Peripheral mechanism of action of antimigraine prophylactic drugs.
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.
Neurological Department and Headache Center, Policlinico S. Pietro, via Forlanini 15, 24036 Ponte San Pietro (BG), Italy. fabio_frediani@yahoo.it
Fabio
F
Frediani
Veronica
V
Villani
Gerardo
G
Casucci
D000700:Analgesics / Q000627:therapeutic use*; D000818:Animals; D006801:Humans; D008881:Migraine Disorders / Q000188:drug therapy* / Q000517:prevention & control*; D010525:Peripheral Nerves / Q000187:drug effects* / Q000503:physiopathology
D000700:Analgesics