Cognitive deficits in Parkinson's disease
Identifieur interne : 001586 ( PascalFrancis/Checkpoint ); précédent : 001585; suivant : 001587Cognitive deficits in Parkinson's disease
Auteurs : B. Dubois [France] ; B. Pillon [France]Source :
- Journal of neurology [ 0340-5354 ] ; 1997.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
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.
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
Pascal:97-0024497Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">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 wicri:level="3"><inist:fA14 i1="01"><s1>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital</s1><s2>75651 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Pillon, B" sort="Pillon, B" uniqKey="Pillon B" first="B." last="Pillon">B. Pillon</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital</s1><s2>75651 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">97-0024497</idno><date when="1997">1997</date><idno type="stanalyst">PASCAL 97-0024497 INIST</idno><idno type="RBID">Pascal:97-0024497</idno><idno type="wicri:Area/PascalFrancis/Corpus">001777</idno><idno type="wicri:Area/PascalFrancis/Curation">001869</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">001586</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">001586</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">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 wicri:level="3"><inist:fA14 i1="01"><s1>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital</s1><s2>75651 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Pillon, B" sort="Pillon, B" uniqKey="Pillon B" first="B." last="Pillon">B. Pillon</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital</s1><s2>75651 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of neurology</title><title level="j" type="abbreviated">J. neurol.</title><idno type="ISSN">0340-5354</idno><imprint><date when="1997">1997</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurology</title><title level="j" type="abbreviated">J. neurol.</title><idno type="ISSN">0340-5354</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cognitive disorder</term><term>Dementia</term><term>Human</term><term>Parkinson disease</term><term>Pathophysiology</term><term>Symptomatology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term><term>Trouble cognition</term><term>Démence</term><term>Symptomatologie</term><term>Physiopathologie</term><term>Homme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0340-5354</s0></fA01><fA02 i1="01"><s0>JNRYA9</s0></fA02><fA03 i2="1"><s0>J. neurol.</s0></fA03><fA05><s2>244</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Cognitive deficits in Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>DUBOIS (B.)</s1></fA11><fA11 i1="02" i2="1"><s1>PILLON (B.)</s1></fA11><fA14 i1="01"><s1>INSERM U 289 and Fédération de Neurologie, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital</s1><s2>75651 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></fA14><fA20><s2>1-8 [7 p.]</s2></fA20><fA21><s1>1997</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4826</s2><s5>354000060743490010</s5></fA43><fA44><s0>0000</s0><s1>© 1997 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>86 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>97-0024497</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurology</s0></fA64><fA66 i1="01"><s0>DEU</s0></fA66><fC01 i1="01" l="ENG"><s0>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.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Trouble cognition</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Cognitive disorder</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Trastorno cognitivo</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Démence</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Dementia</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Demencia</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Symptomatologie</s0><s5>17</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Symptomatology</s0><s5>17</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Sintomatología</s0><s5>17</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Physiopathologie</s0><s5>18</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Pathophysiology</s0><s5>18</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Fisiopatología</s0><s5>18</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Homme</s0><s5>20</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Human</s0><s5>20</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Hombre</s0><s5>20</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>41</s5></fC07><fN21><s1>006</s1></fN21></pA></standard></inist><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Dubois, B" sort="Dubois, B" uniqKey="Dubois B" first="B." last="Dubois">B. Dubois</name></region><name sortKey="Pillon, B" sort="Pillon, B" uniqKey="Pillon B" first="B." last="Pillon">B. Pillon</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PascalFrancis/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001586 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Checkpoint/biblio.hfd -nk 001586 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= PascalFrancis
|étape= Checkpoint
|type= RBID
|clé= Pascal:97-0024497
|texte= Cognitive deficits in Parkinson's disease
}}
| This area was generated with Dilib version V0.6.29. |  |