Cognitive functioning in neurologically symptomatic and asymptomatic forms of Wilson's disease
Identifieur interne : 006539 ( Main/Merge ); précédent : 006538; suivant : 006540Cognitive functioning in neurologically symptomatic and asymptomatic forms of Wilson's disease
Auteurs : Joanna Seni W [Pologne] ; Thomas Bak [Royaume-Uni] ; Jolanta Gajda [Pologne] ; Renata Poniatowska [Pologne] ; Anna Czlonkowska [Pologne]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
English descriptors
- KwdEn :
- Adult, Basal Ganglia (pathology), Basal Ganglia (physiopathology), Brain (pathology), Brain (physiopathology), Cognition Disorders (diagnosis), Cognition Disorders (etiology), Female, Hepatolenticular Degeneration (complications), Hepatolenticular Degeneration (pathology), Hepatolenticular Degeneration (physiopathology), Humans, Male, Neuropsychological Tests, Severity of Illness Index, Wilson's disease, basal ganglia, cognition, dementia.
- MESH :
- complications : Hepatolenticular Degeneration.
- diagnosis : Cognition Disorders.
- etiology : Cognition Disorders.
- pathology : Basal Ganglia, Brain, Hepatolenticular Degeneration.
- physiopathology : Basal Ganglia, Brain, Hepatolenticular Degeneration.
- Adult, Female, Humans, Male, Neuropsychological Tests, Severity of Illness Index.
Abstract
We sought to determine the pattern of cognitive deficits in patients with Wilson's disease (WD) with different type and degree of neurological involvement, and to interpret the findings in relation to the underlying pathology. A total of 67 WD patients were examined with a neuropsychological test battery assessing different aspects of cognitive processing. The patients were subdivided into three groups: neurologically asymptomatic, neurological with pure basal ganglia lesions, and neurological with more extensive pathology. The results were compared with 50 matched healthy controls. Patients with a neurological form of WD showed a mild but definitive impairment in all cognitive functions. In contrast, the neurologically asymptomatic patients showed no deficits when compared with normal controls. Multifocal pathology was associated with more severe cognitive deficits than selective basal ganglia lesions but did not contribute significantly to memory impairment. A range of cognitive functions, including frontal‐executive ability, aspects of memory and visuospatial processing, are affected in the neurologically symptomatic WD patients. In contrast, no subliminal deficits were observed in the asymptomatic patients. The lesions of the basal ganglia seem to be of central importance in explaining the symptomatology. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10195
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-09">2002-09</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1077">1077</biblScope><biblScope unit="page" to="1083">1083</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">75D5845A01858C1892211F3385291F3995BA8B56</idno><idno type="DOI">10.1002/mds.10195</idno><idno type="ArticleID">MDS10195</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Basal Ganglia (pathology)</term><term>Basal Ganglia (physiopathology)</term><term>Brain (pathology)</term><term>Brain (physiopathology)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (etiology)</term><term>Female</term><term>Hepatolenticular Degeneration (complications)</term><term>Hepatolenticular Degeneration (pathology)</term><term>Hepatolenticular Degeneration (physiopathology)</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Severity of Illness Index</term><term>Wilson's disease</term><term>basal ganglia</term><term>cognition</term><term>dementia</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Brain</term><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Brain</term><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Severity of Illness Index</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We sought to determine the pattern of cognitive deficits in patients with Wilson's disease (WD) with different type and degree of neurological involvement, and to interpret the findings in relation to the underlying pathology. A total of 67 WD patients were examined with a neuropsychological test battery assessing different aspects of cognitive processing. The patients were subdivided into three groups: neurologically asymptomatic, neurological with pure basal ganglia lesions, and neurological with more extensive pathology. The results were compared with 50 matched healthy controls. Patients with a neurological form of WD showed a mild but definitive impairment in all cognitive functions. In contrast, the neurologically asymptomatic patients showed no deficits when compared with normal controls. Multifocal pathology was associated with more severe cognitive deficits than selective basal ganglia lesions but did not contribute significantly to memory impairment. A range of cognitive functions, including frontal‐executive ability, aspects of memory and visuospatial processing, are affected in the neurologically symptomatic WD patients. In contrast, no