Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.
Identifieur interne : 002695 ( PubMed/Checkpoint ); précédent : 002694; suivant : 002696Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.
Auteurs : Misuzu Saiki [Japon] ; Shinji Saiki ; Koichiro Sakai ; Ichiro Matsunari ; Kotaro Higashi ; Ken-Ya Murata ; Nobutaka Hattori ; Genjiro HiroseSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Aged, 80 and over, Basal Ganglia Diseases (pathology), Basal Ganglia Diseases (physiopathology), Calcinosis (physiopathology), Family Health, Female, Humans, Male, Metabolism, Inborn Errors (physiopathology), Middle Aged, Positron-Emission Tomography (methods), Tomography, Emission-Computed, Single-Photon (methods), Tomography, X-Ray Computed (methods).
- MESH :
- methods : Positron-Emission Tomography, Tomography, Emission-Computed, Single-Photon, Tomography, X-Ray Computed.
- pathology : Basal Ganglia Diseases.
- physiopathology : Basal Ganglia Diseases, Calcinosis, Metabolism, Inborn Errors.
- Aged, 80 and over, Family Health, Female, Humans, Male, Middle Aged.
Abstract
We report two familial cases of idiopathic basal ganglia calcification. A 60-year-old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82-year-old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism.
DOI: 10.1002/mds.21438
PubMed: 17357130
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.</title><author><name sortKey="Saiki, Misuzu" sort="Saiki, Misuzu" uniqKey="Saiki M" first="Misuzu" last="Saiki">Misuzu Saiki</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Kanazawa Medical University, Ishikawa, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Kanazawa Medical University, Ishikawa</wicri:regionArea><wicri:noRegion>Ishikawa</wicri:noRegion></affiliation></author><author><name sortKey="Saiki, Shinji" sort="Saiki, Shinji" uniqKey="Saiki S" first="Shinji" last="Saiki">Shinji Saiki</name></author><author><name sortKey="Sakai, Koichiro" sort="Sakai, Koichiro" uniqKey="Sakai K" first="Koichiro" last="Sakai">Koichiro Sakai</name></author><author><name sortKey="Matsunari, Ichiro" sort="Matsunari, Ichiro" uniqKey="Matsunari I" first="Ichiro" last="Matsunari">Ichiro Matsunari</name></author><author><name sortKey="Higashi, Kotaro" sort="Higashi, Kotaro" uniqKey="Higashi K" first="Kotaro" last="Higashi">Kotaro Higashi</name></author><author><name sortKey="Murata, Ken Ya" sort="Murata, Ken Ya" uniqKey="Murata K" first="Ken-Ya" last="Murata">Ken-Ya Murata</name></author><author><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name></author><author><name sortKey="Hirose, Genjiro" sort="Hirose, Genjiro" uniqKey="Hirose G" first="Genjiro" last="Hirose">Genjiro Hirose</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="doi">10.1002/mds.21438</idno><idno type="RBID">pubmed:17357130</idno><idno type="pmid">17357130</idno><idno type="wicri:Area/PubMed/Corpus">002819</idno><idno 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K" first="Koichiro" last="Sakai">Koichiro Sakai</name></author><author><name sortKey="Matsunari, Ichiro" sort="Matsunari, Ichiro" uniqKey="Matsunari I" first="Ichiro" last="Matsunari">Ichiro Matsunari</name></author><author><name sortKey="Higashi, Kotaro" sort="Higashi, Kotaro" uniqKey="Higashi K" first="Kotaro" last="Higashi">Kotaro Higashi</name></author><author><name sortKey="Murata, Ken Ya" sort="Murata, Ken Ya" uniqKey="Murata K" first="Ken-Ya" last="Murata">Ken-Ya Murata</name></author><author><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name></author><author><name sortKey="Hirose, Genjiro" sort="Hirose, Genjiro" uniqKey="Hirose G" first="Genjiro" last="Hirose">Genjiro Hirose</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged, 80 and over</term><term>Basal Ganglia Diseases (pathology)</term><term>Basal Ganglia Diseases (physiopathology)</term><term>Calcinosis (physiopathology)</term><term>Family Health</term><term>Female</term><term>Humans</term><term>Male</term><term>Metabolism, Inborn Errors (physiopathology)</term><term>Middle Aged</term><term>Positron-Emission Tomography (methods)</term><term>Tomography, Emission-Computed, Single-Photon (methods)</term><term>Tomography, X-Ray Computed (methods)</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Positron-Emission Tomography</term><term>Tomography, Emission-Computed, Single-Photon</term><term>Tomography, X-Ray Computed</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia Diseases</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Calcinosis</term><term>Metabolism, Inborn Errors</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged, 80 and over</term><term>Family Health</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We report two familial cases of idiopathic basal ganglia calcification. A 60-year-old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82-year-old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17357130</PMID><DateCreated><Year>2007</Year><Month>05</Month><Day>31</Day></DateCreated><DateCompleted><Year>2007</Year><Month>08</Month><Day>03</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>22</Volume><Issue>7</Issue><PubDate><Year>2007</Year><Month>May</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.</ArticleTitle><Pagination><MedlinePgn>1027-30</MedlinePgn></Pagination><Abstract><AbstractText>We report two familial cases of idiopathic basal ganglia calcification. A 60-year-old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82-year-old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism.</AbstractText><CopyrightInformation>(c) 2007 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saiki</LastName><ForeName>Misuzu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Neurology, Kanazawa Medical University, Ishikawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saiki</LastName><ForeName>Shinji</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Sakai</LastName><ForeName>Koichiro</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Matsunari</LastName><ForeName>Ichiro</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Higashi</LastName><ForeName>Kotaro</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Murata</LastName><ForeName>Ken-Ya</ForeName><Initials>KY</Initials></Author><Author ValidYN="Y"><LastName>Hattori</LastName><ForeName>Nobutaka</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Hirose</LastName><ForeName>Genjiro</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><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="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001480">Basal Ganglia Diseases</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002114">Calcinosis</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005192">Family Health</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008661">Metabolism, Inborn Errors</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D049268">Positron-Emission Tomography</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015899">Tomography, Emission-Computed, Single-Photon</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014057">Tomography, X-Ray Computed</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>3</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>8</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>3</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21438</ArticleId><ArticleId IdType="pubmed">17357130</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name><name sortKey="Higashi, Kotaro" sort="Higashi, Kotaro" uniqKey="Higashi K" first="Kotaro" last="Higashi">Kotaro Higashi</name><name sortKey="Hirose, Genjiro" sort="Hirose, Genjiro" uniqKey="Hirose G" first="Genjiro" last="Hirose">Genjiro Hirose</name><name sortKey="Matsunari, Ichiro" sort="Matsunari, Ichiro" uniqKey="Matsunari I" first="Ichiro" last="Matsunari">Ichiro Matsunari</name><name sortKey="Murata, Ken Ya" sort="Murata, Ken Ya" uniqKey="Murata K" first="Ken-Ya" last="Murata">Ken-Ya Murata</name><name sortKey="Saiki, Shinji" sort="Saiki, Shinji" uniqKey="Saiki S" first="Shinji" last="Saiki">Shinji Saiki</name><name sortKey="Sakai, Koichiro" sort="Sakai, Koichiro" uniqKey="Sakai K" first="Koichiro" last="Sakai">Koichiro Sakai</name></noCountry><country name="Japon"><noRegion><name sortKey="Saiki, Misuzu" sort="Saiki, Misuzu" uniqKey="Saiki M" first="Misuzu" last="Saiki">Misuzu Saiki</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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