Pain
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This study investigated the psychometric properties of the Chronic Pain Acceptance Questionnaire (CPAQ) in a mixed chronic pain, Internet sample and sought to develop a valid and reliable short form. Questionnaires were completed by 428 respondents, comprising a sample accessed via the Internet (n=319) and a sample who completed a paper and pencil version of the measures (n=109). Using confirmatory factor analysis (CFA) the two-factor structure of the CPAQ in the Internet sample was supported, though a good model fit was only achieved following the removal of one item. ⋯ Using structural equation modelling both subscales were found to partially mediate the impact of pain severity on pain interference and emotional distress. In this model AE had stronger associations with outcomes while PW accounted for a small portion of the variance in pain interference and anxiety, but not depression. This study confirmed the two-factor structure of the CPAQ in a mixed chronic pain Internet sample and provides preliminary evidence for the psychometric soundness of the CPAQ-8.
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Mental defeat is a psychological construct that has recently been applied to characterize the experience of chronic pain. Elevated levels of mental defeat have been identified in patients with chronic pain, and while its presence distinguishes treatment seeking from non-treatment seeking individuals, the link between mental defeat and disability in chronic pain is yet to be established. The current study investigated the extent to which mental defeat is associated with pain-related interference, distress and disability. ⋯ In a series of regression analyses, mental defeat emerged as the strongest predictor of pain interference, depression and psychosocial disability, whereas catastrophizing was the best predictor of sleep interference, anxiety and functional disability. These findings suggest that mental defeat may be an important mediator of distress and disability in chronic pain. Theoretical and clinical implications are discussed.
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The involvement of the 5-HT(7) receptor in nociception and pain, particularly chronic pain (i.e., neuropathic pain), has been poorly investigated. In the present study, we examined whether the 5-HT(7) receptor participates in some modulatory control of nerve injury-evoked mechanical hypersensitivity and thermal (heat) hyperalgesia in mice. Activation of 5-HT(7) receptors by systemic administration of the selective 5-HT(7) receptor agonist AS-19 (1 and 10mg/kg) exerted a clear-cut reduction of mechanical and thermal hypersensitivities that were reversed by co-administering the selective 5-HT(7) receptor antagonist SB-258719. ⋯ The 5-HT(7) receptor co-localized with GABAergic cells in the dorsal horn of the spinal cord, suggesting that the activation of spinal inhibitory GABAergic interneurons could contribute to the analgesic effects of 5-HT(7) receptor agonists. In addition, a significant increase of 5-HT(7) receptors was found by immunohistochemistry in the ipsilateral dorsal horn of the spinal cord after nerve injury, suggesting a "pain"-triggered regulation of receptor expression. These results support the idea that the 5-HT(7) receptor subtype is involved in the control of pain and point to a new potential use of 5-HT(7) receptor agonists for the treatment of neuropathic pain.
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Randomized Controlled Trial
Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.
Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus-pituitary-adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N=20 healthy drug-free volunteers (median age 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5-13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). ⋯ Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p<.05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity.