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Multiple Sclerosis

Multiple sclerosis (MS) is the second-largest NLUTD population by volume. Approximately 75% of patients develop urinary symptoms during their disease course, most commonly OAB / detrusor overactivity early, evolving toward mixed patterns with impaired emptying and, in a minority, frank detrusor areflexia or DSD as spinal plaques accumulate.[1][3] The reconstructive urologist's role in MS is different from SCI: the lesions are disseminated and evolving, the phenotype can shift, and major reconstruction is uncommon — but botulinum, neuromodulation, and occasionally augmentation / diversion are all in play for the subset with refractory disease.

See Neurogenic Lower Urinary Tract Dysfunction for the general framework.

Epidemiology and Natural History​

  • US prevalence ~1 million; more common in women (~3:1) and young adults.
  • ~75% of MS patients develop urinary symptoms over time; ~50% at presentation in some cohorts.[3]
  • OAB / DO is the most common finding (~60%), followed by detrusor underactivity / impaired emptying (~20%), DSD (~20–30% in spinal-predominant disease), and mixed patterns.
  • Urinary symptoms correlate with disability (EDSS score); they are rarely isolated — usually coexist with bowel, sexual, and mobility impairment.

Pathophysiology​

MS plaques disseminate in time and space. Urinary phenotype depends on the location of lesions, not on time since diagnosis:

  • Cortical / subcortical plaques → OAB / DO (uninhibited detrusor contractions).
  • Cervical / thoracic spinal plaques → DO + DSD (suprasacral phenotype; upper-tract risk if sustained high pressure).
  • Sacral / cauda equina involvement (uncommon) → detrusor underactivity or areflexia, retention, overflow.

Because lesions evolve, a patient's phenotype can shift — e.g., from pure OAB to OAB + 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 + focused neurologic exam (EDSS, mobility, dexterity, cognition)
  • Voiding diary + UA + PVR
  • Renal ultrasound and eGFR

Indications for multichannel urodynamics in MS:

  • 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.

Not always needed at entry in a low-risk, voiding MS patient with mild OAB — start empiric behavioral / pharmacologic therapy and escalate workup if refractory.

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.
  • Antimuscarinics — first-line for OAB. Trospium (minimal CNS penetration) is often preferred in MS given cognitive risk.
  • β3-adrenergic agonists (mirabegron, vibegron) — first-line alternative when anticholinergic side effects are limiting; often preferred in progressive MS with cognitive concerns.
  • Combination therapy when monotherapy inadequate.
  • Desmopressin — selective use for nocturia; monitor sodium, avoid in frail / older patients.
  • α-blockers — help CIC patients with mild DSD or those with bladder-neck dyssynergia.

Catheterization​

  • CIC — required in MS with significant PVR (often defined as >100 mL with LUTS) or with DSD pattern. Many MS patients retain sufficient hand function for CIC well into the disease; visual and cognitive issues are commoner obstacles than motor.
  • Indwelling SPC — when dexterity, spasticity, or caregiver support preclude CIC; preferable to urethral catheter in men and in women with progressive disability.
  • Intermittent vs indwelling debate — CIC minimizes UTI and stone risk but requires independence; SPC is pragmatic in progressive disability.

Intradetrusor onabotulinumtoxinA​

  • 100 U (idiopathic OAB) or 200 U (neurogenic OAB) — highly effective in MS OAB.[2]
  • Prerequisite: patient must be capable of CIC post-injection (or accept this risk).
  • Repeat every ~6–9 months.

Sacral neuromodulation (SNM)​

  • Reasonable in MS with refractory OAB or non-obstructive retention.[2]
  • Test phase before permanent implant; MS lesions can complicate response.
  • MRI compatibility — critical consideration because MS patients require periodic MRI surveillance. Newer SNM devices are MRI-conditional.

Percutaneous tibial nerve stimulation (PTNS)​

Office-based alternative for MS OAB; less durable than SNM but lower invasiveness.

Surgical reconstruction​

  • Augmentation cystoplasty — rare in MS; reserved for refractory high-pressure storage with demonstrable upper-tract risk despite botulinum and SNM.
  • Continent catheterizable channel (Mitrofanoff) — occasionally constructed when hand dexterity for urethral CIC fails but abdominal-wall access is still feasible.
  • Ileal conduit — for patients with severe disability, no practical CIC option, and refractory incontinence. Lower threshold than in SCI because MS is a progressive disease where reconstructive complexity may not match the trajectory.

Special Considerations in MS​

MRI and device selection​

MS patients typically need recurrent brain and spinal-cord MRIs for disease surveillance. Always verify device MRI compatibility before permanent implants (SNM, AUS, suprapubic catheter magnets).

Disease-modifying therapy and perioperative planning​

  • Many MS patients are on immunomodulators (interferons, natalizumab, fingolimod, ocrelizumab). Not usually stopped for elective urologic procedures, but coordinate with the MS neurologist for major reconstructive surgery because of infection and wound-healing implications.
  • Steroid courses for MS relapses increase short-term UTI risk.

Progressive disease and advance care planning​

Urologic management evolves as disability progresses. Preemptively discuss the downstream options (botulinum → SPC → ileal conduit) so that transitions do not happen during an acute deterioration.

UTI in MS​

  • Incidence of symptomatic UTI is higher in MS, especially in those on CIC or with high PVR.
  • Symptomatic UTI is also a common trigger for MS relapse — treat infection aggressively when clinically active; resist treating asymptomatic bacteriuria.

Sexual Function​

  • ~50% of women and ~70% of men with MS report sexual dysfunction.
  • Women: reduced lubrication, anorgasmia, genital sensory changes.
  • Men: erectile dysfunction → PDE5i first-line; intracavernosal injection or prosthesis in refractory cases.
  • 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.
  • Aggressive early management pays off. Empiric behavioral + pharmacologic therapy resolves most early MS urinary symptoms; formal urodynamics reserved for those who fail, have high PVR, or have upper-tract signs.
  • Multidisciplinary team. MS neurologist, urologist, pelvic-floor PT, incontinence / continent-catheter nurse educator, mental health support for the sexual-function domain.

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