gms | German Medical Science

63rd Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Japanese Neurosurgical Society (JNS)

German Society of Neurosurgery (DGNC)

13 - 16 June 2012, Leipzig

Structural, cellular and molecular characterization of focal cortical dysplasia

Meeting Abstract

  • J. Nakagawa - Abteilung Experimentelle Epilepsieforschung, Allgemeine Neurochirurgie, Universitätsklinikum Freiburg, Deutschland; Allgemeine Neurochirurgie, Universitätsklinikum Freiburg, Deutschland
  • S. Fauser - Epilepsiezentrum, Allgemeine Neurochirurgie, Universitätsklinikum Freiburg, Deutschland
  • C. Donkels - Abteilung Experimentelle Epilepsieforschung, Allgemeine Neurochirurgie, Universitätsklinikum Freiburg, Deutschland
  • J. Beckervordersandforth - Department of Pathology, Universiteit Maastricht, The Netherlands
  • J. Zentner - Allgemeine Neurochirurgie, Universitätsklinikum Freiburg, Deutschland
  • C. Haas - Abteilung Experimentelle Epilepsieforschung, Allgemeine Neurochirurgie, Universitätsklinikum Freiburg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocP 021

DOI: 10.3205/12dgnc408, URN: urn:nbn:de:0183-12dgnc4088

Published: June 4, 2012

© 2012 Nakagawa et al.
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Outline

Text

Objective: Focal cortical dysplasia (FCD) is considered as a local, neocortical malformation. FCD are a major cause of pharmaco-resistant focal epilepsy and thus are frequently object of neurosurgical resection. However, little is known about the related histopathologic and molecular phenotypes underlying the cortical dyslamination patterns in human FCD. The structural, molecular and cellular characterization of an impaired cortical composition in FCD and a possible coherence between interneuron status and epileptogenicity of FCD are subject of the current study.

Methods: Layer-specific protein expression (Reelin, Calbindin, SMI32, Parvalbumin, TLE4), interneuron and transmitter status (Reelin, Calbindin, Parvalbumin, Calretinin, GAD65/67, GLT1) were studied by quantitative Western blot analysis and immunohistochemistry. Mild FCD Type I and IIa: n=14 patients, control group with (n=6) or without epilepsy (n=6). Severe FCD Type IIb: n=35 sections of n=29 specimen, in addition analysis of maturation (Vimentin); control group with epilepsy (n=6) and without epilepsy (n=4 post mortem cases, different brain regions per control). Statistical analysis following quantification of layer specific neuronal and interneuronal subpopulations of different neocortical regions was carried out and compared to clinical parameters and postsurgical outcome of mild and severe FCD.

Results: Using lamina-specific markers we found no evidence of an underlying general migration defect in mild FCD. Moreover, there was no significant change in interneuron marker expression or transmitter status as revealed by Western blot analysis. In FCD IIb, however, we observed a strongly disturbed laminar structure, but no dyslamination in general. The extent of dyslamination was relative to the number of balloon cells (BC). A quantitative analysis of layer-specific cell populations with regard to clinical parameters and postsurgical outcome in mild and severe FCD is currently in progress.

Conclusions: Our findings suggest that cortical dyslamination in mild FCD is most likely associated with disturbances in cell proliferation or structural organization but not primarily with a general migration defect. In FCD IIb, high numbers of BC beyond a critical threshold result in a complete disorganization of cortical architecture. In addition, a detailed systematic quantitative analysis of layer-specific protein expression and cell populations in mild and severe FCD has been carried out.