Period pain
Period or menstrual pain is also referred to as dysmenorrhoea, and is usually further classified as primary (no evidence of pathology) or secondary (linked to pathology such as endometriosis). Menstrual pain affects about 60% of women who are menstruating [6], although up to 90% of adolescents can be affected [2]. For a proportion (estimate 2-28%), their pain is severe and distressing with a negative impact on many aspects of life, including missing school/work, reduced physical activity, disrupted sleep and reduced quality of life [5].
Why were we interested in menstrual pain?
We were interested in putting menstrual pain severity under the spotlight, because of the association with other painful conditions like low back pain, fibromyalgia, and irritable bowel syndrome, as well as with psychological conditions [5]. We wanted to try and understand the interactions between menstrual pain severity and tissue sensitivity and examine if musculoskeletal pain explained some of the association.
So what do we know about menstrual pain and tissue sensitivity?
In females with severe menstrual pain, heightened tissue sensitivity in response to different stimuli (pressure, pinch, thermal) is found locally (in the low abdomen/low back) and at sites distant from typical pain referral sites [4]. Sensitivity changes that occur in viscera and in deep tissues like muscles are evident around menses, but also across the menstrual cycle [4].
What about other factors?
Factors that can predispose to menstrual pain or dysmenorrhea include: low body mass index, earlier menarche (< 12 years), longer menstrual cycles, heavy menstrual flow, premenstrual syndrome, sterilisation, clinically suspected pelvic inflammatory disease, and psychological symptoms [5]. Associations between primary dysmenorrhea and women’s age, parity, oral contraceptive use, stress levels and family history are also reported, while the role of modifiable factors including cigarette smoking, diet, obesity, depression, and sexual abuse are less clear [5].
Our study
We tested the association between menstrual pain severity and measures of cold and pressure pain sensitivity, adjusting for potential confounding variables (number of musculoskeletal pain sites, oral contraceptive use, smoking, physical activity, body mass index, psychological distress, and sleep) [8].
Methodology
We used a cross-sectional design to look at the association between menstrual pain severity and sensitivity to pressure and cold stimuli in a community sample of young women (n=432) from the Western Australian Pregnancy Cohort (Raine) Study. This community sample was a good size and captured a representative group of young females making the findings more generalizable.
Menstrual pain severity and oral contraception use and data about multisite pain and other potentially confounding variables of interest were measured from questionnaires already planned for collection at age 20 and 22 year follow ups.
A visual analog scale (VAS; range from 0 (none) to 10 (unbearable)) was used to measure menstrual pain severity at both 20 and 22 years over the 3-year period, with three groups created: 1) no pain/mild pain (VAS 0-3), 2) at least moderate pain at a minimum of one of the two time points (hereafter named ‘mixed’, 3) severe pain (VAS 8-10).
We extended the data capture by using standardised quantitative sensory testing (QST) protocols that allowed us to measure sensitivity to cold and pressure [1]. Pain threshold for cold sensitivity was tested at the wrist (dorsum) and for pressure sensitivity at four sites (wrist, the trapezius muscle along the neck, the low back and the lower leg).
What we found
Severe and ‘mixed’ menstrual pain were positively associated with heightened cold pain sensitivity (distant from menstrual pain referral site) and pressure pain sensitivity (local to menstrual pain referral site). These associations remained after adjusting for all covariates including multisite musculoskeletal pain.
Severe menstrual pain was significantly associated with a predicted cold pain threshold of 7.8 °C (95 % CI 3.1-12.4 °C) lower (i.e.; perceiving cold pain sooner or at a higher temperature) among those with severe pain and 4.3 °C (1.7-7.0 °C) lower among those with mixed pain, compared to the females with no pain or mild pain.
Severe menstrual pain and mixed pain were associated with lower pressure pain thresholds (i.e. more pressure sensitive) at the lumbar spine (severe: -135.6 kPa (-206.1, -65.1); mixed: -61.7 kPa (-100.3, -23.0)).
What it means
We propose that severe menstrual pain may provide a sufficient viscero-visceral/viscero-somatic nociceptive input of a cyclic nature that effectively ‘primes’ the nervous system [3]. We speculate that this ‘priming’ may translate as biologic stress. Prolonged stress can alter central regulatory systems such as the HPA-axis with resultant dysfunction, including blunted cortisol responses [7]. Such dysfunction can trigger a cytokine-mediated sickness response, and at least partly explain the more widespread tissue sensitivity to cold and pressure (a bit like having the flu, which also activates the immune system with widespread sensitivity) and further increase susceptibility to addition nociceptive inputs.
Where to next?
We need longitudinal data to help us better understand the causal relationships underlying these associations and to establish trajectories between menstrual pain severity and other somatic pain conditions. Our data highlight the need for innovative management approaches to attenuate the negative impact of severe menstrual pain in young women.
Acknowledgements: Raine Study participants, RaineStudy Team, University of Western Australia, the Raine Medical Research Foundation, the Telethon Kids Institute, the Women’s and Infant’s Research Foundation, Curtin University, Edith Cowan University, and funding from NH&MRC, Lions Eye Institute and Safework Australia
About Helen Slater
Helen is a clinical researcher and physiotherapist at the School of Physiotherapy and Exercise Science, Curtin University. She’s interested in all things pain but especially findings ways to get evidence about pain into real world clinical settings. Along with colleagues, she researches models of care for people living with musculoskeletal pain; explores ways to use health policy to lever the best evidence into clinical practice; upskills consumers with pain and health professionals about pain; and investigates the ways in which the same clinical problem can present so differently in each individual. She acknowledges the fab team who all worked on bringing together this piece of work. She’s reckons she’s really lucky to work with lots of collegial, really smart, fun people.
References
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