Advances in markers of prodromal Parkinson disease.
Identifieur interne : 000133 ( PubMed/Corpus ); précédent : 000132; suivant : 000134Advances in markers of prodromal Parkinson disease.
Auteurs : Ronald B. Postuma ; Daniela BergSource :
- Nature reviews. Neurology [ 1759-4766 ] ; 2016.
Abstract
Efforts to develop neuroprotective therapy for Parkinson disease (PD) are focusing on the early stages of disease, which offer the best opportunity to intervene. Early PD can be divided into preclinical, prodromal and clinical stages; in this Review, we focus on the prodromal stage and markers that can be used to identify prodromal PD. We consider the necessary properties of a marker, before providing an overview of the proven and potential markers of prodromal PD, including clinical nonmotor markers, clinical motor markers, neuroimaging markers and tissue biomarkers. Markers for which the ability to predict conversion to PD is supported by the strongest evidence include olfactory loss, REM sleep behaviour disorder and constipation. Markers with the highest diagnostic strength include REM sleep behaviour disorder, dopaminergic imaging and subtle motor parkinsonism. The lead time - the period between the appearance of a marker and conversion to PD - is highly variable between markers, ranging from 5 years for impaired motor performance to >20 years for autonomic symptoms. The cost of screening for these markers also varies dramatically: some require just questionnaires, whereas others require sophisticated scanning techniques. Finally, we summarize how prodromal and risk markers can be combined to estimate the probability that an individual has prodromal PD, with a focus on the International Parkinson Disease and Movement Disorders Society (MDS) Prodromal Parkinson Criteria.
DOI: 10.1038/nrneurol.2016.152
PubMed: 27786242
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pubmed:27786242Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Advances in markers of prodromal Parkinson disease.</title><author><name sortKey="Postuma, Ronald B" sort="Postuma, Ronald B" uniqKey="Postuma R" first="Ronald B" last="Postuma">Ronald B. Postuma</name><affiliation><nlm:affiliation>Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal H3G1A4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation><nlm:affiliation>Department of Neurology, Christian-Albrechts-University of Kiel, Arnold-Heller-Straße 3, 24105 Kiel, Germany.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27786242</idno><idno type="pmid">27786242</idno><idno type="doi">10.1038/nrneurol.2016.152</idno><idno type="wicri:Area/PubMed/Corpus">000133</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000133</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Advances in markers of prodromal Parkinson disease.</title><author><name sortKey="Postuma, Ronald B" sort="Postuma, Ronald B" uniqKey="Postuma R" first="Ronald B" last="Postuma">Ronald B. Postuma</name><affiliation><nlm:affiliation>Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal H3G1A4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation><nlm:affiliation>Department of Neurology, Christian-Albrechts-University of Kiel, Arnold-Heller-Straße 3, 24105 Kiel, Germany.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Nature reviews. Neurology</title><idno type="eISSN">1759-4766</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Efforts to develop neuroprotective therapy for Parkinson disease (PD) are focusing on the early stages of disease, which offer the best opportunity to intervene. Early PD can be divided into preclinical, prodromal and clinical stages; in this Review, we focus on the prodromal stage and markers that can be used to identify prodromal PD. We consider the necessary properties of a marker, before providing an overview of the proven and potential markers of prodromal PD, including clinical nonmotor markers, clinical motor markers, neuroimaging markers and tissue biomarkers. Markers for which the ability to predict conversion to PD is supported by the strongest evidence include olfactory loss, REM sleep behaviour disorder and constipation. Markers with the highest diagnostic strength include REM sleep behaviour disorder, dopaminergic imaging and subtle motor parkinsonism. The lead time - the period between the appearance of a marker and conversion to PD - is highly variable between markers, ranging from 5 years for impaired motor performance to >20 years for autonomic symptoms. The cost of screening for these markers also varies dramatically: some require just questionnaires, whereas others require sophisticated scanning techniques. Finally, we summarize how prodromal and risk markers can be combined to estimate the probability that an individual has prodromal PD, with a focus on the International Parkinson Disease and Movement Disorders Society (MDS) Prodromal Parkinson Criteria.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">27786242</PMID><DateCreated><Year>2016</Year><Month>10</Month><Day>27</Day></DateCreated><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1759-4766</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>11</Issue><PubDate><Year>2016</Year><Month>Oct</Month><Day>27</Day></PubDate></JournalIssue><Title>Nature reviews. Neurology</Title><ISOAbbreviation>Nat Rev Neurol</ISOAbbreviation></Journal><ArticleTitle>Advances in markers of prodromal Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>622-634</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/nrneurol.2016.152</ELocationID><Abstract><AbstractText>Efforts to develop neuroprotective therapy for Parkinson disease (PD) are focusing on the early stages of disease, which offer the best opportunity to intervene. Early PD can be divided into preclinical, prodromal and clinical stages; in this Review, we focus on the prodromal stage and markers that can be used to identify prodromal PD. We consider the necessary properties of a marker, before providing an overview of the proven and potential markers of prodromal PD, including clinical nonmotor markers, clinical motor markers, neuroimaging markers and tissue biomarkers. Markers for which the ability to predict conversion to PD is supported by the strongest evidence include olfactory loss, REM sleep behaviour disorder and constipation. Markers with the highest diagnostic strength include REM sleep behaviour disorder, dopaminergic imaging and subtle motor parkinsonism. The lead time - the period between the appearance of a marker and conversion to PD - is highly variable between markers, ranging from 5 years for impaired motor performance to >20 years for autonomic symptoms. The cost of screening for these markers also varies dramatically: some require just questionnaires, whereas others require sophisticated scanning techniques. Finally, we summarize how prodromal and risk markers can be combined to estimate the probability that an individual has prodromal PD, with a focus on the International Parkinson Disease and Movement Disorders Society (MDS) Prodromal Parkinson Criteria.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Postuma</LastName><ForeName>Ronald B</ForeName><Initials>RB</Initials><AffiliationInfo><Affiliation>Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal H3G1A4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Berg</LastName><ForeName>Daniela</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Neurology, Christian-Albrechts-University of Kiel, Arnold-Heller-Straße 3, 24105 Kiel, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of neurodegeneration, Hertie Institute of Clinical Brain Research, Hoppe, Seyler-Straße 3, 72076 Tübingen, 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Version="1">26329429</PMID></CommentsCorrections></CommentsCorrectionsList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27786242</ArticleId><ArticleId IdType="pii">nrneurol.2016.152</ArticleId><ArticleId IdType="doi">10.1038/nrneurol.2016.152</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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