Mechanisms of Migraine Aura Revealed by Functional MRI in Human Visual Cortex

Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Using high-field functional MRI with near-continuous recording during visual aura in three subjects, we observed blood oxygenati...

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Published in:Proceedings of the National Academy of Sciences - PNAS Vol. 98; no. 8; pp. 4687 - 4692
Main Authors: Hadjikhani, Nouchine, del Rio, Margarita Sanchez, Wu, Ona, Schwartz, Denis, Bakker, Dick, Fischl, Bruce, Kwong, Kenneth K., Cutrer, F. Michael, Rosen, Bruce R., Roger B. H. Tootell, Sorensen, A. Gregory, Moskowitz, Michael A.
Format: Journal Article
Language:English
Published: United States National Academy of Sciences 10-04-2001
National Acad Sciences
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Summary:Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Using high-field functional MRI with near-continuous recording during visual aura in three subjects, we observed blood oxygenation level-dependent (BOLD) signal changes that demonstrated at least eight characteristics of CSD, time-locked to percept/onset of the aura. Initially, a focal increase in BOLD signal (possibly reflecting vasodilation), developed within extrastriate cortex (area V3A). This BOLD change progressed contiguously and slowly (3.5 ± 1.1 mm/min) over occipital cortex, congruent with the retinotopy of the visual percept. Following the same retinotopic progression, the BOLD signal then diminished (possibly reflecting vasoconstriction after the initial vasodilation), as did the BOLD response to visual activation. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retino-topic progression of the visual percept. These data strongly suggest that an electrophysiological event such as CSD generates the aura in human visual cortex.
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N.H. and M.S.d.R. contributed equally to this work.
Edited by Marcus E. Raichle, Washington University School of Medicine, St. Louis, MO, and approved February 6, 2001
To whom reprint requests should be addressed at: Stroke and Neurovascular Regulation, Departments of Neurology and Neurosurgery, Massachusetts General Hospital, 149 13th Street, Room 6403, Charlestown, MA 02129. E-mail: moskowitz@helix.mgh.harvard.edu.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.071582498