodies we find a large number of 
organic bodies or derivatives of organic matter, and inorganic sub- 
stances derived from the tissues or from food. 
The reader who desires to examine urine successfully by the aid 
of the microscope must bear in mind that it can only be examined 
satisfactorily after it has stood still in a glass or other vessel for a 
long enough time to allow sedimentation to take place—that is, 
until the objects floating in the fluid have had time to settle. 
Fig. 167. 
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 appa- 
ratus a sediment can be obtained in a few minutes after urine is 
passed. (See Fig. 167 and chapter on Blood.) 
This sediment is to be drawn np into a pipette which has been 
introduced into the urine and a few drops placed upon a glass slide, 
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. 168, 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 392 
THE MANIFESTATION OF DISEASE IN ORGANS. 
epithelial 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, third, 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. 
Fig. 168. 
Casts containing epithelial cells. (Peyer.) 
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 words, of 
parenchymatous nephritis. 
Blood-casts consist of more or less well-preserved blood-corpuscles, 
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 indi- 
cate an acute inflammation of the kidney, acute congestion of this 
organ, or a renal infarction. They are of importance, too, in sepa- 
rating hsematuria arising from other sources than the kidney from 
hemorrhage of this organ, because they are not found unless the 
escape of blood has been into the uriniferous tubules. THE URINARY BLADDER AND THE URINE. 
393 
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 may 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 higher power is used, and they are not quickly 
changed by acids, as are casts composed of other materials. 
The significance of their discovery is that septic infection of the 
kidney is present, as the result, it may be, of septic embolus brought 
from a distant infected part. They are seen in suppurative renal 
inflammation and in cases of pyelonephritis in which the true renal 
tissues are being involved by an extension of the disease. 
Fig. 169. 
a a. Epithelial casts, b b. Opaque granular casts, from a case of acute Bright’s disease. 
(Ro BEETS.) 
Casts, composed of broken-down organic matter, are found as 
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. 169, or light and refractive, dark or 
opaque. Very often the edges of these casts are irregular and the 
ends frayed and uneven. The color of these bodies may be yellow, 
brown, or grayish. 
The significance of granular casts is not as positive as those named 394 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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-poison- 
ing, 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 long, worm-like, transparent 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 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 these 
casts are very large, they may show amyloid degeneration of the 
kidney. They have often been wrongly called 11 waxy ’ ’ casts. 
(Plate XIII., Fig. 1.) 
Fig. 170. 
Cylindroids from albuminous urine. a,'b, and c. Ribbon-like forms, d. Cast-like form, 
with cells upon surface, e. Filamentous forms in a clump. 
Casts are not to be confused with cylindroids or streamers. These 
cylindroids appear in several forms. Most commonly they look PLATE XIII. 
FIG. I. 
FIG. 2. 
Casts, Fatty, Waxy, Hyaline and Granular. 
Crystals of Uric Acid. 
FiG. 3 
FIG. 4. 
Ammonium Urate Crystals. 
Epithelial Cells. 
A, squamous epithelium; B, bladder epithel- 
ium; C, kidney epithelium; D, kidney epithelium THE URINARY BLADDER AND THE URINE. 
395 
like threads or filaments which are transparent and often somewhat 
striated or hyaline in appearance. They are often long enough to 
extend completely across the microscopic field, and if followed out 
to the end will be found to taper off or gradually become more and 
more transparent until they cannot be outlined. For this reason 
too much light should not be 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 
Fig. 171. 
Fig. 172. 
Non-albuminous urine. 
Cast-like forms, with deposit of urates. 
Non-albuminous urine. 
a and b. Cast-like forms, c. Filamentous. 
Fig. 173. 
Filamentous and ribbon-like cylindroids. 
ribbons, or, in other words, they are wider than the thread-like 
masses just described. In still other instances the resemblances to 
true tube-casts are so marked that a differentiation is scarcely pos- 
sible, except that they are sometimes found to have a filiform tail- 
like ending. (See Figs. 170,171, 172, and 173.) The significance 
of cylindroids is not definitely known, but they may be taken as 396 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 litluemia or uricsemia, and in that condition in which we find 
oxaluria. (For further information concerning cylindroids, see 
Stengel’s paper in The Medical News of July 15, 1893.) 
According to Bramwell, the following is the best method of 
staining and mounting tube-casts and other urinary deposits. He 
uses picrocarmine: 
“ 1. An ordinary conical urine glass is filled with ecpial parts of 
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-tube containing the urine and staining-fiuid 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 carefully brought to the 
centre of the field and examined 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 prepa- 
ration the deposit is drawn off as in No. 5, above, and transferred 
to a small tube of Farrant’s medium,1 in which it remains until 
the organic deposit has settled, when it is again drawn off and 
transferred to clear Farrant’s solution, whence it is mounted in the 
usual manner. All organic deposits are thus stained and mounted 
1 Farrant’s solution is made as follows: dissolve 1 grm. of arsenious acid in 200 c.c. of dis- 
tilled water. In this dissolve 130 grms. of gum acacia with frequent stirring, and add 100 c.c. 
of glycerin. Filter the solution through fine Swedish paper upon which has been deposited a 
thin layer of talc. THE URINARY BLADDER AND THE URINE. 
397 
in a perfectly clear medium. Their minute characters can be studied 
with the highest powers of 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 ammo- 
nium and potassium, uric acid, oxalate of lime, the phosphate, car- 
bonate and sulphate of lime, and the so-called triple phosphate 
(ammonio-magnesic phosphate). 
The discovery in a urinary sediment of line shapeless granules, 
which may be crystalline and shaped like a fan, which are generally 
brown or pinkish in hue, indicates acid sodium urate. Urine con- 
taining such deposits is found to become acid on standing, and will 
form a brick-dust deposit as soon as it is cooled. Acid potassium 
urate and acid calcium urate, which occur in an amorphous form, 
are mixed with it in smaller quantities. 
The urates themselves have no particular importance except that 
they are often present in excess in fever, wasting diseases, gastric 
disorders, and in attacks of gout. 
When in a highly acid urine the student finds rhombic or diamond- 
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 ante- 
dates the development of chronic contracted kidney. Uric acid 
also appears in excess in cases suffering from fever and acute in- 
flammations. 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 and refract light strongly, looking somewhat like the 
back of a square envelope at times, are those of oxalate of lime. (See 
Fig. 174.) The significance of oxaluria is quite important, for it 
is often a concomitant symptom of melancholia, depending upon 398 
THE MANIFESTATION OF DISEASE IN ORGANS. 
defective metabolism. The finding of oxaluria separates this class 
of cases from those of the true disease melancholia, and indicates 
the use of nitrohydrochloric acid. These crystals are, however, 
found in the urine of persons who have eaten pears, cabbage, or 
tomatoes, and in that of persons suffering from spermatorrhoea. 
If not due to the ingestion of the foods named, oxaluria indicates 
deficient oxidation of nitrogenous tissues. 
Fig. 174. 
Oxalate of lime crystals. 
Creatin in the urine occurs in very brilliant prisms of a rhomboid 
form, the end of which is often split into a frayed end. (See Fig. 
175, a.) It is not present in normal urine. 
Creatinin also exists in normal urine in small amounts in pris- 
matic, colorless, brilliant crystals of the shape shown in Fig. 175, b. 
When dark-brown spherical masses covered with thorn-like crys- 
tals or sharp spicules are formed in alkaline urine they are composed 
of ammonium urate (Plate XIII., Fig. 3), and they will be found 
associated 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 phosphate. (See Fig. 176.) In 
addition, such urine will contain amorphous calcic phosphate. 
The crystals of the triple phosphate are of some diagnostic im- 
portance, as they do not exist in the normal urine, but are formed 
when ammonia is set free by the decomposition of the urea. If 
such crystals are found in freshly passed urine, they indicate that THE URINARY BLADDER AND THE URINE. 
399 
ammoniacal fermentation is taking place in the bladder, a condi- 
tion often seen in chronic cystitis and in some cases of paraplegia 
arising from injury to the cord or myelitis. A deposit of the 
Fig. 175. 
Crystals of creatin and creatinin. (Charles.) 
a. Crystals of creatin. b. Crystals of creatinin. c. Crystals of chloride of zinc and creatinin. 
triple phosphate and amorphous calcium phosphate, making a 
sediment like that of purulent urine, is sometimes seen in persons 
Fig. 176. 
Triple phosphate crystals. 
suffering from over-work of the nervous system and in cases of 
general debility. 400 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
microscope. In addition, we find spermatozoa in certain cases. 
(See Fig. 179.) 
Thus, we may find the embryos of filaria, echinococcus hooklets 
(Fig. 177), and the eggs of distoma haematobium, which are very 
rarely seen. 
Fig. 177. 
Echinococcus, with two hooklets, and section ot cystic membrane, greatly magnified. 
(Peyer.) 
Tubercle bacilli are to be found by the same staining-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. 
Gonococci indicate the presence of a specific urethritis or vagi- 
nitis, and are found by staining and using a homogeneous immer- 
sion lens with a No. 2 eye-piece. The process of staining is by the THE URINARY BLADDER AND THE URINE. 
401 
use of eosin and methylene-blue. The material on the cover-glass 
is stained for a few seconds in an alcoholic solution of eosin, then 
the excess of stain is washed off, and the slide 
is placed for ten minutes in an aqueous solution 
of methylene-blue. Streptococci appear in chains 
and are stained by the same process. They 
show infection from pus and are found in cases 
of erysipelas. (See Fig. 178.) Staphylococci 
also indicate pus-formation in the urinary tract. 
The presence of spermatozoa is more rare 
than is generally thought. They may be in the 
urine either as the result of a true spermator- 
rhoea, which is rare, or from some of the semen remaining in the 
urethra after an ejaculation in coitus, or from an emission at night 
without intercourse. They appear as small, transparent bodies 
having a head and tail, and, if alive, possess very active move- 
ments. (Fig. 179.) 
Fig. 178. 
Streptococci. (Abbott.) 
Fia. 179 
Spermatozoa, with casts of seminal tubules and spermine crystals. 
Fermentation resulting from the presence of a number of special 
fungi takes place in both healthy and diseased urines after they are 
passed. In normal urine the acidity, which 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 amor- 402 
THE MANIFESTATION OF DISEASE IN ORGANS. 
phous urates. After the urine is exposed still longer it undergoes 
an alkaline fermentation, and there develop in the fluid the micro- 
coccus urese and bacterium ure®. As a result the urea takes up 
water and decomposes with the development of C02 and ammonia. 
No sooner is a positive alkaline reaction established than those in- 
gredients of the urine which are insoluble in an alkaline solution 
are precipitated, namely, amorphous 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 which are covered with spines. 
The crystals of ammonio-magnesic phosphate are shaped like a 
coffin-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 saccharomyces 
albicans, the micro-organism which produces fermentation in ordi- 
nary 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 by the busy practitioner, who can rest assured 
that if he finds no albumin by the heat and nitric-acid test, if prop- 
erly 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 
part 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 to albumin or to 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 be turbid before the test by reason of an excess of 
urates, the fluid can be rendered clear by gently heating all of it. THE URINARY BLADDER AND THE URINE. 
403 
Heller’s test of adding a few drops of urine to HNOs in a test- 
tube is too fallacious to be used, although commonly employed. 
The quantitative tests for albumin are many of them impractical 
for the busy doctor. The best method is by means of percentage- 
tubes placed in a centrifuge-machine. By this means all the albu- 
min is thrown down. The tubes are filled to the 10 c.c. mark with 
urine and 2| c.c. of potassium ferrocyanide solution (one part to 
ten) are added. Next we add 1J c.c. acetic acid and thoroughly 
mix all these liquids, and the tube being placed in the centrifuge 
the machine is worked till all the albumin has settled. Each y 
c.c. mark on the tube represents 1 per cent, by bulk of albumin; 
that is, if the albumin extends up to the 3J 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 necessa- 
rily, 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 inflammatory 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 albu- 
minuria in cases of anaemia and in convalescence from protracted ill- 
ness 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 albumin 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, 
which is not necessarily indicative of renal disease. 
Sugar in the Urine. The presence of sugar is determined 
by a large number of qualitative and quantitative 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; 
thoroughly dissolve the copper salt in the water; add pure gly- 
cerin, 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 added six to 404 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 permanent fluid. 
Whitney’s test is a solution of ammonio-cupric sulphate, of which 
one drachm is decolorized by 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 will 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 the urine should be added more slowly, 
three to five seconds of boiling intervening between each drop. If 
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 
be used for the quantitative estimation of sugar: 
If reduced by 
It contains to the ounce 
Percentage. 
1 drop .... 
3.33 
2 drop?.... 
. 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.1 Usually dia- 
betic urine contains not less than half of 1 per cent, and rarely 
more than 1 per cent. 
As Fehling’s test is so widely used it must be mentioned. 
Wickham Legge thus describes it: 
This solution may be prepared in the following way: 665| grains 
of crystallized potassio-tartrate of sodium are dissolved in five fluid- 
ounces of a solution of caustic potash, sp. gr. 1.120. Into this alka- 
line solution is poured a fluid prepared by dissolving 1331- grains 
of sulphate of copper in ten fluidrachms of water. The solution is 
exceedingly apt to decompose, and must always be kept in stop- 
pered bottles and in a cool place. It is usually, therefore, more 
convenient not to mix the alkali and copper until the solution is 
1 This test, under the name of Aquae Sapphirina, can be had of the Lewis Chemical Co., of 
New York. THE URINARY BLADDER AND THE URINE. 
405 
wanted for use. In this ease a fluidrachm of the sulphate of copper 
solution may be added to half a fluid-ounce of the alkaline solution 
prepared as above. 
About a couple of drachms of this test-solution are poured 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-tube the urine must be 
added to it drop by drop, and the effect watched. A few drops of 
a sample of urine which contains a large percentage of sugar will at 
once give a precipitate of yellow or red suboxide of copper; but if 
no precipitate occur, the urine should be added to the fluid drop by 
drop, any deposit being carefully looked for, until a quantity equal 
to that of the Fehling’s solution employed has been added. If no 
precipitate be found after setting the test-tube aside for an hour, the 
urine may be considered free from sugar. 
Cautions: 1. The test-solution should never be used without boil- 
ing beforehand for a few seconds, the tartrate being exceedingly apt 
to decompose, and the solution then reduces copper as effectually as 
would grape-sugar. 
2. The quantity of urine used in the test should never be greater 
than the quantity of test-solution employed. 
3. After adding urine in volume equal to the Fehling’s solution, 
the boiling of the mixture must not be continued, as other bodies 
present in the urine, besides sugar, will reduce copper at a high 
temperature. 
If the examination for sugar is to be made with the greatest care, 
the urine should always be filtered, at least three times, through 
animal charcoal. This removes all urates and uric acid, which 
often partly reduce the Fehling’s solution, but the sugar goes 
through the filter. 
Sir William Roberts directs that the Fehling’s solution be placed 
in a test-tube to the depth of about one-quarter inch and the filtered 
urine added to the depth of two inches, and the two fluids well 
mixed. The flame of the lamp is then applied to the upper part 
of the urine, as in testing for albumin, and this is briskly boiled 
for a few seconds. The test-tube is now held up to the light, and, 
if sugar is present, the upper part has a yellowish tinge, while the 
earthy phosphates are thrown down in golden-colored flocculi. 406 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The quantitative estimation of sugar is best made by the Whitney 
test, already deseribed, or by the fermentation-method of Roberts, 
which depends upon the principle that grape-sugar is decomposed 
into alcohol, carbon dioxide, etc., by the fermentation set up by 
yeast. As a result of this the urine loses its specific gravity, and 
each degree of specific gravity has been found to equal one grain 
of sugar in the fluidounce. In other words, if the specific gravity 
before the test was 1.035 and after the test 1.015, the amount of 
sugar present would be twenty grains per ounce. Four ounces of 
urine are placed in a twelve-ounce bottle and a lump of German 
yeast added. The bottle is then corked with a perforated cork to 
permit the gas to escape, and placed in a warm place for twenty- 
four hours. By its side is placed a tightly corked bottle of the 
same size, holding four ounces of urine and no yeast. The specific 
gravity of both specimens is taken simultaneously, and the difference 
in degrees represents the number of grains of sugar in each ounce. 
The loss in degrees of specific gravity multiplied by 0.23 will give 
the percentage of sugar. 
The significance of sugar in the urine is various. If it is persistent 
and accompanied by wasting, polydipsia, and polyphagia, it is a sign 
of diabetes mellitus, due to a lesion in the medulla, to morbid func- 
tional activity of the liver, or to changes in the pancreas. If dia- 
betes mellitus occurs in a young person, the prognosis as to life is 
nearly always fatal; if in middle age, it is hopeful; if in persons 
after fifty, it is quite favorable. 
Sugar is sometimes found in small amounts in the urine of very 
obese persons, and its presence under these circumstances does not 
necessarily indicate a grave prognosis ; but, on the other hand, there 
are cases of so-called diabetogenous obesity in which the prognosis 
is very grave. They are to be separated from the class first named 
by the fact that the systemic symptoms of wasting, depraved nutri- 
tion, itching, furunculosis, and profuse diuresis are present. Then, 
too, in the latter form, the disease is usually associated with obesity 
in early life, whereas in the milder form it occurs in the obesity of 
advanced life. Diabetes occurring in old age, or after sixty years 
of age, has not the grave prognosis attached to it that exists in con- 
nection with the disease in earlier life. The younger the patient 
the graver the malady. (See also end of this chapter.) 
The other indications of glycosuria are of little importance. Gly- 
cosuria occurs in the course of ordinary convalescence, many infec- THE URINARY BLADDER AND THE URINE. 
407 
tioas diseases, particularly in typhoid fever, measles, scarlet fever, 
diphtheria, influenza, and malarial disease, and after cerebral an- 
eurism and nervous injuries, and after the ingestion of some poisons, 
notably phloridzin, chloral, arsenic, alcohol, and curare. It also 
sometimes occurs as a result of the ingestion of large amounts of 
sugar and starchy foods in persons who are incompetent to digest 
and assimilate carbohydrate foods in excess. Unless the glycosuria 
is associated with the other symptoms of diabetes mellitus, it is not 
a positive sign of the disease, for glycosuria is a symptom of a num- 
ber of states other than diabetes mellitus, as just pointed out. 
Albumose in the Urine. Albumoses, or peptones, in the urine 
may be tested for and their presence recognized by saturating 
slightly acidified urine with ammonium sulphate, filtering out all 
precipitate, and adding to the filtrate very gently a little solution 
of picric acid, seven grains to the ounce of water. Any precipitate 
is peptone. 
A better method than this, however, is that described by Harris, 
in which one part of albumose in 5000 parts of urine can be recog- 
nized. Before the test is made every trace of coagulable albuminoid 
matter must be removed from the urine to be tested. This is done, 
to use Harris’s words, as follows: 
To 20 c.cm. of (acid) urine1 in a test-tube are added six or eight 
drops of a saturated solution of salicyl-sulphonic acid in distilled 
water, and 1 grm. of chloride of lead. Shake well and boil about 
thirty seconds. Cool by shaking in running water from the cold- 
water tap. 
Filter through ordinary clean, white filter-paper until the urine 
is clear. Now add a few drops of a clear, saturated solution of 
sodium sulphate in distilled water, in order to precipitate what lead 
is held in solution; raise to the boiling-point, and cool under the 
cold-water tap as before. 
Filter again until clear. We should now have a perfectly clear 
urine, absolutely free from every trace of coagulable albuminoids, 
including nucleo-albumin, in which we may search for albumose or 
peptone. This clear filtrate is divided into three equal portions and 
placed in test-tubes, one of which is kept for comparison, the other 
two for further analysis. 
1 The urine must be fresh. If it must stand several hours before it can be examined, it 
should be preserved from the growth of bacteria iu it by the addition of some antiseptic, pre- 
ferably a few drops of formalin, which will keep it several days, and does not interfere with 
subsequent tests. 408 
THE MANIFESTATION OF DISEASE IN ORGANS. 
To one of these are now added three or four drops of a satu- 
rated solution of salicyl-sulpho-tungstate of sodium in distilled 
water. 
If albumose or peptone be present, a cloudiness will appear, vary- 
ing in degree according to the amount of these proteids present. 
As the amount of albumose present is often very minute, it may 
be necessary to compare the tube with the control-tube in order to 
detect the cloudiness. The cloudiness disappears entirely on gently 
heating the test-tube, to reappear on cooling. 
In the third tube the test is varied by allowing about 5 c.cm. of 
a dilute solution of the salicyl-sulpho-tungstate of sodium (made by 
adding about ten drops of the strong solution to 5 c.cm. of distilled 
water) to flow gently down the side of the tube, so as to rest on the 
urine as a separate layer. 
This should be very carefully done so the line of contact will 
be sharp and clear-cut, not diffuse. A cloudy line appears at 
the point of contact of the two liquids if albumose or peptone be 
present. 
When the amount present is very small it may take two or three 
minutes for the line to develop, and shows best, the two liquids 
being clear, when held in front of a dark background. 
As before stated, this test is extremely delicate, 1 part in 5000 
being readily detected; it is simple, and can be easily applied in 
fifteen to twenty minutes. 
Owing to the delicacy of the reactions it is necessary that all test- 
tubes be absolutely clean and the test-solutions perfectly clear, other- 
wise a slight reaction may be easily overlooked. 
The sodium sulphate solution must be added in slight excess in 
order to insure the precipitation of all lead, as any lead left in solu- 
tion would be precipitated by the salicyl-sulpho-tungstate of sodium, 
and thus interfere with the test. This would be easily recognized, 
as the cloudiness in that case would not disappear on heating, but 
would become more marked. 
The boiling during the application of the test, while not abso- 
lutely necessary, very materially facilitates the reactions, and should 
1 Salicyl-sulpho-tungstate of sodium is prepared as foliows : 
To a boiling saturated solution of tungstate of sodium in distilled water salicyl-sulphonic 
acid is gradually added, under constant stirring, until the solution no longer turns red litmus 
blue; or, in other words, until the alkaline tungstate of sodium is completely neutralized. 
Upon cooling the salicyl-sulpho-tungstate of sodium crystallizes. A solution is now made of 
this in cold, distilled water and filtered. A perfectly clear, colorless fluid results. THE URINARY BLADDER AND THE URINE. 
409 
always be done. The cooling, after boiling and before filtering, 
must never be omitted. 
If these few simple points be carefully observed, no difficulties 
will be experienced in applying the test. 
The significance of albumosuria is various. It is present in 
croupous pneumonia, all suppurative processes, empyema, tubercu- 
losis, smallpox, mumps, erysipelas, cancer of the viscera, jaundice, 
and apoplexy, and in typhoid fever and phosphorus-poisoning. 
Jaksch asserts that it is present in epidemic cerebro-spinal 
meningitis and absent in tubercular meningitis, and that it is a posi- 
tive differential sign of the former disease if no ulceration of the 
lung is present. Harris, on the other hand, asserts that albumo- 
suria is simply a manifestation of the action of micro-organisms, and 
is thus only an indication of an infective process. 
It ought not to be forgotten that albumosuria occurs in the nor- 
mal puerperium. 
The Urea in the Urine. The amount of urea is to be esti- 
mated by the process of Lyons, as follows (Fig. 180) :l 
Fig. 180. 
U reometer. 
1. A bottle is provided with perforated rubber cork and delivery 
tube; in this the decomposition of the urea is effected. 
2. A small test-tube to contain the urine, graduated to hold 
4 c.c., the quantity employed in each experiment. 
3. A graduated jar for measuring the gas evolved. The jar is 
provided at the bottom with an “ overflow ” tube, and at the top 
with a vent-tube closed with a rubber cap, to secure accurate adjust- 
ment of the level of the fluid in the jar at the commencement of the 
experiment. 
1 This apparatus, with full directions for use, can he obtained from Parke, Davis & Company, 
Detroit, Mich., for one dollar. 410 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The process is as follows: put into the square bottle 20 c.c. of 
a special solution of chlorinated soda (for formula see below), and 
add 5 c.c. of a 20 per cent, solution of potassium bromide; fill 
the test-tube exactly to the mark (4 c.c.) with the urine to be exam- 
ined, and lower it into the bottle by means of a thread or by the 
aid of a pair of dressing-forceps, taking care that none of its con- 
tents is spilled in the operation. Fill the graduated jar with 
water, which must be of the same temperature as the air of the 
room, to a point a little above the 0° of the scale, supporting the 
extremity of the overflow-tube so that no water can escape. Re- 
move the rubber cap from the vent-tube and connect the apparatus, 
pressing in the rubber corks firmly so as to make the joints air- 
tight. Finally, put on the rubber cap, drawing it down so as to 
force a little water out of the overflow tube, and bring the level of 
the water remaining exactly to the 0° mark, the orifice of the over- 
flow-tube being on the same level. A little practice will make 
this easy. 
To make sure that the connections are all perfectly air-tight, 
lower the end of the overflow tube a few inches; a few drops of 
water will escape from diminished pressure; but if the joints are 
perfect there will be no further dropping. If there is any leakage, 
the defective joint must be found and the difficulty corrected before 
proceeding further with the experiment. Having made sure that 
the connections are perfect, catch the curved end of the overflow- 
tube over the edge of a measuring graduate, as shown in the illus- 
tration (an ordinary bottle or any other receiver may be used in 
place of the graduate). Now, by canting the bottle, cause the urine 
to flow out of the test-tube and mix with the test-solution. Effer- 
vescence is at once produced, and the gas evolved forces a corre- 
sponding volume of water out of the overflow-tube. Shake the 
bottle occasionally to promote the escape of the gas. When the 
action appears to be at an end pour into the measuring-graduate 
enough water to reach above the opening of the overflow-tube, in 
order that cooling of the gas evolved, which at first is quite warm, 
may not draw air into the apparatus. Let the apparatus stand 
fifteen or twenty minutes to cool, then shake the bottle containing 
the urine once more and proceed to read off the result. To do this, 
it is necessary to bring the opening at the end of the overflow-tube 
just to the same level as that of the fluid remaining in the graduated 
cylinder, since raising or lowering the tube slightly affects the THE UR IN A R Y BLADDER AND THE URINE. 
411 
volume of the gas to be measured. The percentage of urea is read 
off without need of any calculation from the scale of the instrument. 
The accompanying table will enable the physician to ascertain from 
the percentage-amount of urea in the specimen examined what is 
the absolute amount of that compound excreted during the day, 
provided, of course, the whole of the urine passed during the twenty- 
four hours has been collected together and carefully measured. 
Per cent of 
Quantity of 
Per cent, of 
Quantity of 
urea by 
urea in grains 
urea by 
urea in grains 
ureometer. 
in 1 fluidounce. 
ureometer. 
in 1 fluidounce. 
0.1 . 
. 0.456 
1.9 . 
. 8.658 
0.2 . 
. 0.911 
2.0 . 
. 9.114 
0.3 . 
. 1.367 
2.1 . 
. 9.570 
0.4 . 
. 1.823 
2.2 . 
. 10.025 
0.5 . 
. 2.279 
2.3 . 
. 10.481 
0.6 . 
. 2.734 
2.4 . 
. 10.937 
0.7 . 
. 3.190 
25 . 
. 11.393 
0.8 . 
. 3.646 
2.6 . 
. 11.848 
0.9 . 
. 4.101 
2.7 . 
. 12.304 
1.0 . 
. 4.557 
2.8 . 
. 12.760 
1.1 . 
. 5.013 
2.9 . 
. 13.215 
1.2 . 
. 5.468 
3.0 . 
. 13,671 
1.3 . 
. 5.924 
3.1 . 
• 14.127 
1.4 . 
. 6.380 
3.2 . 
. 14.582 
1.5 . 
. 6.836 
3.3 . 
. 15.038 
1.6 . 
. 7.291 
3.4 . 
. 15.494 
1.7 . 
. 7.747 
3.5 . 
. 15.950 
1.8 . 
. 8.203 
Example.—The patient has passed 24 fiuidounces of urine, found to contain 2.4 per cent, of 
urea. The total urea excreted will therefore be 10.937 (from the table) X 24 = 262.488 grains. 
For exact estimations the temperature of the room in which the 
experiment is made must be about 70° F. (21° C.). A variation 
from this temperature of 20° will, however, make a difference in 
the result of only about 0.2 per cent., so that the temperature- 
correction may be regarded as unimportant. 
In the process given for the manufacture of the test-solution the 
hypochlorite is changed into hypobromite. 
This mixture gives more uniform and trustworthy results than 
those obtained with the chlorinated soda alone, which is recom- 
mended by Dr. Squibb. It is in fact identical in its action with 
the hypobromite solution, without the great inconvenience of hand- 
ling bromine. A few minutes must be allowed to elapse after the 
mixture is made before mixing the urine with it; but this need occa- 
sion no delay, since the mixture can be put into the bottle before 
filling the cylinder and making the connections. 
The activity of the solution of chlorinated soda can be easily tested 
by adding to a little of it in a test-tube a few drops of the solution 412 
THE MANIFESTATION OF DISEASE IN ORGANS. 
of potassium bromide, and then a little muriate of ammonium, which 
should cause brisk effervescence. If this is not the case, it is too 
much deteriorated for use. 
In some rare instances it will happen that the urine contains a 
larger proportion of urea than the ureometer is capable of indi- 
cating. When this is the case, and in general when the specific 
gravity of the urine exceeds 1.030, sugar being absent, it will be 
best to dilute the urine with an equal volume of water before making 
the test. Four c.c. of the diluted urine will then be used as usual 
in the experiment, but the percentage given by the reading of the 
instrument must be multiplied by two. 
It will be found in practice that an estimation of urea by this 
apparatus consumes very little time, and the results for all prac- 
tical purposes are as accurate as could be wished for. 
Formula for Special Solution of Chlorinated Soda. Shake chlo- 
rinated lime (best quality) 12 grammes with water 100 c.c.; let 
settle and filter into a 250 c.c. bottle. Wash the residue with 
enough water to obtain 130 c.c. of clear filtrate. 
Dissolve sodium carbonate 24 grammes in water 45 c.c. Add 
this solution to the above filtrate, mix thoroughly, and, when reac- 
tion is complete, filter, passing, if necessary, enough water through 
residue on filter to obtain 165 c.c. of filtrate. 
The clinical value of estimating the urea is great in cases of renal 
disease, and it is also of value in diabetes mellitus and during preg- 
nancy or in the puerperium and before surgical operations. The 
quantity of urea excreted in twenty-four hours is increased in nearly 
all fevers and inflammations, and is decreased in any cachectic state 
in which the metabolic changes in the tissues are impaired. It is 
also decreased in diseases which greatly modify the activity of the 
liver, the gland which makes urea. The particular value of esti- 
mating the urea in Bright’s disease and in pregnancy lies in this, 
namely, that the renal disorder in these conditions results in an im- 
perfect elimination of urea, and as a result it, or closely allied pro- 
ducts, are retained in the blood. If, therefore, in a pregnant woman 
or a person suffering from Bright’s disease, analysis shows a con- 
stant diminution in the amount of excreted urea, the physician is 
warned that a uraemic convulsion or other manifestation of uraemic 
disorder is imminent, and can take active measures to relieve the 
patient, for, after the uraemia is developed, treatment is of compara- 
tively little value. THE URINARY BLADDER AND THE URINE. 
413 
Although the quantity of urea varies very greatly in perfect 
health, the mean amount excreted in twenty-four hours by a healthy 
man of twenty to forty years is about 512 grains. Women excrete 
a little less than men, and children still less in actual quantity, but 
more in proportion to their weight. 
It is absolutely necessary in estimating the amount of urea ex- 
creted in twenty-four hours to test a sample of the urine obtained 
from all the quantity passed in that time, as a test of the urine 
passed on one occasion is no guide for the total daily quantity. 
Chlorides in the Urine. The urine in health contains chlo- 
rides of sodium and potassium, and these are to be discovered by 
placing a fluidrachm of urine in a test-tube and then adding a drop 
of nitric acid, and finally a few drops of a solution of nitrate of 
silver. If chlorides are present in considerable quantity, a white 
precipitate of chloride of silver is thrown down, which can easily 
be distinguished from albumin; but if some doubt is felt as to its 
character, the addition of a little caustic ammonium will redissolve 
it if composed of chlorides, and it will be reprecipitated if 
nitric acid is again added. If the same quantities of urine and 
reagents are taken daily and placed in a test-tube of equal dimen- 
sions and the precipitate allowed to settle for twenty-four hours, 
we can gain an approximate estimate of the relative quantity of the 
chlorides. The amount ordinarily passed in twenty-four hours by 
a healthy man is 250 grains. 
The clinical significance of a decrease in the chlorides is not 
great. They are decreased in the acute stages of croupous pneu- 
monia, acute articular rheumatism, and some other fevers; and if 
they gradually increase, they indicate the development of convales- 
cence. 
The Total Quantity of Solids excreted by the kidneys in 
twenty-four hours'can be roughly estimated by what is known as 
Haines’s modification of Haeser’s method. If the solids are much 
decreased, more accurate methods of testing should be resorted to. 
The method just referred to is carried out as follows: the last two 
figures of the specific gravity of the urine are multiplied by the 
number of ounces voided in twenty-four hours, and the product is 
multiplied by one and one-tenth. Thus, if a patient passes 32 
ounces, and the specific gravity of the urine is 1.012, we multiply 
32 by 12, which equals 384, and this is multiplied by 1.1, which 
equals 422, which would be much less than the normal for a person 414 
THE MANIFESTATION OF DISEASE IN ORGANS. 
of, say, 150 pounds, who should pass about 1150 grains of solids in 
twenty-four hours. 
Ehrlich has claimed that a distinct aid to the diagnosis of enteric 
fever can be obtained by the so-called diazo-reaction of the urine, 
although it is to be remembered that this takes place in several 
other conditions of the body, notably pulmonary tuberculosis, 
measles, pyaemia, scarlet fever, and erysipelas. It is usually present 
only in severe cases of these ailments. Further than this, Ehrlich 
asserts that the reaction is usually to be obtained about the fourth 
to seventh day of the disease. A faint reaction is indicative of a 
mild attack. 
The test is as follows : 
1. Take 2 grammes (30 grains) of sulphanilic acid, 50 c.c. of 
hydrochloric acid, and• 1000 c.c. of distilled water. 2. Take a 
solution of sodium nitrite in water of the strength of 0.5 per cent. 
Fifty parts of No. 1 and one part of No. 2 solution are now placed 
in a test-tube and an equal amount of urine added, and this mixture 
is then rendered strongly alkaline by strong ammonia-water. If the 
diazo-reaction is present, the liquid becomes carmine-red in color; 
and if the test-tube is shaken, this color is seen in the foam. This 
coloration of the foam is the point in the reaction, for, if the 
liquid only is red, the test is not positive. After standing a day a 
green precipitate will form in the tube. 
The General Symptoms Associated with Urinary Disorders. 
Having considered the pathological changes found in the urine 
and their significance, we now pass on to a consideration of the gen- 
eral symptoms which will usually be found associated with these 
variations from the normal functional activity of the urinary organs. 
Let us suppose that a patient presents himself complaining that 
he has been seized with pain in the small of the back, and per- 
haps by nausea and chilly sensations, followed by a marked decrease 
in the quantity of urine secreted, which decrease may actually 
amount to suppression of the urine. The urine that is passed is 
high-colored or smoky in hue, sometimes looks like porter, and 
forms a very heavy sediment on standing. If it is filtered and 
tested for albumin, it will be found to contain this abnormal ingre- 
dient in large amount, and a microscopical examination of the sedi- 
ment will reveal a large number of blood-corpuscles, epithelial cells, THE URINARY BLADDER AND THE URINE. 
415 
and casts (hyaline) made up of blood-cells, epithelium, and albumin. 
Scarcely will these signs have been noted when the patient will be 
seen to be anaemic, and puffiness of the face about the eyes will be 
evident. This puffiness will then pass on to a general anasarca, 
but it is to be remembered that the most violent acute diffuse neph- 
ritis may exist without developing anasarca. If the disease be in 
a child and it is due to scarlet fever, anasarca is common, as is also 
uraemia. The pulse in patients with this form of nephritis is usu- 
ally hard and tense, and the sharp and clear sound of the heart, as 
heard at the second right costal cartilage, will indicate the high arte- 
rial tension. The skin is generally dry, and, it may be, harsh to 
the touch. Should the symptoms persist for over a month the 
possibility of the disease becoming chronic renders the prognosis 
doubtful; but, as a rule, particularly in young persons, the prognosis 
of acute diffuse nephritis is favorable. In the acute diffuse neph- 
ritis of pregnancy the prognosis is, of course, grave. The history 
of the case prior to the attack of this ailment will usually be that 
the patient has been exposed to cold or wet, has been or is a sufferer 
from an acute infectious disease, has swallowed or inhaled some 
irritant poison, or has suffered from some severe burn of the surface 
of the body. 
If, instead of an acute attack of illness, the symptoms just de- 
scribed come on gradually and insidiously, and the tendency to 
anasarca is marked and persistent, we have before us a case of 
chronic parenchymatous nephritis, in which the prognosis is most 
grave. Ursemic vomiting and coma may occur in this class of 
patients (see chapter on Vomiting). Blood-cells are also found in 
the sediment of the urine in these cases, but are not so numerous as 
in acute diffuse nephritis. 
A group 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 diffuse parenchymatous 
nephritis, we find it unusually low (only 1.010 to 1.015). Albu- 
min is only found inconstantly and in traces, and is generally to 416 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 paren- 
chymatous nephritis somewhat hypertrophied, is in this disease 
usually markedly hypertrophied, and the second sound at the second 
right costal cartilage is commonly 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. Uraemic symp- 
toms 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 indefi- 
nitely. 
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 presence of syphilis, of prolonged suppuration, or extensive bone 
disease, due, it may be, to tuberculosis, with concomitant enlarge- 
ment 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 of 
the urine will probably reveal the case to be one of diabetes me/litus. 
This will be pointed 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. The other prominent symptoms of dia- 
betes mellitus are furunculosis, 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 Unconsciousness). If the urine has a constant low specific 
gravity and contains no albumin or sugar, the case is probably one 
of diabetes insipidus. 
Should much pus be present in the urine, it is probably derived THE URINARY BLADDER AND THE URINE. 
417 
from a pyelitis or a suppurative inflammation of the pelvis of the 
kidney. The symptoms of this state are, briefly, a constant or in- 
termittent 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 
anaemia 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 urine is acid, in cystitis it is ammoniacal; by the pain 
in the renal region, often unilateral; and by the use of the cysto- 
scope. The prognosis varies. If due to an infectious fever, re- 
covery usually occurs. Tuberculous pyelitis may also recover. CHAPTER XIII. 
THE BOWELS AND FECES. 
Constipation and diarrhoea—The causes of these two symptoms and their diagnosis 
—The diseases in which these symptoms occur—Choleraic diarrhoea—Dysen- 
tery—The color of the feces—Intestinal parasites. 
The consideration of the condition of the bowels and feces as 
indicative of disease affecting the intestines themselves and other 
organs closely associated with their functions can be best divided 
into several parts, namely, the functional disorders of the intestines 
and the organic diseases from which they may suffer, 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 common 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 absorp- 
tion 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 dis- 
ease, producing a deficient biliary flow; and in phosphorus-poison- 
ing, 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 containing large amounts of tannic acid may produce 
similar results because of the astringency of this substance, and 
chronic constipation from the use of large quantities of badly in- 
fused 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 mauifes- THE BOWELS AND FECES. 
419 
tation of diabetes insipidus or diabetes mellitus, because the polyuria 
of these affections drains the body of liquid. Obstinate constipation 
should therefore always call the physician’s attention to these affec- 
tions and to two other possibilities, namely, that the condition de- 
pends upon wilful disregard by the patient 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 constipation 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 in- 
hibitory fibres of the splanchnic nerves may be so irritated that 
peristalsis is impossible. Here a hypodermic injection of morphine 
may make a movement possible. 
The organic diseases of the bowel producing constipation are many 
and of great importance. They consist in intestinal obstruction in 
all its forms, as by bands, by growths, by the process of intussus- 
ception, by volvulus, by cicatricial contractions, and by impacted 
foreign bodies 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 always put the physician 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 constipation, a discussion 
of the various symptoms of intestinal obstruction will be found 
in 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 physician 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. 
Diarrhoea 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 excessive peristalsis; to relaxation of the bloodvessels of the 
intestine, with profuse serous leakage and consequent watery purg- 420 
THE MANIFESTATION OF DISEASE IN ORGANS. 
ing; to acute inflammation, with excessive secretion of mucus; and 
to the endeavor of the system to eliminate poisons in this manner, 
as in cases of sudden profuse diarrhoea, in cases of chronic renal 
disease, in which the purging is an effort at elimination. The last 
named forms of diarrhoea 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 which 
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 gastrointes- 
tinal 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 speedily becomes cold and pinched-looking, exceedingly 
weak, and Anally passes into collapse. The pulse becomes feeble, 
rapid, and running ; the face livid, and finally the patient may 
develop the facies Hippocratica. The urine is greatly decreased or 
entirely suppressed, because of the watery purging, and possibly by 
reason of the effects of certain poisons upon the kidneys. In the 
great majority 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 with curds of milk and green 
masses, looking 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 tenes- 
mus 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 THE BOWELS AND FECES. 
421 
bowels, so that it lies on the lap of the nurse in a relaxed and torpid 
state. The surface of its body is often abnormally cold, and its 
extremities may be pinched and blue; but the temperature of the 
internal organs is generally abnormally high, so that while the axil- 
lary 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 respira- 
tions may be sighing or of the Cheyne-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 
called. Again, the evidences of infection or general systemic dis- 
ease indicate the epidemic malady rather than does a profuse diar- 
rhoea alone. Thus the systemic signs of infection may be so great 
that death from infection in true cholera occurs before diarrhoea 
even begins. Again, it would be possible to determine the presence 
of true cholera if the comma-bacillus could be demonstrated; but 
this requires the examination of the fecal matter to be made by an 
expert who is familiar with the technique of examining fecal 
matter for the germs and with the necessary measures for their arti- 
ficial culture. 
Symptoms identical with the more violent forms of cholera nos- 
tras or true cholera may be produced by acute poisoning by antimony, 
except that in this case we often have profuse sweating and saliva- 
tion early in the attack. The same symptoms of vomiting, purging 
of rice-water stools, collapse, cramps in the calves of the legs, and 
violent pain in the abdomen may be present. A differential diag- 
nosis, without the history of the patient having taken poison is 
impossible, except by a chemical analysis of the vomited matter, 
which with the stools, and the urine, will contain antimony. The 
utmost care should be used that the vessels which receive these mate- 
rials are chemically clean, that they are hermetically sealed until 
ready for the expert analysis, and that they are in the hands of 
thoroughly responsible parties up to the date of analysis. 
While arsenic may cause somewhat similar symptoms to those 
due to antimony, the stools are generally bloody from destruction of 422 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
the gastrointestinal mucous membrane by the drug, llarely certain 
poisonous toadstools produce somewhat similar symptoms. 
If an adult who has not eaten anything which could have produced 
a diarrhoea, as the result of irritation from bad food, is seized with 
profuse watery purging, with very little or no pain, and without 
nausea or vomiting, it is probable that he is suffering from the acute 
nervous diarrhoea which sometimes results from exposure to severe 
nervous strain. To illustrate the character of these cases the author 
may mention the fact that it is quite common for him to see medical 
students, exhausted by a long winter’s work and anxious about their 
examinations, seized by an attack of profuse watery purging in the 
middle of the night preceding the examination of which they stand 
most in dread. 
Care must be taken by the physician in all cases of sudden and 
profuse diarrhoea to which he is called to exclude the presence of 
renal disease, for purging may be an effort at elimination of effete 
materials, and its sudden arrest by drugs may induce uraemic convul- 
sions or coma. 
Sudden attacks of profuse watery diarrhoea in which the patient 
passes great quantities of liquid from the bowel, with or without 
pain in association therewith, may be due to locomotor ataxia, mani- 
festing itself in an “ intestinal crisis.” 
In cases of persistent or obstinate diarrhoea, serous or catarrhal, in 
which there is an excessive peristalsis which hurries the intestinal 
contents along so fast that the food cannot be properly digested, the 
physician should remember that fissure of the anus or some other 
source of irritation may be present in the lower bowel which pro- 
duces reflex excitability of the nerves governing the bowel-move- 
ments. In other cases a stricture in a feeble, dilated rectum will 
cause retention of feces until irritation, tenesmus, and even loose 
mucous movements are produced. 
If, instead of watery or serous movements, the patient is attacked 
by a more or less acute diarrhoea, accompanied by great pain and 
distention of the belly, and if there is marked tenderness on pres- 
sure over the transverse colon and mucus in the feces, which are not 
in very large quantities after the first few movements, there is prob- 
ably present the condition known as entero-colitis, or inflammation 
of the ileum and colon. It is met with in both children and adults, 
and differs in its course from cholera morbus and cholera infantum 
very markedly. The pain is usually more constant, more aching, THE BOWELS AND FECES. 
423 
and less griping in character. Vomiting is not a constant feature, 
as it is in the watery choleraic diarrhoeas, and the course is more 
subacute, the duration of the illness usually being from one to three 
weeks. If food which is difficult of digestion has been eaten, it is 
passed, still undigested, from the bowel and is apt to be coated with 
mucus. Such a diarrhoea is called lienterie diarrhoea. 
Vot far removed from this type of cases are those of a more 
chronic character depending upon more grave and lasting alterations 
in the gastro-intestinal mucosa. As a rule, the greater part of the 
trouble exists in the colon, and more or less griping pain in the 
neighborhood, namely, in the upper umbilical area and left groin, 
may be present before each movement. The abdomen is apt to be 
distended and quite tender on pressure, particularly in certain vari- 
able spots, and considerable loss of bodily weight is apt to ensue, 
chiefly from failure on the part of the digestive tube to absorb the 
food that is eaten. The movements are not markedly watery, but 
are usually unformed and about the consistency of oatmeal gruel or 
a little thicker. Flakes of mucus are often found in large amounts 
in the fecal matter, and the feces may be frothy or flaky as the result 
of fermentation. Blood and pus are very rarely seen in the move- 
ments of these cases, unless the blood escapes from an inflamed 
hemorrhoid. Sometimes, when these cases are very severe in char- 
acter, the mucus takes the shape of long cord-like or worm-like 
strings, or even seems to be membranous in character. In other 
instances the feces, when formed, are passed in ribbon-shaped masses, 
either due to spasm of the muscular fibres of part of the lower 
bowel or to cicatricial contractions, due to the healing of old ulcera- 
tions. In very severe cases the condition of the intestine gradually 
advances from a mild follicular entero-colitis to one of actual deep 
ulceration, and under these circumstances blood and pus may be 
present in the movements. At such times the pain produced by the 
patient having a movement of the bowels, or by the passage of fecal 
matter over the ulcerated surface, may be intense, and the invalid 
will often state that the pain feels as if one spot in the gut were 
made more painful by the feces rubbing over it. Such cases often 
continue for years, while some of them ultimately get well, others 
become chronic invalids from the slow changes in the intestinal 
walls. In this connection the diarrhoea of tuberculosis is not to be 
forgotten, depending, as it does, either upon the general infection or 
upon the development of ulcerations in the intestinal canal. 424 
THE MANIFESTATION OF DISEASE IN ORGANS. 
In some cases in which the patient after exposure to cold or wet 
is seized with violent pain in the epigastrium, and a feeling of 
weight in the rectum, a few loose movements, and then intense 
tenesmus and bearing-down, with only a few drops of mucus in the 
way of a movement, the condition is one of acute rectal catarrh or 
proctitis. 
The cases just named in the preceding paragraphs are to be sepa- 
rated from those in which there is true dysentery. Dysentery is a 
term very loosely applied, by the laity in particular, to any form of 
severe diarrhoea, particularly if there are blood and mucus in the 
movement. In reality the term dysentery should be limited to 
cases due to an infection and very apt to occur in epidemics. As 
Osier says, true dysentery is one of the four great epidemic diseases 
of the world. 
Let us suppose that a patient is seized with diarrhoea and some 
pain in the belly, and with only a slight chill, or in other cases no 
chill may be present. The pain soon becomes more and more col- 
icky and the stools are passed with ever-increasing bearing-down or 
tenesmus. The effort to empty the bowel, after it is in reality thor- 
oughly emptied, results in agonizing bearing-down pains. Fever to 
the extent of from one to three degrees may be present. Thirst is 
excessive, the stomach is usually retentive, and the stools are first 
the ordinary bowel-contents, and then mucus, which may be blood- 
streaked. Soon the mucus becomes jelly-like in appearance and 
more thick and tenacious, and, finally, after several days it begins 
to look muco-purulent, and the stools are less frequent. Sometimes 
small bullet-like hard pieces of fecal matter are shot out of the 
rectum after severe straining. Recovery usually begins at from 
seven to ten days. The entire trouble seems to be in the large 
bowel, and particularly in the sigmoid flexure and rectum. Such 
are the symptoms of ordinary mild dysentery of hot climates or of 
summer weather in the temperate zone. 
