Pain
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Factors underlying individual differences in pain responding are incompletely understood, but are likely to include genetic influences on basal pain sensitivity in addition to demographic characteristics such as age, sex, and ethnicity, and psychological factors including personality. This study sought to explore the relationship between personality traits and experimental pain sensitivity, and to determine to what extent the covariances between these phenotypes are mediated by common genetic and environmental factors. A sample composed of 188 twins, aged 23 to 35years, was included in the study. ⋯ In contrast, associations between HPI and personality seemed weak and unstable, but a significant effect of Angry Hostility (a facet of Neuroticism) emerged in generalized estimating equations analysis. Although the genetic correlation between these phenotypes was essentially zero, a weak but significant individual-specific environmental correlation emerged (re=.21, P<.05). Taken together, these findings suggest that CPI is more consistently related to personality dispositions than HPI, both phenotypically and genetically.
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Calcitonin gene-related peptide (CGRP) is known to play a major role in the pathogenesis of pain syndromes, in particular migraine pain. Here we focus on its implication in a rat pain model of inflammation, induced by injection of complete Freund adjuvant (CFA). The nonpeptide CGRP receptor antagonist BIBN4096BS reduces migraine pain and trigeminal neuronal activity. ⋯ The same amount of reduction occurred after topical administration onto the paw, with resulting systemic plasma concentrations in the low nanomolar range. However, spinal administration of BIBN4096BS did not modify the neuronal activity in the CFA model. Peripheral blockade of CGRP receptors by BIBN4096BS significantly alleviates inflammatory pain.
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This study investigated the effect on observer responses of the presence/absence of information about medical evidence for pain and psychosocial influences on the patient's pain experience. Additionally, the moderating role of the patient's pain expressions and the mediating role of the observer's belief in deception and evaluation of the patient was examined. Sixty-two participants were presented with videos of 4 patients, each accompanied by a vignette describing the presence or absence of both medical evidence for the pain and psychosocial influences on the patient's pain. ⋯ The results indicate that discounting pain in the absence of medical evidence may involve negative evaluation of the patient. Further, the patient's pain expression is a moderating variable, and psychosocial influences negatively impact the degree to which patients' self-reports are taken into account. The results indicate that contextual information impacts observer responses to pain.
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When painful stimuli are evaluated at the time they are experienced, judgments are made not in isolation but with reference to other experienced stimuli. We tested a specific quantitative model of how such context effects occur. Participants experienced 3 blocks of 11 different pressure pain stimuli, and rated each stimulus on a 0-10 scale of intensity. ⋯ Study 2 found that pain ratings were higher in a context where most stimuli were relatively intense, even when the mean stimulus was constant. It is suggested that pain judgments are relative, involve the same cognitive processes as are used in other psychophysical and socioemotional judgments, and are well described by range frequency theory. This approach can further inform the existing body of research on context-dependent pain evaluation.