Fardel. B. C. H.
Corpus striatum and optic thalamus, together . . 22 4
Corpus striatum . . . . . . . . . . . . . . . . . 13 10
Optic thalamus . . . . . . . . . . . . . . . . . 5 3
Corpus striatum, optic thalamus, and middle lobe 2 1
Corpus striatum, optic thalamus, and a
considerable portion, not well defined, of the
hemisphere . . . . . . . . . . . . . . . . . . 12 2
Corpus striatum, optic thalamus, with posterior
lobe . . . . . . . . . . . . . . . . . . . . . 1
Corpus striatum and middle lobe . . . . . . . . . 3 3
Corpus striatum, with a considerable portion of
hemisphere . . . . . . . . . . . . . . . . . . 5 1
Corpus striatum, with an extended portion of base
of ventricle . . . . . . . . . . . . . . . . . 1
Optic thalamus with middle lobe . . . . . . . . . 2 1 {924}
Optic thalamus with posterior lobe . . . . . . . 1
Middle (parietal) lobe . . . . . . . . . . . . . 19 1
Sphenoidal horn of middle lobe (temporal) . . . . 2 4
Anterior (frontal) lobe . . . . . . . . . . . . . 11 3
Posterior (occipital) lobe . . . . . . . . . . . 11 5
A not well-determined extent of one hemisphere . 4 3
The superficies of the convolutions (once with
corpus callosum) . . . . . . . . . . . . . . . 3 1
Insula . . . . . . . . . . . . . . . . . . . . . — 2
Cortex (not further defined) . . . . . . . . . . — 1
Small multiple . . . . . . . . . . . . . . . . . — 3
Meninges (secondarily) . . . . . . . . . . . . . 31 6
Ventricles . . . . . . . . . . . . . . . . . . . 66 8
In the cerebellum, right lobe . . . . . . . . . . 6 |
" " left lobe . . . . . . . . . . 5 | 4
" " middle lobe . . . . . . . . . 2 |
In the protuberance (pons) . . . . . . . . . . . 13 4
Protuberance and brain . . . . . . . . . . . . . 8
Protuberance, crus cerebri, crus cerebelli,
external capsule, fourth ventricle . . . . . . — 1
It would not have been very difficult to increase these figures from
the large number of recorded cases, but there is nothing in later
statistics to invalidate the statement that the corpus striatum,
including both its nuclei, but especially the nucleus lentiformis, the
optic thalamus, and the white substance in their neighborhood, are the
portions of the brain by far the most frequently affected by
hemorrhage, and especially by hemorrhages of considerable size.
There is no essential difference in the frequency of hemorrhage on the
two sides. It may occur on both sides at once. Hughlings-Jackson says
that he saw a patient who escaped with life from the effects of a clot
which had paralyzed both sides of the face as well as all four limbs.
Charcot and Bouchard give the following localities as containing in
decreasing frequency the miliary aneurisms: optic thalami, corpora
striata, the convolutions, the protuberance, the cerebellum, the
centrum ovale, the middle peduncles of the cerebellum, the cerebral
peduncles, and the bulb. The close correspondence of this list with
the table of Durand-Fardel is in itself a strong argument in favor of
the importance of the miliary aneurisms as the principal factors in
determining cerebral hemorrhage.
The arteries supplying the nucleus lenticularis and external capsule
are small branches arising chiefly from the middle cerebral a short
distance from its origin, with some assistance from the anterior and
posterior cerebral. One of the larger of them runs along the outer
side of the nucleus lenticularis where it is covered by the external
capsule—a disposition which may have something to do with the
occurrence of the larger hemorrhages so likely to take place just
outside this nucleus and into the substance of the hemispheres.
The arteries of the optic thalamus arise from the posterior
communicating or the posterior cerebral. Why these two groups should
furnish, as they do, so large a part of cerebral hemorrhages it is
impossible to state, unless it be that from their origin so near to
the larger trunks before their division they are exposed to more
pressure, and hence a greater tendency to form aneurisms. The
functional activity of these regions is another possible reason. The
largest hemorrhages also seem to spring from these sources, and if a
table of large effusions were compiled {925} it would probably show a
greater predilection for this locality than even the general one given
above, which includes those of all sizes.[7]
[Footnote 7: A very careful study of the form and size of foci of
bleeding arising from the various nutrient arteries of the brain will
be found in the well-known elaborate papers of Duret (_Archives de
Physiologie_, 1874).]
