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Parkinson's Disease

Parkinson disease (PD) and related atypical parkinsonism syndromes, most importantly multiple system atrophy (MSA), are a high-volume but generally non-reconstructive NLUTD population. Symptoms are dominantly storage-phase OAB with preserved coordination, and management is largely pharmacologic and behavioral.

See Neurogenic Lower Urinary Tract Dysfunction for the general framework.

Epidemiology​

  • US prevalence of PD >1 million; incidence rises with age.
  • Urinary symptoms are common in PD: published estimates range widely (roughly 27–80%, depending on age, stage and how symptoms are defined), and the EAU guideline reports LUTS in about half of patients at disease onset.[3][4]
  • Urgency and nocturia are the most common symptoms; OAB or detrusor overactivity is the dominant phenotype.[3][4]
  • Urinary symptoms correlate with motor severity and autonomic dysfunction.
  • MSA is rarer and has progressive autonomic dysfunction. The MDS criteria report LUT symptoms as the sole initial manifestation in 18% of patients with MSA, beginning a mean 2.8 years before motor symptoms in that subgroup.[18]

Pathophysiology​

  • PD is a suprapontine disease. Loss of basal ganglia dopaminergic input disinhibits the pontine micturition center, producing detrusor overactivity usually with preserved coordination (true DSD is atypical and merits reassessment). Storage pressures are typically low; upper-tract risk is rare.[2]
  • MSA involves suprapontine and sacral pathways. Storage symptoms may occur early, while PVR tends to rise with progression; some patients have detrusor-sphincter dyssynergia or neurogenic sphincter EMG changes.[18][11] Elevated PVR is an important diagnostic clue.
  • Coexisting BPH. Most PD patients are older men, so mixed PD-OAB and BPH outlet obstruction is common.

Evaluation​

Initial:

  • History: timing of storage symptoms and retention relative to motor features (early severe retention with orthostatic symptoms raises concern for MSA); in men younger than 60, erectile dysfunction with unexplained urge incontinence or voiding difficulty with PVR >100 mL, plus subtle parkinsonian or cerebellar signs, raises concern for possible prodromal MSA.[18] Assess fall risk, medications, cognition, and caregiver status.[4][18]
  • UA, PVR, voiding diary.

Adjunctive (as indicated):

  • Urodynamics. Recommended before prostate surgery in men with PD to distinguish outlet obstruction from PD OAB (changes postoperative expectations), and whenever MSA is suspected.
  • Renal US and eGFR in patients with elevated PVR or MSA phenotype.

PD vs MSA — the urologic clue​

FeaturePDMSA
Onset of urinary symptomsCan occur early[23]Early severe retention is more concerning for MSA[4]
OABYesYes, often severe
PVRUsually lowMay be low early; often rises with progression[18]
Orthostatic hypotensionMay include neurogenic orthostatic hypotensionNeurogenic orthostatic hypotension can occur early but may be absent[18]
Response to dopaminergic therapyOften good (motor)Variable; substantial, persistent benefit argues against MSA[18]
EMG of external anal sphincterUsually normalDenervation pattern in many (less discriminating than PVR in one large series)[5]

Early urinary retention and severe orthostatic hypotension and poor dopamine response should raise concern for MSA and change counseling about prognosis and procedure selection. In a retrospective series of 273 patients with MSA or PD, free-flow PVR >150 mL was associated with MSA (OR 8.7), whereas weak detrusor contraction was not statistically discriminatory.[5] The 2022 MDS criteria include unexplained voiding difficulty with PVR ≥100 mL as one possible autonomic feature of clinically established MSA and allow any residual for clinically probable MSA, with other required features and exclusions.[4][18]

Sphincter EMG can add information when the diagnosis is uncertain, but timing and nonspecificity limit it.[11] In a cohort of 84 probable-MSA patients, a neurogenic change on external anal-sphincter EMG was present in 62% overall, rising from 52% in the first year of disease to 83% by the fifth year.[11] A pathology-confirmed series of 30 MSA cases with a disease duration over five years found an abnormal result in 24, a borderline result in 5, and a normal result in only 1.[12] The reinnervation pattern has also been described in longstanding Parkinson disease, progressive supranuclear palsy, dementia with Lewy bodies, spinocerebellar ataxia type 3, obstetric anal-sphincter injury, and cauda equina lesions.[12][13][14][15][16]

