James Meschter Anders.

A text-book of the practice of medicine online

. (page 149 of 175)
Online LibraryJames Meschter AndersA text-book of the practice of medicine → online text (page 149 of 175)
Font size
QR-code for this ebook

they are prone to develop in ear-disease soon after a cessation in the dis-

Differential Diagnosis. — Brain-tumor usually runs a more chronic
course, and is seldom accompanied by fever, at least not until its final
stage. It may be impossible to differentiate cerebral abscess from men-
ingitis, and the two conditions often coexist, as already stated.

The prognosis is always grave.

Treatment. — When an abscess is diagnosed immediate operation is
indicated. Suspected cases may be treated symptomatically unless focal
symptoms develop. It must be remembered, however, that in a great
many cases no localizing symptoms appear, and, since we know that
most abscesses occur either in the temporo-sphenoidal lobe or in the
cerebellum, when we have reason to suspect the presence of one, these
regions should be explored.


A good deal of doubt exists in the minds of some as to whether diffuse
encephalitis ever exists except as a result of traumatism. Certain it is
that it is less common and much less is known about it than of inflam-
mation of the cord. We meet with it especially in the frontal regions in
certain cases of general paralysis of the insane. The changes often escape
the unaided eye. Microscopically, the vessels will be found injected and
the perivascular spaces distended with leukocytes ; these latter escape
into the surrounding tissue, which becomes softened and edematous.

Symptoms. — It is manifestly impossible to give a definite symp-
tomatology in the present state of our knowledge. Excepting the trau-
matic cases the symptoms are, as a rule, chiefly psychic.

Acute hemorrhagic encephalitis is a condition described by Striimpell.
The brain and soft membranes are hyperemic and slightly edematous,
and throughout the brain-substance there are numerous punctate hemor-
rhages. Perivascular leukocytic infiltration is also present. The eti-
Qlogy is unknown ; but in some cases the disease appears to follow influ-
enza. The symptoms are grave from the first. There are intense head-
ache, fever, unconsciousness, disturbances of motility that are usually
hemiplegic in type, and finally death. In less acute cases there may be
delirium, rapid emaciation, and symptoms of involvement of the cranial
nerves. The diagnosis can rarely be even suspected. The prognosis is
invariably fatal, and no treatment is of any avail.

Acute polioencephalitis, so-called, is a disease of childhood of doubt-
ful pathology. In some of the cases after recovery from the acute


process insular sclerosis or porencephaly is present, with secondary de-
generation in the pyramidal tracts. The etiology is obscure. The
symftoins resemble those of acute poliomyelitis of the cord ; but con-
tractures develop very rapidly in the paralyzed limbs, and reactions of
degeneration are absent from the muscles. The prognosis and treat-
ment are the same as for the disease of the cord.

Non- suppurative encephalitis is by this time well established as a dis-
ease entity, but the symptomatology is not yet clearly defined. The
etiology is indefinite; influenza has preceded some of the cases. The
patlwlogy is variable; there is usually focal softening, often associated
with some vascular alteration, but there may be even cyst formation.
The symptoms are those of focal disease of the brain, usually coming on
gradually — that is, Avithout apoplectiform attack, and, as a rule, sub-
siding without permanent alteration. There may be, therefore, mono-
plegi{Te and disturbances of sensation. The general symptoms are head-
ache, delirium, or coma ; fever, rarely exceeding 103° and sometimes
absent ; and convulsions, often focal in character. The diagnosis is
difficult ; in many cases it cannot be distinguished from meningitis,
cerebral hemorrhage, or tumor except by the outcome. The treatment
is confined to rest, and sedative and antipyretic measures. Operation
is never indicated.


[Cerebral ApojAexy.)

Definition. — Hemorrhage into the brain-substance ; bleeding into
the meninges is generally embraced in the definition.

