Vascular parkinsonism: Deconstructing a syndrome
Identifieur interne : 000177 ( Pmc/Checkpoint ); précédent : 000176; suivant : 000178Vascular 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 [ 0885-3185 ] ; 2015.
Abstract
Progressive ambulatory impairment and abnormal white matter signal on neuroimaging come together under the diagnostic umbrella of vascular parkinsonism. A critical appraisal of the literature, however, suggests that (1) no abnormal structural imaging pattern is specific to vascular parkinsonism; (2) there is poor correlation between brain magnetic resonance imaging hyperintensities
Url:
DOI: 10.1002/mds.26263
PubMed: 25997420
PubMed Central: 4478160
Affiliations:
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<front><div type="abstract" xml:lang="en"><p id="P1">Progressive ambulatory impairment and abnormal white matter signal on neuroimaging come together under the diagnostic umbrella of vascular parkinsonism. A critical appraisal of the literature, however, suggests that (1) no abnormal structural imaging pattern is specific to vascular parkinsonism; (2) there is poor correlation between brain magnetic resonance imaging hyperintensities <italic>and</italic>
microangiopathic brain disease <italic>and</italic>
parkinsonism from available clinicopathologic data; (3) <italic>pure</italic>
parkinsonism from vascular injury (“definite” vascular parkinsonism) consistently results from ischemic or hemorrhagic strokes involving the substantia nigra and/or nigrostriatal pathway but sparing the striatum itself, the cortex, and the intervening white matter; and (4) many cases reported as vascular parkinsonism may represent <italic>pseudovascular</italic>
parkinsonism (e.g., Parkinson disease or another neurodegenerative parkinsonism such as progressive supranuclear palsy with non-specific neuroimaging signal abnormalities), vascular <italic>pseudoparkinsonism</italic>
(e.g., akinetic mutism due to bilateral mesial frontal strokes or apathetic depression from bilateral striatal lacunar strokes), or <italic>pseudovascular pseudoparkinsonism</italic>
(e.g., higher-level gait disorders, including normal pressure hydrocephalus with transependimal exudate). These syndromic designations are preferable over <italic>vascular parkinsonism</italic>
until pathology or validated biomarkers confirm the underlying nature and relevance of the leukoaraiosis.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8610688</journal-id>
<journal-id journal-id-type="pubmed-jr-id">5937</journal-id>
<journal-id journal-id-type="nlm-ta">Mov Disord</journal-id>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Vascular parkinsonism: Deconstructing a syndrome</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Vizcarra</surname>
<given-names>Joaquin A.</given-names>
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<contrib contrib-type="author"><name><surname>Lang</surname>
<given-names>Anthony E.</given-names>
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<contrib contrib-type="author"><name><surname>Sethi</surname>
<given-names>Kapil D</given-names>
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<xref ref-type="aff" rid="A3">3</xref>
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<contrib contrib-type="author"><name><surname>Espay</surname>
<given-names>Alberto J.</given-names>
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<aff id="A1"><label>1</label>
Facultad de Medicina “Alberto Hurtado”, Universidad Peruana Cayetano Heredia, Lima, Peru</aff>
<aff id="A2"><label>2</label>
Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson’s Disease, University Health Network, University of Toronto, Toronto, Canada</aff>
<aff id="A3"><label>3</label>
Georgia Regents University, Department of Neurology, August, Georgia; and Merz Pharmaceuticals, Raleigh, North Carolina, USA</aff>
<aff id="A4"><label>4</label>
Gardner Family Center for Parkinson’s Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio, USA</aff>
<author-notes><corresp id="CR1"><bold>All correspondence to</bold>
: Dr. Alberto J. Espay, University of Cincinnati Academic Health Center, 260 Stetson St., Suite 2300, Cincinnati, OH 45267-0525, USA, P: 513-558-4035 - F: 513-558-7015 - <email>alberto.espay@uc.edu</email>
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<pub-date pub-type="nihms-submitted"><day>29</day>
<month>4</month>
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<pub-date pub-type="epub"><day>21</day>
<month>5</month>
<year>2015</year>
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<pub-date pub-type="ppub"><month>6</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>6</month>
<year>2016</year>
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<volume>30</volume>
<issue>7</issue>
<fpage>886</fpage>
<lpage>894</lpage>
<pmc-comment>elocation-id from pubmed: 10.1002/mds.26263</pmc-comment>
<abstract><p id="P1">Progressive ambulatory impairment and abnormal white matter signal on neuroimaging come together under the diagnostic umbrella of vascular parkinsonism. A critical appraisal of the literature, however, suggests that (1) no abnormal structural imaging pattern is specific to vascular parkinsonism; (2) there is poor correlation between brain magnetic resonance imaging hyperintensities <italic>and</italic>
microangiopathic brain disease <italic>and</italic>
parkinsonism from available clinicopathologic data; (3) <italic>pure</italic>
parkinsonism from vascular injury (“definite” vascular parkinsonism) consistently results from ischemic or hemorrhagic strokes involving the substantia nigra and/or nigrostriatal pathway but sparing the striatum itself, the cortex, and the intervening white matter; and (4) many cases reported as vascular parkinsonism may represent <italic>pseudovascular</italic>
parkinsonism (e.g., Parkinson disease or another neurodegenerative parkinsonism such as progressive supranuclear palsy with non-specific neuroimaging signal abnormalities), vascular <italic>pseudoparkinsonism</italic>
(e.g., akinetic mutism due to bilateral mesial frontal strokes or apathetic depression from bilateral striatal lacunar strokes), or <italic>pseudovascular pseudoparkinsonism</italic>
(e.g., higher-level gait disorders, including normal pressure hydrocephalus with transependimal exudate). These syndromic designations are preferable over <italic>vascular parkinsonism</italic>
until pathology or validated biomarkers confirm the underlying nature and relevance of the leukoaraiosis.</p>
</abstract>
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