to removal, if possible, of its cause, and the treatment of diseased
conditions, if any exist, of the nerve-trunks, as neuritis, mechanical
injuries, etc. Local applications of a stimulating character may be
advantageously used upon the anæsthesic parts. By far the most
effective stimulant to the diseased nerves is the faradic or galvanic
current, and it should be used in the way that will produce the
greatest amount of excitation in the cutaneous end-organs. This is
best done by applying the faradic current to the dry skin with the
metallic brush, or by allowing the cathode of the galvanic current to
rest upon it for some time.
The PROGNOSIS in peripheral anæsthesia is in the main favorable, but
it must, of course, depend much on the gravity of the lesion causing
it, as mechanical injury, pressure, neuritis, cold, etc. Rheumatic
anæsthesia, the result of exposure to cold, is in general readily
recovered from. Vaso-motor anæsthesia yields in most cases without
difficulty to treatment. Washerwoman's anæsthesia and allied cases are
intractable, and often resist the patient and well-conducted
application of remedies.
As a concrete picture of peripheral anæsthesia we will give a
description of anæsthesia of the fifth nerve—the rather that in its
consideration we meet with some of the most interesting and important
complications occurring in connection with paralysis of sensitive
nerves. The fifth nerve may have either of its three branches
separately affected, giving rise to anæsthesia limited to the
distribution of that branch, or all of its fibres may be
simultaneously involved, giving rise to complete anæsthesia of the
nerve. In the latter case the lesion of the nerve in all likelihood
exists at some point of its course between the apparent origin from
the pons and the ganglion of Gasser, which rests upon the apex of the
petrous portion of the temporal bone. Beyond this point the nerve
divides into its three branches. Amongst the causes of trigeminal
anæsthesia are injuries, tumors, syphilitic thickening of the dura
mater, neuritis, etc., affecting the nerve within the cranial cavity.
In complete anæsthesia of the fifth nerve the parts implicated are the
skin of the forehead to the vertex, the nose, the lips, and chin up to
the median line, the cheek and temporal region, including the anterior
portion of the ear, the conjunctiva, the mucous membrane of the nose,
the mucous membrane of the mouth, and partly of the fauces of the same
side. The tongue is deprived not only of common sensation on the
affected side in its anterior two-thirds, but the sense of taste is
also lost over the same region, by reason that the fibres of the
chorda tympani, the nerve of taste for this region of the tongue, are
derived from the fifth nerve. If the whole thickness of the
nerve-trunk is involved, including the small motor root, there is, in
connection with the anæsthesia, paralysis of the muscles of
mastication on the side affected, which may be distinguished by the
want of hardening of the masseter when the jaws are forcibly brought
together, and by the thrusting of the chin over to the paralyzed side
when the mouth is widely opened, caused by the want of action of the
external pterygoid muscle, which allows the condyle on the paralyzed
side to remain in the glenoid fossa, while the condyle of the opposite
side is pulled forward upon the articular eminence by the sound {1202}
pterygoid. The face is of a dusky or livid color, and cooler than
natural. Ulcers of a stubborn character in the mucous membrane of the
cheek may be caused by the patient unconsciously biting the
insensitive parts. An inflammation of the conjunctiva is frequently
set up, which may extend to the cornea, causing ulceration,
perforation, panophthalmitis, and destruction of the eye (ophthalmia
neuro-paralytica). This has been regarded by some as caused by trophic
changes in the tissues, the direct result of irritation or destruction
of trophic fibres connected with the ganglion of Gasser. Experiments
made upon animals, however, seem to show that the inflammation of the
eye depends upon the irritation caused by the intrusion of foreign
bodies, which, owing to the loss of sensation, are not appreciated,
and which from loss of reflex action are not removed by winking nor
washed away by an increased lachrymal secretion, as in the healthy
eye. It may be that although the latter is the true explanation of the
origin of the inflammation, nevertheless the tissues may have lost
their normal power of resistance to its invasion by reason of
nutritive changes consequent upon the lesion of trophic fibres running
in the trunk of the nerve. The reflexes ordinarily induced by
irritation of the parts in their normal state are lost. Irritation of
the conjunctiva causes no winking of the lids nor secretion of tears,
and titillation of the nostrils no movements of the muscles of the
face nor mucous or lachrymal secretion. The movements of the face are
less lively on the affected side, not on account of paralysis of the
muscles, but from the loss of that constant play of reflex activity in
them which takes place in the normal condition. The loss of the
reflexes distinguishes peripheral trigeminal anæsthesia from that of
cerebral origin, in which they may still be excited by irritating the
anæsthesic surfaces. In trigeminal anæsthesia, which sometimes occurs
from the effect of cold upon the surface of the face, the mucous
surfaces are not affected.
