cerebral anæmia which the majority of neurologists regard as of a
different character, has offered a very happy explanation. He says,
“Now, it must be recollected that the brains of anæmic persons are in
very much the same condition as the eyes of those who have for a long
time been shut out from their natural stimulus, light. When the full
blaze of day is allowed to fall upon them retinal pain is produced,
the pupils are contracted, and the lids close involuntarily. The light
must be admitted in a diffused form, and gradually, till the eye
becomes accustomed to the excitation. So it is with the use of alcohol
in some cases of cerebral anæmia. The quantity must be small at first
and administered in a highly diluted form, though it may be frequently
repeated.”]
[Footnote 39: Such as Meneszer Aszu; there is no genuine tokay wine
imported to this country, as far as I am able to learn.]
The cold pack, strongly recommended by some in general anæmia, is not,
in my opinion, beneficial in cases where the nervous phenomena are in
the foreground, particularly in elderly persons. Gentle massage, on
the other hand, has the happiest effects in this very class of cases.
Of late years my attention has been repeatedly directed to cerebral
anæmia of peculiar localization due to malarial poisoning. It has been
{790} noted by others that temporary aphasia and other evidences of
spasm of the cortical arteries may occur as equivalents or sequelæ of
a malarial attack. I have seen an analogous case in which hemianopsia
and hemianæsthesia occurred under like circumstances, and were
recovered from. Whether more permanent lesions, in the way of
pigmentary embolism or progressing vascular disease, causing
thrombotic or other forms of softening, may develop after such focal
symptoms is a matter of conjecture, but I have observed two fatal
cases in which the premonitory symptoms resembled those of one which
recovered, and in which these were preceded by signs of a more general
cerebral anæmia, and in one case had been mistaken for the
uncomplicated form of that disorder. Where a type is observable in the
exacerbation of the vertigo, headache, tinnitus, and lethargy of
cerebral anæmia, particularly if numbness, tingling, or other signs of
cortical malnutrition are noted in focal distribution, a careful
search for evidences of malarial poisoning should be made; and if such
be discovered the most energetic antimalarial treatment instituted. It
is in such cases that arsenic is of special benefit.
The treatment of syncope properly belongs to this article. Where the
signs of returning animation do not immediately follow the assumption
of the recumbent position, the nitrite of amyl, ammonia, or small
quantities of ether should be exhibited for inhalation. The action of
the former is peculiarly rapid and gratifying, though the patient on
recovery may suffer from fulness and pain in the head as after-effects
of its administration. The customary giving of stimulants by the mouth
is to be deprecated. Even when the patient is sufficiently conscious
to be able to swallow, he is usually nauseated, and, as he is
extremely susceptible to strong odors or tastes in his then condition,
this nausea is aggravated by them. By far the greater number of
fainting persons recover spontaneously or have their recovery
accelerated by such simple measures as cold affusion, which, by
causing a reflex inspiration, excites the circulatory forces to a more
normal action. Rarely will the electric brush be necessary, but in all
cases where surgical operations of such a nature as to render the
development of a grave form of cerebral anæmia a possibility are to be
performed, a powerful battery and clysters of hot vinegar, as well as
the apparatus for transfusion, should be provided, so as to be within
reach at a moment's notice.
Inflammation of the Brain.
Before the introduction of accurate methods of examining the diseased
brain the term inflammatory softening was used in a much wider sense
than it is to-day. Most of the disorders ascribed to inflammatory
irritation by writers of the period of Andral and Rush are to-day
recognized as regressive, and in great part passive, results of
necrotic destruction through embolic or thrombic closure of afferent
blood-channels. Two forms of inflammation are universally recognized.
One manifests itself in slow vascular and connective-tissue changes
and in an indurating inflammation. There are two varieties of it: the
first of these, which is associated with furibund vaso-motor
explosions and regressive metamorphosis of the functional
brain-elements, is known from its typical {791} association with grave
motor and mental enfeeblement as paretic dementia or dementia
paralytica. The second, which is focal in the distribution of the
affected brain-areas, is known as sclerosis. The former is treated of
in a separate article; the latter is considered in connection with the
spinal affections which either resemble it in histological character
or complicate its course. The second form of cerebral inflammation is
marked by the formation of the ordinary fluid products of acute
inflammation in other organs of the body; this is the suppurative
form, usually spoken of as abscess of the brain.
In addition to these two generally recognized inflammatory affections
there are a number of rare diseases which are regarded by excellent
authority as also of that character. The vaguely-used term acute
encephalitis has been recently reapplied with distinct limitations to
an acute affection of children by Strümpell. This disease is usually
of acute onset, infants under the sixth year of age being suddenly,
and in the midst of apparently previous good health sometimes,
attacked by fever, vomiting, and convulsions.[40] Occasionally coma
follows, which may last for several days, perhaps interrupted from
time to time by recurring convulsions or delirium. The convalescence
from this condition is rapid, and in some cases is complete; in others
paralysis remains behind in the hemiplegic form. The paralysis is
usually greater in the arm than in the leg; in extreme cases it
involves the corresponding side of the face, and, as the paralyzed
parts are arrested or perverted in growth, considerable deformity,
even extending to asymmetry of the skull, may ensue. The deformity is
aggravated by contractures. Usually there is some atrophy of the
muscles, but in one case I found actual hypertrophy[41] of some
groups, probably in association with the hemiathetoid movements.
[Footnote 40: As in my case of infantile encephalitis followed by
athetoid symptoms (_Journal of Nervous and Mental Diseases_).]
[Footnote 41: This was followed by atrophy. There are never any
qualitative electrical changes.]
The sequelæ of acute infantile encephalitis present us with the most
interesting forms of post-paralytic disturbances of muscular
equilibrium. Hemichorea and hemiathetosis, as well as peculiar
associated movements and hemicontracture, are found in their highest
development with this class of cases. Occasionally epileptiform
symptoms are noted,[42] and in others true epilepsy is developed. It
is under such circumstances that imbecility is apt to be a companion
symptom or result; and this imbecility is prominently noted in the
moral sphere.
[Footnote 42: Which in one case of my own disappeared spontaneously.]
The grave set of symptoms briefly detailed here are attributed by
Strümpell[43] to an acute encephalitis, analogous, in his opinion, to
the acute poliomyelitis of children. Its frequent occurrence after
measles and scarlatina, as well as the fact that Ross[44] in a
carefully-studied case arrived at the opinion that the disease was an
embolo-necrotic result of endocarditis, would lead to the conclusion
that it is a focal affection, probably due to the transportation of
infectious elements to the brain through the blood-vessels. Its
occurrence in children in the midst of apparent health[45] {792} is
consistent with the fact that rheumatism and an attendant slight
endocarditis frequently pass unrecognized in infancy. It is supposed
that a diffuse form of inflammatory non-suppurative softening exists
by some of the Germans, but the proof advanced in favor of this view
is not conclusive.
[Footnote 43: As a surmise, for up to his writing no reliable
autopsies had been made.]
[Footnote 44: _Brain_, October, 1883.]
[Footnote 45: McNutt (_American Journal of Medical Sciences_, January,
1885) cites Strümpell as attributing the theory of an inflammatory
affection, which is analogous to poliomyelitis in its suddenness and
nature, to Benedict, and refers to p. 349 of Strümpell's textbook
under the erroneous date of 1864. This work was published in 1883-84,
and the theory is advanced by Strümpell as his own. It is only a
synonym, hemiplegia spastica infantile, that is attributed to
Benedict.]
A number of rare forms of interstitial encephalitis have been
described. In one, elaborately studied by Danillo, an inflammatory
hypertrophy of the cortex, involving the parenchyma as well as the
connective and vascular structures, was found in a limited area of the
motor province of the right hemisphere. There had been crossed
epileptiform convulsions during life.[46]
[Footnote 46: _Bulletin de la Société de Biologie_, 1883, p. 238.]
