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Fluorodeoxyglucose positron emission tomography in Richardson's syndrome and progressive supranuclear palsy-parkinsonism

Authors

  • Karin Srulijes MD,

    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
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  • Matthias Reimold MD,

    1. Nuclear Medicine and PET Center, University of Tuebingen, Tuebingen, Germany
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    • Karin Srulijes and Matthias Reimold contributed equally to this work.

  • Rajka M. Liscic MD, PhD,

    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
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  • Sarah Bauer,

    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
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  • Elisabeth Dietzel,

    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
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  • Inga Liepelt-Scarfone PhD,

    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
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  • Daniela Berg MD,

    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
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  • Walter Maetzler MD

    Corresponding author
    1. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    2. German Center for Neurodegenerative Diseases, DZNE, University of Tuebingen, Tuebingen, Germany
    3. Robert-Bosch-Hospital, Department of Clinical Gerontology, Stuttgart, Germany
    • Department of Neurodegeneration, University of Tuebingen, Germany, Hoppe Seyler-Strasse 27, 72076 Tuebingen, Germany
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  • Relevant conflicts of interest/financial disclosures: Nothing to report. Full financial disclosures and author roles may be found in the online version of this article.

Abstract

Background:

We hypothesized that postural instability and cognitive decline in patients with Richardson's syndrome could be a consequence of reduced thalamic and frontal metabolism. Severe Parkinsonian signs in patients with progressive supranuclear palsy-parkinsonism may be reflected by alterations in putaminal metabolism.

Methods:

Eleven patients with Richardson's syndrome, 8 patients with progressive supranuclear palsy-parkinsonism, 12 with Parkinson's disease, and 10 controls underwent clinical assessment and fluorodeoxyglucose positron emission tomography (PET).

Results:

Richardson's syndrome patients showed pronounced thalamic hypometabolism, and patients with progressive supranuclear palsy-parkinsonism pronounced putaminal hypometabolism, compared to all other investigated groups. The putamen/thalamus uptake ratio differentiated progressive supranuclear palsy-parkinsonism from Richardson's syndrome (area under the curve = 0.86) and from Parkinson's disease (area under the curve = 0.80) with acceptable accuracy. Frontal hypometabolism was predominantly found in Richardson's syndrome patients.

Conclusions:

Richardson's syndrome, progressive supranuclear palsy-parkinsonism and Parkinson's disease showed different metabolic patterns in fluorodeoxyglucose PET. © 2011 Movement Disorder Society

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