Abnormal involuntary movements induced by subthalamic nucleus stimulation in parkinsonian patients.
Identifieur interne : 004886 ( PubMed/Checkpoint ); précédent : 004885; suivant : 004887Abnormal involuntary movements induced by subthalamic nucleus stimulation in parkinsonian patients.
Auteurs : P. Limousin [France] ; P. Pollak ; D. Hoffmann ; A. Benazzouz ; J E Perret ; A L BenabidSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1996.
English descriptors
- KwdEn :
- Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Bromocriptine (administration & dosage), Bromocriptine (adverse effects), Combined Modality Therapy, Dominance, Cerebral (drug effects), Dominance, Cerebral (physiology), Electric Stimulation Therapy, Female, Humans, Levodopa (administration & dosage), Levodopa (adverse effects), Male, Middle Aged, Motor Activity (drug effects), Motor Activity (physiology), Motor Skills (drug effects), Motor Skills (physiology), Neurologic Examination (drug effects), Parkinson Disease (physiopathology), Thalamic Nuclei (drug effects), Thalamic Nuclei (physiopathology), Treatment Outcome.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Bromocriptine, Levodopa.
- chemical , adverse effects : Antiparkinson Agents, Bromocriptine, Levodopa.
- drug effects : Dominance, Cerebral, Motor Activity, Motor Skills, Neurologic Examination, Thalamic Nuclei.
- physiology : Dominance, Cerebral, Motor Activity, Motor Skills.
- physiopathology : Parkinson Disease, Thalamic Nuclei.
- Combined Modality Therapy, Electric Stimulation Therapy, Female, Humans, Male, Middle Aged, Treatment Outcome.
Abstract
Chronic electrical subthalamic nucleus (STN) stimulation is under investigation for alleviating parkinsonian symptoms. STN alterations may carry the risk of provoking abnormal involuntary movements (AIMs). We took advantage of the reversibility of the stimulation technique to assess the possibility of inducing AIMs, using different electrical variables with or without concomitant levodopa intake. Above a given threshold voltage, stimulation could induce contralateral distal mobile AIMs or hemiballism in the off-drug condition in two patients. AIMs occurred after a latency that varied from a few minutes up to several hours after switching on the stimulator. Hemiballism immediately disappeared upon switching off the stimulator. In these patients, levodopa had never provoked that type of AIMs before surgery. Levodopa-induced AIMs were not modified by electrical stimulation, but off-phase dystonia disappeared in one patient. Stimulation of the STN induced AIMs that resembled both those observed following spontaneous lesions of the STN and levodopa-induced diphasic AIMs in parkinsonian patients. As electrical stimulation provoked AIMs and antiparkinsonian benefit occurred with different electrical variables and different timing, the mechanisms responsible for these two effects could be distinct.
DOI: 10.1002/mds.870110303
PubMed: 8723137
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Abnormal involuntary movements induced by subthalamic nucleus stimulation in parkinsonian patients.</title><author><name sortKey="Limousin, P" sort="Limousin, P" uniqKey="Limousin P" first="P" last="Limousin">P. Limousin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble</wicri:regionArea><wicri:noRegion>Joseph Fourier University of Grenoble</wicri:noRegion><wicri:noRegion>Joseph Fourier University of Grenoble</wicri:noRegion></affiliation></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. Pollak</name></author><author><name sortKey="Hoffmann, D" sort="Hoffmann, D" uniqKey="Hoffmann D" first="D" last="Hoffmann">D. Hoffmann</name></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author><author><name sortKey="Perret, J E" sort="Perret, J E" uniqKey="Perret J" first="J E" last="Perret">J E Perret</name></author><author><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A L" last="Benabid">A L Benabid</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8723137</idno><idno type="pmid">8723137</idno><idno type="doi">10.1002/mds.870110303</idno><idno type="wicri:Area/PubMed/Corpus">004846</idno><idno type="wicri:Area/PubMed/Curation">004846</idno><idno type="wicri:Area/PubMed/Checkpoint">004886</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Abnormal involuntary movements induced by subthalamic nucleus stimulation in parkinsonian patients.</title><author><name sortKey="Limousin, P" sort="Limousin, P" uniqKey="Limousin P" first="P" last="Limousin">P. Limousin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble</wicri:regionArea><wicri:noRegion>Joseph Fourier University of Grenoble</wicri:noRegion><wicri:noRegion>Joseph Fourier University of Grenoble</wicri:noRegion></affiliation></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. Pollak</name></author><author><name sortKey="Hoffmann, D" sort="Hoffmann, D" uniqKey="Hoffmann D" first="D" last="Hoffmann">D. Hoffmann</name></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author><author><name sortKey="Perret, J E" sort="Perret, J E" uniqKey="Perret J" first="J E" last="Perret">J E Perret</name></author><author><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A L" last="Benabid">A L Benabid</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Bromocriptine (administration & dosage)</term><term>Bromocriptine (adverse effects)</term><term>Combined Modality Therapy</term><term>Dominance, Cerebral (drug effects)</term><term>Dominance, Cerebral (physiology)</term><term>Electric Stimulation Therapy</term><term>Female</term><term>Humans</term><term>Levodopa (administration & dosage)</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Middle Aged</term><term>Motor Activity (drug effects)</term><term>Motor Activity (physiology)</term><term>Motor Skills (drug effects)</term><term>Motor Skills (physiology)</term><term>Neurologic Examination (drug effects)</term><term>Parkinson Disease (physiopathology)</term><term>Thalamic Nuclei (drug effects)</term><term>Thalamic Nuclei (physiopathology)</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Bromocriptine</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Bromocriptine</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Dominance, Cerebral</term><term>Motor Activity</term><term>Motor Skills</term><term>Neurologic Examination</term><term>Thalamic Nuclei</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dominance, Cerebral</term><term>Motor Activity</term><term>Motor Skills</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>Thalamic Nuclei</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Combined Modality Therapy</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">Chronic electrical subthalamic nucleus (STN) stimulation is under investigation for alleviating parkinsonian symptoms. STN alterations may carry the risk of provoking abnormal involuntary movements (AIMs). We took advantage of the reversibility of the stimulation technique to assess the possibility of inducing AIMs, using different electrical variables with or without concomitant levodopa intake. Above a given threshold voltage, stimulation could induce contralateral distal mobile AIMs or hemiballism in the off-drug condition in two patients. AIMs occurred after a latency that varied from a few minutes up to several hours after switching on the stimulator. Hemiballism immediately disappeared upon switching off the stimulator. In these patients, levodopa had never provoked that type of AIMs before surgery. Levodopa-induced AIMs were not modified by electrical stimulation, but off-phase dystonia disappeared in one patient. Stimulation of the STN induced AIMs that resembled both those observed following spontaneous lesions of the STN and levodopa-induced diphasic AIMs in parkinsonian patients. As electrical stimulation provoked AIMs and antiparkinsonian benefit occurred with different electrical variables and different timing, the mechanisms responsible for these two effects could be distinct.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8723137</PMID><DateCreated><Year>1996</Year><Month>11</Month><Day>07</Day></DateCreated><DateCompleted><Year>1996</Year><Month>11</Month><Day>07</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>11</Volume><Issue>3</Issue><PubDate><Year>1996</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Abnormal involuntary movements induced by subthalamic nucleus stimulation in parkinsonian patients.</ArticleTitle><Pagination><MedlinePgn>231-5</MedlinePgn></Pagination><Abstract><AbstractText>Chronic electrical subthalamic nucleus (STN) stimulation is under investigation for alleviating parkinsonian symptoms. STN alterations may carry the risk of provoking abnormal involuntary movements (AIMs). We took advantage of the reversibility of the stimulation technique to assess the possibility of inducing AIMs, using different electrical variables with or without concomitant levodopa intake. Above a given threshold voltage, stimulation could induce contralateral distal mobile AIMs or hemiballism in the off-drug condition in two patients. AIMs occurred after a latency that varied from a few minutes up to several hours after switching on the stimulator. Hemiballism immediately disappeared upon switching off the stimulator. In these patients, levodopa had never provoked that type of AIMs before surgery. Levodopa-induced AIMs were not modified by electrical stimulation, but off-phase dystonia disappeared in one patient. Stimulation of the STN induced AIMs that resembled both those observed following spontaneous lesions of the STN and levodopa-induced diphasic AIMs in parkinsonian patients. As electrical stimulation provoked AIMs and antiparkinsonian benefit occurred with different electrical variables and different timing, the mechanisms responsible for these two effects could be distinct.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Limousin</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University of Grenoble, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pollak</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Hoffmann</LastName><ForeName>D</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Perret</LastName><ForeName>J E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Benabid</LastName><ForeName>A L</ForeName><Initials>AL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>3A64E3G5ZO</RegistryNumber><NameOfSubstance UI="D001971">Bromocriptine</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001971">Bromocriptine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003131">Combined Modality Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004292">Dominance, Cerebral</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004599">Electric Stimulation Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009043">Motor Activity</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009048">Motor Skills</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009460">Neurologic Examination</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013787">Thalamic Nuclei</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016896">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>5</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8723137</ArticleId><ArticleId IdType="doi">10.1002/mds.870110303</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country></list><tree><noCountry><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A L" last="Benabid">A L Benabid</name><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name><name sortKey="Hoffmann, D" sort="Hoffmann, D" uniqKey="Hoffmann D" first="D" last="Hoffmann">D. Hoffmann</name><name sortKey="Perret, J E" sort="Perret, J E" uniqKey="Perret J" first="J E" last="Perret">J E Perret</name><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. Pollak</name></noCountry><country name="France"><noRegion><name sortKey="Limousin, P" sort="Limousin, P" uniqKey="Limousin P" first="P" last="Limousin">P. Limousin</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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