2018
DOI: 10.1177/0333102418771350
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Current understanding of meningeal and cerebral vascular function underlying migraine headache

Abstract: Background The exact mechanisms underlying the onset of a migraine attack are not completely understood. It is, however, now well accepted that the onset of the excruciating throbbing headache of migraine is mediated by the activation and increased mechanosensitivity (i.e. sensitization) of trigeminal nociceptive afferents that innervate the cranial meninges and their related large blood vessels. Objectives To provide a critical summary of current understanding of the role that the cranial meninges, their asso… Show more

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Cited by 98 publications
(82 citation statements)
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References 190 publications
(255 reference statements)
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“…Neuropeptides released from sensory nerve endings contribute to vasodilation, plasma protein extravasation (PPE), and activation of immune cell traffic. 25 We evaluated dural mast cells and macrophages, which play a critical role in the generation of dural inflammation. Dural mast cell activation and degranulation can lead to the release of powerful pro-inflammatory mediators.…”
Section: Discussionmentioning
confidence: 99%
“…Neuropeptides released from sensory nerve endings contribute to vasodilation, plasma protein extravasation (PPE), and activation of immune cell traffic. 25 We evaluated dural mast cells and macrophages, which play a critical role in the generation of dural inflammation. Dural mast cell activation and degranulation can lead to the release of powerful pro-inflammatory mediators.…”
Section: Discussionmentioning
confidence: 99%
“…Still, at present there is an ongoing debate what is causing the hyperexcitability of second order neurons in the TCC during migraine. Levy et al noticed that sensory innervation of the cranial meninges and immune and vascular cells may have a major role, but evidence for neurogenic inflammation during migraine and its contribution to meningeal nociception is limited (52). Prolonged or ongoing peripheral nociceptive input via trigger points in pericranial or cervical myofascial structures may contribute to hyperexcitability of second-order neurons at the C1 and C2 dorsal horn of the TCC in TTH, but evidence for this hypothesis is limited (53).…”
Section: Generalized Hyperexcitabilitymentioning
confidence: 99%
“…It is thought that sensitization of dural afferent fibers causes the head pain symptoms typically reported by migraine sufferers (Levy et al, 2018). Neurogenic inflammation, which results from a localized release of neurotransmitters, such as serotonin, histamine, and glutamate as well as neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P, may underlie this sensitization.…”
mentioning
confidence: 99%