Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction
Identifieur interne : 000162 ( Main/Corpus ); précédent : 000161; suivant : 000163Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction
Auteurs : Nicola Pavese ; Vinod Metta ; Subrata K. Bose ; Kallol Ray Chaudhuri ; David J. BrooksSource :
- Brain [ 0006-8950 ] ; 2010-11.
Abstract
Disabling fatigue is a symptom in a number of neurological diseases, including multiple sclerosis, stroke and Parkinsons disease. We used 18F-dopa and 11C-DASB [N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine] positron emission tomography, markers of dopamine storage capacity and serotonin transporter availability, to investigate whether fatigue in Parkinsons disease is associated with dopaminergic and serotonergic dysfunction in basal ganglia and limbic circuits. Ten patients with Parkinsons disease and fatigue and 10 patients without fatigue had a 18F-dopa scan. Seven patients with and eight patients without fatigue also had a 11C-DASB scan. The two groups were matched for age, disease duration and severity and daily intake of levodopa equivalent units. None had a history of depression or sleep disturbance. Using a region of interest analytical approach, we found that patients with fatigue had significantly lower serotonin transporter binding than patients without fatigue in the caudate, putamen, ventral striatum and thalamus. Striatal 18F-dopa uptake was similar in the fatigued and non-fatigued groups. Voxel-based analysis localized further relative serotonin transporter binding reductions in the cingulate and amygdala of the fatigue group, and 18F-dopa uptake reductions in the caudate and insula. We conclude that fatigue in Parkinsons disease is associated with reduced serotonergic function in the basal ganglia and limbic structures. Insular dopaminergic dysfunction could also play a role. These findings imply that strategies to increase brain level of serotonin would be a rational approach for relieving fatigue symptoms in Parkinsons disease and may also be relevant to alleviating fatigue in other clinical conditions.
Url:
DOI: 10.1093/brain/awq268
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction</title><author><name sortKey="Pavese, Nicola" sort="Pavese, Nicola" uniqKey="Pavese N" first="Nicola" last="Pavese">Nicola Pavese</name><affiliation><mods:affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: nicola.pavese@csc.mrc.ac.uk</mods:affiliation></affiliation></author><author><name sortKey="Metta, Vinod" sort="Metta, Vinod" uniqKey="Metta V" first="Vinod" last="Metta">Vinod Metta</name><affiliation><mods:affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Bose, Subrata K" sort="Bose, Subrata K" uniqKey="Bose S" first="Subrata K." last="Bose">Subrata K. Bose</name><affiliation><mods:affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Chaudhuri, Kallol Ray" sort="Chaudhuri, Kallol Ray" uniqKey="Chaudhuri K" first="Kallol Ray" last="Chaudhuri">Kallol Ray Chaudhuri</name><affiliation><mods:affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. 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Bose</name><affiliation><mods:affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Chaudhuri, Kallol Ray" sort="Chaudhuri, Kallol Ray" uniqKey="Chaudhuri K" first="Kallol Ray" last="Chaudhuri">Kallol Ray Chaudhuri</name><affiliation><mods:affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><affiliation><mods:affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-11">2010-11</date><biblScope unit="volume">133</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="3434">3434</biblScope><biblScope unit="page" to="3443">3443</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">FA6512DC0058557D3A0C53467D160AAB9AB6DAE5</idno><idno type="DOI">10.1093/brain/awq268</idno><idno type="ArticleID">awq268</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Disabling fatigue is a symptom in a number of neurological diseases, including multiple sclerosis, stroke and Parkinsons disease. We used 18F-dopa and 11C-DASB [N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine] positron emission tomography, markers of dopamine storage capacity and serotonin transporter availability, to investigate whether fatigue in Parkinsons disease is associated with dopaminergic and serotonergic dysfunction in basal ganglia and limbic circuits. Ten patients with Parkinsons disease and fatigue and 10 patients without fatigue had a 18F-dopa scan. Seven patients with and eight patients without fatigue also had a 11C-DASB scan. The two groups were matched for age, disease duration and severity and daily intake of levodopa equivalent units. None had a history of depression or sleep disturbance. Using a region of interest analytical approach, we found that patients with fatigue had significantly lower serotonin transporter binding than patients without fatigue in the caudate, putamen, ventral striatum and thalamus. Striatal 18F-dopa uptake was similar in the fatigued and non-fatigued groups. Voxel-based analysis localized further relative serotonin transporter binding reductions in the cingulate and amygdala of the fatigue group, and 18F-dopa uptake reductions in the caudate and insula. We conclude that fatigue in Parkinsons disease is associated with reduced serotonergic function in the basal ganglia and limbic structures. Insular dopaminergic dysfunction could also play a role. These findings imply that strategies to increase brain level of serotonin would be a rational approach for relieving fatigue symptoms in Parkinsons disease and may also be relevant to alleviating fatigue in other clinical conditions.