Since the late 1930s and the first demonstration by Graham and Wolff that the ergot drugs were cranial vasoconstrictors, the emphasis in migraine research has been on vasomotion. This is as it should be, and these changes have been well investigated. With the aid of regional cerebral blood-flow measurements using radioactive techniques, the classical theory of preheadache intracranial vasoconstriction and subsequent intracranial and extracranial vasodilation has been proved accurate, though the recent studies of Edmeads2 and Otis et al3 suggest that the vascular changes in migraine may be more persistent than heretofore suspected.
Migraine is characterized by vasodilation, but vasodilation of itself does not produce painful headache. During the last decade, a series of observations has been reported that suggests that in migraine, vasoactive substances are liberated locally about painful and distended blood vessels.4 This combination of vasodilation and sterile inflammation is needed if the clinical syndrome
Dalessio DJ. Migraine, Platelets, and Headache Prophylaxis. JAMA. 1978;239(1):52–53. doi:10.1001/jama.1978.03280280052030
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