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.
The future in peripheral nerve injuries lies in maximizing motor and sensory recovery after nerve injury. Strategies to maintain the neuromuscular junction are important for permitting muscle reinnervation after prolonged muscle denervation, as well as decreasing injury to the cell body.
In traumatic nerve injury with large nerve gaps, nerve allografts may be considered. However, because of the morbidity associated with immunosuppression, the use of the nerve allograft has been limited to otherwise unreconstructable injuries. Investigations to decrease the antigenicity of the allograft or induce tolerance to the nerve allograft are ongoing, and success in these investigations will permit the use of nerve allografts without immunosuppression.
A nerve is composed of neural tissue (axon) and connective tissue. In myelinated nerve fibers, each axon 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. For optimal outcome after surgery, knowledge of motor and sensory fascicular topography within the nerve is essential to ensure correct alignment of the motor and sensory fascicles.
Peripheral nerve injury may result in demyelination, axonal degeneration, or both. Clinically, both demyelination and axonal degeneration result in disruption of sensory function, motor function, or both in the injured nerve. Depending on the severity and degree of nerve injury, recovery of function occurs with remyelination and with axonal regeneration and reinnervation of the sensory receptors, motor end plates, or both. [1, 2, 3]
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.
With restoration of nerve continuity, axons may regenerate and thus reinnervate the motor end plates and sensory receptors. When the nerve injury is very proximal (eg, in brachial plexus injury or sciatic nerve injury), nerve regeneration may not occur quickly enough to permit muscle reinnervation. For example, in a lower trunk brachial plexus injury, reinnervation of the ulnar nerve intrinsic hand muscles is not possible due to the long period of muscle denervation because of the long distance necessary for nerve regeneration.
If, however, surgery is performed within 3-6 months after the nerve injury was sustained, the patient can be expected to recover the use of most muscles, excluding muscles in the hand or foot in injuries at the trunk level or higher. Distal nerve transfers are used to recover distal extremity motor function.
A cross-sectional study evaluated the biomedical and psychosocial factors associated with disability after upper-extremity nerve injury (follow-up period, 6 months to 15 years).  In this study, disability, as assessed on the basis of DASH (Disabilities of the Arm, Shoulder, and Hand) Questionnaire scores, was predicted by pain catastrophizing, sensitivity to cold, time elapsed since injury, employment status, intensity of pain, older age, and the presence of brachial plexus injury.
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