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Chronic Pelvic Pain

Chronic pelvic pain (CPP) is a highly prevalent, multifactorial syndrome (not a single disease) that affects roughly 15–26% of women; chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is one male presentation.[3] ACOG's gynecologic definition uses pelvic pain typically lasting more than six months; EAU uses at least three months of continuous or recurrent pain (more than six months may be appropriate for cyclical pain), and NIH male CP/CPPS research criteria require at least three months of symptoms within the preceding six months.[3][38][48] In about 80% of women with CPP, pain is not gynecologic in origin; common contributors in women include irritable bowel syndrome, bladder pain syndrome or interstitial cystitis, pelvic floor myofascial pain, and endometriosis.[2] The cornerstone of management is a biopsychosocial, multimodal, interdisciplinary approach.[1][2][3][4][5]

For the bladder-specific phenotype, see IC/PBS; for menopause-related pelvic and urogenital pain, see Genitourinary Syndrome of Menopause. In women with CPP without a defined pathology, multimodal physical therapy reduced pain immediately after treatment versus inert or nonconservative comparators (seven trials, 476 women; high certainty).[31]

Part I — Conceptual Framework​

Definition​

  • Women: pain perceived to originate from pelvic organs or structures lasting > 6 months, with negative cognitive, behavioral, sexual, and emotional consequences. Cyclical pain (e.g., dysmenorrhea) is included if it carries significant functional impact.[1][3]
  • Men (CP/CPPS): pelvic pain or discomfort for at least 3 months within the past 6 months in the absence of another identifiable cause. This is the NIH research definition; AUA cautions that strict research definitions should not delay clinical evaluation of compatible symptoms.[4][6][48]
  • EAU 2026 (all patients): chronic pelvic pain is pain perceived in pelvic structures that is continuous or recurrent for at least 3 months (ICD-11). A longer period of more than 6 months may suit cyclical pain. EAU calls the syndrome with no proven infection or other obvious local pathology chronic primary pelvic pain syndrome (CPPPS), and uses primary prostate pain syndrome (PPPS) rather than chronic prostatitis. It classifies bacterial infection, cancer and defined organ disease as specific disease-associated pelvic pain, not CPPPS.[38]

Epidemiology​

  • Women. Prevalence estimates for noncyclic pelvic pain lasting at least 6 months range from 5.7% to 26.6%[1]; CPP accounts for 40% of laparoscopies and about 12% of hysterectomies in the US[2]
  • Men. Prostatitis of any subtype affects approximately 9.3% of men over a lifetime[4]. An older managed-care incidence estimate of 3.3 physician-diagnosed NIH type III cases per 1,000 person-years was extrapolated to about 267,000 annual US cases.[6][50] EAU 2026 cites population-based prevalence of prostatitis symptoms of 2.2–14.2%, notes that symptom-based definitions overlap with BPH and bladder pain and may not reflect true prevalence, and cites a 3.1-fold greater risk at ages 50–59 than at 20–39[38]

Pathophysiology — the biopsychosocial model​

CPP is best understood as a chronic pain syndrome with three interacting domains:[1][2]

  1. Peripheral pain generators. Visceral (gynecologic, urologic, GI) and somatic (musculoskeletal, neural) nociceptive input
  2. Central sensitization. Amplified spinal or brain pain signaling, decreased descending inhibition, viscero-visceral and viscero-somatic convergence
  3. Psychosocial modulation. Mood disorders, trauma, catastrophizing, sleep disruption, social stressors

Central sensitization can contribute to pain persistence after lesion-directed treatment, overlap with other chronic pain conditions, and incomplete response to organ-targeted treatment.[2][5]

Part II — Etiology by Organ System​

A. Gynecologic (women)​

ConditionNotes
EndometriosisDysmenorrhea, dyspareunia, non-menstrual pelvic pain; affects about 10% of reproductive-age women[8][9]; observed, mainly at laparoscopy, in 28.1% of women presenting with CPP in a meta-analysis of 11 observational studies[8]; ACOG cites a mean prevalence of 70% (range 28–93%) in a systematic review of women with CPP evaluated for other conditions[1]
AdenomyosisDysmenorrhea, heavy bleeding, diffusely enlarged uterus; often coexists with endometriosis[3]
VulvodyniaChronic vulvar pain (burning, stinging) without identifiable cause; provoked or unprovoked; 8–16% of women[3]
Pelvic massesFibroids, ovarian cysts — pressure / bulk-related pain
Chronic pelvic infectionHistory of PID; tubal damage and adhesions

