Vascular Parkinsonism: deconstructing a syndrome.
Identifieur interne : 000487 ( PubMed/Curation ); précédent : 000486; suivant : 000488Vascular Parkinsonism: deconstructing a syndrome.
Auteurs : Joaquin A. Vizcarra [Pérou] ; Anthony E. Lang [Canada] ; Kapil D. Sethi [États-Unis] ; Alberto J. Espay [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- classification : Cerebrovascular Disorders, Parkinsonian Disorders.
- pathology : Cerebrovascular Disorders, Parkinsonian Disorders.
- physiopathology : Cerebrovascular Disorders, Parkinsonian Disorders.
- Humans, Syndrome.
Abstract
Progressive ambulatory impairment and abnormal white matter (WM) signal on neuroimaging come together under the diagnostic umbrella of vascular parkinsonism (VaP). A critical appraisal of the literature, however, suggests that (1) no abnormal structural imaging pattern is specific to VaP; (2) there is poor correlation between brain MRI hyperintensities and microangiopathic brain disease and parkinsonism from available clinicopathologic data; (3) pure parkinsonism from vascular injury ("definite" vascular parkinsonism) consistently results from ischemic or hemorrhagic strokes involving the SN and/or nigrostriatal pathway, but sparing the striatum itself, the cortex, and the intervening WM; and (4) many cases reported as VaP may represent pseudovascular parkinsonism (e.g., Parkinson's disease or another neurodegenerative parkinsonism, such as PSP with nonspecific neuroimaging signal abnormalities), vascular pseudoparkinsonism (e.g., akinetic mutism resulting from bilateral mesial frontal strokes or apathetic depression from bilateral striatal lacunar strokes), or pseudovascular pseudoparkinsonism (e.g., higher-level gait disorders, including normal-pressure hydrocephalus with transependimal exudate). These syndromic designations are preferable over VaP until pathology or validated biomarkers confirm the underlying nature and relevance of the leukoaraiosis. © 2015 International Parkinson and Movement Disorder Society.
DOI: 10.1002/mds.26263
PubMed: 25997420
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Vizcarra</name><affiliation wicri:level="1"><nlm:affiliation>Facultad de Medicina "Alberto Hurtado", Universidad Peruana Cayetano Heredia, Lima, Peru.</nlm:affiliation><country xml:lang="fr">Pérou</country><wicri:regionArea>Facultad de Medicina "Alberto Hurtado", Universidad Peruana Cayetano Heredia, Lima</wicri:regionArea></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name><affiliation wicri:level="1"><nlm:affiliation>Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, University Health Network, University of Toronto, Toronto, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, University Health Network, University of Toronto, Toronto</wicri:regionArea></affiliation></author><author><name sortKey="Sethi, Kapil D" sort="Sethi, Kapil D" uniqKey="Sethi K" first="Kapil D" last="Sethi">Kapil D. Sethi</name><affiliation wicri:level="1"><nlm:affiliation>Georgia Regents University, Department of Neurology, August, Georgia, USA; and Merz Pharmaceuticals, Raleigh, North Carolina, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Georgia Regents University, Department of Neurology, August, Georgia, USA; and Merz Pharmaceuticals, Raleigh, North Carolina</wicri:regionArea></affiliation></author><author><name sortKey="Espay, Alberto J" sort="Espay, Alberto J" uniqKey="Espay A" first="Alberto J" last="Espay">Alberto J. Espay</name><affiliation wicri:level="1"><nlm:affiliation>Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio</wicri:regionArea></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cerebrovascular Disorders (classification)</term><term>Cerebrovascular Disorders (pathology)</term><term>Cerebrovascular Disorders (physiopathology)</term><term>Humans</term><term>Parkinsonian Disorders (classification)</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Syndrome</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Cerebrovascular Disorders</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebrovascular Disorders</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebrovascular Disorders</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Syndrome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Progressive ambulatory impairment and abnormal white matter (WM) signal on neuroimaging come together under the diagnostic umbrella of vascular parkinsonism (VaP). A critical appraisal of the literature, however, suggests that (1) no abnormal structural imaging pattern is specific to VaP; (2) there is poor correlation between brain MRI hyperintensities and microangiopathic brain disease and parkinsonism from available clinicopathologic data; (3) pure parkinsonism from vascular injury ("definite" vascular parkinsonism) consistently results from ischemic