Don’t dismiss dysmenorrhea! : PAIN (original) (raw)
With the recent publication of three excellent studies, one in this issue [15], and two previously [13,14], our pain community may, at last, have reached a tipping point regarding primary dysmenorrhea, which is painful menstruation in the absence of pathology. Together, the studies reveal important differences between the brains of otherwise healthy women with moderate-to-severe dysmenorrhea and those of women without it. These differences exist in activity induced by noxious skin stimulation (fMRI; [15]), cerebral metabolism (fluoro-deoxyglucose positron emission tomography; [13]), and cerebral structure (voxel-based morphometry; [14]). Some differences occur not only during the menstrual phase but also in other parts of the cycle, when dysmenorrheic women do not experience menstrual pain. Furthermore, the effects are greater the longer the duration of dysmenorrhea. Although the three studies report different patterns of effects in many brain regions, including those associated with pain, the three outcome measures permit interesting comparisons. For example, Vincent and colleagues [15] showed that the posterior cingulate cortex (PCC) is activated by noxious thermal arm and abdominal skin stimulation, in both non-dysmenorrheic and dysmenorrheic women who experience the same levels of induced pain (lower temperatures used for dysmenorrheic women). However, the dysmenorrheic woman’s PCC has a larger gray-matter volume [14] and does not exhibit the reduction in metabolic activity during the menstrual phase [13] that occurs in non-dysmenorrheic women. Together the findings demonstrate significant changes in how the PCC—which is an area associated with “contextualizing” pain and that exhibits abnormalities in chronic pain [16]—functions in dysmenorrheic compared with non-dysmenorrheic women.
These profound effects support previous data indicating that the impact of dysmenorrhea can extend across the cycle to times when women are not experiencing dysmenorrhea. This impact manifests as increased muscle and visceral sensitivity and as an extension of increased pain sensitivity into body regions outside the uterine referral area [1,2,7]. Of particular interest is that dysmenorrheic women, compared with non-dysmenorrheic women, have a suppressed HPA axis (reduced cortisol) that worsens with symptom duration [15]. Furthermore, dysmenorrheic women report reduced physical, but importantly not mental, quality of life [15], and concomitantly reduce their voluntary physical activity [3]. Thus, despite being a cyclical pain condition, dysmenorrhea clearly fulfills criteria for a chronic pain condition.
Gynecologists acknowledge that “dysmenorrhea is an extremely common and sometimes debilitating condition,” and that best practice is “a multidisciplinary approach…to limit the impact on daily living” [9]. Indeed, 25% of women and up to 90% of adolescent girls worldwide suffer from dysmenorrhea, of whom 15–20% report it as severe or distressing [4,6,10]. Dysmenorrhea also co-occurs with many other chronic pain conditions [12], raising the question whether dysmenorrhea underlies or predisposes women to these other painful conditions.
The answer to this question is unknown. Despite its high prevalence and impact, dysmenorrhea has been virtually ignored by the pain community. PubMed and ScienceDirect searches (4th April 2011) using either “dysmenorrhea” or “pain” (separate searches), showed that only ∼0.1% of “pain” papers dealt with dysmenorrhea (4511/459,762 in PubMed; 6103/669,859 in ScienceDirect). Although ∼0.1% is a surprisingly small percentage, more astonishing were results of a search of pain journals. The NCBI lists 48 “pain” journals, of which 32 are indexed in PubMed, eight in ScienceDirect. In PubMed, only 42 of the 4511 dysmenorrhea papers were published in pain journals; in ScienceDirect, only 166 of the 6103 were published in pain journals. Among pain journals, however, Pain was the runaway winner: 18 papers in PubMed, 90 papers in ScienceDirect.1 Not surprisingly, most dysmenorrhea papers were published in gynecology journals: 12 such journals published 2968 of the 6103 (ScienceDirect).
Consistent with this paucity of published studies (both overall and by pain researchers) is current research effort. NIH RePorter reveals that, while 2988 grants in the USA received funds for “pain” research, only 15 have been funded for research that includes dysmenorrhea: 0.5% of pain research.2 Furthermore, in an informal survey, four lead investigators with knowledge of seven current epidemiological studies concerning chronic pain in the USA and Europe told us that, in all studies, only limited information on dysmenorrhea is collected (severity and/or duration is not included), and that the dysmenorrhea information has not been analyzed or reported.
This situation is appalling, considering the evidence that moderate-to-severe dysmenorrhea not only has a serious and chronic impact on quality of life, but also, as one colleague suggested, is likely “a harbinger of more pain to come later in life.” Furthermore, and importantly, treating dysmenorrhea can reduce pain associated with other co-morbid conditions such as irritable bowel syndrome and urinary calculosis [8].
What might account for the surprising lack of attention to dysmenorrhea? One possibility is that dysmenorrhea is so common that it often goes unreported, as if dysmenorrhea is a “normal” condition unworthy of a report. Another possibility, however, relates to cultural and religious attitudes towards “menstruation” and its associated pain and distress (premenstrual syndrome, premenstrual dysphoric disorder [5,10,11]).3 As a result of these attitudes, in much of the 20th century, menstruation was virtually a “taboo” subject, and in the 1970–1980s was considered by some to be a significant cause of negative opinions regarding women’s abilities to be leaders and their “appropriate” roles in society [5].
