Articles: hyperalgesia.
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Am. J. Med. Genet. B Neuropsychiatr. Genet. · Aug 2003
Association between human mu-opioid receptor gene polymorphism, pain tolerance, and opioid addiction.
Central to both pain responses and opioid addiction is activity at the micro -opioid receptor. To explore the role of the micro -opioid receptor gene (OPRM) in human pain tolerance and opioid addiction, we examined the relationships among OPRM genotype and experimental pain tolerance in opioid addicts in methadone treatment (n = 50) and healthy normal controls (n = 59). Pain phenotype (pain tolerant vs. pain intolerant) was operationalized as tolerance to a standardized noxious stimulus (either thermal or mechanical), and dichotomized based on distribution. ⋯ Although the established relationship between the phenotypes of opioid addiction and pain intolerance was validated (P = 0.02), genotype differed neither between addict-affected vs. control, nor pain tolerant vs. intolerant subjects. The variant A118G was absent in all individuals and the C17T polymorphism appeared in only three African-American individuals (two addicts and one control). The absence of this polymorphism, the small sample size and the heterogeneous ethnic backgrounds of participants in the pilot study allow only tentative conclusions based on the results, thus the role of the opioid receptor in pain and opioid reward response remains uncertain.
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Clin. Pharmacol. Ther. · Aug 2003
Randomized Controlled Trial Clinical TrialPeripheral and central antihyperalgesic effects of diclofenac in a model of human inflammatory pain.
Experimental evidence suggests that the antihyperalgesic effect of nonsteroidal anti-inflammatory drugs may include both peripheral (inflammatory site) and central sites of action. The aim of this study was to assess peripheral and central antihyperalgesic effects of diclofenac in a human experimental pain model. ⋯ The higher antihyperalgesic efficacy of oral diclofenac as compared with topical diclofenac at comparable tissue concentrations suggests that not only peripheral but also central mechanisms are involved in the antihyperalgesic effects of systemically administered diclofenac.
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Comparative Study
Intramuscular injection of tumor necrosis factor-alpha induces muscle hyperalgesia in rats.
The role of proinflammatory cytokines in neuropathic and inflammatory pain is well established. Recent studies suggest that cytokines such as tumor necrosis factor-alpha (TNF) may also be involved in the development of muscle pain. To investigate the pathophysiology of intramuscular TNF, exogenous TNF (0.1-10 microg), formalin (9%) or vehicle was injected into the gastrocnemius or biceps brachii muscles of rats. ⋯ TNF and formalin evoked intramuscular upregulation of CGRP and NGF, whereas PGE2 was increased exclusively after TNF injection. These findings allow us to speculate that endogenous TNF may play a role in the development of muscle hyperalgesia. Targeting proinflammatory cytokines might be beneficial for the treatment of musculoskeletal pain syndromes.
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Experimental neurology · Aug 2003
Gabapentin reverses mechanical allodynia induced by sciatic nerve ischemia and formalin-induced nociception in mice.
The anticonvulsant drug gabapentin has been demonstrated to alleviate symptoms of painful diabetic neuropathy as well as other types of neuropathic pain. The aim of the present study was to investigate the effect of gabapentin in a recently developed mouse model of peripheral neuropathy. This model is based on a photochemical ischemic lesion of the sciatic nerve generated by laser-induced activation of the photosensitizing dye erythrosin B. ⋯ Gabapentin did not affect the tactile withdrawal threshold in intact animals. A dose of gabapentin (100 micromol/kg, sc) that had no effect on allodynia was found to significantly reduce the pain behavior during phase 2 of the formalin test. The present study demonstrates that systemic administration of gabapentin suppresses both allodynia induced by an ischemic lesion of the sciatic nerve and pain behavior in the formalin test.
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J. Pharmacol. Exp. Ther. · Aug 2003
Allodynia and hyperalgesia in adjuvant-induced arthritic rats: time course of progression and efficacy of analgesics.
The complete Freund's adjuvant (CFA)-induced arthritic rat model has extensively served as a laboratory model in the study of arthritic pain. However, the time courses of allodynia and hyperalgesia and the efficacies of different analgesics have not fully been analyzed in this model. Mechanical allodynia, thermal and joint hyperalgesia, and other disease development parameters (body weight, mobility, paw volume, and joint stiffness) were measured on postinoculation days (PIDs) 0 to 28 in rats. ⋯ Amitriptyline significantly reduced thermal and joint hyperalgesia only at sedation-inducing dose. Acetaminophen, carbamazepine, and gabapentin had, at the most, very small efficacies. In conclusion, the present study provided integrated information about the time course of pain and other disease development parameters in the CFA-induced arthritic rats, and clarified acute efficacies of different categories of analgesics for the allodynia and hyperalgesia.