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Brain Advance Access originally published online on May 23, 2008
Brain 2008 131(8):2192-2200; doi:10.1093/brain/awn094
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© The Author (2008). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Migraine headache is not associated with cerebral or meningeal vasodilatation—a 3T magnetic resonance angiography study

G. G. Schoonman1, J. van der Grond2, C. Kortmann1, R. J. van der Geest2, G. M. Terwindt1 and M. D. Ferrari1

1Department of Neurology and 2Department of Radiology, Leiden University Medical Centre, Leiden, The Netherlands

Correspondence to: G. G. Schoonman, MD, Department of Neurology (K5-Q), Leiden University Medical Centre, PO Box 9600, 2300 RC Leiden, The Netherlands E-mail: g.g.schoonman{at}lumc.nl

Migraine headache is widely believed to be associated with cerebral or meningeal vasodilatation. Human evidence for this hypothesis is lacking. 3 Tesla magnetic resonance angiography (3T MRA) allows for repetitive, non-invasive, sensitive assessment of intracranial vasodilatation and blood flow. Nitroglycerine (NTG) can faithfully induce migraine attacks facilitating pathophysiological studies in migraine. Migraineurs (n = 32) randomly received NTG (IV 0.5 µg/kg/min for 20 min; n = 27) or placebo (n = 5; for blinding reasons). Using 3T MRA, we measured: (i) blood flow in the basilar (BA) and internal carotid arteries (ICA) and (ii) diameters of the middle meningeal, external carotid, ICA, middle cerebral, BA and posterior cerebral arteries at three timepoints: (a) at baseline, outside an attack; (b) during infusion of NTG or placebo and (c) during a provoked attack or, if no attack had occurred, at 6 h after infusion. Migraine headache was provoked in 20/27 (74%) migraineurs who received NTG, but in none of the five patients who received placebo. The headache occurred between 1.5 h and 5.5 h after infusion and was unilateral in 18/20 (90%) responders. During NTG (but not placebo) infusion, there was a transient 6.7–30.3% vasodilatation (P < 0.01) of all blood vessels. During migraine, blood vessel diameters were no different from baseline, nor between headache and non-headache sides. There were no changes in BA and ICA blood flow during either NTG infusion or migraine. In contrast to widespread belief, migraine attacks are not associated with vasodilatation of cerebral or meningeal blood vessels. Future anti-migraine drugs may not require vasoconstrictor action.

Key Words: migraine; nitroglycerine; magnetic resonance angiography; cerebral blood flow; middle meningeal artery

Abbreviations: BA, basilar artery; CGRP, calcitonin gene related peptide; ECA, external carotid artery; ICA, internal carotid artery; MCA, middle cerebral artery; MMA, middle meningeal artery; NTG, nitroglycerine; PCA, posterior cerebral artery; 3T MRA, 3 Tesla magnetic resonance angiography

Received February 17, 2008. Revised April 8, 2008. Accepted April 22, 2008.


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