CONCUSSION OF THE BRAIN AND SPINAL CORD.
BY WILLIAM HUNT, M.D.
The writer was asked to contribute a short article upon Concussion of the Brain and Spinal Cord for this work, as these injuries are apt at first to come under the notice, if not charge, of the general practitioner. The article will therefore not be an exhaustive one, and there will be little but the details of personal experience and less quoting of authorities. Much has been written recently upon the subject both in volume and in pamphlet.
Diverse views of equally competent judges of the matter have been put forth, and the brains and spinal cords of the partisans appear to have received as severe a shaking up as the real recipients of the lesions, if absolute lesions there be.
This, in fact, is the point of controversy, for there are those who seem to deny that there can be a jarring or shaking of the cerebro-spinal mass sufficient to cause positive symptoms without producing positive lesions, whilst others are as firm in their convictions that pronounced symptoms may follow a mere disturbing ripple of the nervous elements. How is the question to be settled? The slightly shocked or injured recover rapidly, whilst some who only appear to be as slightly injured or shocked at first, go on to death, during the progress to which event there is no doubt as to the existence of lesion and no difficulty in finding it at the autopsy. Hence, say the lesionists, the first ones had it, but got well, whilst the non-lesionists affirm that it never existed in them.
The logician would think that these differences in opinion were only differences in degree about the same thing, but, nevertheless, the question is one for serious discussion, and is of much greater importance than would appear to be the case to the average layman.
This importance lies in the medico-legal aspects of the suits arising out of the alleged injuries and their consequences. Judges, lawyers, and doctors know them well. In doubtful cases authorities of equal eminence are quoted, and the results of trials are equally as doubtful as to whether justice or injustice has been done. These remarks, as will be seen, are especially applicable to injuries of the spine, but they also may have place in the consideration of consequences arising from concussion of the brain.
Concussion of the Brain.
Whatever doubts there may be as to concussion of the spine, there are none, I believe, who deny the appropriateness of the expression as to the brain, it being, by its anatomical relations, so much more exposed to shock than the spine.
We understand that pure concussion, uncomplicated with fracture, refers to a condition caused by external violence, direct or indirect, which communicates a jar or shock to the cerebral mass, and which expresses itself by certain well-defined symptoms. The nervous system and the circulation are most manifestly involved, but in a pure case it may be said that all of the symptoms arise from central nervous disturbance. Even could it be shown that they were dependent on temporary congestions, these congestions, I think it will be admitted, would be due to vaso-motor derangements.
The anatomical appearances after early death from concussion of the brain are often insufficient for us to comprehend the fatal result, for we know that the organ will bear, both from disease and other kinds of injury, vastly greater inroads upon its structure and surroundings without causing death. Often there is mere localized cerebral congestion, with no ruptures of vessels; then there are slight extravasations shown as points or dots of blood in the nerve-matter; and, again, there is what is called the bruised brain. Sometimes there is nothing abnormal whatever to be found. Most of these cases, under modern criticism, have been justly shut out from the record as having no value; for it has been shown that the post-mortem examinations of them have been very imperfect, the brain only having been inspected, whereas the chest, the abdomen, or the spine might readily have revealed the cause of death.
It is fair, however, to assume that there must be a capacity for serious results in the vibratory jar, as the discoverable lesions in many well-examined cases have been in themselves insufficient to kill. The rapidity of recovery of those who get well also bears weight on this point.
Of nineteen cases of recovery from concussion of the brain of which I have record, the average stay in hospital was eight days. The range of stay was from one to twenty-five days. Many of these were at first profoundly shocked, some of them apparently hopelessly so when we compared their symptoms with those who died. As they recovered, however, in so short a time, there surely could not have been any gross lesion to account for their symptoms. What else, then, can account for them than vibratory jar? and if this can produce such severe results within the line of recovery, why cannot the degree of it be so extended as to involve, for example, the respiratory centres, and so kill without leaving perceptible sign?
The SYMPTOMS of concussion of the brain range from a mere daze or stunning to those of deep unconsciousness. There is no paralysis of the extremities in pure cases. Often the patient is very restless, and throws his limbs about in all directions. When these are quiet there is response to irritation and electricity. Loud speaking to him may elicit some attention, but the answers are mostly incoherent. There is pallor, often extreme, coldness of surface, and sweating. Vomiting is usual, and may come on immediately or later, and it continues as long as there is anything to discharge; sometimes there is retching. In favorable cases the cessation of vomiting is accompanied by a slow return to consciousness, which may be preceded by delirium. This return is never sudden, and the method of it serves to distinguish the case from that of some forms of epilepsy. The pulse is generally frequent and feeble, often irregular; in extreme cases it may be slow and feeble, very rarely, if ever, strong or bounding. After reaction it becomes more natural, and if recovery follows it will not show much variation. The temperature is depressed at first. In one characteristic case it was 98° on the first day, reached 101° on the third day, and receded to 98½° on the eighth day, when the brain symptoms disappeared.
There may be retention of urine and sluggishness of the bowels, but in bad cases coincident with the vomiting there is sometimes involuntary discharge both of feces and urine. The respiration is irregular, sometimes almost ceasing, and then returning with great rapidity.
Much has been said and written about the condition of the pupils in concussion of the brain. I have made this matter a subject of observation, and am convinced that the state of the pupils is of no diagnostic value whatever as to determining the existence of concussion or compression. Their state is of great value in telling us that the functions of certain brain-centres are partially or wholly impaired. The progress of the case will tell us whether the impairment is due to clot or effusion, congestion or jar.
It is wrong, therefore, to say that the pupils are one way in compression and another in concussion. It is right to say that in either case they are sluggish or wholly irresponsive to light. In one person they may be dilated, in another contracted, and in the same person the eyes may present marked contrasts.
In the light of modern physiology this is what might be expected. The condition of the pupils is dependent on that part of their nerve-connections which is involved in the injury, and also upon the method of that involvement. Clinical experience, I think, amply sustains this view.
The reaction from what may be called pure concussion is generally slow. The patient is apt to be dazed for some time, although the pulse and temperature may be normal. When there is a rebound with fever, and florid complexion, and suddenly or gradually another but deeper unconsciousness supervenes, it is almost certain that positive lesion took place at the time of injury, and that the reaction has brought with it great congestion if not extravasation.
Now, really, compression to be followed by inflammation is the condition demanding attention.
DIAGNOSIS.—The history of the case and the symptoms as detailed will enable us to reach a conclusion in most cases as to the existence of concussion of the brain. There are some conditions, however, from which it is to be carefully distinguished. These are simple fracture, with or without depression, compression from any cause, drunkenness, and epilepsy.
There may be such profound shock with fracture that at first concussion symptoms mask those of the lesion, or even keep them for a time completely in abeyance. The head bruises are often very deceptive to the touch in the search for fracture.
I am in the habit of directing students to feel their own scalps, in order that they may appreciate the fact that the touch gives no sensation whatever of the natural thickness of the cranial covering. It seems as though something like a piece of thin parchment only intervenes between the fingers and the bone. The fact is, the scalp varies from an eighth to a quarter of an inch thick, differing in different places, and where muscles, as the temporal, for example, are beneath it, the bone is much deeper. The importance of this observation lies in the fact that a pulpefied bruised mass of scalp will cause the edges of its healthy surrounding part to feel almost precisely like bone around the borders of a depressed fracture. The accompanying general symptoms will mostly not be in accord with this condition, but in some cases the deception is so complete that it is very difficult to persuade those not familiar with the fact that a fracture does not exist, and to induce them to refrain from rash proceedings.
One case I can call to mind where the opinion of the attending physician was only changed by the ultimate favorable result, which left no sign of permanent injury of any kind. These cases are particularly apt to occur with children.
I remember also another source of deception. A boy was severely injured by a blow upon the forehead. Concussion was marked. There was a lacerated wound reaching to the edge of the orbit; fractured bone could be felt, and at first sight what appeared to be brain-matter was oozing from the wound. A hasty unfavorable prognosis was given to the parents. On closer examination it was found that the fracture was of the external wall of the frontal sinus, and the supposed brain-matter was the delicate fat-lobules of the orbit. The patient recovered rapidly.
There is a marked distinction between the ordinary symptoms of concussion and those of compression, whether from depressed fracture or effusion, as of blood in apoplexy. Here there are flushed, often swollen, countenance, stertorous breathing, slow and it may be strong pulse, deep or absolute insensibility, and fixed pupils. The injury, if there is one, is mostly palpable and explanatory. If it is concealed, the other symptoms point to the true nature of the case.
The diagnosis from drunkenness is not always easy, although deep intoxication is more apt to be accompanied with compression than with concussion signs. Drunkards often have bruises on their heads caused by falls, and some of them are pale and sick after debauch. The smell of liquor is not always reliable, for it is so common after accident for friends to administer stimulants before the patient is seen by a medical man that he might be easily misled into too hasty a judgment. The general appearance of the old stager is well known, but in cases where there is the least doubt the patient, whether in hospital or in private, should be kept a sufficient time under observation for the effects of drink to pass off. Then it will be seen whether this has masked a more serious condition. Too hasty conclusions in this matter have led to most unpleasant occurrences. These are well known in police administration and to hospital men.
The convulsions of the epileptic, the foaming mouth, and the quick return to partial or complete consciousness will generally serve to distinguish the case from one of concussion, but at times there are those who require also to be kept under observation for some hours, and even a day or more, in order to come to a correct conclusion.
The PROGNOSIS in concussion is generally favorable, but if complete unconsciousness is present it is doubtful as to the individual so long as this lasts, for, as before intimated, the cases which recover may present as marked symptoms at first as those which prove fatal.
Recovery is mostly complete, but not suddenly so. The after-effects in any case may prove serious.
There is, however, an unwarranted tendency to attribute any defect in character, and even criminal lapses, to a blow upon the head, especially should the history or marks of one be discovered as having occurred at any time, no matter how long, previous to the inquiry.
The blow may be the cause of subsequent epilepsy, chronic inflammations, and insanity or imbecility. These cases have, however, an almost continuous history of trouble from the date of the injury, the manifestations varying in severity from time to time as pathological changes go on or as exciting causes develop them.
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.
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 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 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 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 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.
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 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.
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.
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.
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 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 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
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.
Coats3 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.
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 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
4 Gazette hébdomadaire, May 12, 1876, p. 288.
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
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:
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 it would probably show a greater predilection for this locality than even the general one given above, which includes those of all sizes.7
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. Pagenstecher8 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 of sufficient quantities of water to produce great tension of the occipito-atlantoid membrane, Duret9 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.
8 Centralblatt f. d. Med. Wiss., 1871, p. 706.
9 Centralblatt f. d. Med. Wiss., 1878, p. 454.
Several cases are reported by P. R. Hoy10 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.
10 Journ. Nerv. and Ment. Dis., vol. iv. p. 288.
The natural generalization to be made from these cases and experiments is, that pressure upon the brain-tissue suspends, for the time, its function; but when we find exactly the same symptoms arising from either sudden or gradual occlusion of the vessels where we can hardly imagine increased pressure to exist, except perhaps over a very small area of collateral hyperæmia, we must go a step farther for a common factor; and it seems possible to find one which will not only explain the several conditions spoken of, but also others which closely resemble them. Simple anæmia will cover the cases of hemorrhage and embolism, but certainly not narcotic poisoning and certain other conditions where characteristic apoplectic symptoms exist without discoverable lesion. If, however, we say that a deprivation of a considerable portion of gray matter of its due supply of arterialized and healthy blood suspends for a time its functional activity, we can explain the similarity of results arising from very different causes.
In a case of cerebral hemorrhage of considerable size the pressure is distributed over a space much exceeding the area of the clot itself, and renders a large part of at least one hemisphere anæmic. If the blood finds its way into the ventricles, the conditions are most favorable for compressing nearly the whole brain. The anæmic appearance of the cerebral surface is often remarked at autopsies.
When an embolus lodges in an artery and produces complete occlusion, the portion of brain supplied thereby becomes at once entirely anæmic, since the arteries on the surface have so slight anastomoses that they are entirely unable to supply the deficiency, except to a slight extent around the edges of the vascular territory involved. The anæmia, however, does not extend beyond the territory originally affected, and consequently we may have extensive paralysis from embolism without a marked apoplectic attack. In extreme congestion of the brain the reverse may seem to be the case.
In reality, the hindrance to the proper functions is nearly the same, since blood which is not duly renovated and contains the products of metamorphosis of tissue in excess is worth as little for healthy nutrition as no blood at all. There is no reason to suppose that blood in circulation, no matter in how great quantity, gives rise to unconsciousness. It may cause over-action or disordered action, as in mania, but not arrest of action.
The narcotic poisons also deprive the nerve-tissue of its healthy food; whether by interference with oxygenation and depuration, or by a direct action of the substance itself on the nerve-cells, it is not easy to say. The fact that the completeness and duration of the unconsciousness are not in proportion to the paralysis or anæsthesia shows that they are to some extent independent of each other; and, although it is possible to locate with some precision the lesion which abolishes motor power and conscious sensation, yet we cannot say how much or what part of the brain must be deprived of its function in order to produce that cutting off of all conscious relation with the external world and reduction of a feeling, thinking, remembering, and acting organism to the level of a mere automatic breathing-machine, which we designate as loss of consciousness.
In fact, in the present state of our knowledge as to what consciousness is, any speculation as to its seat would be a waste of time, and we must content ourselves with recognizing that experience seems to show that a large part, rather than any particular part of the brain, must be involved, not necessarily in the primary lesion, but in the resulting pressure or anæmia.
Another theory of unconsciousness is simply that it is due to shock—that the sudden irruption of blood acts like a blow, as it were, and abolishes for a time the function of the nervous structure. This is substituting something indefinite for something comparatively definite; and it is certainly not true that the more sudden the shock the more complete the unconsciousness. It may come on after the paralysis is apparent, and in fact is more commonly gradual than sudden in its onset. The classical instantaneous shock is the rare exception. In the celebrated case where a tamping-iron was driven completely through a man's skull and brain, he himself was able to give a clear description of the accident to the surgeon who first attended him. Several other instances of severe and sudden injury to the brain without loss of consciousness have been recorded.
ETIOLOGY.—As regards the greater number of cases and the most common pathology, the existence of so specific and peculiar lesion as aneurism enables us to distinguish between predisposing and exciting causes, or, in other words, the conditions which lead to the localized periarteritis with its resulting aneurisms and those which cause their rupture. Unfortunately, the aneurisms are not usually looked for, and in the collection of statistics we are obliged to group together cases the pathology of which is not always the same, and which are usually collected under the name of apoplexy.
Age, however, is well known, both on clinical and anatomical grounds, to be the most important factor. Among the predisposing causes of apoplexy, all statistics, both of recent and older date, agree in assigning the period of life beyond forty-five or fifty as that in which the liability to apoplexy is greatly increased. There is no age, however, below this, even to infancy, in which true cerebral hemorrhage may not occur, although the intracranial hemorrhage of children is more usually meningeal. It is probable, however, that in many of these the rupture of the vessel does not depend upon a previous aneurism, but on other lesions. The youngest case in which aneurisms were found by Charcot and Bouchard was twenty.
If we speak of cerebral hemorrhage in general, without reference to the presence of aneurisms, as we unfortunately are obliged to do in the great majority of cases, we may often go much below this point. In youth and childhood, however, it is possible, and often almost proved, that other conditions must have been of greater importance in determining the hemorrhage than aneurism.
In our own small series we find cases of eighteen, twenty-three, twenty-five, twenty-six, twenty-seven years of age, and quite a number from thirty to forty-five. A little further examination shows many of them not to have been of the ordinary kind; thus the patient of eighteen had valvular disease of the heart and advanced parenchymatous nephritis; the one of twenty was, so far as could be seen, typical, but no search was made for aneurisms; that of twenty-five had many small hemorrhages and was a marked case of idiopathic anæmia; that of twenty-six had valvular disease of the heart, an embolus in the middle cerebral artery, which was not in the immediate neighborhood of any hemorrhage, several old hemorrhages, and hemorrhagic infarction in other organs. The case aged twenty-seven had a very large clot in one hemisphere and advanced interstitial nephritis.
Cayley11 describes the case of a girl of eleven with a large cavity in the left middle cerebral lobe, where nothing was discovered abnormal upon the left middle cerebral artery, but when the cerebral matter was washed away with a stream of water, the walls of the vessels were found to be dotted with oil-globules, and in several places studded with round and oval nuclei. This was before miliary aneurisms were known, but the process of preparation was exactly suited to bring them to light had they been present, and they could hardly have escaped observation and mention. Other cases of boys have been reported where the hemorrhage was of the typical kind.
11 Trans. Path. Soc., vol. xx.
Meigs and Pepper speak of nine cases of hemorrhage into the substance of the brain in children, but give none of their own. Of the two cases mentioned by West as coming within his own observation, in one the source of the blood was in the cerebral veins obstructed by the formation of clots in the longitudinal sinus.
C. W. Dulles12 describes a case occurring in his own practice in a child of six months, where a considerable amount of blood was found in the lateral, third, and fourth ventricles. Nothing is said of aneurisms in particular, but the brain was carefully examined without the source of the hemorrhage being found, although it seemed to be in some of the vessels of the velum interpositum. Dulles mentions further a case reported in the books of the Philadelphia Hospital by Joseph Berens, where in the brain of a child ten days old there were found, besides a large meningeal hemorrhage, many points of subarachnoid extravasation, a clot filling all the ventricles, and a clot the size of a pea in the anterior portion of both corpora striata. In addition to these there were scattered points of hemorrhage throughout the brain-substance.
12 Philada. Med. Times, vol. vi. p. 507.
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.
13 Results of Inquiries into Different Proportions of Deaths, etc.
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: 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 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.
Thackrah15 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.
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 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 pericranium16 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.
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.
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 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 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 Bourneville17 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.
