importance among the (possibly remoter) premonitory signs, not only of
cerebral hemorrhage, but of the other lesions treated in this article.
Atheroma and calcification of the tangible arteries place the
existence of peri-endarteritis among the not remote possibilities.
High arterial tension has already been spoken of in connection with
etiology, and its presence should be sought for. An irregular and
enfeebled cutaneous circulation has been spoken of as an indication of
value.
OCCLUSION OF THE CEREBRAL ARTERIES may take place from several causes
other than those which concern us here, as from the pressure of tumors
or endarteritis, usually syphilitic. Thrombosis and embolism are
grouped together from their great anatomical resemblance and their
frequent coexistence, but the symptoms produced, although ultimately
the same, are often different enough to make it necessary to bear in
mind the fact that there is a distinction—that is, that embolism is
rapid and thrombosis is slow.
A cerebral artery may be occluded from the presence of a plug of
fibrin more or less intermixed with the other elements of the blood.
This plug may have been formed in situ, and is then somewhat firmly
attached to the walls of the vessel, and partly decolorized at its
oldest portion, while on each side of it, but especially on the side
away from the heart, it is prolonged by a looser and darker clot of
more recent origin. This is a thrombus.
When the plug has been transported from elsewhere it is embolus.[30]
It may consist of various substances, as described in the article on
General Pathology, but is usually of fibrin which has formed a
thrombus or vegetation elsewhere, and, having been broken off, is
carried by the blood until it comes to a place too narrow for it to
pass, or where it lodges at the bifurcation of a vessel. The piece of
fibrin thus lodged has a strong {947} tendency to cause a still
further deposition—that is, a secondary thrombus—which may progress
until it comes to a place where the blood-current is too strong for
the process to go on any farther. It may in such cases not be obvious
at the first glance whether the whole process is thrombosis or whether
it started from an embolus.
[Footnote 30: The Greek word _εμβολος_ (_εν_, in, and _βαλλω_, to
throw) signifies the beak or rostrum of a ship of war. _Εμβολον_
signifies wedge or stopper, and would certainly seem the appropriate
form to be adopted for anatomical purposes. As uniformity of
nomenclature, however, seems more to be desired than etymological
accuracy, the writer has conformed in this article to the general
usage.]
It is probable that a thrombus forming at one point in a cerebral
vessel may break to pieces and its fragments be carried farther along,
forming a number of small emboli. (See Capillary Embolism.) Embolism
or thrombosis may take place anywhere in the brain or body generally,
but has certain points of preference. Of these, the most usual in the
brain is in the neighborhood where the internal carotid divides into
the anterior and middle cerebral, or in either of these arteries,
especially the middle, beyond this point. The plug may be situated in
the carotid just before this point, or even as low down as its origin
from the common trunk. Emboli lodge in this region, somewhat more
often upon the left side. The brain is said to be third in the order
of frequency with which the different organs are affected by embolism,
the kidneys and spleen preceding it. It has been found that small
emboli experimentally introduced into the carotids are found in much
larger numbers in the middle cerebral than elsewhere. It is the
largest branch, and most nearly in the direct line of the carotid.
Position undoubtedly influences the point at which an embolus lodges,
as it probably moves slowly along the vessels and along their lower
side. It has been remarked that, on account of this course of the
embolus, it is doubtful whether it can get into the carotid when the
patient is standing, but it certainly can do so when he is sitting up;
which, so far as the direction of the carotids is concerned, is the
same thing. The frequency with which a hemiplegia is observed when a
patient awakes in the morning may perhaps be accounted for by the
position favoring the passage of an embolus into the carotid, which
otherwise would reach organs more remote.
The vertebrals and basilar are not infrequently affected.
The sources whence cerebral emboli may spring are various, but cannot
be found outside a certain range. They may, in the first place, be
torn off from vegetations upon either the mitral or aortic valves; and
this source is probably the most common. The appendix of the left
auricle may furnish a plug from the thrombi formed among its
trabeculæ, or the aorta from an aneurism or from parietal thrombi
formed, upon spots roughened by atheroma. The pulmonary veins are
occasionally the source of the embolus, though this is not very
common.
