Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification
Identifieur interne : 001B23 ( Main/Corpus ); précédent : 001B22; suivant : 001B24Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification
Auteurs : Norbert Brüggemann ; Susanne A. Schneider ; Thurid Sander ; Christine Klein ; Johann HagenahSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
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Abstract
We report a 67‐year‐old patient with idiopathic basal ganglia calcification (IBGC). He presented with progressive cognitive impairment, frontal lobe dysfunction, mild leg spasticity, and levodopa (L‐dopa)‐responsive parkinsonism. Transcranial sonography (TCS) revealed marked hyperechogenicity of the basal ganglia and periventricular spaces bilaterally. The detected signal alterations showed a fairly symmetric distribution and corresponded to the hyperintense calcifications depicted on the computer tomography brain scan. The combination of symmetric hyperechogenic areas adjacent to the lateral ventricles and of the basal ganglia may serve as an imaging marker characteristic of IBGC. Hyperechogenicity due to extended basal ganglia calcification as presented here is distinct from the pattern of hyperechogenicity caused by heavy metal accumulation, which is described to be less striking. In addition to atypical parkinsonian syndromes such as progressive supranuclear palsy and multiple system atrophy, IBGC is thus another differential diagnosis of parkinsonism with basal ganglia hyperechogenicity. © 2010 Movement Disorder Society.
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DOI: 10.1002/mds.23264
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He presented with progressive cognitive impairment, frontal lobe dysfunction, mild leg spasticity, and levodopa (L‐dopa)‐responsive parkinsonism. Transcranial sonography (TCS) revealed marked hyperechogenicity of the basal ganglia and periventricular spaces bilaterally. The detected signal alterations showed a fairly symmetric distribution and corresponded to the hyperintense calcifications depicted on the computer tomography brain scan. The combination of symmetric hyperechogenic areas adjacent to the lateral ventricles and of the basal ganglia may serve as an imaging marker characteristic of IBGC. Hyperechogenicity due to extended basal ganglia calcification as presented here is distinct from the pattern of hyperechogenicity caused by heavy metal accumulation, which is described to be less striking. In addition to atypical parkinsonian syndromes such as progressive supranuclear palsy and multiple system atrophy, IBGC is thus another differential diagnosis of parkinsonism with basal ganglia hyperechogenicity. © 2010 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Norbert Brüggemann MD</name><affiliations><json:string>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</json:string><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Susanne A. 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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="2010-11-15"></date><biblScope unit="volume">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2661">2661</biblScope><biblScope unit="page" to="2664">2664</biblScope></imprint></monogr><idno type="istex">75C06FF4860BFAF4F8E9FD85192B7351AE509929</idno><idno type="DOI">10.1002/mds.23264</idno><idno type="ArticleID">MDS23264</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We report a 67‐year‐old patient with idiopathic basal ganglia calcification (IBGC). He presented with progressive cognitive impairment, frontal lobe dysfunction, mild leg spasticity, and levodopa (L‐dopa)‐responsive parkinsonism. Transcranial sonography (TCS) revealed marked hyperechogenicity of the basal ganglia and periventricular spaces bilaterally. The detected signal alterations showed a fairly symmetric distribution and corresponded to the hyperintense calcifications depicted on the computer tomography brain scan. The combination of symmetric hyperechogenic areas adjacent to the lateral ventricles and of the basal ganglia may serve as an imaging marker characteristic of IBGC. Hyperechogenicity due to extended basal ganglia calcification as presented here is distinct from the pattern of hyperechogenicity caused by heavy metal accumulation, which is described to be less striking. In addition to atypical parkinsonian syndromes such as progressive supranuclear palsy and multiple system atrophy, IBGC is thus another differential diagnosis of parkinsonism with basal ganglia hyperechogenicity. © 2010 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>idiopathic basal ganglia calcification</term></item><item><term>transcranial sonography</term></item><item><term>parkinsonism</term></item><item><term>lenticular nucleus</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="2010-01-05">Received</change><change when="2010-04-27">Registration</change><change when="2010-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/75C06FF4860BFAF4F8E9FD85192B7351AE509929/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="150"><doi origin="wiley" registered="yes">10.1002/mds.v25:15</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">15</numbering></numberingGroup><coverDate startDate="2010-11-15">15 November 2010</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="270" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23264</doi><idGroup><id type="unit" value="MDS23264"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-01-05"></event><event type="manuscriptRevised" date="2010-02-21"></event><event type="manuscriptAccepted" date="2010-04-27"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.1.9 mode:FullText" date="2013-01-24"></event><event type="publishedOnlineEarlyUnpaginated" date="2010-08-27"></event><event type="publishedOnlineFinalForm" date="2010-11-10"></event><event type="firstOnline" date="2010-08-27"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">2661</numbering><numbering type="pageLast">2664</numbering></numberingGroup><correspondenceTo>Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23264.