Chapter LXXIX: Introduction: This disease remained unnoticed until twenty years ago, (3)

The TREATMENT consists, at the outset, in rest and position, the local abstraction of blood (in cases where the nerve-trunk is swollen and tender), and the administration of such drugs as we suppose act favorably upon the inflammation of the nerves. Salicylic acid or salicylate of sodium seem to act beneficially in relieving the severe pains in the outset of the disease. Iodide of potassium, gradually increased until large doses are taken, has, in the experience of the writer, seemed to beneficially modify the course of multiple neuritis. The necessary relief of pain is best obtained by hypodermic injections of morphia, supplemented by heat applied to the affected nerves. To these means may be added rubbing with chloroform and applying to the painful parts cloths dipped in a 5 per cent. solution of carbolic acid. After the acute stage has been passed and in chronic cases, just as soon as we have reason to suppose that the degenerative process in the nerves has come to a standstill, we possess in the use of electricity the means of hastening the regeneration of the nerve-fibres, strengthening the paralyzed muscles, and restoring the sensation. The galvanic current is to be preferred, and it is to be applied to the crippled nerves and muscles—sometimes stable for its electrolytic action, sometimes interrupted to obtain its exciting and stimulating effect. The excitement to nerves and muscles by the use of the faradic current has also its uses in hastening recovery. Protracted treatment and much patience are required to overcome contractions and restore the nerves and muscles, and the effects of the disease may be seen for a long time in the weakness and diminished electric reaction of the muscles.

Anæsthesia of Peripheral Origin.

