detailed, and the insidious course of those which as latent abscesses
may exist for many years without producing any noticeable symptoms
whatever, there is every connecting link as to suddenness and slowness
of onset, severity and mildness of symptoms, and rapidity and slowness
of development and progress. It is the encapsulated abscesses which
are properly spoken of as chronic, and which may even constitute an
exception to the almost uniform fatality of the suppurative affections
of the brain. Thus, the symptoms marking their development may
correspond to those of an acute abscess, but coma does not supervene,
temporary recovery ensues, and the patient leaves the hospital or
returns to his vocation. But all this time he appears cachectic, and
there will be found, on accurate observation, pathological variations
of the temperature and pulse. The appetite is poor; the bowels are
usually constipated; there are frequent chilly sensations and
horripilations, and a general malaise. This condition slowly passes
away in the few cases which recover; in others relapses occur, usually
of progressing severity, and terminate life. The period during which
the symptoms of the abscess are latent may be regarded as
corresponding to the latent period which sometimes intervenes between
an injury and the development of the symptoms of acute abscess, and
which, according to Lebert, may comprise several weeks or months. In
other words, the morbid process may be regarded all this time as
progressing under the mask of a remission. It is this latent period
which it is of the highest importance for the diagnostician to
recognize. There is usually headache, which is continuous and does not
change in character, though it may be aggravated in paroxysms. Usually
the temperature rises with these paroxysms, and if they continue
increasing in severity they may culminate in epileptic convulsions.
Many of the symptoms of cerebral abscess—prominently those attending
the rapidly-developed forms and the exacerbations of the chronic
form—are due to cerebral compression. It is the pulse and pupils,
above all, that are influenced by this factor.
In an affection having so many different modes of origin as cerebral
abscess, and occupying such a wide range of possible relations to the
cerebral mechanism, it is natural that there should exist many
different clinical types. So far as the question of the diagnosis of
localized cerebral abscesses is concerned, I would refer to the
article dealing with cerebral localization, in order to avoid
repetition. With regard to the etiological types, they will be
discussed with the respective causal factors.
ETIOLOGY.—Abscess of the brain is so frequently found to be due to
metastatic or other infectious causes that it is to be regarded as
highly improbable that it is ever of idiopathic occurrence. The most
frequent {797} associated conditions are—suppurative inflammation in
neighboring structures, such as the tympanic cavity, the mastoid
cells, the nasal cavity, or inflammation or injury of any part of the
cranium and scalp. The connection of these structures with the brain
through lymphatic and vascular channels is so intimate that the
transmission of a pyogenic inflammatory process from the former to the
latter is not difficult to understand. But disease of far distant
organs, such as gangrene of the lung, and general affections, such as
typhoid fever, occasionally figure among the causes of cerebral
abscess, particularly of the miliary variety.
Among the commonest causes of cerebral abscesses are those which the
surgeon encounters. The injury may be apparently slight and limited to
the soft parts, or the bone may be merely grazed. Gunshot wounds are
particularly apt to be followed by a cerebral abscess; and it has been
noted that those which granulate feebly, whose base is formed by a
grayish, dirty, and fetid material, are most apt to lead to this
ominous complication. The symptoms do not usually develop immediately,
and after the surgeon is led to indulge in the hope that danger is
past, proper reaction sets in, healthy granulations develop—nay, the
wound may close and be undergoing cicatrization—then the patient
complains of feeling faint or drowsy, and with or without this
premonition he has convulsive movements of one side, sometimes
involving both extremities and the corresponding side of the face.
Consciousness is usually preserved, but the spells recur, and the
patient is noted to be absent-minded during and after the convulsive
seizure. On some later day he is noticed to become pale, as in the
initial stage of a true epileptic seizure; total abolition of
consciousness follows, and the clonic spasms, affecting the same limbs
and muscles involved in the first seizures, now recur with redoubled
violence. After such an attack more or less paresis is observed in the
muscles previously convulsed. A number of such seizures may occur, or
a fatal issue terminate any one of them. Not infrequently the field of
the involved muscles increases with each fit. Thus the thumb or a few
fingers may be the first to show clonic spasm; in the next fits, the
entire arm; in succeeding ones, the leg and face may follow suit. In
such a case the periphery first to be convulsed is the first to become
paralyzed, thus showing that where the disease began as an irritative
lesion the cortex is now destroyed, and that around the destructive
focus as a centre the zone of irritation is spreading excentrically,
first to irritate and then to destroy seriatim the functions of the
various cortical fields in their order. According to the teachings
laid down in the article on Localization, the order of invasion and
extension, as well as the nature, of the focal symptoms will vary.
