Internal pachymeningitis is of two kinds: 1st, simple inflammation,

which may be accompanied by purulent exudation and by a corresponding

affection of the pia mater: 2d, hemorrhagic inflammation or hæmatoma

of the dura mater. Simple inflammation of the internal or lower

surface of the dura, without the coexistence of external

pachymeningitis is rarely found in the adult. The morbid appearances

differ but little from that of the external form, and the causes and

the diagnosis are also similar. In children, however, it is not

uncommon, according to Steffen.[2] The pus may discharge itself

spontaneously through the fontanels or the sutures, or caries of the

cranial bones may open a passage for its exit. It has also been

evacuated artificially when the symptoms have indicated its presence.

In other cases more or less extensive firm adhesions {707} between the

dura and pia mater have shown the previous existence of inflammation,

but it would be difficult to say in which membrane it began. In some

instances no symptoms are observed during life; in others the

coexistence of inflammation of the pia, effusion into the ventricles,

etc. prevent an exact diagnosis.

[Footnote 2: “Die Krankheiten des Gehirns in Kindesalter,” von Dr. A.

Steffen, in _Gerhardt's Handb._, 5 B., i. Abt., 2te Hälfte, p. 380.]

The TREATMENT does not differ from that of inflammation of the

external layer of the pia.

Hæmatoma of the Dura Mater.

SYNONYM.—Hemorrhagic pachymeningitis.

DEFINITION.—A chronic inflammation of the dura mater, resulting in the

formation upon its inner surface of successive layers of false

membrane, into and between which there is usually an effusion of

blood, the whole sometimes forming a large solid mass between the dura

and the cavity of the arachnoid.

ETIOLOGY.—Hemorrhagic pachymeningitis never occurs in healthy persons

except from traumatic causes. It is most frequently observed in

advanced life, and especially in the male sex. In a large number of

cases the blood is in an unhealthy condition, and hence the disease is

seen in alcoholism, in scurvy, in acute articular rheumatism, and in

the acute febrile affections, as typhoid fever, pleuro-pneumonia, and

pernicious anæmia, of which last, according to Huguenin,[3] it

complicates one-third of the cases. It is frequent among the chronic

insane. It is occasionally met with in young children, but with them

its causes are mostly unknown; according to Steffen,[4] they may

consist in alterations of the blood resulting from insufficient

nourishment or from the infectious diseases, and from abnormal

blood-pressure, as in whooping cough, asthma, etc., as well as from

blows on the head.

[Footnote 3: G. Huguenin, “Acute and Chronic Inflammations of the

Brain,” in _Ziemssen's Encylop._, Am. translation, New York, 1877,

vol. xii. p. 401 _et seq._]

[Footnote 4: _Op. cit._, p. 386.]

SYMPTOMS.—Many cases of hemorrhagic pachymeningitis complicating other

cerebral diseases can be distinguished by no special symptom from the

original malady. Thus, in cases of chronic insanity its existence may

not be suspected during the lifetime of the patient. Steffen quotes[5]