The severity of the disease is much greater in hot weather, and 
the prognosis is not good in severe cases coming on during an 
epidemic. 
On the other hand, if the patient has an irregular diarrhoea, after, 
or during, a residence in tropical parts, which may or may not have 
a sudden onset, with moderate fever and considerable loss of flesh, 
and has moderate bellyache, which soon becomes much less, and if 
the stools as just described above become more aud more fluid, and THE BOWELS AND FECES. 
425 
the diarrhoea intermits, the physician should think of the case being 
probably one of so-called tropical dysentery, or amoebic dysentery, a 
condition of infection by the so-called amoebae coli. The course of 
the disease is slow, lasting from six to twelve weeks, and the death- 
rate is high. Convalescence is always very slow, and liver-abscess 
due to an hepatic infection by the amoebae coli is very frequent. 
Sometimes abscess of the luug develops. 
A positive diagnosis of this variety of dysentery is made by the 
discovery of the amoebae in the stools. These micro-organisms pos- 
sess active amoeboid movements and are found in greater number 
when the diarrhoea is severe. They are to be sought for in the 
small gelatinous masses which are found in the feces. Sometimes 
the entire stool seems loaded with amoebae, at other times only a 
most careful search will discover them. They are more refractive 
than the cells found in the feces, and contain numerous vacuoles, so 
numerous in some cases that the cells look very granular. These 
must not be mistaken for the compound granular bodies found in 
the feces. When they are active a division into an endosarc and 
an ectosarc can be discovered. Often red blood-cells will be found 
in the amoebae. 
Sometimes a diphtheritic or false membranous dysentery is devel- 
oped in persons having chronic heart disease, and it has been seen 
as a sequel 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 rapidly 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 
diphtheritic dysentery), as they often are filled with blood and 
mucus in dysentery, a condition rarely seen in typhoid fever. 
Dysentery may be confused with the diarrhoea sometimes pro- 
duced by a malignant and ulcerating growth in the sigmoid flexure 
or rectum, but a physical examination will usually reveal the tumor, 
and the cachexia will aid in pointing to it as the cause. 
Syphilitic ulceration of these parts may cause a somewhat similar 
train of symptoms. Again, it is by no means rare to meet with 426 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the passage of several muco-purulent movements each day in per- 
sons who have pulmonary gangrene or pulmonary tuberculosis, 
partly due to the swallowing of fetid sputum or tubercular ulcera- 
tion of the bowels. Diarrhoea is also a symptom of septicaemia. 
Distantly allied to this form of diarrhoea is that seen in persons 
who have dissected a putrid body (“ dissecting-room diarrhoea” 
so called). 
While it does not fall to the lot of this book to discuss the symp- 
toms of the affections of the rectum which are to be relieved by 
surgery, it is proper to speak briefly of the causes of blood in the stools 
in other states than dysentery. In inquiring as to the blood in the 
stools, we should ask whether it is mixed with the feces or is seen 
in streaks, and whether it passes in jets or not. If in jets, it will 
be found in the pan away from the fecal matter. We should ask 
as to the amount of blood and its color. If mixed with the feces, 
it probably results from a slow oozing from a hemorrhoid, or, if the 
feces are formed, from some leaking vessel in an ulcer high up in 
the sigmoid flexure. If in streaks, it probably comes from the wall 
of an ulcer which has been scraped by the fecal mass. If it is 
passed in jets, it probably comes from some vascular but small arte- 
rial tuft of vessels low down near the anus; and, finally, if it is 
dark and tarry-looking, it is probably due to a leaking in the upper 
colon or ileum, whereas if light red in color it is from vessels in the 
rectum. Most commonly it is from hemorrhoids, or from an ulcer- 
ated mucous membrane covering a syphilitic deposit, or else a malig- 
nant growth. (See further on in this chapter.) 
Finally, it is interesting to note that paroxysmal attacks of sero- 
mucous or bloody diarrhoea sometimes come on in case of exoph- 
thalmic goitre. Diarrhoea of a more or less severe type may come 
on in cases of hysteria, often associated with tremendous eructations 
of gas and rumbling in the stomach and bowels. 
Fatly diarrhoea may ensue if feeble persons already suffering from 
irritable bowels take an excess of cod-liver oil, but in other cases it 
possesses great diagnostic importance. If associated with diabetes, 
it gives us reason to believe that there is some disease of the pan- 
creas producing both the glycosuria and the lack of digestion of the 
fats. Sometimes in jaundice, however, fat is found in the stools 
owing to the lack of bile to emulsify it in the intestine. 
The Feces. In this connection we naturally pass on to a discus- 
sion of the diagnostic indications of the feces. In the first place, THE BOWELS AND FECES. 
427 
it must be remembered that the quantity of the feces depends upon 
the quantity of the food, and again that the quantity varies with 
the character of the food, for if the food be such as to be bulky, 
yet contains little nutritive material, there will be a large residue to 
be passed out in the feces; whereas if the food be almost entirely 
composed of materials which can be assimilated very little residue 
is left, and the feces are consequently smaller in bulk. Thus the 
cow eats a large bulk of food and passes large amounts of fecal 
matter, whereas the dog eats meat and passes very small amounts 
of fecal matter. 
Again, it is not to be forgotten that many foods actually increase 
intestinal peristalsis, and so produce large and loose movements, as 
oatmeal and wheaten-grits or apples, while other foods, such as 
cheese, do the opposite. If the stools are large and copious and the 
food which the patient has taken is in reality not of a kind leaving 
a large residue in the bowel, the indication is that there is non- 
absorption of nutritive materials, with consequent wasting of the 
patient. 
The consistency of the feces in health varies from a formed 
“ stool” to a mushy condition; but in disease we have a liquid 
watery stool if the trouble be serous diarrhoea, and a pasty and 
slimy stool if it be due to a catarrhal state of the bowels. The 
passage of hard scybalous masses mixed with liquid indicates that 
the feces have become dried and hard in the sacculations of the 
colon, and are only passed out when they cause so much irritation 
as to produce diarrhoea. If the feces are in narrow bands or flat- 
tened ribbon-shapes, there is probably a stricture of the rectum, 
offering an obstruction to their passage. A mushy or semi-watery 
stool is often seen in typhoid fever. 
The odor of the stools depends very largely upon the food which 
is taken and upon the degree of fermentation present in the bowels. 
In nursing-children the stools often have a faintly sour odor, and 
in the diarrhoea of nurslings with acid fermentation there is an 
odor of the fatty acids. If the process is marked, this odor becomes 
actually foul, and in cholera infantum the stools have a musty, 
mousy odor. If malignant growth of the bowel is present, the 
odor is fetid, as it is also in gangrene of the intestine. Sulphur 
when taken internally causes a very offensive stool, owing to the 
sulphuretted hydrogen gas which is developed in the bowel. 
The color of the stools is of great diagnostic importance in several 428 
THE MANIFESTATION OF DISEASE IN ORGANS. 
conditions. In health the feces should be brown or brownish-black, 
the color being partly due to the food, but chiefly to the bile (hydro- 
bilirubin). Certain fruits render the stools dark in color, and drugs, 
such as iron and bismuth, do likewise, and hsemotoxylon often makes 
them look red. 
In the stools of persons living on a pure milk-diet we usually find 
little color comparatively. Again, in cases of jaundice, phosphorus- 
poisoning, and acute yellow atrophy of the liver, the stools are very 
light in color, owing to their lack of biliary coloring. They are 
also apt to be very light in chronic lead-poisoning. 
Bilious stools are either golden-yellow, greenish, or reddish in 
hue, and if the flow of bile is profuse, they are apt to be watery. 
Greenish stools looking as if they contained chopped spinach are, 
however, a peculiarity of the diarrhoea of fermentation, particularly 
in infants, the color being due to a color-forming micro-organism. 
If the stools are well mixed with mucus, the catarrhal process 
probably exists in the ileum; but if they consist of hard masses of 
"feces coated with mucus, the disease is probably a colitis. 
Bloody stools are most commonly due to hemorrhoids which are 
eroded. The blood may be bright if the hemorrhoid be a small 
arterial bunch, or more dark and grumous if slow oozing has gone 
on for some time prior to the movement. As a rule, the brighter 
the blood in the stool the nearer its source is to the anus, and the 
darker the blood the higher is its source in the bowel. Thus, if the 
stools are tarry-looking, the blood is almost certainly from the small 
intestine, and probably arises from a duodenal or other ulcer or from 
carcinoma of the stomach or bowel; while if it is only somewhat 
changed in appearance, it may be due to an ulcer or ulcerated mor- 
bid growth in the colon. Sometimes, however, where the hemor- 
rhage from the ileum is very profuse, as in typhoid fever, the blood 
comes from the anus only slightly changed in appearance. If 
blood is suspected to be present, we can confirm its presence by 
finding the corpuscles by the microscope or by testing the feces for 
hsemin. (See chapter on Vomiting.) 
Stools containing pus may receive this material from the surfaces 
of ulcers, but usually the source of the purulent matter, if it is 
present in large amount, is an abscess which has ruptured into the 
bowel, as, for example, in peri-rectal abscess. 
Finally, we may find gall-stones in the stools, which, if they are 
passed soon after their escape into the bowel, are found to be faceted. THE BOWELS A ED FECES. 
429 
Stools which are being searched for gall-stones should be washed 
through a sieve in such a way as to catch the stone and let the fecal 
matter through. The iutraliepatic gall-stone is not faceted and 
crumbles easily. 
"Very rarely a portion of the bowel sloughs away, and yet recov- 
ery takes place. This is seen sometimes in intussusception. 
Aside from the character of the stools themselves, we often search 
for the cause of an ailment in the passages, either for foreign bodies, 
such as pebbles or pins, or for intestinal 'parasites (worms). Some- 
times worms may exist for long periods of time in the bowel with- 
out causing any symptoms, and, again, in children in particular, 
they cause great systemic disturbance by producing disorder of the 
digestion or reflex irritation. 
Worms. Under the name of tapeworm or cestodes we find in 
the intestine, and often in the stools, a parasite occurring in seg- 
ments which are flat and ribbon-like, and usually from a quarter 
to one-half inch in length. The worm itself may be several yards 
long. Its head is small, and it maintains its hold on the bowel by 
its head. The segments are usually broken off one by one and 
escape in the stools, and the stools also contain the ova or eggs 
of the parasite, which are developed in each segment, which also 
possesses male and female organs. 
According to the shape of the head and the size of the worm and 
the source of infection, we divide tapeworms into three classes: 
teenia solium, the tsenia mediocanellata, and the bothriocephalus 
latus. 
If the patient passes a worm of from one to three yards in length, 
the head of which is about the size of a pin-head and glistening gray 
in appearance, the rest of the worm being yellowish-white, and if 
upon the head can be seen four pigmented suckers surrounded by a 
crown of hooks, that worm is a tsenia solium, and is probably 
derived by the patient from raw or uncooked pork. The eggs of 
the Uenia solium must be sought for by a microscope. They are 
round and covered by a hard shell, which breaks upon pressure into 
small fragments. In the shells may be found a few booklets. 
These eggs are passed out in the feces by the host, and are then 
swallowed by the pig, in whose muscles the hooklets migrate and 
form cysts. In these cysts the hooklets develop, and when a man 
eats the meat raw they enter his intestine, attach themselves, and 
from them a tapeworm is developed. 430 
THE MANIFESTATION OF DISEASE IN ORGANS. 
If the worm is from four to five yards long and the segments 
after leaving the anus have motile powers, and if the head is larger 
than that of ttenia solium and devoid of booklets about the suckers 
Fig. 181. 
Fig. 182. 
Oxyuris vermicularis, magnified. (Payne.) 
a. Young female. 6. Male. c. Mature female, 
full of eggs. 
Ascaris lumbricoides, dissected and walls 
thrown back. (Heller.) a. Genital orifice. 
b. Intestine, c. Oviducts, d. Longitudinal 
band. e. Ovaries. THE BOWELS AND FECES. 
431 
on its head, it is probably the taenia mediocanellata or saginata. 
The egg is slightly larger than that of the solium. This worm 
usually comes from eating raw beef. The bothriocephalus latus is 
the largest of all tapeworms, often reaching seven to eight yards in 
length. It has a long head with two long, narrow suckers. The 
eggs are oval, very large, and the shell is light brown in color, and 
very easily broken. This parasite is not common in America, but 
Fig. 183. 
Fig. 184 
Trichocephalus dispar, natural size. (Payne.) 
a. Female, b. Male. 
is a very frequent cause of profound anaemia in the 
persons whom it infects. Its joints are only rarely 
thrown off, so its presence is often overlooked, and 
this renders the search for the eggs very important 
in severe anaemia with no ascribable cause. This 
worm is usually derived from fish. A worm which 
is comparatively rare is the tcenia cucumerina, which 
has a head with sixty hooks. It infects dogs, cats, 
and sometimes children. 
A round worm, looking like an ordinary earth- 
worm, appears sometimes in the stools, and is called 
ascaris lumbricoides. It is sometimes vomited, and, 
rarely, causes trouble by crawling into and blocking 
the common biliary duct. 
Fine thread-like worms inhabiting the rectum are 
the oxyuris vermicularis. 
A very important diagnostic find in the feces is a fied. (Bkistowe.) 
worm looking very much like the thread-worm, but a l emale- b- Male- 
somewhat larger, which inhabits the duodenum. It is called the 
ankylostoinum duodenale. The importance of finding it lies in the 
fact that it produces the most profound and acute anaemia by suck- 
ing blood from the intestinal wall. The worms are usually only 
found after a vermifuge is taken, but the eggs are always present in 
Ankylostomum 
duodenale, magni- 432 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the feces as unsymmetrical, thickly covered segmented globules. 
If the stools containing the eggs be set aside in a warm place, the 
embryos can be seen to develop. Bloody stools may be due to the 
presence of this parasite. 
The so-called whip-worm, or trichocephalus dispar, is a fine 
thread-worm without any medical interest. PART II. 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
CHAPTER I. 
FEVER AND SUBNORMAL TEMPERATURES. 
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 which 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 
inserting 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 bulb of the thermometer. Before 
the thermometer is placed in the axilla this space should be care- 
fully 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 insert- 
ing the thermometer into the rectum, and, if this is done, the bulb 
should be passed well inside the external sphincter. Rarely the 
temperature is taken in the vagina. 
The precautions to be taken in all cases 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 inflam- 
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 particularly apt to be the case in diseases of the 434 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
month in children, thus stomatitis may raise the local temperature 
from one to two degrees. Hot liquids, if taken into the month 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 possible 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 tempera- 
ture from a physiological point of view is that the nervous centres 
governing 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 probably aids the body in throwing off or, rather, conquering 
the disease, which has attacked it, in three ways, namely, by pro- 
ducing a temperature less favorable to the growth 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 tem- 
perature the effects of poisons may be rendered nil. This is the 
case, for example, 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 symp- 
tom 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 AND SUBNORMAL TEMPERATURES. 
435 
but sometimes with a cold, wet skin. The latter condition 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 in adults, for children often develop high temperatures from 
slight causes and have speedy 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 in 
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 at times as the result of the 
reflex irritation produced by difficult teething. (See chapter on the 
Tongue.) In many instances, however, the fever of dentition de- 
pends upon a more or less closely related, but overlooked, gastric 
catarrh. Sometimes after a urethral sound or catheter has been 
passed into the urethra of 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. 
Fever in Infectious Diseases.1 Xearly all infectious diseases 
are ushered in by the development of fever of greater or less degree, 
and this is particularly true of the exanthemata. In typhoid fever the 
febrile movement is very characteristic in some cases, although in 
many instances it does not follow the description laid down in text- 
books. After several days of general wretchedness the patient de- 
velops 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 night 
103°, and so on until the morning temperature may be 103° and 
the evening temperature 104° or rarely 105°. The fever usually 
reaches its acme by the end of the first week or ten days, and then 
for another week remains almost unchanged, there being a morning 
fall and evening rise of an almost equal 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, 
1 In this connection the student should also read that part of the chapter on the skin devoted 
to the consideration of the eruptive infectious diseases. 436 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
and then the evening rises fail to reach their former height. Often 
these marked morning remissions are the first indication of the ten- 
dency to recovery. Very high evening temperatures are indicative 
of a severe attack, but are not so indicative of serious illness as are 
high temperatures in the morning. After the third week, in a mod- 
erately severe ease, 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 begin- 
ning 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 such a fall 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 occurring in connection with abortion 
in a female patient. Sometimes, too, without any of these causes, the 
temperature falls very rapidly, and the patient goes into collapse. 
Such cases are very grave and the prognosis is unfavorable. 
Fig. 185. 
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 convales- 
cence from typhoid fever, take solid food too soon, or are excited 
by the visit of a friend. Such rises are but temporary. (Fig. 185.) FEVER AND SUBNORMAL TEMPERATURES. 
437 
Showing a relapse in typhoid fever. 
Fig. 186. 438 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
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 usually, but not always, of a shorter and milder 
character than the first attack. (Fig. 186.) Sometimes a mild, 
irritative fever, perhaps due to anaemia, persists for some weeks, 
but the physician should not rest content with a belief that anaemia 
is the cause until he has excluded all possibility of there being 
pulmonary, pleural, or bone disease, as these conditions very com- 
monly ensue as sequels of typhoid. In other instances, after the 
morning temperature lias 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 of them at St. Agnes’s Hospital in one term of service. 
Striimpell asserts as a rare occurrence that the fever may become 
intermittent, being normal in the morning and as high as 104° at 
night during almost the entire illness. 
The association of such a temperature-curve as just described with 
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 tubei'culosis 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 dis- 
eases is apathetic. Even the respiratory sounds in both diseases in 
their early stages may be apparently only those of a moderate bron- 
chitis; and, finally, abdominal swelling, tympanites, and meteorism 
may occur in both maladies. Under these circumstances the hered- 
itary and recent history of the patient may be of much value, as FEVER AND SUBNORMAL TEMPER A T UR ES. 
439 
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 oftener 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 examined for tubercle bacilli in all doubtful cases. 
Irregular forms of malarial fever, particularly those forms due 
to infection by the sestivo-autumnal parasite (see chapter on the 
Blood), may closely resemble typhoid fever. In many instances 
such cases are diagnosed as typhoid fever, and probably some cases 
of true typhoid fever are thought to be malarial fever. The follow- 
ing differential table, drawn up by Thayer, is of interest in this 
connection. There is no such disease as typho-malarial fever. 
Remittent Fever. 
Onset generally intermittent. 
Irregular remissions 
The temperature may arrive at 40° (104°) 
within twenty-four hours. 
Headache rare in the beginning; of a neu- 
ralgic character, pulsating, variable in its 
position and intensity. Sclera subicteric from 
the onset. 
The apathetic expression of the face, the dry- 
ness of the tongue, sordes upon the teeth are 
not very marked. 
Breath foul. 
The delirium may come on in the early days; 
it is recurrent, hut changes with the exacerba- 
tions of temperature and other symptoms, and 
may give way to grave symptoms related to 
other organs. 
Typhoid Fever. 
Onset gradual and progressive 
Regular, though very slight morning remis- 
sions with evening exacerbations of tempera- 
ture. 
The temperature does not reach 40° (104°) 
before the third or fourth day. 
Headache from the beginning, permanent, 
severe, frontal. Sclera white. 
These symptoms are well-marked and pro- 
gressive. 
Breath has a peculiar mouse-like odor. 
Delirium appears only when the disease is 
well pronounced; it is often persistent and 
variable only in degree. 440 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
Remittent Fever. 
If there he pulmonary congestion, the cough 
and other symptoms come on suddenly; the 
areas affected change from one to the other 
lobe or lung and may disappear and reappear 
again with varying intensity; dyspnoea is very 
pronounced; circulatory disturbances are 
marked, even syncope. 
There are usually restlessness and anxiety 
(jactitatio corporis). 
Peculiar grayish color of skin; sometimes a 
slight jaundice. 
Herpes common. 
Anaemia more or less marked early in the 
course. 
No characteristic exanthem; urticaria not 
uncommon. 
At times there may be transient tympanites 
or ileo-caecal gurgling; they are but slightly 
pronounced and paroxysmal; diarrhoea is 
slight or absent, and has not the characters of 
that in typhoid fever. 
No distinct course. 
Urine high-colored ; may show a trace of bile ; 
Ehrlich’s diazo reaction rarely present. 
Blood shows no leucocytosis; eosinophiles 
not notably diminished ; serum does not cause 
agglomeration of typhoid bacilli (Pfeiffer, Dur- 
ham, and Widal); malarial parasites and pig- 
mented leucocytes present. 
Fever disappears under quinine. 
Is an endemic disease occurring particularly 
in rural districts; rarely epidemic. 
Typhoid Fever. 
Pulmonary congestion is gradual and per- 
sistent ; always hypostatic (the bases and dor- 
sal surfaces of the lungs); the dyspnoea is less 
pronounced and later in appearing, depending 
more upon the abdominal conditions (tym- 
panites, etc.). 
There are usually relaxation, prostration, 
stupor. 
No jaundice. 
Herpes rare. 
Anaemia absent, excepting in later stages. 
Characteristic roseola. 
Tympanites, gurgling, diarrhoea appear 
slowly and may become well marked. 
Has a fairly characteristic course. 
Urine high-colored ; bile absent; diazo-re- 
action present during the height of the process. 
Blood shows no leucocytosis; eosinophiles 
diminished or absent; serum causes agglomer- 
ation of typhoid bacilli; malarial parasites and 
pigment absent. 
Fever uninfluenced by quinine. 
Usually epidemic; prevailing commonly in 
cities. 
The febrile movement and other symptoms of enteric fever are 
often imitated very closely bv 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- 
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- FEVER AND SUBNORMAL TEMPERATURES. 
441 
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. Some- 
times 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 
vehemence than before. Such relapses may occur again and again. 
Violent pain in the joints on moving the body is 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 petechia; before fading, or remain unchanged 
in appearance, the great exhaustion, the severity of the illness, and 
the sudden rise of temperature, followed by a constant fever, point 
to typhus fever. Finally, the conclusion of the febrile movement 
in favorable cases by 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 cases very difficult or impossible at first. 
The temperature of relapsing fever nearly always rises suddenly 
at the beginning of the attack to from 103° to 105°, and remains 
high with slight morning remissions from three to seven days, when 
it suddenly falls as by crisis to the normal or below it, after being 
on the preceding afternoon or evening unusually high. Sometimes 
it falls as low as 92° or 93° F. The patient now remains free from 
fever for from several days to two weeks, when with a sudden leap 
the fever and other symptoms of the first attack recur. A tempera- 
ture of 105° to 106° in relapsing fever rarely indicates a grave out- 
look 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 malarial 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. 442 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
In scarlet fever the temperature suddenly rises on the first day to 
104° to 105° F., and still higher the next day, and then remains 
constant as long 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 slowly 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 persists longer, is probably due to some complications, such as 
otitis, or the “ collar of brawn,” due to enlarged cervical glands. 
(Fig. 187.) The characteristic strawberry punctated rash and 
Fig. 187. 
Chart of scarlet fever. 
scarlet hue appearing 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, 
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. 188.) 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 FEVER AND SUBNORMAL TEMPERATURES. 
443 
the original disease; such a complication, for example, as a bron- 
chial or gastro-duodenal catarrh. 
The fever of rotheln, 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 differ- 
ential diagnosis. (See chapter on the Skin.) 
'Fig. 188. 
Showing initial fever with the subsequent fall and then a rise when the rash is well developed 
in a case of measles. Also shows an ending of the fever by crisis. 
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 fever, pain in the back, severe headache, 
and malaise, the patient takes to his bed if possible, and his tem- 
perature 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 this way, there- 
fore, the temperature-chart of variola differs diametrically from that 
of the eruptive fevers so far discussed, for in these cases the fever 
rises with the appearance of the eruption, whereas in this instance 
the temperature 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 pus- 
tules the temperature rises again in what is called the fever of sup- 
puration, which lasts with greater or less persistence for at least a 444 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
week, when it ends by lysis or a gradual fall. Excessively high 
fever of 108° is a sign of approaching death or at least 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 propor- 
tions entirely out of consonance with the general systemic disturb- 
ance, which is usually very slight in previously healthy children. 
Thus it may rise in children who are prone to active febrile move- 
ments 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 con- 
stantly high through the course of the inflammatory process in the 
skin, goes through marked intermissions or remissions, which fre- 
quently 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 dis- 
comfort, lasting but eight to twelve hours, is in the majority of 
cases that of intermittent malarial fever. The peculiarities of inter- 
mittent 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. 189.) 
The fall of temperature is usually less abrupt than the rise, and 
is sometimes delayed by slight temporary rises or arrests in its 
downward course. The febrile movement is repeated at intervals, 
ranging 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 days, or it may be due to infection with three sets of quar- 
tan parasites. If the attacks occur every other day, they are called FEVER AND SUBNORMAL TEMPERATURES. 
445 
tertian (Fig. 190); 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. 189. 
Showing daily paroxysm due to double tertian infection. One set of parasites segmented 
at 4 p.m. and the second set at 8 p..m. Paroxysm stopped by quinine on fourth day. 
Another point of importance in connection with malarial attacks 
is that they often occur earlier each day by an hoar or more. Rarely, 
they are delayed. 
Fig. 190. 
Showing paroxysms of tertian fever, the segmentation of the organism occurring 
at about twelve o’clock each day. 
Intermittent malarial fever is to be separated from other inter- 
mitting fevers by a number of facts. First, the presence of the 
malarial organism in the blood at the time of the attack, or evidences 
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 on malarial fever produced by the adminis- 
tration of quinine. Care must always be taken that the intermitting 446 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 evening, when, in reality, the 
real cause is an undiscovered pulmonary or abdominal tuberculosis. 
Again, acute ulcerative endocarditis and purulent phlebitis may 
cause similar symptoms, as may also hepatic abscess, impaction of 
gall-stones, 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 abdomen by careful physical exam- 
ination will aid in deciding that the fever is tubercular and not 
malarial in origin. (See chapters on Thorax and on Abdomen.) 
In ulcerative endocarditis the temperature-curve may exactly 
resemble 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 puerperium will reveal the source of 
an infection. (Fig. 191.) In the typhoid type of ulcerative endo- 
carditis 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 feebleness and asthenia, on the one hand, and the result 
of the blood-examination, on the other, aid the diagnosis. The dura- 
tion of the case is not of much value in making a diagnosis, for 
cases of ulcerative endocarditis have lasted from two days to more 
than a year. Iiarely it lasts more than six weeks. Death usually 
occurs in ulcerative 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 point to this 
cause for intermittent fever. 
The fever of catarrhal or suppurative cholangitis often closely 
resembles intermittent fever, but the presence of hepatic symptoms, 
of marked jaundice, of a history of gall-stone 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- FEVER AND SUBNORMAL TEMPERATURES. 
447 
Showing temperature-curves in a case of ulcerative endocarditis. 
Fig. 191. 448 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
covered as a cause," search should be made for tenderness and swelling 
of the liver, due to hepatic abscess. Profuse sweats also will be 
found in such cases, as in most instances of septic fever. The diag- 
nosis of hepatic abscess will be strengthened if there is a history of 
the patient having suffered from dysentery, as hepatic abscess is 
frequently caused by amoebic dysentery. 
The presence of fever preceded by chills, the temperature rising 
to 104° or even 105°, followed by excessive sweats, in a person who 
is profoundly cachectic, may be due to pernicious ancemia or to septic 
poisoning, as already pointed out; but it should be recollected that 
such a temperature-chart is often seen in cases of gastric cancer. 
Similar symptoms as to fever in association with enlargement of 
the lymphatic glands, particularly those of the neck, indicate 
Hodgkin’s disease (see chapter on Blood), or even more commonly 
tuberculous adenitis which, however, is more commonly met with in 
the young and involves the glands near the jaw, while in Hodgkin’s 
disease the glands near the clavicle are affected. Further, in Hodg- 
kin’s disease the swelling is usually bilateral and to be found else- 
where than in the neck. Again, in tubercular disease these glands 
often suppurate. The presence of the tubercle bacillus in an ex- 
cised piece of the swelling will decide the diagnosis. An intermit- 
tent fever may also be seen in suppurative pyelitis, in association 
with pyuria. This pyelitis may or may not be tubercular. 
Remittent fever rising and falling every few days for two or three 
weeks, rarely rising above 103° to 104°, and even falling to the 
normal line, associated with enlargement of the spleen and liver, 
yellowing 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 intermit- 
tent form just described, because it responds less readily to treat- 
ment, and, second, because it is accompanied by more marked 
changes in the viscera. It depends upon infection with what is 
known as the sestivo-autumnal form of the malarial parasite, which 
has an irregular or variable period of growth. The conditions pro- 
duced 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 examina- 
tion of the blood can decide the diagnosis. If small ovoid, moving 
parasites are found in the first week, or crescentic parasites after FEVER AND SUBNORMAL TEMPERATURES. 
449 
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, 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 
disease, 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 with the fact that it is an 
epidemic 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 symp- 
toms of the disease, 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, bilious 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 epi- 
demic, however, the probabilities of the case being bilious remittent 
fever are very great, and the 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 blood, with the partial control of the 
symptoms by quinine in certain stages of remittent fever, point to 
the malarial disease rather than to yellow fever. 450 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
Just as in yellow fever, so iu spotted fever or cerebrospinal men- 
ingitis of an epidemic form, the fever itself is one of the least 
important symptoms, for, aside from the fact that it is apt to be irreg- 
ular and intermitting, it is rarely very high, as compared with 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- 
ever, 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 mani- 
fested. 
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 mani- 
festations, 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 septicaemia 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 point 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 independent of 
taking food, Avould 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 pulmonary tuberculosis, 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. 192.) 
This symptom of fever in any form occurring iu a person with 
suspiciously “ weak lungs” should cause the physician to be confi- FEVER AND SUBNORMAL TEMPERATURES. 
451 
dent that he has overlooked some focus which another careful exam- 
ination may discover, and it possesses another important diagnostic 
significance, namely, that the more active the febrile movement in 
phthisis pulmonalis the more active the disease-process, and the less 
active the fever the less active the process. Fever may, however, 
be almost entirely absent in some tubercular cases with diseased 
lungs. 
The febrile movement 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 involves the meninges of the brain, a hyper- 
pyrexia may be developed, and death speedily occurs in such 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. 192. 
Chart of a case of pulmonary tuberculosis, showing rising and falling of the temperature 
morning and night. 
When fern* is associated with marked catarrhal symptoms, chiefly 
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 influenza or catarrhal 
fever, either of the sporadic or epidemic form. In this condition 
there may be in severe cases great prostration and cardiac failure or 
vomiting and diarrhoea. The febrile movement is of the most irreg- 
ular type, even when some grave complication, such as severe bron- 452 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
chitis or pneumonia, comes on, although croupous pneumonia rarely 
occurs as a complication of “ la grippe.” 
The respiratory symptoms just described are also seen frequently, 
in association with moderate fever, in “Hay Fever,” that condition 
seen in susceptible persons during haying-season or late in the 
summer. 
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. 193.) For the 
next few days, if not modified by the 
antipyretics and the use 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 
suddenly falls by crisis on the seventh 
to ninth day (Fig. 194) and convales- 
cence is established, although the sud- 
den 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 pro- 
longed, or of the typhoid type, the fever may end by lysis. 
It is to be remembered that the fever of catarrhal pneumonia is 
rarely as high as in the croupous form, usually 101° to 103°, and 
ends by lysis, not crisis. (See chapter on the Thorax.) 
The fever of acute bronchitis possesses no 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 simple 
fever, Avith slight morning remissions and evening exacerbations; 
or it may be as remittent as is a malarial remittent fe\Ter; or, again, 
Fig. 193. 
Chart of a case of croupous pneu- 
monia, showing primary rise of tem- 
perature to 103.4° and crisis occurring 
as early as the third day. FEVER AND SUBNORMAL TEMPERATURES. 
453 
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.) 
Fig. 194. 
Chart of a case of croupous pneumonia, with crisis on the seventh day: admitted to 
author’s wards on second day of illness. 
In anthrax (splenic fever) the temperature rises rapidly and 
becomes very high, and in the course of from three to five days be- 
comes 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 enlarge- 
ment of the neighboring lymph-glands, render the diagnosis easy; 
but if any doubt exists, it can be promptly dispelled by a micro- 
scopical 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 be due, particularly in children, to infection by the 
milk of cows suffering from foot-and-mouth disease or epidemic 
stomatitis. The prognosis is generally exceedingly unfavorable. 
In cholera Asiatica during the stage of collapse the surface is 454 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 uncommonly much higher, even to 107° or 
108° in fatal cases. The diarrhoea 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 
diagnosis. It is important to remember in these cases that the skin 
may feel cold and clammy even when the rectal temperature is very 
high. The febrile movement associated with the progress of acute 
parenchymatous 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 diag- 
nosis easy and the cause of the fever evident. Very marked fever 
up to 104° or 105° may develop in the early course of acute infec- 
tious tonsillitis 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 associa- 
tion 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 manifes- 
tations, a rheumatic hyperpyrexia may be developed, when, with 
delirium, convulsions, and cyanosis, the fever rises to 106° and 
even to 108°, after which death often ensues. The history of pre- 
vious attacks of articular rheumatism, the hot, swollen joint or 
joints (usually the large ones), and the successive invasion of other FEVER AND SUBNORMAL TEMPERATURES. 
455 
joints as the ones first affected get well, point to the correct diag- 
nosis. It must not be forgotten, however, that gonorrhoeal and 
other forms of septic arthritis occur with febrile movement. Pyae- 
mia, osteomyelitis, and purpura also may produce a fever with swell- 
ing 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 
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 and Face and Head.) The fever in sunstroke may rise 
as high as 110° or 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 upon 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 suffer- 
ing from rheumatism or influenza, or on the other, in the absence of 
such a history, from the early stages of one of the infectious dis- 
eases. The early appearance of tingling, numbness, loss of power, 
and wasting of the muscles soon decides the diagnosis in favor of 
neuritis. The nervous disease which most closely resembles acute 
febrile neuritis is Landry’s paralysis, and a differential diagnosis 
may be difficult; but in neuritis there are loss of sensation, muscular 
wasting, signs of degeneration, and fever, whereas in Landry’s 
paralysis all these are wanting, excepting the sensory symptoms, 
which in both diseases may be similar. The predominant symptoms 456 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
of Landry’s paralysis are paralysis and loss of reflexes. (See chapter 
on the Legs and Feet.) 
The prognosis of the severe form of febrile neuritis is grave, as 
deatli may ensue from respiratory paralysis. 
The fever of infantile spinal paralysis (anterior poliomyelitis) 
often is the chief symptom ushering in the disease, and rises to 104° 
or even 105° in some cases. There may be convulsions, headache, 
and twitching of the muscles, and, after the acute attack has passed 
off, 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 weakness 
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 Don- 
kin and Goodhart, and the writer has also met with it quite fre- 
quently. This condition has been called gastro-pulmonary 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 pres- 
ent. 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 operation, 
or prolonged anesthetization. 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. FEVER AND SUBNORMAL TEMPERATURES. 
457 
Subnormal temperatures are also seen in some cases of confusional 
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 growths 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 exhaus- 
tion or neurasthenia with or without associated anaemia. These 
may all be 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 stand- 
point, is headache seen in persons suffering from renal disease, 
brain-tumor, and meningitis in its various forms. The remaining 
causes of headache 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 the rheumatic, and of the 
second class those of cranial periostitis, middle-ear disease, and 
acute inflammation of the eye or in the jaw. 
Headaches depending upon disturbance of the digestive system 
are nearly always accompanied by evidences of such disorder, con- 
sisting in gastric or intestinal distress, belching, hiccoughing or 
vomiting, or even by diarrhoea. Often there is a distinct history 
of the ingestion of indigestible food or digestion-disturbing drink, 
but in other cases exposure to cold so congests the abdominal viscera 
that catarrh of the stomach and bowels is induced, and with it con- 
gestion of the liver followed by jaundice. The headache of dis- 
turbed digestion is nearly always frontal, and in many cases conges- 
tive to such an extent that the face may be flushed, or at least the HEADACHE AND VERTIGO. 
459 
intracranial circulation is so disturbed that the patient is unable to 
lower the head, because such a posture increases the pain. Such 
cases are relieved by hot foot-baths, which relieve the congestion of 
the head; nearly always by the act of vomiting, which should be 
induced, if need be, by an emetic or by putting the finger 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 vom- 
iting, and this is an important point in diagnosis, for in renal dis- 
ease 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 abdom- 
inal incision caused a great increase in the flow of blood through the 
carotid arteries. 
Headache due to disorder of the digestion rarely ensues immedi- 
ately 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 
headaches of indigestion are, however, characterized by two impor- 
tant 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 hemian- 
opsia. It is to be remembered, however, that in some cases of hemi- 
crania 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 
depend entirely upon irritation of the stomach and bowel with reflex 
disturbance 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 secre- 460 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
tion ensile than they are formed in large amounts, and enter the 
general blood-stream, owing to the absence of antiseptic bile and 
the coincident 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 suffer- 
ing from paroxysmal haemoglobinuria, for in this state severe head- 
ache, 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 diag- 
nosis of this primary haemoglobinuria. 
In other cases in which no jaundice is present violent headaches, 
which utterly incapacitate the patient,come on from autointoxication. 
Thus a man apparently perfectly well goes to bed on a certain 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 ver- 
tiginous, 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 pur- 
gative he removes the source of his intoxication, and his kidneys 
have time to eliminate the toxins already absorbed. Sometimes 
vomiting comes to his relief, and the emptying of the stomach 
so stimulates his liver and intestines by the efforts of vomiting 
that the process of autointoxication ceases. Some of the intes- 
tinal 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 belladonna, 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 feeble pulse, if no nausea is pres- 
ent, 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. 
Brunton 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 observation. HEADACHE AND VERTIGO. 
461 
The headache of eye-strain is usually due to abnormalities in the 
ocular muscles. Most commonly, according to Noyes, the externi 
(abductors) are the muscles which are the seat of the difficulty, but 
this opinion is not generally shared by other ophthalmologists, who 
assert that the interni are most commonly at fault. Such head- 
aches may be felt in any part of the head, but are most commonly 
said to be in the occipital region. If, in association with such head- 
ache, immediately after or long after reading, there is blurred vision, 
pain in the muscles of the eye on suddenly moving the eyeball, any 
tendency to congestion of the lids, or hypercemia in the conjunctiva 
over the insertion of the muscle, the diagnosis of headache from 
eye-strain is practically certain. (See chapter on Eye.) Violent 
pain in the head may also be due to irritable retina and to astig- 
matism and spasm of the ciliary muscle. Acute inflammatory 
processes in any part of the eye may produce severe headache, 
particularly iritis, the pain of which is very apt to be worse at 
night. 
Whether muscular asthenopia or eye-strain can cause “ sick head- 
ache” by reflex irritation is still undecided, but those ophthalmol- 
ogists who are inclined to carry the theory of refraction 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 unilat- 
eral character, and the sharp, shooting pain causes a false diagnosis 
of neuralgia to be made, or in some cases the patient is thought to 
be suffering from migraine, because in addition to unilateral pain 
there are often nausea, vomiting, and pallor of the face. The exam- 
ination 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 
appearing over the brows. In addition to the pain, which is gen- 
erally not very severe, there is often a sense of constriction about 
the head. Such a headache persists as long as a person who is over- 
worked persists in fatiguing himself, and rapidly disappears when 
rest is taken. More rarely the pain in the head in neurasthenia is 
that of migraine, and is complicated by hemianopsia and hemi- 462 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
crania, often’ by a dilated pupil on the affected side, and flushing 
and pallor of one side of the face. 
Headaches due to rheumatism are often quite severe, and are asso- 
ciated jwith much tenderness of the scalp or muscles covering the 
skull. Similar headaches, but more dull in character, are also seen 
in persons suffering from phosphaturia, and are relieved by ben- 
zoate 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 associ- 
ated 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 uraemia, or they are congestive and due to the high 
arterial tension so often seen as the result of chronic contracted 
kidney with its associated conditions of cardiac hypertrophy. 
Uraemic headache, as pointed out in the chapter on Amounting, is 
often associated 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. Sometimes 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 uraemic headaches may occur in any form of renal disease, 
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 heart 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. The urinary examina- 
tion is of the utmost importance, and no surely correct diagnosis 
can be made in any case of suspected kidney trouble till this 
secretion has been examined and found abnormal. (See chapter 
on Urine.) 
While headache is far less common as a symptom of diabetes than HEADACHE AND VERTIGO. 
463 
of nephritis, it occurs in the former disease either as a dull pain 
with lassitude and depression of spirits or as violent neuralgia. 
Headache which is constant, although it usually varies in degree, 
may be due to brain-tumor, and is one of the most important symp- 
toms to be noted in the diagnosis of a case in which such a lesion is 
suspected. The pain is often worse at night, and is usually more 
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 physician 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 snch 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, 
and 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 paral- 
ysis of the olfactory and oculomotor 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), anaes- 
thesia of the skin and muscles of the eyebrow, forehead, nose, and 464 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
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 oculo- 
motor, the pathetic, the abducens, and the fifth nerve are paralyzed. 
When tumors occur in the posterior fossa they cause paralysis of 
the trifacial, facial, auditory, glosso-pharyngeal, vagus, spinal acces- 
sory, and abducens, or, in other words, cause anaesthesia of the 
upper part of the face, facial paralysis, deafness, loss of taste, irreg- 
ular cardiac action, loss of power in sterno-mastoid and trapezius 
muscles, and internal squint. Tumors of the lenticular and cau- 
date nucleus, the interior portion of the thalamus, the corpus callo- 
sum, the fornix, choroid plexus, and of any part of the cerebellum 
except the vermiform process, may be present without any localiz- 
ing 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 the 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 
probably 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 be a bilateral lesion of the 
optic radiations of the occipital lobes, or in the centre of vision in 
the cortex. (See chapter on Eye.) 
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. HEADACHE AND VERTIGO. 
465 
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 depres- 
sion, sharp exacerbations 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 pain is usually diffuse, 
whereas in tumor or syphilitic gumma it may be localized. Optic 
neuritis, if present, makes the diagnosis of tumor certain. The 
chief symptoms of syphilitic arteritis are headache, giddiness, weak- 
ness 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 chronic 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 symptoms 
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 abscess 
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 the 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 466 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
patient, who may so far recover as to go back to his occupation, for 
it sometimes happens that a remission or latent period develops in 
the subacute forms of abscess. During this apparent remission, 
however, the temperature is rarely constantly normal, and the 
patient is anything 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, 
is probably due 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 
Fig. 195. 
Showing the communications existing between the superior longitudinal and lateral sinuses 
and the external veins, indicated in the figure by *. (Leube.) 
varying length give vent to sharp cries, evidently due to a sudden 
dart of pain. 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, HEADACHE AND VERTIGO. 
467 
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. Pulmonary signs of tuberculous 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 headache, malaise, languor, and remitting delirium are pres- 
ent. The symptoms of meningitis 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 longitudinal 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 oedematous through their close connections with the 
sinus through the emissary veins of Santorini, which escape from 
the skull by way of the parietal foramina. (Fig. 195.) In chil- 
dren there is usually in such cases bulging of the fontanelles and 
heaviness. Somnolence or delirium 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 continued 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 exophthalmos, 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 
chapters on 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 cavernous 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- 468 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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. 196). 
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. 
Fig. 196. 
Showing the communication existing between the lateral and cavernous sinuses and the 
external veins, indicated in the figure by *. (Leube.) 
Not only may cerebral thrombosis present symptoms resembling 
those of meningitis, but in addition those of cerebral abscess. 
Violent headache, with vertigo, staggering, and confusion of HEADACHE AND VERTIGO. 
469 
thought, followed by unconsciousness, may follow meningeal hemor- 
rhage due to disease of the bloodvessels, which are ruptured by 
some strain or by increased blood-pressure under the influence of 
stimulants. Hemiplegia or localized spasms may be present. The 
patient may survive several days in severe cases, or may recover if 
the hemorrhage is small; but usually a, hemorrhage large enough to 
cause marked symptoms is large enough to cause death. 
The individual affected by a meningeal hemorrhage will usually 
be plethoric, and, with the symptoms just described, will suffer from 
photophobia, extreme sensitiveness to the slightest noise, and pain 
radiating down the neck and trunk, which occurs in paroxysms. 
Localized paralysis is rarely present. 
The presence of severe vertical headache in a middle-aged person 
who is insane and who is a male may indicate pachymeningitis 
interna hemorrhagica (hsematoma of the dura); but usually the 
insane patient does not complain, and an ante-mortem diagnosis of 
this state is not made. 
Headache resulting from heat-stroke or thermic fever is usually 
the result of meningeal congestion or inflammation, and is one of 
the most annoying symptoms of convalescence. It is apt to be 
greatly increased by moving the head, and is relieved by venesection. 
The earlier stages of smallpox and pneumonia of the croupous 
type are often periods of violent headache, which symptom in the 
former instance decreases with the appearance of the rash, and in 
the case of croupous pneumonia so closely resembles the headache 
and associated symptoms of meningitis that a correct diagnosis, if 
the pulmonary signs are not sought for, may be impossible. In every 
case in which such symptoms occur the lungs should be examined. 
Headache is a constant symptom in many cases of typhoid fever 
in the early stages, but the peculiar tongue (see chapter on Tougue), 
the tendency to diarrhoea, the general systemic symptoms, and the 
facies of the patient will usually make its cause clear. More or less 
violent headache is often seen in measles, and depends probably to 
a great extent upon the engorgement of the nasal mucous membrane, 
or, in other words, has the same causative factor as has an acute 
“ cold in the head” in producing cephalalgia. 
Gruening is quoted by de Schweinitz as asserting that early 
morning headache is often due to nasal catarrh. This is, of course, 
only true if digestive troubles, which are often due to alcohol, and 
renal disorders are excluded. Severe morning headache, or dull 470 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
headache on just waking up may be due to nocturnal attacks of 
epilepsy, of which the patient is ignorant. If the tongue is bitten 
or the bed wet with urine, this diagnosis receives strong support. 
Violent headache is often present during the febrile stage of 
intermittent fever and is often a complicating symptom of fever of 
the remittent type. In this connection the physician should remem- 
ber that violent neuralgia of the supraorbital nerve is sometimes 
due to malarial poisoning, and is called “ brow ague.” 
Headache is often due to anaemia, whether it be the result of hem- 
orrhage or of the deficient formation of blood. The pain is usually 
frontal; there are often giddiness on movement, palpitation of the 
heart, a peculiar sensation in the head, and pallor of the skin. An 
examination of the blood will usually reveal the cause to be in this 
tissue. 
Headache sometimes results from valvular heart disease. Thus 
in mitral regurgitation it is often associated with vertigo, stupor, 
sleepiness, and, as night approaches, a mild delirium may come on. 
Its probable cause is congestion of the brain. 
Rarely intracranial aneurisms produce headache, and when they 
are of the diffuse miliary variety this symptom may be a prodromal 
one before an attack of apoplexy. Large aneurisms may, however, 
exist without severe headache, and the position of the pain in no 
way indicates the seat of the aneurism, save that aneurism of the 
basilar artery may cause occipital pain. Auscultation might pos- 
sibly reveal a murmur. 
Headache may also arise from disease of the skull bones, either 
caries, ostitis, or periostitis, which result from injury, infection by 
syphilis or other infecting cause, such as typhoid fever or tubercu- 
losis; but there is nothing diagnostic about the headache in these 
cases save that it is generally most severe in the area involved, 
and pressure over that part may elicit more or less pain or tender- 
ness. 
Violent neuralgia or shooting-headache may be produced by 
exposure to cold, with resulting inflammation of the nerve-sheath; 
by dental caries, and by middle-ear disease or disease iu the externaj 
auditory canal. 
When headache is present in the course of croupous pneumonia 
it often lasts till crisis, but in some cases ceases by the third day. 
The chest should always be carefully examined in all cases of severe 
headache with fever for signs of pulmonary disease. HEADACHE AND VERTIGO. 
471 
Vertigo. 
Vertigo is a condition in which the patient feels as if he were 
losing his equilibrium. Sometimes he feels as if he were whirling 
around from right to left or left to right, sometimes as if falling 
forward or backward, and sometimes he seems stationary, while all 
his surroundings whirl round or rise up to or fall away from him. 
