Profile of families with parkinsonism-predominant spinocerebellar ataxia type 2 (SCA2).
Identifieur interne : 003448 ( PubMed/Curation ); précédent : 003447; suivant : 003449Profile of families with parkinsonism-predominant spinocerebellar ataxia type 2 (SCA2).
Auteurs : Sarah Furtado [Canada] ; Haydeh Payami ; Paul J. Lockhart ; Melissa Hanson ; John G. Nutt ; Andrew A. Singleton ; Amanda Singleton ; Jamel Bower ; Ryan J. Utti ; Thomas D. Bird ; Raul De La Fuente-Fernandez ; Yoshio Tsuboi ; Mary L. Klimek ; Oksana Suchowersky ; John Hardy ; Donald B. Calne ; Zbigniew K. Wszolek ; Matthew Farrer ; Katrina Gwinn-Hardy ; A Jon StoesslSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2004.
English descriptors
- KwdEn :
- Antiparkinson Agents (therapeutic use), Brain (blood supply), Brain (metabolism), Brain (pathology), Corpus Striatum (blood supply), Corpus Striatum (metabolism), Dopamine Plasma Membrane Transport Proteins, Dystonia (epidemiology), Humans, Levodopa (therapeutic use), Magnetic Resonance Imaging, Membrane Glycoproteins (metabolism), Membrane Transport Proteins (metabolism), Nerve Tissue Proteins (metabolism), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (epidemiology), Parkinsonian Disorders (genetics), Posture, Spinocerebellar Ataxias (drug therapy), Spinocerebellar Ataxias (epidemiology), Spinocerebellar Ataxias (genetics), Tomography, Emission-Computed, Tomography, Emission-Computed, Single-Photon, Tremor (drug therapy), Tremor (epidemiology).
- MESH :
- chemical , metabolism : Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- blood supply : Brain, Corpus Striatum.
- drug therapy : Parkinsonian Disorders, Spinocerebellar Ataxias, Tremor.
- epidemiology : Dystonia, Parkinsonian Disorders, Spinocerebellar Ataxias, Tremor.
- genetics : Parkinsonian Disorders, Spinocerebellar Ataxias.
- metabolism : Brain, Corpus Striatum.
- pathology : Brain.
- chemical : Dopamine Plasma Membrane Transport Proteins, Humans, Magnetic Resonance Imaging, Posture, Tomography, Emission-Computed, Tomography, Emission-Computed, Single-Photon.
Abstract
Spinocerebellar ataxia type 2 (SCA2) has been recognized recently as an uncommon cause of parkinsonism, an alternate presentation to the typical cerebellar disorder. This research review summarizes the existing literature on parkinsonism-predominant presentation SCA2 and presents new clinical cases of patients with this condition. Various phenotypes are noted in this subtype of SCA2, including parkinsonism indistinguishable from idiopathic Parkinson's disease (PD), parkinsonism plus ataxia, motor neuron disease, and postural tremor. In several kindreds with multiple affected family members, the SCA2 expansion segregated with disease; in addition, several single cases of parkinsonism with and without a family history are also described. The number of repeats in symptomatic patients ranged from 33 to 43. Interruption of the CAG repeat with CAA, CGG, or CCG was found in some individuals, possibly stabilizing the repeat structure and accounting for the relative stability of the repeat size across generations in some families; allele length is not necessarily indicative of trinucleotide repeat architecture. Positron emission tomography scanning in one family showed reduced fluorodopa uptake and normal to increased raclopride binding with a rostrocaudal gradient similar to that found in idiopathic PD. This review emphasizes the importance of testing for SCA2 in patients with parkinsonism and a family history of neurodegenerative disorders. Testing for SCA2 is also important in studies of inherited parkinsonism.
