Mechanisms of Disease: central nervous system involvement in overactive bladder syndrome

The pathophysiology of overactive bladder syndrome (OABS) and detrusor overactivity (DO) is complex and involves both peripheral and central nervous system (CNS) factors. Central in OABS is urgency, the pathophysiology of which is unknown. Increased afferent activity, decreased capacity to process afferent information, decreased suprapontine inhibition, and increased sensitivity to contraction-mediating transmitters are all potential causes of DO and OABS. Because both urgency and initiation of the micturition reflex depend on afferent input from the lower urinary tract, it seems logical that in the search for new therapies for DO/OABS, afferent functions and central control of afferent functions are targets of interest. Voiding and storage reflexes involve several transmitters and transmitter systems that could be targets for the development of drugs that control DO/OABS. Perturbations of these systems are found in CNS disorders associated with DO/OAB, such as stroke, Parkinson's disease, spinal cord injury and multiple sclerosis. This short overview focuses on the afferent pathways and on how the transmitter systems that control micturition can be perturbed by disease to give rise to DO/OABS.