Finally, the attacks become more severe and of longer duration; the
patient does not recover in the intervals, but complains of nausea,
pain, confusion, and head-pressure. He is noted to be dull, his
temperature is slightly raised (100° F.), and the speech may be
affected. Several attacks may occur in a day, each leaving the patient
more and more crippled as to motility and mind. He is delirious and
drowsy at intervals; his temperature may rise after an attack from one
to four degrees, usually remaining near 103°-104° F. in the evening;
and, coma developing, death occurs, the convulsion or paralytic
phenomena continuing at intervals during the moribund period, and the
temperature and pulse sometimes running up rapidly toward the last. On
examining {798} the parts, it is found that the bone is necrotic at
the point of injury, usually only in its outer table, but sometimes in
its entire thickness. In exceptional cases the normal continuity of
the entire table is not interrupted to all appearances, and a small
eroded spot on the inner table is found bathed in pus, or a detached
necrotic fragment may be found in the latter. Corresponding to the
purulent focus on the inner table the dura mater is detached,
discolored, and perforated in one or more places with irregular rents
or holes which have a greenish or blackish border. An abscess is found
in that part of the brain which corresponds to this opening. There is
no question that it was caused by direct infection from the necrotic
spot.
Cases have been noted,[55] apparently of idiopathic origin, in which a
sudden paralysis of a few fingers was the first symptom produced by
the development of a cerebral abscess. In a few days such a paralysis
extends to the other fingers and to the forearm. Occasionally no
convulsive phenomena are noted, or choreic movements indicate, in
their place, that the cortical field is irritated. Such cases usually
run a rapidly fatal course.
[Footnote 55: Arthur E. W. Fox, _Brain_, July, 1885.]
The most frequent cause of cerebral abscess in civil practice is
suppurative inflammation of the middle ear. It may be safely asserted
that the person suffering from this affection is at no time free from
the danger of a cerebral abscess, a purulent meningitis, or a
phlebitic thrombosis of the sinuses. Cases are on record where the
aural trouble had become chronic, and even quiescent, for a period of
thirty years, and at that late date led to abscess with a fatal
termination. Of 6 cases of this character in my experience, 4 of which
were verified by anatomical examination, not one but had occurred at
least four years after the commencement of the ear trouble, and 1
happened in a man aged fifty-four who had contracted the latter
affection in childhood. In 2 there was in addition diffuse purulent
meningitis, limited on the convexity to the side where the abscess was
situated.[56] In 4 the abscess was in the temporal lobe, 1 of them
having in addition an abscess in the cerebellar hemisphere of the same
side; in a fifth the abscess was in the deep white substance of the
cerebral hemisphere, opening into the lateral ventricle, and in the
sixth it was in one cerebellar hemisphere alone.
[Footnote 56: One of these was seen during life by J. R. Pooley; the
other was a paretic dement at the New York City Pauper Asylum.]
The course of this class of abscesses is usually obscure: focal
symptoms are not commonly present, and the constitutional and local
symptoms usually appear as a gradual outgrowth from the aural
troubles. Thus there is at first usually little fever, vertigo, and
chilliness, but considerable tinnitus, and sometimes pain in the ear.
