PRACTICAL DIAGNOSIS: 
THE USE OF SYMPTOMS IN THE 
DIAGNOSIS OF DISEASE. 
THIRD EDITION, REVISED AND ENLARGED. 
BY 
HOBART AMORY HARE, M.D., B.Sc., 
V\\ ’ 7 
PROFESSOR OF THERAPEUTICS IN THE JEFFERSON MEDICAL 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 204 ENGRAVINGS AND 13 COLORED PLATES. 
LEA BROTHERS & CO., 
PHILADELPHIA AND NEW YORK. 
18 98. Entered according to the Act of Congress in the year 1898, by 
LEA BROTHERS & CO., 
In the Office of the Librarian of Congress. All rights reserved 
DORNAN,PRINTER. PREFACE TO THE THIRD EDITION. 
The fact that three large editions of this book have been called 
for in two years indicates that it has found favor with practitioners 
of medicine. No less pleasant to the author is the fact that an 
equal popularity has attended it in Great Britain. These facts 
have served to stimulate him to constant endeavor to maintain its 
usefulness. The text of this the third edition has been carefully 
revised, much important new matter added, and new illustrations, 
taken from life by photography, have been introduced to render 
the text more practically useful. The endeavor has been to make 
this edition prove a companion volume to the seventh edition of 
the author’s Text-book of Practical Therapeutics, which is published 
simultaneously. With these additions the author hopes that the 
volume will continue to deserve the favor with which it has so 
far been received. 
Philadelphia, 222 South Fifteenth Street, 
August, 1898. 
III 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 stand-point 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. 
V 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 the disease supposed to be present, when if the 
description fails to coincide with the symptoms of his case he 
must make another guess aud read another article. In this book, 
however, the discovery of any marked symptom will lead directly 
to the diagnosis. Thus, if the patient is vomiting, in the chapter 
on Vomiting 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 
VII 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 of 
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 deformity—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 55 
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 and legs—The joints—Altera- 
tions in the nutrition of the feet and legs aside from a change in 
the muscles . 87 
CHAPTER IV. 
HEMIPLEGIA 131 
IX X 
CONTENTS. 
CHAPTER V. 
THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
PAGE 
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—Tonsillitis—Diphtheria—Phar- 
yngitis—Diseases of the oesophagus 1-15 
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 
Retinitis—Amblyopia and blindness 164 
CHAPTER VII. 
THE SKIN. 
The color of the skin—Eruptions on the skin—Gangrene, ulcers, and 
sloughs—Scars, sweating, dryness, oedema, hardness—Anaesthesia 
and hemianaesthesia—Parsesthesia, hypersesthesia, itching . . 201 
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 . . 268 
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 328 
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 355 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 haemoglobin of the blood in health and disease — 
The various forms of anaemia—Leukaemia and pseudo-leukaemia— 
Parasites of the blood 363 
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 . . . 388 
CHAPTER XIII. 
THE BOWELS AND FECES. 
Constipation and diarrhoea—The cause of these two symptoms and their 
diagnosis —The diseases in which these symptoms occur—Choleraic 
diarrhoea—Dysentery—The color of the feces—Intestinal parasites 429 
PART II. 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
CHAPTER I. 
CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
The methods of taking the temperature—The significance of fever— 
The febrile movements of various diseases 443 
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 . . . 469 XII 
CONTENTS. 
CHAPTER III. 
PAGE 
COMA OR UNCONSCIOUSNESS .... 485 
CHAPTER IV. 
CONVULSIONS OR GENERAL SPASMS. 
The convulsions of epilepsy in its various forms —Of infancy—Of hys- 
teria—Tetanic convulsions—Spasms —Chorea 493 
CHAPTER V. 
HICCOUGH, VOMITING, REGURGITATION, AND THE CHARACTER OF THE 
VOMIT — DYSPHAGIA. 
Due to uraemia—Cerebral lesions —Intestinal obstruction—Peritonitis— 
Cholera—Gastric disease - Hepatic disease—Poisons—The appear- 
ance of vomit—Difficulty in swallowing 504 
CHAPTER VI. 
COUGH AND EXPECTORATION. 
The varieties of and indications of cough—The causes of cough—The 
sputum—Its pathological significance 537 
CHAPTER VII. 
PAIN. 
The kinds of pain—The significance of its locality—Colic . . . 550 
CHAPTER VIII. 
TENDON-REFLEXES AND MUSCLE-TONE. 
The knee-jerk and ankle-clonus—The arm-jerk—The significance of 
decreased and increased reflexes 563 
CHAPTER IX. 
SPEECH. 
The changes in the speech and voice—Their significance—Aphasia— 
Apraxia—Alexia—Paraphasia 568 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 purpose 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 
possessed 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 
person will probably be one who habitually wears his coat open on 
the coldest days. Again, chronic drunkards, or persons whose 
mental powers are failing, often are exceedingly careless about their 
17 18 
PRACTICAL DIAGNOSIS. 
clothing, 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, the bearing and stride of a patient will often give 
us a clear idea of his general tone. The neurasthenic 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 from 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. 
The breath of the patient may call the physician’s attention to 
some important facts in connection with the case. If it is sweet 
or vinous in odor, this may be due to diabetes mellitus, or if it be 
ammoniacal or urinous, uraemia may be present. The previous 
use of bismuth may give it a garlic-like smell, due to the con- 
taminating tellurium , and various aromatic or volatile drugs, such as 
turpentine or copaiba, may be eliminated in the breath. In cases of 
advanced bronchiectasis the breath is often foul, and is insupport- 
ably so in gangrene of the lung or when an empyema has ruptured 
into a bronchus. It is similarly offensive in gangrenous stomatitis, 
and often very disagreeable in tonsillitis. In diphtheria it has a 
peculiarly sickening and sweetish odor. When the odor is not 
dependent on these causes it may be due to ozsena, or chronic 
atrophic nasal catarrh, to the presence of decaying food between GENERAL DIAGNOSTIC CONSIDERATIONS. 
19 
the teeth or secretions in the crypts of the tonsils. Moderate fetor 
is usually due to disordered digestion and constipation. 
When 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 sufferer 
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 
interest may give the impression of carelessness, or it may inter- 
rupt the story just as a most important symptom is about to be 
described. Even if the patient is unable to convey in words a 
very clear idea of his condition, 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 
exacerbation of the latter. A glance at the face of such a patient, 
revealing 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, indicating capillary stasis and deficient oxidation in the blood. 
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 atmosphere of the patient is better, and the surroundings 
are apt to be more tidy. 20 
PRACTICAL DIAGNOSIS. 
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 so 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 remain on the side 
without moving except partly to 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. Thus, 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 character- 
istic of grave and advanced disease in some instances. Very ill 
persons almost never lie on the side, and the fact that a desperately 
ill case of yesterday is found lying on the side to-day is an encour- 
aging sign. Persons with severe heart disease are rarely, if ever, 
able to lie straight 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 consoli- 
dation, or oedema, require 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. GENERAL DIAGNOSTIC CONSIDERATIONS. 
21 
(For the significance of picking at the bedclothes, 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 
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 pla- 
tonic 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 ques- 
tions which elicit the fact that she has had frequent miscarriages. 
He in this way finds out 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, pro- 
duce 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. 22 
PRACTICAL DIAGNOSIS. 
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 described 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 which 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. 
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 
produces 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 GENERAL DIAGNOSTIC CONSIDERATIONS. 
23 
over-attention by the family and friends. Time should always be 
given the child to grow accustomed to the peculiarities of the vis- 
itor, and, if any instrument for diagnosis is to be employed, it is 
best to hold it in the hand as if it were a plaything before 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 expressions 
of the child; its color, size, nutrition, breathing; the shape and size 
of its head; the condition of its lips, whether moist or dry, red, 
livid, or pale; and, if the child is speaking, the tone of its voice, 
or, if crying, the character of its cry. It is needless to state that 
a child may cry from fright, from pain, auger, or hunger. Con- 
stant 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 
producing 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 and cooing and moving its arms about, and has a happy 
expression on its face; whereas if any cerebral trouble is present, 24 
PRACTICAL DIAGNOSIS. 
it often has an anxious frown, or its hands are placed on 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 physician should always, by careful questioning of the nurse 
or mother, find out how long the illness has lasted, the manner in 
which it began, the fact as to whether a similar attack has 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 hands. 
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 deformity—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 pre- 
vents the patient from making a too close scrutiny of the physician’s 
face with the object of detecting encouragement, 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 finally, 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. 
25 26 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The intellectual face is easily recognized. Sometimes it is deeply 
thoughtful and placid, at others eager or keenly alive to the sur- 
roundings or the conversation, and it separates the man descended 
from several generations of men who have lived as thinkers from 
him whose ancestors have been but recently wage-earners by physi- 
cal labor, involving only ordinary human intelligence. 
Fulness of the lips, particularly of the lower lip, is supposed to 
be present in persons of strong sexual appetite, and often indicates 
a phlegmatic temperament, whereas the thin, mobile lip is typical 
of the high-strung, nervous individual. 
The expression of the lips as a whole is also to be regarded in 
connection with the expression of smiling. The risus sardonicus 
of strychnine-poisoning or tetanus is quite characteristic, and the 
simple smile of hysteria is equally notorious. 
The skin of the face and the expression about the eyes of one 
who has been exposed for years to the weather are so characteristic 
as to need no description, while the face of the clerk, whose life is 
almost entirely spent indoors, is pale and wan. 
Similarly, the face of a person who uses alcohol to excess is 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. AVomen 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 discolorations. A 
pufffness under the eyes, most noticeable in the morning, may indi- 
cate renal lesions or the excessive use of arsenic, or 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 lattei 
disease the faint yellowish-green tinge of the skin in some parts of 
the face, which still retains its plumpness, is quite typical. A 
parchment-like skin stretched over the face so that it appears as 
if dried over the under-structures is seen in some young persons THE FACE AND HEAD. 
27 
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 acetanilid, 
antipyrin, and phenacetin, and it is curious that this effect is best 
seen when the patient is viewed at a little distance. 
(For the indications of facial cyanosis, see chapter on the Skin.) 
In view of the extraordinary variations seen in the expression of 
the face 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 a 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 expres- 
sion 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 some- 
times 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 prac- 
tically 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 probably present some 
digestive or nervous disturbance, perhaps accompanied by moderate 
pain. If in the course of an illness 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 indi- 
cates 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 ten- 
dencies, or even hereditary diseases. Thus we see the light flaxen- 
haired, slimly built child with a refined, spirituelle face and trans- 
parent skin, whose temporal veins can be easily traced and whose 
expression is often thoughtful and deep. Such a child often comes 
of tubercular parents, and is frequently a victim of tuberculosis, in 
one of its rapid forms, as it approaches puberty. Or, again, the 
child is “ 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 tubercular bone 
disease. In other instances, a square projecting forehead with 
faulty bone-development elsewhere indicates rickets, or an immense, 
bulging forehead with a wizened, puny face beneath shows hydro- 
cephalic tendencies. Sometimes a broadness of the bridge of the 
nose or marked flatness of it indicates congenital syphilis. Such a 
child is often much wasted, its features pinched, and its lips thin, 
while the flattened nasal bridge is bluish, and its face is often that of 
a little old man, shrivelled and wrinkled. Mucous patches at the 
corners of the mouth or around the anus are often found in such 
cases, and, if found, confirm the diagnosis of infantile syphilis. 
Finally, in respect to facial expression in childhood, attention must THE FACE AND HEAD. 
29 
be called to the “ fish mouth,” vacuous, and “ nose-pinched” ex- 
pression 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 the possible presence of 
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 pulmo- 
nary phthisis the widely opened eye, the hunted expression, the quiv- 
ering 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 ex- 
pression ; pinched nostrils ; dull eyes ; drooping eyelids; round shoulders. (Hooper.) 
Iii severe croupous 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 diffi- 
culty in respiration, the patient’s lips are seen to be slightly parted 
and dry, and may appear somewhat cyanotic. In children suffer- 
ing 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 with sordes, 
which become brown and blackish by exposure or by discoloration 30 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 he is 
also responsible for the statement that it is best seen in the face of 
the parturient woman in the second stage of labor. 
The facial expression of hysteria may be apathetic, or it is that 
of devotion, rage, or grief, and these expressions are fixed if the 
patient be cataleptic. If she is not cataleptic, not infrequently one 
expression may succeed the other, or in their place there comes that 
curious smile or vacuous expression of the face which is so charac- 
teristic. It should be remembered, however, that this vacant fatu- 
ous 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 “ Parkinson- 
ian visage,” is distressed and pathetic, and yet somewhat intense. 
(See chapter on the Hands and Arms, and part of that on Tremor.) 
A pale, puffy face, generally looking worn and weary, may be 
seen in cases of chronic or subacute renal disease. In children 
there is often in this condition a peculiar transparent or pearly look 
in the lower eyelid, so that it seems somewhat pellucid. Great 
swelling or oedema of the face is seen in erysipelas, dropsy (Fig. 2), 
and simple inflammatory swelling (see chapter on the Skin). In 
tricliiniasis 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 
of the lips, which cannot be approximated, as in whistling, and at THE FACE AND HEAD. 
31 
the same time the patient is unable to close the eyes entirely, 
although the lids droop, the physician should think of the possibility 
of these being the early symptoms of what has been called the 
“ facio-humero-scapular ” type of muscular atrophy (Landouzy and 
D6j6rine). 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 twitch- 
ings seen in spinal progressive muscular atrophy ; there are no 
changes in electrical excitability, except that owing to the loss of 
Fig. 2. 
Face of a patient witn general anasarca due to chronic parenchymatous nephritis. 
(From a patient in the author’s wards—Jefferson Medical College Hospital.) 
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, 
and absence of muscular atrophy separate it from the Landouzy- 32 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Dejerine type of muscular atrophy just described as facio-humero- 
scapular atrophy. (See Ataxia iu chapter on Feet and Legs.) 
The facial expression of cretinism is exceedingly characteristic. 
The nose is broad and flat, the eyelids are swollen, the lips 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 
Fig. 3. 
A cretin. (Dercum.) 
is nearly always in well-developed cases marked lumbar lordosis. 
(Fig. 3.) The facial expression of myxoedema is heavy and listless, 
as a rule. (See page 34 and chapter on Skin.) 
In certain forms of leprosy the face often becomes leonine, 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 
of the lungs or any state associated with profound collapse, such as THE FACE AND HEAD. 
33 
internal hemorrhage. It is accompanied by pallor, cold extremities, 
and difficult breathing. This is called the u Hippocratic face/’ 
and is peculiar in the sinking-in of the temples where the jaw- 
mnscles 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 facial expression, 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 chil- 
Fig. 4. 
Acromegaly, showing the large face 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 34 
THE MANIFESTATION OF DISEASE IN ORGANS. 
wasted in its skin, muscles, bones, color, and hair. Even the eye 
may be sunken and shrunken. Rarely this wasting is bilateral. 
Sometimes in facial hemiatrophy the wasting is accompanied by 
painful 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 also found on this side. Such symptoms as the last 
show involvement of the sympathetic nerve-fibres. The changes 
are probably due to disease of the fifth (trifacial) nerve. 
Fig. 5. 
Myxcedema. (Meltzek.) 
The expression is usually more stupid and apathetic. 
As to whether circumscribed scleroderma (morphoea) and facial 
hemiatrophy are identical—that is, whether the first is a well-devel- 
oped form of the latter—is not decided. Hyde apparently regards 
them as identical. (See chapter on Skin, Scleroderma.) 
Even more rare than facial hemiatrophy is facial hemihyper- 
trophy, one side remaining normal in size and the other becoming 
gigantic. THE FACE AND HEAD. 
35 
The massive face of a person suffering from acromegaly is very 
characteristic. (Fig. 4.) The face has a full-moon broadness in 
myxoedema. (Fig. 5.) The enlargement of the bony parts of the 
skeleton, the kyphosis, and the comparative muscular feebleness 
of acromegaly aid in the diagnosis of that disease, for in myxoedema 
there is no true bony enlargement. The face in osteitis deformans 
is shaped like a triangle with the base upward. In osteitis defor- 
mans the shafts of the long bones become weakened, and their sur- 
faces roughened from periosteal deposits. (See chapter on Hands 
and Arms.) 
Unilateral Facial Paralysis. Very notable changes in the face 
are produced by paralysis, the palsy 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, as already stated, the form of facial paral- 
ysis most commonly seen, and is generally due to injury of the facial 
nerve-trunk. The lesion producing the paralysis may, however, be 
peripheral—that is, in the nerve itself—or central, that is, 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 in- 
flammation of the nerve-sheath as it passes through the stylo-mastoid 
foramen, the loss of function being due to pressure on the axis- 
cylinders owing to the presence of swelling in so limited a canal. 
Such an attack will generally be found 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 follow- 
ing 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 probable that by the extension of inflam- 
mation along the chorda tympani such a paralysis may result. If the 
disease be in the petrous portion of the temporal bone, in addition 36 
THE MANIFESTATION OF DISEASE IN ORGANS. 
to paralysis of the muscles of expression there will also be loss of 
taste in the anterior part of the tongue due to involvement of the 
chorda tympani. The mouth is dry, owing to a lack of saliva, the 
salivary gland being paralyzed, and there may be deafness from paral- 
ysis of the stapedius muscle. Still more rarely facial paralysis results 
from swelling of the parotid gland or from a 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- 
orrhage from the cerebellum during birth, or from pressure of for- 
ceps. (See below.) 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 paral- 
ysis may also arise from locomotor ataxia, the lesion being in the 
pons, and from hysteria. All these forms are very rare, compara- 
tively speaking. The cerebral or medullary lesions which produce 
unilateral facial paralysis usually consist in the results of hemor- 
rhage 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 the peripheral form separates itself 
from facial paralysis of cerebral origin in the course of ten days or 
two weeks, for, if the nerve is inflamed or pressed upon in the fora- 
men, 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 which it supplies. In 
other words, electrical response in the paralyzed side remains normal 
in centric lesions and is lost in peripheral lesions. The only other 
conditions in which there can be developed the reaction of degener- 
ation 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. THE FACE AND HEAD. 
37 
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 
body, and by the development, often before each additional spread of 
the paralysis, of a convulsion. The facial paralysis resulting from 
tumor at the base of the brain differs from that due to cerebral 
tumor or hemorrhage by the fact, already stated, that the reaction 
of degeneration quickly develops in the paralyzed part; that the 
parts supplied by the upper branch of the facial are often quite as 
much paralyzed as are those supplied by the lower branch, which is 
rare in the cerebral lesion; and 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, in asso- 
ciation with this form of facial paralysis there will nearly always 
be found paralysis of the oculo-motor nerve, causing ptosis, a mod- 
erately dilated pupil, and external squint, and there may also be 
paralysis of the abducens or sixth nerve, which causes internal 
squint by paralysis of the external rectus muscle. The optic nerve 
may show choked disk, and there may be disturbance of vision. 
(See chapter on Eye.) If the tumor grows large enough, or is so 
placed as to involve the facial fibres for both sides as well as those 
of the oculo-motor, abducens, and optic nerves on both sides, all 
these symptoms become, of course, bilateral. 
Facial palsy associated with deafness may indicate cerebellar 
tumor, 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 uncomon 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 extravasation 
of blood into the neighborhood of the parotid gland, thereby causing 
pressure on the nerve. The prognosis is usually favorable if due 38 
THE MANIFESTATION OF DISEASE IN ORGANS. 
to such causes; but if the forceps have caused facial palsy by pro- 
ducing 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 
Fig. 6. 
Diagram to show the general arrangement of the motor tract and the effect 
of lesions at various points. (Ormerod.) 
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 elsewhere. 
These are as follows: THE FACE AND HEAD. 
39 
Unilateral facial paralysis very rarely occurs in association with 
monoplegia in acute anterior poliomyelitis. So seldom does it occur 
in this connection that it has been denied an existence. Often it is 
but temporary, while the monoplegia of the arm is permanent. It 
occurs more commonly with the disease in adults than in children. 
Facial paralysis with arm paralysis of the same side, followed in 
a short time by paralysis of the leg of the opposite side, is quite a 
characteristic symptom of syphilitic arteritis at the base of the brain. 
Crossed paralysis—that is, paralysis of the face on one side, and 
of the arm and leg on the other—is due to a lesion in the pons 
above the decussation of the pyramids and below that of the facial 
fibres. (Fig. 6.) Thus it is seen in this figure, on the left side, 
third inscription, that the lesion in the pons cuts off the motor fibres 
in the place indicated, thereby causing the distribution of the paral- 
ysis just named. (See also chapters on Hemiplegia and on Arms 
and Hands.) 
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 press- 
ure 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 his or her condition. The presence of this symptom should call 
to the physician’s mind the various causes which produce it. 
In 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 
is concerned, there will be, in addition to ptosis, paralysis of all the 
external muscles of the eye except the superior oblique and external 
rectus, and in addition there will be a moderately dilated pupil, 40 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
Fig. 7. 
Ptosis in a case of alternate hemiplegia of syphilitic origin. (Dercum.) 
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 palpebrae 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 FACE AND HEAD, 
41 
the side of the cortex opposite 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 Miiller 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 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. (Fig. 7.) 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 the 
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. 42 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 quadrigemina, and the reason for this will be 
Fig. 8. 
Medulla oblongata with the corpora quadrigemina. The numbers IV-XII indicate the super- 
ficial origin of the cranial nerves, while the Arabic numerals (3-12) indicate their deep 
origin—i e., the position of their central nuclei; thus, 3 shows the deep origin of the oculo- 
motor nerve of one side. (Gray.) 
clear when the deep origin of the oculo-motor nerves from their 
nuclei is remembered. (Fig. 8.) Sometimes there will be associ- 
ated with the ptosis internal squint due to paralysis of the abducens 
nerve (sixth), which arises from the near-by nucleus, and is connected 
with that of the oculo-motor. (Fig. 9.) (See also chapter on the 
Eye.) 
If the condition is due to a serious congenital fault, we usually THE FACE AND HEAD. 
43 
find associated with it failure to elevate the eyeballs, and the failure 
is probably due to a nuclear defect. If the ptosis is due to gelse- 
mium or conium, the other symptoms of poisoning by those drugs 
will be present. 
Ptosis, with hemiplegia of the face and limbs, on the opposite side 
of the body, associated it may be with hemiansestliesia, 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.) 
Fig. 9. 
Diagram of the connections of the nucleus of the sixth nerve. (Bruce.) 
A very rare condition, of which there are but twenty-seven cases 
on record according to Darquire, 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 
accommodation, and crossed diplopia. It is seen most frequently 
in women, 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. 44 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
brain producing a tumor or inflammatory thickening, very rarely 
to bilateral inflammation of the stylo-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 the limitation of the paralysis, as a rule, to 
the neighborhood 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 in- 
flammation 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 class 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 “ asthenic 
bulbar paralysis,” and in it we find, as early symptoms, that the 
muscles of swallowing and of speech become easily tired on exer- 
tion, 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; aud clumsy movements of 
the tongue are present, which is a sign that the nuclei of the hypo- THE FACE AND HEAD. 
45 
glossal and twelfth pair are involved. These symptoms are practi- 
cally 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, aud extremities, the fibrillary 
twitching of the affected muscles, aud the loss of electrical irrita- 
bility in these muscles, all of which symptoms belong to true degen- 
erative 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 expression about the eyebrows and forehead (due to 
facial and trifacial failure.) Whether the diagnosis be true degen- 
erative 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 congenital 
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 distrib- 
uted over both sides, and may be clonic or tonic in type. Sometimes 
it occurs only on attempted movement, in other cases it is constant. 46 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 tougue are affected. The disease de- 
pends 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 palpebrae superioris 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 
described are sometimes paralleled by what is called nictitating or 
clonic spasm, which is probably due to some undiscovered 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 sud- 
den bursting out with some blasphemous or filthy word (called 
coprolalia), sometimes is seen in neurotic adult females or children, 
and is often associated with perversion of moral sense. It is called 
1 This term should not be confused with the more common term '‘Graefe’s sign ” used to in- 
dicate the condition in exophthalmic goitre in which the lids fail to follow the eyeballs when 
the patient looks down. THE FACE AND HEAD. 
47 
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 Arras.) 
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 tlie 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 
character, when the history of the presence of an aura, or of uncon- 
sciousness, or biting of the tongue may be discovered. 
Spasm or contractures of the muscles of the face sometimes fol- 
low 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 muscles 
affected. Care should be taken to remember that not very uncom- 
monly 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 heading 
of wry-neck. We find that the head is moved abnormally in nod- 
ding spasm, in chorea, and in tetanus and strychnine-poisoning. It 
is also thrown backward and forward or from side to side in epi- 
lepsy, and in hysteria or in the convulsive seizures occurring in 
young children. 48 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Nodding spasm of the head, depending upon somewhat rhythmical 
contractions of the sterno-mastoid and trapezius muscles, is some- 
times seen in half-fed or rickety children. It also occurs in hyster- 
ical women, and in men who are not hysterical. The nodding 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 be more or less constant though 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 vari- 
ous forms of tic or choreiform spasm. (See chapters on Hands and 
Arms and on Convulsions and Spasms.) 
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 
prognosis, 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 has 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 THE FACE AND HEAD. 
49 
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 
by the attempt 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 
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 en- 
larged glands in the neck may produce such a result. Sometimes, 
too, it occurs after falls without there beiug any other 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 with 
the good ear, and pronounced strabismus may cause a child to so 
carry its head as to improve its sight and avoid diplopia. 
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 
certain 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 50 
THE MANIFESTATION OF DISEASE IN ORGANS. 
occur in acromegaly, osteitis deformans, and in hydrocephalus, micro 
cephalus, rickets, idiocy, myxoedema, and cretinism. 
Fig. 10. 
Acromegaly with goitre (not exophthalmic). (G. R. Murray.) 
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 is flattened. Sometimes in true hydrocephalus the fonta- 
nelle remains pulsating for a long period. Again, in true hydro- THE FACE AND HEAD. 
51 
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 
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. 11. 
Exophthalmic goitre. (Meltzer.) 
the shape of the skull to that of hydrocephalus, we suspect the 
presence 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 addi- 
tion to these changes from the normal, spots of thinned bone in the 
occipital and parietal regions. These may be also somewhat soft- 
ened, and this condition, called “cranio-tabes,” is usually a sign of 52 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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, particu- 
larly in the ribs and legs. 
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 
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.) 
closes very slowly indeed, but after this time has elapsed its edges 
become rapidly approximated. The presence of other fontauelles 
in a child’s skull after it is several months old indicates rickets, 
syphilis, hydrocephalus, or some intracranial growth producing pres- 
sure on the cranial bones, preventing their approximation. Gen- 
erally, 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 until the third or fourth year, and should the rachitic ten- THE FACE AND HEAD. 
53 
dency be developed early in life the edges of the fontanelle may not 
only fail to be approximated, but may actually recede from each other. 
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 hydroceph- 
alus the fontanelle will be markedly bulging. 
If the skin over the fontanelle be found to be bulging temporarily 
to a slight extent, the cause probably lies in some acute disease with 
fever, producing cerebral congestion; whereas, if permanent, and 
if the general dimensions of the skull are not increased, an intracra- 
nial growth may be the cause, or a cerebral hemorrhage, a purulent 
meningitis, or some cystic formation may be present, or sometimes 
a thrombosis of a cerebral sinus produces hydrocephalus and bulg- 
ing. In other cases thrombosis causes sinking-in of the fontanelle. 
This difference in the tension of skin over the fontanelle 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 pneu- 
monia 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. The other symptoms associated with this state 
are usually a sunken appearance of the eyes, slight duskiness of the 
face, a cool skin, and a rapid feeble pulse. The patient is almost 
comatose, and there may be slight convulsive seizures. Such a 
condition has been called the “hydrocephaloid state,” and has been 
confused with symptoms of cerebral effusion arising from tubercular 
meningitis. If there be marked diarrhoea present the following 
table of Symes will serve to clear the diagnois: 
Hydrocephaloid State from Diarrhoea. 
Diarrhoea. 
No ocular paralysis. 
No rise of temperature. 
No headache. 
No tension or bulging of fontanelle. 
No rigidity and 
No retraction of head. 
Cerebral Effusion (as in Tubercular 
Meningitis;. 
Constipation. 
Ocular paralysis and squint. 
Slight feverishness. 
Headache (if old enough to complain). 
Bulging fontanelle. 
Rigidity and retraction of head in many cases. 
Sometimes in rachitic babies auscultation of the fontanelle will 
reveal a murmur, hsemic in origin. This is most frequently heard 54 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
exophthalmic goitre. (See Figs. 11 and 12.) If these symptoms 
are absent, the condition is simply one of overgrowth of the thyroid 
gland. 
Aside from swelling of the glands of the neck due to syphilis, 
Hodgkin’s disease, struma, and tuberculosis, there may be enlarge- 
ment of the parotid gland on one or both sides, just in front of the 
ears and extending under the angle of the jaw. This swelling may 
be due to the specific inflammation involving these glands, known as 
mumps, or be due to other infections, such as typhoid, typhus, and 
pyaemic fever. If the latter be the cause suppuration usually 
ensues. Rarely enlargement of the parotid glands follows trauma 
or disease of the abdominal viscera or pelvic organs. Sometimes the 
enlargement is chronic after the acute inflammation has passed by. 
(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—Tremors 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-black dottings of the 
hand of the miner; and Hirt asserts that atrophy of the antithenar 
eminence often ensues in cabinet-makers, perhaps from the excessive 
use of the plane. Even when no pathological condition exists we 
are wont to regard the heavy aud somewhat thick and clumsy hand 
as an evidence of a phlegmatic temperament, and the thin, wiry, 
dexterous hand as indicative of the nervous temperament. Simi- 
larly, 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. Very 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, and unilateral clubbing 
with incurvation of the nails of one hand is sometimes seen in 
thoracic aneurism. 
From the appearance of the nails we can often gain important 
information; thus, whenever the color of the blood in the capillaries 
under the nails is dusky we know that a deficient pulmonary func- 
55 56 
THE MANIFESTATION OF DISEASE IN ORGANS. 
tion exists or that the circulation is impaired, it may be from feeble- 
ness or from cold. In anaemia the nails are often very pale, 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 parony- 
chia. These conditions may result from skiu lesions, such as eczema 
or lichen ruber, at or near the matrix, or be due to syphilis, and 
Yogi asserts that mere thickening may arise from severe fevers. 
They may also be seen in cases of Raynaud’s disease, or in sclero- 
dactyle, and in cases of pulmonary osteo-arthropathy. 
Atrophy of the nails may apparently arise from causes identical 
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 dacty- 
litis due to syphilis (Fig. 13). Similar deformity, often multiple, THE HANDS AND ARMS. 
57 
also occurs in scrofulosis or tuberculosis. In other cases this is 
replaced by an eruption on the skin of the hand characteristic of 
syphilis. Another indication is seen in the ulcers at the bases of 
the finger-nails, with ecchymotic spots on the skin, produced by the 
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.) 
Fig. 13. 
Dactylitis syphilitica in the infant. (Taylor.) 
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 tendinum). 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 bed- 
clothes,” or carphologia, is given by Shakespeare in his description 
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.” 58 
THE MANIFESTATION OF DISEASE IN ORGANS. 
And again, Hippocrates has well emphasized the gravity of this 
symptom, for he says: “In acute fevers, in peripneumoniae, in 
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 Riintgen 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 be seen 
in the bones 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 finger 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.) 
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 THE HANDS AND ARMS. 
59 
Fig. 15. 
Radiograph of a case of gout in which the gouty deposits affected all the joints of both 
hands, greatly deforming them. The outline of the hand shows the deformity, hut in this 
case it is interesting to note that the gouty deposits do not materially prevent the passage of 
the rays. Marked gouty nodules were present in this case, from which chalky material was 
readily obtained, and the outline of these can be readily discerned in the picture, particularly 
in the forefinger. (From the author’s wards.) 60 
THE MANIFESTATION OF DISEASE IN ORGANS. 
fingers occur through the deposit of urate of sodium in large 
amounts about the joints in their tendons and sheaths, so that the 
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 mate- 
rial looking like wet, powdered chalk. The joint-surfaces them- 
selves 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. The hand to the left is a seal-fin hand. 
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 commonly 
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 manifes- 
tations of the disease, and its character render a differential diag- 
nosis between the hand of gout and that of arthritis deformans a THE HANDS AND ARMS. 
61 
possibility, it should not be forgotten that the deformities of gout 
may take every position assumed by those of arthritis deformans. 
In arthritis deformans the distortion of the hand may be far more 
marked than in 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 still more readily produced. 
(Fig. 20.) As a result there is sometimes developed what is called 
Fig. 17. 
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. (Duckwokth.) 
Nodular swellings (Heberden’s nodes) due 
to gouty arthritis on the forefinger and little 
finger of a woman aged fifty years. (Duck- 
wokth.) 
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). (Figs. 16 and 19.) 
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 immo- 
bility or stiffness. Some persons believe that when the hand wastes 
it does so not from disuse, but through reflex nervous influences. 62 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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.) 
Fig. 19. 
Tophaceous gout of hands, illustrating deflection and torsion of digits and phalanges. 
The figure to the left shows the “ seal-fin ” type. (Duckworth.) THE HANDS AND ARMS. 
63 
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 
Fig. 20. 
A Rontgen ray picture showing the condition of 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 hone of the middle 
and ring fingers with the os magnum and unciform bones, with deposits in the heads of the 
phalanges and dislocations. (From the Medical Chronicle.) 
of the thumb, or in the wrist and carpal joint. The hand is 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 64 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
readily separate acute rheumatism from chronic gout and arthritis 
deformans, and leave it to be separated from sprain, septic arthritis, 
and deep-seated inflammation of the hand proper. The first is ex- 
cluded 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 accompanying 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 sometimes occurs during the fall of temperature in scarlet 
fever, and is often hot 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 instances out of one hundred cases, and only twenty- 
five times in the larger joints out of a hundred cases. The con- 
dition 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 oedema- 
tous in the sense that it can be pitted on pressure. This swelling, 
which may be multiple, red in color, or pale and waxy in appear- 
ance, 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 bv a white and waxy or slate 
color of the fingers, associated with coldness, swelling, and mottling 
of the skin, termed u Raynaud’s disease.” Often this is a passing 
condition, but in its severe forms there is finally developed dry 
gangrene in 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 dis- 
eased and thickened bloodvessels will enable us to decide on the 
latter as the cause; frost-bite, in which the history of exposure will 
be of value, although exposure to cold often precipitates an attack 
of Raynaud’s disease; ergotism, which can be discovered by the 
history of the patient having for a long time taken food which may 
have contained bad rye; leprosy, which will probably be seen more THE HANDS AND ARMS. 
65 
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 pro- 
gressive loss of power in the hand, with atrophy and ulcers about 
the bases of the nails. Sometimes the terminal phalanges undergo 
necrosis, and enlargement of the fingers, through swelling, may be 
very marked. It is probable that this condition represents two 
separate lesions, namely, neuritis and syringomyelia, and it is an 
exceedingly rare disease. 
Swelling of the hand, followed in some months by rupture of the 
skin, may, in a person from the tropics, mean mycetoma, which is, 
however, 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 defor- 
mity depends upon the alterations in the subcutaneous tissues, rather 
than on changes in the bones, so that the hand is swollen or boggy- 
looking, but does not pit on pressure as in true oedema. In acro- 
megaly the enlargement is chiefly osseous, as it is also in pulmonary 
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 particularly well 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 locally 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 66 
THE MANIFESTATION OF DISEASE IN ORGANS. 
from wasting of the muscular tissues, so that hollows or sunken 
places occur, but also from the distortions caused by the contrac- 
tions 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 con- 
tracted, overcoming 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 muscles, the remaining portion of the hand having its normal 
appearance or being only indirectly influenced. 
Fig. 21. 
Claw-hand. (Gray.) 
Under the name of u claw-hand,” or “ main-en-griffe” we find 
a deformity of the hand which is in itself very characteristic, although 
indicative of several causes which all operate in an identical manner. 
The back of the hand loses its normal convexity and becomes some- 
what concave, the tendons on the extensor surface stand out in 
ridges, the proximal phalanges are drawn backward toward the 
wrist, while the second and third phalanges are 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 digitorum produce a 
dorsal flexion of the first phalanges and a complete palmar flexion THE HANDS AND ARMS. 
67 
of the second and third phalanges. A certain amount of immo- 
bility is also caused by the fact that flexion of the hand is impos- 
sible 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 
(generally the former), and there will be evidences of local injury, 
or a history which will indicate that the lesion is peripheral. Further 
than this, there will nearly always be found, in ulnar and median 
injury, sensory as well as motor paralysis; and Hirt asserts the 
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 diagnostic information in suspected cases, and if the patient 
with this disease be watched as he unbuttons 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 68 
THE MANIFESTATION OF DISEASE IN ORGANS. 
fingers. The additional symptoms are some pain or parsesthesia in 
the affected parts prior to the wasting, and the spread of the paral- 
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.) 
)7sis, as its name indicates, from muscle to muscle. (Figs. 23, 24, 
and 25.) Thus, beginning in the ball of the thumb it passes to the THE HANDS AND ARMS. 
69 
interossei, and thence up the forearm and arm. Sometimes, how- 
ever, the forearm muscles escape, and the shoulder muscles are 
attacked secondarily. 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 disease may last for many years. 
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 
the claw-hand of peripheral neuritis of a general and severe type. 
Fig. 25. 
Hand and forearm in chronic spinal muscular atrophy, showing especially wasting of thenar 
and hypothenar eminences. (Dercum.) 
As the result of the acute poliomyelitis of infancy, we may also 
have the hand distorted by contractures, such as forced extension 
in paralysis of the flexors, forced flexion in paralysis of the exten- 
sors, and claw-hand in 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 paral- 
ysis, 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 main-en-griff'e, there 
being a slow symmetrical wasting of the muscles with a drawing of 
the fingers into flexion. There are also analgesia and painless whit- 70 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
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 progres- 
sive 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 
before the physician, such as weariness, stiffness, and loss of power 
in the legs. (See chapter on Legs, 
Paraplegia.) There are also exag- 
gerated 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 gener- 
ally there will be, with this, loss of 
power and disturbance of sensation, 
such as anaesthesia. Often in syrin- 
gomyelia 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 contrac- 
tures, is seen rarely in advanced 
paralysis agitans in place of the 
characteristic tremor. 
In the “ cerebral palsy of chil- 
dren,” 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, 
Fig. 26. 
Right hemiplegia, with contractures 
and retarded growth of arm. Onset of 
disease at eight years of age, following 
typho-malarial fever. (Sachs.) THE HANDS AND ARMS. 
71 
bat are sometimes bilateral. A peculiarity of these cases is that 
the muscles waste very slightly, and do not develop 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 
carious positions with ease, and, if the limb be suddenly flexed, a 
lock-like sensation will be imparted to the physician’s hand. Con- 
vulsive seizures of an epileptiform 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 in 
deformity. These contractions, if they occur early, are an evidence 
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 descending the 
pyramidal tracts. Wasting finally comes on. (For further discus- 
sion of the significance of paralysis in the arm and hand, see suc- 
ceeding pages and chapter on Hemiplegia.) 
Fig. 27. 
Fig. 28. 
Hysterical atrophy of the hand with flexion of 
the last two phalanges into the palm, particu- 
larly the last phalanges of the index and middle 
fingers. (Gilles de la Toukette.) 
Same hand in another view. 
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. 72 
THE MANIFESTATION OF DISEASE IN ORGANS. 
As a rule, the muscles do not waste or develop degenerative reac- 
tions, but rarely such wasting may occur. (Figs. 27 and 28.) Care 
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 either a 
true organic or a false hysterical contracture, much medico-legal in- 
terest 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 produce 
the spasm. 
When in the course of an acute illness in a child the fingers are 
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 THE HANDS AND ARMS. 
73 
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 in 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 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 evidences 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 char- 
acteristic. 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 chil- 
dren. The same term, “ paralytic chorea,” is also applied to a con- 
dition sometimes seen after an apoplectic stroke, choreic movements 
taking place as degenerative changes in the muscles are developed. 
Sometimes choreic movements come on in the latter half of life, 
often preceded by 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 mani- 
acal, 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 hebetude. 
Several other affections which somewhat resemble true chorea are 
sometimes met with, but all of them lack, with one exception, the 74 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
thau 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 it is to be recalled that the movements consist in sudden twitch- 
ings 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. 
Sometimes the muscles in myoclonus are exceedingly irritable. 
Under the name of electric chorea, or “ Dubini’s disease,” Dubini 
described a disease, affecting both sexes and all ages, in which sud- 
den shock-like contractions of the muscles take place, as if they 
were being stimulated by a slowing interrupted faradic current. 
The disease usually begins in the upper extremities, and gradually 
involves 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 convul- 
sive tic or palmus, which has also been called “ the jumpers,” in 
which the movements are not in the slightest degree 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 Huntingdon’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 accompa- THE HANDS AND ARMS. 
75 
niecl by progressive mental deterioration, 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 myo- 
tonia congenita, is what is 
called paramyotonia congen- 
ita, which exists in three 
forms: first, a patient suffer- 
ing from paralysis agitans on 
attempting to move is seized 
with rigidity of the muscles, 
which holds him fixed; sec- 
ond, a patient is suffering 
from ataxia and muscular 
weakness, and is seized with 
an attack of muscular rigid- 
ity; 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 ex- 
posure, and not by intention- 
movement, and may last for 
hours. (See also Athetosis.) 
The position of the hand 
may be very various. Thus, 
the hand may drop edgewise 
from the radius toward the 
ulna from paralysis of the extensors on the radial side of the fore- 
arm, resulting from neuritis or acute infantile poliomyelitis, while 
marked wrist-drop may occur from paralysis of the extensors in 
chronic lead poisoning, or in any form of neuritis, toxic or other- 
wise, involving the nerve supply of these muscles (musculo-spiral 
nerve). (Fig. 29.) Wrist-drop may also be developed by pressure 
upon the musculo-spiral nerve, as in crutch-palsy. If the wrist- 
drop is bilateral, it may be due to toxic neuritis; but if unilateral, 
Fig. 29. 
Boy with multiple neuritis, with double wrist- 
drop and slight foot-drop. (Sachs.) 76 
THE MANIFESTATION OF DISEASE IN ORGANS. 
it is probably, but not positively, due to pressure-paralysis from 
sleeping with the head resting on that arm, or from pressure by a 
crutch, or from 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 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 from the normal will be 
found to be tremor, which may indicate paralysis agitans, dissemi- 
nated sclerosis, general paresis, chronic mercurial, plumbic, or alco- 
holicpoisoning, hysteria, senility, and Graves’s disease. 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 mem- 
ber. 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). Indeed, they may be so coarse 
as to be choreic in type, or even ataxic. 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 symp- THE HANDS AND ARMS. 
77 
toms of disseminated sclerosis are well summarized in the follow- 
ing table drawn up by Charcot. 
I. Spinal Symptoms : 
Tremor on voluntary movements of the extremities—“ intention 
tremor” (arms and head ; more rarely of legs). 
Titubation. 
Paresis (spasmodic) of the extremities. 
Contracture, with exaggeration of the reflexes—spastic rigidity. 
Positive . . . 
Negative .... 
No sensory symptoms, or only very slight disturbance. 
Vesical disturbance none or very slight. 
II. Cerebral Symptoms 
Dysarthria—slowness of speech; scanning of words. 
Nystagmus—blank expression. 
Attacks of vertigo—spasmodic myosis. 
Transitory amblyopia—white atrophy of the papillee. 
Diplopia—associated paralysis of ocular muscles. 
Mental enfeeblement. 
Apoplectiform and epileptiform attacks. 
Difficulty in deglutition. 
III. Abnormal or Unusual Symptoms : 
Trophic Muscular atrophies (amyotrophies), bedsores. 
Lightning pains. 
Romberg symptom. 
Anaesthetic areas. 
Vesical and rectal paresis. 
Gastric crises. 
Tabetic . . . 
Frequent remission of all the symptoms is characteristic of the malady. 
It is not to be expected that all these symptoms will be found 
in one case. But many of them will occur. Charcot taught 
that tremor involving the head indicated disseminated sclerosis, 
and excluded paralysis agitans ; but cases of head tremor in the 
latter disease do occur. (See chapter on Feet and Legs, part on 
Gait.) 
The tremor of mercurial, plumbic, and alcoholic poisoning resem- 
bles 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 mercury may be relieved in a short time 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 symptoms, even preceding the motor disturbance. In 78 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 ppon 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 11 type Rendu,” and 
has a rhythm of seven to nine per second, while the slower hyster- 
ical tremor may be four or five per second. 
Beyond the state of tremor should be recalled the movements of 
chorea (see page 73), 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. 
General Movements of the Hand and Arm. Aside from the 
movements of tremor, careful notes should be made of the move- 
ments of the hand as a whole, of the co-ordination of its fingers 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) THE HANDS AND ARMS. 
79 
is of still graver import (see beginning of this chapter.) Inability 
to write, to play musical instruments requiring the use of the 
fingers, 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 cor-ordination, although loss of power may not be 
present. 
Sometimes in locomotor ataxia as the disease becomes advanced 
paroxysmal twitching of the fingers may come on, or involuntary 
movements of the fingers 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 advanced 
past the object which the patient desires to grasp, or else falls short 
of it. On endeavoring to pick up an object the fingers 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, how- 
ever, 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 occur 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. 
Very rarely athetoid movements of the fingers occur in advanced 
spinal tabes (locomotor ataxia), probably as the result of a related 
lesion, and not from tabes itself. 
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- 
ness, hereditary or acquired, and rarely in hysteria. “ Mirror- 80 
THE manifestation of disease in organs. 
Fig. 30. 
Examples of the positions of the fingers in the movements of athetosis. (StrOmpell.) 
writing ’ ’ may also be present in cases of cerebral paralysis. The 
following example of this, taken from a case reported by Clapham, 
illustrates the character of the handwriting. The patient, a girl of 
twenty-four years, could write all three ways, but mirror-writing 
was easiest to her. (Fig. 31.) THE HANDS AND ARMS. 
81 
Fig. 31. 
Mirror-writing. 
Paralysis of One Arm, or Brachial Monoplegia. Absolute 
loss of power in one hand and arm without the necessary develop- 
ment 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 sub- 
cortical; that is, in the surface of the brain or in the internal cap- 
sule, or between the cortex and the capsule in the corona radiata. 
As a rule, however, monoplegia is cortical in origin, for below the 
cortex the motor fibres run so closely together that only a very 
small lesion can involve one without involving all, and so producing 
a hemiplegia. These cortical lesions when they do occur are gener- 
ally, but not always, associated with a convulsive seizure in the 82 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 convul- 
sion and loss of consciousness, and lacking in signs of involvement 
of lower nervous centres, is, therefore, cortical, 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 otherwise, 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 yet 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 
increase 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 
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 THE HANDS AND ARMS. 
83 
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, a sudden 
inflammatory process is set up in the tissues surrounding a tumor, 
and this 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 becom- 
ing puffy and swollen. The presence of a neurotic temperament 
and other hysterical signs, coupled with the prompt development 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 anesthesia 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 the cut- 
ting 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, 
which supplies the triceps; whereas if the power to flex the forearm 
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 84 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 com- 
paratively 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 monoplegia 
may depend upon fracture or dislocation of the head of the humerus, 
and 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 sen- 
sation in 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, Striimpell has re- 
ported cases of musculo-spiral paralysis from this cause, and Remak 
and Hirt record cases in which the median nerve has been affected, 
so that not only loss of power but wasting of the muscles has re- 
sulted. 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 Eye.) Widespread muscular atrophy of 
the arm sometimes takes place in locomotor ataxia as a result of a 
coincident neuritis. 
There are still to be considered two comparatively rare forms of 
brachial monoplegia of the plexus type, namely, that due to press- 
ure 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, 
bracliialis anticus, and supinator longus and brevis, and the supra- 
and infra-spinatus muscles. The adult form is often associated with 
anaesthesia 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 THE HANDS AND AEMS. 
85 
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 anaesthesia 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 11 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 appar- 
ently perfectly 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, but there may be some 
pain and crepitation on moving the arm. The cause of these symp- 
toms lies in the fact that there has been a separation of the epiphyses 
from the shafts of the bones, with consequent helplessness. Some- 
times general 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 are supplied by the musculo-cutaneous, and the third by the 
musculo-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 86 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 supi- 
nator 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 paralyzed 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 Parsesthesia. 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 involve- 
ment. Thus, if the function of the nerve is merely impaired, the 
sensation may be that of tingling or pain; if still further impaired, 
the sensation may be that of numbness; and if the sensory fibres be 
totally destroyed or paralyzed, absolute anaesthesia and analgesia 
may be present. (See Anaesthesia, chapter on Skin.) CHAPTER III. 
THE 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 and legs—The joints—Alterations in the nutrition of the feet 
and leg 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-poisoning, syphilis, or peripheral neuritis arising from other 
causes, Friedreich’s ataxia, general paresis, chronic myelitis, lateral 
sclerosis, acute poliomyelitis, pseudo-muscular hypertrophy, cerebral 
infantile palsy, mulitiple sclerosis, paralysis agitans, cerebellar dis- 
ease, organic and hysterical hemiplegia, and osteomalacia, and the 
gaits caused by rickets and other bony defects. 
87 88 
THE MANIFESTATION OF DISEASE IN ORGANS. 
In locomotor ataxia the gait is unsteady and waveringly uncer- 
tain, resembling that of a blindfolded person who is told that he is 
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 of 
Dr. Dercum, made simultaneously from two different points of view by Muybridge. 
The gait of pseudo-tabes is sometimes identical with that just 
described, is usually associated with a history of alcoholic excess, 
and is due to multiple neuritis. In a majority of the cases, 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, THE FEET AND LEGS. 
89 
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 
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 (WestphaPs sign), the history of 
gastric, laryngeal, or vesical crises, the presence of numbness in the 
feet, the slow onset of the disease, and the absence of any history of 
exposure to the causes of neuritis just named. If all these signs are 
present, and are combined with that most important symptom, the 
Argyll-Robertson pupil, the diagnosis is practically certain. 
Grube has, however, recently reported three cases of diabetes 
mellitus producing a pseudo-tabes due to neuritis which had the 
Argyll-Robertson pupil, and in addition attacks of abdominal pain 
like the crises of true ataxia. 
The Stages of Tabes Dorsalis. 
Initial Period. 
Second Stage. 
Final Station. 
Inco-ordination,but no change 
of gait. 
Greater inco-ordination, and 
marked ataxic gait. 
Cannot walk because of aiaxia. 
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. 90 
THE MANIFESTATION OF DISEASE IN ORGANS. 
The preceding 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. 
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. 
Prom a prognostic and therapeutic stand-point it is interesting to 
note that about 80 per cent, of all cases of tabes dorsalis are syph- 
ilitic. (Duckworth.) 
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 be remembered that 
the lesions of locomotor ataxia are found in the peripheral nerves as well. 
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. (Fig. 33.) For these reasons the reflex arc is 
destroyed and the co-ordination of the muscles lost. The patient 
cannot tell how to use his muscles unless he can see them and co- 
ordinate them by the aid of the eye. The sensations of formication 
or numbness are also due to these sensory lesions. (For descrip- 
tions of motor and sensory tracts of the spinal cord, see early part 
of chapter on Hemiplegia, and the chapter on the Skin.) 
Sometimes not only the gait, but the entire set of the ordinary 
symptoms of locomotor ataxia are aped by hysteria so closely that THE FEET AND LEGS. 
91 
a diagnosis may be almost impossible, but the Argyll-Robertson 
pupil, the lost knee-jerks, and the optic atrophy will not be present 
if hysteria be the cause of the symptoms. On the other hand, 
Romberg’s symptom may be marked to an extraordinary degree. 
The patient who is hysterical, in falling nearly always falls the 
same way, keeping her frame stiff like a board. (See chapter on 
Eye for differential ocular symptoms.) 
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 
feebleness in the paretic case, or at least evidences of delusions, and 
if the disease is at all advanced there will be a history of the patient 
having had convulsions or apoplectiform attacks. Sometimes there 
will be found present in paretic dementia increased knee-jerks and 
many of the symptoms of ataxic paraplegia, but the associated mental 
failure and fine intention-tremor of the hands decide the diagnosis 
in favor of paretic dementia. 
In 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 is told to stand still, 
swaying at once develops. If the eyes be closed, the swaying may 
greatly increase. 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 hered- 
ity, there are a slow and jerky articulation, scoliosis, and talipes 
equiuo-varus, but there is no Argyll-Robertson pupil. (Fig. 34.) 
The following table shows the differential points between loco- 
motor ataxia and Friedreich’s ataxia: 
Locomotok Ataxia. 
Argyll-Robertson pupils. 
No nystagmus. 
Painful crises. 
Intellect unimpaired. 
Gait ataxic. 
Speech normal. 
No head tremor. 
Friedreich’s Ataxia. 
No Argyll-Robertson pupils. 
Present late in disease. 
Crises usually absent. 
Becomes impaired. 
Cerebellar ataxic gait. 
Speech halting. 
Head tremor present. 
Friedreich’s ataxia must be separated from another rare disease in 
which the gait is ataxic and the disease hereditary, namely, heredi- 
tary cerebellar ataxia, in which we have the following symptoms not 92 
THE MANIFESTATION OF DISEASE IN ORGANS. 
seen in Friedreich’s disease, namely, normal or exaggerated knee- 
jerks, Argyll-Robertson pupils, and a beginning of the malady after 
Fig. 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). 
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. 
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. Docs 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; “ i ntentional. ’ ’ 
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. THE FEET AND LEGS. 
93 
Hereditary Spinal Ataxia. 
Friedreich's disease. 
8. Nystagmus is a very common late symp- 
tom, 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 bot and spinal curvature, very common. 
Hereditary Cerebellar Ataxia. 
8. Eyes : twitching of the eyeballs very com- 
mon, but not nystagmus. Optic atrophy, pro- 
gressive 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 extremity and spine, 
such as pied hot or scoliosis, do not occur or 
are very rare. 
Hereditary cerebellar ataxia may also be confused with dissemi- 
nated sclerosis, as is shown in the following table prepared by Stieg- 
litz. Hereditary cerebellar ataxia is, however, much more rare than 
sclerosis. The differential points are shown in italics. 
Hereditary Cerebellar Ataxia. 
1. Gait: ataxic, groggy ; feet wide apart. 
2. Station : Romberg’s symptom absent. 
3. Arms: ataxy and some intention tremor. ! 
4. Oscillations and jerky movements of the 
head and trunk. 
5. Exaggerated contractions of facial mus- j 
cles during speaking. 
6. Speech: hesitating and abrupt, or simply 
monotonous. 
7. Eyes: jerky nystagmus; optic atrophy, 
contracted field of vision. The external recti 
muscles may be paretic or paralyzed. 
8. Myotatic irritability increased, knee- 
jerks exaggerated, ankle-clonus ; contractures j 
and muscular rigidity. 
9. Mental impairment in varying degrees. 
10. Vertigo sometimes. 
11. Vesical f unctions rarely affected. 
12. Apoplectiform seizures do not occur. 
13. Heredity common. 
Disseminated Sclerosis. 
1. (a) Spastic paraplegia; feet close together. 
(6) Ataxic, groggy ; feet wide apart, (c) Ataxic 
paraplegia (a + 6). 
2. Romberg symptom may be present. 
3. Intention tremor; sometimes ataxy. 
4. Oscillations and jerky movements of the 
head and trunk. 
5. Twitching in facial muscles during 
speaking. 
6. Laborious, scanning, or monotonous 
speech. 
7. Jerky nystagmus; optic atrophy, con- 
tracted field of vision; ocular nerve palsies. 
8. Myotatic irritability increased; knee- 
jerks exaggerated, ankle-clonus; contractures 
and muscular rigidity. 
9. Mental impairment in varying degrees. 
10. Vertigo common. 
11. Vesical functions more frequently dis- 
turbed. 
12. Apoplectiform seizures occur in a small 
proportion of cases. 
13. Heredity uncommon. 
Stieglitz has also pointed out that in certain cases of acute dis- 
seminated myelitis and encephalomyelitis following the acute infec- 
tious diseases, the symptoms of an acute or subacute multiple 
sclerosis are presented, more especially the intention-tremor, the 
increased reflexes, and the scanning speech. The disease may ulti- 
mately form the basis of a typical chronic insular sclerosis with its 
recurrent attacks, etc. It may, however—and this is a point of 
importance—subside after a shorter or longer period and end in 
recovery.  THE MANIFESTATION OF DISEASE IN ORGANS. 
94 
In chronic myelitis in the early stages, while motion is still pre- 
served the gait is typically that of feebleness, and the legs respond 
slowly to the cerebral desires, being dragged along after the patient, 
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. THE FEET AND LEGS. 
95 
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.) 
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 floor 
and on going up and down stairs. 
The patient in all his movements 
shows a marked loss of power in the 
legs with a great apparent 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 features 
of the case which may mislead the 
physician are that the child, if fat, 
will have bulging legs, as if the mus- 
cles were hypertrophied, and lor- 
dosis due to spinal weakness. In 
the rickety case, however, the knee- 
jerk is preserved, and in the case of 
pseudo-muscular hypertrophy it is 
lost. 
The gait of a child suffering from 
infantile cerebral paralysis is quite 
characteristic. In the first place, it 
is spastic, and the patient walks on 
the toes, or in some cases club-foot 
develops. The heels are everted and 
the toes turned inward, the knees 
being so closely approximated that 
the clothes may become worn be- 
tween them from the rubbing. So great is the extension of the 
legs that the toes are very apt to drag, and, finally, the adduction 
Fig. 3G. 
Typical pseudo-muscular hypertrophy. 
(Dercum.) 96 
THE MANIFESTATION OF DISEASE IN ORGANS. 
spasm may be so great that the legs overlap each other as walking 
is attempted. (Fig. 37.) 
The gait in disseminated 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 
Fig. 37. 
Fig. 38. 
Spastic paraplegia; crossed-legged pro- 
gression. (Prom 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. (Dercum.) 
his fingers there are tremor and oscillation of the hand. Scanning 
speech and nystagmus develop later on in these cases. It is, how- 
ever, important to remember that multiple cerebro-spinal syphilis 
may closely simulate multiple, or disseminated, sclerosis. Some- 
times they may be differentiated by the fact that in disseminated 
sclerosis there is apt to be paresthesia, whereas in syphilis there is THE FEET AND LEGS. 
97 
more apt to be pain. An important differential symptom is that 
nystagmus is rare in syphilis, common in disseminated sclerosis, and 
ocular palsies are common in syphilis, rarely so severe in sclerosis, 
so that complete oculo-motor palsy with ptosis and squint would be 
more likely syphilitic than sclerotic. (See chapter on the Eye.) 
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 festination. 
The gait is also somewhat trotting or toddling. (Fig. 38.) (See 
chapter on Hands and Arms, part of on Tremor.) 
In cerebellar disease the gait may closely resemble that of a 
drunken man, and the patient has the greatest difficulty in keeping 
from sheering off 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 
are associated with paralysis of the oculo-motor nerves and other 
symptoms of brain-tumor, there is a growth in the corpora quadri- 
gemina. 
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 para- 
plegic 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 
hypersesthesia. Again, in the gait of hysterical paralysis the patient 
is apt to be excessively laborious in her progress, and will exhaust 
her muscles in her strained movements. An altered gait due to 
irregularly distributed paralysis of groups of muscles is nearly 
always hysterical, and sometimes the patient who has hysterical loss 
of power will suddenly fall through giving way of her knees. 
A condition of the gait and station of the patient varying from 98 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 reg- 
ularly 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 per- 
formed perfectly. The 
knee-jerks are rarely lost, 
and in addition the gen- 
eral 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. This symptom 
generally follows some 
severe shock, and is most 
commonly seen in young 
persons, usually young 
women. 
In osteomalacia there 
is increasing difficulty of 
walking, partly due to 
pain and partly to mus- 
cular 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 FEET AND LEGS. 
99 
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 
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, result- 
ing in localized palsies. These paralyses often produce deformities, 
as will be shown shortly. 
Paraplegia. Given a case of paraplegia, what may be its cause? 
It may arise from a cerebral lesion, which is very rare, except in 
children, when it is common,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 cap- 
sules. 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 “ “ 
Medullary. 
1. Organic disease . . 
Meningitis “ “ 
Meningeal hemorrhage 
Injuries 
Tumors 
Meningeal. 
Caries of bone 
Tumors of bone 
Osseous. 
Hysterical. 
Reflex. 
Malarial and anaemic. 
Dependent on idea. 
2 Functional . . 
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.) 100 
THE manifestation of disease in organs. 
Spastic Paraplegia. The paraplegia of cerebral infantile 
paralysis is spastic, and follows difficult labors or injuries to the 
child before or after birth. Contractures nearly always ensue, and 
exist chiefly in the adductors of the thighs, so that the attitude is 
very characteristic. (Fig. 40.) Epileptic convulsions very often 
complicate these cases. Often these paraplegias are not manifested 
for some months, or eveu longer, after birth. In many cases they 
are first noticed when the child attempts to walk. 
Fig. 40. 
Spastic diplegia, congenital, presenting choreiform and athetoid movements. (Derccm.) 
(Philadelphia Hospital.) 
Cerebral spastic paraplegia in infants also sometimes comes on 
in cases of so-called arrested development. Such infants present no 
abnormality for the first few months of life, then cease to develop 
iu mental brightness, fail to recognize the nurse or mother, cease 
to play, gradually lose their vision, and develop nystagmus. Death 
usually takes place in oue or two years at the latest. Convulsions 
do not occur in this state, but tremors are often present in the arms. 
There is no history in such cases of difficult labor or premature 
delivery. In both this and the infantile cerebral form of spastic 
paraplegia the pyramidal tracts are degenerated. It is important 
to remember that cerebral paraplegia is not associated with the de- 
velopment of the reactions of degeneration in the paralyzed part, 
and is associated with comparatively little wasting, thereby differing 
from the deformities of the lower extremities resulting from polio- 
myelitis or acute infantile palsy. 
Care should be taken that the spastic paraplegia of rickets is not 
mistaken for a birth-palsy. THE FEET AND LEGS. 
101 
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- 
mus, and vertiginous, epileptiform, or apoplectiform seizures, with 
staccato speech, and local areas of loss of power elsewhere, associated 
with the spastic paraplegia, renders the diagnosis easy. (See early 
part of this chapter.) 
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. This absence of con- 
vulsions and defective mental power in this form of spastic para- 
plegia 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 contrac- 
tures, but the bladder and rectum escape the paralysis, and there 
are no trophic changes. The reflexes are increased. The disease 
is rare. 
In transverse myelitis there is often in the later stages of the 
malady spastic paraplegia as a result of the irritability of the spinal 
centres below the seat of the lesion, and this may cause a spastic 
state of the muscles. In distinction from lateral sclerosis we find 
in myelitis that there are girdle-pains, 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 102 
THE manifestation of disease in organs. 
from Setschenow’s reflex inhibitory centre in the medulla oblongata 
are destroyed in the lateral pyramidal tracts. In amyotrophic lat- 
Fig. 41. 
Shading shows areas involved in lateral sclerosis, viz., the crossed pyramidal tracts. 
Fig. 42. 
Showing areas of spinal cord involved in amyotrophic lateral sclerosis. 1. Crossed pyramidal 
tracts. 2. Anterior horns of gray matter containing the trophic ceils. 
eral sclerosis similar symptoms associated with wasting of the mus- 
cles are present in the later stages, but in the early stages the arms THE FEET AND LEGS. 
103 
are chiefly affected by the wasting and paralysis. (Fig. 42.) (See 
chapter on Hands and Arms.) 
Spastic paraplegia may also be due to spinal pachymeningitis, 
and the associated symptoms may so closely resemble those of mye- 
litis that a diagnosis is impossible; but the spastic character of the 
paraplegia, the early appearance and severity of the pain, and the 
comparatively slow development of the symptoms in pachymen- 
ingitis 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 condition. If the inflammatory process becomes widespread, 
there may be sensory disorders and trophic sloughs, owing to inva- 
sion 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 menin- 
geal 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 
ensiform cartilage at the fourth or fifth dorsal vertebra. Early in 
the disease pressure on the spinal cord may increase the reflexes. 
The area of the cord involved can be determined by the symptoms 
as detailed on pages 106 and 107. The prognosis is not always 
unfavorable, as extraordinary recoveries take place. 
Non-spastic Paraplegia. Passing from spastic paraplegia we 
come to those forms of paraplegia lacking this peculiarity. They 
are quite numerous and important. If the paraplegia comes on 
suddenly, the cause may be hemorrhage into the substance of the 
cord or into the spinal membranes, or be due to compression or 
destruction of the cord by injuries of the back, whereby there is 104 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 myelitis, 
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, 
neuritis, and pressure due to disease of the vertebrae or to spinal 
tumors. Finally, we have what are called reflex and hysterical 
paraplegias. 
Hemorrhage into the spinal cord is an exceedingly rare condi- 
tion unless preceded by grave disease of its tissues. Indeed, the 
existence 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 sufficient 
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. 
D filer 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. THE FEET AND LEGS. 
105 
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 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 involved 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, delirium 
may develop. The prognosis is unfavorable. Acute central mye- 
litis 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 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 cases the reflexes do not return if the lesion is completely 
transverse. The patient is speedily bedridden, 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 106 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
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 3Iedicine shows 
the effect of a lesion in the spinal cord in transverse myelitis. 
Symptoms in Transverse Myelitis. 
The darkened portion represents the seat of lesion. 
Spinal cord 
Reflexes normal 
Band of hyperaesthesia.... 
Reflexes normal. 
Band of hyperaesthesia. 
Muscles palsied, waste and lose 
their electrical reactions. 
Reflexes lost. 
Muscles palsied, waste, and lose 
their electrical reactions . . 
Reflexes lost 
Sensation lost 
Tender spines. 
Tender spines. 
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 Panesthesia 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-sensa- 
tion on the trunk becomes well developed (see chapter on Skin). 
The bladder, which at first was irritable, may now be toneless, THE FEET AND LEGS. 
107 
paralyzed, 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 abol- 
ished, but very soon some of them return, only those reflexes the 
centres for which are destroyed by the transverse lesion being abol- 
ished; that is, the reflexes recover after the first shock of the attack, 
and those muscles and tendons having spinal centres below the lesion 
have their reflexes increased because they are cut off from the inhib- 
iting 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 bullae, 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 pre- 
vents the sensory impulse from reaching the brain (see chapter on 
Skin). When the entire cord is not evenly involved in the trans- 
verse lesion certain groups of muscles partly escape. It is asserted 
that the extensors escape oftener than the flexors. The height of the 
paralysis also depends upon the situation of the lesion of 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 supposed 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 condi- 108 
THE manifestation of disease in organs. 
tion: there is complete paralysis of his arms and legs, with paralysis 
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 reten- 
tive. All these symptoms point to a transverse lesion of the spinal 
cord in the cervical region, probably between the fifth cervical and 
first dorsal vertebrae. 
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 height of lesion. 
2. Legs. 
Neck-muscles, dia- 
phragm, arms, trunk, 
and legs. 
Sensation. 
Pains in legs, or girdle-pains 
around loins; hypersesthe- 
tic zone around loins ; an- 
aesthesia of legs, complete 
or uneven distribution. 
Girdle-pain and hyperass- 
thetic zone between ensi- 
form cartilage and pubes. 
Hypersesthesia and 
pains in certain 
nerve-distributions 
of arms ; below this 
auaesthesia 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. 
Sameasin dorsal mye- 
litis. 
Reflexes, 
superficial, 
Lost. 
Temporary loss, then rapid 
increase. 
Same as in dorsal mye- 
litis. 
Reflexes, 
deep. 
Lost. 
Temporary Loss, then slow 
increase. 
Same as in dorsal mye- 
litis. 
Priapism. 
Absent. 
Often present. 
Often present. 
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 mus- 
cles, and the other symptoms just named are present, combined with 
1 From Prince’s article in Dercum’s Nervous Diseases. THE FEET AND LEGS. 
109 
degeneration of the muscles of the trunk, the lesion is probably 
somevvhere between the second and twelfth dorsal vertebrae. 
Again, if the paralysis of motion and sensation be only in the 
lower limbs, and there be flaccidity of the muscles (where before 
we discovered spastic contraction), with muscular degeneration, loss 
of reflexes, and paralysis of the bladder and rectum, the lesion is in 
the lumbar cord. 
Still further, if there be loss of power with degeneration of the 
small muscles of the feet, and loss of sensation of the outside of the feet 
and toes, and of the skin about the anus, with preservation of power 
in 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 amesthesia. 
This subject is still further subdivided and elucidated by the 
following table and by the illustration (Fig. 43, p. 111). 
Localization of the Functions of the Segments of the Spinal 
Coed. (According to Starr ) 
Segment. 
Muscles. 
Reflex. 
Sensation. 
II. and III. 
C. 
Sterno-mastoid. 
Trapezius. 
Sealeni 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-brach ialis. 
Supinator longus. 
Khomboid. 
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. 110 
the manifestation of disease in organs. 
Segment 
Muscles. 
Reflex. 
Sensation. 
VII. C. 
Triceps (long head). 
Extensors of wrist and 
fingers. 
Pronators of wrist. 
Flexors of wrist. 
Subscapular. 
Pectoralis (costal part). 
Latissimus dorsi. 
Teres major. 
Anterior wrist. 
7th to 8th cervical. 
Tapping anterior tendons 
causes flexion of wrist. 
Palmar. 7 th cervical to 1st 
dorsal. 
Stroking palm causes closure 
of fingers. 
Inner side and back of 
arm and forearm. 
Radial half of the 
hand. 
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. 
Forearm, inner half. 
Ulnar distribution to 
hand. 
II. to XII. 
D. 
Muscles of back and abdo- 
men. 
Erectores spinas. 
Epigastric. 4th to 7th dorsal. 
Tickling mammary region 
causes retraction of the 
epigastrium. 
Abdominal. 7th to 11th dor- 
sal. 
Stroking side of abdomen 
causes retraction of belly. 
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. 2d 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 A rgy 11 - Robe r tson 
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 FEET AND LEGS. 
111 
The symptoms of lateral sclerosis and amyotrophic lateral scle- 
rosis have already been discussed under Gait and Spastic Paraple- 
gia, but in the paraplegia called “ ataxic paraplegia,” also already 
discussed, there are in association lateral sclerosis and posterior 
sclerosis, and for this reason some of the symptoms of both are 
found to be present. 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, titubation, and 
sometimes vomiting. 
Fig. 43. 
Showing the surface-areas of the back corresponding approximately to the areas of the 
spinal cord supplying the trunk and limbs. 
The onset of the 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 convul- 
sions, all point to the cause being poliomyelitis of a severe type. 112 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 (ante- 
rior cornua) remain paralyzed. There is no loss of sensation, 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 devel- 
opment of coldness in these areas, which is due to the destruction 
of the trophic centres in the spinal cord. 
Paraplegia resulting from tumor of the cord or its membranes 
only ensues when the growth is so placed as to cut off all the motor 
tracts supplying both limbs, which is rarely accomplished until after 
a long history of more or less well-developed motor and sensory 
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 chap- 
ter 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 irritation 
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 removal 
of the source of irritation. Even worms in the intestine have pro- 
duced such a paralysis, and their removal has been followed 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 exaggeration of the reflexes. Probably 
these severe cases are always due to a coincident myelitis rather 
than to a 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 THE FEET AND LEGS. 
113 
not only great loss of motion, but exaggerated or lost reflexes, relax- 
ation or spastic contraction of the muscles, anaesthesia and hyper- 
aesthesia, pain or no pain. The very occurrence of such irregular 
manifestations in a young, neurotic girl, the facts that the anaesthetic 
areas constantly tend to shift their position, and, finally, that the 
contractures, if present from hysteria, disappear on administering 
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 it is 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 hmmaturia or bloody 
stools may appear. 
Pseudo-paraplegia may occur in rickety children from faulty mus- 
cular and bony development. It is to be separated from the ordi- 
nary paraplegias of childhood by the state of the bones, the presence 
of knee-jerks, and the absence of local wasting or spasm, and 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 sen- 
sory disturbances and marked muscular and nerve-trunk tender- 
ness; 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, toxic neuritis produces loss of power in 
the arms. Very rarely paraplegia of the lower extremities results 114 
THE MANIFESTATION OF DISEASE IN ORGANS. 
from diabetes mellitus, the lesion being in all probability a multiple 
neuritis. 
Monoplegia of a lower extremity may be due to cerebral 
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- 
cental 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 amesthesia (see Skin), and the other hysterical 
signs, or a tumor pressing on the crural nerve in the pelvis, or sec- 
tion 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 darkened mass represents the site of the lesion.) 
Spinal cord 
Reflexes normal 
Band of hypersesthesia.... 
Band of anaesthesia 
Reflexes lost 
Motor palsy . 
Hypersesthesia 
Reflexes increased 
Temperature above that of the 
rest of the body 
Reflexes normal. 
Band of hypersesthesia. 
Band of anaesthesia. 
Motor power unaffected. 
Anaesthesia. 
Reflexes unaffected. 
Temperature same as that of 
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 de- 
generative changes. The most typical symptom of this lesion is, 
however, the crossed character of the sensory paralysis. That is to THE FEET AND LEGS. 
115 
say, there is loss of sensation in the limb opposite that in wdiich 
motion is lost, and in the limb in which motion is lost there is 
hvperaesthesia, so that the lightest touch may be very painful. The 
cause of 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 supposed heretofore. There is, however, a symmetrical band 
of anaesthesia round the body at the level of the lesions, and a 
similar band of hyperaesthesia above the lesions. The reflexes of 
the parts supplied by the diseased area are lost, but those supplied 
by the area below the lesions are increased as in ordinary myelitis. 
