A Scan Without Evidence Is Not Evidence of Absence: Scans Without Evidence of Dopaminergic Deficit in a Symptomatic Leucine-Rich repeat Kinase 2 Mutation Carrier
Identifieur interne : 000846 ( Pmc/Curation ); précédent : 000845; suivant : 000847A Scan Without Evidence Is Not Evidence of Absence: Scans Without Evidence of Dopaminergic Deficit in a Symptomatic Leucine-Rich repeat Kinase 2 Mutation Carrier
Auteurs : Daryl J. Wile [Canada] ; Katie Dinelle [Canada] ; Nasim Vafai [Canada] ; Jessamyn Mckenzie [Canada] ; Joseph K. Tsui [Canada] ; Paul Schaffer [Canada] ; Yu-Shin Ding [États-Unis] ; Matthew Farrer [Canada] ; Vesna Sossi [Canada] ; A. Jon Stoessl [Canada]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2015.
Abstract
The basis for SWEDD is unclear, with most cases representing PD mimics but some later developing PD with a dopaminergic deficit.
We studied a patient initially diagnosed with SWEDD (based on 18F-dopa PET) who developed unequivocal PD associated with a leucine-rich repeat kinase 2 p.G2019S mutation. Repeat multitracer PET was performed at 17 years’ disease duration, including (+)[11C]dihydrotetrabenazine, [11C](N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine (which binds the serotonin transporter), and 18F-dopa.
The patient showed bilateral striatal dopaminergic denervation (right putamen 28% of age-matched normal, left putamen 33%). 18F-dopa uptake was decreased, particularly on the left (mean 31% of normal vs. 45% on the more affected right side). Serotonin transporter binding was relatively preserved in the putamen (right mean 90% of normal, left 81%) and several cortical regions.
SWEDD can occur in genetically determined PD and may, in some cases, be the result of compensatory nondopaminergic mechanisms operating in early disease.
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DOI: 10.1002/mds.26450
PubMed: 26685774
PubMed Central: 4894497
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Wile</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Dinelle, Katie" sort="Dinelle, Katie" uniqKey="Dinelle K" first="Katie" last="Dinelle">Katie Dinelle</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Vafai, Nasim" sort="Vafai, Nasim" uniqKey="Vafai N" first="Nasim" last="Vafai">Nasim Vafai</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Mckenzie, Jessamyn" sort="Mckenzie, Jessamyn" uniqKey="Mckenzie J" first="Jessamyn" last="Mckenzie">Jessamyn Mckenzie</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Tsui, Joseph K" sort="Tsui, Joseph K" uniqKey="Tsui J" first="Joseph K." last="Tsui">Joseph K. Tsui</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Schaffer, Paul" sort="Schaffer, Paul" uniqKey="Schaffer P" first="Paul" last="Schaffer">Paul Schaffer</name><affiliation wicri:level="1"><nlm:aff id="A2">TRIUMF, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>TRIUMF, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Ding, Yu Shin" sort="Ding, Yu Shin" uniqKey="Ding Y" first="Yu-Shin" last="Ding">Yu-Shin Ding</name><affiliation wicri:level="1"><nlm:aff id="A3">New York University School of Medicine, New York, New York, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>New York University School of Medicine, New York, New York</wicri:regionArea></affiliation></author><author><name sortKey="Farrer, Matthew" sort="Farrer, Matthew" uniqKey="Farrer M" first="Matthew" last="Farrer">Matthew Farrer</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A. Jon" last="Stoessl">A. Jon Stoessl</name><affiliation wicri:level="1"><nlm:aff id="A1">University of British Columbia, Vancouver, BC, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of British Columbia, Vancouver, BC</wicri:regionArea></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Introduction</title><p id="P1">The basis for SWEDD is unclear, with most cases representing PD mimics but some later developing PD with a dopaminergic deficit.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We studied a patient initially diagnosed with SWEDD (based on <sup>18</sup>F-dopa PET) who developed unequivocal PD associated with a leucine-rich repeat kinase 2 p.G2019S mutation. Repeat multitracer PET was performed at 17 years’ disease duration, including (+)[11C]dihydrotetrabenazine, [11C](N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine (which binds the serotonin transporter), and <sup>18</sup>F-dopa.</p></sec><sec id="S3"><title>Results</title><p id="P3">The patient showed bilateral striatal dopaminergic denervation (right putamen 28% of age-matched normal, left putamen 33%). <sup>18</sup>F-dopa uptake was decreased, particularly on the left (mean 31% of normal vs. 45% on the more affected right side). Serotonin transporter binding was relatively preserved in the putamen (right mean 90% of normal, left 81%) and several cortical regions.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">SWEDD can occur in genetically determined PD and may, in some cases, be the result of compensatory nondopaminergic mechanisms operating in early disease.</p></sec></div></front></TEI><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>
