The natural history of treated Parkinson's disease in an incident, community based cohort
Identifieur interne : 000541 ( Main/Corpus ); précédent : 000540; suivant : 000542The natural history of treated Parkinson's disease in an incident, community based cohort
Auteurs : Jonathan R. Evans ; Sarah L. Mason ; Caroline H. Williams-Gray ; Thomas Foltynie ; Carol Brayne ; Trevor W. Robbins ; Roger A. BarkerSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2011-10.
Abstract
Background Our understanding of the natural history of idiopathic Parkinson's disease (PD) remains limited. In the era of potential disease modifying therapies, there is an urgent need for studies assessing the natural evolution of treated PD from onset so that relevant outcome measures can be identified for clinical trials. No previous studies have charted progression in unselected patients followed from the point of diagnosis. Methods A representative cohort of 132 PD patients was followed from diagnosis for up to 7.9 years (mean 5.2 years). Comprehensive clinical and neuropsychological evaluations were performed every 18 months. Disease progression was evaluated using well validated clinical measures (motor progression and development of dyskinesia on the Unified PD Rating Scale and Hoehn–Yahr scale, dementia onset according to DSM-IV criteria). Multi-level linear modelling was used to chart the nature and rate of progression in parkinsonian symptoms and signs over time. The prognostic importance of baseline demogr`aphic, clinical and genetic variables was evaluated using survival analysis. Results Axial (gait and postural) symptoms evolve more rapidly than other motor features of PD and appear to be the best index of disease progression. Conversely, conventional outcome measures are relatively insensitive to change over time. Earlier onset of postural instability (Hoehn–Yahr stage 3) is strongly associated with increased age at disease onset and has a significant impact on quality of life. Conclusions Dementia risk is associated with increased age, impaired baseline semantic fluency and the MAPT H1/H1 genotype. The efficacy of disease modifying therapies may be more meaningfully assessed in terms of their effects in delaying the major milestones of PD, such as postural instability and dementia, since it is these that have the greatest impact on patients.
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DOI: 10.1136/jnnp.2011.240366
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Mason</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Williams Gray, Caroline H" sort="Williams Gray, Caroline H" uniqKey="Williams Gray C" first="Caroline H" last="Williams-Gray">Caroline H. Williams-Gray</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Foltynie, Thomas" sort="Foltynie, Thomas" uniqKey="Foltynie T" first="Thomas" last="Foltynie">Thomas Foltynie</name><affiliation><mods:affiliation>Institute of Neurology, University College London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Brayne, Carol" sort="Brayne, Carol" uniqKey="Brayne C" first="Carol" last="Brayne">Carol Brayne</name><affiliation><mods:affiliation>Institute of Public Health, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Robbins, Trevor W" sort="Robbins, Trevor W" uniqKey="Robbins T" first="Trevor W" last="Robbins">Trevor W. Robbins</name><affiliation><mods:affiliation>Department of Experimental Psychology, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A" last="Barker">Roger A. Barker</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6441532380F3047211C43FDBCE1D97A725AEE92F</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1136/jnnp.2011.240366</idno><idno type="url">https://api.istex.fr/document/6441532380F3047211C43FDBCE1D97A725AEE92F/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000541</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">The natural history of treated Parkinson's disease in an incident, community based cohort</title><author><name sortKey="Evans, Jonathan R" sort="Evans, Jonathan R" uniqKey="Evans J" first="Jonathan R" last="Evans">Jonathan R. Evans</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jonathanevans@doctors.org.uk</mods:affiliation></affiliation></author><author><name sortKey="Mason, Sarah L" sort="Mason, Sarah L" uniqKey="Mason S" first="Sarah L" last="Mason">Sarah L. Mason</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Williams Gray, Caroline H" sort="Williams Gray, Caroline H" uniqKey="Williams Gray C" first="Caroline H" last="Williams-Gray">Caroline H. Williams-Gray</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Foltynie, Thomas" sort="Foltynie, Thomas" uniqKey="Foltynie T" first="Thomas" last="Foltynie">Thomas Foltynie</name><affiliation><mods:affiliation>Institute of Neurology, University College London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Brayne, Carol" sort="Brayne, Carol" uniqKey="Brayne C" first="Carol" last="Brayne">Carol Brayne</name><affiliation><mods:affiliation>Institute of Public Health, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Robbins, Trevor W" sort="Robbins, Trevor W" uniqKey="Robbins T" first="Trevor W" last="Robbins">Trevor W. Robbins</name><affiliation><mods:affiliation>Department of Experimental Psychology, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A" last="Barker">Roger