Articles: hyperalgesia.
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The Journal of physiology · Nov 2010
Magnesium attenuates chronic hypersensitivity and spinal cord NMDA receptor phosphorylation in a rat model of diabetic neuropathic pain.
Neuropathic pain is a common diabetic complication affecting 8-16% of diabetic patients. It is characterized by aberrant symptoms of spontaneous and stimulus-evoked pain including hyperalgesia and allodynia. Magnesium (Mg) deficiency has been proposed as a factor in the pathogenesis of diabetes-related complications, including neuropathy. ⋯ Magnesium supplementation failed to reduce hyperglycaemia, polyphagia and hypermagnesiuria, or to restore intracellular Mg levels and body growth, but increased insulinaemia and reduced polydipsia. Moreover, it abolished thermal and tactile allodynia, delayed the development of mechanical hypersensitivity, and prevented the increase in spinal cord dorsal horn pNR1. Thus, neuropathic pain symptoms can be attenuated by targeting the Mg-mediated blockade of NMDA receptors, offering new therapeutic opportunities for the management of chronic neuropathic pain.
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Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) that selectively inhibits cyclooxygenase-2 (COX-2). Like most NSAIDs, celecoxib exhibits analgesic effects in models of inflammatory pain but these appear to be dependent on endogenous opioid release. Therefore, this study has assessed the ability of celecoxib to induce tolerance in rats, comparable to that induced by morphine. ⋯ Naltrexone prevented induction of tolerance to morphine or celecoxib. The present results strengthen the possibility that celecoxib has also mechanisms of analgesia unrelated to COX inhibition but dependent on endogenous opioid release. Our results also imply the existence of a new class of analgesics without the deleterious effects of COX inhibitors.
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Reg Anesth Pain Med · Nov 2010
Randomized Controlled TrialEffect of a preemptive femoral nerve block on cytokine release and hyperalgesia in experimentally inflamed skin of human volunteers.
Tissue injury is associated with the local release of inflammatory and nociceptive mediators and the development of hyperalgesia. It is unclear whether interrupting neuronal signaling using regional anesthetic techniques at the time of the injury modifies local nociceptive and inflammatory processes. The aim of this study was to determine whether a peripheral nerve block at the time of tissue injury could modify the development of wound hyperalgesia and the local release of inflammatory and nociceptive mediators. ⋯ These findings suggest that a preemptive, single-shot peripheral nerve block minimally affects wound hyperalgesia and inflammation. Continuous nerve block techniques may be better suited to alter nociceptive and inflammatory events in wounds beyond the duration of the block.
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Opioids are commonly used for pain control; however, they can cause hyperalgesia. The reason why this can happen is not known. The objective of this review was to describe the mechanisms, factors implicated, and drug modulation. ⋯ This is a very complex subject, which involves a series of pathophysiological mechanisms that could contribute for OIH and patient discomfort, bringing disastrous consequences.
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Mixed evidence exists regarding whether irritable bowel syndrome (IBS) patients show increased somatic pain perception compared with controls. The current study used a deep, tonic somatic pain stimulus (ischemic pain) to evaluate somatic hypersensitivity in IBS patients. ⋯ The results of this study suggest that a widespread alteration in central pain processing in IBS patients may be present as they display hypersensitivity to ischemic arm pain, and ischemic pain threshold was associated with clinical symptoms. These findings could reflect a dysfunction in inhibitory pain systems in IBS patients, as ischemic (deep) pain may be under tonic inhibitory control.