It is rather doubtful whether an embolus can find its way from the
systemic veins through the lungs to the brain, but it is possible that
small emboli may do so, and increase in size from the addition of
fresh fibrin when floating in the blood-current. The occurrence of
pyæmic abscesses in the brain would suggest the possibility of this,
though it is, on the other hand, possible that the brain abscesses are
secondary to older ones in the lungs. In some cases, however, a
careful examination does not disclose the source of the embolus.
In the blood-current the embolus may give rise to no symptoms
whatever, and even after its arrival in the cerebral circulation it
may lodge in such a way as not entirely to obstruct the current. In
most instances, however, it does not stop until it plugs the vessel
completely and arrests {948} the current of blood beyond it for a
moment. Whether it shall completely deprive the portion of brain to
which it is distributed depends upon its situation as regards
anastomoses and upon the formation of secondary thrombus. Hence the
knowledge of the distribution of the arteries supplying the brain—that
is, the two carotids and two vertebrals—is of more importance in
reference to embolism and thrombosis than to cerebral hemorrhage,
where the effusion takes place from quite small branches.
The anterior portion of the brain, including the anterior and
posterior central convolutions and the first temporal, are supplied
with blood by the two terminal branches of the internal carotid, the
anterior and middle cerebral, the ganglia underlying these portions of
the cortex being supplied, as already stated, by small branches
arising near the origin of these two trunks, and principally the
second. The anterior cerebrals of the two sides are connected by the
anterior communicating, which is a short and usually wide vessel.
Sometimes one anterior cerebral branches in the longitudinal fissure,
and supplies a part of both sides. Hence in plugging of one internal
carotid which does not reach its bifurcation a collateral supply may
be received from the other side. If, however, an embolus or thrombus
has penetrated beyond the origin of the middle cerebral, this vessel
can no longer receive a supply from the anterior.
The posterior communicating arteries are two small vessels which
connect on each side the posterior cerebrals and either the carotid,
just as it gives off its two chief cerebral branches, or else the
middle cerebral close to its origin. These arteries may be of quite
unequal size, that upon the right usually being the larger, and
sometimes so large as to give the appearance of being the principal
origin of the posterior cerebral. When this happens the part of the
posterior cerebral which arises from the basilar may be reduced to a
minute arteriole, and the basilar, almost entire, goes to supply the
left side of the brain. This condition of the posterior communicating
may exist to some extent on both sides in the same brain. It is
probable that in many cases these arteries are too small to be of
great value in re-establishing the circulation in the anterior portion
of the brain when it is suddenly interrupted by an embolus.
When the large trunks leave the circle of Willis to be distributed
upon the surface of the brain, after giving off from the first
centimeter or two of their course the nutrient arteries for the
deep-seated ganglia, they break up into several branches which ramify
upon the surface, but, as Duret has shown, undergo very few
anastomoses. Instead of forming, as was once supposed, a richly
inosculating network, small branches penetrate into the
brain-substance perpendicularly from the superficial vessels, but
these do not communicate freely with each other by vessels larger than
capillaries.
From these anatomical conditions it happens that when a vascular
territory is deprived of its normal supply by an embolus, it cannot be
supplied with blood from surrounding districts. A certain limited
amount of collateral supply is possible through the capillaries and
the rare anastomoses, but it is only around the edges, and the centre
of the territory becomes destitute of circulating blood. Thus an
embolus does not in the brain produce, as it does in other organs with
more abundant collateral supply, a large hemorrhagic infarction.
{949} Small hemorrhages may, however, take place around the edges of
the softening, and when a number of small emboli are present, so as to
afford a number of overlapping areas with their borders of congestion,
a red softening may be the result. When the emboli are very small, and
at the same time not numerous enough to occlude all the ultimate
ramifications of a trunk, the vascular compensation may be rapidly
completed.
The change produced in the cerebral substance from cutting off its
supply of blood is known as anæmic necrosis, and includes what has
been known as white softening, with probably some yellow, and possibly
a little red softening, the latter in case where simple softening has
been complicated by hemorrhage.
