title: Cortical electrophysiology in migraine and possible pathogenetic implications.
abstract: According to recent evoked potential studies a fundamental, probably protective, feature of cortical information processing, i.e., response habituation during stimulus repetition, is abnormal in migraine between attacks. The deficient habituation is found for different sensory modalities and experimental paradigms: pattern-reversal visual evoked potentials (same stimulus at a constant intensity), cortical auditory evoked potentials (same stimulus at increasing intensities), and auditory event-related potential obtained in a passive "oddball" paradigm (novel stimulus). The abnormal information processing is an interictal cortical dysfunction most likely due to inadequate control by the so-called "state-setting, chemically-addressed pathways" originating in the brain stem, in particular by the serotonergic pathway, leading to a low preactivation level of sensory cortices. We propose that it may play a pivotal role in migraine pathogenesis in conjunction with the reported decrease of brain mitochondrial energy reserve, by favouring a rupture of metabolic homeostasis and biochemical shifts capable of activating the trigeminovascular system and, thus, of producing a migraine attack. We postulate that both the deficient habituation in information processing and the deranged oxygen metabolism may have behavioral correlates. Which of these abnormalities are inherited, acquired, or both remains to be determined.
authors.affiliation: Department of Neurology, University of Liège, CHR Citadelle, Liège, Belgium. Schoenen.J@innet.be
authors.forename: J
authors.initials: J
authors.lastname: Schoenen
mesh_terms: D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology; D005072:Evoked Potentials, Auditory / Q000502:physiology*; D005074:Evoked Potentials, Visual / Q000502:physiology*; D006185:Habituation, Psychophysiologic; D006801:Humans; D008606:Mental Processes / Q000502:physiology; D008881:Migraine Disorders / Q000209:etiology / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000502:physiology
chemical_list: D018377:Neurotransmitter Agents