Bladder contractility and idiopathic detrusor instability in the female.

Twenty females with pure stress urinary incontinence (Group A) were studied clinically and urodynamically together with 20 stress incontinent women with idiopathic detrusor instability (Group B) and 20 controls (Group C). Forty females with the idiopathic urge syndrome, 20 with detrusor instability (motor urgency, Group D) and 20 with stable bladders (sensory urgency, Group E) were also investigated. Detrusor contractility, assessed on the basis of strength and velocity parameters derived from pressure flow data, was increased in the unstable groups. In particular, the maximum mechanical power (per unit of bladder wall surface area) generated by the contracting detrusor during voiding was higher in the unstable patients, this was also the case when estimating maximum bladder contraction velocity. No significant difference in these parameters was found in the patients with sensory urgency when compared with the controls and with the women with stress urinary incontinence, nor was there any significant difference between patients with motor urgency and the stress incontinent patients with detrusor instability. The enhanced contractile capability could be explained in the unstable stress incontinent group by a reduced threshold of stretch receptors in the urethral walls. If this were the case, urine running through the urethra at the beginning of voiding would be able to activate a urethrovesical reflex which may augment micturition contractions. In the group with the idiopathic urge syndrome one could speculate that sensory and motor urgency are due to the same neurological disorder (i.e. possibly a reduction in a tonic inhibitory or modulatory device) that would affect detrusor mechanics at different levels of the nervous system, resulting in different contractile capabilities.