Before proceeding to a minute account of the symptoms accompanying
cerebral hemorrhage, a consideration of the relation between extensive
lesions and the most fully-developed clinical phenomena will be of
value—in other words, the pathology of hemorrhagic or sanguineous
apoplexy. This will naturally demand a reference to the cases where
the same symptoms are present with a different lesion.
The most marked symptom, one which is essential to the definition of
apoplexy, is the sudden, or more frequently rapid, loss of
consciousness, and next, in a great proportion of cases, a unilateral
paralysis or paresis. The latter, in many cases, finds a sufficient
explanation in the rupture of fibres connecting the motor centres in
the brain with the spinal cord; but this does not cover all cases, for
it is well known that we may have paralysis without any laceration. In
fact, in many cases paralysis may disappear so rapidly as to put aside
at once any such explanation. Sufficient pressure upon contracting
fibres is entirely competent to arrest their conductivity, and this
pressure may be diffused over a considerably wider area than that
where total destruction of tissue has taken place. Meningeal
hemorrhage, where, of course, no laceration takes place, may be
attended by a well-marked hemiplegia when the effusion is wholly or
chiefly on one side.
The writer recalls a case of a man, of whose history little or nothing
was known, found unconscious with a very distinct difference in the
amount of motion to be provoked by irritation of the two sides. The
diagnosis naturally inclined to the more common causes of hemiplegia,
but the autopsy showed a purulent meningitis of the vertex, with a
layer of pus considerably thicker on the side opposed to the
paralysis.
A very similar statement may be made in regard to the symptom of
unconsciousness, which seldom occurs more rapidly and completely than
in cases of meningeal hemorrhage (not from injury), where, of course,
there is no question of laceration.
F. Pagenstecher[8] succeeded in producing phenomena closely allied to
apoplexy by injecting at a known pressure, between the skull and dura
mater in dogs, masses of melted wax and tallow. In the first group of
cases the result was somnolence, great depression of the psychical
capacity, and general muscular weakness. The second group showed,
besides the condition of sopor, unilateral paralysis; and the third
contained cases in a part of which death followed in a few hours after
the setting in of coma, and in another part partial recovery took
place after scooping out the waxy mass. The symptoms in these cases
are referred to the pressure upon the vessels; and it is stated that
in order to destroy life the pressure had to be equal to that of the
blood. Convulsions were present in some cases where the pressure was
not steady. The temperature showed a notable peculiarity in that,
after the initial fall, in which it resembles the course in human
apoplexy, it kept on falling in the fatal cases, instead of rapidly
rising, as in man. After injection into the brain of animals {926} of
sufficient quantities of water to produce great tension of the
occipito-atlantoid membrane, Duret[9] found the respiration to cease
and the heart to be slowed. On tearing the membrane so as to allow the
water to escape, respiration began again, and the animals gradually
recovered consciousness. Similar effects could, however, be produced
by blows on the head.
[Footnote 8: _Centralblatt f. d. Med. Wiss._, 1871, p. 706.]
[Footnote 9: _Centralblatt f. d. Med. Wiss._, 1878, p. 454.]
Several cases are reported by P. R. Hoy[10] where pressure upon the
brain produced an arrest of function, which was resumed when the
pressure was removed. In the first of these a piece of bone had been
removed, but the dura was intact. If the patient were asked a question
and the finger immediately pressed upon the dura, no answer was made,
but as soon as the finger was removed the reply came. In two other
cases, which are not without their parallels, the patients resumed
after trephining the mental attitude in which they had been surprised
by the injury—in one case hours, and in the other years, before.
[Footnote 10: _Journ. Nerv. and Ment. Dis._, vol. iv. p. 288.]
The natural generalization to be made from these cases and experiments
is, that pressure upon the brain-tissue suspends, for the time, its
function; but when we find exactly the same symptoms arising from
either sudden or gradual occlusion of the vessels where we can hardly
imagine increased pressure to exist, except perhaps over a very small
area of collateral hyperæmia, we must go a step farther for a common
factor; and it seems possible to find one which will not only explain
the several conditions spoken of, but also others which closely
resemble them. Simple anæmia will cover the cases of hemorrhage and
embolism, but certainly not narcotic poisoning and certain other
conditions where characteristic apoplectic symptoms exist without
discoverable lesion. If, however, we say that a deprivation of a
considerable portion of gray matter of its due supply of arterialized
and healthy blood suspends for a time its functional activity, we can
explain the similarity of results arising from very different causes.
