Volume 5 — DISEASES OF THE NERVOUS SYSTEM. (continued 26)

Cerebral Anæmia.

The oft-confirmed observation of Treviranus, that the brain is paler in the sleeping than in the waking state, supplemented as it has been by more elaborate observations, which show that the difference between the intracranial blood-amounts, as estimated in these opposite states, is equivalent to one-twenty-fourth part of the total blood-amount of the body, has been made the basis of much dazzling theory and premature speculation. Hyperæmia of the central nervous apparatus or of certain of its provinces becomes regarded as synonymous with over-activity, and anæmia, general or provincial, as the expression of the opposite functional state. Elaborate directions may be found, even in recent treatises on the subject, how to diagnose, not alone hyperæmia and anæmia of the brain and spinal cord, but also of special lobes of the former and particular columns of the latter. These directions are in most instances based on assumptions which are not supported by direct or tangible evidence, and the consequence is that they have failed to stand the tests of experience, where this gauge is applicable, and necessarily failed to advance in any way either our theoretical or practical knowledge of those states of the brain mechanism which are due to alterations in its nutrition.

Much of the unsatisfactory state of our knowledge on this head is due to the grouping together of the physiological anæmia of sleep and the pathological anæmia with which the physician has to deal. The anæmia of the brain in a sleeping person is probably a secondary factor; it ensues after the person falls asleep, the first step in the latter process being probably an altered dynamic state of the brain which lessens the requirements of that organ for blood. This can be readily demonstrated in the case of infants whose anterior fontanelle has not yet closed. In deep sleep the fontanelle is deeply sunken in, but this sinking in does not occur simultaneously with the child's falling asleep, but shortly thereafter. On the other hand, the fontanelle does not rise simultaneously with the child's awakening, unless it cry, which adds a disturbing factor. There are a number of other facts which show that while a comparison between the sleeping state and cerebral anæmia may be made for the purposes of theoretical discussion, yet there are many important points in which they are at variance. To illustrate this I need but refer to the fact that in deep sleep the pupils are in a state of immobility and pinhole contraction,¹⁴ while in chronic cerebral anæmia of young persons a dilated and mobile pupil is the commoner condition. In acutely-produced cerebral anæmia an initial contraction has been noted, but it is not then persistent.

¹⁴ Inability to counterfeit this feature is one of the most reliable tests of simulation, and served to convince me that in the well-known case of a colored cadet, who was tried by a court-martial on charges involving simulation, the latter was proven. There are persons who can voluntarily contract the pupils, but as they are compelled to innervate all the muscles supplied by the third pair, in so doing they are compelled to converge the optic axes—an act which does not take place in sleep.

One of the main reasons of our imperfect knowledge of the nutritive disorders of the brain is the unsatisfactory state of their post-mortem evidence. Little has been learned in this field, except in those extreme cases where the suddenness and intensity of the circulatory catastrophe were sufficient to prove fatal. Even where all observations made during life justify us in supposing that the amount of blood sent to the brain is small, that the velocity of its current is reduced, and its quantity poor, the autopsy may reveal conditions apparently conflicting with the supposition based on ante-mortem observations. This is amply illustrated by the experience of alienists who have studied the relation between nutritive states of the brain and certain forms of insanity. It is generally held that in so far as the antithetical forms of mental disorder known as anæmia and melancholia can be connected with nutritive disorders, the former is indicative of hyperæmia and the latter of anæmia. A number of facts can be adduced in support of this view, particularly as regards the latter condition. It is found, however, in some examinations made of the brains of patients dying melancholic that the brain is apparently hyperæmic; the length of time elapsing before an autopsy is made, the form of somatic disease with which the patient dies, the position of the body after death,—all these may play a part in the production of cerebral injections which do not correctly indicate the condition of the brain as it existed prior to the moribund period, and when the symptoms of supposed anæmia or hyperæmia could be satisfactorily differentiated.

ETIOLOGY.—The best studied form of cerebral anæmia is that ensuing after extensive hemorrhages or from compression and ligature of either of the common carotid arteries.¹⁵ In the latter case symptoms are produced which are in harmony with the doctrine of localization, and permit us to form a conception of the mode in which a diminution of the cerebral blood-supply influences the functions of the brain. The chief symptoms are noted on the side of the body opposite to that on which the common carotid artery is tied. Thus if the left artery be tied, there is at first felt a tingling or pricking feeling on the right half of the body; this is followed by a warm, sometimes a cold, and ultimately by a numb, feeling. This sensory disturbance may become of what might be called the capsular type—that is, a complete hemianæsthesia; but at first it is distinctly like that which is found with cortical and subcortical disease, being limited to the muscular sense and the intelligent contact-perceptions of objects, the æsthesiometer showing but little or no impairment of the cutaneous space-sense. With the loss of muscular sense the movements become heavy, and later true paresis may appear with perhaps total anæsthesia. Aphasia is sometimes noted in such cases, and, in obedience to the predominant location of the speech-faculty in the left side of the brain, is rarely if ever found¹⁶ when the right common carotid artery is the one ligated.

¹⁵ As the conditions of the cerebral circulation resulting from surgical and other rare causes are not apt to be brought to the physician's attention separately from conditions of more immediate importance, their symptoms are discussed in the etiological portion of this section in order to avoid complicating the semeiological picture of cerebral anæmia of every-day experience. For similar reasons the anomalies of the cerebral circulation of an embolic and thrombotic nature, and those associated with eclampsia and epilepsy, are not mentioned in this connection, as their full discussion properly belongs to other portions of this work.

¹⁶ I am unaware of the record of any case where aphasia occurred with ligature of the right common carotid artery. There is a singular observation by Hagen-Torn of permanent paralysis of the right hypoglossal nerve after such an operation, but the report to which I have access does not state whether this may not have been due to some peripheral involvement of that nerve.

In this series of symptomatic sequelæ it is seen that the functional manifestations of the highest centres are the first to be involved, and this establishes that of all parts of the cerebrum the cortex and subcortical tracts are the more vulnerable to the influence of a deficient blood-supply.¹⁷ As we shall see, it is precisely to the insufficient nutrition of these parts that the more important symptoms of the cerebral anæmia of ordinary practice are attributable.

¹⁷ To this there is an apparent exception: when blindness occurs in consequence of ligature of one carotid artery, it is monocular and limited to the side of the ligation. The visual disturbance of cortical and subcortical disease is bilateral, being of the character known as hemianopsic. The blindness due to tying of the carotid is, however, not due to cerebral, but to retinal, anæmia, and its monocular character does not therefore invalidate the observation in the text. Litten and Hirschberg (Berliner klinische Wochenshrift, 1885, No. 20) found complete bilateral amaurosis in a chlorotic girl of fifteen, and on ophthalmoscopic examination the peripheral origin of the blindness was conclusively proven by the existence of an exquisite choked disc. Both the morbid ophthalmoscopic appearance and the amaurosis disappeared under tonic regimen. It is well to recollect that choked disc may occur in chlorosis, and thus be perhaps erroneously attributed to a coexisting hysteria, as was done in some cases at least by Rosenthal in his textbook.

With bilateral ligature¹⁸ of the primary carotids—and this applies in the main to cerebral anæmia from profuse hemorrhages or sudden changes in the blood-pressure, such as occur in enteric affections, ruptures of aneurisms, in obstetric practice, and after brusque tapping for ascites—the same phenomena noted with unilateral compression are observed on both sides of the body, and usually in slighter intensity. In addition, there is a profound and characteristic disturbance of respiration; a cold sweat breaks out; the senses of sight and hearing become greatly impaired or perverted; the mind becomes clouded, consciousness blurred; complete syncope may ensue, and pass to a fatal termination. In other cases vertigo preponderates or vomiting, and finally convulsions appear. It would seem that the respiratory centre exceeds even the cortex in susceptibility to the evil influence of anæmia. It differs from them in two features: firstly, it appears to require bilateral involvement of the brain for its production; secondly, although the respiratory disturbance precedes that of the higher cerebral functions, it does not become as intense, for at a time when the intellectual functions are abolished, as in anæmic coma and syncope, the respiratory function, however disturbed, is in most cases sufficiently well carried on to bear the organism safely through the crisis. The disturbance is marked by the following characters: The respiration is at first deep and sighing, perhaps frequent; it later becomes slow, and is associated with a subjective sense of oppression; the patient feels as if he could not fill his lungs properly; there is an unsatisfied sensation, as if a deeper breath should be taken, and when, in obedience to this subjective need, a full deep breath is taken, the patient feels as if he had stopped short of completing the act, and remains as unsatisfied as before.¹⁹ Yawning and moaning are often accompaniments of this symptom.²⁰ As we shall see, these signs are often among the chief sources of complaint in the less grave forms of anæmia of every-day experience. In the serious condition before us the Cheyne-Stokes phenomena may follow.

¹⁸ I exclude the observations of Flemming, Hammond, and Corning on carotid compression by external pressure, owing to the difficulty of determining whether or no, and what, other important structures are compressed at the same time.

¹⁹ The occurrence of this functional respiratory trouble is a feature of toxic as well as of anæmic irritation of the respiratory centre; it is accordingly found in cases of profound alcoholic poisoning.

²⁰ It is somewhat difficult to understand why in cases of anæmia induced in both carotid districts the symptoms of anæmia should be marked in the functions of that part of the brain-axis which through the basilar trunk derives its blood from the vertebral arteries. Here the blood-current must necessarily be increased. That the disturbance of breathing, the yawning, and the sighing belong to the group of irritative symptoms due to anæmia is in harmony with the general physiological law which is illustrated in the initial contraction of the pupil, which is found in experimental cerebral anæmia. Observations on anæmia of the brain-axis are too few, and, so far as noted, have been so rapidly fatal that it is not possible to derive from them any facts bearing on the physiological reactions of the respiratory centre to high-graded anæmia. One of the curiosities of medicine appertaining to this subject is the observation recorded in Virchow's Archiv, lxix. p. 93, of the case of a man who had fractured the base of the skull in its posterior fossa, and, the basilar artery becoming caught and pinched in the crack, death occurred rapidly with all the signs of cerebral anæmia, verified by the post-mortem appearances.