The SYMPTOMS and DIAGNOSIS of peripheral paralysis having been already
given under the heads of Injuries of Nerves and Neuritis, a
consideration of the distribution of any motor nerve will enable us to
anticipate the distinguishing features of the paralysis dependent upon
it. With each the picture will be modified according to the position
of the muscles paralyzed and the motor functions destroyed. It now
remains to give the symptoms, diagnosis, and treatment of the
paralysis of an individual motor nerve, which may serve as an example
and paradigm, in the consideration of which points of interest and
instruction may be touched upon applicable to all other cases.
Peripheral Paralysis of the Facial Nerve (Bell's Paralysis).
Of all the peripheral paralyses, probably that of the seventh is the
one we are most frequently called upon to treat and the symptoms of
which are the most complex and interesting. The frequency of its
paralysis is due to the length and peculiarity of its course, enclosed
as it is in a bony canal which permits no increase of its volume
without compression, the run of its terminal branches through parts
liable to inflammation and disease (parotid gland), and their final
distribution to parts exposed to all vicissitudes of heat and cold and
in constant danger of mechanical injury. {1203} The complexity and
interest of the symptoms of its paralysis depend in a great measure
upon the intimate connections it forms at different points of its
course with the fibres of other nerves of entirely different functions
(acoustic and fifth).
The seventh nerve is liable not only to intercranial compression from
tumors, inflammation of the meninges, syphilitic processes, etc., but
its long course through the petrous portion of the temporal bone
renders it liable to injury from fracture or caries, and its close
proximity to the middle ear causes it often to suffer from the
diseased conditions of the bony walls or mucous lining membrane of
that chamber, its paralysis being not infrequently the result of
simple aural catarrh. After the exit of the nerve from the
stylo-mastoid foramen it is imbedded in the parotid gland, and
sometimes suffers from compression produced by an inflammation or
abscess in that organ or by enlarged lymphatic glands in the
neighborhood. Surgical operations, so often demanded for disease of
the bones or soft parts of the face, may necessitate the lesion of its
trunk or branches. The exposed position of this nerve is sometimes the
occasion of its injury at the very outset of the life of the
individual, when the application of the forceps to the head has been
resorted to in delivery. But the most frequent cause of facial
paralysis appears to be the exposure of one side of the face directly
to cold—as sleeping in a draught of air, sitting at the open window of
a railroad coach, etc. Here the causal connection appears evident from
the rapidity with which the paralysis usually follows, although cases
occur in which an interval of hours or days elapses after the exposure
before the paralysis declares itself. Although this is usually
designated rheumatic paralysis, there is nothing to connect it with
that disease, nor are rheumatics more liable to it than others. Under
such circumstances the paralysis is probably brought about by the
occurrence of a neuritis of the nerve-trunk, which is compressed by
the hyperæmia, and it may be by an inflammatory exudation against the
bony walls surrounding it, until not only does it lose the power of
conduction, but its fibres undergo the degenerative process. In some
cases the neuritis thus excited by exposure to cold attacks the nerve
after it has issued from the bony canal, and then the resulting injury
to the fibres is much less grave. Although in some cases there are
prodromal symptoms, as stiffness or pain in the face, generally the
paralysis occurs suddenly, very often being first observed upon
awaking. The patient may be first made aware of the paralysis by an
inability to drink without the fluid dribbling from the affected side
of the mouth or by the overflow of tears from the eye of the same
side. When the paralysis is recent and the face in complete repose,
there may be little or no deformity to mark the condition of the
muscles. When, however, the patient speaks or the slightest emotional
or reflex movements of the face are excited, as laughing, frowning,
etc., it becomes obvious from the bizarre grimace caused by a
one-sided contraction. After the paralysis has existed for some time
the contrast of the two sides of the face is marked. The paralyzed
side is characterized by a vacancy of expression to which the staring,
unwinking eye contributes. From loss of the tonicity of the muscles
