The natural history of parkinson's disease
Identifieur interne : 000274 ( Main/Corpus ); précédent : 000273; suivant : 000275The natural history of parkinson's disease
Auteurs : Poewe ; G. K. WenningSource :
- Annals of Neurology [ 0364-5134 ] ; 1998-09.
Abstract
There are still insufficient data on the natural course of Parkinson's disease (PD) owing to lack of standardized longitudinal follow‐up studies. Reported progression rates in early PD vary considerably by a factor of 2 to 3. Similarly, data from sequential [18F]dopa PET studies in PD patients have produced variable decline rates of PET indices ranging between 7 and 70% per decade. Risk factors for rapid progression include old age at onset, concomitant major depression, dementia, and akinetic‐rigid symptom presentation. The introduction of levodopa into the routine treatment of PD patients had a dramatic impact on symptomatic control without affecting the underlying rate of disease progression. By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow‐up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa‐induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co‐morbidity, disease stage at study entry, and diagnostic accuracy. However, the most recent follow‐up from the DATATOP cohort suggests normal life expectancy in carefully selected patients without significant co‐morbidity and with adequate treatment and expert follow‐up.
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DOI: 10.1002/ana.410440703
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Wenning</name><affiliation><mods:affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:3CD4C175B98DF2D00C5999356CA7702F16F27018</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/ana.410440703</idno><idno type="url">https://api.istex.fr/document/3CD4C175B98DF2D00C5999356CA7702F16F27018/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000274</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The natural history of parkinson's disease</title><author><name sortKey="Poewe" sort="Poewe" uniqKey="Poewe" last="Poewe">Poewe</name><affiliation><mods:affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G. K." last="Wenning">G. K. Wenning</name><affiliation><mods:affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-09">1998-09</date><biblScope unit="volume">44</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="supplement">1</biblScope><biblScope unit="page" from="S1">S1</biblScope><biblScope unit="page" to="S9">S9</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">3CD4C175B98DF2D00C5999356CA7702F16F27018</idno><idno type="DOI">10.1002/ana.410440703</idno><idno type="ArticleID">ANA410440703</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There are still insufficient data on the natural course of Parkinson's disease (PD) owing to lack of standardized longitudinal follow‐up studies. Reported progression rates in early PD vary considerably by a factor of 2 to 3. Similarly, data from sequential [18F]dopa PET studies in PD patients have produced variable decline rates of PET indices ranging between 7 and 70% per decade. Risk factors for rapid progression include old age at onset, concomitant major depression, dementia, and akinetic‐rigid symptom presentation. The introduction of levodopa into the routine treatment of PD patients had a dramatic impact on symptomatic control without affecting the underlying rate of disease progression. By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow‐up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa‐induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co‐morbidity, disease stage at study entry, and diagnostic accuracy. However, the most recent follow‐up from the DATATOP cohort suggests normal life expectancy in carefully selected patients without significant co‐morbidity and with adequate treatment and expert follow‐up.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr Poewe MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>G. K. 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By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow‐up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa‐induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co‐morbidity, disease stage at study entry, and diagnostic accuracy. 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Reported progression rates in early PD vary considerably by a factor of 2 to 3. Similarly, data from sequential [18F]dopa PET studies in PD patients have produced variable decline rates of PET indices ranging between 7 and 70% per decade. Risk factors for rapid progression include old age at onset, concomitant major depression, dementia, and akinetic‐rigid symptom presentation. The introduction of levodopa into the routine treatment of PD patients had a dramatic impact on symptomatic control without affecting the underlying rate of disease progression. By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow‐up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa‐induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co‐morbidity, disease stage at study entry, and diagnostic accuracy. However, the most recent follow‐up from the DATATOP cohort suggests normal life expectancy in carefully selected patients without significant co‐morbidity and with adequate treatment and expert follow‐up.