Document Detail


A hypothesis regarding the pathogenesis and epileptogenesis of pediatric cortical dysplasia and hemimegalencephaly based on MRI cerebral volumes and NeuN cortical cell densities.
MedLine Citation:
PMID:  17910584     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study compared MRI cerebral volumes and Neuronal-Nuclei (NeuN) cell densities in pediatric epilepsy surgery patients with cortical dysplasia (CD; n = 25) and hemimegalencephaly (HME; n = 14). Our purpose was to deduce possible mechanisms of pathogenesis and epileptogenesis based on an understanding of normal developmental corticoneurogenesis. We used MRI to measured cerebral hemisphere volumes, and NeuN staining to determine grey and white matter cell densities and cell sizes in the molecular layer, grey, and white matter. CD and HME surgical cases were compared with autopsy or non-CD cases (n = 20). Total MRI brain volumes were similar between non-CD, CD, and HME cases. However, in HME patients, the affected cerebral hemisphere was larger and the nonaffected side smaller than non-CD cases. Compared with autopsy cases, NeuN cell densities and cell sizes in CD and HME patients were increased in the molecular layer, upper grey matter, and white matter. In CD and HME cases, total cerebral hemisphere volumes were normal in size and there were more cortical neurons in upper layers than expected. The increase in cortical neuronal densities is consistent with the hypothesis that CD and HME pathogenesis involves increased neurogenesis in the late (not early) phases of cortical formation. In addition, more neurons in the molecular layer and white matter supports the concept that CD and HME pathogenesis also involves incomplete programmed cell death in the remnant cells occupying the preplate and subplate regions. Based on our anatomical and previous electrophysiological findings, we propose that in CD and HME seizure generation is the consequence of incomplete cerebral development with abnormal interactions between immature and mature cells and cellular networks.
Authors:
Gary W Mathern; Marissa Andres; Noriko Salamon; P Sarat Chandra; Veronique M Andre; Carlos Cepeda; Michael S Levine; Joao P Leite; Luciano Neder; Harry V Vinters
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Epilepsia     Volume:  48 Suppl 5     ISSN:  0013-9580     ISO Abbreviation:  Epilepsia     Publication Date:  2007  
Date Detail:
Created Date:  2007-10-03     Completed Date:  2007-11-13     Revised Date:  2008-01-16    
Medline Journal Info:
Nlm Unique ID:  2983306R     Medline TA:  Epilepsia     Country:  United States    
Other Details:
Languages:  eng     Pagination:  74-8     Citation Subset:  IM    
Affiliation:
Division of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, USA. 90095-1769
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MeSH Terms
Descriptor/Qualifier:
Adult
Apoptosis / physiology
Brain / abnormalities*,  pathology
Cell Count
Cerebral Cortex / abnormalities*,  pathology
Child
Child, Preschool
Coloring Agents / diagnostic use
Epilepsy / etiology,  pathology*
Humans
Infant
Magnetic Resonance Imaging / statistics & numerical data
Models, Neurological
Neocortex / metabolism,  pathology
Nerve Tissue Proteins / drug effects,  metabolism
Spasms, Infantile / etiology,  pathology
Tomography, X-Ray Computed
Grant Support
ID/Acronym/Agency:
P05 NS02808/NS/NINDS NIH HHS; R01 NS38992/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Coloring Agents; 0/Nerve Tissue Proteins
Comments/Corrections
Erratum In:
Epilepsia. 2007 Dec;48(12):2380

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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