which it would be difficult to substantiate. It is not, of course, the
quality of the work, but its relation to the capacity of the
individual brain, which makes any amount of thought a special strain.
The cases of Dieulafoy, in which the hereditary tendency was so
strongly marked, were mostly hospital cases, among which class the
so-called intellectual occupations do not specially preponderate. A
life of constant cerebral excitement, like that of a speculator or
stockbroker, certainly seems more likely to give rise to overstrain of
the vessels than the more quiet and regular, but certainly more
intellectual, labor of the professional or literary man.
Thackrah[15] speaks of affections of the head as frequent among
professional men, but does not advert to cerebral hemorrhage in
particular. He evidently considers a want of sufficient exercise in
the open air a far more potent factor than mental excitement.
[Footnote 15: _Health and Longevity_, p. 183.]
It is very difficult to get statistics which bear upon the influence
of mental labor on the brain, since the recorded occupation of an
individual furnishes but a very rough estimate of the amount of
thought evolved from his brain, and a very much less accurate one of
what is probably of far greater importance—the amount of friction and
anxiety with which it is done.
Hemorrhagic diseases may, for the sake of completeness, be once more
mentioned as among the predisposing causes.
The exciting causes of cerebral hemorrhage are those which give rise
to rupture of the fragile walls either of the aneurisms or fattily
degenerated arterioles. They are to be found chiefly among such
conditions as increase the pressure in the cerebral vessels, chiefly,
though not wholly, from the arterial side. The connection of an attack
of apoplexy with hypertrophy of the heart means, as has already been
shown, in a great many cases, their mutual dependence upon arterial
disease, as in chronic interstitial nephritis, but it seems probable
also that an unusually powerful action of such a heart might be the
immediate cause of the rupture. An excited action of the heart,
connected with a dilatation of the cerebral vessels, naturally
increases the strain on the weak portions, and we have thus the
explanation of those instances where sudden or great excitement brings
on the attack.
Apoplexy is less frequent in summer than in the other seasons, and it
is especially remarked that sudden changes of temperature are likely
to be accompanied by an unusual number of cases. Changes in the
arterial tension consequent upon the varying amount of blood
circulating in the skin are the probable connecting link.
Obstruction to the venous outflow, either alone or in conjunction with
the preceding condition, has undoubtedly a marked effect. In addition
to the cases of hemorrhage from veins obstructed by thrombi, already
mentioned, instances of this method of production are to be found in
{932} the effects of severe muscular effort, as in lifting, in
straining at stool, or, as has occasionally happened, in coitu. It has
been objected to the congestion theory of apoplexy that even in severe
paroxysms of whooping cough, where the face becomes cyanosed and
congested, nothing like unconsciousness or paralysis occurs; but cases
have been reported where aphasia and cerebral hemorrhage into the
optic thalamus and cortex have accompanied whooping cough. Violent
convulsions may be the cause of cerebral hemorrhage, as in puerperal
eclampsia.
Obstruction to the circulation in the neck by tight clothing may be a
means of increasing the back pressure from the veins. It is said that
deaths from apoplexy have been unusually frequent among soldiers who
have been obliged to wear tight stocks for the sake of imparting what
was supposed to be a more military bearing. Probably some of the
hemorrhages found with valvular disease of the heart are to be
explained by venous congestion, although others are due to embolism.
Blows and shocks to the head, not producing fractures, are occasional
causes of cerebral and ventricular as well as of meningeal hemorrhage.
Important medico-legal questions are likely to arise where both
bruises externally and internal hemorrhage are found. It is important
to recollect that ecchymoses of the pericranium[16] have been found in
cases of apoplexy where no violence has been used. These may occur
with occlusion of the cerebral vessels, as well as with hemorrhage,
and are most likely to be situated on the paralyzed side, being
sometimes distinctly limited at the median line. They have been
supposed to be due to the general tendency of the blood toward the
head, and to be of the same pathological origin as the cerebral lesion
they accompany; but the fact that they may not be associated with
hemorrhage proves that this explanation is inadequate. Another
explanation attributes their causation to vaso-motor paralysis,
together with some unknown factor present in only a certain number of
cases. They may be compared to the subconjunctival hemorrhages seen
after violent convulsions.
