We explored the effects of valproate treatment on visual cortex excitability changes in migraine with aura patients. Abnormal cortical excitability has been suggested to play an important role in the etiopathogenesis of migraine; in particular, it has been suggested a failure of inhibitory circuits in migraine with aura. Valproate acts as a central GABA agonist and it is reasonable suppose that VPA could modify cortical excitability state. Phosphene threshold (PT) was assessed at baseline and after 1Hz rTMS before and after one month therapy. We found that low-frequency rTMS in drug-free migraineurs decreased PT, while the treatment with the GABA agonist valproate is able to revert the effect of 1Hz rTMS over the occipital cortex. If the paradoxical increasing of PT to 1Hz rTMS is consequent upon the deficiency of intracortical inhibitory circuits in migraine, it seems reasonable to suppose that the effect of valproate is due to a recovery of activity of these circuits.