Profile of Cognitive Impairment in Parkinson's Disease
Identifieur interne : 000429 ( Main/Corpus ); précédent : 000428; suivant : 000430Profile of Cognitive Impairment in Parkinson's Disease
Auteurs : G. Stennis Watson ; James B. LeverenzSource :
- Brain Pathology [ 1015-6305 ] ; 2010-05.
English descriptors
Abstract
Cognitive impairment (CI) is a common nonmotor complication of Parkinson's disease (PD), and is associated with significant disability for patients and burden for caregivers. Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy‐related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease‐specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.
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DOI: 10.1111/j.1750-3639.2010.00373.x
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Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy‐related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease‐specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.</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>cognitive impairment</term></item><item><term>neuropsychology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E424CEAFBE02F536E818594AFAEAFBED7CCC4034/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1750-3639</doi><issn type="print">1015-6305</issn><issn type="electronic">1750-3639</issn><idGroup><id type="product" value="BPA"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="BRAIN PATHOLOGY">Brain Pathology</title></titleGroup></publicationMeta><publicationMeta level="part" position="05003"><doi origin="wiley">10.1111/bpa.2010.20.issue-3</doi><numberingGroup><numbering type="journalVolume" number="20">20</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2010-05">May 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="15" status="forIssue"><doi origin="wiley">10.1111/j.1750-3639.2010.00373.x</doi><idGroup><id type="unit" value="BPA373"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">MINI‐SYMPOSIUM: Dementia in Parkinson's Disease</title></titleGroup><copyright>Journal Compilation © 2010 International Society of Neuropathology. No claim to original US government works</copyright><eventGroup><event type="firstOnline" date="2010-04-12"></event><event type="publishedOnlineFinalForm" date="2010-04-12"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-05-18"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-08"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-15"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="640">640</numbering><numbering type="pageLast" number="645">645</numbering></numberingGroup><correspondenceTo>James B. Leverenz, MD, VA Puget Sound Health Care System, MIRECC (116MIRECC), 1660 S. Columbian Way, Seattle, WA 98108 (E‐mail: <email>leverenz@u.washington.edu</email>) </correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:BPA.BPA373.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 11 December 2009; accepted 31 December 2009.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="58"></count><count type="wordTotal" number="5662"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Profile of Cognitive Impairment in Parkinson's Disease</title><title type="shortAuthors">Watson & Leverenz</title><title type="short">Cognitive Impairment in Parkinson's Disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a3 #a5"><personName><givenNames>G. Stennis</givenNames><familyName>Watson</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2 #a4 #a5" corresponding="yes"><personName><givenNames>James B.</givenNames><familyName>Leverenz</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Mental Illness,</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Parkinson's Disease and</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Geriatric Research Education and Clinical Centers, VA Puget Sound Health Care System, Seattle Division, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Departments of Neurology, and</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="US"><unparsedAffiliation>Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">dementia</keyword><keyword xml:id="k3">cognitive impairment</keyword><keyword xml:id="k4">neuropsychology</keyword></keywordGroup><supportingInformation><p><b>Table S1.</b> Summary of cognitive domains, impaired cognitive functions and representative cognitive tests.</p><p>Please note: Wiley‐Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.</p><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:10156305:media:bpa373:BPA_373_sm_tableS1"></mediaResource><caption>Supporting info item</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Cognitive impairment (CI) is a common nonmotor complication of Parkinson's disease (PD), and is associated with significant disability for patients and burden for caregivers. Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy‐related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease‐specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Profile of Cognitive Impairment in Parkinson's Disease</title></titleInfo><titleInfo type="abbreviated"><title>Cognitive Impairment in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Profile of Cognitive Impairment in Parkinson's Disease</title></titleInfo><name type="personal"><namePart type="given">G. Stennis</namePart><namePart type="family">Watson</namePart><affiliation>Geriatric Research Education and Clinical Centers, VA Puget Sound Health Care System, Seattle Division, Seattle, WA</affiliation><affiliation>Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">James B.</namePart><namePart type="family">Leverenz</namePart><affiliation>Mental Illness,</affiliation><affiliation>Parkinson's Disease and</affiliation><affiliation>Departments of Neurology, and</affiliation><affiliation>Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA</affiliation><description>Correspondence: James B. Leverenz, MD, VA Puget Sound Health Care System, MIRECC (116MIRECC), 1660 S. Columbian Way, Seattle, WA 98108 (E‐mail: )</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-05</dateIssued><edition>Received 11 December 2009; accepted 31 December 2009.</edition><copyrightDate encoding="w3cdtf">2010</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">1</extent><extent unit="references">58</extent><extent unit="words">5662</extent></physicalDescription><abstract lang="en">Cognitive impairment (CI) is a common nonmotor complication of Parkinson's disease (PD), and is associated with significant disability for patients and burden for caregivers. Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy‐related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease‐specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>dementia</topic><topic>cognitive impairment</topic><topic>neuropsychology</topic></subject><relatedItem type="host"><titleInfo><title>Brain Pathology</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Table S1. Summary of cognitive domains, impaired cognitive functions and representative cognitive tests. Please note: Wiley‐Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. Table S1. Summary of cognitive domains, impaired cognitive functions and representative cognitive tests. Please note: Wiley‐Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.Supporting Info Item: Supporting info item - </note><identifier type="ISSN">1015-6305</identifier><identifier type="eISSN">1750-3639</identifier><identifier type="DOI">10.1111/(ISSN)1750-3639</identifier><identifier type="PublisherID">BPA</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>640</start><end>645</end><total>6</total></extent></part></relatedItem><identifier type="istex">E424CEAFBE02F536E818594AFAEAFBED7CCC4034</identifier><identifier type="DOI">10.1111/j.1750-3639.2010.00373.x</identifier><identifier type="ArticleID">BPA373</identifier><accessCondition type="use and reproduction" contentType="copyright">Journal Compilation © 2010 International Society of Neuropathology. 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