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Myofascial Pelvic Pain

Myofascial pelvic pain (MFPP) is a chronic regional pain condition driven by hyperirritable trigger points within taut bands of the pelvic floor musculature — most commonly the levator ani (puborectalis, pubococcygeus and iliococcygeus), adjacent coccygeus, and obturator internus. It is reported in 22–94% of chronic pelvic pain populations depending on the case mix and rigor of the pelvic-floor exam, and can be missed when a structured pelvic-floor myofascial examination is omitted.[1][2][3]

For the broader chronic pelvic pain framework (etiology by organ system, UPOINT phenotyping, pelvic congestion, pudendal neuralgia), see Chronic Pelvic Pain. For the bladder-specific phenotype, see IC/PBS. First-line management centers on Pelvic Floor Physical Therapy (down-training, not strengthening).

Pathophysiology and Presentation​

MFPP arises from dysfunction of the pelvic-floor muscles with development of myofascial trigger points (MTrPs) producing localized and referred pain. It may exist independently or co-occur with endometriosis, IC/BPS, vulvodynia, IBS, dyspareunia / vaginismus, and CP/CPPS in men, with viscero-somatic convergence amplifying both the pelvic-floor and visceral symptom burden.[1][2][4]

A recently described entity — myofascial urinary frequency syndrome — captures the subset of patients in whom pelvic-floor myofascial dysfunction drives lower-urinary-tract symptoms (frequency, urgency, sensation of incomplete emptying, suprapubic/bladder pressure) that are routinely misclassified as overactive bladder or IC/BPS.[5]

Typical clinical features:

  • Pelvic, perineal, vulvar, or suprapubic pain
  • Dyspareunia, post-coital pain, sexual dysfunction
  • Urinary frequency, urgency, hesitancy, or incomplete emptying
  • Pain with prolonged sitting
  • Referred pain to low back, thighs, abdomen, and rectum

Diagnosis​

Diagnosis is clinical and exam-based. There is no validated imaging, biomarker, or laboratory test.[6]

Pelvic-floor myofascial examination​

  • Single-digit transvaginal (or transrectal) palpation of the levator-ani complex and obturator internus, sweeping each muscle group and laterality.[6]
  • Assess for taut bands, trigger points, hypertonicity, and reproduction of the patient's typical pain with focal pressure.
  • The ACOG Practice Bulletin 218 explicitly directs particular attention to the abdominal and pelvic neuromusculoskeletal exam.[7]

Persistency Index​

The Persistency Index (Ackerman 2023) is a screening tool to help identify patients who warrant examination for myofascial dysfunction — incorporating the persistent nature of incomplete-emptying sensation, dyspareunia, and age. A score ≥ 7 discriminates myofascial dysfunction from non-myofascial LUTS (AUC 0.74), allowing primary clinicians to triage patients to a structured pelvic-floor exam.[5]

Stepwise Management​

ACOG supports multimodal management and AUA supports manual PT for IC/BPS with pelvic-floor tenderness. The 2024 high-tone pelvic-floor algorithm is expert Delphi consensus, not a set of AUA/ACOG graded recommendations for every intervention. PFPT is first line; subsequent options require shared decisions and reassessment.[7][8][2][40]

StepInterventionTrigger to escalate
1PFPT, relaxation and a home programFirst-line; address access barriers with guided home or virtual care
2Local-anesthetic TPIs, cognitive behavioral therapy, selected muscle-relaxant trialsPersistent symptoms or inability to tolerate manual therapy; medication evidence is limited
3Off-label onabotulinumtoxinASelected refractory patients; discuss negative larger RCTs and phenotype-specific uncertainty
4Specialist reassessmentReconsider diagnosis and comorbid pain mechanisms; the consensus reserves SNM mainly for coexisting urgency/frequency

Avoid unsupervised Kegel strengthening during symptomatic hypertonicity. PFPT initially emphasizes relaxation and down-training; later exercise is individualized to examination findings.[9][7] Opioids are not recommended.[7][2]

I. Pelvic Floor Physical Therapy​

PFPT is the cornerstone and the consensus first-line treatment. Evidence from multimodal physiotherapy in female CPP supports short-term pain reduction, but should not be generalized to every isolated modality or patient phenotype.[7][2][9]

