An integral theory of female urinary incontinence. Experimental and clinical considerations.

TLDR: The complex interplay of the specific structures involved in female urinary continence are analyzed and the effects of age, hormones, and iatrogenically induced scar tissue on these structures are discussed specifically with regard to understanding the proper basis for treatment of urinary incontinence.

Abstract: In this Theory paper, the complex interplay of the specific structures involved in female urinary continence are analyzed. In addition the effects of age, hormones, and iatrogenically induced scar tissue on these structures, are discussed specifically with regard to understanding the proper basis for treatment of urinary incontinence. According to the Theory stress and urge symptoms may both derive, for different reasons from the same anatomical defect, a lax vagina. This laxity may be caused by defects within the vaginal wall itself, or its supporting structures i.e. ligaments, muscles, and their connective tissue insertions. The vagina has a dual function. It mediates (transmits) the various muscle movements involved in bladder neck opening and closure through three separate closure mechanisms. It also has a structural function, and prevents urgency by supporting the hypothesized stretch receptors at the proximal urethra and bladder neck. Altered collagen/elastin in the vaginal connective tissue and/or its ligamentous supports may cause laxity. This dissipates the muscle contraction, causing stress incontinence, and/or activation of an inappropriate micturition reflex, (“bladder instability”) by stimulation of bladder base stretch receptors. The latter is manifested by symptoms of frequency, urgency, nocturia with or without urine loss.