subliminal deficits were observed in the asymptomatic patients. The lesions of the basal ganglia seem to be of central importance in explaining the symptomatology. © 2002 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.10195"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cognitive functioning in neurologically symptomatic and asymptomatic forms of Wilson's disease</title><author><name sortKey="Seni W, Joanna" sort="Seni W, Joanna" uniqKey="Seni W J" first="Joanna" last="Seni W">Joanna Seni W</name></author><author><name sortKey="Bak, Thomas" sort="Bak, Thomas" uniqKey="Bak T" first="Thomas" last="Bak">Thomas Bak</name></author><author><name sortKey="Gajda, Jolanta" sort="Gajda, Jolanta" uniqKey="Gajda J" first="Jolanta" last="Gajda">Jolanta Gajda</name></author><author><name sortKey="Poniatowska, Renata" sort="Poniatowska, Renata" uniqKey="Poniatowska R" first="Renata" last="Poniatowska">Renata Poniatowska</name></author><author><name sortKey="Czlonkowska, Anna" sort="Czlonkowska, Anna" uniqKey="Czlonkowska A" first="Anna" last="Czlonkowska">Anna Czlonkowska</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:75D5845A01858C1892211F3385291F3995BA8B56</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1002/mds.10195</idno><idno type="url">https://api.istex.fr/document/75D5845A01858C1892211F3385291F3995BA8B56/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000D60</idno><idno type="wicri:Area/Istex/Curation">000D60</idno><idno type="wicri:Area/Istex/Checkpoint">002E25</idno><idno type="wicri:doubleKey">0885-3185:2002:Seni W J:cognitive:functioning:in</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Cognitive functioning in neurologically symptomatic and asymptomatic forms of Wilson's disease</title><author><name sortKey="Seni W, Joanna" sort="Seni W, Joanna" uniqKey="Seni W J" first="Joanna" last="Seni W">Joanna Seni W</name><affiliation wicri:level="1"><country xml:lang="fr">Pologne</country><wicri:regionArea>Institute of Psychiatry and Neurology, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation></author><author><name sortKey="Bak, Thomas" sort="Bak, Thomas" uniqKey="Bak T" first="Thomas" last="Bak">Thomas Bak</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Cognition and Brain Sciences Unit, Cambridge</wicri:regionArea><wicri:noRegion>Cambridge</wicri:noRegion></affiliation></author><author><name sortKey="Gajda, Jolanta" sort="Gajda, Jolanta" uniqKey="Gajda J" first="Jolanta" last="Gajda">Jolanta Gajda</name><affiliation wicri:level="1"><country xml:lang="fr">Pologne</country><wicri:regionArea>Institute of Psychiatry and Neurology, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation></author><author><name sortKey="Poniatowska, Renata" sort="Poniatowska, Renata" uniqKey="Poniatowska R" first="Renata" last="Poniatowska">Renata Poniatowska</name><affiliation wicri:level="1"><country xml:lang="fr">Pologne</country><wicri:regionArea>Institute of Psychiatry and Neurology, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation></author><author><name sortKey="Czlonkowska, Anna" sort="Czlonkowska, Anna" uniqKey="Czlonkowska A" first="Anna" last="Czlonkowska">Anna Czlonkowska</name><affiliation wicri:level="1"><country xml:lang="fr">Pologne</country><wicri:regionArea>Institute of Psychiatry and Neurology, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Pologne</country><wicri:regionArea>Department of Clinical and Experimental Pharmacology, Medical Academy, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-09">2002-09</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1077">1077</biblScope><biblScope unit="page" to="1083">1083</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">75D5845A01858C1892211F3385291F3995BA8B56</idno><idno type="DOI">10.1002/mds.10195</idno><idno type="ArticleID">MDS10195</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Wilson's disease</term><term>basal ganglia</term><term>cognition</term><term>dementia</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We sought to determine the pattern of cognitive deficits in patients with Wilson's disease (WD) with different type and degree of neurological involvement, and to interpret the findings in relation to the underlying pathology. A total of 67 WD patients were examined with a neuropsychological test battery assessing different aspects of cognitive processing. The patients were subdivided into three groups: neurologically asymptomatic, neurological with pure basal ganglia lesions, and neurological with more extensive pathology. The results were compared with 50 matched healthy controls. Patients with a neurological form of WD showed a mild but definitive impairment in all cognitive functions. In contrast, the neurologically asymptomatic patients showed no deficits when compared with normal controls. Multifocal pathology was associated with more severe cognitive deficits than selective basal ganglia lesions but did not contribute significantly to memory impairment. A range of cognitive functions, including frontal‐executive ability, aspects of memory and visuospatial processing, are affected in the neurologically symptomatic WD patients. In contrast, no subliminal deficits were observed in the asymptomatic patients. The lesions of the basal ganglia seem to be of central importance in explaining the symptomatology. © 2002 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cognitive functioning in neurologically symptomatic and asymptomatic forms of Wilson's disease.