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dc.contributor.authorLopes, M
dc.contributor.authorRichardson, MP
dc.contributor.authorAbela, E
dc.contributor.authorRummel, C
dc.contributor.authorSchindler, K
dc.contributor.authorGoodfellow, M
dc.contributor.authorTerry, J
dc.date.accessioned2018-03-07T15:34:15Z
dc.date.issued2018-03-01
dc.description.abstractRecent 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.en_GB
dc.description.sponsorshipML, MG, MR, and JT gratefully acknowledge funding from the Medical Research Council via grant MR/K013998/1. MG, MR, and JT further acknowledge the financial support of the EPSRC via grant EP/N014391/1. The contribution of MG and JT was further generously supported by a Wellcome Trust Institutional Strategic Support Award (WT105618MA). MR and EA are supported by the National Institute for Health Research (NIHR) Biomedical Research Centre at the South London and Maudsley NHS Foundation Trust. KS gratefully acknowledges support by the Swiss National Science Foundation (SNF 32003B_155950).en_GB
dc.identifier.citationVol. 9: 98en_GB
dc.identifier.doi10.3389/fneur.2018.00098
dc.identifier.urihttp://hdl.handle.net/10871/31945
dc.language.isoenen_GB
dc.publisherFrontiers Mediaen_GB
dc.rights© 2018 Lopes, Richardson, Abela, Rummel, Schindler, Goodfellow and Terry. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en_GB
dc.titleElevated ictal brain network ictogenicity enables prediction of optimal seizure controlen_GB
dc.typeArticleen_GB
dc.date.available2018-03-07T15:34:15Z
dc.identifier.issn1664-2295
dc.descriptionThis is the final version of the article. Available from Frontiers Media via the DOI in this record.en_GB
dc.identifier.journalFrontiers in Neurologyen_GB


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