treatment of otitis media and early attention to inflammation in the
mastoid cells, with incision or trephining as may be necessary.
After a thrombus has formed there is little to be done toward its
removal.
It has been claimed[68] that the preparations of ammonia are capable
of diminishing considerably the coagulability of the blood when it is
morbidly augmented. Though this cannot be considered proved, yet since
the tendency of these salts is also to quicken the blood-current, a
trial in a case where other indications are wanting is, to say the
least, justifiable.
[Footnote 68: Lidell, _Am. Journ. Med. Sci._, July, 1874, p. 101.]
In a case reported by O'Hara,[69] where the symptoms pointed very
strongly toward thrombosis of the cavernous sinuses, recovery took
place under mercurials, iodide of potassium, and purgatives. The
reporter was inclined to consider the cause of trouble specific.
[Footnote 69: _N. Y. Med. Record_, vol. xvii. p. 617.]
Considering the fact that cases with such marked and decisive symptoms
as those last recorded have recovered, it is certainly the duty of the
physician to prolong the life of his patient to the utmost, that
absorption and condensation may go on as long as possible and
collateral circulation be developed. Probably most physicians can
recall cases of obscure cerebral disease going on to recovery contrary
to all expectation, in which thrombosis furnishes an explanation quite
as plausible as any other.
Softening of the Brain
is a name which it is yet too early to omit altogether from a
systematic work, although in treating of it we have more to do with
nomenclature and classification than with pathological anatomy. The
phrase may be said to have both an anatomical and a clinical
signification, which do not coincide at all points. Clinically and
among the laity it is used to express various symptoms and groups of
symptoms more or less referable to the brain, some of them connected
with one and some with another lesion, and many purely functional—if
the word may be used—or at any rate unconnected with any known or
definite lesion.
Vertigo, dull headache, sleeplessness, or, on the other hand,
drowsiness, failure of memory, failure of power of concentration, of
steady application, mental depression, fatigue, and even slight
aphasia or actual slight hemiplegia, may any of them be considered
symptoms or forerunners of softening of the brain. As nearly as
anything, the popular notion of this affection corresponds to general
paralysis of the insane or senile dementia, or even mere exhaustion.
Many of these symptoms may, of course, be connected with the real
softening described as the result of embolism or {990} thrombosis, but
it is hardly necessary to say that a symptomatology based on these
elements alone is either too vague or else too much like that of
diseases already described to be considered useful as a separate
clinical grouping.
On the anatomical side softening of the brain has had a definite
meaning, and for many years a part of its pathology has been well
known. A general softening of the whole brain, such as seems to be the
condition supposed when the phrase is used, does not and cannot exist,
since a vascular lesion sufficient to cause anæmic necrosis of the
whole brain must cause death long before softening would have time to
take place. Nearly all the works and reports on softening have been
based upon cases such as are now referred to definite lesions of the
blood-vessels; and a good idea of the change in nomenclature and
pathological views may be obtained by noticing the dates given in the
extensive literature of the subject in the _Index Catalogue_ of the
Surgeon-General's library, which are nearly all previous to 1860 or
1865.
Localized softening has already been described under the heads of
hemorrhage, embolism, and thrombosis, venous and arterial. Whether it
may occur from diseases of the cerebral vessels without actual
occlusion is not certain, but, remembering the difficulty of detecting
thrombi in minute vessels, and also the fact that it is not a great
many years that occlusions have been systematically sought for at
autopsies, it is better for the present to assume, in cases where
softening is found in the usual form and the usual situations for the
results of thrombosis and embolism, that one of these accidents is the
cause, even if the actual point of occlusion is not found.
Softening may take place secondarily from tumors in the brain, and the
name is also sometimes applied to a local encephalitis, which is an
early stage of abscess. When, however, these various forms of disease
are removed from the general heading of softening and referred to
their proper pathological classes, there is a residuum in which the
softening seems to be the primary affection, so far as the brain is
concerned, though depending on other constitutional conditions.
In new-born infants softening of the brain, besides the rare cases in
which it may be dependent on the same conditions which may cause it in
the adult, is observed in two forms, as described by Parrot:[70] _A_.
White softening in multiple foci, dependent upon fatty degeneration,
of which it constitutes the last stage, is found almost exclusively in
the centres of the hemispheres. _B_. Red softening, which affects the
same region, but more extensively, and is accompanied by hemorrhage
into the lymphatic sheaths with rupture.
[Footnote 70: _Arch. de Phys._, 1873, p. 302.]
These two forms may exist with each other, and with other intracranial
lesions, such as thrombi of the sinuses and exudation under the
arachnoid and around the veins.
