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  • Title: Some reflections and hypotheses on the pathophysiology of female urinary incontinence.
    Author: Ulmsten U.
    Journal: Acta Obstet Gynecol Scand Suppl; 1997; 166():3-8. PubMed ID: 9253370.
    Abstract:
    It is proposed that opening and closure of the proximal urethra and bladder neck are regulated by a battery of surrounding structures, the most important being the pubourethral-vesical ligaments, the suburethral vaginal wall, 'the hammock', the pubococcygeus muscles, the levator plate and the connective tissue which like glue connects these structures to each other. Inappropriate function in one of these structures can, to some extent, be compensated for by an improved function in another hereby maintaining continence. However, a significantly deteriorated function in the support of urethra--normally maintained by the pubourethral/pubovesical ligaments, the pubococcygeus muscles and suburethral vaginal wall--will result in pronounced stress incontinence. Severe defects in these structures can generally not be compensated for by exercises of the pelvic muscles. This is true, in particular, if there is also a defect function in the connective tissue which 'glues' the urogenital structures to each other. Under such circumstances surgical procedures have to be considered to alleviate the patients symptoms. What is said so far must not exclude the importance of recognizing the role of the internal urethral structures to maintain continence, in particular the quality of urethral muscles, connective tissue and vascularization. In some specific cases of mixed incontinence it can be speculated whether the urge symptom can be caused by an anatomical dysfunction causing the proximal urethra and the bladder neck to remain involuntarily open or to open promptly at even minor pressure provocations. If so distension of the bladder neck and proximal urethra may activate stretch receptors located here which will induce uninhibited detrusor contractions. The presence of estrogen receptors in many of the structures involved in preserving continence may explain the increased prevalence of dysfunctions in the urogenital tract in postmenopausal patients, in particular in those not on hormone replacement therapy.
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