ABSTRACT
Migraine is a highly prevalent chronic episodic illness. The true cause of migraine has proved elusive, and thus effective treatments, especially preventive, have been slow to emerge. Welch et al. suggested in 1989 that multiple causal factors for migraine converge onto a common hyperexcitable brain state, which constitutes the fundamental susceptibility to migraine attacks (1), underscored by recent genetic findings in familial hemiplegic migraine (FHM), which have introduced three strong but separate causal factors. (2-4) Perhaps the most persuasive argument for brain hyperexcitability constituting the basic susceptibility to migraine is that triggers of an attack initiate a depolarizing electrical and metabolic event originating in brain likened to the spreading depression (SD) of Lea˜o (5). SD is believed to be the underlying mechanism of aura (6), which in turn activates the headache and associated features of the attack. Factors that increase or decrease brain excitability form the threshold for triggering attacks. Prevention of migraine attacks with antiepileptic drugs (AEDs) that decrease excitability of cell membranes thus seems a logical approach toward managing severe and frequent migraine. Evidence for hyperexcitability in the interictal phase of the illness, encompassing clinical observations strengthened by noninvasive electrophysiological and functional brain imaging techniques, is reviewed first, followed by discussion of the effectiveness and current place of AEDs in migraine treatment.
CLINICAL INVESTIGATION
