Abstract
Localization of the epileptogenic zone (EZ) is crucial in the surgical treatment of focal epilepsy. Recently, EEG studies have revealed that the EZ exhibits abnormal connectivity, which has led investigators to now consider connectivity as a biomarker to localize the EZ. Further, abnormal connectivity of the EZ may provide an explanation for the impact of focal epilepsy on more widespread brain networks involved in typical cognition and development. Stereo-electroencephalography (sEEG) is a well-established method for localizing the EZ that has recently been applied to examine altered brain connectivity in epilepsy. In this manuscript, we review recent computational methods for identifying the EZ using sEEG connectivity. Findings from previous sEEG studies indicate that during interictal periods, the EZ is prone to seizure generation but concurrently receives inward connectivity preventing seizures. At seizure onset, this control is lost, allowing seizure activity to spread from the EZ. Regulatory areas within the EZ may be important for subsequently ending the seizure. After the seizure, the EZ appears to regain its influence on the network, which may be how it is able to regenerate epileptiform activity. However, more research is needed on the dynamic connectivity of the EZ in order to build a biomarker for EZ localization. Such a biomarker would allow for patients undergoing sEEG to have electrode implantation, localization of the EZ, and resection in a fraction of the time currently needed, preventing patients from having to endure long hospital stays and induced seizures.
Highlights
Focal epilepsy is the most common type of epilepsy [1]
Building on a strong premise of previous work, we present connectivity findings from several sEEG papers and provide a framework for a model of ictogenesis that could be used to identify a biomarker for the epileptogenic zone (EZ) [26, 27]
In patients who were seizure-free postsurgery, the seizure onset zone (SOZ) colocalized more with nodes with high betweenness centrality in the gamma band during seizures compared to those of patients who still had seizures after surgery [37]. This finding suggests that regions involved in generating epileptogenic activity display high gamma band connectivity in ictal periods, which is supported by phase-amplitude coupling studies mentioned earlier and studies showing that fast gamma band activity and suppression of lower frequency activity during seizure onset can localize the EZ [38, 39]
Summary
Focal epilepsy is the most common type of epilepsy [1]. seizure onset is confined to a focus comprising one or a few areas, several lines of evidence demonstrate that focal epilepsy is a network disorder with widespread influence rather than a disorder of an isolated area [2, 3]. The bilateral posterior cingulate cortex (PCC) has been shown to have the highest outward connectivity in controls during resting state, the ipsilateral hippocampus had the highest outward connectivity in patients with temporal lobe epilepsy (TLE) using electrical source imaging from high-density EEG [19] This finding indicates that the hippocampus (the EZ) seems to be the predominant source of influence outflow in TLE even in the absence of seizures, and it may be disrupting other functional networks, such as those controlled by the PCC. A recent sEEG study of focal epilepsy measured the Pearson correlation coefficient during resting state and calculated node strength, which measures the average connection between a contact to all other contacts, for each contact [28]. Can measure directionality Does not assume a linear relationships between signals Resistant to spurious connectivity detections due to noise
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