Chapter LXXVIII: Introduction: This disease remained unnoticed until twenty years ago, (2)

If the continuity of the fibres of a mixed nerve be destroyed at some point in its course by cutting, bruising, pressure, traction, the application of cold, the invasion of neighboring disease, etc., there will be an immediate loss of the functions dependent on the nerve in the parts to which it is distributed. The muscles which are supplied by its motor fibres are paralyzed; they no longer respond by contraction to the impulse of the will. No reflex movements can be excited in them either from the skin or the tendons. They lose their tonicity, which they derive from the spinal cord, and are relaxed, soft, and flabby. As the interrupted sensory fibres can no longer convey impressions to the brain, we might naturally look for an anæsthesia, a paralysis of sensation, in the parts to which they are distributed, as complete as is the loss of function in the muscles. Such, however, is not the fact. Long ago cases were observed in which, although sensitive nerves were divided, the region of their distribution retained more or less sensation, or seemed to recover it so {1183} quickly that an explanation was sought in a supposed rapid reunion of the cut fibres. Recent investigations, moreover, show that in a large number of cases where there is complete interruption of continuity in a mixed nerve the region to which its sensitive fibres are distributed retains, or rapidly regains, a certain amount of sensation, and that absolute anæsthesia is confined to a comparatively small area, while around this area there is a zone in which the sensations of pain, touch, and heat are retained, though in a degree far below the normal condition; in short, that there is not an accurate correspondence between the area of anæsthesia consequent upon cutting a sensitive nerve and the recognized anatomical distribution of its fibres. We find the explanation of this partly in the abnormal distribution of nerves, but principally in the fact of the frequent anastomoses of sensitive nerves, especially toward their peripheral distribution, thus securing for the parts to which the cut nerve is distributed a limited supply of sensitive fibres from neighboring nerves which have joined the trunk below the point of section. This seems proved not only by direct anatomical investigation, but also from the fact that the peripheral portion of the divided nerve may be sensitive upon pressure, and that the microscope shows normal fibres in it after a time has elapsed sufficiently long to allow all the divided fibres to degenerate, in accordance with the Wallerian law. Some of the sensation apparently retained in parts the sensitive nerve of which has been divided may be due to the excitation of the nerves in the adjacent uninjured parts, caused by the vibration or jar propagated to them by the mechanical means used to test sensation, as tapping, rubbing, stroking, etc.[3] It is to be observed that this retained sensation after the division of nerves exists in different degrees in different regions of the body; thus it is greatest in the hands, least in the face.

[Footnote 3: Létiévant, _Traité des Sections nerveuses_.]

As the vaso-motor and trophic nerve-fibres run in the trunks of the cerebro-spinal nerves, destructive lesions of these trunks cut off the influence of the centres with which those fibres are connected, and hence they are followed by changes in the circulation, calorification, and nutrition of the parts to which they are distributed. Thus, the loss of the vaso-motor influence is at first shown in the dilation of the vessels and the unvarying warmth and[4] congestion of the part.[5] This gives way in time to coldness, due to sluggish circulation and diminished nutritive activity. Marked trophic changes occur in the paralyzed muscles. They atrophy, their fibres becoming smaller and losing the striations, while the interstitial areolar tissues proliferates, and finally contracts cicatricially. The skin is sometimes affected in its nutrition, becoming rough and scaly. Other trophic changes of the skin resembling those produced by irritation of a nerve are very rarely seen, and they may probably be referred to irritation of fibres with which the part is supplied from neighboring trunks.

[Footnote 4: A remarkable exception is seen, however, in the effect of gradual pressure experimentally applied to nerve-trunks until there is complete interruption of sensation and motion, in which case the temperature invariably falls.]

[Footnote 5: In a case of gunshot wound that came under the writer's care in 1862, the leg and foot, which were paralyzed from lesion of the popliteal nerve, remained warm and natural in color during repeated malarial chills, which caused coldness and pallor of the rest of the body.]

