Which pelvic floor defects cause stress incontinence?

University Of Michigan At Ann Arbor, Ann Arbor MI

Investigators

Linked publications & trials

Abstract

The lack of scientific understanding of the basic mechanism underlying stress urinary incontinence (SUI) is impeding preventing, treatment and research. New findings reveal birth-induced injuries that may explain the higher prevalence of this condition in women than men. We propose studying women with SUI who present for treatment to determine the type and location of pelvic floor failure responsible for this priority condition in women's health. Our hypothesis maintains that SUI occurs through individual defects and specific combinations of defects. We will quantify and compare vesical neck support and urethral sphincter function in classes; women with SUI, and controls; similar women without SUI, to test this hypothesis. Aim 1: Using these data we will demonstrate that the occurrence of SUI is a function of both support stiffness and sphincter constriction and that the threshold for having SUI is an interaction of these two types of measures that explains SUI better than either sphincter or support function alone. Aim 2: Define the anatomic abnormalities that are responsible for these functional problems. Using MR imaging we will show that, 1) Loss of support involves loss of levator and bulk measurable on MRI as decrease in size of the levator ani and/or breaks in connective tissue supports and 2) Sphincteric weakness results from quantifiable loss of sphincter bulk in the smooth and striated sphincter muscles. Correlation between anatomic measurements and functional parameters listed in the primary hypotheses will determine the cause of functional abnormalities. Aim 3: Evaluate other personal and medical variables that may influence incontinence. The importance of this research lies in its providing insights that should help form the basis for rational treatment selection in women with SUI, devise injury prevention, understand where deterioration occurs, and form a basis for organ , cell, and molecular research into these disease processes.