Overactive Bladder

Table of Contents

1. Overview
2. Epidemiology
3. Pathophysiology
4. Etiology and Risk Factors
5. Clinical Presentation
6. Diagnosis
7. Treatment
8. Complications
9. Prognosis
10. Prevention
11. Recent Research
12. Key Research Papers
13. Connections
14. Featured Videos

1. Overview

Overactive Bladder (OAB) is a clinical syndrome defined by the International Continence Society (ICS) as urinary urgency, usually accompanied by increased daytime frequency (eight or more voids per day) and/or nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection or other obvious pathology. The cardinal symptom is urgency — a sudden, compelling desire to void that is difficult to defer — which distinguishes OAB from simple urinary frequency or stress incontinence.

OAB is subclassified into two phenotypes based on the presence or absence of leakage: OAB-wet (urgency with urge incontinence) and OAB-dry (urgency without incontinence). OAB-wet carries greater quality-of-life burden and is more commonly the presenting complaint driving patients to seek care. Approximately 16% of adults in the general population fulfill symptomatic criteria for OAB, making it one of the most prevalent lower urinary tract conditions worldwide.

2. Epidemiology

Overactive bladder affects an estimated 33 million adults in the United States, with prevalence rising markedly with advancing age. The NOBLE (National Overactive Bladder Evaluation) program and subsequent national surveys consistently demonstrate that approximately 16% of adults over age 18 report OAB symptoms, a figure that increases to 40% of women and 30% of men over age 75. Despite this high prevalence, fewer than half of affected individuals seek medical attention, largely due to embarrassment, acceptance of symptoms as a normal consequence of aging, or unawareness that effective treatments exist.

Sex-specific epidemiology differs by symptom subtype: OAB-wet is more prevalent in women across all age groups, while urgency frequency without incontinence is roughly equally distributed between sexes. In men, OAB commonly coexists with bladder outlet obstruction from benign prostatic hyperplasia (BPH), complicating both diagnosis and management. Internationally, the EPIC study, a population survey in five countries (Canada, Germany, Italy, Sweden and the United Kingdom), found an overall OAB prevalence of 11.8%, with similar rates in men and women, rising with age.

3. Pathophysiology

The pathophysiology of OAB centers on abnormal detrusor muscle activity and altered afferent bladder signaling, though the precise mechanisms remain incompletely understood.

Detrusor Overactivity

Urodynamically, OAB frequently (though not invariably) correlates with detrusor overactivity (DO) — involuntary phasic contractions of the detrusor muscle during the filling phase of the micturition cycle, occurring at a pressure exceeding 6–15 cmH2O. DO is classified as neurogenic (arising from identifiable neurological disease, such as stroke, multiple sclerosis, or spinal cord injury) or idiopathic (occurring in the absence of demonstrable neurological or local pathology). The majority of OAB cases are idiopathic.

M3 Muscarinic Receptor Signaling

Detrusor smooth muscle contraction is mediated predominantly through M3 muscarinic acetylcholine receptors, which couple to Gq proteins, activate phospholipase C, and increase intracellular calcium via IP3-mediated release from the sarcoplasmic reticulum. In OAB, spontaneous acetylcholine release from detrusor myocytes (the "myogenic hypothesis") or heightened muscarinic receptor sensitivity generates propagated detrusor contractions during the filling phase. M3 receptor subtype selectivity is the pharmacological rationale underlying antimuscarinic drug development.

Urothelial Afferent Pathway

The urothelium is now recognized as an active sensory and signaling structure, not merely a passive barrier. In response to stretch during bladder filling, urothelial cells release adenosine triphosphate (ATP), acetylcholine, nitric oxide, and substance P, which activate purinergic P2X3 receptors and transient receptor potential (TRP) channels on subepithelial afferent C-fibers and A-delta fibers. In OAB, enhanced urothelial adenosine triphosphate release and upregulated TRP channel expression (especially TRPV1 and TRPA1) amplify afferent urgency signaling before physiologic bladder capacity is reached.

Pudendal and Tibial Nerve Roles

Sacral spinal cord circuits integrating afferent input from the bladder and somatic input from the pudendal nerve modulate the micturition reflex. The tibial nerve (L4–S3 root origin), which carries somatic afferents to the same sacral segments that control bladder function, provides the anatomical rationale for percutaneous tibial nerve stimulation (PTNS) as a neuromodulatory OAB treatment. Dysfunction of descending inhibitory control from the pontine micturition center (PMC) and prefrontal cortex contributes to urgency in both neurogenic and idiopathic OAB.

