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Mechanisms of epileptogenicity in cortical dysplasias

From the Cleveland Clinic Foundation (Drs. Najm and Ying), Cleveland, OH; Wayne State University (Dr. Babb), Detroit, MI; University of Pennsylvania (Dr. Crino), Philadelphia, PA; Vanderbilt University (Dr. Macdonald), Nashville, TN; University of California (Dr. Mathern), Los Angeles, CA; and Istituto Nazionale Neurologico "C. Besta" (Dr. Spreafico), Milan, Italy.

Address correspondence and reprint requests to Dr. Imad Najm, 9500 Euclid Avenue, S51, Cleveland, OH 44195; e-mail: najmi{at}ccf.org

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 -amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and -aminobutyric acid receptors identified in animal models and resected human neocortex.

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