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Underactive Bladder

Underactive bladder (UAB) is a symptom complex of slow stream, hesitancy, straining, and prolonged voiding, with or without a feeling of incomplete emptying; storage symptoms may coexist.[16] Elevated PVR is a measured finding, not part of the symptom definition. Detrusor underactivity (DU) is the urodynamic diagnosis: a detrusor contraction of reduced strength and/or duration, causing prolonged emptying or failure to empty completely within a normal time span.[1][2]

UAB describes symptoms; pressure-flow urodynamics supports a DU diagnosis when detrusor contraction, flow, outlet resistance, and voiding pattern are assessed together.[1][16] Low flow alone does not distinguish DU from bladder outlet obstruction (BOO), and many patients have both.

Terminology​

TermMeaningPractical use
Underactive bladder (UAB)Symptom complex associated with impaired emptyingClinical syndrome; analogous to OAB
Detrusor underactivity (DU)Urodynamic diagnosis of weak and/or short detrusor contractionRequires pressure-flow testing
Acontractile detrusor (ACD)No demonstrable detrusor contraction on urodynamicsWorst contractility phenotype; catheter dependence more likely
Impaired detrusor contractilityReduced detrusor strength, speed, or persistenceBroader physiologic concept
DHICDetrusor hyperactivity with impaired contractilityStorage overactivity plus poor emptying

DU is not synonymous with retention. A patient can void with low efficiency, empty by abdominal straining, or have apparently acceptable PVR early in the disease.

Voiding mechanism also varies among women without a distinct disease process. In a urodynamic study of 13 women with stress incontinence, five initiated voiding with Valsalva, three mainly by lowering maximal urethral pressure, and five by the pattern observed in healthy controls.[24] In a separate study of 70 women before and after retropubic urethropexy, 35 (50%) voided without a detrusor contraction preoperatively; of these, half developed a detrusor contraction once surgery raised urethral resistance, and the other half continued to strain, with more flow reduction and a longer need for postoperative bladder drainage.[25]

Epidemiology​

True prevalence is unknown because most data come from referral cohorts undergoing urodynamics.[1][3]

Approximate ranges in urodynamic series:

  • Men with non-neurogenic LUTS: 10-48% (EAU 2026 cites 10% in men referred for videourodynamics, up to 48% at age 70 or older)[23]
  • Older women with non-neurogenic LUTS undergoing urodynamic evaluation: 12-45%[1]
  • Women undergoing urodynamics for pelvic floor disorders: 4.1-37.0% in one 2,092-woman cohort, depending on the definition used[35]
  • Institutionalized older adults with incontinence: DU and DHIC are common contributors

Ambulatory urodynamic series in women put DU nearer 12-19%, and about 30% of older women in one series had detrusor overactivity with DU.[17] Prevalence is definition-sensitive. A strict pressure-flow index captures a different population than a voiding-efficiency definition, and many published thresholds were derived in men before being applied to women.

Pathophysiology​

DU is a final common pathway.

Myogenic failure​

  • Loss of detrusor smooth muscle cells
  • Collagen deposition and fibrosis
  • Impaired excitation-contraction coupling
  • Reduced contraction speed, duration, and reserve power

Neurogenic failure​

  • Sacral / cauda equina lesions
  • Peripheral neuropathy, especially diabetes
  • Pelvic autonomic nerve injury after radical pelvic surgery
  • Spinal cord disease, multiple sclerosis, stroke, Parkinson disease, and other NLUTD phenotypes
  • Impaired afferent sensation: bladder fills but the patient does not generate an adequate voiding reflex

Vascular and metabolic injury​

Microvascular disease, diabetes, aging, and cardiovascular disease may reduce detrusor blood supply and impair neural and muscular reserve.[4]

A three-stage model of bladder remodeling with BOO has been hypothesized from limited human evidence:[5]

  1. Hypertrophy. The detrusor works against higher outlet resistance.
  2. Compensation. Voiding pressure rises; filling-phase detrusor overactivity may appear.
  3. Decompensation. Contractility fails, PVR rises, and DU develops.[5]

This is why outlet surgery can help some men with DU: removing obstruction may let a weak but still viable detrusor empty better. It will not rescue an acontractile, insensate bladder reliably.

Risk Factors and Etiology​

CategoryExamples
Age-relatedDetrusor muscle aging, sensory decline, comorbidity accumulation
Metabolic / vascularDiabetes, metabolic syndrome, cardiovascular disease, microvascular disease
NeurogenicSpinal cord injury, cauda equina syndrome, multiple sclerosis, stroke, Parkinson disease, peripheral neuropathy
IatrogenicRadical pelvic surgery, hysterectomy, rectal surgery, pelvic radiation, medications
Outlet-relatedChronic BPH/BPO, urethral stricture, bladder neck contracture, dysfunctional voiding
Medication-relatedAnticholinergics, opioids, antihistamines, sympathomimetics, tricyclics, some antipsychotics

In practice, the most common patient is mixed: older, diabetic or vascular, exposed to anticholinergic medications, with some degree of outlet obstruction or pelvic-floor dysfunction.

Clinical Presentation​

Voiding symptoms​

  • Weak stream
  • Hesitancy
  • Intermittency
  • Straining
  • Prolonged voiding time
  • Terminal dribbling
  • Need to double void

Post-micturition symptoms​

  • Incomplete emptying
  • Post-void dribbling
  • Early return of urge after voiding

The sensation of incomplete emptying can reflect retained urine, altered bladder sensation, or a detrusor after-contraction (a post-void rise in detrusor pressure, most often seen with detrusor overactivity). In a series of 331 symptomatic women undergoing ambulatory urodynamics, after-contractions were identified in 37% and were associated with detrusor overactivity.[26]

Storage symptoms​

  • Frequency
  • Nocturia
  • Urgency
  • Urgency incontinence

Storage symptoms can reflect DHIC, chronic retention, recurrent infection, high residual volumes, or coexisting OAB.

Signs​

  • Elevated PVR
  • Palpable bladder
  • Overflow incontinence
  • Recurrent UTI
  • Reduced or absent bladder sensation
  • Hydronephrosis in severe chronic retention

DU vs BOO​

Symptoms overlap heavily. The reconstructive trap is assuming that every weak stream is obstruction or that every low-flow tracing is DU.

FeatureMore suggestive of DUMore suggestive of BOO
SensationReduced filling sensation, delayed first desireNormal sensation, urgency from obstruction
FlowLow flow with low detrusor pressureLow flow with high detrusor pressure
PVROften high, may be very highVariable; rises with decompensation
Prostate / urethraPatent outlet on anatomic and functional assessmentBPH, stricture, bladder neck contracture, sling obstruction, primary bladder neck obstruction, or dysfunctional voiding[16][23]
UrodynamicsLow Pdet@Qmax, low voiding efficiencyHigh pressure-low flow

Pressure-flow urodynamics is the decisive test when the diagnosis will change treatment.

DHIC​

Detrusor hyperactivity with impaired contractility (DHIC) is the combination of detrusor overactivity during filling and impaired contractility during voiding. It is common in frail older adults and may present as incontinence, urgency, recurrent cystitis, retention, or both.[6]

OAB drugs may worsen emptying, while cholinergic drugs do not reliably improve emptying. Treatment usually prioritizes safe emptying first, then storage control.

Practical sequence:

  1. Measure PVR before starting antimuscarinic or botulinum therapy.
  2. Treat infection, constipation, and medication contributors.
  3. Establish reliable emptying if PVR is high: CIC, caregiver catheterization, or suprapubic tube.
  4. Add storage therapy cautiously: beta-3 agonist, low-burden antimuscarinic, or botulinum only if catheterization is feasible.

Evaluation​

Initial assessment​

  • LUTS history: voiding, storage, post-micturition, duration, bother
  • Retention history: acute retention, catheter episodes, failed void trials
  • Neurologic history: spine disease, diabetes, stroke, MS, Parkinson disease, pelvic surgery
  • Medication review
  • Bowel function and constipation
  • Pelvic / prostate / neurologic exam
  • Urinalysis and urine culture when symptomatic
  • PVR measurement, repeated at least once if unexpectedly high (fluid intake, incomplete voiding time, or straining can produce a false-positive reading, and no single PVR value defines chronic retention in women)
  • In suspected non-neurogenic chronic urinary retention, obtain serum creatinine and renal ultrasonography to assess renal function and upper-tract dilation.[34]
  • Uroflowmetry
  • Voiding diary when frequency or nocturia is prominent

Urodynamics​

Urodynamics is required for a definitive diagnosis of DU.[1][7]

Typical findings:

  • Low Qmax
  • Low Pdet@Qmax
  • Slowly rising or brief detrusor contraction
  • Intermittent or unsustained contraction
  • Large PVR
  • Low voiding efficiency
  • Reduced bladder sensation
  • Abdominal straining during voiding

Contractility metrics​

No single criterion is universally accepted.

