Causal influence of epileptic network during spike-and-wave discharge in juvenile myoclonic epilepsy

초록

Electroencephalographic (EEG) characteristic of juvenile myoclonic epilepsy (JME) is spike-and-wave discharge (SWD), which is dominant in the frontal region. However, activity in the parietal area, including the precuneus, has also been documented for several seconds before and during SWD. The aim of this study was to identify the role of the parietal region, especially the precuneus, and to clarify the causal dynamics among cortical regions during SWD. EEGs were obtained from seven patients with JME. Each SWD was divided into six distinct temporal phases: spike onset, spike peak, slow-wave onset, slow-wave ascending, slow-wave peak, and slow-wave descending phases. Based on the cortical current source distribution and the results of a previous study, we selected the medial frontal, orbitofrontal, anterior cingulate, and mesial temporal cortices and the precuneus as regions of interest (ROIs). To assess epileptic networks and the causal relationships among ROIs during SWD, the directed transfer function (DTF), a measure of multivariate causality, was calculated for each phase of SWD. During spike onset, the maximal outdegree region in all patients was the precuneus. The spike-peak and slow-wave onset phases did not show a consistently dominant outflow region. Outflow from the anterior cingulate cortex was dominant in four patients during the slow-wave ascending phase, and the precuneus showed the maximal outdegree in six patients during the slow-wave peak. In the slow-wave descending phase, four patients showed maximal outflow from the temporal cortex. Our findings suggest that the precuneus is likely a key region for SWD despite the small amount of neural activity observed. The precuneus was the region with the maximal outdegree during both the spike onset and slow-wave peak phases, indicating that SWD in JME is initiated and sustained by a network involving the frontal cortex, precuneus, and thalamus. (C) 2013 Elsevier B.V. All rights reserved.

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