Reduced dopamine transporter binding predates impulse control disorders in Parkinson's disease.
Identifieur interne : 000502 ( PubMed/Curation ); précédent : 000501; suivant : 000503Reduced dopamine transporter binding predates impulse control disorders in Parkinson's disease.
Auteurs : Chris Vriend [Pays-Bas] ; Anna H. Nordbeck ; Jan Booij ; Ysbrand D. Van Der Werf ; Tommy Pattij ; Pieter Voorn ; Pieter Raijmakers ; Elisabeth M J. Foncke ; Elsmarieke Van De Giessen ; Henk W. Berendse ; Odile A. Van Den HeuvelSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Dopamine (metabolism), Dopamine Plasma Membrane Transport Proteins (metabolism), Female, Humans, Impulse Control Disorders (complications), Impulse Control Disorders (diagnosis), Impulse Control Disorders (metabolism), Male, Middle Aged, Parkinson Disease (complications), Parkinson Disease (metabolism), Retrospective Studies, Tomography, Emission-Computed, Single-Photon.
- MESH :
- chemical , metabolism : Dopamine, Dopamine Plasma Membrane Transport Proteins.
- complications : Impulse Control Disorders, Parkinson Disease.
- diagnosis : Impulse Control Disorders.
- metabolism : Impulse Control Disorders, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Retrospective Studies, Tomography, Emission-Computed, Single-Photon.
Abstract
Impulse control disorders (ICD) are relatively common in Parkinson's disease (PD) and generally are regarded as adverse effects of dopamine replacement therapy, although certain demographic and clinical risk factors are also involved. Previous single-photon emission computed tomography (SPECT) studies showed reduced ventral striatal dopamine transporter binding in Parkinson patients with ICD compared with patients without. Nevertheless, these studies were performed in patients with preexisting impulse control impairments, which impedes clear-cut interpretation of these findings. We retrospectively procured follow-up data from 31 medication-naïve PD patients who underwent dopamine transporter SPECT imaging at baseline and were subsequently treated with dopamine replacement therapy. We used questionnaires and a telephone interview to assess medication status and ICD symptom development during the follow-up period (31.5 ± 12.0 months). Eleven patients developed ICD symptoms during the follow-up period, eight of which were taking dopamine agonists. The PD patients with ICD symptoms at follow-up had higher baseline depressive scores and lower baseline dopamine transporter availability in the right ventral striatum, anterior-dorsal striatum, and posterior putamen compared with PD patients without ICD symptoms. No baseline between-group differences in age and disease stage or duration were found. The ICD symptom severity correlated negatively with baseline dopamine transporter availability in the right ventral and anterior-dorsal striatum. The results of this preliminary study show that reduced striatal dopamine transporter availability predates the development of ICD symptoms after dopamine replacement therapy and may constitute a neurobiological risk factor related to a lower premorbid dopamine transporter availability or a more pronounced dopamine denervation in PD patients susceptible to ICD.
DOI: 10.1002/mds.25886
PubMed: 24832846
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Nordbeck</name></author><author><name sortKey="Booij, Jan" sort="Booij, Jan" uniqKey="Booij J" first="Jan" last="Booij">Jan Booij</name></author><author><name sortKey="Van Der Werf, Ysbrand D" sort="Van Der Werf, Ysbrand D" uniqKey="Van Der Werf Y" first="Ysbrand D" last="Van Der Werf">Ysbrand D. Van Der Werf</name></author><author><name sortKey="Pattij, Tommy" sort="Pattij, Tommy" uniqKey="Pattij T" first="Tommy" last="Pattij">Tommy Pattij</name></author><author><name sortKey="Voorn, Pieter" sort="Voorn, Pieter" uniqKey="Voorn P" first="Pieter" last="Voorn">Pieter Voorn</name></author><author><name sortKey="Raijmakers, Pieter" sort="Raijmakers, Pieter" uniqKey="Raijmakers P" first="Pieter" last="Raijmakers">Pieter Raijmakers</name></author><author><name sortKey="Foncke, Elisabeth M J" sort="Foncke, Elisabeth M J" uniqKey="Foncke E" first="Elisabeth M J" last="Foncke">Elisabeth M J. Foncke</name></author><author><name sortKey="Van De Giessen, Elsmarieke" sort="Van De Giessen, Elsmarieke" uniqKey="Van De Giessen E" first="Elsmarieke" last="Van De Giessen">Elsmarieke Van De Giessen</name></author><author><name sortKey="Berendse, Henk W" sort="Berendse, Henk W" uniqKey="Berendse H" first="Henk W" last="Berendse">Henk W. Berendse</name></author><author><name sortKey="Van Den Heuvel, Odile A" sort="Van Den Heuvel, Odile A" uniqKey="Van Den Heuvel O" first="Odile A" last="Van Den Heuvel">Odile A. Van Den Heuvel</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24832846</idno><idno type="pmid">24832846</idno><idno type="doi">10.1002/mds.25886</idno><idno type="wicri:Area/PubMed/Corpus">000502</idno><idno type="wicri:Area/PubMed/Curation">000502</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Reduced dopamine transporter binding predates impulse control disorders in Parkinson's disease.