MetricFormula / conceptUse
BCIPdet@Qmax + 5 x Qmax[20]Common in men; BCI <100 is the usual research surrogate for DU, though DU is a spectrum and no single cutoff is universally accepted
Voiding efficiencyVoided volume / bladder capacitySimple functional endpoint; useful across sexes
Pdet@QmaxDetrusor pressure at maximum flowSeparates low-pressure-low-flow from high-pressure-low-flow
Video-UDSPressure-flow plus fluoroscopyBest for mixed DU/BOO, bladder neck dysfunction, sphincter non-relaxation

Schäfer-nomogram-derived metrics such as BCI were developed in men and can overestimate detrusor contractility in women.[27] A modified index, PIP1 (Pdet@Qmax + Qmax), was derived retrospectively from baseline data in 100 symptomatic women 53 years or older with urge incontinence; PIP1 typically ranged from 30 to 75 cm H2O in that population.[27] In the same cohort, a continuous mechanical stop test was more reliable than a voluntary stop test for measuring detrusor contraction strength, though interrupting flow adds a step that limits routine use.[28]

When to obtain video-urodynamics​

  • Prior outlet surgery or pelvic reconstruction
  • Suspected BOO plus weak detrusor
  • Neurogenic disease
  • Elevated PVR before continence surgery
  • Women with suspected sling obstruction or dysfunctional voiding
  • Men with small prostate and severe low-flow symptoms
  • Failed outlet surgery or unexpected postoperative retention

Management Principles​

For non-neurogenic chronic urinary retention, the AUA consensus stratifies first by high or low risk, then by symptomatic or asymptomatic status; high-risk features include hydronephrosis, stage 3 chronic kidney disease, and recurrent symptomatic, culture-proven UTI or urosepsis.[34]

The goals are:

  1. Prevent overdistension, UTI, stones, hydronephrosis, and renal injury.
  2. Make bladder emptying reliable.
  3. Treat storage symptoms without worsening retention.
  4. Avoid unnecessary outlet surgery in acontractile or insensate bladders.

Conservative and Drainage Management​

Clean intermittent catheterization​

Clean intermittent catheterization (CIC) is the preferred long-term drainage strategy when emptying is inadequate and the patient or caregiver can perform it; AUA/SUFU recommends it over indwelling catheters in NLUTD , and EAU makes it a strong recommendation with thorough training in technique and risks.[8][9][16] In a tertiary retrospective cohort of 133 patients already performing CIC for DU or acontractility, 75% still required bladder drainage long term.[8] Learning success also varies by age and sex: in one service teaching CIC with structured before-visit information, supervised practice, and follow-up support, 6-week success was 91% in men and 80% in women under 65, and 86% in men and 68% in women 65 or older.[29]

Advantages:

  • Lower urethral erosion risk than indwelling catheter
  • May reduce stone burden and urethral complications; symptomatic UTI susceptibility does not clearly differ from indwelling drainage in the general neuro-urological population.[15][23]
  • Preserves sexual function and mobility better than urethral catheter
  • Allows measured emptying schedule

In a 2026 randomized trial of 386 people performing CIC for urinary retention, reusable catheters disinfected daily in 2% sodium hypochlorite met the UTI noninferiority margin against single-use catheters over about 12 months (0.050 vs 0.054 UTIs per patient-month in the modified intention-to-treat analysis); 72/185 (39%) in the reusable arm discontinued, mainly because of handling difficulty or urethral irritation.[39]

Practical targets:

  • Catheterize often enough to avoid painful distension and high residual volumes.
  • Use hydrophilic or closed systems when recurrent trauma or UTI is an issue.
  • Match plan to dexterity, cognition, caregiver support, and urethral anatomy.
  • Warn patients, particularly women with Fowler-type sphincter non-relaxation, that catheterization can be uncomfortable: 69% of 91 women with Fowler's syndrome reported a gripping sensation and discomfort, particularly on withdrawal, in one survey.[30] Teach with an experienced clinician and consider alternative drainage if CIC is not tolerated.

Suprapubic catheter​

Use when CIC is not feasible, urethral catheterization is traumatic, or long-term drainage is required. SPC is generally preferable to chronic urethral catheterization when a durable catheter route is needed.