Anæmia of the brain may develop at any period of life, not excluding the intra-uterine period. Kundrat and Binswanger regard the deformity of the brain known as porencephaly as the result of an anæmic (non-embolic) necrosis of brain-substance, developed either in the fœtal or the infantile period. The occasional symmetry of the deformity is in favor of this view. That there are other conditions of cerebral malnutrition,²¹ masking themselves in defective development and imperfect isolation of the conducting tracts, and that the consequent differing rate of maturation of these tracts has some relation to the absence or presence of a predisposition to chorea and other disturbances of nervous equilibrium so common at this period of life, I regard as at least probable. But it is at the period of puberty that we encounter the most important discrepancies between the requirements of brain-nutrition and the furnished blood-supply. The disposition to uncomplicated cerebral anæmia is greatest at this period of life and in the female sex. Beneke²² has shown that as the human being grows the arteries, which in children are very large in proportion to the length of the body, get to be relatively smaller and smaller toward the period of puberty—that after this period they widen to again attain a large circumference at old age. There is thus added to the other and more obscure factors which may determine general anæmia at puberty a diminished calibre of the arteries in both sexes. To some extent the disadvantageous influence of (relatively) narrow vascular channels may be overcome by increased cardiac action, and the almost sudden increase in size of the heart about this period is probably the result of the demand made upon its compensatory power. But, as we learn from the same observer that the female heart remains relatively as well as absolutely smaller than that of the male, we can understand why the female should be less able to overcome the pubescent disposition to cerebral (and general) anæmia than the male. Menstruation, which in a certain proportion of girls scarcely maintains the semblance of a physiological process, acting rather as a drain than a functional discharge, is added to the anæmia-producing factors. It is among those who marry in the ensuing condition, who bring forth child after child in rapid succession, perhaps, in addition, flooding considerably at each confinement, that we find the classical symptoms of chronic cerebral anæmia developed.

²¹ I have found in three children under fourteen months of age, who died with symptoms not unlike those of slowly-developed tubercular meningitis, including convulsions, strabismus, temperature disturbance (slight), and terminal coma, without nuchal contracture or pupillary anomalies, a remarkably anæmic brain. The sulci gaped; there were few or no puncta vasculosa; the cortex extremely pale, and the white substance almost bluish-white. On attempting to harden the brain of the youngest of these children, using every precaution and a sufficient number of sets of hardening fluids, including the chromic salts and alcohol, I found that small cavities formed in the cortex, varying from the scarcely visible to two-thirds of a millimeter in diameter. Their existence were demonstrable the day after the death and almost immediate autopsy performed in this case. There had been no antecedent disease in any one of these cases; the children had been lethargic, inactive, and the oldest had made no attempt to walk or talk. There was no morphological or quantitative defect in cerebral or cranial development, and microscopic examination showed that the cavities were not perivascular. In all these cases the patients belonged to the tenement-house population.

²² An excellent abstract of Beneke's original monograph, by N. A. P. Bowditch, will be found in volume i. Transactions of the Massachusetts Medico-Legal Society.

In the male sex the period of adolescence has not the same profound influence in producing cerebral anæmia that it has in females. To some extent, however, habitual self-abuse and early sexual excess of the former produce results similar to those occurring in consequence of perverted physiological processes in the latter. Many of the symptoms presented by the inveterate masturbator are probably due to cerebral anæmia; there are, however, in his case and in that of the early libertine certain vaso-motor complications frequently present which render the clinical picture a mixed one.²³ In addition, abuse of the sexual apparatus has a direct—probably dynamic and impalpable—exhausting effect on the central nervous apparatus.

²³ Kiernan of Chicago has described peculiar trophic disturbances—dermato-neuroses, color-changes of the hair, etc.—in a case of masturbatory mental trouble associated with marked anæmia. The patient whenever he flushed up heard a noise as of a pistol snapped near the mastoid region. In the case of a young man of eighteen who—the pampered son of wealthy parents—became his own master at fifteen, and had at that age indulged in sexual orgies which were continued to an almost incredible extent, it was found that he gradually lost his memory, and on one occasion had a violent epileptiform attack. During his convalescence from the stuporous state which followed it was noted that the patient was quite bright in the morning, but that after he had been up a while he relapsed into a state of apathy, with amnesia, which, decreasing in intensity from week to week, was eventually only noted toward evening, and finally disappeared, the case terminating in complete recovery.

In the vast majority of cases anæmia of the brain is but a part of general anæmia, and all conditions which tend to impoverish the character of the blood and to reduce the rapidity of movement and fulness of the cerebral blood-column are apt to be associated with signs of cerebral malnutrition. As early an observer as Addison noticed the wandering of the mind in pernicious anæmia, in which disorder anæmia and wasting of the brain have been found post-mortem. In two cases of extreme chlorosis I heard the sound known as the cephalic soufflé with great distinctness;²⁴ this sound, when the other morbid conditions that may lead to it can be excluded, indicates a high degree of anæmia. Both patients were somnolent and subject to fainting-spells. In leucocythæmia a rambling delirium is not infrequently noted toward the close of the patient's life, and the habitual sadness and depression of many leukæmic patients is due, as are also certain phases of melancholia, to cerebral malnutrition. In some stages of most, and in all stages of some, forms of renal disease the conditions of cerebral anæmia are present; and it is reasonable to attribute to it some share in the production of the head symptoms of Bright's disease; but here, as in cases of cardiac disease, symptoms due to other influences—uræmia in the former, and insufficient oxygenation of the blood in the latter instance—obscure or conceal those due to the anæmia strictly speaking.

²⁴ When an anæmic murmur at the base of the heart coexists with the cephalic soufflé, the latter may be regarded as an evidence of anæmia; but where the former is absent—that is, when the cephalic soufflé is an isolated, independent symptom—there is reason to suspect the existence of a tumor or some other cause of compression of the carotid artery at or after its entry into the cranium. In one of the cases referred to in the text, pressing on one or the other carotid produced numbness and tingling in the opposite arm, leg, and cheek. Similar observations were made by Tripier (Revue de Médecine, March, 1881), who strenuously maintains the existence of the cephalic soufflé in the adult, against Henry Roger, and in consonance with the observations of Fisher and Whitney. In the last-mentioned case of mine the sound could be heard a distance from the head.

All exhausting diseases, many febrile affections, notably typhoid, starvation from any cause, and exhausting discharges, may produce cerebral anæmia. Under the latter head belong the diarrhœal affections of childhood, which not infrequently lead to an aggravated form of anæmia of the brain known as hydrocephaloid. In addition to the provoking causes of cerebral anæmia there are certain accessory ones: prominent among these is the upright position and sudden rising. The reason of this influence is self-evident, as is also the fact that it is most apt to manifest itself in cases of cardiac enfeeblement. Many a convalescent from an exhausting fever or other disease has on rising from bed fainted; some have fallen dead from cerebral anæmia already existing, but fatally intensified by this sudden change of position. A number of cases are on record by Abercrombie, Forbes Winslow, J. G. Kiernan, and others where persons manifested the symptoms of cerebral anæmia only when in the upright position and even in lying on one side or the other; these are, however, far rarer than is claimed by some later writers.

The purest form of acute cerebral anæmia, aside from that produced by surgical interference with the cerebral circulation or extensive hemorrhages, is that induced by mental influences, such as fright, a disagreeable odor, or a disgusting or harrowing spectacle. Some persons, not suffering from general anæmia or any diseased condition thus far mentioned, on experiencing the emotional influences named will be observed to turn pale, to breathe heavily, and either sink into a chair or fall on the floor partly or entirely unconscious. They are then suffering from a spasm of the cerebral arteries resulting in acute and high-graded cerebral anæmia or syncope. This condition is marked by some of the symptoms previously mentioned as occurring with bilateral ligature of the carotids: thus, the feeling of oppression on the chest, vertigo, heaviness of the limbs, nausea, and vomiting are characteristic; a cold sweat breaks out on the forehead; the visual field becomes darkened; and hearing is rendered difficult by the tinnitus.²⁵ The pulse is small and of low tension, but regular.

²⁵ Most authors claim that the sense of hearing is blunted, as that of vision is. This is so in some, but certainly not in a large number of other cases. I have now under observation a girl whose physical conformation—her neck is very long and her shoulders tapering—and extreme susceptibility combine to favor the occurrence of syncope. She faints in my office whenever an examination is made, even though it be entirely verbal; and after recovering frequently lies down to answer by deputy, as experience has shown her that she is less likely to faint in this position. I have repeatedly satisfied myself from her subsequent statements that she heard what was said, while she appeared to be quite unconscious and “saw everything black or through a cloud.” It is not improbable that the impressions which most writers on the subject convey were derived from the experience of novices in fainting; these, in the alarm and anxiety of their condition, and confused by the tinnitus, might well fail to hear what the bystanders said, particularly as on many such occasions the fainting person is apt to be surrounded by a confused Babel of tongues. While the auditory nerve is as sensitive to the irritative influence of anæmia as any, and there is a case of a boy on record (Abercrombie) who could only hear well when lying down, and was deaf when he stood up, yet the conclusions of other authorities who have studied the subject would lead one to think that there are individual differences in this respect. How often does not the dying person, after feeling for the hands of a relative whom he cannot see, converse with him responsively! And how much need is there not of the humane physician to remember that the sense of hearing is the last intellectual sense to die, lest he speak unguardedly at the bedside!

As a rule, the subjects of simple syncope recover, the horizontal position, which is assumed perforce in most cases, carrying with it the chief remedial influence—namely, the facilitating of the access of a fuller blood-supply to the brain. While, as stated, the tendency to syncope may exist in healthy non-anæmic individuals, it is far more common with those who suffer either from chronic cerebral anæmia or from many of its predisposing conditions. The arterial spasm which causes syncope is an exaggeration of what occurs within physiological limits²⁶ in all persons when subjected to emotional or violent external impressions of any kind.