Parrot compares this form of softening to that occurring in the other
extreme of life, dependent on vascular lesions; but although he
supposes the method of production to be unlike in the two cases, it is
by no means so certain, either from his conclusions or his cases, that
it is always so. In some of his cases the vessels are said not to be
abnormal, but in others old thrombi are distinctly mentioned. As
secondary consequences may {991} be observed intracranial dropsy, with
perhaps hydrocephalic cranium and degeneration of the pons, bulb, and
medulla.
Two cases of red softening of the cerebellum have been reported.[71]
In one of them the pia was adherent, in the other thickened and
covered with exudation. The microscopic details are not given nor the
state of vessels mentioned. They are probably not strictly analogous
to those described by Parrot.
[Footnote 71: _Jahrbuch. f. Kinderheilkunde_, 1877.]
The occurrence of granular corpuscles in the brain of the new-born is
described by Virchow, and it is thought by him to be pathological and
of an irritative character (encephalitis congenita). It is somewhat
doubtful if this process is characterized by any distinct symptoms.
The ETIOLOGY is impaired nutrition, deficient or improper feeding, and
depressing diseases, frequently tubercle.
The SYMPTOMS and DIGNOSIS of this form of softening are even more
obscure than those of venous thrombosis in the same class of cases.
Vague cerebral symptoms arising in an infant poorly nourished and
suffering from acute disease may be due to this condition, but a
positive diagnosis is out of the question. In the two cases of
softening of the cerebellum just mentioned, in one, aged five, there
was dilatation of the pupil, difficulty of hearing, and vertigo; in
the other, aged six, vertigo, inclination to vomit, and clonic spasm
of the left facial muscles. Parrot says that in the greater number of
patients the encephalopathic troubles observed during life cannot be
referred to it (softening), and in no case can it be diagnosticated.
Under these circumstances it is obvious that remarks upon the
PROGNOSIS and TREATMENT must be purely works of the imagination.
Atheroma of the Cerebral Arteries
has already been spoken of as one of the most important factors in
thrombosis, and perhaps of considerable consequence in embolism and
hemorrhage. Its symptoms, when one of these accidents has taken place,
are hardly to be separately considered; and if atheroma have produced
complete occlusion, even without the assistance of a clot, the
symptoms could not be distinguished from those of an ordinary
thrombosis, and would follow the same course.
In some cases, however, the thickening of the artery may interfere
with, without completely interrupting, the circulation in the part to
which it is distributed, and the degree of the interference may vary
from time to time. If, then, in a person whose age and general
physical condition, as shown by the state of the tangible arteries,
arcus senilis, complexion, and so forth, render the existence of
atheromatous arteries in the brain probable, cerebral symptoms of an
ill-defined character arise, it is very probable that they are the
result of irregularities in the circulation dependent on atheroma.
This state of things is to be distinguished from the more clearly
marked conditions which have already been described, partly by the
incompleteness of the attack, and partly by its changes in severity
and character from time to time—a paralysis undergoing alternations of
{992} improvement and the reverse from day to day, delirium appearing
and disappearing in correspondence with the general health, the vigor
of the heart, and the state of the digestive organs.
The diagnosis between these incomplete anæmias and an almost precisely
similar result of syphilitic endarteritis is to be made chiefly by the
history and age. In middle-aged persons general paralysis might
present a not very different set of phenomena. A tolerably distinct,
but not severe, hemiplegia in an old person, subsiding in a few hours
under the influence of a cathartic, and perhaps returning more than
once, may often be due to a local and temporary anæmia from atheroma,
as well as to slight hemorrhage or a not completely occluding
thrombus.
On the other hand, extensive atheroma may exist without serious
impairment of the cerebral functions, provided it be evenly
distributed and do not interfere with the passage of blood in any one
vessel.
The prophylaxis of atheroma has already been considered. We do not
know of any drug that can change the nature or extent of the processes
going on in the arterial walls, but if any influence can be exerted it
is through dietetic and hygienic means.
The consequences of rigidity of the arterial walls, as productive of
resistance to the passage of blood, can be warded off to some extent
by promoting the vigor of the heart. Treatment should therefore be
directed to the improvement of the nutrition of the body in general
and the heart in particular. Heart tonics and laxatives are the
classes of medicaments most likely to be useful. Perhaps it is to its
effect in increasing the force of the heart contractions, like
digitalis, that coffee owes its reputation as a preservative from
apoplexy.
{993}
ATROPHY AND HYPERTROPHY OF THE BRAIN.
BY H. D. SCHMIDT, M.D.
ATROPHY OF THE BRAIN.
INTRODUCTION AND DEFINITION.—Atrophy of the brain may originate during
intra-uterine life or by defective development during the early
periods of childhood, or it may occur during adult life, when the
organ is fully developed. The atrophy is characterized by a diminution
of the normal bulk of the brain-substance, in consequence of which the
latter does not entirely fill the cavity of the cranium, but leaves a
greater or less space to be occupied by a serous fluid. Generally, the
atrophy affects, in a symmetrical or asymmetrical manner, larger or
smaller portions of the brain; an atrophy symmetrically affecting all
parts of the brain has never been observed, even in microcephalia.
