Migraine is a debilitating neurological disorder, which affects approximately 10% of the general population. Recent advances in functional neuroimaging as well as accumulating data obtained from animal studies have provided important clues to the pathophysiology of migraine. In the past, it was believed that migraine was a vascular disorder, such that migraine aura was induced by vasoconstriction with ensuing abnormal vasodilation responsible for the development of headache. However, it is now clear that brain abnormalities are primarily implicated in migraine pathogenesis. Migraine-associated prodrome is likely to reflect aberrant activity of the hypothalamus and the limbic system, whereas migraine aura is caused by a unique electrical brain phenomenon termed cortical spreading depolarization/depression. Migraine headache is likely to be caused by abnormal activation of the trigeminovascular system; wherein calcitonin gene-related peptide plays a pivotal role. Collectively, migraine symptomatology should be interpreted in relation to underlying biological mechanisms on a phase-to-phase basis.