by its name. As the hemiplegia disappears, irregular movements are
developed in the paralyzed limbs, sometimes closely resembling
ordinary chorea, and at others consisting of irregular movements, as
closing and spreading of the fingers, with curious and bizarre
stiffenings, extensions, and contractions, sometimes known as
athetosis, or in others still a tremor resembling paralysis agitans.
These usually cease during sleep. It is very apt to be associated with
hemianæsthesia more or less complete, though this may be represented
by only a certain amount of numbness. A hemiathetosis has been
observed to be gradually developed from a post-hemiplegic hemichorea
of the more ordinary form.[44]
[Footnote 44: _Archiv für Psychiatrie_, xii. 516.]
This affection is not a common one, and Weir Mitchell states that it
is common in inverse proportion to the age. He thinks it possible that
some of the congenital choreas may be the result of, or at least
closely connected with, intra-uterine cerebral paralysis. It remains
for years or for life. In the absence of history such a case might
present difficulties of diagnosis from the more usual hemichorea,
which is not infrequently accompanied by considerable weakness of the
affected side.
The temperature in the early days of both hemorrhage and embolism has
been described. At a later period of the hemiplegia it remains in the
neighborhood of normal. The temperature of the affected side is often
higher than that of the sound one for an indefinite period, but in
many cases sinks below if atrophy takes place. The time at which the
change occurs is extremely variable. Out of ten cases reported by
Folet,[45] in two of them for three years and one year after the
attack the paralyzed {961} side was eight-tenths and six-tenths of a
degree respectively the warmer. In three others, of twenty months,
four and six years, it was the same on both sides, and in the
remaining five the paralyzed limb was a little the cooler. In the last
eight there was more or less atrophy.
[Footnote 45: _Gaz. hébd._, 1867.]
The coincidence of rise of temperature with vascular relaxation has
already been noted under the head of Cerebral Hemorrhage. It is not
difficult to explain why a vascular paralysis in a comparatively
well-nourished limb, especially when the heart is vigorous, may, by
allowing a larger amount of warm blood to circulate, raise the
temperature, when the same paralysis with atrophied muscles, weak
heart, and impaired general health, merely furnishes a larger
reservoir in which the slowly-moving blood may be cooled. The
accompanying charts represent the difference of temperature between
the two sides in two cases of hemiplegia, the first, O. G. T. (Fig.
41), from embolism, and the second, J. B. (Fig. 42), from hemorrhage,
the observation being made within two or three weeks of the attack.
The dotted line is from the paralyzed side. A subjective feeling of
coldness is not uncommon in paralyzed limbs.
[Illustration: FIG. 41.]
[Illustration: FIG. 42.]
The modifications undergone by the urine in a case of cerebral
hemorrhage are increase of quantity amounting to polyuria, the urine
becoming limpid and afterward returning to the usual color; a
diminution in the quantity of urea coinciding with the fall of
temperature, and afterward a return to the normal or even above it.
When this augmentation is considerable, it constitutes at the same
time with a marked elevation of temperature an unfavorable prognostic
sign.[46] In a case under the observation of the writer, probably of
thrombosis, the acid urine has been {962} remarkable for the amount of
mucus contained in it, so that it pours from one vessel to another
like white of egg. There is a small amount of pus, but no vesical
irritation whatever.
[Footnote 46: Ollivier, _Archives de Physiol._, 1876.]
Since the trophic centres for the muscles are situated in the spinal
cord, cerebral hemiplegia, which does not cut off their connection,
does not produce the rapid wasting seen in some cases of spinal
paralysis, unless descending degeneration involves the anterior gray
columns. The limbs preserve their fulness for a time, although the
muscular masses become flabby and slowly atrophy for want of use. This
atrophy, however, seldom becomes extreme. The skin of the hands
becomes dry, the folds at the knuckles disappear, and the hand loses
its expression, looking more like a stuffed glove. The change,
however, is not much greater than may be seen in a hand kept for a
long time in a bandage. The growth of the nails is retarded, as may be
seen by staining them with nitric acid.
