Neurological Sciences

, Volume 29, Supplement 1, pp 127–130

Peripheral mechanism of action of antimigraine prophylactic drugs

  • Fabio Frediani
  • Veronica Villani
  • Gerardo Casucci
Current Reality in Headache Treatments

DOI: 10.1007/s10072-008-0903-8

Cite this article as:
Frediani, F., Villani, V. & Casucci, G. Neurol Sci (2008) 29: 127. doi:10.1007/s10072-008-0903-8


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.


MigrainePeripheral actionProphylactic drugs

Copyright information

© Springer-Verlag Italia 2008

Authors and Affiliations

  • Fabio Frediani
    • 1
  • Veronica Villani
    • 2
  • Gerardo Casucci
    • 3
  1. 1.Neurological Department and Headache CenterPoliclinico “S. Pietro”Ponte San Pietro (BG)Italy
  2. 2.Neurology UnitS. Andrea Hospital “La Sapienza” UniversityRomeItaly
  3. 3.Casa di Cura S. FrancescoTelese Terme (BN)Italy