the case, reported by Moses, of a child seven months old who died of

catarrhal pneumonia, and who exhibited no symptom which could suggest

any disease of the brain or its membranes. The autopsy revealed a

pachymeningitic cyst extending over the anterior half of the right

hemisphere. When symptoms are present they vary in different cases

according to the acuteness of the inflammatory process, the amount and

situation of the effusion, and the participation of the pia mater and

brain in the disease. In the beginning they are usually indefinite,

headache being the most common and often the only complaint. This may

continue for weeks without any other indication of disease, but it is

frequently accompanied by tinnitus aurium, vertigo, muscular weakness,

and contraction of the pupils. Wakefulness and restlessness at night

and slight twitching of the facial muscles or of the limbs sometimes

occur. There may be no change in the condition of the patient for a

{708} considerable length of time (weeks or months), or he may improve

to some extent, owing to the absorption of the serous portion of the

effusion or to the tolerance of the foreign body acquired by the

brain. Sooner or later a fresh hemorrhage is followed by a recurrence,

and usually an aggravation, of all the symptoms. Sometimes the patient

becomes comatose, and dies speedily with apoplectic symptoms, but this

is not common at an early period. The extravasation of blood generally

takes place in small quantities at a time, without giving rise to

unconsciousness or paralysis. After a period of uncertain duration,

when the tumor has attained considerable dimensions a condition of

somnolence may take place, the patient sometimes sleeping twenty-four

hours or longer at a time. Distinct paralysis rarely occurs, though

hemiplegia is sometimes seen, and the paralysis has been observed on

the same side with the lesion. When symptoms of compression appear the

pupils become dilated. Toward the end of life the patient is usually

in a state of profound coma, the pulse is slow and irregular, and the

sphincters are relaxed.

[Footnote 5: _Op. cit._, p. 394.]

The distinctive features of internal pachymeningitis, therefore, so

far as they are at present known, are those which would depend upon a

primary cerebral irritation, followed by those of compression of the

brain—persistent, often severe, headache, with contracted pupils, and

occasionally motor and sensory disturbances; afterward, coma, dilated

pupils, and involuntary discharges from the bowels and bladder.

The DURATION of the disease is exceedingly variable, extending from a

few days to more than a year. According to a table made from carefully

observed cases by Huguenin, 74 per cent. of patients die within thirty

days; 18 per cent. live from one to six months; 4 per cent. live from

six months to one year; and 4 per cent. live over one year.

PATHOLOGY.—A difference of opinion has existed among pathologists

concerning the true nature of hemorrhagic effusions of the inner

surface of the dura mater, especially as to whether the membrane in

which they are enclosed is formed by a deposit of fibrin from the

effused blood itself, or whether the disease consists essentially in

an inflammation of the dura, followed by a pseudo-membranous deposit

into which blood is afterward extravasated. The latter explanation,

offered by Virchow, has been generally accepted, but Huguenin, whose

opportunities for observing the disease were unusually good, believes

that the first stage of hæmatoma is not the formation of connective

tissue, but simply an extravasation of blood.

The disease begins with hyperæmia of the dura mater in the area of

distribution of the middle meningeal artery, followed by the formation

upon its inner surface of an extremely delicate membrane in small

patches of a yellowish color and studded with innumerable bloody

points. If the membrane be carefully raised, it is found to be

connected with the dura by very delicate blood-vessels, and to contain

an immense number of very wide and thin-walled vessels, much larger

than ordinary capillaries.[6] At a later stage we find the membranes

to be made up of several distinct layers, of which the innermost

exhibits the character of the primary deposit, being thin and

abundantly supplied with blood-vessels, while those of older formation

have become successively thicker and are {709} composed of tough,

lustrous fibres of connective tissue almost as dense as that of the

dura mater itself. The delicate structure of the false membranes and

of the vessels which they contain leads almost inevitably to the

effusion of blood, which increases in quantity with the thickness of

the whole growth, so that in an advanced stage it is not uncommon to

find large pools of blood, partly clotted and partly fluid,

constituting what is called hæmatoma of the dura mater. The small

bloody points are within the substance of the false membrane; the

extravasations are interstitial, the largest being always found

between the youngest membrane and the older layers. In some cases

serous transudations also occur between the false membranes. In still

rarer instances no blood or serum is found between or beneath the

layers. Occasionally small quantities of blood escape by leakage

through the delicate membrane into the cavity of the arachnoid.

[Footnote 6: See Rindfleisch's _Manual of Pathological Histology_, New

Sydenham Soc.'s translation, 1873, vol. ii. p. 302.]

The usual situation of internal pachymeningitis is the vault of the

cranium, near the median line, the upper or external layer of the

tumor being in relation with the dura mater, to which it is adherent,

and the lower or internal with the arachnoid and pia mater. If the

effusion be extensive, it spreads downward over the frontal and

occipital lobes of the brain, and laterally toward the fissure of

Sylvius. In the majority of cases the disease occupies both sides of

the median line symmetrically, but it may be limited to one side only.

According to Huguenin, 56 per cent. of the cases embrace the surfaces

of both hemispheres; 44 per cent., that of one only. Hæmatoma very

rarely occupies the base of the cranium. The thickness and consistency

of the deposit vary in different cases, depending upon the number of

successive exudations, and hence are most marked in cases of the

longest duration.