Very commonly 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 wabble, to use a crude term. This is 
sometimes called a “ Punchinello leg.” There is no tendency to  THE MANIFEST A TION OF DISEASE IN ORGANS. 
116 
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 
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 cere- 
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.) 
bral paralysis and anterior poliomyelitis are so clearly separated in 
well-marked cases that no error can be made, particularly if the his- 
tory 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 cere- 
bral and spinal diseases in the child. (Figs. 45 and 46.) In acute 
infantile paralysis of spinal origin the right lower extremity is most THE FEET AND LEGS. 
117 
frequently affected, after this, a close second, the left leg. Some- 
times 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 ex- 
clude 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 en- 
largement seems to be due to hypertrophy of all the tissues com- 
posing the foot, whereas, on the other hand, in myxoedema the foot, 
though enlarged, is puffed and swollen in appearance through hyper- 
trophy 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 metatarsal 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 118 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
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 
Fig. 47. 
Fig. 48. 
Pes equinus in a boy five years of age, from 
atrophy of tibialis anticus. (Sachs.) 
“Claw-foot” from atrophy of interossei 
and other intrinsic muscles of foot. (Du- 
CHENNE.) 
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 which affects the leg chiefly 
and rarely in volves the foot proper first. The extensor muscles of the 
toes lose their power, the interossei waste, the foot may be flattened 
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. This state of the foot must be carefully THE FEET AND LEGS. 
119 
separated 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 hyperextended, and the foot is very 
broad when viewed from side to side at the metatarsal joints. It 
is stated that this sign is considered characteristic of the early de- 
velopment 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 short- 
ening of the peroneus longus. (Fig. 49.) In other instances the 
Fig. 49. 
Fig. 50. 
Plantar surface exhibiting changes due to contracture of peroneus longus, shortening of 
transverse diameter, A, C, and torsion of foot, D. (Sachs.) 
deformities undergo marked changes as the disease progresses, so 
that they not 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 Fried- 
reich’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, 120 
THE manifest a tion of disease in organs. 
farther, that in neuritis there is no history of heredity. From 
poliomyelitis we separate it by the fact that in this peroneal type of 
paralysis the onset is more slow and by the fact that there is a loss 
of 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 elec- 
trical changes in the muscles. 
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 Figs. 49 and 52 hyperextension of the fingers and of the big toe is very striking. 
(Thomson and Bruce.) 
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. 
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.) THE FEET AND LEGS. 
121 
Wasting of the muscles of the inner surface of the foot affecting 
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 
there is strong extension, as 
in this figure. (Fig. 53.) 
A shrivelled, undeveloped 
foot and leg with drawing up 
and deformity are seen most 
commonly as the ultimate re- 
sult of the acute cerebral par- 
alysis of infancy. (Fig. 54.) 
Acute cerebral paralysis of 
infancy is to be separated 
from spinal paralysis of acute 
or subacute poliomyelitis an- 
terior of infancy, or the rare 
poliomyelitis 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 cerebral paralysis there 
are spastic rigidity and spastic contractures, no atrophy of the 
muscles, until by disuse or secondary changes in the cord the mus- 
cles 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 pecu- 
liarly lax, flabby, and lifeless; contractions with resulting deformity 
only arising from the action of healthy muscles robbed of their 
natural antagonists. The contractures of the leg which occur in 
acute infantile paralysis of spinal origin are not spastic, and are 
often only developed upon intention-movements or by the unop- 
posed healthy muscles. 
A very important form of contracture following paralysis or 
occurring without it, which is apt to lead to a mistake in diagnosis, 
Fig. 53. 
Tabetic foot. (Shingleton Smith.) 122 
THE MANIFESTATION OF DISEASE IN ORGANS. 
is that seen in hysteria (Figs. 55 and 57). As a rule, the contrac- 
tures come on in association with paraplegia. Sometimes, however, 
they affect the arms or an arm. It is a characteristic of these con- 
tractures due to hysteria that they set in 
suddenly, and are always accompanied by 
such hysterical symptoms as borborygmi, 
ovarian tenderness, and often areas of an- 
aesthesia. Weir Mitchell has divided these 
cases into two forms. The first only in- 
volves single parts or limited muscle-groups, 
and, though the contractures may last for 
years, joint- or muscle-changes do not occur. 
In the second class, one limb after another is 
attacked 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 ill- 
ness, the presence of anaesthesia (see chapter 
on Skin), and hyperesthesias. 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 in- 
volves antagonistic muscles. Sleep does not 
always cause a relaxation of hysterical con- 
traction, 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 joints. The muscular wasting under 
these circumstances may arise from neuritis, which is associated 
with the arthritis, but its cause is often difficult to discover. 
Very rarely universal muscular atrophy follows joiut-changes. 
The Joints. The joints of the lower limbs may be swollen from 
an arthritis arising from many causes, such as locomotor ataxia, 
hemiplegia, rheumatoid arthritis (arthritis deformans), acute mye- 
litis, cerebro-spinal meningitis, Morvan’s disease, septicaemia, or the 
Fig. 54. 
Shrivelled foot of infantile 
cerebral paralysis. (Hirt.) THE FEET AND LEGS. 
123 
Hysterical spasm and contracture, showing the condition of the affected leg in the recumbent position. (Bramwell.) 124 
THE MANIFESTATION OF DISEASE IN ORGANS. 
infectious processes, such as acute articular rheumatism and typhoid 
fever. 
The most marked alterations in the joints are those produced by 
advanced locomotor ataxia, and are called arthropathies. Often 
Fig. 56. 
Fig. 57. 
Fig. 56.—A case of universal muscular atrophy following arthritis. The right hand is a 
“seal-fin” hand. From the author’s wards 
Fig. 57.—Hysterical spasm and contracture, showing attitude in erect position. (Bramwell.) 
they are associated with spontaneous fractures of the bones. The 
knees are most commonly involved, then the ankles and hips. A THE FEET AND LEGS. 
125 
joint or several joints may become suddenly swollen with or without 
paiu, and without apparent cause until the swelling becomes quite 
massive. There are then developed osseous hyperplasia and a ten- 
dency to dislocation with crepitation on movement, and the ends 
of the bone become 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, leav- 
ing the articulating surfaces roughened, uneven, and deformed, but 
there are no deposits of urate of sodium as in gout, the deformities 
being due to alterations in the articulating surfaces themselves, and 
the periarticular development of bone. The disease always remains 
in the joint originally attacked, although new joints are involved. 
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 
involved varies greatly, but the involvement is generally sym- 
metrical. 
Sometimes this disease, which is generally gradual in its onset, 
becomes very acute, speedily involving many joints, causing swell- 
ing of the synovial sheaths and bursae, and being accompanied by 
some febrile movement. The suddenness of its onset, the febrile 
movement 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 signs 
of the disease renders its cause evident. The joints are many of 126 
THE MANIFESTATION OF DISEASE IN ORGANS. 
them affected simultaneously with swelling, paiu, and serous or 
purulent 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 
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 
offensive 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. 
Great swelling of the thigh or leg occurring in a child may be 
due to subperiosteal hsematoma (Moller-Barlow’s disease). Aspira- 
tion of the swelling will reveal the character of its contents, and 
the child will usually be a sufferer from rickets. 
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 : 
a. Arthralgic, in which there are wandering pains about the 
joints, without redness or swelling. These persist for a long time. 
b. 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 sev- 
eral become swollen and tender. In this form cerebral and cardiac 
complications may occur. 
c. Acute gonorrhoeal arthritis, in which a single articulation 
becomes suddenly involved. The paiu is severe, the swelling ex- THE FEET AND LEGS. 
127 
tensive 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 super- 
venes. 
d. Chronic hydrarthrosis. This is usually monarticular, 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 bursae and the periosteum. The articu- 
lations may not be affected. The bursae 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 long period unchanged in one joint, and is a process accompanied 
by fever. 
Although gout is capable of causing deformity in the lower 
extremities, it has one fact about it which is of practical impor- 
tance, namely, that it involves the small joints of the foot, while 
rheumatism attacks the large joints, such as the knee, by preference. 
Gout involves the feet most commonly, while rheumatism is more 
frequently 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, if possible, similar manifesta- 
tions in acute rheumatism, there is often an additional and per- 
manent cause of deformity in the chalk-stones which are deposited 
about the joints, and vdiich are never seen in rheumatism. The 
history of frequently recurring attacks lasting but a few days, accom- 
panied by enlargement 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 wre 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 far greater effusion into the 128 
THE manifestation of disease in organs. 
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 osteo-arthritis 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, 
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 pic- 
ture. 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 haemo- 
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 contrary, 
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 temperature 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- THE FEET AND LEGS. 
129 
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 per- 
forating ulcer of the foot occurs during the course of diabetes mel- 
litus, but it is probable in many such cases that locomotor ataxia is 
associated with diabetes. (Fig. 58.) 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 diagno- 
sis (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 
gangrene generally affects the 
inner side of the foot, espe- 
cially the big toe, and is a dry 
gangrene, renders the diag- 
nosis 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 exophthalmic goitre. 
More rarely gangrene of the foot and hand follows embolism due 
to cardiac valvular disease. It is usually a moist gangrene, ex- 
tremely painful, and septic fever may ensue. 
In this connection mention may be made of “ Madura foot,” 
or mycetoma, a chronic local disease of tropical climates, and called 
Fig. 58. 
Tabetic ulcer. (Suing leton Smith.) 130 
THE MANIFESTATION OF DISEASE IN ORGANS. 
u fungus foot disease” in India. A small tumor develops on 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. 
Ain hum is a disease peculiar to dark-skinned races, characterized 
by gradual drying up and separation of the toes (by a constric- 
tion), usually the little toe. It has been thought to be related to 
leprosy, but this is doubtful. 
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. PLATE I. 
FIG. 1. 
Chart of Localization of Cortical Centres determined on External 
Surface of Cerebrum. (Gray.) 
FIG. 2. 
Chart of Localization of Cortical Centres determined on Medial 
Surface of Cerebrum. (Gray.) CHAPTER IV 
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 hemi- 
plegia, 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 illness 
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 throm- 
bosis of some vessel supplying important areas. Still other causes 
of hemiplegia are brain-tumors, meningeal hemorrhage, degenera- 
tive 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 w’ith 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 governing 
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 
131 132 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Fig. 59. 
Diagram showing the fibres from the cortex forming the corona radiata, which after they are 
approximated pass into thednternal capsule. It also shows the decussation of the pyramid of 
the left side, which passes to the right side of the spinal cord, and the direct or uncrossed tract. 
Finally it also shows 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. (Modified from Van Gehuchten.) HEMIPLEGIA. 
133 
Fig. 60. 
Outline of horizontal section of brain, 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. OT, optic thalamus, showing the median, lateral, and anterior 
nuclei; NL, nucleus lenticularis, showing the putamen large, and the inner division of the 
globus pallidus very small; Ac, nucleus caudatus, the large head in front of and the dimin- 
ishing tail near the thalamus; O, the knee of the internal capsule. From “Eye" to “ Digits" 
marks the position of the pyramidal tract as a whole, and the several letters indicate broadly 
the relative positions of the several constituents of the tract, named according to the 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 Reil, and the operculum or convolution overlapping the 
island of Reil. P is inserted to show which is the hind part of the section. 134 
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 
(the corona radiata). Thus we see in Plate II. how the fibres arising 
from the middle area of the cortex cerebri pass down through the 
Fig. 61. 
-Posterior 
division 
of Sylvian 
fissure. 
-Temporo- 
splienoidal 
lobe. 
(After Gray.) 
lenticular nucleus into the knee or angle of what is called the inter- 
nal capsule. This is a lateral view. In Fig. 59, which also shows 
the results of a lesion in the capsule, we get an antero-posterior view. 
These fibres are arranged in such a way that those arising from the 
lower part of the cortex, as in the face-centre, lie nearest the knee PLATE II. 
Diagram showing Course of Motor Fibres from the Cerebrum 
and Cord to the Periphery. (Flatau.) HEMIPLEGIA. 
135 
of the capsule, and those highest, furthest from this point. (Fig. 
60.) After the motor fibres have passed through the internal cap- 
sule they pass into the crus cerebri of that side, which (the crus 
cerebri) connects the hemisphere of the same side with the cerebel ■ 
Fig. 62. 
Diagram showing the general arrangement of the motor tract and the effect of lesions at 
various points. (Obmekod.) 
lum 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. 61), diverge as 
they pass upward and outward to enter the under part of each hemi- 
sphere, as if stretching out to receive the motor fibres from the inter- 136 
THE MANIFESTATION OF DISEASE IN ORGANS. 
nal capsule. From the crura cerebri the motor fibres pass downward 
into the pons Varolii. Here the fibres which have hitherto travelled 
together divide into two parts, namely, those from 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, 
Fig. 68. 
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 II the hypoglossus would be affected on one side, with hemiplegia on the other. (Modified 
from Ed ingee.) 
leg, and trunk of the body, which continue on down to the medulla 
oblongata, where they form the so-called pyramids, and having 
done so most of the fibres cross to the opposite side of the spinal 
cord (the crossing of the pyramids), and so form the crossed or lateral 
pyramidal tracts. (Fig- 59-) A smaller number of fibres, how- HEMIPLEGIA. 
137 
ever, pass directly down to the spinal cord from the medulla oblon- 
gata, and form what is called the direct or anterior pyramidal tract. 
Direct, because it does not cross; anterior, because it lies along the 
edge of the anterior fissure of the cord; pyramidal, because it conies 
down from the pyramid. This is sometimes called Tiirck’s column. 
(Fig. 59.) It is by means of these two tracts in the spinal cord 
that motor impulses pass down to the nerve-trunks and muscles. 
Fig. 64. 
Showing tracts in spinal cord. 1. Anterior horns of gray matter, which contain the cells 
governing the nutrition of the muscles and give rise to the motor roots. 2. Posterior horns of 
gray matter, which receive the sensory roots. 3. Crossed lateral pyramidal or chief motor 
tracts from cortex of brain. 4. Columns of Burdach, or the outer sensory tracts, carrying 
impulses upward. 5. Columns of Goll, or inner sensory tracts, carrying 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 Tiirck, or direct anterior pyramidal tract, which carries impulses of 
motion downward. 9. Lateral mixed tracts same as 7. 
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. Tims, as seen in 
Fig. 62, a clot at the arm-centre would only involve the arm-fibres. 
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 138 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
widely separated areas in the body, and, if large enough, produce 
hemiplegia. (Figs. 62 and 63, lesion A.) If the lesion be situated 
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. 62 and 63, M), it will, under these circumstances, 
destroy the facial fibres after they have crossed, and the remaining 
motor fibres before they cross. The various tracts, motor and sen- 
sory, in the spinal cord are shown in Fig. 64. 
Fig. 65. 
Diagram of the arteries of the base of the brain, showing, LO., the lenticular optic, and, LS., 
lenticular striate set of arteries. One of the latter is called the artery of cerebral hemorrhage. 
V. Arteria vertebralis. S.a. Spinalis anterior. S.p. Spinalis posterior. B. Basilaris, with 
median branches. C.b.s. Cerebralis superior. C.i. Cerebelli inferior. C.p. Cerebralis posterior 
(profunda cerebri). C.o.m. p. Communicantes posteriores. C.ci.i. Carotis interna, o. Ophthal- 
mica. C.m. Cerebralis media (A. fossae Sylvii). i. Insularis. cst. Corp striati. C.a. Cerebralis 
anterior. C.o.m. Communicans anterior. C.c.a.ll. Corp. callosi. (Dkrcum.) 
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 
decreased and the deep reflexes increased, but the bladder and rec- 
tum are not usually paralyzed, although in the first shock of the 
accident there may be vesical and rectal incontinence. The mental HEMIPLEGIA. 
139 
disturbance usually amounts to a rapidly oncoming unconsciousness 
in hemorrhagic hemiplegia. 
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 de- 
scribed. 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 
perforates the internal capsule, and ends in the caudate nucleus, and 
this artery is so commonly ruptured that Charcot has called it the 
“ artery of cerebral hemorrhage.” (Fig. 65.) 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 
paralysis 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. 60.) The 
symptoms associated with hemiplegia due to this cause often become 
very severe, because the hemorrhage is so profuse that the lateral 
ventricles become filled with blood, and from them the blood passes 
to the third and from there to the fourth ventricle, where, by press- 
ure on the vital centres, it speedily produces death. In such cases 
deep unconsciousness, stertorous breathing, a slow, full pulse, and a 
flushed skiu, becoming somewhat cyanotic, may be present. Recov- 
ery never occurs, for the secondary inflammation, or softening, fol- 
lowing 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 pro- 
truded may tend to go over to one side. If the case does not pass 
to such favorable results, instead of recovery of power at this time 
there are developed contractures and seoondary rigidity from degen- 140 
THE MANIFESTATION OF DISEASE IN ORGANS. 
erative processes extending to the pyramidal tracts. (See Fig. 59.) 
Hitzig has shown that these conditions are apt to be least marked 
in the morning. Wasting of the paralyzed muscles only ensues 
from the disuse, and not from true 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 backward 
till it involves the sensory fibres in the internal capsule, and, finally, 
breaks into the lateral ventricle, soon after which death ensues. 
When a hemiplegia is followed by rigidity very early, with sen- 
sory 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 
commonly, 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 convulsions, with 
difficulty in swallowing and in speech, the lesion is to be found in 
the pons Varolii on the side opposite the paralysis. This is due to 
the fact that the injury is below the decussation of the facial nerve. 
(Figs. 62 and 63.) 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 gid- 
diness, vomiting, conjugate spasm with nystagmus, albuminuria, 
glycosuria, and marked disturbances in the respiration and heart. 
Pontile hemorrhages are, however, very rare, and usually are rapidly 
fatal. HEMIPLEGIA. 
141 
Finally, if there is hemiplegia involving the lower part of the 
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 sen- 
sibility and vasomotor changes in the limbs, the lesion is probably 
in the crus cerebri on the side of the upper facial paralysis—that 
is, on the same side as the ptosis; but this is only true if the two 
paralyses have been 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 
hemianesthesia (see chapter on Skin), and hemianopsia (see chapter 
on Eye). Generally, however, such changes result from a thrombus. 
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. Some- 
times the leg is from the beginning more affected than the arm, and 
remains paralyzed long after the face and arm have recovered. 
The leg may become rigid and distorted by contractures, and there 
will often be found present marked anaesthesia of the skin of the 
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 
result from rupture of the lenticulo-optic artery. When the arm 142 
THE MANIFESTATION OF DISEASE IN ORGANS. 
suffers most the symptoms just described as in the leg are seen in 
it, and motor aphasia, if the lesion is ou 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 cap- 
sule. 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 ou. The presence of hemiplegia in a young man, therefore, is 
probably not due to a thrombosis. Again, hemorrhage occurs often 
after exertion or the drinking of stimulants, and occurs rarely in 
sleep, whereas thrombosis not rarely comes on under these circum- 
stances, and often develops during the night, so that the patient 
awakes paralyzed, but a patient may have both thrombosis and apo- 
plexy. In hemorrhage, consciousness is generally lost, whereas in 
thrombosis 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 hem- 
orrhage than in thrombosis. The history of syphilitic infection, 
producing an endarteritis, also points to thrombosis, although hem- 
orrhage may arise from this cause also. 
The diagnosis of embolism producing hemiplegia from the paral- 
ysis due to hemorrhage is always more or less difficult, but the pres- 
ence of chronic or ulcerative endocarditis or their results, or other 
cause for the formation of emboli, aids the diagnosis. Where 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 HEMIPLEGIA. 
143 
history, to have come on gradually. Thus, the history may be that 
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 
intense 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 twitellings 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 dissemi- 
nated sclerosis, the pathological process involving the side of the 
pons and spinal cord, but the intention-tremor, the peculiar speech, 144 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the nystagmus, and the very excessive reflexes aid us in the diag- 
nosis of this cause of the loss of power. (See chapter on Hands 
and Arms, part on Tremor.) 
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 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 ursemia. 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 pysemic 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 V. 
THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
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— 
Tonsillitis—Diphtheria—Pharyngitis—Disease of the oesophagus. 
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 
physician 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 
movements. 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 becmes 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 mauy 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 fungiform or medi- 
ate, 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 ante- 
rior surface of the tongue, are very minute, and arranged in lines 
corresponding in direction with the two rows of the circumvallate 
papillae. From their apices project many fine, filiform processes 
which are of a whitish tint owing to the density of the epithelium 
145  THE MANIFESTATION OF DISEASE IN ORGANS. 
146 
of which they are composed. There are, in addition, many simple 
papillae which cover the surface between the peculiar ones already 
described. The fungiform papillae are those seen most commonly 
in cases of disease, for they become large and prominent, and be- 
cause 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 consist 
of dead epithelial cells, micro-organisms of many kinds, and abnor- 
mally shaped living epithelium. Small particles of food may also 
be present. Butlin believes that the coating is chiefly due to micro- 
organisms. The question as to how characteristic of a particular 
disease any one coating or fur may be has been warmly discussed. 
Some have gone so far as to assert that the coating of the tongue 
is not indicative of any state in particular, while others, of whom 
the author is one, are convinced that, while an absolute diagnosis of 
disease in other organs cannot be based upon the appearance of the 
tongue, great aid can be gained by its study. 
There are, however, very few conditions of the coating of the 
tongue which are pathognomonic of any one disease, since 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 circumvallate 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 tips 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 derangements, depends chiefly on three factors: 
first, immobility of the tongue, so that it is not kept clean by rub- 
bing; 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 sali- 
vary secretion. Additional local causes are a decayed or ragged 
tooth or follicular tonsillitis, which infects the lingual epithelium, 
lack of cleanliness, and habits, such as smoking. In the last class PLATE III. 
Fig. 1. 
Fig. 2. 
Typhoid Tongue. 
Bilious Tongue, with Yellow Coating. 
Fig. 8 
Fig. 4. 
Tongue of Mucous Disease or Chronic 
Catarrh of Stomach. 
Tongue of Chronic Gastric Catarrh 
with Anemia. THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
147 
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 coat- 
ing 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, which 
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 conva- 
lescence is established; but if the disease runs a severe course, the 
coating becomes very heavy, more dry, rough and brown from expo- 
sure to air and medicine. The furred appearance becomes almost 
shaggy at the back portion, and the drying proceeds until the under- 
lying epithelial layer is cracked and fissured, so tnat tiny exudations 
of blood add to the lingual discoloration. The reddened edges 
become dusky in hue, and may be cracked and fissured also. (Fig. 
1, Plate III.) The tongue is very slowly protruded on request, 
partly from mental apathy, partly from feebleness and because its 
surface is so stiffened that to move it is difficult. It is equally 
slowly withdrawn for similar reasons, and while protruded is often 
markedly tremulous. Toward the close of the attack the tongue 
cleans off through exfoliation of the dead epithelial accumulation, 
and this is a favorable or unfavorable sign according to whether the 
remaining surface is red and moist or dusky and dry. Sometimes 
these characteristic 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 simi- 
lar 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 148 
THE MANIFESTATION OF DISEASE IN ORGANS. 
cases, because, as Fothergill asserts, the coat has been stained by 
the taurocholic acid eliminated by the salivary glands. The cir- 
cumvallate papillae are often prominent and stand above the coat- 
ing, 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 a person who takes 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 circum vallate 
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 membranes. (Fig. 3, Plate III.) 
If, on the other hand, there is a comparatively light coating, dotted 
irregularly by bright-red spots, which are not raised above the sur- 
face, but are very numerous, and the patient is a child, the diag- 
nosis 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 THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
149 
fungiform papillae, which have been deprived of their epithelial 
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 covered 
by an excess of living and dead epithelial cells; it may denote grave 
disease of the viscera, but in rare instances possesses no diagnostic 
importance, unless coupled with other symptoms. This tongue is 
sometimes seen in scrofulous children in whom strumous manifesta- 
tions are marked. 
Should the tongue be denuded not only of coating, but, in addi- 
tion, of its normal epithelium, so that it appears dry, hard, and 
harsh to the touch, it denotes, as a rule, grave and advanced disease 
of an exhausting nature, such as renal, hepatic, or gastric disorder 
about to cause the death of the patient. Sometimes this condition 
is seen in advanced phthisis or gastric carcinoma, and is of evil 
omen. When 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 dis- 
comfort of cases of advanced pulmonary tuberculosis or acute peri- 
tonitis. 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- 150 
THE MANIFESTATION OF DISEASE IN ORGANS. 
stances as to be entirely changed in appearance. If the coating be 
black, the color may be due to the ingestion of iron, of bismuth, 
charcoal, ink, or blackberries, mulberries, cherries, or red wine. 
In very rare cases it is black, not from the growth of a fungus, as 
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, 
from licorice, nuts, 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 haemoglo- 
bin, 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 
difficulty. 
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 papillae at the base are unusually large. 
When sulphuric acid has been swallowed the tongue has a parch- 
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 it are brownish if impure acid has been swal- THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
151 
lowed, or white if the pare acid has been taken. In the course of 
a few hours this spot becomes surrounded by a red zone, and finally 
becomes dark brown or black in the centre. After 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. Can- 
tharidal poisoning produces large lingual blisters and sores. 
Aside from the coating and color of the tongue, its surfaces 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 furrows are 
very deep, they may indicate the early stages of what Wunderlich 
has called dissecting-glossitis, which in turn may be due to syphilis,1 
although, as a rule, the fissures of the tongue due to syphilis are 
deepest at the edges of the organ, and are due to pressure by and 
from irritation from the teeth or to ulceration, and subsequent cica- 
trization of small syphilitic nodules or gummata. The cervical 
glands are rarely involved in such cases. If only one ulcer is 
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 
syphilitic ulcers heal sclerosis of the tongue may develop. 
Multiple ulceration of the tongue may be due to tubercular dis- 
ease, which is very rarely primary, but rather secondary to its 
1 This is denied by Demarquay and doubted by Butlin. 152 
THE MANIFESTATION OF DISEASE IN ORGANS. 
presence elsewhere. The sores are often stellate in shape, and there 
is always swelling of the cervical lymphatics, whereas in multiple 
syphilitic ulceration of the tongue the glands generally escape. The 
diagnosis between tubercular ulcer and that due to epithelioma is 
more difficult, since in both diseases the cervical glands are 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 rarely to lupus. A 
very similar tongue is seen in a tropical disease with intestinal 
disorder called by Thin 11 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 with 
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 glosso-labio-pharyngeal paralysis.1 
The surface of the tongue may be attacked by various eruptions, 
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, PHARYNX, AND (ESOPHAGUS. 
153 
such as measles, variola, eczema, herpes, erysipelas, pemphigus, 
zoster, or hydroa, and from the rupture of the vesicles or bullse so 
formed ulcers may arise. 
If the sore is herpetic, de Mussy asserts that the eruption will be 
found in the distribution of the lingual branch of the chorda tym- 
pani 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 some- 
times called “smokers’ patch.” It may extend over the whole 
tongue and last for years. 
When the tongue has on its dorsum and edges dull-white or slate- 
colored dots, patches, or lines, which are elevated, hard and horny 
to the touch, but not painful, the condition is known as leucokera- 
tosis 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 commonly 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 154 
THE MANIFESTATION OF DISEASE IN ORGANS. 
marked by rings or areas on the dorsum, which gradually enlarge 
until they reach the edge or coalesce. In appearance they are red 
and smooth, deprived of filiform papillae, but not of the fungiform 
variety. Often the border of the circle is more red than the centre, 
and the very edge is often yellowish. This condition is sometimes 
called wandering rash, geographical tongue, or annulus migrans. 
Little if anything is known of its cause, save that delicate children 
are most often affected by it. 
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. 
(Edema of the tongue, with the development upon it of vesicles, 
and, finally, sloughs, may occur, and is probably identical with the 
foot-and-mouth disease of domestic animals. 
Bilateral atrophy of the tongue is due to disease affecting the 
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 and 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 involv- 
ing 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 may 
also be due to dermoid cysts, fibroma, lipoma, papilloma, angioma, 
myxoma, osteoma, and enchondroma. When it is due to acute 
glossitis 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, MOUTH, PHARYNX, AND (ESOPHAGUS. 
155 
The tongue may be greatly enlarged by actinomycosis, this condi- 
tion in olden times being called angina Ludovici. Great enlarge- 
ment 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 to move parts of the body fail to produce a response. In the 
various forms of coma due to apoplexy, diabetes, ur£emia, and cere- 
bral congestion, this condition obtains, and it is very characteristic 
of typhoid fever. Often the tongue which has been partially pro- 
truded 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 be- 
tween the teeth and cheek by means of his tongue, and complains 
that the power of speech is interfered with, because the tongue is 
clumsy in its movements, he may be suffering from the disease known 
as glosso-labio-pharvngeal paralysis or progressive bulbar paralysis. 
These lingual disorders are often the earliest signs of the disease. 
More rarely this disability of the tongue may arise from pseudo- 
bulbar paralysis, or what has been called glosso-labio-pharyngeal 
cerebral paralysis, a disease in which foci of softening occur in that 
portion of the cortico-muscular tract in which are the fibres which 
supply the muscles used in swallowing and speaking. This false 
type is separated from the true bulbar palsy by its sudden onset, an 
apoplectiform seizure, and other evidences of cortical disease. The 
tongue affords the most important points for differential diagnosis 
when a differential diagnosis is to be made under these circum- 
stances, for in the false disease it does not waste or develop the 
reactions of degeneration, whereas in true bulbar paralysis these 
changes always speedily develop. 
Paralysis of the Tongue. In apoplexy the tongue is protruded 
toward the paralyzed side, as it is also in the condition, already 
described, of hemiatrophy. The lesions of the hypoglossus which 
produce paralysis may be of cortical origin (unilateral), in which 
case the hemorrhage or other injury may be situated where the 
middle and inferior frontal convolutions form the anterior central 156 
THE MANIFESTATION OF DISEASE IN ORGANS. 
convolution,1 or in the supra-nuclear tract between the cortex and 
the medulla, or in the hypoglossal nucleus, or, again, in the intra- 
nuclear tract within the medulla. Insular sclerosis may very rap- 
idly cause lingual paralysis. Paralysis of the tongue may also 
result from injury to the hypoglossal fibres outside the medulla 
through meningitis or syphilitic or other growths. In still other 
cases pressure upon the nerve in its foramen may cause unilateral 
paralysis, or wounds of the neck, caries of the first cervical verte- 
brae, or cervical tumors may so result. Often in such a case the 
spinal accessory nerve is also involved. Very rarely, indeed, the 
tongue may be paralyzed by a hypoglossal neuritis (Erb). In rare 
instances hemiatrophy of the 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 situated that even a small lesion involves both of them, or 
it may be due to symmetrical disease of both sides of the cortex, 
the so-called pseudo-bulbar paralysis already spoken of. 
It should not be forgotten that paralysis of the tongue may occur 
as the result of diphtheria. 
Hirt asserts that the reaction of degeneration may be found in 
the tongue whether the lesion be cortical or in the nucleus. If the 
lesion is only cerebral, this reaction will probably 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, PHARYNX, AND (ESOPHAGUS. 
157 
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 move- 
ments 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 associated with this tremor it will be noted that 
the protrusion of the organ is uncertain or in jerks. 
Spasm of the tongue may be unilateral or bilateral, most com- 
monly the latter. It is seen very commonly in cases of chorea, 
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, 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. 158 
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. 
We can sometimes gain some information from the teeth as to 
the state of the patient. Normally the two lower central incisors are 
cut about the sixth to the eighth month, then the four upper incisors 
from the eighth to the tenth month, and the lower lateral and all 
the front molars from the twelfth to the fourteenth month. The 
canines are cut from the eighteenth to the twentieth month, and 
the posterior molars at two to two and one-half years. The first 
permanent teeth usually begin to come in about the sixth year. In 
children who are sufferers from rickets the teeth decay very early 
and rapidly, and if they be sufferers from inherited syphilis, the 
teeth are often cut in the early months of extra-uterine life. 
Caries of the teeth to an undue extent is also seen in many preg- 
nant women and in cases of diabetes mellitus. 
Fig. 66. 
Hutchinson teeth. 
If the permanent upper incisors are notched or peg-shaped 
with notches in the free edge, as if cut out with a small gouge, they 
are a fairly sure indication of syphilis of an 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.” 
The staining of teeth by tobacco or other materials held in the 
mouth may reveal certain habits of the patient, and a blue line on 
the gums where they join the teeth is an indication of the presence 
of chronic lead-poisoning. Loosening of the teeth, with bleeding, THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
159 
spongy gums should call to the physician’s mind the possibility of 
scurvy or scorbutus, and the spongy gums are particularly indica- 
tive of this affection in bottle-fed babies. If loosening of the teeth 
occurs in adults, it may be due to mercurial salivation. 
Grinding of the teeth in sleep in children usually indicates gastro- 
intestinal irritation from indigestion or worms, and it is sometimes 
seen in the advanced stages of respiratory diseases, as from pneu- 
monia or diphtheria associated with dyspnoea. It takes place in 
adults in hysteria, maniacal attacks, and in epilepsy. 
Difficulty in swallowing may arise from involvement of the 
pharyngeal muscles in diphtheritic paralysis, or from glosso-labio- 
pharyngeal paralysis (see chapter on Face, or retro-oesophageal 
abscess). Much more commonly it results from tonsillitis or phar- 
yngitis. Not rarely it is due to a stricture of the oesophagus, and 
sometimes to a morbid growth in the walls of this tube, or to the 
pressure of such a growth situated in the surrounding tissues. If 
the difficulty in swallowing is due to diphtheritic paralysis the his- 
tory will be that there had recently been an attack of diphtheria. 
If due to a lesion of the bulb there will be the symptoms described 
in the chapter on the Face, as referred to above. The presence of 
an inflammation of the pharynx or the tonsils is easily discovered 
by observation of the back part of the mouth, as is also retro- 
oesophageal abscess, which will generally be found associated with 
disease of the cervical vertebrae. If these states be excluded the 
diagnosis now lies between a stricture and a growth, and as the 
growth may be an aneurism the patient’s chest should be carefully 
examined and the other signs of aneurism sought for, for should 
this be overlooked and an oesophageal sound passed, the aneurism, 
if present, may be ruptured. This examination may also disclose 
the existence of a mediastinal growth or enlargement of the retro- 
oesophageal glands. If these causes be eliminated the actual search 
for stricture may be begun. First the physician should listen over 
the cardiac orifice of the stomach while the patient takes a swallow 
of water. If the act of swallowing is properly performed this 
single swallow of water will be heard to descend to the cardiac 
orifice, and then pause there for six seconds before it falls into the 
stomach. If there is a stricture this fall will be delayed ; if there 
be atony of the cardia it will be hastened. An ordinary oesopha- 
geal bougie may be passed. If a point of resistance is discovered 
that part of the bougie-stem opposite the upper incisor teeth is 160 
THE MANIFESTATION OF DISEASE IN ORGANS. 
marked, and then the instrument is withdrawn. In this manner we 
are enabled to tell the part of the oesophagus affected. Ordinarily 
the distance from the upper incisors to the cardia is, in adults, 40 
centimetres, and from the incisors to the beginning of the oesophagus, 
15 centimetres. From the teeth to the point where the oesophagus 
crosses the bronchus the distance is 23 centimetres. 
If a stricture exists it may be due to a cicatrix the result of an old 
burn, from the ingestion of alkalies or acids, or from an ulcer due 
to another cause. In other cases the lesion is due to syphilis. 
If the obstruction be due to cancer the passage of a bougie may do 
great damage, and, therefore, if any intimation of the existence of 
such a growth is present, great gentleness must be used. It should 
also be remembered that the bougie may be arrested by its passage 
into a diverticulum, or, in other cases, the instrument, by coiling on 
itself, may give a wrong impression as to the site of the obstruction. 
If a diverticulum is present the food which is obtained from it is 
usually alkaline, as it has never entered the stomach, and milk 
derived from a diverticulum, in which it has tarried a short time 
after attempted swallowing, will not be coagulated. 
Finally, the physician should not forget, if his patient be a young 
woman, that there may be hysterical spasm of the oesophagus. 
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 Avhich 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 THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
161 
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 
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 
bleeding surface behind it, and it has not the dusky, dirty look of 
diphtheritic 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 examination of the throat in scarlet fever shows the intense 
redness of the pharyngeal mucous membrane with comparatively 
slight enlargement of the tonsils. The intense redness of the throat 
in scarlatina and the development of the rash on the skin aid in 
making a differential diagnosis. The lymphatic glands of the neck 
may be enlarged in scarlet fever, but are rarely so in tonsillitis. 
If the patient complains of dysphagia, and, on examination, the 
pharynx is red and the tonsils are covered with patches which 
speedily spread, as just described, so that by forty-eight or seventy- 
two hours the tonsils, pillars, and soft palate are covered by a gray 
membrane, the case should always be diagnosed as diphtheria and 162 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 differentiation 
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, often 
exist simultaneously. Rarely the formation of a false membrane 
due to streptococcus 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 
becomes 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 distinguished 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. THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 
163 
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 (see illustration in chapter on Face), 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. 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—Retinitis—Amblyopia and blindness. 
The eye affords more information for diagnostic purposes con- 
cerning the condition of other organs of the body than any single 
part which can be examined. We gather from it not only a clear 
idea as to its own state, and the state of the nervous centres more 
or less intimately connected with the government of its movements 
and its special functions, but in addition we often gain positive 
information 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 the 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 con- 
junctival hemorrhage may result from violent coughing. In old 
persons such a hemorrhage, if not due to injury, may indicate 
degenerative 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 find more or less enlargement of the thyroid 
gland, an irritable heart, and a very rapid pulse, throbbing carotid 
arteries, marked general nervousness, often mental depression, and 
insomnia. In well-marked or advanced cases of exophthalmic goitre 
164 THE EYE. 
165 
we often have a condition in which the upper eyelid does not follow 
the eyeball in its downward movement. This is sometimes called 
u Graefe’s symptom.” Again, there may be almost total absence 
of winking as an involuntary act, u Stell wag’s symptom.” Or, 
again, there is insufficiency of convergence, so that a near point 
cannot be seen with both eyes 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 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. Such a pupil is also seen in 
fright, in some hysterical seizures, and in glaucoma and whenever 
the vision is lost, unless the pupil be contracted by disease of the iris. 
A contracted pupil indicates the use of a myotic or the existence of 
central nervous 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 differen- 
tiate the condition from true coma, in which the pupils are usually 
dilated. If, however, the coma be due to cerebral inflammation or 
meningitis, the pupils may be contracted; or if it be due to intra- 
cranial pressure, they are usually dilated. (See Paralysis of the 
Intraocular Muscles.) 
In addition to these objective symptoms we have also a very 
important 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. 166 
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 im- 
pression made on the well side is the “ true image,” as it is called, 
and that in the diseased eye is called the “ false image.” Any 
cause which interferes with the fixation of each eye on the same 
point produces dipolpia, 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 
diplopia—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 
diagnosis 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 pal- 
pebrse is particularly apt to be paralyzed in this disease, we may 
find ptosis. 
Diplopia is also found in cases of ptomaine-poisoning, and in 
poisoning by belladonna, spigelia, conium, and gelsemium, owing 
to their effects on the ocular nerves. THE EYE. 
167 
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 
maintain the horizontal equilibrium of the eyeball. If the internal 
rectus is completely paralyzed in one eye, we have developed a uni- 
lateral external squint, the eye looking toward the outer side of the 
orbit; and if the external rectus fails, the eyeball is turned toward 
the nose. If these muscles are affected in both eyes, we have a 
divergent squint in the first case and a convergent squint in the 
second. Not only do the muscles of each eyeball govern the eye- 
movements of that side, but by the nervous centres governing the 
eye-muscles the two sets of eye-muscles are co-ordinated, so that 
they move as one organ in health. 
Just here it is well for the reader to make a clear distinction 
between concomitant and paralytic squint, for they are two very 
different things in origin, symptoms, course, and prognosis. A 
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 mus- 
cles which are paralyzed in whole or in part. When the attempt 
1 In the preparation of this chapter free use has been made of the article of my friend, Dr. 
de Schweinitz, on “ Diseases of the Cranial Nerves,” in Dercum’s “Nervous Diseases.” 168 
THE MANIFESTATION OF DISEASE IN ORGANS. 
is made, the eye with the sound muscles turns as it should, while 
the eye with a 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 
degree 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 
approaches his 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 internus 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 or ten 
inches from the eyes and below the horizontal, and one eye is covered 
by a card or 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 insuffi- 
ciency 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” (Randall). If 
the internus is insufficient, and the covered eye moves in to fix in 
several distinct impulses, each impulse should be multiplied into 
the foregoing result. 
A very useful, and the simplest, apparatus for testing the func- 
tional balance 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 should “ 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 
[vertically] through the flame, there is orthophoria (equipoise), as 
far as the horizontal movements of the eyes are concerned. Should THE EYE. 
169 
the line lie to either side of the flame, as in most people it will, 
there is either latent convergence or latent divergence: the former 
if the line is the same side as the rod (homonymous diplopia), the 
latter if to the other side (crossed diplopia).” (Maddox.) (Fig. 67.) 
Fig. 67. 
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 frame. 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. 68.) 
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 glases, 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. 
170 
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 68. 
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 oeular muscles consist in the fol- 
lowing 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 moves 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 
erroneous localization of the objects in the field of vision. Altered 
carriage of the head, due to the fact that the patient tries to turn 
his head in the direction in 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 THE EYE. 
171 
must be made by a study of the double images. This is made by 
placing before the patient, at a distance of from three to five yards, 
a caudle 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 are 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 diplo- 
•pia being present if other muscles are used. Again, the image which 
Fig. 69. 
Paralysis of left abducens in a case of hemiplegia of syphilitic origin. (Dercum.) 
belongs to the affected eye is projected in the direction toward which 
the paralyzed muscle normally turns the eye, and, finally, the dis- 
tance 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 aud at the 
level of his eyes, the double images of two candles will appear 
as in Fig 70, 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. 71. Further, if the 172 
THE MANIFESTATION OF DISEASE IN ORGANS. 
object is moved to the right in the first condition, the false 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 diplopia, because 
the word homonymous indicates that the false image is seen on the 
same side as the eye affected. 
Fig. 70. 
Fig. 71. 
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. 72, the internal rectus of the left eye is para- 
lyzed, 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 be to the left side of the true one. (Fig. 73.) Further, if the 
object is moved to the right in the first case, the two images sepa- 
rate more and more widely; or if the right interims is involved, 
and the object is moved to the left, the same thing occurs. This is 
called crossed diplopia, because the image of the right eye appears 
on the left side, and the image of the left eye appears on the right 
side. 
Fig. 72. 
Fig. 73. 
Fig. 74. 
Fig. 75. 
The false image is in outline, (de Schweinitz.) 
Supposing, again, that the images are seen as in Fig. 74, then the 
left superior rectus is involved (downward squint); while if they 
appear as in Fig. 75, 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. THE EYE. 
173 
If the images appear as in Fig. 76, the left inferior rectus is 
affected; or if as in Fig. 77, the right inferior rectus muscle. This 
is also crossed diplopia, chiefly in the lower field, because the infe- 
rior rectus muscle rotates the eyeball downward. 
Fig. 76. 
Fig. 77. 
The false image is in outline, (de Schweinitz.) 
Again, if the images appear as in Fig. 78, 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. 
79. 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. 80; and if as in Fig. 81, the right is affected. There is 
an upward and inward squint, and there is a homonymous diplopia 
chiefly in the lower field. 
Fig. 78. 
Fig. 79. 
Fig. 80. 
Fig. 81. 
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. 174 
THE MANIFESTATION OF DISEASE IN ORGANS. 
1. Homonymous diplopia indicates paralysis of an external rectus. 
a. Images separating to the right indicate paralysis of the ex- 
ternus of the right eye. 
b. Images separating to the left indicate paralysis of the externus 
of the left eye. 
2. Crossed images indicate paralysis of an intern us. 
a. Images separating to the right indicate paralysis of the inter- 
nus of the left eye. 
b. Images separating to the left indicate paralysis of the inter- 
ims 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 
oblique 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 oblique. 
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 mus- 
cles are defective, we must determine the diagnostic indications pre- 
sented by this examination. In other words, we must seek the 
cause of the paralysis or loss of power. 
Paralysis of the ocular muscles may be due to a lesion in one of THE EYE. 
175 
several places. Thus it may arise from 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, aris- 
ing from syphilis, tuberculosis, ptomaine-poisoning, alcoholic and 
sulphuric-acid poisoning. Such cases are usually rapidly fatal. 
A less fatal form follows injuries, and the effects of nicotine, lead, 
carbonic acid, or such diseases as diabetes, syphilis, and epidemic 
influenza. Sometimes 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 unsym- 
metrical, 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 locomotor ataxia, paretic dementia, disseminated sclerosis, pro- 
gressive muscular atrophy, chronic bulbar paralysis, and in connec- 
tion with paralysis of the frontalis and orbicularis palpebrarum, 
which are innervated by the facial nerve. The cause may be tuber- 
culosis or syphilis, but in some cases no cause can be found. 
If the cause of the paralysis of one or two muscles be basilar 
lesions, these may arise from hemorrhage, pachymeningitis, menin- 
gitis, both simple and tubercular, chiefly the latter; purulent men- 
ingitis, abscess as the result of middle-ear disease, and ansemia. 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. 176 
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?1 
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. 82.) 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 sphe- 
noid bone, passes through the clinoid process, enters the cavernous 
sinus, and, finally, enters the orbit through the sphenoidal fissure 
between the heads of the external rectus. If this form of squint 
is 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. 
177 
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. 82. 
The base of the brain and the cranial nerves, crura, pons, and medulla. (Allen Thompson.) 
I to All. 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. 
Jl. 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. 83.) Complete paralysis of the 
externus may, therefore, be due to a nuclear lesion; for if the lesion 178 
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 
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. 
Fig. 83. 
Semicircular 
Canals 
Diagram of the connections of the nucleus of the sixth nerve. (Bruce.) 
Again, let us suppose that the internal rectus is paralyzed, caus- 
ing 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. 82.) 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. 84, after Bruce, where, how- THE EYE. 
179 
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 brandies enters the orbit through the sphenoidal 
fissure. The upper branch supplies the superior rectus and the 
levator palpebrse, 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. 84. 
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, iii.r. Third nerve. M. Median nucleus, a. Anterior 
nucleus, interior part. ax. Anterior nucleus, lower part of main nucleus. a2. Anterior 
nucleus, intermediate portion. a3. Anterior nucleus, upper portion, p.i. Postero-internal 
nucleus, p.e. Posterior-exterior 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.j, iv r.j, 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 
paralysis, 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 180 
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 hemi- 
plegia of the opposite side of the body, the lesion, according to 
Mauthner, probably affects the fascicular fibres—that is, those 
between the cortex and the nuclei. There may be associated with 
this form of oculomotor paralysis loss of power in the hypoglossal 
and facial nerves. On the other hand, if the oculomotor paralysis 
is complete, the lesion is almost certainly at the base of the brain, 
and this diagnosis becomes practically certain if there is associated 
with it paralysis of other cranial nerves. Paralysis of the 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 approx- 
imated that they are readily involved together. It will be recalled 
that the course of these nerves is as follows: the oculomotor nerve, 
having arisen from the nucleus in the corpora quadrigemina, pierces 
the dura mater below the posterior clinoid process, passes along the 
outer wall of the cavernous sinus, and there divides into two branches. THE EYE. 
181 
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 sphenoidal bone, passes 
through the clinoid process, and enters the cavernous sinus, finally 
reaching the orbit through the sphenoidal fissure. It is thus seen 
that a lesion at the sphenoid fissure and pressure in the cavernous 
sinus would cause all the symptoms described above. This occurs 
in cases of thrombosis of the cavernous sinus. Where there is an 
arterio-venous aneurism of this sinus there will be pulsating exoph- 
thalmos. 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 ihe result of an apo- 
plexy, 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 con- 
jugate 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 
hemiplegia, the eyes will be turned to the left by the action of the 
unaffected left external rectus and the right internal rectus; while 
if the lesion be on the right side of the brain, the reverse will occur. 
If, however, the lesion be irritative (as a 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, 182 
THE MANIFESTATION OF DISEASE IN ORGANS. 
and the eyes are, therefore, turned by the muscles which remain 
intact. In the second instance the eyes are turned toward the con- 
vulsed side because the internal and external rectus are spasmod- 
ically 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. 85.) 
Fig. 85. 
1. Left ext. rectus. 2. Left int. rectus. 3. Eight 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 produce 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. 
183 
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 cerebel- 
lum 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 functions of 
the extraocular muscles, we next proceed to a consideration of 
these facts in connection with the intraocular muscles. These con- 
sist, it will be remembered, in the muscular fibres 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 ophthal- 
mic or upper branch of the fifth nerve. From this ganglion ex- 
tend 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 oculo- 
motor 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 he named. 184 
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 normal pupil is about four milli- 
metres 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 con- 
traction 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 consensual 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 communicating fibres 
(Meynert’s fibres) between these bodies and the oculomotor centres 
to the centre for the sphincter pupillse or circular muscle-centre, and 
from there to the ciliary ganglion, the ciliary nerves, and the mus- 
cles of the iris. (Fig. 86.) 
Not only does the pupil change its size by reason of the ordinary 
light-reflex, but it also contracts or dilates in association with the 
other muscles governing accommodation and convergence, namely, 
the ciliary muscle and internal recti. This is the associated reaction 
of the pupils, and is tested by causing the patient to direct his eyes 
to a near object—for example, the point of a pencil. If the sight 
is intact, contraction 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. 
185 
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 test- 
ing the ocular reflexes in the manner already described we find that 
the pupil of one eye when uncovered does not contract, and imme- 
diately does so as soon as the other eye is uncovered, what is the 
indication? It indicates that there is disease of the optic nerve of 
that eye which does not convey the impulse of light from the retina; 
Fig. 86. 
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.) 
whereas if it contracts when the other eye is uncovered, it shows 
that the rest of the mechanism involved in the reflex is intact. 
Accommodative reaction of the pupil is intact also. Again, sup- 
posing 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 quad- 
rigemina to the oculomotor nuclei. (See Fig. 86.) 
This condition is seen in locomotor ataxia, general paralysis of 
the insane, sometimes in cerebral syphilis and as the result of poison- 186 
THE manifesta tion of disease in organs. 
ing by the bisulphide of carbon. Recently Grube has reported 
three cases in which the Argyll-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 oculo- 
motor nucleus. If the eyes fail to react to light and to accommo- 
dation, 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. 
Sachs asserts that immobility of the pupil is very characteristic 
of syphilitic cerebro-spinal disease, and if the diagnosis lies between 
multiple sclerosis on the one hand, and cerebro-spinal syphilis on 
the other, the discovery of immobility of one or both pupils should 
decide in favor of its being a syphilitic case. He also asserts that 
persistent pupillary immobility in a case of hemiplegia indicates a 
syphilitic endarteritis. It is important in this connection to remem- 
ber that the pupillary changes due to syphilis often suddenly im- 
prove, while those due to sclerosis are absolutely permanent. 
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 regurgitation, 
and irritation of the cervical sympathetic, as by aneurism. A dilated 
pupil is also often seen in idiotic children. 
Dilatation of the pupil results from two causes, opposite in 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 is 
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 THE EYE. 
187 
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 “ Wer- 
nicke’s pupil,” we sometimes, though rarely, meet with a condition 
associated with hemianopsia, or blindness in one-half of the eye, 
which is demonstrated in the following manner : the patient is seated 
in a dark room and one eye is covered. The other eye is now illu- 
minated by just sufficient light from a flat mirror to enable the 
physician to see the eye. By means of the concave mirror of an 
ophthalmoscope the physician now directs into the uncovered eye a 
bright beam of light, taking care that it falls upon one side of the 
retina, or, in other words, enters the 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 quadrigemina; but if there is a pupillary 
reaction, the lesion must be further back in the visual centres, back 
of the reflex arc. When the lesion is found back of the reflex arc 
it may indicate a lesion of the optic tract, the posterior segment of 
the thalamus, the posterior part of the chiasm, or rarely it may be 
caused by a lesion of the optic nerve if the hemianopsia be monoc- 
ular, which is rarely the case. 
Finally, a rhythmical contraction and dilatation of the pupil, 
called “ hippus,” is 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 by Rampoldi to be an early and almost 
constant sign of pulmonary tuberculosis. He believes 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 188 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
destroys the peripheral ocular sense-organ (the eye), the optic nerves, 
the optic tracts, or the receptive and perceptive centres of sight. It 
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. 87. 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 back- 
ward 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. 87.) 
Hemianopsia. As lesions of the nervous centres frequently 
produce 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 hemi- 
anopsia or partial or complete blindness of one-half of the retina. 
Usually hemianopsia is bilateral—that is, in both eyes; and it is THE EYE. 
189 
usually homonymous—that is, on the same side of each eye; or, 
in other words, if it is in the outer half of the left eye, it will be in 
Fig. 87. 
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. Substantia nigra of crus. L. Lemniscus in 
crus. kn. Red nucleus, in. Third nerves, p, q, k, s, u. Lesions in the occipital lobe and 
in front of it, producing left homonymous lateral hemianopsia. 190 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 hemianop- 
sia; if the blindness is found in the nasal side of both eyes, it 
is called binasal hemianopsia. It must be remembered, however, 
that the apparent blindness of the outer side of the eye is really 
due to disease of the fibres supplying the opposite side of the retina, 
as is shown in Fig. 88. The presence of hemianopsia in any form 
is determined by the following method of examination : the patient 
tEFT VISUAL FIELD. RIGHT VISUAL FIELD. 
Fig. 88. 
Fixation Point. 
Fixation Point. 
(Oliver.) 
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. 
We measure the field of vision more accurately by means of what THE EYE. 
191 
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 
Fig. 89. 
Chart of F. V. of right eye. 
number of degrees at which the object is seen and marks it on a 
chart. (See Fig. 89.) 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 
field, as shown in Fig. 90. 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 inter- 
nal capsule, in the primary optic centres, or in the optic tract. Fig. 192 
THE MANIFESTATION OF DISEASE IN ORGANS. 
87 shows the sites of these lesions and why they cause left homony- 
mous hemianopsia. Supposing, on the other hand, that instead of 
Fig. 90. 
Left homonymous hemianopsia from a case of gunshot-wound, with suspected lesion of the 
right cuneus. (de Schweinitz.) 
left homonymous hemianopsia we find bitemporal hemianopsia (Fig. 
91), this indicates that the patient has a lesion of the optic tracts in 
Fig. 91, 
Bitemporal hemianopsia from a case of acromegaly 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.) 
the crossing fibres in the middle of the chiasm (see “ H ” in Fig. 
87); or if binasal hemianopsia, that he has a lesion on both sides of THE EYE. 
193 
the chiasm or one on the outer side of each optic nerve. This is 
a very rare lesion. 
Hemianopsia of the homonymous form is very rarely found in 
hysteria, generally in association with hysterical hemianaesthesia, in 
which condition the conjunctiva is usually anaesthetic, thereby differ- 
ing from the condition of the conjunctiva of persons suffering from 
hemiansesthesia of an organic origin. 
In some cases in place of hemianopsia we have simply an altera- 
tion in the visual fields for color. It will be remembered that the 
Fig. 92. 
WHITE- 
BLUE - 
RED - 
GREEN - 
Chart of F. V. of left eye. (Landolt.) 
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 
of the visual field in ordinary daylight we find that blue is the color 
first seen, its boundary being 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. 92. These fields are determined by means of small 194 
THE MANIFESTATION OF DISEASE IN ORGANS. 
pieces of colored paper passed around the perimeter in the manner 
already described. 
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 versa. The fields 
for all the colors are also markedly narrowed in hysteria. This 
transposition, rather than loss of color-sense, helps us sometimes to 
a distinction between the ocular symptoms of hysteria and those of 
true tabes dorsalis, 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 pre- 
served and the Argyll-Robertson pupil is not seen. The following 
table from Charcot’s lectures for 1888-’89 summarizes these differ- 
ential points : 
Tabes. 
Hysteria. 
Motor apparatus of the 
Paralysis from lesion of a motor 
1. Sometimes associated paralysis. 
eye. 
nerve of the eye (bulbar or per- 
2. Blepharospasm. 
Pupillary disturbances. 
Optic disk. 
ipheral); consequent diplopia. 
Argyll-Robertson pupil. 
Atrophy. 
3. Monocular diplopia ; micropsia 
and macropsia. 
Symptoms due to affec- 
1. Irregular concentric contrac- 
1. Regular concentric contraction 
tions of the optic nerve 
tion of the visual fields. 
of the visual fields. 
or visual centres. 
2. Tabetic achromatopsia or dys- 
chromatopsia, affecting first 
green and red, yellow and blue 
being preserved to the last. 
2. Dyschromatopsia from simple 
contraction of the visual fields 
for colors. Frequently percep- 
tion of red alone persists. 
3. Progressive blindness. 
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 eve 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 EYE. 
195 
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 oph- 
thalmoscope 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 
ophthalmoscope, and by means of the concave mirror on the face of 
the instrument he reflects the light into the eye through the pupil. 
Fig. 93. 
Relative position of physician and patient whilst employing the direct method. 
(Norms and Oliver.) 
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 impor- 
tance in the diagnosis of the case, it is justifiable to use homatropine 
to dilate the pupil and prevent the alterations of accommodation by 
paralyzing this function. The ophthalmoscope and the head of the 196 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 93. If the light be now directed slightly 
toward the nasal side of the eye, the optic nerve will be seen, or in 
its stead a retinal bloodvessel will be seen across the field of vision, 
and this should be traced along its course to its origin in the papilla. 
If the patient or the physician is short-sighted (myopic), the oph- 
thalmoscope must be adjusted to correct this error by placing over 
the aperture a concave lens; but if ordinary degrees of far-sighted- 
ness (hypermetropia) are present, the use of a convex lens is not 
necessary, because the accommodation of the eye makes up for the 
error in refraction. If the hypermetropia is so great that accom- 
modation cannot overcome it, then a convex lens must be used. 
The view of the eye which is obtained ordinarily by a beginner is 
clouded, not because of myopia or hypermetropia, 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 PLATE IV 
FIG. l. 
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 At- 
rophy of the Optic Nerve. Modi- 
fied from Juler. (de Schweinitz ) THE EYE. 
197 
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 under- 
lying 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 gran- 
ular, 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 
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 
papillary region or near it, occurring in flame-like shapes. These 
are the signs of optic neuritis, and optic neuritis depends upon intra- 
orbital 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, 198 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
what is called tobacco-amblyopia or toxic amblyopia, with failure 
of vision from these causes. In such cases there is a central sco- 
toma between the macula and the optic nerve where the senses of 
red and green are lost. The ophthalmoscope may reveal in such 
cases discoloration 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 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 it is a valuable one in the diagnosis of this grave disorder, 
separating it from pseudo-tabes due to ordinary peripheral neuritis. 
The diagram (Fig. 94) on page 199, taken from de Schweinitz’s 
article on this subject, shows the relation between age, severe ocular 
symptoms, and atrophy of the optic nerve. 
The more advanced forms of optic atrophy with a hazy outline of PLATE V. 
Embolic Atrophy of the Optic Nerve. From a ease in the Jef- 
ferson Medical College Hospital, (de Sehweinitz.) THE EYE. 
199 
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. 
Fig. 94. 
Upper curve, frequency of tabes. Middle curve, frequency of severe ocular symptoms. 
Lower curve, frequency of atrophy of the optic nerve. (Berger.) 
Again, if on the use of the ophthalmoscope we find that there is 
a faint haziness of the retina, that whitish streaks are seen 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 show 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 in addition to these symptoms the vitreous humor is opaque, 
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. 200 
THE MANIFESTATION OF DISEASE IN ORGANS. 
By far the most important of these forms of retinitis from a diag- 
nostic stand-point 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 the first suspicion of renal trouble is 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 eases 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. 
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 
usually find 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 cen- 
tres, 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 hemianaesthesia— 
Paraesthesia, hyperaesthesia, itching. 
Much information can be obtained by careful examination of the 
skin in many cases of disease. The examiner should make a note 
of the color*of the integument, of its general nutrition, of its pliabil- 
ity, and of its sensibility. Naturally the eye at once takes in any 
eruption or scars which may mar its naturally smooth surface, and, 
as eruptions and scars are often the manifestations of more or less 
active systemic disorders, an insight into the presence of internal 
disease may be obtained from them. 
The color of the skin in health in the white race depends upon 
the presence of pigment in the cells of the 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 cir- 
culation. With these normal alterations in color, however, we have 
little to do, for it is the abnormal colorations which interest us from 
a diagnostic stand-point. 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 mela- 
notic 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 u pigmentation ” we sometimes see 
201 202 
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 bronz- 
ing of the skin in Addison’s disease, and the slate-blue hue of argyria 
or chronic silver-poisoning. (See further on in this chapter.) 
The changes in color depending upon disturbance of the subcu- 
taneous 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. ’ Consider- 
able cyanosis of the face and hands in a case of tuberculosis of the 
lungs is a very grave symptom. Again, we see in pneumonia a 
peculiar dusky red flushing of one cheek or of the entire face, and 
in erysipelas the zone of hypersemic 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 yellow- 
ing 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 remem- 
bered that jaundice may be hepatogenous—that is, arise from dis- 
order 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 com- 
mon cause of this form of jaundice is catarrhal inflammation of the 
smaller ducts and common bile-duct which generally occurs in asso- 
ciation with gastro-duodenal catarrh. THE SKIN. 
203 
As a result of this catarrhal process the bile-duct becomes blocked 
by the swollen mucous membrane and the mucus which is secreted; 
the biliary coloring-matter is absorbed into the hepatic circulation 
and general circulation, and is by this means distributed over the 
body. Another common cause of hepatogenous jaundice is the 
obstruction offered to the flow of bile by the presence of a gallstone 
or gallstones 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, summar- 
izes the causes of hepatogenous jaundice : 
Tabular View of the Causes of Hepatogenous Jaundice. 
f , „ . . . . . . .5 
1. Gallstones and inspissated bile 
In common duct, 
in radicles of duct. 
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 
J syphilis. 
1 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 204 
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 from 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 obstruc- 
tion is below the opening of the cystic duct it may be possible some- 
times to discover by abdominal palpation a pear-like swelling due 
to a distended gall-bladder. 
The jaundice of gallstone 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 hypochondrium, 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 
gallstone colic, the presence of gallstones 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 gallstone 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. 
205 
fever high, the failure in strength may be most alarming, while the 
repeated rigors and sweats increase the distress of the patient. 
Jaundice very rarely arises from pressure on the ducts by an 
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, with displacement of the liver in such a way 
that the adhesions cause twisting or dragging on the ducts. 
The juaudice 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 skiu. 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 muscu- 
lar twitching occur the symptoms may resemble acute yellow 
atrophy of the liver, and that all forms of jaundice produce head- 
ache and may cause delirium. In acute yellow atrophy of the liver 
(see below) the liver is greatly reduced in size, whereas in hyper- 
trophy 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 obstruction to 
the flow of bile. 
In amyloid disease of the liver Bartholow states that jaundice 
occurs in about one-tentli of the cases as a result of enlargement of 
the lymphatics in the hilus with pressure on the hepatic duct. In 206 
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 
only about one-third 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 pressing 
on the common duct may cause jaundice, and, as is now well known, 
widespread disease of the pancreas may cause diabetes. Jaundice in 
a case of diabetes should, therefore, direct attention to the pancreas. 
In this connection it is well to remember that Hanot, under the 
name of bronze, has described a pigmentation of the skin 
which contains iron (that of Addison’s disease and melansemia does 
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 glyco- 
suria 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 gallstones impacted in the ducts, and pro- 
ducing irritation or ulceration of their lining so that septic absorp- 
tion 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 inter- 
mittent fever. As these symptoms sometimes develop 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 gallstone produces active suppura- 
tion the fever becomes more like remittent fever and the patient 
rapidly emaciates and presents all the signs of active suppuration. THE SKIN. 
207 
The urine in all cases of hepatogenous jaundice is heavily bile- 
stained (see Urine), and the stools arc 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 re- 
covery has been known to occur. The stools during the attack are 
clay-colored, and the urine contains leucin in disks 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 pro- 
ducts, chlorate of potassium, glycerin, 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. 
Yellow fever. 
Typhus fever. 
Scarlet fever. 
Relapsing fever. 
r Fevers . . 
Animal 
Snake bite. 
Pyaemia. 
N on-obstructiv e 
(feces normal 
in color) 
Poisons. . 
Phosphorus, copper, 
mercury, antimony, 
chloroform, ether. 
Chemical 
Acute atrophy of liver. 
Neurosis: joy, grief, fear, passion. 
Cirrhosis of liver in its later stages. 
Jaundice sometimes occurs after severe hemorrhage of a prolonged 
character and in prolonged exhausting fevers, and is then due not 208 
THE manifestation of disease in organs. 
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 juandice 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 pysemic 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 newborn, 
usually within the first or second day of life (icterus neonatorum), 
which some believe to be due to a decrease in the blood-pressure in 
the portal vessels subsequent to the arrest of the placental circula- 
tion, 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 hepa- 
titis due to hereditary syphilis. In any of these latter causes death 
will probably occur, whereas in the mild form of icterus neonatorum 
the prognosis is very favorable, even though the discoloration lasts THE SKIN. 
209 
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 malarial 
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 sometimes 
appear in the course of diabetes (Hutchinson, Besnier), and under 
these circumstances generally develop suddenly, and spontaneously 
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-poison- 
ing. This discoloration is so characteristic as to admit of no diffi- 
culty in diagnosis, since the absence of any circulatory or respiratory 
embarrassment excludes the possibility of its being due to cyanosis. 
Owing to the decrease in the amount of silver given internally by 
physicians chronic argyria is becoming more and more rare. The 
discoloration is due to a deposit of oxide of silver in the rete Mal- 
pigliii. 
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 tuber- 
cular in character. A greasy, yellowish skin does, however, occur 
as an accompaniment of some cases of pulmonary phthisis, 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 210 
THE manifestation of disease in organs. 
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 pigmentation of the skin results from many causes, both 
local and systemic, direct and indirect. When brownish-yellow 
spots or streaks appear on the face, so that 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 externally 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 coales- 
cence 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- 
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 THE SKIN. 
211 
rete Malpighii, and pressure lias no effect on it. The symptoms of 
Addison’s disease to be found associated with these skin-changes are 
“ anaemia, 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 unusu- 
ally 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 path- 
ognomonic of carcinoma, although it may also be present to some 
extent in far-advanced cases of pernicious anaemia or sarcoma. 
Pallor of the skin is due to absence of the normal pigment, to 
deficient blood, to central or local vasomotor disturbance as is typified 
by fainting, and far more rarely by Raynaud’s disease. As a type 
of the pallor due to lack of pigment in the skin we see 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 anaemia 
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 
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 212 
THE manifest a tion of disease in organs. 
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-hue to an almost black hue. The lobes of the ears, the tongue, 
the scrotum, and the toes show the color most deeply. It is impor- 
tant to remember that this form of cyanosis is greatly decreased, as 
a rule, by placing the child on its right side. Anything which pro- 
duces excitement increases the cyanosis greatly, whereas cyanosis 
due to other causes is not subject to great variations. In the cya- 
nosis of the newly born, males are far more frequently affected than 
females, in the proportion of about 2 to 1 or 3 to 1, and it is a note- 
worthy 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 congenital 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 . . It 
5. One auricle and one ventricle 12 
6. Two auricles and one ventricle 4 
7. A single auriculo-ventricular opening ; interauricular and interventricular 
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 chances are about ten to one that in cyanosis of the newborn 
the lesion is absence of a properly developed interauricular or 
interventricular wall. 
In the adult or child cyanosis may be produced by serious cardiac THE SKIN. 
213 
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 iu 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 dusk-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 diseases 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 ‘ mewling and puking ’ infant we meet 
with sclerema and cedema neonatorum, the ‘ red gum ’ or strophulus 
of the older writers, intertrigo, eczema, urticaria papillosa (lichen 
urticatus), urticaria pigmentosa, xeroderma pigmentosum, and im- 
petigo; the ‘ schoolboy,’ with his chilblains and ringworms, alopecia 
areata, pityriasis rosea, ecthyma, and ‘ football 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 1 lean and slippered pantaloon,’with rodent 
ulcer and ‘ gouty’ eczema; ‘ last scene of all, sans teeth, sans eyes, 
sans taste, sans everything’—except an incessant and intolerable 
itching of the skin which we call senile prurigo.” 
There are two conditions of the skin in which valuable evidence 214 
THE MANIFESTATION OF DISEASE IN ORGANS. 
is given that the 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 rheu- 
matic poisoning. Sometimes this eruption may be the only mani- 
festation other than cardiac involvement, and when the marginate 
eruption is present severe cardiac involvement is commonly seen. 
The papulate 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 remem- 
bered that these forms of erythema may be distributed anywhere 
over the body in rheumatism, but that they become especially diag- 
nostic 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 luemorrhagica, 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 
purpura 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 preg- 
nant women. The chief symptoms consist in hemorrhages from 
the mucous membrane, purpuric spots, high fever, and a general 
class of symptoms resembling those of sepsis, as chills, pyrexia, and 
exhaustion. In other instances active hemorrhages, take place into 
the viscera, and if into the meninges of the brain cause cerebral 
symptoms at once. The liver and spleen are nearly always enlarged. 
The subacute type, while severe, runs a far more favorable course 
as to its manifestations and results. It usually attacks children or 
young adult males from twenty to thirty years of age. The patient, 
after a feeling of wretchedness, and perhaps a chill, followed by the 
purpuric eruption, is attacked by swelling of the joints and perhaps 
hemorrhages from the kidneys, bowels, and mucous membranes. If THE SKIN. 
215 
the hemorrhage be from the gams, 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 
manner, 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 hyper- 
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 
erythema exudativum multiforme. The attacks are apt to be recur- 
rent. Sometimes the skin-manifestations are absent. 
Subcutaneous fibroid nodules sometimes occur in cases of rheu- 
matism 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, 
chloral, 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 216 
THE manifestation of disease in organs. 
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 
petechise, result from snake-poisoning, septicaemia, cerebro-spinal 
meningitis, iodism, ergotism, and after inhaling the vapor of ben- 
zine. They are also seen in scurvy and in some cases of profound 
wasting, as in the course of phthisis and carcinoma. 
Petechial rashes closely resembling those of malignant smallpox, 
typhoid fever, or cerebro-spinal fever may be due to the presence 
of acute ulcerative endocarditis. 
Hemorrhages 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 haematoma auris, a condi- 
tion in which a free extravasation of blood takes place into and 
beneath the skin of the ear. The color of the swollen ear is quite 
red, if the hemorrhage has been recent, or dark blue if it is an old 
occurrence. The left ear is more commonly affected than the right, 
and it is seen more commonly in males than females. 
Intense redness of the skin is seen in acute inflammations of the 
skin or the subcutaneous tissues, and as the result of hot applica- 
tions, the redness being more and more marked as the heat is pro- 
longed 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 blush- 
ing, we should remember the general flushing seen so commonly in 
persons 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 cerebralea condition of vasomotor disorder in which THE SKIN. 
217 
when the finger is gentlv 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.'1'’ 
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 
importance. 
The development of a diffuse, punctated rose-rash on the skin of 
a person who is suffering from malaise, fever, nervous disturbance, 
and sore throat should direct the physician’s attention to the possible 
presence of two infectious diseases, namely, scarlet fever, which is 
more common in childhood, and syphilis, which is more frequent in 
adults. The rash of scarlet fever is of a very bright-red color, and 
shows itself at the end of the first or on the second day of the dis- 
ease, first appears on the chest and neck, and then speedily 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 redness depends upon an acute hypersemia 
of the skin, which though removed by pressure instantly returns 
when the finger is withdrawn. A noteworthy point is its punctate 
and mottled appearance, for, while the entire skin may be red, there 
are points which are more red than the rest of the skin, and also 
certain areas which are particularly so. The skin is often slightly 
swollen and feels tense, and itching is commonly present. The rasli 
usually lasts three or four days, and then fades, desquamation of the 
cuticle speedily setting in, which is complete in about two weeks. 
Sometimes, however, it remains for ten days to three weeks. Often 
when the rash can scarcely be seen on the skin its full development 
will be found on the pharyngeal wall. In the malignant types of 
scarlet fever petechise and subdermal hemorrhages occur. 
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 218 
THE manifestation of disease in organs. 
papular 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 iu 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 cater- 
pillars. 
Another condition closely resembling scarlet fever is rarely seen, 
namely, acute exfoliating dermatitis, called, in its mild form, ery- 
thema searlatiniform, which has a sudden onset with febrile movement 
and a rash which rapidly spreads over the entire body and lasts four 
or five days, finally ending in desquamation. So closely may this 
disease resemble scarlet fever that a diagnosis during the first attack 
may be impossible for the first few days, but the condition of the 
throat and tongue does not resemble the condition seen in scarlatina. 
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 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 THE SKIN. 
219 
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, and 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 in 
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 press- 
ure. 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 
puffiness 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. 
It also appears sometimes in cases of smallpox previous to the 
outbreak of the true eruption. Under the latter circumstance 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. 220 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 Vakious Exanthemata. 
Day. 
Disease. 
Area 
First to second day .... 
ROtheln or German measles. 
Varicella or chickenpox. 
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 of scarlet fever four days, will aid the diagnosis 
if a history of exposure can 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 
persists. 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 absorption. 
The presence of a very high temperature, of nervous irritability, 
and the predominance of the throat-lesions of scarlet fever ought to 
decide the diagnosis in favor of scarlet fever. 
The physician should also recall the fact that the injection of 
anti-diphtheritic serum sometimes causes a roseolous eruption, asso- 
ciated, it may be, with pains in the joints. The general illness caused THE SKIN. 
