title: Hyperalgesic pain: a review.
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 E(2) (PGE(2)) and prostacyclin (PGI(2)), 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.
authors.affiliation: University of California, San Francisco.
authors.forename: J D
authors.initials: JD
authors.lastname: Levine
authors.forename: Y O
authors.initials: YO
authors.lastname: Taiwo
mesh_terms: D001095:Arachidonic Acids / Q000502:physiology; D011464:Epoprostenol / Q000502:physiology; D006801:Humans; D006930:Hyperalgesia / Q000503:physiopathology*; D007975:Leukotriene B4 / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology; D011458:Prostaglandins E / Q000502:physiology
chemical_list: D001095:Arachidonic Acids; D011458:Prostaglandins E; D007975:Leukotriene B4; D011464:Epoprostenol; D009638:Norepinephrine