Chapter C: W. Dulles12 describes a case occurring in his own practice in a (1)

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.

Intellectual pursuits have been considered a disposing cause—a theory 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.]

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.

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.]

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.

One of the most significant signs is the conjugate deviation of the eyes, both eyes and the head being turned strongly to one side or the other. When the lesion is above the pons and is irritative, as in the early stage of hemorrhage, the deviation is toward the side of the body affected and away from the lesion; when paralysis is established, away from the paralysis and toward the lesion. Below the pons the rule is reversed. The spastic stage of conjugate deviation may coincide with stiffness (early rigidity) of the paralyzed limbs. This deviation must not be mistaken for an accidental position of the head. The patient should be addressed from the side away from which he is looking. Sometimes the eyes can be brought to the median line, and not beyond. An attempt to turn the head forcibly beyond the median line occasionally causes pain. The value of this symptom in diagnosis has been denied, but a part at least of the apparent contradictions have arisen from the neglect to notice whether it were of a paralytic or spastic character.

As the condition of unconsciousness gradually passes off, the face regaining, at least in part, its natural and more intelligent expression, the eyes trying to follow the movements of surrounding persons, an attempt being made, perhaps only by an unintelligible sound or by a nod, to answer questions, the tongue being protruded, or at least an attempt toward it made, and some motions being made with the limbs,—the exact extent and intensity of the paralysis become more apparent. Conjugate deviation, if it have existed, may disappear before the other symptoms, or, if it has been of the rigid form depending on an irritative lesion, it may become paralytic, and is then in the opposite direction. The patient is then usually found to be in a condition of hemiplegia, and at this point the history of hemorrhagic apoplexy becomes identical with that of paralysis from hemorrhage where no truly apoplectic condition has been present.

Lidell states that in more than one-third of all cases of cerebral hemorrhage hemiplegia is developed without loss of consciousness or coma. In some, the paralysis precedes unconsciousness, which then slowly supervenes.

{940} Hemiplegia (_ἥμι_, half, _πληγη_ blow) is a paralysis or paresis of a part of the voluntary muscles of one side of the body, and a few, in some cases, on the other, and is undoubtedly to be referred to a lesion interrupting the nervous communication between the cortical centres of motion and the nuclei of the motor nerves, cerebral and spinal; the conductors passing through the corpora striata, the internal capsule, the peduncles, and crossing in great part to the other side above or at the lower border of the medulla oblongata, and passing down the crossed pyramidal tracts of the cord, to be finally connected with the anterior gray columns of the cord. The portion which does not decussate passes down the inner border of the anterior columns under the name of columns of Türck. The amount of decussation which takes place varies somewhat, and the suggestion has been made, in order to explain certain cases of paralysis occurring on the same side with the lesion, that possibly in some rare cases there may be no decussation. It has never been shown, however, that this condition, highly exceptional if even it ever occurs, is present in such cases.

It may be said in a general way, although exceptions to the rule can be found, that it is those muscles trained to separate, specialized, or non-associated movements which are chiefly affected, while those which are habitually associated in function with those of the other side are less or not at all so. It would not, however, be in the least correct to say that specialized or educated movements of any set of muscles are alone paralyzed, since the fingers, which are trained to the most independent movements, are often just as incapable of making the slightest movement of simple flexion as of writing or sewing.

We have in ordinary hemiplegia more or less paralysis of the upper facial, the patient not being able to close his eye or to wink quite so well as on the paralyzed side. The forehead may be smoother on the paralyzed side. This condition is usually slight and of short duration, but varies in different cases. Paralysis of the lower facial angle of the mouth and cheek is usually better marked, but not absolute. The corner of the mouth droops, perhaps permits the saliva to escape; the naso-labial fold is less deep, and the glabella deviated away from the paralyzed side. The cheek flaps with respiration. The difference between this facial paralysis connected with hemiplegia and that dependent upon a lesion of the trunk or distribution of the nerve (Bell's), as in caries of the temporal bone or the so-called rheumatic paralysis, is very striking, the latter being so much more complete, and, by affecting the orbicularis palpebrarum so as to prevent closure of the eye, giving a very peculiar expression to the countenance. This distinction between the two portions of the facial seems to make an exception to the rule stated above, since in most persons the movements of the corner of the mouth and of the cheek are quite as closely bilaterally associated as those of the eyelids.

