Whatever the possible relation between ictal CSD and interictal VEP might be, the pathophysiological mechanisms underlying VEP habituation are not permanently influenced by the ictal phenomena, even in MA+ patients. In the latter, indeed, like in MwA patients overall and in migraine without aura [15], the VEP habituation deficit is obvious between attacks. Moreover, in MA+, but not in MA patients, it worsens progressively with time elapsed since the last migraine attack and decreases with increased attack frequency; in other words, VEP habituation increases with proximity to an attack. To explain this difference between MA+ and MA, we speculate that MA+ patients are carrying the most pronounced genetic load predisposing them to more prominent pathophysiological dysfunctions. For instance, we intend to explore the possibility that MA+ is the migraine with aura phenotype with the most pronounced deficit of short-range lateral inhibition within the visual cortex, an abnormality that we also found directly related to the distance from the last attack in a previous study of a mixed group of migraine with and without aura patients [15]. Taken together with our present results, this would indicate that the inhibitory performance and habituation with stimulus repetition decreases with the distance from the last migraine attack. A psychophysical study using visual metacontrast masking test, found a similar correlation between inhibitory processes and the number of days elapsed since the last attack [72]. The biochemical correlate of impaired inhibitory mechanisms could be lactate-induced downregulation of GABA activity in the visual cortex. As mentioned, in MA+ lactate levels increase in the occipital cortex during visual stimulation [20] there is emerging evidence that lactate, besides its role as energy substrate, has a concentration-dependent downregulating effect on GABAergic neurotransmission [22].