the angle of the mouth droops, and the expressive furrows and lines
about the brow, below the eye, and beside the nose are smoothed out
and obliterated. Speech is affected, inasmuch as the paralysis of the
{1204} lip interferes with the pronunciation of the labials, and all
attempts to purse up the mouth, as in whistling, is abortive. The eye
not only remains open, the lids motionless, but there is partial
eversion of the lower lid (lagophthalmos), and the tears, no longer
directed to the punctum (paralysis of Horner's muscle), flow over the
cheek. The natural impulse to reflex winking caused by evaporation
from the conjunctiva or by the contact of particles of dust is
answered by a rolling of the eyeball upward to wipe the cornea beneath
the momentarily relaxed and drooping upper lid. Excited respiration
causes no movement of the ala of the nose on the affected side, but in
deep inspiration, in contrast to the normal elevation of the ala, it
is flattened down by the suction of the inrushing current of air. In
masticating, the cheek bulges out from want of power in the paralyzed
buccinator to press the food inward against the opposing movements of
the tongue. In persons who have the rather unusual power of
voluntarily moving the ear we may detect the paralysis of the muscles
concerned in those movements—a useful point in diagnosis. Moreover, on
the sound side of the face the features have not entirely the natural
appearance. The angle of the mouth is drawn upward and the naso-labial
line more deeply impressed than natural. This results not from
excessive contraction, but from the muscles remaining in the position
they have taken during contraction, the antagonistic tonic traction
from the opposite side, which would have restored them to their normal
position, being wanting. This may be in a measure remedied by
mechanical appliances which will keep up an elastic pull from the
paralyzed side, or by restoring the muscles after contraction to
position with the hand. The tongue rests symmetrically in the floor of
the mouth, and is thrust out straight, although in appearance it is
pushed toward the side paralyzed—a deceptive appearance produced by
the asymmetrical position of the mouth. In some cases there is partial
paralysis of the velum palati, the half arch on the affected side
hanging lowest, and if we cause the patient to make the sound of _ah_
the opposite side of the palate is alone drawn upward. The uvula may
also participate in the paralysis, but the explanation of its
position, sometimes directed away from, sometimes toward, the side of
the paralysis, cannot be given. In proportion to the amount of the
paralysis of the soft palate will be the prominence of the symptoms
caused by it, such as difficulty in deglutition, a nasal tone in
speaking, and the escape of fluids through the nostril in swallowing.
The sense of hearing is often affected coincidently with facial
paralysis. Thus by reason of their close juxtaposition the same cause
may in common affect the acoustic and the facial, causing imperfect
hearing, subjective noises, etc. The hearing is frequently affected by
diseased conditions of the middle ear, which also cause a facial
paralysis. Still another defect of hearing, however, is caused by the
paralysis of the facial nerve itself. The stapedius muscle, supplied
by a branch of the facial, is the antagonist of the tensor tympani,
and when it is paralyzed the over-tense tympanic membrane vibrates
more readily to sound-waves, and a condition of uncomfortably
exaggerated sensitiveness to sounds is the result (hyperacuisis). The
rarely-occurring symptom of dryness of the mouth on the side of the
paralysis receives its explanation in the well-known fact of the
presence of secretory fibres for the salivary gland in the chorda
tympani, which are derived from the facial. We observe sometimes, in
connection with facial paralysis, that the patient {1205} complains of
certain subjective sensations of taste, as sour or metallic, and an
examination will in some cases reveal that the sense of taste is lost
on the anterior two-thirds of the tongue on the side of the paralysis.
The fibres which convey the sense of taste pass centripetally from the
tongue in the chorda tympani nerve, join the facial just within the
stylo-mastoid foramen, and continue united with it to the geniculate
ganglion of the facial, at which point they leave it to pass in the
great superficial petrosal to the spheno-palatine ganglion, and thence
to the trunk of the fifth nerve. Loss of sensation over the face only
occurs in cases where the fifth nerve has been simultaneously affected
with the facial, which may occur from exposure to cold.
