Peripheral mechanism of action of antimigraine prophylactic drugs

Fabio Frediani, Veronica Villani, Gerardo Casucci

Research output: Contribution to journalArticle

Abstract

Migraine is a visceral pain. According to current theories, activation of trigeminocervical nerve endings releases calcitonin gene-related peptide and substance P, inducing vasodilation and plasma protein extravasation, leading to 'neurogenic' inflammation. Activation of the trigeminovascular system is followed by sensitisation of trigeminocervical fibres, maintaining a condition of hypersensitivity to non-noxious stimuli that support persistent pain during migraine attack. Other neurotransmitters (nitric oxide, bradykinins, 5-HT, etc.) play a role in regulating this complex mechanism. In this brief review, we consider the effect of drugs that, acting on the different transmitters involving in pain perception, can stop or inhibit these pathogenetic mechanisms.

Original languageEnglish
JournalNeurological Sciences
Volume29
Issue numberSUPPL. 1
DOIs
Publication statusPublished - May 2008

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Keywords

  • Migraine
  • Peripheral action
  • Prophylactic drugs

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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