Nevertheless, when the atrophy affects both hemispheres of the
cerebrum, it is generally called total, whilst it is designated
partial when it is limited to only one hemisphere or to other
individual parts of the brain, such as the cerebellum, the large
cerebral ganglia, etc.
For the sake of convenience we shall treat the atrophy of the brain
occurring during childhood, when the organ is still developing,
separately from that of the fully-developed brain of the adult.
1. Atrophy of the Brain during Childhood.
When congenital or originating during infancy the atrophy is either
primarily due to certain pathological processes taking place in the
substance of the brain, or secondary, being due to lesions of the
skull, such as premature ossification of the sutures. Total atrophy of
the brain at this period of life leads to an early death, while
children affected with partial atrophy may continue to live, though
almost always in a state of idiocy. The forms mostly observed in
children are unilateral or bilateral atrophy of the cerebrum, partial
or almost entire absence of the cerebellum, imperfect development of
the large cerebral ganglia, and slight partial atrophy of the medulla
oblongata. The large commissures as well as the crura cerebri are very
seldom found atrophied.
The most frequent and, from a practical point of view, the most
important of these forms is the unilateral atrophy of the cerebrum,
for the reason that in a mild form it is to a certain degree
consistent with the {994} mental and physical development of the
child. It is mostly found on the left side. In some cases the atrophy
extends evenly throughout the hemisphere, while in others it affects
more or less one or the other lobe. The loss in the bulk of the
hemisphere may amount to only a slight diminution, or to as much as to
one-half of the normal size. Its thickness above the ventricle may be
reduced to a few millimeters; in some cases even the membranes of the
brain may lie in contact with the ependyma. The ventricle of the
atrophied hemisphere is almost always enlarged. The convolutions of
the cerebrum are very narrow, sometimes quite indistinct. One or both
of the corpora striata also are generally found atrophied. In many
cases even the atrophy extends to one of the crura cerebri and to the
pyramid of the same side, and to the anterior and lateral columns of
the spinal cord on the opposite side. Frequently, one or the other
lateral half of the cerebellum also is found affected. The condition
of the substance of the cerebrum is nearly the same as in the senile
atrophy of the brain to be described hereafter. The skull is mostly
thickened on the side of the atrophy, and frequently asymmetrical.
SYMPTOMS.—In most cases the mental capacity is below the normal
standard, and frequently borders on or represents a state of idiocy.
The temperament of the patient is generally irritable and very
excitable. The most prominent symptom is an incomplete paralysis on
the side opposite to the atrophied hemisphere, which is the more
pronounced the more the corpus striatum, thalamus opticus, and crus
cerebri are involved. Frequently, there are contractures of the flexor
and pronator muscles of both extremities, particularly of the upper;
the muscles of the trunk remain free; sometimes one or the other half
of the face is also paralyzed. Epileptic convulsions also are
frequently present. Blindness and deafness, with a defective sense of
smell and a blunted sensibility of the paralyzed limbs, as well as
neuralgia of the latter, and headache, have also been observed.
CAUSES.—Besides the causes already mentioned, atrophy of the brain
occurring in children after birth may be induced by injuries of the
head, inflammation of the enveloping membranes, of the ependyma, or of
the substance of the brain itself.
TREATMENT.—Atrophy of the brain in children is perhaps, in the
majority of cases, incurable; it is therefore only in the milder cases
that the patient may be benefited by treatment. Electricity and
gymnastic exercises have been recommended. At any rate, it must be
pursued in a very systematic manner, and based upon the principles
established and practised by the late E. Seguin of New York in his
Physiological School for Weak-minded Children, consisting in improving
the mind, first by training the child to the use of his limbs by means
of light mechanical work, etc.
2. Atrophy of the Fully-developed Brain.
In the brain of the adult the atrophy may be partial or total,
symmetrical or asymmetrical, in the same sense as before used in
connection with the atrophy of the brain of children. It may, further,
be stationary, {995} when the atrophying process remains limited to
the part where it originated; or, progressive, when it extends to
other parts of the brain. Generally, partial, asymmetrical, and
stationary atrophy is due to certain accidental pathological
processes, producing a destruction or loss of portions of the
substance of the brain, such as apoplexy, softening, etc., by which
the nutrition of the neighboring parts becomes disturbed. Total,
symmetrical, and progressive atrophy, on the other hand, actually
depends upon certain constitutional disturbances of the nutritive
process in general, such as chronic alcoholic intoxication, etc.