There is some question among pathologists as to the recognition of
Virchow's encephalitis of the new-born. Certainly a part of Virchow's
material was derived from the imperfect study of a condition of
infantile brain-development which, as Jastrowitz showed, is
physiological, and on which Flechsig based his important researches of
tract-development. More recent studies, however, demonstrate that
there is a form of miliary encephalitis in new-born children due to
septic causes, such as, for example, suppuration of the umbilical
cord. The demonstration by Zenker of the occurrence of metastatic
parasitic emboli in cases of aphthous stomatitis, and by Letzerich of
a diphtheritic micrococcus invasion in the brain of his own child,
show that the subject of early infantile encephalitis merits renewed
consideration.[47]
[Footnote 47: The attempt of Jacusiel to revive Virchow's encephalitis
of the new-born (_Berliner klinische Wochenschrift_, 1883, No. 7)
under the title of interstitial encephalitis does not seem to have met
with encouragement, for, besides Jastrowitz, Henoch and Hirschberg
opposed this view in the discussion.]
Strictly speaking, the reactive changes which occur in the
brain-substance bordering on tumors, hemorrhagic and softened foci,
belong to the domain of encephalitis; but as they are considered in
conjunction with the graver lesions to which they are secondary both
in occurrence and importance, it is not necessary to more than refer
to them here.
Abscess of the Brain.
As indicated in the last article, there formerly existed much
confusion in the minds of pathologists regarding the terms softening
and abscess of the brain. As long as softening was regarded as an
inflammation, so long was abscess of the brain regarded as a
suppurative form of softening. Aside from the fact that there is some
resemblance in mechanical consistency between a spot of ordinary
softening and one of inflammatory softening, there is no essential
similarity of the two conditions. True softening is to-day regarded as
the result of a death of brain-tissue produced by interference with
the blood-supply; it is therefore a passive process. Inflammatory
softening, of which abscess is a form, is due to an irritant, usually
of an infectious nature. It is to the results of such irritation that
the term suppurative encephalitis should be limited.
MORBID ANATOMY.—In all well-established inflammatory brain {793}
troubles the active part is taken by the blood-vessels and connective
tissue; the ganglionic elements undergo secondary, usually regressive
or necrotic, changes. The brain, considered as a parenchymatous organ,
is not disposed to react readily in the way of suppurative
inflammation unless some septic elements are added to the inflammatory
irritant. Foreign bodies, such as knitting-needles, bullets, and
slate-pencils, have been found encapsulated in this organ or
projecting into it from the surrounding bony shell without
encapsulation and without any evidences of inflammatory change. As a
rule, a foreign body which enters the brain under aseptic conditions
will, if the subject survive sufficiently long, be found to have made
its way to the deepest part of the brain, in obedience to the law of
gravity, and through an area of so-called inflammatory red softening
which appears to precede it and facilitate the movement downward. This
form of softening derives its color from the colored elements of the
blood, which either escape from the vessels in consequence of the
direct action of the traumatic agent; secondly, in consequence of
vascular rupture from the reduced resistance of the perivascular
tissue in consequence of inflammatory œdema and infiltration; or,
thirdly, in obedience to the general laws governing simple
inflammation.