4. Etiology and Risk Factors

• Neurological conditions: Stroke (disrupts descending inhibitory pathways from PMC to sacral cord), multiple sclerosis (demyelination of corticospinal and spinobulbar tracts), Parkinson's disease (basal ganglia dopaminergic deficit impairs voiding inhibition), and spinal cord injury are major causes of neurogenic OAB.
• Diabetes mellitus: Diabetic cystopathy initially presents as detrusor underactivity, but autonomic neuropathy and altered urothelial signaling can manifest as urgency and OAB symptoms, particularly in long-standing disease.
• Bladder outlet obstruction (BOO): Benign prostatic hyperplasia in men is the commonest cause of acquired BOO; chronic obstruction induces detrusor hypertrophy, altered smooth muscle properties, and DO in approximately 50–70% of men with benign prostatic hyperplasia.
• Pelvic floor weakness: Weakened pelvic floor musculature, particularly after childbirth or pelvic surgery, reduces urethral support and may heighten urgency perception via altered afferent input.
• Caffeine and alcohol: Caffeine is a direct detrusor stimulant and diuretic; alcohol inhibits antidiuretic hormone, increasing urine output. Both worsen OAB symptoms acutely and are modifiable risk factors.
• Aging: Age-related changes include reduced bladder compliance, decreased detrusor contractility interspersed with overactivity, increased nocturnal urine production (nocturnal polyuria), and heightened sensory thresholds. Aging is the most consistent independent predictor of OAB prevalence.
• Obesity: Elevated intra-abdominal pressure and metabolic effects of adiposity exacerbate bladder dysfunction; weight loss of 5–10% body weight reduces OAB symptom severity.
• Medications: Diuretics, alpha-adrenergic agonists (decongestants), and cholinesterase inhibitors can precipitate or worsen urgency symptoms.

5. Clinical Presentation

The four cardinal symptoms of OAB form the ICS-defined symptom complex:

• Urgency (cardinal symptom): A sudden, compelling urge to void that is difficult or impossible to defer. Unlike the normal physiologic urge, OAB urgency is poorly suppressible and may arrive with little warning, limiting the time available to reach a toilet. Urgency is the defining feature that distinguishes OAB from other lower urinary tract syndromes.
• Urinary frequency: Eight or more micturitions per 24-hour period. Patients often describe voiding "just in case" to preempt urgency episodes, which further reduces functional bladder capacity over time through a learned behavioral cycle.
• Nocturia: Waking one or more times per night to void. Two or more nocturia episodes per night are associated with significant sleep disruption, daytime fatigue, and, in older adults, an increased risk of falls and fractures during nocturnal toilet trips.
• Urgency urinary incontinence (OAB-wet): Involuntary urine leakage accompanied by or immediately preceded by urgency. Leakage volume ranges from small dribbles to complete bladder emptying. Present in approximately 35–40% of OAB patients seeking care.

Validated Assessment Tools

• OAB Questionnaire (OAB-q): A 33-item patient-reported outcome measure with a symptom bother subscale and a health-related quality-of-life subscale; validated across multiple languages and widely used in clinical trials.
• ICIQ-OAB (International Consultation on Incontinence Questionnaire — OAB module): Brief, validated tool assessing urgency, frequency, nocturia, and incontinence with impact scores.
• Voiding diary (bladder diary): 3- to 7-day diary recording time and volume of each void, urgency episodes, incontinence events, and fluid intake. Provides objective baseline data and distinguishes OAB from global polyuria or nocturnal polyuria (nocturnal urine output exceeding 33% of 24-hour total).
• Urgency Perception Scale (UPS): 3-point scale quantifying urgency severity per void; simpler than OAB-q for rapid clinical assessment.

6. Diagnosis

OAB is a clinical diagnosis based on symptom criteria. The American Urological Association and Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction (AUA/SUFU) guideline emphasizes ruling out reversible causes before initiating treatment.

Urinalysis and Urine Culture

Urinalysis with microscopy is the essential first-line test to exclude urinary tract infection (UTI) as a reversible cause of urgency and frequency. Pyuria with bacteriuria warrants culture and targeted antibiotic therapy. Microscopic hematuria (defined in the 2020 AUA/SUFU microhematuria guideline as 3 or more red blood cells per high-power field on microscopic evaluation of a single specimen) mandates urological evaluation to exclude bladder malignancy before attributing symptoms to OAB.

