prevent or arrest the inflammation; 2d, to modify its violence and
shorten its duration when arrest is no longer possible; and 3d, to
place the patient in the best condition to withstand the violence of
the disease and to recover from its effects. It is only by prompt
action that we can hope to attain the first object, that of preventing
the passage of hyperæmia into inflammation. The patient should be
placed in a cool and well-ventilated apartment of good size, from
which a bright light is excluded. His head, moderately raised, should
be kept cool by means of pounded ice enclosed in a rubber bag or a
bladder. One or more leeches, according to his age, should be applied
behind the ears, or blood may be drawn from the temples or back of the
neck by means of cupping. The bleeding should be encouraged by
poultices if necessary, but with young children the abstraction of
blood should be done with caution. An active purge should be given,
such as ten grains each of calomel and jalap, followed by castor oil
or infusion of senna; for {721} children, from three to six grains,
according to age, followed by oil, would be sufficient. The medicine
should be repeated in a few hours if there be no effect.
Counter-irritation by means of blisters is recommended by most
authorities as a valuable aid in the first stage of the disease.
Unless the application be very extensive, it is not likely to be of
any avail, and extensive blistering would hardly fail to greatly
reduce the strength of the patient, and also is likely to irritate the
kidneys. There are no medicines which can be relied upon to arrest the
inflammatory process. Nevertheless, the tincture of aconite-root, in
the dose of from one to three drops, according to the age of the
patient, every two hours, might be given early, with the view of
fulfilling the second indication by its sedative property. The bromide
of potassium or of sodium, combined with small doses of chloral
hydrate or of sulphate of morphia, will also calm the excitement and
pain, and diminish convulsions. The success which sometimes follows
the employment of ergot in the epidemic cerebro-spinal meningitis
warrants its trial. Bartholow recommends the wet sheet two or three
times a day if the temperature is high. Steffen advises four grains of
sulphate of quinine with one grain of salicylate of soda, from two to
four times daily, for young children, and in double these doses for
older ones. The alimentation of the patient should be carefully
attended to during this stage. Nourishing liquid food, such as milk,
gruel, broth, eggs, with stimulants if indicated, should be given at
proper intervals, care being taken not to overload the stomach, as is
frequently done. When the patient can no longer swallow the food must
be given by the rectum. During the stage of compression it is useless,
in the present state of our knowledge, to expect any benefit from the
further administration of drugs, and the treatment then consists
mainly in giving small quantities of food at regular intervals, and in
such external applications as the bodily temperature may require. The
bladder must be relieved by the catheter when necessary. Simple
enemata are generally sufficient to prevent constipation.
Chronic Cerebral Meningitis.
Chronic inflammation of the pia mater rarely follows the acute form,
but is generally secondary to other conditions, such as inflammation
and tumors of the dura, tumors and abscess of the brain, disease of
the vessels of the brain, suppurative otitis, and to constitutional
diseases, especially alcoholism, syphilis, and pulmonary tuberculosis.
It is one of the most common lesions found after death from general
paralysis of the insane. As a distinct affection, unconnected with
constitutional disease, it is extremely rare, though less so,
according to Flint,[19] than the acute form. He cites a case in which
the symptoms were intermittent. The patient, fifteen years old, died
after a month's illness. The autopsy showed cerebral hyperæmia, lymph
at the base of the brain, and distension of the ventricles with
transparent fluid. There were no tubercles. In most cases in which the
results of chronic meningitis are found after death the cortical
substance of the brain is involved in the disease; hence {722} the
difficulty in defining its symptoms, which are usually extremely
vague, and not always distinctive of cerebral disease. The principal
are pain in the head, vertigo, vomiting, impairment of the memory,
mental apathy, drowsiness, and muscular weakness. The anatomical
changes are thickening and opacity of the membrane by the deposit of
lymph upon its surface and into the connective tissue, adhesions to
the dura and to the cortical substances of the brain, together with
hyperæmia of the latter. These appearances are usually distributed in
irregular patches of greater or less extent.
