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Deep brain stimulation (DBS) can alleviate the movement disorders likeParkinson's disease (PD). Indeed, it is known that aberrant beta(13-30Hz)oscillations and the loss of dopaminergic neurons in the basalganglia-thalamus (BGTH) and cortex characterize the akinesia symptoms of PD.However, the relevant biophysical mechanism behind this process still remainsunclear. Based on the prior striatal inhibitory model, we propose an extendedBGTH model incorporating medium spine neurons (MSNs) and fast-spikinginterneurons (FSIs) along with the effect of DBS. We are focusing in this paperon an open-loop DBS mode, where the stimulation parameters stay constantindependent of variations in the disease state, and modifications of parametersrely mainly on trial and error of medical experts. Additionally, we propose anovel combined model of the cerebellar-basal-ganglia thalamocortical network,MSNs, and FSIs, and show new results that indicate that Parkinsonianoscillations in the beta-band frequency range emerge from the dynamics of sucha network. Our model predicts that DBS can be used to suppress betaoscillations in globus pallidus pars interna (GPi) neurons. This research willhelp our better understanding of the changes in brain activity caused by DBS,providing new insight for studying PD in the future.

Deep brain stimulation with a computational model for the cortex-thalamus-basal-ganglia system and network dynamics of neurological disorders