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 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
18 Guy's Hosp. Rep., 1882.
FIG. 37.
The chart W. H. (Fig. 37) is from a man aged fifty who fell in the street while returning from work at noon, and whose axillary temperature was taken at 5 P.M. and every two hours thereafter until death. The hemiplegia was not very marked, but the hemorrhage was extensive, involving the pons and left crus cerebri, the external capsule, left crus cerebelli, and medulla, bursting through into the fourth ventricle.
FIG. 38.
The chart M. M. (Fig. 38), as taken from Bourneville, represents the course of the temperature in a rapid case: each perpendicular line denotes an hour.
The difference in the temperature of the two sides has been variously stated, and probably depends on a number of factors besides the length of time that has elapsed since the first attack. There is probably, however, a tendency to excess of heat on the paralyzed side soon after the attack, owing to vaso-motor paralysis; and this difference will be more marked in the hands than in the axillæ. After a length of time which may be from days to months the temperature becomes equalized, or more frequently the relation is reversed, the paralyzed side being colder as atrophy takes place. Lepine19 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 paralyzed side was six-tenths of a degree (Cent.) hotter than the other, in both being inferior to the rectal (107° Cent.).20
19 Mémoires de Société de Biol., 1867.
20 The chart in the original, and as reproduced by Bourneville, is wrongly lettered. The text says that the left side was the hotter.
FIG. 39.
The chart C. M. (Fig. 39) shows the excess of temperature in a case of meningeal hemorrhage. The dotted line is from the paralyzed side. The first observation was made two and a half hours after the attack.
A very interesting case is reported by Johnson21 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.
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 Ollivier23 in cerebral apoplexy, are probably to be referred to vaso-motor disturbances.
22 Med. Times and Gaz., Dec. 4, 1869.
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 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.
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.
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, 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, 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 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 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.
Bull25 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.
25 Am. Journ. Med. Sci., July, 1879.
In a case reported by Amidon26 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.
26 N. Y. Med. Rec., 1878, xiv. 13.
The highly interesting observation has been made by Lionville27 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.
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 Savage28 in a case which terminated soon after in apoplexy.
28 Journ. Ment. Sci., 1883, xxix. 90.
There are few symptoms which are more likely to excite alarm and apprehension of a stroke of paralysis than vertigo or attacks of dizziness, but it is too common under a great variety of circumstances to have much value, and is, as a matter of fact, rarely a distant precursor of intracranial hemorrhage, although it frequently appears among the almost initiatory symptoms, especially when the lesion is in the cerebellum, so that, if continuous, it is not likely to mean that anything worse is coming. It has been said to be strongly significant if occurring without the digestive derangements or circulatory disturbances likely to cause it, and be unconnected with disease of the ear. Unfortunately for diagnosis, but fortunately for the patients, the so-called vertigo a stomacho læso, may arise in cases where the stomach trouble is very difficult or impossible to detect, and it often continues for weeks or months after the most careful regulation of the diet, and yet is followed by no cerebral lesion. Although a vertigo for which every other cause can be excluded certainly justifies a suspicion of cerebral trouble, the tendency to exaggerate its prognostic importance should not be encouraged by the physician, as it may exist a long time, and disappear without another sign of the catastrophe which has been keeping the patient in dread.
Among the more significant and immediate symptoms are to be reckoned paræsthesiæ of the side about to be paralyzed, such as numbness or tickling. Headache of great severity is often, but not invariably, present. It has nothing characteristic about it, except that it may be different from those the patient has been in the habit of having, or may be of unusual severity, so that the patient says it is going to kill him. Such a headache in a person in whom there is good reason, from age, interstitial nephritis, or other symptoms, to suspect the existence of vascular lesions is likely to be an immediate precursor of a hemorrhage. Persistent early waking with a slight headache, which passes off soon after rising, is said by Thompson29 to be a somewhat frequent premonition. Vomiting is hardly a premonitory, but may be an initial, symptom, especially in hemorrhage of the cerebellum.
29 N. Y. Med. Record, 1878, ii. p. 381.
Reference is had in these statements chiefly to the ordinary form of cerebral hemorrhage. Of course if, during a leucocythæmia or purpura, large hemorrhages occur elsewhere, it may be taken as a hint that possibly the same thing may take place in the brain.
These signs of arterial disease must be considered as of the highest importance among the (possibly remoter) premonitory signs, not only of cerebral hemorrhage, but of the other lesions treated in this article. Atheroma and calcification of the tangible arteries place the existence of peri-endarteritis among the not remote possibilities. High arterial tension has already been spoken of in connection with etiology, and its presence should be sought for. An irregular and enfeebled cutaneous circulation has been spoken of as an indication of value.
OCCLUSION OF THE CEREBRAL ARTERIES may take place from several causes other than those which concern us here, as from the pressure of tumors or endarteritis, usually syphilitic. Thrombosis and embolism are grouped together from their great anatomical resemblance and their frequent coexistence, but the symptoms produced, although ultimately the same, are often different enough to make it necessary to bear in mind the fact that there is a distinction—that is, that embolism is rapid and thrombosis is slow.
A cerebral artery may be occluded from the presence of a plug of fibrin more or less intermixed with the other elements of the blood. This plug may have been formed in situ, and is then somewhat firmly attached to the walls of the vessel, and partly decolorized at its oldest portion, while on each side of it, but especially on the side away from the heart, it is prolonged by a looser and darker clot of more recent origin. This is a thrombus.
When the plug has been transported from elsewhere it is embolus.30 It may consist of various substances, as described in the article on General Pathology, but is usually of fibrin which has formed a thrombus or vegetation elsewhere, and, having been broken off, is carried by the blood until it comes to a place too narrow for it to pass, or where it lodges at the bifurcation of a vessel. The piece of fibrin thus lodged has a strong tendency to cause a still further deposition—that is, a secondary thrombus—which may progress until it comes to a place where the blood-current is too strong for the process to go on any farther. It may in such cases not be obvious at the first glance whether the whole process is thrombosis or whether it started from an embolus.
30 The Greek word εμβολος (εν, in, and βαλλω, to throw) signifies the beak or rostrum of a ship of war. Εμβολον signifies wedge or stopper, and would certainly seem the appropriate form to be adopted for anatomical purposes. As uniformity of nomenclature, however, seems more to be desired than etymological accuracy, the writer has conformed in this article to the general usage.
It is probable that a thrombus forming at one point in a cerebral vessel may break to pieces and its fragments be carried farther along, forming a number of small emboli. (See Capillary Embolism.) Embolism or thrombosis may take place anywhere in the brain or body generally, but has certain points of preference. Of these, the most usual in the brain is in the neighborhood where the internal carotid divides into the anterior and middle cerebral, or in either of these arteries, especially the middle, beyond this point. The plug may be situated in the carotid just before this point, or even as low down as its origin from the common trunk. Emboli lodge in this region, somewhat more often upon the left side. The brain is said to be third in the order of frequency with which the different organs are affected by embolism, the kidneys and spleen preceding it. It has been found that small emboli experimentally introduced into the carotids are found in much larger numbers in the middle cerebral than elsewhere. It is the largest branch, and most nearly in the direct line of the carotid. Position undoubtedly influences the point at which an embolus lodges, as it probably moves slowly along the vessels and along their lower side. It has been remarked that, on account of this course of the embolus, it is doubtful whether it can get into the carotid when the patient is standing, but it certainly can do so when he is sitting up; which, so far as the direction of the carotids is concerned, is the same thing. The frequency with which a hemiplegia is observed when a patient awakes in the morning may perhaps be accounted for by the position favoring the passage of an embolus into the carotid, which otherwise would reach organs more remote.
The vertebrals and basilar are not infrequently affected.
The sources whence cerebral emboli may spring are various, but cannot be found outside a certain range. They may, in the first place, be torn off from vegetations upon either the mitral or aortic valves; and this source is probably the most common. The appendix of the left auricle may furnish a plug from the thrombi formed among its trabeculæ, or the aorta from an aneurism or from parietal thrombi formed, upon spots roughened by atheroma. The pulmonary veins are occasionally the source of the embolus, though this is not very common.
It is rather doubtful whether an embolus can find its way from the systemic veins through the lungs to the brain, but it is possible that small emboli may do so, and increase in size from the addition of fresh fibrin when floating in the blood-current. The occurrence of pyæmic abscesses in the brain would suggest the possibility of this, though it is, on the other hand, possible that the brain abscesses are secondary to older ones in the lungs. In some cases, however, a careful examination does not disclose the source of the embolus.
In the blood-current the embolus may give rise to no symptoms whatever, and even after its arrival in the cerebral circulation it may lodge in such a way as not entirely to obstruct the current. In most instances, however, it does not stop until it plugs the vessel completely and arrests the current of blood beyond it for a moment. Whether it shall completely deprive the portion of brain to which it is distributed depends upon its situation as regards anastomoses and upon the formation of secondary thrombus. Hence the knowledge of the distribution of the arteries supplying the brain—that is, the two carotids and two vertebrals—is of more importance in reference to embolism and thrombosis than to cerebral hemorrhage, where the effusion takes place from quite small branches.
The anterior portion of the brain, including the anterior and posterior central convolutions and the first temporal, are supplied with blood by the two terminal branches of the internal carotid, the anterior and middle cerebral, the ganglia underlying these portions of the cortex being supplied, as already stated, by small branches arising near the origin of these two trunks, and principally the second. The anterior cerebrals of the two sides are connected by the anterior communicating, which is a short and usually wide vessel. Sometimes one anterior cerebral branches in the longitudinal fissure, and supplies a part of both sides. Hence in plugging of one internal carotid which does not reach its bifurcation a collateral supply may be received from the other side. If, however, an embolus or thrombus has penetrated beyond the origin of the middle cerebral, this vessel can no longer receive a supply from the anterior.
The posterior communicating arteries are two small vessels which connect on each side the posterior cerebrals and either the carotid, just as it gives off its two chief cerebral branches, or else the middle cerebral close to its origin. These arteries may be of quite unequal size, that upon the right usually being the larger, and sometimes so large as to give the appearance of being the principal origin of the posterior cerebral. When this happens the part of the posterior cerebral which arises from the basilar may be reduced to a minute arteriole, and the basilar, almost entire, goes to supply the left side of the brain. This condition of the posterior communicating may exist to some extent on both sides in the same brain. It is probable that in many cases these arteries are too small to be of great value in re-establishing the circulation in the anterior portion of the brain when it is suddenly interrupted by an embolus.
When the large trunks leave the circle of Willis to be distributed upon the surface of the brain, after giving off from the first centimeter or two of their course the nutrient arteries for the deep-seated ganglia, they break up into several branches which ramify upon the surface, but, as Duret has shown, undergo very few anastomoses. Instead of forming, as was once supposed, a richly inosculating network, small branches penetrate into the brain-substance perpendicularly from the superficial vessels, but these do not communicate freely with each other by vessels larger than capillaries.
From these anatomical conditions it happens that when a vascular territory is deprived of its normal supply by an embolus, it cannot be supplied with blood from surrounding districts. A certain limited amount of collateral supply is possible through the capillaries and the rare anastomoses, but it is only around the edges, and the centre of the territory becomes destitute of circulating blood. Thus an embolus does not in the brain produce, as it does in other organs with more abundant collateral supply, a large hemorrhagic infarction.
Small hemorrhages may, however, take place around the edges of the softening, and when a number of small emboli are present, so as to afford a number of overlapping areas with their borders of congestion, a red softening may be the result. When the emboli are very small, and at the same time not numerous enough to occlude all the ultimate ramifications of a trunk, the vascular compensation may be rapidly completed.
The change produced in the cerebral substance from cutting off its supply of blood is known as anæmic necrosis, and includes what has been known as white softening, with probably some yellow, and possibly a little red softening, the latter in case where simple softening has been complicated by hemorrhage.
When the circulation ceases the substance that should have been nourished loses its firmness and acquires a custard-like consistency. The gray and white substances are no longer so distinct in appearance, the latter losing its milky-white color, the whole surface of a section becoming of a dirty yellowish-white, somewhat shining, and looking as if it contained more moisture than normal. When a considerable portion of the interior of the hemisphere is thus affected, the brain outside, with its membranes, bags down, looks swollen, and feels to the fingers as if there were present a sacful of fluid. The boundaries of such an area of softening are marked off from the healthy substance with some distinctness, though less than that of a hemorrhage. There may be some hemorrhage around the edges or into the cavity, so that the presence of a little blood-pigment is no proof that the original lesion was not softening from occlusion. In the further progress the contents of the cavity become more fluid, and finally a somewhat distinct cyst is formed, not unlike that from a hemorrhage, with an internal areolar structure from the remains of connective tissue, and contents of a slightly yellowish or brownish color, or often of a chalky white. These cysts have little to distinguish them, when old, from similar ones left by hemorrhage, except the much greater amount of pigment in the latter. The smaller spots of softening may after a time lose their fluidity, and remain as yellowish patches as firm as, or firmer than, the surrounding brain. The region of the brain involved becomes atrophied, the convolutions shrink, and the membranes become filled with serous fluid, to compensate for the sinking of the surface.
The microscope shows gradually increasing fatty degeneration, disorganization of the nervous tissue, and degeneration of its elements. The pyramidal cells are sometimes distinctly recognizable by their form, and show gradual transition into the indeterminate round granulation-corpuscles. The vessels exhibit fatty degeneration of their coats, as well as accumulation of fatty granules between the vessel and the lymphatic sheath. The clot which blocks the artery becomes adherent to its walls, and the vessel with its contents forms a round solid cord.
In a few instances the thrombi have become perforated through the centre, so that a channel is formed for a renewal of the circulation. There is no reason to suppose that this takes place soon enough to be of any advantage in restoring the nutrition of the necrosed portions of brain.
The region involved in softening depends upon the artery which is plugged and the location of the obstructing body. The place of election seems to be the carotid near its separation into its large branches, or these branches after the separation, especially the middle cerebral, this being peculiarly liable because it is the largest branch and is the continuation in a direct line of the carotid. It is more frequent upon the left side. Cases have been observed where the whole of one hemisphere was softened from obstruction of the carotid at its bifurcation; which may be accounted for, as Charcot suggests, by an unusual distribution of the arteries, as described above, the posterior cerebral as well as the other two being derived almost entirely from the carotid. In a case recently observed by the writer the whole right cerebral hemisphere, with the exception of the tip of the frontal and tip of the occipital lobes, was softened to the consistency of custard, a thrombus extending from the bifurcation of the common carotid into all the ramifications of the middle cerebral. The most common form, however, is where more or less of the brain around the fissure of Rolando and fissure of Sylvius, with or without the underlying ganglia, is softened. This happens from a lodgment of the embolus in the middle cerebral. If the obstruction be close to the origin of the artery, the corpus striatum suffers, from the mouths of its small nutrient arteries arising in this part of its course being stopped, while if it have passed along a little farther, these remain open, and the cortex, to which the larger branches are distributed, alone is softened.
The anterior cerebral is not infrequently affected, either alone or with the middle, and in these arteries as well as the posterior the embolus, if of small size originally, may penetrate so far as to give rise only to quite a limited anæmia. The basilar is an artery not very rarely occluded, though more commonly by thrombus than embolus. This occlusion may be so limited as to affect only the nutrient arteries of the pons and cause a very limited softening, the parts before and behind it being supplied by the unobstructed portion or by collateral circulation from the carotids. Occlusion of the cerebellar arteries and softening of the cerebellum are among the rarer forms. The vertebrals themselves are sometimes plugged. A thrombosis has been observed in the only inferior cerebellar artery which existed, causing softening in both lobes. There was atheroma of the heart and arteries, and a thick calcareous plate in that which was occluded.31
31 Progrès méd., 1876, 373.
In a general way, it may be said, with many exceptions on both sides, that thrombosis and embolism tend to affect the cortex, and hemorrhage the central ganglia.
What has just been written applies to the simple mechanical action of emboli. If, however, they have a septic origin, as notably in cases of ulcerative endocarditis, the region in which they lodge becomes, instead of a simple spot of necrosis, a septic focus or abscess, with its results of compression or irritation. In such a case there are likely to be abscesses of similar origin in other organs, and the cerebral lesion is only a part of the general pyæmic condition.
ETIOLOGY.—So far as the lodgment of an embolus in an artery is concerned, it can hardly be said that there is any etiology, for the detachment of the plug from its place of origin is purely a matter of accident, and may take place at any time. As to its origin in the form of fibrinous deposit on the valves of the heart or a roughened spot on the aorta, we must refer to the article on General Pathology. The most important condition for embolism is disease of the valves of the heart, rheumatic or otherwise. Next comes arterial disease, producing roughening of the inner coat and subsequent deposition of fibrin. So far as we can tell, the causes leading to endarteritis or atheroma are essentially the same as those which produce the periarteritis described in connection with cerebral hemorrhage, and we may therefore put down old age, alcohol, and strain as among the causes of cerebral embolism. Injuries of the lungs leading to thrombosis of the veins may be considered as possible sources for the formation of an embolus, and we might suppose that phthisis and pneumonia would furnish plugs which would lodge in the brain, though as a matter of fact they seldom do so.
