Extrahippocampal Desynchronization in Nonlesional Temporal Lobe Epilepsy


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Jesús Pastor, Eduardo G. Navarrete, Rafael G. Sola, and Guillermo J. Ortega


Introducción:
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 “focal” model suggests that a single pathological region in the mesial temporal lobe is responsible for seizure origin, establishing a link between the presence of MS and the region of seizure onset [8]. (2) The “network” model states that seizures in MTLE result from an alteration of limbic network, which implies atrophy in other structures different from hippocampus [9]; this model suggests that the abnormal interaction between EC, hippocampal formation, and subiculum may be responsible for the seizures [10].

In a high percentage of MTLE patients (60%–80%), clinical seizures cannot be eliminated by drug treatment. In such cases, surgery is the only curative/palliative alternative. Even with the advent of imaging techniques that are now routinely applied in the preevaluation of drug-resistant TLE patients, neurophysiological assessment remains the main diagnostic method at the time of locating epileptogenic areas. Besides traditional electroencephalography (EEG), invasive and semi-invasive neurophysiological methods are justified in most cases when imaging techniques fail in the localization/lateralization of the epileptic focus. Traditional neurophysiological analysis, whether noninvasive, semi-invasive, or fully invasive, depends mainly on the analysis of interictal epileptogenic discharges (IED), which are the hallmark of epileptic activity [11]. However, IED appears in the so-called irritative area, which often does not coincide with the true epileptogenic area. Thus, ictal neurophysiological patterns, such as spikes and sharp waves, must be studied in order to obtain a correct diagnosis. Moreover, as we have recently highlighted [12], analysis of IED in a neurophysiological signal, although very valuable, can only account for a very low percentage of the full information carried by a pathological signal. In order to obtain such recordings, v-EEG (EEG combined with an invasive technique and video recording) is used in most centers. This approach requires hospital admission for several days in order to record and analyze a suitable quantity of seizures to locate the focus.

In this work we analyze foramen ovale electrodes (FOEs) recordings in seven TLE patients with normal presurgical MRI, without taking into account IED activity. Very recently we have shown [12] the existence of interictal mesial synchronization imbalance in TLE patients, mostly with pathologic findings in MRI studies. In the present work, by using part of the already developed methodology, we extend the preceding work in several directions.
(a) We analyze, for the first time, both interictal and ictal mesial synchronization in TLE patients.
(b) We use here a homogenous sample of seven nonlesional TLE patients, in order to discard the causality relation of lesion-desynchronization.
(c) Six out of seven patients presented MTLE, as assessed by previously evaluating FOEs ictal IED analysis; the remaining patient presented LTLE, thus, the issue of mesial synchronization imbalance against mesial or lateral TLE is also addressed.

By analyzing records of ictal and interictal activity in a homogenous sample of nonlesional TLE patients we were able to provide new information regarding the synchronization imbalance in this pathology, as we will show below.

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