A carefully planned electrodiagnostic study is critical for determining the localization, completeness, and pathophysiology of nerve injuries. Both nerve conduction studies and the needle electromyography (EMG) portion of the test contribute. However, the utility of nerve conduction studies to assess nerve injuries can be limited by the availability of conventional studies and stimulation sites. In general, sensory conduction studies are affected earlier and more severely than motor studies in nerve injuries, and a low-amplitude or absent sensory response from an affected nerve is the most sensitive indication of peripheral nerve injury. Normal sensory responses are seen with nerve root injuries, even from clinically anesthetic regions, because the injured nerve segment is proximal to the dorsal root ganglion. In neurapraxic injuries, the compound muscle action potential elicited from stimulation of a motor nerve distal to the lesion is normal, with partial or complete conduction block from proximal stimulation. Late responses (F-waves) are occasionally useful with extremely proximal lesions where it is not possible to directly stimulate proximal to the injured segment. Once an axonal injury has fully evolved, nerve conduction studies will show low-amplitude responses from both proximal and distal stimulation (Fig. 8.1 and Table 8.2). Nerve injuries will cause reduced or absent motor unit potential recruitment in denervated muscles on needle electromyography (EMG) examination. The mere presence of any voluntary motor unit potentials in a clinically paralyzed muscle always indicates that the nerve injury, at least the branch or fascicle supplying that individual muscle, is partial and not complete. Abnormal spontaneous activity on needle EMG examination in the form of fibrillation potentials appears in muscles denervated by axonal nerve injury over 2–3 weeks.

In sum, although electrodiagnostic studies can be performed at any time after nerve injuries, maximal information can be obtained after 2–3 weeks, when the presence of conduction block on nerve conduction studies indicated neurapraxia, and the presence of low-amplitude motor and sensory responses and abnormal spontaneous activity on needle EMG examination indicate the degree of axonal loss (Table 8.2). Obviously every electrodiagnostic evaluation is tailored to the particular clinical situation. However, in general the study should include motor and sensory nerve conduction studies and proximal (F-wave) responses from affected nerves and from the contralateral limbs to compare amplitudes as well as a needle EMG examination of affected muscles to distinguish complete from incomplete injuries and neurapraxia from axonotmesis. In the case of axonal injuries, a repeat study may be indicated in 2–3 months to look for increased evoked amplitudes on nerve conduction studies as well as nascent or reinnervating motor unit potentials on needle EMG examination, both of which indicate ongoing recovery [2]. Planning for surgical repair should be considered for the case of complete injury or where there is significant injury with the lack of ongoing reinnervation after 2–3 months. Even after nerve graft repair, recovery must occur by axonal regrowth from the proximal stump which occurs at a rate of 1 mm/day. Reinnervation must occur before the muscle undergoes irreversible muscle atrophy (within 12 months). In other words, nerve graft repair must be accomplished within 6 months, 3 months for proximal injuries, in order to obtain meaningful results.