CAUSES.—As already mentioned, the causes of atrophy of the brain in
the adult may be direct or indirect. The former are generally
represented by certain pathological processes which directly affect
the substance of the brain, as, for instance, apoplectic hemorrhagic
effusions into the brain-substance, thrombosis or embolism of the
cerebral arteries, encephalitis, chronic serous effusions into the
ventricles, inflammation and œdema of the pia mater, etc. To the
latter or indirect causes, which affect the organ by disturbing or
lowering the nutrition of its substance, belong the retrogressive
processes of old age or of insanity; the introduction into the system
of certain noxious substances, such as lead or alcohol; furthermore,
certain wasting diseases, such as phthisis, Bright's disease, etc.
PATHOLOGICAL ANATOMY.—The cerebrum particularly is found diminished in
volume. While the convolutions are thinner than normal, their
intervening sulci are broader. The white substance presents a
dirty-white color, and is abnormally dense and tough, especially near
the ventricles. The latter are enlarged and filled with serum; their
ependyma is thickened and frequently covered with granulations. The
cortical layer appears of a dirty, rusty-brown or yellow color, is
pale, soft, or hard, and frequently is found to adhere to the pia
mater. In very pronounced cases the white substance is almost as tough
as leather, and contracts upon section, especially in the
convolutions; its cut surface is rendered concave. Sometimes the
surface of the convolutions, after the removal of the pia mater,
appears finely shrivelled. The dura mater is often found thickened and
adhering to the skull. The space created in the cavity of the cranium
by the atrophy of the brain is filled by serous effusions into the
tissue of the pia mater, the subarachnoidal space, arachnoid sac, and
ventricles.
The histological changes associated with atrophy of the brain differ
in the different forms. In cases of partial atrophy caused by
hemorrhages, etc. the destructive process generally embraces all the
tissues at first, while the secondary degenerations particularly
affect the nervous elements. In total atrophy the pathological process
appears to commence in the connective tissue, and to involve the
nervous elements subsequently; though in a number of cases, especially
of senile atrophy, the nervous elements appear to be primarily
affected. The blood-vessels also undergo certain changes, giving rise
to the contraction of the brain-substance.
SYMPTOMS.—In partial atrophy of the brain the primary symptoms
resemble those which characterize the particular destructive process
to which the atrophy is due. The most prominent are the symptoms of
motor disturbance, which are always semilateral and correspond to the
extent and seat of the lesion; frequently they remain stationary. The
{996} sensibility of the paralyzed parts is but slightly diminished,
and the mind generally undisturbed. But when the effects of the
original lesion extend, in the form of a secondary degeneration of the
nervous elements, to neighboring parts, or even to the other
hemisphere, the cerebral functions may become secondarily disturbed.
In senile atrophy of the brain, which represents the most simple form
of total atrophy of this organ, the first symptoms frequently appear
toward the end of some intercurrent disease. They consist in a very
slow and gradually increasing derangement of the cerebral functions,
associated with a general loss of innervation, manifesting itself by
talkative wanderings of the mind, restless sleep, hallucinations,
foolish activity, attacks of tremor senilis, etc. The intellectual
functions diminish and the memory is lost. The physical forces also
gradually sink, the tremor senilis increases, and the patient, no more
able to walk, becomes confined to bed. Finally, a relaxation of the
sphincters takes place, and death is produced by the disturbance of
the automatic functions of deglutition and respiration.
Total atrophy of the brain, when due to an extensive meningitis or to
a general disturbance of the nutrition, as is met with in drunkards,
may finally lead to a condition known as general paralysis of the
insane. This disease, however, will be found treated elsewhere in this
work.
TREATMENT.—There is no special treatment for atrophy of the brain; all
that can be done is to palliate and combat the symptoms as they arise.
HYPERTROPHY OF THE BRAIN.
INTRODUCTION.—Notwithstanding the numerous measurings and weighings of
human brains made in the course of time by different investigators, no
absolute standard measure or weight has as yet been established by
which we can accurately determine a pathological increase or decrease
in the size and weight of this organ. The want of such a standard is
principally due to the difference generally existing in the dimensions
and weights of even a certain number of brains taken from individuals
belonging to the same race or nation. The same difficulties are met
with in the attempt at establishing a rule by which to measure the
mental capacity of a certain brain, for the question has as yet not
been solved whether this capacity depends upon the quantity or quality
of the brain-substance. In speaking of hypertrophy of the brain,
therefore, we must keep in mind that a large brain must not be
considered hypertrophied unless there exists a disproportion between
its size and that of the cavity from which it was removed; in other
words, when its growth or hypertrophy meets a resistance at the inner
walls of the cranial cavity. According to Virchow, a further
distinction must be made between the increase (hyperplasia) of the
nervous elements themselves and that of the supporting connective
tissue, the neuroglia. To the latter condition particularly
corresponds the peculiar doughy consistence of the white substance of
hypertrophied brains.