The anatomy of a peripheral nerve trunk is
shown in Fig. 34.1. Nerve impulses are conducted by axons.
The nerve contains many axons which are supported by connective tissue
structures. Neurons consist of a cell body, associated dendrites and usually one
axon. In order to remain viable an axon must be connected to its cell body. All
axons are surrounded by Schwann cells. In myelinated fibres the Schwann cells
form an insulating sheath, each Schwann cell being associated with only one
axon. Integrity of the myelin sheath is
Response
of a nerve to injury
If trauma to a nerve is sufficient to disrupt
axons then the distal part of the nerve undergoes Wallerian degeneration. In
this process there is lysis of the axoplasm and fragmentation of myelin sheaths
leaving an endoneurial tube containing Schwann cells. The axons in the proximal
part of the nerve have the potential to regenerate into the endoneurial tubes of
the distal segment and subsequently make connections with target organs. The
regeneration proceeds slowly with axons growing at only 1—2 mm/day in humans.
The extent of damage to the supporting connective tissue layers influences the
quality of recovery and is, hence, the basis of the classification of nerve
injuries.
Classification
of nerve injuries
The most widely used classification of nerve
injuries in the UK was described by Seddon (1942) after study of a large number
of battle casualties during World War II. There are three types of injury of
increasing severity:
•
neuropraxia;
•
axonotmesis;
•
neurotmesis.
Neuropraxia
(nerve not working)
This is a local block to conduction of nerve
impulses at a discrete area along the course of a nerve. The axons are in continuity
and therefore Wallerian degeneration does not occur. Nerve conduction distal to
the site of injury remains normal. Experimental work suggests that the
conduction block results from localised demyelination of fibres in the damaged
segment of nerve. Neuropraxia is a relatively mild injury typically caused
by moderate compression such as that caused by a tourniquet, slight stretching
or the passage of a missile close to a nerve. Recovery is complete providing the
cause is removed, but the time varies from days to several weeks.
Axonotmesis
(axons divided)
This represents an anatomical disruption of the
axons and their myelin sheaths. However, the supporting connective tissue
structures including the endoneurial tubes, perineurlum and epineurium are
still intact. Wallerian degeneration occurs distal to the site of injury and,
hence, distal conduction is lost. Arxonotmesis results from a more severe blow
or stretch injury to a nerve. For example, radial nerve palsy associated with
fracture of the humerus is usually an axonotmesis. Recovery occurs by axon
regeneration proceeding at a rate of 1—2 mm/day. Axons regenerate along the
same endoneurial tube and therefore connect with the same end organ as before
injury. The prognosis is good, restoring near-normal sensory and motor function.
Neurotmesis
(whole nerve divided)
This is the state where the nerve has been
completely severed or is so seriously disorganised that spontaneous recovery is
not possible. The axons and the supporting connective tissue structures are
disrupted, and Wallerian degeneration occurs distal to the site of injury.
Typically neurotmesis occurs as a result of an open injury such as a stab wound
but high-energy traction, injection of noxious drugs and ischaemia can also
destroy a nerve in this way.
If
appropriate surgical repair is carried out then recovery may occur by axonal
regeneration at a rate of 1—2 mm/day. In contrast to axonotmesis, the quality
of recovery is never perfect after neurotmesis. This is probably the result of
the failure of correct ‘rewiring’. Because the endoneurial tubes and other
connective tissue structures have been disrupted, even with the best repair,
regenerated nerve fibres connect with muscles or sensory organs which they did
not previously innervate.
Sunderland’s
classification
In 1951 Sunderland defined five degrees of
nerve injury on the basis of increasing anatomical disruption of the nerve trunk
(see Table 34.1). Although Seddon’s classification is simpler and more widely
used in the UK, Sunderland’s classification is useful in its distinction
between third- and fourth-degree injuries when exploring a damaged nerve. If the
fascicles are in continuity (not worse than third-degree injury) then spontaneous
recovery is possible, whereas if the fascicles are disrupted (fourth-degree
injury) then spontaneous recovery will not occur and immediate nerve grafting
may be considered.