When the circulation ceases the substance that should have been
nourished loses its firmness and acquires a custard-like consistency.
The gray and white substances are no longer so distinct in appearance,
the latter losing its milky-white color, the whole surface of a
section becoming of a dirty yellowish-white, somewhat shining, and
looking as if it contained more moisture than normal. When a
considerable portion of the interior of the hemisphere is thus
affected, the brain outside, with its membranes, bags down, looks
swollen, and feels to the fingers as if there were present a sacful of
fluid. The boundaries of such an area of softening are marked off from
the healthy substance with some distinctness, though less than that of
a hemorrhage. There may be some hemorrhage around the edges or into
the cavity, so that the presence of a little blood-pigment is no proof
that the original lesion was not softening from occlusion. In the
further progress the contents of the cavity become more fluid, and
finally a somewhat distinct cyst is formed, not unlike that from a
hemorrhage, with an internal areolar structure from the remains of
connective tissue, and contents of a slightly yellowish or brownish
color, or often of a chalky white. These cysts have little to
distinguish them, when old, from similar ones left by hemorrhage,
except the much greater amount of pigment in the latter. The smaller
spots of softening may after a time lose their fluidity, and remain as
yellowish patches as firm as, or firmer than, the surrounding brain.
The region of the brain involved becomes atrophied, the convolutions
shrink, and the membranes become filled with serous fluid, to
compensate for the sinking of the surface.
The microscope shows gradually increasing fatty degeneration,
disorganization of the nervous tissue, and degeneration of its
elements. The pyramidal cells are sometimes distinctly recognizable by
their form, and show gradual transition into the indeterminate round
granulation-corpuscles. The vessels exhibit fatty degeneration of
their coats, as well as accumulation of fatty granules between the
vessel and the lymphatic sheath. The clot which blocks the artery
becomes adherent to its walls, and the vessel with its contents forms
a round solid cord.
In a few instances the thrombi have become perforated through the
centre, so that a channel is formed for a renewal of the circulation.
There is no reason to suppose that this takes place soon enough to be
of any advantage in restoring the nutrition of the necrosed portions
of brain.
The region involved in softening depends upon the artery which is
plugged and the location of the obstructing body. The place of
election seems to be the carotid near its separation into its large
branches, or these {950} branches after the separation, especially the
middle cerebral, this being peculiarly liable because it is the
largest branch and is the continuation in a direct line of the
carotid. It is more frequent upon the left side. Cases have been
observed where the whole of one hemisphere was softened from
obstruction of the carotid at its bifurcation; which may be accounted
for, as Charcot suggests, by an unusual distribution of the arteries,
as described above, the posterior cerebral as well as the other two
being derived almost entirely from the carotid. In a case recently
observed by the writer the whole right cerebral hemisphere, with the
exception of the tip of the frontal and tip of the occipital lobes,
was softened to the consistency of custard, a thrombus extending from
the bifurcation of the common carotid into all the ramifications of
the middle cerebral. The most common form, however, is where more or
less of the brain around the fissure of Rolando and fissure of
Sylvius, with or without the underlying ganglia, is softened. This
happens from a lodgment of the embolus in the middle cerebral. If the
obstruction be close to the origin of the artery, the corpus striatum
suffers, from the mouths of its small nutrient arteries arising in
this part of its course being stopped, while if it have passed along a
little farther, these remain open, and the cortex, to which the larger
branches are distributed, alone is softened.
The anterior cerebral is not infrequently affected, either alone or
with the middle, and in these arteries as well as the posterior the
embolus, if of small size originally, may penetrate so far as to give
rise only to quite a limited anæmia. The basilar is an artery not very
rarely occluded, though more commonly by thrombus than embolus. This
occlusion may be so limited as to affect only the nutrient arteries of
the pons and cause a very limited softening, the parts before and
behind it being supplied by the unobstructed portion or by collateral
circulation from the carotids. Occlusion of the cerebellar arteries
and softening of the cerebellum are among the rarer forms. The
vertebrals themselves are sometimes plugged. A thrombosis has been
observed in the only inferior cerebellar artery which existed, causing
softening in both lobes. There was atheroma of the heart and arteries,
and a thick calcareous plate in that which was occluded.[31]
[Footnote 31: _Progrès méd._, 1876, 373.]