Experience shows that embolism, unlike hemorrhage, is not specially a disease of advanced life, but is distributed over different periods, with preference for old age less marked than with hemorrhage. Andral gives the ages of patients with softening—which, however, includes thrombosis as well as embolism—as follows: the average would undoubtedly be displaced in the direction of youth if thrombosis could be taken out of the list:
| Andral: Beginning of softening in 27 cases. | Andral: Death with softening in 153 cases. | Cases (with autopsies) of embolism, thrombosis, and softening—25 cases. |
| 17–20 4 27 2 30–37 2 43–45 2 53–59 4 63–69 7 76–78 6 | 15–20 10 20–30 18 30–40 11 40–50 19 50–60 27 60–70 34 70–80 30 80–89 4 | 20–30 4 30–40 3 40–50 3 50–60 1 60–70 5 70–80 2 Young 1 Middle-aged 1 Old 5 |
In the etiology of cerebral arterial thrombus there seem to be two factors of prime importance, although there are cases which seem to demand a third, and Charcot32 suggests the possibility of some hæmic dyscrasia favoring the formation of a thrombus, and relates a case of thrombosis of the middle cerebral, with three others of the same process in other arteries, occurring in patients with uterine cancer, where all the usual sources of emboli were explored with negative results. The first of the two is disease of the cerebral arteries, not necessarily extensive, but sufficient to form a starting-point on the inner wall for the deposit of fibrin. In this respect the etiology of thrombosis may be various. Syphilitic endarteritis, for instance, may very easily give rise to this lesion, but it is likely to be accompanied by others, and has a symptomatology more or less peculiar to itself. It is not, of course, to be included with the form we are considering.
32 Comptes Rendus Soc. de Biol., 1865, p. 24.
The second factor—one which is perhaps capable of giving rise to coagulation of the blood or deposit of fibrin without any arterial disease—is weakness of the heart, connected or not with anæmia. The causes of this condition may be manifold, and are likely to lead to many other consequences than cerebral thrombosis. A thrombus may form upon a very small basis of atheroma. Several of these points are illustrated in the following case: A lady, aged about sixty-five, had had for many months vague symptoms of want of strength, fatigue, want of appetite, and so on, with complaints of distress and fulness in the abdomen, for which no special cause could be found. On one occasion she was unusually long in dressing, and her expression was noticed to be changed and her voice altered for a few moments. The pulse was habitually 60 or less, and at times irregular, but nothing abnormal could be detected in the sounds or position of the heart. Fatty degeneration was suspected. One morning, after going to bed in her usual health, she was found on the floor of her room unconscious and with left hemiplegia. She lived about thirty-six hours. The autopsy showed nothing abnormal in the abdomen except a considerable accumulation of fat; and in the thorax the heart appeared normal, and was not fatty. There was very little atheroma. In the end of the internal carotid artery was a thrombus, of which the lower and firmest part was connected with a very small spot of roughening just at the point where the artery comes through the base of the skull. It extended just beyond the origin of the middle cerebral artery, which was of course occluded. The corresponding region of the brain was converted into a vast mass of softened tissue.
The SYMPTOMS of the lodgment of an embolus in the brain may closely resemble, or even be precisely the same as, those of hemorrhage. Unless, however, an embolus makes a pause on its journey, giving rise to a partial obstruction before there is a complete one, or unless the obstruction is not absolute until after the formation of a secondary thrombus, the attack may be absolutely sudden.
A thrombus, however, is slower in its formation, and may produce gradually increasing anæmia of the region of brain supplied before it is absolutely complete, with a gradually increasing paralysis and loss of consciousness slowly approaching. Thus we may have the early symptoms in the form of headache, vertigo, heaviness, and drowsiness, peculiar sensations in the limbs about to be paralyzed or in the head, delirium of various kinds, or hysterical manifestations. Prévost and Cotard33 lay special stress upon the importance of severe vertigo (étourdissement) as a prodrome or warning of softening, especially in the aged. It is dependent upon anæmia of the brain, and this, in its turn, upon atheroma of the arteries, and sometimes at least upon feebleness of the circulation, both of these being conditions likely to cause the deposit of a thrombus. As, however, the thrombus does not necessarily result from these conditions, and as the vertigo may arise from other sources, as stated under the head of Cerebral Hemorrhage, it is to be looked upon with special suspicion chiefly in those cases where other symptoms might lead in the same direction, and when other causes can be excluded.
33 Mémoires de la Soc. de Biol., 1865, p. 171.
The same authors also speak of less defined symptoms, like delirium and stupor, occurring among the inhabitants of the Salpêtrière (old women), with intervals of comparative health, as being premonitory.
It is possible, however, for the symptoms of thrombus to be developed rapidly when, as in the case last described, the thrombus begins to form in a place which does not entirely interrupt the current, but afterward reached the mouth of a large vessel, which it closes.
The loss of consciousness, coma, and all the phenomena of the apoplectic attack, with the possible exception of early rigidity, may be as fully developed from occlusion of the cerebral vessels as from their rupture; but it must be said that it is more common to meet with them in cases of large hemorrhage than with either embolism or thrombosis.
The general functions are even less disturbed than with a hemorrhage producing an equal extent of paralysis. The temperature follows nearly the same course as in hemorrhage, except that the initial fall, if present—which is not always the case—is said to be less than with cerebral hemorrhage. To this succeeds a rapid rise, which, even in cases which are to terminate fatally, gives place to a fall to the neighborhood of normal, and another rise before death. These are the statements of Bourneville. The rise is said not to be so high as with hemorrhage.
The annexed chart is from a man (W. I. W.) who was in the hospital with ill-defined nervous symptoms, and was suddenly attacked with convulsions, vomiting, and unconsciousness. He had a small tumor at the point of the right temporal lobe, and softening of the left corpus striatum. The apoplectic symptoms occurred on the 15th—that is, as will be seen by the chart, one day after the temperature began to rise. The pulse and respiration show no characteristic changes.
FIG. 40.
It is much more common for the embolus or thrombus to give rise to a set of symptoms less severe than a fully-developed apoplectic fit. During such a fit—or, more clearly, as it is passing off—we find more or less marked paralytic symptoms, but these are quite as frequently present without the loss of consciousness. The patient states that he waked up and found one side of his body helpless, or that he was reading the paper when it fell from his hand, and upon trying to walk found that he could not do so. Loss of speech may be an initial symptom. It has been spoken of as premonitory, but it is probable that it is in reality only the beginning, which, in some cases may go no farther, but is usually succeeded by more extensive paralysis, which makes its meaning unmistakable. These symptoms may be hours or even days in developing, with occlusion as well as with hemorrhage. Very slight attacks may occur which hardly excite attention, and lesions are found after death in many cases to which there is nothing in the history to correspond.
Improvement may begin very rapidly in some cases where the lesion is small, a sufficient amount of collateral circulation being developed to prevent the structure from being disorganized. In others a specially favorable anastomosis may preserve even a larger area, but in others still it is not easy to account on entirely anatomical grounds for the amount of improvement which takes place.
From this point onward the history of hemorrhagic and of embolic and thrombotic paralysis is essentially the same, and the description of the principal phenomena and progress of hemiplegia will apply to all.
SYMPTOMS AND PROGRESS OF HEMIPLEGIA DEPENDING ON CEREBRAL HEMORRHAGE OR OCCLUSION OF THE CEREBRAL VESSELS.—The cerebral cortex represents the centres for many of the higher nervous functions, spread out in such a way that they may be more or less separately affected, while the corpora striata and internal capsules are the regions where the various conductors are crowded together, so that embolism, when affecting small vessels and limited areas of the cortex, more frequently gives rise to narrowly-defined groups of symptoms than hemorrhage, which, taking place oftener in the central ganglia, is able to cut off the communication from large masses of cerebral tissue at once. This is a general remark, tending to explain why aphasia, for instance, is often spoken of as especially a symptom of embolism, while it is in reality common to all the lesions that affect the proper locality.
The motor paralysis, more or less complete, which has been described under the head of Hemorrhage continues indefinitely. It may disappear rapidly, so that motion begins to return in a day or two, and goes on to complete recovery in a short time. On the other hand, it may be months before the flexion of a finger or a toe gives the slightest token of the will resuming its control. The face often recovers its symmetry before the limbs are fully restored, but the leg may be used in locomotion before the complete recovery from paralysis, since the tone of the muscles is sufficient to keep the knee straight enough for support, as if the leg were all in one piece, while it is swung around at each step by the pelvic muscles. We may meet with all degrees of recovery—from that which is absolutely complete and comparatively rare, through the case where a little want of play upon one side of the face, a little thickness of speech, a feeble or awkward grasp of the hand, betrays what has happened, or that of the man so often seen in the streets with a mournful or stolid face, the arm in a sling or dangling straight down by the side, and swinging one leg awkwardly around, to the helpless paralytic lifted in and out of his chair or lying almost motionless in bed, and living only to be fed and be kept clean.
Involuntary movements may take place in limbs entirely incapable of voluntary ones, and may occur under conditions of excitement or with other involuntary movements, such as gaping. On the other hand, the patient often moves the well hand while making utterly ineffectual attempts on the paralyzed side. Involuntary twitching of the feet may be annoying. Reflex movements, especially of the feet, are often exaggerated, and in fact the twitching just spoken of is often excited by some trifling, perhaps unperceived, irritation. A touch with the point of a penknife upon the sole of the foot may call out a movement which the patient is utterly incapable of executing by the force of the will, and the appearance of volition is often increased by the grimace or exclamation of pain or annoyance.
Epileptiform attacks may be a sequence of hemiplegia, occurring at irregular intervals, and not of great severity. Sometimes the patient seems depressed or less talkative for a day or two previously, and relieved after the fit has occurred, as in true epilepsy.
Comparatively little attention has been given to the condition of sensation in hemiplegia. In the more complete apoplectic stupor it is apparently abolished, like nearly all the functions above those of respiration and circulation, but it often happens when the patient is unable or unwilling to make any voluntary response to the voice, and lies apparently perfectly indifferent, that any moderate irritation like a pinch will bring out evidence of sensation. It is often stated that in hemiplegia the sensation is not at all affected; and this is probably true of many cases, but a more attentive examination will often disclose a decided diminution on the affected side. Broadbent, who has tested with pricking, touch, the compasses, and hot substances, says that it is frequently diminished, and often greatly so, and not only in the limbs, but in the face, chest, and abdomen. Tripier34 says that a lesion of the larger part of the fronto-parietal region determines at the same time a paralysis of motion and a diminution of sensibility; and one may conclude that this region holds under its dependence sensitive as well as motor phenomena intimately connected with each other. The zone called motor, of which the limits are difficult to fix, may with more reason be called sensori-motor.
34 Revue mensuelle de Méd. et Chir., 1880, p. 18.
Anæsthesia probably in most instances disappears more rapidly than motor paralysis, which accounts for its being frequently overlooked. The more common location of lesions causing motor paralysis—i.e. the corpus striatum and the motor portion of the cortex—is one not likely, unless extensive, to concern sensation; but there are cases where a very complete hemianæsthesia, including the special senses, may be found; and when, in such cases, the motor paralysis is slight, a picture is presented almost identical with that of hysterical hemianæsthesia with great diminution or abolition of the special senses, hearing, taste, smell, with concentric diminution of the field of vision and of the color-field, or complete color-blindness on the affected side.
A man aged thirty-five while at work suddenly felt a prickling sensation upon his left side, and became unconscious. The bystanders say he was convulsed. On returning to consciousness after three hours he had lost his speech, which, however, was rapidly recovered, and his left side was not so strong as his right, though there was no distinct history of paralysis. Two or three days afterward it was noticed that sensation was much diminished upon the left side, two sharp points of the æsthesiometer being felt as one at two inches on the forearm and three-quarters of an inch on the tongue. He could feel the touch of a spoon, but could not tell whether it was cold or hot. Odors were not recognized upon the left side of the nose, except faintly ammonia and chloroform, and a watch was heard on that side only when in contact with the ear. The field of vision was much diminished and color-blindness was almost complete. A few days later the field of vision had increased, and there was color-sense, the field of perception for the different colors being arranged almost exactly as laid down by Charcot, vision for red being largest, but not so large as for simple perception of objects; those for blue, green, and yellow nearly the same and smaller; and that for violet limited to a small space in the centre of the field.
Less regular forms of anæsthesia may be met with, as well as hyperæsthesia. These are said to be especially connected with various lesions of the pons.35 A case is recorded36 of complete hemianæsthesia in a man, coming on like a blow. There was no loss of motor power; the face was symmetrical, sight and hearing unimpaired. Taste was lost and smell doubtful. There was aortic and mitral disease. Hughlings-Jackson speaks of a man who experienced a severe apoplectiform attack which it was thought would be fatal in a few hours. He recovered, however, with almost complete loss of hearing.
35 Conty, Centralblatt f. d. Med. Wiss., 1878, 571.
36 Med. Times and Gaz., 1871, i. 246.
Neuralgic pains of long continuance are not infrequent accompaniments of hemiplegia, and may be lasting even after nearly complete recovery from the paralysis. A peculiar restlessness, a constant desire for change of position, has been referred to derangement of the muscle-sense. It is sometimes very distressing, and causes much annoyance to attendants as well as to the sufferer, as the patient is no sooner placed in one position, no matter how comfortable, than he desires to change it.
The mental condition seldom fails to suffer more or less in cases of hemiplegia, but the limits are very wide between a slight emotional excitability on the one hand and almost dementia on the other. This is, of course, applicable to cases where the lesion is a single or limited one, and not where a hemorrhage or thrombus is merely a part of a general vascular degenerative change with chronic meningitis or atrophy of the brain, where the mental decay can hardly be called the result of any single lesion. In cases of aphasia the mental condition is harder to make out, from the peculiar inability to communicate ideas if present. It is very safe to say, however, that many such patients possess much greater intelligence than would appear to a casual observer, and yet the apathy with which they often bear the deprivation of speech and consequent isolation speaks more strongly in favor of some blunting of the perceptions than of Christian resignation. A patient whose general appearance is that of tolerable comfort is likely to cry when attention is called to the helpless condition of the hand. It is probable that memory suffers in such cases, if not the reasoning faculties.
Trousseau cites the case of Lordat, who became aphasic, and after recovery described his own case. The learned professor claims to have been in full possession of his faculties, and to have arranged a lecture with the divisions and subdivisions of the subject, and all this without the thought of a single word passing through his mind. Trousseau ventures to doubt the possibility of carrying on complicated mental processes without words, and thinks Lordat may have overestimated the precision of his mental processes. It appears in confirmation of this view that after his attack he always read his lectures, whereas before he had been distinguished as an extempore speaker.
McCready, in an excellent article in the New York Journal of Medicine (September, 1857), discusses this subject at length, and details a number of cases where it was evident that paralytics and aphasics (who, however, he did not know by that name, nor the special lesion connected with their condition) possessed not only ordinary intelligence, but excellent business judgment and ability. He says that the confusion of mind and difficulty in pursuing a train of thought of which apoplectics are apt to complain is, to a great extent, the mere result of diminished nervous energy—that they comprehend well and judge correctly. It is fair to say that while the mind is almost certainly impaired, it is not necessarily in exact proportion to the severity of other symptoms, aphasia included. The memory, either special or general, is most apt to be impaired.
The testamentary capacity of a person who has had an apoplectic fit or who is paralyzed at the time of making a will may be called in question. The only general remark to be made is that these facts alone are not sufficient to prove incapacity; neither should the presence of aphasia or agraphia do so without further evidence of want of comprehension of the meaning of language used by others; so that if, for instance, a person were seized with hemiplegia and aphasia between the drawing up of a will and its signature, it should not be invalidated unless there be further evidence to show that the testator was incapable of understanding it when read over to him. In cases of word-blindness, a patient, like one described by Magnan, may be able to draw up a will with full comprehension of what he is doing, and yet be unable to read it understandingly. Inability to signify intelligibly assent or dissent would, of course, entirely disqualify one from signing a will.
It is seldom that a paralytic attack fails to leave its mark, though perhaps slight, for years, if not for the remainder of life. An extreme ease of shedding tears is a very common symptom, and sometimes laughter comes on very slight provocation.
Among the most interesting groups of phenomena connected with hemiplegia, and sometimes the sole representative of this condition—that is, existing alone without any motor paralysis—is that embracing the means of communicating with the outer world by means of language spoken or written. Corresponding to, and usually but not always connected with, right motor paralysis we have the inability to use words in speaking, known as aphasia, aphemia, alalia, and others. The first of these names is the one most frequently used. Agraphia is the inability to use words in writing.
On the receptive side we have the inability to understand language as presented to the eye (word- or psychic blindness) or to the ear (word- or psychic deafness). A case of the former condition has already been spoken of. One still more singular was reported by Mdlle. Skwortzoff,37 where the patient, not being blind, could not understand letters presented to the eye, but could read with the fingers and understand raised letters like those used by the blind. In a case of the latter kind a man whose ears were normal, and who could distinguish different sounds, answered questions, but entirely at random, though he could read and understand what was written. All these defects are manifestly connected with a peculiar loss of memory, and hence the word amnesia is used sometimes to cover part of the group, and amnesic as an adjective to qualify aphasia.
37 Comptes Rendus de la Société de Biologie, 1883, p. 319.
It should, of course, be understood that the muscles are not paralyzed, so that glottis, lips, tongue, and fingers are capable of making the necessary movements to produce words, and, on the other hand, that the senses of sight and hearing are intact. Aphasia was confounded by some of the older writers with paralysis of these organs, and the whole grouped together under the name of alalia. Even now the distinction is not always clearly observed.
The act of speaking, according to Kussmaul,38 consists in three stages or processes: the preparation in the intelligence and feelings of the matter to be uttered; the diction, or the formation of the words internally, together with their syntax; the articulation, or formation of words outwardly, irrespective of their connection with one another in the matter spoken. Defects in the first condition have already been spoken of. In the entire absence of mind, as in the deepest apoplexy, aphasia can hardly be said to exist, and it is only later that it becomes manifest. If the second stage is defective, amnesic aphasia exists, and if the third, ataxic. In the great majority of cases of aphasia the loss of memory is the most important factor; and as this exists whatever be the mode in which it is desired to express the idea, amnesic aphasia is accompanied by agraphia. In those cases, however, in which the patient retains a few words, they are not always the same for speech and writing. Occasionally an instance is found where a person can write perfectly well and possesses complete intelligence, but is unable to speak a word. This is pure ataxic aphasia, and is certainly rare. An ataxic agraphia is less easy to detect, since the aphasic patient is likely to be paralyzed upon the right side, and thus unable to write, even if he remembers the words, until educated upon the left side.
