Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation.
Identifieur interne : 001158 ( PubMed/Corpus ); précédent : 001157; suivant : 001159Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation.
Auteurs : Elena Moro ; Rianne J A. Esselink ; Alim Louis Benabid ; Pierre PollakSource :
- Brain : a journal of neurology [ 0006-8950 ] ; 2002.
English descriptors
- KwdEn :
- Adult, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Dose-Response Relationship, Drug, Down-Regulation (physiology), Dyskinesia, Drug-Induced (physiopathology), Dyskinesia, Drug-Induced (therapy), Electric Stimulation Therapy, Female, Functional Laterality (physiology), Humans, Levodopa (administration & dosage), Levodopa (adverse effects), Male, Middle Aged, Parkinson Disease (physiopathology), Parkinson Disease (therapy), Recovery of Function (physiology), Subthalamic Nucleus (physiology), Subthalamic Nucleus (surgery), Treatment Outcome.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Levodopa.
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- physiology : Down-Regulation, Functional Laterality, Recovery of Function, Subthalamic Nucleus.
- physiopathology : Dyskinesia, Drug-Induced, Parkinson Disease.
- surgery : Subthalamic Nucleus.
- therapy : Dyskinesia, Drug-Induced, Parkinson Disease.
- Adult, Dose-Response Relationship, Drug, Electric Stimulation Therapy, Female, Humans, Male, Middle Aged, Treatment Outcome.
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.
PubMed: 12390968
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<record><TEI><teiHeader><fileDesc><titleStmt><title 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><nlm:affiliation>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France.</nlm: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></author><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim Louis" last="Benabid">Alim Louis Benabid</name></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12390968</idno><idno type="pmid">12390968</idno><idno type="wicri:Area/PubMed/Corpus">001158</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001158</idno></publicationStmt><sourceDesc><biblStruct><analytic><title 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><nlm:affiliation>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France.</nlm: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></author><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim Louis" last="Benabid">Alim Louis Benabid</name></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="ISSN">0006-8950</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Dose-Response Relationship, Drug</term><term>Down-Regulation (physiology)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Dyskinesia, Drug-Induced (therapy)</term><term>Electric Stimulation Therapy</term><term>Female</term><term>Functional Laterality (physiology)</term><term>Humans</term><term>Levodopa (administration & dosage)</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Recovery of Function (physiology)</term><term>Subthalamic Nucleus (physiology)</term><term>Subthalamic Nucleus (surgery)</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Down-Regulation</term><term>Functional Laterality</term><term>Recovery of Function</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Dose-Response Relationship, Drug</term><term>Electric Stimulation Therapy</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Treatment Outcome</term></keywords></textClass></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12390968</PMID><DateCreated><Year>2002</Year><Month>10</Month><Day>22</Day></DateCreated><DateCompleted><Year>2002</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8950</ISSN><JournalIssue CitedMedium="Print"><Volume>125</Volume><Issue>Pt 11</Issue><PubDate><Year>2002</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Response to levodopa in parkinsonian patients with bilateral subthalamic nucleus stimulation.</ArticleTitle><Pagination><MedlinePgn>2408-17</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moro</LastName><ForeName>Elena</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University, CHU de Grenoble, Grenoble, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Esselink</LastName><ForeName>Rianne J A</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Benabid</LastName><ForeName>Alim Louis</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Pollak</LastName><ForeName>Pierre</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004599" MajorTopicYN="Y">Electric Stimulation Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007839" MajorTopicYN="N">Functional Laterality</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020127" MajorTopicYN="N">Recovery of Function</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>10</Month><Day>23</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>12</Month><Day>17</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>10</Month><Day>23</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12390968</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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