encouraged to rise and use moderate exertion. This, if well borne,
should be increased day by day, for it will be soon found whether the
efforts are injurious or not. All the requirements are present in
these cases to produce chronic hysterical invalids, both male and
female. It is therefore incumbent upon the medical attendant to
protect his patient from discouraging surroundings of any kind. It is
also his duty to so act that while he will be careful to work no
injustice, he will at the same time be on the watch for malingering,
for this will often be practised, especially by those who are among
the expectants already mentioned in this article.
{917}
INTRACRANIAL HEMORRHAGE AND OCCLUSION OF THE CEREBRAL VESSELS,
APOPLEXY, SOFTENING OF THE BRAIN, CEREBRAL PARALYSIS.
BY ROBERT T. EDES, M.D.
The various subjects embraced in this article are so closely united to
each other, both in a clinical and in a pathological point of view,
that they must be considered to a certain extent in common. It is of
course more systematic to group them entirely according to the obvious
and final lesion, as hemorrhage, thrombosis, or embolism; but when it
is considered how very closely the symptoms of one affection may
counterfeit those of another—so closely, in fact, that a diagnosis
with absolute certainty is not only difficult, but often
impossible—and also that similar conditions of the vessels may give
rise either to rupture or occlusion, so that not infrequently two sets
of lesions may be found in the same brain, and, finally, that the
basis of prognosis and of the later treatment is not unlike in
different lesions,—we are surely justified in bringing them, at least
in the beginning, under a common head.
Intracranial hemorrhage, and especially cerebral hemorrhage, is the
lesion which more frequently than any other gives rise to the group of
symptoms known as apoplexy, and from this fact has arisen the frequent
incorrect application of the word apoplexy, in a pathological as well
as a clinical sense, to indicate an extravasation of blood, as in the
so-called pulmonary apoplexy, where the anatomical lesion, being an
extensive effusion of blood into the tissues of the lung, bears an
apparent resemblance to the state of the brain often found in apoplexy
primarily and properly so called, the symptoms, however, being
entirely different. This error receives additional support from the
fact that in some injuries to the brain, especially to the base,
pulmonary hemorrhage may secondarily take place. Apoplexy, however, is
not always the result of hemorrhage, but occurs with many cases of
embolism and of thrombosis, and is sometimes, so far as we can tell,
dependent upon neither of these conditions, recovery in one set of
cases taking place so rapidly as to preclude the supposition of a
considerable organic lesion, and in others, which are fatal, nothing
being found beyond an excess of serum or of vascularity, and sometimes
not even that. The first of these conditions has been called simple
apoplexy, but with our present knowledge its simplicity seems to
border closely on ignorance, or at any rate is not of a character
{918} to satisfy the inquiring mind. It is therefore better to retain
the term apoplexy strictly as a convenient term for a certain set of
symptoms, but, whenever possible to substitute for it an anatomical
description of the lesion found post-mortem or diagnosticated with
reasonable probability during life.
The practitioner may very properly, and without laying himself open to
criticism of his diagnostic accuracy, return the cause of death in a
case of sudden death, or where his opportunity for observation has
been limited, or where no post-mortem examination has been held, as
being apoplexy; but in others, where the symptoms were decisive or a
post-mortem has disclosed the exact lesion, the condition of the
cranial contents should be stated. It is also a not uncommon
mistake—or rather piece of carelessness—to speak of small hemorrhages
in the brain as small apoplexies. A small extravasation may give rise
to slight symptoms or next to none, but a real apoplexy can hardly be
small, although it may be short.
The root from which the word apoplexy is derived seems to have been
used by the classic writers in something like its present clinical
signification (_Απορληκτος_, seized with (apoplexy or)
stupor—Aristophanes; mad—Demosthenes; _Αποπλησσομαι_, to be struck
with amazement—Sophocles). Morbus attonitus, another of its names,
expresses a somewhat similar idea.
Morgagni was familiar with cerebral hemorrhage, and Bonetus in the
_Sepulchretum_ gives several cases. The allusions of Galen and
Hippocrates supposed to refer to this lesion are not unequivocal,
although the Father of medicine could hardly have helped being
familiar with the symptoms of so striking a form of disease.
Cerebral softening has been recognized since the early part of the
present century, and in some of the cases thirty years ago an
efficient cause, in the form of arterial disease, assigned to it; but
the complete theory of its causation forms a part of the general
doctrine of embolism and thrombosis which was so largely developed and
systematized by Virchow. Andral and Durand-Fardel had apparently no
idea of the exact mechanism of its origin, the latter supposing it to
depend upon inflammation, while Todd mentions a case where softening
giving rise to paralysis depended upon a dissecting aneurism of the
carotid. He seems to have generalized so far as to say that white
softening is atrophic, but the precise way in which this localized
atrophy was usually brought about evidently escaped him. According to
him, the suddenness of the attack was owing to a gradual
disorganization of the brain-substance with few or no symptoms, and
then a sudden rupture of diseased fibres by some accidental cause or
by their having reached the extreme limit of cohesion.
Intracranial hemorrhage may be situated outside of the dura mater,
separating this membrane from the bones of the skull and producing
more or less compression of the brain. It is usually the result of a
blow, but not necessarily of a fracture of the skull. When a fracture
is present, blood may pass through it from the interior and give rise
to an external extravasation in addition to that which is likely to be
the direct result of the blow upon the skin and subjacent soft parts.
The middle meningeal artery is a frequent source of this hemorrhage.
Hemorrhage in this position will naturally give rise to symptoms of
compression, and, if the fact of the blow be not known or the fracture
manifest, may be mistaken for some of the deeper-seated forms.
{919} Blood may be effused upon the surface of the brain in the
so-called cavity of the arachnoid—that is, outside of the pia mater—or
in the meshes of this membrane, following its course along the sulci.
This also is not infrequently the result of violence either with or
without fracture of the bone. Its source is likely to be found in the
veins which empty into the longitudinal sinus from the surface of the
brain. Rupture of a lateral sinus from a not very severe blow has been
the source of large and fatal hemorrhage.[1] Blows upon the head, with
or without fracture of the cranial bones, are likely to cause rupture
of the cerebral substance with hemorrhage, and this may find its way
to the outside and cover more or less of the surface. Such injuries to
the brain, it is important to note, do not necessarily correspond
immediately to the place of the blow or to the external ecchymoses.
Meningeal hemorrhage in this region may, however, be observed when no
injury has been received, or at least when there is neither history
nor external traces of any.
[Footnote 1: _Cincinnati Clinic_, p. 135, 1874.]
The conditions under which it occurs may not vary greatly from those
of the more ordinary intracerebral effusion. In two instances under
the observation of the writer the source of hemorrhage has been a
vessel of small, but not the smallest, calibre (artery), situated near
the fissure of Sylvius, in the lower parietal or temporo-occipital
lobe. In children meningeal hemorrhage is, with only a few exceptions,
the usual lesion of apoplexy. The blood is usually dark and coagulated
in recent cases. Blood found under the membranes where no fracture has
taken place is, however, more likely to have been derived from the
brain-substance and to form part of a cerebral hemorrhage.
Hemorrhagic pachymeningitis, indicated by a layer of fibrin included
between the dura on the one hand and a false membrane on the other, is
met with in connection with meningeal and cerebral hemorrhages. It is
supposed to depend on a small and thin hemorrhage upon the surface of
the brain, which forms, by its irritant action, a false membrane about
itself. It is found usually over the vertex.
Hemorrhage into the ventricles is nearly always the consequence of a
hemorrhage in the brain-substance breaking through, although it may in
rare cases originate in the vessels of the choroid plexus, velum
interpositum, or meninges. Its source, however, is sometimes so near
the surface as to cause but little laceration of the cerebral tissue.
The blood breaking into any one of the ventricles may be found in one
or all of them (except the fifth), and form quite an accurate cast of
their shape.
