Peripheral Nerve Injuries 

Paul of Aegina (625-690) was the first to describe approximation of the nerve ends with wound closure. Hueter (1871, 1873) introduced the concept of primary epineurial nerve suture, and Nelaton described secondary nerve repair in 1864. Even at an early time, the idea of decreasing tension on the nerve suture was important. In 1882, Mikulicz described sutures that reduced tension, and Loebke described bone shortening to decrease nerve tension in 1884. In 1876, Albert described grafting nerve gaps. A great deal of information regarding the evaluation and treatment of traumatic nerve injuries came with the experience of treating wartime injuries.

Peripheral nerve injuries may result in loss of motor function, sensory function, or both.^{[1, 2, 3]}

Frequency

Limited reported data are available to determine the incidence of peripheral nerve injuries. In North America, data taken from a trauma population in Canada revealed that approximately 2-3% of patients had a major nerve injury. In New South Wales, Australia, 2% of patients were reported to have a major nerve injury.

Peripheral nerve injuries may occur as a result of trauma (eg, a blunt or penetrating wound, trauma) or acute compression.

Peripheral nerve injury may result in demyelination or axonal degeneration. Clinically, both demyelination and axonal degeneration result in disruption of the sensory and/or motor function of the injured nerve. Recovery of function occurs with remyelination and with axonal regeneration and reinnervation of the sensory receptors, muscle end plates, or both.^[4]

The clinical appearance of an injured nerve depends on the nerve affected. Injury to a motor nerve results in a loss of muscle function, and injury to a sensory nerve results in a loss of sensation to the affected nerve's sensory distribution and/or neuromatous or causalgia pain.^[2]

Classification of nerve injury was described by Seddon in 1943^[5] and by Sunderland in 1951.^[6] The classification of nerve injury described by Seddon comprised neurapraxia, axonotmesis, and neurotmesis. Sunderland expanded this classification system to 5 degrees of nerve injury.

First-degree nerve injury

A first-degree injury or neurapraxia involves a temporary conduction block with demyelination of the nerve at the site of injury. Electrodiagnostic study results are normal above and below the level of injury, and no denervation muscle changes are present. No Tinel sign is present. Once the nerve has remyelinated at that area, complete recovery occurs. Recovery may take up to 12 weeks.

Second-degree nerve injury

A second-degree injury or axonotmesis results from a more severe trauma or compression. This causes wallerian degeneration distal to the level of injury and proximal axonal degeneration to at least the next node of Ranvier.^[7] In more severe traumatic injuries, the proximal degeneration may extend beyond the next node of Ranvier. Electrodiagnostic studies demonstrate denervation changes in the affected muscles, and in cases of reinnervation, motor unit potentials (MUPs) are present. Axonal regeneration occurs at the rate of 1 mm/d or 1 in/mo and can be monitored with an advancing Tinel sign. The endoneurial tubes remain intact, and therefore, recovery is complete with axons reinnervating their original motor and sensory targets.

Third-degree injury

A third-degree injury was introduced by Sunderland to describe an injury more severe than second-degree injury. Similar to a second-degree injury, wallerian degeneration occurs, and electrodiagnostic studies demonstrate denervation changes with fibrillations in the affected muscles. In cases of reinnervation, MUPs are present. Regeneration occurs at 1 mm/d, and progress may be monitored with an advancing Tinel sign. However, with the increased severity of the injury, the endoneurial tubes are not intact, and regenerating axons therefore may not reinnervate their original motor and sensory targets.

The pattern of recovery is mixed and incomplete. Reinnervation occurs only if sensory fibers reach their sensory end organs and motor fibers reach their muscle targets. Even within a sensory nerve, recovery can be mismatched if sensory fibers reinnervate a different sensory area within the nerve's sensory distribution. If the muscle target is a long distance from the site of injury, nerve regeneration may occur, but the muscle may not be completely reinnervated because of the long period of denervation.

Fourth-degree injury

A fourth-degree injury results in a large area of scar at the site of nerve injury and precludes any axons from advancing distal to the level of nerve injury. Electrodiagnostic studies reveal denervation changes in the affected muscles, and no MUPs are present. A Tinel sign is noted at the level of the injury, but it does not advance beyond that level. No improvement in function is noted, and the patient requires surgery to restore neural continuity, thus permitting axonal regeneration and motor and sensory reinnervation.

Fifth-degree injury

A fifth-degree injury is a complete transection of the nerve. Similar to a fourth-degree injury, it requires surgery to restore neural continuity. Electrodiagnostic findings are the same as those for a fourth-degree injury.

Sixth-degree injury

A sixth-degree injury was introduced by Mackinnon to describe a mixed nerve injury that combines the other degrees of injury.^[8] This commonly occurs when some fascicles of the nerve are working normally while other fascicles may be recovering, and other fascicles may require surgical intervention to permit axonal regeneration.

Indications for nerve injury surgery are as follows:

• Closed nerve injury: With no evidence of recovery either clinically or with electrodiagnostic studies at 3 months following injury, surgery is recommended.
• Open nerve injury (ie, laceration): Surgical exploration is recommended as soon as possible. All lacerations with a reported loss of sensation or motor weakness should be surgically explored.
• Crush nerve injury: Surgical exploration of the nerve may be delayed for as long as several weeks. However, after 3 months with no evidence of reinnervation electrically (motor unit potentials [MUPs] present) or clinically, surgical reconstruction with repair or graft is indicated.

Nerve is composed of neural and connective tissue. In myelinated axons, each nerve fiber is surrounded by the endoneurium. Groups of nerve fibers are surrounded by the perineurium to form fascicles, and groups of fascicles are surrounded by the internal and external epineurium. Knowledge of motor and sensory fascicular topography within the nerve is essential to ensure correct alignment of the motor and sensory fascicles.

In contaminated or crush nerve injuries, delayed reconstruction may be indicated.