Aberrant Cells and Synaptic Circuits in Pediatric Epilepsy Surgery Patients

Carlos Cepeda, Véronique M. André, Irene Yamazaki, Max Kleiman-Weiner, Robin S. Fisher, Harry V. Vinters, Michael S. Levine and and Gary W. Mathern

in From Development to Degeneration and Regeneration of the Nervous System

Published in print December 2008 | ISBN: 9780195369007
Published online May 2009 | e-ISBN: 9780199865253 | DOI:
 Aberrant Cells and Synaptic Circuits in Pediatric Epilepsy Surgery Patients

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This chapter discusses studies on the properties of abnormal cells and synaptic circuits in pediatric cortical dysplasia (CD). It provides a working hypothesis concerning how CD tissue may be able to generate epileptic discharges. CD pathogenesis probably involves partial failure of events occurring during later phases of corticogenesis resulting in incomplete cortical development. The timing of these events during cortical development would explain the different forms of CD. Developmental alterations during the late second or early third trimester would account for severe CD with numerous dysmorphic and cytomegalic cells (CDII Type A and B), whereas events occurring closer to birth after the subplate has nearly degenerated would explain mild CD (CD Type I). As a consequence, subplate and radial glial degeneration and transformation would be prevented, giving the appearance of abnormal dysmorphic cells in the postnatal human brain. Failure of late cortical maturation could explain the presence of thickened, abnormally placed gyri with indistinct cortical gray-white matter junctions in postnatal CD tissue.

Keywords: pediatric cortical dysplasia; epileptic discharges; cerebral cortex; seizures; subplate; CD; CD Type I

Chapter.  7905 words.  Illustrated.

Subjects: Neuroscience

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