young persons competing for admission to higher institutions of
learning in New York City through the channel of a competitive
examination died with symptoms of cerebral irritation; the death
certificates in several such cases assigned meningitis or cerebral
congestion as the cause of death, and attributed the disorder to
mental overstrain. It is not so much the intellectual effort that has
proved hurtful to the pupils as the emotional excitement attending on
all competitive work, the dread of failure, the fear of humiliation,
and anxiety developed by the evident futility of the cramming process.
Some years ago I recorded the results of some inquiries on this head
in the following words: “The mental-hygiene sensationalists, who
periodically enlighten the public through the columns of the press
whenever an opportune moment for a crusade against our schools and
colleges seems to have arrived, are evidently unaware of the existence
of such a disease as delirium grave, and ignorant of the fact that the
disorder which they attribute to excessive study is in truth due to a
generally vitiated mental and physical state, perhaps inherited from a
feeble ancestry. Our school system is responsible for a good deal of
mischief, but not for meningitis” (_Insanity, its Classification,
Diagnosis, and Treatment_). Since then I had an opportunity of
obtaining an excellent description of such a case which had been
attributed to the combined effects of malaria and educational
overstrain, presenting opisthotonos, fulminating onset, and an
eruption!]
[Footnote 3: _Virchow's Archiv_, lxiv.]
[Footnote 4: The observations of Gärntner (_Medicinische Jahrbucher_,
1884, 1) harmonize with this. He found that radiant heat contracts the
blood-vessels of the frog's mesentery.]
[Footnote 5: The same applies to conditions which are discussed under
this head in textbooks, although they have either only a medico-legal
bearing or are inconstant factors, such as the injection of the brain
in death from strangulation. I need but instance the vascular
condition of brains of criminals executed by hanging. In the case of
one where the strangulation had been slow I found an engorgement of
all the vessels and arachnoidal as well as endymal hemorrhages; in a
second, where the criminal had been carried half fainting to the drop,
and death ensued quickly and without signs of distress, the brain was
decidedly anæmic.
It has been also considered best to omit treating of the collateral
hyperæmia of the brain sometimes found with erysipelas of the face and
scalp. This I regard as essentially of the same nature as the
metastatic meningitis of erysipelas, if it be not in reality a first
stage of the latter.]
ETIOLOGY.—An individual predisposition to cerebral congestion was one
of the unquestioned facts of the older medical writers. It undoubtedly
exists, and to-day we attribute it to inherited vascular conditions
either affecting the calibre and coats of the blood-vessels or the
vigor of the vaso-motor apparatus. I have remarked the transmission of
that weakness of the latter which underlies the congestive phenomena
of later life much more frequently in the female than in the male sex.
It has been claimed that external refrigeration produces hyperæmia of
the brain, as of other internal organs, and that this accounts for the
greater frequency of the disorder in cold weather. Niemeyer indeed
speaks of persons who, suffering from this condition, appear and act
in such a way as to convince the laity that they are intoxicated; and
Andral, Falret, and Hammond note the occurrence of a much larger
number of cases in the winter than in the summer months. I apprehend
that the condition described by Niemeyer must be extremely uncommon,
both from individual experience and the rarity of its mention as an
independently observed fact. With regard to the alleged greater
frequency of the disorder in winter, it must be remembered that all
the three observers cited include in their computation a number of
cases in which congestion was a collateral feature; they did not limit
themselves to the disorder as {766} spoken of here. Certainly, the
physician will see few if any persons who consult him because of the
hyperæmia-producing effects of a cold day.
The suppression of habitual discharges, of the hemorrhoidal flux, and
the cessation of menstruation are associated in many instances with
the more formidable grades of cerebral hyperæmia. Many phenomena of
so-called climacteric insanity depend on congestive states. The sudden
closure of an old ulcer or the removal of hemorrhoids in advanced life
has in some well-established instances provoked alarming seizures not
unlike those noted with paretic dementia. The chain of proof
establishing the direct influence of physiological and pathological
discharges on the vascular controlling apparatus of the brain is most
complete. Not alone cumulative clinical observation, but the
occasional happy result of therapeutical procedure based on this
supposed interdependence, support it. Thus, the congestive cerebral
state is recovered from when the menstrual or hemorrhoidal flow is
re-established, or an issue is formed in the nape of the neck, or an
old ulcer is allowed to reopen.[6]
[Footnote 6: The treatment of paretic dementia, particularly of the
congestive type, is also based on this relation. The irritating
antimonial ointment and issues in the nape of the neck, etc. have been
lauded by older observers, and in two of my own cases had the best
results—in one, indeed, with established restitutio ad integrum of now
nearly two years' duration. I am inclined to suppose that its
abandonment is due to an improper selection of cases; in the ordinary
premature senility and syphilitic types such treatment is altogether
ineffective. It is applicable to but a minority of cases at best, and
to them only at an early period. It is probably to a similar form of
congestion that Bouchut refers when (“Les Nèvroses congestives de
l'Encéphale,” _Gazette des Hôpitaux_, 1869) he speaks of a cerebral
hyperæmia developing under the mask of a meningitis—an expression that
may be allowed if understood in the same sense as the comparison
between hydrocephaloid and hydrocephalus.]