DOI: 10.1002/mds.20074
PubMed: 15197699
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pubmed:15197699Le document en format XML
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Lockhart</name></author><author><name sortKey="Hanson, Melissa" sort="Hanson, Melissa" uniqKey="Hanson M" first="Melissa" last="Hanson">Melissa Hanson</name></author><author><name sortKey="Nutt, John G" sort="Nutt, John G" uniqKey="Nutt J" first="John G" last="Nutt">John G. Nutt</name></author><author><name sortKey="Singleton, Andrew A" sort="Singleton, Andrew A" uniqKey="Singleton A" first="Andrew A" last="Singleton">Andrew A. Singleton</name></author><author><name sortKey="Singleton, Amanda" sort="Singleton, Amanda" uniqKey="Singleton A" first="Amanda" last="Singleton">Amanda Singleton</name></author><author><name sortKey="Bower, Jamel" sort="Bower, Jamel" uniqKey="Bower J" first="Jamel" last="Bower">Jamel Bower</name></author><author><name sortKey="Utti, Ryan J" sort="Utti, Ryan J" uniqKey="Utti R" first="Ryan J" last="Utti">Ryan J. Utti</name></author><author><name sortKey="Bird, Thomas D" sort="Bird, Thomas D" uniqKey="Bird T" first="Thomas D" last="Bird">Thomas D. Bird</name></author><author><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raul" last="De La Fuente-Fernandez">Raul De La Fuente-Fernandez</name></author><author><name sortKey="Tsuboi, Yoshio" sort="Tsuboi, Yoshio" uniqKey="Tsuboi Y" first="Yoshio" last="Tsuboi">Yoshio Tsuboi</name></author><author><name sortKey="Klimek, Mary L" sort="Klimek, Mary L" uniqKey="Klimek M" first="Mary L" last="Klimek">Mary L. Klimek</name></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></author><author><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name></author><author><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B" last="Calne">Donald B. 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Wszolek</name></author><author><name sortKey="Farrer, Matthew" sort="Farrer, Matthew" uniqKey="Farrer M" first="Matthew" last="Farrer">Matthew Farrer</name></author><author><name sortKey="Gwinn Hardy, Katrina" sort="Gwinn Hardy, Katrina" uniqKey="Gwinn Hardy K" first="Katrina" last="Gwinn-Hardy">Katrina Gwinn-Hardy</name></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</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="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (therapeutic use)</term><term>Brain (blood supply)</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Corpus Striatum (blood supply)</term><term>Corpus Striatum (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Dystonia (epidemiology)</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Magnetic Resonance Imaging</term><term>Membrane Glycoproteins (metabolism)</term><term>Membrane Transport Proteins (metabolism)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Parkinsonian Disorders (drug therapy)</term><term>Parkinsonian Disorders (epidemiology)</term><term>Parkinsonian Disorders (genetics)</term><term>Posture</term><term>Spinocerebellar Ataxias (drug therapy)</term><term>Spinocerebellar Ataxias (epidemiology)</term><term>Spinocerebellar Ataxias (genetics)</term><term>Tomography, Emission-Computed</term><term>Tomography, Emission-Computed, Single-Photon</term><term>Tremor (drug therapy)</term><term>Tremor (epidemiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Brain</term><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinsonian Disorders</term><term>Spinocerebellar Ataxias</term><term>Tremor</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Dystonia</term><term>Parkinsonian Disorders</term><term>Spinocerebellar Ataxias</term><term>Tremor</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinsonian Disorders</term><term>Spinocerebellar Ataxias</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Posture</term><term>Tomography, Emission-Computed</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Spinocerebellar ataxia type 2 (SCA2) has been recognized recently as an uncommon cause of parkinsonism, an alternate presentation to the typical cerebellar disorder. This research review summarizes the existing literature on parkinsonism-predominant presentation SCA2 and presents new clinical cases of patients with this condition. Various phenotypes are noted in this subtype of SCA2, including parkinsonism indistinguishable from idiopathic Parkinson's disease (PD), parkinsonism plus ataxia, motor neuron disease, and postural tremor. In several kindreds with multiple affected family members, the SCA2 expansion segregated with disease; in addition, several single cases of parkinsonism with and without a family history are also described. The number of repeats in symptomatic patients ranged from 33 to 43. Interruption of the CAG repeat with CAA, CGG, or CCG was found in some individuals, possibly stabilizing the repeat structure and accounting for the relative stability of the repeat size across generations in some families; allele length is not necessarily indicative of trinucleotide repeat architecture. Positron emission tomography scanning in one family showed reduced fluorodopa uptake and normal to increased raclopride binding with a rostrocaudal gradient similar to that found in idiopathic PD. This review emphasizes the importance of testing for SCA2 in patients with parkinsonism and a family history of neurodegenerative disorders. Testing for SCA2 is also important in studies of inherited parkinsonism.