Apathy in Parkinson's disease: clinical features, neural substrates, diagnosis, and treatment.
Identifieur interne : 000513 ( PubMed/Corpus ); précédent : 000512; suivant : 000514Apathy in Parkinson's disease: clinical features, neural substrates, diagnosis, and treatment.
Auteurs : Javier Pagonabarraga ; Jaime Kulisevsky ; Antonio P. Strafella ; Paul KrackSource :
- The Lancet. Neurology [ 1474-4465 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- diagnosis : Parkinson Disease.
- physiopathology : Parkinson Disease.
- therapy : Parkinson Disease.
- Apathy, Humans, Male, Middle Aged.
Abstract
Normal maintenance of human motivation depends on the integrity of subcortical structures that link the prefrontal cortex with the limbic system. Structural and functional disruption of different networks within these circuits alters the maintenance of spontaneous mental activity and the capacity of affected individuals to associate emotions with complex stimuli. The clinical manifestations of these changes include a continuum of abnormalities in goal-oriented behaviours known as apathy. Apathy is highly prevalent in Parkinson's disease (and across many neurodegenerative disorders) and can severely affect the quality of life of both patients and caregivers. Differentiation of apathy from depression, and discrimination of its cognitive, emotional, and auto-activation components could guide an individualised approach to the treatment of symptoms. The opportunity to manipulate dopaminergic treatment in Parkinson's disease allows researchers to study a continuous range of motivational states, from apathy to impulse control disorders. Parkinson's disease can thus be viewed as a model that provides insight into the neural substrates of apathy.
DOI: 10.1016/S1474-4422(15)00019-8
PubMed: 25895932
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pubmed:25895932Le document en format XML
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Strafella</name><affiliation><nlm:affiliation>Morton and Gloria Shulman Movement Disorder Unit, E.J. Safra Parkinson Disease Program, Toronto Western Hospital and Research Institute, UHN, ON, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, CAMH, University of Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Krack, Paul" sort="Krack, Paul" uniqKey="Krack P" first="Paul" last="Krack">Paul Krack</name><affiliation><nlm:affiliation>Movement Disorder Unit, Department of Psychiatry and Neurology, CHU de Grenoble, Joseph Fourier University, Grenoble, France; INSERM, Unit 836, Grenoble Institut des Neurosciences, Grenoble, France. 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Strafella</name><affiliation><nlm:affiliation>Morton and Gloria Shulman Movement Disorder Unit, E.J. Safra Parkinson Disease Program, Toronto Western Hospital and Research Institute, UHN, ON, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, CAMH, University of Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Krack, Paul" sort="Krack, Paul" uniqKey="Krack P" first="Paul" last="Krack">Paul Krack</name><affiliation><nlm:affiliation>Movement Disorder Unit, Department of Psychiatry and Neurology, CHU de Grenoble, Joseph Fourier University, Grenoble, France; INSERM, Unit 836, Grenoble Institut des Neurosciences, Grenoble, France. Electronic address: Paul.Krack@ujf-grenoble.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The Lancet. Neurology</title><idno type="eISSN">1474-4465</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apathy</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apathy</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Normal maintenance of human motivation depends on the integrity of subcortical structures that link the prefrontal cortex with the limbic system. Structural and functional disruption of different networks within these circuits alters the maintenance of spontaneous mental activity and the capacity of affected individuals to associate emotions with complex stimuli. The clinical manifestations of these changes include a continuum of abnormalities in goal-oriented behaviours known as apathy. Apathy is highly prevalent in Parkinson's disease (and across many neurodegenerative disorders) and can severely affect the quality of life of both patients and caregivers. Differentiation of apathy from depression, and discrimination of its cognitive, emotional, and auto-activation components could guide an individualised approach to the treatment of symptoms. The opportunity to manipulate dopaminergic treatment in Parkinson's disease allows researchers to study a continuous range of motivational states, from apathy to impulse control disorders. Parkinson's disease can thus be viewed as a model that provides insight into the neural substrates of apathy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25895932</PMID><DateCreated><Year>2015</Year><Month>04</Month><Day>21</Day></DateCreated><DateCompleted><Year>2015</Year><Month>07</Month><Day>06</Day></DateCompleted><DateRevised><Year>2015</Year><Month>04</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1474-4465</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>5</Issue><PubDate><Year>2015</Year><Month>May</Month></PubDate></JournalIssue><Title>The Lancet. Neurology</Title><ISOAbbreviation>Lancet Neurol</ISOAbbreviation></Journal><ArticleTitle>Apathy in Parkinson's disease: clinical features, neural substrates, diagnosis, and treatment.</ArticleTitle><Pagination><MedlinePgn>518-31</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/S1474-4422(15)00019-8</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1474-4422(15)00019-8</ELocationID><Abstract><AbstractText>Normal maintenance of human motivation depends on the integrity of subcortical structures that link the prefrontal cortex with the limbic system. Structural and functional disruption of different networks within these circuits alters the maintenance of spontaneous mental activity and the capacity of affected individuals to associate emotions with complex stimuli. The clinical manifestations of these changes include a continuum of abnormalities in goal-oriented behaviours known as apathy. Apathy is highly prevalent in Parkinson's disease (and across many neurodegenerative disorders) and can severely affect the quality of life of both patients and caregivers. Differentiation of apathy from depression, and discrimination of its cognitive, emotional, and auto-activation components could guide an individualised approach to the treatment of symptoms. The opportunity to manipulate dopaminergic treatment in Parkinson's disease allows researchers to study a continuous range of motivational states, from apathy to impulse control disorders. Parkinson's disease can thus be viewed as a model that provides insight into the neural substrates of apathy.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pagonabarraga</LastName><ForeName>Javier</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Movement Disorders Unit, Neurology Department, Sant Pau Hospital and Biomedical Research Institute, Barcelona, Spain; Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación en Red-Enfermedades Neurodegenerativas, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kulisevsky</LastName><ForeName>Jaime</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Movement Disorders Unit, Neurology Department, Sant Pau Hospital and Biomedical Research Institute, Barcelona, Spain; Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación en Red-Enfermedades Neurodegenerativas, Madrid, Spain; Universitat Oberta de Catalunya, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Strafella</LastName><ForeName>Antonio P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Morton and Gloria Shulman Movement Disorder Unit, E.J. Safra Parkinson Disease Program, Toronto Western Hospital and Research Institute, UHN, ON, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, CAMH, University of Toronto, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krack</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Movement Disorder Unit, Department of Psychiatry and Neurology, CHU de Grenoble, Joseph Fourier University, Grenoble, France; INSERM, Unit 836, Grenoble Institut des Neurosciences, Grenoble, France. 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