Volume 5 — DISEASES OF THE NERVOUS SYSTEM. (continued 33)

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.

ATROPHY AND HYPERTROPHY OF THE BRAIN.

BY H. D. SCHMIDT, M.D.

ATROPHY OF THE BRAIN.

INTRODUCTION AND DEFINITION.—Atrophy of the brain may originate during intra-uterine life or by defective development during the early periods of childhood, or it may occur during adult life, when the organ is fully developed. The atrophy is characterized by a diminution of the normal bulk of the brain-substance, in consequence of which the latter does not entirely fill the cavity of the cranium, but leaves a greater or less space to be occupied by a serous fluid. Generally, the atrophy affects, in a symmetrical or asymmetrical manner, larger or smaller portions of the brain; an atrophy symmetrically affecting all parts of the brain has never been observed, even in microcephalia. Nevertheless, when the atrophy affects both hemispheres of the cerebrum, it is generally called total, whilst it is designated partial when it is limited to only one hemisphere or to other individual parts of the brain, such as the cerebellum, the large cerebral ganglia, etc.

For the sake of convenience we shall treat the atrophy of the brain occurring during childhood, when the organ is still developing, separately from that of the fully-developed brain of the adult.

1. Atrophy of the Brain during Childhood.

When congenital or originating during infancy the atrophy is either primarily due to certain pathological processes taking place in the substance of the brain, or secondary, being due to lesions of the skull, such as premature ossification of the sutures. Total atrophy of the brain at this period of life leads to an early death, while children affected with partial atrophy may continue to live, though almost always in a state of idiocy. The forms mostly observed in children are unilateral or bilateral atrophy of the cerebrum, partial or almost entire absence of the cerebellum, imperfect development of the large cerebral ganglia, and slight partial atrophy of the medulla oblongata. The large commissures as well as the crura cerebri are very seldom found atrophied.

The most frequent and, from a practical point of view, the most important of these forms is the unilateral atrophy of the cerebrum, for the reason that in a mild form it is to a certain degree consistent with the mental and physical development of the child. It is mostly found on the left side. In some cases the atrophy extends evenly throughout the hemisphere, while in others it affects more or less one or the other lobe. The loss in the bulk of the hemisphere may amount to only a slight diminution, or to as much as to one-half of the normal size. Its thickness above the ventricle may be reduced to a few millimeters; in some cases even the membranes of the brain may lie in contact with the ependyma. The ventricle of the atrophied hemisphere is almost always enlarged. The convolutions of the cerebrum are very narrow, sometimes quite indistinct. One or both of the corpora striata also are generally found atrophied. In many cases even the atrophy extends to one of the crura cerebri and to the pyramid of the same side, and to the anterior and lateral columns of the spinal cord on the opposite side. Frequently, one or the other lateral half of the cerebellum also is found affected. The condition of the substance of the cerebrum is nearly the same as in the senile atrophy of the brain to be described hereafter. The skull is mostly thickened on the side of the atrophy, and frequently asymmetrical.

SYMPTOMS.—In most cases the mental capacity is below the normal standard, and frequently borders on or represents a state of idiocy. The temperament of the patient is generally irritable and very excitable. The most prominent symptom is an incomplete paralysis on the side opposite to the atrophied hemisphere, which is the more pronounced the more the corpus striatum, thalamus opticus, and crus cerebri are involved. Frequently, there are contractures of the flexor and pronator muscles of both extremities, particularly of the upper; the muscles of the trunk remain free; sometimes one or the other half of the face is also paralyzed. Epileptic convulsions also are frequently present. Blindness and deafness, with a defective sense of smell and a blunted sensibility of the paralyzed limbs, as well as neuralgia of the latter, and headache, have also been observed.

CAUSES.—Besides the causes already mentioned, atrophy of the brain occurring in children after birth may be induced by injuries of the head, inflammation of the enveloping membranes, of the ependyma, or of the substance of the brain itself.

TREATMENT.—Atrophy of the brain in children is perhaps, in the majority of cases, incurable; it is therefore only in the milder cases that the patient may be benefited by treatment. Electricity and gymnastic exercises have been recommended. At any rate, it must be pursued in a very systematic manner, and based upon the principles established and practised by the late E. Seguin of New York in his Physiological School for Weak-minded Children, consisting in improving the mind, first by training the child to the use of his limbs by means of light mechanical work, etc.

