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Pudendal nerve function in normal and encopretic children
S M Sentovich1, S S Kaufman, R L Cali
1Section of Colon and Rectal Surgery, Creighton University School of Medicine, Omaha, Nebraska, USA.
Insights
Pudendal nerve function is normal in children with encopresis (involuntary defecation). External anal sphincter non-relaxation is common in encopretic children, but pudendal neuropathy is not a significant cause.
Area of Science:
- Pediatric Gastroenterology
- Neuroscience
- Urology
Background:
- Abnormal pudendal nerve function is linked to fecal issues in adults.
- The role of pudendal neuropathy in childhood encopresis requires investigation.
Purpose of the Study:
- To evaluate pudendal nerve function in children with encopresis.
- To compare pudendal nerve function between encopretic and healthy children.
Main Methods:
- Pudendal nerve terminal motor latency was measured in 23 encopretic and 23 control children.
- Anal manometry and electromyography were performed on all participants.
Main Results:
- Pudendal nerve latency was similar in encopretic and control groups.
- External anal sphincter non-relaxation occurred in 75% of encopretic children.
- Anorectal manometry showed lower pressures in encopretic children, but few had significantly abnormal sphincter pressures.
Conclusions:
- Pudendal nerve function is not significantly impaired in childhood encopresis.
- External anal sphincter dysfunction is a key finding in encopretic children.
- Pudendal neuropathy is unlikely to be a primary cause 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.