Injection
injuries
Injection of toxic substances directly into a
nerve leads to a very intense fibrotic reaction in the nerve. Immediate
exploration, incision of the epineurium and irrigation of the nerve trunk is
recommended, but the outcome is poor.
Clinical
features of nerve disorders
As with other medical and surgical problems,
diagnosis of conditions affecting nerves is based upon history, examination and
special investigations. In the case of trauma it is particularly important to
establish the mechanism. High-velocity and open injuries produce more severe
nerve injuries.
The
clinical findings on examination of patients with nerve injury include motor and
sensory dysfunction but depend, in part, upon the grade of injury. With
neurapraxia there is usually complete paralysis of the appropriate muscle groups
but some sensation and autonomic function is preserved. In the case of
axonotmesis and neurotmesis there is complete loss of muscle power, sensation
and autonomic function. The latter is most easily shown by lack of sweating in
the distribution of the nerve. This is a useful objective sign as it does not
require a co-operative patient. The nerve injured and the level at which the
injury has occurred can be worked out from a careful physical examination and
knowledge of the anatomical distribution of the nerves. Nonetheless, there is
significant crossover in sensory function and also in some motor function,
particularly when considering nerve roots (Table 34.2 and Fig.
34.2).
It
is useful to grade the level of dysfunction of nerves, particularly in
the assessment of recovery and the results of treatment. The system widely
used is the 1975 update of the 1954 Medical Research Council (MRC)
classification (Tables 34.3 and 34.4). This grading system is good, and widely
used, but is still a rather coarse measure of muscle function and sensation.
Investigation
While the most important assessment of nerve
pathology is undoubtedly clinical, useful additional information can sometimes
be obtained from neurophysiological studies or imaging.
Neurophysiological
investigations require complex stimulation and recording apparatus.
Interpretation of the results requires experience and is reliant upon the skill
of the neurophysiologist. There are two types of test available.
•
Nerve conduction studies —
these involve
recording sensory or motor nerve action potentials and calculating the
conduction velocity for given anatomical segments. Compression neuropathy can be
identified by slowing of conduction.
•
Electromyography (EMG) —
in this test
muscle action potentials are recorded in response to voluntary activity.
Denervation can be diagnosed and distinguished from reinnervation.
Using
these tests it is possible to distinguish between a nerve injury where axons
have not degenerated distal to the lesion (neurapraxia) and one were Wallerian
degeneration has occurred (axonotmesis or neurotmesis). Axonotmesis and
neurotmesis cannot be distinguished.
Magnetic
resonance imaging (MRI) is showing some promise in displaying peripheral nerve
pathology and is likely to be used routinely in the future. Currently, its main
application is in imaging cervical nerve roots after brachial plexus injuries.
Treatment
Open
injuries
If there is clinical evidence of a nerve injury
associated with a wound, then it should be assumed that the nerve is divided
until proven otherwise.
Surgical
exploration of the nerves is advisable, once life-threatening haemorrhage has been controlled and providing the
general condition of the patient allows operation. In addition, wounds in areas
where important nerves are vulnerable to damage should be routinely explored
even in the absence of obvious neurological deficit, for example the flexor
compartment of the forearm. Early repair of any divided nerves should be
performed if possible. Exploration should therefore be undertaken by a surgeon
with appropriate experience to carry out repair of nerves if necessary. If a
vascular repair is required then nerve repair should normally be carried out
at the same time. If the injury is in a site which is difficult to expose
surgically, for example the brachial plexus, then transfer to a specialist unit
should be arranged as soon as possible.
