PET imaging of the pre‐synaptic dopamine uptake sites in rapid‐onset dystonia‐parkinsonism (RDP)
Identifieur interne : 007994 ( Main/Merge ); précédent : 007993; suivant : 007995PET imaging of the pre‐synaptic dopamine uptake sites in rapid‐onset dystonia‐parkinsonism (RDP)
Auteurs : Allison Brashear [États-Unis] ; G. Keith Mulholland [États-Unis] ; Qi-Huang Zheng [États-Unis] ; Martin R. Farlow [États-Unis] ; Eric R. Siemers [États-Unis] ; Gary D. Hutchins [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 1999-01.
English descriptors
- KwdEn :
- Dopamine, Dystonia, PET, Parkinsonism, RDP.
Abstract
BACKGROUND: Rapid‐onset dystonia‐parkinsonism (RDP) is a genetic movement disorder characterized by abrupt onset over hours to days of bradykinesia, postural instability, dysphagia, dysarthria, and severe dystonic spasms with decreased levels of the dopamine metabolite, homovanillic acid (HVA), in cerebrospinal fluid (CSF). METHODS: We imaged the dopamine re‐uptake system with [O‐methyl‐11C]β‐CFT ([11C]β‐CFT) in three severely affected individuals with RDP and four patients with idiopathic Parkinson's disease (IPD). Results were compared with those of age‐matched normal volunteers. RESULTS: Positron emission tomography images from those patients with IPD demonstrated a dramatic reduction in the volume of distribution of [11C]β‐CFT whereas patients with RDP showed slightly elevated values. CONCLUSIONS: The data suggest that patients with RDP do not have a decrease in the number of dopamine re‐uptake sites. Our findings suggest that, unlike the situation in IPD, low CSF HVA concentrations seen in RDP patients are not the result of degeneration of striatal dopamine terminals or loss of dopamine re‐uptake sites.
Url:
DOI: 10.1002/1531-8257(199901)14:1<132::AID-MDS1022>3.0.CO;2-J
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Siemers</name></author><author><name sortKey="Hutchins, Gary D" sort="Hutchins, Gary D" uniqKey="Hutchins G" first="Gary D." last="Hutchins">Gary D. 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Farlow</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, and the Division of Imaging Sciences, Department of Radiology, Indiana University School of Medicine, Indianapolis, Indiana</wicri:regionArea><placeName><region type="state">Indiana</region></placeName></affiliation></author><author><name sortKey="Siemers, Eric R" sort="Siemers, Eric R" uniqKey="Siemers E" first="Eric R." last="Siemers">Eric R. Siemers</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, and the Division of Imaging Sciences, Department of Radiology, Indiana University School of Medicine, Indianapolis, Indiana</wicri:regionArea><placeName><region type="state">Indiana</region></placeName></affiliation></author><author><name sortKey="Hutchins, Gary D" sort="Hutchins, Gary D" uniqKey="Hutchins G" first="Gary D." last="Hutchins">Gary D. Hutchins</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Imaging Sciences, Department of Radiology, Indiana University School of Medicine, Indianapolis, Indiana</wicri:regionArea><placeName><region type="state">Indiana</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="1999-01">1999-01</date><biblScope unit="vol">14</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="132">132</biblScope><biblScope unit="page" to="137">137</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">DCCFF22FD077624EAE39149AED7B25B49BFE59A0</idno><idno type="DOI">10.1002/1531-8257(199901)14:1<132::AID-MDS1022>3.0.CO;2-J</idno><idno type="ArticleID">MDS1022</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine</term><term>Dystonia</term><term>PET</term><term>Parkinsonism</term><term>RDP</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">BACKGROUND: Rapid‐onset dystonia‐parkinsonism (RDP) is a genetic movement disorder characterized by abrupt onset over hours to days of bradykinesia, postural instability, dysphagia, dysarthria, and severe dystonic spasms with decreased levels of the dopamine metabolite, homovanillic acid (HVA), in cerebrospinal fluid (CSF). METHODS: We imaged the dopamine re‐uptake system with [O‐methyl‐11C]β‐CFT ([11C]β‐CFT) in three severely affected individuals with RDP and four patients with idiopathic Parkinson's disease (IPD). Results were compared with those of age‐matched normal volunteers. RESULTS: Positron emission tomography images from those patients with IPD demonstrated a dramatic reduction in the volume of distribution of [11C]β‐CFT whereas patients with RDP showed slightly elevated values. CONCLUSIONS: The data suggest that patients with RDP do not have a decrease in the number of dopamine re‐uptake sites. Our findings suggest that, unlike the situation in IPD, low CSF HVA concentrations seen in RDP patients are not the result of degeneration of striatal dopamine terminals or loss of dopamine re‐uptake sites.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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