2. Atrophy of the Fully-developed Brain.

In the brain of the adult the atrophy may be partial or total, symmetrical or asymmetrical, in the same sense as before used in connection with the atrophy of the brain of children. It may, further, be stationary, when the atrophying process remains limited to the part where it originated; or, progressive, when it extends to other parts of the brain. Generally, partial, asymmetrical, and stationary atrophy is due to certain accidental pathological processes, producing a destruction or loss of portions of the substance of the brain, such as apoplexy, softening, etc., by which the nutrition of the neighboring parts becomes disturbed. Total, symmetrical, and progressive atrophy, on the other hand, actually depends upon certain constitutional disturbances of the nutritive process in general, such as chronic alcoholic intoxication, etc.

CAUSES.—As already mentioned, the causes of atrophy of the brain in the adult may be direct or indirect. The former are generally represented by certain pathological processes which directly affect the substance of the brain, as, for instance, apoplectic hemorrhagic effusions into the brain-substance, thrombosis or embolism of the cerebral arteries, encephalitis, chronic serous effusions into the ventricles, inflammation and œdema of the pia mater, etc. To the latter or indirect causes, which affect the organ by disturbing or lowering the nutrition of its substance, belong the retrogressive processes of old age or of insanity; the introduction into the system of certain noxious substances, such as lead or alcohol; furthermore, certain wasting diseases, such as phthisis, Bright's disease, etc.

PATHOLOGICAL ANATOMY.—The cerebrum particularly is found diminished in volume. While the convolutions are thinner than normal, their intervening sulci are broader. The white substance presents a dirty-white color, and is abnormally dense and tough, especially near the ventricles. The latter are enlarged and filled with serum; their ependyma is thickened and frequently covered with granulations. The cortical layer appears of a dirty, rusty-brown or yellow color, is pale, soft, or hard, and frequently is found to adhere to the pia mater. In very pronounced cases the white substance is almost as tough as leather, and contracts upon section, especially in the convolutions; its cut surface is rendered concave. Sometimes the surface of the convolutions, after the removal of the pia mater, appears finely shrivelled. The dura mater is often found thickened and adhering to the skull. The space created in the cavity of the cranium by the atrophy of the brain is filled by serous effusions into the tissue of the pia mater, the subarachnoidal space, arachnoid sac, and ventricles.

The histological changes associated with atrophy of the brain differ in the different forms. In cases of partial atrophy caused by hemorrhages, etc. the destructive process generally embraces all the tissues at first, while the secondary degenerations particularly affect the nervous elements. In total atrophy the pathological process appears to commence in the connective tissue, and to involve the nervous elements subsequently; though in a number of cases, especially of senile atrophy, the nervous elements appear to be primarily affected. The blood-vessels also undergo certain changes, giving rise to the contraction of the brain-substance.

SYMPTOMS.—In partial atrophy of the brain the primary symptoms resemble those which characterize the particular destructive process to which the atrophy is due. The most prominent are the symptoms of motor disturbance, which are always semilateral and correspond to the extent and seat of the lesion; frequently they remain stationary. The sensibility of the paralyzed parts is but slightly diminished, and the mind generally undisturbed. But when the effects of the original lesion extend, in the form of a secondary degeneration of the nervous elements, to neighboring parts, or even to the other hemisphere, the cerebral functions may become secondarily disturbed.

In senile atrophy of the brain, which represents the most simple form of total atrophy of this organ, the first symptoms frequently appear toward the end of some intercurrent disease. They consist in a very slow and gradually increasing derangement of the cerebral functions, associated with a general loss of innervation, manifesting itself by talkative wanderings of the mind, restless sleep, hallucinations, foolish activity, attacks of tremor senilis, etc. The intellectual functions diminish and the memory is lost. The physical forces also gradually sink, the tremor senilis increases, and the patient, no more able to walk, becomes confined to bed. Finally, a relaxation of the sphincters takes place, and death is produced by the disturbance of the automatic functions of deglutition and respiration.