ModalityTechniqueGoal
Internal myofascial releaseSingle-digit transvaginal/transrectal palpation of levator ani and obturator internus with sustained pressure to taut bands and MTrPs; 30–60 min sessions, 1–2× per week for 8–12 weeksRelease fascial restrictions, reduce trigger-point irritability
Biofeedback (down-training)Surface or intracavitary EMG with real-time feedbackTrain pelvic-floor relaxation, not strength
Electrical stimulationLow-frequency TENS or interferential current, external or intravaginalPain modulation, muscle relaxation
Pelvic-floor stretching / home programReverse Kegels, child's pose, deep squat, diaphragmatic breathingSustain in-clinic gains

A 2025 trial of postpartum pelvic-floor hypertonia found that lifestyle intervention + biofeedback/electrical stimulation + manual myofascial release achieved a 94.3% effective rate, significantly superior to electrical stimulation/biofeedback alone (87%) or lifestyle alone (37.7%) — supporting combined rather than single-modality protocols.[10]

II. Trigger Point Injections (TPIs)​

ACOG Practice Bulletin 218 recommends TPIs (Level B) to improve pain and functional ability in myofascial CPP — alone or with other modalities.[7] Needling and contextual effects may contribute to benefit; small heterogeneous studies do not establish equivalence of every injectant.[7][11]

Injectant options​

InjectantNotesEvidence
Local anesthetic (lidocaine, bupivacaine, levobupivacaine, mepivacaine)Most commonly used; well-studiedMultiple cohorts and RCTs[12][13][14]
Local anesthetic + corticosteroid (triamcinolone, betamethasone)Common in postpartum and refractory MFPPA 2025 RCT found levobupivacaine alone non-inferior to levobupivacaine + betamethasone for postpartum myofascial perineal pain[13]; ASRA/AAPM guidance favors considering anesthetic alone because routine steroid addition offers little established benefit; its earlier evidence search preceded the postpartum RCT[15]
Magnesium-based formulationNovel approachSmall underpowered RCT (44 participants; magnesium, lidocaine and waitlist arms) did not establish superiority over lidocaine[11]
Normal salineMechanical / needling effectMay produce a needling/contextual response; absence of superiority does not establish universal equivalence[7]
OnabotulinumtoxinAFor refractory / repeated-TPI patientsSee Section III

Office-based transvaginal TPI — published protocols​

ProtocolInjectantVolume per TrPDelivery
Langford 20070.25% bupivacaine 10 mL + 2% lidocaine 10 mL + triamcinolone 40 mg / 1 mL5 mL per trigger point5.5" Iowa-trumpet pudendal needle guide; office, no sedation[12]
Leitch 2022 (RCT)1% lidocaine 10 mL or magnesium-based formulationPer trigger pointTransvaginal, office; 8 sessions over 12 weeks[11]
Solano Calvo 2025 (RCT)Levobupivacaine 5 mg/mL ± betamethasone 3 mg/mLPer trigger pointTransvaginal, office[13]
Moya Esteban 2019Mepivacaine 2% (8 mL) + betamethasone acetate (2 mL)Per trigger pointTransvaginal, office[14]

These are historical study formulations, not universal prescribing instructions. Calculate the total dose across every injection site and any accompanying block, accounting for additive local-anesthetic toxicity, body size and comorbidity. Steroid is not routinely required.[15]

Step-by-step technique​

  1. Position: dorsal lithotomy; sedation usually not required.
  2. Exam: single-digit transvaginal palpation of pubococcygeus, iliococcygeus, coccygeus, and obturator internus bilaterally; identify trigger points by reproduction of the patient's pain.[12][6]
  3. Needle guidance: Iowa-trumpet pudendal needle guide (5.5") or pudendal-block kit (≈ 1 cm depth of penetration); the guide is held transvaginally with the index finger directing the needle tip onto the trigger point.[12]
  4. Injection: advance into the trigger point under digital guidance; aspirate and inject incrementally with monitoring. Negative aspiration does not exclude intravascular placement. Choose aliquots and the number of sites within the calculated total-dose limit.
  5. Post-procedure: brief observation; teach pelvic-floor stretching for home use; resume PFPT.[12]