</title><author><name sortKey="Vriend, Chris" sort="Vriend, Chris" uniqKey="Vriend C" first="Chris" last="Vriend">Chris Vriend</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands; Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands; Neuroscience Campus Amsterdam, VU/VUmc, Amsterdam, The Netherlands.</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands; Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands; Neuroscience Campus Amsterdam, VU/VUmc, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Nordbeck, Anna H" sort="Nordbeck, Anna H" uniqKey="Nordbeck A" first="Anna H" last="Nordbeck">Anna H. Nordbeck</name></author><author><name sortKey="Booij, Jan" sort="Booij, Jan" uniqKey="Booij J" first="Jan" last="Booij">Jan Booij</name></author><author><name sortKey="Van Der Werf, Ysbrand D" sort="Van Der Werf, Ysbrand D" uniqKey="Van Der Werf Y" first="Ysbrand D" last="Van Der Werf">Ysbrand D. Van Der Werf</name></author><author><name sortKey="Pattij, Tommy" sort="Pattij, Tommy" uniqKey="Pattij T" first="Tommy" last="Pattij">Tommy Pattij</name></author><author><name sortKey="Voorn, Pieter" sort="Voorn, Pieter" uniqKey="Voorn P" first="Pieter" last="Voorn">Pieter Voorn</name></author><author><name sortKey="Raijmakers, Pieter" sort="Raijmakers, Pieter" uniqKey="Raijmakers P" first="Pieter" last="Raijmakers">Pieter Raijmakers</name></author><author><name sortKey="Foncke, Elisabeth M J" sort="Foncke, Elisabeth M J" uniqKey="Foncke E" first="Elisabeth M J" last="Foncke">Elisabeth M J. Foncke</name></author><author><name sortKey="Van De Giessen, Elsmarieke" sort="Van De Giessen, Elsmarieke" uniqKey="Van De Giessen E" first="Elsmarieke" last="Van De Giessen">Elsmarieke Van De Giessen</name></author><author><name sortKey="Berendse, Henk W" sort="Berendse, Henk W" uniqKey="Berendse H" first="Henk W" last="Berendse">Henk W. Berendse</name></author><author><name sortKey="Van Den Heuvel, Odile A" sort="Van Den Heuvel, Odile A" uniqKey="Van Den Heuvel O" first="Odile A" last="Van Den Heuvel">Odile A. Van Den Heuvel</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term><term>Female</term><term>Humans</term><term>Impulse Control Disorders (complications)</term><term>Impulse Control Disorders (diagnosis)</term><term>Impulse Control Disorders (metabolism)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (metabolism)</term><term>Retrospective Studies</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Impulse Control Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Impulse Control Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Impulse Control Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Retrospective Studies</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Impulse control disorders (ICD) are relatively common in Parkinson's disease (PD) and generally are regarded as adverse effects of dopamine replacement therapy, although certain demographic and clinical risk factors are also involved. Previous single-photon emission computed tomography (SPECT) studies showed reduced ventral striatal dopamine transporter binding in Parkinson patients with ICD compared with patients without. Nevertheless, these studies were performed in patients with preexisting impulse control impairments, which impedes clear-cut interpretation of these findings. We retrospectively procured follow-up data from 31 medication-naïve PD patients who underwent dopamine transporter SPECT imaging at baseline and were subsequently treated with dopamine replacement therapy. We used questionnaires and a telephone interview to assess medication status and ICD symptom development during the follow-up period (31.5 ± 12.0 months). Eleven patients developed ICD symptoms during the follow-up period, eight of which were taking dopamine agonists. The PD patients with ICD symptoms at follow-up had higher baseline depressive scores and lower baseline dopamine transporter availability in the right ventral striatum, anterior-dorsal striatum, and posterior putamen compared with PD patients without ICD symptoms. No baseline between-group differences in age and disease stage or duration were found. The ICD symptom severity correlated negatively with baseline dopamine transporter availability in the right ventral and anterior-dorsal striatum. The results of this preliminary study show that reduced striatal dopamine transporter availability predates the development of ICD symptoms after dopamine replacement therapy and may constitute a neurobiological risk factor related to a lower premorbid dopamine transporter availability or a more pronounced dopamine denervation in PD patients susceptible to