Abstract

IN 1937 Wolff and Graham1 demonstrated that the pain of the migraine attack was associated with dilatation of branches of the cranial vasculature. Ergotamine tartrate was found to be effective in controlling this pain by virtue of its capacity to cause significant and prolonged constriction of the affected blood vessels. In 1957 Ostfeld et al.,2 in a series of ingenious experiments, indicated that vasodilatation per se was not the sole cause of headache but that it must be accompanied by the presence locally of a noxious agent that lowered the pain threshold. The elucidation of the exact chemical nature of . . .

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