Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease
Identifieur interne : 002536 ( Main/Corpus ); précédent : 002535; suivant : 002537Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease
Auteurs : M. Faist ; J. Xie ; D. Kurz ; W. Berger ; C. Maurer ; P. Pollak ; C. H. Lu CkingSource :
- Brain [ 0006-8950 ] ; 2001-08.
English descriptors
- KwdEn :
Abstract
The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with l-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and l-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean ± SD age 48.1 ± 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 ± 2.4 years, mean stimulation time 15.4 ± 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of l-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. l-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received l-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with l-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.
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DOI: 10.1093/brain/124.8.1590
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Lu Cking</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1093/brain/124.8.1590</idno><idno type="url">https://api.istex.fr/document/8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002536</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</title><author><name sortKey="Faist, M" sort="Faist, M" uniqKey="Faist M" first="M." last="Faist">M. Faist</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author><author><name sortKey="Xie, J" sort="Xie, J" uniqKey="Xie J" first="J." last="Xie">J. Xie</name><affiliation><mods:affiliation></mods:affiliation></affiliation><affiliation><mods:affiliation>18, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Kurz, D" sort="Kurz, D" uniqKey="Kurz D" first="D." last="Kurz">D. Kurz</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author><author><name sortKey="Berger, W" sort="Berger, W" uniqKey="Berger W" first="W." last="Berger">W. Berger</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author><author><name sortKey="Maurer, C" sort="Maurer, C" uniqKey="Maurer C" first="C." last="Maurer">C. Maurer</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P." last="Pollak">P. Pollak</name><affiliation><mods:affiliation></mods:affiliation></affiliation><affiliation><mods:affiliation>18, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Lu Cking, C H" sort="Lu Cking, C H" uniqKey="Lu Cking C" first="C. H." last="Lu Cking">C. H. Lu Cking</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2001-08">2001-08</date><biblScope unit="volume">124</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1590">1590</biblScope><biblScope unit="page" to="1600">1600</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F</idno><idno type="DOI">10.1093/brain/124.8.1590</idno><idno type="PII">1460-2156</idno><idno type="local">1241590</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>GPi = internal globus pallidus</term><term>Parkinson's disease</term><term>STN = subthalamic nucleus</term><term>STN stimulation</term><term>UPDRS = Unified Parkinson's Disease Rating Scale</term><term>gait analysis</term><term>gait disorders</term><term>movement disorders</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with l-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and l-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean ± SD age 48.1 ± 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 ± 2.4 years, mean stimulation time 15.4 ± 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of l-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. l-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received l-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with l-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>M. Faist</name><affiliations><json:string>Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany,</json:string></affiliations></json:item><json:item><name>J. Xie</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, University Hospital of Grenoble and</json:string><json:string>INSERM Unit 318, Joseph Fourier University, Grenoble, France</json:string></affiliations></json:item><json:item><name>D. Kurz</name><affiliations><json:string>Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany,</json:string></affiliations></json:item><json:item><name>W. Berger</name><affiliations><json:string>Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany,</json:string></affiliations></json:item><json:item><name>C. Maurer</name><affiliations><json:string>Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany,</json:string></affiliations></json:item><json:item><name>P. Pollak</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, University Hospital of Grenoble and</json:string><json:string>INSERM Unit 318, Joseph Fourier University, Grenoble, France</json:string></affiliations></json:item><json:item><name>C. H. Lücking</name><affiliations><json:string>Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>gait disorders</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>movement disorders</value></json:item><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>gait analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STN stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GPi = internal globus pallidus</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 fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with l-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and l-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean ± SD age 48.1 ± 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 ± 2.4 years, mean stimulation time 15.4 ± 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of l-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. l-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received l-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with l-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 791 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>2472</abstractCharCount><pdfWordCount>6660</pdfWordCount><pdfCharCount>42843</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>377</abstractWordCount></qualityIndicators><title>Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</title><genre><json:string>research-article</json:string></genre><host><volume>124</volume><pages><last>1600</last><first>1590</first></pages><issn><json:string>0006-8950</json:string></issn><issue>8</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>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1093/brain/124.8.1590</json:string></doi><id>8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2001</date></publicationStmt><notesStmt><note>Dr Michael Faist, Department of Clinical Neurology and Neurophysiology, University of Freiburg, Breisacherstr 64, D-79106 Freiburg, Germany E-mail: faist@nz11.ukl.uni-freiburg.de</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</title><author><persName><forename type="first">M.</forename><surname>Faist</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">J.</forename><surname>Xie</surname></persName><affiliation></affiliation><affiliation>18, Joseph Fourier University, Grenoble, France</affiliation></author><author><persName><forename type="first">D.</forename><surname>Kurz</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">W.</forename><surname>Berger</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">C.</forename><surname>Maurer</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">P.