[Footnote 16: Lepine, _Archives de Physiologie_, tome ii., 1869, p.
667.]
Cerebral hemorrhage depending upon a blow is likely to be accompanied
by meningeal bleeding; to be situated at some point of the cortex, and
not in the regions more frequently affected; and to consist of the
effusion of no great amount of blood, mixed with cerebral substance.
There are also very often more than one. All the circumstances should
be carefully weighed when, as not infrequently happens, there is doubt
as to whether a blow was the cause of a hemorrhage, or whether a
person found insensible, with a bruise upon his head, may have fallen
down suddenly from an apoplectic attack. In the following case it
would be difficult to be sure of the sequence: A negro man aged fifty
fell backward from the first step of a ladder. He got up and went to
work again, but soon became unconscious. He became partially conscious
again in the accident-room of the hospital, but died in a few hours.
There was no sign of injury to the head, but there was a rupture of an
aneurism (not miliary) of the left middle cerebral artery, and
hemorrhage into the meninges and all the ventricles. If the first fall
had occurred in a scuffle, and the autopsy had been made in such way
as not to disclose the aneurism, it might have been considered a case
of homicide.
{933} Alcohol, besides not infrequently counterfeiting apoplexy, and
besides acting as one of the predisposing causes, is occasionally an
exciting cause. The dilatation of cerebral vessels, perhaps present as
an habitual condition, is added to by the effect of the temporary
narcotism and produces the rupture. In many cases these factors have
their activity much increased by heavy sleep, very likely in a
constrained posture, causing pressure on the veins of the neck and
consequent venous congestion, which is in its turn intensified by the
confined air of a station-house or the cold of the weather. The man
who has possibly a vessel ready to burst in his brain should have,
even if demonstrably drunk, the advantage at least of good air and an
unconstrained position.
Other poisons, less frequently taken, may perhaps have a similar
influence. In one case under the observation of the writer a number of
small hemorrhages were found in various parts of the brain of a man
who was found in his room some forty-eight hours after taking a
quantity of opium, and having had, of course, no treatment during that
time. He was aroused in the hospital without great difficulty, but
died after a day or two with his brain in the condition above
described, and bronchitis with inhalation pneumonia. There had been no
paralysis, and the hemorrhages were probably not the immediate cause
of death.
Durand-Fardel gives a table of supposed causes in 21 cases of persons
over fifty: 8 of these were connected with either habitual use of
liquor or a debauch; 9 had an attack immediately after a meal.
After naming all these causes, it must be said that in many cases it
is impossible to find any reason for the occurrence of the hemorrhage
at the particular moment it comes. A person may go to bed in apparent
health, and be found some hours afterward unconscious and comatose, or
unable to stir hand or foot on one side, or to speak. Gendrin, as
quoted by Aitken, states that of 176 cases, 97 were attacked during
sleep. The attack may come on when the patient is making no special
muscular effort and under no special excitement. It is simply the
gradual progress of the lesion, which has reached its limit.
SYMPTOMATOLOGY.—If we take as a point of departure the fully-developed
attack, such as most frequently is found with a large and rapid
hemorrhage into the cerebral hemispheres, pons, or cerebellum, the
symptoms are those usually spoken of as an apoplectic attack, shock,
or stroke, or, as the Germans say, Hemorrhagische Insult. Trousseau
quotes as a satisfactory definition the words of Boerhaave: “Apoplexia
dicitur adesse, quando repente actio quinque sensuum externorum, tum
internorum, omnesque motus voluntarii abolentur, superstite pulsu
plerumque forti, et respiratione difficili, magna, stertente, una cum
imagine profundi perpetuique somni.”
