Chapter C: W. Dulles12 describes a case occurring in his own practice in a (2)

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.

{946} 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 Thompson[29] to be a somewhat frequent premonition. Vomiting is hardly a premonitory, but may be an initial, symptom, especially in hemorrhage of the cerebellum.

[Footnote 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 {947} tendency to cause a still further deposition—that is, a secondary thrombus—which may progress until it comes to a place where the blood-current is too strong for the process to go on any farther. It may in such cases not be obvious at the first glance whether the whole process is thrombosis or whether it started from an embolus.

[Footnote 30: The Greek word _εμβολος_ (_εν_, in, and _βαλλω_, to throw) signifies the beak or rostrum of a ship of war. _Εμβολον_ signifies wedge or stopper, and would certainly seem the appropriate form to be adopted for anatomical purposes. As uniformity of nomenclature, however, seems more to be desired than etymological accuracy, the writer has conformed in this article to the general usage.]

It is probable that a thrombus forming at one point in a cerebral vessel may break to pieces and its fragments be carried farther along, forming a number of small emboli. (See Capillary Embolism.) Embolism or thrombosis may take place anywhere in the brain or body generally, but has certain points of preference. Of these, the most usual in the brain is in the neighborhood where the internal carotid divides into the anterior and middle cerebral, or in either of these arteries, especially the middle, beyond this point. The plug may be situated in the carotid just before this point, or even as low down as its origin from the common trunk. Emboli lodge in this region, somewhat more often upon the left side. The brain is said to be third in the order of frequency with which the different organs are affected by embolism, the kidneys and spleen preceding it. It has been found that small emboli experimentally introduced into the carotids are found in much larger numbers in the middle cerebral than elsewhere. It is the largest branch, and most nearly in the direct line of the carotid. Position undoubtedly influences the point at which an embolus lodges, as it probably moves slowly along the vessels and along their lower side. It has been remarked that, on account of this course of the embolus, it is doubtful whether it can get into the carotid when the patient is standing, but it certainly can do so when he is sitting up; which, so far as the direction of the carotids is concerned, is the same thing. The frequency with which a hemiplegia is observed when a patient awakes in the morning may perhaps be accounted for by the position favoring the passage of an embolus into the carotid, which otherwise would reach organs more remote.

The vertebrals and basilar are not infrequently affected.

The sources whence cerebral emboli may spring are various, but cannot be found outside a certain range. They may, in the first place, be torn off from vegetations upon either the mitral or aortic valves; and this source is probably the most common. The appendix of the left auricle may furnish a plug from the thrombi formed among its trabeculæ, or the aorta from an aneurism or from parietal thrombi formed, upon spots roughened by atheroma. The pulmonary veins are occasionally the source of the embolus, though this is not very common.

It is rather doubtful whether an embolus can find its way from the systemic veins through the lungs to the brain, but it is possible that small emboli may do so, and increase in size from the addition of fresh fibrin when floating in the blood-current. The occurrence of pyæmic abscesses in the brain would suggest the possibility of this, though it is, on the other hand, possible that the brain abscesses are secondary to older ones in the lungs. In some cases, however, a careful examination does not disclose the source of the embolus.

In the blood-current the embolus may give rise to no symptoms whatever, and even after its arrival in the cerebral circulation it may lodge in such a way as not entirely to obstruct the current. In most instances, however, it does not stop until it plugs the vessel completely and arrests {948} the current of blood beyond it for a moment. Whether it shall completely deprive the portion of brain to which it is distributed depends upon its situation as regards anastomoses and upon the formation of secondary thrombus. Hence the knowledge of the distribution of the arteries supplying the brain—that is, the two carotids and two vertebrals—is of more importance in reference to embolism and thrombosis than to cerebral hemorrhage, where the effusion takes place from quite small branches.

The anterior portion of the brain, including the anterior and posterior central convolutions and the first temporal, are supplied with blood by the two terminal branches of the internal carotid, the anterior and middle cerebral, the ganglia underlying these portions of the cortex being supplied, as already stated, by small branches arising near the origin of these two trunks, and principally the second. The anterior cerebrals of the two sides are connected by the anterior communicating, which is a short and usually wide vessel. Sometimes one anterior cerebral branches in the longitudinal fissure, and supplies a part of both sides. Hence in plugging of one internal carotid which does not reach its bifurcation a collateral supply may be received from the other side. If, however, an embolus or thrombus has penetrated beyond the origin of the middle cerebral, this vessel can no longer receive a supply from the anterior.