38 Ziemssen's Cyclopædia.
There are many degrees and kinds of amnesic aphasia, and, in fact, every case is a study by itself. The slightest might be called physiological; at any rate, it is sufficiently common among people supposed to be well, and consists in the failure to recollect in time for use the name, most frequently of a person, but sometimes of a thing, which is really well known, is recognized at once if suggested, and perhaps returns spontaneously at a later period. Another person may forget only some words which are not recalled at any time, or parts of words. A man appeared among the out-patients at St. Bartholomew's Hospital who had his name written on a piece of paper, because he could not say it, but could carry on a long conversation. There were a few other words he could not say. The more complete cases have no vocabulary at all, or only a few words or syllables applied to all purposes, and perhaps an exclamation or two. In these cases the patient may know perfectly well that he is not expressing his ideas, and he may recognize perfectly well the word when it is told to him or reject a wrong one. If he be, as happens in nearly all cases, unable to pronounce the word after he has recognized it as the one he wished for, there is a combination of ataxic and amnesic aphasia. Incorrect or deficient words may be corrected or supplemented by gestures or intonation. “Yes” may do duty without confusion for “yes” or “no,” according to the tone.
Oaths may be retained, and sometimes an exclamation may be uttered with perfect propriety of application which cannot be repeated deliberately a moment afterward. This emotional use of words may be considered akin to the movement executed by paralyzed limbs under the stimulus of a movement taking place elsewhere, and may lead to an erroneous prognosis of recovery. This curious fact, that more or less automatic expressions are possible when deliberately-willed pronunciation is not, is a probable explanation for the observation which has occasionally been made that an aphasic patient is able to sing words which he cannot speak.
Paraphasia is the use of the wrong words, or of phrases which carry an entirely different meaning from that intended, as when Trousseau's patient receives a guest with politeness and invites her to be seated with the words “cochon, animal, fichue bête,” or an old paralytic, when a lady declines to drive with him, answers with great suavity, “It don't make any damnation to me whether you go or not.”
Word-blindness is more common than word-deafness, and is a frequent accompaniment of aphasia. Rostan, the well-known author of the work on softening of the brain, experienced an attack of aphasia lasting a few hours. The symptom which first attracted his attention was the inability to understand the book, by no means abstruse, which he was reading. He was, however, able carefully to observe his own symptoms, and made signs to be bled, which operation was followed by relief.
Gouty aphasia has been described in a man aged thirty-seven who on several occasions became aphasic, with recovery in a short time. This condition was connected with localized paralysis, and once with entire right hemiplegia. Afterward it was accompanied by convulsions. In the intervals the patient was in fair health.39 It is difficult to imagine the lesion in this case. The reporter speaks of “sudden blocking by a gouty thrombus,” but nothing is known of any thrombus which can disappear so rapidly. Ball40 describes twelve attacks of aphasia occurring within nine months, and accompanied by slight paresis and convulsive movements in the right hand. The patient suffered habitually from migraine. He supposes the cause to have been a temporary anæmia.
39 Brit. Med. Journ., Aug. 28, 1880.
40 L'Encephale, 1883, 2.
Aphasia may be entirely unconnected with motor paralysis, and is then likely to be of shorter duration, though just as complete. Most of these cases probably do not depend upon a lesion of the same kind as when aphasia is only one of several severe symptoms. It shows how delicate a function of the brain memory for words may be, and is possibly the result of a temporary malnutrition or a change in the vascular supply. It has been observed in various conditions of debility and after acute disease. Rostan was diabetic. It has been seen after chloroform narcosis, after santonin (5 cgr.), after fright, and is said to be one of the ordinary symptoms after the bite of venomous serpents. Aphasia and paraphasia may be met with in thorough bromization, and, naturally enough, may be part of the symptomatology of general paralysis. In other cases, even when it is the principal symptom, it depends upon an organic lesion, and is not infrequently the precursor of a more fully-developed attack. The diagnosis is of great importance, and other traces of paralysis should be carefully sought for. This symptom is far more common with occlusion of the vessels than with hemorrhage, though not unknown with the latter.41
41 Lancet, Oct. 11, 1884, p. 655.
By far the most common situation of the softening or hemorrhage which gives rise to aphasia is in the third left frontal convolution (convolution of Broca) or the white substance immediately underlying it. The island of Reil may be involved in some cases where but little damage is done to the third frontal.
In a respectable minority of cases aphasia may be associated with left hemiplegia. A case where a tumor in the third right frontal convolution was found in a case of aphasia is reported by Habershon.42 It is not stated whether the patient was left-handed. Some of these cases constitute those exceptions which prove the rule, inasmuch as the patient is left-handed, and Hughlings-Jackson has shown that the relationship of aphasia to the side which is congenitally pre-eminent, and which is in the vast majority of human beings the right side, is not destroyed by a partial education of the other side to such acts as writing or using a knife.
42 Med. Times and Gaz., 1881, i.
A lesion in the pons may give rise to aphasia or something closely resembling it, but it is probable that a careful distinction of true aphasia, both amnesic and aphasic, from paralysis or inco-ordination of the muscles of speech, would reduce the number of these cases, and bring the symptom into closer relations with the usual cortical lesions.
A case of congenital aphasia with right hemiplegia has been described.43 When six years old the boy was well developed, though less so on the paralyzed side; intelligent; heard well, but could say only a few words, and those badly. Whatever the lesion, which is thought by the author to have been in the speech-centre, but which may not improbably have been in the pons, it is interesting, as showing that the development of the speech-centre is certainly not accomplished by education.
43 Centralblatt f. d. Med. Wiss., 1873, p. 299.
Post-paralytic chorea is an affection the nature of which is indicated by its name. As the hemiplegia disappears, irregular movements are developed in the paralyzed limbs, sometimes closely resembling ordinary chorea, and at others consisting of irregular movements, as closing and spreading of the fingers, with curious and bizarre stiffenings, extensions, and contractions, sometimes known as athetosis, or in others still a tremor resembling paralysis agitans. These usually cease during sleep. It is very apt to be associated with hemianæsthesia more or less complete, though this may be represented by only a certain amount of numbness. A hemiathetosis has been observed to be gradually developed from a post-hemiplegic hemichorea of the more ordinary form.44
44 Archiv für Psychiatrie, xii. 516.
This affection is not a common one, and Weir Mitchell states that it is common in inverse proportion to the age. He thinks it possible that some of the congenital choreas may be the result of, or at least closely connected with, intra-uterine cerebral paralysis. It remains for years or for life. In the absence of history such a case might present difficulties of diagnosis from the more usual hemichorea, which is not infrequently accompanied by considerable weakness of the affected side.
The temperature in the early days of both hemorrhage and embolism has been described. At a later period of the hemiplegia it remains in the neighborhood of normal. The temperature of the affected side is often higher than that of the sound one for an indefinite period, but in many cases sinks below if atrophy takes place. The time at which the change occurs is extremely variable. Out of ten cases reported by Folet,45 in two of them for three years and one year after the attack the paralyzed side was eight-tenths and six-tenths of a degree respectively the warmer. In three others, of twenty months, four and six years, it was the same on both sides, and in the remaining five the paralyzed limb was a little the cooler. In the last eight there was more or less atrophy.
45 Gaz. hébd., 1867.
The coincidence of rise of temperature with vascular relaxation has already been noted under the head of Cerebral Hemorrhage. It is not difficult to explain why a vascular paralysis in a comparatively well-nourished limb, especially when the heart is vigorous, may, by allowing a larger amount of warm blood to circulate, raise the temperature, when the same paralysis with atrophied muscles, weak heart, and impaired general health, merely furnishes a larger reservoir in which the slowly-moving blood may be cooled. The accompanying charts represent the difference of temperature between the two sides in two cases of hemiplegia, the first, O. G. T. (Fig. 41), from embolism, and the second, J. B. (Fig. 42), from hemorrhage, the observation being made within two or three weeks of the attack. The dotted line is from the paralyzed side. A subjective feeling of coldness is not uncommon in paralyzed limbs.
FIG. 41.
FIG. 42.
The modifications undergone by the urine in a case of cerebral hemorrhage are increase of quantity amounting to polyuria, the urine becoming limpid and afterward returning to the usual color; a diminution in the quantity of urea coinciding with the fall of temperature, and afterward a return to the normal or even above it. When this augmentation is considerable, it constitutes at the same time with a marked elevation of temperature an unfavorable prognostic sign.46 In a case under the observation of the writer, probably of thrombosis, the acid urine has been remarkable for the amount of mucus contained in it, so that it pours from one vessel to another like white of egg. There is a small amount of pus, but no vesical irritation whatever.
46 Ollivier, Archives de Physiol., 1876.
Since the trophic centres for the muscles are situated in the spinal cord, cerebral hemiplegia, which does not cut off their connection, does not produce the rapid wasting seen in some cases of spinal paralysis, unless descending degeneration involves the anterior gray columns. The limbs preserve their fulness for a time, although the muscular masses become flabby and slowly atrophy for want of use. This atrophy, however, seldom becomes extreme. The skin of the hands becomes dry, the folds at the knuckles disappear, and the hand loses its expression, looking more like a stuffed glove. The change, however, is not much greater than may be seen in a hand kept for a long time in a bandage. The growth of the nails is retarded, as may be seen by staining them with nitric acid.
If there is any tendency to œdema, as when nephritis is complicated with hemiplegia, the swelling is likely to be much greater upon the paralyzed side. In the adult, of course, there can be no question of the growth of limbs, but when a child becomes hemiplegic from cerebral disease, the limbs grow more slowly and remain smaller, as in a case of ordinary infantile palsy or anterior poliomyelitis.
Much importance has been attached to the fact that large sloughs form with great rapidity upon the nates of the paralyzed side, and Charcot says that this tendency is greater than can be accounted for in any mechanical way. He therefore thinks that a direct trophic influence of the brain upon nutrition is shown. At the very most, however, that can only be a contributory cause, and the freedom of other portions from a similar condition—and that, too, in regions farther removed from the centres of circulation—makes it highly improbable that anything more is necessary to account for it than the less sensitiveness of that side to irritation from urine, roughnesses in the bed, or pressure, and hence neglect. The writer, among a very considerable number of hemiplegias, fatal and otherwise, does not remember to have seen a well-marked case of the kind. Scrupulous cleanliness and changing the position sufficiently often make the preference for the paralyzed side a very slight one.
Arthropathies, consisting in a vegetating, and sometimes an exudative, synovitis, and accompanied by swelling, redness, and pain, are sometimes observed, especially in the upper extremity. They do not appear until fifteen days or a month after the attack.
The most significant change which occurs in the course of a hemiplegia is the development of increased reflexes and rigidity and contracture. After some weeks or months, during which the aspect of the case has not essentially changed, the limbs remaining in the same condition, it will be found on examination that the patellar reflex has become quite energetic, and ankle clonus developed upon the paralyzed side; the arm reflexes from the triceps, biceps, and supinator longus are much exaggerated. This has the same meaning as when similar phenomena are found with spinal disease, and signifies descending degeneration of the postero-lateral columns of the spinal cord, the crossed peduncular tracts. This degeneration may sometimes be traced completely down from the situation of the lesion in the cortical motor centres through the basal ganglia, crura, decussation, and cord. The fuller development of this condition is the contracture or rigidity, which was at one time referred to secondary changes taking place in the neighborhood of the original lesion, as well as to a purely reflex action having no relation to the degeneration of the cord.
The arms are usually flexed at the elbow, the wrists on the arm, and the fingers in the hand. Sometimes, however, the arm is straight. The leg, which is not always affected to the same extent, is generally in extension, though the toes are likely to be flexed. Attempts to move the limbs are resisted strongly, and in such a way as to show the reflex nature of the phenomenon. If an attempt be made to open the fingers of a contractured hand slowly and carefully, it can be often accomplished and the hand held open with but little pressure, but if it is twitched the fingers resist like a spring. The violent attempt to overcome rigidity is often painful.
In some rare cases rapid atrophy of the muscles of one limb may take place. This has been found to coincide with extension of degenerative changes in the cord to the anterior gray columns.
Late rigidity is an unfortunately clear symptom. There is little if any hope of complete recovery of the use of the limb after it has made its appearance, though it does not prevent walking. After long-continued contracture the activity of the muscles diminishes, but the increase of connective tissue and changes in the joints hold the limb in its fixed position, and the contracture is a more passive one. The electrical reactions of the muscles and their nerves in cerebral hemiplegia are not materially altered, but the neuro-muscular irritability may be somewhat increased for a time by the irritating influence of the cerebral lesion.
In most cases of flaccid cerebral hemiplegia the electrical irritability is somewhat decreased, though retaining the normal character with both currents. Since the muscles and their nerves retain their connection with the spinal nuclei which are their trophic centres, and these nuclei are uninjured, their nutrition does not undergo the changes which affect electric excitability.
When descending degeneration takes place there may be found, coinciding with increased reflex activity and contracture, increased sensitiveness to the electric currents. If the degeneration extend to the anterior columns, as happens in rare cases, the muscles waste rapidly and exhibit the reactions of anterior poliomyelitis—i.e. degenerative.
What has just been said applies to the muscles paralyzed by a central lesion. If, however, with or without a complete hemiplegia, a limited lesion, as in the pons, affects the nucleus of a nerve, the peripheral distribution of that nerve is cut off from its nutritive centre, and it undergoes the usual changes which lead to the reaction of degeneration, so that, in some unusual forms of paralysis, the two kinds of reaction, normal and degenerative, may be present in different sets of muscles.
DIAGNOSIS.—The apoplectiform attack due to hemorrhage or occlusion of the cerebral arteries is to be distinguished from narcotic poisoning, specially by opium or alcohol, or by coal gas; epilepsy with its succeeding coma; uræmia (so called) or cerebral symptoms connected with renal disease; comatose form of pernicious intermittent; diabetic coma; sunstroke; hysteria, and various other forms of intracranial disease, especially meningitis; concussion and compression of the brain, which often involve hemorrhage; the apoplectiform attacks of intracranial syphilis and of general paralysis, as well as the congestive attacks (coup de sang, rush of blood to the head).
The first of these distinctions is, in a practical point of view, among the most important and often the most difficult, so that distinguished authorities insist not only on the difficulty, but impossibility, of making a positive diagnosis in every case. The physician who is most familiar with all the different conditions which may cause coma is least likely to jump at a conclusion.
Persons are constantly being picked up in the street partially or wholly unconscious, or found alone in a room without history and away from friends. The physician must then form his opinion from the present condition, which without a history may be very obscure, though with one it might present no difficulty. An empty laudanum- or whiskey-bottle may be of assistance, the former of much, but the latter of less. The smell of the breath may give a hint, but even if the smell of alcohol be detected, considering the widespread belief in its virtues as a panacea, it may be as well the result of amateur therapeutic attempts as an indication of the cause of the attack. Neither does it follow that because a man has been or is drunk he has no organic disease in his brain. Alcohol should simply make us more careful to examine for possible injuries. In regard to both these poisons—and in fact in the diagnosis of these conditions generally—the first thing to be sought for, after assuring one's self that the patient can breathe and is likely to do so for a few minutes, is some evidence of hemiplegia. This is not so easy as it might appear at first sight, since the general muscular relaxation may be so complete as to cover up local manifestations. The face, however, may show inequality in its lines or one cheek flap more loosely than the other. The patient is not likely to undertake voluntary movements at the request of the physician, but he may make semi-voluntary ones if annoyed by the examination. The flaccidity of the arms may vary. Irregularity of the pupils is a piece of evidence to be received with some caution, as it may be habitual or the result of disease in the eye. Conjugate deviation of the eyes and head is a form of paralysis, or sometimes of unilateral spasm, which when present is of great significance. In opium-poisoning—and to a less extent in alcoholic coma—the pupils are much contracted, while they are not always so in apoplexy. Respiration is usually much more rapid in apoplexy than in opium-poisoning, and this, in the absence of distinct signs of hemiplegia, would be one of the most important means of distinction. The pulse is more nearly normal in frequency, while that of opium is either slow and hard or more often frequent and feeble.
After the time for the initial depression has passed, rapidly-rising temperature is very strong evidence in favor of apoplexy. If the patient be only partially unconscious and able to protest against being handled, to make some short answers, or even be inclined to be combative, this is not to be taken as evidence of alcohol. Hemiplegia may then be noticed. This condition of excitement may be observed in the early stage of an apoplectic attack before it deepens into coma. Unfortunately, when the lesion is situated in certain portions of the brain, as in the extremities of either the frontal or occipital lobes, there may be no paralysis, but then also there is less likelihood of the extreme symptoms we are supposing to be present. In the cerebellum, however, the symptoms may be very severe without hemiplegia, and the diagnosis correspondingly difficult. Vomiting, not caused by the presence of large quantities of food or liquor, and persisting after the stomach is once emptied, would be of some value in this case, but it would often be necessary to wait for a diagnosis. Cerebellar hemorrhage is, however, a very rare accident, and cerebellar embolism sufficiently large to cause apoplectiform symptoms still more so. A limited lesion in the pons may cause gradually-increasing stupor without distinct paralysis.
Chloroform, especially if swallowed, and chloral might possibly give rise to difficulties in the way of diagnosis, and would have to be distinguished on the same general principles as alcohol and opium.
The poisonous gases arising from burning coal, consisting chiefly of carbonic oxide and dioxide, or illuminating gas, consisting of carburetted hydrogen with a little carbonic oxide, cause unconsciousness, coma, and sometimes convulsions and vomiting. In case of a person found unconscious in bed the possibility of poisoning by one of these should not be lost sight of, nor, on the contrary, assumed to be a cause without investigation. A case has been reported where, after acute poisoning by coal gas, there occurred, presumably as the result of local anæmia, alternate paralysis, convulsions, and aphasia.47 The new water-gas process is said to furnish a product considerably richer in the poisonous carbonic oxide than that now most in use.
