Closed-Loop Control of Absence Seizures Inspired by Feedback Modulation of Basal Ganglia to the Corticothalamic Circuit.

Abstract

Basal ganglia (BG) has been demonstrated to play the role of modulation for absence seizure generated in the corticothalamic (CT) circuit. But it is unknown what the principle of modulation is and how to improve the modulation if BG fails to hold back the absence seizures. Although neurostimulation has been surgically employed to improve the clinical symptom of patients with epilepsy, the mechanism underlying the neurostimulation regulation is still unclear. In addition, it is not clear what sort of the spatiotemporal patterned stimulation protocols can effectively abate absence seizures with less side effect and energy consumption. Here, we address these issues on the previously proposed BG-CT model. In particular, we develop a reduced corticothalamic (RCT) moldel by viewing BG as a 2I:3O feedback modulator. By calculating the mean firing rate (MFR) and triggering mean firing rate (TMFR), we find that absence seizures can be induced or abated using the neurostimulations through driving the MFRs of the related neurons to fall into or be kicked out of the regions bounded by the TMFRs. In particular, closed-loop m:n ON-OFF anodic-cathodic-cathodic (ACC) triphase coordinated resetting stimulation (CRS) applied on the CT circuit and designed with the TMFR of subthalamic nucleus (STN) in BG could achieve the satisfying abatement effects of absence seizures with the least current consumption.