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

    17 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

    Fingerprint

    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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    author = "H.G.E. Meijer and M. Krupa and H. Cagnan and M.A.J. Lourens and T. Heida and H.C.F. Martens and L.J. Bour and {van Gils}, S.A.",
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    language = "English",
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    journal = "Journal of neural engineering",
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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

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    JO - Journal of neural engineering

    JF - Journal of neural engineering

    SN - 1741-2560

    IS - 6

    M1 - 066005

    ER -