[Opioid-induced analgesia and hyperalgesia].
Opioids are frequently used for the treatment of moderate to severe acute and chronic pain. However, clinical evidence suggests that opioids can elicit increased sensitivity to noxious stimuli suggesting that administration of opioids can activate both, pain inhibitory and pain facilitatory systems. Acute receptor desensitization via uncoupling of the receptor from G proteins, upregulation of the cAMP pathway, activation of the N-methyl-D-aspartate (NMDA) receptor system and descending facilitation have been proposed as potential mechanisms underlying opioid-induced hyperalgesia. The tolerance results from a pain sensitization process more than from a decrease in the opioid effectiveness. Opioid-induced hyperalgesia and tolerance are observed both in animal and human experimental models. Brief exposures to mu-receptor agonists induce long-lasting hyperalgesic effects for days. Furthermore, the prolonged use of opioids in patients often requires increasing doses and may be accompanied by the development of abnormal pain. Successful strategies that may decrease or prevent opioid-induced hyperalgesia include the concomitant administration of drugs such as NMDA antagonists, alpha(2)-agonists, or nonsteroidal anti-inflammatory drugs (NSAID), opioid rotation, or combinations of opioids with different receptor selectivity.
Koppert
W
W
Klinik für Anästhesiologie, Universitätsklinikum, Erlangen. koppert@kfa.imed.uni-erlangen.de
D000698:Analgesia; D006801:Humans; D006930:Hyperalgesia / Q000139:chemically induced*; D008959:Models, Neurological; D009294:Narcotics / Q000494:pharmacology* / Q000627:therapeutic use; D010146:Pain / Q000517:prevention & control; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology
D009294:Narcotics; D016194:Receptors, N-Methyl-D-Aspartate