Frequency and pairing with PFPT​

  • Frequency is individualized; the Leitch RCT used 8 sessions over 12 weeks, not a universal every-2–4-week regimen.[11]
  • In a retrospective cohort of 87 women, TPI followed immediately by myofascial-release PFPT was associated with a median VAS reduction of 4 points vs 2 points with TPI alone (p = 0.042); 77% vs 45% achieved ≥ 3-point improvement (p = 0.008).[16]

III. OnabotulinumtoxinA (Botox)​

OnabotulinumtoxinA (BTA) may be discussed for selected refractory patients after PFPT; access barriers alone are not evidence of benefit or an indication to escalate.[17][18] This is an off-label use — pelvic-floor MFPP is not on the FDA label.[17]

Dosing​

DoseDilutionApproachAnesthesiaNote
200 U (published protocol)200 U in 20 mL normal saline (10 U/mL)TransvaginalConscious sedation or generalWhitmore 2025 protocol[17]; Dessie RCT[19]
80 UVariableTransvaginalGeneralAbbott 2006 RCT[20]
50–200 U rangeVariableTransvaginalVariableObservational dosing experience; an optimal dose and reliable dose-response relationship remain unestablished[21][22]

Step-by-step technique (Whitmore 2025)​

  1. Awake exam — palpate pubococcygeus, iliococcygeus, and obturator internus bilaterally; mark hypertonic / tender targets.[17]
  2. Sedation — conscious sedation or general anesthesia; some centers use local-only office protocols.
  3. Reconstitution — 200 U onabotulinumtoxinA in 20 mL normal saline (10 U/mL).
  4. Needle — pudendal-block kit, ~1 cm depth of penetration.
  5. Injection — sequentially deliver 1–2 mL (10–20 U) at multiple sites along each affected muscle, distributed across pubococcygeus, iliococcygeus, and obturator internus bilaterally.
  6. Image-guided alternative — 4D transperineal ultrasound can confirm intramuscular needle placement and visualize fluid tracking along muscle fibers.[23]
  7. Standardized ten-point method — a retrospective study published in the 2026 volume compared a fixed ten-site pattern with trigger-point injection (91 patients; 64 propensity-matched). No significant outcome difference establishes neither equivalence nor a superior learning curve in a randomized comparison.[24]

Concurrent pudendal nerve block — limited benefit​

  • A 12-year, 182-patient retrospective cohort found no difference in clinical outcomes, re-intervention, or AEs between BTA alone vs BTA + pudendal block.[18]
  • A 96-event subgroup analysis found no difference in PACU pain (VAS 1.7 vs 1.9), PACU time, or opioid requirements.[25]

Onset, duration, retreatment​

  • Assess response at 2–4 weeks, as suggested by the expert consensus; studies also assess outcomes at 6–12 weeks. These assessment times are not a universal six-week pharmacologic onset or a reason to withhold PFPT.[17][26][40]
  • Duration: ~3–6 months; median time to re-intervention 6 months.[17][18]
  • Mean number of total injections per patient: 1.6–1.7 in a large cohort — many require retreatment.[18]

Efficacy — mixed​

StudyDesign / NResult
Spruijt 2025 RCTn = 94; 100 U vs placebo, then four PFPT sessions≥33% pain reduction: 33% vs 20% (p=0.19); global improvement 17% in both groups. Resting activity improved, but pain benefit was not demonstrated.[41]
Karp 2026 phase 2 RCTn = 29 with endometriosis-associated pain and pelvic-floor spasm despite treatment; 100 U vs salineAt one month, self-reported benefit 11/15 (73%) vs 4/14 (29%), p=0.027. Small, selected phenotype; subsequent open injections prevent interpreting one-year outcomes as a sustained randomized comparison.[42]
Dessie 2019 RCTn = 59; 200 U BTA vs saline (all received PFPT from week 4)Not superior to saline for pain on palpation at 2/4/12 weeks; BTA more likely to report PGI-I global improvement at 4 weeks (p = 0.03)[19]
Abbott 2006 RCTn = 60; 80 U BTASignificantly reduced pelvic-floor resting pressure (49 → 32 cmH₂O) and dyspareunia VAS[20]
Jha 2021 observationaln = 4874% improvement; no efficacy difference across 50–200 U dose range[21]
Mooney 2021 pilotn = 21Improvement in dyspareunia, sexual function, QoL; 4 previously apareunic patients regained penetrative intercourse[26]
Lewis 2023 12-year cohortn = 182Median time to re-intervention 6 months; safety profile across long-term repeat dosing[18]

