Meeting Highlights Central & Peripheral Nervous Systems: 8th World Pain Congress Vancouver, 17-22 August, 1996

Abstract

No significant new drugs nor pharmacological strategies were revealed, whilst all trade stands and symposia stressed the use of existing agents (sometimes in new formulations). The cyclo-oxygenase (COX)-2 inhibitors probably constituted the only real innovation in drug therapy since the last Congress in 1993. However, basic research has been productive, and a number of emerging strategies are likely to lead to novel analgesics. Key areas of interest included: neuropeptides; with bradykinin, substance P (SP), calcitonin gene related peptide (CGRP), galanin, and opioids receiving significant attention. N-Methyl-D-aspartate (NMDA) receptor antagonism was a favoured topic in both preclinical and clinical presentations, and there was much enthusiasm for the idea of an NMDA receptor antagonist with an improved therapeutic index (should this be possible) as an analgesic strategy. The idea that morphine tolerance was in part due to protein kinase C (PKC) induction, leading to NMDA receptor phosphorylation and removal of Mg2+ blockade, and that NMDA antagonists could therefore block morphine tolerance was popular. The ion channel area showed something of a resurgence, with papers on the cloning of PN3 channels from Syntex/Roche and presentations suggesting that lamotrigine and gabapentin offered advantages over other anticonvulsants in the treatment of peripheral neuropathies. Growth factors received much attention; in particular, the observation that hyperalgesia in neuropathies could be due to the action of endogenous nerve growth factor (NGF) and could, therefore, be reversible with antibodies to Trk-A or to NGF itself. In addition, studies in knock-out mice implicated the low affinity P75 receptor for NGF in the control of nociceptive threshold. A complementary proposal was that the neurocytokines, fibroblast growth factor (FGF) and leukaemia inhibitory factor (LIF) might serve as endogenous constraining factors after nerve damage, and that removal of their influence would lead to upregulation of galanin synthesis (for example) and consequent neuropathic changes (as evidenced by autotomy in rats). There was much interest in sympathetically maintained pain and the role of α-adrenoceptors in neuropathic pain. Headache was not heavily featured at this congress, but there was interest in the specialised function of trigeminal systems in the context of head and neck pain.