221 
by diphtheria, plus these symptoms, may point to a complicating 
scarlet fever or measles. The antitoxin rash is not, as a rule, so 
persistent as that of scarlet fever, lasts a short time, and is rarely 
followed by desquamation, except iu fine scales. While it may 
resemble measles in its characteristics, the patient does not present 
the eruption on the pharyngeal mucous membrane nor the peculiar 
coryza of that disease, nor the bronchitis or other evidences of res- 
piratory catarrh. 
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 straw- 
berry-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 become 
slightly papular. In this connection it should not be forgotten that 
the rose-rash of typhoid fever may be so profuse, particularly in 222 
THE manifestation of disease in organs. 
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, that the 
exhaustion following an attack of scarlet fever may render the gen- 
eral 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 
petechise. 
In Bright’s disease a roseola often appears over the feet and 
ankles, wrists, and hands, and sometimes spreads to the skin of the 
chest and abdomen. Desquamation may take place, but absence of 
febrile movements and the presence of renal trouble render the diag- 
nosis 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 lines of demar- 
cation feel 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 bullae form, the oedema of the skin becomes very profound, and 
finally suppuration may occur, forming what is known as phlegmo- 
nous erysipelas (see also Glanders). Erysipelatous inflammation of 
the skin without systemic disturbance may follow the application of 
arnica. A condition also closely resembling erysipelas in its raised 
surface is urticaria, which, however, 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. THE SKIN. 
223 
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 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 diagnosis of syph- 
ilitic 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 kness, 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 strychnine, 
and a scarlatiniform rash sometimes appears in blotches over the 
face and body in persons who are taking turpentine. 224 
TIIE MANIFESTATION OF DISEASE IN ORGANS. 
Roseola also ensues in some persons after the application of sur- 
gical dressings containing iodoform, corrosive sublimate, and car- 
bolic acid, being due either to a local effect of these drugs or to their 
absorption from the dressings. Arnica tincture applied for sprains 
or bruises may produce marked roseola, or eveu 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 con- 
vulsions from overdoses of atropine, thus making the resemblance 
to the onset of scarlet fever very striking. The brief duration 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 
ointment produces a widespread rash resembling measles, and this 
resemblance 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 generally 
sudden in its onset and profuse in its distribution. The base of the 
pimple is bright red, the top speedily becomes pustular, and Four- 
nier states that it may be hemorrhagic. Stopping the ingestion 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. THE SKIN. 
225 
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 char- 
acteristic of smallpox and chickenpox. The eruption of smallpox 
appears on the second or third day in the form of tiny specks, 
resembling flea-bites. These rapidly become papules, which have 
an indurated base, so that they feel as if shot were under the skin. 
(Fig. 95.) After about thirty-six hours these papules become vesi- 
Fig. 95. 
Smallpox eruption on the seventh day. 
cles, containing a turbid fluid, which speedily becomes purulent, 
forming a pustule. (Figs. 96 and 97.) Generally this process of 
maturation takes three days and, with the development of the pus, 
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 lias been severe or the skin delicate, deeply 
pitted scars. Although the eruption of smallpox appears on the 
forehead, which is the favorite seat of acne in many cases, a differ- 
ential diagnosis is not difficult, since the grave systemic disturbance, 226 
THE MANIFESTATION OF DISEASE IN ORGANS. 
febrile movement, and rapid involvement of the whole surface of 
the body speedily indicate the true nature of the disease. The early 
Fig. 90. 
Smallpox eruption on the eighth day. 
Fig. 97. 
Smallpox eruption on the eleventh day. The pock is seen to he umbilicated. THE SKIN. 
227 
appearance of the rash on the hands in variola is also a diagnostic 
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. 
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 rash is not measles. 
Fig. 98. 
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 228 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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- 
rounded by an areola of rosy red of several inches in width. Rarely 
severe inflammation and sloughing ensue. (Fig* 98.) 
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 umbili- 
cated, and rarely leaves pits in the skin unless the vesicles are picked 
at by the finger-nails. Neither do the vesicles become pustules 
unless iufected by picking or the child is in a condition of debility 
or suffers from struma. Varicella 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 smallpox 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 dis- 
ease 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 fact 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 iii the back, the grave systemic dis- THE SKIN. 
229 
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 
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. 
This symptom rather excludes tuberculosis, typhoid fever, and 
simple pleurisy from the case in instances in which the diagnosis is 
doubtful. 
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 debil- 
ity, 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 subcu- 
taneous 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 230 
THE manifestation of disease in organs. 
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 pus- 
tule. 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. 
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 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 oil 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 preseuce 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 
contain dark bloody fluid and are situated upon a limb in which 
there is an abnormally high temperature, are peculiarly indicative 
of central nervous lesions, particularly if there is a tendency to 
dilatation of the capillaries of the skin on slight irritation; but if 
the temperature of the entire body be raised, the physician should 
remember 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. THE SKIN. 
231 
Bnliae 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 
smoothed out and it appears unduly shiny, often results from 
chronic disease involving some portion of the nervous system con- 
nected with the government of nutrition. Very commonly it 
results from peripheral neuritis. In addition to glossiness there 
are often redness and marked thinning or thickening of the cuticle 
and subcutaneous 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 aud 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 big toe or 
on the sole or dorsum of the foot. Previous to the development 
of gangrene there are developed bullae and other inflammatory 
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 232 
THE MANIFESTATION OF DISEASE IN ORGANS. 
ulcers and a lupus-like formation, also occurs in diabetes. Per- 
forating 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 
removed by the use of an Eshmarch bandage. 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 
haemoglobinuria. 
The development of gangrene of the fingers and toes sometimes 
follows the prolonged use of bread made from rye which is infected 
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. 
Bed-sores 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, iu the course of acute traus- THE SKIN. 
233 
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, bed-sores often form 
on the buttocks, and in paraplegia from other causes than transverse 
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 Avith 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 circular, 
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 indu- 
ration, 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 ulcerate 
and become deep sores, and finally form on healing well-marked 
cicatrices, tertiary syphilis is to be considered the probable cause. 
If, again, 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  THE MANIFESTATION OF DISEASE IN ORGANS. 
234 
may be clue 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. 
Scabs 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 
evidence 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 convalescence 
from some grave disease, such as typhoid fever. 
Sweating of the skin, aside from the normal and almost 
imperceptible exhalation of moisture, takes place in health as a 
result of severe muscular exertion, whereby the peripheral circu- 
lation 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 THE SKIN. 
235 
occurrence of a profuse sweat (generally associated with a fall of 
temperature) gives us the first sigu of beginning convalescence, and 
in irritative fevers, or those due to cold and congestion, the artificial 
production of 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, pyaemia, acute 
ulcerative endocarditis, phthisis, malarial fever of the distinctly 
periodic type, and of typhoid fever and collapse. Constant 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 rheu- 
matism the febrile movement may even increase during the sweat 
rather decrease. 
Profuse so-called colliquative sweats often occur at night in debili- 
tated persons without the presence of any febrile movement, and are 
an evidence of profound nervous and vasomotor relaxation. Mod- 
erate sweating sometimes is seen from similar causes in feeble per- 
sons 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 Ray- 
naud’s disease. They depend upon perverted vasomotor influences 
sent to the glands and their supplying vessels in particular 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 cer- 
vical 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 236 
THE MANIFESTATION OF DISEASE IN ORGANS. 
cholera and diabetes, in which diseases the drvness is largely the 
result of 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 miliara 
or sudamina. 
When the skin is dry and harsh, and the naturally thickened por- 
tions have in their folds a peculiar white appearance as if filled with 
meal, diabetes should be sought for. llarely 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 
effusion 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 
important 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 
differentiated from myxoedema by the facts that in the latter disease 
the onset is very slow, the swelling does not pit on pressure and is 
universal 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 anaesthesia of the skin. When the 
subcutaneous tissues are distended by air, instead of liquid, they 
are even less resistant than in dropsy, the swelling is usually very 
localized 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- THE SKIN. 
237 
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 
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 anasarca after 
renal disease is heart disease. When due to this cause it will be 
found that the ghastly pallor of renal anasarca is replaced by cya- 
nosis, 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 multiple peripheral 
neuritis, and it also occurs as a symptom of beri-beri and from the 
excessive use 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 general anasarca in 
cases of advanced cancerous cachexia, and care must be exercised 
that the hsemic murmur due to anaemia does not mislead the physi- 
cian 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 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 hypertrophic cirrhosis of the 238 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 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 
standing with little muscular movement during many hours in the 
pursuit of their occupation, as in type-setters and salesmen, or in 
young persons who have subjected themselves to excessively severe 
muscular exercise. In other instances, very much more frequently, 
oedema of the feet and legs conies on in the course of profound 
anaemia resulting from slow hemorrhages or other causes. It is also 
seen in the cachectic stage of cancer, owing to the anaemia which is 
present. General swelling of a leg in a puerperal woman is prob- 
ably due to phlegmasia 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 conies 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 THE SKIN. 
239 
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 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 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 gro*wth. 
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 sub- 
cutaneous 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 commonlv affects 240 
THE manifest a tion of disease in organs. 
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 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 sclero- 
derma 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 takes 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 drowisness 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 jaw 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 closely 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 
itching, an important difference from true urticaria, but the part 
affected may be tense or hot to the patient. These attacks are gen- THE SKIN. 
241 
erally 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 
interference 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 
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 per- 
versions 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 practically 
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, 242 
THE MANIFESTATION OF DISEASE IN ORGANS. 
which seems devoid of sense on ordinary touch, is found to be 
excessively hyperresthetic if the hand is drawn lightly over it. 
The best apparatus for testing tactile sensibility is the sesthesi- 
ometer of Carroll, which is a pair of double-pointed compasses con- 
nected by a graduated scale. (Fig. 99.) 
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. 
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 integument. 
Fig. 99. 
Carroll’s sesthesiometer. 
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 bauds simultaneously. With one hand 
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 instrument must be of the 
same temperature as the body. 
Disturbances in the sensation of the skin may arise from functional 
or organic disease involving the peripheral nerves, the sensory 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 PLATE VI. 
Diagram showing Course of Sensory Fibres from Periphery to 
Cord, Cerebrum and Cerebellum. (Flatau.) THE SKIN. 
243 
with the peripheral sense-organ in the skin, or elsewhere, and after 
forming part of the nerve trank and entering the ganglion on the 
posterior root, enter the spinal cord by what is called the posterior 
root, which is shown in Fig. 101 near the words “ Lissauer’s 
zone.” (See Figs. 100 and 101.) 
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. 100. 
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. 244 
THE MANIFESTATION OF DISEASE IN ORGANS. 
These nuclei which have received the fibres of the two sensory 
columns give origin to fibres which pass to the brain. They sweep 
Fig. 101. 
Chart showing the sensory tracts in the spinal cord with entrance of the sensory nerve-roots. THE SKIN. 
245 
forward to the front of the central canal of the medulla and decus- 
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 
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, aud 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, mye- 
litis (transverse), locomotor ataxia, cerebro-spinal meningitis, spinal 
meningitis; compression of the cord by vertebral caries, by frac- 
tures, by dislocations; and hemorrhage into its membranes. Addi- 
tional 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. 246 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Hemianesthesia occurs most frequently as a result of hysteria, 
next commonly from lesion of the posterior part of the internal 
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 aud there may be patches of hyperesthesia or tenderness, dotted 
like oases in the midst of the absence of sensation. This anesthesia 
is often unaccompanied by motor paralysis, aud 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 suddenly 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 hyperaes- 
thesia on the opposite side increases the contrast which exists between 
it and that in which sensation is lost. (See Hyperaesthesia.) 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, aud 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 existence by most authori- 
ties, 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 hyster- THE SKIN. 
247 
ical symptoms detailed farther on in this chapter, will generally 
decide the diagnosis in favor of hysteria. 
A form of hysterical hemianaesthesia very apt to lead to an error 
in diagnosis is that seen in persons who have suffered from infantile 
cerebral paralysis with the resulting deformity (a disease not char- 
acterized by 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 hemianaesthe- 
sia, may occur in the course of chorea. The presence of chorea in 
its motor manifestations clears up the diagnosis as to the cause of 
the loss of sensation. 
Hemianaesthesia when not hysterical is nearly always due to an 
organic lesion in the posterior part of the hinder limb of the internal 
capsule on the opposite side of the brain from the anaesthesia, and 
the additional symptoms which sometimes accompany it depend for 
their existence upon whether the lesion is large enough to involve, 
not only the fibres from the cutaneous areas, but also those of special 
sense, such as sight, hearing, or taste. Nearly always the area de- 
stroyed is sufficiently large to result not only in hemianaesthesia, but 
also in 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 20 248 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 lesions 
in the neighborhood of the fissure of Rolando, and in tumors involv- 
ing the posterior parietal region and the posterior part of the internal 
capsule. 
Autopsies and experiments show that liemianaesthesia 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 anaesthesia 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 anaesthesia 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 has 
involved the nucleus of the fifth nerve. (See Anaesthesia of Face.) 
Anaesthesia of irregular distribution or confined to one limb may 
result from cerebral or spinal lesions, or be due to a neuritis, of 
which 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 sensation 
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 THE SKIN. 
249 
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 
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 hyperaemia 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 the 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 
—can 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 
intentiqn of the patient, but owing to the fact that the sensory 
centres 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 Browu-S6quard, 250 
THE MANIFESTATION OF DISEASE IN ORGANS. 
which has recently been doubted owing to the studies of Mott and 
others. Thus, until recently, it was considered as proved that sen- 
sory impulses entering the cord crossed to the opposite side almost 
at once, at least in greater part, passing to the lateral columns in 
front of the pyramidal tract, and that a very small 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 col- 
umns, 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 anaesthetic. Anaesthesia of 
this variety, corresponding in the sensory organs to what we call 
paraplegia 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 
anaesthesia of the skin of the legs and trunk are, first and most 
prominent, locomotor ataxia; second, myelitis; and, finally, hemor- 
rhages, tumor of the cord or its membranes, meningitis, or injuries THE SKIN. 
251 
which cause pressure on the sensory tracts by producing fracture of 
the vertebrae or dislocation. Very rarely, however, a lesion of the 
pons may so result. 
Anaesthesia of the lower portions of the body and legs occurs in 
the later stages of locomotor ataxia, and is usually preceded by forms 
of paraesthesia. (See Paraesthesia.) The anaesthetic areas are most 
marked in the soles of the feet and about the malleoli, according to 
Belmont. In other words, blunting of sensibility is seen in nearly 
all cases of tabes dorsalis late in the disease. In some cases the 
sense of touch is preserved and the sense of pain lost (analgesia), 
while in others the opposite condition is present. Again, we find 
loss of tactile sense and of pain-sense without loss of heat and cold 
sense, and vice versa. A very characteristic sensory symptom of 
tabes is the delay in the recognition of an irritation of the sensory 
nerves, so that if the patient be blindfolded and then pricked with 
a pin he will not make an exclamation or draw his foot away for 
several seconds. In other instances the patient complains of repeated 
pricks when only one has been given, or, when asked the number of 
points pricking him, states that there are four or five instead of the 
one really present. If, in addition to these sensory disturbances, 
we find Romberg’s symptom (see Legs), Argyll-Robertson 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 anaesthesia is easily made. 
Slight anaesthesia, retardation of the transmission of sensory 
impulses 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 devel- 
oped. 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 252 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 important point, too, in regard to the anaesthesia 
of acute myelitis is this, namely, that, while in the upper extremities 
the loss of sensation and motion is associated, so that both functions 
are lost in the same area, in the lower extremities these two func- 
tions are not lost in the same areas. Thus myelitis of the lumbar 
enlargement in its lower part is accompanied by anaesthesia of the 
Fig. 102. 
Sensory chart, showing 
areas of 
Thermo-Anaesthesia, 
Analgesia, 
Thermo-Anaesthesia 
and Analgesia 
Tactile Anaesthesia, and areas in which the patient’s answer to tests of temperature 
showed reversal 
Cold-Hot; 
Hot-Cold. (Dercum ) 
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 muscles of the thigh. (See chapter on Feet and Legs, part 
on Myelitis.) THE SKIN. 
253 
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. Anaes- 
thesia, or the milder perversions of normal sensibility of the skin, 
may be present in cases of compression of the cord by caries, and 
by spinal curvature, tumors, or aneurisms producing erosion. Some- 
times, while tactile anaesthesia 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. 
Fig. 103. 
1st to 7th cervical segment. 
1st to 12th dorsal segment. 
1st to 5th lumbar 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. 
Partial anaesthesia of the skin of the trunk and arras of a bilat- 
eral character, associated with progressive muscular atrophy, scoli- 
osis, and trophic lesions in the skin, points strongly to syringomyelia. 
The loss of pain- and temperature-sense is usually the first symp- 
tom. The areas of anaesthesia are best shown in Fig. 102. 254 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 by Horsley and many others; but the field is only partly 
covered, and some of our uncertainties depend upon lack of knowl- 
edge 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, hand, 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. 
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 spinal injury or disease are best 
described by Starr’s well-known article and diagrams, from which 
we quote. In this connection the reader should refer to the tables 
on pages 109 and 110, showing the localization of the functions of 
the segments of the spinal cord. (See chapter on Legs and Feet.) 
The anaesthetic areas included in zones I. and II. in Fig. 104 are 
due to a lesion involving the conus medullaris and the fourth and 
fifth sacral segments of the cord. These zones include the perito- 
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 A7, 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 THE SKIN. 
255 
side of the leg and foot, sometimes ending at the ankle, some- 
times 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 segment, 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. 104. If the foot is involved, the 
Fig. 104. 
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 hi. 
IV. Sacral i. 
V. Lumbar v. 
VI. Lumbar hi. 
VII. Lumbar II. 
lesion in the lumbar cord is probably above the third lumbar seg- 
ment. 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 seg- 
ment is probably 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  the manifestation of disease in organs. 
256 
space already mentioned, of two to three inches for the interlacing 
anastomosis of the nerve-fibres of the posterior roots. 
They are about as follows, according to Thorburn : when the 
amesthesia is as high as the anterior inferior spine of the ilium, the 
lesion is at the twelfth dorsal vertebra; if at the umbilicus, at the 
eleventh and twelfth dorsal vertebrse; if up to the lowest floating 
rib, the whole eleventh dorsal vertebra; if from 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. 105. 
Areas of anaesthesia from lesions at 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. 105.) When the anaesthesia extends to the 
arms and is found upon the inner side of the arm and foreariji, 
reaching 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, 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 after Starr.) 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 Head.) THE SKIN. 
257 
the second dorsal region is the site of the lesion. If the anaesthetic 
area includes the ulnar side of the hand, the palmar and dorsal sur- 
faces of the same, and the little finger, and extends in a narrow 
strip 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 figure 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 surfaces 
to the axilla is affected, the lesion is at the sixth cervical vertebra, 
while anaesthesia of the forearm and arm on the outer surface as 
high as the deltoid insertion indicates that the fifth cervical verte- 
bral 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 be due not only 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, hypersesthesia 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 
pressure over the nerve-trunks supplying the affected area, trophic 
changes in the tissues of the part, with the development of reac- 
tions of degeneration and pain in the involved nerves or parts sup- 
plied by them. Somewhat similar symptoms occur in anterior 
poliomyelitis, but pain is not commonly present in this disease, and  THE MANIFESTATION OF DISEASE IN ORGANS. 
258 
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 
poisoning by arsenic, lead, alcohol, or mercury, from septic states 
of the body, and from the infectious diseases, particularly diph- 
theria, 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 bv 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 sensation 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 THE SKIN. 
259 
anastomosis, and where they are present they usually disappear, 
more rapidly than the motor loss, as recovery takes place. 
Fig. 106. 
Fig. 107. 
Showing areas of sensory loss in injuries of the median nerve. (Bowlby.) 
Fig. 108. 
Fig. 109. 
Showing areas of sensory loss in injuries of the ulnar nerve. (Bowlby.) 
The following facts are, therefore, of diagnostic interest. If the 
anaesthesia is found to be due to a neuritis and to involve the palmar 260 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
surface of the thumb, fore and middle fingers, the median nerve is 
probably the one at fault (Figs. 106 and 107), and the area may 
even include in rare instances the backs of these fingers at their 
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. 
108 and 109). (See also chapter on Hands.) The nerve-supply of 
the skin of the entire upper extremity is well seen in Fig. 110. 
Fig. 110. 
Cutaneous nerve-supply of the trunk and upper extremity. (Fowler.) sa. Supraclavicular 
nerve, iid. Second dorsal, rs. 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, is as follows : When there is perverted sensation of 
the inner side of the foot from the tip of the big toe to the heel, THE SKIN. 
261 
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 
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 
Fig. Ill 
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, mcs. Musculo-cutaneous. at. Branches of anterior tibial. pt. Branches 
of posterior tibial. 
of function in the external saphenous, which is composed of the 
cutaneous branches of the external and internal popliteal nerves. 
Disturbed sensation on the posterior surface of the calf also indi- 
cates trouble in the external saphenous nerve and communicans 262 
THE MANIFESTATION OF DISEASE IN ORGANS. 
peronei, while when the sensation of the skin of the heel is dis- 
turbed 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, the upper eyelid, the conjunc- 
tiva, 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 are anaesthetic, the 
inferior 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 accom- 
panied by trophic changes in the anaesthetic parts. The most com- 
mon cause of anaesthesia of the trifacial is, however, neuritis. 
Romberg makes the following differential statement: 
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. 
263 
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 syringo- 
myelia, 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 paraesthesia, hyper- 
aesthesia, and analgesia. 
Paraesthesia—numbness, tingling, or 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 were about 
the patient is common. These are the subjective disturbances of 
sensation in tabes dorsalis, and, as they are often the earliest mani- 
festations of the disease, possess great diagnostic importance. The 
objective sensory perversions consist in the discovery by the physi- 
cian, when studying the sensibility of the skin, of areas of anaes- 
thesia, analgesia, and hyperaesthesia which are usually bilateral. 
Belmont has stated that we also find these areas in spinal syphilis, 
either on one or both sides. Numbness, tingling, and formications 264 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
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 involve- 
ment of all or part of the sensory tracts in the cord. Similar symp- 
toms 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 
classes of aconite-poisoning, and when the hands have been exposed 
to carbolic acid. Paraesthesias 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 acropanesthesia or walking numb- 
ness. This state is usually seen in women past middle life, but 
may occur in men. On waking in the morning marked formication 
and numbness 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 anaesthesia, strictly speaking, 
the disturbed sense of touch renders sewing or performing any 
small act with the fingers almost impossible. These sensations may 
be confined 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 
excitability is usually associated with the local manifestations. 
Sometimes the scalp may be the area involved. 
Acroparsesthesia 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. 
265 
condition is usually unilateral, and by the absence of the characteristic 
general hysterical symptoms. From organic disease it is separated 
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 11 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 promi- 
nent 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.) 
Hypercesthesia 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 confirm 
a diagnosis most positively. The most important and curious of 
these hyperesthesias 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 convulsiye 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 the hair pain or extreme sen- 
sitiveness 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  THE MANIFESTATION OF DISEASE IN ORGANS. 
266 
hysteria, and the personal history and characteristics of the indi- 
vidual aid still further in separating the two conditions. 
Hyperaesthesia 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 
sensory 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 
eruptions, in that very rare condition called chronic leptomeningitis. 
Motor symptoms are nearly always present if the cord becomes 
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 paral- 
yzed. 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 fre- 
quently 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 hyperaesthetic that the slightest 
touch causes pain. The whole breast is, moreover, tender, and 
movement of the arm may be impossible, owing to pain thereby 
caused in the gland. This hysterical breast can be separated from THE SKIN. 
267 
the 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 hypersesthesia of chronic alcoholism may be both dermal and 
deep, and is well marked along the course of the peripheral nerves, 
particularly where they emerge from deeper 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 hypersesthesia 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 hypersesthesia or tenderness upon the skin, which 
mav 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 iu its manifestations, and nearly 
always is due to functional nervous troubles. Duhring has noted 
a boring sensation in some cases. It should direct the physician’s 
attention to the possibility of hysteria or tabes dorsalis. 
Pruritus or intense itching of the skin may be due to contact 
with some irritant, but its presence, if persistent, particularly if 
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 iu 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 
results of using inspection, palpation, percussion, and auscultation in health 
and disease—The characteristic signs and symptoms of the various diseases of 
the thoracic organs. 
The chief 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 they exist in such an indefinite manner that 
the physician’s attention is not attracted to them, and as a result im- 
portant thoracic changes from the normal are overlooked or made 
light of. We base our diagnosis of the character of a case on the 
changes which we find in the surface of the thorax as to its contour 
and as to its movements, on the respiratory and cardiac sounds, and 
on 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 supraclavicular 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 con- 
vexity varies considerably according to the muscular development 
of the individual, the formation of the bony portion of the chest- 
wall, and the deposit of fat in the subcutaneous tissues of the chest. 
268 THE THORAX AND ITS VISCERA. 
269 
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. 112. 
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 270 
THE manifestation of disease in organs. 
the clavicles downward through the nipple are called the mammil- 
lary lines. (Fig. 112.) 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 the locality of signs and 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 left clavicle is the beginning of the innominate vein, and 
Fig. 113. 
Position of heart in relation to ribs and sternum. (Tyson.) 
back of this, again, the common carotid artery. On the right side 
the innominate artery bifurcates just behind the junction 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. 113.) 
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 AND ITS VISCERA. 
271 
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. 114. 
Fig. 115. 
The alar chest of phthisis. 
Side view of same patient, 
The most familiar of these is the so-called phthisical chest, which 
has been called the 11 alar chest,” because the scapulae stand out 272 
the manifestation of disease in organs. 
from the back like wings. (Fig. 114.) The antero-posterior diam- 
eter, particularly in the upper two-thirds, is very slight, and instead 
of convexity of the anterior surface there may be flattening or hol- 
lowness. (Fig. 115.) This area scarcely moves on inspiration, but 
the lower third, which is bulging, moves markedly with the respi- 
ratory 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 phthisical chest fall downward toward the belly from their 
points of origin, instead of coming forward in a normal curve. 
(Fig. 116.) 
Fig. 116. 
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 bulging is fairly uni- 
form, the shoulders being elevated, the back rounded, and the neck 
short in appearance from the raised shoulders, the patient is prob- 
ably a sufferer from emphysema of the lungs. This chest is often THE THORAX AND ITS VISCERA. 
273 
called the “ barrel-shaped chest.” (Fig. 117.) The chest-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 pressure 
(Fig. 118); from pericardial effusion; and, finally, from mediastinal 
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. 
Fro. 117. 
Fig. 118. 
Emphysema of the 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 respi- 
ration of a more or less chronic character during the time the chest- 
wall was soft and capable of being moulded. Sometimes on each 
side of the sternum, over the costal cartilages, there is seen a groove 274 
TIIE MANIFESTATION OF DISEASE IN ORGANS. 
Rhacbitic rosary. (Barbour.' THE THORAX AND ITS VISCERA. 
275 
or depression as the result of rickets. In other 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. 119.) 
Fig. 120. 
Fig. 121 
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. 120 and 121). It is sometimes seen 276 
THE manifestation of disease in organs. 
over the diseased area in pulmonary tuberculosis, and may be appa- 
rently jiresent, but in reality due to Avasting 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; systolic pulsa- 
tion 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 clavi- 
cles, and the veins of the trunk and arms may be engorged. Intra- 
thoracic growths produce similar symptoms.1 Pulsation in the 
cervical vessels is also sometimes seen in cases of severe anaemia, 
and in cases of aortic dilatation with regurgitation. 
Marked enlargement of the mammary gland on the affected side 
is sometimes seen in pulmonary tuberculosis, particularly in males. 
Respiration. 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 
breathing when their attention is called to it. Generally the eye 
can detect the frequency of the breathing by simply watching the 
movement 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 dis- 
ease it may be one to one. 
Rapid respirations not due to any recent sudden exertion are 
nearly always indicative of respiratory trouble, primary or second- 
ary. If the primary trouble be in the lung, it will probably be 
1 See “ Mediastinal Disease,” by the author. Fothergillian Prize Essay of Medical Society of 
London for 1888. THE THORAX AND ITS VISCERA. 
277 
due to croupous pneumonia, catarrhal pneumonia, severe bronchitis, 
asthma, tuberculosis, pulmonary abscess, or tumors of the lungs. 
If it be due to secondary lesions in the lung, it may rise from pul- 
monary 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. 
Usually in these states the respirations will be not only more rapid 
than normal, but difficult or labored. Sometimes in hysterical rapid 
breathing the respirations reach 150 per minute. This is not volun- 
tary, and the diaphragm moves very little, the chief breathing being 
costal. 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, 
or aneurism 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 repre- 
sents 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 pro- 
longed. This prolongation is also sometimes very marked in cases 
of paralysis of the posterior crico-arytenoid muscles. If there is 278 
THE manifest a tion of disease in organs. 
difficulty in expelling the air, the expiration is prolonged, as in 
asthma and in emphysema. 
Labored breathing (dyspnoea) is seen in all cases in which the 
blood cannot be provided with sufficient oxygen owing to obstruc- 
tion to the entrance of air into the chest, to spasm of the bron- 
chioles, or to the occluding of the air-vesicles by any form of 
exudate, croupous, 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 is anxious. The posture of the patient is that 
of sitting up in bed. 
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 and irregularly owing 
to the obstruction. 
The most remarkable change in rhythm is the so-called Clieyne- 
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 haematuric 
malarial fever. Rarely it occurs in cases of acute febrile disease, 
as typhoid fever, scarlet fever, pneumonia, whooping-cough, and 
puerperal septicaemia. It may also 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 THORAX AXD ITS VISCERA. 
279 
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 tuber- 
culosis or pleurisy, or old pleural adhesions which bind down the 
chest-wall. 
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 natu- 
rally 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 280 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 varia- 
tions in fremitus in health we have a number of causes in disease 
which greatly modify vocal fremitus. It must be remembered, too, 
that this vibration is more marked in men than in women and chil- 
dren, 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 supplying 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 correspond- 
ing left bronchial tube.” Sometimes this upper tube comes off the 
trachea directly. 
The conditions of disease which cause a decrease in vocal fremitus 
are pleural effusions of any kind, which not only cut off the trans- 
mission of sound, but by their contact prevent vibration of the chest- 
wall; pneumothorax, which causes collapse of the transmitting 
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 a cavity or of tumor in the thorax touching 
the chest-wall. Fremitus is increased in these conditions because 
the consolidated lung transmits the vibrations of the air in the 
bronchial tubes to the chest-wall, or, in the case of a cavity, the 
sound is 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 Auscultation.) 
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 THE THORAX AND ITS VISCERA. 
281 
Fig. 128.) 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 pleural cavity on the left side, to pulmonary emphy- 
sema causing abnormal descent of the diaphragm, and with it car- 
diac 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 peri- 
cardial effusions or adhesions following inflammation, by pleural 
adhesions or effusions, by abdominal effusion (ascites), by tumors, by 
distention of the colon with gas, and by great enlargement of the 
spleen. Displacement of the apex-beat to the left is generally asso- 
ciated with downward displacement, and is generally due to hyper- 
trophy 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 
page 291.) 
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 apex-beat in health depends largely upon 
the depth of the chest and the thickness of its wall. In disease it 
is increased in hypertrophy of the heart, and decreased in cases of 
feebleness 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 very rare, or aneurism of the descending 
part of the aorta. 
In this connection we should remember the pulsation felt in the 282 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 heav- 
ing impulse to the chest; and the external, in which there is a pul- 
sating tumor external to the chest-wall. Sometimes this is called 
“ pulsating pleurisy. ” 
Percussion of the chest is commonly performed by placing one 
finger, generally the middle one of the left hand, on the chest-wall 
and tapping it on the back with the tip of the bent finger of the 
right hand, the movement of the striking hand being entirely a 
wrist-movement. Sometimes percussion is made by directly striking 
the chest with the fingers or palm of the hand (direct percussion). 
Many physicians also employ a percussion-hammer with a rubber 
head and a 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 percussion 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 pneumo- 
nia is suspected and the results of the percussion will deckle the 
diagnosis. Care should be taken in performing percussion: first, 
that similar points on the chest-wall on each side are carefully com- 
pared; 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 tilings : 
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 be considered 
as a factor only 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 the 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 THORAX AND ITS VISCERA. 
283 
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 
we find the dulness. The area of partial and absolute hepatic 
dulness is shown in Fig. 153, in the chapter on the Abdomen. 
Fig. 122. 
•Skodaic resonance on percussion. 
■Compressed lung and dulness. 
Tympany and coin resonance. 
-Air. 
Succussion on shaking. 
Fluid. 
•Flat on percussion. 
■Loss of vocal resonance and fremitus. 
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.) 
Posteriorly we find on percussion of the right chest 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 scapulae. For this reason pulmonary 
resonance is best developed posteriorly at the bases of the lungs 
below the scapulae. Before percussing the back the patient should 
be made to lean forward and fold the arms, in order to stretch the 
tissues and make them tense and as thin as possible. 
We can divide the normal sounds produced by percussion into 284 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the tympanitic, the dull, and the flat. We can also develop by 
percussion of the chest in disease what is known as a (< cracked- 
pot sound.” 
A tympanitic sound is best produced in its most typical form by 
percussing the epigastrium when the stomach and colon contain 
some gas. We obtain this sound when the chest is percussed if 
there is present in the lung a large cavity, and also in pneumo- 
thorax (see Fig. 122), 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- 
acter of the note will change when the mouth is closed or opened. 
(Fig. 123.) If the case be one of peumothorax, with fluid in the 
Fig. 123. 
Increased vocal resonance 
and fremitus. 
Pectoriloquy, 
Cavity with cavernous 
breathing and gurgling 
rales. 
Consolidated area. 
Fremitus increased. 
Hyper-resonance on per- 
cussion. 
Vocal resonance increased, 
Dulness on percussion. 
Consolidation—bronchial 
breathing. 
Increased fremitus and 
resonance. 
Dulness on percussion. 
Tubercular infiltration. 
Impaired resonance on 
percussion. 
Congestion—crepitant and 
subcrepitant rales. 
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 
and tuberculosis (Figs. 124 and 125), 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, 
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- THE THORAX AND ITS VISCERA. 
285 
tions not being stopped as in health by the tense septa and vesicular 
walls. It is best heard in cases of pleural effusion over the apex 
of the chest, into which the collapsed lung has been pushed by the 
Fig. 124. 
Showing at x moderate dulness over tubercular infiltration. (Gibson and Russell.) 
effusion. This is sometimes called u skodaie 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. 
Fig. 125. 
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.) 
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 286 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 opening 
externally or into a bronchus, in a few cases of pleural effusion in 
thin-chested persons, and in rare instances before consolidation has 
occurred in pneumonia. 
In cases of pleural effusion a flat note on percussion is heard over 
the effusion, and it is of very much the same character as the sound 
elicited by percussion of the solid tissues of the thigh. (Fig. 122.) 
Fig. 126. 
Position of heart uncovered by lungs, A shows the area of superficial cardiac dulness. 
(Aitken.) 
Cardiac Dulness. On percussing the chest anteriorly on the left 
side it will be found that the normal resonance is decreased by the 
presence of the heart. At the apex of the chest on this side 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 THE THORAX AND ITS VISCERA. 
287 
by the presence of a solid organ, the heart. The impairment of reso- 
nance is not complete at the upper border of the heart, because of 
the fact that the edge of the lung intervenes between the heart 
and the chest-wall, and so the note which results on percussion is 
neither the normal resonance of the lung nor the dulness produced 
by the presence of the heart. (Fig. 126.) 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 “ car- 
diac triangles.” (Fig. 127.) 
Fig. 127. 
Diagram showing cardiac triangles. Compare this figure with Fig. 126, 
The large triangle begins at the level of the second left costal 
cartilage, and extends down the midsternal line to the level of the 
sixth costal cartilage. The base then extends to the apex-beat, 
normally situated in the fifth interspace just inside of the 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 with the third costal cartilage 288 
THE manifestation of disease in organs. 
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. 126.) 
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. 128.) 
Firs. 128. 
Position of heart in relation to ribs and sternum. 
When hypertrophy or dilatation of the heart occurs it will be 
found that the area of cardiac dulness extends to the right of the 
sternal line and to the left of the long side of the triangle, while 
the apex-beat is apt to be displaced downward and to the left. Great 
distortion of the triangles occurs as the result of pericardial effusion 
(Fig. 129), 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 THE THORAX AND ITS VISCERA. 
289 
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 Rotcli, namely, that any considerable 
Fig. 129. 
Outline of percussion-dulness in a ease of extensive pericardial effusion 
(Bramwell, after Sibson.) 
dulness in the fifth right intercostal space near the sternum means 
pericardial effusion, provided pulmonary consolidation and pleural 
effusions or adhesions are excluded. The writer has, however, often 
seen this sign present in marked cardiac dilatation. 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, is 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- 
beat 
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. 290 
THE manifestation of disease in organs. 
Relation of dulness 
to left apex-beat . 
Dulness may extend to the left 
of the apex-beat. 
Pericarditis with Effusion. 
Dulness does not extend to the left 
of the left apex-beat. 
Dilatation of the Heart. 
Pain over preecordia 
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. 
Etiology 
Usually acute, in course of 
acute rheumatism, cirrhotic 
Bright’s disease, etc. 
Usually chronic ; often associated 
with chronic valvular lesions, 
fatty and fibroid degeneration. 
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 : 
Pericarditis with Effusion. 
Hypertrophy. 
Rate of development 
Usually rapid. 
Usually slow. 
Impulse, when present, is in 
the third or fourth left inter- 
space, and is feeble ; apex 
tilted upward and outward, 
or beat effaced. 
Impulse powerful; if left ventricle 
hypertrophied, apex displaced 
downward and outward ; if right 
ventricle hypertrophied, apex 
displaced downward and inward 
beat may be in the epigastrium. 
Impulse; apex-heat. 
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. 
PnW 
Weak and quick ; may be ir- 
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. 
The various valvular and other lesions of the heart result in 
alterations 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 hyper- 
trophy), and aortic stenosis also causes the same enlargement, as a 
rule, in less degree. Mitral regurgitation causes hypertrophy and THE THORAX AND ITS VISCERA. 
291 
dilatation of the left ventricle and some enlargement of the left 
auricle, and the left auricle is also enlarged in mitral stenosis. 
Fig. 130. 
Fig. 131. 
Diagram of the normal heart, the continu- 
ous line indicating the outline of the right, 
and the incomplete of the left cavities. 
(Sansom.) 
Diagram of the heart of aortic obstruction 
and regurgitation. The dotted lines indicate 
enlargement of the left cavities, especially 
the ventricle. The liver-area only slightly 
increased. (Sansom.) 
Tricuspid regurgitation causes hypertrophy and dilatation of the 
right auricle and hypertrophy of the right ventricle, and mitral 
Fig. 132. 
Fig. 133. 
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.) 
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 above diagrams from Sansom will illustrate the  THE manifestation of disease in organs. 
292 
deformity of the cardiac triangles under these various conditions. 
(See Figs. 130, 131, 132, and 133.) 
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 fingers 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 sets of sounds : 
the respiratory and cardiac, and two chief varieties of breath- 
sonuds, namely, vesicular breathing and bronchial breathing. The 
vesicular sound 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 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 in its entire 
circumference is in close contact with the chest-wall. 
The respiratory sounds consist, as already stated, in the vesicular 
murmur and the bronchial or blowing sounds, which are sometimes 
designated by the term 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 
expiratory sounds. Normally in the perfectly healthy chest the 
ratio of the expiratory sound to the inspiratory sound is as one to 
three, although if the volume of air itself be measured the duration THE THORAX AND ITS VISCERA. 
293 
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 tuber- 
culosis, 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 thinness of the chest-wall. If it is exaggerated in a child 
or present in the area of normal vesicular breathing in adults, it 
usually indicates some irritation of the bronchial mucous mem- 
brane. If it is found in the apices of the lungs in a marked degree, 
and expiration is prolonged, it is an important and fairly sure sign 
of early pulmonary tuberculosis. 
Sometimes physicians speak of 11 broncho-vesicular breathing,” 
meaning a breath-sound consisting of both bronchial and vesicular 
sounds. It is sometimes heard in a healthy person when he breathes 
superficially, and in disease usually indicates the early stages of 
pneumonia or early tuberculosis of the lungs. It is of value as a 
diagnostic sign only when 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 
latter expiration holds its normal ratio to inspiration, whereas in 
disease it is greatly prolonged. 
Irregular, u cog-wheel,” 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, and 
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 294 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 nor- 
mally heard, is, therefore, a sign of tubercular or pneumonic con- 
solidation (Fig. 134) or of compression or collapse of the lung above 
a pleural effusion. Bronchial breathing is also heard in that area of 
the chest in which vesicular sounds normally predominate, 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 tissue and cavities transmit sound better 
than the normal vesicular portion of the lung, which is a combina- 
tion of air and vesicular wall. If the cavity be large, we have a 
Fig. 134. 
Increased vocal resonance and 
fremitus on auscultation and 
palpation. Dulness on percus- 
sion 
Bronchial breathing. 
Pneumonia of the inferior lobe with the physical signs characteristic of consolidation 
(Gibson and Russell.) 
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 
what is called “amphoric breathing”—that is, a sound like that 
produced by blowing over the mouth of an empty bottle. This 
sound is also rarely heard in cases of pneumothorax in which the TIIE THORAX AND ITS VISCERA. 
295 
bronchial tubes, running near to the pleural cavity, transmit their 
sound to the air in the pleural space. 
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 
tli is 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. 
There are a number of other sounds heard in the chest in cases 
of disease of the air-passages. These consist in rales 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 important 
sign of croupous pneumonia in its early stages before consolidation 
has occurred. It also is heai’d in cases of pulmonary collapse and 
oedema, but not always in any of these diseased conditions. 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 postei’iorly. 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 296 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
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 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. 122.) 
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 fine 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 sibilant, 
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 
diagnosis 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 glide over one an- 
other noiselessly, but when they become roughened by disease a 
sound of friction is developed. The friction-sound is sometimes so 
slight as to be almost inaudible, and again so harsh as to sound like 
a loud creaking, which not only can be 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-souud is heard at the apex of the 
chest, tuberculosis will often be the cause of its existence in this THE THORAX AND ITS VISCERA. 
297 
locality. Care should always be taken that fine rales are not mis- 
taken for frietion-sounds. They can be separated one from the 
other by the recollection of the facts that rales are modified by 
coughing, are 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 its frequency and 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 rode for the first time. Sometimes 
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 frem- 
itus 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 exam- 
iner 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 vetebral 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 vesic- 
ular breathing, the sound of the voice will be still more modified, 
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 298 
THE MANIFESTATION OF DISEASE IN ORGANS. 
in the healthy lung and in the diseased area cannot be distinguished. 
Usually we get the patient to speak by asking him to repeat his 
name or to count u one, two, three.” The unemployed ear of the 
physician should always be closed, and the counting or speaking 
should be continued only 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 the 
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. 117.) Vocal resonance, however, 
may be increased over pleural effusions, particularly the resonance 
of the whispered voice. This is called “ Baccelli’s sign,” and 
Baccelli claims that it serves to separate serous effusions from pu- 
rulent 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 
u 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 by compression and partial 
occlusion of a bronchus. 
Finally, in pvo- 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 
1 This sign is mentioned here for what it is worth. The writer has never been able to use it 
with success. THE THORAX AND ITS VISCERA. 
299 
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. 
Pneumonia. Let us suppose that a patient, previously in health 
or without any serious pulmonary complaint, is found, after a physi- 
cal examination of his chest, to have rapid breathing, a somewhat 
anxious expression, a bright eye, and a dusky flush on one or both 
cheeks. Palpation 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 impairment of resonance over the area where fremitus was 
found most 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 so 
fast as the respiration would lead us to suspect, for it is a character- 
istic 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 sputa, or, as the disease progresses, purulent sputa, 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 prob- 
ably 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- 300 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
Care should be taken in all suspected cases of croupous pneumonia 
that another common cause of the same symptoms does not mislead 
the physician. This cause or condition is acute pneumonic phthisis. 
In many cases only the finding of tubercle bacilli in the sputum, and 
the fact that the lung remains consolidated for a long time and 
finally breaks down and forms a cavity, will permit a diagnosis of 
acute tuberculosis to be made. 
The condition of croupous pneumonia cannot readily be confused 
with any other disease except acute pneumonic phthisis, because of 
its characteristic symptoms, but catarrhal pneumonia and tubercu- 
losis of the lung often are confused. 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 elicited in croupous pneu- 
monia, and only impairment of resonance may be developed. There 
is increased vocal fremitus on palpation and increased vocal reso- 
nance 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 THE THORAX AND ITS VISCERA. 
301 
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 rales, the signs of the 
Fig. 135. 
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). 
breaking down of lung-tissue. Finally, when a cavity is developed 
the percussion-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 typi- 
cally. (Fig. 135.) Prolongation of expiration is also present, and 
sweats, irregular hectic fever, and great loss of flesh ensue. 302 
THE MANIFEST A TION OF DISEASE IN ORGANS. 
Pulmonary Abscess. The history of the case and its symp- 
toms are our chief means of separating pulmonary abscess from 
pulmonary tuberculosis with the development of cavity, for the 
physical signs are about the same. In cases of abscess we find that 
the patient has suffered from pneumonia or from pyaemia with 
embolic infarction. In other cases discharges from the nose and 
Fig. 136. 
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. 
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 found at the apex or in the upper 
lobe. The constitutional disturbance in abscess is often very slight, 
whereas in tuberculosis it is usually severe. In abscess the sputum 
is copious and purulent, aud often coughed up in gushes, whereas in THE THORAX AND ITS VISCERA. 
303 
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. 
Bronchiectasis with fetid breath is occasionally met with, but the 
foetor 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 
pneumonia, particularly of the croupous type, and in pulmonary 
tuberculosis, which are apt to be overlooked, namely, the axilla and 
the septum between the upper and middle lobe on the right side, an 
area exposed to percussion and auscultation only 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. 136.) 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 
dulness on percussion or, on auscultation, rales, and the other physi- 
cal 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. 
Pulmonary (Edema. 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, the crepitant rales, the limi- 
tation of these signs to the lower part of the chest, combined with 
dulness on percussion, the absence of fever, the frothy sputum, and, 
it may be, the presence of renal or cardiac disease, all point to the 
true state of affairs. 
There is another state that gives dulness on percussion’, crepitant 
rales, and the other physical signs of pneumonia, namely, pulmonary 
congestion dependent upon the action of a feeble heart in the course 
of prolonged exhausting fevers; but the history of the illness, the  THE MANIFESTATION OF DISEASE IN ORGANS. 
304 
feeble heart, and the development of these signs in the dependent 
parts of the chest effectually preclude the idea of any acute inflam- 
matory process in the lung. 
Finally, we frequently have after a pulmonary apoplexy an area 
of consolidation in the lungs; but if this be the case, we also have, 
as a rule, a history of haemoptysis. This condition is, however, 
comparatively rare. 
Pleuritis. To cite another form of thoracic disease, let us sup- 
pose 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 aus- 
cultation 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 diappears, and that the affected side, previously almost 
normally 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- 
cussion 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 
au 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-shaped). Above the level of the 
effusion percussion over the compressed lung gives a somewhat hol- 
low note or hyperresonance, 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. Iu auscultiug the THE THORAX AND ITS VISCERA. 
305 
chest in the area in which flatness has been developed by percus- 
sion very distant breath-sounds are audible, except in the back near 
the vertebral column, where there may be marked blowing breath- 
ing. If the patient speaks, there will be found loss of vocal reso- 
nance and of fremitus over the effusion, but along the margin of 
the spine on the diseased side there may be heard in some cases 
bronchophony, or even the bleating voice-sound called aegophony. 
Inspection and palpation will show the apex-beat of the heart dis- 
placed 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 effusion 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 
succussion 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 
“coin percussion.” This consists in having an assistant place a large 
silver coin 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 coin with the edge of another silver coin. If the coins 
be struck together below the surface of the effusion, very little of 
the metallic sound will be transmitted through the chest. If the 
coins 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 transmis- 
sion 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. 306 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Finally, if the effusion is absorbed by unaided nature, the area 
of flatness on percussion becomes less and less great from above 
downward, the expansion of the chest on inspiration increases, the 
interspaces 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 eases 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 insidious in its onset and devoid of prodromes, 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 
effusion 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 
inflammation by the method of Pohl and Rosenbach. This con- 
sists in withdrawing some of the fluid by an aspirating-needle after 
the patient has 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 not 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 effusion occurs in THE THORAX AND ITS VISCERA. 
307 
otherwise healthy men without these causes. The possibility of the 
hemorrhagic effusion being due to a leaking aneurism, or to leakage 
from an ulcerated bloodvessel in tubercular disease of the lung, is 
to be remembered. 
Bronchitis. If after exposure to cold there is a sense of sore- 
ness in the chest, with more or less oppression and a hard cough, 
which seems to tear the bronchial tubes, the cough being without 
associated expectoration 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 
scapulae, 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 rales, 
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. 
Should the case become chronic, the sounds of coarse and more 
or less sonorous rales will persist and 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 “ 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. 
Emphysema. 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 auscultation of the chest we find marked prolongation of expi- 
ration, diminished vocal resonance and fremitus, and increased reso- 
nance on percussion. The face is often quite cyanotic, the super- 
ficial veins of the neck turgescent, the abdominal respiratory move-  THE MANIFESTATION OF DISEASE IN ORGANS. 
308 
ments abnormally 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 regur- 
gitation 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. 
Asthma. If it is asthma, there will be labored breathing in 
which all the accessory muscles of respiration in the neck and trunk 
aid the ordinary respiratory muscles. The posture of the patient 
will usually be that of sitting up in bed and somewhat leaning for- 
ward. The face will be flushed, the vessels of the face and neck 
turgid, and the 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 he 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 
rales 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 blow- 
ing breathing, musical notes, or squeaking or creaking noises, both 
on inspiration and expiration. Finally, as secretion begins to be 
established, musical and cooing rales may be heard, in well-marked 
cases, all over the chest before the ear is placed against the patient. THE THORAX AND ITS VISCERA. 
309 
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 Curschman’s spirals and Charcot-Levden 
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 test 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 pass- 
ing away; but if, on the other hand, the attack is beginning, the 
prolonged expiration, with comparatively few rales, the harsh bron- 
chial breathing, and the general objective symptoms of the case will 
explain the cause of the pulmonary condition. 
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 true 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 me- 
diastinum 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 a 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 obstruc- 
tion is in the larynx, if unable to speak. Such obstruction when 
seen in children is, as a rule, due to spasmodic croup, and, if so, 310 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 to growths in the mediastinum pro- 
ducing 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 con- 
solidation by causing an exudation in the lung-tissue. 
The diseased conditions from which it is necessary we should 
distinguish 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 ean 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.) THE THORAX AND ITS VISCERA. 
311 
Unfortunately, the most common age for aneurism is much the 
same as that for mediastinal disease, although mediastinal disease 
seems to occur more frequently iu 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 equal 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 iu 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 mediastinal abscess the diagnosis of mediastinal tumors is 
much more readily made. Iu the first place, in abscess we gener- 
ally have a history of traumatism, or, if the case be one of cold 
abscess, it is commonly associated with a history of struma. If the 
abscess be acute, there is generally the history of pain, followed by 
a chill more or less severe, and fever; or, if cold, then we frequently 
have irregular febrile movements, with long-continued anorexia and 
loss of flesh. Cold abscess, too, is generally in the posterior medi- 
astinum, 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 pro- 
duced 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 312 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 abso- 
lutely impossible to make a diagnosis unless by symptoms of press- 
ure 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 medias- 
tinal disorder rather than one confined to the lungs. If the heart 
be displaced in either direction, the odds point to mediastinal tumor; 
but the presence or absence of a haemoptysis, as has just been stated, 
influences the diagnosis not at all. 
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 irregu- 
lar and varying. 
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 sound of the words “ lub dup;” the “lub” 
being the so-called first sound of the heart, produced by the contrac- 
tion of the heart-muscle and the tense valves, and the “ dup ” being 
caused by the slapping to of the aortic valves. After listening in 
this region we next place the ear over the second right costal carti- 
lage, in order to come as near as possible to the point of origin of 
Heart-sounds and Signs. THE THORAX AND ITS VISCERA. 
313 
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 c: lub” is feeble, and 
the u dup ” sound is also feeble, because the valves do not slap back 
into place with as much force as is normal. If, on the other hand, 
the heart is hypertrophied or stimulated, we find these sounds 
accentuated, and it is of importance to remember that marked accent- 
uation 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. 
Fig. 137. 
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. 
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 regurgi- 
tation and in some cases of pneumonia and emphysema. 
The sounds produced at the various orifices of the heart are heard 
best at the following points (Fig. 137): The mitral valve is heard 
best at the apex-beat; the aortic valve at the second right costal 314 
THE MANIFESTATION OF DISEASE IN ORGANS. 
cartilage, the tricuspid valve over the sternum on a line drawn from 
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. 
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 
Having found that there is a murmur, aud, 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 car- 
tilage (second right). If the murmur be mitral in origin, it will 
not be heard at this place, unless it be so loud as to be transmitted. 
If it is aortic in origin, it will be louder here than at the apex. If 
it is tricuspid, it will be loudest in the tricuspid area; if pulmonary, 
loudest at the pulmonary area. As murmurs at the tricuspid and 
pulmonary valves are rare, we nearly always have to deal with 
aortic or mitral murmurs, or both. In this way, therefore, 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 deter- 
mine whether it is that of mitral regurgitation or obstruction, or, 
as they are also called, incompetence and stenosis. The probabili- 
ties are that it is the regurgitant murmur, because this lesion is by 
far the most common murmur heard in the heart; and if 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 
1 It must not be forgotten that murmurs due to endarteritis also are frequently found in 
choreic children. THE THORAX AND ITS VISCERA. 
315 
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 dis- 
ease are present, it is almost certainly one of mitral regurgitation. 
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. 138. 
Fig. 138. 
Showing at x the apex-heat where the murmurs of mitral regurgitation and obstruction can 
be 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. 
In adults inspection and palpation will rarely reveal much of a 
thrill over the prsecordium 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 316 
THE MANIFESTATION OF DISEASE IN ORGANS. 
chapter) is broadened, extending beyond the right edge of the ster- 
num and to the left of the mammillary line. 
If the pulse is irregular and asynchronous with the heart-beats, 
the heart enlarged by dilatation, and the urine scanty, we recognize 
that compensation is lacking and treatment needed. 
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 prsecor- 
dium 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 by a very 
irregular action of the heart, the first sound becoming accentuated 
and the murmur disappearing or being inconstant, because the 
auricle is too feeble to drive the blood forcibly through the orifice. 
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. 
Cyanosis, jugular distention, congestion of the lungs, and dysp- 
noea also indicate a failing heart, for the venous system is engorged 
and the arterial system starved. 
In the diagnosis of mitral obstruction the physician must not be 
misled by the possible presence of what is known as Flint’s mur- 
mur, a presystolic murmur heard in the sternal area, and due to 
relaxation of the mitral valves, which are thrown into vibration 
during diastole by blood regurgitating from the aorta in aortic 
regurgitation. 
If, however, we have found the murmur to be aortic, we must 
exclude aneurism, and then determine whether it is that of aortic 
regurgitation or obstruction. 
The characteristic symptoms of aortic aneurism vary greatly with 
the site of the lesion, as will be pointed out below. The most 
typical signs are a “bruit” or angry murmur systolic in point of 
time, thrill over the growth, dulness on percussion over the area of THE THORAX AND ITS VISCERA. 
317 
this thrill, dyspnoea, cardiac hypertrophy, and functional disturbance. 
Finally, a history of alcoholism, syphilis, and severe strain or injury 
will be a valuable indication of a causative factor. It is to be 
remembered that small aneurisms deeply situated, which do not 
press upon other organs, may produce no symptoms for years, and 
Fig. 139. 
mo shows area of greatest intensity of a mitral obstructive murmur, tr shows area of 
greatest intensity of a tricuspid regurgitant murmur. (From the author’s wards.) 
finally be discovered only at autopsy. When the ordinary signs of 
aneurism are not clear, an examination of the radial pulses may 
reveal that one of them is delayed. 
Although these are the general symptoms of aortic aneurism, 
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 that arm. The heart may be pushed downward 
and to the left, and the voice may be lost or partially impaired by 
pressure on the recurrent laryngeal nerve of the right side. The 318 
THE MANIFESTATION OF DISEASE IN ORGANS. 
pupil of the eye may be widely dilated through irritation of the 
sympathetic, and there may be unilateral pallor of the face from 
this cause. If the pupil is contracted then the cilio-spinal fibres are 
paralyzed by pressure. In such a case pain is apt to be a promi- 
nent symptom and so severe as to be almost like that of true angina. 
Percussion over the second right interspace will give impaired reso- 
nance, and auscultation of the area of the pulmonary valve may 
show a pulmonic systolic murmur, due to pressure on the pulmo- 
Fig. 140. 
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 an arrest of the growth of the 
aneurism by electrolysis. 
nary artery, which in turn causes hypertrophy and dilatation of the 
right ventricle. There may be bulging of the first, second, or third 
interspace on the right side. Generally 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. 
Again, let us suppose that the patient has a ringing, brassy cough, 
difficulty in swallowing, and expansile pulsation in the episternal THE THORAX AND ITS VISCERA. 
319 
space and epiclavicular space of the left side, and dulness on per- 
cussion over the first and second left intercostal space. The left 
side of the face and neck may be engorged from pressure on the 
left innominate vein. Pupillary symptoms similar to those already 
named may be present. There is difficulty in breathing, particu- 
larly on inspiration, owing to the pressure of the growth on the 
trachea, the paralysis of the left vocal cord, and the pressure on the 
left bronchus, and there is dysphagia due to pressure on the oesopha- 
gus. The voice is altered from pressure on the left recurrent laryn- 
geal nerve. These symptoms indicate a lesion of the transverse 
arch. If, however, none of these important signs are present ante- 
riorly, we must search for some of them posteriorly, particularly the 
bruit and the expansile pulsation, and, if these are found to the 
left of the vertebral column opposite the angle of the scapula, we 
can rest assured that the aneurism involves the descending aorta. 
Severe intercostal pain is often felt in these cases. 
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 but not in all. 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 emphasized 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 mur- 
mur occurs with the systole of the ventricles, and the carotid pulse 
and apex-beat; it is harsh, as a rule, and is transmitted up into 
the carotid and it may be into other arteries of less importance. 
(See Fig. 141.) It is produced by the contraction of the ventricle 
driving the blood through a narrowed or roughened aortic orifice. 
Considerable hypertrophy of the left ventricle is usually present, 
and the apex-beat is strong and forcible if compensatory hyper- 
trophy is present. A similar murmur may arise from vegetations 
on the aortic valves, or, in other instances, morbid atheromatous 
changes in the aorta may produce a systolic aortic murmur. 
If, on the other hand, the murmur occurs after the systole or the 320 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 plainly heard at the 
apex. (See Fig. 142.) In this condition we have usually marked 
dilatation 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 valves, which allows the blood to 
regurgitate into the heart after it is driven out into the aorta. 
Fig. 142. 
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 in association with this murmur we find irregularity of the action 
of the heart, a lack of sharpness in its sounds, displacement of the 
apex-beat downward and to the left, extension of cardiac dulness 
to the right, and a feeble pulse, then we know that the heart is fail- 
ing. Finally, a soft mitral systolic murmur and the development 
of rales in the chest at the base of the lungs show still greater 
failure. 
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- THE THORAX AND ITS VISCERA. 
321 
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 in the left. 
Actual disease of the pulmonary valve is exceedingly rare, and 
the regurgitant form of lesion is almost never met with. The 
murmurs sometimes heard, and the thrills sometimes felt, in this 
area are generally due to anaemia, the puerperal state, *or some 
neurosis, or to congenital narrowing of the pulmonary artery, or 
to compression of the vessel by the heart. If 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 orifices 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 derived from the London 
hospitals are usually accepted as correct. His results are as fol- 
lows, 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 regurgi- 
tation. 
7. Mitral regurgitation and tricuspid regurgitation. 
8. Aortic regurgitation and stenosis; mitral regurgitation; tri- 
cuspid 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 regurgita- 
tion. 
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 regur- 
gitation. 322 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
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 
general symptoms depends entirely upon the question of compensa- 
tion by hypertrophy. If there is a leak in a valve or a constriction 
of an orifice, this leak or obstruction must be overcome by compen- 
satory 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- THE THORAX AND ITS VISCERA. 
323 
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 
be comfortable only when sitting up. Dropsy of the lower extremi- 
ties now comes on and the liver becomes enlarged from portal con- 
gestion, 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 addi- 
tion 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. Very 
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 the bloodvessels. 
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 with palpitation 
and a sense of cardiac oppression, we often have a great deal of car- 
diac 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  THE MANIFESTATION OF ELS EASE IN ORGANS. 
324 
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 
interesting signs of this heart-lesion, chief among which is the 
“ water-hammer’ ’ or “ trip-hammer ” or “Corrigan pulse,” the 
throbbing 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 the same capillary pulsation will be found. Ophthalmo- 
scopic examination 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 him- 
self 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 extraordinary 
exertion, generally of a prolonged character, rather than a brief and 
sudden effort, which would perhaps cause aneurism. Since that 
time his symptoms of heart-failure have been marked. He may 
perhaps have attacks of syncope. Examination of his heart reveals 
on inspection a diffuse thrill in the region of the apex; but this 
thrill is too feeble to be felt, though well marked to the eye if his 
chest is thin. Percussion shows that the area of cardiac dulness is 
increased vertically and laterally, and auscultation will discover 
feeble heart-sounds; and if the dilatation of the muscular portion 
of the heart is associated with dilatation of the orifices, a murmur 
may be present, most commonly that of mitral regurgitation. Some- 
times 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 by 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 THE THORAX AND ITS VISCERA. 
325 
sedentary lives in the winter, develop irregular eardiae action, pal- 
pitation, and some shortness of breath. Examination of the prte- 
cordium 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 dillness is also found. 
Again, let us suppose that a patient presents himself with the 
statement that he has attacks in which he suffers from a very rapidly 
beating heart. His skin is alternately red and pale, and sweats 
without cause, but a careful examination of the heart fails to reveal 
any murmurs or organic abnormality. There are considerable short- 
ness 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, 
perhaps only thirty or even as slowly as twelve times a minute. 
Bradycardia, or great slowness of the heart, may be due not only 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- 
thalmos 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 326 
THE MANIFESTATION OF DISEASE IN ORGANS. 
embolism or thrombus of one of the coronary arteries. If the 
vessel is suddenly plugged, death occurs; but if the process is 
gradual, an anaemic 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 pres- 
ence of fatty degeneration of the more superficial organs, such as the 
arcus senilis in the eye,1 the presence of atheromatous bloodyessels, 
the feeble heart-sounds at all times, and the evident feebleness 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 per- 
nicious anaemia. It is not possible to make a differential 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. 
When 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. Valvular disease may, of 
course, be found associated with the myocardial lesion. Such cases 
make up the greater number of sudden deaths, called popularly 
“ death by sudden cardiac failure.” 
Great feebleness of the heart and of the general system, loss of 
flesh (or sometimes maintenance of weight), and 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 
1 Ophthalmologists and many clinicians deny that arcus senilis has any significance of this 
character. THE THORAX AND ITS VISCERA. 
327 
child is the subject of congenital malformation of the heart. The 
following rules, laid down by Hochsinger, may be used for their 
diagnosis: 
1. In childhood loud, rough, musical heart-murmurs, with 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- 
carditis in 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 endo- 
carditis. 
4. An abnormally weak second pulmonic sound associated with 
a distinct systolic murmur is a symptom which, in early childhood, 
is to be explained only by the assumption of a congenital pulmonary 
stenosis, and possesses, therefore, an importance from a point of 
differential diagnosis which is not to be underestimated. 
5. Absence of a palpable thrill, despite loud murmurs which are 
heard over the whole prsecordial region, is rare, except with con- 
genital defects in the septum, and it speaks therefore against 
an acquired cardiac affection. 
6. Loud, especially vibratory, systolic murmurs, with the point 
of maximum intensity over the upper third of the sternum, asso- 
ciated 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 abdom- 
inal 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. 143. 
The regions of the abdomen and their contents. (Gray.) (Edge of costal cartilages in 
dotted outline.) 
auscultation. For the purposes of inspection the surface of the 
abdomen has been arbitrarily divided by diagnosticians into a num- 
328 THE ABDOMEN AND THE ABDOMINAL VISCERA. 
329 
ber of spaces, which are best shown in the accompanying figure 
(Fig. 143), 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.1 
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. On inspecting the abdominal surface the physician 
should look for eruptions which may indicate some general disease, 
as typhoid fever; for localized swelling, which may be due to hernia; 
for strise, indicating that the skin has been stretched by excessive 
fat, by great swelling from ascites, or by pregnancy. He should 
also in a case of suspected early pregnancy look for the dark line 
in the linea alba. If the umbilicus is protruding and tense it may 
indicate distention due to grave abdominal disease, or it may be 
infiltrated by a morbid growth which has been primarily hepatic. 
If it be a secondary growth the navel will be “ moored fast.” 
Sometimes it is much swollen from chafing and eczema. Umbilical 
hernia may be found. 
The general abdominal wall is protruded and retracted in nor- 
mal respiration in both sexes, but more markedly so in males. It 
is pushed outward or protruded by many perfectly normal causes, 
1 For changes in the skin of the abdomen, see chapter on the Skin. 330 
THE MANIFESTATION OF DISEASE IN ORGANS. 
such as an unusual amount of fat in the omentum, pregnancy, and 
an accumulation of liquid and food in the stomach after a heavy 
meal. It is also convex to an abnormal degree in cases iu 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. 
(See Figs. 145, 146.) In children a protruding pot-belly, “ the 
frog-belly” of the French, is seen in cases of scrofula or tubercu- 
losis of the mesenteric glands, and in those cases which suffer from 
chronic gastro-intestinal catarrh. It is claimed in a recently pub- 
lished 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, concave, 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. Thus excessive summer diarrhoea may produce 
such a result. We also find a retracted belly-wall in nearly all 
cases of advanced wasting diseases, such as carcinoma or 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 reual or hepatic colic or lead colic. Marked concavity and 
retraction of the belly-wall are also seen sometimes in cases of 
tubercular meningitis. 
Sometimes peristaltic waves are to be seen traversing the abdom- 
inal surface as the result of violent movements of the bowels in 
thin subjects. These waves are most commonly seen in cases of 
intestinal obstruction, and, if in the epigastrium, may be due to a 
dilated stomach. If the waves are from below upward and in the 
right side, they are probably arising in the ascending colon; if from 
above downward and in the left side, in the descending colon and 
sigmoid flexure. Again, gastric waves pass from left to right, while 
those in the transverse colon pass from right to left. 
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 THE ABDOMEN AND THE ABDOMINAL VISCERA. 
331 
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 where the 
intestines containing gas are floated up against the anterior belly- 
wall above the effusion. Sometimes, however, if the large intestine 
be empty of fecal matter, percussion in the flank behind the midax- 
illary line will reveal tympany, because the peritoneum walls off the 
liquid from the posterior surface of the bowel. Palpation will also 
reveal fluctuation 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. With the finger-tips of the right hand the oppo- 
site flank of the patient is struck a blow as in performing ordinary 
percussion, when the impulse if fluid is present will be transmitted 
to the fingers of the left hand. To prevent a transmission of the 
impulse through the abdominal wall, an assistant may press with 
the edge of his hand over the linea alba. As the result of grad- 
ually increasing intra-abdominal pressure the floating ribs become 
pushed outward, 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 muscles becoming separated, the peristaltic movements 
of the bowels can be readily felt through the intervening skin. 
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. 154). 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 be caused by tubercular peritonitis, by 332 
THE MANIFESTATION OF DISEASE IN ORGANS. 
obstruction of the thoracic duct, by valvular disease of the heart 
causing an obstruction to the flow of blood in the vena cava, or 
finally, by acute 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 albu- 
minuria. 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). 
Fig. 144. 
Dotted line shows area of cancerous liver extending far beyond 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.) 
There is an additional source of information to be utilized as 
to the cause of the ascites, 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 probably due to hepatic cirrhosis, whereas if due to the press- 
ure of a tumor the specific gravity is usually about 1.012 and the 
albumin nearly 2 per cent. Such a specific gravity and proportion THE ABDOMEN AND THE ABDOMINAL VISCERA. 
333 
of albumin may 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 disease 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 peri- 
toneal cavity, as carcinoma of the peritoneum or of the abdominal 
viscera, or tubercular peritonitis with or without pus, the specific 
gravity is much higher than just stated, namely, from 1.018 to 
Fig. 145. 
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.) 
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 Pohl and 
Rosenbach that the effusions due to venous engorgement, heart dis- 
ease, and renal lesions can be separated from those due to disease 
in the peritoneum affecting this membrane directly by a test follow- 334 
THE MANIFESTATION OF DISEASE IN ORGANS. 
ing 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 peri- 
toneum which have been named, it will not appear. The fluid to 
be tested is placed in a test-tube and some nitric acid and chloro- 
form added, when if iodine is present its characteristic color will 
appear. Should the cause of the ascites be a ruptured ovarian cyst 
Fig. 146. 
A case of enormous enlargement of the spleen in splenic leuksemia. (From a private patient.) 
the diagnosis of its cause, except from the history of a previous 
localized swelling, is exceedingly 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 iu the 
instances in which the specific gravity of the fluid is very low the 
swelling is due to a cyst of the broad ligament. THE ABDOMEN AND THE ABDOMINAL VISCERA. 
335 
Very often in cases of ascites, particularly when this condition 
arises from hepatic cirrhosis, there is developed on the anterior 
belly-wall a more or less well-defined bunch of veins, which is 
sometimes called the caput Medusce, as the result of an attempt at 
collateral circulation, to compensate for the obstructed flow caused 
by the changes in the liver. Sometimes a mediastinal growth will 
cause a somewhat similar development. When the obstruction is 
lower down than the liver the superficial veins of the lower part of 
the abdomen (hypogastrium) will be found distended. 
Fig, 147. 
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.) 
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, 
will arise under the floating ribs on the right side, aud 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 336 
THE MANIFESTATION OF DISEASE IN ORGANS. 
umbilical area to the opposite side of the abdomen, as in Fig. 144. 
In enlargement of the spleen similar signs, springing from the 
floating ribs well over to the left side, may be developed (see Figs. 
146 and 147), and large cystic kidney on either side may cause 
abdominal bulging, particularly if the kidney be floating. (See 
Floating Kidney and Spleen.) 
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 mediastinal and retro-peritoneal glands. Again, 
distention of the epigastrium is apt to be caused by enlargement of 
the left lobe of the liver. In ovarian tumors the growth often 
gradually distends the entire belly equally; but, as already stated, 
the 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 
swelling 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 distended by liquid and gas. (See Percussion in this 
chapter.) 
AVre 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.) 
Another useful method 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- THE ABDOMEN AND THE ABDOMINAL VISCERA. 
337 
tionary outer tube; a cable covered with tight-fitting rubber tube; 
and a sponge-spiral attached to the cable. 
Tiirck says: u 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 
Fig. 148. 
Tiirck’s gyromele. 
ci 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. 
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 pal- 
pation through the abdominal wall. A stiffer cable (No. 2) is then 
used, and pushed onward until it meets with resistance at the lesser 
curvature, and its length is noted. The lengths are compared, and 
their difference shows the degree of distensibility. The degree of 
distention also is found by palpation through the abdominal wall.” 
(For the symptoms of gastric dilatation, see the chapter on Vom- 
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 dis- 338 
THE MANIFESTATION OF DISEASE IN ORGANS. 
ease 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 con- 
tents is the use of gentle palpation, the fingers being gradually 
worked down into the abdominal cavity in such a way as not to 
cause pain or excite the muscles of the abdominal wall to resistance. 
The hand should always be carefully warmed before palpation is 
attempted, and the object of the examiner is to discover, first, the 
hardness or resistance to pressure; secondly, the consistency and 
form of the organs which he can touch; and, thirdly, whether any 
swellings which he feels are movable, bound down and immovable, 
pulsating, soft or hard, nodular or smooth. The patient whose 
abdomen is to be palpated must be placed flat on his back, with the 
knees draw 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 else- 
where than in the belly, while the examination is made, as in this 
way voluntary muscular resistance is removed to some extent. He 
should be made to breathe easily through his opened mouth; and 
if the belly-wall remains so rigid that a perfect examination is im- 
possible, and yet the results of such an examination are very impor- 
tant, ether or chloroform should be given to relax the muscles. 
After the abdominal contents have been carefully examined, the 
patient being on his back, he should be placed first upon his left 
side and then upon his right and the abdominal contents again pal- 
pated. This is particularly necessary when examining the belly 
for growths or when enlargement or displacement of the liver, 
spleen, or kidneys is suspected. 
Great resistance of the rigid abdominal muscles is found when- 
ever peritonitis is present in an acute form, in some cases of renal THE ABDOMEN AND THE ABDOMINAL VISCERA. 
339 
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 
tenderness of the abdomen, the drawn lip, the thirst, and the dis- 
tention or rigidity of the belly-wall, is pain of a severe character; 
unless it be septic peritonitis, when pain may be absent. There are 
also the drawing up of the limbs to relieve abdominal tension, obsti- 
nate constipation, moderate fever, and a very rapid, quick pulse. 