Pathology and l^tiology. — In intracerebral hemorrhage the blood
will be found to have infiltrated the brain-substance, and, if extensive, it
may have penetrated into the ventricle. In such cases the white matter is
torn asunder, leaving a ragged space that is more or less filled with recent
clot and fragmentary gray matter ; if the ventricles have been entered, blood
may escape from the lowest into the subarachnoid space. In less severe
cases the territory involved is less extensive, and the blood may occupy a
single space or several small spaces, forming mere separations of the nerve-
fibers. Other changes take place according to the duration of the case.
The blood changes color and gradually grows lighter, while reactive in-
flammation about the lesion results in the formation of a wall. The cyst
— for such it has become through fatty degeneration of its contents — may
remain as such, or when the lesion is a small one connective tissue may
form within and a scar result. The larger arteries are generally atherom-
atous, and an aneurysm is occasionally met with ; many miliary aneur-
ysms may be seen in the course of the smaller vessels. It is very seldom
that the actual source of the hemorrhage can be discovered.

Secondary degeneration follows a lesion occuiTing in the motor region
(the cortex or internal capsule), so that sclerotic changes can be traced
from the cortex through the corona radiata, internal capsule, crura, pons,
and medulla to the termination of the fibers in the cord.

Cerebral hemorrhage is generally of arterial or capillary origin. It is


rarely venous, and in the latter case is due almost always either to trau-
matism or to rupture. Spontaneous rupture generally results from exten-
sion of some neighboring focus of disease to the vessel-wall.

Andral states that varicose veins occur in the pia and that they occa-
sionally rupture. Capillary hemorrhage may follow the plugging of a
large vein, and of the larger vessels any one or more may be involved,
but it has been observed that hemorrhage tends to take place at par-
ticular places. In more than one-half of all cases the lenticulo-striate
artery (Charcot's artery of cerebral hemorrhage) gives way, and damages
the lenticular nucleus and internal capsule. Other regions in the order
in which hemorrhage occurs are as follows : centrum ovale, cortex, pons,
peduncle, cerebellum, optic thalamus, and the posterior and anterior
parts of the hemispheres. Hemorrhage into the cerebrum occurs twenty
times more often than hemorrhage into the cerebellum ; it may take
place into the brain-substance, into the ventricles, or into the meninges,
the latter form having already been considered. Ventricular hemor-
rhage in a great number of cases is caused by a more or less extensive
laceration of brain-matter, thus permitting the blood to escape into the
ventricles. Not only the lateral ventricles, but the third and fourth
also, may contain blood.

Symptoms. — Generally the patient is seized without any Avarning,
but in other cases headache, depression, possibly choreiform movements,
and more or less paresthesia precede an attack. The loss of conscious-
ness is usually the first manifestation, though for a few moments before,
motor weakness, with or without spasmodic movements, may exist. In
very slight attacks consciousness may be preserved throughout. The
cause of the unconsciousness is still an open question. Niemeyer re-
garded it as due to pressure acting either directly upon the convolutions
or by limiting the blood-supply. This view is scarcely tenable, how-
ever, for unconsciousness occurs even when the hemorrhage is too small
to exert pressure, and, moreover, the hemorrhage and loss of conscious-
ness are usually simultaneous. The symptoms are in direct proportion
to the extent and position of the hemorrhage. The patient falls, the
face is usually congested, one side often expressionless, and the cheek
flaps during respiration. Breathing is stertorous and, in grave cases,
of the Cheyne-Stokes type ; the pulse is generally feeble for a few mo-
ments, but soon becomes full and bounding in character. The pupils
vary, and may either be contracted or dilated. There is frequently a
relaxation of the sphincters, and on raising the limbs it will be found
that those of one side offer absolutely no resistance. The temperature
is slightly lowered at first, but after a feAv hours rises to, or just above,
normal. In grave cases it will either remain low or will mount up to
106° F. (41.1° C.) or even higher. Such cases are usually fatal. Con-
jugate deviation of the head and eyes takes place in some cases, the
deviation being toward the lesion and away from the paralyzed side ; in
pontine hemorrhage the opposite to this occurs. As a rule, the symp-
toms that we group under the term apoplexy — viz. loss of consciousness,
motor power, and sensation, with or without relaxation of the sphincters
— pass off in twelve to twenty-four hours. In fatal cases the coma
deepens, but death rarely ensues under twelve hours. In hemorrhage
into the medulla or ventricles it may be more rapid.