{1184} Anatomical Changes in the Divided Nerve and Muscles.—The peripheral portion of a divided nerve separated from its nutritive centres degenerates and loses its characteristic appearance, looking to the naked eye like a grayish cord, and being shrunken to one-fourth of its natural size. The changes which take place in the degeneration of the nerve-fibres, and which proceed from the point of lesion toward the periphery, are, first, an alteration of the white substance of Schwann, which breaks into fragments, these melting into drops of myeline, and finally becoming reduced to a granular mass. The central axis at a later period likewise breaks up, and is lost in the granular contents of the sheath of Schwann. Meanwhile, absorption of the débris of the fibres goes on, until, finally, there remains but the empty and collapsed sheath of Schwann with its nuclei, the whole presenting a fibrous appearance. When this has taken place the degenerated motor nerve-fibres can no longer be excited, and no stimulation applied to them can cause the muscles to contract. At the same time, the muscles atrophy and undergo degenerative changes in their tissue. The fibres become smaller and their transverse striæ indistinct, with the appearance of fatty degeneration, and finally there is proliferation of the interstitial cellular tissue. They do not, however, lose their contractility, and upon a mechanical stimulus being applied directly to them they contract in a degree that is even exaggerated, but with a slowness that is abnormal. If, now, we apply the stimulus of electricity to the muscles themselves, we encounter phenomena of the greatest interest and importance. The application of the faradic current, however strong, elicits no contraction; there is loss of faradic excitability. But if the galvanic current be applied the muscles contract, and that, too, in reply to a current too weak to excite healthy muscles to action; there is increased galvanic excitability. The kind of contraction thus induced is peculiar, differing from that ordinarily seen in muscles. Instead of its being short, and immediately followed by relaxation, as when we make or break the galvanic current in healthy muscles, it is sluggish, long-drawn out, and almost peristaltic in appearance. This is characteristic of degenerated muscles, and is the degenerative reaction. But there is also a change in the manner in which the degenerated muscles reply to the two poles of the galvanic current. Instead of the strongest contraction being elicited, as in the normal condition, by the application of the negative pole to the muscle (C. C. C., cathode closing contraction), an equally strong or stronger is obtained by the application of the positive pole (A. C. C., anode closing contraction), while the contraction normally caused on opening the circuit by removal of the positive pole (A. O. C., anode opening contraction) becomes weaker and weaker, until it is at last exceeded by the contraction upon opening the current by the removal of the negative pole (C. O. C., cathode opening contractions). In short, the formula for the reply of the healthy muscles to galvanic excitation is reversed; there is a qualitative galvanic change in the paralyzed and degenerated muscles.

If no regeneration of the nerve takes place, the reaction of the muscles to the galvanic current is finally lost, and they exhibit those rigid contractions which probably result from a sclerotic condition of the intramuscular areolar tissue.

After complete destruction of the fibres of a nerve at some point of its {1185} course, even when a considerable length of it is involved, and after the consequent degeneration of the peripheral portion has taken place, we have, with lapse of time, restoration of its function, consequent upon its regeneration and the re-establishment of its continuity. The histological changes by which the degenerated fibres are restored and the divided ends reunited have not been made out with such certainty as to preclude difference of opinion as to the details. But the process in general seems to be a proliferation of the nuclei in the sheath of Schwann, with increase of the protoplasm which surrounds them, filling the sheath of Schwann with the material from which the new fibre originates. In this mass within the sheath is formed first the central axis of the new fibre, which is later surrounded by the white substance of Schwann. With the regeneration of the nerve-fibres the functions of the nerve return, but in the order of sensation first, and afterward the power of transmitting the volitional impulse to the muscles. Even after regeneration has so far advanced that the muscles may be made to contract by an exercise of the will, the newly-formed fibres fail to respond to other stimuli; thus, the faradic current applied to the nerve does not cause the muscles to contract; the stimulation is not transmitted along the imperfectly restored fibres.

It may be here remarked that after regeneration has restored the functions of a divided nerve the muscles to which it is distributed may still exhibit for a time the degenerative reaction in consequence of unrepaired changes in themselves. In the end we may look for complete restoration in both nerve and muscles.

The time required for the regeneration and reunion of a divided nerve depends somewhat upon the manner in which the destruction has been caused. Thus, a nerve which has been divided by a clean cut, and where the cut ends remain in apposition or close proximity, unites much more readily than one in which bruising, tearing, or pressure has destroyed an appreciable length of its fibres or the divided ends have been thrust apart.

In complete division of a nerve we must not look for regeneration and restoration of its functions, even in favorable circumstances, before the lapse of several months, although cases have been recorded where the process has been much more rapid.

