According to the traditional view,1 migraine is due to spasm in one or more major cerebral arteries causing cerebral ischemia, which as the spasm disappears, gives way to hyperperfusion. In this phase, atonic arteries, especially extracranially, cause the pain experience. For many years, there was little experimental evidence in favor of this theory but also little evidence against it. Hence, it remained for decades in virtually every textbook of medicine or neurologogy. Due to its appealing simplicity, the hypothesis has easily been grasped by students, and it has been very useful as patient information. It has also caused the search for new migraine drugs to be directed exclusively toward vasoactive compounds.
With ample new evidence at hand, it now becomes necessary to reevaluate the classic hypothesis, and to discuss common migraine and classic migraine separately.
It has always been difficult, not to say impossible, to encompass the
Olesen J. The Ischemic Hypotheses of Migraine. Arch Neurol. 1987;44(3):321–322. doi:10.1001/archneur.1987.00520150061023
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