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 1 Hz 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 1 Hz rTMS over the occipital cortex. If the paradoxical increasing of PT to 1 Hz 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. © 2009 Elsevier Ireland Ltd. All rights reserved.
Palermo, A., Fierro, B., Giglia, G., Cosentino, G., Puma, A.R., Brighina, F. (2009). Modulation of visual cortex excitability in migraine with aura: effects of valproate therapy. NEUROSCIENCE LETTERS, 467(1), 26-29 [10.1016/j.neulet.2009.09.054].
Modulation of visual cortex excitability in migraine with aura: effects of valproate therapy
PALERMO, Antonio;FIERRO, Brigida;GIGLIA, Giuseppe;COSENTINO, Giuseppe;PUMA, Angela Rita;BRIGHINA, Filippo
2009-01-01
Abstract
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 1 Hz 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 1 Hz rTMS over the occipital cortex. If the paradoxical increasing of PT to 1 Hz 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. © 2009 Elsevier Ireland Ltd. All rights reserved.
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