Acute and chronic pharmacological models of generalized absence seizures.
This article reviews the contribution of pharmacologically induced acute and chronic animal models to our understanding of epilepsies featuring non-convulsive generalized seizures, the typical and atypical absence seizures. Typical absences comprise about 5% of all epilepsies regardless of age and the atypical ones are even more common. Although absence epilepsy was thought to be relatively benign, children with childhood epilepsy (CAE) turn out to have a high rate of pretreatment attention deficits that persist despite seizure freedom. The phenomenon of the absence seizure has long attracted research interest because of the clear temporal relationship of the conspicuous EEG rhythm of 3 Hz generalized spike and wave discharges (GSWD) and the parallel transient "loss of consciousness" characterizing these seizures which is time-locked with the GSWD. Indeed, clinical epileptologists, basic scientists and neurophysiologists have long recognized in GSWD a unique electrographic and behavioral marker of the genetic predisposition to most types of epilepsy. Interestingly, the subject is still controversial since it has recently been proposed that both classification terms of CAE currently in use: idiopathic and primary generalized, be abandoned - a point of debate. Both issues - underlying mechanisms and focal origin of absence seizures - may be further enlightened by observations in valid animal models.
Division of Neurology, Neuroscience and Mental Health Program, SickKids Research Institute, Hospital for Sick Children, Department of Paediatrics, University of Toronto, Toronto, Ontario, Canada.
Miguel A
MA
Cortez
Department of Physiology, Medical School, University of Patras, Patras, Greece.
George K
GK
Kostopoulos
Division of Neurology, Neuroscience and Mental Health Program, SickKids Research Institute, Hospital for Sick Children, Department of Paediatrics, University of Toronto, Toronto, Ontario, Canada. Electronic address: carter.snead@sickkids.ca.
O Carter
OC
Snead
D000208:Acute Disease; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000503:physiopathology; D018678:Cholinergic Agents; D002908:Chronic Disease; D003292:Convulsants; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000187:drug effects*; D004832:Epilepsy, Absence / Q000139:chemically induced* / Q000503:physiopathology*; D018756:GABA Antagonists; D009415:Nerve Net / Q000187:drug effects / Q000503:physiopathology; D026902:Potassium Channel Blockers
D018678:Cholinergic Agents; D003292:Convulsants; D018756:GABA Antagonists; D026902:Potassium Channel Blockers
Acute; Animal; Behavior; Chronic; Drugs; ECoG; Generalized seizures; Models