Behavioral measures​

  • Timed voiding
  • Double voiding
  • Avoid bladder overdistension
  • Treat constipation
  • Reduce sedating and anticholinergic medication burden
  • Avoid Valsalva voiding as the only plan in high-risk or obstructed patients

Valsalva voiding may empty an areflexic, low-resistance outlet, but it is a poor solution when outlet resistance is high, pelvic organ prolapse is present, or upper-tract risk exists. Warn women who strain to void that it raises prolapse risk.[16] EAU gives weak recommendations against routine intravesical electrical stimulation for women with UAB and against intravesical prostaglandins for female retention outside a well-regulated, closely monitored research study.[16] An 8-year single-center retrospective series of 105 patients with detrusor underactivity of mixed cause treated with intravesical electrical stimulation reported a greater-than-50% reduction in postvoid residual in 47% of the 89 patients with pre/post measurements.[31] In a 76-patient, four-week randomized trial, active stimulation reduced mean PVR by 97 mL versus 11 mL with an open-circuit control; between-group differences in daily CIC frequency and patient-reported scores were not statistically significant.[38]

Pharmacologic Therapy​

Drug therapy for DU is disappointing. The EAU Neuro-Urology guideline (2026) strongly recommends against prescribing parasympathomimetics for underactive detrusor; the EAU non-neurogenic female LUTS guideline (2026) strongly recommends against their routine use for women with UAB.[15][16] Its evidence review found that oral agents do not improve clinical or urodynamic parameters and can cause gastrointestinal upset, blurred vision, bronchospasm, and bradycardia.[15][16] A 2022 meta-analysis found low-quality evidence with short follow-up: an early post-void volume reduction that was gone by one month.[21]

TreatmentRoleCaveat
Bethanechol / cholinergic agonistsLegacy therapy for detrusor atonyLimited efficacy, frequent adverse effects; rarely transformative[10]
Distigmine / anticholinesterase agentsUsed in some regionsSide effects and limited evidence
Alpha blockersReduce bladder neck / prostatic smooth muscle toneAUA/SUFU allows them to improve voiding parameters in NLUTD patients who void spontaneously , EAU strongly recommends them to lower outlet resistance in NLUTD and weakly suggests offering them to women with UAB before invasive options (small studies)[9][15][16]
Alpha blocker + cholinergic agentIn one 4-week Japanese trial (n=119), the combination raised flow and lowered PVR; cholinergic alone did not, and the alpha blocker alone lowered IPSS and PVR[11]—
Beta-3 agonists / antimuscarinicsTreat storage symptoms or DHICCheck and monitor PVR; catheterization plan must be clear

Medication works best when the problem is mixed DU plus functional outlet resistance, not a truly acontractile detrusor.

Sacral Neuromodulation​

Sacral neuromodulation (SNM) is one of the few therapies with meaningful evidence for non-obstructive urinary retention and selected DU.[12][13] AUA/SUFU 2021 says clinicians may offer SNM to selected NLUTD patients with urgency, frequency, or urgency incontinence and should not offer it in SCI or spina bifida ; EAU Neuro-Urology 2026 recommends considering SNM in selected neurological patients .[9][15]

Best candidates:

  • Non-obstructive retention
  • Preserved bladder sensation
  • Some preserved contractility
  • Younger patients
  • No fixed anatomic obstruction
  • Able to participate in trial-phase voiding diary and catheter-volume tracking

Less favorable:

  • Acontractile detrusor
  • Absent bladder sensation
  • Severe chronic overdistension
  • Advanced neurogenic disease with poor sacral reflex arc
  • Uncorrected outlet obstruction

Published series report roughly half of DU patients responding to the test phase (51% in one 69-patient series; 33% with acontractile detrusor versus 57% with measurable contractility).[12] Younger age also predicted response.[12] EAU strongly recommends SNM for women with UAB refractory to conservative management; trial-phase response ranges 33-90% and permanent-implant success 55-100%.[16]

Outlet-Directed Treatment​

Outlet treatment can help a weak bladder if outlet resistance is meaningfully contributing.

Men​

Consider outlet surgery when video-UDS or cystoscopy shows:

  • BPH or BPO with obstruction
  • Tight bladder neck
  • Urethral stricture
  • Bladder neck contracture

Poor external-sphincter relaxation requires a functional-voiding assessment and targeted therapy; it is not by itself an indication to incise a structurally normal outlet.

