Chapter M: M——, was a stout Irish woman about forty years of age. She had (27)

TREATMENT.—Absolute simple rest in bed is all that is necessary in mild cases of concussion. The patient should be well watched for any symptoms which might supervene and show that the injury was more severe than at first supposed. On the other hand, serious symptoms may be present without indicating any great gravity in the case. Children, for example, often have convulsions from the slightest cause. I have attended them when these set in immediately after the injury, but in a day or two there was entire recovery.

The more serious cases equally require rest, but also something more. To bring about reaction from shock, sinapisms to the extremities, to the nape of the neck, and over the stomach should be used. Hot-water bags should be placed along the sides of the body and limbs. Alcoholic stimulants must be sparingly used, if at all: they are rarely necessary. The stomach will often reject them unless in minute doses. If too much is absorbed, unpleasant consequences to the brain may follow. In extreme cases hypodermic injections of brandy or ether may be administered. Ammonia, camphor, and other diffusible stimulants may be useful, either externally or internally.

If the reaction is regular, with gradual restoration to consciousness and no noticeable rise in temperature, nothing further is required but a continuance of the rest and the use of cooling drinks and spare diet. The bowels and bladder must be attended to; the catheter may have to be used.

Restlessness, with or without delirium, is not unusual, but it generally subsides under full doses of bromide of potassium.

When reaction is followed by high fever, and especially when there is with it a passing on into secondary unconsciousness independent of true sleep, we have almost surely internal compression from congestion, effusion of serum, or hemorrhage to deal with. Now, blood may be taken generally or locally with great benefit. Cups, both dry and wet, to the temples and back of the neck are very useful. Leeching also is an efficient method of depletion. Ice in bags or towels, or cold water, should be applied to the head. Hot water, say about 120° to 130°, to the head is often of great service and very soothing.

{912} The choice between cold and hot water is to be determined by the effects produced. Sometimes surprisingly good results come from alternating their use. Hot mustard foot-baths may be given in bed while the patient is kept lying on his back with the limbs flexed.

The result only in these severe cases will determine whether the symptoms were due to great congestion or to extravasation, possibly with brain lesion. Complete recovery takes place in the first condition. In the latter a fatal termination is much more probable, and if there is recovery it is apt to be only partial, and the patient may be the victim of nervous troubles more or less pronounced throughout a long life.

Concussion of the Spine.

John G. Johnson of New York is authority for the statement that English railways paid in five years two million two hundred thousand pounds, or eleven million of dollars, as damages awarded by juries in cases of concussion of the spine. The statement appears almost incredible, but the facts are ample to sustain it.

It also illustrates the powerful influence of one great authority (Erichsen) better than anything I know of in the history of the medical profession. After this celebrated surgeon's lectures and work on concussion of the spine, etc. were published, dating back to 1866, the great body of medical men received them as the standard and guide in all such cases. They were a godsend to plaintiffs and prosecuting attorneys, and the defendant had a poor chance with juries when the possible miseries of any one who claimed compensation for injury to the spine was pathetically pictured to them.

That the defendants have suffered injustice in a great number of cases I think there can be no doubt. Is it any wonder, therefore, that a reaction has occurred of late, and that the views formerly held by professional men have been subjected to sharp criticism founded upon a much more scientific and practical knowledge of the subject at issue?

As in all reactions, extreme views have been reached by certain observers, and there are those who seem to hold that concussion of the spine cannot occur. By spine here is meant the spinal cord or marrow.

It has been well remarked, I think by Page, that we do not speak of concussion of the skull. We always say concussion of the brain. The use of the term spine has given rise to much confusion, but the professional man will understand what is meant when so-called concussion of the spine is under discussion.

The advocates of the rarity or even impossibility of the injury call attention with much force to the anatomical facts. First, to the immense strength, pliability, and cushioning of the bony and ligamentous encasement or column; then to the ample calibre of the canal in which the nervous cord is suspended, and to the pliant structures intervening between its inner walls and the cord itself. From without inward, in the canal, we have fat, watery connective tissue, and the plexus of spinal vessels; then comes the dura mater, loosely investing the cord and unattached to the bone, not forming here, as in the skull, the internal periosteum. Within the dura mater is the arachnoid, its visceral layer {913} separated by a wide interval from the viscus or cord, which interval contains the cerebro-spinal fluid; then the pia mater or vascular membrane, which closely invests the cord.

Besides these structures there is the ligamentum denticulatum passing from the dense pia mater to the parietes of the canal and supporting the cord and roots of the nerves in the most efficient way—pliable enough to yield and break the force of vibrations, and strong enough to sustain.

Thus we see that the cord is much more securely protected from the effects of external violence than the brain, and we can understand that there is reason for the doubt of the sceptics as to the frequency of the injury described as concussion of the spine.