A. Barker</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2011-10">2011-10</date><biblScope unit="volume">82</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1112">1112</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">6441532380F3047211C43FDBCE1D97A725AEE92F</idno><idno type="DOI">10.1136/jnnp.2011.240366</idno><idno type="href">jnnp-82-1112.pdf</idno><idno type="ArticleID">jnnp240366</idno><idno type="PMID">21593513</idno><idno type="Related-article-Href">10.1136/jnnp.2011.246835</idno><idno type="related-article-ID">RA1</idno><idno type="local">jnnp;82/10/1112</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background Our understanding of the natural history of idiopathic Parkinson's disease (PD) remains limited. In the era of potential disease modifying therapies, there is an urgent need for studies assessing the natural evolution of treated PD from onset so that relevant outcome measures can be identified for clinical trials. No previous studies have charted progression in unselected patients followed from the point of diagnosis. Methods A representative cohort of 132 PD patients was followed from diagnosis for up to 7.9 years (mean 5.2 years). Comprehensive clinical and neuropsychological evaluations were performed every 18 months. Disease progression was evaluated using well validated clinical measures (motor progression and development of dyskinesia on the Unified PD Rating Scale and Hoehn–Yahr scale, dementia onset according to DSM-IV criteria). Multi-level linear modelling was used to chart the nature and rate of progression in parkinsonian symptoms and signs over time. The prognostic importance of baseline demogr`aphic, clinical and genetic variables was evaluated using survival analysis. Results Axial (gait and postural) symptoms evolve more rapidly than other motor features of PD and appear to be the best index of disease progression. Conversely, conventional outcome measures are relatively insensitive to change over time. Earlier onset of postural instability (Hoehn–Yahr stage 3) is strongly associated with increased age at disease onset and has a significant impact on quality of life. Conclusions Dementia risk is associated with increased age, impaired baseline semantic fluency and the MAPT H1/H1 genotype. The efficacy of disease modifying therapies may be more meaningfully assessed in terms of their effects in delaying the major milestones of PD, such as postural instability and dementia, since it is these that have the greatest impact on patients.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Jonathan R Evans</name><affiliations><json:string>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</json:string><json:string>E-mail: jonathanevans@doctors.org.uk</json:string></affiliations></json:item><json:item><name>Sarah L Mason</name><affiliations><json:string>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item><json:item><name>Caroline H Williams-Gray</name><affiliations><json:string>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item><json:item><name>Thomas Foltynie</name><affiliations><json:string>Institute of Neurology, University College London, London, UK</json:string></affiliations></json:item><json:item><name>Carol Brayne</name><affiliations><json:string>Institute of Public Health, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item><json:item><name>Trevor W Robbins</name><affiliations><json:string>Department of Experimental Psychology, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item><json:item><name>Roger A Barker</name><affiliations><json:string>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Research paper</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>JNNP Patients' choice</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Background Our understanding of the natural history of idiopathic Parkinson's disease (PD) remains limited. In the era of potential disease modifying therapies, there is an urgent need for studies assessing the natural evolution of treated PD from onset so that relevant outcome measures can be identified for clinical trials. No previous studies have charted progression in unselected patients followed from the point of diagnosis. Methods A representative cohort of 132 PD patients was followed from diagnosis for up to 7.9 years (mean 5.2 years). Comprehensive clinical and neuropsychological evaluations were performed every 18 months. Disease progression was evaluated using well validated clinical measures (motor progression and development of dyskinesia on the Unified PD Rating Scale and Hoehn–Yahr scale, dementia onset according to DSM-IV criteria). Multi-level linear modelling was used to chart the nature and rate of progression in parkinsonian symptoms and signs over time. The prognostic importance of baseline demogr`aphic, clinical and genetic variables was evaluated using survival analysis. Results Axial (gait and postural) symptoms evolve more rapidly than other motor features of PD and appear to be the best index of disease progression. Conversely, conventional outcome measures are relatively insensitive to change over time. Earlier onset of postural instability (Hoehn–Yahr stage 3) is strongly associated with increased age at disease onset and has a significant impact on quality of life. Conclusions Dementia risk is associated with increased age, impaired baseline semantic fluency and the MAPT H1/H1 genotype. The efficacy of disease modifying therapies may be more meaningfully assessed in terms of their effects in delaying the major milestones of PD, such as postural instability and dementia, since it is these that have the greatest impact on patients.