How to diagnose dementia with Lewy bodies: State of the art
Identifieur interne : 001799 ( Main/Corpus ); précédent : 001798; suivant : 001800How to diagnose dementia with Lewy bodies: State of the art
Auteurs : Felix Geser ; Gregor K. Wenning ; Werner Poewe ; Ian MckeithSource :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
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- KwdEn :
Abstract
Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia in older people that has only been recognized in the past decade and that remains widely underdiagnosed. At postmortem examination, affected patients show numerous α‐synuclein‐positive Lewy bodies (LB) in many parts of the cerebral cortex, particularly neocortical and limbic areas in addition to the nigral LB degeneration characteristic of Parkinson's disease (PD). Clinical presentation, unlike PD, is with progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function accompanied by usually only mildly to moderately severe parkinsonism, which is often akineto‐rigid without the classical parkinsonian rest‐tremor. Further accompanying features include spontaneous recurrent visual hallucinations and conspicuous fluctuations in alertness and cognitive performance. The two main differential diagnoses are Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). To improve the differential diagnosis of DLB, consensus criteria have been developed that establish possible and probable levels of clinical diagnostic accuracy. Generally, their sensitivity is variable and low but their specificity is high. Current consensus is to restrict a diagnosis of DLB only to patients with parkinsonism who develop dementia within 12 months of the onset of motor symptoms. Using operationalized criteria, DLB can be diagnosed clinically with an accuracy similar to that achieved for AD or PD. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. We review the present state of the best practice in the clinical diagnosis of DLB. Future modifications of diagnostic criteria would ideally include the full range of clinical presentations that can be associated with LB disease. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20535
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At postmortem examination, affected patients show numerous α‐synuclein‐positive Lewy bodies (LB) in many parts of the cerebral cortex, particularly neocortical and limbic areas in addition to the nigral LB degeneration characteristic of Parkinson's disease (PD). Clinical presentation, unlike PD, is with progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function accompanied by usually only mildly to moderately severe parkinsonism, which is often akineto‐rigid without the classical parkinsonian rest‐tremor. Further accompanying features include spontaneous recurrent visual hallucinations and conspicuous fluctuations in alertness and cognitive performance. The two main differential diagnoses are Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). To improve the differential diagnosis of DLB, consensus criteria have been developed that establish possible and probable levels of clinical diagnostic accuracy. Generally, their sensitivity is variable and low but their specificity is high. Current consensus is to restrict a diagnosis of DLB only to patients with parkinsonism who develop dementia within 12 months of the onset of motor symptoms. Using operationalized criteria, DLB can be diagnosed clinically with an accuracy similar to that achieved for AD or PD. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. We review the present state of the best practice in the clinical diagnosis of DLB. Future modifications of diagnostic criteria would ideally include the full range of clinical presentations that can be associated with LB disease. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Felix Geser MD, PhD</name><affiliations><json:string>Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Gregor K. Wenning MD, PhD</name><affiliations><json:string>Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Ian McKeith MD</name><affiliations><json:string>University of Newcastle upon Tyne, Wolfson Research Centre, Newcastle General Hospital, Newcastle, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>dementia with Lewy bodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>clinical diagnosis</value></json:item></subject><articleId><json:string>MDS20535</json:string></articleId><language><json:string>eng</json:string></language><abstract>Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia in older people that has only been recognized in the past decade and that remains widely underdiagnosed. At postmortem examination, affected patients show numerous α‐synuclein‐positive Lewy bodies (LB) in many parts of the cerebral cortex, particularly neocortical and limbic areas in addition to the nigral LB degeneration characteristic of Parkinson's disease (PD). Clinical presentation, unlike PD, is with progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function accompanied by usually only mildly to moderately severe parkinsonism, which is often akineto‐rigid without the classical parkinsonian rest‐tremor. Further accompanying features include spontaneous recurrent visual hallucinations and conspicuous fluctuations in alertness and cognitive performance. The two main differential diagnoses are Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). To improve the differential diagnosis of DLB, consensus criteria have been developed that establish possible and probable levels of clinical diagnostic accuracy. Generally, their sensitivity is variable and low but their specificity is high. Current consensus is to restrict a diagnosis of DLB only to patients with parkinsonism who develop dementia within 12 months of the onset of motor symptoms. Using operationalized criteria, DLB can be diagnosed clinically with an accuracy similar to that achieved for AD or PD. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. We review the present state of the best practice in the clinical diagnosis of DLB. 