European journal of pain : EJP
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Spinal cord injury (SCI) results in the development of chronic pain that is refractory to conventional treatment. Progesterone, a neuroprotective steroid, may offer a promising perspective in pain modulation after central injury. Here, we explore the impact of progesterone administration on the post-injury inflammatory cascade involving the enzymes cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) at the spinal cord level. We also analyse pain behaviours, the profile of glial cell activation, and IκB-α mRNA levels, as an index of NF-κB transactivation. ⋯ Our results suggest that progesterone, by modulating early neuroinflammatory events triggered after SCI, may represent a useful strategy to prevent the development of central chronic pain.
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Annexin 1, a glucocorticoid (GC)-inducible protein, can play an important role via formyl peptide receptor like 1 (FPR2/ALX, also known as FPRL1) in inflammatory pain modulation. The aim of this review is to analyze different lines of evidence for the role of ANXA1 with different mechanisms on inflammatory pain and describe the profile of ANXA1 as a potential analgesic. A Medline (PUBMED) search using the terms 'Annexin 1 distribution OR expression, FPR2/ALX distribution OR expression, Annexin 1 AND pain, Annexin 1 AND FPR2/ALX AND pain' was performed. ⋯ The antinociception of ANXA1 has been evaluated in diverse pain models. It has been suggested that ANXA1 may exerts its action via: (1) inhibiting vital cytokines involved in pain transmission, (2) inhibiting neutrophil accumulation through preventing transendothelial migration via an interaction with formyl peptide receptors, (3) facilitating tonic opioid release from neutrophil in inflammatory site, (4) interrupting the peripheral nociceptive transmission by suppressing neuronal excitability. In general, ANXA1 is a potential mediator for anti-nociception and the role with its receptor constitute attractive targets for developing anesthesia and analgesic drugs, and their interaction may prove to be a useful strategy to treat inflammatory pain.
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High-frequency electrical stimulation (HFS) of the human forearm evokes analgesia to blunt pressure in the ipsilateral forehead, consistent with descending ipsilateral inhibitory pain modulation. The aim of the current study was to further delineate pain modulation processes evoked by HFS by examining sensory changes in the arm and forehead; investigating the effects of HFS on nociceptive blink reflexes elicited by supraorbital electrical stimulation; and assessing effects of counter-irritation (electrically evoked pain at the HFS-conditioned site in the forearm) on nociceptive blink reflexes before and after HFS. ⋯ These findings suggest that HFS concurrently triggers hemilateral inhibitory and facilitatory influences on nociceptive processing over and above more general effects of counter-irritation. The inhibitory influence may help limit the spread of sensitization in central nociceptive pathways.
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Treating bone cancer pain continues to be a major clinical challenge, and the underlying mechanisms of bone cancer pain remain elusive. Protease-activated receptor 2 (PAR2) has been reported to be involved in neurogenic inflammation, nociceptive pain and hyperalgesia. Here, we investigated the role of PAR2 in bone cancer pain development. ⋯ These findings suggest that PAR2 may be a key mediator for peripheral sensitization of bone cancer pain. Inhibiting PAR2 activation, especially during the early phase, may be a new therapy for preventing/suppressing development of bone cancer pain.
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Randomized Controlled Trial
Cognitive exposure versus avoidance in patients with chronic pain: Adherence matters.
Behavioural exposure methods can reduce pain-avoidance behaviours, but outcomes vary. One possible explanation is that patients employ cognitive (experiential) avoidance during behavioural exposure. If so, reducing cognitive avoidance during behavioural exposure should help. One option is interoceptive exposure (IE), which involves sustained exposure (via attention) to pain sensations. In order to test if IE could improve outcomes from behavioural exposure, this study with mixed chronic pain patients compared outcomes from a cognitive behavioural therapy (CBT) pain management programme incorporating either IE or distraction from pain. ⋯ The addition of IE to behavioural exposure did not improve outcomes. However, higher adherence to either attentional strategy was associated with larger effect sizes on all measures, suggesting factors shared by the two treatments could have contributed to the outcomes. Taken as a whole, the results suggest that increasing adherence to treatment strategies, possibly by motivational measures, would improve the overall outcomes of these interventions.