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OBJECTIVE: Fecal incontinence in women is thought to be associated with sphi nc ter laceration or pudendal nerve damage. A prolonged pudendal nerve terminal mot or latency is evidence of profound nerve damage, but pudendal nerve terminal mot or latency can be normal even when nerve injury has been sustained. We performed quantitative electromyography (EMG) to compare multiple motor unit action poten tial parameters between recently postpartum women and nulliparous women. METHODS : Standardized examinations were prospectively performed on 2 groups: 1) healthy nulliparous women without pelvic floor disorders (n=28) and 2) asymptomatic wom en who were postpartum following vaginal delivery of their first child (n = 23). The examinations included pelvic organ prolapse quantification measurements, e ndoanal ultrasonography, pudendal nerve terminal motor latency, sacral reflexes, and concentric needle EMG using multiple motor unit action potential analysis. RESULTS: A mean of 11.5 (standard deviation [SD] 1.1) weeks had elapsed since fi rst vaginal deliveries in the postpartum group. The mean fetal weight at deliver y was 3,495 (SD 458) grams. There were no sphincter defects seen by ultrasonogra phy. Compared with the nulliparous women, pudendal nerve terminal motor latency and sacral reflexes (clitoral-anal reflex, urethral-anal reflex) were not incr eased in the postpartum group. Each of the quantitative parameters (duration, am plitude, area, turns, and phases), measured from motor unit action potentials in the postpartum group, were larger than in the nulliparous group (P ≤.004, nest ed analysis of variance [ANOVA]). CONCLUSION: Quantitative EMG using multiple mo tor unit action potential analysis can detect the presence after vaginal childbi rth of subtle nerve injury not demonstrable by pudendal nerve terminal motor lat ency. Even asymptomatic women show evidence of pelvic floor nerve injury after u ncomplicated deliveries.
OBJECTIVE: Fecal incontinence in women is thought to be associated with sphi nc lace or pudendal nerve damage. A prolonged pudendal nerve terminal mot or latency is evidence of profound nerve damage, but pudendal nerve terminal mot or latency can be normal even when nerve injury METHODS: Standardized examinations were prospectively performed on 2 groups: 1) healthy nulliparous women without pelvic floor disorders (n = 28) and 2) asymptomatic wom en who were postpartum following vaginal delivery of their first child (n = 23). The examinations included pelvic organ prolapse quantification measurements, e ndoanal ultrasonography, pudendal nerve terminal motor latency, sacral reflexes, and concentric needle EMG using multiple motor unit action potential analysis. RESULTS: A mean of 11.5 (standard d The mean fetal weight at deliver y was 3,495 (SD 458) grams. There were no sphincter defects seen by ultrasonogra phy. Compared with the nulliparous women, pudendal nerve terminal motor latency and sacral reflexes (clitoral-anal reflex, urethral-anal reflex) were not incr eased in the postpartum group. Each of the quantitative parameters (duration, am plitude, area, turns, and phases), measured from motor unit action potentials in the postpartum group, were larger than in the nulliparous group (P ≤ 0.004, nest ed analysis of variance [ANOVA]). CONCLUSION: Quantitative EMG using multiple mo tor unit action potential analysis can detect the presence after vaginal childbi rth of subtle nerve injury not demonstrable by pudendal nerve terminal motor lat ency. Even asymptomatic women show evidence of pelvic floor nerve injury after u ncomplicated deliveries.