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Qiu et al. Plast Aesthet Res 2022;9:19 https://dx.doi.org/10.20517/2347-9264.2021.126 Page 3 of 17

A detailed sensory and motor exam should be performed to characterize the degree of nerve injury and
localize the lesion. Sensory exam should include light touch, sharp-dull sensation, two-point discrimination,
and monofilament testing. The presence of neuropathic pain and evaluation for a symptomatic neuroma
can also be helpful in localizing lesions. Pain in a defined neural anatomic distribution, a positive Tinel sign,
and a positive response to local anesthetic injection all increase the likelihood of a sensory neuroma
[10]
indicating nerve injury . Motor exam should utilize the Medical Research Council (MRC) grading system,
and should be assessed across the hip, knee, ankle, and toes in all planes of active motion. Additional exam
maneuvers that help further localize the lesion include searching for a Tinel sign along an injured nerve and
straight leg raise and reflex testing to identify lumbosacral radiculopathies. Finally, observation of gait may
identify stereotypical associations with patterns of PNI and help contextualize the deficits. In cases of
unclear or absent injury and inconsistent localization of the neurologic lesion, functional neurological exam
maneuvers may identify psychogenic weakness and avoid unnecessary surgery. One such test is Hoover’s
sign, in which psychogenic weakness of hip extension is revealed when the involuntary, forceful hip
extension is elicited during voluntary flexion of the contralateral hip .
[11]
Electrodiagnostics and imaging are helpful in localizing and characterizing the extent of nerve injury. Serial
electrodiagnostic testing can inform on the degree of reinnervation, or the lack thereof, to aid surgical
decision making. In the senior author’s practice, it is standard to obtain a nerve conduction study and
electromyography at 2-3 months after injury, at which point Wallerian degeneration has occurred and
electrical abnormalities will be detectable. A loss of distal conduction or the presence of fibrillations and
positive sharp waves within the affected muscle groups indicates critical axonal loss and denervation .
[12]
Either magnetic resonance or ultrasound imaging has become standard tools used in the workup of
traumatic nerve injuries, as they provide valuable information regarding gross nerve morphology and
architecture to help differentiate partial and complete injuries. Magnetic resonance neurography (MRN)
protocols are gaining ground as a powerful mode of nerve imaging, achieving finer resolution at the
fascicular level [13,14] . However, sensitivity for MRN in detected closed nerve injuries is only 40%-70%,
meaning that workup should not be precluded by a normal or negative MRN study [15,16] . Ultrasound can be
an inexpensive and useful method for diagnosing injuries to more superficial nerves, such as the common
peroneal nerve (CPN), but the efficacy of this imaging modality remains user and institutional dependent.

GENERAL TREATMENT PRINCIPLES
Watchful waiting with close observation for clinical or electrodiagnostic evidence of recovery is appropriate
in certain clinical scenarios in which the potential exists for spontaneous recovery. In general, this is the
preferred management for closed nerve injuries in which there is no evidence of nerve transection or gross
injury on imaging. Physical therapy should be initiated during this observation period when possible,
including braces and passive range of motion exercises to prevent contractures while deficits persist.
Surgical intervention is typically indicated if no clinical functional recovery or electrodiagnostic evidence of
reinnervation is observed 3-5 months following injury.

When exploring a closed nerve injury in a delayed fashion, the surgeon should be prepared to employ
different surgical approaches depending on the specific findings that are encountered. If nerve
macroarchitecture is preserved and there is no visible injury identified along the traumatized nerve, then
exploration should be limited to neurolysis and release of distant compression sites. Neurolysis can be
“external” - release of fibrotic tissue around the epineurium - or “internal” - release of interfascicular fibrotic
tissue. While the exact mechanisms of neurolysis leading to improved function are not well described, the
alleviation of compressing forces is thought to facilitate axonal transport, perineural vascular flow,
myelination, and axonal regeneration, enabling more rapid and robust reinnervation of target muscles [17,18] .