From Parkinsonian thalamic activity to restoring thalamic relay using deep brain stimulation: new insights from computational modeling

H.G.E. Meijer, M. Krupa, H. Cagnan, M.A.J. Lourens, T. Heida, H.C.F. Martens, L.J. Bour, S.A. van Gils

Research output: Contribution to journalArticleAcademicpeer-review

16 Citations (Scopus)

Abstract

We present a computational model of a thalamocortical relay neuron for exploring basal ganglia thalamocortical loop behavior in relation to Parkinson's disease and deep brain stimulation (DBS). Previous microelectrode, single-unit recording studies demonstrated that oscillatory interaction within and between basal ganglia nuclei is very often accompanied by synchronization at Parkinsonian rest tremor frequencies (3–10 Hz). These oscillations have a profound influence on thalamic projections and impair the thalamic relaying of cortical input by generating rebound action potentials. Our model describes convergent inhibitory input received from basal ganglia by the thalamocortical cells based on characteristics of normal activity, and/or low-frequency oscillations (activity associated with Parkinson's disease). In addition to simulated input, we also used microelectrode recordings as inputs for the model. In the resting state, and without additional sensorimotor input, pathological rebound activity is generated for even mild Parkinsonian input. We have found a specific stimulation window of amplitudes and frequencies for periodic input, which corresponds to high-frequency DBS, and which also suppresses rebound activity for mild and even more prominent Parkinsonian input. When low-frequency pathological rebound activity disables the thalamocortical cell's ability to relay excitatory cortical input, a stimulation signal with parameter settings corresponding to our stimulation window can restore the thalamocortical cell's relay functionality.
Original languageEnglish
Article number066005
Number of pages13
JournalJournal of neural engineering
Volume8
Issue number6
DOIs
Publication statusPublished - 12 Oct 2011

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Deep Brain Stimulation
Basal Ganglia
Brain
Microelectrodes
Parkinson Disease
Neurons
Synchronization
Tremor
Action Potentials

Keywords

  • PACS-87.17.Aa
  • PACS-87.19.L
  • PACS-87.19.R
  • IR-79408
  • PACS-87.80.y
  • EWI-21225
  • METIS-284985
  • PACS-87.19.X

Cite this

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title = "From Parkinsonian thalamic activity to restoring thalamic relay using deep brain stimulation: new insights from computational modeling",
abstract = "We present a computational model of a thalamocortical relay neuron for exploring basal ganglia thalamocortical loop behavior in relation to Parkinson's disease and deep brain stimulation (DBS). Previous microelectrode, single-unit recording studies demonstrated that oscillatory interaction within and between basal ganglia nuclei is very often accompanied by synchronization at Parkinsonian rest tremor frequencies (3–10 Hz). These oscillations have a profound influence on thalamic projections and impair the thalamic relaying of cortical input by generating rebound action potentials. Our model describes convergent inhibitory input received from basal ganglia by the thalamocortical cells based on characteristics of normal activity, and/or low-frequency oscillations (activity associated with Parkinson's disease). In addition to simulated input, we also used microelectrode recordings as inputs for the model. In the resting state, and without additional sensorimotor input, pathological rebound activity is generated for even mild Parkinsonian input. We have found a specific stimulation window of amplitudes and frequencies for periodic input, which corresponds to high-frequency DBS, and which also suppresses rebound activity for mild and even more prominent Parkinsonian input. When low-frequency pathological rebound activity disables the thalamocortical cell's ability to relay excitatory cortical input, a stimulation signal with parameter settings corresponding to our stimulation window can restore the thalamocortical cell's relay functionality.",
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From Parkinsonian thalamic activity to restoring thalamic relay using deep brain stimulation : new insights from computational modeling. / Meijer, H.G.E.; Krupa, M.; Cagnan, H.; Lourens, M.A.J.; Heida, T.; Martens, H.C.F.; Bour, L.J.; van Gils, S.A.

In: Journal of neural engineering, Vol. 8, No. 6, 066005, 12.10.2011.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - From Parkinsonian thalamic activity to restoring thalamic relay using deep brain stimulation

T2 - new insights from computational modeling

AU - Meijer, H.G.E.

AU - Krupa, M.

AU - Cagnan, H.

AU - Lourens, M.A.J.

AU - Heida, T.

AU - Martens, H.C.F.

AU - Bour, L.J.

AU - van Gils, S.A.

PY - 2011/10/12

Y1 - 2011/10/12

N2 - We present a computational model of a thalamocortical relay neuron for exploring basal ganglia thalamocortical loop behavior in relation to Parkinson's disease and deep brain stimulation (DBS). Previous microelectrode, single-unit recording studies demonstrated that oscillatory interaction within and between basal ganglia nuclei is very often accompanied by synchronization at Parkinsonian rest tremor frequencies (3–10 Hz). These oscillations have a profound influence on thalamic projections and impair the thalamic relaying of cortical input by generating rebound action potentials. Our model describes convergent inhibitory input received from basal ganglia by the thalamocortical cells based on characteristics of normal activity, and/or low-frequency oscillations (activity associated with Parkinson's disease). In addition to simulated input, we also used microelectrode recordings as inputs for the model. In the resting state, and without additional sensorimotor input, pathological rebound activity is generated for even mild Parkinsonian input. We have found a specific stimulation window of amplitudes and frequencies for periodic input, which corresponds to high-frequency DBS, and which also suppresses rebound activity for mild and even more prominent Parkinsonian input. When low-frequency pathological rebound activity disables the thalamocortical cell's ability to relay excitatory cortical input, a stimulation signal with parameter settings corresponding to our stimulation window can restore the thalamocortical cell's relay functionality.

AB - We present a computational model of a thalamocortical relay neuron for exploring basal ganglia thalamocortical loop behavior in relation to Parkinson's disease and deep brain stimulation (DBS). Previous microelectrode, single-unit recording studies demonstrated that oscillatory interaction within and between basal ganglia nuclei is very often accompanied by synchronization at Parkinsonian rest tremor frequencies (3–10 Hz). These oscillations have a profound influence on thalamic projections and impair the thalamic relaying of cortical input by generating rebound action potentials. Our model describes convergent inhibitory input received from basal ganglia by the thalamocortical cells based on characteristics of normal activity, and/or low-frequency oscillations (activity associated with Parkinson's disease). In addition to simulated input, we also used microelectrode recordings as inputs for the model. In the resting state, and without additional sensorimotor input, pathological rebound activity is generated for even mild Parkinsonian input. We have found a specific stimulation window of amplitudes and frequencies for periodic input, which corresponds to high-frequency DBS, and which also suppresses rebound activity for mild and even more prominent Parkinsonian input. When low-frequency pathological rebound activity disables the thalamocortical cell's ability to relay excitatory cortical input, a stimulation signal with parameter settings corresponding to our stimulation window can restore the thalamocortical cell's relay functionality.

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KW - PACS-87.19.L

KW - PACS-87.19.R

KW - IR-79408

KW - PACS-87.80.y

KW - EWI-21225

KW - METIS-284985

KW - PACS-87.19.X

U2 - 10.1088/1741-2560/8/6/066005

DO - 10.1088/1741-2560/8/6/066005

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JO - Journal of neural engineering

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SN - 1741-2560

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