The origin of most cases that are brought to the physician's attention
is more or less complicated. A business-man, lawyer, or student
suffering from worry incident to his profession, living so irregularly
as to provoke gastric disturbances, becomes afflicted with insomnia,
and in addition is also constipated. Straining at stool, he finds a
dull, heavy sensation affecting the upper part of his head; attempting
to resume his work, this is aggravated, and after a series of
temporary remissions the condition to be later described becomes
continuous. In such a case the insomnia, usually due to neural
irritability, if not aggravated by an existing dyspepsia, leads to
such a one, and a circulus vitiosus familiar to all physicians is
established. Each of the factors concerned involves strain of the
cerebral vaso-motor apparatus, but none more so than the insomnia. It
is not so much the intensity of the strain as its long duration and
the exhaustion of the centre which in sleep is supposed to be at
comparative rest. This rest is not obtained, and, in conformity to the
laws of neural exhaustion, that centre becomes morbidly irritable.
Now, gastric irritation is competent to produce a reflex influence on
even the healthy cerebral organ; to do so it must be a severe one; but
with the class of persons alluded to the slightest indiscretion in
food or drink is sufficient to set up reflex vertigo or headache. The
current theory regarding these symptoms is that they are due to
stimulation of the vaso-constrictors and ensuing cerebral anæmia; but
the subjects before us will usually be found to flush up instead of
becoming pale, as in simple vertigo a stomacho læso, or if there be
initial paleness, there is a {767} secondary flush, as if the tired
arterial muscle had become exhausted by the effort at obeying the
reflex stimulus. In addition, a profuse perspiration sometimes breaks
out on the upper part of the body.
The influence of traumatic causes and insolation in producing a
tendency to repeated and severe cerebral congestion is recognized,
particularly among alienists. It is supposed that an abnormal
irritability of the vaso-motor apparatus is provoked by these causes.
Abundant evidences are sometimes found in the brains of such persons
of an altered state of nutrition of the brain and its membranes, and
which point in the direction of congestion.
In the conditions thus far alluded to it can be fairly assumed that
the determination of blood to the cerebral blood-vessels is more or
less active. Passive congestion due to impeded return circulation is
of secondary interest, as the primary disease, be it a pertussis or a
laryngeal, cardiac, pulmonary, or surgical condition, will constitute
the main object of recognition and management. Certain
quasi-physiological acts, as coughing, hurried breathing, holding the
breath while straining at stool, and placing the head in a dependent
position while acting in the direction of passive hyperæmia, are to be
considered in connection with the active forms of congestion which
they may momentarily aggravate.
MORBID ANATOMY.—Owing to the non-fatality of the commoner forms of
cerebral hyperæmia, no pathological observations of them are at our
disposal, nor can we assume from analogy that the appearances would be
well marked if they could be made. What little knowledge we have is
derived from a study of more serious conditions of which cerebral
hyperæmia is an initial, collateral, or episodial feature.
In pronounced cerebral hyperæmia the entire brain is, as it were,
tumefied, so that the dura appears tensely stretched over its surface
and the gyri are flattened; both the meningeal vessels proper and
those of the pia are injected. According as the hyperæmia is active or
passive the color of this injection varies, being of a brighter red in
the former, of a purple or bluish color in the latter case. The purest
instances of active cerebral hyperæmia which I have seen were found in
patients dying in the apoplectiform phases of paretic dementia
(progressive paralysis of the insane). Here the cortex on section
exhibited a beautiful rosy tint, which was distributed in darker and
lighter strata in correspondence with the distributional areas of the
short and the long cortical arteries; there were numerous puncta
vasculosa both in the cortex and in the white substance, and in some
instances the arachnoid or the ventricular fluid was tinged with
blood, albeit no vascular rupture could be discovered. The red
blood-corpuscles undoubtedly escape by diapedesis from the surface as
well as the endymal vessels; the same thing occurs in the
intracerebral blood-vessels, whose adventitial spaces are often
crowded with accumulations of red blood-discs, while groups or single
ones are found scattered in the surrounding parenchyma, and even in
the periganglionic spaces. Occasionally accumulations of pigment found
near the vascular channels remain to attest the former existence of
other hyperæmias, and indeed slight accumulations of this kind are
found in the brains of most persons who have reached adult life. These
are to be regarded as remnants of the physiological hyperæmias to
which all active individuals are subject. It is only when the
accumulations become considerable and numerous, as in the chronic
insane, or are associated with those changes in the blood-vessels
{768} which are discussed in the articles on thrombotic and
hemorrhagic cerebral disease, that they can be regarded as indications
of a pathological condition.
