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Multiple Sclerosis

Multiple sclerosis (MS) is the second-largest NLUTD population by volume. Lower urinary tract symptoms become more common with MS duration and are reported by almost all patients 10 years or more after symptom onset. OAB or detrusor overactivity can occur early and coexist with impaired emptying; a minority have detrusor areflexia or DSD as spinal plaques accumulate.[1][3]

See Neurogenic Lower Urinary Tract Dysfunction for the general framework. For the procedural options that come into play in refractory MS, see Intradetrusor OnabotulinumtoxinA, Sacral Neuromodulation, Percutaneous Tibial Nerve Stimulation, Bladder Augmentation, and the Ileal Conduit.

Epidemiology and Natural History​

  • US prevalence about 1 million; more common in women (about 3:1) and young adults.
  • About 10% of patients have voiding dysfunction at onset and about 75% develop it after 10 years of disease (EAU 2026).[6]
  • Urodynamic series (EAU 2026 summary) report neurogenic detrusor overactivity in 43–65%, DSD in about 35% and detrusor underactivity in about 25%; overlapping patterns are common, so the categories do not sum to 100%.[6]
  • Urinary symptoms track disability and disease duration. LUTS correlate with age, clinical course, disease duration, EDSS disability and fatigue.[6] They are rarely isolated and usually coexist with bowel, sexual and mobility impairment.

Pathophysiology​

MS plaques disseminate in time and space. Urinary phenotype depends chiefly on the location of lesions, although it also drifts with disease duration and disability:

  • Cortical or subcortical plaques give OAB or DO (uninhibited detrusor contractions).
  • Cervical or thoracic spinal plaques give DO and DSD (suprasacral phenotype; upper-tract risk if sustained high pressure).
  • Sacral cord / conus involvement may impair detrusor contraction. Cauda-equina disease is a peripheral lesion; do not automatically attribute it to MS without evaluating another cause.

Because lesions evolve, a patient's phenotype can shift (for example, from pure OAB to OAB with incomplete emptying), requiring re-evaluation when symptoms change.

Evaluation​

Initial workup is the AUA/SUFU framework.[1] Most MS patients are unknown-risk at entry and should have baseline:

  • History and focused neurologic exam (EDSS, mobility, dexterity, cognition)
  • Voiding diary and UA and PVR
  • Renal ultrasound and eGFR
  • Multichannel urodynamics to complete unknown-risk classification

Additional reasons to reassess with multichannel urodynamics:

  • Refractory symptoms despite empirical therapy
  • Elevated PVR suggesting DSD or underactivity
  • Upper-tract deterioration
  • Before botulinum injection, SNM, or reconstructive surgery
  • Recurrent febrile UTI

Video-urodynamics specifically documents DSD and VUR, both of which change management.

In a neurourology clinic series of patients with MS, 66 of 113 referred patients had both urodynamics and screening renal ultrasonography at initial evaluation. Eleven (16.7%) had abnormal ultrasound findings, mostly focal caliectasis, and none had more than mild hydronephrosis.[14] No demographic factor, serum creatinine or urodynamic finding, including DSD and the threshold or amplitude of detrusor overactivity, was associated with an abnormal ultrasound.[14]

AUA/SUFU calls for renal function assessment, upper-tract imaging and multichannel urodynamics to classify unknown-risk NLUTD. For stable moderate risk, perform annual focused history, examination, symptom and renal function assessment, with upper-tract imaging every 1–2 years. For stable high risk, perform annual focused history, examination, symptom and renal function assessment plus annual upper-tract imaging, and repeat multichannel urodynamics when clinically indicated (both Moderate Recommendations, Grade C).[1]

