Evidence has recently been presented which suggests that the mechanism of migraine headache is similar to that of the so-called histamine headache, first described by Pickering.1 It is the purpose of this study to investigate other aspects of the relation. Headache following sudden intravenous injection of small amounts of histamine phosphate is considered to be due to the resultant hypotonicity of branches of the internal and external carotid arteries.2 Apparently the increased amplitude of the arterial pulsations resulting from the relaxed vessel walls stimulates the periarterial nerve plexus.2a Such stimulation when transmitted centrally by the trigeminal nerve and along other as yet undetermined pathways is interpreted as pain.2b Other observations have revealed that migraine headache is accompanied by a similar increase in the amplitude of cranial arterial pulsations, limited, however, to branches of the external carotid artery.3 It has been demonstrated that the amplitude of