Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia.
Identifieur interne : 000C04 ( PubMed/Corpus ); précédent : 000C03; suivant : 000C05Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia.
Auteurs : Richard Camicioli ; Jennifer Sabino ; Myrlene Gee ; Thomas Bouchard ; Nancy Fisher ; Chris Hanstock ; Derek Emery ; W R Wayne MartinSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Aged, Atrophy (etiology), Atrophy (pathology), Brain (physiopathology), Cerebral Ventricles (physiopathology), Cognition Disorders (diagnosis), Cognition Disorders (etiology), Dementia (complications), Dementia (pathology), Dilatation, Female, Humans, Image Processing, Computer-Assisted, Longitudinal Studies, Magnetic Resonance Imaging, Male, Mental Status Schedule, Neuropsychological Tests, Parkinson Disease (complications), Parkinson Disease (pathology), Statistics as Topic, Time Factors.
- MESH :
- complications : Dementia, Parkinson Disease.
- diagnosis : Cognition Disorders.
- etiology : Atrophy, Cognition Disorders.
- pathology : Atrophy, Dementia, Parkinson Disease.
- physiopathology : Brain, Cerebral Ventricles.
- Aged, Dilatation, Female, Humans, Image Processing, Computer-Assisted, Longitudinal Studies, Magnetic Resonance Imaging, Male, Mental Status Schedule, Neuropsychological Tests, Statistics as Topic, Time Factors.
Abstract
Age-related ventricular enlargement is accelerated in Alzheimer's disease, but its relationship to cognitive decline in Parkinson's disease is less clear, even though dementia is common in Parkinson's disease. Our goals were to determine if greater enlargement of the ventricles and gray or white matter atrophy occurred in Parkinson's disease patients developing cognitive decline. Older nondemented patients with Parkinson's disease (33) and age- and sex-matched controls (39) were recruited and prospectively assessed for the development of significant cognitive decline over 36 months. Magnetic resonance imaging was obtained every 18 months, and ventricular volume and total brain gray and white matter volumes were measured using reliable segmentation of T1-weighted volumetric scans. Subjects with incidental intracranial abnormalities, an atypical course, and stroke as well as dropouts were excluded from a cohort of 52 patients and 50 controls. Among 33 patients and 39 controls, 10 patients and 3 controls developed significant cognitive impairment or dementia. Ventricular change and Parkinson's disease status were significantly associated with dementia. Ventricular change was significantly correlated with change in Mini-Mental Status Examination in the Parkinson's disease with dementia group (r = 0.87, P = .001). Gray matter atrophy was greater in Parkinson's disease with dementia, with similar change over time in both Parkinson's disease and Parkinson's disease with dementia. White matter volumes were not significantly different between Parkinson's disease and Parkinson's disease with dementia; however, the decrease over time might be greater in Parkinson's disease with dementia. Ventricular dilatation occurs early in the course of significant cognitive decline in patients with Parkinson's disease, possibly reflecting both cortical gray and white matter loss.
DOI: 10.1002/mds.23700
PubMed: 21442661
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pubmed:21442661Le document en format XML
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first="Nancy" last="Fisher">Nancy Fisher</name></author><author><name sortKey="Hanstock, Chris" sort="Hanstock, Chris" uniqKey="Hanstock C" first="Chris" last="Hanstock">Chris Hanstock</name></author><author><name sortKey="Emery, Derek" sort="Emery, Derek" uniqKey="Emery D" first="Derek" last="Emery">Derek Emery</name></author><author><name sortKey="Martin, W R Wayne" sort="Martin, W R Wayne" uniqKey="Martin W" first="W R Wayne" last="Martin">W R Wayne Martin</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21442661</idno><idno type="pmid">21442661</idno><idno type="doi">10.1002/mds.23700</idno><idno type="wicri:Area/PubMed/Corpus">000C04</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000C04</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia.</title><author><name sortKey="Camicioli, Richard" sort="Camicioli, Richard" uniqKey="Camicioli R" first="Richard" last="Camicioli">Richard Camicioli</name><affiliation><nlm:affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada. rcamicio@ualberta.ca</nlm:affiliation></affiliation></author><author><name sortKey="Sabino, Jennifer" sort="Sabino, Jennifer" uniqKey="Sabino J" first="Jennifer" last="Sabino">Jennifer Sabino</name></author><author><name sortKey="Gee, Myrlene" sort="Gee, Myrlene" uniqKey="Gee M" first="Myrlene" last="Gee">Myrlene Gee</name></author><author><name sortKey="Bouchard, Thomas" sort="Bouchard, Thomas" uniqKey="Bouchard T" first="Thomas" last="Bouchard">Thomas Bouchard</name></author><author><name sortKey="Fisher, Nancy" sort="Fisher, Nancy" uniqKey="Fisher N" first="Nancy" last="Fisher">Nancy Fisher</name></author><author><name sortKey="Hanstock, Chris" sort="Hanstock, Chris" uniqKey="Hanstock C" first="Chris" last="Hanstock">Chris Hanstock</name></author><author><name sortKey="Emery, Derek" sort="Emery, Derek" uniqKey="Emery D" first="Derek" last="Emery">Derek Emery</name></author><author><name sortKey="Martin, W R Wayne" sort="Martin, W R Wayne" uniqKey="Martin W" first="W R Wayne" last="Martin">W R Wayne Martin</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="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Atrophy (etiology)</term><term>Atrophy (pathology)</term><term>Brain (physiopathology)</term><term>Cerebral Ventricles (physiopathology)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (etiology)</term><term>Dementia (complications)</term><term>Dementia (pathology)</term><term>Dilatation</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Mental Status Schedule</term><term>Neuropsychological Tests</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (pathology)</term><term>Statistics as Topic</term><term>Time Factors</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Atrophy</term><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Atrophy</term><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Cerebral Ventricles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Dilatation</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Mental