Post-Void Residual (PVR) Measurement

Bladder ultrasound or in-and-out catheterization to measure PVR is recommended to exclude urinary retention and incomplete bladder emptying, which can mimic OAB symptoms. A PVR exceeding 150–200 mL indicates impaired bladder emptying and alters the management approach, particularly before initiating anticholinergic medications that further impair detrusor contractility.

Urodynamics

Multichannel filling cystometry is the gold-standard method for demonstrating detrusor overactivity — phasic involuntary detrusor contractions during bladder filling. Urodynamic evaluation is indicated when the diagnosis is uncertain, when empiric therapy has failed, when neurological disease is present, or when invasive therapy (neuromodulation, botulinum toxin, surgery) is planned. Urodynamic DO is identified in approximately 60–70% of patients with symptomatic OAB, but its absence does not exclude OAB, and its presence in asymptomatic individuals does not establish the diagnosis.

Cystoscopy

Not required for routine OAB evaluation but indicated when hematuria is present, when bladder pathology (carcinoma in situ, bladder stones, foreign body) must be excluded, or when Hunner lesions of interstitial cystitis are suspected on clinical grounds. Cystoscopy findings in uncomplicated OAB are typically normal.

7. Treatment

The current 2024 AUA/SUFU guideline on idiopathic OAB covers non-invasive therapies, medicines, minimally invasive therapies, invasive therapies and indwelling catheters, and no longer ranks them as first- to fourth-line steps. Its conclusion is that the clinician and the patient should, through shared decision-making, formulate a personalized treatment approach that takes account of the evidence and the patient's values and preferences. The superseded 2012 version arranged treatments in tiers; the sections below follow that order, from least to most invasive.

Behavioral Therapies

• Bladder training: Patients are instructed to void on a fixed schedule and progressively increase inter-void intervals by 15–30 minutes per week, targeting 3–4 hour inter-void intervals. Behavioral training reduces urgency episodes and incontinence by 50–80% in motivated patients and is commonly offered to all patients with OAB before medicines.
• Pelvic floor muscle exercises (Kegel exercises): Voluntary pelvic floor contractions during urgency episodes inhibit detrusor contraction reflexively via the guarding reflex. Regular pelvic floor muscle training (3 sets of 10–15 contractions daily) reduces urgency, frequency, and leakage and is especially effective in women with concurrent stress incontinence.
• Fluid management: Reducing total fluid intake to 1.5–2.0 liters per day (avoiding over-restriction), eliminating caffeine and alcohol, and distributing fluid intake throughout the day reduces urgency frequency and nocturia. Bladder diary data guides individualized fluid counseling.
• Weight loss: In the PRIDE trial in overweight and obese women, an average 8% weight loss over 6 months cut weekly incontinence episodes by 47%, compared with 28% in the control group; the fall was in stress-incontinence episodes, while urge-incontinence episodes did not fall significantly.

Pharmacotherapy

Two pharmacological classes with distinct mechanisms are available for OAB:

• Anticholinergics (antimuscarinics): Block M3 muscarinic receptors in the detrusor, reducing involuntary contractions. Available agents include oxybutynin (immediate-release (IR) and extended-release (ER)), tolterodine (IR and ER), solifenacin, fesoterodine, trospium, and darifenacin. Extended-release formulations have superior tolerability versus IR. Class-wide adverse effects include dry mouth (most common), constipation, blurred vision, urinary retention, and — critically — cognitive impairment and increased dementia risk with long-term use in elderly patients, attributed to central nervous system (CNS) M1 receptor blockade and blood-brain barrier (BBB) penetration. Trospium (quaternary ammonium compound, minimal central nervous system penetration) and darifenacin (M3-selective) have relatively more favorable central nervous system profiles. Anticholinergics are relatively contraindicated in patients with narrow-angle glaucoma, urinary retention, or cognitive impairment.
• Beta-3 adrenergic agonists: Mirabegron and vibegron activate beta-3 receptors on detrusor smooth muscle, increasing cyclic AMP and promoting detrusor relaxation during bladder filling without inhibiting the voiding contraction. This mechanism confers several advantages over antimuscarinics: no dry mouth or constipation as class effects, no adverse cognitive effects, and no contraindication in patients with glaucoma. Mirabegron (25–50 mg daily) is modestly associated with elevated blood pressure and caution is warranted in uncontrolled hypertension. Vibegron (75 mg daily) has a lower drug-interaction profile than mirabegron (does not inhibit cytochrome P450 2D6, CYP2D6) and may be preferred in polypharmacy patients. Combinations of mirabegron 25 mg or 50 mg plus solifenacin 5 mg were tested in the SYNERGY trial (results below).

