Chronic pain remains an area of great unmet medical need, with epidemiological studies finding a prevalence of about 20% in Europe and the US and large numbers of these failing to receive adequate relief from existing therapies.
Several possible new opportunities to develop analgesic drugs have emerged from a realisation of the importance of the immune system in driving chronic pain responses. One body of evidence relates to the role of peripheral inflammatory processes in chronic pain. While this role has been long appreciated (pain is one of the cardinal defining features of inflammation) only recently has there been recognition of novel peripheral pain meditators being identified originating from immune cells. The most clinically advanced data relates to the role of NGF (nerve growth factor) but recent data also suggests the important role played by several chemokines.
A second area of current interest lies in the role of the CNS microglia in pain. Long regarded as passive surveyors of tissue environment, it now appears that they can in some circumstances (particularly associated with peripheral nerve injury) become highly reactive and the source of several centrally acting pain mediators – molecules that alter pre- and/or post-synaptic processing of pain-related stimuli.
These developments will be reviewed in this lecture.
Disclosure of Interest None Declared
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