Cases of this important form of neuritis have been observed and recorded since 1864, but the resemblance of its symptoms to those of certain diseases of the central nervous system (poliomyelitis, Landry's paralysis, etc.) has prevented its general recognition, and it is only within the last few years that its distinctive pathological lesions have been demonstrated and its diagnosis made with considerable certainty. We can hardly overrate the importance of this in view of the great difference in gravity of prognosis between it and other diseases with which it may be confounded.
Multiple neuritis consists in a simultaneous or more or less rapidly succeeding inflammation of several or many usually bilaterally situated nerves, with a greatly preponderating, almost exclusive, lesion of the motor fibres. Commonly the disease attacks the lower extremities and progresses upward, although occasionally it has been seen to begin in the arms. It does not confine itself to the nerves of the extremities and trunk, but often involves the phrenics, causing paralysis of the diaphragm, and frequently invades one or more of the cranial nerves, notably the vagus, thus giving rise to the rapid heart-beat so often seen in the disease. In the cases of multiple neuritis observed the muscles of deglutition have never been paralyzed. The sphincter ani and bladder have likewise escaped. All degrees of acuteness are observed in the course it runs, from the cases terminating rapidly in death to those in which the disease extends over months, slowly involving nerve after nerve, until nearly all of the muscles of the body are paralyzed, when death may result or a more or less complete recovery take place. The invasion of the disease is in most cases sudden, even when its subsequent course is chronic, and is often marked by decided constitutional disturbance, as rigors, fever, delirium, albuminuria, etc. Disturbances of sensation are prominent among the initial symptoms, and are of great importance for the diagnosis of the disease. Severe, spontaneous, paroxysmal pain of a shooting, tearing character has ushered in most of the cases on record, remitting, however, during their progress. Pain is not always present, nevertheless, and cases not infrequently occur which run a painless course. In some cases which have come under the writer's notice spontaneous pain did not occur until some days after the disease was fully declared by other symptoms. More constantly present, and more characteristic of multiple neuritis, are the disturbances of sensation which show themselves in subjective feelings of numbness, tingling, pins and needles, coldness, burning, and other paræsthesiæ, which appear at its outset and continue to be present more or less during its course. Anæsthesia, not of a high degree nor at all coextensive with the paralysis of the muscles—sometimes, indeed, confined to very circumscribed areas—may be said to exist always in multiple neuritis—a fact of great diagnostic value. Hyperæsthesia of the skin is frequently seen. Hyperalgesia and analgesia are sometimes observed. Hyperæsthesia of the muscles is a very marked symptom in almost every case, and shows itself not only upon direct pressure being made, but also in the pain elicited by passive movements of the parts affected. Pressure upon nerve-trunks does not cause pain asinvariably as might have been expected from the location of the disease. Delayed sensation has been frequently observed.
Paresis of muscles, often commencing suddenly, is early seen in multiple neuritis, and increases until there is more or less complete paralysis, the most important feature of the disease. The paralyzed muscles present the flabby condition characteristic of muscles deprived of the tonic influence of the spinal cord. Atrophy, which is not commensurate, however, with the paralysis, soon begins, and may go on to an extreme degree. As the paralysis develops the tendon reflexes are lost, and there may be diminution or loss of the skin reflexes also. The paralyzed muscles lose their faradic contractility, and exhibit diminution of electric excitability to the galvanic current, and, finally, the various forms of degenerative reaction. It is remarkable that neither the impairment of sensation nor the paralysis is, as a rule, strictly confined to the areas of distribution of particular nerves, but is diffused over regions of the body. Thus in the limbs the motor and sensory symptoms are most marked at their extremities, gradually diminishing toward the trunk. In some cases multiple neuritis appears to have occasioned the inco-ordinate movements of locomotor ataxy. In the progress of the disease a rigidity and contracted condition of muscles may be developed, occasioning a fixed flexion of some of the joints. Profuse sweating, œdema of the hands and feet, trophic changes in the skin, mark at times the implication of trophic and vaso-motor nerves. Bed-sores do not occur.
The pathological changes in pure cases of multiple neuritis are found in the nerve-trunks, mainly toward their peripheral terminations, and in their muscular branches, the evidences of disease diminishing toward the larger trunks, the nerve-roots being unaffected and the spinal cord showing no lesions. Sometimes the affected nerves present, even to the naked eye, unmistakable proof of acute inflammation. They are reddened by hyperæmia, swollen by exudation, and small extravasations of blood may be seen among their fibres. The microscope shows congestion of the blood-vessels, exudation of the white corpuscles, even to the formation of pus, alteration of the endo- and perineurium; in short, all the evidence of an interstitial inflammation, the nerve-fibres being comparatively little altered, and suffering, as it were, at second hand. In most of the cases, however, the nerves macroscopically present little or nothing giving indication of disease. The microscopic changes, however, are extensive, and pertain almost exclusively to the nerve-fibres themselves. These are altered and degenerated, giving an appearance almost precisely the same as already described in treating of the changes occurring in nerves separated by injury from the centres—Wallerian degeneration.8There is no hyperæmia, thickening, or change in the endoneurium. So great are these differences in the microscopic appearance of the nerves in different cases of multiple neuritis that objection has been raised to classing the two varieties together, and it has been argued that we cannot with right designate the cases in which hyperæmia and other evidence ofa general inflammation are absent as neuritis. It has been, however, argued—apparently, to the writer, with better reason—that the same morbid influence which at one time affects the blood-vessels, causing their congestion and the passage through their walls of the white corpuscles and the exudation of inflammation, may at another time, by a direct and isolated influence upon the nerve-fibres, cause their degeneration; in other words, that there may be a parenchymatous neuritis, which shall affect only the nerve-fibres. The vastly disproportionate implication of the motor fibres would point to the fact of a selective infection in multiple neuritis of certain fibres, as there is a selective infection in poliomyelitis of the motor cells of the anterior horns of the spinal gray matter.
