Early Menstrual Pain Impact on Multisensory Hypersensitivity

该拟议补充允许对参与者进行延长随访和分析，以获得EEG 月经初潮后关键时间点的月经数据。月经疼痛的早期轨迹 强度和长期暴露于月经疼痛对慢性盆腔疼痛（CPP）风险的影响 是未知的，尽管痛经的患病率很高。观察性研究表明， 经期疼痛和过度的一般身体症状意识是CPP的强危险因素。由于电流 CPP的治疗成功有限，针对已知风险因素的预防策略仍然是一种有效的方法。 迫切的、未满足的需求。月经疼痛或痛经本身对生活质量有深远的负面影响 对于许多女性来说，并且在10-20%的青少年中难以治疗。在青春期发育期间， 神经可塑性可以允许重复的不良感觉经历，从中度到重度的月经疼痛， 在青春期建立多感觉过敏，增加慢性疼痛的风险。然而，在这方面， 需要确定哪些月经疼痛模式造成了这种脆弱性，以及它们如何影响神经系统。 变化因此，本研究的目的1将纵向描述痛经的轨迹模式 在月经初潮后的两年内，并确定定义这些轨迹的生物心理社会因素。到 为了确定持续性痛经加重的危险因素，将对女孩进行为期两年的随访研究 月经初潮后，使用前瞻性月经症状日记沿着仔细的月经分类， 心理社会和发展因素。目的2然后将测试是否最坏的，持续性痛经 两年后，轨迹有最高的多感觉超敏反应的后续风险， 是完全成熟的CPP的前体。此外，该目的将评估多感觉超敏反应风险的变化 重复的月经疼痛是由特定的脊柱或中枢机制介导的。多感官 超敏反应将通过包括自我报告症状 清单和实验诱发反应的标准电池不同的感官刺激测试。 作为介质测试的具体机制包括前额叶和初级感觉皮层活动， 使用定量感觉的疼痛和外周压力疼痛敏感性的脑干下行调制 测试和高密度EEG方法。测量多感官的创新实验方法 超敏反应（包括用于测量内脏敏感性的非侵入性方法），同时伴有kid- 友好的大脑活动电生理测量，建立在联合研究所使用的工具上， 该团队广泛从事子宫和儿科疼痛评估。成功完成本 一个针对慢性盆腔疼痛脆弱性的发展时间轴的项目，可能会定义理想的窗口 为未来的预防性干预和完善工具，以评估内脏和多感官的敏感性。 本研究的发现对于理解急性疼痛向慢性疼痛的转变具有重要意义。

This proposed supplement allows for extended follow up and analysis of participants to obtain EEG data and menstrual data at a critical time point after menarche. The early trajectory of menstrual pain intensity and the long-term impact of repeated exposure to menstrual pain on chronic pelvic pain (CPP) risk are 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. 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 risk for chronic pain. However, which patterns of menstrual pain create this vulnerability need to be determined, and how they effect 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 biopsychosocial 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 valuable for understanding the transition from acute to chronic pain.