Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation
Identifieur interne : 000F02 ( Main/Corpus ); précédent : 000F01; suivant : 000F03Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation
Auteurs : Elena Moro ; Rianne J. A. Esselink ; Alim Louis Benabid ; Pierre PollakSource :
- Brain [ 0006-8950 ] ; 2002-11.
English descriptors
- KwdEn :
Abstract
The response to levodopa changes over time in Parkinson’s disease, probably due to alterations in the dopaminergic system, progression of the disease and pulsatile oral intake of the drug. Bilateral high‐frequency stimulation of the subthalamic nucleus (STN) allows a large reduction or the complete cessation of levodopa intake in patients with advanced Parkinson’s disease. We studied variation in the motor short‐duration response (SDR) during a levodopa challenge in bilaterally STN‐stimulated patients. Twenty‐eight consecutive patients with a mean duration of Parkinson’s disease of 16.6 ± 6.0 years at the time of surgery were enrolled. Fourteen patients were evaluated both before STN stimulation and 3 months after surgery (group 1) whereas the other 14 patients were assessed before implantation and after a mean of 3 years of STN stimulation (group 2). After drug withdrawal for one night, the hand‐tapping test (TT) was carried out every 15 min, together with evaluation of dyskinesias using a modified Goetz scale. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was assessed every 30 min. In operated patients, STN stimulation was stopped 15 min before starting the clinical evaluations. A suprathreshold oral levodopa dose was given after one motor evaluation and two TTs. The clinical evaluation was carried out until the TT score returned to the baseline. In group 1, six patients continued without levodopa after surgery and the other eight received a daily mean dose of 337 mg; in group 2, seven patients continued without levodopa and the other seven received a daily mean dose of 386 mg. The main change in the levodopa SDR was a significant reduction in levodopa‐induced dyskinesias in both groups. In those patients of group 1 who did not receive levodopa after surgery, the motor UPDRS magnitude decreased and the ‘on’ UPDRS motor score worsened. In group 2, the results were similar, but in the patients who continued to receive levodopa after surgery the TT magnitude increased. On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. These results suggest that continuous STN stimulation induces long‐term plastic changes of the dopaminergic system, with slow and partial desensitization. In addition, the persistence of levodopa intake after surgery might hinder this beneficial process.
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DOI: 10.1093/brain/awf249
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Esselink</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim Louis" last="Benabid">Alim Louis Benabid</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:32195035FCE3CBB97AF065117F9C33C82BC31770</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1093/brain/awf249</idno><idno type="url">https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000F02</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</title><author><name sortKey="Moro, Elena" sort="Moro, Elena" uniqKey="Moro E" first="Elena" last="Moro">Elena Moro</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Esselink, Rianne J A" sort="Esselink, Rianne J A" uniqKey="Esselink R" first="Rianne J. A." last="Esselink">Rianne J. A. Esselink</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim Louis" last="Benabid">Alim Louis Benabid</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name><affiliation><mods:affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</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="2002-11">2002-11</date><biblScope unit="volume">125</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2408">2408</biblScope><biblScope unit="page" to="2417">2417</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">32195035FCE3CBB97AF065117F9C33C82BC31770</idno><idno type="DOI">10.1093/brain/awf249</idno><idno type="local">awf249</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abbreviations: LEDD = levodopa equivalent daily dose; LDR = long‐duration response; SDR = short‐duration response; STN = subthalamic nucleus; TT = tapping test; UPDRS = Unified Parkinson’s Disease Rating Scale</term><term>Keywords: levodopa; subthalamic nucleus; deep‐brain stimulation; Parkinson’s disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The response to levodopa changes over time in Parkinson’s disease, probably due to alterations in the dopaminergic system, progression of the disease and pulsatile oral intake of the drug. Bilateral high‐frequency stimulation of the subthalamic nucleus (STN) allows a large reduction or the complete cessation of levodopa intake in patients with advanced Parkinson’s disease. We studied variation in the motor short‐duration response (SDR) during a levodopa challenge in bilaterally STN‐stimulated patients. Twenty‐eight consecutive patients with a mean duration of Parkinson’s disease of 16.6 ± 6.0 years at the time of surgery were enrolled. Fourteen patients were evaluated both before STN stimulation and 3 months after surgery (group 1) whereas the other 14 patients were assessed before implantation and after a mean of 3 years of STN stimulation (group 2). After drug withdrawal for one night, the hand‐tapping test (TT) was carried out every 15 min, together with evaluation of dyskinesias using a modified Goetz scale. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was assessed every 30 min. In operated patients, STN stimulation was stopped 15 min before starting the clinical evaluations. A suprathreshold oral levodopa dose was given after one motor evaluation and two TTs. The clinical evaluation was carried out until the TT score returned to the baseline. In group 1, six patients continued without levodopa after surgery and the other eight received a daily mean dose of 337 mg; in group 2, seven patients continued without levodopa and the other seven received a daily mean dose of 386 mg. The main change in the levodopa SDR was a significant reduction in levodopa‐induced dyskinesias in both groups. In those patients of group 1 who did not receive levodopa after surgery, the motor UPDRS magnitude decreased and the ‘on’ UPDRS motor score worsened. In group 2, the results were similar, but in the patients who continued to receive levodopa after surgery the TT magnitude increased. On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. These results suggest that continuous STN stimulation induces long‐term plastic changes of the dopaminergic system, with slow and partial desensitization. In addition, the persistence of levodopa intake after surgery might hinder this beneficial process.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Elena Moro</name><affiliations><json:string>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France, 2Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and 3Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Rianne J. A. Esselink</name><affiliations><json:string>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France, 2Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and 3Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Alim Louis Benabid</name><affiliations><json:string>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France, 2Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and 3Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Pierre Pollak</name><affiliations><json:string>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France, 2Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and 3Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Keywords: levodopa; subthalamic nucleus; deep‐brain stimulation; Parkinson’s disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Abbreviations: LEDD = levodopa equivalent daily dose; LDR = long‐duration response; SDR = short‐duration response; STN = subthalamic nucleus; TT = tapping test; UPDRS = Unified Parkinson’s Disease Rating Scale</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The response to levodopa changes over time in Parkinson’s disease, probably due to alterations in the dopaminergic system, progression of the disease and pulsatile oral intake of the drug. Bilateral high‐frequency stimulation of the subthalamic nucleus (STN) allows a large reduction or the complete cessation of levodopa intake in patients with advanced Parkinson’s disease. We studied variation in the motor short‐duration response (SDR) during a levodopa challenge in bilaterally STN‐stimulated patients. Twenty‐eight consecutive patients with a mean duration of Parkinson’s disease of 16.6 ± 6.0 years at the time of surgery were enrolled. Fourteen patients were evaluated both before STN stimulation and 3 months after surgery (group 1) whereas the other 14 patients were assessed before implantation and after a mean of 3 years of STN stimulation (group 2). After drug withdrawal for one night, the hand‐tapping test (TT) was carried out every 15 min, together with evaluation of dyskinesias using a modified Goetz scale. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was assessed every 30 min. In operated patients, STN stimulation was stopped 15 min before starting the clinical evaluations. A suprathreshold oral levodopa dose was given after one motor evaluation and two TTs. The clinical evaluation was carried out until the TT score returned to the baseline. In group 1, six patients continued without levodopa after surgery and the other eight received a daily mean dose of 337 mg; in group 2, seven patients continued without levodopa and the other seven received a daily mean dose of 386 mg. The main change in the levodopa SDR was a significant reduction in levodopa‐induced dyskinesias in both groups. In those patients of group 1 who did not receive levodopa after surgery, the motor UPDRS magnitude decreased and the ‘on’ UPDRS motor score worsened. In group 2, the results were similar, but in the patients who continued to receive levodopa after surgery the TT magnitude increased. On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. These results suggest that continuous STN stimulation induces long‐term plastic changes of the dopaminergic system, with slow and partial desensitization. In addition, the persistence of levodopa intake after surgery might hinder this beneficial process.