Association between dysmenorrhea and chronic pain: a systematic review and meta-analysis of population-based studies.

OBJECTIVE: The objective of the study was to synthesize the epidemiological findings for the associations between dysmenorrhea, including primary dysmenorrhea and endometriosis-associated dysmenorrhea and any chronic pain conditions, including chronic pelvic pain, and chronic nonpelvic pain. DATA SOURCES: The data sources included PubMed, Embase, and CINAHL from inception to December 2019. STUDY ELIGIBILITY CRITERIA: The study criteria included observational population-based studies in which the relationship between dysmenorrhea and the presence or severity of chronic pain was examined. STUDY APPRAISAL AND SYNTHESIS METHODS: Each study was double coded and evaluated for bias based on the modified Newcastle and Ottawa Scale. Random-effect meta-analyses were conducted to quantify the associations between dysmenorrhea and the presence of chronic pelvic and nonpelvic pain. RESULTS: Out of 9452 records, 32 studies were included, with 14 reporting associations between dysmenorrhea and chronic pelvic pain, and 20 for dysmenorrhea and chronic nonpelvic pain. Primary dysmenorrhea and endometriosis-associated dysmenorrhea were examined in 7 studies, respectively. More than 30% of the studies were categorized as poor quality, 56% as moderate, and 12.5% as high. Dysmenorrhea was positively associated with both the presence and severity of chronic pelvic and nonpelvic pain conditions. Based on 6689 women from 8 studies, those with chronic pelvic pain had 2.43 (95% confidence interval, 1.98-2.99, I2, 42%) times the odds of having dysmenorrhea compared with those without. Based on 3750 women from 11 studies, those with chronic nonpelvic pain had 2.62 (95% confidence interval, 1.84-3.72, I2, 72%) times the odds of having dysmenorrhea compared with those without. Overall, dysmenorrhea was associated with 2.50 (95% confidence interval, 2.02-3.10) times the odds of chronic pain, which did not differ by chronic pelvic vs chronic nonpelvic pain, community vs clinical populations, or different geographical regions. CONCLUSIONS: Dysmenorrhea may be a general risk factor for chronic pain, although whether primary dysmenorrhea increases the risk for chronic pain is unclear. Given that adolescence is a sensitive period for neurodevelopment, elucidating the role of primary dysmenorrhea in pain chronicity in future longitudinal studies is important for preventing both chronic pelvic and nonpelvic pain.

Dysmenorrhea catastrophizing and functional impairment in female pelvic pain.

Background: Dysmenorrhea is suggested to increase the risk of chronic pain by enhancing central sensitization. However, little is known about whether emotional and cognitive responses induced by dysmenorrhea contribute to chronic pain interference. This study examined the association between catastrophizing specific to dysmenorrhea and both dysmenorrhea and chronic pelvic pain (CPP)-associated pain interference. Methods: Women (N = 104) receiving care for CPP through a tertiary gynecological pain clinic between 2017 and 2020 were recruited. They completed the Pain Catastrophizing Scale, the Brief Pain Inventory-pain interference, and a separate questionnaire regarding dysmenorrhea symptoms and treatment preceding the development of CPP. Dysmenorrhea catastrophizing and interference measures were developed and tested for internal consistency and construct validity. Multiple linear regression models examined dysmenorrhea catastrophizing in association with dysmenorrhea interference and CPP-associated pain interference. Results: Dysmenorrhea catastrophizing and interference measures demonstrated excellent internal consistency (Cronbach's Alpha = 0.93 and 0.92 respectively) and evidence of construct validity (correlated with dysmenorrhea severity and treatment, Ps < 0.01). Dysmenorrhea catastrophizing was moderately correlated with pain catastrophizing (ρ = 0.30, P = 0.003), and was associated with greater dysmenorrhea interference (P < 0.001) and CPP-associated pain interference (P = 0.032) accounting for general pain catastrophizing and other outcome-specific confounders. Dysmenorrhea intensity was most predictive of dysmenorrhea catastrophizing. Conclusion: Among our clinical sample of women with CPP, dysmenorrhea catastrophizing was associated with greater dysmenorrhea interference and subsequent CPP-associated pain interference. More research is needed to determine whether reduction in dysmenorrhea catastrophizing leads to reduced pain interference associated with female pelvic pain.