Adverse events​

AEIncidenceNotes
Constipation6.6–10.1%Most common; usually transient[17][18]
Urinary incontinenceup to 22%More common at higher doses[17][22]
Urinary retention3.8%[18]
Urinary tract infection2.7–9%[18]
Fecal incontinence2.7%Transient (~2 weeks); more frequent at higher doses[18][22]
Worsening pelvic pain11.5%[18]

IV. Compounded Intravaginal Pharmacotherapy​

These are off-label, non-FDA-approved, and rely on compounding-pharmacy formulations whose bioavailability and stability vary between pharmacies. They are adjuncts within a multimodal plan — not stand-alone therapies — and the evidence base is dominated by small studies, case reports, and expert opinion.[2][27][9]

Intravaginal diazepam — most studied​

  • Published doses: 5–10 mg compounded suppositories; this is not a validated routine regimen for MFPP.
  • Pharmacokinetics (eight healthy volunteers): vaginal administration produces a lower peak (Cmax ~31 ng/mL at ~3.1 h) and lower bioavailability (70.5%) than oral, but a prolonged half-life (~82 h) with active nordiazepam metabolite peaking at ~132 h. Steady-state takes ~1 week — accumulation favors intermittent dosing (e.g., before PT or intercourse) rather than daily use.[28]
  • Evidence is mixed:
    • Observational series report subjective improvement in 71–96% with improved pelvic-floor tone on perineometry.[29]
    • A triple-blinded RCT (10 mg nightly × 28 days) found no improvement in resting EMG, FSFI, or VAS vs placebo as monotherapy.[30]
    • In women with vestibulodynia receiving TENS, vaginal diazepam improved dyspareunia and relaxation outcomes, but not the between-group VAS pain outcome.[31]
    • A systematic review found two small placebo-controlled trials without significant pain benefit and the limited TENS findings above. Benefit as a PFPT adjunct remains uncertain; the evidence does not establish it as a routinely effective treatment.[32]
  • Safety: meaningful systemic absorption and accumulation remain possible; fatigue occurred in 3/8 volunteers. Apply benzodiazepine precautions for sedation, dependence and concurrent opioids or other sedatives.[28]

Intravaginal / topical baclofen​

  • GABA-B receptor agonist with antispastic and analgesic effects.[33]
  • Formulations: topical creams have been reported with palmitoylethanolamide (PEA) or amitriptyline; no established evidence-based vaginal dose exists.
  • Evidence: limited to case reports and small series in vulvodynia and proctodynia (>50% symptom reduction with 5% cream + PEA; resumption of sexual activity).[34][35] Amitriptyline-baclofen creams have shown pre-to-post improvement in non-RCT vulvodynia studies.[36] No RCTs of intravaginal baclofen alone for pelvic-floor MFPP.
  • Mechanism: acts at peripheral GABA-B receptors on nociceptor terminals and modulates nociceptor / immunocompetent / epithelial cross-talk in vulvar / vaginal mucosa; centrally reduces spasticity.[33][35]
  • Safety: formal vaginal-baclofen pharmacokinetic data are lacking, so reduced systemic risk cannot be assumed. Oral baclofen causes sedation and dizziness and can cause withdrawal after abrupt cessation.[33]

Intravaginal / topical ketamine​

  • NMDA-receptor antagonist; rationale is modulation of peripheral sensitization at nociceptor afferents.[37]
  • Formulation: compounded topical combinations are described, but neither an effective vaginal dose nor equivalence between cream concentrations and suppository doses is established.
  • Evidence is weak:
    • A 2025 Cochrane review found very uncertain evidence that topical ketamine improves pain vs placebo (MD 1.90, 95% CI −18.73 to 22.53, immediate-term).[38]
    • Small studies of topical ketamine alone show no statistically significant benefit for neuropathic pain.
    • Combination topical formulations (ketamine + amitriptyline, ketamine + lidocaine) show 40–75% response in retrospective non-placebo-controlled analyses; optimal dosing and combinations remain unclear.
    • No RCTs of intravaginal ketamine for MFPP or vulvodynia.
  • Safety: psychomimetic effects, unclear long-term cognitive impact, addiction risk. Chronic systemic ketamine causes ketamine cystitis (bladder inflammation / fibrosis) — particularly relevant in the urologic context, and absence of reported cases with vaginal formulations does not establish their long-term safety.[37]