²⁶ It has been experimentally determined by Istomanow (St. Petersburg Dissertation, 1885) in persons whose brain-surface had become partially accessible to observation through traumatic causes that pain, warmth, pleasant smells, and sweet tastes cause a contraction of the cerebral vessels and a sinking in of the brain-surface, while tickling, unpleasant odors, bitter and sour tastes, produce the reverse condition; that is, bulging of the brain-surface and increased injection of the vessels. Istomanow's results are verified by other observations, particularly by the fact that with the latter class of impressions there is an increase in the general blood-pressure, with sinking of the surface-temperature, and, as measured by Mosso's method, decrease in the volume of the extremities. While there is a general correspondence between these observations and clinical experience, there are a few unexplained discrepancies.

MORBID ANATOMY.—In those severe cases of cerebral anæmia which terminate fatally the entire brain appears bloodless. Since the color of this organ under ordinary circumstances is in great part due to the vascular injection, it appears very different when this admixture is lessened or removed. Then the gray substance, instead of presenting a reddish-gray tint, is of a pale buff color in infants, and a pale gray in adults who have died of acute or intense cerebral anæmia. The white substance exhibits few or no puncta vasculosa, and there is no indication of the faint rosy tinge which even the white substance has in the normal brain. All these appearances can be imitated in the brain of an animal that is bled to death; they are also met with in those who have died of inanition, particularly in cases of melancholia attonita, the subjects of which had long refused food. Most writers state that the ventricular and subarachnoid fluids are increased in amount,²⁷ and that the sulci appear wider in anæmic than in normal brains. That these fluids must be increased to compensate for the diminished blood-amount is evident. But it is not unlikely that exaggerated estimates of the increase have been made; and for this reason: Since the meninges and choroid plexuses are comparatively bloodless, the cerebro-spinal fluids are more likely to present themselves free from that admixture of blood which renders the obtaining and measuring of their quantity so difficult under ordinary circumstances. The gaping of the sulci has not been verified by me either in animals that had been bled to death or in cases of cerebral anæmia in rapidly-fatal atonic and phthisical melancholia. In protracted cases of this nature I frequently found gaping of the sulci: here, from the nature of the cases, the patients dying either from self-starvation, imperfect assimilation, or wasting diseases, the occurrence of a certain amount of atrophy of the brain-substance proper could not be excluded.²⁸

²⁷ Hammond, on the other hand (Diseases of the Nervous System, p. 77), has the ventricles generally empty.

²⁸ Up to within a very short time ago it would have appeared heretical to claim that any considerable amount of brain-wasting could ensue from starvation alone, as the oft-cited experiments of Chossat seemed to show that mammals, birds, reptiles, and amphibians lose in body-weight while being starved, but that the brain-weight is not disturbed to any appreciable extent. Six years ago I examined the brain of a tortoise (Cestudo Virginica) which had starved fully a year through ignorance of the keeper of an aquarium. The atrophy of the brain was so marked that it had undergone demonstrable changes of contour. Since then Rosenbach (Archiv für Psychiatrie, xvi. p. 276) has demonstrated that brain-wasting and other changes do occur in starved rabbits.

With protracted fevers accompanied by inanition—and this applies particularly to the later period of typhoid fever—a condition of cerebral anæmia is found which is of the greatest interest to the clinician. The brain as a whole is bloodless; there may or may not be apparently hyperæmic districts, but the injection is altogether on the surface; the consistency of the brain is considerably diminished, and this organ is often distinctly œdematous. In exceptional cases the œdema is so great that softening results, the white substance becoming fluidified at the cortical limit near the base of the sulci and at the ventricular walls. This is due perhaps as much to post-mortem maceration as to pre-mortem œdema, but that the latter condition exists is shown by the condition of the brain as a whole. The loss of memory, the difficulty of correlating the past and present, the rambling, incoherent conversation, and anenergic stupor observed in the decline of typhoid and other exhausting fevers, especially in older subjects, may be properly attributed to the injurious effects of post-febrile anæmia and anæmic œdema of the brain. Aside from fevers, œdema is apt to be associated with anæmia where venous stagnation is a complicating feature; consequently, it is not uncommon with certain uncompensated valvular lesions, emphysema, and other chronic pulmonic troubles.

Positive observations of tissue-changes from simple cerebral anæmia have not been recorded. Even in extreme cases the essential nervous structures, the ganglionic bodies, the nerve-fibres, their sheaths, and the neuroglia, appear healthy. The adventitial and pericellular spaces are sometimes enlarged, and variations in the number and distribution of the free nuclei of the neuroglia and the border bodies of the periadventitial districts have been observed by me, but not with such constancy as to justify more than this mere mention. In his researches on starvation Rosenbach found the brain œdematous and the ventricles dilated; there were also microscopical changes which indicated a profound disturbance of nutrition; the large cells of the anterior spinal horn and cerebellum had lost their transparency, being in a condition resembling cloudy swelling. The neuroglia appeared to be in a similar condition as that of nerve-cells. Singular as it may appear on first sight, the capillaries were found crowded with blood-corpuscles, and there were many evidences of diapedesis of such. This may indicate a passive accumulation due to deficient cardiac and vascular contractility. The changes, as a whole, were not unlike those found in myelitis,²⁹ except in so far as no actual inflammatory signs were present.

²⁹ Several distinguished neurologists, notably Westphal, who were present when Rosenbach presented his conclusions, were unable to recognize so profound a deviation from the normal structural conditions as he claimed (Archiv für Psychiatrie, xvi. p. 279).

SYMPTOMS.—The clinical phenomena of acute cerebral anæmia have been in the main related in connection with the etiology of this disorder. We shall now proceed to detail those which occur with cases more likely to engage the attention of the practitioner either on account of their gravity or protracted duration.

Uncomplicated Chronic Cerebral Anæmia of Adolescents and Adults.—This condition is one of the common manifestations of general anæmia. Most anæmic persons are languid, drowsy, suffer from insomnia, tinnitus aurium, and other signs of imperfect cerebral irrigation. In some these troubles become alarmingly prominent and may approach the confines of mental derangement. This is particularly apt to occur with women who have borne and nursed a large number of children. In addition to the typical signs of cerebral anæmia, they exhibit depression, may suffer from hallucinations, and even become afflicted with lachrymose or suicidal melancholia (insanity of lactation of the somato-etiological school). Depression of the mental functions is the most constant symptom of cerebral anæmia, and the one which most frequently directs the physician's attention to its existence; its subjects appear mentally blunted, the apperceptive powers are diminished, and it is difficult for the patient to interest himself in anything, or when interested to keep up a mental effort—that is, his attention—any length of time. In more severe grades of the trouble the patients become somnolent in the daytime. Contrary to what those who regard sleep as essentially due to cerebral anæmia might expect, sleep is disturbed, and the patient is wakeful or suffers from vivid and frightful dreams, or even deliria. Others pass a quiet night, but are rather in a trance-like condition than a healthy sleep. Lethargic as the cerebral anæmic person is on the whole, and unable as he feels himself to exert his will-power (aboulia), yet he is often irritable, perverse, and petulant in consequence of that morbid excitability which is a universal attribute of the overworked or imperfectly nourished nerve-element. The younger the patient the more likely is the condition apt to impress one as a stupor, while with older patients irritability is more prominent. In the former the obtuseness is often rapidly overcome when the patient assumes the horizontal position.

It was supposed by Abercrombie that an acute exacerbation of cerebral anæmia of this form in weakly and aged individuals might terminate in death. This condition corresponded to the so-called serous apoplexy of the old writers. With increasing accuracy in our autopsies this condition is more and more rarely recorded, although the possibility of its occurrence as a pathological rarity cannot be denied. As a rule, the chronic form of cerebral anæmia when it terminates fatally, which is exceptional, is marked by a deepening coma and gradual extinction of the vital processes, the Cheyne-Stokes phenomenon preceding this.

Patients suffering from chronic cerebral anæmia are afflicted with morbid irritability of the optic and auditory nerves. Loud sounds and bright lights are very annoying to them. Roaring, buzzing, and beating sounds in the ear are common, and scintillations, muscæ volitantes, and temporary darkening of the visual field—particularly noticed when the head is suddenly raised—are complained of in all cases. It is often found that the tinnitus disappears and the hearing power improves on assuming the horizontal position.

Headache of greater or less severity is found in the majority of cases: it is more severe in the rapidly-developed forms, and I have found it to be complained of in agonizing intensity by women who had risen from childbed and who had flooded considerably. As a rule, the headache, whether severe or mild, is symmetrical and verticalar, in some cases associated with an ache subjectively appearing as if it extended to the back of the orbit. It is remarkable for its constancy, and its exacerbations are often complicated with vertigo and nausea, so that it is not infrequently interpreted as a reflex evidence of gastric disorder. A stitch-like feeling, located in both temples, is often associated with it.

Occasionally sufferers from chronic cerebral anæmia experience seizures, or rather exacerbations, of their disorder which approach in character, while not equalling in degree, an attack of syncope. Whether in bed or in a chair, they then feel as if their limbs were of lead; they deem that they cannot stir hand or foot; the other symptoms related are aggravated; they yawn and breathe deeply, but hear all that is said by those near them, and do not lose consciousness. They express themselves as feeling as if everything around them were about to pass away. One of my patients would frequently find that if this condition overtook her while lying on one side, that side would remain numb for some time and be the seat of a tingling sensation which disappeared on the parts being rubbed. The same was noticed when she awoke in the morning in a similar position. To what extent these features were due to the general anæmia is doubtful. As previously stated, true syncope occurs in chronic cerebral anæmia, but much less frequently in those subjects of this disorder who have reached middle life than in adolescents.

The radial pulse in cerebral anæmia does not necessarily show the anæmic character; not infrequently the general blood-pressure is increased at the onset of the acute form, and if long continued this may be followed by a decrease of the same. The pulse-character may therefore vary greatly in frequency, resistance, and fulness. In protracted cases it is soft, easily compressible, and rapid.

