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      Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

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          Abstract

          Deep brain stimulation (DBS) is highly effective for both hypo- and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson’s disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal ganglia-thalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

          Electronic supplementary material

          The online version of this article (doi:10.1007/s13311-016-0426-6) contains supplementary material, which is available to authorized users.

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          Author and article information

          Contributors
          twichma@emory.edu
          Journal
          Neurotherapeutics
          Neurotherapeutics
          Neurotherapeutics
          Springer US (New York )
          1933-7213
          1878-7479
          8 March 2016
          April 2016
          : 13
          : 2
          : 264-283
          Affiliations
          [1 ] GRID grid.189967.8, ISNI 0000000109416502, Department of Neurology, , Emory University School of Medicine, ; Atlanta, GA USA
          [2 ] GRID grid.189967.8, ISNI 0000000109416502, Yerkes National Primate Research Center, , Emory University, ; Atlanta, GA USA
          Article
          PMC4824026 PMC4824026 4824026 426
          10.1007/s13311-016-0426-6
          4824026
          26956115
          57d70474-48dd-4bd7-8422-ce7f52ad879a
          © The American Society for Experimental NeuroTherapeutics, Inc. 2016
          History
          Categories
          Review
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          © The American Society for Experimental NeuroTherapeutics, Inc. 2016

          Basal ganglia circuits,Pathophysiology,Synchrony,Oscillation,Deep brain stimulation,Dystonia,Parkinson’s disease

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