Pain
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Review Meta Analysis
The effect of bodily illusions on clinical pain: A systematic review and meta-analysis.
This systematic review and meta-analysis critically examined the evidence for bodily illusions to modulate pain. Six databases were searched; 2 independent reviewers completed study inclusion, risk of bias assessment, and data extraction. Included studies evaluated the effect of a bodily illusion on pain, comparing results with a control group/condition. ⋯ Conflicting results were found for virtual walking illusions (both active and inactive control comparisons). Single studies suggest no effect of resizing illusions on pain evoked by noxious stimuli, no effect of embodiment illusions, but a significant pain decrease with synchronous mirrored stroking in nonresponders to traditional mirror therapy. There is limited evidence to suggest that bodily illusions can alter pain, but some illusions, namely mirror therapy, bodily resizing, and use of functional prostheses show therapeutic promise.
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Comparative Study
Test-retest reliability of pain-related functional brain connectivity compared to pain self-report.
Test-retest reliability, or reproducibility of results over time, is poorly established for functional brain connectivity (fcMRI) during painful stimulation. As reliability informs the validity of research findings, it is imperative to examine, especially given recent emphasis on using functional neuroimaging as a tool for biomarker development. Although proposed pain neural signatures have been derived using complex, multivariate algorithms, even the reliability of less complex fcMRI findings has yet to be reported. ⋯ Intraclass correlations coefficients for VAS scores ranged from .906 to .947. Overall, self-reported pain was more reliable than fcMRI data. These results highlight that fMRI findings might be less reliable than inherently assumed and have implications for future studies proposing pain markers.
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We have recently shown that repeated exposure of the peripheral terminal of the primary afferent nociceptor to the mu-opioid receptor (MOR) agonist DAMGO ([D-Ala, N-Me-Phe, Gly-ol]-enkephalin acetate salt) induces a model of transition to chronic pain that we have termed type II hyperalgesic priming. Similar to type I hyperalgesic priming, there is a markedly prolonged response to subsequent administration of proalgesic cytokines, prototypically prostaglandin E2 (PGE2). However, type II hyperalgesic priming differs from type I in being rapidly induced, protein kinase A (PKA), rather than PKCε dependent, not reversed by a protein translation inhibitor, occurring in female as well as in male rats, and isolectin B4-negative neuron dependent. ⋯ In this study, we demonstrate that priming induced by repeated exposure to this A1-adenosine receptor agonist shares the same mechanisms, as MOR-agonist induced priming. However, the prolongation of PGE2 hyperalgesia induced by repeated administration of CPA depends on G-protein αi subunit activation, differently from DAMGO-induced type II priming, in which it depends on the β/γ subunit. These data implicate a novel form of Gi-protein signaling pathway in the type II hyperalgesic priming induced by repeated administration of an agonist at A1-adenosine receptor to the peripheral terminal of the nociceptor.