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.