Native American Pain Disparities: Exploring Nociceptive Processing Differences

描述（由申请人提供）：探索伤害性加工差异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的疼痛研究缺乏，30多年来仅发表了28篇关于疼痛的论文。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），中枢敏化（CNS中增强的疼痛信号）和/或CNS疼痛抑制（下行疼痛调节）是否导致这种差异。我们的试验数据表明，相对于非西班牙裔白人，NAs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（即伤害性屈曲反射的时间累积）上表现出较低的中枢敏化（降低的中枢神经系统对疼痛的反应）。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。具体来说，较低的疼痛敏感性可能使NAs面临慢性疼痛的风险，因为它们可能难以检测和预防组织损伤和/或一旦发生组织损伤就无法保护组织损伤。然而，这些试点数据的结果需要在更大的样本中得到复制。目的1将确定与非西班牙裔白人对照组（n=120）相比，健康、无痛的美洲原住民（n=120）是否具有较低的疼痛敏感性、较低的中枢致敏性和增强的疼痛抑制过程。测试将在两个会议中进行，使用经过验证的，最先进的，定量的感觉测试方法，从主观（例如，疼痛报告）和生理（伤害性屈曲反射）疼痛结果评估疼痛处理。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）的反应进行全面评估。中枢致敏性将从以下方面进行评估：1)热痛的时间累积（致敏性的主观测量），2)伤害性屈曲反射阈值（NFR，脊髓伤害性的生理测量），以及3)NFR的时间累积（脊髓高兴奋性的生理测量）。中枢神经系统对疼痛和NFR的抑制将从以下方面进行评估：1)条件疼痛调节（即疼痛抑制疼痛）和2)伤害感受的情绪控制（即愉快情绪抑制疼痛，不愉快情绪增强疼痛）。目的2是确定导致NAs疼痛处理改变的个体差异。因此，疼痛应对（例如，疼痛灾难化）、社会文化变量（例如，种族认同）和遗传（例如，血液量水平）将被检查，以确定它们是否与疼痛的群体差异有关。本研究预计将在至少5个方面影响少数民族健康差异：1)确定导致NAs疼痛差异的机制，2)确定NAs疼痛差异是否源于生理过程（例如，中枢神经系统疼痛抑制），3)提供证据证明NAs的疼痛风险在生理上是不同的，从而确定有针对性的干预措施的必要性，4)为评估有慢性疼痛风险的NAs提供方法，5)促进消除NAs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.