| Mechanisms of epileptogenicity in cortical dysplasias. | |
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MedLine Citation:
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PMID: 15037672 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cortical dysplasias (CDs) increasingly are recognized as pathologic substrates in patients with medically intractable epilepsy. Several studies have demonstrated the intrinsic epileptogenicity of these lesions, but the cellular and molecular mechanisms responsible for seizure initiation remain unknown. The increased availability of surgically resected neocortical tissue has provided the opportunity for direct histopathologic and electrocorticographic correlations. Moreover, the description of various animal models of CDs allowed the testing of various mechanistic hypotheses. It is likely that the mechanisms of epileptogenicity in CDs are multifactorial. In this article, the authors summarize current knowledge of the molecular and cellular mechanisms of epileptogenicity in focal CDs based on human and animal data. In particular, they focus on the roles of glutamate (NMDA and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and gamma-aminobutyric acid receptors identified in animal models and resected human neocortex. |
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Authors:
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I Najm; Z Ying; T Babb; P B Crino; R Macdonald; G W Mathern; R Spreafico |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review |
Journal Detail:
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Title: Neurology Volume: 62 ISSN: 1526-632X ISO Abbreviation: Neurology Publication Date: 2004 Mar |
Date Detail:
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Created Date: 2004-03-23 Completed Date: 2004-04-29 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0401060 Medline TA: Neurology Country: United States |
Other Details:
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Languages: eng Pagination: S9-13 Citation Subset: AIM; IM |
Affiliation:
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Cleveland Clinic Foundation, Cleveland, OH, USA. najmi@ccf.org |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Brain Diseases / complications*, physiopathology Electrophysiology Epilepsy / etiology*, physiopathology Humans Nervous System Malformations / complications*, physiopathology Neurotransmitter Agents / physiology Receptors, Glutamate / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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K08 MH01658/MH/NIMH NIH HHS; K08 NS02046/NS/NINDS NIH HHS; P01 NS02808/NS/NINDS NIH HHS; R01 NS38992/NS/NINDS NIH HHS; R21 NS42354/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Neurotransmitter Agents; 0/Receptors, Glutamate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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