Clinical observation is, I think, of far greater value in determining questions of the kind than any theory, however strongly supported by anatomical facts. Does transient concussion of the spine occur as transient concussion of the brain occurs? Page, if I understand him, says not. In his work on _Injuries of the Spine and Spinal Cord_ (London, 1883), in criticising a well-known case as to the claim of persistent paraplegia without discoverable lesion, he says: “We italicize the word persistent, for simple concussion of the brain may give rise to a transient unconsciousness, and, if the analogy holds good, concussion of the spine should per se produce a transient paraplegia. _We know of no case, nor can we discover the history of any case, where this has happened._”

I italicise the last sentence. In 1881 a boy came under my care who was shot in the back three inches to the right of the third or fourth dorsal vertebra. He at once had characteristic symptoms in the legs of being wounded in the spine in such a way as to affect the cord somehow. There was partial paraplegia, with pains in both limbs. Under rest these symptoms soon disappeared. In a few days I made a deep incision and removed some clothing and fragments of bone, and then from the depths of the spinal gutter I took a large conical ball which was resting against the bony bridge of a vertebra. The boy recovered rapidly. I saw him some months afterward perfectly well.

Surely, this was a case of spinal shock or concussion with transient paraplegia, and the cause of it could have been nothing else than the impact of the ball against the column, producing vibratory jar sufficient to affect the cord. The immediate symptoms and the rapid and complete recovery are, in my opinion, inconsistent with any theory of congestion or pronounced lesion of the medulla.

Here is another case of transient paraplegia also occurring in 1881, and, to my mind, still more significant: A man fell from a height of about twenty feet and landed directly on his feet. He was immediately paraplegic. On examination no injury to the spinal column could be detected, but there was fracture of both calcanea. The spinal symptoms were thoroughly marked. Besides the paralysis of the limbs there was loss of control of the bladder and bowels, and the other accessories in such cases. But all went on to recovery. Pari passu with the fractures the spinal symptoms improved. It is not necessary here to give further details, but simply to state that in four months, the time required being chiefly due to the fractures, the patient was discharged able to walk and well in every other respect.

If this is not a case of transient paraplegia owing to spinal shock or {914} concussion, I am willing to admit that I do not know the requirements of the critics when they ask for such cases. I think that it is no matter how the blow or shock to the column is received, whether direct or indirect, so that it is shown that the medulla is influenced within the line of recovery, without having suffered fairly presumable lesion.

President Garfield surely suffered from transient spinal shock produced immediately by impact of the bullet upon the column. The symptoms soon passed off, and at the post-mortem the cord was healthy in every respect. The differences between his case and the others I have mentioned were those of degree only, his concussion not being severe enough to cause paraplegia.

Spinal concussion or shock from railway collisions does not differ from forms of the same injury received in other ways. It is absurd, therefore, to give a peculiar pathological history to so-called railway spine. That the injury occurs, I have no doubt; that the medulla is seriously affected in the vast majority of cases, I have very great doubt.

I cannot now, after thirty years of hospital and private practice, call to mind a single case of concussion of the spine arising from other accidents than on railways which has had the terrible after-history that is so often attributed to them; and I have seen in that time many cases of spinal injuries of all kinds.

There is another fact of personal experience. I have examined many cases of claimed irreparable or serious injury to the spine in private, both for plaintiff and defendant, in impending suits, but I cannot remember a single application of a patient for admission to the hospital to be treated for the after-effects of concussion of the spine, the original injury having been received in a railway collision.

As all sorts of people ride on railways, it is strange that the numerous recipients of concussions of the spine are pecuniarily independent of hospitals. One old fraud I do remember who fell from a street-car and claimed lasting injury to the upper part of the spine and the head, and adequate compensation for it in court. I was not called as a witness at the trial, and the plaintiff recovered very heavy damages. These were afterward reduced to a much smaller amount when it was discovered what I knew about the case.

Other structures of the spine besides the medulla are much more subjected to injury than it is, and their consequences often mislead both patient and doctor, especially the former.

The ligaments and muscles are exposed to contusions, strains, ruptures, and twists which are wrongly attributed to concussion. From these injuries and from so-called concussions the patient recovers rapidly or slowly according to their extent. If damages are looked for from a corporation, he is in a state of what may be called expectant pecuniosity, and shows no amendment until the question is settled. Otherwise, he gets well, as those do who are injured but have no expectations.

There is a striking want of confirmation by post-mortem examination of the terrible effects which are said to follow concussion of the spine.

In fact, the records of such examinations are so few, notwithstanding the immense number of those who have claimed to have the injury that the sceptics are somewhat justified in attributing the few cases which have shown great pathological changes in the cord and its membranes to the {915} coincidence of disease, as myelitis or syphilis, or to much graver injuries than concussion.

I have reported a case in full in the _Medical News and Abstract_ (Philada., Nov., 1881) which illustrates how coincidence might easily play its part in a supposed concussion. This feature of it is not alluded to in that paper. A gentleman began to complain of pain posteriorly at the root of the neck. Paralytic symptoms gradually developed. It is unnecessary to repeat the details here, but the history was a most dreadful one, and precisely that of the few serious ones described in the works on concussion. Within a year the patient died. The autopsy revealed a meningitis and softening and destruction of the cord to the extent of two and a half inches of its brachial enlargement. There was no other disease. Now, this patient frequently travelled on railways, and if he had been subjected to the slightest accidental shock it would have been received on all sides as the cause of the disease. There was, however, no such history, nor was anything ever known to account for the fact that a man in otherwise perfect health should have two and a half inches of his spinal cord as it were spontaneously destroyed.

I will state in passing that this case did not confirm the views of Johnson and others as to there not being any severe pain on pressure in myelitis. It showed also that clinical observation is not always in accord with plausible anatomical facts or reasoning.