Paralyses of the third, fourth, and sixth pairs upon one side of the body are comparatively rare in hemiplegia, and when present are usually referable to localized lesions in the pons. They are to be looked upon as something superadded to the ordinary hemiplegia. These nerves, however, are affected in the peculiar way already spoken of as conjugate deviation, which phenomenon would seem to denote that muscles accomplishing combined movements in either lateral direction of both eyes, {941} rather than all the muscles of each, are innervated from opposite sides—_i.e._ that the right rectus externus and the left rectus internus are innervated from the left motor centres, and vice versâ. Exactly the same remark will apply to the muscles of the neck which cause the rotation of the head seen together with the deviation of the eyes. The muscles controlling deviation to one side, although situated upon both sides of the median line, are apparently innervated from the side of the brain toward which the head is turned in paralysis.

The tongue is usually protruded with its point toward the paralyzed side; and this is simply for the reason that it is pushed out instead of pulled, and the stronger muscle thrusts the tongue away from it. The motor portion of the fifth is, according to Broadbent, affected to a certain extent, the bite upon the paralyzed side being less strong.

The hand and the foot are the parts most frequently and most completely affected, but one or the other may be partially or wholly spared, though the latter is rare. The muscles of the limbs nearer the trunk may be less affected, so that the patient may make shoulder or pelvis movements when asked to move hand or foot. In severe cases even the scapular movements may be paralyzed. The muscles of the trunk are but slightly affected, though Broadbent states that a difference in the abdominal muscles on the two sides may be perceived as the patient rises from a chair. The respiratory movements are alike on the two sides. A woman in the hospital service of the writer had a quite complete left hemiplegia at about the seventh month of pregnancy. There was some return of motion at the time of her confinement. None of the attendants could perceive any difference in the action of the abdominal muscles of the two sides, although, of course, the usual bracing of the hand and foot upon the left side was wanting. The pains were, however, generally inefficient, and she was delivered by turning. Muscular weakness often exists, and in some cases the non-paralyzed side shows a diminution of power.

The sphincters of the bladder and rectum frequently, and in severe cases almost invariably, lose their activity for a time. It is possible, however, that in some cases of alleged inability to retain urine and feces the defect is really mental, and akin to the dirty habits of the demented. The involuntary muscles probably take no part in hemiplegia, with the very important exception of the muscular coats of the arteries, which apparently share to a certain extent, and sometimes the iris.

Speech may be attempted, and the words be correct, so far as they can be understood, though the patient is apt to confine his remarks to the shortest possible answering of questions. It is, however, thick and indistinct, since the muscles of the tongue and lips are but imperfectly under the control of the will. This condition may be connected with paralysis of either side, and is to be sharply distinguished from aphasia or mental inability to select the proper word or to determine the necessary movements for its pronunciation. Aphasia is almost invariably connected with paralysis of the right side, and will be minutely spoken of hereafter. There is, of course, nothing to prevent the coexistence of the two conditions, but aphasia cannot well be shown to exist until we have reason to suppose, first, that the patient has ideas to express, and secondly, that the paralysis of the muscles of the lips and tongue has more or less completely disappeared. The patient may indistinctly mumble a word which, {942} however, can be understood to be appropriate to the occasion (defective articulation, glosso-labial paralysis), or, on the other hand, pronounce with distinctness an entire wrong word or a number of sounds without meaning (aphasia).

Sensibility—that is, ordinary cutaneous sensation—and, so far as we can judge, the special senses, are not greatly affected after the deep coma has passed off, but exceptions to this rule will be noted later.

Having described this most typical but not most common form of cerebral hemorrhage—that is, the form in which both lesion and symptoms are most distinct and can be most clearly connected—we have a point of departure for conditions less clearly marked and less easily explained.

It is probable that cerebral hemorrhage is much less likely than cerebral embolism to take place without any disturbance of consciousness or abnormal sensations; but there can also be little doubt that a certain amount of paralysis is often accompanied by no other symptoms, and post-mortem appearances often show the remains of small hemorrhages which have passed unnoticed or are lightly estimated. It is highly probable that small hemorrhages may give rise to symptoms which pass for only a little accidental vertigo or a slight feeling of faintness, until a later and more serious attack gives a more definite explanation.

