On the possible relation of spreading cortical depression to classical migraine.
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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.
Original language | English |
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Journal | Cephalalgia : an international journal of headache |
Volume | 5 Suppl 2 |
Pages (from-to) | 47-51 |
Number of pages | 5 |
ISSN | 0333-1024 |
DOIs | |
Publication status | Published - 1 Jan 1985 |
ID: 201457932