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Skeletal Muscle Relaxants

Skeletal muscle relaxants (SMRs) are used in urology to relax three different anatomic targets — the external urethral sphincter (in detrusor sphincter dyssynergia), the pelvic floor musculature (in high-tone pelvic floor dysfunction and myofascial pelvic pain), and indirectly the detrusor (via spinal-cord-acting agents). Botulinum toxin A is covered separately: evidence and licensing differ between intradetrusor treatment and off-label sphincter or pelvic-floor injection. This page addresses systemic SMRs (baclofen, dantrolene, diazepam, cyclobenzaprine) and compounded vaginal diazepam, whose urologic evidence is generally limited.[1][2]

For agents covered separately:

Anatomic targets​

TargetMuscle typeAgent classes
External urethral sphincterStriatedBaclofen (oral, intrathecal); dantrolene; intrasphincteric BoNT-A
Pelvic floor (levator ani, obturator internus)StriatedDiazepam (oral, vaginal); cyclobenzaprine (off-label); BoNT-A injection
Detrusor (indirectly)SmoothIntrathecal baclofen (spinal-cord effect on EUS motoneurons and detrusor reflexes); intradetrusor BoNT-A
Bladder neck / prostate / ureterSmoothAlpha-blockers (covered separately)

Baclofen — for DSD and neurogenic spasticity​

A GABA-B receptor agonist used principally for limb spasticity in spinal-cord pathology, with possible secondary effects on detrusor sphincter dyssynergia (DSD) and bladder reflexes. A limb-spasticity indication does not establish reliable bladder benefit.[3]

Mechanism in urology​

  • Oral: central GABA-B agonism depresses pudendal-to-pudendal nerve reflex via spinal cord presynaptic hyperpolarization → reduced external urethral sphincter resistance[4]
  • Intrathecal (ITB): direct lumbosacral GABA-B activation in the nucleus of Onuf inhibits EUS motoneurons → urethral relaxation during detrusor contraction. Experimental work in spinal-cord-injured rats suggests different dose responses for urethral and detrusor effects; it does not establish a human bladder-specific therapeutic window[5][6]

Oral baclofen evidence​

In an older uncontrolled series of 25 SCI patients with DSD, oral baclofen reduced post-void residual significantly in 73% of cases within ~5 weeks. This is the proportion reported to improve, not a 73% reduction in each patient or proof of equivalence to sphincterotomy.[4] The principal limitation is poor blood–brain barrier penetration: tolerable oral doses often produce sedation and weakness without reaching effective spinal cord concentrations for DSD.[3]

Intrathecal baclofen for genitourinary effects​

In a prospective study of 10 patients with severe spasticity from spinal-cord pathology, acute bolus testing was blinded against placebo; chronic infusion was compared with pretreatment values:[5]

  • Eliminated uninhibited bladder contractions in all patients with irritative voiding and urge incontinence
  • Abolished DSD in 40%
  • Achieved 72% increase in bladder capacity and 16% improvement in compliance (in non-cervical SCI patients)
  • 1 of 3 patients with an indwelling catheter converted to clean intermittent self-catheterization

Interpretation: mean capacity, compliance, sensation and voiding pressures were not significantly different across the whole small cohort. The capacity/compliance percentages above apply to a subgroup. Reassess bladder emptying and storage after ITB changes; benefit is not assured and pumps should not be implanted solely on these historical bladder findings.[3][5]

Adverse effects relevant to LUT[7]​

Sedation, weakness, dizziness, headache; LUT-specific: urinary frequency (2–6%) and rarely enuresis, urinary retention, dysuria, impotence, ejaculatory failure, nocturia. Baclofen is predominantly renally eliminated: impaired kidney function can produce accumulation, profound sedation and respiratory depression, requiring dose reduction or an alternative. Abrupt withdrawal of oral or especially intrathecal treatment can cause seizures, hyperthermia, severe spasticity and multiorgan failure. Avoid abrupt discontinuation; pump interruption requires urgent specialist management.

