Nerves are liable to inflammations from the action of irritants of various sorts. In the causation of such inflammations two distinct categories may be distinguished. We have, in the first place, a group in which a poison is circulating in the blood and affects the nerve stems, and in the second place we have cases in which the lesion is local, being due either to an extension from some existing inflammation or to the direct action on particular nerves of an infective or other agent which produces the inflammation. The former group may be distinguished as toxic, and the latter as localized.
The poison is in solution, and acts on the nerves as a chemical or chemico-vital irritant. It may be a metallic poison, such as lead or arsenic, but is more frequently a toxine resulting from the action of microbes. It may perhaps be permitted to include alcohol in the latter category, as it is the product of the action of vegetable organisms closely allied to the bacteria. In toxic neuritis the irritant, being in solution in the blood, acts on the whole nerves at once, the neuritis is therefore usually multiple and symmetrical. It is, however, to be noted that the various irritants show special elective affinities for particular nerves, this fact being consistent with what is known in general as to the action of poisons.
The various poisons act, for the most part, on the nerve structures proper, and hence these inflammations are mostly parenchymatous. They are characterized by breaking up of the medullary sheaths, and other changes analogous to those described as following division of nerve stems. It is, however, to be noted that, while in the case where a nerve has been divided, all the fibres of the peripheral end suffer a like and simultaneous degeneration, since all of them are alike separated from their trophic centres, it is otherwise in the case we are considering, for it is easy to conceive that all may not be alike vulnerable to the toxic agent, nor simultaneously attacked, so that m such a nerve, fibres may be found side by side in very different states, and illustrative of the various phases of the Wallerian degeneration. The lesion is, in the first instance, limited to portions of the stems affected, but as the result is to interrupt, more or less, the conductivity of the nerves, there may be secondary changes in the peripheral distribution such as ensue on the division of nerves. There is also wasting of muscles in cases where the motor nerves are involved. Several forms of toxic neuritis have been distinguished.
In lead poisoning the -agent attacks particular nerves, and it affects the motor fibres much more than the sensory. The commonest seats of the affection are the nerves of the forearms and hands, and the characteristic symptom is "drop-wrist." This is usually bilateral, but may be more marked on one side than the other. There is a curious omission of the nerve to the supinator longus in the affection. The neuritis is not limited to these nerves, but may affect the nerves of the larynx, the eye, etc. The condition of the nerves is that of parenclvymatous neuritis, with wasting of the muscles.
In arsenical poisoning the affection of the nerves is also localized, but the sensory nerves are more frequently affected along with the motor than in lead poisoning. There is greater variety in the symptoms, and these may also be complicated by the cord being affected.
This includes a considerable number of forms in which an organic poison is present in the blood. Many nerves are affected, and the change is parenchymatous. More or less extensive paralysis with muscular wasting results. In this country the most frequent form is Alcoholic neuritis, and in this form there may be wide-spread lesions affecting many nerves, and leading to extensive paralysis and atrophy of muscles.
The acute specific fevers are sometimes followed by multiple neuritis. It is a rare result in typhoid and typhus fevers, is more frequent in malaria, but is especially common as a result of diphtheria. The neuritis seems to be the consequence of the action of the poison evolved by the infective agent, and not of the latter itself. This is proved, at least in the case of diphtheria, by the fact that the toxine obtained from cultures is capable of inducing the paralysis without the bacteria being present.
The disease known in India as Beri-beri, and in Japan as Kak-ke, is apparently a multiple neuritis, due to a specific infection. It is endemic in certain localities, and particular forms of microbes have been asserted by some authors.
The condition of the spinal cord in cases of neuritis, especially in the toxic forms, has been much discussed, and there are records by Dejerine of changes in the cells of the anterior horns in cases of diphtheritic neuritis examined by him. A like condition has been found in cases of alcoholic neuritis, while atrophy of these cells has been noted also in the forms depending on lead intoxication. Quite recently the question has been again considered by Marinesco and Lugaro, with the aid of Nissl's method of staining, and both have found changes in these cells in such cases.
This is due to an agent acting locally. It may be the result of direct injury to a nerve, as by the broken end of a bone. Cold is also an occasional cause, as in the sciatic nerve. Inflammations may extend by contiguity to a nerve stem, or an infective agent may fix on particular nerves and produce local lesions. Many of these forms are chronic, and these, as in the case of chronic inflammations in general, are characterized by new-formation of connective tissue. The inflammation is in this way interstitial, the perineurium and endoneurium being thickened. There is consequent atrophy of the nerve fibres with the results in the nerves themselves and in the muscles which ensue on division of nerves. Several forms merit a special description.
Acute suppurative inflammations do not readily extend to peripheral nerve stems. A nerve may be bathed in pus, and almost isolated by the suppuration around, but there may be almost no infiltration of the nerve itself. The explanation of this is that the perineurium forms a barrier between the lymph spaces of the nerve and those of surrounding parts. If a nerve in a living animal be exposed, and the wound filled with water in which vermilion is suspended, then the leucocytes which accumulate take up the vermilion and carry it in various directions, but not into the nerve. But if a nerve in a suppurating wound be itself wounded so as to lay open its internal structure, then suppuration will readily extend into it.
An exception to this condition is afforded by the nerves before their exit from the skull or spinal canal. These are much less protected by an external sheath, and in consequence acute inflammations, such as simple and tubercular leptomeningitis, readily involve the substance of those nerves.
Chronic inflammations also extend, by contiguity, to nerves. Thus an inflammation of a joint, or a dysenteric inflammation of the intestine may give rise to a neuritis. It is most frequent as a result of inflammation of the pelvic organs, the bladder, uterus, etc. It is important to observe that inflammations originating thus may extend up the nerves, and we may have an Ascending neuritis which may extend even to the spinal cord and its membranes. It is to be presumed that the irritant having obtained entrance, gradually finds its way along the lymph-spaces of the nerve, which we have seen to be somewhat independent of those around. .
This is characterized by the specific leprous new-formation which occurs in the nerve-stems, as already described, the condition being a specific interstitial neuritis with atrophy of the nerve fibres and consequent sensory and motor phenomena (see pp. 319-320).
This mostly occurs in the cranial nerves, where a gumma or gummatous inflammation of the meninges involves a nerve in its transit from the brain to its foramen.