Thus, Johnson says: “It is a mistake to suppose that meningitis or myelitis is accompanied by pain on pressure: the spinal cord is surrounded by a bony wall thicker than the bones of the skull, and you might as well press on the head to see if the brain is diseased.”

Now, in this case the pain was simply atrocious and greatly increased by pressure. To relieve both it and the disease the actual cautery was applied on both sides of the spinous processes; and some estimate may be made of the sufferings of the patient, who would not take ether, when he exclaimed as the hot irons were burning through his tissues, “Oh, that is better than the pain.”

To sum up, then, I think I have shown that concussion of the spinal cord proper occurs. I also believe it may occur in a railway collision just as it occurred in the man who fell twenty feet. Why should not a traveller sitting in a peculiar position—with his feet, for example, firmly against a partition or wall of the car—suffer it in a collision.

On the other hand, the great majority of those who after accidents claim injury to the spinal cord as the cause of their disabilities are wholly mistaken. The question is of great importance, for upon it depends the testimony as to whether the patient has sustained temporary or permanent injury.

Each case must be studied on its own merits. There is no class of injuries so full of opportunity for the exaggerator or malingerer. The history of many of them is by no means complimentary to human honesty. Those interested can study the special works on the subject: space is not given to detail them in this paper.

The SYMPTOMS and PROGNOSIS of concussion of the spine may be almost inferred from what has been written above. There are tinglings, pain, and sometimes cramps in the limbs; there may be partial or complete paraplegia which is transient in character. Complete paraplegia is {916} very rare, and when it exists it almost always indicates a more serious injury than concussion. The case I have cited is an exceptional one.

The bladder is almost always affected; there is either suppression or incontinence. The bowels are sluggish for a time. The pulse is mostly quickened; the temperature does not vary much from the normal. Priapism, which is so frequently present in wounds involving the spinal column and cord, is not present in concussion.

I have in the _Medical News_ (Nov., 1881) given my reasons for believing this symptom to be due to a coincident impression or laceration of the sympathetic nerve when there is a fracture or other injury of the vertebra. This view I have been able to sustain by a case reported in the _Medical News_ (Philada., Feb. 25, 1882).

The PROGNOSIS of concussion of the spine is generally favorable. The recovery is slow in pronounced cases. Where such terrible consequences follow as are described in some of the cases which have been caused by railway collision, there is reason to believe that the original injury was either too severe to come under the head of concussion, or that some coincident deterioration was present at the time of the accident.

The DIAGNOSIS from fractures and dislocations is mostly easy. In these cases the local and general symptoms are nearly always so definite as to give no trouble in coming to a conclusion as to their nature. In obscure cases time will develop the truth.

In the TREATMENT of concussion of the spine the great remedy is rest. Under this alone the slight cases will rapidly recover. The more severe ones will require other aids, such as cupping, both wet and dry, to the spine over and about the chief seat of complaint. Sinapisms, blisters, and iodine are useful in the order named. Opium will be borne much better for the relief of pain and restlessness than in like injuries of the head. The natural functions must be looked after. Both the catheter and enemata may be required. Great care must be taken to provide against chafing of the skin and bed-sores. For this I know of nothing better than repeated sponging with alcohol, and drying the surface at once by a good rubbing. The points of pressure should be frequently changed by shifting the patient.

As soon as the acute symptoms pass away the patient should be encouraged to rise and use moderate exertion. This, if well borne, should be increased day by day, for it will be soon found whether the efforts are injurious or not. All the requirements are present in these cases to produce chronic hysterical invalids, both male and female. It is therefore incumbent upon the medical attendant to protect his patient from discouraging surroundings of any kind. It is also his duty to so act that while he will be careful to work no injustice, he will at the same time be on the watch for malingering, for this will often be practised, especially by those who are among the expectants already mentioned in this article.

{917}

INTRACRANIAL HEMORRHAGE AND OCCLUSION OF THE CEREBRAL VESSELS, APOPLEXY, SOFTENING OF THE BRAIN, CEREBRAL PARALYSIS.

BY ROBERT T. EDES, M.D.

The various subjects embraced in this article are so closely united to each other, both in a clinical and in a pathological point of view, that they must be considered to a certain extent in common. It is of course more systematic to group them entirely according to the obvious and final lesion, as hemorrhage, thrombosis, or embolism; but when it is considered how very closely the symptoms of one affection may counterfeit those of another—so closely, in fact, that a diagnosis with absolute certainty is not only difficult, but often impossible—and also that similar conditions of the vessels may give rise either to rupture or occlusion, so that not infrequently two sets of lesions may be found in the same brain, and, finally, that the basis of prognosis and of the later treatment is not unlike in different lesions,—we are surely justified in bringing them, at least in the beginning, under a common head.

