Over the years, there has been a considerable amount of controversy as to whether the vascular component of migraine pain arises from the intracranial or the extracranial vessels or both. Some have even questioned whether vasodilatation even plays a significant role in migraine pain and have described it as an unimportant epiphenomenon. In this review, evidence is presented that confirms (1) vasodilatation is indeed a source of pain in migraine; (2) this dilatation does not involve the intracranial vasculature; (3) the extracranial terminal branches of the external carotid artery are a significant source of pain in migraine.

This study yields the first evidence for the existence of a TRPV1-LI innervation in human scalp arteries and provides the first quantitative assessment of the TRPV1-LI, CGRP-LI and SP-LI innervation of those vessels. The increase of TRPV1-LI periarterial nociceptive fibres of scalp arteries may represent, at least in some participants, a structural condition favouring CM (and possibly migraine), for example, by causing a higher sensitivity to algogenic agents.

The pain of migraine is not related to dilatation of the dural meningeal arteries.

IntroductionMigraine is a common disorder with a lifetime prevalence of 16%, worldwide, and a last-year prevalence of 10% [1,2]. Although the pathogenesis of the migraine headache remains poorly understood, current theories suggest that a primary, genetically determined, central nervous system dysfunction is involved in the initiation of migraine headache, with subsequent activation of the trigeminovascular system [3, 4]. We review clinical and experimental evidence showing how nociceptive input from the cervical muscles may contribute to the activation of the trigeminovascular system as part of the pathogenesis of the migraine headache. Pathogenesis of the migraine headacheClinical and experimental considerations suggest that the pathogenesis of the migraine headache is intimately linked to the trigeminal innervation of the cranial blood vessels [5]. Dilation of these blood vessels and the consequent stimulation of the surrounding trigeminal sensory nerve fibres represent key mechanisms in the generation of the pain of the migraine headache [6]. Orthodromic conduction along the trigeminovascular nerve fibres transmits the nociceptive information centrally, via the trigeminal nucleus caudalis onto third-order neurones in the thalamus and from there on to cortical structures where the pain is perceived [7]. Elliot Shevel Egilius H. SpieringsAbstract The pathogenesis of migraine headache is poorly understood but the trigeminovascular system seems to play an important role in it. The trigeminal nucleus caudalis is sensitised by noxious sensory stimuli, often from convergent afferents originating from a variety of tissues. In this paper, we review evidence to support the view that the cervical muscles play a role in the pathogenesis of the migraine headache as well by facilitating the mechanism of central sensitisation.

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