Olanzapine treatment for dopaminergic‐induced hallucinations
Identifieur interne : 000A11 ( Main/Corpus ); précédent : 000A10; suivant : 000A12Olanzapine treatment for dopaminergic‐induced hallucinations
Auteurs : William G. Ondo ; Joel K. Levy ; Kevin Dat Vuong ; Christine Hunter ; Joseph JankovicSource :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
English descriptors
Abstract
Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P < 0.05) and timed tapping (P < 0.01) worsened while on drug compared to placebo. Bradykinesia (P < 0.01) and gait (P < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10217
Links to Exploration step
ISTEX:4441E152BD20AC9092A3A945BE23A457F95BFB16Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Olanzapine treatment for dopaminergic‐induced hallucinations</title><author><name sortKey="Ondo, William G" sort="Ondo, William G" uniqKey="Ondo W" first="William G." last="Ondo">William G. Ondo</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Levy, Joel K" sort="Levy, Joel K" uniqKey="Levy J" first="Joel K." last="Levy">Joel K. Levy</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Vuong, Kevin Dat" sort="Vuong, Kevin Dat" uniqKey="Vuong K" first="Kevin Dat" last="Vuong">Kevin Dat Vuong</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Hunter, Christine" sort="Hunter, Christine" uniqKey="Hunter C" first="Christine" last="Hunter">Christine Hunter</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4441E152BD20AC9092A3A945BE23A457F95BFB16</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1002/mds.10217</idno><idno type="url">https://api.istex.fr/document/4441E152BD20AC9092A3A945BE23A457F95BFB16/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000A11</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Olanzapine treatment for dopaminergic‐induced hallucinations</title><author><name sortKey="Ondo, William G" sort="Ondo, William G" uniqKey="Ondo W" first="William G." last="Ondo">William G. Ondo</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Levy, Joel K" sort="Levy, Joel K" uniqKey="Levy J" first="Joel K." last="Levy">Joel K. Levy</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Vuong, Kevin Dat" sort="Vuong, Kevin Dat" uniqKey="Vuong K" first="Kevin Dat" last="Vuong">Kevin Dat Vuong</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Hunter, Christine" sort="Hunter, Christine" uniqKey="Hunter C" first="Christine" last="Hunter">Christine Hunter</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-09">2002-09</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1031">1031</biblScope><biblScope unit="page" to="1035">1035</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">4441E152BD20AC9092A3A945BE23A457F95BFB16</idno><idno type="DOI">10.1002/mds.10217</idno><idno type="ArticleID">MDS10217</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>atypical antipsychotics</term><term>olanzapine</term><term>organic psychosis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P < 0.05) and timed tapping (P < 0.01) worsened while on drug compared to placebo. Bradykinesia (P < 0.01) and gait (P < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>William G. Ondo MD</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</json:string></affiliations></json:item><json:item><name>Joel K. Levy PhD</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</json:string></affiliations></json:item><json:item><name>Kevin Dat Vuong MA</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</json:string></affiliations></json:item><json:item><name>Christine Hunter RN</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</json:string></affiliations></json:item><json:item><name>Joseph Jankovic MD</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>organic psychosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>olanzapine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>atypical antipsychotics</value></json:item></subject><articleId><json:string>MDS10217</json:string></articleId><language><json:string>eng</json:string></language><abstract>Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P > 0.05) and timed tapping (P > 0.01) worsened while on drug compared to placebo. Bradykinesia (P > 0.01) and gait (P > 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society</abstract><qualityIndicators><score>5.934</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1643</abstractCharCount><pdfWordCount>2518</pdfWordCount><pdfCharCount>16585</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>243</abstractWordCount></qualityIndicators><title>Olanzapine treatment for dopaminergic‐induced hallucinations</title><genre><json:string>article</json:string></genre><host><volume>17</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>1035</last><first>1031</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Brief Reports</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1002/mds.10217</json:string></doi><id>4441E152BD20AC9092A3A945BE23A457F95BFB16</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/4441E152BD20AC9092A3A945BE23A457F95BFB16/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/4441E152BD20AC9092A3A945BE23A457F95BFB16/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/4441E152BD20AC9092A3A945BE23A457F95BFB16/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Olanzapine treatment for dopaminergic‐induced hallucinations</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><availability><p>WILEY</p></availability><date>2002</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Olanzapine treatment for dopaminergic‐induced hallucinations</title><author><persName><forename type="first">William G.</forename><surname>Ondo</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: 6550 Fannin, Ste 1801, Houston, TX 77030</p></note><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation></author><author><persName><forename type="first">Joel K.