Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease
Identifieur interne : 001976 ( Main/Corpus ); précédent : 001975; suivant : 001977Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease
Auteurs : Thomas D. H Lbig ; Stephanie Assuras ; Judy Creighton ; Joan C. Borod ; Winona Tse ; Pasquale G. Frisina ; Andrei Voustianiouk ; Jean-Michel Gracies ; C. Warren OlanowSource :
- Movement Disorders [ 0885-3185 ] ; 2011-08-01.
English descriptors
Abstract
Consistent with the hypothesis that dopamine is implicated in the processing of salient stimuli relevant to the modification of various behavioral responses, Parkinson's disease is associated with emotional blunting. To address the hypothesis that emotional attention and memory are modulated by dopaminergic neurotransmission in Parkinson's disease, we assessed 15 nondemented patients with Parkinson's disease while on and off dopaminergic medication and 15 age‐matched healthy controls. Visual stimuli were presented, and recognition was used to assess emotional memory. Response latency was used as a measure of emotional attention modulation. Stimuli were varied based on valence (pleasant, neutral, and unpleasant) and arousal (high and low) dimensions. Controls had significantly better memory for positive than negative stimuli, whereas patients with Parkinson's disease tested off medication had significantly better memory for negative than positive items. This negativity bias was lost when they were tested while on dopaminergic medication. Reaction times in patients with Parkinson's disease off medication were longer than in healthy controls and, paradoxically, were even longer when on medication. Further, although both healthy controls and patients with Parkinson's disease in the “off” state had arousal‐induced prolongation of reaction time, this effect was not seen in patients with Parkinson's disease on medication. These data indicate that dopaminergic neurotransmission is implicated in emotional memory and attention and suggest that dopamine mediates emotional memory via the valence dimension and emotional attention via arousal. Furthermore, our findings suggest that emotional changes in Parkinson's disease result from the effects of both the disease process and dopaminergic treatment. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23728
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H Lbig</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neuropsychiatry, Charité University Medical Center, Berlin, Germany</mods:affiliation></affiliation></author><author><name sortKey="Assuras, Stephanie" sort="Assuras, Stephanie" uniqKey="Assuras S" first="Stephanie" last="Assuras">Stephanie Assuras</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Creighton, Judy" sort="Creighton, Judy" uniqKey="Creighton J" first="Judy" last="Creighton">Judy Creighton</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Borod, Joan C" sort="Borod, Joan C" uniqKey="Borod J" first="Joan C." last="Borod">Joan C. 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To address the hypothesis that emotional attention and memory are modulated by dopaminergic neurotransmission in Parkinson's disease, we assessed 15 nondemented patients with Parkinson's disease while on and off dopaminergic medication and 15 age‐matched healthy controls. Visual stimuli were presented, and recognition was used to assess emotional memory. Response latency was used as a measure of emotional attention modulation. Stimuli were varied based on valence (pleasant, neutral, and unpleasant) and arousal (high and low) dimensions. Controls had significantly better memory for positive than negative stimuli, whereas patients with Parkinson's disease tested off medication had significantly better memory for negative than positive items. This negativity bias was lost when they were tested while on dopaminergic medication. Reaction times in patients with Parkinson's disease off medication were longer than in healthy controls and, paradoxically, were even longer when on medication. Further, although both healthy controls and patients with Parkinson's disease in the “off” state had arousal‐induced prolongation of reaction time, this effect was not seen in patients with Parkinson's disease on medication. These data indicate that dopaminergic neurotransmission is implicated in emotional memory and attention and suggest that dopamine mediates emotional memory via the valence dimension and emotional attention via arousal. Furthermore, our findings suggest that emotional changes in Parkinson's disease result from the effects of both the disease process and dopaminergic treatment. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thomas D. 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Frisina PhD</name><affiliations><json:string>Department of Research & Quality Management, Kessler Institute for Rehabilitation, West Orange, New Jersey, USA, and Department of Geriatrics & Adult Development, Mount Sinai School of Medicine, New York, New York, USA</json:string></affiliations></json:item><json:item><name>Andrei Voustianiouk PhD</name><affiliations><json:string>Dysautonomia Research Laboratory, New York University School of Medicine, New York, New York, USA</json:string></affiliations></json:item><json:item><name>Jean‐Michel Gracies MD, PhD</name><affiliations><json:string>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</json:string></affiliations></json:item><json:item><name>C. Warren Olanow MD</name><affiliations><json:string>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>emotional processing</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>memory</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><articleId><json:string>MDS23728</json:string></articleId><language><json:string>eng</json:string></language><abstract>Consistent