Prevailing hypotheses for the mechanisms of migraine are reviewed. Models of aura mechanisms include transient cerebral ischemia and spreading depression. Models of headache involve trigeminovascular and brainstem mechanisms. The ability to trigger an attack may depend on a threshold of brain excitability. Mitochondrial disorder, magnesium deficiency, and abnormality of presynaptic calcium channels may be responsible for neuronal hyperexcitability between attacks. It remains to be determined whether cortical or brainstem centers generate the attack.