Open Access

CGRP and migraine: neurogenic inflammation revisited

  • P. Geppetti1, 2Email author,
  • J. G. Capone1,
  • M. Trevisani2,
  • P. Nicoletti2,
  • G. Zagli2 and
  • M. R. Tola1
The Journal of Headache and Pain20056:153

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

Received: 23 February 2005

Accepted: 23 February 2005

Published: 8 April 2005

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.

Key words

Calcitonin gene–related peptideNeurogenic inflammationTransient receptor potential vanilloid–1MigraineVasodilatation