Injuries of mixed nerves, with incomplete destruction of the fibres, give rise to many and varied symptoms, some of which are the direct result of the injury—many others of subsequent changes of an inflammatory character (neuritis) in the nerves or in the parts to which they are distributed. Pain is one of the most prominent symptoms immediately resulting from nerve-injury, although as a rule it soon subsides. There is sometimes merely numbness or tingling, or there may be no disturbance of sensation at the moment of injury. Rarely is spasm of muscles an immediate effect. Generally, motion is at first very much impaired, but if the injury is not grave enough to cause a lasting paralysis, the muscles may rapidly regain their activity. In observing the effects of injuries of mixed nerves one remarkable fact strikes us: it is the very much greater liability of the motor fibres to suffer loss or impairment of function. Thus, it is common to see sensation but little or only transiently affected by injuries which cause marked paralysis of muscles. {1186} So in the progress of recovery the sensory disturbances usually disappear long before restoration of the motor function; indeed, sensation may be entirely restored while the muscular paralysis remains permanent. Direct experimental lesions of the mixed nerve-trunks of animals give the same result.[6] For this immunity of the sensitive nerve-fibres no explanation can be given other than an assumed difference in their inherent endowments.

[Footnote 6: Luderitz, _Zeitschrift für klin. Med._, 1881.]

According to the amount of damage the nerve has sustained will there remain after the immediate effects of the injury have passed off more or less of the symptoms already described as due to loss of conductivity in the fibres—viz. paralysis of motion, and anæsthesia. Sometimes the impairment of conductivity in the sensitive fibres shows itself by an appreciable time required for the reception of impressions transmitted through them, giving rise to the remarkable phenomenon of delayed sensation. Degeneration of the nerve peripherally from the point of lesion, and consequently of the muscles, will likewise take place in a greater or less degree, according to the amount of the injury and the subsequent morbid changes, and give rise to the degenerative reaction which has been already described. We will not, however, always encounter the degenerative reaction in the typical form which presents itself after the complete division of nerves. Many variations from it have been observed; as, for instance, Erb's middle form of degenerative reaction, in which the nerve does not lose the power of replying to the faradic or galvanic current, but the muscles show both the loss of the faradic with increased galvanic excitability, with also the qualitative change in regard to the poles of the galvanic current. Such irregularities may be explained by the supposition of an unequal condition of degeneration in the nerve and the muscles. A rare modification has been recorded which has once come under the writer's observation, in which the muscles reply with the sluggish contraction characteristic of the degenerative reaction to the application of the faradic current.

A highly important class of symptoms arise later in injuries of nerves, due not so much to a loss as to an exaggeration or perversion of their functions: they are the result of molecular changes in the nerves, giving rise to the condition called irritation. Irritation of motor nerves shows itself in muscular spasm, or contractions of a tonic or clonic character, or in tremor. If the sensitive fibres are irritated by an injury or the subsequent changes in the nerve resulting from it, we may have hyperæsthesia of the skin, in which, although the sense of touch may be blunted, the common sensation is exaggerated, it may be, to such a degree that the slightest contact with the affected part gives rise to pain or to an indescribable sensation of uneasiness almost emotional in its character—something of the nature of the sensation of the teeth being on edge. There may be hyperæsthesia of the muscles, shown by a sensitiveness upon deep pressure, in which the skin has no part. Pain, spontaneous in its character, is a very constant result of nerve-irritation, whether caused by gross mechanical interference or by the subtler processes of inflammation in the nerve-tissue. It is generally felt in the distribution of the branches of the nerve peripheral to the point of lesion, although it is occasionally located at the seat of the injury. Neuralgias are a common result of the irritation of nerves from injuries.

{1187} Causalgia, a burning pain, differing from neuralgia, and sometimes of extreme severity, is very frequent after injuries of nerves, especially in parts where the skin has undergone certain trophic changes (glossy skin). A number of abnormal sensations (paræsthesiæ) result from the irritation of sensitive fibres, and are common after nerve injuries. Among these we may mention a sensation of heat (not the burning pain of causalgia) in the region of the distribution of the nerve, which does not coincide with the actual temperature of the part; it occurs not unfrequently after injury to a nerve-trunk, and may be of value in diagnosis.

The effect of irritative lesions of mixed nerves upon nutrition is very marked, and sometimes gives rise to grave complications and disastrous results. Any or all of the tissues of the part to which the injured nerve is distributed may be the seat of morbid nutritive changes.

In the skin we may have herpetic or eczematous eruptions or ulcerations. It may become atrophied, thin, shining, and, as it were, stretched tightly over the parts it covers, its low nutrition showing itself in the readiness with which it ulcerates from trifling injuries. This condition, called glossy skin, usually appears about the hands or feet, and is very frequently associated with causalgia. The hair may drop off, or, as has been occasionally seen, be increased in amount and coarsened, and the nails become thickened, crumpled, and distorted.

The subcutaneous cellulo-adipose tissue sometimes becomes œdematous, sometimes atrophies, and rarely has been known to become hypertrophied. The bones and joints, finally, may, under the influence of nerve-irritation, undergo nutritive changes, terminating in various deformities.

With regard to the trophic changes, as well as to the pain and paræsthesiæ resulting from nerve-injury, we must bear in mind that they may be attributed not only to the direct irritation of trophic and sensitive fibres in the injured nerve, but also, in part, to influences reflected from abnormally excited nutritive centres in the spinal cord, and to the spread of the sensitive irritation conveyed to the brain by the injured fibres to neighboring sensitive centres, thus multiplying and exaggerating the effect, causing, as it were, sensitive echoes and reverberations. Indeed, the variety of the symptoms resulting from apparently similar nerve lesions would seem to point to the introduction of other factors in their causation than the simple injuries of the nerve-fibres themselves.

DIAGNOSIS OF NERVE INJURIES.—Although in the great majority of cases the circumstances attending nerve injuries render their diagnosis a matter of little difficulty, it is yet important to keep in mind those symptoms which distinguish them from lesions or diseases of the brain and spinal cord, inasmuch as in cases of multiple lesion, injuries to the spinal column, or where the history of the case is imperfect, it may be difficult to determine to which part of the nervous system, peripheral or central, some of the gravest resulting troubles are due. Paralysis, spasm, anæsthesia, atrophy, etc. may be of central or spinal as well as peripheral origin, and an intelligent prognosis and rational treatment alike demand that we should distinguish between them. Moreover, many diseased conditions of the peripheral nerves of whose pathology we are ignorant, and in which localizing symptoms—_i.e._ those indicating the exact point at which the nerve is implicated—are wanting, can only be distinguished as peripheral affections by the occurrence of symptoms which we {1188} recognize as identical with those arising from injuries of nerves, in which definite histological changes are known to occur. Indeed, cases of disease of the nervous system are not infrequent in which a careful study of their symptomatology leads to a difference of opinion in the minds of the best observers as to whether their seat is central or peripheral. We will notice here some of the prominent symptoms resulting from nerve injuries which may be useful in distinguishing peripheral from central lesions, although in many cases it is only by the careful consideration of all symptoms and the impartial weighing of all attending circumstances that a probable conclusion can be arrived at.

The rapid loss of muscular tone and the early atrophy of the muscles is a mark of paralysis from nerve-injury which distinguishes it from cerebral paralysis, even when the latter occupies circumscribed areas, as is sometimes the case in cortical brain lesion. In spinal paralysis also the muscles retain their tone and volume (the latter being slightly diminished by disuse), except in extensive destruction of gray matter, when all tonicity is lost, and in lesions of the anterior horns of gray matter (poliomyelitis), when there is loss of muscular tone and marked atrophy. The first of these spinal affections may be distinguished by the profound anæsthesia and by the paralysis being bilateral—by the implication of bladder and rectum and the tendency to the formation of bed-sores; such symptoms being only possible from nerve-injury when the cauda equina is involved. In poliomyelitis the complete integrity of sensation—which is almost always interfered with at some period after nerve-injury—and the history of previous constitutional disturbance will aid us in recognizing the diseased condition. While the reflexes are wanting in peripheral, they are, as a rule, retained, and often exaggerated, in cerebral and spinal paralysis; the exceptions being in the two lesions of the cord above mentioned, in which the reflex arc is of course destroyed by the implication of the gray matter. Loss or alteration of sensation, where it occurs from nerve-injury, generally shows itself in the distribution of the nerve, while the sensitive disturbances from disease or injury of the brain or spinal cord are less strictly confined to special nerve territories. The trophic disturbances arising from nerve-irritation are distinctively characteristic of nerve-injury.