On the other hand, we have a set of cases in which all the symptoms of cerebral hemorrhage may be present without the lesion. Many of these are of course due to embolism, which will be considered later; but besides this condition, recognized as softening for many years, we find described under the head of simple, congestive, serous, and nervous apoplexy cases where sudden or rapid loss of consciousness occurs with general muscular relaxation, which, when fatal, show nothing beyond changes in the circulation—_i.e._ in the amount of blood in the cerebral vessels or of serum in the meshes of the pia or at the base of the brain.

Besides these, there are cases of temporary unconsciousness with complete recovery—the coup de sang of the French, or rush of blood to the head, which are attributed to congestion of the brain—a theory difficult to prove or disprove, but not in itself unreasonable. Trousseau, without denying the possibility, or even probability, of such a condition, says that which has been called apoplectiform cerebral congestion is in the greater number of cases an epileptic or eclamptic accident, sometimes a syncope. Simple epileptic vertigoes, vertigoes connected with a bad condition of the stomach or diseases of the ear, are wrongly considered as congestions of the brain. He speaks of various conditions, such as violent attacks of whooping cough, the expulsive efforts of women in labor, the congested faces of laborers under heavy burdens, to show that cerebral congestion does not give rise to an apoplectiform attack; and it is undoubtedly true that, as a rule, no long-continued attack is the result; but it must be within the personal experience of almost every one that decided cerebral disturbance is produced for a few moments by such efforts, as, for instance, blowing a fire with the head down. Besides this, a laborer under a heavy load is presumably healthy and accustomed to his work, so that his arteries may be supposed capable of maintaining a due balance between arterial and venous blood in the brain; and, again, although the ordinary efforts of women in labor do not cause unconsciousness, puerperal {943} convulsions, involving a longer period of violent muscular action, may do so, and even give rise to hemiplegia.

Whatever name we may adopt for the temporary cases which recover, there are others, and fatal ones, which are not explained by any change in nomenclature. Epilepsy may, it is true, occur under such circumstances that no convulsion is observed, but, on the other hand, convulsions may accompany not only an attack of unconsciousness, but actual cerebral hemorrhage.

Cases of sudden death with no discoverable lesion furnish abundant opportunity and temptation for conjecture, and it is well known that too much dependence must not be placed upon the post-mortem appearances as to the amount of blood in the brain before death, and probably just as little upon the amount of serum, except as indicating a condition of atrophy.

Syncope, either from over-stimulation of the pneumogastric or from simple failure of the heart, may be put forward to explain some cases of sudden death, but seems to have no advantage as a universal theory over the older one, which meets with so little favor. Lidell gives no less than seventeen cases which he classifies as congestive or serous apoplexy. They are not all equally conclusive, and were almost all of alcoholics. In some of these there were absolutely no appearances which could account for death. The two most characteristic of congestive apoplexy were, first, a young negress who experienced a violent fit of passion, became unconscious, with stertorous breathing, and died, having had some tonic spasms. The brain contained a large amount of blood in the vessels, but no effusion. Second, a semi-intoxicated woman, aged thirty, became very angry, fell insensible, and expired almost immediately. The brain contained an excess of blood, with no effusion. In both these cases the patients were subject to fits under the influence of strong excitement, but in both the author took pains to inquire into and negative the probability of epilepsy of the ordinary kind; and a change of name does not go far toward clearing up the pathology.

Lidell's case (XXII.) was that of a man accustomed to alcohol, thin and pale, who had an apoplectic fit with coma and hemiplegia. He regained consciousness on the second day, and the hemiplegia disappeared in a fortnight. This rapid and complete recovery, exceptional to be sure, cannot be regarded as proof of the absence of hemorrhage or embolism. In fact, the latter is highly probable. It is possible that the clot may have been partially dislodged, so as to allow some blood to pass by it, or that an exceptionally favorable anastomosis allowed a better collateral circulation than usual to be established.

The following case occurred in the service of the writer: An elderly negress, who had extensive anasarca and signs of enfeebled action of the heart without any valvular lesion being detected, after washing her face was heard to groan, and found speechless and unable to swallow, with complete right hemiplegia. There was a slight improvement in a few hours, but she died two days later. The autopsy disclosed some hypertrophy and dilatation of the heart without valvular lesion. A careful search failed to discover any change in the brain or obstruction in its vessels, although there was chronic endarteritis.

The relations between epilepsy, apoplexy, and syncope are interesting {944} and important, but are certainly far from clear. Little is gained by shifting obscure cases from one category to the other. If sudden deaths be synonymous with apoplexy, we shall certainly have to admit that apoplexy does not always demand for its cause cerebral changes sufficiently marked to be recognizable after death. If, on the other hand, we refer them to heart disease, we shall have to admit that a heart without valvular disease or extensive changes in its muscular substance may cease to beat under influences as yet not well understood.