In from twenty-four to forty-eight hours after the onset febrile reac-
tion sets in, with irritative symptoms due to the inflammatory changes
occurrincr about the oricrinal lesion. There are fever, often delirium,
twitchings or spasmodic movements of a more pronounced type, and
sometimes rigidity in the aflFected limbs. The temperature of the para-
lyzed side is often from one-half to two degrees higher than the tem-
perature on the sound side. Trophic changes in the form of vesicles,
or even sloughing, may occur. Death may take place during this
stage. Cases are generally fatal also in which a second "stroke"
follows closely upon the first, indicating a fresh hemorrhage. After
the reactionary period a stationary period follows ; sooner or later con-
trol of the damaged membranes is then gradually, but not perfectly,
regained. The degree of recovery is dependent upon the resumption
of function of slightly damaged tissue or upon the compensatory activity
of the other side of the brain. In well-marked cases the movements of
the affected side are subsequently ataxic. In certain cases the struct-
ural damage has been too great, and permanent paralysis remains, with
rigidity, wasting, and secondary contractures.

Ingravescent Apoplexy. — In certain cases the onset is slow, conscious-
ness being lost gradually. Coma deepens and the case, as a rule, termi-
nates fatally.

Simple Apoplexy. — The term " simple apoplexy " is almost obsolete.

Serous Apoplexy. — The cases present clinical evidences of apoplexy,
but the only jyostmortem finding is an excess of serum, and this is in no
way responsible for the apoplexy. These cases probably belong in the
same category as those just mentioned, but occur in old persons whose
brains have atrophied.

Hemiplegia. — When this is complete one side of the face and the arm
and leg of one side, generally the same, are all involved. The facial
palsy is not complete, the frontalis and orbicularis oculi escaping. The
tongue when protruded deviates toward the paralyzed side. As a rule
the arm is affected to a greater extent than the leg, and, indeed, in
some cases the face and arm may alone be paralyzed. The trunk-mus-
cles always escape, possibly owing, as Broadbent suggested, to the func-
tional unison of the spinal nuclei of the two sides that preside over them,
and, since they habitually act together, he supposed that they might be
stimulated from either hemisphere.

Sensation is, of course, absent during the period of unconsciousness.
Subsequent sensory disturbances are not constant for all cases. Spots
of anesthesia often exist for a brief period, but hemianesthesia is rare.
Occasionally dissociation of sensation is present, tactile sensation being
preserved, whilst muscular and thermal sensation is lost or diminished.
The stereognostic sense is often seriously disturbed in these cases. A
lesion in or about the posterior part of the posterior limb of the inter-
nal capsule is specially prone to give rise to disturbances of sensation.

The special senses may be temporarily perverted or their functions
in abeyance, but rarely do permanent disturbances occur. Transient
crossed hemianopsia usualW occurs, even if the optic tract has not been
directly involved. More or less mental deterioration may be perma-
nent, however. The deep reflexes are increased on the paralyzed side,
and the superficial reflexes are absent.

Crossed Hemiplegia. — When a lesion occurs in the lower part of the


pons the fibers of the facial nerve that are involved hav6 already decus-
sated ; hence facial palsy occurs on the same side as the lesion. The
fibers coming from the cortex are implicated before their decussation, so
that paralysis of the limbs occurs on the side opposite to the lesion.
Lesion of the crus may lead to oculo-motor palsy of the same side, and
palsy of the face, arm, and leg of the opposite side.

Course and Terminations. — As previously intimated, the course
depends on the position and extent of the lesion. In the most extensive
cases death rarely takes place under several hours. Hemorrhage into
the medulla may prove fatal more quickly. In the slightest cases, per-
fect recovery may take place in a few days or weeks. Generally, how-
ever, when little or no improvement occurs in two or three months, per-
manent changes result. The facial muscles soon recover, and next the
leg, while at first the patient is able merely to move the toes. Daily
improvement then follows until he can support his weight ; dragging of
the foot, however, is marked at first, and rarely disappears absolutely.
In the mean time a less pronounced change for the better has been taking
place in the arm. This member very rarely recovers, however, to the
same extent as the leg, and secondary contractures develop in time, the
arm and hand becoming flexed, whilst the leg is extended. The hand
is usually bluish and cold, and swells if kept in a dependent position.
More or less ataxia is constant, and rheumatoid pains are apt to occur
during this stage. Other late manifestations that are only occasionally
met with are athetosis, arthropathies, post-hemiplegic chorea, and

There is no wasting of the aifected muscles as a rule ; nor are there
electric changes, except during the irritative period, when the response
to stimulation is heightened. Occasionally marked atrophy occurs, and
is due in some cases, as Charcot has shown, to changes in the cells of
the anterior horns. In others no such change is found, and we are
forced to regard the wasting as cerebral.