with the hypothesis that dopamine is implicated in the processing of salient stimuli relevant to the modification of various behavioral responses, Parkinson's disease is associated with emotional blunting. To address the hypothesis that emotional attention and memory are modulated by dopaminergic neurotransmission in Parkinson's disease, we assessed 15 nondemented patients with Parkinson's disease while on and off dopaminergic medication and 15 age‐matched healthy controls. Visual stimuli were presented, and recognition was used to assess emotional memory. Response latency was used as a measure of emotional attention modulation. Stimuli were varied based on valence (pleasant, neutral, and unpleasant) and arousal (high and low) dimensions. Controls had significantly better memory for positive than negative stimuli, whereas patients with Parkinson's disease tested off medication had significantly better memory for negative than positive items. This negativity bias was lost when they were tested while on dopaminergic medication. Reaction times in patients with Parkinson's disease off medication were longer than in healthy controls and, paradoxically, were even longer when on medication. Further, although both healthy controls and patients with Parkinson's disease in the “off” state had arousal‐induced prolongation of reaction time, this effect was not seen in patients with Parkinson's disease on medication. These data indicate that dopaminergic neurotransmission is implicated in emotional memory and attention and suggest that dopamine mediates emotional memory via the valence dimension and emotional attention via arousal. Furthermore, our findings suggest that emotional changes in Parkinson's disease result from the effects of both the disease process and dopaminergic treatment. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.389</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1850</abstractCharCount><pdfWordCount>4389</pdfWordCount><pdfCharCount>28176</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>255</abstractWordCount></qualityIndicators><title>Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>7</total><last>1683</last><first>1677</first></pages><issn><json:string>0885-3185</json:string></issn><issue>9</issue><subject><json:item><value>Research 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type="main" xml:lang="en">Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease</title><author><persName><forename type="first">Thomas D.</forename><surname>Hälbig</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Charité University Medical Center, Department of Neuropsychiatry, Campus Charité Mitte, S152B, Charitéplatz 1, D‐10117 Berlin, Germany</p></note><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><affiliation>Department of Neuropsychiatry, Charité University Medical Center, Berlin, Germany</affiliation></author><author><persName><forename type="first">Stephanie</forename><surname>Assuras</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">Judy</forename><surname>Creighton</surname></persName><roleName type="degree">MA</roleName><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">Joan C.</forename><surname>Borod</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><affiliation>Department of Psychology, Queens College and the Graduate Center, City University of New York, Flushing, New York, USA</affiliation></author><author><persName><forename type="first">Winona</forename><surname>Tse</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">Pasquale G.</forename><surname>Frisina</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Research & Quality Management, Kessler Institute for Rehabilitation, West Orange, New Jersey, USA, and Department of Geriatrics & Adult Development, Mount Sinai School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">Andrei</forename><surname>Voustianiouk</surname></persName><roleName type="degree">PhD</roleName><affiliation>Dysautonomia Research Laboratory, New York University School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">Jean‐Michel</forename><surname>Gracies</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">C. Warren</forename><surname>Olanow</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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To address the hypothesis that emotional attention and memory are modulated by dopaminergic neurotransmission in Parkinson's disease, we assessed 15 nondemented patients with Parkinson's disease while on and off dopaminergic medication and 15 age‐matched healthy controls. Visual stimuli were presented, and recognition was used to assess emotional memory. Response latency was used as a measure of emotional attention modulation. Stimuli were varied based on valence (pleasant, neutral, and unpleasant) and arousal (high and low) dimensions. Controls had significantly better memory for positive than negative stimuli, whereas patients with Parkinson's disease tested off medication had significantly better memory for negative than positive items. This negativity bias was lost when they were tested while on dopaminergic medication. Reaction times in patients with Parkinson's disease off medication were longer than in healthy controls and, paradoxically, were even longer when on medication. Further, although both healthy controls and patients with Parkinson's disease in the “off” state had arousal‐induced prolongation of reaction time, this effect was not seen in patients with Parkinson's disease on medication. These data indicate that dopaminergic neurotransmission is implicated in emotional memory and attention and suggest that dopamine mediates emotional memory via the valence dimension and emotional attention via arousal. Furthermore, our findings suggest that emotional changes in Parkinson's disease result from the effects of both the disease process and dopaminergic treatment. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>emotional processing</term></item><item><term>dopamine</term></item><item><term>memory</term></item><item><term>basal ganglia</term></item><item><term>Parkinson's disease</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="2010-08-09">Received</change><change when="2011-03-01">Registration</change><change when="2011-08-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D2EB33A8887241AF7D05FA967F9B95043B7BBF40/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="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi origin="wiley" registered="yes">10.1002/mds.v26.9</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2011-08-01">1 August 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="160" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23728</doi><idGroup><id type="unit" value="MDS23728"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-08-09"></event><event type="manuscriptRevised" date="2011-01-06"></event><event type="manuscriptAccepted" date="2011-03-01"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2011-12-16"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-06-02"></event><event type="publishedOnlineFinalForm" date="2011-08-09"></event><event type="firstOnline" date="2011-06-02"></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">1677</numbering><numbering type="pageLast">1683</numbering></numberingGroup><correspondenceTo>Charité University Medical Center, Department of Neuropsychiatry, Campus Charité Mitte, S152B, Charitéplatz 1, D‐10117 Berlin, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23728.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="41"></count><count type="wordTotal" number="5605"></count></countGroup><titleGroup><title type="main" xml:lang="en">Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease<link href="#fn4"></link><link href="#fn5"></link><link href="#fn6"></link></title><title type="short" xml:lang="en">Dopamine and Emotional Processing</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Thomas D.</givenNames><familyName>Hälbig</familyName><degrees>MD</degrees></personName><contactDetails><email>thomas.haelbig@charite.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Stephanie</givenNames><familyName>Assuras</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Judy</givenNames><familyName>Creighton</familyName><degrees>MA</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Joan C.</givenNames><familyName>Borod</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Winona</givenNames><familyName>Tse</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Pasquale G.</givenNames><familyName>Frisina</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Andrei</givenNames><familyName>Voustianiouk</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jean‐Michel</givenNames><familyName>Gracies</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C. Warren</givenNames><familyName>Olanow</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neuropsychiatry, Charité University Medical Center, Berlin, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Psychology, Queens College and the Graduate Center, City University of New York, Flushing, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Research & Quality Management, Kessler Institute for Rehabilitation, West Orange, New Jersey, USA, and Department of Geriatrics & Adult Development, Mount Sinai School of Medicine, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Dysautonomia Research Laboratory, New York University School of Medicine, New York, New York, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">emotional processing</keyword><keyword xml:id="kwd2">dopamine</keyword><keyword xml:id="kwd3">memory</keyword><keyword xml:id="kwd4">basal ganglia</keyword><keyword xml:id="kwd5">Parkinson's disease</keyword></keywordGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23728:MDS_23728_sm_suppinfoappendixA"></mediaResource><caption>Supporting Information</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23728:MDS_23728_sm_suppinfoappendixB"></mediaResource><caption>Supporting Information</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Consistent with the hypothesis that dopamine is implicated in the processing of salient stimuli relevant to the modification of various behavioral responses, Parkinson's disease is associated with emotional blunting. To address the hypothesis that emotional attention and memory are modulated by dopaminergic neurotransmission in Parkinson's disease, we assessed 15 nondemented patients with Parkinson's disease while on and off dopaminergic medication and 15 age‐matched healthy controls. Visual stimuli were presented, and recognition was used to assess emotional memory. Response latency was used as a measure of emotional attention modulation. Stimuli were varied based on valence (pleasant, neutral, and unpleasant) and arousal (high and low) dimensions. Controls had significantly better memory for positive than negative stimuli, whereas patients with Parkinson's disease tested off medication had significantly better memory for negative than positive items. This negativity bias was lost when they were tested while on dopaminergic medication. Reaction times in patients with Parkinson's disease off medication were longer than in healthy controls and, paradoxically, were even longer when on medication. Further, although both healthy controls and patients with Parkinson's disease in the “off” state had arousal‐induced prolongation of reaction time, this effect was not seen in patients with Parkinson's disease on medication. These data indicate that dopaminergic neurotransmission is implicated in emotional memory and attention and suggest that dopamine mediates emotional memory via the valence dimension and emotional attention via arousal. Furthermore, our findings suggest that emotional changes in Parkinson's disease result from the effects of both the disease process and dopaminergic treatment. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn4"><p><b>Funding agencies:</b> This work was supported by a fellowship award (to T.D.H.) from the Bachmann‐Strauss Dystonia & Parkinson Foundation, New York, NY.</p></note><note xml:id="fn5"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn6"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopamine and Emotional Processing</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Differential role of dopamine in emotional attention and memory: Evidence from Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Thomas D.</namePart><namePart type="family">Hälbig</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><affiliation>Department of Neuropsychiatry, Charité University Medical Center, Berlin, Germany</affiliation><description>Correspondence: Charité University Medical Center, Department of Neuropsychiatry, Campus Charité Mitte, S152B, Charitéplatz 1, D‐10117 Berlin, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephanie</namePart><namePart type="family">Assuras</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Judy</namePart><namePart type="family">Creighton</namePart><namePart type="termsOfAddress">MA</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joan C.</namePart><namePart type="family">Borod</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><affiliation>Department of Psychology, Queens College and the Graduate Center, City University of New York, Flushing, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Winona</namePart><namePart type="family">Tse</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pasquale G.</namePart><namePart type="family">Frisina</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Research & Quality Management, Kessler Institute for Rehabilitation, West Orange, New Jersey, USA, and Department of Geriatrics & Adult Development, Mount Sinai School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrei</namePart><namePart type="family">Voustianiouk</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Dysautonomia Research Laboratory, New York University School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Michel</namePart><namePart type="family">Gracies</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. Warren</namePart><namePart type="family">Olanow</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA</affiliation><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">2011-08-01</dateIssued><dateCaptured encoding="w3cdtf">2010-08-09</dateCaptured><dateValid encoding="w3cdtf">2011-03-01</dateValid><copyrightDate encoding="w3cdtf">2011</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">3</extent><extent unit="tables">1</extent><extent unit="references">41</extent><extent unit="words">5605</extent></physicalDescription><abstract lang="en">Consistent with the hypothesis that dopamine is implicated in the processing of salient stimuli relevant to the modification of various behavioral responses, Parkinson's disease is associated with emotional blunting. To address the hypothesis that emotional attention and memory are modulated by dopaminergic neurotransmission in Parkinson's disease, we assessed 15 nondemented patients with Parkinson's disease while on and off dopaminergic medication and 15 age‐matched healthy controls. Visual stimuli were presented, and recognition was used to assess emotional memory. Response latency was used as a measure of emotional attention modulation. Stimuli were varied based on valence (pleasant, neutral, and unpleasant) and arousal (high and low) dimensions. Controls had significantly better memory for positive than negative stimuli, whereas patients with Parkinson's disease tested off medication had significantly better memory for negative than positive items. This negativity bias was lost when they were tested while on dopaminergic medication. Reaction times in patients with Parkinson's disease off medication were longer than in healthy controls and, paradoxically, were even longer when on medication. Further, although both healthy controls and patients with Parkinson's disease in the “off” state had arousal‐induced prolongation of reaction time, this effect was not seen in patients with Parkinson's disease on medication. These data indicate that dopaminergic neurotransmission is implicated in emotional memory and attention and suggest that dopamine mediates emotional memory via the valence dimension and emotional attention via arousal. Furthermore, our findings suggest that emotional changes in Parkinson's disease result from the effects of both the disease process and dopaminergic treatment. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: This work was supported by a fellowship award (to T.D.H.) from the Bachmann‐Strauss Dystonia & Parkinson Foundation, New York, NY.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>emotional processing</topic><topic>dopamine</topic><topic>memory</topic><topic>basal ganglia</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information - Supporting Information - </note><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1677</start><end>1683</end><total>7</total></extent></part></relatedItem><identifier type="istex">D2EB33A8887241AF7D05FA967F9B95043B7BBF40</identifier><identifier type="DOI">10.1002/mds.23728</identifier><identifier type="ArticleID">MDS23728</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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