Abstract

Pudendal neuropathy causes idiopathic fecal incontinence. We thus designed a new operation for idiopathic fecal incontinence based on the hypothesis that a conversion from innervation by the neuropathic pudendal nerve to that by the normal somatic peripheral nerve innervating a larger skeletal muscle might enable the anal sphincter to recover from neuropathic muscular atrophy. This study was undertaken to investigate the muscular change of the external anal sphincter after such an operation. On 14 sides of eight dogs, the transected proximal end of the nerve innervating the biceps femoris muscle was microsurgically cross-transferred to the distal end of the transected pudendal nerve. The external anal sphincter was analyzed by electromyography and adenosine 5'-triphosphatase staining at three months after surgery. On 13 of 14 sides, the external anal sphincter was well preserved and the evoked potential was clearly recorded. The external anal sphincter in these dogs, however, had neither any basal electrical activity nor any increased electrical activity. The percentage of Type 1 muscle fibers of the external anal sphincter innervated by the nerve to the biceps femoris muscle (30.9 +/- 9.8 percent) was significantly higher than that of the normal external anal sphincter (15.2 +/- 8.5 percent; P < 0.001) and also significantly lower than that of the normal biceps femoris muscle (38.5 +/- 7.5 percent; P = 0.006). The diameter of the muscle fibers (Types 1 and 2) of the external anal sphincter (expressed as mean +/- standard deviation) innervated by the nerve to the biceps femoris muscle (32.9 +/- 6.2 microm) was also significantly larger than that of the normal external anal sphincter (29.9 +/- 5.1 microm; P = 0.021) and significantly smaller than that of the normal biceps femoris muscle (36.1 +/- 6.1 microm; P = 0.028). The cross-nerve transfer procedure in a dog model was found to prevent muscular atrophy of the external anal sphincter when performed immediately after pudendal nerve transection.

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