Although vertigo is a symptom which in itself lacks danger, it always 
produces great discomfort, if not fear. Functional vertigo arises 
from the patient being subjected to a whirling motion, from rough 
sea-voyages, and from indigestion, deficient circulation, or excessive 
cerebral congestion. Often it is due to cerebral anaemia arising from 
excessive hemorrhage. When it arises from indigestion it is prob- 
ably 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 cerebel- 
lum, 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 mat 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, such 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 discovering any cause. Some authorities believe the disease to 
be due to a neurosis of the vasomotor nerves supplying the semi- 
circular 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 
cousciousnesss. CHAPTER III. 
COMA OR UNCONSCIOUSNESS. 
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 or 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 
poisonous doses of other narcotics. Thirdly, it may arise from 
autointoxication, as iu 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 symptom 
or sequel of hemorrhage into the brain (apoplexy), as the result of 
an epileptic attack, of 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 they are the cause of the coma. 
The coma of acute alcoholic poisoning is characterized by profound 
insensibility, great muscular relaxation, loss of the ocular reflexes, 
and great fulness of the bloodvessels of the neck and face in the 
early stages, but finally ghastly pallor of the face as the coma 
deepens on the approach of death. The skin is moist and warm at 
first, but afterward becomes cold. The pupils are usually moder- 
ately dilated; the pulse is rapid, at first strong, then more and more 
feeble; and the respiration stertorous and heavy. The sphincters, COMA OR UNCONSCIOUSNESS. 
473 
as a rule, are not relaxed, although they may be so iu rare cases. 
The bodily temperature iu severe alcoholic poisoning progressively 
falls from 1° to 6° F. below normal. 
Alcoholic coma is to be separated from that due to opium-poison- 
ing by the absence of the contracted pupils and slow breathing of 
the latter condition, in addition to the other symptoms named below 
in discussing that condition: from coma due to cranial fracture by 
the absence of any history or sign of head-injury';1 from chloral- 
poisoning by the history, the greater fall of body-temperature, and 
the great feebleness of the heart and respiration produced by chloral. 
It may be impossible to separate alcoholic poisoning from that of 
cannabis-indica-poisoning except for the fairly strong pulse gener- 
ally found in the latter condition, and the history of the patient 
having taken the hemp or complained of the peculiar sense of pro- 
longation of time before the coma came on. 
The symptoms accompanying the coma of opium-poisoning are 
heavy sleep, preceding the deep unconsciousness, during which the 
patient can usually be aroused by shouting in his ear or by violent 
shaking, but sinks back into slumber at once on being undisturbed. 
The face is suffused and reddened and may be finally distinctly 
cyanotic, and the breathing puffing and stertorous. When the pa- 
tient is awakened he breathes more rapidly, and for this reason the 
duskiness of the face disappears and the normal hue returns. Death 
never occurs iu the second stage of opium-poisoning from the poison 
alone; but, if disease is present, death may take place at this time. 
The pupils are contracted to pin-points. The third or fatal stage 
emerges from the second by a gradual process, so that no abrupt line 
of separation can be noted. The face becomes at first more cyanotic, 
then pale and livid; the respirations, which have been eight to ten 
in the minute, are now only four or five ; and, finally, such prolonged 
pauses occur that all hope of another respiration is lost by the attend- 
ant. While the slow breathing is at first deep, it now rapidly be- 
comes shallow, and relaxation is present to the greatest degree. The 
skin, previously dry, is wet with the sweat of death ; the patient is 
so deeply narcotized that nothing can arouse him, and he dies from 
respiratory failure, although the heart ceases almost simultaneously 
from the asphyxia. The pupils do not dilate in the third stage, 
except in the relaxation of death. 
1 The physician must not forget that a fall from alcoholism may result in cranial fracture. 474 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
In view of the frequency with which alcoholic and opium-poison- 
ing are confused, the following table is appended, which will be 
found of value in making a differential diagnosis as to the condition 
of the patient : 
Opium-poisoning and Alcoholism. 
Opium-poisoning. 
1. Pupils contracted. 
2. Respiration and pulse slow and full. 
3. Face suffused and cyanosed. 
4. Skin warmer than in alcoholic poisoning. 
5. Pulse slow, strong, and full till late in 
poisoning. 
Alcoholism. 
1. Pupils normal or dilated. 
2. Respiration nearly normal; pulse rapid, 
and finally feeble. 
3. Face may be pallid. 
4. Skin cool, perhaps moist. 
5. Pulse rapid, at first strong, then weak. 
There is scarcely any difference as to consciousness in these two 
conditions. 
When a poisonous dose of chloral is taken by man the person 
soon falls asleep and then sinks into a deep coma. The respirations 
become at first slow and labored, then shallow and feeble. The 
pulse, at first perhaps a little slowed, soon becomes rapid, thready, 
and shuttle-like, and is finally lost at the wrist. The face is white 
and livid, the forehead and the hands covered with a cold sweat, and 
the pupils, which are at first contracted, soon become widely dilated. 
Absolute muscular relaxation is present, and it is impossible to 
arouse the patient. 
The coma of uraemia may come on gradually, but most com- 
monly its onset is sudden and follows a uraemic convulsion. It 
possesses no diagnostic sign or signs which clearly separate it from 
the unconsciousness or coma following epileptic attacks, and, as the 
uraemic convulsion is often typically epileptic in character, the 
differential diagnosis is very difficult. An examination of the urine, 
if it can be obtained by the catheter or otherwise, will indicate, but 
not prove, the presence of uraemia if albumin be found in either 
large or small amounts, and the presence of very little urine in the 
bladder, indicating anuria, may be of some diagnostic significance. 
On the other hand, if the uraemia be due to chronic contracted kidney, 
the urine may be plentiful, the albumin scanty, but the low specific 
gravity be noteworthy. The pulse is usually very slow, often but 
forty to fifty, but the arterial tension is high, so that the artery feels 
hard aud unyielding. The temperature of the body is usually very 
low in those severe cases which are free from convulsions and have 
a progressively downward course; so low a point as 91° to 95° being 
sometimes reached, at which time the patient is usually moribund from COMA OR UNCONSCIOUSNESS. 
475 
collapse. When convulsions are present the temperature may rise as 
high as 108°, and there may be in some cases a severe chill, followed 
by fever, and this again by collapse. The respiration is nearly 
always very deep, and sometimes very much quickened. If a pre- 
ceding history of prolonged nausea, attacks of colliquative diarrhoea, 
and vertiginous symptoms can be discovered as symptoms leading 
up to unconsciousness, these will add to the array of uraemic prob- 
abilities. The coma of uraemia is not necessarily a fatal symptom. 
Even in very severe cases remarkable recoveries sometimes occur. 
Coma resulting from diabetes mellitus is of far graver import, as 
it commonly terminates the patient’s life. There may not be any 
prodromes, and there may not be any history of au exciting 
cause for the coma. Sometimes it is provoked by severe exercise 
or great mental strain or emotion. When unconsciousness does 
not come on at once the patient, after suffering from nausea, 
headache, and respiratory oppression, suddenly becomes anxious, 
delirious and violent, then drowsy and deeply comatose. The pulse 
is not particularly noteworthy, but is usually full and not very tense. 
The respirations are deep and often very noisy, but at about the 
normal rate, although sometimes they may be rapid in the con- 
dition called diabetic dyspnoea. The body-temperature falls very 
greatly, even below 90° F. The respiratory changes and those in 
temperature may, therefore, be very much like those of uraemia; 
but in association with the coma of diabetes mellitus there are two 
pathognomonic symptoms: first, the sweet odor of the breath, 
which smells like the aroma of a pear or an apple, or a faint odor of 
chloroform ; and, second, the presence of sugar in the urine, which 
secretion becomes dark red on the addition of chloride of iron. 
Ordinary coma is rare in typhoid fever ; it is usually replaced by 
what is called coma-vigil, in which the patient, in a semi-uncon- 
scious state, keeps muttering day or night. It is a grave sign. 
The coma of acute yellow atrophy of the liver is generally preceded 
by headache, nausea, anorexia, and perhaps fever, followed by 
nervous excitement or restlessness, and then mental hebetude, which 
is often accompanied by a noisy delirium which may amount to 
mania. Finally, after several days, coma comes on and gradually 
becomes more and more profound till death takes place. Some of 
these symptoms resemble those of uraemia or diabetic poisoning, but 
the coma of acute yellow atrophy has in addition these characteristic 
signs, namely, jaundice, bile-stained urine, marked shrinking of the 476 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
liver-dulness, enlargement of the spleen, and hemorrhages into the 
skin, or these effusions may take place into the bowels and stomach. 
The urine is singularly free from urea, but contains leucin and 
tyrosin in large amounts. (See chapter on Urine for description of 
leucin and tyrosin crystals.) 
The coma of apoplexy may be sudden or gradual in its onset; 
generally it rapidly appears after the first symptoms of cerebral 
hemorrhage develop. The loss of consciousness may be partial or 
absolute, generally the latter if the leakage from a ruptured vessel 
be great. The respirations become stertorous, generally more rapid 
than normal, and, if a fatal result is in prospect, are rhythmically 
irregular; that is, they are now very slow, then gain in speed gradu- 
ally till they become very fast, then the speed and vigor gradually fall 
till they are as feeble and slow as before (Cheyne-Stokes respiration). 
The history of preceding paralysis on one side of the body, or the 
absence of this loss of power if it can be demonstrated, the unequal 
pupils, the drawing of the face away from the paralyzed side, a 
strong, bounding pulse, and generally raised temperature complete the 
clinical picture of the coma of cerebral hemorrhage. If death does 
not ensue, consciousness may return, and the patient progress to re- 
covery ; but sometimes after several days of apparent convalescence 
a secondary fatal irritative coma comes on, associated with high 
fever. This is usually of ominous portent and is readily recognized 
because of the history. (See chapters on the Arms and on the Legs 
and on Hemiplegia.) 
The coma of cerebral hemorrhage is unfortunately often taken 
for acute alcoholism, particularly as the latter state often produces 
the hemorrhage. The following table is designed to separate them: 
Alcoholism. 
1. Pulse rapid, compressible, and weak.. 
2. Skin moist, or relaxed and cool. 
3. Bodily temperature lowered. 
4. Pupils equally contracted or dilated ; gen- 
erally dilated. 
5. No hemiplegia. 
6. Breathing not so stertorous nor so one-sided 
in lips. 
7. No facial palsy. 
8. Unconsciousness may not be complete. 
Acute Alcoholism and Apoplexy. 
Cerebral Hemorrhage. 
1. Pulse apt to be strong and slow. 
2. Skin hot or dry. 
3. Bodily temperature raised. 
4. Pupils unequal. 
5. Hemiplegia; one side tossed, the other 
remaining motionless. 
6. Respiration stertorous, the lips being 
inflated on one side on expiration. 
7. Facial palsy. 
8. Unconsciousness complete. 
The smell of alcohol in the breath is no guide, as acute alcoholism 
may have caused the rupture of a cerebral bloodvessel. COMA OB UNCONSCIOUSNESS. 
477 
Coma due to cerebral softening, following embolism or thrombosis, 
has no signs other than those discussed in 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, nystagamus, and lockjaw, 
stiffness of the neck, and clonic spasms. If the caveruous sinus is 
thrombosed, there will generally be found stasis of the veins in the 
eye, which means retinal congestion. The eyeball may be protruded, 
the eyelids swollen, and perhaps loss of function in the oculomotor 
nerve may be present, causing ptosis, and, if the abducens is affected, 
causing internal strabismus from paralysis of the 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 ob- 
structed, 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 
(pachymeningitis interna hemorrhagica) is peculiar in the fact that 
its onset is usually very slow, and the sigus 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. Sudden unconsciousness with hemi- 
plegia and vomiting may also come on in Raynaud’s disease. 
Coma from cerebral. abscess is accompanied by symptoms closely 
resembling those of acute meningitis. The patient is dull and de- 
lirious ; has headache, fever, and often has a hyperpyrexia. The 
sensibility becomes less and less, and deepens into the coma which 
ends in death if relief is not given. The localizing symptoms of 
paralysis may indicate that a lesion is in a certain part of the brain ; 
but generally these signs are absent, because cerebral abscess is usu- 
ally 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. 478 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
The coma of purulent lepto-meningitis resembles that of abscess in 
many of its associated symptoms, but the intense headache, the rapid 
development of delirium and unconsciousness, the stiffness of the 
neck, the optic neuritis and disturbed movements of the ocular mus- 
cles, combined 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 development of coma by produc- 
ing hemorrhage, embolism, arteritis, tumor of the brain, or almost 
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 proba- 
bility of syphilis as a cause very great. Scars on the skin (see chap- 
ter on Skin) may show specific taint. 
When coma results from general paralysis 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 with 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 dis- 
ease, and it often develops very suddenly. 
Heatstroke produces coma as one of its almost constant symptoms. 
The history of exposure to heat and the hyperpyrexia are the two 
diagnostic points of importance. (See Fever.) Sudden uncon- 
sciousness may arise from heart-failure due to disease or fright ; we COMA OB UNCONSCIOUSNESS. 
479 
call this fainting. Frequent attacks of this character 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 renal difficulty. Sometimes sudden uncon- 
sciousness will be due to petit mal or minor epilepsy. CHAPTER IV.1 
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 those 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 ex- 
citation of the motor tracts in the spinal cord. The clonic variety 
of convulsions are represented by idiopathic, traumatic, reflex, and 
syphilitic 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 suc- 
cessfully the epileptic 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 commouly it is sensory, and is as if a cloud or wave was 
passing up the body to the head. As the sensation reaches the 
head the patient mav utter the peculiar epileptic cry or sigh, and 
with this sound the patient becomes rigid from momentary tonic 
spasm of the muscles. This spasm now relaxes for an instant, and 
then the patient’s muscles pass into a state of alternate relaxation 
and contraction which throws the patient’s body from one place to 
another. 
The primary tonic spasm of the face produces risus sardonicus in 
1 For local spasms, see chapters dealing with Face and Head, Hands and Arms, Feet and 
Legs. CONVULSIONS OB GENERAL SPASMS. 
481 
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 are strongly flexed at the elbows, the 
hands 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 overcoming 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 clonic spasms, already described, which are 
ushered in by more or less violent tossings, but whose onset is fore- 
warned by peculiar vibratory thrills which run through all the 
affected muscles. The eyelids tremble, the body changes its posi- 
tion ever so slightly, and then, as if the vibrations gained greater 
and greater power with each moment, the fibrillary tremors give 
way to muscular contraction. 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 protruded and drawn back, and, as a consequence, is 
often caught between the teeth and lacerated. The excessive move- 
ments 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 move- 
ments 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 constantly borne in mind that the pro- 
longation 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 oxygenated, 
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, 482 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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- 
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 separate 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. Jacksonian 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 convulsion 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 in- 
volved, or, if not this, the attack is, at most, only unilateral. 
Further than this, it is always associated with the symptoms 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 should be remembered that hemi- 
plegia often follows ordinary idiopathic epilepsies; 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 epi- 
lepsy, being produced by the convulsion. In a considerable number 
of cases of epilepsy it will be found that the convulsions succeeded CONVULSIONS OR GENERAL SPASMS. 
483 
an attack of paralysis, which was sadden in onset and possessed the 
characteristics of vascular rapture. 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 patient with the convulsive 
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 called idiopathic 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 rheu- 
matism, syphilis, and puerperal sepsis may all produce a softening 
of the cortex, with au epileptic state following the paralysis. 
We can 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, and 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 hypoth- 
esis. Indeed, they tend to overcome 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, 
and repeated post-mortem examinations have confirmed the possi- 
bility of this occurrence. 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 a 
male child. A priori reasoning would seem to show, therefore, that 
the heads of male children would, accordingly, have instruments 
applied most frequently, and consequently that infantile cerebral 
trouble would be the result more commonly in males than in 484 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
females ; but, as has been said, this conclusion is contradicted by 
the facts. Another symptom of great interest is that the paralysis 
in the 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 an interval may occur between the attack and the subsequent 
paroxysm. The chronic recurrent fits date from the onset in about 
one-third the cases, but it is not uncommon for the paralysis to oc- 
cur in infancy and the epilepsy to begin at puberty. It would seem 
that cells injured in early life may lay undisturbed till the increased 
demands 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 
Jacksonian 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 uinety-seven suffered from it. 
In the eighty cases collected by Gaudard eleven children had hemi- 
plegic epilepsy, and sixty-six children out of one hundred cases col- 
lected by Walleuburg 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 affections 
which afflict those who may be so unfortunate as to contract this dis- 
ease. There can be no doubt that syphilis produces an enormous 
amount of epilepsy in adults, and the presence of epilepsy in a 
person in whom the slightest suspicion of a specific taint exists 
should cause him to be instantly placed under antisyphilitic treat- 
ment. That this is true is evidenced by the statements of the fore- 
most neurologists the world has ever known, for we find no less 
noted a writer than Charcot stating that epilepsy is the most fre- 
quent manifestation of cerebral syphilis, and the equally eminent CONVULSIONS OR GENERAL SPASMS. 
485 
syphilographer, Fournier, lias insisted most strongly on this point, 
as have also Bravis and M. Lagneau. In England, Hughlings- 
Jackson, Broadbent, Todd, and Buzzard have promulgated this 
doctrine, and in America Weir Mitchell, Spitzka, Wood, and 
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. 
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 symp- 
toms of headache in forty-five males and thirty-eight females, or 
70.30 per cent, of them all. 
In fifty-nine patients prtucordial 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 and eight females suffered 
from pain in the temples, while nine males and 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 exacer- 
bated toward nightfall or during the night, generally getting worse 
until the convulsion 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, never- 
theless, baffles the descriptions that one would like to give of it. 
Once 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 live- 
liness with an iron heel. If spoken to, the man, who has been 
resting his head on the hands, will either answer slowly and pain- 
fully in monosyllables, or, gradually raising the face to that of the 
questioner, give an answer, and once more return to his former 486 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
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 generally 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- 
toms, slight loss of memory, unwonted slowness of speech, general 
lassitude, and especially a lack of willingness to make mental 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 ex- 
amined, 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 
hysterical, are in the syphilitic almost pathognomonic of brain- 
involvement—a momentary weakness in one arm ; a slight drawing 
of the face to one side, which disappears in a few hours ; a tem- 
porary dragging of the toe ; a partial aphasia which appears and 
disappears ; a squint which to-morrow leaves no trace behind it. A 
symptom which has been asserted as being frequent in this disease is 
the common occurrence of nocturnal attacks; indeed, cases have 
been reported by Charcot and Lagueau 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- 
turbances with incomplete palsies, which, curiously enough, rarely 
involve the crauial nerves, as has been particularly noted by Heub- 
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 CONVULSIONS OR GENERAL SPASMS. 
487 
itself is concerned, it is not possible to separate them. If, however, 
we can obtain any history, the matter becomes much more simple. 
It is characteristic of syphilis to have severe darting or aching pains 
in the tibiae, particularly at night; and it is also characteristic of 
syphilitic epilepsy to have severe frontal headache before the 
attack, while in idiopathic epilepsy this pain generally follows the 
seizure. 
Fournier, in his lectures on epilepsy, in the Louvain, in Paris, in 
1875, gave a summary of his views as follows : 
1. In the syphilitic epilepsy there is nearly always absence of the 
shrill cry at the onset, so characteristic of the idiopathic variety. 
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 success, 
is the administration of iodide of potassium in large doses. If the 
epilepsy be syphilitic, it will rapidly become less severe, and enor- 
mous 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 involved, 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 patheticus nerves. 
The diagnosis of syphilitic epilepsy from the idiopathic form is of 
the utmost importance, since the ultimate result must be largely 
governed 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 par- 
oxysms, it will generally yield to specific remedies. Cyanosis is 488 
THE manifestation of disease by symptoms. 
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 ex- 
anthem 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 
manifestly impossible. 
Alcoholic epilepsy consists of two distinct varieties produced 
by overindulgence in intoxicating drinks. In one of these the con- 
vulsions 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 originate 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 ac- 
companied 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 con- 
vulsions 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 convul- 
sions. 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 dis- 
turbances result rather in suicidal than homicidal tendencies, which 
is just the reverse of the insanity following simple epilepsy. It is 
very important that the reader remember that alcoholism in produc- 
ing epilepsy very frequently produces a permanent nervous disorder 
which the withdrawal of the poison will not remove. 
The symptoms of an uraemic 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 re- CONVULSIONS OR GENERAL SPASMS. 
489 
suit in au 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 phy- 
sician to bear in mind that certain drugs when taken in poisonous 
doses produce well-developed epileptic convulsions. This is particu- 
larly true of the so-called cardiac sedatives or depressants, such as 
aconite, veratrum viride, sabadilla, hydrocyanic acid, and one or two 
similar substances. Suffice it to say that experimental researches 
seem to prove 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 who 
has had for a few days a feeling of weight in the head, or headache, 
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 pre- 
ceded by any aura whatever, but previous to the headache, already 
mentioned, the patient may have had amaurosis, and ophthalmo- 
scopic 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. 
Malaria] epilepsy is an uncommon disorder, even in countries and 
regions which are notoriously malarial, but it has undoubtedly oc- 
curred, 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 
region, 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 MANIFESTATION OF DISEASE BY SYMPTOMS. 
490 
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. Below 
are arranged all these disorders in a table, which briefly and suc- 
cinctly shows the different points between them, although, of neces- 
sity, it is somewhat arbitrary on account of the lack of space. 
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,1 etc. 
Signs. 
Epilepsy. 
Hysteria. 
Uraemia. 
Petit mal. 
Alcoholic 
epilepsy. 
Tetanus. 
Syncope. 
Apparent 
cause. 
None. 
Emotion. 
None. 
None. 
None. 
None. 
Mental 
shock. 
Aura or 
Generally 
Globus 
Headache, 
Faintness 
Tremors. 
Nervous- 
Not so well 
prodro- 
mata. 
present, 
but short. 
hytericus; 
palpi tat’n ; 
choking. 
vomiting, 
and dys- 
pepsia. 
and dim- 
ness of 
vision. 
ness. 
defined 
as in epi- 
lepsy. 
Onset. 
Sudden. 
Often gra- 
dual. 
Often gra- 
dual. 
Sudden. 
Sudden or 
gradual. 
Gradual; 
begins 
in jaw. 
Sudden or 
gradual. 
Scream. 
At onset 
and sud- 
den. 
During 
attack. 
Frequently 
none. 
Frequently 
none. 
May or may 
not be 
present. 
None. 
None. 
Convul- 
sion. 
First tonic, 
then 
clonic. 
Rigidity 
more pro- 
nounced, 
with more 
aching. 
Rigidity 
generally 
absent. 
Ko rigidity. 
Movements 
more clonic 
than tonic. 
Always 
tonic. 
None. 
Biting. 
Tongue. 
People, 
tongue, 
lips, and 
hands. 
Tongue. 
None. 
Rarely. 
None. 
None. 
Micturi- 
tion. 
Frequent. 
Never. 
Never. 
Rarely, ex- 
cept when 
bladder is 
affected. 
Rarely. 
Some- 
times. 
Never. 
Defecation. 
Occasion- 
ally. 
Never. 
Never. 
Never. 
Rarely. 
Rarely. 
Never. 
Talking. 
Never. 
Frequent. 
Muttering. 
Never. 
Never. 
Never. 
None. 
Duration. 
A few 
minutes. 
Generally 
many 
minutes. 
From a 
minute 
to hours. 
Momen- 
tary. 
May be 
prolonged.* 
Hours. 
Indefinite 
time. 
Conscious- 
ness. 
Lost. 
Generally 
preserved. 
Lost. 
Not lost 
always, but 
clouded. 
Lost. 
Pre- 
served. 
Lost. 
Termina- 
Spontane- 
May be in- 
Spontane- 
Spontane- 
Spontane- 
Spon- 
Gradual, 
tion. 
ous. 
duced by 
shock. 
OUS. 
OUS. 
OUS. 
taneous. 
with no 
somno- 
lence. 
1 This table is taken from the author’s essay on Epilepsy, the prize essay of the Royal 
Academy of Medicine in Belgium, January, 1889. CONVULSIONS OR GENERAL SPASMS. 
491 
The very irregularity of true epilepsy makes it extremely difficult 
to give clear and well-defined outlines of it against auother disease, 
particularly when we remember that epilepsy and hysteria often go 
hand in hand. 
By far the most important differential point between the two dis- 
orders just named, when not complicated with still another disease, 
is the character of the movements. As already pointed out, in epi- 
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 
frequently there is prolonged tonic contraction of the muscles, 
giving rise to the assumption of positions which bear more or less 
resemblance to normal attitudes. In hysteria, also, consciousness is 
impaired sometimes, but never so completely as in true epilepsy. 
Indeed, most commonly the individual knows all that goes on 
around her, for, while she may give no sign of consciousness by 
words or looks during the attack, she may afterward be able to 
narrate all that has occurred. Less commonly, however, a condi- 
tion known as automatic consciousness exists, in which, during the 
paroxysm, the patient understands all that is said, but forgets every- 
thing on the return to quietness 
The fact that the patient is a female cannot be regarded as affirm- 
ative evidence of hysteria in the least, but the condition occurring 
in a male may be taken as fairly positive evidence of its being epi- 
lepsy ; 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 
possess 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 surrounding furniture. 
Another 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 re- 
membered 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 mayr show a second tonic stage. This can 
be separated, however, by the fact that it is followed by clonic move- 
ments, whereas the secondary tonic stage of hysteria is usually fol- 
lowed by relaxation and temporary recovery. 492 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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, pain, or entreaty, may seem to be 
gazing at some object very far off. In some very well developed 
cases the expression of pleasure is followed by a look of paiu, with 
painful movements, or an appearance of intense voluptuous entreaty, 
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 attend- 
ants or herself. Such is the history of a fully developed attack of 
hysteria. 
Hysterical convulsions in their fully developed form are com- 
paratively 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 upon the fact that in both cases 
he has given only the most typical characteristics of the dis- 
eases, 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 
attacks 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 CONVULSIONS OB GENERAL SPASMS. 
493 
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 breath 
hysteria. Very commonly areas of anaesthesia and hypersesthesia 
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 unilateral, 
and may extend entirely over one-half of the body, the line of de- 
marcation of the anaesthesia or hypersesthesia from the sound area 
being clearly aud abruptly defined, generally at the median line of 
the front and back of the trunk. (See chapter on the Skin; that 
part dealing with anaesthesia.) 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, and, 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 
Salpetriere. 
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. 
Hyster o-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 delirium, may be 
hallucinations. 
Mental power preserved. 
Emotional attitudes. 
A very useful differential point, strongly insisted upon by Charcot 
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- 494 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 uraemia is much more readily 
made, for there is usually a previous history of symptoms point- 
ing to renal trouble, as, for example, some oedema, or somnolence, 
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 uraemia 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 vomit- 
ing, occasional attacks of asthma, and failure of general health is 
found to be present, the correct diagnosis probably will be uraemia. 
The preservation 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, conscious- 
ness 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 the 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; and, in a large number of cases of chronic contracted 
kidney, 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 administer iodide of potassium and study its eliminations. It is 
affirmed that, after a full dose, this drug can in an hour be readily 
recognized in the urine by adding nitric acid and then starch; but 
when contracted kidney exists the iodide fails to appear or is ex- 
creted only in very small quantities. The temperature of the body 
may also be used to differentiate between uraemia and epilepsy. In CONVULSIONS OB GENERAL SPASMS. 
495 
1865 Kien called attention to the fact that even when nrsemic con- 
vulsions are most violent they are accompanied by a fall of temper- 
ature of as marked a character as the rise noted in respect to epi- 
lepsy. Since then this has been confirmed by Roberts, Hirtz, 
Hutchinson, Charcot, Bourneville, and Teinurier. 
The diagnosis between 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 
during the puerperal state. This is not a place for the discussion of 
the identity of uraemia and puerperal eclampsia, although we believe 
that uraemia is generally responsible for the nervous disturbance. If 
the convulsions are uraemic, the temperature, according to the in- 
vestigators just quoted, should fall; and according to Bourneville, 
puerperal 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 uraemia. 
It is unnecessary to state once more that petit mal is but a variety 
or modification of haut 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 
paitent, 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 be- 
tween the symptoms applicable to all cases. Generally one seizure 
of alcoholic epilepsy follows the other every few minutes until three 
or four have taken place, when the paroxysms cease. It is-not to 496 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 remembered 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 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 determining 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, ex- 
ceedingly valuable evidence, but it should not be forgotten that in 
many cases this history is wanting. Thus, the poison may be de- 
rived from a hair-dye, or cosmetic, or from water which contains 
lead from pipes, or from an endless line of similar hidden and ob- 
scure sources. Amaurosis may be present in some cases, or optic 
neuritis with atrophy may occur. Where double wrist-drop is pres- 
ent the diagnosis is much more easy. 
It is exceedingly important to differentiate between those convul- 
sions which arise from the uraemia 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, but there are some points of difference. In the first place, 
the convulsion of uraemia is, as a general rule, not so violent in its CONVULSIONS OR GENERAL SPASMS. 
497 
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 urine 
in uraemic convulsions will show a decreased amount of urates in 
proportion to the quantity of urine passed, while in plumbic epilepsy 
just the reverse will be true, unless the kidneys are affected pari 
passu with the cerebrum. If albumin be present, uraemia 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, 
which may or may not be the cause of the nervous disturbance. 
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; aud 
it is related of Fournier that, after his expressing an opinion that 
a man could always tell them apart, one of his assistants threw him- 
self to the floor on his next visit in a pretended attack, whereupon 
Fournier, completely misled, exclaimed, “ Poor M—; he is epi- 
leptic ! ” upon which the assistant, smiling, arose to his feet and 
confuted the statement. 
Very serious injuries are sometimes submitted to by these persons 
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 bystander 
can readily straighten the thumbs out, aud that they remain so ; 
whereas in epilepsy they instantly become flexed again. 
Suggestions, as to movements, are sometimes followed by maling- 
erers, 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. 
Convulsions appearing in infants or young children may result from 
injuries to the brain in birth, from the presence of growths, or from 
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 iritation produced by teething in children eu- 498 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
tirely free from rickets and from gastro-intestiual 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 treat- 
ment. 
There is one variety of infantile convulsive seizure due to menin- 
gitis which is in itself often tubercular and associated with retraction 
of the head and squint ; and another variety in which the symp- 
toms very closely resemble those due to actual meningeal lesions, but 
in reality are quite independent of them. This condition 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 somnolent or comatose, and 
fever may or may not be present. The prognosis in the first class of 
cases is very bad. In the second class it is bad enough, but recovery 
quite often occurs if the treatment generally employed in the first 
class is set aside and a highly nutritious and supporting treatment is 
instituted. 
If a child 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 later 
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 
stigmata, or the signs manifested bv the skin, and when examination CONVULSIONS OR GENERAL SPASMS. 
499 
can be made between attacks, of the eyes (see chapters on Skin and 
on 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 
history 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 
swallowed. 
The differential diagnosis between strychnine-poisoning and 
hysterical 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 disease. 
The history of the patient, if obtainable, will throw much light on 
the case and aid very materially in the separation of the two condi- 
tions. 
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 ex- 
tended, 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 
“ Trousseau’s symptom.” The pressure must be applied for several 
minutes in some cases, and the best place to apply it is the bicipital 
sulcus or the crural sulcus. Sometimes pressure on the brachial 
plexus or on the popliteal space will be provocative of an attack. 
It is not a constant symptom, but pathognomonic if found. Another 
equally useful diagnostic sign is called Chvostek’s facial symptom. 
This results from the fact that the facial muscles are irritable, so 
that when they are tapped by the finger-tip, or a hammer, contrac- 
tion results. The tapping is usually applied over the zygomatic 
arch in its anterior portion, and this will result in a spasm of the 
upper lid of the eye and the alee nasi. In other cases stroking 
the area over the parotid will have the same effect. The muscles in 
tetany also have an increased electrical excitability. (Erb’s Symp- 
tom.) 
It is worthy of note that both Trousseau’s and Chvostek’s symp- 500 
THE manifestation of disease by symptoms. 
toms are sometimes met with in rachitic children, particularly if 
they have craniotabes (see chapter on the Head). Laryngismus 
stridulus will often be found associated with tetany and rickets. 
(See chapter on the Hauds and Arms; accoucher’s hand.) 
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 hydatid 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. 
Obviously 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 whooping-cough at the time 
of the paroxysm. 
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 Hands and 
Arms 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 condition is prob- 
ably chorea minor. Often the speech is seriously disturbed by 
reason of the choreic movements of the lips and tongue or jaws, CONVULSIONS OR GENERAL SPASMS. 
501 
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 be readily recognized 
in most cases; but it sometimes has to be separated from dissemi- 
nated sclerosis, progressive muscular atrophy, hysteria, and Fried- 
reich’s ataxia. The movements in disseminated sclerosis are, how- 
ever, fine muscular tremors, instead of minor jerking movements; 
and there are present nystagmus and scanning speech in sclerosis, 
but not in chorea. Again, in progressive muscular atrophy there 
is fibrillary muscular tremor, but not twitching of a marked form, 
and the 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 hysteria (see chapters ou Skin and on 
Eyes) renders a diagnosis of the latter condition easy. 
Friedreich’s ataxia is to be separated from chorea by the scanning 
speech, scoliosis, slow inco-ordinate movements and the family 
history of the disease. 
Rarely, when there is some paresis with chorea, the patient may 
present symptoms of acute poliomyelitis; but the paralysis in the 
latter affection is more marked, and there are no movements in the 
affected muscles, such as occur in chorea. 
Chorea insaniens 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 
(“ Parkinsonian visage ”). Senile trembling is usually an affection 
limited to the head, and consists in a tremor and not in marked 
twitching. (See chapter on Hands and Arms, part on Tremors.) 
A rare form of chorea has been called Huntington? s chorea. It 
occurs in adults about the age of thirty to forty years. It is heredi- 
tary ; that is, there is generally a history of the same trouble in the 
ancestors of the patient, and finally as it progresses psychical dis- 502 
THE manifestation of bisea.se by symptoms. 
turbances 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 infec- 
tion involves the legs a characteristic gait is developed of a dancing 
or “ hop, skip, and jump” character. Sometimes, earlv in the 
malady, the movements can be controlled by the will. The face 
passes through slowly formed grimaces, and the gait may be stag- 
gering. The speech becomes indistinct, and enunciation is not clear. 
Finally, dementia closes the scene. The movements of Hunting- 
ton’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 
abdominal muscles, producing the so-called salaam convulsions or 
chorea major. 
A still more rare malady is electric chorea or “ Dubinins 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 
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 
movement 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 to four 
to 120 per minute, but are generally about 50 per minute. The 
symmetrical 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 CONVULSIONS OR GENERAL SPASMS. 
503 
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 dis- 
ease 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 twitchings. 
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 11 saltatoric spasm” to those cases 
which possess no imitative features. In such cases the disease is far 
more moderate in its manifestations. 
Quite 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 
movements, but ultimately develop a tonic spasm, so that walking 
is at first almost impossible, but the limbs limber up on exercise. 
This is a rare affection, called Thomsen’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 V. 
VOMITING, REGURGITATION, AND THE CHARACTER OF 
THE VOMIT. 
Due to uraemia—Cerebral lesions—Intestinal obstruction—Peritonitis—Cholera— 
Gastric disease—Hepatic disease—Poisonous—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 uraemia the vomiting sometimes encountered is the result of irrita- 
tion of the centre by some unknown poison, and when apomorphine 
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 ab- 
dominal disorders 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 uraemia, 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, peri- 
tonitis, nephritic colic, hepatic jaundice, hepatic colic, in cholera, 
yellow fever, and a host of other ailments. Sometimes the onset of 
one of the acute infectious diseases of childhood is characterized by 
vomiting. Not infrequently this symptom associated with diarrhoea 
masks the presence of the real cause of the attack, as in some cases 
of croupous pneumonia. 
The vomiting of uraemia 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 consid- 
ered to be suffering from some slight indiscretion in diet. Its associa- VOMITING. 
505 
tion either as a preceding, concomitant, or consequent symptom of con- 
vulsions renders a diagnosis of uraemia probable, while a history of 
uraemic amaurosis, colliquative diarrhoea, and failure of the general 
health will be very important points in reaching a decision. No 
pathognomonic symptom of uraemic vomiting exists unless we con- 
sider the urinary evidence a symptom, but in some cases the vomited 
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. Uraemic 
vomiting 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 ex- 
amination 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 
vomiting due to cerebral tumor is generally preceded by the charac- 
teristic severe and constant headache, vertigo, a slow pulse, impaired 
memory, and sometimes by epileptiform convulsions. Further than 
this, the important diagnostic ocular symptom called u choked disk ” 
of the optic nerve is to be sought for, and if found is of great posi- 
tive value. Tumor of the brain, if near the base, often causes, too, 
involvement of the various cranial nerves. The vomiting of cere- 
bral tumor is independeut of taking food, and commonly comes on 
early in the morning, thereby differing from some of the forms of 
vomiting due to gastric disorder. The vomiting arising from cere- 
bral abscess has symptoms precisely like those just named, so that a 
differential diagnosis 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 cranial 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 506 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
may be localized. Vomiting sometimes results from profound cere- 
bral ancemia of au acute type due to hemorrhage, iu faiuting or in 
chronic anaemia, as in chlorosis. Generally, however, the symptom 
is only a constant nausea. The presence of great pallor and other 
evidences of anaemia aid in the diagnosis, but it must not be for- 
gotten that some severe anaemias are accompanied by febrile move- 
ment and by marked choked disk, which should not mislead the 
physician into a diagnosis 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, ou ophthalmoscopic examination, with 
disordered vision. 
The vomiting of meningitis is quite 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 the spine ; 
by the rigidity of the dorsal muscle, 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, slowly 
reacting pupils, which may be unequal, nystagmus, 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 physical 
signs of tuberculosis of the lungs, and, very important, the 
peculiarly severe dyspnoea, for which no adequate cause can be dis- 
covered on physical examination, all point to the general infection. 
If a skilful examination of the eye can be made with the ophthal- 
moscope, 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. Iu some of these conditions vomiting is of little impor- 
tance, except for its gravity if the patient is exhausted; in other 
words, it is simply a disagreeable symptom. In others the symp- 
tom vomiting is of considerable diagnostic value as indicating the VOMITING. 
507 
grave mischief which produces it. One of the most important of 
the latter conditions is intestinal obstruction, whether it arises from 
intussusception, constrictions by bands, volvulus, or impactions. 
In intussusception vomiting is practically a constant symptom, oc- 
curring with the sudden pain, or, at times, even preceding it. In 
children it continues till shortly before death, and is rarely feculent. 
In the adult, and in the chronic form, there may be complete 
absence of vomiting, though this is certainly exceedingly rare. 
Leichtenstern takes exception to the statement that the seat of ob- 
struction 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 the 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 con- 
tinues. This is followed by a return of the paiu, 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 intervals 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 re- 
lieve the pain. 
Blood-stained mucous evacuations are a symptom of intestinal 
obstruction which, in children, is rarely wanting. 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 de- 
veloped, of blood and mucus, and is usually exceediugly 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 508 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
necrosed intussusception. Where this slough is extensive it may be 
lodged in a lower portion of the bowel and cause fatal obstruction.1 
In connection with the muco-sanguinolent evacuations the tenes- 
mus or straining is a symptom so common that it is of some diag- 
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 com- 
plete obstruction. Brinton has shown that this symptom is seldom 
developed except in the ileo-csecal and colon invaginations. 
A much rarer condition, and one which Leichtenstern ascribes to 
the secondary effect of intense teuesmus, 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 parietes 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 left 
iliac region, or by the finger passed into the anus. The ileo-caecal 
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 elud- 
ing the most careful search. Duchaussoy 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 become as well marked as in obstruction from any 
other cause. 
Dance calls attention to an inequality in the shape of the abdo- 
men 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 observation. 
In the chronic form of invagination the symptoms are less violent 
in onset; there may be nothing more characteristic of the attack 
than recurring paroxysms of pain, meteorism, and obstruction, with 
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. VOMITING. 
509 
symptoms of intestinal stricture constantly manifesting themselves. 
These eases 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 upon which a diagnosis of vomiting 
from intussusception is to be based are the acute onset of colicky 
pain, and its intermittent character; passages from the bowels con- 
taining blood and mucus; the presence of 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 um- 
bilicus, 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 passages 
representing the contents of the bowel below the seat of obstruction; 
after that the constipation is absolute, not even flatus passing by the 510 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
anus. Treves has suggested that the evacuations sometimes observed 
toward the termination of the case, and not due to the relief of ob- 
struction, 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 sugges- 
tive as 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 symp- 
tom to locate the obstruction with some certainty. 
The violeut 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 
traumatism would respectively assign an adherent vermiform ap- 
pendix, peritoneal bands, or rents in the omentum or mesentery as 
the causative 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 temper- 
ature and frequent pulse, the obstinate, absolute constipation, the 
persistent, repeated 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. VOMITING. 
511 
Palpation and percussion should not be omitted, as thereby the 
seat of obstruction has been distinctly located. 
Volvulus is the most frequent form of intestinal obstruction after 
intussusception and that due to strangulation. Vomiting occurs, but 
is not so constant a symptom as in those forms first named. Thus 
it occurred in from 8 per cent, in Brinton’s statistics to 2.5 per cent, 
in those of Treves, and 4 per cent, in Martin’s and the author’s. 
It is nearly always seen in men in middle life. The vomiting is 
rarely fecal, is very slight in many cases, and sometimes does not 
appear at all. 
Vomiting, on the other hand, is quite commonly seen in cases of 
obstruction from impaction or obstruction from foreign bodies. This 
underlying cause of the emesis can be diagnosed by the history of a 
foreign body having been swallowed, of attacks of hepatic colic, or, 
where a gall-stone ulcerates through into the bowel, of some local 
peritonitis about the region of the liver. A history can commonly 
be elicited of sharp, colicky pain, of partial obstruction, and of 
vomiting. The distention is slight, the amount of systemic shock 
far less than in other forms of obstruction, and the duration of the 
attack somewhat longer than usually obtains in this class of affec- 
tions. The symptoms of obstruction are frequently only partial, the 
vomiting being moderate in amount and not stercoraceous, the con- 
stipation not being absolute. 
Except in the case of enteroliths and very large foreign bodies 
a tumor can rarely be felt. 
It is often impossible to diagnose this form of obstruction from 
that depending upon a narrowing of the lumen of the bowel, such 
as is produced by cancer or stricture. The previous history is 
always of great importance. The presence of indican1 rather than 
albumin in the urine, the comparative mildness of the attack, the 
moderate meteorism, and the slow course of the disease, all help to 
exclude internal strangulation or volvulus. It is, however, mainly 
upon the history that the diagnosis will be founded. 
Vomiting, loss of appetite, thirst, cough, hectic fever, and sweats, 
with the development of marked cachexia, sometimes occur from 
obstruction of the rectum. 
When vomiting arises from peritonitis it is often one of the 
earliest symptoms of the malady. It is almost always present, 
i For the test of indican, see chapter on the Urine. 512 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
and is often a very severe symptom, and is associated with, or 
replaced by a constant retching, which adds to the exhaustion of the 
patient. At first it may only follow the swallowing of food, but 
often it occurs without such a cause, and after the stomach is emptied 
of its ordinary contents glairy, watery mucus is expelled, which is 
often of a distinct greenish tint. The great tenderness of the belly 
in acute peritonitis, the moderate fever, the rapid pulse, the anxious 
face, and the cold skin as collapse approaches, all render the diag- 
nosis easy; but it is to be remembered that the distention of the 
belly by an overfilled bladder or pregnant uterus may mislead the 
physician into thinking that peritonitis is present because of the 
swelling, the pain, and the vomiting. Vomiting is not a severe 
symptom of appendicitis unless the peritoneum has become involved 
in the inflammatory process, although it may occur once or twice 
when the pain in the appendix is most severe. The localization of 
the symptoms in the neighborhood of the appendix makes the diag- 
nosis possible. (See chapter on Abdomen.) When vomiting occurs 
in typhoid fever it is usually a symptom of bad feeding or imperfect 
digestion, and is rarely of grave importance except under two con- 
ditions. The first of these is when it occurs as a result and symp- 
tom of intestinal perforation, an accident commonly seen late in the 
diease ; and, second, when it takes place as an obstinate and exhaust- 
ing symptom after the fever has practically passed by, from 
unknown causes, probably reflex in character. The symptoms of 
perforation other than vomiting can be found in the chapter on the 
Abdomen and Abdominal Viscera. 
Vomiting as a symptom of cholera is accompanied by serous 
diarrhoea of a profuse character, by the development of collapse, 
cramps in the muscles, anuria, and great circulatory failure. It 
must be separated from the vomiting due to cholera morbus or 
severe indigestion, antimonial poisoning, and arsenical poisoning. 
Cholera morbus is to be separated from cholera, first, by the absence 
of the comma-bacillus in the stools; second, by the fact that there 
is a history of exposure to cold or damp; third, by the absence of 
an epidemic; and, fourth, by the milder manifestations. Vo one 
can be skilful enough to separate symptoms of poisoning by antimony 
from those due to cholera, for they are identical in every way. 
Nothing but the history of the ingestion of the poison and the dis- 
covery of antimony in the secretions can prove the case to be one of 
antimonial poisoning, particularly if an epidemic of cholera is present. VOMITING. 
513 
In arsenical poisoning the association of vomiting with bloody 
stools separates the symptoms from those of cholera. 
Vomiting is a very severe and early symptom of cholera infantum 
(see chapters on Abdomen and on Bowels and Feces), and it occurs 
in attacks of true dysentery as a common symptom, when its under- 
lying cause is readily discovered. (See Abdomen.) The disease 
of the stomach causing vomiting are cancer, ulcer, gastritis, catarrh 
(acute and chronic), true gastritis, and dilatation. 
The vomiting of gastric cancer at first consists in the expulsion 
from the stomach of its contents—mixed particles of food, mucus, 
water, and sometimes bile. The vomit may be tasteless or sour 
from fermeutation, 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 coffee-grounds, producing “ coffee-ground vomit.” This 
coffee-ground vomit is not pathognomonic of gastric cancer, but is 
very characteirstic of this disease. Microscopically the vomited 
materials 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 generally 
brought on by taking food, and so occurs soon after eating. The 
food is, therefore, only slightly digested, and evidences of fermenta- 
tion are absent to a great extent. If blood is present, it is nearly 
always bright red and in considerable quantity, and indicates 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, combined with the 
other symptoms (see chapter on Abdomen), complete the diagnostic 
array of facts. 
There*are, however, other causes of vomiting of blood or lne- 
matemesis than gastric ulcer and cancer. Thus it occurs from ob- 
struction to the portal circulation from hepatic cirrhosis, and from 514 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
growths and splenic affections which result in varicosity of the blood- 
vessels of the stomach. Ha3matemesis 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 de- 
veloped in small degree by any form of violent vomiting which 
strains the stomach, particularly if an irritant substance has already 
destroyed the mucous membrane. Again, haematemesis 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 influenza of 
the epidemic type, and in relapsing fever. Ilsematemesis may also 
occur in purpura hemorrhagica, in haemophilia, and as a result of 
vicarious meustruation. 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. Ekematemesis is to be separated from hse- 
moptysis 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 haemoptysis 
oftener than in haematemesis. 
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 sudden 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. It may also be a symptom of Raynaud’s disease. 
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 back (see Hepatitis, 
in this chapter), and great restlessness, prsecordial distress, dyspncea, 
and faintness are present. The matters vomited are greenish, clear, VOMITING. 
515 
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 meleena neonatorum there is a condition of 
lisematemesis occurring in children within the first few days or weeks 
of life. This condition has been thought by Leube to be due to 
gastric and duodenal ulcers, and his views are indorsed by Buhl and 
Huhu, Spiegelberg, Binz, and Landau. In one of the latter’s cases 
thrombosis of the umbilical vein was present, and it has been 
thought that when expansion of the chest takes place in the new- 
born 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- 
jioisoning. The symptoms associated with ingestion of the poison 
may not come on for some hours. At the end of that time the 
peculiar 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 vomit is at first made up of food, then 
mucus, then bile, then perhaps blood. All 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 prognosis. 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 re- 
newed vigor. The matters vomited are often the color of “ coffee- 
grounds,” due to exuded and altered blood. The bowels are abso- 
lutely confined, or the few hard masses passed are white and clay- 
like, because of the absence of biliary coloring-matter. There is 
no bile in the vomit in this stage, because the hepatic ducts have 516 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 convulsions occur just before dissolu- 
tion. Even if the patient survive the acute stage, he generally dies 
of the changes produced in his vital organs, which consist in wide- 
spread fatty degeneration, even in the acute stages. Atrophy of the 
liver, destruction of the gastric tubules, pancreatic involvement, and 
kidney degenerations aid in producing the ultimately fatal result. 