[Footnote 19: Austin Flint, M.D., _Principles and Practice of
Medicine_, 5th ed., Philada., 1881, p. 701.]
The DIAGNOSIS of chronic meningitis is often obscure or impossible.
Long-continued pain in the head, accompanied by vertigo, impairment of
memory, drowsiness, mental apathy, etc., without paralysis, would be
suggestive of it, especially if there were occasional intermissions of
the symptoms. The probability would be greatly increased if the
patient had a syphilitic or alcoholic history. The diagnosis should
exclude tumor of the brain, chronic pachymeningitis, and chronic
hydrocephalus, but as these diseases are often complicated with
chronic meningitis, the distinction might be very difficult. As
already stated, chronic meningitis is almost a constant lesion in
general paralysis, as well as in other forms of chronic insanity, but
there are no special symptoms by which its presence can be ascertained
during life.
TREATMENT.—Our aim should be to relieve pain, diminish congestion, and
favor absorption. Counter-irritation to the head and nucha by means of
small blisters or croton oil should be employed with moderation.
Bromide of potassium, or, if necessary, small doses of morphia, may be
given if the pain be severe. Should there be symptoms of cerebral
congestion, such as acute delirium, flushing, and heat of head, an
ice-bag should be applied to the head and leeches behind the ears, or
blood may be drawn from the temples or nucha by cupping. As an
absorbent the iodide of potassium is much recommended, but it is not
likely to be effectual, except in syphilitic cases. The bowels should
be kept free, but without active purging. The general health of the
patient should be promoted by suitable diet and regimen, by relief
from excitement and fatigue, or by change of scene and of climate. For
the treatment of chronic meningitis complicating syphilis, alcoholism,
and tuberculosis, the reader is referred to the articles treating of
those diseases.
{723}
TUBERCULAR MENINGITIS.
BY FRANCIS MINOT, M.D.
DEFINITION.—Inflammation of the pia mater of the brain, with effusion
of lymph and pus, caused by the deposit of miliary tubercles upon its
surface or into its substance.
SYNONYMS.—Scrofulous meningitis, Granular meningitis, Basilar
meningitis, Acute hydrocephalus, Dropsy of the brain.
HISTORY.[1]—It is only within a comparatively recent time that
tubercular meningitis has been distinguished from other cerebral
diseases. Up to the eighteenth century the term hydrocephalus was
employed not only for the dropsical diseases of the head, including
internal and external hydrocephalus, but also for meningeal
inflammations, both simple and tubercular, and for congestion of the
brain and of the membranes; the accumulation of water in the
ventricles or between the membranes being looked upon as the disease,
and not as one of its consequences. The term was even applied to
external tumors, as cephalæmatoma and caput succedaneum. We owe the
first accurate account of the symptomatology of acute hydrocephalus,
or ventricular dropsy, to Robert Whytt of Edinburgh, whose remarkable
monograph, entitled _Observations on the Dropsy of the Brain_, first
published in 1768, after his death, was founded upon the study of 20
cases with 10 autopsies. No addition of importance has been made by
later observers to his graphic description of the disease or to his
rules for its diagnosis. Whytt, however, had no clear notion of its
pathogeny, and it was not till 1815 that Gölis pointed out that acute
ventricular dropsy was a secondary condition depending upon previous
inflammation of the membranes or vessels of the brain.
[Footnote 1: See W. Hughes Willshire's valuable paper, entitled
“Historic Data on Scrofulous Meningitis,” in _Brit. and For.
Med.-Chir. Review_, Oct., 1854.]
In 1827, Guersant remarked that the inflammation of the meninges
constituting acute hydrocephalus presented such peculiarities as led
him to denominate it granular meningitis. He did not, however, connect
the granular deposit with tubercle. This was left for Papavoine to
effect, who in 1830 published two cases of tuberculous arachnitis, in
one of which effusion into the ventricles, or hydrocephalus, existed.