Neuromodulation

• Percutaneous tibial nerve stimulation (PTNS): A fine-gauge needle electrode is inserted near the tibial nerve at the ankle, and electrical stimulation is delivered for 30 minutes per session weekly for 12 weeks (the PTNS protocol validated in the SUmiT trial), followed by maintenance therapy every 3–4 weeks. PTNS reduces urgency episodes, frequency, and incontinence by approximately 55–60% in responders. It is well-tolerated, minimally invasive, and does not require anesthesia, making it suitable for patients unable to tolerate pharmacotherapy or surgery.
• Sacral neuromodulation (SNM): A programmable implanted pulse generator connected to a sacral nerve root (S3) lead modulates afferent and efferent sacral nerve traffic to restore normal bladder-brain communication. The two-stage procedure (test stimulation phase followed by permanent implantation in responders) yields 50–80% improvement in OAB symptoms and 40–50% complete dryness rates in carefully selected patients. Rechargeable systems offer battery longevity exceeding 15 years. SNM is preferred over PTNS for patients desiring a durable, low-maintenance neuromodulation option.

OnabotulinumtoxinA Intradetrusor Injection

OnabotulinumtoxinA (100 U for non-neurogenic OAB; 200 U for neurogenic OAB) is injected into multiple detrusor sites via cystoscopic guidance under local or general anesthesia. The toxin cleaves SNAP-25 synaptosomal protein, blocking vesicular acetylcholine release from efferent motor terminals and impairing afferent adenosine triphosphate/substance-P release from urothelial sensory fibers. In a phase 3 placebo-controlled trial of the 100 U dose (Nitti et al., 2013), daily urinary incontinence episodes fell by 2.65 versus 0.87 with placebo, and 22.9% of patients (versus 6.5% with placebo) became completely continent. Duration of effect is 6–12 months, necessitating repeat injections. Urinary retention requiring clean intermittent self-catheterization occurs in 6–12% of patients with non-neurogenic OAB at the 100 U dose; for this reason, patients are counseled on self-catheterization, and need to be capable of it, before treatment.

8. Complications

• Urgency urinary incontinence: The most socially disabling complication, associated with pad use, protective clothing, and avoidance of social situations. Severe OAB-wet significantly impairs sexual function, occupational performance, and interpersonal relationships.
• Sleep disruption: Nocturia-associated sleep fragmentation produces daytime fatigue, impaired cognitive function, reduced immune competence, and exacerbation of mood disorders. Two or more nocturia episodes per night doubles insomnia prevalence.
• Falls and fractures in elderly patients: Nocturia-related nocturnal ambulation in older adults with reduced balance, altered sensorium, or polypharmacy exposure is a well-established independent risk factor for falls and hip fractures. Estimates suggest nocturia accounts for 25% of falls in elderly populations.
• Social isolation and depression: Anxiety about leakage in public settings leads to progressive restriction of activities — travel, exercise, social gatherings, and sexual intimacy. Depression is two to three times more prevalent in patients with OAB than in age-matched controls without lower urinary tract symptoms.
• Anticholinergic cognitive burden in the elderly: Long-term anticholinergic use for OAB is associated with accelerated cognitive decline and increased dementia risk in older patients (OR approximately 1.5–2.0 for dementia with cumulative anticholinergic exposure). The American Geriatrics Society Beers Criteria lists anticholinergic drugs as potentially inappropriate medications in older adults. For this reason, beta-3 agonists or non-drug therapies are commonly chosen for patients over 65.
• Skin complications: Persistent urinary incontinence causes incontinence-associated dermatitis (IAD), perineal skin breakdown, and increased risk of pressure injuries in patients with limited mobility.

9. Prognosis

OAB is a chronic condition that follows a fluctuating course but rarely resolves completely without active management. Approximately 60–70% of patients achieve significant symptom improvement with combined behavioral and pharmacological therapy, and response rates are higher when treatments are combined rather than used sequentially. Behavioral therapy alone produces durable benefit in 50–80% of motivated patients who complete structured programs.

