Dysautonomia and cognitive dysfunction in Parkinson's disease.
Identifieur interne : 002850 ( PubMed/Checkpoint ); précédent : 002849; suivant : 002851Dysautonomia and cognitive dysfunction in Parkinson's disease.
Auteurs : Werner Poewe [Autriche]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Cognition Disorders (diagnosis), Cognition Disorders (epidemiology), Constipation (epidemiology), Diagnosis, Differential, Female, Female Urogenital Diseases (epidemiology), Humans, Male, Male Urogenital Diseases (epidemiology), Parkinson Disease (diagnosis), Parkinson Disease (epidemiology), Shy-Drager Syndrome (epidemiology).
- MESH :
- diagnosis : Cognition Disorders, Parkinson Disease.
- epidemiology : Cognition Disorders, Constipation, Female Urogenital Diseases, Male Urogenital Diseases, Parkinson Disease, Shy-Drager Syndrome.
- Diagnosis, Differential, Female, Humans, Male.
Abstract
Nonmotor symptoms have recently become a focus of renewed clinical interest and research in Parkinson's disease (PD). Autonomic and cognitive dysfunction are among the most prevalent of these nonmotor aspects of the disease. Although exact clinico-pathological correlations have not been established, alpha-synuclein pathology with Lewy body formation in the central and peripheral autonomic nervous system as well as in neocortical areas are generally believed to be driving factors for autonomic failure and cognitive decline in PD. Recent pathological and clinical studies have suggested greater prevalence of clinical dysautonomia and cardiac sympathetic denervation in PD dementia and dementia with Lewy bodies as compared with PD without dementia. This raises the possibility that spread of synuclein pathology to involve neocortical areas producing cognitive decline could be somehow linked to involvement of the autonomic nervous system in PD.
DOI: 10.1002/mds.21681
PubMed: 18175399
Affiliations:
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Autonomic and cognitive dysfunction are among the most prevalent of these nonmotor aspects of the disease. Although exact clinico-pathological correlations have not been established, alpha-synuclein pathology with Lewy body formation in the central and peripheral autonomic nervous system as well as in neocortical areas are generally believed to be driving factors for autonomic failure and cognitive decline in PD. Recent pathological and clinical studies have suggested greater prevalence of clinical dysautonomia and cardiac sympathetic denervation in PD dementia and dementia with Lewy bodies as compared with PD without dementia. This raises the possibility that spread of synuclein pathology to involve neocortical areas producing cognitive decline could be somehow linked to involvement of the autonomic nervous system in PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18175399</PMID><DateCreated><Year>2008</Year><Month>01</Month><Day>04</Day></DateCreated><DateCompleted><Year>2008</Year><Month>02</Month><Day>20</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>22 Suppl 17</Volume><PubDate><Year>2007</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Dysautonomia and cognitive dysfunction in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>S374-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.21681</ELocationID><Abstract><AbstractText>Nonmotor symptoms have recently become a focus of renewed clinical interest and research in Parkinson's disease (PD). Autonomic and cognitive dysfunction are among the most prevalent of these nonmotor aspects of the disease. Although exact clinico-pathological correlations have not been established, alpha-synuclein pathology with Lewy body formation in the central and peripheral autonomic nervous system as well as in neocortical areas are generally believed to be driving factors for autonomic failure and cognitive decline in PD. Recent pathological and clinical studies have suggested greater prevalence of clinical dysautonomia and cardiac sympathetic denervation in PD dementia and dementia with Lewy bodies as compared with PD without dementia. This raises the possibility that spread of synuclein pathology to involve neocortical areas producing cognitive decline could be somehow linked to involvement of the autonomic nervous system in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Poewe</LastName><ForeName>Werner</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. werner.poewe@uibk.ac.at</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003072">Cognition Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003248">Constipation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003937">Diagnosis, Differential</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D052776">Female Urogenital Diseases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D052801">Male Urogenital Diseases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012791">Shy-Drager Syndrome</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>42</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>1</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>2</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>1</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18175399</ArticleId><ArticleId IdType="doi">10.1002/mds.21681</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Autriche</li></country><region><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="Autriche"><region name="Tyrol (Land)"><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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