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Updated: Jan 17, 2026

Inducing Post-Traumatic Epilepsy in a Mouse Model of Repetitive Diffuse Traumatic Brain Injury
Published on: February 10, 2020
Dynamics study of double-column model and its application in epilepsy EEG
Yuhua Xu1, Ying Du1, Xuying Xu1
1School of Mathematics, East China University of Science and Technology, Shanghai, China.
Abstract:
The human brain constitutes a highly complex nonlinear network, comprising billions of interconnected neurons capable of rapid and precise responses to diverse internal and external perturbations. Disruptions in neural connectivity or functional impairments within this network can lead to neurological disorders, including epilepsy. In this study, we propose an improved double-column neural model, derived from the Jansen-Rit (JR) framework, to investigate the effects of external stimuli on epileptiform electroencephalogram (EEG) across multiple cortical regions. Our model specifically targets the signal transmission delays and dynamic synaptic interactions within and between cortical columns. Simulations demonstrate that the improved double-column model successfully reproduces diverse EEG phenomena, including alpha rhythms and epileptiform discharges, across distinct cortical layers. When configured within the same cortical region, the model exhibits symmetry dynamics governed by two connection constants, which is predictable within the symmetry framework of the system, validating its plausibility. Notably, in inter-cortical double-column simulations, parametric modulation of coupling strengths generated varied prefrontal cortical epileptiform discharge patterns. Most significantly, applying targeted external stimuli to visual cortex columns induced a state transition in prefrontal cortex column activity, shifting from epileptic like discharges to stable alpha rhythm, which did not occur in the single-column experiment. These findings suggest that focal neuromodulation of specific cortical regions could serve as a potential therapeutic strategy for suppressing pathological activity in epilepsy.
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