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J Neurol Neurosurg Psychiatry 2005;76:426-428 doi:10.1136/jnnp.2004.043547
  • Short report

Altered subthalamo-pallidal synchronisation in parkinsonian dyskinesias

  1. G Foffani1,
  2. G Ardolino1,
  3. B Meda2,
  4. M Egidi1,
  5. P Rampini1,
  6. E Caputo3,
  7. G Baselli2,
  8. A Priori1
  1. 1Department of Neurological Sciences, Università di Milano, IRCCS Ospedale Maggiore di Milano, 20122 Milan, Italy
  2. 2Department of Biomedical Engineering, Politecnico di Milano, 20133 Milan, Italy
  3. 3Department of Clinical Neurology, Ospedale San Paolo, 20142 Milan, Italy
  1. Correspondence to:
 Professor Alberto Priori
 Dipartimento di Scienze Neurologiche, Clinica Neurologica, Padiglione Ponti, Ospedale Maggiore Policlinico, Via F. Sforza 35, Milano, 20122 Italy; alberto.prioriunimi.it
  • Received 19 April 2004
  • Accepted 25 June 2004
  • Revised 8 June 2004

Abstract

The aim of this work was to study the role of subthalamo-pallidal synchronisation in the pathophysiology of dyskinesias. We recorded local field potentials (LFPs) in a patient with Parkinson’s disease and left surgery induced dyskinesias with double, bilateral deep brain stimulation electrode implants in the subthalamic nucleus (STN) and the globus pallidus internus (GPi). Synchronisation was studied through coherence analysis. In the nuclei contralateral to the dyskinetic side of the body there was decreased STN-GPi coherence in the high beta range (20–30 Hz) and an enhanced coherence at low frequencies (<10 Hz). Despite the possible limitations arising from single-case observations, our findings suggest that parkinsonian dyskinesias are related to altered synchronisation between different structures of the basal ganglia. Firing abnormalities within individual basal ganglia nuclei are probably not enough to account for the complex balance between hypokinetic and hyperkinetic symptoms in human parkinsonian dyskinesias and altered interactions between nuclei should also be considered.

Footnotes

  • This study was supported by the IRCCS Ospedale Maggiore di Milano, the Centro Dino Ferrari for Neurodegenerative Disorders, the Ministero della Sanità, and the Ministero dell’Università e della Ricerca Scientifica e Tecnologica. G Foffani was partially supported by the “Professor Guglielmo Scarlato Award” 2003 from the Società Italiana di Neurologia (S.I.N.). A Priori was partly supported by travel grant N00014-04-1-4004 from the US Department of the Navy, Office of Naval Research International Field Office.

  • Competing interests: none declared

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