In a general way, it may be said, with many exceptions on both sides,
that thrombosis and embolism tend to affect the cortex, and hemorrhage
the central ganglia.
What has just been written applies to the simple mechanical action of
emboli. If, however, they have a septic origin, as notably in cases of
ulcerative endocarditis, the region in which they lodge becomes,
instead of a simple spot of necrosis, a septic focus or abscess, with
its results of compression or irritation. In such a case there are
likely to be abscesses of similar origin in other organs, and the
cerebral lesion is only a part of the general pyæmic condition.
ETIOLOGY.—So far as the lodgment of an embolus in an artery is
concerned, it can hardly be said that there is any etiology, for the
detachment of the plug from its place of origin is purely a matter of
accident, and may take place at any time. As to its origin in the form
of fibrinous deposit on the valves of the heart or a roughened spot on
the aorta, we must refer to the article on General Pathology. The most
important {951} condition for embolism is disease of the valves of the
heart, rheumatic or otherwise. Next comes arterial disease, producing
roughening of the inner coat and subsequent deposition of fibrin. So
far as we can tell, the causes leading to endarteritis or atheroma are
essentially the same as those which produce the periarteritis
described in connection with cerebral hemorrhage, and we may therefore
put down old age, alcohol, and strain as among the causes of cerebral
embolism. Injuries of the lungs leading to thrombosis of the veins may
be considered as possible sources for the formation of an embolus, and
we might suppose that phthisis and pneumonia would furnish plugs which
would lodge in the brain, though as a matter of fact they seldom do
so.
Experience shows that embolism, unlike hemorrhage, is not specially a
disease of advanced life, but is distributed over different periods,
with preference for old age less marked than with hemorrhage. Andral
gives the ages of patients with softening—which, however, includes
thrombosis as well as embolism—as follows: the average would
undoubtedly be displaced in the direction of youth if thrombosis could
be taken out of the list:
-----------------+-------------------+------------------------
Andral: | Andral: | Cases (with autopsies)
Beginning of | Death with | of embolism,
softening in 27 | softening in 153 | thrombosis, and
cases. | cases. | softening—25 cases.
-----------------+-------------------+------------------------
17-20 4 | 15-20 10 | 20-30 4
27 2 | 20-30 18 | 30-40 3
30-37 2 | 30-40 11 | 40-50 3
43-45 2 | 40-50 19 | 50-60 1
53-59 4 | 50-60 27 | 60-70 5
63-69 7 | 60-70 34 | 70-80 2
76-78 6 | 70-80 30 | Young 1
| 80-89 4 | Middle-aged 1
| | Old 5
-----------------+-------------------+------------------------
In the etiology of cerebral arterial thrombus there seem to be two
factors of prime importance, although there are cases which seem to
demand a third, and Charcot[32] suggests the possibility of some hæmic
dyscrasia favoring the formation of a thrombus, and relates a case of
thrombosis of the middle cerebral, with three others of the same
process in other arteries, occurring in patients with uterine cancer,
where all the usual sources of emboli were explored with negative
results. The first of the two is disease of the cerebral arteries, not
necessarily extensive, but sufficient to form a starting-point on the
inner wall for the deposit of fibrin. In this respect the etiology of
thrombosis may be various. Syphilitic endarteritis, for instance, may
very easily give rise to this lesion, but it is likely to be
accompanied by others, and has a symptomatology more or less peculiar
to itself. It is not, of course, to be included with the form we are
considering.
[Footnote 32: _Comptes Rendus Soc. de Biol._, 1865, p. 24.]
