[A causative role of vasodilation in migraine? Yes]

The role of vasodilatation in migraine pathophysiology is still debated with three hypotheses. The first is that vasodilatation of meningeal or intracranial arteries are the primary cause of pain. The second is that vasodilatation is secondary to neuronal activation, but can sustain or increase pain through sensitized perivascular nociceptors. The third is that vasodilatation is an epiphenomenon neither sufficient nor necessary for pain. We review in this part the arguments in favor of the old hypothesis that vasodilation is the primary cause of pain. Finally we show that there is a mild vasodilation during the attacks provoked by CGRP infusion.