Management​

Behavioral and pharmacologic first line​

  • Fluid management (avoid late-evening intake for nocturia).
  • Bowel regimen. MS constipation is common and worsens urinary symptoms.
  • Pelvic-floor muscle training. Modest benefit in MS; AUA/SUFU allows it in appropriately selected patients, particularly those with MS or cerebrovascular accident .[2]
  • Antimuscarinics. EAU strongly recommends antimuscarinics or β3 agonists for neurogenic OAB and calls antimuscarinics its first-line choice for urodynamically confirmed NDO.[6] Trospium (minimal CNS penetration) is often preferred in MS given cognitive risk.
  • β3-adrenergic agonists (mirabegron, vibegron) are an alternative when anticholinergic side effects or cognitive concerns are limiting; EAU 2026 advises switching to a β3 agonist or other therapy if cognition is affected. Short MS/SCI studies of mirabegron report symptom benefits similar to antimuscarinics, without significant improvement in detrusor pressure or cystometric capacity. A retrospective SCI cohort reported improved capacity and compliance with vibegron, but MS urodynamic benefit and upper-tract protection remain unestablished; EAU 2026 strongly recommends against using β3 agonists to reduce urodynamically proven NDO.[6]
  • Combination therapy when monotherapy inadequate.
  • Desmopressin. Selected nocturnal-polyuria cases after renal, sodium and fluid-intake assessment; older age raises hyponatremia risk. Evidence in MS is heterogeneous and low quality, hyponatremia is frequent, and EAU 2026 strongly recommends screening and monitoring serum sodium.[6][9] Use the drug-specific safety and monitoring guidance.
  • α-blockers. May improve voiding parameters in selected patients who spontaneously void.[2]

Catheterization​

  • CIC. Consider for clinically important incomplete emptying, unsafe voiding or an agreed continence plan. For CIC, assess capacity, repeat volumes, symptoms, infections and pressures; a single PVR >100 mL or DSD label does not automatically establish an indication.[5] Counsel before starting: in one retrospective MS cohort with PVR >100 mL (n = 37; 19 started CIC, 18 received medical therapy), starting CIC was associated with about seven times the odds of at least one UTI over one year (OR 6.8) and a lower recorded rate of any urinary symptom improvement than medical therapy at one year (26% versus 72%; symptom status was reassessed in 26/37 patients).[6][13] Assess hand dexterity, positioning, vision, cognition and caregiver support before CIC; reassess catheterization ability as MS progresses.[5][6]
  • Indwelling SPC. When dexterity, spasticity, or caregiver support preclude CIC; AUA/SUFU recommends suprapubic over urethral drainage in appropriately selected patients who need a chronic indwelling catheter , and CIC over indwelling catheters for emptying (statement 35, strong, Grade C).[2]
  • Intermittent versus indwelling drainage. Assess ability, caregiver support, complications and treatment burden.[5] CIC may be assisted; SPC is an option when the intermittent regimen is not feasible.[5]

Intradetrusor onabotulinumtoxinA​

For refractory adult detrusor overactivity associated with MS, the US NDO dose is 200 U; the 100-U idiopathic OAB regimen is a different indication.[18] Assess retention risk and confirm a feasible catheterization plan before injection. In patients not routinely catheterizing, measure PVR within two weeks after injection and periodically as medically appropriate for up to 12 weeks, particularly in MS.[18] BOTOX is contraindicated for intradetrusor injection with a UTI, or with urinary retention or PVR >200 mL in a patient not routinely performing CIC.[18] Consider retreatment when the effect wanes, no sooner than 12 weeks after the preceding injection.[18] AUA/SUFU strongly recommends onabotulinumtoxinA for MS or SCI refractory to oral medication (statement 40, Grade A) and requires discussion of retention risk and possible CIC before treatment in patients who void .[2] EAU 2026 strongly recommends intradetrusor botulinum toxin A when antimuscarinic therapy fails; effect lasts about nine months and repeat injections remain effective.[6]

Trial (MS-relevant)DoseResult
Ginsberg 2012 (MS and SCI, n = 416)[10]200 U or 300 U vs placeboAt week 6, incontinence fell about 21–23 vs 9 episodes/week; among patients not catheterizing at baseline, 35% (200 U) and 42% (300 U) started CIC, vs 10% on placebo; no added benefit from 300 U
Tullman 2018 (MS, non-catheterizing, n = 144)[11]100 U vs placeboAt week 6, incontinence fell 3.3 vs 1.1 episodes/day; CIC started in 15.2% vs 2.6% during treatment cycle 1; protocol-defined UTI during the first 12 weeks (culture plus leukocyturia, symptoms not required) 25.8% (17/66) vs 6.4% (5/78); symptomatic UTI 13.6% (9/66) vs 1.3% (1/78)

In the 100-U trial of noncatheterizing patients with MS, 15.2% initiated CIC because of retention; the authors report 31.4% after 200 U in earlier trials.[11] The labeled adult NDO dose is 200 U, and patients who void should be counseled about retention and possible CIC.[19] See indications, dosing and follow-up.[2]

