AUTHOR=Müller Eli J. , Robinson Peter A. TITLE=Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols JOURNAL=Frontiers in Computational Neuroscience VOLUME=Volume 12 - 2018 YEAR=2018 URL=https://www.frontiersin.org/journals/computational-neuroscience/articles/10.3389/fncom.2018.00098 DOI=10.3389/fncom.2018.00098 ISSN=1662-5188 ABSTRACT=A neural field model of the corticothalamic-basal ganglia system is developed that describes enhanced beta activity within subthalamic and pallidal circuits in Parkinson's disease~(PD) via system resonances. A model of deep brain stimulation (DBS) of typical clinical targets, the subthalamic nucleus (STN) and globus pallidus internus~(GPi), is added and studied for several distinct stimulation protocols that are used for treatment of the motor symptoms of PD and that reduce pathological beta band activity (13-30 Hz) in the corticothalamic-basal ganglia network. The resulting impact of DBS on enhanced beta activity in the STN and GPi, as well as cortico-subthalamic and cortico-pallidal coherence, are studied. Both STN-DBS and GPi-DBS are found to be effective for suppressing peak STN and GPi power in the beta band, with GPi-DBS being slightly more effective in both the STN and the GPi for all stimulus protocols tested. The largest decrease in cortico-STN coherence is observed during STN-DBS, whereas GPi-DBS is most effective for reducing cortico-GPi coherence. A reduction of the pathologically large STN connection strengths that define the parkinsonian state results in enhanced 6 Hz activity and could thus represent a compensatory mechanism that has the side effect of driving parkinsonian tremor-like oscillations. This model provides a method for systematically testing effective DBS protocols that agrees with experimental and clinical findings, and can be calibrated against large scale brain activity measures. Furthermore, the model suggests GPi-DBS and STN-DBS have distinct impacts on elevated synchronization between the basal ganglia and motor cortex in PD.