Pain
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Cognitive-behavioral models of chronic pain hypothesize that how a person copes with pain influences how well he or she adjusts to the pain. Several measures have been developed to assess pain coping, but no studies have yet examined whether these measures are complementary or redundant. In the current study, two pain coping measures (the Chronic Pain Coping Inventory, CPCI, and the Coping Strategies Questionnaire, CSQ) were completed by a large number (N=564) of primarily male veterans referred to a chronic pain program. ⋯ The findings of this study are consistent with cognitive-behavioral models of pain. Future research will need to determine whether changes in coping responses (catastrophizing and guarding, in particular) merely reflect, or actually influence, adjustment to chronic pain. In the meantime, clinicians would be wise to give these coping responses particular attention in chronic pain programs.
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Excitotoxic spinal cord injury (SCI) causes anatomic, physiologic and molecular changes within the spinal cord and brain. Intraspinal injection of quisqualic acid (QUIS) produces an excitotoxic injury that leads to the onset of behavioral syndromes, believed to be related to the clinical condition of chronic pain. The opioid system, classically involved in the suppression of pain transmission, has been associated with the onset of pain-related behaviors and changes in spinal opioid peptide expression have been demonstrated in various models of SCI and chronic pain. ⋯ In addition, PPE expression in the anterior cingulate cortex and PPD expression in the contralateral parietal cortex were significantly higher in grooming vs. non-grooming animals. These results support previous conclusions that both spinal and supraspinal regulation of endogenous opioid peptide expression plays a role in the response to or onset of post-SCI pain. These results also suggest that the opioid peptides are regulated independently and serve different functions in response to SCI.
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Randomized Controlled Trial Clinical Trial
Heat, but not mechanical hyperalgesia, following adrenergic injections in normal human skin.
The development of adrenergic sensitivity in nociceptors has been suggested as a mechanism of neuropathic pain. We sought to determine if nociceptors in the skin of normal subjects exhibit adrenergic sensitivity. We investigated the effects of intradermal administration of norepinephrine, phenylephrine, and brimonidine on heat pain sensitivity. ⋯ In addition, occlusion of blood flow with a blood pressure cuff did not lead to heat hyperalgesia. Thus, the heat hyperalgesia observed with the adrenergic agonists is not due to a decrease in perfusion associated with the injection. These results indicate that alpha(1)- and alpha(2)-adrenoceptor-mediated mechanisms may play a role in sensitization of nociceptors to heat stimuli in normal skin.
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Clinical Trial Controlled Clinical Trial
Hyperalgesic responses in methadone maintenance patients.
Opioid substitution treatment for dependence may alter sensitivity to pain. Previous studies on pain sensitivity in methadone maintenance patients have yielded contradictory results. This study compared nociceptive responses between 16 patients on stable, once daily, doses of methadone and 16 matched control subjects. ⋯ Pain tolerance to pain detection ratios for methadone patients were significantly lower than controls for the cold pressor test at 0 and 3 h, and for electrical stimulation at 0 h only. In summary, the relative pain sensitivity of methadone maintenance patients is determined by the nature of the nociceptive stimulus (e.g. cold pressor test versus electrical stimulation), the plasma methadone concentration (trough versus peak plasma concentration), and whether thresholds are determined for detection of pain or pain tolerance. Although responding to changes in plasma methadone concentration, maintenance patients are markedly hyperalgesic to pain induced by the cold pressor test.
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Randomized Controlled Trial Clinical Trial
A cognitive-behavioral group intervention as prevention for persistent neck and back pain in a non-patient population: a randomized controlled trial.
Given the demand for interventions that may prevent the development of persistent musculoskeletal pain problems, we investigated the effects of a cognitive-behavioral program in a group of non-patients with neck or back pain symptoms. Two hundred and fifty-three people selected from a population study were invited to participate. These people had experienced four or more episodes of relatively intense spinal pain during the past year but had not been out of work more than 30 days. ⋯ Group comparisons indicated that the cognitive-behavioral group, relative to the comparison group, had significantly better results with regard to fear-avoidance beliefs, number of pain-free days, as well as the key variable of sick leave. Participation in the cognitive behavioral group reduced the risk for long-term sick leave during the follow-up by threefold. Thus, despite the strong natural recovery rate for back pain, the cognitive-behavioral intervention produced a significant preventive effect with regard to disability.