In this issue of the Scandinavian Journal of Pain Jakob Møller Hansen and coworkers  report the effect of sumatriptan on circulating levels of two neuropeptides, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating peptide-38 (PACAP-38) to provide new insights into migraine pathogenesis.1Trigeminovascular system in migraineDysfunction of the trigeminovascular system is one of many factors that have been considered in the pathogenesis of migraine . It has long been known that the headache phase of migraine, at least in part, is associated with release of vasoactive substances and neuropeptides . The role of several neuropeptides (e.g. substance P, calcitonin gene-related peptide (CGRP) and VIP) and a possible impact of these peptides on vascular and neuronal mechanisms associated with migraine have already been investigated [4, 5]. Neuropeptides can cause dural neurogenic vasodilatation, plasma protein extravasation and sensitization of nociceptors, which have been documented in animal studies [6, 7]. In humans, elevated concentrations of neuropeptides such as CGRP, VIP, and neurokinin A (NKA) have been found in plasma samples during migraine attacks [4, 8, 9, 10]. Hence, one strategy to abort migraine is to block the release of neuropeptides or their receptor activation. Abortive agents in acute migraine management exert
Scandinavian Journal of Pain – de Gruyter
Published: Oct 1, 2013
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