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.