evidently be affected by the causes that determine its duration, the
grade of the disease, the development and extent of the lesions, etc.;
but it is certain that, except in those imperfect and, as it were,
shadowy cases which denote a very slight action of the morbid cause,
its subjects do not recover rapidly. The essential lesion of the
fully-formed disease requires time for its removal, just as in typhoid
fever the intestinal ulcers are often slow of healing, and hence
become a cause of tardy recovery and even of unlooked-for death. The
convalescence, then, from the disease we are now studying is slow and
irregular, is attended often with debility and emaciation, and
sometimes with persistent headache, neuralgia, convulsions, stiffness
of the neck and pain in moving it, hyperæsthesia of portions of the
skin, palpitation of the heart, dyspepsia, etc. Relapses are very far
from being uncommon.
Among the causes of tardy convalescence in this disease are those
lesions and disorders which may be embraced by the term sequelæ.
Impaired vision, due to various affections of the eyes, has already
been considered among the symptoms proper of the disease, but they are
not infrequently developed after the acute attack has subsided. Thus,
in a case reported by Larrabie:[45] "Just as convalescence seemed
beginning the left eye became affected in all its parts, with entire
loss of vision and also complete deafness. After a short remission
hydrencephaloid symptoms appeared, followed by the same changes in the
hitherto sound eye, complete blindness and deafness, general cachexia
and marasmus, rigid flexion of the right limbs, and death by
exhaustion at the end of sixteen weeks." The impairment of hearing,
which also was described as a symptom of the acute attack, is apt to
become more marked after the acute stage has passed by, and, as before
stated, is very often permanent. Occurring in young children, it then
involves deaf-mutism. It is in many cases associated with defective
vision, weakness or loss of memory, mania, impairment of intelligence,
persistent pains in the head or chronic hydrocephalus. Sometimes to
one or more of these symptoms is added more or less general paresis or
complete paralysis. Southhall[46] mentions the case of a child two
years old whose attack was followed by incomplete paralysis, and death
at the end of eight months with softening {820} of the brain. Gordon
thus describes the conclusion of a case: "The man has gradually passed
into a state of almost organic life; he eats, drinks, and sleeps well;
he passes solid feces and urine without giving any notice, yet,
evidently, not unconsciously; ... he seems to understand, but cannot
answer; ... he can draw up his legs and arms, but he cannot use his
hands at all." Hirsch has remarked that disorders of speech are met
with, due apparently to an inability to articulate certain sounds. Von
Ziemssen regards chronic hydrocephalus as not a rare consequence of
epidemic meningitis, and as one not absolutely or immediately fatal.
Its symptoms include severe paroxysmal pain in the head or neck or
extremities, with vomiting, loss of consciousness, convulsions, and
involuntary evacuation of excrements. Between the paroxysms, which
sometimes occur periodically, the patient generally suffers from
neuralgic pains, hyperæsthesia, and various motor and even mental
disorders; but in other cases the intervals are free, or nearly so,
from all morbid manifestations. Davis (1872) and many others speak of
severe neuralgic pains following this disease; according to Dr. D.,
they are most frequent at the heads of the gastrocnemii muscles, in
the abdomen, and the head; a very fretful disposition, variable
appetite, and disturbed sleep are often observed. Relapses have been
noticed in almost all the epidemics, and it seems probable that they
are often due to the influence of accidental exciting causes, mental
or physical, in renewing the inflammation around the cerebro-spinal
lesions. Miner (1825) remarked that they were most apt to occur within
the first week, but that when the disease had once run its course
there were very few relapses during convalescence. But, he adds, there
were several repeated attacks after the most perfect recovery, and
several of the patients had had the disease the preceding year.
[Footnote 45: _Richmond Journal of Med._, Dec., 1872, p. 779.]
[Footnote 46: _Ibid._, Aug., 1872, p. 141.]
Like other epidemic diseases, meningitis presents itself with every
possible degree of gravity between that of a slight indisposition and
that of a malignant and deadly malady. The mortality in a number of
epidemics compared by Hirsch varied between 20 per cent. and 75 per
cent. It changes with the locality. Thus, nearly at the same time that
the death-rate from this disease in Massachusetts was 61 per cent., it
was but 33 per cent. in the Philadelphia Hospital. In 1872 the whole
number of deaths caused by it in Philadelphia was 133, while at St.
