EDITORIAL COMMENT

The urodynamic observation of detrusor underactivity (DU) and the related clinical disorder of detrusor hyperreflexia with impaired contractility (DHIC) are common contributors to urinary incontinence, voiding disorders, and overactive bladder symptoms especially in the aged. While DU can be due to chronic obstructive or neurologic damage, in many cases the etiology is unknown. The nominally implied detrusor motor dysfunction is generally attributed to either impaired parasympathetic outflow or structural changes of the detrusor muscle resulting in diminished muscular contractile capabilities. However, animal and human evidence is not conclusive regarding a primary age-associated loss of detrusor contractile capabilities. Authors hypothesized that the observation of DU, with or without detrusor overactivity, as a primary urodynamic finding would be associated with higher volüme sensory thresholds when compared to other common nonobstructive, non-neurologic urodynamic conditions. Data from each urodynamic record abstracted into a spreadsheet, included age, gender, volume and pressures at each sensation, voiding volumes and flow rates, and maximum Watts Factor (WFmax) as calculated over the voiding phase by the urodynamic software. Wall stress at each sensation was calculated as the product of detrusor pressure and volume. Examination suggests a diminished rate of response to volume, pressure and wall stress in DU patients (except for pressure in DO, as discussed above) as the bladder reaches larger volumes, in contrast to a more linear response in ormal voiders. Authors conclude that DU is associated with altered perceptions of bladder volume, and not necessarily diminished detrusor contractility. This diminished sensitivity to bladder volumes may be mediated by dysfunctional central processing of afferent information provided by the filling bladder.

Oğuz Mertoğlu MD