Pain
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It is frequently necessary for patients to undergo multiple painful medical interventions as part of their diagnosis and care. Predictors of future pain report have yet to be established although initial pain level, affect, and memory of the procedure are often implicated. The purpose of this research was to establish a predictive model of future pain reporting using a standardized experimental pain stimulus. ⋯ An additional 13% of the variance was shared between Session 1 maximum pain intensity and remembered maximum pain intensity. The level of remembered Session 1 pain was significantly exaggerated from the initial pain report (p < or = .05) but not significantly different from the level of pain reported at Session 2. These findings provide strong evidence for a post-pain modulation phenomenon in which cognitive processes influence both pain recall and future pain reporting.
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Comparative Study
Glucocorticoid inhibition of vascular abnormalities in a tibia fracture rat model of complex regional pain syndrome type I.
Tibia fracture in rats evokes chronic hindpaw warmth, spontaneous extravasation, edema, allodynia, and periarticular bone loss, a syndrome resembling complex regional pain syndrome type I (CRPS I). Glucocorticoids such as methylprednisolone (MP) are probably effective analgesic and anti-edematous agents in patients suffering from CRPS and this study examined the effects of chronic MP treatment in the rat CRPS I model. Bilateral hindpaw thickness, temperature, and nociceptive thresholds were determined, and the hindlimb bone density was measured using dual-energy X-ray absorptiometry (DXA). ⋯ Furthermore, there was an increase in spontaneous protein extravasation and an enhanced substance P evoked extravasation and edema response in the hindpaw at 4 weeks that was inhibited by MP infusion. Glucocorticoid treatment had no effect on the allodynia, hindpaw unweighting, or the periarticular bone loss observed after tibia fracture. We postulate that post-junctional facilitation of substance P signaling contributes to the hindpaw warmth, edema, and the enhanced spontaneous protein extravasation observed in this CRPS I model, and that the anti-edematous effects of glucocorticoid treatment are due to inhibition of post-junctional neuropeptide signaling.
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Comparative Study
Synergism between paracetamol and nonsteroidal anti-inflammatory drugs in experimental acute pain.
The antinociception induced by the intraperitoneal coadministration of combinations of paracetamol with the nonsteroidal anti-inflammatory drugs (NSAIDs) diclofenac, ibuprofen, ketoprofen, meloxicam, metamizol, naproxen, nimesulide, parecoxib and piroxicam was studied by isobolographic analysis in the acetic acid abdominal constriction test of mice (writhing test). The effective dose that produced 50% antinociception (ED50) was calculated from the log dose-response curves of fixed ratio combinations of paracetamol with each NSAID. ⋯ As shown by isobolographic analysis, all the combinations were synergistic, the experimental ED50s being significantly smaller than the theoretically calculated ED50s. The results of this study demonstrate potent interactions between paracetamol and NSAIDs and validate the clinical use of combinations of these drugs in the treatment of pain conditions.
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Although peripheral nerve function is strongly dependent on energy stores, the role of the mitochondrial electron transport chain, which drives ATP synthesis, in peripheral pain mechanisms, has not been examined. In models of HIV/AIDS therapy (dideoxycytidine), cancer chemotherapy (vincristine), and diabetes (streptozotocin)-induced neuropathy, inhibitors of mitochondrial electron transport chain complexes I, II, III, IV, and V significantly attenuated neuropathic pain-related behavior in rats. While inhibitors of all five complexes also attenuated tumor necrosis factor alpha-induced hyperalgesia, they had no effect on hyperalgesia induced by prostaglandin E2 and epinephrine. ⋯ Neither of these inhibitors, however, affected tumor necrosis factor alpha, prostaglandin E2 or epinephrine hyperalgesia. These experiments demonstrate a role of the mitochondrial electron transport chain in neuropathic and some forms of inflammatory pain. The contribution of the mitochondrial electron transport chain in neuropathic pain is ATP dependent.