Abstract
Three primary mechanisms have been suggested as an explanation of migraine; a neuronal event, a vascular event and a mechanism focussing on the trigeminal nerve and its supply to intra- and extracranial blood vessels. None of these theories has been adequately proven yet. A neuronal point of impact, rather than a vascular one, seems to be responsible for migraine prophylaxis with calcium antagonists. Primarily vasoactive substances such as nimodipine are not or only marginally effective, whereas flunarizine with a limited vascular activity is effective. Data on other calcium antagonists are insufficient to conclude on a migraine-prophylactic activity. The only calcium antagonist that has been extensively tested for vertigo is flunarizine. In placebo-controlled trials, the drug showed to be effective in labyrinthine vertigo. The mechanism behind this effect is unclear.

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