During the course of poisoning by phosphorus the urine is scanty 
and perhaps albuminous, and is peculiar because of the unusual 
substances found in it. The most unusual of these is sarco-lactie 
acid, which results from the breaking-down of muscular tissues. 
Leucin and tyrosin are also found, and tube-casts, with fatty glob- 
ules in them, are seen. Free fat-globules may also occur. Bile 
acids and bile coloring-matter are 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 children, 
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 pres- 
sure. 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 then is called 
the “ morning vomiting of drunkards.” (See chapter on the 
Tongue.) 
Vomiting due to true gastritis or inflammation of the stomach in 
its deeper layers is very rare, except as a result of the ingestion of 
an irritant poison or hot liquid. VOMITING. 
517 
Perhaps the vomiting occurring in dilatation of the stomach is more 
typical in its character than any other. This act is always a prominent 
symptom of gastric ectasy, the matters vomited being often greenish 
and extremely fetid, and nearly always profuse in amount. Examina- 
tion of the ejecta will generally show food swallowed days before, 
owing to the imperfect digestive action of the stomach, and this 
very inability of the stomach to act on the food generally gives, for 
a long period of time, a sense of weight and fulness often amounting 
to pain, and complained of bitterly. There is tenderness over the epi- 
gastrium on pressure, and the displacement produced by the palpation 
often brings on either acid or yeasty eructations or even the vomit- 
ing already named. Nausea preceding the vomiting is by no means 
common, there being simply a gush of foul liquids from the mouth. 
After such an occurrence the vomiting fails to recur for from 
twenty-four to forty-eight hours, or perhaps not for a week—i. e., 
until the viscus becomes overladen once more. The gases which are 
given off on eructation are exceedingly acrid, nauseous, and bitter. 
Sometimes they are offensive, but more rarely odorless. They are 
often inflammable, and consist of oxygen, nitrogen, hydrogen, and 
carbonic acid. Sometimes sulphuretted hydrogen is present in large 
quantity. The reaction of the vomit is almost always acid, lactic 
and butyric being the acids most commonly found, but the normal 
hydrochloric acid is usually absent. Fibres of meat or masses of 
semi-digested and semi-decomposed food can be seen by the naked 
eye or under the microscope, and sarcinse and many forms of bacteria 
swarm in the mass. Particular search should be made for the yeast 
fungus, torula cerevisice, the presence of which is a certain evidence 
of active fermentation. 
(For further information in regard to the symptoms of gastric 
dilatation, see the chapter on the Abdomen.) 
ATomiting due to gastric dilatation should not at once lead the 
physician into a diagnosis of stenosis of pylorus from growth or 
constrictions in this part of the stomach, or from innate feebleness 
of the gastric walls, for similar conditions may follow growths of 
the pancreas, which by pressure occlude the pyloric opening (see 
chapter on Abdomen); and if cancer is present, an examination of 
the gastric contents after a test-meal will fail to reveal the smallest 
trace of hydrochloric acid. 
Sarcinse ventriculi are found not only in the frothy, dirty-looking 
vomit of gastric dilatation, but in that of chronic gastric catarrh, 518 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
cancer, and ulcer of the stomach. If iodine or iodide of potassium 
is added to the vomit, the sareinae becomes mahogany-red or brown, 
and are easily recognized, occurring in squares which are separated 
by dividing-lines. (Fig. 197.) 
Fig. 197. 
Sarcinse ventriculi, with starch-granules and oil-globules, from vomited matters. 
(Otto Funke.) 
Vomiting also arises from neuroses of the stomach in several 
forms. Thus it is frequently seen in hysteria, in neurasthenia, preg- 
nancy, and sometimes occurs in the form of what Gee has called 
“cyclical vomiting.” It also comeson in association with gastric 
crises in locomotor ataxia. The vomiting of hysteria is generally 
characterized by its character, often lasting for months, 
and yet the patient often maintains her normal weight to a surpris- 
ing degree, either because the food which is taken is only vomited 
. in small part or because she surreptitiously obtains food when her 
attendants do not know it, which she retains. It is generally asso- 
ciated with so many of the hysterical stigmata as to be readily diag- 
nosed. The vomiting of neurasthenia is seen in both sexes, and is 
particularly apt to follow any nervous muscular exertion. Thus in 
one case of the writer’s even short railroad journeys taken by an 
overworked man produced attacks of spinal tenderness with vomit- 
ing, which lasted several days. The vomiting of pregnancy is usu- 
ally a morning vomiting, though it may persist all through the day. 
It has no particular diagnostic features in itself, save that there are 
rarely any signs of gastric indigestion. The presence of pregnancy, 
of course, makes the diagnosis clear; but in such cases, if the preg- 
nancy is advanced, the physician should always examine the urine, 
since the ordinary vomiting of pregnancy is a symptom of the first 
few months, while that occurring later on may indicate grave renal 
complications. (See Unemia, in chapter on Coma and in chapter on 
Convulsions.) VOMITING. 
519 
The cyclical vomiting already mentioned is generally seen in chil- 
dren, and is of rare occurrence. It is characterized by attacks of 
vomiting recurring after intervals of uncertain length, during which 
the patient may seem entirely well. The attack may last from a 
few hours to a few days. There are often pain in the epigastrium 
and constipation. Sometimes retching is the main symptom. It is 
generally seen in neurotic patients. 
Vomiting of a nervous type is a common complication of exoph- 
thalmic goitre, and when it occurs sometimes develops into a danger- 
ously severe symptom, owing to its constancy, violence, and resist- 
ance to treatment. Oftentimes serous diarrhoea is associated with 
it, and these two associated symptoms should not mislead the phy- 
sician into a diagnosis of cholera morbus nor of jaundice, for icterus 
often comes ou. 
Meniere’s disease is associated with vomiting, the contents of the 
stomach being expelled after the attack of vertigo and tinnitus aurium. 
The affections of the liver which result in vomiting are chiefly 
catarrhal and obstructive jaundice, hepatitis, and pylephlebitis. The 
rapid development of jaundice, hepatic tenderness, and swelling, or 
a history of violent hepatic pain (colic), renders the diagnosis possi- 
ble in the case of jaundice. (See chapter on Skin.) Hepatitis— 
that is, hepatic abscess—is often accompanied by or produces vomit- 
ing which is apt to be very obstinate. The swelling of the liver, 
the tenderness in the hypochondrium on palpation, the pain in the 
hepatic region, often referred to the neighborhood of the right 
shoulder, and the febrile movement, which is intermittent, sweeping 
up to 104° or 105°, then down to normal, are the chief character- 
istic symptoms. (See chapter on Abdomen.) Vomiting accom- 
panied by a similar train of symptoms also occurs in cases suffering 
from pylephlebitis. 
Violeut vomiting associated with great pain in the loin, radiating 
down into the testicle or inside of the thigh, indicates the presence 
of a renal calculus, either in the pelvis of the kidney or in the ureter. 
Haemoglobinaemia is sometimes accompanied by vomiting. The 
attacks are paroxysmal, and are often ushered in by persistent yawn- 
ing, with pain iu the limbs, headache, nausea, and vomiting, fol- 
lowed by moderate fever, which is preceded or accompanied by a 
chill. Pain may be felt in the liver, but, more pathognomonic than 
all, the urine is soon found to be dark, brownish-red, or even black, 
owing to the presence in it of haemoglobin. 520 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
Vomiting is a frequent coincident symptom of headache, because 
in many cases the headache depends for its existence upon a dis- 
ordered stomach or disordered bowels ; but it also appears as a 
characteristic symptom of a condition in which the stomach is pri- 
marily not at fault, namely, in migraine or hemicrania, in which, in 
addition to violent pain in the head on one side, we have hemian- 
opsia, scotomata, and sometimes great pallor or flushing of the face. 
(See Pain.) In acute yellow atrophy of the liver vomiting is a con- 
stant symptom, with jaundice, violent headache, and finally convul- 
sions and subcutaneous ecchymoses. (See chapter on Convulsions.) 
When vomiting occurs in yellow fever, the presence of an epidemic, 
the suffusion of the eyes, the headache, the black character of the 
vomit, the slow pulse, scanty urine, and prostration, all point to the 
real cause of the symptom. In Addison’s disease vomiting is often 
present, and may be so severe as to prove beyond control. The 
peculiar pigmentation of the skin (see Skin), the mental inactivity, 
headache, vertigo, and anaemia without loss of weight in many cases, 
all aid in the diagnosis. 
Vomiting is a frequent symptom in some cases of phthisis, par- 
ticularly if laryngeal tuberculosis is present. It also occurs as a 
result of swallowing the sputum instead of expectorating it, and 
very commonly excessive cough produces vomiting, especially if the 
cough follows closely after a meal. 
Closely associated with the vomiting due to these causes is that 
occurring in cases of pulmonary gangrene. 
Vomiting often takes place in children suffering from whooping- 
cough at the close of the paroxysm, and is due to the spasmodic 
movements of the chest and diaphragm. 
Finally, it is not to be forgotten that vomiting often ushers in 
any oue of the eruptive diseases, such as the fevers, syphilis in its 
early secondary stages, and erysipelas. 
Under the name of merycismus cases of voluntary regurgitation 
of food have been reported. The patients have been nervous or 
hysterical persons. 
The Vomit. 
Aside from the diagnostic significance of the act of vomiting, the 
physician should remember that the vomit itself may give him in- 
formation as to the condition of his patient. 
Under the head of gastric dilatation we have spoken of the sig- VOMITING. 
521 
nificance of vomiting large amounts of liquid and undigested food, 
so that it is not necessary to speak of this point here; but it is well 
to remember that small amounts of vomited material ofteu possess 
considerable diagnostic importance. Thus, in the case of drunkards 
it is by no means rare for the patient to vomit in the morning small 
amounts of watery and sour material, and in the severe retching of 
cerebral disease or uraemia very little material is gotten rid of. In 
cases in which small quantities of exceedingly sour, clear liquid are 
vomited, we ofteu find that the attack is due to migraine or nervous 
headache. If watery liquid and mucus are vomited, there is prob- 
ably gastric catarrh. The vomiting of bile is usually only seen 
when repeated retching has drawn this secretion up into the stomach. 
The liquid may be either golden yellow or greenish in hue. Some- 
what like this vomit is that seen in peritonitis, in which disease 
grass-green material is often expelled. Similar 
material is also vomited in cases of intestinal ob- 
struction before stercoraeeous vomiting comes on. 
The significance of bloody vomit has already 
been described. It only remains to name the test 
for heemin, which, if present, shows that the color 
of the ejecta is really due to blood. Some of the 
vomited material is filtered, and a little of the 
filtrate is evaporated on a watch-glass. This dried 
material is now scraped off the glass, mixed with 
a trace of finely powdered common salt, and placed on a glass 
slide. The powder is now covered by a cover-glass and one or 
two drops of glacial acetic acid allowed to flow under the cover- 
glass. This is then dried by exposing it to gentle heat, and after 
the drying is absolute a drop or two of pure water is touched to the 
edge of the cover-glass. Very minute crystals of hsemin are now 
seen with the aid of the microscope (see Fig. 198). 
The vomit of uraemia is often ammoniacal from the decomposed 
urea in it, and that of intestinal obstruction is fecal in odor for 
obvious reasons. If odorous poisons have been taken, it smells of 
the poison ; and if there be phosphorus present, the vomit not only 
smells of it, but in addition is luminous in the dark. 
Fig. 198. 
Hsemin crystals. CHAPTER VI. 
COUGH AND EXPECTORATION. 
The varieties of and indications of cough—The causes of cough—The sputum— 
Its pathological significance. 
The significance of cough as a symptom is very important, and, 
though it may arise from many causes, in the majority of instances 
it points to trouble in the chest, in the trachea or the larynx, in the 
pharynx or in the nose. Rarely it is a purely nervous trick, and 
equally rarely it arises from irritation in the stomach (“ stomach- 
cough,” so called). A cough is said to be dry and hacking when it 
fails to bring up into the throat or mouth any secretion, or when it is 
short and sharp. Often such a cough is paroxysmal ; in other cases 
it consists in single but fairly frequently repeated, short, and forcible 
expiratory efforts, as if the patient was trying to clear his throat. 
A loose cough is nearly always paroxysmal; that is, it occurs u in 
spells,” and at nearly every paroxysm results in the raising of some 
mucus. The first variety of cough is that seen in the early stages 
of phthisis pulmonalis, acute bronchitis, or pneumonia, before any 
exudation has taken place; in the early part of a paroxysm of 
asthma; in the early portion of an attack of whooping-cough, and 
when the cough arises from irritation in the upper air-passages, 
whether this be due to the inhalation of dust or the presence of 
some growth, as a laryngeal papilloma. The loose variety of cough 
is seen in the later stages of acute bronchitis, pneumonia, asthma, 
whooping-cough, and in cases of emphysema with bronchiectasis, 
and in the stage of pulmonary tuberculosis associated with the break- 
ing down of lung-tissue, the formation of cavity, and the develop- 
ment of bronchitis with it, and in gangrene of the lung. There are 
two peculiar forms of cough to be mentioned, namely, the so-called 
barking, brassy, laryngeal cough, which we hear most typically 
in false or spasmodic croup, and the cough of whooping-cough, which 
is, as its name implies, the most typical which we meet with. Sud- 
denly the child begins to give a series of quick, sharp coughs, which 
become more aud more rapid until the chest is emptied of air. In COUGH AND EXPECTORATION. 
523 
the early stages of the disease this is all that occurs, and unimpeded 
inspiration ensues; but later the cough no sooner ceases from ex- 
haustion of the lungs of air than with the attempt of deep inspira- 
tion the glottis closes spasmodically, and the air is sucked in through 
the chink with a whooping sound. The flushed or cyanotic face of 
the child, associated with these paroxysmal attacks, renders the diag- 
nosis easy. 
There is nothing distinctive in the cough of early stages of pul- 
monary inflammation, whether it be bronchial or vesicular, although, 
if the bronchitis be very intense or the pulmonary inflammation also 
affect the pleura, the cough may be partly smothered or suppressed 
by the patient, who endeavors to control or stop it in order to escape 
the pain it causes. To this end he sits or lies in bed, endeavors to 
fix the muscles of his chest so that they will not respond to the 
reflex cough-impulse, and shuts his lips to hold his breath in, 
although very often the reflex irritation overcomes his will-power 
and the cough bursts through his compressed lips with an expression 
of pain. Such a cough is always indicative of pain. 
In all forms of dry cough there is now and again a small plug of 
mucus expelled from some part of the respiratory mucous membrane. 
Such coughs possess no value to the patient, being merely a sign of 
reflex irritation; but a loose cough, unless it is very excessive, is of 
the greatest possible use to the patient, for it is an effort on the part 
of nature to rid the lungs of abnormal exudations or secretions. For 
this reason this symptom is not to be removed completely in cases 
of resolving pneumonia, pulmonary tuberculosis, or bronchiectasis 
with excessive secretion, since, if drugs are given which stop the 
cough, the lungs are speedily filled with the secretion; and in the 
case of tuberculosis or gangrene or muco-purulent bronchitis septic 
absorption with systemic infection results. Similar good results are 
reached by the cough heard in cases of pulmonary abscess, and 
when an empyema has broken into a bronchial tube. When the 
patient complains of chronic cough, which is worse in, or confined 
entirely to, the morning hours, and tells us that the cough finally 
causes the discharge of much secretion, and that tin's is followed by 
freedom from cough for many hours, the case may be one of tu- 
berculosis with cavity; pulmonary abscess; empyema, which has 
ruptured into a bronchus; or sacculated bronchiectasis. Such 
coughs come on in paroxysms whenever the lung must be relieved, 
and the length of paroxysm depends upon the looseness of the secre- 524 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
tion and its situation in the lung. Thus, if the secretion be in the 
larger bronchial tubes, it is easily expelled ; whereas if it be in 
smaller bronchioles, or in the vesicles, or at the bottom of a cavity, 
great and frequently repeated effort will be required before the 
liquid can be raised into the mouth for expectoration. 
The presence of an obstinate cough due to bronchitis, which re- 
sists all ordinary treatment, should lead the physician strongly to 
suspect that one of two ailments is present, namely, undiscovered 
tuberculosis, or, if there is puff ness under the eyes, Bright’s disease. 
Cough brought on by changing the position of the patient often 
arises because of the alteration in position of a pleural effusion. 
Violent and constant cough often comes on during aspiration of the 
chest for pleural effusion. 
The cough of acute laryngitis may be quite severe, and occurs in 
short, sharp barks of a harsh or brassy character (like spasmodic 
cough) which is so typical as to be called a laryngeal cough. The 
association with this cough of partial or complete loss of voice and 
pain in the larynx, with a history of exposure to cold and dust, or 
the excessive use of the larynx in speech or singing, renders the 
diagnosis clear even if the laryngoscope is not used to discover con- 
gestion and inflammation of the laryngeal mucous membrane. In 
the false croup of children, which is always associated with laryn- 
geal irritation, the barking, ringing cough is so characteristic as to 
render a diagnosis possible as soon as the sound is heard, and with 
it there is dyspnoea due to obstruction to breathing. 
The cough of the laryngeal phthisis is not so typically brassy and 
ringing as that of acute laryngitis, but the presence of pain in the 
larynx, hoarseness, and persistent laryngeal dryness and difficulty 
should lead to a search for tuberculosis by the laryngoscope, and an 
examination of the chest for physical signs of trouble in the lungs 
and of the sputum for tubercle bacilli. 
Sometimes cough of a laryngeal character is due to an aneurism 
pressiug upon the larynx. In other cases the cough depends not 
upon the pressure of an aneurism, but upon the pressure produced 
by carcinoma of the oesophagus, by a mediastinal tumor, or is due 
to the inhalation of irritant dusts or vapors. This cough, laryn- 
geal or bronchial, is often present in girls who work in carpet 
factories, in the air of which there are immense quantities of fine 
particles of wool. Again, it is seen in knife-grinders, needle- 
workers, coal-miners, and in workers in arsenical and lead pigments. COUGH AND EXPECTORATION. 
525 
Sometimes in paralysis of the pharyngeal muscles (glosso-labio- 
pharyngeal paralysis) cough is produced by the slow passage of food, 
which may in fact enter the larynx. 
A night or evening cough is very commonly seen in cases of res- 
piratory catarrh or more grave disease. It is often absent all day, 
only to return in the evening in cases of laryngitis and in phthisis; 
and, iu those cases in which it follows getting into bed, it is due to 
chilliug of the skin by the cold sheets, which results in congestion 
of the inflamed mucous membrane. 
Quite frequently children suffering from chronically enlarged 
tonsils suffer from cough on going to sleep, especially if the uvula 
is relaxed or elongated. The cause of this cough is that in the re- 
laxation of sleep the tonsils touch one another or tickle the uvula. 
As soon as the child wakes muscular contraction separates the ap- 
proximating surfaces and the cough soon ceases. 
Sometimes in hysteria a peculiar barking cough is produced by 
pinching the skin of the neck or elsewhere in the body, and it may 
also come on in paroxysms independent of such causes in neurotic 
children of both sexes about the time of puberty. 
In regard to coughs in general, it can be said that in the absence 
of the early stages of acute inflammation of the respiratory appa- 
ratus a dry, hacking cough is either nervous or is due to reflex irri- 
tation in the ear or stomach, or to some hyperiesthetic spot in the 
nasal, pharyngeal, or laryngeal mucous membrane ; whereas a loose 
cough may arise both in adults and children from congestion and 
engorgement of the lingual tonsil. Such a cough is frequent, dry, 
and paroxysmal, and seems to arise from a sticking or pricking sen- 
sation in the throat; whereas a loose and prolonged cough depends 
upon causes of greater gravity further down in the respiratory 
organs. Generally, if the stomach is at fault, a low grade of pharyn- 
gitis will be found. The physician should also remember that 
valvular disease of the heart, by the secondary changes which it 
causes in the lungs, may produce cough, and Sansom states in his 
book that cough was present iu 45 per cent, of the cases of heart 
disease taken by him as illustrative. 
There is another variety of cough seen in persons who have 
paralysis of the diaphragm. The cough under these circumstances 
is produced for the purpose of expelling air from the chest, and is 
seen in persons with paralysis of the diaphragm from the removal 
of large ovarian tumors, which have pressed upon it and stretched 526 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
it and the chest-walls to which it is attached, so that when the press- 
ure is removed the muscle is too slack to contract. It is also seen iu 
injuries to the phrenic nerve and to the spinal cord. 
The cessation of cough in advanced phthisis, suffocative bronchitis, 
or the bronchorrhoea with bronchiectasis of old persons, or in severe 
pneumonia, indicates exhaustion, collapse, or approaching uncon- 
sciousness, and is a bad sign. 
The Expectoration. 
A careful examination of the materials expectorated by the pa- 
tient, or, in other words, of the sputum, is of the utmost importance 
in all cases of disease of the respiratory tract, whether the abnormal 
process be primary or secondary. The methods which we resort to 
in examining sputum are macroscopic, or those of the naked-eye, 
and microscopic. Of these the microscopic are by far the most im- 
portant. Sputum varies greatly in its general character on ordinary 
examination, sometimes being very fluid and even watery in consist- 
ency, and sometimes thick or tenacious. In some instances it is 
clear and glairy-looking, resembling somewhat partly beaten white 
of egg; in others it is yellow and opaque. Placed on a clean linen 
cloth the sputum may evaporate to almost nothing, or leave a heavy 
muco-purulent deposit after all moisture is gone. 
The naked-eye appearances of sputum are, however, quite char- 
acteristic in several conditions. Thus, in the later stages of acute 
bronchitis the sputum is apt to be thick and yellowish and to con- 
tain lumps of half-inspissated mucus. In croupous pneumonia it 
is rusty in color, is peculiarly free from watery ingredients, and is 
gelatinous to such an extent that it adheres to the spit-cup, so that 
when this vessel is well filled its contents do not readily fall out even 
when the cup is tipped upside down. The brightness of the blood in 
the sputum in cases of pneumonia is also a guide to prognosis. Thus 
Sir William Jenner said, u the less the weight for a given height, the 
more red blood in the sputum, the better the chance for the patient.” 
Later on it may be less adhesive after resolution is well advanced. 
If the pneumonia is chronic, the sputum has such a dark color that 
it is often called “ prune-juice sputum.” A third variety is that 
seen in pulmonary hemorrhage or haemoptysis. In this condition, 
after having, perhaps for a short time, a salty taste in the mouth, 
the patient suddenly brings up, with or without much preceding COUGH AND EXPECTORATION. 
527 
cough, a gush of nearly pure blood or blood freely mixed with ordi- 
nary sputum. The blood is bright red, not dark or prune-juice in 
appearance, and the liquid is frothy, while the cough, which is 
always present after the hemorrhage has occurred, is suppressed and 
resisted by the patient, who fears further bleeding. This haemoptysis 
may be caused, first, by pulmonary tuberculosis; second, by val- 
vular cardiac disease, generally involving the mitral valves, and 
resulting in pulmonary infarction ; third, by aortic aneurism ; fourth, 
in persons suffering from severe purpura; fifth, from persons suffer- 
ing from haemophilia; sixth, from vicarious menstruation; and, 
seventh, in rare cases of hemorrhagic smallpox. 
Bloody sputum must be separated from bloody vomit due to gas- 
tric hemorrhage from ulcer or cancer (see Vomiting). This can be 
done by the cough, by the frothy character of the expectoration, by 
the presence of physical signs in the lungs, and by the history of 
pulmonary disease. It may, however, be confused with slight 
hemorrhage from a dilated and ruptured vessel on the posterior 
pharyngeal wall, in which case, after a little coughing, there may be 
expelled on a handkerchief a little blood-tinged saliva. Examina- 
tion of the throat will usually reveal the source of the blood or 
other vessels dilated, but still intact. For a number of days after 
an attack of haemoptysis there may be expelled in the sputum dark 
clots of blood. So-called “currant-jelly” clots are expelled by 
coughing in many cases of malignant growths of the lungs. 
Other causes of blood-streaked sputum are aortic aneurism with 
leakage by oozing into a bronchus or the trachea; and particularly 
in children do we see streaks of blood in the sputum if there be 
present pulmonary gangrene. Care should always be taken to dis- 
cover whether the materials spat up are really tinged with blood, for 
they may be colored by some dye-stuff or the blood of some animal 
for purposes of deception. 
Finally, it is well to remember that a reddish-brown or brick- 
dust looking sputum is sometimes coughed up in cases of hepatic 
abscess communicating with the lung ; and the sudden expectoration 
of a brownish, purulent-looking sputum by a person who has been 
a sufferer from dysentery should cause the physician to examine the 
sputum for the amoeba coli, in order to discover if the case is one 
of pulmonary abscess secondary to amoebic dysentery. Symptoms 
of hepatic abscess may also be present. This has been called 
“ anchovy-sauce” sputum. 528 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
In addition to the sputum already described we sometimes see a 
peculiar semi-liquid sputum in cases of pulmonary phthisis, in 
which the sputum promptly separates into two layers on standing, 
the lower one being light and flocculent, unless there is a well- 
marked bronchial catarrh present, when it may be markedly muco- 
purulent, or, if a large cavity is present, its purulent character may 
be even more marked. To this list may be added several others, 
namely, the purulent sputum of pulmonary abscess or empyema, of 
mediastinal abscess, subphrenic abscess, hepatic abscess, pronounced 
bronchiectasis, and, finally, that from a large tubercular cavity in 
the lung. Of these the more common are bronchiectasis, tubercular 
cavity, and empyema breaking into a bronchus. In the first of 
these the cough is paroxysmal, and after it has been kept up for 
some time a gush of purulent sputum is suddenly brought up into 
the mouth, and the accumulation of pus is removed for a time. 
In the other the sputum is very fluid, and is so free that its expec- 
toration rapidly fills the spit-cup, provided that the patient is strong 
enough to bring it up. A very liquid watery sputum is seen in 
pulmonary oedema, particularly that seen in cases of Bright’s disease 
or heart-failure, and in some of the pulmonary forms of epidemic 
influenza. 
Sputum which, on standing, separates into three layers, the top 
one frothy and dirty-looking, the next clear and filled with shreds, 
and the lowest consisting of a sediment of pus and broken-down- 
looking materials, is seen in cases of pulmonary gangrene, and if 
the sputum when placed in a vessel containing water sinks to the 
bottom in disk-like masses or globules the disease may be tuber- 
culosis. 
The sputum expelled by an asthmatic at the time of the attack 
also has characteristics not so easily seen at a glance, but neverthe- 
less demonstrable by the naked eye. Small pearls or plugs of 
mucus of the size of a sago-pearl are seen in the sputum, and if 
these are placed on a plate of glass under which is a black surface, 
and then teased out, they will be found to be rolled-up fibres, which 
when unrolled are found to be in the forms of curls or spirals. 
These are sometimes called Curschmanu’s spirals (Fig. 199), and 
they are rarely seen in several other conditions than asthma, namely, 
in chronic pulmonary tuberculosis and croupous pneumonia. Through 
the central core of the curl runs a bright and refractive filament, 
which is waxy, and is probably not an entity, but an optical effect. COUGH AND EXPECTORATION. 
529 
Between the spiral fibres can be seen in many cases slight, bluish, 
octahedral crystals varying greatly in size, sometimes requiring a 
high-power lens to distinguish them. They are said by Salkowski 
to be composed of a mucous substance, but others believe them to 
be oxalate of lime, a phosphate of an unknown base or ethylenimin. 
These are called Charcot-Leyden crystals, and are also seen in the 
sputum of chronic croupous pneumonia, chronic pulmonary tuber- 
culosis, and in acute bronchitis. 
Fig. 199. 
Curschmann’s spirals. (Von Nooeden.) 
Sometimes, in cases of diphtheria, casts of the larynx and upper 
bronchial tubes are expelled by coughing. Small casts are also seen 
in the sputum of that rare affection, fibrinous bronchitis. Some- 
times these casts consist of a perfect mould of several branching 
bronchial tubes and bronchioles, and they may be white, yellowish, 
or even pinkish in color from bloody exudation. Sometimes they 
are onlv visible to the naked eye if placed in wrater and shaken, 
when what has appeared to be a roll of mucus spreads out into the 
characteristic shape of the tubes from which it comes. Casts of the 
finer tubes can sometimes _be found in the sputum of cases of croup- 
ous pneumonia. 530 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
The examination of sputum by the aid of the microscope should 
be made with care. A portion of the sedimentary part of any 
sample may be carefully separated from the rest by means of a 
pipette; but to facilitate the examination of sputum for tubercle 
bacilli when but few exist, and for the rapid and thorough examina- 
tion of the sputum for elastic fibres, which has been heretofore a 
tedious and complicated process, and for the discovery of Charcot- 
Leyden crystals and fibrinous coagula the centrifuge is a much better 
apparatus. (See chapters on Urine and Blood.) The tubes used 
for the precipitation of the sputum are 50 mm. long, with 2J mm. 
lumen, and are fitted into the haematocrit frame. 
A small quantity of sputum is placed in a clean porcelain dish 
and actively stirred for a few minutes with a glass rod until it be- 
comes thin and free from lumps and apparently homogeneous. With- 
out any dilution whatever the sputum is drawn into the sputum- 
tubes by means of a medicine-dropper connected with a small rubber 
tube. The two precipitating tubes, filled with sputum in this way, 
are placed in the haematocrit frame and revolved for at least three 
minutes, making about fifteen thousand revolutions. The solid por- 
tions of the sputum collect in the distal extremity of the tubes. A 
small portion of the sediment is placed ou a slide and examined 
microscopically for elastic fibres, Charcot-Leyden crystals, etc. The 
sediment from the second tube cau be stained for tubercle bacilli or 
other micro-organism as desired. 
When the centrifuge is not used and a small particle of sputum 
is placed upon a glass slide under a cover-glass and gently pressed 
there will be seen, if the sputum be mucus or muco-purulent, threads 
of mucus and mucous corpuscles with white blood-corpuscles, which 
are particularly numerous if the sputum be purulent. These latter 
are granular, fatty, and sometimes pigmented by soot or other sub- 
stances which have been inhaled. Epithelial cells derived from the 
respiratory passages are also found in large numbers, often broken 
down and fissured, granular, and generally a nucleus can be distin- 
guished in their centre. Of far more importance than these, how- 
ever, are the particles of elastic fibre or elastic threads, which, if 
present, show positively that a breaking-down process is going ou 
in the lung, or more rarely in the bronchial tubes. These are usu- 
ally seen in the sputum of advanced or rapidly progressing tuber- 
culosis of the lung and in that of abscess and gaugreue of the lung. 
If there is doubt as to their presence because they are sparse, we COUGH AND EXPECTORATION. 
531 
obtain them by the following process : boil equal parts of the sus- 
pected sputum and a 10 per cent, solution of caustic potash, and 
dilute the jelly-like mass which results with water. After this has 
stood for twenty-four hours the elastic fibres may be found in the 
sediment as swollen threads, for which, however, small particles of 
food which may come from the mouth may be mistaken. 
The appearance of fine, needle-like crystals of fatty (margaric) 
acid, which may be bent like a curved needle and often grouped iu 
bunches, may indicate pulmonary gangrene or purulent bronchitis. 
They are found chiefly in the plugs or lumps which the patient 
expels in his sputum, but they possess no indicativeness of the 
pulmonary changes just named if follicular tonsillitis, either acute 
or chronic, is present, since the plugs derived from the follicles of 
the tonsils also contain similar crystals. Again, they are of no 
diagnostic value if found in stale, muco-purulent sputum, as they 
may form in this after it has been expectorated. The peculiar 
crystals called Charcot-Leyden crystals have already been described. 
Fig. 200, 
Actinomyces, 
There are four remaining objects to be seen in sputum of dis- 
eased persons, all of which are of great diagnostic importance when 
found. The first of these is very rare, namely, the eggs of the dis- 
toma pulmonum, which are found in the sputum. This parasite 
sometimes produces haemoptysis without any physical signs of pul- 
monary change, and is rarely if ever seen in this country, but is 
common in Japan, Corea, Formosa, and in China. The second is 
the evidence of echinococcus infection by the appearance of portions 
of the cysts or of the hooks of the scolices when the cyst bursts into 532 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
a bronchus from the lung or adjacent structures. Such cases are 
rare in this country. The third condition, which is also very rare 
when involving the lung, is actinomycosis, in which infection we find 
radiated fungi or actinomyces in the sputum. This fungus appears 
as a number of club-shaped projections attached to a heterogeneous 
mass of irregular-looking material. (Fig. 200.) 
The fourth and most important of all these finds in sputum is 
the tubercle bacillus, both from the point of diagnosis, prognosis, 
and treatment, and because the disease tuberculosis is so widely dis- 
tributed in every class, in every part of the country, and is so con- 
stantly prevalent. The discovery of these bacilli in a sample of 
sputum which has not been exposed to the entrance of bacilli after 
it has been expectorated, is a positive sign of tuberculous infection 
unless there be tuberculous disease of the upper air-passages or 
mouth. While their presence gives positive evidence, their absence 
in a given sample of sputum is not negative evidence of an absolute 
character, for that particular specimen may be free from bacilli or 
they may have escaped the staining or the eye of the examiner. 
The method for examining sputum for tubercle bacilli is as fol- 
lows: The specimen which is brought to the physician is poured 
into a shallow glass vessel having a blackened bottom, or into a 
glass saucer placed on a piece of blackened paper. If this sputum 
is now closely examined, it will be fouud to contain small, yellowish 
masses, one of which should be picked up by means of a spoon or 
platinum needle, freeing it as much as possible from the mucus sur- 
rounding it. A very small part of this mass is now placed on a 
cover-glass and well distributed over its surface by means of a 
needle or teasers, or it is spread by placing another cover-glass 
over the first and pressing them together with a to-and-fro move- 
ment. The quantity of sputum used must not be large enough to 
extend over the edges of the glass. This having been done, the 
glasses are now separated by a gliding movement, and the thin film 
of sputum covering each one is allowed to dry by exposure to the 
air, after which, being held by forceps, it is passed through the 
flame of an alcohol lamp to fix the coatiug. Care must be taken 
that too much heat is not used. Some carbol-fuchsiu stain1 is now 
placed in a watch-glass and the cover-glasses are immersed in it. 
As soon as this is done the cover-glass is held over a flame until the 
1 Carbol-fuchsin stain, or Ziehl’s solution, is made by dissolving 1 gramme of fucbsin in 10 
c.c. of alcohol, and adding 100 c.c. of a 5 per cent, solution of carbolic acid. COUGH AND EXPECTORATION. 
533 
steam begins to rise from it, when it is withdrawn, then heated again 
until this process has been repeated several times. The cover-glass 
is now washed in water, and the film covering it will be found to 
have an evenly distributed red color. The glass is next placed for 
a moment in a 25 per cent, solution of nitric or sulphuric acid in 
water and gently moved about to decolorize the deposit on the sur- 
face of the glass. As a result the albumin and cells on the glass are 
decolorized, but the bacilli are not. The glass is next washed in 
dilute alcohol (60 per cent.) to remove any free fuchsin. Should 
the decolorization be imperfect, so that the film still has a red color, 
it must be still further decolorized by returning the glass to the acid 
solution and then washed again in the dilute alcohol and water. 
The cover-glass is now placed in a solution of methylene-blue (satu- 
rated watery solution). The glass is then finally washed in water 
and afterward examined under the microscope, or dried and mounted 
in Canada balsam for permanent preservation. The tubercle bacilli 
are distinguished by the fact that they retain the red color from the 
fuchsin solution, while other bacteria, having been decolorized by 
the acid solution, take the contrast-stain and appear blue. 
Fig. 201. 
Tuberculous sputum stained by Gabbett’s method. Tubercle bacilli seen as red rods; 
all else is stained blue. (Abbott.) 
Another method (Gabbett’s modification of Fraenkel’s) is perhaps 
more useful than that just given. It consists in staining, as already 
directed, with the carbol-fuchsin solution, and then placing the cover- 
glass in a second solution, which contains the acid for decolorizing 
and the contrast-stain. This latter solution is composed of 20 parts 534 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
of nitric acid, 30 parts of alcohol, 50 parts of water, and sufficient 
methylene-blue to make a saturated solution, equalling above one or 
two parts in a hundred. The cover-glasses are left in this solution 
for a couple of minutes, and then washed in water. When placed 
under the microscope the tubercle bacilli will appear as red rods in 
strong contrast to the blue background. CHAPTER VII. 
PAIN.1 
The kinds of pain—The significance of its locality—Colic. 
It is manifest that it will be impossible for the author iu this 
volume to enumerate all kinds of pain, both as to the situation, de- 
gree, and character. He can only mention those forms which pos- 
sess considerable diagnostic importance. It should always be 
remembered that pain is the sign adopted by nature to notify the 
individual of some abnormal condition iu his body, and in many 
instances pain is only developed when the attempt is made to 
remove a part which from its condition had much better be allowed 
to rest. 
Pain is generally described as darting or stabbing in character, 
when it occurs in a single or repeated paroxysm; as throbbing or 
pulsating, when it rises and falls in severity with the pulse-beat; 
as dull and aching, when it resembles the feeling associated with a 
bruise. Sometimes stabbing or darting pains are called lancinating, 
and often the patient will state that the pain is tearing and rending 
in character. All pain is associated with direct and indirect irrita- 
tion of nervous matter, and, if the nerve or nervous centres con- 
nected with a part be destroyed organically or in function, we have 
a condition called anaesthesia. (See chapter on Skin.) 
Almost invariably dartiug or stabbing pain is associated closely 
with actual disease of nervous tissue, which may be primary or 
caused by the pressure or irritation of a growth or some foreign 
body. Such pains are seen in neuralgias due to inflammation of 
the sheath of a nerve or its surroundings as it passes through a bony 
foramen; in neuralgia due to meningeal thickening; in the agon- 
izing lightning or tearing pains of locomotor ataxia; of pressure 
upon the spinal nerves by spinal disease or in that caused by frac- 
tured bones. Again, we often meet with violent pain as the result 
of true neuritis, whether it be produced by infection, by injury, or 
by poisoning. 
1 See also chapter on Headache. 536 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
Throbbing pain is nearly always associated with the presence of 
congestion or local swelling in the part where the pain originates, 
and arises from the fact that the peripheral nerves are subjected to 
pressure, which is increased with each additional beat of the heart. 
Dull, aching pain is often produced by slow inflammatory or path- 
ological processes in organs not well endowed with sensory nerves. 
There are two forms of pain yet to be considered which are pecu- 
liar in their character, namely, that due to a blow or injury to the 
testicle and ovary and that which occurs in cases of inflammation or 
morbid growth affecting bony tissues, particularly in the long bones. 
There is another point in connection with the study of pain as a 
symptom of disease, namely, that pain is often referred to a point far 
away from the source of the symptom. Thus, the child with hip- 
disease complains of pain in the knee or in the ankle; the one with 
dorsal caries of pain in the intercostal nerves anteriorly; and a stone 
in the kidney may cause violent pain in the penis or testicle. 
The physician should always remember that the degree of pain 
must be determined in part by the expression of the face and move- 
ments of the body, for often these features of a case will show that 
the pain described so vividly in words is much exaggerated. The 
general systemic signs of pain are a tense pulse, if the pain be recent 
in onset and acute; a somewhat accelerated respiration unless the 
pleurae or lungs are involved, when it may be retarded ; dilatation 
of the pupil; more or less sweating, particularly on the forehead; 
faintness; and sometimes the passage of clear, limpid urine if the 
pain be abdominal. 
The first kind of pain which will be discussed is the darting or 
paroxysmal pains in that division which may be called the neural- 
gias. These depend upon one of three causes, and, though they may 
occur in any nerve of the body, are most commonly seen in the 
nerves of the head; or in nervous women in the nerves of the 
pelvic organs and external genitals. The three causes are generally 
debility with anaemia, reflex irritation, and irritation of the nerve 
by poisons or by the presence of growths. 
Violent neuralgia of the head is commonly seen in overworked 
or young women, who lack sufficient sleep and fresh 
air and who are anaemic. It also arises from the reflex irritation 
of a decayed tooth, or from inflamed or overstrained eyes, or of a 
diseased ear, so that an examination of any oue of these parts may 
reveal the cause of an obstinate neuralgic pain. Similarly we see PA IX 
537 
cases of neuralgia, particularly of the supraorbital nerve, which are 
due to chronic poisoning by one of the metallic poisons, such as lead 
and arsenic, aod also as a result of malarial infection (brow ague). 
If the neuralgic pain be due to neuritis, it will not only be typical 
of neuralgia, but along the track of the nerve marked tenderness 
will be developed on pressure, and often an eruption will appear on 
the skin, as a herpes zoster. Pure neuralgia, on the other hand, is 
often relieved by pressure upon the nerve involved. 
When the fifth cranial nerve is affected by neuralgia we find that 
if the upper branch is involved the pain is felt in the forehead, the 
eyebrow, and the eyeball, the conjunctiva often becoming injected. 
If the pain be in the upper lip, the posterior nares, and the cheek, 
the infraorbital or second branch is affected ; while if the pain is in 
the lower jaw and chin, the third division of the fifth nerve is in- 
volved. 
A peculiar form of neuralgic pain coming on in attacks or par- 
oxysms of great severity is migraine or megrim, in which the pain 
is usually confined to one side of the head, is associated with great 
tenderness of the scalp, and preceded in many cases by disorders of 
vision, such as hemianopsia or dimness of visual perception. Asso- 
ciated with this pain at its zenith we frequently see vomiting and 
retching, faintness, with sweating localized to the pain-area or dif- 
fused, and great facial pallor. Pressure by the fingers upon the 
painful area often gives no more pain or even partial relief, but a 
light touch will often cause marked increase in the pain. Rarely 
a somewhat similar condition to migraine, which is not unilateral 
but bilateral, is found in connection with rheumatism of the scalp. As 
migraine may be due to, and this last-named condition arises from the 
rheumatic diathesis, care in making a differential diagnosis is neces- 
sary. The pain of migraine is, however, unilateral, more severe, 
more transitory, and associated with the symptoms named, whereas 
in the rheumatic head-pain the history of rheumatic tendencies of a 
marked character, the diffuse pain, the increased soreness on ex- 
posure to cold or changes in the weather, aid in separating it from 
migraine. When syphilis or injury causes a periostitis of the skull, 
violent pain of a neuralgic character may be present, particularly at 
night; but the local symptoms are manifest, and when compared 
with the history make the diagnosis possible. 
It is also necessary to separate the headache of cerebral tumor or 
cerebral abscess from neuralgia of the head. The pain of such a 538 
THE MANIFESTATION OF DISEASE BY SYMPTOMS 
cerebral condition is constant; the headache is sometimes worse at 
night, sometimes in the daytime, and greatly increased by physical 
or mental effort. The danger of confusing the pain of neuralgia 
with that due to tumor is great unless the physician remembers that 
the constant pain of tumor may vary from slight headache to sharp 
paroxysms of pain. The occurrence of convulsions points strongly 
to tumor if associated with headache of this character, and, finally, 
the presence of tumor as a cause of headache and not ordinary neu- 
ralgia is decided upon by evidences of optic neuritis, vomiting, vertigo, 
and the development of focal symptoms of localized paralysis. (See 
chapters on Headache and on Vomiting, Convulsions and Spasms.) 
The most common seat for neuralgic pain in the head, other than 
in the brow, is the occipital region, the posterior branch of the second 
cervical nerve or great occipital being the one most affected. As 
this nerve supplies all the occipital region and the posterior part of 
the parietal regions, all these areas may be involved in the painful 
manifestations, and all these parts may be tender to the touch. Brush- 
ing the hair may be impossible, because of the pain produced by the 
brush touching the scalp. Occipital neuralgia is oftentimes bilat- 
eral. It may simply arise from cold or injury; but, if persistent 
and severe, caries of the cervical vertebra should be sought for as a 
possible cause. 
Pain of a neuralgic or dartiug character in the neighborhood of 
the heart is found as the result of several causes, as a rule in the 
following order of frequency: 1. Pain, with palpitation in the 
prsecordium from the accumulation of flatus in the transverse colon 
just as it turns to descend. Many patients who come to the physi- 
cian complaining of heart disease only suffer from this condition, 
due to fermentation. Again, the pain due to gastralgia, or, as it 
has been called, cardialgia, may be referred to the heart by the 
patient. 2. To intercostal neuralgia due to debility. In these cases 
a tender spot will often be found, one in the prsecordium, another 
in the outer edge of the scapula, and a third on the vertebral col- 
umn. These are sometimes called the “ spots of Valleix.” In 
other cases it will be due to spinal trouble, anajmia, or the tight 
lacing of corsets. 3. To pseudo-angina. 4. To true angina pec- 
toris. 5. To locomotor ataxia. 
Pain of a character somewhat resembling true angina pectoris is 
also sometimes met with in patients who have that rare disease, 
acute aortitis. The pain is constant under the sternum, but it has PAIN. 
539 
terrible exacerbations, and a sensation of rending of the retro-sternal 
tissues. Death may occur in an attack. It is seen chiefly in gouty 
patients aud in syphilitics. Very rarely it is seen in patients who 
have suffered from malarial poisoning. 
Pain is felt much more commonly in disease of the aortic orifice 
than in lesions of the mitral orifice of the heart. 
Pseudo-angina occurs most commonly in anaemic, nervous girls, 
or young women whose vessels are normal, but who have hysterical 
tendencies. True angina occurs in those of middle age or advanced 
life or in young persons whose vessels are affected by syphilis. In 
the false form the sensation is as if the heart would burst. In the 
real form it feels as if the heart was squeezed tightly in a vise. In 
this form, too, the bloodvessels will usually be found hard aud 
corded, atheromatous, and the blood-pressure high. The addi- 
tional diagnostic points in favor of true angina pectoris are that the 
principal seat of pain is somewhat to the left of the lower and 
middle sternum, from which spot it may extend to the axilla and 
back and turn off to the occiput or extend down the arms to the 
hands, where a sensation of coldness may be felt. Sometimes even 
the abdominal organs and testicles seem to be affected. The patient 
is motionless, the face anxious and covered with a cold sweat, and 
respiration is shallow. The disease is usually seen in persons over 
forty years of age. The thoracic pain of locomotor ataxia is rarely 
in the prsecordium, but commonly in the axilla, aud it rarely radiates 
down the arm. The other symptoms of tabes dorsalis should be 
sought for in all doubtful cases. (See chapter on Legs and Feet.) 
True angina pectoris is far more rare in women than in men. 
Violent pain, exactly resembling that of true angina pectoris, is 
met with, according to Vergely, in diabetes mellitus. 
Very severe pain, paroxysmal or constant, felt in the chest may 
also be due to aortic aneurism, and, if so, will be found associated 
with pain shooting down the arm on the left side, dilatation of the 
pupil, unilateral sweating of the face and neck, and the physical 
signs described in the chapter on the Thorax. 
Severe pain of a darting character felt in the chest, not due to 
angina or the causes just named, is nearly always an indication of 
one of four things: 1. Intercostal neuralgia, already named. 2. 
Pleuritis, with or without pneumonia. 3. Pericarditis, if it is felt 
in the prsecordium. 4. A morbid growth in the chest, particularly 
a mediastinal tumor or enlarged bronchial glands. 540 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
Both intercostal neuralgia and 'pleurisy are associated with severe 
pain, increased by taking a deep breath, the pain occurring some- 
times with inspiration and sometimes with expiration. They are 
to be separated from one another by the presence of cough, fever, 
aud of a friction-sound in pleuritis, and by the fact that the entire 
side is more or less tender to the touch in this state. When the 
pain is constant and lasts for a long time, it may be due to a low- 
grade pleuritis, resulting from pulmonary tuberculosis, particularly 
of the apex of the lung, the morbid process affecting the pleura. 
Pericarditis is frequently caused by pneumonia, and is painful. 
Pain felt at the right of the left scapula or between the shoulders 
is often due to gastric ulcer or dyspepsia. 
The pain of mediastinal growth is due to pressure on nerve-trunks, 
and the diagnosis may be very difficult unless bulging and dulness 
on percussion are present. 
