ABSTRACT
CGRP is a po ten t vasodilator o f cranial b lo o d vessels an d is th o u g h t to be involved in the pathogenesis o f m igraine headache since plasm a levels o f CGRP are elevated during m igraine attacks.1 M echani cal distension o f the dura-m ater, particularly a round b lood vessels, is intensely painful and it has been proposed tha t du ring m i graine CGRP released from dural perivas cular afferent fibres results in a painful dila tion o f dural b lood vessels. M igraineurs also often report tenderness and sensitivity o f the face and scalp during m igraine attacks. This m ay be due to a central convergence o f cra nial and extracranial sensation, since preclinical anatom ical2 and electrophysiological3,4 stud ies show th a t n eu rones o f the trigem inal nucleus caudalis receive conver gent nociceptive inputs from the craniovasculature and extracranial tissues. We have investigated the effects o f dural vasodilation on the activity o f neurones in the trigem i nal nucleus caudalis tha t receive dural inpu t and how this vasodilation m ight affect the activity o f neurones tha t receive convergent dural/facial inputs.
