From off-period dystonia to peak-dose chorea
Identifieur interne : 002D67 ( Main/Corpus ); précédent : 002D66; suivant : 002D68From off-period dystonia to peak-dose chorea
Auteurs : Paul Krack ; Pierre Pollak ; Patricia Limousin ; Abdelhamid Benazzouz ; Gu Nther Deuschl ; Alim-Louis BenabidSource :
- Brain [ 0006-8950 ] ; 1999-06.
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- KwdEn :
Abstract
The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.
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DOI: 10.1093/brain/122.6.1133
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from="1133">1133</biblScope><biblScope unit="page" to="1146">1146</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">8F037AEB01C2F6CB70E4BD26EC8AF299425834CC</idno><idno type="DOI">10.1093/brain/122.6.1133</idno><idno type="local">1221133</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>GPi = globus pallidus internus</term><term>HFS = high-frequency stimulation</term><term>LID = levodopa-induced dyskinaesias</term><term>Parkinson's disease</term><term>STN = subthalamic nucleus</term><term>UPDRS = Unified Parkinson's Disease Rating Scale</term><term>deep brain stimulation</term><term>dystonia</term><term>levodopa-induced dyskinaesias</term><term>subthalamic nucleus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Paul Krack</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</json:string><json:string>Neurology Department, Christian Albrecht Universität, Kiel, Germany and</json:string></affiliations></json:item><json:item><name>Pierre Pollak</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</json:string></affiliations></json:item><json:item><name>Patricia Limousin</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</json:string><json:string>MRC Human Movement and Balance Unit, Queen Square, London, UK</json:string></affiliations></json:item><json:item><name>Abdelhamid Benazzouz</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</json:string></affiliations></json:item><json:item><name>Günther Deuschl</name><affiliations><json:string>Neurology Department, Christian Albrecht Universität, Kiel, Germany and</json:string></affiliations></json:item><json:item><name>Alim-Louis Benabid</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</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>levodopa-induced dyskinaesias</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subthalamic nucleus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deep brain stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GPi = globus pallidus internus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HFS = high-frequency stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LID = levodopa-induced dyskinaesias</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STN = subthalamic nucleus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>UPDRS = Unified Parkinson's Disease Rating Scale</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.</abstract><qualityIndicators><score>8</score><pdfVersion>1.1</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>10</keywordCount><abstractCharCount>2977</abstractCharCount><pdfWordCount>9965</pdfWordCount><pdfCharCount>65196</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>408</abstractWordCount></qualityIndicators><title>From off-period dystonia to peak-dose chorea</title><genre><json:string>research-article</json:string></genre><host><volume>122</volume><pages><last>1146</last><first>1133</first></pages><issn><json:string>0006-8950</json:string></issn><issue>6</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2156</json:string></eissn><title>Brain</title></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1999</publicationDate><copyrightDate>1999</copyrightDate><doi><json:string>10.1093/brain/122.6.1133</json:string></doi><id>8F037AEB01C2F6CB70E4BD26EC8AF299425834CC</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/8F037AEB01C2F6CB70E4BD26EC8AF299425834CC/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/8F037AEB01C2F6CB70E4BD26EC8AF299425834CC/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8F037AEB01C2F6CB70E4BD26EC8AF299425834CC/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">From off-period dystonia to peak-dose chorea</title><title level="a" type="sub" xml:lang="en">The clinical spectrum of varying subthalamic nucleus activity</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>1999</date></publicationStmt><notesStmt><note>P. Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany E-mail: p.krack@neurologie.uni-kiel.de</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">From off-period dystonia to peak-dose chorea</title><title level="a" type="sub" xml:lang="en">The clinical spectrum of varying subthalamic nucleus activity</title><author><persName><forename type="first">Paul</forename><surname>Krack</surname></persName><affiliation></affiliation><affiliation></affiliation></author><author><persName><forename type="first">Pierre</forename><surname>Pollak</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">Patricia</forename><surname>Limousin</surname></persName><affiliation></affiliation><affiliation></affiliation></author><author><persName><forename type="first">Abdelhamid</forename><surname>Benazzouz</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">Günther</forename><surname>Deuschl</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">Alim-Louis</forename><surname>Benabid</surname></persName><affiliation></affiliation></author></analytic><monogr><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1999-06"></date><biblScope unit="volume">122</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1133">1133</biblScope><biblScope unit="page" to="1146">1146</biblScope></imprint></monogr><idno type="istex">8F037AEB01C2F6CB70E4BD26EC8AF299425834CC</idno><idno type="DOI">10.1093/brain/122.6.1133</idno><idno type="local">1221133</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1999</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Parkinson's disease</term></item><item><term>levodopa-induced