Status Schedule</term><term>Neuropsychological Tests</term><term>Statistics as Topic</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Age-related ventricular enlargement is accelerated in Alzheimer's disease, but its relationship to cognitive decline in Parkinson's disease is less clear, even though dementia is common in Parkinson's disease. Our goals were to determine if greater enlargement of the ventricles and gray or white matter atrophy occurred in Parkinson's disease patients developing cognitive decline. Older nondemented patients with Parkinson's disease (33) and age- and sex-matched controls (39) were recruited and prospectively assessed for the development of significant cognitive decline over 36 months. Magnetic resonance imaging was obtained every 18 months, and ventricular volume and total brain gray and white matter volumes were measured using reliable segmentation of T1-weighted volumetric scans. Subjects with incidental intracranial abnormalities, an atypical course, and stroke as well as dropouts were excluded from a cohort of 52 patients and 50 controls. Among 33 patients and 39 controls, 10 patients and 3 controls developed significant cognitive impairment or dementia. Ventricular change and Parkinson's disease status were significantly associated with dementia. Ventricular change was significantly correlated with change in Mini-Mental Status Examination in the Parkinson's disease with dementia group (r = 0.87, P = .001). Gray matter atrophy was greater in Parkinson's disease with dementia, with similar change over time in both Parkinson's disease and Parkinson's disease with dementia. White matter volumes were not significantly different between Parkinson's disease and Parkinson's disease with dementia; however, the decrease over time might be greater in Parkinson's disease with dementia. Ventricular dilatation occurs early in the course of significant cognitive decline in patients with Parkinson's disease, possibly reflecting both cortical gray and white matter loss.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21442661</PMID><DateCreated><Year>2011</Year><Month>11</Month><Day>04</Day></DateCreated><DateCompleted><Year>2012</Year><Month>02</Month><Day>29</Day></DateCompleted><DateRevised><Year>2011</Year><Month>11</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>8</Issue><PubDate><Year>2011</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia.</ArticleTitle><Pagination><MedlinePgn>1443-50</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23700</ELocationID><Abstract><AbstractText>Age-related ventricular enlargement is accelerated in Alzheimer's disease, but its relationship to cognitive decline in Parkinson's disease is less clear, even though dementia is common in Parkinson's disease. Our goals were to determine if greater enlargement of the ventricles and gray or white matter atrophy occurred in Parkinson's disease patients developing cognitive decline. Older nondemented patients with Parkinson's disease (33) and age- and sex-matched controls (39) were recruited and prospectively assessed for the development of significant cognitive decline over 36 months. Magnetic resonance imaging was obtained every 18 months, and ventricular volume and total brain gray and white matter volumes were measured using reliable segmentation of T1-weighted volumetric scans. Subjects with incidental intracranial abnormalities, an atypical course, and stroke as well as dropouts were excluded from a cohort of 52 patients and 50 controls. Among 33 patients and 39 controls, 10 patients and 3 controls developed significant cognitive impairment or dementia. Ventricular change and Parkinson's disease status were significantly associated with dementia. Ventricular change was significantly correlated with change in Mini-Mental Status Examination in the Parkinson's disease with dementia group (r = 0.87, P = .001). Gray matter atrophy was greater in Parkinson's disease with dementia, with similar change over time in both Parkinson's disease and Parkinson's disease with dementia. White matter volumes were not significantly different between Parkinson's disease and Parkinson's disease with dementia; however, the decrease over time might be greater in Parkinson's disease with dementia. Ventricular dilatation occurs early in the course of significant cognitive decline in patients with Parkinson's disease, possibly reflecting both cortical gray and white matter loss.</AbstractText><CopyrightInformation>Copyright © 2011 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Camicioli</LastName><ForeName>Richard</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada. rcamicio@ualberta.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sabino</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Gee</LastName><ForeName>Myrlene</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Bouchard</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Fisher</LastName><ForeName>Nancy</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Hanstock</LastName><ForeName>Chris</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Emery</LastName><ForeName>Derek</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>W R Wayne</ForeName><Initials>WR</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>03</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001284" MajorTopicYN="N">Atrophy</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002552" MajorTopicYN="N">Cerebral Ventricles</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003072" MajorTopicYN="N">Cognition Disorders</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003704" MajorTopicYN="N">Dementia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004106" MajorTopicYN="N">Dilatation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007091" MajorTopicYN="N">Image Processing, Computer-Assisted</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008609" MajorTopicYN="N">Mental Status Schedule</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009483" MajorTopicYN="N">Neuropsychological Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013223" MajorTopicYN="N">Statistics as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>10</Month><Day>19</Day></PubMedPubDate><PubMedPubDate 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