Dissociable dorsal and ventral frontostriatal working memory circuits: evidence from subthalamic stimulation in Parkinson's disease.
Identifieur interne : 000591 ( PubMed/Curation ); précédent : 000590; suivant : 000592Dissociable dorsal and ventral frontostriatal working memory circuits: evidence from subthalamic stimulation in Parkinson's disease.
Auteurs : Jocelyne Ventre-Dominey [France] ; Stéphanie Bourret ; Hélène Mollion ; Emmanuel Broussolle ; Peter Ford DomineySource :
- Human brain mapping [ 1097-0193 ] ; 2014.
English descriptors
- KwdEn :
- Adult, Association Learning (physiology), Brain Mapping, Case-Control Studies, Corpus Striatum (diagnostic imaging), Corpus Striatum (physiopathology), Deep Brain Stimulation (methods), Female, Humans, Male, Memory, Short-Term (physiology), Middle Aged, Neural Pathways (physiopathology), Parkinson Disease (diagnostic imaging), Parkinson Disease (pathology), Parkinson Disease (therapy), Positron-Emission Tomography, Prefrontal Cortex (diagnostic imaging), Prefrontal Cortex (physiopathology), Reaction Time, Subthalamus (physiology).
- MESH :
- diagnostic imaging : Corpus Striatum, Parkinson Disease, Prefrontal Cortex.
- methods : Deep Brain Stimulation.
- pathology : Parkinson Disease.
- physiology : Association Learning, Memory, Short-Term, Subthalamus.
- physiopathology : Corpus Striatum, Neural Pathways, Prefrontal Cortex.
- therapy : Parkinson Disease.
- Adult, Brain Mapping, Case-Control Studies, Female, Humans, Male, Middle Aged, Positron-Emission Tomography, Reaction Time.
Abstract
In this study, we investigated the neural substrates involved in visual working memory (WM) and the resulting effects of subthalamic nucleus (STN) stimulation in Parkinson's disease (PD). Cerebral activation revealed by positron emission tomography was compared among Parkinson patients with (PD-ON) or without (PD-OFF) STN stimulation, and a group of control subjects (CT) in two visual WM tasks with spatial (SP) and nonspatial (NSP) components. PD-OFF patients displayed significant reaction time (RT) deficits for both memory tasks. Although there were no significant differences in RT between patients with PD-ON and -OFF stimulation, patients with PD-ON stimulation performed comparably to controls. The memory tasks were executed with normal error rates in PD-ON and -OFF stimulation. In contrast to these behavioral results, whether the corresponding prefrontal activation was differentially affected by deep brain stimulation status in patients depended on whether the WM modality was SP versus NSP. Thus, SP WM was associated with (1) abnormal reduction in dorsolateral prefrontal activity in PD-OFF and -ON stimulation and (2) abnormal overactivation in parieto-temporal cortex in PD-OFF and in limbic circuits in PD-ON stimulation. In NSP WM, normal activation of the ventral prefrontal cortex was restored in PD-ON stimulation. In both visual modalities the posterior cerebral regions including fusiform cortex and cerebellum, displayed abnormally reduced activity in PD. These results indicate that PD induces a prefrontal hypoactivation that STN stimulation can partially restore in a modality selective manner by additional recruitment of limbic structures in SP WM or by recovery of the ventral prefrontal activation in NSP WM.