Endometriosis affects about 10% of reproductive-age women (about 9 million in the US); 90% report pelvic pain; diagnostic delay averages 5–12 years.[8] Pain mechanisms include nociceptive (inflammation), neuropathic (nerve infiltration or neurogenesis), and nociplastic (central sensitization), explaining why lesion burden correlates poorly with pain severity and why about 25% have recurrent pain after hysterectomy.[8][9]

B. Urologic (all patients)​

Bladder pain syndrome / interstitial cystitis (BPS/IC)​

  • Persistent or chronic discomfort perceived as bladder origin, with urgency or frequency, lasting > 6 weeks with negative urine cultures[10]
  • More commonly diagnosed in women; increasingly recognized in men (often misdiagnosed as CP/CPPS)[10][11]
  • Hunner lesions (EAU 2026 reports 5–50% across studies and says the proportion of lesion versus non-lesion disease is unclear) represent a distinct phenotype with different treatment responses[10][12][38]
  • The 2022 AUA IC/BPS guideline replaced tiered treatment lines with categorical management; see IC/PBS for the full algorithm[10][11][13]

Ketamine-associated uropathy​

Chronic prostatitis / chronic pelvic pain syndrome (CP/CPPS) — men​

AUA 2025 distinguishes CP/CPPS from chronic scrotal content pain (CSCP). Perineal, bilateral scrotal, penile or suprapubic pain, dysuria, or ejaculatory pain supports CP/CPPS; isolated unilateral chronic scrotal pain without other pelvic pain or urinary symptoms supports CSCP .[48]

  • The most common urologic diagnosis in men < 50[4][14]
  • Diagnosis of exclusion. History, examination, urine testing and PVR guide evaluation; concerning findings require additional investigation[4]
  • NIH-CPSI measures symptom severity (0–43 scale); a 6-point change is clinically meaningful[4]
  • Pelvic floor myalgia or tenderness in 27–64% of CP/CPPS patients[4]. EAU 2026 cites muscle tenderness in 51% of men with prostatitis versus 7% of controls in the Chronic Prostatitis Cohort Study, and pelvic floor dysfunction in 92.2% of men attending one tertiary pain center[38]
  • Higher rates of fibromyalgia, chronic fatigue, IBS, depression, anxiety, and panic disorder[6]
  • Dysfunctional high-pressure voiding. In 48 men with treatment-refractory NIH category IIIb (non-inflammatory) CPPS, 29 (60%) had endoscopic bladder-neck hypertrophy, with higher detrusor opening pressure, higher detrusor pressure at maximal flow, lower maximal flow and higher postvoid residual than the men without it; dyssynergic high-pressure voiding is one proposed route to chronic neuropathic pelvic pain.[45] A classic carbon-particle instillation study separately demonstrated retrograde intraprostatic reflux of urine at voiding, proposed as a route for both infection in bacterial prostatitis and the inflammatory process in the abacterial form.[45][46]

C. Gastrointestinal​

  • Irritable bowel syndrome (IBS). Most common GI cause of CPP; reported in roughly 8–41% of women with CPP across series[3]
  • Diverticular colitis, IBD and celiac disease may all contribute[1]

D. Musculoskeletal and myofascial​

  • Musculoskeletal pain or dysfunction is reported in 50–90% of women evaluated at specialized CPP centers; pelvic-floor myalgia or tenderness is reported in 27–64% of men with CP/CPPS.[2][4] Focus on visceral causes alone leads to prolonged pain and unnecessary surgery.[2]
  • For the dedicated technical reference (pelvic-floor exam, PFPT down-training, trigger-point injection protocols, onabotulinumtoxinA dosing and outcomes, and compounded intravaginal diazepam or baclofen or ketamine), see Myofascial Pelvic Pain.
  • Abdominal-wall myofascial pain. Trigger points in rectus and obliques; positive Carnett sign.
  • Lower back, sacroiliac joints and pubic symphysis belong in the palpation examination; women who do not improve with pelvic floor physical therapy may have a treatable musculoskeletal disorder identified by a physiatrist.[1]

E. Neurologic​

Pudendal neuralgia​

Chronic neuropathic pain in the pudendal nerve distribution (perineum, vulva or scrotum, perianal region).[15][16][17]

Nantes diagnostic criteria:[15][16]

  1. Pain in the anatomical territory of the pudendal nerve
  2. Pain worsened by sitting
  3. Pain does not wake the patient at night
  4. No objective sensory loss on exam
  5. Positive response to a diagnostic pudendal nerve block