Differential Diagnosis. — Apoplexy is to be distinguished from
other conditions causing unconsciousness, such as cardiac syncope, epi-
lepsy, alcohol or opium-poisoning, insolation, or uremia. If some pre-
vious history can be obtained, the difficulty of the diagnosis is lessened,
though it may still be great. In syncopal attacks the pulse is very
feeble and the face is pale, respiration being shallow and often sus-
pended. The sphincters are hardly ever relaxed ; the reflexes are usu-
ally preserved, and the skin is often moist. In epilepsy there is a his-
tory of previous attacks, or, failing to obtain this, one can usually learn
that a convulsion has immediately preceded the coma. With alcoholism
the case is more difiicult. The odor of alcohol on the breath is of no
value, as spirits may have been given by a bystander ; moreover, hem-
orrhage is common in alcoholics (vide table of difi"erential diagnosis, p.
969). In opium-poisoniny the coma comes on gradually, and when not
too profound the patient can be aroused when shaken or shouted at.
The respirations, which are very slow and deep at other times, become
somewhat quicker and shallower when he is aroused. In insolation the
temperature suffices as a rule, though, as stated, high temperature may
occur in apoplexy. The presence of albumin is not conclusive evidence
of uremic poisoning unless the centrifuge and the microscope reveal
the presence of casts or other indications of renal change ; even then



the case may be one of apoplexy in a subject of nephritis. In the case
of diabetic coma the presence of sugar in the urine serves to make the
diagnosis. When we meet with a comatose case in which there is abso-
lutely no resistance when the limbs of one side are raised, while those
of the other still exhibit some tonicity, particularly if the deep reflexes are
exaggerated on the flaccid side, the probability is that it is an apoplectic
attack. It is generally not possible to tell whether the condition is due
to hemorrhage, embolism, or thrombosis, though the tabulated points of
distinction (after Leube, vide infra) Avill aftbrd material aid :


Early adult life.

Previous development of atheroma, car-
diac disease following acute rheuma-
tism, sepsis, chronic valvular disease,
fatty heart, general cardiac weakness,

Detection of emboli in other organs.

During the attack there is an absence of
congestion of the face ; the pulse is
normal ; in cardiac affections it is ac-
celerated and irregular.

Temperature normal, but shortly after
the attack it begins to rise, without
making an unfavorable prognosis.

The attack, as a rule, is short ; if there is
a protracted embolic infarction, the
duration is long ; usually the circula-
tion adjusts itself promptly.

Remote effects are infrequent. Hemi-
• plegia is right-sided, with aphasia.


Late adult life ; in early life very rare.
Atheroma with cardiac hypertrophy.

History that the patient up to the time
of attack was well ; also the finding of
casts in urine and other symptoms of
chronic nephritis.

During the attack there are noted flushes
(reddish) of the face, pulsating carotids,
and slow pulse.

Temperature during the attack is sub-
normal, but just previous to death there
is an antemortem rise.

The duration is, as a rule, longer. Coma
of long duration (about two days) gives
a very unfavorable prognosis.

Remote effects quite frequent ; alteration
in the urine — albuminuria, polyuria.

At times the ophthalmoscope reveals
either a recent or an old embolus in the
arteria centralis retinae.

Ophthalmoscopic Examination.

The retinal arteries may show various
stages of atheromatous degeneration ;
as a result there may be a hemorrhagic
retinitis or there may be a thrombus
of the central vein of the retinae. In a
few instances, in which the hemorrhage
occurred in tiie ventricle, the pupils
were contracted.

It is not an uncommon occurrence to have patients brought to a hos-
pital dazed and smelling of liquor. These should always be carefully
watched, for mistakes readily occur, and many such cases have been
condemned to a prison-cell when they were really suffering from cerebral

Prognosis. — Sufficient has already been said on this point.