Neuralgia of the pelvic viscera in women is frequently seen as the 
result of functional or organic disease. It may be ovarian, when it 
is very apt to occur with greatest severity half-way between the 
menstrual epochs or just before them. Sometimes the neuralgia 
may be present in the labia majora or in the perineum. It usually 
occurs simply as a sudden, darting pain, which does not last and, 
indeed, rarely continues more than a moment, although there is 
usually associated with it more or less constant uterine or ovarian 
tenderness. Care should be taken that these pains are not thought 
to be due to cancer or other severe organic lesion. Pain in the 
sacral region is often an indication of uterine or rectal disease. If 
higher up the back, it is often due to myalgia or lumbago; and 
lumbago, if not due to rheumatic tendencies, is often due to the 
colon being loaded with feces. 
If the patient is a child, pain in the back should cause us to sus- 
pect spinal caries, rickets, or scurvy. If the former, any jar will 
greatly increase the pain; but if the child be placed over the knees, 
face downward, and the knees separated so that intervertebral pres- 
sure is removed, the pain disappears. Such a child if told to jump 
down from a stool will not obey, but will take care to slide off 
gradually and gently on to the floor. 
When a patient suffers from violent pain, increased by motion, 
extending from the sciatic notch in the buttock down the posterior 
part of the thigh, even to the ankle or heel, the pain signifies an 
attack of sciatic neuralgia in an adult, or if it occurs in a child gives PAIJS 
541 
grave reason for suspecting hip-disease. If it is not sciatic neural- 
gia, it is clue to sciatic neuritis, or, rarely, to a growth in the pelvis 
pressing upon the nerve before it emerges from the pelvis. The 
pain is fairly constant, generally worse at night, and becomes agon- 
izing at times, even if the patient remains absolutely quiet and does 
not move the limb. The following points will, when pressed on, in- 
crease the pain if it be neuritis: the point of exit of the nerve 
from the pelvis, the lower part of the sacrum, the head of the fibula, 
and behind the malleolus on the outside of the ankle. If these 
points are found, combined with a history of exposure to cold, in- 
jury to the nerve, rheumatic tendencies, and a persistency and ten- 
dency to return, the diagnosis of sciatica is clear. If the pain be 
due to sciatic neuritis, there may be found wasting in the muscles 
supplied by the nerve, and some anaesthesia of the skin, and herpetic 
eruptions may appear on the skin along the course of the nerves. 
There will be also a history of long duration, and the leg will be 
apt to feel numb and tense from effusions into the sheath of the 
nerve. (See chapters on Skin and Feet and Legs.) When the 
pain is a pure neuralgia, which is rare, it will not be increased 
by moving the limb, there is little or no tenderness on pressure 
on the nerve-trunk, and the patient often has neuralgia of other 
nerves. 
Sciatica is much more common in men than in women, and far 
more usual in middle or advauced age than in the young. 
Double sciatic pain should arouse suspicion of locomotor ataxia, 
of malignant growth pressing on the spinal cord or on both nerves 
in the pelvis, or the presence of lumbar abscess. 
When there is a hysterical, painful joint at the knee or hip in a 
woman, care is necessary to discover that the pain is over the entire 
leg rather than in the course of the nerve. Care must also be taken 
that rheumatism of the muscles of the thigh be not taken for sciatica. 
This can be separated from sciatica by the diffuse character of the 
pain and tenderness and by the fact that in the rheumatic condition 
the slightest muscular movement causes pain all over the thigh. 
Sometimes a malignant growth of the femur may produce symptoms 
of sciatica, and the writer not long since had under his care a case 
of osteosarcoma of the thigh bone which had been treated for sciatica 
for several months. 
Finally, renal calculus may cause violent pain to pass down the 
leg. (See below.) 542 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
It should also be remembered that malingerers, particularly 
soldiers desiring to shirk duty, often pretend to have sciatica. 
Abdominal Pain. Neuralgic pain in the back and abdominal 
parietes very closely resembling, if severe, renal or hepatic colic is 
sometimes seen in gastrcilgia, and the paroxysms may be very sudden 
in onset. In other instances the pain is in the epigastrium or hypo- 
gastrium, and is associated with so much tenderness on light press- 
ure as to impress the careless with the belief that a gastric ulcer or 
cancer is the cause. Neuralgic spots can generally be isolated in 
such persons if the skin is carefully tested for its degrees of sensa- 
tion, and will be found to exist near where the nerves are given off 
from the spine or over the spine of the ilium. There are other causes 
of these lightning abdominal pains than simple functional neuralgia, 
so called, and renal and hepatic colic, which should never be for- 
gotten in the diagnosis of a case, namely, locomotor ataxia manifested 
in gastric crises, lead-poisoning shown by a neuralgia due to a neu- 
ritis, and disease of the vertebrae causing pressure on the nerve-trunks. 
Further than this, we are to remember that cancer and ulcer of the 
stomach often cause exceedingly severe, painful attacks ; that abdom- 
inal aneurism may cause severe pain by pressure on nerves; and that 
uterine and periuterine disease also cause, reflexly, epigastric pains. 
By colic we mean a sudden, griping pain in the belly. It is met 
with chiefly in cases of stone in the ureter or gall-duct, but it is 
often due to irritating food, to wind, and to chronic lead-poisoning, 
to fecal impaction, intestinal obstruction, intestinal perforation, and 
ulcer of the bowels. 
Reference has already been made to the pain of renal and hepatic 
colic. The characteristic symptoms of these conditions are as fol- 
lows: in renal colic the patient is suddenly seized with violent pain 
in the kidney on one side, which passes down to the groin and even 
to the end of the penis. It is paroxysmal in character, and so 
excessively severe that it often produces sweating, vomiting, and 
even fainting. The condition is seen much more frequently in men 
than in women. The pain often suddenly subsides, leaving only a 
sense of soreness and tenderness in its track. The urine may be 
partly suppressed and bloody if the stone injures the ureter to any 
great, extent. Pain simulating renal colic may be due to neuralgia 
or arise from several organic causes not connected with calculus. 
Thus, Habershon has stated that in valvular disease of the heart, 
particularly of the aortic valve, severe and colicky pains frequently PAIN. 
543 
radiate down into the right hypochondriac region, and Ralfe says 
into the renal region. Again, pain in this part may be due to 
aneurism of the aorta or of the mesenteric artery. Further, the 
accumulation of hard fecal matter in the colon may cause nephralgia. 
Finally, Ralfe calls attention to the renal pain felt generally in the 
right kidney by women who have exercised violently while wearing 
a tight corset, which has pressed upon the liver and kidney with great 
force on making a jump or sudden bend of the trunk. Sometimes 
sudden “ storm ” of uric acid or an accumulation of oxalic acid in 
the kidney causes pain and tenderness. When the pain is due to 
pyelitis the urine will always show pus and perhaps blood. 
In hepatic colic the patient often, after some days of wretchedness 
and “ biliousness,” is seized by sudden and violent pain in the right 
hypochondrium, which is paroxysmal in character and causes quite 
as profound general symptoms of disorder as does the renal colic. 
Jaundice very commonly ensues in such cases with more or less rap- 
idity, and fever of an irregular type is more often seen than in the 
renal form. The pains just described are so severe and character- 
istic in their distribution that they cannot well be confused with 
those of intestinal indigestion, in which condition we have a history 
of the ingestion of bad food, a state of more or less flatulent disten- 
tion of the entire belly, and, it may be, diarrhoea. Sometimes violent 
belly pain is due to aneurism. If the pain be due to chronic lead- 
poisoniug, it centres about the umbilicus, and is of a twisting, knotty 
character, “ as if the bowels were being twisted around a stick.” There 
is a history of exposure to lead in many cases, and a blue-line on the 
gums can often be found. If due to fecal impaction, we will have 
a history of a continued tendency to constipation, with dry, hard 
stools, and a lump of hardened feces may perhaps be felt through 
the belly-wall. In perforation of the bowel the patient speedily 
becomes collapsed, and suffers severe pain. This accident generally 
occurs in persons convalescing from typhoid fever. If due to in- 
testinal obstruction, the pain has no characteristic seat in any part 
of the abdomen, as a rule; but the general symptoms of this con- 
dition will be found present in the case. (See chapter on Abdomen 
and that on Vomiting.) 
The pain of colic due to flatulence can be separated from that of 
peritonitis by the fact that pressure gives comfort in the first instance 
and is unbearable in the latter disease. 
Pain in the abdomen of the darting neuralgic type, other than 544 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
that due to gall-stones, renal calculi, ordinary gastralgia, lead-pois- 
oning, euteralgia, or malignant growth, may be due to locomotor 
ataxia. This should never be forgotten, and the fact that the 
patient is full-grown, complains of the most violent pain in the 
belly, and has no other abdominal signs, should make us search 
him for the other sigus of tabes dorsalis. Generally, these attacks 
will be of a tearing, rending character, are beyond description in 
severity, and leave the man in a condition of nervous wreck after them. 
Sometimes the pain is in the stomach, sometimes in the bladder. 
Grube has recently reported cases showing that diabetes may pro- 
duce violent abdominal attacks of pain resembling the crises of an 
ataxia. 
The following table summarizes the subject as already discussed 
in these pages: 
Abdominal Conditions in which Sudden and Acute Pain forms a 
Prominent Symptom.1 
Character of pain. 
Mode of 
Tenderness and 
Disease. 
onset. 
In kind. 
In inten- 
sity. 
Seat of pain. 
pressure. 
Acute intestinal 
obstruction: 
a. Strangula- 
tion due to 
bauds. 
Very sud- More or less 
den. continuous. 
Most in- 
tense, 
agonizing. 
Epigastric or um- 
bilical region. 
Pressure at first re- 
lieves, afterward 
aggravates. 
b. Acute intus- 
susception. 
Sudden Paroxysmal. 
to very | 
sudden 
Severe 
Epigastric or um- 
bilical region. 
Pressure at first re- 
lieves, afterward 
aggravates. 
c. Acute volvu- 
lus. 
Sudden. Paroxysmal, 
but less than 
b. 
Moderate. 
Umbilical or over 
heart. 
Pressure never 
causes pain. 
d. Due to gall- 
stone or 
stricture. 
Less sud- Paroxysmal 
den, gra- later, 
dual. 
Moderate. 
Often near seat of 
obstruction. 
Tenderness over 
obstruction. 
Appendicitis. 
Very sud-1 Quite con- 
den. tinuous. 
Agonizing. 
At first periumbili- 
cal, later about 
appendix. 
Greatest over ap- 
pendix or in left 
groin. 
Acute peritonitis. 
Very sud- Continuous, 
den. 
Very severe 
All over belly, but 
chiefly epigastric 
or umbilical. 
Very tender every- 
where except at 
very first. 
Hepatic colic. 
Sudden. Aching, tear 
ing, parox- 
ysmal. 
Agonizing. 
Epigastric, radi- 
ating to between 
shoulders or to 
shoulder-blade. 
Pressure at first re- 
lieves, then un- 
bearable over 
gall-bladder. 
Renal colic. 
Sudden. Aching, tear- 
ing, parox- 
ysmal. 
Agonizing. 
Affected loin, pass- 
ing down in front 
into testicle and 
bladder. 
Tenderness over 
affected kidney. 
Intestinal colic. 
Sudden Paroxysmal, 
or 
gradual. 
Varies in 
severity. 
Varies in position. 
Relieved by pres- 
sure. 
1 Andrew’s table, slightly modified. PAIN. 
545 
Generally diffused pain of a constant severe character felt all over 
the abdomen or localized at first to some particular spot, and greatly 
increased by pressure, should lead the physician to examine the case 
for a possible 'peritonitis. Nothing else causes such violent, diffuse 
pain unless it be acute enteritis. The well-flexed legs, the anxious 
face, the drawn upper lip, quick pulse, exquisitely tender abdominal 
surface, the thirst, the moderate fever, and the rapid onset of collapse 
in fatal cases render the diagnosis easy. 
Circumscribed abdominal pain of a constant character and gener- 
ally of less severity than that just described, may be due to dysmen- 
orrhoea, to an abdominal tumor (see Abdomen), to an ovaritis, to 
cystitis, hepatitis, ulcer of the stomach or bowel, typhlitis, peri- 
typhlitis, appendicitis, and cholangitis. In appendicitis the onset 
is usually very sudden and severe, and is only equalled by that of 
gallstone colic, renal colic, and perforation of the bowel by neu- 
ralgia and by a crisis in ataxia. It is also seen in a very violent 
form in acute pancreatitis, which may give rise, with the other 
symptoms, to a diagnosis of peritonitis. In dysmenorrhcea the pain 
is sometimes so severe as to render the patient almost insane, but it 
differs from that of inflammation in that it is paroxysmal and that 
there is no real tenderness on pressure; and, again, the patient 
does not lie still, but tosses from side to side in the bed. The pain 
of tumor is usually produced by pressure on a nerve, and is increased 
by palpation in some cases, as is also that of ovaritis. In cystitis 
the pain is deep in the pelvis, radiating upward, and is associated 
with tenderness, vesical spasm, and tenesmus. In hepatitis the pain 
is distinctly in the hypochondrium, although if the condition be 
suppurative it may be well diffused. The pain of ulcer of the 
stomach is not only gastric, but is often associated with a tender or 
painful spot at the angle of the scapula. In typhlitis, perityphlitis, 
and appendicitis it is chiefly in the right groin, and in cholangitis 
in the hepatic area anteriorly. Care should be taken that the pain 
in this region is not taken for hepatitis, when it is in reality due to 
a subphrenic abscess. In pancreatitis the pain is sudden in onset, 
violent, and often felt chiefly in the left upper zone of the abdomen. 
The belly is distended, nausea and vomiting are present, and fever 
may be present also; delirium may come on, and death generally 
speedily ensues. 
The pain of fissure of the anus is not at all proportionate to the 
lesion producing it. This pain may be atrocious and agonizing, and 546 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
often is produced by a movement of the bowels, after which it lasts 
for some hours. 
(For abdominal pain due to conditions associated with movements 
of the bowels, see chapter on Bowels and Feces.) 
Neuralgia of the toe and foot is not a very rare condition, and is 
sometimes called “ Morton’s painful toe,” or metatarsal neuralgia. 
Severe pain at the base of the fourth toe comes on suddenly, and 
may radiate up the anterior aspect of the leg. Sometimes it is only 
dull, but at others it is so sharp and excruciating as to cause the 
patient to scream. It is separated from gout by the absence of any 
signs of inflammation in the part, by the fact that the big toe is not 
affected, and by the age and history of the patient. At times the 
base of the second toe is affected. Such a case will usually indicate 
that the patient has worn an ill-fitting boot. 
Finally, in connection with this class of cases there should not 
be forgotten two others, namely, those in which, idiopathically or 
otherwise, growths form on nerves and cause pain; and, secondly, 
cases in which the arm or leg having been amputated, a neuroma 
or catching of the end of the nerve in the scar causes violent pain 
in the lost part, according to the patient’s sensation, because the 
perceptive centres have been trained to regard pain-impulses coming 
along this nerve as from its peripheral end. Thus a man whose leg 
may have been amputated years before will complain of severe pain 
in the amputated foot, although he knows it is off. 
The pain of inflammation is often very severe and throbbing in 
character; but, if the nerves be affected in the area involved, it may 
be darting in its nature. We have already discussed pain due to 
inflammation in the tissues of the head and in the nerves. We now 
have to consider the indications of pain due to inflammation in the 
chest and abdomen. 
Pain in the back is often very severe in the early stages of small- 
pox, of epidemic influenza, and in lumbago. One of the most mis- 
leading forms of pain of a severe character, involving the entire 
body, with fever, delirium, and a variable skin eruption and swell- 
ing of the joints, may in the early stage be thought to be smallpox 
or rheumatic fever, when in reality it is due to dengue or break'bone 
fever. CHAPTER VIII. 
TENDON-REFLEXES AND MUSCLE-TONE. 
The knee-jerk and ankle-clonus—The arm-jerk—The significance of decreased and 
increased reflexes. 
We have already had occasion, particularly in those chapters de- 
voted to the Legs and Feet and the Arms and Hands, to speak of what 
are called the reflexes or“ muscle-jerks.” There is much discussion 
as to whether the muscular contractions produced by tapping the 
tendon attached to a muscle are the result of a reflex action, in which 
the spinal cord is directly involved, or whether it depends upon 
muscle irritability or tone. It is not necessary for purposes of diag- 
nosis to enter iuto a discussion of this character, because the facts in 
our possession prove conclusively that variations in these muscle- 
jerks are of great diagnostic importance in diseases of the nervous 
system, whether they be true reflexes or not. The knee-jerk, or, 
as it has been called, the patellar reflex, is the diagnostic sign most 
frequently sought in studying nervous diseases associated with lesions 
in the spinal cord, because it is most easily developed. 
This knee-jerk is best developed by directing the patient to sit in 
an ordinary chair and to cross the legs, the foot which touches the 
floor being kept near the rounds of the chair rather than well for- 
ward, and the upper leg being allowed to swing perfectly free over 
the under knee. By means of the finger-tips, the side of the hand, 
or a small rubber hammer, a blow is now struck upon the tendon of 
the quadriceps extensor midway between the patella and the inser- 
tion of the tendon below the knee, and, if the man is healthy, the 
hanging leg and foot are at once thrown forward; that is, the knee- 
jerk is developed. 
If there be produced by the patient at the moment of the tap on 
his tendon a strong muscular effort, as by sudden clinching of the 
hands, this movement of the leg is exaggerated, or, to use the com- 
mon term, the knee-jerk is “ re-enforced.” 
The production of pain or a sensory stimulation will also increase 
the knee-jerk, as will also the stirring of the emotions as by lively 548 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
music. On the other hand, enervating weather, loss of sleep, 
hunger, or anything which decreases general systemic and muscular 
tone decreases the knee-jerk. 
The second most important test of the muscular tone is the test 
for what is called “ ankle-clonus.” If a healthy person while sit- 
ting rests the weight of the leg on the ball of the foot, the leg is 
very apt, in a short time, to begin to tremble, and finally to develop 
clonic movements. In disease these movements often develop as 
soon as the foot is placed in this position, and are at once developed 
if, while the leg is so placed, a sharp blow is struck above the knee 
or sudden pressure is made on the leg. In other cases the clonus is 
tested for by grasping the ankle with one hand and the toes with 
the other and bending the foot up toward the knee with 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 reflex, 
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 absent or abnormally 
increased. 
A loss of knee-jerk is not characteristic of any disease unless this 
loss is associated with other symptoms which ouly need the discovery 
of this symptom to confirm the diagnosis. The nervous conditions 
in which we find the reflexes decreased or lost, taking the patellar 
reflex as a type, are locomotor ataxia; peripheral neuritis; polio- 
myelitis, 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 injuries, immediately after the accident; epilepsy, immediately 
after an attack; and chorea. We also fiud a total loss of reflexes 
in advanced diabetes mellitus and sometimes in diabetes insipidus. 
By far the most common cause of the loss of the knee-jerk is loco- 
motor ataxia, but any lesion involving the posterior columus of the 
cord or the posterior nerve-roots in the second, third, or fourth lum- 
bar segment will produce the same results. Therefore, loss of knee- 
jerk is symptomatic of transverse myelitis of this region as well as 
of ataxia. Again, if the motor tract of the cord at these levels is TENDON-REFLEXES AND MUSCLE-TONE. 
549 
diseased, the knee-jerk is lost, as, for example, in acute and chronic 
poliomyelitis or myelitis involving the motor part of the reflex arc; 
and, finally, peripheral neuritis, which blocks the pathway from the 
periphery to the cord, and from the cord to the muscles, also cause 
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 
usually be a child if the disease is acute. If the loss be due to 
transverse myelitis of the second, third, and fourth lumbar seg- 
ments, 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 
history 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 the attack; disseminated sclerosis; cerebral palsy 
of childhood ; paretic dementia (not constant) ; primary lateral scle- 
rosis ; amyotrophic lateral sclerosis; ataxic paraplegia; hysterical 
paraplegia; 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 the recovery 
from first shock ; pressure on spinal cord above the reflex arc ; hered- 550 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
itary 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 dissemi- 
nated 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 diag- 
nosis. In lateral sclerosis the spastic rigidity, excessive exaggera- 
tion 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 peculiar 
facies, the areas of anaesthesia and hypercesthesia, and the peculiar 
gait point 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 
exhausted. 
Leaving the knee-jerk as a type 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 page 551, from Taylor’s Index of Medi- 
cine, 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 progres- 
sive muscular atrophy the reflexes of the arms are lost, while those 
of the legs are preserved, and in tubercular meningitis the reflexes 
are 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 lateral sclerosis, in dissemi- TENDON-REFLEXES AND MUSCLE-TONE. 
551 
nated sclerosis, and in amyotrophic lateral sclerosis. A false clonus 
is sometimes seen in hysteria. 
Keflex. 
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 
dorsal 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. 
Absent in disease only. CHAPTER 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 amount of diagnostic information to the physician. 
While in many diseases no marked alterations from the normal 
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 whispering voice. In persons suffering from pul- 
monary tuberculosis the development of hoarseness and whispering, 
or labored speech tells us only too well of the fact that the grave 
and distressing complication called laryngeal tuberculosis 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 hysteria, 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 hoarseness 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, rapid radial 
pulses, we should suspect aortic aneurism or a mediastinal tumor 
which is pressing on his recurrent laryngeal nerve. 
Hysterical mutism may occur in both males and females. It 
usually follows a fright or violent emotion, or it may follow an 
hysterical seizure. Sometimes it develops without any such history. 
The condition lasts from a few hours to months or years, and re- 
covery is often as sudden and unsuspected as the onset. As a 
rule, the tongue, lips, and jaws are unimpaired in their functions. 
Sometimes, however, these parts are affected by hysterical spasm. 
Often there will be hysterical anaesthesia with the mutism. Usually 
there is no evidence of cerebral lesion in such cases in the sense of 
impairment of intellect. SPEECH. 
553 
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, hesitating 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 complaint, 
which renders his breath short, so that he hurries through his sen- 
tence in order to be able to breathe freely again. Thus, in cases of 
pneumonia or of pulmonary oedema this hurried speech is a very 
constant sign. 
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 
develops a slow, scanning speech, with intention-tremors (see chapter 
on Hands), 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, Friedreich’s ataxia; but the facts that this dis- 
ease begins in childhood, that several members of the family are apt 
to be affected, that there are ataxic symptoms and early talipes 
equinus, render it easy to separate this affection from insular scle- 
rosis. (See Paraplegia, in chapter on Feet and Legs.) 
A hesitating, halting speech associated with Argy 11-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 dementia. 
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 
suffering from this disease. 
A very indistinct speech of a mumbling character, great difficulty 
being experienced in the pronouncing of dental and lingual sounds, 554 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 may 
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, piping 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 aud 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 couveys the sound 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 developed 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 howto say certain words, and the lesion is in the third left frontal 
(Broca’s) convolution. He can read t(f 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 repeat a word imme- 
diately after you have said it by a purely imitative process. Gen- 
erally we find with aphasia a condition called agraphia, in which SPEECH. 
555 
the patient cannot write voluntarily, but can copy perfectly. In 
the great majority of cases of aphasia, however, the patient is par- 
alyzed in his right hand, so that the symptoms of agraphia cannot be 
demonstrated. Under the name of paraphasia we sometimes meet 
with a condition in which the patient 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 which the patient can spell out words from a page set before 
him, but he cannot read, because the words convey no idea to him. 
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-deafness.” 
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. 
Aphasia is quite frequently met with as a symptom of hysteria, 
and may occur independently of any organic lesion, so far as we 
know, in children during convalescence from an attack of a severe 
infectious disease. In the latter cases speech may return many 
months after. 
The following plan of testing a patient, devised by Eskridge from 
a shorter one by M. Allen Starr, may be followed with ad vantage : 
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. 556 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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. 
13. The power to write voluntarily. 
14. The power to write at dictation. 
15. The power to copy, and the manner of copying, printing, and 
writing. 
16. The power to write the names 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 being guided by another. 
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. 
23. Does the patient recognize his mistakes in speaking and 
writing, and can he correct them ? 
24. Can the patient think in speech (propositionize) ? 
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. SPEECH. 
557 
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. 
It is not to be forgotten that speechlessness is often present in 
melancholia and dementia. Further, temporary speechlessness or 
apparent aphasia may follow severe typhoid fever as a result of 
cortical exhaustion without the development of hemorrhage, em- 
bolus, or thrombus. The prognosis is favorable. INDEX. 
A BADIE’S sign, 45 
xi. Abdomen, 320 
causes of distention of, 322 
of localized bulging of wall 
of, 323 
of pain in, 540, 542 
of protrusion of wall of, 321 
of retraction of wall of, 321 
of swelling in epigastrium, 
326 
frog-belly, 321 
inequality in shape of, due to me- 
teorism in intussusception, 508 
palpation of, 328 
regions of, 321 
tumors of, 336 
Abscess, cerebral, choked disk not gen- 
erally present in, 191, 505 
character of pain in, 537 
coma in, 477 
diagnosis of, 505 
fever in, 505 
gangrene in, 225 
symptoms of, 465, 477 
tache cerebrale, a sign of, 211 
vomiting in, 505 
hepatic, brick-dust sputum in, if 
communicating with the lung, 
527 
character of pain in, 545 
symptoms and signs of pysemic, 
341 
symptoms and signs of tropical, 
341 
vomiting in, 519 
lumbar, sciatic pain in, 541 
mastoid, oedema back of the ear in, 
233 
mediastinal, purulent sputum in, 528 
perinephritic, bulging of flank in, 
338 
pulmonary, chronic morning cough 
in, 523 
copious and purulent sputum in, 
294, 528 
diagnosis between mediastinal 
growths and, 303 
elastic fibres in sputum of, 530 
following amoebic dysentery, an- 
chovy-sauce sputum in, 527 
Abscess, pulmonary, history, signs, and 
symptoms of, 294 
pyo-pneumothorax subphrenicus, 336 
subphrenic, purulent sputum in, 
528 
“Accoucheur’s hand” in tetany, 71 
Acne due to bromine or iodine, 218 
due to iron, 218 
due to working in paraffin, 218 
of forehead, purulent, in syphilis, 
221 
Acromegaly, enlargement of feet in, 114 
of tongue in, 151 
face of, 34 
head in, 49 
spade-like hand in, 64 
Acroparesthesia, 258 
diagnosis of, 258 
Actinomycosis, actinomyces in sputum in, 
531 
enlargement of tongue in, 151 
Acute yellow atrophy of the liver. See 
Yellow Atrophy of the Liver, Acute 
Addison’s disease, appearance of tongue 
in, 146 
diagnosis of coma in, 478 
heart in, 318 
pigmentation of buccal mucous 
membrane in, 156, 318 
of skin in, 204, 318 
symptoms of, 205, 520 
vomiting in, 520 
JEgophony over pleural effusions, 291 
iEsthesiometer, 235 
Agraphia, 555 
location of lesion in, 555 
Albuminuria, anemic, 403 
boiling-test for, 402 
cyclic, 403 
due to renal congestion, 403 
Heller’s test for, 403 
indicative of renal disease, 403 
marked, or absent, in amyloid kid- 
ney, 415 
quantitative test for, by centrifuge, 
403 
transient, in chronic interstitial 
nephritis, 415 
Albumosuria, Harris’s test for, 407 
in normal puerperium, 409 560 
INDEX. 
Albumosuria said to be due to the action! 
of microorganisms, 409 
significance of, 409 
Alcoholism, convulsions due to, 488, 495 
hyperesthesia in chronic, 261 
morning vomiting in, 516 
symptoms of acute, 476 
Alexia, 555 
location of lesion of, 555 
Allochiria in hysteria, 258 
in multiple sclerosis, 258 
in myelitis, 258 
in paralysis agitans, 258 
in tabes dorsalis, 258 
Amaurosis, 194 
significance of, in brain-tumor, 464 
Amblyopia, 192 
Amoeba coli, 425 
Amphoric breathing, rarely heard in 
pneumothorax, 287 
in small cavity, 287 
Amyloid disease of kidney, 416 
hyaline, fatty, and granular j 
casts in urine in, 416 
syphilis, prolonged suppu- 
ration, and extensive bone 
disease accompanying, 
416 . 
urine in, 415 
of liver, enlargement and 
smoothness of liver in, 
340, 341 
history of prolonged suppu- 
ration elsewhere in, 341 
jaundice occurring in, 199 
Anaemia, albuminuria in, 403 
appearance of nails in, 54 
of tongue in, 146 
bothriocephalus latus, a cause of, 434 
cerebral, choked disk in, 506 
vertigo in, 471 
vomiting in profound, 505 
dropsy of feet and legs in, 231 
headache in, 470 
hyperaesthesia in, 261 
in acute diffuse nephritis, 418 
in anchylostomum duodenale, 366, 
434 
in atrophy of gastric tubules, 364 
in bleeding hemorrhoids, 365 
in cancer, 366 
in chronic indigestion, 365 
lead- or arsenic-poisoning, 366 
in convalescence from infectious dis- 
ease, 364 
in gastric ulcer, 366 
in hemorrhage, 365 
in malaria, 366 
in renal disease, 366 
in sarcoma, 366 
in tapeworm, 366 
in tubei’culosis, 366 
Anaemia in uraemic poisoning, 366 
oedema in, 231 
pallor of conjunctiva in, 158 
papillitis in, 191 
pernicious, cardiac palpitation in, 
365 
change in red blood-corpuscles 
in, 365 
chills followed by fever in, 448 
gradually increasing dyspnoea 
in, 365 
indicanuria in, 390 
jaundice in, 201 
marked pallor without loss of 
flesh in, 365 
pulsating cervical vessels in, 269 
venous murmurs in, 365 
vertigo in, 365 
purpuric eruptions in, 210 
Anaesthesia, 239 
bilateral, in Friedreich’s ataxia, 245 
in hemorrhage of the cord, 246 
in hysteria, 244 
in injuries of the cord, 244 
in lesions of the pons, 244 
in locomotor ataxia, 245 
in meningitis, spinal, 244 
in myelitis, 245 
in spinal disease, 244 
in syringomyelia, 249 
never in cerebral lesions, 244 
crossed, in lesion of one side of the 
cord, 243 
of peduncle, 243 
of pons, 243 
differential diagnosis in facial, 256 
distribution of, in special nerve in- 
volvement, 253 
dolorosa, in cancer of spine, 247 
gauntlet or stocking form of, in hys- 
teria, 242 
in 50 per cent of neuritis due to 
diphtheria, 252 
location of lesion of, in the spinal 
cord, 247 
of body and legs, in locomotor ataxia, 
245 
of Friedreich’s ataxia, 245 
of myelitis, 245 
of toxic peripheral neuritis, 251 
patches of, in leprosy, 257 
in syringomyelia, 247, 257 
reflexes preserved in cerebral, 243 
signs of, due to neuritis, 251 
zones of, 249 
Analgesia in locomotor ataxia, 245 
in Morvan’s disease, 68 
Anascara, general. See General Ana- 
sarca. 
Anatomy of brain, 127 
of optic nerve, 183 
of sensory tracts, 236, 247 INDEX. 
561 
Anatomy of tongue, 141 
Anchylostomum duodenale, anaemia due 
to, 366, 434 
Aneurism, aortic, blood-streaked sputum 
due to leakage from aorta in, 
527 
bulging of chest in, 267 
dilatation of pupil in, 180 
haemoptysis in, 527 
pain in, 539 
brassy bough due to pressure on 
larynx by, 310, 524 
bruit in, 309 
dyspnoea or dysphagia in, 309 
enlarged cervical vessels in, 269 
hemorrhagic pleural effusion in, 299 
history of syphilis in, 309 
hoarseness of voice due to pressure 
on recurrent laryngeal nerve by, 
552 
intracranial headache due to, 470 
laryngeal spasm due to pressure on 
recurrent laryngeal nerve by, 302 
loss of pulsation in peripheral ves- 
sels in, 311 
oedema of upper extremities in, 232 
pain in abdominal, 542 
pressure on bile-duct causing jaun- 
dice in, 199 
sweating of side of head in, 229 
symptoms of, 309 
tracheal tugging in, 311 
Angina pectoris, causes of, 347 
character and position of pain 
in, 539 
symptoms of, 539 
Angioneurotic oedema, appearance of 
hands in, 63 
of skin in, 234 
Ankle-clonus, false, in amyotrophic lat- 
eral sclerosis, 550 
how best elicited, 548 
in ataxic paraplegia, 91 
in hysteria, 551 
in lateral sclerosis, 550 
most marked in disseminated scle- 
rosis, 550 
Annulus migrans, 150 
senilis, 159 
Anthrax maligna, anthrax bacilli found 
as cause of, 453 
character of fever in, 453 
symptoms of, 223, 453 
simplex. See Carbuncle. 
Aorta, aneurism of abdominal, 337 
descending, symptoms of, 
311 
greater curvature of ascend- 
ing, symptoms of, 311 
transverse portion of arch 
of, symptoms of, 311 
Aortitis, acute, causes of, 528 
Aortitis, acute, character of pain in, 528 
Apex-beat, 273 
Aphasia due to hematoma near island of 
Eeil, 137 
due to hemorrhage into island of 
Reil, 137 
Aphonia in hysteria, 552 
Aphthongia, spasm of tongue in, 153 
Apoplexy, albuminuria in, 409 
Cheyne-Stokes breathing in, 271 
coma in, 476 
conjugate lateral paralysis of ocular 
muscles in, 175 
contractions following, 69 
diagnosis between coma of, and alco- 
holism, 466 
ingravescent, 136 
involuntary passage of urine in, 386 
knee - jerk exaggerated some time 
after shock, 550 
increased immediately after 
shock, 548 
skin-reflexes lost when deep reflexes 
exaggerated, 521 
vertigo before, 471 
Appendicitis, character of fever in, 454 
of vomiting in, 512 
pain in, 546 
Appetite, wayward, in chlorosis, 366 
Apraxia, 555 
location of lesion in, 555 
Arcus senilis, 159, 318 
Argyll-Robertson pupil, 87, 179 
not present in ataxic paraplegia, 
91 
in Friedreich’s ataxia, 88 
present in diabetes mellitus 
rarely, 180 
in true ataxia, 179 
Argyria, 203 
Arms, movements of, 69 
spastic rigidity of, an early sign of 
chronic hydrocephalus, 71 
tremors of, 75 
Arrested development, 97 
cerebral spastic paraplegia in, 
97 
Arterial tension, 347 
causes of high, 348 
of low, 348 
high in acute diffuse nephritis, 
415 
Arteritis, symptoms of syphilitic, 464 
Arthritis deformans, distortion of fingers 
in, 57 
enlargement of joints in, 121 
formation of osteophytes in, 122 
knee-jerk increased in, 550 
seal-fin hand of, 61 
gonorrhoeal, 124 
septic, appearance of hands in, 62 
Arthropathies, 121 562 
INDEX. 
Ascaris lumbricoides, 431 
Ascites, apex-beat raised in, 273 
Caput Medusae in hepatic cirrhosis 
causing, 325 
diagnosis of, 322 
examination of withdrawn fluid in, 
324 
rapid respiration in, 270 
skin of abdomen in, 227 
Asthenic bulbar paralysis. See Paralysis, 
Asthenic Bulbar. 
Asthma, catarrhal pneumonia following, 
301 
character of rales in, 301 
due to cardiac lesions, 301 
due to .gastric disorders, 301 
due to reflex nasal irritation, 301 
due to renal disease, 301 
erect position in, 300 
expiration prolonged in, 270, 301 
physical signs and symptoms of, 
300 
rapid respiration in, 269 
sputum of, Charcot-Leyden crystals 
in, 301 
Curschmann’s spirals in, 301 
pearls of Laennec in, 528 
Asymmetry, facial, 33 
Ataxia, Friedreich’s. See Friedreich’s 
Ataxia. 
hereditary cerebellar, 89 
spinal. See Friedreich’s Ataxia, 
locomotor See Locomotor Ataxia. 
Atheroma, headache in, 471 
in chronic interstitial nephritis, 416 
in old age, 347 
in syphilis, 347 
symptoms of, 347 
Athetosis, 77 
reflexes increased in, 551 
Atrophy, acute yellow, coma in, 475 
jaundice in, 201 
bilateral, of tongue, causes of, 150 
facio-humero-scapular type of, 30 
idiopathic muscular, ptosis in, 41 
of gastric tubules, anaemia in, 362 
of nails, 55 
optic, 192 
progressive muscular, 66 
Aran-Duchenne type of, 117 
claw-hand in, 66 
condition of reflexes in, 550 
excessive sweating of hand 
in, 55 
fibrillary twitch in, 77 
leg-symptoms of, 115 
-type of, 115 
peroneal leg-type of, 117 
Aura, 480 
Autointoxication, headache in, 460 
poisons causing, 460 
symptoms of, 460 
BACCELLI’S sign, 291 
Bacilli, anthrax, 453 
in preputial smegma, 401 
in stools in cholera, 421 
in tubercular pyelitis, 417 
methods of examining for, 531 
of Eberth, in stools of typhoid 
fever, 439 
of tuberculosis in urine, 421 
Bedsores in acute transverse myelitis, 226 
in hemiplegia, 226 
Behavior in advanced hepatic and renal 
cirrhosis, 20 
in opium-poisoning, 20 
of child with cerebral trouble, 23 
of healthy child, 23 
Bergeron’s chorea, 73 
Beri-beri, general anasarca in, 231 
Bilious remittent fever. See Malaria, 
Remittent. 
Biceps tendon reflex, how developed, 548 
Bilateral anaesthesia, 244 
facial paralysis, 43 
ptosis, 41 
Bladder, causes of incontinence of urine 
in the, 379 
of retention of urine in the, 378 
character of blood in urine from the, 
385 
nervous, 382 
paralysis of, 379 
stone in, 382 
symptoms of disease of, 378 
of inflammation of, 381 
-symptoms of myelitis, 379 
of paretic dementia, 381 
of tabes, 381 
Blood, estimation of hemoglobin in, by 
hemoglobinometer of v. Fleischl, 
363 
in sputum, 527 
in stools, 426 
character and significance of, 426 
in dysentery, 424 
in entero-colitis, 423 
in urine, 384 
Heller’s test for, 385 
in vomitus, 513 
method of staining with Ehrlich’s 
triple stain, 356 
normal constitution of, 353 
parasites of, 368 
red corpuscles of, change in, in anae- 
mia, 365 
coloring-matter of, decreased 
in oligochromaemia, 354 
decreased in myelogenous 
leukaemia, 369 
in oligocythaemia, 353 
estimation of, by hemato- 
cy tome ter, 358 
with hematocrit, 360 INDEX. 
563 
Blood, red corpuscles of, extraordinary 
decrease of, in pernicious 
ansemia, 365 
increased in polycythemia, 
353 
megaloblasts, 358 
megalocytes, 354 
microblasts, 356 
microcytes, 354 
normoblasts, 354 
nucleated, 354 
poikilocytes, 354 
shadow corpuscles, 354 
varieties of, 353 
white corpuscles of, amoeboid move- 
ment of, impaired in leu- 
kaemia, 355 
eosinophiles, 355 
estimation of, with hemato- 
cytometer, 358 
increase of, 355 
lymphocytes alone increased 
in lymphatic leukaemia, 
354 
mononuclear leucocytes, 355 
multinuclear leucocytes, 355 
neutrophiles, 355 
polymorphous leucocytes, 
355 
polynuclear leucocytes, 355 
proportion of, to red, 354 
Toison’s solution for count- 
ing, 359 
Blowing breathing. See Bronchial Breath- 
ing. 
Boils in diabetes mellitus, 223 
in paraffin-workers, 223 
in tar-workers, 223 
Bothriocephalus latus, 429 
Bowels, constipated, in jaundice, 197 
patient’s idea as to regularity of, 21 
Brachial monoplegia, 79 
apparent, 83 
causes of cortical lesions in, 89 
due to cortical lesions, 79 
due to crutch-paralysis, 83 
due to fracture or dislocation of 
the head of the humerus, 82 
due to growth in neck or axilla, 
82 
due to hysteria, 81 
due to injury of the brachial 
plexus or important branches, 
81 
due to lead-poisoning, 83 
due to locomotor ataxia, 82 
due to primary brachial neuritis, 
82 
Erb’s paralysis, 82 
Klumpke’s paralysis, 83 
paralysis of special muscles in, 
83 
Brachial monoplegia, signal - symptoms 
of cortical, causes of, 80 
parsesthesia, 84 
Bradycardia, 317, 352 
in jaundice, 317 
in typhoid fever, 317 
Bramwell’s method of staining and 
mounting casts in urine, 396 
Breakbone fever. See Dengue. 
Breath in bronchiectasis, 295 
in diphtheria, 23 
in empyema opening into bronchus, 
23 
in fever, 23 
in gastric disorders, 23 
in gangrenous stomatitis, 23 
in healthy child, 23 
in pulmonary gangrene, 294 
in tonsillitis, 23 
shortness of, in heart disease, 314 
Breathing, amphoric, 287 
blowing, 286 
bronchial, 284 
broncho-vesicular, 286 
puerile, 285 
vesicular, 284 
Bright’s disease. See also Kidneys and 
Nephritis. 
complications of, 415 
obstinate cough in, 524 
retinal hemorrhage in, 193 
retinitis in, 193 
roseola in, 216 
secondary diphtheritic dysen- 
tery in, 425 
value of estimation of urea in, 412 
Bromidrosis, cold, clammy hands in, 56 
in hysteria, 229 
Bronchial breathing, 284 
due to compression of lungs over 
pleural effusion, 284 
in cavity, 284 
in catarrhal pneumonia, 284 
in consolidation, 284 
Bronchiectasis, fetid breath of, 295 
purulent sputum in, 528 
sacculated, loose morning cough in, 
524 
Bronchitis, acute, character of sputum in 
later stages of, 526 
bronchorrhoea in, 300 
bubbling rales in, 288 
Charcot-Leyden crystals in, 529 
chronic, in chronic interstitial ne- 
phritis, 416 
distended cervical vessels in chronic, 
269 
Dittrich’s plugs in sputum of putrid, 
300 
fibrinous, small casts of bronchioles 
coughed up in, 530 
hard, dry cough in, 299 564 
INDEX. 
Bronchitis, moderate, early in typhoid 
fever, 438 
physical signs of, 299 
purulent, crystals of margaric acid 
in sputum of, 531 
putrid, 300 
rales in, 299, 300 
rapidity of respiration in severe, 269 
Broncho-vesicular breathing, 286 
Bronchophony in tuberculosis of the 
lungs, 293 
Brow ague in malaria, 537 
Bullse, due to antipyrin or iodine, 224 
due to pemphigus, 224 
due to trophic lesions in disease of 
central nervous system, 224 
CACHEXIA, general anasarca in can- 
cerous, 230 
Calculus. See Stone. 
renal, character of pain in, 541 
vomiting in, 541 
salivary, 154 
vesical, symptoms of, 382 
Caput Medusae, 325 
Carbuncle, 223 
Carcinoma, appearance of skin in, 204 
cheesy pallor of face in, 205 
expression of face in, 27 
gastric, anaemia in, 366 
character of vomiting in, 513 
coffee-ground vomit in, 331,513 
fever in, 448 
indicanuria in, 390 
most frequent at pylorus, 329 
hemorrhagic effusion in pleura in, 299 
melanotic, black urine in, 384 
oesophageal, brassy cough due to 
pressure on larynx by, 524 
of caput coli, 343 
of pancreas, diabetes mellitus in, 336 
jaundice in, 199, 336 
oily stools in, 335 
symptoms of. 336 
of pylorus, diagnosis of, 330 
between gastric ulcer and, 
333 
dilatation of stomach due to, 335 
excess of lactic acid in stomach 
in, 332 
symptoms of, 331 
renal hematuria in, 387 
retraction of abdominal wall in, 322 
visceral, albumosuria in, 409 
Cardiac crises, 317 
dulness, alterations in, due to val- 
vular lesion, 283 
increase of, due to hypertrophy 
or dilatation of heart, 282 
due to pericardial effusion, 
282 
Cardiac dulness lessened by emphysema, 
283 
normal extent of, 279 
feebleness, 318 
Caries of bones of skull, headache in, 470 
spinal, pain in back in children with, 
338, 540 
Carphologia, 56, 77 
Carpo-pedal spasm in rickety, hydro- 
cephaloid children, 71 
Casts, Bramwell’s method of mounting 
and staining, 396 
centrifuge in examining, 391 
composition of, 390 
Farrant’s solution for staining, 396 
fatty, 394 
hyaline, 394 
of blood-cells, 392 
of bronchioles found in sputum, 529 
of epithelial cells, 391 
of granular matter, 393 
of micrococci, 393 
of pus-cells, 393 
resemblance of cylindroids to, 394 
Catalepsy, 30 
CataiTh, acute gastric, appearance of 
tongue in, 144, 516 
symptoms of, 516 
vomiting, 516 
chronic gastric, morning vomiting 
of drunkards in, 516 
vomiting due to excessive 
tea-drinking in, 516 
gastro-intestinal, fever in mild, in 
children, 438 
frog-belly in children with, 321 
uric acid excess in urine of, 397 
laryngeal spasm due to, 310 
nasal, character of headache due to, 
469 
of middle ear in syphilis, 155 
persistence of fever in measles due to 
bronchial or gastro-intestinal, 444 
respiratory, cough at night in, 525 
Catarrhal fever. See Influenza. 
pneumonia See Pneumonia, catar- 
rhal. 
Cavernous breathing, 285 
Cavity of lung, Hippocratic succussion in 
large, partly filled with liquid, 
289 
pectoriloquy in, 289 
tubercular, purulent sputum in, 
528 
Centrifuge in examination of blood, 360 
of urine, 391 
quantitative test for albumin with, 
403 
Cephalalgia. See Headache. 
Cerebellar hemorrhage, 137 
titubation, 193 
Cerebral palsy of children, 69 INDEX 
565 
Cerebral palsy of children, athetosis in, 77 
epileptiform convulsions in, 
69 
flexion of hands in, 69 
intention-tremor in, 69 
softening, coma of, 477 
symptoms of, 477 
Cerebro-spinal meningitis, 450 
albumosuria of great importance 
in diagnosis of, 409 
character of fever in, 450 
convulsions in, 450 
diagnosis between croupous 
pneumonia, otitis media, tu- 
bercular infection and, 450 
headache in, 478 
herpes labialis in, 223 
hyperaesthesia in, 259 
joints in, 122 
petechiae in, 210 
rigidity of back of neck in, 450 
vomiting in, 450 
Charcot-Leyden crystals in acute bron- 
chitis, 529 
in asthmatic attacks, 529 
in chronic croupous pneumonia, 
529 
in pulmonary tuberculosis, 529 
Charcot’s fever, 200 
Cheek, swelling of, in noma, 154 
in peliosis rheumatica, 154 
in salivary calculus, 154 
in Schonlein’s disease, 54 
in stomatitis, 154 
Chenzynski’s solution for staining mala- 
rial organisms, 372 
Chest, auscultation of, 284 
barrel-shaped, of emphysema, 266 
beaded ribs of, in rickets, 268 
bulging of, causes of, 267 
sternum in pigeon-breast, 267 
expansion, 272 
Harrison’s grooves in, 268 
inspection of normal, 262 
localized bulging of, causes of, 267 
pain in, shown by pinched nose in 
children, 28 
palpation of, 272 
percussion of, 274 
phthisical or alar, 265 
shrinking of, 269 
variation in shape of, in health, 262 
Cheyne-Stokes respiration, causes of, 271 
prognostic value of, 271 
Chickenpox, appearance of eruption in, 
214, 222 
character of fever in, 444 
disparity between height of fever 
and degree of illness in, 444 
Chill in acute pleurisy, 295 
in croupous pneumonia, 453 
in intermittent malarial fever, 435 
Chill in pernicious anaemia, 431 
in pyelitis, 417 
in septic poisoning, 419 
slight, in dysentery, 427 
Chilly sensations and nausea in acute dif- 
fuse nephritis, 414 
Chin, position of, in wry-neck, 48 
Chlorosis, constipation in, 366 
disorders of menstruation in, 366 
dyspnoea in, 366 
greenish-yellow color in, 204, 205 
hemoglobin decreased in, 365 
humming-top murmur in jugular 
vein in, 366 
irregular heart in, 366 
peculiar pallor of, 25 
poikilocytosis in, 366 
slight fever in, 366 
wayward appetite in, 366 
Choked disk. See Papillitis. 
in cerebellar tumor, 506 
in cerebral tumor, 505 
in profound cerebral anaemia, 
505 
not generally seen in cerebral 
abscess, 505 
Cholangitis, catarrhal or suppurative, 
character of fever in, 446 
gallstone colic in, 446 
marked jaundice in, 446 
Cholera Asiatica. comma bacillus in, 421 
diagnosis of, 421 
Hippocratic face in impending 
death in, 33 
indicanuria in, 389 
roseola in, 215 
subnormal temperature in, 456 
systemic infection in, 421 
temperature in, 453 
vomiting in, 512 
infantum, character of fever in, 453 
Cheyne-Stokes respiration in, 
421 
cold skin and high rectal tem- 
perature in, 453 
diarrhoea in, 453 
disparity between axillary and 
rectal temperatures in, 421 
mousy, musty odor of stools in, 
427 
obstinate vomiting in, 453, 513 
sinking in of fontanelles in, 53 
subnormal temperature in se- 
vere, 456 
symptoms of, 420 
morbus, subnormal temperature in 
severe, 456 
symptoms of, 420 
nostras. See Cholera Morbus. 
