Intact presupplementary motor area function in early, untreated Parkinson's disease.
Identifieur interne : 000F50 ( PubMed/Curation ); précédent : 000F49; suivant : 000F51Intact presupplementary motor area function in early, untreated Parkinson's disease.
Auteurs : W R Wayne Martin [Canada] ; Marguerite Wieler ; Myrlene Gee ; Christopher C. Hanstock ; Richard M. CamicioliSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Aged, Aspartic Acid (analogs & derivatives), Aspartic Acid (analysis), Case-Control Studies, Choline (analysis), Creatine (analysis), Female, Humans, Magnetic Resonance Spectroscopy (methods), Male, Middle Aged, Motor Cortex (metabolism), Motor Cortex (physiopathology), Parkinson Disease (pathology), Parkinson Disease (physiopathology).
- MESH :
- chemical , analogs & derivatives : Aspartic Acid.
- chemical , analysis : Aspartic Acid, Choline, Creatine.
- metabolism : Motor Cortex.
- methods : Magnetic Resonance Spectroscopy.
- pathology : Parkinson Disease.
- physiopathology : Motor Cortex, Parkinson Disease.
- Aged, Case-Control Studies, Female, Humans, Male, Middle Aged.
Abstract
Although motor symptoms of Parkinson's disease (PD) are initially responsive to dopamine replacement therapy, nonresponsive features develop over time, suggesting that impaired dopaminergic function alone may not be wholly responsible for all the motor features of the disease. Previous studies suggest impaired function in the presupplementary motor area (pre-SMA) in PD. Our objective was to determine whether pre-SMA abnormalities are present in untreated patients with early disease. We measured N-acetyl aspartate (NAA)/creatine (Cr) and choline (Cho)/Cr ratios in pre-SMA in 26 untreated patients with early PD (disease duration 3.0 +/- 2.0 yr) and 15 control subjects with single voxel magnetic resonance spectroscopy. Neither NAA/Cr nor Cho/Cr ratios differed significantly between groups. These observations suggest that, although pre-SMA function is impaired in moderately advanced PD, it is relatively spared in early disease. We suggest that pre-SMA dysfunction is in part responsible for the dopamine nonresponsive features associated with disease progression.
DOI: 10.1002/mds.22101
PubMed: 18709678
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Hanstock</name></author><author><name sortKey="Camicioli, Richard M" sort="Camicioli, Richard M" uniqKey="Camicioli R" first="Richard M" last="Camicioli">Richard M. 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Hanstock</name></author><author><name sortKey="Camicioli, Richard M" sort="Camicioli, Richard M" uniqKey="Camicioli R" first="Richard M" last="Camicioli">Richard M. Camicioli</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="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aspartic Acid (analogs & derivatives)</term><term>Aspartic Acid (analysis)</term><term>Case-Control Studies</term><term>Choline (analysis)</term><term>Creatine (analysis)</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Spectroscopy (methods)</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (metabolism)</term><term>Motor Cortex (physiopathology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aspartic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Aspartic Acid</term><term>Choline</term><term>Creatine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Motor Cortex</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Magnetic Resonance Spectroscopy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Motor Cortex</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Case-Control Studies</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">Although motor symptoms of Parkinson's disease (PD) are initially responsive to dopamine replacement therapy, nonresponsive features develop over time, suggesting that impaired dopaminergic function alone may not be wholly responsible for all the motor features of the disease. Previous studies suggest impaired function in the presupplementary motor area (pre-SMA) in PD. Our objective was to determine whether pre-SMA abnormalities are present in untreated patients with early disease. We measured N-acetyl aspartate (NAA)/creatine (Cr) and choline (Cho)/Cr ratios in pre-SMA in 26 untreated patients with early PD (disease duration 3.0 +/- 2.0 yr) and 15 control subjects with single voxel magnetic resonance spectroscopy. Neither NAA/Cr nor Cho/Cr ratios differed significantly between groups. These observations suggest that, although pre-SMA function is impaired in moderately advanced PD, it is relatively spared in early disease. We suggest that pre-SMA dysfunction is in part responsible for the dopamine nonresponsive features associated with disease progression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18709678</PMID><DateCreated><Year>2008</Year><Month>10</Month><Day>02</Day></DateCreated><DateCompleted><Year>2009</Year><Month>04</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>12</Issue><PubDate><Year>2008</Year><Month>Sep</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Intact presupplementary motor area function in early, untreated Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1756-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22101</ELocationID><Abstract><AbstractText>Although motor symptoms of Parkinson's disease (PD) are initially responsive to dopamine replacement therapy, nonresponsive features develop over time, suggesting that impaired dopaminergic function alone may not be wholly responsible for all the motor features of the disease. Previous studies suggest impaired function in the presupplementary motor area (pre-SMA) in PD. Our objective was to determine whether pre-SMA abnormalities are present in untreated patients with early disease. We measured N-acetyl aspartate (NAA)/creatine (Cr) and choline (Cho)/Cr ratios in pre-SMA in 26 untreated patients with early PD (disease duration 3.0 +/- 2.0 yr) and 15 control subjects with single voxel magnetic resonance spectroscopy. Neither NAA/Cr nor Cho/Cr ratios differed significantly between groups. These observations suggest that, although pre-SMA function is impaired in moderately advanced PD, it is relatively spared in early disease. We suggest that pre-SMA dysfunction is in part responsible for the dopamine nonresponsive features associated with disease progression.</AbstractText><CopyrightInformation>(c) 2007 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>W R Wayne</ForeName><Initials>WR</Initials><AffiliationInfo><Affiliation>Division of Neurology, University of Alberta, Edmonton, Alberta, Canada. wayne.martin@ualberta.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wieler</LastName><ForeName>Marguerite</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Gee</LastName><ForeName>Myrlene</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Hanstock</LastName><ForeName>Christopher C</ForeName><Initials>CC</Initials></Author><Author ValidYN="Y"><LastName>Camicioli</LastName><ForeName>Richard M</ForeName><Initials>RM</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><ChemicalList><Chemical><RegistryNumber>30KYC7MIAI</RegistryNumber><NameOfSubstance UI="D001224">Aspartic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>997-55-7</RegistryNumber><NameOfSubstance UI="C000179">N-acetylaspartate</NameOfSubstance></Chemical><Chemical><RegistryNumber>MU72812GK0</RegistryNumber><NameOfSubstance UI="D003401">Creatine</NameOfSubstance></Chemical><Chemical><RegistryNumber>N91BDP6H0X</RegistryNumber><NameOfSubstance UI="D002794">Choline</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001224" MajorTopicYN="N">Aspartic Acid</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002794" MajorTopicYN="N">Choline</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003401" MajorTopicYN="N">Creatine</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009044" MajorTopicYN="N">Motor Cortex</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>8</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>4</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>8</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18709678</ArticleId><ArticleId IdType="doi">10.1002/mds.22101</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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