If there is any tendency to œdema, as when nephritis is complicated
with hemiplegia, the swelling is likely to be much greater upon the
paralyzed side. In the adult, of course, there can be no question of
the growth of limbs, but when a child becomes hemiplegic from cerebral
disease, the limbs grow more slowly and remain smaller, as in a case
of ordinary infantile palsy or anterior poliomyelitis.
Much importance has been attached to the fact that large sloughs form
with great rapidity upon the nates of the paralyzed side, and Charcot
says that this tendency is greater than can be accounted for in any
mechanical way. He therefore thinks that a direct trophic influence of
the brain upon nutrition is shown. At the very most, however, that can
only be a contributory cause, and the freedom of other portions from a
similar condition—and that, too, in regions farther removed from the
centres of circulation—makes it highly improbable that anything more
is necessary to account for it than the less sensitiveness of that
side to irritation from urine, roughnesses in the bed, or pressure,
and hence neglect. The writer, among a very considerable number of
hemiplegias, fatal and otherwise, does not remember to have seen a
well-marked case of the kind. Scrupulous cleanliness and changing the
position sufficiently often make the preference for the paralyzed side
a very slight one.
Arthropathies, consisting in a vegetating, and sometimes an exudative,
synovitis, and accompanied by swelling, redness, and pain, are
sometimes observed, especially in the upper extremity. They do not
appear until fifteen days or a month after the attack.
The most significant change which occurs in the course of a hemiplegia
is the development of increased reflexes and rigidity and contracture.
After some weeks or months, during which the aspect of the case has
not essentially changed, the limbs remaining in the same condition, it
will be found on examination that the patellar reflex has become quite
energetic, and ankle clonus developed upon the paralyzed side; the arm
reflexes from the triceps, biceps, and supinator longus are much
exaggerated. This has the same meaning as when similar phenomena are
found with spinal disease, and signifies descending degeneration of
the postero-lateral columns of the spinal cord, the crossed peduncular
tracts. This degeneration may sometimes be traced completely down from
the situation of the lesion in the cortical motor centres through the
basal ganglia, crura, decussation, and cord. The fuller development of
this condition is the {963} contracture or rigidity, which was at one
time referred to secondary changes taking place in the neighborhood of
the original lesion, as well as to a purely reflex action having no
relation to the degeneration of the cord.
The arms are usually flexed at the elbow, the wrists on the arm, and
the fingers in the hand. Sometimes, however, the arm is straight. The
leg, which is not always affected to the same extent, is generally in
extension, though the toes are likely to be flexed. Attempts to move
the limbs are resisted strongly, and in such a way as to show the
reflex nature of the phenomenon. If an attempt be made to open the
fingers of a contractured hand slowly and carefully, it can be often
accomplished and the hand held open with but little pressure, but if
it is twitched the fingers resist like a spring. The violent attempt
to overcome rigidity is often painful.
In some rare cases rapid atrophy of the muscles of one limb may take
place. This has been found to coincide with extension of degenerative
changes in the cord to the anterior gray columns.
Late rigidity is an unfortunately clear symptom. There is little if
any hope of complete recovery of the use of the limb after it has made
its appearance, though it does not prevent walking. After
long-continued contracture the activity of the muscles diminishes, but
the increase of connective tissue and changes in the joints hold the
limb in its fixed position, and the contracture is a more passive one.
The electrical reactions of the muscles and their nerves in cerebral
hemiplegia are not materially altered, but the neuro-muscular
irritability may be somewhat increased for a time by the irritating
influence of the cerebral lesion.
In most cases of flaccid cerebral hemiplegia the electrical
irritability is somewhat decreased, though retaining the normal
character with both currents. Since the muscles and their nerves
retain their connection with the spinal nuclei which are their trophic
centres, and these nuclei are uninjured, their nutrition does not
undergo the changes which affect electric excitability.
