Abstracts

Rationale: Mesial temporal sclerosis (MTS) is the most common lesion observed in patients with intractable temporal lobe epilepsy (TLE) and it is consistently found in 60-70% of the surgical canditates. Neuropathologically, the most characteristic features of MTS are the loss of hippocampal pyramidal and dentate hilar neurons with extensive gliosis as well as varying involvement of the amygdala and other mesial temporal structures. The etiology of MTS is not known. However, it has been stated that 53% of MTS patients had a history of febrile seizure as the most common type of seizure in childhood. The possible role of febrile seizures in the genesis of MTS has been a long-standing debate. Based on the results from epidemiological studies, we know that only a small percentage of children are susceptible to the disease. The purpose of this presentation is to analyze the data on morphological findings in the blood-brain barrier (BBB) of the hippocampus in intractable patients with MTS. Methods: Our study involves 20 patients (8 F/ 12 M) with intractable MTLE who had undergone selective amygdalahippocampectomy (7 right, 13 left). Specimens from the patients’ hippocampi were obtained between the years 2005 and 2007. The mean age of the patients was 30.2±8.6 years. The age at onset of epilepsy was 16±6.3 years. The mean duration between the onset of epilepsy and surgery was 13±10.3 years. As is common in such studies, all the patients submitted their written consent. We also used c-Fos and VEGF, two immediate early genes important in signal transduction linking environmental stimuli to neuron and regulation of angiogenesis, immunohistochemistry to examine patterns of neuronal activation and their relationship to seizure expression. Results: Morphologically, narrowed microvessel lumen, disordered luminal membrane or surface infoldings and swelling of endothelial cells were frequently observed. Endothelial tight junctions were also found to be intact. Ultrastructurally, a network of basal lamina-like electron-dense materials of variable thickness encircled the vessel lumina. Neurons presenting electron microscopic features of necrotic neuronal cell death, including shrunken cell bodies and a slightly darkened and vacuolar cytoplasm with severely swollen mitochondria were detected. The cytoplasm of these astrocytes revealed swelling of mitochondria and many vacuoles. In addition to altered reactive astrocytes, related to perivascular edema swollen endfoot of astrocytes were noticeable. There were particular lipofuscin structures in neuron, glia and also in endothelial cells of BBB. Immunohistochemistry for c-fos showed that TLE neurons in the hippocampal area express c-fos in their nuclei. Conclusions: In this study, we suggest that morphological alterations in neurons and astroglia as well as microvasculature in hippocampus of intractable patients with mesial temporal lobe epilepsy may alter neuronal environment in this region rendering it liable to epileptogenesis.