A prominent and important symptom of the lesion of peripheral nerves is the diminution and loss of cutaneous sensibility. Besides the {1199} anæsthesia caused by the affections of the fibres themselves, which has been touched upon in the preceding pages, it may be produced by morbid states of the peripheral end-organs or cutaneous terminations of the nerves. Cold applied to a nerve-trunk may produce alterations which for days after cause numbness and paræsthesia in the surface to which it is distributed, and the application of cold to the surface of the body, as we know from common observation, causes blunting of the cutaneous sensations, especially that of touch. In this way, from exposure to the atmosphere at low temperatures, to cold winds, or by the immersion of the body in cold water, the end-organs of the nerves in the skin are morbidly affected, and anæsthesia results, the so-called rheumatic anæsthesia. Many substances, as acids, notably carbolic acid, alkalies, narcotics, etc., act upon the cutaneous end-organs in a way to destroy their capacity for receiving or transmitting impressions and produce a more or less persistent anæsthesia of the skin. In the anæsthesia so often observed in the hands and forearms of washerwomen we have an example of the action probably of several of these causes, as the frequent plunging of the hands into cold water and the action upon the skin of alkalies and alkaline soaps. The diminution or interruption of the circulation through the skin, as in ischæmia from spasm of the minute arteries due to an affection of the vaso-motor nerves, is also a cause of cutaneous anæsthesia. In lepra anæsthetica (Spedalskhed) the cutaneous anæsthesia is dependent upon a neuritis of the minute branches in the skin. The local anæsthesia met with so often in syphilis, though its pathology is doubtful, is not improbably sometimes caused by an affection of the peripheral nerves (neuritis?) and their end-organs. After many acute diseases, diphtheria, typhoid fever, etc., we have cutaneous anæsthesia in connection with muscular paralysis, the cause of both being a neuritis. The patient is made aware of the loss of sensation by some interference with his usual sensations and movements. If he puts a glass to his lips, the sensation is as if a bit were broken out of the rim; his accustomed manipulations are awkward, because of the want of distinct appreciation of the objects he holds; he fumbles in buttoning his clothes or he stumbles unless looking to his steps. An examination, nevertheless, almost always reveals that the anæsthesia is greater than would have been supposed from the subjective feelings of the patient; indeed, cases occur in which he is not aware of an existing defect of sensation. But a careful examination is not only required to determine the extent, but by it alone can we arrive at a knowledge of the quality of the anæsthesia—viz. whether there is a loss of all of the different kinds of sensation, whether they are affected in an unequal degree, or whether some have entirely escaped. Thus we must test for the acuteness of the simple sense of touch by comparing the sensations elicited by the contact of small surfaces of unequal size, as the point and head of a pin or pencil, observing the appreciation by touch of the patient for different substances, as woollen, silk, linen, cloth, or comparing the sensation of the anæsthesic part with the same part on the opposite healthy side of the body. The sense of locality and space may be examined by placing at the same instant upon the skin of the patient, his eyes being closed, two points (the anæsthesiometer or the points of a compass), and observing his capacity for appreciating the impression as double. As there is an enormous difference of acuteness of the {1200} space-sense in the skin of different parts of the body (see textbooks of physiology)—ranging from the tip of the tongue, where the touch of two points separated 1.2 mm. gives a double sensation, to the thigh, where the points must be separated 77 mm. to be felt as two—we must be careful to consider in making the examination the normal space-perception of the region. Care must be taken not to repeat the test too often, as a rapid education of the surface to a more delicate appreciation of the impressions is the result. In certain abnormal conditions from spinal disease we have a condition of polyæsthesia in which the impression of one point is felt as two or more. The sense by which we appreciate the pressure of objects must be tested by placing upon the surface to be examined, in succession, objects of different weight, care being taken to have the area which touches the skin and the temperature the same in each. The parts to be tested must be firmly supported, and all muscular contraction on the part of the patient prevented. The temperature sense is examined by the application of hot and cold water or bodies of different temperature. We sometimes meet with a perversion of this sense in which the application of a cold surface to the skin gives the sensation of warmth, and the contrary. In testing the sense of temperature and the sense of pressure it is not the absolute capacity of appreciating on the part of the patient that we investigate, but the power of discriminating between different degrees of temperature or pressure. The sense of pain must likewise be tested, since morbid conditions occur in which it may be caused more readily than is normal by exciting the cutaneous nerves, and that, too, in parts which have in a great measure or quite lost the sense of touch; or, on the other hand, touch may be retained, while irritation of the skin can excite no feeling of pain (analgesia). We have in the faradic current an excellent means of testing the cutaneous sensibility, inasmuch as it excites the skin over the various parts of the body about equally, and it can be employed in very gradually increasing or decreasing strength. Its effects on the affected part must be compared with those produced on the healthy surface of other parts of the patient's body or on healthy individuals.

Frequently accompanying cutaneous anæsthesia, but constituting no part of it, are various paræsthesiæ, as formication, pins and needles, burning, etc. Pain, sometimes of great intensity, is not infrequently connected with it (anæsthesia dolorosa). The paræsthesiæ and pain are the result of irritation in some portion of the conducting tracts, and, together with the trophic changes so often seen in connection with nerve-injuries, they have been already considered under that head.

It is a very important point to make the diagnosis between central and peripheral anæsthesia, but it is often a matter of great difficulty, and sometimes not to be made at all. The history of the case must be carefully considered, and an examination made for symptoms of brain or spinal disease, the existence of nerve lesions, or if there is a history of toxic influences, etc. In peripheral anæsthesia the reflexes which may be normally excited from the affected surface are wanting, in contradistinction to anæsthesia of central origin, in which they are most generally retained or even increased. Concomitant trophic changes speak strongly for a peripheral origin, as do also paralysis and atrophy of muscles. {1201} Loss of some of the forms of sensation, with retention of others—_i.e._ partial paralysis of sensation—indicate a central origin.

The TREATMENT of peripheral anæsthesia must look, in the first place, 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.

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 {1207} 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 {1208} 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.

