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.