Native American Pain Disparities: Exploring Nociceptive Processing Differences

描述（由申请人提供）：探索伤害性处理差异7.0。美洲原住民（NAs）的疼痛患病率高于非西班牙裔白人和其他美国少数民族。然而，NAs缺乏疼痛研究，30多年来只有28篇关于疼痛的论文发表。此外，没有研究评估疼痛处理，以确定疼痛敏感性（有意识的疼痛体验），中枢致敏（CNS中增强的疼痛信号）和/或CNS疼痛抑制（下行疼痛调制）是否有助于这种差异。我们的试点数据表明，相对于非西班牙裔白人，NA具有较低的疼痛敏感性（例如，更高的疼痛耐受性）并且在生理测量上显示降低的中枢致敏（降低的CNS对疼痛的反应）（即，伤害性屈曲反射的时间总和）。这表明他们的中枢神经系统对有害输入的反应不同，这可能具有重要的临床意义。具体而言，对疼痛不太敏感可能会使NA处于慢性疼痛的风险中，因为一旦发生组织损伤，它们可能难以检测和预防组织损伤和/或保护组织损伤。然而，这些试点数据的结果需要在更大的样本中复制。目的1是确定健康、无痛的美洲原住民（n=120）相对于非西班牙裔白色对照组（n= 120）是否具有降低的疼痛敏感性、降低的中枢致敏性和增强的疼痛抑制过程。测试将在两个阶段进行，使用经过充分验证的、最先进的定量感觉测试方法，从主观（例如，疼痛报告）和生理（伤害性屈曲反射）疼痛结果。疼痛敏感性将从疼痛阈值、耐受性和对多种刺激方式（热、冷、机械压力、缺血、皮肤电刺激）的反应报告进行全面评估。中枢致敏将从以下方面进行评估：1）热痛的时间总和（致敏的主观测量），2）伤害性屈曲反射阈值（NFR，脊髓伤害性感受的生理测量），和3）NFR的时间总和（脊髓过度兴奋的生理测量）。疼痛和NFR的CNS抑制将从以下方面进行评估：1）条件性疼痛调节（即，疼痛抑制疼痛）和2）伤害感受的情绪控制（即，愉快的情绪抑制疼痛，不愉快的情绪加剧疼痛）。目的2是确定个体差异，有助于改变疼痛处理的NAs。因此，疼痛应对（例如，疼痛灾难化），社会文化变量（例如，种族身份），和遗传（即，血量子水平）以确定它们是否与疼痛的组间差异有关。这项研究预计将在至少5个方面影响少数民族的健康差异：1）确定导致NAs疼痛差异的机制，2）确定NAs疼痛差异是否由生理过程（例如，CNS疼痛抑制），3）提供证据表明疼痛风险在NA中具有生理学差异，因此确定了定制干预措施的需求，4）提供评估慢性疼痛风险的NA的方法，以及5）促进干预措施以消除NA中的疼痛差异。

DESCRIPTION (provided by applicant): Exploring Nociceptive Processing Differences 7.0. Project Summary/Abstract Native Americans (NAs) have a higher prevalence of pain than non-Hispanic whites and other U.S. minority groups. Yet, there is a lack of pain research in NAs, with only 28 papers on pain published in over 30 years. Moreover, no study has assessed pain processing to identify whether pain sensitivity (conscious pain experience), central sensitization (augmented pain signaling in the CNS), and/or CNS pain inhibition (descending pain modulation) contribute to this disparity. Our pilot data indicate that relative to non-Hispanic whites, NAs have lower pain sensitivity (e.g., higher pain tolerance) and show reduced central sensitization (reduced CNS response to pain) on a physiological measure (i.e., temporal summation of the nociceptive flexion reflex). This suggests their CNS responds differently to noxious input, which could have significant clinical implications. Specifically, being less pain sensitive may place NAs at risk for chronic pain because they could have difficulty detecting and preventing tissue damage and/or protecting tissue damage once it has occurred. However, results from these pilot data need to be replicated in a larger sample. Aim 1 will be to determine whether healthy, pain-free Native Americans (n=120) have lowered pain sensitivity, reduced central sensitization, and enhanced pain inhibitory processes relative to a non-Hispanic white control group (n=120). Testing will occur across two sessions using well-validated, state-of-the-art, quantitative sensory testing methods to assess pain processing from subjective (e.g., pain report) and physiological (nociceptive flexion reflex) pain outcomes. Pain sensitivity will be comprehensively assessed from pain threshold, tolerance, and report in response to multiple stimulus modalities (heat, cold, mechanical pressure, ischemia, electrocutaneous). Central sensitization will be assessed from: 1) temporal summation of heat pain (a subjective measure of sensitization), 2) nociceptive flexion reflex threshold (NFR, a physiological measure of spinal nociception), and 3) temporal summation of NFR (a physiological measure of spinal cord hyperexcitability). CNS inhibition of pain and NFR will be assessed from: 1) conditioned pain modulation (i.e., pain inhibits pain) and 2) emotional controls of nociception (i.e., pleasant emotions inhibit pain, unpleasant emotions enhance pain). Aim 2 is to identify individual differences that contribute to altered pain processing in NAs. Thus, pain coping (e.g., pain catastrophizing), sociocultural variables (e.g., ethnic identity), and heredity (i.e., blood quantu level) will be examined to determine whether they are associated with group differences in pain. This research is expected to impact minority health disparities in at least 5 ways: 1) identify mechanisms contributing to pain disparities in NAs, 2) determine if pain disparities in NAs result from physiological processes (e.g., CNS pain inhibition), 3) provide evidence that pain risk is physiologically different in NAs thus identifying the need for tailored interventions, 4) inform methods to assess NAs at-risk for chronic pain, and 5) promote interventions to eliminate pain disparity in NAs.