Chorea, anaemic murmurs in children in, 
306 
Bergeron’s, 73 566 
INDEX. 
Chorea, character of spasms in, 500 
diagnosis of, 501 
electric, 72, 502 
expression in, 30 
facial spasm in, 45 
heart disease in, 306 
hemiansesthesia in, 241 
hereditary, 73 
Huntington’s, 73, 501 
hysterical, 73 
incoherent speech in, 552 
insaniens, 501 
loss of knee-jerk in, 544 
major, 531 
maniacal, 72 
nodding spasm in, 47 
paralytic, 72 
post-hemiplegic, lesion of, 138 
senile, 72 
spasm of tongue in, 153 
Chronic poliomyelitis, claw-hand in, 66 
Chvostek’s symptom of tetany, 499 
Chyluria, caused by filaria sanguinis ho- 
minis, 374 
test for, 382 
Cirrhosis, hepatic, ascites in, 342 
caput Medusae in ascites caused 
by, 326 
disorders of digestion in, 342 
enlargement of spleen in, 342 
hematemesis in, 342 
symptoms due to, 342 
uric acid in excess in urine of, 
397 
Claw-hand, 65 
-foot, 115 
Clothing, diagnostic significance of, 17, 18 
Coffee-ground vomit in gastric cancer, 513 
in locomotor ataxia, 513 
in phosphorus-poisoning, 515 
Colic, causes of abdominal, 542 
character of crying in children caused 
by abdominal, 23 
convulsions in, 500 
gallstone, in catarrhal cholangitis, 
449 
hepatic, 542 
lead, pain in, 542 
renal, character of pain in, 542 
diagnosis of, 542 
retraction of abdominal wall in re- 
nal, hepatic, and lead, 322 
sometimes due to strongylus gigas, 
388 
ureteral, 384 
Coma, ability to protrude tongue in, when 
other orders fail to gain response, 
151 
causes of, 472 
in acute alcoholic poisoning, 472 
yellow atrophy of the liver, 475 
in Addison’s disease, 478 
Coma in apoplexy, 476 
in cerebral abscess, 477 
disease, 19 
softening, 477 
syphilis, 478 
in chloral-poisoning, 474 
in chronic parenchymatous neph- 
ritis, 415 
in diabetes, 416, 473 
in epidemic cerebro-spinal menin- 
gitis, 478 
in general paralysis, 478 
in heart-failure, 478 
in multiple sclerosis, 478 
in opium-poisoning, 473 
in petit mat, 479 
in purulent leptomeningitis, 478 
in renal disease, 19 
in subdural hemorrhage, 477 
in sunstroke, 478 
in typhoid fever, 475 
in uraemia, 474 
rapidity of respiration in diabetic or 
uraemic, 270 
slowness of breathing in uraemic or 
diabetic, 270 
Concomitant squint, 161 
Congestion, pulmonary, 296 
physical signs and history of, 296 
renal, albuminuria in, 403 
blood-casts in, 384, 392 
irritation of bladder in, 381 
Constipation, causes of, 418 
in chlorosis, 366 
in chronic lead-poisoning, 419 
in diabetes insipidus, 419 
mellitus, 419 
in intestinal obstruction, 419 
in jaundice, 418 
in reflex irritation, 419 
indicanuria in, 419 
Continued fever See Malaria, Remit- 
tent. 
Contractures in hysteria, 70, 119 
Convulsions in acute articular rheuma- 
tism with hyperpyrexia, 454 
in Addison’s disease, later stages, 498 
in anterior poliomyelitis, 456 
in cerebro-spinal meningitis, 450 
in uraemia, 505 
clonic, in acute alcoholism, 488, 495 
in cardiac sedatives, 489 
in chronic lead-poisoning, 489 
in epilepsy, 480 
in eruptive fevers, 488 
in general paresis, 90 
in hemicrania, 496 
in hysteria, 491 
in Jacksonian epilepsy, 482 
in malaria, 489 
in malingerers, 497 
in post-hemiplegic epilepsy, 483 INDEX. 
567 
Convulsions, clonic, in puerperal eclamp - 
sia, 495 
in syphilitic epilepsy, 485 
in syncope, 496 
epileptiform, in cerebral palsy of 
children, 69 
erotic, in phosphorus-poisoning, 516 
of infants, in meningitis, 498 
in pseudo-meningitis, 498 
in reflex irritation, 497 
salaam, 501 
tetanic, in acute yellow atrophy of 
liver, 500 
in gallstone colic, 500 
in hematoma of dura mater, 500 
in hydatid cyst of cerebral cor- 
tex, 500 
in irrigation of pleural cavity, 
500 
in multiple cirrhosis, 500 
in strychnine-poisoning, 499 
in tetanus, 499 
in tetany, 499 
Convulsive tic, facial spasm in, 45 
Coprolalia, 46, 73 
Corpuscles of Ehrlich, 365 
Coryza, action of child toward breast in, 
23 
in influenza, 451 
Cough, causes of night, 525 
character of, in acute laryngitis, 524 
in aneurism of transverse arch 
of aorta, 310 
in false croup, 522, 524 
in laryngeal phthisis, 524 
chronic loose, morning, in empyema 
rupturing into bron- 
chus, 523 
in pulmonary abscess, 
523 
in sacculated bronchi- 
ectasis, 523 
in tuberculosis with 
cavity, 523 
due to change of position in pleurisy 
with effusion, 524 
during aspiration of fluid in pleurisy, 
524 
followed by cry in pneumonia or 
pleurisy, in children, 23 
hard and dry, in acute bronchitis, 
299 
hysterical, 525 
in paralysis of diaphragm, 525 
in whooping-cough, 522 
laryngeal, due to irritant dust or 
vapors, 524 
due to mediastinal tumors, 524 
due to pressure by aneurism, 524 
by carcinoma of oesophagus, 
524 
nervous or reflex, 525 
Cough, obstinate, in Bright’s disease, 524 
significance of cessation of, in ad- 
vanced phthisis, 526 
smothered or suppressed, in pleuro- 
pulmonary inflammation, 523 
value of loose, 523 
varieties of, 522 
Cracked-pot sound, 278 
Cranio-tabes, 51 
Cretinism, facial expression in, 32 
Crisis, apparent, in relapsing fever, 441 
fever in erysipelas ending by either 
lysis or, 445 
gastric, in locomotor ataxia, 513 
in croupous pneumonia, 453 
in typhus fever, 442 
intestinal, 422 
subnormal temperature in many 
diseases at, 457 
with fading of eruption in measles, 
444 
Crossed anaesthesia, 243 
in lesion of one side of cord, 243 
of peduncle, 243 
of pons, 243 
Croup, spasmodic, character of cough in, 
522, 524 
inspirations prolonged in, 271 
laryngeal spasm in, 302 
Croupous pneumonia. See Pneumonia, 
Croupous 
Crutch-palsy, 74 
Crying in children, absence of, in pneu- 
monia, 23 
causes of, 23 
constant, due to earache or 
hunger, 23 
of earache, not pacified by offer 
of breast, 23 
of four months old, without 
shedding tears, an unfavor- 
able sign, 23 
Crystals, ammonium urate, 398 
amorphous phosphates, 399 
blood, of Teichmann, 385 
Charcot-Leyden, 528 
creatin, 398 
creatinin, 398 
hemin, 521 
leucin and tyrosin in phosphorus- 
poisoning, 516 
margaric acid, 531 
oxalate of lime, 397 
triple phosphates, 398 
urates, 397 
uric acid, 397 
Curschmann’s spirals, in asthmatic 
attacks, 528 
rarely in croupous pneumonia, 
528 
in pulmonary tuberculosis, 
528 568 
INDEX. 
Curvature of spine, unilateral bulging 
of chest in, 268 
Cyanosis, causes of, 206 
due to drugs, as antipyrin or ace- 
tan ilid, 207 
• in acute articular rheumatism with 
hyperpyrexia, 455 
in acute miliary tuberculosis, 452 
in cardiac dyspnoea, 29 
in laryngeal obstruction, 207 
in newborn, 206 
relative frequency of cause of 
lesions of, 206 
in pulmonary diseases, 207 
in serious cardiac disease, 206 
Cyclical vomiting, other symptoms, de- 
pendent on, 518 
Cylindroids, significance of, 395, 396 
varieties of, 395 
Cyst, echinococcus of liver, 341 
hematuria in renal, 387 
of kidney, 338 
of pancreas, 337 
ovarian, diagnosis of, 322 
Cystitis, character of pain in, 545 
chronic, triple phosphates m urine 
in, 398 
darting pain in urethra in, 381 
purulent, symptoms of septic fever 
in, 378 
tenesmus in, 381 
Dactylitis, 55 
Deformity of feet and legs, 114 
in acute cerebral paralysis of 
infancy, 118 
Delirium, a bad omen in croupous pneu- 
monia, 292 
in acute articular rheumatism with 
hyperpyrexia, 455 
in acute yellow atrophy of liver, 
475 
in thrombosis of cerebral sinuses, 
467 
incoherent speech in, 553 
low, muttering, in tvphoid fever, 
30 
mild, in mitral regurgitation, 470 
mild, in phosphorus-poisoning, 475 
Dementia, paretic, Argyll-Robertson 
pupil in, 179 
delusions of grandeur in, 553 
diplopia in, 160 
gangrene in, 225 
hemiplegia in, 140 
hemorrhage into skin in, 210 
hesitating, halting speech in, 
553 
knee-jerk in, 549 
localized sweating in, 229 
optic atrophy in, 192 
Dementia, paretic, perforating nicer of 
foot in, 225 
tache cerebrate in, 211 
tremor of tongue in, 553 
Dengue, an epidemic disease, 449 
character of fever in, 449 
erythema in, 212 
hematemesis in, 514 
jaundice in, 201 
joint-involvements in, 124 
pain involving entire body in, 546 
Dentition, fever in difficult, 435 
Diabete bronze, 200 
Diabetes insipidus, constipation in, 419 
great increase of urine in, 383 
loss of knee-jerk in some cases 
of, 548 
urine of, 416 
mellitus, Argyll-Robertson pupil in, 
180 
boils in, 233, 406 
caries of teeth in, 157 
cataract in, 158, 194 
Chevne-Stokes respiration in, 
271 
color of urine in, 416 
coma in, 416 
constipation in, 417 
development of, in carcinoma of 
pancreas, 336 
diagnosis of coma in, 475 
dry harsh skin in, 416 
fermentation of urine in. due to 
saccharomyces albicans, 401 
gangrene in, 225 
great increase of urine in, 383 
headache rarely in, 462 
heavv, sweet odor of urine in, 
382 
high specific gravity of urine 
in, 383. 
jaundice in, 200 
knee-jerk lost in advanced, 548 
ocular palsy in. 169 
paraplegia rare in, 110 
perforating ulcer of foot in, 125 
polydipsia in, 406 
polyphagia in, 406 
prognosis of, 406 
if associated with obesity, 
406 
influence of age on, 406 
pruritus in, 261, 406 
retinitis in, 193 
roseola in, caused by urine, 216 
rosette crystals of uric acid in 
urine of, 397 
wasting in, 406 
white spots on trousers in, 18 
urine in, 416 
vomiting rare in, 504 
Diarrhoea, causes of, 419 INDEX. 
569 
Diarrhoea, colliquative, in uraemia, 504 
decrease of urine due to, 383 
dissecting-room, 426 
fatty, due to cod-liver oil, 426 
due to disease of pancreas, 426 
in jaundice, 426 
in abdominal pain, 21 
in cholera infantum, 420 
morbus, 420 
in dysentery, 424 
in entero-colitis, 422 
in fissure of the anus, 422 
in hysteria, 426 
in influenza, 452 
in leukaemia, 369 
in locomotor ataxia, 422 
in malignant ulceration, 426 
in proctitis, 424 
in pulmonary gangrene or tubercu- 
losis, 426 
in renal disease, 422 
in septicaemia, 426 
in syphilitic ulceration, 425 
in tuberculosis, 423 
lienteric, 423 
may be caused by purgatives, 21 
nervous, 422 
paroxysmal, sero-mucous or bloody, 
in exophthalmic goitre, 426 
Diazo-reaction, 414 
Dilatation of heart, symptoms and physi- 
cal signs of, 316 
of stomach, atrophy of gastric 
tubules in. 332 
character of vomiting in, 517 
constitution of vomitus in, 517 
in pressure by growths of pan- 
creas, 517 
in tetany, 71 
methods of examining in, 325, 
327, 329 
sarcinae ventriculi in vomitus in, 
517 
total absence of hydrochloric 
acid in, 517 
torula cerevisiae, causing fer- 
mentation in, 328, 516 
Diphtheria, anaesthesia in 50 per cent, of 
cases of, due to neuritis, 252 
casts of larynx and upper bronchial 
tubes at times coughed up in, 531 
double oculomotor paralysis in, 174 
nasal, 156 
paralysis of tongue following, 152 
paraplegia a sequel to, 110 
roseola in, 214 
sickening, sweet odor of breath in, 
23 
symptoms of, 155 
Diplopia, crossed, 163, 168 
explanation of, 160 
homonymous, 163, 166, 168 
Diplopia, in poisoning, 160 
symptom of Friedreich’s ataxia, 160 
of lesion at base of brain, 160 
of cerebral cortex, 160 
of cranial nerve nuclei, 
160 
of nerve in its course, 160 
of locomotor ataxia, 160 
of paretic dementia, 160 
vertical, 168 
Distoma haematobium, eggs of, in urine, 
400 
hematuria due to, 388 
pulmonum, 531 
Dropsy. See (Edema and General Ana- 
sarca. 
general, in arsenic-poisoning, 231 
in beri-beri, 231 
in blood diseases, 230 
in cancerous cachexia, 230 
in disordered nervous control of 
vessels, 230 
in emboli, 230 
in heart disease, 230, 231 
in multiple neuritis, 230 
in renal disease, 230 
in scurvy, 231 
in thrombi, 230 
in vascular disease, 230 
localized, in anaemia, 231 
in aneurism, 232 
in angioneurotic oedema, 232 
in arsenic-poisoning, 232 
in cardiac failure, 231 
in cerebral thrombosis, 232 
in hepatitis or cirrhosis, 231 
in mastoid abscess, 233 
in neuralgia, 232 
in occupations requiring a 
standing position, 231 
in phlegmasia alba dolens, 232 
in pressure on great vein, 231 
in p_yothorax, 233 
in relapsing fever, 233 
in renal disease, 231 
in thrombosis, 232, 233 
in typhoid fever, 233 
of eyelids in renal disease, 232 
in other affections, 232 
of feet and legs in anaemia, 231 
in abdominal growths 
causing pressure, 231 
in renal disease, 231 
Dubini’s chorea, 72. See Electric Chorea. 
Dupuytren’s contraction, 59 
Dysentery, acute primary, of a diph- 
theritic character, 425 
amoebic, amoeba coli the cause of, 425 
liver abscess in, 425 
symptoms of, 424 
arthritis in, 124 
character of stools in, 424 570 
INDEX. 
Dysentery, fever in, 424 
secondary diphtheritic, a complica- 
tion of Bright’s disease, 
425 
in acute croupous pneumo- 
nia, 425 
in chronic heart disease, 425 
slight chill in, 424 
thirst in, 424 
vomiting in, 513 
Dysmenorrhoea, pain in, 545 
Dyspnoea from foreign body in air-pas- 
sages, 301 
in anaemia, 365 
in aortic insufficiency, 315 
in asthma, 300 
in chlorosis, 366 
in heart disease, 29 
in laryngeal spasm, 302 
in leukaemia, 369 
in miliary tuberculosis, 506 
position due to, 20 
worse at night in chronic interstitial 
nephritis, 415 
EARACHE, character of crying in 
children with, 23 
rubbing of hand over affected side 
of head in, 23 
Echolalia, 46, 73 
Eclampsia, puerperal. See Puerperal 
Eclampsia. 
Eczema, appearance of nails in, 55 
due to chloral, 223 
due to mercury, 223 
due to potassium iodide, 223 
due to quinine, 223 
Ehrlich, corpuscles of, 365 
diazo reaction in urine of, 414 
myelocyte of, 366 
triple blood-stain of, 367 
Electric chorea, 73, 502 
Bergeron’s, 73 
Elephantiasis, sometimes caused by filaria 
sanguinis hominis, 375 
symptoms of, 233 
Embolism, cerebral, Cheyne-Stokes respi- 
ration in, 271 
gangrene in. 126 
vomiting in, 505 
of coronary arteries, 317 
of kidney, casts of micrococci in, 393 
haematuria in, 386 
oedema in, 230 
of pons Yarolii, 455 
of superior mesenteric artery, symp- 
toms of, 514 
Emphysema, appearance of hands in, 54 
barrel-shaped chest of, 266, 300 
distended cervical vessels in, 269,300 
expiration prolonged in, 270, 300 
Emphysema, lessened area of cardiac dull- 
ness in, 283, 300 
percussion resonance increased in, 
300 
pulmonary and cardiac hypertrophy 
causing depression of apex-beat 
in, 273 
rales in, 300 
spleen and liver displaced downward 
in, 300 
systolic tricuspid murmur in, 300 
vocal fremitus diminished in, 300 
resonance diminished in, 291, 
300 
Emprosthotonos in hysteria. 492 
Empyema, albumosuria in 409 
communicating with bronchus, loose 
morning cough in, 523 
odor of breath in, 23 
pulsation of chest-wall in some cases 
of, 274 
purulent sputum in, 528 
Endocarditis, acute ulcerative, character 
of fever in, 446 
diagnosis between typhoid 
fever and, 440 
duration of, 446 
jaundice in, 203 
petechial rashes in, 210 
prognosis of, 446 
retinal hemorrhage in, 193 
sweating in, 228 
Enteric fever. See Typhoid Fever. 
Enterocolitis, flakes of mucus in stools 
of, 423 
mild follicular, 423 
ribbon-shaped stools in, 423 
symptoms of, 422 
ulcerative, 423 
Enteroliths, 511 
Eosinophile corpuscles, 355 
numerous in myelogenous leu- 
kaemia, 355 
Epigastrium, distention of, 326 
Epilepsy, alcoholic, 488 
aura in, 480 
biting of tongue in, 148 
caused by drugs, 489 
lead, 489 
malaria, 489 
character of convulsions in, 480 
cutaneous hemorrhage in, 210 
diagnosis of, 490 
expression of face in, 480 
facial spasm in, 45, 46 
fever after seizure of, 456, 493 
hippusin,181 
Jacksonian, character of convulsions 
in, 482 
knee-jerk in, 548 
minor, diagnosis of, 495 
unconsciousness in, 479 INDEX. 
571 
Epilepsy, minor, vertigo the only symp- 
tom of, 471 
muscae volitantes in, 194 
nystagmus a rare symptom of, 177 
post-hemiplegic, 483 
scars on head in suspected traumatic, 
228 
spasm of heart in, 148 
syphilitic, character of headache in, 
485 
diagnosis of, 485 
symptoms of, 487 
tache cerebrale in, 211 
vertigo a premonitory symptom of, 
471 
Epiphysitis of infancy, acute, symptoms 
of, 122, 123 
Equina. See Glanders. 
Erb’s paralysis, 82 
symptom, 499 
Ergotism, gangrene in, 63 
Eruption, date of, in various diseases, 214 
herpetic, along nerve-trunk in sciatic 
neuritis, 541 
in anthrax maligna, 223 
in erysipelas, 225 
in glanders, 224 
in impetigo contagiosa, 222 
in measles, 214 
in rotheln, 213 
in smallpox, 214, 218, 443 
in syphilis, 227 
in typhus, 216, 441 
in vaccinia, 222 
pemphigus-like, due to salicylic acid 
or copaibia, 224 
pharyngeal and buccal in measles, 
156 
purpuric, from drugs, 209 
from diseases, 210 
resulting from quinine, 222 
vesicular, about mouth, in foot-and- 
mouth disease in man, 150 
Erysipelas, albumosuria in, 409 
appearance of eruption in, 216, 225 
diazo-reaction in severe, 414 
fever in, ending by either crisis or 
lysis, 444 
marked remissions and inter- 
missions of, 444 
sudden rise of, 444 
inflammation of skin similar to, from 
arnica, 216 
symptoms of, 216 
vomiting in, 520 
Erythema. See Roseola. 
exudativum multiforme, symptoms 
of, 209 
following operation, 215 
parturition, 215 
vaccination, 218 
in dengue, 212 
Erythema in diphtheria, 214 
in rheumatism, 208 
in scarlet fever, 211 
in syphilis, 215 
in typhoid fever, 215 
roseola, symptoms of, 212 
scarlatiniform, symptoms of, 212 
Esophoria, 161 
Ewald’s test-breakfast, 335 
Examination, method of, in consulting- 
room, 25 
of abdomen, 320 
of blood by hematocytometer, 358 
by hematocrit, 360 
by hemoglobinometer, 363 
for micro-organisms of malaria, 
372 
in leukaemia, 368 
of children, 22 
of eye by ophthalmoscope, 159, 
188 
of field of vision, 184 
of functional activity of ocular 
muscles, 162 
of hemianopsia, 184 
of pulse, 345 
of pupillary reflex, 178 
of skin for jaundice, 196 
of sputum, 538 
of stomach, 327 
of tongue, 141 
Exophoria, 161 
Exophthalmic goitre. See Goitre, Ex- 
ophthalmic. 
Expectoration See Sputum. 
Expression, of face as an early symptom 
of facio humero scapular type 
of muscular atrophy, 31 
elated, of paretic dementia, 30 
excited, of acute mania, 30 
fatuous, of hysteria, 30 
fixed, of catalepsy, 30 
how formed, 25 
modified, 25 
in acute peritonitis, 30 
in cretinism, 32 
in epileptic seizures, 480 
in Friedreich’s ataxia, 31 
in healthy, sleeping child, 27 
in- malignant disease, 27 
in melancholia, 30 
in moderate pain in children, 
28 
in nervous exhaustion, 30 
in typhoid fever, 29 
intellectual, 26 
Eye, ability to close, in cerebral facial 
paralysis, 36 
alteration of color-field of, 186 
amaurosis, 194 
anatomy of optic nerve of, 183 
annulus senilis, 159 572 
INDEX 
Eye, appearance of healthy eye-ground, 
190 
arcus senilis, 159 
causes of paralysis of, 167 
conjunctival hemorrhage, from 
coughing, 158 
from degenerative vascular 
changes, 158 
from injury, 158 
dark areas under, during menstrua- 
tion, 26 
diagnosis between ocular symptoms 
of tabes and hysteria, 186 
diplopia, 160 
examination of, ophthalmoscopic, 
159, 188 
exophthalmos in goitre, 158 
in lesion of oculomotor nerve, 
40 
Graefe’s symptom, 159 
hemianopsia, 183 
homonymous and crossed diplopia, 
163 
iritis, 193 
lesion of optic nerve in locomotor 
ataxia, 192 
method of determining paralysis of, 
164 
of examining functional activity 
of muscles of, 162 
muscae volitantes, 194 
orthophoria, 162 
papillitis, 191 
puftiness about, from excessive use of 
arsenic, 26 
in acute diffuse nephritis, 414 
retinitis, 193 
retrobulbar neuritis, 191 
rod-test of Maddox, 162 
squint, 161 
Eyelids, closed in healthv sleeping child, 
29 
oedematous, in angioneurotic oedema, 
232 
from arsenic, 232 
in cerebral thrombosis, 232 
in neurotics, 232 
painful twitchings of, accompanying 
facial hemiatrophy, 34 
pallor of, in anaemia, 158 
pigmentation of, early in pregnancy, 
27 
puffy, in cardiac disease. 158 
in overuse of arsenic, 158 
in renal disease, 158 
in trichinosis, 158 
showing glazed conjunctivae, 28 
slightly parted in sleeping child, 
showing congestive or nervous 
pain, 28 
swollen in cretinism, 132 
twitching, in nervous irritation, 28 
FACE. See Expression. 
anaesthesia of, due to involvement of 
the fifth nerve or its nucleus, 256 
anxious and covered with sweat in 
angina pectoris, 539 
asymmetry of, congenital, 33 
blurring of features of, in children 
with lesions of mitral valve, 29 
diagnosis of anaesthesia of, 256 
facio-humero-scapular type of mus- 
cular atrophy, 31 
full-moon, of myxoedema, 32, 34 
gray or bluish, from overdose of 
coal-tar products, 27 
heavy, cheesy-looking, in children, 
28 
hemiatrophy of, 32 
hemihypertrophy of, 34 
Hippocratic, of impending death, 33 
hysterical, 26, 30 
intellectual, 26 
leonine, of leprosy, 32 
massive, of acromegaly, 34 
oedema or great swelling of, in 
dropsy, 30 
in erysipelas, 30 
of carcinoma, 27 
of catalepsy, 30 
of chorea in children, 30 
of chronic or subacute renal disease, 
30 
of congenital syphilis, 28 
of cretinism, 32 
of disseminated sclerosis, early stages 
of, 30 
of Friedreich’s ataxia, 31 
of paralysis agitans, 30 
of pneumonia, severe, 29 
of those exposed to weather, 26 
of those living indoors, 26 
of those using alcohol to excess, 26 
of typhoid fever, 29 
pallor of, in chlorosis, 26 
in fright, 26 
in hemorrhage, 26 
paralysis of, bilateral, 43 
unilateral, 35 
parchment-like skin of, in syphilis 
and alcoholic hepatic cirrhosis, 26 
pellucid, in renal disease in chil- 
dren, 30 
spasm of, 45 
triangular, in osteitis deformans, 35 
Farrant’s solution, 396 
Fatty degeneration in pliophorus-poison- 
ing, 516 
heart, 317 
Feces. See Stools. 
causes of variation in quantity of, 
426 
color of, 427 
consistency of, 427 INDEX. 
573 
Feces, impaction of, 337 
odor of, 427 
Feet, claw-, 114 
contractures of, in diphtheria, 119 
deformity of, due to acute cerebral j 
paralysis of infancy, 118 
due to poliomyelitis, 118 
due to progressive renal or mus- j 
cular atrophy, 116 
distribution of anaesthesia of, in neu- \ 
ritis, 254 
enlarged, due to deformity, 114 
in acromegaly 114 
in myxoedema, 114 
in pulmonary osteo-arthropathy, 
114 
flat-, in locomotor ataxia, 117 
numbness of, in locomotor ataxia, 87 
perforating ulcer of, in diabetes, 125 
in senile gangrene, 125 
in tabes dorsalis, 125 
sciopedy, 114 
tabetic, 118 
Fehling’s test for sugar in the urine, 404 
Festination, 93 
Fever, absence of, in pulmonary oedema, i 
296 
appearance of nails in, 55 
causes of tertian, quartan, and sestivo- 
autumnal, 369, 371 
cold, wet skin of evil import in, 435 
character of, in acute appendicitis, 
454 
articular rheumatism, 454 
miliary tuberculosis, 451 
multiple neuritis, 455 
myelitis, 456 
pulmonary tuberculosis, 450 
in anthrax, 453 
in catarrhal pneumonia, 452 
in cerebral abscess, 450 
in cerebro-spinal meningitis, 450 
in chickenpox, 444 
in cholangitis, catarrhal or sup- 
purative, 446 
in cholera Asiatica, 453 
infantum, 453 
in croupous pneumonia, 452 
in dengue, 124, 449 
in difficult dentition, 435 
in dysentery, 424 
in epilepsy, 456, 493 
in erysipelas, 444 
in foot-and-mouth disease, 453 
in gastro-pulmonary fever, 456 
in hsemoglobinsemia, 519 
in hay fever, 451 
in hepatic abscess, 448 
in Hodgkin’s disease, 448 
in hysteria, 455 
in infantile spinal paralysis, 456 
in influenza, 451 
Fever, character of, in injuries to cervical 
portion of spinal cord, 455 
in intermittent malarial fever, 
444 
in Malta fever, 441 
in measles, 442 
in mild gastro-intestinal catarrh 
in children, 437 
in obstruction of the rectum, 
511 
in parenchymatous nephritis, 
454 
in pemphigus, 224 
in pernicious anaemia, 448 
in pyelitis, 417, 448 
in relapsing fever, 441 
in remittent malarial fever, 448 
in rotheln, 443 
in scarlet fever, 442 
in septic poisoning, 448 
in septicaemia, 450 
in smallpox, 443 
in syphilis, 452 
in tetanus, 454 
in thermic fever, 455 
in tonsillitis, 454 
in trichinosis, 441, 443 
in typhoid fever, 435 
in typhus fever, 441 
in ulcerative endocarditis, 446 
in Weil’s disease, 449 
in yellow fever, 449 
Charcot’s, 200 
chlorides decreased in some, 413 
increased during convalescence 
from, 413 
dry, hot skin in, 434 
high specific gravity of urine in, 383 
rapid pulse in, 351 
respiration in, 270 
secondary, in smallpox, 220 
septic, in purulent cystitis, 378 
sighing or arhythmic respiration in, 
in children, 23 
significance of, 434 
in children, 435 
slight, in chlorosis, 366 
in leukaemia, 369 
sour breath in, 23 
urates in excess in urine of, 397 
urea increased in urine of, 413 
uric acid increased in urine of, 397 
urine decreased in, 383 
Filaria sanguinis hominis, chyluria and 
elephantiasis caused by, 
3/5 
description of, 375 
embryos of, in urine, 400 
haematuria in, 387 
diurna, 373 
loa, 374 
nocturna, 373 574 
INDEX. 
Gait in cerebellar tumor, 508 
in chronic myelitis, 91 
in Friedreich's ataxia, 89 
in general paresis, 89 
in gout, 85 
in health, 18 
in hemiplegia, 94 
in hereditary cerebellar ataxia, 90 
in hysteria, 89 
in infantile cerebral paralysis, 92 
in lateral sclerosis, 91 
in locomotor ataxia, 85 
cause of, 88 
in multiple sclerosis, 92 
in neurasthenia, 18 
in osteomalacia, 95 
in paralysis agitans, 93 
in pseudo-muscular hypertrophy, 92 
-tabes, 86 
in rheumatism, 85 
in rickets, 92, 95 
in sciatica, 85 
Gall-bladder, diagnosis of obstruction of, 
342 
Gallstone in stools, 428 
jaundice in, 198 
Gallop-rhythm in mitral stenosis, 308 
Gangrene in central nervous lesion, 225 
in diabetes, 225 
in embolism, 126 
in ergotism, 63 
in exophthalmic goitre, 126 
in frost-bite, 63 
in leprosy, 63 
in nerve injury, 225 
in Raynaud’s disease, 63, g25 
of extremities, following infectious 
fevers, 126 
of intestines, fetid odor of stools in, 
430 
pulmonarv, character of sputum in, 
294, 527, 528 
crystals of inargaric acid in spu- 
tum of, 531 
due to putrid bronchitis, 300 
elastic fibres in sputum of, 530 
fetid breath in, 294 
muco-purulent stools in, 426 
vomiting in, 520 
senile, perforating ulcer of foot in, 
125 
spontaneous, in hysteria, 63, 225 
Gastralgia, character of pain in, 542 
diagnosis of, 542 
neuralgic spots in, 542 
Gastric crisis in locomotor ataxia, 87 
dilatation. See Dilatation of the 
Stomach. 
ulcer, anaemia in, 366 
pain in, 542 
symptoms of, 333, 513 
vomiting of blood in, 513 
Filaria perstans, 373 
Fingers, appearance of, diagnostic of 
chloral-habit, 56 
clubbed in heart disease, 314 
distorted and twisted in gout and 
arthritis deformans, 57 
fixation of joints of, by deposit of 
urate of sodium, 57 
in syphilitic dactylitis, 55 
spasm of, due to occupation, 71 
Fissure of the anus, character of pain in, 
545 
diarrhoea in, 422 
Flat-foot in locomotor ataxia, 117 
Floating kidney, 337 
spleen, 338 
Fontanelle, pulsation of, 49, 51, 52, 53 
Foot-and-mouth disease in man, symp- 
toms of, 453 
Foot-drop, 112 
Forehead, immense and bulging, with a 
wizened, puny face beneath, indi- 
cating hydrocephalic tendencies, 
28 
square and projecting, indicative of 
rickets, 28 
wrinkled, indicating pain in the 
head, 28 
Foreign body in air-passages, 301 
in bowel, 337 
Fremitus, vocal, decrease of, causes of, 
273 
increase of, causes of, 273 
mode of production of, 272 
Friction-sounds, 289 
as a rule, due to pleuritis, 289 
at apex of chest, usually due to tu- 
berculosis, 289 
best heard in axilla, 289 
pericardial, 289 
Friedreich’s ataxia, claw-foot in, 116 
diagnosis of, 549 
diplopia a symptom of, 160 
face of, 31 
gait of, 89 
loss of knee-jerk in, 548 
movement of hands in, 77 
nystagmus in, 177 
sensory disturbance of skin late 
in, 245 
slow, scanning speech in, 553 
table of symptoms of, 90 
Frost-bite, gangrene in, 63 
Fungus foot disease. See Mycetoma. 
GABBETT’S method of staining for 
tubercle bacilli, 533 
Gait, 85 
“ astasia abasia,” 91 
in acute poliomyelitis, 91 
in cerebellar disease, 93 INDEX. 
575 
Gastritis, vomiting rare in, excepting 
when due to an irritant, 516 
Gastro-diaphane of Einhorn, 327 
-duodenal catarrh, jaundice in, 197 
-pulmonary fever, etiology of, 456 
gastric symptoms of, 456 
marked fever in, 456 
pulmonary symptoms of, 
456 
General anasarca in advanced cancerous 
cachexia, 230 
in arsenic-poisoning, 231 
in beri beri, 231 
in children with acute diffuse 
nephritis, 415 
in chronic parenchymatous ne- 
phritis, 415 
in heart disease, 230, 231 
in multiple peripheral neuritis, 
231 
in renal disease, 230, 231 
paresis. See Paresis, General. 
Geographical tongue, 150 
Gerhardt’s symptom, 468 
German measles. See Rotheln. 
Girdle-sensation, 259 
in locomotor ataxia, 259 
in myelitis, 259 
in tumors of cord and meninges, 
259 
Glanders, eruption of, 224 
symptoms of, 224 
Glaucoma, dilated pupil in, 159 
headache in, 461 
Glossitis, acute, 150 
dissecting, 149 
Glossodynia exfoliativa, 149 
Glycosuria, Fehling’s test for, 404 
Haines’s test for, 403 
Roberts’s yeast-test for, 406 
significance of, 406 
Whitney’s test for, 404 
Gmelin’s test for bile in urine, 389 
Goitre, exophthalmic, Abadie’s sign in, 46 
brown pigmentation an occa- 
sional symptom of, 204 
diminished electrical resistance 
in, 317 
exophthalmos in, 53, 158 
gangrene in, 126 
Graefe’s symptoms of, 159 
localized sweating in, 221 
Moebius’s sign of, 159 
paroxysmal bloody, mucous 
diarrhoea in, 518 
Stellwag’s symptom in, 159 
symptoms of, 158 
tache cerebrale in some cases of, 
211 
tachycardia in, 53, 317 
thrill over carotid arteries in, 
317 
Goitre, exophthalmic, vomiting in, 519 
Gonococci, indicative of specific urethri- 
tis or vaginitis, 400 
method of staining, 400 
Gonorrhoeal arthritis, symptoms of, 123 
Gout, aortitis in, 538 
appearance of nails in, 55 
distortion of fingers in, 57 
hypersesthesia of scalp in, 260 
joint-affections in, 124 
limping gait of, 85 
pain in great toe in, 544 
pruritus in, 261 
retinal hemorrhages in, 193 
urates in urine of, 397 
uric acid in urine of, 397 
Gouty diathesis, appearance of nails in, 
55 
“Grisolle” sign of smallpox, 214 
Graefe’s spots, 46 
symptom, 159 
Gums, blue line on, in lead-poisoning, 
157 
spongy, in salivation, 159 
in scurvy, 159 
Gyromele of Turck, 327 
Habit-chorea, 72 
Habit-spasm, 45 
Haines’s modification of Haeser’s method 
for computing total quantity of 
solids in urine, 413 
test for sugar in urine, 403 
Hands, “accoucheur’s” in tetany, 71 
changes in shape of, in chronic rheu- 
matism, 61 
choreic movements of, and of arms, 
in children with chorea minor, 72 
claw-, due to disease of median and 
ulnar nerves, 65 
of cells of cerebral cortex in 
hand-area, 65 
of cells of spinal cord, 65 
cold and clammy, due to bromidro- 
sis, 56 
due to local innervation of 
sweat-glands, 56 
contractions of, following apoplexy, 
69 
from hysteria, 70 
distribution of anaesthesia of, in neu- 
ritis, 253 
Dupuytren’s contraction of, 59 
excessive sweating of, in progressive 
muscular atrophy, 56 
flexion Of, in cerebral palsy of chil- 
dren, 69 
gangrene of, in ergotism, 63 
in frost-bite, 63 
in leprosy, 63 
in Morvan’s disease, 63 576 
INDEX. 
Hands, gangrene of, in neuritis, 63 
in Raynaud’s disease, 63 
in syringomyelia, 63 
senile, 63 
in acute articular rheumatism, 61 
in angioneurotic oedema, 63 
in child with cerebral trouble, 23 
with heart disease, 65 
in emphysema and chronic phthisis, 
54 
in heart disease, 19 
lateral drop of, in neuritis or acute 
infantile poliomyelitis, 74 
movement of, 76 
position of, in meningeal congestion 
or hydrocephalus in children, 71 
seal-tin, in arthritis deformans and 
gout, 61 
spade-like, in acromegaly, 64 
in myxoedema, 64 
in pulmonary osteo-arthropathy, 
64 
spasm of, from cold and exposure, 71 
in ataxia, 73 
in paralysis agitans, 73 
in Thomsen’s disease, 73 
swelling and rupture of, in myce- 
toma, 64 
tumors of, 75 
wasting of, in diabetes mellitus, 64 
in nervous lesions, 64 
in old age, 64 
in phthisis, 64 
with anaesthesia, in syringomy- 
elia, 69 
with flexion and rigidity rarely 
seen in paralysis agitans, 69 
Harris’s test for albumose in urine, 407 
Harrison’s grooves in rickets, 268 
Hay fever, 452 
Head, activity of, with fixation of body, 
in peritonitis, 19 
excessive sweating of, 53 
in acromegaly, 45 
in cholera infantum, 421 
in chorea minor, 47 
in hydrocephalus, 49 
in idiocy, 49 
in microcephalus, 49 
in myxoedema, 49 
in osteitis deformans, 49 
in rickets, 47 
position of, in advanced strabismus, 
49 
in chronic deafness, 49 
in mental depression, 49 
retraction of, in attack of indigestion 
in neurotic babies, 49 
generally due to basal menin- 
gitis, 49 
may be due to caries of cervical 
vertebrae, 49 
Head, retraction of, may be due to cerebro- 
spinal fever in adults, 49 
may be due to a fall, 49 
may be due to tender and en- 
larged glands of neck, 49 
Headache, causes of, 458 
from use of drugs, 462 
in acute parenchymatous nephritis, 
454 
in Addison’s disease, 520 
in anaemia, 470 
in anterior poliomyelitis, 456 
in autointoxication, 460 
in brain abscess, 465 
tumor, 462 
in cerebral tumors, 505 
in cerebro-spinal meningitis, 450 
in croupous pneumonia, early stages, 
469 
in dental caries, 470 
in diabetes, 462 
in digestive disturbances, 458 
in disease of cranial bones, 470 
in ear disease, 470 
in eye-strain, 461 
in exposure to cold, 470 
in gastro-pulmonary fever, 457 
in glaucoma, 461 
in hemoglobinsemia, 519 
in intracranial aneurism, 470 
in jaundice, 460 
in malaria, 470 
in Malta fever, 441 
in measles, 469 
in meningeal hemorrhage, 469 
in meningitis, 466, 507 
in migraine, 462 
in nasal catarrh, 469 
in neurasthenia, 461 
in nocturnal epilepsy, 470 
in paroxysmal hemoglobinuria, 460 
in phosphaturia, 462 
in phosphorus-poisoning, 515 
in renal disease, 462 
in rheumatism. 462 
in sunstroke, 469 
in syphilitic arteritis, 465 
epilepsy, 465 
in tubercular meningitis, 466 
in typhoid fever, 469 
in typhus fever, 441 
in uraemia, 462 
in valvular heart disease, 470 
vertical, in hematoma of dura, 470 
vomiting in, 520 
Heart, alterations in area of dulnessof, 280 
apex-beat of, area of, 274 
depression of, due to pulmonary 
emphysema, pericardial or 
pleural effusion, tumors in 
the chest, and cardiac hyper- 
trophy, 273 INDEX 
577 
Heart, apex-beat of, displacement of, to 
left, by hypertrophy 
of left ventricle, 274 
by pleural adhesions, 
274 
effusions, 274 
to right, by hypertrophy or 
dilatation of right ven- 
tricle. 274 
normal position of, 273 
raised by ascites, 274 
by distention of colon, 274 
by enlargement of spleen, 
274 
by hypertrophy of heart, 
274 
by intra-abdominal growths, 
274 
strength of, 274 
asthma due to lesions of, 301 
blood-streaked sputum in valvular 
lesion of, 527 
causes of pain in neighborhood of. 
538 
congenital malformations of the, 318 
rules for diagnosis of, 318, 
319 
cough in valvular disease of, 525 
dilatation of, 282, 316 
disease of, appearance of hands in 
children in, 65 
jaundice in chronic valvular, 199 
oedema in, 230. 231 
patient’s position in, 19, 20 
retinitis in, 193 
enlarged cervical vessels in tricuspid 
regurgitation of. 2'9 
-failure, in influenza. 451 
unconsciousness in, 478 
fatty degeneration of, 317 
deposition on, 318 
general malformation of, 319 
greatly hypertrophied in chronic in- 
terstitial nephritis, 416 
headache in valvular disease of, 470 
hypertrophy of. 316 
irregular, in children, 366 
location of murmurs of, 305 
neuroses of, 316 317 
secondary diphtheritic dysentery in 
chronic disease of, 425 
slightly dilated, in acute diffuse ne- 
phritis, 415 
hypertrophied, in chronic pa- 
renchymatous nephritis, 416 
-sounds, 305 
accentuation of, 305 
reduplication of, 306 
where best heard, 305, 306 
symptoms associated with murmurs 
off 314 
thrills of 274 
Heart, thrills of, causes of, 274 
Heat-exhaustion, subnormal temperature 
in, 457 
-stroke- See Sunstroke. 
Heller’s test for albumin in urine, 403 
for blood in urine, 385 
Hematemesis, as vicarious menstruation, 
514 
diagnosis between hemoptysis and, 
514 
diseases in which it occurs, 514 
due to swallowed blood, 514 
in cirrhosis of liver, 513 
in gastric cancer, 513 
ulcer, 513 
in heart disease, 514 
in injury of stomach, 514 
in locomotor ataxia, 513 
in malingerers, 514 
in melaena neonatorum, 515 
in scurvy, 514 
Hematocrit, 360 
Hematocytometer of Thoma-Zeiss, 358 
Hematoma auris, 210 
of dura maier, convulsions due ,to, 
500 
Hematozoa malaria;, 368 
Hematuria, acute, due to embolism, 386 
due to irritating drugs, 386 
due to malaria 386 
due to scarlet fever, 386 
blood-casts in, 392 
character of blood from bladder in, 
385 
from kidney in, 884 
from urethra in, 385 
chronic, due to chronic hemorrhagic 
nephritis, 387 
due to cyst of kidney, 387 
due to distoma hematobium, 388 
due to filaria sanguinis hominis, 
387 
due to renal cancer, 387 
due to stone in kidney, 387 
due to strongylus gigas, 388 
due to tuberculosis of kidney, 
387 
other causes for, 388 
Hemiachromatopsia, 187 
Hemiansesthesia in capsular disease, 241 
in chorea, 241 
in cortical lesions, 241 
in disseminated sclerosis, 241 
in hysteria, 239 
superimposed in infantile cere- 
bral paralysis, 241 
in softening of brain, 241 
in tumor of brain, 24l 
partial, with partial hemiplegia on 
opposite side, may be due to lesions 
of one side of cord, 243 
Hemianopsia, 183 
for blood in urine, 385 578 
INDEX. 
Hemianopsia, binasal, 183 
bitemporal, 183 
homonymous, 186 
in brain-tumor, 463 
in hysteria, rarely, 186, 240 
in migraine, 460 • 
location of lesion in, 186 
method of determining, 183 
significance of, 186 
use of perimeter in determining, 184 
Hemiatrophy, facial, 33 
Hemicrania. See Migraine. 
Hemidyschromatopsia, 187 
homonymous, 187 
in hysteria, 187 
Hemihypertrophy, facial, 34 
Hemin, test for, 521 
Hemiplegia, anatomy of brain-areas in- 
volved in, 127 
appearance of nails in, 55 
of tongue in, 145 
bedsores in, 226 
crossed, due to bulbar lesions, 140 
diagnosis of, 138 
from acute infantile paralysis, 139 
from cerebellar hemorrhage, 137 
from cerebral hemorrhage, 134 
in crus cerebri, 136 
in frontal lobe 137 
in island of Reil, 137 
in occipital lobe, 137 
in parietal lobe, 137 
in pons Varolii, 136 
location of lesion in, 134 
syphilis, 139 
from diffuse cerebral sclerosis of one 
hemisphere, 139 
from hematoma of dura mater, 139 
from multiple sclerosis, 139 
gait in, 94 
hypersesthesia in, 260 
in ingravescent apoplexy, 136 
in locomotor ataxia, 139 
in paretic dementia, 140 
in purulent meningitis, 140 
in renal disease with uraemia, 140 
irregular forms of, 138 
spastic, 138 
symptoms associated with, 135, 136, 
138 
Hemoglobin greatly decreased in chloro- 
sis, 365 
in leuka?mia, 367 
of individual red blood corpuscles 
greater than normal in pernicious 
anaemia, 365 
Hemoglobinsemia accompanied by vom- 
iting, 519 
symptoms of, 519 
urine in, 519 
Hemoglobinometer of von Fleischl, 360 
Hemoglobinuria, causes of, 388 
Hemoglobinuria, headache in, 460 
signs of, 385 
symptoms associated with, 460 
Hemometer See Hsemoglobinometer. 
Hemophilia, 388 
hematemesis in, 514 
hematuria in, 388 
hemoptysis in, 527 
hemorrhage into retina in, 193 
joint-involvements in, 125 
Hemoptysis, causes of, 314, 527, 531 
diagnosis of, 514, 527 
significance of currant-jelly clots in, 
327 
Hemorrhage, anaemia in, 365 
cerebral, vomiting in, 505 
from mucous membranes in yellow 
fever, 449 
from nose in leukaemia, 262 
in typhoid fever, 436 
indicated by anxious restlessness, 19 
into brain, causing hemiplegia, 134 
ocular paralysis, 177 
diplopia a symptom of, 160 
into membranes or cord, 347 
into retina, 193 
into skin, 210 
jaundice after severe prolonged, 202 
meningeal, symptoms of, 468 
movements minute, though active 
in, 19 
pallor of face in, 26 
pulmonary diseases in which it oc- 
curs, 527 
pulse of *' empty arteries” in severe, 
350 
subdural, cause of, 477 
Hemorrhagic pleurisy, 299 
Hemorrhoids, anaemia in bleeding, 365 
pruritus due to, 261 
Henoch’s disease, 209 
Hepatitis. See Abscess, Hepatic. 
Hereditary cerebellar ataxia, 89 
table of symptoms of, 90 
chorea, 73 
Hernia, umbilical, 328, 339 
Herpes labialis in croupous pneumonia, 
29, 223 
in epidemic spinal meningitis, 
223 
in salicylic acid, 223 
zoster, 224 
Hip-disease, character of pain in, 21,541 
Hippocratic face, 33, 420 
succussion, 291 
Ilippus, 191 
Hodgkin’s disease, enlargement of cer- 
vical lymphatic glands in, 448 
temperature in, 448 
Hunger, character of child’s cry in, 23 
Huntington’s chorea, 73, 501 
Hutchinson teeth, 157 INDEX. 