DOI: 10.1002/hbm.22205
PubMed: 23097317
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dissociable dorsal and ventral frontostriatal working memory circuits: evidence from subthalamic stimulation in Parkinson's disease.</title><author><name sortKey="Ventre Dominey, Jocelyne" sort="Ventre Dominey, Jocelyne" uniqKey="Ventre Dominey J" first="Jocelyne" last="Ventre-Dominey">Jocelyne Ventre-Dominey</name><affiliation wicri:level="1"><nlm:affiliation>INSERM Unit 846, Stem Cell and Brain Research Institute, 69675 Bron, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM Unit 846, Stem Cell and Brain Research Institute, 69675 Bron</wicri:regionArea></affiliation></author><author><name sortKey="Bourret, Stephanie" sort="Bourret, Stephanie" uniqKey="Bourret S" first="Stéphanie" last="Bourret">Stéphanie Bourret</name></author><author><name sortKey="Mollion, Helene" sort="Mollion, Helene" uniqKey="Mollion H" first="Hélène" last="Mollion">Hélène Mollion</name></author><author><name sortKey="Broussolle, Emmanuel" sort="Broussolle, Emmanuel" uniqKey="Broussolle E" first="Emmanuel" last="Broussolle">Emmanuel Broussolle</name></author><author><name sortKey="Dominey, Peter Ford" sort="Dominey, Peter Ford" uniqKey="Dominey P" first="Peter Ford" last="Dominey">Peter Ford Dominey</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:23097317</idno><idno type="pmid">23097317</idno><idno type="doi">10.1002/hbm.22205</idno><idno type="wicri:Area/PubMed/Corpus">000613</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000613</idno><idno type="wicri:Area/PubMed/Curation">000591</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000591</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dissociable dorsal and ventral frontostriatal working memory circuits: evidence from subthalamic stimulation in Parkinson's disease.</title><author><name sortKey="Ventre Dominey, Jocelyne" sort="Ventre Dominey, Jocelyne" uniqKey="Ventre Dominey J" first="Jocelyne" last="Ventre-Dominey">Jocelyne Ventre-Dominey</name><affiliation wicri:level="1"><nlm:affiliation>INSERM Unit 846, Stem Cell and Brain Research Institute, 69675 Bron, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM Unit 846, Stem Cell and Brain Research Institute, 69675 Bron</wicri:regionArea></affiliation></author><author><name sortKey="Bourret, Stephanie" sort="Bourret, Stephanie" uniqKey="Bourret S" first="Stéphanie" last="Bourret">Stéphanie Bourret</name></author><author><name sortKey="Mollion, Helene" sort="Mollion, Helene" uniqKey="Mollion H" first="Hélène" last="Mollion">Hélène Mollion</name></author><author><name sortKey="Broussolle, Emmanuel" sort="Broussolle, Emmanuel" uniqKey="Broussolle E" first="Emmanuel" last="Broussolle">Emmanuel Broussolle</name></author><author><name sortKey="Dominey, Peter Ford" sort="Dominey, Peter Ford" uniqKey="Dominey P" first="Peter Ford" last="Dominey">Peter Ford Dominey</name></author></analytic><series><title level="j">Human brain mapping</title><idno type="eISSN">1097-0193</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>Association Learning (physiology)</term><term>Brain Mapping</term><term>Case-Control Studies</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (physiopathology)</term><term>Deep Brain Stimulation (methods)</term><term>Female</term><term>Humans</term><term>Male</term><term>Memory, Short-Term (physiology)</term><term>Middle Aged</term><term>Neural Pathways (physiopathology)</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (therapy)</term><term>Positron-Emission Tomography</term><term>Prefrontal Cortex (diagnostic imaging)</term><term>Prefrontal Cortex (physiopathology)</term><term>Reaction Time</term><term>Subthalamus (physiology)</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Prefrontal Cortex</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Association Learning</term><term>Memory, Short-Term</term><term>Subthalamus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Neural Pathways</term><term>Prefrontal Cortex</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Brain Mapping</term><term>Case-Control Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term><term>Reaction Time</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In this study, we investigated the neural substrates involved in visual working memory (WM) and the resulting effects of subthalamic nucleus (STN) stimulation in Parkinson's disease (PD). Cerebral activation revealed by positron emission tomography was compared among Parkinson patients with (PD-ON) or without (PD-OFF) STN stimulation, and a group of control subjects (CT) in two visual WM tasks with spatial (SP) and nonspatial (NSP) components. PD-OFF patients displayed significant reaction time (RT) deficits for both memory tasks. Although there were no significant differences in RT between patients with PD-ON and -OFF stimulation, patients with PD-ON stimulation performed comparably to controls. The memory tasks were executed with normal error rates in PD-ON and -OFF stimulation. In contrast to these behavioral results, whether the corresponding prefrontal activation was differentially affected by deep brain stimulation status in patients depended on whether the WM modality was SP versus NSP. Thus, SP WM was associated with (1) abnormal reduction in dorsolateral prefrontal activity in PD-OFF and -ON stimulation and (2) abnormal overactivation in parieto-temporal cortex in PD-OFF and in limbic circuits in PD-ON stimulation. In NSP WM, normal activation of the ventral prefrontal cortex was restored in PD-ON stimulation. In both visual modalities the posterior cerebral regions including fusiform cortex and cerebellum, displayed abnormally reduced activity in PD. These results indicate that PD induces a prefrontal hypoactivation that STN stimulation can partially restore in a modality selective manner by additional recruitment of limbic structures in SP WM or by recovery of the ventral prefrontal activation in NSP WM.