Cognitive deficits in Parkinson's disease.
Identifieur interne : 001550 ( PubMed/Corpus ); précédent : 001549; suivant : 001551Cognitive deficits in Parkinson's disease.
Auteurs : B. Dubois ; B. PillonSource :
- Journal of neurology [ 0340-5354 ] ; 1997.
English descriptors
- KwdEn :
- Aging (physiology), Cerebral Cortex (pathology), Cerebral Cortex (physiopathology), Cognition Disorders (etiology), Cognition Disorders (pathology), Cognition Disorders (physiopathology), Humans, Lewy Bodies (pathology), Lewy Bodies (physiology), Parkinson Disease (complications), Parkinson Disease (pathology), Parkinson Disease (physiopathology).
- MESH :
- complications : Parkinson Disease.
- etiology : Cognition Disorders.
- pathology : Cerebral Cortex, Cognition Disorders, Lewy Bodies, Parkinson Disease.
- physiology : Aging, Lewy Bodies.
- physiopathology : Cerebral Cortex, Cognition Disorders, Parkinson Disease.
- Humans.
Abstract
Neuropsychological investigations of patients with Parkinson's disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catecholaminergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease.
PubMed: 9007738
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Pillon</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9007738</idno><idno type="pmid">9007738</idno><idno type="wicri:Area/PubMed/Corpus">001550</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001550</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cognitive deficits in Parkinson's disease.</title><author><name sortKey="Dubois, B" sort="Dubois, B" uniqKey="Dubois B" first="B" last="Dubois">B. Dubois</name><affiliation><nlm:affiliation>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 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 neurology</title><idno type="ISSN">0340-5354</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (physiology)</term><term>Cerebral Cortex (pathology)</term><term>Cerebral Cortex (physiopathology)</term><term>Cognition Disorders (etiology)</term><term>Cognition Disorders (pathology)</term><term>Cognition Disorders (physiopathology)</term><term>Humans</term><term>Lewy Bodies (pathology)</term><term>Lewy Bodies (physiology)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebral Cortex</term><term>Cognition Disorders</term><term>Lewy Bodies</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Aging</term><term>Lewy Bodies</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term><term>Cognition Disorders</term><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">Neuropsychological investigations of patients with Parkinson's disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catecholaminergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9007738</PMID><DateCreated><Year>1997</Year><Month>04</Month><Day>03</Day></DateCreated><DateCompleted><Year>1997</Year><Month>04</Month><Day>03</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0340-5354</ISSN><JournalIssue CitedMedium="Print"><Volume>244</Volume><Issue>1</Issue><PubDate><Year>1997</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of neurology</Title><ISOAbbreviation>J. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Cognitive deficits in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>2-8</MedlinePgn></Pagination><Abstract><AbstractText>Neuropsychological investigations of patients with Parkinson's disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catecholaminergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dubois</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 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>Germany</Country><MedlineTA>J Neurol</MedlineTA><NlmUniqueID>0423161</NlmUniqueID><ISSNLinking>0340-5354</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><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="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016631" MajorTopicYN="N">Lewy Bodies</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>86</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9007738</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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