ABSTRACT

The pathologic mechanisms underlying neurogenic detrusor overactivity (NDO) may be classified into abnormally increased afferent activity from the bladder and urethra, or abnormal handling of afferent signals in the brain. Two hypotheses have been proposed to explain increased afferent activity and therefore overactive bladder (OAB) symptoms—the urothelium-based hypothesis and the myogenic hypothesis. The urothelium and suburothelium is a metabolically active integrated functional unit that plays an important role in modulating bladder activity. According to the neurogenic hypothesis, abnormal handling of afferent signals in the brain can lead to OAB and NDO. Functional brain imaging has recently emerged as a useful tool for understanding neural activity in different brain cortical regions and has been used to study the control of the lower urinary tract functions.