Summary of compounded intravaginal agents​

AgentDose evidenceMechanismEvidenceClinical implication
Diazepam5–10 mg studiedGABA-A modulatorSmall RCTs and observational studiesRoutine benefit unproven; systemic absorption and accumulation[28][30][31][32]
BaclofenNo established vaginal doseGABA-B agonistCase reports / seriesVaginal efficacy and pharmacokinetics uncertain[34][35]
KetamineNo established vaginal doseNMDA antagonistVery low certaintyTopical effect uncertain; no basis for routine vaginal combinations[38]

V. Practical Treatment Ladder​

  1. Start with individualized PFPT, relaxation and a home program. Select oral treatments for a defined comorbid pain phenotype; routine gabapentin for unexplained female CPP is not supported by the GaPP2 trial (see the CPP hub).[7][2][9]
  2. Persistent focal tenderness or inability to tolerate manual therapy: consider local-anesthetic TPIs. Immediate PFPT may be feasible, but its added benefit rests on retrospective evidence; steroid addition is not routine.[12][15][16]
  3. Refractory symptoms: reassess diagnosis, comorbidities and goals before considering off-label Botox. Explain the negative larger trial and the positive small endometriosis-specific trial; neither warrants automatic escalation.[40][41][42]
  4. Compounded vaginal drugs: consider only through shared decisions about uncertain benefit, formulation variability and systemic adverse effects; avoid treating them as a mandatory stage.[28][32][35][38]
  5. Multidisciplinary reassessment is appropriate for persistent disability. An uncontrolled 186-woman series of nerve blocks, TPIs and PFPT reported improvement, but cannot isolate treatment effects or establish this combination as the standard protocol.[7][39]

Key Principles​

  • Include a structured pelvic-floor examination when evaluating pelvic pain; prevalence varies widely by case mix.[1][2][6]
  • Start with relaxation-focused PFPT; avoid unsupervised strengthening during symptomatic hypertonicity.[9][40]
  • TPIs can be considered for focal refractory tenderness; small studies do not establish injectant equivalence or require immediate post-injection PT.[7][11][16]
  • Botox is off-label, with mixed randomized evidence and no established optimal dose. Observational pudendal-block comparisons do not prove that a block can never help an individual patient.[18][22][25][41][42]
  • Compounded vaginal diazepam, baclofen and ketamine have uncertain benefit and require attention to systemic exposure and formulation safety.[28][30][32][38]
  • Routine opioids are not recommended for MFPP.[7][2]

See Also​

Videos​

Pelvic Floor Trigger Point Injections for Myofascial Pain
Green Journal (2025)

References​

1. Ross V, Detterman C, Hallisey A. Myofascial pelvic pain: an overlooked and treatable cause of chronic pelvic pain. J Midwifery Womens Health. 2021;66(2):148-160. doi:10.1111/jmwh.13224.

2. Namazi G, Chauhan N, Handler S. Myofascial pelvic pain: the forgotten player in chronic pelvic pain. Curr Opin Obstet Gynecol. 2024;36(4):273-281. doi:10.1097/GCO.0000000000000966.

3. Steen JP, Jaiswal KS, Kumbhare D. Myofascial pain syndrome: an update on clinical characteristics, etiopathogenesis, diagnosis, and treatment. Muscle Nerve. 2025;71(5):889-910. doi:10.1002/mus.28377.

4. Lamvu G, Carrillo J, Ouyang C, Rapkin A. Chronic pelvic pain in women: a review. JAMA. 2021;325(23):2381-2391. doi:10.1001/jama.2021.2631.

5. Ackerman AL, Torosis M, Jackson NJ, et al. The Persistency Index: a novel screening tool for identifying myofascial pelvic floor dysfunction in patients seeking care for lower urinary tract symptoms. Am J Obstet Gynecol. 2023;229(6):667.e1-667.e11. doi:10.1016/j.ajog.2023.08.017.