Intracranial hemorrhage, and especially cerebral hemorrhage, is the lesion which more frequently than any other gives rise to the group of symptoms known as apoplexy, and from this fact has arisen the frequent incorrect application of the word apoplexy, in a pathological as well as a clinical sense, to indicate an extravasation of blood, as in the so-called pulmonary apoplexy, where the anatomical lesion, being an extensive effusion of blood into the tissues of the lung, bears an apparent resemblance to the state of the brain often found in apoplexy primarily and properly so called, the symptoms, however, being entirely different. This error receives additional support from the fact that in some injuries to the brain, especially to the base, pulmonary hemorrhage may secondarily take place. Apoplexy, however, is not always the result of hemorrhage, but occurs with many cases of embolism and of thrombosis, and is sometimes, so far as we can tell, dependent upon neither of these conditions, recovery in one set of cases taking place so rapidly as to preclude the supposition of a considerable organic lesion, and in others, which are fatal, nothing being found beyond an excess of serum or of vascularity, and sometimes not even that. The first of these conditions has been called simple apoplexy, but with our present knowledge its simplicity seems to border closely on ignorance, or at any rate is not of a character {918} to satisfy the inquiring mind. It is therefore better to retain the term apoplexy strictly as a convenient term for a certain set of symptoms, but, whenever possible to substitute for it an anatomical description of the lesion found post-mortem or diagnosticated with reasonable probability during life.

The practitioner may very properly, and without laying himself open to criticism of his diagnostic accuracy, return the cause of death in a case of sudden death, or where his opportunity for observation has been limited, or where no post-mortem examination has been held, as being apoplexy; but in others, where the symptoms were decisive or a post-mortem has disclosed the exact lesion, the condition of the cranial contents should be stated. It is also a not uncommon mistake—or rather piece of carelessness—to speak of small hemorrhages in the brain as small apoplexies. A small extravasation may give rise to slight symptoms or next to none, but a real apoplexy can hardly be small, although it may be short.

The root from which the word apoplexy is derived seems to have been used by the classic writers in something like its present clinical signification (_Απορληκτος_, seized with (apoplexy or) stupor—Aristophanes; mad—Demosthenes; _Αποπλησσομαι_, to be struck with amazement—Sophocles). Morbus attonitus, another of its names, expresses a somewhat similar idea.

Morgagni was familiar with cerebral hemorrhage, and Bonetus in the _Sepulchretum_ gives several cases. The allusions of Galen and Hippocrates supposed to refer to this lesion are not unequivocal, although the Father of medicine could hardly have helped being familiar with the symptoms of so striking a form of disease.

Cerebral softening has been recognized since the early part of the present century, and in some of the cases thirty years ago an efficient cause, in the form of arterial disease, assigned to it; but the complete theory of its causation forms a part of the general doctrine of embolism and thrombosis which was so largely developed and systematized by Virchow. Andral and Durand-Fardel had apparently no idea of the exact mechanism of its origin, the latter supposing it to depend upon inflammation, while Todd mentions a case where softening giving rise to paralysis depended upon a dissecting aneurism of the carotid. He seems to have generalized so far as to say that white softening is atrophic, but the precise way in which this localized atrophy was usually brought about evidently escaped him. According to him, the suddenness of the attack was owing to a gradual disorganization of the brain-substance with few or no symptoms, and then a sudden rupture of diseased fibres by some accidental cause or by their having reached the extreme limit of cohesion.

Intracranial hemorrhage may be situated outside of the dura mater, separating this membrane from the bones of the skull and producing more or less compression of the brain. It is usually the result of a blow, but not necessarily of a fracture of the skull. When a fracture is present, blood may pass through it from the interior and give rise to an external extravasation in addition to that which is likely to be the direct result of the blow upon the skin and subjacent soft parts. The middle meningeal artery is a frequent source of this hemorrhage. Hemorrhage in this position will naturally give rise to symptoms of compression, and, if the fact of the blow be not known or the fracture manifest, may be mistaken for some of the deeper-seated forms.

{919} Blood may be effused upon the surface of the brain in the so-called cavity of the arachnoid—that is, outside of the pia mater—or in the meshes of this membrane, following its course along the sulci. This also is not infrequently the result of violence either with or without fracture of the bone. Its source is likely to be found in the veins which empty into the longitudinal sinus from the surface of the brain. Rupture of a lateral sinus from a not very severe blow has been the source of large and fatal hemorrhage.[1] Blows upon the head, with or without fracture of the cranial bones, are likely to cause rupture of the cerebral substance with hemorrhage, and this may find its way to the outside and cover more or less of the surface. Such injuries to the brain, it is important to note, do not necessarily correspond immediately to the place of the blow or to the external ecchymoses. Meningeal hemorrhage in this region may, however, be observed when no injury has been received, or at least when there is neither history nor external traces of any.

[Footnote 1: _Cincinnati Clinic_, p. 135, 1874.]

The conditions under which it occurs may not vary greatly from those of the more ordinary intracerebral effusion. In two instances under the observation of the writer the source of hemorrhage has been a vessel of small, but not the smallest, calibre (artery), situated near the fissure of Sylvius, in the lower parietal or temporo-occipital lobe. In children meningeal hemorrhage is, with only a few exceptions, the usual lesion of apoplexy. The blood is usually dark and coagulated in recent cases. Blood found under the membranes where no fracture has taken place is, however, more likely to have been derived from the brain-substance and to form part of a cerebral hemorrhage.

Hemorrhagic pachymeningitis, indicated by a layer of fibrin included between the dura on the one hand and a false membrane on the other, is met with in connection with meningeal and cerebral hemorrhages. It is supposed to depend on a small and thin hemorrhage upon the surface of the brain, which forms, by its irritant action, a false membrane about itself. It is found usually over the vertex.

