Randomised, double‐blind, placebo‐controlled trial to assess the potential of cannabinoid receptor stimulation in the treatment of dystonia
Identifieur interne : 003166 ( Istex/Corpus ); précédent : 003165; suivant : 003167Randomised, double‐blind, placebo‐controlled trial to assess the potential of cannabinoid receptor stimulation in the treatment of dystonia
Auteurs : Susan H. Fox ; Mark Kellett ; A. Peter Moore ; Alan R. Crossman ; Jonathan M. BrotchieSource :
- Movement Disorders [ 0885-3185 ] ; 2002-01.
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- KwdEn :
Abstract
Cannabis may have medicinal uses in a variety of diseases. The neural mechanisms underlying dystonia involve abnormalities within the basal ganglia—in particular, overactivity of the lateral globus pallidus (GPl). Cannabinoid receptors are located presynaptically on GABA terminals within the GPi, where their activation reduces GABA reuptake. Cannabinoid receptor stimulation may thus reduce overactivity of the GPl and thereby reduce dystonia. A double‐blind, randomised, placebo‐controlled, crossover study using the synthetic cannabinoid receptor agonist nabilone in patients with generalised and segmental primary dystonia showed no significant reduction in dystonia following treatment with nabilone. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1280
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<affiliation>Manchester Movement Disorders Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, and Motac Neuroscience Ltd., Manchester Incubator Building, Manchester, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Jonathan M.</namePart>
<namePart type="family">Brotchie</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Manchester Movement Disorders Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, and Motac Neuroscience Ltd., Manchester Incubator Building, Manchester, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<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">2002-01</dateIssued>
<dateCaptured encoding="w3cdtf">2001-03-10</dateCaptured>
<dateValid encoding="w3cdtf">2001-07-12</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">2</extent>
<extent unit="references">28</extent>
<extent unit="words">2488</extent>
</physicalDescription>
<abstract lang="en">Cannabis may have medicinal uses in a variety of diseases. The neural mechanisms underlying dystonia involve abnormalities within the basal ganglia—in particular, overactivity of the lateral globus pallidus (GPl). Cannabinoid receptors are located presynaptically on GABA terminals within the GPi, where their activation reduces GABA reuptake. Cannabinoid receptor stimulation may thus reduce overactivity of the GPl and thereby reduce dystonia. A double‐blind, randomised, placebo‐controlled, crossover study using the synthetic cannabinoid receptor agonist nabilone in patients with generalised and segmental primary dystonia showed no significant reduction in dystonia following treatment with nabilone. © 2001 Movement Disorder Society.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>dystonia</topic>
<topic>cannabis</topic>
<topic>globus pallidus</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
</titleInfo>
<titleInfo type="abbreviated"><title>Mov. Disord.</title>
</titleInfo>
<subject><genre>article category</genre>
<topic>Brief Report</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>1</number>
</detail>
<extent unit="pages"><start>145</start>
<end>149</end>
<total>5</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">820A66911789DED586603BDE2C38BCABB5D36D7C</identifier>
<identifier type="DOI">10.1002/mds.1280</identifier>
<identifier type="ArticleID">MDS1280</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorder Society</accessCondition>
<recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
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<serie></serie>
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