Gilles de la Tourette's syndrome in twins: clinical and neurochemical data.
Identifieur interne : 004F46 ( PubMed/Corpus ); précédent : 004F45; suivant : 004F47Gilles de la Tourette's syndrome in twins: clinical and neurochemical data.
Auteurs : C G Goetz ; C M TannerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1990.
English descriptors
- KwdEn :
- MESH :
- chemical , cerebrospinal fluid : Homovanillic Acid, Hydroxyindoleacetic Acid.
- cerebrospinal fluid : Tourette Syndrome.
- genetics : Diseases in Twins, Tourette Syndrome.
- physiopathology : Tourette Syndrome.
- Child, Humans, Male.
Abstract
A pair of identical twins (probability of monozygosity by genetic marking = 99.99%) with Gilles de la Tourette's syndrome (GTS) were studied clinically and neurochemically. The two boys were distinguished within the family by dramatic differences in their behavior and tics. Twin 1 had severe motor tics, loud vocalizations, coprolalia, and school behavior problems, whereas twin 2 was only mildly affected. Neither boy had ever been treated with medication for his tic disorder. Lumbar puncture was performed on each after a night of bed rest. In spite of the marked clinical differences between the two boys, the major indices of dopamine and serotonin turnover in the cerebrospinal fluid were equivalent. Homovanillic acid levels were 65 and 60 ng/ml, respectively, and 5-hydroxyindoleacetic acid levels were 36 and 39 ng/ml. Observation of these twins suggests that the phenotypic expression of GTS relates to more factors than inheritance. Neurochemical metabolites of dopamine and serotonin did not reflect the comparative clinical severity of GTS in these boys.
DOI: 10.1002/mds.870050216
PubMed: 1691443
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The two boys were distinguished within the family by dramatic differences in their behavior and tics. Twin 1 had severe motor tics, loud vocalizations, coprolalia, and school behavior problems, whereas twin 2 was only mildly affected. Neither boy had ever been treated with medication for his tic disorder. Lumbar puncture was performed on each after a night of bed rest. In spite of the marked clinical differences between the two boys, the major indices of dopamine and serotonin turnover in the cerebrospinal fluid were equivalent. Homovanillic acid levels were 65 and 60 ng/ml, respectively, and 5-hydroxyindoleacetic acid levels were 36 and 39 ng/ml. Observation of these twins suggests that the phenotypic expression of GTS relates to more factors than inheritance. Neurochemical metabolites of dopamine and serotonin did not reflect the comparative clinical severity of GTS in these boys.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">1691443</PMID><DateCreated><Year>1990</Year><Month>05</Month><Day>24</Day></DateCreated><DateCompleted><Year>1990</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>5</Volume><Issue>2</Issue><PubDate><Year>1990</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Gilles de la Tourette's syndrome in twins: clinical and neurochemical data.</ArticleTitle><Pagination><MedlinePgn>173-5</MedlinePgn></Pagination><Abstract><AbstractText>A pair of identical twins (probability of monozygosity by genetic marking = 99.99%) with Gilles de la Tourette's syndrome (GTS) were studied clinically and neurochemically. The two boys were distinguished within the family by dramatic differences in their behavior and tics. Twin 1 had severe motor tics, loud vocalizations, coprolalia, and school behavior problems, whereas twin 2 was only mildly affected. Neither boy had ever been treated with medication for his tic disorder. Lumbar puncture was performed on each after a night of bed rest. In spite of the marked clinical differences between the two boys, the major indices of dopamine and serotonin turnover in the cerebrospinal fluid were equivalent. Homovanillic acid levels were 65 and 60 ng/ml, respectively, and 5-hydroxyindoleacetic acid levels were 36 and 39 ng/ml. Observation of these twins suggests that the phenotypic expression of GTS relates to more factors than inheritance. Neurochemical metabolites of dopamine and serotonin did not reflect the comparative clinical severity of GTS in these boys.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Goetz</LastName><ForeName>C G</ForeName><Initials>CG</Initials><AffiliationInfo><Affiliation>Department of Neurological Sciences, Rush Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tanner</LastName><ForeName>C M</ForeName><Initials>CM</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>54-16-0</RegistryNumber><NameOfSubstance UI="D006897">Hydroxyindoleacetic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>X77S6GMS36</RegistryNumber><NameOfSubstance UI="D006719">Homovanillic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Mov Disord. 1991;6(4):384</RefSource><PMID Version="1">1758465</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002648">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004200">Diseases in Twins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006719">Homovanillic Acid</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000134">cerebrospinal fluid</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006897">Hydroxyindoleacetic Acid</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000134">cerebrospinal fluid</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005879">Tourette Syndrome</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000134">cerebrospinal fluid</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1990</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1990</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1990</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1691443</ArticleId><ArticleId IdType="doi">10.1002/mds.870050216</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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