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the eye. The eye-grounds often show a slight perineuritis without
choked discs, and perhaps one or more miliary tubercles. The leuko-
cytes are slightly, if at all increased. There is rarely rigidity of the
neck. In other forms of meningitis this appears early. The optic
nerve shows intense inflammation and there is usually pronounced
leukocytosis. Quincke, -in 1890, introduced his method of lumbar
puncture. This is of comparatively simple application, and has become
a well-recognized measTire. The tubercle bacillus and streptococcus
pyogenes, also the pneumococcus and micrococcus meningitidis, have
been found in the fluid withdrawn.



DISTURBANCES OF CIRCULATION OF THE BRAIN. 1111

Prognosis. — This is always grave. A percentage of cases of epi-
demic cerebrospinal meningitis, varying with the nature of the epi-
demic, may recover. In all other forms any termination, except in
death, is exceedingly exceptional. Remissions frequently occur in the
symptoms, and the course may be very prolonged. That even tubercu-
lous cases may recover is proved, however, by that of West, and even
more strikingly by that of Baumann and Senile, who found the tubercle
bacillus in the cerebro-spinal fluid. The case recovered, but died some
months later from an intercurrent affection ; the diagnosis gained addi-
tional confirmation from the postmortem findings.

Treatment. — This has been previously considered. It is only neces-
sary to add that we are able to do no more in this form than in the
tuberculous. We have no specific, and all that can be done is to meet
the symptomatic indications. In certain cases — e. g. those secondary
to middle-ear disease — operation may seem justifiable. When in doubt
the physician should not delay action until too late, but should call in a
surgeon while some benefit may still be hoped for.



DISTURBANCES OF CIRCULATION OF THE BRAIN.

HYPEREMIA.

Definition. — An abnormal increase in the amount of blood in the
cerebral capillaries. The condition is not in any Avay associated with
the primary phenomena of inflammation.

What has already been mentioned in the case of hyperemia of the
cord is equally true in this case — viz. that while congestion undoubtedly
may take place, there is nothing symptomatically pathognomonic in the
fact, and hence we do not recognize it as a definite clinical entity.
" Congestion of the brain " is rather a " diagnostic haven " and satisfies
the patient, while at the same time, provided the assumption is not
made on too superficial evidence, it harms no one. Two forms of
hyperemia have been described :

1. Active hyperemia is met with in men more frequently than in
women, and results from over-action of the heart and widespread ob-
struction to the circulation, as when the surface capillaries contract, or
there is arterial dilatation, due to excessive mental activity from any
cause or to drugs — alcohol, amyl nitrite, nitroglycerin.

2. Passive congestion is met with in cases of obstruction of the cere-
bral sinuses and veins, and is due to pressure on the superior cava or
the innominate or jugular veins by tumors or aneurysms ; also in suffo-
cation and strangling, in cases of excessive strain, and in tricuspid in-
sufiiciency.

Pathology. — There are no marked changes in the brain in these
cases. In the active form the gray matter will appear somewhat darker
than normal, and a macroscopic section of the white matter shows the
puncta vasculosa to be increased. It often leaves no trace jjostmortem.
In passive congestion the veins and sinuses are engorged and more or
less edema may be present.

The symptoms are described under two headings — 1, those of irri-
tation, and, 2, of depression. Among the former arc headache, vertigo,



1112 DISEASES OF THE NERVOUS SYSTEM.

irritahility, rapid pulse, restlessness, insomnia, and special nervous phe-
nomena, as flashes of light, hyperacusis, and even convulsive movements.
The latter is manifested by the obtunding of the senses ; in fact, the
antithesis of the other. The cerebral symptoms met with in febrile
processes are probably due either to faulty metabolism or to some toxin,
and should not be regarded as the result of hyperemia.

Treatment. — The recumbent posture is of great importance.
Leeching, wet-cupping, and venesection are sometimes employed. Cold
applications to the head, bromids internally, and attention to the bowels
will be of assistance. Freedom from annoyance and worry of all kinds
is necessary.

ANEMIA.

Definition. — A condition in which an insufficient amount of blood
circulates in the cerebral capillaries.

It is due to exhausting discharges (diarrhea), an abnormally slow
pulse or weak heart, to hemorrhage, obstructive endarteritis of the ves-
sels supplying the brain, and to syncopal attacks and dilatation of the
intestinal vessels, owing to the too rapid withdrawal of ascitic fluid.

