Normal bladder function is controlled by the central nervous system (CNS) and any peripheral contribution to bladder control is believed to be small. Nevertheless, anatomically and functionally, such a contribution might exist. Taking account of this evidence, we propose that the detrusor muscle is arranged into modules, which are circumscribed areas of muscle active during the filling phase of the micturition cycle. These modules might be controlled by a peripheral myovesical plexus, consisting of intramural ganglia and interstitial cells. Detrusor overactivity is the occurrence of abnormal increases in pressure during bladder filling, which the patient cannot inhibit. This disorder is thought to be a consequence of abnormal expression of the micturition reflex or changes in the properties of the smooth muscle. We propose that detrusor overactivity results from exaggerated symptomatic expression of peripheral autonomous activity, resulting from a shift in the balance of excitation and inhibition in smooth muscle modules. These structures responsible for origin and spread of peripheral autonomous activity could be targeted to help develop new therapeutic strategies.