Hemorrhagic pachymeningitis is occasionally met with in young

children, but much more rarely than in adults. The disease is usually

more acute than in older persons, but the anatomical appearances are

essentially the same.[7]

[Footnote 7: For an able description of the lesions of hemorrhagic

pachymeningitis in children see the third edition of Rilliet and

Barthez's _Maladies des Enfants_, by Barthez and Sanné, Paris, 1884,

vol. i. p. 152.]

PROGNOSIS.—The great majority of cases end fatally. A few instances of

recovery are reported in which the diagnosis seems justified by the

symptoms. Moreover, it is not very rare to find, on post-mortem

examination of those who have died of other diseases, evidence of the

former existence of hemorrhagic pachymeningitis. According to Steffen,

while the prognosis of simple pachymeningitis in children is

frequently good, owing to the favorable conditions for the exit of pus

through the open fontanels and sutures, in hemorrhagic pachymeningitis

recovery is rare.

DIAGNOSIS.—In a disease whose symptoms are so vague the diagnosis must

of necessity be difficult and often impossible. The chief elements for

the formation of the diagnosis are the slow and interrupted progress

of the affection, persistent headache, tendency to prolonged slumber,

and final coma; the absence of paralysis of the cranial nerves, of

vomiting, and of general convulsions; the age of the patient, the

coexistence of alcoholism, chronic insanity, or acute rheumatism, and

traumatism. The diseases for which hæmatoma would be most likely

mistaken are acute inflammation of the meninges, apoplexy from

cerebral hemorrhage, tumor in the substance of the brain, and

necrobiosis from thrombus or embolus. {710} The absence of symptoms

characteristic of these affections might lead to a probable diagnosis

by exclusion, but in many cases the existence of the disease cannot be

determined with certainty. In children it is most likely to be

confounded with tubercular meningitis, from which it may be

distinguished by the fact that it is most common under the age of two

years, the other being rare before that period, and that the

characteristic symptoms of tubercular meningitis (prodromic period,

vomiting, irregularity of pulse, etc.) are wanting. But the tubercular

disease in young infants may closely resemble hæmatoma, a profound

coma replacing all other symptoms. Here the existence of tuberculous

disease in the parents or other near relatives would point strongly to

tubercular meningitis, while the absence of such antecedents would

suggest hæmatoma.

TREATMENT.—If the disease be a complication of alcoholism, anæmia,

scurvy, rheumatism, etc., the treatment appropriate to those

affections should be employed, along with remedies addressed to the

local disease. For the early symptoms of irritation, perfect rest in

bed, cold to the head, bromide of potassium internally, sinapisms to

the back of the neck, together with simple and nutritious diet, are

the most efficient means. The bowels must be regulated, but purging is

not necessary. The abstraction of blood from the head by leeches to

the temples or behind the ears, or by cupping, is recommended by most

authorities, especially if there be much heat of the head. Mercury may

be tried, care being taken not to salivate the patient. It is obvious

that this treatment, in order to be of any avail, must be instituted

at the earliest stage of the disease. After the probable formation of

the hæmatoma an effort should be made to promote its absorption, which

sometimes actually takes place, as is proved by the autopsies of

patients who, having previously suffered from this affection, have

died from other causes. The iodide of potassium or the iodide of

sodium should be employed perseveringly for this purpose, in the dose

of from ten to thirty grains three times daily. The bromide should

also be continued if necessary. The acne which sometimes accompanies

the continued use of these remedies may be prevented or cured by the

use of three to five drops of the liquor potassæ arsenitis, given once

or twice daily after meals. Counter-irritation to the scalp by means

of stimulating liniments or croton oil, and small blisters to the

temples, are likely to do good. In alcoholic subjects the amount of

wine or spirit taken should be regulated by allowing enough to support

the strength, without too suddenly withdrawing the accustomed

stimulant. In the stage of coma the treatment must be purely

expectant. The state of the bladder must be regularly examined, and

the catheter employed when necessary. Liquid nourishment should be

carefully given as long as the patient is able to swallow.