Sacral neuromodulation (SNM)​

  • Reasonable in selected MS patients with refractory OAB or non-obstructive retention ; EAU 2026 notes MS patients with NDO are often good responders, but disease-specific evidence is limited and urodynamic effects are uncertain.[2][6]
  • Test phase before permanent implant; MS lesions can complicate response.
  • MRI compatibility. MS patients require periodic MRI surveillance, which makes compatibility a required consideration. MRI-conditional generator and lead combinations permit surveillance imaging under their specified conditions. Older systems may allow head-only MRI, which does not meet a need for spinal surveillance; verify the generator, lead, field strength and scan region against current local labeling before implantation.[16] See the SNM page.[6]

Percutaneous tibial nerve stimulation (PTNS)​

An option for selected spontaneously voiding patients with urgency, frequency or urgency incontinence .[2] A meta-analysis of eight small, uncontrolled MS studies reported improved PVR and symptom outcomes.[5][12]

Cannabinoids​

Nabiximols (Sativex, oromucosal THC/CBD) is not approved for bladder indications in the US. In the 135-patient RCT in MS-related OAB the primary endpoint (incontinence episodes) did not differ from placebo, though nocturia, voids per day and global impression improved.[7] An exploratory pooled analysis of two randomized trials and one open-label study (426 patients enrolled; a control group was constructed for the open-label study) found a small reduction in incontinence (mean difference −0.35 episodes/24 h) with frequent mild adverse events; EAU 2026 calls the evidence preliminary.[6][8]

Surgical reconstruction​

  • Stress incontinence and outlet surgery. When stress leakage coexists with MS-related storage dysfunction, establish acceptable storage parameters and a feasible emptying plan before sling or AUS surgery; concurrent bladder management may be needed.[2][6]
  • Augmentation cystoplasty. AUA/SUFU states that clinicians may offer augmentation to selected patients with NLUTD, including MS, whose detrusor overactivity or poor compliance is refractory to or intolerant of less invasive therapy . Assess patient or caregiver hand and cognitive function for regular CIC before surgery, and counsel about stones, perforation, bowel dysfunction, and lifelong follow-up.[2]
  • Continent catheterizable channel (Mitrofanoff). Occasionally constructed when hand dexterity for urethral CIC fails but abdominal-wall access is still feasible.
  • Ileal conduit. Consider when catheterization is infeasible, incontinence remains intractable, upper tracts are severely compromised, or other treatments cannot provide safe storage; severe disability and caregiver support shape the choice.[2][6] Selection depends on the individual’s disease trajectory, goals and ability to sustain bladder care.

Special Considerations in MS​

MRI and device selection​

MS surveillance commonly uses serial brain MRI, with spinal-cord MRI for selected clinical indications.[20] Always verify device MRI compatibility before permanent implants (for example, SNM or AUS).

Disease-modifying therapy and perioperative planning​

  • Many MS patients are on immunomodulators (interferons, natalizumab, fingolimod, ocrelizumab). Coordinate medication-specific perioperative decisions with the MS neurologist, considering infection, immune status and relapse or rebound risk. Some immunosuppressive MS treatments increase UTI risk and need particular attention when hypogammaglobulinemia is present.[15]
  • Relapse steroids. The French MS Society found no increased UTI incidence after high-dose methylprednisolone in the available MS studies (Level C); assess and treat symptomatic UTI before relapse treatment.[15]

Progressive disease and advance care planning​

Urologic management evolves as disability progresses.

UTI in MS​

  • Incidence of symptomatic UTI is higher in MS, especially in those on CIC or with high PVR.
  • Pseudo-relapse. Febrile UTI can transiently worsen existing MS symptoms without new inflammatory activity. Evaluate fever and urinary symptoms alongside neurologic change; treat symptomatic UTI and avoid treating asymptomatic bacteriuria.[4][6]

Sexual Function​

  • Sexual dysfunction: in one 217-person MS questionnaire study, 56% of women and 75% of men reported sexual dysfunction.[17]
  • Women: reduced lubrication, anorgasmia, genital sensory changes.
  • Men: EAU strongly recommends oral PDE5 inhibitors as first-line and intracavernosal injections as second-line medical treatment for neurogenic erectile dysfunction, and reserves prostheses for selected cases in which conservative treatment has failed.[6]
  • Ejaculatory dysfunction is common; fertility workup as indicated.

Clinical Correlations for the Reconstructive Urologist​

  • Symptoms change with disease. Reassess any MS patient whose urinary pattern shifts; a previously effective regimen can become inadequate with new spinal plaques.
  • MRI compatibility drives device choice. SNM MRI-conditional models, AUS, and any implant require verification against the patient's MS-surveillance MRI protocol.
  • Cognitive load of medications matters. Prefer β3 agonists and trospium over other anticholinergics in MS with cognitive symptoms.
  • Early management. Behavioral measures or medication may address early urinary symptoms, but unknown-risk MS still requires renal function assessment, upper-tract imaging and multichannel urodynamics.[1][6]
  • Multidisciplinary team. MS neurologist, urologist, pelvic-floor PT, incontinence / continent-catheter nurse educator, mental health support for the sexual-function domain.