In a case of cerebral hemorrhage of considerable size the pressure is
distributed over a space much exceeding the area of the clot itself,
and renders a large part of at least one hemisphere anæmic. If the
blood finds its way into the ventricles, the conditions are most
favorable for compressing nearly the whole brain. The anæmic
appearance of the cerebral surface is often remarked at autopsies.
When an embolus lodges in an artery and produces complete occlusion,
the portion of brain supplied thereby becomes at once entirely anæmic,
since the arteries on the surface have so slight anastomoses that they
are entirely unable to supply the deficiency, except to a slight
extent around the edges of the vascular territory involved. The
anæmia, however, does not extend beyond the territory originally
affected, and consequently we may have extensive paralysis from
embolism without a marked apoplectic attack. In extreme congestion of
the brain the reverse may seem to be the case.
In reality, the hindrance to the proper functions is nearly the same,
since blood which is not duly renovated and contains the products of
metamorphosis of tissue in excess is worth as little for healthy
nutrition as no blood at all. There is no reason to suppose that blood
in {927} circulation, no matter in how great quantity, gives rise to
unconsciousness. It may cause over-action or disordered action, as in
mania, but not arrest of action.
The narcotic poisons also deprive the nerve-tissue of its healthy
food; whether by interference with oxygenation and depuration, or by a
direct action of the substance itself on the nerve-cells, it is not
easy to say. The fact that the completeness and duration of the
unconsciousness are not in proportion to the paralysis or anæsthesia
shows that they are to some extent independent of each other; and,
although it is possible to locate with some precision the lesion which
abolishes motor power and conscious sensation, yet we cannot say how
much or what part of the brain must be deprived of its function in
order to produce that cutting off of all conscious relation with the
external world and reduction of a feeling, thinking, remembering, and
acting organism to the level of a mere automatic breathing-machine,
which we designate as loss of consciousness.
In fact, in the present state of our knowledge as to what
consciousness is, any speculation as to its seat would be a waste of
time, and we must content ourselves with recognizing that experience
seems to show that a large part, rather than any particular part of
the brain, must be involved, not necessarily in the primary lesion,
but in the resulting pressure or anæmia.
Another theory of unconsciousness is simply that it is due to
shock—that the sudden irruption of blood acts like a blow, as it were,
and abolishes for a time the function of the nervous structure. This
is substituting something indefinite for something comparatively
definite; and it is certainly not true that the more sudden the shock
the more complete the unconsciousness. It may come on after the
paralysis is apparent, and in fact is more commonly gradual than
sudden in its onset. The classical instantaneous shock is the rare
exception. In the celebrated case where a tamping-iron was driven
completely through a man's skull and brain, he himself was able to
give a clear description of the accident to the surgeon who first
attended him. Several other instances of severe and sudden injury to
the brain without loss of consciousness have been recorded.
ETIOLOGY.—As regards the greater number of cases and the most common
pathology, the existence of so specific and peculiar lesion as
aneurism enables us to distinguish between predisposing and exciting
causes, or, in other words, the conditions which lead to the localized
periarteritis with its resulting aneurisms and those which cause their
rupture. Unfortunately, the aneurisms are not usually looked for, and
in the collection of statistics we are obliged to group together cases
the pathology of which is not always the same, and which are usually
collected under the name of apoplexy.
Age, however, is well known, both on clinical and anatomical grounds,
to be the most important factor. Among the predisposing causes of
apoplexy, all statistics, both of recent and older date, agree in
assigning the period of life beyond forty-five or fifty as that in
which the liability to apoplexy is greatly increased. There is no age,
however, below this, even to infancy, in which true cerebral
hemorrhage may not occur, although the intracranial hemorrhage of
children is more usually {928} meningeal. It is probable, however,
that in many of these the rupture of the vessel does not depend upon a
previous aneurism, but on other lesions. The youngest case in which
aneurisms were found by Charcot and Bouchard was twenty.
If we speak of cerebral hemorrhage in general, without reference to
the presence of aneurisms, as we unfortunately are obliged to do in
the great majority of cases, we may often go much below this point. In
youth and childhood, however, it is possible, and often almost proved,
that other conditions must have been of greater importance in
determining the hemorrhage than aneurism.
