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.