Overactive bladder (OAB) is a syndrome characterized by symptoms of urinary urgency with or without urgency urinary incontinence (UUI), usually with frequency and nocturia. OAB affects approximately 17% of women in the United States and Europe. The causes of OAB, as with many bladder disorders, are multifactorial and are not completely understood. The primary functions of the lower urinary tract (bladder and bladder outlet mechanism) are storage and evacuation of urine. The bladder and the micturition cycle are under complex neural control involving both the sympathetic and parasympathetic nervous systems. Micturition may occur in response to the activation of receptors in the bladder muscle and detection of chemical stimuli by receptors within the bladder lining. Neurogenic or myogenic bladder dysfunction can lead to the symptoms of urgency, frequency, and UUI that characterize OAB. The consequences of this condition are far-reaching and include direct medical consequences and coping strategies that adversely affect quality of life. Although the prevalence of OAB increases with age, it is not a normal consequence of aging. Antimuscarinic agents (e.g., oxybutynin, tolterodine, trospium, solifenacin, and darifenacin) have demonstrated efficacy for the treatment of OAB symptoms in multiple clinical trials. This review explores the physiological basis for OAB, the effects of OAB on health-related quality of life, and the pharmacotherapies that may provide relief to patients with this distressing condition.