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.