A cerebral abscess may present itself to the pathological anatomist in
one of three phases—the formative, the crude, and the encapsulated. In
the first it is not dissimilar to a focus of yellow softening, being,
like the latter, a diffuse softened area varying from almost
microscopical dimensions to the size of a walnut, and of a distinctly
yellow tinge. Microscopic examination, however, shows a profound
difference. In pure yellow softening there are no pus-cells; in the
suppurative encephalitic foci they are very numerous, and congregated
around the vessels and in the parenchyma in groups. The crude abscess
is the form usually found in cases rapidly running to a fatal
termination. Here there is an irregular cavity in the brain, usually
the white central substance of the cerebrum or cerebellum, formed by
its eroded and pulpy tissue; it is filled with yellow, greenish, and
more rarely brownish pus. In the most furibund cases broken-down
brain-detritus may be found in the shape of whitish or reddish
flocculi, but in slowly-formed abscesses the contents are free from
such admixture, and thus the third phase is produced, known as the
encapsulated abscess. The cavity of the abscess becomes more regular,
usually spheroid or ovoid; the pus is less fluid, more tenacious, and
slightly transparent; and the walls are formed by a
pseudo-membrane[48] which is contributed by the sclerosing
brain-substance, which merges gradually into the outlying normal
tissue. I have seen one acute cerebral abscess from ear disease which
might be appropriately designated as hemorrhagic; the contents were
almost chocolate-colored; on closer inspection it was found that they
were true pus, mingled with a large number of red blood-discs and some
small flocculi of softened brain-substance. This hemorrhagic admixture
was not due to the erosion of any {794} large vessel, for the abscess
had ruptured into the lateral ventricle at that part where it was most
purely purulent. In a case of tubercular meningitis, Mollenhauer in my
laboratory found an abscess in the white axis of the precentral gyrus,
with a distinct purulent infiltration following the line of one of the
long cortical vessels. The abscess was not encapsulated, the
surrounding white substance exhibited an injected halo, and the
consistency of the contents was that of mucoid material.
[Footnote 48: There is considerable dispute as to the real nature of
the tissue encapsulating cerebral abscesses. It is known, through the
careful observations of R. Meyer, Goll, Lebert, Schott, and Huguenin,
that the capsule may form in from seven to ten weeks in the majority
of cases, about eight weeks being the presumable time, and that at
first the so-called capsule of Lallemand does not deserve the name,
being a mucoid lining of the wall. At about the fiftieth day,
according to Huguenin, this lining becomes a delicate membrane
composed of young cells and a layer of spindle-shaped connective
elements.]
In cases where the symptoms accompanying the abscess during life had
been very severe it is not rare to find intense vascular injection of
the parts near the abscess, and it is not unlikely that the reddish or
chocolate color of the contents of some acutely developed abscesses is
due to blood admixture derived from the rupture of vessels in this
congested vicinity. Sometimes the entire segment of the brain in which
the abscess is situated, or the whole brain, is congested or
œdematous. In a few cases meningitis with lymphoid and purulent
exudation has been found to accompany abscesses that had not ruptured.
It is impossible to say whether in this case there was any relation
between the focal and the meningeal inflammation, as both may have
been due to a common primary cause.[49] In such cases, usually
secondary to ear disease, thrombosis of the lateral sinus may be found
on the same side. Where rupture of an abscess occurs, if the patient
have survived this accident long enough—for it is usually fatal in a
few minutes or hours—meningitis will be found in its most malignant
form. A rupture into the lateral and other ventricles has been noted
in a few cases.[50]
[Footnote 49: Otitis media purulenta in the two cases of this kind I
examined.]
[Footnote 50: In one, observed together with E. G. Messemer, intense
injection of the endymal lining, with capillary extravasations,
demonstrated the irritant properties of the discharged contents.]
Some rare forms of abscess have been related in the various journals
and archives which have less interest as objects of clinical study
than as curiosities of medical literature. Thus, Chiari[51] found the
cavity of a cerebral abscess filled with air, a communication with the
nose having become established by its rupture and discharge.
[Footnote 51: _Zeitschrift für Heilkunde_, 1884, v. p. 383. In this
remarkable rase the abscess, situated in the frontal lobe, had
perforated in two directions—one outward into the ethmoidal cells, the
other inward into the ventricles, so that the ventricles had also
become filled with air. This event precipitated a fatal apoplectiform
seizure.]
The contents of a cerebral abscess usually develop a peculiarly fetid
odor. It has been claimed that this odor is particularly marked in
cases where the abscess was due to some necrotic process in the
neighborhood of the brain-cavity. The only special odor developed by
cerebral abscesses, as a rule, is identical with that of putrid
brain-substance, and it must therefore depend upon the presence of
brain-detritus in the contents of the abscess or upon the rapid
post-mortem decomposition of the neighboring brain-substance.