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Nicola Pavese</name><affiliations><json:string>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</json:string><json:string>E-mail: nicola.pavese@csc.mrc.ac.uk</json:string></affiliations></json:item><json:item><name>Vinod Metta</name><affiliations><json:string>2 Kings College and Lewisham Hospitals, Kings College, London, UK</json:string></affiliations></json:item><json:item><name>Subrata K. Bose</name><affiliations><json:string>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</json:string></affiliations></json:item><json:item><name>Kallol Ray Chaudhuri</name><affiliations><json:string>2 Kings College and Lewisham Hospitals, Kings College, London, UK</json:string></affiliations></json:item><json:item><name>David J. Brooks</name><affiliations><json:string>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Original Articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>fatigue</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>F-dopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DASB</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Disabling fatigue is a symptom in a number of neurological diseases, including multiple sclerosis, stroke and Parkinsons disease. We used 18F-dopa and 11C-DASB [N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine] positron emission tomography, markers of dopamine storage capacity and serotonin transporter availability, to investigate whether fatigue in Parkinsons disease is associated with dopaminergic and serotonergic dysfunction in basal ganglia and limbic circuits. Ten patients with Parkinsons disease and fatigue and 10 patients without fatigue had a 18F-dopa scan. Seven patients with and eight patients without fatigue also had a 11C-DASB scan. The two groups were matched for age, disease duration and severity and daily intake of levodopa equivalent units. None had a history of depression or sleep disturbance. Using a region of interest analytical approach, we found that patients with fatigue had significantly lower serotonin transporter binding than patients without fatigue in the caudate, putamen, ventral striatum and thalamus. Striatal 18F-dopa uptake was similar in the fatigued and non-fatigued groups. Voxel-based analysis localized further relative serotonin transporter binding reductions in the cingulate and amygdala of the fatigue group, and 18F-dopa uptake reductions in the caudate and insula. We conclude that fatigue in Parkinsons disease is associated with reduced serotonergic function in the basal ganglia and limbic structures. Insular dopaminergic dysfunction could also play a role. These findings imply that strategies to increase brain level of serotonin would be a rational approach for relieving fatigue symptoms in Parkinsons disease and may also be relevant to alleviating fatigue in other clinical conditions.</abstract><qualityIndicators><score>8.44</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612.68 x 790.866 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1759</abstractCharCount><pdfWordCount>6200</pdfWordCount><pdfCharCount>40772</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>245</abstractWordCount></qualityIndicators><title>Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction</title><genre><json:string>research-article</json:string></genre><host><volume>133</volume><pages><last>3443</last><first>3434</first></pages><issn><json:string>0006-8950</json:string></issn><issue>11</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2156</json:string></eissn><title>Brain</title></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1093/brain/awq268</json:string></doi><id>FA6512DC0058557D3A0C53467D160AAB9AB6DAE5</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/FA6512DC0058557D3A0C53467D160AAB9AB6DAE5/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/FA6512DC0058557D3A0C53467D160AAB9AB6DAE5/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/FA6512DC0058557D3A0C53467D160AAB9AB6DAE5/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2010-09-30</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction</title><author corresp="yes"><persName><forename type="first">Nicola</forename><surname>Pavese</surname></persName><email>nicola.pavese@csc.mrc.ac.uk</email><affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</affiliation></author><author><persName><forename type="first">Vinod</forename><surname>Metta</surname></persName><affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</affiliation></author><author><persName><forename type="first">Subrata K.</forename><surname>Bose</surname></persName><affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</affiliation></author><author><persName><forename type="first">Kallol Ray</forename><surname>Chaudhuri</surname></persName><affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</affiliation></author><author><persName><forename type="first">David J.