Cardiac sympathetic denervation correlates with clinical and pathologic stages of Parkinson's disease
Identifieur interne : 000828 ( Main/Corpus ); précédent : 000827; suivant : 000829Cardiac sympathetic denervation correlates with clinical and pathologic stages of Parkinson's disease
Auteurs : Hiroshige Fujishiro ; Roberta Frigerio ; Melinda Burnett ; Kevin J. Klos ; Keith A. Josephs ; Anthony Delledonne ; Joseph E. Parisi ; J. Eric Ahlskog ; Dennis W. DicksonSource :
- Movement Disorders [ 0885-3185 ] ; 2008-06-15.
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- KwdEn :
Abstract
Attention has been drawn to cardiac sympathetic denervation in Parkinson's disease (PD) based on clinical studies using [123I] metaiodobenzylguanidine scintigraphy; however, the histologic correlates and time course of cardiac sympathetic denervation are poorly understood. To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD. Cardiac sympathetic innervation was significantly less in PD than in normal controls and cases with iLBs (P < 0.05). There was also a decrease in TH‐immunoreactive fibers in iLB cases compared to normal controls (P < 0.01). TH‐immunoreactive fibers correlated with the PD stage (r = −0.75, P < 0.001), as well as with Hoehn & Yahr clinical stage (r = −0.61, P < 0.001), and disease duration (r = −0.63, P < 0.001). Immunohistochemistry for α‐synuclein showed neurites in epicardium in PD and iLB cases, but not in normal controls. The density of α‐synuclein neurites correlated with Braak PD stage (r = 0.38, P < 0.05), Hoehn & Yahr clinical stage (r = 0.44, P < 0.05), and disease duration (r = 0.42, P < 0.05). This study demonstrates that cardiac sympathetic degeneration and α‐synuclein pathology is present in presymptomatic phase of PD, and that both increase with disease duration and severity. © 2008 Movement Disorder Society.
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DOI: 10.1002/mds.21989
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Klos</name><affiliation><mods:affiliation>Neurological Associates of Tulsa, Tulsa, Oklahoma</mods:affiliation></affiliation></author><author><name sortKey="Josephs, Keith A" sort="Josephs, Keith A" uniqKey="Josephs K" first="Keith A." last="Josephs">Keith A. Josephs</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</mods:affiliation></affiliation></author><author><name sortKey="Delledonne, Anthony" sort="Delledonne, Anthony" uniqKey="Delledonne A" first="Anthony" last="Delledonne">Anthony Delledonne</name><affiliation><mods:affiliation>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</mods:affiliation></affiliation></author><author><name sortKey="Parisi, Joseph E" sort="Parisi, Joseph E" uniqKey="Parisi J" first="Joseph E." last="Parisi">Joseph E. Parisi</name><affiliation><mods:affiliation>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota</mods:affiliation></affiliation></author><author><name sortKey="Ahlskog, J Eric" sort="Ahlskog, J Eric" uniqKey="Ahlskog J" first="J. Eric" last="Ahlskog">J. Eric Ahlskog</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</mods:affiliation></affiliation></author><author><name sortKey="Dickson, Dennis W" sort="Dickson, Dennis W" uniqKey="Dickson D" first="Dennis W." last="Dickson">Dennis W. 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To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD. Cardiac sympathetic innervation was significantly less in PD than in normal controls and cases with iLBs (P < 0.05). There was also a decrease in TH‐immunoreactive fibers in iLB cases compared to normal controls (P < 0.01). TH‐immunoreactive fibers correlated with the PD stage (r = −0.75, P < 0.001), as well as with Hoehn & Yahr clinical stage (r = −0.61, P < 0.001), and disease duration (r = −0.63, P < 0.001). Immunohistochemistry for α‐synuclein showed neurites in epicardium in PD and iLB cases, but not in normal controls. The density of α‐synuclein neurites correlated with Braak PD stage (r = 0.38, P < 0.05), Hoehn & Yahr clinical stage (r = 0.44, P < 0.05), and disease duration (r = 0.42, P < 0.05). This study demonstrates that cardiac sympathetic degeneration and α‐synuclein pathology is present in presymptomatic phase of PD, and that both increase with disease duration and severity. © 2008 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Hiroshige Fujishiro MD, PhD</name><affiliations><json:string>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</json:string><json:string>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</json:string></affiliations></json:item><json:item><name>Roberta Frigerio MD</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Rochester, Minnesota</json:string></affiliations></json:item><json:item><name>Melinda Burnett MD</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Rochester, Minnesota</json:string></affiliations></json:item><json:item><name>Kevin J. Klos MD</name><affiliations><json:string>Neurological Associates of Tulsa, Tulsa, Oklahoma</json:string></affiliations></json:item><json:item><name>Keith A. Josephs MD, MST</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Rochester, Minnesota</json:string></affiliations></json:item><json:item><name>Anthony DelleDonne PhD</name><affiliations><json:string>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</json:string><json:string>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</json:string></affiliations></json:item><json:item><name>Joseph E. Parisi MD</name><affiliations><json:string>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota</json:string></affiliations></json:item><json:item><name>J. Eric Ahlskog MD, PhD</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Rochester, Minnesota</json:string></affiliations></json:item><json:item><name>Dennis W. Dickson