The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial
High levels of vicarious exposure bias pain judgments.
The present study evaluated the effects of exposure to facial expression of pain, on observers' perceptions of pain expression. Participants were undergraduates shown brief video clips of the facial expressions of shoulder-pain patients displaying no pain or moderate pain. Participants were randomly allocated to either a high preexposure condition in which each clip was preceded by 10 other clips showing strong pain or a no-exposure control. On each test trial, participants indicated whether they thought the person they saw was in pain or not. Data were analyzed using signal detection theory methods. High prior exposure to pain was unrelated to sensitivity to pain expression, but did significantly diminish the likelihood of judging the other to be in pain. Results are discussed in terms of their implications for pain judgments of health-care professionals, adaptation-level theory, and the psychophysical method of selective adaptation. ⋯ This paper provides an experimental demonstration that, when people have large amounts of exposure to others' expressions of pain, their estimation of others' pain is reduced. The findings offer 1 explanation for the widely observed underestimation bias in pain judgments and may suggest ways of changing it.
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Considerable evidence has linked catastrophizing to pain responses, and recent experimental pain research has suggested that situational catastrophizing, measured during or immediately after laboratory pain procedures, is strongly related to pain ratings of standardized noxious stimuli. However, given that most experimental pain protocols involve "static" assessments of pain ratings and catastrophizing at a single time point, the direction by which these factors may affect each other remains unclear. Does catastrophizing influences one's subsequent pain responses or do individual differences in the perceived severity of pain lead to differential rates of catastrophizing? Little is known regarding the course of these variables. Using a cross-lagged panel analysis, we evaluated whether changes in situation-specific catastrophizing preceded changes in laboratory-induced pain responses, or vice versa, during tonic capsaicin pain stimulation. Topical application of a 10% capsaicin cream was applied to the dorsal aspect of the nondominant hand of 38 healthy participants. Situation-specific catastrophizing and pain ratings were obtained at Early (0 to 15 minutes), Mid (15 to 30 minutes), and Final (30 to 35 minutes) periods during capsaicin pain. Analyses revealed that Early-to-Mid changes in catastrophizing ratings prospectively accounted for unique variance in subsequent Mid-to-Final changes in pain ratings, whereas Early-to-Mid changes in pain ratings did not account for unique variance in Mid-to-Final changes in catastrophizing ratings. That is, participants who showed the largest initial increases in catastrophizing reported the greatest subsequent increases in pain. Controlling for the reported change in stress did not affect this pattern of results. These findings provide empirical evidence that a situation-specific catastrophizing process might precede and contribute to subsequent increases in pain experience. Limitations of the present study and possible future research directions are discussed. ⋯ The present study adds to a growing literature on prospective associations between catastrophizing and pain. These results provide initial evidence, in healthy individuals, that changes in catastrophizing may precede changes in pain response.
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Randomized Controlled Trial
The association of single nucleotide polymorphisms in the catechol-O-methyltransferase gene and pain scores in female patients with major depressive disorder.
We tested the hypothesis that single nucleotide polymorphisms (SNPs) in the catechol-O-methyltransferase (COMT) gene are associated with baseline pain levels in patients with major depressive disorder (MDD). Pain levels were quantified using a visual analog scale (VAS) for pain. Data from 159 female and 93 male self-reported white patients with MDD were analyzed. The associations between a haplotype previously associated with pain sensitivity created using COMT SNPs rs6269, rs4633, rs4818, and rs4680, and the proportion of female patients with "Pain While Awake" and "Overall Pain" at baseline were statistically significant (P < .05). In male patients, no statistically significant associations between COMT haplotypes and baseline pain scores were seen. The rs165599 SNP, which has previously been associated with response of depressive symptoms to treatment in patients with MDD, did not impact baseline pain in either gender. In conclusion, baseline pain levels appear to be associated with the COMT pain sensitivity haplotype in female patients with MDD. ⋯ This article presents associations of the COMT pain sensitivity haplotype and baseline pain levels in female patients with MDD. This finding could potentially help clinicians who seek to assess how genetic polymorphisms may contribute to a patient's pain experience.
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Individuals with chronic craniofacial pain experience symptoms that are consistent with central sensitization. In fact, central sensitization may constitute the major disease process in these conditions, particularly if the original injury has healed or the condition is idiopathic. To understand central sensitization we have developed a conjugate of substance P and cholera toxin (SP-CTA). SP-CTA is selectively taken up by cells that express neurokinin receptors. Twenty-four hours following intracisternal administration of SP-CTA, wild-type rats and mice demonstrated signs of persistent background nociception, but when tested for facial cold sensitivity, they did not differ from controls. However, treating the SP-CTA-injected animals with naloxone exposed cold hypersensitivity in the face. Mu-opioid receptor knockout mice treated with SP-CTA demonstrated hypersensitivity without naloxone treatment. These findings suggest that central sensitization leads to activation of an endogenous opioid system. The data also demonstrate that the intracisternal administration of SP-CTA in rodents is a useful model for studying central sensitization as a disease process without having to induce a peripheral injury. ⋯ Central sensitization is a concern in many craniofacial pain conditions. In this project, we utilize a conjugate of substance P and the catalytic subunit of cholera toxin to induce central sensitization in the nucleus caudalis of rodents. The data indicate that the injected animals become hypersensitive in the face.