The posterior communicating arteries are two small vessels which connect on each side the posterior cerebrals and either the carotid, just as it gives off its two chief cerebral branches, or else the middle cerebral close to its origin. These arteries may be of quite unequal size, that upon the right usually being the larger, and sometimes so large as to give the appearance of being the principal origin of the posterior cerebral. When this happens the part of the posterior cerebral which arises from the basilar may be reduced to a minute arteriole, and the basilar, almost entire, goes to supply the left side of the brain. This condition of the posterior communicating may exist to some extent on both sides in the same brain. It is probable that in many cases these arteries are too small to be of great value in re-establishing the circulation in the anterior portion of the brain when it is suddenly interrupted by an embolus.

When the large trunks leave the circle of Willis to be distributed upon the surface of the brain, after giving off from the first centimeter or two of their course the nutrient arteries for the deep-seated ganglia, they break up into several branches which ramify upon the surface, but, as Duret has shown, undergo very few anastomoses. Instead of forming, as was once supposed, a richly inosculating network, small branches penetrate into the brain-substance perpendicularly from the superficial vessels, but these do not communicate freely with each other by vessels larger than capillaries.

From these anatomical conditions it happens that when a vascular territory is deprived of its normal supply by an embolus, it cannot be supplied with blood from surrounding districts. A certain limited amount of collateral supply is possible through the capillaries and the rare anastomoses, but it is only around the edges, and the centre of the territory becomes destitute of circulating blood. Thus an embolus does not in the brain produce, as it does in other organs with more abundant collateral supply, a large hemorrhagic infarction.

{949} Small hemorrhages may, however, take place around the edges of the softening, and when a number of small emboli are present, so as to afford a number of overlapping areas with their borders of congestion, a red softening may be the result. When the emboli are very small, and at the same time not numerous enough to occlude all the ultimate ramifications of a trunk, the vascular compensation may be rapidly completed.

The change produced in the cerebral substance from cutting off its supply of blood is known as anæmic necrosis, and includes what has been known as white softening, with probably some yellow, and possibly a little red softening, the latter in case where simple softening has been complicated by hemorrhage.

When the circulation ceases the substance that should have been nourished loses its firmness and acquires a custard-like consistency. The gray and white substances are no longer so distinct in appearance, the latter losing its milky-white color, the whole surface of a section becoming of a dirty yellowish-white, somewhat shining, and looking as if it contained more moisture than normal. When a considerable portion of the interior of the hemisphere is thus affected, the brain outside, with its membranes, bags down, looks swollen, and feels to the fingers as if there were present a sacful of fluid. The boundaries of such an area of softening are marked off from the healthy substance with some distinctness, though less than that of a hemorrhage. There may be some hemorrhage around the edges or into the cavity, so that the presence of a little blood-pigment is no proof that the original lesion was not softening from occlusion. In the further progress the contents of the cavity become more fluid, and finally a somewhat distinct cyst is formed, not unlike that from a hemorrhage, with an internal areolar structure from the remains of connective tissue, and contents of a slightly yellowish or brownish color, or often of a chalky white. These cysts have little to distinguish them, when old, from similar ones left by hemorrhage, except the much greater amount of pigment in the latter. The smaller spots of softening may after a time lose their fluidity, and remain as yellowish patches as firm as, or firmer than, the surrounding brain. The region of the brain involved becomes atrophied, the convolutions shrink, and the membranes become filled with serous fluid, to compensate for the sinking of the surface.

The microscope shows gradually increasing fatty degeneration, disorganization of the nervous tissue, and degeneration of its elements. The pyramidal cells are sometimes distinctly recognizable by their form, and show gradual transition into the indeterminate round granulation-corpuscles. The vessels exhibit fatty degeneration of their coats, as well as accumulation of fatty granules between the vessel and the lymphatic sheath. The clot which blocks the artery becomes adherent to its walls, and the vessel with its contents forms a round solid cord.

In a few instances the thrombi have become perforated through the centre, so that a channel is formed for a renewal of the circulation. There is no reason to suppose that this takes place soon enough to be of any advantage in restoring the nutrition of the necrosed portions of brain.

The region involved in softening depends upon the artery which is plugged and the location of the obstructing body. The place of election seems to be the carotid near its separation into its large branches, or these {950} branches after the separation, especially the middle cerebral, this being peculiarly liable because it is the largest branch and is the continuation in a direct line of the carotid. It is more frequent upon the left side. Cases have been observed where the whole of one hemisphere was softened from obstruction of the carotid at its bifurcation; which may be accounted for, as Charcot suggests, by an unusual distribution of the arteries, as described above, the posterior cerebral as well as the other two being derived almost entirely from the carotid. In a case recently observed by the writer the whole right cerebral hemisphere, with the exception of the tip of the frontal and tip of the occipital lobes, was softened to the consistency of custard, a thrombus extending from the bifurcation of the common carotid into all the ramifications of the middle cerebral. The most common form, however, is where more or less of the brain around the fissure of Rolando and fissure of Sylvius, with or without the underlying ganglia, is softened. This happens from a lodgment of the embolus in the middle cerebral. If the obstruction be close to the origin of the artery, the corpus striatum suffers, from the mouths of its small nutrient arteries arising in this part of its course being stopped, while if it have passed along a little farther, these remain open, and the cortex, to which the larger branches are distributed, alone is softened.