579 
Hydrocephalus, contraction of hands and 
arms in, 71 
face in, 28 
head in, 49 
nystagmus in, 177 
open fontanelle in, 51 
spastic rigidity of arms in, 71 
Hydrochloric acid, test for, in stomach- 
contents, 335 
Hydronephrosis, 338 
Hydropneumothorax, dollar percussion 
in, 298 
Hippocratic succussion in, 291 
metallic tinkling in, 288 
physical signs of, 297 
Hyperesthesia, 259 
in brain-tumor, 260 
in cerebro-spinal meningitis, 260 
in chronic alcoholism, 261 
leptomeningitis, 260 
in gout, 260 
in hemiplegia, 260 
in hysteria, 259 
in leprosy, an early sign of, 261 
in locomotor ataxia, 260 
in menopause, 260 
in neuralgia, 260 
in neurasthenia, 259 
in peripheral neuritis, 260 
in relapsing fever, 260 
in transverse myelitis, 260 
in typhoid fever, at convalescence, 
260 
Hyperpyrexia, causes of, 435 
Hypertrophy, cardiac, associated with 
chronic contracted kidney, in- 
crease of urine in, 384 
diagnosis of, 316 
great, force of pulse in, 352 
great, in chronic interstitial ne- 
phritis, 414 
limited bulging of chest in, 
267 
symptoms and signs of, 423 
Hysteria, allochiria in, 258 
alterations of color-fields in, 187 
aphonia in, 552 
bilateral anaesthesia in, 244 
borborygmi in, 426 
brachial monoplegia in, 81 
bromidrosis in, 229 
character of convulsions in, 491 
of cough in, 525 
of temperature in, 455 
contractions of hands, feet, and legs 
in, 70, 119 
diagnosis of, 490 
dilated pupil in, 159 
facial spasm in, 45 
false clonus in, 551 
fatuous expression in, 30 
gait in paralysis of, 94 
Hysteria, gauntlet or stocking form of 
anaesthesia in, 242 
hemianaesthesia in, 239 
hemianopsia rare in, 186 
hemidyschromatopsia in, 187 
hippus rare in, 181 
hysterogenous zones of hypersesthe- 
sia in, 259 
localized sweating in, 229 
mirror-writing rare in, 78 
ocular symptoms of, 186 
pain, cutaneous, in, 259 
painful joints in, 540 
paraplegia in, 109 
phantom tumor in, 338 
ptosis in, 41 
spasm of tongue in, 153 
spontaneous gangrene of skin in, 225 
squint in, 174 
subnormal temperature in some cases 
of, 457 
tremor of hands in, 75 
visual changes in, 240 
vomiting in, 518 
Hystero-epilepsy, diagnosis of, 493 
Hysterogenous zones, 259 
T CTE RUS. See Jaundice. 
1 neonatorum, 202 
urobilin, 202 
Idiosyncrasy to drugs, 18, 209 
hemoglobinuria of, 388 
Impetigo contagiosa, appearance of erup- 
tion in, 222 
symptoms of, 222 
Incontinence of urine, ammoniacal odor 
in, 18 
due to concentrated urine, 379 
due to excessive reflex irritation 
of bladder-walls, 379 
due to insensitive urethra, 379 
due to loss of power of sphinc- 
ter, 379 
nocturnal, in children, 381 
trousers stained in, 18 
Incubation-period of eruptive diseases, 
214 
Indicanuria, diseases in which it occurs, 
390 
in intestinal obstruction due to im- 
paction, 511 
test for, 390 
Infantile spinal paralysis. See Anterior 
Poliomyelitis. 
Infarction, renal, blood-casts in, 391 
Influenza, epidemic, cardiac failure in, 451 
catarrhal symptoms of, 451 
character of fever in, 451 
of sputum in, 528 
complications of, 451 
diarrhoea of, 451 580 
INDEX. 
Influenza, epidemic, great prostration in, 
451 
hsematemesis in, 514 
hyperaesthesia in 260 
ocular palsy in, 169 
pain in back in early stages of, 
546 
vomiting in, 451 
Indigestion, anaemia in chronic, 365 
character of respiration of child with, 
22 
erythema in, 212 
headache associated with, 446 
muscae volitantes in severe, 194 
sour breath in, 23 
vertigo in, 518 
Ingravescent apoplexy, 136 
Injury, expression of anxiety after severe, 
27 
iritis due to, 193 
spinal, knee-jerk decreased imme- 
diately after, 548 
Insomnia in Malta fever, 442 
Insufficiency of convergence in exoph- 
thalmic goitre, 159 
Intention-tremor of cerebral palsy of 
children, 69 
Intestinal obstruction, 336 
albumin in urine in, 510 
constipation in, 419 
due to cancer or stricture, 511 
due to impaction of foreign body, 
indicanuria in, 511 
symptoms of, 611 
vomiting in, 511 
due to intussusception, blood- 
stained mucous evacua- 
tions of children in, 
507 
detection of tumor in, 508 
distention of abdomen in, 
508 
inequality of shape of ab- 
domen in, 508 
pain, character of, in 507 
patulous condition of anus 
in, 508 
symptoms of chronic, 508 
tenesmus in, 508 
vomiting early in, in invag- 
ination, 507 
due to completeness of 
obstruction, 507 
due to strangulation by bands, 
509 
character of constipation in, 
509 
of localized tenderness 
and percussion-dul- 
ness in, 510 
of pulse in, 509 
of vomiting in, 509 
Intestinal obstruction due to strangulation 
by bands, Meckel’s diver- 
ticulum a cause of, 510 
pain in, 509 
temperature in, 509 
tympanitic distention in, 
510 
urine diminished in, 510 
due to volvulus, vomiting not a 
constant symptom of, 511 
indicanuria in, 389 
of rectum, symptoms of, 511 
Iritis due to injury, 193 
due to rheumatism, 193 
due to syphilis, 193 
headache due to, 461 
immobile pupil in, 159 
JAUNDICE, 196 
J albumosuria in, 409 
bradycardia in, 317 
cause of, 202 
complicating diabetes, 200 
of constipation occurring in, 418 
of hematogenous, 201 
of hepatogenous, 197 
Charcot’s fever in, 200 
color of urine in, 201, 389 
diabete bronze in, 200 
fatty diarrhoea in, 426 
headache in, 460 
hematogenous, 201 
hepatogenous, 196 
in acute phosphorus-poisoning, 199 
yellow atrophy, 201 
in amyloid liver, 199 
in chronic valvular heart disease, 
199 
in cirrhosis of liver, 199 
in malignant disease, 199 
in newborn, 202 
in pressure from aneurism, 199 
in remittent malarial fever, 448 
method of examining for, 196 
persistent and progressive in carci- 
noma of pancreas, 335 
pruritus in, 261 
purpuric eruption in severe, 210 
stools light colored in, 201 
symptoms of catarrhal, 197 
of hepatogenous, 200 
urine in, 201 
vomiting in, 519 
Joints, alterations of, in locomotor ataxia, 
121 
different modes of infection of, in 
gonorrhoeal arthritis, 123 
enlargement of, in rheumatoid arth- 
ritis, 121 
hypertrophic osteo-arthritis, follow- 
ing typhoid fever, 124 INDEX. 
581 
Joints in acute epiphysitis of infancy, 123 
synovitis, 124 
in central myelitis, 122 
in cerebro-spinal meningitis, 122 
in chronic lead poisoning, 124 
in dengue, 124 
in epidemic dysentery, 124 
in gout, 124 
in hemophilia, 125 
in milk-leg, 125 
in osteomyelitis, 122 
in scarlet fever, 124 
in Schonlein’s disease, 124 
in reflex arthritis, 122 
involvement of, with fever, in osteo- 
myelitis, 455 
in purpura, 455 
in pyaemia, 455 
small, affected in Morvan’s disease, 
124 
in syringomyelia, 122 
violent pain on motion of, in Malta 
fever, 441 
Jumpers, the. See Saltatoric Spasm. 
KIDNEY, blood-casts in acute inflam- 
mation of, 392 
character of blood in urine from, 384 
fatty casts in fatty degeneration of, 
393 
floating, 326, 337 
hematuria due to stone in, 387 
hydronephrosis, 338 
irritation of, cylindroids found in, 
395 
septic infection of, casts of micro- 
cocci in, 393 
slow degeneration of parenchyma of, 
granular casts in, 394 
Klumpke’s paralysis, 83 
Knee-jerk, diseases in which decreased, 
548 
in which increased, 549 
how best elicited, 547 
reinforced, 547 
T A GRIPPE See Influenza. 
Ju Lactic acid, test for, in stomach-con- 
tents, 332 
Landouzy-Dej erine type of muscular atro- 
phy, 31 
Landry’s paralysis, diagnosis of, 455 
loss of knee-jerk in, 548 
loss of reflexes predominant 
symptom of, 455 
non-spastic paraplegia in, 101 
Laryngeal crisis in locomotor ataxia, 87 
Laryngitis, night-cough in, 525 
partial or complete loss of voice in, 
524 
Laryngitis, short, sharp, brassy cough in, 
524 
whispering voice in, 553 
Laveran, malarial germ of, 369 
Leprosy, appearance of hands in, 63 
gangrene in, 63 
leonine face of, 32 
patches of anaesthesia in, 257 
Leptomeningitis, diagnosis of coma in 
purulent, 478 
hyperaesthesia in chi’onic, 260 
Leucocythaemia. See Leukaemia. 
Leucocytosis, 355 
in pneumonia, 355 
Leucoderma in goitre, 205 
Leucokeratosis, 149 
Leukaemia, lymphatic, enlargement of 
superficial lymph-glands in, 
368 
lymphocytes alone increased in, 
356. 368 
spleno - medullary, enlargement of 
spleen in, 343 
blood in, 355, 367 
symptoms of, 367 
Lichen planus, appearance of tongue in, 
149 
ruber, appearance of nails in, 55 
Lineae albicantes. 328 
Lips, blueness of, in heart disease, 314 
fulness of, in persons of strong sexual 
appetite, 26 
indicating phlegmatic tempera- 
ment, 26 
greatly thickened in cretinism, 32 
immobility of, due to mucous patches 
or ulceration of buccal mucous 
membrane, 29 
pendulous, in progressive bulbar par- 
alysis, 44 
slightly parted, dry, and cyanotic in 
chronic pulmonary or cardiac dis- 
ease, 29 
thin and mobile, in nervous indi- 
viduals, 26 
twitching of raised upper, in perito- 
nitis or pain below diaphragm, 
28 
Lithsemia, cylindroids in urine in, 396 
Liver, acute yellow atrophy of. See Yel- 
low Atrophy, Acute, 
causes of tenderness of, 341 
enlarged, position in, 20 
and smooth, in amyloid disease, 
341 
of kidney, 417 
enlargement of, 326 
headache in congestion of, 459 
indicanuria in cancer of, 390 
nodules and umbilication of, in ma- 
lignant disease of, 340 
percussion-note over, 339 582 
INDEX. 
Liver pushed down by right-sided pleural 
effusion, 342 
rough, in cirrhosis, 340 
swelling of, in Weil’s disease, 449 
symptoms of cirrhosis of, 341, 342 
of malignant disease of, 341 
of tropical abscess of, 341 
Localization of functions of segments of 
spinal cord, 106 
Locomotor ataxia, 87 
allochiria in, 258 
alteration of joints in, 121 
anaesthesia of lower portion of 
body and of legs in, 245 
analgesia in, 245 
Argyll-Robertson pupil in, 87, 
179 
athetoid movements in ad- 
vanced, 79 
bilateral atrophy of tongue in, 150 
bladder-symptoms of, 379 
blunted and delayed sensation 
in, 245 
brachial monoplegia in, 82 
cardiac feebleness in, 317 
coffee-ground vomit in gastric 
crisis of, 513 
contracted pupil in, 159 
cutaneous hemorrhages in, 210 
diagnosis of, 549 
diarrhoea as an intestinal crisis 
of, 422 
diplopia in, 41 
double sciatic pain in, 540 
flat-foot in, 117 
gait of, 86 
cause of, 86 
gastric crisis of, 87 
girdle-sensation in, 259 
hemiplegia in, 139 
hypersesthesia in, 260 
inability to use fingers and hands 
in, 77 
laryngeal crisis of, 87 
spasm in, 302 
lesion of optic nerve in, 192 
loss of knee-jerk in, 245, 548 
muscular atrophy of arm in, 82 
numbness of feet in, 87 
nystagmus in advanced, 177 
ocular symptoms of, 192 
optic atrophy in, 192 
pain in, 535, 541 
of skin in, 258 
parsesthesia in, 257 
paraplegia in, 107 
perforating ulcer in, 125 
ptosis in, 41 
retention of urine in, 378 
Romberg’s symptom of, 87 
swaying of body with eyes closed 
in, 87 
Locomotor ataxia, syphilis a frequent 
cause of, 88 
table of symptoms of, 87 
thoracic pain in, 539 
twitching of fingers in, 77 
vesical crisis of, 87 
Westphal’s sign of, 87 
Lordosis in cretinism, 32 
in progressive muscular atrophy, 66 
Lumbago, pain in, 539, 545 
Lyons’ method of estimating urea, 409 
Lysis, fever in erysipelas ending by 
crisis or, 444 
in scarlet fever, ending by, 442 
in smallpox, ending by, 444 
in typhoid, ending by, 443 
in catarrhal pneumonia, 452 
rare in croupous pneumonia, 452 
MADDOX’S rod-test, 162 
Madura foot, 64, 126 
Main-en-griffe, 65 
Malaria, anaemia in, 366 
aortitis rare in, 538 
brow-ague in, 537 
Chenzynski’s solution for staining 
organisms of, 372 
Cheyne-Stokes breathing in hema- 
turic, 271 
convulsions due to, 489 
enlargement of spleen in, 343 
headache in, 470 
hematemesis rare in, 514 
hematuria in, 386 
hemoglobinuria in, 388 
intermittent, attacks occurring earlier 
each day in, 445 
characteristic of fever, quartan, 
444 
quotidian, 444 
tertian, 444 
chill, fever, and sweats in, 444 
diagnosis of, 445 
effect of quinine on, 445 
method of examining organism of, 
372 
of staining organism of, 372 
muddy yellow skin in chronic, 203 
parasite of sestivo-autumnal, 371 
of quartan, 369 
of tertian, 369, 371 
remittent, bilious vomiting in, 448 
character of fever in, 448 
diagnosis between yellow fever 
and, 449 
due to aestivo-autumnal parasite, 
448 
jaundice in, 448 
sweating in, 228 
synonyms of, 448 
retinal hemorrhage in, 193 INDEX. 
583 
Malaria, roseola in, 214 
Malarial germ of Laveran, 368 
Malignant pustule. See Anthrax, Malig- 
nant. 
Malingering, convulsions in, 497 
hematemesis in, 514 
inability to ape facies of disease in, 27 
merycismus in, 520 
sciatica in, 541 
Malta fever, anorexia in, 441 
character of fever in, 441 
frequency of relapse in, 441 
headache in, 441 
insomnia in, 441 
pain on motion in 441 
Marasmus, sinking in of fontanelle in, 53 
Measles, character of fever in, 442 
date of eruption in, 214 
diazo-reaction in urine of severe, 414 
persistence of fever in, due to bron- 
chial or gastro-duodenal catarrh, 
443 
rash of, 213 
on pharynx and buccal mucous 
membrane, 156 
symptoms of, 213 
Meckel’s diverticulum, 510 
Mediastinal growths, bulging of chest in, 
267 
caput Medusa; in some cases of, 
326 
diagnosis of, from abscess, 303 
from aneurism, 303 
from chronic pneumonia, 
304 
from pericarditis, 305 
from pleural effusion, 304 
hoarseness of voice due to press- 
ure by, 554 
laryngeal cough due to pressure 
on larynx by, 524 
pain in, 545 
signs and symptoms of, 302 
Megaloblasts, called corpuscles of Ehr- 
lich, 365 
in advanced leukaemia, 363 
in pernicious anaemia, 363, 366 
Megrim. See Migraine. 
Melaena neonatorum, causes of, 515 
vomiting in, 515 
Melancholia with oxaluria, diagnosis of, 
398 
Meniere’s disease, symptoms of 471 
vomiting following tinnitus au- 
rium and vertigo in, 519 
Meningitis, basilar, lesions causing ocular 
paralysis in, 164 
papillitis in, 191 
bulging fontanelle in purulent, 52 
cerebro-spinal. See Cerebro-spinal 
Meningitis. 
contracted pupil in, 159 
Meningitis, contraction of hand in, 71 
diplopia in, 160 
facial spasm in, 45, 46 
hippus in early stages of acute, 181 
hyperaesthesia in cerebro-spinal, 260 
nystagmus occasionally in, 177 
occipital headache in, 506 
symptoms of, 506 
pain in nape of neck in, 506 
piercing cry in, 23 
purulent, hemiplegia in, 140 
vomiting in, 505 
rigidity of dorsal muscles in, 506 
scaphoid belly in tubercular, 322 
spinal, bilateral anaesthesia, in 244 
loss of knee-jerk, 548 
symptoms of, 466 
tache cerebrate in, 211 
tubercular albumosuria not present 
in, 409 
reflexes in, 548 
retraction of abdominal wall in, 
322 
subnormal temperature in some 
cases of, 457 
symptoms of, 466 
vomiting in, 506 
Menstruation, anaemia due to profuse, 365 
dark areas under eye during, 26 
disorders of, in chlorosis, 366 
hematemesis as vicarious, 514 
hemoptysis as vicarious, 527 
Merycismus, 520 
Metallic tinkling heard over the stomach, 
288 
over chest, in cavity, 288 
over hydropneumothorax, 
288 
Microblasts. 363 
Migraine, hemianopsia in, 460 
hyperaesthesia in, 260 
muscae volitantes in, 194 
scotomata in, 519 
sweating of head in, 229 
symptoms of, 537 
vomiting in, 520 
Miliaria, 229 
Milk-leg, joints in, 125 
Mirror-writing, 77 
Miscarriage, a symptom of syphilis, 159 
Moebius’s sign, 159 
Mono-anaesthesia, 242 
Monoplegia, brachial. See Brachial 
Monoplegia. 
Morbilli. See Measles. 
Morphoea as a cause of facial hemi- 
atrophy, 34 
Morton’s painful toe, 546 
Morvan’s disease, 68 
gangrene of hands in, 63 
hand similar to claw-hand in, 68 
small joints affected in, 122 584 
INDEX. 
Muscular atrophy, idiopathic. See Atro- 
phy, Idiopathic Muscular. 
Mutism, hysterical, 552 
Myalgia, pain in, 539 
Mycetoma, 64, 126 
swelling of hand followed by rup- 
ture in, 64 
Myelitis, acute ascending, bedsores in, 
225 
character of fever in, 456 
symptoms of, 101, 431 
transverse, allochiria in, 258 
anaesthesia in, 246 
bilateral anaesthesia in, 
245 
bladder-symptoms of, 379 
collateral symptoms of, 381 
diagnosis of cervical, dorsal, 
and lumbar, 105 
effect of lesion in. 102 
girdle-sensation in, 98, 259 
hyperaesthesia in, 260 
knee jerk in, 548, 550 
location of lesion in, 104 
non-spastic paraplegia in, 
101 
paraesthesia in, 258 
sensory paralysis in, 98 
spastic paraplegia in, 98 
chronic, gait of, 91 
subacute symptoms of, 103 
traumatic, retention of urine in, 
410 
Myelocyte of Ehrlich, in spleno-medul- 
lary leukaemia, 367 
Myoclonus multiplex, 72 
Myosis in facial hemiatrophy, 34 
Myotonia congenita. See Thomsen’s Dis- 
ease. 
Myxoedema, diagnosis between dropsy 
and, 230 
enlargement of feet in, 114 
of tongue in, 151 
face of, 32, 34 
skin in, 233 
spade-like hand in, 64 
symptoms of, 233 
NAILS, appearance of, in anaemia, 54 
in chloral-habit, 56, 226 
in eczema. 55 
in gout, 65 
in hemiplegia, 55 
in lichen ruber, 55 
in prolonged illness, 55 
in psoriasis, 55 
in pulmonary osteo-arthropathy, 
55 
in Raynaud’s disease, 55 
in sclerodactyle, 55 
in syphilis, 55 
Mouth-breathers, 29 
Mouth, chapter on, 141 
constant opening of, in heart disease, 
29 
fish-, nasal twang of voice in, 552 
pigmentation of, 318 
Mowing gait, 94 
Mucous patches about mouth and anus in 
infantile syphilis, 28 
immobility of lips due to, 28 
Mumps, albumosuria in, 409 
Murmur, aortic regurgitant, 311 
capillary pulsation of, 315 
Corrigan’s pulse in, 312,315 
dyspnoea in, 315 
ox-heart in, 312 
pulsation of retinal arteries 
in, 315 
pulse-wave of, 351 
short and sharp pulse in, 349 
symptoms of, due to failing 
compensation, 315 
water-hammer pulse in, 312 
stenosis, 811 
small and hard pulse in, 
349 
symptoms of, due to failing 
compensation, 315 
hemic, over fontanelle in rickets, 52 
humming-top, in jugular vein in 
chlorosis, 366 
mitral regurgitation, 307 
small volume of pulse in, 
349 
symptoms of, due to failing 
compensation, 314 
thrill in, 308 
stenosis, 308 
gallop-rhythm in, 308 
pulse-wave of, 351 
small volume of pulse in, 
349 
symptoms of, due to failing 
compensation, 314 
thrill in, 308 
pulmonary regurgitation, 312 
stenosis, 312 
splenic, in leukaemia, 368 
tricuspid regurgitation, 312 
stenosis, 312 
Murmurs, relative frequency of associated, 
313 
gravity of, 314 
venous, in anaemia, 365 
Muscae volitantes, 194 
Muscles, contraction of, in paramyoclonus 
multiplex, 72 
in electric chorea of Bergeron ,72 
in “jumpers,’’ 72 
in Huntington’s chorea, 72 
shock-like, in Dubini’s disease, 
72 INDEX. 
585 
Nails, appearance of, in syringomyelia, 
injury, or neuritis, 55 
atrophy of, 54 
hypertrophy of, 55 
white spots on, 55 
Nephritis. See also Kidneys and Bright’s 
Disease. 
acute, diarrhoea in, 422 
diffuse, anaemia in, 415 
anasarca in, in children, 415 
heart slightly dilated in, 415 
high arterial tension in, 415 
nausea and chilly sensations 
preceding, 415 
prognosis of, 415 
puffiness of face about eyes 
in, 415 
pulse hard and tense in, 415 
shortness of breath most 
marked at night in, 415 
skin harsh and dry in, 415 
symptoms and signs of, 414 
urine in, 414 
hemorrhagic effusions into 
pleura in, 299 
irritation of bladder in, 378 
parenchymatous, decrease of 
urine in, 383 
epithelial casts in urine a 
positive sign of, 392 
fever in, 454 
symptoms of, 454 
chronic hemorrhagic, hematuria in, 
387 
interstitial, albumin transient 
in, 415 
atheroma of bloodvessels in, 
416 
chronic bronchitis in, 416 
dropsy rare in, 416 
excess of uric acid in urine 
often antedates, 397 
frequency of urination in, 
415 
headache in, 462 
heart markedly hypertro- 
phied in, 416 
high tension of pulse in, 416 
hyaline casts in urine of, 
395 
low specific gravity of urine 
in, 383 
nocturnal urination in, 415 
pruritus in, 261 
pulmonary oedema in, 416 
parenchymatous, decrease of 
urine in, 383 
heart somewhat hypertro- 
phied in, 416 
marked tendency to ana- 
sarca in, 415 
prognosis in, 415 
Nephritis, chronic parenchymatous, urae- 
mic vomiting and coma may occur in, 
415 
Nervous bladder, 382 
Neuralgia, causes of, 536 
due to lead- or arsenic-poisoning, 537 
due to malaria, 537 
hypersesthesia in, 260 
intercostal, causes of, 539 
pain in, 539 
spots of Yalleix in, 538 
Morton’s painful toe in, 546 
occipital, causes of, 538 
diagnosis of, 544 
pain in, 538 
oedema in, 232 
of fifth nerve, infra-orbital, symp- 
toms of, 537 
third division, symptoms 
of, 537 
upper branch, symptoms of, 
537 
of foot, 543 
of head, due to decayed teeth, 536 
due to diseased ear, 536 
due to overstrained eyes, 536 
in anaemic, overworked women, 
536 
of labia majora or perineum, 539 
of pelvic viscera in women, 540 
pain in, 536 
supraorbital, diagnosis of, from neu- 
ritis, 537 
Neurasthenia, headache in, 461 
hypersesthesia in, 259 
knee-jerk increased in, 550 
paraesthesia in, 258 
vomiting in, 518 
Neuritis, acute multiple, character of 
fever in, 455 
knee-jerk lost in, 550 
symptoms and signs of, 455 
anaesthesia in toxic peripheral, 252 
in 50 per cent, of diphtheritic, 
252 
claw-hand in peripheral, 67 
diagnosis of, 549 
diphtheritic, 252 
general anasarca in multiple periph- 
eral, 231 
hyperaesthesia in peripheral, 260 
in foot, leg, and thigh, distribution 
of anaesthesia in, 254 
in hand, distribution of anaesthesia 
in, 253 
optic. See Papillitis, 
retro-bulbar. Nee Retro bulbar Neu- 
ritis. 
sciatic, diagnosis of, 541 
limping gait of, 85 
pain in, 541 
symptoms of, 541 586 
INDEX. 
Neuritis, sciatic, tender joints in, 541 
toxic peripheral, 251 
Neuroma, character of pain in, 546 
Neutrophile corpuscles, 355, 367 
Nictitating spasm, 46 
Nodding spasm, 47 
Noma, 154 
Nose, anaemia due to hemorrhage from, 
365 
asthma due to reflex irritation in, 
301 
broad and flat, in cretinism, 32 
broadness of bridge of, an indication 
of congenital syphilis, 28 
dilated nostril in heart disease, 29 
hemorrhage from, in leukaemia, 368 
obstruction of, in mouth-breathers, 
29 
pinched and drawn, indicating pain 
in chest in children, 28 
Nystagmus, 176 
in acute meningitis, 177 
in children otherwise normal, 177 
with imperfect vision, 177 
in disseminated sclerosis, 177 
in epilepsy, 177 
in Friedreich’s ataxia, 177 
in growths in cerebellum or pons, 177 
in hydrocephalus 177 
in locomotor ataxia, advanced, 177 
in mining and other occupations, 177 
in multiple sclerosis, 177 
OBEKMEIER, spirillum of, 441 
Obstruction, intestinal. See Intes- 
tinal Obstruction. 
Occupation spasm, 71 
Oculo-facial paralysis, 45 
(Edema. See also Dropsy and General 
Anasarca, 
localized, 231 
neonatorum, 234 
pulmonary, absence of fever in, 296 
character of sputum in, 296 
crepitant and bubbling rales in, 
288 
due to acute disease of lungs, 296 
due to injury of vagus, 296 
dulness on percussion in, 296 
feeble, hesitating speech in se- 
vere, 553 
frothy sputum in, 296 
in chronic interstitial nephritis, 
415 
Oligochromsemia, 354 
Oligocythsemia, 333 
Onychogyrophosis, 55 
Ophthalmoplegia, 40 
Ophthalmoscopy, 188 
Opisthotonos in hysteria, 492 
in severe meningitis, 506 
Optic atrophy, 192 
neuritis. See Papillitis 
Orthophoria, 162 
Osteitis deformans, head in, 49 
of cranial bones, headache in, 
470 
triangular face of, 35 
Osteomalacia, gait of, 95 
Osteomyelitis, acute, arthritis in, 122 
joint involvement with pain in, 
455 
Osteophytes, formation of, in rheumatoid 
arthritis, 122 
Otitis in scarlet fever, 442 
media, connected with thrombosis of 
cavernous sinus, 467 
diagnosis between cerebro-spinal 
meningitis and, 441 
vertigo in, 471 
Ovaritis, character of pain in, 545 
Oxaluria accompanying spermatorrhoea, 
398 
concomitant symptoms of melan- 
cholia, 398 
cylindroids in urine of, 396 
due to ingestion of pears, cabbage, 
and tomatoes, 398 
Oxyuris vermicularis, 431 
PAIN below diaphragm, twitching of 
upper lip in, 30 
best manner of discovering true seat 
of, 21 
bilateral of rheumatism of scalp,537 
burning, in oesophagus, stomach, and 
abdomen in phosphorus-poisoning, 
515 
causes of circumscribed abdominal, 
540 
in back in children, 540 
in neighborhood of heart, 538 
in sacral region, 539 
neuralgic, 536, 538 
sciatic, 540 
supraorbital neuralgic, 537 
colicky, extending to right shoulder 
in acute pancreatitis, 514 
in embolism of superior mesen- 
teric artery, 514 
concomitant symptoms of abdom- 
inal, 21 
crisis of, in tabes, 87 
darting, in urethra, in cystitis, 381 
distribution of, in neuralgia of fifth 
nerve, 537 
expression about eyes in children 
due to, 28 
of face due to, 28 
in abdominal colic, 542 
in acute aortitis, 538 
bellyache, 19 INDEX 
587 
Pain in acute pleurisy, 296 
in angina pectoris, 539 
in back, causes of, 546 
in belly in children, 544 
in cerebral tumor or abscess, 538 
in chest in aortic aneurism, 539 
in coxalgia, 21, 541 
in dengue, 546 
in diabetes mellitus, 544 
in dysmenorrhcea, 545 
in entero-colitis, 423 
in fecal impaction, 543 
in fissure of the anus, 545 
in gastralgia, 542 
in gastric cancer and ulcer, 542 
in head in children, 28 
in hemoglobinaemia, 519 
in hepatic colic, 542 
in intestinal obstruction, 507 
in intussusception, 507 
in jaundice, due to gallstones, 198 
in lead-colic, 543 
in locomotor ataxia, 541 
in lumbar region, due to pyelitis, 378 
due to perinephritic, dis- 
ease, 378 
due to stone in kidney or 
ureter, 378 
in mediastinal growths, 545 
in meningeal hemorrhage, 468 
in neuralgia of foot, 546 
of pelvic viscera, 540 
in neuromata, 546 
in one side of head, in migraine, 537 
in pancreatitis, 545 
in peritonitis, 545 
in pseudo-angina pectoris, 539 
in pulmonary disease in children, 21 
in renal calculus, 541 
colic, 542 
in skin in tabes dorsalis or hysteria, 
258 
in syphilitic periostitis of skull, 537 
often referred to point distant from 
its source, 536 
significance of, 535 
signs of, 536 
tearing, burning, in hemorrhage into 
membranes of cord, 247 
thoracic, in locomotor ataxia, 538 
throbbing, in inflammation, 536, 546 
varieties of, 535 
Pallor of face in chlorosis, 26 
in fright, 26 
in hemorrhage, 26 
of skin in absence of pigment, 265 
in anaemia, 365 
in vasomotor disturbance, 205 
Palmus, 73 
Pancreas, abscess of, 336 
carcinoma of, 335 
cysts of, 336 
Pancreas, fatty diarrhoea due to disease 
of, 426 
hemorrhagic inflammation of, 836 
inflammation of, 336 
symptoms of, 514 
Pancreatitis, acute hemorrhagic, charac- 
ter of pain in, 514, 545 
malignant, 336 
symptoms of, 514, 545 
vomiting in, 514 
Papillitis, 191 
in acute febrile disorders, 191 
in anaemia, 191 
in brain-tumor, 191 
in cerebral abscess, 191 
in meningitis, 191 
tubercular, 191 
in rheumatism, 191 
in syphilis, 191 
in toxaemia from alcohol, 191 
from lead, 191 
Paraesthesia. See also Allochiria. 
from exposure to carbolic acid, 258 
in aconite poisoning, 258 
in brain tumor, 258 
in cocaine-habit, 258 
in locomotor ataxia, 257 
in myelitis, 258 
in neurasthenia, 258 
in spinal syphilis, 257 
Paralysis agitans, gait in, 93 
Parkinsonian visage in, 30 
speech in, 554 
tremor of hands in, 75 
wasting, rigidity, and flexion of 
hands in, 69 
asthenic bulbar, 44 
diagnosis between progressive 
bulbar paralysis and, 44 
speech of, 553 
bilateral facial, 43 
in acute bulbar paralysis, 43 
in bilateral inflammation at 
stylo-mastoid foramen, 43 
in bilateral lesion of cere- 
brum, 43 
in bilateral lesion of pons, 
due to disease of basilar 
artery, 43 
in cold or double otitis, 43 
in diphtheritic multiple 
neuritis, 43 
in lesion of pons, 43 
in progressive bulbar paral- 
ysis, 43 
in syphilis at base of brain, 
43 
in toxic peripheral neuritis, 
43 
bulbar, 44 
cerebral, acute infantile, causing 
hemiplegia, 139 INDEX. 
588 
Paralysis, cerebral, deformity of foot in 
acute, 118 
diagnosis between paralysis of 
leg in, and polio- 
myelitis, 113 
hereditary spastic pa- 
ralysis and, 97 
spinal paralysis and, 
118 
epileptic convulsions in, 97 
gait of infantile, 92 
mirror-writing in, 78 
movements of hand in, 77 
spastic paraplegia in, 96 
due to traumatic myelitis, 109 
glosso - labio - pharyngeal, bilateral 
atrophy of tongue in, 150 
biting the tongue in, 148 
cardiac feebleness coming on 
suddenly in, 317 
cough in, 525 
diagnosis of, 553 
faulty movements of tongue in, 
151 
fibrillary tremor of tongue in, 
152 
indistinct speech of mumbling 
character in, 553 
hereditary spastic, 98 
infantile spinal. See Poliomyelitis, 
Anterior 
oculo-facial, 45 
of bladder with retention, due to 
pressure during childbirth, 379 
of diaphragm, causes of, 525 
cough in, 525 
of intraocular muscles, 177 
of muscles of jaw, 39 
of ocular muscles, 161 
causes of conjugate lateral, 
175 
due to acute or chronic 
lesions of nuclei, 164, 169 
due to basilar lesions, 164 
due to hemorrhage of cere- 
bral cortex, 169 
due to lesion of nerve- 
trunks, 164, 170 
between cortex and nu- 
clear origin of nerve, 
164,169 
due to poison, 164, 169 
due to sclerosis of cerebral 
cortex, 169 
Maddox’s rod-test for, 162 
method of determining in- 
dividual muscles in- 
volved in, 164 
of determining partial. 
162 
significance of conjugate 
lateral, 175 
Paralysis of ocular muscles, signs of, 
164 
symptoms of thrombosis of 
cavernous signs causing, 
175. 
varieties of, location of le- 
sion in,170 
progressive bulbar, 44 
causing paralysis of muscles 
of mastication, 39 
diagnosis between asthenic 
bulbar paralysis and, 44 
recurrent, of oculomotor nerve of 
one side, 42 
sometimes found instead of occupa- 
tion-spasm, 71 
unilateral facial, 35 
absence of trophic changes 
in cerebral, 36 
appearance of face when 
smiling in, 35 
associated with monoplegia 
in acute anterior polio- 
myelitis, 37 
caused by exposure to cold, 
35 
by fracture at base of 
skull, 35 
by hemorrhage from 
cerebellum, 36 
by hysteria, 36 
by inflammation of 
nerve-sheath at stylo- 
mastoid foramen, 35 
by injuries, 35 
by otitis media. 35 
by pressure of forceps, 
36 
of growth at base 
of skull, 35 
by primary hemor- 
rhage into nerve- 
sheath, 36 
by swelling of parotid 
gland, 35 
difficulty of whispering 
and pronouncing labial 
sounds in, 35 
in crossed paralysis, 38 
in syphilitic arteritis caus- 
ing other paralyses, 38 
location of cause of, 36 
nerve-degeneration in peri- 
pheral, 36 
peculiar distribution of, in 
some cases, 37 
power of closing eye and 
wrinkling forehead re- 
mains in cerebral form 
of, 36 
prognosis of, when due to 
pressure by forceps, 37 INDEX. 
589 
Paralysis, unilateral facial, reactions of 
degeneration in, caused by tumor in- 
volving facial fibres below or destroy- 
ing facial nucleus, 36 
Paralytic squint, 161 
Paramyoclonus multiplex, 72 
diagnosis of, 502 
Paramyotonia, 73 
forms of, 73 
Paraplegia, 96 
ataxic, 91 
knee-jerk exaggerated in, 550 
causes of, 96 
hysterical, knee-jerk exaggerated in, 
550 
non-spastic, in acute transverse mye- 
litis, 102 
in chronic transverse myelitis, 
104 
in compression from fracture or 
dislocation of vertebrae, 109 
in diabetes mellitus, rarely, 110 
in hemorrhage into the spinal 
cord or its membranes, 101 
in hereditary spastic paralysis, 
97 
in injury of the cord or mye- 
litis, triple phosphates in 
urine of, 398 
in Landry’s paralysis, 101 
in locomotor ataxia, 107 
in neuritis, 110 
in poliomyelitis, 108 
in polyneuritis, 101 
in subacute transverse myelitis, 
103 
in tumor of cord or membranes, 
109 
partial, following diphtheria, 
110 
pseudo-, in rickets, 110 
in scorbutus in infancy, 110 
of rickets, 97 
reflex, 109 
spastic, 96 
in arrested development, 97 
in rickets, 97 
in spinal lesions, 97 
pachymeningitis, 99 
syphilis, 100 
Parasites, anaemia due to ankylostomum 
duodenale, 366 
due to tapeworm, 366 
intestinal, ankylostomum duodenale, 
431 
ascaris lumbricoides, 431 
bothriocephalus latus, 429 
oxyuris vermicularis, 431 
taenia cucumerina, 431 
mediocanellata, 429 
solium, 429 
trichocephalus dispar, 431 
Parasites of lung, distoma pulmonum, 531 
echinococcus, 531 
of malaria, sestivo-autumnal, 371 
quartan, 369 
tertian, 369, 371 
of urine, distoma hematobium, 388 
filaria sanguinis hominis, 373 
Paresis, general, delusions of grandeur 
in, 381 
diagnosis of coma of, 178 
diplopia a symptom of, 161 
fine intention-tremor in, 90 
gait of, 90 
Jacksonian epilepsy in, 482 
spasm of tongue in, 153 
tremor of hands in, 75 
vesical symptoms of, 381 
Parkinsonian visage, 30, 501 
Paronychia, 55 
Parotitis in typhoid fever, 441 
in ulcerative endocarditis, 441 
Pectoriloquy over cavity connected with 
a bronchial tube, 291 
Peliosis rheumatica. See Purpura. 
Pemphigus, eruption of, 224 
Percussion-note, cracked-pot sound, 278 
dollar-test in hydropneumothorax, 
298 
dull, in consolidation of lung in 
pneumonia, 277 
in pulmonary congestion, 296 
oedema, 296 
flat, over liver, 339 
pleural effusion, 296 
method of eliciting, 274 
normal, 275 
tympanitic, in lung, due to collapse 
or adhesion of lung, 276 
due to consolidation, 276 
due to large cavity, 276 
due to pneumothorax, 276 
Pericarditis, pain in. 540 
with effusion, diagnosis of, 305 
bulging of chest in, 267 
displaced apex beat in, 273 
signs and symptoms of, 283 
Peritonitis, character of pain in, 540, 545 
drawing up of limbs to relieve pain 
in, 329 
expression of anxiety in, 27, 30 
fever in, 512 
indicanuria in, 390 
muscular rigidity in, 329 
position of body and head in, 19 
retraction of abdominal wall with 
pain in, 322 
small, wiry pulse in, 350 
symptoms of acute, 329, 543 
vomiting in, 511 
Perityphlitis, pain in, 546 
Petechise from drugs, 210 
in acute ulcerative endocarditis, 210' 590 
INDEX. 
Petech he in cerebro-spinal meningitis, 
210 
in scurvy, 210 
in septicaemia, 210 
in snake-bite, 210 
in typhus fever, 441 
in wasting, 210 
Petit mal. See Epilepsy, Minor. 
Phantom tumor, 338 
Pharyngitis, associated with stomach- 
cough, 525 
simple acute, not to be confounded 
with scarlet fever or measles, 156 
symptoms of acute, 156 
Phlegmasia alba dolens, 232 
oedema in, 232 
Phosphaturia, headache associated with, 
462 
Phthisis. See also Tuberculosis, 
alar chest of, 265 
cause of night-cough in, 525 
character of cough in laryngeal, 
524 
of sputum in, 527 
diminished expansion of chest in, 
272 
facial expression in acute, 29 
flushing of face in, 196 
greasy, yellow skin in some cases of, 
203 
hands in chronic, 54 
laryngeal, whispering voice in, 552 
night-sweats of, 229 
vomiting in, 520 
Piles. See Hemorrhoids. 
Pin-point pupil in opium-poisoning, 159 
Pitting a sign of dropsy, 230 
Pleurisy, acute, character of pain in, 296 
diminished chest-expansion in, 
272 
friction-sound often best heard 
in axilla in, 289 
position in, 20 
symptoms and signs of, 296, 297 
tenderness over rib in, 260 
hemorrhagic, 299 
in acute infectious diseases, 299 
in aneurism, 299 
in carcinoma, 299 
in nephritis, 299 
in tuberculosis, 299 
with effusion, 296 
segophony above effusion in, 291 
Bacelli’s signs above effusion in, 
291 
bronchial breathing due to com- 
pression in, 286 
bulging of chest in, 267, 297 
changes in level of effusion in, 
297 
convulsions during irrigation of 
pleura in, 500 
Plurisy with effusion, cough during aspir- 
ation of fluid in, 524 
on change of position in, 
524 
cracked-pot sound in, 278 
decreaseof vocal fremitus in, 273 
resonance in, 291 
diminished chest-expansion in, 
271 
displacement of apex-beat in, 
273, 297 
distant breath-sounds over effu- 
sion in, 297 
method of testing for cause of, 
299 
oedema over ribs in purulent, 
233 
of left side, obliteration of 
Traube’s semilunar 
space in, 297 
spleen displaced down- 
ward in, 343 
of right side, liver pushed down 
in, 342 
pulsating, 274 
sigmoid line marking top of 
effusion in, 297 
skodaic resonance above effusion 
in, 278, 297 
symptoms and signs of, 296, 297 
Pneumonia, acute catarrhal, character of 
fever in, 452 
difficulty of diagnosis be- 
tween pulmonary tuber- 
culosis and, 292, 293 
symptoms and signs of, 292 
croupous, casts of finer bronchial 
tubes sometimes found in 
sputum of, 529 
bronchial breathing in, 292 
bubbling rales in resolution in, 288 
character of crying in children with, 
23 
Cheyne-Stokes respiration in, 271 
chill in, 452 
chlorides decreased in urine in acute 
stages of, 413 
increased, indicating conva- 
lescence from, 413 
chronic, Charcot-Leyden crystals in 
sputum of, 529 
cracked-pot sound in, 278 
crepitant rale an early sign of, 288 
crisis on third to ninth day in, 292 
delirium a bad symptom of, 292 
diagnosis and symptoms of, 291, 292 
between mediastinal growths 
and, 304 
diminished expansion of chest in, 
272 
expression of anxiety in some cases 
of, 27 INDEX. 
591 
Pneumonia, face of, 29 
feeble heart a bad symptom in, 292 
hesitating speech in severe, 553 
great increase in urine in conva- 
lescence from, 383 
headache in early stages of, 469 
herpetic blisters about mouth, with 
fever in. 29, 223, 292 
increase of vocal fremitus in, 273 
resonance in, 291 
jaundice in, 201 
leucocytosis in, 355 
necessity for examining axilla and 
septum between upper and middle 
lobe of right lung in, 295 
percussion-note dull in, 277 
prune-juice or purulent sputum a 
bad symptom late in, 292 
pseudo-crisis in, 292 
rale redux in, 292 
rapidity of respiration in, 269 
rusty, sticky sputum in, 291 
secondary diphtheritic dysentery due 
to, 425 
subnormal temperature following 
crisis of, 456 
sweat at crisis in, 228 
vocal resonance in. 291 
wavy breathing of, 272 
Pneumothorax, amphoric breathing 
rarely heard in, 287 
cracked-pot sound in, 278 
decrease of vocal fremitus in, 273 
tympanitic note in, 277 
Pohl and Kosenbach’s test, 299 
Poikilocytosis in chlorosis, 366 
in pernicious anaemia, 366 
Poisoning, acute alcohol, symptoms of, 472 
albumosuria in phosphorus, 409 
anaemia in chronic lead and arsenic, 
366 
anaesthesia in toxic peripheral neu- 
ritis, caused by arsenic, lead, alco- 
hol, mercury, 252 
appearance of tongue in acid or 
alkali, 146 
Argyll-Eobertson pupil in bisul- 
phide of carbon, 179 
autointoxication, 460 
blue-line on gums in lead, 157 
brachial monoplegia in lead, 83 
cannabis indica, diagnosis of, 473 
chloral, symptoms of, 474 
chronic silver, 203 
constipation in phosphorus, 418 
contraction of pupil in opium, 180 
convulsions due to aconite, veratrum 
viride, hydrocyanic acid, ignatia, 
strychnine, sabadilla, chronic lead, 
489, 498 
diplopia in ptomain, spigelia, co- 
nium, belladonna, gelsemium, 160 
Poisoning, fatty casts in urine due to phos- 
phorus, arsenic, antimony, iodo- 
form, 394 
fever in septic, 448, 450 
hemoglobinuria in mushroom, coal- 
tar, potassium chlorate, glycerin, 
388 
hyperaesthesia in lead and arsenic, 
261 
jaundice in phosphorus, 199 
in any poisoning causing ex- 
cessive hemolysis, 201 
joint-affections in chronic lead, 124 
light-colored stools in phosphorus, 
515 
neuralgia of head in lead and arsenic, 
537 
obstinate constipation in chronic 
lead, 419 
ocular paralysis in ptomain, alco- 
hol, sulphuric acid, nicotin, lead, 
and carbonic acid, 169 
oedema in arsenic, 231, 232 
papillitis in alcohol and lead, 191 
parsesthesia in aconite and cocaine, 
258 . 
pin-point pupil in opium, 159 
pruritus in lead and opium, 261 
ptosis in gelsemium and conium, 42 
slowness of breathing in opium, 
chloral, aconite, chloroform, anti- 
mony, 270 
symptoms of acute antimonial, 421 
of arsenical, 421 
of opium, 473 
of phosphorus, 515 
tremors of hand in chronic alcohol, 
lead, and mercurial, 73, 75 
unilateral atrophy of tongue in 
chronic lead, 150 
urine in santonin and carbolic acid, 
389. 
vomiting in antimonial, phosphorus, 
and arsenical, 512, 513, 515 
wrist-drop in lead, 74 
Poliomyelitis, absence of vesical symp- 
toms in, 381 
character of fever in, 456 
claw-hand in, 67 
convulsions, headache, and muscular 
twitching in, 456 
crural monoplegia in, 110 
diagnosis between paralysis of leg 
in and acute cerebral paralysis, 113 
foot-drop in, 112 
gait in acute, 91 
lateral wrist-drop in, 74 
loss of knee-jerk in, 549 
of power in several muscles of 
limb later in disease in, 456 
paraplegia in, 108 
‘‘Punchinello” leg in, 112 592 
INDEX. 
