Primary Dysmenorrhea: Diagnosis and Therapy

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Hellman and colleagues argue that primary dysmenorrhea involves multisensory hypersensitivity and central pain processing changes, emphasizing the need for objective neurobiological features to predict risk for chronic pelvic pain conditions like endometriosis.

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This letter critiques a 2020 review on primary dysmenorrhea for overlooking neural frameworks of chronic pain, arguing that abnormal sensory function explains poor treatment responses. The authors present data showing that women with moderate-to-severe dysmenorrhea exhibit multisensory hypersensitivity and impaired conditioned pain modulation despite lacking chronic pain symptoms. They propose that these neurobiological features represent early aberrant changes in threat processing networks rather than a central sensitization syndrome affecting the majority of women. Relevance to endometriosis: The paper is centrally about endometriosis — specifically as one of several chronic pelvic pain conditions linked to dysmenorrhea where early identification may prevent pain emergence.

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As the co-directors of a clinical translational research program studying female visceral pain, we commend the Ferries-Rowe et al for the extensive update on the etiology and management of dysmenorrhea in the November 2020 issue.1 However, we also challenge both the authors and the general readership to be aware of some additional key developments in our understanding of dysmenorrhea’s mechanisms that were not captured in this review. Oddly, the pathophysiology of menstrual pain historically has not been viewed using the overarching neural framework of chronic pain. An inadequate understanding of abnormal sensory function in dysmenorrhea may explain why so many menstrual pain sufferers do not respond to nonsteroidal anti-inflammatories or hormonal suppression. While we and others have found evidence that dysmenorrhea is linked to a higher risk of developing a chronic pelvic pain syndrome, it is somewhat illogical to refer to dysmenorrhea as a central sensitization syndrome, as that would mean 40–90% of women have an abnormal physiological state.2,3 Indeed, our research shows that in general, women with moderate-to-severe dysmenorrhea, without chronic pain symptoms, still report mild levels of daily nonmenstrual pelvic pain (average 25/100). However, they do not have evidence of impaired conditioned pain modulation, an indicator of central sensitization commonly observed in chronic pain conditions.4 On deeper inspection, a fifth of such moderate-to-severe dysmenorrhea sufferers, despite being chronic-pain–free, harbor silent evidence of multisensory hypersensitivity when provoked with a simple noninvasive bladder distension task, and impaired conditioned pain modulation with quantitative sensory testing. In the absence of chronic pain symptoms, such multisensory hypersensitivity may reflect early, aberrant changes in either the threat processing networks of the cerebral cortex, or the spinal dorsal horn, ultimately found in several chronic pelvic pain conditions.5–7 The authors astutely emphasize that identifying dysmenorrhea and providing effective treatment is essential to limit chronic pelvic pain emergence, including endometriosis-associated pelvic pain and bladder pain syndromes. To be most effective, that prevention strategy will need us to further define dysmenorrhea with objective, reproducible neurobiological features that convey excessive risk for chronic pelvic painP emergence, perhaps paralleling the framework widely practiced to identify preinvasive cervical disease. Financial Disclosure Kevin Hellman disclosed that money was paid to his institution from the Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD) R01HD098193. The other author did not report any potential conflicts of interest. References - 1.Ferries-Rowe E, Corey E, Archer JS. Primary dysmenorrhea: diagnosis and therapy. Obstet Gynecol. 2020;136:1047–58. 10.1097/AOG.0000000000004096 [DOI] [PubMed] [Google Scholar] - 2.Zondervan KT, Yudkin PL, Vessey MP, Jenkinson CP, Dawes MG, Barlow DH, et al. Chronic pelvic pain in the community--symptoms, investigations, and diagnoses. Am J Obstet Gynecol. 2001;184:1149–55. 10.1067/mob.2001.112904 [DOI] [PubMed] [Google Scholar] - 3.Westling AM, Tu FF, Griffith JW, Hellman KM. The association of dysmenorrhea with noncyclic pelvic pain accounting for psychological factors. Am J Obstet Gynecol 2013;209:422.e1–422.e10. 10.1016/j.ajog.2013.08.020 [DOI] [PMC free article] [PubMed] [Google Scholar] - 4.Hellman KM, Roth GE, Dillane KE, Garrison EF, Oladosu FA, Clauw DJ, et al. Dysmenorrhea subtypes exhibit differential quantitative sensory assessment profiles. Pain 2020;161:1227–36. [DOI] [PMC free article] [PubMed] [Google Scholar] - 5.Wei S-Y, Chao H-T, Tu C-H, Li W-C, Low I, Chuang C-Y, et al. Changes in functional connectivity of pain modulatory systems in women with primary dysmenorrhea. Pain. 2016;157(1):92–102. 10.1097/j.pain.0000000000001826 [DOI] [PubMed] [Google Scholar] - 6.Vincent K, Warnaby C, Stagg CJ, Moore J, Kennedy S, Tracey I. Dysmenorrhoea is associated with central changes in otherwise healthy women. Pain 2011;152:1966–75. 10.1016/j.pain.2011.03.029 [DOI] [PubMed] [Google Scholar] - 7.Winnard KP, Dmitrieva N, Berkley KJ. Cross-organ interactions between reproductive, gastrointestinal, and urinary tracts: modulation by estrous stage and involvement of the hypogastric nerve. Am J Physiol Regul Integr Comp Physiol 2006;291:R1592–601. 10.1152/ajpregu.00455.2006 [DOI] [PubMed] [Google Scholar]

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dysmenorrhea

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Dysmenorrhea Dysmenorrhea Dysmenorrhea Dysmenorrhea Female Humans

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