It is not uncommon to find indications of a slight unilateral preponderance of the signs of cerebral anæmia. In one case which terminated in recovery, and was otherwise pure, vertigo was not produced on turning from the left to the right, but it was produced to a distressing degree on turning in the opposite direction; in a second, equally typical, there was for a long time a subjective sensation of falling over toward the right side.

There appears to be much less constancy in the relationship of the deficient blood-supply to the severity of the symptoms than is usually supposed. Much depends upon the time of life at which the disorder develops: a brain that has acquired stability through education and exercise is less vulnerable to the influence of general anæmia than one that has not. The nerve-centres appear, to some extent at least, to regulate their own blood-supply; and whether it be through a change in the blood-current rapidity or some other factor neutralizing the evil effects of the intrinsically inferior quality of the blood, we must attribute to the self-regulating nutrition power of the brain the not uncommon phenomena of an active mind in an anæmic body. And where the general anæmia reaches so high a degree as to involve the brain, under such circumstances we find that irritability to sensory impressions and fretfulness are more prominent than the lethargy and indifference which characterize the juvenile chlorotic form. Although this distinction is less marked between these two classes in regard to acutely-produced anæmia, yet it is observable even there. If in a youth or girl while undergoing phlebotomy cerebral anæmia were to reach such a degree as to cause subjective sounds, they would either approach or fall into a faint; but Leuret, the distinguished cerebral anatomist, while being subjected to the same procedure, hearing a hissing sound, did not lose consciousness, but complained that some one must have upset a bottle of acid on a marble table in the same room, as he supposed he was hearing the sound of effervescence thus produced.

Much, too, appears to depend on dynamic and other thus far undiscovered intrinsic conditions of the brain-tissue itself, irrespective of the mere amount and rapidity of the blood-current. If the subject be exposed to wasting diseases, to blood-poisons, or to vicissitudes of temperature and to physical exhaustion in addition to the causes producing cerebral malnutrition, deliria of a cortical nature are more apt to characterize the case than in simple anæmia. These are known as the deliria of inanition, and present themselves under two forms. The first has been frequently observed in sailors, travellers, and others who have undergone starvation in exposed situations, and is tinctured by the psychical influences incident to such a condition. Just as the Greeley survivors at Cape Sabine, when reduced to their miserable rations of seal-skin boot-leather and shrimps, entertained each other with the enumeration of imaginary culinary luxuries, so others who have suffered in the same way declaim about gorgeous banquets in the midst of a howling wilderness, or, as occurred to a miner who lost his way in Idaho a few winters ago, experienced hallucinatory visions of houses, kitchen utensils, and persons with baskets of provisions. In others the terror of the situation leads to the development of rambling and incoherent delusions of persecution.

The second form, regarded as a variety of starvation delirium, is found in the post-febrile periods of typhoid and other exhausting fevers. In aged persons it may even develop shortly after the onset of the disease. It is usually unsystematized, of a depressive cast, and may be associated with a condition resembling melancholia agitata. In a small proportion of cases insanity of the ordinary types, but more commonly of the special kinds comprised in the group of post-febrile insanity, develops from the anæmic fever delirium as its starting-point.

The spurious hydrocephalus (hydrocephaloid, hydrencephaloid) of Marshall Hall and Abercrombie, referred to in the section on Etiology, is an important condition for the diagnostician to recognize. A child suffering from this disorder presents many symptoms which are customarily regarded as characteristic of tubercular meningitis or of chronic hydrocephalus; thus the pupils are narrow—sometimes unequal;³⁰ there is strabismus, and there may be even nuchal opisthotonos, while the somnolent state in which the little patient usually lies may deepen into a true coma, in which the pupils are dilated, do not react to light, nor do the eyelids close when the cornea is touched. Ominous as this state appears, it may be completely recovered from under stimulating and restorative treatment. On inquiry it is found that the symptoms above mentioned were preceded by cholera infantum or some other exhausting complaint, such as a dysentery or diarrhœa, and that the somnolent condition in which infants are often found toward the close of such complaints passed gradually into the more serious condition described.³¹ The infants thus affected do not, however, sleep as healthy children do, but moan and cry, while apparently unconscious of their surroundings. The surface of the body is cool and pale; the pulse and respiration are normal, except in the comatose period, but the former is easily compressible. The chief points distinguishing hydrocephaloid from true hydrocephalus and other diseases associated with similar symptoms are the following: 1st, There is no rise of temperature; 2d, the pupils are equal; 3d, the fontanelle is sunken in; 4th, the pulse and respiration, with the exception stated, are natural; 5th, there is an antecedent history of an exhausting abdominal disorder; 6th, also a facial appearance characteristic of the latter.

³⁰ This is not admitted by most writers, but does occur exceptionally.

³¹ It should not be forgotten, however, that very similar symptoms occur after cholera infantum, with a much graver pathological condition—namely, marantic thrombosis of the sinuses.

One of the gravest and rarest forms of cerebral anæmia is one which occurs as a result of extreme general anæmia in very young infants. In a remarkable case which I have had an opportunity of studying, the abolition of certain cerebral functions reached such a degree that the opinion of a number of physicians was in favor of tubercular meningitis.³² There was at the time of my examination complete extremity hemiplegia, and there had been conjugated deviation, restlessness in sleep, and dulness in the waking hours: all these symptoms except the hemiplegia disappeared whenever a more assimilable and nutritious food was used than the one previously employed. On one occasion there were evidences of disturbed vaso-motor innervation; on several, convulsive movements. This history, associated with ordinary evidences of general anæmia, covered a period of eighteen months, without the slightest abnormality of temperature being noted or discoverable during that period. The mucous surfaces of this child were almost colorless, certainly without any indication of the normal tinge; the mother had nursed it, and her milk had been found to possess scarcely any nutritive value. The case terminated fatally at the age of twenty months.

³² It was stated by an experienced practitioner that death occurred with unmistakable symptoms of tubercular meningitis. Certainly, the absence of temperature disturbance at the time of the hemiplegic and other exacerbations, as well as other important features for a period exceeding a year, shows that whatever favorable soil the earlier condition may have furnished for the secondary development of such or other gross structural disease, tubercular meningitis did not exist at the time; while the absence of pupillary and optic-nerve symptoms, as well as the rapid changes from day to day or week to week under dietetic treatment, militate against the assumption of any other organic affection incident to childhood.

Partial Cerebral Anæmia.—Most writers on cerebral anæmia discuss a number of varieties of partial cerebral anæmia as distinguished from the acute and chronic general forms. Some of the conditions thus described properly appertain to the angio-spastic form of hemicrania, others to epilepsy, and the majority to circulatory disturbances dependent on arterial disease. Aside from the partial cerebral anæmia resulting from surgical causes, I am acquainted with but one evidence of limited cerebral anæmia which can be regarded as independent of the neuroses or of organic disease, and that is the scintillating scotoma. This symptom, in the only case in which I observed it, occurred in a medical student, accompanied by pallor and nausea in consequence of the disgust produced in him by the combined odors of a dissecting-room and of a neighboring varnish-factory. The totally blind area of the visual field was strictly hemianopsic in distribution and bounded by a colored zone scintillating, to use the sufferer's words, like an aurora borealis. The attack, probably protracted by his great alarm at being blind in one-half of the visual field, lasted three hours. As the cause in this case was a psychical impression and accompanied by the ordinary signs of that fainting which is not an uncommon occurrence in the dissecting-room; as, furthermore, the individual in question never had a headache except in connection with febrile affections, and then in the lightest form, and is neither neurotic himself nor has a neurotic ancestry or relatives,—I regard it as the result of a simple arterial spasm intensified in the visual field of one hemisphere, analogous to the more general spasm of ordinary syncope.³³

³³ It may be remembered that Wollaston had scintillating scotomata, and that after his death a small focus of softening was found in the one visual field. Ordinarily, this disturbance is associated with hemicrania.

DIAGNOSIS.—There is so little difficulty in recognizing the nature of those cases of acute cerebral anæmia which depend on recognizable anæmia-producing causes that it is unnecessary to point out their special diagnostic features. With regard to chronic cerebral anæmia, and its differentiation from other circulatory brain disorders, I refer to the last article. In this place it will be necessary only to point to some of the symptoms which, individually considered, are found in other disorders, and may therefore be misinterpreted. The chief of these is vertigo, which, as already stated, being associated with nausea, and even vomiting, is not infrequently confounded with stomachic vertigo, while the opposite error is also, though less frequently, fallen into. The chief differential points are—that stomachic vertigo is relieved by vomiting, and anæmic vertigo is not; that the former is rather episodical, the latter more continuous; that in the free intervals of the former, while there may be some dulness, there is not the lethargy found with anæmia; that the headache with the former is either over the eyes or occipital, and most intense after the passage of a vertiginous seizure, while anæmic headache is verticalar or general, and not subject to marked momentary changes. It is unnecessary to indicate here the positive evidences of gastric disorder which are always discoverable in persons suffering from stomachic vertigo; but it is also to be borne in mind that such disorder is frequently associated with the conditions underlying general and cerebral anæmia, particularly in the prodromal period of some pulmonary troubles.

There are a number of organic affections of the brain which are in their early periods associated with symptoms which are in a superficial way like those of cerebral anæmia. As a rule, focal or other pathognomonic signs are present which render the exclusion of a purely nutritive disorder easy; but with some tumors, as is generally admitted, these signs may be absent. It is not difficult to understand why a tumor not destructive to important brain-centres, nor growing sufficiently rapid to produce brain-pressure, yet rapidly enough to compress the blood-channels, may produce symptoms like those of simple cerebral anæmia. It is claimed that with such a tumor the symptoms are aggravated on the patient's lying down, while in simple anæmia they are ameliorated.³⁴ The latter proposition holds good as a general rule; as to the former, I have some doubts. Not even the ophthalmoscope, although of unquestionable value in ascertaining the nature of so many organic conditions of the brain and its appendages, can be absolutely relied on in this field. Until quite recently, optic neuritis, if associated with cerebral symptoms, was regarded as satisfactory proof that the latter depended on organic disease; but within the year it has been shown by Juler³⁵ that it may occur in simple cerebral anæmia, and both the latter and the associated condition of the optic nerve be recovered from.

