Pain
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Histone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). ⋯ The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain.
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Emerging evidence suggests that perceived injustice is a risk factor for adverse outcomes associated with chronic pain. To date, however, the processes by which perceived injustice impacts on pain outcomes remain speculative. Evidence from several lines of research suggests that anger may mediate the relationship between injustice and pain outcomes. ⋯ Hierarchical regression analyses indicated that anger variables completely mediated the relationship between perceived injustice and pain intensity, and partially mediated the relationship between perceived injustice and depressive symptoms. Anger did not mediate the relationship between perceived injustice and self-reported disability. The Discussion addresses the theoretical and clinical implications of the findings.
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Chronic widespread pain (CWP) is a complex condition characterized by central hyperexcitability and altered descending control of nociception. However, nociceptive input from deep tissues is suggested to be an important drive. N-Acylethanolamines (NAEs) are endogenous lipid mediators involved in regulation of inflammation and pain. ⋯ This is the first study demonstrating that CNSP and CWP differ in levels of NAEs in response to a low-force exercise which induces pain. Increases in pain intensity as a consequence of low-force exercise were associated with low levels of PEA and SEA in CNSP and CWP. These results indicate that PEA and SEA have antinociceptive roles in humans.
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Review Meta Analysis
Relationship between quantitative sensory testing and pain or disability in people with spinal pain-A systematic review and meta-analysis.
Sensitization of the nervous system can present as pain hypersensitivity that may contribute to clinical pain. In spinal pain, however, the relationship between sensory hypersensitivity and clinical pain remains unclear. This systematic review examined the relationship between pain sensitivity measured via quantitative sensory testing (QST) and self-reported pain or pain-related disability in people with spinal pain. ⋯ Fair correlations were found for the relationship between pain intensity and thermal temporal summation (0.26, 95% CI: 0.09 to 0.42) or pain tolerance (-0.30, 95% CI: -0.45 to -0.13), but only a few studies were available. Our study indicates either that pain threshold is a poor marker of central sensitization or that sensitization does not play a major role in patients' reporting of pain and disability. Future research prospects are discussed.