Dantrolene — for external sphincter hypertonicity (largely historical)​

The only peripherally acting oral SMR — interferes with calcium release from the sarcoplasmic reticulum to reduce excitation–contraction coupling in skeletal muscle.[8][9]

Selectivity matters​

Dantrolene acts on striated muscle only: it has no significant effect on detrusor smooth-muscle contractility, which makes it conceptually attractive for isolated EUS hypertonicity that spares the detrusor.[10]

Evidence​

  • In 15 SCI patients with PVR > 150 mL secondary to EUS hypertonicity (urethral closure pressures > 100 cm H₂O), 8 of 15 (53%) benefited from dantrolene — successful patients had a mean urethral pressure decrease of 77 cm H₂O (49%). However, 5 of the 8 responders received doses up to 600 mg/day. These historical doses exceed the current oral label ceiling and are not a prescribing recommendation[8]
  • Early reports also showed efficacy for non-neurogenic external sphincter spasm causing functional outlet obstruction[9]
  • Reported as a salvage option for refractory neurogenic detrusor overactivity in cerebral palsy when combined with antimuscarinics and β3-agonists[11]

Limitations​

  • Fatal and nonfatal hepatitis is a boxed-warning risk; the current oral label ceiling is 100 mg four times daily, with baseline/ongoing liver assessment, lowest effective dosing and discontinuation if no benefit within 45 days[12]
  • Generalized muscle weakness limits functional utility, particularly in incomplete SCI where ambulation is preserved
  • Intrasphincteric BoNT-A is an off-label alternative in selected DSD, with transient effects and limited evidence; systemic toxin effects remain possible[23]
  • Detrusor hyporeflexia frequently coexists and contributes to treatment failure

Current role​

Urologic sphincter use is historical and off-label. A single cerebral-palsy case report does not establish dantrolene as an NDO salvage treatment. Active hepatic disease, or spasticity needed for posture/function, contraindicates oral use.[11][12]

Diazepam — for high-tone pelvic floor dysfunction​

The most-studied SMR for myofascial pelvic pain and high-tone pelvic floor disorders, available as oral tablets and as compounded vaginal suppositories (10 mg in several small studies; no FDA-approved vaginal formulation).[1][13]

Pharmacokinetics — vaginal vs oral​

Compounded 10 mg vaginal diazepam has a distinctive PK profile: peak concentration 31.0 ng/mL at ~3.1 h, bioavailability 70.5%, and a terminal half-life of 82 hours in eight healthy volunteers. Three reported fatigue. Lower peaks do not mean absent systemic exposure; repeated daily dosing accumulates. This PK study does not demonstrate clinical efficacy or validate a routine schedule.[14]

Evidence — mixed at best​

StudyDesignResult
Stone systematic review[13]5 studies (2 observational, 3 RCTs)Observational studies report 71–96% subjective improvement; RCTs found no significant difference in FSFI or VAS pain scores
Crisp triple-blinded RCT (n = 21)[15]10 mg vaginal diazepam nightly × 4 wk vs placeboNo improvement in resting pelvic-floor EMG or subjective outcomes
Murina RCT — vestibulodynia[16]Vaginal diazepam + TENS vs placebo + TENSImproved dyspareunia and relaxation measures, but no significant between-group VAS pain improvement
Rogalski retrospective (n = 26)[17]Vaginal diazepam + PT + trigger-point injectionsImproved pelvic-floor muscle tone at rest, squeeze, and relaxation phases

Practical interpretation: small studies do not establish a routine benefit, including as an adjunct. NICE NG210 explicitly recommends not offering vaginal diazepam for pelvic-floor dysfunction, even with high tone. Discuss the uncertainty if considering specialist off-label use; pelvic-floor physical therapy remains central.[24][1][13][15]

Oral diazepam​

Pelvic-floor use is off-label. Oral and systemically absorbed vaginal diazepam carry sedation, cognitive, dependence and withdrawal risks. Opioids, alcohol and other CNS depressants increase respiratory-depression/overdose risk; an established course should be tapered rather than abruptly stopped.[25] In vitro work shows diazepam has no direct effect on human bladder smooth-muscle contractility — its urologic effects are centrally mediated.[18]

Cyclobenzaprine and Other Centrally Acting Antispasmodics​

A tricyclic-related agent prescribed off-label for myofascial pelvic pain and CP/CPPS, with very limited supporting evidence.[1][19][20]

  • No high-quality studies demonstrate improvement in pelvic-pain scales with cyclobenzaprine specifically
  • Anticholinergic adverse effects (dry mouth, urinary retention, sedation) can worsen voiding dysfunction. The label concerns short-term acute musculoskeletal spasm (up to 2–3 weeks), not chronic pelvic pain; avoid MAOIs within 14 days, relevant cardiac conduction/heart-failure conditions and hyperthyroidism. Serotonergic combinations can cause serotonin syndrome[19]
  • Other centrally acting agents (methocarbamol, metaxalone, carisoprodol) have no established urologic role
  • The ACOG Chronic Pelvic Pain Practice Bulletin notes that SMRs have limited high-quality evidence for chronic myofascial pelvic pain and should be used as part of multimodal management rather than as primary therapy[2]

For the broader pelvic-pain pharmacotherapy framework, see Antispasmodics.