³⁴ The increased flow of blood to the brain in anæmia is not always momentarily remedial: if, for example, the patient stoop down, he flushes more easily than a normal person, and suffers more than the latter. The same is observed with regard to stimulants.

³⁵ British Medical Journal, Jan. 30, 1886. In the case reported suppression of the catamenia is spoken of, as well as the fact that treatment was directed to the menstrual disturbance. It is not evident from the brief report at my disposal whether the suspension of the menstrual flow was symptomatic of general anæmia or of a local disturbance. Optic neuritis has been recorded as having been present in a large number of cases with no other assignable cause than a uterine disorder. As previously stated, Hirschberg and Litten found choked disc under like circumstances.

The claim of Hammond and Vance that ordinary anæmia of the brain may be recognized through the ophthalmoscope is almost unanimously disputed by experienced ophthalmoscopists, nor is it unreservedly endorsed by any authority of weight among neurologists. That there may be color-differences to indicate anæmia is, however, not impossible; and the fact that a concentric limitation of the visual field sometimes occurs should not be forgotten. It is distinguished from that found with organic diseases by its variability through the day and in different positions of the body.

TREATMENT.—Chronic as well as acute cerebral anæmia, dependent on general anæmia, usually requires no other medicinal treatment than that rendered necessary by the general anæmic state of which it is a part. This has been discussed at length in the third volume of this work: it remains to speak of certain special precautions and procedures rendered necessary by the nervous symptoms predominating in such cases. As the insufficiently nourished brain is not capable of exertion, mental as well as physical rest is naturally indicated. And this not only for the reason that it is necessary to avoid functional exhaustion, but also because the anæmic brain when overstrained furnishes a favorable soil for the development of morbid fears, imperative impulses, and imperative conceptions. This fact does not seem to have been noticed by most writers. The mind of the anæmic person is as peculiarly sensitive to psychical influences as the anæmic visual and auditory centres are to light and sound; and in a considerable proportion of cases of this kind the origin of the morbid idea has been traced to the period of convalescence from exhausting diseases. The prominent position which masturbation occupies among the causes of cerebral anæmia perhaps explains its frequent etiological relationship to imperative conceptions and impulsive insanity.

Although the radical and rational treatment of cerebral anæmia is covered by the treatment of the general anæmia, there are certain special symptoms which call for palliative measures. Most of these, such as the vertigo, the optic and aural phenomena, improve, as stated, on assuming the horizontal position. The headache if very intense will yield to one of three drugs: nitrite of amyl, cannabis indica, or morphine. I am not able to furnish other than approximative indications for the use of remedies differing so widely in their physiological action. Where the cerebral anæmia and facial pallor are disproportionately great in relation to the general anæmia, and we have reason to suppose the existence of irritative spasm of the cerebral blood-vessels—a condition with which the cephalalgia is often of great severity—nitrite of amyl acts as wonderfully as it does in the analogous condition of syncope.³⁶ Where palpitations are complained of, and exist to such a degree as to produce or aggravate existing insomnia, small doses of morphine will act very well, due precautions being taken to reduce the disturbance of the visceral functions to a minimum, and to prevent the formation of a drug habit by keeping the patient in ignorance of the nature of the remedy. When trance-like conditions and melancholic depression are in the foreground, cannabis indica with or without morphia will have the best temporary effect: it is often directly remedial to the cephalalgia. Chloral and the bromides are positively contraindicated, and untold harm is done by their routine administration in nervous headache and insomnia, irrespective of their origin. Nor are hypnotics, aside from those previously mentioned, to be recommended; the disadvantages of their administration are not counterbalanced by the advantages.³⁷ Frequently, in constitutional syphilis, insomnia resembling and probably identical with the insomnia of cerebral anæmia will call for special treatment. In such cases the iodides, if then being administered, should be suspended, and if the luetic manifestations urgently require active measures, they should be restricted to the use of mercury in small and frequent dosage, while the vegetable alteratives may be administered if the state of the stomach permit.

³⁶ There are disturbances in the early phases of cerebral syphilis, whose exact pathological character is not yet ascertained, which so closely resemble the condition here described that without a knowledge of the syphilitic history, and misled by the frequently coexisting general anæmia, it is regarded as simple cerebral anæmia. Under such circumstances, as also with the cerebral anæmia of old age, amyl nitrite should not be employed.

³⁷ Urethran and paraldehyde have failed in my hands with anæmic persons.

Among the measures applicable to the treatment of general anæmia there are three which require special consideration when the cerebral symptoms are in the foreground: these are alcoholic stimulants, the cold pack, and massage. It is a remarkable and characteristic feature of cerebral anæmia that alcoholic stimulants, although indicated, are not well borne³⁸—at least not in such quantities as healthy persons can and do take without any appreciable effect. I therefore order them—usually in the shape of Hungarian extract wines,³⁹ South Side madeira, or California angelica—to be given at first in such small quantities as cannot affect the cerebral circulation unpleasantly, and then gradually have the quantity increased as tolerated. In fact, both with regard to the solid nourishment and the stimulating or nourishing fluids and restorative drugs the division-of-labor principle is well worth following. The cerebral anæmic is not in a position to take much exercise, his somatic functions are more or less stagnant, and bulky meals are therefore not well borne. Small quantities of food, pleasingly varied in character and frequently administered, will accomplish the purpose of the physician much better.

³⁸ Hammond, who classes many disorders under the head of cerebral anæmia which the majority of neurologists regard as of a different character, has offered a very happy explanation. He says, “Now, it must be recollected that the brains of anæmic persons are in very much the same condition as the eyes of those who have for a long time been shut out from their natural stimulus, light. When the full blaze of day is allowed to fall upon them retinal pain is produced, the pupils are contracted, and the lids close involuntarily. The light must be admitted in a diffused form, and gradually, till the eye becomes accustomed to the excitation. So it is with the use of alcohol in some cases of cerebral anæmia. The quantity must be small at first and administered in a highly diluted form, though it may be frequently repeated.”

³⁹ Such as Meneszer Aszu; there is no genuine tokay wine imported to this country, as far as I am able to learn.

The cold pack, strongly recommended by some in general anæmia, is not, in my opinion, beneficial in cases where the nervous phenomena are in the foreground, particularly in elderly persons. Gentle massage, on the other hand, has the happiest effects in this very class of cases.

Of late years my attention has been repeatedly directed to cerebral anæmia of peculiar localization due to malarial poisoning. It has been noted by others that temporary aphasia and other evidences of spasm of the cortical arteries may occur as equivalents or sequelæ of a malarial attack. I have seen an analogous case in which hemianopsia and hemianæsthesia occurred under like circumstances, and were recovered from. Whether more permanent lesions, in the way of pigmentary embolism or progressing vascular disease, causing thrombotic or other forms of softening, may develop after such focal symptoms is a matter of conjecture, but I have observed two fatal cases in which the premonitory symptoms resembled those of one which recovered, and in which these were preceded by signs of a more general cerebral anæmia, and in one case had been mistaken for the uncomplicated form of that disorder. Where a type is observable in the exacerbation of the vertigo, headache, tinnitus, and lethargy of cerebral anæmia, particularly if numbness, tingling, or other signs of cortical malnutrition are noted in focal distribution, a careful search for evidences of malarial poisoning should be made; and if such be discovered the most energetic antimalarial treatment instituted. It is in such cases that arsenic is of special benefit.

The treatment of syncope properly belongs to this article. Where the signs of returning animation do not immediately follow the assumption of the recumbent position, the nitrite of amyl, ammonia, or small quantities of ether should be exhibited for inhalation. The action of the former is peculiarly rapid and gratifying, though the patient on recovery may suffer from fulness and pain in the head as after-effects of its administration. The customary giving of stimulants by the mouth is to be deprecated. Even when the patient is sufficiently conscious to be able to swallow, he is usually nauseated, and, as he is extremely susceptible to strong odors or tastes in his then condition, this nausea is aggravated by them. By far the greater number of fainting persons recover spontaneously or have their recovery accelerated by such simple measures as cold affusion, which, by causing a reflex inspiration, excites the circulatory forces to a more normal action. Rarely will the electric brush be necessary, but in all cases where surgical operations of such a nature as to render the development of a grave form of cerebral anæmia a possibility are to be performed, a powerful battery and clysters of hot vinegar, as well as the apparatus for transfusion, should be provided, so as to be within reach at a moment's notice.

Inflammation of the Brain.

Before the introduction of accurate methods of examining the diseased brain the term inflammatory softening was used in a much wider sense than it is to-day. Most of the disorders ascribed to inflammatory irritation by writers of the period of Andral and Rush are to-day recognized as regressive, and in great part passive, results of necrotic destruction through embolic or thrombic closure of afferent blood-channels. Two forms of inflammation are universally recognized. One manifests itself in slow vascular and connective-tissue changes and in an indurating inflammation. There are two varieties of it: the first of these, which is associated with furibund vaso-motor explosions and regressive metamorphosis of the functional brain-elements, is known from its typical association with grave motor and mental enfeeblement as paretic dementia or dementia paralytica. The second, which is focal in the distribution of the affected brain-areas, is known as sclerosis. The former is treated of in a separate article; the latter is considered in connection with the spinal affections which either resemble it in histological character or complicate its course. The second form of cerebral inflammation is marked by the formation of the ordinary fluid products of acute inflammation in other organs of the body; this is the suppurative form, usually spoken of as abscess of the brain.

