Pain
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EphBs receptors and ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Ours and other studies have demonstrated that spinal ephrinBs/EphBs signaling was involved in the modulation of nociceptive information and central sensitization. However, the role of ephrinBs/EphBs signaling in peripheral sensitization is poorly understood. ⋯ EphrinB1-Fc-induced hyperalgesia is accompanied with the NMDA receptor-mediated increase of expression in peripheral and spinal phosphorylated mitogen-activated protein kinases (phospho-MAPKs) including p-p38, pERK and pJNK, and also is prevented or reversed by the inhibition of peripheral and spinal MAPKs. Furthermore, in formalin inflammation pain model, pre-inhibition of EphBs receptors by the injection of EphB1-Fc reduces pain behavior, which is accompanied by the decreased expression of peripheral p-p38, pERK and pJNK. These data provide evidence that ephrinBs may act as a prominent contributor to peripheral sensitization, and demonstrate that activation of peripheral ephrinBs/EphBs system induces hyperalgesia through a MAPKs-mediated mechanism.
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Multicenter Study
Post-trauma ratings of pre-collision pain and psychological distress predict poor outcome following acute whiplash trauma: a 12-month follow-up study.
Patients with acute whiplash trauma were followed to examine if post-trauma ratings of pre-collision pain and psychological distress were associated with reduced work capability and neck pain at 12 months follow-up. The study included 740 consecutive patients (474 females, 266 males) referred from emergency departments or primary care after car accidents in four counties in Denmark. After the collision patients received a questionnaire on psychological distress, unspecified pain and socio-demographics and 12 months later a follow-up on work capability and neck pain was performed. ⋯ In conclusion unspecified as opposed to specified pain (neck pain) before the collision is associated with poor recovery and high accumulation of pre-collision psychological distress is associated with considerable neck pain at follow-up. However, no conclusions on causality can be drawn. Personal characteristics before the collision are important for recovery and attention to pre-collision characteristics may contribute to the prevention of poor recovery after acute whiplash trauma.
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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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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.