Although nonsteroidal antiinflammatory drugs can alleviate menstrual pain, about 18% of women with dysmenorrhea are unresponsive, leaving them and their physicians to pursue less well-studied strategies. The goal of this review is to provide a background for treating menstrual pain when first-line options fail. Research on menstrual pain and failure of similar drugs in the antiplatelet category suggested potential mechanisms underlying nonsteroidal antiinflammatory drug resistance. Based on these mechanisms, alternative options may be helpful for refractory cases. This review also identifies key pathways in need of further study to optimize menstrual pain treatment.

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OBJECTIVE To determine if women with chronic pelvic pain and variable degrees of endometriosis demonstrate altered pain sensitivity relative to pain-free healthy controls, and whether such differences are related to the presence or severity of endometriosis or comorbid pain syndromes. METHODS Four patient subgroups (endometriosis with chronic pelvic pain (n=42), endometriosis with dysmenorrhea (n=15), pain-free endometriosis (n=35), and chronic pelvic pain without endometriosis (n=22)) were each compared to 30 healthy controls in this cross-sectional study. All patients completed validated questionnaires regarding pain symptoms and underwent screening for comorbid pain disorders. Pain sensitivity was assessed by applying discrete pressure stimuli to the thumbnail using a previously validated protocol. RESULTS While adjusting for age and education, pain thresholds were lower in all subgroups of women with pelvic pain, relative to healthy controls (all p-values <0.01). There was no difference in pain thresholds when comparing endometriosis patients without pelvic pain to healthy controls (mean difference 0.02 kg/m2, 95% confidence interval -0.43, 0.47). The presence and severity of endometriosis and number of comorbid pain syndromes were not associated with a difference in pain thresholds. CONCLUSION Women with chronic pelvic pain demonstrate increased pain sensitivity at a nonpelvic site compared to healthy controls, which is independent of the presence or severity of endometriosis or comorbid pain syndromes. These findings support the notion that central pain amplification may play a role in the development of pelvic pain, and may explain why some women with pelvic pain do not respond to therapies aimed at eliminating endometriosis lesions.

Women who develop bladder pain syndrome (BPS), irritable bowel syndrome, or dyspareunia frequently have an antecedent history of dysmenorrhea. Despite the high prevalence of menstrual pain, its role in chronic pelvic pain emergence remains understudied. We systematically characterized bladder, body, and vaginal mechanical sensitivity with quantitative sensory testing in women with dysmenorrhea (DYS, n = 147), healthy controls (HCs) (n = 37), and women with BPS (n = 25). Previously, we have shown that a noninvasive, bladder-filling task identified a subset of women with both dysmenorrhea and silent bladder pain hypersensitivity, and we repeated this to subtype dysmenorrhea sufferers in this study (DYSB; n = 49). DYS, DYSB, and BPS participants had lower vaginal mechanical thresholds and reported more pain to a cold stimulus during a conditioned pain modulation task and greater pelvic examination after-pain than HCs (P's < 0.05). DYSB participants also had reduced body mechanical thresholds and less conditioned pain modulation compared to HCs and DYS participants (P's < 0.05). Comparing quantitative sensory testing results among the DYS and HC groups only, provoked bladder pain was the only significant predictor of self-reported menstrual pain (r = 0.26), bladder pain (r = 0.57), dyspareunia (r = 0.39), and bowel pain (r = 0.45). Our findings of widespread sensory sensitivity in women with dysmenorrhea and provoked bladder pain, much like that observed in chronic pain, suggest a need to study the trajectory of altered mechanisms of pain processing in preclinical silent visceral pain phenotypes to understand which features convey inexorable vs modifiable risk.