The most common form of intracranial hemorrhage, however, which most
nearly concerns us here, and which is generally meant when sanguineous
apoplexy is spoken of, has its principal seat in the brain itself,
which is, of course, more or less lacerated. Such hemorrhages may vary
greatly in size, from a mere red point (punctate or capillary), of
which many may be present at once, to one of many ounces, filling a
large cavity of nearly the length of one hemisphere, and pushing the
torn and compressed brain-substance before it in every direction. The
amount of laceration produced of course varies greatly; sometimes it
seems as if nothing more than a pushing aside of fibres without
rupture had taken place, while at others large masses of tissue are
torn away and mixed up with the blood into a pulp.
{920} In a recent hemorrhage the clot itself, speaking of those of a
size above the capillary, is usually homogeneous, the brain-substance
surrounding it ragged, œdematous, yellowish or red, and frequently
containing many minute secondary hemorrhages. The rest of the brain is
frequently found anæmic from pressure, the convolutions flattened, the
surface dry, and the section exhibiting a diminished quantity of
blood. In older cases, however, and probably also in some where
atrophy, senile or otherwise, has preceded the hemorrhage, this
condition is not found, and we may have the convolutions shrunken and
the meshes of the pia containing an excess of serum.
If death does not take place speedily, the clot undergoes degenerative
changes. Its color becomes somewhat lighter, chocolate color,
reddish-yellow, or yellowish-red. A portion is absorbed, and after a
time the cerebral substance in the neighborhood forms about it a wall
of some density, so that finally nothing is left but a cyst with fluid
or semifluid contents, and often remains of connective tissue.
Sometimes the absorption of a clot of moderate size is so complete
that only a firm mass of a reddish or yellowish-brown color marks the
seat of an old hemorrhage. The brain-substance in the neighborhood may
be more or less atrophied, and a distinct depression may be noted over
the position. The microscope shows in a fresh hemorrhage only
broken-down nerve-tissue and blood and vessels more or less
degenerated. In an older one the blood-corpuscles have disappeared,
but masses of pigment of a dark yellow or a brownish-red remain to
show the former presence of blood. This pigment occurs in the form of
rounded granules or of small rhombic crystals, and has received the
name of hæmatoidin. The light-yellow masses often found along the
course of the cerebral vessels are not evidence of hemorrhage, but of
congestion merely. The so-called inflammation or granulation
corpuscles, which are simply the fattily degenerated cells of the
organ in which they are found, and which usually possess no
distinctive form, being simply round masses of fat-drops, are often
met with in the brain in hemorrhage or softening. It is sometimes
perfectly evident, however, from their form, triangular or pyramidal,
that they are degenerated nerve-cells. The blood-vessels, those just
above the size of capillaries, are usually in a condition of fatty
degeneration, masses of dark granules occupying more or less densely
the line of their walls. A mere deposit of fatty granules inside the
perivascular sheath, but outside of and not involving the walls of the
arteries, may present the appearance of a degeneration of the walls
themselves. This condition may be a consequence of any lesion
involving degeneration of brain-tissue, and in no way a cause.
The intermediate stages of transformation in a hemorrhage are less
frequently found than the recent or old ones, since the patient, if he
does not die within a few days, is likely to live for some weeks or
months.
The changes taking place in the clot itself within the first few days
are not very marked, but the walls of the cavity may become softer and
more deeply colored, at first red and afterward yellow. Blood-crystals
have been detected on the seventeenth day (Virchow). The following
descriptions have been given of clots of different ages: Eleven
days—reddish-yellow softening clot, with brain-tissue stained for half
an inch in depth, and brain rather hard in vicinity. Eighteen
days—cavity with its {921} edges anteriorly and superiorly sharply
defined, with the edges posteriorly ragged and yellowish, filled with
a tolerably firm brick-red mass adherent to surrounding brain, and
showing in the centre a softened clot about the size of a pea.
Twenty-eight to thirty-five days—soft, brownish, and semifluid.