Times, however, have changed. Whereas in the mid-20th century, menstruation was often called “the curse,” today most women younger than 35 (informally surveyed by the authors) never heard of the term and do not consider menstruation or dysmenorrhea taboo subjects. Our times, however, should change further. It is time for our pain community, like the gynecology community, to give moderate-to-severe dysmenorrhea its rightful place as an unfortunately-common chronic pain condition. Thus, we should tackle dysmenorrhea vigorously with basic and clinical research, incorporate dysmenorrhea into our epidemiological studies (particularly longitudinal ones), and, like any chronic pain condition, treat dysmenorrhea aggressively as early as possible—without diminishing in any way the status of the individuals (i.e., women) who suffer from it.
Conflict of interest statement
The authors have no conflicts of interest to report.
References
[1]. Bajaj P, Bajaj P, Madsen H, Arendt-Nielsen L. A comparison of modality-specific somatosensory changes during menstruation in dysmenorrheic and nondysmenorrheic women. Clin J Pain. 2002;18:180-190.
[2]. Brinkert W, Dimcevski G, Arendt-Nielsen L, Drewes AM, Wilder-Smith OH. Dysmenorrhoea is associated with hypersensitivity in the sigmoid colon and rectum. Pain. 2007;132:S46-S51.
[3]. Chantler I, Mitchell D, Fuller A. Actigraphy quantifies reduced voluntary physical activity in women with primary dysmenorrhea. J Pain. 2009;10:38-46.
[4]. Davis AR, Westhoff CL. Primary dysmenorrhea in adolescent girls and treatment with oral contraceptives. J Pediatr Adolesc Gynecol. 2001;14:3-8.
[5]. Delaney J, Lupton MJ, Toth E., 1988. The curse, revised ed. University of Illinois Press, Chicago, 334pp.
[6]. Durain D. Primary dysmenorrhea: assessment and management update. J Midwifery Womens Health. 2004;49:520-528.
[7]. Giamberardino MA, Berkley KJ, Iezzi S, de Bigontina P, Vecchiet L. Pain threshold variations in somatic wall tissues as a function of menstrual cycle, segmental site and tissue depth in non-dysmenorrheic women, dysmenorrheic women and men. Pain. 1997;71:187-197.
[8]. Giamberardino MA, Costantini R, Affaitati G, Fabrizio A, Lapenna D, Tafuri E, Mezzetti A. Viscero-visceral hyperalgesia: characterization in different clinical models. Pain. 2010;151:307-322.
[9]. Lefebvre G, Pinsonneault O. SOGS clinical practice guideline. December JGC, December, 2005, No. 169. Available from: http://www.sogc.org/jogc/documents/cpd_abstract_jogc-dec-05.pdf.
[10]. Rapkin AJ, Winer SA. Premenstrual syndrome and premenstrual dysphoric disorder: quality of life and burden of illness. Expert Rev Pharmacoecon Outcomes Res. 2009;9:157-170.
[11]. Steiner M, Peer M, Palova E, Freeman EW, Macdougall M, Soares CN. The Premenstrual Symptoms Screening Tool revised for adolescents (PSST-A): prevalence of severe PMS and premenstrual dysphoric disorder in adolescents. Arch Womens Ment Health. 2011;14:77-81.
[12]. Stratton P, Berkley KJ. Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications. Hum Reprod Update. 2011;17:327-346.
[13]. Tu CH, Niddam DM, Chao HT, Liu RS, Hwang RJ, Yeh TC, Hsieh JC. Abnormal cerebral metabolism during menstrual pain in primary dysmenorrhea. Neuroimage. 2009;47:28-35.
[14]. Tu CH, Niddam DM, Chao HT, Chen LF, Chen YS, Wu YT, Yeh TC, Lirng JF, Hsieh JC. Brain morphological changes associated with cyclic menstrual pain. Pain. 2010;150:462-468.
[15]. Vincent K, Warnaby C, Stagg CJ, Moore J, Kennedy S, Tracey I. Dysmenorrhoea is associated with central changes in otherwise healthy women. Pain. 2011;152:1966-1975.
[16]. Weissman-Fogel I, Moayedi M, Tenenbaum HC, Goldberg MB, Freeman BV, Davis KD. Abnormal cortical activity in patients with temporomandibular disorder evoked by cognitive and emotional tasks. Pain. 2011;152:384-396.
1We do not know the reason for the different search result numbers.
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2If we expand the search to include endometriosis pain (which is mainly dysmenorrhea), then the percent for dysmenorrhea increases to 1.3% (38 grants). For comparison, 17.5% of funded pain grants concern cancer pain, and 3.3% concern fibromyalgia pain.
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3In Christian and Jewish faiths, the passage Genesis 3:13 has been interpreted as God’s punishment of women for Eve’s sin of having eaten from the tree of knowledge. The passage refers to pain in childbirth, but has been extended by some religious denominations to menstruation.
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