SMRs for Postoperative Urinary Retention​

Methocarbamol, meprobamate, chlormezanone, diazepam, and carisoprodol have all been studied for postoperative urinary retention (POUR) on the rationale that they reduce reflex pelvic-floor and EUS contracture (or anxiety-related voiding inhibition). The Cochrane review found insufficient evidence to support routine use of any drug — including SMRs — for the treatment of POUR. That 2010 review included only seven studies / 494 participants and did not establish efficacy for alpha-blocker monotherapy in treating established POUR. Prevention trials are a different question; drugs must not delay decompression of a significantly distended bladder.[21]

Evidence Summary​

AgentSettingEvidenceBottom line
Oral baclofenDSD in SCIPVR improved in 73% of cases in a 25-patient series[4]Uncontrolled historical evidence; renal/CNS toxicity limits use
Intrathecal baclofenDSD + detrusor hyperreflexia in SCI10-patient study: DSD abolished in 40%; capacity improvement confined to a subgroup[5]Reassess bladder effects; not consistent across the whole cohort
DantroleneEUS hypertonicity in SCI8/15 benefited in an old series; some received doses above today’s label ceiling[8]Historical/off-label; hepatotoxicity and weakness are limiting
Vaginal diazepamHigh-tone pelvic floor dysfunctionStone meta: no benefit in RCTs; helpful adjunct in some series[13][15][16][17]No established routine benefit; NICE recommends against use
CyclobenzaprineMyofascial CPPNo high-quality urologic data[1]Off-label; consider only as multimodal adjunct
POUR (any SMR)Postoperative urinary retentionCochrane: insufficient evidence[21]Not recommended as primary therapy
Functional BOO in NLUTD (any approach)Surgical / medical managementCochrane: limited evidence for any single approach[22]Multimodal, individualized strategy

Clinical Positioning​

  • Intradetrusor BoNT-A has established OAB/NDO indications; intrasphincteric DSD treatment is off-label with limited evidence. These are separate clinical decisions — see Botulinum toxin.[23]
  • Baclofen may affect bladder function when treating neurologic spasticity; monitor emptying and storage rather than promising secondary urologic improvement.
  • Dantrolene is historical/off-label for urinary sphincter dysfunction; do not extrapolate an old high-dose series or a case report into a modern rescue protocol.
  • Vaginal diazepam has substantial systemic absorption and no established routine efficacy; NICE recommends against its use for pelvic-floor dysfunction.[24]
  • Cyclobenzaprine and other antispasmodics lack high-quality urologic evidence — and their anticholinergic burden can worsen voiding dysfunction
  • No SMR is routinely indicated for postoperative urinary retention[21]
  • The urologic adverse effects of systemically administered SMRs (urinary retention with baclofen and dantrolene; anticholinergic effects with cyclobenzaprine) must be considered when these agents are prescribed for non-urologic indications in patients with pre-existing LUTS[7][12][19]

See Also​

References​

1. Flatow V, Uy-Kroh J, Carey ET, Ascher-Walsh C, Khalil S. "Skeletal muscle relaxants for the treatment of myofascial pelvic pain and high tone pelvic floor disorders." Curr Opin Obstet Gynecol. 2023;35(4):311–315. doi:10.1097/GCO.0000000000000894

2. American College of Obstetricians and Gynecologists. "Chronic pelvic pain: ACOG Practice Bulletin, Number 218." Obstet Gynecol. 2020;135(3):e98–e109. doi:10.1097/AOG.0000000000003716

3. Verduzco-Gutierrez M, Raghavan P, Pruente J, et al. "AAPM&R consensus guidance on spasticity assessment and management." PM R. 2024;16(8):864–887. doi:10.1002/pmrj.13211

4. Leyson JF, Martin BF, Sporer A. "Baclofen in the treatment of detrusor-sphincter dyssynergia in spinal cord injury patients." J Urol. 1980;124(1):82–84. doi:10.1016/s0022-5347(17)55307-0

5. Steers WD, Meythaler JM, Haworth C, Herrell D, Park TS. "Effects of acute bolus and chronic continuous intrathecal baclofen on genitourinary dysfunction due to spinal cord pathology." J Urol. 1992;148(6):1849–1855. doi:10.1016/s0022-5347(17)37048-9