</abstract><qualityIndicators><score>8.457</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>2</keywordCount><abstractCharCount>1890</abstractCharCount><pdfWordCount>4957</pdfWordCount><pdfCharCount>33273</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>275</abstractWordCount></qualityIndicators><title>The natural history of treated Parkinson's disease in an incident, community based cohort</title><pmid><json:string>21593513</json:string></pmid><genre><json:string>research-article</json:string></genre><host><volume>82</volume><pages><first>1112</first></pages><issn><json:string>0022-3050</json:string></issn><issue>10</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & Psychiatry</title></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1136/jnnp.2011.240366</json:string></doi><id>6441532380F3047211C43FDBCE1D97A725AEE92F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6441532380F3047211C43FDBCE1D97A725AEE92F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6441532380F3047211C43FDBCE1D97A725AEE92F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6441532380F3047211C43FDBCE1D97A725AEE92F/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">The natural history of treated Parkinson's disease in an incident, community based cohort</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>2011-05-18</date></publicationStmt><notesStmt><note>See Editorial commentary, p 1065</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">The natural history of treated Parkinson's disease in an incident, community based cohort</title><author corresp="yes"><persName><forename type="first">Jonathan R</forename><surname>Evans</surname></persName><email>jonathanevans@doctors.org.uk</email><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation></author><author><persName><forename type="first">Sarah L</forename><surname>Mason</surname></persName><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation></author><author><persName><forename type="first">Caroline H</forename><surname>Williams-Gray</surname></persName><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation></author><author><persName><forename type="first">Thomas</forename><surname>Foltynie</surname></persName><affiliation>Institute of Neurology, University College London, London, UK</affiliation></author><author><persName><forename type="first">Carol</forename><surname>Brayne</surname></persName><affiliation>Institute of Public Health, University of Cambridge, Cambridge, UK</affiliation></author><author><persName><forename type="first">Trevor W</forename><surname>Robbins</surname></persName><affiliation>Department of Experimental Psychology, University of Cambridge, Cambridge, UK</affiliation></author><author><persName><forename type="first">Roger A</forename><surname>Barker</surname></persName><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2011-10"></date><biblScope unit="volume">82</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1112">1112</biblScope></imprint></monogr><idno type="istex">6441532380F3047211C43FDBCE1D97A725AEE92F</idno><idno type="DOI">10.1136/jnnp.2011.240366</idno><idno type="href">jnnp-82-1112.pdf</idno><idno type="ArticleID">jnnp240366</idno><idno type="PMID">21593513</idno><idno type="Related-article-Href">10.1136/jnnp.2011.246835</idno><idno type="related-article-ID">RA1</idno><idno type="local">jnnp;82/10/1112</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011-05-18</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background Our understanding of the natural history of idiopathic Parkinson's disease (PD) remains limited. In the era of potential disease modifying therapies, there is an urgent need for studies assessing the natural evolution of treated PD from onset so that relevant outcome measures can be identified for clinical trials. No previous studies have charted progression in unselected patients followed from the point of diagnosis. Methods A representative cohort of 132 PD patients was followed from diagnosis for up to 7.9 years (mean 5.2 years). Comprehensive clinical and neuropsychological evaluations were performed every 18 months. Disease progression was evaluated using well validated clinical measures (motor progression and development of dyskinesia on the Unified PD Rating Scale and Hoehn–Yahr scale, dementia onset according to DSM-IV criteria). Multi-level linear modelling was used to chart the nature and rate of progression in parkinsonian symptoms and signs over time. The prognostic importance of baseline demogr`aphic, clinical and genetic variables was evaluated using survival analysis. Results Axial (gait and postural) symptoms evolve more rapidly than other motor features of PD and appear to be the best index of disease progression. Conversely, conventional outcome measures are relatively insensitive to change over time. Earlier onset of postural instability (Hoehn–Yahr stage 3) is strongly associated with increased age at disease onset and has a significant impact on quality of life. Conclusions Dementia risk is associated with increased age, impaired baseline semantic fluency and the MAPT H1/H1 genotype. The efficacy of disease modifying therapies may be more meaningfully assessed in terms of their effects in delaying the major milestones of PD, such as postural instability and dementia, since it is these that have the greatest impact on patients.