The pharmacotherapy of migraine. Despite remarkable progress in understanding the pathophysiological mechanism of migraine in recent decades, the prophylaxis of this recurrent neurovascular disorder, as well as the therapy of acute migraine attacks are only partly efficient. Like epilepsy, migraine reflects the state of neuronal hypersensitivity stemming from an imbalance between inhibitory and excitatory amino acids, the dysfunction of metabolic processess and ion homeostasis.The above findings provide a rationale for the use of antiepileptic drugs such as valproate, topiramate, tiagabine, gabapentin, or zonisamide to prevent migraine attacks. The prophylaxis of migraine also includes application of some beta-blockers, calcium channel antagonists (flunarizine, verapamil) and tricyclic antidepressants such as amitryptyline, nortriptyline and trazodone. On the other hand, the drugs useful in relieving acute attacks of migraine are these which can interfere with disturbances in the trigeminovascular system and subsequent perivascular neurogenic inflammation. Apart from antiemetics and analgesics, classical antimigraine drugs include ergotamine and dihydrorergotamine. The molecular and functional characteristics of serotonin receptors enabled the introduction of a new generation of highly efficient antimigraine drugs, i.e. 5-HT1B/D agonists (triptans), 5-HT1F agonists devoid of vasoconstrictor activity and 5-HT2B antagonists. Triptans presynaptically inhibit the release of proinflammatory and vasodilatatory agents (CGRP, SP, neurokinins), and - via 5-HT-1B receptors - constrict blood vessels. They are characterized by a rapid onset of action and a favorable profile of side-effects. The clinical efficacy of other potential antimigraine agents such as calcitonin gene-related peptide (CGRP) antagonists, adenosine A1 receptor agonists, nitric oxide synthesis inhibitors, the botulin toxin or magnesium is still to be proven in well-controlled clinical trials.