Cortical hyperexcitability is thought to explain the more enhanced contingent negative variation (CNV) amplitudes and impaired CNV habituation that have been found during the interictal period in migraine without aura. These CNV characteristics have been shown to normalize to the level of healthy controls during an attack. This study aimed to replicate the interictal findings, and additionally examine whether migraineurs show reduced CNV amplitudes during the postattack period. Of 12 patients with migraine without aura and their sex-and agematched healthy controls, CNV characteristics were recorded once in an interictal period, once during the postattack period within 30 hours after an attack that was treated with sumatriptan, and once after an attack that was treated with habitual nonvasoactive medication (counterbalanced). The present results did not confirm the enhanced CNV early and late wave amplitudes or impaired habituation, and cortical hyperexcitability that have previously been reported in the interictal period in patients with migraine without aura. During the postattack period, a decrease in CNV early and late amplitudes was found but only after sumatriptan use. This reduction in CNV amplitudes was most prominent over the frontal cortex and could reflect cortical hypoexcitability, possibly related to a suppression of central catecholaminergic activity by sumatriptan.Key words: migraine, contingent negative variation, sumatriptan Abbreviations: CNV contingent negative variation, WS warning stimulus, RS response signal ( Headache 2001;41:72-78) Individuals with migraine have been hypothesized to be characterized by cortical hyperexcitability reflected in enhanced contingent negative variation (CNV) amplitude. The CNV is an event-related slow brain potential that is characterized by an augmenting negativity recorded on the surface of the scalp during the foreperiod that separates a warning stimulus and a response stimulus. 1 The CNV is comprised of an early and a late component that become clearly visible if the foreperiod is longer than 2 seconds. 2 These components have a different brain topography and seem to be related to different behavioral processes 2-6 such as orienting and motor preparation. The CNV is thought to be controlled by noradrenergic and dopaminergic systems within the central nervous system, 7-12 where noradrenergic pathways may have a dominant role in the early wave, and dopaminergic structures mainly contribute to the late wave. 8 Various studies have demonstrated a more negative CNV in patients with migraine during foreperiods that are shorter than 2 seconds. 10,13,14 Studies employing longer foreperiods predominantly report a higher early wave amplitude in migraine without aura, 13,15-17 but higher late wave amplitudes have been reported as well. 13 These higher CNV amplitudes are believed to emerge as a result of the slow habituation over trials. 10,11,15,17 Research in cortical electrophysiology such as that embracing the thalamic gating model 18 or the threshold regulation ...