Clinicians have long suspected that migraine may be mediated through involvement of the cranial arteries. Many patients have discovered that pressure on the particular artery supplying the painful area will ameliorate the pain. Furthermore, Cushing1 commented on the striking dilatation of the temporal arteries and veins seen during an attack of migraine. It remained for Wolff2 and his co-workers to establish this relationship. In a series of experiments they were able to show that in many cases of migraine the fundamental difficulty was vascular dilatation. They demonstrated that changes in the intensity of headache are related to changes in the amplitude of pulsations in the cranial arteries, chiefly the branches of the external carotid, i. e., the superficial temporal and the occipital. Mechanical experimental distention of the superficial temporal artery by increasing the intravascular pressure produced pain of a migrainous type. It seems probable, however, that pial and