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23097317</PMID><DateCreated><Year>2014</Year><Month>01</Month><Day>14</Day></DateCreated><DateCompleted><Year>2014</Year><Month>09</Month><Day>02</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-0193</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Human brain mapping</Title><ISOAbbreviation>Hum Brain Mapp</ISOAbbreviation></Journal><ArticleTitle>Dissociable dorsal and ventral frontostriatal working memory circuits: evidence from subthalamic stimulation in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>552-66</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/hbm.22205</ELocationID><Abstract><AbstractText>In this study, we investigated the neural substrates involved in visual working memory (WM) and the resulting effects of subthalamic nucleus (STN) stimulation in Parkinson's disease (PD). Cerebral activation revealed by positron emission tomography was compared among Parkinson patients with (PD-ON) or without (PD-OFF) STN stimulation, and a group of control subjects (CT) in two visual WM tasks with spatial (SP) and nonspatial (NSP) components. PD-OFF patients displayed significant reaction time (RT) deficits for both memory tasks. Although there were no significant differences in RT between patients with PD-ON and -OFF stimulation, patients with PD-ON stimulation performed comparably to controls. The memory tasks were executed with normal error rates in PD-ON and -OFF stimulation. In contrast to these behavioral results, whether the corresponding prefrontal activation was differentially affected by deep brain stimulation status in patients depended on whether the WM modality was SP versus NSP. Thus, SP WM was associated with (1) abnormal reduction in dorsolateral prefrontal activity in PD-OFF and -ON stimulation and (2) abnormal overactivation in parieto-temporal cortex in PD-OFF and in limbic circuits in PD-ON stimulation. In NSP WM, normal activation of the ventral prefrontal cortex was restored in PD-ON stimulation. In both visual modalities the posterior cerebral regions including fusiform cortex and cerebellum, displayed abnormally reduced activity in PD. These results indicate that PD induces a prefrontal hypoactivation that STN stimulation can partially restore in a modality selective manner by additional recruitment of limbic structures in SP WM or by recovery of the ventral prefrontal activation in NSP WM.</AbstractText><CopyrightInformation>Copyright © 2012 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ventre-Dominey</LastName><ForeName>Jocelyne</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>INSERM Unit 846, Stem Cell and Brain Research Institute, 69675 Bron, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bourret</LastName><ForeName>Stéphanie</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mollion</LastName><ForeName>Hélène</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Broussolle</LastName><ForeName>Emmanuel</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Dominey</LastName><ForeName>Peter Ford</ForeName><Initials>PF</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>10</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Hum Brain Mapp</MedlineTA><NlmUniqueID>9419065</NlmUniqueID><ISSNLinking>1065-9471</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001245" MajorTopicYN="N">Association Learning</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001931" MajorTopicYN="N">Brain Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D046690" MajorTopicYN="N">Deep Brain Stimulation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008570" MajorTopicYN="N">Memory, Short-Term</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009434" MajorTopicYN="N">Neural Pathways</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="N">Positron-Emission Tomography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017397" MajorTopicYN="N">Prefrontal Cortex</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011930" MajorTopicYN="N">Reaction Time</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020530" MajorTopicYN="N">Subthalamus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">PET</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">dissociated prefrontal activation</Keyword><Keyword MajorTopicYN="N">subthalamic stimulation</Keyword><Keyword MajorTopicYN="N">visual working memory</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>03</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>08</Month><Day>27</Day></PubMedPubDate><PubMedPubDate 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