Hemorrhage into the ventricles is nearly always the consequence of a hemorrhage in the brain-substance breaking through, although it may in rare cases originate in the vessels of the choroid plexus, velum interpositum, or meninges. Its source, however, is sometimes so near the surface as to cause but little laceration of the cerebral tissue. The blood breaking into any one of the ventricles may be found in one or all of them (except the fifth), and form quite an accurate cast of their shape.

The most common form of intracranial hemorrhage, however, which most nearly concerns us here, and which is generally meant when sanguineous apoplexy is spoken of, has its principal seat in the brain itself, which is, of course, more or less lacerated. Such hemorrhages may vary greatly in size, from a mere red point (punctate or capillary), of which many may be present at once, to one of many ounces, filling a large cavity of nearly the length of one hemisphere, and pushing the torn and compressed brain-substance before it in every direction. The amount of laceration produced of course varies greatly; sometimes it seems as if nothing more than a pushing aside of fibres without rupture had taken place, while at others large masses of tissue are torn away and mixed up with the blood into a pulp.

{920} In a recent hemorrhage the clot itself, speaking of those of a size above the capillary, is usually homogeneous, the brain-substance surrounding it ragged, œdematous, yellowish or red, and frequently containing many minute secondary hemorrhages. The rest of the brain is frequently found anæmic from pressure, the convolutions flattened, the surface dry, and the section exhibiting a diminished quantity of blood. In older cases, however, and probably also in some where atrophy, senile or otherwise, has preceded the hemorrhage, this condition is not found, and we may have the convolutions shrunken and the meshes of the pia containing an excess of serum.

If death does not take place speedily, the clot undergoes degenerative changes. Its color becomes somewhat lighter, chocolate color, reddish-yellow, or yellowish-red. A portion is absorbed, and after a time the cerebral substance in the neighborhood forms about it a wall of some density, so that finally nothing is left but a cyst with fluid or semifluid contents, and often remains of connective tissue. Sometimes the absorption of a clot of moderate size is so complete that only a firm mass of a reddish or yellowish-brown color marks the seat of an old hemorrhage. The brain-substance in the neighborhood may be more or less atrophied, and a distinct depression may be noted over the position. The microscope shows in a fresh hemorrhage only broken-down nerve-tissue and blood and vessels more or less degenerated. In an older one the blood-corpuscles have disappeared, but masses of pigment of a dark yellow or a brownish-red remain to show the former presence of blood. This pigment occurs in the form of rounded granules or of small rhombic crystals, and has received the name of hæmatoidin. The light-yellow masses often found along the course of the cerebral vessels are not evidence of hemorrhage, but of congestion merely. The so-called inflammation or granulation corpuscles, which are simply the fattily degenerated cells of the organ in which they are found, and which usually possess no distinctive form, being simply round masses of fat-drops, are often met with in the brain in hemorrhage or softening. It is sometimes perfectly evident, however, from their form, triangular or pyramidal, that they are degenerated nerve-cells. The blood-vessels, those just above the size of capillaries, are usually in a condition of fatty degeneration, masses of dark granules occupying more or less densely the line of their walls. A mere deposit of fatty granules inside the perivascular sheath, but outside of and not involving the walls of the arteries, may present the appearance of a degeneration of the walls themselves. This condition may be a consequence of any lesion involving degeneration of brain-tissue, and in no way a cause.

The intermediate stages of transformation in a hemorrhage are less frequently found than the recent or old ones, since the patient, if he does not die within a few days, is likely to live for some weeks or months.

The changes taking place in the clot itself within the first few days are not very marked, but the walls of the cavity may become softer and more deeply colored, at first red and afterward yellow. Blood-crystals have been detected on the seventeenth day (Virchow). The following descriptions have been given of clots of different ages: Eleven days—reddish-yellow softening clot, with brain-tissue stained for half an inch in depth, and brain rather hard in vicinity. Eighteen days—cavity with its {921} edges anteriorly and superiorly sharply defined, with the edges posteriorly ragged and yellowish, filled with a tolerably firm brick-red mass adherent to surrounding brain, and showing in the centre a softened clot about the size of a pea. Twenty-eight to thirty-five days—soft, brownish, and semifluid. Forty-one days—spot of softening filled with brownish material. One hundred days—somewhat darker, and a little more distinctly marked from surrounding tissues; by microscope granular corpuscles, groups of fatty granules along the swollen vessels, granules of pigment. Eighty-three years—old hemorrhagic focus in right optic thalamus, color yellowish, and areolar structure.

The thirtieth day is given as about the time at which the walls of the cyst become more firm and distinct. The following statement is prepared from a considerable number of cases given by Durand-Fardel: From four to six weeks, the clot is dark-colored, from black to ochrey or reddish-yellow. It varies in firmness. The capsule is tolerably firm. From two to four months, it seems to be generally softer, pultaceous, grumous, or the clot still remaining swimming in serum; in some cases lighter in color. In six months it has lost more in color, and the cavity may be smaller. In a year there is still considerable color left. In a few cases after some years the blood has been found in the form of a dried mass, not changed or darker in color.

Hemorrhages of several months' standing may be indicated either by a brownish-red patch somewhat firmer in texture than the surrounding brain-substance, or by a cavity with firm walls, which often has strings and septa of connective tissue running across it, so as to convert it into a kind of spongy mass filled with brownish fluid.