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 790 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>2</keywordCount><abstractCharCount>2436</abstractCharCount><pdfWordCount>5893</pdfWordCount><pdfCharCount>37568</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>367</abstractWordCount></qualityIndicators><title>Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</title><genre><json:string>research-article</json:string></genre><host><volume>125</volume><pages><last>2417</last><first>2408</first></pages><issn><json:string>0006-8950</json:string></issn><issue>11</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>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1093/brain/awf249</json:string></doi><id>32195035FCE3CBB97AF065117F9C33C82BC31770</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2002</date></publicationStmt><notesStmt><note>Correspondence to: Pierre Pollak, Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble, CHU, Service de Neurologie, BP 217 38043 Grenoble, France E‐mail: pierre.pollak@ujf‐grenoble.fr</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</title><author><persName><forename type="first">Elena</forename><surname>Moro</surname></persName><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</affiliation></author><author><persName><forename type="first">Rianne J. A.</forename><surname>Esselink</surname></persName><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</affiliation></author><author><persName><forename type="first">Alim Louis</forename><surname>Benabid</surname></persName><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</affiliation></author><author><persName><forename type="first">Pierre</forename><surname>Pollak</surname></persName><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</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="2002-11"></date><biblScope unit="volume">125</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2408">2408</biblScope><biblScope unit="page" to="2417">2417</biblScope></imprint></monogr><idno type="istex">32195035FCE3CBB97AF065117F9C33C82BC31770</idno><idno type="DOI">10.1093/brain/awf249</idno><idno type="local">awf249</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The response to levodopa changes over time in Parkinson’s disease, probably due to alterations in the dopaminergic system, progression of the disease and pulsatile oral intake of the drug. Bilateral high‐frequency stimulation of the subthalamic nucleus (STN) allows a large reduction or the complete cessation of levodopa intake in patients with advanced Parkinson’s disease. We studied variation in the motor short‐duration response (SDR) during a levodopa challenge in bilaterally STN‐stimulated patients. Twenty‐eight consecutive patients with a mean duration of Parkinson’s disease of 16.6 ± 6.0 years at the time of surgery were enrolled. Fourteen patients were evaluated both before STN stimulation and 3 months after surgery (group 1) whereas the other 14 patients were assessed before implantation and after a mean of 3 years of STN stimulation (group 2). After drug withdrawal for one night, the hand‐tapping test (TT) was carried out every 15 min, together with evaluation of dyskinesias using a modified Goetz scale. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was assessed every 30 min. In operated patients, STN stimulation was stopped 15 min before starting the clinical evaluations. A suprathreshold oral levodopa dose was given after one motor evaluation and two TTs. The clinical evaluation was carried out until the TT score returned to the baseline. In group 1, six patients continued without levodopa after surgery and the other eight received a daily mean dose of 337 mg; in group 2, seven patients continued without levodopa and the other seven received a daily mean dose of 386 mg. The main change in the levodopa SDR was a significant reduction in levodopa‐induced dyskinesias in both groups. In those patients of group 1 who did not receive levodopa after surgery, the motor UPDRS magnitude decreased and the ‘on’ UPDRS motor score worsened. In group 2, the results were similar, but in the patients who continued to receive levodopa after surgery the TT magnitude increased. On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. These results suggest that continuous STN stimulation induces long‐term plastic changes of the dopaminergic system, with slow and partial desensitization. In addition, the persistence of levodopa intake after surgery might hinder this beneficial process.