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="14"></count><count type="wordTotal" number="2090"></count></countGroup><titleGroup><title type="main" xml:lang="en">Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification<link href="#fn3"></link></title><title type="short" xml:lang="en">TCS in Basal Ganglia Calcification</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Norbert</givenNames><familyName>Brüggemann</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Susanne A.</givenNames><familyName>Schneider</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Thurid</givenNames><familyName>Sander</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Christine</givenNames><familyName>Klein</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Johann</givenNames><familyName>Hagenah</familyName><degrees>MD</degrees></personName><contactDetails><email normalForm="johann.hagenah@neuro.uni-luebeck.de">johann.hagenah@neuro.uni‐luebeck.de</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">idiopathic basal ganglia calcification</keyword><keyword xml:id="kwd2">transcranial sonography</keyword><keyword xml:id="kwd3">parkinsonism</keyword><keyword xml:id="kwd4">lenticular nucleus</keyword></keywordGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23264:MDS_22364_sm_suppinfovideo"></mediaResource><caption>Supporting Information Video</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We report a 67‐year‐old patient with idiopathic basal ganglia calcification (IBGC). He presented with progressive cognitive impairment, frontal lobe dysfunction, mild leg spasticity, and levodopa (<sc>L</sc>‐dopa)‐responsive parkinsonism. Transcranial sonography (TCS) revealed marked hyperechogenicity of the basal ganglia and periventricular spaces bilaterally. The detected signal alterations showed a fairly symmetric distribution and corresponded to the hyperintense calcifications depicted on the computer tomography brain scan. The combination of symmetric hyperechogenic areas adjacent to the lateral ventricles and of the basal ganglia may serve as an imaging marker characteristic of IBGC. Hyperechogenicity due to extended basal ganglia calcification as presented here is distinct from the pattern of hyperechogenicity caused by heavy metal accumulation, which is described to be less striking. In addition to atypical parkinsonian syndromes such as progressive supranuclear palsy and multiple system atrophy, IBGC is thus another differential diagnosis of parkinsonism with basal ganglia hyperechogenicity. © 2010 Movement Disorder Society.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>TCS in Basal Ganglia Calcification</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification</title></titleInfo><name type="personal"><namePart type="given">Norbert</namePart><namePart type="family">Brüggemann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</affiliation><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susanne A.</namePart><namePart type="family">Schneider</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</affiliation><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thurid</namePart><namePart type="family">Sander</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</affiliation><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>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</affiliation><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Johann</namePart><namePart type="family">Hagenah</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany</affiliation><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><description>Correspondence: Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief communication" displayLabel="shortCommunication"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-11-15</dateIssued><dateCaptured encoding="w3cdtf">2010-01-05</dateCaptured><dateValid encoding="w3cdtf">2010-04-27</dateValid><copyrightDate encoding="w3cdtf">2010</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">1</extent><extent unit="references">14</extent><extent unit="words">2090</extent></physicalDescription><abstract lang="en">We report a 67‐year‐old patient with idiopathic basal ganglia calcification (IBGC). He presented with progressive cognitive impairment, frontal lobe dysfunction, mild leg spasticity, and levodopa (L‐dopa)‐responsive parkinsonism. Transcranial sonography (TCS) revealed marked hyperechogenicity of the basal ganglia and periventricular spaces bilaterally. The detected signal alterations showed a fairly symmetric distribution and corresponded to the hyperintense calcifications depicted on the computer tomography brain scan. The combination of symmetric hyperechogenic areas adjacent to the lateral ventricles and of the basal ganglia may serve as an imaging marker characteristic of IBGC. Hyperechogenicity due to extended basal ganglia calcification as presented here is distinct from the pattern of hyperechogenicity caused by heavy metal accumulation, which is described to be less striking. In addition to atypical parkinsonian syndromes such as progressive supranuclear palsy and multiple system atrophy, IBGC is thus another differential diagnosis of parkinsonism with basal ganglia hyperechogenicity. © 2010 Movement Disorder Society.</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>idiopathic basal ganglia calcification</topic><topic>transcranial sonography</topic><topic>parkinsonism</topic><topic>lenticular nucleus</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information Video - </note><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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2661</start><end>2664</end><total>4</total></extent></part></relatedItem><identifier type="istex">75C06FF4860BFAF4F8E9FD85192B7351AE509929</identifier><identifier type="DOI">10.1002/mds.23264</identifier><identifier type="ArticleID">MDS23264</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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