The tongue speedily becomes dry and parched, and collapse may 
soon ensue in severe cases. It is not to be forgotten that local- 
ized peritonitis 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 examination, may cause great rigidity 
of the belly-wall without there being any abnormal condition pres- 
ent. This can be generally overcome by gentleness in palpation and 
by resting the palm of the hand on the belly and partly flexing the 
fingers, rather than by attempting to insert the finger-tips between 
the abdominal muscles. The writer has 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, we find a swelling. In 
the first place, we must decide as to whether it is in the abdom- 
inal 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 by 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 peri- 
toneum. 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 340 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 tuber- 
cular 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 carci- 
nomatous 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 years); 
will have a history of constantly increasing pain and discomfort in 
the stomach; there will have been much sour belching, and perhaps 
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 circum- 
stances, 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 gradu- THE ABDOMEN AND THE ABDOMINAL VISCERA. 
341 
ally accumulated, will be expelled. The probable diagnosis of 
gastric cancer and of gastric dilatation can usually be confirmed by 
percussion, 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 
Fig. 149. 
Outline of normal position and size of stomach in an adult when distended with gas. 
(After Meinert.) 
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 342 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 obstruc- 
tion, there will be impairment of resonance wherever the pylorus 
may be situated. While this is a somewhat indefinite statement, 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. 149 shows the normal gastric 
area when the stomach is distended with gas. The following 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. 150, 151, and 152.) 
Fig. 150. 
Profile view of the abdomen of a woman, aged sixty-five years, showing the tumor 
formed by the dilated stomach. (Osler.) 
Many of these cases of gastric dilatation are also associated with 
atrophy of the gastric tubules, or at least an absence of any secre- 
tion of normal gastric juice. The matters vomited, or washed out THE ABDOMEN AND THE ABDOMINAL VISCERA. 
343 
Fig. 151. 
Showing the position and size of the stomach. (Osler.) 
Fig. 152. 
Tumor of the abdomen caused by a dilated stomach. (Osler.) 344 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 chloride solution are mixed with one or two drops of pure 
carbolic acid, 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 
abdominal wall. In such instances the points which aid us in sepa- 
rating the condition from gastric cancer are the fact that the patient 
is young and usually a woman; that the vomiting occurs immedi- 
ately after taking food, for in gastric cancer it is only seen in most 
cases several hours after food has been taken; that there is no sign 
of gastric obstruction; that there is an excess of hydrochloric acid 
in the gastric contents in cases of ulcer, and an absence of this acid 
in cases of cancer; and, finally, that there is no cachexia in cases of 
gastric ulcer, though there may be ansemia. 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 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 present- 
ing 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 ABDOMEN AND THE ABDOMINAL VISCERA. 
345 
The solution of phloroglucin and vanillin is made as follows: 
Phloroglucin gr. xxx. 
Vanillin gr. xv. 
Absolute alcohol fSj. 
This solution is pale yellow in hue. It must 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 distributed 
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 
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 scirrhous cancer, and may 
be primary or secondary. Segre found that of 627 cases of carci- 
noma of the upper abdominal organs cancer of the pancreas occurred 
in 127, but in only 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  THE MANIFESTATION OF DISEASE IN ORGANS. 
346 
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 u 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 reso- 
nant on percussion. Abscess in this region also follows abscess of 
the pancreas or fat-necrosis of this organ in rare instances. 
Sometimes, too, we have marked enlargement of the head of the 
pancreas due to a malignant pancreatitis. This is particularly apt 
to be associated with cholelithiasis. 
The appearance of sudden swelling in the neighborhood of the 
pancreas, associated with intense pain, nausea, and vomiting, may 
be due either to acute hemorrhagic pancreatitis, to intestinal 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, although the history of 
the patient may aid us in deciding the cause of the illness. (See 
chapter on Vomiting for symptoms of intestinal obstruction.) 
Either palpation or inspection may reveal pulsation in the epigas- 
tric area. This may be due to distention or enlargement of the 
right ventricle or to excessive aortic pulsation or to venous pulsa- 
tion in the liver. If due to the action of the ventricle there will 
be additional signs of cardiac disturbance on examining the heart, 
and in hepatic pulsation there will not only be found tricuspid 
regurgitation, but a pulsation below the floating ribs at the lower 
border of the liver. An excessive aortic pulsation is often met 
with in hysterical or neurasthenic persons without any abdominal 
lesion. Epigastric pulsation is also often transmitted from the 
aorta to the hand by enlarged abdominal glands or tumor-masses. 
If the pulsation of the aorta is not transmitted by glands or tumors, 
impulse may be due to aneurism of the abdominal aorta, the diag- 
nosis of which is established if, in addition to a pulsating sensa- 
tion, we also find on palpation a marked thrill, an expansile move- THE ABDOMEN AND THE ABDOMINAL VISCERA. 
347 
ment 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 prominent symptom. Some- 
times a horseshoe kidney extending across the vertebral column 
will mislead one into a diagnosis of an intra-abdominal tumor, for 
horseshoe kidney is not very rare, being found as often as once in 
1650 autopsies. 
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. Such a 
growth occurs most frequently in the caecum, when the tumor will 
be found in the right groin, or in the sigmoid flexure, when it will 
be found in the left groin. 
Tumors or foreign bodies in the bowel can nearly always be 
moved about unless bound down by inflammatory adhesions, so 
differing from growths which involve the immovable parts, such as 
the retroperitoneal glands. Very rarely we find a cancerous tumor 
of the omentum, but when it is present it usually becomes retracted 
and indurated so that its hardened edges can be felt extending 
across the abdominal cavity. More commonly when multiple nod- 
ules are found in the omentum or studded over the surface of the 
bowels, they are due to peritoneal tuberculosis. Not rarely these 
nodular masses are also found studded over the mesentery. 
Floating kidney may also cause a marked movable swelling or 
tumor-like mass in the upper zone of the abdomen. It may be 
mistaken for a tumor of the uterus, or of the liver, omentum, ovary, 
or spleen, or even for a much-distended gall-bladder. If the belly- 
walls are thin, the peculiar shape of the kidney can sometimes be 
outlined by palpation, 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 pal- 
pation of the flank, if the kidney has floated away from its normal 
seat, may reveal lessened resistance in this area, and bimanual pal- 
pation, one hand being placed at the back and the other in front, 
may reveal the presence 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. In other 
instances, the patient lying on her back with the thighs flexed, the 
physician grasps the side between the rib and the iliac spine and  THE MANIFESTATION OF DISEASE IN ORGANS. 
348 
directs the patient to take a full breath, when the kidney, if mov- 
able from its normal resting place, can be felt passing down between 
the thumb in front and the fingers behind. The fingers should be 
in the flank and the thumb over the side of the abdomen. If the 
kidney be pressed upon gently it can be slipped back into place on 
expiration. The condition of floating kidney is more common in 
women than in men, but may occur in both sexes. It is generally 
found on the right side, although dislocation of the left kidney is 
not very rare. 
When the kidney is enlarged from cystic degeneration, from 
ordinary hydronephrosis, and from echinococcus cysts, it may be 
readily felt in the umbilical area in many instances. Hydrone- 
phrosis has been mistaken, in children particularly, for sarcoma 
of the kidney, and in adult females for ovarian tumor. The diag- 
nosis in some of these cases can be made only by tapping. The 
fluid obtained in hydronephrosis will usually be somewhat turbid 
and contain epithelial cells. It should not be forgotten that the 
condition of hydronephrosis may be intermittent, for, if this is not 
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. This intermittence in the size of the tumor 
may be of considerable diagnostic aid, for sudden decrease in size 
would indicate the escape of fluid through a temporarily patulous 
ureter, and its redevelopment would indicate that this pathway of 
escape was again closed. Should the fluid escape into the bladder 
free urination would naturally take place shortly after the tumor 
decreased in size. Hydronephrosis may be bilateral. In 13 out 
of 20 cases collected by Roberts this was the case. 
A fluctuating swelling in the epigastrium or flank may also arise 
from cysts of the mesentery. These may grow to a very large size. 
In other cases a cystic hydroma of the tissues near the kidney may 
be present. Hawkins has recorded a case in which a large cyst, 
with an atrophic third kidney attached to it, filled nearly the entire 
right side of the belly, and from which after death five pints of 
clear fluid, devoid of albumin and casts, were removed. As already 
indicated, much diagnostic aid can often be given by tapping an 
obscure abdominal cyst. 
Bulging of the flank, with pain, fever, and perhaps fluctuation, 
indicates perinephritic abscess or caries of the spine with cold 
abscess. THE ABDOMEN AND THE ABDOMINAL VISCERA. 
349 
In connection with the subject of abdominal tumors, 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 pres- 
ence of resonance on percussion over the area of normal splenic 
dulness will confirm the diagnosis that the spleen has become dis- 
placed. 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 twisting of its 
pedicle and secondary engorgement, its size may be enormous; but 
if this condition 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. 
u Phantom tumor” is generally found in hysterical women, and 
often leads to ludicrous errors in diagnosis. It is due to persistent 
dilatation of a knuckle of intestine by gas, thereby forming a mod- 
erately hard and more or less constant mass, which may resemble a 
real tumor. Examination of the patient under ether will usually 
reveal its true character. Localized 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. 153, and that as we percuss above it on the ribs 350 
the manifestation of disease in organs. 
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 
Fig 153. 
Showing absolute and relative percussion dulness of liver and heart. 1. Relative dulness ot 
liver. 2. Absolute dulness. 3. Relative dulness of heart. 4. Absolute dulness. 
they begin as high as the nipple, or above it, and then cease at a 
line drawn across the abdomen about midway between the ensiform 
cartilage and umbilicus. To the left of the middle line of the ster- 
num the liver-dulness merges into the cardiac dulness. (See Fig. 
153.) 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. THE ABDOMEN AND THE ABDOMINAL VISCERA. 
351 
When a hard and firm mass with a smooth surface can be felt in 
the right hypochondrium or right umbilical area, which is movable, 
and which has an edge which can be readily felt on deep palpation, 
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 enlarge- 
ment 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 sensation to the 
hand when the abdominal wall is moved over the organ. In malig- 
nant growth large and small nodules may often be found, and depres- 
sions or umbilications of its surface may be marked. (Fig. 144.) 
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 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 fluctuation 
will be found, as a rule; whereas, if it is large and single, fluctua- 
tion is sometimes felt. Further, the enlargement of the liver in 
the pyaemic form is uniform, whereas in the single abscess there is 
often one spot which is swollen or enlarged. If a single large pyri- 
form 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 gallstones be the cause of the swelling, there will be a his- 
tory of gallstone 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 Avith the result of 
examining the fluid aspirated from the swelling, will decide the 
diagnosis. Further than this, hydatid cyst yields on percussion a 
peculiar vibratory thrill called the hydatid thrill. Three fingers  THE MANIFESTATION OF DISEASE IN ORGANS. 
352 
are placed over the area, the middle one being pressed firmly upon 
the growth and the lateral ones but lightly. The middle finger is 
now percussed with the other hand and allowed to remain in situ, 
when an after thrill may be felt in the lateral fingers. 
The consistency of the liver is usually very hard in cases of cirrho- 
sis, carcinoma, and amyloid degeneration. In cirrhosis there will be 
some ascites in many cases, some swelling of the legs perhaps, and 
dull pain in the hepatic region. The digestion will be disordered, 
there will be marked loss of flesh and often haematemesis. Some- 
times 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. Ten- 
derness 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 gallstones 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 hyper- 
trophic or atrophic form, the organ presents no symptoms in itself 
save 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 digestion 
and assimilation of food, or from changes in the blood-supplv 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. 154.) 
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, THE ABDOMEN AND THE ABDOMINAL VISCERA. 
353 
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. 
Fig. 154. 
To illustrate symptoms of cirrhosis of liver. 
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 out- 
lined by percussion in persons not inordinately fat. Its normal 
position is best shown in the accompanying figure (155). 
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 per- 
cussing the spleen heavy percussion is to be avoided, since this may 
develop the resonance of the stomach 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 leucocythtemia of the 
spleno-medullary variety; in amyloid disease, as that after long 
suppuration; in early syphilitic infection; and in any disease which 
causes venous engorgement of the abdominal viscera, such as car- 
diac disease or hepatic cirrhosis. Sometimes displacement of the 354 
THE MANIFESTATION OF DISEASE IN ORGANS. 
spleen downward arises from emphysema of the lungs or left-sided 
pleural effusion. 
Acute splenic swelling sometimes comes on in cases of general 
septicaemia. 
Nearly always the splenic surface is smooth, except for the notch 
in its surface (see Fig. 145), unless the disease be the rare condition 
of hydatid disease or carcinoma. 
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 tenderness are present, points 
strongly to appendicitis or to inflamma- 
tion about the caput coli. Sometimes, 
however, the presence of a distinct 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 per- 
son well advanced in years, carcinoma 
is also to be regarded as possible, for the 
sigmoid flexure is a frequent seat of such 
growths. In a young person or a child 
impaction of feces, a foreign body, or in- 
testinal obstruction is to be considered. 
(See chapters on Vomiting and on the 
Bowels.) 
For the diagnosis of renal disease ref- 
erence is to be made to the chapters on 
the Bladder and Urine, the Blood, the 
Bloodvessels and the Pulse, aud 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 aud Spasms. 
For further information in regard to the diagnosis of disease 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. 
Fig. 155 
Normal position of the spleen. CHAPTER X. 
THE BLOODVESSELS AND PULSE. 
The condition of the bloodvessels on palpation—Feeling and counting the pulse— 
The quality, force, and volume of the pulse in health and disease. 
One of the first things that 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 
debility of the patient. By feeling the pulse we also gather valu- 
able 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 are 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 ner- 
vous individuals to wait for sedation to follow the excitement of 
meeting the physician. 
Often when called to see a sick child or a nervous woman, who 
may be sleeping at the moment of the physician’s arrival, a true 
estimate of the 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. 
355 356 
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 prse- 
cordium for the apex-beat. 
Before considering the qualities of the pulse in health or disease, 
it is well to understand what it is due to and the manner in which 
the circulation is carried on. The bloodvessels consist of the arte- 
ries, arterioles, capillaries, venules, and veins. These vessels also 
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 dis- 
tended. Behind the column of blood, which being a fluid confined 
laterally is practically a solid, for fluids are incompressible, is the 
heart, and in the arterioles are muscular fibres, which by their con- 
traction 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 per- 
verted, for the rate of flow in the capillaries depends largely upon 
the blood-pressure in the arteries. As the capacity of the capillary THE BLOODVESSELS AND PULSE. 
357 
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 
individual pulse-beat is not a wave of blood sent out by the heart, 
but it is the transmission of the force of the heart-beat sent along 
the blood-column, and the character of the beat gives us, therefore, 
an idea of how forcibly the heart is driving another quantity of 
blood into the aorta, and also how much blood is being sent out at 
each beat. 
Supposing, therefore, that on feeling the radial pulse we find that 
the artery is tense and hard, and that the individual beat is strong 
and its volume great: this signifies that there is an excited vaso- 
motor 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 
a bloodvessel will burst in its weakest spot, or the spasm of the 
arterioles will give way. It is the first result which we meet in 
cases of true angina pectoris, for in this state we find great arte- 
rial 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 hardening of 
the bloodvessels as the result of old age, syphilis, or chronic vessel- 
changes, the very inelasticity of the vessel, associated, perhaps, 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 accent- 
uated. 
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 358 
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 ail- 
ment 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. It is often met with in mitral stenosis and 
indeed in all forms of cardiac disease with ruptured compensation. 
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 78, and from twenty to fifty years about 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, by 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. The 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 to the THE BLOODVESSELS AND PULSE. 
359 
finger, “trip-hammer/’ “water-hammer,” or “ Corrigan'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. 156. 
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 /. 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 the box h. The paper is 
thus 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 irregu- 
lar in force but regular in rhythm, we have developed what is called 
a pulsus alterans.  THE manifestation of disease in organs. 
360 
A dierotic 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. 150.) 
The normal pulse-wave is shown in Fig. 157. 
Fig. 157. 
a b. Percussion upstroke, a b c. Percussion-wave, c d e. Tidal wave, ef g. Dicrotic wave. 
d ef. Aortic notch. / 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 tin's 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 a 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 bloodvessels being thrown into vibrations by a forcible pulse- 
wave. 
In Fig. 158 is shown the typical pulse-wave of aortic regurgita- 
tion; and in Fig. 159 that of mitral stenosis, which is irregular in 
time and volume. 
The rapidity and force of the pulse also depend largely on the THE BLOODVESSELS AND PULSE. 
361 
condition of the bloodvessel-walls, particularly the rapidity. The 
latter also is influenced by the activity of the pneumogastric nerves 
in regulating the beat of the heart. Thus, if the arterial pressure 
be very high, through spasm of the arterioles, the difficulty experi- 
enced 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. 158. 
Tracing from a case of aortic regurgitation. (Musser.) 
Fig. 159. 
Tracing from a case of mitral stenosis, showing increased tension and some irregularity. 
(Mussek.) 
The vagus or pneuraogastric 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-press- 
ure 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 ves- 
sels. 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, produced by pressure or disease, or by drugs, such as 
digitalis. 
The term bradycardia is applied to a very slow pulse. The pulse 
may be as slow as twelve a minute. 362 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 stimu- 
lant effect of heat upon this viscus and its depressant effect on the 
vagus. 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 blood- 
vessels, or more rarely to depression of the pneumogastric nerves. 
As a symptom of organic disease it is a frequent manifestation of 
exophthalmic goitre. 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 by 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—Leukae- 
mia and pseudo-leukaemia—Parasites of the blood. 
As already pointed out in the chapter devoted to the skin, marked 
changes in the blood speedily produce manifest alterations in 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, iu 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 polycythaemia; if de- 
creased, the condition is called oligocythaemia. One of the most 
marked instances of polycythaemia which occurs is the very extraor- 
dinary increase of red blood-cells which is often met with in cases 
of congenital cardiac disease in children, amounting to as many as 
8,000,000 to the cubic millimetre. A similar increase is seen in 
phosphorus-poisoning. Beside the ordinary red blood-cells we 
find in health small red cells supposed to be immature red cells and 
363 364 
THE MANIFESTATION OF DISEASE IN ORGANS. 
called microcytes, and sometimes, though rarely, we find also 
megalocytes or very large red cells. Not only may the red blood- 
cells change in number, but the quantity of their haemoglobin may 
also vary. Normal blood should contain 100 per cent, of haemo- 
globin, but often we find perfect health when the haemoglobin is 
estimated at only 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 
“normoblasts;” and, finally, we find other red cells pigmented or 
vacuolized, or, again, so dim in appearance as to be called “ shadow 
corpuscles.” The diseases 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 cor- 
puscles 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 before supper, 1 to 544; 
and two hours after supper, 1 to 1227. In general, the proportion 
is about 1 in 280. 
Proceeding, then, to the study of the blood for diagnostic pur- 
poses, we examine it not only by the microscope, but also by color- 
tests. The object of the microscopic examination is to determine 
the quality and character of the red and the 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 Con- 
tinent of Europe, a Number 7 Hartuack or a D. Zeiss; and for THE BLOOD. 
365 
examinations for parasites a 1-12 oil-immersion lens for use with a 
condenser. The eye-pieces used are usually Nos. 2 and 4. 
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 
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 hsematocy- 
Fig. 160. 
Thoma-Zeiss blood-counting apparatus. A heavy glass slip (a), in the middle of which is a 
cell (£) exactly ]/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 V20 mm. Dark lines mark 
out large squares containing twenty-five small squares. Thick, carefully ground cover-glasses 
(D) are provided in the ease. 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 1 c.mm. 
tometer, of which the best is the Thoma-Zeiss apparatus, which 
consists in part of a glass capillary tube, about 10 cm. long, with 
an expansion 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. 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. 160 and 161.) 366 
TIIE MANIFESTATION OF DISEASE IN ORGANS. 
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 3 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- 
Fig. 161. 
Appearance of blood in the Thoma-Zeiss cell 
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 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 num- 
ber of squares. This number in turn is multiplied 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 THE BLOOD. 
367 
line of a given square, and may, therefore, be counted twice or left 
out altogether. For this reason it is customary to include those 
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 cells 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-riolet 0.03 grain) 
Neutral glycerin 30.0 (1 ounce) 
Distilled water 80.0 (2% ounces) 
Mix thoroughly and add 
Chloride of sodium 1.0 (15 grains) 
Sulphate of sodium. . . . . . . . 8.0 (2 drachms) 
Distilled water 80.0 (2% ounces) 
This is then filtered; it requires about eleven minutes for the white corpuscles 
to he stained by it. 
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 multi- 
ply by 40,000 instead of 400,000. 
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. 163), 
which takes the place of the test-tube holders shown in Fig. 162. 368 
TIIE manifest a tion of disease in organs. 
This instrument is an improvement upon the Blitz-Hedin hsema- 
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 luematocrit to make 
Fig. 162. 
Centrifuge. 
5000 revolutions per minute. This enormous speed is attained with 
only moderate exertion on the part of the operator. The liaemato- 
crit attachment consists of a metallic frame, carrying two graduated 
capillary glass tubes, 50 mm. long, \ 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, A A, so that there is no possible danger of THE BLOOD. 
369 
losing the tubes during rotation. By drawing back the milled heads 
B, B the tubes are instantly released and as quickly clamped again 
into position. (Fig. 163.) This apparatus should be made of alumi- 
num, 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 “ the centrifugal forces of 
Fig. 163. 
Hsematocrit attachment for centrifuge. 
two equal bodies, moving with equal velocity at different distances 
from the 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 cen- 
trifuge, 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 con- 
stricted dropper (Fig. 164) with rubber-bulb connection, and by 
this means placed in the hsematocrit, which is rapidly revolved for 
at least one minute. 
Fig. 164. 
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. 
The white corpuscles, next in specific gravity, will occupy a posi- 
tion between the red corpuscles and the liquor sanguinis, which is THE MANIFESTATION OF DISEASE IN ORGANS. 
370 
found in the proximal end of the tube, quite clear and free from 
corpuscles. 
When the column of red blood-corpuscles extends to mark 50 we 
have, as a rule, about five million red corpuscles per cubic milli- 
metre; but if the precipitated corpuscles reach only mark 30, there 
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. 
Fig. 165. 
Von Fleischl’s hiemometer. 
Having discovered the number and the quality of the corpuscles, 
au equally important measure is to discover the quantity of haemo- 
globin which they contain. We do this best by the use of the 
haemoglobinometer 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. THE BLOOD. 
371 
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 at 
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 ouly pure water, by a thumb-screw. 
Under the glass and cylinder is a white reflector to direct the rays 
of light through them. (Fig. 165.) 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 
haemometer container, by directing through the tube a stream of 
distilled water from a fine-pointed pipette. Both compartments 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 inaccuracies in the results 
obtained. The apparatus is then exposed to gaslight or lamplight, 
because with daylight the hue of the glass does not match blood- 
color, and the frame is moved backward under the side of the cylin- 
der which contains only pure water, until the glass seems to the eye 
to match the fluid containing the blood on the side through which 
the pure light streams. If the glass matches the blood-color when 
the mark on the frame is at 50, it shows that the haemoglobin equals 
only 50 per cent, of normal; or if it is at 85, it signifies 85 per cent. 
As a matter of fact, an examination of perfectly healthy blood will 
often give not more than 85 to 90 per cent, of haemoglobin with 
this apparatus. 
Care should be taken in regard to three points: first, to be sure 
that all the blood is washed out of the capillary tube into the water; 
second, to be sure that the two halves of the cylinder are filled to 
the brim with water, so that there is neither a positive nor a nega- 
tive meniscus; and, third, to be careful to cleanse the entire appa- 
ratus thoroughly after each use of it before putting it away. 
Proceeding, then, to the study of the blood for diagnostic pur- 
poses, we find that a very important part of this study consists in 372 
THE MANIFESTATION OF DISEASE IN ORGANS. 
the differentiation of the various forms of white blood-cells. These 
cells appear in the blood of healthy individuals in five forms: 
1. They occur as white cells as small as, or smaller than, the 
ordinary red cells. Each of these small white cells contains a nucleus 
so large that it almost completely fills the body of the cell and pre- 
vents us from seeing any surrounding protoplasm. They are called 
lymphocytes. They form about 20 per cent, of the total number 
of white cells in health. They are increased in number after food, 
and diminished by starvation. They are not phagocytic, nor do 
they exhibit amceboid movement. 
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 
protoplasm. Sometimes these cells show a change in the shape of 
the nucleus, and are then called (3) transitional leucocytes. These 
mononuclear cells make about 10 per cent, of the white blood-cells. 
4. 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 contains 
fine granules, which stain when brought in contact with neutral dyes, 
and for this reason these cells are often called neutrophiles. A neu- 
trophile, a polymorphous leucocyte, and a polynuclear leucocyte are, 
therefore, one and the same tiling. They equal about 60 per cent, 
of the white blood-cells; are actively amoeboid and phagocytic. 
5. 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 eosinophilic, and are 
very limited in number or entirely absent in many cases. These 
cells possess amoeboid movement, but are not phagocytes. They 
make up in some individuals about 2 per cent, of the leucocytes. 
When they are considerably increased this indicates leukaemia. 
In disease MTe find variations from these types as to proportional 
and actual number, and in addition other white cells are present. 
In 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 PLATE X. 
FIG. 1. 
FIG. 2. 
Severe Anemia with Leueoeytosis. 
Dry. preparation. Fixed with picric acid. 
Stained with hsematoxylin 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 Mikroskopie des Blutes.") 
Splenic-Myelogenic Leukaemia. 
Eosin-haematoxylin, x 300. Red corpuscles rosy- 
red, of nearly uniform size, round. To the left a 
normoblast with eccentrically placed nucleus. 
Many large mononuclear leucocytes (myelocytes) 
and three eosiuophiles seen. (Rieder.) 
FIG. 3 
FIG. 4. 
Splenic-Myelogenie Leukaemia. 
Same case. Eosi n-hae m atoxy 1 i n, x noo. One 
normoblast, one polynuclear leucocyte, one mye- 
locyte, two eosinophiles. The neutrophilic gran- 
ules of the polynuclear leucocyte and of the mye- 
locyte do not show with this stain. The large 
mononuclear eosinophile 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. 
373 
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,” 1-25 c.c.; saturated hydro-alcoholic (20 per 
cent, of alcohol) solution of acid fuchsin, 125 c.c. These ingre- 
dients having been mixed gradually and thoroughly shaken, the 
following; constituents are added, the shaking being continued: satu- 
rated watery solution of methyl-green, 125 c.c.; absolute alcohol, 
75 c.c. 
Recently 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, 300 
parts. This solution should stand for several weeks to allow of 
sedimentation; it improves with age; and when it is used the super- 
natant 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 hardened over an 
alcohol flame or on a hot stage made of sheet copper, and kept at 212° 
F. for from fifteen minutes to two hours. After this they are placed 
in the staining-fluid for from one to four minutes, then washed in 
pure water, dried, and mounted in Canada balsam or cedar oil. The 
Canada balsam should not be prepared with chloroform, as it will 
decolorize the specimen. The glass is then ready for microscopic 
examination with a one-twelfth oil-immersion lens. The eosinophile 
granules in the corpuscles will be stained a reddish hue, the neu- 
trophile granules purple, and the nuclei bluish-green or blue. 
(Plate X.) 374 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
diseases. Practically all conditions of the blood which are patho- 
logical 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 anaemia 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 sur- 
roundings, 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 pres- 
ent 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 
repeated 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 THE BLOOD. 
375 
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 are gradually increasing dyspnoea, failure of strength, cardiac 
palpitation, venous murmurs, some vertigo, and roaring in the ears. 
The blood shows a most extraordinary and continually diminishing 
number 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 projections and constrictions on their surfaces (poiki- 
locytes); fourth, there are present microcytes, or red blood-cells 
which are smaller than normal; fifth, nucleated red blood-cells (nor- 
moblasts); and sixth, and quite constantly, there are other large cells 
like the megalocytes, named megaloblasts, which have a plain stain- 
ing nucleus. These last are often larger than the megalocytes, and 
are sometimes called the “ corpuscles of Ehrlich,”1 since he regards 
them as pathognomonic of pernicious amemia. The white blood- 
corpuscles are normal in number, or slightly decreased, although the 
great diminution in the red cells renders the proportion of white to 
red greater than normal. 
Ansemia depending upon lack of haemoglobin in the corpuscles, 
rather than a decrease in their actual number, is seen most typically 
in that condition called chlorosis. In this state the corpuscular dimi- 
nution is so slight that it may be ignored; but the decrease in haemo- 
globin is extraordinary, sometimes falling as low as 20 per cent, of 
the normal or below it. The red corpuscles are, however, very com- 
monly irregular in form—that is, there is more or less poikilocy- 
tosis, but the white corpuscles remain normal in number or slightly 
increase. Normoblasts are quite constantly found in chlorosis 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 facts that the patient is generally a girl of from 
fourteen to twenty-five years, that the skin is peculiar in its pallor 
(see chapter on Skin), and that there is often little if any men- 
strual flow, which is usually only faintly pink in hue. Dyspnoea, 
1 These are not to he confused with the myelocytes of Ehrlich, which are large white cells. 376 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 ” mur- 
mur. Febrile movement of slight degree may also be present. 
In addition to these causes of anaemia 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 impor- 
tant 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 con- 
dition the blood may resemble that of pernicious anaemia, and gastric 
ulcer, in which the loss of corpuscles may also be extraordinary, 
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 tape- 
worm, anchylostomum duodenale, and last, but by no means least, 
from malarial infection, either as manifested by acute attacks, fre- 
quently repeated, or by slow poisoning with the development of 
cachexia. (See further on in this chapter.) 
Estimations of haemoglobin and red cells are of value in certain 
acute conditions. If a patient is brought to the physician in a state 
of advanced anaemia, acute or chronic, and needs an operative pro- 
cedure for relief, and the haemoglobin is below 35 per cent., it is 
well to remember the rule of Mikulicz, which is, “ Do not operate.” 
Again, a great decrease in haemoglobin and red cells would aid in 
separating the collapse of concealed hemorrhage, as in a case of 
rupture of the tube in extra-uterine pregnancy, from other condi- 
tions of collapse not dependent on loss of blood. 
There yet remain to be considered those conditions in which we 
find not only the states already described, but, in addition, marked 
alterations in the white blood-corpuscles as well as the red, altera- 
tions of such moment that they become the salient features of the 
blood when it is examined, and these are of great diagnostic im- 
portance. 
The points of importance in examining blood in regard to the 
white corpuscles are their number and their peculiarities and kinds. 
The discovery that the proportion of white to red corpuscles is far 
too great, varying from the normal (1 to 450, approximately), should THE BLOOD. 
377 
cause the physician, first, to exclude all possibility of transient 
causes of variation by making an examination at various times of 
day, or by excluding the presence of acute infectious disease char- 
acterized by leucocytosis—that is, the presence of an unusually large 
number of white corpuscles of the polymorphonuclear variety. This 
can be done not only by excluding the presence of infection, but also 
by the fact that in leucocytosis in infectious diseases the increase is 
solely in the polynuclear neutrophile 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, dysp- 
noeic, and feeble, with a marked and constant increase in the propor- 
tion of his white corpuscles, what does it mean ? It probably means 
that the patient is a sufferer 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. 
AVhen the disease leukaemia is present in its spleno-medullary 
form, the typical change in the blood is a slight increase in the large 
mononuclear leucocytes and in the presence of the so-called myelo- 
cyte of Ehrlich, a large white corpuscle with a single pale-staining 
nucleus of even outline, usually placed to one side, 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 pro- 
toplasm of the mononuclear leucocyte is clear. The ordinary large 
mononuclear cells are not greatly increased, and the polymorphous 
or polynuclear cells are rather decreased. The myelocyte of 
Ehrlich is a giant-cell, without amoeboid movement. Eosinophile 
cells may or may not be present. At one time they were supposed 
to be pathognomonic of this disease, but they are not so considered at 
this time. When stained with Ehrlich’s tri-acid stain the granules 
of the eosinophilic leucocyte appear as coarse reddish-bronze gran- 
ules scattered through the protoplasm of the cell, and often super- 
imposed 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 also decreased. The pro- 378 
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 to be differentiated 
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, however, the blood 
condition separates the affections. (See chapter on Fevers.) 
We study the white cells as to their number and character for 
other diagnostic purposes, namely, for the discovery and separation 
of acute infectious diseases. Thus, in nearly all infections associated 
with acute inflammation we find an increase in the white cells, or 
leucocytosis. The particular white cell increased is the polymor- 
phonuclear cell, aud rarely we find eosinophiles. Acute croupous 
pneumonia is particularly apt to produce this state unless the infec- 
tion is very malignant, when it fails to occur. By studying leu- 
cocytosis we can often decide as to the presence of deep-seated 
abscesses. Thus in doubtful cases of appendicitis a study of leu- 
cocytosis will aid the diagnosis and separate it from obscure non- 
inflammatory states. If an increased leucocytosis is present we can 
exclude gallstone colic, renal colic, and fecal colic, intestinal ob- 
struction, and ovarian neuralgia, unless there is associated with one 
of these affections an acute inflammation. Should, however, the 
leucocytosis be absent and yet appendicitis present, the inflamma- PLATE XI. 
The Parasite of Tertian Fever 
The Parasite of Quartan Fever. THE BLOOD. 
379 
tory process will be either very mild, or, on the other hand, very- 
severe—too mild to so result, or too severe for the system to react. 
So, too, if leucocytosis gradually increases it is a sign of spreading 
inflammation. Leucocytosis is usually absent in typhoid fever, 
malaria, severe septicaemia, tuberculosis in all its forms, in influenza, 
and in measles. 
Parasites of the Blood. We still have for consideration the 
parasitic diseases of the blood. These consist in the malarial germ 
of Laveran, or, as it is more properly called, the “ hsematozoon 
malariae” of Marchiafava and Celli, and the filaria sanguinis 
hominis. 
Malarial Organisms. No more important addition to the 
study of disease from a diagnostic stand-point has been made than 
the discovery of the presence of a parasite in the blood of persons 
suffering from malarial fever, a parasite which is always present 
under these circumstances, and in all probability acts as the cause 
of all malarial manifestations. These parasites are varieties of 
sporozoa, which live inside the red blood-corpuscles of the indi- 
vidual attacked.1 
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 lestivo-autumnal fever. The tertian parasite is a small 
hyaline, colorless body, which occupies but a slight extent of the 
interior of the red blood-corpuscle. (Plate XI., Figs. 2, 3, and 4.)2 
When quiet it is round, like the corpuscle in which it lies; but if 
the specimen examined be fresh, it may be seen to possess active 
amoeboid movements, thereby changing its shape. 
Soon this amoeboid body grows in size and begins to develop 
reddish-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 cor- 
puscle which contains the parasite becomes more and more pale, and 
at the same time swells up or expands, and the amoeboid movements 
1 In this country the chief investigators into the life-history of the malarial parasites have 
been Osier, Councilman, and, more recently. Thayer and Hewetson, from whose exhaustive 
and able monograph of ‘ ‘ The Malarial Fevers of Baltimore ” much of the information in the 
text of this book is derived. 
2 No. 1. is a normal red corpuscle. Plates XI. and XII. are taken from Thayer and Hewet- 
son’s monograph. 380 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 previously 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 
becomes 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 seg- 
menting 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 
will 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. It soon, however, develops 
the following differences: first, it develops a sharper outline; 
second, it is more refractive; third, the amoeboid movements are 
slower (Plate XI., Fig. 26); fourth, the pigment-granules are 
coarser and darker (Plate XI., Fig. 27), and, more important 
still, they lie very quietly around the edge of the parasite; fifth, 
the corpuscle acting as host does not increase in size, and finally PLATE XII. 
The Parasite of Aestivo-Autumnal Fever THE BLOOD. 
381 
disappear, as it does when affected by the tertian type, but grows 
smaller and darker, more refractive and metallic looking (Plate XI., 
Figs. 28 to 34). Reaching its complete development in about 
sixty-four to seventy-two hours, it appears as a small, round body, 
taking up nearly all the space in the corpuscle in which it lives, 
or it appears 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 become 
more and more separated from one another, and simultaneously 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; a degenerative form 
may also appear, and vacuoles may develop. (Plate XI., Fig. 42.) 
Finally, flagella may develop, as in the tertian organism (Plate XI., 
Fig. 41), and they differ from the tertian form in being smaller, 
and their granules are coarser. 
In the third form of infection (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 amceboid 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, are 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-autum- 
nal 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 para- 
site 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 382 
THE MANIFESTATION OF DISEASE IN ORGANS. 
days we find in the blood larger parasites, of an egg-shape or cres- 
cent-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. 
JEstivo-autunxnal. 
Develops in 24 to 48 hours. 
Has 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. 
Tbe 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 are 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 1-12 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 THE BLOOD. 
383 
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 abso- 
lute alcohol and ether for two hours, to “fix” the preparations. 
The specimens are then dried and stained by Lofler’s methylene- 
blue mixture, which consists of concentrated alcoholic solution of 
methylene-blue, 30 c.c.; solution of caustic potash (1 to 10,000), 100 
c.c. The specimens are immersed in this stain for one-half to one 
minute, then washed in pure water, dried by placing them between 
two pieces of filter-paper, and then mounted in oil or balsam. The 
nuclei of the parasite and of the leucocytes will appear blue and the 
red cells will be unstained. 
We can also 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 water 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 
hsematozoa 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. 
It has already been stated that the paroxysm of the malarial dis- 
ease takes place at the time when the parasite is breaking up into 
segments. In other words, the attacks occur whenever the cycle of 
growth of a set of parasites is completed, which in tertian fever is 
every forty-eight hours, and in quartan fever every seventy-two 
hours. If there be two sets of parasites in the 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 
successive days, then a day of intermission ensues. If three sets 
of parasites of this type are present, the attacks may be daily for 
three days—triple quartan infection. (See chapter on Fever.) 
The parasite of sestivo-autunmal fever is irregular in its develop- 384 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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. 
Malarial infection differs from most infections, the symptoms of 
which resemble it, in that there is no increase in leucocytosis, 
whereas in sepsis a great increase is usually present. This gives us 
an important aid in differential diagnosis. (See chapter on Fever.) 
When the malarial organisms cannot be found the presence of leuco- 
cytes bearing pigment granules may indicate the breaking down of 
the red cells by the parasite, and so point to the probable presence 
of malaria. 
Widal's test for typhoid or enteric fever depends upon the fact that 
the blood-serum of a patient suffering from typhoid fever exercises 
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 abso- 
lutely 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 u 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 rap- 
idly form clumps. If the patient has not typhoid fever this clump- 
ing 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 lymphatics. 
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 nodurna ; 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 nodurna solely or chiefly during the night; while 
the filaria perstans is constantly present in the capillaries of the 
integument. The filaria diurna and filaria perstans are confined, 
thus far, to the west coast of Africa and adjoining districts, while 
the filaria nodurna is pandemic in the tropics and endemic in cer- 
tain sections of the United States. The adults of filaria nodurna THE BLOOD. 
385 
have been frequently found; that of filaria perstans never, so far as 
Henry has been able to ascertain. Manson has also described 
another parasite, the filaria Demarquayi, which is less than half the 
Fig. 166. 
Filaria alive in the blood. Instantaneous photomicrograph. Four hundred diameters 
magnification. Four millimetres Zeiss apochromatic. (Henry’s case.) 
size of the filaria nocturna, and another form which he calls the filaria 
Ozzendi. In the opinion of Manson, the filaria loa of the eye of the 
Fig. 167. 
Filaria in the blood. Eight hundred diameters. (Henry’s case.) 
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 386 
THE manifestation of disease in organs. 
be discovered, for the embryos of the loa must escape from the body 
of their host through the medium of the circulation. The filaria 
perstans has been practically proved by Manson to be the cause of 
the fatal u sleeping-sickness” of the Congo region. 
The second is the one ordinarily seen in blood obtained from the 
peripheral circulation during sleep or at night. (Figs. 166 and 
167.) The male filaria measures 83 millimetres long by 0.407 
millimetre broad, and the tail is twisted into a spiral form. The 
female measures 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 
micromillimetres 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 night 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 Gowers liaemoglo- 
binometer 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 haemoglobinometer 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. THE BLOOD. 
387 
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 nor- 
mal 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 evi- 
dence in regard to obscure affections that a correct diagnosis is at 
once possible, and in other cases its examination, as a matter of 
routine, will discover important facts the existence of which has 
been unsuspected. Again and again will a diagnosis prove erro- 
neous 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 are 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 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 the chapter on the Skin, part 
on oedema and color of the skin, and the chapter on the Face, part 
on expression.) Aside from these evidences of renal disease no 
388 THE URINARY BLADDER AND THE URINE. 
389 
alteration can usually be noted unless it be loss of weight, which 
may be replaced by a gain if dropsy develops. 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 perinephritic troubles are present, when pain becomes 
an important sign. 
Fig, 168. 
1st to 7th cervical segment. 
J- 1st to 12th dorsal segment. 
!- 1st to 5th lumbar 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, limbs, and bladder. 
The Bladder. The objective symptoms of bladder difficulties 
are generally local, unless they are very chronic, when the face may 
appear worn and weary, aud, 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 function 
of the cells in the spinal cord which govern the contraction of the 390 
THE MANIFESTATION OF DISEASE IN ORGANS. 
muscles involved in expelling urine from the bladder. These centres 
are situated at or about the level at which are given off the second, 
third, and fourth sacral nerves. (Fig. 108.) 
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, reten- 
tion of urine may arise from paralysis of the muscular part of the 
vesical walls by pressure produced in severe labor (childbirth). 
Retention sometimes comes on in locomotor ataxia, in which 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 its walls 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-mus- 
cles and retention-muscles are both paralyzed, so that the urine 
accumulates 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 pres- 
ence 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. 
On the other hand, if the portion of the cord which is involved THE URINARY BLADDER AND THE URINE. 
391 
happens 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 con- 
trol may be regained before any marked improvement can be found 
elsewhere. 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 circum- 
stances 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 situ- 
ated. 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 spasmodically 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 spinal centre for the control of the walls of the 
bladder is situated 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 reten- 
tion. Precisely similar vesical symptoms occur in cases of spinal 
tumor producing transverse lesions of the cord (see chapter on Feet 
and Legs, Paraplegia), 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 abdominal 
muscles before he can evacuate the bladder. As a result of this, 392 
THE MAN/FES HA TION OF DISEASE IN ORGANS. 
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 forcibly 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 sneezing, owing to lack of com- 
plete control of the bladder and its sphincter; or, again, after many 
attempts to urinate, the patient gives up the effort, only to be humili- 
ated by an involuntary passage of urine immediately after his penis 
has been withdrawn into his clothes. 
These symptoms differ so materially from myelitis as to make a 
diagnosis as to their cause nearly always possible. 
In obscure cases of ataxia the vesical symptoms may aid the diag- 
nosis quite markedly; thus the presence of bladder-symptoms would 
confirm a diagnosis of ataxia as against pseudo-tabes due to periph- 
eral neuritis. Again, in myelitis the presence of vesical symptoms 
points to that disease, and excludes from the diagnosis such affec- 
tions as poliomyelitis and lateral sclerosis, affections in which vesical 
paralysis rarely, if ever, occurs. Precisely similar vesical symptoms 
are sometimes seen in cases of general paralysis of the insane, but 
the delusions of grandeur or melancholia and other characteristic, 
signs of this disease separate it at once from ataxia. 
The sensory disturbances of the bladder will be found discussed 
in the chapter on Pain, but it is worth noting here that accompany- 
ing the symptoms already named as characteristic of locomotor ataxia 
vesical crises of spasm and pain frequently occur. 
When there is pain in the bladder, made worse by the attempted 
act of micturition, and tenesmus, with darting pain into the urethra, 
there is probably present a cystitis; but the physician should remem- 
ber that cystitis may be present with almost no painful manifesta- 
tions, even when in its acute form. In other cases this condition 
arises from concentration of urine, which produces irritation of the 
viscus, such as is seen in cases of acute nephritis or renal congestion. 
In children this concentration of the urine is the most common cause 
of nocturnal urinary incontinence. 
Involuntary passage of the urine sometimes occurs in idiots, in 
some cases of insanity, in attacks of apoplexy, or any condition of 
abnormal unconsciousness, and sometimes in very severe infectious 
diseases, such, for example, as diphtheria. Oftentimes it results in THE URINARY BLADDER AND THE URINE. 
393 
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, in old men, that most com- 
monly met with cause of difficult micturition, enlargement of the 
prostate, is to be remembered. 
Aside from these causes of interference with the passage of urine, 
we must not forget the possibility of its obstruction by stricture of 
the urethra, nor should the physician ignore the fact that some per- 
sons have “ nervous bladders,” which will not respond to an effort 
of the will if any person is near by, although the urine is instantly 
passed as soon as the patient is alone. 
The Condition of the Urine itself is determined, first, by its 
general appearance, quantity, odor, specific gravity; second, by 
its microscopical appearance; and, third, by its chemical reaction 
and responses to tests. Any changes in this fluid of an abnormal 
character are solely symptomatic, and point with more or less dis- 
tinctness to disorders of bodily metabolism, disease or disorder of 
the kidneys, ureters, bladder, or urethra, and sometimes of the 
prostate, testicles, vagina, or uterus. 
The urine which is to be tested should always be passed directly 
into the vessel in which it is brought to the physician, and this 
bottle should be scrupulously clean; or, if the urine is passed into 
any other vessel, care must be taken that it is perfectly clean. 
When it is thought that urethral disease may obscure the investiga- 
tion a catheter should be passed, all urine'in the bladder drawn off, 
and then the catheter allowed to remain in place, so that the urine 
will trickle directly from the ureters to the catheter, and so to a 
receiving vessel. This is very important when the urine is voided 
involuntarily. If the condition of the bladder is bad, this viscus 
should be washed out 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 MANIFESTATION OF DISEASE IN ORGANS. 
394 
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 with 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 kidneys are stimulated to increased effort by the action of 
drugs, such as digitalis, caffein, or alcohol. We also find an increase 
in urinary secretion, without its possessing any grave significance, 
in convalescence from such diseases as typhoid fever and pneumonia. 
The quantity of the urine is diminished in cases in which the 
heart fails to 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. Persistent 
vomiting also has a similar effect. Parenchymatous nephritis, both 
acute and chronic, greatly diminishes the urine, and in grave, fatal 
illnesses urinary suppression also takes place. 
The odor of freshly passed urine is faint, but characteristic. 
What is often called a “urine odor” is really due to the development 
of ammonia in urine which has decomposed. The odor is altered by 
many drugs and foods, notably by copaiba, turpentine, eucalyptus, 
valerian, musk, asafoedita, and by asparagus. Diabetic urine pos- 
sesses 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 con- 
tracted kidney if no dietetic cause can be found, while a persistently 
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 prob- 
ably diabetes mellitus, the high specific gravity being due to the 
sugar which it contains. 
The naked-eye appearance of the urine often gives very impor- 
tant information, if its clearness, opacity, and color are studied. Its 
clearness and color are modified by the presence of blood or other 
pigments derived from outside sources, such as the educts of carbolic 
acid or salicylic acid, of senna or lneinatoxylon, and bile, urobilin, THE URINAR Y BLADDER AND THE URINE. 
395 
and many other substances coining 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 discol- 
oration 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. (See below.) 
If the color be due to blood or hcematuria, 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, aud 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 indicates 
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 
clinging 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 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 396 
THE MANIFESTATION OF DISEASE IN ORGANS. 
urine comes from the healthy kidney. A sudden profuse hemor- 
rhage 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 papillary growth or to injury. Rarely in certain cases of loco- 
motor ataxia, hsematuria develops after the vesical crises which we 
have already described (see Bladder in this chapter). This is a 
capillary hemorrhage from the bladder-walls. 
When the blood comes in the first part of the urine passed and 
not in the last part, it almost certainly comes from the urethra. The 
urine, when not discolored by blood, may be discolored by the pres- 
ence of the coloring-matter of the blood. This is called hsemoglo- 
binuria. Microscopical examination of the urine in such cases will 
show no corpuscles, although the urine will be coagulated by the 
acid test; but the coagulum 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 this urine be placed on a watch-glass, and 
a drop of strong acetic acid be added, the blood-crystals of Teich- 
mann will be found, showing that the coloring-matter is haemo- 
globin. 
If the discoloration of the urine be due to blood, a microscopical 
examination will reveal red blood-corpuscles, white blood-corpuscles, 
and perhaps fine filaments of clots; but the corpuscles will not be 
found in rouleaux, as in ordinary blood outside the body, and they 
may be crenated and distorted in shape, particularly if the urine is 
alkaline. 
The test which can be most easily applied to determine the pres- 
ence of blood, if the microscope cannot be used, is Heller’s test, 
which consists in adding to a few c.c. of urine a little caustic soda, 
so as to render the liquid strongly alkaline. The urine is now 
heated to boiling, and if blood is present a bottle-green color is 
produced, and the phosphates fall to the bottom of the test-tube in 
fine flakes, tinged brownish-red by the coloring-matter of the blood. 
The significance of hasmaturia is various, since any solution of 
continuity in the bloodvessels of the genito-urinary tract may pro- 
duce it. When the blood comes from the kidney some of the pos- 
sible causes are acute parenchymatous nephritis, resulting from any 
one of the severe infectious diseases, such as scarlet fever or mala- 
rial fever; from embolism, resulting from ulcerative or other forms THE URINARY BLADDER AND THE URINE. 
397 
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 
eruption will render the diagnosis easy. 
Haematuria 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 
certain 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 association 
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 bloocly-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 hsemoglobinuria, arising 
from dissolution of the red blood-cells in the bloodvessels or blood- 
making organs. 
Finally, there is a type of malarial hajmaturia which is produced 
by the administration of quinine (Ivaramitsas et al.). 
All these forms of hsematuria can be diagnosed by the presence 
of the malarial germs in the blood (see Blood) and the characteristic 
malarial symptoms, except that which occurs in persons who have a 
dyscrasia from old malarial poisoning. 398 
THE MANIFESTATION OF DISEASE IN ORGANS. 
If the haematuria be due to embolic infarction of the kidney, an 
examination of the heart will probably reveal signs of valvular 
disease, 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. Sometimes 
thrombosis of a renal vein occurs iu feeble, wasted infants, and so 
causes haematuria. If heart-disease is not present, the history of 
the ingestion of an irritating drug will be the diagnostic guide, or, 
if injuries be the cause, a history of traumatism is all that is needed 
to elucidate the case. 
The 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 kidney, 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 albu- 
minuria. 
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 hsematuria is the 
distoma haematobium of Egypt and Abyssinia. (Fig. 169.) This 
produces what has been called tropical haematuria. The third cause 
is even more rare in man, namely, the strongylus gigas, which also THE URINARY BLADDER AND THE URINE. 
399 
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, lisematuria may also appear as a symptom of purpura haemor- 
rhagica, haemophilia, and very rarely in leukaemia. 
Fig. 169. 
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 poisonous doses of certaiu 
coal-tar derivatives, or of chlorate of potassium, or glycerin. Mala- 
rial poisoning sometimes causes it instead of hsematuria. One form 
of malarial haemoglobinuria is intermittent, the urine being at one 
hour limpid, the next hour bloody, and the third hour clear again. 
The possibility of confusing the hsemoglobinuria of idiosyncrasy 
about to be described, when in a severe form, with true and severe 
malarial poisoning, is very great. The history of paroxysmal 
haemoglobinuria teems with reports of cases in which the chief 
manifestations 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 
human blood, and occurs in paroxysmal hemoglobinuria, a condi- 
tion 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 
be carmine, due to the chrysophan in this drug; but this discolora- 
tion only appears if the urine is alkaline. Precisely similar changes 400 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 
confused with luemoglobinuria or hsematuria, is that produced by 
carbolic 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 enumerated, 
may be owing to an excess of urates (except urate of sodium, which 
is usually white). If on the addition of nitric acid the urine be- 
comes brown where the fluids join, the coloration is due to urates; 
but if all the fluid is brown, the patient has probably been taking 
iodine or compounds of iodine 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 after 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 
(indigotin) or into a red hue (indirubin). If chromogen is present 
in large amount, shaking the urine with air will develop a violet- 
blue color, or this change may take place in the bladder. If urine 
containing iudican be treated with two or three times its volume of 
hydrochloric acid, it will turn a violet hue. THE URINARY BLADDER AND THE URINE. 
401 
Indicauuria is present in intestinal obstruction, general peritonitis, 
cholera, cancer of the liver or stomach, and pernicious anaemia. It 
may, however, be present in health as a result of constipation. 
Blue urine is also caused 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 surface, 
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 milky-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 facts that it remains markedly 
acid for a long time after it is passed and that it has a high specific 
gravity point still more to its being diabetic, and the diagnosis is 
confirmed if the characteristic reaction with Haines’s, Whitney’s, 
or Fehling’s solution is obtained. (See Tests in this chapter.) 
Microscopic Appearance 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 appear- 
ance of this secretion, for, very commonly, a sample of urine which 
looks quite normal to the naked eye is loaded with microscopic 
objects of the greatest pathological significance. The most impor- 
tant of these objects are what are called “ casts”—that is, moulds 
of the uriniferous tubules, formed as a result of the disease-process 
present in the kidney. These casts consist of epithelial cells, blood- 402 
THE MANIFESTATION OF DISEASE IN ORGANS. 
and pas-corpuscles, masses of micro-organisms, or of broken-down 
organic matter, as in fatty casts, and in hyaline or transparent 
bodies, or moulds which are made up of unknown material, but 
often covered by corpuscles, pus-corpuscles, or epithelial cells. In 
addition to these bodies we find a large number of organic bodies or 
derivatives of organic matter, and inorganic substances 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. 170. 
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. By the use of this 
apparatus a sediment can be obtained in a few minutes after urine 
is passed. (See Fig. 170 and chapter on Blood.) 
The sediment is to be drawn up into a pipette which has been 
introduced into the urine and a few drops placed upon a glass slide, 
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. 171, and are due to proliferation or exfoliation 
of the epithelium lining the uriniferous tubules. The cells look 
swollen and granular and may contain globules of fat. These epi- 
thelial casts occur in three forms : first, they may appear as hollow 
casts of the tubule when the epithelium has exfoliated en masse (that THE URINARY BLADDER AND THE URINE. 
403 
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 refrac- 
tive of light and are not altered by chemical substances as easily as 
are the other casts about to be described. 
Fig. 171. 
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-corpus- 
cles attached to one another in a mould of the tube in which they 
have escaped. They are rarely seen and are masked by freely float- 
ing cells. The significance of these blood-casts is great, as they 
indicate an acute inflammation of the kidney, acute congestion of 
this organ, or a renal infarction. They are of importance, too, in 
separating hsematuria arising from other sources than the kidney 
from hemorrhage from this organ, because they are not found unless 
the escape of blood has been into the uriniferous tubules. 
Casts composed of pus-corpuscles are still more rarely seen, but, 
if constantly present, may indicate multiple abscess of the kidneys. 404 
THE MANIFESTATION OF DISEASE IN ORGANS. 
When masses of micrococci become grouped together in the tubules 
they may be expelled in casts, and under a low power look somewhat 
like granular casts (see below). They can be seen to consist of micro- 
cocci 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. 172. 
a, a. Epithelial casts, b, b. Opaque granular casts from a case of acute Bright’s disease. 
(Roberts.) 
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. 172, 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 
so far, but they often indicate a slow degenerative process in the renal 
parenchyma. PLATE XIII 
FIG. 1. 
FIG. 2. 
Casts, Fatty, Waxy, Hyaline and 
Granular. 
Crystals of Uric Aeid 
FIG. 3. 
FIG. 4 
Ammonium Urate Crystals. 
Epithelial Cells. 
A, Squamous Epithelium ; B, Bladder Epithel 
ium ; C, Kidney Epithelium ; 1), Kiduey Epithel 
iutn (fatty). THE URINAR Y BLADDER AND THE URINE. 
405 
Fatty casts, composed of minute globules of oil, cohering to one 
another or attached to a central core of epithelium, or fat-crystals, 
are found in cases of widespread fatty degeneration, as the result of 
disease or poisoning, as in the case of large white kidney, on the one 
hand, or phosphorus, arsenical, antimonial, or iodoform-poisoning, 
on the other. They show the presence of a very slow process if due 
to disease, but have not the same significance if caused by poison. 
(Plate XIII., Fig. 1.) 
Hyaline casts are 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 “waxy” casts. 
(Plate XIII., Fig. 1.) 
Fig. 173. 
Cylindroids from albuminous urine, a, b, and c. Ribbon-like forms, d. Cast-like form, 
with cells upon its 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 like 
threads or filaments which are transparent and often somewhat stri- 
ated or hyaline in appearance. They are often long enough to extend 406 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 a lens of 
too high a power be used. These cylindroids often are grouped in 
bunches. In other instances we find cylindroids in the form of 
Fig. 174. 
Fig. 175. 
Non-albuminous urine. 
Cast-like forms with deposit of urates. 
Non-albuminous urine, 
a and 6. Cast-like forms, c. Filamentous. 
Fig. 176. 
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. 173, 174, 175, and 176.) The significance 
of cylindroids is not definitely known, but they may be taken as an 
indication of irritation of the kidneys, even if albumin and true THE URINARY BLADDER AND THE URINE. 
407 
casts cannot be found in the urine. They are often seen in the renal 
irritation following or, rather, accompanying the conditions called 
lithsemia or uricsemia, and in that condition in which we find oxa- 
lnria. (For further information concerning cylindroids, see Sten- 
gel’s paper in The Medical News of July 15, 1893.) 
According to Bramwell, the following is the best method of stain- 
ing and mounting tube-casts and other urinary deposits. He uses 
picrocarmine. 
“ 1. An ordinary conical urine-glass is filled with equal 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-fluid is then 
set aside to stand for twenty-four hours. 
“ 5. The deposit, which has by that time settled at the bottom of 
the test-tube, is then drawn off by a fine-mouthed pipette, placed on 
a slide, covered, and examined under a low power. 
“ If any tube-casts are present, they are very easily detected by 
this method. 
u 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 charac- 
teristic rose-pink reaction with methyl-violet. For permanent prep- 
aration 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 trans- 
ferred to clear Farrant’s solution, whence it is mounted in the usual 
manner. All organic deposits are thus stained and mounted in a 
perfectly clear medium. Their minute characters can be studied 
with the highest powers of the microscope.” 
1 Farrant’s solution is made as follows : Dissolve 1 grm. of arsenous 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 manifest a tion of disease in organs. 
408 
The most important sedimentary substances for diagnostic pur- 
poses, other than casts, are the products of tissue-chauges, or are 
derived from articles of food. These substances are chiefly the acid 
urate of sodium and potassium and alkaline urate of ammonium 
and potassium, uric acid, oxalate of lime, the phosphate, carbonate, 
and sulphate of lime, and the so-called triple phosphate (ammonio- 
magnesic phosphate). 
The discovery in a urinary sediment of fine 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 iu fever, wasting diseases, gastric 
disorders, and in attacks of gout. 
When in a highly acid urine the student finds rhombic or dia- 
mond-shaped plates (Plate XIII., Fig. 2), or plates of a similar 
shape with the lateral angles rounded off, or quadrate crystals or 
square plates, or plates like double-headed arrows, or rosettes of 
crystals, or bundles of crystals like bundles of kindling-wood, these 
forms are uric acid. Any urine will deposit such crystals if it 
stands for many hours (say ten hours), as its acidity increases, and 
therefore the discovery of these crystals only possesses significance 
if they are found in from four to six hours, as this shows an excess 
of uric acid, which in turn is found in gouty or rheumatic persons 
or in those who eat to excess and take no exercise. Often an excess 
of uric acid in the urine antedates the development of chronic con- 
tracted kidney. Uric acid also appears in excess in cases suffering 
from fever and acute inflammations. It is also eliminated in excess 
in leukaemia, splenic enlargement, hepatic cirrhosis, and gastro- 
intestinal catarrh. The rosette crystals just named are often found 
in diabetic urine. 
Small, square, brilliant octahedral crystals which are perfectly 
transparent and refract light strongly, looking somewhat like the 
back of a square envelope at times, are those of oxalate of lime. 
(See Fig. 177.) The significance of oxaluria is quite important, for 
it is often a concomitant symptom of melancholia depending upon 
defective metabolism. The finding of oxaluria separates this class THE URINARY BLADDER AND THE URINE. 
409 
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 oxi- 
dation of nitrogenous tissues. 
Fig. 177. 
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. 
178, 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. 178, 6. 
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. 179.) In 
addition, such urine will contain amorphous calcic phosphate. 
The crystals of the triple phosphate are of some diagnostic impor- 
tance, 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 crys- 
tals are found in freshly passed urine, they indicate that ammoniacal 410 
THE MANIFESTATION OF DISEASE IN ORGANS. 
fermentation is taking place in the bladder, a condition often seen 
in chronic cystitis and in some cases of paraplegia arising from 
Fig. 178. 
Crystals of creatin and creatinin. (Charles.) 
a. Crystals of creatin. b. Crystals of creatinin. c. Crystals of chloride of zinc and creatinin. 
injury to the cord or myelitis. A deposit of the triple phosphate 
and amorphous calcium phosphate, making a sediment like that of 
Fig. 179. 
Triple phosphate crystals. 
purulent urine, is sometimes seen in persons suffering from over- 
work of the nervous system and in cases of general debility. THE URINARY BLADDER AND THE URINE. 
411 
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. 182.) 
Thus, we may find the embryos of filaria, echinococcus hooklets 
(Fig. 180), and the eggs of distoma haematobium, which are very 
rarely seen. 
Fig. 180. 
Echinococcus, with two hooklets, and section of cystic membrane, greatly magnified, 
(Peyek.) 
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 yL homogeneous immer- 
sion lens with a No. 2 eye-piece. The process of staining is by the 
use of eosin and methylene-blue. The material on the cover-glass 412 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 pro- 
cess. They show infection from pus and are 
found in cases of erysipelas. (See Fig. 181.) 
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 spermatorrhoea, 
which is rare, or from some of the semen remain- 
ing 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 movements. (Fig. 182.) 
Fermentation resulting from the presence of a number of special 
fungi takes place in both healthy and diseased urines after they are 
Fig. 181. 
Streptococci. (Abbott.) 
Fig. 182. 
Spermatozoa, with casts of seminal tubules and spermine crystals. 
passed. In normal urines 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 THE URINARY BLADDER AND THE URINE. 
413 
amorphous urates. After the urine is exposed still longer it under- 
goes an alkaline fermentation, and there develop in the fluid the 
micrococcus urese and bacterium lire*. As a result, the urea takes 
up water and decomposes with the development of C02 and ammo- 
nia. No sooner is a positive alkaline reaction established than those 
ingredients of the urine which are insoluble in an alkaline solution 
are precipitated, namely, amorphous calcic phosphate, ammonium 
urate, and amnionio-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 saccharomyces albi- 
cans, the micro-organism which produces fermentation in ordinary 
solutions of glucose. 
Chemical Tests. The chemical tests of the urine give us much 
important information. We commonly test it for albumin and for 
sugar, and if we wish still further information, we examine it for 
its percentage of urea, uric acid, and for its peptones, or, to use a 
better term, its albumoses. 
Albuminuria. There are a great number of tests for albumin 
and sugar. Many of them are open to fallacies, and they are, there- 
fore, to be avoided 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, 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. 414 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 albumin 
is thrown down. The tubes are filled to the 10 c.c. mark with 
urine and 2J c.c. of potassium ferrocyanide solution (one part to ten) 
are added. Next we add 1| 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 c.c. mark on 
the tube represents 1 per cent, by bulk of albumin; that is, if the 
albumin extends up to the 3| cubic centimetre mark the albumin 
amounts to 35 per cent. 
The significance of albumin is not as grave in all cases as it was 
considered at one time, nor is its quantity of great import neces- 
sarily, 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 
illness 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 inter- 
mittent, little-understood form of albuminuria, called cyclic albu- 
minuria, 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 glycerin, one-half 
ounce, which is to be thoroughly mixed; and then add liquor potassae, 
five ounces. One drachm of this is to be placed in a test-tube and 
gently boiled, and to this are added six to eight drops of the urine, THE URINARY BLADDER AND THE URINE. 
415 
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 of 
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 drops . 
8 
1.67 
3 “ ... 
5.33 
1.11 
4 “ ... 
4 
0.83 
5 “ ... 
3.20 
0.67 
6 “ ... 
0.56 
7 “ ... 
2.29 
0.48 
8 “ ... 
2 
0.32 
9 “ ... 
1.78 
0.37 
10 “ ... 
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 pure water, and the amount 
found in the table multiplied by the amount of dilution.1 Usually 
diabetic 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. Wick- 
ham 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 poatash, sp. gr. 1.120. Into this alka- 
line solution is poured a fluid prepared by dissolving 133J grains of 
sulphate of copper in ten fluidrachms of water. The solution is 
exceedingly apt to decompose, and must always be kept in stoppered 
bottles and in a cool place. It is usually, therefore, more conven- 
ient not to mix the alkali and copper until the solution is wanted 
1 This test, under the name of Aquse Sapphirina, can be had of the Lewis Chemical Co., of 
New York. THE MANIFESTATION OF DISEASE IN ORGANS. 
416 
for use. In this case a fluidrachm of the sulphate of copper solution 
may be added to half a fluidounce 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'larnp 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, beside sugar, will reduce copper at a high tem- 
perature. 
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, aud, if 
sugar is present, the upper part has a yellowish tinge, while the 
earthy phosphates are thrown down in golden-colored flocculi. THE URINARY BLADDER AND THE URINE. 
417 
The quantitative estimation of sugar is best made by the Whitney 
test, already described, 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 per- 
centage of sugar. 
The significance of sugar in the urine is various. If it is persist- 
ent and accompanied by wasting, polydipsia, and polyphagia, it is a 
sign of diabetes mellitus, due to a lesion in the medulla, to morbid 
functional activity of the liver, or to changes in the pancreas. If 
diabetes 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 connec- 
tion with the disease in earlier life, as just stated. 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 from many 418 
THE MANIFESTATION OF DISEASE IN ORGANS. 
infectious diseases, particularly in typhoid fever, measles, scarlet 
fever, diphtheria, influenza, and malarial disease, after cerebral 
hemorrhage 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 
number of states other than diabetes mellitus, as just pointed out. 
Finally, it is not to be forgotten that a condition known as alkapto- 
nuria may exist. In this state the urine reduces alkaline solutions 
of copper and on exposure to the air absorbs oxygen in the presence 
of an alkali and becomes of a dark-brown or black hue. The specific 
gravity of the urine is low, 1.014 to 1.020, and there is no marked 
polyuria. While such a urine reduces Fehling’s test, it will not 
give the reaction with bismuth, the phenylhydrazine, the fermen- 
tation or polariscope tests for sugar. This coudition of alkaptonuria 
has no direct pathological significance so far as is known. It is 
often found in several members of the same family. 
Albumose ix 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 
1 The urine should be fresh. If it must stand several hours before it can be examined, it 
should be preserved from the growth of bacteria in it by the addition of some antiseptic, pref- 
erably a few drops of formalin, which will keep it several days, and does not interfere with 
subsequent tests. THE URINAR Y BLABBER AND THE URINE. 
419 
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. 
To one of these are now added three or four drops of a saturated 
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 sodium1 (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- 
1 Salicyl-sulpho-tungstate of sodium is prepared as follows: 
To a boiling saturated solution of tungstate of sodium in distilled water salicyl-sulphonie 
acid is gradually added, under constant stirring, until the solution no longer turns red litmus 
blue, or, in other words, luntil 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. 420 
THE MANIFESTATION OF DISEASE IN ORGANS. 
tion would be precipitated by the salicyl-sulpho-tungstate of sodium, 
aud 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 
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 crou- 
pous pneumonia, all suppurative processes, empyema, tuberculosis, 
smallpox, mumps, erysipelas, cancer of the viscera, jaundice, and 
apoplexy, and in typhoid fever and phosphorus-poisoning. Von 
Jaksch asserts that it is present in epidemic cerebro-spinal menin- 
gitis and absent in tubercular meningitis, and that it is a positive 
differential sign of the former disease if no ulceration of the lung 
is present. Harris asserts that albumosuria is simply a manifesta- 
tion of the action of micro-organisms, and is thus only an indication 
of an infective process, but Fitz holds that its persistent presence 
nearly always points to a fatal ending. It ought not to be forgotten 
that albumosuria occurs in the normal puerperium. 
The Urea in the Urine. The amount of urea is to be esti- 
mated by the process of Lyons, as follows (Fig. 183) i1 
Fig. 183. 
Ureomecer. 
1. A bottle is provided with perforated rubber cork and delivery 
tube; in this the decomposition of the urea is effected. 
1 This apparatus, with full directions for use, can be obtained from Parke, Davis & Company, 
Detroit, Mich., for one dollar. THE URINARY BLADDER AND THE URINE. 
421 
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. 
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 examined, 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 contents 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. Remove 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 overflow-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 connec- 
tions are perfect, catch the curved end of the overflow-tube over the 
edge of a measuring graduate, as shown in the illustration (an ordi- 
nary bottle or any other receiver may be used in place of the grad- 
uate). Now, by canting the bottle, cause the urine to flow out of 
the test-tube and mix with the test-solution. Effervescence is at 
once produced, and the gas evolved forces a corresponding 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 422 
THE MANIFESTATION OF DISEASE IN ORGANS. 
apparatus. Let the apparatus stand fifteen or twenty minutes to 
cool, then shake the bottle containing the urine once more and pro- 
ceed 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 volume of the gas to be meas - 
ured. The percentage of urea is read off without need of any cal- 
culation 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 
O.S 
. 1.367 
2.1 . 
. 9.570 
0.4 
. 1.823 
2.2 
. 10.025 
05 
. 2.279 
2.3 
. 10.481 
0.6 
. 2.734 
2.4 
. 10.937 
0.7 
. 3.190 
2.5 
. 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 fluidounces of urine, found to contain 2.4 per cent, of 
urea. The total urea excreted will therefore be 10.937 (from the table) X 21 
= 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 URINARY BLADDER AND THE URINE. 
423 
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 of potassium bromide, and then a little muriate of ammo- 
nium, 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 practical 
purposes are as accurate as could be wished for. 
Formula f07' Special Solution of Chlorinated Soda. Shake chlori- 
nated 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 
imperfect elimination of urea, and as a result it, or closely allied 424 
THE MANIFESTATION OF DISEASE IN ORGANS. 
products, are retained in the blood. If, therefore, in a pregnant 
woman or a person suffering from Bright’s disease, analysis shows 
a constant 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 uraemia is developed, treatment is of compara- 
tively little value. 
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 
excreted 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 fluidrachin 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 ammonia 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 dimensions 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 pneumonia, acute 
articular rheumatism, and some other fevers; and if they gradually 
increase, they indicate the development of convalescence. 
The Total Quantity of Solids excreted by the kidneys in 
twenty-four hours can be roughly estimated by what is known as 
Haine’s modification of Ilaeser’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 THE URINARY BLADDER AND THE URINE. 
425 
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 
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 from the fourth to the 
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 solu- 
tion 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 mix- 
ture 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 perhaps 
by nausea and chilly sensations, followed by a marked decrease in 
the quantity of urine secreted, which decrease may actually amount  THE MANIFESTATION OF DISEASE IN ORGANS. 
426 
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 ingredient in 
large amount, and a microscopical examination of the sediment will 
reveal a large number of blood-corpuscles, epithelial cells, 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 nephritis 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 usually hard and 
tense, and the sharp and clear sound of the heart, as heard at the 
second right costal cartilage, will indicate the high arterial 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 neph- 
ritis is favorable. In the acute diffuse nephritis 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 infec- 
tious 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. Uraemia, 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 THE URINARY BLADDER AND THE URINE. 
427 
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). Albumin 
is only found inconstantly and in traces, and is generally to be sought 
for in the urine passed by the patient when first arising from bed. 
The pulse is usually much increased in tension, and atheroma of the 
bloodvessels is more or less marked. This high-tension pulse is a 
valuable diagnostic sign. The heart, which in acute diffuse neph- 
ritis may be slightly dilated, or in chronic parenchymatous nephritis 
somewhat hypertrophied, is in this disease usually markedly hyper- 
trophied, 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 symptoms are more commonly seen in this class 
of cases than in any other, and violent vomiting difficult of control 
should always make the physician test the urine to discern renal 
mischief. Unlike parenchymatous nephritis, dropsy is a rare com- 
plication 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 pres- 
ence of syphilis, of prolonged suppuration, or extensive bone dis- 
ease, due, it may be, to tuberculosis, with concomitant enlargement 
of the liver and spleen, separates it from any other ailment. Albu- 
minuria may be a marked or an absent symptom. 
Let us suppose, however, that a patient comes to us with a history 
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 mellitus. 
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  THE MANIFESTATION OF DISEASE IN ORGANS. 
428 
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 
from a pyelitis or a suppurative inflammation of the pelvis of the 
kidney. The symptoms of this state are, briefly, a constant or inter- 
mittent pyuria, usually an acid reaction of the urine, chills and 
fever, which may mislead the physician into a diagnosis of malarial 
poisoning, or, in other cases, if the pyelitis be tubercular, hectic fever 
may be present. Sometimes violent attacks of pain resembling renal 
colic are passing symptoms, and not uncommonly 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 suppura- 
tive 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 cystoscope. 
The prognosis varies. If due to an infectious fever, recovery usually 
occurs. Tuberculous pyelitis may also recover. CHAPTER XIII. 
THE BOWELS AND FECES. 
Constipation and diarrhoea—The cause 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 infused 
or boiled tea made with hard water is frequently met with. When 
too rapid absorption of the liquids takes place from the feces the 
cause may be lack of liquid ingested, and the remedy be full 
draughts of pure water; or, again, constipation occurs as a manifes- 
tation of diabetes insipidus or diabetes mellitus, because the polyuria 
429 430 
THE MANIFESTATION OF DISEASE IN ORGANS. 
of these affections drains the body of liquid. Obstinate constipa- 
tion should, therefore, always call the physician’s attention to these 
affections and to two other possibilities, namely, that the condition 
depends 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 inhibi- 
tory fibres of the splanchnic nerves may be so irritated that peri- 
stalsis 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, growths, by the process of intussuscep- 
tion, by volvulus, by cicatricial contractions, and by impacted for- 
eign 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 intes- 
tine 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; relaxation of the bloodvessels of the intes- 
tine, with profuse serous leakage and consequent watery purging; 
acute inflammation, with excessive secretion of mucus; and the THE BOWELS AND FECES. 