MD</name><affiliations><json:string>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</json:string><json:string>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>presymptomatic</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tyrosine hydroxylase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>α‐synuclein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiac</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinsons</value></json:item></subject><articleId><json:string>MDS21989</json:string></articleId><language><json:string>eng</json:string></language><abstract>Attention has been drawn to cardiac sympathetic denervation in Parkinson's disease (PD) based on clinical studies using [123I] metaiodobenzylguanidine scintigraphy; however, the histologic correlates and time course of cardiac sympathetic denervation are poorly understood. To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD. Cardiac sympathetic innervation was significantly less in PD than in normal controls and cases with iLBs (P > 0.05). There was also a decrease in TH‐immunoreactive fibers in iLB cases compared to normal controls (P > 0.01). TH‐immunoreactive fibers correlated with the PD stage (r = −0.75, P > 0.001), as well as with Hoehn & Yahr clinical stage (r = −0.61, P > 0.001), and disease duration (r = −0.63, P > 0.001). Immunohistochemistry for α‐synuclein showed neurites in epicardium in PD and iLB cases, but not in normal controls. The density of α‐synuclein neurites correlated with Braak PD stage (r = 0.38, P > 0.05), Hoehn & Yahr clinical stage (r = 0.44, P > 0.05), and disease duration (r = 0.42, P > 0.05). 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Eric</forename><surname>Ahlskog</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</affiliation></author><author><persName><forename type="first">Dennis W.</forename><surname>Dickson</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Neuropathology Laboratory, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224</p></note><affiliation>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</affiliation><affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD. Cardiac sympathetic innervation was significantly less in PD than in normal controls and cases with iLBs (P < 0.05). There was also a decrease in TH‐immunoreactive fibers in iLB cases compared to normal controls (P < 0.01). TH‐immunoreactive fibers correlated with the PD stage (r = −0.75, P < 0.001), as well as with Hoehn & Yahr clinical stage (r = −0.61, P < 0.001), and disease duration (r = −0.63, P < 0.001). Immunohistochemistry for α‐synuclein showed neurites in epicardium in PD and iLB cases, but not in normal controls. The density of α‐synuclein neurites correlated with Braak PD stage (r = 0.38, P < 0.05), Hoehn & Yahr clinical stage (r = 0.44, P < 0.05), and disease duration (r = 0.42, P < 0.05). This study demonstrates that cardiac sympathetic degeneration and α‐synuclein pathology is present in presymptomatic phase of PD, and that both increase with disease duration and severity. © 2008 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>presymptomatic</term></item><item><term>tyrosine hydroxylase</term></item><item><term>α‐synuclein</term></item><item><term>cardiac</term></item><item><term>Parkinsons</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-07-18">Received</change><change when="2008-01-22">Registration</change><change when="2008-06-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B2D178713218F90FD26FD418975AA3283957D11C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><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)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="80"><doi origin="wiley" registered="yes">10.1002/mds.v23:8</doi><numberingGroup><numbering type="journalVolume" number="23">23</numbering><numbering type="journalIssue">8</numbering></numberingGroup><coverDate startDate="2008-06-15">15 June 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="30" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21989</doi><idGroup><id type="unit" value="MDS21989"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2008 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2007-07-18"></event><event type="manuscriptRevised" date="2007-10-23"></event><event type="manuscriptAccepted" date="2008-01-22"></event><event type="publishedOnlineEarlyUnpaginated" date="2008-04-28"></event><event type="firstOnline" date="2008-04-28"></event><event type="publishedOnlineFinalForm" date="2008-06-24"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1085</numbering><numbering type="pageLast">1092</numbering></numberingGroup><correspondenceTo>Neuropathology Laboratory, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21989.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="32"></count><count type="wordTotal" number="4749"></count></countGroup><titleGroup><title type="main" xml:lang="en">Cardiac sympathetic denervation correlates with clinical and pathologic stages of Parkinson's disease</title><title type="short" xml:lang="en">Cardiac Denervation in Presympomatic PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Hiroshige</givenNames><familyName>Fujishiro</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Roberta</givenNames><familyName>Frigerio</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Melinda</givenNames><familyName>Burnett</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Kevin J.</givenNames><familyName>Klos</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Keith A.</givenNames><familyName>Josephs</familyName><degrees>MD, MST</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Anthony</givenNames><familyName>DelleDonne</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Joseph E.