Etiologies: entrapment (Alcock canal, sacrospinous / sacrotuberous ligaments), childbirth, pelvic surgery, cycling, sacroiliac abnormalities.[15][17][18] EAU 2026 describes possible sites of pudendal nerve damage at the sacrospinous/sacrotuberous ligaments in 42% of cases, Alcock's canal in 26%, and multiple levels in 17%; six in ten cases are observed in women.[38] Childbirth-related pudendal neuralgia resolves in most women within months. Pelvic surgery, including sacrospinous fixation, and prolonged sitting are the commonest associations in pain centers.[38]

Stepwise management:[15][16][17]

  1. Conservative. Avoid prolonged sitting, cushion, pelvic floor PT
  2. Pharmacologic. TCAs or gabapentinoids first-line; opioids ineffective[16]
  3. Pudendal nerve blocks. Diagnostic and sometimes therapeutic; 29/31 patients in one uncontrolled CT-guided series reported a positive response at six weeks.[15] EAU 2026 describes the evidence base for nerve blocks in chronic pain as weak and, for suspected peripheral nerve pain, prefers image- or nerve-locator-guided local anesthetic injection to imaging or neurophysiology for diagnosis [38]
  4. Pulsed radiofrequency. Case reports and uncontrolled series describe responses in selected refractory cases.[15][19] In one randomized trial of 80 patients with pudendal neuralgia, pulsed radiofrequency plus nerve block produced a lower three-month pain score than block alone (mean VAS 3.9 versus 5.2 among 77 followed).[58]
  5. Surgical decompression. Approaches include transgluteal, transischiorectal, transperineal and laparoscopic release. EAU 2026 cites a randomized transgluteal trial with 66% improvement when pain had lasted under 6 years versus 40% after more than 6 years, and notes persistent symptoms in many operated patients.[15][16][38] AUA 2025's ungraded Future Directions discussion advises against open release because of scarring and re-entrapment; it describes laparoscopic and robotic reports without a graded recommendation.[39]
  6. Sacral or pudendal neuromodulation. Refractory cases[16][17]

Persistent genital arousal disorder / genito-pelvic dysesthesia (PGAD/GPD). Unwanted genital arousal with or without burning, tingling or pain can arise from the pudendal nerve, sacral roots or other sites; see PGAD/GPD for the five-region evaluation and the limited procedural evidence.

Other neuralgias. Ilioinguinal, iliohypogastric, genitofemoral entrapment, particularly after pelvic or abdominal surgery or mesh.[2]

Small-fiber polyneuropathy. In a retrospective study of 39 patients referred to subspecialty clinics for complex chronic pelvic pain (refractory to initial treatment, or with comorbid pain syndromes at presentation), lower-extremity skin biopsy was positive for small-fiber polyneuropathy in 25 (64%). Distal sensory loss or hyperalgesia, autonomic symptoms and overlapping chronic pain syndromes are proposed clues that may prompt specialist assessment for this phenotype.[47]

F. Vascular — pelvic congestion syndrome (PCS)​

For a dedicated deep dive (including SVP classification, escape points, IVUS-guided iliac stenting, the POTS or orthostatic-intolerance association, and the deep uterine vein as a surgical landmark), see Pelvic Venous Disorders.

  • Chronic pelvic pain associated with pelvic varicosities from incompetent ovarian / pelvic vein valves[20][21][22][23]
  • Estimated to account for up to 30% of CPP in women,[20] although ACOG notes the evidence is insufficient to confirm a causal relationship[1]
  • Phenotype: dull aching pelvic pain worsened by prolonged standing, post-coital pain, premenstrual exacerbation; predominantly premenopausal, parous women[20][21][23]
  • Pathophysiology: ovarian or pelvic vein valve incompetence leads to retrograde flow, then venous hypertension and dilation; may be secondary to nutcracker (left renal vein compression) or May-Thurner (iliac vein compression)[21][22]
  • Diagnosis:[20][22][24]
    • TVUS. First-line; ovarian vein diameter > 7–8 mm, slow or retrograde flow, dilated myometrial veins (> 5 mm)[20]
    • Venography. Gold standard but invasive[21]
    • MRI or CT. In a retrospective single-institution series of 2,384 women receiving abdominopelvic CT, dilated ovarian veins (with or without para-uterine vein dilation) were found in 293 (12%): 118/559 (21%) premenopausal and 175/1,825 (10%) postmenopausal women[24]
    • Caveat: laparoscopy has limited sensitivity because CO₂ pneumoperitoneum compresses the veins[20]
  • Treatment:[21][22][23]
    • Ovarian vein embolization. Minimally invasive option for symptomatic ovarian or pelvic vein reflux after assessment for coexisting renal or iliac venous obstruction; series report high technical and clinical success.[21][22]
    • Hormonal suppression. Medroxyprogesterone may reduce pain
    • Venous intervention. Specialist assessment of symptomatic, confirmed obstruction; incidental renal or iliac vein compression alone is not a stenting indication
    • Hysterectomy and BSO. Historical; largely replaced by embolization