Occasionally local signs of a septic metastasis of the otitis, such as
œdema over the mastoid or painful tumefaction of the cervical glands,
are visible. The pain previously referred to the region of the ear now
becomes general; commonly—even where the abscess is in the temporal
lobe—it becomes progressively aggravated in the frontal and sometimes
in the nuchal region, and under an increase of the febrile phenomena
death may exceptionally occur without further complication. Even large
abscesses in one half of the cerebellum occur without producing
Ménière's symptom—a fact {799} which leads to the suspicion that the
purulent deposit must have been of slow and gradual development. In
one case distinct symptoms indicating an affection of the subcortical
auditory tract were observed. As a rule, this class of abscesses are
accompanied toward the close by active general symptoms—convulsions,
coma, narrowing and impaired light-reaction of the pupils. Delirium,
when a prominent symptom from the beginning, indicates the probable
association of meningitis with the abscess.[57] Occasionally severe
pain, rigor, high temperature, and paralysis may be absent even with
rapidly-developed abscess from otitis.[58]
[Footnote 57: The same is probably true of oculo-motor paralysis,
which Ross (_loc. cit._, vol. ii. p. 735) refers to uncomplicated
abscess.]
[Footnote 58: This was the case with an abscess containing five ounces
of pus recorded by C. S. Kilham at the Sheffield Medical Society
(_British Medical Journal_, February 13, 1886). As illustrating what
was stated about the non-correspondence of the pain and the location
of the abscess, it may be stated that notwithstanding this large
abscess was in the temporal lobe, what pain was present was in the
forehead.]
Ulcerative endocarditis, infectious osteomyelitis, pulmonary gangrene,
general pyæmia, and, as is claimed by a few authors, typhoid fever,
are often accompanied by multiple abscesses in the brain-substance.
Usually the foci are small, as may be readily inferred from the fact
that they are of embolic origin, the emboli being usually so small as
to lodge in very small vessels, and that the fatality of the primary
disease is so great as to cut short life before the abscess can reach
larger dimensions. For the same reasons the symptoms they produce are
rarely distinctive. In chronic lung affections accompanied by
putrescence in bronchiectatic or other cavities cerebral abscesses are
not uncommon occurrences. Under these circumstances, although we must
assume an embolic origin, the abscess is rarely multiple, and the
symptoms are as marked as in the ordinary varieties. Thus a patient
suffering from chronic phthisis, with or without prodromal malaise or
somnolence, experiences formications and pain in his right leg; he
then notices a slight halt in walking; twitches appear in the affected
extremity; it becomes distinctly paretic. The arm then becomes
affected in like manner; the pupils become unequal; a severe chill
occurs, followed by delirium, convulsions, coma, and death.
DIAGNOSIS.—There is little difficulty in recognizing the existence of
a cerebral abscess in which well-marked focal and constitutional
symptoms coincide, or where a distinct abscess-producing cause, such
as an ear trouble, a head injury, or a putrid bronchiectasis,
coexists.[59] But there are a number of cases, varying from the latent
form to forms with obscure general symptoms, whose recognition is
impossible or at best a matter of conjecture. Such cases may be
readily confounded with certain tumors. The existence of febrile
symptoms, although not excluding tumor, as some tumors are accompanied
by such, is greatly in favor of abscess. On the other hand, choked
disc, which is rare with abscess and found only with the very largest,
is in favor of tumor.
[Footnote 59: Yet a leading and careful authority was misled into
making the diagnosis of abscess in a case of ear disease complicated
by a cerebral tumor.]
PROGNOSIS AND TREATMENT.—The majority of cerebral abscesses must, from
the nature of the case, be regarded as not influenceable by medicinal
measures or surgical treatment. The miliary and other abscesses due to
general septic causes or to mycotic invasion, being in the nature of
{800} the case but features of intrinsically dangerous or fatal
primary diseases, do not call for special measures. It is different
with those due to local trouble about the head and to surgical causes.
Remarkable advances have been made in the operative treatment of
cerebral abscesses, chiefly owing to the increasing accuracy of the
localization of the affected areas through the disturbance of their
function, and to the perfection of surgical methods. A number of cases
by Gussenbauer, Wernicke, and others have shown that some abscesses
may be accurately located during life by the focal symptoms produced
by their presence. Wernicke's observation of a large abscess in the
occipital lobe showed two facts. First, it permitted the study of the
effect of large abscesses on the cerebral movements, as it was found
after trephining that the pulsation movement of the brain was lost and
the dura tensely bulging, thus indicating a high degree of cerebral
pressure. Secondly, the operation showed that an abscess can be
emptied of its contents, under moderate aseptic precautions, without
provoking contiguous inflammatory reaction or infecting the meninges.
