Hemiballismus: Study of a case using positron emission tomography with 18f1uoro-2-deoxyg1ucose

Authors

  • Richard M. Dubinsky,

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland
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  • Michael Baker,

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland
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  • Dr. Mark Hallett,

    Corresponding author
    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland
    • NINDS, NIH, Building 10, Room 5N226, Bethesda, MD 20892, U.S.A.
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  • Michael Greenberg,

    1. Neuroimaging Section, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland
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  • Giovanni di Chiro

    1. Neurology Service, Malcolm Grow United States Air Force Medical Center, Washington, D.C., U.S.A.
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Abstract

A 64-year-old man had right-sided persistent hemiballismus. Cerebral computed tomography (CT) and 0.5-T magnetic resonance imaging (MRI) showed no abnormalities, but 1.5-T MRI showed decreased signal intensity of the putamina, greater on the left than on the right. The subthalamic area was normal on CT and MRI. Positron emission tomography with 18fluoro- 2-deoxyglucose showed marked hypometabolism of the left putamen (60% of the right) and hypermetabolism of the left parietal lobe (138% of the right). The decreased metabolism of the left putamen may indicate a reduction in neuronal firing. The pathophysiology of the hemiballismus in this case may be loss of tonic inhibition of the lateral globus pallidus from the putamen, leading in turn to greater inhibition of the subthalamic nucleus, less excitation of the medial globus pallidus, and less inhibition of the thalamus and motor cortex, and thus allowing expression of the ballistic movements. allowing expression of the ballistic movements.

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