Sequential changes in voiding dynamics related to the development of detrusor instability in women with stress urinary incontinence
A. Cucchi
Abstract
A. Cucchi
Abstract
We evaluated 31 women who had undergone a conservative treatment regimen for stress urinary incontinence and who, during the treatment period, were assessed twice urodynamically (by cystometry and pressure/flow study) at an interval of months between the two examinations. Seventeen (Group 1) had stable bladders at time 1 and detrusor instability (DI) after a mean of 12 months (time 2). Fourteen (Group 2) had stable bladders both at time 1 and after a mean of 15 months. Of the urodynamic parameters evaluated, the opening detrusor pressure (pdet.op) reflected the height of the bladder neck pressure rise that normally occurs during the opening phase of micturition and that is overcome by the detrusor contraction pressure at the onset of flow. At the second testing, Group 1 patients showed greater detrusor strength. They also showed a more elevated pdet.op (= a more elevated bladder neck pressure rise during the onset of voiding detrusor contraction), which may have been necessary to ensure an enhanced bladder contractility level. Indeed, a higher rise in pressure, hence in muscular tension, at the bladder neck region should obviously lead to increased afferent signals from tension receptors, and positive feedback to the detrusor of such increased signals may yield more intense neural stimulation. This would amplify the facilitating effect on bladder contractility of a possible DI-related decrease in electrical resistance between the detrusor smooth muscle cells.
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We evaluated 31 women who had undergone a conservative treatment regimen for stress urinary incontinence and who, during the treatment period, were assessed twice urodynamically (by cystometry and pressure/flow study) at an interval of months between the two examinations. Seventeen (Group 1) had stable bladders at time 1 and detrusor instability (DI) after a mean of 12 months (time 2). Fourteen (Group 2) had stable bladders both at time 1 and after a mean of 15 months. Of the urodynamic parameters evaluated, the opening detrusor pressure (pdet.op) reflected the height of the bladder neck pressure rise that normally occurs during the opening phase of micturition and that is overcome by the detrusor contraction pressure at the onset of flow. At the second testing, Group 1 patients showed greater detrusor strength. They also showed a more elevated pdet.op (= a more elevated bladder neck pressure rise during the onset of voiding detrusor contraction), which may have been necessary to ensure an enhanced bladder contractility level. Indeed, a higher rise in pressure, hence in muscular tension, at the bladder neck region should obviously lead to increased afferent signals from tension receptors, and positive feedback to the detrusor of such increased signals may yield more intense neural stimulation. This would amplify the facilitating effect on bladder contractility of a possible DI-related decrease in electrical resistance between the detrusor smooth muscle cells.
Key concepts: Medicine, Detrusor instability, Cystometry, Urology, Detrusor muscle, Urination, Contractility, Neck of urinary bladder