</givenNames><familyName>Parisi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>J. Eric</givenNames><familyName>Ahlskog</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Dennis W.</givenNames><familyName>Dickson</familyName><degrees>MD</degrees></personName><contactDetails><email>dickson.dennis@mayo.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Neurological Associates of Tulsa, Tulsa, Oklahoma</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">presymptomatic</keyword><keyword xml:id="kwd2">tyrosine hydroxylase</keyword><keyword xml:id="kwd3">α‐synuclein</keyword><keyword xml:id="kwd4">cardiac</keyword><keyword xml:id="kwd5">Parkinsons</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Attention has been drawn to cardiac sympathetic denervation in Parkinson's disease (PD) based on clinical studies using [123I] metaiodobenzylguanidine scintigraphy; however, the histologic correlates and time course of cardiac sympathetic denervation are poorly understood. To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD. Cardiac sympathetic innervation was significantly less in PD than in normal controls and cases with iLBs (<i>P</i> < 0.05). There was also a decrease in TH‐immunoreactive fibers in iLB cases compared to normal controls (<i>P</i> < 0.01). TH‐immunoreactive fibers correlated with the PD stage (r = −0.75, <i>P</i> < 0.001), as well as with Hoehn & Yahr clinical stage (r = −0.61, <i>P</i> < 0.001), and disease duration (r = −0.63, <i>P</i> < 0.001). Immunohistochemistry for α‐synuclein showed neurites in epicardium in PD and iLB cases, but not in normal controls. The density of α‐synuclein neurites correlated with Braak PD stage (r = 0.38, <i>P</i> < 0.05), Hoehn & Yahr clinical stage (r = 0.44, <i>P</i> < 0.05), and disease duration (r = 0.42, <i>P</i> < 0.05). This study demonstrates that cardiac sympathetic degeneration and α‐synuclein pathology is present in presymptomatic phase of PD, and that both increase with disease duration and severity. © 2008 Movement Disorder Society.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cardiac sympathetic denervation correlates with clinical and pathologic stages of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Cardiac Denervation in Presympomatic PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cardiac sympathetic denervation correlates with clinical and pathologic stages of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Hiroshige</namePart><namePart type="family">Fujishiro</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</affiliation><affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roberta</namePart><namePart type="family">Frigerio</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Melinda</namePart><namePart type="family">Burnett</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kevin J.</namePart><namePart type="family">Klos</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurological Associates of Tulsa, Tulsa, Oklahoma</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Keith A.</namePart><namePart type="family">Josephs</namePart><namePart type="termsOfAddress">MD, MST</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anthony</namePart><namePart type="family">DelleDonne</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</affiliation><affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph E.</namePart><namePart type="family">Parisi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. Eric</namePart><namePart type="family">Ahlskog</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dennis W.</namePart><namePart type="family">Dickson</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology (Neuropathology), Mayo Clinic, Jacksonville, Florida</affiliation><affiliation>Department of Neuroscience, Mayo Clinic, Jacksonville, Florida</affiliation><description>Correspondence: Neuropathology Laboratory, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-06-15</dateIssued><dateCaptured encoding="w3cdtf">2007-07-18</dateCaptured><dateValid encoding="w3cdtf">2008-01-22</dateValid><copyrightDate encoding="w3cdtf">2008</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">4</extent><extent unit="tables">2</extent><extent unit="references">32</extent><extent unit="words">4749</extent></physicalDescription><abstract lang="en">Attention has been drawn to cardiac sympathetic denervation in Parkinson's disease (PD) based on clinical studies using [123I] metaiodobenzylguanidine scintigraphy; however, the histologic correlates and time course of cardiac sympathetic denervation are poorly understood. To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD. Cardiac sympathetic innervation was significantly less in PD than in normal controls and cases with iLBs (P < 0.05). There was also a decrease in TH‐immunoreactive fibers in iLB cases compared to normal controls (P < 0.01). TH‐immunoreactive fibers correlated with the PD stage (r = −0.75, P < 0.001), as well as with Hoehn & Yahr clinical stage (r = −0.61, P < 0.001), and disease duration (r = −0.63, P < 0.001). Immunohistochemistry for α‐synuclein showed neurites in epicardium in PD and iLB cases, but not in normal controls. The density of α‐synuclein neurites correlated with Braak PD stage (r = 0.38, P < 0.05), Hoehn & Yahr clinical stage (r = 0.44, P < 0.05), and disease duration (r = 0.42, P < 0.05). This study demonstrates that cardiac sympathetic degeneration and α‐synuclein pathology is present in presymptomatic phase of PD, and that both increase with disease duration and severity. © 2008 Movement Disorder Society.</abstract><subject lang="en"><genre>Keywords</genre><topic>presymptomatic</topic><topic>tyrosine hydroxylase</topic><topic>α‐synuclein</topic><topic>cardiac</topic><topic>Parkinsons</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. 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