When descending degeneration takes place there may be found,
coinciding with increased reflex activity and contracture, increased
sensitiveness to the electric currents. If the degeneration extend to
the anterior columns, as happens in rare cases, the muscles waste
rapidly and exhibit the reactions of anterior poliomyelitis—_i.e._
degenerative.
What has just been said applies to the muscles paralyzed by a central
lesion. If, however, with or without a complete hemiplegia, a limited
lesion, as in the pons, affects the nucleus of a nerve, the peripheral
distribution of that nerve is cut off from its nutritive centre, and
it undergoes the usual changes which lead to the reaction of
degeneration, so that, in some unusual forms of paralysis, the two
kinds of reaction, normal and degenerative, may be present in
different sets of muscles.
DIAGNOSIS.—The apoplectiform attack due to hemorrhage or occlusion of
the cerebral arteries is to be distinguished from narcotic poisoning,
specially by opium or alcohol, or by coal gas; epilepsy with its
succeeding coma; uræmia (so called) or cerebral symptoms connected
with renal disease; comatose form of pernicious intermittent; diabetic
coma; sunstroke; hysteria, and various other forms of intracranial
disease, especially meningitis; concussion and compression of the
brain, which often {964} involve hemorrhage; the apoplectiform attacks
of intracranial syphilis and of general paralysis, as well as the
congestive attacks (coup de sang, rush of blood to the head).
The first of these distinctions is, in a practical point of view,
among the most important and often the most difficult, so that
distinguished authorities insist not only on the difficulty, but
impossibility, of making a positive diagnosis in every case. The
physician who is most familiar with all the different conditions which
may cause coma is least likely to jump at a conclusion.
Persons are constantly being picked up in the street partially or
wholly unconscious, or found alone in a room without history and away
from friends. The physician must then form his opinion from the
present condition, which without a history may be very obscure, though
with one it might present no difficulty. An empty laudanum- or
whiskey-bottle may be of assistance, the former of much, but the
latter of less. The smell of the breath may give a hint, but even if
the smell of alcohol be detected, considering the widespread belief in
its virtues as a panacea, it may be as well the result of amateur
therapeutic attempts as an indication of the cause of the attack.
Neither does it follow that because a man has been or is drunk he has
no organic disease in his brain. Alcohol should simply make us more
careful to examine for possible injuries. In regard to both these
poisons—and in fact in the diagnosis of these conditions generally—the
first thing to be sought for, after assuring one's self that the
patient can breathe and is likely to do so for a few minutes, is some
evidence of hemiplegia. This is not so easy as it might appear at
first sight, since the general muscular relaxation may be so complete
as to cover up local manifestations. The face, however, may show
inequality in its lines or one cheek flap more loosely than the other.
The patient is not likely to undertake voluntary movements at the
request of the physician, but he may make semi-voluntary ones if
annoyed by the examination. The flaccidity of the arms may vary.
Irregularity of the pupils is a piece of evidence to be received with
some caution, as it may be habitual or the result of disease in the
eye. Conjugate deviation of the eyes and head is a form of paralysis,
or sometimes of unilateral spasm, which when present is of great
significance. In opium-poisoning—and to a less extent in alcoholic
coma—the pupils are much contracted, while they are not always so in
apoplexy. Respiration is usually much more rapid in apoplexy than in
opium-poisoning, and this, in the absence of distinct signs of
hemiplegia, would be one of the most important means of distinction.
The pulse is more nearly normal in frequency, while that of opium is
either slow and hard or more often frequent and feeble.
After the time for the initial depression has passed, rapidly-rising
temperature is very strong evidence in favor of apoplexy. If the
patient be only partially unconscious and able to protest against
being handled, to make some short answers, or even be inclined to be
combative, this is not to be taken as evidence of alcohol. Hemiplegia
may then be noticed. This condition of excitement may be observed in
the early stage of an apoplectic attack before it deepens into coma.