The meningeal granulations or tubercles were described with care, and
their coincidence with tuberculous deposit elsewhere was remarked
upon, as also the apparent occurrence of the former previous to the
inflammatory action in the meninges, and in one case the existence of
the tuberculous granules without the sequence of inflammation. The
important pathological element of acute hydrocephalus thus clearly
pointed out by Papavoine {724} now became apparent to observers, and
obtained almost universal assent. The attention of the profession in
this country was first called to it by W. W. Gerhard of Philadelphia
in 1833, in an admirable paper published in the _American Journal of
the Medical Sciences_,[2] containing the reports of thirty-two cases
with autopsies. In every case but two tubercles were found in other
organs besides the meninges. In one of these two, gangrenous cavities
were found in the lungs without tubercles, though perfectly
characterized miliary tubercles existed in the membranes; in the other
case the lungs were not examined with care, Gerhard not being present
at the autopsy.
[Footnote 2: Vols. xiii. and xiv., 1833-34.]
Finally, the distinction between tubercular and simple meningitis was
pointed out by Guersant in 1839, and clearly established by Barthez
and Rilliet in 1843 in their systematic work on the diseases of
children; and it was further elucidated by Rilliet in 1847.
ETIOLOGY.—The causes of tubercular meningitis are predisposing and
exciting. Among the former are hereditary tendency to tuberculosis and
to the so-called scrofulous diathesis; the previous existence of
tubercle in any part of the body, especially in the lungs; and the
presence of caseous degeneration in the bronchial, the mesenteric, and
other glands, or in the parenchyma of various organs, as the lung, the
testicle, the liver, the spleen, etc. The dependence of miliary
tuberculosis of the pia upon previously-existing caseous or other
inflammatory deposits in some part of the body is acknowledged by most
modern pathologists. Seitz[3] states that out of 130 cases, with
autopsies, of adults, upon which his work is based, such deposits were
found in 93.5 per cent. General constitutional weakness, either
congenital or resulting from grave disease or from overwork, from
insufficient or unwholesome food, and from bad hygienic surroundings,
also favors the deposit of tubercle in the meninges. Sometimes two or
more predisposing causes exist at once. Thus, a child born of
tuberculous parents may be fed with artificial diet instead of being
nursed, or may live in a house whose sanitary condition is bad. Hence
the disease is common among the poor, although by no means rare in the
higher classes of society. In some cases it is difficult or impossible
to assign any predisposing cause. A single child out of a numerous
family may be stricken with the disease, while the rest of the
children, as well as the parents and other ascendants, are healthy.
For instance, while writing this article I had under observation a
little boy six years old whose parents are living and healthy, with no
pulmonary disease in the family of either. The only other child, an
older brother, is healthy. While apparently in perfect health the
child was attacked with tubercular meningitis, and died in seventeen
days with all the characteristic symptoms of the disease. At the
autopsy there was found much injection of the cerebral pia everywhere,
a large effusion of lymph at the base of the brain and extending down
the medulla, abundance of miliary tubercles in the pia and
accompanying the vessels in the lateral regions of the hemispheres,
lateral ventricles distended with nearly clear fluid, ependyma smooth,
choroid plexuses covered with granulations, convolutions of brain much
flattened. Careful investigation, however, will usually {725} enable
us to detect some lurking primary cause, either in the family
predisposition or in the history of the patient himself.
[Footnote 3: _Die Meningitis Tuberculosa der Erwachsenen_, von Dr.
Johannes Seitz, Berlin, 1874, p. 317.]
Season appears to have but little influence on the production of the
disease. The largest number of cases is observed during winter and
spring, owing doubtless to the influence of the temperature and
weather, and to the exclusion from fresh air, in favoring the
development of tubercle and the scrofulous diathesis. Males, both
children and adults, are somewhat more frequently attacked than
females.