The anterior cerebral is not infrequently affected, either alone or with the middle, and in these arteries as well as the posterior the embolus, if of small size originally, may penetrate so far as to give rise only to quite a limited anæmia. The basilar is an artery not very rarely occluded, though more commonly by thrombus than embolus. This occlusion may be so limited as to affect only the nutrient arteries of the pons and cause a very limited softening, the parts before and behind it being supplied by the unobstructed portion or by collateral circulation from the carotids. Occlusion of the cerebellar arteries and softening of the cerebellum are among the rarer forms. The vertebrals themselves are sometimes plugged. A thrombosis has been observed in the only inferior cerebellar artery which existed, causing softening in both lobes. There was atheroma of the heart and arteries, and a thick calcareous plate in that which was occluded.[31]

[Footnote 31: _Progrès méd._, 1876, 373.]

In a general way, it may be said, with many exceptions on both sides, that thrombosis and embolism tend to affect the cortex, and hemorrhage the central ganglia.

What has just been written applies to the simple mechanical action of emboli. If, however, they have a septic origin, as notably in cases of ulcerative endocarditis, the region in which they lodge becomes, instead of a simple spot of necrosis, a septic focus or abscess, with its results of compression or irritation. In such a case there are likely to be abscesses of similar origin in other organs, and the cerebral lesion is only a part of the general pyæmic condition.

ETIOLOGY.—So far as the lodgment of an embolus in an artery is concerned, it can hardly be said that there is any etiology, for the detachment of the plug from its place of origin is purely a matter of accident, and may take place at any time. As to its origin in the form of fibrinous deposit on the valves of the heart or a roughened spot on the aorta, we must refer to the article on General Pathology. The most important {951} condition for embolism is disease of the valves of the heart, rheumatic or otherwise. Next comes arterial disease, producing roughening of the inner coat and subsequent deposition of fibrin. So far as we can tell, the causes leading to endarteritis or atheroma are essentially the same as those which produce the periarteritis described in connection with cerebral hemorrhage, and we may therefore put down old age, alcohol, and strain as among the causes of cerebral embolism. Injuries of the lungs leading to thrombosis of the veins may be considered as possible sources for the formation of an embolus, and we might suppose that phthisis and pneumonia would furnish plugs which would lodge in the brain, though as a matter of fact they seldom do so.

Experience shows that embolism, unlike hemorrhage, is not specially a disease of advanced life, but is distributed over different periods, with preference for old age less marked than with hemorrhage. Andral gives the ages of patients with softening—which, however, includes thrombosis as well as embolism—as follows: the average would undoubtedly be displaced in the direction of youth if thrombosis could be taken out of the list:

-----------------+-------------------+------------------------
Andral: | Andral: | Cases (with autopsies)
Beginning of | Death with | of embolism,
softening in 27 | softening in 153 | thrombosis, and
cases. | cases. | softening—25 cases.
-----------------+-------------------+------------------------
17-20 4 | 15-20 10 | 20-30 4
27 2 | 20-30 18 | 30-40 3
30-37 2 | 30-40 11 | 40-50 3
43-45 2 | 40-50 19 | 50-60 1
53-59 4 | 50-60 27 | 60-70 5
63-69 7 | 60-70 34 | 70-80 2
76-78 6 | 70-80 30 | Young 1
| 80-89 4 | Middle-aged 1
| | Old 5
-----------------+-------------------+------------------------

In the etiology of cerebral arterial thrombus there seem to be two factors of prime importance, although there are cases which seem to demand a third, and Charcot[32] suggests the possibility of some hæmic dyscrasia favoring the formation of a thrombus, and relates a case of thrombosis of the middle cerebral, with three others of the same process in other arteries, occurring in patients with uterine cancer, where all the usual sources of emboli were explored with negative results. The first of the two is disease of the cerebral arteries, not necessarily extensive, but sufficient to form a starting-point on the inner wall for the deposit of fibrin. In this respect the etiology of thrombosis may be various. Syphilitic endarteritis, for instance, may very easily give rise to this lesion, but it is likely to be accompanied by others, and has a symptomatology more or less peculiar to itself. It is not, of course, to be included with the form we are considering.

[Footnote 32: _Comptes Rendus Soc. de Biol._, 1865, p. 24.]