431 
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 cheek 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 finally 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 
bowel, 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  THE MANIFESTATION OF DISEASE IN ORGANS. 
432 
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 de- 
scribed 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 points 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 artificial culture. 
Symptoms identical with the more violent forms of cholera nostras 
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 
materials 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 the 
gastro-intestinal mucous membrane by the drug. Rarely certain 
poisonous toadstools produce somewhat similar symptoms. 
If an adult who has not eaten anything which could have pro- THE BOWELS AND FECES. 
433 
duced a diarrhoea, as the result of irritation from bad food, is seized 
with profuse watery purging, with very little or no pain, and with- 
out nausea and 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 ursemic con- 
vulsions 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 pressure 
over the transverse colon and mucus in the feces, which are not in 
very large quantities after the first few movements, there is probably 
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, and 
less griping in character. Vomiting is not a constant feature, as it 
is in the watery choleraic diarrhoeas, and the course is more sub- 
acute, the duration of the illness usually being from one to three 434 
THE MANIFESTATION OF DISEASE IN ORGANS. 
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 lienteric diarrhoea. 
Not far removed from this type of cases are those of a more 
chronic character depending upon more grave and lasting altera- 
tions 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, 
due either to spasm of the muscular fibres of part of the lower bowel 
or to cicatricial contractions from the healing of old ulcerations. 
In very severe cases the condition of the intestines 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 intes- 
tinal walls. In this connection the diarrhoea of tuberculosis is not 
to be forgotten, depending, as it does, either upon the general infec- 
tion or upon the development of ulcerations in the intestinal canal. 
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 THE BOWELS AND FECES. 
435 
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 
colicky and the stools are passed with ever-increasing bearing-down 
or tenesmus. The effort to empty the bowel, after it is in reality 
thoroughly 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 jellv-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 and more fluid, and 
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- 436 
THE MANIFESTATION OF DISEASE IN ORGANS. 
rate is high. Convalescence is always very slow, and liver-abscess 
due to an hepatic infection by the amoebae coli is very frequent. 
Sometimes secondary abscess of the lung develops. 
A positive diagnosis of this variety of dysentery is made by the 
discovery of the amoebae in the stools. These micro-organisms possess 
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 amoebse; 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 numer- 
ous 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 
amoebse. 
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 the 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 diph- 
theritic 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 produced 
by a malignant and ulcerating growth in the sigmoid flexure or rec- 
tum, 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 the 
passage of several muco-purulent movements each day in persons 
who have pulmonary gangrene or pulmonary tuberculosis, partly 
due to the swallowing of fetid sputum or tubercular ulceration of 
the bowels. Diarrhoea is also a symptom of septicaemia. Distantly THE BO WELS AND FECES. 
437 
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 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 ulcerated mucous 
membrane covering a syphilitic deposit, or else a malignant 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 cases of exophthal- 
mic 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. 
Fatty 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 dis- 
cussion of the diagnostic indications of the feces. In the first place, 
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 com- 438 
TIIE MANIFESTATION OF DISEASE IN ORGANS. 
posed 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-absorp- 
tion 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 saceulations of the 
colon, and are passed out only 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 actu- 
ally 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 
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 hsematoxylon often makes 
them look red. 
In the stools of persons living on a pure milk-diet we usually find THE BOWELS AND FECES. 
439 
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 color-forming micro-organims; 
but a greenish stool may also be produced in an infant by the per- 
sistent administration of sodium bicarbonate. 
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 ulcer- 
ated morbid growth in the colon. Sometimes, however, where the 
hemorrhage 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 with the microscope or by testing the feces 
for haem in. (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 gallstones in the stools, which, if they are 
passed soon after their escape into the bowel, are found to be faceted. 
Stools which are being searched for gallstones should be washed 
through a sieve in such a way as to catch the stone and let the fecal 
matter through. The intrahepatic gallstone is not faceted and crum- 
bles easily. 440 
THE MANIFESTATION OF DISEASE IN ORGANS. 
Very rarely a portion of the bowel sloughs away, and yet recovery 
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 without 
causing any symptoms, and, again, in children in particular, they 
cause great systemic disturbance by producing disorder of the diges- 
tion 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 segments 
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 para- 
site, 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: the taenia 
solium, the taenia 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 taenia solium, and is probably 
derived by the patient from raw or uncooked pork. The eggs of 
the taenia solium must be sought for by a microscope. They are 
round and covered by a hard shell, which upon pressure breaks 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 swal- 
lowed 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. 
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 taenia solium and devoid of hooklets about the suckers 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 THE BOWELS AND FECES. 
441 
from eating raw beef. The botliriocephalus 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, 
Fig. 184. 
Fig. 185. 
Ascaris lumbricoides, dissected and walls 
thrown hack. (Heller.) a. Genital orifice. 
b. Intestine, c. Oviducts, d. Longitudinal 
hand. e. Ovaries. 
Oxyuris vermicularis, magnified. (Payne.) 
a. Young female, b. Male. c. Mature female, 
full of eggs,  THE MANIFESTATION OF DISEASE IN ORGANS. 
442 
very large, and the shell is light brown in color, and very easily 
broken. This parasite is not common in America, but is a very 
Fig. 186. 
Fig. 187. 
Triehocephalus dispar, natural size. (Payne.) 
a. Female, b. Male. 
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 ren- 
ders 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 com- 
paratively rare is the taenia 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 
worm looking very much like the thread-worm, but 
somewhat larger, which inhabits the duodenum. It is called the 
ankylostomum 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 
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 trichoceph- 
alus dispar, is a fine thread-worm without any medical interest. 
Ankylostomum 
duodenale, magni- 
fied. (Bristowe.) 
a. Female, b. Male. PART II. 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
CHAPTER I. 
CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
The methods of taking the temperature—The significance of fever—The febrile 
movements of various diseases. 
A chill is of very considerable diagnostic importance when 
observed by the physician, or even when reported as having occurred 
in the immediate history of the patient. It may follow prolonged 
exposure to cold without the subsequent development of disease, 
or be a precursor of pneumonia or even severe bronchitis. Often 
it is an early symptom of the onset of one of the acute infectious dis- 
eases, such as croupous pneumonia, erysipelas, or scarlet fever. In 
other instances it is an early symptom of the development of a puru- 
lent or pysemic process. When chills recur repeatedly they may be 
due to malarial infection, in which case they may be controlled by 
using quinine as a therapeutic test, as a result of deep-seated ab- 
scesses and general pyaemia, and finally, but less frequently, they 
may indicate tuberculosis or suppurative endocarditis. 
Fever is that state of the human body in which its temperature 
is raised above the normal limit, or 98.8° F., blit variations from 
97.8° to 99.5° may occur without indicating disease. From 99.5° 
to 100.4° the temperature is spoken of as subfebrile, from 100.4° 
to 101.3° as mildly febrile, while the term decidedly febrile is 
applied to temperatures varying from 103.1° to 105°. Hyper- 
pyrexia is a term applied to a febrile movement in which the tem- 
perature rises as high as 106° F., although cases are on record of a 
temperature of 115° or even more. 
The method of taking the temperature consists in placing a self- 
registering clinical thermometer in the mouth under the side of the 
tongue, the lips being then closed tightly about its stem; or of insert- 
443 444 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
mg 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 carefully 
wiped dry, since if perspiration is present its evaporation will so 
chill the thermometer that a false record will be made by the index. 
Sometimes the temperature of the patient is taken by inserting the 
thermometer into the rectum, and, if this is done, the bulb should 
be passed well inside the external sphincter. Rarely the tempera- 
ture 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 
mouth in children: thus, stomatitis may raise the local temperature 
from one to two degrees. Hot liquids, if taken into the mouth just 
previous to or during the time at which the thermometer is inserted, 
will so raise the temperature of the local tissues as to make the 
thermometer 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 impos- 
sible, and advises that the temperature shall never be taken in the 
mouth if it is possible to take it elsewhere. 
The face of a patient with fever is apt to be red or flushed, and 
sometimes if the disease be distinctly infectious, as in pneumonia or 
acute rheumatism, it is covered with sweat. The pulse is quickened 
and there are usually thirst and a somewhat scanty urine. 
Febrile movements are generally associated with a dry, hot skin, 
but sometimes with a cold, wet skin. The latter condition is of evil 
significance, as a rule, and must be overcome if possible. 
The significance of fever is great. Tt 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 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
445 
determine its cause. The significance of a raised bodily temperature 
from a physiological point of view is that the nervous centres gov- 
erning heat-production and heat-dissipation are disturbed by some 
substance criculating in the blood or by reflex irritation, or perhaps 
by both. The danger of high fever is that it may cause coagulation 
of the protoplasm of the heart or vital centres in the base of the 
brain, but the danger of ordinary febrile temperatures has been 
greatly exaggerated. Indeed, in some cases moderate fever prob- 
ably aids the body in throwing off or, rather, conquering the disease, 
which has attacked it, in three ways, namely, by producing a tem- 
perature 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 ma- 
terials; and, finally, by virtue of the increased temperature the 
effects of poisons may be rendered nil. This is the case, for exam- 
ple, 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 dura- 
tion of fever has more to do with its importance as a symptom than 
has its degree, for a temperature of 105° for a few hours may be 
borne with immunity, whereas one of 103° for many days cannot 
fail to produce evil effects. 
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 446 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
hoars he develops a severe chill, followed by a fever which may be 
quite high, but does not last long. 
Fever accompanied by apathy and listlessness is not of itself of 
grave omen, but if such symptoms change into a state of active 
fever with delirium and jactitation the change is to be regarded as 
dangerous. 
Fever in Infectious Diseases.1 Nearly all infectious dis- 
eases are ushered in by the development of fever of greater or less 
degree, and this is particularly true of the exanthemata. Inquiry 
should, therefore, be made by the physician as to the previous his- 
tory of infectious disease. If one or more of the eruptive fevers 
have already been present, they can usually be excluded from the 
diagnosis of the illness at the time of the visit. If, on the other 
hand, there is a history of old pulmonary disease or acute articular 
rheumatism, this may indicate that another attack is coming on. 
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 wretched- 
ness the patient develops a slight fever of from 100° in the morn- 
ing 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 tem- 
perature 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, and then the evening rises fail to 
reach their former height. Often these marked morning remissions 
are the first indication of the tendency 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 morn- 
ing. After the third week, in a moderately severe case, the tem- 
perature falls gradually till by the twenty-eighth day it usually 
reaches the normal. In very rare cases the temperature speedily 
reaches its acme at the very beginning of the disease, and then 
passes through the course already described. Such cases are gener- 
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. CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
447 
ally 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. 188. 
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 iu 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. 188.) 
More rarely, as a result of getting out of bed too soon, or bad feed- 
ing, or other cause, 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. 189.) 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, acute renal, or bone disease, as these con- 
ditions very commonly ensue as sequels of typhoid. In other 448 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
Showing a relapse in typhoid fever. 
Fig. 189. CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
449 
instances, after the morning temperature has reached normal, the 
evening temperature remains pyretic for a number of days, and it 
may persist for some time. 
If the fever of typhoid rises as high as 107° or 108°, the prog- 
nosis 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 that as a rare occurrence the fever in this disease 
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 tuberculosis from typhoid fever 
may be quite difficult in certain cases. When the symptoms of the 
two conditions are compared this is not difficult to believe, for we 
often have in both diseases headache, epistaxis, a very similar 
temperature-chart, and a feeble pulse, while there may be in both 
conditions 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 stage 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 
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 on percussion to be enlarged. 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 typhoid fever they 
are apt to be ochre-colored; and, again, in tuberculosis the loss 
of flesh is often exceedingly rapid, and profuse sweats and high fever 
are frequently seen. The finding of Widal’s reaction in the blood, 450 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
or the discovery of the bacillus of Eberth in the feces and the pres- 
ence of the diazo-reaction in the urine would, of course, indicate 
typhoid fever. (See chapter on Urine.) An absence of leucocytosis 
would also indicate typhoid fever, for this condition is usually 
present in acute tuberculosis. Finally, careful and repeated exam- 
inations of the chest xvill usually, iu the course of the disease, demon- 
strate 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 eestivo-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 con- 
nection. There is no such disease as typho-malarial fever. 
Remittent Fever. 
Onset generally intermittent. 
Irregular remissions. 
The temperature may arrive at 40° C. (104° 
F.) within twenty-four hours. 
Headache rare in the beginning; of a neu- 
ralgic character, pulsating, variable in its 
position and intensity. Sclera subicteric from j 
the onset. 
The apathetic expression of the face, the dry- J 
ness of the tongue, and sordes upon the teeth j 
are not very marked. 
Breath foul. 
The delirium may come on in the early days; 
it is recurrent, but changes with the exacerba- 
tions of temperature and other symptoms, and 
may give way to grave symptoms related to 
other organs. 
If there be pulmonary congestion, the cough 
aud 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 j 
marked, even syncope. 
There are usually restlessness and anxiety 
(jactitatio corporis). 
Peculiar grayish color of skin ; sometimes a 
slight jaundice. 
Herpes common. 
Typhoid Fever. 
Onset gradual and progressive. 
Regular, though very slight morniug remis- 
sions with evening exacerbations of tempera- 
ture. 
The temperature does not reach 40° C. (104° 
F.) 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. 
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, 
and stupor. 
No jaundice. 
Herpes rare. CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
451 
Remittent Fever. 
Anaemia more or less marked early in the 
course. 
No characteristic exanthem; urticaria not 
uncommon. 
At times there may be transient tympanites 
or ileo-csecal gurgling; they are but slightly 
pronounced and paroxysmal ; diarrhcea 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, 
Durham, and Widal); malarial parasites and 
pigmented leucocytes present. 
Fever disappears under quinine. 
Is an endemic disease occurring particularly 
in rural districts; rarely epidemic. 
Typhoid Fever 
Anaemia absent, excepting in later stages. 
Characteristic roseola. 
Tympanites, gurgling, and 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 leucocytes; 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 by those of ulcerative endocarditis of a 
typhoid type. In addition to an irregular fever, there may be diar- 
rhoea, parotitis, stupor, and progressive feebleness in both diseases. 
An examination of the heart may reveal the presence of endocar- 
ditis; or the existence of some focus of infection, such as a wound, 
a septic process, or the fact that the patient is in the puerperium, 
will, in combination with the sudden development of endocarditis, 
render a diagnosis possible. 
An irregular fever with muscular pains and a great deal of dis- 
comfort in the belly, the case simulating typhoid fever, may occur 
in cases of trichinosis. 
A febrile movement closely resembling that of typhoid fever, a 
resemblance which is increased by the association with it of head- 
ache, insomnia, and anorexia, may be Malta fever, a disease which 
can be excluded in the vast majority of cases if there is no history 
of exposure to the exciting cause in the island of Malta. 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 tem- 
perature falls, but in a few days all the symptoms return witli even 
greater vehemence than before. Such relapses may occur again and 
again. Violent pain in the joints on moving the body is often 
present. 452 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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, head- 
ache, 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 petechise 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 in the early stages. 
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 relapsi ug fever in America, the frequency of mala- 
rial fever in certain parts, the presence of the spirillum of Obermeier 
in the blood in relapsing fever, and the malarial germ in the blood 
of intermittent fever, all make the diagnosis possible. 
In scarlet fever the temperature suddenly rises on the first day to 
104° to 105° F., and still higher on 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 per- 
sists longer, is probably due to some complications, such as otitis, 
or the “ collar of brawn,” due to enlarged cervical glands. (Fig. CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
453 
190.) The characteristic strawberry punctated rash and scarlet hue 
appearing on the first or second day, the ultimate dermal desquama- 
tion, 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.) 
Fig. 190. 
Chart of scarlet fever. 
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. 191.) With the fading of the 
rash the temperature also falls by crisis. If fever persists to any 
extent, it is always due to some complicating cause other than the 
original disease; such a complication, for example, as a bronchial or 
gastro-duodenal catarrh. 
The fever of rbtheln, if any occurs, is very seldom more than 
102°, and lias no typical preliminary rise as has measles, so that the 
temperature-chart of the disease may aid materially in a differential 
diagnosis. (See chapter on the Skin.) 
The febrile movement of smallpox is with the exception of that of 
typhoid the most characteristic of all the eruptive diseases. With 
a sudden onset of fever, pain in the back, severe headache, and 
malaise, the patient takes to his bed if possible, and his temperature 
if taken will be found speedily to rise even to 105° or more in some 454 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
cases, and then falls back to almost normal for two or three days, 
during which time the eruption appears. In this way, therefore, 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 pustules the tem- 
perature rises again in what is called the fever of suppuration, which 
lasts with greater or less persistence for at least a week, when it 
ends by lysis or a gradual fall. Excessively high fever of 108° 
is a sign of approaching death or at least of very grave import. 
Fig. 191. 
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 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 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
455 
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 
Fig. 192. 
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. 
whole term of acute illness, if we exclude general physical discom- 
fort, lasting but eight to twelve hours, is in the majority of cases 
that of intermittent malarial fever. The peculiarities of intermittent 
malarial fever, aside from those just named, are that the febrile 
movement begins to decline before the stage of sweating begins, and 
in some cases it begins to rise before the sensation of chilliness of 
the first stage leaves the patient. (Fig. 192.) 
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 456 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
to infection by two sets of tertian parasites which undergo segmen- 
tation on alternate days, or it may be due to infection with three 
sets of quartan parasites. If the attacks occur every other day, they 
are called tertian (Fig. 193); if on the third day, quartan; if on 
the fourth, quintan. If two attacks come on the same day, it is 
called double quotidian. 
Another point of importance in connection with malarial attacks 
is that they often occur earlier each day by an hour or more. 
Rarely, they are delayed. 
Fig. 193. 
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 evi- 
dences 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 
administration of quiuine. 
As stated in the chapter on the Blood, an examination of this 
fluid will reveal in practically every form of infection, except mala- 
ria and typhoid fever, an increased leucocytosis; but in malarial 
infection the leucocytes are not increased in number. 
Care must always be taken that the intermitting fever of the 
various forms of sepsis is 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 tuberculsois. Again, 
acute, ulcerative endocarditis and purulent phlebitis may cause sim- CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
457 
Showing temperature-curves in a case ot ulcerative endocarditis. (From a case in author’s wards.) 
Fio. 194. 458 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
ilar symptoms, as may also hepatic abscess, impaction of gallstones, 
with suppurative cholangitis, causing the so-called Charcot’s fever 
(see below). The absence of a history of malarial exposure, the 
possible presence of a cough, and the discovery of a tubercular 
lesion in the chest or abdomen by careful physical examination 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. 194.) In the typhoid type of ulcerative endo- 
carditis the profound asthenia and general prostration will separate 
the diseases even if the temperature-chart be useless. 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 
duration 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. Rarely it lasts more than six weeks. Death 
usually occurs in ulcerative endocarditis, unless there has been pre- 
viously 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 gallstone colic, and of exceed- 
ingly severe rigors, enables us to separate them. 
When fever of an intermittent type has been observed, and inter- 
mittent malarial fever, tuberculosis, and cholangitis cannot be dis- 
covered as a cause, search should be made for tenderness and swelling 
of the liver, due to hepatic abscess. Profuse sweats also 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. CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
459 
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 pe?'nioious anaemia 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 Hodg- 
kin’s disease (see chapter on Blood), or even more commonly tuber- 
culous 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 excised 
piece of the swelling will decide the diagnosis. An intermittent 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, indicate 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 examination 
of the blood can decide the diagnosis. If small ovoid, moving para- 
sites are found in the first week, or crescentic parasites after that time, 
this will decide that the case is malarial. (See chapter on the Blood.) 
Care should be taken to recollect the fact that when typhoid fever 
develops in a young child the temperature may be so markedly 
remittent that an erroneous diagnosis of malarial infection may 
be made. In other words, “ infantile remittent fever” is really 
typhoid fever.  THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
460 
A febrile process somewhat closely resembling remittent malarial 
fever, yet so rare, comparatively, as never to be confused with it, is 
WeiVs 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 epi- 
demic disease, separate it from malarial fever. Dengue and influ- 
enza, of an epidemic type, closely resemble one another, but in 
dengue there is rarely marked involvement of the respiratory tract 
as there is in influenza; there is an eruption which is not seen in 
influenza, and it is not followed or accentuated by such grave com- 
plications as we see in the more severe cases of influenza. Dengue 
is a disease of the South and influenza one of the North. 
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 pecu- 
liarity, 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 the disease to convalescence or death is run in about one week. 
There are only two other diseases which can be readily confused 
with yellow fever, namely, dengue and bilious remittent fever. 
Dengue has been confused with yellow fever many times, and even 
the most experienced physicians have had great difficulty in sepa- 
rating them when the yellow fever has been mild. The most im- 
portant points in their differentiation are the facts that in dengue 
there is usually a second onset of fever several days after the first CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
461 
onset, whereas this does not occur in yellow fever. Again, the 
eruption on the skin is not seen in yellow fever, and a rapid pulse 
is present in dengue, whereas in yellow fever the pulse is usually 
not very rapid. On the other hand, in yellow fever we usually 
meet with jaundice, albuminuria or suppressed urine, and a hemor- 
rhagic tendency of a marked degree, all of which are absent in 
deugue. Further, death from dengue is very rare. 
A case of bilious remittent fever occurring during an epidemic of 
yellow fever is almost certain to be incorrectly diagnosed. In the 
absence of an epidemic, 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 diagnosis of malarial disease rather than to 
yellow fever. 
Just as in yellow fever, so in spotted fever or cerebrospinal men- 
ingitis of an epidemic form, the fever itself is one of the least impor- 
tant symptoms, for, aside from the fact that it is apt to be irregular 
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 symp- 
foms in an epidemic does more to confirm a diagnosis than the 
febrile movement. In some cases of spotted fever, however, of a 
very grave type, the fever becomes a hyperpyrexia, but in cases 
tending toward recovery the temperature usually begins to fall by 
lysis before any moderation in the other symptoms is manifested. 
Even in the presence of an epidemic of spotted fever it should 
never be forgotten that middle-ear disease often causes marked 
meningeal symptoms, and that croupous pneumonia often produces 
a similar train of manifestations, probably by infection with its par- 
ticular micro-organism. The possibility of tubercular infection pro- 
ducing such symptoms 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. 
The fever due to septiccemia may produce a temperature-chart 
which closely resembles that of enteric fever, but septic fever gener- 
ally possesses one characteristic which, in the face of other symptoms 
suggesting sepsis, is of great importance, namely, the extraordinary 462 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
rises 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 inde- 
pendent of taking food, would point to cerebral abscess, particularly 
if a history of injury could be obtained. 
A somewhat similar chart to this may occur in connection with 
cases of active pulmonary tuberculosis, when the lesions are well 
developed and septic absorption is active; but usually in the hectic 
fever of phthisis we have an approximately normal morning tem- 
perature, with a rise from two to three degrees, or even more, toward 
night. (Fig. 195.) 
Fig. 195. 
Chart ot a case of pulmonary tuberculosis, showing rising and falling of the temperature 
morning and night. 
This symptom of fever in any form occurring in a person with 
suspiciously “ weak lungs” should cause the physician to be confi- 
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 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
463 
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. 
When fever 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 fail- 
ure or vomiting and diarrhoea. The 
febrile movement is of the most irreg- 
ular type, even when some grave com- 
plication, such as severe bronchitis or 
pneumonia, comes on, although croup- 
ous pneumonia rarely occurs as a com- 
plication of “ la grippe.” 
The respiratory symptoms just de- 
scribed are also seen frequently in 
association with moderate fever, in “hay fever,” that condition 
seen in susceptible persons during the 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. 196.) 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. 197) and 
convalescence is established, although the sudden fall of fever may 
FrG. 196. 
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. 464 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
throw the patient into dangerous collapse. Sometimes convales- 
cence is broken by brief and slight febrile movements. If the 
case has been prolonged, or of the typhoid type, the fever may end 
by lysis. 
Fig. 197. 
Chart of a case of croupous pneumonia, with crisis ou the seventh day; admitted to 
author’s wards on second day of illness. 
It is to be remembered that the fever of catarrhal pneumonia is 
rarely as high as in the croupous form, 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 ma- 
laise. This febrile movement may then follow one of three courses: 
it may never rise above 101°, and proceed as does a simple fever, 
with slight morning remissions and evening exacerbations; or it 
may be as remittent as is a malarial remittent fever; or, again, it 
may resemble a malarial intermittent, rising to a high point and 
then falling almost to the normal. Phillips, of London, has reported 
a case of syphilitic fever in which this febrile movement lasted for 
weeks, and, after being treated by quinine as a supposed tertian CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
465 
ague, ended at once under antisyphilitic medication. (See chapter 
on Skin, Eruptions.) 
In anthrax (splenic fever) the temperature rises rapidly and 
becomes very high, and in the course of from three to five days 
becomes subnormal, when death occurs. The history of exposure 
to possibly infected hides or hair, the early development of a pap- 
ule, vesicle, and pustule, surrounded by brawny swelling, and 
enlargement of the neighboring lymph-glands, render the diagnosis 
easy; but if any doubt exists, it can be promptly dispelled by a 
microscopical examination of the fluid from the pustule, when, if 
the disease be anthrax, the anthrax bacilli will be found. (See 
chapter on Skin.) 
Fever with a vesicular eruption about the lips and on the mucous 
membrane of the mouth accompanied by disorder of the stomach and 
bowels may 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 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 diag- 
nosis. 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 paren- 
chymatous nephritis may or may not be preceded by a chill. The 
temperature may rise to from 100° to 104°, but the course of the 
fever itself is of no diagnostic import. The pulse, pain in the back, 
headache, perhaps drowsiness and coma, and the diminished urinary 
secretion, bloody urine, and albuminuria, render the diagnosis easy 
and the cause of the fever evident. 
Very marked fever up to 104° or 105° may develop in the early 
course of acute infectious 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°. 466 
THE manifestation of disease by symptoms. 
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 
characteristics; but in very severe forms of the disease with cere- 
bral manifestations, 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 previous attacks of articular rheumatism, the hot, swollen joint 
or joints (usually the large ones), and the successive invasion of 
other joints as the ones first affected get well, point to the correct 
diagnosis. It must not be forgotten, however, that gonorrhoeal and 
other forms of septic arthritis occur with febrile movement. Pyse- 
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 been reported as occurring 
in hysteria, but in a certain number of cases these records are really CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 
467 
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, mus- 
cular 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 symp- 
toms 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 
death 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 pres- 
ent 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 
Donkin and Goodhart, and the writer has also met with it quite 
frequently. This condition has been called gastro-pulmomary fever ; 
but as either pulmonary or gastric signs may be absent, this term 468 
THE manifestation of disease by symptoms. 
does not apply to all eases. 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. 
A subnormal temperature of a dangerous degree is met with in the 
algid type of pernicious malarial infection, and can only be satisfac- 
torily differentiated from other conditions by a blood examination. 
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. 
A temperature below 92.3° is nearly always fatal in its prognosis, 
but subnormal temperatures above this degree are not necessarily 
followed by death. A temperature of 95° is spoken of as one of 
moderate collapse. 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 con- 
ditions 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 
exhaustion 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 diag- 
nostic 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 dis- 
ease, 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, consisting 
in gastric or intestinal distress, belching, hiccoughing or vomiting, 
or even by diarrhoea. Often there is a distinct history of the inges- 
tion 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 congestion of the 
liver followed by jaundice. The headache of disturbed digestion is 
nearly always frontal, and in many cases congestive to such an extent 
that the face may be flushed, or at least the intracranial circulation 
is so disturbed that the patient is unable to lower the head, because 
469 470 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 into the back of the throat. Vomit- 
ing makes such headaches very much worse for a time, owing to the 
congestion of the head following the efforts at vomiting, and this 
is an important point in diagnosis, for in renal disease or some 
other states the vomiting is sometimes so easily performed that no 
straining ensues. 
That disturbances of the digestive tube are capable of altering 
the intracranial circulation is proved by numerous facts. Thus 
Brunton quotes the experiments of Ludwig and Dogiel, who showed 
that moving the intestines by the finger introduced through an 
abdominal incision caused a great increase in the flow of blood 
through the 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, sev- 
eral 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 con- 
stipation 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 hemiau- 
opsia. It is to be remembered, however, that in some cases of 
hemicrania of nervous origin the sickness at the stomach seems to 
be secondary to the severe pain in the head. 
Headaches resulting from digestive disturbance do not always 
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 ouly to be destroyed by 
the liver, or are developed in too small quantities to have any 
effect; but no sooner do congestion of the liver and deficient biliary 
secretion ensue than they are formed in large amounts, and enter the HEADACHE AND VERTIGO. 
471 
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 hsemoglobinuria, 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 hsemoglobinuria. 
In other cases in which no jaundice is present violent headaches, 
which utterly incapacitate the patient, come on from auto-intoxica- 
tion. 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 
vertiginous, but is able to eat his breakfast as heartily as usual. In 
the course of a few hours the mental heaviness becomes more marked 
and a pain in the brow develops, which gradually gets worse and 
worse till it is unbearable. The ordinary remedies for neuralgic 
headache are futile, and he finds no relief until by the use of a 
purgative he removes the source of his intoxication, and his kidneys 
have time to eliminate the toxins already absorbed. 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 auto-intoxication ceases. Some of the intestinal poisons 
have been isolated by Brieger, Harnack,and others, and have a physi- 
ological 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, faint- 
ness, and a feeble pulse, if no nausea is present, the presence of the 
aconite-like toxin. Persons suffering from headache of this type 
are nearly always much freer from discomfort in the head after such 
an attack 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. 
The headache of eye-strciin is usually due to abnormalities in the 472 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 headaches 
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 headache, 
immediately after or long after reading, there is blurred vision, pain 
in the muscles of the eye on suddenly moving the eyeball, any ten- 
dency to congestion of the lids, or hyperaemia 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 astigma- 
tism 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 ophthalmolo- 
gists who are inclined to carry the theory of refraction errors in the 
production of morbid symptoms to excess believe that it cau. 
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 iii 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 hemicrania, 
often by a dilated pupil ou the affected side, aud flushing and pallor 
of one side of the face. HEADACHE AND VERTIGO. 
473 
Headaches due to rheumatism are often quite severe, and are asso- 
ciated with 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 benzoate 
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. 
Those due to renal disease are of two classes, in that they are an 
evidence of ursemia, or they are congestive and due to the high arterial 
tension so often seen as the result of chronic contracted kidney with 
its associated conditions of cardiac hypertrophy and arterio-sclerosis. 
Ursemic headache, as pointed out in the chapter on Vomiting, 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 ursemic headaches may occur in any form of renal disease, 
acute or chronic, which results in ursemia; 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 exami- 
nation is of the utmost importance, and no surely correct diagnosis 
can be made in any case of suspected kidney trouble till this secre- 
tion has been examined and found abnormal. (See chapter on Urine.) 
While headache is far less common as a symptom of diabetes than 
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, 474 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 caus- 
ing 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 lias been found in the frontal lobes. Tumors of the base of 
the brain cause focal symptoms most commonly, and in addition to 
unilateral choked disk we find in many such cases ptosis from paral- 
ysis of the oculomotor nerve, disturbances in the functions of the 
trifacial nerve in its sensory filaments, so that painful tic (see chap- 
ter 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, 
internal squint from paralysis of the abducens (sixth), and anaesthesia 
of the skin and muscles of the eyebrow, forehead, nose, and eye, 
from involvement of the first division of the trifacial. A tumor of 
the middle fossa above the dura causes oculomotor palsy (ptosis), 
patheticus paralysis (downward deviation of eyeball from paralysis HEADACHE AND VERTIGO. 
475 
of the superior oblique), and amaurosis from pressure on the chiasm. 
On the other hand, if it is below the dura, the oculomotor, the 
pathetic, the abducens, and the fifth nerve are paralyzed. When 
tumors occur in the posterior fossa they cause paralysis of the tri- 
facial, facial, auditory, glosso-pharyngeal, vagus, spinal accessory, 
and abducens, or, in other words, cause anaesthesia of the upper part 
of the face, facial paralysis, deafness, loss of taste, irregular cardiac 
action, loss of power in the sterno-mastoid and trapezius muscles, 
and internal squint. Tumors of the lenticular and caudate nucleus, 
the interior portion of the thalamus, the corpus callosum, the fornix, 
choroid plexus, and of any part of the cerebellum except the vermi- 
form process, may be present without any localizing signs. 
Still more localizing symptoms are early paralysis of the oculo- 
motor nerve from a lesion in the crus, hemianopsia in tumor of the 
occipital lobe, and tonic convulsions with preservation of conscious- 
ness and a staggering gait in tumor of the vermis of the cerebellum. 
Should amaurosis be present, very valuable data as to the position 
of the growth are to be had from a study of the fmictions of the eye. 
If the pupils react properly to light, this shows that the optic nerves 
and tracts 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, 
particularly when the patient sleeps, a slow pulse, and, as the 
growth increases, symptoms of cerebral compression. It ought to be 
remembered that brain-tumor may be closely masked by the results 
of chronic nephritis, for in the latter disease we find headache, local 
palsies or spasms, and, more important than all, an optic papillitis, 
which used to be thought pathognomonic of brain-tumor. Albu- 476 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
minuria may be present in botli diseases,but tube-casts can be found in 
renal disease and not in tumor. Both diseases may exist side by side. 
Care should be taken in a case of constant and severe headache 
that it be not thought due to brain-tumor until the possibility of 
its being caused by a syphilitic gumma, syphilitic arteritis, or syph- 
ilitic meningitis is excluded, for mental depression and crashing head 
pains occur in all of these states. The differentiation of gumma- 
tous tumor from cerebral tumor due to other causes may be impos- 
sible unless there be a history of specific infection or manifestations 
of this disorder in scars or other external signs of syphilis. Im- 
provement in the symptoms under the use of iodides and mercury 
would indicate syphilis rather than a growth due to other causes. 
The presence of optic neuritis would indicate tumor or menin- 
gitis and would exclude arteritis, and in tumor the pain is apt to be 
localized, while in arteritis and meningitis it may be diffuse. The 
chief symptoms of arteritis are those indicating failure of a proper 
blood-supply to the brain, as evidenced by giddiness, weakness of 
groups of muscles, difficulty in speech, so that the words are dropped 
out, and it may be symptoms like general paresis. In meningitis, 
on the other hand, the symptoms are irritative, such as spasmodic 
paralysis and irritative fever. 
The following differential diagnostic table aids in making a diag- 
nosis; but it is to be remembered that all these conditions may be 
very obscure : 
Syphilitic Gumma. 
Headache usually localized. 
Distinct focal paralysis com- 
mon. Paralysis associated with 
rigidity and spasm. 
Choked disk often present. 
Hallucinations rare. 
Syphilitic Arteritis. 
Headache diffuse, often ab- 
sent ; not severe. Not started 
by pressure on cranium. 
Hemiplegia or monoplegia 
frequent. Muscles affected are 
flaccid, and reflexes are ab- 
sent. Paralysis often fleeting 
and limited to a few groups of 
muscles. 
Optic papilla usually normal, 
sometimes syphilitic retinitis 
is present. 
Partial epilepsy rare. 
Aphasia is transitory and in- 
termittent. 
Hallucinations rare. 
Pain in limbs rare and fleet- 
ing. 
Intellectual functions feeble. 
No active delirium. 
Syphilitic Meningitis. 
Headache diffuse and rarely 
wanting; sometimes localized. 
Started by pressure or by per- 
cussion on head. Very severe. 
Paralysis, if present, associ- 
ated with rigidity and con- 
tracture, involuntary spasms, 
exaggerated reflexes. Paral- 
ysis more widespread. 
Optic retinitis with marked 
neuro-retinitis and abundant 
exudation along the vessels. 
Partial epilepsy common. 
Aphasia less complete but 
more permanent. 
Hallucinations common. 
Severe pain in limbs of cen- 
tral origin. 
Intellectual functions not 
feeble, but may be drowsy. 
Active delirium often present. HEADACHE AND VERTIGO. 
477 
Syphilitic Gumma. 
Ocular symptoms of gumma 
involve ocular cranial nerves 
(see text). 
Paralysis of cranial nerves if 
gumma is so placed as to injure 
them. 
Temperature very rarely 
raised. 
Syphilitic Arteritis. 
Ocular symptoms rare. 
Disorders of sensation are 
fleeting. 
Paralysis of cranial nerves 
not common. 
Temperature may be raised. 
Syphilitic Meningitis. 
Bitemporal hemianopsia due 
to compression of the chiasm. 
Homonymous hemianopsia. 
I Amaurosis from pressure on 
optic tracts. 
Permanent zones of hyper- 
1 eesthesia, anaesthesia, and par- 
; aesthesia. 
j Paralysis ot any cranial 
! nerve. 
Temperature quite frequently 
I raised. 
In connection with this table it must be remembered that, should 
the arteritis result in degenerative changes descending the pyramidal 
tracts, or in thrombosis with degeneration, the flaccid paralysis char- 
acteristic of arteritis may become spastic. Again, should aneurism 
arise from the arteritis the pressure upon a cranial nerve may pro- 
duce paralysis, as does meningitis. Then, too, the meningeal symp- 
toms may be varied. If the lesion is acute and at the base, there 
will be vertigo, compression of the cranial nerves, polyuria, and 
bulbar phenomena, and finally fatal coma. If it be at the convexity, 
then noisy delirium, convulsions, hallucinations, and paralysis in the 
form of hemiplegia or monoplegia appear. Death comes in coma. 
If it is chronic meningitis of the base, then we may have slowly 
developing alternate hemiplegia, crossed paralysis of the face and 
body, anaesthesia of one side of the face, and paralysis of motion on 
the opposite side of the body. If the convexity be affected then 
great irritability of the intellect, sensation, and motion may be 
present. Paralytic strokes are common, but coma is rare. 
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 
headache are almost if not quite identical in both cases. One of  THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
478 
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 pillow7, or, if 
the child is still about the room, 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 patient, 
who may so far recover as to go back to his occupation, for it some- 
times happens that a remission or latent period develops in the sub- 
acute forms of abscess. During this apparent remission, however, 
the temperature is rarely constantly normal, and the patient is any- 
thing but well, and chilly sensations may be present. 
Severe headache well diffused over the skull, coming on rather 
rapidly and associated with fever, stiffness of the back of the neck, 
vomiting, photophobia, delirium, and finally, stupor and paralysis, 
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. The differentiation 
of the former from the latter is sometimes difficult, but the finding 
of some local tuberculous focus, the insidious nature of the onset in 
some cases, the family history, and a set of symptoms pointing 
strongly to involvement of the base of the brain indicate that the ba- 
cillus tuberculosis is the cause of the disease. The fact that these 
symptoms are due in some cases to the onset of one of the acute 
exanthemata is established promptly by the appearance of a rash. 
If the disease be tubercular meningitis, the head-pains will often 
be paroxysmal in character, so that the patient will at intervals of 
varying length give vent to sharp cries, evidently due to a sudden 
dart of pain. Vomiting may also be present and ocular symptoms 
develop, such as ptosis, strabismus, and unequal pupils, which have 
a sluggish reaction. The febrile movement will be irregular, now7 
high, 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, HEADACHE AND VERTIGO. 
479 
and even if absent a focus of tubercular disease can often be found 
elsewhere. 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 present. 
In children these symptoms of tubercular meningitis may be so 
marked as to lead the physician to the diagnosis of this disease 
almost at once. Usually for some two or three weeks before the 
Fig. 198. 
Int. jugular 
vein 
Showingthe communications existing between the superior longitudinal and lateral sinuses 
and the external veins, indicated in the figure by *. (Leube.} 
onset of the severe symptoms the child will have been feverish and 
cross. Vomiting of a more or less obstinate form now comes on, 
and constipation is present. The pulse becomes slow and irregular, 
a mild fever is present, and emaciation may be rapid. The gen- 
eral nervous state is one of apathy, but finally may be disturbed by 
the sharp hydrocephalic cry. Often the child makes chewing or 
sucking movements. The fact, however, that several otner condi- 
tions produce identical signs in this class of patients renders caution 
necessary. It has just been pointed out that the onset of an infec- 480 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
tious disease may so result, and it is to be remembered that inflam- 
mation of the middle ear of an acute type may cause every one of 
the symptoms just described. Such cases are often incorrectly diag- 
nosed until a discharge from the ear with great relief to the patient 
clears up all doubt as to the malady. Then, again, in some cases of 
croupous pneumonia all pulmonary symptoms may be masked in 
the violence of the meningeal manifestations, and, finally, it is not to 
be forgotten that in some cases of severe gastro-intestinal disorder 
there may be signs of meningeal inflammation, such as coma, squint, 
convulsions, myosis, Cheyne-Stokes breathing, and a depressed fon- 
tanel! e. 
The symptoms of meningitis are 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 
ccdematous through their close connections with the sinus through 
the emissary veins of Santorini, which escape from the skull by 
way of the parietal foramina. (Tig. 198.) In children there is 
usually in such cases bulging of the fontanelles and heaviness. 
Somnolence or delirium may be present with many of the charac- 
teristic 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 chap- 
ters on Face and Head and on the Eye, paralysis of the oculomotor 
nerve, the ophthalmic branch of the fifth nerve, and of the abducens 
and patheticus may occur, as these nerves pass through the cavern- 
ous sinus or in its walls. Nearly always thrombosis of the cavernous 
sinus results from some disease 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 HEADACHE AND VERTIGO. 
481 
marked oedema back of the ear, owing to the clot extending to the 
small veins of the scalp, which pass through the mastoid and pos- 
terior condyloid foramina. The external jugular vein on the affected 
side is partly collapsed, particularly on full inspiration (Gerhardt’s 
symptom). Rarely this vein may be unduly distended (Fig. 199). 
Fig. 199. 
Showing the communications existing between the lateral and cavernous sinuses and the 
external veins, indicated in the figure by *. (Leube.) 
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. 482 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
thought, followed by unconsciousness, may follow meningeal hem- 
orrhage 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 hsemorrhagica (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. 
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 is a constant symptom in many cases of typhoid fever 
in the early stages, but the peculiar tongue (see chapter on Tongue), 
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 HEADACHE AND VERTIGO. 
483 
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 cephalgalia. 
Gruening is quoted by de Schweinitz as asserting that early morn- 
ing 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 headache 
on first 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 inter- 
mittent fever and is often a complicating symptom of fever of the 
remittent type. In this connection the physician should remember 
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 
hemorrhage 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. This 
in mitral regurgitation 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 tenderness. 
Violent neuralgia or shooting headache may be produced by expo- 
sure to cold, with resulting inflammation of the nerve-sheath; by 484 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
dental caries, and by middle-ear disease or disease in the external 
auditory canal. 
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 indiges- 
tion it is probably due to reflex irritation, and perhaps to the absorp- 
tion 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 quadri- 
gemina. Vertigo also is not only a premonitory sign of an epileptic 
attack, but in the epileptic state called petit mal or minor epilepsy it 
is often the only symptom. In persons with atheromatous arteries 
it is very common, and sometimes it is a persistent symptom for 
some days before an apoplectic seizure. It is also present in dis- 
seminated 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. 
A form of vertigo unknown 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 consciousness. 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 otherwise 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 auto-intoxica- 
tion, as in uraemia resulting from renal disease; in cases of profound 
exhausting disease, like typhoid fever or ulcerative endocarditis; 
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 vari- 
ous 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, to ascertain that any head-injuries found to be 
present are not the result of a fall due to the onset of sudden un- 
consciousness, rather than 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 by 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, 
as a rule, are not relaxed, although they may be so in rare cases. 
485 486 
THE MANIFEST A TION OF DISEASE B Y SYMPTOMS. 
The bodily temperature in severe alcoholic poisoning progressively 
falls from 1° to G° 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 cyan- 
otic, and the breathing puffing and stertorous. When the patient is 
awakened he breathes more rapidly, and for this reason the duski- 
ness of the face disappears and the normal hue returns. Death 
never occurs in 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 attendant. While the slow breathing is at first deep, it 
now rapidly becomes shallow, and relaxation is present to the great- 
est 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. 
In view of the frequency with which alcoholic and opium-poison- 
1 The physician must not forget that a fall from alcoholism may result in a cranial fracture. COMA OR UNCONSCIOUSNESS. 
487 
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. Pace 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 impos- 
sible to arouse the patient. 
The coma of uraemia may come on gradually, but most commonly 
its onset is sudden and follows a uraemic convulsion. It possesses 
no diagnostic sign or signs which clearly separate it from the uncon- 
sciousness 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 blad- 
der, 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 and 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 mori- 488 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
bund from 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 preceding 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 
probabilities. The coma of uraemia is not necessarily a fatal symp- 
tom. 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 an 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 respi- 
ratory 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 condition called diabetic dysp- 
noea. 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 addi- 
tion 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- 
unconscious 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 ner- 
vous 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 OR UNCONSCIOUSNESS. 
489 
coma of acute yellow atrophy has in addition these characteristic 
signs, namely, jaundice, bile-stained urine, marked shrinking of the 
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.) 
When coma comes on as the result of pernicious malarial infec- 
tion, it is most apt to be ascribed to sunstroke, uraemia, or apoplexy, 
for its onset is usually sudden. Only a history of exposure to mala- 
rial influences, the presence of slight jaundice and anaemia, and of an 
enlarged spleen will serve to separate it from these conditions, and 
an examination of the blood for the malarial organism may be 
necessary before a positive differentiation can be made, for the diag- 
nosis is by no means easy. 
The coma of apoplexy may be sudden or gradual in its onset; gen- 
erally it rapidly appears after the first symptoms of cerebral hemor- 
rhage 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 nor- 
mal, and, if a fatal result is in prospect, are rhythmically irregular; 
that is, they are now very slow, then gain in speed gradually 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 recovery; but sometimes after several days of apparent convales- 
cence a secondary fatal irritative coma comes on, associated with 
high fever. This is usually of ominous portent and is readily recog- 
nized 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 pro- 
duces the hemorrhage. The following table is designed to separate 
them : 490 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
Acute Alcoholism and Apoplexy. 
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. 
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 re- 
maining motionless. 
6. Respiration stertorous, the lips being in- 
flated 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 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 fol- 
lowing diagnostic symptoms, namely, irritation or paralysis of the 
cranial nerves resulting in strabismus, nystagmus, and lockjaw, stiff- 
ness of the neck, and clonic spasms. If the cavernous 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 
obstructed, the proximal part of the vein collapses. Thrombosis of 
the superior longitudinal sinus causes epistaxis and engorgement of 
the temporal veins. Thrombosis of any of these sinuses, however, 
may be present without these signs. Coma due to subdural hemor- 
rhage (pachymeningitis interna h Hemorrhagica) is peculiar in the fact 
that its onset is usually very slow, and the signs of nervous irrita- 
tion last a long time and are quite violent, often amounting to epi- 
leptic 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 hemiplegia and vomiting may also come on in Raynaud’s 
disease. 
Coma from cerebral abscess is accompanied by symptoms closely COMA OB UNCONSCIOUSNESS. 
491 
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 
usually in the frontal lobes. If there is a history of injury, puru- 
lent otitis, infectious disease involving other parts, such as septicae- 
mia 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. 
The coma of 'purulent leptomeningitis 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 
muscles, combined with the absence of a history of septic absorp- 
tion, may make a differential diagnosis possible. Purulent lepto- 
meningitis 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 mvo- 
sis. The face is often painfully distorted. The presence of an 
epidemic, of course, makes the diagnosis clear. 
It is well to remember that coma may be present from other forms 
of meningitis and arise in several conditions presenting similar 
symptoms, such as pneumonia of the meningeal type, otitic abscess, 
and gastro-enteritis. (See chapter on Headache and Vertigo.) 
Cerebral syphilis may result in the development of coma by pro- 
ducing 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 prob- 
ability of syphilis as a cause very great. Scars on the skin (see 
chapter on Skin) may show specific taint. 492 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
disease, and it often develops very suddenly. 
Heat-stroke produces coma as one of its almost constant symp- 
toms. The history of exposure to heat and the hyperpyrexia are 
the two diagnostic points of importance. (See Fever.) Sudden 
unconsciousness may arise from heart-failure due to disease or 
fright; we 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 
unconsciousness 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 
excitation 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, 
uraemic convulsions, and those convulsions which arise from the 
presence of growths or other sources of irritation in the cerebral 
cortex. Certain poisons may also rarely produce such attacks, 
notably lead and alcohol, and sometimes malingerers imitate very 
successfully the 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 commonly it is sensory, and is as if a cloud or wave was pass- 
ing up the body to the head. As the sensation reaches the head the 
patient may utter the peculiar epileptic cry or sigh, and with this 
sound the patient becomes rigid from momentary tonic 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 con- 
traction which throws the patient’s body from one place to another. 
The primary tonic spasm of the face produces risus sardonicus in 
some cases: the head is often drawn to one side, the eyes commonly 
1 For local spasms or tremors, see chapters dealing with Face and Head, Hands and Arms, 
Feet and Legs. 
493 494 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 wrists, and the fingers bent into the palms of the 
hands with great force. As a rule, the evidences of the powerful 
flexors overcoming the extensor muscles predominate; but some- 
times 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 movements now 
becomes less and less marked; well-developed remissions occur 
between each toss of the body, until the movements cease entirely; 
but it should be constantly borne in mind that the prolongation of 
the remissions does not produce any decrease in the severity of the 
intervening spasm, the final spasm often being even more violent 
than the first. 
The intense discoloration of the face begins to pass away as soon 
as the remissions, by their length, permit the blood to be oxygen- 
ated, its disappearance being temporarily arrested by each parox- 
ysm. Finally, the spasms having ceased, the patient lies before us 
relaxed, unconscious, and exhausted, and passes into a deep sleep or 
coma, which lasts a variable length of time, and from which he 
cannot be aroused, except very rarely, and then with great difficulty. 
When one part of the body is involved in an epileptic paroxysm, 
the rest of it escaping, the condition is one of Jacksonian epilepsy. CONVULSIONS OR GENERAL SPASMS. 
495 
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 
involved. 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. 
Epileptform 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 
involved, 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 epilepsy, 
being produced by the convulsion. In a considerable number of 
cases of epilepsy it will be found that the convulsions succeeded an 496 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
attack of paralysis* which was sudden in onset and possessed the 
characteristics of vascular rupture. In some persons the history of 
this attack is very indistinct, owing to its occurrence in early life; 
while in others the paralysis has been so slight or temporary as not 
to bear any relation in the mind of the 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 atten- 
tion to the fact that the palsy and convulsions are not always due to 
hemorrhage, but to any pathological cerebral change. Heart dis- 
ease, by causing embolism, may bring them on, and rheumatism, 
syphilis, and puerperal sepsis may all produce a softening of the 
cortex, with an epileptic state following the paralysis. 
We 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 hypothesis. Indeed, they tend to overcome many of our pre- 
conceived 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 
possibility of this occurrence. On the other hand, every obstetri- 
cian 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 females; 
but, as has been said, this conclusion is contradicted by the facts. CONVULSIONS OR GENERAL SPASMS. 
497 
Another symptom of great interest is that the paralysis in the infan- 
tile 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 of the cases, but it is not uncommon for the paralysis to 
occur in infancy and the epilepsy to begin at puberty. It would 
seem that cells injured in early life may lie 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 ninety-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 Wallenberg were epileptic after hemiplegia. In another 
series of cases collected by Osier fifteen children out 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 
disease. There can be no doubt that syphilis produces an enormous 
amount of epilepsy in adults, and the presence of epilepsy in a per- 
son in whom the slightest suspicion of a specific taint exists should 
cause him to be instantly placed under antisyphilitic treatment. 
That this is true is evidenced by the statements of the foremost 
neurologists the world has ever known, for we find no less noted a 
writer than Charcot stating that epilepsy is the most frequent mani- 
festation of cerebral syphilis, and the equally eminent syphilog- 
rapher, Fournier, has insisted most strongly on this point, as have 498 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 prsecordial 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 suf- 
fered from pain in the temples, while nine males and seven females 
suffered 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 description 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 rest- 
ing his head on the hands, will either answer slowly and painfully 
in monosyllables, or, gradually raising the face to that of the ques- 
tioner, give an answer, and once more return to his former position. 
These symptoms are not, of course, pathognomonic, but they are CONVULSIONS OB GENERAL SPASMS. 
499 
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, particu- 
larly 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 exam- 
ined, for in many, but not all, cases evidence of brain disease may 
be noted in the eye. This is particularly true of syphilitic epilepsy 
as contrasted with its other forms. 
There is also one symptom which may occur early in syphilitic 
epilepsy, or sometimes only late in the disease, namely, repeated par- 
tial, passing palsies, which while they may be in some cases hyster- 
ical, 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 temporary 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 occur- 
rence of nocturnal attacks; indeed, cases have been reported by 
Charcot and Lagneau in which this was the case, but there are 
similar instances by the score in ordinary idiopathic cases. 
In syphilitic epilpesy there are often well-marked psychical dis- 
turbances with incomplete palsies, which, curiously enough, rarely 
involve the cranial 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 convul- 
sion itself is concerned, it is not possible to separate them. If, how- 
ever, we can obtain any history, the matter becomes much more 500 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
simple. It is characteristic of syphilis to have severe darting or 
aching pains in the tibiae, particularly at night; and it is also char- 
acteristic 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, which is due not 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 paroxysms, 
it will generally yield to specific remedies. Cyanosis is less fre- 
quent and pallor is more common in syphilitic epilepsy than in the 
ordinary disease. CONVULSIONS OR GENERAL SPASMS. 
501 
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 exan- 
them occurs the character of the attack is evident. 
Epileptic convulsive disorders may arise owing to the action of a 
very large number of toxic substances, of which the writer shall 
here consider only a few, as an enumeration of all of them is mani- 
festly impossible. 
Alcoholic epilepsy consists of two distinct varieties produced by 
over-indulgence in intoxicating drinks. In one of these the convul- 
sions are symptomatic of acute poisoning, and come on during a 
drunken orgy or immediately after a single large draught of liquor. 
In the second variety the convulsion does not 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 
accompanied by hallucinations or by dementia or imbecility. In 
the alcoholic convulsion the symptoms may closely resemble those 
of true epilepsy, and not rarely the attack is ushered in by headache, 
gastric embarrassment, disorders of vision, and excessive tremors or 
some similar prodrome which may be looked upon as partaking of 
the nature of an aura. As a general rule, these alcoholic convul- 
sions occur in paroxysms—two, three, four, or more, one after the 
other, at intervals of a few minutes. Hot 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 pro- 
ducing epilepsy very frequently produces a permanent nervous dis- 
order which the withdrawal of the poison will not remove. 
The symptoms of an ursemic convulsion will be spoken of further 
when studying its differential diagnosis in connection with epilepsy. 
As some cases of sudden epileptiform convulsions are apt to result 
in an official investigation as to their cause, and as the character of 
the treatment of the case before death may influence the question of 502 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
life and death for the accused very greatly, it is well for the physi- 
cian to bear in mind that certain drugs when taken in poisonous 
doses produce well-developed epileptiform convulsions. This is par- 
ticularly 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 head- 
ache, is suddenly seized with most violent convulsions, which are 
often fatal, and which during their presence resemble ordinary epi- 
lepsy so closely as not to be separated from it. They end in coma, 
and are separated from each other by intervals of nervousness and 
disquiet. In some cases one convulsion follows the other so rapidly 
that death ensues from exhaustion, but in much more rare instances 
the attacks may resemble Jacksonian epilepsy very closely, and there 
may be no loss of consciousness. If such a condition occur, it is 
almost sure to be followed by a more violent fit. The attacks are 
not preceded by any aura whatever, but previous to the headache, 
already mentioned, the patient may have had amaurosis, and oph- 
thalmoscopic examination of the eyes may show choked disk and 
neuritis of the optic nerve. As a general rule, such cases are fatal, 
but they may recover under careful treatment. 
Malarial epilepsy is an uncommon disorder, even in countries and 
regions which are notoriously malarial, but it has undoubtedly 
occurred, particularly in the southern part of the United States and 
in Brazil. The only cases which the writer can find recorded are 
by American or English observers, namely, Jacobi, Payne, and 
Hamilton. 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, at- 
tended by great preliminary rise of temperature and intense con- 
gestion of the face and head. He was unusually somnolent, and 
in the intervals frequently suffered from facial neuralgia. Change 
of the place of habitation and the use of quinine removed the dis- 
ease entirely. 
The differential diagnosis between idiopathic epilepsy, that which CONVULSIONS OR GENERAL SPASMS. 
503 
is due to demonstrable cause, and the diseases which resemble it, is 
quite possible in many eases. 
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. 
Nevertheless, it is hoped that it will be clear enough to be of ser- 
vice, 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. 
hystericus 
pal pi tat’n 
choking. 
vomiting, 
and dys- 
pepsia. 
and dim- 
ness of 
vision. 
ness. 
defined as 
in epilepsy. 
Onset. 
Sudden. 
Often 
gradual. 
Often 
gradual. 
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. 
No 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- 
Sponta- 
Gradual, 
tion. 
ous. 
duced by 
shock. 
OUS. 
OUS. 
OUS. 
neous. 
with no 
somno- 
lence. 
The very irregularity of true epilepsy makes it extremely difficult 
to give clear and well-defined outlines of it against another disease, 
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. 504 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
epilepsy they are typically at variance with those of daily life, while 
in hysteria they are almost equally typical of ordinary muscular 
contractions, 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 condition known as 
automatic consciousness exists, in which, during the paroxysm, the 
patient understands all that is said, but forgets everything on the 
return to quietness. 
The fact that the patient is a female cannot be regarded as affirma- 
tive evidence of hysteria in the least, but the condition occurring in 
a male may be taken as fairly positive evidence of its being epilepsy; 
and yet it should always be remembered that males may suffer from 
hysterical attacks. 
The movements of the hysterical patient after the tonic condition 
has passed away are as clonic as those of the epileptic, but still pos- 
sess some purposive characteristics, and are not so bizarre as are 
those of the true disease. Thus the head, arms, and legs are struck 
with evident endeavor against the floor or surrounding furniture. 
Another point, which, when it occurs, is very distinctive, is the 
onset, toward the close of an hysterical convulsion, of a second stage 
of tonic spasm, such as occurred at the beginning. It will be remem- 
bered that this does not occur in epilepsy, although it must be borne 
in mind that in cases of the “ status epilepticus ’ ’ the rapid onset of 
another attack may show a second tonic stage. This can be sepa- 
rated, however, by the fact that it is followed by clonic movements, 
whereas the secondary tonic stage of hysteria is usually followed by 
relaxation and temporary recovery. 
In the secondary hysterical tonic contractions emprosthotonus and 
opisthotonus may occur, and are even more rigid in their character CONVULSIONS OR GENERAL SPASMS. 
505 
than they are in the first attack in some cases. Finally, too, in hys- 
teria 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 pain, 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 compara- 
tively rarely seen among Americans, Germans, Belgians, or corre- 
sponding races, but are very frequently observed by French practi- 
tioners 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 diseases, and he repeats 
that all cases are not by any means so well defined. He would also 
remind the reader that the chief difficulty in making a diagnosis lies 
in the fact that frequently it must be made without any previous 
history of the case, as when a patient is brought into a hospital, in 
a fit, for treatment. Where the history is obtainable or where the 
diagnosis can be put off until the case may be studied, the question 
becomes more easily solved. 
If a large number of patients suffering from these hysterical 
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 
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.  THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
506 
Again, the expression of the face in hysteria is, between the attacks, 
often very characteristic, and the surrounding atmosphere of the 
patient seems, even to the inexperienced, to breathe hysteria. Very 
commonly areas of anaesthesia and hyperaesthesia occur in these 
patients, and are of all degrees of intensity and limitation. Search 
for them generally shows their presence after attacks of convulsions, 
but they may exist from one attack to the other, or develop sponta- 
neously. In nearly all cases these areas are unilateral, and may 
extend entirely over one-half of the body, the line of demarcation 
of the anaesthesia or hyperaesthesia from the sound area being clearly 
and 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 sometimes they even 
occur during the attacks. They are always associated 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 Sal- 
: 
True Epilepsy. 
Aura short. 
Cry is violent. 
Spasms first tonic, then clonic, then followed 
by stertor. 
Sometimes after fit of delirium or violent im- 
pulse or mania. 
Mental power is lost. 
No emotional attitudes. 
Hystero-epilepsy. 
Aura extremely prolonged. 
Cry is more moderate and prolonged. 
Ataxic contractions, extension of limbs, turn- 
ing of head, clonic movements, slight stertor. 
Bizarre contractions, no 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- 
tion of the two conditions in frequency of occurrence is, according 
to Gowers, 815 to 185 in every 1000 cases. CONVULSIONS OR GENERAL SPASMS. 
507 
The differentiation of epilepsy from urcemia is much more readily 
made, for there is usually a previous history of symptoms pointing 
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 con- 
ditions 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 vomiting, occasional 
attacks of asthma, and failure of general health is found to be pres- 
ent, the correct diagnosis probably will be uraemia. The preserva- 
tion or loss of consciousness in uraemic convulsions is . variable. 
Generally, if the convulsion is widespread and severe, the intellec- 
tion is lost; but if it be only a slight attack, consciousness may be 
preserved. So long ago as 1840 Dr. Bright described cases of urae- 
mia, on the other hand, in which furious convulsions occurred with- 
out 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 
believed 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 kid- 
ney, albumin may be absent from the urine for long periods of time. 
The specific gravity of the urine should be carefully noted, and in 
very doubtful cases careful estimations of the urea be made. If 
the specific gravity is constantly below 1.010, the kidney will nearly 
always be contracted unless diabetes insipidus exists. Tests of the 
urine passed at different times of the day should always be made. 
Another means of testing the integrity of the kidney is to admin- 
ister iodide of potassium and study its 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 con- 
tracted kidney exists the iodide fails to appear or is excreted only 
in very small quantities. The temperature of the body may also 
be used to differentiate between uraemia and epilepsy. In 1865 
Kien called attention to the fact that even when uraemic convul- 
sions are most violent they are accompanied by a fall of temperature 
of as marked a character as the rise noted in respect to epilepsy. 508 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
believe that uraemia is generally responsible for the nervous disturb- 
ance. If the convulsions are uraemic, the temperature, according 
to the investigators 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 re- 
mains 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 symp- 
toms go. An important and useful point, first discovered by the 
celebrated neurologist, Weir Mitchell, is that, whereas the inhalation 
of amyl nitrite stops true epilepsy, the use of this drug increases the 
severity of an attack of petit mal. 
Alcoholic epilepsy occurring during an attack of mania a potu is, 
of course, easily diagnosed, and the general appearance of the patient, 
combined with his history, suffices to make the physician’s decision. 
The movements are more clonic than tonic, and often are lacking in 
force. There is, however, no constant distinction between the symp- 
toms applicable to all cases. Generally one seizure of alcoholic 
epilepsy follows the other every few minutes until three or four have 
taken place, when the paroxysms cease. It is not to be forgotten 
that alcohol may produce all degrees of epilepsy, from the mildest 
petit mal to the most severe paroxysms, and it is also to be remem- 
bered that hallucinations of terror are very commonly present. CONVULSIONS OR GENERAL SPASMS. 
509 
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 cer- 
tainly lead-poisoning; but its absence is no proof that lead is not 
present. The administration of iodide of potassium also will so 
increase the elimination of the poison as to benefit the case and 
render it more easy to recover lead from the urine. 
The history of exposure to lead in any form is, of course, exceed- 
ingly valuable evidence, but it should not be forgotten that in many 
cases this history is wanting. Thus, the poison may be derived from 
a hair-dye, or cosmetic, or from water which cod tains lead from 
pipes, or from an endless line of similar hidden and obscure sources. 
Amaurosis may be present in some cases, or optic neuritis with 
atrophy may occur. Where double wrist-drop is present the diag- 
nosis is much more easy. 
It is exceedingly important to differentiate between those convul- 
sions which arise from 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 pre- 
sented, 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 
movements nor so sudden iu its onset. It is generally preceded by 
a few days of somnolence, or weeks of gastric disorder and head- 
ache, while lead epilepsy is geuerally sudden or preceded by ceph- 
alalgia by only a few days or hours. Again, examination of the urine 510 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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; and 
it is related by 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, u Poor M—; he is epilep- 
tic !” upon which the assistant, smiling, arose to his feet and con- 
futed 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, and that they remain so; 
whereas in epilepsy they instantly become flexed again. 
Suggestions as to movements are sometimes followed by malin- 
gerers, and the movements generally lack the bizarre character so 
typical of epilepsy. 
If tobacco or ammonia be held to the nose of the fraud, he gen- 
erally 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 alimen- 
tary canal. In these cases they may be reflexly produced. Cer- 
tainly they often arise from the reflex irritation produced by teething 
in children entirely free from rickets and from gastro-intestinal irri- 
tation due to the ingestion of improper foods. Whether adherent 
prepuce and other causes of peripheral irritation ever result in con- 
vulsive seizures is a matter of doubt, some authorities believing CONVULSIONS OB GENERAL SPASMS. 
511 
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 produced. Stevens asserts that insufficiency of the 
ocular muscles very frequently causes epilepsy, and he is not alone 
in this belief. Certainly in cases in which such possible causes of 
nervous excitation exist the physician should remove them as his 
first attempt at treatment. 
There is one variety of infantile convulsive seizure due to menin- 
gitis -which is in itself often tubercular and associated with retrac- 
tion of the head and squint; and another variety in which the 
symptoms very closely resemble those due to actual meningeal 
lesions, but in reality are quite independent of them. This condi- 
tion has been called “ pseudo-meningitis ” or “ hydrocephaloid dis- 
ease,” 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 the last few pages in respect to the symptoms of hys- 
terical convulsions, and finally by the discovery of the hysterical 
stigmata, or the signs manifested by the skin, and, when examination 
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 512 
THE MANIFESTATION OF DISEASE B Y SYMPTOMS. 
comes first, while in strychnine-poisoning it comes last. The con- 
vulsions of tetanus rarely, if ever, completely relax, while those of 
strychnine do have periods of relaxation. There is a different his- 
tory in each case: in one, perhaps, of an injury, as of a nail run 
into the foot; in the other, of a dose of poison having been swal- 
lowed. 
The differential diagnosis between strychnine-poisoning and hys- 
terical convulsions is more difficult. The convulsions are rarely so 
persistently tonic in hysteria as in strychnine-poisoning, and the 
peculiar expression of the hysterical face is often seen in this dis- 
ease. The history of the patient, if obtainable, will throw much 
light on the case and aid very materially in the separation of the 
two conditions. 
AVhen 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, and the lower arm is flexed, while 
the legs are extended and 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 ham- 
mer, contraction 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 a he 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 
symptoms.) 
It is worthy of note that both Trousseau’s and Chvostek’s symp- 
toms are sometimes met with in rhachitic 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 Hands and Arms, accoucheur’s hand.) CONVULSIONS OR GENERAL SPASMS. 
513 
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 gallstone colic, 
and they also sometimes usher in the acute poliomyelitis of childhood 
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-neu- 
roses. There are other localized spasms from nervous disease, such 
as facial spasm and wryneck, 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 probably 
chorea minor. Often the speech is seriously disturbed by reason of 
the choreic movements of the lips and tongue or jaws, and some loss 
of power may be manifest in certain muscles. This true chorea or 
St. Vitus’s dance may affect the whole body or only one arm or leg, 
but generally it is diffused. Commonly it ceases at night when the 
child sleeps, but it often persists day and night, and then becomes a 
serious malady, because of the exhaustion produced. It often fol- 
lows fright, prolonged bad weather, and other causes which may 514 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 disseminated sclerosis, 
progressive muscular atrophy, hysteria, and Friedreich’s ataxia. 
The movements in disseminated sclerosis are, however, fine muscular 
tremors, instead of minor jerking movements; and there are present 
nystagmus and scanning speech in sclerosis, 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 stig- 
mata of hysteria (see chapters on 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 incoordinate movements, and the family his- 
tory of the disease. 
Rarely when there is some paresis with chorea, the patient may 
present symptoms of acute poliomyelitis; but the paralysis iu 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 (“ Park- 
insonian 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 Huntingdon’s chorea. It 
occurs in adults about the age of thirty to forty years. It is hered- 
itary; that is, there is generally a history of the same trouble in the 
ancestors of the patient, and finally as it progresses psychical distur- 
bances ensue. Irregular movements first appear in the hands, which 
movements become markedly iucoordinated, the arms are thrown 
about in excessive and rapid jerkings, and when the infection involves 
the legs a characteristic gait is developed of a dancing or u hop, skip, 
and jump” character. Sometimes, early in the malady, the move- 
ments can be controlled by the will. The face passes through slowly CONVULSIONS OR GENERAL SPASMS. 
515 
formed grimaces, and the gait may be staggering. The speech be- 
comes indistinct, and enunciation is not clear. Finally, dementia 
closes the scene. The movements of Huntingdon’s chorea are not 
sudden as in true chorea; it is a disease of adult life, and mental 
disturbance is a prominent symptom. These facts separate it from 
ordinary chorea. 
When the patient involuntarily bends over in a profound bow the 
cause of his movements may be rhythmical contraction of his abdom- 
inal muscles, producing the so-called salaam convulsions or chorea 
major. 
A still more rare malady is electric chorea or “ Dubini’s disease,” 
in which the muscles of the arm and then the leg on the same side 
are affected with a sudden muscular spasm or shock, such as is pro- 
duced by the electrical current. Wasting of the affected muscles, 
loss of faradic irritability, occasional epileptic convulsions, and rarely 
elevation of temperature come on. The disease is a fatal one, and 
generally occurs in malarial regions in Italy. 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 or 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 
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 516 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 u 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 Huntingdon’s chorea in that voluntary movements with the 
hands may be performed perfectly, and from chorea minor by the 
absence of small incoordinated 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 “ 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. 
HICCOUGH, VOMITING, REGURGITATION, AND THE CHARAC- 
TER OF THE VOMIT. 
Dae to uraemia—Cerebral lesions—Intestinal obstruction—Peritonitis—Cholera— 
Gastric disease—Hepatic disease—Poisonous—The appearance of vomit. 
Hiccough or singultus may or may not possess considerable clin- 
ical significance. Often it arises from slight indigestion. In other 
cases it is produced by the drinking of sparkling wines or waters. 
When hiccough becomes persistent it is a symptom to be re- 
garded with interest, for if it continues for a long period of time 
it is usually significant of hysteria or uraemia, while if it develops 
in a patient exhausted by some prolonged or severe illness it shows 
deep depression of nervous tone, and is itself dangerous because of 
the exhaustion it speedily produces. Sometimes it is said to be an 
annoying symptom after passing catheters or bougies in cases of 
stricture in the urethra. Sometimes hiccough develops in peritonitis, 
and is a most distressing symptom. It is also seen in cases of intes- 
tinal obstruction or when growths are developing. Singultus also 
takes place in some cases of cerebral hemorrhage, in myelitis affecting 
the upper parts of the spinal cord, and in very rare instances because 
of severe mediastino-pericarditis involving the phrenic nerve. It 
also occurs as a result of central nervous irritation in persons suffer- 
ing from advanced anaemia, and in cases of suppurative hepatitis. 
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 the 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 irritation of the centre by some unknown poison, and when apo- 
morphine 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 
abdominal disorders may reflexly produce very persistent emesis, 
517 518 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
and for these reasons vomiting is of considerable diagnostic impor- 
tance. 
As vomiting is produced by many maladies, it is a symptom fre- 
quently met with. It occurs with a certain degree of constancy as 
a complication or symptom of ureemia, diabetes, apoplexy, brain- 
tumor, brain-abscess, Meniere’s disease, tubercular meningitis, hys- 
teria, intestinal obstruction from all its various causes, gastric and 
intestinal indigestion, gastritis, gastric ulcer, gastric cancer, perito- 
nitis, nephritic colic, hepatic jaundice, hepatic colic, in cholera, 
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 con- 
sidered to be suffering from some slight indiscretion in diet. Its 
association either as a preceding, concomitant, or consequent symp- 
tom of convulsions 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 deci- 
sion. No pathognomonic symptom of uraemic vomiting exists unless 
we consider 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. Urae- 
mic vomiting is, therefore, not only due to centric irritation by a 
poision in the blood, but to irritation of the stomach by the urea 
which is excreted into it. Diabetes comparatively rarely produces 
vomiting by the toxaemia which it causes, but in any case the urinary 
examination and polyuria decide the diagnosis. 
When vomiting results from cerebral hemorrhage, embolism, or 
thrombosis, the focal or hemiplegic symptoms characteristic of apo- 
plexy are present. Possibly the vomiting is more indicative of 
hemorrhage than of plugging of the vessel. A sudden attack of 
vomiting in a previously healthy man of advanced years, or in one 
who is young but has a specific history, should raise the question as 
to the possible presence of one of these lesions; provided, of course, VOMITING. 
519 
that ordinary gastric disorder is not present as a cause. The vom- 
iting due to cerebral tumor is generally preceded by the characteristic 
severe and constant headache, vertigo, a slow pulse, impaired mem- 
ory, and sometimes by epileptiform convulsions. Further than this, 
the important diagnostic ocular symptom called “ choked disk” of 
the optic nerve is to be sought for, and if found is of great positive 
value. Tumor of the brain, if near the base, often causes, too, 
involvement of the various cranial nerves. (See chapter on the Eye.) 