But it is in the behavior of the nerves and muscles to electricity that we find some of the strongest points on which to base a diagnosis of nerve-injury, and, although not always conclusive as to the seat of lesion, it enables us to reduce within very narrow limits the field for discrimination. The degenerative reaction which we have seen takes place in muscles the continuity of whose nerves have been destroyed, or in which degenerative changes have taken place in consequence of injury to their nerves, is never found in muscles paralyzed from the brain. In spinal paralysis resulting from transverse myelitis the electrical excitability of the nerves and muscles may be increased or diminished, but there is no degenerative reaction. In progressive muscular atrophy a careful electrical examination may discover the degenerative reaction in the affected muscles; but it is too obscure, and there are besides too many characteristic symptoms in that disease, to allow of a practical difficulty in diagnosis from its presence. In poliomyelitis anterior (infantile paralysis and the kindred affection in the adult) we have, it is true, the quantitative, {1189} qualitative changes of degenerative reaction, such as are seen after nerve-injury, and in such cases its presence is not conclusive of peripheral lesion. Here we may be assisted by remembering that while in poliomyelitis sensation is intact, in nerve-injury it is almost always affected in a greater or less degree, although it may have been recognizable but for a short time. In lead paralysis we also have the degenerative reaction, but whether the seat of lesion in that affection is central or peripheral is an undecided question.

TREATMENT OF NERVE-INJURIES.—The therapeutics of nerve-injuries belong largely to surgery. When there is complete division of a nerve the ends should be united by suture at the time of injury. When this has not been done, and after the lapse of time no return of function is observed, the ends of the nerve should be sought for, refreshed with the knife, and brought together by suture. There is the more hope that such a procedure will be successful as we know that after a time the fibres of the peripheral portion of the nerve may be regenerated, even when there has been no reunion, and thus be in a condition to render the operation successful. It is a matter for consideration whether in injuries in which a certain portion of the nerve, not too great in extent, has been crushed or otherwise obviously destroyed, it would not be best to excise the destroyed portion and bring the ends together. Whether the use of electricity, the galvanic current, hastens the regeneration and restitution of the injured nerves cannot be affirmed with certainty, although in practice this has seemed to us to be the case, and the known catalytic action of the current gives us a possible explanation of such beneficial effects. But, however this may be, it is certain that with the first symptoms of returning function in the nerves and muscles the use of electricity obviously accelerates the improvement. And, again, in the treatment of the results of nerve-injury, such as paralysis, anæsthesia, pain, it is in the careful and very patient use of the electric currents, both faradic and galvanic, that most confidence is to be placed; the galvanic being generally most applicable and giving the better results. The symptoms of nerve-irritation are amongst those most difficult to treat successfully. Counter-irritation, heat, cold, electricity, may all be tried in vain, and as a last resource against pain, ulceration, and perverted nutrition we may be obliged to resort to nerve-stretching, or neurotomy. Under the head of Neuritis much must be said of treatment applicable to the inflammation, acute and chronic, resulting from nerve-injuries.

INFLAMMATION OF NERVES.

Neuritis.

Although inflammation of the nerves has been for a long time a recognized disease, its frequency and the extent and importance of its results have been appreciated only within a comparatively short time. The observations upon neuritis were formerly almost exclusively confined {1190} to acute cases, the results of traumatic lesions or the invasion of neighboring disease, while the more obscure forms occurring from cold, toxic substances in the circulation, constitutional disease, etc., or those apparently of spontaneous origin, escaped attention, or were classed according to their symptoms simply as neurosis, functional disease of the nerves, or affections of the spinal cord. Hence the classic picture of neuritis is made to resemble exclusively the acute inflammation of other tissues, and tends to blind as to the subtler but not less important morbid processes in the nerves which at present we must classify as inflammation, though wanting, it may be, in some of the striking features seen in connection with inflammatory processes elsewhere. In short, we must not look for heat, redness, pain, and swelling as absolutely necessary to a neuritis.

Entering into the structure of the peripheral nerves we have the true nervous constituent, the fibres, and the non-nervous constituent, the peri- and endoneurium, in which are found the blood-vessels and lymph-channels. Though intimately combined, these tissues, absolutely distinct structurally and functionally, may be separately invaded by disease; and although it may not be practicable nor essential in every case to decide if we have to do with a parenchymatous or interstitial (peri-) neuritis, it is necessary to keep in mind how much the picture of disease may be modified according as one or the other of the constituents of the nerve are separately or predominantly involved. Thus, a different group of symptoms will be seen when the vascular peri- and endoneurium is the seat of inflammation from that which appears when the non-vascular nerve-fibres are themselves primarily attacked and succumb to the inflammatory process with simple degeneration of their tissue. Furthermore, it is not too speculative to consider that the different kinds of nerve-fibres may be liable separately or in different degrees to morbid conditions, so that when mixed nerves are the seat of neuritis, motor, sensitive, or trophic symptoms may have a different prominence in different cases in proportion as one or other kind of fibres is most affected.

