properly considered in connection with the traumatic neuroses and
certain forms of insanity. But there are some milder cases in which
the symptoms remain within such compass as is comprised in this
section. The patient, after a fall or a blow on the head, suffers from
insomnia, has a sensation of fulness and ache in the head, complains
of a pulsating feeling in the occipital region and an inability to
concentrate his thoughts on subjects which previously were parts of
his routine. Under appropriate treatment recovery ensues, but there
remains behind an intolerance of alcoholic beverages, and at times the
patient experiences momentary fits of abstraction, which may be
regarded as mild analogies of the more serious episodes of the
full-blown traumatic neurosis. Thus, he may be walking along the
street and suddenly lose his train of thought for an instant, to
regain it on observing that he has inadvertently made a misstep. Or in
the midst of an address a previously fluent orator in attempting to
find a certain by-law in the rules of a society is unable to recollect
which he was in search of, and is compelled to take his seat with a
rambling apology. But for the fact that similar sequelæ are noted in
cerebral hyperæmia from other causes, it would be questionable whether
it be proper to attribute them to the congestive element engendered by
the traumatic influence. They are usually noted when the hyperæmic
phenomena proper have become latent or disappear, and, with other
symptoms customarily treated of as mere results of circulatory
trouble, may be regarded as signs of neural exhaustion or inadequacy
rather than of insufficient ensanguination.
A more serious form of cerebral hyperæmia occurs in females in
conjunction with the climacteric period, and in both sexes in
consequences of the suppression of any habitual discharge in advanced,
and exceptionally in middle and juvenile, life. The advent of the
symptoms is rapid, a few hours or days sufficing for the development
of the attack. The face is flushed, the carotids throb violently, the
general cutaneous surface is congested, and the patient is
incoherently talkative. The one side, usually the right, is heavy and
tremulous, the fingers are devoid of their usual skill, and the speech
is more or less thick. The sleep is disturbed or replaced by a
stuporous condition, whose similitude to an apoplectiform seizure is
sometimes heightened by stertorous breathing. After one or several
days the patient emerges from this condition by degrees or suddenly
with complete restitutio ad integrum. But the attack may recur, and
ultimately it is noted in the event of repeated attacks that the
return to the normal state is slower and less complete: the disorder
then undergoes a transition into the congestive type of paretic
dementia described in another portion of this volume.
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.
--------------------+----------------------+------------------------
Symptomatic State. | In Cerebral Anæmia. | In Cerebral Hyperæmia.
--------------------+----------------------+------------------------
Pupils. | Usually dilated and | Usually small or
| mobile. | medium.
--------------------+----------------------+------------------------
Respiration. | Often interrupted by | Normal.
| sighing or by a deep |
| breath, even when at |
| rest. |
--------------------+----------------------+------------------------
Headache. | Either sharp and | If localized,
| agonizing, and then | accompanied by a
| in a limited area, | subjective and
| or a general dull | objective (always?)
| ache, intensified in | feeling of heat; if
| the temples and over | general, is compared to
| or behind the eyes. | a bursting or steady
| | pressure.
--------------------+----------------------+------------------------
Activity. | There is lassitude. | There is indisposition
| | to exertion, yet
| | patient is restless.
--------------------+----------------------+------------------------
Temperament. | Lethargic, with | Choleric, with
| exceptions. | exceptions.
--------------------+----------------------+------------------------
Intellect. | Inability to exert. | Rather confusion than
| | inability of.
--------------------+----------------------+------------------------
Sleep. | Insomnia, interrupted| Insomnia, with great
| by trance-like | restlessness,
| conditions, in which | variegated by
| the patient is | unpleasant and confused
| comparatively | dreams.
| comfortable. Dreams |
| often pleasant. |
--------------------+----------------------+------------------------
Influence of | Aggravates all the | Either without
upright position | symptoms. | influence or
of body. | | beneficial.
--------------------+----------------------+------------------------
Influence of | Amelioration. | Aggravation.
recumbent position | |
of body and | |
dependent position | |
of head. | |
--------------------+----------------------+------------------------
Influence of acts | If any, a sharp | Aggravated.
involving deep | headache may ensue, |
inspiration, such | but the other |
as blowing, | symptoms are not |
straining at stool, | aggravated. |
sneezing, etc. | |
--------------------+----------------------+------------------------
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.]