Numerical simulation of novel stimulation strategies in the modulation of absence seizures based on an improved BGCT model

An absence seizure is a common neurological disorder primarily associated with abnormal interactions between the corticothalamic network and the basal ganglia. In order to better understand how the basal ganglia contributes to absence seizure regulation, we use an improved mean field model of the basal ganglia-corticothalamo (BGCT) by introducing a direct projection from the glutamatergic mediated subthalamic nucleus to the striatum (STN-D). The results indicate that enhancing the excitatory coupling strength of the STN-D pathway significantly suppresses spike-wave discharges (SWDs) by increasing striatal activation levels, which promotes the transition from the pathological state to either simple oscillations or low firing state. We propose a new stimulation paradigm, namely a four-phase pulse stimulation (FPS), which sequentially delivers four pulses to the striatum (D), thus targeting the cortical excitatory neurons (EPN), specific relay nuclei (SRN), STN, and D. The results indicate that FPS can successfully replace the original inputs to the D and effectively control absence seizures by adjusting the anodal pulse amplitudes ($ A_1 $, $ A_2 $, and $ A_3 $), which correspond to the excitatory inputs to the D from SRN-D, EPN-D, and SRN-D. These findings offer new insights into understanding the pathophysiology of an absence seizure and its precise therapeutic interventions.