Degradation of emotion processing ability in corticobasal syndrome and Alzheimer's disease.
Identifieur interne : 003349 ( PubMed/Corpus ); précédent : 003348; suivant : 003350Degradation of emotion processing ability in corticobasal syndrome and Alzheimer's disease.
Auteurs : Fiona Kumfor ; Laurie-Anne Sapey-Triomphe ; Cristian E. Leyton ; James R. Burrell ; John R. Hodges ; Olivier PiguetSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Alzheimer Disease (pathology), Alzheimer Disease (physiopathology), Amygdala (pathology), Amygdala (physiopathology), Atrophy (pathology), Basal Ganglia Diseases (pathology), Basal Ganglia Diseases (physiopathology), Cerebral Cortex (pathology), Cerebral Cortex (physiopathology), Emotions (physiology), Facial Expression, Female, Humans, Limbic System (pathology), Limbic System (physiopathology), Male, Middle Aged, Neurodegenerative Diseases (pathology), Neurodegenerative Diseases (physiopathology), Social Perception, Syndrome.
- MESH :
- pathology : Alzheimer Disease, Amygdala, Atrophy, Basal Ganglia Diseases, Cerebral Cortex, Limbic System, Neurodegenerative Diseases.
- physiology : Emotions.
- physiopathology : Alzheimer Disease, Amygdala, Basal Ganglia Diseases, Cerebral Cortex, Limbic System, Neurodegenerative Diseases.
- Aged, Facial Expression, Female, Humans, Male, Middle Aged, Social Perception, Syndrome.
Abstract
Disturbed emotion processing and difficulty with social interactions are present to variable degrees in dementia. They are characteristic features of frontotemporal dementia, whereas these deficits tend to be mild in Alzheimer's disease, reflecting the different patterns of neurodegeneration seen in these disorders. Corticobasal syndrome is an atypical parkinsonian disorder clinically and pathologically related to frontotemporal dementia. Corticobasal syndrome typically presents as a motor disturbance, although cognitive and behavioural changes are now recognized. Pathological changes are found in frontoparietal cortical regions and in the basal ganglia; regions that are heavily involved in emotion processing. Despite the overlap with frontotemporal dementia and the observed regions of brain atrophy, emotion processing has not been systematically explored in corticobasal syndrome. This study aimed to (i) comprehensively examine emotion processing in corticobasal syndrome in comparison to Alzheimer's disease, to determine whether emotion processing deficits exist in this syndrome, beyond those seen in Alzheimer's disease; and (ii) identify the neural correlates underlying emotion processing in corticobasal syndrome and Alzheimer's disease. Sixteen patients with corticobasal syndrome, 18 patients with Alzheimer's disease and 22 matched healthy control subjects were assessed on a comprehensive battery of face and emotion processing tasks. Behavioural analyses revealed deficits in both basic face processing and high-level emotion processing tasks in patients with corticobasal syndrome. Notably, the emotion processing disturbance persisted even after controlling for face processing deficits. In contrast, patients with Alzheimer's disease were impaired on high-level complex and cognitively demanding emotion recognition tasks (Ekman 60, The Awareness of Social Inference Test) only. Neuroimaging analyses using FreeSurfer revealed that emotion processing deficits in corticobasal syndrome were associated with basal ganglia volume loss as well as cortical thinning of the left paracentral gyrus/precuneus region. In Alzheimer's disease, however, emotion processing deficits were associated with atrophy in a different set of brain regions, including the right cingulate and the bilateral insulae, as well as the hippocampi, right amygdala and nucleus accumbens bilaterally. Our results demonstrate that patients with corticobasal syndrome experience widespread deficits in emotion processing, and these deficits are related to changes in brain regions known to be crucial for emotion processing. These findings have important clinical implications for the treatment and management of these patients.