In two cases of miliary abscess which, as far as an imperfect
examination showed, depended on an invasion of micro-organisms, an
odor was noticed by me which was of so specific a character that on
cutting open the second brain it instantly suggested that of the first
case, examined six years previous, although up to that moment I had
not yet determined the nature of the lesion.[52]
[Footnote 52: Owing to the lack of proper methods of demonstrating
micro-organisms, the first case whose clinical history was known was
imperfectly studied; of the second case, accidentally found in a brain
obtained for anatomical purposes, the examination is not yet
completed.]
{795} That form of abscess which, from its situation in or immediately
beneath the surface, has latterly aroused so much interest from its
important relations to localizations is usually metastatic, and
directly connected with disease of the overlying structures, notably
the cranial walls. In this case the membranes are nearly always
involved. The dura shows a necrotic perforation resembling that found
with internal perforation of a mastoid or tympanic abscess. The pia is
thickened and covered with a tough fibro-purulent exudation;
occasionally the dura and leptomeninges are fused into a continuous
mass of the consistency of leather through the agglutinating
exudation. The abscess is usually found open, and it is not yet
determined whether it begins as a surface erosion, and, bursting
through the cortex, spreads rapidly on reaching the white substance,
or not. The white substance is much more vulnerable to the assault of
suppurative inflammation than the gray, and not infrequently the
superficial part of the cortex may appear in its normal contiguity
with the pia, but undermined by the cavity of the abscess, which has
destroyed the subcortical tissue. Possibly the infecting agent, as in
some cases of ear disease, makes its way to the brain-tissue through
the vascular connections, which, however sparse at the convexity of
the brain, still exist.
CLINICAL HISTORY.—The symptoms of a cerebral abscess depend on its
location, size, and rapidity of formation. There are certain parts of
the brain, particularly near the apex of the temporal lobe and in the
centre of the cerebellar hemisphere, where a moderately large abscess
may produce no special symptoms leading us to suspect its presence.
There are other localities where the suppurative focus[53] indicates
its presence, and nearly its precise location and extent, by the
irritative focal symptoms which mark its development and by the
elimination of important functions which follows its maturation. It is
also in accordance with the general law governing the influence of new
formations on the cerebral functions that an acutely produced abscess
will mark its presence by more pronounced symptoms than one of slow,
insidious development. Indeed, there are found abscesses in the brain,
even of fair dimensions, that are called latent because their
existence could not have been suspected from any indication during
life, while many others of equal size are latent at some time in their
history.
[Footnote 53: Practically, our knowledge of localization of functions
in the human brain begins with the observation by Hitzig of a
traumatic abscess in a wounded French prisoner at Nancy named Joseph
Masseau. The year of the publication of this interesting case
constitutes an epoch in advancing biological knowledge, which will be
remembered when even the mighty historical events in which Hitzig's
patient played the part of an insignificant unit shall have become
obsolete. This, the first case in the human subject where a reliable
observation was made was an unusually pure one; the abscess involved
the facial-hypoglossal cortical field (_Archiv für Psychiatrie_, iii.
p. 231).]
An acute cerebral abscess is ushered in by severe, deep, and dull
headache, which is rarely piercing, but often of a pulsating
character. The pain is sometimes localized, but the subjective
localization does not correspond to the actual site of the morbid
focus.[54] It is often accompanied {796} by vertigo or by a tendency
to dig the head into the pillow or to grind it against the wall. With
this there is more or less delirium, usually of the same character as
that which accompanies acute simple meningitis. As the delirium
increases the slight rise in temperature which often occurs in the
beginning undergoes an increase; finally coma develops, and the
patient dies either in this state or in violent convulsions. The case
may run its course in this way in a few days, but usually one to three
weeks intervene between the initial symptoms and death.
[Footnote 54: Although Ross seems to be of a contrary opinion, it is
the exception for the pain to correspond in location to the abscess.]