A new strategy for the treatment of inflammatory pain. Prevention or elimination of central sensitization.
The optimal treatment of pain requires an understanding of the mechanisms involved. Pain is a sensory end-point that can be generated by a number of dissimilar processes. Consequently, the concept of treating pain as a unitary symptom is obsolete. The mechanisms responsible for specific types of pain need to be understood, and particular treatments should be aimed selectively at the various subtypes of pain. A major breakthrough in our understanding of pain has come from the appreciation that clinical pain is qualitatively quite different from physiological or nociceptive pain and is characterised by the appearance of abnormal hypersensitivity. Clinical pain is more than a reflection of sustained peripheral input and it is, to a large extent, the expression of changes produced in the CNS, including the phenomenon of central sensitization. We need to treat both the disease/injury process in the periphery and the changes it induces or triggers in the CNS. Prevention of central sensitization will substantially eliminate the hyperalgesia and allodynia that patients find so distressing, and it offers new possibilities for the development of novel analgesics or antihypersensitivity drugs.
Woolf
C J
CJ
Department of Anatomy and Developmental Biology, University College London, England.
D000700:Analgesics / Q000627:therapeutic use; D002490:Central Nervous System / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D009020:Morphine / Q000627:therapeutic use; D009619:Nociceptors / Q000502:physiology*; D010146:Pain / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D010147:Pain Measurement; D017288:Pain Threshold / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
D000700:Analgesics; D009020:Morphine