On the possible relation of spreading cortical depression to classical migraine.
During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3 mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro- and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4-6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.
D000818:Animals; D002560:Cerebrovascular Circulation; D013181:Cortical Spreading Depression; D006801:Humans; D008881:Migraine Disorders / Q000209:etiology / Q000503:physiopathology*; D051381:Rats; D014661:Vasoconstriction; D014664:Vasodilation