Familial idiopathic strio‐pallido‐dentate calcifications with late onset extrapyramidal syndrome
Identifieur interne : 003788 ( Istex/Corpus ); précédent : 003787; suivant : 003789Familial idiopathic strio‐pallido‐dentate calcifications with late onset extrapyramidal syndrome
Auteurs : P. Martinelli ; S. Giuliani ; M. Ippoliti ; Martinelli ; A. Sforza ; St. FerrariSource :
- Movement Disorders [ 0885-3185 ] ; 1993.
English descriptors
Abstract
A family with autosomal dominant inheritance of idiopathic strio‐pallidodentate calcifications and late onset of extrapyramidal symptoms is reported. Clinical features consisted of parkinsonism in one member and postural tremor in two. Depression and dysarthria were present in all cases. All symptomatic members showed a peculiar biochemical abnormality consisting of reduced 25‐OH vitamin D3 with normal levels of 1,25(OH)2 vitamin D3, suggesting an inborn error of Vitamin D metabolism. The biochemical, clinical, and genetic pattern of this family distinguishes this syndrome from the larger group of secondary familial basal ganglia calcifications.
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DOI: 10.1002/mds.870080221
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ISTEX:0A612954BAAF64E3F8E4B1DF14207FA29197A1C6Le document en format XML
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Ippoliti</name><affiliation><mods:affiliation>Institute of Clinical Neurology, University of Bologna</mods:affiliation></affiliation></author><author><name sortKey="Martinelli" sort="Martinelli" uniqKey="Martinelli" last="Martinelli">Martinelli</name><affiliation><mods:affiliation>Institute of Clinical Neurology, University of Bologna</mods:affiliation></affiliation></author><author><name sortKey="Sforza, A" sort="Sforza, A" uniqKey="Sforza A" first="A." last="Sforza">A. 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Clinical features consisted of parkinsonism in one member and postural tremor in two. Depression and dysarthria were present in all cases. All symptomatic members showed a peculiar biochemical abnormality consisting of reduced 25‐OH vitamin D3 with normal levels of 1,25(OH)2 vitamin D3, suggesting an inborn error of Vitamin D metabolism. The biochemical, clinical, and genetic pattern of this family distinguishes this syndrome from the larger group of secondary familial basal ganglia calcifications.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>P. Martinelli</name><affiliations><json:string>Institute of Clinical Neurology, University of Bologna</json:string></affiliations></json:item><json:item><name>S. Giuliani</name><affiliations><json:string>Institute of Clinical Neurology, University of Bologna</json:string></affiliations></json:item><json:item><name>M. Ippoliti</name><affiliations><json:string>Institute of Clinical Neurology, University of Bologna</json:string></affiliations></json:item><json:item><name>Prof. Martinelli</name><affiliations><json:string>Institute of Clinical Neurology, University of Bologna</json:string></affiliations></json:item><json:item><name>A. Sforza</name><affiliations><json:string>Endorcrinology Department, Maggiore Hospital, Bologna</json:string></affiliations></json:item><json:item><name>St. Ferrari</name><affiliations><json:string>Institute of Biochemistry, University of Modena, Modena, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Basal ganglia calcifications</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Vitamin D metabolism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Extrapyramidal syndrome</value></json:item></subject><language><json:string>eng</json:string></language><abstract>A family with autosomal dominant inheritance of idiopathic strio‐pallidodentate calcifications and late onset of extrapyramidal symptoms is reported. Clinical features consisted of parkinsonism in one member and postural tremor in two. Depression and dysarthria were present in all cases. All symptomatic members showed a peculiar biochemical abnormality consisting of reduced 25‐OH vitamin D3 with normal levels of 1,25(OH)2 vitamin D3, suggesting an inborn error of Vitamin D metabolism. 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Foscolo 7, Bologna, Italy</p></note><affiliation>Institute of Clinical Neurology, University of Bologna</affiliation></author><author><persName><forename type="first">A.</forename><surname>Sforza</surname></persName><affiliation>Endorcrinology Department, Maggiore Hospital, Bologna</affiliation></author><author><persName><forename type="first">St.</forename><surname>Ferrari</surname></persName><affiliation>Institute of Biochemistry, University of Modena, Modena, Italy</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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Clinical features consisted of parkinsonism in one member and postural tremor in two. Depression and dysarthria were present in all cases. All symptomatic members showed a peculiar biochemical abnormality consisting of reduced 25‐OH vitamin D3 with normal levels of 1,25(OH)2 vitamin D3, suggesting an inborn error of Vitamin D metabolism. 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Clinical features consisted of parkinsonism in one member and postural tremor in two. Depression and dysarthria were present in all cases. All symptomatic members showed a peculiar biochemical abnormality consisting of reduced 25‐OH vitamin D<sub>3</sub> with normal levels of 1,25(OH)2 vitamin D<sub>3</sub>, suggesting an inborn error of Vitamin D metabolism. The biochemical, clinical, and genetic pattern of this family distinguishes this syndrome from the larger group of secondary familial basal ganglia calcifications.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Familial idiopathic strio‐pallido‐dentate calcifications with late onset extrapyramidal syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>FAMILIAL IDIOPATHIC SPDC</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Familial idiopathic strio‐pallido‐dentate calcifications with late onset extrapyramidal syndrome</title></titleInfo><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Martinelli</namePart><affiliation>Institute of Clinical Neurology, University of Bologna</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Giuliani</namePart><affiliation>Institute of Clinical Neurology, University of Bologna</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Ippoliti</namePart><affiliation>Institute of Clinical Neurology, University of Bologna</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Prof.</namePart><namePart type="family">Martinelli</namePart><affiliation>Institute of Clinical Neurology, University of Bologna</affiliation><description>Correspondence: Istituto di Clinica Neurologica, Via U. Foscolo 7, Bologna, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Sforza</namePart><affiliation>Endorcrinology Department, Maggiore Hospital, Bologna</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">St.</namePart><namePart type="family">Ferrari</namePart><affiliation>Institute of Biochemistry, University of Modena, Modena, Italy</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">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</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">1</extent><extent unit="references">23</extent></physicalDescription><abstract lang="en">A family with autosomal dominant inheritance of idiopathic strio‐pallidodentate calcifications and late onset of extrapyramidal symptoms is reported. Clinical features consisted of parkinsonism in one member and postural tremor in two. Depression and dysarthria were present in all cases. All symptomatic members showed a peculiar biochemical abnormality consisting of reduced 25‐OH vitamin D3 with normal levels of 1,25(OH)2 vitamin D3, suggesting an inborn error of Vitamin D metabolism. The biochemical, clinical, and genetic pattern of this family distinguishes this syndrome from the larger group of secondary familial basal ganglia calcifications.</abstract><subject lang="en"><genre>Keywords</genre><topic>Basal ganglia calcifications</topic><topic>Vitamin D metabolism</topic><topic>Extrapyramidal syndrome</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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