PAIN REGULATORY SYSTEM DYSFUNCTION IN CHRONIC PAIN

点击翻译按钮获取中文摘要

Elevated resting blood pressure (BP) is consistently related to diminished acute pain sensitivity. Ibis cardIovascular-related antinociception (mediated in part by endogenous opioids) is an important component of adaptation to pain in healthy individuals. it is unknown whether these antinociceptive mechanisms operate normally in chronic pain patients. Previous research indicates deficits in endogenous opioid levels in chronic pain patients, although little is known about the functional impact (e.g., diminished analgesia) of these deficits. Given the mediating role of endogenous opioids in cardiovascular-related antinociception and likely opioid deficits in chronic pain conditions, it is hypothesized that chronic pain patients will display alterations in these normally adaptive cardiovascular-pain regulatory relationships. The long-term objective of these studies is to explore the nature of dysfunction in the endogenous pain regulatory systems of chronic pain patients. improved understanding of the mechanisms contributing to chronic pain has the potential to lead to improved treatment for chronic pain patients. The specific aims of these studies are threefold: 1) examine the relationship between resting blood pressure and acute pain sensitivity in both neuropathic and nociceptive chronic pain patients as contrasted to normals, 2) examine possible differences in degree of endogenous opioid mediation of the relationship between resting blood pressure and acute pain sensitivity across the pain patient and normal control subgroups, and 3) examine whether endogenous opioid dysfunction in chronic pain is progressive and therefore related to pain duration. Sixty chronic pain patients (study l=neuropathic back pain, study 2=nociceptive back pain) and 60 healthy controls will undergo a laboratory ischemic pain stimulus once under placebo and once under opioid blockade with naloxone (randomized, counterbalanced order). in both sessions, resting BP will be determined at baseline. Pain patients will also rate their clinical pain before and after drug administration. it is expected that controls will display significant negative correlations between resting BP and acute pain sensitivity, which is at least partially eliminated by naloxone. Pain patients are expected to demonstrate no correlation or a positive correlation between resting BP and acute pain responsiveness, and will be unresponsive to opioid blockade. Greater pain duration is expected to be associated with smaller changes in the BP/pain relationship in response to opioid blockade.