Pathology. — The gray matter is quite pale ; the puncta vasculosa
are diminished, and sometimes cannot be seen ; the cerebro-spinal fluid
is frequently increased.

Syinptoms. — The most exaggerated type is met with after a pro-
fuse hemorrhage. There are pallor, weakness, vertigo, headache, flashes
of light, subjective noises, rapid respiration, cool skin, possibly profuse
sweating, and in extreme cases coma, convulsions, and death. We are
more familiar with the ordinary fainting-attack. When cerebral ane-
mia is brought about more slowly "irritable weakness" results. The
patient is either somnolent, dull, and apathetic ; or he may be a victim
of iyisomnia. Headache, vertigo, tinnitus aurmm, musca volitantes, and
lowered muscular power are present. The patient becomes irritable on
the slightest provocation. Marshall Hall has described a group of symp-
toms as *■' hydrocephaloid " from their resemblance to hydrocephalus;
they occur especially in young children after diarrhea. There are pal-
lor, hehetude, contracted pupils, and depressed fontanels. The somno-
lence may deepen into a coma that often becomes more profound until
death results.

The treatment varies with the cause. The recumbent posture is
always indicated, and in some cases it is necessary to depress the head,
administer stimulants, and even transfuse or inject a normal saline solu-
tion. A light and easily assimilable diet should be given during con-
valescence.

EDEMA OF THE BRAIN.

Definition. — An infiltration of serum into the subarachnoid space
and a greater or less increase of ventricular fluid, with or without infil-
tration into the brain-substance.

Pathology. — The fluid is chiefly in the meshes and beneath the
membrane. The ventricular fluid is increased in amount ; the brain-
substance is pale, and in some cases infiltrated and softened. Micro-
scopically, lacunae may be seen in the cerebral tissue, the perivascular
spaces are dilated, and some slight degree of nerve-cell degeneration is
often present.



EMBOLISM AND THROMBOSIS. 1113

Ktiology. — Edema is met with in Brigbt's disease, in senile cere-
bral atropby, 'and as a result of active or passive byperemia.

Sytnptoms. — In general the symptoms are those of anemia though
nothing definite is known of them. Since the condition is always sec-
ondary, it may be that symptoms directly referable to the edema are
masked by the primary condition. Cases of apoplexy are seen occasion-
ally, in which the only postmortem finding is an effusion of fluid into
the pia and ventricles. This has been termed " serous apoplexy."

The treatment is that of the primary condition.

EMBOLISM AND THROMBOSIS.

( Cerebral Softening.)

Kmbolistn. — Definition and Etiology. — The obstruction of arteries
or capillaries by material brought to the spot from some other part by
the blood-current. The material, generally fibrin, usually comes from
the heart, and is either a vegetation of a recent endocarditis or, more
commonly, of chronic valvular disease; it may possibly be a fragment
of the valve plus the fibrin in ulcerative endocarditis. In the latter
case the plug is generally septic, giving rise to suppurative processes.
An embolus may be washed from the auricular recesses, from an aneur-
ysm of the aorta or carotid, or from atheromatous patches ; rarely from
the pulmonary veins.

In puerperal women, and in certain febrile processes (diphtheria and
pneumonia) the coagulability of the blood is increased. Heart-clots
form, and fragments may be washed into the cerebral vessels. Owing
to the direction of the vessels the embolus most frequently enters the
left carotid, whence it usually passes to the left middle cerebral. Al-
most any cerebral artery may be obstructed, but the cerebellar very
rarely. Embolism occurs most frequently between the tenth and forti-
eth years of life. The middle cerebrals are most frequently involved,
and next in order the internal carotid and anterior cerebrals.

Pathology. — That region of the brain that is cut off from its blood-
supply by the embolus undergoes softening. The cortical changes are
less marked than those of the central ganglia, since in the former case
more or less anastomosis exists, and none in the latter. When the em-
bolus is septic one or more metastatic abscesses result. The degree of
softening varies in different cases within wide limits. There may be
nothing more than a slight diminution in the consistence, the affected area
being somewhat paler than normal, or absolute dissolution may occur,
the myelin breaking up into granules, while the tissue becomes infil-
trated with serum, and the vessels undergo hyaline or more often fatty
change. The color of the part varies with the amount of blood. In
recent cases it is red. As the hemoglobin is absorbed a yellow color
appears, and soon predominates. Red and yellow softening are found
chiefly in the cortex. The so-called white softening is met with particu-
larly in the white matter. A variety of red softening in which numer-
ous small hemorrhages exist has been termed capillary apoplexy, while
plaques jaunes is the term given by the French to a form of yellow soft-
ening often seen in the cortex of old people. The ultimate changes de-
pend in a great measure upon the extent of the lesion. If this is small,



1114 DISEASES OF THE NERVOUS SYSTEM.

the granular debris is absorbed, and the proliferation of connective tis-
sue results in the formation of a scar. On the other hand, if large the
solid elements are removed, and the cavity that remains contains more
or less fluid (a cyst). In many instances fibers, trabeculae, and even
vessels that have escaped destruction, pass through the cyst.