Cerebral Meningeal Hemorrhage.

SYNONYM.—Meningeal apoplexy of the brain. Hemorrhage of or upon the

membranes of the brain is closely connected with intracerebral

hemorrhage. Both arise from similar causes, and the former may result

directly from the latter. It is for convenience of arrangement that

the two subjects are treated separately in this work.

{711} ETIOLOGY.—The causes of meningeal apoplexy are predisposing and

immediate. The most important predisposing cause consists in disease

of the cerebral vessels, especially the arteries, which favors the

formation of so-called miliary aneurisms, as demonstrated by Charcot

and Bouchard in the case of cerebral apoplexy. Disease of the vessels

in its turn arises from various conditions, among which alcoholism in

adults holds a prominent place from its tendency to favor a fatty

degeneration of the vascular walls. In subjects of purpura or

hæmophilia (the so-called bleeders), in whom, from an inherent

weakness of the capillary vessels or a deficiency of the fibrin of the

blood, or both combined, there is a tendency to extravasation of the

blood in various parts, hemorrhage into the arachnoid cavity may

occur.[8] A new-born child under my observation had bleeding at the

navel and ecchymoses in various parts of the body. Suddenly it became

comatose, and it died with signs of cerebral compression. There was no

autopsy, but it seems probable that hemorrhage into the cavity of the

arachnoid had taken place. A sister of the patient had also had

spontaneous hemorrhage from the navel and from other parts shortly

after birth, but recovered. Chronic general arthritis and gout also

probably predispose to the affection, as well as old age, which is

accompanied by atrophy of all the tissues. The disease is most

frequently met with in the two extremes of life; according to

Durand-Fardel,[9] in adults the largest number of cases occurs between

the ages of seventy and eighty years.

[Footnote 8: A case of this kind is cited in the article “Pathologie

des Méninges” in _Nouv. Dict. de Méd. et de Chirurg. pratiques_,

Paris, 1876, vol. xxii. p. 101.]

[Footnote 9: _Traité clinique et pratique des Maladies des

Vieillards_, par M. Durand-Fardel, Paris, 1854, p. 283.]

The exciting causes comprise injuries to the head, both with and

without fracture; strong muscular effort, as in lifting, straining at

stool or in labor; powerful action of the heart in cases of

hypertrophy. An interesting case is reported[10] by S. G. Webber of

Boston, in which the effusion was evidently caused by vomiting; a clot

of blood covered the greater part of the posterior two-thirds of the

right hemisphere. Sometimes meningeal hemorrhage may arise from the

bursting of an intracerebral apoplexy into the arachnoid cavity, as in

a remarkable case occurring in the practice of Morris Longstreth of

Philadelphia, of bilateral effusion.[11] Outside the dura,

corresponding with the left middle cerebral lobe, was a considerable

amount of blood connected with a fracture of the skull, and on the

right side a large quantity of blood in the cavity of the arachnoid,

originating in the middle lobe, which was torn up. The patient had

fallen in the street; he was stupid, there was no paralysis, active

delirium came on, followed by coma and death in twenty-four hours.

Here was cerebral apoplexy bursting into the cavity of the arachnoid

on the right side, and causing the fall, which was the occasion of the

fracture and hemorrhage on the left side.

[Footnote 10: _Boston Med. and Surg. Journal_, Jan. 17, 1884.]

[Footnote 11: _Ibid._, Dec. 28, 1882.]

In young children, especially in the new-born, meningeal hemorrhage

may follow difficult and instrumental labor, either from injury to the

skull or from delay in the establishment of respiration, as in breech

presentation, though it sometimes occurs in cases in which the labor

has been normal. In a case of breech presentation under my care in

1873 {712} the child, a female weighing nine pounds, did not cry or

breathe for some minutes after birth, although delivery had not been

much delayed. Soon afterward it was noticed that it did not move the

right arm, although it moved the hand and the fingers. In the course

of twenty-four hours, during which time it cried much more than usual,

it became comatose, and remained so until its death, three days after

birth. The whole surface was livid, and the child had two or three

short convulsions. At the autopsy a clot about the size of a grape was

found in the pia mater on the upper surface of the cerebellum, in the

immediate vicinity of the pons Varolii. The brain was so soft that the

amount of injury received by the cerebellum could not be exactly

ascertained, but it was probable that the clot extended into the

fourth ventricle.