Treatment. — The patient should be kept as quiet as possible and
in the recumbent position, with the head somewhat elevated. The
clothing about the neck should be loosened to prevent constriction.
An ice-bag may be put to the head and hot bricks or a hot-water bottle
to the feet, while sinapisms may be placed on the back of the neck or
on other parts of the body. If the pulse is strong, full, and incom-


pressible, and the face is congested — venesection is probably justifiable,
particularly if the age and condition of the vessels support the idea
that hemorrhage is taking place. It must not be done without consid-
eration, however, since it would be useless in embolism and thrombosis.
The bowels should be made to move freely ; a cathartic may be exhibited
by the mouth (croton oil, gtt. j or ij), and at the same time an enema
may be given. When consciousness returns the patient should be kept
absolutely quiet for several days, and only liquid food permitted. Later
an endeavor should be made to keep up the tone of the affected muscles
by massage and electricity. It is questionable if the iodids or any other
drugs have an influence over the subsequent changes.


Definition. — Impairment or total suppression of the power of
speech, due to cerebral disease. This is a complex subject, and cannot
be more than touched upon here ; but the chief disturbances will be
briefly mentioned, omitting any further description of the form due to
disease of the bulb (anarthria), since it has already been dealt with in
speaking of Bulbar Palsy (vide p. 1098).

The majority of cases of aphasia are met with in connection with
hemiplegia. They are apt to be more marked in the beginning, owing to
the general obtunding of the psychic processes that is induced by the
shock. Speech is the expression of thought in words, and is the result
of external stimulation in which the impulse awakens in the mind a
recollection of similar impulses that have preceded it — e. g. the sight of
a dog, sound of a bell, or certain odors {vide Fig. 70). Bastian, however,
believes that it is not necessary to postulate the existence of a separate
center for conceptions or ideas. He believes that a better knowledge of
the functional activity of the auditory and visual word-centers obviates it,
and gives the following three ways in which the perceptive center may be
called into activity : (1) By voluntary recall of past impressions, as in an
act of recollection ; (2) by association — that is, by impulses communi-
cated from another center during some act of perception or during some
thought-process ; and (3) by means of external impressions.

Two principal forms of aphasia exist : (1) Motor, and (2) Seiisory. I
shall consider these forms of aphasia separately, although before doing
so it seems necessary to indicate by means of the accompanying schematic
diagram (Pig. 71) the diff"erent paths on which the individual acts for the
occurrence of speech are fulfilled. This will also serve to furnish an easy
explanation of the symptomatology of the individual forms of aphasia and
the means by which their discrimination (from each other) is possible.

Motor Aphasia. — As stated, we meet with aphasia most frequently
in hemiplegia. It is also met with in certain cases of embolism and
thrombosis and as a result of softening from any cause ; also in certain cases
of brain-tumor and in deaf-mutes. The latter cases are not strictly in-
cluded in the definition given, for, while brain-injuries at birth may and
do occasionally cause aphasia either by damaging the brain as a whole (im-
becility) or in a more circumscribed fashion, I refer particularly to those
cases in which the child is aphasic because he is deaf, for unless trained



through his visual or tactile sense he has no memory-picture of words
from which to draw. A child may acquire the power of speech and
retain it for several years, and then become deaf. He will then receive
no more auditory impressions, and, unless trained as in the preceding
group, will become aphasic. Certain cases of congenital speech-defect
have been described by Hodden under the name " idioglossia." Here
the children utter peculiar sounds, constant for the same words. As a
rule, their intelligence is not up to the normal. In hemiplegia the lesion
is usually in the motor, or emissive, center in the foot of the third frontal
convolution (Broca's region). In right-handed people this is on the left


A<^- -^L

a "

u I

Fig. 74.— Diagram for the explanation of
the process of speech (Leube) : A, auditory
perceptive center (center for the recognition
of sounds) ; a A, acoustic tract (auditory
tract) ; L, center of motor speech ; L I, motor
speech tract (path for the innervation of the
muscles of plionation) ; J, center of ideation
(higher concept center).



Fig. 75.— Diagram for the explanation of aphasia
(Leube) : A, a A, L, LI, J, the same as in Fig. 71 ;
A J L A, circle by which speech is controlled;
a A LI, path used for automatic speech; J LI,
path used for voluntary speech ; a A J, path used
for the recognition of words ; =, interruption of
conduction; 1-.3, forms of sensory aphasia (1, cor-
tical ; 2, subcortical ; 3, transcortical) ; 4-6, forms
of conduction-aphasia (1, cortical; 2, subcortical;

Online LibraryJames Meschter AndersA text-book of the practice of medicine → online text (page 149 of 175)