Pain
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Back schools are interventions that comprise exercise and education components. We aimed to systematically review the randomized controlled trial evidence on back schools for the treatment of chronic low back pain. By searching MEDLINE, Embase, and Cochrane Central as well as bibliographies, we identified 31 studies for inclusion in our systematic review and 5 of these for inclusion in meta-analyses. ⋯ No meta-analysis was feasible for the comparison of back schools vs other active treatments. Adverse events were poorly reported so that no reliable conclusions regarding the safety of back schools can be drawn, although some limited reassurance in this regard may be derived from the fact that few adverse events and no serious adverse events were reported in the back school groups in the studies that did report on safety. Overall, the evidence base for the use of back schools to treat chronic low back pain is weak; in nearly a half-century since back schools were first trialled, no unequivocal evidence of benefit has emerged.
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Pain modulates rhythmic neuronal activity recorded by Electroencephalography (EEG) in humans. Our laboratory previously showed that rat models of acute and neuropathic pain manifest increased power in primary somatosensory cortex (S1) recorded by electrocorticography (ECoG). In this study, we hypothesized that pain increases EEG power and corticocortical coherence in different rat models of pain, whereas treatments with clinically effective analgesics reverse these changes. ⋯ Electroencephalography power is not affected by ibuprofen in the acute pain model. However, pregabalin and mexiletine reverse the changes in power and S1-PFC coherence in the inflammatory and neuropathic pain models. These data suggest that quantitative EEG might be a valuable predictor of pain and analgesia in rodents.
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Although conduction failure has been observed in nociceptive C-fibers, little is known regarding its significance or therapeutic potential. In a previous study, we demonstrated that C-fiber conduction failure, which is regarded as an intrinsic self-inhibition mechanism, was reduced in circumstances of painful diabetic neuropathy. In this study, we extend this finding in the complete Freund's adjuvant model of inflammatory pain and validate that the degree of conduction failure decreased and led to a greater amount of pain signals conveyed to the central nervous system. ⋯ ZD7288 promoted conduction failure by suppressing Ih as a mechanism to reduce the rising slope of the after-hyperpolarization potential. Moreover, perineuronal injection of ZD7288 inhibited abnormal mechanical allodynia and thermal hyperalgesia without affecting motor function or heart rate. Our data highlight the analgesic potential of local ZD7288 application and identify conduction failure as a novel target for analgesic therapeutic development.