Abstract
Excessive beta band (13-30 Hz) oscillations have been observed in the basal ganglia (BG) of patients with Parkinson's disease (PD). Understanding the origin and transmission of beta band oscillations are important to improve treatments of PD, such as closed-loop deep brain stimulation (DBS). This paper proposed a model-based closed-loop GPi stimulation system to suppress pathological beta band oscillations of BG. The feedback nucleus was selected through the analysis of GPi oscillations variation when different synaptic currents were blocked, mainly projections from globus pallidus external (GPe), the subthalamic nucleus (STN) and striatum. Since simulation results proved the important role of synaptic current from GPe in shaping the excessive GPi beta band oscillations, the local field potential (LFP) of GPe was chosen as the feedback signal. That is to say, the feedback nucleus was selected based on the origin analysis of the pathological GPi beta band oscillation. The closed-loop algorithm was the multiplication of linear delayed feedback of the filtered GPe-LFP and modeled synaptic dynamics from GPe to GPi. Thus, the formed stimulation waveform was synaptic current like shape, which was proved to be more energy efficient than open-loop continuous DBS in suppressing GPi beta band oscillation. With the development of DBS devices, the efficiency of this closed-loop stimulation could be testified in animal model and clinical.
Highlights
T HE core pathology of Parkinson’s disease (PD) is the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), which trigger cellular and synaptic dysfunctions of the cortex-basal ganglia-thalamus network [1], [2]
When the stimulation frequency was larger than 40Hz, the excessive beta oscillations of subthalamic nucleus (STN)/globus pallidus interma (GPi) could be gradually lowered
Simulation results indicated that the existence of synaptic current from globus pallidus external (GPe) to GPi was important in maintaining the pathological beta oscillations of GPi, which was consistent with previous findings [35]
Summary
T HE core pathology of Parkinson’s disease (PD) is the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), which trigger cellular and synaptic dysfunctions of the cortex-basal ganglia-thalamus network [1], [2]. Understanding the origin and transmission of beta oscillations in the cortex-basal ganglia-thalamus network is important to help improve treatments for PD [9]. Current studies about beta band oscillations mainly focus on subnetworks of cortex-basal ganglia-thalamus network, e.g. the subthalamic nucleus (STN) - globus pallidus external (GPe) network, the GPe-striatum network. The output nucleus of BG-the globus pallidus interma (GPi) occupies a pivotal position in the circuitry of BG, they receive direct excitatory synaptic input from STN and inhibitory synaptic input from striatum and GPe [15].
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