Overactive bladder (OAB) is a condition that affects potentially 46 million American adults. The most common symptoms of OAB include the experience of sudden urges to urinate that cannot be controlled, frequent urination, and urinary incontinence due to involuntary contractions of the detrusor muscle. While several conditions may contribute to signs and symptoms of overactive bladder, the underlying cause of OAB remains unclear.
Individuals with OAB are frequently undiagnosed due to embarrassment or the misperception that there are no approved treatments. Patients who do receive treatment are most frequently prescribed anticholinergic medications, which inhibit the binding of acetylcholine to the muscarinic receptors in the detrusor, thereby reducing involuntary bladder contractions. Unfortunately, the majority of patients receiving such treatment have a suboptimal response to this class of drugs and experience anticholinergic side-effects, such as dry mouth, constipation, and blurred vision., Consequently, a high proportion of patients discontinue anticholinergic therapy, with fewer than 25% remaining on treatment at one year. Moreover, a growing body of evidence links longer-term treatment with anticholinergic medications to cognitive decline and dementia in older individuals., Most prescriptions written for anticholinergics for the treatment of OAB are for individuals over the age of 60, who may already be at elevated baseline risk of cognitive impairment.
A smaller, but growing, number of patients with OAB are treated with a β3-adrenergic agonist. β3 agonism is a novel mechanism to treat OAB via relaxation of the detrusor muscle of the bladder. β3 agonists appear to lack many of the classic anticholinergic side-effects. To date there has been no published evidence linking β3 agonists to increased risk of cognitive impairment.
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