Patients with MSA may experience syncope or presyncope after voiding. In a study of 25 patients with MSA and 16 age-matched controls, MSA patients had a smaller systolic blood-pressure rise during bladder filling and a prolonged fall after voiding (mean systolic reduction about 15 mmHg from baseline and about 29 mmHg below controls). The fall was greater in patients who strained to void or reported micturition syncope or presyncope.[17] Ask about symptoms after voiding, especially with straining, and counsel on sitting to void.

Management​

For the procedural therapies referenced below, see Intradetrusor OnabotulinumtoxinA, Sacral Neuromodulation, and Percutaneous Tibial Nerve Stimulation; for refractory MSA, the Ileal Conduit is the salvage option.

Behavioral and pharmacologic first line​

  • Timed voiding, bowel program, fluid management.
  • Pelvic-floor training and urge suppression. Offer a structured behavioral program to patients who can participate. A 12-week randomized noninferiority trial (77 people with PD; 84% men) found nurse-led behavioral treatment noninferior to solifenacin for ICIQ-OAB symptoms (mean score 5.5 versus 5.8 at 12 weeks; prespecified 15% margin). Six falls were reported in the solifenacin arm versus none in the behavioral arm, an exploratory safety observation; patients with MoCA <18 or PVR ≥150 mL were excluded.[24]
  • β3-adrenergic agonists (mirabegron, vibegron). Often attractive when avoiding anticholinergic burden. AUA/SUFU permits antimuscarinics, beta-3 agonists or both ; it does not require a beta-3-first sequence for all PD patients.[1] Disease-specific evidence is stronger for mirabegron than for assuming a class-wide effect: the PaDoMi RCT (117 randomized patients with parkinsonism) improved OAB symptoms at weeks 4 and 8, with PVR increasing to about 64 mL at visit 4 and one acute urinary-retention event, and a Medicare cohort associated antimuscarinic initiation with more non-elective hospitalizations or emergency visits within 90 days than beta-3-agonist initiation (HR 1.23).[8][9][3][1] Check blood pressure and PVR at baseline; mirabegron can raise blood pressure, and PD patients often have orthostatic hypotension, so review the full antihypertensive and dopaminergic regimen. Vibegron has limited PD-specific data.[4]
  • Antimuscarinics. Individualize benefit versus cognition, constipation, retention and total anticholinergic burden. Avoid oxybutynin IR in cognitively impaired patients. The AGS Beers Criteria advise avoiding strongly anticholinergic drugs in patients with dementia or cognitive impairment, which covers most antimuscarinics for PD dementia or Lewy body disease; if cognition declines on treatment, switch to a beta-3 agonist or non-drug measures.[10][4] Dopaminergic drugs can improve or worsen LUTS, so review timing of dose changes against symptoms.[3]
  • Alpha-blockers. Helpful for documented obstruction, but avoid them when orthostatic hypotension is documented, as advised by the 2025 NEUROGED guideline.[26] Otherwise, follow each agent's product-specific dosing instructions; check supine and standing blood pressure when starting or increasing treatment, and discuss nighttime falls if an evening dose is chosen.[19][20]
  • Desmopressin. Consider selectively for documented nocturnal polyuria after addressing reversible causes. The EAU guideline strongly recommends screening serum sodium before treatment and monitoring it during use; hyponatremia was frequent in heterogeneous neurologic studies. Weigh age, frailty, and fall risk in selection.[4]