Total atrophy of the brain, when due to an extensive meningitis or to a general disturbance of the nutrition, as is met with in drunkards, may finally lead to a condition known as general paralysis of the insane. This disease, however, will be found treated elsewhere in this work.

TREATMENT.—There is no special treatment for atrophy of the brain; all that can be done is to palliate and combat the symptoms as they arise.

HYPERTROPHY OF THE BRAIN.

INTRODUCTION.—Notwithstanding the numerous measurings and weighings of human brains made in the course of time by different investigators, no absolute standard measure or weight has as yet been established by which we can accurately determine a pathological increase or decrease in the size and weight of this organ. The want of such a standard is principally due to the difference generally existing in the dimensions and weights of even a certain number of brains taken from individuals belonging to the same race or nation. The same difficulties are met with in the attempt at establishing a rule by which to measure the mental capacity of a certain brain, for the question has as yet not been solved whether this capacity depends upon the quantity or quality of the brain-substance. In speaking of hypertrophy of the brain, therefore, we must keep in mind that a large brain must not be considered hypertrophied unless there exists a disproportion between its size and that of the cavity from which it was removed; in other words, when its growth or hypertrophy meets a resistance at the inner walls of the cranial cavity. According to Virchow, a further distinction must be made between the increase (hyperplasia) of the nervous elements themselves and that of the supporting connective tissue, the neuroglia. To the latter condition particularly corresponds the peculiar doughy consistence of the white substance of hypertrophied brains.

ETIOLOGY.—Hypertrophy of the brain is sometimes congenital, and then associated with dwarfishness and a defective development of the cranium. Generally, however, it is an extra-uterine affection, originating mostly during infancy and childhood, though it is also met with at the age of puberty, and even in adult life. The male sex is more predisposed to the affection than the female. When hypertrophy of the brain occurs during infancy, it is almost always associated with an excessive development of the lymphatic glands, with a defective involution of the thymus gland, and with rachitis, but generally without cachexia. No special exciting cause can be assigned to the affection during youth or adult age, though it has been stated that during these periods of life the disease may supervene upon tubercle or carcinoma of the brain. Repeated active or passive congestion (Rokitanski, Andral), as well as the introduction of lead into the system, has also been supposed to incite the disease.

PATHOLOGICAL ANATOMY.—Directly after the removal of the vault of the cranium, and on cutting through the dura mater, the brain, as if liberated from pressure, is observed to swell out to such a degree as to render the replacement of the removed skull-cap impossible. The enveloping membranes are found closely adapted to one another and to the brain; they are very thin, bloodless, and dry, and their vessels are empty and pressed flat. The hemispheres of the cerebrum are large, and their convolutions, mutually pressing against one another, are flattened at their surfaces, so that the intervening sulci are hardly recognizable. After the removal of the brain from the skull the abnormal dimensions of the cerebrum present a remarkable contrast to the normal size of the cerebellum, pons, and medulla oblongata, which also appear flat and broad from pressure. When a horizontal section is made through the hemispheres of the cerebrum and a little above the corpus callosum, the centrum ovale appears unusually large. The cavities of the ventricles are very narrow, their walls touching one another. There is no serum in the pia mater or in the ventricles. The substance of the brain is pale, bloodless, and dry. The white substance, upon which the hypertrophy particularly depends, is of a doughy consistence, comparable to the boiled white of an egg or cheese, whilst the gray substance is so pale as to be hardly distinguishable from the former.

The condition of the skull is, according to Rokitanski,¹ as follows: In cases in which the hypertrophy of the brain has advanced to a high degree, and in which the sutures of the skull are united, the bones of the cranium are found thinner and their inner table roughened by absorption. This is especially the case in the bones which form the vault of the cranium. The holes or other deficiencies found at the base of the cranium in the plates of the frontal, ethmoid, and sphenoid bones are not entirely due to the absorbing process, but rather to the thinness of these bones. In infants the cavity of the cranium enlarges in proportion to the hypertrophy of its contents; the head then resembles in form so much that of hydrocephalus that it may lead to errors in diagnosis. In some cases in which the disease rapidly develops to a high degree there is observed on the infant's skull a loosening and separation of the sutures of the cranial vault, with red coloration and suffusion of their cartilages.

¹ Lehrbuch der Pathologischen Anatomie, 3d ed., 1855, vol. ii. p. 431.

SYMPTOMS.—There is a gradually increasing muscular weakness, manifesting itself especially in the lower extremities, and giving rise to an unsteady, stumbling gait and frequent falling, caused perhaps by the excessive weight of the head, and also an inability of securely grasping objects. Besides these disturbances of motion, epileptic spasms appear, at first light in degree and at long intervals, but becoming later on in the course of the disease more frequent and severe. Continuous or intermittent attacks of headache almost always accompany the disease, and, furthermore, vertigo, tinnitus aurium, photophobia, and dimness of sight with dilatation of the pupil; general sensation also becomes blunted, but without ever amounting to anæsthesia. In a number of cases there is no disturbance of the psychical functions, though in others symptoms of mental excitement amounting even to delirium have been observed. Most frequently the intelligence sinks from the beginning of the disease, to end in complete idiocy. The pulse also has been observed to fall considerably during the last stage.

The COURSE of the disease is, according to Andral and Hasse,² almost always chronic, and if an acute development of the affection has been spoken of, it may be supposed that the latter has commenced a considerable time previous to the manifestation of the symptoms during the last stage. Andral divides the disease into two stages, of which the first is chronic and frequently latent, whilst the other is more acute and leads to a rapid fatal termination. In most cases death is caused by such intercurrent affections as give rise to irritation and hyperæmia of the brain, and thus increase the already abnormal pressure upon this organ.

² “Krankheiten des Nervensystems,” 2d ed., 1869, in Handbuch der Speciellen Pathologie und Therapie, edited by R. Virchow, vol. iv. 1st div., p. 578.

DIAGNOSIS, PROGNOSIS, AND TREATMENT.—It has already been mentioned that errors in diagnosis may very easily be committed on account of the great resemblance in the form of the head in cases of hypertrophy of the brain and of hydrocephalus, though it has been stated that in the former affection convulsions, in the form of epileptic spasms, predominate, to be followed during the last stage by symptoms of depression; whilst in hydrocephalus the symptoms of depression manifest themselves from the beginning of the disease, and, moreover, the rachitic deformities are more prominently shown in the form of a chicken-breast. A positive diagnosis can only be made by the autopsy.

There are no remarks to be made on the prognosis and treatment of hypertrophy of the brain.

SYPHILITIC AFFECTIONS OF THE NERVE-CENTRES.

BY H. C. WOOD, M.D., LL.D.

Introduction.

Syphilitic affections of the nerve-centres are best studied by separating those of the spinal cord from those of the cerebrum, and in the present article this natural division of the subject is adopted. Further, cerebral syphilis in its most characteristic or gummatous form usually attacks the brain-membranes, or perhaps in some cases the perivascular sheaths of the vessels, and only secondarily affects the tissue of the brain itself. The question of the occurrence of specific disease of the brain-cortex is so important that it shall have a separate discussion. It is perfectly well proven that with or without other brain lesion the vessels of the brain may undergo an atheromatous degeneration as the direct result of a syphilitic dyscrasia; but such disease links itself on the one hand with the subject of syphilitic disease of the general vascular system, and on the other hand with cerebral apoplexies, softenings, and other degenerations. Moreover, the space here allotted to brain syphilis is very insufficient. I, therefore, shall not enter upon the further discussion of syphilitic degeneration of the brain-vessels. The etiology of brain and spinal syphilis is best discussed under one heading.

GENERAL ETIOLOGY.—We do not know why in any individual case syphilis selects one portion of the nervous centres rather than another for attack; indeed, it is only rarely that any exciting cause can be discovered.

It is not unnatural to expect that any agency which is capable of exciting an inflammation of a nerve-centre may, when present in a syphilitic person, provoke a specific disease of such centre. Thus, thermic fever is a very common cause of chronic meningitis, and in the Journ. de Méd. et Chir. (Paris, 1879, p. 191) a case is reported in which cerebral syphilis followed a sunstroke; I have myself seen one similar instance, and in Roberts's case of precocious cerebral syphilis (see p. 804) the first convulsion came whilst the man was fishing on a very hot day, and may have been precipitated by the exposure.