</title><author><name sortKey="Seni W, Joanna" sort="Seni W, Joanna" uniqKey="Seni W J" first="Joanna" last="Seni W">Joanna Seni W</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Psychiatry and Neurology, Warsaw, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Institute of Psychiatry and Neurology, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation></author><author><name sortKey="Bak, Thomas" sort="Bak, Thomas" uniqKey="Bak T" first="Thomas" last="Bak">Thomas Bak</name></author><author><name sortKey="Gajda, Jolanta" sort="Gajda, Jolanta" uniqKey="Gajda J" first="Jolanta" last="Gajda">Jolanta Gajda</name></author><author><name sortKey="Poniatowska, Renata" sort="Poniatowska, Renata" uniqKey="Poniatowska R" first="Renata" last="Poniatowska">Renata Poniatowska</name></author><author><name sortKey="Czlonkowska, Anna" sort="Czlonkowska, Anna" uniqKey="Czlonkowska A" first="Anna" last="Czlonkowska">Anna Czlonkowska</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12360563</idno><idno type="pmid">12360563</idno><idno type="doi">10.1002/mds.10195</idno><idno type="wicri:Area/PubMed/Corpus">003938</idno><idno type="wicri:Area/PubMed/Curation">003938</idno><idno type="wicri:Area/PubMed/Checkpoint">003B55</idno><idno type="wicri:Area/Ncbi/Merge">000913</idno><idno type="wicri:Area/Ncbi/Curation">000913</idno><idno type="wicri:Area/Ncbi/Checkpoint">000913</idno><idno type="wicri:doubleKey">0885-3185:2002:Seni W J:cognitive:functioning:in</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cognitive functioning in neurologically symptomatic and asymptomatic forms of Wilson's disease.</title><author><name sortKey="Seni W, Joanna" sort="Seni W, Joanna" uniqKey="Seni W J" first="Joanna" last="Seni W">Joanna Seni W</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Psychiatry and Neurology, Warsaw, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Institute of Psychiatry and Neurology, Warsaw</wicri:regionArea><wicri:noRegion>Warsaw</wicri:noRegion></affiliation></author><author><name sortKey="Bak, Thomas" sort="Bak, Thomas" uniqKey="Bak T" first="Thomas" last="Bak">Thomas Bak</name></author><author><name sortKey="Gajda, Jolanta" sort="Gajda, Jolanta" uniqKey="Gajda J" first="Jolanta" last="Gajda">Jolanta Gajda</name></author><author><name sortKey="Poniatowska, Renata" sort="Poniatowska, Renata" uniqKey="Poniatowska R" first="Renata" last="Poniatowska">Renata Poniatowska</name></author><author><name sortKey="Czlonkowska, Anna" sort="Czlonkowska, Anna" uniqKey="Czlonkowska A" first="Anna" last="Czlonkowska">Anna Czlonkowska</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Basal Ganglia (pathology)</term><term>Basal Ganglia (physiopathology)</term><term>Brain (pathology)</term><term>Brain (physiopathology)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (etiology)</term><term>Female</term><term>Hepatolenticular Degeneration (complications)</term><term>Hepatolenticular Degeneration (pathology)</term><term>Hepatolenticular Degeneration (physiopathology)</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Severity of Illness Index</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Brain</term><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Brain</term><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We sought to determine the pattern of cognitive deficits in patients with Wilson's disease (WD) with different type and degree of neurological involvement, and to interpret the findings in relation to the underlying pathology. A total of 67 WD patients were examined with a neuropsychological test battery assessing different aspects of cognitive processing. The patients were subdivided into three groups: neurologically asymptomatic, neurological with pure basal ganglia lesions, and neurological with more extensive pathology. The results were compared with 50 matched healthy controls. Patients with a neurological form of WD showed a mild but definitive impairment in all cognitive functions. In contrast, the neurologically asymptomatic patients showed no deficits when compared with normal controls. Multifocal pathology was associated with more severe cognitive deficits than selective basal ganglia lesions but did not contribute significantly to memory impairment. A range of cognitive functions, including frontal-executive ability, aspects of memory and visuospatial processing, are affected in the neurologically symptomatic WD patients. In contrast, no subliminal deficits were observed in the asymptomatic patients. The lesions of the basal ganglia seem to be of central importance in explaining the symptomatology.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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