Stress urinary incontinence: An alternative concept of pathogenesis

Abstract

A urodynamic study was done on 14 normal subjects and 24 with stress urinary incontinence (SUI), aiming to elucidate SUI etiology. All were multiparous women; 8 of the SUI patients also had partial fecal incontinence. The investigations comprised measuring the vesical and urethral pressures before and after testing external urethral sphincter anesthesia, determination of the functional urethral length and recording of the external urethral sphincter EMG, the straining-urethral reflex and the perineal nerve terminal motor latency (PNTML). The results in both normal and SUI subjects showed that coughing caused both vesical and urethral pressure increase, while an increase in vesical pressure only on external urethral sphincter anesthesia. In SUI patients, the urethral pressure at rest and on coughing was significantly lower (P<0.001) and the functional length shorter than in normal subjects (P<0.01). The external urethral sphincter EMG activity was below normal. The latency of the straining-urethral reflex as well as the PNTML were longer than normal (P<0.01). Results suggest that urethral pressure increase on coughing is effected by external urethral sphincter contraction and is not transmitted by increased intraabdominal pressure, as evidenced by the urethral sphincter anesthesia test and physioanatomic studies. The vesical and urethral descent in SUI is likely to be related to levator subluxation and sagging, which causes levator dysfunction. The cause of the weak external urethral sphincter and the prolonged straining-urethral reflex latency seems to be neurogenic, due probably to stretch of the pudendal nerve in the pudendal canal, as evidenced by the prolonged PNTML.