DOI: 10.1093/brain/awu246
PubMed: 25227744
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pubmed:25227744Le document en format XML
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Leyton</name><affiliation><nlm:affiliation>1 Neuroscience Research Australia, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia 6 Faculty of Health Sciences, The University of Sydney, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Burrell, James R" sort="Burrell, James R" uniqKey="Burrell J" first="James R" last="Burrell">James R. Burrell</name><affiliation><nlm:affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Hodges, John R" sort="Hodges, John R" uniqKey="Hodges J" first="John R" last="Hodges">John R. 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Leyton</name><affiliation><nlm:affiliation>1 Neuroscience Research Australia, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia 6 Faculty of Health Sciences, The University of Sydney, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Burrell, James R" sort="Burrell, James R" uniqKey="Burrell J" first="James R" last="Burrell">James R. Burrell</name><affiliation><nlm:affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Hodges, John R" sort="Hodges, John R" uniqKey="Hodges J" first="John R" last="Hodges">John R. Hodges</name><affiliation><nlm:affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Piguet, Olivier" sort="Piguet, Olivier" uniqKey="Piguet O" first="Olivier" last="Piguet">Olivier Piguet</name><affiliation><nlm:affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Alzheimer Disease (pathology)</term><term>Alzheimer Disease (physiopathology)</term><term>Amygdala (pathology)</term><term>Amygdala (physiopathology)</term><term>Atrophy (pathology)</term><term>Basal Ganglia Diseases (pathology)</term><term>Basal Ganglia Diseases (physiopathology)</term><term>Cerebral Cortex (pathology)</term><term>Cerebral Cortex (physiopathology)</term><term>Emotions (physiology)</term><term>Facial Expression</term><term>Female</term><term>Humans</term><term>Limbic System (pathology)</term><term>Limbic System (physiopathology)</term><term>Male</term><term>Middle Aged</term><term>Neurodegenerative Diseases (pathology)</term><term>Neurodegenerative Diseases (physiopathology)</term><term>Social Perception</term><term>Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Amygdala</term><term>Atrophy</term><term>Basal Ganglia Diseases</term><term>Cerebral Cortex</term><term>Limbic System</term><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Emotions</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Alzheimer Disease</term><term>Amygdala</term><term>Basal Ganglia Diseases</term><term>Cerebral Cortex</term><term>Limbic System</term><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Facial Expression</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Social Perception</term><term>Syndrome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Disturbed emotion processing and difficulty with social interactions are present to variable degrees in dementia. They are characteristic features of frontotemporal dementia, whereas these deficits tend to be mild in Alzheimer's disease, reflecting the different patterns of neurodegeneration seen in these disorders. Corticobasal syndrome is an atypical parkinsonian disorder clinically and pathologically related to frontotemporal dementia. Corticobasal syndrome typically presents as a motor disturbance, although cognitive and behavioural changes are now recognized. Pathological changes are found in frontoparietal cortical regions and in the basal ganglia; regions that are heavily involved in emotion processing. Despite the overlap with frontotemporal dementia and the observed regions of brain atrophy, emotion processing has not been systematically explored in corticobasal syndrome. This study aimed to (i) comprehensively examine emotion processing in corticobasal syndrome in comparison to Alzheimer's disease, to determine whether emotion processing deficits exist in this syndrome, beyond those seen in Alzheimer's disease; and (ii) identify the neural correlates underlying emotion processing in corticobasal syndrome and Alzheimer's disease. Sixteen patients with corticobasal syndrome, 18 patients with Alzheimer's disease and 22 matched healthy control subjects were assessed on a comprehensive battery of face and emotion processing tasks. Behavioural analyses revealed deficits in both basic face processing and high-level emotion processing tasks in patients with corticobasal syndrome. Notably, the emotion processing disturbance persisted even after controlling for face processing deficits. In contrast, patients with Alzheimer's disease were impaired on high-level complex and cognitively demanding emotion recognition tasks (Ekman 60, The Awareness of Social Inference Test) only. Neuroimaging analyses using FreeSurfer revealed that emotion processing deficits in corticobasal syndrome were associated with basal ganglia volume loss as well as cortical thinning of the left paracentral gyrus/precuneus region. In Alzheimer's disease, however, emotion processing deficits were associated with atrophy in a different set of brain regions, including the right cingulate and the bilateral insulae, as well as the hippocampi, right amygdala and nucleus accumbens bilaterally. Our results demonstrate that patients with corticobasal syndrome experience widespread deficits in emotion processing, and these deficits are related to changes in brain regions known to be crucial for emotion processing. These findings have important clinical implications for the treatment and management of these patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25227744</PMID><DateCreated><Year>2014</Year><Month>10</Month><Day>25</Day></DateCreated><DateCompleted><Year>2015</Year><Month>02</Month><Day>09</Day></DateCompleted><DateRevised><Year>2014</Year><Month>10</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>137</Volume><Issue>Pt 11</Issue><PubDate><Year>2014</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Degradation of emotion processing ability in corticobasal syndrome and Alzheimer's disease.