In regard to the exciting causes it may be said that where a
disposition to the deposit of tubercle exists, anything which tends to
lower the vitality of the individual is likely to hasten the event. In
infants with hereditary tendency to tubercle, an improper diet is
especially liable to develop meningeal tubercle. In older children,
besides unwholesome or insufficient food and unfavorable hygienic
surroundings, the acute diseases common to that period of life, such
as the eruptive fevers, intestinal disorders, whooping cough, etc.,
often act as immediate causes. Sometimes the development of the
disease may be traced to over-stimulation of the nervous system by
excessive study, often aided by imperfect ventilation or overheating
of the school-room. Caries of the temporal bone from disease of the
middle ear may act as an immediate cause of tubercular meningitis,
although simple meningitis is of course a more frequent result of that
condition. The disease has been known to follow injuries of the head
from blows or falls. In a larger number of cases the exciting cause is
not discoverable, especially when the meningeal affection is simply an
extension of the disease from some other part of the body, as the
lungs, the bronchial or mesenteric glands, etc. This is often the
case, both in adults and in children, when tubercular meningitis
complicates pulmonary consumption.
SYMPTOMS.—The disease is most frequently observed in children between
the ages of two and seven years. It is much less common in adults, who
are generally attacked between the ages of twenty and thirty years. In
the majority of cases the invasion of the malady is preceded by a
prodromic stage, usually occupying from a few days to several weeks,
though sometimes extending over a considerably longer period. This
stage probably represents the process of deposit of miliary tubercles
in the pia mater before their presence has given rise to much
structural change in the tissue. The characteristic symptoms of the
prodromic stage consist chiefly in an alteration of the character and
disposition of the patient, varying in extent in different cases. In
general, it may be said that he becomes sad, taciturn, apathetic,
irritable, indisposed to play, often sitting apart from his
companions, gazing in a strange way into vacancy. There is diminution
or loss of appetite and some emaciation. He is restless at night, is
disturbed by nightmare, or grinds his teeth. The digestion is
deranged. Usually there is constipation, but occasionally diarrhœa, or
these conditions may alternate with each other. Squinting and
twitching of the facial muscles are sometimes noticed. Headache may
occur early in this stage, but it is usually observed later, and it
then forms a prominent symptom. Vomiting is also frequent, usually not
preceded by nausea, sometimes provoked by sudden movement, as in
sitting up in bed, and is apt to occur when the stomach contains
little or no food. These symptoms vary much in degree, and they are
often so slight {726} that they pass unnoticed by the parents or
friends. Occasionally the patient, if a child, will manifest a strange
perversity or an unusual disobedience, for which he is perhaps
punished under the belief that his misconduct is intentional. In older
children and in adults delirium, especially at night, sometimes
followed by delusions which may be more or less permanent, is frequent
at this stage. The above symptoms often remit from time to time, and
during the interval the patient may seem to have recovered his health.
The prodromic symptoms are rarely altogether wanting in children,
although they may have escaped notice from lack of opportunity of
observation on the part of the physician. On the other hand, as
Steffen[4] justly observes, the most characteristic symptoms may be
present, and lead even an experienced observer to a confident
diagnosis of tubercular meningitis during the early stage of a case of
typhoid fever or of cerebral congestion without tuberculosis.
[Footnote 4: “Meningitis Tuberculosa,” by A. Steffen, in _Gerhardt's
Handb. der Kinderkrankheiten_, 5 B., 1ste Abth., 2te Hälfte, p. 465.]
For convenience of description it is customary to divide the disease
proper, after the prodromal period, into three stages—viz. of
irritation, compression, and collapse. In some cases it is not
difficult to observe these divisions, but it must be borne in mind
that in others the symptoms do not follow any regular sequence, so
that no division is possible. In infants profound slumber may be the
only morbid manifestation throughout the entire disease. Steffen
records such a case, and I have seen two similar ones.
