Migraine is as old as civilisation itself, its first recorded description dating back to Hippocrates. In spite of its antiquity, little was known about the disorder until Wolff and his colleagues (Ostfeld and Wolff, 1955; Tunis and Wolff, 1953) established that the symptoms and signs of the attack are closely associated with changes in the calibre of the cranial vessels. Whilst the preheadache phenomena of migraine are probably due to intracranial vasoconstriction, the headache of the attack is due to dilatation of the extra cranial vessels. It is generally accepted that in migrainous subjects, there is an hereditary vascular instability as shown by the following:1) The amplitude of pulsation of the superficial temporal arteries, between attacks, is larger and more variable in migrainous patients than in normal subjects.2) In the prodromal phase of migraine, the amplitude of pulsation of the scalp arteries diminishes, and during headache it increases on the affected side, the form of the pulse wave indicating overdistension from vasodilatation and increased peripheral resistance.3) The amplitude of pulsation of the superficial temporal arteries falls sharply in migrainous subjects when they rise from the recumbent to the upright posture, unlike the relatively constant amplitude maintained in normal subjects.4) The conjunctival vessels dilate on the side of the headache during migraine and show reduced response to topical noradrenaline. The neural control of the scalp vessels in man is confined to vasodilatation, an active process, and this appears to be impaired in migraine. Normally, the forearm blood vessels dilate in response to heating the trunk, whereas in the majority of migrainous subjects this response is deficient or absent.