</ArticleTitle><Pagination><MedlinePgn>3061-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awu246</ELocationID><Abstract><AbstractText>Disturbed emotion processing and difficulty with social interactions are present to variable degrees in dementia. They are characteristic features of frontotemporal dementia, whereas these deficits tend to be mild in Alzheimer's disease, reflecting the different patterns of neurodegeneration seen in these disorders. Corticobasal syndrome is an atypical parkinsonian disorder clinically and pathologically related to frontotemporal dementia. Corticobasal syndrome typically presents as a motor disturbance, although cognitive and behavioural changes are now recognized. Pathological changes are found in frontoparietal cortical regions and in the basal ganglia; regions that are heavily involved in emotion processing. Despite the overlap with frontotemporal dementia and the observed regions of brain atrophy, emotion processing has not been systematically explored in corticobasal syndrome. This study aimed to (i) comprehensively examine emotion processing in corticobasal syndrome in comparison to Alzheimer's disease, to determine whether emotion processing deficits exist in this syndrome, beyond those seen in Alzheimer's disease; and (ii) identify the neural correlates underlying emotion processing in corticobasal syndrome and Alzheimer's disease. Sixteen patients with corticobasal syndrome, 18 patients with Alzheimer's disease and 22 matched healthy control subjects were assessed on a comprehensive battery of face and emotion processing tasks. Behavioural analyses revealed deficits in both basic face processing and high-level emotion processing tasks in patients with corticobasal syndrome. Notably, the emotion processing disturbance persisted even after controlling for face processing deficits. In contrast, patients with Alzheimer's disease were impaired on high-level complex and cognitively demanding emotion recognition tasks (Ekman 60, The Awareness of Social Inference Test) only. Neuroimaging analyses using FreeSurfer revealed that emotion processing deficits in corticobasal syndrome were associated with basal ganglia volume loss as well as cortical thinning of the left paracentral gyrus/precuneus region. In Alzheimer's disease, however, emotion processing deficits were associated with atrophy in a different set of brain regions, including the right cingulate and the bilateral insulae, as well as the hippocampi, right amygdala and nucleus accumbens bilaterally. Our results demonstrate that patients with corticobasal syndrome experience widespread deficits in emotion processing, and these deficits are related to changes in brain regions known to be crucial for emotion processing. These findings have important clinical implications for the treatment and management of these patients.</AbstractText><CopyrightInformation>© The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kumfor</LastName><ForeName>Fiona</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia f.kumfor@neura.edu.au.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sapey-Triomphe</LastName><ForeName>Laurie-Anne</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>1 Neuroscience Research Australia, Sydney, Australia 4 Brain Dynamics and Cognition, Lyon Neuroscience Research Centre, INSERM U1028, CNRS UMR 5292, Lyon, France 5 Ecole Normale Supérieure de Lyon, Lyon, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leyton</LastName><ForeName>Cristian E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>1 Neuroscience Research Australia, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia 6 Faculty of Health Sciences, The University of Sydney, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burrell</LastName><ForeName>James R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hodges</LastName><ForeName>John R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piguet</LastName><ForeName>Olivier</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>1 Neuroscience Research Australia, Sydney, Australia 2 School of Medical Sciences, The University of New South Wales, Sydney, Australia 3 ARC Centre of Excellence in Cognition and its Disorders, The University of New South Wales, Sydney, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>09</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000679" MajorTopicYN="N">Amygdala</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001284" MajorTopicYN="N">Atrophy</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001480" MajorTopicYN="N">Basal Ganglia Diseases</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004644" MajorTopicYN="N">Emotions</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005149" MajorTopicYN="Y">Facial Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008032" MajorTopicYN="N">Limbic System</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019636" MajorTopicYN="N">Neurodegenerative Diseases</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012938" MajorTopicYN="N">Social Perception</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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