Memory and executive function in sporadic and familial Parkinson's disease
Identifieur interne : 001221 ( Main/Corpus ); précédent : 001220; suivant : 001222Memory and executive function in sporadic and familial Parkinson's disease
Auteurs : Kathy Dujardin ; Luc Defebvre ; Christine Grunberg ; Estelle Becquet ; Alain Deste ESource :
- Brain [ 0006-8950 ] ; 2001-02.
English descriptors
- KwdEn :
- MDRS = Mattis Dementia Rating Scale, UKPDBB = United Kingdom Parkinson's Disease Brain Bank, UPDRS = Unified Parkinson's Disease Rating Scale, VIQ = verbal intelligence quotient, WAIS-R = Wechsler Adult Intelligence Scale—revised, WCST = Wisconsin Card Sorting Test, dysexecutive syndrome, familial Parkinson's disease, frontostriatal circuit.
Abstract
Some studies have demonstrated that the motor symptomatology in sporadic and familial Parkinson's disease was identical. From a physiopathological point of view, and perhaps in the future from a therapeutic point of view, it seems important to determine whether sporadic and familial Parkinson's disease are also similar with regard to cognitive impairment. The aim of the present study was to assess cognitive functions in patients suffering from sporadic and familial Parkinson's disease. Executive functions and memory were investigated in particular. Two groups of 12 patients with Parkinson's disease (sporadic and familial) and 12 healthy controls performed a set of tasks known to evaluate different aspects of executive function and memory. One-way analysis of variance tested for significant group effects, and when justified, post hoc analysis was performed. Cognitive impairment was different in sporadic and familial forms of Parkinson's disease. Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. Cholinergic deprivation is considered in particular.
Url:
DOI: 10.1093/brain/124.2.389
Links to Exploration step
ISTEX:817CE9DAB893BA333B39ECA3F23B2A3D4DF9150BLe document en format XML
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From a physiopathological point of view, and perhaps in the future from a therapeutic point of view, it seems important to determine whether sporadic and familial Parkinson's disease are also similar with regard to cognitive impairment. The aim of the present study was to assess cognitive functions in patients suffering from sporadic and familial Parkinson's disease. Executive functions and memory were investigated in particular. Two groups of 12 patients with Parkinson's disease (sporadic and familial) and 12 healthy controls performed a set of tasks known to evaluate different aspects of executive function and memory. One-way analysis of variance tested for significant group effects, and when justified, post hoc analysis was performed. Cognitive impairment was different in sporadic and familial forms of Parkinson's disease. Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. Cholinergic deprivation is considered in particular.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Kathy Dujardin</name><affiliations><json:string>Neurologie A, Clinique Neurologique, CHU de Lille,</json:string><json:string>Psychology Department, Charles de Gaulle University, Lille, France</json:string></affiliations></json:item><json:item><name>Luc Defebvre</name><affiliations><json:string>Neurologie A, Clinique Neurologique, CHU de Lille,</json:string></affiliations></json:item><json:item><name>Christine Grunberg</name><affiliations><json:string>Neurologie A, Clinique Neurologique, CHU de Lille,</json:string></affiliations></json:item><json:item><name>Estelle Becquet</name><affiliations><json:string>Neurologie A, Clinique Neurologique, CHU de Lille,</json:string></affiliations></json:item><json:item><name>Alain Destée</name><affiliations><json:string>Neurologie A, Clinique Neurologique, CHU de Lille,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>familial Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dysexecutive syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>frontostriatal circuit</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MDRS = Mattis Dementia Rating Scale</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>UKPDBB = United Kingdom Parkinson's Disease Brain Bank</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>UPDRS = Unified Parkinson's Disease Rating Scale</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>VIQ = verbal intelligence quotient</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>WAIS-R = Wechsler Adult Intelligence Scale—revised</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>WCST = Wisconsin Card Sorting Test</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Some studies have demonstrated that the motor symptomatology in sporadic and familial Parkinson's disease was identical. 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Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. 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Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. Cholinergic deprivation is considered in particular.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>familial Parkinson's disease</term></item><item><term>dysexecutive syndrome</term></item><item><term>frontostriatal circuit</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>MDRS = Mattis Dementia Rating Scale</term></item><item><term>UKPDBB = United Kingdom Parkinson's Disease Brain Bank</term></item><item><term>UPDRS = Unified Parkinson's Disease Rating Scale</term></item><item><term>VIQ = verbal intelligence quotient</term></item><item><term>WAIS-R = Wechsler Adult Intelligence Scale—revised</term></item><item><term>WCST = Wisconsin Card Sorting Test</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-02">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/817CE9DAB893BA333B39ECA3F23B2A3D4DF9150B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><abbrev-journal-title abbrev-type="publisher">Brain</abbrev-journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">1240389</article-id><article-id pub-id-type="doi">10.1093/brain/124.2.389</article-id><article-id pub-id-type="pii">1460-2156</article-id><title-group><article-title>Memory and executive function in sporadic and familial Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Dujardin</surname><given-names>Kathy</given-names></name><xref