</p></abstract><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>JNNP Patients' choice</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-05-18">Created</change><change when="2011-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6441532380F3047211C43FDBCE1D97A725AEE92F/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-id journal-id-type="publisher-id">jnnp</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><abbrev-journal-title>J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">jnnp240366</article-id><article-id pub-id-type="doi">10.1136/jnnp.2011.240366</article-id><article-id pub-id-type="other">jnnp;82/10/1112</article-id><article-id pub-id-type="other">jnnp;jnnp.2011.240366</article-id><article-id pub-id-type="pmid">21593513</article-id><article-id pub-id-type="other">1112</article-id><article-id pub-id-type="other">jnnp.2011.240366</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research paper</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>JNNP Patients' choice</subject></subj-group></article-categories><title-group><article-title>The natural history of treated Parkinson's disease in an incident, community based cohort</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Evans</surname><given-names>Jonathan R</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Mason</surname><given-names>Sarah L</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Williams-Gray</surname><given-names>Caroline H</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Foltynie</surname><given-names>Thomas</given-names></name><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Brayne</surname><given-names>Carol</given-names></name><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Robbins</surname><given-names>Trevor W</given-names></name><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Barker</surname><given-names>Roger A</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib></contrib-group><aff id="aff1"><label>1</label>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</aff><aff id="aff2"><label>2</label>Institute of Neurology, University College London, London, UK</aff><aff id="aff3"><label>3</label>Institute of Public Health, University of Cambridge, Cambridge, UK</aff><aff id="aff4"><label>4</label>Department of Experimental Psychology, University of Cambridge, Cambridge, UK</aff><author-notes><corresp><label>Correspondence to</label> Dr J R Evans, Cambridge Centre for Brain Repair, University of Cambridge, Forvie Site, Robinson Way, Cambridge CB2 0SD, UK; <email>jonathanevans@doctors.org.uk</email></corresp><fn fn-type="other"><p><bold>See Editorial commentary, p <related-article id="RA1" related-article-type="commentary" ext-link-type="doi" xlink:href="10.1136/jnnp.2011.246835">1065</related-article></bold></p></fn></author-notes><pub-date pub-type="epub-original"><day>18</day><month>5</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>10</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>18</day><month>5</month><year>2011</year></pub-date><volume>82</volume><volume-id pub-id-type="other">82</volume-id><volume-id pub-id-type="other">82</volume-id><issue>10</issue><issue-id pub-id-type="other">jnnp;82/10</issue-id><issue-id pub-id-type="other">10</issue-id><issue-id pub-id-type="other">82/10</issue-id><fpage>1112</fpage><history><date date-type="received"><day>4</day><month>1</month><year>2011</year></date><date date-type="rev-recd"><day>9</day><month>3</month><year>2011</year></date><date date-type="accepted"><day>4</day><month>4</month><year>2011</year></date></history><permissions><copyright-statement>© 2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</copyright-statement><copyright-year>2011</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-82-1112.pdf"></self-uri><abstract><sec><title>Background</title><p>Our understanding of the natural history of idiopathic Parkinson's disease (PD) remains limited. In the era of potential disease modifying therapies, there is an urgent need for studies assessing the natural evolution of treated PD from onset so that relevant outcome measures can be identified for clinical trials. No previous studies have charted progression in unselected patients followed from the point of diagnosis.</p></sec><sec><title>Methods</title><p>A representative cohort of 132 PD patients was followed from diagnosis for up to 7.9 years (mean 5.2 years). Comprehensive clinical and neuropsychological evaluations were performed every 18 months. Disease progression was evaluated using well validated clinical measures (motor progression and development of dyskinesia on the Unified PD Rating Scale and Hoehn–Yahr scale, dementia onset according to DSM-IV criteria). Multi-level linear modelling was used to chart the nature and rate of progression in parkinsonian symptoms and signs over time. The prognostic importance of baseline demogr`aphic, clinical and genetic variables was evaluated using survival analysis.