The true neuromas are again subdivided into those in which the nerve-tissue composing them resembles exactly the fibres of the peripheral nerves, showing with the microscope the double-contoured white substance of Schwann surrounding an axis-cylinder, and those in which the tumor is made up of fibres which Virchow has shown to be non-medullated nerve-fibres—_i.e._ the axis-cylinder without the white substance of Schwann. These two forms have been distinguished by the names myelinic and non-myelinic. The true neuromas are non-malignant, although showing the tendency to recur after extirpation, are of slow growth, and as a rule do not increase to a very great size. The best type of the myelinic neuromas is found in the spherical or spindle-shaped enlargements at the cut ends of nerves, particularly in the stumps of amputated limbs, where they are found oftenest intimately connected with the cicatricial tissue, though sometimes lying free. They consist of true medullated fibres mixed with some fibrous tissue. The fibres composing them are derived partly from splitting up and proliferation of the fibres of the nerve itself, partly are of new formation, the appearances strongly recalling the process of regeneration in nerves. Myelinic neuromas consist of fibres and nuclei so closely resembling in microscopic appearance the fibromas that they have hitherto been confounded with them; and there is a difference among the highest authorities as to the certainty of their diagnosis, and, in consequence, of the frequency of their occurrence. The true neuromas may include in their structure all of the fibres of the nerve-trunk or only a portion of them (partial neuroma)—a fact of importance in their symptomatology. Of the false neuromas, the fibromas are by far the most frequently met with. They appear as knots, more or less hard, upon the course of the nerve-trunk, which they may involve completely or partially. They are often excessively painful to the touch or spontaneously, most of the so-called tubercula dolorosa belonging to the fibro-neuromas. Fibromas sometimes occur along the trunk and branches of a nerve, forming a plexus of knotted cords (plexiform neuroma). Fibro-sarcomas are not an infrequent form of neuroma.

{1209} Myxomas often occur upon the peripheral nerves, and are frequently multiple, their points of predilection being the larger trunks, as the sciatic, ulnar, etc. They show their characteristic soft structure, and are usually spindle-shape, assuming a rounder form as they attain a large size. The various forms of sarcoma occasionally form tumors upon the nerves, attacking generally the large trunks. Carcinomatous tumors beginning upon the nerves sometimes occur, but as a rule these growths involve the nerve by extension to it from adjacent parts.

Syphilitic gummata have been found almost exclusively upon the intracranial portion of the cranial nerves.

Gliomas appear to affect only the optic and acoustic nerves. Lepra nervorum (lepra anæsthetica) produces usually a spindle-form thickening upon the nerve-trunks, but sometimes there are more distinct knots, which may be felt beneath the skin, bead-like, along the course of the nerves of the extremities.

Like the true neuromas, the false neuromas, developing from the neurilemma and perineurium, may involve the whole or only a part of the fibres of a nerve, or the nerve-fibres may run at the side of the tumor—different conditions, which may alter materially the effects produced upon the nerve.

Neuromas, both false and true, may occur not only singly, but often in large numbers, many hundreds having been counted upon an individual. Sometimes they are numerous upon a single nerve-trunk and its branches, and again they may appear scattered over nearly all of the nerves of the body, even to the cauda equina and roots of the nerves. According to Erb,[9] isolated neuromas are more frequent in females, while multiple neuromas are found almost exclusively in men. Neuromas vary greatly in size, as we might expect from the very great difference of their nature and structure; sometimes no larger than a pea, they may attain the size of a child's head.

[Footnote 9: _Ziemssen's Handbuch_.]

ETIOLOGY.—In cases of multiple neuromata it would seem as if there was a constitutional condition or diathesis as the foundation of the affection. This we may the more readily believe as there appears good evidence to show that the tendency to the formation of these nerve-tumors is sometimes hereditary, and some of them are congenital.

Idiots and cretins have been observed to suffer in undue proportion with multiple neuromas. We find a direct exciting cause of neuromas in mechanical injuries of nerves, wounds, blows, pressure, etc. Thus, as has been already seen, true neuromas occur in the divided ends of the nerves after amputations or otherwise where a nerve-trunk has been divided (cicatricial neuroma). As such neuromas are in some degree the result of inflammation, it is probable that they may sometimes be caused by chronic neuritis.

