Pain
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The experience of pain in humans is modulated by endogenous opioids, but it is largely unknown how the opioid system adapts to chronic pain states. Animal models of chronic pain point to upregulation of opioid receptors (OpR) in the brain, with unknown functional significance. We sought evidence for a similar relationship between chronic pain and OpR availability in humans. ⋯ These findings are consistent with the view that chronic pain may upregulate OpR availability to dampen pain. Finally, patients with arthritis pain, compared with healthy controls, had overall less OpR availability within the striatum specifically, consistent with the greater endogenous opioid binding that would be expected in chronic pain states. Our observational evidence points to the need for further studies to establish the causal relationship between chronic pain states and OpR adaptation.
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Surgical nerve injury sometimes leads to chronic postsurgical neuropathic pain (CPSNP). The risk factors for this condition are not well understood. We prospectively assessed 46 patients scheduled for iliac crest bone harvest, 2 days (D2) and 3 months (M3) after surgery, to determine the time course of nerve fiber degeneration and expression of the TNF-α and NGF genes in skin punch biopsies. ⋯ However, in patients with CPSNP, burning, compression, and pain provoked by brushing were correlated with IENFD at M3, suggesting a possible association between partial nerve lesions and more intense CPSNP, than with total nerve lesion. Furthermore, preoperative pain and opioid use were higher in patients who developed CPSNP than in those without CPSNP. These findings suggest that the predictors of CPSNP development are clinical rather than histological or biochemical.
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Clinical and human experimental pain studies often include so-called "healthy" controls in investigations of sensory abnormalities, using quantitative sensory testing (QST) as an outcome measure. However, the criteria for what is considered "healthy" vary among the different studies and between study centers and investigators, partly explaining the high variability of the results. Therefore, several aspects should be considered during inclusion of healthy volunteers in QST-based trials to have homogenous groups of healthy controls with less variability between human experimental studies, so that results are less likely to be false negative or false positive because of subject-related factors. ⋯ These suggestions are believed to help researchers interpret their results in comparison with others and improve the quality of clinical studies including healthy volunteers as controls or in human experimental pain studies. They aim to reduce any confounding factors. Furthermore, the acquired information will allow post hoc analyses of variance for different potential influencing factors.
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Multilevel modeling was used to examine the effects of morning pain intensity and morning positive and negative affect on pain's interference with afternoon work goal pursuit and with evening work goal progress in a community sample of 132 adults who completed a 21-day diary. The moderating effects of pain acceptance and pain catastrophizing on the associations between morning pain intensity and afternoon work goal interference were also tested. Results revealed that the positive relationship between morning pain intensity and pain's interference with work goal pursuit was significantly moderated by pain acceptance, but not by pain catastrophizing. ⋯ Thus, it appears that high pain acceptance significantly attenuates pain's capacity to disrupt work goal pursuit. Moreover, morning positive affect appears to operate as a protective factor. Additional interpretations and potential explanations for some inconsistent outcomes are discussed along with limitations, clinical implications, and suggestions for future studies.
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In the past, nocebo manipulations have been found to modulate pain perception and influence long-term habituation to pain. Recently, neural correlates accompanying this finding have been identified: habituation over days is mirrored by decreased activity in pain-processing brain areas, whereas nocebo-specific modulation specifically involves the opercular cortex. Focusing on duration and central network characteristics of nocebo information in a longitudinal heat pain paradigm, we investigated 40 healthy participants over a period of 21 consecutive days, whereof sessions on days 1, 8, 14, and 21 were performed during functional magnetic resonance imaging scanning. ⋯ Consistent with previous results, the nocebo manipulation not only modulated pain perception but also was accompanied by the activation of the operculum over an extended period of time. Importantly, the operculum exhibited changes in coupling during nociceptive input over time, as demonstrated by decreased connectivity with the basal ganglia and pinpoints differences, depending on whether a nocebo context was given. These data suggest that negative verbal suggestions prognosticating increasing pain may prevail by modulating basal ganglia-thalamocortical loops.