Premise: Migraine is a complex neurologic disorder that leads to significant disability, yet remains poorly understood. Problem: One potential triggering mechanism in migraine with aura is cortical spreading depression, which can activate the trigeminal nociceptive system both peripherally and centrally in animal models. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent vasodilatory peptide and is currently a major therapeutic target for migraine treatment. Despite the importance of both cortical spreading depression and calcitonin gene-related peptide in migraine, the relationship between these two players has been relatively unexplored. However, recent data suggest several potential vascular and neural connections between calcitonin gene-related peptide and cortical spreading depression. Conclusion: This review will outline calcitonin gene-related peptide-cortical spreading depression connections and propose a model in which cortical spreading depression and calcitonin gene-related peptide act at the intersection of the vasculature and cortical neurons, and thus contribute to migraine pathophysiology.
CITATION STYLE
Close, L. N., Eftekhari, S., Wang, M., Charles, A. C., & Russo, A. F. (2019, March 1). Cortical spreading depression as a site of origin for migraine: Role of CGRP. Cephalalgia. SAGE Publications Ltd. https://doi.org/10.1177/0333102418774299
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