Pain
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The acid sensing ion channel 3 (ASIC3) is critical for the development of secondary hyperalgesia as measured by mechanical stimulation of the paw following muscle insult. We designed experiments to test whether ASIC3 was necessary for the development of both primary and secondary mechanical hyperalgesia that develops after joint inflammation. We used ASIC3 -/- mice and examined the primary (response to tweezers) and secondary hyperalgesia (von-Frey filaments) that develops after joint inflammation comparing to ASIC3 +/+ mice. ⋯ ASIC3 was found, however, in synoviocytes of the knee joint of uninflamed mice. In ASIC3 +/+ mice with joint inflammation, ASIC3 co-localized with PGP 9.5 or CGRP in joint afferents innervating the synovium. We conclude that the decreased pH that occurs after inflammation would activate ASIC3 on primary afferent fibers innervating the knee joint, increasing the input to the spinal cord resulting in central sensitization manifested behaviorally as secondary hyperalgesia of the paw.
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Given the high prevalence of depression in individuals with chronic pain and the negative outcomes associated with such comorbidity, the importance of assessing depressive symptoms is widely acknowledged by chronic pain specialists. The BDI-II is a commonly employed measure of depressive symptomatology at pain centres; however, little is known about its psychometric properties in this population. This study evaluated factorial validity, internal consistency, and gender invariance of the BDI-II in 481 patients with chronic pain. ⋯ Overall, results support the construct validity and internal consistency of the BDI-II for assessing depressive symptoms in both women and men with chronic pain. Results support the appropriateness of computing a total score and/or subscale scores. These results impact chronic pain researchers and clinicians, particularly given current trends toward empirically supported assessment.
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In previous studies we demonstrated that protein kinase D1 (PKD1/PKCmu) could directly phosphorylate the transient receptor potential V1 (TRPV1) at its N-terminal region and enhance the function of TRPV1 in CHO cells stably transfected with TRPV1. In the current study we assessed the involvement of PKD1 in pain modulation and explored the possible interaction between PKD1 and TRPV1 in rat inflammatory heat hypersensitivity. PKD1 was translocated to cytoplasmic membrane fraction and was trans-phosphorylated only in membrane fraction but not in cytoplasmic fraction of dorsal root ganglia (DRG) at 2 and 6h after Complete Freund's Adjuvant (CFA) treatment. ⋯ The average magnitude of the peak inward current evoked by capsaicin was greater in the DRG overexpressing PKD1 than in those expressing DN-PKD1. Furthermore, overexpressed PKD1 could up regulate, whereas PKD1 antisense could knock down TRPV1 content in DRG through posttranscriptional regulation manner. We concluded that PKD1 in DRG, through interaction with TRPV1, is involved in developing and maintaining inflammatory heat hypersensitivity.
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Randomized controlled trials and meta-analyses provide evidence for the efficacy of cognitive-behaviourally informed treatment (CBT) programmes for chronic pain. The current study aims to provide practice-based evidence for the effectiveness of CBT in routine clinical settings. Over a 10-year period 1013 pain patients were accepted into a 4 week in-patient pain management programme. ⋯ There was also evidence that a small percentage of patients (1-2%) reliably deteriorated during the period of treatment. The limitations in the inferences that can be drawn from this study and of the methodology are discussed. A case is made for the application of benchmarking methods using data from RCTs in order to more fully evaluate practice and to generate better quality practice based evidence.