Blows and other traumatisms would be expected to figure largely as exciting causes of nervous syphilis, but they, in fact, are only rarely present. I have seen one or two cases of specific brain disease attributed to violence by the patient, and several cases of possibly specific spinal disease—one in which a poliomyelitis followed a fall on the ice; one in which, after a fall from a cart and marked spinal concussion, a local myelitis developed;¹ and one of a general myelitis following an injury by a horse. The only records of such cases are those of Broadbent² and those collected by Heubner.³

¹ Univers. Hosp. Dispen. Service-Book, x., 1875, p. 58.

² Lond. Lancet, 1876, ii. p. 741.

³ Ziemssen's Encyclopædia, xii. 301.

Various authorities attach much influence to over-study and other forms of cerebral strain in exciting brain syphilis. Engelstedt is stated to have reported cases having such etiological relations, and Fournier⁴ affirms that he has especially seen the disease in professional men and other persons habitually exercising their brains to excess. Neither in private nor public practice have I met with an instance where over-brainwork could be considered a distinct etiological factor, whilst I have seen some hundreds of cases from amongst the laboring classes, in whom the intellectual faculties are chiefly dormant.

⁴ La Syphilis du Cerveau.

The drift of the evidence in medical literature is so pronounced, and so in accord with my own experience, that I believe it may be positively affirmed that in the vast majority of cases of nervous syphilis no exciting cause can be found.

Inherited syphilis seems to be less prone than the acquired diathesis to attack the nervous system, but is certainly capable of so acting. As early as 1779, Joseph Glenck⁵ reported a case of a girl, six years old, cured by a mercurial course of an epilepsy of three years' standing and of other manifestations of hereditary syphilis. Graefe found gummatous tumors in the cerebrum of a child nearly two years old.⁶ O. Huebner⁷ details the occurrence of pachymeningitis hæmorrhagica in a syphilitic infant under a year old. Hans Chiari⁸ reports a case in which very pronounced syphilitic degeneration of the brain-vessels was found in a child fourteen months old. Both Barlow⁹ and T. S. Dowse¹⁰ report cases of nerve syphilis in male infants of fifteen months. For other similar cases the reader is referred to an article by J. Parrott,¹¹ and to a paper by M. E. Troisier.¹²

⁵ Doctrina de Morbis Venereis, Vienna.

⁶ Arch. f. Ophthalm., Bd. i. Erst Abth.

⁷ Virchow's Archiv, Bd. lxxxiv. 269.

⁸ Wien. Med. Wochenschrift, xxxi. 1881, 17.

⁹ Lond. Patholog. Soc. Trans., 1877.

¹⁰ The Brain and its Diseases, vol. i. p. 76.

¹¹ Archiv. de Physiologie, 1871-72, p. 319; also to his “Leçons sur le Syphilis hered.,” Progrès méd., 1877 and 1878.

¹² Arch. de Tocologie, x. 411.

Recorded cases prove decisively that even after puberty specific nervous affections may primarily attack the unfortunate offspring. Thus, Nettleship reports¹³ the development of a cerebral gumma in a girl of ten years, and J. A.. Ormerod¹⁴ of a tumor of the median nerve (probably gummatous) in a woman of twenty-three, both the subjects of inherited syphilis. Thomas S. Dowse¹⁵ details a case of cerebral gumma at the age of ten years, and Samuel Wilks¹⁶ one of epilepsy, from inherited taint, in a boy of fourteen. J. Hughlings-Jackson reports¹⁷ paraplegia with epilepsy in a boy of eight, hemiplegia in a girl of eighteen, and hemiplegia in a woman of twenty-two;¹⁸ the nervous affection in each case being associated with or dependent upon inherited syphilis. E. Mendel reports¹⁹ a case of a child who had inherited syphilis, and developed in her fifteenth year a maniacal attack with hallucinations. I have seen cerebral syphilis occur at twenty-one years of age as the first evident outbreak of the inherited disorder.

¹³ Trans. Lond. Path. Soc., xxxii. 13.

¹⁴ Ibid., p. 14.

¹⁵ Loc. cit., p. 71.

