Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification.
Identifieur interne : 002E26 ( Ncbi/Merge ); précédent : 002E25; suivant : 002E27Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification.
Auteurs : Norbert Brüggemann [Allemagne] ; Susanne A. Schneider ; Thurid Sander ; Christine Klein ; Johann HagenahSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Aged, Basal Ganglia (pathology), Basal Ganglia (ultrasonography), Basal Ganglia Diseases (pathology), Basal Ganglia Diseases (ultrasonography), Calcinosis (pathology), Calcinosis (ultrasonography), Cognition Disorders (pathology), Cognition Disorders (ultrasonography), Humans, Male, Parkinsonian Disorders (pathology), Parkinsonian Disorders (ultrasonography), Ultrasonography, Doppler, Transcranial.
- MESH :
- pathology : Basal Ganglia, Basal Ganglia Diseases, Calcinosis, Cognition Disorders, Parkinsonian Disorders.
- ultrasonography : Basal Ganglia, Basal Ganglia Diseases, Calcinosis, Cognition Disorders, Parkinsonian Disorders.
- Aged, Humans, Male, Ultrasonography, Doppler, Transcranial.
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.
DOI: 10.1002/mds.23264
PubMed: 20803519
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Schneider</name></author><author><name sortKey="Sander, Thurid" sort="Sander, Thurid" uniqKey="Sander T" first="Thurid" last="Sander">Thurid Sander</name></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name></author><author><name sortKey="Hagenah, Johann" sort="Hagenah, Johann" uniqKey="Hagenah J" first="Johann" last="Hagenah">Johann Hagenah</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.23264</idno><idno type="RBID">pubmed:20803519</idno><idno type="pmid">20803519</idno><idno type="wicri:Area/PubMed/Corpus">001591</idno><idno type="wicri:Area/PubMed/Curation">001591</idno><idno type="wicri:Area/PubMed/Checkpoint">001935</idno><idno type="wicri:Area/Ncbi/Merge">002E26</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification.</title><author><name sortKey="Bruggemann, Norbert" sort="Bruggemann, Norbert" uniqKey="Bruggemann N" first="Norbert" last="Brüggemann">Norbert Brüggemann</name><affiliation wicri:level="1"><nlm:affiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck</wicri:regionArea><wicri:noRegion>Lübeck</wicri:noRegion><wicri:noRegion>Lübeck</wicri:noRegion><wicri:noRegion>Lübeck</wicri:noRegion></affiliation></author><author><name sortKey="Schneider, Susanne A" sort="Schneider, Susanne A" uniqKey="Schneider S" first="Susanne A" last="Schneider">Susanne A. Schneider</name></author><author><name sortKey="Sander, Thurid" sort="Sander, Thurid" uniqKey="Sander T" first="Thurid" last="Sander">Thurid Sander</name></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name></author><author><name sortKey="Hagenah, Johann" sort="Hagenah, Johann" uniqKey="Hagenah J" first="Johann" last="Hagenah">Johann Hagenah</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Basal Ganglia (pathology)</term><term>Basal Ganglia (ultrasonography)</term><term>Basal Ganglia Diseases (pathology)</term><term>Basal Ganglia Diseases (ultrasonography)</term><term>Calcinosis (pathology)</term><term>Calcinosis (ultrasonography)</term><term>Cognition Disorders (pathology)</term><term>Cognition Disorders (ultrasonography)</term><term>Humans</term><term>Male</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonian Disorders (ultrasonography)</term><term>Ultrasonography, Doppler, Transcranial</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Basal Ganglia Diseases</term><term>Calcinosis</term><term>Cognition Disorders</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="ultrasonography" xml:lang="en"><term>Basal Ganglia</term><term>Basal Ganglia Diseases</term><term>Calcinosis</term><term>Cognition Disorders</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Humans</term><term>Male</term><term>Ultrasonography, Doppler, Transcranial</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20803519</PMID><DateCreated><Year>2010</Year><Month>11</Month><Day>11</Day></DateCreated><DateCompleted><Year>2011</Year><Month>02</Month><Day>25</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>15</Issue><PubDate><Year>2010</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification.</ArticleTitle><Pagination><MedlinePgn>2661-4</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23264</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>© 2010 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brüggemann</LastName><ForeName>Norbert</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Schilling Section of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schneider</LastName><ForeName>Susanne A</ForeName><Initials>SA</Initials></Author><Author ValidYN="Y"><LastName>Sander</LastName><ForeName>Thurid</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Klein</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Hagenah</LastName><ForeName>Johann</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001479">Basal Ganglia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000736">ultrasonography</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001480">Basal Ganglia Diseases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000736">ultrasonography</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002114">Calcinosis</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000736">ultrasonography</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003072">Cognition Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000736">ultrasonography</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000736">ultrasonography</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017585">Ultrasonography, Doppler, Transcranial</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>8</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>8</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>2</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23264</ArticleId><ArticleId IdType="pubmed">20803519</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Hagenah, Johann" sort="Hagenah, Johann" uniqKey="Hagenah J" first="Johann" last="Hagenah">Johann Hagenah</name><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><name sortKey="Sander, Thurid" sort="Sander, Thurid" uniqKey="Sander T" first="Thurid" last="Sander">Thurid Sander</name><name sortKey="Schneider, Susanne A" sort="Schneider, Susanne A" uniqKey="Schneider S" first="Susanne A" last="Schneider">Susanne A. Schneider</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Bruggemann, Norbert" sort="Bruggemann, Norbert" uniqKey="Bruggemann N" first="Norbert" last="Brüggemann">Norbert Brüggemann</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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