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15197699</PMID><DateCreated><Year>2004</Year><Month>06</Month><Day>15</Day></DateCreated><DateCompleted><Year>2004</Year><Month>10</Month><Day>28</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>19</Volume><Issue>6</Issue><PubDate><Year>2004</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Profile of families with parkinsonism-predominant spinocerebellar ataxia type 2 (SCA2).</ArticleTitle><Pagination><MedlinePgn>622-9</MedlinePgn></Pagination><Abstract><AbstractText>Spinocerebellar ataxia type 2 (SCA2) has been recognized recently as an uncommon cause of parkinsonism, an alternate presentation to the typical cerebellar disorder. This research review summarizes the existing literature on parkinsonism-predominant presentation SCA2 and presents new clinical cases of patients with this condition. Various phenotypes are noted in this subtype of SCA2, including parkinsonism indistinguishable from idiopathic Parkinson's disease (PD), parkinsonism plus ataxia, motor neuron disease, and postural tremor. In several kindreds with multiple affected family members, the SCA2 expansion segregated with disease; in addition, several single cases of parkinsonism with and without a family history are also described. The number of repeats in symptomatic patients ranged from 33 to 43. Interruption of the CAG repeat with CAA, CGG, or CCG was found in some individuals, possibly stabilizing the repeat structure and accounting for the relative stability of the repeat size across generations in some families; allele length is not necessarily indicative of trinucleotide repeat architecture. Positron emission tomography scanning in one family showed reduced fluorodopa uptake and normal to increased raclopride binding with a rostrocaudal gradient similar to that found in idiopathic PD. This review emphasizes the importance of testing for SCA2 in patients with parkinsonism and a family history of neurodegenerative disorders. Testing for SCA2 is also important in studies of inherited parkinsonism.</AbstractText><CopyrightInformation>Copyright 2004 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Furtado</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. furtado@ucalgary.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Payami</LastName><ForeName>Haydeh</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Lockhart</LastName><ForeName>Paul J</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Hanson</LastName><ForeName>Melissa</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Nutt</LastName><ForeName>John G</ForeName><Initials>JG</Initials></Author><Author ValidYN="Y"><LastName>Singleton</LastName><ForeName>Andrew A</ForeName><Initials>AA</Initials></Author><Author ValidYN="Y"><LastName>Singleton</LastName><ForeName>Amanda</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Bower</LastName><ForeName>Jamel</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Utti</LastName><ForeName>Ryan J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Bird</LastName><ForeName>Thomas D</ForeName><Initials>TD</Initials></Author><Author ValidYN="Y"><LastName>de la Fuente-Fernandez</LastName><ForeName>Raul</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Tsuboi</LastName><ForeName>Yoshio</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Klimek</LastName><ForeName>Mary L</ForeName><Initials>ML</Initials></Author><Author ValidYN="Y"><LastName>Suchowersky</LastName><ForeName>Oksana</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Hardy</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Calne</LastName><ForeName>Donald B</ForeName><Initials>DB</Initials></Author><Author ValidYN="Y"><LastName>Wszolek</LastName><ForeName>Zbigniew K</ForeName><Initials>ZK</Initials></Author><Author ValidYN="Y"><LastName>Farrer</LastName><ForeName>Matthew</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Gwinn-Hardy</LastName><ForeName>Katrina</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A Jon</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS36960</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000098">blood supply</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003342">Corpus Striatum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000098">blood supply</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D050483">Dopamine Plasma Membrane Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004421">Dystonia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008279">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008562">Membrane Glycoproteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D026901">Membrane Transport Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009419">Nerve Tissue Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011187">Posture</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020754">Spinocerebellar Ataxias</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014055">Tomography, Emission-Computed</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015899">Tomography, Emission-Computed, Single-Photon</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014202">Tremor</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>28</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>6</Month><Day>16</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>10</Month><Day>29</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>6</Month><Day>16</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15197699</ArticleId><ArticleId IdType="doi">10.1002/mds.20074</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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