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CGRP and migraine: neurogenic inflammation revisited

Abstract

For more than a century neurogenic inflammation has been proposed to have a role in various human diseases. The present review will cover the conceptual steps of the itinerary that has led to the conclusion that neurogenic inflammation is important in migraine. Of particular relevance for the object of this article is the observation that tachykin–independent neurogenic inflammatory responses are evident in rodents, but much less pronounced or absent in other mammal species, including man, whereas neurogenic vasodilatation, most likely mediated by CGRP, occurs in most mammalian species and also in man. Recent evidence that a CGRP receptor antagonist was effective in the treatment of migraine attack supports the hypothesis that neurogenic vasodilatation is a major underlying mechanism of migraine.

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Correspondence to P. Geppetti.

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Open Access This is an open access article distributed under the terms of the Creative Commons Attribution Noncommercial License ( https://creativecommons.org/licenses/by-nc/2.0 ), which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

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Geppetti, P., Capone, J.G., Trevisani, M. et al. CGRP and migraine: neurogenic inflammation revisited. J Headache Pain 6, 61–70 (2005). https://doi.org/10.1007/s10194-005-0153-6

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  • DOI: https://doi.org/10.1007/s10194-005-0153-6

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