Dopaminergic and non-dopaminergic pharmacological hypotheses for gait disorders in Parkinson's disease.
Identifieur interne : 000A69 ( PubMed/Corpus ); précédent : 000A68; suivant : 000A70Dopaminergic and non-dopaminergic pharmacological hypotheses for gait disorders in Parkinson's disease.
Auteurs : David Devos ; L. Defebvre ; R. BordetSource :
- Fundamental & clinical pharmacology [ 1472-8206 ] ; 2010.
English descriptors
- KwdEn :
- Antiparkinson Agents (adverse effects), Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Clinical Trials as Topic, Dopamine (metabolism), Gait Disorders, Neurologic (drug therapy), Gait Disorders, Neurologic (etiology), Gait Disorders, Neurologic (metabolism), Gait Disorders, Neurologic (physiopathology), Humans, Norepinephrine (metabolism), Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Pedunculopontine Tegmental Nucleus (drug effects), Pedunculopontine Tegmental Nucleus (metabolism), Pedunculopontine Tegmental Nucleus (physiopathology), Subthalamic Nucleus (drug effects), Subthalamic Nucleus (metabolism), Subthalamic Nucleus (physiopathology), Treatment Outcome.
- MESH :
- chemical , adverse effects : Antiparkinson Agents.
- chemical , metabolism : Dopamine, Norepinephrine.
- chemical , pharmacology : Antiparkinson Agents.
- chemical , therapeutic use : Antiparkinson Agents.
- complications : Parkinson Disease.
- drug effects : Pedunculopontine Tegmental Nucleus, Subthalamic Nucleus.
- drug therapy : Gait Disorders, Neurologic, Parkinson Disease.
- etiology : Gait Disorders, Neurologic.
- metabolism : Gait Disorders, Neurologic, Parkinson Disease, Pedunculopontine Tegmental Nucleus, Subthalamic Nucleus.
- physiopathology : Gait Disorders, Neurologic, Parkinson Disease, Pedunculopontine Tegmental Nucleus, Subthalamic Nucleus.
- Clinical Trials as Topic, Humans, Treatment Outcome.
Abstract
Gait disorders form one component of the axial disorders observed in Parkinson's disease (PD). Indeed, short steps with a forward-leaning stance are diagnostic criteria for PD in the early stages of the condition. Gait disorders also represent a major source of therapeutic failure in the advanced stages of PD (with the appearance of freezing of gait and falls) because they do not respond optimally to the two hand late-stage therapeutics--levodopa and electrical subthalamic nucleus (STN) stimulation. The late onset of doparesistance in these disorders may be linked to propagation of neurodegeneration to structures directly involved in gait control and to non-dopaminergic neurotransmitter systems. The coeruleus locus (a source of noradrenaline) is rapidly and severely affected, leading to a major motor impact. The pedunculopontine nucleus (PPN) and lateral pontine tegmentum (rich in acetylcholine) are both involved in gait. Degenerative damage to the serotoninergic raphe nuclei appears to be less severe, although serotonin-dopamine interactions are numerous and complex. Lastly, dopaminergic depletion leads to glutamatergic hyperactivity of the efferent pathways from the the STN to the PPN. However, the relationships between the various parkinsonian symptoms (and particularly gait disorders) and these pharmacological targets have yet to be fully elucidated. The goal of this review is to develop the various pathophysiological hypotheses published to date, in order to underpin and justify ongoing fundamental research and clinical trials in this disease area.
DOI: 10.1111/j.1472-8206.2009.00798.x
PubMed: 20163480
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pubmed:20163480Le document en format XML
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Bordet</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20163480</idno><idno type="pmid">20163480</idno><idno type="doi">10.1111/j.1472-8206.2009.00798.x</idno><idno type="wicri:Area/PubMed/Corpus">000A69</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000A69</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dopaminergic and non-dopaminergic pharmacological hypotheses for gait disorders in Parkinson's disease.</title><author><name sortKey="Devos, David" sort="Devos, David" uniqKey="Devos D" first="David" last="Devos">David Devos</name><affiliation><nlm:affiliation>Department of Neurology and Movement Disorders, EA2683, IMPRT, IFR 114, Faculty of Medicine Lille 2, University of Lille Nord de France, Lille University Hospital, Lille, France. d-devos@chru-lille.fr</nlm:affiliation></affiliation></author><author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. Defebvre</name></author><author><name sortKey="Bordet, R" sort="Bordet, R" uniqKey="Bordet R" first="R" last="Bordet">R. Bordet</name></author></analytic><series><title level="j">Fundamental & clinical pharmacology</title><idno type="eISSN">1472-8206</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Clinical Trials as Topic</term><term>Dopamine (metabolism)</term><term>Gait Disorders, Neurologic (drug therapy)</term><term>Gait Disorders, Neurologic (etiology)</term><term>Gait Disorders, Neurologic (metabolism)</term><term>Gait Disorders, Neurologic (physiopathology)</term><term>Humans</term><term>Norepinephrine (metabolism)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (physiopathology)</term><term>Pedunculopontine Tegmental Nucleus (drug effects)</term><term>Pedunculopontine Tegmental Nucleus (metabolism)</term><term>Pedunculopontine Tegmental Nucleus (physiopathology)</term><term>Subthalamic Nucleus (drug effects)</term><term>Subthalamic Nucleus (metabolism)</term><term>Subthalamic Nucleus (physiopathology)</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Norepinephrine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Pedunculopontine Tegmental Nucleus</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Gait Disorders, Neurologic</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Gait