6. Miyazato M, Sasatomi K, Hiragata S, et al. "Suppression of detrusor-sphincter dyssynergia by GABA-receptor activation in the lumbosacral spinal cord in spinal cord-injured rats." Am J Physiol Regul Integr Comp Physiol. 2008;295(1):R336–R342. doi:10.1152/ajpregu.90315.2008

7. Baclofen oral solution prescribing information. DailyMed. Accessed September 12, 2026.

8. Hackler RH, Broecker BH, Klein FA, Brady SM. "A clinical experience with dantrolene sodium for external urinary sphincter hypertonicity in spinal cord injured patients." J Urol. 1980;124(1):78–81. doi:10.1016/s0022-5347(17)55305-7

9. Murdock MM, Sax D, Krane RJ. "Use of dantrolene sodium in external sphincter spasm." Urology. 1976;8(2):133–137. doi:10.1016/0090-4295(76)90340-x

10. Harris JD, Benson GS. "Effect of dantrolene sodium on canine bladder contractility." Urology. 1980;16(2):229–231. doi:10.1016/0090-4295(80)90095-3

11. Bulchandani S, Toozs-Hobson P, Kennedy A, Sturman S. "Dantrolene an unusual option for detrusor overactivity: observations of a patient with cerebral palsy." Eur J Obstet Gynecol Reprod Biol. 2015;194:255–256. doi:10.1016/j.ejogrb.2015.08.012

12. Dantrium oral capsules prescribing information. DailyMed. Accessed September 12, 2026.

13. Stone RH, Abousaud M, Abousaud A, Kobak W. "A systematic review of intravaginal diazepam for the treatment of pelvic floor hypertonic disorder." J Clin Pharmacol. 2020;60(Suppl 2):S110–S120. doi:10.1002/jcph.1775

14. Larish AM, Dickson RR, Kudgus RA, et al. "Vaginal diazepam for nonrelaxing pelvic floor dysfunction: the pharmacokinetic profile." J Sex Med. 2019;16(6):763–766. doi:10.1016/j.jsxm.2019.03.003

15. Crisp CC, Vaccaro CM, Estanol MV, et al. "Intra-vaginal diazepam for high-tone pelvic floor dysfunction: a randomized placebo-controlled trial." Int Urogynecol J. 2013;24(11):1915–1923. doi:10.1007/s00192-013-2108-9

16. Murina F, Felice R, Di Francesco S, Oneda S. "Vaginal diazepam plus transcutaneous electrical nerve stimulation to treat vestibulodynia: a randomized controlled trial." Eur J Obstet Gynecol Reprod Biol. 2018;228:148–153. doi:10.1016/j.ejogrb.2018.06.026

17. Rogalski MJ, Kellogg-Spadt S, Hoffmann AR, Fariello JY, Whitmore KE. "Retrospective chart review of vaginal diazepam suppository use in high-tone pelvic floor dysfunction." Int Urogynecol J. 2010;21(7):895–899. doi:10.1007/s00192-009-1075-7

18. Ayyat FM, Lloyd LK, Kuhlemeier KV. "Effect of skeletal muscle relaxants on bladder smooth muscle." J Urol. 1984;132(2):372–375. doi:10.1016/s0022-5347(17)49630-3

19. Cyclobenzaprine hydrochloride extended-release prescribing information. DailyMed. Accessed September 12, 2026.

20. Pena VN, Engel N, Gabrielson AT, Rabinowitz MJ, Herati AS. "Diagnostic and management strategies for patients with chronic prostatitis and chronic pelvic pain syndrome." Drugs Aging. 2021;38(10):845–886. doi:10.1007/s40266-021-00890-2

21. Buckley BS, Lapitan MC. "Drugs for treatment of urinary retention after surgery in adults." Cochrane Database Syst Rev. 2010;(10):CD008023. doi:10.1002/14651858.CD008023.pub2

22. Utomo E, Groen J, Blok BF. "Surgical management of functional bladder outlet obstruction in adults with neurogenic bladder dysfunction." Cochrane Database Syst Rev. 2014;(5):CD004927. doi:10.1002/14651858.CD004927.pub4

23. EAU. Neuro-urology Guidelines. 2026; botulinum toxin and bladder-outlet sections. Guideline.

24. NICE. Pelvic floor dysfunction: prevention and non-surgical management. NG210, recommendation 1.6.33. Recommendations.

25. FDA. Boxed warning updated to improve safe use of benzodiazepines. September 23, 2020. Safety communication.