rid="AFF1">1</xref><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Defebvre</surname><given-names> Luc</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Grunberg</surname><given-names> Christine</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Becquet</surname><given-names> Estelle</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Destée</surname><given-names>Alain</given-names></name><xref rid="AFF1">1</xref></contrib><aff id="AFF1"><label>1</label>Neurologie A, Clinique Neurologique, CHU de Lille, </aff><aff id="AFF2"><label>2</label>Psychology Department, Charles de Gaulle University, Lille, France</aff></contrib-group><author-notes><corresp>Kathy Dujardin, Neurologie A, Hôpital Salengro, CHU de Lille, 59037 Lille Cedex France E-mail: <ext-link xlink:href="kdujardin@nordnet.fr" ext-link-type="email">kdujardin@nordnet.fr</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>2</month><year>2001</year></pub-date><volume>124</volume><issue>2</issue><fpage>389</fpage><lpage>398</lpage><history><date date-type="accepted"><day>09</day><month>10</month><year>2000</year></date><date date-type="received"><day>24</day><month>07</month><year>2000</year></date><date date-type="rev-recd"><day>03</day><month>10</month><year>2000</year></date></history><copyright-statement>© Oxford University Press 2001</copyright-statement><copyright-year>2001</copyright-year><abstract xml:lang="en"><p>Some studies have demonstrated that the motor symptomatology in sporadic and familial Parkinson's disease was identical. From a physiopathological point of view, and perhaps in the future from a therapeutic point of view, it seems important to determine whether sporadic and familial Parkinson's disease are also similar with regard to cognitive impairment. The aim of the present study was to assess cognitive functions in patients suffering from sporadic and familial Parkinson's disease. Executive functions and memory were investigated in particular. Two groups of 12 patients with Parkinson's disease (sporadic and familial) and 12 healthy controls performed a set of tasks known to evaluate different aspects of executive function and memory. One-way analysis of variance tested for significant group effects, and when justified, <italic>post hoc</italic> analysis was performed. Cognitive impairment was different in sporadic and familial forms of Parkinson's disease. Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. Cholinergic deprivation is considered in particular.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>familial Parkinson's disease</kwd><kwd>dysexecutive syndrome</kwd><kwd>frontostriatal circuit</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd> MDRS = Mattis Dementia Rating Scale</kwd><kwd> UKPDBB = United Kingdom Parkinson's Disease Brain Bank</kwd><kwd> UPDRS = Unified Parkinson's Disease Rating Scale</kwd><kwd> VIQ = verbal intelligence quotient</kwd><kwd> WAIS-R = Wechsler Adult Intelligence Scale—revised</kwd><kwd> WCST = Wisconsin Card Sorting Test</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>389</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Memory and executive function in sporadic and familial Parkinson's disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Memory and executive function in sporadic and familial Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Kathy</namePart><namePart type="family">Dujardin</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luc</namePart><namePart type="family">Defebvre</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Grunberg</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Estelle</namePart><namePart type="family">Becquet</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alain</namePart><namePart type="family">Destée</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2001-02</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Some studies have demonstrated that the motor symptomatology in sporadic and familial Parkinson's disease was identical. From a physiopathological point of view, and perhaps in the future from a therapeutic point of view, it seems important to determine whether sporadic and familial Parkinson's disease are also similar with regard to cognitive impairment. The aim of the present study was to assess cognitive functions in patients suffering from sporadic and familial Parkinson's disease. Executive functions and memory were investigated in particular. Two groups of 12 patients with Parkinson's disease (sporadic and familial) and 12 healthy controls performed a set of tasks known to evaluate different aspects of executive function and memory. One-way analysis of variance tested for significant group effects, and when justified, post hoc analysis was performed. Cognitive impairment was different in sporadic and familial forms of Parkinson's disease. Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. Cholinergic deprivation is considered in particular.</abstract><note type="author-notes">Kathy Dujardin, Neurologie A, Hôpital Salengro, CHU de Lille, 59037 Lille Cedex France E-mail: kdujardin@nordnet.fr</note><subject lang="en"><genre>KWD</genre><topic>familial Parkinson's disease</topic><topic>dysexecutive syndrome</topic><topic>frontostriatal circuit</topic></subject><subject lang="en"><genre>ABR</genre><topic>MDRS = Mattis Dementia Rating Scale</topic><topic>UKPDBB = United Kingdom Parkinson's Disease Brain Bank</topic><topic>UPDRS = Unified Parkinson's Disease Rating Scale</topic><topic>VIQ = verbal intelligence quotient</topic><topic>WAIS-R = Wechsler Adult Intelligence Scale—revised</topic><topic>WCST = Wisconsin Card Sorting Test</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><titleInfo type="abbreviated"><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><identifier type="PublisherID-nlm-ta">Brain</identifier><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>124</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>389</start><end>398</end></extent></part></relatedItem><identifier type="istex">817CE9DAB893BA333B39ECA3F23B2A3D4DF9150B</identifier><identifier type="DOI">10.1093/brain/124.2.389</identifier><identifier type="PII">1460-2156</identifier><identifier type="local">1240389</identifier><accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press 2001</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/817CE9DAB893BA333B39ECA3F23B2A3D4DF9150B/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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