Selective dysfunction of basal ganglia subterritories: From movement to behavioral disorders.
Identifieur interne : 000318 ( PubMed/Corpus ); précédent : 000317; suivant : 000319Selective dysfunction of basal ganglia subterritories: From movement to behavioral disorders.
Auteurs : Léon Tremblay ; Yulia Worbe ; Stéphane Thobois ; Véronique Sgambato-Faure ; Jean FégerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- pathology : Basal Ganglia, Mental Disorders, Movement Disorders, Nerve Net.
- physiopathology : Basal Ganglia.
- Animals, Humans.
Abstract
Historically, Parkinson's disease (PD) was defined as a pure movement disorder. Currently, it is widely accepted that this disease is also characterized by nonmotor signs, such as depression, apathy, and anxiety. On the other hand, the consideration of Gilles de la Tourette syndrome (GTS) as a neuropsychiatric disorder has also been debated. In this review, we will focus on these two disorders, which combine both motor and behavioral features and in which dysfunction of cortical and subcortical regions was suggested. Anatomical, experimental, and clinical data are reported to support the involvement of basal ganglia (BG) in cognitive and motivational functions in addition to motor control. In PD, the nonmotor signs could result from the heterogeneity of dopaminergic lesions and excessive activation of the dopamine receptors, particularly within the limbic neuronal networks. Experimental results obtained on nonhuman primates using local disinhibition within functional territories of BG allowed the precise mapping of their motor and nonmotor functions. Thus, impairment of inhibitory control inside specific striatal territories induced behavioral disorders and abnormal movements, which had striking similarities to clinical expressions of GTS. Establishing such a relationship between BG subterritories and motor and behavioral disorders could potentially be helpful for future target choices for DBS in many neuropsychiatric disorders. Furthermore, it is also of great interest for therapeutic research and for the efficient targeting of symptom relief to determine the precise pharmacological effects of the two main modulators of BG function, which are dopamine and serotonin.
DOI: 10.1002/mds.26199
PubMed: 25772380
Links to Exploration step
pubmed:25772380Le document en format XML
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Currently, it is widely accepted that this disease is also characterized by nonmotor signs, such as depression, apathy, and anxiety. On the other hand, the consideration of Gilles de la Tourette syndrome (GTS) as a neuropsychiatric disorder has also been debated. In this review, we will focus on these two disorders, which combine both motor and behavioral features and in which dysfunction of cortical and subcortical regions was suggested. Anatomical, experimental, and clinical data are reported to support the involvement of basal ganglia (BG) in cognitive and motivational functions in addition to motor control. In PD, the nonmotor signs could result from the heterogeneity of dopaminergic lesions and excessive activation of the dopamine receptors, particularly within the limbic neuronal networks. Experimental results obtained on nonhuman primates using local disinhibition within functional territories of BG allowed the precise mapping of their motor and nonmotor functions. Thus, impairment of inhibitory control inside specific striatal territories induced behavioral disorders and abnormal movements, which had striking similarities to clinical expressions of GTS. Establishing such a relationship between BG subterritories and motor and behavioral disorders could potentially be helpful for future target choices for DBS in many neuropsychiatric disorders. Furthermore, it is also of great interest for therapeutic research and for the efficient targeting of symptom relief to determine the precise pharmacological effects of the two main modulators of BG function, which are dopamine and serotonin.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25772380</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>17</Day></DateCreated><DateCompleted><Year>2016</Year><Month>06</Month><Day>08</Day></DateCompleted><DateRevised><Year>2015</Year><Month>09</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>9</Issue><PubDate><Year>2015</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Selective dysfunction of basal ganglia subterritories: From movement to behavioral disorders.</ArticleTitle><Pagination><MedlinePgn>1155-70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26199</ELocationID><Abstract><AbstractText>Historically, Parkinson's disease (PD) was defined as a pure movement disorder. Currently, it is widely accepted that this disease is also characterized by nonmotor signs, such as depression, apathy, and anxiety. On the other hand, the consideration of Gilles de la Tourette syndrome (GTS) as a neuropsychiatric disorder has also been debated. In this review, we will focus on these two disorders, which combine both motor and behavioral features and in which dysfunction of cortical and subcortical regions was suggested. Anatomical, experimental, and clinical data are reported to support the involvement of basal ganglia (BG) in cognitive and motivational functions in addition to motor control. In PD, the nonmotor signs could result from the heterogeneity of dopaminergic lesions and excessive activation of the dopamine receptors, particularly within the limbic neuronal networks. Experimental results obtained on nonhuman primates using local disinhibition within functional territories of BG allowed the precise mapping of their motor and nonmotor functions. Thus, impairment of inhibitory control inside specific striatal territories induced behavioral disorders and abnormal movements, which had striking similarities to clinical expressions of GTS. Establishing such a relationship between BG subterritories and motor and behavioral disorders could potentially be helpful for future target choices for DBS in many neuropsychiatric disorders. Furthermore, it is also of great interest for therapeutic research and for the efficient targeting of symptom relief to determine the precise pharmacological effects of the two main modulators of BG function, which are dopamine and serotonin.</AbstractText><CopyrightInformation>© 2015 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tremblay</LastName><ForeName>Léon</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Centre de Neurosciences Cognitives-UMR 5229, CNRS-Université de Lyon 1, Bron, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Worbe</LastName><ForeName>Yulia</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>UPMC Université Paris 6, UMR-S975, CRICM-Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thobois</LastName><ForeName>Stéphane</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Centre de Neurosciences Cognitives-UMR 5229, CNRS-Université de Lyon 1, Bron, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hospices Civils de Lyon, Hopital Neurologique Pierre Wertheimer, Neurologie C, Lyon, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université de Lyon, Université Claude Bernard Lyon 1, Faculté de Médecine Lyon Sud Charles Mérieux, Lyon, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sgambato-Faure</LastName><ForeName>Véronique</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Centre de Neurosciences Cognitives-UMR 5229, CNRS-Université de Lyon 1, Bron, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Féger</LastName><ForeName>Jean</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>UPMC Université Paris 6, UMR-S975, CRICM-Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Paris, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>03</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000473" 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