Loss of consciousness, abolition of voluntary motion and sensation,
and usually stertor, the appearance of the patient being that of one
in deep sleep, are found in the extreme cases. In others the loss of
consciousness and sensation are not complete; the patient can be
aroused enough to utter a grunt or raise a hand to his face in order
to brush away a fly or the hand of the physician who is trying to
raise his eyelids, or can make a grimace to show that he is hurt, the
face returning to its indifferent expression as soon as the cause of
irritation is removed. Although the grade of action, both sensitive
and motor, seems to be a little above the {934} purely reflex, it is
but very slightly so, and probably is not sufficient to remain an
instant in the memory.
The rapidity with which this condition comes on varies widely, from a
very few minutes, or even seconds, to some hours. It may even diminish
for a time and return. The cases in which unconsciousness is most
rapidly produced are apt to be meningeal and ventricular, and
presumably depend upon the rupture of vessels of considerable size,
although the location among the deeper ganglia, where the conductors
of a large number of nervous impulses are gathered into a small space,
will, of course, make the presence of a smaller clot more widely felt.
Even in these, however, the onset is not absolutely instantaneous, and
the very sudden attack is rather among the exceptions. Trousseau
denies having seen, during fifteen years of hospital and consulting
practice, a single case in which a patient was suddenly attacked as if
knocked down with a hammer, and that since he had been giving lectures
at the Hotel Dieu he had seen but two men and one woman in whom
cerebral hemorrhage presented itself from the beginning with
apoplectiform phenomena. In each of these the hemorrhage had taken
place largely into the ventricles.
Lidell gives the following case: A colored woman, aged forty-nine, was
engaged in rinsing clothes, and while in a stooping posture suddenly
fell down upon her left side as if she had been struck down by a
powerful blow. She was picked up insensible, and died in ten or
fifteen minutes. The hemorrhage was chiefly meningeal, and especially
abundant about her pons and medulla oblongata. The fourth ventricle
was full of blood, and there were clots in the lateral ventricles.
A woman, aged about forty, had been hanging out clothes in an August
sun. She was observed to run out of the house screaming, and fell to
the ground unconscious. This was at 1 P.M., and she died at 3.30 P.M.
Her temperature just after death was 107.2°. The neighborhood of the
posterior surface of the pons Varolii was occupied by a
broken-down-looking mass, appearing like an aggregation of small
apoplexies (hemorrhages), involving and breaking down the middle crura
of the cerebellum. There was no fatty degeneration nor any miliary
aneurism. (I do not know upon how thorough an examination this last
statement rests.)
In a large number of cases it is difficult to say, in the absence of
any observation, intelligent or otherwise, exactly how rapid the onset
of the symptoms may have been, but in those which occur where the
patient is watched or is in the company of observant persons it is
almost invariable to meet with symptoms less than unconsciousness
which denote the actual beginning of the hemorrhage. From the nature
of the lesion it can rarely give rise to symptoms which justify the
epithet of fulminating in the sense of struck with a thunderbolt. The
unconsciousness, so far as can be known, does not depend on the injury
of any one special small point of the brain in which consciousness
resides, but upon the compression of a considerable portion, which
must necessarily take place gradually, but with a rapidity
proportioned to the size of the current which issues from the ruptured
vessel and the ease with which pressure can diffuse itself over a
large area. It is undoubtedly the greater facility offered to such
diffusion by the communication of the hemorrhage with the so-called
cavity of the arachnoid and the ventricles which gives to {935} these
forms a peculiar severity. The difference between a hemorrhage
spreading through all the ventricles or over a large surface of the
brain, and one which is limited to a focus in the substance of one
hemisphere, being restrained by more or less firm tissue, may be
illustrated by the gain in power in the hydraulic press from the
transfer of the stream of water from a small cylinder to a larger one.
Vomiting is a symptom of some importance in diagnosis, being not very
common in cerebral hemorrhage, but very frequent in cerebellar.