The second factor—one which is perhaps capable of giving rise to coagulation of the blood or deposit of fibrin without any arterial disease—is weakness of the heart, connected or not with anæmia. The causes of this condition may be manifold, and are likely to lead to many other consequences than cerebral thrombosis. A thrombus may form upon a very small basis of atheroma. Several of these points are illustrated in the {952} following case: A lady, aged about sixty-five, had had for many months vague symptoms of want of strength, fatigue, want of appetite, and so on, with complaints of distress and fulness in the abdomen, for which no special cause could be found. On one occasion she was unusually long in dressing, and her expression was noticed to be changed and her voice altered for a few moments. The pulse was habitually 60 or less, and at times irregular, but nothing abnormal could be detected in the sounds or position of the heart. Fatty degeneration was suspected. One morning, after going to bed in her usual health, she was found on the floor of her room unconscious and with left hemiplegia. She lived about thirty-six hours. The autopsy showed nothing abnormal in the abdomen except a considerable accumulation of fat; and in the thorax the heart appeared normal, and was not fatty. There was very little atheroma. In the end of the internal carotid artery was a thrombus, of which the lower and firmest part was connected with a very small spot of roughening just at the point where the artery comes through the base of the skull. It extended just beyond the origin of the middle cerebral artery, which was of course occluded. The corresponding region of the brain was converted into a vast mass of softened tissue.

The SYMPTOMS of the lodgment of an embolus in the brain may closely resemble, or even be precisely the same as, those of hemorrhage. Unless, however, an embolus makes a pause on its journey, giving rise to a partial obstruction before there is a complete one, or unless the obstruction is not absolute until after the formation of a secondary thrombus, the attack may be absolutely sudden.

A thrombus, however, is slower in its formation, and may produce gradually increasing anæmia of the region of brain supplied before it is absolutely complete, with a gradually increasing paralysis and loss of consciousness slowly approaching. Thus we may have the early symptoms in the form of headache, vertigo, heaviness, and drowsiness, peculiar sensations in the limbs about to be paralyzed or in the head, delirium of various kinds, or hysterical manifestations. Prévost and Cotard[33] lay special stress upon the importance of severe vertigo (étourdissement) as a prodrome or warning of softening, especially in the aged. It is dependent upon anæmia of the brain, and this, in its turn, upon atheroma of the arteries, and sometimes at least upon feebleness of the circulation, both of these being conditions likely to cause the deposit of a thrombus. As, however, the thrombus does not necessarily result from these conditions, and as the vertigo may arise from other sources, as stated under the head of Cerebral Hemorrhage, it is to be looked upon with special suspicion chiefly in those cases where other symptoms might lead in the same direction, and when other causes can be excluded.

[Footnote 33: _Mémoires de la Soc. de Biol._, 1865, p. 171.]

The same authors also speak of less defined symptoms, like delirium and stupor, occurring among the inhabitants of the Salpêtrière (old women), with intervals of comparative health, as being premonitory.

It is possible, however, for the symptoms of thrombus to be developed rapidly when, as in the case last described, the thrombus begins to form in a place which does not entirely interrupt the current, but afterward reached the mouth of a large vessel, which it closes.

The loss of consciousness, coma, and all the phenomena of the {953} apoplectic attack, with the possible exception of early rigidity, may be as fully developed from occlusion of the cerebral vessels as from their rupture; but it must be said that it is more common to meet with them in cases of large hemorrhage than with either embolism or thrombosis.

The general functions are even less disturbed than with a hemorrhage producing an equal extent of paralysis. The temperature follows nearly the same course as in hemorrhage, except that the initial fall, if present—which is not always the case—is said to be less than with cerebral hemorrhage. To this succeeds a rapid rise, which, even in cases which are to terminate fatally, gives place to a fall to the neighborhood of normal, and another rise before death. These are the statements of Bourneville. The rise is said not to be so high as with hemorrhage.

The annexed chart is from a man (W. I. W.) who was in the hospital with ill-defined nervous symptoms, and was suddenly attacked with convulsions, vomiting, and unconsciousness. He had a small tumor at the point of the right temporal lobe, and softening of the left corpus striatum. The apoplectic symptoms occurred on the 15th—that is, as will be seen by the chart, one day after the temperature began to rise. The pulse and respiration show no characteristic changes.

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 {954} 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.

{955} 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. Tripier[34] 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.

[Footnote 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 {956} 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 recorded[36] 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.

[Footnote 35: Conty, _Centralblatt f. d. Med. Wiss._, 1878, 571.]

[Footnote 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, {957} 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.

[Footnote 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 {958} 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.

[Footnote 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 {959} 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. Ball[40] 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.

[Footnote 39: _Brit. Med. Journ._, Aug. 28, 1880.]

[Footnote 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]

[Footnote 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 {960} (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.

[Footnote 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.

[Footnote 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]

[Footnote 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 {961} 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.

[Footnote 45: _Gaz. hébd._, 1867.]