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Botulinum Toxin (Neuromodulation Adjunct)

OnabotulinumtoxinA (Botox) has FDA-labeled uses for adult idiopathic OAB (100 U) and adult neurogenic detrusor overactivity (NDO; 200 U) after inadequate response to or intolerance of anticholinergics. Pediatric NDO is labeled from age 5 with weight-based dosing (see below). Its off-label applications include IC/BPS, detrusor-sphincter dyssynergia (DSD), primary bladder-neck obstruction, pelvic-floor and pudendal myofascial pain, and chronic prostatitis / CPPS.[1][2] It is the only chemodenervation agent with urologic FDA approvals — abobotulinumtoxinA and incobotulinumtoxinA are not interchangeable and carry no urologic labels.

For related classes, see Anticholinergics, β3-agonists, and Topical compounded agents.

Mechanism — why dual efferent + afferent matters​

OnabotulinumtoxinA cleaves SNAP-25, blocking SNARE-complex-mediated vesicle fusion at presynaptic terminals. In the lower urinary tract this produces three simultaneous effects that together explain why BoNT-A improves not just leakage but also urgency, frequency, and pain:[3][4]

PathwayEffect
Efferent (motor)Blocks acetylcholine release at the detrusor neuromuscular junction; blocks ATP release from purinergic efferent nerves — reduces involuntary detrusor contraction
Afferent (sensory)Markedly reduces urothelial ATP release and increases NO release; inhibits release of substance P, CGRP, and glutamate from sensory terminals; downregulates TRPV1 and P2X3 on C-fiber afferents; decreases urothelial NGF
Anti-inflammatoryReduces neurogenic inflammation by suppressing neuropeptide release; modulates mast-cell degranulation

Simple muscle paralysis cannot account for the urgency and pain reductions observed clinically — the afferent effect is a core mechanism, not a byproduct. Investigational non-injection delivery aims to affect sensory pathways while reducing motor effects; small studies do not establish an afferent-only mechanism or eliminate retention risk.[4]

Agents in this class​

AgentFDA urologic indicationUrologic role
OnabotulinumtoxinA (Botox)Adult OAB 100 U; adult NDO 200 U; pediatric NDO ≥5 y: 200 U if ≥34 kg, 6 U/kg if <34 kgThe only approved agent; all urologic data below[1][2]
AbobotulinumtoxinA (Dysport)NoneNot interchangeable with onabotA; no urologic label
IncobotulinumtoxinA (Xeomin)NoneNot interchangeable; no urologic label
RimabotulinumtoxinB (Myobloc)NoneSerotype B; not used in urology

FDA indication #1 — idiopathic OAB (100 U)​

Guideline position​

The AUA/SUFU OAB guideline (2024) places intradetrusor onabotulinumtoxinA alongside sacral neuromodulation (SNM) and percutaneous tibial nerve stimulation (PTNS) as minimally invasive options (Statement 25; Moderate Recommendation, Grade A) and now explicitly allows bypassing oral pharmacotherapy in patients who cannot tolerate or do not wish to try antimuscarinics or β3-agonists. Clinicians may offer minimally invasive therapies without requiring trials of behavioral or pharmacologic management (Expert Opinion). PVR must be measured before injection; pivotal RCTs used PVR ≥100–200 mL as exclusion criteria.[5]

Pivotal phase 3 — Nitti 2013​

The registration trial (n = 557 adults with OAB / urge urinary incontinence refractory to antimuscarinics) remains the anchor data:[6]

  • UI reduction: −2.65 episodes/day (onabotA 100 U) vs −0.87 (placebo); p < 0.001
  • Positive treatment benefit: 60.8% vs 29.2% (p < 0.001)
  • Complete continence: 22.9% vs 6.5%
  • Significant improvements across urgency, frequency, nocturia, and QoL (I-QOL, KHQ)
  • Most common AEs: UTI and urinary retention; urinary retention 5.4% in this trial; retention and initiation of clean intermittent catheterization (CIC) are distinct outcomes

Long-term efficacy — 3.5-year extension​

The open-label extension (Nitti 2016, up to 6 treatments):[7]

  • Consistent mean UI reductions of −3.1 to −3.8 episodes/day across repeat injections
  • Durable symptom and QoL improvement
  • Median duration of effect 7.6 months
  • De novo CIC 4.0% after first treatment, falling to 0.6–1.7% on subsequent treatments
  • No new safety signal in the extension cohort; this does not guarantee indefinite response in all patients

