Clinical and positron emission tomography findings of chorea associated with primary antiphospholipid antibody syndrome
Identifieur interne : 002F58 ( Main/Curation ); précédent : 002F57; suivant : 002F59Clinical and positron emission tomography findings of chorea associated with primary antiphospholipid antibody syndrome
Auteurs : Steve W. Wu [États-Unis] ; Brent Graham [États-Unis] ; Michael J. Gelfand [États-Unis] ; Ralph E. Gruppo [États-Unis] ; Argirios Dinopolous [États-Unis] ; Donald L. Gilbert [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-09-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adolescent, Antiphospholipid antibody syndrome, Attention Deficit Disorder with Hyperactivity (complications), Cardiolipins (immunology), Chorea, Chorea (etiology), Chorea (immunology), Chorea (radionuclide imaging), Emission tomography, Fluorodeoxyglucose F18 (diagnostic use), Humans, Immunoglobulin G (blood), Male, Nervous system diseases, Neurologic Examination, PET imaging, Platelet, Positron emission tomography, Positron-Emission Tomography (methods), Steroid, antiphospholipid antibody syndrome, beta 2-Glycoprotein I (immunology), chorea, steroid.
- MESH :
- chemical , blood : Immunoglobulin G.
- chemical , diagnostic use : Fluorodeoxyglucose F18.
- chemical , immunology : Cardiolipins, beta 2-Glycoprotein I.
- complications : Attention Deficit Disorder with Hyperactivity.
- etiology : Chorea.
- immunology : Chorea.
- methods : Positron-Emission Tomography.
- radionuclide imaging : Chorea.
- Adolescent, Humans, Male, Neurologic Examination.
Abstract
A fourteen‐year‐old right‐handed male with a history of attention deficit hyperactivity disorder (ADHD) presented with alternating hemichorea. Laboratory findings included elevated anticardiolipin IgG and anti‐β2‐glycoprotein I IgG, which were consistent with primary antiphospholipid antibody syndrome. Positron emission tomography (PET) imaging revealed altered striatal metabolism in his left putamen while he was exhibiting right‐sided hemichorea. His symptoms resolved on prednisone; however, his antiphospholipid antibody profile remained markedly abnormal despite being symptom‐free for 26 months. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21657
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<front><div type="abstract" xml:lang="en">A fourteen‐year‐old right‐handed male with a history of attention deficit hyperactivity disorder (ADHD) presented with alternating hemichorea. Laboratory findings included elevated anticardiolipin IgG and anti‐β2‐glycoprotein I IgG, which were consistent with primary antiphospholipid antibody syndrome. Positron emission tomography (PET) imaging revealed altered striatal metabolism in his left putamen while he was exhibiting right‐sided hemichorea. His symptoms resolved on prednisone; however, his antiphospholipid antibody profile remained markedly abnormal despite being symptom‐free for 26 months. © 2007 Movement Disorder Society</div>
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<front><div type="abstract" xml:lang="en">A fourteen-year-old right-handed male with a history of attention deficit hyperactivity disorder (ADHD) presented with alternating hemichorea. Laboratory findings included elevated anticardiolipin IgG and anti-β<sub>2</sub>
-glycoprotein I IgG, which were consistent with primary antiphospholipid antibody syndrome. Positron emission tomography (PET) imaging revealed altered striatal metabolism in his left putamen while he was exhibiting right-sided hemichorea. His symptoms resolved on prednisone; however, his antiphospholipid antibody profile remained markedly abnormal despite being symptom-free for 26 months.</div>
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<author><name sortKey="Gruppo, Ralph E" sort="Gruppo, Ralph E" uniqKey="Gruppo R" first="Ralph E." last="Gruppo">Ralph E. Gruppo</name>
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<author><name sortKey="Dinopolous, Argirios" sort="Dinopolous, Argirios" uniqKey="Dinopolous A" first="Argirios" last="Dinopolous">Argirios Dinopolous</name>
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<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Clinical and positron emission tomography findings of chorea associated with primary antiphospholipid antibody syndrome</title>
<author><name sortKey="Wu, Steve W" sort="Wu, Steve W" uniqKey="Wu S" first="Steve W." last="Wu">Steve W. Wu</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Graham, Brent" sort="Graham, Brent" uniqKey="Graham B" first="Brent" last="Graham">Brent Graham</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Rheumatology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gelfand, Michael J" sort="Gelfand, Michael J" uniqKey="Gelfand M" first="Michael J." last="Gelfand">Michael J. Gelfand</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Radiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gruppo, Ralph E" sort="Gruppo, Ralph E" uniqKey="Gruppo R" first="Ralph E." last="Gruppo">Ralph E. Gruppo</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Dinopolous, Argirios" sort="Dinopolous, Argirios" uniqKey="Dinopolous A" first="Argirios" last="Dinopolous">Argirios Dinopolous</name>
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<wicri:regionArea>Division of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gilbert, Donald L" sort="Gilbert, Donald L" uniqKey="Gilbert D" first="Donald L." last="Gilbert">Donald L. Gilbert</name>
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<wicri:regionArea>Division of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
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<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>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2007-09-15">2007-09-15</date>
<biblScope unit="vol">22</biblScope>
<biblScope unit="issue">12</biblScope>
<biblScope unit="page" from="1813">1813</biblScope>
<biblScope unit="page" to="1815">1815</biblScope>
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<idno type="DOI">10.1002/mds.21657</idno>
<idno type="ArticleID">MDS21657</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term>
<term>Attention Deficit Disorder with Hyperactivity (complications)</term>
<term>Cardiolipins (immunology)</term>
<term>Chorea (etiology)</term>
<term>Chorea (immunology)</term>
<term>Chorea (radionuclide imaging)</term>
<term>Fluorodeoxyglucose F18 (diagnostic use)</term>
<term>Humans</term>
<term>Immunoglobulin G (blood)</term>
<term>Male</term>
<term>Neurologic Examination</term>
<term>PET imaging</term>
<term>Positron-Emission Tomography (methods)</term>
<term>antiphospholipid antibody syndrome</term>
<term>beta 2-Glycoprotein I (immunology)</term>
<term>chorea</term>
<term>steroid</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Immunoglobulin G</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Fluorodeoxyglucose F18</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cardiolipins</term>
<term>beta 2-Glycoprotein I</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Attention Deficit Disorder with Hyperactivity</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Chorea</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Chorea</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Positron-Emission Tomography</term>
</keywords>
<keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Chorea</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adolescent</term>
<term>Humans</term>
<term>Male</term>
<term>Neurologic Examination</term>
</keywords>
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<langUsage><language ident="en">en</language>
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<front><div type="abstract" xml:lang="en">A fourteen‐year‐old right‐handed male with a history of attention deficit hyperactivity disorder (ADHD) presented with alternating hemichorea. Laboratory findings included elevated anticardiolipin IgG and anti‐β2‐glycoprotein I IgG, which were consistent with primary antiphospholipid antibody syndrome. Positron emission tomography (PET) imaging revealed altered striatal metabolism in his left putamen while he was exhibiting right‐sided hemichorea. His symptoms resolved on prednisone; however, his antiphospholipid antibody profile remained markedly abnormal despite being symptom‐free for 26 months. © 2007 Movement Disorder Society</div>
</front>
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