</forename><surname>Brooks</surname></persName><affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</affiliation></author></analytic><monogr><title level="j">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-11"></date><biblScope unit="volume">133</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="3434">3434</biblScope><biblScope unit="page" to="3443">3443</biblScope></imprint></monogr><idno type="istex">FA6512DC0058557D3A0C53467D160AAB9AB6DAE5</idno><idno type="DOI">10.1093/brain/awq268</idno><idno type="ArticleID">awq268</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010-09-30</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Disabling fatigue is a symptom in a number of neurological diseases, including multiple sclerosis, stroke and Parkinsons disease. We used 18F-dopa and 11C-DASB [N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine] positron emission tomography, markers of dopamine storage capacity and serotonin transporter availability, to investigate whether fatigue in Parkinsons disease is associated with dopaminergic and serotonergic dysfunction in basal ganglia and limbic circuits. Ten patients with Parkinsons disease and fatigue and 10 patients without fatigue had a 18F-dopa scan. Seven patients with and eight patients without fatigue also had a 11C-DASB scan. The two groups were matched for age, disease duration and severity and daily intake of levodopa equivalent units. None had a history of depression or sleep disturbance. Using a region of interest analytical approach, we found that patients with fatigue had significantly lower serotonin transporter binding than patients without fatigue in the caudate, putamen, ventral striatum and thalamus. Striatal 18F-dopa uptake was similar in the fatigued and non-fatigued groups. Voxel-based analysis localized further relative serotonin transporter binding reductions in the cingulate and amygdala of the fatigue group, and 18F-dopa uptake reductions in the caudate and insula. We conclude that fatigue in Parkinsons disease is associated with reduced serotonergic function in the basal ganglia and limbic structures. Insular dopaminergic dysfunction could also play a role. These findings imply that strategies to increase brain level of serotonin would be a rational approach for relieving fatigue symptoms in Parkinsons disease and may also be relevant to alleviating fatigue in other clinical conditions.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Original Articles</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson</term></item><item><term>fatigue</term></item><item><term>serotonin</term></item><item><term>F-dopa</term></item><item><term>DASB</term></item><item><term>PET</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-09-30">Created</change><change when="2010-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/FA6512DC0058557D3A0C53467D160AAB9AB6DAE5/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/brain/awq268</article-id><article-id pub-id-type="publisher-id">awq268</article-id><article-categories><subj-group><subject>Original Articles</subject></subj-group></article-categories><title-group><article-title>Fatigue in Parkinson’s disease is linked to striatal and limbic serotonergic dysfunction</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Pavese</surname><given-names>Nicola</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Metta</surname><given-names>Vinod</given-names></name><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bose</surname><given-names>Subrata K.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Chaudhuri</surname><given-names>Kallol Ray</given-names></name><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Brooks</surname><given-names>David J.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib></contrib-group><aff id="AFF1">1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</aff><aff id="AFF2">2 Kings College and Lewisham Hospitals, Kings College, London, UK</aff><author-notes><corresp>Correspondence to: Nicola Pavese, MD, Hammersmith Hospital, Cyclotron Building, DuCane Road W12 0NN, London, UK E-mail: <email>nicola.pavese@csc.mrc.ac.uk</email></corresp></author-notes><pub-date pub-type="ppub"><month>11</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>30</day><month>9</month><year>2010</year></pub-date><volume>133</volume><issue>11</issue><fpage>3434</fpage><lpage>3443</lpage><history><date date-type="received"><day>10</day><month>5</month><year>2010</year></date><date date-type="rev-recd"><day>2</day><month>8</month><year>2010</year></date><date date-type="accepted"><day>2</day><month>8</month><year>2010</year></date></history><permissions><copyright-statement>© The Author (2010). