Comparative Study
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A surprisingly low prevalence of demonstrable stress urinary incontinence and pelvic organ prolapse in women with multiple sclerosis followed at a tertiary neurogenic bladder clinic.

PURPOSE: We report the prevalence of stress urinary incontinence and pelvic organ prolapse in patients with multiple sclerosis referred to a tertiary care neurogenic bladder clinic.

MATERIALS AND METHODS: We queried an institutional review board approved neurogenic bladder database for urodynamic and demographic data on patients with multiple sclerosis followed for lower urinary tract symptoms in a 12-year period. Demographic information included multiple sclerosis classification, age at initial visit, body mass index, parity and pelvic examination findings. Prolapse was defined as stage 2 prolapse or greater. Stress urinary incontinence was defined as urodynamic stress incontinence and/or incontinence on a supine stress test.

RESULTS: Included in analysis were 280 women with a mean age of 50 years and a mean 13-year history of multiple sclerosis. Relapse remitting multiple sclerosis was noted in 40% of patients, while 45 (16%) had stress urinary incontinence. Women with stress urinary incontinence had a higher average maximum urine flow (14 vs 9 ml per second, p <0.003), higher voided volume (272 vs 194 cc, p = 0.018) and higher body mass index (30 vs 25 kg/m(2), p <0.005). Overall, 23 women (9%) had pelvic organ prolapse, including 2 (9%) with posterior prolapse only, 8 (35%) with anterior prolapse only and 13 (56%) with posterior and anterior prolapse. There was no difference in age, body mass index or multiple sclerosis subtype between women with vs without pelvic organ prolapse.

CONCLUSIONS: The 14% prevalence of demonstrable stress urinary incontinence and 9% rate of pelvic organ prolapse are markedly lower than published historical data on an age matched cohort without multiple sclerosis. The surprisingly low prevalence of stress urinary incontinence and pelvic organ prolapse in women with multiple sclerosis may be attributable to decreased activity, a neurogenically enhanced vesicourethral unit or other functional or anatomical etiologies.

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