Unfortunately, when the lesion is situated in certain portions of the
brain, as in the extremities of either the frontal or occipital lobes,
there may be no paralysis, but then also there is less likelihood of
the extreme symptoms we are supposing {965} to be present. In the
cerebellum, however, the symptoms may be very severe without
hemiplegia, and the diagnosis correspondingly difficult. Vomiting, not
caused by the presence of large quantities of food or liquor, and
persisting after the stomach is once emptied, would be of some value
in this case, but it would often be necessary to wait for a diagnosis.
Cerebellar hemorrhage is, however, a very rare accident, and
cerebellar embolism sufficiently large to cause apoplectiform symptoms
still more so. A limited lesion in the pons may cause
gradually-increasing stupor without distinct paralysis.
Chloroform, especially if swallowed, and chloral might possibly give
rise to difficulties in the way of diagnosis, and would have to be
distinguished on the same general principles as alcohol and opium.
The poisonous gases arising from burning coal, consisting chiefly of
carbonic oxide and dioxide, or illuminating gas, consisting of
carburetted hydrogen with a little carbonic oxide, cause
unconsciousness, coma, and sometimes convulsions and vomiting. In case
of a person found unconscious in bed the possibility of poisoning by
one of these should not be lost sight of, nor, on the contrary,
assumed to be a cause without investigation. A case has been reported
where, after acute poisoning by coal gas, there occurred, presumably
as the result of local anæmia, alternate paralysis, convulsions, and
aphasia.[47] The new water-gas process is said to furnish a product
considerably richer in the poisonous carbonic oxide than that now most
in use.
[Footnote 47: _Boston Med. and Surg. Journal_, Nov. 26, 1885.]
The stupor succeeding an epileptic convulsion resembles apoplexy, and
the fact that cerebral hemorrhage may be accompanied by some
convulsions increases the possible similarity, but it requires only a
short time for epilepsy to make itself manifest, either by a renewal
of the convulsions or a rapid recovery without paralysis. According to
Trousseau, however, many attacks of so-called congestion of the brain
are really epilepsy. Puerperal eclampsia comes under the same head,
but when convulsions are violent they may give rise to actual
hemorrhage. Unilateral epileptiform convulsions are likely to be
dependent on organic disease of the brain, usually not of the kind at
present under consideration, but more frequently of a tumor.
Among the cerebral symptoms connected with renal disease, and not
involving organic change in the brain, may be found unconsciousness,
deep coma, and convulsions. It is obvious that the presence of a few
hyaline casts and a little albumen will not decide the matter, since
these may be present from many causes, and especially the changes in
the circulation accompanying apoplexy. Neither will the most
indubitable evidence of Bright's disease, such as dropsy, hypertrophy
of the heart, rigid arteries, with fatty and waxy casts in the urine,
do so, for, as we have already seen, not only is there nothing in the
presence of nephritis to exclude apoplexy, but the very form, the
interstitial, which, from the supervention of coma not preceded by
other very severe symptoms, most nearly counterfeits apoplexy, is also
the most likely to give rise to actual cerebral hemorrhage. The
extreme and frequent cephalalgia which is so distressing a symptom in
cases where there is no cerebral lesion may also be the precursors of
hemorrhage.
If we have a history, the gradual onset of the symptoms, deepening
{966} unconsciousness without any paralytic or unilateral symptoms,
especially if accompanied by a diminution in the amount of urine or
contained urea or a marked change in the character of the casts,
renders it probable that we are dealing with so-called uræmia alone.
In the absence of history hemiplegia must be the chief dependence, but
it would not be difficult to imagine a case of embolism of the basilar
artery with softening of the pons which would defy a positive
diagnosis.
Pernicious intermittent fever appears in a so-called comatose form,
which, if it were to be accompanied, as in a case related by Bemiss in
the second volume of this work, by paralysis of one arm, might present
difficulties of diagnosis. If it were known that the attack had been
only of short duration, the elevation of temperature would, as in the
case of sunstroke, decide in favor of the fever, but if it had lasted
some hours, this symptom would be of no value, as the temperature may
rise to an equal height in apoplexy.