The vomiting of cerebral tumor is independent 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 cerebral 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 collec- 
tion may be localized. Vomiting sometimes results from profound 
cerebral anaemia of an acute type due to hemorrhage, in fainting or 
in chronic anaemia, as in chlorosis. Generally, however, the symp- 
tom is only a constant nausea. The presence of great pallor and 
other evidences of anaemia aid in the diagnosis, but it must not be 
forgotten that some severe anaemias are accompanied by febrile 
movement 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, on 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 occip- 
ital type; by the pain in the nape of the neck and in the spine; by 
the rigidity of the dorsal muscles, so that opisthotonus may be caused 
in severe cases; and, finally, by the disordered functions of the 520 
THE MANIFEST A TION OF DISEASE BY SYMPTOMS. 
cranial nerves, as a result of which there are found trouble in the 
oculomotor nerve, strabismus, double or single ptosis, slowly react- 
ing 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 tlm 
very onset of the malady, and is associated with obstinate consti- 
pation, 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 vis- 
cera. In some of these conditions vomiting is of little importance, 
except for its gravity if the patient is exhausted; in other words, it 
is simply a disagreeable symptom. In others the symptom vomit- 
ing is of considerable diagnostic value as indicating the grave mis- 
chief which produces it. One of the most important of the latter 
conditions is intestinal obstruction, whether it arises from intussus- 
ception, constrictions by bands, volvulus, or impactions. In intus- 
susception vomiting is practically a constant symptom, occurring 
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 
obstruction is indicated by the period at which vomiting is devel- 
oped. 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 depend, 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, 
usually placed in the ileo-caecal or umbilical region. After a few 
hours in children, a much longer interval in the adult, the pain VOMITING. 
521 
ceases, often as suddenly as it commenced, and there is an interval 
in which there is little to suggest that the pathological condition still 
continues. This is followed by a return of the pain, the paroxysms 
becoming more violent and prolonged, the intervals less marked as 
the disease progresses, or in the adult, if it passes into the chronic 
form, and intervals even of days may elapse between the parox- 
ysms. The pain is frequently accompanied by tenderness, but this 
is an exceedingly variable symptom, and at times pressure seems to 
relieve the pain. 
Blood-stained mucous evacuations are a symptom of intestinal 
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 devel- 
oped, of blood and mucus, and is usually exceedingly offensive. In 
children diarrhoea is common throughout the whole course of the 
c?ise. At times, following complete constipation and feculent vom- 
iting, there will suddenly appear copious evacuations from the 
bowel, mingled with blood, in which may be found evidences of 
the necrosed intussusception. Where this slough is extensive it 
may be lodged in a lower portion of the bowel and cause fatal 
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 tenesmus, is a patulous condition of 
the anus due to paralysis and dependent upon invagination of the 
descending colon and rectum. This is never produced by invagi- 
nation 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-csecal 
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. 522 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
may appear 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 
symptoms of intestinal stricture constantly manifesting themselves. 
These cases terminate either in cure by reduction or by extrusion of 
a slough, or perish from exhaustion, inanition, or in the course of 
an acute attack. In over one-half of the recorded cases a correct 
diagnosis was not made. 
The additional symptoms 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. VOMITING. 
523 
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 passsages 
representing the contents of the bowel below the seat of obstruction; 
after that the constipation is absolute, not even flatus passing by 
the anus. Treves has suggested that the evacuations sometimes 
observed toward the termination of the case, and not due to the relief 
of obstruction, may be dependent upon the beginning of peritonitis. 
5. Tympanitic distention. Where there is a large segment of 
gut involved in the strangulation its early distention may give rise 
to a localized abdominal enlargement, which is exceedingly 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 symptom 
to locate the obstruction with some certainty. 
The violent peristalsis and repeated vomiting prevent the extreme 
meteorism characteristic of intestinal paralysis. 
6. Localized tenderness and percussion-dulness. When present 
these signs are of exceeding great importance, since they denote the 
position of the strangulated bowel. 
Exceptionally a tumor may be felt, formed by the congested gut 
or the matting together of the intestinal coils. 524 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
The urine is diminished in quantity and may be suppressed. In 
acute strangulation it commonly contains albumin, and it is stated 
that this is of diagnostic value. 
In this connection the history is of great importance. 
Other congenital deformities would suggest the possibility of 
Meckel’s diverticulum as a cause. 
A preceding typhlitis, pelvic peritonitis, or severe abdominal trau- 
matism would respectively assign an adherent vermiform appendix, 
peritoneal bands, or rents in the omentum or mesentery as the causa- 
tive agents in the production of the symptoms. 
The age of the patient should also be considered, since this form of 
obstruction usually occurs between the twentieth and fortieth years. 
The sudden onset of violent, persistent pain, subnormal tempera- 
ture, and frequent pulse, the obstinate, absolute constipation, the per- 
sistent, 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. 
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 the cases 
of obstruction from impaction or obstruction from foreign bodies. 
This underlying cause of the emesis can be diagnosed by the his- 
tory of a foreign body having been swallowed, of attacks of hepatic 
colic, or, where a gallstone 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 
affections. The symptoms of obstruction are frequently only par- VOMITING. 
525 
tial, the vomiting being moderate in amount and not stercoraceous, 
the constipation 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, maiuly 
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, and is often 
a very severe symptom, and is associated with or replaced by a con- 
stant 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 ordi- 
nary 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 diagnosis 
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 symp- 
toms in the neighborhood of the appendix makes the diagnosis 
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 
1 For the test of indican, see chapter qp the Urine. 526 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
disease; and, second, when it takes place as an obstinate and ex- 
hausting 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 diar- 
rhoea 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 indi- 
gestion, 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. No 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. 
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 diseases 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 fermentation, and may have an offensive odor from similar 
causes. Often it contains blood, either in bright-red streaks or as a 
brownish-red fluid, or in similarly colored clots, which may be brown 
when they have been in the stomach for some time. Often the 
exuded blood, changed by mixture with the stomach-contents, looks 
like coffee-grounds, producing “ coffee-ground vomit.” This coffee- 
ground vomit is not pathognomonic of gastric cancer, but is very 
characteristic of this disease. Microscopically the vomited materials 
are seen to consist of particles of food, yeast-cells, cocci, and broken- VOMITING. 
527 
down blood-corpuscles. (For the other symptoms of gastric cancer, 
see chapter on the Abdomen.) 
Coffee-ground vomit is also sometimes seen in cases of locomotor 
© 
ataxia following a gastric crisis. 
Vomiting due to gastric ulcer is preceded by pain, and is gener- 
ally brought on by taking food, and so occurs soon after eating. 
The food is, therefore, only slightly digested, and evidences of fer- 
mentation are absent to a great extent. If blood is present, it is 
nearly always bright red and iu 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 vomit- 
ing by irritating and distending this viscus. The history of vom- 
iting 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 hrema- 
temesis than gastric ulcer and cancer. Thus it occurs from obstruc- 
tion to the portal circulation from hepatic cirrhosis, and from growths 
and splenic affections which result in varicosity of the bloodvessels 
of the stomach. Hsematemesis also follows severe blows, kicks, and 
other injuries to the epigastrium. Sometimes it takes place in cases 
of heart disease in which there has resulted hepatic engorgement 
with secondary gastric congestion, and it may be developed in small 
degree by any form of violent vomiting which strains the stomach, 
particularly if an irritant substance has already destroyed the 
mucous membrane. Again, hsematemesis is seen in scurvy, typhus, 
yellow fever, and acute yellow atrophy of the liver, as a result of 
breaking down or destruction of the coats of the vessels. Some- 
times it is seen in cases of dengue, in influenza of the epidemic type, 
and in relapsing fever. Hsematemesis may also occur in purpura 
hemorrhagica, in hemophilia, and as a result of vicarious menstrua- 
tion. 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- 528 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
lowed by a malingerer. Hsematemesis is to be separated from 
haemoptysis by the fact that in the latter there are physical signs in 
the lungs, the sputum is frothy and bloody, there is absence of retch- 
ing or vomiting-movements, and the blood is bright red in haemop- 
tysis 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, proecordial distress, dyspnoea, and 
faintness are present. The matters vomited are greenish, clear, and 
viscid, and the efforts at vomiting increase the pain. There is no 
jaundice, and death soon comes to the relief of the patient. 
As an early diagnosis of acute pancreatitis may permit surgical 
interference with possible recovery of the patient, the diagnosis is 
important. The mistake commonly made is to consider the case 
one of intestinal obstruction. 
Under the name of melaena neonatorum there is a condition of 
haematemesis 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 Huhn, 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 palce in 
the newborn child small clots may escape from this vessel through 
the ductus arteriosus into the descending aorta and gastric arteries, 
and thus cause an ulcer of the stomach by embolism. 
Vomiting of a peculiar character is always present in phosphorus- 
poisoning. The symptoms associated with ingestion of the poison 
may not come on for some hours. At the end of that time the 
peculiar taste of phosphorus may be noticed in the mouth, the 
breath is heavily laden with its odor, and burning pain in the VOMITING. 
529 
oesophagus, stomach, and abdomen ensues. Vomiting and purging 
now assert themselves, and the matters vomited and those passed 
from the bowels may be luminous in the dark, owing to the pres- 
ence 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 renewed 
vigor. The matters vomited are often the color of “ coffee-grounds/’ 
due to exuded and altered blood. The bowels are absolutely con- 
fined, or the few hard masses passed are white and clay-like, because 
of the absence of biliarv coloring-matter. There is no bile in the 
vomit in this stage, because the hepatic ducts have been closed by 
the inflammation set up in the liver. After this nervous symptoms 
ensue. Muscular twitchings, headache, vertigo, wild delirium, 
erotic convulsions, and finally unconsciousness and death occur. 
Sometimes the convulsions occur just before dissolution. Even if 
the patient survive the acute stage, he generally dies of the changes 
produced in his vital organs, which consist in widespread fatty 
degeneration, even in the acute stages. Atrophy of the liver, de- 
struction 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 sub- 
stances found in it. The most unusual of these is sarco-lactic acid, 
which results from the breaking-down of muscular tissues. Leucin 
and tyrosin are also found, and tube-casts, with fatty globules in 
them, are seen. Free fat-globules may also occur. Bile acids and 
bile coloring-matter are found in large amount, and the urine is gen- 
erally 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. 530 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
The vomiting of acute gastric catarrh is generally seen in chil- 
dren, and is often preceded by great nausea. The contents of the 
stomach are first gotten rid of, then mucus, water, and bile may be 
ejected, and finally exhausting retching ensues if the attack is severe. 
The tongue in such cases is coated and dotted with red spots from 
the enlarged fungiform papillae, and the epigastrium is tender on 
pressure. There may or may not be fever and looseness of the 
bowels. The attack usually follows indiscretions in diet or exposure 
to cold. 
Vomiting from chronic gastric catarrh is usually a condition met 
with in adults, and when seen in the male is most frequently the 
result of a frequent use of alcoholic beverages to excess. In women 
it often develops from excessive tea-drinking associated with errors 
in diet. When due to alcoholism, the vomiting is often present only 
in the morning before or after taking food, and 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. 
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. Examination of the ejecta will generally show food swal- 
lowed 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 epigastrium on pressure, and the displacement 
produced by the palpation often brings on either acid or yeasty eruc- 
tations or even the vomiting 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 
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, nitro- 
gen, hydrogen, and carbonic acid. Sometimes sulphuretted hydro- 
gen is present in large quantity. The reaction of the vomit is 531 
VOMITING. 
almost always acid, lactic and butyric being the acids most com- 
monly 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.) 
Vomiting 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. 
Fig. 200. 
Sarcinae ventriculi, with starch-granules and oil-globules, from vomited matters. 
(Otto Funke.) 
Sarcinse ventriculi are found not only in the frothy, dirty-looking 
vomit of gastric dilatation, but in that of chronic gastric catarrh, 
cancer, and ulcer of the stomach. If iodine or iodide of potassium 
is added to the vomit, the sarcinse become mahogany-red or brown, 
and are easily recognized, occurring in squares which are separated 
by dividing lines. (Fig. 200.) 
Vomiting also arises from neuroses of the stomach in several forms. 
Thus it is frequently seen in hysteria, in neurasthenia, pregnancy, 
and sometimes occurs in the form of what Gee has called “ cyclical 
vomiting.” It also comes on in association with gastric crises in 
locomotor ataxia. The vomiting of hysteria is generally character- 
ized by its persistent character, often lasting for months, and yet the 532 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
patient often maintains her normal weight to a surprising degree, 
either because the food which is taken is only vomited in small 
part or because she surreptitiously obtains food when her attend- 
ants do not know it, which she retains. It is generally associated 
with so many of the hysterical stigmata as to be readily diagnosed. 
The vomiting of neurasthenia is seen in both sexes, and is particu- 
larly apt to follow any nervous muscular exertion. Thus in one 
case of the writer’s even short railroad journeys taken by an over- 
worked man produced attacks of spinal tenderness with vomiting, 
which lasted several days. In some neurotic cases the vomiting 
takes place as soon as the food is swallowed. The vomiting of 
'pregnancy is usually 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 pregnancy 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 Uraemia, in chapter 
on Coma and in chapter on Convulsions.) 
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 resistance 
to treatment. Oftentimes serous diarrhoea is associated with it, and 
these two associated symptoms should not mislead the physician into 
a diagnosis of cholera morbus nor of jaundice, for icterus often 
comes on. 
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 swell- VOMITING. 
533 
ing, or a history of violent hepatic pain (colie), renders the diagnosis 
possible in the case of jaundice. (See chapter on Skin.) Hepatitis 
—that is, hepatic abscess—is often accompanied by or produces 
vomiting 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 accompa- 
nied by a similar train of symptoms also occurs in cases suffering 
from pylephlebitis. 
Violent 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. 
Hsemoglobinoemia is sometimes accompanied by vomiting. The 
attacks are paroxysmal, and are often ushered in by persistent 
yawning, with pain in the limbs, headache, nausea, and vomiting, 
followed 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. 
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 char- 
acteristic symptom of a condition in which the stomach is primarily 
not at fault, namely, in migraine or hemicrania, in which, in addition 
to violent pain in the head on one side, we have hemianopsia, scoto- 
mata, and sometimes great pallor or flushing of the face. (See Pain.) 
In acute yellow atrophy of the liver vomiting is a constant symptom, 
with jaundice, violent headache, and finally convulsions and subcu- 
taneous 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 pigmeutation 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- 534 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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. 
In children suffering from whooping-cough vomiting often takes 
place 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 one 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 
information as to the condition of his patient. 
Under the head of gastric dilatation we have spoken of the sig- 
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 often 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 exceed- 
ingly sour, clear liquid are vomited, we often find 
that the attack is due to migraine or nervous head- 
ache. If watery liquid and mucus are vomited, 
there is probably 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. Somewhat 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 intes- 
tinal obstruction before stercoraceous vomiting comes on. 
Fig. 201. 
Hsemin crystals. VOMITING. 
535 
The significance of bloody vomit has already been described. It 
only remains to name the test for hsemin, 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. 201). 
The vomit of uraemia is often ammoniacal from the decomposed 
urea in it, and that of intestinal obstruction is fecal in odor for obvi- 
ous reasons. If odorous poisons have been taken, the vomit 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. 
Difficulty in swallowing usually arises from hysteria, severe in- 
flammation of the pharynx or oesophagus, stricture of the oesophagus, 
or glosso-labio-pharyngeal paralysis. If it occurs in a neurotic girl 
the possibility of hysteria is to be seriously regarded, whereas if it 
occurs in an adult of advanced years it is more apt to be due to 
stricture or morbid growth of the gullet or in the adjacent parts. 
Not rarely an aneurism produces difficult deglutition by pressure. 
If we believe that the difficulty is due to obstruction, the usual 
method of diagnosis is to pass an oesophageal bougie slowly and 
gently, when if an oesophageal stricture, growth, or diverticulum 
exists the bougie will be arrested before it reaches the stomach. 
Usually pain will be felt at the point where the bougie is stopped. 
Care must be exercised that muscular spasm of the oesophagus does 
not mislead the physician to a diagnosis of stricture, the difference 
between the two states being that in one case the spasm can be grad- 
ually overcome and in the other is persistent. If it be a stricture 
it is usually situated about six inches from the teeth, or where the 
left bronchus crosses the gullet about eight to nine inches from the 
teeth, or at the cardiac orifice, which is seventeen inches from the 
teeth in an adult. If there be a diverticulum the tube may pass 
freely at one time and be arrested at another. When there is a 
growth present some of its surface, if ulcerated, may be brought up 
in the eyelet of a stomach-tube. The physician may also direct the  THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
536 
patient to take one swallow of water after having applied his ear to 
the patient’s epigastrium. If there is no obstruction a gurgling 
sound will take place till the water reaches the cardiac opening. 
Then it will cease as the water is arrested, and after a period of six 
seconds the sound of the water dropping into the stomach may be 
heard. Any delay in these sounds indicates obstruction or paralysis. 
A second swallow will at once precipitate the water, first taken, into 
the stomach. The patient must be warned not to take more than 
one swallow, as if he does so the test fails. 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, aud 
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 pneu- 
monia, before any exudation has taken place; in the early part of 
a paroxysm of asthma; in the early portion of an attack of whoop- 
ing-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, pneu- 
monia, asthma, whooping-cough, and in cases of emphysema with 
bronchiectasis, and in the stage of pulmonary tuberculosis associated 
with the breaking down of lung-tissue, the formation of cavity, and 
the development 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. Suddenly the child begins to give a series of quick, sharp 
coughs, which become more and more rapid until the chest is emp- 
537 538 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
tied of air. In the early stages of the disease this is all that occurs, 
and unimpeded inspiration ensues; but later the cough no sooner 
ceases from exhaustion of the lungs of air than with the attempt of 
deep inspiration the glottis closes spasmodically, and the air is sucked 
through the chink with a whooping sound. The flushed or cyanotic 
face of the child, associated with these paroxysmal attacks, renders 
the diagnosis 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 if the pulmonary inflammation 
also affect the pleura, the cough may be partly smothered or sup- 
pressed 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, en- 
deavors 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 expres- 
sion of pain. Such a cough is always indicative of pain. 
In all forms of dry cough there is nowand 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 bronchi- 
ectasis 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 this 
is followed by freedom from cough for many hours, the case may 
be one of tuberculosis 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 COUGH AND EXPECTORATION. 
539 
of the secretion 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 
resists all ordinary treatment, should lead the physician strongly to 
suspect that one of two ailments is present, namely, undiscovered 
tuberculosis, or, if there is puffiness 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 laryngeal 
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 
pressing 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, laryngeal 
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. 540 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
respiratory 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, in those cases in which it follows getting into bed, it 
is due to chilling of the skin by the cold sheets, which results in 
congestion of the inflamed mucous membrane. 
Quite frequently children suffering from chronically enlarged ton- 
sils suffer from cough on going to sleep, especially if the uvula is 
relaxed or elongated. The cause of this cough is that in the relax- 
ation of sleep the tonsils touch one another or tickle the uvula. As 
soon as the child wakes muscular contraction separates the approxi- 
mating surfaces and the cough soon ceases. 
If this cause of cough cannot be eliminated we must look further 
for its origin. Not infrequently hypertrophy of the mucous mem- 
brane over the turbinated bones, so that it presses on the nasal sep- 
tum, may cause cough, and irritation of the inferior and middle 
turbinated bodies and the septum opposite the inferior turbinated 
body may cause reflex cough. So, too, enlargement of the pharyn- 
geal tonsil may cause this symptom, as may also elongation of the 
uvula. When chronic enlargement of the tonsils, with follicular 
accumulations, is present, cough frequently results. 
Sometimes in hysteria a peculiar barking cough is produced by 
pinching the skin of the neck or elsewhere in the body, and this 
symptom 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 apparatus 
a dry, hacking cough is either nervous or is due to reflex irritation 
in the ear or stomach, or to some hypersesthetic spot in the nasal, 
pharyngeal, or laryngeal mucous membrane; whereas a loose cough 
may arise both in adults and children from congestion and engorge- 
ment of the lingual tonsil. Such a cough is frequent, dry, and 
paroxysmal, and seems to arise from a sticking or pricking sensa- 
tion 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 phar- 
yngitis will be found. The physician should also remember that GOUGH AND EXPECTORATION. 
541 
valvular disease of the heart, by the secondary changes which it 
causes in the lungs, may produce cough, and Sansom states that 
cough was present in 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 paral- 
ysis 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 it 
and the chest-walls to which it is attached, so that when the pressure 
is removed the muscle is too slack to contract. It is heard in 
injuries to the phrenic nerve and to the spinal cord. 
The cessation of cough in advanced phthisis, suffocative bron- 
chitis, or the bronchorrhoea with bronchiectasis of old persons, or in 
severe pneumonia, indicates exhaustion, collapse, or approaching 
unconsciousness, and is a bad sign. 
The Expectoration. 
A careful examination of the materials expectorated by the patient, 
or, in other words, of the sputum, is of the utmost importance in all 
cases of disease of the respiratory tract, whether the abnormal pro- 
cess 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 impor- 
tant. Sputum varies greatly in its general character on ordinary 
examination, sometimes being very fluid and even watery in con- 
sistency, 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 542 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
in the sputum in cases of pneumonia is also a guide to prognosis. 
Thus Sir William Jenner said, “ 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, a gush of nearly pure blood or blood freely mixed 
with ordinary 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; sec- 
ond, by valvular 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 suffering from haemophilia; sixth, from vicarious men- 
struation ; and, seventh, in rare cases of hemorrhagic smallpox. 
Bloody sputum must be separated from bloody vomit due to gas- 
tric hemorrhage arising from ulcer or cancer (see Vomiting). This 
can be done by the cough, by the frothy character of the expectora- 
tion, 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 ruptured vessel 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 cough- 
ing 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 discover whether the materials 
spit up are really tinged with blood, for they may be colored by some 
dye-stuffs or the blood of some animal for the purposes of deception. COUGH AND EXPECTORATION. 
543 
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 u anchovy- 
sauce” sputum. 
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 
upper 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 medias- 
tinal abscess opening into a bronchus, subphrenic abscess, hepatic 
abscess, pronounced bronchiectasis, and 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 expectora- 
tion 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 dis- 
ease or heart-failure, and in some of the pulmonary forms of epi- 
demic 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 tubercu- 
losis. 
The sputum expelled by an asthmatic at the time of the attack 
also has characteristics not so easily seen at a glance, but nevertheless 
demonstrable by the naked eye. Small pearls or plugs of mucus of 544 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 Curschmann’s spirals (Fig. 202), 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. 
Fig. 202. 
Curschmann’s spirals. (Von Noorden.) 
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. 
Sometimes, in cases of diphtheria, casts of the larynx and upper 
bronchial tubes are expelled by coughing. Small casts are also seen GOUGH AND EXPECTORATION. 
545 
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 only visible to the naked eye if placed in water 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 
croupous pneumonia. 
The examination of the 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 exami- 
nation 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 2| 
mm. lumen, and are fitted into the hsematocrit 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 
becomes thin and free from lumps and apparently homogeneous. 
Without 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 hsematocrit frame and revolved for at 
least three minutes, making about fifteen thousand revolutions. The 
solid portions of the sputum collect in the distal extremity of the 
tubes. A small portion of the sediment is placed on a slide and 
examined microscopically for elastic fibres, Charcot-Leyden crystals, 
etc. The sediment from the second tube can be stained for tubercle 
bacilli or other micro-organisms 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 mucous 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 546 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 on 
in the lung, or more rarely in the bronchial tubes. These are usually 
seen in the sputum of advanced or rapidly progressing tuberculosis 
of the lung and in that of abscess and gangrene of the lung. If 
there is doubt as to their presence because they are sparse, we obtain 
them by the following process: boil equal parts of the suspected 
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 in 
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 pecu- 
liar crystals called Charcot-Leyden crystals have already been 
described. 
There are four remaining objects to be seen in the 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 
distoma 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 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 
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 actiuomyces in the sputum. This fungus COUGH AND EXPECTORATION. 
547 
appears as a number of club-shaped projections attached to a hetero- 
geneous mass of irregular-looking material. (Fig. 203.) 
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 distrib- 
uted in every class, in every part of the country, and is so constantly 
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 
Fig. 203. 
Actinomyces. 
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 found 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 movement. 
The quantity of sputum used must not be large enough to extend 548 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 coating. Care must be taken that too 
much heat is not used. Some carbol-fuchsin 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 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 
Fig. 204. 
Tuberculous sputum stained by Gabbett’s method. Tubercle bacilli seen as red rods; 
all else is stained blue. (Abbott.) 
in a 25 per cent, solution of nitric or sulphuric acid in water and 
gently moved about, to decolorize the deposit on the surface of 
the glass. As a result the albumin and cells on the glass are decol- 
orized, but the bacilli are not. The glass is next washed in dilute 
alcohol (60 per cent.) to remove any free fuchsin. Should the decol- 
orization be imperfect, so that the film still has a red color, it must 
be still further decolorized by returning the glass to the acid solu- 
tion and then washed again in the dilute alcohol and water. The 
cover-glass is now placed in a solution of methylene-blue (saturated 
1 Carbol-fuchsin stain, or Ziehl’s solution, is made by dissolving 1 gramme of fuchsin in 10 
c.c. of alcohol, and adding 100 c.c. of a 5 per cent, solution of carbolic acid. GOUGH AND EXPECTORATION. 
549 
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. 
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 
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 in this 
volume to enumerate all kinds of pain, both as to the situation, 
degree, and character. He can only mention those forms which 
possess considerable diagnostic importance. It should always be 
remembered that pain is the sign adopted by nature to notify the 
individual of some abnormal condition in his body, and in many 
instances pain is only developed when the attempt is made to move 
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 aniesthesia. (See chapter on Skin.) 
Almost invariably darting 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 agoniz- 
ing lightning or tearing pains of locomotor ataxia; of pressure upon 
the spinal nerves by spinal disease or in that caused by fractured 
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. 
Throbbing pain is nearly always associated with the presence of 
550 
1 See also chapter on Headache. PAIN. 
551 
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 patho- 
logical 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; dilata- 
tion of the pupil; more or less sweating, particularly on the fore- 
head; 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 pain 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 overdanced 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 from a dis- 
eased ear, so that an examination of any one of these parts may 
reveal the cause of an obstinate neuralgic pain. Similarly we see 552 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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, and 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 
iuvolved. 
A peculiar form of neuralgic pain coming on in attacks or parox- 
ysms 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 a rheumatic taint, and this last-named con- 
dition arises from the rheumatic diathesis, care in making a differ- 
ential diagnosis is necessary. 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 exposure 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 PAIN. 
553 
cerebral abscess from neuralgia of the head. The pain of such a 
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, ver- 
tigo, 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. 
Brushing the hair may be impossible, because of the pain produced 
by the brush touching the scalp. Occipital neuralgia is oftentimes 
bilateral. It may simply arise from cold or injury; but, if persist- 
ent and severe, caries of the cervical vertebra should be sought for 
as a possible cause. 
Pain of a neuralgic or darting 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 of the 
heart from the accumulation of flatus in the transverse colon just 
as it turns to descend. Many patients who come to the physician 
complaining of heart disease only suffer from this condition, due to 
fermentation in the large bowel. 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 
column. These are sometimes called the “ spots of Valleix.” In 
other cases the pain will be due to spinal trouble, ansemia, or the 
tight lacing of corsets. 3. To pseudo-angina. 4. To true angina 
pectoris. 5. To locomotor ataxia. 
Pain of a character somewhat resembling true angina pectoris is 554 
THE MANIFESTATION OF DISEASE BY SYMPTOMS 
also sometimes met with in patients who have that rare disease, 
acute aortitis. The pain is constant under the sternum, but it has 
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 and 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 ansemic, 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 and 
corded, atheromatous, and the blood-pressure high. The additional 
diagnostic points in favor of true angina pectoris are that the prin- 
cipal 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 felt in the prae- 
cordium, but commonly in the axilla, and 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 PAIN. 
555 
in the prsecordium. 4. A morbid growth in the chest, particularly 
a mediastinal tumor or enlarged bronchial glands. 
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, and 
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. Pericar- 
ditis 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 
suspect 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 press- 
ure 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 grad- 
ually 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 556 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
grave reason for suspecting hip-disease. If it is not sciatic neural- 
gia, it is due 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 ago- 
nizing at times, even if the patient remains absolutely quiet and does 
not move the limb. The following points will, when pressed on, 
increase 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, injury 
to the nerve, rheumatic tendencies, and a persistency and tendency 
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 erup- 
tions 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 aud Feet and Legs.) Again, in sciatic neu- 
ritis, if the leg be extended, and then while in extension flexed at the 
hip till it is at a right angle with the trunk, pain will be felt at the 
sciatic notch. When the pain is a pure neuralgia, which is rare, it 
will not be increased by moving the limb, there is little or no ten- 
derness 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, which is 
the reverse of all other nerve pains of like character, and far more 
usual in middle or advanced 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, the presence of lumbar abscess or of diabetes mellitus. 
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 sci- 
atica. 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 PAIN 
557 
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.) 
It should also be remembered that malingerers, particularly sol- 
diers 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 gastralgia, and the paroxysms may be very sud- 
den in onset. In other instances the pain is in the epigastrium or 
hypogastrium, and is associated with so much tenderness on light 
pressure 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 forgotten in the diagnosis of a case, namely, locomotor ataxia 
manifested in gastric crises, lead-poisoning shown by a neuralgia 
due to a neuritis, 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 558 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
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 
radiate down into the right hypochondriac region, and Ralfe says 
into the renal region. Again, pain in this part may be due to aneu- 
rism of the aorta or of the mesenteric artery. Further, the accu- 
mulation 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. Some- 
times a 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 
rapidity, and fever of an irregular type is more often seen than in 
the renal form. The pains just described are so severe and charac- 
teristic 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 vio- 
lent belly pain is due to aneurism. If the pain be due to chronic 
lead-poisoning, 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 impac- 
tion, 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 intestinal obstruction, the pain has no characteristic seat in 
any part of the abdomen, as a rule; but the general symptoms of PAIN. 
559 
this condition 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. 
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 
Mode of 
Character of pain. 
Seat of pain. 
Tenderness and 
Disease. 
onset. 
In kind. 
In inten- 
sity. 
pressure. 
Acute intestinal 
obstruction: 
a. Strangula- 
tion due to 
bands. 
Very sud- 
den. 
More or less 
continuous. 
Most in- 
tense, 
agonizing. 
Epigastric or um- 
bilical region. 
Pressure at first re- 
lieves, afterward 
aggravates. 
b. Acute intus- 
susception. 
Sudden 
to very 
sudden. 
Paroxysmal. 
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- 
den, gra- 
dual. 
Paroxysmal 
later. 
Moderate. 
Often near seat of 
obstruction. 
Tenderness over 
obstruction. 
Appendicitis. 
Very sud- 
den. 
Quite con- 
tinuous. 
Agonizing. 
At first periumbili- 
cal, later about 
appendix. 
Greatest over ap- 
pendix or in left 
groin. 
Acute peritonitis. 
Very sud- 
den. 
Continuous. 
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 
or 
gradual. 
Paroxysmal. 
Varies in 
severity. 
Varies in position. 
Relieved by press- 
ure. 
Pain in the abdomen of the darting neuralgic type, other than 
that due to gallstones, renal calculi, ordinary gastralgia, lead- 
poisoning, enteralgia, or malignant growth, may be due to locomotor 
ataxia. This should never be forgotten, and the fact that the patient 
1 Andrew’s table, slightly modified.  the MANIFEST A TION OF DISEASE BY SYMPTOMS. 
560 
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 signs 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. Some- 
times 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. 
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, the exquisitely tender ab- 
dominal 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 gall- 
stone colic, renal colic, and perforation of the bowel by neuralgia, 
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 dysmenorrlioea 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 ou 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 gas- 
tric, 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 PAIN. 
561 
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 
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, at other times 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 per- 
ceptive 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- 562 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
pox, of epidemic influeuza, 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 breakbone 
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 
devoted to the Legs and Feet and the Anns 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 tap- 
ping 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 diagnosis to enter into 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 
563 564 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
music. On the other hand, enervating weather, loss of sleep, hun- 
ger, 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 sitting 
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 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 only need the discovery 
of this symptom to confirm the diagnosis. The nervous conditions 
in which we find the reflexes decreased or lost, taking the patella 
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, immedi- 
ately after an attack; and chorea. We also find 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 
locomotor ataxia, but any lesion involving the posterior columns of 
the cord or the posterior nerve-roots in the second, third, or fourth 
lumbar segment will produce the same results. Therefore, loss of 
knee-jerk is symptomatic of transverse myelitis of this region as TENDON-REFLEXES AND MUSCLE-TONE. 
565 
well as of ataxia. Again, if the motor tract of the cord at these 
levels is 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 path- 
way from the periphery to the cord, and from the cord to the mus- 
cles, also causes loss of knee-jerk. 
If the cause of loss of knee-jerk be locomotor ataxia, we will 
probably find in addition to this symptom some difficulty in walk- 
ing, 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, 
laryngeal 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 566 
THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
recovery from first shock; pressure on spinal cord above the reflex 
arc; hereditary 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 diag- 
nosis clear unless the attack be one of the apoplectiform attacks of 
disseminated sclerosis, in which case there will be present a history 
of the intention-tremor, nystagmus, and the syllabic speech, so that 
though the knee-jerk is exaggerated in both diseases the diagnosis 
can be readily made. In the cerebral palsy of childhood the age of 
the patient, the contractures and gait, with the history, decide the 
diagnosis. In lateral sclerosis the spastic rigidity, excessive exag- 
geration of the knee-jerks, absence of sensory disturbances, and 
ocular symptoms, all render the diagnosis possible. Similar exag- 
geration is also seen in amyotrophic lateral sclerosis, in which dis- 
ease there is wasting of the muscles, particularly of the hand. In 
both these ailments the exaggeration of the knee-jerk is due to dis- 
ease of the lateral pyramidal tracts, which block the inhibitory 
fibres from the higher centres. For similar reasons we find exag- 
gerated knee-jerk in ataxic paraplegia. 
In hysterical paraplegia the age and sex of the patient, the pecu- 
liar facies, the areas of anaesthesia and hvperaesthesia, 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-jerks 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 567, from Taylor’s 
Index of Medicine, shows the area of skin-reflexes very well. 
In glosso-labio-pharyngeal paralysis the reflexes of the tongue 
and throat are lost and those of the face sometimes increased; in 
progressive muscular atrophy the reflexes of the arms are lost, while 
those of the legs are preserved, and in 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. 
567 
nated sclerosis, and in amyotrophic lateral sclerosis. A false clonus 
is sometimes seen in hysteria. 
A Table of the Beflexes. 
Reflex. 
Point of stimulation. 
Situation of centre. 
Significance. 
1. Plantar, 
Irritating skin of soles. 
Extreme end of cord. 
Usual in health. 
2. Gluteal, 
Irritating skin of but- 
tocks. 
Origin of 4th and 5th 
lumbar nerves. 
Rare in health. 
3. Cremasteric, 
Irritating skin of inner 
side of thighs. 
Origin of 1st and 2d lum- 
bar 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 dor- 
sal nerves. 
Frequently absent. 
5. Epigastric, 
Irritating skin of chest 
in 5th and 6th spaces. 
Origin of 4th to 6th dor- 
sal nerves. 
May be absent in health. 
6. Erector spinse, 
Irritating skin from sca- 
pula to crest of ilium. 
Origin of all the dorsal 
nerves. 
Rare in health; frequent 
in wasting disease. 
7. Interscapular, 
Irritating skin between 
scapulae. 
Origin of 6th cervical to 
3d dorsal. 
Rare in health. 
8. Palmar, 
Palms of hands. 
Cervical bulb. 
Only in infants. 
9. Cranial: 
Conjunctival, 
Sclerotic, or inner sur- 
face of eyelid. 
Medulla. 
Absent in disease of 5th 
nerve only. 
Iris (to light), 
Pupil. 
Anterior portion of ocu- 
lomotor nucleus. 
Absent in disease only. 
Palate, 
Soft palate and uvula. 
Medulla. 
Absent in disease only. 
Nasal (sneez- 
ing), 
Naso-respiratory pas- 
sages. 
Medulla. 
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 
convey 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 pulmonary 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 condition are absent and the patient has none of the 
signs of tuberculosis, we should examine the larynx for a papillo- 
matous growth. Again, if hoarseness or a whispering voice is mani- 
fested by a male of adult years, who is also suffering from dyspnoea, 
unilateral flushing or sweating of the face and neck, and unequal, 
rapid radial pulses, we should suspect aortic aneurism or a medias- 
tinal tumor which is pressing on his recurrent laryngeal nerve. 
There are also other causes of hoarseness due to nervous lesions 
arising from the long and tortuous course of the nerves supplying 
it. These have been well grouped together by Felix Semon in the 
following table. It is interesting to note that in suspected cases 
of disease of the parts herein named it is well to make a laryngeal 
examination, since this may reveal a paralyzed cord, although the 
voice has not indicated such a condition, because by great retraction 
of the opposite cord the laryngeal opening is kept patulous and 
phonation is possible. 
568 SPEECH. 
569 
Table Showing the Possible Causes of Laryngeal Paralysis. 
I. Bulbar and Bulbo-spinal Affections. 
1. Hemorrhage and softening. 
2. Syphilitic processes. 
3. Tumors. 
4. Diphtheria. 
5. Progressive bulbar paralysis. 
6. That curious form of systemic central 
nervous disease first described by Hughlings 
Jackson and Morell Mackenzie, in which one- 
half of the tongue, the corresponding half of 
the palate, the corresponding vocal cord, 
and, in a number of cases, the corresponding 
trapezius and sterno mastoid muscles are 
affected. 
7. Amyotrophic lateral sclerosis. 
8. Disseminated cerebro-spinal sclerosis. 
9. Syringomyelia. 
10. Tabes dorsalis. 
II. Peripheral Affections. 
1. Acute rheumatic influences. 
2. Catarrhal neuritis. 
3. Toxic influences (lead, arsenic, etc.). 
4. Tumors in the posterior cavity of the 
skull or in the foramen lacerum or foramen 
jugulare. 
5. Pachymeningitis. 
6. Traumatism (unintentional ligature of 
nerves, injection of iodine into a goitre, cut 
throat, stabbing, injury during extirpation of 
goitre, etc.). 
7. Tumors of neck (goitre, peritracheal 
glands, etc.). 
8. Aneurisms of the arch of the aorta, In- 
nominate, subclavian, carotid. 
9. Mediastinal tumors (malignant, tubercu- 
lous, calcification of bronchial glands, etc.). 
10. Pericarditis. 
11. Pleurisy. 
12. Tuberculosis and pleuritic thickening ot 
apex of right lung. 
13. Chronic pulmonary affections (chronic 
pneumonia, anthracosis, etc.). 
14. Infectious fevers (typhoid, etc.). 
15. (Esophageal carcinoma. 
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 recov- 
ery is often as sudden and unsuspected as the onset. As a rule, 
the tongue, lips, and jaws are unimpaired in their functions. Some- 
times, however, these parts are affected by hysterical spasm. Often 
there will be hysterical ansesthesia with the mutism. Usually there 
is no evidence of cerebral lesion in such cases in the sense of impair- 
ment of intellect. 
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. 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 pnlmonary com- 
plaint, which renders his breath short, so that he hurries through  THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
570 
his sentence in order to be able to breathe freely again. Thus, in 
cases of pneumonia or of pulmonary oedema this hurried speecli is 
a very constant sign. 
Again, in cases of typhoid fever, when the tongue is dry and 
immobile from accumulated sordes, a mumbling character of the 
speech is present, even if the brain is entirely clear, and in severe 
stomatitis 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 con- 
dition in which a slow, scanning speech is of great diagnostic 
importance is in that rare disease, Friedreich’s ataxia; but the facts 
that this disease begins in childhood, that several members of the 
family are apt to be affected, that there are ataxic symptoms and 
early talipes equinus, render it easy to separate this affection from 
insular sclerosis. (See Paraplegia, in chapter on Feet and Legs.) 
A hesitating, halting speech associated with Argyll-Robertson 
pupils, unequal pupils, delusions of grandeur, and tremor of the 
tongue, which last symptom may be so marked as to cause the 
speech to be indistinct and blurred, is indicative of paretic 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 suf- 
fering from this disease. 
A very indistinct speech of a mumbling character, great difficulty 
being experienced in the pronouncing of dental and lingual sounds, 
and perhaps associated with feebleness of the voice, if the larynx is 
involved, is seen in cases of glosso-labio-pharyngeal paralysis. If 
the cause of the defective speech be this disease there will be found, 
as associated symptoms, wasting of the tongue, lingual tremors, some 
dribbling of saliva from the mouth, and immobility of the lips, the 
face about the mouth being expressionless. 
Somewhat similar symptoms due to paralysis of the lips, with 
escape of the tongue and pharynx, at least for a long time after SPEECH. 
571 
labial paralysis develops, are 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 a rapid volley of words, is 
sometimes seen in paralysis agitans. 
By far the most interesting speech-defect is that called aphasia. 
It is divided into motor aphasia and sensory aphasia. 
Before studying these conditions we must discuss the nervous 
mechanism of speech. When a child learns to talk it performs a 
purely imitative act. Its auditory nerve conveys the 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 howto 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 hemi- 
sphere 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 mem- 
ory of how to say certain words, and the lesion is in the third left 
frontal (Broca’s) convolution. He can read to himself, because he 
has not forgotten the meaning of the words, and for this reason he 
understands what is said to him, and may be able to repeat a word 
immediately after you have said it by a purely imitative process. 
Generally we find with aphasia a condition called agraphia, in which 
the patient cannot write voluntarily, but can copy perfectly. In the 
great majority of cases of aphasia, however, the patient is paralyzed 
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  THE MANIFESTATION OF DISEASE BY SYMPTOMS. 
572 
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 and 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 advantage: 
1. The power to recognize objects seen, heard, felt, tasted, smelt, 
and their uses. 
2. The power to recall the spoken names of objects seen, heard, 
felt, tasted, and smelt. 
3. The power to understand sounds other than speech. 
4. The power to understand speech and music. 
5. The power to call to mind objects named and point them out 
at request. 
6. If word-deaf, can he recognize his own name when it is spoken ? 
7. The power to recognize a word spelled aloud. 
8. The power to call up mentally the sound of a note, figure, 
letter, or word. 
The examination thus far will test the various sensory areas, but 
more especially the auditory and the association tracts between the 
different sensory areas connected with speech. SPEECH. 
573 
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. 
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 cor- 
tical exhaustion without the development of hemorrhage, embolus, 
or thrombus. The prognosis is favorable. INDEX. 
A BADIE’S sign, 46 
£1. Abdomen, 328 
causes of distention of, 330 
of localized bulging of wall 
of, 335 
of pain in, 557, 559 
of protrusion of wall of, 330 
of retraction of wall of, 330 
of swelling in epigastrium, 
3o6 
frog-belly, 330 
inequality in shape of, due to me- 
teorism in intussusception, 522 
inspection of, 329 
palpation of, 338 
regions of, 328 
scaphoid, 330 
tumors of, 345 
Abscess, cerebral, choked disk not gen- 
erally present in, 198, 519 
character of pain in, 553 
coma in, 490 
diagnosis of, 519 
fever in, 519 
gangrene in, 231 
symptoms of, 477, 490 
tache cerebrale, a sign of, 216 
vomiting in, 519 
hepatic, brick-dust sputum in, if 
communicating with the lung, 
543 
character of fever in, 458 
of pain in, 560 
dysentery a cause of, 458 
sweating in, 458 
symptoms and signs of pyaemic, 
351 
of tropical, 351 
vomiting in, 533 
lumbar, sciatic pain in, 556 
mastoid, oedema back of the ear in, 
239 
mediastinal, purulent sputum in, 543 
perinephritic, bulging of flank in, 
348 
pulmonary, chronic morning cough 
in, 538 
copious and purulent sputum in, 
302, 543 
diagnosis between mediastinal 
growths and, 311 
Abscess, pulmonary, elastic fibres in spu- 
tum of, 546 
following amoebic dysentery, an- 
chovy-sauce sputum in, 543 
history, signs, and symptoms of, 
302 
pyo-pneumothorax subphrenicus,346 
retro-oesophageal. See Retro-oesopha- 
geal abscess. 
subphrenic, purulent sputum in, 543 
“Accoucheur’s hand” in tetany, 72 
Acne due to bromine or iodine, 224 
due to iron, 224 
due to working in paraffin, 225 
of forehead, purulent, in syphilis, 
227 
Acromegaly, enlargement of feet in, 117 
of tongue in, 155 
face of, 35 
head in, 50 
spade-like hand in, 65 
Acroparsesthesia, 264 
diagnosis of, 264 
Actinomycosis, actinomyces in sputum 
of, 546 
enlargement of tongue in, 155 
Acuity of vision, changes in, 188 
Acute yellow atrophy of the liver. See 
Yellow atrophy of the liver, acute. 
Addison’s disease, appearance of tongue 
in, 150 
coma in, 492 
heart in, 326 
pigmentation of buccal mucous 
membrane in, 163, 326 
of skin in, 210, 326 
symptoms of, 211, 533 
vomiting in, 533 
iEgophony over pleural effusions, 298 
i'Esthesiometer, 242 
Agraphia, 571 
location of lesion in, 572 
Ainhuin, 130 
Albuminuria, anaemic, 414 
boiling-test for, 413 
cyclic, 414 
due to renal congestion, 414 
Heller’s test for, 414 
indicative of renal disease, 414 
marked, or absent, in amyloid kid- 
ney, 427 
575 576 
INDEX. 
Albuminuria, quantitative test for, by 
centrifuge, 414 
transient, in chronic interstitial ne- 
phritis, 427 
Albumosuria, Harris’s test for, 418 
in normal puerperium, 420 
said to be due to the action of micro- 
organisms, 420 
significance of, 420 
Alcoholism, convulsions due to, 501, 503, 
508 
hyperesthesia in chronic, 267 
morning vomiting in, 530 
symptoms of acute, 490 
Alexia, 572 
location of lesion of, 572 
Alkaptonuria, 418 
Allochiria in hysteria, 264 
in multiple sclerosis, 264 
in myelitis, 264 
in paralysis agitans, 264 
in tabes dorsalis, 264 
Amaurosis, 200 
significance of, in brain fever, 475 
Amblyopia, 198 
Amoeba coli, 435 
Amphoric breathing, rarely heard in 
pneumothorax, 294 
in small cavity, 294 
Amyloid disease of kidney, 427 
hyaline, fatty, and granular 
casts in urine in, 427 
syphilis, prolonged suppu- 
ration, and extensive bone 
disease accompanying, 
427 
urine in, 427 
of liver, enlargement and 
smoothness of liver in, 
351, 352 
history of prolonged sup- 
puration elsewhere in, 
352 
jaundice occurring in, 205 
Anaemia, albuminuria in, 414 
appearance of nails in, 56 
of tongue in, 150 
bothriocephalus latus a cause of, 442 
cerebral, choked disk in, 519 
vertigo in, 484 
vomiting in profound, 519 
dropsy of feet and legs in, 237 
headache in, 483 
liyperaesthesia in, 267 
in acute diffuse nephritis, 426 
in anchylostomum duodenale, 376, 
442 
in atrophy of gastric tubules, 374 
in bleeding hemorrhoids, 374 
in cancer, 376 
in chronic indigestion, 374 
lead- or arsenic-poisoning, 376 
Anaemia in convalescence from infectious 
disease, 374 
in gastric ulcer, 376 
in hemorrhage, 374 
in malaria, 376 
in renal disease, 376 
in sarcoma, 376 
in tapeworm, 376 
in tuberculosis, 376 
in uraemic poisoning, 376 
oedema in, 237 
pallor of conjunctiva in, 164 
papillitis in, 198 
pernicious, cardiac palpitation in, 
375 
change in red blood corpuscles 
in, 375 
chills followed by fever in, 459 
gradually increasing dyspnoea 
in, 375 
indicanuria in, 401 
jaundice in, 207 
marked pallor without loss of 
flesh in, 375 
pulsating cervical vessels in, 276 
venous murmurs in, 375 
vertigo in, 375 
purpuric eruptions in, 215 
Anaesthesia, 245 
bilateral, in Friedreich’s ataxia, 251 
in hemorrhage of the cord, 253 
in hysteria, 250 
in injuries of the cord, 250 
in lesions of the pons, 251 
in locomotor ataxia, 251 
in meningitis, spinal, 250 
in myelitis, 251 
in spinal disease, 250 
in syringomyelia, 253 
never in cerebral lesions, 250 
causes of, 245 
crossed, in lesions of one side of the 
cord, 249 
of peduncle, 249 
of pons, 249 
differential diagnosis in facial, 262 
distribution of, in special nerve in- 
volvement, 259 
dolorosa, in cancer of spine, 253 
gauntlet or stocking form of, in hys- 
teria, 248 
in 50 per cent, of neuritis due to 
diphtheria, 258 
location of lesion of, in the spinal 
cord, 254 
of body and legs in locomotor ataxia, 
251 
of Friedreich’s ataxia, 251 
of myelitis, 251 
of toxic peripheral neuritis, 258 
patches of, in leprosy, 263 
in syringomyelia, 253, 263 INDEX. 
577 
Anaesthesia, reflexes preserved in cere- j 
bral, 249 
signs of, due to neuritis, 257 
unilateral, 248 
varieties of, 245 
zones of, 254 
Analgesia in locomotor ataxia, 251 
in Morvan’s disease, 69 
Anasarca, general. See General ana- 
sarca. 
Anatomy of brain, 131 
of optic nerve, 188 
of sensory tracts, 242, 254 
of tongue, 145 
Anchylostomum duodenale, anaemia due 
to, 376, 442 
Aneurism, aortic, blood-streaked sputum 
due to leakage from aorta in, 
• 542 
bulging of chest in, 273 
dilatation of pupil in, 186 
haemoptysis in, 542 
pain in, 318, 554 
appearance of hands in, 55 
brassy cough due to pressure on 
larynx by, 318, 539 
bruit in, 316, 318 
dyspnoea or dysphagia in, 159, 319 
enlarged cervical vessels in, 276 
hemorrhagic pleural effusion in, 307 
history of syphilis in, 317 
hoarseness of voice due to pressure 
on recurrent laryngeal nerve by, 
317, 568 
intracranial, headache due to, 483 
laryngeal spasm due to pressure on 
recurrent laryngeal nerve by, 310 
loss of pulsation in peripheral ves- 
sels in, 319 
oedema of upper extremities in, 238 
of abdominal aorta, 346 
pain in abdominal, 558 
pressure on bile-duct causing jaun- 
dice in, 205 
sweating of side of head in, 235 
symptoms of, 316 
tracheal tugging in, 319 
Angina pectoris, causes of, 357 
character and position of pain 
in, 554 
symptoms of, 554 
Angioneurotic oedema, appearance of 
hands in, 64 
of skin in, 240 
Ankle-clonus, how best elicited, 564 
in amyotrophic lateral sclerosis, 566 
in ataxic paraplegia, 94 
in hysteria, 567 
in lateral sclerosis, 566 
most marked in disseminated scle- 
rosis, 566 
Annulus migrans, 154 
Annulus senilis, 165 
Anthrax maligna, anthrax bacilli found 
as cause of, 465 
character of fever in, 465 
symptoms of, 230, 465 
simplex. See Carbuncle. 
Antidiphtheritic serum, roseola due to 
injection of, 220 
Aorta, aneurism of abdominal, 346 
of descending, symptoms of, 319 
of greater curvature of ascending, 
symptoms of, 318 
of transverse portion of arch of, 
symptoms of, 319 
Aortic valvular disease, 319 
Aortitis, acute, causes of, 554 
character of pain in, 553 
Apex-heat, 281 
Aphasia due to hsematoma near island of 
Keil, 141 
due to hemorrhage into island of 
Eeil, 141 
Aphonia in hysteria, 568 
Aphthongia, spasm of tongue in, 157 
Apoplexy, albuminuria in, 420 
Cheyne-Stokes breathing in, 278, 
489 
coma in, 489 
conjugate lateral paralysis of ocular 
muscles in, 181 
contractions following, 71 
diagnosis between coma of, and alco- 
holism, 489 
ingravescent, 140 
involuntary passage of urine in, 392 
knee-jerk exaggerated some time 
after shock, 566 
increased immediately after 
shock, 564 
paralytic chorea following stroke of, 
73 
skin-reflexes lost when deep reflexes 
exaggerated, 566 
vertigo before, 484 
Appendicitis, character of fever in, 466 
of vomiting in, 525 
leucocytosis in, 378 
pain in, 560 
Appetite, wayward, in chlorosis, 375 
Apraxia, 572 
location of lesion in, 572 
Arcus senilis, 165, 326 
Argyll-Robertson pupil, 89, 185 
not present in ataxic paraplegia, 
94 _ 
in Friedreich’s ataxia, 
91 
present in diabetes mellitus 
rarely, 89, 186 
in true ataxia, 185 
Argyria, 209, 211 
Arms, movements of, 70 578 
INDEX. 
Arms, spastic rigidity of, an early sign of 
tremors of, 76 
Arrested development, 100 
cerebral spastic paraplegia in, 
100 
Arterial tension, 357 
causes of high, 357 
of low, 358 
high in acute diffuse nephritis, 
427 
Arteritis, symptoms of syphilitic, 476 
Arthritic muscular atrophy, 122 
Arthritis deformans, distortion of fingers 
in, 58 
enlargement of joints in, 125 
formation of osteophytes in, 125 
knee-jerk increased in, 565 
seal-fin hand of, 61 
gonorrhoeal, 126 
septic, appearance of hands in, 64 
Arthropathies, 124 
Ascaris lumbricoides, 442 
Ascites, apex-beat raised in, 281 
caput medusae in hepatic cirrhosis 
causing, 335 
causes of, 331 
diagnosis of, 331 
examination of withdrawn fluid in, 
332 
rapid respiration in, 277 
skin of abdomen in, 234 
Asthenic bulbar paralysis. See Paralysis, 
asthenic bulbar. 
Asthma, catarrhal pneumonia following, 
309 
character of rales in, 308 
due to cardiac lesions, 309 
due to gastric disorders, 309 
due to reflex nasal irritation, 309 
due to renal disease, 309 
erect position in, 308 
expiration prolonged in, 278, 309 
physical signs and symptoms of, 
308 
rapid respiration in, 276 
sputum of, Charcot-Leyden crystals 
in, 309, 544 
Curschmann’s spirals in, 309 
pearls of mucus in, 544 
Asymmetry, facial, 33 
Ataxia, differential diagnosis of, 93 
Friedreich’s. See Friedreich’s ataxia, 
hereditary cerebellar, 92 
spinal. See Friedreich’s ataxia, 
locomotor. See Locomotor ataxia. 
Atheroma, headache in, 473 
in chronic interstitial nephritis, 427 
in old age, 357 
in syphilis, 357 
symptoms of, 357 
Athetosis, 79, 
reflexes increased in, 566 
Atrophy, acute yellow, of the liver, coma 
in, 488 
jaundice in, 207 
bilateral, of tongue, causes of, 154 
facio-humero-scapular type of, 30 
idiopathic muscular, ptosis in, 41 
of gastric tubules, anaemia in, 374 
of nails, 56 
optic, 198 
progressive muscular, 67 
Aran-Duchenne tvpeof, 120 
claw-hand in, 67 
condition of reflexes in, 564 
excessive sweating of hand 
in, 57 
fibrillary twitch in, 79 
leg symptoms of, 118 
-type of, 118 
peroneal leg-type of, 120 
Aura, 493 
Auto-intoxication, headache in, 471 
poisons causing, 471 
symptoms of, 471 
BACCELLI’S sign, 298 
Bacilli, anthrax, 465 
in preputial smegma, 411 
in stools in cholera, 432 
in tubercular pyelitis, 428 
of Eberth, in stools of typhoid 
fever, 449 
tubercle, in urine, 411 
in sputum, methods of exam- 
ining for, 547 
Bedsores in acute transverse miyelits, 232 
in hemiplegia, 233 
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, 74 
Beri-beri, general anasarca in, 237 
Biceps tendon reflex, how developed, 564 
Bilateral anaesthesia, 250 
facial paralysis, 44 
ptosis, 41 
Bilious remittent fever. See Malaria, 
remittent. 
Biliousness, appearance of tongue in, 147 
Bladder, causes of incontinence of urine 
in the, 390 
of retention of urine in the, 389 
character of blood in urine from the, 
396 
nervous, 393 
paralysis of, 390 
stone in, 393 
symptoms of disease of, 389 
of inflammation of, 392 
-symptoms of myelitis, 390 INDEX. 
579 
Bladder-symptoms of paretic dementia, 
392 
of tabes, 391 
Blindness, causes of, 188 
sometimes from influence of drugs, 
200 
Blood, changes in, in infectious diseases, 
378 
circulation of, 356 
estimation of haemoglobin in, by 
haemoglobinometer of v. Fleischl, 
370 
in sputum, 542 
in stools, 437, 439 
character and significance of, 
433 
in dysentery, 435, 436 
in entero-colitis, 434 
in urine, 395 
Heller’s test for, 396 
in vomitus, 527 
method of staining with Ehrlich’s 
triple stain, 373 
normal constitution of, 363 
of diagnostic value in appendicitis, 
378 
parasites of, 379 
red corpuscles of, change in, in anae- 
mia, 375 
coloring-matter of, decreased 
in oligochromaemia, 364 
decreased in myelogenous 
leukaemia, 377 
in oligocythaemia, 363 
estimation of, by haemato- 
cvtometer, 365 
with haematocrit, 367 
extraordinary decrease of, 
in perniciousanaemia, 374 
increased in polycythaemia, 
363 
megaloblasts, 375 
megalocytes, 364 
microcytes, 364 
normoblasts, 364 
nucleated, 364 
poikilocytes, 364 
proportion of, to white, 364 
shadow corpuscles, 364 
varieties of, 363 
white corpuscles of, amoeboid move- 
ments of, 372 
eosinophiles, 372 
estimation of, with haemato- 
cytometer, 367 
increase of, 372, 376 
lymphocytes alone increased 
in lymphatic leukaemia, 
378 ' 
mononuclear leucocytes, 372 
multinuclear leucocytes, 372 
neutrophiles, 372 
Blood, white corpuscles of, polymorph- 
ous leucocytes, 372 
polynuclear leucocytes, 372 
proportion of, to red, 364 
Toison’s solution for count- 
ing, 367 
Blowing breathing. See Bronchial breath- 
ing._ 
Boils in diabetes mellitus, 229 
in paraffin-workers, 229 
in tar-workers, 229 
Bothriocephalus latus, 441 
Bowels, consideration of, 429 
constipated, in jaundice, 204 
patient’s idea as to regularity of, 22 
Brachial monoplegia, 81 
apparent, 85 
causes of cortical lesions in, 82 
due to cortical lesions, 81 
due to crutch-paralysis, 85 
due to fracture or dislocation of 
the head of the humerus, 84 
due to growth in neck or axilla, 
84 
due to hysteria, 83 
due to injury of the brachial 
plexus or important branches, 
83 
due to lead-poisoning, 85 
due to locomotor ataxia, 84 
due to primary brachial neu- 
ritis, 83 
Erb’s paralysis, 84 
Klumpke’s paralysis, 85 
paralysis of special muscles in, 
> 83, 85 
signal - symptoms of cortical, 
causes of, 81 
paraesthesia, 86 
Bradycardia, 325, 361 
in jaundice, 325 
in typhoid fever, 325 
Brain, areas of, 131 
tumors of, anaesthesia in, 247 
convulsions in, 474 
diagnosis of, 474 
deferential diagnosis between 
chronic nephritis and, 475 
headache in, 473 
liyperaesthesia in, 266 
papillitis of optic nerve in, 197, 
474 
paraesthesia in, 263 
paralysis in, 474 
slow breathing in, 475 
pulse in, 475 
vomiting in, 474 
Bramwell’s method of staining and 
mounting casts in urine, 407 
Breakbone fever. See Dengue. 
Breast, enlarged, in tuberculosis, 276 
pigeon-, 273 580 
INDEX. 
Breath in bronchiectasis, 18, 303 
in diphtheria, 18 
in empyema opening into bronchus, 
18 
in fever, 18 
in gangrenous stomatitis, 18 
in gastric disorders, 18 
in healthy child, 276 
in pulmonary gangrene, 18, 303 
in tonsillitis, 18 
shortness of, in heart disease, 323 
Breathing, amphoric, 294 
blowing, 294 
bronchia], 292 
broncho-vesicular, 293 
cog-wheel, 293 
puerile, 293 
vesicular, 292 
Bright’s disease. See also Kidneys and 
Nephritis. 
complications of, 426 
obstinate cough in, 539 
retinal hemorrhage in, 200 
retinitis in, 200 
roseola in, 222 
secondary diphtheritic dysen- 
tery in, 436 
value of estimation of urea in, 
423 
Bromidrosis, cold, clammy hands in, 57 
in hysteria, 235 
Bronchial breathing, 292 
due to compression of lungs over 
pleural effusion, 294 
in catarrhal pneumonia, 294 
in cavity, 294 
in consolidation, 294 
Bronchiectasis, fetid breath of, 303 
purulent sputum in, 543 
sacculated, loose, morning cough in, 
538 
Bronchitis, acute, character of sputum in 
later stages of, 541 
bronchorrhcea in, 307 
bubbling rales in, 295 
Charcot-Leyden crystals in, 544 
chronic, in chronic interstitial ne- 
phritis, 427 
distended cervical vessels in chronic, 
276 
Dittrich’s plugs in sputum of putrid, 
307 _ 
fever in, 464 
fibrinous, small casts of bronchioles 
coughed up in, 544 
hard, dry cough in, 307 
moderate, early in typhoid fever, 
449 
physical signs of, 307 
purulent, crystals of margaric acid 
in sputum of, 546 
putrid, 307 
Bronchitis, rales in, 307 
rapidity of respiration in severe, 276 
Broncho-vesicular breathing, 293 
Bronchophony in tuberculosis of the 
lungs, 301 
Brow ague in malaria, 552 
Bullae, due to antipyrin or iodine, 231 
due to pemphigus, 230 
due to trophic lesions in disease of 
central nervous system, 230 
CACHEXIA, general anasarca in can- 
cerous, 237 
Calculus. See Stone. 
renal, character of pain in, 557 
vomiting in, 557 
salivary, 160 
vesical, symptoms of, 393 
Caput coli, diseases of the, 354 
Medusae, 335 
Carbuncle, 230 
Carcinoma, appearance of skin in, 211 
cheesy pallor of face in, 210 
expression of face in, 27 
gastric, anaemia in, 376 
character of vomiting in, 526 
coffee-ground vomit in, 340, 526 
fever in, 459 
indicanuria in, 401 
most frequent at pylorus, 340 
hemorrhagic effusion in pleura in, 
306 
melanotic, black urine in, 395 
oesophageal, brassy ccugh due to 
pressure on larynx by, 539 
of caput coli, 354 
of pancreas, diabetes mellitus in, 
345 
jaundice in, 205, 345 
oily stools in, 345 
symptoms of, 345 
of pylorus, diagnosis of, 340 
between gastric ulcer and, 
344 
dilatation of stomach due to, 340 
excess of lactic acid in stomach 
in, 342 
symptoms of, 340 
renal, hematuria in, 398 
retraction of abdominal wall in, 330 
visceral, albumosuria in, 420 
Cardiac crises, 326 
dulness, alterations in, due to valvu- 
lar lesion, 290 
increase of, due to hypertrophy 
or dilatation of heart, 288 
due to pericardial effusion, 
288 
lessened by emphysema, 290 
normal extent of, 287 
feebleness, 326 INDEX. 
581 
Caries of bones of skull, headache in, 483 
of cervical vertebrae, retraction of 
head in, 49 
spinal, signs or symptoms of, 348, 
555 
Carphologia, 57, 78 
Carpo-pedal spasm in rickety, hydro- 
cephaloid children, 72 
Casts, Bramwell’s method of mounting 
and staining, 407 
centrifuge in examining, 402 
composition of, 401 
Farrant’s solution for staining, 407 
fatty, 405 
hyaline, 405 
of blood-cells, 403 
of bronchioles found in sputum, 544 
of epithelial cells, 402 
of granular matter, 404 
of micrococci, 404 
of pus-cells, 403 
resemblance of cylindroids to, 405 
Catalepsy, 30 
Cataract sometimes the result of diabetes 
mellitus, 200 
Catarrh, acute gastric, appearance of 
tongue in, 148, 530 
symptoms of, 530 
vomiting, 530 
chronic gastric, morning vomiting 
of drunkards in, 530 
vomiting due to excessive 
tea-drinking in, 530 
gastro-intestinal, fever in mild, in 
children, 445 
frog-belly in children with, 330 
uric acid excess in urine of, 408 
laryngeal spasm due to, 309 
nasal, character of headache due to, 
483 
of middle ear in syphilis, 158 
persistence of fever in measles due to 
bronchial or gastro-intestinal, 453 
respiratory, cough at night in, 540 
Catarrhal fever. See Influenza. 
pneumonia. See Pneumonia, catar- 
rhal. 
Cavernous breathing, 294 
Cavity of lung, Hippocratic succussion in 
large, partly filled with liquid, 
298 
pectoriloquy in, 298 
tubercular, purulent sputum in, 
543 
Centrifuge in examination of blood, 367 
of urine, 402 
quantitative test for albumin with, 
414 
Cephalalgia. See Headache. 
Cerebellar hemorrhage, 141 
titubation, 97 
Cerebral effusion. 53 
Cerebral palsy of children, 70 
athetosis in, 79 
epileptiform convulsions in, 
71 
flexion of hands in, 70 
intention-tremor in, 71 
softening, coma of, 490 
symptoms of, 490 
Cerebro-spinal meningitis, 461 
albumosuria of great importance 
in diagnosis of, 420 
character of fever in, 461 
convulsions in, 461 
diagnosis between croupous 
pneumonia, otitis media, tu- 
bercular infection and, 461 
headache in, 461 
herpes labialis in, 229 
hypersesthesia in, 267 
joints in, 125 
petechise in, 216 
rigidity of back of neck in, 461 
vomiting in, 461 
Changes in acuity of vision, 188 
Charcot-Leyden crystals in acute bron- 
chitis, 544 
in asthmatic attacks, 544 
in chronic croupous pneumonia, 
544 
in pulmonary tuberculosis, 544 
Charcot’s fever, 206 
Cheek, swelling of, in noma, 160 
in peliosis rheumatica, 160 
in salivary calculus, 160 
in Schonlein’s disease, 160 
in stomatitis, 160 
Chenzynski’s solution for staining mala- 
rial organisms, 383 
Chest, auscultation of, 292 
barrel-shaped, of emphysema, 273 
beaded ribs of, in rickets, 275 
bulging of, causes of, 273 
of sternum in pigeon-breast, 273 
expansion, 279 
Harrison’s grooves in, 275 
inspection of abnormal, 271 
of normal, 268 
localized bulging of, causes of, 273 
pain in, shown by pinched nose in 
children, 28 
palpation of, 279 
percussion of, 282 
phthisical or alar, 271 
resonance of, 282 
shrinking of, 275 
variation in shape of, in health, 271 
Chewing or sucking movements in men- 
ingitis, 479 
Cheyne-Stokes respiration, causes of, 278 
prognostic value of, 278 
pupillary reaction associated 
with, 187 INDEX. 
582 
Chickenpox, appearance of eruption in, 
220, 228 
character of fever in, 454 
disparity between height of fever 
and degree of illness in, 454 
Children, ages at which the different 
teeth appear, 158 
appearance of hands of, in heart- 
disease, 55 
causes of fever in, 445 
cerebral palsy of, 70 
congenital malformation of heart in, 
323 
crying of, 23 
earache in, 23 
gastro-pulmonary fever of, 467 
grinding of teeth by, significance of, 
159 
hydrocephaloid disease of, 511 
languor in cerebral trouble of, 23 
pleurisy in, 23 
pneumonia in, 23 
poliomyelitis in, 111 
respiration of, 24 
rose-rash in, 218 
stomatitis in, 23 
syphilis in, 23 
typhoid fever in, 459 
winning confidence of, 22 
Chill in acute pleurisy, 304 
in croupous pneumonia, 463 
in intermittent malarial fever, 455 
in pernicious anaemia, 459 
in pyelitis, 428 
in septic poisoning, 459 
slight, in dysentery, 435 
Chills, 443 
Chilly sensations and nausea in acute dif- 
fuse nephritis, 425 
Chin, position of, in wry-neck, 48 
Chlorosis, constipation in, 376 
disorders of menstruation in, 375 
dyspnoea in, 375 
greenish-yellow color in, 211 
haemoglobin decreased in, 375 
humming-top murmur in jugular 
vein in, 376 
irregular heart in, 376 
peculiar pallor of, 26 
poikilocytosis in, 375 
slight fever in, 376 
wayward appetite in, 376 
Choked disk, 197 
in cerebellar tumor, 198, 519 
in cerebral tumor, 197, 519 
in profound cerebral anaemia, 
519 
not generally seen in cerebral 
abscess, 519 
Cholangitis, catarrhal or suppurative, 
character of fever in, 458 
gallstone collie in, 458 
Cholangitis, marked jaundice in, 458 
Cholera Asiatica, comma bacillus in, 432 
diagnosis of, 432 
Hippocratic face in impending 
death in, 33 
indicanuria in, 401 
roseola in, 221 
subnormal temperature in, 468 
systemic infection in, 432 
temperature in, 465 
vomiting in, 526 
infantum, character of fever in, 465 
Chevne-Stokes respiration in, 
432 
cold skin and high rectal tem- 
perature in, 465 
diarrhoea in, 465 
disparity between axillary and 
rectal temperatures in, 432 
mousv, musty odor of stools in, 
438 
obstinate vomiting in, 465, 526 
sinking in of fontanelles in, 53 
subnormal temperature in se- 
vere, 468 
symptoms of, 431 
morbus, subnormal temperature in 
severe, 468 
symptoms of, 431 
nostras. See Cholera morbus. 
Chorea, anaemic murmurs in children in, 
314 
Bergeron’s, 74 
character of spasms in, 513 
diagnosis of, 514 
electric, 74, 515 
expression in, 30 
facial spasm in, 45 
heart disease in, 314 
liemiansesthesia in, 247 
hereditary, 74 
Huntington’s, 74, 514 
hysterical, 74 
incoherent speech in, 570 
insaniens, 514 
loss of knee-jerk in, 564 
major, 514 
maniacal, 73 
nodding spasm in, 47 
paralytic, 73 
post-hemiplegic, lesion of, 142 
senile, 73 
spasm of tongue in, 157 
Chronic poliomyelitis, claw-hand in, 69 
Chvostek’s symptom of tetany, 512 
Chyluria, caused by filaria sanguinis 
hominis, 386 
test for, 401 
Circulation of the blood, 356 
Cirrhosis, hepatic, ascites in, 352 
caput Medusae in ascites caused 
by, 335 INDEX. 
583 
Cirrhosis, hepatic, disorders of digestion 
in, 352 
enlargement of spleen in, 353 
haematemesis in, 352 
symptoms due to, 352 
uric acid in excess in urine of, 
408 
Claw-foot, 118 
-hand, 66 
Clothing, diagnostic significance of, 17,18 
Clubbed fingers, 55, 323 
Coflee-ground vomit in gastric cancer, 
526 
in locomotor ataxia, 527 
in phosphorus-poisoning, 529 
Cog-wheel breathing, 293 
Colic, causes of abdominal, 557 
character of crying in children caused 
by abdominal, 23 
convulsions in, 513 
gallstone, in catarrhal cholangitis, 
458 
hepatic, 204, 558 
lead, pain in, 558 
renal, character of pain in, 557 
diagnosis of, 557 
retraction of abdominal wall in re- 
nal, hepatic, and lead, 330 
sometimes due to strongylus gigas, 
398 
ureteral, 395 
Collapse, profuse sweating a sign of, 235 
Coma, ability to protrude tongue in, when 
other orders fail to gain response, 
155 
causes of, 485 
following pernicious malarial fever, 
489 
in acute alcoholic poisoning, 485 
differential diagnosis 
of, 486 
yellow atrophy of the liver, 488 
in Addison’s disease, 491 
in apoplexy, 489 
in cannibas indica poisoning, 486 
in cerebral abscess, 490 
disease, 20 
softening, 490 
syphilis, 490 
in chloral-poisoning, 487 
in chronic parenchymatous nephritis, 
426 
in diabetes, 427, 488 
in epidemic cerebro-spinal menin- 
gitis, 490 
in general paralysis, 492 
in heart-failure, 491 
in heat-stroke, 491 
in multiple sclerosis, 492 
in opium-poisoning, 486 
in petit mat, 491 
in purulent leptomeningitis, 491 
Coma in Raynaud’s disease, 490 
in renal disease, 20 
in subdural hemorrhage, 490 
in thrombosis of brain sinuses, 490 
in typhoid fever, 488 
in uraemia, 487 
rapidity of respiration in diabetic or 
uraemic, 277, 488 
slowness of breathing in uraemic or 
diabetic, 277, 488 
-vigil, 488 
Concomitant squint, 167 
Congestion, pulmonary, 303 
physical signs and history of,303 
renal, albuminuria in, 414 
blood-casts in, 395, 403 
irritation of bladder in, 392 
Consciousness, loss of, in cerebral hemor- 
rhage, 139, 140 
Constipation, causes of, 429 
in chlorosis, 375 
in chronic lead-poisoning, 430 
in diabetes insipidus, 429 
mellitus, 429 
in intestinal obstruction, 430 
in jaundice, 429 
in reflex irritation, 430 
indicanuria in, 40l 
Continued fever. See Malaria, remit- 
tent. 
