Ineffective subthalamic nucleus stimulation in levodopa-resistant postischemic parkinsonism.
Identifieur interne : 001309 ( PubMed/Corpus ); précédent : 001308; suivant : 001310Ineffective subthalamic nucleus stimulation in levodopa-resistant postischemic parkinsonism.
Auteurs : P. Krack ; P L Dowsey ; A L Benabid ; N. Acarin ; A. Benazzouz ; G. Künig ; K L Leenders ; J A Obeso ; P. PollakSource :
- Neurology [ 0028-3878 ] ; 2000.
English descriptors
- KwdEn :
- Antiparkinson Agents (therapeutic use), Drug Resistance, Electric Stimulation, Globus Pallidus (pathology), Humans, Levodopa (therapeutic use), Male, Middle Aged, Myocardial Ischemia (complications), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (etiology), Parkinson Disease, Secondary (surgery), Subthalamic Nucleus (pathology), Subthalamic Nucleus (surgery).
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- complications : Myocardial Ischemia.
- drug therapy : Parkinson Disease, Secondary.
- etiology : Parkinson Disease, Secondary.
- pathology : Globus Pallidus, Subthalamic Nucleus.
- surgery : Parkinson Disease, Secondary, Subthalamic Nucleus.
- Drug Resistance, Electric Stimulation, Humans, Male, Middle Aged.
Abstract
The authors report a patient with postischemic parkinsonism who responded neither to levodopa nor to bilateral subthalamic nucleus (STN) stimulation. MRI revealed bilateral lesions of the substantia nigra, the striatum, the external pallidum, and part of the internal pallidum. PET showed reduced striatal dopa-decarboxylase activity, D2 receptor binding, and glucose metabolism. Perioperative microrecording showed low-frequency activity of STN cells. This case suggests that parkinsonian patients who do not have a good response to levodopa or in whom a postsynaptic dopaminergic lesion can be shown may not be good candidates for STN surgery.
PubMed: 10851392
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pubmed:10851392Le document en format XML
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Benazzouz</name></author><author><name sortKey="Kunig, G" sort="Kunig, G" uniqKey="Kunig G" first="G" last="Künig">G. Künig</name></author><author><name sortKey="Leenders, K L" sort="Leenders, K L" uniqKey="Leenders K" first="K L" last="Leenders">K L Leenders</name></author><author><name sortKey="Obeso, J A" sort="Obeso, J A" uniqKey="Obeso J" first="J A" last="Obeso">J A Obeso</name></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. 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Krack</name><affiliation><nlm:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France. p.krack@neurologie.uni-kiel.de</nlm:affiliation></affiliation></author><author><name sortKey="Dowsey, P L" sort="Dowsey, P L" uniqKey="Dowsey P" first="P L" last="Dowsey">P L Dowsey</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><author><name sortKey="Acarin, N" sort="Acarin, N" uniqKey="Acarin N" first="N" last="Acarin">N. Acarin</name></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author><author><name sortKey="Kunig, G" sort="Kunig, G" uniqKey="Kunig G" first="G" last="Künig">G. Künig</name></author><author><name sortKey="Leenders, K L" sort="Leenders, K L" uniqKey="Leenders K" first="K L" last="Leenders">K L Leenders</name></author><author><name sortKey="Obeso, J A" sort="Obeso, J A" uniqKey="Obeso J" first="J A" last="Obeso">J A Obeso</name></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. Pollak</name></author></analytic><series><title level="j">Neurology</title><idno type="ISSN">0028-3878</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (therapeutic use)</term><term>Drug Resistance</term><term>Electric Stimulation</term><term>Globus Pallidus (pathology)</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Myocardial Ischemia (complications)</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (etiology)</term><term>Parkinson Disease, Secondary (surgery)</term><term>Subthalamic Nucleus (pathology)</term><term>Subthalamic Nucleus (surgery)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Myocardial Ischemia</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Globus Pallidus</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Parkinson Disease, Secondary</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Drug Resistance</term><term>Electric Stimulation</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The authors report a patient with postischemic parkinsonism who responded neither to levodopa nor to bilateral subthalamic nucleus (STN) stimulation. MRI revealed bilateral lesions of the substantia nigra, the striatum, the external pallidum, and part of the internal pallidum. PET showed reduced striatal dopa-decarboxylase activity, D2 receptor binding, and glucose metabolism. Perioperative microrecording showed low-frequency activity of STN cells. This case suggests that parkinsonian patients who do not have a good response to levodopa or in whom a postsynaptic dopaminergic lesion can be shown may not be good candidates for STN surgery.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10851392</PMID><DateCreated><Year>2000</Year><Month>07</Month><Day>13</Day></DateCreated><DateCompleted><Year>2000</Year><Month>07</Month><Day>13</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0028-3878</ISSN><JournalIssue CitedMedium="Print"><Volume>54</Volume><Issue>11</Issue><PubDate><Year>2000</Year><Month>Jun</Month><Day>13</Day></PubDate></JournalIssue><Title>Neurology</Title><ISOAbbreviation>Neurology</ISOAbbreviation></Journal><ArticleTitle>Ineffective subthalamic nucleus stimulation in levodopa-resistant postischemic parkinsonism.</ArticleTitle><Pagination><MedlinePgn>2182-4</MedlinePgn></Pagination><Abstract><AbstractText>The authors report a patient with postischemic parkinsonism who responded neither to levodopa nor to bilateral subthalamic nucleus (STN) stimulation. MRI revealed bilateral lesions of the substantia nigra, the striatum, the external pallidum, and part of the internal pallidum. PET showed reduced striatal dopa-decarboxylase activity, D2 receptor binding, and glucose metabolism. Perioperative microrecording showed low-frequency activity of STN cells. This case suggests that parkinsonian patients who do not have a good response to levodopa or in whom a postsynaptic dopaminergic lesion can be shown may not be good candidates for STN surgery.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Krack</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France. p.krack@neurologie.uni-kiel.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dowsey</LastName><ForeName>P L</ForeName><Initials>PL</Initials></Author><Author ValidYN="Y"><LastName>Benabid</LastName><ForeName>A L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Acarin</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Künig</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Leenders</LastName><ForeName>K L</ForeName><Initials>KL</Initials></Author><Author ValidYN="Y"><LastName>Obeso</LastName><ForeName>J A</ForeName><Initials>JA</Initials></Author><Author ValidYN="Y"><LastName>Pollak</LastName><ForeName>P</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurology</MedlineTA><NlmUniqueID>0401060</NlmUniqueID><ISSNLinking>0028-3878</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="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004351" MajorTopicYN="N">Drug Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005917" MajorTopicYN="N">Globus Pallidus</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017202" MajorTopicYN="Y">Myocardial Ischemia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="Y">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>6</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>7</Month><Day>15</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>6</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10851392</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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