For a large number of neuromas no cause can be assigned, and we must at present consider them as originating spontaneously.

SYMPTOMS.—The position and connections of neuromas being so different, sometimes simply in contact with the nerve; sometimes situated in the thickness of the nerve-trunk, the fibres being pressed aside and spread out upon the surface of the tumor; sometimes involving in their tissue a part or the whole of the nerve-fibres,—we cannot but expect a {1210} very marked difference in their clinical history. Not a few cases occur in which the presence of neuromas, even in large numbers, gives rise to no symptoms during life, and their existence has been revealed only upon a post-mortem examination.

The symptom most common to neuromas, and one to be expected from their mechanical interference with the nerves, is neuralgic pain—sometimes extreme, local or shooting along the course of the nerves, stubborn, and hardly to be alleviated by remedies. It is paroxysmal, notwithstanding the unvarying character of its cause, in consonance with the tendency to periodical activity which prevails in the nervous system. Sometimes the pain is increased notably by atmospheric changes. The pain may sometimes be arrested by firm pressure upon the nerve above the seat of the tumor. In some cases pressure upon the neuroma, or even handling it, causes great pain. The intensity of the pain does not depend upon the size of the tumor, some of the smallest having earned the appropriate name of tubercula dolorosa. The continued irritation of a neuroma sometimes produces a condition of general nervous excitability, which shows itself in hysterical and even in true epileptic convulsions. Occasionally there are abnormal sensations (paræsthesiæ), formication, numbness, etc., in the distribution of the nerve affected, and when from pressure or histological changes the fibres are destroyed anæsthesia results.

The interference with the conductivity of the motor fibres, which occurs less frequently than alterations of sensation, shows itself in cramps, tumors, paresis, and paralysis, according to its degree.

Neuromas may destroy life by the continued excessive pain, which wears down the strength and depresses the vitality. Death may be caused by their peculiar situation; as, for instance, upon the cauda equina, where they produce paraplegia, paralysis of the sphincter and bladder, and trophic changes.

The DIAGNOSIS of neuromas can only be made when they are sufficiently superficial to be recognized by the touch, and along with the symptoms above detailed the tumor is situated upon the known course of a nerve, to which, moreover, its attachment allows a lateral movement.

The only TREATMENT available for neuromas is extirpation, which must be conducted with a view to sparing any fibres of the nerve not involved in the tumor. Where it is necessary to divide the nerve in the removal of the tumor, as small a portion as possible must be excised, with the hope of a regeneration and reuniting of the cut ends. The success of extirpation depends largely upon the nature of the neuroma. The true neuromas, while they often show a strong tendency to recur after removal, are benign and show no metastasis. For the false neuromas the prognosis will be in accordance with their benign or malignant character.

{1211}

NEURALGIA.

BY J. J. PUTNAM, M.D.

DEFINITION.—It is customary to describe as neuralgic those pains for which no adequate cause can be assigned in any irritation of the sensory nerves from outside, which recur paroxysmally, are unattended by fever, and are distributed along the course of one or more nerves or nerve-branches.

The general use of the term neuralgia further implies the common belief that there is a disease or neurosis, not covered by any other designation, of which these pains are the characteristic symptom. Of the pathological anatomy of such a disease, however, nothing is known; and if it could be shown for any given group of cases that the symptoms which they present could be explained by referring them to pathological conditions with which we are already familiar, these cases would no longer properly be classified under the head of neuralgia.

The attempt has frequently been made, and on good grounds, in obedience to this reasoning, to cut down the list of the neuralgias, strictly so called, and to account for many of the groups of symptoms usually classified under that head by referring them to anæmia or congestion of the sensory nerves, to neuritis, etc.

