Pain
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Age differences in the experience of chronic pain remain unclear. A serious barrier to progress in the field of pain and aging arises from the lack of data regarding the psychometric properties of pain scales for use with the elderly. The present study was designed to assess age differences in pain intensity and quality and to compare the psychometric properties of the McGill Pain Questionnaire (MPQ) in young and elderly chronic pain patients. ⋯ Finally, the latent structure, internal consistency, and pattern of subscale correlations of the MPQ were very similar in the young and elderly groups. Possible explanations for the discrepancy in the pattern of age differences on measures of pain intensity and quality are explored. The implications of this pattern of age differences for basic pain mechanisms and pain management should be given serious empirical attention.
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Injury to peripheral nerves often produces non-physiological, long-lasting spontaneous pain, hyperalgesia and allodynia that are refractory to standard treatment and often insensitive to opioids, such as morphine. Recent studies demonstrate spinal glial activation and increased proinflammatory cytokines in animal models of neuropathic pain. When these data are considered together, a unifying hypothesis emerges which implicates a role of central neuroimmune processes in the etiology of neuronal and behavioral hypersensitivity. ⋯ These findings directly correlated with the ability of propentofylline to inhibit glial activation and enhanced spinal proinflammatory cytokines following peripheral nerve injury. These findings along with our earlier observations of an anti-allodynic activity of propentofylline using the identical animal model of mononeuropathy supports the concept that modulation of glial and neuroimmune activation may be potential therapeutic targets to treat or prevent neuropathic pain. Further, restoration of the analgesic activity of morphine by propentofylline treatment suggests that increased glial activity and proinflammatory cytokine responses may account for the decreased analgesic efficacy of morphine observed in the treatment of neuropathic pain.
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A patient's readiness to adopt a self-management approach to pain has been suggested as a construct that may explain differences among patients in coping, adjustment, and response to multidisciplinary pain treatment. The pain stages of change questionnaire (PSOCQ; Pain, 72 (1997) 227) was designed to assess four components of this construct. ⋯ The findings supported the first hypothesis and provided mixed support for the second. The implications of the findings for understanding the readiness to self-manage pain construct and the validity of the PSOCQ for assessing this construct are discussed.
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Randomized Controlled Trial Comparative Study Clinical Trial
Negative affect: effects on an evaluative measure of human pain.
Prior work indicates that exposure to fear-inducing shock inhibits finger-withdrawal to radiant heat in humans (hypoalgesia), whereas anxiety induced by threat of shock enhances reactivity (hyperalgesia; Pain 84 (2000) 65-75). Although finger-withdrawal latencies are thought to reflect changes in pain sensitivity, additional measures of pain are needed to determine whether pain perception is altered. The present study examined the impact of negative affect on visual analog scale (VAS) ratings of fixed duration thermal stimuli. ⋯ Results suggest that both negative affect manipulations reduced pain. Manipulation checks indicated that the emotion-induction treatments induced similar levels of fear but with different arousal levels. Potential mechanisms for affect induced changes in pain are discussed.
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Comparative Study
Intramuscular injection of tumor necrosis factor-alpha induces muscle hyperalgesia in rats.
The role of proinflammatory cytokines in neuropathic and inflammatory pain is well established. Recent studies suggest that cytokines such as tumor necrosis factor-alpha (TNF) may also be involved in the development of muscle pain. To investigate the pathophysiology of intramuscular TNF, exogenous TNF (0.1-10 microg), formalin (9%) or vehicle was injected into the gastrocnemius or biceps brachii muscles of rats. ⋯ TNF and formalin evoked intramuscular upregulation of CGRP and NGF, whereas PGE2 was increased exclusively after TNF injection. These findings allow us to speculate that endogenous TNF may play a role in the development of muscle hyperalgesia. Targeting proinflammatory cytokines might be beneficial for the treatment of musculoskeletal pain syndromes.