or hemorrhagic strokes involving the SN and/or nigrostriatal pathway, but sparing the striatum itself, the cortex, and the intervening WM; and (4) many cases reported as VaP may represent pseudovascular parkinsonism (e.g., Parkinson's disease or another neurodegenerative parkinsonism, such as PSP with nonspecific neuroimaging signal abnormalities), vascular pseudoparkinsonism (e.g., akinetic mutism resulting from bilateral mesial frontal strokes or apathetic depression from bilateral striatal lacunar strokes), or pseudovascular pseudoparkinsonism (e.g., higher-level gait disorders, including normal-pressure hydrocephalus with transependimal exudate). These syndromic designations are preferable over VaP until pathology or validated biomarkers confirm the underlying nature and relevance of the leukoaraiosis. © 2015 International Parkinson and Movement Disorder Society.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25997420</PMID><DateCreated><Year>2015</Year><Month>06</Month><Day>23</Day></DateCreated><DateCompleted><Year>2016</Year><Month>04</Month><Day>04</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>7</Issue><PubDate><Year>2015</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Vascular Parkinsonism: deconstructing a syndrome.</ArticleTitle><Pagination><MedlinePgn>886-94</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26263</ELocationID><Abstract><AbstractText>Progressive ambulatory impairment and abnormal white matter (WM) signal on neuroimaging come together under the diagnostic umbrella of vascular parkinsonism (VaP). A critical appraisal of the literature, however, suggests that (1) no abnormal structural imaging pattern is specific to VaP; (2) there is poor correlation between brain MRI hyperintensities and microangiopathic brain disease and parkinsonism from available clinicopathologic data; (3) pure parkinsonism from vascular injury ("definite" vascular parkinsonism) consistently results from ischemic or hemorrhagic strokes involving the SN and/or nigrostriatal pathway, but sparing the striatum itself, the cortex, and the intervening WM; and (4) many cases reported as VaP may represent pseudovascular parkinsonism (e.g., Parkinson's disease or another neurodegenerative parkinsonism, such as PSP with nonspecific neuroimaging signal abnormalities), vascular pseudoparkinsonism (e.g., akinetic mutism resulting from bilateral mesial frontal strokes or apathetic depression from bilateral striatal lacunar strokes), or pseudovascular pseudoparkinsonism (e.g., higher-level gait disorders, including normal-pressure hydrocephalus with transependimal exudate). These syndromic designations are preferable over VaP until pathology or validated biomarkers confirm the underlying nature and relevance of the leukoaraiosis. © 2015 International Parkinson and Movement Disorder Society.</AbstractText><CopyrightInformation>© 2015 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vizcarra</LastName><ForeName>Joaquin A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Facultad de Medicina "Alberto Hurtado", Universidad Peruana Cayetano Heredia, Lima, Peru.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Anthony E</ForeName><Initials>AE</Initials><AffiliationInfo><Affiliation>Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, University Health Network, University of Toronto, Toronto, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sethi</LastName><ForeName>Kapil D</ForeName><Initials>KD</Initials><AffiliationInfo><Affiliation>Georgia Regents University, Department of Neurology, August, Georgia, USA; and Merz Pharmaceuticals, Raleigh, North Carolina, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Espay</LastName><ForeName>Alberto J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K23 MH092735</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>05</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2006 Jan;21(1):124-5</RefSource><PMID Version="1">16229001</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroepidemiology. 1994;13(3):108-12</RefSource><PMID Version="1">8015663</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 1997 May;12(3):302-5</RefSource><PMID Version="1">9159723</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Magn Reson Med Sci. 2006 Jul;5(2):99-104</RefSource><PMID Version="1">17008766</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Sci. 2008 Apr 15;267(1-2):166-9</RefSource><PMID Version="1">17996905</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2015 Feb;138(Pt 2):284-92</RefSource><PMID Version="1">25527826</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Adv Neurol. 1996;69:293-303</RefSource><PMID Version="1">8615141</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosurgery. 1996 Aug;39(2):292-9; 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