Pain
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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.
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Peripheral nerve injury causes neuropathic pain including mechanical allodynia and thermal hyperalgesia due to central and peripheral sensitization. Spontaneous ectopic discharges derived from dorsal root ganglion (DRG) neurons and from the sites of injury are a key factor in the initiation of this sensitization. Numerous studies have focused primarily on DRG neurons; however, the injured axons themselves likely play an equally important role. ⋯ The function of these accumulated channels was verified by local application of ZD7288, a specific HCN blocker, which significantly suppressed the ectopic discharges from injured nerve fibers with no effect on impulse conduction. Moreover, mechanical allodynia, but not thermal hyperalgesia, was relieved significantly by ZD7288. These results suggest that axonal HCN channel accumulation plays an important role in ectopic discharges from injured spinal nerves and contributes to the development of mechanical allodynia in neuropathic pain rats.
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When faced with the problem of pain one can attempt a solution aimed at relief (assimilation) or a solution aimed at acceptance (accommodation). Using this dual process model of adaptation to pain, this study compares acute and chronic pain patients on their approach to problem solving. Three hundred and sixty-four patients were recruited from clinical settings, 303 with chronic pain and 61 with acute pain, and completed a range of measures of both affect and pain-related behavior, including the Pain Solutions Questionnaire. ⋯ Only in the case of catastrophic thinking about pain was it found that the effects of assimilative coping were moderated by pain duration. For chronic pain patients, catastrophic thinking about pain was greater when assimilative coping was higher. These results are discussed within the context of a goal directed motivational model of adaptation to chronic pain.
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Chronic pain is often associated with reduced tactile acuity. A relationship exists between pain intensity, tactile acuity and cortical reorganisation. When pain resolves, tactile function improves and cortical organisation normalises. ⋯ Pain and TPD were lower after the discrimination phase [mean (95% CI) effect size for pain VAS = 27 mm (14-40 mm) and for TPD = 5.7 mm (2.9-8. ), p < 0.015 for both]. These gains were maintained at three-month follow-up. We conclude that tactile stimulation can decrease pain and increase tactile acuity when patients are required to discriminate between the type and location of tactile stimuli.