Cerebral metabolism of glucose in benign hereditary chorea
Identifieur interne : 001D92 ( Istex/Corpus ); précédent : 001D91; suivant : 001D93Cerebral metabolism of glucose in benign hereditary chorea
Auteurs : Oksana Suchowersky ; Hayden ; W. R. Wayne Martin ; A. Jon Stoessl ; Anne M. Hildebrand ; Brian D. PateSource :
- Movement Disorders [ 0885-3185 ] ; 1986.
English descriptors
- KwdEn :
Abstract
Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. There is marked clinical variability in this disease with some subjects having onset in infancy and others with onset in early adulthood. In contrast to Huntington's disease (HD), there is no dementia. Computed tomography is normal in all subjects with no evidence of caudate nucleus atrophy. We present the results of positron emission tomography using 18F‐2‐fluorodeoxyglucose on three patients with this disorder from two families. Cerebral glucose metabolism in one patient was decreased in the caudate nucleus, as previously reported in HD. The other two persons from a second family showed a relative decrease in metabolic rates of glucose in the caudate when compared with the thalamus. It appears that caudate hypometabolism is not specific for HD. These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.
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DOI: 10.1002/mds.870010105
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<front><div type="abstract" xml:lang="en">Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. There is marked clinical variability in this disease with some subjects having onset in infancy and others with onset in early adulthood. In contrast to Huntington's disease (HD), there is no dementia. Computed tomography is normal in all subjects with no evidence of caudate nucleus atrophy. We present the results of positron emission tomography using 18F‐2‐fluorodeoxyglucose on three patients with this disorder from two families. Cerebral glucose metabolism in one patient was decreased in the caudate nucleus, as previously reported in HD. The other two persons from a second family showed a relative decrease in metabolic rates of glucose in the caudate when compared with the thalamus. It appears that caudate hypometabolism is not specific for HD. These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.</div>
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<p>Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. There is marked clinical variability in this disease with some subjects having onset in infancy and others with onset in early adulthood. In contrast to Huntington's disease (HD), there is no dementia. Computed tomography is normal in all subjects with no evidence of caudate nucleus atrophy. We present the results of positron emission tomography using <sup>18</sup>
F‐2‐fluorodeoxyglucose on three patients with this disorder from two families. Cerebral glucose metabolism in one patient was decreased in the caudate nucleus, as previously reported in HD. The other two persons from a second family showed a relative decrease in metabolic rates of glucose in the caudate when compared with the thalamus. It appears that caudate hypometabolism is not specific for HD. These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.</p>
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<noteGroup><note xml:id="fn1"><p>A videotape segment accompanies this article.</p>
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<!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Cerebral metabolism of glucose in benign hereditary chorea</title>
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<titleInfo type="abbreviated" lang="en"><title>GLUCOSE METABOLISM IN BENIGN HEREDITARY CHOREA</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cerebral metabolism of glucose in benign hereditary chorea</title>
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<name type="personal"><namePart type="given">Oksana</namePart>
<namePart type="family">Suchowersky</namePart>
<affiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="termsOfAddress">Dr.</namePart>
<namePart type="family">Hayden</namePart>
<affiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
<affiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
<description>Correspondence: Department of Medical Genetics, Health Sciences Centre Hospital, 2211 Wesbrook Mall, University of British Columbia, Vancouver, British Columbia, Canada V6T 2B5</description>
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<name type="personal"><namePart type="given">W. R. Wayne</namePart>
<namePart type="family">Martin</namePart>
<affiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">A. Jon</namePart>
<namePart type="family">Stoessl</namePart>
<affiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Anne M.</namePart>
<namePart type="family">Hildebrand</namePart>
<affiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Brian D.</namePart>
<namePart type="family">Pate</namePart>
<affiliation>Faculty of Pharmaceutical Sciences, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation>
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<dateIssued encoding="w3cdtf">1986</dateIssued>
<copyrightDate encoding="w3cdtf">1986</copyrightDate>
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<extent unit="figures">4</extent>
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<extent unit="references">25</extent>
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<abstract lang="en">Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. There is marked clinical variability in this disease with some subjects having onset in infancy and others with onset in early adulthood. In contrast to Huntington's disease (HD), there is no dementia. Computed tomography is normal in all subjects with no evidence of caudate nucleus atrophy. We present the results of positron emission tomography using 18F‐2‐fluorodeoxyglucose on three patients with this disorder from two families. Cerebral glucose metabolism in one patient was decreased in the caudate nucleus, as previously reported in HD. The other two persons from a second family showed a relative decrease in metabolic rates of glucose in the caudate when compared with the thalamus. It appears that caudate hypometabolism is not specific for HD. These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.</abstract>
<note type="content">*A videotape segment accompanies this article.</note>
<subject lang="en"><genre>Keywords</genre>
<topic>Benign hereditary chorea</topic>
<topic>Huntington's disease</topic>
<topic>Positron emission tomography</topic>
<topic>Computed tomography</topic>
<topic>Glucose metabolism</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<topic>Original Article</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part><date>1986</date>
<detail type="volume"><caption>vol.</caption>
<number>1</number>
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<detail type="issue"><caption>no.</caption>
<number>1</number>
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<extent unit="pages"><start>33</start>
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<identifier type="DOI">10.1002/mds.870010105</identifier>
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<accessCondition type="use and reproduction" contentType="copyright">Copyright © 1986 Movement Disorder Society</accessCondition>
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