G. Psychosocial​

  • Major depression criteria are met in approximately 12–33% of women living with or seeking care for CPP[1]
  • Trauma history. Pelvic pain and dyspareunia are more prevalent in women with a history of abuse, mental illness, lack of support, social stressors or relationship discord[1]; military sexual trauma and adverse childhood events are also associated[2]
  • Catastrophizing and anxiety independently predict pain severity and disability[25]
  • Psychosocial factors do not change the physical pain generators but amplify the symptom burden and impair recovery[1]

Part III — Clinical Phenotyping (Men): UPOINT​

The UPOINT system is the most widely adopted clinical phenotyping tool for CP/CPPS, sorting patients into six domains to drive individualized, multimodal therapy.[25][26][27][28][29]

DomainDescriptionTargeted treatment
U — UrinaryVoiding / storage symptomsAlpha-blockers (tamsulosin, alfuzosin)
P — PsychosocialDepression, catastrophizing, anxiety, maladaptive copingCBT, antidepressants, psychological support
O — Organ-specificProstate / bladder tenderness, Hunner lesionsAnti-inflammatories, quercetin, intravesical therapy
I — InfectionDocumented localized infectionTargeted antibiotics — only if proven[28]
N — Neurologic / SystemicWidespread pain, fibromyalgia, central sensitizationPain-mechanism education; consider gabapentinoids or SNRIs for a selected neuropathic component, recognizing limited CPP-specific efficacy evidence and the negative gabapentin trial in women with unexplained CPP[1][32][37][41]
T — TendernessPelvic floor muscle tenderness, trigger pointsPelvic floor PT, myofascial release

The number of positive UPOINT domains correlates with NIH-CPSI severity. Cluster analysis identifies a pelvic-predominant cluster (U, O, T) and a systemic cluster (N, I, P); the dominant pain drivers across patients are pelvic floor tenderness, depression, and catastrophizing.[25] UPOINT was proposed by Shoskes and colleagues in 2009,[42] and a sexual-dysfunction domain (S) added in European cohorts (UPOINTS) improved the correlation with symptom severity.[43] EAU 2026 cites both and adds the domain to its own symptom classification.[38]

Part IV — Diagnostic Evaluation​

Women​

  1. Biopsychosocial history. Pain (onset, location, quality, severity, triggers, menstrual relationship), urinary, gastrointestinal and sexual symptoms, trauma history, mood, sleep, prior pelvic surgery or mesh implants, and prior treatments.[2][3][5][38]
  2. Red-flag screening. Acute abdomen, unintentional weight loss, postmenopausal bleeding, hematuria, rectal bleeding, new neurologic deficit prompt urgent evaluation
  3. Physical exam. Abdominal (Carnett test for abdominal-wall pain); pelvic musculoskeletal exam of levator ani, obturator internus, and piriformis for trigger points and hypertonicity; neurosensory mapping; speculum and bimanual exam for masses, tenderness, prolapse, endometriosis nodularity
  4. Targeted diagnostics. Pregnancy testing when relevant; UA/culture, STI testing and ultrasound according to symptoms and examination
  5. Advanced imaging. Transvaginal ultrasound is generally the first imaging study for suspected endometriosis; in symptomatic premenopausal or early postmenopausal patients, add posterior-compartment views, uterine and ovarian positioning, and the uterine sliding sign to assess deep disease.[8][54] MRI can assess deep or extrapelvic disease, adenomyosis, or complex masses when indicated, including when transvaginal imaging is infeasible or inconclusive; normal imaging does not exclude superficial endometriosis.[8][3][54] Use TVUS with vascular assessment for suspected PCS.[20][22]
  6. Assess for central sensitization. Widespread pain, multiple pain syndromes, allodynia or hyperalgesia, sleep or mood disturbance

Men​

  1. History. Pain location or quality or duration, voiding symptoms, sexual dysfunction, psychosocial impact[4][28][48]
  2. Physical exam. Examine the scrotum; a DRE may be performed to evaluate the prostate; palpate pelvic-floor muscles transrectally for tenderness . Screen the pelvis, hips and lower spine for neurological and musculoskeletal abnormalities, with specialist referral when identified . Scrotal ultrasound may be performed .[48]
  3. Urinalysis and urine culture to evaluate infection; PVR to assess emptying.[48]
  4. NIH-CPSI for symptom severity
  5. UPOINT phenotyping to guide treatment
  6. Additional testing. Cystoscopy, urodynamics or imaging may be used when the diagnosis is unclear . A two-glass or four-glass localization test may help distinguish chronic bacterial prostatitis from CP/CPPS when uncertainty persists .[48]

