Peripheral nerves contain sensory or motor axons (or both), most of which are myelinated. Each axon is surrounded by fine collagen fibers, the endoneurium. Groups of axons called fasciculi are bound together by the perineurium, which consists of Schwann cells and fine collagen fibrils. The epineurium, made of thicker collagen fibrils, surrounds the fasciculi. This layer is thought to elaborate the fibroblastic reaction that is the primary cause of fibrosis subsequent to nerve injury.
The four major causes of traumatic peripheral nerve lesions are laceration, contusion, stretch, and compression. Less commonly, nerves may be injured inadvertently when an injection is given. Irrespective of cause, localized injuries fall into one of three categories: neurotmesis, axonotmesis, and neurapraxia. In neurotmesis (eg, nerve laceration), axons and endoneurial tubes are disrupted. The proximal nerve end first swells and then, to a variable degree, undergoes retrograde degeneration. Subsequently, a neuroma develops, composed of connective tissue and a tangle of regenerating axons. The axons in the distal end die (wallerian degeneration), the endoneurial tubes shrink, collagen is deposited, and an end-bulb glioma forms. In axonotmesis, there is wallerian degeneration, but because the endoneurial tubes are retained, effective axonal regeneration can occur unless it is impeded by a connective tissue fibroblastic reaction (neuroma in continuity).
Following nerve injury, the history suggests the type of pathology while the neurologic examination localizes the lesion. A standard neuroanatomy textbook should be available for review of specific motor and sensory innervation and possible anatomic variations. A complete neurologic examination must be done, with emphasis on the nerves involved. Motor, sensory, and reflex deficits must be correlated to determine severity and distribution of involvement. The sensory findings are the least reliable because of overlap from adjacent uninjured nerves. Electromyography and nerve conduction studies establish a baseline for monitoring subsequent recovery but are not helpful until 2–3 weeks after an acute injury.
An accurate history and a meticulous examination are the key elements. The history will help differentiate traumatic neuropathies from those of infectious origin (diphtheria, mumps, influenza, malaria, syphilis, typhoid, typhus, dysentery, tuberculosis, gonorrhea) or toxic or metabolic origin (diabetes, rheumatic fever, gout, leukemia, vitamin deficiency, polyarteritis nodosa, drug reaction, heavy metals, carbon monoxide).
Pain resulting from nerve injury (neuropathic pain) can be caused by neuroma formation, by involvement of the sympathetic nervous system, or by alterations in peripheral and central processing of sensory information. Painful neuromas produce pain when pressure is applied locally. Pain associated with CRPS (formerly known as causalgia) is burning and dysesthetic and is associated with hyperpathia and trophic skin and joint changes. Early aggressive treatment of CRPS is essential to avoid permanent disability. Local anesthetic blocks of the peripheral and sympathetic nerves may be helpful in diagnosing and treating these problems. Medical management includes tricyclic antidepressants, anticonvulsants (carbamazepine or gabapentin), mexiletine, or sympathetic blocking agents. Surgical treatment includes neurolysis, resection of the neuroma away from sites of mechanical trigger, sympathectomy, or electrical stimulation of the proximal nerve or the spinal cord.
Treatment of Traumatic Peripheral Nerve Lesions
The treatment depends on the nature of the nerve injury. Early exploration and repair should be used for clean lacerations. When associated injuries are present (major arterial laceration, shock) or when there is gross contamination, it is better to tag the nerve endings with nonabsorbable suture to prevent excessive retraction and to facilitate subsequent repair. Such injuries should be approached within 10 days if the patient’s condition warrants. Patients with nerves injured by stretch or contusion should be followed for clinical signs of recovery. If no recovery is seen within 3 months, exploration is indicated. Intraoperative electrical studies help distinguish between axonotmetic injuries in the process of recovery (compound nerve action potential present) and those with no evidence of recovery. Recovering nerves should be left intact, but in those with no evidence of function, the damaged segment should be resected. Although this approach sometimes results in exploration when the nerves would have recovered spontaneously, initiation of early repair is important in nerve that will not recover. Because nerve regeneration is relatively slow and because intraneural fibrosis eventually prevents axonal growth (approximately 18 months), waiting too long may eliminate the chance for recovery.
The techniques of nerve anastomosis depend on whether the primary nerve endings are in close proximity; if so, epineurial repair should be performed with microscopic magnification and fine (8-0 or finer) suture. Nerve repair must be done without tension. If the gap between endings is too long for primary repair, nerve grafts (usually sural) should be used in an interfascicular repair.
Some lesions resulting from contusion or compression are improved by neurolysis. The same is true of some injection neuropathies (depending upon the substance injected).
Only careful grading of sensorimotor function following injury will allow accurate evaluation of recovery, especially after surgical repair. Thus, improvement may not be noted for many months, and the patient must be psychologically prepared. Recovery of function should proceed smoothly from proximal to distal; maximum recovery may take 1–2 years.
Patients must understand that their role in treatment is an active one, and their motivation must be maintained. Early rehabilitation is important to maintain full joint range of motion while awaiting functional return. Later, physical therapy will help maximize the return of useful function.