Thrombus of the sinuses of the dura mater, and less frequently of the

cerebral arteries, is the origin, in a considerable number of cases,

of meningeal hemorrhage in children, in consequence of pressure upon

the delicate vessels of the membranes caused by the obstructed

circulation. Bouchut[12] reports an observation of hemorrhage produced

in this way.

[Footnote 12: E. Bouchut, _Clinique de l'Hôpital des Enfants

maladies_, Paris, 1884, p. 263. See, also, Steffen, _op. cit._, p.

352.]

SYMPTOMS.—In some cases the attack is preceded by indications of

congestion, such as headache, vertigo, staggering, confusion of ideas,

noises in the ears, feeling of weight in the head, delirium, stupor.

At the time of the attack the patient frequently complains of severe

pain in the head, just as in cerebral hemorrhage, and then falls to

the ground with complete loss of consciousness. Sometimes the symptoms

come on gradually. Hemiplegia occurs in a notable proportion of cases.

Convulsions may occur at any time after the attack. In Webber's case,

already referred to, the first symptom was sharp pain in the head and

neck; this was followed by very severe headache and pain on motion of

the head. Intelligence gradually diminished; on the sixth day there

was almost no consciousness, and the patient died in about eight days.

She had occasional spasms, in which both eyes were turned toward the

left in extreme conjugate deviation, and the left side of the face was

distorted. The spasms were followed by suspension of respiration for

nearly a minute, cyanosis, and paralysis of the left hand and leg.

Both the nature of the lesion and its seat were correctly

diagnosticated during the patient's lifetime.

As a rule, the condition of unconsciousness continues up to the time

of death, but in some cases there are intermissions during which the

patient responds to questions more or less promptly. Death takes place

at a period varying between a few hours and several days.

Durand-Fardel[13] reports a case in which the patient lived a month

from the first attack, with preservation of the intellect and of

motion. An inmate of the Home for Aged Women in Boston, eighty-eight

years old, previously in good health, complained of severe pain in the

head one morning before rising. She took her breakfast in bed, and

immediately afterward vomited copiously. From that moment she became

insensible, and remained so until her death, seven days and three

hours afterward. During this time there was no stertor. No decided

paralysis could be discovered, but there was some rigidity of the left

arm. At the autopsy an effusion of {713} blood was found in the

arachnoid cavity extending from below upward on each side to a level

with the top of the ear. There was a large amount of blood at the base

of the brain, and both lateral ventricles were distended with bloody

serum. The vessels were generally in an atheromatous condition. There

was no laceration of the brain. The source of the hemorrhage could not

be ascertained. In such a case the condition of the patient in respect

to power of movement often cannot be ascertained with certainty, in

consequence of the abolition of consciousness. Complete muscular

resolution is most common when the effusion is bilateral, but when the

hemorrhage is limited to one side more or less paralysis of the

opposite limbs may exist. Should the blood make its way into the

spinal canal, it might give rise to special symptoms, but this is not

probable in view of the large amount of the cerebral effusion under

the circumstances, which would produce complete insensibility or

speedily cause death by pressure on the medulla.

[Footnote 13: _Op. cit._, p. 202.]

The temperature of the body immediately after a copious cerebral or

meningeal hemorrhage falls below the normal point, and remains so for

several hours, after which it rises, its degree varying according to

circumstances. In fatal cases the elevation is extreme, and remains so

until death. If the patient recover, it gradually returns to the

normal standard.

Vomiting is a frequent symptom at the beginning of the attack, just as

in intracerebral hemorrhage, owing probably to compression of the

pneumogastric by the effusion at the base of the brain. In Webber's

case the vomiting was evidently the cause of the hemorrhage, and not

its consequence, since it had been a frequent symptom for several days

before the attack, and was probably due to the presence of a calculus

in the pelvis of the right kidney, which was found at the autopsy, and

there was no blood at the base of the brain.

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