The early trajectory of menstrual pain intensity and the long-term impact of repeated exposure to menstrual
pain on chronic pelvic pain (CPP) risk is unknown, despite the high prevalence of dysmenorrhea.
Observational studies implicate both heightened menstrual pain and excess general bodily symptom
awareness as strong risk factors for CPP emergence. Since current treatments for CPP have limited success,
preventative strategies, targeting known risk factors, remain an urgent, unmet need. Menstrual pain, or
dysmenorrhea, itself has a profound negative impact on quality of life for many women, and is refractory to
treatment in 10-20% of adolescents. During pubertal development, neuroplasticity could permit repeated
adverse sensory experiences from moderate-to-severe menstrual pain to establish multisensory
hypersensitivity during adolescence, increasing the future risk for development of chronic pain. However, which
patterns of menstrual pain create this vulnerability need to be determined, and how they effect such neural
changes. Therefore, Aim 1 of this study will characterize the trajectory patterns of dysmenorrhea longitudinally
over the two years post-menarche and determine the physiological and psychological factors defining these
trajectories. To determine risk factors for persistent heightened dysmenorrhea, girls will be studied for two
years of follow-up after menarche, using prospective menstrual symptom diaries along with careful cataloging
of menstrual, psychosocial and developmental factors. Aim 2 will then test whether the worst, persistent
dysmenorrhea trajectory has the highest subsequent risk for multisensory hypersensitivity two years later, as a
likely precursor to full blown CPP. Additionally, this aim will assess if change in risk of multisensory
hypersensitivity following repeated menstrual pain is mediated by specific spinal or central mechanisms.
Multisensory hypersensitivity will be measured by composite latent variable encompassing both self-reported
symptom inventories and experimentally evoked responses to a standard battery of different sensory
provocation tests. Specific mechanisms to be tested as mediators include prefrontal and primary sensory
cortex activity, brainstem descending modulation of pain and peripheral pressure pain sensitivity using
quantitative sensory testing and high-density EEG methods. The innovative experimental methods for
measuring multisensory hypersensitivity (including non-invasive methods for measuring visceral
sensitivity), with simultaneous kid-friendly electrophysiological measurements of brain activity, build
on tools used by the combined research team, that is extensively engaged in uterine and pediatric pain
assessment. Successful completion of this project, targeting the developmental timeline of chronic pelvic pain
vulnerability, likely will define ideal windows for future preventative interventions and refine tools for evaluating
visceral and multisensory sensitivity. Findings in this study will be uniquely valuable for understanding the
transition from acute to chronic pain, a major public health priority.