INTRODUCTION AND HYPOTHESIS: Although still a matter of debate, stress urinary incontinence (SUI) may be accompanied by damage to urethral and pelvic floor innervations, thus promoting dysfunctions of the urethral support and sphincteric closure mechanisms. The aim of this study was to analyze the pelvic floor and urethral innervations through pelvic electrophysiological tests to identify whether neurological alterations interfere with urinary continence and urethral functional activity. METHODS: This prospective study included 52 women, 33 with clinically and urodynamically proven SUI and 19 continent volunteers matched for age, height, parity, and number of vaginal deliveries by the propensity score method. The patients were divided according to the severity of urinary loss evaluated by measuring abdominal leak point pressure (ALPP). Pudendal nerve terminal motor latency (PNTML), pudendal somatosensory evoked potential (SSEP) latencies, urethral and clitoral sensory thresholds, and urethroanal reflex latency were tested. RESULTS: SUI and control subjects did not differ in PNTML, SSEP latency, and clitoral sensory thresholds. However, reduced responsiveness to urethral electrosensitivity and prolonged urethroanal reflex latency were detected in most incontinent patients. In addition, urethral electrosensitivity was altered in suspected intrinsic sphincteric dysfunction. CONCLUSIONS: Urethral afferent pathways can be altered in women with SUI and may play an important role in evoking intrinsic sphincteric dysfunction.
INTRODUCTION AND HYPOTHESIS: Although still a matter of debate, stress urinary incontinence (SUI) may be accompanied by damage to urethral and pelvic floor innervations, thus promoting dysfunctions of the urethral support and sphincteric closure mechanisms. The aim of this study was to analyze the pelvic floor and urethral innervations through pelvic electrophysiological tests to identify whether neurological alterations interfere with urinary continence and urethral functional activity. METHODS: This prospective study included 52 women, 33 with clinically and urodynamically proven SUI and 19 continent volunteers matched for age, height, parity, and number of vaginal deliveries by the propensity score method. The patients were divided according to the severity of urinary loss evaluated by measuring abdominal leak point pressure (ALPP). Pudendal nerve terminal motor latency (PNTML), pudendal somatosensory evoked potential (SSEP) latencies, urethral and clitoral sensory thresholds, and urethroanal reflex latency were tested. RESULTS: SUI and control subjects did not differ in PNTML, SSEP latency, and clitoral sensory thresholds. However, reduced responsiveness to urethral electrosensitivity and prolonged urethroanal reflex latency were detected in most incontinentpatients. In addition, urethral electrosensitivity was altered in suspected intrinsic sphincteric dysfunction. CONCLUSIONS: Urethral afferent pathways can be altered in women with SUI and may play an important role in evoking intrinsic sphincteric dysfunction.
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