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2010</copyright-year></permissions><abstract><p>Disabling fatigue is a symptom in a number of neurological diseases, including multiple sclerosis, stroke and Parkinson’s disease. We used <sup>18</sup>F-dopa and <sup>11</sup>C-DASB [<italic>N,N</italic>-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine] positron emission tomography, markers of dopamine storage capacity and serotonin transporter availability, to investigate whether fatigue in Parkinson’s disease is associated with dopaminergic and serotonergic dysfunction in basal ganglia and limbic circuits. Ten patients with Parkinson’s disease and fatigue and 10 patients without fatigue had a <sup>18</sup>F-dopa scan. Seven patients with and eight patients without fatigue also had a <sup>11</sup>C-DASB scan. The two groups were matched for age, disease duration and severity and daily intake of levodopa equivalent units. None had a history of depression or sleep disturbance. Using a region of interest analytical approach, we found that patients with fatigue had significantly lower serotonin transporter binding than patients without fatigue in the caudate, putamen, ventral striatum and thalamus. Striatal <sup>18</sup>F-dopa uptake was similar in the fatigued and non-fatigued groups. Voxel-based analysis localized further relative serotonin transporter binding reductions in the cingulate and amygdala of the fatigue group, and <sup>18</sup>F-dopa uptake reductions in the caudate and insula. We conclude that fatigue in Parkinson’s disease is associated with reduced serotonergic function in the basal ganglia and limbic structures. Insular dopaminergic dysfunction could also play a role. These findings imply that strategies to increase brain level of serotonin would be a rational approach for relieving fatigue symptoms in Parkinson’s disease and may also be relevant to alleviating fatigue in other clinical conditions.</p></abstract><kwd-group><kwd>Parkinson</kwd><kwd>fatigue</kwd><kwd>serotonin</kwd><kwd>F-dopa</kwd><kwd>DASB</kwd><kwd>PET</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Fatigue in Parkinsons disease is linked to striatal and limbic serotonergic dysfunction</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Nicola</namePart><namePart type="family">Pavese</namePart><affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</affiliation><affiliation>E-mail: nicola.pavese@csc.mrc.ac.uk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vinod</namePart><namePart type="family">Metta</namePart><affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Subrata K.</namePart><namePart type="family">Bose</namePart><affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kallol Ray</namePart><namePart type="family">Chaudhuri</namePart><affiliation>2 Kings College and Lewisham Hospitals, Kings College, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><affiliation>1 Department of Medicine, Centre for Neuroscience, Imperial College, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Original Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2010-11</dateIssued><dateCreated encoding="w3cdtf">2010-09-30</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Disabling fatigue is a symptom in a number of neurological diseases, including multiple sclerosis, stroke and Parkinsons disease. We used 18F-dopa and 11C-DASB [N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine] positron emission tomography, markers of dopamine storage capacity and serotonin transporter availability, to investigate whether fatigue in Parkinsons disease is associated with dopaminergic and serotonergic dysfunction in basal ganglia and limbic circuits. Ten patients with Parkinsons disease and fatigue and 10 patients without fatigue had a 18F-dopa scan. Seven patients with and eight patients without fatigue also had a 11C-DASB scan. The two groups were matched for age, disease duration and severity and daily intake of levodopa equivalent units. None had a history of depression or sleep disturbance. Using a region of interest analytical approach, we found that patients with fatigue had significantly lower serotonin transporter binding than patients without fatigue in the caudate, putamen, ventral striatum and thalamus. Striatal 18F-dopa uptake was similar in the fatigued and non-fatigued groups. Voxel-based analysis localized further relative serotonin transporter binding reductions in the cingulate and amygdala of the fatigue group, and 18F-dopa uptake reductions in the caudate and insula. We conclude that fatigue in Parkinsons disease is associated with reduced serotonergic function in the basal ganglia and limbic structures. Insular dopaminergic dysfunction could also play a role. These findings imply that strategies to increase brain level of serotonin would be a rational approach for relieving fatigue symptoms in Parkinsons disease and may also be relevant to alleviating fatigue in other clinical conditions.</abstract><subject><genre>Keywords</genre><topic>Parkinson</topic><topic>fatigue</topic><topic>serotonin</topic><topic>F-dopa</topic><topic>DASB</topic><topic>PET</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>133</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>3434</start><end>3443</end></extent></part></relatedItem><identifier type="istex">FA6512DC0058557D3A0C53467D160AAB9AB6DAE5</identifier><identifier type="DOI">10.1093/brain/awq268</identifier><identifier type="ArticleID">awq268</identifier><accessCondition type="use and reproduction" contentType="copyright">The Author (2010). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. 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