Cerebral metabolism and atrophy in huntington's disease determined by 18FDG and computed tomographic scan

Authors

  • Dr David E. Kuhl MD,

    Corresponding author
    1. Laboratory of Nuclear Medicine, the Divisions of UCLA School of Medicine, Los Angeles, CA 90024
    2. Nuclear Medicine UCLA School of Medicine, Los Angeles, CA 90024
    • Laboratory of Nuclear Medicine, UCLA School of Medicine, Los Angeles, CA 90024
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  • Michael E. Phelps PhD,

    1. Laboratory of Nuclear Medicine, the Divisions of UCLA School of Medicine, Los Angeles, CA 90024
    2. Nuclear Medicine UCLA School of Medicine, Los Angeles, CA 90024
    3. Biophysics UCLA School of Medicine, Los Angeles, CA 90024
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  • Charles H. Markham MD,

    1. Section of Ultrasound and Body Computed Tomography of the Department of Radiological Sciences UCLA School of Medicine, Los Angeles, CA 90024
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  • E. Jeffrey Metter MD,

    1. Laboratory of Nuclear Medicine, the Divisions of UCLA School of Medicine, Los Angeles, CA 90024
    2. Section of Ultrasound and Body Computed Tomography of the Department of Radiological Sciences UCLA School of Medicine, Los Angeles, CA 90024
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  • Walter H. Riege PhD,

    1. Section of Ultrasound and Body Computed Tomography of the Department of Radiological Sciences UCLA School of Medicine, Los Angeles, CA 90024
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  • James Winter MD, PhD

    1. Department of Neurology, UCLa school of Medicine, Los Angeles, CA 90024
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Abstract

Patterns of local cerebral glucose utilization were measured with positron emission computed tomography using the 18F-fluorodeoxyglucose method in 13 patients with Huntington's disease (HD), 15 subjects at risk for HD, and 40 normal control subjects. These data were compared with computed tomographic measures of cerebral atrophy, with age, and with duration and severity of symptoms. The results indicate that in HD there is a characteristic decrease in glucose utilization in the caudate and putamen and that this local hypometabolism appears early and precedes bulk tissue loss. In contrast to patients with senile dementia, in these HD patients glucose utilization typically was normal throughout the rest of the brain, regardless of the severity of symptoms and despite apparent shrinkage of brain tissue. Our results suggest the possibility that the caudate may be hypometabolic in some asymptomatic subjects who are potential carriers of the autosomal dominant gene for HD.

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