47 Boston Med. and Surg. Journal, Nov. 26, 1885.
The stupor succeeding an epileptic convulsion resembles apoplexy, and the fact that cerebral hemorrhage may be accompanied by some convulsions increases the possible similarity, but it requires only a short time for epilepsy to make itself manifest, either by a renewal of the convulsions or a rapid recovery without paralysis. According to Trousseau, however, many attacks of so-called congestion of the brain are really epilepsy. Puerperal eclampsia comes under the same head, but when convulsions are violent they may give rise to actual hemorrhage. Unilateral epileptiform convulsions are likely to be dependent on organic disease of the brain, usually not of the kind at present under consideration, but more frequently of a tumor.
Among the cerebral symptoms connected with renal disease, and not involving organic change in the brain, may be found unconsciousness, deep coma, and convulsions. It is obvious that the presence of a few hyaline casts and a little albumen will not decide the matter, since these may be present from many causes, and especially the changes in the circulation accompanying apoplexy. Neither will the most indubitable evidence of Bright's disease, such as dropsy, hypertrophy of the heart, rigid arteries, with fatty and waxy casts in the urine, do so, for, as we have already seen, not only is there nothing in the presence of nephritis to exclude apoplexy, but the very form, the interstitial, which, from the supervention of coma not preceded by other very severe symptoms, most nearly counterfeits apoplexy, is also the most likely to give rise to actual cerebral hemorrhage. The extreme and frequent cephalalgia which is so distressing a symptom in cases where there is no cerebral lesion may also be the precursors of hemorrhage.
If we have a history, the gradual onset of the symptoms, deepening unconsciousness without any paralytic or unilateral symptoms, especially if accompanied by a diminution in the amount of urine or contained urea or a marked change in the character of the casts, renders it probable that we are dealing with so-called uræmia alone. In the absence of history hemiplegia must be the chief dependence, but it would not be difficult to imagine a case of embolism of the basilar artery with softening of the pons which would defy a positive diagnosis.
Pernicious intermittent fever appears in a so-called comatose form, which, if it were to be accompanied, as in a case related by Bemiss in the second volume of this work, by paralysis of one arm, might present difficulties of diagnosis. If it were known that the attack had been only of short duration, the elevation of temperature would, as in the case of sunstroke, decide in favor of the fever, but if it had lasted some hours, this symptom would be of no value, as the temperature may rise to an equal height in apoplexy.
Diabetic coma is a much less common affection than apoplexy. The peculiar odor (aceton) of the breath, if present—which is not always the case—might be diagnostic. The peculiar long and deep respirations would awaken suspicion which would be confirmed by an examination of the urine.
Sunstroke, with its sudden onset, complete unconsciousness, and rapidly rising temperature, may present a very close resemblance for a while to apoplexy, and in fact has been known as heat apoplexy. Age, temperature, and surroundings would give strong probabilities one way or the other, and if the temperature of the patient were at first below the normal and did not rise for an hour or two, it would certainly not be sunstroke and would be apoplexy, while if the temperature were very high a few minutes after the patient had been observed to cease work or become unconscious, the evidence in favor of sunstroke would be equally strong.
It might appear that hysteria need hardly enter into our consideration, and could hardly be mistaken for apoplexy, but most experienced physicians could relate instances where serious organic disease has been made light of under the name of hysteria, and many inexperienced ones could tell of the opposite and safer mistake. An occasional case of deep coma presents itself where, although the age and sex of the patient awaken strong suspicion, we cannot at once be sure that no organic lesion is present; and if, in addition, the patient should be affected with hemiplegia—a combination which, although rare, is by no means beyond the limits attainable by this perplexing disease—an immediate positive diagnosis would be difficult. Absence of facial paralysis, which might be made manifest by some irritation like pinching or an attempt to raise the eyelids, would be of much value under these circumstances. The hysterical physiognomy might be well enough marked to be almost conclusive by itself. The urine and feces are not likely to be passed involuntarily in hysteria, as they are in apoplexy.
Injuries to the head should be carefully looked for in any case with unknown history. Actual fracture, which perhaps leads to no depression of bone, may give rise to hemorrhage, probably meningeal, which will cause the usual symptoms, and a shock which is not accompanied by fracture may cause considerable laceration of the brain with consequent hemorrhage. In the latter case, however, unless the brain be already predisposed by arterial disease, the laceration and hemorrhage will not be extreme and the symptoms will be those of concussion. The diagnosis can hardly be said to be between hemorrhage and concussion, but whether the hemorrhage be the result of concussion—a question which can hardly be answered without the history and observation of the further progress. Cuts and bruises may result from a fall caused by the shock, and pericranial ecchymoses may result from cerebral hemorrhage through the vaso-motor system without the intervention of accident.
Rapid meningitis of the vertex, with predominance of the effusion upon one side, may closely simulate compression from hemorrhage. At the base, by the time it has become severe enough to cause unconsciousness, it is likely to have affected the ocular muscles, and perhaps given rise to other paralyses less regular in their distribution than the ordinary hemiplegia. Ophthalmoscopic examination would be of value in these cases if—which is not very likely to happen—there is no history. The temperature in meningitis is more likely to be irregular and less rapidly and uniformly rising than in a severe hemorrhage or occlusion. In many cases emaciation, dry tongue, and constipation with sunken abdomen will testify to a previous illness, while after a few hours' observation the progress of the case will make the diagnosis more clear.
In differentiating cerebral hemorrhage or ordinary embolism from the apoplectiform attacks met with in syphilitic intracranial disease, it is rather a question of etiology than of diagnosis in the narrower sense, since unconsciousness and hemiplegia coming on with syphilis are often dependent upon a condition of the vessels closely resembling that which gives rise to the ordinary forms; that is, we are dealing in either case with an endarteritis which has furnished the basis for the deposit of a thrombus, and the question is, Of what nature is the endarteritis? It is obvious that this is only to be answered by a knowledge of the history, not necessarily of a primary or secondary lesion, but of previous disease. The syphilitic taint may often be suspected from the irregularity of the paralysis, the cranial nerves, for instance—especially the ocular—being much more frequently affected in syphilitic than in ordinary hemiplegia. After partial recovery or amendment the characteristics of irregularity and changeableness will be more strongly marked.
The pathology of hemiplegia and apoplectiform attacks, often transitory, in the course of general paralysis is not certain, but it is probable that they are due to sudden congestions of regions of some extent already in a condition of chronic periencephalitis or to cerebral œdema. The question of the existence of the previous disease can only be settled after the return of the patient to consciousness. Usually, these attacks are not of the severest kind, and are not necessarily attended with loss of consciousness, which, when it occurs, is usually not of long duration. An apoplectiform attack occurring in a young or middle-aged person who has neither cardiac nor renal disease, rapidly recovered from or changing its character, should awaken strong suspicions of either general paralysis or syphilis, or both.
The characteristic of the so-called congestion of the brain, or coup de sang, is a close resemblance to ordinary apoplexy, but without hemiplegia and usually with a rapid and complete recovery. A diagnosis from apoplexy cannot be made at once, except so far as hemiplegia can be shown to be either distinctly present or absent.
As has already been stated, the doctrine of the dependence of real apoplectiform attacks upon cerebral congestion alone has been vigorously combated by distinguished clinicians; and certainly the diagnosis of congestive (and the same may be stated even more strongly of so-called serous) apoplexy should never be made until after the rigorous exclusion of every other possibility.
After the severer apoplectic symptoms have passed off, and in cases where they have never been present, the diagnosis, so far as most of the conditions mentioned above is concerned, is divested of many of its difficulties when we are dealing with cases of well-marked hemiplegia. The chief points left are the distinctions from the apoplectiform attacks of general paralysis, cerebral syphilis, and cerebral tumor, which are to be made as already pointed out.
Slighter and more localized paralyses, such as may occur with limited lesion of the pons or where a hemorrhage having a large focus in the substance has escaped under the membranes and presses on some cranial nerve, would present more difficulties. Paralyses which are very limited, and at the same time complete, are not likely to arise from hemorrhage or embolism, though it is possible that they may do so, but the diagnosis is to be considered rather under the head of local palsies than of cerebral disease. General rules cannot be laid down for slighter cases, and each case must be diagnosticated for itself. In many of them the electrical diagnosis would be of great value and often decisive.
Hysteria remains, as always, ready to counterfeit anything, but the following case shows that the error is not always on that side: F. S——, a young woman, was brought to the hospital, apparently conscious and understanding what was going on, but unable or unwilling to speak or to protrude her tongue. There was no history except that she had probably been in the same condition for thirty-six hours. There was paralysis of the right side, including the face, and marked anæsthesia of the same side, quite distinctly limited at the median line; temperature 97.8°, pulse 60, respiration 20. The next day she seemed perfectly conscious, but did not speak. The faradic brush to her face caused loud outcries, and the facial paralysis was diminished. This condition remained nearly the same, the patient appearing half conscious, but passing urine in bed. Four days later there was marked diminution of sensation and motion on the left (previously sound) side, as well as the right. The note two days later was, “Shuts and opens her eyes when told, and moves eyeballs in every direction, but there is apparently no voluntary motion except slight of the head. Incontinence of urine and feces.” A week later the temperature rose to 100.4°, pulse 140, and she died. The autopsy showed red adherent thrombus in the left carotid, extending into the cerebrals, with extensive anæmic necrosis of the cortex and a part of the corpus striatum. On the right there was a grayish thrombus and softening of the cortex, while the great ganglia were not affected.
A woman of thirty-two had repeated attacks of loss of consciousness and somnolence lasting several hours, but leaving her apparently well. The case was considered hysteria, but the patient died in a similar attack. Degeneration of the cerebral arteries and hemorrhage were found.48
48 Christian, Centralblatt f. d. Med. Wiss., 1873, 864.
Post-paralytic chorea might present difficulties of diagnosis from hysteria or malingering, though the difficulty is quite as likely to be on the other side.
The diagnosis, however, is not complete until the lesion is located with some precision and its nature determined, although it must be confessed that when we have got as far as this the diagnosis in most cases is of more interest to the physician than to anybody else, except to a slight extent for prognosis, so that the event may be anticipated by a few hours. As to the localization of the lesion, recent experiments and observations, involving not only lesions of the kind we are here discussing, but tumors and injuries as well, permit this to be done with a reasonable degree of certainty. The general article on Cerebral Localization may be referred to by the reader for the minuter points, but certain groups of symptoms may be indicated here which are available to some extent before the complete return of the patient to consciousness.
In the vast majority of cases the lesion is situated upon the side of the brain opposite to the paralysis, except in some instances of cerebellar lesion, while in the peculiar form known as alternate paralysis due to lesion of the pons it is on the opposite side to the paralysis of the limbs and on the same side with the facial. It should be distinctly stated, however, that there are exceptions which are inexplicable on the present basis of cerebral anatomy. It is well known that only a part of the motor tracts cross to the other side of the cord at the decussation, and also that the proportion between the fibres which do and those which do not cross is a variable one. It has been suggested, in some cases of the kind mentioned, that all the motor fibres, instead of only a minority, as is usual, pass down on the same side of the cord as their origin. This has not been demonstrated. The number of such cases are so small that it need not be taken into account in diagnosis, and if the practitioner should make a mistake on this basis, he will have the recompense of knowing that he has assisted in a very rare case, in which it was next to impossible for him to be right. This condition is said to be found more frequently when the brain lesion and paralysis are on the right side.
Severe pain in the head, followed by gradually but rapidly deepening coma and paralysis of one side, becoming more and more complete, probably means a hemorrhage into or just outside of the great ganglia and involving a large extent of one of the hemispheres.
If there have been moderate loss of power or complete paralysis lasting some hours, with, afterward, sudden loss of consciousness and general muscular relaxation, with sudden fall, soon followed by rapid rise, of temperature, it is very probable that a hemorrhage has broken through into the ventricles or beneath the membranes, and is still going on.
Rapidly-deepening unconsciousness, with general muscular relaxation and gradual manifestations of more paralysis on one side than the other, may come from meningeal hemorrhage.
Very sudden and complete hemiplegia without prodromata, with deep unconsciousness coming on rapidly or suddenly, but a little after the paralysis, is likely to denote the occlusion of the middle (and perhaps anterior cerebral) artery of the opposite side at a point sufficiently low down to produce extensive anæmia of the motor centres along the fissure of Rolando as well as the underlying great ganglia.
Aphasia with hemiplegia, often without the slightest disturbance of consciousness, is in a considerable proportion of cases connected with a lesion of the third left frontal convolution, and in a somewhat larger proportion with the frontal lobes in general and the island of Reil. This lesion is in a great majority of cases occlusion of the artery. Difficulty of speech, connected with difficulty of swallowing and associated with a certain amount of amnesic aphasia, has been found with lesions of the pons. As aphasia, however, may occur without any fatal lesions at all, it is not certain in all these cases that the obvious lesion of the pons is a direct cause of all the symptoms.
Word-blindness is associated, according to a case reported by Skworzoff and a few others,49 with a lesion of the angular gyrus, pli courbe (P2 of Ecker), and word-deafness with a lesion of the first temporal (T1). These localizations agree with those experimentally determined.
49 West, Brit. Med. Journ., June 20, 1885.
Conjugate deviation is of importance as a localizing symptom, chiefly because it may be manifest when other signs of hemiplegia are difficult to elicit. I do not find it mentioned in twenty-seven cases of cerebellar hemorrhage not included in the table of Hillairet, but it is not infrequent with lesions of the pons; and when the lesion is in the lower third, it is in the opposite direction to that described as usual with lesions of the hemispheres.
Hemianæsthesia involving the organs of special sense, unilateral amblyopia, and color-blindness is supposed to be connected with a lesion of the posterior third of the internal capsule, or the thalamus in its immediate vicinity, sometimes also with a lesion of the pons. Bilateral hemiopia—blindness of the corresponding sides of both eyes—is apt to be connected with a lesion of the occipital lobe of the opposite side. Rendu and Gombault remark that hemianæsthesia of the limbs and face may be met with in certain lesions of the cerebral peduncles, but in this case the higher special senses (sight, smell) remain unaltered. Hemichorea points to the same localization as the more complete hemianæsthesia.
Alternate hemiplegia is due to a lesion of the pons upon the side of the facial paralysis, and opposed to the paralysis of the limbs and in the posterior or lower half. Care should be taken not to confound this with the accidental addition of a facial paralysis to a hemiplegia of the other side.
Irregular ocular paralyses are very likely to be due to lesion of the same region. In some of these forms an investigation of the electrical condition with reference to the presence of the degeneration reaction may be of great assistance.
With extensive lesions profound coma and relaxation without distinct hemiplegia are likely to be due to injury of the pons. A thrombus of the basilar artery may lead not only to rapid, but even to sudden, death. A phthisical patient died suddenly while eating his supper, and a thrombosis of the basilar artery, with softening of the pons, was found. Of course the lesion must have been of older date.50 Bright51 thought that when symptoms pointing to disease of the intracranial vessels were present the diagnosis was confirmed, and the location of the lesion in the vertebral arteries rendered highly probable, by a persistent occipital pain. In the upper part of one side of the pons the hemiplegia is not alternate, but of the ordinary form.
50 Bull. de Société anatomique, 1875.
51 Guy's Hospital Reports, 1836.
Any extensive lesion of the medulla must cause death so rapidly as almost to defy diagnosis, but such rarely occurs. The very rapid termination of certain cases of hemorrhage into the pons and cerebellum is due to the escape of blood into the fourth ventricle and consequent compression of the medulla.
Lesions of the lower and inner part of the crus are indicated by paralysis of the third nerve of the same, and hemiplegia of the opposite side of the body.
Obstinate vomiting, severe occipital headache, and vertigo, with or without a distinct paralysis, render a cerebellar hemorrhage probable, though no one of these symptoms is necessarily present or pathognomonic. Vomiting is very much more common with cerebellar hemorrhage than with cerebral. Ocular symptoms, like nystagmus and strabismus, accompany cerebellar lesions.
A difference in the temperature of the paralyzed and non-paralyzed sides, when amounting to one and a half to two degrees and lasting for a long time, is thought by Bastian to indicate a lesion of the optic thalamus.
The severe and rapid sloughing of the nates sometimes seen in rapidly-fatal cases is stated by Joffroy to be most frequently connected with a lesion of the occipital lobes.52
52 Arch. gén., Jan., 1876.
It is plain, from what has been said about the symptoms of the different kinds of lesion, that a distinction may be often very difficult, and at times impossible; and in this connection all observers are agreed, the apoplectiform shock, the hemiplegia, and the slighter attacks being common to two or three lesions. The diagnosis can be made, if at all, only by the consideration of more or less secondary symptoms and the careful weighing of the various probabilities against each other. Most of the statements of differences of symptoms are only relatively true.
A glance at the nature of the pathological processes involved may serve to systematize our observations.
Hemorrhage is a sudden accident, with a severity increasing as the amount of effusion increases. It has been prepared for by arterial disease, but this disease is one which may have no previous symptoms. It is at first an irritative lesion.
Embolism is a sudden attack which may be as severe at first as even a few minutes afterward. It is also prepared for by disease of other organs, which may or may not have symptoms according to the origin of the embolus. As embolism affects especially those regions where the motor centres are spread out, while hemorrhage attacks more frequently the conductors in their locality of concentration, the paralyses arising from the former affection may be more narrowly limited.
Thrombosis is a gradual affection, which may, however, manifest itself suddenly, from the obstruction reaching a certain point and suddenly cutting off the supply of blood. This also depends on previous disease which has more or less definite symptoms.
