Cerebral and systemic endothelial dysfunction in migraine: Current knowledge and perspective

Abstract

Migraine still causes a high rate of disability and is reported to increase the risk of cardiovascular and cerebrovas-cular diseases. Endothelial dysfunction is considered to be one of the underlying mechanisms linking migraine and vascular disorders. Investigation of endothelial function in migraine includes a variety of examinations including biomarkers and ultrasonography-based studies. Several proposed biomarkers for endothelial dysfunction are endothelial progenitor cells (EPCs), von Willebrand factor (vWF), nitric oxide (NO), tissue-type plasminogen activator antigen (tPA antigen), C-reactive protein (CRP), endothelin-1 (ET-1), and vascular endothelial growth factor (VEGF). Brachial flow-mediated dilatation (FMD) is quite commonly used to reflect systemic endothelial dysfunction, while cerebral endothelial function can be assessed using breath holding index (BHI) on transcranial Doppler (TCD). The results of most studies in migraine sufferers indicate that endothelial dysfunction is found locally in the cerebral circulation, especially at the posterior circulation, while evidence for endothelial dysfunction in the systemic circulation remains controversial.