Since the paralysis arising from hemorrhage resembles so closely in its progress that dependent upon occlusion of the cerebral vessels, a further description will be deferred until the latter lesion has been described; but this remark does not apply to the premonitory and initiative symptoms, which may be of great importance, and which are not always the same with the two or three sets of lesions. There are many of them, but, unfortunately, no one among them taken alone can be considered of high significance, unless we except what are sometimes called premonitory attacks, which are in all probability frequently genuine hemorrhages of so slight extent that they produce no unconsciousness, and but slight paralysis easily overlooked. A little indistinctness of speech or a forgetfulness of words, a droop of one angle of the mouth, or heaviness in the movement of a foot or hand, lasting but a few moments, may be real but slight attacks, which may be followed either by a much more severe one, by others of the same kind, or by nothing at all for a long time. They are sufficient to awaken apprehension, and to show in what direction danger lies, but they give little information as to the time of any future attack.

Retinal hemorrhage is admitted by all modern authors to be connected with disease of the vascular system, and hence also with renal inflammation and cerebral lesions. The writer is greatly indebted to Hasket Derby for the following facts: Out of 21 patients who had retinal hemorrhage, and of whose subsequent career he had information, 9 had some sort of apoplectic or paralytic attack; 1 had had such an attack before she was examined; 3 died of heart disease, 1 suddenly, the cause being variously assigned to heart disease or apoplexy; and 6 were alive when heard from, one of these, a man of forty-eight, being alive and well fourteen years after.

Bull[25] describes four cases of his own where retinal hemorrhage was followed by cerebral hemorrhage, demonstrated or supposed in three, while in the fourth other symptoms rendered a similar termination by no means improbable. He quotes others of a similar character. The total number of cases which were kept under observation for some years is, unfortunately, not given. In a case under the observation of the writer a female patient, aged fifty-seven, who had irregularity of the pulse with some cardiac hypertrophy, was found to have a retinal hemorrhage two and a half years before an attack of hemiplegia. The hemorrhage was not accompanied by the white spots which often accompany retinitis albuminuria.

[Footnote 25: _Am. Journ. Med. Sci._, July, 1879.]

In a case reported by Amidon[26] retinal and cerebral hemorrhages seem to have been nearly simultaneous a few hours before death. There was diffuse neuro-retinitis and old hemorrhages besides the recent one.

[Footnote 26: _N. Y. Med. Rec._, 1878, xiv. 13.]

{945} The highly interesting observation has been made by Lionville[27] that when miliary aneurisms are present in the brain, they may often be found in the retina also. In one case where they were very numerous in the cerebrum, cerebellum, pons, and meninges, aneurismal dilatations were found also in the pericardium, mesentery, cervical region, and carotids (the latter not being more minutely described). There was very general atheroma and numerous points of arteritis. The retinal aneurisms varied in size from those requiring a power of ten or twenty diameters to be examined up to the size of a pin's head or a millet-seed. He thinks they might have been recognized by the ophthalmoscope.

[Footnote 27: _Comptes Rendus de l'Acad. des Sci._, 1870.]

The hemorrhages accompanying idiopathic anæmia and other diseases with a similar tendency are not to be taken into this account. Hemorrhage accompanying optic neuritis is likely to be due to some disease of the brain other than the one under consideration.

Mental disturbances of various kinds have been considered as significant, and Forbes Winslow gives a great many instances of different forms, but they are to be looked upon rather as indicating chronic cerebral changes which may result in various conditions, of which hemorrhage may be one, than as furnishing any definite indication of what is to be expected. Loss of memory should be regarded in this way. Some acute or temporary conditions of depression may affect the nutrition of the brain in such a way, without having anything to do with hemorrhage actual or anticipated.

Aberrations of the special senses are often observed, such as noises in the ears more or less definite, the sight of colors (red), or being unable to see more than a portion of an object. The fact to which these testify is probably a localized disturbance of the circulation which may not precede rupture of the vessels.

Distinct hallucinations of hearing, followed by those of smell and succeeding irritability, sleeplessness, were observed by Savage[28] in a case which terminated soon after in apoplexy.

[Footnote 28: _Journ. Ment. Sci._, 1883, xxix. 90.]