<pmc-dir>properties manuscript</pmc-dir>
<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><journal-id journal-id-type="iso-abbrev">Mov. Disord.</journal-id><journal-title-group><journal-title>Movement disorders : official journal of the Movement Disorder Society</journal-title></journal-title-group><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn></journal-meta><article-meta><article-id pub-id-type="pmid">26685774</article-id><article-id pub-id-type="pmc">4894497</article-id><article-id pub-id-type="doi">10.1002/mds.26450</article-id><article-id pub-id-type="manuscript">NIHMS790350</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>A Scan Without Evidence Is Not Evidence of Absence: Scans Without Evidence of Dopaminergic Deficit in a Symptomatic Leucine-Rich repeat Kinase 2 Mutation Carrier</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wile</surname><given-names>Daryl J.</given-names></name><degrees>MD, MSc</degrees><xref ref-type="aff" rid="A1">1</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib><contrib contrib-type="author"><name><surname>Dinelle</surname><given-names>Katie</given-names></name><degrees>MSc</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Vafai</surname><given-names>Nasim</given-names></name><degrees>MASc</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>McKenzie</surname><given-names>Jessamyn</given-names></name><degrees>LPN</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tsui</surname><given-names>Joseph K.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Schaffer</surname><given-names>Paul</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Ding</surname><given-names>Yu-Shin</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Farrer</surname><given-names>Matthew</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Sossi</surname><given-names>Vesna</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Stoessl</surname><given-names>A. Jon</given-names></name><degrees>MD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>University of British Columbia, Vancouver, BC, Canada</aff><aff id="A2"><label>2</label>TRIUMF, Vancouver, BC, Canada</aff><aff id="A3"><label>3</label>New York University School of Medicine, New York, New York, USA</aff><author-notes><corresp id="FN1"><label>*</label>Correspondence to: Dr. Daryl J. Wile, Pacific Parkinson’s Research Center, M36-2221 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5; <email>daryl.wile@ubc.ca</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>27</day><month>5</month><year>2016</year></pub-date><pub-date pub-type="epub"><day>21</day><month>12</month><year>2015</year></pub-date><pub-date pub-type="ppub"><month>3</month><year>2016</year></pub-date><pub-date pub-type="pmc-release"><day>06</day><month>6</month><year>2016</year></pub-date><volume>31</volume><issue>3</issue><fpage>405</fpage><lpage>409</lpage><pmc-comment>elocation-id from pubmed: 10.1002/mds.26450</pmc-comment>
<abstract><sec id="S1"><title>Introduction</title><p id="P1">The basis for SWEDD is unclear, with most cases representing PD mimics but some later developing PD with a dopaminergic deficit.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We studied a patient initially diagnosed with SWEDD (based on <sup>18</sup>F-dopa PET) who developed unequivocal PD associated with a leucine-rich repeat kinase 2 p.G2019S mutation. Repeat multitracer PET was performed at 17 years’ disease duration, including (+)[11C]dihydrotetrabenazine, [11C](N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine (which binds the serotonin transporter), and <sup>18</sup>F-dopa.</p></sec><sec id="S3"><title>Results</title><p id="P3">The patient showed bilateral striatal dopaminergic denervation (right putamen 28% of age-matched normal, left putamen 33%). <sup>18</sup>F-dopa uptake was decreased, particularly on the left (mean 31% of normal vs. 45% on the more affected right side). Serotonin transporter binding was relatively preserved in the putamen (right mean 90% of normal, left 81%) and several cortical regions.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">SWEDD can occur in genetically determined PD and may, in some cases, be the result of compensatory nondopaminergic mechanisms operating in early disease.</p></sec></abstract><kwd-group><kwd>SWEDD</kwd><kwd>LRRK2</kwd><kwd>Parkinson’s disease</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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