Jamie L. Rhudy - US grants

[unreadable] DESCRIPTION (provided by applicant): Fibromyalgia syndrome (FMS) is an insidious disease that results in disability for 70% of those who suffer from it and tremendous loss of work and productivity. It is estimated that 8-12 million adults in the U.S. are affected by FMS, making it the most common chronic widespread pain syndrome. The exact mechanisms leading to the development and maintenance of fibromyalgia are unknown. But, accumulating evidence suggests abnormal nociceptive processing in the central nervous system (CNS) that could result from aberrations in supraspinal modulation. Our laboratory has developed procedures to assess supraspinal modulation of physiological and subjective nociceptive reactions (nociceptive flexion reflex, skin conductance, heart rate, pain report). A standardized picture-viewing paradigm is used to experimentally manipulate emotional valence (unpleasant, neutral, pleasant), and physiological-emotional manipulation checks verify emotional reactions. During picture-viewing, noxious electric stimuli are delivered (balanced across picture valence) and nociceptive reactions are recorded and averaged by picture valence. In healthy controls, we have shown that nociceptive reactions are reliably modulated in parallel by picture valence. Unpleasant pictures facilitate nociceptive reactions and pleasant pictures inhibit nociceptive reactions (an effect that explains 47-52% of the combined variance in the reactions). Because the nociceptive flexion reflex (a spinal reflex) is modulated, this suggests descending modulatory circuits are involved. Therefore, these procedures provide a non-invasive way to study supraspinal modulation. The present study will use the picture-viewing paradigm to study supraspinal modulation in FMS patients, rheumatoid arthritis (RA) patients, and no-pain controls. RA patients provide important controls for chronic pain history and other comorbid variables (eg, psychological distress, health/physical functioning, maladaptive coping) that could influence the emotion-pain relationship. Also, emotional factors are important in RA and FMS pain, but it is unclear whether emotion plays an equally potent role in both conditions. Further, there is limited human evidence for dysfunctional supraspinal modulation in RA, although RA is also associated with hyperalgesia. The specific aims of this study are: (1) To examine supraspinal modulation of nociceptive reactions in FMS patients and (2) To assess for hyperalgesia in FMS and RA patients. [unreadable] [unreadable] [unreadable]

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.