Central neuronal mechanisms in cancer-induced bone pain.
OBJECTIVE
To consider distinct neuropharmacological substrates that underlie transmission of impulses from the periphery to the central nervous system in cancer pain.


RESULTS
Advances reveal that plasticity, the ability of the nervous system to alter in response to external events, leads to changes throughout the pathways involved in the perception of pain. Exploitation of pharmacological, functional, molecular and genomic techniques is a basis for new insights into the molecular and cellular mechanisms that contribute to the pain that follows pathophysiology. Characteristic changes experienced with chronic or persistent pain from various causes include expanded receptive fields, allodynia and spontaneous pain in the absence of external stimuli. In addition there are the affective and emotional responses that have to be considered along with these sensory aspects of pain.


CONCLUSIONS
It is clear that although the sensory and psychological aspects of pain are separable, the neural pathways that contribute to these aspects of pain are interlinked. Furthermore, at both peripheral and central sites, there are mechanisms that amplify and prolong the painful stimulus--this can result in severe pain in the presence of relatively minor peripheral pathology. This review considers these signalling systems and changes therein in the context of pain in cancer.
Gordon-Williams
Richard M
RM
Department of Pharmacology, University College London, London, UK. r.gordon-williams@ucl.ac.uk
Dickenson
Anthony H
AH
D000208:Acute Disease; D000818:Animals; D001842:Bone and Bones / Q000187:drug effects / Q000503:physiopathology*; D002490:Central Nervous System / Q000378:metabolism / Q000503:physiopathology*; D002908:Chronic Disease; D006801:Humans; D009369:Neoplasms / Q000150:complications* / Q000628:therapy; D009473:Neuronal Plasticity / Q000502:physiology*; D010146:Pain / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology*