Earlier explanations of the mechanism of the action of ergotamine tartrate in ending migraine headache claimed a sedative effect mainly on the sympathetic nervous system.1The number of the bodily disturbances accompanying a migraine headache attack that could be attributed to autonomic overactivity were used as support for this view. Later, it was suggested that the cranial sympathetic nerves were implicated in the cranial vascular pain, and that their activity would be blocked by ergotamine tartrate. However, resection and division of the cervical sympathetic nerves supplying the cranial vessels failed to eliminate headache.2 In 1936 the dominant role of vasodilatation of the cranial vessels in the mechanism of migraine headache was demonstrated. It was shown that the administration of ergotamine tartrate was followed by a decrease in the amplitude of pulsations of the cranial arteries, mainly of the extracranial, with a concomitant reduction in intensity of the headache.