Thrombosis. — Definition. — Obstruction of a vessel due to clotting
in situ. This may occur (a) in the arteries or (h) in the veins and
sinuses.

In the Arteries. — Etiology. — Thrombosis results from disease of
the vessel-wall, atheroma, endarteritis, or syphilitic arteritis, extension
from surrounding diseased areas, traumatism, in aneurysms, in depraved
blood-states, and at the seat of lodgement of an embolus. Thrombosis
of a cerebral vessel may rarely follow ligation of the carotid. In gen-
eral we may say thrombosis results from (1) changes in the vessel-wall,
(2) retardation of the blood-current, and (3) hypercoagulability of the
blood. It occurs most frequently in the middle cerebral, basilar, in-
ternal carotid, and vertebral arteries.

Pathology. — The changes in the brain-tissue are precisely those de-
scribed under Embolism. Within the vessel a clot is found adherent
to the vessel-wall, and extending from the nearest large branch on the
proximal side to the contracted branches on the distal side. If of
recent and rapid formation, it is always of a red color. The slower the
formation the paler the color. Such clots are often laminated. The
ultimate changes are contraction and atrophy, or, more rarely, calcifica-
tion, or even softening and removal, the vessel again becoming patulous.

Ix THE Veixs axd Sixuses. — Etiology. — Thrombosis may be (1)
primary, due to general causes, or [2) the result of local changes.

Primary thrombosis is less common than the secondary variety.
It is met with in marasmic children (one of the causes of infantile
hemiplegia — Gowers), in which the clot is called marantic throm-
bosis, cachexia, phthisis, carcinoma, and in blood-dyscrasise (anemia,
chlorosis).

Secondary thrombosis usually results from an extension of neigh-
boring forms of inflammation, caries of the bone, middle-ear disease, or
meningitis. It may also be due to fracture of the skull or compression
of a sinus by a tumor.

Pathology. — In primary thrombosis the most common seat is the su-
perior longitudinal sinus. From this it spreads into the veins of both
sides, and frequently also into the lateral sinuses of one or both sides.
In secondary thrombosis the sinus nearest the local disease sufi"ers.
The veins emptying into the sinus involved become distended, often
rupture, and in consequence the brain-tissue and pia become infiltrated.
When the veins of Galen are blocked serum escapes into the ventricles.
Eed, yellow, and white softening is met with as a final result of the ex-
travasation. Secondary thrombi are usually septic, and give rise to
abscess formation.

Symptoms. — Folio-wing Embolism or Thrombosis of Arteries. — The
symptoms necessarily depend upon the position and extent of the lesion.
Often it is discovered postmortem^ not having been suspected during
life. We meet with many such cases occurring in late adult life. Then,
too, extensive lesions may occur in those portions of the brain that
never yield any localizing symptoms — the frontal region, for instance.



