LOCALIZED PERIPHERAL NERVE (PN) injuries are very common and arise from a wide range of etiologies. They are seen in healthy individuals and also may arise from complications from other disorders or traumatic injuries. PN injuries may accompany or complicate rehabilitation management of other disorders, for example, nerve compressions due to use of assistive devices or bracing, or overuse injuries in less impaired extremities. An understanding of the anatomic course and innervation of peripheral nerves and common sites of entrapment is important in recognizing and diagnosing these injuries. As PN injuries can accompany other musculoskeletal disorders and trauma, their existence can sometimes be initially masked. Therefore, it is important to recognize high-risk scenarios for nerve injury as they may impede expected recovery from the traumatic injury.

The peripheral nervous system contains 12 pairs of cranial and 31 pairs of spinal nerves that supply specific sensory territories and muscle groups, known as dermatomes and myotomes, respectively (Fig. 12–1). After leaving the spinal cord as nerve roots, the spinal nerves in the cervical and lumbosacral regions form plexuses. Different root levels then intermingle in the plexus to form individual peripheral nerves innervating the upper and lower extremities. When a spinal root, portion of the plexus, or peripheral nerve is injured, characteristic patterns of sensory and motor abnormalities will be seen.

The neural structure is composed of an axon (the nerve fiber) which is enclosed in a Schwann cell. A single Schwann cell may encircle a multiple axons, in which case it is referred to as an unmyelinated axon. When a Schwann cell associates with a single axon, wrapping around it several times, the resultant fiber is referred to as myelinated. The myelinated fiber is invested by multiple Schwann cells in succession, which are separated by small uncovered regions called nodes of Ranvier (Fig. 12–2). This allows nerve depolarization to “jump” from node to node in a process known as saltatory conduction. This results in far more rapid conduction of the nerve impulse than in unmyelinated fibers (50 to 60 m/s vs. 1 to 2 m/s). The nerve fiber and its Schwann cells are enclosed in an endoneurium. Several of these are grouped into fascicles surrounded by a perineurium. Along its course individual axons may cross from one fascicle to another. The fascicles are then all enclosed within an epineurium which makes up the entire peripheral nerve (Fig. 12–3).

PN injuries, mononeuropathies, are classified by the degree to which to the axon and its supporting structures are affected. The two classic classification systems are the Seddon system¹ and the Sunderland system.² The least severe injury is focal injury of the myelin resulting in conduction block without injury to the underlying axon. This corresponds to neuropraxia in the Seddon system. Axonotmesis occurs when the axon is damaged with resultant Wallerian degeneration, but the supporting endoneurium and perineurium are preserved. The most severe injury involves the axon, myelin, and the supporting nerve structures, often with loss of axonal continuity; this process is referred to as neurotmesis. The Sunderland system further subdivides neurotmesis based on extent of damage to the supporting structures (Table 12–1).

Neuropraxic injuries, only involving the myelin sheath, have good prognosis for recovery within 2 to 3 months, given removal of the source of the injury as the axon remyelinates. It should be noted, however, that the repaired myelin may not be as robust and some slowing of nerve conduction may persist.³ When the axon is injured, prognosis for recovery is related to the degree to which the supporting structures are involved and the number of axons affected. Sunderland grade 3 and 4 injuries have a much lower chance of recovery than grade 2 (axonotmesis). If there is significant disruption of the fascicles with local tissue fibrosis at the site of injury, there is very poor chance of axonal regrowth to the target end organ. The distance of the site of axonal injury to its target muscles and sensory territory also affects prognosis for regrowth. When neural supporting structures are preserved (axonotmesis), the axon can regrow down the neural tube at an estimated rate of 1 to 5 mm/day.² If the injury is at a distance from the site of injury, the axon tube may degenerate and the target muscle may become fibrotic before the axon reaches it and thus not be viable for reinnervation. In addition to primary reinnervation from the damaged axon, regenerating intact axons in nearby territories can reinnervate denervated muscle fibers through collateral sprouting. Motor neurons can reinnervate about five times its normal motor fiber territory.⁴ Complete loss of axonal continuity, such as with laceration of the nerve, is unlikely to repair without surgical intervention.

History and Physical Examination

A detailed history is the first step in localizing the level of injury. The pattern of weakness, sensory loss, and pain usually follows a characteristic distribution pointing to the nerve involved and site of injury. History of onset and associated traumatic event, occupational demands, hobbies, or medical procedure is often revealing, as is exacerbating and relieving factors. The physical examination will show deficits in specific areas consistent with the nerve’s motor and sensory distribution; therefore, an understanding of the anatomic distribution of specific nerves, their course, and areas of mechanical vulnerability is important. Various provocative maneuvers may reproduce the patient’s symptoms such as percussing over common entrapment or injury sites (Tinel sign) or either compressing or stretching the nerve at site of injury.