Intradetrusor onabotulinumtoxinA​

    • Four small uncontrolled series with PD-specific data (n=4, 20, 9, and 10) describe improvement in storage symptoms after intradetrusor onabotulinumtoxinA (100–200 U; follow-up 12 weeks to six months); PD-specific randomized efficacy has not been established.[21] In the United States, BOTOX is indicated for adults with OAB symptoms of urge urinary incontinence, urgency, and frequency or with urinary incontinence from neurologic detrusor overactivity after inadequate response to or intolerance of an anticholinergic medication; the recommended adult doses are 100 U for OAB and 200 U for neurologic detrusor overactivity.[22] Counsel that retention may require CIC.[22][4] AUA/SUFU states that clinicians may offer onabotulinumtoxinA to oral-refractory NLUTD patients other than those with SCI or MS and must discuss retention risk and possible CIC beforehand in patients who void .[1]
  • Caution. Check for UTI and PVR before treatment; the BOTOX label contraindicates intradetrusor injection with active UTI or urinary retention/PVR >200 mL without routine CIC. Confirm CIC feasibility in light of motor and caregiver limitations, and check PVR within two weeks and periodically as indicated through 12 weeks in patients who do not catheterize.[22]

Prostate / outlet surgery in men with PD​

  • For urodynamically confirmed prostatic obstruction in men with PD, consider outlet surgery after assessing for MSA and counseling about uncertain PD-specific outcomes. The cited review reports PD-focused outcomes for TURP and mixed-cohort data for transurethral incision; it does not report PD-specific outcomes for HoLEP or simple prostatectomy.[3][6] Evidence is small and biased: a 2024 review counted study-defined success in 19/70 (27.1%) men with PD data from two PD-focused studies and one mixed neurologic cohort (reported median follow-ups 9.2 months, two years, and three years).[6] De novo urge incontinence occurred in 6/30 (20%) previously continent men in one older cohort.[6]
  • Counsel about persistent OAB symptoms post-op.
  • In MSA, avoid routine outlet surgery. One high-bias TURP cohort reported de novo incontinence in 12/20 men (60%); if surgery is considered for verified obstruction, assess sphincter function and counsel about this risk.[4][6]

Catheter-based management​

  • Indwelling urethral catheter. Sometimes the pragmatic choice in late PD or MSA with severe mobility limitation and caregiver support.
  • CIC. Feasible in early PD with intact dexterity; becomes harder as tremor progresses.
  • Suprapubic catheter. AUA/SUFU recommends suprapubic over urethral drainage in appropriately selected patients who need a chronic indwelling catheter .[1]

Sacral neuromodulation and PTNS​

  • SNM is a reasonable option in PD with refractory OAB; AUA/SUFU allows it for selected NLUTD patients with urgency, frequency or urgency incontinence .[1]
  • Tibial nerve stimulation. AUA/SUFU permits PTNS in selected spontaneously voiding NLUTD patients with urgency, frequency or urgency incontinence .[1] In the PD-specific STRIPE trial (148 randomized), Geko transcutaneous stimulation did not outperform sham on ICIQ-OAB at 12 weeks.[25] In Uroparktens, 100 people with parkinsonian syndromes (85 with idiopathic PD) were randomized; 30 (64%) receiving transcutaneous stimulation versus 38 (72%) receiving sham reported improvement after three months (p = 0.399).[28]
  • MRI compatibility. PD patients often have co-indications for brain imaging (e.g., if DBS surgery is planned); verify device MRI-conditional status.
  • DBS interaction. Subthalamic DBS does not impair bladder function and may increase cystometric capacity (mean +124 mL in meta-analysis); coordinate with the movement-disorders team.[7]
  • Usually not used in MSA because of the aggressive autonomic phenotype.

Reconstructive surgery​

  • Rare in PD. For a patient with PD and documented low bladder compliance or refractory neurogenic detrusor overactivity, augmentation may be considered after less invasive treatment fails; the EAU makes a strong recommendation for augmentation in these NLUTD phenotypes.[4]
  • MSA. Occasionally needs urinary diversion for refractory combined retention and incontinence, but advanced care planning and prognosis often drive the decision.

Common Scenarios​

PD with OAB and mixed BPH​

Pragmatic pathway: (1) behavioral measures and an individualized β3 agonist; consider an α-blocker for coexisting obstructive symptoms after assessing orthostasis; (2) pressure-flow testing before outlet surgery to assess bladder function and distinguish prostatic obstruction from dynamic functional outlet resistance; (3) outlet surgery for documented prostatic obstruction, with continued treatment of residual OAB; (4) intradetrusor onabotulinumtoxinA after discussing retention risk and confirming a feasible CIC plan.[1][3][4][6][27]

PD with nocturia​

Very common and multifactorial (fluid intake, peripheral edema redistribution, sleep fragmentation, depression). Treat the modifiable factors first (elevation, compression, evening fluid restriction) before adding desmopressin.

