Neuroleptic‐induced Parkinsonism: Clinicopathological study
Identifieur interne : 000A39 ( Pmc/Curation ); précédent : 000A38; suivant : 000A40Neuroleptic‐induced Parkinsonism: Clinicopathological study
Auteurs : Umar A. Shuaib ; Ali H. Rajput ; Christopher A. Robinson ; Alex RajputSource :
- Movement Disorders [ 0885-3185 ] ; 2015.
Abstract
Drug‐induced parkinsonism is a well‐known complication of several different drugs—the most common being neuroleptic‐induced parkinsonism. However, very few autopsies have been reported in such cases.
Patients assessed at Movement Disorders Clinic Saskatchewan are offered brain autopsy. Detailed clinical records are kept.
Brains were obtained from 7 drug‐induced parkinsonism patients with parkinsonian symptom onset coinciding with use of drugs known to produce parkinsonism. Six were on antipsychotics and 1 was on metoclopramide. Three cases were treated with levodopa for parkinsonism. In two cases, parkinsonian features reversed after stopping the offending agent. Both had autopsy evidence of preclinical PD. In 4 of the remaining 5, dopamine‐blocking drugs were continued until death. In 4 of those 5, brain histology revealed no cause for the parkinsonism, but 1 had mild SN neuronal loss without Lewy bodies.
This study shows that reversal of parkinsonism after discontinuing offending drugs does not indicate absence of underlying pathology. Neuroleptics can unmask preclinical PD in patients with insufficient SN damage for the disease to manifest clinically. Though the mechanism of sustained parkinsonian features after discontinuing neuroleptics remains to be established, it is unlikely that dopamine receptor block leads to retrograde SN neuronal degeneration. Furthermore,
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DOI: 10.1002/mds.26467
PubMed: 26660063
PubMed Central: 5064745
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Robinson</name><affiliation><nlm:aff id="mds26467-aff-0003"></nlm:aff></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation><nlm:aff id="mds26467-aff-0002"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">26660063</idno><idno type="pmc">5064745</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064745</idno><idno type="RBID">PMC:5064745</idno><idno type="doi">10.1002/mds.26467</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000A39</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000A39</idno><idno type="wicri:Area/Pmc/Curation">000A39</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000A39</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Neuroleptic‐induced <styled-content style="fixed-case">P</styled-content>arkinsonism: <styled-content style="fixed-case">C</styled-content>linicopathological study</title><author><name sortKey="Shuaib, Umar A" sort="Shuaib, Umar A" uniqKey="Shuaib U" first="Umar A." last="Shuaib">Umar A. Shuaib</name><affiliation><nlm:aff id="mds26467-aff-0001"></nlm:aff></affiliation></author><author><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H." last="Rajput">Ali H. Rajput</name><affiliation><nlm:aff id="mds26467-aff-0002"></nlm:aff></affiliation></author><author><name sortKey="Robinson, Christopher A" sort="Robinson, Christopher A" uniqKey="Robinson C" first="Christopher A." last="Robinson">Christopher A. Robinson</name><affiliation><nlm:aff id="mds26467-aff-0003"></nlm:aff></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation><nlm:aff id="mds26467-aff-0002"></nlm:aff></affiliation></author></analytic><series><title level="j">Movement Disorders</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"><title>ABSTRACT</title><sec id="mds26467-sec-0001"><title>Background</title><p>Drug‐induced parkinsonism is a well‐known complication of several different drugs—the most common being neuroleptic‐induced parkinsonism. However, very few autopsies have been reported in such cases.</p></sec><sec id="mds26467-sec-0002"><title>Methods</title><p>Patients assessed at Movement Disorders Clinic Saskatchewan are offered brain autopsy. Detailed clinical records are kept.</p></sec><sec id="mds26467-sec-0003"><title>Results</title><p>Brains were obtained from 7 drug‐induced parkinsonism patients with parkinsonian symptom onset coinciding with use of drugs known to produce parkinsonism. Six were on antipsychotics and 1 was on metoclopramide. Three cases were treated with levodopa for parkinsonism. In two cases, parkinsonian features reversed after stopping the offending agent. Both had autopsy evidence of preclinical PD. In 4 of the remaining 5, dopamine‐blocking drugs were continued until death. In 4 of those 5, brain histology revealed no cause for the parkinsonism, but 1 had mild SN neuronal loss without Lewy bodies.