Head-to-head vs combined oral pharmacotherapy (Hsieh 2025, RCT, 74 enrolled / 66 completed)​

In women with urodynamically confirmed DO refractory to single pharmacotherapy:[8]

  • OnabotA 100 U and solifenacin 5 mg + mirabegron 25 mg had no statistically significant between-group difference in urgency reduction (median 2.0 episodes / 24 h at 12 weeks; p = 0.925; this superiority trial did not establish equivalence)
  • Frequency, nocturia, UUI, and QoL improvements were similar
  • Adverse events (dry mouth, constipation, blurred vision) were significantly more common with combination pharmacotherapy (all p < 0.05)

FDA indication #2 — neurogenic detrusor overactivity (200 U)​

Guideline position​

The AUA/SUFU NLUTD guideline (2021):[9]

  • Statement 40 (Strong Recommendation; Grade A): in NLUTD patients with SCI or MS refractory to oral medications, offer onabotulinumtoxinA to improve storage parameters, decrease incontinence, and improve QoL
  • No efficacy difference between 200 U and 300 U, but a dose-dependent increase in retention risk — 200 U is standard
  • Repeated injections restore first-injection benefit; efficacy does not diminish over time in most patients
  • Statement 41 (Conditional; Grade C): in non-SCI/MS neurogenic patients (PD, CVA, spina bifida), BoNT-A may be offered but evidence is limited

Pivotal phase 3 — MS and SCI​

The registration program (Sanford 2014 review) produced:[10]

  • Significant reductions in UI episodes and MCC increases with matching detrusor-pressure reductions
  • Most common AEs: UTI and urinary retention
  • Among noncatheterizing adults in the label’s pooled NDO trials, 30.6% required CIC after 200 U versus 6.7% with placebo; discuss the relevant population and possible prolonged catheterization.[1]

Low-dose 100 U for noncatheterizing MS — Tullman 2018​

Placebo-controlled evidence supports symptom benefit from 100 U in noncatheterizing MS patients; 200 U remains the recommended adult NDO label dose:[11]

  • UI reduction −3.3 episodes/day vs −1.1 placebo (p < 0.001)
  • CIC initiation was 15.2% versus 2.6% with placebo; comparisons with the 200 U studies are indirect
  • A specialist may discuss the lower off-label dose with selected patients; it does not remove the need for a catheterization plan

4-year durability — Rovner 2016​

Long-term extension in NDO:[12]

  • Consistent UI reduction −3.4 to −3.9 episodes/day across all 4 years
  • 86.6–94.1% achieved ≥50% UI reduction annually; 43.6–57.4% achieved 100% UI reduction each year
  • I-QOL improvements sustained year-to-year
  • Median duration of effect ≥9.0 months (range 3.0–49.2); ≥26% experienced ≥12-month duration
  • No accumulating safety signal

Personalization (Wang 2026 narrative review)​

Practical levers for NLUTD dosing:[13]

  • Baseline voiding status — CIC status changes the practical consequences of retention but does not remove dose-related or systemic adverse effects
  • Self-catheterization ability — the go / no-go criterion for most non-CIC patients
  • Age — older patients carry higher retention risk
  • Reduced injection-site templates and trigone-inclusive techniques are active areas of investigation

ROSETTA — onabotulinumtoxinA vs sacral neuromodulation​

Amundsen 2016 (JAMA, 381 randomized / 364 in the primary analysis) compared SNM with 200 U, a dose above the labeled 100 U OAB dose; it is not a direct comparison of SNM with standard-dose OAB Botox:[14]

  • UUI reduction: −3.9 (onabotA 200 U) vs −3.3 (SNM) episodes/day — mean difference 0.63 favoring onabotA (p = 0.01)
  • Complete UUI resolution: 20% vs 4% (p < 0.001)
  • UTI was 35% versus 11%; Botox-group CIC use was 8% at one month and 2% at six months. SNM revision/removal occurred in 3%

Longitudinal fluctuation (Hendrickson 2024) — over 6 months, 61% of onabotA vs 51% of SNM patients maintained persistent objective success. OnabotA had lower 30-day transition probability from success to failure (10% vs 14%; ratio 0.75). Roughly 2 in 5 women's symptoms fluctuated regardless of modality.[15]

2025 network meta (Roman, 12 studies, 2,645 patients) — onabotA reduced UUI more than placebo or SNM; ≥75% UUI reduction was more likely with onabotA. However, complete UUI resolution favored SNM (p < 0.05). Adverse events predictably split — UTI and CIC with BoNT-A; device / reprogramming with SNM.[16]

