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dc.contributor.authorDalkara, Turgay
dc.contributor.authorNozari, Ala
dc.contributor.authorMoskowitz, Michael A.
dc.date.accessioned2019-12-10T11:25:20Z
dc.date.available2019-12-10T11:25:20Z
dc.date.issued2010
dc.identifier.issn1474-4422
dc.identifier.urihttps://doi.org/10.1016/S1474-4422(09)70358-8
dc.identifier.urihttp://hdl.handle.net/11655/15705
dc.description.abstractMigraine attacks with auras are sometimes associated with underlying hereditary or acquired cerebrovascular disorders. A unifying pathophysiological explanation linking migraine to these conditions has been difficult to identify. On the basis of genetic and epidemiological evidence, we suggest that changes in blood vessels, hypoperfusion disorders, and microembolisation can cause neurovascular dysfunction and evoke cortical spreading depression, an event that is widely thought to underlie aura symptoms. In fact, recent experimental data have indicated that focal, mild, and transient ischaemia can trigger cortical spreading depression without an enduring tissue signature. Although migraine with aura has many causes (eg, neuronal network excitability), it seems that migraine and stroke might both be triggered by hypoperfusion and could therefore exist on a continuum of vascular complications in a subset of patients who have these hereditary or acquired comorbid vascular conditions.
dc.language.isoen
dc.publisherElsevier Science Inc
dc.relation.isversionof10.1016/S1474-4422(09)70358-8
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNeurosciences & Neurology
dc.titleMigraine Aura Pathophysiology: The Role Of Blood Vessels And Microembolisation
dc.typeinfo:eu-repo/semantics/article
dc.relation.journalLancet Neurology
dc.contributor.departmentNöroloji
dc.identifier.volume9
dc.identifier.issue3
dc.identifier.startpage309
dc.identifier.endpage317
dc.description.indexWoS


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