EMBOLISM AXD THROMBOSIS. 1115

Apart from the etiologic differences, the clinical pictures of embolism
and thi-ombosis diifer as follows : In the former the 07iset is sudden,
without premonitory signs, and is in many cases accompanied by loss
of consciousness. In addition to symptoms arising directly through
implication of the particular part involved, there are those of shock.
In the less severe cases consciousness soon returns and the apoplectic
symptoms pass off. When more severe, coma supervenes and may prove
fatal. When hyperemia occurs in or about the motor region the irrita-
tion may«give rise to convulsions. In other cases delirium is a promi-
nent feature ; hence three varieties of softening are described by some
writers — the apoplectic, convulsive, and delirious, from the prevailing
feature. Thrombosis may commence abruptly, but as a rule the onset
is slow, the patient meanwhile complaining of vague pains, numbness,
tingling, headache, and vertigo. It is observed that a gradually in-
creasing impairment of the mind is going on, and that motor weakness,
slight at first, increases until the function is lost. The special symp-
toms are, as stated, dependent upon the location of the obstruction. If
this is in the middle cerebral artery, the most common seat, there will be
Jiemiplegia, owing to destruction of the internal capsule. The trunk may
be spared and one of its branches stopped. The latter run to the third
frontal, ascending parietal, supramarginal, angular, or temporal gyri.
Thus, then, we can account for the aphasia so often met with in these
cases by the plugging of the branch that supplies the third frontal con-
volution of the left side. If both middle cerebrals are plugged, symp-
toms develop that are indistinguishable from hemorrhage into the ven-
tricles. This condition is generally fatal. Thrombotic obstruction of
the anterior and posterior cerebral arteries rarely causes symptoms, owing
to compensatory circulation. " Hebetude and dulness of intellect may
occur " (Osier), with obstruction of the anterior cerebral. Hemianopsia
may arise from a lesion of the posterior cerebral, since it supplies the
cuneus. The left cerebral is more often involved than the right. In
either case bulbar symptoms develop.

Cerebellar softening is rare. When it does occur it is usually in the
region supplied by the posterior cerebral artery. There may be no
symptoms if only one hemisphere is involved : otherwise they are sim-
ilar to those of cerebellar disease due to other lesions.

Thrombosis in veins and sinuses causes variable symptoms. Those
directly due to the vascular disturbance are severe headache, optic neur-
itis, delirium, or convulsions, and, later, great depression. Hemiplegia
may result. When the superior longitudinal sinus is affected, epistaxis
is common, while in lateral-sinus involvement post-auricular edema oc-
curs. In secondary cases, moreover, we have to reckon with the cause.
Since this is so often septic, septicemic symptoms are the rule.

Treatment. — Of Embolism and Thrombosis of Arteries. — Very
little can be done in brain-softening. In the early stages, however,
while it is absolutely impossible to repair the tissue already damaged,
an effort should be made to prevent the spread of the process. Rest in
bed with the head slightly elevated should be insisted on. When shock
is present it must be met by gentle stimulation, ammonium carbonate,
and even by alcohol and digitalis in some cases ; hot-water bottles may
be applied to the body. Venesection is contraindicated. The bowels
should be made to move gently and purgation should be avoided. Later,



1116 DISEASES OF THE XEBVOUS SYSTE3L

as stated, symptoms of irritation often appear. In such cases the bro-
mids should be given, and also a diaphoretic mixture, or ice should be
placed to the head. In any case in which syphilis, rheumatism, gout,
chorea, or other malady capable of causing or adding to the trouble ex-
ists, the original disease should be treated promptly and thoroughly. In
the mean time efforts should be made to improve the patient's general
tone by the strict observance of hygienic and dietetic rules.

Of Throjnhosis of Veins and Sinuses. — Treatment in these cases de-
pends largely on the cause. In the primary form it is that of the sys-
temic disease. Good, wholesome, and easily assimilable food should be
given, together with a tonic treatment. In secondary thrombosis care-
ful search should be made for pent-up inflammatory products, which
should be liberated at the earliest possible moment. The emunctories
must act freely. Counter-irritation, applied to the neck, is of question-
able value, but internally quinin, iron, and strychnin, and, if stimulation
is necessary, ammonia and alcohol, will all be useful.

VASCULAR DEGENERATION.

Arterial.-i— The cerebral arteries undergo a more or less decided de-
generative change in the majority of people past middle life (Bichat
said seven-tenths). It is met with much earlier, however, as a result of
disease. Bright's disease, rheumatism, gout, alcoholism — in fact, any
irritation of the vessel-wall, whether autogenous, the result of faulty
metabolism, or whether introduced from without, as alcohol — is capable
of bringing about a change of the inner seat of the vessel, to which
Virchow gave the name " endarteritis deformans.'' The circle of Willis
and its branches are the most frequent seats. Various stages may be
met with in different vessels or even in the same vessel — viz. hyaline
degeneration, fatty degeneration, liquefaction-necrosis, atheromatous
ulcers, and calcification.

Syphilitic arteritis is not a true degenerative process. It is rather a
proliferative process in which both intima and adventitia are involved.

Venous. — The veins are less liable to disease than arteries, possibly
because they are more yielding, yet the same pathologic changes may be
met with in them. They are more commonly damaged by extension of
inflammation from neighboring tissues or by pressure.