John's College, Little Rock, Ark., 21 cases out of 29 were fatal
(Southhall). It differs, also, at different periods; for while ten
epidemics in various places, occurring between 1838 and 1848,
presented an average mortality of 70 per cent., a similar number,
occurring between 1855 and 1865, gave an average mortality of only 30
per cent. It must, however, be confessed that such statistics cannot
be relied upon as accurate, for in private practice many cases occur
that are never reported unless they end fatally.
MORBID ANATOMY.--The lesions found after death from epidemic
meningitis consist essentially of congestion or inflammation of the
cerebro-spinal meninges, but they also include in many cases
hemorrhage, serous effusion, plastic exudation, and tissue-changes in
the brain and spinal marrow, and in many other cases an impaired
constitution of the blood. As the signs of the latter, and not the
former, alterations are met with in the more malignant cases, it is
evident that, looking at the disease as a {821} whole, it must involve
a toxic element of whose operation the various post-mortem lesions are
only effects. These lesions, on the whole, vary with the type of the
disease, and also with its duration, but some are chiefly met with in
cases of a malignant and others in cases of an inflammatory type.
The exterior of the body after death in the early stages of this
disease almost always presents the marks of transudation of the
contents of the blood-vessels. The dependent parts of the body exhibit
large livid patches or a uniform discoloration of the same hue. In
acute cases the muscles are more deeply colored than natural, and when
the attack is prolonged they are said to have their cohesion impaired
by fatty degeneration. Congestion of the brain is an unfailing
accompaniment of the first stage of the disease; its blood-vessels are
all distended with dark blood; the sinuses of the dura mater are
usually filled with coagula of the same hue, though sometimes very
dense. Serum abounds in the arachnoid cavity and in the ventricles of
the brain; it may be clear or milky, and sometimes it is quite
purulent. It is alleged by one reporter that no less than three pints
of turbid serum escaped in a case in which, however, death did not
occur until the thirty-fifth day. Craig found eight and twelve ounces
of a limpid fluid in two cases; and Tourdes found pus in more than
one-half of his cases, either unmixed or forming a milky liquid. J. L.
Smith refers to the case of an infant who had the disease at the age
of five months, and two months subsequently great prominence of the
anterior fontanelle, and other symptoms which indicated the presence
of a considerable amount of effusion within the cranium. In a case in
Dublin,[47] there was no meningeal lesion except in a "few dark spots
like sanguineous effusion under the arachnoid." White[48] mentions the
case of an adult that terminated fatally in thirty-six hours, in which
the vessels of the pia mater were very much congested, and sanguineous
effusions existed above and below the cerebellum, and a clot of blood
three inches long and external to the theca extended downward from the
lowest portion of the medulla oblongata. In all of these instances,
then, congestion, the first stage of inflammation, existed. That such
was its real nature is proved by what follows.
[Footnote 47: _Dublin Jour._, July, 1867, p. 441.]
[Footnote 48: _Med. Record_, iii. 198.]
The most characteristic lesion is a fibrinous or purulent exudation in
the meshes of the pia mater. American physicians described it as early
as 1806 in such terms as these: "The dura mater and pia mater in
several places adhered together and to the substance of the brain; ...
between the dura mater and the pia mater was a fluid resembling pus"
(Danielson and Mann). In 1810, Bartlett and Wilson found "an
extravasation of lymph on the surface of the brain;" and in the same
year Jackson and his colleagues, after describing the congestion and
serous effusion found within the cranium "in those who perished within
twelve hours of the first invasion," state that the arachnoid and pia
mater present an effusion between them of "coagulated lymph or
semi-purulent lymph" both on the convexity and at the base of the
brain. These descriptions correspond in all respects with those of
Mathey relating to the epidemic at Geneva in 1805, for he says: "The
meningeal blood-vessels were strongly injected. A jelly-like exudation
tinged with blood covered the surface of the brain; ... on its lower
surface and in the ventricles a {822} yellowish puriform matter was
found." Such lesions have been described by a long line of
observers--by Wilson in 1813, Gamage in 1818, Ames and Sargent in
1848; by Squire, Upham, and a host of others since 1860 in the United
States, and by Tourdes, Gilchrist, Ferrus, Wilks, Gordon, Banks,
Gaskoin, Niemeyer, Burdon-Sanderson, and many more in Europe.
