Decreased striatal dopamine transporter binding in a patient with extrapontine myelinolysis
Identifieur interne : 003323 ( Istex/Corpus ); précédent : 003322; suivant : 003324Decreased striatal dopamine transporter binding in a patient with extrapontine myelinolysis
Auteurs : Joong-Seok Kim ; Kwang-Soo Lee ; Si-Ryung Han ; Yong-An ChungSource :
- Movement Disorders [ 0885-3185 ] ; 2003-03.
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Abstract
We describe the case of a 61‐year‐old woman who developed extrapontine myelinolysis (EPM) with parkinsonism. Decreased striatal dopamine transporter binding assessed by [123I]N‐(3‐iodopropen‐2‐yl)‐2β‐carbomethoxy‐3β‐(4‐chlorophenyl) tropane and single photon emission computed tomography ([123I]IPT) SPECT) were observed in the patient, suggesting that osmotic injury causes the demyelination of nigrostriatal dopaminergic neurons and that such injury may be involved in the pathogenesis of EPM with parkinsonism.
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DOI: 10.1002/mds.10331
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ISTEX:C66C79ABD3426B8B5EF65CACF617FA234099243ALe document en format XML
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Decreased striatal dopamine transporter binding assessed by [<sup>123</sup>I]N‐(3‐iodopropen‐2‐yl)‐2β‐carbomethoxy‐3β‐(4‐chlorophenyl) tropane and single photon emission computed tomography ([<sup>123</sup>I]IPT) SPECT) were observed in the patient, suggesting that osmotic injury causes the demyelination of nigrostriatal dopaminergic neurons and that such injury may be involved in the pathogenesis of EPM with parkinsonism.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Decreased striatal dopamine transporter binding in a patient with extrapontine myelinolysis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopamine Binding and Extrapontine Myelinolysis</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Decreased striatal dopamine transporter binding in a patient with extrapontine myelinolysis</title></titleInfo><name type="personal"><namePart type="given">Joong‐Seok</namePart><namePart type="family">Kim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kwang‐Soo</namePart><namePart type="family">Lee</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea</affiliation><description>Correspondence: Movement Clinic, Department of Neurology, Kangnam St. Mary's Hospital, 505 Banpo‐Dong, Seocho‐Ku, Seoul 130‐701, South Korea</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Si‐Ryung</namePart><namePart type="family">Han</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yong‐An</namePart><namePart type="family">Chung</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Nuclear Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">shortCommunication</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2003-03</dateIssued><dateCaptured encoding="w3cdtf">2002-03-08</dateCaptured><dateValid encoding="w3cdtf">2002-08-06</dateValid><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="references">19</extent><extent unit="words">1995</extent></physicalDescription><abstract lang="en">We describe the case of a 61‐year‐old woman who developed extrapontine myelinolysis (EPM) with parkinsonism. Decreased striatal dopamine transporter binding assessed by [123I]N‐(3‐iodopropen‐2‐yl)‐2β‐carbomethoxy‐3β‐(4‐chlorophenyl) tropane and single photon emission computed tomography ([123I]IPT) SPECT) were observed in the patient, suggesting that osmotic injury causes the demyelination of nigrostriatal dopaminergic neurons and that such injury may be involved in the pathogenesis of EPM with parkinsonism.</abstract><subject lang="en"><genre>Keywords</genre><topic>extrapontine myelinolysis</topic><topic>parkinsonism</topic><topic>IPT SPECT</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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