Crossover — SNM after failed BoNT-A (Yang 2020 meta-analysis) showed 58.5% success, no statistically significant difference from prior-BoNT-naive comparators (RR 0.96; 95% CI 0.72–1.26). Prior Botox failure does not exclude SNM, but this does not prove identical subsequent success.[17]

Who does worse? ROSETTA secondary analysis (Richter 2017) — older women with multiple comorbidities and lower baseline QoL had lower response and satisfaction with onabotA vs SNM; higher BMI was associated with reduced odds of achieving ≥50% UUI reduction with either treatment (adjusted OR 0.82 per 5 BMI points).[18]

Dose, administration and label safeguards​

Use the current US prescribing information for reconstitution and administration. Units cannot be converted between toxin products.[1]

PopulationLabeled bladder dose / dilution
Adult OAB100 U in 10 mL; 20 detrusor injections of 0.5 mL
Adult NDO200 U in 30 mL; 30 detrusor injections of 1 mL
Pediatric NDO, age ≥5 y≥34 kg: 200 U; <34 kg: 6 U/kg; follow the pediatric 10 mL dilution and injection instructions

The cumulative adult limit is 400 U in three months across indications; pediatric cumulative exposure is limited to the lesser of 10 U/kg or 340 U. These are overall ceilings, not a reason to exceed a bladder-indication dose. Reinject when effect wanes, no sooner than 12 weeks; there is no mandatory six-month interval.[1]

Do not inject with active UTI, relevant hypersensitivity or injection-site infection. Intradetrusor use is contraindicated with retention or PVR >200 mL in a patient not routinely catheterizing. Arrange catheterization if needed and check PVR within two weeks in noncatheterizing patients, then as appropriate through 12 weeks.[1]

The adult bladder label specifies prophylactic antibiotics excluding aminoglycosides for 1–3 days before, on the day, and 1–3 days after treatment. This differs from some stewardship pathways: resolve the regimen with local policy rather than silently treating it as a universal single-dose procedure. Antithrombotic decisions require a coordinated individual plan.[1]

Eilber’s 2025 expert consensus and Rovner’s 2014 practical review describe variations in office anesthesia and injection distribution. Fewer sites, alternative dilution or trigonal inclusion should be identified as deviations from the labeled template, with their evidence limits.[19][20] A small transabdominal-injection trial is investigational; a nonsignificant efficacy comparison does not establish equivalence or justify routine substitution for cystoscopic delivery.[21]

Systemic toxin effects

The boxed warning covers distant spread, including generalized weakness, dysphagia and breathing difficulty, potentially hours to weeks after injection. Neuromuscular disease, respiratory compromise and interacting agents (including aminoglycosides or muscle relaxants) require particular attention. A bladder dose is not a guarantee against systemic effects.[1]

Adverse effects and predictors of response​

Adverse effectOAB (100 U)NDO (200 U)Notes
UTI15–35%25–49%Most common; mostly uncomplicated[6][10]
CIC for retention in label trials6.5% versus 0.4% placebo30.6% versus 6.7% placebo among patients not using CIC at baselineDifferent populations; not an individualized risk estimate[1]
Elevated PVR~20%Expected in CIC-dependent patientsCheck PVR at 7–14 days[20]
Dysuria, hematuriaCommon, transientCommon, transientProcedure-related[6]
Autonomic dysreflexiaN/ARare in high-SCI patientsMonitor during injection[9]
Systemic weakness / dysphagiaSerious potential riskSerious potential riskSee boxed warning; no safe-dose threshold eliminates it

Predictors of poor response / CIC need — Abrar 2020 (n = 74)[22]​

  • Male sex — the only predictor of poor response (OR 5.45; 95% CI 1.83–16.47; p = 0.002) and also the strongest predictor of CIC need (OR 5.14; p = 0.013)
  • Lower Qmax predicted CIC need (OR 0.91 per mL/s; p = 0.023)
  • Prior hysterectomy in women predicted CIC (OR 4.55; p = 0.038)
  • CIC use predicted UTI (OR 5.26; p = 0.015)

Factors associated with efficacy — Hsiao 2016 (n = 80)[23]​

  • Overall success 63.8%
  • Female sex was the only independent predictor of success (OR 3.75)
  • Low baseline OABSS and OAB-wet predicted better efficacy
  • Low baseline voiding efficiency (<0.67) predicted need for CIC

