%0 Journal Article
%T Extrahippocampal Desynchronization in Nonlesional Temporal Lobe Epilepsy
%A Jes¨˛s Pastor
%A Eduardo G. Navarrete
%A Rafael G. Sola
%A Guillermo J. Ortega
%J Epilepsy Research and Treatment
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/823683
%X Although temporal lobe epilepsy (TLE) is traditionally associated with both hypersynchronous activity in the form of interictal epileptic discharges and hippocampal sclerosis, recent findings suggest that desynchronization also plays a central role in the dynamics of this pathology. The objective of this work is to show the imbalance existing between mesial activities in patients suffering from mesial TLE, with normal mesial structures. Foramen ovale recordings from six patients with mesial TLE and one with lateral TLE were analyzed through a cluster analysis and synchronization matrices. None of the patients present findings in the MRI presurgical evaluation. Numerical analysis was carried out in three different situations: awake and sleep interictal and also during the preictal stage. High levels of desynchronization ipsilateral to the epileptic side were present in mesial TLE patients. Low levels of desynchronization were present in the lateral TLE patient during the interictal stage and almost zero in the preictal stage. Implications of these findings in relation with seizure spreading are discussed. 1. Introduction Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy, where the epileptogenic area is located at some part of the temporal lobe. Mesial TLE (MTLE) refers to those cases where the suspected source of epileptogenic activity is located in the mesial area of the temporal lobe [1], and lateral TLE (LTLE), instead, where the focus is located in the lateral side. MTLE is often associated with structural lesions and/or functional deficiency in one or several (dual pathology) mesial structures of the temporal lobe, with hippocampal sclerosis (HS) as the most common underlying abnormality [2]. However, pathological findings of damage in the amygdala and parahippocampal region, which in turn is subdivided into the entorhinal cortex (EC), perirhinal cortex (PC), and parahippocampal cortex (PPC), are also reported [3, 4]. A significant minority of MTLE patients have no pathological findings on magnetic resonance imaging (MRI), even though lateralization may be correctly performed by neurophysiological methods [5, 6]. Normal underlying mesial structures play a key role in our understanding of the pathogenesis of MTLE, as they oblige us to ask whether mesial sclerosis (MS) is either the cause or the effect in MTLE [7]. Pathophysiology in MTLE can be explained according to two models: (1) the ˇ°focalˇ± model suggests that a single pathological region in the mesial temporal lobe is responsible for seizure origin, establishing a link
%U http://www.hindawi.com/journals/ert/2012/823683/