Pain
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Randomized Controlled Trial
The Pain Course: a randomised controlled trial of a clinician-guided Internet-delivered cognitive behaviour therapy program for managing chronic pain and emotional well-being.
The present study evaluated the efficacy of a clinician-guided Internet-delivered cognitive behaviour therapy (iCBT) program, the Pain Course, to reduce disability, anxiety, and depression associated with chronic pain. Sixty-three adults with chronic pain were randomised to either a Treatment Group or waitlist Control Group. Treatment consisted of 5 iCBT-based lessons, homework tasks, additional resources, weekly e-mail or telephone contact from a Clinical Psychologist, and automated e-mails. ⋯ These outcomes were sustained at follow-up and participants rated the program as highly acceptable. Overall, the clinician spent a total mean time of 81.54 minutes (SD 30.91 minutes) contacting participants during the program. The results appear better than those reported in iCBT studies to date and provide support for the potential of clinician-guided iCBT in the treatment of disability, anxiety, and depression for people with chronic pain.
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Peripheral neuropathy is a common adverse effect of paclitaxel treatment. To analyze the contribution of transient receptor potential vanilloid 1 (TRPV1) in the development of paclitaxel-induced thermal hyperalgesia, TRPV1 expression in the rat dorsal root ganglion (DRG) was analyzed after paclitaxel treatment. Behavioral assessment using the tail-flick test showed that intraperitoneal administration of 2 and 4 mg/kg paclitaxel induced thermal hyperalgesia after days 7, 14, and 21. ⋯ TRPV1 immunostaining was up-regulated in paw skin day 14 after paclitaxel treatment. Moreover, in situ hybridization histochemistry revealed that most of the TRPV1 mRNA-labeled neurons in the DRG were small or medium in size. These results suggest that paclitaxel treatment increases TRPV1 expression in DRG neurons and may contribute to functional peripheral neuropathic pain.
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Bradykinin (BK) is an inflammatory mediator that can evoke oedema and vasodilatation, and is a potent algogen signalling via the B1 and B2 G-protein coupled receptors. In naïve skin, BK is effective via constitutively expressed B2 receptors (B2R), while B1 receptors (B1R) are purported to be upregulated by inflammation. The aim of this investigation was to optimise BK delivery to investigate the algesic effects of BK and how these are modulated by inflammation. ⋯ We have optimised a versatile experimental model by which BK and its analogues can be administered to human skin. We have found that there is an early phase of BK-induced pain which partly depends on the release of inflammatory mediators by MCs; however, subsequent hyperalgesia is not dependent on MC degranulation. In naïve skin, B2R signaling predominates, however, cutaneous inflammation results in enhanced B1R responses.