Background & Aims

Primary dysmenorrhea (PD) is menstrual pain with no identified pathology, affecting 71.1% of girls and women [1]. Menstrual pain is a risk factor for chronic pain [2, 3], but the factors associated with this transition are still poorly understood [4]. Central sensitization of pain may play a role in this process, and extant research in adolescents with PD has demonstrated heightened pain sensitivity [5] and alterations in structural and functional connectivity of brain networks [6]) compared with non-PD populations. Emerging research also shows that individuals with PD display sensitivity to non-pain (e.g., visual, auditory, tactile, and visceral) sensory modalities, known as multisensory sensitivity (MSS) [7-11], which has been shown to predict the development of pelvic pain [10]. The purpose of this study was to explore the relationship of MSS in adolescents with and without PD to menstrual pain severity and widespread pain [12] over 12 months.

Methods

One hundred forty-one adolescent girls (ages 13-19; mean age 17.2 years; SD 1.9) completed self-report measures of menstrual pain severity using a 0 (none) to 10 (worst pain possible) numeric rating scale (NRS) [13, 14] and indicated the presence of pain in body locations (over the prior month when not menstruating) using a body map [12] at baseline and monthly for 12 months. MSS was assessed with the Sensory Hypersensitivity Scale (SHS) [15], which was completed at baseline. The SHS is a 25-item measure assessing sensitivity related to allergies, heat, cold, light, pain, smell, hearing, taste, and touch.

Results

We ran a 3-way linear mixed model assessing the predictive value of time, menstrual pain, and SHS score on the number of endorsed body map locations. There were no significant differences in menstrual pain levels at baseline between those who showed no increase in menstrual pain (M = 5.40) and those who had increased menstrual pain (M = 5.40), t(123.87) = 1.086, p = 0.2792, over the study period. Within this model, there was a significant main effect of SHS score on number of body map locations (? = 2.159, t(159.186) = 2.720, p= 0.007). Additionally, for girls whose menstrual pain increased over the study period, high SHS scores were associated with increased endorsement of body map pain locations over the study period (? = 0.287, t(125.468) = 2.308, p = 0.022).

Conclusions

These data demonstrate that higher SHS scores predict an overall greater number of body map pain locations over 12 months, regardless of whether menstrual pain increased or did not increase. However, for those with increasing levels of menstrual pain, higher SHS scores were associated with increased endorsement of body pain locations. Taken together, these data suggest that MSS is an important factor affecting the trajectory of body pain, independent of the trajectory of menstrual pain, in adolescents with varying levels of PD. MSS could reflect a greater overall sensitization of the central nervous system and may represent a phenotype at risk for chronic pain.

References

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Presenting Author

Laura Payne

Poster Authors

Laura Payne

PhD

McLean Hospital/Harvard Medical School

Lead Author

Ariel Handy

PhD

McLean Hospital

Lead Author

Laura Seidman

BS

McLean Hospital

Lead Author

Robert Edwards

PhD

Brigham & Women's Hospital/Harvard Medical School

Lead Author

Topics

  • Specific Pain Conditions/Pain in Specific Populations: Abdominal and Pelvic Pain