Whether of sudden, rapid, or slow development, the apoplectic attack
is, in its main features, described in the aphorism of Boerhaave given
above. The muscular relaxation of the face imparts to it an
expressionless, mask-like character; the limbs lie motionless by the
side, unless they can be excited to some slight movement by some
painful irritation or are agitated by convulsions, or in a condition
of rigid spasm; the face may be pale or flushed; the cheeks flap
nervelessly—le malade fume la pipe.
Swallowing, in the deepest coma, is not attempted. The fluid poured
into the mouth remains, and distributes itself according to the laws
of gravity without exciting reflex movements of the pharynx. When the
depression is less profound, it may excite coughing or be swallowed.
An attempt to swallow when the spoon touches the lips indicates a
considerably higher degree of nervous activity. Respiration may be
slow, but when the case is to terminate fatally rises with the pulse
and temperature. It is often stertorous and difficult, the obstruction
consisting partly in the gravitation backward of the soft palate and
tongue, and partly in the accumulation of fluids in the pharynx. Hence
stertor is in some cases only an accidental phenomenon, depending upon
the position of the patient on the back, and can be relieved by
turning him on his side and wiping out the mouth as far back as can be
reached. Cheyne-Stokes respiration occurs in severe cases, though not
confined to necessarily fatal ones.
The general temperature in cerebral hemorrhage has been studied enough
to make it of considerable value, especially in prognosis. In a case
which extends over a sufficiently long time several stages can be
distinguished which in shorter ones may be wanting. An initial period
of depression is described by Bourneville[17] as occurring immediately
after an attack, in which the temperature falls a degree or two below
the normal, and, according to his view, continues depressed if death
takes place rapidly. He gives the case of a man who died very shortly
after an attack (his second one), where the temperature, taken in the
rectum at the moment of death, was 35.8°. In cases which survive
longer this initial fall passes either into a stage where it
oscillates within the neighborhood of the normal or immediately begins
to rise; the latter occurrence indicates an impending fatal
termination (unless, of course, something else can be found to account
for it). In the former condition we find patients whose life may be
indefinitely prolonged for days or weeks, when, if a fatal termination
is to result, the thermometer again indicates a rise.
[Footnote 17: _Études cliniques et thermométriques sur les Maladies du
Système nerveux_, 1872.]
The initial fall of temperature is not so likely to be observed except
in institutions like the Salpêtrière, where large numbers of old
persons are collected and under close medical surveillance; and,
indeed, it {936} {937} may be doubted, even from Bourneville's own
table, whether the rule is one without exceptions. At any rate, the
rise is a more important phenomenon than the fall. When the rise of
temperature is interrupted by a fall, and then continues again, it is
due, according to the author already quoted, to a renewal of the
hemorrhage.
These changes of temperature may be noted with various locations of
the lesion, but it seems probable that further study might make them
useful in diagnosis as well as prognosis. Hale White reports the case
of a boy aged six and a half years, who was found unconscious with
right hemiplegia, and who afterward had many and various paralyses
with hyperpyrexia, the highest temperature being 107°. He lived long
enough for secondary degeneration to extend down the crura and into
the anterior cornua. A small soft patch a quarter of an inch in
diameter existed at the anterior part of each corpus striatum.[18]
[Footnote 18: _Guy's Hosp. Rep._, 1882.]
[Illustration: FIG. 37.]
The chart W. H. (Fig. 37) is from a man aged fifty who fell in the
street while returning from work at noon, and whose axillary
temperature was taken at 5 P.M. and every two hours thereafter until
death. The hemiplegia was not very marked, but the hemorrhage was
extensive, involving the pons and left crus cerebri, the external
capsule, left crus cerebelli, and medulla, bursting through into the
fourth ventricle.
[Illustration: FIG. 38.]
The chart M. M. (Fig. 38), as taken from Bourneville, represents the
course of the temperature in a rapid case: each perpendicular line
denotes an hour.