</p></sec><sec id="mds26467-sec-0004"><title>Conclusion</title><p>This study shows that reversal of parkinsonism after discontinuing offending drugs does not indicate absence of underlying pathology. Neuroleptics can unmask preclinical PD in patients with insufficient SN damage for the disease to manifest clinically. Though the mechanism of sustained parkinsonian features after discontinuing neuroleptics remains to be established, it is unlikely that dopamine receptor block leads to retrograde SN neuronal degeneration. Furthermore, <sc>l</sc>‐dopa does not appear to be toxic to SN. © 2015 International Parkinson and Movement Disorder Society</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Lang, Ae" uniqKey="Lang A">AE Lang</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Factor, Sa" uniqKey="Factor S">SA Factor</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Factor, Sa" uniqKey="Factor S">SA Factor</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Fahn, S" uniqKey="Fahn S">S Fahn</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Marsden, Cd" uniqKey="Marsden C">CD Marsden</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Mcdowell, Fh" uniqKey="Mcdowell F">FH McDowell</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Factor, Sa" uniqKey="Factor S">SA Factor</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mov Disord</journal-id><journal-id journal-id-type="iso-abbrev">Mov. Disord</journal-id><journal-id journal-id-type="doi">10.1002/(ISSN)1531-8257</journal-id><journal-id journal-id-type="publisher-id">MDS</journal-id><journal-title-group><journal-title>Movement Disorders</journal-title></journal-title-group><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn><publisher><publisher-name>John Wiley and Sons Inc.</publisher-name><publisher-loc>Hoboken</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26660063</article-id><article-id pub-id-type="pmc">5064745</article-id><article-id pub-id-type="doi">10.1002/mds.26467</article-id><article-id pub-id-type="publisher-id">MDS26467</article-id><article-categories><subj-group subj-group-type="overline"><subject>Research Article</subject></subj-group><subj-group subj-group-type="heading"><subject>Research Articles</subject></subj-group></article-categories><title-group><article-title>Neuroleptic‐induced <styled-content style="fixed-case">P</styled-content>arkinsonism: <styled-content style="fixed-case">C</styled-content>linicopathological study</article-title><alt-title alt-title-type="right-running-head">Neuroleptic‐induced Parkinsonism</alt-title><alt-title alt-title-type="left-running-head">Shuaib et al</alt-title></title-group><contrib-group><contrib id="mds26467-cr-0001" contrib-type="author"><name><surname>Shuaib</surname><given-names>Umar A.</given-names></name><degrees>MBBS</degrees><xref ref-type="aff" rid="mds26467-aff-0001"><sup>1</sup></xref></contrib><contrib id="mds26467-cr-0002" contrib-type="author"><name><surname>Rajput</surname><given-names>Ali H.</given-names></name><degrees>MBBS, FRCPC</degrees><xref ref-type="aff" rid="mds26467-aff-0002"><sup>2</sup></xref></contrib><contrib id="mds26467-cr-0003" contrib-type="author"><name><surname>Robinson</surname><given-names>Christopher A.</given-names></name><degrees>MD, FRCPC</degrees><xref ref-type="aff" rid="mds26467-aff-0003"><sup>3</sup></xref></contrib><contrib id="mds26467-cr-0004" contrib-type="author"><name><surname>Rajput</surname><given-names>Alex</given-names></name><degrees>MD, FRCPC</degrees><xref ref-type="aff" rid="mds26467-aff-0002"><sup>2</sup></xref></contrib></contrib-group><aff id="mds26467-aff-0001"><label><sup>1</sup></label><named-content content-type="organisation-division">Saskatchewan Movement Disorders Program</named-content><institution>Royal University Hospital</institution><named-content content-type="city">Saskatoon</named-content><named-content content-type="country-part">Saskatchewan</named-content><country country="CA">Canada</country></aff><aff id="mds26467-aff-0002"><label><sup>2</sup></label><named-content content-type="organisation-division">Division of Neurology, Saskatchewan Movement Disorders Program</named-content><institution>University of Saskatchewan, Saskatoon Health Region</institution><named-content content-type="city">Saskatoon</named-content><named-content content-type="country-part">Saskatchewan</named-content><country country="CA">Canada</country></aff><aff id="mds26467-aff-0003"><label><sup>3</sup></label><named-content content-type="organisation-division">Neuropathology, Department