Part V — Management​

Overarching principles (all patients)[1][2][3][30]​

  • Multimodal interdisciplinary care addresses coexisting pain contributors. In men, AUA permits multimodal and multidisciplinary management, usually beginning nonsurgically, with reassessment and discontinuation of ineffective treatments (Statements 13–15; Clinical Principles).[48]
  • Patient education about pain mechanisms (especially central sensitization) is needed
  • Shared decision-making with functional goal-setting
  • Treat all contributing domains simultaneously. Visceral, myofascial, neurologic, psychosocial
  • Opioids are not recommended for CPP (ACOG).[1] EAU 2026 allows them only after multidisciplinary assessment and after other reasonable treatments have failed , initiated by an appropriately trained specialist and with psychiatric or psychological input when drug misuse is suspected[38]

A. Non-pharmacologic therapies​

TherapyEvidence
Pelvic floor PTACOG recommends referral for pelvic floor PT, sex therapy or CBT, alone or combined, for the myofascial and psychosocial contributors to CPP (Level B)[1]; multimodal PT in women: short-term pain SMD −1.69 (high certainty in the cited meta-analysis); male myalgia evidence is less certain[30][31][32]
CBT / psychological therapyAddresses catastrophizing, depression, anxiety and sexual function; in women with CPP, predominantly psychological approaches did not lower pain intensity in the meta-analysis (SMD −0.18, moderate certainty) but slightly improved sexual function. AUA lists CBT as a conditional adjunct in CP/CPPS (Grade C)[2][31][32]
Sex therapyAdjunct to PT for dyspareunia and genito-pelvic pain[1]
Self-managementModerate physical activity, stress management, mindfulness, dietary modification[2]
AcupunctureMay be considered, with yoga, for CPP of musculoskeletal etiology (ACOG Level C); evidence inconsistent[1][33]

B. Pharmacologic therapies​

ClassAgentsEvidence / indication
Alpha-blockersTamsulosin, alfuzosinOffer for CP/CPPS with voiding symptoms ; ΔNIH-CPSI −10.8 to −4.8 vs placebo in the JAMA review, but the Cochrane review rates the certainty as very low (pooled MD −5.0), with more dizziness and postural hypotension[4][26][32]
NSAIDsIbuprofen, naproxenModest benefit in CP/CPPS (ΔNIH-CPSI −2.5 to −1.7); AUA permits use within multimodal CP/CPPS pain management ; modest benefit in dysmenorrhea; no proven benefit in endometriosis[4][8][9][32]
SNRIsDuloxetine, venlafaxineRecommended for neuropathic CPP (ACOG Level B)[1][2]; a double-blind, eight-week RCT randomized 69 women with CPP syndrome to duloxetine or amitriptyline, but had no placebo arm[55]
GabapentinoidsGabapentin, pregabalinSelected neuropathic phenotypes only; GaPP2 found no benefit and more adverse effects in women with unexplained CPP. In men with CP/CPPS, pregabalin did not improve the 6-point NIH-CPSI responder endpoint over placebo (6-week RCT, n = 324)[37][41]. AUA 2025 lists gabapentinoids, TCAs and SSRIs together as conditional options (Grade C)[32]
TCAsAmitriptyline, nortriptylineAmitriptyline is an IC/BPS option; TCAs may be considered for neuropathic pain, with tolerability review [2][10][32]
Hormonal therapyCOCs, progestins, GnRH agonists / antagonistsCOCs and progestins are first-line for endometriosis-related CPP; GnRH agonists / antagonists are second-line; continuous COC use preferred[8][9][34][35]
PhytotherapyPollen extract (Cernilton)Modest benefit in CP/CPPS (ΔNIH-CPSI −2.49); AUA permits pollen extract, quercetin or saw palmetto [26][32]
PDE5 inhibitorsTadalafilDaily tadalafil is an AUA 2025 option with or without ED [32]
Muscle relaxantsCyclobenzaprine, intravaginal diazepamInsufficient / inconsistent evidence for myofascial CPP[2]
  • First-line: combined oral contraceptives (continuous use preferred) or progestins (norethindrone acetate, dienogest, LNG-IUS); clinically significant pain reduction (network meta-analysis of 15 trials, n = 1,680: mean differences of about −13 to −18 points on a 0–100 VAS versus placebo)[8]
  • Second-line: GnRH agonists (leuprolide) or antagonists (elagolix, relugolix combination) with add-back therapy
  • Third-line: aromatase inhibitors (letrozole, anastrozole); off-label
  • Limitation: 25–34% recur within 12 months of stopping hormonal therapy; 11–19% have no pain reduction with hormonal medications[8]