Biomarker signal — Hanna 2026​

Baseline urinary cytokine profiling suggests older women are less likely to respond; the authors propose pre-treatment cytokine panels as a future selection tool.[24]

Off-label urologic applications​

Interstitial cystitis / bladder pain syndrome​

AUA IC/BPS guideline (2022) — Statement 20 (Option; Grade C): intradetrusor onabotulinumtoxinA may be administered after other treatments have failed; patients must accept the possibility of CIC.[25]

Intratrigonal injection (Pinto 2018, RCT, n = 19) — 10 trigonal injections of 100 U significantly reduced pain vs placebo at week 12 (Δ −3.8 vs −1.6; p < 0.05), with parallel improvements in frequency, urgency, and QoL.[26] Injection-site variability across studies (trigonal, lateral, posterior) and the scarcity of placebo-controlled trials remain the principal interpretive limits — see Intravesical IC/BPS agents for the broader armamentarium.

Detrusor-sphincter dyssynergia​

Goel 2020 systematic review and meta-analysis (11 studies, n = 353):[27]

  • BoNT-A reduces PVR, mean detrusor pressure, DLPP, and urethral pressure in 60–78% of patients at 1 month
  • Most need reinjection at 4–9 months
  • A 2013 expert evidence review assigned Level B using the AAN classification scale; this is not a current AAN guideline recommendation[28]

Concomitant detrusor + external urethral sphincter injection (Huang 2022, n = 20 male SCI) — 200 U detrusor + 100 U EUS reduces both maximal detrusor pressure and urethral pressure, raises MCC, and improves QoL without increasing PVR ratio or CIC frequency in this small cohort; this does not establish a standard approach for preserving spontaneous voiding.[29]

Predictors of sphincter-injection success (Lee 2025, n = 207) — overall success 33.8%; DSD grade 1 had 65.7% success vs grade 2 at 14.3% and grade 3 at 7.1%. Higher Qmax and lower PVR predicted response. These retrospective predictors are not a validated universal selection rule.[30]

Primary bladder-neck obstruction​

Sacco 2014 (n = 30 men) — transurethral 200 U into the bladder neck in medically refractory PBNO dropped IPSS from 21.9 → 7.8 at 2 months (p < 0.001), with durable but reduced benefit at 6 months (10.3).[31]

Lee 2025 (n = 41) — bladder-neck BoNT-A for both neurogenic and non-neurogenic BND yielded 65.9% satisfactory outcomes at 6 months (26.8% successful + 39.0% improved); non-neurogenic BND had the highest satisfaction; higher baseline BOOI predicted failure.[32]

BPH / LUTS — does not work​

Two large phase 2 RCTs are decisive:

  • Marberger 2013 (n = 374) — 100, 200, or 300 U intraprostatic onabotA: IPSS, Qmax, and prostate-volume improvements were matched by placebo, with a large placebo effect from the injectable procedure itself[33]
  • McVary 2014 (n = 315) — 200 U vs placebo: IPSS −6.3 vs −5.6 (no difference) despite a sham-injection run-in designed to suppress placebo response[34]

Phase 3 was not pursued. OnabotulinumtoxinA should not be used for BPH / LUTS outside of study.[35][36]

Chronic prostatitis / CPPS and pelvic-floor myofascial pain​

  • Falahatkar 2015 (RCT, n = 60) — transurethral intraprostatic BoNT-A dropped the NIH-CPSI pain subscale by 64.8% / 75.6% / 80.0% at 1, 3, and 6 months vs no placebo improvement (all p < 0.001) — striking signal but small and unreplicated[37]
  • Franco 2019 Cochrane — intraprostatic BoNT-A may decrease prostatitis symptoms (MD −25.80; low-quality evidence, one trial). Pelvic-floor injection showed little to no effect (MD −2.60; low-quality)[38]
  • Panunzio 2022 pooled meta (18 studies, 896 patients) — benefit across CPPS subtypes (bladder, prostate, gynecologic) but heterogeneity limits firm conclusions[39]

Women — pelvic-floor injection for chronic pelvic pain:

  • Spruijt 2022 systematic review / meta-analysis (8 studies, n = 289 women) — at 24–26 weeks, 15-point VAS reduction for non-menstrual pelvic pain and 13-point reduction for dyspareunia, plus reduced pelvic-floor resting pressure and improved QoL[40]
  • Dessie 2019 RCT (n = 59) — 200 U trigger-point injection was not superior to saline on the primary endpoint (muscle pain on palpation); participants were more likely to report overall improvement at 4 weeks (p = 0.03); de novo constipation 10.1%, incontinence 22%[41]
  • Practical technique (Whitmore 2025) — 200 U in 20 mL saline; inject pubococcygeus, iliococcygeus, and obturator internus using a pudendal nerve kit (1 cm needle depth); effect 3–6 months; pain reduction onset at ~6 weeks; AEs include constipation, incontinence, UTI, retention[42]
  • Overall read (Karp 2025) — numerous uncontrolled series are positive; the few RCTs are equivocal. These are different conditions and study populations; the small trials do not establish a routine intraprostatic treatment standard.[43]

Spruijt 2025 added a four-center placebo-controlled trial of 94 women, using 100 U plus pelvic-floor muscle therapy. Neither clinical primary outcome differed significantly: ≥33% pain reduction occurred in 33% versus 20% (p=0.19), and 17% in each arm reported marked improvement. Reduced resting muscle activity did not translate into established additional pain relief.[51]

See Chronic Pelvic Pain and IC/PBS.

Novel delivery — injection-free approaches​

The dual-compartment mechanism (efferent + afferent) raises an obvious engineering question: can you get BoNT-A into the urothelium without a cystoscopic needle? Three approaches are in development.

Liposome-encapsulated BoNT-A (lipotoxin)​

Liposomes adsorb to and fuse with urothelial cell membranes, delivering toxin across the urothelium without injection — and the approach aims for sensory effects with less detrusor weakness; absence of retention in small studies does not prove no risk.[44][45]

  • Chuang 2014 multicenter RCT (n = 62) — intravesical 200 U lipo-BoNT-A reduced micturitions (Δ −4.64 vs −0.19; p = 0.025) and urgency severity (p = 0.018) vs placebo at 4 weeks, with no retention signal. UUI effects inconclusive.[46]
  • Kuo 2014 pilot RCT (n = 24) — significant frequency and urgency reduction; no PVR or UTI increase; immunohistochemistry showed decreased P2X3 expression in responders.[47]
  • Mechanism contrast (Liu 2015) — injection effectively cleaves SNAP-25 in both urothelium and detrusor; lipotoxin acts in the urothelium only, consistent with the afferent-only clinical profile.[48]

TC-3 thermosensitive hydrogel​

Liquid at room temperature, solid at body temperature — prolongs intravesical dwell time. Early RCT data show frequency, urgency, and incontinence improvement in OAB.[49]

Energy-assisted delivery​

Suprapubic energy shock wave (ESW) after BoNT-A instillation demonstrates cleaved SNAP-25 in bladder tissue on immunohistochemistry — proof-of-concept that ESW can drive toxin across the urothelium. Not clinically deployed.[49]

Status: all three are investigational. Sensory-selective delivery is a research aim; these methods are not validated alternatives for patients unable to manage retention.

Special populations​

Pediatric NDO (≥5 y)​

Pediatric NDO is FDA-labeled from age 5 after inadequate response to or intolerance of anticholinergics: 200 U if weight ≥34 kg, 6 U/kg below 34 kg. Use the pediatric dilution and procedural instructions rather than transferring the adult NDO template.[1]

Parkinson's disease and post-stroke​

Most authors use 100 U (not 200 U) for PD and post-stroke patients to preserve efficacy while limiting retention — ~20% retention rate keeps post-stroke use largely experimental.[50]

Elderly and men​

Older women with comorbidities had lower response and satisfaction with onabotA compared with SNM in ROSETTA secondary analysis.[18][24] One small retrospective series associated male sex with poorer response and CIC; do not use its fivefold odds estimate as the expected risk for all men.[22]

Clinical Positioning​

  • OAB and NDO have strong efficacy evidence, but doses, trial populations and catheterization risks differ. Use the indication-specific label and a retention plan.
  • AUA 2024 allows shared selection of minimally invasive OAB treatment without requiring prior behavioral or drug trials; this recommendation does not rewrite the product’s labeled indication.[5]
  • ROSETTA compared SNM with 200 U Botox. Its small six-month difference in UUI episodes and higher UTI risk should not be generalized to all doses or long-term superiority.[14]
  • IC/BPS, sphincter/bladder-neck injection, and pelvic-floor treatment are off-label. Small cohorts or exploratory predictors do not establish routine use. The newer pelvic-floor RCT did not establish additional pain relief.[25][51]
  • Intraprostatic Botox has not shown convincing benefit for BPH in large placebo-controlled trials.[33][34]
  • Repeat dosing follows clinical response, the ≥12-week interval and cumulative limits; investigational delivery techniques do not remove label safety precautions.

