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Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols
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 nu...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297248/ https://www.ncbi.nlm.nih.gov/pubmed/30618692 http://dx.doi.org/10.3389/fncom.2018.00098 |
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author | Müller, Eli J. Robinson, Peter A. |
author_facet | Müller, Eli J. Robinson, Peter A. |
author_sort | Müller, Eli J. |
collection | PubMed |
description | 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. Furthermore, the model suggests GPi-DBS and STN-DBS have distinct impacts on elevated synchronization between the basal ganglia and motor cortex in PD. |
format | Online Article Text |
id | pubmed-6297248 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-62972482019-01-07 Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols Müller, Eli J. Robinson, Peter A. Front Comput Neurosci Neuroscience 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. Furthermore, the model suggests GPi-DBS and STN-DBS have distinct impacts on elevated synchronization between the basal ganglia and motor cortex in PD. Frontiers Media S.A. 2018-12-11 /pmc/articles/PMC6297248/ /pubmed/30618692 http://dx.doi.org/10.3389/fncom.2018.00098 Text en Copyright © 2018 Müller and Robinson. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Müller, Eli J. Robinson, Peter A. Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols |
title | Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols |
title_full | Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols |
title_fullStr | Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols |
title_full_unstemmed | Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols |
title_short | Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols |
title_sort | suppression of parkinsonian beta oscillations by deep brain stimulation: determination of effective protocols |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297248/ https://www.ncbi.nlm.nih.gov/pubmed/30618692 http://dx.doi.org/10.3389/fncom.2018.00098 |
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