PATHOLOGICAL ANATOMY.—The chief points of interest in the morbid

anatomy relate to the seat and source of the effusion, the amount and

condition of the blood, the state of the vessels and that of the

brain, including the ventricles. In respect to the seat, the

hemorrhage may occupy the space between the cranial bones and the dura

mater; it may be found on the lower surface of the latter, in the

arachnoid cavity, or in the meshes of the pia mater, the so-called

subarachnoid space. Blood found upon the outer surface of the dura,

between that membrane and the bones, is almost always the result of

traumatic causes, such as blows or other injuries, with or without

fracture, or of caries of the skull. If below the dura, but between

that and the so-called parietal layer of the arachnoid, the lesion

comes under the title of pachymeningitis interna, already described as

an inflammatory disease of the dura with hemorrhagic effusion. The

arachnoid cavity and meshes of the pia are by far the most common

situations in which the blood is found in meningeal hemorrhage. The

origin of the effusion is either the rupture of a capillary aneurism

of one of the arterioles of the membrane or of one of the vessels

themselves in consequence of atheromatous or other degenerations of

its walls. On account of the minute size of the vessels it is seldom

possible to discover the exact point at which the rupture took place.

In rare instances the source of the hemorrhage is within the brain,

the blood being forced through the cerebral tissue, either into the

meshes of the pia {714} or upon the surface of that membrane. The

amount of hemorrhage varies according to conditions which are mostly

unknown, but is probably dependent upon the size of the ruptured

vessel and the conditions under which the accident occurs, such as

muscular effort, cardiac action, etc. In some cases it is so small as

to give rise to no definite symptoms, as is evident from post-mortem

examinations of those who have died from other causes. In these cases

there may be either a single effusion or several. The amount is

largest when the arachnoid cavity is the seat of the extravasation.

The blood, which may be either liquid or more or less coagulated,

according to the time which has elapsed since the hemorrhage, is

usually found upon the convexity of the hemispheres, most frequently

on one side only, and oftenest on the left. But if the rupture have

taken place at the base, it often ascends on each side, as in a case

mentioned above. Where a large vessel has given way, its contents may

cover a great part of the surface of the brain. The coagulum is found

in a thin layer, which at the end of a few days is covered with a

transparent envelope, evidently composed of a deposit or separation of

fibrin. Should the patient survive long enough, this membrane may

become organized, receiving vessels from the adjacent pia, and in turn

become the seat of new hemorrhages, exactly as in the hæmatoma of

internal pachymeningitis. In cases in which absorption of most of the

fluid part of the effusion takes place, the membrane remains more or

less dense and vascular, and usually contains a small quantity of

recently-effused blood within its meshes. Small cysts, containing

transparent or reddish-brown serum, are also occasionally observed

enclosed between the layers of the membrane. In very young children,

whose fontanels are not yet ossified, these cysts sometimes attain to

a large size, containing several pints of fluid, which is more or less

limpid from absorption of the coloring matter of the blood,

constituting the so-called dropsy of the arachnoid.[14] The

convolutions of the brain are more or less flattened according to the

amount of the effusion, and the cortical substance is correspondingly

anæmic from pressure. The blood may make its way, if extravasated in

large quantities, into the ventricles, over the medulla, into the

spinal arachnoid cavity, or even into the central canal of the spinal

cord. The arteries of the brain, especially at the base, are

frequently in a state of atheromatous degeneration, and thrombi often

occupy the sinuses of the dura mater.

[Footnote 14: Charles West, M.D., _Lectures on the Diseases of

Childhood and Infancy_, 6th ed., London, 1874, p. 62. These large

cysts are much more frequently (perhaps solely) found in cases of

hemorrhagic pachymeningitis. (See Barthez and Sanné, _op. cit._, vol.

i. p. 157.)]

DIAGNOSIS.—The distinction between meningeal hemorrhage and cerebral

apoplexy is always difficult, and in the majority of cases impossible.

