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. 1990 Mar-Jun;37(2-3):133–135.

Hyperalgesic Pain: A Review

Jon D Levine, Yetunde O Taiwo
PMCID: PMC2190333  PMID: 1964769

Abstract

Pain induced by a stimulus that is normally not painful is referred to as hyperalgesic pain. Inhibition of arachidonic acid metabolism and/or sympathectomy have been found to be effective treatment for this type of pain. We propose that the lowered pain threshold is induced by arachidonic acid metabolites produced in inflamed tissue or by sympathetic postganglionic neurons after nerve injury. The most extensively studied hyperalgesic mediators are prostaglandin E2 (PGE2) and prostacyclin (PGI2), products of the cyclooxygenase pathway of arachidonic acid metabolism, whose production is inhibited by nonsteroidal antiinflammatory analgesics (NSAIAs). Recent studies, however, have demonstrated that products of the NSAIA-resistant lipoxygenase pathway of arachidonic acid metabolism are also hyperalgesic. Their production is inhibited by corticosteroids and current experimental agents.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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