Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia
Identifieur interne : 000914 ( Main/Corpus ); précédent : 000913; suivant : 000915Ventricular 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 [ 0885-3185 ] ; 2011-07.
English descriptors
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. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23700
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ISTEX:1C13AD81052040F7F91234DE32AA9AC7A4C0DBC3Le document en format XML
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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. 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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. 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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. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>dementia</term></item><item><term>magnetic resonance imaging</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-10-19">Received</change><change when="2011-02-08">Registration</change><change when="2011-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/1C13AD81052040F7F91234DE32AA9AC7A4C0DBC3/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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Wayne</givenNames><familyName>Martin</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Department of Medicine, University of Calgary, Calgary, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="CA" type="organization"><unparsedAffiliation>Division of Neurosciences, Alberta Health Services, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="CA" type="organization"><unparsedAffiliation>Department of Radiology and Diagnostic Imaging, University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">dementia</keyword><keyword xml:id="kwd3">magnetic resonance imaging</keyword></keywordGroup><supportingInformation><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23700:MDS_23700_sm_authorroles"></mediaResource><caption>Author Roles and Disclosures</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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 (<i>r</i> = 0.87, <i>P</i> = .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 <i>decrease</i> 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. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn2"><p>The study was supported through an operating grant from the Canadian Institutes for Health Research.</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Ventricular Dilatation In PD Dementia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Ventricular dilatation and brain atrophy in patients with Parkinson's disease with incipient dementia</title></titleInfo><name type="personal"><namePart type="given">Richard</namePart><namePart type="family">Camicioli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</affiliation><description>Correspondence: E223, Glenrose Rehabilitation Hospital, 10230 111th Avenue, Edmonton, Alberta, Canada T5G 0B7</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jennifer</namePart><namePart type="family">Sabino</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myrlene</namePart><namePart type="family">Gee</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Bouchard</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</affiliation><affiliation>Department of Medicine, University of Calgary, Calgary, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nancy</namePart><namePart type="family">Fisher</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Division of Neurosciences, Alberta Health Services, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chris</namePart><namePart type="family">Hanstock</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Derek</namePart><namePart type="family">Emery</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</affiliation><affiliation>Department of Radiology and Diagnostic Imaging, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.R. Wayne</namePart><namePart type="family">Martin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-07</dateIssued><dateCaptured encoding="w3cdtf">2010-10-19</dateCaptured><dateValid encoding="w3cdtf">2011-02-08</dateValid><copyrightDate encoding="w3cdtf">2011</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">3</extent><extent unit="tables">3</extent><extent unit="references">37</extent><extent unit="words">7420</extent></physicalDescription><abstract 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. © 2011 Movement Disorder Society</abstract><note type="additional physical form">Author Roles and Disclosures</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*The study was supported through an operating grant from the Canadian Institutes for Health Research.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>dementia</topic><topic>magnetic resonance imaging</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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