The severity of the attack is not conclusive, though the completely developed apoplectic attack is more frequent with hemorrhage. Rapidly increasing severity, especially if there have been prodromata, is in favor of hemorrhage. Convulsions, early rigidity, and conjugate deviation of the eyes of the spastic form, especially if afterward becoming paralytic, are strongly in favor of hemorrhage, and the latter possibly conclusive. Hughlings-Jackson states that he cannot call to mind a single case of hemiplegia from clot in a young person in which there were not convulsions.
Sudden paralysis without cerebral prodromata, unconsciousness, or pain can hardly be anything else than embolism; but, unfortunately for diagnosis, the initial paralysis from the embolus may be slight, and afterward added to by the secondary thrombus, so as to put on the appearance of more gradual approach.
Aphasia, and especially aphasia associated with but little or no paralysis, is very much more frequent with embolism than with hemorrhage.
The temperature, if we could always have it recorded from the very beginning, might be of value, as the initial depression is said to be less with embolism than with hemorrhage, but Bourneville,53 who lays down this rule, gives so many cases where no great depression occurred with hemorrhage that it cannot be considered decisive. Besides this, we are not likely to get the information at the time it is of the most value.
53 Op. cit.
Etiological information may have a very practical bearing on this part of the diagnosis. Age gives a slight amount of predominance to the chances of hemorrhage, and youth a considerably greater one to the chances of embolism. Interstitial nephritis with hypertrophy of the heart, after the exclusion of uræmia, gives a strong probability in favor of hemorrhage. Valvular disease of the heart, especially a more or less recent endocarditis, is strongly in favor of embolism. A feeble action of the heart, slow and irregular pulse, are more likely to be connected with thrombosis.
Atheroma and calcification, as detected by examination of the visible and tangible arteries like the radial and temporal, is a condition either connected with the periarteritis aneurysmatica which gives rise to hemorrhage, or one which furnishes a suitable spot for the deposition of a thrombus; hence it can be considered conclusive in neither direction.
Arcus senilis, even of the fatty variety, can only show some probability of arterial degeneration.
Retinal hemorrhage, if present, favors the presence of a similar cerebral lesion, but nothing can be argued from its absence. Landesberg54 has reported a case in which embolism of the central artery of the retina, easily diagnosticated by the ophthalmoscope, preceded by a few days a similar accident in the middle cerebral; and Gowers55 another in which the two arteries were occluded simultaneously.
54 Archiv für Ophthalmologie, xv. p. 214.
55 Lancet, Dec. 4, 1875.
If a sudden paralysis arises in connection with a septic process, we may diagnosticate an embolus with a good deal of confidence; but it is not unusual to meet with small abscesses of septic origin which have given rise to no special symptoms whatever, or only to such as are covered up by the more general constitutional ones.
PROGNOSIS.—The prognosis quoad vitam of cases of apoplexy still in the unconscious state is based upon the general severity of the symptoms as indicated by general muscular relaxation, or, at a later period, the extent of the paralysis, the amount of affection of the heart and respiration, and especially the progress during the first few hours. Too much weight should not be placed upon a very slight improvement at first, since this often takes place in cases soon to prove fatal.
Stertorous respiration with perfect tolerance of mucus in the throat, absolute loss of the reflexes, and immobility of the pupils signifies profound depression of the organic nervous centres, and is consequently of unfavorable augury.
The temperature is a valuable guide. In proportion as it moves steadily and rapidly upward is the prospect of an early fatal result. A person may die during the initial fall of temperature, but in such a case there would hardly be need of a prognosis.
In general, the prognosis from hemorrhage, supposing the symptoms to increase in severity for an hour or two, is worse than that from occlusion.
Age, aside from the fact that it makes hemorrhage more probable than occlusion, is not of great importance in prognosis, certainly not out of proportion to the general impairment of vigor in advanced years.
A renewal of the hemorrhage within a few hours cannot be predicted. It may be indicated by another fall of the temperature, which, if it have been previously on the rise, renders, of course, the prognosis more unfavorable.
After recovery, more or less complete, from the apoplectic condition the prognosis is favorable, for a time at least, except so far as one attack may be looked upon as the forerunner of another. After the temperature has reached a sort of standstill in the neighborhood of normal, its subsequent rise will furnish among the earliest indications of an approaching fatal termination.
Urinary trouble, retention, incontinence, or, much more, cystitis, is to be looked upon as a complication which materially increases the gravity of the situation. Bed-sores or abrasions may be placed in the same class, except that the early and extensive sloughing of the nates described by Charcot is of almost absolutely fatal significance.
After some days or weeks the progress of the paralysis either toward better or worse may be exceedingly slow, and as time goes on the danger to be apprehended from the latter becomes less and less.
When paralysis takes place in young persons and the primary attack is recovered from, it is doubtful if the chances of a long life are materially diminished. A case has already been referred to in this article where the consequences of a cerebral hemorrhage occurring in infancy were found in a woman of eighty-three in the form of atrophied limbs and an old pigmentary deposit in the brain.
Hemorrhage into the cerebellum would appear, from statistics, to be exceedingly fatal, but it is certain from old lesions occasionally found that it is not absolutely so, and its apparent severity is partly caused by the fact that it is very seldom diagnosticated except at the autopsy.
The prognosis quoad restitutionem ad integrum cannot be made to advantage at an early period. After the immediate danger to life has passed it is safe to say, if pressed for an answer, that it is highly probable that some recovery from paralysis may take place, but that it is highly improbable that it will be absolutely complete, and just how far improvement may go it is impossible to predict with accuracy at first. Time must be given, in the first place, for pressure to subside, compressed nerve-fibres to be restored, and for such collateral circulation as is possible to be established. How recovery takes place beyond this it is not easy to say. It is hardly supposable that any considerable portion of nerve-structure is renewed. A certain amount of substitution, by which one part of the brain takes up the functions of another part, is among the most plausible suppositions; but how this is accomplished it is hardly worth while in the present condition of cerebral physiology to speculate.
Practically, it may be said that physicians are apt to consider a paralysis absolute at too early a period, while the patient and his friends continue to hope for a complete restoration after it is evident that no really useful increase of power is to be looked for. Weeks, and even months, may elapse before any return of motion can be perceived in cases which are really susceptible of considerable improvement, and a year most certainly does not cover the limit of the time during which it may go on.
The most unfavorable symptom, one which probably precludes all hope of useful recovery in the limbs affected, is contracture, heralded for a time by increase of the deep reflexes, indicating degeneration of the motor tract in the white substance of the cord. Until this begins, certainly for many weeks, the patient may be fairly encouraged that some improvement is possible, though after a few weeks the chances diminish as time goes on. In the rare cases where the muscles undergo rapid wasting the prognosis is, if possible, worse still. The localization of the lesion after the early symptoms are passed does not greatly influence the prognosis.
A rapid recovery taking place in either hand or foot, and especially of the hand first, without corresponding improvement in the other limb, is of unfavorable import for the latter, and, in general, the prognosis is not exactly the same for both limbs involved. In the rare cases of hemiplegia from acute brain disease occurring in children the nutritive disturbances in the form of arrest of growth should be taken into the account in prognosis, since the result may be nearly or quite the same as is found after infantile paralysis from disease of the cord.
In regard to the slighter forms of paralysis, it may be said that the less extensive the original paralysis is, and the sooner improvement begins, the better is the chance of complete recovery.
TREATMENT, INCLUDING PROPHYLAXIS.—Cerebral Hemorrhage.—As the condition upon which the usual form of cerebral hemorrhage depends is so frequently aneurism, and probably nearly always some arterial disease, the prophylaxis must evidently consist in such a mode of life as will least tend to this degeneration, or at least put it off as long as possible. This, of course, means the avoidance of all the special causes described under the head of Etiology. It is a disease of old age, but in a pathological sense old age begins in different persons after a different number of years. Fortunately for rules of hygiene, there is little that is contradictory in those to be given for most chronic and degenerative diseases. Abstinence from alcohol, as an agent tending at once to paralysis and dilatation of the vessels, is one of the most important rules and insisted upon by nearly all writers. The avoidance of over-eating, and especially of nitrogenous food as tending to lithæmia—a generally recognized cause of arterial degeneration—is perhaps the next. Over-eating is of course to be understood as a relative term, and to be estimated with reference to the habits of exercise of each person. Practically, it will be decided by its effects; that is, if careful thought be given to the matter and the statements of the gourmand as to his immunity from all risk of trouble are not accepted as of scientific value. On the other hand, insufficient food, producing anæmia, may be a factor in arterial degeneration. Keeping one's self free from anxiety, and getting through the world with as little experience of its roughnesses as possible, might be, properly enough, added in a purely theoretical point of view if any one ever asked a physician's advice in youth as to avoidance of the diseases of age, or if any one could or would profit by this advice if it were given.
Intellectual pursuits have been credited with a special tendency to apoplexy, but there is no good reason to suppose that healthy exercise of the mind is otherwise than beneficial to its organ. Hurry, over-anxiety, and mental tension are undoubtedly potent factors in general breakdown, but do not necessarily lead to this form. They are certainly not to be found by preference in those persons who lead an intellectual life.
Syphilis, one of the most important of the causes of organic cerebral disease, and that too in the form of thrombosis, is not specially concerned in the etiology of the forms here under consideration.
If symptoms have occurred that justify the apprehension of apoplexy or paralysis, such as frequent headaches in an elderly person, hemiopia, temporary aphasia, or slight and temporary paralyses, or if one have reached a time of life at which the risk of cerebral hemorrhage becomes considerable, a stricter attention to the rules laid down above, and even to some to which but little heed would be given in health, is not out of place. A certain amount of limitation of diet, moderate and regular but not violent exercise, clothing suitable to the season, and especially warm enough in winter, and, most of all, rest if the patient be doing wearing and anxious work, should be enjoined. Finally, it should be said that the real prophylaxis of cerebral hemorrhage is to be begun in early life.
Among the exciting causes to be avoided are those which obstruct the flow of blood from the head, like tight clothing around the neck. Increase of the arterial pressure by severe or prolonged muscular effort, as in lifting or straining at stool, is to be avoided, as well as violent fits of passion. The condition of the bowels should be regulated by mild laxatives.
When the apoplectic attack has actually occurred, treatment, though apparently urgently demanded, is really of little avail. If a patient is about to die in an hour or two from rapidly increasing pressure, nothing within the reach of medical science can stop him.
There is one danger, however, easily avoided, but probably often overlooked. A patient may die from suffocation. The stertor is often a result of the paralysis of the tongue and palate and of the amount of fluids collecting in the pharynx from the almost invariable position of the patient on his back; that is, if he have been seen by some one who wished to do something for him, but did not know what. Insensibility and paralysis combine to favor this accumulation, which obstructs the respiration, and which may find its way to the lungs, together with brandy and milk, and set up an inhalation-pneumonia. The simple and obvious thing to do is to place the patient sufficiently on his side, with the face somewhat downward, for the tongue and palate and secretions to fall forward, instead of backward into the pharynx. Swabbing out the pharynx may be of some use, but cannot be so thorough. An easy position and proper ventilation should be secured in all cases of unconsciousness, even at the risk of treating a drunkard with undue consideration. Police-stations should be provided with rooms where these conditions can be secured, and the necessity avoided of placing persons picked up in the streets in the narrow, close, and perhaps distant cells provided for malefactors. The writer recalls the cases of two young men—one who had been drinking some time before, and the second roaring drunk—who were locked up in a suburban station-house in the evening, and found the next morning—one dying and the other dead.
Artificial respiration may be used to prolong life in some cases until the nervous centres have sufficiently recovered their functions to carry on the process without assistance. The condition of the bladder should be ascertained, and the urine drawn if necessary, though it is more frequently passed involuntarily.
Although it is manifestly impossible to remove the clot from the interior of the brain, it may appear that the further flow of blood may be stopped and the amount of damage done limited. For this purpose two remedies are proposed—namely, bleeding and purgatives. Both of these act to diminish arterial pressure, which is forcing the blood out of the rupture. Though the treatment seems reasonable, it would not be difficult to imagine a condition where sudden and premature diminution of pressure in the brain, which of course exists outside of the arteries as well as inside, would tend to set going again the flow which has ceased from the very force of the pressure it itself exerts, very much as if a tampon were prematurely removed from a bleeding cavity elsewhere. As the conditions are somewhat complicated, and at the same time only remotely to be estimated, it is safer to be guided by experience in the use of these remedies than by abstract reasoning. In some of the cases of temporary aphasia, as notably that of Rostan narrated by Trousseau, bleeding seems to have given immediate relief. Trousseau, however, is no advocate of that method of treatment. Most modern authors speak of venesection as to be used in cases where the pulse is strong and full and the face red, but not to be thought of in the opposite class. When a case presents the appearances of plethora and an attack has come on suddenly, the loss of a few ounces of blood can certainly do no harm. Other forms of bleeding, such as cups and leeches, are not rapid enough to be of great value, though a large number of leeches about the head might be useful. Some French writers recommend leeches to the anus as revulsives. Cathartics may be more freely used, although they should be given cautiously when there is any tendency to cardiac depression. It can be clearly shown that a brisk purgative lowers the arterial tension decidedly. In case of cerebral tumor or injury with occasional so-called congestive attacks, the relief afforded by cathartics is very great, and, although the conditions are not exactly parallel, it is fair to assume a similar action in the congestion accompanying cerebral hemorrhage. From one to three drops of croton oil may be placed far back on the tongue or it may be diluted with a neutral oil. Ail enema may be desirable for the unloading of the bowels, but has a much less marked effect on the tension of the cerebral circulation.
In most cases of apoplectiform cerebral hemorrhage, and probably in all of simple paralysis, no very active treatment is called for. Measures directed to the prevention of another hemorrhage, and to allay any irritation that may supervene during the changes taking place about the clot and the formation of its capsule, are of the simplest, and consist in keeping the head high and cool, the clothing sufficient for warmth, and offering no obstruction to respiration or circulation, laxatives sufficient to keep the bowels in good order, and a diet not highly nitrogenous, but sufficient and digestible.
That which will tax most severely, however, the care and patience of attendants is the scrupulous and minute attention to cleanliness and pressure over the bony prominences which is necessary when a patient is helpless and unable to control the discharges from the rectum and bladder. Frequent change of clothing, bathing, change of position, and avoidance of wrinkles and roughnesses in the bed may be successful in keeping the patient free from bed-sores. Bathing with alcohol hardens the skin and makes it less susceptible to pressure.
Surgical interference may perhaps be of value in cases where the portion of the clot outside the brain can be clearly demonstrated; and this would apply with special force where the hemorrhage arises from injury.
Trephining and removal of the clot has been done in a few cases of meningeal hemorrhage, though with indifferent success (3 cases—2 deaths, 1 unknown.)56 An intracerebral clot is obviously a step beyond, though possibly in some cases not absolutely without, the reach of the surgeon.
56 Med. Press and Circular, Oct. 14, 1885.
Treatment of Cerebral Embolism.—The prophylaxis is in the avoidance of such conditions as give rise to the formation of detachable vegetations or clots. Unfortunately, these are numerous, not completely known, and not always avoidable. Arterial disease is to be looked upon as of some importance, but cardiac valvular lesions of much greater, and the causes of these, like rheumatism, scarlet fever, and the puerperal condition, are not always to be escaped. The presence of a detachable piece of fibrin in the pulmonary veins, heart, or aorta being granted, nobody can possibly say what will prevent its being loosened and lodging in one of the cerebral arteries; so that, practically, the prophylaxis of embolism consists in the judicious treatment of acute rheumatism and the other conditions just mentioned. The treatment of the first attack must consist solely in the relief of respiration, bladder, and bowels, if they have not taken care of themselves. Stimulants may be of use for a short time, but there cannot be any call for even the slight amount of depletion suggested for some cases of hemorrhage. Bed-sores are to be looked out for, just as in hemorrhage, and the subsequent treatment conducted on the same principles. As regards the primary lesion, we can do nothing about it either in the way of removal of the embolus or restoration of the necrosed brain-tissue.
Treatment of Cerebral Thrombosis.—There being two factors in this affection, both of which are to a certain extent under control, something may be done toward diminishing the risk of its occurrence. Arterial disease and its prophylaxis have already been spoken of. The other condition which is necessary to the production of thrombosis—namely, an enfeebled circulation—is to some extent under the control of general hygienic rules: a nutritious, not too highly nitrogenous, diet, and especially sufficient exercise and the avoidance of completely sedentary habits. If there is a crasis which predisposes to the formation of coagula in the vessels, it is not known that there is any special treatment, medical or otherwise, which can prevent it. The attack is to be treated exactly on the principles already laid down. Bleeding is about the last thing to be thought of. Stimulants, though they cannot dislodge the clot, may be of use for a time to sustain the heart under the shock. The secretions and the condition of the skin are to be looked out for.
After a few weeks of waiting the patient and his friends not unnaturally feel as if something ought to be done to hasten recovery, and certain measures may be taken, in addition to careful hygiene, which have this object in view. It is very doubtful, however, whether anything really shortens the time necessary for such repair as is possible or diminishes the amount of damage which is to be permanent. As has already been said, improvement may go on slowly for months. In the first place, it is sometimes considered desirable to practise shampooing and massage of the affected muscles in order to keep them in as good a condition of nutrition as possible. This, as well as the regular use of the faradic battery if it be not begun too early, will prevent a certain moderate amount of atrophy, but could not have any influence in those rare cases where rapid wasting depends upon secondary degeneration of the anterior gray columns. It may be doubted, however, whether it is necessary to pay much attention to the condition of the muscles, as they do not ordinarily atrophy to the extent of becoming unsusceptible to the nervous stimulus from the brain so soon as it shall be transmitted to them. Faradism, like many other agencies, such as magnets, metals, pieces of wood, and so forth, is said to produce a transfer of sensibility in cases of hemianæsthesia.
