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N. Vijayan, MD
Headache and Neurology Clinic 2600 Capitol Ave Sacramento, CA 95816

Arch Neurol. 1989;46(6):605.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—In their recent article Andersen et al¹ have further clarified the regional cerebral blood flow patterns in classic migraine. As the authors conclude the focal hypoperfusion is responsible for the neurologic accompaniments of classic migraine, thus confirming the original hypothesis of Wolff.² However, no correlation was found between the onset of headache and the development of hyperemia that occurred long after the onset of headache and persisted much longer than the headache phase. As a result, the authors¹ concluded that "it is unlikely that the headache is triggered by hyperemia."

This latter conclusion may be somewhat premature because it was believed by Wolff² that the headache resulted from primarily dilatation of the extracranial vessels. Therefore, the lack of correlation between regional cerebral blood flow and headache may not be surprising. Is there a method by which the same techniques can be applied to the . . . [Full Text PDF of this Article]

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