Menstrual Pain and Visual Sensitivity Are Related to Different Neural Mechanisms in Adolescent Girls

A substantial body of evidence exists demonstrating central pain mechanisms involved in the experience of menstrual pain. Yet, the neurobiological underpinnings are not yet known and have not yet been studied in adolescents. Further, no study has investigated the relationship of menstrual pain to non-physical pain (i.e., noxious visual stimuli) and examined brain connectivity in networks commonly associated with pain. Forty-six adolescent girls (ages 14 to 18) completed a 6-min resting state MRI scan and then completed a visual sensitivity task involving viewing a blue and yellow checkerboard stimulus. Visual unpleasantness ratings and self-reported average menstrual pain ratings were collected. Thirty-five resting-state networks was estimated using a multivariate data-driven method for group Independent Component Analysis (GICA). Cingulo-opercular (CN), prefrontal salience (pfSN) and default mode (DMN) networks were selected as a priori, as they are often associated with pain. Using dual regression approach, we extracted subject-specific network maps corresponding to each a priori network. Statistical models were analyzed using Randomise in FSL to investigate the association of menstrual pain and visual sensitivity scores with the connectivity of these networks. Menstrual pain was negatively associated with connectivity of wide-spread prefrontal areas within the DMN, thalamus, insula, and striatum. In contrast, visual sensitivity was positively associated with connectivity of the medial temporal subnetwork of the DMN. These data suggest that different pain experiences may result from unique neural mechanisms. For visual sensitivity, increased connectivity of medial temporal lobe DMN regions with anterior DMN may be a mechanism in which affective experience of noxious stimuli is linked with self-reported pain. For menstrual pain, dysregulated connectivity within the DMN and between the DMN and pain-related regions might lead to impaired regulation of other pain constructs and put some individuals at risk for chronic pain. Grant support from NIH/NICHD R01 HD093680.