D. Interventional therapies​

  • Trigger point injections of saline, local anesthetic, steroid or opioid, alone or combined, are recommended by ACOG to improve pain and function in myofascial CPP (Level B); botulinum toxin has a separate, uncertain evidence base; for protocols see Myofascial Pelvic Pain[1][2]
  • Pudendal nerve blocks. Diagnostic and sometimes therapeutic; 29/31 patients in one uncontrolled CT-guided series reported a positive response at six weeks.[15]
  • Sacral neuromodulation. Emerging evidence for refractory IC/BPS and CPP[13]
  • Pulsed radiofrequency. Investigational or selected refractory use; reported responder proportions do not mean 95% reduction in pain intensity[15][19]
  • Ovarian vein embolization. An option for symptomatic ovarian or pelvic vein reflux after assessment for venous outflow obstruction.[21][22]

E. Surgical therapies​

Women:

  • Laparoscopic excision of endometriosis when hormonal therapies are ineffective or contraindicated; about 25% have recurrent pain even after hysterectomy[8][36]
  • Hysterectomy. Consider for treatment-resistant endometriosis when future pregnancy is not desired, with excision of visible endometriosis lesions; refractory adenomyosis is a separate uterine indication. Preserve normal ovaries when feasible, particularly before menopause.[8][36][3] Before surgery for CPP, explore pain beliefs and treatment expectations, then counsel about the rationale, uncertain outcomes, and the possibility of unchanged or worse pain (SOGC Guideline 445, Recommendation 16; strong recommendation, moderate-certainty evidence).[52]
  • Laparoscopic adhesiolysis. ACOG recommends against routine use solely for CPP (Level A), citing no benefit over diagnostic laparoscopy and potential harms including bowel injury, but notes that bowel stricture or dense adhesions tethering the uterus may support targeted lysis.[1][30] In a Cochrane review of women with CPP without an identifiable cause, pain outcomes for adhesiolysis came from one 43-woman trial and remained uncertain at 3, 6, and 12 months; adverse events were inadequately reported.[7]
  • LUNA and presacral neurectomy are not routine treatments for nonspecific CPP: ACOG finds limited evidence for either, a large RCT found no improvement in pain scores or quality of life after LUNA, and most presacral neurectomy studies enrolled patients with dysmenorrhea; disease-specific indications and risks require separate assessment[1][30]
  • Pudendal nerve decompression. Refractory pudendal neuralgia after failed conservative or interventional therapy; open transgluteal, transischiorectal, and transperineal approaches exist alongside a laparoscopic transperitoneal approach (see Laparoscopic Pudendal Nerve Decompression for technique and outcomes)[15][16]

Men:

  • The 2025 AUA male CPP guideline builds care around non-surgical, multimodal therapy[32][39]
  • Prostate surgery is not offered to relieve pain: the guideline states that clinicians should not perform radical prostatectomy or BPH outlet procedures for pelvic pain, though these may be discussed within multimodal care for coexisting prostate cancer or bladder outlet obstruction . It also advises against long-term oral glucocorticoids .[39]
  • CSCP procedures. Diagnostic spermatic cord or ilioinguinal block may be used for isolated unilateral CSCP .[48] Microsurgical denervation of the spermatic cord may be offered, especially after a favorable cord-block response .[49] Vasectomy reversal for post-vasectomy pain, epididymectomy for focal epididymal pain after conservative treatment fails, and inguinal orchiectomy with removal of the entire cord for refractory CSCP after a relieving spermatic cord block are selected options ; these are distinct from prostate surgery for CP/CPPS.[48][49] See Chronic Scrotal Content Pain and Microdenervation of the Spermatic Cord for the full workup and operative detail.

F. AUA male CPP guideline (2025) — multimodal pathway[4][28][32]​

The guideline supports shared decisions across modalities, not a fixed sequence. Alpha-blockers address voiding symptoms; for CP/CPPS with voiding symptoms from BPH or prostate enlargement on imaging or PSA, AUA also permits a 5-alpha-reductase inhibitor .[39] Anti-inflammatories may supplement multimodal care.[39] Daily tadalafil, selected neuropathic medicines and phytotherapeutics are conditional options. For men with pelvic-floor or abdominopelvic muscle myalgia, manual therapy is a Conditional Recommendation, Grade C (Statement 29); EMG biofeedback for increased resting tone is Expert Opinion (Statement 30).[32] CBT can be added. In patients with CP/CPPS, clinicians should discuss low-intensity shockwave therapy .[32] For CP/CPPS, lifestyle change may be discussed (Grade C); anti-inflammatories, daily tadalafil and phytotherapeutics may be prescribed (Grade B); CBT may be offered as an adjunct (Grade C); and TENS and acupuncture may be offered (Grade B).[32] These are Conditional Recommendations (Statements 17, 20–25, 27–28).[32][39]

