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Vascular Contributions to Migraine: Time to Revisit?
Journal article   Open access   Peer reviewed

Vascular Contributions to Migraine: Time to Revisit?

Bianca N Mason and Andrew F Russo
Frontiers in cellular neuroscience, Vol.12, pp.233-233
08/03/2018
DOI: 10.3389/fncel.2018.00233
PMCID: PMC6088188
PMID: 30127722
url
https://doi.org/10.3389/fncel.2018.00233View
Published (Version of record) Open Access

Abstract

Migraine is one of the most prevalent and disabling neurovascular disorders worldwide. However, despite the increase in awareness and research, the understanding of migraine pathophysiology and treatment options remain limited. For centuries, migraine was considered to be a vascular disorder. In fact, the throbbing, pulsating quality of the headache is thought to be caused by mechanical changes in vessels. Moreover, the most successful migraine treatments act on the vasculature and induction of migraine can be accomplished with vasoactive agents. However, over the past 20 years, the emphasis has shifted to the neural imbalances associated with migraine, and vascular changes have generally been viewed as an epiphenomenon that is neither sufficient nor necessary to induce migraine. With the clinical success of peripherally-acting antibodies that target calcitonin gene-related peptide (CGRP) and its receptor for preventing migraine, this neurocentric view warrants a critical re-evaluation. This review will highlight the likely importance of the vasculature in migraine.
Neuroscience migraine vasodilation inflammation vasoconstriction vascular CGRP

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