Abstract

Evidence supports hyperexcitability as a cause of migraine in the affected brain. This hyperexcitability may have its origins in many factors including low magnesium levels in serum, cerebrospinal and other fluids, mitochondrial and energy metabolism abnormalities, excessive nitric oxide levels or sensitivity to nitric oxide, and channel protein mutations. New imaging technologies, such as positron-emission tomography, have provided clues to the sequence of events in migraine and may offer clues for developing additional avenues of treatment. Better understanding of the physiologic and molecular events in migraine may lead to even better targets for therapy.

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