First Stage: The interval between the prodromic period and the first
stage is usually so gradual that no distinction between the two can be
detected. In other cases the disease is ushered in suddenly by some
striking symptom, such as an attack of general convulsions, with
dilated pupils and loss of consciousness. This is not often repeated,
though partial twitchings of the limbs or of the muscles of the face
may follow at intervals. In young children a comatose condition, with
unequal pupils, is apt to take the place of these symptoms. The
principal phenomena of the first stage are headache, sensitiveness to
light and sound, vomiting, and fever. The latter varies much in
intensity from time to time, but is not usually high, the temperature
seldom rising above 103° F., and usually, but not always, higher at
night than in the morning; but there is no characteristic curve. The
pulse varies in rate, but is usually slow and irregular or
intermittent. The respiration is irregular, with frequent sighing. The
tongue is dryish and covered with a thin white coat. The bowels are
costive. Delirium is frequent at night, and the sleep is disturbed,
the patient tossing about and muttering or crying out. The eyes are
half open during sleep. These symptoms become more marked from day to
day. The pain in the head is more frequent and severe; the patient
presses the hands to the forehead or rests the head against some
support if sitting up. During sleep he occasionally utters a loud,
sharp cry, without waking. There is increasing apathy, and some
intolerance of light, shown by an inclination to turn toward the wall
of the room or to lie with the face buried in the pillow. The appetite
is lost, the constipation becomes more obstinate, the slowness and
irregularity of the pulse persist. With the rapid emaciation the belly
sinks in, so that the spinal column can be easily felt. Soon the child
falls into a state of almost {727} continual somnolence, from which,
however, he can be awakened in full consciousness, and will answer
correctly, generally relapsing again immediately into slumber. His
restlessness diminishes or ceases altogether, and he lies continuously
on the back with the head boring into the pillow. He becomes more
passive under the physician's examination, in strong contrast to his
previous irritability. At the end of a week or more from the beginning
of this stage symptoms of irritation of some of the cerebral nerves
begin to show themselves, in consequence of pressure from the
increasing exudation at the base of the brain and into the ventricles.
Strabismus (usually convergent), twitching of the facial muscles and
grimaces, grinding of the teeth, or chewing movements of the mouth are
noticed. The somnolence deepens into sopor, from which it becomes more
and more difficult to arouse the patient, who gradually becomes
completely insensible.
Notwithstanding the alarming and often hopeless condition which this
assemblage of symptoms indicates, intervals of temporary amendment not
unfrequently take place. The child may awake from his lethargy,
recognize those about him, converse rationally, take his food with
relish, and exhibit such symptoms of general improvement that the
parents and friends are led to indulge in fallacious hopes, and
sometimes the physician himself ventures to doubt the accuracy of his
diagnosis. Such hopes are of short duration; the unfavorable symptoms
always return after a brief interval. The duration of the first stage
may be reckoned at about one week.
Second Stage: This period is not separated from the preceding one by
any distinct change in symptoms. The patient lies in a state of
complete insensibility, from which he can no longer be aroused by any
appeal. The face is pale or of an earthen tint, the eyes are half
closed. If the anterior fontanel be still open, the integument
covering it is distended by the pressure beneath. Often one knee is
flexed, the opposite leg extended; one hand applied to the genitals,
the other to the head. Sometimes one leg or arm is alternately flexed
and extended. The head is apt to be retracted and bores into the
pillow. The pupils are dilated, though often unequal and insensible to
light: the sclerotica are injected; a gummy exudation from the
Meibomian glands forms on the edges of the lids. The patient sighs
deeply from time to time, and occasionally utters a loud, piercing
cry. Paralysis, and sometimes rigidity of one or more of the
extremities, are often observed, and occasionally there is an attack
of general convulsions. The pulse continues to be slow and irregular,
the emaciation progresses rapidly, and the abdomen is deeply
excavated. The discharges from the bladder and rectum are involuntary.
The average duration of the second stage is one week.