Articles: hyperalgesia.
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Pro-inflammatory cytokine production after nociceptive stimuli is pivotal for hyperalgesia. As macrophage migration inhibitory factor (MIF), a pleiotropic cytokine produced mainly by nonneuronal tissue, has been involved in the regulation of neuronal functions, herein we examined the role for MIF in formalin-induced inflammatory pain model. MIF critically contributed to nociceptive behaviors following formalin injection. ⋯ Mechanistic studies revealed that MIF upregulated the expression of the spinal NMDA receptor subunit NR2B via the MAPK signaling pathway. Moreover, microglial cells were found to be the major source of spinal MIF after formalin administration by fluorescence colocalization. These data highlight spinal MIF plays a critical role in the pathogenesis of formalin-induced inflammatory pain and suggest MIF may be a potential target for therapy of such pathological condition.
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Animal models for mechanical pressure or heat nociception usually only measure the threshold response latency. In this study, the effect of typical sensitising treatments on the lasting nocifensive behaviour elicited after a supra-threshold heating stimulus - the hyperpathic component of hypernociception - was assessed. Male Wistar rats received either intra-plantar (i.pl.) injection of 350ng PGE(2) (50microL) or topical application (t.a.) of 100% dimethylsulfoxide (DMSO), and 10mM capsaicin. ⋯ Capsaicin neonatal treatment (CNT) (50mg/kg) reduced the sensitisation induced by DMSO and capsaicin (P<0.01), but not that induced by PGE(2). These data suggest that the heat-induced lasting nociception is probably conveyed by Aeth nociceptors, and PGE(2) seems to be more selective to induce this phenomenon than the thermal threshold lowering. In addition, this hyperpathic effect induced by DMSO and capsaicin seems to be indirectly mediated by PGE(2) and C-fibres.
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Following spinal cord injury (SCI), individuals lose normal sensation and often develop debilitating neuropathic pain. Basic research has helped to elucidate many of the underlying mechanisms, but unanswered questions remain concerning how sensation changes after SCI and potential negative consequences of regenerative therapies. Mouse models provide an opportunity to explore these questions using genetic markers and manipulations. ⋯ On the trunk, mechanical and pin prick testing revealed diminished sensitivity at and below the injury level, while responses above the level of the injury were unchanged. The contrast in injury severity threshold for thermal and mechanical hypersensitivity in the hind paws suggests that these responses have different underlying mechanisms. These results establish essential baseline information for murine studies of pain and changes in sensation after SCI.
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Case Reports
Clinical course of pain in a patient with neuropathic pain induced by ligation of an intercostal nerve.
A patient with severe right chest pain and mechanical allodynia induced by an intercostal drainage tube to his chest is presented. It was not relieved by treatment with diclofenac sodium and was worsened by movement and touch to the right chest wall. Mechanical allodynia was also present. The patient's wrenching pain disappeared immediately after stitch removal, but the dull pain and mechanical allodynia persisted, gradually decreasing to zero in 7 days.
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To compare a central analgesic mechanism known as diffuse noxious inhibitory controls (DNIC) using somatic test stimuli and somatic conditioning stimuli, (CS) in irritable bowel syndrome (IBS) patients and healthy controls. ⋯ These data demonstrate deficient DNIC in IBS. This is the first study to adequately control for alternative explanations of pain reduction during counterirritation. Only by controlling for nonspecific effects can evidence of deficient DNIC be attributed to dysregulation in endogenous analgesic mechanisms.