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At postmortem examination, affected patients show numerous α‐synuclein‐positive Lewy bodies (LB) in many parts of the cerebral cortex, particularly neocortical and limbic areas in addition to the nigral LB degeneration characteristic of Parkinson's disease (PD). Clinical presentation, unlike PD, is with progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function accompanied by usually only mildly to moderately severe parkinsonism, which is often akineto‐rigid without the classical parkinsonian rest‐tremor. Further accompanying features include spontaneous recurrent visual hallucinations and conspicuous fluctuations in alertness and cognitive performance. The two main differential diagnoses are Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). To improve the differential diagnosis of DLB, consensus criteria have been developed that establish possible and probable levels of clinical diagnostic accuracy. Generally, their sensitivity is variable and low but their specificity is high. Current consensus is to restrict a diagnosis of DLB only to patients with parkinsonism who develop dementia within 12 months of the onset of motor symptoms. Using operationalized criteria, DLB can be diagnosed clinically with an accuracy similar to that achieved for AD or PD. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. We review the present state of the best practice in the clinical diagnosis of DLB. 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At postmortem examination, affected patients show numerous α‐synuclein‐positive Lewy bodies (LB) in many parts of the cerebral cortex, particularly neocortical and limbic areas in addition to the nigral LB degeneration characteristic of Parkinson's disease (PD). Clinical presentation, unlike PD, is with progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function accompanied by usually only mildly to moderately severe parkinsonism, which is often akineto‐rigid without the classical parkinsonian rest‐tremor. Further accompanying features include spontaneous recurrent visual hallucinations and conspicuous fluctuations in alertness and cognitive performance. The two main differential diagnoses are Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). To improve the differential diagnosis of DLB, consensus criteria have been developed that establish possible and probable levels of clinical diagnostic accuracy. Generally, their sensitivity is variable and low but their specificity is high. Current consensus is to restrict a diagnosis of DLB only to patients with parkinsonism who develop dementia within 12 months of the onset of motor symptoms. Using operationalized criteria, DLB can be diagnosed clinically with an accuracy similar to that achieved for AD or PD. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. We review the present state of the best practice in the clinical diagnosis of DLB. Future modifications of diagnostic criteria would ideally include the full range of clinical presentations that can be associated with LB disease. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>How to diagnose dementia with Lewy bodies: State of the art</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>How to Diagnose Dementia with Lewy Bodies</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>How to diagnose dementia with Lewy bodies: State of the art</title></titleInfo><name type="personal"><namePart type="given">Felix</namePart><namePart type="family">Geser</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria</affiliation><description>Correspondence: Clinical Department of Neurology, Medical University Innsbruck, Anichstrasse 35, A‐6020 Innsbruck, Austria</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregor K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ian</namePart><namePart type="family">McKeith</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Newcastle upon Tyne, Wolfson Research Centre, Newcastle General Hospital, Newcastle, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-08</dateIssued><copyrightDate encoding="w3cdtf">2005</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="tables">1</extent><extent unit="references">109</extent><extent unit="words">7752</extent></physicalDescription><abstract lang="en">Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia in older people that has only been recognized in the past decade and that remains widely underdiagnosed. At postmortem examination, affected patients show numerous α‐synuclein‐positive Lewy bodies (LB) in many parts of the cerebral cortex, particularly neocortical and limbic areas in addition to the nigral LB degeneration characteristic of Parkinson's disease (PD). Clinical presentation, unlike PD, is with progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function accompanied by usually only mildly to moderately severe parkinsonism, which is often akineto‐rigid without the classical parkinsonian rest‐tremor. Further accompanying features include spontaneous recurrent visual hallucinations and conspicuous fluctuations in alertness and cognitive performance. The two main differential diagnoses are Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). To improve the differential diagnosis of DLB, consensus criteria have been developed that establish possible and probable levels of clinical diagnostic accuracy. Generally, their sensitivity is variable and low but their specificity is high. Current consensus is to restrict a diagnosis of DLB only to patients with parkinsonism who develop dementia within 12 months of the onset of motor symptoms. Using operationalized criteria, DLB can be diagnosed clinically with an accuracy similar to that achieved for AD or PD. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. We review the present state of the best practice in the clinical diagnosis of DLB. Future modifications of diagnostic criteria would ideally include the full range of clinical presentations that can be associated with LB disease. © 2005 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>dementia with Lewy bodies</topic><topic>Alzheimer's disease</topic><topic>Parkinson's disease dementia</topic><topic>clinical diagnosis</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart></name><name type="personal"><namePart type="given">Gregor</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD, PhD</namePart></name><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>S12</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>S12</number></detail><extent unit="pages"><start>S11</start><end>S20</end><total>10</total></extent></part></relatedItem><identifier type="istex">0E3787F075403488B0AC6D9DD4920F5C8642A791</identifier><identifier type="DOI">10.1002/mds.20535</identifier><identifier type="ArticleID">MDS20535</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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