In a male video-urodynamic DU cohort, voiding efficiency above 66.7% was reached in 68% after outlet surgery, 59% after urethral botulinum toxin, and 18% with conservative care alone.[14] Across all treatment groups, 59/143 men (41.3%) with detrusor acontractility and 5/28 (17.9%) with absent bladder sensation achieved voiding efficiency >66.7% within one year.[14] A meta-analysis of BPE surgery (17 nonrandomized comparative studies) found no significant perioperative retention difference between DU and normal contractility, with worse Qmax and IPSS at 3–6 months but similar IPSS and quality of life from 12 months.[18] A newer meta-analysis (14 studies; 2,060 men with DU and 2,285 controls) found higher postoperative retention with DU (OR 1.63, 95% CI 1.21–2.20); most studies were retrospective.[32] In a small HoLEP series with at least 24 months of follow-up, 89% of men with DU and 63% with acontractility were catheter-free, and some still needed intermittent catheterization for high PVR.[19] Counsel that catheter dependence can persist.

EAU 2026 male LUTS guideline recommendations for men (all weak unless stated):[23]

  • Start intermittent catheterization when PVR exceeds 300 mL or the upper tract is at risk.[23] EAU notes that UTI risk rises above 300 mL.[23] Use an indwelling catheter only when other drainage has failed or is unsuitable, and prefer a suprapubic catheter to avoid traumatic hypospadias.
  • EAU describes double voiding and pelvic floor relaxation for men with underactive bladder, and weakly recommends offering an alpha blocker before more invasive techniques.[23]
  • Offer an alpha blocker before more invasive treatment. Evidence is limited (level 4). Do not routinely recommend parasympathomimetics (strong).
  • Counsel men with DU or an acontractile detrusor and concomitant prostatic enlargement about the potential benefit of prostate surgery. EAU cites a systematic review with IPSS changes of −3 to −19.5 points and mixed comparisons against men without DU. It reports worse outcomes after PVP or TURP than after HoLEP, and with older age, absent obstruction, detrusor overactivity and lower contractility. Case series in men with DU or acontractility and concomitant prostatic obstruction report return of contractility in 78% at 6 months after HoLEP (94.7% voiding spontaneously); a TURP/TUIP series reported improved quality of life and voiding efficiency >50% in 81.7%, with durability data limited.[23]
  • In men with DU and no prostatic obstruction, offer a sacral neuromodulation test phase. In a multicenter retrospective series of 35 men, 51.4% responded to the first stage and 72% of implanted men had a favorable response.[23] In a separate 69-patient cohort of men and women, residual contractility was associated with better trial response than acontractility.[12]

Women​

Look for:

  • Prior sling obstruction
  • Pelvic organ prolapse
  • Fowler-type sphincter non-relaxation
  • Dysfunctional voiding
  • Urethral stricture
  • Medication-induced retention

Sling incision or urethrolysis helps obstruction; it does not treat primary DU and may unmask stress incontinence.

Transurethral bladder neck incision has been described in an earlier retrospective series of 31 women with refractory DU.[22] In a later 82-woman series (59 with neurogenic etiology; median follow-up five years), 40 (48.8%) achieved spontaneous voiding with voiding efficiency of at least 50%; five (6.1%) developed SUI and two (2.4%) developed vesicovaginal fistula.[16][33] EAU gives it no recommendation and advises against routine latissimus dorsi detrusor myoplasty, which rests on one group's retrospective multicentre series.[16]

Botulinum toxin to outlet​

Urethral sphincter botulinum toxin may help selected patients with poor sphincter relaxation, DSD, or functional outlet obstruction. EAU describes retrospective case series with relief typically lasting three months and weakly recommends offering external-sphincter onabotulinumtoxinA to women with UAB before more invasive options, with disclosure that the evidence is low quality.[16] In a trial that randomized 73 adults with non-neurogenic voiding dysfunction, 62 completed the one-month assessment (31 with DU); a ≥2-point improvement in Patient Perception of Bladder Condition followed one 100 U injection in 14/38 (36.8%) versus 13/24 (54.2%) after saline, with DU subgroup rates of 7/22 (31.8%) versus 3/9 (33.3%).[36]

