Pain
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Controlled Clinical Trial
Oral opioid use alters DNIC but not cold pain perception in patients with chronic pain - new perspective of opioid-induced hyperalgesia.
Opioids can elicit unexpected changes in pain sensitivity, known as opioid-induced hyperalgesia (OIH). The aim of this study was to explore whether OIH exists in patients with chronic pain treated with oral opioids (OP) versus non-opioid (NOP) analgesics. The sensitivity to cold pain and the magnitude of diffuse noxious inhibitory control (DNIC) were evaluated in 73 OP and 37 NOP treated patients. ⋯ A regression analysis showed that opioid dosage and treatment duration had a significant negative effect on the magnitude of DNIC in OP treated men (beta=-2.175, p=0.036 and beta=-2.061, p=0.047, respectively). In conclusion, oral opioids usage for the treatment of chronic pain does not result in abnormal sensitivity to cold pain, but seems to alter pain modulation. The use of 'advanced' psychophysics tests such as evaluation of DNIC can help understanding the phenomenon of OIH.
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A prognostic approach to defining chronic pain has been proposed as an alternative to traditional definitions based on retrospective duration of pain. While this new approach performs well in low back pain (LBP), headache and orofacial pain, it is not known whether it translates to regional pain syndromes with an underlying pathological component, such as osteoarthritis (OA). We investigated the performance of this approach in a population-based cohort of older adults reporting knee pain, with a spectrum of radiographic knee OA. 676 adults (50 years+) attended a research clinic and were followed up at 18 months and 3 years. ⋯ The derived cut-points suggested a lower threshold for each of the risk groups than the previous LBP work. This prognostic approach to defining chronic pain appears to translate well to knee pain. Different cut-points for defining risk groups may be needed for different pain syndromes.
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Previous research supports the fear-avoidance model in explaining the transition from acute to chronic non-specific musculoskeletal pain. However, there is still little knowledge on when this vicious circle of pain, disability, pain catastrophizing and fear of movement starts. We performed a daily diary study in 42 patients with acute whiplash injury. ⋯ We also examined the reverse association, that is, whether the changes in pain predict changes in the next day's fear of movement and pain catastrophizing. Although for the fear of movement the model reached significance, the amount of explained variance was negligible. In conclusion, this study provides evidence that already in the early stages of whiplash-related complaints, significant associations between fear of movement and pain intensity and disability occur, and that this association may be predictive of the persistence of pain.
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Both trait anger-in (managing anger through suppression) and anger-out (managing anger through direct expression) are related to pain responsiveness, but only anger-out effects involve opioid mechanisms. Preliminary work suggested that the effects of anger-out on postoperative analgesic requirements were moderated by the A118G single nucleotide polymorphism of the mu opioid receptor gene. This study further explored these potential genotypexphenotype interactions as they impact acute pain sensitivity. ⋯ No genetic moderation was observed for anger-in, although significant main effects on MPQ-Affective ratings were noted (p<.005). Anger-in main effects were due to overlap with negative affect, but anger-outxA118G interactions were not, suggesting unique effects of expressive anger regulation. Results support opioid-related genotypexphenotype interactions involving trait anger-out.