Closed
injuries
Management of closed injuries where nerves have
been subjected to stretch or compression is more difficult because the severity
of nerve injury may not be clear. Neurapraxia and axonotmesis will recover
spontaneously providing the cause, for example compression, is removed. However,
surgical repair of the nerve is necessary for there to be any chance of
recovery after neurotmesis. Results are markedly better if this repair is
carried out early after injury.
Exploration
and repair of nerves may be combined with fixation of any associated skeletal
injury. In cases of low-energy injury it is reasonable to observe the nerve
injury initially, unless operation is being carried for fracture fixation in
which case the opportunity should not be missed to confirm nerve continuity.
Cases managed nonoperatively should be followed up carefully. If there is clear
evidence of recovery after 2—3 months then nonoperative management can
continue. If not, then surgical exploration should be considered without
further delay. Neurophysiology may be helpful in making the decision in some
cases as the tests may detect early recovery which is not evident clinically.
Surgical
repair
The essence of a good surgical repair of a
nerve is accurate coaptation of the nerve ends without tension in a healthy bed
of tissue. At operation the nerve ends are exposed, carefully avoiding further
injury. If there has been a clean division of a nerve, then little dissection is
usually required and direct suture can be carried out. However, if the nerve
ends are ragged or the disruption has been caused by blunt trauma, it is
necessary to trim the nerve back to healthy tissue with bulging nerve bundles.
In delayed repairs significant scarring and retraction of the nerve ends may
have occurred and it is,
Timing
of nerve repair
Early nerve repair provides the best chance of
satisfactory recovery and should be carried out provided that a well-trained
surgeon and suitable equipment are available. Occasionally, if a wound is very
contaminated then primary nerve repair may not be appropriate. In most
circumstances it is possible to carry out early repair if sufficient wound debridement
is carried out and plastic surgical expertise is available to provide flap cover
of soft-tissue defects. If primary repair is not carried out then it is useful
to apply one or two nonabsorbable sutures, either to hold nerve ends together or
to suture a nerve end to local soft tissue, thereby minimising retraction and
aiding identification at later surgery.
Direct
nerve suture
When repairing a nerve, a microscope should be
used to aid accurate alignment of the nerve and placement of sutures, which
range in the order of 6/0 for large nerves (such as the sciatic nerve), 8/0 for
the median nerve in the forearm, and 9/0 or 10/0 for digital nerves. It is
important to orientate the nerve ends with the correct rotation in order to
minimise crossover during recovery. The pattern of nerve fascicles and surface
blood vessels can be used as guides for alignment. Sutures are usually placed in
the epineurium (epineurial repair). There is probably no advantage in
performing interfascicular repair except at distal sites where the nerve is
dividing into terminal branches. Sufficient sutures are inserted to provide
epineurial cover for all nerve bundles (Fig. 34.3).
Nerve
grafting
When direct nerve suture is not possible an
interpositional nerve graft is necessary. This involves harvesting a length of
Postoperative
management
After wound closure, the limb is immobilised to
minimise any tension on the suture line with appropriate flexion of proximal
and distal joints. These are held in a cast for a minimum of 3 weeks. It may
then be appropriate progressively to extend the proximal and distal joints, thus
gradually restoring normal tension to the nerves. After 6 weeks, free mobilisation
is permitted, assisted by appropriate physiotherapy.
Follow-up
management
After nerve repair patients should have regular
physiotherapy to maintain the passive range of movement in all joints prior to
muscle recovery. In addition, patients should be monitored clinically to check
that nerve recovery is occurring at the expected rate. Tinel’s sign is useful
in monitoring axon regeneration and should advance at about 1 mm/day.
(Elicited by percussing over the course of the nerve, the patient feels tingling
in the distribution of the nerve.) In the event of nerve recovery not
progressing, then re-exploration of the nerve may be justified.
General
factors affecting prognosis
The factors governing the prognosis of nerve
repair are both general to all nerves and specific to certain nerves.