One of the best and most recent statements of this view is that of Hallopeau,[1] who, although he does not wholly deny the existence of a neurosis which may manifest itself as neuralgia, goes so far as to maintain that the gradual onset and decline and more or less protracted course so common in the superficial neuralgias, such as sciatica, suggest rather the phases of an inflammatory process than the transitions of a functional neurotic outbreak, and that, in general terms, a number of distinct affections are often included under the name of neuralgia which are really of different origin, one from the other, and resemble each other only superficially. This subject will be discussed in the section on Pathology, and until then we shall, for convenience' sake, treat of the various neuralgic attacks as if they were modifications of one and the same disease.

[Footnote 1: _Nouveau Dict. de Méd. et de Chir. pratiques_, art. “Névalgies.”]

GENERAL SYMPTOMATOLOGY.—The neuralgias may be conveniently divided into—1, external or superficial; 2, visceral; 3, migraine and the migrainoid headaches.

Superficial Neuralgia.

The most prominent symptom of a neuralgic attack of the superficial {1212} nerves is of course the pain, and sometimes, from first to last, no other sign of disease is present. In an acute attack the pain is usually ushered in by a sense of discomfort, which the patient vainly tries to shake off, or by a feeling of weight and pressure or of numbness and prickling, or of itching. Sometimes, though far less often than in the case of migraine, there are prodromal signs of a more general character, such as a feeling of thirst[2] or of mental depression or drowsiness.

[Footnote 2: Spoken of by Mitchell's patient with neuralgia of the stump (see below).]

A dart of pain may then be felt, which soon disappears, but again returns, covering this time a wider area or occupying a new spot as well as the old. The intensity, extension, and frequency of the paroxysms then increase with greater or less rapidity, but, as a rule, certain spots remain as foci of pain, which radiates from them in various directions, principally up or down in the track of the nerve-trunk mainly implicated. The pain rarely or never occupies the whole course and region of distribution of a large nerve or plexus, but only certain portions, which may be nearly isolated from one another.

In an acute attack the affected parts may at first look pale and feel chilly, and later they frequently become congested and throb. Mucous surfaces or glandular organs in the neighborhood often secrete profusely, sometimes after passing through a preliminary stage of dryness.

The skin often becomes acutely sensitive to the touch, even though firm, deep pressure may relieve the suffering. Movement of the painful parts, whether active or passive, is apt to increase the pain. When the attack is at its height, the pain is apt to be felt over a larger area than at an earlier or a later period, and may involve other nerves than those first attacked. Thus, a brachial becomes a cervico-brachial neuralgia or involves also the mammary or intercostal nerves. A peculiarly close relationship exists between the neuralgias of the trigeminal and of the occipital nerves. It is said that when the attack is severe the corresponding nerves of the opposite side may become the seat of pain. This is perhaps remotely analogous to the complete transference of the pain from one side to the other which is so characteristic of periodical neuralgic headaches, especially if they last more than one day.

Some cutaneous neuralgias pass away after a few hours' or a night's rest, after the manner of a migraine or a headache, and patients in whom this takes place are, as a rule, constitutionally subject to neuralgia or other neuroses. Toward the end of such an attack there is often a copious secretion of pale, limpid urine. In a large class of cases, on the other hand, the attack is of several days' or weeks', or even months' or years', duration, with remissions or intermissions and exacerbations, which may be either periodical or irregular.

The most marked periodicity of recurrence is seen with the neuralgias of malarial origin, which may take on any one of the typical forms of that disease.

These malarial neuralgias affect pre-eminently, though not exclusively, the supraorbital branch of the fifth nerve; but it should not be forgotten that there is also a typically periodical supraorbital neuralgia of non-malarial origin, of which the writer has seen several pronounced examples, the pain usually recurring regularly every morning at eight or nine o'clock and passing away early in the afternoon. The same periodicity {1213} is seen, though less often, in other neuralgias. Thus, Trousseau[3] speaks of neuralgic attacks from cancer of the uterus in a young woman, which recurred daily at exactly the same hour. Some of the traumatic neuralgias show the same peculiarity to a marked degree.