</p></sec><sec><title>Results</title><p>Axial (gait and postural) symptoms evolve more rapidly than other motor features of PD and appear to be the best index of disease progression. Conversely, conventional outcome measures are relatively insensitive to change over time. Earlier onset of postural instability (Hoehn–Yahr stage 3) is strongly associated with increased age at disease onset and has a significant impact on quality of life.</p></sec><sec><title>Conclusions</title><p>Dementia risk is associated with increased age, impaired baseline semantic fluency and the MAPT H1/H1 genotype. The efficacy of disease modifying therapies may be more meaningfully assessed in terms of their effects in delaying the major milestones of PD, such as postural instability and dementia, since it is these that have the greatest impact on patients.</p></sec></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>The natural history of treated Parkinson's disease in an incident, community based cohort</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>The natural history of treated Parkinson's disease in an incident, community based cohort</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Jonathan R</namePart><namePart type="family">Evans</namePart><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation><affiliation>E-mail: jonathanevans@doctors.org.uk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sarah L</namePart><namePart type="family">Mason</namePart><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Caroline H</namePart><namePart type="family">Williams-Gray</namePart><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Foltynie</namePart><affiliation>Institute of Neurology, University College London, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carol</namePart><namePart type="family">Brayne</namePart><affiliation>Institute of Public Health, University of Cambridge, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Trevor W</namePart><namePart type="family">Robbins</namePart><affiliation>Department of Experimental Psychology, University of Cambridge, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roger A</namePart><namePart type="family">Barker</namePart><affiliation>Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><genre>hwp-journal-coll</genre><topic>JNNP Patients' choice</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2011-10</dateIssued><dateCreated encoding="w3cdtf">2011-05-18</dateCreated><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Background Our understanding of the natural history of idiopathic Parkinson's disease (PD) remains limited. In the era of potential disease modifying therapies, there is an urgent need for studies assessing the natural evolution of treated PD from onset so that relevant outcome measures can be identified for clinical trials. No previous studies have charted progression in unselected patients followed from the point of diagnosis. Methods A representative cohort of 132 PD patients was followed from diagnosis for up to 7.9 years (mean 5.2 years). Comprehensive clinical and neuropsychological evaluations were performed every 18 months. Disease progression was evaluated using well validated clinical measures (motor progression and development of dyskinesia on the Unified PD Rating Scale and Hoehn–Yahr scale, dementia onset according to DSM-IV criteria). Multi-level linear modelling was used to chart the nature and rate of progression in parkinsonian symptoms and signs over time. The prognostic importance of baseline demogr`aphic, clinical and genetic variables was evaluated using survival analysis. Results Axial (gait and postural) symptoms evolve more rapidly than other motor features of PD and appear to be the best index of disease progression. Conversely, conventional outcome measures are relatively insensitive to change over time. Earlier onset of postural instability (Hoehn–Yahr stage 3) is strongly associated with increased age at disease onset and has a significant impact on quality of life. Conclusions Dementia risk is associated with increased age, impaired baseline semantic fluency and the MAPT H1/H1 genotype. The efficacy of disease modifying therapies may be more meaningfully assessed in terms of their effects in delaying the major milestones of PD, such as postural instability and dementia, since it is these that have the greatest impact on patients.</abstract><note type="footnotes">See Editorial commentary, p 1065</note><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>82</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1112</start></extent></part></relatedItem><identifier type="istex">6441532380F3047211C43FDBCE1D97A725AEE92F</identifier><identifier type="DOI">10.1136/jnnp.2011.240366</identifier><identifier type="href">jnnp-82-1112.pdf</identifier><identifier type="ArticleID">jnnp240366</identifier><identifier type="PMID">21593513</identifier><identifier type="Related-article-Href">10.1136/jnnp.2011.246835</identifier><identifier type="related-article-ID">RA1</identifier><identifier type="local">jnnp;82/10/1112</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/6441532380F3047211C43FDBCE1D97A725AEE92F/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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