Notwithstanding these favorable local conditions, the patient died.
Gussenbauer[60] was more fortunate. He surmised from the fluctuation
of some symptoms and the predominance of others that his patient had
an abscess in the frontal lobe. The suspicion was verified: an abscess
of the size of an apple was found, opened, and emptied of its
contents. The patient recovered without any immediate untoward
symptom.[61]
[Footnote 60: _Prager medizinische Wochenschrift_, 1885, Nos. 1, 2,
and 3.]
[Footnote 61: Epileptic and focal spasms subsequently developed, which
shows that a new inflammatory or other destructive process may have
set in in the vicinity of the emptied sac.]
The uncertainties of localization in some districts of the brain are
so great that a number of attempts to repeat the explorations and
aspiration of Wernicke and Gussenbauer have failed. In one case
recently operated on in New York City the aspirating-needle was run
into the brain-substance in several different directions without
striking the pus. It is a question under such circumstances whether
the chances of an abscess becoming latent, minimal though they be in
cases with pronounced signs, are not to be preferred to those which an
uncertain operation can give. The superficial encephalitic foci offer
far better opportunities for surgical triumphs. Here not only the
symptoms are much more constant, and point more unerringly to the site
of the morbid spot, but there are often other signs, such as the
evidences of impaction of a foreign body, local tenderness on
percussion, or bone disease, which aid in determining the proper spot
for the application of the trephine. Several operations where
traumatic encephalitis existed with or without leptomeningitis of the
convexity, followed by complete recovery, were performed by
Macewen.[62]
[Footnote 62: _The Lancet_, 1885, vol. i. p. 881.]
The medicinal treatment of abscess of the brain is limited to
derivative methods, whose aim is the relief of pressure—an aim whose
fulfilment is more frequently illusory than otherwise.
Benefit has been claimed from the energetic use of mercury, chiefly in
the form of calomel, by older writers; and recently Handfield Jones
has endorsed its administration, attributing to it a remission in a
case in which it was employed. It must be remembered, however, that
remissions occur spontaneously in this disease, and that the purgative
action of calomel may act well for the time being in an affection so
apt to be {801} associated with hyperæmia and increased cerebral
pressure as is an abscess of the brain.[63] In the nature of the case,
even this latter momentarily beneficial effect is at the best
temporary.
[Footnote 63: _Brain_, October, 1884, p. 398.]
The prophylaxis of cerebral abscess can be carried out only in cases
due to cranial and aural affections. The importance of treating all
scalp and cranial injuries under aseptic[64] precautions is recognized
by all surgeons. It is generally admitted that the trephining of a
bone suspected to be the site of an ostitic or necrotic process
involves fewer risks than the allowing it to remain. Similar
principles govern the treatment of the inflammatory involvement of the
mastoid cells often complicating otitis media. If trephined at all,
these should be trephined at the earliest moment. It was a belief
among the older aurists that the sudden cessation of an aural
discharge was of evil augury, and that cerebral complications were
more apt to follow under such circumstances than when the ear
discharged freely. Von Tröltsch, Politzer, Gruber, and Toynbee have
opposed the exclusive application of the old dogma. In so far as the
older ear-surgeons regarded a profuse aural discharge as an
encouraging sign, in this respect they were of course wrong. But their
observation of the frequent concurrence of cerebral sequelæ with
suppression of discharge is, I think, borne out by a large number of
cases. It does not apply, however, to the suppression of discharge by
the rational employment of aseptic injections.
[Footnote 64: This term is used in its widest sense here.]
Spinal Hyperæmia.
