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Tom Skyhøj Olsen, MD; Lars Friberg, MD
Department of Clinical Physiology and Nuclear Medicine Bispebjerg Hospital Bispebjerg Bakke 23 DK-2400 Copenhagen, Denmark

Arch Neurol. 1990;47(2):125-127.

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In Reply.

—Unitl 1981, it was widely accepted that the neurological deficits that occurred during attacks of classic migraine (CM) were caused by reduced blood flow and ischemia during the aura phase. However, in 1981 Olesen et al¹ described seven patients in whom cerebral blood flow (CBF) was recorded during the aura. The authors concluded that "the reduction in rCBF [regional cerebral blood flow] was not of sufficient magnitude to explain the symptoms except in one of seven patients." In 1983, Lauritzen et al² described rCBF studies in nine patients in whom, during migraine aura, "the mean regional perfusion in the oligemic areas was 40 mL/100 g per minute, well above the threshold for producing neuronal damage by ischemia," concluding that "this quantitative consideration supports our conclusion that ischemia is not of primary importance in the development of focal migraine symptoms." Small areas of ischemia were, however, observed . . . [Full Text PDF of this Article]

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