Concurrent Deep Brain Stimulation Reduces the Direct Cortical Stimulation Necessary for Motor Output.

Parkinson's disease; deep brain stimulation; direct cortical stimulation; hyperdirect pathway; motor-evoked potential; hypokinetic sequalae

Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
12 2020
Historique:
received: 06 03 2020
revised: 09 07 2020
accepted: 03 08 2020
pubmed: 12 9 2020
medline: 28 4 2021
entrez: 11 9 2020
Statut: ppublish

Résumé

Converging literatures suggest that deep brain stimulation (DBS) in Parkinson's disease affects multiple circuit mechanisms. One proposed mechanism is the normalization of primary motor cortex (M1) pathophysiology via effects on the hyperdirect pathway. We hypothesized that DBS would reduce the current intensity necessary to modulate motor-evoked potentials from focally applied direct cortical stimulation (DCS). Intraoperative subthalamic DBS, DCS, and preoperative diffusion tensor imaging data were acquired in 8 patients with Parkinson's disease. In 7 of 8 patients, DBS significantly reduced the M1 DCS current intensity required to elicit motor-evoked potentials. This neuromodulation was specific to select DBS bipolar configurations. In addition, the volume of activated tissue models of these configurations were significantly associated with overlap of the hyperdirect pathway. DBS reduces the current necessary to elicit a motor-evoked potential using DCS. This supports a circuit mechanism of DBS effectiveness, potentially involving the hyperdirect pathway that speculatively may underlie reductions in hypokinetic abnormalities in Parkinson's disease. © 2020 International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND
Converging literatures suggest that deep brain stimulation (DBS) in Parkinson's disease affects multiple circuit mechanisms. One proposed mechanism is the normalization of primary motor cortex (M1) pathophysiology via effects on the hyperdirect pathway.
OBJECTIVES
We hypothesized that DBS would reduce the current intensity necessary to modulate motor-evoked potentials from focally applied direct cortical stimulation (DCS).
METHODS
Intraoperative subthalamic DBS, DCS, and preoperative diffusion tensor imaging data were acquired in 8 patients with Parkinson's disease.
RESULTS
In 7 of 8 patients, DBS significantly reduced the M1 DCS current intensity required to elicit motor-evoked potentials. This neuromodulation was specific to select DBS bipolar configurations. In addition, the volume of activated tissue models of these configurations were significantly associated with overlap of the hyperdirect pathway.
CONCLUSIONS
DBS reduces the current necessary to elicit a motor-evoked potential using DCS. This supports a circuit mechanism of DBS effectiveness, potentially involving the hyperdirect pathway that speculatively may underlie reductions in hypokinetic abnormalities in Parkinson's disease. © 2020 International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 32914888
doi: 10.1002/mds.28255
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2348-2353

Informations de copyright

© 2020 International Parkinson and Movement Disorder Society.

Références

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Auteurs

Kurt E Weaver (KE)

Department of Radiology, University of Washington School of Medicine, Seattle, Washington, USA.
Graduate Program in Neuroscience, University of Washington School of Medicine, Seattle, Washington, USA.
Center for NeuroTechnologies, University of Washington School of Medicine, Seattle, Washington, USA.

David J Caldwell (DJ)

Graduate Program in Neuroscience, University of Washington School of Medicine, Seattle, Washington, USA.
Department of BioEngineering, University of Washington School of Medicine, Seattle, Washington, USA.

Jeneva A Cronin (JA)

Graduate Program in Neuroscience, University of Washington School of Medicine, Seattle, Washington, USA.
Department of BioEngineering, University of Washington School of Medicine, Seattle, Washington, USA.

Chao-Hung Kuo (CH)

Department of Neurosurgery, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
School of Medicine, National Yang-Ming University, Taipei, Taiwan.

Michael Kogan (M)

Department of Neurosurgery, University of Buffalo, Buffalo, New York, USA.

Brady Houston (B)

Dept of Electrical Engineering, University of Washington School of Medicine, Seattle, Washington, USA.

Victor Sanchez (V)

Department of Radiology, University of Washington School of Medicine, Seattle, Washington, USA.

Vicente Martinez (V)

Department of Rehabilitative Medicine, University of Washington School of Medicine, Seattle, Washington, USA.

Jeffrey G Ojemann (JG)

Graduate Program in Neuroscience, University of Washington School of Medicine, Seattle, Washington, USA.
Center for NeuroTechnologies, University of Washington School of Medicine, Seattle, Washington, USA.
Department of Neurological Surgery, University of Washington School of Medicine, Seattle, Washington, USA.

Swati Rane (S)

Department of Radiology, University of Washington School of Medicine, Seattle, Washington, USA.

Andrew L Ko (AL)

Graduate Program in Neuroscience, University of Washington School of Medicine, Seattle, Washington, USA.
Center for NeuroTechnologies, University of Washington School of Medicine, Seattle, Washington, USA.
Department of Neurological Surgery, University of Washington School of Medicine, Seattle, Washington, USA.

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