Sacral neuromodulation (SNM) offers the most durable long-term outcomes among procedural options. Approximately 30% of SNM patients achieve complete continence. OnabotulinumtoxinA provides substantial relief with a 6–12 month durability that requires planned repeat injections; sustained benefit over multiple injection cycles is well-documented. Overall, fewer than 10% of patients require major reconstructive surgery for OAB.

Prognosis is less favorable when OAB is secondary to progressive neurological disease (multiple sclerosis (MS), Parkinson's), where symptomatic control is managed alongside the underlying condition's trajectory. Elderly patients with cognitive impairment face additional challenges due to limited pharmacotherapy options and difficulties adhering to behavioral regimens.

10. Prevention

While OAB cannot always be prevented, several modifiable lifestyle factors reduce the risk of developing the condition or attenuate symptom severity:

• Weight management: Maintaining healthy body weight reduces intra-abdominal pressure on the bladder and mitigates metabolic drivers of bladder dysfunction. A 5–10% weight reduction in overweight patients reduces OAB incidence and severity.
• Regular pelvic floor exercises: Habitual Kegel exercises throughout adulthood preserve pelvic floor tone, prevent pelvic organ prolapse, and reduce the likelihood of urgency incontinence development, particularly in women following childbirth.
• Limiting caffeine and alcohol: Reducing or eliminating caffeine (target less than 100 mg/day) and alcohol minimizes direct bladder irritation and diuresis-driven urgency episodes.
• Adequate fluid intake: Paradoxically, under-hydration concentrates urine, increasing urothelial irritation. Maintaining 1.5–2.0 liters of fluid intake per day (predominantly water, avoiding bladder irritants) is preferable to fluid restriction.
• Treating underlying conditions: Prompt management of diabetes, benign prostatic hyperplasia, and neurological conditions reduces the risk of developing secondary OAB. Optimizing glycemic control in diabetes limits bladder autonomic neuropathy progression.
• Smoking cessation: Smoking is associated with bladder irritation, chronic cough (which precipitates incontinence), and bladder carcinoma risk. Quitting removes these urological risks.

11. Recent Research

Vibegron (75 mg): Approved by the U.S. Food and Drug Administration (FDA) in 2020, vibegron is a highly selective beta-3 agonist with a favorable drug-interaction profile compared to mirabegron, particularly relevant in OAB patients taking tamsulosin (an alpha-1 blocker commonly used for benign prostatic hyperplasia). The EMPOWUR trial demonstrated significant reductions in urgency incontinence episodes, urinary urgency, and micturition frequency versus placebo, with efficacy maintained at 52 weeks in the double-blind extension study. Vibegron does not inhibit cytochrome P450 2D6 and does not raise blood pressure, expanding its use in patients with cardiovascular comorbidities.

Combination mirabegron plus solifenacin (SYNERGY trial): The SYNERGY phase 3 randomized controlled trial evaluated combination therapy with mirabegron 25 mg or 50 mg plus solifenacin 5 mg versus either agent alone in 3527 patients with OAB. The combination of mirabegron 50 mg plus solifenacin 5 mg was statistically superior to solifenacin 5 mg alone for incontinence episodes, but did not reach statistical superiority over mirabegron 50 mg alone in the primary analysis (P = 0.052), with a safety and tolerability profile not significantly worse than solifenacin alone. This combination is now incorporated into guideline algorithms for patients with inadequate response to monotherapy.

Transcranial magnetic stimulation (TMS) for central sensitization: Emerging evidence positions OAB, particularly refractory idiopathic OAB, within the spectrum of centrally sensitized syndromes. TMS targeting the dorsomedial prefrontal cortex and anterior cingulate cortex — regions implicated in descending inhibitory control of the micturition reflex — has produced statistically significant reductions in urgency and frequency in pilot trials. The mechanism is hypothesized to involve modulation of corticoreticulospinal inhibitory pathways that govern supraspinal suppression of detrusor overactivity.

Intravesical botulinum toxin versus SNM: The ABC (Anticholinergic versus Botulinum toxin Comparison) trial compared anticholinergic pills with onabotulinumtoxinA injection. The ROSETTA (Refractory Overactive Bladder: Sacral Neuromodulation versus Botulinum Toxin Assessment) trial compared SNM with onabotulinumtoxinA in women with refractory urgency incontinence: at 6 months onabotulinumtoxinA gave a slightly greater reduction in urgency incontinence episodes (3.9 vs. 3.3 fewer per day), a difference the investigators called of uncertain clinical importance, and was associated with more urinary tract infections (35% vs. 11%) and with transient self-catheterization (8% at 1 month). Patient preference and functional capacity for self-catheterization guide treatment selection between these options.