¹⁶ Lectures on Dis. of Nerv. Syst., Philada., 1878, p. 333.

¹⁷ Journ. Ment. and Nerv. Diseases, 1875, p. 516.

¹⁸ Brit. Med. Journal, May 18, 1872.

¹⁹ Archiv f. Psychiatrie, Bd. i. 313.

When a nervous affection develops first at a comparatively late period, and no very apparent evidences of the inherited taint are present, there is great danger of the case being misunderstood; indeed, in some instances an immediate diagnosis may be scarcely possible. It is probable that in most of the reported recoveries from alleged tubercular meningitis the disease has been syphilitic.

Some time since I saw, in an orphan of fourteen, a chronic basal meningitis, and in the absence of any history and of any evidences of syphilis gave the fatal prognosis of tubercular disease; but, to my astonishment, under the long-continued and free use of iodide of potassium complete recovery occurred. Another child, reported by a very good practitioner as cured of tubercular meningitis, and afterward for a long time under my own care, I believe suffered from hereditary syphilis. Cases of this character have also been reported by F. Dreyfous.²⁰

²⁰ Revue mensuelle des Malad. des Enfants, 1883, i. 497; see also Gaz. hébdom. Sci. méd. de Montpellier, 1883, v. 89.

It is of course very important to diagnose between a tubercular meningitis and one due to hereditary syphilis. Without a history certainty is not possible, but a general indefiniteness of symptoms and slowness of progression should arouse suspicion, especially if the absence of the pulse-retardation indicated that the vault rather than the base of the cranium was involved.

The relation of inherited syphilis to various nervous affections not distinctly specific cannot yet be determined. Arrested development, and the consequent epilepsy, idiocy,²¹ early brain sclerosis, are probably sometimes due to the inheritance; and the cases collected by E. Mendel²² show that chronic hydrocephalus is frequently of specific origin.²³

²¹ See Brain, vol. vii. 409.

²² Archiv f. Psychiatrie, Bd. i. 309.

²³ See, also, Virchow's Archiv, Bd. xxxviii. p. 129.

Another very important question connected with the etiology of these disorders is as to the time of their development. Nervous diseases following acquired syphilitic infection certainly belong to the advanced stages of the disorder. Huebner reports²⁴ a case in which thirty years elapsed between the contraction of the chancre and the nervous explosion. I have seen a similar period of thirty years. Fournier reports intervals of twenty-five years, and thinks from the third to the tenth year is the period of maximum frequency of nervous accidents.

²⁴ Ziemssen's Encyclopædia, xii. 298, New York ed.

The fact that nervous syphilis may occur many years after the cessation of all apparent evidences of the diathesis is of great practical importance, especially as the nervous system is more prone to be attacked when the secondaries have been very light than when the earlier manifestations have been severe. I have repeatedly seen nervous syphilis in persons whose secondaries have been so slight as to have been entirely overlooked or forgotten, and who honestly asserted that they never had had syphilis, although they acknowledged to gonorrhœa or to repeated exposure, and confessed that their asserted exemption was due to good fortune rather than to chastity.

The following citations prove that this experience is not peculiar. Dowse²⁵ says: “Often have I had patients totally ignorant of having at any time acquired or experienced the signs or symptoms of syphilis in its primary and secondary stages, yet the sequelæ have been made manifest in many ways, particularly in many of the obscure diseases of the nervous system.” Buzzard²⁶ reports a case of nervous syphilis where the patient was unconscious of the previous existence of a chancre or of any secondaries. Rinecker also calls attention²⁷ to the frequency of nervous syphilis in persons who afford no distinct history of secondary symptoms.

²⁵ The Brain and its Diseases, London, 1879, vol. i. p. 7.

²⁶ Syphilitic Nervous Affections, London, 1874, p. 80.

²⁷ Archiv f. Psychiatrie, vii. p. 241.

Although syphilis is prone to attack the nervous system many years after infection, it would be a fatal mistake to suppose that nervous disease may not rapidly follow the chancre. What is the minimum possible intermediate period we do not know, but it is certainly very brief, as is shown by the following cases of this so-called precocious nervous syphilis. Alfrik Ljunggrén of Stockholm reports²⁸ the case of H. R——, who had a rapidly-healed chancre in March, followed in May of the same year by a severe headache, mental confusion, and giddiness. Early in July H. R—— had an epileptic attack, but was finally cured by active antisyphilitic treatment. Although the history is not explicit, the nervous symptoms appear to have preceded the development of distinct secondaries other than rheumatic pains.

