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Objectives: A significant body of knowledge implicates menopausal estrogen levels in the pathogenesis of the ommon pelvic floor disorders (PFDs). These health conditions substantially decrease quality of life, increase depression, social isolation, caregiver burden, and economic costs to the individuals and society. Methods: This review summarizes the epidemiology of the individual PFDs with particular attention to the understanding of the relationship between each PFD and menopausal estrogen levels, and the gaps in science and clinical care that affect menopausal women. In addition, we review the epidemiology of recurrent urinary tract infection (rUTI)—a condition experienced frequently and disproportionately by menopausal women and hypothesized to be potentiated by menopausal estrogen levels. Results: The abundance of estrogen receptors in the urogenital tract explains why the natural reduction of endogenous estrogen, the hallmark of menopause, can cause or potentiate PFDs and rUTIs. A substantial body of epidemiological literature suggests an association between menopause, and PFDs and rUTIs; however, the ability to separate this association from age and other comorbid conditions makes it difficult to draw definitive conclusions on the role of menopause alone in the development and/or progression of PFDs. Similarly, the causative link between the decline in endogenous estrogen levels and the pathogenesis of PFDs and rUTIs has not been well-established. Conclusions: Innovative human studies, focused on the independent effects of menopausal estrogen levels, uncoupled from tissue and cellular senescence, are needed.

Electrical stimulation is an effective and well-tolerated treatment for overactive bladder. Initial work in animals indicated the potential of this treatment, and early clinical experience in Europe further supported its likely efficacy. Although the mechanism of action of electrical stimulation remains unproven in humans, it is believed to be a neuromodulating therapy which affects the neural signaling that controls continence. There is also strong evidence that electrical stimulation affects striated muscle. The therapy can cause hypertrophy of skeletal muscle fibers, possibly by the recruitment of faster-conducting motor units, which would not normally be recruited during voluntary efforts. In addition, electrical stimulation can alter the expression of myosin isoforms, favoring a conversion to type I muscle. Despite our incomplete understanding of the mechanism of action of electrical stimulation, clinical devices have been developed quickly. Case series have been reported throughout Europe. These were followed by controlled clinical trials in the United States. There is good evidence that the use of vaginal electrical stimulators can reduce the occurrence of symptoms of overactive bladder in about half of the patients treated. Multiple uses of nonimplanted stimulation, including thigh stimulation, anal stimulation, and direct pelvic muscle stimulation, have been reported. In these trials, it is common for objective findings to be poorly correlated with subjective reports of improvements or cure. Patients frequently report that the urge-to-Ieak time improves, but this is difficult to measure objectively. The use of nonimplanted devices is effective and well tolerated, and should precede the use of implanted devices. A direct comparison with other effective methods of treatment for overactive bladder is warranted. UROLOGY 55 (Suppl SA): 17-23, 2000.

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