8Gombault's observations (Arch. de Névrologie, 1880) would seem to show that there is a difference in the lesion of the fibres in neuritis from that in simple Wallerian degeneration, inasmuch as that in the former the first alteration is seen about the nodes of Ranvier, and occurs at points separated from each other by healthy fibre, and also in the more tardy destruction of the axis-cylinder.
ETIOLOGY.—Much in the symptomatology of multiple neuritis, especially of its invasion, strongly urges us to the conclusion that it is a constitutional disease caused by an unknown morbid influence, the stress of which falls upon the nervous system. This view receives strong support from the history of the Japanese kak-ke or Indian beriberi, a disease at times epidemic in those countries, and which has the undoubted symptoms and the characteristic pathological alterations of multiple neuritis. After many acute infectious diseases neuritis of individual nerves is not uncommon, but the distinctive characteristics of multiple neuritis have, so far, been observed almost exclusively after diphtheria, to which it is not infrequently a sequel. It has been observed as the result at least occurring in intimate connection with polyarthritis, and the frequency with which it has occurred in the phthisical is remarkable. There have been not a few cases of multiple neuritis recorded as having been produced by chronic alcohol-poisoning. A well-marked case has come under the writer's observation in which the immediate cause was acute poisoning by arsenious acid, a very large amount having been taken at one dose by mistake. The poison of syphilis has been regarded as standing in a causal relation to multiple neuritis. For the rest, the exciting causes (probably acting in connection with a peculiar condition of the system) have appeared to be exposure to cold, great muscular exertion, direct mechanical injury to the nerves, as the rough jolting of a wagon, or the inflammation of a nerve which has in some unknown way extended to others.
TheDIAGNOSISof multiple neuritis in certain cases presents great difficulty, from the close resemblance of its symptoms to those of poliomyelitis. The prominent symptoms in the muscular system—viz. paralysis, atrophy, the degenerative reaction—are the same in both. It may be remarked, however, that in multiple neuritis the paralysis is more generally diffused over the muscles of the affected limbs, while in poliomyelitis it is more confined to the areas of distribution of particular nerve-branches. Pain is common to the beginning of both diseases, but it generally passes off more quickly and completely in poliomyelitis. The persistent hyperæsthesia of the muscles is wanting in poliomyelitis. But it is in the diminution and alteration of sensation that we have the surest means of distinguishing between the two affections. This symptom seldom or never fails to show itself in multiple neuritis, although its area may be circumscribed and it may be slight in degree, while it certainly makes no part of the symptomatologyof poliomyelitis. It has been asserted that the implication of the cranial nerves so often seen in multiple neuritis never occurs in poliomyelitis. When we consider the intimate connection of the anterior horns of the spinal gray matter with the motor nerve-fibres, it appears highly probable that the same morbid influence may invade both simultaneously or in quick succession, thus producing a complex of symptoms rendering a diagnosis very difficult, and probably giving rise to some confusion in the recorded symptoms of multiple neuritis. From Landry's paralysis multiple neuritis is to be distinguished by the impairment of sensibility, the loss of faradic contractility, and absence of the tendon reflex; from progressive muscular atrophy, by the loss of sensibility and the much more obvious degenerative reaction.
ThePROGNOSISof multiple neuritis is in the great majority of cases not grave, so far as life is concerned, even when there is extensive paralysis. Death may occur early in the acute form of the disease or it may take place at the end of chronic cases. When the disease proves fatal, it is from paralysis of the diaphragm and the other muscles of respiration. Where the paralysis and atrophy have been great, showing profound alteration of the nerves, a long time is required for recovery, and more or less paralysis, contracture, or defective sensibility may permanently remain.
TheTREATMENTconsists, 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.
A prominent and important symptom of the lesion of peripheral nerves is the diminution and loss of cutaneous sensibility. Besides theanæsthesia 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 thespace-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.Loss of some of the forms of sensation, with retention of others—i.e.partial paralysis of sensation—indicate a central origin.
TheTREATMENTof 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.
ThePROGNOSISin 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 soundpterygoid. 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.
TheSYMPTOMSandDIAGNOSISof 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.
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 thelip 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 ofahthe 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 patientcomplains 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 clearestindications 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 TREATMENTof 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 electricitymust 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 aboutthe 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.
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.