BACKGROUND: Abnormal pudendal nerve function contributes to fecal retention and incontinence in adults. To determine the role of pudendal neuropathy in childhood, we prospectively evaluated pudendal nerve function in normal and encopretic children. METHODS: We studied pudendal nerve terminal motor latency in 23 encopretic children and in an equal number of similarly aged, normal children. Anal manometry and electromyography were also obtained in all children. RESULTS: Pudendal nerve latency in the encopretic children equaled 1.58 +/- 0.33 msec, which was the same as that in control children. Of the 75 pudendal nerves tested, latency was prolonged in only one encopretic child. In contrast, anal electromyography demonstrated nonrelaxation of the external anal sphincter in 75% of the encopretic children but in only 13% of the normal children (p < 0.001). Anorectal manometry demonstrated, on average, lower and sphincter pressures at rest and with squeezing in the encopretic children (p < 0.01), but only 17% had sphincter pressures more than two standard deviations below normal. CONCLUSIONS: Other than poor relaxation response of the external anal sphincter during evacuation, these data reveal a paucity of functionally important abnormalities in encopretic children. In particular, we find no evidence that abnormal pudendal nerve function is important in the etiology or pathogenesis of encopresis in children.
BACKGROUND: Abnormal pudendal nerve function contributes to fecal retention and incontinence in adults. To determine the role of pudendal neuropathy in childhood, we prospectively evaluated pudendal nerve function in normal and encopretic children. METHODS: We studied pudendal nerve terminal motor latency in 23 encopretic children and in an equal number of similarly aged, normal children. Anal manometry and electromyography were also obtained in all children. RESULTS: Pudendal nerve latency in the encopretic children equaled 1.58 +/- 0.33 msec, which was the same as that in control children. Of the 75 pudendal nerves tested, latency was prolonged in only one encopretic child. In contrast, anal electromyography demonstrated nonrelaxation of the external anal sphincter in 75% of the encopretic children but in only 13% of the normal children (p < 0.001). Anorectal manometry demonstrated, on average, lower and sphincter pressures at rest and with squeezing in the encopretic children (p < 0.01), but only 17% had sphincter pressures more than two standard deviations below normal. CONCLUSIONS: Other than poor relaxation response of the external anal sphincter during evacuation, these data reveal a paucity of functionally important abnormalities in encopretic children. In particular, we find no evidence that abnormal pudendal nerve function is important in the etiology or pathogenesis of encopresis in children.