It is evident, therefore, that in a certain number of fatal cases only
sanguineous congestion of the membranes of the brain and spinal cord
are found, and in certain others--constituting, it may be added,
nine-tenths of the whole number--evidences exist of cerebro-spinal
meningitis. Hence the natural conclusion is that the congestive
lesions represent the first stage of a process which if prolonged and
perfected occasions the lesions peculiar to inflammation. For the
development of the latter two factors would seem to be essential--not
only a fibrinous condition of the blood, but also sufficient time for
exudation to occur. But when we come to study the actual results of
examinations post-mortem, it is found that the duration of the attack
does not determine absolutely the nature of the lesions. On the one
hand, in a case which terminated fatally after a week's illness there
was found reddish serum between the arachnoid and the pia mater and in
the lateral ventricles, with intense injection of the pia mater of the
base, medulla oblongata, and upper part of the spinal cord, but no
exudation of lymph.[49] And, on the other hand, numerous cases have
been published in which, although death occurred within twenty-four
hours from the onset of the attack, coagulated lymph and also pus were
found upon the brain and spinal marrow. For example, during the winter
of 1861-62, in the army, that then lay near Washington, D.C., a
soldier was attacked with a chill, severe fever, and headache,
followed by opisthotonos and repeated convulsions before his death,
which occurred in about twenty-four hours. No eruption or
discoloration of the skin is mentioned in the history. On examination
there was found beneath the arachnoid a thin layer of lymph and
abundant exudation over the posterior lobes of the cerebrum, and also
at the base of the brain and on the medulla oblongata.[50] In a case
reported by Gordon[51] the entire duration of the illness was under
five hours, and after death the cerebral arachnoid was more or less
opaque, and in some spots had a layer of very thin purulent matter
beneath it. And, again, not only may the symptoms belonging to
blood-dissolution be consistent with a certain prolongation of life,
but also with decidedly inflammatory tissue-changes. Thus, in another
case of Gordon's the duration of the illness was at least six days,
and the patient presented all the characteristic symptoms of the
disease, including "a most wonderful and uniform curve of the spine
and head backward," "spots black as ink," "bullæ which rapidly became
opaque and dusky," "herpetic eruption, etc." After death the body had
a very frightful appearance. It was still prominently arched forward.
It was of a dusky blue color, with a copious eruption of black spots
of various sizes, and one or two of them were gangrenous.... When the
theca vertebralis was opened purulent matter flowed out, and a
purulent effusion was found in patches on the brain. {823} The
cerebral arachnoid was all opaque, the lateral ventricles were filled
with serum, and the blood in all the cavities was very fluid and dark
colored. From all that precedes, therefore, it must be inferred that
the nature of the lesions in this disease depends not on the type
alone, nor on the duration merely, of the attack--that a very brief
course is compatible with marked inflammatory lesions, and a prolonged
one with profound alterations in the condition of the blood. In other
words, it seems that there must be something besides the appreciable
lesions that influences, if it does not determine, the issue of an
attack of this affection. While bringing forward prominently this
proposition, and the facts on which it rests, we have no intention of
under-estimating the relative significance of the two most conspicuous
types of the disease, the purely inflammatory and the adynamic, or
calling in question the fact that the evolution of the former is most
usually comparatively slow and regular, and of the latter rapid and
irregular. In the one, when death takes place early, congestive
changes are found, and when later these have merged into exudative
lesions; in the other or adynamic cases congestion and liquid
transudation prevail, and the results of complete inflammation are
seldom seen. When the disease has been very much prolonged the
exudation becomes tough, adherent, and shrivelled.
[Footnote 49: Davis, _Richmond Med. Jour._, June, 1872, p. 709.]
[Footnote 50: Frothingham, _Amer. Med. Times_, Apr., 1864, p. 207.]
[Footnote 51: _Dublin Quart. Jour._, May, 1867, p. 409.]
