Epidemiology of Parkinson's disease—An overview
Identifieur interne : 000075 ( Main/Corpus ); précédent : 000074; suivant : 000076Epidemiology of Parkinson's disease—An overview
Auteurs : J. Marttila ; K. RinneSource :
- Journal of Neural Transmission [ 0300-9564 ] ; 1981-03-01.
Abstract
Summary: Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful. Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.
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DOI: 10.1007/BF01664011
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Rinne</name><affiliation><mods:affiliation>Department of Neurology, University of Turku, Turku, Finland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:CD82B2DC4F254BE37158AF4ABBF19364FCA5E906</idno><date when="1981" year="1981">1981</date><idno type="doi">10.1007/BF01664011</idno><idno type="url">https://api.istex.fr/document/CD82B2DC4F254BE37158AF4ABBF19364FCA5E906/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000075</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Epidemiology of Parkinson's disease—An overview</title><author><name sortKey="Marttila, J" sort="Marttila, J" uniqKey="Marttila J" first="J." last="Marttila">J. Marttila</name><affiliation><mods:affiliation>Department of Neurology, University of Turku, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Rinne, K" sort="Rinne, K" uniqKey="Rinne K" first="K." last="Rinne">K. Rinne</name><affiliation><mods:affiliation>Department of Neurology, University of Turku, Turku, Finland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission</title><title level="j" type="sub">Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</title><title level="j" type="abbrev">J. Neural Transmission</title><idno type="ISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1981-03-01">1981-03-01</date><biblScope unit="volume">51</biblScope><biblScope unit="issue">1-2</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="148">148</biblScope></imprint><idno type="ISSN">0300-9564</idno></series><idno type="istex">CD82B2DC4F254BE37158AF4ABBF19364FCA5E906</idno><idno type="DOI">10.1007/BF01664011</idno><idno type="ArticleID">Art10</idno><idno type="ArticleID">BF01664011</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-9564</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful. Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>R. J. Marttila</name><affiliations><json:string>Department of Neurology, University of Turku, Turku, Finland</json:string></affiliations></json:item><json:item><name>U. K. Rinne</name><affiliations><json:string>Department of Neurology, University of Turku, Turku, Finland</json:string></affiliations></json:item></author><articleId><json:string>Art10</json:string><json:string>BF01664011</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful. Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.</abstract><qualityIndicators><score>6.981</score><pdfVersion>1.3</pdfVersion><pdfPageSize>432 x 648 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>2070</abstractCharCount><pdfWordCount>3981</pdfWordCount><pdfCharCount>26242</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>302</abstractWordCount></qualityIndicators><title>Epidemiology of Parkinson's disease—An overview</title><genre><json:string>research-article</json:string></genre><host><volume>51</volume><pages><last>148</last><first>135</first></pages><issn><json:string>0300-9564</json:string></issn><issue>1-2</issue><subject><json:item><value>Pharmacology/Toxicology</value></json:item><json:item><value>Neurology</value></json:item><json:item><value>Psychiatry</value></json:item></subject><journalId><json:string>702</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1435-1463</json:string></eissn><title>Journal of Neural Transmission</title><publicationDate>1981</publicationDate><copyrightDate>1981</copyrightDate></host><publicationDate>1981</publicationDate><copyrightDate>1981</copyrightDate><doi><json:string>10.1007/BF01664011</json:string></doi><id>CD82B2DC4F254BE37158AF4ABBF19364FCA5E906</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/CD82B2DC4F254BE37158AF4ABBF19364FCA5E906/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/CD82B2DC4F254BE37158AF4ABBF19364FCA5E906/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/CD82B2DC4F254BE37158AF4ABBF19364FCA5E906/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Epidemiology of Parkinson's disease—An overview</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><availability><p>SPRINGER</p></availability><date>1980-12-29</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Epidemiology of Parkinson's disease—An overview</title><author><persName><forename type="first">R.</forename><surname>Marttila</surname></persName><affiliation>Department of Neurology, University of Turku, Turku, Finland</affiliation></author><author><persName><forename type="first">U.</forename><surname>Rinne</surname></persName><affiliation>Department of Neurology, University of Turku, Turku, Finland</affiliation></author></analytic><monogr><title level="j">Journal of Neural Transmission</title><title level="j" type="sub">Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</title><title level="j" type="abbrev">J. Neural Transmission</title><idno type="JournalID">702</idno><idno type="pISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><idno type="IssueArticleCount">13</idno><idno type="VolumeIssueCount">4</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1981-03-01"></date><biblScope unit="volume">51</biblScope><biblScope unit="issue">1-2</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="148">148</biblScope></imprint></monogr><idno type="istex">CD82B2DC4F254BE37158AF4ABBF19364FCA5E906</idno><idno type="DOI">10.1007/BF01664011</idno><idno type="ArticleID">Art10</idno><idno type="ArticleID">BF01664011</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1980-12-29</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful. Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Neurology</term></item><item><term>Psychiatry</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1980-12-29">Created</change><change when="1981-03-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-1">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/CD82B2DC4F254BE37158AF4ABBF19364FCA5E906/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Vienna</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>702</JournalID><JournalPrintISSN>0300-9564</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission</JournalTitle><JournalSubTitle>Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</JournalSubTitle><JournalAbbreviatedTitle>J. Neural Transmission</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject><JournalSubject Type="Secondary">Psychiatry</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>51</VolumeIDStart><VolumeIDEnd>51</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Combined"><IssueInfo TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>2</IssueIDEnd><IssueArticleCount>13</IssueArticleCount><IssueHistory><CoverDate><DateString>1981</DateString><Year>1981</Year><Month>3</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1981</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art10"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01664011</ArticleID><ArticleDOI>10.1007/BF01664011</ArticleDOI><ArticleSequenceNumber>10</ArticleSequenceNumber><ArticleTitle Language="En">Epidemiology of Parkinson's disease—An overview</ArticleTitle><ArticleFirstPage>135</ArticleFirstPage><ArticleLastPage>148</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>4</Month><Day>25</Day></RegistrationDate><Received><Year>1980</Year><Month>12</Month><Day>29</Day></Received></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1981</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>702</JournalID><VolumeIDStart>51</VolumeIDStart><VolumeIDEnd>51</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>2</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>R.</GivenName><GivenName>J.</GivenName><FamilyName>Marttila</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>U.</GivenName><GivenName>K.</GivenName><FamilyName>Rinne</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Department of Neurology</OrgDivision><OrgName>University of Turku</OrgName><OrgAddress><City>Turku</City><Country>Finland</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future.</Para><Para>Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing.</Para><Para>Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful.</Para><Para>Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.</Para></Abstract></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Epidemiology of Parkinson's disease—An overview</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Epidemiology of Parkinson's disease—An overview</title></titleInfo><name type="personal"><namePart type="given">R.</namePart><namePart type="given">J.</namePart><namePart type="family">Marttila</namePart><affiliation>Department of Neurology, University of Turku, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U.</namePart><namePart type="given">K.</namePart><namePart type="family">Rinne</namePart><affiliation>Department of Neurology, University of Turku, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1980-12-29</dateCreated><dateIssued encoding="w3cdtf">1981-03-01</dateIssued><copyrightDate encoding="w3cdtf">1981</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful. 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