Storage & Overactive Bladder Pharmacotherapy
Pharmacologic therapy for overactive bladder (OAB) and neurogenic lower urinary tract dysfunction (NLUTD) works through two complementary mechanisms at the detrusor: blocking cholinergic contraction (antimuscarinics) or stimulating sympathetic relaxation (β3-agonists). A third distinct agent — desmopressin — addresses nocturnal polyuria rather than storage per se.
This subcategory covers the three drug classes relevant to storage-phase pharmacotherapy. For the full clinical framework see the AUA/SUFU OAB guideline and the OAB clinical-condition article.
- Anticholinergic / Antimuscarinic AgentsSix FDA-approved agents — oxybutynin, tolterodine, solifenacin, darifenacin, fesoterodine, trospium. Mechanism, efficacy (Cochrane 2023 data), head-to-head comparisons, dry mouth burden, the dementia controversy (SUFU 2022 white paper), and contemporary AUA positioning.
- β3-Adrenergic Receptor AgonistsMirabegron and vibegron — mechanism (β3 → cAMP → detrusor relaxation), FDA indications including the 2024 vibegron BPH-OAB expansion (COURAGE trial), efficacy comparable to antimuscarinics with superior tolerability, combination therapy with solifenacin, and the absence of the dementia association.
- DesmopressinSynthetic vasopressin analogue for nocturnal polyuria and nocturia. Oral and nasal routes, sex-specific dosing (lower doses in women), hyponatremia monitoring, AUA-approved indications, and the NOCDURNA FDA approval.
Contemporary Stepped Therapy (AUA/SUFU 2024)
- Behavioral therapy (pelvic-floor muscle training, fluid management, bladder retraining) → first-line for all OAB patients
- Pharmacotherapy: β3-agonist OR antimuscarinic (the 2024 AUA guideline slightly favors β3-agonists due to better tolerability and absence of dementia association)
- Combination therapy (antimuscarinic + β3-agonist) for suboptimal response to monotherapy
- Third-line: intradetrusor onabotulinumtoxinA, sacral neuromodulation, posterior tibial nerve stimulation