Cortical hyperexcitability in migraine has been suggested to play a pivotal role in triggering migraine attacks, possibly via generation of spreading depression. Low levels of plasma, intracellular and brain magnesium as well as increased amplitudes of visual evoked potentials support this theory. More recent data on evoked and even related potentials, i. e. lack of habituation and low initial amplitudes during repetitive stimulation, however, may indicate reduced levels of cortical excitability. Transcranial magnetic stimulations of motor and visual cortices, a direct method to assess cortical excitability, yielded contradictory results. Lower or elevated motor threshold, amplitudes and/or phosphene prevalence or even no significant differences at all were demonstrated suggesting also cortical hypo- rather than hyperexcitability in migraine. Methodological differences, selection of subjects, and timing of investigations might partly explain these marked differences. Clinical and genetic heterogeneity of migraine, for instance via opposite influence on neuronal excitability caused by recently described ion-channel mutations, might provide further explanation.