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Keywords: levodopa; subthalamic nucleus; deep‐brain stimulation; Parkinson’s disease</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>Abbreviations: LEDD = levodopa equivalent daily dose; LDR = long‐duration response; SDR = short‐duration response; STN = subthalamic nucleus; TT = tapping test; UPDRS = Unified Parkinson’s Disease Rating Scale</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2002-11">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-14">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/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">awf249</article-id><article-id pub-id-type="doi">10.1093/brain/awf249</article-id><title-group><article-title>Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Moro</surname><given-names>Elena</given-names></name><xref rid="AFF1">1</xref><xref rid="AFF1">2</xref></contrib><contrib contrib-type="author"><name><surname>Esselink</surname><given-names>Rianne J. A.</given-names></name><xref rid="AFF1">1</xref><xref rid="AFF1">3</xref></contrib><contrib contrib-type="author"><name><surname>Benabid</surname><given-names>Alim Louis</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Pollak</surname><given-names>Pierre</given-names></name><xref rid="AFF1">1</xref></contrib><aff id="AFF1"><target target-type="aff" id="AWF249A1"></target><label>1</label>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France, <target target-type="aff" id="AWF249A2"></target><label>2</label>Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and <target target-type="aff" id="AWF249A3"></target><label>3</label>Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</aff></contrib-group><author-notes><corresp>Correspondence to: Pierre Pollak, Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble, CHU, Service de Neurologie, BP 217 38043 Grenoble, France E‐mail: <ext-link xlink:href="pierre.pollak@ujf-grenoble.fr" ext-link-type="email">pierre.pollak@ujf‐grenoble.fr</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>11</month><year>2002</year></pub-date><volume>125</volume><issue>11</issue><fpage>2408</fpage><lpage>2417</lpage><history><date date-type="accepted"><day>23</day><month>05</month><year>2002</year></date><date date-type="received"><day>25</day><month>01</month><year>2002</year></date><date date-type="rev-recd"><day>19</day><month>05</month><year>2002</year></date></history><copyright-year>2002</copyright-year><abstract xml:lang="en"><p>The response to levodopa changes over time in Parkinson’s disease, probably due to alterations in the dopaminergic system, progression of the disease and pulsatile oral intake of the drug. Bilateral high‐frequency stimulation of the subthalamic nucleus (STN) allows a large reduction or the complete cessation of levodopa intake in patients with advanced Parkinson’s disease. We studied variation in the motor short‐duration response (SDR) during a levodopa challenge in bilaterally STN‐stimulated patients. Twenty‐eight consecutive patients with a mean duration of Parkinson’s disease of 16.6 ± 6.0 years at the time of surgery were enrolled. Fourteen patients were evaluated both before STN stimulation and 3 months after surgery (group 1) whereas the other 14 patients were assessed before implantation and after a mean of 3 years of STN stimulation (group 2). After drug withdrawal for one night, the hand‐tapping test (TT) was carried out every 15 min, together with evaluation of dyskinesias using a modified Goetz scale. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was assessed every 30 min. In operated patients, STN stimulation was stopped 15 min before starting the clinical evaluations. A suprathreshold oral levodopa dose was given after one motor evaluation and two TTs. The clinical evaluation was carried out until the TT score returned to the baseline. In group 1, six patients continued without levodopa after surgery and the other eight received a daily mean dose of 337 mg; in group 2, seven patients continued without levodopa and the other seven received a daily mean dose of 386 mg. The main change in the levodopa SDR was a significant reduction in levodopa‐induced dyskinesias in both groups. In those patients of group 1 who did not receive levodopa after surgery, the motor UPDRS magnitude decreased and the ‘on’ UPDRS motor score worsened. In group 2, the results were similar, but in the patients who continued to receive levodopa after surgery the TT magnitude increased. On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. These results suggest that continuous STN stimulation induces long‐term plastic changes of the dopaminergic system, with slow and partial desensitization. In addition, the persistence of levodopa intake after surgery might hinder this beneficial process.