Sudden pain in the head, vomiting, and lowering of the bodily

temperature (the thermometer should be placed in the rectum), followed

by loss of consciousness, are strongly suggestive of hemorrhage within

the cranium, either cerebral or meningeal. If these symptoms are

followed by coma and resolution without obvious paralysis, the

diagnosis would be almost impossible between intra- and extra-cerebral

extravasation. If the loss of consciousness be not complete, so that

the presence or absence of paralysis can be ascertained, we can

sometimes distinguish the situation of the hemorrhage. Right-sided

hemiplegia, with paralysis of the face or tongue, or with aphasia, is

most probably owing to hemorrhage or {715} embolism somewhere in the

left motor tract, and hence within the brain. If the absence of

paralysis can be certainly ascertained, the probabilities are in favor

of meningeal apoplexy. Convulsions affecting the face or limbs of one

side would point to irritation of the cortical centres of those parts,

and so far to extravasation on the surface of the brain (on the

opposite side), as in Webber's case. Where the amount of hemorrhage is

small it furnishes no diagnostic indications. In the case of new-born

children the presumption is in favor of meningeal effusion.

PROGNOSIS.—If the effusion be considerable in amount, as indicated by

prolonged coma with resolution, the issue is almost inevitably fatal,

though life is occasionally prolonged for a surprising length of time.

Slight hemorrhages are doubtless recovered from, but there are no

means for their certain diagnosis.

TREATMENT.—The treatment, which is essentially the same as that for

cerebral congestion, has for its object the arrest of the hemorrhage,

and, if that can be effected, the absorption of the effused blood. In

view of the former, the patient's head should be elevated and kept

cool by the application of ice. Unless the bowels have previously been

freely moved, saline laxatives, followed by enemata if necessary, must

be given. The state of the bladder must be carefully attended to.

Liquid nourishment alone, in moderate quantities at regular intervals,

is permissible, with stimulants if there be signs of exhaustion. For

the absorption of the effusion mild counter-irritation to the scalp

and the administration of the iodide of potassium may be employed.

Congestion of the Cerebral Pia Mater.

The pia mater consists of two layers, separated by a loose connective

tissue. The outer layer, being that which was formerly called the

visceral layer of the arachnoid, is stretched smoothly over the

convolutions of the brain without dipping into the sulci; the inner

layer is closely connected with the surface of the brain, whose

inequalities it follows. The two layers are more firmly united

together over the convolutions than between them; in the latter

situation the connection is loose, and the space which separates the

surfaces is called the meshes of the pia. The membrane extends into

the ventricles, investing the ependyma and the choroid plexuses, and

over the medulla oblongata and spinal cord. In the normal condition it

is loosely attached to the brain, from which it can be stripped off

without loss of substance. The meshes of the pia, together with the

ventricles, constitute a series of cavities connected with each other,

containing a variable amount of cerebro-spinal fluid, and they

communicate with the lymph-spaces surrounding the blood-vessels.

Pressure within the cranial cavity, from congestion of the vessels or

from the products of inflammation, is thus relieved in a measure by

displacement of the cerebro-spinal fluid, which is driven out through

the perivascular lymph-spaces.

Congestion or hyperæmia of the pia mater probably never occurs

independently of that of the external surface of the brain, on account

of the intimate vascular connection of the two. In the adult it can

only exist to a limited extent, on account of the unyielding nature of

the cranial {716} walls and of the limited compensatory action of the

cerebro-spinal fluid. In young children the incomplete ossification of

the skull and the delicate structure of the vessels are more favorable

to congestion.

ETIOLOGY.—The causes of hyperæmia of the pia mater are in the main the

same as those of congestion of the dura.

SYMPTOMS.—Since congestion of the pia always coexists with that of the

corresponding part of the external portion of the brain, it is

impossible to separate the symptoms belonging to each. They are

therefore usually included under the head of Cerebral Congestion, to

which article the reader is referred.

PATHOLOGICAL ANATOMY.—Arterial hyperæmia of the pia is seldom

discovered after death, the elasticity of the vessels causing

transudation of the fluid part of the blood through their walls.

Venous congestion of the pia is more frequently noticed, usually in

connection with that of the dura, the sinuses with their accompanying

veins being distended with blood, and in cases of long standing often

containing thrombi. Simple hyperæmia of the pia being rarely or never

fatal of itself, these appearances are usually accompanied by those of

inflammation of the membrane or of the cortical layer of the brain

(effusion of lymph or pus), or by hemorrhage.

TREATMENT.—In a case of suspected congestion of the pia the treatment

would be the same as that of cerebral congestion.

Inflammation of the Cerebral Pia Mater.

