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. 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 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 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 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.
The TREATMENT of peripheral facial paralysis must begin with the effort to remove its cause. If syphilis is suspected, mercury and iodide of potassium must be freely used. If the cause is an affection of the middle ear, this must be treated. Wounds or traumatic injuries must receive the necessary surgical attention. In addition, in such cases electricity must be employed in the manner presently to be described. In cases of rheumatic facial paralysis the treatment will vary with their gravity. In the lighter form in which the nerve is affected outside of the Fallopian canal, recovery takes place in a comparatively short time, even without treatment, but is hastened by the use of the faradic or galvanic current daily along the branches of the nerve. In the severe form we must open the treatment by an attempt to combat the condition of inflammation—of inflammatory exudation—which we suppose exists within the Fallopian canal. Local blood-letting by leeching upon the mastoid process may be appropriately used in the very first outset of the paralysis. Iodide of potassium, given persistently in large doses during the earlier period of the disease, appears to act beneficially independently of any syphilitic taint. Electricity is the remedy, however, on which most reliance is to be placed in the treatment of rheumatic facial paralysis, and the manner of its application may be taken as a model of how it should be employed in all cases of peripheral paralysis. The galvanic current, on account of its power of penetrating to the deeper parts and its catalytic action, is to be preferred for the direct electrical treatment of the nerve which should be instituted in recent cases. Its action is best obtained by placing the positive pole behind the ear on the affected side, the cathode behind the opposite ear, and passing a moderate current across the base of the skull (the affected nerve being thus in the course of the current) for one or two minutes. Occasionally the position of the poles may be reversed. Besides this direct application of galvanism to the point of lesion, it is necessary to make a peripheral application of electricity to the branches of the nerve and to the paralyzed muscles. For this we use both the faradic and galvanic currents. The galvanic current is used by applying the positive pole stationary behind the ear, while the negative pole, with an electrode of suitable size, is stroked over each branch of the nerve and applied to each muscle, a current being used sufficiently strong to produce decided contractions. This peripheral application should be made once daily, the time of application being from two to five minutes. The application of the faradic current is made by simply placing one electrode upon an indifferent spot, and moving the other over the face, with a current strong enough to cause contractions if the muscles still respond to it, or if they do not of such strength as the patient can bear without discomfort. Without doubt, one of the beneficial effects of peripheral electrization is the reflex excitement of the facial above the point of lesion through the irritation of the terminations of the fifth nerve in the skin. A certain advantage derived from it is that it maintains the tone of the paralyzed muscles, which in the case of the orbicularis palpebrarum is of great importance in preventing the eversion of the lower lid and the overflow of the tears. As it is impossible during the first days succeeding the paralysis to distinguish severe cases from those of the middle form, it is best to begin the treatment of all cases in the manner above described. The use of strychnia in rheumatic facial paralysis, both internally and by hypodermic injection, may be mentioned on account of the widespread preposession in its favor, and to point out distinctly its utter futility.
Mechanical appliances and manipulation are used with advantage in the treatment of facial paralysis to prevent the paralyzed muscles about the mouth and cheek from being drawn out of place and over-stretched by the action of the sound ones of the opposite side, thus having their tonicity and nutrition impaired.
Contractions and rigidity of muscles receive little benefit from the use of electricity, and must be treated by mechanical procedures, such as stretching, massage, etc.
Neuromata.
The term neuromata was applied to all tumors involving the nerve-trunks at a time when their histological differences had not been studied and they were all supposed to be composed of nerve-tissue; and even yet the name is conveniently retained, because, although differing widely histologically, tumors situated upon the nerves have a very similar clinical history.
Neuromas must be divided into true and false, the true consisting of nerve-tissue, the false, or pseudo-neuromas, being composed of many varieties, having this only in common, that they are seated upon the nerves.