The spinal cord is found to vary considerably in color in different
individuals. To some extent this difference is influenced by the
position occupied by the body after death, but not as markedly as in
the case of the brain. Thus it will be paler in a body which has been
kept in the prone than in one which has been kept in the supine
position.[65] It is usually found more injected in persons who have
died of febrile affection than in those who have died of exhausting
diseases; notably is this the case with typhus fever and with subjects
who die with congestive malarial chill. But the most intense
congestion, where the gray substance instead of having the normal rosy
hue appears like a blood-soaked sponge, and the white substance
instead of the tint to which it owes its name has a pink shade, is
found in subjects dying in convulsive disorders complicated by
asphyxia, such as epileptic status, tetanus, and certain toxic
disorders.
[Footnote 65: I have not seen it noticed anywhere, but it is a fact
readily demonstrable in any autopsy made in a well-preserved body that
when a short segment of cord is observed at the moment of section the
section surface appears pale; but if it be again examined after a few
moments, it will show a reddish tinge, marked as a faint injection
would be; this tinge distinctly deepens under the eye. I have observed
this in specimens which were not held in the hand, so that the
influence of pressure can be excluded. Nor do I believe that the
elasticity of the tissues is such as to account for the phenomenon.]
In attempting to apply the fact that varying degrees of vascular
injection are found on post-mortem examinations of the spinal cord to
the elucidation of certain clinical phenomena, we encounter the same
difficulties and sources of error that confronted us in the study of
nutritive {802} brain disorders. The majority of writers have
therefore contented themselves with making a careful clinical study of
the mostly subjective signs of disorders which, once designated as
spinal anæmia and hyperæmia, are now classified under the
non-committal titles of spinal irritation and exhaustion
(neurasthenia), as in this volume. A number of these disorders, like
the so-called anæmic paralysis of Bouchut, Leroy d'Etiolles, Beroliet,
Baimer, and Brandis, would to-day be considered as hysterical or
reflex; and a few of the instances cited by their contemporaries as
cases of spinal hyperæmia have been since demonstrated to resemble the
initial phases of organic diseases of the cord.
The causes of active spinal hyperæmia are either direct, as when the
spinal centres are overtasked by muscular strain either through
over-exertion or through toxic convulsions, surprised by violent
shocks, such as concussion accidents, or collateral, as when a
physiological discharge (menstruation) or a pathological one
(hemorrhoidal flux) is suddenly checked. A few cases are reported
where carbonic-oxide-gas poisoning provoked spinal hyperæmia. But,
like the alleged cases of spinal hyperæmia after continued and
exanthematic fevers, they were probably cases of incipient or
established myelitis. Hammond claims that surface chilling exerts the
same congesting influence on the cord which he claims for the brain;
but no definite observations have been made in this direction.
Passive spinal hyperæmia has been attributed to obstructive cardiac
and chronic pulmonary affections. In such cases, as with most causes
acting on the circulation of blood in the nerve-centres, the
coexisting cerebral congestion usually masks the spinal. It is a
question how far the intense hyperæmia of the cord found in some cases
of tetanus, strychnia-poisoning, and the condition called
hydrophobia[66] is primary and an indication of neural
hyperexcitability, and how far it is secondary to the asphyxia
attending the last phases of these convulsive states. The weight of
opinion is in favor of an acceptation of the latter as the chief or
only factor.
[Footnote 66: In a case of hydrophobia clinically as well marked as
has been recorded, which I had the privilege of examining through the
courtesy of Kretschmar, both brain and cord were found remarkably
anæmic.]
Over-exertion and sexual excesses are frequently followed by a
sensation of fulness and tension in the sacral and lumbar regions,
which may be relieved by lying prone, while it is aggravated while
lying supine.[67] From the location of this pain it is evident that it
is not due to congestion of the cord or its membranes, but to fulness
of the vertebral and spinal veins of the lower segment of the
vertebral column. A similar sensation, which may be relieved by the
same change in position or by a hemorrhoidal flux, is complained of by
patients suffering from portal obstruction. The veritable symptoms of
hyperæmia manifest themselves in the parts which receive their nervous
supply from the affected districts. The reflexes are usually more
active; paræsthesias of different kinds, such as formication,
tingling, and creeping sensations, are common; and {803} there is more
or less motor weakness, the limbs feeling heavy and sometimes being
the seat of an acute pain. As a rule, these symptoms are limited to
the lower half of the body.