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Center for Neuromagnetism, Department of Physiology and Neuroscience, New York University Medical Center, NY (Dr. Volkmann) (Dr. Joliot) (Dr. Mogilner) (Dr. Lado) (Dr. Ribary) (Dr. Llinás)
Department of Neurology, New York University Medical Center, NY (Dr. Fazzini)
Department of Physics, The Open University, Milton Keynes, UK (Dr. Ioannides)
Institute for Medicine, Research Center Jülich, Jülich, Germany (Dr. Ioannides)
Service Hospitalier Frédéric Joliot, DRIPP-CEA, Orsay, France (Dr. Joliot)
Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany. (Dr. Volkmann)
Address correspondence and reprint requests to Dr. R. Llinás or Dr. U. Ribary, Department of Physiology and Neuroscience, NYU Medical Center, 550 First Avenue, New York, NY, 10016.
A variety of clinical and experimental findings suggest that parkinsonian resting tremor results from the involuntary activation of a central mechanism normally used for the production of rapid voluntary alternating movements. However, such central motor loop oscillations have never been directly demonstrated in parkinsonian patients. Using magnetoencephalography, we recorded synchronized and tremor-related neuromagnetic activity over wide areas of the frontal and parietal cortex. The spatial and temporal organization of this activity was studied in seven patients suffering from early-stage idiopathic Parkinson's disease (PD). Single equivalent current dipole (ECD) analysis and fully three-dimensional distributed source solutions (magnetic field tomography, MFT) were used in this analysis. ECD and MFT solutions were superimposed on high-resolution MRI. The findings indicate that 3 to 6 Hz tremor in PD is accompanied by rhythmic subsequent electrical activation at the diencephalic level and in lateral premotor, somatomotor, and somatosensory cortex. Tremor-evoked magnetic activity can be attributed to source generators that were previously described for voluntary movements. The interference of such slow central motor loop oscillations with voluntary motor activity may therefore constitute a pathophysiologic link between tremor and bradykinesia in PD. NEUROLOGY 1996;46:1359-1370
Supported by Biomagnetic Technology, Inc., San Diego, California.
Received March 21, 1995. Accepted in final form August 10, 1995.
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