A system of practical medicine. By American authors. Vol. 5

Chapter M: M——, was a stout Irish woman about forty years of age. She had (18)

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DIFFERENTIAL DIAGNOSIS.—In some of its clinical aspects cerebral hyperæmia closely resembles cerebral anæmia. This is not surprising {772} when we bear in mind that both constitute nutritive disturbances of the same organ, and that, notwithstanding the apparent difference in the surface injection of an anæmic and a hyperæmic brain, the state of affairs in the ultimate capillary districts may be much more alike than might be anticipated on theoretical grounds. In congestion we have wider vessels, and perhaps, though not necessarily, a better quality of blood; but at the same time the intracranial pressure may be such that the venous emunctories can labor but slowly: the result will be that although there is more blood in the brain, the lessened rate of flow places the nerve-elements under nearly the same nutritive disadvantage that they are placed under with the narrower and vitiated but more rapid blood-column of ordinary anæmia.[10] It is particularly the symptoms dependent on those nerve-centres and tracts which are, so to speak, dynamically sensitive, which resemble each other so much that an intrinsic difference—both being placed side by side—is not always determinable. This is true of the aural and optic symptoms. Tinnitus, photophobia, scotomata, and blurring or darkening of the visual field occur in both, and in about the same varieties. In my experience the acuteness of hearing is more apt to be interfered with by the subjective sounds with hyperæmic than with anæmic tinnitus. The scotomata of hyperæmia are more distinct and coarser than those of anæmia; darkening of the visual field is more apt to occur with sudden rising in anæmia, while in hyperæmia it is provoked by coughing, straining at stool, or other cause operating directly or indirectly on the return circulation. It may be stated, as a general rule, that if any of these symptoms are aggravated on lying down or stooping, they are due to hyperæmia; while if the same procedures are resorted to in anæmia, amelioration ensues. But in many chronic cases these symptoms seem to continue as indications of a permanently altered activity of the nerve-elements themselves; that is, as a sort of pathological habit. In that case the position test may not be decisive. In one respect there is a decided difference between the anæmic and hyperæmic forms; there is never amaurosis in the latter, while it is approached, and occasionally fully developed, in the former. Much more importance attaches to the differentiation of tinnitus due to nutritive brain disorders and that due to aural disease. As a rule, the tinnitus from cerebral hyperæmia is symmetrical; if unilateral, it is of short duration. The procedure of Valsalva[11] aggravates the tinnitus of hyperæmia, and relieves that which is due to the commoner forms of ear disease; the former is aggravated and the latter relieved by noise.

[Footnote 10: It is also admitted that the blood stagnating in the larger veins and accumulating in the arteries, the limits of compressibility of the other cerebral contents being passed, the capillaries will suffer, so that with injected and turgescent arterioles and venules there may be capillary anæmia.]

[Footnote 11: I would caution against Politzer's method in cases of ear disease coexisting with cerebral congestion. In a patient now under my treatment each session at the aurist's was followed by a distinct exacerbation of the cerebral symptoms.]

In the table on p. 773 I have attempted to formulate the principal differential relations of the protracted forms of cerebral anæmia and hyperæmia.

There are a number of so-called functional nervous states which, aside from the fact that they are unwarrantably confounded with cerebral congestion, do not require mention in a differential relation. Such are the {773} masturbatory neurosis, certain hysterical states, and the asthenia resulting from nervous shock and overwork. These states have found a provisional resting-place under the comprehensive and non-committing title of neurasthenia or nervous exhaustion—a term which includes conditions fully recognized by Robert Whytt and Isenflamm in the last century.

TREATMENT.—Ergot of rye with its preparations may be regarded as the cardinal drug in cerebral hyperæmia. There are few drugs in the domain of neurological therapeutics which are so directly antithetical to the pathological state as this one. There is scarcely a case of cerebral hyperæmia that is brought to the physician's attention but may be regarded as being in part due to an over-distension of the cerebral vascular tubes. This is directly overcome by ergot, and the quantity which such patients will sometimes bear without showing signs of ergotism is something remarkable, in notable contrast with the subjects of cerebral anæmia, who are usually very sensitive to it. About three grains of Bonjean's ergotin may be regarded as a safe trial-dose for an adult, and unless a distinct effect is produced within two or three days this dose may be raised to six grains twice or three times within twenty-four hours. It is not advisable to combine strychnia with the ergotin, as is often done; the effect of that alkaloid is to increase the psychical and sensorial irritability of the patient. Chloral hydrate or bromide, or both in combination, is as useful an adjuvant here as it would be hurtful in cerebral anæmia.

