Abstract
Parkinson's disease (PD) is treated by means of deep brain stimulation (DBS), a therapy based on the injection of current on a regular basis into the basal ganglia, a set of small subcortical nervous system nuclei. DBS is effective in relief of motor symptoms and leads to a notable reduction of drug dose. From an engineering viewpoint, it also raises several optimization-related issues, like energy consumption minimization and stimulation effectiveness. How DBS really works, however, is still unknown, even though several hypotheses and experiments have been reported in literature. To shed some light on the function of DBS, we focused in [1] on those brain nuclei involved in the genesis of PD motor symptoms and developed for them conductance-based models to mimic quantitative data from different in vitro experiments. Now, we use such models in a network scheme to reproduce the main existing anatomical connections between and within the basal ganglia and the resulting macroscopic behaviors reported in literature both for normal and Parkinsonian state. The overall model is proposed as a simulatioParkinson's disease (PD) is treated by means of deep brain stimulation (DBS), a therapy based on the injection of current on a regular basis into the basal ganglia, a set of small subcortical nervous system nuclei. DBS is effective in relief of motor symptoms and leads to a notable reduction of drug dose. From an engineering viewpoint, it also raises several optimization-related issues, like energy consumption minimization and stimulation effectiveness. How DBS really works, however, is still unknown, even though several hypotheses and experiments have been reported in literature. To shed some light on the function of DBS, we focused in (S. Santaniello et al., 20007) on those brain nuclei involved in the genesis of PD motor symptoms and developed for them conductance-based models to mimic quantitative data from different in vitro experiments. Now, we use such models in a network scheme to reproduce the main existing anatomical connections between and within the basal ganglia and the resulting macroscopic behaviors reported in literature both for normal and Parkinsonian state. The overall model is proposed as a simulation instrument to better understand the functional mechanisms currently explaining the basal ganglia physiology and the cellular effects of DBS.n instrument to better understand the functional mechanisms currently explaining the basal ganglia physiology and the cellular effects of DBS.
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