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DOI: 10.1055/s-2006-949699
Peroneal Nerve Stretch/Traction Zone of Injury Extends to Neuromuscular Regions of Muscle, Preventing Success of Nerve Grafting for Foot Drop
Since Millesi began reporting the results of nerve grafting to correct the foot drop of common peroneal nerve palsy, the results have been poor, such that Dr. Millesi himself recommended doing a tendon transfer concomitant with the nerve grafting. Recent surgical reports confirm success for nerve grafting without tendon transfer in just 33% of patients with a nerve gap of < 6 cm, and 16% for a nerve gap of > 6 cm. In contrast, success (M3 to M4 +) of 85 to 90%) has been reported recently when tendon transfer is added to the nerve grafting.
The present study was carried out to investigate the hypothesis that the failure of nerve grafting for severe stretch/traction injury to the common peroneal nerve is due to extension of the zone of injury from the nerve into the muscle entry zone of the terminal axons.
From a patient who was 3 months post disruption of the common peroneal nerve at the knee from a stretch/traction injury, the distal portion of the nerve and its entry into the foot/ankle extensor muscles was excised en bloc and submitted for histopathologic analysis. Staining included H&E, trichrome, S-100, and neurofilament immunohistochemistry. The pathology was compared to a non-injured human specimen obtained from an above-knee amputation.
The injured common peroneal nerve had no neurofilament staining, but intense S-100 staining consistent with Wallerian degeneration. There were no nerve bundles in continuity within the muscle. All muscle fibers demonstrated denervation atrophy. There was diffuse collagenization of the region between the nerve and the muscle, consistent with injury at the nerve-to-muscle entry zone. This was in contrast to the histology of the normal nerve/muscle interface.
Based on the histopathology demonstrated in this single human specimen, it is likely that the reason for failure of nerve grafting for common peroneal nerve disruption due to stretch/traction, is that the zone of injury has transformed the normal relationship of the terminal motor axons and muscle into a region of collagen, thereby preventing even an expertly done interposition interfascicular nerve graft from having regenerating axon sprouts reach the target end-organ, the denervated muscle. Conceptually, this problem can be overcome by direct neurotization of the muscle, instead of doing interposition interfascicular nerve grafting.