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Neural origin of evoked potentials during thalamic deep brain stimulation.

Publication ,  Journal Article
Kent, AR; Grill, WM
Published in: Journal of neurophysiology
August 2013

Closed-loop deep brain stimulation (DBS) systems could provide automatic adjustment of stimulation parameters and improve outcomes in the treatment of Parkinson's disease and essential tremor. The evoked compound action potential (ECAP), generated by activated neurons near the DBS electrode, may provide a suitable feedback control signal for closed-loop DBS. The objectives of this work were to characterize the ECAP across stimulation parameters and determine the neural elements contributing to the signal. We recorded ECAPs during thalamic DBS in anesthetized cats and conducted computer simulations to calculate the ECAP of a population of thalamic neurons. The experimental and computational ECAPs were similar in shape and had characteristics that were correlated across stimulation parameters (R(2) = 0.80-0.95, P < 0.002). The ECAP signal energy increased with larger DBS amplitudes (P < 0.0001) and pulse widths (P < 0.002), and the signal energy of secondary ECAP phases was larger at 10-Hz than at 100-Hz DBS (P < 0.002). The computational model indicated that these changes resulted from a greater extent of neural activation and an increased synchronization of postsynaptic thalamocortical activity, respectively. Administration of tetrodotoxin, lidocaine, or isoflurane abolished or reduced the magnitude of the experimental and computational ECAPs, glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D(-)-2-amino-5-phosphonopentanoic acid (APV) reduced secondary ECAP phases by decreasing postsynaptic excitation, and the GABAA receptor agonist muscimol increased the latency of the secondary phases by augmenting postsynaptic hyperpolarization. This study demonstrates that the ECAP provides information about the type and extent of neural activation generated during DBS, and the ECAP may serve as a feedback control signal for closed-loop DBS.

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Published In

Journal of neurophysiology

DOI

EISSN

1522-1598

ISSN

0022-3077

Publication Date

August 2013

Volume

110

Issue

4

Start / End Page

826 / 843

Related Subject Headings

  • Valine
  • Thalamus
  • Tetrodotoxin
  • Sodium Channel Blockers
  • Neurons
  • Neurology & Neurosurgery
  • Muscimol
  • Male
  • Lidocaine
  • GABA-A Receptor Agonists
 

Citation

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Kent, A. R., & Grill, W. M. (2013). Neural origin of evoked potentials during thalamic deep brain stimulation. Journal of Neurophysiology, 110(4), 826–843. https://doi.org/10.1152/jn.00074.2013
Kent, Alexander R., and Warren M. Grill. “Neural origin of evoked potentials during thalamic deep brain stimulation.Journal of Neurophysiology 110, no. 4 (August 2013): 826–43. https://doi.org/10.1152/jn.00074.2013.
Kent AR, Grill WM. Neural origin of evoked potentials during thalamic deep brain stimulation. Journal of neurophysiology. 2013 Aug;110(4):826–43.
Kent, Alexander R., and Warren M. Grill. “Neural origin of evoked potentials during thalamic deep brain stimulation.Journal of Neurophysiology, vol. 110, no. 4, Aug. 2013, pp. 826–43. Epmc, doi:10.1152/jn.00074.2013.
Kent AR, Grill WM. Neural origin of evoked potentials during thalamic deep brain stimulation. Journal of neurophysiology. 2013 Aug;110(4):826–843.

Published In

Journal of neurophysiology

DOI

EISSN

1522-1598

ISSN

0022-3077

Publication Date

August 2013

Volume

110

Issue

4

Start / End Page

826 / 843

Related Subject Headings

  • Valine
  • Thalamus
  • Tetrodotoxin
  • Sodium Channel Blockers
  • Neurons
  • Neurology & Neurosurgery
  • Muscimol
  • Male
  • Lidocaine
  • GABA-A Receptor Agonists