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd><bold>Keywords</bold>: levodopa; subthalamic nucleus; deep‐brain stimulation; Parkinson’s disease</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd><bold>Abbreviations</bold>: LEDD = levodopa equivalent daily dose; LDR = long‐duration response; SDR = short‐duration response; STN = subthalamic nucleus; TT = tapping test; UPDRS = Unified Parkinson’s Disease Rating Scale</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>2408</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>Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation</title></titleInfo><name type="personal"><namePart type="given">Elena</namePart><namePart type="family">Moro</namePart><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rianne J. A.</namePart><namePart type="family">Esselink</namePart><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alim Louis</namePart><namePart type="family">Benabid</namePart><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Pollak</namePart><affiliation>8, Joseph Fourier University, CHU de Grenoble, Grenoble, France, Department of Neurology, Niguarda Ca’ Granda Hospital, Milan, Italy and Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands</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">2002-11</dateIssued><copyrightDate encoding="w3cdtf">2002</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 response to levodopa changes over time in Parkinson’s disease, probably due to alterations in the dopaminergic system, progression of the disease and pulsatile oral intake of the drug. Bilateral high‐frequency stimulation of the subthalamic nucleus (STN) allows a large reduction or the complete cessation of levodopa intake in patients with advanced Parkinson’s disease. We studied variation in the motor short‐duration response (SDR) during a levodopa challenge in bilaterally STN‐stimulated patients. Twenty‐eight consecutive patients with a mean duration of Parkinson’s disease of 16.6 ± 6.0 years at the time of surgery were enrolled. Fourteen patients were evaluated both before STN stimulation and 3 months after surgery (group 1) whereas the other 14 patients were assessed before implantation and after a mean of 3 years of STN stimulation (group 2). After drug withdrawal for one night, the hand‐tapping test (TT) was carried out every 15 min, together with evaluation of dyskinesias using a modified Goetz scale. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was assessed every 30 min. In operated patients, STN stimulation was stopped 15 min before starting the clinical evaluations. A suprathreshold oral levodopa dose was given after one motor evaluation and two TTs. The clinical evaluation was carried out until the TT score returned to the baseline. In group 1, six patients continued without levodopa after surgery and the other eight received a daily mean dose of 337 mg; in group 2, seven patients continued without levodopa and the other seven received a daily mean dose of 386 mg. The main change in the levodopa SDR was a significant reduction in levodopa‐induced dyskinesias in both groups. In those patients of group 1 who did not receive levodopa after surgery, the motor UPDRS magnitude decreased and the ‘on’ UPDRS motor score worsened. In group 2, the results were similar, but in the patients who continued to receive levodopa after surgery the TT magnitude increased. On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. These results suggest that continuous STN stimulation induces long‐term plastic changes of the dopaminergic system, with slow and partial desensitization. In addition, the persistence of levodopa intake after surgery might hinder this beneficial process.</abstract><note type="author-notes">Correspondence to: Pierre Pollak, Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble, CHU, Service de Neurologie, BP 217 38043 Grenoble, France E‐mail: pierre.pollak@ujf‐grenoble.fr</note><subject lang="en"><genre>KWD</genre><topic>Keywords: levodopa; subthalamic nucleus; deep‐brain stimulation; Parkinson’s disease</topic></subject><subject lang="en"><genre>ABR</genre><topic>Abbreviations: LEDD = levodopa equivalent daily dose; LDR = long‐duration response; SDR = short‐duration response; STN = subthalamic nucleus; TT = tapping test; 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>2002</date><detail type="volume"><caption>vol.</caption><number>125</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>2408</start><end>2417</end></extent></part></relatedItem><identifier type="istex">32195035FCE3CBB97AF065117F9C33C82BC31770</identifier><identifier type="DOI">10.1093/brain/awf249</identifier><identifier type="local">awf249</identifier><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/32195035FCE3CBB97AF065117F9C33C82BC31770/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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