Disorders, Neurologic</term><term>Parkinson Disease</term><term>Pedunculopontine Tegmental Nucleus</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Gait Disorders, Neurologic</term><term>Parkinson Disease</term><term>Pedunculopontine Tegmental Nucleus</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Clinical Trials as Topic</term><term>Humans</term><term>Treatment Outcome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gait disorders form one component of the axial disorders observed in Parkinson's disease (PD). Indeed, short steps with a forward-leaning stance are diagnostic criteria for PD in the early stages of the condition. Gait disorders also represent a major source of therapeutic failure in the advanced stages of PD (with the appearance of freezing of gait and falls) because they do not respond optimally to the two hand late-stage therapeutics--levodopa and electrical subthalamic nucleus (STN) stimulation. The late onset of doparesistance in these disorders may be linked to propagation of neurodegeneration to structures directly involved in gait control and to non-dopaminergic neurotransmitter systems. The coeruleus locus (a source of noradrenaline) is rapidly and severely affected, leading to a major motor impact. The pedunculopontine nucleus (PPN) and lateral pontine tegmentum (rich in acetylcholine) are both involved in gait. Degenerative damage to the serotoninergic raphe nuclei appears to be less severe, although serotonin-dopamine interactions are numerous and complex. Lastly, dopaminergic depletion leads to glutamatergic hyperactivity of the efferent pathways from the the STN to the PPN. However, the relationships between the various parkinsonian symptoms (and particularly gait disorders) and these pharmacological targets have yet to be fully elucidated. The goal of this review is to develop the various pathophysiological hypotheses published to date, in order to underpin and justify ongoing fundamental research and clinical trials in this disease area.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20163480</PMID><DateCreated><Year>2010</Year><Month>07</Month><Day>23</Day></DateCreated><DateCompleted><Year>2010</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1472-8206</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>4</Issue><PubDate><Year>2010</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Fundamental & clinical pharmacology</Title><ISOAbbreviation>Fundam Clin Pharmacol</ISOAbbreviation></Journal><ArticleTitle>Dopaminergic and non-dopaminergic pharmacological hypotheses for gait disorders in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>407-21</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1472-8206.2009.00798.x</ELocationID><Abstract><AbstractText>Gait disorders form one component of the axial disorders observed in Parkinson's disease (PD). Indeed, short steps with a forward-leaning stance are diagnostic criteria for PD in the early stages of the condition. Gait disorders also represent a major source of therapeutic failure in the advanced stages of PD (with the appearance of freezing of gait and falls) because they do not respond optimally to the two hand late-stage therapeutics--levodopa and electrical subthalamic nucleus (STN) stimulation. The late onset of doparesistance in these disorders may be linked to propagation of neurodegeneration to structures directly involved in gait control and to non-dopaminergic neurotransmitter systems. The coeruleus locus (a source of noradrenaline) is rapidly and severely affected, leading to a major motor impact. The pedunculopontine nucleus (PPN) and lateral pontine tegmentum (rich in acetylcholine) are both involved in gait. Degenerative damage to the serotoninergic raphe nuclei appears to be less severe, although serotonin-dopamine interactions are numerous and complex. Lastly, dopaminergic depletion leads to glutamatergic hyperactivity of the efferent pathways from the the STN to the PPN. However, the relationships between the various parkinsonian symptoms (and particularly gait disorders) and these pharmacological targets have yet to be fully elucidated. The goal of this review is to develop the various pathophysiological hypotheses published to date, in order to underpin and justify ongoing fundamental research and clinical trials in this disease area.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Devos</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Neurology and Movement Disorders, EA2683, IMPRT, IFR 114, Faculty of Medicine Lille 2, University of Lille Nord de France, Lille University Hospital, Lille, France. d-devos@chru-lille.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Defebvre</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Bordet</LastName><ForeName>R</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>02</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Fundam Clin Pharmacol</MedlineTA><NlmUniqueID>8710411</NlmUniqueID><ISSNLinking>0767-3981</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>X4W3ENH1CV</RegistryNumber><NameOfSubstance UI="D009638">Norepinephrine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="Y">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002986" MajorTopicYN="N">Clinical Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020233" MajorTopicYN="N">Gait Disorders, Neurologic</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009638" MajorTopicYN="N">Norepinephrine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045042" MajorTopicYN="N">Pedunculopontine Tegmental Nucleus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20163480</ArticleId><ArticleId IdType="pii">FCP798</ArticleId><ArticleId IdType="doi">10.1111/j.1472-8206.2009.00798.x</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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