In addition to these two generally recognized inflammatory affections there are a number of rare diseases which are regarded by excellent authority as also of that character. The vaguely-used term acute encephalitis has been recently reapplied with distinct limitations to an acute affection of children by Strümpell. This disease is usually of acute onset, infants under the sixth year of age being suddenly, and in the midst of apparently previous good health sometimes, attacked by fever, vomiting, and convulsions.⁴⁰ Occasionally coma follows, which may last for several days, perhaps interrupted from time to time by recurring convulsions or delirium. The convalescence from this condition is rapid, and in some cases is complete; in others paralysis remains behind in the hemiplegic form. The paralysis is usually greater in the arm than in the leg; in extreme cases it involves the corresponding side of the face, and, as the paralyzed parts are arrested or perverted in growth, considerable deformity, even extending to asymmetry of the skull, may ensue. The deformity is aggravated by contractures. Usually there is some atrophy of the muscles, but in one case I found actual hypertrophy⁴¹ of some groups, probably in association with the hemiathetoid movements.

⁴⁰ As in my case of infantile encephalitis followed by athetoid symptoms (Journal of Nervous and Mental Diseases).

⁴¹ This was followed by atrophy. There are never any qualitative electrical changes.

The sequelæ of acute infantile encephalitis present us with the most interesting forms of post-paralytic disturbances of muscular equilibrium. Hemichorea and hemiathetosis, as well as peculiar associated movements and hemicontracture, are found in their highest development with this class of cases. Occasionally epileptiform symptoms are noted,⁴² and in others true epilepsy is developed. It is under such circumstances that imbecility is apt to be a companion symptom or result; and this imbecility is prominently noted in the moral sphere.

⁴² Which in one case of my own disappeared spontaneously.

The grave set of symptoms briefly detailed here are attributed by Strümpell⁴³ to an acute encephalitis, analogous, in his opinion, to the acute poliomyelitis of children. Its frequent occurrence after measles and scarlatina, as well as the fact that Ross⁴⁴ in a carefully-studied case arrived at the opinion that the disease was an embolo-necrotic result of endocarditis, would lead to the conclusion that it is a focal affection, probably due to the transportation of infectious elements to the brain through the blood-vessels. Its occurrence in children in the midst of apparent health⁴⁵ is consistent with the fact that rheumatism and an attendant slight endocarditis frequently pass unrecognized in infancy. It is supposed that a diffuse form of inflammatory non-suppurative softening exists by some of the Germans, but the proof advanced in favor of this view is not conclusive.

⁴³ As a surmise, for up to his writing no reliable autopsies had been made.

⁴⁴ Brain, October, 1883.

⁴⁵ McNutt (American Journal of Medical Sciences, January, 1885) cites Strümpell as attributing the theory of an inflammatory affection, which is analogous to poliomyelitis in its suddenness and nature, to Benedict, and refers to p. 349 of Strümpell's textbook under the erroneous date of 1864. This work was published in 1883-84, and the theory is advanced by Strümpell as his own. It is only a synonym, hemiplegia spastica infantile, that is attributed to Benedict.

A number of rare forms of interstitial encephalitis have been described. In one, elaborately studied by Danillo, an inflammatory hypertrophy of the cortex, involving the parenchyma as well as the connective and vascular structures, was found in a limited area of the motor province of the right hemisphere. There had been crossed epileptiform convulsions during life.⁴⁶

⁴⁶ Bulletin de la Société de Biologie, 1883, p. 238.

There is some question among pathologists as to the recognition of Virchow's encephalitis of the new-born. Certainly a part of Virchow's material was derived from the imperfect study of a condition of infantile brain-development which, as Jastrowitz showed, is physiological, and on which Flechsig based his important researches of tract-development. More recent studies, however, demonstrate that there is a form of miliary encephalitis in new-born children due to septic causes, such as, for example, suppuration of the umbilical cord. The demonstration by Zenker of the occurrence of metastatic parasitic emboli in cases of aphthous stomatitis, and by Letzerich of a diphtheritic micrococcus invasion in the brain of his own child, show that the subject of early infantile encephalitis merits renewed consideration.⁴⁷

⁴⁷ The attempt of Jacusiel to revive Virchow's encephalitis of the new-born (Berliner klinische Wochenschrift, 1883, No. 7) under the title of interstitial encephalitis does not seem to have met with encouragement, for, besides Jastrowitz, Henoch and Hirschberg opposed this view in the discussion.

Strictly speaking, the reactive changes which occur in the brain-substance bordering on tumors, hemorrhagic and softened foci, belong to the domain of encephalitis; but as they are considered in conjunction with the graver lesions to which they are secondary both in occurrence and importance, it is not necessary to more than refer to them here.

Abscess of the Brain.

As indicated in the last article, there formerly existed much confusion in the minds of pathologists regarding the terms softening and abscess of the brain. As long as softening was regarded as an inflammation, so long was abscess of the brain regarded as a suppurative form of softening. Aside from the fact that there is some resemblance in mechanical consistency between a spot of ordinary softening and one of inflammatory softening, there is no essential similarity of the two conditions. True softening is to-day regarded as the result of a death of brain-tissue produced by interference with the blood-supply; it is therefore a passive process. Inflammatory softening, of which abscess is a form, is due to an irritant, usually of an infectious nature. It is to the results of such irritation that the term suppurative encephalitis should be limited.

MORBID ANATOMY.—In all well-established inflammatory brain troubles the active part is taken by the blood-vessels and connective tissue; the ganglionic elements undergo secondary, usually regressive or necrotic, changes. The brain, considered as a parenchymatous organ, is not disposed to react readily in the way of suppurative inflammation unless some septic elements are added to the inflammatory irritant. Foreign bodies, such as knitting-needles, bullets, and slate-pencils, have been found encapsulated in this organ or projecting into it from the surrounding bony shell without encapsulation and without any evidences of inflammatory change. As a rule, a foreign body which enters the brain under aseptic conditions will, if the subject survive sufficiently long, be found to have made its way to the deepest part of the brain, in obedience to the law of gravity, and through an area of so-called inflammatory red softening which appears to precede it and facilitate the movement downward. This form of softening derives its color from the colored elements of the blood, which either escape from the vessels in consequence of the direct action of the traumatic agent; secondly, in consequence of vascular rupture from the reduced resistance of the perivascular tissue in consequence of inflammatory œdema and infiltration; or, thirdly, in obedience to the general laws governing simple inflammation.

A cerebral abscess may present itself to the pathological anatomist in one of three phases—the formative, the crude, and the encapsulated. In the first it is not dissimilar to a focus of yellow softening, being, like the latter, a diffuse softened area varying from almost microscopical dimensions to the size of a walnut, and of a distinctly yellow tinge. Microscopic examination, however, shows a profound difference. In pure yellow softening there are no pus-cells; in the suppurative encephalitic foci they are very numerous, and congregated around the vessels and in the parenchyma in groups. The crude abscess is the form usually found in cases rapidly running to a fatal termination. Here there is an irregular cavity in the brain, usually the white central substance of the cerebrum or cerebellum, formed by its eroded and pulpy tissue; it is filled with yellow, greenish, and more rarely brownish pus. In the most furibund cases broken-down brain-detritus may be found in the shape of whitish or reddish flocculi, but in slowly-formed abscesses the contents are free from such admixture, and thus the third phase is produced, known as the encapsulated abscess. The cavity of the abscess becomes more regular, usually spheroid or ovoid; the pus is less fluid, more tenacious, and slightly transparent; and the walls are formed by a pseudo-membrane⁴⁸ which is contributed by the sclerosing brain-substance, which merges gradually into the outlying normal tissue. I have seen one acute cerebral abscess from ear disease which might be appropriately designated as hemorrhagic; the contents were almost chocolate-colored; on closer inspection it was found that they were true pus, mingled with a large number of red blood-discs and some small flocculi of softened brain-substance. This hemorrhagic admixture was not due to the erosion of any large vessel, for the abscess had ruptured into the lateral ventricle at that part where it was most purely purulent. In a case of tubercular meningitis, Mollenhauer in my laboratory found an abscess in the white axis of the precentral gyrus, with a distinct purulent infiltration following the line of one of the long cortical vessels. The abscess was not encapsulated, the surrounding white substance exhibited an injected halo, and the consistency of the contents was that of mucoid material.

⁴⁸ There is considerable dispute as to the real nature of the tissue encapsulating cerebral abscesses. It is known, through the careful observations of R. Meyer, Goll, Lebert, Schott, and Huguenin, that the capsule may form in from seven to ten weeks in the majority of cases, about eight weeks being the presumable time, and that at first the so-called capsule of Lallemand does not deserve the name, being a mucoid lining of the wall. At about the fiftieth day, according to Huguenin, this lining becomes a delicate membrane composed of young cells and a layer of spindle-shaped connective elements.

In cases where the symptoms accompanying the abscess during life had been very severe it is not rare to find intense vascular injection of the parts near the abscess, and it is not unlikely that the reddish or chocolate color of the contents of some acutely developed abscesses is due to blood admixture derived from the rupture of vessels in this congested vicinity. Sometimes the entire segment of the brain in which the abscess is situated, or the whole brain, is congested or œdematous. In a few cases meningitis with lymphoid and purulent exudation has been found to accompany abscesses that had not ruptured. It is impossible to say whether in this case there was any relation between the focal and the meningeal inflammation, as both may have been due to a common primary cause.⁴⁹ In such cases, usually secondary to ear disease, thrombosis of the lateral sinus may be found on the same side. Where rupture of an abscess occurs, if the patient have survived this accident long enough—for it is usually fatal in a few minutes or hours—meningitis will be found in its most malignant form. A rupture into the lateral and other ventricles has been noted in a few cases.⁵⁰

⁴⁹ Otitis media purulenta in the two cases of this kind I examined.

⁵⁰ In one, observed together with E. G. Messemer, intense injection of the endymal lining, with capillary extravasations, demonstrated the irritant properties of the discharged contents.

Some rare forms of abscess have been related in the various journals and archives which have less interest as objects of clinical study than as curiosities of medical literature. Thus, Chiari⁵¹ found the cavity of a cerebral abscess filled with air, a communication with the nose having become established by its rupture and discharge.

⁵¹ Zeitschrift für Heilkunde, 1884, v. p. 383. In this remarkable rase the abscess, situated in the frontal lobe, had perforated in two directions—one outward into the ethmoidal cells, the other inward into the ventricles, so that the ventricles had also become filled with air. This event precipitated a fatal apoplectiform seizure.