Diabetic coma is a much less common affection than apoplexy. The
peculiar odor (aceton) of the breath, if present—which is not always
the case—might be diagnostic. The peculiar long and deep respirations
would awaken suspicion which would be confirmed by an examination of
the urine.
Sunstroke, with its sudden onset, complete unconsciousness, and
rapidly rising temperature, may present a very close resemblance for a
while to apoplexy, and in fact has been known as heat apoplexy. Age,
temperature, and surroundings would give strong probabilities one way
or the other, and if the temperature of the patient were at first
below the normal and did not rise for an hour or two, it would
certainly not be sunstroke and would be apoplexy, while if the
temperature were very high a few minutes after the patient had been
observed to cease work or become unconscious, the evidence in favor of
sunstroke would be equally strong.
It might appear that hysteria need hardly enter into our
consideration, and could hardly be mistaken for apoplexy, but most
experienced physicians could relate instances where serious organic
disease has been made light of under the name of hysteria, and many
inexperienced ones could tell of the opposite and safer mistake. An
occasional case of deep coma presents itself where, although the age
and sex of the patient awaken strong suspicion, we cannot at once be
sure that no organic lesion is present; and if, in addition, the
patient should be affected with hemiplegia—a combination which,
although rare, is by no means beyond the limits attainable by this
perplexing disease—an immediate positive diagnosis would be difficult.
Absence of facial paralysis, which might be made manifest by some
irritation like pinching or an attempt to raise the eyelids, would be
of much value under these circumstances. The hysterical physiognomy
might be well enough marked to be almost conclusive by itself. The
urine and feces are not likely to be passed involuntarily in hysteria,
as they are in apoplexy.
Injuries to the head should be carefully looked for in any case with
unknown history. Actual fracture, which perhaps leads to no depression
of bone, may give rise to hemorrhage, probably meningeal, which will
cause the usual symptoms, and a shock which is not accompanied by
fracture may cause considerable laceration of the brain with
consequent hemorrhage. In the latter case, however, unless the brain
be already {967} predisposed by arterial disease, the laceration and
hemorrhage will not be extreme and the symptoms will be those of
concussion. The diagnosis can hardly be said to be between hemorrhage
and concussion, but whether the hemorrhage be the result of
concussion—a question which can hardly be answered without the history
and observation of the further progress. Cuts and bruises may result
from a fall caused by the shock, and pericranial ecchymoses may result
from cerebral hemorrhage through the vaso-motor system without the
intervention of accident.
Rapid meningitis of the vertex, with predominance of the effusion upon
one side, may closely simulate compression from hemorrhage. At the
base, by the time it has become severe enough to cause
unconsciousness, it is likely to have affected the ocular muscles, and
perhaps given rise to other paralyses less regular in their
distribution than the ordinary hemiplegia. Ophthalmoscopic examination
would be of value in these cases if—which is not very likely to
happen—there is no history. The temperature in meningitis is more
likely to be irregular and less rapidly and uniformly rising than in a
severe hemorrhage or occlusion. In many cases emaciation, dry tongue,
and constipation with sunken abdomen will testify to a previous
illness, while after a few hours' observation the progress of the case
will make the diagnosis more clear.
In differentiating cerebral hemorrhage or ordinary embolism from the
apoplectiform attacks met with in syphilitic intracranial disease, it
is rather a question of etiology than of diagnosis in the narrower
sense, since unconsciousness and hemiplegia coming on with syphilis
are often dependent upon a condition of the vessels closely resembling
that which gives rise to the ordinary forms; that is, we are dealing
in either case with an endarteritis which has furnished the basis for
the deposit of a thrombus, and the question is, Of what nature is the
endarteritis? It is obvious that this is only to be answered by a
knowledge of the history, not necessarily of a primary or secondary
lesion, but of previous disease. The syphilitic taint may often be
suspected from the irregularity of the paralysis, the cranial nerves,
for instance—especially the ocular—being much more frequently affected
in syphilitic than in ordinary hemiplegia. After partial recovery or
amendment the characteristics of irregularity and changeableness will
be more strongly marked.