The brain-tissue has generally been found softer than natural, and,
although in some cases this diminished consistence might be attributed
to post-mortem changes, yet on the whole it must be associated with
the inflammatory lesions of the meninges. As a rule, it is greater the
longer the attack has lasted, and is by no means equally diffused, but
is more marked where the meningeal alterations are greatest. Ames
found softening in nine out of eleven cases, and chiefly in the
cortical substance, but also in the fornix and septum lucidum; and
Chauffard states that in protracted cases "the interior surface of the
ventricles, the fornix, and septum lucidum, were reduced to a
pultaceous and creamy consistence." But it is by no means true that
softening is met with in all cases of long duration.
The lesions of the spinal marrow and its membranes correspond with
those of the brain. The dura mater is often very dark, its
blood-vessels engorged, its arachnoid cavity distended with serum more
or less bloody, turbid, or purulent. Two ounces of pus have been
removed from it through a puncture. Fibrinous and purulent exudation
fills the meshes of the pia mater, and is usually most abundant in the
cervical and dorsal portions, and generally upon the posterior rather
than upon the anterior surface of the organ; but sometimes large
accumulations of lymph and pus are found at the lower end of the cord.
Gordon[52] relates of a case that "when an opening was made into the
lower part of the theca vertebralis purulent matter flowed out, and
the entire surface of the pia mater was covered with a coating of thin
purulent matter, which, like a thin layer of butter, remained adherent
to it." Occasionally the cavity of the spinal arachnoid contains
blood. Softening of the spinal cord has been often noticed. Chauffard
states that in some cases of particularly long duration it was reduced
to a mere pulp, and he adds, "in the place of portions of the spinal
marrow, completely destroyed, was found only a yellowish liquid, or
the empty membranes fell into contact where it was {824} wanting."
Similar disorganization has been described by Ames, Klebs, and others.
Fronmüller reports the case of a girl aged fourteen years in whom the
central canal of the spinal cord was distended with pure pus.
[Footnote 52: _Dublin Quart. Jour._, xliii. 414.]
The lesions of the internal auditory apparatus consist of softening in
the fourth ventricle and of the root of the auditory nerve, yet such
lesions are said to have been found even when no defect of hearing had
existed. In other cases in which deafness did occur the lesions
consisted of inflammatory changes in the cavity of the tympanum and
suppuration of the labyrinth. They probably arose from an extension of
inflammation from the pia mater along the trunk of the auditory nerve
(Von Ziemssen). In like manner, the inflammatory and destructive
changes in the eye which have been elsewhere described arise from an
analogous cause affecting the optic nerves.
It is unnecessary to dwell upon the condition in which other organs
are found after death from epidemic meningitis. In cases that present
a typhoid type, and even in such as are rapidly fatal with ecchymotic
discoloration of the skin, the various organs present no distinctive
tissue-change, but only such engorgement as is common to all diseases
of a similar type. It deserves to be particularly mentioned that in
this affection the spleen is not enlarged, as it always is in a
greater or less degree in diseases whose primary stage involves an
altered condition of the blood. This fact becomes all the more
important in view of the remarkable contrast which the constitution of
the blood presents in epidemic meningitis and in various typhous
affections.
The state of the blood in this disease is one of peculiar interest,
dominating as it does its whole pathology and determining its
nosological position. It is the blood of a phlegmasia rather than of a
pyrexia. This fact was early established by American physicians who
observed the disease, and the opportunities for doing so were not
wanting, since venesection was used by every one who treated it. In
1807-09 a rapidly fatal case or two was found in which the "blood was
darker and had a larger proportion of serum than usual," but in others
"it did not present any uncommon appearance, and no inflammatory buff,
nor was it dissolved" (Fish). In 1811, Arnell stated that "the blood
drawn in the early stage appeared like that of a person in full
health; there was no unusual buffy coat, neither was the crassamentum
broken down or destroyed." In the epidemic studied by Mannkopff (1866)
he found that blood obtained by venesection gave a clot with a thick
buffy coat. Andral, seeking to establish the law that in every acute
inflammation there is an increase in the fibrin of the blood, remarks
that in a case of cerebro-spinal meningitis it was very marked.[53]
Ames states that "the blood taken from the arm and by cups from the
back of the neck" "coagulated with great rapidity." "Its color was
generally bright--in a few cases nearly approaching to that of
arterial blood; it was seldom buffed; in thirty-seven cases in which
its appearance was noted it was buffed in only four." Analyses were
made in four cases, "the blood being taken early in the disease from
the arm, and was the first bleeding in each case. They furnished the
following results: {825}
Fibrin. Corpuscles.
