Brain parenchyma sonography detects preclinical parkinsonism
Identifieur interne : 002892 ( Istex/Corpus ); précédent : 002891; suivant : 002893Brain parenchyma sonography detects preclinical parkinsonism
Auteurs : Uwe Walter ; Christine Klein ; Ruediger Hilker ; Reiner Benecke ; Peter P. Pramstaller ; Dirk DresslerSource :
- Movement Disorders [ 0885-3185 ] ; 2004-12.
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- KwdEn :
Abstract
Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society
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DOI: 10.1002/mds.20232
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Brain parenchyma sonography detects preclinical parkinsonism</title><author><name sortKey="Walter, Uwe" sort="Walter, Uwe" uniqKey="Walter U" first="Uwe" last="Walter">Uwe Walter</name><affiliation><mods:affiliation>Department of Neurology, University of Rostock, Rostock, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><mods:affiliation>Department of Neurology, University of Luebeck, Luebeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hilker, Ruediger" sort="Hilker, Ruediger" uniqKey="Hilker R" first="Ruediger" last="Hilker">Ruediger Hilker</name><affiliation><mods:affiliation>Department of Neurology, University of Cologne, Koeln, Germany</mods:affiliation></affiliation></author><author><name sortKey="Benecke, Reiner" sort="Benecke, Reiner" uniqKey="Benecke R" first="Reiner" last="Benecke">Reiner Benecke</name><affiliation><mods:affiliation>Department of Neurology, University of Rostock, Rostock, Germany</mods:affiliation></affiliation></author><author><name sortKey="Pramstaller, Peter P" sort="Pramstaller, Peter P" uniqKey="Pramstaller P" first="Peter P." last="Pramstaller">Peter P. 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We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Uwe Walter MD</name><affiliations><json:string>Department of Neurology, University of Rostock, Rostock, Germany</json:string></affiliations></json:item><json:item><name>Christine Klein MD</name><affiliations><json:string>Department of Neurology, University of Luebeck, Luebeck, Germany</json:string></affiliations></json:item><json:item><name>Ruediger Hilker MD</name><affiliations><json:string>Department of Neurology, University of Cologne, Koeln, Germany</json:string></affiliations></json:item><json:item><name>Reiner Benecke MD</name><affiliations><json:string>Department of Neurology, University of Rostock, Rostock, Germany</json:string></affiliations></json:item><json:item><name>Peter P. Pramstaller MD</name><affiliations><json:string>Department of Neurology, Regional General Hospital, Bolzano, Italy</json:string></affiliations></json:item><json:item><name>Dirk Dressler MD</name><affiliations><json:string>Department of Neurology, University of Rostock, Rostock, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>brain parenchyma sonography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>parkin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARK2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>substantia nigra hyperechogenicity</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-12"></date><biblScope unit="vol">19</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1445">1445</biblScope><biblScope unit="page" to="1449">1449</biblScope></imprint></monogr><idno type="istex">769495CF95B685EB89CE82DC55B762FABE1D9898</idno><idno type="DOI">10.1002/mds.20232</idno><idno type="ArticleID">MDS20232</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>brain parenchyma sonography</term></item><item><term>Parkinson's disease</term></item><item><term>parkin</term></item><item><term>PARK2</term></item><item><term>substantia nigra</term></item><item><term>substantia nigra hyperechogenicity</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-11-28">Received</change><change when="2004-02-16">Registration</change><change when="2004-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/769495CF95B685EB89CE82DC55B762FABE1D9898/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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xml:id="kwd6">substantia nigra hyperechogenicity</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic <i>parkin</i> mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with <i>parkin</i> mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney <i>U</i> test, <i>P</i> = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, <i>P</i> = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal <sup>18</sup>F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society</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>Brain parenchyma sonography detects preclinical parkinsonism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Sonography in Preclinical Parkinsonism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Brain parenchyma sonography detects preclinical parkinsonism</title></titleInfo><name type="personal"><namePart type="given">Uwe</namePart><namePart type="family">Walter</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Rostock, Rostock, Germany</affiliation><description>Correspondence: Department of Neurology, University of Rostock, Gehlsheimer Str. 20, D‐18147 Rostock, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Klein</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Luebeck, Luebeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ruediger</namePart><namePart type="family">Hilker</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Cologne, Koeln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Reiner</namePart><namePart type="family">Benecke</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Rostock, Rostock, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter P.</namePart><namePart type="family">Pramstaller</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Regional General Hospital, Bolzano, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dirk</namePart><namePart type="family">Dressler</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Rostock, Rostock, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2004-12</dateIssued><dateCaptured encoding="w3cdtf">2003-11-28</dateCaptured><dateValid encoding="w3cdtf">2004-02-16</dateValid><copyrightDate encoding="w3cdtf">2004</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="tables">2</extent><extent unit="references">16</extent><extent unit="words">2892</extent></physicalDescription><abstract lang="en">Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>brain parenchyma sonography</topic><topic>Parkinson's disease</topic><topic>parkin</topic><topic>PARK2</topic><topic>substantia nigra</topic><topic>substantia nigra hyperechogenicity</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><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>2004</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>1445</start><end>1449</end><total>5</total></extent></part></relatedItem><identifier type="istex">769495CF95B685EB89CE82DC55B762FABE1D9898</identifier><identifier type="DOI">10.1002/mds.20232</identifier><identifier type="ArticleID">MDS20232</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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