PD with dementia / functional incontinence​

Shifts emphasis to caregiver-directed toileting schedules, incontinence products, and careful medication review (anticholinergic burden, diuretics). Avoid aggressive pharmacologic management that risks cognitive or fall side effects.

MSA with retention​

Teach CIC early while dexterity remains; plan for SPC as progression limits function.

Clinical Correlations for the Reconstructive Urologist​

  • Differentiate PD from MSA. Early urinary retention with severe orthostasis and anal-sphincter EMG denervation suggests MSA.
  • Choose storage medication individually. Limit anticholinergic burden when choosing storage medication for cognitively vulnerable patients.
  • Urodynamics before outlet surgery in men with PD. OAB and BPH mix is common; operating without documenting obstruction leaves an unhappy patient.
  • CIC is often impractical in late PD. Plan drainage around that reality (SPC rather than ongoing CIC failure).
  • Functional incontinence is often bigger than neurogenic incontinence in late PD. Caregiver strategies, toilet transfer aids, clothing modifications, and scheduled voiding matter more than drugs.
  • MRI-compatibility and DBS coexistence drive implant selection.

See Also​

Videos​

Behavioral vs Drug Therapy for OAB in Parkinson Disease
Grand Rounds in Urology

References​

1. 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

2. 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

3. Sakakibara R, Panicker J, Finazzi-Agro E, et al.; ICS Parkinson Disease Subcommittee. A guideline for the management of bladder dysfunction in Parkinson’s disease and other gait disorders. Neurourol Urodyn. 2016;35:551–563. doi:10.1002/nau.22764.

4. European Association of Urology. EAU Guidelines on Neuro-Urology (Limited Update). March 2026.

5. Yamamoto T, Asahina M, Yamanaka Y, et al. Postvoid residual predicts the diagnosis of multiple system atrophy in Parkinsonian syndrome. J Neurol Sci. 2017;381:230-234. doi:10.1016/j.jns.2017.08.3262

6. Charalampous I, et al. Does surgical treatment for benign prostate enlargement (BPE)-related bladder outlet obstruction (BOO) benefit patients with central nervous system diseases? A systematic review. J Clin Med. 2024;13(19):5846. doi:10.3390/jcm13195846

7. Jörg E, Sartori AM, Hofer AS, et al. Deep brain stimulation effects on lower urinary tract function: Systematic review and meta-analysis. Parkinsonism Relat Disord. 2020;79:65-72. doi:10.1016/j.parkreldis.2020.08.032

8. Cho SY, Jeong SJ, Lee S, et al. Mirabegron for treatment of overactive bladder symptoms in patients with Parkinson's disease: A double-blind, randomized placebo-controlled trial (PaDoMi Study). Neurourol Urodyn. 2021;40(1):286-294. doi:10.1002/nau.24552

9. Abraham DS, Pham Nguyen TP, Newcomb CW, et al. Comparative safety of antimuscarinics versus mirabegron for overactive bladder in Parkinson disease. Parkinsonism Relat Disord. 2023;115:105822. doi:10.1016/j.parkreldis.2023.105822

10. By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2023;71(7):2052-2081. doi:10.1111/jgs.18372

11. Yamamoto T, Sakakibara R, Uchiyama T, et al. When is Onuf's nucleus involved in multiple system atrophy? A sphincter electromyography study. J Neurol Neurosurg Psychiatry. 2005;76(12):1645-1648. doi:10.1136/jnnp.2004.061036

12. Paviour DC, Williams D, Fowler CJ, Quinn NP, Lees AJ. Is sphincter electromyography a helpful investigation in the diagnosis of multiple system atrophy? A retrospective study with pathological diagnosis. Mov Disord. 2005;20(11):1425-1430. doi:10.1002/mds.20584

13. Libelius R, Johansson F. Quantitative electromyography of the external anal sphincter in Parkinson's disease and multiple system atrophy. Muscle Nerve. 2000;23(8):1250-1256. doi:10.1002/1097-4598(200008)23:8<1250::aid-mus14>3.0.co;2-w