I 6.40 140.29
II 5.20 112.79
III 3.64 123.45
IV 4.56 129.50
The first was from a laboring man thirty-five years old; the second
from a boy twelve years old, while comatose; and the two others from
stout women between thirty and thirty-five."[54] Tourdes, whose
analyses follow, states that "blood drawn from a vein was rarely
buffed; if a buffy coat existed, it was thin, and generally a mere
iridization upon the surface of the clot."[55]
Fibrin. Corpuscles.
I 4.60 134.00
II 3.90 135.54
III 3.70 143.00
IV 5.63 137.84
Maillot gives, as the result of an analysis of six cases, an increase
of fibrin to six parts and more in a thousand. This summary
represents, as far as is known, all of the analyses of blood taken
from living patients in this disease, and it shows that in every case
the proportion of fibrin exceeded that of healthy blood, and
corresponded exactly to that observed in the blood of inflammatory
diseases, while the proportion of red corpuscles varied within the
normal limits. How different is this condition of the blood from that
of typhus fever, in which there is a marked diminution of fibrin, and
a falling off in the red corpuscles as well, or from that of typhoid
fever, in which neither element declines until the disease affects the
body by inanition! (Murchison).
[Footnote 53: _Path. Hæmatology_, p. 73.]
[Footnote 54: _New Orleans Med. and Surg. Jour._, Nov., 1848.]
[Footnote 55: _Epidemie de Strasbourg_, p. 160.]
* * * * *
In regard to the condition of the blood after death the historians of
the disease are not so well agreed; nevertheless, the preponderance of
the testimony is in favor of the statement that the blood presents
appearances resembling those belonging to the continued fevers rather
than to the inflammations. It is true that even in this the agreement
is neither general nor complete. Tourdes, for example, states that in
an autopsy "the blood was remarkable for the abundance and toughness
of the fibrinous clots," but the greater number have reported it as
being dark and liquid. Such was its condition in the epidemic which we
studied at the Philadelphia Hospital in 1866-67, and it has been
correctly described by Dr. Githens as follows: "The blood was fluid,
of the color and appearance of port-wine lees; under the microscope
the corpuscles were shrivelled and crenated, and there was a space
apparent between them as they were arranged in rouleaux. There were in
two cases white, firm, fibrinous heart-clots extending through both
ventricles and auricles and into the vessels leading to and from the
heart."[56] It may be added that the red corpuscles are often crenated
and shrivelled when the case has been protracted, and it has been
stated--from limited observation, indeed--that "the white corpuscles
are three times more numerous than the red."[57] The blood has been
scrutinized to discover, if possible, some of those bodies which are
judged by Koch and his disciples to differentiate {826} general
diseases, but it is stated that the investigation has been without
definite result.[58]
[Footnote 56: _Amer. Jour. of Med. Sci._, July, 1867, p. 23.]
[Footnote 57: _Dublin Quart. Jour._, May, 1867, p. 441.]
[Footnote 58: Jaffé, _Phila. Med. Times_, xii. 599.]
It does not seem difficult to reconcile the conflicting statements now
given of the condition of the blood in epidemic meningitis. One of
them points to an excess and the other to a loss of the spontaneously
coagulable element of the blood. It is evident that venesection, which
was necessary for procuring the living blood for analysis, would only
be performed when the type of the disease authorized it--that is, when
the type was sthenic; whereas the blood examined after death had
necessarily undergone changes which tended to, if they did not
actually, occasion death. Hence we find among the former cases, when
fatal, the most extensive and massive exudation, and always among the
latter less evidence of inflammation, but, on the other hand, a
greater or less manifestation of those appearances which denote a loss
of the vitality and organization of the blood. In the one case death
may fairly be attributed, above all other causes, to the pressure
upon, and the disorganization of, the cerebro-spinal organs essential
to life; in the other, primarily, to the death of the vital elements
of the blood produced by the specific cause of the disease. It is
probable that the post-mortem fluidity of the blood exists under two
conditions. In the one the morbid cause is powerful enough from the
very commencement rapidly to destroy the life of that fluid, and in
the other it acts less violently, but continuously, to exhaust the
powers of life.