Native American Pain Disparities: Exploring Nociceptive Processing Differences

描述(申请人提供)：探索伤害性加工差异7.0。项目摘要/摘要美洲原住民(Nas)的疼痛患病率高于非西班牙裔白人和其他美国少数群体。然而，NAS缺乏对疼痛的研究，在30多年的时间里只发表了28篇关于疼痛的论文。此外，还没有研究评估疼痛处理来确定疼痛敏感性(有意识的疼痛体验)、中枢敏感化(中枢神经系统中增强的疼痛信号)和/或中枢神经系统疼痛抑制(下行疼痛调制)是否导致这种差异。我们的试验数据表明，与非西班牙裔白人相比，非西班牙裔白人具有较低的疼痛敏感性(例如，较高的疼痛耐受性)，并在生理指标(即，伤害性屈曲反射的时间总和)上显示出中枢敏感度降低(中枢神经系统对疼痛的反应减少)。这表明它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。具体地说，疼痛敏感度较低可能会使NAS面临慢性疼痛的风险，因为一旦发生组织损伤，他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重复。目标1将确定与非西班牙裔白人对照组(n=120)相比，健康、无疼痛的美洲原住民(n=120)是否降低了疼痛敏感度，减少了中枢敏感化，并增强了疼痛抑制过程。测试将在两个疗程中进行，使用经过充分验证的、最先进的定量感觉测试方法来评估主观(例如，疼痛报告)和生理(伤害性屈曲反射)疼痛结果的疼痛处理。将从痛阈值、耐受性和报告对多种刺激方式(热、冷、机械压力、缺血、电刺激)的反应来综合评估疼痛敏感性。中枢敏感化将从以下几个方面进行评估：1)热痛的暂时总和(敏化的主观测量)，2)伤害性屈曲反射阈值(NFR，脊髓伤害性的生理学测量)，以及3)NFR的暂时总和(脊髓过度兴奋的生理学测量)。中枢神经系统对疼痛和NFR的抑制将从以下两个方面进行评估：1)条件性疼痛调制(即，疼痛抑制疼痛)和2)伤害性感受的情绪控制(即，愉快的情绪抑制疼痛，不愉快的情绪增强疼痛)。目标2是确定导致NAS疼痛处理改变的个体差异。因此，将对疼痛应对(例如，疼痛灾害化)、社会文化变量(例如，种族认同)和遗传(例如，血液量子水平)进行检查，以确定它们是否与疼痛的群体差异有关。这项研究预计将以至少5种方式影响少数群体的健康差异：1)确定导致NAS疼痛差异的机制，2)确定NAS中的疼痛差异是否是生理过程(如中枢神经系统疼痛抑制)造成的，3)提供证据表明NAS中的疼痛风险在生理上不同，从而确定需要量身定做的干预措施，4)提供评估NAS慢性疼痛风险的方法，以及5)促进消除NAS中疼痛差异的干预措施。

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.