MICROSCOPIC HIPPOCAMPAL MALFORMATION IN PATIENTS WITH MESIAL TEMPORAL SCLEROSIS
Abstract number :
1.069
Submission category :
Year :
2004
Submission ID :
4170
Source :
www.aesnet.org
Presentation date :
12/2/2004 12:00:00 AM
Published date :
Dec 1, 2004, 06:00 AM
Authors :
1Alexandre V. Silva, 1Elza M.T. Yacubian, 1Henrique Carrete Jr, 1Ricardo S. Centeno, 1Jo[atilde]o N. Stavale, 3Mauro Canzian, 2Americo C. Sakamoto, and 1Esper A. Caval
Mesial temporal sclerosis (MTS) is the most frequent substrate of refractory epilepsy in adult patients. Despite the recent progress in epileptology, the question whether MTS represents the cause or the consequence of repeated seizures in temporal lobe epilepsy (TLE) remains open to more accurate studies. To address this issue, we studied surgical specimens from seventeen TLE patients and five necropsy controls. Hippocampal and neocortical sections were processed for immunocytochemistry using monoclonal antibodies against neuronal and glial components. All patients had detailed anamnesis, interictal and ictal video-EEG recordings for seizure detection and electroclinical correlation and MRI studies, including volumetric evaluation of the hippocampi. Typical MTS findings on MRI and routine histopathological examination were observed in all patients. The immunocytochemical study of the hippocampi demonstrated the presence of dysmorphic neurons, persistent Cajal-Retzius cells and bilamination of the dentate gyrus in 7/17 (41%) of cases. Neocortical temporal lobe abnormalities included cortical dyslamination (3/17), excess of white matter heterotopic neurons (6/17), numerous Cajal-Retzius cells in layer 1 (7/17), and focal or diffuse cortical astrogliosis (11/17). Temporal pole MRI abnormalities were present in 10 out of 14 patients in whom this could be evaluated and included atrophy, white matter hypersignal and inaccurate limits between gray and white matter. Altogether, our results indicate that subtle malformation of cortical development (not detectable in routine histopathological examination) involving mesial/hippocampal and lateral/neocortical structures may constitute an important physiopathological substrate underlying TLE. (Supported by Funda[ccedil][atilde]o de Amparo [agrave] Pesquisa do Estado de S[atilde]o Paulo (FAPESP).)