It is obviously of importance in cases of facial paralysis to
determine if they are of central or peripheral origin. The most
prominent symptoms which mark a peripheral paralysis are the
implication of all the branches of the nerve, the loss of the
reflexes, the development of the degenerative reaction, and atrophy of
the muscles. In facial paralysis of cerebral origin the frontal and
orbital branches are not at all or but slightly affected, leaving the
eye with its natural appearance, in contrast to the lagophthalmos, and
the open eye which does not close even in sleep. In cerebral paralysis
the reflexes are normal and the muscles retain their natural electric
reaction. Accompanying brain symptoms assure the diagnosis. In facial
paralysis of bulbar origin the electric reactions are diminished, and
we have a complex of symptoms made up in a great measure by the
implication of neighboring nerves. After the diagnosis of a peripheral
facial paralysis has been made, by a careful consideration of the
symptoms we may with more or less accuracy determine at which point of
the nerve the lesion is situated. If there is paralysis of all the
muscles of the face, without alteration of taste or hearing, the
electric reaction of nerve and muscles normal, the nerve is affected
outside of the stylo-mastoid foramen. This is usually the form of
slight rheumatic paralysis. If we discover that the muscles of the
external ear are paralyzed, it shows that the point of lesion is just
within the stylo-mastoid foramen, where the posterior auricular branch
is given off from the facial. If with paralysis of the face there is
alteration of the sense of taste, with dryness of the mouth, without
interference with hearing, the trunk of the nerve is affected within
the Fallopian canal, involving the chorda tympani fibres below the
point where the stapedius nerve is given off. If to the above symptoms
there is added over-sensitiveness to sounds, hyperacuisis, and there
is no paralysis of the palate, we have the nerve affected still higher
up, but below the geniculate ganglion. If the geniculate ganglion is
involved, there is, in addition to the foregoing, symptoms of
paralysis of the palate. If, now, the lesion is above the geniculate
ganglion, we will have eliminated the symptom due to implication of
the chorda tympani, which leaves the trunk of the facial at the
geniculate ganglion, and the sense of taste is unaffected, while there
remains paralysis of the face, dryness of the mouth (the secretory
fibres run in the trunk of the seventh), hyperacuisis, and paralysis
of the palate.
It was in facial paralysis that the first observations upon the
degenerative reaction in muscles were made, and it is in that
affection that these electric phenomena have been best studied, and
give us the clearest {1206} indications for prognosis and treatment in
peripheral paralysis generally. In rheumatic facial paralysis, the
most common form of peripheral facial paralysis, the electric
reactions of the paralyzed muscles enable us to classify the cases
into three groups, the prognosis and duration of which vary very much.
In the first group are the slight forms of facial paralysis. Here the
faradic or galvanic current, applied to nerve or muscles, causes an
ordinary contraction; the electric reactions are normal. These cases
scarcely require treatment, and recover in two or three weeks. In a
second group are those cases in which within a short time after the
invasion of the paralysis (two weeks) complete degenerative reaction
is observed. This degenerative reaction, with the accompanying
anatomical changes in nerve and muscle, has already been treated of in
this article, and it is sufficient here to say that it is marked by
total loss of electric excitability, both faradic and galvanic, in the
nerve, loss of faradic and increased galvanic excitability in the
paralyzed muscles, with a reversal of the normal reply of the muscles
to the different poles of the galvanic battery. These cases constitute
the severe form of rheumatic facial paralysis, and the prognosis is
grave, recovery takes place only after months, and even after the
lapse of years traces of the disease remain in the imperfect action of
the muscles. A third group of cases are of a gravity intermediate
between these two. In them is present the milder form of degenerative
reaction; that is, there is a diminution, but not a total loss, of
electric excitability in the nerve for both the galvanic and faradic
currents; but in the muscles there is a marked increase of galvanic
excitability, with qualitative change—_i.e._ greater contraction upon
application to them of the positive than of the negative pole. These
cases may be expected to recover in from four to eight weeks, the
muscles still exhibiting the degenerative reaction after voluntary
motion has returned. Among the symptoms to be particularly noticed in
the progress of the severe forms of facial paralysis are spasmodic
twitchings or spasms of the muscles on the affected side of the face,
about the angle of the mouth, and around the eye, occurring
spontaneously or when voluntary movements are made. Also a state of
tonic contraction and rigidity may develop in some of the muscles,
causing a permanent elevation of the angle of the mouth, a narrowing
of the opening of the eye, or a rigidity of the cheek. These symptoms
have been erroneously attributed to the use of electricity in the
treatment, but they occur as frequently in cases in which it has not
been employed. Traumatic facial paralysis, as from wounds, surgical
operations, use of the forceps in delivery, or paralysis from
compression of the nerve, as from tumors, syphilitic thickening of the
dura mater, etc., do not require a detailed mention here, as such
cases come under the head of nerve-injuries, already discussed.
Paralysis of both facials (diplegia facialis), in so far as it is
caused by peripheral nerve lesion, is an accidental occurrence, and
need not be considered as a separate form of facial paralysis. It is
often the result of central disease.