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A relatively high number of different medications is currently used for migraine prevention in clinical practice. Although these compounds were initially developed for other indications and differ in their mechanisms of action, some general themes can be identified from the mechanisms at play. Efficacious preventive drugs seem to either suppress excitatory nervous signaling via sodium and/or calcium receptors, facilitate GABAergic inhibition, reduce neuronal sensitization, block cortical spreading depression and/or reduce circulating levels of CGRP. We here review such mechanisms for the different compounds.
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