In our own small series we find cases of eighteen, twenty-three,
twenty-five, twenty-six, twenty-seven years of age, and quite a number
from thirty to forty-five. A little further examination shows many of
them not to have been of the ordinary kind; thus the patient of
eighteen had valvular disease of the heart and advanced parenchymatous
nephritis; the one of twenty was, so far as could be seen, typical,
but no search was made for aneurisms; that of twenty-five had many
small hemorrhages and was a marked case of idiopathic anæmia; that of
twenty-six had valvular disease of the heart, an embolus in the middle
cerebral artery, which was not in the immediate neighborhood of any
hemorrhage, several old hemorrhages, and hemorrhagic infarction in
other organs. The case aged twenty-seven had a very large clot in one
hemisphere and advanced interstitial nephritis.
Cayley[11] describes the case of a girl of eleven with a large cavity
in the left middle cerebral lobe, where nothing was discovered
abnormal upon the left middle cerebral artery, but when the cerebral
matter was washed away with a stream of water, the walls of the
vessels were found to be dotted with oil-globules, and in several
places studded with round and oval nuclei. This was before miliary
aneurisms were known, but the process of preparation was exactly
suited to bring them to light had they been present, and they could
hardly have escaped observation and mention. Other cases of boys have
been reported where the hemorrhage was of the typical kind.
[Footnote 11: _Trans. Path. Soc._, vol. xx.]
Meigs and Pepper speak of nine cases of hemorrhage into the substance
of the brain in children, but give none of their own. Of the two cases
mentioned by West as coming within his own observation, in one the
source of the blood was in the cerebral veins obstructed by the
formation of clots in the longitudinal sinus.
C. W. Dulles[12] describes a case occurring in his own practice in a
child of six months, where a considerable amount of blood was found in
the lateral, third, and fourth ventricles. Nothing is said of
aneurisms in particular, but the brain was carefully examined without
the source of the hemorrhage being found, although it seemed to be in
some of the vessels of the velum interpositum. Dulles mentions further
a case reported in the books of the Philadelphia Hospital by Joseph
Berens, where in the brain of a child ten days old there were found,
besides a large meningeal hemorrhage, many points of subarachnoid
extravasation, a clot filling all the ventricles, and a clot the size
of a pea in the anterior portion of both corpora striata. In addition
to these there were scattered points of hemorrhage throughout the
brain-substance.
[Footnote 12: _Philada. Med. Times_, vol. vi. p. 507.]
{929} Cerebellar hemorrhage seems to show a certain preference for
younger ages than the more usual forms. In a list of 25 cases from
various sources I find the ages given thirty-two, twenty, nineteen,
sixteen, thirteen and a half, eight. In the seven cases detailed by
Hillairet there were two aged fifteen and twenty-six respectively.
These exceptions, however, do not invalidate the rule that cerebral
hemorrhage of the ordinary type is pre-eminently a disease of later
middle or advanced life.
The male sex is more liable than the female. Durand-Fardel gives 54
cases of men, 37 of women (old persons); our own list, 31 men, 15
women. Falret, cited by Rochoux and Durand-Fardel, gives 1670 cases of
apoplexy among men and 627 among women. This, however, is only a rough
approximation as regards cerebral hemorrhage, as it undoubtedly
includes many cases not dependent upon this lesion. The same remark
applies to Lidell's statement that there died in New York during three
years, of apoplexy, 598 males and 440 females. This moderate
predominance is ascribable to greater muscular effort, and probably
also to the greater prevalence of alcoholic intoxication. Greenhow, in
a Parliamentary report,[13] states that in England and Wales the
number of deaths from apoplexy in 100,000 of population is 46 males to
44 females. From paralysis the figures are 42 and 44, so that the
total from the diseases registered under these two heads is alike for
the two sexes—viz. 88 to 88. In London alone the discrepancy is a
little greater on the male side—108 to 101; but in certain districts
of England the excess is on the other side. Race is of little
influence. High altitudes (7000 feet) favor the prevalence of apoplexy
in the population,[14] as in Peru and Mexico. Warm climates are
somewhat, but less markedly, opposed to it.
[Footnote 13: _Results of Inquiries into Different Proportions of
Deaths, etc._]
[Footnote 14: Hirsch, _Handbuch der Hist. Geoqr. Pathologie_, vol.
ii.]
