4.7 Article

Motor activation in multiple system atrophy and Parkinson disease A PET study

Journal

NEUROLOGY
Volume 75, Issue 13, Pages 1174-1180

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181f4d78f

Keywords

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Funding

  1. GE Healthcare
  2. Novartis
  3. UCB
  4. Lundbeck Inc.
  5. Boehringer Ingelheim
  6. GlaxoSmithKline
  7. Orion Pharma
  8. Teva Pharmaceutical Industries Ltd.
  9. SERVIER
  10. PHRC
  11. France Parkinson
  12. Michael J. Fox Foundation

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Background: Multiple system atrophy (MSA) is an atypical parkinsonian syndrome including cerebellar impairment and poor response to levodopa. We assessed right hand motor activation in patients with MSA before and after an acute levodopa challenge in comparison with patients with PD and healthy volunteers (HVs). Methods: Eighteen patients with MSA, 8 patients with PD, and 10 age-matched HVs were included. Regional cerebral blood flow measurements with H(2)(15)O PET were performed at rest and during a right hand movement. Statistical parametric mapping was used to analyze motor vs rest in OFF and ON conditions and the effect of levodopa on motor activation. Results: Before levodopa, patients with MSA activated most known cerebral motor areas. Compared with HVs, patients with MSA exhibited less bilateral cerebellar activation and greater left superior parietal activation. They also had less bilateral cerebellar and greater supplementary motor and left superior parietal activation than patients with PD. Conversely, patients with PD had greater activation than HVs in the right cerebellum and less in the supplementary motor cortex. After levodopa, patients with MSA exhibited reduced activation in anterior cingulate, whereas patients with PD had greater activation in the right cerebellum. Conclusion: Patients with MSA and patients with PD recruited different motor networks. Patients with PD preferentially activated cerebellar pathways, possibly to compensate for basal ganglia dysfunction. This was not observed in patients with MSA, probably because of cerebellar dysfunction; other frontoparietal cortical areas were recruited. Neurology (R) 2010; 75: 1174-1180

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