There is no sufficient reason to suppose that any drug is of any value in the restoration of the nervous structure. Iodide of potassium may possibly prove to have some effect as a sorbefacient. Very favorable results have been claimed for ammonia salts in the restoration of aged persons to a nearly complete use of paralyzed limbs. Phosphorus has been spoken of as assisting in repair, but the writer is not aware upon how wide a basis of facts. Silver and gold have been said to counteract the sclerosing myelitis. Strychnia is certainly useless, and probably worse. It may make the paralyzed limbs twitch, but this does just as little good as the involuntary spasmodic movements, which have never been considered desirable, except as awakening in the patient false notions of immediate recovery, and which are frequently a very annoying symptom. The galvanic current has been applied with a view to a sorbefacient or restorative action directly to the brain, or rather to the pericranium.
Something can be done for the comfort of such patients: the rubbing and kneading of the paralyzed limbs, if they do not hasten the recovery of motion, relieve many of the painful and unpleasant feelings. Since we do not know how far one part of the brain may supplement another, attempts at motion after it has once appeared to ever so slight a degree should not be abandoned by the patient. He should walk with crutches frequently as soon as he can, though not to the point of fatigue.
There is one faculty which seems capable of re-education to some extent: that is of speech in cases of ataxic aphasia, and even in others the attempt should be made to teach the patient the names of things. A very interesting case has been reported by Bristowe57 of a man who came under his observation after an attack which may have been anterior poliomyelitis with extensive paralysis, able to write well and intelligently, but unable to say anything. By gradual education, first in the sound and formation of letters and afterward of words, he reacquired the use of language. It is obvious that in this case there could have been no loss of memory for the words themselves, but simply the loss of the knowledge of how to produce them. When his speech returned he spoke with his original American accent.
57 Clin. Soc. Trans., iii. p. 92.
In short, the therapeutics of hemiplegia from arterial disease in the brain is good nursing and attention to symptoms, with a moderate amount of care of the paralyzed muscles.
Capillary Embolism.
It may be remarked, in the first place, that the lesions known by this name are not necessarily strictly capillary, but are situated in the very small arteries. The microscope marks the transition from the larger to these smaller embolisms.
More is known about very small embolisms experimentally than clinically, since they have been produced by the injection of small seeds and insoluble particles of various kinds. Embolisms arising from natural causes and deposited in the minutest arteries may have very similar origin to the larger ones already described, but there are also other conditions which give rise to particles which pass through larger arteries without any disturbance, and are arrested in smaller ones. The softening of thrombi is undoubtedly one source. The same thrombus which, if detached en masse, would block the carotid artery, may, if broken up into a number of minute fragments of fibrin and fat, pass into the ultimate distribution of the cerebrals. The same thing may of course happen if the thrombus have already undergone one transportation.
Cases of localized softening are seen where no cause has been found, except perhaps a thrombus in the heart, which has discharged its softened and puriform contents; and it is probable that the connecting links exist in the form of embolisms so minute as to escape ordinary observation.
The consequences of capillary emboli if they block every minute ramification of an arterial branch must be essentially the same as if the branch itself were stopped; but if only a part are thus affected, the resulting anæmia is not so complete, since the zones of capillary congestion surrounding the part the supply of which is cut off may be sufficient entirely to cover it and make more or less complete compensation. The experimental emboli, in the form of tobacco-seed and other insoluble substances, which have been traced into the brain in considerable numbers, often give rise to no distinct lesions in the cases where the immediate effects are recovered from.
Among the other sources, ulcerative endocarditis may be mentioned as of special importance, not from the size but the character of detached emboli, which will give rise, not to simple anæmia, nor, on the other hand, to merely negative results, but to septic changes at the place of lodgment.
Aside from these conditions, which are almost the same on a small scale as we find with the large emboli, we have several peculiar substances formed in the body and floating in the blood which lodge in the capillaries of the brain. These are pigment, fat, lime salts, and white corpuscles. Every one of these, however, is much better known anatomically than clinically.
Pigment scales, flakes, granules, or cells containing them, are formed in the course of severe malarial fever, and deposits consisting of this pigment are found in the spleen, liver, kidneys, heart, lungs, and lymphatic glands, as well as the brain and spinal cord. The brain, when a deposit of pigment has taken place, is of a slaty-grayish or chocolate color, which is marked only in the cortical substance, the white being unaffected. The pigment is found in the capillaries, and, according to Frerichs, fibrinous coagula are often associated. Punctiform hemorrhages in the brain have been seen, as well as meningeal hemorrhages, in connection with this degeneration.
The point at which these masses are formed is still a matter of theory. If the liver, as has been supposed, is one of the places of formation, or if they originate in the blood, it is of course easy to see how they reach the brain. If in the spleen, they must pass through the wide portal capillaries before they are arrested in the narrower ones of the brain.
It is by no means certain, however, that pigment reaches the brain in the form of emboli. It is quite as probable that it is found in many organs which undergo repeated congestions from the local destruction of blood-corpuscles and changes in their pigment. The very general deposition seems to point to a process of this kind rather than to a local origin and a distribution through the blood. The punctiform extravasations which may be found with deposits of pigment are also found without it.
Minute particles of fat have been found in cerebral capillaries, but are much less common here than in the lungs. They may be derived from the decomposition of a thrombus, as described above, or they may come from a fractured bone, when, of course, only particles fine enough to pass through the pulmonary capillaries can reach the brain. This form of embolism has an interest in connection with diabetic coma.
Collections of white corpuscles in considerable number have been observed to form an embolus. These cannot be considered to differ very widely in character from the ordinary fibrinous embolus, which contains white corpuscles. It is, however, not certain that such emboli are deposited during life.
Calcareous masses formed from the decomposition of bone have been seen in cerebral arteries.
About the symptomatology of such emboli little is known. An array of minute emboli from the breaking up of a thrombus in the left auricle, carotid, or even aorta, might possibly so block up large numbers of arterial twigs as to give rise to the ordinary symptoms of embolism; but considering the possibility of the re-establishment of circulation, provided a certain proportion of the minutest vessels escape, complete anæmia of a large tract produced in this way must be rare. It is possible that some of the slighter and more transitory attacks of hemiplegia or of more or less vague cerebral symptoms may be referred to a lesion of this kind, the first action of a large number of emboli being to cause an anæmia, which is compensated for much more rapidly and thoroughly than would be the case if a single considerable vessel were obliterated.
Various attempts have been made to connect definite and peculiar diseases with capillary embolisms. Chorea in particular has been said to depend upon a lesion of this kind, but, although cases have been observed where the symptoms and lesion coexisted, yet they are very far from being the rule, or even from constituting a respectable minority of cases. The lesion of chorea in the great majority of cases is not known, although attention has been directed to this theory long enough to have established its truth.
The same may be said of the relationship between pernicious attacks of intermittent and pigment embolism. There is occasional coexistence, but far from invariable. Cerebral symptoms of the same kind and severity occur without as with the pigment deposit. If pigment embolism is the cause of coma, delirium, etc. in pernicious fever, it is difficult to see why such cases can recover so rapidly, and why no symptoms referable to a localized cerebral lesion are observed after the primary unconsciousness.
Even less proof can be adduced as to any connection between leukæmic embolisms and the cerebral symptoms occurring toward the end of severe acute disease.
Calcareous embolism is a pathological curiosity.
DIAGNOSIS.—In the case of multiple capillary embolism it would be impossible, if it were complete, to distinguish it from a blocking of the main branch.
Cerebral symptoms arising in the course of ulcerative endocarditis might be referred, with a high degree of probability, to an embolus, but if they were distinct enough to be referred to a localized lesion, the probability of a single embolus would be much greater than that of a multitude of capillary ones occluding the same vascular territory. The diagnosis of pigment embolism might be a probable, or at any rate a possible, one if in a long-continued case of paludal fever, where the liver and spleen were enlarged and the skin had the slaty hue marking the deposit of pigment, there were decisive cerebral symptoms. It could not, however, be a positive one.
Fatty embolism might be suspected in a case of diabetic coma, though even if the condition were found it would not establish the relation of causation.
PROGNOSIS AND TREATMENT can hardly have a definite basis in the absence of all ground for a satisfactory diagnosis, but do not differ essentially from those of the larger occlusions.
Thrombosis of the Cerebral Veins and Sinuses.
It has for centuries been known that coagulation of the blood might take place in the sinuses in a way different from the ordinary post-mortem clots, but this was looked upon rather as an anatomical curiosity than as a fact of practical importance and clinical significance, and it is chiefly among observers of the present century that we find a growing knowledge of the conditions under which it occurs and the symptoms to which it gives rise.
Thrombi in the cerebral sinuses are not essentially different from those formed elsewhere, and the reader is referred to the account given in the article on General Pathology for a history of their formation, growth, appearances, and transformations. For our purposes it is sufficient to recall that they may be white, red, or striated, either partly or wholly obstructing, and that they may become degenerated and partly or wholly washed away. The most important distinction of all, however, is that into two classes, of which the first consists of those which are simply depositions of fibrin in a comparatively healthy vessel, and the second of those which are dependent on a phlebitis.
In order that a thrombus may form it is necessary that there should be, in the first place, a special condition of the walls of the veins—not necessarily, however, inflammation, though this is one of the most frequent and probably the most active form; second, a slackening of the blood-current; and, third, perhaps a peculiar state of the blood, though this latter is not certain. A thrombus tends strongly to grow, and when already formed furnishes a most favorable point for the deposition of more fibrin.
The cerebral veins furnish a very suitable place for the coagulation of the blood for several reasons: they are roomy in proportion to the amount of blood they carry; they are tortuous and abundantly anastomosing, so that the current of blood is almost reversed at some points, and can easily stagnate; the veins of the diploë are held open by their bony walls, and the sinuses by their stiff membranous ones, so that they cannot collapse and thus limit the extension of a thrombus once formed.
The sinuses most frequently affected, though none are free from the liability, are the cavernous, superior longitudinal, and lateral.
The results of thrombosis of the sinuses and veins are not equivalent to those of a similar process in the arteries, and they may be said in a general way to be more diffused, as might be expected from the much greater freedom of anastomosis. Limited softening is rarely a consequence of occlusion even of a considerable number of veins, but it has been observed. A large area of softening of one hemisphere, not involving the temporal and occipital lobes, has been seen with thrombosis of the parietal veins58 (the internal capsule and ganglia were not affected).
58 Gaz. des Hôp., 1880, 1066.
Passive congestion in the brain, as elsewhere, although apparently entirely incompatible with the normal function, seems to be able to sustain a low form of structural integrity.
Bleeding may take place from the congested veins behind the obstruction, constituting a distinct form of cerebral hemorrhage which does not depend upon an arteritis, although if miliary aneurisms were present the occurrence of thrombosis would undoubtedly tend to their rupture. The writer, however, is not aware of such a coincidence having been actually observed. Hemorrhages are usually diffuse, composed of or accompanied by a number of small effusions, and situated on or near the surface of the brain or distinctly meningeal. Punctiform hemorrhages are exceedingly common.
Phlebitis of the cerebral veins is very likely to run into meningitis, and the two affections are often so closely united that it is difficult to say which was the first. Œdema is a consequence of venous obstruction in the brain as well as elsewhere, and is seen also around some of the peripheral veins connected with the sinuses.
ETIOLOGY.—Venous thrombosis in the brain depends chiefly on three sets of causes, though it must be admitted that there are a few cases where the origin cannot be distinctly traced and where no previous disease has existed. In the marantic form, occurring chiefly in the very old and in children, as well as in cases of wasting and depressing diseases in adults, a simple thrombosis without inflammation takes place. Two conditions, and sometimes three, are combined here to produce the result—feebleness of the blood-current from a corresponding state of the heart, diseased endothelium of the vessels from defective nutrition, and possibly, where profuse watery discharges have been going on for some time, an increased tendency to coagulation from the inspissation of the blood.
Rilliet and Barthez and Von Dusch59 give the following tables of ages at which this form of thrombosis has been observed. The observations of the former were made in a children's hospital, and hence do not affect the question of its frequency in later life. Perhaps the rules of admission may account for the absence of cases under one year of age, of which Von Dusch collected several:
| Rilliet and Barthez. | Von Dusch. | |
| Under 1 year | ... | 5 |
| 2 years | 2 | 1 |
| 4 years | 4 | 1 |
| 5 years | 1 | 1 |
| 6 years | 1 | |
| 7 years | 1 | |
| 9 years | 2 | |
| 10 years | 1 | |
| 11 years | 1 | |
| 12 years | ... | 1 |
| 14 years | ... | 1 |
| Adults (20, 23, unknown) | ... | 3 |
| 53 years | ... | 1 |
| Aged women | ... | 2 |
59 Sydenham Society's translation.
The special diseases in which thrombosis is most likely to be met with are given by Bouchut as follows. The same remark is to be made about these as about those of Rilliet and Barthez. The table is given as convulsions from thrombosis of sinuses:60
| Chronic enteritis | 5 |
| Measles and catarrhal pneumonia | 2 |
| Chronic pneumonia | 5 |
| Phthisis | 8 |
| Anasarca without albuminuria | 1 |
| Chronic albuminuria | 2 |
| Whooping cough and pneumonia | 7 |
| Scrofula, tubercle of bones, etc. | 1 |
| Gangrene of mouth | 1 |
| Diphtheritis | 2 |
Von Dusch gives a number of cases of the same kind, as do many subsequent writers, but without tabulation. Virchow61 reports a case of congenital variola with thrombosis of the sinuses of the dura mater, the superior and inferior cava, and vessels of the cord.
60 Gazette des Hôpitaux, 1879.
61 Arch., 1859, 367.
It is probable that simple anæmia may, here as elsewhere, either alone or with other debilitating influences, lead to thrombosis. Von Dusch remarks that quickly operating and debilitating influences lead to thrombosis, and gives as an instance a case where a puerperal peritonitis, for the cure (?) of which repeated copious abstractions of blood were made during nine days, was supposed to be the cause. The puerperal condition seems to have a tendency in this direction in a way not always to be explained by the ordinary rules of the transmission of emboli or of phlebitis. Although in those reported by Ducrest62 phlebitis of the pelvic veins existed or was suspected, in the first of these five cases the lesion may have been, so far as the description goes, arterial instead of venous thrombosis; and in the second it is possible that the succession of events was uterine phlebitis (with the addition of a large sacral slough), lobular pneumonia surrounded and traversed by veins which were affected with phlebitis, emboli in the arteries of the cortex, and consequent venous thrombosis. In the third, fourth, and fifth the connection between the uterine phlebitis and the inflammation of the cerebral veins (in two cases meningitis) cannot easily be made out, except by the rather vague assumption of a general tendency to phlebitis, which was shown in one by a similar condition in the vein of the arm where the patient was bled. Empyema has been followed by hemiplegia, cerebral softening, and thrombosis of the lateral sinus. The venous thrombosis in such a case may be secondary.
62 Archives générales, 1847, p. 1.
Marantic thromboses are more likely to occur upon one side, and that the side upon which the patient habitually lies.
The second class of cases embraces those where a simple obstruction, partial or complete, of the current of the blood gives the starting-point for a thrombus in the veins. Such an obstruction may be formed by an embolus, but in the veins this cannot be considered an important factor, although a portion of a thrombus may be detached and become lodged in a narrower vessel or branch farther along. In this way the propagation of thrombosis for a short distance toward the heart may be accounted for.
A tumor or inflammatory exudation may press upon a vein or intrude into it, but most cases of obstruction-thrombosis are traumatic in origin. Thromboses arising in connection with tubercular meningitis may be looked upon as having both an obstructive and marantic cause. In many wounds of the vertex, gunshot and other, the walls of the superior longitudinal sinus are pressed upon by pieces of bone, and sometimes spiculæ have directly penetrated it. This class of injuries is also likely to cause phlebitis without any actual penetration or compression of the sinus, simply as a result of the inflammation of tissues in the neighborhood. The thrombi formed in these cases are not necessarily completely occluding. Where direct injury to the sinus or in its immediate neighborhood gives rise to phlebitis and consequent thrombosis, we have a condition closely resembling that of the third class, where disease of an inflammatory character in the tissues of the skull, neck, or face sets up a phlebitis and thrombosis which are transmitted to the intracranial veins and sinuses.
The most frequent source of this third form of inflammatory thrombosis is the chronic inflammation of the middle ear with the mastoid cells. The inflammation may be propagated through a carious or necrosed portion of the temporal bone to the petrosal and lateral sinuses, or may, without disease of the bone, be carried by the small veins which open into the sinuses from the petrous and mastoid portion of the temporal in this region. Abscesses in the neck may set up a phlebitis extending up the jugular to the lateral sinuses, to which a meningitis may possibly be added.
Carbuncles about the root of the nose, face, and so far down as the upper lip are very prone to give rise to thrombosis propagated through the ophthalmic vein to the cavernous sinus; and it is probably this risk which gives to carbuncles in this situation their well-known peculiar gravity. The divide or watershed between the regions which drain backward through the cranium and those which are connected with the facial vein below is apparently situated about the level of the mouth, so that a carbuncle of the lower lip is much less dangerous. Billroth, however, gives a case where a carbuncle in this situation was followed rapidly by cerebral symptoms and death, and where a thrombo-phlebitis was not improbable. He mentions another case where a carbuncle upon the side of the head set up an inflammation which travelled along a vein into the cellular tissue of the orbit, and thence through the optic foramen and superior orbital fissure into the skull.
Erysipelas of the scalp apparently causes phlebitis in some cases, and even eczema in the same situation seems to have done so. When the erysipelas is situated about the upper part of the face, the path of transmission is through the ophthalmic vein; but when upon the vertex, it may be propagated through the small veins that penetrate the bone. This result is certainly a rare one in facial erysipelas of the ordinary and superficial kind, which is a notoriously benign disease for one of such apparent severity. It may, however, be more frequent than ordinarily supposed, since cerebral symptoms occasionally appear at a date too late to be accounted for by the fever and too slight to be referred to extensive interference with the cerebral circulation; the lesion to account for which, as they do not cause death, can be only inferred, though it is not unreasonable to suppose it to be a limited thrombosis.