Reconstructive Decision Points​

  • Before SUI surgery: measure PVR and consider urodynamics when symptoms suggest impaired emptying. A sling or AUS in an underactive bladder can convert borderline emptying into retention.
  • Before BPH surgery: distinguish BOO from DU. If both are present, counsel that surgery may improve emptying but urgency, weak stream, or catheter need may persist.
  • Before botulinum for OAB: confirm the patient can catheterize if retention worsens.
  • Before urinary diversion or bladder neck closure: establish whether the issue is unsafe storage, unsafe emptying, outlet incompetence, or patient-care logistics.
  • After pelvic surgery: new retention can be neuropraxia, pain or opioids, hematoma, sling obstruction, or true denervation. After female stress-incontinence surgery, the 2024 CUA guideline recommends 1–2 days of catheterization followed by a repeat voiding trial; for persistent retention after a midurethral sling, it recommends sling loosening within one week or incision at 4–6 weeks when possible .[37]

Prognosis​

Long-term prognostic factors for recovery from DU are poorly established.[16][23] In a retrospective cohort of 298 men with DU, normal or increased bladder sensation and measurable detrusor contraction were associated with higher rates of voiding efficiency >66.7% within one year after treatment; absent sensation and acontractility had lower rates. Videourodynamic outlet narrowing informed outlet-directed treatment. Baseline PVR was not associated with treatment outcome in that cohort.[14]

Record retention duration and baseline PVR; assess prolonged overdistension, diabetes, and neurologic disease as possible contributors to DU.[16][34] In chronic retention, recurrent culture-proven UTI, stones, and hydronephrosis warrant assessment as complications; ability of the patient or a caregiver to perform CIC informs the drainage plan.[34]

Complications of untreated DU include recurrent UTI, acute retention, overflow incontinence, bladder stones, upper-tract dilation, and renal deterioration.

See Also​

References​

1. Osman NI, Chapple CR, Abrams P, et al. "Detrusor Underactivity and the Underactive Bladder: A New Clinical Entity? A Review of Current Terminology, Definitions, Epidemiology, Aetiology, and Diagnosis." Eur Urol. 2014;65(2):389-398. doi:10.1016/j.eururo.2013.10.015

2. Drake MJ, Williams J, Bijos DA. "Voiding Dysfunction Due to Detrusor Underactivity: An Overview." Nat Rev Urol. 2014;11(8):454-464. doi:10.1038/nrurol.2014.156

3. Osman NI, Esperto F, Chapple CR. "Detrusor Underactivity and the Underactive Bladder: A Systematic Review of Preclinical and Clinical Studies." Eur Urol. 2018;74(5):633-643. doi:10.1016/j.eururo.2018.07.037

4. Taylor JA, Kuchel GA. "Detrusor Underactivity: Clinical Features and Pathogenesis of an Underdiagnosed Geriatric Condition." J Am Geriatr Soc. 2006;54(12):1920-1932. doi:10.1111/j.1532-5415.2006.00917.x

5. Bosch R, Abrams P, Averbeck MA, et al. "Do Functional Changes Occur in the Bladder Due to Bladder Outlet Obstruction? - ICI-RS 2018." Neurourol Urodyn. 2019;38 Suppl 5:S56-S65. doi:10.1002/nau.24076

6. Resnick NM, Yalla SV. "Detrusor Hyperactivity With Impaired Contractile Function. An Unrecognized but Common Cause of Incontinence in Elderly Patients." JAMA. 1987;257(22):3076-3081. doi:10.1001/jama.257.22.3076

7. Gammie A, Kaper M, Dorrepaal C, Kos T, Abrams P. "Signs and Symptoms of Detrusor Underactivity: An Analysis of Clinical Presentation and Urodynamic Tests From a Large Group of Patients Undergoing Pressure Flow Studies." Eur Urol. 2016;69(2):361-369. doi:10.1016/j.eururo.2015.08.014

8. Dewulf K, Meurice A, Duvillier T, et al. "Detrusor Underactivity and Acontractile Bladder Patients Performing Clean Intermittent Catheterization in a Single Tertiary Referral Center: What Is Happening in Real Life?" Int Urogynecol J. 2025;36(7):1533-1540. doi:10.1007/s00192-025-06181-3

9. Ginsberg DA, Boone TB, Cameron AP, et al. "The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-Up." J Urol. 2021;206(5):1106-1113. doi:10.1097/JU.0000000000002239

10. Gaitonde S, Malik RD, Christie AL, Zimmern PE. "Bethanechol: Is It Still Being Prescribed for Bladder Dysfunction in Women?" Int J Clin Pract. 2019;73(8):e13248. doi:10.1111/ijcp.13248