Poliomyelitis, symptoms of, 549 
Polycythsemia, due to congenital cardiac 
disease in children, 353 
Polydipsia, a symptom of diabetes mel- 
litus, 406 
Polyneuritis, differential diagnosis be- 
tween paraplegia in, and Landry’s 
paralysis, 102 
Polyphagia, a symptom of diabetes mel 
litus, 406 
Position as an encouraging sign, 20 
due to action of drugs, 19 
in acute bellyache, 19 
in nausea, 19 
pleurisy, 20 
in coma, 19 
in dyspnoea due to asthma, 300 
in enlarged liver, 20 
in grave or advanced disease, 20 
in heart-disease, 19 
severe, 20 
in hemorrhage, external or internal, 
19 
in large growths in abdominal cavity, 
20 
in oedema of lungs, 20 
in peritonitis, 19 
in pleurisy with effusion, 20 
in pulmonary consolidation, 20 
indicative of convalescence, 19 
persistently on the side, 19 
Pott’s disease, 100 
spastic paraplegia in, 100 
Pregnancy, caries of teeth in, 157 
chloasma of, 204 
discomfort due to, 21 
grave prognosis of acute diffuse 
nephritis in, 415 
pigmentation of eyelids during, 26 
proportion of white corpuscles to red 
altered during, 354 
value of estimation of urea during, 
412 
vomiting in, 518 
Presystolic mitral murmur, 308 
Prevost’s symptom, 175 
Proctitis, symptoms of, 424 
Prostate, enlarged, a cause of interfer- 
ence with passage of urine, 382 
Pruritus, about anus, from opium, 
261 
in chronic lead-poisoning, 261 
in contracted kidney, 261 
in diabetes, 261 
in gout, 261 
in jaundice, 261 
in piles, 261 
Pseudo-angina pectoris, pain in, 539 
-bulbar paralysis, diagnosis of, 44, 
553 
-meningitis, convulsions in children 
in, 498 
Pseudo-muscular hypertrophy, gait in, 
92 
-ptosis, caused by paralysis of the 
unstriped fibres of Muller, 40 
-tabes, 82, 88 
gait in, 86 
Psoriasis, nails in, 55 
Ptosis, alternate, in so-called nervous 
syphilis, 41, 43 
associated with internal squint, 41 
caused by affection of the sym- 
pathetic, 40 
by cerebral hemorrhage, 40 
by disease of the corpora quad- 
rigemina, 41 
by lesion of oculomotor nerve 
or nucleus, 39 
in angular gyrus, 40 
by nervous syphilis, 41 
by reflex irritation, 40 
complicating tetanus, 41 
concomitant symptoms of, if oculo- 
motor nerve is destroyed, 40 
congenital, 39, 41 
definition of, 39 
in feeble, overworked women in the 
morning, 41 
in hysteria, 41 
in idiopathic muscular atrophy, 41 
in locomotor ataxia, 41 
in meningitis, 506 
in oculo-facial paralysis, 45 
in recurrent paralysis of oculomotor 
nerve on one side, 42 
in tubercular or syphilitic changes 
at base of brain, 41 
transient, in poisoning by gelsemium 
or conium, 42 
with hemiplegia of face and limbs 
on opposite sides of body, 42 
Puerile breathing, 285 
Puerperal eclampsia, diagnosis of con- 
vulsions in, 495 
Pulmonary abscess, 294 
apoplexy, 296 
congestion, 296 
consolidation, position in, 20 
gangrene, 295 
oedema, 296 
osteo-arthropathy, appearance of 
nails in, 55 
enlargement of feet in, 114 
spade-like hands in, 64 
Pulsating pleurisy, 274 
Pulse, best taken in children when asleep, 
24 
causes of rapid, 352 
slow, 351 
character of, 341 
Corrigan, 349 
dicrotic, 350 
examination of, 345 INDEX. 
593 
Pulse, feeble, rapid, and running, in 
cholera morbus, 420 
force of, 351, 352 
hard and tense, in acute diffuse 
nephritis, 415 
high tension, in chronic interstitial 
nephritis, 416 
method of production of, 346 
normal wave of, 350 
of empty arteries in severe hemor- 
rhage, 350 
pulsus alterans, 350 
paradoxus, 346 
rapid and weak, in intestinal ob- 
struction, 509 
due to stimulation of heart, 
351 
rate of, 348 
slow in cerebral tumor, 505 
of digitalis, 341 
trip-hammer, 349 
volume of, 348 
water-hammer, 349 
“Punchinello” leg, 112 
Pupil, Argyll-Robertson, 179 
contracted, 159 
from bulbar paralysis, 180 
from central nervous disease, 
159 
from cerebral inflammation, 159 
tumor, 180 
from corneal inflammation, 
causing photophobia, 159 
from embolism, 180 
from false paretic dementia of 
syphilis, 180 
from locomotor ataxia, 180 
from meningitis, 159, 180 
from paretic dementia, 180 
contraction and dilatation of, with 
Cheyne-Stokes breathing, 181 
dilated, from aneurism, 180 
from aortic regurgitation, 180 
from blindness, 159 
from fright, 159, 180 
from glaucoma, 159, 180 
from hysteria, 159 
from intracranial pressure caus- 
ing coma, 159 
from irritation of cervical sym- 
pathetic, 180 
of upper part of spinal- 
cord, 180 
from mydriatic, 159, 180 
from neurasthenia, i80 
from paralysis of centre of third 
nerve, 180 
hippus, 181 
immobile, from iritis, 159 
method of testing, 178 
pin-point, in opium-poisoning, 159, 
473 
Pupil, reaction of, to accommodation, 178 
to light, 178 
size of normal, 178 
transitory unequal dilatation of, in 
tuberculosis, 181 
Wernicke’s sign of hemiopic inaction 
of, 180 
Purpura hemorrhagica, 208 
hematemesis in, 514 
hematuria in, 388 
hemoptysis in severe, 527 
Henoch’s disease in, 209 
in rheumatism, 208 
joint involvement with fever in, 
455 
Pyaemia, diazo reaction in severe, 414 
jaundice in, 202 
joint involvement with fever in, 455 
profuse sweating in, 228 
Pyelitis, character of fever in, 417, 448 
of pain in, 417 
chills and fever in, 417, 448 
diagnosis of, 417 
may be caused by strongylus gigas, 
388 
pain in lumbar region in, 378 
pyuria,constant or intermittent in, 417 
urine, acid in, 417 
Pyelonephrosis, casts iof micrococci in, 
393 
Pylephlebitis, vomiting in, 519 
Pyopneumothorax, dollar percussion in, 
298 
Hippocratic succussion in, 291 
metallic tinkling in, 288 
subphrenicus, 336 
Rales, 288 
altered by coughing if not crepitant, 
289 
bubbling, in bronchitis, 288 
in convalescence from asthmatic 
attack, 288 
from pneumonia, 288 
in pulmonary oedema, 288 
in resolution in pneumonia, 288 
in tuberculosis, 288 
character of, in asthma, 301 
crepitant, in early stages of croupous 
pneumonia, 288 
in pulmonary collapse or oedema, 
288 
congestion, 296 
in tubercular breaking down, 
288 
redux, in pneumonia, 294 
Raynaud’s disease, appearance of hands 
in, 55 
coma in, 477 
gangrene of hands in, 63, 225 
hemoglobinuria in, 388 594 
INDEX. 
Raynaud’s disease, localized sweating in, 
229 
symptoms of, 225 
vomiting in, 514 
Reflex iridoplegia- See Argyll-Robert- 
son Pupil. 
Reflexes, 547 
ankle clonus, how elicited, 548 
biceps tendon, how tested, 548 
diseases in which decreased, 548 
in which increased, 549 
knee-jerk, how best elicited, 547 
reinforced, 547 
of skin, table of, 551 
Relapse, frequency of, in Malta fever, 441 
in typhoid fever, 438 
Relapsing fever, character of fever in, 
441 
hematemesis in, 514 
hyperaesthesia in, 260 
jaundice in. 201 
oedema of legs and wrists in, 
233 
spirillum of Obermeier in blood 
in, 441 
sweating in, 228 
tongue in, 143 
Remittent fever. See Malaria, Remit- 
life tent. 
Resonance, vocal, 290 
Baccelli’s sign, 291 
decreased, causes of, 291 
increased, causes of, 291 
Respiration, causes of labored, 272 
of rapid, 269, 270 
of slow, 270 
Cheyne-Stokes, 271 
costal, 271 
diaphragmatic, 271 
inspiration prolonged in spasmodic 
croup, 270 
method of studying, in children, 23, 
24 
prolonged expiration in asthma and 
emphysema, 270 
rhythm of, 270 
wavy, in pneumonia, 272 
Retention of urine in locomotor ataxia, 
379 
in overdistention, 379 
in pressure during childbirth, 
379 
in traumatic myelitis, 279 
Retinitis, albuminuric, 193 
hemorrhagic, 193 
in diabetes, 193 
in leukaemia, 362 
in syphilis, 379 
Retro bulbar neuritis, 191 
Rheumatism, acute articular, appearance 
of hands in, 61 
of tongue in, 144 
Rheumatism, acute articular, acid sweats 
of, 229 
character of fever in, 454 
chlorides decreased in, 413 
increased in, in conva- 
lescence, 413 
convulsions in, 454 
cyanosis in, 454 
erythema in, 208 
headache in, 462 
iritis in, 123 
joint affections in, 454 
papillitis in, 191 
purpura in, 208 
subcutaneous fibrous nod- 
ules in, 209 
uric acid in urine of, 397 
urticaria in, 210 
with hyperpyrexia, de- 
lirium in, 454 
chronic, changes in shape of hand 
in, 61 
limping gait in, 85 
of scalp, symptoms of, 537 
Rheumatoid arthritis. See Arthritis De- 
formans 
Rhonchi, 288 
Rickets, beaded ribs of, 268 
carpo-pedal spasm in, 71 
cranio-tabes in, 51 
deficient bony development in, 51 
early decay of teeth in, 156 
excessive sweating of head in, 53 
gait in. 92, 95 
Harrison’s grooves in, 268 
head in, 28, 50 
hyperaesthesia in, 260 
l&ryngeal spasm in, 302 
nodding-spasm in, 47 
open fontanelle in, 51 
pain in back in, 540 
pseudo-paraplegia in, 110 
spastic paraplegia in, 97 
sweating of head in, 229 
tenderness of skin in, 260 
Risus sardonicus in tetanus or strychnine- 
poisoning, 26, 146 
Roberts’s yeast-test for sugar in urine, 
406 
Romberg’s symptom, 87 
Roseola See also Erythema. 
due to drugs, 217, 218, 222, 223 
in Bright’s disease, 216 
in chickenpox, 214, 222 
in cholera, 215 
in diabetes, 216 
in diphtheria, 214 
in German measles, 213 
in malaria, 214 
in measles, 213 
in septicaemia, 215 
in smallpox, 214, 218 INDEX. 
595 
Roseola in syphilis, 215 
in tubercular peritonitis, 217 
in typhoid fever, 215 
in typhus fever, 216 
in vaccination, 221 
Rose-rash. See Erythema and Roseola 
Rotheln, appearance of rash in, 213, 214 
fever in, 443 
symptoms of, 213 
Rubella. See Rotheln. 
Rubeola. See Measles. 
0 ACCHAROMYCES albicans, causing 
O fermentation in diabetic urine, 402 
St. Vitus’s dance See Chorea. 
Salaam convulsions, 501 
Saltatoric spasm, 73, 503 
Sarcinse ventriculi, in vomitus from 
chronic gastric catarrh, 
517 
from gastric cancer, 518 
dilatation, 517 
ulcer, 518 
test for, 517 
Sarcoma, anaemia due to, 366 
purpura in multiple, 310 
Scarlet fever, arthritis in, 124 
character of fever in, 442 
collar of brawn in, 442 
date of eruption in, 214 
diazo-reaction in severe, 414 
enlargement of spleen in, 343 
erythema in, 211, 212 
hematuria in, 386 
lysis in fever of, 442 
otitis in, 442 
pleurisy with effusion compli- 
cating, apt to become puru- 
lent, 298 
prognosis from fever of, 442 
sore-throat in, 155 
strawberry tongue in, 144 
synovitis in, 62 
Scars, 228 . 
Schonlein’s disease, joint-involvement, 
in,124 
symptoms of, 209 
ulcerations of tongue in, 148 
ulcers of buccal mucous mem- 
brane in, 154 
Sciatica. See Neuritis, Sciatic. 
Sciopedy, 114 
Sclerema neonatorum, symptoms of, 234 
Sclerodactyle, nails in, 55 
Scleroderma, skin in, 34, 234 
Sclerosis, amyotrophic lateral, 68 
alteration of hands in, 68 
ankle-clonus in, 551 
character of speech in, 554 
knee-jerk increased in, 550 
spastic paraplegia in, 99 
Sclerosis, disseminated, ankle-clonus in, 
550 
expression of face in early stages 
of, 30 
hemianaesthesia in, 241 
hippusin, 181 
knee-jerk increased in, 550 
nystagmus in, 177 
optic atrophy in, 192 
slow, scanning speech in, 553 
symptoms of. 75 
tremor of hands in, 75 
vertigo in, 471 
lateral, absence of vesical symptoms 
in, 381 
ankle-clonus in, 550, 551 
causes of increased reflexes in, 
99 
gait in, 91 
spastic paraplegia in, 99 
multiple, allochiria in, 258 
coma in, 478 
convulsions in, 500 
gait in, 92 
hemiplegia resulting from, 13, 
hippus in, 191 
spastic paraplegia in, 97. 
| Scorbutus See Scurvy. 
Scotoma, 192 
Scurvy, corneal ulceration in, 194 
dropsy in, 231 
hematemesis in, 514 
hematuria in, 388 
loosening of teeth in, 157 
pain in back in, 540 
petechise in, 210 
pseudo-paralysis in, in infancy, 110 
sponginess of gums in, 157 
Senility, tremor of hands in, 75 
Septicaemia, character of fever in, 448, 
450 
diarrhoea in, 426 
great variations in temperature in, 
450 
jaundice in, 201 
rose-rash in, 215 
Skin, anaesthesia of, 239 
cadaveric, in pyaemia, 204 
cold and moist, with high rectal tem- 
perature, in sunstroke, 455 
and wet, a bad symptom in fever, 
435 
color of, in health and disease, 195 
cyanosis of, 206 
dropsy and swelling of, 230 
dry and hot, in fever, 434 
eruptions of, in disease, 212 
excess of dryness of, 229 
gangrene of, 225 
glossiness of, 224 
grassy-yellow in phthisis and chronic 
liver disease, 203, 204 596 
INDEX. 
Skin, greenish-yellow in chlorosis, 204, 
205 
harsh and dry, in acute diffuse ne- 
phritis, 414 
in diabetes, 229 
hemorrhages into, 210 
hypersesthesia of, 259 
in acute alcohol poisoning, 472 
in Addison’s disease, 204 
in angioneurotic oedema, 234 
in argyria, 203 
in carcinoma of internal organs, 204 
in chloasma of pregnancy, 204 
in elephantiasis, 233 
in influenza, 261 
in jaundice, 195 
in kidney disease, 205 
in oedema neonatorum, 234 
in opium-poisoning, 261 
in profound anaemia, 261 
in sclerema neonatorum, 234 
in scleroderma, 234 
in tuberculosis, 205 
increased sensibility of, due to ergot, 
261 
leucoderma, in true goitre, 205 
muddy-yellow, in chronic malaria 
and prolonged suppuration, 203 
pain of, 261 
pallor of, 205 
in myxcedema, 206 
paraesthesia of, 257 
parchment-like, in syphilis, 26 
pigmentation of, 204, 318 
pruritus of, 261 
redness of, 210 
scars of, 228 
sensation in, 235 
sweating of, 228 
table of reflexes of, 551 
tache cerebrate, 211 
meningeale, 211 
tenderness of, in disease of internal 
organs, 260 
in rickets, 260 
waxy, in cretinism, 32 
yellow, in xanthoma, 203 
and greasy, in paretic dementia, 
204 
Skodaic resonance, 278 
Smallpox, appearance of eruption in, 214, 
218, 443 
date of eruption in, 214 
fever in, 443 
grisolle sign of, 214 
headache in early stage of, 469 
hemoptysis in hemorrhagic, 527 
pain in back in onset of, 443, 546 
Spasm, nodding. See Nodding Spasm. 
Spasms, blepharo-facial, 45 
Graefe’s spots in, 46 
carpo-pedal, 71 
Spasms, facial, Abadie’s sign in, 46 
cause of functional, 45 
of organic, 45 
following exposure to cold, 46 
paralysis, 47 
in hysteria, 45 
in adults, due to locomotor ataxia, 
302 
due to mediastinal growths, 
302 
in children, due to croup, 302 
due to digestive disturbances, 
302 
due to laryngeal catarrh, 302 
due to rickets, 302 
in chorea insaniens, 501 
minor, 500 
in electric chorea, 502 
in Huntingdon’s chorea, 501 
in lesion of middle peduncle of cere- 
bellum, 503 
in paramyclonus multiplex, 502 
in Thomsen’s disease, 503 
in true chorea, 501 
laryngeal, in adults, due to aneurism 
pressing on recurrent 
laryngeal nerve, 302 
due to enlargement of retro- 
bronchial glands, 302 
of fingers due to occupation, 71 
of tongue, 153 
varieties of, 500 
Spastic paraplegia. See Paraplegia, Spas- 
tic. 
Speech, 552. See also Voice 
defects of, 555 
agraphia, 555 
alexia, 555 
aphasia, 554 
aphonia, 555 
apraxia, 555 
paraphasia, 555 
tests for, 555 
word-deafness, 555 
feeble, hesitating, in pneumonia of 
pulmonary oedema, 553 
halting, hesitating, in paretic de- 
mentia, 553 
incoherent, in chorea in children, 
553 
in delirium, 553 
indistinct, mumbling, in amyotrophic 
lateral sclerosis, 554 
in glosso-labio-pharyngeal 
paralysis, 553 
in stomatitis, 553 
in typhoid fever, 553 
nasal, in adenoid vegetations, 553 
nervous mechanism of, 554 
scanning, in multiple sclerosis, 93 
shrill, piping, in paralysis agitans, 
554 INDEX. 
597 
Speech, slow, scanning, in disseminated 
sclerosis, 553 
in Friedreich’s ataxia, 553 
tests for defects of, 555 
whispering, causes of, 552 
Spermatorrhoea accompanying oxaluria, 
398 
spermatozoa found in, 401 
Spermatozoa in urine, significance of, 401 
Sphygmograph, 350 
Spinal cord, great rise in temperature 
due to injuries to cervical por- 
tion of, 455 
localization of functions of seg- 
ments of, 106 
location of lesion of, in anaes- 
thesia, 247 
Spirillum of Obermeier in blood in re- 
lapsing fever, 441 
Spleen, causes of enlargement of, 343 
extension downward of, 343 
enlarged, in amyloid disease of kid- 
ney, 416 
in typhoid fever, 439 
in leukaemia, 368 
method of examination of, 343 
normal position of, 343 
swelling of, in septicaemia, 343 
in Weil’s disease, 449 
uric acid in excess in enlargement 
_ of, 397 
Splenic fever. See Anthrax. 
Spots of Valleix, 538 
Spotted fever. See Cerebro-spinal Me- 
ningitis. 
Sputum, actinomyces in, 532 
anchovy sauce, in amoebic abscess, 527 
blood-streaked in leakage from aortic 
aneurism, 527 
in pulmonary gangrene in chil- 
dren, 527 
in valvular heart disease, 527 
bloody, in hemoptysis, 527 
in ruptured bloodvessels in pos- 
terior pharyngeal wall, 527 
brick-dust, in hepatic abscess com- 
municating with lung, 527 
brownish, in gangrene of lung, 294 
casts of bronchioles in, in fibrinous 
bronchitis, 529 
of larynx and bronchi in, in 
diphtheria, 529 
of smaller bronchioles found oc- 
casionally in, in croupous 
pneumonia, 529 
Charcot-Leyden crystals in asth- 
matic, 399, 528 
copious and purulent, in pulmonary 
abscess, 294 
crystals of margaric acid in pulmon- 
ary gangrene, purulent bronchitis, 
and follicular tonsillitis, 531 
Sputum, Curschmann’s spirals in asth- 
matic, 399, 528 
Dittrich’s plugs in, in purulent bron- 
chitis, 300 
eggs of distoma pulmonum in, 531 
elastic fibres in, in abscess of lung, 
530 
in gangrene of lung, 530 
in tuberculosis of lung, 530 
examination of, for elastic fibres, 531 
with centrifuge, 530 
frothy, in pulmonary oedema, 528 
hooks of echinococcus in, 531 
in asthmatic attack, 528 
in chronic bronchitis, 310 
in pulmonary gangrene, 528 
liquid and watery, in epidemic influ- 
enza, 528 
in pulmonary oedema, 528 
method of staining for tubercle ba- 
cilli in, 532 
microscopical examination of, 530 
prune-juice in chronic pneumonia, 
526 
purulent, causes of, 528 
rusty, sticky, in croupous pneumonia, 
526 
Squint, diagnosis between concomitant 
and paralytic, 161 
of conditions of producing, 167 
in hysteria, 176 
in meningitis, 506 
in ocular palsy, 42, 164 
significance of external, 172 
Stellwag’s symptom, 159 
Steppage gait in pseudo-tabes, 86 
Stomach, cough due to reflex irritation 
from, 525 
distention of, by gas, 331 
indicanuria in cancer of, 390 
method of examining with gastro- 
diaphane, 327 
with gyromele, 328 
test of contents for hydrochloric acid, 
335 
for lactic acid, 332 
for urates in urine in disorders 
of, 397 
vomiting in dilatation of, 517 
Stomatitis, action of child with, toward 
breast, 23 
appearance of tongue in ulcerative, 
148 
buccal mucous membrane affected in, 
154 
epidemic, symptoms of, 453 
impetiginosa, 150 
malignant ulcerative, 154 
offensive odor of breath in, 23 
temperature of mouth raised in, 434 
Stone in bladder, interference with pas- 
sage of urine due to, 382 598 
INDEX\ 
Stools. See also Feces. 
almost devoid of mucus in cholera- 
morbus, 420 
bilious, 428 
bloody, 428 
clay colored, in hepatogenous jaun- 
dice, 201 
in Weil’s disease, 449 
gall-stones in, 428 
in cholera, comma bacilli in, 421 
infantum, 420 
in dysentery, 424 
in intussusception in children, 507 
in proctitis, 423 
intestinal parasites in, 429 
mixed with mucus, 428 
oily, in carcinoma of pancreas, 
335 
ribbon-shaped, in follicular entero- 
colitis. 423 
rice water, in antimonial poisoning, 
421 
significance and character of blood 
in, 426 
tarry, in yellow fever, 449 
Strabismus See Squint. 
Strongylus gigas, hematuria due to, 388 
Stupor in typhoid fever, 438 
in ulcerative endocarditis, 438 
Subsultus tendinum, 56, 77 
Succussion, Hippocratic, 291 
Sudamina, 229 
Sugar in the blood, 375 
Williamson’s test for, 375 
in the urine. See Glycosuria and 
Urine 
Sunstroke, character of fever in, 455 
diagnosis of coma in, 477 
headache of, 469 
skin cold and moist with high rectal 
temperature in, 455 
hot and dry in, 455 
Sweating, in acute miliary tuberculosis, 
452 
ulcerative endocarditis, 228 
bile-stained, in jaundice, 229 
in antimonial poisoning, 421 
in collapse, 229 
in crises in fevers, 228 
in debility, 229 
in health, 228 
in hepatic abscess, 341, 451 
in intermittent malarial fever, 228 
in malaria, 228 
in obstruction of rectum, 511 
in phthisis, 228 
in pneumonia at crisis, 228 
in pyaemia, 228 
in relapsing fever, 228 
in typhoid fever, 229 
in uraemia, 229 
localized, 229 
Sweating, localized, in exophthalmic 
goitre, 229 
in hysteria, 229 
in migraine, 229 
in paretic dementia, 229 
in Raynaud’s disease, 229 
in rickets, 229 
in thoracic aneurism, 229 
uriniferous, in deficient renal activity, 
229 
Syncope, diagnosis of, 496 
Syphilis, action of child with, toward 
breast, 23 
alternate ptosis in, 41, 43 
aortitis in, 538 
appearance of fingers in dactylitis in, 
55 
of nails in, 55 
Argyll-Robertson pupil in cerebral, 
180 
associated with amyloid kidney, 416 
at base of brain causing bilateral 
facial paralysis, 43 
atheroma in, 347 
broadness of bridge of nose in con- 
genital, 28 
diagnosis of coma in, 478 
of epilepsy due to, 485 
earlv cutting of teeth in inherited, 
157 
enlargement of spleen in early, 343 
eruptions of, 227 
fever in, intermittent, 453 
remittent, 452 
simple continued, 452 
fissures and chancres of tongue in, 
147 
gummatous swelling and periosteal 
thickening of shins in, 126 
hemiplegia in cerebral, 139 
Hutchinson teeth in, 157 
iritis in, 193 
miscarriage a symptom of, 21 
mucous patches about mouth and 
anus in infantile, 28 
ocular paralysis in, 179 
of intestinal tract, diarrhoea due to, 
425 
open fontanelle in, 51 
pain in periostitis of skull in, 537 
papillitis in, 191 
paraesthesia in spinal, 258 
parchment-like skin of, 26 
pseudo-palsy in, 83 
ptosis in changes at base of brain in, 
41 
purpura in, 210 
purulent acne of forehead in, 221 
retinitis in, 193 
rose-rash in, 211, 215 
scars in, 227 
spastic paraplegia in spinal, 100 INDEX. 
599 
Syphilis, symptoms of arteritis due to, 465 
triad of, 157 
Syphilitic triad, 157 
Syringomyelia, appearance of nails in, 55 
loss of pain and temperature-sense 
in, 247 
necrosis of terminal phalanges in, 63 
partial anaesthesia in, 247 
patches of anaesthesia in, 247, 257 
small joints affected in, 122 
symptoms of, 247 
wasting of hands with anaesthesia in, 
68 
TABES dorsalis. See Locomotor Ataxia. 
Tabetic atrophy, 192 
Tache cerebrale, 211 
meninc/eale, 211 
Tachycardia, 317, 352 
Taenia cucumerina, 431 
mediocanellata, 429 
solium, 429 
Tapeworm. See Parasites. 
Taste, decrease of acuity of, in facial 
hemiatrophy, 34 
Teeth, blue line around, in lead-poison- 
ing, 157 
caries of, in diabetes mellitus, 157 
in pregnancy, .157 
cut early in inherited syphilis, 157 
early decay of, in rickets, 156 
Hutchinson, 157 
loosening of, in salivation, 157 
in scurvy 157 
staining of, 157 
Teichmann’s crystals in hemoglobinuria, 
385 
Temperature. See also Fever. 
causes of sudden fall of, in typhoid 
fever, 436 
great rise of, in injuries to cervical 
cord, 455 
high, with cold skin in cholera 
Asiatica, 453 
in cholera infantum, 453 
in sunstroke, 455 
in acute alcohol-poisoning, 472 
in diabetic coma, 475. 
in intestinal obstruction, 509 
methods of taking, 434 
subnormal, causes of, 456 
in cretinism, 32 
in heat-exhaustion, 457 
in injuries to dorsal portion of 
spinal cord, 457 
Tenesmus in bladder-trouble, 381 
in cholera infantum, 420 
in dysentery, 424 
in intussusception, 508 
in proctitis, 423 
in stricture of rectum, 422 
Test, Ehrlich’s diazo-reaction, 414 
for albumin in urine, boiling, 402 
Heller’s, 403 
quantitative, by centrifuge, 
403 
for albumose, Harris’s, 407 
for chlorides, 413 
for chyle in urine, 390 
for defects, intellectual, 555 
for elastic fibres in lungs, 530 
for hemin crystals, 521 
for hydrochloric acid in stomach, 
335 
for indicanuria, 390 
for lactic acid in stomacn, 332 
for sarcinse ventriculi, 517 
for sugar in urine, Fehling’s, 404 
Haines’s, 403 
Roberts’s, 406 
Whitney’s, 404 
for tubercle bacilli, 532 
for urates, 389 
for urea, Lyons’s, 409 
Gabbett’s modification of FraenkeFs 
method for tubercle bacilli, 533 
Gmelin’s, for bile in urine, 389 
Haines’s modification of Haeser’s 
method for total quantity of solids 
in urine, 413 
Heller’s, for blood in urine, 385 
Widal’s, for typhoid fever, 372 
Williamson’s, for sugar in the blood, 
375 
Tetanus, character of convulsions in, 499 
of fever in. 454 
facial spasm in. 45, 46 
head or cephalic, 48 
knee-jerk increased in, 550 
ptosis in, 41 
risus sardonicus in, 26 
Tetany, “accoucheur’s hand” in, 71 
character of convulsions in, 499 
Chvostek’s symptom of, 499 
Erb’s symptom of, 499 
gastric dilatation in 71 
thyroid wasting in, 71 
Trousseau’s symptom of, 499 
Thermic fever. See Sunstroke. 
Thoma-Zeiss’s hematocytometer, 358 
Thomsen’s disease, diagnosis of, 503 
spasm of hand in, 73 
of tongue in, 153 
Thorax, aneurism of, diagnosis between 
mediastinal growths and, 303 
localized sweating in, 229 
spongy, venous masses above 
clavicle due to, 269 
Thrill, causes of, 274 
diffuse and feeble in cardiac dilata- 
tion, 316 
in aortic aneurism, 339 
in carotid arteries, 317 600 
INDEX. 
Thrill in mitral regurgitation in child- 
ren, 308 
stenosis, 308 
Thrombosis, cerebral, 232 
of cavernous sinus, 175 
symptoms of, 175 
of coronary artery, 317 
of femoral vein, 125 
of lateral sinus, 467 
of umbilical vein in melaena neona- 
torum, 515 
vomiting in, 505 
Thrush, appearance of tongue in, 144 
Tic, convulsive, 73 
facial spasm in, 45 
in pulmonary disease, 146 
in relapsing fever, 143 
Tinnitus aurium in Meniere’s disease, 
519 
Toison’s solution for counting white cor- 
puscles, 359 
Tongue, anatomy of the, 141 
annulus migrans of, 150 
appearance of, in acute articular 
rheumatism, 144 
in acute catarrhal jaundice, 143 
gastric catarrh, 144 
in children, 144 
glossitis, 150 
in Addison’s disease, purple spots 
on, 146 
in advanced disease of exhaust- 
ing nature, 145 
in anaemia, 146 
in biliousness, 143 
in cardiac disease, 146 
in cretinism, 32 
in dysentery, 145 
in grave disease of the viscera, 
145 
in hepatic abscess, 145 
in mucous disease, worm-eaten, 
144 
in persons taking large amounts 
of milk, 144 
in poisoning by acids, 146 
by alkalies, 146 
by cantharides, 147 
by corrosive sublimate, 146 
in pulmonary disease, 146 
in relapsing fever, 143 
in scarlet fever, strawberry, 144 
in scrofulosis, 145 
in stomatitis impetiginosa, 150 
in syphilis, 147 
in thrush, 144 
in tonsillitis, 142, 143 
in typhoid fever, in typhoid 
state, 143 
in ulcerative stomatitis, 148 
bilateral atrophy of, due to disease 
affecting hypoglossal nerve, 150 
Tongue, bilateral atrophy of, in chronic 
lead-poisoning, 150 
in glosso-labio-pharyngeal 
paralysis, 150 
in locomotor ataxia, 150 
in paretic dementia, 150 
in progressive muscular 
atrophy, 150 
biting of, in epilepsy, 148 
in glosso labio pharyngeal par- 
alysis, 148 
chancre of, 147 
chronic superficial glossitis of, 149 
coating of, causes of, 142 
composition of, 142 
unilateral, due to decayed teeth 
or hemiplegia, 145 
dryness or moisture of, prognostic 
value of, 145 
enlargement of, in acromegaly, 151 
in acute inflammation, 150 
in inflammatory hypertrophy, 
150 
in macroglossia, 150 
in myxoedema, 151 
in new growths, 150 
in syphilis. 150 
epithelioma of, 147 
eruptions of, 148 
examination of, 141 
in children best when crying, 
24 
fibrillary tremor of, in labio-glosso- 
pharyngeal paralysis, 153 
fissures of, due to age, chewing to- 
bacco, or abuse of alcohol or 
tea, 147 
deep, in dissecting glossitis, 147 
geographical, 150 
glossodynia exfoliativa of, 149 
hemiatrophy of, 151 
ichthyosis of, 149 
leucokeratosis of, 149 
leucoma of, 149 
lichen planus of, 149 
movements of, 151 
in coma, 151 
in feeble minded, 151 
in glosso-labio pharyngeal par- 
alysis. 151 
in nervous individuals, 151 
in pseudo bulbar paralysis, 151 
in typhoid fever, 151 
mucous patches of, 147 
mycosis of, 144 
oedema of, 150 
paralysis of, in diphtheria, 152 
in injury of hypoglossal or tri- 
facial nerve, 151 
location of lesion in, 152 
parrot , in dysentery or hepatic ab- 
scess, 145 INDEX. 
601 
Tongue, patches on, in chronic superficial 
glossitis, 149 
in leucoma, 149 
in smokers, 149 
purple spots on, in Addison’s disease, 
146 
scleroderma of, 149 
sclerosis of, following syphilitic ul- 
ceration, 147 
smoker’s patch on, 149 
spasm of, in aphthongia, 153 
in chorea, 153 
in general paralysis of the in- 
sane, 153 
in hysteria, 153 
in insular sclerosis, 153 
in irritation of hypoglossal 
nerve, 153 
in puerperal mania, 153 
in Thomsen’s disease, 153 
stains of, 144, 145, 146 
strawberry, in scarlet fever, 144 
tremor of, in alcoholism, 153 
in glosso-labio-pharyngeal pa- 
ralysis, 153 
in typhoid fever, 153 
ulceration of, in epithelioma, 147 
in lupus, 148 
in psilosis, 148 
in Schonlein’s disease, 148 
in stomatitis, 148 
in syphilis, 148 
in wounds, 147 
multiple, in tuberculosis, 147 
of frsenum of, in whooping- 
cough, 148 
unilateral atrophy of, in chronic 
lead-poisoning, 150 
urticaria of, 149 
wandering rash of, 150 
worm-eaten, in mucous disease, 144 
xanthelasma of, 146 
xeroderma pigmentosum of, 149 
Tonsillitis, chronic night-cough in, 525 
crystals of margaric acid in follicu- 
lar, 531 
diagnosis between diphtheria, scarlet 
fever and, 155 
sickening sweet odor of breath in, 23 
symptoms of follicular, 154 
of suppurative, 155 
Tonsils, chronic cough in enlarged 
lingual, 525 
night cough in enlarged faucial, 
525 
pain in calculus of, 155 
symptoms of chronic enlargement of, 
155 
Tracheal tugging in aneurism, 311 
Traube’s semilunar space obliterated in j 
left-sided pleural effusion, 297 
Tremor of hands and arms, 75 
Tremor of hands and arms in mercurial 
poisoning, 73 
railroad-bridge type of, 76 
of tongue, 153 
of type Rendu, 76 
post-hemiplegic, 76 
sometimes found instead of occupa- 
tion spasm, 71 
Trichiniasis, diagnosis of, 440 
puffy eyelids in, 30 
Trichinosis. See Trichiniasis. 
Trichocephalus dispar, 431 
Trousseau’s symptom of tetany, 499 
Tube-casts. See Casts. 
Tubercular glands, symptoms of, 335 
pyelitis, 417 
Tuberculosis, anaemia in, 366 
albumosuria in, 409 
amphoric breathing in, 287 
bronchial breathing and consolida- 
tion in, 286 
bronchitis(?) a cause of death in, 21 
bronchophony in, 293 
bubbling rales in, 288 
Charcot-Leyden crystals in sputum 
of, 529 
Cheyne-Stokes breathing in menin- 
geal, 271 
chronic loose morning cough in 
cavity in, 523 
cracked-pot sound in, 278 
crepitant rales and breaking down 
of lung-tissue in, 288 
dactylitis in, 55 
diagnosis between catarrhal pneu- 
monia and pulmonary, 293 
diarrhoea of, 423 
diazo-reaction in severe pulmonary, 
414 
elastic fibres in sputum of, 530 
expiration prolonged in, 293 
fever in acute miliary, 451 
pulmonary, 4-50 
heavy face in bone disease in, 28 
hectic fever in, 293 
hemoptysis in, 527 
hemorrhagic pleurisy in, 299 
hollow-chested build in, 18 
loss of flesh in, 293 
metallic tinkling in, 288 
multiple ulceration of tongue in, 
147 
necessity of examining axilla in, 
295 
ocular palsy in, 169 
of bones in amyloid kidney, 416 
of kidney, hematuria in, 387 
pectoriloquy in, 291, 293 
percussion -note dull in consolidation 
due to, 277 
pleurisy complicating, apt to become 
purulent, 298 602 
INDEX. 
Tuberculosis pleurisy, with effusion com- 
ing on insidiously in undiscovered, 
298 > 
ptosis in changes at base of brain due 
to, 41 
puerile breathing an early sign of, 
286 
rapidity of breathing in, 269 
retraction of abdominal wall in, 
322 
scars on neck from suppurating 
glands in, 228 
spirituelle face of children with 
diathesis of, 28 
sputum, Curschmann’s spirals rarely 
seen in, 528 
sweating in, 293 
transitory unequal dilatation of 
pupils in, 181 
vocal fremitus and resonance in- 
creased in, 291, 293 
vomiting in acute miliary, 506, 520 
Tumor, abdominal, pain in, 545 
brain-, Cheyne-Stokes breathing in, 
271 
hypersesthesia in, 260 
impaired memory in, 505 
papillitis in, 191, 505 
paraesthesia in, 258 
severe headache in, 505 
slow pulse in, 505 
symptoms of, 463 
unilateral anaesthesia in 241 
vertigo in, 471, 505 
vomiting independent of taking 
food in, 505 
detection of, in intussusception, 508 
diagnosis of fatty, of abdominal wall, 
330 
of abdomen, 336 
of bladder, 382 
of cord, bladder symptoms of, 380 
girdle-sensation in, 259 
paraplegia in, 109 
of lung, rapid respiration in, 269 
of mediastinum, 302 
of nerves, pain in, 546 
phantom, 338 
pontine, anaesthesia in, 242 
Typhoid fever, albumosuria in, 409 
appearance of eruption in, 224 
bacillus of Eberth the cause of, 
439 
bloody stools in, 428 
bradycardia in, 317 
carphologia in, 77 
causes of mumbling speech in, 
553 
of recrudescence of fever 
in, 436 
of vomiting in, 512 
character of coma in, 475 
Typhoid fever, character of fever in, 435 
date of eruption in, 214 
delirium in, 30, 438 
diagnosis of, 438 
between acute miliary tu- 
berculosis and, 452 
acute tuberculosis and, 
438 
Malta fever and, 441 
remittent fever and, 
439 
trichiniasis and, 440 
ulcerative endocarditis 
and, 440 
Ehrlich’s diazo-reaction in, 414 
enlargement of spleen in, 343 
face in, 29 
fever in, 438 
headache in, 469 
hypersesthesia in convalescence 
from, 260 
hypertrophic osteoarthritis fol- 
lowing, 124 
increase of urine in convales- 
cence from, 383 
lesions of lungs generally at base 
in, 439 
meteorism in, 438 
moderate bronchitis early in, 
438 
mushy stool in, 427 
oedema of thigh over deep mus- 
cular abscess following, 233 
parotitis in, 441 
pleurisy with effusion compli- 
cating, apt to become puru- 
lent, 298 
relapse in, 438 
roseola in, 215 
stupor in, 438 
subsultus tendinum in, 77 
sudden fall in temperature due 
to hemorrhage 
of any sort in, 
436 
due to intestinal 
hemorrhage in, 
436 
due to intestinal 
perforation in, 
436 
sweating in, 228 
tongue in, 142 
tympanites in, 322, 438 
Widal’s test for, 372 
without fever, 438 
Typho-malarial fever. See Malaria, Re- 
mittent. 
Typhus fever, character of fever in, 441 
crisis in, 441 
eruption in, 214, 216, 441 
great exhaustion in, 441 INDEX. 
603 
Typhus fever, headache in, 441 
hematemesis in, 514 
ULCER, perforating, 125 
Ulcers at base of finger-nails due to 
chloral, 226 
on buccal mucous membrane in 
Schonlein’s disease, 154 
on cornea in scrofula, 194 
on tongue, 147 
perforating, in diabetes, senility, 
and tabes dorsalis, 125 
syphilitic, in intestinal tract 
causing diarrhoea, 425 
Unconsciousness. See Coma. 
Unilateral facial paralysis. See Paralysis, 
Unilateral Facial. 
Uraemia See also Coma, 
amaurosis in, 194 
anaemia, in, 368 
Cheyne-Stokes breathing in, 271 
colliquative diarrhoea in, 504 
coma in, 474 
occurring in chronic interstitial 
nephritis, 416 
convulsions in, 505 
diagnosis of, 494 
headache in, 462 
retching in, 520 
sweating in, producing scales of urea, 
229 
symptoms of, 474 
vomiting in, 475, 504 
odor of carbonate of ammonium 
in, 505 
Urethra, character of blood in hemor- 
rhage from, 385 
fever due to passage of sound into, 
435 
gonococci in specific inflammation of, 
400 
incontinence of urine due to insensi- 
tive, 379 
interference with passage of urine in 
stricture of, 382 
Urethritis, specific, gonococci in, 400 
Uricsemia. See Lithsemia. 
Urine, acid fermentation of, 402 
albumin in, boiling test for, 402 
Heller’s test for, 403 
quantitative test for, by centri- 
fuge, 403 
albuminuria, significance of, 403 
albumose in, Harris’s test for, 407 
significance of, 409 
alkaline fermentation of, 402 
bile-stained, in hepatogenous jaun- 
dice, 201 
casts in, blood, 384, 392 
epithelial, 391 
fatty, 394 
Urine, casts in, granular, 393 
hyaline, 394 
of micrococci, 393 
of pus, 393 
causes of incontinence of, 379 
of retention of, 378 
chlorides in, significance of increase 
and decrease of, 413 
test for, 413 
color of, blue, 389 
brown, 389 
causes of black, 384, 390 
due to blood, 384 
green, 389 
in diabetes, 390 
in jaundice, 389 
red, 384, 388, 389 
white or milky, 390 
yellow, 389 
conditions in which decreased, 383 
in which increased, 383 
crystals in, creatin, 398 
creatinin, 398 
oxalate of lime, 397 
triple phosphates, 398 
urate, 397 
uric acid, 397 
cylindroids in, 394, 395 
diazo-reaction of Ehrlich iD, 414 
embryos of parasites in, 400 
epithelial cells in, 400 
fermentation of, 401, 402 
Gmelin’s test for bile in, 389 
gonococci in, 400 
Heller’s test for blood in, 385 
in acute diffuse nephritis, 414 
in amyloid kidney, 415 
in cholera morbus, severe, decreased 
in, 420 
in chronic interstitial nephritis, 416 
in diabetes insipidus, 416 
mellitus, 416 
in phosphorus-poisoning, 516 
in pyelitis, 417 
interference with passage of, due to 
enlarged prostate, 382 
due to nervous bladder, 382 
due to stone in bladder, 382 
due to stricture of urethra, 
382 
due to tumors of bladder, 
382 
involuntary passage of, in apoplexy, 
381 
in idiots, 381 
in infectious diseases, 382 
in irritation of foreskin or 
vagina in children, 382 
in seat-worms, 382 
in some cases of insanity, 
381 
method of collecting, for testing, 382 604 
INDEX. 
Urine, odor of, causes of alteration of, 383 
specific gravity of, causes of high, 
383 
of low, 383 
spermatozoa in, 400, 401 
staphylococci and streptococci in, 
indicating pus, 400 
sugar in, Fehling’s test for, 404 
Haines’s test for 403 
quantitative yeast-test of Rob- 
erts for, 406 
significance of, 406 
Whitney’s test for, 404 
total quantity of solids in, Haines’s 
modification of Haeser’s method 
for computing, 413 
tubercle bacilli in, 400 
urates in, 397 
urea in, amount excreted in health, 
413 
causes of increase and decrease 
of, 412 
Lyon’s method of estimating, 
409 
value of estimating in renal 
disease during pregnancy and 
before surgical operations, 
412 
uric acid in, 397 
variations in quantity of, 383 
Urticaria, 216 
from drugs, 210 
in rheumatism, 210 
of tongue, 149 
VACCINATION, appearance of erup- 
tion of, 221 
roseola following, 213 
Vaginitis, specific, gonococci in, 400 
Valvular heart disease. See Heart. 
Varicella. See Chickenpox. 
Variola. Nee Smallpox. 
Vertigo, 471 
causes of, 471 
due to drugs, 471 
in Addison’s disease, 520 
in anaemia, 365, 471 
in apoplexy, 471 
in cerebral tumor, 471 
in epilepsy, 471 
in Meniere’s disease, 471 
in middle-ear disease, 471 
in ocular palsy, 164 
in paretic dementia, 140 
in phosphorus poisoning, 515 
paralyzing, 471 
Vesical crises in locomotor ataxia, 87 
Vesicular breathing, 284 
Vocal fremitus. See Fremitus, Vocal. 
resonance. See Resonance, Vocal. 
Volvulus, 337 
Vomiting, associated with headache, 520 
bilious, in remittent malarial fever, 
448 
black, in yellow fever, 449 
centric, from chloroform or ether, 
504 
coffee-ground, in chronic gastric 
catarrh, 516 
in gastric cancer, 331, 513 
in locomotor ataxia, 513 
in phosphorus-poisoning, 515 
cyclical, 518, 519 
decrease of urine by persistent, 383 
in acute gastric catarrh, 516 
miliary tuberculosis, 506 
pancreatitis, 514 
yellow atrophy of liver, 520 
in appendicitis, 512 
in catarrhal or obstructive jaundice, 
519 
in cerebral disease, 505 
in cerebro-spinal meningitis, 430 
in cholera Asiatica, 512 
infantum, 420, 512 
morbus, 420, 512 
in diabetes, rarely, 504 
in dysentery, 513 
in early secondary syphilis, 520 
in embolism of superior mesenteric 
artery, 514 
in enterocolitis, not common, 526 
in erysipelas, 520 
in exophthalmic goitre, 519 
in gastric cancer, 513 
ulcer, 513 
in gastro-pulmonary fever, 456 
in hemiplegia, due to hematoma of 
dura mater, 139 
in hemoglobinaemia, 519 
in hemorrhagic pressure on brain, 
138 
in hepatic abscess, 519 
cirrhosis, 513 
in hepatitis, 519 
in hysteria, 518 
in influenza, 451 
in intestinal obstruction, 507 
in mela?na neonatorum, 515 
in Meniere’s disease, 519 
in meningitis, 506 
in merycismus, 520 
in migraine, 520 
in neurasthenia, 518 
in neuroses of stomach, 518 
in peritonitis, 511 
in phosphorus-poisoning, 515 
in phthisis, 520 
in poisoning by arsenic and anti- 
mony, 515 
in pregnancy, 518 
in profound cerebral anaemia, 506 
in pulmonary gangrene, 520 INDEX. 
605 
Vomiting in purulent meningitis, 505 
in pylephlebitis, 519 
in Raynaud’s disease, 514 
in true gastritis, rare, 516 
in renal calculus, 519 
in typhoid fever, 512 
in uraemia, 504 
in whooping-cough, 520 
in yellow fever, 52 
of blood. See Hematemesis. 
uraemic, in chronic parenchymatous 
nephritis, 415 
ushering in eruptive diseases, 520 
Von Fleischl’s hemoglobinometer, 360 
WEIL’S disease, almost total absence 
of gastro-intestinal symp- 
toms in, 449 
character of fever in, 449 
clay-colored stools in, 449 
jaundice in, 199, 449 
swelling of liver and spleen in, 
449 
Wernicke’s pupil, 180, 464 
Westphal’s sign, 87 
Whitlow, painless, in Morvan’s disease, 
68 
Whooping-cough, cough in. 522 
ulcer on frsenum in, 148 
vomiting in, 520 
Widal’s test for typhoid fever, 373 
Williamson’s test for sugar in blood, 375 
Word-blindness, 555 
-deafness, 555 
Worms, seat-, involuntary passage of 
urine due to, 382 
Wrist-drop, causes of, 74 
-jerk, marked, in amyotrophic lateral 
sclerosis, 69 
Wry-neck, clonic or tonic, 48 
congenital or acquired, 48 
definition of, 48 
diagnosis of, 48 
facial asymmetry in connection with, 
33 
XANTHELASMA, 146 
Xanthoma, 203 
YELLOW atrophy of liver, acute,'con- 
vulsions in,500 
coma in, 475 
hematemesis in, 516 
jaundice in, 201 
symptoms of, 201, 515, 520 
fever, black vomit in, 449 
character of fever in, 449 
diagnosis of, 449 
between bilious remittent 
fever and, 449 
hematemesis in, 514 
hemorrhage from mucous mem- 
branes in, 449 
jaundice in, 199, 449 
symptoms of, 520 
tarry stools in, 449 
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ESSIG (CHARLES J.). PROSTHETIC DENTISTRY. See American Text-hooks 
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GRAY (HENRY). ANATOMY, DESCRIPTIVE AND SURGICAL. A new 
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HAMILTON (FRANK H.)., A PRACTICAL TREATISE ON FRACTURES 
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