Brain, Vol. 124, No. 8, 1601-1609,
August 2001
© 2001 Oxford University Press
Networks mediating the clinical effects of pallidal brain stimulation for Parkinson's disease
A PET study of resting-state glucose metabolism
1 Center for Neurosciences, North Shore-Long Island Jewish Research Institute, Manhasset, 2 Department of Neurology, New York University School of Medicine, 3 Department of Psychiatry, Columbia College of Physicians and Surgeons, New York, 4 Department of Neurology, Oregon Health Science University, Portland, Oregon, 5 University of Miami Medical Center, Miami, Florida, USA and 6 The Toronto Western Hospital, Toronto, Ontario, Canada
Correspondence to:
Dr D. Eidelberg, Center for Neurosciences, North Shore-Long Island Jewish Research Institute, 350 Community Drive, Manhasset, NY 11030, USA E-mail: david1{at}nshs.edu
Employing [18F]fluorodeoxyglucose (FDG) and PET, we have found previously that stereotaxic ablation of the internal globus pallidus (GPi) for Parkinson's disease causes resting metabolic changes in brain regions remote from the lesion site. In this study we determined whether similar metabolic changes occur in Parkinson's disease patients treated with deep brain stimulation (DBS) of the GPi. We studied seven Parkinson's disease patients with FDG-PET to measure resting regional cerebral glucose utilization on and off GPi stimulation. We used statistical parametric mapping to identify significant changes in regional brain metabolism that occurred with this intervention. We also quantified stimulation-related changes in the expression of a specific abnormal Parkinson's disease-related pattern of metabolic covariation (PDRP) that had been identified in earlier FDG-PET studies. Metabolic changes with DBS were correlated with clinical improvement as measured by changes in Unified Parkinson's Disease Rating Scale (UPDRS) motor ratings off medication. GPi DBS improved UPDRS motor ratings (36%, P < 0.001) and significantly increased regional glucose metabolism in the premotor cortex ipsilateral to stimulation and in the cerebellum bilaterally. GPi DBS also resulted in a significant (P < 0.01) decline in PDRP activity ipsilateral to stimulation, which correlated significantly with clinical improvement in UPDRS motor ratings (P < 0.03). Clinical improvement with GPi DBS is associated with reduced expression of an abnormal Parkinson's disease-related metabolic network involving elements of the cortico-striato-pallido-thalamocortical and the cerebello-cortical motor loops.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. Hilker, J. Voges, T. Weber, L. W. Kracht, J. Roggendorf, S. Baudrexel, M. Hoevels, V. Sturm, and W. D. Heiss STN-DBS activates the target area in Parkinson disease: An FDG-PET study Neurology, September 2, 2008; 71(10): 708 - 713. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Hirano, K. Asanuma, Y. Ma, C. Tang, A. Feigin, V. Dhawan, M. Carbon, and D. Eidelberg Dissociation of Metabolic and Neurovascular Responses to Levodopa in the Treatment of Parkinson's Disease J. Neurosci., April 16, 2008; 28(16): 4201 - 4209. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Feigin, M. G. Kaplitt, C. Tang, T. Lin, P. Mattis, V. Dhawan, M. J. During, and D. Eidelberg Modulation of metabolic brain networks after subthalamic gene therapy for Parkinson's disease PNAS, December 4, 2007; 104(49): 19559 - 19564. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Asanuma, C. Tang, Y. Ma, V. Dhawan, P. Mattis, C. Edwards, M. G. Kaplitt, A. Feigin, and D. Eidelberg Network modulation in the treatment of Parkinson's disease Brain, October 1, 2006; 129(10): 2667 - 2678. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. M. Halliday, V. Macdonald, and J. M. Henderson A comparison of degeneration in motor thalamus and cortex between progressive supranuclear palsy and Parkinson's disease Brain, October 1, 2005; 128(10): 2272 - 2280. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sestini, S. Ramat, A. R. Formiconi, F. Ammannati, S. Sorbi, and A. Pupi Brain Networks Underlying the Clinical Effects of Long-Term Subthalamic Stimulation for Parkinson's Disease: A 4-Year Follow-up Study with rCBF SPECT J. Nucl. Med., September 1, 2005; 46(9): 1444 - 1454. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Habeck, J. W. Krakauer, C. Ghez, H. A. Sackeim, D. Eidelberg, Y. Stern, and J. R. Moeller A New Approach to Spatial Covariance Modeling of Functional Brain Imaging Data: Ordinal Trend Analysis Neural Comput., July 1, 2005; 17(7): 1602 - 1645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Feigin, M. F. Ghilardi, M. Carbon, C. Edwards, M. Fukuda, V. Dhawan, C. Margouleff, C. Ghez, and D. Eidelberg Effects of levodopa on motor sequence learning in Parkinson's disease Neurology, June 10, 2003; 60(11): 1744 - 1749. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Feigin, M. F. Ghilardi, M. Fukuda, M. J. Mentis, V. Dhawan, A. Barnes, C. P. Ghez, and D. Eidelberg Effects of levodopa infusion on motor activation responses in Parkinson's disease Neurology, July 23, 2002; 59(2): 220 - 226. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Feigin, M. Fukuda, V. Dhawan, S. Przedborski, V. Jackson-Lewis, M.J. Mentis, J.R. Moeller, and D. Eidelberg Metabolic correlates of levodopa response in Parkinson's disease Neurology, December 11, 2001; 57(11): 2083 - 2088. [Abstract] [Full Text] [PDF]
|
|