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Introduction</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-09">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3CD4C175B98DF2D00C5999356CA7702F16F27018/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component found"><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)1531-8249</doi><issn type="print">0364-5134</issn><issn type="electronic">1531-8249</issn><idGroup><id type="product" value="ANA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title><title type="short">Ann Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="70"><doi origin="wiley" registered="yes">10.1002/ana.v44.1s</doi><titleGroup><title type="supplementTitle">Cell Death and Neuroprotection in Parkinson's Disease</title></titleGroup><numberingGroup><numbering type="journalVolume" number="44">44</numbering><numbering type="journalIssue">S1</numbering><numbering type="supplement" number="1">1</numbering></numberingGroup><coverDate startDate="1998-09">September 1998</coverDate></publicationMeta><publicationMeta level="unit" type="miscellaneous" position="3" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.410440703</doi><idGroup><id type="unit" value="ANA410440703"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Introduction</title><title type="tocHeading1">Introductions</title></titleGroup><copyright ownership="publisher">Copyright © 1998 Wiley‐Liss, Inc.</copyright><eventGroup><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.2.9 mode:FullText" date="2014-02-20"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.2.9 mode:FullText" date="2014-02-20"></event><event type="firstOnline" date="2014-02-21"></event><event type="publishedOnlineFinalForm" date="2014-02-21"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">S1</numbering><numbering type="pageLast">S9</numbering></numberingGroup><correspondenceTo>Department of Neurology, University Hospital, Anichstrasse 35, 6020 Innsbruck, Austria</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA410440703.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="0"></count></countGroup><titleGroup><title type="main" xml:lang="en">The natural history of parkinson's disease</title><title type="short" xml:lang="en">Natural History of PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr</honorifics><givenNames>W. H.</givenNames><familyName>Poewe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>G. K.</givenNames><familyName>Wenning</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AT" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital, Innsbruck, Austria</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>There are still insufficient data on the natural course of Parkinson's disease (PD) owing to lack of standardized longitudinal follow‐up studies. Reported progression rates in early PD vary considerably by a factor of 2 to 3. Similarly, data from sequential [<sup>18</sup>F]dopa PET studies in PD patients have produced variable decline rates of PET indices ranging between 7 and 70% per decade. Risk factors for rapid progression include old age at onset, concomitant major depression, dementia, and akinetic‐rigid symptom presentation. The introduction of levodopa into the routine treatment of PD patients had a dramatic impact on symptomatic control without affecting the underlying rate of disease progression. By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow‐up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa‐induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co‐morbidity, disease stage at study entry, and diagnostic accuracy. 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K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="other" displayLabel="miscellaneous"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-09</dateIssued><copyrightDate encoding="w3cdtf">1998</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">2</extent><extent unit="tables">1</extent></physicalDescription><abstract lang="en">There are still insufficient data on the natural course of Parkinson's disease (PD) owing to lack of standardized longitudinal follow‐up studies. Reported progression rates in early PD vary considerably by a factor of 2 to 3. Similarly, data from sequential [18F]dopa PET studies in PD patients have produced variable decline rates of PET indices ranging between 7 and 70% per decade. Risk factors for rapid progression include old age at onset, concomitant major depression, dementia, and akinetic‐rigid symptom presentation. The introduction of levodopa into the routine treatment of PD patients had a dramatic impact on symptomatic control without affecting the underlying rate of disease progression. By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow‐up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa‐induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co‐morbidity, disease stage at study entry, and diagnostic accuracy. However, the most recent follow‐up from the DATATOP cohort suggests normal life expectancy in carefully selected patients without significant co‐morbidity and with adequate treatment and expert follow‐up.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Introduction</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>44</number></detail><detail type="issue"><caption>no.</caption><number>S1</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>1</number></detail><extent unit="pages"><start>S1</start><end>S9</end><total>9</total></extent></part></relatedItem><identifier type="istex">3CD4C175B98DF2D00C5999356CA7702F16F27018</identifier><identifier type="DOI">10.1002/ana.410440703</identifier><identifier type="ArticleID">ANA410440703</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Wiley‐Liss, Inc.</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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