Forty-one days—spot of softening filled with brownish material. One
hundred days—somewhat darker, and a little more distinctly marked from
surrounding tissues; by microscope granular corpuscles, groups of
fatty granules along the swollen vessels, granules of pigment.
Eighty-three years—old hemorrhagic focus in right optic thalamus,
color yellowish, and areolar structure.
The thirtieth day is given as about the time at which the walls of the
cyst become more firm and distinct. The following statement is
prepared from a considerable number of cases given by Durand-Fardel:
From four to six weeks, the clot is dark-colored, from black to ochrey
or reddish-yellow. It varies in firmness. The capsule is tolerably
firm. From two to four months, it seems to be generally softer,
pultaceous, grumous, or the clot still remaining swimming in serum; in
some cases lighter in color. In six months it has lost more in color,
and the cavity may be smaller. In a year there is still considerable
color left. In a few cases after some years the blood has been found
in the form of a dried mass, not changed or darker in color.
Hemorrhages of several months' standing may be indicated either by a
brownish-red patch somewhat firmer in texture than the surrounding
brain-substance, or by a cavity with firm walls, which often has
strings and septa of connective tissue running across it, so as to
convert it into a kind of spongy mass filled with brownish fluid.
The most important changes which are found in most if not all cases of
ordinary hemorrhages (_i.e._ such as do not depend upon violence or
cachexia) are those of the blood-vessels. They are not, however,
visible in the ordinary inspection of the brain at an autopsy, but
require to be carefully sought for, either with the microscope or a
somewhat tedious process of washing. For this reason there are no
trustworthy statistics of large numbers to determine in how large a
proportion of all the cases alterations in the blood-vessels are to be
found, and in what form. There can be but little doubt, however, that
those cases in which no form of arterial disease is present (if, with
the reservation just noted as to violence or cachexia, such exist) are
to be looked upon as rare exceptions.
The presence of miliary aneurisms in the brain had been noted in some
cases, and even in cerebral hemorrhage, without the great importance
of the observation having been perceived; but the extended and careful
observations of Charcot and Bouchard first showed how extremely common
their presence is, while in many instances they were found actually
ruptured. These aneurisms are present in the largest numbers in the
regions of the brain where hemorrhage is most frequent, and at the age
when death from apoplexy is most likely to occur. They have been found
at the age of twenty, but very rarely at early ages, while after forty
they are not uncommon. It is of course not always that they have gone
on to rupture, but may occasionally be found where no hemorrhages have
taken place. It is not going far, however, to infer that in such cases
the hemorrhage was not very distant.
These aneurisms are dependent upon a periarteritis which is diffused
{922} more or less widely over the cerebral arteries, but not over
those of the rest of the body. The larger arteries get a thin and
shining appearance, compared by Charcot and Bouchard to the skin of an
onion, while the smaller ones present besides distinct aneurisms,
bulgings and irregularities of outline. This condition may be—and, as
would be at once suggested from the age at which both lesions are met
with, is—very likely to be associated with atheroma, but it is not the
same thing, since the development of the aneurisms depends upon a
periarteritis, and that of atheroma upon an endarteritis. It may be
remarked, also, that atheroma usually does not affect the very small
arteries which bear the aneurisms and give rise to the hemorrhage.
These aneurisms are visible to the naked eye, being from two-tenths to
one millimeter, or a little more, in diameter, while the artery to
which they are attached can be seen by the naked eye or with a lens
magnifying two or three diameters. They may be strung along a small
artery like beads or be found in groups like a bunch of grapes.
Charcot and Bouchard found them in every case of cerebral hemorrhage
which they examined, and, although the possibility of other sources
was admitted, concluded that in by far the greater number of cases,
excluding those dependent upon traumatism or hemorrhagic diseases, the
blood effused in the brain has its origin in one of these aneurisms.
