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57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

12. - 15.09.2012, Erlangen

57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

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Focal Cortical Dysplasias in patients with Pharmacoresistant Temporal Lobe Epilepsy

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  • presenting/speaker Juana Villeda - Instituto Nacional De Neurologia, Neuropatologia Experimental, Mexico City, Mexico
  • Mario Arturo Alonso-Vanegas - Instituto Nacional De Neurología, Neuropatología Experimental, México, Mexico; Instituto Nacional De Neurologia, Neuropatologia Experimental, México, Mexico; Instituto Nacional De Neurologia, Servicio De Neurocirugia, México, Mexico
  • Luisa Rocha - Instituto Nacional De Neurología, Neuropatología Experimental, México, Mexico; Instituto Nacional De Neurologia, Neuropatologia Experimental, México, Mexico; Instituto Nacional De Neurologia, Servicio De Neurocirugia, México, Mexico; Centro De Investigacion De Estudios Avanzados Ipn, Farmacobiologia, México, Mexico
  • Sandra Orozco-Suarez - Instituto Nacional De Neurología, Neuropatología Experimental, México, Mexico; Instituto Nacional De Neurologia, Neuropatologia Experimental, México, Mexico; Instituto Nacional De Neurologia, Servicio De Neurocirugia, México, Mexico; Centro De Investigacion De Estudios Avanzados Ipn, Farmacobiologia, México, Mexico; Centro Medico Nacional Siglo Xxi, Enfermedades Neurologicas, México, Mexico
  • Victoria Campos Peña - Instituto Nacional De Neurología, Neuropatología Experimental, México, Mexico; Instituto Nacional De Neurologia, Neuropatologia Experimental, México, Mexico; Instituto Nacional De Neurologia, Servicio De Neurocirugia, México, Mexico; Centro De Investigacion De Estudios Avanzados Ipn, Farmacobiologia, México, Mexico; Centro Medico Nacional Siglo Xxi, Enfermedades Neurologicas, México, Mexico; Instituto Nacional De Neurologia, Enfermedades Neurodegenerativas, México, Mexico

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPp6.11

doi: 10.3205/12dgnn122, urn:nbn:de:0183-12dgnn1224

Published: September 11, 2012

© 2012 Villeda et al.
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Outline

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Rationale: In the present study we characterized focal cortical dysplasia (FCD) in cases of refractory temporal lobe epilepsy (TLE).

Methods: We studied 257 cases with pharmacoresistant-TLE, 16 patients with cavernomas and TLE, 79 patients with tumors and TLE, 72 with TLE and mesial sclerosis (MS), and 90 with TLE without MS. All patients were studied according to standardized presurgical protocol and submitted to lesionectomy/corticectomy, temporal lobectomy with/without amigalohippocampectomy. We studied the immunocitochemical expression and distribution of GFAP, nestin, vimentin and NueN, and characterized FCD in the temporal lobe.

Results: We found marked dislamination in all areas of the neocortex, neuronal loss, amylaceous bodies, and neuronal cytomegaly with cytoskeletal disorganization containing dense fibrillar cytoplasmic aggregates, nodular heterotopias, dysplastic and large neurons with high-Nissl staining, often with binucleation, and abundant glassy eosinophilic and shrunken cytoplasm, intermixed with balloon-cells, condensed, fragmented and atypical nuclei. FCDs were found in 75% of patients in the cavernomas group, in 67% of the tumors group, 82% of the TLE with MS group and 77% of the TLE without MS group. Nestin, vimentin and NeuN were highly expressed in the dysplastic, hypertrophic, dimorphic, and balloon-cells of the cortical neurons.

Conclusions: These results demonstrated a very high association (dual pathology) of FCD and cavernomas, tumors and MS as well as a high prevalence of FCD in TLE. This situation prompted us to recognize this association and study the neocortical surgical specimens more carefully as well as to utilize the new ILAE classification of FCD. Are these FCD responsible for the TLE syndrome, or just a random association?

This study was supported by the CONACYT of Mexico (grants J010.0170/2010) and Academy of Sciences of Hungary (grantsETT577/2006, RET67/2005).