Heredity seems to play an important part in the same sense as in
tuberculosis; that is, in the establishment of a tendency, which of
course means, anatomically speaking, periarteritis. Many deaths from
cerebral hemorrhage may sometimes be found among the members of a
single family. Dieulafoy has been able to trace this disposition
through several generations. Among several instances, Mme. G—— died in
three hours of paraplegia with loss of consciousness. Her mother had
hemiplegia at the age of fifty-two, and two uncles and an aunt were
also paralyzed at ages not stated. A commercial traveller, aged
thirty-nine, was in the hospital with left hemiplegia, second attack;
his mother, aged sixty-six, had an attack a few weeks before, and his
grandmother died at seventy-five of fulminating apoplexy. A woman aged
forty-six was hemiplegic for two months. Her mother, her maternal
aunt, and uncle are all hemiplegic, and her son had a left hemiplegia
at the age of seventeen. According to the cases of Dieulafoy, it is
especially through the female side that the hemorrhagic disease is
transmitted. Of course, the tendency may remain, and usually does so,
latent until the age at which in the average of cases it becomes
manifest by an apoplectic or paralytic attack; but the last two series
given above show that it may develop at an earlier period of life in
the younger than in the older generation.
Alcohol is universally stated by authorities to be one of the most
potent factors in different races in establishing the hemorrhagic
tendency: {930} but it is not easy to get exact facts on this point,
as so large a share of hospital patients are more or less alcoholic,
and in private practice observations of this kind accumulate so slowly
as not to be readily available. The greater frequency of this
affection among the male sex may point in this direction. Two of the
usual effects produced by the long-continued use of alcoholic drinks
in excess probably combine to produce this result: first, the
degeneration of tissues and tendency to low forms of inflammation of
the tissues in general and arteries in particular; and secondly, the
repeated dilatations of vessels under its paralyzing influence on the
vaso-motor nerves, resulting in chronic congestion. This preparatory
influence is distinct from the effect an occasional debauch may have
in precipitating the attack.
Another highly important cause of cerebral hemorrhage is Bright's
disease of the kidneys, in the form known as chronic interstitial
nephritis, contracted, granular, cirrhotic, or atrophied kidney; or,
as it would be perhaps more correct to say, cerebral hemorrhage is one
of the results of the arterial lesion which almost invariably
accompanies interstitial nephritis. As to the supposed or possible
identity or relation of the arterio-capillary fibrosis of Gull and
Sutton with the periarteritis of Charcot and Bouchard, the writer does
not feel competent to express an opinion.
The connection between cerebral hemorrhage and hypertrophy of the
heart was noticed and commented on long before it was known that the
great majority of cases of hypertrophy, where no lesion of valves or
of the aorta was present, were really cases of Bright's disease. The
influence which might be exerted by the high arterial tension in the
rupture of an aneurism is obvious enough theoretically, but it is far
from certain that the effect of the renal disease, or rather the
common cause of renal and cerebral disease, is not a more subtile one
than this, and prepares the way for, as well as hastens along, the
impending catastrophe.
This result, however, is not an extremely common one. Among 43 fatal
cases of interstitial nephritis, well-marked cerebral hemorrhage was
found in 4; in another, cysts and brownish indurations of small size
were found which might have been partly the results of embolism. This
patient had had a distinct paralytic attack. In a fifth the symptoms
pointed unequivocally to a large rapid hemorrhage, although it was not
demonstrated by an autopsy.
Looking at it from the other side, it was found that (in another
series) of 48 cases of cerebral hemorrhage with autopsy, contracted
kidneys were present in 17; and the writer is of the opinion, although
he has not at his command a sufficient number of facts to make such an
opinion conclusive, that if a series of cases were taken of persons
under forty or fifty, excluding those where a hemorrhagic disease or a
valvular disease of the heart might be present, the proportion of
interstitial nephritis to cerebral hemorrhage would be greatly
increased; and especially so if large hemorrhages into the great
ganglia or the interior of the cerebral lobes were alone considered.
The so-called apoplectic constitution should be mentioned here; that
is, the stout, thick-set build with short neck and florid complexion.
The popular notions as to the peculiar dangers of this condition seem
to have arisen rather from suppositions as to what might be supposed
to take place, from inferring a similar state of things to exist in
the brain to {931} what exists in the countenance, than from any
observation as to what has actually occurred. Cerebral hemorrhage may
take place with any sort of complexion or any figure, and there is no
sufficient evidence that persons of the physique above described are
specially liable to it. Many recent writers distinctly deny any such
connection.