SYNONYMS.—Meningitis, Leptomeningitis, Acute non-tubercular

hydrocephalus.

Meningitis (by which is generally understood inflammation of the pia)

appears under an acute, a chronic, and an epidemic form. The latter,

being a zymotic disease, is described in a separate article, to which

the reader is referred.

ETIOLOGY.—Meningitis occurs both as a primitive disease and as

secondary to other affections. The former is rare, the latter is more

frequent. The causes of idiopathic meningitis are for the most part

unknown. Exposure to the sun's rays and excessive indulgence in

alcoholic liquors are thought to excite it in some instances. It has

been known to follow blows and falls on the head which have produced

no injury to the skull. It is rather more commonly observed in early

manhood than at other periods of life. Secondary meningitis may follow

injury or disease of the cranial bones or of the dura, and of the

brain. A frequent cause is extension of disease of the ear to the

membranes and substance of the brain. The reader is referred to the

article on MEDICAL OTOLOGY for information concerning the symptoms of

that formidable complication. Certain diseases are known to be

occasionally complicated with meningitis—acute articular rheumatism;

erysipelas of the scalp and of the face; Bright's disease, especially

the chronic interstitial form; peritonitis; ulcerative endocarditis;

pyæmia; the eruptive fevers; the puerperal state; and syphilis.

Meningitis following or complicating acute rheumatism is generally

supposed to be not uncommon, but the number of cases in which the

existence of inflammation of the meninges has been {717} proved by

autopsy is small. Fuller,[15] along with three cases in which

dissection showed suppurative inflammation of the pia, cites several

others in which no cerebral disease was found after death, although

the symptoms gave every indication of it. True meningitis is rare in

chronic Bright's disease, the symptoms resembling it being caused, in

the majority of cases, by uræmia. Meningitis complicating pneumonia is

also rare, although cerebral symptoms are common enough in that

disease, especially in young children with inflammation of the upper

lobes. C. Neuwerk[16] reports seventeen cases of purulent meningitis

complicating acute pneumonia. It was more frequent in men, especially

in alcoholic subjects, than in women. The meningitis was generally

total. The lungs were in a state of gray or yellow hepatization.

[Footnote 15: H. W. Fuller, M.D., _On Rheumatism, Rheumatic Gout, and

Sciatica_, 3d ed., Philada., 1864, p. 271. See also E. Leudet,

_Clinique médicale de l'Hôtel Dieu de Rouen_, Paris, 1874, p. 133.]

[Footnote 16: _Deutsches Archiv für klin. Med._, xxix., 1881, p. 1;

and _Schmidt's Jahrbücher_, Band cxcviii., 1883, Nov. 5.]

SYMPTOMS.—The symptoms of acute leptomeningitis vary much in the

course of the disease. This is readily explained by the complex

character of the functions of the parts involved in the inflammation.

It may be assumed that the cortical layer of the brain is implicated

in every case unless of the most transient and limited kind; the

substance of the brain, cerebellum, and medulla are subjected to

pressure from the afflux of blood, from the effused lymph and pus, and

from the accumulation of serum in the ventricles; the cranial nerves

are exposed to pressure from the deposit of lymph, which may give rise

to irritation or to suspension of function or both; parts at a

distance from the seat of lesion may be functionally disordered by

reflex action through communicating filaments. Finally, the general

system suffers from the effects of the high fever upon the blood and

the nutrition.

It is customary to speak of a stage of excitement followed by one of

depression as characteristic of the course of the disease; but

although active symptoms generally prevail in the early period, to be

succeeded later by coma and paralysis, this disposition is by no means

uniform. Sometimes sopor and paralysis constitute almost the only

symptoms throughout the disease—this is especially noticed in

infants—or active delirium and convulsions may persist until the fatal

termination. More frequently the two conditions alternate several

times with each other. A prodromic period of short duration, a few

hours or a day or two, is sometimes observed in primitive meningitis,

the patients complaining of headache, vertigo, vomiting, restlessness,

or lassitude. Infants are irritable or drowsy, with heat of the head,

quick pulse, and occasional vomiting. In secondary meningitis this

period is usually masked by the symptoms of the primitive disease. In

the majority of cases the beginning of acute meningitis is abrupt.

