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| Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology. |
From the Anticonvulsant Screening Project, Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT.
Address correspondence and reprint requests to Dr. H. Steve White, Anticonvulsant Screening Project, Dept. Pharmacology and Toxicology, University of Utah, 20 S. 2030 E., Room 408, Salt Lake City, UT 84112; e-mail: swhite{at}hsc.utah.edu
Advances in our understanding of the molecular biology of human epileptogenesis and secondary hyperexcitability have resulted in part from the development and characterization of animal models of mesial temporal lobe epilepsy, trauma-induced epilepsy, and age-specific models of febrile seizures and neonatal hypoxia-induced seizures. Each of these models displays similarities to and differences from their human counterparts and will undoubtedly prove useful for evaluating novel therapies aimed at preventing the development, or halting the progression, of epilepsy or insult-induced secondary hyperexcitability. This article briefly reviews those models that most closely parallel human mesial temporal lobe epilepsy, trauma-induced epilepsy, febrile seizures, and hypoxia-induced seizures. Particular attention is paid to the underlying pathology, the presence or absence of a latent period, and development of spontaneous seizures.
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