Recognizing physiologic variations in sensory anatomy is clinically significant because accurate EMG or NCV studies rely on the correct mapping of nerves.[11] Knowledge of anatomic variations of sensory nerves is especially useful for the surgeon harvesting skin flaps that need an accessible donor sensory nerve.[12] Examples of variations recorded in the literature include the lateral antebrachial cutaneous nerve innervating the radial border of the dorsum of the hand instead of the superficial radial nerve.[13] The most extensive literature of sensory nerve variation is of the hand with median, ulnar, and radial nerves.[14][15][16]

Peripheral nerve surgery includes repair of acute nerve injuries, entrapment neuropathies, and nerve sheath tumor resection. Acute nerve injury can result from stretching, compression, or laceration. An example of nerve stretching is brachial plexus injury during vaginal delivery of an infant with shoulder dystocia resulting in Erb palsy.[17] Nerve stretching is typically treated conservatively with surgical exploration reserved for severe cases where spontaneous recovery with physical therapy does not happen after several months, or if tearing of nerves is suspected.[18] Entrapment neuropathies occur when a nerve is externally compressed causing compromise of blood supply and local ischemia. Symptoms include paresthesia or muscle weakness. Examples of entrapment/compression neuropathy requiring surgical intervention include carpal or tarsal tunnel syndrome, herniated disc compressing nerve roots, or thoracic outlet syndrome.[19]

Peripheral nerve sheath tumors (PNST) can be benign or malignant. Benign tumors include neurofibromas or schwannomas, and malignant PNST are typically sarcomatous. Surgical consideration of the nerve fascicle that gave rise to the PNST involves intraoperative neurophysiologic monitoring to establish if the associated fascicle has a motor function because that determines whether to do a complete or partial resection. Malignant PNST involves wide local excision, sometimes consisting of proximal amputation. Studies have shown that pre-operative biopsy of PNST results in increased risk of postoperative neurologic deficit, suggesting that referral for surgery without biopsy is recommended.[20][21] Finally, there is the management of nerve laceration, usually due to trauma. Sharp transection, such as seen with a stab wound, has a better prognosis than a crush injury. Repair involves surgical approximation of the damaged epineurium in a tension-free manner. For defects great than 5cm, the gold standard is autologous nerve grafting.[22]

The morbidity of peripheral nerve injury is highest in trauma patients, specifically the upper extremity with the radial nerve the most commonly injured. Approximately 34% of discharged upper extremity trauma patients require support services, and 16% require rehabilitation according to a recent international survey of surgeons.[23] The wide variation in clinical outcomes after peripheral nerve injury makes it difficult to compare data, especially considering the high rate of co-morbidities in these trauma patients. The sensory exam is subjective, and so the examiner must be thorough when doing the sensory exam. 

The best clinical tools for objective measurement of the extent of peripheral nerve injury include EMG and nerve conduction velocity (NCV). Characteristic findings of a compressive neuropathy on EMG include positive sharp waves representing fibrillations from denervation of muscle fibers. NCV in focal compression will show increased latency, decreased conduction velocity, reduced amplitude of motor action potential and sensory nerve action potential.[24]

The Seddon classification system of nerve injury can be used to predict the complexity of nerve regeneration.[25] This system includes neurapraxia, axonotmesis, and neurotmesis. Neurapraxia is nerve contusion due to focal nerve compression resulting in reversible local ischemia without Wallerian degeneration, in which the segment of axon distal to the injury degrades. An example would be meralgia paresthetica which is compression of the lateral femoral cutaneous nerve from tight clothing on an obese person that can often be easily be relieved by wearing looser clothing or losing weight. Axonotmesis is more severe resulting in Wallerian degeneration, but the endoneurium remains intact, and the damage is still reversible. This degeneration begins 24 to 36 hours after injury. A “stinger” is neurapraxia of the proximal upper trunk of the brachial plexus due to stretching. Spontaneous recovery occurs at a rate of 1mm per day and is usually complete as long as the fibers regenerate along their original endoneurial tubes. Nonoperative management with serial electromyography (EMG) is indicated for neurapraxia and axonotmesis.[26] Finally, neurotmesis is complete nerve division that is irreversible without surgical repair. As discussed previously, primary repair of the epineurium is crucial to ensure proper regeneration of the original fiber pattern with the best prognosis for recovery of function. About 2.5% of all peripheral nerve injuries today cannot be surgically repaired.[27]

The differential for non-traumatic peripheral neuropathy includes:

• Immune-mediated
• Metabolic
• Hereditary
• Toxic
• Infectious
• Entrapment

Sensory neuropathies can represent the neurologic manifestations of systemic disease.[27] Ascending, symmetric sensory loss in the context of recent infection with albuminocytologic dissociation on CSF analysis represents acute inflammatory demyelinating polyneuropathy (AIDP/GBS). Mononeuropathy multiplex, which is neuropathy of individual peripheral nerves in a multifocal distribution, can be seen in Churg-Strauss, polyarteritis nodosa, and Wegener granulomatosis. The most common metabolic neuropathy is seen in diabetes mellitus presenting as distal symmetric polyneuropathy. The A-delta and C fibers are the first involved since they are the smallest, so the insidious onset of symmetric loss of temperature and light touch sensation in a “stocking and glove” distribution is the common initial presentation. This neuropathy distribution is also characteristic of vitamin B12 deficiency.[28] Other vitamin deficiencies characterized by peripheral neuropathies include B1, B6, vitamin E, and niacin. Hereditary neuropathies include neurocristopathies such as neurofibromatosis and Charcot-Marie-Tooth.[29] Neurofibromatosis type I (NF1) is associated with cutaneous neurofibromas and NF2 involves bilateral acoustic schwannomas. Charcot-Marie-Tooth is a chronic demyelinating disease of the peripheral nerves associated with foot deformities like pes cavus, foot drop due to lower extremity weakness, and sensory deficits especially along the distribution of the peroneal nerve. Other hereditary diseases with peripheral neuropathy include the sphingolipidoses like Krabbe disease, metachromatic leukodystrophy, and Fabry disease. Neuropathies associated with infections include HIV distal sensory polyneuropathy due to neurotoxic side effects of anti-retroviral therapy and mononeuropathy associated with other infections like CMV. Lyme disease can cause facial neuropathy, unilateral or bilateral. Leprosy is the most common infectious cause of neuropathy in the world, presenting with painful mononeuropathies of cool areas like the nose, ears, and distal limbs.[30] Finally, entrapment and compressive neuropathies like carpal tunnel syndrome (median neuropathy) or peroneal neuropathy (meralgia paresthetica) can occur and be addressed surgically if sufficiently severe.