Excitatory and inhibitory pain mechanisms during the menstrual cycle in healthy women (original) (raw)
Related papers
Indian journal of physiology and pharmacology
A b s t r a c t : G e n d e r d i f f e r e n c e s i n p a i n p e r c e p t i o n h a v e b e e n r e p o r t e d i n literature. However, most such studies have ignored the role of female sex hormones in influencing pain response across menstrual cycle (MC). In this study, we have investigated the variation in pain response on different days o f t h e m e n s t r u a l c y c l e . N i n e t y s u b j e c t s ( 6 0 f e m a l e s ) w e r e s u b j e c t e d t o experimental pain of cold pressor task, on days 1, 7, 14, and 21 of the MC (females), and on four consecutive Mondays of a month (males). Male subjects showed no variation in pain response. Females reported higher pain sensitivity on days 7 and 14 of MC. We suggest that experimental pain studies involving female menstruating subjects should be carried out only during a particular phase of the cycle, and this phase should be reported in literature to increase the reproducibility of the experiment.
Menstrual cycle phase does not influence gender differences in experimental pain sensitivity
European Journal of Pain, 2010
Influence of menstrual cycle phase on experimental pain sensitivity in women and on gender differences in pain sensitivity was examined in 48 men and 49 women in response to cold pressor, heat, and ischemic pain. Each woman was tested at three points in their menstrual cycle in randomized order, the early follicular, late follicular, and luteal phases, while men were also tested three times, controlling for number of days between test sessions. Cycle phase was confirmed via serum hormone levels. As expected, women were significantly more sensitive to cold pain (p < .01), to heat pain (p < .0001), and to ischemic pain (p < .01) than men. However, pain perception during each task was not influenced by the menstrual cycle in women, nor did the menstrual cycle influence the magnitude of the gender differences in pain sensitivity. These results indicate that although women are more sensitive to a variety of noxious stimuli than men, menstrual cycle phase does not appear to moderate those differences in healthy men and women.
A meta-analytic review of pain perception across the menstrual cycle
Pain, 1999
The purpose of this article is to review the sixteen published studies that examine associations between the perception of experimentally induced pain across menstrual cycle phases of healthy females. We also performed a meta-analysis to quantitatively analyze the data and attempt to draw conclusions. The results suggest that there are relatively consistent patterns in the sensitivity to painful stimulation. These patterns are similar across stimulus modality with the exception of electrical stimulation. The magnitude of the effect was approximately 0.40 across all stimulation. For pressure stimulation, cold pressor pain, thermal heat stimulation, and ischemic muscle pain, a clear pattern emerges with the follicular phase demonstrating higher thresholds than later phases. When the effect size was pooled across studies (excluding electrical) comparisons involving the follicular phase were small to moderate (periovulatory phase, d thr = 0.34; luteal phase, d thr = 0.37; premenstrual phase, d thr = 0.48). The pattern of effects was similar for tolerance measures. Electrical stimulation was different than the other stimulus modalities, showing the highest thresholds for the luteal phase. When the effect size was pooled across studies for electrical stimulation, effect sizes were small to moderate (menstrual (d thr = −0.37), follicular d thr = −0.30) periovulatory d thr = −0.61), and premenstrual d thr = 0.35) phases. This paper raises several important questions, which are yet to be answered. How much and in wha way does this menstrual cycle effect bias studies of female subjects participating in clinical trials? Furthermore, how should studies of clinical pain samples control for menstrual related differences in pain ratings and do they exist in clinical pain syndromes? What this paper does suggest is that the menstrual cycle effect on human pain perception is too large to ignore.
Menstrual Variation in Experimental Pain: Correlation with Gonadal Hormones
Neuropsychobiology, 2010
menstrual cycle with the highest thresholds on day 22, except for the cold pain thresholds, which peaked on day 14. There were no such changes regarding heat pain and all the detection thresholds. The correlations separately computed for each of the 4 days between salivary estrogen as well as testosterone on the one hand and the detection or pain thresholds on the other hand failed to show significant levels, except for the coupling of testosterone and electrical pain thresholds on day 1. Conclusions: The pain thresholds for all the physical stressors increased after menstruation. The acrophases were located in the follicular (cold pain threshold) or in the luteal phase (pressure and electrical pain thresholds). The results of our correlation analyses indicate only minimal influences of the physiological levels of gonadal hormones on pain sensitivity in women.
Annals of Behavioral Medicine, 2012
Background The menstrual cycle influences pain, with symptoms often increasing during the premenstrual (lateluteal) phase. Deficiencies in endogenous inhibition of afferent nociception at the spinal level might contribute to menstrual phase-related changes in pain. Purpose This study assessed whether conditioned pain modulation (CPM) of spinal nociception differs between mid-follicular and late-luteal phases. Methods CPM was evoked by a blood pressure cuff affixed to the right forearm and inflated to induce ischemia in 41 healthy women during both menstrual phases. Suprathreshold electric stimuli were delivered to the left sural nerve to evoke pain and the nociceptive flexion reflex (NFR) before, during, and after forearm ischemia. Results Forearm ischemia produced CPM of electrocutaneous pain and NFR, but inhibition did not differ across mid-follicular and late-luteal phases. Conclusions Mechanisms contributing to changes in experimental pain across mid-follicular and late-luteal phases in healthy women are not due to deficits in CPM of spinal nociception.
Phase and Sex Effects in Pain Perception: A Critical Review
Psychology of Women Quarterly, 1985
The psychological literature in pain perception is reviewed to clarify the influence of sex and menstrual phase on the phenomenon of pain. An attempt is made to resolve some of the discrepancies in the reported findings by taking special note of the methodological differences in the pain studies. The appropriateness of the measures of pain threshold, pain tolerance, discrimination accuracy, and of response bias to the study of pain are discussed.
Brain morphological changes associated with cyclic menstrual pain
Pain, 2010
Primary dysmenorrhea (PDM) is the most prevalent gynecological disorder for women in the reproductive age. PDM patients suffer from lower abdominal pain that starts with the onset of the menstrual flow. Prolonged nociceptive input to the central nervous system can induce functional and structural alterations throughout the nervous system. In PDM, a chronic viscero-nociceptive drive of cyclic nature, indications of central sensitization and altered brain metabolism suggest a substantial central reorganization. Previously, we hypothesized that disinhibition of orbitofrontal networks could be responsible for increased pain and negative affect in PDM. Here, we further tested this hypothesis. We used an optimized voxel-based morphometry (VBM) approach to compare total and regional gray matter (GM) increases and decreases in 32 PDM patients with 32 healthy age and menstrual cycle matched (peri-ovulatory phase) controls. Abnormal decreases were found in regions involved in pain transmission, higher level sensory processing, and affect regulation while increases were found in regions involved in pain modulation and in regulation of endocrine function. Moreover, GM changes in regions involved in top-down pain modulation and in generation of negative affect were related to the severity of the experienced PDM pain. Our results demonstrate that abnormal GM volume changes are present in PDM patients even in the absence of pain. These changes may underpin a combination of impaired pain inhibition, increased pain facilitation and increased affect. Our findings highlight that longer lasting central changes may occur not only in sustained chronic pain conditions but also in cyclic occurring pain conditions. Ó
Endogenous pain inhibition during menstrual cycle in migraine
European Journal of Pain, 2014
Background: Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. Methods: Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. Results: Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. Conclusions: Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.