Abstract
Recent studies have shown that mathematical models can be used to analyze brain networks by quantifying how likely they are to generate seizures. In particular, we have introduced the quantity termed brain network ictogenicity (BNI), which was demonstrated to have the capability of differentiating between functional connectivity (FC) of healthy individuals and those with epilepsy. Furthermore, BNI has also been used to quantify and predict the outcome of epilepsy surgery based on FC extracted from pre-operative ictal intracranial electroencephalography (iEEG). This modeling framework is based on the assumption that the inferred FC provides an appropriate representation of an ictogenic network, i.e., a brain network responsible for the generation of seizures. However, FC networks have been shown to change their topology depending on the state of the brain. For example, topologies during seizure are different to those pre- and post-seizure. We therefore sought to understand how these changes affect BNI. We studied peri-ictal iEEG recordings from a cohort of 16 epilepsy patients who underwent surgery and found that, on average, ictal FC yield higher BNI relative to pre- and post-ictal FC. However, elevated ictal BNI was not observed in every individual, rather it was typically observed in those who had good post-operative seizure control. We therefore hypothesize that elevated ictal BNI is indicative of an ictogenic network being appropriately represented in the FC. We evidence this by demonstrating superior model predictions for post-operative seizure control in patients with elevated ictal BNI.
Highlights
Resective surgery is a treatment option for pharmacoresistant epilepsy patients
We observed a sharp increase in brain network ictogenicity (BNI) at seizure onset, but, interestingly, BNI remained at similar levels to those of the ictal epoch for about 1 min into the clinically defined post-ictal epoch
We found elevated ictal BNI in both peri-ictal epochs of eight individuals, with the remaining eight individuals not displaying a significant increase in BNI during the ictal period in at least one of the peri-ictal epochs
Summary
The paradigm of epilepsy surgery is to identify and remove the brain tissue responsible for the generation of seizures; the epileptogenic zone [1]. Elevated BNI and Epilepsy Surgery recognized that even presumed “focal” epilepsies can emerge from distributed ictogenic networks [4,5,6]. This new understanding may explain in part why surgery is often unsuccessful and long-term positive outcome may be lower than 25% in extratemporal cases [7, 8]
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