6. Meister MR, Shivakumar N, Sutcliffe S, Spitznagle T, Lowder JL. Physical examination techniques for the assessment of pelvic floor myofascial pain: a systematic review. Am J Obstet Gynecol. 2018;219(5):497.e1-497.e13. doi:10.1016/j.ajog.2018.06.014.

7. Committee on Practice Bulletins—Gynecology. Chronic pelvic pain: ACOG Practice Bulletin, Number 218. Obstet Gynecol. 2020;135(3):e98-e109. doi:10.1097/AOG.0000000000003716.

8. 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.

9. Wallace SL, Miller LD, Mishra K. Pelvic floor physical therapy in the treatment of pelvic floor dysfunction in women. Curr Opin Obstet Gynecol. 2019;31(6):485-493. doi:10.1097/GCO.0000000000000584.

10. Xu Y, Li C, Li J. Comparison of the efficacy of three intervention schemes for postpartum pelvic floor muscle hypertonia. Int Urogynecol J. 2025. doi:10.1007/s00192-025-06128-8.

11. Leitch J, Webb A, Pudwell J, et al. Magnesium-based trigger point infiltrations versus local anaesthetic infiltrations in chronic pelvic myofascial pain: a randomized, double-blind, controlled study. J Obstet Gynaecol Can. 2022;44(8):877-885. doi:10.1016/j.jogc.2022.02.129.

12. Langford CF, Udvari Nagy S, Ghoniem GM. Levator ani trigger point injections: an underutilized treatment for chronic pelvic pain. Neurourol Urodyn. 2007;26(1):59-62. doi:10.1002/nau.20393.

13. Solano Calvo JA, Barreiro García JM, González Hinojosa J, et al. Treatment of postpartum myofascial perineal pain and dyspareunia through local anaesthetic infiltrations compared to anaesthetic and corticosteroids: a randomised double-blind clinical trial. J Clin Med. 2025;14(9):3228. doi:10.3390/jcm14093228.

14. Moya Esteban BM, Solano Calvo JA, Torres Morcillo C, et al. Retrospective case review of combined local mepivacaine and steroid injections into vaginal trigger points for the management of moderate-to-severe perineal pain after childbirth. Arch Gynecol Obstet. 2019;299(2):501-505. doi:10.1007/s00404-018-5000-5.

15. Benzon HT, Elmofty D, Shankar H, et al. Use of corticosteroids for adult chronic pain interventions: sympathetic and peripheral nerve blocks, trigger point injections — guidelines from the ASRA, AAPM, ASIPP, and IPSIS. Reg Anesth Pain Med. 2025. doi:10.1136/rapm-2024-105593.

16. Lewis GK, Chen AH, Craver EC, Crook JE, Carrubba AR. Trigger point injections followed by immediate myofascial release in the treatment of pelvic floor tension myalgia. Arch Gynecol Obstet. 2023;307(4):1027-1035. doi:10.1007/s00404-022-06880-y.

17. Whitmore GT, Tam J, Orlando M. Onabotulinumtoxin A injections for patients with pelvic floor dysfunction. J Minim Invasive Gynecol. 2025. doi:10.1016/j.jmig.2025.07.005.

18. Lewis GK, Carrubba AR, Stanton AP, et al. OnabotulinumtoxinA injections for the treatment of myofascial pelvic pain: 12-year experience at a tertiary care academic center. Gynecol Obstet Invest. 2023;88(1):37-46. doi:10.1159/000528177.

19. Dessie SG, Von Bargen E, Hacker MR, Haviland MJ, Elkadry E. A randomized, double-blind, placebo-controlled trial of onabotulinumtoxin A trigger point injections for myofascial pelvic pain. Am J Obstet Gynecol. 2019;221(5):517.e1-517.e9. doi:10.1016/j.ajog.2019.06.044.

20. Abbott JA, Jarvis SK, Lyons SD, Thomson A, Vancaille TG. Botulinum toxin type A for chronic pain and pelvic floor spasm in women: a randomized controlled trial. Obstet Gynecol. 2006;108(4):915-23. doi:10.1097/01.AOG.0000237100.29870.cc.

21. Jha S, Toozs-Hobson P, Roper JC, et al. Botulinum injections for myofascial pelvic pain. Int Urogynecol J. 2021;32(5):1151-1156. doi:10.1007/s00192-020-04435-w.

