Entheseal pain of levator ani muscle: A novel etiology in chronic pelvic pain and lower urinary tract symptoms-A urodynamic perspective.

Abstract

Background: Although evidence suggests that levator ani muscle (LAM) entheseal pain is a novel etiology of chronic pelvic pain (CPP), its association with lower urinary tract symptoms (LUTS) remains underexplored. This study examined the urodynamic manifestations of LUTS in patients with LAM entheseal pain.

Methods: In this retrospective cohort, women with chronic pelvic pain (CPP) and LUTS underwent standardized palpation and were divided into three groups: an isolated LAM muscular pain, an isolated LAM entheseal pain, and a combined muscle and entheseal pain group. Between-group differences in symptom prevalence and urodynamic parameters were analyzed.

Results: A total of 307 female patients were enrolled. Enthesis-related pain groups exhibited significantly higher prevalences of urinary symptoms, including urinary frequency (muscle pain, n = 81 vs entheseal pain, n = 32 vs combined pain, n = 194: 82.7% vs 87.5% vs 85.1%, p = 0.011), residual urinary sensation (46.9% vs 65.6% vs 63.4%, p < 0.001), and painful bladder symptoms (45.7% vs 59.4% vs 61.9%, p < 0.001). Additionally, these groups demonstrated significantly higher rates of pain-related comorbidities, including bearing-down sensation (33.3% vs 37.5% vs 49.0%, p < 0.001), dysmenorrhea (22.2% vs 25.0% vs 35.1%, p < 0.001), irritable bowel syndrome (29.6% vs 32.4% vs 44.3%, p < 0.001), and systemic myofascial pain (28.4% vs 40.6% vs 52.6%, p < 0.001). However, direct comparison between isolated muscular and entheseal pain groups revealed no significant differences in LUTS or pain comorbidities, whereas combined pain group demonstrated the highest symptom prevalence. Notably, no significant intergroup differences were observed in urodynamic parameters.

Conclusion: LAM entheseal pain represents a distinct, clinically palpable entity in CPP. Its urodynamic similarity to myofascial pain suggests that LUTS reflect a shared final pathway of central sensitization rather than peripheral structural dysfunction. Moreover, its unique association with morning stiffness supports a divergent pathophysiology.