One can only speculate on the possible relation between the ictal phenomena, i.e. CSD and its spreading, and the VEP abnormalities found interictally. We know of only one study in photosensitive subjects with a photo-paroxysmal response to intermittent photic stimulation where increased VEP amplitude was correlated with spread of the paroxysmal EEG activity to more anterior brain areas [63]. In photo-paroxysmal responses and photically induced seizures, this could be the electrophysiological correlate of increased functional connectivity between occipital and parieto-temporo-frontal networks under the control of the thalamus [64–66]. A recent study showing in animals that CSD can activate the thalamic reticular nuclei that controls the flow of sensory information to the cortex, is therefore of major interest [67]. Translated to migraine pathophysiology, one may hypothesize that repeated thalamic activation by CSD could worsen the interictal impairment of thalamic/thalamocortical activity in migraine with complex auras [14, 68–71]. Studies correlating aura frequency and duration of the disorder with thalamic/thalamocortical activity in MwA are necessary to test this hypothesis.