The difference in the temperature of the two sides has been variously
stated, and probably depends on a number of factors besides the length
of time that has elapsed since the first attack. There is probably,
however, a tendency to excess of heat on the paralyzed side soon after
the attack, owing to vaso-motor paralysis; and this difference will be
more marked in the hands than in the axillæ. After a length of time
which may be from days to months the temperature becomes equalized, or
more frequently the relation is reversed, the paralyzed side being
colder as atrophy takes place. Lepine[19] gives a case where the
axillary temperatures of the two sides continued the same within a
small fraction of a degree for three days, and then separated very
slowly, until at death the {938} paralyzed side was six-tenths of a
degree (Cent.) hotter than the other, in both being inferior to the
rectal (107° Cent.).[20]
[Footnote 19: _Mémoires de Société de Biol._, 1867.]
[Footnote 20: The chart in the original, and as reproduced by
Bourneville, is wrongly lettered. The text says that the left side was
the hotter.]
[Illustration: FIG. 39.]
The chart C. M. (Fig. 39) shows the excess of temperature in a case of
meningeal hemorrhage. The dotted line is from the paralyzed side. The
first observation was made two and a half hours after the attack.
A very interesting case is reported by Johnson[21] of crossed
hemiplegia, where the temperature was about a degree higher on the
paralyzed side of the body, and, corresponding to this, the
sphygmograph showed a great diminution of tension; the lesion is
supposed to have been a hemorrhage in the pons. Johnson, in commenting
on the statement of Lorain that in all cases of hemiplegia the pulse
is more full on the paralyzed side, says that it is incorrect for
ordinary cases of hemorrhage into the corpus striatum, though true in
his own case.
[Footnote 21: _Brit. Med. Journ._, Jan. 6, 1877.]
The most marked differences of temperature have been observed where
the lesion has been in the neighborhood of the pons, crus cerebri, or
medulla oblongata. In a case reported by Allbutt there was a
difference of 1.6°; the radial pulse was softer and fuller on the
paralyzed side, and the cheek upon that side was flushed.[22] The
pulmonary hemorrhages which have been noticed by Brown-Séquard and
others in animals after cerebral lesions, and the extravasation,
congestion, subpleural ecchymoses noted by Ollivier[23] in cerebral
apoplexy, are probably to be referred to vaso-motor disturbances.
[Footnote 22: _Med. Times and Gaz._, Dec. 4, 1869.]
[Footnote 23: _Archives générales_, 1873, 167.]
Much more attention has been paid to the pulse than to the
temperature, but it is less easy to lay down definite rules in regard
to it. It may vary in either direction. When the case is approaching a
fatal termination the pulse is apt to accompany the temperature in a
general way in its rise, though not necessarily following exactly, as
is seen in the chart in Fig. 38.
The throbbing or bounding of the arteries often described may indicate
increased activity of heart, but means at the same time vaso-motor
relaxation. The urine and feces are often passed involuntarily.
In some rare cases symptoms closely resembling those produced in
animals by section of the sympathetic have been seen. These are false
ptosis, narrowing of the palpebral opening and sinking of the globe of
the eye {939} into the orbit, diminution in the size of the pupil,
higher temperature on the paralyzed side of the face and the
corresponding ear, abnormal secretion of the eye, nose, and mouth on
the same side.[24] They are supposed to indicate a paralysis of the
sympathetic.
[Footnote 24: Nothnagel, quoted by Grasset.]
The condition of general relaxation may be so profound as to cover up
everything else, but in many cases true paralytic symptoms may be
discovered or provoked, which even at an early period give us
information as to the locality and nature of the lesion.
A greater degree of muscular relaxation may be manifest on one side of
the face than the other; the forehead may be a little smoother on one
side, the corner of the mouth drooping, the downward line from the ala
of the nose flattened, and the cheek flapping. There may be a little
greater resistance to passive motion of the limbs on one side; one
hand on being raised may drop helplessly back to the bed, while the
other is laid slowly down; the right hand when pinched lies motionless
and without power to escape the pain until the left comes to its
assistance. Irregularity of the pupils, if present, is an important
sign, but its absence signifies nothing.