Clinical aspects of peripheral nerve surgery

With the advent of adjuvant therapy and aggressive resuscitative measures in trauma, surgical amputation for extremity malignancies/injuries is no longer the time honored treatment. It is this change in the purview of cancer/trauma treatment that has increased the need for peripheral nerve reconstruction and subsequently the restoration of the quality of life, form and function. Failure to restore sacrificed or injured nerves can lead to the loss of muscle function, impaired sensation and/or painful neuropathies. Current surgical strategies for repair of critical nerves involves the transfer of normal donor nerve from an uninjured body location. Frequently however these “gold standard” methods for tissue restoration are limited by tissue availability, risk of disease spread, secondary deformities and potential differences in tissue structure and size. When a nerve injury is small (<5-10 mm), the gap can usually be closed by an end-to-end neurography. Surgical repair involves the direct reconnection of nerve ends or of individual nerve fascicles, and is successful if tension is minimized and technique optimized. However, if the nerve defect is large (>10 mm), alternative methods are required. These larger functional nerve defects have traditionally been reconstructed by autografting, the surgical transfer and sacrifice of healthy nerve from an uninjured location to the injured site. Allografts and immunosuppression have been substituted for autogenous nerve grafts. However, functional capability following nerve restoration with allografting has not approached that following autografting. Furthermore, considerations of oncologic and traumatic morbidity frequently preclude the use of allografting because of the necessity for immunosuppression. Despite the current “gold standard” of nerve autografting, complete functional recovery is seldom achieved. One possible alternative to autogenous tissue replacement is the development of engineered constructs to replace those elements necessary for axonal proliferation and include: a scaffold, support cells, induction factors and extracellular matrices