David Moore
St James Hospital, Ireland
Title: The Role of the Neuroimmune Interface in Neuropathic Pain and Therapeutic Implications in the Clinical Scenario.
Biography
Biography: David Moore
Abstract
Neuropathic pain poses a significant burden on the individual and society, because of a lack of effective pharmacological therapies. Interventional pain therapies may be more effective in a select cohort of patients. Neuropathic pain results from a lesion or disease of the somatosensory system. Traditionally neuropathic pain was attributed to dysfunctional activity and hypersensitivity of the neuron. However a maladaptive immune response is increasingly recognised as contributing to the maintenance of chronic neuroapthic pain (1). Glial cell activation and altered peptide biosynthesis are implicated in the maintence of persistent neuropathic pain. Human data suggests that NGF, VEGF and BDNF play a role here. This neuroimmune process is maitained by cellular and neuropeptide biosynthetic responses which become pathological. Intrathecal opioids and steroids are associated with alterations in cell signalling and the levels of inflammatory mediators at the neuroimmune interface in humans in vivo (2,3). Markers of glial and immune cell activity, up-regulated in neuropathic pain states, are down-regulated in spinal cord stimulator patients (4). Pulsed radiofrequency of the dorsal root ganglion in patients with radicular pain alters CSF lymphocyte subsets and peptide comcentrations (unpublished data).