Contraction of pupil of the eye, 186 
Contractures in hysteria, 71, 121 
Convulsions or general spasms, 493 
in acute articular rheuma- 
tism with hyperpyrexia, 
466 
in Addison’s disease, later 
stages, 511 
in anterior poliomyelitis, 
467 
in brain-tumor, 474 
in cerebro-spinal menin- 
gitis, 461 
in uraemia, 518 
clonic, in acute alcoholism, 501, 508 
in cardiac sedatives, 502 
in chronic lead-poisoning, 502 
in epilepsy, 493 
in eruptive fevers, 501 
in general paresis, 91 
in hemicrania, 509 
in hysteria, 503 
in Jacksonian epilepsy, 494 
in malaria, 502 
in malingerers, 510 
in post-hemiplegic epilepsy, 496 
in puerperal eclampsia,- 508 
in syphilitic epilepsy, 499 
in syncope, 509 
epileptiform, in cerebral palsy of 
children, 71 
erotic, in phosphorus-poisoning, 529 584 
INDEX. 
Convulsions of infants in meningitis, 511 
in pseudo-meningitis, 511 
in reflex irritation, 510 
salaam, 515 
tetanic, in acute yellow atrophy of 
liver, 513 
in gallstone colic, 513 
in ha;matoma of dura mater, 513 
in hydatid cyst, of cerebral cor- 
tex, 513 
in irrigation of pleural cavity, 
513 
in multiple sclerosis, 513 
in strychnine-poisoning:, 511 
in tetanus, 511 
in tetany, 512 
Convulsive tic, facial spasm in, 46 
Coprolalia, 46, 74 
Corneal ulceration in scrofulosis, 200 
Corpuscles of Ehrlich, 375 
Corrigan’s pulse, 320 
Coryza, action of child toward breast in, 
23 
in influenza, 463 
Cough and expectoration, 537 
causes of night, 540 
character of, in acute laryngitis, 539 
in aneurism of transverse arch 
of aorta, 318 
in false croup, 537, 539 
in laryngeal phthisis, 539 
chronic loose, morning, in empyema 
rupturing into bron- 
chus, 538 
in pulmonary abscess, 
538 
in sacculated bronchi- 
ectasis, 538 
in tuberculosis with 
cavity, 538 
due to change of position in pleurisy 
with effusion, 539 
during aspiration of fluid in pleurisy, 
539 
followed by cry in pneumonia or 
pleurisy, in children, 23 
hard and dry, in acute bronchitis, 307 
hysterical, 540 
in paralysis of diaphragm, 541 
in whooping-cough, 537 
laryngeal, due to irritant dust or 
vapors, 539 
due to mediastinal tumors, 539 
due to pressure by aneurism, 539 
by carcinoma of oesopha- 
gus, 539 
nervous or reflex, 540 
obstinate, in Bright’s disease, 539 
produced by enlarged tonsils, en- 
larged uvula, hypertrophy of mu- 
cous membrane of the nose, etc., 
540 
Cough, significance of cessation of, in ad- 
vanced phthisis, bronchorrhoea of 
the old, and severe pneumonia,541 
smothered or suppressed, in pleuro- 
pulmonary inflammation, 538 
value of loose, 538 
varieties of, 537 
Cracked-pot sound, 285 
Cranio-tahes, 51 
Cretinism, facial expression in, 32 
“ Cri hydrocephalique,” 479 
Crisis, apparent, in relapsing fever, 452 
fever in erysipelas ending by either 
lysis or, 455 
gastric, in locomotor ataxia, 527 
in croupous pneumonia, 463 
in typhus fever, 452 
intestinal, 433 
subnormal temperature in many 
diseases at, 468 
with fading of eruption in measles, 453 
Crossed anaesthesia, 249 
in lesion of one side of cord, 249 
of peduncle, 249 
of pons, 249 
Croup, spasmodic, character of cough in, 
537, 539 
inspirations prolonged in, 277 
laryngeal spasm in, 309 
Croupous pneumonia. See Pneumonia, 
croupous. 
Crutch-palsy, 75 
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 child over four months old, with- 
out shedding tears, an unfavor- 
able sign, 23 
Crystals, ammonium urate, 409 
amorphous phosphates, 410 
blood, of Teichmann, 396 
Charcot-Leyden, 544 
creatin, 409 
creatinin, 409 
hsemin, 535 
leucin and tyrosin, in phosphorus- 
poisoning, 529 
margaric acid, 546 
oxalate of lime, 408 
triple phosphates, 410 
urates, 408 
uric acid, 403 
Curschmann’s spirals, in asthmatic 
attacks, 544 
rarely in croupous pneumonia, 
544 
in pulmonary tuberculosis, 
544 INDEX. 
585 
Curvature of spine, unilateral bulging 
of chest in, 275 
Cyanosis, causes of, 211, 213 
due to drugs, as antipyrin or ace 
tanilid, 213 
in acute articular rheumatism with 
hyperpyrexia, 466 
in acute miliary tuberculosis, 463 
in cardiac dyspnoea, 29 
in laryngeal obstruction, 213 
in new-born, 212 
relative frequency of cause of 
lesions of, 212 
in pulmonary diseases, 213 
in serious cardiac disease, 212 
Cyclical vomiting, other symptoms de- 
pendent on, 532 
Cylindroids, significance of, 406 
varieties of, 405 
Cyst, echinococcus, of liver, 351 
hsematuria in renal, 398 
of kidney, 348 
of pancreas, 345 
ovarian, diagnosis of, 331 
Cystitis, character of pain in, 560 
chronic, triple phosphates in urine 
in, 409 
darting pain in urethra in, 392 
purulent, symptoms of septic fever 
in, 389 
tenesmus in, 392 
Dactylitis, 56 
Deformity of feet and legs, 117 
in acute cerebral paralysis of 
infancy, 121 
Delirium, a bad omen in croupous pneu- 
monia, 299 
in acute articular rheumatism with 
hyperpyrexia, 466 
in acute yellow atrophy of liver, 
488 
in thrombosis of cerebral sinuses, 
480 
incoherent speech in, 570 
low, muttering, in typhoid fever, 
29,570 
mild, in mitral regurgitation, 483 
wild, in phosphorus-poisoning, 529 
Dementia, paretic, Argyll - Robertson 
pupil in, 185 
diplopia in, 166 
gangrene in, 231 
hemiplegia in, 144 
hemorrhage into skin in, 216 
hesitating, halting speech in, 
570 
knee-jerk in, 565 
localized sweating in, 235 
optic atrophy in, 198 
perforating ulcer of foot in, 232 
Dementia, paretic, tache cerebrate in, 216, 
217 
tremor of tongue in, 570 
Dengue, an epidemic disease, 460 
character of fever in, 460 
differential diagnosis of, 460 
erythema in, 218 
hsematemesis in, 527 
jaundice in, 207 
joint-involvements in, 128 
pain involving entire body in, 562 
Dentition, fever in difficult, 445 
Diabete bronze, 206 
Diabetes insipidus, constipation in, 429 
great increase of urine in, 394 
loss of knee-jerk in some cases 
of, 564 
urine of, 428 
mellitus, Argyll-Robertson pupil in, 
186 
boils in, 229, 417 
caries of teeth in, 158 
cataract in, 164, 200 
Cheyne Stokes respiration in, 
278 
color of urine in, 394, 427 
coma in, 427 
constipation in, 429 
development of, in carcinoma of 
pancreas, 345 
diagnosis of coma in, 488 
dry, harsh skin in, 427 
fermentation of urine in, due to 
saccharomyces albicans, 413 
gangrene in, 231 
great increase of urine in, 394 
headache rarely in, 473 
heavy, sweet odor of urine in, 
394 
high specific gravity of urine 
in, 394 
jaundice in, 206 
knee-jerk lost in advanced, 564 
ocular palsy in, 175 
paraplegia rare in, 114 
perforating ulcer of foot in, 129 
polydipsia in, 417 
polyphagia in, 417 
prognosis of, 417 
if associated with obesity, 
417 
influence of age on, 417 
pruritus in, 267, 417 
retinitis in, 200 
roseola in, caused by urine, 223 
rosette crystals of uric acid in 
urine of, 408 
urine in, 427 
vomiting rare in, 518 
wasting in, 417 
white spots on trousers in, 18 
Diarrhoea, causes of, 430 586 
INDEX. 
Diarrhoea, colliquative, in uraemia, 518 
decrease of urine due to, 394 
dissecting-room, 437 
fatty, due to cod-liver oil, 437 
due to disease of pancreas, 437 
in jaundice, 437 
in abdominal pain, 22 
in cholera infantum, 431 
morbus, 431 
in dysentery, 435 
in entero-colitis, 433 
in fissure of the anus, 433 
in hysteria, 437 
in influenza, 463 
in leukaemia, 378 
in locomotor ataxia, 433 
in malignant ulceration, 436 
in proctitis, 435 
in pulmonary gangrene or tubercu- 
losis, 436 
in renal disease, 433 
in septicaemia, 436 
in syphilitic ulceration, 436 
in tuberculosis, 434 
lienteric, 434 
may be caused by purgatives, 22 
nervous, 433 
paroxysmal, sero-mucous or bloody, 
in exophthalmic goitre, 437 
Diazo-reaction, 425 
Dilatation of heart, symptoms and physi- 
cal signs of, 324 
of pupil of the eye, 186 
of stomach, atrophy of gastric tu- 
bules in, 342 
character of vomiting in, 530 
constitution of vomitus in, 531 
in pressure by growths of pan- 
creas, 531 
in tetany, 72 
methods of examining in, 341, 
342 
sarcinae ventriculi in vomitus in, 
531 
torula cerevisiae, causing fer- 
mentation in, 531 
total absence of hydrochloric 
acid in, 531 
Diphtheria, anaesthesia in 50 per cent, of 
cases of, due to neuritis, 258 
casts of larynx and upper bronchial 
tubes at times coughed up in, 544 
difficult swallowing due to paralysis 
from, 159 
double oculomotor paralysis in, 180 
nasal, 162 
paralysis of tongue following, 156 
paraplegia a sequel to, 113 
roseola in, 220 
sickening, sweet odor of breath in, 
18 
symptoms of, 161 
Diplopia, crossed, 169, 172 
explanation of, 166 
homonymous, 169, 172, 174. 
in poisoning, 166 
symptom of Friedreich’s ataxia, 166 
of lesion at base of brain, 166 
of cerebral cortex, 166 
of cranial nerve nuclei, 166 
of nerve in its course, 166 
of locomotor ataxia, 166 
of paretic dementia, 166 
vertical, 174 
Distoma haematobium, eggs of, in urine, 
411 
haematuria due to, 398 
pulmonum, 546 
Dittrich’s plugs, 307 
Dropsy. See CEdema and general ana- 
sarca. 
general, in arsenic-poisoning, 237 
in beri-beri, 237 
in blood diseases, 237 
in cancerous cachexia, 237 
in disordered nervous control of 
vessels, 237 
in emboli, 236 
in heart disease, 237 
in multiple neuritis, 237 
in renal disease, 237 
in scurvy, 237 
in thrombi, 236 
in vascular disease, 236 
localized, in anaemia, 237 
in aneurism, 238, 239 
in angioneurotic oedema, 238 
in arsenic-poisoning, 238 
in cardiac failure, 237 
in cerebral thrombosis, 238 
in hepatitis or cirrhosis, 237 
in mastoid abscess, 239 
in neuralgia, 238 
in occupations requiring a stand- 
ing position, 238 
in phlegmasia alba dolens, 238 
in pressure on great vein, 237 
in pyothorax, 239 
in relapsing fever, 239 
in renal disease, 237 
in thrombosis, 238, 239 
in typhoid fever, 239 
of eyelids in renal disease, 238 
in other affections, 238 
of feet and legs in abdominal 
growths causing 
pressure, 237 
in anaemia, 238 
in renal disease, 237 
Dryness of the skin, 235 
Dubini’s chorea, 74, 502 
Dupuytren’s contraction, 60 
Dysentery, acute primary, of a diphthe- 
ritic character, 436 INDEX. 
587 
Dysenterv, amoebic, amoeba coli the cause 
_ of, 436 
liver abscess in, 436 
symptoms of, 435 
arthritis in, 128 
character of stools in, 435 
fever in, 435 
secondary diphtheritic, a complica- 
tion of Bright’s disease, 
436 
in acute croupous pneumo- 
nia, 436 
in chronic heart disease, 
436 
slight chill in, 435 
thirst in, 435 
tongue in, 149 
vomiting in, 526 
Dysmenorrhoea, pain in, 560 
Dysphagia, causes of, 159, 535 
Dyspnoea from foreign body in air-pas- 
sages, 309 
in anaemia, 375 
in aortic insufficiency, 323 
in asthma, 308 
in chlorosis, 375 
in heart disease, 29 
in laryngeal spasms, 309 
in leukaemia, 378 
in miliary tuberculosis, 520 
inspection of chest in, 270 
position due to, 20 
worse at night in chronic interstitial 
nephritis, 427 
EARACHE, character of crying in chil- 
dren with, 23 
rubbing of hand over affected side 
of head in, 23 
Echolalia, 46, 74 
Eclampsia, puerperal. See Puerperal 
eclampsia. 
Eczema, appearance of nails in, 56 
due to chloral, 229 
due to mercury, 229 
due to potassium iodide, 229 
due to quinine, 229 
Ehrlich, corpuscles of, 375 
diazo-reaction in urine of, 425 
myelocyte of, 377 
triple blood-stain of, 373 
Electric chorea, 74, 515 
Bergeron’s, 74 
Elephantiasis, sometimes caused by filaria 
sanguinis hominis, 386 
symptoms of, 239 
Embolism, cerebral, Cheyne-Stokes res- 
piration in, 278 
gangrene in, 129 
vomiting in, 518 
of coronary arteries, 325 
Embolism of kidney, casts of, micrococci 
in, 404 
hsematuria in, 398 
oedema in, 236 
of pons Varolii, 466 
of superior mesenteric artery, symp- 
toms of, 528 
Emphysema, appearance of hands in, 55 
barrel-shaped chest of, 272, 307 
distended cervical vessels in, 276, 307 
expiration prolonged in, 278, 307 
lessened area of cardiac dulness in, 
290, 308 
percussion resonance increased in, 
307 
pulmonary and cardiac hypertrophy 
causing depression of apex-beat in, 
281 
rales in, 308 
spleen and liver displaced downward 
in, 308 w 
systolic tricuspid murmur in, 308 
vocal fremitus diminished in, 307 
resonance diminished in, 298, 
307 
Emprosthotonos in hysteria, 504 
Empyema, albumosuria in, 420 
communicating with bronchus, loose 
morning cough in, 538 
odor of breath in, 18 
pulsation of chest-wall in some cases 
of, 281 
purulent sputum in, 543 
Endocarditis, acute ulcerative, character 
of fever in, 451, 458 
diagnosis between typhoid 
fever and, 451 
duration of, 458 
jaundice in, 209 
petechial rashes in, 216 
prognosis of, 458 
retinal hemorrhage in, 200 
sweating in, 235 
Enteric fever. See Typhoid fever. 
Enterocolitis, flakes of mucus in stools of, 
434 
mild follicular, 434 
ribbon-shaped stools in, 434 
symptoms of, 433, 434 
ulcerative, 434 
Enteroliths, 525 
Eosinophile corpuscles, 372, 377 
in myelogenous leukaemia, 377 
Epigastrium, distention of, 336 
pulsation in region of, 346 
Epilepsy, alcoholic, 501, 508 
aura in, 493, 497 
biting of tongue in, 152, 494 
caused by drugs, 502 
by lead, 502, 509 
by malaria, 502 
character of convulsions in, 493 588 
INDEX. 
Epilepsy, cutaneous hemorrhage in, 216 
diagnosis between attacks simulated 
by malingerers and, 510 
between hysteria and, 503 
between uraemia and, 507 
expression of face in, 493, 494 
facial spasm in, 46, 47 
fever after seizure of, 467, 506 
hippus in, 187 
Jacksonian, character of convulsions 
in, 494, 495 
knee-jerk in, 565 
minor, diagnosis of, 508 
unconsciousness in, 492 
vertigo the only symptom of, 
484 
muscse volitantes in, 200 
nystagmus a rare symptom of, 183 
post-hemiplegic, 496 
scars on head in suspected traumatic, 
234 
spasm of heart in, 492 
syphilitic, 497 
diagnosis of, 498, 499 
symptoms of, 498 
tache cerebrate in, 216 
vertigo, a premonitory symptom of, 
484 
Epileptiform convulsions from cerebral 
hemorrhage, 495 
from other causes, 496 
Epiphysitis of infancy, acute, symptoms 
of, 126 
Equina. See Glanders. 
Erb’s paralysis, 84 
symptom, 512 
Ergotism, gangrene in, 64 
Eruption, date of, in various diseases, 
220 
herpetic, along nerve-trunk in sciatic 
neuritis, 556 
in anthrax maligna, 230 
simplex, 229 
in chickenpox, 228 
in erysipelas, 222, 230 
in glanders, 230 
in impetigo contagiosa, 228 
in measles, 220 
in rheumatism, 213 
in rotheln, 218 
in smallpox, 219, 225, 454 
in syphilis, 233 
in typhus, 222, 452 
in vaccinia, 227 
of skin in regard to age, 213 
pemphigus-like, due to salicylic acid 
or copaibia, 231 
pharyngeal and buccal in measles, 
162 
purpuric, from diseases, 215 
from drugs, 215 
resulting from quinine, 229 
Eruption, vesicular, about mouth, in foot- 
and-mouth disease in man, 154 
Erysipelas, albumosuria in, 420 
appearance of eruption in, 222, 230 
diazo-reaction in severe, 425 
fever in, ending by either crisis or 
lysis, 455 
marked remissions and inter- 
missions of, 455 
sudden rise of, 454 
inflammation of skin similar to, from 
arnica, 222 
symptoms of, 222 
vomiting in, 534 
Erythema. See Roseola. 
exudativum multiforme, symptoms 
of, 215 
following operation, 221 
parturition, 221 
vaccination, 219 
in Bright’s disease, 222 
in dengue, 218 
in diphtheria, 220 
in rheumatism, 214 
in scarlet fever, 217 
in smallpox, 219 
in syphilis, 221 
in typhoid fever, 221 
produced by drugs, 223, 229 
roseola, symptoms of, 218 
scarlatiniform, symptoms of, 218 
Esophoria, 167 
Ewald’s test-breakfast, 344 
Examination, method of, in consulting- 
room, 25 
of abdomen, 329 
of blood by hsematocrit, 367 
by hsematocytometer, 365 
by hsemoglobinometer, 370 
for micro-organisms of malaria, 
382 
in leukaemia, 377 
of children, 22 
of eye by ophthalmoscope, 165, 194 
of field of vision, 190 
of functional activity of ocular 
muscles, 168 
of hemianopsia, 190 
of pulse, 355 
of pupillary reflex, 184 
of skin for jaundice, 202 
of sputum, 545 
of stomach, 336 
of tongue, 145 
Exhaustion from hiccough, 517 
Exophoria, 167 
Exophthalmic goitre. See Goitre, ex- 
ophthalmic. 
Expectoration. See Sputum. 
Expression of face as an early symptom 
of facio-humero-scapular type of mus- 
cular atrophy, 31 INDEX. 
589 
Expression of face, elated, of paretic de- 
mentia, 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, 493 
in Friedreich’s ataxia, 31 
in healthy, sleeping child, 27 
in malignant disease, 27 
in melancholia, 30 
in moderate pain in children, 28 
in myxcedema, 32, 34 
in nervous exhaustion, 30 
in renal disease, 30 
in typhoid fever, 29 
intellectual, 26 
of anxiety in grave disease, 27 
of “mouth breathers,” 29 
Eye, ability to close, in cerebral facial 
paralysis, 36 
alteration of color-field of, 193 
amaurosis, 200 
anatomy of optic nerve of, 188 
annulus senilis, 165 
appearance of healthy eye-ground, 
196 
arcus senilis, 165 
causes of paralysis of, 169 
conjunctival hemorrhage, from 
coughing, 164 
from degenerative vascular 
changes, 164 
from injury, 164 
dark areas under during menstrua- 
tion, 26 
diagnosis between ocular symptoms 
of tabes and hysteria, 193 
diplopia, 166 
examination of, ophthalmoscopic, 
165, 194 
exophthalmos in goitre, 164 
in lesion of oculomotor nerve, 
40 
Graefe’s symptom, 165 
hemianopsia, 188 
homonymous and crossed diplopia, 
169 
intraocular muscles of, 183 
iritis, 200 
lesion of optic nerve in locomotor 
ataxia, 198 
method of determining paralysis of, 
170 
of examining functional activity 
of muscles, 168 
muscse volitantes, 200 
orthophoria, 168 
papillitis, 197 
Eye, puffiness about, from excessive use 
of arsenic, 26 
in acute diffuse nephritis, 426 
retinitis, 199 
retrobulbar neuritis, 198 
rod test of Maddox, 168 
squint, 167 
Eyelids, closed in healthy sleeping child, 
27 
oedematous, in angioneurotic oedema, 
236 
from arsenic, 236 
in cerebral thrombosis, 236 
in neurotics, 236 
painful twitchings of, accompanying 
facial hemiatrophy, 34 
pallor of, in anaemia, 164 
pigmentation of, early in pregnancy, 
26 
puffy, in cardiac disease, 164 
in overuse of arsenic, 164 
in renal disease, 164 
in trichinosis, 30 
showing glazed conjunctivse, 28 
slightly parted in sleeping child, 
showing congestive or nervous 
pain, 28 
swollen in cretinism, 32 
twitching in nervous irritation, 28 
FACE. See Expression. 
anaesthesia of, due to involvement of 
the fifth nerve or its nucleus, 262 
anxious and covered with sweat in 
angina pectoris, 554 
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 
flushed in fever, 444 
full moon, of myxcedema, 32, 34, 
35 
gray or bluish, from overdose of coal- 
tar products, 27 
heavy, cheesy-looking, in children, 
28 
hemiatrophy of, 33 
hemihypertrophy of, 34 
Hippocratic, of impending death, 33 
hysterical, 26, 30 
intellectual, 26 
leonine, of leprosy, 32 
massive, of acromegaly, 33, 35 
oedema or great swelling of, in 
dropsy, 30 
in erysipelas, 30 
of carcinoma, 27 
of catalepsy, 30 
of chorea in children, 30 590 
INDEX. 
Face 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, 44 
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, 407 
Fatty degeneration in phosphorus- 
poisoning, 529 
heart, 326 
Feces. See Stools. 
causes of variation in quantity of, 
437 
color of, 438 
consistency of, 438 
impaction of, 347 
odor of, 438 
Feet, claw-, 118 
contractures of, in hysteria, 122 
deformity of, due to acute cerebral 
paralysis of infancy, 121 
due to poliomyelitis, 121 
due to progressive muscular 
atrophy, 118 
distribution of anaesthesia of, in neu- 
ritis, 254 
enlarged, due to deformity, 117 
in acromegaly, 117 
in myxoedema, 117 
in pulmonary osteo-artliropathy, 
117 
flat-, in locomotor ataxia, 120 
numbness of, in locomotor ataxia, 89 
perforating ulcer of, in diabetes, 129 
in senile gangrene, 129 
in tabes dorsalis, 129 
sciopedy, 117 
tabetic, 121 
Fehling’s test for sugar in the urine, 415 
Festination, 97 
Fever, absence of, in pulmonary oedema, 
303 
appeai'ance of nails in, 56 
Fever, causes of tertian, quartan, and 
sestivo-autumnal, 379, 380, 381 
cold, wet skin of evil import in, 444 
character of, in acute appendicitis, 
406 
articular rheumatism, 466 
miliary tuberculosis, 462 
multiple neuritis, 467 
myelitis, 467 
pulmonary tuberculosis, 462 
in anthrax, 465 
in catarrhal pneumonia, 464 
in cerebral abscess, 462 
in cerebro-spinal meningitis, 461 
in chicken pox, 454 
in cholangitis, catarrhal or sup- 
purative, 458 
in cholera Asiatica, 465 
infantum, 465 
in croupous pneumonia, 463 
in dengue, 128, 460 
in difficult dentition, 445 
in dysentery, 435 
in epilepsy, 467, 506 
in erysipelas, 454 
in foot-and-mouth disease, 465 
in gastro-pulmonary fever, 467 
in hsemoglobinsemia, 533 
in hay fever, 463 
in hepatic abscess, 458 
in Hodgkin’s disease, 459 
in hysteria, 466 
in infantile spinal paralysis, 467 
in influenza, 463 
in injuries to cervical portion of 
spinal cord, 466 
in intermittent malarial fever, 
455 
in Malta fever, 451 
in measles, 453 
in mild gastro-intestinal catarrh 
in children, 445 
in obstruction of the rectum, 
525 
in parenchymatous nephritis, 
465 
in pemphigus, 230 
in pernicious anaemia, 459 
in pyelitis, 428, 459 
in relapsing fever, 452 
in remittent malarial fever, 459 
in rotheln, 453 
in scarlet fever, 452 
in septic poisoning, 459 
in septicaemia, 461 
in smallpox, 453 
in syphilis, 464 
in teething, 445 
in tetanus, 465 
in thermic fever, 466 
in tonsillitis, 465 
in trichinosis, 451 INDEX. 
591 
Fever, character of, in typhoid fever, 
44(5 
in typhus fever, 452 
in ulcerative endocarditis, 458 
in Weil’s disease, 4(50 
in vellow fever, 460 
Charcot’s, 206 
chlorides decreased in some, 424 
increased during convalescence 
from, 424 
definition of, 443 
dry, hot skin in, 444 
flushed face in, 444 
high specific gravity of urine in, 394 
infantile remittent, 459 
rapid pulse in, 362 
respiration in, 277 
secondary, in smallpox, 225 
septic, in purulent cystitis, 389 
sighing or arhvthmic respiration in, 
in children, 24 
significance of, 444 
in children, 445 
slight, in chlorosis, 376 
in leukaemia, 378 
urates in excess in urine of, 408 
urea increased in urine of, 423 
urethral, from passing sounds, 445 
uric acid increased in urine of, 408 
* urine decreased in, 394 
Filaria Demarquayi, 385 
description of, 384 
diurna, 384 
embryos of, in urine, 411 
haematuria in, 398 
loa, 385 
nocturna, 384 
Ozzendi, 385 
perstans, 384, 386 
sanguinis hominis, chyluria and 
elephantiasis caused by, 386 
Fingers, appearance of, diagnostic of 
chloral habit, 57 
clubbed in heart disease, 55, 323 
distorted and twisted in gout and 
arthritis deformans, 58 
fixation of joints of, by deposit of 
urate of sodium, 58 
in syphilitic dactylitis, 56 
spasm of, due to occupation, 72 
Fissure of the anus, character of pain in, 
561 
diarrhoea in, 433 
Flat-foot in locomotor ataxia, 120 
Flint’s murmur, 316 
Floating kidney, 347 
spleen, 349 
Fontanelle, condition of, diagnostic, 50, 
51, 52, 53 
Foot-and-mouth disease in man, symp- 
toms of, 465 
Foot-drop, 115 
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, 309 
in bowel, 347 
Fovea centralis, 197 
Fremitus, vocal, decrease of, causes of, 
280 
increase of, causes of, 280 
mode of production of, 279 
Friction-sounds, 296 
as a rule, due to pleuritis, 296 
at apex of chest, usually due to tu- 
berculosis, 296 
best heard in axilla, 296 
pericardial, 297 
Friedreich’s ataxia, claw-foot in, 119 
diagnosis of, 565 
differential points between loco- 
motor ataxia and, 91 
diplopia a symptom of, 166 
face of, 31 
gait of, 91 
loss of knee-jerk in, 564 
movement of hands in, 79 
nystagmus in, 183 
sensory disturbance of skin late 
in, 251 
slow, scanning speech in, 570 
table of symptoms of, 91, 93 
Frost-bite, gangrene in, 64 
Fungus foot disease. See Mycetoma. 
GABBETT’S method of staining for 
tubercle bacilli, 549 
Gait, 87 
“astasia abasia,” 98 
in acute poliomyelitis, 95 
in cerebellar disease, 97 
tumor, 96, 475 
in chronic myelitis, 94 
in disseminated sclerosis, 93 
in Friedreich’s ataxia, 91, 93 
in general paresis, 91 
in gout, 87 
in health, 18 
in hemiplegia, 97 
in hereditary cerebellar ataxia, 91, 
92, 93 
in hysteria, 97 
in infantile cerebral paralysis, 95 
in lateral sclerosis, 94 
in locomotor ataxia, 88, 91 
cause of, 90 
in multiple sclerosis, 93, 96 
in neurasthenia, 18 592 
INDEX. 
Gait in osteomalacia, 98 
in paralysis agitans, 97 
in pseudo-muscular hypertrophy, 95 
-tabes, 88 
in rheumatism, 87 
in rickets, 95, 99 
in sciatica, 87 
Gall bladder, diagnosis of obstruction of, 
353 
Gallop-rhythm in mitral stenosis, 316 
Gallstone in stools, 439 
jaundice in cases of, 204 
Gangrene in central nervous lesion, 231 
in diabetes, 231 
in embolism, 129 
in ergotism, 64 
in exophthalmic goitre, 129 
in frost-bite, 64 
in leprosy, 64 
in nerve injury, 231 
in Raynaud’s disease, 64, 232 
of extremities, following infectious 
fevers, 129 
of intestines, fetid odor of stools in, 
438 
pulmonary, character of sputum in, 
303, 542, 543 
crystals of margaric acid in spu- 
tum of, 546 
due to putrid bronchitis, 307 
elastic fibres in sputum of, 546 
fetid breath in, 303 
muco-purulent stools in, 436 
vomiting in, 534 
senile, perforating ulcer of foot in, 
129 
spontaneous, in hysteria, 231 
Gastralgia, character of pain in, 557 
diagnosis of, 557 
neuralgic spots in, 557 
Gastric cancer, anaemia in, 376 
fever in, 459 
indicanuria in, 401 
most frequent at pylorus, 340 
vomiting in, 340, 526 
crisis in locomotor ataxia, 89 
dilatation. See Dilatation of the 
stomach. 
ulcer, anaemia in, 344, 376 
pain in, 344, 557 
symptoms of, 344, 527 
vomiting of blood in, 527 
Gastritis, vomiting rare in, excepting 
when due to an irritant, 530 
Gastro diaphane of Einhorn, 336 
-duodenal catarrh, jaundice in, 202 
-pulmonary fever, etiology of, 467 
gastric symptoms of, 468 
marked fever in, 468 
pulmonary symptoms of, 468 
General anasarca in advanced cancerous 
cachexia, 237 
General anasarca in arsenic-poisoning, 
237 
in beri-beri, 237 
in children with acute diffuse 
nephritis, 42b 
in chronic pai’enchymatous ne- 
phritis, 426 
in heart disease, 236, 237 
in multiple peripheral neuritis, 
237 
in renal disease, 237 
paresis. See Paresis, general. 
Geographical tongue, 154 
Gerhardt’s symptom, 481 
German measles. See Rotheln. 
Girdle-sensation, 265 
in locomotor ataxia, 265 
in myelitis, 265 
in tumors of cord and meninges, 
265 
Glanders, blood in, 355 
eruption of, 230 
symptoms of, 230 
Glaucoma, dilated pupil in, 165, 186 
headache in, 472 
Glossitis, acute, 154 
dissecting, 153 
Glossodynia exfoliativa, 153 
Glycosuria, Fehling’s test for, 415 
Haines’ test for, 414 
Roberts’ yeast-test for, 417 
significance of, 417 
Whitney’s test for, 415 
Gmelin’s test for bile in urine, 400 
Goitre, exophthalmic, Abadie’s sign in, 
46 
brown pigmentation an occa- 
sional symptom of, 210 
diminished electrical resistance 
in, 325 
exophthalmos in, 54, 164 
gangrene in, 129 
Graefe’s symptom of, 165 
localized sweating in, 235 
Moebius’s sign of, 165 
paroxysmal bloody, mucous 
diarrhoea in, 437 
Stellwag’s symptom in, 165 
symptoms of, 1(54 
tache cerebrate in some cases of, 
216 
tachycardia in, 54, 325 
thrill over carotid arteries in, 
325 
vomiting in, 532 
Gonococci, indicative of specific urethri- 
tis or vaginitis, 411 
method of staining, 411 
Gonorrhoeal arthritis, symptoms of, 126 
Gout, aortitis in, 554 
appearance of nails in, 56 
distortion of fingers in, 58 INDEX. 
593 
Gout, hyperaesthesia of scalp in, 266 
joint-affections in, 127 
limping gait of, 87 
pain in great toe in, 561 
pruritus in, 267 
retinal hemorrhages in, 200 
urates in urine of, 408 
uric acid in urine of, 408 
Gouty diathesis, appearance of nails in, 
56 
Graefe’s spots, 46 
symptom, 165 
“Grisolle” sign of smallpox, 220 
Gums, blue line on, in lead-poisoning, 
158 
spongy, in salivation, 159 
in scurvy, 159 
Gyromele of Tiirck, 336 
Habit-chorea, 74 
-spasm, 45 
Haines’ modification of Haeser’s method 
for computing total quantity of 
solids in urine, 424 
test for sugar in urine, 414 
Hands, “accoucheur’s,” in tetany, 72 
changes in shape of, in chronic rheu- 
matism, 61 
choreic movements of, and of arms, 
in children with chorea minor, 73 
claw-, 66, 67, 68 
cold and clammy, due to bromidro- 
sis, 57 
due to local innervation of 
sweat-glands, 57 
contractions of, following apoplexy, 
71 
from hysteria, 71 
distribution of anaesthesia of, in neu- 
ritis, 260 
Dupuytren’s contraction of, 60 
excessive sweating of, in progressive 
muscular atrophy, 57 
flexion of, in cerebral palsy of chil- 
dren, 70 
gangrene of, in ergotism, 64 
in frost-bite, 64 
in leprosy, 64 
in Morvan’s disease, 65 
in neuritis, 65 
in Raynaud’s disease, 64 
in syringomyelia, 65 
senile, 64 
in acute articular rheumatism, 63 
in angioneurotic oedema, 64 
in child with cerebral trouble, 24 
with heart disease, 55 
in emphysema and chronic phthisis, 
55 
in heart disease, 19 
in thoracic aneurism, 55 
Hands, lateral drop of, in neuritis or acute 
infantile poliomyelitis, 75 
movement of, 76 
position of, in meningeal congestion 
or hydrocephalus in children, 72 
seal-fin, in arthritis deformans and 
gout, 61 
spade-like, in acromegaly, 65 
in mvxoedema, 65 
in pulmonary osteo-arthropathy, 
65 
spasm of, from cold and exposure, 75 
in ataxia, 75 
in paralysis agitans, 75 
in Thomsen’s disease, 75 
swelling and rupture of, in myce- 
toma, 65 
tremors of, 76 
wasting of, in diabetes mellitus, 66 
in nervous lesions, 66 
in old age, 66 
in phthisis, 66 
with anaesthesia, in syringomy- 
elia, 70 
with flexion and rigidity rarely 
seen in paralysis agitans, 70 
Harris’ test for albumose in urine, 418 
Harrison’s grooves in rickets, 275 
Hay fever, 463 
Head, activity of, with fixation of body, 
in peritonitis, 20 
examination of, 47 
excessive sweating of, 54 
in acromegaly, 50 
in cholera infantum, 432 
in chorea minor, 48 
in hydrocephalus, 50 
in idiocy, 51 
in microcephalus, 51 
in myxcedema, 50 
in osteitis deformans, 50 
in rickets, 48, 51 
position of, in advanced strabismus, 
49 
in chronic deafness, 49 
in mental depression, 49 
retraction of, in attack of indiges- 
tion in neurotic babies, 49 
generally due to basal menin- 
gitis, 49 
may be due to caries of cervical 
vertebrae, 49 
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, 469 
from use of drugs, 473 
in acute parenchymatous nephritis, 
465 
in Addison’s disease, 533 INDEX. 
594 
Headache in anaemia, 483 
in anterior poliomyelitis, 467 
in auto-intoxication, 470, 471 
in brain abscess, 477 
tumor, 473, 474 
in cerebral tumors, 519 
in cerebro-spinal meningitis, 461 
in croupous pneumonia, early stages, 
482 
in dental caries, 484 
in diabetes, 473 
in digestive disturbances, 469 
in disease of cranial bones, 483 
in ear disease, 484 
in exposure to cold, 483 
in eye-strain, 471 
in gastro-pulmonary fever, 468 
in glaucoma, 472 
in hsematoma of the dura, 482 
in hsemoglobinsemia, 533 
in intracranial aneurism, 483 
in jaundice, 471 
in malaria, 483 
in Malta fever, 451 
in measles, 482 
in meningeal hemorrhage, 482 
tumors, 474 
in meningitis, 478 
in migraine, 470 
in nasal catarrh, 483 
in neurasthenia, 472 
in nocturnal epilepsy, 483 
in paroxysmal hsemoglobinuria, 471 
in phosphaturia, 473 
in phosphorus-poisoning, 529 
in renal disease, 473 
in rheumatism, 473 
in smallpox, early stages, 482 
in sunstroke, 482 
in syphilitic arteritis, 476 
epilepsy, 498 
gumma, 476 
meningitis, 476 
in tubercular meningitis, 478 
in typhoid fever, 482 
in typhus fever, 452 
in uraemia, 473 
in valvular heart disease, 483 
vomiting in, 533 
Heart, alterations in area of dulness of, 
286 
apex-beat of, area of, 280, 281 
depression of, due to pulmonary 
emphysema, pericardial or 
pleural effusion, tumors in 
the chest, and cardiac hyper- 
trophy, 281 
displacement of, to left, by 
hypertrophy of left 
ventricle, 281 
by pleural adhesions, 
Heart, apex-beat of, displacement of, to 
left, by pleural effusions, 
281 
to right, by hypertrophy or 
dilatation of right ven- 
tricle, 281 
normal position of, 281 
raised by ascites, 281 
by distention of colon, 281 
by enlargement of spleen, 
281 
by hypertrophy of heart, 
281 
by iutra-abdominal growths, 
281 
strength of, 281 
asthma due to lesions of, 309 
blood-streaked sputum in valvular 
lesion of, 542 
causes of pain in neighborhood of, 
553 _ 
congenital malformations of the, 326 
rules for diagnosis of, 327 
cough in valvular disease of, 540 
dilatation of, 289, 324 
disease of, appearance of hands in 
children in, 55 
jaundice in chronic valvular, 205 
oedema, in, 236, 237 
patient’s position in, 19, 20 
retinitis in, 199 
enlarged cervical vessels in tricuspid 
regurgitation of, 276 
-failure, in influenza, 463 
unconsciousness in, 492 
fatty degeneration of, 326 
deposition on, 326 
general malformation of, 327 
greatly hypertrophied in chronic in- 
terstitial nephritis, 427 
headache in valvular disease of, 483 
hypertrophy of, 324 
irregular, in children, 314 
location of murmurs of, 314 
neuroses of, 325 
secondary diphtheritic dysentery in 
chronic disease of, 436 
slightly dilated, in acute diffuse ne- 
phritis, 427 
hypertrophied, in chronic pa- 
renchymatous nephritis, 427 
-sounds, 312 
accentuation of, 313 
reduplication of, 314 
where best heard, 313 
symptoms associated with murmurs 
of, 322 
thrills of, 281 
causes of, 281 
Heat-exhaustion, subnormal temperature 
in, 468 
-stroke. See Sunstroke. INDEX. 
595 
Heller’s test for albumin in urine, 414 
for blood in urine, 396 
Hematemesis, as vicarious menstruation, 
527 
diagnosis between haemoptysis and, 
528 
diseases in which it occurs, 527 
due to swallowed blood, 527 
in cirrhosis of liver, 527 
in embolism in the superior mesen- 
teric artery, 528 
in gastric cancer, 526 
ulcer, 527 
in heart disease, 527 
in injury of stomach, 527 
in locomotor ataxia, 527 
in malaria, 527 
in malingerers, 527 
in melaena neonatorum, 528 
in scurvy, 527 
Hematocrit, 368 
Hematocytometer of Thoma-Zeiss, 365 
Hematoma auris, 216 
of dura mater, convulsions due to, 
513 
subperitoneal, in children, 126 
Hematozoa malarise, 379 
Hematuria, acute, due to embolism, 396 
due to irritating drugs, 396 
due to malaria, 396, 397 
due to scarlet fever, 396 
blood-casts in, 403 
character of blood from bladder in, 
396 
from kidney in, 395 
from urethra in, 396 
chronic, due to chronic hemorrhagic 
nephritis, 398 
due to cyst of kidney, 398 
due to distoma haematobium,398 
due to filaria sanguinis hominis, 
398 
due to renal cancer, 398 
due to stone in kidney, 398 
due to strongylus gigas, 398 
due to tuberculosis of kidney, 
398 
other causes for, 399 
Hemiachromatopsia, 194 
Hemianaesthesia in capsular disease, 247 
in chorea, 247 
in cortical lesions, 247 
in disseminated sclerosis, 247 
in hysteria, 246 
superimposed in infantile cere- 
bral paralysis, 247 
in softening of brain, 247 
in tumor of brain, 247 
partial, with partial hemiplegia on 
opposite side, may be due to le- 
sions of one side of cord, 249 
Hemianopsia, 188 
Hemianopsia, binasal, 190 
bitemporal, 190 
homonymous, 193 
in brain-tumor, 475 
in hysteria, rarely, 193, 246 
in migraine, 470 
location of lesion in, 191 
method of determining, 190 
significance of, 191 
use of perimeter in determining, 191 
Hemiatrophy, facial, 33 
Hemicrania. See Migraine. 
Hemidyschromatopsia, 194 
homonymous, 194 
in hysteria, 194 
Hemihypertrophy, facial, 34 
Hemin, test for, 535 
Hemiopic pupillary inaction, 187 
Hemiplegia, anatomy of brain-areas in- 
volved in, 131 
appearance of nails in, 56 
of tongue in, 149 
bedsores in, 233 
crossed, due to bulbar lesions, 144 
diagnosis of, 140, 141 
from acute infantile paralysis, 143 
from cerebellar hemorrhage, 141 
from cerebral hemorrhage, 138 
in crus cerebri, 139 
in frontal lobe, 139 
in island of Eeil, 139 
in occipital lobe, 139 
in parietal lobe, 139 
in pons Varolii, 139 
location of lesion in, 139 
syphilis, 143 
from diffuse cerebral sclerosis of one 
hemisphere, 143 
from disseminated sclerosis, 143 
from haematoma of dura mater, 143 
gait in, 97 
hypersesthesia in, 266 
in ingravescent apoplexy, 140 
in locomotor ataxia, 143 
in paretic dementia, 144 
in purulent meningitis, 144 
in renal disease with uraemia, 144 
irregular forms of, 141 
pupillary immobility in, 180 
spastic, 142 
symptoms associated with, 138, 139, 
140 
Hemoglobin greatly decreased in chloro- 
sis, 375 
in leukaemia, 377 
of individual red blood-corpuscles 
greater than normal in pernicious 
anaemia, 375 
Hemoglobinaemia accompanied by vomit- 
ing, 533 
symptoms of, 533 
urine in, 533 596 
INDEX. 
Hemoglobinometer of von Fleischl, 370 
Hemoglobinuria, causes of, 399 
headache in, 471 
signs of, 396 
symptoms associated with, 471 
Hemometer. Sie Hsemoglobinometer. 
Hemophilia, 399 
hematemesis in, 527 
hematuria in, 399 
hemoptysis in, 542 
hemorrhage into retina in, 200 
joint-involvements in, 128 
Hemoptysis, causes of, 323, 542, 546 
diagnosis of, 528, 542 
significance of currant-jelly clots in, 
542 
Hemorrhage, anaemia in, 374 
cerebral, vomiting in, 518 
facies in, 33 
from mucous membrane in yellow 
fever, 460 
from nose in leukaemia, 378 
in typhoid fever, 447 
indicated by anxious restlessness, 20 
into brain, causing hemiplegia, 138 
ocular paralysis, 181 
diplopia a symptom of, 166 
into membranes of cord, 253 
into retina, 200 
into skin, 216 
jaundice after severe prolonged, 207 
meningeal, symptoms of, 482 
movements minute, though active 
in, 20 
pallor of face in, 26 
pulmonary diseases in which it oc- 
curs, 542 
pulse of “ empty arteries” in severe, 
360 
subdural, cause of, 490 
Hemorrhagic pleurisy, 306 
Hemorrhoids, anaemia in bleeding, 374 
blood in stools caused by, 439 
pruritus due to, 267 
Henoch’s disease, 215 
Hepatic colic, 204 
Hepatitis. See Abscess, hepatic. 
Hereditary, cerebellar ataxia, 92 
chorea, 74 
spinal ataxia, 92 
Hernia, umbilical, 338, 349 
Herpes labialis after salicylic acid, 229 
in croupous pneumonia, 29, 229 
in epidemic spinal meningitis, 
229 
zoster, 231 
Hiccough, 517 
causes of, 517 
significance of persistent, 517 
Hip-disease, character of pain in, 22, 556 
Hippocratic face, 33, 431 
succussion, 298 
Hippus, 187 
Hodgkin’s disease, enlargement of cer- 
vical lymphatic glands in, 459 
temperature in, 459 
Hunger, character of child’s cry in, 23 
Huntington’s chorea, 74, 514 
Hutchinson teeth, 158 
Hydrocephaloid disease, 511 
state, 53 
Hydrocephalus, contraction of hands and 
arms in, 72 
face in, 28 
head in, 50 
nystagmus in, 183 
open fontanelle in, 52 
spastic rigidity of arms in, 72 
Hydrochloric acid, test for, in stomach- 
contents, 344 
Hydronephrosis, 348 
Hvdropneumothorax, coin percussion in, 
305 
Hippocratic succussion in, 298 
metallic tinkling in, 296 
physical signs of, 306 
Hypersesthesia, 265 
following the use of drugs, 267 
in brain-tumor, 266 
in cerebro-spinal meningitis, 266 
in chronic alcoholism, 267 
leptomeningitis, 266 
in gout, 266 
in hemiplegia, 266 
in hysteria, 265 
in leprosy, an early sign of, 267 
in locomotor ataxia, 266 
in menopause, 266 
in neuralgia, 266 
in neurasthenia, 265 
in peripheral neuritis, 266 
in poisoning by lead and arsenic, 267 
in relapsing fever, 266 
in transverse myelitis, 266 
in typhoid fever, at convalescence, 
266 
Hyperpyrexia, causes of, 445 
Hypertrophy, cardiac, associated with 
chronic contracted kidney, in- 
crease of urine in, 394 
diagnosis of, 324 
great, force of pulse in, 362 
great, in chronic interstitial ne- 
phritis, 427 
limited bulging of chest in, 273 
symptoms and signs of, 324 
Hysteria, allochiria in, 264 
alterations of color fields in, 194 
aphonia in, 569 
bilateral anaesthesia in, 250 
borborygmi in, 122 
brachial monoplegia in, 83 
bromidrosis in, 235 
character of convulsions in, 504 INDEX. 
597 
Hysteria, character of cough in, 540 
of temperature in, 466 
contractions of hands, feet, and legs 
in, 72, 121 
diagnosis of, 503, 504 
dilated pupil in, 165 
facial spasm in, 47 
false clonus in, 567 
fatuous expression in, 30 
fever in, 466 
gait in paralysis of, 97 
gauntlet or stocking form of anaes- 
thesia in, 249 
hemiansesthesia in, 246 
hemianopsia rare in, 193 
hemidyschromatopsia in, 194 
hiccough in, 517 
hippus rare in, 187 
hysterogenous zones of hyperaesthe- 
sia in, 265 
localized sweating in, 235 
mirror-writing rare in, 79 
ocular symptoms of, 194 
pain, cutaneous in, 267 
painful joints in, 556 
paraplegia in, 112 
phantom tumor in, 349 
ptosis in, 41 
respirations in, 277 
spasm of oesophagus in, 160 
of tongue in, 157 
spontaneous gangrene of skin in, 231 
squint in, 182 
subnormal temperature in some cases 
of, 468 
tremor of hands in, 78 
visual changes in, 246 
vomiting in, 531 
Hystero-epilepsy, diagnosis of, 506 
Hysterogenous zones, 265 
TCTERUS. See Jaundice. 
1 neonatorum, 208 
urobilin, 208 
Idiocy, 50, 51 
Idiosyncrasy to drugs, 18, 215 
hsemoglobinuria of, 399 
Impetigo contagiosa, appearance of erup- 
tion in, 228 
symptoms of, 228 
Incontinence of urine, ammoniacal odor 
in, 18 
due to concentrated urine, 390 
due to excessive reflex irritation 
of bladder walls, 390 
due to insensitive urethra, 390 
due to loss of power of sphinc- 
ter, 390 
erythema of thighs in, 223 
nocturnal, in children, 390 
trousers stained in, 18 
Incubation-period of eruptive diseases? 
220 
Indicanuria, diseases in which it occurs, 
401 
in intestinal obstruction due to im- 
paction, 525 
test for, 400 
Indigestion, anaemia in chronic, 374 
character of respiration of child 
with, 24 
erythema in, 218 
headache associated with, 470 
muscae volitantes in severe, 200 
retraction of head in neurotic chil- 
dren with, 49 
vertigo in, 484 
Infantile remittent fever, 459 
spinal paralysis. See Anterior poli- 
omyelitis. 
Infarction, renal, blood-casts in, 403 
Influenza, epidemic, cardiacfailurein, 463 
catarrhal symptoms of, 463 
character of fever in, 463 
of sputum in, 543 
complications of, 463 
diarrhoea, 463 
differential diagnosis from den- 
gue, 460 
great prostration in, 463 
haematemesis in, 527 
hyperaesthesia in, 267 
ocular palsy in, 175 
pain in back in early stages of, 
561 
vomiting in, 463 
Ingravescent apoplexy, 140 
Injury, expression of anxiety after severe, 
27 
iritis due to, 200 
spinal, knee-jerk decreased imme- 
diately after, 564 
Insomnia in Malta fever, 451 
Inspection of chest, 268 
of abdomen, 329 
Insufficiency of convergence in exoph- 
thalmic goitre, 165 
Intention-tremor of cerebral palsy of 
children, 71 
Intestinal obstruction, 347 
albumin in urine in, 524 
constipation in, 430 
due to cancer or stricture, 525 
due to impaction of foreign body, 
indicanuria in, 524, 525 
symptoms of, 524, 525 
vomiting in, 524 
due to intussusception, blood- 
stained mucous evacua- 
tions of children in, 521 
detection of tumor in, 521 
distention of abdomen in, 598 
INDEX. 
Intestinal obstruction due to intussuscep- 
tion, inequality of shape 
of abdomen in, 522 
pain, character of, in, 520 
patulous condition of anus 
in, 521 
symptoms of chronic, 522 
tenesmus in, 521 
vomiting early in, in invag 
ination, 520 
due to completeness of 
obstruction, 520 
due to strangulation by bands, 
523 
characterof constipation in, 
523 
of localized tenderness 
and percussion-dul- 
ness in, 523 
of pulse in, 523 
of vomiting in, 523 
due to strangulation by bands, 
Meckel’s diverticulum a 
cause of, 524 
pain in, 523 
temperature in, 523 
tympanitic distention in, 
523 
urine diminished in, 524 
due to volvulus, vomiting not a 
constant symptom of, 524 
hiccough in, 517 
indicanuria in, 401 
Iritis due to injury, 200 
due to rheumatism, 200 
due to syphilis, 200 
headache due to, 472 
immobile pupil in, 165 
1AUNDICE, 202 
J albumosuria in, 420 
bradycardia in. 325 
catarrhal, 204 
cause of, 207 
complicating diabetes, 206 
of constipation occurring in,429 
of hsematogenous, 207 
of hepatogenous, 202 
Charcot’s fever in, 206 
color of urine, 207, 400 
diabete bronze in, 206 
fatty diarrhoea in, 437 
haematogenous, 207 
headache in, 471 
hepatogenous, 202 
in acute phosphorus poisoning, 205 
yellow atrophy, 207 
in amyloid liver, 205 
in chronic valvular heart disease, 
205 
in cirrhosis of liver, 205 
Jaundice in malignant disease, 206 
in new-born, 208 
in pressure from aneurism, 205 
in remittent malarial fever, 459 
in Weil’s disease, 205 
in yellow fever, 205 
method of examining for, 202 
obstructive, 204 
persistent and progressive in carci- 
noma of pancreas, 345 
pruritus in, 267 
purpuric eruption in severe, 215 
stools in, 207 , 208 
symptoms of catarrhal, 203 
of hepatogenous, 206 
urine in, 207 
vomiting in, 532 
Joints, alterations of, in locomotor ataxia, 
124 
different modes of infection of, in 
gonorrhoeal arthritis, 126 
enlargement of, in rheumatoid ar- 
thritis, 125 
hypertrophic osteo-arthritis, follow- 
ing typhoid fever, 128 
in acute epiphysitis of infancy, 126 
synovitis, 127 
in central myelitis, 125 
in cerebro-spinal meningitis, 125 
in chronic lead-poisoning, 127 
in dengue, 128 
in epidemic dysentery, 128 
in gout, 127 
in haemophilia, 128 
in milk-leg, 128 
in osteomyelitis, 126 
in rheumatoid arthritis, 125 
septic, 126 
in scarlet fever, 128 
in Sclionlein’s disease, 128 
involvement of, with fever, in osteo- 
myelitis, 466 
in purpura, 466 
in pyaemia, 466 
small, affected in Morvan's disease, 
126 
in syringomyelia, 126 
violent pain on motion of, in Malta 
fever, 451 
Jumpers, the. See Saltatoric spasm. 
KIDNEY, blood-casts in acute inflam- 
mation of, 403 
character of blood in urine from, 395 
fatty casts in fatty degeneration of, 
405 
floating, 336, 347 
haematuria due to stone in, 398 
hydronephrosis, 348 
irritation of, cylindroids found in, 
406 INDEX. 
599 
Kidney, septic infection of, casts of mi- 
crococci in, 404 
slow degeneration of parenchyma of, 
granular casts in, 404 
Klumpke’s paralysis, 85 
Knee jerk, diseases in which decreased, 
564 
in which increased, 565 
how best elicited, 563 
reinforced, 563 
1 A GRIPPE. See Influenza. 
Jj Lactic acid, test for, in stomach con- 
tents, 344 
Landouzy Dejerine type of muscular atro- 
phy, 31 
Landry’s paralysis, diagnosis of, 467 
loss of knee-jerk in, 564 
loss of reflexes, predominant 
symptom of, 467 
non-spastic paraplegia in, 104 
Laryngeal crisis in locomotor ataxia, 89 
paralysis, table showing causes of, 
569 
spasm, 309 
Laryngitis, night-cough in, 540 
par tial or com plete loss of voice in, 539 
short, sharp, brassy cough in, 539 
whispering voice in, 568 
Laveran, malarial germ of, 379 
Leprosy, appearance of hands in, 64 
gangrene in, 64 
leonine face of, 32 
patches of anaesthesia in, 263 
Leptomeningitis, diagnosis of coma in 
purulent, 491 
hyperaesthesia in chronic, 266 
Leucocythaemia. See Leukaemia. 
Leucocytosis, 377 
in pneumonia and other infectious 
diseases, 377, 378 
Leucoderma in goitre, 211 
Leucokeratosis, 153 
Leukaemia, lymphatic, enlargement of 
superficial Ivmph glands in, 
378 
lymphocytes alone increased in, 
378 
spleno-medullary, blood in, 377 
enlargement of spleen in, 
353, 378 
symptoms of, 378 
Lichen pianus, appearance of tongue in, 
153 
ruber, appearance of nails in, 56 
Lineae albicantes, 329 
Lips, blueness of, in heart disease, 323 
fulness of, in persons of strong sexual 
appetite, 26 
indicating phlegmatic tempera- 
ment, 26 
Lips 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 peri- 
tonitisor pain below diaphragm, 28 
Lithsemia, cylindroids in urine in, 406 
Liver, acute yellow atrophy of. See Yel- 
low atrophy, acute, 
causes of tenderness of, 351 
enlarged, position in, 20 
and smooth, in amyloid disease, 
351 
of kidney, 427 
enlargement of, 335 
headache in congestion of, 470 
indicanuria in cancer of, 401 
nodules and umbilication of, in ma- 
lignant disease of, 351 
percussion note over, 349 
pushed down by right-sided pleural 
effusion, 352 
rough, in cirrhosis, 351 
swelling of, in Weil’s disease, 460 
symptoms of cirrhosis of, 352 
of malignant disease of, 352 
of tropical abscess of, 351 
Localization of functions of segments of 
spinal cord, 109 
Locomotor ataxia, 89 
allochiria in, 264 
alteration of joints in, 124 
anaesthesia of lower portion of 
body and of legs in, 251 
analgesia in, 251 
Areyll-Robertson pupil in, 89, 
185 
athetoid movements in ad- 
vanced, 79 
bilateral atrophy of tongue in, 
154 
bladder-symptoms of, 391 
blunted and delayed sensation 
in, 251 
brachial monoplegia in, 84 
cardiac feebleness in, 326 
coffee ground vomit in gastric 
crisis of, 527 
contracted pupil in, 165 
cutaneous hemorrhages in, 216 
diagnosis of, 565 
diarrhoea as an intestinal crisis 
of, 433 
differential points between 
Friedreich’s ataxia and, 89 600 
INDEX. 
Locomotor ataxia, diplopia in, 41 
double sciatic pain in, 556 
flat-foot in, 120 
gait of, 88, 91 
cause of, 88 
gastric crisis of, 89 
girdle-sensation in, 265 
hemiplegia in, 143 
hyperaesthesia in, 266 
inability to use fingers and hands 
in, 79 
laryngeal crisis of, 89 
spasm in, 310 
lesion of optic nerve in, 198 
loss of knee-jerk in, 564 
muscular atrophy of arm in, 84 
numbness of feet in, S9 
nystagmus in advanced, 183 
ocular symptoms of, 198 
optic atrophy in, 198 
pain in, 550, 556 
of skin in, 267 
paraesthesia in, 263 
paraplegia in, 110 
perforating ulcer in, 129 
ptosis in, 41 
retention of urine in, 390 
Romberg’s symptom of, 89 
swaying of body with eyes closed 
in, 89 
syphilis a frequent cause of, 90 
table of symptoms of, 89 
thoracic pain in, 554 
twitching of fingers in, 79 
vesical crisis of, 89 
Westphal’s sign of, 89 
Lordosis in cretinism, 32 
in progressive muscular atrophy, 69 
Lumbago, pain in, 555, 561 
Lyons’ method of estimating urea, 420 
Lysis, fever in erysipelas ending by crisis 
or, 455 
in scarlet fever, ending by, 452 
in smallpox, ending by, 454 
in typhoid, ending by, 446 
in catarrhal pneumonia, 464 
rare in croupous pneumonia, 464 
Macula lutea, 197 
Maddox’s rod-test, 168 
Madura foot, 65, 129 
Main-en griffe, 66 
Malaria, anaemia in, 376 
aortitis rare in, 554 
blood in, 355, 368 
brow-ague in, 552 
Chenzynski’s solution for staining 
organisms of, 383 
Cheyne-Stokes breathing in haema- 
turic, 278 
coma in, 489 
Malaria, convulsions due to, 502 
enlargement of spleen in, 353 
haematemesis rare in, 527 
haematuria in, 397 
haemoglobinuria in, 399 
headache in, 483 
intermittent, attacks occurring earlier 
• each day in, 456 
characteristic of fever, quartan, 
456 
quotidian, 455 
tertian, 456 
chill, fever, and sweats in, 455 
diagnosis of, 456 
effect of quinine on, 456 
method of examining organism of, 
382 
of staining organism of, 383 
muddy yellow skin in chronic, 209 
parasite of sestivo-autumnal, 381 
of quartan, 380 
of tertian, 379, 381 
remittent, bilious vomiting in, 459 
character of fever in, 459 
diagnosis between typhoid fever 
and, 450 
between yellow fever and, 
461 
due to sestivo-autumnal parasite, 
459 
jaundice in, 459 
sweating in, 235 
synonyms of, 459 
retinal hemorrhage in, 200 
roseola in, 220 
Malarial germ of Laveran, 379 
Malignant pustule. See Anthrax, malig- 
nant. 
Malingering, convulsions in, 510 
hsematemesis in, 527 
inability to ape facies of disease in, 
27 
merycismus in, 534 
sciatica in, 557 
Malta fever, anorexia in, 451 
character of fever in, 451 
frequency of relapse in, 451 
headache in, 451 
insomnia in, 451 
pain on motion in, 451 
Mammary gland, enlargement of, in pul- 
monary tuberculosis, 276 
Marasmus, sinking in of fontanelle in, 53 
Measles, character of fever in, 453 
date of eruption in, 219 
diazo-reaction in urine of severe, 425 
persistence of fever in, due to bron- 
chial or gastro-duodenal catarrh, 
453 
rash of, 218 
on pharynx and buccal mucous 
membrane, 162 INDEX. 
601 
Menstruation, disorders of, in chlorosis, 
375 
haematemesis as vicarious, 527 
haemoptysis as vicarious, 542 
Merycismus, 534 
Metallic tinkling heard over chest, in 
cavity, 296 
over hydropneumothorax, 
296 
over stomach, 296 
Microblasts, 375 
Microcephalus, 51 
head in, 50 
Migraine, haemianopsia in, 470 
hyperaesthesia in, 266 
muscae volitantes in, 200 
scotamata in, 533 
sweating of head in, 235 
symptoms of, 552 
vomiting in, 533 
Miliaria, 236 
Milk-leg, joints in, 128 
Mirror-writing, 79 
Miscarriage, a symptom of syphilis, 21 
Mitral disease, 314 
Moebius’s sign, 165 
Mono-anaesthesia, 248 
Monoplegia, 81, 114 
Morbilli. See Measles. 
Morphoea as a cause of facial haemi- 
atrophy, 34 
Morton’s painful toe, 561 
Morvan’s disease, 69 
gangrene of hands in, 65 
hand similar to claw hand in, 
69 
small joints affected in, 126 
Mouth, chapter on, 145 
constant opening of, in heart disease, 
29 
dryness of, in paralysis of salivary 
glands, 36 
pigmentation of, 326 
Mouth-breathers, 29 
nasal twang of voice in, 569 
Mowing gait, 97 
Mucous patches about mouth and anus in 
infantile syphilis, 28 
immobility of lips due to, 29 
Multiple sclerosis. See Sclerosis, dissemi- 
nated. 
Mumps, albumosuria in, 420 
enlarged parotid glands in, 54 
Murmur, aortic regurgitant, 319 
capillary pulsation in, 324 
Corrigan’s pulse in, 320, 
324 
dyspnoea in, 323 
ox-heart in, 320 
pulsation of retinal arteries 
in, 324 
pulse-wave of, 360 
Measles, symptoms of, 219 
Meckel’s diverticulum, 524 
Mediastinal growths, bulging of chest in, 
273 
caput Medusae in some cases of, 
335 
diagnosis of, from abscess, 311 
from aneurism, 310 
from chronic pneumonia, 
312 
from pericarditis, 312 
from pleural effusion, 311 
dysphagia in, 157 
hoarseness of voice due to press- 
ure by, 568 
laryngeal cough due to pressure 
on larynx by, 539 
pain in, 555 
signs and symptoms of, 310 
Megaloblasts, called corpuscles of Ehr- 
lich, 375 
in pernicious anaemia, 375 
Megrim. See Migraine. 
Melaena neonatorum, causes of, 528 
vomiting in, 528 
Melancholia with oxyluria, diagnosis of, 
408 
Meniere’s disease, symptoms of, 484 
vomiting following tinnitus au- 
rium and vertigo in, 532 
Meningitis, albumosuria not present in 
tubercular, 420 
basilar, lesions causing ocular paral- 
ysis in, 175 
papillitis in, 198 
bilateral anaesthesia in, 250 
loss of knee-jerk, 564 
bulging fontanelle in purulent, 53 
cerebro-spinal. See Cerebro-spinal 
meningitis. 
contracted pupil in, 165 
contraction of hand in, 72 
diplopia in, 166 
facial spasm in, 46, 47 
hippus in early stages of acute, 187 
hyperaesthesia in cerebro-spinal, 266 
nystagmus occasionally in, 183 
occipital headache in, 519 
pain in nape of neck in, 519 
piercing cry in, 23 
pseudo-, 511 
purulent, hemiplegia in, 144 
reflexes in, 564 
rigidity of dorsal muscles in, 519 
scaphoid belly in tubercular, 330 
subnormal temperature in some cases 
of, 468 
symptoms of, 478 
tache cerebrate in, 216 
vomiting in, 519 
Menstruation, anaemia due to profuse, 374 
dark areas under eye during, 26 INDEX. 
602 
Murmur, aortic regurgitant, short and 
sharp pulse in, 359 
symptoms of, due to failing 
compensation, 323 
water-hammer pulse in, 320 
stenosis, 319 
small and hard pulse in, 
359 
symptoms of, due to failing 
compensation, 323 
haemic, over fontanelle in rickets, 53 
humming-top, in jugular vein in 
chlorosis, 376 
mitral regurgitation, 314 
small volume of pulse in, 
359 
symptoms of, due to failing 
compensation, 323 
thrill in, 315 
stenosis, 316 
gallop-rhythm in, 316 
pulse-wave of, 360 
small volume of pulse in, 
359 
symptoms of, due to failing 
compensation, 323 
thrill in, 316 
pulmonary regurgitation, 321 
stenosis, 321 
splenic, in leukaemia, 378 
tricuspid regurgitation, 321 
stenosis, 321 
Murmurs, relative frequency of associated, 
321 
gravity of, 322 
venous, in anaemia, 375 
Muscae volitantes, 200 
Muscle-tone, 563 
Muscles, contraction of, in paramyoclonus 
multiplex, 74 
in electric chorea of Bergeron, 
74 
in Huntington’s chorea, 74 
in “jumpers,” 74 
intraocular, 183 
shock-like, in Dubini’s disease, 
74 
Muscular atrophy, arthritic, 122 
idiopathic. See Atrophy, idiopathic 
muscular. 
Mutism, hvsterical, 568 
Myalgia, pain in, 555 
Mycetoma, 65, 129 
swelling of hand followed by rupture 
in, 65 
Myelitis, acute ascending, bedsores in, 
233 
character of fever in, 467 
symptoms of, 105, 467 
transverse, allochiria in, 264 
anaesthesia in, 252 
bilateral anaesthesia in, 251 
Myelitis, acute transverse, bladder symp- 
toms of, 390 
collateral symptoms of, 392 
diagnosis of cervical, dor- 
sal, and lumbar, 108 
effect of lesion in, 106 
girdle-sensation in, 101, 265 
hyperaesthesia in, 266 
knee jerk in, 564, 566 
location of lesion in, 107 
non-spaotic paraplegia in, 
104 
paresthesia in, 263 
sensory paralysis in, 101 
spastic paraplegia in, 101 
chronic, gait of, 94 
subacute, symptoms of, 106 
traumatic, retention of urine in, 390 
Myelocyte of Ehrlich, in spleno-medul- 
lary leukaemia, 377 
Myoclonus multiplex, 74 
Myosis in facial hemiatrophy, 34 
Myotonia congenita, 75, 503 
Myxoedema, diagnosis between dropsy 
and, 236 
enlargement of feet in, 117 
of tongue in, 155 
face of, 32, 35 
skin in, 239 
spade-like hand in, 65 
symptoms of, 239 
NAILS, appearance of, in anaemia, 56 
in chloral-habit, 57, 229 
in eczema, 56 
in gout, 56 
in hemiplegia, 56 
in lichen ruber, 56 
in prolonged illness, 56 
in psoriasis, 56 
in pulmonary osteo-arthropathy, 
56 
in Raynaud’s disease, 56 
in sclerodactyle, 56 
in syphilis, 56 
appearance of, in syringomelia, in- 
jury, or neuritis, 56 
atrophy of, 56 
hypertrophy of, 56 
white spots on, 56 
Neck, spasm of the muscles of the, 47, 48 
Nephritis. See also Kidneys and Bright’s 
disease. 
acute, diarrhoea in, 433 
diffuse, anaemia in, 426 
anasarsa in, in children, 426 
heart slightly dilated in, 426 
high arterial tension in, 426 
nausea and chilly sensations 
preceding, 425 
prognosis of, 426 INDEX. 
603 
Nephritis, acute diffuse, puffiness of face 
about eyes in, 426 
pulse hard and tense in, 426 
skin harsh and dry in, 426 
symptoms and signs of, 425 
urine in, 426 
hemorrhagic effusions into 
pleura in, 306 
irritation of bladder in, 392 
parenchymatous, decrease of 
urine in, 394 
epithelial casts in urine a 
positive sign of, 403 
fever in, 465 
symptoms of, 465 
chronic hemorrhagic, hsematuria in, 
398 
interstitial, albumin transient 
in, 427 
atheroma of bloodvessels in, 
427 
chronic bronchitis in, 427 
diagnosis between brain 
tumor and, 475 
dropsy rare in, 427 
excess of uric acid in urine 
often antedates, 408 
frequency of urination in, 
426 
headache in, 473 
heart markedly hypertro- 
phied in, 427 
high tension of pulse in, 427 
hyaline casts in urine of, 
405 
low specific gravity of urine 
in, 394 
nocturnal urination in, 426 
pruritus in, 267 
pulmonary oedema in, 427 
shortness of breath most 
marked at night in, 427 
parenchymatous, decrease of 
urine in, 394 
heart somewhat hypertro 
phied in, 427 
marked tendency to ana- 
sarca in, 426 
prognosis in, 426 
uraemic vomiting and coma 
may occur in, 426 
Nervous bladder, 393 
Neuralgia, causes of, 551 
due to lead- or arsenic-poisoning, 552 
due to malaria, 552 
hyperaesthesia in, 266 
intercostal, causes of, 553 
pain in, 553 
spots of Valleix in, 553 
Morton’s painful toe in, 561 
occipital, causes of, 553 
diagnosis of, 553 
Neuralgia, occipital, pain in, 553 
oedema in, 238 
of fifth nerve, infra-orbital, symp- 
toms of, 552 
third division, symptoms 
of, 552 
upper branch, symptoms of, 
552 
of foot, 561 
of head, due to decayed teeth, 551 
due to diseased ear, 551 
due to overstrained eyes, 551 
in anaemic, overworked women, 
551 
of labia majora or perineum, 555 
of pelvic viscera in women, 555 
pain in, 551 
supraorbital, diagnosis of, from neu- 
ritis, 552 
Neurasthenia, headache in, 472 
hyperaesthesia in, 265 
knee jerk increased in, 565 
paraesthesia in, 264 
vomiting in, 532 
Neuritis, acute multiple, character of 
fever in, 467 
knee-jerk lost in, 565 
symptoms and signs of, 467 
anaesthesia in toxic peripheral, 258 
in 50 per cent, of diphtheritic, 
258 
as a cause of anaesthesia, 257 
claw-hand in peripheral, 67 
diagnosis of, 565 
diphtheritic, 258 
general anasarca in multiple periph- 
eral, 237 
hypera-sthesia in peripheral, 266 
in foot, leg, and thigh, distribution 
of anaesthesia in, 260 
in hand, distribution of anaesthesia 
in, 250 
optic. See Papillitis, 
retro-bulbar, 198 
sciatic, diagnosis of, 556 
limping gait of, 87 
pain in, 555 
symptoms of, 555 
tender joints in, 556 
toxic peripheral, 258 
Neuroma, character of pain in, 561 
Neutrophile corpuscles, 372, 377 
Nictitating spasm, 46 
Nodding spasm, 47 
Noma, 160 
Nose, anaemia due to hemorrhage from, 
374 
asthma due to reflex irritation in, 
309 
broad and flat, in cretinism, 32 
broadness of bridge of, an indication 
of congenital syphilis, 28 604 
INDEX. 
Nose, dilated, in heart disease, 29 
hemorrhage from, in leuksemia, 378 
obstruction of, in mouth breathers, 
29 
pinched and drawn, indicating pain 
in chest in children, 28 
Nystagmus, 182 
in acute meningitis, 183 
in children otherwise normal, 183 
with imperfect vision, 183 
in disseminated sclerosis, 183 
in epilepsy, 183 
in Friedreich’s ataxia, 183 
in growths in cerebellum or pons, 183 
in hydrocephalus, 183 
in locomotor ataxia, advanced, 183 
in multiple sclerosis, 183 
OBERMEIER, spirillum of, 452 
Obstruction, intestinal. See Intes- 
tinal obstruction, 
of the rectum, 525 
symptoms of, 525 
Occupation-spasm, 73 
Oculo-facial paralysis, 45 
(Edema. See also Dropsy and general 
anasarca, 
localized, 237 
neonatorum, 240 
pulmonary, absence of fever in, 303 
character of sputum in, 303 
crepitant and bubbling rales in, 
295 
due to acute disease of lungs, 303 
due to injury of vagus, 303 
dulness on percussion in, 303 
feeble, hesitating speech in se- 
vere, 570 
frothy sputum in, 303 
in chronic interstitial nephritis, 
427 
(Esophagus, cancer of, 160 
diverticulum of, 160 
hysterical spasms of, 160 
stricture of, 159, 535 
causes of, 160 
diagnosis of, 159, 535 
dysphagia in, 535 
Oligochromsemia, 364 
Oligocythsemia, 363 
Onychogyrophosis, 56 
Ophthalmoplegia, 40 
Ophthalmoscopy, 194 
Opisthotonos in hysteria, 504 
in severe meningitis, 519 
Opium-poisoning, 486 
differential diagnosis between 
poisoning from alcohol and, 
487 
Optic atrophy, 198 
nerve, 194 
Optic neuritis, 197 
Orthophoria, 168 
Osteitis deformans, head in, 50 
of cranial bones, headache in, 
483 
triangular face of, 35 
Osteomalacia, gait of, 98 
Osteomyelitis, acute, arthritis in, 126 
joint involvement with fever in, 
466 
Osteophytes, formation of, in rheumatoid 
arthritis, 125 
Otitis in scarlet fever, 452 
media, connected with thrombosis of 
cavernous sinus, 480 
diagnosis between cerehro spinal 
meningitis and, 461 
vertigo in, 484 
Ovaritis, character of pain in, 560 
Oxaluria accompanying spermatorrhoea, 
409 
concomitant symptom of melan- 
cholia, 408 
cylindroids in urine of, 407 
due to ingestion of pears, cabbage, 
and tomatoes, 409 
Oxyuris vermicularis, 442 
PAIN below diaphragm, twitching of 
upper lip in, 30 
best manner of discovering true seat 
of, 22 
bilateral, of rheumatism of scalp, 552 
burning, in oesophagus, stomach, and 
abdomen in phosphorus poisoning, 
528 
causes of circumscribed abdominal, 
557 
in back in children, 555 
in neighborhood of heart, 553 
in sacral region, 555 
neuralgic, 551, 553 
sciatic, 555, 556 
supraorbital neuralgic, 552 
colicky, extending to right shoulder 
in acute pancreatitis, 528 
in embolism of superior mesen- 
teric artery, 528 
concomitant symptoms of abdom- 
inal, 22 
crisis of, in tabes, 89 
darting, in urethra, in cystitis, 392 
distribution of, in neuralgia of fifth 
nerve, 552 
expression about eyes in children 
due to, 28 
of face due to, 28 
in abdominal colic, 557 
in acute aortitis, 554 
bellyache, 20 
pleurisy, 304, 555 INDEX. 
605 
Pain in aneurism, 318 
in angina pectoris, 554 
in back, causes of, 561 
in cerebral tumor or abscess, 552 
in chest in aortic aneurism, 554 
in coxalgia, 22, 556 
in dengue, 562 
in diabetes mellitus, 560 
in dysmenorrhoea, 560 
in entero-colitis, 433 
in fecal impaction, 558 
in fissure of the anus, 561 
in gastralgia, 557 
in gastric cancer and ulcer, 557 
in hsemoglobinsemia, 533 
in head in children, 28 
in hepatic colic, 558 
in intercostal neuralgia, 555 
in intestinal obstruction, 520, 521 
in intussusception, 420 
in jaundice, due to gallstones, 204 
in lead-colic, 558 
in locomotor ataxia, 554, 559 
in lumbar region, due to perinephritic 
disease, 389 
due to pyelitis, 389 
due to stone in kidney or 
ureter, 389 
in mediastinal growths, 555 
in meningeal hemorrhage, 482 
in migraine, 552 
in neuralgia of foot, 561 
of head, 551 
of pelvic viscera, 555 
in neuromata, 561 
in occipital neuralgia, 553 
in one side of head, in migraine, 552 
in pancreatitis, 561 
in peritonitis, 560 
in pseudo-angina pectoris, 554 
in pulmonary diseases in children, 22 
in renal calculus, 557 
colic, 557 
in skin in tabes dorsalis or hysteria, 
267 
in syphilitic periostitis of skull, 552 
often referred to point distant from 
its source, 551 
significance of, 550 
signs of, 551 
summary of conditions producing 
acute, sudden, 559 
tearing, burning, in hemorrhage 
into membranes of cord, 253 
thoracic, in locomotor ataxia, 554 
throbbing, in inflammation, 550, 561 
varieties of, 550 
Pallor of face in advanced stage of acute 
alcohol poisoning, 485 
in chlorosis, 26, 211, 375 
in fright, 26 
in hemorrhage, 26 
Pallor of skin in absence of pigment, 
213 
in anaemia, 375 
in vasomotor disturbance, 211 
in vitiligo, 211 
Palmus, 74 
Palsy, cerebral, of children, 70 
Pancreas, abscess of, 346 
carcinoma of, 345 
cysts of, 345 
fatty diarrhoea due to disease of, 437 
hemorrhagic inflammation of, 346 
inflammation of, 346 
symptoms of, 528, 561 
vomiting in, 528 
Papillitis, 197 
in acute febrile disorders, 198 
in anaemia, 198 
in brain-tumor, 198, 474 
in cerebral abscess, 198 
in meningitis, 198 
tubercular, 198 
in rheumatism, 198 
in syphilis, 198 
in toxaemia from alcohol, 198 
from lead, 198 
Paraesthesia. See also Allochiria. 
from exposure to carbolic acid, 264 
in aconite poisoning, 264 
in brain-tumor, 263 
in cocaine intoxication, 264 
in locomotor ataxia, 263 
in myelitis, 264 
in neurasthenia, 264 
in spinal syphilis, 263 
Paralysis agitans, gait in, 97 
Parkinsonian visage in, 30 
speech and voice in, 571 
tremor of hands in, 76 
wasting, rigidity, and flexion of 
hands in, 70 
asthenic bulbar, 44 
diagnosis between progressive 
bulbar paralysis and, 45 
speech of, 570 
bilateral facial, 44 
in acute bulbar paralysis, 44 
in bilateral inflammation at 
stylo-mastoid foramen, 44 
in bilateral lesion of cere- 
brum, 44 
in bilateral lesion of pons, 
due to disease of basilar 
artery, 44 
in cold or double otitis, 44 
in diphtheritic multiple 
neuritis, 44 
in lesion of pons, 44 
in progressive bulbar paral- 
ysis, 44 
in syphilis at base of brain, 606 
INDEX 
Paralysis, bilateral facial, in toxic peri- 
pheral neuritis, 44 
bulbar, 44 
cerebral, acute infantile, causing 
hemiplegia, 143 
deformity of foot in acute, 121 
diagnosis between paralysis of 
leg in, and poliomyelitis, 
116 
between hereditary spastic- 
paralysis and, 101 
between spinal paralysis 
and, 121 
epileptic convulsions in, 101 
gait of infantile, 95 
mirror-writing in, 79 
movements of hand in, 78 
spastic paraplegia in, 100 
due to myelitis, 105 
due to tumor of brain, 474 
glosso - labio - pharyngeal, bilateral 
atrophy of tongue in, 154 
biting the tongue in, 152 
cardiac feebleness coming on 
suddenly in, 326 
cough in, 540 
diagnosis of, 570 
dysphagia in, 159 
faulty movements of tongue in, 
155 
fibrillary tremor of tongue in, 
157 
indistinct speech of mumbling 
character in, 570 
hereditary spastic, 101 
infantile spinal. See Poliomyelitis, 
anterior. 
laryngeal, causes of, 569 
oculo-facial, 45 
of bladder with retention, due to 
pressure during childbirth, 390 
of diaphragm, causes of, 541 
cough in, 541 
of intraocular muscles, 183 
of muscles of jaw, 39 
of ocular muscles, 167 
causes of conjugate lateral, 
181 
due to acute or chronic 
lesions of nuclei, 170,175 
due to basilar lesions, 170 j 
due to hemorrhage of cere- 
bral cortex, 175 
due to lesion of nerve- 
trunks, 170, 176 
between cortex and nu- 
clear origin of nerve, 
170, 175 
due to poison, 170, 175 
due to sclerosis of cerebral 
cortex, 175 
Maddox’s rod-test for, 168 
Paralysis of ocular muscles, method of 
determining individ- 
ual muscles involved 
in, 170 
of determining partial, 
168 
significance of conjugate, 
lateral, 181 
signs of, 170 
symptoms of thrombosis of 
cavernous signs causing, 
181 
varieties of, location of le- 
sion in, 176 
of salivary glands, causing dryness 
of mouth, 36 
progressive bulbar, 44 
causing paralysis of muscles 
of mastication, 39 
diagnosis between asthenic 
bulbar paralysis and, 45 
recurrent, of oculomotor nerve of 
one side, 43 
sometimes found instead of occupa- 
tion-spasm, 73 
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, 39 
caused by exposure to cold, 
35 
by fracture at base of 
skull, 36 
by hemorrhage from 
cerebellum, 36 
by hysteria, 36, 38 
by inflammation of 
nerve-sheath atstylo- 
mastoid foramen, 35 
by injuries, 35 
by otitis media, 35 
by pressure of forceps, 
36, 37 
of growth at base 
of skull, 36 
by swelling of parotid 
gland, 36 
difficulty of whistling and 
pronouncinglabial sounds 
in, 35 
in crossed paralysis, 39 
in syphilitic arteritis caus- 
ing other paralyses, 39 
location of cause of, 36 
nerve-degeneration in pe- 
ripheral, 36 
peculiar distribution of, in 
some cases, 37 INDEX. 
607 
Paralysis, unilateral facial, power of 
closing eye and wrinkling 
forehead remains in cere- 
bral form of, 36 
prognosis of, when due to 
pressure by forceps, 37 
reactions of degeneration in, 
caused by tumor involv- 
ing facial fibres below or 
destroying facial nucleus, 
36 
Paralytic squint, 167 
Paramyoclonus multiplex, 74 
diagnosis of, 515 
Paramyotonia, 75 
Paraplegia, 99 
ataxic, 94 
knee-jerk exaggerated in, 566 
causes of, 99 
hysterical, knee-jerk exaggerated in, 
566 
non-spastic, in acute transverse mye- 
litis, 104 
in chronic transverse myelitis, 
107 
in compression from fracture or 
dislocation of vertebrae, 112 
in diabetes mellitus, rarely, 114 
in hemorrhage into the spinal 
cord or its membranes, 103 
in hereditary spastic paralvsis, 
101 
in injury of the cord or myelitis, 
triple phosphates in urine of, 
410 
in Landry’s paralysis, 104 
in locomotor ataxia, 110 
in neuritis, 113 
in poliomyelitis, 111 
in polyneuritis, 104 
in subacute transverse myelitis, 
106 
in tumor of cord or membranes, 
112 
partial, following diphtheria, 
113 
pseudo-, in rickets, 113 
in scorbutus in infancy, 113 
of rickets, 100 
reflex, 112 
spastic, 100 
in arrested development, 100 
in rickets, 100 
in spinal lesions, 101 
pachymeningitis, 103 
syphilis, 103 
Parasites, anaemia due to ankylostomum 
duodenale, 376, 442 
due to tapeworm, 376, 442 
intestinal, ankylostomum duodenale, 
442 
ascaris lumbricoides, 442 
Parasites, intestinal, bothriocephalus 
latus, 441 
oxyuris vermicularis, 442 
taenia cucumerina, 442 
mediocanellata, 440 
solium, 440 
trichocephalus dispar, 442 
of lung, distoma pulmonum, 546 
echinococcus, 546 
of malaria, aestivo-autumnal, 381, 
382 
quartan, 380, 382 
tertian, 379, 381, 382 
of urine, distoma haematobium, 398 
tilaria sanguinis hominis, 384 
Paresis, general, delusions of grandeur 
in, 392 
diagnosis of coma of, 492 
diplopia a symptom of, 166 
fine intention-tremor in, 91 
gait of, 91 
Jacksonian epilepsy in, 495 
spasm of tongue in, 157 
tremor of hands in, 78 
vesical symptoms of, 392 
Parkinsonian visage, 30, 514 
Paronychia, 56 
Parotitis in pyaemic fever, 54 
in typhoid fever, 54, 451 
in typhus fever, 54 
in ulcerative endocarditis, 451 
Pectoriloquy over cavity connected with 
a bronchial tube, 298 
Peliosis rheumatica. See Purpura. 
Pemphigus, eruption of, 230 
Percussion-note, cracked-pot sound, 285 
coin-test in hydropneumothorax, 305 
dull, in consolidation of lung in 
pneumonia, 284 
in pulmonary congestion, 303 
oedema, 303 
flat, over liver, 349 
over pleural effusion, 286 
method of eliciting, 282 
normal, 283 
tympanitic, in lung, due to collapse 
or adhesion of lung, 284 
'due to consolidation, 284 
due to large cavity, 284 
due to pneumothorax, 284 
Pericarditis, pain in, 555 
with effusion, diagnosis of, 312 
bulging of chest in, 273 
displaced apex-beat in, 281 
signs and symptoms of, 289 
Peristaltic waves, 322 
Peritonitis, character of pain in, 339, 560 
drawing up of limbs to relieve pain 
in, 339 
expression of anxiety in, 27, 30 
fever in, 525 
hiccough in, 517 608 
INDEX. 
Peritonitis, indicanuria in, 401 
muscular rigidity in, 339 
position of body and head in, 20 
retraction of abdominal wall with 
pain in, 330 
small, wiry pulse in, 359 
symptoms of acute, 339, 560 
vomiting in, 525 
Perityphlitis, pain in, 560 
Petechise from drugs, 216 
in acute ulcerative endocarditis, 216 
in cerebro-spinal meningitis, 216 
in scurvy, 216 
in septicaemia, 216 
in snake-bite, 216 
in typhus fever, 452 
in wasting, 216 
Petit mal. See Epilepsy, minor. 
Phantom tumor, 349 
Pharyngitis, associated with stomach- 
cough, 540 
simple acute, not to be confounded 
with scarlet fever or measles, 162 
symptoms of acute, 162 
Phlebitis, fever in, 456, 458 
Phlegmasia alba dolens, 239 
oedema in, 239 
Phloroglucin-vanillin test, 344 
Phosphaturia, headache associated with, 
473 
Phthisis. See also Tuberculosis, 
alar chest of, 271 
cause of night-cough in, 540 
character of cough in laryngeal, 539 
of sputum in, 543 
diminished expansion of chest in, 
279 
facial expression in acute, 29 
flushing of face in, 216 
greasy, yellow skin in some cases of, 
209 
hands in chronic, 55 
laryngeal, whispering voice in, 568 
night-sweats of, 235 
vomiting in, 533 
Pigeon breast, 273 
Piles. See Hemorrhoids. 
Pin-point pupil in opium-poisoning, 165 
Pitting a sign of dropsy, 236 
Pleurisy, acute, character of pain in, 304 
diminished chest-expansion in, 
279 
friction-sound often best heard 
in axilla in, 296, 304 
position in, 20 
symptoms and signs of, 304 
tenderness over rib in, 266 
hemorrhagic, 306 
in acute infectious diseases, 306 
in aneurism, 307 
in carcinoma, 306 
in nephritis, 306 
Plenrisy, hemorrhagic, in tuberculosis, 306 
with effusion, 304 
segophony above effusion in, 298, 
305 
Baccelli’s sign above effusion in, 
298 
bronchial breathing due to com- 
pression in, 294 
bulging of chest in, 273, 304 
changes in level of effusion in, 
304 
convulsions during irrigation of 
pleura in, 513 
cough during aspiration of fluid 
in, 539 
on change of position in, 
539 
cracked-pot sound in, 286 
decrease of vocal fremitus in, 280 
resonance in, 298 
diminished chest-expansion in, 
279 
displacement of apex-beat in, 
281, 305 
distant breath-sounds over effu- 
sion in, 305 
method of testing for cause of, 
306 
oedema over ribs in purulent, 
239 
of left side, obliteration of 
Traube’s semilunar 
space in, 305 
spleen displaced down- 
ward in, 353 
of right side, liver pushed down 
in, 352 
pulsating, 282 
sigmoid line marking top of ef- 
fusion in, 304 
skodaic resonance above effu- 
sion in, 285, 304 
symptoms and signs of, 304, 305 
Pleuritus. See Pleurisy. 
Pneumonia, acute catarrhal, character of 
fever in, 464 
difficulty of diagnosis be- 
tween pulmonary tuber- 
culosis and, 300 
symptoms and signs of, 300 
croupous, casts of finer bronchial 
tubes sometimes found in 
sputum of, 545 
character of fever in, 463 
bronchial breathing in, 299 
bubbling rales in resolution in, 295 
character of crying in children with, 
23 
Cheyne-Stokes respiration in, 278 
chill in, 463 
chlorides decreased in urine in acute 
stages of, 424 INDEX. 
609 
Pneumonia, chlorides increased, indica 
ting convalescence from, 424 
chronic, Charcot-Leyden crystals in 
sputum of, 544 
cracked-pot sound in, 286 
crepitant rale an early sign of, 295 
crisis on third to ninth day in, 299 
delirium a bad symptom of, 299 
diagnosis and symptoms of, 299, 300 
between mediastinal growths 
and, 312 
between pulmonic phthisis and, 
300 
diminished expansion of chest in, 
279 
expression of anxiety in some cases 
of, 27 
face of, 29 
feeble heart a bad symptom in, 299 
great increase in urine in conva- 
lescence from, 394 
headache in early stages of, 480 
herpetic blisters about mouth, with 
fever in, 29, 229, 299 
increase of vocal fremitus in, 280 
resonance in, 298 
jaundice in, 207 
leucocytosis in, 378 
necessity for examining axilla and 
septum between upper and middle 
lobe of right lung in, 303 
percussion-note dull in, 284 
prune-juice or purulent sputum a 
bad symptom late in, 299 
pseudo-crisis in, 299 
rale redux in, 299 
rapidity of respiration in, 276 
rusty, sticky sputum in, 299 
secondary diphtheritic dysentery due 
to, 436 
subnormal temperature following 
crisis of, 468 
sweat at crisis in, 235 
vocal resonance in. 299 
wavy breathing of, 279 
Pneumonic phthisis, acute, 300 
Pneumothorax, amphoric breathing 
rarely heard in, 294 
cracked-pot sound in, 286 
decrease of vocal fremitus in, 280 
tympanitic note in, 284 
Pohl and Rosenbach’s test, 306 
Poikilocytosis in chlorosis, 375 
in pernicious anaemia, 375 
Poisoning, acute alcohol, symptoms of, 
485 
albumosuria in phosphorus, 420 
anaemia in chronic lead and arsenic, 
376 
anaesthesia in toxic peripheral neu- 
ritis, caused by arsenic, lead, alco- 
hol, mercury, 258 
Poisoning, appearance of tongue in acid 
or alkali, 150, 151 
Argyll-Robertson pupil in bisul- 
phide of carbon, 18b 
atrophy of tongue in chronic lead, 
154 
auto-intoxication, 471 
blue line on gums in lead, 158 
brachial monoplegia in lead, 85 
cannabis indica, diagnosis of, 486 
chloral, symptoms of, 487 
chronic silver, 209, 211 
constipation in phosphorus, 429 
contraction of pupil in opium, 187, 
486 
convulsions due to aconite, veratrum 
viride, hydrocyanic acid, ignatia, 
strychnine, sabadilla, chronic lead, 
502, 511 
diplopia in ptomain, spigelia, co- 
nium, belladonna, gelsemium, 166 
fatty casts in urine due to phos- 
phorus, arsenic, antimony, iodo- 
form, 405 
fever in septic, 459, 461 
haemoglobinuria in mushroom, coal- 
tar, potassium chlorate, glycerin, 
399 
liypersesthesia in lead and arsenic, 
267 
jaundice in phosphorus, 205 
in any poisoning causing ex- 
cessive haemolysis, 207 
joint-affections in chronic lead, 127 
light-colored stools in phosphorus, 
529 
neuralgia of head in lead and arsenic, 
551 
obstinate constipation in chronic 
lead, 430 
ocular paralysis in ptomain, alcohol, 
sulphuric acid, nicotin, lead, and 
carbonic acid, 175 
oedema in arsenic, 237, 238 
papillitis in alcohol and lead, 198 
paraesthesia in aconite and cocaine, 
264 
pin-point pupil in opium, 165, 486 
pruritus in lead and opium, 267 
ptosis in gelsemium and conium, 43 
skin in malarial, 209 
slowness of breathing in opium, 
chloral, aconite, chloroform, anti- 
mony, 277 
symptoms of acute antimonial, 432 
of arsenical, 432 
of opium, 486 
of phosphorus, 528 
tremors of hand in chronic alcohol, 
lead, and mercurial, 75, 77 
urine in santonin and carbolic acid, 
400 610 
INDEX. 
Poisoning, vomiting in antimonial, phos- 
phorus and arsenical, 526, 528 
wrist-drop in lead, 75 
Poliomyelitis, absence of vesical symp- 
toms in, 392 
character of fever in, 467 
claw-hand in, 69 
convulsions, headache, and muscular 
twitching in, 467 
crural monoplegia, 114 
diagnosis between paralysis of leg in 
and acute cerebral paralysis, 116 
foot-drop in, 115 
gait in acute, 95 
lateral wrist-drop in, 75 
loss of knee-jerk in, 565 
of power in several muscles of 
limb later in disease in, 467 
paraplegia in, 111 
“Punchinello” leg in, 115 
symptoms of, 111, 565 
Polycythsemia, due to congenital cardiac 
disease in children, and phosphorus 
poisoning, 363 
Polydipsia, a symptom of diabetes mel- 
litus, 417 
Polyneuritis, differential diagnosis be- 
tween paraplegia in, and Landry’s 
paralysis, 104 
Polyphagia, a symptom of diabetes mel- 
litus, 417 
Position as an encouraging sign, 20 
due to action of drugs, 20 
in acute bellyache, 20 
nausea, 20 
pleurisy, 20 
in coma, 20 
in dyspnoea due to asthma, 308 
in enlarged liver, 20 
in grave or advanced disease, 20 
in heart-disease, 19 
severe, 20 
in hemorrhage, external or internal, 
20 
in large growths in abdominal cavity, 
20 
in oedema of lungs, 20 
in peritonitis, 20 
in pleurisy with effusion, 20 
in pulmonary consolidation, 20 
indicative of convalescence, 19 
persistently on the side, 20 
Pott’s disease, 103 
spastic paraplegia in, 103 
Pregnancy, caries of teeth in, 158 
chloasma of, 210 
discomfort due to, 21 
grave prognosis of acute diffuse 
nephritis in, 426 
pigmentation of eyelids during, 26 
value of estimation of urea during, 
423 
Pregnancy, vomiting in, 532 
Presystolic mitral murmur, 316 
Prevost’s symptom, 181 
Proctitis, symptoms of, 434 
Prostate, enlarged, a cause of interfer- 
ence with passage of urine, 393 
Pruritus about anus, from opium, 267 
in chronic lead-poisoning, 267 
in contracted kidney, 267 
in diabetes, 267 
in gout, 267 
in jaundice, 267 
in piles, 267 
Pseudo-angina pectoris, pain in, 554 
-bulbar paralysis, diagnosis of, 44, 
571 
-meningitis, convulsions in children 
in, 511 
-muscular hypertrophy, gait in, 95 
-ptosis, caused by paralysis of the 
unstriped fibres of Muller, 41 
-tabes, 84, 88 
gait in, 88 
Psoriasis, nails in, 56 
Ptosis, alternate, in so-called nervous 
syphilis, 40, 41, 43 
associated with internal squint, 42 
caused by affection of the sympa- 
thetic, 41 
by cerebral hemorrhage, 40 
by disease of the corpora quad- 
rigemina, 42 
by lesion of oculomotor nerve 
or nucleus, 39 
in angular gyrus, 40 
by nervous syphilis, 41 
by reflex irritation, 41 
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, 519 
in oculo-facial paralysis, 45 
in recurrent paralysis of oculomotor 
nerve on one side, 43 
in tubercular or syphilitic changes 
at base of brain, 41 
transient, in poisoning by gelsemium 
or conium, 43 
with hemiplegia of face and limbs 
on opposite sides of the body, 43 
Puerile breathing, 293 
Puerperal eclampsia, diagnosis of con- 
vulsions in, 508 
Pulmonary abscess, 302 
apoplexy, 304 INDEX. 
611 
Pulmonary congestion, 303 
consolidation, position in, 20 
gangrene, 303 
oedema, 303 
osteo-arthropathy, appearance of 
nails in, 56 
enlargement of feet in, 117 
resonance in, 282 
spade-like hands in, 65 
Pulsating pleurisy, 282 
Pulsation, of cervical vessels, 276 
epigastric, 346 
Pulse, best taken in children when 
asleep, 24 
causes of rapid, 362 
of slow, 361 
Corrigan, 359 
dicrotic, 360 
examination of, 355 
feeble, rapid, and running, in rup- 
tured compensation of heart mus- 
cles, and in cholera morbus, 316, 
431 
force of, 357, 360 
hard and tense, in acute diffuse ne- 
phritis, 426 
high tension, in chronic interstitial 
nephritis, 427 
in acute alcohol-poisoning, 485 
in chloral-poisoning, 486 
in opium-poisoning, 486 
in uraemic coma, 486 
low tension in exhausting diseases, 
358 
in mitral stenosis, 358 
in ruptured compensation, 
358 
method of production of, 356 
normal wave of, 360 
of empty arteries in severe hemor- 
rhage, 360 
pulsus alterans, 359 
paradoxus, 359 
rapid and weak, in intestinal obstruc- 
tion, 523 
due to stimulation of heart, 362 
rate of, 358 
slow in cerebral tumor, 519 
of digitalis, 359 
trip-hammer, 359 
volume of, 358 
water-hammer, 359 
“ Punchinello ” leg, 115 
Pupil, Argyll-Robertson, 185 
contracted, 165 
from bulbar paralysis, 186 
from central nervous disease, 165 
from cerebral inflammation, 165 
tumor, 186 
from corneal inflammation, caus- 
ing photophobia, 165 
from embolism, 186 
Pupil, contracted, from false paretic de- 
mentia of syphilis, 186 
from locomotor ataxia, 186 
from meningitis, 165, 186 
from paretic dementia, 186 
contraction and dilatation of, with 
Cheyne-Stokes breathing, 187 
dilated, from aneurism, 186, 310 
from aortic regurgitation, 186 
from blindness, 165 
from fright, 165, 186 
from glaucoma, 165, 186 
from hysteria, 165 
from intracranial pressure caus- 
ing coma, 165 
from irritation of cervical sym- 
pathetic, 186 
of upper part of spinal cord, 
186 
from mydriatic, 165, 186 
from neurasthenia, 186 
from paralysis of centre of third 
nerve, 186 
hippus, 187 
immobile, 165, 180, 186 
method of testing, 184 
pin-point, in opium-poisoning, 165, 
486 
reaction of, to accommodation, 184 
to light, 184 
size of normal, 184 
transitory unequal dilatation of, in 
tuberculosis, 187 
Wernicke’s sign of hemiopic inaction 
of, 187 
Purpura hsemorrhagica, 214 
hsematemesis in, 527 
hsematuria in, 399 
haemoptysis in severe, 542 
Henoch’s disease in, 215 
in rheumatism, 214 
joint involvement with fever in, 
466 
Pyaemia, diazo reaction in severe, 425 
jaundice in, 208 
joint involvement with fever in, 
466 
parotitis in, 54 
profuse sweating in, 235 
Pyelitis, character of fever in, 428, 459 
of pain in, 428 
chills and fever in, 428, 459 
diagnosis of, 428 
may be caused by strongylus gigas, 
398 
pain in lumbar region in, 389 
pyuria constant or intermittent in, 
428 
urine acid in, 428 
Pyelonephrosis, casts of micrococci in, 
404 
Pylephlebitis, vomiting in, 532 612 
INDEX. 
Pyopneumothorax, coin percussion in, 
305 
Hippocratic succussion in, 298 
metallic tinkling in, 296 
subphrenicus, 346 
Rales, 295 
altered by coughing if not crepitant, 
296 
bubbling, in bronchitis, 295 
in convalescence from asthmatic 
attack, 296 
from pneumonia, 295 
in pulmonary oedema, 295 
in resolution in pneumonia, 295 
in tuberculosis, 296 
character of, in asthma, 308 
crepitant, in breaking down of tuber- 
cular lung tissue, 295 
in early stages of croupous pneu- 
monia, 295 
in pulmonary collapse or oedema, 
295 
congestion, 303 
redux, in pneumonia, 299 
Rash of scarlet feyer, 217 
Raynaud’s disease, appearance of hands 
in, 56 
coma in, 490 
gangrene in, 64, 232 
hsemoglobinuria in, 399 
localized sweating in, 235 
symptoms of, 232 
vomiting in, 528 
Reflex iridoplegia. See Argyll-Robert- 
son pupil. 
Reflexes, ankle clonus, how elicited, 564 
biceps tendon, how tested, 564 
diseases in which decreased, 564 
in which increased, 565 
knee-jerk, how best elicited, 563 
reinforced, 563 
loss of ocular, in acute alcoholic poi- 
soning, 485 
of skin, table of, 566, 567 
tendon, 547 
Relapse, frequency of, in Malta fever, 
451 
in typhoid fever, 447 
Relapsing fever, character of fever in, 
452 
hsematemesis in, 527 
hypersesthesia in, 266 
jaundice in, 207 
oedema of legs and wrists in, 
239 
spirillum of Obermeier in blood 
in, 452 
sweating in, 235 
tongue in, 147 
Remittent fever. See Malaria, remittent. 
Resonance, vocal, 297 
Baccelli’s sign, 298 
decreased, causes of, 298 
increased, causes of, 298 
Respiration, causes of labored, 278 
of rapid, 276 
of slow, 277 
Cheyne-Stokes, 278 
costal, 279 
counting, 276 
diaphragmatic, 279 
in chloral-poisoning, 487 
in coma of apoplexy, 489 
in diabetic coma, 488 
in uraemic coma, 488 
inspiration prolonged in spasmodic 
croup, 277 
method of studying in children, 23, 
24 
prolonged expiration in asthma and 
emphysema, 278 
ratio of pulse to, 276 
rhythm of, 277 
stertorous, in acute alcohol-poison- 
ing, 485 
in opium-poisoning, 486 
wavy, in pneumonia, 279 
Retention of urine in locomotor ataxia, 
390 
in myelitis, 390 
in overdistention, 390 
in pressure during childbirth, 
390 
Retinitis, 199 
albuminuric, 200 
hemorrhagic, 200 
in diabetes, 200 
in leukaemia, 378 
in syphilis, 199 
Retraction of head in children, causes of, 
49 
Retro-bulbar neuritis, 198 
Retro oesophageal abscess sometimes 
causes dysphagia, 159 
Rheumatism, acute articular, appearance 
of hands in, 63 
of tongue in, 148 
character of fever in, 466 
chlorides decreased in, 424 
increased in, in conva- 
lescence, 424 
convulsions in, 466 
cyanosis in, 466 
erythema in, 214 
headache in, 473 
iritis in, 200 
joint affections in, 466 
papillitis in, 198 
purpura in, 214 
subcutaneous fibrous nod- 
ules in, 215 
sweating of, 235 INDEX. 
613 
Rhumatism, acute articular, uric acid in 
urine of, 408 
urticaria in, 216 
with hyperpyrexia, delir- 
ium in, 466 
chronic, changes in shape of hand 
in, 61 
limping gait in, 87 
of scalp, symptoms of, 552 
Rheumatoid arthritis. See Arthritis de- 
formans. 
Rhonchi, 295 
Rickets, beaded ribs of, 275 
carpo-pedal spasm in, 72 
cranio-tabes in, 51 
deficient bony development in, 52 
early decay of teeth in, 158 
excessive sweating of head in, 54 
gait in, 95, 99 
Harrison’s grooves in, 275 
head in, 28, 50 
hyperaesthesia in, 266 
laryngeal spasm in, 309 
nodding spasm in, 48 
open fontanelle in, 52 
pain in back in, 555 
pseudo-paraplegia in, 113 
spastic paraplegia in, 100 
sweating of head in, 235 
tenderness of skin in, 266 
Risus sardonicus in tetanus or strychnine- 
poisoning, 26, 47 
Roberts’s yeast-test for sugar in urine, 417 
Romberg’s symptom, 89 
Roseola. See also Erythema. 
due to antidiphtheritic serum, 220 
due to drugs, 223, 224, 229 
in Bright’s disease, 222 
in chickenpox, 220, 228 
in cholera, 221 
in diabetes, 223 
in diphtheria, 220 
in German measles, 218 
in malaria, 220 
in septicaemia, 221 
in smallpox, 219, 225 
in syphilis, 221 
in tubercular peritonitis, 223 
in typhoid fever, 221 
in typhus fever, 222 
in vaccination, 227 
Rose rash. See Erythema and roseola. 
Rotheln, appearance of rash in, 218 
fever in, 453 
symptoms of, 219 
Rubella. See Rotheln. 
Rubeola. See Measles. 
OACCHAROMYCES albicans, causing 
0 fermentation in diabetic urine, 413 
St. Vitus’s dance. See Chorea. 
Salaam convulsions, 515 
Saltatoric spasm, 74, 516 
Sarcinae ventriculi, in vomitus from 
chronic gastric catarrh, 
531 
from gastric cancer, 531 
dilatation, 531 
ulcer, 531 
test for, 531 
Sarcoma, anaemia due to, 376 
enlargement of liver in, 339 
purpura in multiple, 210 
Scarlet fever, arthritis in, 128 
character of fever in, 452 
collar of brawn in, 452 
date of eruption in, 220 
diazo-reaction in severe, 425 
enlargement of spleen in, 353 
erythema in, 217, 218 
haematuria in, 397 
lysis in fever of, 452 
otitis in, 452 
pleurisy with effusion compli- 
cating, apt to become puru- 
lent, 306 
prognosis from fever of, 453 
sore-throat in, 161 
strawberry tongue in, 149 
synovitis in, 64 
Scars of the skin, 234 
Schonlein’s disease, joint-involvement in, 
128 
symptoms of, 215 
ulcerations of tongue in, 152 
ulcer of buccal mucous mem- 
brane in, 160 
Sciatica See Neuritis, sciatic. 
Sciopedy, 117 
Sclerema neonatorum, symptoms of, 240 
Sclerodactyle, nails in, 56 
Scleroderma, skin in, 34, 240 
Sclerosis, amyotrophic lateral, 70 
alteration of hands in, 70 
ankle-clonus in, 566 
character of speech in, 570 
knee-jerk increased in, 566 
spastic paraplegia in, 102 
disseminated, allochiria in, 264 
ankle-clonus in, 566 
coma in, 492 
convulsions in, 513 
differential diagnosis of, 90, 93, 
96, 186 
expression of face in early stages 
of, 30 
gait in, 96 
hemianaesthesia in, 247 
hemiplegia resulting from, 143 
hippus in, 187 
knee-jerk increased in, 566 
nystagmus in, 183 
optic atrophy in, 198 614 
INDEX. 
Sclerosis, disseminated, slow, scanning 
speech in, 570 
symptoms of, 76, 77 
tremor of hands in, 76 
of head in, 77 
vertigo in, 484 
lateral, absence of vesical symptoms 
in, 392 
ankle-clonus in, 566 
causes of increased reflexes in, 
101 
gait in, 93 
spastic paraplegia in, 101 
Scorbutus. See Scurvy. 
Scotoma, 198 
Scrofulosis, 33 
abdomen in, 330 
dactylitis in, 56 
tongue in, 149 
Scurvy, corneal ulceration in, 200 
dropsy in, 237 
hsematemesis in, 527 
haematuria in, 399 
loosening of teeth in, 159 
pain in back in, 555 
petechiae in, 216 
pseudo-paralysis in, in infancy, 113 
sponginess of gums in, 159 
Senility, tremor of hands in, 76 
Sensation, disturbances of, 263 
Sensibility, disturbances of, 241 
method of testing, 241 
tactile, 241 
thermic, 241 
perverted, 245 
Septicaemia, blood in, 355 
character of fever in, 459, 461 
diarrhoea in, 436 
great variations in temperature in, 
461 
jaundice in, 207 
rose-rash in, 221 
Singultus, 517 
causes of, 517 
Skin, anaesthesia in, 245 
cadaveric, in pyaemia, 210 
cold and moist, with high rectal tem- 
perature, in sunstroke, 466 
and wet, a bad symptom in 
fever, 444 
color of, in health and disease, 201, 
209 
cyanosis of, 211 
dropsy and swelling of, 236 
dry and hot, in fever, 444 
eruptions of, in disease, 218 
excess of dryness of, 235 
gangrene of, 231 
glossiness of, 231 
grassy-yellow in phthisis and chronic 
liver disease, 209 
greenish-yellow in chlorosis, 210 
Skin, harsh and dry, in acute diffuse ne- 
phritis, 426 
in diabetes, 236 
hemorrhages into, 216 
hyperaesthesia of, 265 
in acute alcohol poisoning, 485 
in Addison’s disease, 210 
in angioneurotic oedema, 240 
in argyria, 209, 211 
in carcinoma of internal organs, 211 
in chloasma of pregnancy, 210 
in elephantiasis, 239 
in influenza, 267 
in jaundice, 202 
in kidney disease, 211 
in oedema neonatorum, 240 
in opium-poisoning, 267 
in profound anaemia, 267 
in sclerema neonatorum, 240 
in scleroderma, 240 
in tuberculosis, 211 
increased sensibility of, due to ergot, 
267 
leucoderma, in true goitre, 211 
muddy-yellow, in chronic malaria 
and prolonged suppuration, 209 
pain of, 267 
pallor of, 211 
in myxoedema, 211 
paraesthesia of, 263 
parchment-like, in syphilis, 26 
pigmentation of, 210, 329 
pruritus of, 267 
redness of, 216 
scars of, 234 
sensation of, 241 
sweating of, 234 
table of reflexes of, 567 
tache cerebrate, 216 
meningeale, 217 
tenderness of, in diseases of internal 
organs, 266 
in rickets, 266 
waxy, in cretinism, 32 
yellow, in xanthoma, 209 
and greasy, in paretic dementia, 
210 
Skodaic resonance, 285, 304 
Smallpox, appearance of eruption in, 
219, 225, 454 
date of eruption in, 220 
fever in, 453 
grisolle sign of, 220 
haemoptysis in hemorrhagic, 542 
headache in early stage of, 482 
pain in back in onset of, 453, 561 
spasms, 513 
Spasm, hysterical, of oesophagus, 160 
nodding. See Nodding spasm. 
Spasms, 513 
blepharo-facial, 46 
Graefe’s spots in, 46 INDEX. 
615 
Spasms, carpo-pedal, 72 
facial, Abadie’s sign in, 46 
cause of functional, 45 
of organic, 45 
following exposure to cold, 47 
paralysis, 47 
in hysteria, 45, 47 
in adults, due to locomotor ataxia, 
310 
due to mediastinal growths, 310 
in children, due to croup, 309 
due to digestive disturbances, 
309 
due to laryngeal catarrh, 309 
due to rickets, 309 
in chorea insaniens, 514 
minor, 513 
in electric chorea, 515 
in Huntington’s chorea, 514 
in lesion of middle peduncle of cere- 
bellum, 516 
in paramyoclonus multiplex, 515 
in tetanus, 47 
in Thomsen’s disease, 516 
in true chorea, 513 
laryngeal, in adults, due to aneurism 
Dressing on recurrent 
laryngeal nerve, 310 
due to enlargement of retro- 
bronchial glands, 310 
of fingers due to occupation, 72 
of tongue, 157 
saltatoric, 516 
varieties of, 513 
Spastic paraplegia. See Paraplegia, 
spastic. 
Speech, 568. See also Voice, 
defects of, 571 
agraphia, 571 
alexia, 572 
aphasia, 571 
aphonia, 572 
apraxia, 572 
paraphasia, 571 
tests for, 572 
word-deafness, 572 
feeble, hesitating, in pneumonia of 
pulmonary oedema, 569 
halting, hesitating, in paretic de- 
mentia, 570 
incoherent, in chorea in children, 
570 
in delirium, 570 
indistinct, mumbling, in amyotrophic 
lateral sclerosis, 571 
in glosso-labio-pharyngeal 
paralysis, 570 
in stomatitis, 570 
in typhoid fever, 570 
nasal, in adenoid vegetations, 569 
nervous mechanism of, 571 
scanning, in multiple sclerosis, 96 
Speech, shrill, piping, in paralysis agi- 
tans, 571 
slow, scanning, in disseminated scle- 
rosis, 570 
in Friedreich’s ataxia, 570 
tests for defects of, 572 
whispering, causes of, 568 
Spermatorrhoea, 412 
accompanying oxaluria, 409 
spermatozoa found in, 412 
Spermatozoa in urine, significance of, 
412 
Sphygmograph, 360 
Spinal cord, great rise in temperature 
due to injuries to cervical 
portion of, 466 
localization of functions of seg- 
ments of, 109 
location of lesion of, in anaes- 
thesia, 254 
Spirillum of Obermeier in blood in re- 
lapsing fever, 452 
Spleen, causes of enlargement of, 353 
extension downward of, 353 
enlarged, in amyloid disease of kid- 
ney, 427 
in leukaemia, 378 
in typhoid fever, 353, 449 
method of examination of, 353 
normal position of, 353 
swelling of, in septicaemia, 354 
in Weil’s disease, 460 
uric acid in excess in enlargement 
. of, 408 
Splenic fever. See Anthrax. 
Spots of Valleix, 553 
Spotted fever. See Cerebro-spinal men- 
ingitis. 
Sputum, actinomyces in, 546 
anchovy sauce, in amoebic abscess, 
543 
blood-streaked in leakage from aortic 
aneurism, 541 
in pulmonary gangrene in chil- 
dren, 542 
in valvular heart disease, 542 
bloody, diagnosis between bloody 
vomit and, 542 
in haemoptysis of aortic aneu- 
rism, 542 
in ruptured bloodvessels in pos- 
terior pharyngeal wall, 542 
of haemophilia, 542 
of hemorrhagic smallpox rarely, 
542 
of pulmonary tuberculosis, 542 
of severe purpura, 542 
of valvular cardiac disease, 542 
of vicarious menstruation, 542 
brick-dust, in hepatic abscess com- 
municating with lung, 543 
brownish, in gangrene of lungs, 303 616 
INDEX. 
Sputum, casts of bronchioles in, in fibrin- 
ous bronchitis, 545 
of larynx and bronchi in, in 
diphtheria, 544 
of smaller bronchioles found oc- 
casionally in, in croupous 
pneumonia, 545 
Charcot-Leyden crystals in asth- 
matic, 302, 544 
copious and purulent, in pulmonary 
abscess, 302 
crystals of margaric acid in pulmon- 
ary gangrene, purulent bronchitis, 
and follicular tonsillitis, 546 
Curschmann’s spiral in asthmatic, 
309, 544 
Dittrich’s plugs in, in purulent bron- 
chitis, 307 
eggs of distoma pulmonum in, 546 
elastic fibres in, in abscess of lung, 
546 
in gangrene of lung, 546 
in tuberculosis of lung, 546 
examination of, for elastic fibres, 546 
with centrifuge, 545 
hooks of echinococcus in, 546 
in asthmatic attack, 543 
in chronic bronchitis, 307 
in pulmonary gangrene, 543 
liquid and watery, in epidemic influ- 
enza, 543 
in pulmonary oedema, 543 
method of staining for tubercle ba- 
cilli in, 548 
microscopical examination of, 545, 
547 < 
prune-juice in chronic pneumonia, 
542 
purulent, causes of, 543 
rusty, sticky, in croupous pneumonia, 
541 
semi-liquid, in pulmonary phthisis, 
543 
Squint, diagnosis between concomitant 
and paralytic, 167 
of conditions producing, 174 
external and internal, due to tumor 
at base of brain, 474 
in hysteria, 182 
in meningitis, 519 
in ocular palsy, 42, 170 
significance of external, 178 
Stellwag’s symptom, 165 
Steppage gait, 88 
Stomach, cancer of, 340 
cough due to reflex irritation from, 
540 
dilatation of, 342 
distention of, by gas, 341 
indicanuria in cancer of, 401 
method of examining with gastro- 
diaphane, 336 
Stomach, method of examining, with 
gyromele, 336 
palpation and percussion of, 338 
test of contents for hydrochloric acid, 
344 
for lactic acid, 344 
for urates in urine in disorders 
of, 408 
ulcer of, 344 
vomiting in dilatation of, 531 
Stomatitis, action of child with, toward 
breast, 23 
appearance of tongue in ulcerative, 
152 
buccal mucous membrane affected in, 
160 
epidemic, symptoms of, 465 
impetiginosa, 154 
malignant ulcerative, 160 
offensive odor of breath in, 18 
temperature of mouth raised in, 444 
Stone in bladder, interference with pas- 
sage of urine due to, 393 
Stools. See also Feces. 
almost devoid of mucus in cholera- 
morbus, 431 
bilious, 439 
bloody, 439 
clay colored, in hepatogenous jaun- 
dice, 207 
in Weil’s disease, 460 
gallstones in, 439 
in cholera, comma bacilli in, 432 
infantum, 431 
in dysentery, 435 
in intussusception in children, 521, 
522 
in proctitis, 435 
intestinal parasites in, 440 
mixed with mucus, 439 
oily, in carcinoma of pancreas, 345 
ribbon-shaped, in follicular entero- 
colitis, 434 
rice-water, in antimonial poisoning, 
432 
significance and character of blood 
in, 437 
tarry, in yellow fever, 460 
Strabismus. See Squint. 
Stricture of oesophagus. See (Esophageal 
stricture. 
Strongylus gigas, haematuria due to, 398 
Stupor in typhoid fever, 451 
in ulcerative endocarditis, 451 
Subsultus tendinum, 57, 78 
Succussion, Hippocratic, 298 
Sucking movements in meningitis, 479 
Sudaniina, 236 
Sugar in the blood, 386 
Williamson’s test for, 386 
in the urine. See Glycosuria and 
urine. INDEX. 
617 
Sunstroke, character of fever in, 466 
diagnosis of coma in, 489 
headache of, 482 
skin cold and moist with high rectal 
temperature in, 466 
hot and dry in, 466 
Swallowing, difficult. See Dysphagia. 
Sweat, bile-stained, in jaundice, 235 
Sweating in acute miliary tuberculosis, 
463 
ulcerative endocarditis, 235 
in antimonial poisoning, 432 
in collapse, 235 
in crises in fevers, 235 
in debility, 235 
in health, 234 
in hepatic abscess, 351, 456 
in intermittent malarial fever, 235 
in malaria, 235 
in obstruction of rectum, 525 
in phthisis, 235 
in pneumonia at crisis, 235 
in pysemia, 235 
in relapsing fever, 235 
in typhoid fever, 235 
in uraemia, 235 
localized, 235 
in exophthalmic goitre, 235 
in hysteria, 235 
in migraine, 235 
in paretic dementia, 235 
in Raynaud’s disease, 235 
in rickets, 235 
in thoracic aneurism, 235 
uriniferous, in deficient renal ac- 
tivity, 235 
Syncope, diagnosis of, 509 
Syphilis, action of child with, toward 
breast, 23 
alternate ptosis in, 41, 43 
aortitis in, 554 
appearance of fingers in dactylitis in, 
56 . 
of nails in, 56 
Argyll-Robertson pupil in cerebral, 
185 
associated with amyloid kidney, 427 
at base of brain causing bilateral 
facial paralysis, 44 
atheroma in, 357 
broadness of bridge of nose in con- 
genital, 28 
diagnosis between cerebro - spinal 
syphilis and disseminated 
sclerosis, 96, 186 
of coma in, 491 
of epilepsy due to, 497 
early cutting of teeth in inherited, 
158 
enlargement of spleen in early, 353 
eruptions of, 221, 227, 233 
fever in, intermittent, 464 
Syphilis, fever in, remittent, 464 
simple continued, 464 
fissures and chancres of tongue in, 
151 
gummatous swelling and periosteal 
thickening of shins in, 130 
hemiplegia in cerebral, 143 
Hutchinson teeth in, 158 
immobility of pupil in, 186 
iritis in, 197 
miscarriage a symptom of, 21 
mucous patches about mouth and 
anus in infantile, 28 
of intestinal tract, diarrhoea due to, 
436 
open fontanelle in, 51 
pain in periostitis of skull in, 552 
papillitis in, 198 
parsesthesia in spinal, 263 
parchment-like skin of, 26 
pseudo-palsy in, 85 
ptosis in changes at base of brain in, 
41 
purpura in, 215 
purulent acne of forehead in, 227 
retinitis in, 199 
rose-rash in, 217, 221 
scars in, 234 
spastic paraplegia in spinal, 103 
symptoms of arteritis due to, 476 
Syphilitic arteritis, 476 
gumma, 476 
meningitis, 476 
triad, 158 
Syringomyelia, appearance of nails in, 56 
loss of pain and temperature-sense 
in, 253 
necrosis of terminal phalanges in, 
65 
partial anaesthesia in, 253 
patches of anaesthesia in, 253, 263 
small joints affected in, 126 
symptoms of, 253 
wasting of hands with anaesthesia 
in, 70 
TABES dorsalis. See Locomotor ataxia. 
Tabetic atrophy, 192 
Table of reflexes, 567 
Tache cerebrate, 216 
meningeale, 217 
Tachycardia, 317, 362 
Taenia cucumerina, 442 
mediocanellata, 440 
solium, 440 
Tapeworm. See Parasites; Taenia. 
Taste, decrease of acuity of, in facial 
haemiatrophy, 34 
loss of, in anterior portion of tongue 
in disease of petrous portion of 
temporal bone, 36 618 
INDEX. 
Teeth, ages at which different teeth ap- 
pear in children, 158 
blue line around, in lead-poisoning, 
158 
caries of, in diabetes mellitus, 158 
in pregnancy, 158 
cut early in inherited syphilis, 158 
early decay of, in rickets, 158 
grinding of, in children, 159 
Hutchinson, 158 
loosening of, in salivation, 159 
in scurvy, 159 
staining of, 158 
Teichmann’s crystals in haemoglobinuria, 
396 
Temperature. See also Fever. 
causes of sudden fall of, in typhoid 
fever, 447 
great rise of, in injuries to cervical 
cord, 466 
high, in cholera infantum, 465 
in sunstroke, 468 
with cold skin in cholera Asia- 
tica, 465 
in acute alcohol-poisoning, 486 
in diabetic coma, 488 
in intestinal obstruction, 524 
in uraemic coma, 487, 488 
methods of taking, 443 
subfebrile, mildly febrile, decidedly 
febrile, 443 
subnormal, causes of, 468 
in algid type of pernicious ma- 
laria, 468 
in cretinism, 32 
in heat-exhaustion, 468 
in injuries to dorsal portion of 
spinal cord, 468 
Tendon-reflexes, 563 
Tenesmus in bladder-trouble, 389 
in cholera infantum, 431 
in dysentery, 435 
in intussusception, 522 
in proctitis, 434 
in stricture of rectum, 433 
Test, coin-, in hydro-pneumothorax, 305 
Ehrlich’s diazo-reaction, 425 
for albumin in urine, boiling, 413 
Heller’s, 414 
quantitative by centrifuge, 
414 
for albumose, Harris’, 418 
for chlorides, 424 
for chyle in urine, 401 
for defects, intellectual, 572 
for elastic fibres in lungs, 545 
for haemin crystals, 535 
for hydrochloric acid in stomach, 
344 
for indicanuria, 400 
for lactic acid in stomach, 344 
for sarcinae ventriculi, 531 
Test for stricture of oesophagus, 159 
for sugar in urine, Fehling’s, 415 
Haines’, 414 
Roberts’s, 416 
Whitney’s, 415 
for tubercle bacilli, 547 
for urates, 400 
for urea, Lyons’, 420 
Gabbett’s modification of Fraenkel’s 
method for tubercle bacilli, 549 
Gmelin’s, for bile in urine, 400 
Haines’ modification of Haesser’s 
method for total quantity of solids 
in urine, 424 
Heller’s, for blood in urine, 396 
of Maddox, rod-, 168 
of pupils, 184 
Widal’s, for typhoid fever, 384 
Williamson’s, for sugar in the blood, 
386 
Tetanus, character of convulsions in, 511 
of fever in, 465 
facial spasm in, 47 
head or cephalic, 49 
knee-jerk increased in, 566 
ptosis in, 41 
risus sardonicus in, 26 
Tetany, “accoucheur’s hand” in, 72 
character of convulsions in, 512 
Chvostek’s symptom of, 512 
Erb’s symptom of, 512 
gastric dilatation in, 72 
thyroid wasting in, 72 
Trousseau’s symptom of, 512 
Thermic fever. See Sunstroke. 
Thoma-Zeiss’s hsematocytometer, 365 
Thomsen’s disease, diagnosis of, 516 
spasm of hand in, 75 
of tongue in, 157 
Thorax, aneurism of, diagnosis between 
medicinal growths and, 310 
localized sweating in, 235 
spongy, venous masses above 
clavicle due to, 276 
Thrill, causes of, 281 
diffuse and feeble in cardiac dilata- 
tion, 324 
in aortic aneurism, 316, 346 
in carotid arteries, 325 
in mitral regurgitation in children, 
315 
stenosis, 316 
Thrombosis, cerebral, 53, 238 
of cavernous sinus, 181 
symptoms of, 181 
of coronary artery, 325 
of femoral vein, 129 
of lateral sinus, 480 
of umbilical vein in melsena neona- 
torum, 528 
vomiting in, 518 
Thrush, appearance of tongue in, 148 INDEX. 
619 
Tic, convulsive, 74 
facial spasm in, 46 
in pulmonary disease, 146 
in relapsing fever, 143 
Tinnitus aurium in Meniere’s disease, 
532 
Tobacco-heart, 325 
Toes, separation of, in ainhum, 130 
Toflier’s methylene-blue mixture, 383 
Toison’s solution for counting white cor- 
puscles, 367 
Tongue, anatomy of the, 145 
annulus migrans of, 154 
appearance of, in acute articular 
rheumatism, 148 
catarrhal jaundice, 147 
gastric catarrh, 148 
in children, 148 
glossitis, 154 
in Addison’s disease, purple 
spots on, 150 
in advanced disease of exhaust- 
ing nature, 149 
in ansemia, 150 
in biliousness, 147 
in cardiac disease, 150 
in cretinism, 32 
in dysentery, 149 
in grave disease of the viscera, 
149 
in hemiplegia, 149 
in hepatic abscess, 149 
in mucous disease, worm-eaten, 
148 
in persons taking large amounts 
of milk, 148 
in poisoning by acids, 150 
by alkalies, 151 
by cantharides, 151 
by corrosive sublimate, 150 
in pulmonary disease, 150 
in relapsing fever, 147 
in scarlet fever, strawberry, 149 
in scrofulosis, 149 
in stomatitis impetiginosa, 154 
in syphilis, 151 
in thrush, 148 
in tonsillitis, 146, 147 
in typhoid fever, in typhoid 
state, 147 
in ulcerative stomatitis, 152 
bilateral atrophy of, due to dis- 
ease affecting hypoglossal 
nerve, 154 
in chronic lead-poisoning, 
154 
in glosso labio-pharyngeal 
paralysis, 154 
in locomotor ataxia, 154 
in paretic dementia, 154 
in progressive muscular 
atrophy, 154 
Tongue, biting of, in epilepsy, 152 
in glosso-labio-pharyngeal par- 
alysis, 152 
chancre of, 151 
chronic superficial glossitis of, 153 
coating of, causes of, 146 
composition of, 146 
unilateral, due to decayed teeth 
or hemiplegia, 149 
dryness or moisture of, prognostic 
value of, 149 
enlargement of, in acromegaly, 155 
in acute inflammation, 154 
in inflammatory hypertrophy, 
154 
in macroglossia, 154 
in myxcedema, 155 
in new growths, 154 
in syphilis, 154 
epithelioma of, 151 
eruptions of, 152 
examination of, 145 
in children best when crying, 24 
fibrillary tremor of, in labio glosso- 
pharyngeal paralysis, 157 
fissures of, due to age, chewing to- 
bacco, or abuse of alcohol or 
tea, 151 
deep, in dissecting glossitis, 151 
geographical, 154 
glossodynia exfoliativa of, 153 
hemiatrophy of, 155 
ichthyosis of, 153 
leucokeratosis of, 153 
leucoma of, 153 
lichen planus of, 153 
movements of, 155 
in coma, 155 
in feeble minded, 155 
in glosso-labio-pharyngeal par- 
alysis, 155 
in nervous individuals, 155 
in pseudo-bulbar paralysis, 155 
in typhoid fever, 155 
mucous patches of, 151 
mycosis of, 148 
oedema of, 154 
paralysis of, in diphtheria, 156 
in injury of hypoglossal or tri- 
facial nerve, 155 
location of lesion in, 156 
parrot, in dysentery or hepatic ab- 
scess, 149 
patches on, in chronic superficial glos- 
sitis, 153 
in leucoma, 153 
in smokers, 153 
purple spots on, in Addison’s disease, 
150 
scleroderma of, 153 
smoker’s patch on, 153 
spasm of, in aphthongia, 157 620 
INDEX. 
Tongue, spasm of, in chorea, 157 
in general paralysis of the in- 
sane, 157 
in hysteria, 157 
in insular sclerosis, 157 
in irritation of hypoglossal 
nerve, 157 
in puerperal mania, 157 
in Thomsen’s disease, 157 
stains of, 148, 149, 150 
strawberry, in scarlet fever, 149 
tremor of, in alcoholism, 157 
in glosso-labio-pharyngeal pa- 
ralysis, 157 
in typhoid fever, 157 
ulceration of, in epithelioma, 151 
in lupus, 152 
in psilosis, 152 
in Schonlein’s disease, 152 
in stomatitis, 152 
in syphilis, 152 
in wounds, 151 
multiple, in tuberculosis, 151 
of frsenum of, in whooping- 
cough, 152 
unilateral atrophy of, in chronic 
lead-poisoning, 154 
urticaria of, 153 
wandering rash of, 154 
worm-eaten, in mucous disease, 148 
xanthelasma of, 150 
xeroderma pigmentosum of, 153 
Tonsillitis, chronic night-cough in, 540 
crystals of margaric acid in follicu- 
lar, 546 
diagnosis between diphtheria, scarlet 
fever, and, 161 
fever in, 465 
odor of breath in, 18, 23 
symptoms of follicular, 161 
of suppurative, 161 
tongue in, 146, 147 
Tonsils, chronic cough in enlarged lin- 
gual, 540 
night cough in enlarged faucial, 540 
pain in calculus of, 163 
symptoms of chronic enlargement of, 
163 
Tracheal tugging in aneurism, 319 
Traube’s semilunar space obliterated in 
left-sided pleural effusion, 305 
Tremor of hands and arms, 76 
in mercurial poisoning, 77 
railroad-bridge type of, 78 
of tongue, 157 
of type Rendu, 78 
post-hemiplegic, 78 
sometimes found instead of occupa- 
tion spasm, 73 
Trichiniasis, diagnosis of, 451 
puffy eyelids in, 30 
Trichinosis. See Trichiniasis. 
Trichocephalus dispar, 442 
Trousseau’s symptom of tetany, 512 
Tube-casts. See Casts. 
Tubercular glands, symptoms of, 345 
meningitis, 478 
differential diagnosis of, 478 
headache in, 478 
in children, 479 
pyelitis, 428 
Tuberculosis, albumosuria in, 420 
amphoric breathing in, 294 
anaemia in, 376 
bronchial breathing and consolida- 
tion in, 294 
bronchitis a cause of death in, 21 
bronchophony in, 301 
bubbling rales in, 295, 301 
Cliarcot-Leyden crystals in sputum 
of, 544 
Cheyne-Stokes breathing in menin- 
geal, 278 
chronic loose morning cough in 
cavity in, 538 
cracked-pot sound in, 286 
crepitant rales and breaking down 
of lung-tissue in, 295 
dactylitis in, 56 
diagnosis between catarrhal pneu- 
monia and pulmonary, 300 
diarrhoea of, 434 
diazo-reaction in severe pulmonary, 
425 
elastic fibres in sputum of, 546 
expiration prolonged in, 30f 
fever in acute miliary, 462 
pulmonary, 462 
haemoptysis in, 542 
heavy face in bone disease in, 28 
hectic fever in, 301 
hemorrhagic pleurisy in, 306 
hollow chested build in, 18 
leucocvtosis in, 450 
loss of flesh in, 301 
mammary gland enlarged in, 276 
metallic tinkling in, 296 
multiple ulceration of tongue in, 
151 
necessity of examining axilla in, 
303 
ocular palsy in, 175 
of bones in amyloid kidney, 427 
of kidney, hasmaturia in, 398 
pectoriloquy in, 298, 301 
percussion-note dull in consolidation 
due to, 284 
pleurisy complicating, apt to become 
purulent, 306 
with effusion coming on insidi- 
ously in undiscovered, 306 
ptosis in changes at base of brain due 
to, 41 
puerile breathing an early sign of, 293 INDEX. 
621 
Tuberculosis, rapidity of breathing in, 27 6 
retraction of abdominal wall in, 330 
scars on neck from suppurating 
glands in, 234 
spirituelle face of children with 
diathesis of, 28 
sputum, Curschmann’s spirals rarely 
seen in, 544 
sweating in, 301 
transitory unequal dilatation of 
pupils in, 187 
vocal fremitus and resonance in- 
creased in, 298, 301 
vomiting in acute miliary, 520, 533 
Tumor, abdominal, pain in, 560 
at base of brain, symptoms of, 37 
brain-, Cheyne-Stokes breathing in, 
278 
hyperaesthesia in, 266 
impaired memory in, 519 
papillitis in, 197, 519 
parsesthesia in, 263 
severe headache in, 519 
slow pulse in, 519 
symptoms of, 474 
unilateral anaesthesia in, 247 
vertigo in, 484, 519 
vomiting independent of taking 
food in, 519 
detection of, in intussusception, 521 
diagnosis of fatty, of abdominal wall, 
339 
of abdomen, 345 
of bladder, 393 
of cord, bladder symptoms of, 391 
girdle-sensation in, 265 
paraplegia in, 112 
of lung, rapid respiration in, 276 
of mediastinum, 310 
of nerves, pain in, 561 
phantom, 349 
pontine, anaesthesia in, 248 
Tympanites in flatulent colic, 330 
in peritonitis, 330 
in typhoid fever, 330, 438 
Typhoid fever, albumosuria in, 420 
appearance of eruption in, 221 
bacillus of Eberth the cause of, 
449 
blood in, 379 
bloody stools in, 439 
bradycardia in, 325 
carphologia in, 78 
causes of mumbling speech in, 
570 
of recrudescence of fever 
in, 447 
of vomiting in, 525 
character of coma in, 488 
of fever in, 446 
date of eruption in, 220 
delirium in, 30, 449 
Typhoid fever, diagnosis, 449 
between acute miliary tu- 
berculosis and, 449 
between Malta fever and, 
451 
between remittent fever 
and, 450 
between trichiniasis and, 
451 
between ulcerative endocar- 
ditis and, 451 
Ehrlich’s diazo-reaction in, 425 
enlargement of spleen in, 353 
face in, 29 
headache in, 482 
hyperaesthesia in convalescence 
from, 266 
hypertrophic osteo-arthritis fol- 
lowing, 128 
in children, 459 
increase of urine in convales- 
cence from, 394 
lesions of lungs generally at base 
in, 449 
meteorism in, 449 
moderate bronchitis early in, 
449 
mushy stool in, 438 
oedema of thigh over deep mus- 
cular abscess following, 239 
parotitis in, 451 
pleurisy with effusion compli- 
cating, apt to become puru- 
lent, 306 
recrudescence in, 447 
relapse in, 447 
roseola in, 221 
stupor in, 449 
subsultus tendinum in, 78 
sudden fall in temperature due 
to hemorrhage 
of any sort in, 
447 
due to intestinal 
hemorrhage in, 
447 
due to intestinal 
perforation in, 
447 
sweating in, 235 
tongue in, 147 
tympanites in, 330, 449 
Widal’s test for, 384, 439 
without fever, 449 
Typho-malarial fever. See Malaria, re- 
mittent. 
Typhus fever, character of fever in, 452 
crisis in, 452 
eruption in, 220, 222, 452 
great exhaustion in, 452 
haematemesis in, 527 
headache in, 452 622 
INDEX. 
ULCER, perforating, 129 
Ulcers at base of finger-nails due to 
chloral, 57, 232 
on buccal mucous membrane in 
Schonlein’s disease, 160 
on cornea in scrofula, 200 
on tongue, 152 
perforating, in diabetes, senility, 
and tabes dorsalis, 129 
syphilitic, in intestinal tract 
causing diarrhoea, 436 
Unconsciousness. See Coma. 
Unilateral facial paralysis. See Paralysis, 
unilateral facial. 
Uraemia. See also Coma, 
amaurosis in, 200 
anaemia in, 376 
Cheyne-Stokes breathing in, 278 
colliquative diarrhoea in, 518 
coma in, 487 
occurring in chronic interstitial 
nephritis, 427 
convulsions in, 518 
diagnosis of, 507 
headache in, 473 
hiccough in, 517 
sweating in, producing scales of urea, 
235 
symptoms of, 487 
vomiting in, 488, 518 
odor of carbonate of ammonium 
in, 518 
Urethra, character of blood in hemor- 
rhage from, 396 
fever due to passage of sound into, 
445 
gonococci in specific inflammation of, 
411. 
incontinence of urine due to insensi- 
tive, 390 
interference with passage of urine in 
stricture of, 393 
Urethritis, specific, gonococci in, 411 
Uricsemia. See Lithsemia. 
Urine, acid fermentation of, 412 
albumin in, boiling test for, 413 
Heller’s test for, 414 
quantitative test for, by centri- 
fuge, 414 
albuminuria, significance of, 414 
albumose in, Harris’s test for, 418 
significance of, 420 
alkaline fermentation of, 413 
bile-stained, in hepatogenous jaun- 
dice, 207 
casts in, blood, 395, 403 
epithelial, 402 
fatty, 405 
granular, 404 
hyaline, 405 
of microccoci, 404 
of pus, 403 
Urine, causes of incontinence of, 390 
of retention of, 389 
chlorides in, significance of increase 
and decrease of, 424 
test for, 424 
color of, blue, 400 
brown, 400 
causes of black, 395, 401 
due to blood, 395 
green, 400 
in diabetes, 401 
in jaundice, 400 
red, 395, 399, 400 
white or milky, 401 
yellow, 400 
conditions in which decreased. 394 
in which increased, 394 
crystals in, creatin, 409 
creatinin, 409 
oxalate of lime, 408 
triple phosphates, 409 
urate, 408, 409 
uric acid, 408 
cylindroids in, 405, 406 
diazo-reaction of Ehrlich in, 425 
embryos of parasites in, 411 
epethelial cells in, 411 
fermentation of, 412, 413 
Gmelin’s test for bile in, 400 
gonococci in, 411 
Heller’s test for blood in, 396 
in acute diffuse nephritis, 426 
in amyloid kidney, 427 
in cholera morbus, severe, decreased 
in, 431 
in chronic interstitial nephritis, 426 
in diabetes insipidus, 428 
mellitus, 427 
in phosphorus-poisoning, 529 
in pyelitis, 428 
in uraemia, 487 
interference with passage of, due to 
enlarged prostate, 393 
due to nervous bladder, 393 
due to stone in bladder, 393 
due to stricture of urethra, 
393 
due to tumors of bladder, 
393 
involuntary passage of, in apoplexy, 
392 
in idiots, 392 
in infectious diseases, 392 
in irritation of foreskin or 
vagina in children, 393 
in seat-worms, 393 
in some cases of insanity, 
392 
method of collecting, for testing, 393 
odor of, causes of alteration of, 394 
specific gravity of, causes of high, 
394 INDEX. 
623 
Urine, specific gravitv of, causes of low, 
394 
spermatozoa in, 411, 412 
staphylococci and streptococci in, in- 
dicating pus, 412 
sugar in, Fehling’s test for, 415 
Haines’ test for, 414 
quantitative yeast test of Rob- 
erts for, 417 
significance of, 417 
Whitney’s test for, 415 
total quantity of solids in, Haines’ 
modification of Haesser’s method 
for computing, 424 
tubercle bacili in, 411 
urates in, 408, 409 
urea in, amount excreted in health, 
424 
causes of increase and decrease 
of, 423 
Lyon’s method of estimating, 
420 
value of estimating in renal dis 
ease during pregnancy and 
before surgical operations, 423 
uric acid in, 408 
variations in quantity of, 393 
Urobilin icterus, 208 
Urticaria, 222 
from drugs, 216 
in rheumatism, 216 
of tongue, 153 
\ VACCINATION, appearance of erup- 
V tion of, 227 
roseola following, 219 
Vaginitis, specific, gonococci in, 411 
Valvular heart disease. See Heart. 
Varicella. See Chickenpox. 
Variola. See Smallpox. 
Vertigo, 484 
causes of, 484 
due to drugs, 484 
in Addison’s disease, 533 
in anaemia, 375, 484 
in apoplexy, 484 
in brain tumors, 484 
in disseminated sclerosis, 484 
in epilepsy, 484 
in indigestion, 484 
in ingravescent apoplexy, 140 
in Meniere’s disease, 484 
in middle-ear disease, 484 
in ocular palsy, 170 
in paretic dementia, 144 
in phosphorus poisoning, 529 
paralyzing, 484 
Vesical crises in locomotor ataxia, 89 
Vesicular breathing, 292 
Vision, changes in acuity of, 188 
failure of, 188 
Vocal fremitus. See Fremitus, vocal. 
resonance. See Resonance, vocal. 
Voice, 568 
hoarseness of, 568 
in aneurism, 568 
in paralysis agitans, 571 
in typhoid fever, 570 
loss of, or mutism, 569 
nasal, causes of, 569 
whispering, causes of, 568 
Volvulus, 347, 524 
vomiting caused by, 524 
Vomit, 531 
of chronic gastric catarrh, 534 
of gastric cancer, 340, 526, 531 
dilatation, 530, 531 
ulcer, 527 
of uraemia, 535 
significance of, 534 
test for haemin in, 532 
sarcinae in, 531 
Vomiting, 517 
associated with headache, 533 
bilious, in remittent malarial fever, 
459 
black, in yellow fever, 460 
centric, from chloroform or ether, 
517 
coffee-ground, in chronic gastric ca- 
tarrh, 530 
in gastric cancer, 340, 526 
in locomotor ataxia, 527 
in phosphorus-poisoning, 528 
cyclical, 531, 532 
decrease of urine by persistent, 394 
due to injuries to the epigastrium, 
527 
in acute gastric catarrh, 530 
miliary tuberculosis, 520 
pancreatitis, 528 
yellow atrophy of liver, 533 
in appendicitis, 525 
in brain tumor, 474 
in catarrhal or obstructive jaundice, 
532 
in cerebellar tumor, 519 
in cerebral disease, 518 
in cerebro-spinal meningitis, 461 
in cholera Asiatica, 526 
infantum, 431, 526 
morbus, 431, 526 
in diabetes, rarely, 518 
in dilatation of the stomach, 530 
in dysentery, 526 
in early secondary syphilis, 534 
in embolism of superior mesenteric 
artery, 528 
in enterocolitis, not common, 433 
in erysipelas, 534 
in exophthalmic goitre, 532 
in gastric cancer, 526 
ulcer, 527 624 
INDEX. 
Vomiting in gastro-pulmonary fever, 
467 
in haemoglobinsemia, 533 
in hemiplegia, due to hsematoma of 
dura mater, 143 
in hemorrhagic pressure on brain, 
142 
in hepatic abscess, 533 
cirrhosis, 527 
in hepatitis, 533 
in hysteria, 531 
in influenza, 463 
in ingravescent apoplexy, 140 
in intestinal obstruction, 520 
in intussusception, 520 
in melaena neonatorum, 528 
in Meniere’s disease, 532 
in meningitis, 467, 519 
in merycismus, 534 
in migraine, 533 
in neurasthenia, 532 
in neuroses of stomach, 531 
in peritonitis, 525 
in phosphorus-poisoning, 528 
in phthisis, 533 
in poisoning by arsenic and anti- 
mony, 526 
in pregnancy, 532 
in profound cerebral anaemia, 519 
in pulmonary gangrene, 534 
in purulent meningitis, 519 
in pylephlebitis, 532 
in Raynaud’s disease, 528 
in renal calculus, 533 
in true gastritis, rare, 530 
in typhoid fever, 525 
in uraemia, 517, 518 
in whooping-cough, 534 
in yellow fever, 533 
of blood. See Haematemesis. 
reflexly produced by gastric, intesti- 
nal, or other abdominal disorders, 
517, 520 
uraemic, in chronic parenchymatous 
nephritis, 426 
ushering in eruptive diseases, 534 
Von Fleischl’s haemoglobinometer, 370 
WEIL’S disease, almost total absence 
of gastro-intestinal symp- 
toms in, 460 
character of fever in, 460 
clay-colored stools in, 460 
jaundice in, 205, 460 
Weil’s disease, swelling of liver and 
spleen in, 460 
Wernicke’s pupil, 187, 475 
Westphal’s sign, 89 
Whitlow, painless, in Morvan’s disease, 
69 
Whooping-cough, cough in, 537 
ulcer on fraenum in, 152 
vomiting in, 534 
Widal’s test for typhoid fever, 384, 439 
Williamson’s test for sugar in blood, 386 
Word-blindness, 572 
-deafness, 572 
Worms, 440 
involuntary passage of urine due to 
seat-, 393 
Wrist-drop, causes of, 75 
-jerk, marked, in amyotrophic lat- 
eral sclerosis, 70 
Wry-neck, causes of, 48 
clonic or tonic, 48 
congenital or acquired, 48 
definition of, 48 
diagnosis of, 48 
facial asymmetry in connection with, 
33 
VANTHELASMA, 150 
-A- Xanthoma, 209 
YELLOW atrophy of liver, acute, con- 
vulsions in, 513 
coma in, 488 
hsematemesis in, 527 
jaundice in, 207 
symptoms of, 207, 529, 533 
fever, black vomit in, 460 
character of fever in, 460 
diagnosis of, 460 
between bilious remittent 
fever and, 461 
between dengue and, 460 
hsematemesis in, 527 
hemorrhage from mucous mem- 
branes in, 460 
jaundice in, 205, 460 
symptoms of, 533 
tarry stools in, 460 
spot of the eye, 197 
ZIEHL’S solution for staining tubercle 
bacilli, 548 Catalogue of Sooks 
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GERRISH (FREDERIC H.). A TEXT-BOOK OF ANATOMY. By American 
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