The pathophysiological determinants of different aura phenotypes and related differences in interictal visual evoked potential profiles remain speculative. Cortical spreading depression (CSD) is thought to be the pathophysiological substrate of the migraine aura. CSD is an electrochemical wave that usually starts in the posterior regions of the brain and spreads anteriorly at approx. 3 mm/min, accompanied by biphasic cerebral blood flow changes [4]. In several brain imaging studies performed during attacks, though not in all, [49, 50] the vascular and metabolic changes accompanying the migraine aura spread more anteriorly in patients with complex neurological symptoms and hemiplegia than in those with only visual disturbances. The recovery from CSD depends largely on intact neurovascular coupling to match the increased energy demand and to restore ion gradients via the Na+/K+ ATPase pump [51]. The distance, to which CSD spreads during MwA attacks, and thus the clinical phenotype of the aura, depends on the balance between factors that predispose the brain to CSD and others that inhibit CSD and allow the parenchyma to recover.