The globus pallidus, deep brain stimulation, and Parkinson's disease.
Identifieur interne : 001508 ( PubMed/Corpus ); précédent : 001507; suivant : 001509The globus pallidus, deep brain stimulation, and Parkinson's disease.
Auteurs : Jonathan O. Dostrovsky ; William D. Hutchison ; Andres M. LozanoSource :
- The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry [ 1073-8584 ] ; 2002.
English descriptors
- KwdEn :
- Animals, Dopamine (metabolism), Electric Stimulation Therapy, Globus Pallidus (metabolism), Globus Pallidus (physiopathology), Globus Pallidus (surgery), Humans, Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Parkinson Disease (surgery), Parkinson Disease (therapy), Substantia Nigra (physiopathology), gamma-Aminobutyric Acid (metabolism).
- MESH :
- chemical , metabolism : Dopamine, gamma-Aminobutyric Acid.
- metabolism : Globus Pallidus, Parkinson Disease.
- physiopathology : Globus Pallidus, Parkinson Disease, Substantia Nigra.
- surgery : Globus Pallidus, Parkinson Disease.
- therapy : Parkinson Disease.
- Animals, Electric Stimulation Therapy, Humans.
Abstract
Parkinson's disease (PD) is caused by the degeneration of the dopaminergic neurons in the substantia nigra. Loss of dopaminergic innervation leads to hyperactivity in the internal segment of the globus pallidus (GPi), the main output nucleus of the basal ganglia and to a profound disturbance in the function of motor circuits. Lesions of the GPi (or in its upstream modulator, the subthalamic nucleus) can greatly improve the motor symptoms of PD presumably by reducing this pathological activity. Paradoxically, high-frequency electrical stimulation of the GPi (deep brain stimulation, DBS) mimics the effects of pallidotomy and has become an accepted therapeutic technique. The mechanisms underlying the beneficial effects of pallidal DBS are not known. Various mechanisms that might account for inhibiting or disrupting the pathological pallidal outflow by high-frequency DBS have been proposed ranging from depolarization block to stimulation-evoked release of GABA, and these are discussed.
DOI: 10.1177/1073858402008003014
PubMed: 12061508
Links to Exploration step
pubmed:12061508Le document en format XML
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Dostrovsky</name><affiliation><nlm:affiliation>Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada. j.dostrovsky@utoronto.ca</nlm:affiliation></affiliation></author><author><name sortKey="Hutchison, William D" sort="Hutchison, William D" uniqKey="Hutchison W" first="William D" last="Hutchison">William D. Hutchison</name></author><author><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M" last="Lozano">Andres M. 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Loss of dopaminergic innervation leads to hyperactivity in the internal segment of the globus pallidus (GPi), the main output nucleus of the basal ganglia and to a profound disturbance in the function of motor circuits. Lesions of the GPi (or in its upstream modulator, the subthalamic nucleus) can greatly improve the motor symptoms of PD presumably by reducing this pathological activity. Paradoxically, high-frequency electrical stimulation of the GPi (deep brain stimulation, DBS) mimics the effects of pallidotomy and has become an accepted therapeutic technique. The mechanisms underlying the beneficial effects of pallidal DBS are not known. Various mechanisms that might account for inhibiting or disrupting the pathological pallidal outflow by high-frequency DBS have been proposed ranging from depolarization block to stimulation-evoked release of GABA, and these are discussed.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12061508</PMID><DateCreated><Year>2002</Year><Month>06</Month><Day>13</Day></DateCreated><DateCompleted><Year>2002</Year><Month>12</Month><Day>27</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1073-8584</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><Issue>3</Issue><PubDate><Year>2002</Year><Month>Jun</Month></PubDate></JournalIssue><Title>The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry</Title><ISOAbbreviation>Neuroscientist</ISOAbbreviation></Journal><ArticleTitle>The globus pallidus, deep brain stimulation, and Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>284-90</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease (PD) is caused by the degeneration of the dopaminergic neurons in the substantia nigra. Loss of dopaminergic innervation leads to hyperactivity in the internal segment of the globus pallidus (GPi), the main output nucleus of the basal ganglia and to a profound disturbance in the function of motor circuits. Lesions of the GPi (or in its upstream modulator, the subthalamic nucleus) can greatly improve the motor symptoms of PD presumably by reducing this pathological activity. Paradoxically, high-frequency electrical stimulation of the GPi (deep brain stimulation, DBS) mimics the effects of pallidotomy and has become an accepted therapeutic technique. The mechanisms underlying the beneficial effects of pallidal DBS are not known. Various mechanisms that might account for inhibiting or disrupting the pathological pallidal outflow by high-frequency DBS have been proposed ranging from depolarization block to stimulation-evoked release of GABA, and these are discussed.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dostrovsky</LastName><ForeName>Jonathan O</ForeName><Initials>JO</Initials><AffiliationInfo><Affiliation>Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada. j.dostrovsky@utoronto.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hutchison</LastName><ForeName>William D</ForeName><Initials>WD</Initials></Author><Author ValidYN="Y"><LastName>Lozano</LastName><ForeName>Andres M</ForeName><Initials>AM</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neuroscientist</MedlineTA><NlmUniqueID>9504819</NlmUniqueID><ISSNLinking>1073-8584</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>56-12-2</RegistryNumber><NameOfSubstance UI="D005680">gamma-Aminobutyric Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004599" MajorTopicYN="Y">Electric Stimulation Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005917" MajorTopicYN="N">Globus Pallidus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005680" MajorTopicYN="N">gamma-Aminobutyric Acid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>46</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>6</Month><Day>14</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>12</Month><Day>28</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>6</Month><Day>14</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12061508</ArticleId><ArticleId IdType="doi">10.1177/1073858402008003014</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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