M igraine is a common, multifactorial, neurovascular disorder, characterized by recurrent disabling attacks of moderate to severe headache, nausea, vomiting, photophobia, and phonophobia, and also, in up to one third of patients, neurologic aura symptoms. 12 It is known that migraine is characterized by a state of central neuronal hyperexcitability, 30 which involves overactivity of the excitatory amino acids. Higher concentrations of excitatory amino acids (mainly glutamic and aspartic acid) were observed in the cerebrospinal fluid, 23 in the saliva, 26 in the plasma, 2,13 and in the platelets 9 of patients with migraine.Recently it has been proposed that the throbbing pain of migraine, which is the pulsating pain aggravated by routine physical activities, is mediated by sensitization of peripheral trigeminovascular neurons, and that cutaneous allodynia (CA) of migraine, which means pain resulting from a non-noxious stimulus to normal skin, is mediated by sensitization of central trigeminovascular neurons. 4,22 The development of hyperalgesia has been shown after the injection of kainic acid. The hyperalgesic effect of kainic acid appears to be mediated by activity at aminomethylisoxazole-propionic acid/kainate receptors that are located outside the spinal cord, perhaps on primary afferents in trigeminal ganglia. 27 Intraperitoneal injection of kainic acid induces a persistent hyperalgesia in mice and rats. 18 Glutamate, an excitatory neurotransmitter, produces