Lauritzen M
Cephalalgia. 1985 May;5 Suppl 2:47-51. doi: 10.1177/03331024850050S208.
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.
在典型偏头痛发作的最初1至2小时内，会出现一种灌注不足，这种灌注不足始于脑后部，并以每分钟2 - 3毫米的速度向前发展。灌注不足在勾勒主要皮质宏观和微观结构变化的初级脑沟处停止，但似乎不受皮质结构其他变化的抑制。低血流区域位于皮质，低血流持续4 - 6小时，直至发作缓解。高灌注区域要么较小，要么不存在。一种类似的表现特征存在于皮质扩散性抑制的速度和演变模式中，皮质扩散性抑制是皮质神经元功能的一种短暂扰动，对皮质血流有深远且持久的影响。本文简要总结了近年来提出的观点，这些观点认为扩散性抑制是偏头痛的发病机制。
