• G Demarquay.
• Service de neurologie, hôpital de la Croix-Rousse, Hospices Civils de Lyon, 103, grande rue de la Croix-Rousse, 69004 Lyon, France; Service de neurologie fonctionnelle et épileptologie, hôpital neurologique, Hospices Civils de Lyon, 59, boulevard Pinel, 69500 Bron, France; Inserm U 1028, CNRS UMR 5292, centre de recherche en neurosciences de Lyon (CRNL), Research Center, Brain Dynamics and Cognition Team, 69000 Lyon, France. Electronic address: genevieve.demarquay@chu-lyon.fr.
• Rev Neurol France. 2014 Aug 1; 170 (8-9): 490-4.

IntroductionThe hypothesis that migraine pain is caused by vasodilation has been challenged by clinical and experimental evidence.State Of ArtThe most convincing arguments against the vascular hypothesis come from neuroimaging data. Magnetic resonance imaging studies show that spontaneous migraine attacks are not accompanied by extracranial vasodilation, and by only slight dilation of the intracranial arteries. Pharmacologically-induced migraine attacks also provide further evidence against the role of vasodilation in migraine. Vasodilators such as sildenafil and nitroglycerine trigger attacks without dilation of the middle cerebral artery diameter, whereas VIP (vasoactive intestinal peptide) markedly dilates intra- and extracranial arteries but does not induce migraine attacks. Clinical studies also show a lack of correspondence between the subjective experience of throbbing headache and the arterial pulse. Moreover, many acute anti-migraine agents are not vasoconstrictors.PerspectivesFurther studies are necessary to clarify the mechanisms of migraine headache generation.ConclusionsContrary to a longstanding and widespread belief, vasodilatation is neither sufficient nor necessary to cause migraine headache and is probably an epiphenomenon.Copyright © 2014 Elsevier Masson SAS. All rights reserved.

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