부산대학교 도서관

To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1468-2982.2009.01940.x Byline: AH Stam (1), J Haan (1,2), AMJM van den Maagdenberg (1,3), MD Ferrari (1), GM Terwindt (1) Keywords: migraine; RVCL; TREX1; CADASIL; comorbidity; ischaemic stroke Abstract: It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine. Author Affiliation: Departments of(1)Neurology and (3)Human Genetics, Leiden University Medical Centre, Leiden, and (2)Department of Neurology, Rijnland Hospital, Leiderdorp, the Netherlands Article note: Gisela M. Terwindt, MD, PhD, Department of Neurology, Leiden University Medical Centre, PO Box 9600, 2300 RC Leiden, the Netherlands. Tel +31 71 5262895, fax +31 71 5248253, e-mail g.m.terwindt@lumc.nl