The contents of a cerebral abscess usually develop a peculiarly fetid odor. It has been claimed that this odor is particularly marked in cases where the abscess was due to some necrotic process in the neighborhood of the brain-cavity. The only special odor developed by cerebral abscesses, as a rule, is identical with that of putrid brain-substance, and it must therefore depend upon the presence of brain-detritus in the contents of the abscess or upon the rapid post-mortem decomposition of the neighboring brain-substance.

In two cases of miliary abscess which, as far as an imperfect examination showed, depended on an invasion of micro-organisms, an odor was noticed by me which was of so specific a character that on cutting open the second brain it instantly suggested that of the first case, examined six years previous, although up to that moment I had not yet determined the nature of the lesion.⁵²

⁵² Owing to the lack of proper methods of demonstrating micro-organisms, the first case whose clinical history was known was imperfectly studied; of the second case, accidentally found in a brain obtained for anatomical purposes, the examination is not yet completed.

That form of abscess which, from its situation in or immediately beneath the surface, has latterly aroused so much interest from its important relations to localizations is usually metastatic, and directly connected with disease of the overlying structures, notably the cranial walls. In this case the membranes are nearly always involved. The dura shows a necrotic perforation resembling that found with internal perforation of a mastoid or tympanic abscess. The pia is thickened and covered with a tough fibro-purulent exudation; occasionally the dura and leptomeninges are fused into a continuous mass of the consistency of leather through the agglutinating exudation. The abscess is usually found open, and it is not yet determined whether it begins as a surface erosion, and, bursting through the cortex, spreads rapidly on reaching the white substance, or not. The white substance is much more vulnerable to the assault of suppurative inflammation than the gray, and not infrequently the superficial part of the cortex may appear in its normal contiguity with the pia, but undermined by the cavity of the abscess, which has destroyed the subcortical tissue. Possibly the infecting agent, as in some cases of ear disease, makes its way to the brain-tissue through the vascular connections, which, however sparse at the convexity of the brain, still exist.

CLINICAL HISTORY.—The symptoms of a cerebral abscess depend on its location, size, and rapidity of formation. There are certain parts of the brain, particularly near the apex of the temporal lobe and in the centre of the cerebellar hemisphere, where a moderately large abscess may produce no special symptoms leading us to suspect its presence. There are other localities where the suppurative focus⁵³ indicates its presence, and nearly its precise location and extent, by the irritative focal symptoms which mark its development and by the elimination of important functions which follows its maturation. It is also in accordance with the general law governing the influence of new formations on the cerebral functions that an acutely produced abscess will mark its presence by more pronounced symptoms than one of slow, insidious development. Indeed, there are found abscesses in the brain, even of fair dimensions, that are called latent because their existence could not have been suspected from any indication during life, while many others of equal size are latent at some time in their history.

⁵³ Practically, our knowledge of localization of functions in the human brain begins with the observation by Hitzig of a traumatic abscess in a wounded French prisoner at Nancy named Joseph Masseau. The year of the publication of this interesting case constitutes an epoch in advancing biological knowledge, which will be remembered when even the mighty historical events in which Hitzig's patient played the part of an insignificant unit shall have become obsolete. This, the first case in the human subject where a reliable observation was made was an unusually pure one; the abscess involved the facial-hypoglossal cortical field (Archiv für Psychiatrie, iii. p. 231).

An acute cerebral abscess is ushered in by severe, deep, and dull headache, which is rarely piercing, but often of a pulsating character. The pain is sometimes localized, but the subjective localization does not correspond to the actual site of the morbid focus.⁵⁴ It is often accompanied by vertigo or by a tendency to dig the head into the pillow or to grind it against the wall. With this there is more or less delirium, usually of the same character as that which accompanies acute simple meningitis. As the delirium increases the slight rise in temperature which often occurs in the beginning undergoes an increase; finally coma develops, and the patient dies either in this state or in violent convulsions. The case may run its course in this way in a few days, but usually one to three weeks intervene between the initial symptoms and death.

⁵⁴ Although Ross seems to be of a contrary opinion, it is the exception for the pain to correspond in location to the abscess.

Between the rapid and violent course of acute cerebral abscess detailed, and the insidious course of those which as latent abscesses may exist for many years without producing any noticeable symptoms whatever, there is every connecting link as to suddenness and slowness of onset, severity and mildness of symptoms, and rapidity and slowness of development and progress. It is the encapsulated abscesses which are properly spoken of as chronic, and which may even constitute an exception to the almost uniform fatality of the suppurative affections of the brain. Thus, the symptoms marking their development may correspond to those of an acute abscess, but coma does not supervene, temporary recovery ensues, and the patient leaves the hospital or returns to his vocation. But all this time he appears cachectic, and there will be found, on accurate observation, pathological variations of the temperature and pulse. The appetite is poor; the bowels are usually constipated; there are frequent chilly sensations and horripilations, and a general malaise. This condition slowly passes away in the few cases which recover; in others relapses occur, usually of progressing severity, and terminate life. The period during which the symptoms of the abscess are latent may be regarded as corresponding to the latent period which sometimes intervenes between an injury and the development of the symptoms of acute abscess, and which, according to Lebert, may comprise several weeks or months. In other words, the morbid process may be regarded all this time as progressing under the mask of a remission. It is this latent period which it is of the highest importance for the diagnostician to recognize. There is usually headache, which is continuous and does not change in character, though it may be aggravated in paroxysms. Usually the temperature rises with these paroxysms, and if they continue increasing in severity they may culminate in epileptic convulsions.

Many of the symptoms of cerebral abscess—prominently those attending the rapidly-developed forms and the exacerbations of the chronic form—are due to cerebral compression. It is the pulse and pupils, above all, that are influenced by this factor.

In an affection having so many different modes of origin as cerebral abscess, and occupying such a wide range of possible relations to the cerebral mechanism, it is natural that there should exist many different clinical types. So far as the question of the diagnosis of localized cerebral abscesses is concerned, I would refer to the article dealing with cerebral localization, in order to avoid repetition. With regard to the etiological types, they will be discussed with the respective causal factors.

ETIOLOGY.—Abscess of the brain is so frequently found to be due to metastatic or other infectious causes that it is to be regarded as highly improbable that it is ever of idiopathic occurrence. The most frequent associated conditions are—suppurative inflammation in neighboring structures, such as the tympanic cavity, the mastoid cells, the nasal cavity, or inflammation or injury of any part of the cranium and scalp. The connection of these structures with the brain through lymphatic and vascular channels is so intimate that the transmission of a pyogenic inflammatory process from the former to the latter is not difficult to understand. But disease of far distant organs, such as gangrene of the lung, and general affections, such as typhoid fever, occasionally figure among the causes of cerebral abscess, particularly of the miliary variety.

Among the commonest causes of cerebral abscesses are those which the surgeon encounters. The injury may be apparently slight and limited to the soft parts, or the bone may be merely grazed. Gunshot wounds are particularly apt to be followed by a cerebral abscess; and it has been noted that those which granulate feebly, whose base is formed by a grayish, dirty, and fetid material, are most apt to lead to this ominous complication. The symptoms do not usually develop immediately, and after the surgeon is led to indulge in the hope that danger is past, proper reaction sets in, healthy granulations develop—nay, the wound may close and be undergoing cicatrization—then the patient complains of feeling faint or drowsy, and with or without this premonition he has convulsive movements of one side, sometimes involving both extremities and the corresponding side of the face. Consciousness is usually preserved, but the spells recur, and the patient is noted to be absent-minded during and after the convulsive seizure. On some later day he is noticed to become pale, as in the initial stage of a true epileptic seizure; total abolition of consciousness follows, and the clonic spasms, affecting the same limbs and muscles involved in the first seizures, now recur with redoubled violence. After such an attack more or less paresis is observed in the muscles previously convulsed. A number of such seizures may occur, or a fatal issue terminate any one of them. Not infrequently the field of the involved muscles increases with each fit. Thus the thumb or a few fingers may be the first to show clonic spasm; in the next fits, the entire arm; in succeeding ones, the leg and face may follow suit. In such a case the periphery first to be convulsed is the first to become paralyzed, thus showing that where the disease began as an irritative lesion the cortex is now destroyed, and that around the destructive focus as a centre the zone of irritation is spreading excentrically, first to irritate and then to destroy seriatim the functions of the various cortical fields in their order. According to the teachings laid down in the article on Localization, the order of invasion and extension, as well as the nature, of the focal symptoms will vary. Finally, the attacks become more severe and of longer duration; the patient does not recover in the intervals, but complains of nausea, pain, confusion, and head-pressure. He is noted to be dull, his temperature is slightly raised (100° F.), and the speech may be affected. Several attacks may occur in a day, each leaving the patient more and more crippled as to motility and mind. He is delirious and drowsy at intervals; his temperature may rise after an attack from one to four degrees, usually remaining near 103°–104° F. in the evening; and, coma developing, death occurs, the convulsion or paralytic phenomena continuing at intervals during the moribund period, and the temperature and pulse sometimes running up rapidly toward the last. On examining the parts, it is found that the bone is necrotic at the point of injury, usually only in its outer table, but sometimes in its entire thickness. In exceptional cases the normal continuity of the entire table is not interrupted to all appearances, and a small eroded spot on the inner table is found bathed in pus, or a detached necrotic fragment may be found in the latter. Corresponding to the purulent focus on the inner table the dura mater is detached, discolored, and perforated in one or more places with irregular rents or holes which have a greenish or blackish border. An abscess is found in that part of the brain which corresponds to this opening. There is no question that it was caused by direct infection from the necrotic spot.

Cases have been noted,⁵⁵ apparently of idiopathic origin, in which a sudden paralysis of a few fingers was the first symptom produced by the development of a cerebral abscess. In a few days such a paralysis extends to the other fingers and to the forearm. Occasionally no convulsive phenomena are noted, or choreic movements indicate, in their place, that the cortical field is irritated. Such cases usually run a rapidly fatal course.