Aneurysm. — Dilatation of a vessel results from any of the causes
above mentioned. The aneurysms may be very small — miliary — or
often as large as a filbert-nut, and rarely as large as a hen's egg. They
occur more commonly in males than in females. The middle cerebrals
and basilar are most frequently attacked, and next come the internal
carotid, the vertebral, and the anterior and posterior cerebrals. Miliary
aneurysms are frequently found in enormous numbers upon the basilar
branches of the cerebral arteries.

Symptoms of Aneurysm. — There may be none ; but in any case they
are due to pressure exerted by the mass, and are therefore comparable to
tumors of the brain. In many cases the first evidence of any trouble is
an apoplectic attach, and it is scarcely necessary to add that this is usually
fatal. In other cases headache, vertigo, and optic neuritis are present,
and more rarely a subjective murmur. Still more rarely an objective
murmur may exist.



INFLAMMATION OF THE BRAIN. 1117

INFLAMMATION OF THE BRAIN.

{Encephalitis.)

Definition. — Encephalitis, strictly speaking, is an inflammation of
the brain-substance, and does not include inflammation of the meninges,
though in many instances the two conditions coexist as the result of a
common cause, or one may precede and give rise to the other. Encepha-
litis is met Avith in two forms — [a) Focal, and (h) Difiuse.

FOCAL ENCEPHALITIS.
{Abscess.)

Pathology. — In very acute cases no time is given for encapsulation ;
when of longer duration, however, the abscess is well circumscribed,
having a well-defined wall, within which there are cell-detritus, pus, and
sometimes more or less altered blood. It may be ofiensive. About it
the brain-substance is generally softened and edematous. The abscess is
generally single, except in pyemic cases, and varies greatly in size in
difierent instances.

Ktiology. — Abscess of the brain is a more or less circumscribed
process, due to (1) Injury. — In the majority of cases of abscess following
head-injuries either a compound fracture of the skull exists, with or with-
out hernia cerebri (fungus cerebri), or a punctured wound has been made.
Less commonly it may follow a simple fracture, and rarely it is said to
occur when neither a fracture nor even an abrasion of the scalp has been
produced. Meningitis is an almost invariable concomitant. (2) Exten-
sion from some neigliboring inflammatory focus, as from orbital, nasal, or
aural disease, in which the bones have usually become aff"ected. (3)
Pyemia., in which case the abscesses are apt to be small and multiple.
It is also met with occasionally in gangrene of the lung, bronchiectasis,
ulcerative endocarditis, suppurative hepatitis, or bone-disease, and rarely
in chronic septic processes. (4) Congenital Heart-disease. — Little is
known of this condition. Within the past two or three years Northrup,
Packard, Sir Dyce Duckworth, and Osier have reported such cases. (5)
Obstruction of an artery., vein, or sinus, whether of spontaneous origin
or the result of ligature, may give rise to abscess. Generally, however,
the cerebral change is that of softening, and not of true suppuration.
(6) Intracranial tumors. (7) Infectious fevers.

Symptoms. — These at first are generally vague ; but in traumatic
cases, and more especially in those in which a compound fracture of the
skull has resulted, the course may be most acute, and /ever, headache,
delirium, and possibly vomiting may be seen quite early. These are fol-
lowed by other evidences of irritation, soon by compression Avith convul-
sions, and then by coma and death. In the more chronic cases the symp-
toms depend upon the size and location of the abscess and whether or not
a vent exists. In such cases an intermission in the symptoms is occa-
sionally met with, due to filling and emptying of the sac. Apart from
the headache, pyrexia (not always present), twitching, and drowsiness,
that occur in the course of these cases, more or less hemiparesis commonly
exists, except in abscess of the frontal lobes. The latter are spoken of
as "silent regions." An abscess may be "latent," however, in almost



1118 DISEASES OF THE NERVOUS SYSTEM.

any region, these latent abscesses being typified in certain cases of con-
genital heart-disease. I do not think they were suspected during life in
any of the cases reported thus far, and therefore optic neuritis has not
been looked for ; in other cases this latter symptom is commonly present.

Diagnosis. — In the acute cases following injury little difficulty pre-
sents as a rule, though even in this group a latent period may exist.
With such a history, however, the onset of headache, fever, delirium,
and convulsive movements is decidedly suspicious, and, should optic
neuritis also exist, practically no doubt can remain. When dural or
nasal disease exists the head-symptoms should be carefully studied, since



Online LibraryJames Meschter AndersA text-book of the practice of medicine → online text (page 148 of 175)