See Also​

References​

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2. Nitti V, Haag-Molkenteller C, Kennelly M, et al. "Treatment of neurogenic detrusor overactivity and overactive bladder with Botox (onabotulinumtoxinA): development, insights, and impact." Medicine. 2023;102(S1):e32377. doi:10.1097/MD.0000000000032377

3. Lin YH, Chiang BJ, Liao CH. "Mechanism of action of botulinum toxin A in treatment of functional urological disorders." Toxins. 2020;12(2):E129. doi:10.3390/toxins12020129

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5. Cameron AP, Chung DE, Dielubanza EJ, et al. "The AUA/SUFU guideline on the diagnosis and treatment of idiopathic overactive bladder." J Urol. 2024;212(1):11–20. doi:10.1097/JU.0000000000003985

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11. Tullman M, Chartier-Kastler E, Kohan A, et al. "Low-dose onabotulinumtoxinA improves urinary symptoms in noncatheterizing patients with MS." Neurology. 2018;91(7):e657–e665. doi:10.1212/WNL.0000000000005991

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14. Amundsen CL, Richter HE, Menefee SA, et al. "OnabotulinumtoxinA vs sacral neuromodulation on refractory urgency urinary incontinence in women: a randomized clinical trial." JAMA. 2016;316(13):1366–1374. doi:10.1001/jama.2016.14617

15. Hendrickson WK, Zhang C, Jelovsek JE, Nygaard IE, Presson AP. "Longitudinal fluctuations in treatment response after onabotulinumtoxinA and sacral neuromodulation for refractory urgency incontinence." J Urol. 2024;211(1):134–143. doi:10.1097/JU.0000000000003746

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18. Richter HE, Amundsen CL, Erickson SW, et al. "Characteristics associated with treatment response and satisfaction in women undergoing onabotulinumtoxinA and sacral neuromodulation for refractory urgency urinary incontinence." J Urol. 2017;198(4):890–896. doi:10.1016/j.juro.2017.04.103

19. Eilber KS, Brucker BM, Pezzella A, et al. "Expert opinions on best practices for overactive bladder management with onabotulinumtoxinA." Toxins. 2025;17(4):207. doi:10.3390/toxins17040207

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22. Abrar M, Stroman L, Malde S, Solomon E, Sahai A. "Predictors of poor response and adverse events following botulinum toxin-A for refractory idiopathic overactive bladder." Urology. 2020;135:32–37. doi:10.1016/j.urology.2019.08.054

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24. Hanna MG, Shah AM, Li W, et al. "Urinary cytokines in predicting intradetrusor onabotulinumtoxin-A response." Neurourol Urodyn. 2026;45(4):845–852. doi:10.1002/nau.70261

25. Clemens JQ, Erickson DR, Varela NP, Lai HH. "Diagnosis and treatment of interstitial cystitis/bladder pain syndrome." J Urol. 2022;208(1):34–42. doi:10.1097/JU.0000000000002756

26. Pinto RA, Costa D, Morgado A, et al. "Intratrigonal onabotulinumtoxinA improves bladder symptoms and quality of life in patients with bladder pain syndrome/interstitial cystitis: a pilot, single-center, randomized, double-blind, placebo-controlled trial." J Urol. 2018;199(4):998–1003. doi:10.1016/j.juro.2017.10.018

27. Goel S, Pierce H, Pain K, et al. "Use of botulinum toxin A (BoNT-A) in detrusor external sphincter dyssynergia (DESD): a systematic review and meta-analysis." Urology. 2020;140:7–13. doi:10.1016/j.urology.2020.03.007

28. Chancellor MB, Elovic E, Esquenazi A, et al. "Evidence-based review and assessment of botulinum neurotoxin for the treatment of urologic conditions." Toxicon. 2013;67:129–140. doi:10.1016/j.toxicon.2013.01.020

29. Huang YH, Chen SL. "Concomitant detrusor and external urethral sphincter botulinum toxin-A injections in male spinal cord injury patients with detrusor overactivity and detrusor sphincter dyssynergia." J Rehabil Med. 2022;54:jrm00264. doi:10.2340/jrm.v54.122

30. Lee CL, Kuo HC. "Video urodynamic predictors of outcomes after urethral sphincter botulinum toxin A injection in spinal cord-injured patients with detrusor sphincter dyssynergia." Toxins. 2025;17(8):412. doi:10.3390/toxins17080412

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