Rigor is sometimes the first symptom observed, and in children is

usually represented by a convulsion. More commonly, however, the

disease is ushered in by severe headache, which is often referred to

the forehead. The head is hot, the face is flushed, the eyes are

brilliant, the pupils are contracted, the pulse is quick and hard, the

temperature high (104° F. or upward). The patient is wakeful,

restless, and irritable, sensitive to light and to sound. The skin is

hyperæsthetic, {718} especially that of the legs. There may be

wandering or even active delirium. Vomiting is not unfrequent. There

is thirst, but no desire for food. The urine is scanty and

high-colored, the bowels constipated. These symptoms gradually

increase in intensity, especially the pain in the head and the

delirium, and in many cases they are followed by convulsions, at first

in the form of twitchings of the facial muscles or of the limbs,

grinding the teeth, etc., which give place to tonic contractions of

the limbs or of the trunk, often confined at first to one or both

members of the same side, but afterward becoming general; the flexors

of the forearms and of the legs are most usually affected. The upper

dorsal muscles may become contracted, so that the head is drawn

backward, and more rarely trismus occurs.

A diminution in the rapidity of the pulse, which may fall to the

normal rate, or even below that, notwithstanding the persistence of

the high temperature, indicates the beginning of the stage of

depression. This change is sometimes sudden, though more often gradual

in its approach. The activity of the delirium subsides, giving place

to a somnolence which may seem to the inexperienced observer a

favorable indication, but which soon deepens into coma. The face

becomes pale, the features are sunken. Only an occasional grimace or a

movement of the hand to the head shows that the patient is to some

extent conscious of suffering. This condition may alternate with the

previous one from time to time, the comatose state being interrupted

by noisy delirium and tonic or clonic convulsions, or even a partial

return of consciousness, giving rise to fallacious hopes on the part

of the friends, and sometimes deceiving the physician himself into a

belief that a favorable issue is at hand. Before long, however, the

symptoms of brain-compression become permanent. The rigidity of the

limbs gives place to complete resolution. The patient lies absolutely

unconscious, with dilated pupils. The pulse becomes again rapid in

consequence of compression of the medulla, and thread-like and

irregular; for the same reason the respirations increase to 40, 50, or

60 in the minute. The sphincters are relaxed, and the patient dies

without any recurrence of the active symptoms. In rare cases recovery

takes place, although almost never after the symptoms of compression

have continued without interruption for any considerable length of

time. Moreover, it is seldom that recovery takes place in the adult

without leaving some traces of permanent damage, such as general

debility, paralysis of one or more limbs, deafness, mental weakness,

epilepsy, etc. Many cases of general paralysis of the insane and other

forms of so-called mental disease are the result of meningitis.

DURATION.—In the adult usually the disease lasts about a week or ten

days; exceptionally, it may last two or three weeks.

COURSE.—In young children the course of meningitis differs somewhat

from that which is observed in adults, though the symptoms are

essentially the same. It is more sudden in its onset and shorter in

its duration. The prodromal stage may be brief or hardly noticeable;

but in older children restlessness, sensitiveness to light and sound,

wakefulness, slight twitchings of the features or of the limbs, a

half-open condition of the eyelids during sleep, occasional vomiting,

etc., are more commonly noticed. Convulsions are more common than in

the adult, and sometimes constitute the chief symptom. They may be

confined to a single extremity, but in {719} general they shift from

one limb to another. The muscles of the eyeball are usually

implicated, causing strabismus. Retraction of the head is rarely

absent, especially in young infants. These convulsions are almost

always tonic, but occasionally they alternate with clonic ones.

Distension and increased pulsation of the anterior fontanel is always

observed in infants a few months old affected with this disease. When

meningitis is secondary to some other disease, the first symptom

noticed in children is apt to be vomiting, with delirium. According to

Steffen, pneumonia is the disease most frequently complicated with

meningitis in children. As in tubercular meningitis, the most

prominent symptom may be mere sopor, sometimes with intervals of

intelligence. Simple meningitis in children is generally a rapid

disease, proving fatal in most cases within a week, and sometimes even

in a few hours. Exceptionally, it may last much longer. A case

occurring in a girl six years old, the duration of which was

fifty-five days, is reported by J. Bokai, Jr.;[17] the diagnosis was

substantiated by autopsy. Another case, which recovered after seven

weeks, is mentioned by Henoch.[18]

[Footnote 17: _Jahrb. f. Kinderkrankheiten_, N. F., xviii. 1, p. 105;

and _Schmidt's Jahrb._, 1882, No. 6, p. 269.]

