The detection of preclinical Parkinson's disease: what is the role of positron emission tomography?
Identifieur interne : 004C20 ( PubMed/Curation ); précédent : 004C19; suivant : 004C21The detection of preclinical Parkinson's disease: what is the role of positron emission tomography?
Auteurs : G V Sawle [Royaume-Uni]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
- Blood-Brain Barrier, Brain (metabolism), Brain (physiopathology), Brain (radionuclide imaging), Diagnosis, Differential, Dopamine (metabolism), Female, Humans, Levodopa (pharmacokinetics), Lewy Bodies, Male, Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Parkinson Disease (radionuclide imaging), Prospective Studies, Tomography, Emission-Computed (methods).
- MESH :
- chemical , metabolism : Dopamine.
- metabolism : Brain, Parkinson Disease.
- methods : Tomography, Emission-Computed.
- chemical , pharmacokinetics : Levodopa.
- physiopathology : Brain, Parkinson Disease.
- radionuclide imaging : Brain, Parkinson Disease.
- Blood-Brain Barrier, Diagnosis, Differential, Female, Humans, Lewy Bodies, Male, Prospective Studies.
Abstract
On clinical criteria alone, the diagnosis of early Parkinson's disease can be difficult and, by definition, the prospective recognition of preclinical Parkinson's disease is impossible. Positron emission tomography (PET) using [18F]dopa as tracer has been proposed as a means of identifying patients with preclinical disease. The number of subjects detected to date has been few; most have been identified by serendipity or during the course of family studies. This review examines the significance of a single abnormal scan in an apparently healthy subject in terms of the relationship between normal and abnormal values and the time course of the disease.
DOI: 10.1002/mds.870080304
PubMed: 8341290
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Positron emission tomography (PET) using [18F]dopa as tracer has been proposed as a means of identifying patients with preclinical disease. The number of subjects detected to date has been few; most have been identified by serendipity or during the course of family studies. This review examines the significance of a single abnormal scan in an apparently healthy subject in terms of the relationship between normal and abnormal values and the time course of the disease.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8341290</PMID><DateCreated><Year>1993</Year><Month>09</Month><Day>02</Day></DateCreated><DateCompleted><Year>1993</Year><Month>09</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><Issue>3</Issue><PubDate><Year>1993</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>The detection of preclinical Parkinson's disease: what is the role of positron emission tomography?</ArticleTitle><Pagination><MedlinePgn>271-7</MedlinePgn></Pagination><Abstract><AbstractText>On clinical criteria alone, the diagnosis of early Parkinson's disease can be difficult and, by definition, the prospective recognition of preclinical Parkinson's disease is impossible. Positron emission tomography (PET) using [18F]dopa as tracer has been proposed as a means of identifying patients with preclinical disease. The number of subjects detected to date has been few; most have been identified by serendipity or during the course of family studies. This review examines the significance of a single abnormal scan in an apparently healthy subject in terms of the relationship between normal and abnormal values and the time course of the disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sawle</LastName><ForeName>G V</ForeName><Initials>GV</Initials><AffiliationInfo><Affiliation>Clinical Sciences Section, Hammersmith Hospital, London, England.</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><ChemicalList><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001812">Blood-Brain Barrier</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003937">Diagnosis, Differential</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000493">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016631">Lewy Bodies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011446">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014055">Tomography, Emission-Computed</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000379">methods</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>67</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1993</Year><Month>7</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8341290</ArticleId><ArticleId IdType="doi">10.1002/mds.870080304</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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