of Pathology</named-content><institution>University of Saskatchewan, Saskatoon Health Region</institution><named-content content-type="city">Saskatoon</named-content><named-content content-type="country-part">Saskatchewan</named-content><country country="CA">Canada</country></aff><author-notes><corresp id="correspondenceTo"><bold>Correspondence to</bold>: Dr. Ali H. Rajput, Royal University Hospital, Room 1663, Saskatoon, Saskatchewan, Canada, S7N 0W8; <email>ali.rajput@saskatoonhealthregion.ca</email></corresp></author-notes><pub-date pub-type="epub"><day>11</day><month>12</month><year>2015</year></pub-date><pub-date pub-type="ppub"><month>3</month><year>2016</year></pub-date><volume>31</volume><issue>3</issue><issue-id pub-id-type="doi">10.1002/mds.v31.3</issue-id><fpage>360</fpage><lpage>365</lpage><history><date date-type="received"><day>25</day><month>6</month><year>2015</year></date><date date-type="rev-recd"><day>29</day><month>9</month><year>2015</year></date><date date-type="accepted"><day>05</day><month>10</month><year>2015</year></date></history><permissions><pmc-comment> © 2016 International Parkinson and Movement Disorder Society </pmc-comment>
<copyright-statement content-type="article-copyright">© 2015 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.</copyright-statement><license license-type="creativeCommonsBy"><license-p>This is an open access article under the terms of the <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution</ext-link> License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="file:MDS-31-360.pdf"></self-uri><abstract><title>ABSTRACT</title><sec id="mds26467-sec-0001"><title>Background</title><p>Drug‐induced parkinsonism is a well‐known complication of several different drugs—the most common being neuroleptic‐induced parkinsonism. However, very few autopsies have been reported in such cases.</p></sec><sec id="mds26467-sec-0002"><title>Methods</title><p>Patients assessed at Movement Disorders Clinic Saskatchewan are offered brain autopsy. Detailed clinical records are kept.</p></sec><sec id="mds26467-sec-0003"><title>Results</title><p>Brains were obtained from 7 drug‐induced parkinsonism patients with parkinsonian symptom onset coinciding with use of drugs known to produce parkinsonism. Six were on antipsychotics and 1 was on metoclopramide. Three cases were treated with levodopa for parkinsonism. In two cases, parkinsonian features reversed after stopping the offending agent. Both had autopsy evidence of preclinical PD. In 4 of the remaining 5, dopamine‐blocking drugs were continued until death. In 4 of those 5, brain histology revealed no cause for the parkinsonism, but 1 had mild SN neuronal loss without Lewy bodies.</p></sec><sec id="mds26467-sec-0004"><title>Conclusion</title><p>This study shows that reversal of parkinsonism after discontinuing offending drugs does not indicate absence of underlying pathology. Neuroleptics can unmask preclinical PD in patients with insufficient SN damage for the disease to manifest clinically. Though the mechanism of sustained parkinsonian features after discontinuing neuroleptics remains to be established, it is unlikely that dopamine receptor block leads to retrograde SN neuronal degeneration. Furthermore, <sc>l</sc>‐dopa does not appear to be toxic to SN. © 2015 International Parkinson and Movement Disorder Society</p></sec></abstract><kwd-group kwd-group-type="author-generated"><kwd id="mds26467-kwd-0001">parkinsonism</kwd><kwd id="mds26467-kwd-0002">drug induced</kwd><kwd id="mds26467-kwd-0003">pathology</kwd><kwd id="mds26467-kwd-0004">substantia nigra</kwd><kwd id="mds26467-kwd-0005">neuroleptic‐induced</kwd></kwd-group><counts><page-count count="6"></page-count></counts><custom-meta-group><custom-meta><meta-name>source-schema-version-number</meta-name><meta-value>2.0</meta-value></custom-meta><custom-meta><meta-name>component-id</meta-name><meta-value>mds26467</meta-value></custom-meta><custom-meta><meta-name>cover-date</meta-name><meta-value>March 2016</meta-value></custom-meta><custom-meta><meta-name>details-of-publishers-convertor</meta-name><meta-value>Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:14.10.2016</meta-value></custom-meta></custom-meta-group></article-meta><notes><fn-group><fn id="mds26467-note-0001"><p><bold>Relevant conflicts of interest/financial disclosures</bold>: Nothing to report.</p></fn><fn id="mds26467-note-0002"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></fn></fn-group></notes></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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