22. Karp BI, Tandon H, Vigil D, Stratton P. Methodological approaches to botulinum toxin for the treatment of chronic pelvic pain, vaginismus, and vulvar pain disorders. Int Urogynecol J. 2019;30(7):1071-1081. doi:10.1007/s00192-018-3831-z.

23. Nesbitt-Hawes EM, Dietz HP, Abbott JA. Four-dimensional ultrasound guidance for pelvic floor botulinum toxin-A injection in chronic pelvic pain: a novel technique. Ultrasound Obstet Gynecol. 2018;51(3):396-400. doi:10.1002/uog.17537.

24. Yang J, Ma X, Luo C, et al. The significance of type A botulinum toxin ten-point injection therapy in the treatment of chronic pelvic pain caused by muscle spasms in women. Int Urogynecol J. 2026;37(4):963-972. doi:10.1007/s00192-025-06346-0.

25. Coombs P, Lewis G, Chen AH, Ma Y, Carrubba AR. Does pudendal nerve block improve perioperative pain following onabotulinumtoxinA injection for myofascial pelvic pain? Eur J Obstet Gynecol Reprod Biol. 2025;306:64-68. doi:10.1016/j.ejogrb.2024.12.055.

26. Mooney SS, Readman E, Hiscock RJ, et al. Botulinum toxin A (Botox) injection into muscles of pelvic floor as a treatment for persistent pelvic pain secondary to pelvic floor muscular spasm: a pilot study. Aust N Z J Obstet Gynaecol. 2021;61(5):777-784. doi:10.1111/ajo.13396.

27. 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.

28. 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.

29. 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):895-9. doi:10.1007/s00192-009-1075-7.

30. 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):1915-23. doi:10.1007/s00192-013-2108-9.

31. 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.

32. 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.

33. Fromm GH. Baclofen as an adjuvant analgesic. J Pain Symptom Manage. 1994;9(8):500-9. doi:10.1016/0885-3924(94)90111-2.

34. Keppel Hesselink JM, Kopsky DJ, Sajben NL. Vulvodynia and proctodynia treated with topical baclofen 5% and palmitoylethanolamide. Arch Gynecol Obstet. 2014;290(2):389-93. doi:10.1007/s00404-014-3218-4.

35. Keppel Hesselink JM, Kopsky DJ, Sajben N. New topical treatment of vulvodynia based on the pathogenetic role of cross talk between nociceptors, immunocompetent cells, and epithelial cells. J Pain Res. 2016;9:757-762. doi:10.2147/JPR.S115407.

36. Schlaeger JM, Glayzer JE, Villegas-Downs M, et al. Evaluation and treatment of vulvodynia: state of the science. J Midwifery Womens Health. 2023;68(1):9-34. doi:10.1111/jmwh.13456.

37. Pickering G, Morel V, Voute M. Managing chronic pain: the ketamine option. CNS Drugs. 2025. doi:10.1007/s40263-025-01234-z.

38. Ferraro MC, Cashin AG, Visser EJ, et al. Ketamine and other NMDA receptor antagonists for chronic pain. Cochrane Database Syst Rev. 2025;8:CD015373. doi:10.1002/14651858.CD015373.pub2.

39. Patil S, Daniel G, Vyas R, et al. Neuromuscular treatment approach for women with chronic pelvic pain syndrome improving pelvic pain and functionality. Neurourol Urodyn. 2022;41(1):220-228. doi:10.1002/nau.24799.

40. Torosis M, Carey E, Christensen K, et al. A treatment algorithm for high-tone pelvic floor dysfunction. Obstet Gynecol. 2024;143(4):595–602. doi:10.1097/AOG.0000000000005536.

41. Spruijt MA, Klerkx WM, Notten K, et al. The efficacy of botulinum toxin A injection in pelvic floor muscles in chronic pelvic pain patients: a double-blinded randomised controlled trial. BJOG. 2025. doi:10.1111/1471-0528.17991.

42. Karp BI, Tandon HK, Sinaii N, et al. Botulinum toxin for endometriosis-associated chronic pelvic pain: a randomised, double-masked, parallel, phase 2 trial. EClinicalMedicine. 2026;91:103740. doi:10.1016/j.eclinm.2025.103740.