Implication of the subthalamic nucleus in the pathophysiology and pathogenesis of Parkinson's disease.
Identifieur interne : 001340 ( PubMed/Corpus ); précédent : 001339; suivant : 001341Implication of the subthalamic nucleus in the pathophysiology and pathogenesis of Parkinson's disease.
Auteurs : A. Benazzouz ; B. Piallat ; Z G Ni ; A. Koudsie ; P. Pollak ; A L BenabidSource :
- Cell transplantation [ 0963-6897 ]
English descriptors
- KwdEn :
- Animals, Basal Ganglia (physiopathology), Cell Death, Electric Stimulation Therapy, Humans, Parkinson Disease (etiology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Parkinsonian Disorders (etiology), Parkinsonian Disorders (physiopathology), Parkinsonian Disorders (therapy), Rats, Subthalamic Nucleus (physiopathology).
- MESH :
- etiology : Parkinson Disease, Parkinsonian Disorders.
- physiopathology : Basal Ganglia, Parkinson Disease, Parkinsonian Disorders, Subthalamic Nucleus.
- therapy : Parkinson Disease, Parkinsonian Disorders.
- Animals, Cell Death, Electric Stimulation Therapy, Humans, Rats.
Abstract
The subthalamic nucleus (STN) has been shown to play an important role in the control of movement and has been considered as a key structure in the functional organization of the basal ganglia. Several studies postulated that the STN plays a critical role in the pathophysiology of Parkinson's disease and that its inhibition or its lesioning can reverse the cardinal motor symptoms. Nevertheless, the beneficial effect was accompanied by dyskinetic abnormal movements. In order to avoid unpleasant and irreversible side effects we used high-frequency stimulation (HFS) of the STN instead of lesions. We have shown that parkinsonian motor symptoms, akinesia, rigidity, and tremor can be alleviated by HFS of the STN in the nonhuman primate model. Side effects were controllable and appeared only at intensities higher than that inducing the improvement of motor symptoms. In severe parkinsonian patients, bilateral STN-HFS greatly improved parkinsonian motor symptoms. Motor fluctuations were attenuated and patients became independent in most activities of daily living. It appears that STN-HFS mimics the effects of lesions by inhibiting its neuronal activity. In a rat model of parkinsonism, we studied the implication of the STN in the excitotoxicity of nigral dopamine cells. We showed that kainic acid lesioning of the STN can protect nigral dopaminergic cells against 6-hydroxydopamine-induced toxicity. The evidence reviewed in the present article clearly demonstrates that the STN is implicated in the pathophysiology and pathogenesis of Parkinson's disease.
PubMed: 10811394
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pubmed:10811394Le document en format XML
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Pollak</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="????"><PubDate><MedlineDate>2000 Mar-Apr</MedlineDate></PubDate></date><idno type="RBID">pubmed:10811394</idno><idno type="pmid">10811394</idno><idno type="wicri:Area/PubMed/Corpus">001340</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001340</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Implication of the subthalamic nucleus in the pathophysiology and pathogenesis of Parkinson's disease.</title><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name><affiliation><nlm:affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, Grenoble, France. 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Pollak</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">Cell transplantation</title><idno type="ISSN">0963-6897</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Basal Ganglia (physiopathology)</term><term>Cell Death</term><term>Electric Stimulation Therapy</term><term>Humans</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Parkinsonian Disorders (etiology)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Parkinsonian Disorders (therapy)</term><term>Rats</term><term>Subthalamic Nucleus (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Death</term><term>Electric Stimulation Therapy</term><term>Humans</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The subthalamic nucleus (STN) has been shown to play an important role in the control of movement and has been considered as a key structure in the functional organization of the basal ganglia. Several studies postulated that the STN plays a critical role in the pathophysiology of Parkinson's disease and that its inhibition or its lesioning can reverse the cardinal motor symptoms. Nevertheless, the beneficial effect was accompanied by dyskinetic abnormal movements. In order to avoid unpleasant and irreversible side effects we used high-frequency stimulation (HFS) of the STN instead of lesions. We have shown that parkinsonian motor symptoms, akinesia, rigidity, and tremor can be alleviated by HFS of the STN in the nonhuman primate model. Side effects were controllable and appeared only at intensities higher than that inducing the improvement of motor symptoms. In severe parkinsonian patients, bilateral STN-HFS greatly improved parkinsonian motor symptoms. Motor fluctuations were attenuated and patients became independent in most activities of daily living. It appears that STN-HFS mimics the effects of lesions by inhibiting its neuronal activity. In a rat model of parkinsonism, we studied the implication of the STN in the excitotoxicity of nigral dopamine cells. We showed that kainic acid lesioning of the STN can protect nigral dopaminergic cells against 6-hydroxydopamine-induced toxicity. The evidence reviewed in the present article clearly demonstrates that the STN is implicated in the pathophysiology and pathogenesis of Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10811394</PMID><DateCreated><Year>2000</Year><Month>08</Month><Day>07</Day></DateCreated><DateCompleted><Year>2000</Year><Month>08</Month><Day>07</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0963-6897</ISSN><JournalIssue CitedMedium="Print"><Volume>9</Volume><Issue>2</Issue><PubDate><MedlineDate>2000 Mar-Apr</MedlineDate></PubDate></JournalIssue><Title>Cell transplantation</Title><ISOAbbreviation>Cell Transplant</ISOAbbreviation></Journal><ArticleTitle>Implication of the subthalamic nucleus in the pathophysiology and pathogenesis of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>215-21</MedlinePgn></Pagination><Abstract><AbstractText>The subthalamic nucleus (STN) has been shown to play an important role in the control of movement and has been considered as a key structure in the functional organization of the basal ganglia. Several studies postulated that the STN plays a critical role in the pathophysiology of Parkinson's disease and that its inhibition or its lesioning can reverse the cardinal motor symptoms. Nevertheless, the beneficial effect was accompanied by dyskinetic abnormal movements. In order to avoid unpleasant and irreversible side effects we used high-frequency stimulation (HFS) of the STN instead of lesions. We have shown that parkinsonian motor symptoms, akinesia, rigidity, and tremor can be alleviated by HFS of the STN in the nonhuman primate model. Side effects were controllable and appeared only at intensities higher than that inducing the improvement of motor symptoms. In severe parkinsonian patients, bilateral STN-HFS greatly improved parkinsonian motor symptoms. Motor fluctuations were attenuated and patients became independent in most activities of daily living. It appears that STN-HFS mimics the effects of lesions by inhibiting its neuronal activity. In a rat model of parkinsonism, we studied the implication of the STN in the excitotoxicity of nigral dopamine cells. We showed that kainic acid lesioning of the STN can protect nigral dopaminergic cells against 6-hydroxydopamine-induced toxicity. The evidence reviewed in the present article clearly demonstrates that the STN is implicated in the pathophysiology and pathogenesis of Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, Grenoble, France. 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