ICD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24832846</PMID><DateCreated><Year>2014</Year><Month>06</Month><Day>13</Day></DateCreated><DateCompleted><Year>2015</Year><Month>02</Month><Day>26</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>7</Issue><PubDate><Year>2014</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Reduced dopamine transporter binding predates impulse control disorders in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>904-11</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25886</ELocationID><Abstract><AbstractText>Impulse control disorders (ICD) are relatively common in Parkinson's disease (PD) and generally are regarded as adverse effects of dopamine replacement therapy, although certain demographic and clinical risk factors are also involved. Previous single-photon emission computed tomography (SPECT) studies showed reduced ventral striatal dopamine transporter binding in Parkinson patients with ICD compared with patients without. Nevertheless, these studies were performed in patients with preexisting impulse control impairments, which impedes clear-cut interpretation of these findings. We retrospectively procured follow-up data from 31 medication-naïve PD patients who underwent dopamine transporter SPECT imaging at baseline and were subsequently treated with dopamine replacement therapy. We used questionnaires and a telephone interview to assess medication status and ICD symptom development during the follow-up period (31.5 ± 12.0 months). Eleven patients developed ICD symptoms during the follow-up period, eight of which were taking dopamine agonists. The PD patients with ICD symptoms at follow-up had higher baseline depressive scores and lower baseline dopamine transporter availability in the right ventral striatum, anterior-dorsal striatum, and posterior putamen compared with PD patients without ICD symptoms. No baseline between-group differences in age and disease stage or duration were found. The ICD symptom severity correlated negatively with baseline dopamine transporter availability in the right ventral and anterior-dorsal striatum. The results of this preliminary study show that reduced striatal dopamine transporter availability predates the development of ICD symptoms after dopamine replacement therapy and may constitute a neurobiological risk factor related to a lower premorbid dopamine transporter availability or a more pronounced dopamine denervation in PD patients susceptible to ICD.</AbstractText><CopyrightInformation>© 2014 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vriend</LastName><ForeName>Chris</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands; Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands; Neuroscience Campus Amsterdam, VU/VUmc, Amsterdam, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nordbeck</LastName><ForeName>Anna H</ForeName><Initials>AH</Initials></Author><Author ValidYN="Y"><LastName>Booij</LastName><ForeName>Jan</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>van der Werf</LastName><ForeName>Ysbrand D</ForeName><Initials>YD</Initials></Author><Author ValidYN="Y"><LastName>Pattij</LastName><ForeName>Tommy</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Voorn</LastName><ForeName>Pieter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Raijmakers</LastName><ForeName>Pieter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Foncke</LastName><ForeName>Elisabeth M J</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>van de Giessen</LastName><ForeName>Elsmarieke</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Berendse</LastName><ForeName>Henk W</ForeName><Initials>HW</Initials></Author><Author ValidYN="Y"><LastName>van den Heuvel</LastName><ForeName>Odile A</ForeName><Initials>OA</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>05</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D050483">Dopamine Plasma Membrane Transport Proteins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007174">Impulse Control Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012189">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015899">Tomography, Emission-Computed, Single-Photon</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">dopamine replacement therapy</Keyword><Keyword MajorTopicYN="N">dopamine transporter</Keyword><Keyword MajorTopicYN="N">impulse control</Keyword><Keyword MajorTopicYN="N">neuropsychiatry</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>12</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>2</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>3</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2014</Year><Month>5</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>5</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>5</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>2</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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