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From the Departments of Psychiatry (Dr. Hershey), Neurology (Drs. Hershey, Revilla, Videen, and Perlmutter, and A.R. Wernle, L. McGee-Minnich, and J.V. Antenor), Neurological Surgery (Drs. Revilla and Dowling), Radiology (Drs. Videen and Perlmutter), and Anatomy and Neurobiology (Dr. Perlmutter), Washington University School of Medicine, St. Louis, MO; and Departments of Neurology, Neurobiology, and Pediatrics (Dr. Mink), University of Rochester Medical Center, Rochester, NY.
Address correspondence and reprint requests to Dr. J.S. Perlmutter, Campus Box 8111, Washington University School of Medicine, 4525 Scott Avenue, St. Louis, MO 63110; e-mail: joel{at}npg.wustl.edu
Objective: To assess whether subthalamic nuclei (STN) stimulations primary mechanism of action is to drive or inhibit output neurons.
Methods: Cerebral blood flow responses to STN stimulation were measured using PET in 13 patients with Parkinson disease. Patients were scanned with stimulators off and on (six scans each condition). Clinical ratings, EMG, and videotaping of movements were obtained at each scan. Scans with observable tremor or movement were eliminated from analysis. Brain regions where STN stimulation significantly altered blood flow were identified.
Results: STN stimulation increased blood flow in midbrain (including STN), globus pallidus, and thalamus, primarily on the left side, but reduced blood flow bilaterally in frontal, parietal, and temporal cortex.
Conclusions: These data suggest that STN stimulation increases firing of STN output neurons, which increases inhibition of thalamocortical projections, ultimately decreasing blood flow in cortical targets. STN stimulation appears to drive, rather than inhibit, STN output neurons.
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