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Treatment strategies for stress incontinence are based on the concept that urethral mobility is the predominant causal factor with sphincter function a secondary contributor. To our knowledge the relative importance of these 2 factors has not been assessed in properly controlled studies.The Research on Stress Incontinence Etiology project is a case-control study that compared 103 women with stress incontinence and 108 asymptomatic controls in groups matched for age, race, parity and hysterectomy. Urethral closure pressure, urethral and pelvic organ support, levator ani muscle function and intravesical pressure were measured and analyzed using logistic regression and multivariable modeling.Mean ± SD maximal urethral closure pressure was 42% lower in cases (40.8 ± 17.1 vs 70.2 ± 22.4 cm H2O, d = 1.47). Lesser effect sizes were seen for support parameters, including resting urethral axis and urethrovaginal support (d = 0.41 and 0.50, respectively). Other pelvic floor parameters, including genital hiatus size and urethral axis during muscle contraction (d = 0.60 and 0.58, respectively), differed but levator strength and levator defect status did not. Maximum cough pressure, which is an assessment of stress on the continence mechanism, was also different (d = 0.43). After adjusting for body mass index the maximal urethral closure pressure alone correctly classified 50% of cases. Adding the best predictors for urethrovaginal support and cough strength to the model added 11% of predictive ability.The finding that maximal urethral closure pressure and not urethral support is the factor most strongly associated with stress incontinence implies that improving urethral function may have therapeutic promise.