ETIOLOGY.—Traumatic and mechanical injuries of nerves are the most common and best understood causes of neuritis. Not only may it be occasioned by wounds, blows, compression, and other insults to the nerves themselves, but jolting and concussion of the body, and even sudden and severe muscular exertion, have been recorded as giving rise to it. We readily understand how neuritis is caused by the nerves becoming involved in an inflammation extending to them from adjacent parts, although the nerves in many instances show a remarkable resistance to surrounding disease. Less easily understood but undoubted causes of neuritis are to be found in the influence of cold, especially when the body is subjected to it after violent exertion. Although the causal connection is unexplained, we find neuritis a frequent sequel of acute diseases, as typhoid fever, diphtheria, smallpox, etc. In the course of many chronic constitutional affections, as syphilis, gout, elephantiasis græcorum, we encounter neuritis so frequently as to make us look for its cause in these diseases. Finally, neuritis may develop apparently spontaneously in one or many nerves.

MORBID ANATOMY.—The macroscopic appearance of nerves affected by neuritis is very varied, according as the disease is more interstitial or parenchymatous, acute or chronic. Sometimes the nerve is swollen, red, {1191} or livid, the blood-vessels distended, with here and there points of hemorrhage, the glistening white of the fibres being changed to a dull gray. Sometimes the nerves are reduced to gray shrunken cords. When the perineurium has been the principal seat of the inflammation we may have swellings at intervals along the course of the nerve (neuritis nodosa, perineuritis nodosa acuta) or, as in chronic neuritis, the trunk of the nerve may be hard and thickened from proliferation of the connective tissue, sclerosis of the nerve. The nerve does not always present the appearance of continuous inflammation, but the evidence of neuritis may be seen at points along its course which are separated by sound tissue. These points of predilection are usually exposed positions of the nerve or near joints. Often the nerve appears to the naked eye normal, and the characteristic changes of neuritis are only revealed by the microscope. The microscopical changes in neuritis may extend to all of the constituents of the nerve, and present the ordinary picture of acute inflammation, hyperæmia, exudation, accumulation of white corpuscles in the tissues, and even the formation of pus, the nerve-fibres exhibiting in various degrees the destruction of the white substance of Schwann and the axis-cylinder. Or, as in chronic neuritis, the alterations may consist in the more gradual proliferation of the peri- and endoneurium, which, contracting, renders the nerve dense and hard and destroys the nerve-fibres by compression. In acute as well as in chronic neuritis the perineurium may be exclusively affected, the fibres remaining normal (Curschman and Eisenlohr). The nerve-fibres themselves may be the primary and almost exclusive seat of the neuritis, exhibiting more or less complete destruction of all their constituent parts, except the sheath of Schwann, without hyperæmia and with little or no alteration of the interstitial tissue. Sometimes the fibres are affected at intervals, the degeneration occupying a segment between two of Ranvier's nodes, leaving the fibre above and below normal (nèvrite segmentaire peri-axile, Gombault). All of these lesions of the nerve-fibres may be recovered from by a process of regeneration, the fibres showing a remarkable tendency to recover their normal structure and function.

SYMPTOMS OF NEURITIS.—When a mixed nerve is the seat of an acute neuritis, with hyperæmia of its blood-vessels, it becomes swollen by inflammatory exudation, and can be felt as a hard cord amongst the surrounding tissues. It is not only highly sensitive to direct pressure, but muscular exertion, or even passive movement of the part, excites pain. Spontaneous pain is one of the most prominent symptoms, and is sometimes so severe and continuous as to destroy the self-control of the patient, and demand the employment of every agent we possess for benumbing sensibility and quieting the excited system. At first there may be hyperæsthesia of the skin in the region of the distribution of the nerve, but a much more constant and significant symptom is cutaneous anæsthesia, which generally makes its appearance early in the course of the disease. The degree and extent of the anæsthesia varies very much in different cases, but is seldom total, except over small areas, even when the inflammation has seriously damaged the nerve-fibres. This is explained by the sensibility supplied to the part by neighboring nerves, as already described in treating of traumatic nerve-injuries. Very characteristic of acute neuritis are various abnormal sensations (paræsthesiæ) which are {1192} developed in a greater or less degree during the progress of the disease, and are described by the patients as numbness, tingling, pins and needles, burning, etc. In a case of acute neuritis of the ulnar nerve seen by the writer the patient was much annoyed by a persistent sensation of coldness in the little and ring fingers, which caused him to keep them heavily wrapped up even in the warm weather of summer. When motor symptoms make their appearance they begin with paresis of the muscles, which may increase rapidly to paralysis. As this is the result of destructive changes, more or less complete, in the motor nerve-fibres, we will have, as would be expected, accompanying the paralysis the symptoms already detailed in the consideration of nerve-injuries with destruction of continuity—namely, absence of muscular tone, loss of skin and tendon reflexes, increased mechanical excitability, atrophy of muscles, and the different forms of degenerative reaction, with loss of faradic contractility. When spasm or tremor has been observed in acute neuritis of mixed nerves, it is a matter of doubt whether it is not to be explained by reflex action of the cord excited by irritated centripetal fibres. Various trophic symptoms may show themselves, as herpes zoster or acute œdema. Erythematous streaks and patches are sometimes observed upon the skin along the course of the inflamed nerve-trunks. In chronic neuritis, into which acute neuritis generally subsides or which arises spontaneously, the symptoms above described are very much modified; indeed, cases occur which exist for a long time almost without symptoms. While the affected nerve may be hard and thickened by proliferation of its connective tissue, pain, spontaneous or elicited by pressure, is not of the aggravated character present in acute neuritis, and may be quite a subordinate symptom. It has more of a rheumatic character, is less distinctly localized, more paroxysmal, and has a greater tendency to radiate to other nerves. It is probable that many ill-defined, so-called rheumatic pains which are so frequently complained of are the result of obscure chronic neuritis. Anæsthesia and various paræsthesiæ are often more prominent symptoms than pain. Sometimes there is a hyperæsthesic condition of the skin, in which touching or stroking the affected part causes a peculiarly disagreeable nervous thrill, from which the patient shrinks, but which, however, is not described as pain.

The motor symptoms in chronic neuritis of mixed nerves often remain for a remarkably long time in abeyance or may be altogether wanting. They may appear as tremor, spasm, or contraction, these, however, being probably reflex phenomena. Most commonly there is paresis, which may deepen into paralysis with atrophy of muscles and degenerative reaction. The trophic changes dependent on chronic neuritis are frequently very prominent and important. The skin sometimes becomes rough and scaly, sometimes atrophied, smooth, and shining (glossy skin). Œdema of the subcutaneous cellular tissue is often seen, for example, on the dorsum of the hand, where it may be very marked. The hair of the affected part shows sometimes increased growth, sometimes it falls off. The nails may become thickened, ridged, and distorted. Deformity of joints with enlargement of the ends of the bones is not infrequently met with as the result of chronic neuritis. In short, we may meet with all of those trophic changes which have been described as arising from nerve-irritation, and which occur in chronic neuritis as the result of compression of {1193} nerve-fibres by the contraction of the proliferated connective tissue in the nerve-trunk.

The symptom-complex varies greatly in neuritis, so that there is hardly a symptom which may not be greatly modified or even wanting in some cases—a fact, which, as we have already said, may be explained by the morbid process fixing itself exclusively or in different degrees upon one or other of the component parts of the nerve-trunk, or, it may be, upon fibres of different functional endowment. Thus pain, usually one of the most prominent symptoms of neuritis, may be quite subordinate, or even absent, in cases of neuritis acute in invasion and progress. In a case of neuritis of the ulnar nerve seen by the writer, beginning suddenly with numbness and paresis, and rapidly developing paralysis, atrophy of muscles, loss of faradic contractility, with degenerative reaction, there was no pain during the disease, which ended in recovery.[7] On the other hand, in mixed nerves the sensitive fibres may be long affected, giving rise to pain and various paræsthesiæ before the motor fibres are implicated, or these last may escape altogether.

[Footnote 7: “Two Cases of Neuritis of the Ulnar Nerve,” _Maryland Medical Journal_, Sept., 1881.]

The swollen condition of the nerve, so characteristic in many cases of neuritis where the perineurium is the seat of a hyperæmia, is wanting in cases where the stress of the attack is upon the nerve-fibres themselves. Again, the trophic changes induced in the tissues by a neuritis may predominate greatly over the sensitive or motor alterations. Thus, in the majority of cases in which herpes zoster occurs it is without pain or paræsthesia. Indeed, in chronic neuritis the symptoms show such variations in different cases that it is difficult to give a general picture of the disease sufficiently comprehensive and at the same time distinctive. The prognosis in acute neuritis is generally favorable, although it must depend in a great measure upon the persistence of the cause producing it. Thus, if it has been excited by the inflammation of neighboring organs it cannot be expected to disappear while these continue in their diseased condition. In other cases the symptoms may subside with comparative rapidity; and so great is the capacity of the nerve-fibres for regeneration that recovery may be complete and nothing remain to indicate the previous inflammation. The nerve, however, that has once suffered from neuritis shows for a long time a tendency to take on an inflammatory action from slight exciting causes. If there has resulted an atrophy of muscles, we must expect some time to elapse before they recover their functional activity and normal electric reaction.

