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This version was published on February 1, 2008
The Neuroscientist, Vol. 14, No. 1, 78-90 (2008)
DOI: 10.1177/1073858407301681

Late-Onset Epileptogenesis and Seizure Genesis: Lessons From Models of Cerebral Ischemia

Jérôme Epsztein

INMED (Institut de Neurobiologie de la Méditerranée), INSERM (Institut National de la Santé et de la Recherche Médicale Unité 29), and Université de La Méditerranée, Marseille Cedex, France

Yehezkel Ben-Ari

INMED (Institut de Neurobiologie de la Méditerranée), INSERM (Institut National de la Santé et de la Recherche Médicale Unité 29), and Université de La Méditerranée, Marseille Cedex, France

Alfonso Represa

INMED (Institut de Neurobiologie de la Méditerranée), INSERM (Institut National de la Santé et de la Recherche Médicale Unité 29), and Université de La Méditerranée, Marseille Cedex, France

Valérie Crépel

INMED (Institut de Neurobiologie de la Méditerranée), INSERM (Institut National de la Santé et de la Recherche Médicale Unité 29), and Université de La Méditerranée, Marseille Cedex, France, crepel{at}inmed.univ-mrs.fr

Patients surviving ischemic stroke often express delayed epileptic syndromes. Late poststroke seizures occur after a latency period lasting from several months to years after the insult. These seizures might result from ischemia-induced neuronal death and associated morphological and physiological changes that are only partly elucidated. This review summarizes the long-term morphofunctional alterations observed in animal models of both focal and global ischemia that could explain late-onset seizures and epileptogenesis. In particular, this review emphasizes the change in GABAergic and glutamatergic signaling leading to hyperexcitability and seizure genesis. NEUROSCIENTIST 14(1):78—90, 2008.

Key Words: Epileptogenesis • Poststroke seizure • Ischemia • Stroke


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