[Footnote 3: _Clin. Méd._]

In many neuralgias, on the other hand, the exacerbations are worse at night, like the pains of neuritis. In the intervals between the attacks the pain may be wholly absent, or may persist, usually as a dull aching.

After a neuralgia has lasted a few days—sometimes, indeed, from the outset if the attack is severe—it is usually found that definite spots of tenderness have made their appearance at certain limited points on the course of the nerve. These are the famous points douloureux which Valleix described with such minute accuracy, believing them to be invariably present in true neuralgias. This is certainly not strictly the case, though they are very common. They are not necessarily coincident with the foci of spontaneous pain, as Valleix supposed, but do correspond in general to the points at which the affected nerve emerges from its bony canal or from deep muscles and fascia, and to portions of its area of distribution in the skin. The spinous process corresponding to an affected spinal nerve may also become tender, but this is probably to be looked on, like the same symptom in so-called spinal irritation, not as a sign of local disease, but as due to a general reaction on the part of the nervous system, and as a fact of a different order from the tenderness along the nerve.

The termination of an acute neuralgic attack is usually gradual, like its onset, although in some cases of headache, and in other neuralgias to a less degree, there comes a moment when the patient suddenly declares that he is free from pain.

Neuralgic attacks are usually characterized, besides the pain, by a highly-interesting series of symptoms, which are in part transitory and functional, and in part due to structural changes in the tissues.[4]

[Footnote 4: See Notta, _Arch. gén. de Méd._, 1854; Anstie, _Neuralgia and its Counterfeits_.]

The spasm and subsequent dilatation of blood-vessels in the affected area have already been alluded to. A disturbance of secreting organs in the neighborhood of the painful region, the lachrymal gland, the skin, the mucous membranes, the salivary glands, is of equally common occurrence, and is probably in great measure due to direct irritation of the glandular nerves, since the increased secretion is said to occur sometimes unattended by congestion.

The hair may become dry and brittle and inclined to fall out, or may lose its color rapidly, regaining it after the attack has passed.

The increased secretion of urine already alluded to attends not only renal neuralgias, but those of the fifth pair, intercostal, and other nerves. There may be unilateral furring of the tongue (Anstie).

The muscles supplied by the branches of the affected nerve or of related nerves may be the seat of spasm, or, on the other hand, may become paretic; and this is true even of the large muscles of the extremities.

Vision may be temporarily obscured or lost in the eye of the affected side in neuralgia of the fifth pair, and hearing, taste, and smell are likewise deranged, though more rarely. I am not aware that distinct {1214} hemianopsia is observed except in cases of true migraine, where it forms an important prodromal symptom.

In connection with these disorders of the special senses the occasional occurrence of typical anæsthesia of the skin of one-half of the body should be noted, which several observers have found in connection with sciatica. The writer has seen a cutaneous hyperæsthesia of one entire half of the body in a case of cervico-occipital neuralgia of long standing. These symptoms are probably analogous to the hemianæsthesia which comes on after epileptic or other acute nervous seizures, or after concussion accidents, as has lately been observed both in this country and in Europe, and it is perhaps distantly related to the hemianæsthesia of hysteria. Local disorders of the sensibility in the neuralgic area are far more common than this, and, in fact, are usually present in some degree. The skin is at first hyperæsthetic, but becomes after a time anæsthetic; and this anæsthesia offers several interesting peculiarities. When this loss of sensibility is well marked, areas within which the anæsthesia is found are apt to be sharply defined, but they may be either of large size or so small as only to be discovered by careful searching (Hubert-Valleroux). The sensibility within these areas may be almost wanting, but in spite of this fact it can often be restored by cutaneous faradization around their margins, and the functional or neurosal origin of the anæsthesia is thus made apparent. Where the anæsthesia is due, as sometimes happens, to the neuritis with which the neuralgia is so often complicated, it is more lasting, but usually less profound and less sharply defined.