²⁸ Archiv f. Dermatol. u. Syphilis, 1870, ii. p. 155.

Davaine is said²⁹ to have seen paralysis of the portio dura “a month after the first symptoms of constitutional syphilis.” E. Leyden³⁰ found advanced specific degeneration of the cerebral arteries in a man who had contracted syphilis one year previously. R. W. Taylor details a case in which epilepsy occurred five months after the infection.³¹ In the case of M. X——, reported by Ad. Schwarz,³² headache came on the fortieth day after the appearance of the primary sore, and a hemiplegia upon the forty-sixth day. S. L——³³ had a paralytic stroke without prodromes six months after the chancre. A. P. L——³⁴ had an apoplectic attack seven months after the chancre; A. S——, one five months after her chancre. In a case which recently occurred in the practice of A. Sydney Roberts of this city the chancre appeared after a period of incubation of twenty-six days, and two months and eight days subsequent to this came the first fit; eight days after the first the second convulsion occurred, with a distinct aura, which preceded by some minutes the unconsciousness. An interesting observation in this connection is that of Ern. Gaucher³⁵ of a spinal syphilis occurring six months after the appearance of a chancre.

²⁹ Buzzard, Syphilitic Nervous Affections, London, 1874.

³⁰ Zeitschrift f. klin. Med., Bd. v. 165.

³¹ Journ. Nervous and Mental Dis., 1876, p. 38.

³² De l'Hémiplegia syphilitique Prêcoce, Inaug. Diss., Paris, 1880.

³³ Ibid.

³⁴ Ibid.

³⁵ Revue de Méd., 1882, ii. 678.

This citation of cases might be much extended, but is sufficient to show that nervous syphilis occurs not very rarely within six months after infection, and may be present in two months.

Gummatous Brain Syphilis.

CLINICAL HISTORY.—Brain syphilis of the type now under consideration may declare itself with great suddenness. An apoplectic attack, a convulsive paroxysm, a violent mania, or a paralytic stroke may be the first detected evidence of the disease. In most of these cases the coming storm ought to have been foreseen, and to a greater or less degree averted. The onset of cerebral syphilis is, however, generally more gradual, the symptoms coming on slowly and successively. Proper treatment, instituted at an early stage, is usually successful, so that a careful study of these prodromes is most important. They are generally such as denote cerebral disturbance, and, although they should excite suspicion, are not diagnostic, except as occurring in connection with a specific history or under suspicious circumstances.

Headache, slight failure of memory, unwonted slowness of speech, general lassitude, and especially lack of willingness to mental exertion, sleeplessness or excessive somnolence, attacks of momentary giddiness, vertiginous feelings when straining at stool, yelling or in any way disturbing the cerebral circulation, alteration of disposition,—any of these, and, a fortiori, several of them, occurring in a syphilitic subject, should be the immediate signal of alarm, and lead to the examination of the optic discs, for in some cases the eye-ground will be found altered even during the prodromic stage. Of course if choked disc be found the diagnosis becomes practically fixed, but the absence of choked disc is no proof that the patient is free from cerebral syphilis. In regard to the individual prodromic symptoms, my own experience does not lend especial importance to any one of them, although, perhaps, headache is the most common. There is one symptom which may occur during the prodromic stage of cerebral syphilis, but is more frequent at a later stage—a symptom which is not absolutely characteristic of the disease, but which, when it occurs in a person who is not hysterical, should give rise to the strongest suspicion. I refer to the occurrence of repeated, partial, passing palsies. A momentary weakness of one arm, a slight drawing of the face disappearing in a few hours, a temporary dragging of the toe, a partial aphasia which appears and disappears, a squint which to-morrow leaves no trace, may be due to a non-specific brain tumor, to miliary cerebral aneurisms, or to some other non-specific affection; but in the great majority of cases where such phenomena occur repeatedly the patient is suffering from syphilis or hysteria.