Acute and chronic effects of clozapine in essential tremor
Identifieur interne : 001E45 ( Istex/Corpus ); précédent : 001E44; suivant : 001E46Acute and chronic effects of clozapine in essential tremor
Auteurs : Roberto Ceravolo ; Stefania Salvetti ; Paola Piccini ; Claudio Lucetti ; Gianna Gambaccini ; Ubaldo BonuccelliSource :
- Movement Disorders [ 0885-3185 ] ; 1999-05.
English descriptors
Abstract
Patients with essential tremor (ET) may not respond to commonly used drugs. Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p <0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p <0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. Our results suggest that in selected drug‐resistant ET cases, clozapine should be considered before resorting to neurosurgical options.
Url:
DOI: 10.1002/1531-8257(199905)14:3<468::AID-MDS1013>3.0.CO;2-M
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ISTEX:1D26A034CBFC106C2766EAA83ACA73DAAAA01126Le document en format XML
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Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p <0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p <0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. Our results suggest that in selected drug‐resistant ET cases, clozapine should be considered before resorting to neurosurgical options.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Roberto Ceravolo MD</name><affiliations><json:string>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Stefania Salvetti MD</name><affiliations><json:string>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Paola Piccini MD</name><affiliations><json:string>Department of Neurology, Imperial College School of Medicine, Hammersmith Hospital, London, U.K.</json:string></affiliations></json:item><json:item><name>Claudio Lucetti MD</name><affiliations><json:string>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Gianna Gambaccini MD</name><affiliations><json:string>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Ubaldo Bonuccelli MD</name><affiliations><json:string>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Essential tremor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Clozapine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Acute and chronic administration</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Patients with essential tremor (ET) may not respond to commonly used drugs. Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p >0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p >0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. 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Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p <0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p <0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. Our results suggest that in selected drug‐resistant ET cases, clozapine should be considered before resorting to neurosurgical options.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Essential tremor</term></item><item><term>Clozapine</term></item><item><term>Acute and chronic administration</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-07-16">Received</change><change when="1999-01-29">Registration</change><change when="1999-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/1D26A034CBFC106C2766EAA83ACA73DAAAA01126/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>John Wiley & Sons, Inc.</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. 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Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p <0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p <0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. Our results suggest that in selected drug‐resistant ET cases, clozapine should be considered before resorting to neurosurgical options.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Acute and chronic effects of clozapine in essential tremor</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Clozapine in Essential Tremor</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Acute and chronic effects of clozapine in essential tremor</title></titleInfo><name type="personal"><namePart type="given">Roberto</namePart><namePart type="family">Ceravolo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stefania</namePart><namePart type="family">Salvetti</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Piccini</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Imperial College School of Medicine, Hammersmith Hospital, London, U.K.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claudio</namePart><namePart type="family">Lucetti</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gianna</namePart><namePart type="family">Gambaccini</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ubaldo</namePart><namePart type="family">Bonuccelli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroscience, Clinical Neurology, University of Pisa, Italy</affiliation><description>Correspondence: Department of Neuroscience, Clinical Neurology, University of Pisa, via Rome 67, 56100 Pisa, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">1999-05</dateIssued><dateCaptured encoding="w3cdtf">1998-07-16</dateCaptured><dateValid encoding="w3cdtf">1999-01-29</dateValid><copyrightDate encoding="w3cdtf">1999</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">3</extent><extent unit="references">42</extent><extent unit="words">3054</extent></physicalDescription><abstract lang="fr">Patients with essential tremor (ET) may not respond to commonly used drugs. Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p <0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p <0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. Our results suggest that in selected drug‐resistant ET cases, clozapine should be considered before resorting to neurosurgical options.</abstract><subject lang="en"><genre>Keywords</genre><topic>Essential tremor</topic><topic>Clozapine</topic><topic>Acute and chronic administration</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><subject><genre>article category</genre><topic>Article</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>1999</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>468</start><end>472</end><total>5</total></extent></part></relatedItem><identifier type="istex">1D26A034CBFC106C2766EAA83ACA73DAAAA01126</identifier><identifier type="DOI">10.1002/1531-8257(199905)14:3<468::AID-MDS1013>3.0.CO;2-M</identifier><identifier type="ArticleID">MDS1013</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1999 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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