title: A brief history on the oscillating roles of thalamus and cortex in absence seizures.
abstract: This review summarizes the findings obtained over the past 70 years on the fundamental mechanisms underlying generalized spike-wave (SW) discharges associated with absence seizures. Thalamus and cerebral cortex are the brain areas that have attracted most of the attention from both clinical and experimental researchers. However, these studies have often favored either one or the other structure in playing a major role, thus leading to conflicting interpretations. Beginning with Jasper and Penfield's topistic view of absence seizures as the result of abnormal functions in the so-called centrencephalon, we witness the naissance of a broader concept that considered both thalamus and cortex as equal players in the process of SW discharge generation. Furthermore, we discuss how recent studies have identified fine changes in cortical and thalamic excitability that may account for the expression of absence seizures in naturally occurring genetic rodent models and knockout mice. The end of this fascinating tale is presumably far from being written. However, I can confidently conclude that in the unfolding of this "novel," we have discovered several molecular, cellular, and pharmacologic mechanisms that govern forebrain excitability, and thus consciousness, during the awake state and sleep.
authors.affiliation: Montreal Neurological Institute and Departments of Neurology & Neurosurgery, and of Physiology, McGill University, Montreal, Quebec, Canada. massimo.avoli@mcgill.ca
authors.forename: Massimo
authors.initials: M
authors.lastname: Avoli
mesh_terms: D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D002540:Cerebral Cortex / Q000503:physiopathology*; D004569:Electroencephalography; D004832:Epilepsy, Absence / Q000235:genetics / Q000266:history* / Q000473:pathology*; D049671:History, 18th Century; D049673:History, 20th Century; D049674:History, 21st Century; D006801:Humans; D051379:Mice; D013788:Thalamus / Q000503:physiopathology*