Age
Children recover much better than adults and
this is probably the most important prognostic factor. Nonetheless, the
secondary consequences of paralysis in children may be worse because of the
associated growth abnormalities. Age over 50 years is a particularly poor
prognostic factor for proximal nerve injuries.
The
severity of in jury to the nerve
Seddon’s classification of nerve injuries
relates the severity of injury to the prognosis. However, there are varying
grades of neurotmesis which affect the chance of recovery after repair. A
clean-cut nerve injury has the best prognosis, whereas
The
level of in jury
In general, proximal lesions do worse than
distal lesions although there do appear to be some exceptions to this rule.
The
type of
nerve
The classic teaching is that nerves with both
sensory and motor fibres fare worse than pure sensory or motor nerves. The
latter do not truly exist, as all motor nerves have some afferents from muscle
spindles. However, it is
certainly true that motor nerves to large muscle groups not requiring fine
control have a better prognosis than motor nerves supplying the small muscles of
the hand.
Associated
injuries
Nerve repairs with associated vascular
injuries, soft-tissue damage and fractures are less likely to heal with a
satisfactory result. It is important that associated vessels and other
structures are repaired as far as possible.
Delay
Early repair of nerves, that is within a few
days of injury, gives the best results and is one of the main factors which the
surgeon can influence.
Special
types of nerve injury
Compression
neuropathy
This is the term used to describe chronic
dysfunction of a nerve as a result of local compression at some point along its
course. Compression neuropathy is one of the most frequent single conditions
presenting to orthopaedic and hand clinics. The most common sites of compression
are the median nerve at the carpal tunnel and the ulnar nerve at the cubital
tunnel or Guyon’s canal. These are anatomical sites where the nerve is
surrounded by unyielding bone and ligaments. Sometimes there is an identifiable
cause such as tenosynovitis within the carpal tunnel, but in many cases there is
no obvious cause. Compression of a nerve has a direct effect on the myelin
sheaths, as well as causing ischaemia of the nerve with consequent fibrosis.
It also appears that damage results from loss of mobility of the nerve at the
point of entrapment. The patient initially complains of pain and altered
sensation in the distribution of the affected nerve. In more advanced cases
there is loss of sensory and motor function. Most compression neuropathies
respond to surgical decompression of the affected nerve.
Irradiation
Radiation neuritis can occur up
to 20 years after the radiation, the classic site being
the infraclavicular
brachial plexus following radiation for breast cancer. Fortunately, this is
rare. Characteristically, there is severe pain with some motor and sensory changes. The pain is cry
difficult to treat. Surgical exploration and release of nerves has been
beneficial in some patients.
Pain
The pain following nerve injuries or other
nerve pathology can be of the most severe intractable type, leading to requests
for amputation and even depression and suicide. The cause of this pain is poorly
understood. Local nonoperative treatment includes encouraging use and movement
of the limb, and transcutaneous electrical nerve stimulation (TFNS~. This works
as a counter-stimulus to the pain. In addition to simple systemic analgesics,
medication to suppress nerve excitability, such as carbamazepine, and
antidepressants, such as amitryptilline, can be useful. There are certain
occasions where pain of nerve origin may be influenced by surgical intervention.
Cusalgia is pain as a result of an injury (often partial) to a major nerve. The pain typically has an intense burning character. This pain tends to improve with nerve recovery and therefore any surgical measures should be aimed at facilitating this. Sympathectomy may be helpful in resistant cases
Nerve
compression may
cause severe pain (neurostenalgia).
Reflex
sympathetic dystrophy (algodystrophy)
— this
is a specific syndrome which can occur after trauma or surgery where a cycle of
pain and dysfunction is set up and leads to a chronic state associated with
sympathetic over-activity. The limb involved becomes painful and tender to
normal stimuli. This leads to disuse, stiffness and trophic changes. It is
important to recognise the condition as early as possible and to break the
vicious cycle. In addition to standard analgesics, guanathedine blockade to
suppress sympathetic activity is useful to facilitate vigorous physiotherapy.