</forename><surname>Pollak</surname></persName><affiliation></affiliation><affiliation>18, Joseph Fourier University, Grenoble, France</affiliation></author><author><persName><forename type="first">C. H.</forename><surname>Lücking</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="2001-08"></date><biblScope unit="volume">124</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1590">1590</biblScope><biblScope unit="page" to="1600">1600</biblScope></imprint></monogr><idno type="istex">8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F</idno><idno type="DOI">10.1093/brain/124.8.1590</idno><idno type="PII">1460-2156</idno><idno type="local">1241590</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with l-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and l-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean ± SD age 48.1 ± 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 ± 2.4 years, mean stimulation time 15.4 ± 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of l-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. l-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received l-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with l-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>gait disorders</term></item><item><term>movement disorders</term></item><item><term>Parkinson's disease</term></item><item><term>gait analysis</term></item><item><term>STN stimulation</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>GPi = internal globus pallidus</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="2001-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F/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">1241590</article-id><article-id pub-id-type="doi">10.1093/brain/124.8.1590</article-id><article-id pub-id-type="pii">1460-2156</article-id><title-group><article-title>Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Faist</surname><given-names>M.</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Xie</surname><given-names>J.</given-names></name><xref rid="AFF2">2</xref><xref rid="AFF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Kurz</surname><given-names>D.</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Berger</surname><given-names>W.</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Maurer</surname><given-names>C.</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Pollak</surname><given-names>P.</given-names></name><xref rid="AFF2">2</xref><xref rid="AFF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Lücking</surname><given-names>C. H.</given-names></name><xref rid="AFF1">1</xref></contrib><aff id="AFF1"><label>1</label>Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany, </aff><aff id="AFF2"><label>2</label>Department of Clinical and Biological Neurosciences, University Hospital of Grenoble and </aff><aff id="AFF3"><label>3</label>INSERM Unit 318, Joseph Fourier University, Grenoble, France</aff></contrib-group><author-notes><corresp>Dr Michael Faist, Department of Clinical Neurology and Neurophysiology, University of Freiburg, Breisacherstr 64, D-79106 Freiburg, Germany E-mail: <ext-link xlink:href="faist@nz11.ukl.uni-freiburg.de" ext-link-type="email">faist@nz11.ukl.uni-freiburg.de</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>8</month><year>2001</year></pub-date><volume>124</volume><issue>8</issue><fpage>1590</fpage><lpage>1600</lpage><history><date date-type="accepted"><day>18</day><month>04</month><year>2001</year></date><date date-type="received"><day>31</day><month>01</month><year>2001</year></date><date date-type="rev-recd"><day>18</day><month>04</month><year>2001</year></date></history><copyright-statement>© Oxford University Press 2001</copyright-statement><copyright-year>2001</copyright-year><abstract xml:lang="en"><p>The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with <sc>l</sc>-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and <sc>l</sc>-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean ± SD age 48.1 ± 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 ± 2.4 years, mean stimulation time 15.4 ± 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of <sc>l</sc>-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. <sc>l</sc>-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received <sc>l</sc>-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with <sc>l</sc>-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>gait disorders</kwd><kwd>movement disorders</kwd><kwd>Parkinson's disease</kwd><kwd>gait analysis</kwd><kwd>STN stimulation</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd>GPi = internal globus pallidus</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>1590</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>Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Effect of bilateral subthalamic nucleus stimulation on gait in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Faist</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Xie</namePart><affiliation></affiliation><affiliation>18, Joseph Fourier University, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Kurz</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Berger</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Maurer</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Pollak</namePart><affiliation></affiliation><affiliation>18, Joseph Fourier University, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. H.</namePart><namePart type="family">Lücking</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">2001-08</dateIssued><copyrightDate encoding="w3cdtf">2001</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 fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with l-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and l-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean ± SD age 48.1 ± 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 ± 2.4 years, mean stimulation time 15.4 ± 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of l-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. l-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received l-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with l-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.</abstract><note type="author-notes">Dr Michael Faist, Department of Clinical Neurology and Neurophysiology, University of Freiburg, Breisacherstr 64, D-79106 Freiburg, Germany E-mail: faist@nz11.ukl.uni-freiburg.de</note><subject lang="en"><genre>KWD</genre><topic>gait disorders</topic><topic>movement disorders</topic><topic>Parkinson's disease</topic><topic>gait analysis</topic><topic>STN stimulation</topic></subject><subject lang="en"><genre>ABR</genre><topic>GPi = internal globus pallidus</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>2001</date><detail type="volume"><caption>vol.</caption><number>124</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1590</start><end>1600</end></extent></part></relatedItem><identifier type="istex">8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F</identifier><identifier type="DOI">10.1093/brain/124.8.1590</identifier><identifier type="PII">1460-2156</identifier><identifier type="local">1241590</identifier><accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press 2001</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/8A0AF7CAC90A941DAC8DBB0D51486D8CBE7E4D4F/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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