14. Sakakibara R, Ito T, Uchiyama T, et al. Lower urinary tract function in dementia of Lewy body type. J Neurol Neurosurg Psychiatry. 2005;76(5):729-732. doi:10.1136/jnnp.2004.046243

15. Miao Y, Wang K, Han J, et al. Differential value of external anal- and urethral-sphincter electromyography in multiple system atrophy cerebellar type and spinocerebellar ataxias. J Clin Neurosci. 2020;80:16-22. doi:10.1016/j.jocn.2020.07.067

16. Vodusek DB. Sphincter EMG and differential diagnosis of multiple system atrophy. Mov Disord. 2001;16(4):600-607. doi:10.1002/mds.1121

17. Uchiyama T, Sakakibara R, Asahina M, Yamanishi T, Hattori T. Post-micturitional hypotension in patients with multiple system atrophy. J Neurol Neurosurg Psychiatry. 2005;76(2):186-190. doi:10.1136/jnnp.2004.040972

18. Wenning GK, Stankovic I, Vignatelli L, et al. "The Movement Disorder Society Criteria for the Diagnosis of Multiple System Atrophy." Mov Disord. 2022;37(6):1131-1148. doi:10.1002/mds.29005

19. NuCare Pharmaceuticals, Inc. "Tamsulosin hydrochloride capsules: prescribing information." DailyMed. Repackaged label updated October 26, 2022. Drug label.

20. Aphena Pharma Solutions - Tennessee, LLC. "Doxazosin tablets: prescribing information." DailyMed. Repackaged label updated March 6, 2018. Drug label.

21. Arshad H, Nuha R, Khashaba S, et al. "Mirabegron and Intradetrusor OnabotulinumtoxinA for Overactive Bladder in Parkinson's Disease: A Systematic Review and Meta-Analysis." Neurourol Urodyn. 2026. doi:10.1002/nau.70322

22. Sportpharm LLC. "BOTOX (onabotulinumtoxinA): prescribing information." DailyMed. Repackaged label updated February 2, 2026. Drug label.

23. Schrag A, Horsfall L, Walters K, Noyce A, Petersen I. "Prediagnostic presentations of Parkinson's disease in primary care: a case-control study." Lancet Neurol. 2015;14(1):57-64. doi:10.1016/S1474-4422(14)70287-X

24. Vaughan CP, Morley JF, Lehosit J, et al. "Behavioral Compared With Drug Therapy for Overactive Bladder Symptoms in Parkinson Disease: A Randomized Noninferiority Trial." JAMA Neurol. 2025;82(9):925-931. doi:10.1001/jamaneurol.2025.1904

25. Smith MD, Portlock GE, Cullen A, et al. "Transcutaneous Tibial Nerve Stimulation for Overactive Bladder Symptoms in Parkinson's Disease: Results from a Phase II Randomized Control Trial (STRIPE)." Mov Disord. 2025;40(7):1291-1296. doi:10.1002/mds.30186

26. Panicker JN, Fanciulli A, Krbot Skoric M, et al. "European Academy of Neurology (EAN)/European Federation of Autonomic Societies (EFAS)/International Neuro-Urology Society (INUS) guidelines for practising neurologists on the assessment and treatment of neurogenic urinary and sexual symptoms (NEUROGED guidelines)." Eur J Neurol. 2025;32(4):e70119. doi:10.1111/ene.70119

27. Vírseda-Chamorro M, Salinas-Casado J, Adot-Zurbano JM, Méndez-Rubio S, Moreno-Sierra J. "Can We Differentiate Between Organic and Functional Bladder Outlet Obstruction in Males With Parkinson's Disease?" Neurourol Urodyn. 2025;44(1):171-177. doi:10.1002/nau.25599

28. Castel-Lacanal E, Peyronnet B, Karsenty G, et al. "Evaluation of transcutaneous electrical tibial nerve stimulation in lower urinary tract dysfunction secondary to a parkinsonian syndrome: Uroparktens—a multicenter randomized placebo-controlled study." World J Urol. 2025;43(1):214. doi:10.1007/s00345-025-05597-2