Earlier studies have indicated that the dilatation and distention of cranial arteries form the basis of the headache produced by a variety of factors.1 The purpose of this communication is to analyze further the mechanism of such headache and to ascertain which cranial arteries are responsible for the headache in each instance.
EFFECT OF VARIOUS AGENTSIt was shown1b that the termination of attacks of migraine headache by ergotamine tartrate regularly paralleled the decrease in amplitude of pulsations of the cranial arteries, chiefly certain branches of the external carotid artery. Pressure over the common carotid artery on the side of the headache reduced the severity of the attack during the pressure. The amelioration was associated with decreased amplitude of pulsations of the temporal artery. Conversely, the distention of the walls of the cranial arteries, for example, experimental distention of the temporal and the middle meningeal arteries,