Identifying Influential Nodes in a Network Model of Epilepsy
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Identifying Influential Nodes in a Network Model of Epilepsy Joseph Emerson1 · Amber Afelin2 · Viesulas Sliupas3 · Christian G. Fink4 Received: 8 September 2018 / Accepted: 3 April 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019
Abstract A significant proportion of individuals with epilepsy suffer from intractable forms of the disease. Current evidence suggests that pathological brain connectivity could be a major contributor to the propagation of focal seizures, constituting a possible cause for some forms of intractable epilepsy. Currently, however, the precise network structures that underpin epileptic brain connectivity are poorly understood. In this study, we use a computational model to simulate focal seizure spread in the macaque cortical connectome. We then use the results to propose a novel network centrality measure (called “Ictogenic Centrality”) that accurately identifies which nodes are most effective in propagating seizures. In the framework presented, ictogenic centrality outperforms other standard centrality measures in correctly identifying ictogenic nodes, exhibiting high accuracy (0.947), specificity (0.939), and sensitivity (0.964). Ictogenic centrality is degree based and relies on only a single free parameter, making it useful and efficient to compute for large networks. Our results suggest that baseline brain connectivity may predispose the temporal and frontal lobes toward ictogenicity even in the absence of any overtly pathological network reorganization. Keywords Epilepsy · Seizure · Connectome · Centrality Mathematics Subject Classification 92B20 · 92B25 · 05C82
1 Introduction Epilepsy is the fourth-most prevalent neurological disorder (behind cerebrovascular disease, dementia, and migraine disorders), affecting at least 0.5% of all people worldwide (World Health Organization 2006). While approximately two-thirds of this population can be effectively treated through medication (Kwan and Sander 2004), and another 8–10% through surgical intervention, the remainder fall to attain full
Communicated by Paul Newton. Extended author information available on the last page of the article
123
Journal of Nonlinear Science
seizure control (Mormann et al. 2006), reflecting our inadequate understanding of the manifold mechanisms underpinning seizure generation. One possibility is that some forms of intractable epilepsy are the result of pathological brain connectivity (Spencer 2002; Bartolomei et al. 2017). Thalamocortical connections (Crunelli and Leresche 2002; Kim et al. 2014) and interhemispheric connections (Ji et al. 2014) may be compromised in instances of generalized epilepsy, in which seizures arise in both hemispheres simultaneously. Focal epilepsies, on the other hand, are a diverse group of conditions in which seizures originate in localized region(s) of the brain before potentially spreading. Focal epilepsies can be notoriously resistant to anti-epileptic drugs (Semah et al. 1998; Engel et al. 2003; Sørensen and Kokaia 2013). In the past few decades, both b
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