</forename><surname>Levy</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation></author><author><persName><forename type="first">Kevin Dat</forename><surname>Vuong</surname></persName><roleName type="degree">MA</roleName><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation></author><author><persName><forename type="first">Christine</forename><surname>Hunter</surname></persName><roleName type="degree">RN</roleName><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation></author><author><persName><forename type="first">Joseph</forename><surname>Jankovic</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-09"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1031">1031</biblScope><biblScope unit="page" to="1035">1035</biblScope></imprint></monogr><idno type="istex">4441E152BD20AC9092A3A945BE23A457F95BFB16</idno><idno type="DOI">10.1002/mds.10217</idno><idno type="ArticleID">MDS10217</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P < 0.05) and timed tapping (P < 0.01) worsened while on drug compared to placebo. Bradykinesia (P < 0.01) and gait (P < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>organic psychosis</term></item><item><term>olanzapine</term></item><item><term>atypical antipsychotics</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Brief Reports</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-06-15">Received</change><change when="2002-02-19">Registration</change><change when="2002-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/4441E152BD20AC9092A3A945BE23A457F95BFB16/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/mds.v17:5</doi><numberingGroup><numbering type="journalVolume" number="17">17</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2002-09">September/October 2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="210" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.10217</doi><idGroup><id type="unit" value="MDS10217"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Brief Reports</title><title type="tocHeading1">Brief Report</title></titleGroup><copyright ownership="thirdParty">Copyright © 2002 Movement Disorders Society</copyright><eventGroup><event type="manuscriptReceived" date="2001-06-15"></event><event type="manuscriptRevised" date="2002-01-09"></event><event type="manuscriptAccepted" date="2002-02-19"></event><event type="firstOnline" date="2002-04-16"></event><event type="publishedOnlineFinalForm" date="2002-09-26"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1031</numbering><numbering type="pageLast">1035</numbering></numberingGroup><correspondenceTo>6550 Fannin, Ste 1801, Houston, TX 77030</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS10217.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="21"></count><count type="wordTotal" number="2435"></count></countGroup><titleGroup><title type="main" xml:lang="en">Olanzapine treatment for dopaminergic‐induced hallucinations</title><title type="short" xml:lang="en">Treatment for Dopaminergic‐Induced Hallucinations</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>William G.</givenNames><familyName>Ondo</familyName><degrees>MD</degrees></personName><contactDetails><email>wondo@bcm.tmc.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Joel K.</givenNames><familyName>Levy</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Kevin Dat</givenNames><familyName>Vuong</familyName><degrees>MA</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christine</givenNames><familyName>Hunter</familyName><degrees>RN</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Joseph</givenNames><familyName>Jankovic</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">organic psychosis</keyword><keyword xml:id="kwd3">olanzapine</keyword><keyword xml:id="kwd4">atypical antipsychotics</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of <i>on</i> and <i>off</i> time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total <i>on</i> UPDRS motor scores (<i>P</i> < 0.05) and timed tapping (<i>P</i> < 0.01) worsened while on drug compared to placebo. Bradykinesia (<i>P</i> < 0.01) and gait (<i>P</i> < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Olanzapine treatment for dopaminergic‐induced hallucinations</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Treatment for Dopaminergic‐Induced Hallucinations</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Olanzapine treatment for dopaminergic‐induced hallucinations</title></titleInfo><name type="personal"><namePart type="given">William G.</namePart><namePart type="family">Ondo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><description>Correspondence: 6550 Fannin, Ste 1801, Houston, TX 77030</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joel K.</namePart><namePart type="family">Levy</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kevin Dat</namePart><namePart type="family">Vuong</namePart><namePart type="termsOfAddress">MA</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Hunter</namePart><namePart type="termsOfAddress">RN</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Jankovic</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-09</dateIssued><dateCaptured encoding="w3cdtf">2001-06-15</dateCaptured><dateValid encoding="w3cdtf">2002-02-19</dateValid><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">21</extent><extent unit="words">2435</extent></physicalDescription><abstract lang="en">Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P < 0.05) and timed tapping (P < 0.01) worsened while on drug compared to placebo. Bradykinesia (P < 0.01) and gait (P < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>organic psychosis</topic><topic>olanzapine</topic><topic>atypical antipsychotics</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Brief Reports</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>1031</start><end>1035</end><total>5</total></extent></part></relatedItem><identifier type="istex">4441E152BD20AC9092A3A945BE23A457F95BFB16</identifier><identifier type="DOI">10.1002/mds.10217</identifier><identifier type="ArticleID">MDS10217</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorders Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A11 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000A11 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:4441E152BD20AC9092A3A945BE23A457F95BFB16
|texte= Olanzapine treatment for dopaminergic‐induced hallucinations
}}
| This area was generated with Dilib version V0.6.23. |  |