Recent clinical practice has found that the spike-wave discharge (SWD) scopes of absence seizures change from small cortical region to large thalamocortical networks, which has also been proved by theoretical simulation. The best biophysics explanation is that there are interactions between coupled cortico-thalamic and thalamocortical circuits. To agree with experiment results and describe the phenomena better, we constructed a coupled thalamocortical model with bidirectional channel (CTMBC) to account for the causes of absence seizures which are connected by the principle of two-way communication of neural pathways. By adjusting the coupling strength of bidirectional pathways, the spike-wave discharges are reproduced. Regulatory mechanism for absence seizures is further applied to CTMBC via four different targeted therapy schemes, such as deep brain stimulation (DBS), charge-balanced biphasic pulse (CBBP), coordinated reset stimulation (CRS) 1 : 0, and (CRS) 3 : 2. The new CTMBC model shows that neurodiversity in bidirectional interactive channel could supply theory reference for the bidirectional communication mode of thalamocortical networks and the hypothesis validation of pathogenesis.

中文翻译：

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通过不同靶向治疗方案在双向交互丘脑皮质模型中失神发作的调控机制

最近的临床实践发现，失神发作的棘波放电（SWD）范围由小皮层区域向大丘脑皮层网络变化，理论模拟也证明了这一点。最好的生物物理学解释是耦合的皮质-丘脑和丘脑皮质回路之间存在相互作用。为了与实验结果一致并更好地描述现象，我们构建了具有双向通道（CTMBC）的耦合丘脑皮质模型来解释失神发作的原因，该模型通过神经通路的双向通信原理连接。通过调节双向通路的耦合强度，重现尖峰波放电。失神发作的调节机制通过四种不同的靶向治疗方案进一步应用于 CTMBC，