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      Modulation of Beta Oscillations in the Subthalamic Nucleus with Prosaccades and Antisaccades in Parkinson's Disease

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          Abstract

          Increased oscillations in the beta band are thought to be related to motor symptoms of Parkinson's disease (PD). Previous studies have shown that beta-band desynchronization in the subthalamic nucleus (STN) is reduced just before and during limb movements. While the STN is part of the basal ganglia (BG)-thalamocortical circuit controlling limb movements, it is also part of the BG-brainstem projection controlling saccadic eye movements. Late-stage PD patients have deficits in saccades in addition to difficulties with limb movements arising from impaired functions of the BG. We investigated saccade-related changes in beta-band (15–30 Hz) oscillatory activities in the human STN while PD patients performed visually guided prosaccades and antisaccades, the latter requiring suppression of reflexive responses and volitional initiation of saccades. We recorded local field potentials from deep brain stimulation electrodes implanted in the STN in human PD patients 1–5 d after surgery and compared prosaccades and antisaccades with these and with limb movements. Saccade-related beta-band desynchronizations were observed just before and during saccades in all subjects, suggesting that reduction of beta-band oscillatory activity in the STN is related to preparation and execution of saccades. Furthermore, beta-band desynchronizations for antisaccades started earlier, were sustained for longer periods, were of greater magnitude, and were observed more often than prosaccades. Beta-band desynchronization in the STN may reflect the additional processes associated with suppression of reflexive responses and volitional execution of saccades in the opposite direction.

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          Author and article information

          Journal
          J Neurosci
          J. Neurosci
          jneuro
          jneurosci
          J. Neurosci
          The Journal of Neuroscience
          Society for Neuroscience
          0270-6474
          1529-2401
          17 April 2013
          : 33
          : 16
          : 6895-6904
          Affiliations
          [1] 1Division of Neurology, Toronto Western Research Institute, and the Edmond J. Safra Program in Parkinson's Disease,
          [2] 2Division of Neurosurgery, and Toronto Western Research Institute, and
          [3] 3Department of Physiology, University of Toronto, Toronto, Ontario M5T 2S8, Canada
          Author notes
          Correspondence should be addressed to Akihiro Yugeta, Department of Neurology, The University of Tokyo Hospital, 7–3-1 Hongo, Bukyo-ku, Tokyo, 113–8655, Japan. yugetaa-tky@ 123456umin.ac.jp

          Author contributions: A.Y., W.D.H., and R.C. designed research; A.Y., W.D.H., C.H., U.S., A.M.L., M.H., E.M., and R.C. performed research; A.Y. and W.D.H. contributed unpublished reagents/analytic tools; A.Y. and W.D.H. analyzed data; A.Y., W.D.H., and R.C. wrote the paper.

          E. Moro's present address is Movement Disorder Unit, Department of Psychiatry and Neurology, Centre Hospitalier Universitaire de Grenoble, 38043 Grenoble, France.

          Article
          PMC6618858 PMC6618858 6618858 2564-12
          10.1523/JNEUROSCI.2564-12.2013
          6618858
          23595748
          46012c5d-ef6d-428d-ab65-01cf12de49f5
          Copyright © 2013 the authors 0270-6474/13/336895-10$15.00/0
          History
          : 28 May 2012
          : 28 February 2013
          : 2 March 2013
          Categories
          Articles
          Behavioral/Cognitive

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