Electrodiagnostic Studies

Electrodiagnostic studies are very helpful in diagnosis of peripheral nerve injury. A well-crafted and properly interpreted study can identify the affected nerve and assist in localizing the site of injury as well as the severity and chronicity of the nerve injury. Electromyography (EMG) also can give helpful information on prognosis for recovery. As compound muscle action potentials (CMAP) are proportional to the number of muscle fibers depolarized, it can reflect motor axonal injury. If conduction block is present, however, the CMAP will be low when stimulating proximal (across) the site of demyelination, with stimulation distal to the site resulting in large CMAP amplitude, reflecting severity of the conduction block. It should be noted, however, that after an axonal injury it can take up to 7 days for loss of CMAP amplitude to be detectable.⁵ Similarly sensory nerve amplitude potentials take approximately 10 days to reach maximal loss. After several months the CMAP amplitude can improve due to collateral sprouting, without actual primary axonal regrowth. Conduction velocity slowing suggests demyelination, though in axonal injury some slowing may be present due to preferential damage to faster conducting fibers. A drop in conduction velocity between a distal and proximal site is useful in localizing where the nerve injury has occurred, though in many cases, particularly in proximal injuries, there are technical limitations in stimulating across suspected site of damage. Presence of a conduction block with relatively preserved distal amplitude is actually a favorable prognostic factor, indicating that the injury is primarily demyelinating and thus more likely to improve than an axonal insult. Needle studies (EMG) detect denervated muscle (axonal loss). Early on after axonal injury, at 10 days to 4 weeks depending of distance from injury, fibrillation potentials and positive sharp waves will appear. The degree of fibrillation potentials do not correlate with the severity of axonal loss.⁶ Voluntary motor unit action potential (MUAP) recruitment is an indication of the number of motor units available to volitional control and thus the degree of axonal preservation. The presence of relatively preserved recruitment distal to the site of injury is a good prognostic indicator. The reverse, however, is not as prognostic, as poor or absent recruitment may also reflect conduction block. Needle EMG is also helpful in assessing nerves lesions that are technically difficult or impossible to assess by typical nerve conduction studies, such as the nerves deep in the pelvis like the obturator nerve or gluteal nerves.

Imaging Studies

Radiographs should be obtained in the setting of traumatic injuries. In most cases the presenting fracture will be the initial cause for evaluation, with the accompanying peripheral nerve injury secondary. Nerve injures commonly associated with fractures include radial nerve injury with humeral facture, peroneal nerve with fibular head fractures, and the sciatic nerve with hip fracture and dislocation. Magnetic resonance imaging (MRI) and computerized tomography (CT) can further characterized fractures, as well as identify soft tissue masses, tumors, and hematomas compressing the nerve. MRI can also visualized larger nerves such as the sciatic nerve and also evaluate for changes in muscles characteristic of denervation. MRI of the spine is also helpful to evaluate for radiculopathy, which may be difficult to differentiate from PN injury. Ultrasound (US) is increasingly being used to visualize nerves. This is particularly useful in more peripheral and superficial nerve locations such as the median nerve at the wrist and the fibular nerve at the fibular head. An advantage of US is that it can be used dynamically to look at the nerve in motion, for example, abnormal subluxation of the ulnar nerve at the elbow. Use of US is limited in nerves that are more deeply located.

Median Nerve

The most common peripheral nerve injury is that of the median nerve at the wrist, or carpal tunnel syndrome (CTS). The median nerve is formed from contributions from the sixth through eighth cervical roots via the medial and lateral cords of the brachial plexus. It innervates the pronator teres, flexor digitorum superficialis, and flexor carpi radialis. The median nerve then gives off the anterior interosseous nerve supplying the lateral portion of the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus. The median nerve continues through the carpal tunnel to innervate the first and second lumbricals and the opponens pollicis and abductor pollicis in the thenar eminence (Fig. 12–4A). The sensory territory of the median nerve involves the skin over the thenar eminence, supplied by the palmar cutaneous branch, given off before the carpal tunnel, and the first three and lateral aspect of the fourth fingers (Fig. 12–5). The most common site of compression of the median nerve is in the carpal tunnel, which is made up of the carpal bones and the transverse carpal ligament. The canal contains the median nerve and the tendons of the flexor digitorum profundus and superficialis and flexor pollicis (Fig. 12–6). Less commonly the nerve can be compressed at the pronator muscle or at the anterior interosseous nerve under a fibrous arch formed by the flexor digitorum superficialis and the pronator teres.

Median mononeuropathy at the wrist (CTS) is the most common compressive mononeuropathy. It is more common in women and often associated with repetitive hand and wrist motions, vibration exposure, and keyboarding. The condition is often bilateral and more severe in the dominant hand.⁷ Most cases are idiopathic but there are a number of medical conditions that predispose to CTS, including diabetes, rheumatoid arthritis, and hypothyroidism.⁸ Other associated conditions include pregnancy and obesity.⁹ Occasionally a ganglion cyst or other mass can cause compression.

CTS classically presents with numbness and paresthesia affecting the second and third finger and variably the first and fourth. Usually the thenar eminence is spared as the palmar cutaneous branch comes off before the carpal canal. Nocturnal symptoms typically predominate. Use of the hands, particularly gripping activities, exacerbates symptoms. The patient may note overt weakness of thumb abduction or opposition, or functional difficulties and report dropping things. Atrophy of the thenar eminence may be seen when axonal loss is severe. Strength of the long finger flexors and pronation of the forearm and wrist should be normal. Positive provocative maneuvers include Phalen and reverse Phalen. Phalen sign is provoked by pressing the palms to together with the wrists extended for 30 to 60 seconds to reproduce numbness into the second and third fingers (Fig. 12–7). Reverse Phalen is performed by pressing the dorsum of the hands together causing forced flexion of the wrist, similarly reproducing symptoms. A Tinel sign may be provoked by tapping over the median nerve 1 to 2 cm distal to the wrist crease. Sensory abnormalities may be appreciated to light touch and pinprick in the second, third, and lateral side of the fourth digits. Conditions that can mimic CTS include more proximal median nerve injuries, brachial plexopathy, or C6 or C7 radiculopathies. These conditions maybe suspected if the distribution of the motor abnormality affects nonmedian innervated muscles or long finger or wrist flexors. Muscle stretch reflexes should be normal in CTS.