Propagation Effect of Epileptic Seizures in a Coupled Thalamocortical Network

Luyao Yan, Honghui Zhang, Zhongkui Sun, Zilu Cao, Zhuan Shen, Lin Du
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Abstract

Epileptic seizures have spatial features related to the propagation of seizure waves. As the main characteristic of absence seizures, 2–4[Formula: see text]Hz spike-wave discharges (SWDs) originate from the cortices and are maintained by the thalamus. In this study, we explore the onset and propagation effect of absence seizures based on a thalamocortical model. First, we develop a two-compartment model and consider the autapse of the thalamic reticular nucleus as a crucial parameter to investigate transition behaviors. Moreover, we present dynamical mechanisms through bifurcation analysis. Simulation results show that the absence seizures can be induced and advanced as the coupling strength increases. Second, we investigate excitatory and inhibitory coupling functions in a three-compartment model. Our research indicates that the excitatory coupling function can lead to SWDs when all the compartments are initially saturated. In the process of propagation, excitatory coupling also gives rise to SWDs in normal compartments, whereas inhibitory coupling plays a limited role. Finally, we reproduce the above results in a 10-compartment model and verify the robustness against the variation of the number of modules. This work may shed new light on the field of seizure propagation and provide potential dynamical mechanisms.
耦合丘脑皮质网络中癫痫发作的传播效应
癫痫发作具有与发作波传播相关的空间特征。作为失神癫痫发作的主要特征,2-4[公式:见文本]Hz的尖峰波放电(SWDs)起源于大脑皮层,由丘脑维持。在这项研究中,我们探讨了基于丘脑皮质模型的失神发作的发生和传播效应。首先,我们建立了一个双室模型,并将丘脑网状核的自垂作为研究过渡行为的关键参数。此外,我们还通过分岔分析给出了其动力机制。仿真结果表明,随着耦合强度的增大,缺勤发作会被诱发并加剧。其次,我们在一个三室模型中研究了兴奋和抑制耦合功能。我们的研究表明,当所有隔室初始饱和时,兴奋耦合功能可导致SWDs。在繁殖过程中,兴奋性偶联也会引起正常胞室的SWDs,而抑制性偶联作用有限。最后,我们在10室模型中重现上述结果,并验证了对模块数量变化的鲁棒性。这项工作可能为癫痫发作传播领域提供新的思路,并提供潜在的动力学机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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