The most important changes which are found in most if not all cases of ordinary hemorrhages (_i.e._ such as do not depend upon violence or cachexia) are those of the blood-vessels. They are not, however, visible in the ordinary inspection of the brain at an autopsy, but require to be carefully sought for, either with the microscope or a somewhat tedious process of washing. For this reason there are no trustworthy statistics of large numbers to determine in how large a proportion of all the cases alterations in the blood-vessels are to be found, and in what form. There can be but little doubt, however, that those cases in which no form of arterial disease is present (if, with the reservation just noted as to violence or cachexia, such exist) are to be looked upon as rare exceptions.

The presence of miliary aneurisms in the brain had been noted in some cases, and even in cerebral hemorrhage, without the great importance of the observation having been perceived; but the extended and careful observations of Charcot and Bouchard first showed how extremely common their presence is, while in many instances they were found actually ruptured. These aneurisms are present in the largest numbers in the regions of the brain where hemorrhage is most frequent, and at the age when death from apoplexy is most likely to occur. They have been found at the age of twenty, but very rarely at early ages, while after forty they are not uncommon. It is of course not always that they have gone on to rupture, but may occasionally be found where no hemorrhages have taken place. It is not going far, however, to infer that in such cases the hemorrhage was not very distant.

These aneurisms are dependent upon a periarteritis which is diffused {922} more or less widely over the cerebral arteries, but not over those of the rest of the body. The larger arteries get a thin and shining appearance, compared by Charcot and Bouchard to the skin of an onion, while the smaller ones present besides distinct aneurisms, bulgings and irregularities of outline. This condition may be—and, as would be at once suggested from the age at which both lesions are met with, is—very likely to be associated with atheroma, but it is not the same thing, since the development of the aneurisms depends upon a periarteritis, and that of atheroma upon an endarteritis. It may be remarked, also, that atheroma usually does not affect the very small arteries which bear the aneurisms and give rise to the hemorrhage.

These aneurisms are visible to the naked eye, being from two-tenths to one millimeter, or a little more, in diameter, while the artery to which they are attached can be seen by the naked eye or with a lens magnifying two or three diameters. They may be strung along a small artery like beads or be found in groups like a bunch of grapes. Charcot and Bouchard found them in every case of cerebral hemorrhage which they examined, and, although the possibility of other sources was admitted, concluded that in by far the greater number of cases, excluding those dependent upon traumatism or hemorrhagic diseases, the blood effused in the brain has its origin in one of these aneurisms. The presence of these aneurisms has been abundantly established by other observers, and the fact that they are not usually demonstrated proves nothing except the amount of care and time necessary to find them. One does, however, find occasionally noted that they were sought for and not found. The statements of Charcot and Bouchard relate, so far as their own observations are concerned, and as they themselves remark, chiefly to aged persons, but in their first series of 66 cases there is found 1 of twenty and 1 of forty years of age. The patient of twenty was a semi-imbecile and a drunkard. Extensive cerebral hemorrhage, with atheroma, in the circle of Willis has been found in an apparently healthy and well-nourished boy of fifteen.[2]

[Footnote 2: Baker, _Annals of Anat. and Surg. Soc. Brooklyn_, 1879, p. 40.]

Larger aneurisms, often multiple, are not very infrequent upon the arteries at the base of the brain. They may before their rupture give rise to symptoms of pressure like any other tumor, and may also be the source of hemorrhage, which is usually meningeal. They are not infrequently symmetrical, and a place of election is one of the early bifurcations of the middle cerebral.

Coats[3] states that aneurism of the larger arteries is the most frequent source of hemorrhage in persons under fifty. They may be due to embolism, producing, when the occlusion is not complete, mechanical injury to the walls of the vessels by the constant hammering upon them of the embolus under the impulse of the blood. If this etiology is a common one, it accounts for the frequent situation of these aneurisms in the middle cerebral arteries.

[Footnote 3: _Glasgow Med. Journ._, 1882, xvii. 109.]

Small vessels in a condition of fatty degeneration are often found in the neighborhood of a cerebral hemorrhage. In some cases, undoubtedly, the degeneration is a consequence of the injury to which the cerebral substance has been subjected, but they have also been found too soon {923} after the hemorrhage for this explanation to hold; and in cases where no aneurisms are present the older supposition, that hemorrhage results from this kind of degeneration, seems to have a certain foundation, even if only in a minimum of cases.

In several cases of cerebral hemorrhage in purpura, where the general character of the disease was shown by hemorrhages in other organs, fatty degeneration of the cerebral vessels has been found, together with extensive steatosis of the liver, kidneys, muscles, and heart.[4] In a cerebral hemorrhage found in the brain of a girl of eleven the walls of the vessels were dotted with fat-globules and dark granules, and several of them studded with round and oval nuclei closely resembling the nuclei (small cells?) commonly found in tubercle. There was no trace of tubercle in any part of the body.[5]

[Footnote 4: _Gazette hébdomadaire_, May 12, 1876, p. 288.]

[Footnote 5: _Trans. Path. Soc._, Cayley.]

There is no possible means of determining in which way any given bleeding has arisen, except a very minute search, and this may fail to show the actual point of rupture. It seems highly probable, from the connection of some cases of hemorrhage with valvular disease of the heart, that embolism may give rise to effusions of blood, especially capillary and multiple ones. In such cases the emboli may be deposited in arteries far too small to be obvious in the ordinary process of dissection. (See Capillary Embolism.)