It is not usually necessary to employ special hypnotics in cerebral congestion. The same drug whose beneficial effect is so potently marked during the daytime that tinnitus, cerebral pressure, and subjective drowsiness will disappear before it, if not as rapidly, more enduringly, than the symptoms of cerebral anæmia disappear before nitrate of amyl, will also overcome the insomnia in the majority of cases. Where it fails, warm pediluvia or sitz-baths will prove more efficient than the majority of hypnotics. Their use, at all events, involves no hurtful effect on a—possible already—disordered stomach, and their certainty of action is {774} much more even. Their temperature should be about 40-42° Centigrade, and the immersion continue from fifteen to twenty-five minutes.[12]

[Footnote 12: A number of experiments, the most recent of which were by Musso and Bergesio (_Rivista sperimentale di Freniatria e di Medicina legale_, 1885, xi. p. 124), have shown that in such baths the cerebral pulsations become less excursive and that the volume of the brain decreases. The same applies to general warm baths.]

In those cases where the subject sensations accompanying hyperæmia, active or passive, are intensified in the posterior segment of the head or the nuchal region, leeches at the mastoid process, or cupping, wet or dry according to the severity of the symptoms, will often give immediate relief. Burning with the actual cautery, or, what is equivalent and a much neater application, the heated glass rod, has an equally happy effect in that class of cases where throbbing and pain are intensified low down. It should be done as near the spot indicated by the patient's complaints as possible.[13]

[Footnote 13: In a case of gliomatous hypertrophy of the pons oblongata transition marked by the development of numerous tortuous and enlarged blood-vessels the episodes of the disease were found to be of the congestive type, and yielded to no other treatment than that with the cautery.]

The diet of patients who are suffering from or subject to cerebral hyperæmia should not be stimulating nor difficult of digestion. It is much more important to avoid distension or overstrain of the stomach than to reduce the nutritive value of the food in the majority of cases, for true plethora is much less common than is supposed. The bowels should be so regulated that the patient have at least one, and that an easy, movement a day. The saline cathartics, particularly the Carlsbad salt, are to be used to effect this if necessary. The clothing around the neck should be free and not compress the parts.

In those severe forms of cerebral congestion attending the climacteric period, or occurring in consequence of the suppression of discharges, and similar causes, the symptoms are often so alarming as to render energetic measures, such as bleeding, immediately necessary. This may be affected by applying leeches to the nose, the temples, or by bleeding at the arm. If due to the suppression of hemorrhoidal discharges or menstruation, the leeches should be applied to the anus and hot sitz-baths taken. In the milder forms a pill composed of aloes, podophyllin, and ox-gall, recommended by Schroeder van der Kolk, will be found effective.

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 {775} 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.

[Footnote 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 {776} 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 found[16] when the right common carotid artery is the one ligated.

[Footnote 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.]

[Footnote 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.

[Footnote 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.]

{777} With bilateral ligature[18] 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.

[Footnote 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.]

[Footnote 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.]

[Footnote 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 {778} 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. Beneke[22] 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.

[Footnote 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.]

[Footnote 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 {779} 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.

[Footnote 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.

[Footnote 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 {780} 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.

[Footnote 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 limits[26] in all persons {781} when subjected to emotional or violent external impressions of any kind.

[Footnote 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]

[Footnote 27: Hammond, on the other hand (_Diseases of the Nervous System_, p. 77), has the ventricles generally empty.]

[Footnote 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 {782} 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.

[Footnote 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). {783} 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 {784} 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 {785} 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 {786} antecedent history of an exhausting abdominal disorder; 6th, also a facial appearance characteristic of the latter.

[Footnote 30: This is not admitted by most writers, but does occur exceptionally.]

[Footnote 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.

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A system of practical medicine. By American authors. Vol. 5Chapter M: M——, was a stout Irish woman about forty years of age. She had (18)

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