Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-10-20
pubmed:abstractText
Chronic pain, which is associated with prolonged tissue damage or injuries to the peripheral or central nervous system, results from a number of complex changes in nociceptive pathways. These include alterations of cell phenotype and changes in the expression of proteins such as receptors, transmitters and ion channels, as well as modifications of neural structure, for example, cell loss, nerve regeneration and synaptic reorganizations. The resultant increase in neural excitability can be reduced with receptor-selective drugs that block peripheral or central chemical mediators or that control ectopic activity or cellular phenotype changes. In this article, Andy Dray, Laszlo Urban and Anthony Dickenson focus on some current mechanistic aspects of chronic pain imposed by inflammation and peripheral neuropathy, and review in particular the molecular changes involving the pharmacology of nociceptive pathways since these have important implications for the management of pain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0165-6147
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
190-7
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Pharmacology of chronic pain.
pubmed:affiliation
Sandoz Institute for Medical Research, London, UK.
pubmed:publicationType
Journal Article, Review