Neurapraxia denotes injury to myelin alone, with electrodiagnostic findings of conduction block and, later, conduction velocity slowing along the involved segment of nerve.

Axonotmesis describes injury to axons resulting in wallerian degeneration. Early electrodiagnostic findings include loss of nerve conduction across the site of the injury (indistinguishable from neurapraxia). Later findings of decreased or absent evoked potential amplitudes distal to the site of injury are seen as wallerian degeneration occurs.

Neurotmesis is complete disruption of the nerve, with injury to axons and wallerian degeneration as well as disruption of the supporting connective tissue. This type of injury carries a poor prognosis for recovery and usually requires urgent surgical intervention.

Electrodiagnostic testing cannot differentiate between complete axonotmetic lesions and neurotmesis because the difference between these types of lesions is in the integrity of the supporting structures, which have no electrophysiologic function.

Organizes injury type based on the nerve anatomy involved.

Class 1: Injury to myelin alone (i.e., neurapraxia). Prognosis for recovery is excellent.

Class 2: Axonotmesis with injury to axons with intact endoneurium, perineurium, and epineurium. Prognosis is good in general but varies depending on percentage of axons injured and distance of lesion from muscle.

Class 3: Axonotmesis with injury to the endoneurium and sparing of the perineurium and epineurium. Prognosis is poor. Surgery may be required.

Class 4: Axonotmesis with injury to the endoneurium and perineurium and sparing of the epineurium. Prognosis is poor. Surgery is required to restore nerve continuity.

Class 5: Neurotmesis. Complete transection of the peripheral nerve. Surgery is required to restore nerve continuity. Prognosis for recovery is particularly poor (38).

Timing of testing depends on the question being asked.

Immediate to 7 days: Localization of injury with NCS, identifying conduction block versus axonotmesis (2,38).

1-2 weeks: Distinguishes complete lesions from incomplete lesions. May also distinguish axonal from demyelinating lesions (axonotmesis and neurotmesis from neurapraxia) (2).

3-4 weeks: Able to characterize lesion as EMG becomes useful. A single study at this point will yield the most information (2). Although EMG cannot accurately quantify axonal damage, it is the most sensitive indicator that axonal damage has occurred.

3-4 months: Detects reinnervation of previously denervated muscles (2,38).

Prognosis is based on severity and type of damage to the nerve. Although purely neurapraxic (demyelinating) lesions have an excellent prognosis for fast and complete recovery, axonotmetic and neurotmetic lesions have variable outcomes based on the number of axons injured.

Axonal loss results in decreased evoked potential amplitudes. The best determination for degree of axonal loss is comparison to asymptomatic contralateral amplitude. A side-to-side amplitude difference of 50% is generally indicative of significant axonal loss.

EMG can determine complete versus partial functional denervation based on the absence or presence of motor unit action potentials. EMG can also demonstrate evidence of reinnervation based on the amplitude, phases, and duration of motor unit action potentials.

Most prognostication for motor recovery after peripheral nerve injury is extrapolated from a study of injured facial nerve compound motor action potential amplitudes in comparison with the asymptomatic contralateral side (45). Results indicated:

Mechanism of injury also contributes to prognosis, with avulsion-type injuries having the worst prognosis and compression injuries having the best prognosis (38).

Peripheral nerve injuries are unfortunately common in volleyball, with the most common being suprascapular nerve entrapment at the spinoglenoid notch.

This presents as painless weakness and atrophy of the infraspinatus in the dominant serving arm of the player.

Prevalence has been documented to range from 33% to 45% of symptomatic international-level players and to be 12% in asymptomatic players at the same level (17,19,53).

EMG reveals isolated infraspinatus denervation and motor unit loss (32,53). Possible etiologies of this specific nerve entrapment related to volleyball serving include increased shoulder range of motion and impingement of the infraspinatus branch of the suprascapular nerve between the edge of the spine of the scapula and the medial tendinous margin between the infraspinatus and supraspinatus muscles (40,53).

Cycling is commonly associated with two peripheral nerve injuries: ulnar neuropathy at the wrist, or “cyclist’s palsy,” and pudendal neuropathy.

Cyclist’s palsy presents as numbness and paresthesias in the ulnar distribution of the hand (small finger and ulnar half of the ring finger) and weakness of hand intrinsic muscles (24).

Ulnar neuropathy at the wrist is highly prevalent in long-distance cyclists and is independent of handlebar design (24,34)

Injury is due to compression of the ulnar nerve at the wrist. NCSs have demonstrated significantly increased distal motor latencies in the deep branch of the ulnar nerve after a long-distance cycling event, suggesting the possibility of acute trauma (1,24).