AUA advises against repeated antimicrobial courses with negative urine cultures, negative STI tests, or after vasectomy .[39] It permits one 10-day antimicrobial trial for antibiotic-naive CSCP .[39] EAU differs for initial treatment: it strongly recommends a quinolone or tetracycline for at least six weeks in treatment-naïve primary prostate pain syndrome lasting less than one year, while emphasizing avoidance of unnecessary antibiotics, local resistance patterns and a change in strategy after one unsuccessful six-week course.[38] EAU notes that culture, leukocyte and antibody findings do not predict response and that the trials showed only modest effects, mostly below clinical significance.[38][39]

G. EAU 2026 chronic pelvic pain guideline (limited update, March 2026)[38]​

EAU builds care around a biopsychosocial model, multimodal treatment and early multidisciplinary involvement. Strengths below are EAU's own.

  • General (strong): take a full history and exclude a treatable cause; assess functional, emotional, behavioral and sexual effects early; and refer for pain-focused psychological treatment when distress is significant. EAU weakly recommends screening patients with symptoms suggestive of chronic primary pelvic pain syndrome for abuse without implying that abuse causes the pain.[38]
  • Primary prostate pain syndrome. Offer multimodal, phenotypically directed treatment (weak). Use an alpha blocker (strong) or a quinolone or tetracycline for at least 6 weeks (strong) when PPPS has lasted under 1 year. Offer acupuncture (strong), high-dose oral pentosan polysulfate (weak) with a baseline retinal examination within six months of starting treatment and periodic examinations during long-term use for dose-associated pigmentary maculopathy, and NSAIDs with attention to long-term side effects (weak).[56][57] Evidence levels: alpha blockers, antimicrobials, NSAIDs, phytotherapy and acupuncture 1a; pregabalin not effective (1b); botulinum toxin into the pelvic floor or prostate may have a modest effect (2b); posterior tibial nerve stimulation probably effective (1b); shock wave therapy probably effective over the short term (1b). EAU does not recommend 5-ARIs for PPPS in general, and finds insufficient data for bladder neck incision, TURP or radical prostatectomy for PPPS.[38]
  • Pelvic floor. Apply myofascial treatment as first-line therapy (weak) and offer biofeedback as an adjunct in anal pain with an overactive pelvic floor (strong).[38] Actively look for myofascial trigger points (weak); no accepted standard defines them. For trigger point release, EAU finds it neither supported nor refuted that needling beats placebo, and finds no evidence that manual techniques beat no treatment.
  • Pudendal neuralgia. Use standard neuropathic pain approaches (strong). If a peripheral nerve syndrome is suspected, refer early to an expert in a multidisciplinary team (weak).
  • Mesh. Refer every patient with complications after mesh insertion to a multidisciplinary service that includes pain medicine and surgery (strong).[38]
  • Gynecologic. Involve a gynecologist for hormonal therapy or surgery in well-defined disease (strong), and use a multidisciplinary approach in persistent disease (strong).

Gabapentinoid caution: GaPP2 randomized 306 women with CPP and no obvious pelvic pathology; gabapentin did not improve worst or average pain versus placebo at 13–16 weeks, and serious adverse events were more frequent (7% versus 2%).[37]

Part VI — Special Topics​

Chronic overlapping pain conditions (COPCs)​

CPP frequently coexists with other chronic pain syndromes, reflecting shared central-sensitization mechanisms:[2][5][6]

  • Fibromyalgia
  • IBS
  • IC/BPS
  • Chronic fatigue syndrome
  • Migraine / tension headaches
  • Temporomandibular disorders
  • Vulvodynia

Multiple COPCs prompt assessment of nociplastic mechanisms and broader rehabilitation, sleep and psychological needs.[2][5] Assess treatable peripheral causes.[2][5]

Vestibulodynia — cotton-swab test and clock-face mapping​

The bedside diagnostic test for provoked vestibulodynia (PVD) is cotton-swab palpation: with the patient adequately exposed, a moistened swab is touched to the vestibular mucosa in a clock-face pattern while the patient rates pain 0–10 at each position and the examiner notes erythema and visible gland ostia. A 2023 review describes localized provoked vestibular pain as usually posterior, around 5–7 o’clock.[53] Posterior-only vestibular tenderness prompts separate examination of the hymenal ring and pelvic-floor muscles; among 72 women with posterior-only tenderness in a 113-woman insertional-dyspareunia cohort, 37 had a constricting hymenal ring and the remaining 35 were classified as a hypertonic-tenderness subgroup.[51] Provoked, spontaneous, and mixed pain describe the relationship to contact.[44] Localized PVD refractory to conservative and medical management is the indication for vestibulectomy.

