Abstract
Although the pathogenesis of migraine headache is still a matter of speculation rather than of understanding, clinical and experimental evidence has long focused attention on pathological processes involving the perivascular innervation of mainly intracranial blood vessels (i.e. pial and durai vessels) as the likely source of the pain in this disease [1– 3]. The discovery of neuropeptides in perivascular nerve fibres during recent years has had a major influence here, and greatest interest has been directed to the possible actions of two vasoactive peptides found in trigeminal sensory neurons, calcitonin gene-related peptide (CGRP) and substance P (SP). Though meningeal as well as extracranial vessels are innervated by trigeminal nerve fibres containing these neuropeptides [4, 5] and extracranial vascular mechanisms may partly be involved [6], experimental and clinical work, initiated by the pioneering studies of Ray and Wolff [7] and Penfield and McNaughton in 1940 [8], implicated a dominant role of intracranial blood vessels, i.e. arteries of the dura mater encephali, the sagittal sinus, and to some extent basal intracerebral arteries, in the generation of headaches [3, 9]. Therefore the dura mater has become the preferential target for studying mechanisms of meningeal nociception and vascular headache [9– 12]. The neurogenic inflammation of the meninges in particular (an experimental inflammation characterized by oedema, hyperaemia, activation of platelets, endothelium and mast cells following antidromic stimulation of trigeminal afferents [13,14]), has attracted the attention of several investigators.
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Messlinger, K., Pawlak, M. (1999). Regulation of meningeal blood flow by neuropeptides: Relevance to migraine. In: Brain, S.D., Moore, P.K. (eds) Pain and Neurogenic Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8753-3_13
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