Pain
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The purpose of this study was to examine racial/ethnic-related differences in a four-stage model of the processing of chronic pain. The subjects were 1557 chronic pain patients (White=1084, African American=473) evaluated at a pain management clinic at a large southeastern university medical center. Using an analysis of covariance controlling for pain duration and education, African American patients reported significantly higher levels of pain unpleasantness, emotional response to pain, and pain behavior, but not pain intensity than Whites. ⋯ The groups differed by approximately 1.0 visual analogue scale unit, a magnitude that may be clinically significant. Racial/ethnic differences in the linear relationship between stages were also tested using structural equation modeling and LISREL-8. The results indicate differences in linear associations between pain measures with African Americans showing a stronger link between emotions and pain behavior than Whites.
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Meta Analysis Comparative Study
Interference due to pain following spinal cord injury: important predictors and impact on quality of life.
Two studies were designed to examine important predictors of pain following spinal cord injury (SCI), and the impact of pain on self-reported quality of life (QOL). Pain was defined as "interference in day-to-day activities secondary to pain". In order to determine risk factors associated with the development of pain interference, Study 1 examined the predictive validity of multiple demographic, medical, and QOL variables at year 1 post-SCI to self-reported pain interference 2 years post-injury. ⋯ More specifically, those developing pain interference (group 2) from year 1 to year 2 reported decreased life satisfaction, physical health, and mental health, whereas, those with resolving pain interference from year 1 to year 2 reported an increase in these same domains. Unexpectedly, change in pain interference status was unrelated to change in self-reported handicap. Implications and future directions are discussed.
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Clinical Trial
The contribution of pain, reported sleep quality, and depressive symptoms to fatigue in fibromyalgia.
The major objective of this research was to evaluate the predictors of fatigue in patients with fibromyalgia (FM), using cross-sectional and daily assessment methodologies. In the cross-sectional phase of the research involving a sample of 105 FM patients, greater depression and lower sleep quality were concurrently associated with higher fatigue. While pain was correlated with fatigue, it did not independently contribute to fatigue in the regression equation. ⋯ A path analytic framework was tested with disaggregated (removing between subjects variability) data in which pain was predicted to contribute to lower sleep quality which, in turn, was predicted to lead to greater fatigue. The results revealed that poor sleep quality fully accounted for the positive relationship between pain and fatigue, thus substantiating the mediational role of sleep quality. The findings are indicative of a dysfunctional, cyclical pattern of heightened pain and non-restful sleep underlying the experience of fatigue in FM.
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Spinal antinociception produced by delta 9-tetrahydro-cannabinol (Delta(9)-THC) and other cannabinoid agonists has been suggested to be mediated by the release of dynorphin acting at the kappa opioid receptor. Alternatively, as cannabinoid receptors are distributed appropriately in the pain transmission pathway, cannabinoid agonists might act directly at the spinal level to inhibit nociception, without requiring dynorphin release. Here, these possibilities were explored using mice with a deletion of the gene encoding prodynorphin. ⋯ However, the same dose of nor-BNI used blocked U50,488H-induced antinociception in both wild-type and prodynorphin knock-out mice, confirming kappa opioid receptor activity. Pretreatment with SR141716A, a cannabinoid receptor antagonist blocked the antinociceptive actions of both WIN 55,212-2 and Delta(9)-THC. These data support the conclusion that antinociception produced by spinal cannabinoids are likely to be mediated directly through activation of cannabinoid receptors without the requirement for dynorphin release or activation of kappa opioid receptors.