Vestibulodynia — UPDATe results posted in 2026​

The completed UPDATe trial randomized 209 participants to nortriptyline, topical lidocaine/estradiol, both, or matched placebos. The registry’s week-16 primary pain analyses used 170 participants with paired data and found no significant difference across groups for tampon-test pain (p = 0.3630) or SF-MPQ change (p = 0.9859).[40]

Sex-specific differences​

WomenMen
Prevalence15–26%[3]Prostatitis symptoms 2.2–14.2% (definition-dependent)[38]
Most common causesIBS, IC/BPS, endometriosis, myofascialCP/CPPS, IC/BPS, myofascial
Hormonal contributionMajor (endometriosis, adenomyosis, cyclic pain)Minor
Musculoskeletal / pelvic-floor findingsMusculoskeletal pain or dysfunction in 50–90% of women with CPP[2]Pelvic-floor myalgia or tenderness in 27–64% of men with CP/CPPS[4]
Phenotyping toolBiopsychosocial frameworkUPOINT(S) system
Surgical optionsEndometriosis excision, hysterectomy (refractory)CP/CPPS: usually nonsurgical; no prostate surgery solely for pain. CSCP: selected cord denervation, vasectomy reversal, epididymectomy or inguinal orchiectomy[39][49]
Psychological burdenDepression 12–33%; trauma history common[1]Depression, anxiety, panic disorder elevated[39]

Key Principles​

  • CPP is a syndrome, not a single disease. Most patients have multiple contributing conditions[2][3]
  • Central sensitization is the unifying mechanism explaining pain persistence, COPC overlap, and poor response to organ-specific treatment alone[2]
  • Musculoskeletal pain or dysfunction is reported in 50–90% of women evaluated at specialized CPP centers, and pelvic-floor myalgia or tenderness in 27–64% of men with CP/CPPS. Myofascial dysfunction is often overlooked[2][4]
  • Biopsychosocial, multimodal, interdisciplinary treatment is needed[1][2]
  • Multimodal physical therapy reduced pain immediately after treatment in women with CPP without a defined pathology (7 RCTs, 476 women; SMD −1.69 versus inert or nonconservative comparators; high certainty). Benefit at 12–36 weeks after treatment had moderate certainty (5 RCTs, 381 women; SMD −1.82).[31]
  • Opioids are not recommended for routine use in CPP.[1][2][38][39] ACOG recommends against them in women and advises weaning those already taking them (Level B); the AUA male CPP guideline leaves opioids out of its analgesic statement and advises that patients with chronic pain syndromes be referred to pain physicians rather than receive opioids from urologists[1][2][38][39]
  • Hormonal therapy with combined oral contraceptives or progestin-only options is first-line for endometriosis-related pain in symptomatic premenopausal women not currently seeking pregnancy[8]
  • Alpha-blockers should be offered for CP/CPPS with voiding symptoms .[4][32]
  • Avoid repeated empirical antibiotics in CP/CPPS or CSCP with negative urine cultures, negative STI tests, or after vasectomy ; the CSCP single-trial exception and EAU initial-course position are discussed above.[28][39]
  • Routine adhesiolysis is not recommended (ACOG Level A)[1]; pelvic denervation is not a routine treatment for nonspecific CPP[1][30]
  • Pelvic congestion syndrome may account for up to 30% of CPP in women but remains controversial[20]; ACOG considers the evidence insufficient to confirm causation[1]

See Also​

Podcasts​

Update Series (2026) Lesson 27: Case-Based Discussion of the Male Chronic Pelvic Pain Guideline
AUAUniversity Podcast, Ep. 387 (2026)
cme.auanet.org
Chronic Pelvic Pain: Evaluation & Treatment Options
BackTable OBGYN, Ep. 94 (2025) · Aakriti R. Carrubba, Mark Hoffman
backtable.com
Pelvic Pain Syndromes: Clinical Assessment & Strategies
BackTable Urology, Ep. 291 (2026) · Susan MacDonald, George Koch
backtable.com

Videos​

Trigger Point Injections for Chronic Pelvic Pain
OBGYN Academy (2023)

References​

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