Purpose The purpose of this study was to create symptom indices – that is, scores derived from questionnaires – to accurately and efficiently measure symptoms of interstitial cystitis/bladder pain syndrome and chronic prostatitis/chronic pelvic pain syndrome, collectively referred to as urologic chronic pelvic pain syndromes (UCPPS). We created these indices empirically, by investigating the structure of symptoms using exploratory factor analysis. Materials and Methods As part of the Multi-Disciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network, participants (N = 424) completed questionnaires including the Genitourinary Pain Index (GUPI), the Interstitial Cystitis Symptom Index (ICSI), and the Interstitial Cystitis Problem Index (ICPI). Individual items from questionnaires about bladder and pain symptoms were evaluated by principal components and exploratory factor analysis to identify indices with fewer questions to comprehensively quantify symptom severity. Additional analyses included correlating symptom indices with symptoms of depression, a known comorbidity of patients with pelvic pain. Results and Conclusions Exploratory factor analyses suggested that two factors, pain severity and urinary severity, provided the best psychometric description of items contained in the GUPI, the ICSI, and the ICPI. These factors were used to create two symptom indices for pain and urinary symptoms. Pain, but not urinary symptoms, was associated with symptoms of depression in a multiple regression analysis, suggesting that these symptoms may impact patients with UCCPS differently; for pain severity, B (SE) = 0.24 (0.04), 95% CI of B = 0.16–0.32, β = 0.32, p < .001. Our results suggest that pain and urinary symptoms should be assessed separately, rather than combined into one total score. Total scores that combine the separate factors of pain and urinary symptoms into one score may be limited for clinical and research purposes.

Endometriosis may exert a profound negative influence on the lives of individuals with the disorder, adversely affecting quality of life, participation in daily and social activities, physical and sexual functioning, relationships, educational and work productivity, mental health, and well-being. Over the course of a lifetime, these daily challenges may translate into limitations in achieving life goals such as pursuing or completing educational opportunities; making career choices or advancing in a chosen career; forming stable, fulfilling relationships; or starting a family, all of which ultimately alter one's life trajectory. The potential for endometriosis to impact the life course is considerable, as symptom onset generally occurs at a time of life (menarche through menopause, adolescence through middle age) when multiple life-changing and trajectory-defining decisions are made. Using a lifecourse approach, we examine how the known effects of endometriosis on life-domain satisfaction may impact health and well-being across the life course of affected individuals. We provide a quasi-systematic, narrative review of the literature as well as expert opinion on recommendations for clinical management and future research directions.

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OBJECTIVE The factors that underlie pelvic pain are poorly understood. Specifically, the relative influence of dysmenorrhea and psychological factors in the etiology of noncyclic pelvic pain conditions, such as interstitial cystitis and irritable bowel syndrome, is unknown. To further characterize pelvic pain, we compared the frequency of menstrual, somatosensory, and psychological risk factors between women with and without severe noncyclic pelvic pain symptoms. STUDY DESIGN A total of 1012 reproductive-aged women completed a 112-item questionnaire with domains including mood, fatigue, physical activity, somatic complaint, and pain. Questionnaire items included existing items for menstrual distress and newly written items derived from qualitative interviews. The relationship of dysmenorrhea and noncyclic pelvic pain complaints (dyspareunia, dyschezia, or dysuria) was modeled using quantile regression. RESULTS Among women who menstruate regularly, those with dysmenorrhea had disproportionally more severe noncyclic pelvic pain (54/402, 13%) than women without dysmenorrhea (5/432, 1%; odds ratio, 13; 95% confidence interval, 5–33). In a multivariate-adjusted model, dysmenorrhea (β = .17), activity capability (β = .17), somatic complaint (β = .17), and bodily pain (β = .12) were the primary predictors of noncyclic pelvic pain. Depression (β = .03) and anxiety (β = .01) were not significantly predictive. The presence of dysmenorrhea, somatic complaint, and low activity capability predicted 90% of the cases of women with noncyclic pelvic pain. CONCLUSION The association between dysmenorrhea and noncyclic pelvic pain suggests that menstrual pain is an etiological factor in noncyclic pelvic pain, whereas depression and anxiety may be secondary effects. Longitudinal studies are needed to determine whether dysmenorrhea causally influences development of noncyclic pelvic pain or shares common underlying neural mechanisms.