of their irritability, which may go to the extent that neither rest in
the one case nor stimulation in the other can restore it. If a
galvanic current is passed through a nerve in its length, the
irritability of the fibres is increased in the region of
catelectrotonus—viz. in the part near the cathode—and diminished in
the region of anelectrotonus—viz. in the part near the anode. Certain
substances, as veratria, first increase and then destroy the
irritability of the nerves; others, as woorara, rapidly destroy it.
{1181} The fibres of the peripheral nerves are divided into two
classes: first, those which conduct impressions or stimuli to the
nerve-centres, the afferent or centripetal fibres; and, secondly,
those which conduct impulses from the centres to peripheral organs,
the efferent or centrifugal fibres. Belonging to the first class are
(1) sensitive fibres, whose stimulation sets up changes in the
nerve-centres which give rise to a sensation; (2) excito-motor fibres,
whose stimulation sets up in the nerve-centres changes by which
impulses are sent along certain of the centrifugal fibres to
peripheral end-organs, causing muscular contraction, secretion, etc.
Belonging to the second class are (1) motor fibres, through which
impulses are sent from the nerve-centres to muscles, causing their
contraction; (2) secretory fibres, through which impulses from
nerve-centres stimulate glands to secretion; (3) trophic fibres,
through which are conveyed influences from the centres, affecting the
nutritive changes in the tissues; (4) inhibitory fibres, through which
central influences diminish or arrest muscular contraction or
glandular activity. No microscopic or other examination reveals any
distinction between these various fibres.
Every nerve-fibre has the power of conducting both centripetally and
centrifugally, but the organs with which they are connected at their
extremities permit the exhibition of their conductivity only in one
direction. Thus, if a nerve-fibre in connection with a muscle at one
end and a motor nerve-cell at the other be stimulated, although the
stimulus is conducted to both ends of the fibre, the effect of the
stimulus can only be exhibited at the end in connection with the
muscle, causing the muscle to contract. Or if a fibre in connection
with a peripheral organ of touch be stimulated, we can only recognize
the effects of such stimulation by changes in the nerve-cells at its
central end which give rise to a sensation.
When we consider the extensive distribution and exposed position of
the peripheral nerves, their liability to mechanical injury and to the
vicissitudes of heat and cold, we cannot but anticipate that they will
be the frequent seat of lesions and morbid disturbances. It may be
that not a few of their diseased conditions have escaped observation
from a too exclusive looking to the central nervous system as the
starting-point of morbid nervous symptoms. This occurs the more
readily as many of the symptoms of disease of the peripheral nerves,
as paralysis of muscles, anæsthesia, hyperæsthesia, etc., may equally
result from morbid conditions of the brain or spinal cord, and not
unfrequently the peripheral and central systems are conjointly
affected in a way which leaves it doubtful in which the disease began
or whether both systems were simultaneously affected.
The elucidation of such cases involves some of the most difficult
problems in diagnosis, and requires not only a thorough acquaintance
with the normal functions of the peripheral nerves, but also the
knowledge of how those functions are modified and distorted in
disease.
The symptoms arising from injuries and diseases of the peripheral
nerves are referable to a loss, exaggeration, or perversion of their
functions, and we often see several of these results combined in a
single disease or as the result of an injury.
The fibres may lose their conductivity or have it impaired, causing
feebleness or loss of motion (paralysis), or diminution or loss of
sensation {1182} (anæsthesia). Or there may be induced a condition of
over-excitability, giving rise to spasm of muscles and sensations of
pain upon the slightest excitation, not only from external agents, but
from the subtler stimulation of molecular changes within themselves
(hyperæsthesia). Or diseased conditions may induce a state of
irritation of the nerve-fibres, which shows itself in apparently
spontaneous muscular contraction or in sensations abnormal in their
character, and not corresponding to those ordinarily elicited by the
particular excitation applied, as formication or tingling from simple
contact, etc. (paræsthesiæ), or in morbid alterations of nutrition in
the tissues to which the fibres are distributed (trophic changes).
If we could recognize the causes of all these varied symptoms and
discover the histological changes invariably connected with them, it
would enable us to separate and classify the diseases of the
peripheral nerves, and give us a sound basis for accurate observation
and rational therapeutics. But, although the progress of investigation
is continually toward the discovery of an anatomical lesion for every
functional aberration, we are still so far from a complete
pathological anatomy of the peripheral nerves that of many of their
diseases we know nothing but their clinical history. We are therefore
compelled in treating of the diseases of the peripheral nerves to hold
still to their classification into anatomical and functional, as being
most useful and convenient, remembering, however, that the two classes
merge into each other, so that a rigid line cannot be drawn between
them, and that such a classification can only be considered as
provisional, and for the purpose of more clearly presenting symptoms
which we group together, not as entities, but as pictures of diseased
conditions which may thus be more readily observed and studied.
It is well to begin the study of the diseases of the peripheral nerves
by a consideration of nerve-injuries, because in such cases we are
enabled to connect the symptoms which present themselves with known
anatomical alterations, and thus obtain important data for the
elucidation of those cases of disease in which, although their
symptomatology is similar, their pathological anatomy is imperfectly
or not at all known.
Injuries of the Peripheral Nerves.
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.