Articles: hyperalgesia.
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Randomized Controlled Trial
Influence of high-dose intraoperative remifentanil with intravenous ibuprofen on postoperative morphine consumption in patients undergoing pancreaticoduodenectomy: a randomized trial.
High-dose remifentanil during surgery paradoxically increases postoperative pain intensity and morphine consumption. Cyclooxygenase inhibitors decrease prostaglandin synthesis, thereby antagonizing N-methyl-d-aspartate receptor activation, and may reduce hyperalgesia. This study was performed to evaluate whether postoperative morphine consumption increased following intraoperative continuous remifentanil infusion and whether this could be prevented by intravenous ibuprofen pretreatment. ⋯ We found no influence on postoperative pain after high-dose remifentanil in patients undergoing pancreaticoduodenectomy. Addition of intravenous ibuprofen did not reduce postoperative morphine consumption or pain intensity.
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Anesthesia and analgesia · Dec 2016
The Effects of Electroacupuncture on the Apelin/APJ System in the Spinal Cord of Rats With Inflammatory Pain.
Electroacupuncture (EA) is widely applied for pain management, but the analgesic effects of EA have not been fully elucidated. In this study, we investigated the effect of EA on inflammatory pain caused by intraplantar injection of complete Freund's adjuvant (CFA) and apelin/APJ expression in the spinal cord of rats. ⋯ EA stimulation could alleviate inflammatory pain, at least in part, by restoring apelin and APJ mRNA and protein expression levels, which are downregulated in the CFA pain model.
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Experimental neurology · Dec 2016
A new model of nerve injury in the rat reveals a role of Regulator of G protein Signaling 4 in tactile hypersensitivity.
Tactile hypersensitivity is one of the most debilitating symptoms of neuropathic pain syndromes. Clinical studies have suggested that its presence at early postoperative stages may predict chronic (neuropathic) pain after surgery. Currently available animal models are typically associated with consistent tactile hypersensitivity and are therefore limited to distinguish between mechanisms that underlie tactile hypersensitivity as opposed to mechanisms that protect against it. ⋯ Moreover, tactile hypersensitivity after modified spared nerve injury was most frequently persistent for at least four weeks and associated with higher reactivity of glial cells in the lumbar dorsal horn. Based on these data we suggest that this new animal model of nerve injury represents an asset in understanding divergent neuropathic pain outcomes, so far unravelling a role of RGS4 in tactile hypersensitivity. Whether this model also holds promise in the study of the transition from acute to chronic pain will have to be seen in future investigations.
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Quantitative sensory testing (QST) has been used to characterize pain sensitivity in individuals with and without pain conditions. Research remains limited in pediatric populations, hindering the ability to expand the utility of QST toward its potential application in clinical settings and clinical predictive value. The aims of this study were to examine pain sensitivity using QST in adolescents with chronic pain compared to adolescents without chronic pain and identify predictors of pain sensitivity. ⋯ Exploratory analyses revealed several associations between clinical pain characteristics and QST responses within the chronic pain cohort. Findings from this large pediatric sample provide comprehensive data that could serve as normative data on QST responses in adolescents with and without chronic pain. These findings lay the groundwork toward developing future QST research and study protocols in pediatric populations, taking into consideration sex and psychological distress.
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It is now widely recognized that in many chronic pain syndromes the intensity and severity of individually perceived pain does not correlate consistently with the degree of peripheral nervous system tissue damage or with the intensity of primary afferent or spinal nociceptive neurone activity. In particular, stress and anxiety exert modulatory influences on pain depending on the nature, duration and intensity of the stressor and developmental influences on the maturation of the stress as well as the pain system. ⋯ We summarise the studies investigating the neural substrates and neurobiological mechanisms of stress-induced hyperalgesia (SIH) in animals and humans. The review provides new perspectives and challenges for the current and future treatment of chronic pain.