The second factor—one which is perhaps capable of giving rise to
coagulation of the blood or deposit of fibrin without any arterial
disease—is weakness of the heart, connected or not with anæmia. The
causes of this condition may be manifold, and are likely to lead to
many other consequences than cerebral thrombosis. A thrombus may form
upon a very small basis of atheroma. Several of these points are
illustrated in the {952} following case: A lady, aged about
sixty-five, had had for many months vague symptoms of want of
strength, fatigue, want of appetite, and so on, with complaints of
distress and fulness in the abdomen, for which no special cause could
be found. On one occasion she was unusually long in dressing, and her
expression was noticed to be changed and her voice altered for a few
moments. The pulse was habitually 60 or less, and at times irregular,
but nothing abnormal could be detected in the sounds or position of
the heart. Fatty degeneration was suspected. One morning, after going
to bed in her usual health, she was found on the floor of her room
unconscious and with left hemiplegia. She lived about thirty-six
hours. The autopsy showed nothing abnormal in the abdomen except a
considerable accumulation of fat; and in the thorax the heart appeared
normal, and was not fatty. There was very little atheroma. In the end
of the internal carotid artery was a thrombus, of which the lower and
firmest part was connected with a very small spot of roughening just
at the point where the artery comes through the base of the skull. It
extended just beyond the origin of the middle cerebral artery, which
was of course occluded. The corresponding region of the brain was
converted into a vast mass of softened tissue.
The SYMPTOMS of the lodgment of an embolus in the brain may closely
resemble, or even be precisely the same as, those of hemorrhage.
Unless, however, an embolus makes a pause on its journey, giving rise
to a partial obstruction before there is a complete one, or unless the
obstruction is not absolute until after the formation of a secondary
thrombus, the attack may be absolutely sudden.
A thrombus, however, is slower in its formation, and may produce
gradually increasing anæmia of the region of brain supplied before it
is absolutely complete, with a gradually increasing paralysis and loss
of consciousness slowly approaching. Thus we may have the early
symptoms in the form of headache, vertigo, heaviness, and drowsiness,
peculiar sensations in the limbs about to be paralyzed or in the head,
delirium of various kinds, or hysterical manifestations. Prévost and
Cotard[33] lay special stress upon the importance of severe vertigo
(étourdissement) as a prodrome or warning of softening, especially in
the aged. It is dependent upon anæmia of the brain, and this, in its
turn, upon atheroma of the arteries, and sometimes at least upon
feebleness of the circulation, both of these being conditions likely
to cause the deposit of a thrombus. As, however, the thrombus does not
necessarily result from these conditions, and as the vertigo may arise
from other sources, as stated under the head of Cerebral Hemorrhage,
it is to be looked upon with special suspicion chiefly in those cases
where other symptoms might lead in the same direction, and when other
causes can be excluded.
[Footnote 33: _Mémoires de la Soc. de Biol._, 1865, p. 171.]
The same authors also speak of less defined symptoms, like delirium
and stupor, occurring among the inhabitants of the Salpêtrière (old
women), with intervals of comparative health, as being premonitory.
It is possible, however, for the symptoms of thrombus to be developed
rapidly when, as in the case last described, the thrombus begins to
form in a place which does not entirely interrupt the current, but
afterward reached the mouth of a large vessel, which it closes.
The loss of consciousness, coma, and all the phenomena of the {953}
apoplectic attack, with the possible exception of early rigidity, may
be as fully developed from occlusion of the cerebral vessels as from
their rupture; but it must be said that it is more common to meet with
them in cases of large hemorrhage than with either embolism or
thrombosis.
The general functions are even less disturbed than with a hemorrhage
producing an equal extent of paralysis. The temperature follows nearly
the same course as in hemorrhage, except that the initial fall, if
present—which is not always the case—is said to be less than with
cerebral hemorrhage. To this succeeds a rapid rise, which, even in
cases which are to terminate fatally, gives place to a fall to the
neighborhood of normal, and another rise before death. These are the
statements of Bourneville. The rise is said not to be so high as with
hemorrhage.
The annexed chart is from a man (W. I. W.) who was in the hospital
with ill-defined nervous symptoms, and was suddenly attacked with
convulsions, vomiting, and unconsciousness. He had a small tumor at
the point of the right temporal lobe, and softening of the left corpus
striatum. The apoplectic symptoms occurred on the 15th—that is, as
will be seen by the chart, one day after the temperature began to
rise. The pulse and respiration show no characteristic changes.
[Illustration: FIG. 40.]