[Footnote 18: Eduard Henoch, _Vorlesungen über Kinderkrankheiten_,

Berlin, 1881, p. 277.]

PATHOLOGICAL ANATOMY.—The lesions, which are rarely general, may

occupy a greater or less extent of the membrane. They are usually

disposed symmetrically with regard to the two hemispheres, or occupy

corresponding regions of the base. The vessels are in the beginning of

the disease distended, the finest ramifications being injected, giving

a red color to the membrane, which varies in different places from

crimson to light pink. The perivascular spaces of the larger vessels

are filled with a grayish or yellowish fluid composed of extravasated

liquor sanguinis and white blood-corpuscles. The meshes between the

two layers of the pia are soon infiltrated with pus, and the thickened

membrane can be stripped off from the surface of the brain, which is,

however, adherent to it in places and is torn in the process.

Sometimes a thin layer of pus, which can be scraped off with the

knife, is found upon the surface of the pia. The extent of the lesion

varies much in different cases. It may be confined to a limited region

of the hemispheres, or it may spread to the fissure of Sylvius, where

two surfaces become adherent. Sometimes the concrete pus and fibrin

are deposited in thick masses upon the base of the brain, often

completely surrounding the cranial nerves, and even the medulla. The

inflammation may extend to the lateral ventricles, which become filled

with a turbid fluid containing pus-cells, and sometimes wholly

purulent. The choroid plexuses are often covered with flecks of pus.

When the distension of the ventricles is very great, the gyri of the

brain are more or less flattened by compression against the cranium,

and the outer layer of the cerebral substance is bloodless and

œdematous. The cerebral sinuses are distended with blood, and

frequently contain thrombi due to an early stage of the inflammatory

process, besides recent coagula.

DIAGNOSIS.—The diagnosis of acute meningitis is often difficult, and

sometimes impossible, especially in the early stages, when the line

between congestion and inflammation cannot be drawn, and in

complicated cases. The typical symptoms are sudden and acute pain in

the head, with {720} sensitiveness to light and sound, contracted

pupils, rapid pulse, and vomiting, followed by delirium, convulsions,

and coma. If these symptoms were observed in an individual previously

in good health, they would be strongly suggestive of the disease, and

yet many of them are often present in the beginning of pneumonia,

erysipelas, typhoid, typhus, and other eruptive fevers, uræmia, and

poisoning from narcotic substances. Hence it is important to eliminate

these sources of error before coming to a conclusion, and a neglect of

this precaution is a not infrequent source of error in the diagnosis.

A careful examination of the urine will generally enable us to exclude

uræmia. The presence or absence of the eruptive fevers can usually be

determined by the attendant circumstances, and yet cases of

scarlatina, typhoid fever, variola, etc., beginning with active

cerebral symptoms, are sometimes hastily pronounced to be meningitis

by inexperienced observers. In poisoning by narcotics the history will

often aid us in the diagnosis; moreover, except in the case of opium,

the pupils are dilated instead of being contracted. In traumatic

cases, with fracture of the cranial bones, it is always difficult, and

often impossible, to distinguish between the symptoms of meningitis

and those due to other lesions. In concussion without fracture we must

be guided in our diagnosis by the same rules as in idiopathic cases.

The distinction between extreme congestion of the pia mater and

meningitis must be based chiefly upon the duration of the symptoms.

The former is usually brief in its course; the latter lasts one or two

weeks, and in cases which recover is often followed by after-effects

which are more or less permanent in their duration, such as paralysis

or rigidity of the limbs, mental defects, etc. Rapid recovery from the

acute symptoms would be strongly suspicious of congestion, and

doubtless in many such cases the treatment has been credited with a

success to which it was not entitled. The diagnosis from tubercular

meningitis will be reserved for the article on that disease.

PROGNOSIS.—Acute meningitis is fatal in the majority of cases, though

recovery is possible. A gradual diminution of the severity of the

symptoms, especially in respect to temperature, pulse, pain in the

head, and other cerebral phenomena, would afford encouragement, but we

must not trust too much to the brief appearances of amendment so often

observed.

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