Do cognitive changes of Parkinson's disease result from dopamine depletion?
Identifieur interne : 001650 ( PubMed/Corpus ); précédent : 001649; suivant : 001651Do cognitive changes of Parkinson's disease result from dopamine depletion?
Auteurs : B. Dubois ; B. PillonSource :
- Journal of neural transmission. Supplementum [ 0303-6995 ] ; 1995.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Dopamine.
- etiology : Cognition Disorders.
- physiopathology : Cerebral Cortex, Cognition Disorders, Frontal Lobe, Parkinson Disease.
- psychology : Parkinson Disease.
- Humans.
Abstract
Cognitive changes have long been observed in patients with Parkinson's disease: visuo-spatial deficits, memory disorders, dysexecutive syndrome. Given the modulatory role of the basal ganglia and related structures, these deficits might result from more fundamental disorders concerning the allocation of attentional resources, the temporal organization of behavior, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.
PubMed: 8748606
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Pillon</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1995">1995</date><idno type="RBID">pubmed:8748606</idno><idno type="pmid">8748606</idno><idno type="wicri:Area/PubMed/Corpus">001650</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001650</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Do cognitive changes of Parkinson's disease result from dopamine depletion?</title><author><name sortKey="Dubois, B" sort="Dubois, B" uniqKey="Dubois B" first="B" last="Dubois">B. Dubois</name><affiliation><nlm:affiliation>Fédération de Neurologie and INSERM U 289, Hopital de la Salpétrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Pillon, B" sort="Pillon, B" uniqKey="Pillon B" first="B" last="Pillon">B. Pillon</name></author></analytic><series><title level="j">Journal of neural transmission. Supplementum</title><idno type="ISSN">0303-6995</idno><imprint><date when="1995" type="published">1995</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cerebral Cortex (physiopathology)</term><term>Cognition Disorders (etiology)</term><term>Cognition Disorders (physiopathology)</term><term>Dopamine (physiology)</term><term>Frontal Lobe (physiopathology)</term><term>Humans</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (psychology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term><term>Cognition Disorders</term><term>Frontal Lobe</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cognitive changes have long been observed in patients with Parkinson's disease: visuo-spatial deficits, memory disorders, dysexecutive syndrome. Given the modulatory role of the basal ganglia and related structures, these deficits might result from more fundamental disorders concerning the allocation of attentional resources, the temporal organization of behavior, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8748606</PMID><DateCreated><Year>1996</Year><Month>10</Month><Day>23</Day></DateCreated><DateCompleted><Year>1996</Year><Month>10</Month><Day>23</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0303-6995</ISSN><JournalIssue CitedMedium="Print"><Volume>45</Volume><PubDate><Year>1995</Year></PubDate></JournalIssue><Title>Journal of neural transmission. Supplementum</Title><ISOAbbreviation>J. Neural Transm. Suppl.</ISOAbbreviation></Journal><ArticleTitle>Do cognitive changes of Parkinson's disease result from dopamine depletion?</ArticleTitle><Pagination><MedlinePgn>27-34</MedlinePgn></Pagination><Abstract><AbstractText>Cognitive changes have long been observed in patients with Parkinson's disease: visuo-spatial deficits, memory disorders, dysexecutive syndrome. Given the modulatory role of the basal ganglia and related structures, these deficits might result from more fundamental disorders concerning the allocation of attentional resources, the temporal organization of behavior, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dubois</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Fédération de Neurologie and INSERM U 289, Hopital de la Salpétrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pillon</LastName><ForeName>B</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Austria</Country><MedlineTA>J Neural Transm Suppl</MedlineTA><NlmUniqueID>0425126</NlmUniqueID><ISSNLinking>0303-6995</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003072" MajorTopicYN="N">Cognition Disorders</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005625" MajorTopicYN="N">Frontal Lobe</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000523" MajorTopicYN="Y">psychology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>28</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1995</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1995</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1995</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8748606</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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