Pain
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The aim of the study was to examine the presence of hyperalgesia to heat stimuli within the zone of secondary hyperalgesia to punctate mechanical stimuli. A burn was produced on the medial part of the non-dominant crus in 15 healthy volunteers with a 50 x 25 mm thermode (47 degrees C, 7 min), and assessments were made 70 min and 40 min before, and 0, 1, and 2 h after the burn injury. Hyperalgesia to mechanical and heat stimuli were examined by von Frey hairs and contact thermodes (3.75 and 12.5 cm2), and pain responses were rated with a visual analog scale (0-100). ⋯ Further, the heat pain response was more intense in the zone of primary hyperalgesia than in the zone of secondary hyperalgesia (P = 0.004), in contrast to the mechanical pain response, which was not significantly different between the two zones of hyperalgesia. In conclusion, secondary hyperalgesia in man is not restricted to mechanical stimuli, as significant hyperalgesia to heat developed within the zone of secondary hyperalgesia to punctate mechanical stimuli. The data, combined with other evidence, suggest differences in the mechanisms accounting for primary hyperalgesia to heat and mechanical stimuli, whereas secondary hyperalgesia to heat and mechanical stimuli may be explained by a common central mechanism.
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Comparative Study
Anti-hyperalgesic and anti-allodynic effects of intrathecal nociceptin/orphanin FQ in rats after spinal cord injury, peripheral nerve injury and inflammation.
We examined the effects of intrathecal nociceptin, the endogenous ligand for the orphan opioid receptor-like receptor, on abnormal pain-related behaviors in rats after carrageenan-induced inflammation and photochemically-induced peripheral nerve or spinal cord ischemic injury. Intrathecal nociceptin dose-dependently alleviated mechanical and cold allodynia-like behavior in the two models of neuropathic pain. The heat hyperalgesia associated with peripheral inflammation was also significantly reduced, although the efficacy of the antihyperalgesic effect of nociceptin in the inflammation model was decreased. ⋯ However, the antinociceptive effect of nociceptin was significantly reduced in rats with peripheral nerve injury. These results indicated that spinally administered nociceptin has anti-allodynic and anti-hyperalgesic effects in animal models of tonic or chronic pain of different origins. Peripheral inflammation and nerve injury may induce spinal plasticity which leads to altered potency and efficacy of nociceptin.
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Randomized Controlled Trial Comparative Study Clinical Trial
Peripheral morphine analgesia in dental surgery.
The recent identification of opioid receptors on peripheral nerve endings of primary afferent neurons and the expression of their mRNA in dorsal root ganglia support earlier experimental data about peripheral analgesic effects of locally applied opioids. These effects are most prominent under localized inflammatory conditions. The clinical use of such peripheral analgesic effects of opioids was soon investigated in numerous controlled clinical trials. ⋯ No serious side effects were reported. Our results show that 1 mg of morphine added to a local anesthetic for dental surgery results in significant improvement of postoperative analgesia. Since the majority of dental surgeries is accompanied with an inflammatory reaction, supplemental morphine may be of benefit for the relief of postoperative dental pain.
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This study used streptozotocin (STZ; 50 mg/kg i.p.) diabetic rats and monitored weekly thermal and mechanical nociceptive thresholds for 8 weeks diabetes. Rats developed mechanical hyperalgesia as soon as 2 weeks after STZ injection. Thermal nociceptive threshold was not altered up to 8 weeks after STZ injection. ⋯ An increased release of glutamate and activation of the NMDA receptor, would maintain the hyperalgesic state. Reduced activity of both opioidergic and GABA(B)ergic inhibitory systems, might exacerbate the increased excitation thus contributing to the ongoing pain. It is suggested that NMDA receptor antagonists may constitute an alternative therapy for diabetic neuropathic pain.
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Randomized Controlled Trial Clinical Trial
Nimodipine-enhanced opiate analgesia in cancer patients requiring morphine dose escalation: a double-blind, placebo-controlled study.
The ability of nimodipine, a dihydropyridine calcium antagonist, to reduce the daily dose of oral morphine in cancer patients who had developed dose escalation, was tested in 54 patients under randomized, double-blind, placebo-controlled conditions. We selected patients that required at least two successive increments of morphine to maintain pain relief. A possible pharmacokinetic interaction between nimodipine and morphine was also studied in 14 patients by assaying steady-state serum levels of morphine and its 3- and 6-glucuronides. ⋯ One week after introducing nimodipine or placebo, while the dose of morphine remained similar to that of the pre-test week, the serum levels of morphine and its glucuronides were not modified significantly. We conclude that the introduction of nimodipine in patients chronically treated with morphine may be a safe alternative to reduce the daily requirements of the opioid. It is suggested that interference with Ca2+-related events may attenuate the development and/or expression of tolerance to morphine in a clinically relevant way.