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Deep brain stimulation effect on freezing of gait

Identifieur interne : 000831 ( Main/Corpus ); précédent : 000830; suivant : 000832

Deep brain stimulation effect on freezing of gait

Auteurs : Murielle U. Ferraye ; Bettina Debû ; Pierre Pollak

Source :

RBID : ISTEX:715529C6080CF0315467069436DC7AE98A850632

English descriptors

Abstract

The majority of patients with Parkinson's disease suffer from freezing of gait (FOG), which responds more or less to levodopa. Thalamic stimulation, mainly used in the treatment of tremor dominant Parkinson's disease is ineffective in FOG. GPi stimulation moderately improves FOG, but this effect may abate in the long term. STN stimulation was reported to improve levodopa‐responsive FOG. In some patients, the benefit from levodopa is greater than that from STN stimulation, and levodopa and STN stimulation can have additive effects. On the contrary, STN stimulation is ineffective on levodopa‐resistant FOG. In the few cases of levodopa‐induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Stimulation of the pedunculopontine nucleus has recently been performed in small groups of patients suffering from both off‐ and on‐levodopa gait impairments. The first results appear encouraging, but they need to be confirmed by controlled studies in larger series of patients. © 2008 Movement Disorder Society

Url:
DOI: 10.1002/mds.21975

Links to Exploration step

ISTEX:715529C6080CF0315467069436DC7AE98A850632

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<p>The majority of patients with Parkinson's disease suffer from freezing of gait (FOG), which responds more or less to levodopa. Thalamic stimulation, mainly used in the treatment of tremor dominant Parkinson's disease is ineffective in FOG. GPi stimulation moderately improves FOG, but this effect may abate in the long term. STN stimulation was reported to improve levodopa‐responsive FOG. In some patients, the benefit from levodopa is greater than that from STN stimulation, and levodopa and STN stimulation can have additive effects. On the contrary, STN stimulation is ineffective on levodopa‐resistant FOG. In the few cases of levodopa‐induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Stimulation of the pedunculopontine nucleus has recently been performed in small groups of patients suffering from both off‐ and on‐levodopa gait impairments. The first results appear encouraging, but they need to be confirmed by controlled studies in larger series of patients. © 2008 Movement Disorder Society</p>
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<name type="personal">
<namePart type="given">Murielle U.</namePart>
<namePart type="family">Ferraye</namePart>
<namePart type="termsOfAddress">MSc</namePart>
<affiliation>INSERM, U836, Grenoble Institute of Neuroscience, Grenoble, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
<description>Correspondence: CHU de Grenoble, Pavillon de neurologie, BP 217, 38043 Grenoble Cedex 9, France</description>
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<name type="personal">
<namePart type="given">Bettina</namePart>
<namePart type="family">Debû</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>INSERM, U836, Grenoble Institute of Neuroscience, Grenoble, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Pierre</namePart>
<namePart type="family">Pollak</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>INSERM, U836, Grenoble Institute of Neuroscience, Grenoble, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
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<roleTerm type="text">author</roleTerm>
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<dateIssued encoding="w3cdtf">2008</dateIssued>
<dateCaptured encoding="w3cdtf">2007-09-20</dateCaptured>
<dateValid encoding="w3cdtf">2008-01-15</dateValid>
<copyrightDate encoding="w3cdtf">2008</copyrightDate>
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<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<abstract lang="en">The majority of patients with Parkinson's disease suffer from freezing of gait (FOG), which responds more or less to levodopa. Thalamic stimulation, mainly used in the treatment of tremor dominant Parkinson's disease is ineffective in FOG. GPi stimulation moderately improves FOG, but this effect may abate in the long term. STN stimulation was reported to improve levodopa‐responsive FOG. In some patients, the benefit from levodopa is greater than that from STN stimulation, and levodopa and STN stimulation can have additive effects. On the contrary, STN stimulation is ineffective on levodopa‐resistant FOG. In the few cases of levodopa‐induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Stimulation of the pedunculopontine nucleus has recently been performed in small groups of patients suffering from both off‐ and on‐levodopa gait impairments. The first results appear encouraging, but they need to be confirmed by controlled studies in larger series of patients. © 2008 Movement Disorder Society</abstract>
<note type="content">*No potential conflict of interest.</note>
<note type="funding">Michael J. Fox Foundation</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>Parkinson disease</topic>
<topic>freezing of gait</topic>
<topic>deep brain stimulation</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>
<name type="personal">
<namePart type="termsOfAddress">Dr.</namePart>
<namePart type="family">Giladi</namePart>
</name>
<name type="personal">
<namePart type="termsOfAddress">Dr.</namePart>
<namePart type="family">Nieuwboer</namePart>
</name>
<genre type="Journal">journal</genre>
<subject>
<genre>article category</genre>
<topic>Review</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>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>23</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>S2</number>
</detail>
<detail type="supplement">
<caption>Suppl. no.</caption>
<number>S2</number>
</detail>
<extent unit="pages">
<start>S489</start>
<end>S494</end>
<total>6</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">715529C6080CF0315467069436DC7AE98A850632</identifier>
<identifier type="DOI">10.1002/mds.21975</identifier>
<identifier type="ArticleID">MDS21975</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
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