Hemorrhage arises in some rare cases from the backing up of blood in the veins when they are obstructed by thrombosis. A case has been described where meningeal and ventricular hemorrhage resulted from a rupture of the straight sinus at its juncture with the torcular Herophili.[6]

[Footnote 6: Mullar, _Lancet_, 1849, i. 607.]

In many diseases like purpura, idiopathic anæmia, and leucocythæmia many hemorrhages may take place in the brain as well as elsewhere throughout the body. Their importance under these circumstances is usually not great.

The usual localities of cerebral hemorrhage are stated with much minuteness in the following table from Durand-Fardel, which, although not very recent (1854), is not the less accurate on that account. No subsequent statistics have essentially altered its most important conclusions. In 139 cases the hemorrhage was situated in the hemispheres 119 times; in the protuberance (pons), 21; in the cerebellum, 13; total, 153.

I have placed beside these a small number of cases from the records of the Boston City Hospital and my own practice, and, to avoid the multiplication of headings, have entered some multiple hemorrhages under two or more heads, so that from the whole number of cases (46) there are 81 entries:

Durand-
Fardel. B. C. H.
Corpus striatum and optic thalamus, together . . 22 4
Corpus striatum . . . . . . . . . . . . . . . . . 13 10
Optic thalamus . . . . . . . . . . . . . . . . . 5 3
Corpus striatum, optic thalamus, and middle lobe 2 1
Corpus striatum, optic thalamus, and a
considerable portion, not well defined, of the
hemisphere . . . . . . . . . . . . . . . . . . 12 2
Corpus striatum, optic thalamus, with posterior
lobe . . . . . . . . . . . . . . . . . . . . . 1
Corpus striatum and middle lobe . . . . . . . . . 3 3
Corpus striatum, with a considerable portion of
hemisphere . . . . . . . . . . . . . . . . . . 5 1
Corpus striatum, with an extended portion of base
of ventricle . . . . . . . . . . . . . . . . . 1
Optic thalamus with middle lobe . . . . . . . . . 2 1 {924}
Optic thalamus with posterior lobe . . . . . . . 1
Middle (parietal) lobe . . . . . . . . . . . . . 19 1
Sphenoidal horn of middle lobe (temporal) . . . . 2 4
Anterior (frontal) lobe . . . . . . . . . . . . . 11 3
Posterior (occipital) lobe . . . . . . . . . . . 11 5
A not well-determined extent of one hemisphere . 4 3
The superficies of the convolutions (once with
corpus callosum) . . . . . . . . . . . . . . . 3 1
Insula . . . . . . . . . . . . . . . . . . . . . — 2
Cortex (not further defined) . . . . . . . . . . — 1
Small multiple . . . . . . . . . . . . . . . . . — 3
Meninges (secondarily) . . . . . . . . . . . . . 31 6
Ventricles . . . . . . . . . . . . . . . . . . . 66 8
In the cerebellum, right lobe . . . . . . . . . . 6 |
" " left lobe . . . . . . . . . . 5 | 4
" " middle lobe . . . . . . . . . 2 |
In the protuberance (pons) . . . . . . . . . . . 13 4
Protuberance and brain . . . . . . . . . . . . . 8
Protuberance, crus cerebri, crus cerebelli,
external capsule, fourth ventricle . . . . . . — 1

It would not have been very difficult to increase these figures from the large number of recorded cases, but there is nothing in later statistics to invalidate the statement that the corpus striatum, including both its nuclei, but especially the nucleus lentiformis, the optic thalamus, and the white substance in their neighborhood, are the portions of the brain by far the most frequently affected by hemorrhage, and especially by hemorrhages of considerable size.

There is no essential difference in the frequency of hemorrhage on the two sides. It may occur on both sides at once. Hughlings-Jackson says that he saw a patient who escaped with life from the effects of a clot which had paralyzed both sides of the face as well as all four limbs. Charcot and Bouchard give the following localities as containing in decreasing frequency the miliary aneurisms: optic thalami, corpora striata, the convolutions, the protuberance, the cerebellum, the centrum ovale, the middle peduncles of the cerebellum, the cerebral peduncles, and the bulb. The close correspondence of this list with the table of Durand-Fardel is in itself a strong argument in favor of the importance of the miliary aneurisms as the principal factors in determining cerebral hemorrhage.

The arteries supplying the nucleus lenticularis and external capsule are small branches arising chiefly from the middle cerebral a short distance from its origin, with some assistance from the anterior and posterior cerebral. One of the larger of them runs along the outer side of the nucleus lenticularis where it is covered by the external capsule—a disposition which may have something to do with the occurrence of the larger hemorrhages so likely to take place just outside this nucleus and into the substance of the hemispheres.

The arteries of the optic thalamus arise from the posterior communicating or the posterior cerebral. Why these two groups should furnish, as they do, so large a part of cerebral hemorrhages it is impossible to state, unless it be that from their origin so near to the larger trunks before their division they are exposed to more pressure, and hence a greater tendency to form aneurisms. The functional activity of these regions is another possible reason. The largest hemorrhages also seem to spring from these sources, and if a table of large effusions were compiled {925} it would probably show a greater predilection for this locality than even the general one given above, which includes those of all sizes.[7]

[Footnote 7: A very careful study of the form and size of foci of bleeding arising from the various nutrient arteries of the brain will be found in the well-known elaborate papers of Duret (_Archives de Physiologie_, 1874).]

