1. Headache Group, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, U.K.
2. ^*Wellcome Department of Cognitive Neurology, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, U.K.

Correspondence: Peter J Goadsby, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, U.K.

Received 12 February 2001; Revised 22 May 2001; Accepted 22 May 2001.

Abstract

For much of the twentieth century migraine and cluster headache have been considered as vascular headaches whose pathophysiology was determined by changes in cranial vascular diameter. To examine nociceptive neural influences on the cranial circulation, the authors studied healthy volunteers' responses to injection of the pain-producing compound capsaicin in terms of the caliber of the internal carotid artery. The study was conducted using magnetic resonance angiographic techniques. Injection of capsaicin into the skin innervated by the ophthalmic (first) division of the trigeminal nerve elicited 40% 27% (mean SD) increase in vascular cross-sectional area in the right (ipsilateral) internal carotid artery when compared with the mean baseline (P < 0.001). Injection of capsaicin into the skin of the chin to stimulate the mandibular (third) division of the trigeminal nerve and into the leg led to a similar pain perception and failed to produce any significant change in vessel caliber. The data suggest that there is a highly functionally organized, somatotopically congruent trigeminal innervation of the cranial vessels, with a potent vasodilator effect of the ophthalmic division on the large intracranial vessels. The data are consistent with the notion that pain drives changes in vessel caliber in migraine and cluster headache, not vice versa. These conditions therefore should be regarded as primary neurovascular headaches not as vascular headaches.