The presence of these aneurisms has been abundantly established by
other observers, and the fact that they are not usually demonstrated
proves nothing except the amount of care and time necessary to find
them. One does, however, find occasionally noted that they were sought
for and not found. The statements of Charcot and Bouchard relate, so
far as their own observations are concerned, and as they themselves
remark, chiefly to aged persons, but in their first series of 66 cases
there is found 1 of twenty and 1 of forty years of age. The patient of
twenty was a semi-imbecile and a drunkard. Extensive cerebral
hemorrhage, with atheroma, in the circle of Willis has been found in
an apparently healthy and well-nourished boy of fifteen.[2]
[Footnote 2: Baker, _Annals of Anat. and Surg. Soc. Brooklyn_, 1879,
p. 40.]
Larger aneurisms, often multiple, are not very infrequent upon the
arteries at the base of the brain. They may before their rupture give
rise to symptoms of pressure like any other tumor, and may also be the
source of hemorrhage, which is usually meningeal. They are not
infrequently symmetrical, and a place of election is one of the early
bifurcations of the middle cerebral.
Coats[3] states that aneurism of the larger arteries is the most
frequent source of hemorrhage in persons under fifty. They may be due
to embolism, producing, when the occlusion is not complete, mechanical
injury to the walls of the vessels by the constant hammering upon them
of the embolus under the impulse of the blood. If this etiology is a
common one, it accounts for the frequent situation of these aneurisms
in the middle cerebral arteries.
[Footnote 3: _Glasgow Med. Journ._, 1882, xvii. 109.]
Small vessels in a condition of fatty degeneration are often found in
the neighborhood of a cerebral hemorrhage. In some cases, undoubtedly,
the degeneration is a consequence of the injury to which the cerebral
substance has been subjected, but they have also been found too soon
{923} after the hemorrhage for this explanation to hold; and in cases
where no aneurisms are present the older supposition, that hemorrhage
results from this kind of degeneration, seems to have a certain
foundation, even if only in a minimum of cases.
In several cases of cerebral hemorrhage in purpura, where the general
character of the disease was shown by hemorrhages in other organs,
fatty degeneration of the cerebral vessels has been found, together
with extensive steatosis of the liver, kidneys, muscles, and heart.[4]
In a cerebral hemorrhage found in the brain of a girl of eleven the
walls of the vessels were dotted with fat-globules and dark granules,
and several of them studded with round and oval nuclei closely
resembling the nuclei (small cells?) commonly found in tubercle. There
was no trace of tubercle in any part of the body.[5]
[Footnote 4: _Gazette hébdomadaire_, May 12, 1876, p. 288.]
[Footnote 5: _Trans. Path. Soc._, Cayley.]
There is no possible means of determining in which way any given
bleeding has arisen, except a very minute search, and this may fail to
show the actual point of rupture. It seems highly probable, from the
connection of some cases of hemorrhage with valvular disease of the
heart, that embolism may give rise to effusions of blood, especially
capillary and multiple ones. In such cases the emboli may be deposited
in arteries far too small to be obvious in the ordinary process of
dissection. (See Capillary Embolism.)
Hemorrhage arises in some rare cases from the backing up of blood in
the veins when they are obstructed by thrombosis. A case has been
described where meningeal and ventricular hemorrhage resulted from a
rupture of the straight sinus at its juncture with the torcular
Herophili.[6]
[Footnote 6: Mullar, _Lancet_, 1849, i. 607.]
In many diseases like purpura, idiopathic anæmia, and leucocythæmia
many hemorrhages may take place in the brain as well as elsewhere
throughout the body. Their importance under these circumstances is
usually not great.
The usual localities of cerebral hemorrhage are stated with much
minuteness in the following table from Durand-Fardel, which, although
not very recent (1854), is not the less accurate on that account. No
subsequent statistics have essentially altered its most important
conclusions. In 139 cases the hemorrhage was situated in the
hemispheres 119 times; in the protuberance (pons), 21; in the
cerebellum, 13; total, 153.
I have placed beside these a small number of cases from the records of
the Boston City Hospital and my own practice, and, to avoid the
multiplication of headings, have entered some multiple hemorrhages
under two or more heads, so that from the whole number of cases (46)
there are 81 entries: