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.