dyskinaesias</term></item><item><term>dystonia</term></item><item><term>subthalamic nucleus</term></item><item><term>deep brain stimulation</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>GPi = globus pallidus internus</term></item><item><term>HFS = high-frequency stimulation</term></item><item><term>LID = levodopa-induced dyskinaesias</term></item><item><term>STN = subthalamic nucleus</term></item><item><term>UPDRS = Unified Parkinson's Disease Rating Scale</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1999-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/8F037AEB01C2F6CB70E4BD26EC8AF299425834CC/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><abbrev-journal-title abbrev-type="publisher">Brain</abbrev-journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">1221133</article-id><article-id pub-id-type="doi">10.1093/brain/122.6.1133</article-id><title-group><article-title>From off-period dystonia to peak-dose chorea</article-title><subtitle>The clinical spectrum of varying subthalamic nucleus activity</subtitle></title-group><contrib-group><contrib contrib-type="author"><name><surname>Krack</surname><given-names>Paul</given-names></name><xref rid="AFF1">1</xref><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Pollak</surname><given-names>Pierre</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Limousin</surname><given-names>Patricia</given-names></name><xref rid="AFF1">1</xref><xref rid="AFF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Benazzouz</surname><given-names>Abdelhamid</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Deuschl</surname><given-names>Günther</given-names></name><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Benabid</surname><given-names>Alim-Louis</given-names></name><xref rid="AFF1">1</xref></contrib><aff id="AFF1"><label>1</label>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France, </aff><aff id="AFF2"><label>2</label>Neurology Department, Christian Albrecht Universität, Kiel, Germany and </aff><aff id="AFF3"><label>3</label>MRC Human Movement and Balance Unit, Queen Square, London, UK</aff></contrib-group><author-notes><corresp>P. Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany E-mail: <ext-link xlink:href="p.krack@neurologie.uni-kiel.de" ext-link-type="email">p.krack@neurologie.uni-kiel.de</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>6</month><year>1999</year></pub-date><volume>122</volume><issue>6</issue><fpage>1133</fpage><lpage>1146</lpage><history><date date-type="accepted"><day>06</day><month>01</month><year>1999</year></date><date date-type="received"><day>10</day><month>07</month><year>1998</year></date><date date-type="rev-recd"><day>26</day><month>09</month><year>1998</year></date><date date-type="rev-recd"><day>06</day><month>01</month><year>1999</year></date></history><copyright-statement>© Oxford University Press 1999</copyright-statement><copyright-year>1999</copyright-year><abstract xml:lang="en"><p>The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>Parkinson's disease</kwd><kwd>levodopa-induced dyskinaesias</kwd><kwd>dystonia</kwd><kwd>subthalamic nucleus</kwd><kwd>deep brain stimulation</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd>GPi = globus pallidus internus</kwd><kwd>HFS = high-frequency stimulation</kwd><kwd>LID = levodopa-induced dyskinaesias</kwd><kwd>STN = subthalamic nucleus</kwd><kwd>UPDRS = Unified Parkinson's Disease Rating Scale</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>1133</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>From off-period dystonia to peak-dose chorea</title><subTitle>The clinical spectrum of varying subthalamic nucleus activity</subTitle></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>From off-period dystonia to peak-dose chorea</title><subTitle>The clinical spectrum of varying subthalamic nucleus activity</subTitle></titleInfo><name type="personal"><namePart type="given">Paul</namePart><namePart type="family">Krack</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Pollak</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patricia</namePart><namePart type="family">Limousin</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Abdelhamid</namePart><namePart type="family">Benazzouz</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Günther</namePart><namePart type="family">Deuschl</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alim-Louis</namePart><namePart type="family">Benabid</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1999-06</dateIssued><copyrightDate encoding="w3cdtf">1999</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.</abstract><note type="author-notes">P. Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany E-mail: p.krack@neurologie.uni-kiel.de</note><subject lang="en"><genre>KWD</genre><topic>Parkinson's disease</topic><topic>levodopa-induced dyskinaesias</topic><topic>dystonia</topic><topic>subthalamic nucleus</topic><topic>deep brain stimulation</topic></subject><subject lang="en"><genre>ABR</genre><topic>GPi = globus pallidus internus</topic><topic>HFS = high-frequency stimulation</topic><topic>LID = levodopa-induced dyskinaesias</topic><topic>STN = subthalamic nucleus</topic><topic>UPDRS = Unified Parkinson's Disease Rating Scale</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><titleInfo type="abbreviated"><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><identifier type="PublisherID-nlm-ta">Brain</identifier><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>122</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1133</start><end>1146</end></extent></part></relatedItem><identifier type="istex">8F037AEB01C2F6CB70E4BD26EC8AF299425834CC</identifier><identifier type="DOI">10.1093/brain/122.6.1133</identifier><identifier type="local">1221133</identifier><accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press 1999</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/8F037AEB01C2F6CB70E4BD26EC8AF299425834CC/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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