Acute neuritis most frequently passes into the chronic form, and it may then drag on indefinitely, stubbornly resisting treatment and giving rise to permanent derangement of sensibility, loss of muscular power, or perverted nutrition. Neuritis shows a tendency to spread along the affected nerve centripetally, sometimes reaching the spinal cord, and, as it has appeared in some cases, even the brain, causing tetanus or epilepsy.

Reflex paralyses, which at one time were believed to be the not infrequent result of nerve-irritation and inflammation, affecting from a distance the functions of the spinal cord, have been shown to be the effect of an extension of the lesion of the inflamed nerve to the cord, causing organic disease. Instances of the extension of a neuritis to distant nerves, as those of an opposite extremity, without the implication of the spinal {1194} cord (neuritis sympathica), are most probably cases of multiple neuritis, to be considered farther on.

The DIAGNOSIS of cases of traumatic neuritis can scarcely present a difficulty. Acute neuritis with spontaneous pain, swelling, and tenderness of the nerve, presents distinctive features hardly to be confounded with any other affection, although thrombosis of certain veins, as the saphenous, may present some of its symptoms. To distinguish chronic neuritis or the cases wanting those obvious symptoms just indicated (many cases of sciatica) from neuralgia is a more difficult task. The following distinctive points may be noted: In neuritis the persistent and continuous character of the pain helps us to distinguish it from the more paroxysmal exacerbations of neuralgia, and its tendency, often seen, to spread centripetally spontaneously or when pressure is made on the nerve, may be also considered as characteristic of neuritis. Cutaneous anæsthesia, paresis, and atrophy of muscles are distinctive in any case of a neuritis rather than a neuralgia. Herpes zoster and other trophic changes speak strongly for a neuritis.

In the TREATMENT of neuritis the first indication is to get rid, as far as possible, of such conditions as may cause or keep up the inflammation, as, for instance, the proper treatment of wounds, the removal of foreign bodies, the adjustment of fractures, the reduction of dislocations, the extirpation of tumors, etc. Absolute repose of the affected part in the position of greatest relaxation and rest is to be scrupulously enforced. In acute neuritis local abstraction of blood by leeches and cups in the beginning of the affection is of the greatest advantage and should be freely employed. The application of heat along the course of the inflamed nerve has appeared to us preferable to the use of ice, although this also may be employed with excellent effect. The agonizing pain must be relieved by narcotics, and the hypodermic injection of morphia is the most efficient mode of exhibition. Salicylic acid or salicylate of sodium in large doses contributes to control the pain. Iodide of potassium in large doses appears to act beneficially, even in cases with no syphilitic complications. In subacute or chronic neuritis local bloodletting is not as imperatively demanded as in the acute form, although it is sometimes useful. Here counter-irritation in its various forms and degrees, even to the actual cautery, is to be recommended. An excellent counter-irritation is produced by the application of the faradic current with the metallic brush. It appears from general experience that the counter-irritation has the best effect when applied at a little distance from the inflamed nerve, and not directly over its course. In the galvanic current we possess one of the very best means not only for relieving the symptoms of chronic neuritis, but for modifying the morbid processes in the nerve and bringing about a restoration to the healthy condition. Its application is best made by placing the anode or positive pole as near as possible to the seat of the disease, while the cathode or negative pole is fixed upon an indifferent spot at a convenient distance. The positive pole may be held stationary or slowly stroked along the nerve. Finally, in protracted cases nerve-stretching may be resorted to with great benefit. It probably owes its good effects to the breaking up of minute adhesions which have formed between the sheath of the nerve and the surrounding tissues, and which act as sources of irritation.

{1195} Multiple Neuritis, Multiple Degenerative Neuritis, Polyneuritis.

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 as {1196} invariably 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.[8] There 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 of {1197} a 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.

[Footnote 8: Gombault'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.

The DIAGNOSIS of 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 symptomatology {1198} of 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.

The PROGNOSIS of 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.