See Also​

References​

1. Ginsberg DA, Boone TB, Cameron AP, et al. "The AUA/SUFU Guideline on Adult NLUTD: Diagnosis and Evaluation." J Urol. 2021;206(5):1097–1105. doi:10.1097/JU.0000000000002235

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

3. Panicker JN, Fowler CJ, Kessler TM. "Lower Urinary Tract Dysfunction in the Neurological Patient: Clinical Assessment and Management." Lancet Neurol. 2015;14(7):720–732. doi:10.1016/S1474-4422(15)00070-8

4. National Multiple Sclerosis Society. Urinary Dysfunction and MS, infection and pseudo-exacerbation. Accessed September 11, 2026.

5. Panicker JN, Fanciulli A, Skoric MK, et al. NEUROGED Guidelines. Eur J Neurol. 2025. doi:10.1111/ene.70119. Full text.

6. European Association of Urology. EAU Guidelines on Neuro-Urology (limited update). March 2026. uroweb.org

7. Kavia RB, De Ridder D, Constantinescu CS, et al. Randomized controlled trial of Sativex to treat detrusor overactivity in multiple sclerosis. Mult Scler. 2010;16(11):1349-59. doi:10.1177/1352458510378020

8. Abo Youssef N, Schneider MP, Mordasini L, et al. Cannabinoids for treating neurogenic lower urinary tract dysfunction in patients with multiple sclerosis: a systematic review and meta-analysis. BJU Int. 2017;119(4):515-521. doi:10.1111/bju.13759

9. Phé V, Schneider MP, Peyronnet B, et al. Desmopressin for treating nocturia in patients with multiple sclerosis: A systematic review: A report from the Neuro-Urology Promotion Committee of the International Continence Society (ICS). Neurourol Urodyn. 2019;38(2):563-571. doi:10.1002/nau.23921

10. Ginsberg D, Gousse A, Keppenne V, et al. Phase 3 efficacy and tolerability study of onabotulinumtoxinA for urinary incontinence from neurogenic detrusor overactivity. J Urol. 2012;187(6):2131-9. doi:10.1016/j.juro.2012.01.125

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

12. Guitynavard F, Mirmosayyeb O, Razavi ERV, et al. Percutaneous posterior tibial nerve stimulation (PTNS) for lower urinary tract symptoms (LUTSs) treatment in patients with multiple sclerosis (MS): A systematic review and meta-analysis. Mult Scler Relat Disord. 2022;58:103392. doi:10.1016/j.msard.2021.103392

13. Corona LE, Sion NR, Cameron AP, et al. Intermittent catheterization and urinary tract infection in multiple sclerosis patients. Can J Urol. 2020;27(4):10294-10299. PMID 32861254

14. Lemack GE, Hawker K, Frohman E. Incidence of upper tract abnormalities in patients with neurovesical dysfunction secondary to multiple sclerosis: analysis of risk factors at initial urologic evaluation. Urology. 2005;65(5):854-857. doi:10.1016/j.urology.2004.11.038

15. Donzé C, Papeix C, Lebrun-Frenay C, et al. "Urinary tract infections and multiple sclerosis: Recommendations from the French Multiple Sclerosis Society." Rev Neurol (Paris). 2020;176(10):804-822. doi:10.1016/j.neurol.2020.02.011

16. Medtronic. "Neuromodulation MRI safety status." December 2025. MRI safety chart.

17. Valleroy ML, Kraft GH. "Sexual dysfunction in multiple sclerosis." Arch Phys Med Rehabil. 1984;65(3):125–128. PubMed.

18. Allergan. "BOTOX (onabotulinumtoxinA) prescribing information." Revised November 2023. DailyMed.

19. Allergan, Inc. BOTOX (onabotulinumtoxinA) prescribing information. DailyMed. Revised November 2023; SPL version 62 published August 3, 2026. Label.

20. Wattjes MP, Ciccarelli O, Reich DS, et al. "2021 MAGNIMS-CMSC-NAIMS consensus recommendations on the use of MRI in patients with multiple sclerosis." Lancet Neurol. 2021;20(8):653-670. doi:10.1016/S1474-4422(21)00095-8