Acute simple meningitis is ushered in by cerebral hyperæmia of the
active form. This is not alone demonstrated by the early symptoms of
this disease, but also by the fact, which I have observed in two
cases, that where this form of meningitis originates on one side, as
from extension of the middle-ear trouble, the opposite cerebral
hemisphere exhibited intense congestion of the ideal type.
In that serious form of mental disease known variously as grave or
acute delirium and typhomania (Luther Bell) a form of cerebral
hyperæmia is observed which in its intensity approximates inflammatory
congestion. The surface of the brain appears marbled and mottled;
blood seems to exude from the gyri after the pia is removed; the
cortical lamination is invisible, owing to the hyperæmic discoloration
of the gray substance; and the parenchymatous elements themselves
appear to be in a state of cloudy swelling. In one case I have
observed transudation of a hyaline proteinaceous substance and an
exudation of fibrin around the larger arterioles. In some cases of
typhus fever a less intense but similar congestive hyperæmia is found.
The hyperæmias of paretic dementia, of acute delirium, and of typhus
fever agree in this one feature: that all districts of the brain, from
the cortex and white substance of the cerebral hemispheres to the
medulla oblongata, are involved nearly to the same degree. In the
hyperæmia of simple meningitis of the convexity it is chiefly confined
to the pia mater and the most superficial cortical strata.
Congestion of the brain from stagnation of the venous return
circulation should not be confounded with active hyperæmia. With this
condition, which may be due to thrombosis of the sinuses, morbid
growths near the jugular foramen or in the neck around the internal
jugular veins, or, finally, to certain cardiac and pulmonary
disorders, there is rather a lesser than a greater amount of blood
sent to the brain; and it is not infrequently found that while the
surface of the brain appears congested, owing to the prominence of the
cerebral veins, the deeper parts are quite anæmic; and if the
injection be general, it will be found that the blood, whether in
arteries or veins, has the venous character. An excellent example of
this form of congestion is afforded by persons dying in the status
epilepticus. In their brains the venous channels stand out, filled to
their extreme capacity with blood almost black in color; and in
prepared sections, particularly such as are taken from the pons and
medulla oblongata, a beautiful natural injection of the vessels is
found. But that rosy color which is so characteristic of active
hyperæmia is absent, the tissues appearing purplish, bluish, or
chocolate-colored.
SYMPTOMATOLOGY.—There are few symptoms attributable to the nervous
system which have not been enumerated among the characteristics or the
occasional manifestations of cerebral hyperæmia. Thus, Hammond not
only follows Andral in enumerating apoplectic, convulsive, comatose,
and maniacal symptoms as acute manifestations of active cerebral
congestion, but assures us that aphasia may occur under the same
circumstances. In the course of his work on the subject, “an absolute
want of power to get correct ideas of even simple matters,” confusion
of ideas, weakening of the judgment, vacillation of purpose,
diminished logical power, {769} illusions and hallucinations of every
sense, delusions, morbid apprehension of impending evil, imperative,
suicidal, and other impulses, suspicion, hypochondriasis, furious
delirium, and the use of profane and obscene language, are enumerated
among the characteristic or prominent symptoms of various forms and
cases of cerebral hyperæmia.[7] Not one but several of the recognized
forms of insanity have yielded a fair quota of their symptoms to this
long array. Among somatic signs he in like manner names neuralgic
pains, numbness, spasms, paralysis, false impotence, hyperæmia of the
tympanum, choked disc, abolition or perversion of the sense of smell,
taste, and sight, fibrillary or fascicular twitches, various states of
the urinary excretions, diplopia, and monoplegias. It is here equally
evident that the initial symptoms of a considerable number of organic
and clearly defined affections have been included. It is on account of
the confusion engendered by this wide interpretation of the meaning of
the term congestion of the brain that I have determined to limit the
term as previously indicated, and to consider only the active form
here.
[Footnote 7: _A Treatise on the Diseases of the Nervous System_, 7th
ed., pp. 1-53. The natural inference following a perusal of this
chapter, as well as the monographs to which their author refers, is
that he has gathered together all states in which cerebral hyperæmia
was an associated factor, as well as those in which he appears to
assume its existence on theoretical grounds, and designated them as
cerebral congestion. In some instances he uses the terms hypochondria
and cerebral hyperæmia interchangeably (p. 50, _loc. cit._).]
A feeling of head-pressure, associated with a more or less severe dull
pain, aggravated by mental exertion, by stooping down, by straining at
stool, or when out of breath, and accompanied by a subjective sense of
mental dulness, is the most constant feature of the ordinary cases.