Dowse63 describes the case of a robust man who fell on the back of his head, but walked home. After a few days he had a severe headache, chill, and total loss of vision. His temperature rose; he had erysipelas and partial coma, but no convulsions. There was thickening of the scalp, but no fracture of the skull and no adhesions of the membranes. The superior longitudinal lateral sinuses were free from thrombi, though there was a roughness about the latter, as if there had been a fibrinous deposit. The cavernous sinuses were almost completely occluded with adherent fibroid masses, and there was hemorrhage in the anterior lobe. There was some degeneration of the brain-structure, but no disease of the arteries.
63 Trans. Clin. Soc., 1876.
Ulcerations in the nasal passages and ozæna have proved starting-points for thrombosis.64
64 Med. Times and Gaz., 1878, i. 614.
Thrombosis of the jugular veins and corresponding cavernous sinus, with paralytic symptoms, has been observed in the horse.
The symptoms produced by venous thrombosis, as might be supposed from their varying location and extent, and also from the fact of their being almost invariably connected with other diseases having marked and severe symptoms of their own, are not always easy to pick out from among many others, but they are sometimes very well marked and characteristic. A distinction must obviously be made between the symptoms of simple thrombosis depending on interruption of the cerebral circulation and those of phlebitis, which give rise in addition to febrile phenomena common to phlebitis in any of the large veins.
The symptoms which indicate venous obstruction, without reference to its inflammatory or non-inflammatory character, are of two kinds: first, those dependent upon the disturbance of the functions of the brain; and, secondly, those which depend upon congestion and compression of other structures.
According to the locality and completeness of the obstruction we meet with brain symptoms.
In the marantic thrombosis of children these may be very vague, and consist either in restlessness, followed by somnolence and coma, or, most especially, in convulsions. The convulsions may be partial and involve the face only; they may affect one side only, or, what is more usually the case, be general. There is almost always strabismus. There may be conjugate deviation. This latter phenomenon is said by Bouchut to be of no value in children, as it may take place in either direction, from or toward the lesion, but possibly the distinction between the spastic and paralytic forms was not duly observed by him. The condition of the fontanelles is spoken of as yielding and depressed, with the edges of the bones overlapping. They may, however, become again tense in the course of the disease from exudation or hemorrhage taking place. Paralysis is not so marked as in adults, but may be present.
In adults delirium takes the place of convulsions, due to a disturbance of circulation over a considerable area, rather than to a total suppression in a more limited one. Paralyses are not infrequently met with, either in the form of a hemiplegia or more localized. Hemorrhage will naturally be followed by its usual consequences, according to its location. Headache, often very severe, is among the early symptoms.
It is evident that none of these symptoms can be considered highly characteristic. They can only furnish a certain amount of probability in cases where the general course of the disease has made it likely that thrombosis may take place.
There is another set, however, which, when present, offer the strongest kind of confirmation: these are due to the pressure from the veins themselves.
Œdema about the points at which the intracranial circulation is connected with that of the face and neck may give rise to protrusion of the eyeball, conjunctival ecchymoses, swelling of the upper lip, and even of the upper part of the face, which sometimes becomes slightly cyanosed from the congestion. Epistaxis has been noted. Œdema may be noticed about the mastoid process when the thrombosis is situated in the lateral sinuses, but it would be important in many cases to distinguish this from inflammatory œdema directly due to disease of the bone.
Œdema of the optic disc, as shown by obscuration of its outlines, with large and pale vessels, has been observed by Bouchut.
Veins closely connected with those within the cranium may be thrombosed, and felt as hard cords by the finger. This may occur in the facial veins about the orbit, in those around the mastoid, or in the jugulars. On the other hand, if one cavernous sinus is filled with a coagulum which does not go down into the jugular, this vein will naturally be empty or receive only a small amount of blood from other veins.
When the cavernous sinuses are affected, we are likely to have a set of phenomena due to the pressure of the clot upon the nerves which pass through it—i.e. the third and fourth, part of the fifth and sixth—with filaments of the sympathetic accompanying the carotid artery. Hence dilatation of the pupil, strabismus, or ptosis, and other ocular paralyses may be the symptoms observed.
It is possible that a headache upon the side of the affected sinus may be due to vascular dilatation from paralysis of the sympathetic, or to a direct pressure upon the first branch of the fifth pair.
DIAGNOSIS.—The diagnosis of venous thrombosis may be almost entirely a conjectural one in those cases where the cerebral symptoms are vague or mixed with others peculiar to the causative disease. Where wasting disease has existed, the patient is much emaciated, and profuse discharges have diminished the fluidity of the blood, the rapid supervention of coma with slight spasms or general convulsions will render it highly probably that thrombosis is taking place. Unilateral symptoms would greatly increase this probability, and if any accessible veins about the head, neck, or face could be definitely distinguished as filled with firm coagula, the diagnosis would approach certainty.
In cases of this kind the only condition likely to put on the appearance of thrombosis is the simple inanition or so-called hydro-encephaloid disease, which comes on in exactly the same sort of cases. Localized phenomena must be the chief point of difference. Fortunately, the distinction is practically not an important one.
In wounds of the vertex affecting the longitudinal sinus the question likely to arise where cerebral symptoms supervene is that of thrombosis or abscess. Here the more definite localization is likely to be upon the side of the abscess, although, as is well known, this may remain latent or nearly so for a considerable time, and in general is much more chronic in its course than thrombosis.
The swelling of the external veins, epistaxis, œdema of the lid, protrusion of the eyeball, with œdema of the optic papilla, with only moderate fever, would favor the diagnosis of thrombosis, while optic neuritis, if present, with chills, would render the abscess more probable. Unless the wound were sufficiently severe to fracture a piece of bone into the sinus, or unless the subsequent inflammation were of an unhealthy character, the abscess in a person of middle age and previous good health may be considered the more probable of the two. In the case of Dowse, already mentioned, the diagnosis between abscess and thrombus must have been very difficult, and, as it seems to the writer, would have been more likely to rest upon abscess or meningitis than upon the condition afterward found to exist.
Where inflammatory diseases exist which are known to lead to thrombosis with phlebitis, the practitioner, if on the lookout, can often make a diagnosis with a high degree of probability in its favor. The cerebral symptoms with the venous swelling, collateral inflammatory œdema in the more immediate neighborhood of the lesion, and slight œdema and congestion at more distant points, and a febrile movement indicating a distinct inflammatory exacerbation, will point very strongly to thrombo-phlebitis.
An absolute distinction between such a condition of the veins and a meningitis arising under exactly the same circumstances may not always be possible, and is the less important since the two affections are likely to coexist and form a part of the same disease.
The localization of the thrombus is to be determined partly by the paralytic symptoms, if such exist, but principally by the situation of the secondary œdema and from the lesion which forms the starting-point. It has been said that the jugular vein of the side on which thrombosis exists is less full; and this point might be of value when the lateral sinus is affected.
PROGNOSIS.—From the character of the lesion itself, as well as from the diseases with which thrombosis is usually connected, it will readily be seen that the prognosis is in general a highly unfavorable one; but it is possibly regarded as too inevitably so, for the reason that a positive diagnosis may be in slighter cases a matter of considerable uncertainty, so that the practitioner, even if attempting to make an accurate anatomical explanation of obscure cerebral symptoms, is as likely to think that he has been mistaken as that his patient has recovered from so serious a disease.
Cases, however, have been reported where the diagnosis seems as clear as it can be made without an autopsy, and recovery has taken place.
A case is reported by Voorman65 of a child aged six months who had diarrhœa and vomiting, much prostration, sunken fontanelles, overlapping cranial bones, trembling of the tongue, slight spasm of the right arm and leg, head drawn back, and strabismus. The head afterward increased in size, the temporal vein was swollen and hard, with œdema of the skin in its neighborhood. There was gradual improvement and recovery, though when the patient was four and a half years old its mental development corresponded to that of a child two years younger.
65 Centralb. f. d. Med. Wis., 1883.
In another, by Kolb,66 a child of seventeen, well nourished, had a purulent discharge from the right ear. Besides headache, delirium, hyperæsthesia, convulsions, and then sleepiness and loss of consciousness, the following symptoms pointed toward thrombosis of the sinuses: Chills, inflammatory swelling over the right mastoid, with fulness of a cutaneous vein passing over it; a purely œdematous swelling in the neighborhood of the internal jugular or temporal fossa, forehead, and both upper eyelids, with exophthalmos on the right side; photophobia, blepharospasm, and cloudy vision; nose-bleed. There was no elevation of temperature, and recovery took place.
66 Berl. klin. Woch., Nov. 13, 1876.
A case of thrombo-phlebitis following otitis and terminating in recovery is reported at length by Wreden.67
67 Archives of Ophth. and Otol., 1874, lii. (translation).
The PROGNOSIS in any particular case can be based only on the severity of the symptoms and on the character of the preceding disease.
TREATMENT.—The prophylaxis of this affection evidently consists in the proper treatment of the diseases upon which it depends, and might therefore be made to embrace nearly the whole range of tonic, roborant, antiphlogistic, and antiseptic measures, to say nothing of surgery and obstetrics. The proper nourishment of infants and children, the cutting short, when possible, of their acute diseases, or preventing their debilitating effects, will reduce marantic thrombosis to a minimum. At a later period of life the proper surgical management of carbuncle, abscess in the neck, and of the puerperal condition will tend to avoid this risk.
The most important point of all, however, is undoubtedly the careful treatment of otitis media and early attention to inflammation in the mastoid cells, with incision or trephining as may be necessary.
After a thrombus has formed there is little to be done toward its removal.
It has been claimed68 that the preparations of ammonia are capable of diminishing considerably the coagulability of the blood when it is morbidly augmented. Though this cannot be considered proved, yet since the tendency of these salts is also to quicken the blood-current, a trial in a case where other indications are wanting is, to say the least, justifiable.
68 Lidell, Am. Journ. Med. Sci., July, 1874, p. 101.
In a case reported by O'Hara,69 where the symptoms pointed very strongly toward thrombosis of the cavernous sinuses, recovery took place under mercurials, iodide of potassium, and purgatives. The reporter was inclined to consider the cause of trouble specific.
69 N. Y. Med. Record, vol. xvii. p. 617.
Considering the fact that cases with such marked and decisive symptoms as those last recorded have recovered, it is certainly the duty of the physician to prolong the life of his patient to the utmost, that absorption and condensation may go on as long as possible and collateral circulation be developed. Probably most physicians can recall cases of obscure cerebral disease going on to recovery contrary to all expectation, in which thrombosis furnishes an explanation quite as plausible as any other.
Softening of the Brain
is a name which it is yet too early to omit altogether from a systematic work, although in treating of it we have more to do with nomenclature and classification than with pathological anatomy. The phrase may be said to have both an anatomical and a clinical signification, which do not coincide at all points. Clinically and among the laity it is used to express various symptoms and groups of symptoms more or less referable to the brain, some of them connected with one and some with another lesion, and many purely functional—if the word may be used—or at any rate unconnected with any known or definite lesion.
Vertigo, dull headache, sleeplessness, or, on the other hand, drowsiness, failure of memory, failure of power of concentration, of steady application, mental depression, fatigue, and even slight aphasia or actual slight hemiplegia, may any of them be considered symptoms or forerunners of softening of the brain. As nearly as anything, the popular notion of this affection corresponds to general paralysis of the insane or senile dementia, or even mere exhaustion. Many of these symptoms may, of course, be connected with the real softening described as the result of embolism or thrombosis, but it is hardly necessary to say that a symptomatology based on these elements alone is either too vague or else too much like that of diseases already described to be considered useful as a separate clinical grouping.
On the anatomical side softening of the brain has had a definite meaning, and for many years a part of its pathology has been well known. A general softening of the whole brain, such as seems to be the condition supposed when the phrase is used, does not and cannot exist, since a vascular lesion sufficient to cause anæmic necrosis of the whole brain must cause death long before softening would have time to take place. Nearly all the works and reports on softening have been based upon cases such as are now referred to definite lesions of the blood-vessels; and a good idea of the change in nomenclature and pathological views may be obtained by noticing the dates given in the extensive literature of the subject in the Index Catalogue of the Surgeon-General's library, which are nearly all previous to 1860 or 1865.
Localized softening has already been described under the heads of hemorrhage, embolism, and thrombosis, venous and arterial. Whether it may occur from diseases of the cerebral vessels without actual occlusion is not certain, but, remembering the difficulty of detecting thrombi in minute vessels, and also the fact that it is not a great many years that occlusions have been systematically sought for at autopsies, it is better for the present to assume, in cases where softening is found in the usual form and the usual situations for the results of thrombosis and embolism, that one of these accidents is the cause, even if the actual point of occlusion is not found.
Softening may take place secondarily from tumors in the brain, and the name is also sometimes applied to a local encephalitis, which is an early stage of abscess. When, however, these various forms of disease are removed from the general heading of softening and referred to their proper pathological classes, there is a residuum in which the softening seems to be the primary affection, so far as the brain is concerned, though depending on other constitutional conditions.
In new-born infants softening of the brain, besides the rare cases in which it may be dependent on the same conditions which may cause it in the adult, is observed in two forms, as described by Parrot:70 A. White softening in multiple foci, dependent upon fatty degeneration, of which it constitutes the last stage, is found almost exclusively in the centres of the hemispheres. B. Red softening, which affects the same region, but more extensively, and is accompanied by hemorrhage into the lymphatic sheaths with rupture.
70 Arch. de Phys., 1873, p. 302.
These two forms may exist with each other, and with other intracranial lesions, such as thrombi of the sinuses and exudation under the arachnoid and around the veins.
Parrot compares this form of softening to that occurring in the other extreme of life, dependent on vascular lesions; but although he supposes the method of production to be unlike in the two cases, it is by no means so certain, either from his conclusions or his cases, that it is always so. In some of his cases the vessels are said not to be abnormal, but in others old thrombi are distinctly mentioned. As secondary consequences may be observed intracranial dropsy, with perhaps hydrocephalic cranium and degeneration of the pons, bulb, and medulla.
Two cases of red softening of the cerebellum have been reported.71 In one of them the pia was adherent, in the other thickened and covered with exudation. The microscopic details are not given nor the state of vessels mentioned. They are probably not strictly analogous to those described by Parrot.
71 Jahrbuch. f. Kinderheilkunde, 1877.
The occurrence of granular corpuscles in the brain of the new-born is described by Virchow, and it is thought by him to be pathological and of an irritative character (encephalitis congenita). It is somewhat doubtful if this process is characterized by any distinct symptoms.
The ETIOLOGY is impaired nutrition, deficient or improper feeding, and depressing diseases, frequently tubercle.
The SYMPTOMS and DIGNOSIS of this form of softening are even more obscure than those of venous thrombosis in the same class of cases. Vague cerebral symptoms arising in an infant poorly nourished and suffering from acute disease may be due to this condition, but a positive diagnosis is out of the question. In the two cases of softening of the cerebellum just mentioned, in one, aged five, there was dilatation of the pupil, difficulty of hearing, and vertigo; in the other, aged six, vertigo, inclination to vomit, and clonic spasm of the left facial muscles. Parrot says that in the greater number of patients the encephalopathic troubles observed during life cannot be referred to it (softening), and in no case can it be diagnosticated.
Under these circumstances it is obvious that remarks upon the PROGNOSIS and TREATMENT must be purely works of the imagination.
Atheroma of the Cerebral Arteries
has already been spoken of as one of the most important factors in thrombosis, and perhaps of considerable consequence in embolism and hemorrhage. Its symptoms, when one of these accidents has taken place, are hardly to be separately considered; and if atheroma have produced complete occlusion, even without the assistance of a clot, the symptoms could not be distinguished from those of an ordinary thrombosis, and would follow the same course.
In some cases, however, the thickening of the artery may interfere with, without completely interrupting, the circulation in the part to which it is distributed, and the degree of the interference may vary from time to time. If, then, in a person whose age and general physical condition, as shown by the state of the tangible arteries, arcus senilis, complexion, and so forth, render the existence of atheromatous arteries in the brain probable, cerebral symptoms of an ill-defined character arise, it is very probable that they are the result of irregularities in the circulation dependent on atheroma.
This state of things is to be distinguished from the more clearly marked conditions which have already been described, partly by the incompleteness of the attack, and partly by its changes in severity and character from time to time—a paralysis undergoing alternations of improvement and the reverse from day to day, delirium appearing and disappearing in correspondence with the general health, the vigor of the heart, and the state of the digestive organs.
The diagnosis between these incomplete anæmias and an almost precisely similar result of syphilitic endarteritis is to be made chiefly by the history and age. In middle-aged persons general paralysis might present a not very different set of phenomena. A tolerably distinct, but not severe, hemiplegia in an old person, subsiding in a few hours under the influence of a cathartic, and perhaps returning more than once, may often be due to a local and temporary anæmia from atheroma, as well as to slight hemorrhage or a not completely occluding thrombus.
On the other hand, extensive atheroma may exist without serious impairment of the cerebral functions, provided it be evenly distributed and do not interfere with the passage of blood in any one vessel.
The prophylaxis of atheroma has already been considered. We do not know of any drug that can change the nature or extent of the processes going on in the arterial walls, but if any influence can be exerted it is through dietetic and hygienic means.
The consequences of rigidity of the arterial walls, as productive of resistance to the passage of blood, can be warded off to some extent by promoting the vigor of the heart. Treatment should therefore be directed to the improvement of the nutrition of the body in general and the heart in particular. Heart tonics and laxatives are the classes of medicaments most likely to be useful. Perhaps it is to its effect in increasing the force of the heart contractions, like digitalis, that coffee owes its reputation as a preservative from apoplexy.