Before proceeding to a minute account of the symptoms accompanying cerebral hemorrhage, a consideration of the relation between extensive lesions and the most fully-developed clinical phenomena will be of value—in other words, the pathology of hemorrhagic or sanguineous apoplexy. This will naturally demand a reference to the cases where the same symptoms are present with a different lesion.

The most marked symptom, one which is essential to the definition of apoplexy, is the sudden, or more frequently rapid, loss of consciousness, and next, in a great proportion of cases, a unilateral paralysis or paresis. The latter, in many cases, finds a sufficient explanation in the rupture of fibres connecting the motor centres in the brain with the spinal cord; but this does not cover all cases, for it is well known that we may have paralysis without any laceration. In fact, in many cases paralysis may disappear so rapidly as to put aside at once any such explanation. Sufficient pressure upon contracting fibres is entirely competent to arrest their conductivity, and this pressure may be diffused over a considerably wider area than that where total destruction of tissue has taken place. Meningeal hemorrhage, where, of course, no laceration takes place, may be attended by a well-marked hemiplegia when the effusion is wholly or chiefly on one side.

The writer recalls a case of a man, of whose history little or nothing was known, found unconscious with a very distinct difference in the amount of motion to be provoked by irritation of the two sides. The diagnosis naturally inclined to the more common causes of hemiplegia, but the autopsy showed a purulent meningitis of the vertex, with a layer of pus considerably thicker on the side opposed to the paralysis.

A very similar statement may be made in regard to the symptom of unconsciousness, which seldom occurs more rapidly and completely than in cases of meningeal hemorrhage (not from injury), where, of course, there is no question of laceration.

F. Pagenstecher[8] succeeded in producing phenomena closely allied to apoplexy by injecting at a known pressure, between the skull and dura mater in dogs, masses of melted wax and tallow. In the first group of cases the result was somnolence, great depression of the psychical capacity, and general muscular weakness. The second group showed, besides the condition of sopor, unilateral paralysis; and the third contained cases in a part of which death followed in a few hours after the setting in of coma, and in another part partial recovery took place after scooping out the waxy mass. The symptoms in these cases are referred to the pressure upon the vessels; and it is stated that in order to destroy life the pressure had to be equal to that of the blood. Convulsions were present in some cases where the pressure was not steady. The temperature showed a notable peculiarity in that, after the initial fall, in which it resembles the course in human apoplexy, it kept on falling in the fatal cases, instead of rapidly rising, as in man. After injection into the brain of animals {926} of sufficient quantities of water to produce great tension of the occipito-atlantoid membrane, Duret[9] found the respiration to cease and the heart to be slowed. On tearing the membrane so as to allow the water to escape, respiration began again, and the animals gradually recovered consciousness. Similar effects could, however, be produced by blows on the head.

[Footnote 8: _Centralblatt f. d. Med. Wiss._, 1871, p. 706.]

[Footnote 9: _Centralblatt f. d. Med. Wiss._, 1878, p. 454.]

Several cases are reported by P. R. Hoy[10] where pressure upon the brain produced an arrest of function, which was resumed when the pressure was removed. In the first of these a piece of bone had been removed, but the dura was intact. If the patient were asked a question and the finger immediately pressed upon the dura, no answer was made, but as soon as the finger was removed the reply came. In two other cases, which are not without their parallels, the patients resumed after trephining the mental attitude in which they had been surprised by the injury—in one case hours, and in the other years, before.

[Footnote 10: _Journ. Nerv. and Ment. Dis._, vol. iv. p. 288.]

The natural generalization to be made from these cases and experiments is, that pressure upon the brain-tissue suspends, for the time, its function; but when we find exactly the same symptoms arising from either sudden or gradual occlusion of the vessels where we can hardly imagine increased pressure to exist, except perhaps over a very small area of collateral hyperæmia, we must go a step farther for a common factor; and it seems possible to find one which will not only explain the several conditions spoken of, but also others which closely resemble them. Simple anæmia will cover the cases of hemorrhage and embolism, but certainly not narcotic poisoning and certain other conditions where characteristic apoplectic symptoms exist without discoverable lesion. If, however, we say that a deprivation of a considerable portion of gray matter of its due supply of arterialized and healthy blood suspends for a time its functional activity, we can explain the similarity of results arising from very different causes.

In a case of cerebral hemorrhage of considerable size the pressure is distributed over a space much exceeding the area of the clot itself, and renders a large part of at least one hemisphere anæmic. If the blood finds its way into the ventricles, the conditions are most favorable for compressing nearly the whole brain. The anæmic appearance of the cerebral surface is often remarked at autopsies.

When an embolus lodges in an artery and produces complete occlusion, the portion of brain supplied thereby becomes at once entirely anæmic, since the arteries on the surface have so slight anastomoses that they are entirely unable to supply the deficiency, except to a slight extent around the edges of the vascular territory involved. The anæmia, however, does not extend beyond the territory originally affected, and consequently we may have extensive paralysis from embolism without a marked apoplectic attack. In extreme congestion of the brain the reverse may seem to be the case.