There is usually a vertiginous sensation, and an irritability of the
eye and ear not unlike that described in the article on Cerebral
Anæmia. Sleep is at first disturbed by vivid and sometimes frightful
dreams; later, it becomes interrupted, and ultimately complete
insomnia may develop. The action of the heart is accelerated and
exaggerated in some cases; in that event increased pulsation of the
carotids, flushing of the face, injection of the conjunctiva, and a
subjective sense of heat in the head and face are experienced.
Hammond, in accord with Hasse and Krishaber, believes that febrile
symptoms may develop under these circumstances; most authorities,
however, deny this for the uncomplicated form. I have never found an
objective rise of the general temperature.
Such a condition as that described is usually slowly produced, several
weeks, or even months, being occupied in its development. At first the
unpleasant symptoms occur only at certain hours of the day, with
temporary exacerbations and remissions. It may be arrested with
comparative ease at any time; if neglected, the mental faculties
become affected, not in the grave sense in which Hammond and the older
authors describe it, so as to carry the patient into actual dementia
or delusional insanity, but rather in the way of diminished
working-power. It is more difficult to fix attention, to recollect
words, names, and figures, or to keep up a protracted mental effort,
than in health, but the formal judgment does not suffer. I have known
patients to be in this condition for many months, and several for more
than one year, without any grave deterioration. It is true that in the
prodromal periods of some forms of insanity, such as acute mania,
there is a condition very similar to that of these patients; {770} and
this has led to regarding mania as a possible phase of cerebral
hyperæmia. But the very fact that, typically, mania is preceded by
such a stage—which is always of brief duration—that maniacal
excitement is a constant and unavoidable consequence upon it, while,
as far as known, the condition here described may last for years
without leading to a true psychosis, should prevent one regarding the
two conditions as identical, however similar they may be for the time
being.
In sufferers from cerebral hyperæmia who pass into the chronic state
of this disorder the disturbance of sleep and of the digestive organs
becomes very prominent, and continually reinforces the acting causes
of the disorder. In a large number of cases the head-sensations become
more or less localized; that is, while the general feeling of pressure
or dull ache may continue, a special area, which can be covered by the
palm of one hand, either in the middle part or to one side—usually the
left—of that part of the vertex, is the seat of a more severe pain,
complained of as a hot pressure. The patients frequently claim that
the temperature is higher at this spot, and, contrary to what might be
anticipated on a priori grounds, the statement will be confirmed, not
alone by the coarse method of using the hand, but by the surface
thermometer. The locality where this occasional rise of temperature
and the more common sense of pressure are experienced corresponds to
that part of the longitudinal sinus where the largest cerebral veins
enter. It is a noteworthy fact that nearly all the important
admunctories of this sinus empty into it within the short space of two
inches at this point.
Not all sufferers from cerebral hyperæmia give a history of a gradual
development of their symptoms. A few date their trouble from some
single intellectual, physical, or emotional strain. In one case,
complicated by marked evidences of cerebro-spinal exhaustion, the
patient, a lady, had during an illness of her husband, being deserted
by her servants, and the water-supply having been cut off, carried all
the water required for the invalid and domestic as well as sanitary
purposes up three flights of stairs for two unusually hot days in
July. In two others, strikingly similar in many details of their
cases, both being cornet-players, both attributing their illness to an
extra call upon their instrument, it was brought on in the older
patient within a few hours after playing on a hot day at the State
Camp at Peekskill, and in the second at Narragansett Pier as he left
the sultry concert-room and became exposed to a draught. In both these
cases, as in a large number since examined, some stomach trouble could
be positively determined to have antedated these symptoms. I mention
this because it is only in such cases that I have found the nausea or
vomiting which some writers regard as an occasional occurrence of, and
due to, the lighter form of cerebral hyperæmia.
There are no ophthalmoscopic evidences of cerebral hyperæmia of this
form. I have never found the optic disc presenting variations in tint
beyond those found within normal limits, except in a case of saturnine
encephalopathy with predominant signs of cerebral congestion. I
believe that the statement of Hammond[8] as to the existence of choked
disc in cerebral hyperæmia is generally regarded as due to the
interpretation of organic diseases as congestive states. It is not
confirmed by authorities.
[Footnote 8: _Loc. cit._, p. 41, lines 29-36.]
I have never found the tympanic membrane hyperæmic independently {771}
of ear disease, even when tinnitus was marked. It is claimed to exist
by Hammond, and he adduces as analogous the observation of Roosa that
quinine produces an injection around the handle of the malleus.[9]
[Footnote 9: It certainly is not necessary to look to the injection of
the tympanum as an explanation for the tinnitus of cerebral hyperæmia,
based on such an analogy. The tinnitus of cinchonism is more central
in location, being producible in persons who have pathological or no
tympanic membranes, just as the tinnitus of cerebral hyperæmia occurs
indifferently under like circumstances.]