Key Research Papers

1. Abrams P, Cardozo L, Fall M, et al., 2002 — ICS standardisation of lower urinary tract function terminology. — PubMed PMID: 11857671
2. Coyne KS, Sexton CC, Vats V, et al., 2011 — National community prevalence of overactive bladder in the United States stratified by sex and age. — PubMed PMID: 21256571
3. Irwin DE, Milsom I, Hunskaar S, et al., 2006 — Population-based survey of urinary incontinence, overactive bladder, and other lower urinary tract symptoms in five countries: results of the EPIC study. — PubMed PMID: 17049716
4. Gormley EA, Lightner DJ, Burgio KL, et al., 2012 — Diagnosis and treatment of overactive bladder (non-neurogenic) in adults: AUA/SUFU guideline. — PubMed PMID: 23098785
5. Cameron AP, Chung DE, Dielubanza EJ, et al., 2024 — The AUA/SUFU guideline on the diagnosis and treatment of idiopathic overactive bladder. — PubMed PMID: 38651651
6. Barocas DA, Boorjian SA, Alvarez RD, et al., 2020 — Microhematuria: AUA/SUFU guideline. — PubMed PMID: 32698717
7. Chapple CR, Kaplan SA, Mitcheson D, et al., 2013 — Phase 3 study of mirabegron (beta-3 agonist) 12-month safety and efficacy in OAB. — PubMed PMID: 23195283
8. Peters KM, Carrico DJ, Perez-Marrero RA, et al., 2010 — Randomized trial of percutaneous tibial nerve stimulation versus sham efficacy in the treatment of overactive bladder syndrome: results from the SUmiT trial. — PubMed PMID: 20171677
9. Brubaker L, Richter HE, Visco A, et al., 2008 — Refractory idiopathic urge urinary incontinence and botulinum A injection. — PubMed PMID: 18499184
10. Nitti VW, Dmochowski R, Herschorn S, et al., 2013 — OnabotulinumtoxinA for the treatment of patients with overactive bladder and urinary incontinence: results of a phase 3, randomized, placebo controlled trial. — PubMed PMID: 23246476
11. Burgio KL, Goode PS, Locher JL, et al., 2002 — Behavioral training with and without biofeedback in the treatment of urge incontinence in older women: a randomized controlled trial. — PubMed PMID: 12425706
12. Dmochowski R, Chapple C, Nitti VW, et al., 2010 — Efficacy and safety of onabotulinumtoxinA for idiopathic overactive bladder: a double-blind, placebo controlled, randomized, dose ranging trial. — PubMed PMID: 20952013
13. Kelleher CJ, Cardozo L, Chapple CR, et al., 2005 — Improved quality of life in patients with overactive bladder symptoms treated with solifenacin. — PubMed PMID: 15638900
14. Herschorn S, Chapple CR, Abrams P, et al., 2017 — Efficacy and safety of combinations of mirabegron and solifenacin compared with monotherapy and placebo in patients with overactive bladder (SYNERGY study). — PubMed PMID: 28418102
15. Amundsen CL, Richter HE, Menefee SA, et al., 2016 — OnabotulinumtoxinA vs sacral neuromodulation on refractory urgency urinary incontinence in women: a randomized clinical trial. — PubMed PMID: 27701661
16. Subak LL, Wing R, West DS, et al., 2009 — Weight loss to treat urinary incontinence in overweight and obese women. — PubMed PMID: 19179316
17. Staskin D, Frankel J, Varano S, et al., 2021 — Once-daily vibegron 75 mg for overactive bladder: long-term safety and efficacy from a double-blind extension study of the international phase 3 trial (EMPOWUR). — PubMed PMID: 33356445

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Connections

• Urology
• How You Pee: The Bladder & Its Reflex — interactive animation
• Urinary Incontinence
• Interstitial Cystitis
• Benign Prostatic Hyperplasia
• Urinary Tract Infections
• Multiple Sclerosis
• Parkinson's Disease
• Kidney Stones
• Urinalysis
• Depression
• Anxiety
• Type 2 Diabetes
• Stroke
• Herbs covered on this site that discuss this condition: Uva Ursi · Cat’s Whiskers / Java Tea (Orthosiphon aristatus) · Horsetail

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