⁵⁵ Arthur E. W. Fox, Brain, July, 1885.

The most frequent cause of cerebral abscess in civil practice is suppurative inflammation of the middle ear. It may be safely asserted that the person suffering from this affection is at no time free from the danger of a cerebral abscess, a purulent meningitis, or a phlebitic thrombosis of the sinuses. Cases are on record where the aural trouble had become chronic, and even quiescent, for a period of thirty years, and at that late date led to abscess with a fatal termination. Of 6 cases of this character in my experience, 4 of which were verified by anatomical examination, not one but had occurred at least four years after the commencement of the ear trouble, and 1 happened in a man aged fifty-four who had contracted the latter affection in childhood. In 2 there was in addition diffuse purulent meningitis, limited on the convexity to the side where the abscess was situated.⁵⁶ In 4 the abscess was in the temporal lobe, 1 of them having in addition an abscess in the cerebellar hemisphere of the same side; in a fifth the abscess was in the deep white substance of the cerebral hemisphere, opening into the lateral ventricle, and in the sixth it was in one cerebellar hemisphere alone.

⁵⁶ One of these was seen during life by J. R. Pooley; the other was a paretic dement at the New York City Pauper Asylum.

The course of this class of abscesses is usually obscure: focal symptoms are not commonly present, and the constitutional and local symptoms usually appear as a gradual outgrowth from the aural troubles. Thus there is at first usually little fever, vertigo, and chilliness, but considerable tinnitus, and sometimes pain in the ear. Occasionally local signs of a septic metastasis of the otitis, such as œdema over the mastoid or painful tumefaction of the cervical glands, are visible. The pain previously referred to the region of the ear now becomes general; commonly—even where the abscess is in the temporal lobe—it becomes progressively aggravated in the frontal and sometimes in the nuchal region, and under an increase of the febrile phenomena death may exceptionally occur without further complication. Even large abscesses in one half of the cerebellum occur without producing Ménière's symptom—a fact which leads to the suspicion that the purulent deposit must have been of slow and gradual development. In one case distinct symptoms indicating an affection of the subcortical auditory tract were observed. As a rule, this class of abscesses are accompanied toward the close by active general symptoms—convulsions, coma, narrowing and impaired light-reaction of the pupils. Delirium, when a prominent symptom from the beginning, indicates the probable association of meningitis with the abscess.⁵⁷ Occasionally severe pain, rigor, high temperature, and paralysis may be absent even with rapidly-developed abscess from otitis.⁵⁸

⁵⁷ The same is probably true of oculo-motor paralysis, which Ross (loc. cit., vol. ii. p. 735) refers to uncomplicated abscess.

⁵⁸ This was the case with an abscess containing five ounces of pus recorded by C. S. Kilham at the Sheffield Medical Society (British Medical Journal, February 13, 1886). As illustrating what was stated about the non-correspondence of the pain and the location of the abscess, it may be stated that notwithstanding this large abscess was in the temporal lobe, what pain was present was in the forehead.

Ulcerative endocarditis, infectious osteomyelitis, pulmonary gangrene, general pyæmia, and, as is claimed by a few authors, typhoid fever, are often accompanied by multiple abscesses in the brain-substance. Usually the foci are small, as may be readily inferred from the fact that they are of embolic origin, the emboli being usually so small as to lodge in very small vessels, and that the fatality of the primary disease is so great as to cut short life before the abscess can reach larger dimensions. For the same reasons the symptoms they produce are rarely distinctive. In chronic lung affections accompanied by putrescence in bronchiectatic or other cavities cerebral abscesses are not uncommon occurrences. Under these circumstances, although we must assume an embolic origin, the abscess is rarely multiple, and the symptoms are as marked as in the ordinary varieties. Thus a patient suffering from chronic phthisis, with or without prodromal malaise or somnolence, experiences formications and pain in his right leg; he then notices a slight halt in walking; twitches appear in the affected extremity; it becomes distinctly paretic. The arm then becomes affected in like manner; the pupils become unequal; a severe chill occurs, followed by delirium, convulsions, coma, and death.

DIAGNOSIS.—There is little difficulty in recognizing the existence of a cerebral abscess in which well-marked focal and constitutional symptoms coincide, or where a distinct abscess-producing cause, such as an ear trouble, a head injury, or a putrid bronchiectasis, coexists.⁵⁹ But there are a number of cases, varying from the latent form to forms with obscure general symptoms, whose recognition is impossible or at best a matter of conjecture. Such cases may be readily confounded with certain tumors. The existence of febrile symptoms, although not excluding tumor, as some tumors are accompanied by such, is greatly in favor of abscess. On the other hand, choked disc, which is rare with abscess and found only with the very largest, is in favor of tumor.

⁵⁹ Yet a leading and careful authority was misled into making the diagnosis of abscess in a case of ear disease complicated by a cerebral tumor.

PROGNOSIS AND TREATMENT.—The majority of cerebral abscesses must, from the nature of the case, be regarded as not influenceable by medicinal measures or surgical treatment. The miliary and other abscesses due to general septic causes or to mycotic invasion, being in the nature of the case but features of intrinsically dangerous or fatal primary diseases, do not call for special measures. It is different with those due to local trouble about the head and to surgical causes. Remarkable advances have been made in the operative treatment of cerebral abscesses, chiefly owing to the increasing accuracy of the localization of the affected areas through the disturbance of their function, and to the perfection of surgical methods. A number of cases by Gussenbauer, Wernicke, and others have shown that some abscesses may be accurately located during life by the focal symptoms produced by their presence. Wernicke's observation of a large abscess in the occipital lobe showed two facts. First, it permitted the study of the effect of large abscesses on the cerebral movements, as it was found after trephining that the pulsation movement of the brain was lost and the dura tensely bulging, thus indicating a high degree of cerebral pressure. Secondly, the operation showed that an abscess can be emptied of its contents, under moderate aseptic precautions, without provoking contiguous inflammatory reaction or infecting the meninges. Notwithstanding these favorable local conditions, the patient died. Gussenbauer⁶⁰ was more fortunate. He surmised from the fluctuation of some symptoms and the predominance of others that his patient had an abscess in the frontal lobe. The suspicion was verified: an abscess of the size of an apple was found, opened, and emptied of its contents. The patient recovered without any immediate untoward symptom.⁶¹

⁶⁰ Prager medizinische Wochenschrift, 1885, Nos. 1, 2, and 3.

⁶¹ Epileptic and focal spasms subsequently developed, which shows that a new inflammatory or other destructive process may have set in in the vicinity of the emptied sac.

The uncertainties of localization in some districts of the brain are so great that a number of attempts to repeat the explorations and aspiration of Wernicke and Gussenbauer have failed. In one case recently operated on in New York City the aspirating-needle was run into the brain-substance in several different directions without striking the pus. It is a question under such circumstances whether the chances of an abscess becoming latent, minimal though they be in cases with pronounced signs, are not to be preferred to those which an uncertain operation can give. The superficial encephalitic foci offer far better opportunities for surgical triumphs. Here not only the symptoms are much more constant, and point more unerringly to the site of the morbid spot, but there are often other signs, such as the evidences of impaction of a foreign body, local tenderness on percussion, or bone disease, which aid in determining the proper spot for the application of the trephine. Several operations where traumatic encephalitis existed with or without leptomeningitis of the convexity, followed by complete recovery, were performed by Macewen.⁶²

⁶² The Lancet, 1885, vol. i. p. 881.

The medicinal treatment of abscess of the brain is limited to derivative methods, whose aim is the relief of pressure—an aim whose fulfilment is more frequently illusory than otherwise.

Benefit has been claimed from the energetic use of mercury, chiefly in the form of calomel, by older writers; and recently Handfield Jones has endorsed its administration, attributing to it a remission in a case in which it was employed. It must be remembered, however, that remissions occur spontaneously in this disease, and that the purgative action of calomel may act well for the time being in an affection so apt to be associated with hyperæmia and increased cerebral pressure as is an abscess of the brain.⁶³ In the nature of the case, even this latter momentarily beneficial effect is at the best temporary.

⁶³ Brain, October, 1884, p. 398.

The prophylaxis of cerebral abscess can be carried out only in cases due to cranial and aural affections. The importance of treating all scalp and cranial injuries under aseptic⁶⁴ precautions is recognized by all surgeons. It is generally admitted that the trephining of a bone suspected to be the site of an ostitic or necrotic process involves fewer risks than the allowing it to remain. Similar principles govern the treatment of the inflammatory involvement of the mastoid cells often complicating otitis media. If trephined at all, these should be trephined at the earliest moment. It was a belief among the older aurists that the sudden cessation of an aural discharge was of evil augury, and that cerebral complications were more apt to follow under such circumstances than when the ear discharged freely. Von Tröltsch, Politzer, Gruber, and Toynbee have opposed the exclusive application of the old dogma. In so far as the older ear-surgeons regarded a profuse aural discharge as an encouraging sign, in this respect they were of course wrong. But their observation of the frequent concurrence of cerebral sequelæ with suppression of discharge is, I think, borne out by a large number of cases. It does not apply, however, to the suppression of discharge by the rational employment of aseptic injections.

⁶⁴ This term is used in its widest sense here.

Spinal Hyperæmia.

The spinal cord is found to vary considerably in color in different individuals. To some extent this difference is influenced by the position occupied by the body after death, but not as markedly as in the case of the brain. Thus it will be paler in a body which has been kept in the prone than in one which has been kept in the supine position.⁶⁵ It is usually found more injected in persons who have died of febrile affection than in those who have died of exhausting diseases; notably is this the case with typhus fever and with subjects who die with congestive malarial chill. But the most intense congestion, where the gray substance instead of having the normal rosy hue appears like a blood-soaked sponge, and the white substance instead of the tint to which it owes its name has a pink shade, is found in subjects dying in convulsive disorders complicated by asphyxia, such as epileptic status, tetanus, and certain toxic disorders.