In 2002, the International Continence Society defined the term overactive bladder (OAB) as a symptom syndrome that is accompanied by urgency with or without urge incontinence, frequency and nocturia. A proven urinary tract infection or other obvious pathologies must be excluded. The pathophysiology of OAB has not been clarified in detail and is the subject of ongoing research, so partially overlapping hypotheses exist. The urothelium-based hypothesis suggests functional changes of urothelial receptors as well as functional changes regarding the sensitivity and coupling of the suburothelial myofibroblasts, which ultimately lead to increasing activity of afferent signals and urgency. The myogenic hypothesis is based on the assumption that unstable detrusor contractions may be triggered by changes in their excitability and coupling with other myocytes or myofibroblasts. Unstable detrusor contractions generate increased afferent activity followed by symptoms of overactive bladder. The hypothesis of abnormal processing of afferent signals assumes that damage to central inhibitory pathways and/or sensitisation of afferent nerves lead to the activation of the micturition reflex, which, in turn, induces unstable detrusor contractions. In addition, hormonal and psychological influences are discussed.