11. Yamanishi T, Yasuda K, Kamai T, et al. "Combination of a Cholinergic Drug and an Alpha-Blocker Is More Effective Than Monotherapy for the Treatment of Voiding Difficulty in Patients With Underactive Detrusor." Int J Urol. 2004;11(2):88-96. doi:10.1111/j.1442-2042.2004.00753.x

12. Chan G, Qu LG, Gani J. "Evaluation of Pre-Operative Bladder Contractility as a Predictor of Improved Response Rate to a Staged Trial of Sacral Neuromodulation in Patients With Detrusor Underactivity." World J Urol. 2021;39(6):2113-2119. doi:10.1007/s00345-020-03380-z

13. Onur R, Tayebi S, Salehi-Pourmehr H, et al. "Sacral Neuromodulation in Patients With Detrusor Underactivity: Is Biological Sex an Indicator?" Neurourol Urodyn. 2022;41(3):847-859. doi:10.1002/nau.24893

14. Lee CL, Jhang JF, Ho HC, et al. "Therapeutic Outcome of Active Management in Male Patients With Detrusor Underactivity Based on Clinical Diagnosis and Videourodynamic Classification." Sci Rep. 2022;12(1):362. doi:10.1038/s41598-021-04237-0

15. European Association of Urology. EAU Guidelines on Neuro-Urology. Limited update March 2026. Section 3.4.2 (drugs for voiding symptoms). Guideline.

16. European Association of Urology. EAU Guidelines on Management of Non-neurogenic Female Lower Urinary Tract Symptoms (LUTS). Limited update March 2026. Section 4.4 (underactive bladder). Guideline.

17. European Association of Urology. EAU Guidelines on Management of Non-neurogenic Female LUTS. 2026. Section 4.4.1 (epidemiology of underactive bladder). Guideline.

18. Wroclawski ML, Takemura LS, Santos HOD, et al. "Functional and Safety Outcomes After Benign Prostatic Enlargement Surgeries in Men With Detrusor Underactivity Compared With Normal Detrusor Contractility: Systematic Review and Meta-Analysis." Neurourol Urodyn. 2024;43(1):126-143. doi:10.1002/nau.25336

19. Lomas DJ, Krambeck AE. "Long-Term Efficacy of Holmium Laser Enucleation of the Prostate in Patients With Detrusor Underactivity or Acontractility." Urology. 2016;97:208-211. doi:10.1016/j.urology.2016.07.010

20. Abrams P. "Bladder Outlet Obstruction Index, Bladder Contractility Index and Bladder Voiding Efficiency: Three Simple Indices to Define Bladder Voiding Function." BJU Int. 1999;84(1):14-15. doi:10.1046/j.1464-410x.1999.00121.x

21. Moro C, Phelps C, Veer V, et al. "The Effectiveness of Parasympathomimetics for Treating Underactive Bladder: A Systematic Review and Meta-Analysis." Neurourol Urodyn. 2022;41(1):127-139. doi:10.1002/nau.24839

22. Jhang JF, Jiang YH, Kuo HC. "Transurethral Incision of the Bladder Neck Improves Voiding Efficiency in Female Patients With Detrusor Underactivity." Int Urogynecol J. 2014;25(5):671-676. doi:10.1007/s00192-013-2279-4

23. European Association of Urology. EAU Guidelines on the Management of Non-neurogenic Male LUTS. 2026 (March update). Official full guideline. See sections 5.7.1 to 5.7.6.

24. Rud T, Ulmsten U, Andersson KE. "Initiation of Voiding in Healthy Women and Those With Stress Incontinence." Acta Obstet Gynecol Scand. 1978;57(5):457-462. doi:10.3109/00016347809156528

25. Bhatia NN, Bergman A, Karram M. "Changes in Urethral Resistance After Surgery for Stress Urinary Incontinence." Urology. 1989;34(4):200-204. doi:10.1016/0090-4295(89)90372-5

26. Veeratterapillay R, Coates J, Leonard A, et al. "Detrusor After-Contraction on Ambulatory Urodynamics in Symptomatic Women." Int J Urol. 2015;22(11):1058-1062. doi:10.1111/iju.12887

27. Tan TL, Bergmann MA, Griffiths D, Resnick NM. "Stop Test or Pressure-Flow Study? Measuring Detrusor Contractility in Older Females." Neurourol Urodyn. 2004;23(3):184-189. doi:10.1002/nau.20020

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