Delayed Feedback-Based Suppression of Pathological Oscillations in a Neural Mass Model.

Suppression of excessively synchronous beta frequency (12-35 Hz) oscillatory activity in the basal ganglia is believed to correlate with the alleviation of hypokinetic motor symptoms of the Parkinson's disease. Delayed feedback is an effective strategy to interrupt the synchronization and has been used in the design of closed-loop neuromodulation methods computationally. Although tremendous efforts in this are being made by optimizing delayed feedback algorithm and stimulation waveforms, there are still remaining problems in the selection of effective parameters in the delayed feedback control schemes. In most delayed feedback neuromodulation strategies, the stimulation signal is obtained from the local field potential (LFP) of the excitatory subthalamic nucleus (STN) neurons and then is administered back to STN itself only. The inhibitory external globus pallidus (GPe) nucleus in the excitatory-inhibitory STN-GPe reciprocal network has not been involved in the design of the delayed feedback control strategies. Thus, considering the role of GPe, this paper proposes three schemes involving GPe in the design of the delayed feedback strategies and compared their effectiveness to the traditional paradigm using STN only. Based on a neural mass model of STN-GPe network having capability of simulating the LFP directly, the proposed stimulation strategies are tested and compared. Our simulation results show that the four types of delayed feedback control schemes are all effective, even if with a simple linear delayed feedback algorithm. But the three new control strategies we propose here further improve the control performance by enlarging the oscillatory suppression space and reducing the energy expenditure, suggesting that they may be more effective in applications. This paper may guide a new approach to optimize the closed-loop deep brain stimulation treatment to alleviate the Parkinsonian state by retargeting the measurement and stimulation nucleus.