Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus
Identifieur interne : 000673 ( Istex/Corpus ); précédent : 000672; suivant : 000674Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus
Auteurs : Ned Jenkinson ; Dipanker Nandi ; Kalai Muthusamy ; Nicola J. Ray ; Ralph Gregory ; John F. Stein ; Tipu Z. AzizSource :
- Movement Disorders [ 0885-3185 ] ; 2009-02-15.
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Abstract
The pedunculopontine nucleus is composed of cholinergic and non‐cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post‐mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.22189
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Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post‐mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ned Jenkinson PhD</name><affiliations><json:string>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</json:string><json:string>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</json:string><json:string>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</json:string></affiliations></json:item><json:item><name>Dipanker Nandi DPhil</name><affiliations><json:string>Imperial College London, Division of Neuroscience and Mental Health, Charing Cross Campus, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Kalai Muthusamy MSurg</name><affiliations><json:string>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</json:string><json:string>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</json:string></affiliations></json:item><json:item><name>Nicola J. 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Aziz DMedSci</name><affiliations><json:string>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</json:string><json:string>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>PPN</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pedunculopontine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>anatomy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>physiology</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The pedunculopontine nucleus is composed of cholinergic and non‐cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post‐mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. 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The CME activity including form, can be found online at http://www.movementdisorders.org/education/journalcme/</note><note>Medical Research Council UK</note><note>Charles Wolfson Charitable Foundation</note><note>Oxford Biomedical Research Centre</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus</title><author><persName><forename type="first">Ned</forename><surname>Jenkinson</surname><roleName type="degree">PhD</roleName></persName><note type="correspondence"><p>Correspondence: Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom</p></note><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation></author><author><persName><forename type="first">Dipanker</forename><surname>Nandi</surname><roleName type="degree">DPhil</roleName></persName><affiliation>Imperial College London, Division of Neuroscience and Mental Health, Charing Cross Campus, London, United Kingdom</affiliation></author><author><persName><forename type="first">Kalai</forename><surname>Muthusamy</surname><roleName type="degree">MSurg</roleName></persName><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation></author><author><persName><forename type="first">Nicola J.</forename><surname>Ray</surname><roleName type="degree">DPhil</roleName></persName><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation></author><author><persName><forename type="first">Ralph</forename><surname>Gregory</surname><roleName type="degree">FRCP</roleName></persName><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation></author><author><persName><forename type="first">John F.</forename><surname>Stein</surname><roleName type="degree">FRCP</roleName></persName><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation></author><author><persName><forename type="first">Tipu Z.</forename><surname>Aziz</surname><roleName type="degree">DMedSci</roleName></persName><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>PPN</term></item><item><term>pedunculopontine</term></item><item><term>Parkinson's disease</term></item><item><term>anatomy</term></item><item><term>physiology</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-05-06">Received</change><change when="2008-06-01">Registration</change><change when="2009-02-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F8A804FC7A5031E670C1DF07EEB78B934B925243/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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#af3"><personName><givenNames>Kalai</givenNames><familyName>Muthusamy</familyName><degrees>MSurg</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Nicola J.</givenNames><familyName>Ray</familyName><degrees>DPhil</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ralph</givenNames><familyName>Gregory</familyName><degrees>FRCP</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>John F.</givenNames><familyName>Stein</familyName><degrees>FRCP</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Tipu Z.</givenNames><familyName>Aziz</familyName><degrees>DMedSci</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="GB" type="organization"><unparsedAffiliation>Imperial College London, Division of Neuroscience and Mental Health, Charing Cross Campus, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">PPN</keyword><keyword xml:id="kwd2">pedunculopontine</keyword><keyword xml:id="kwd3">Parkinson's disease</keyword><keyword xml:id="kwd4">anatomy</keyword><keyword xml:id="kwd5">physiology</keyword></keywordGroup><fundingInfo><fundingAgency>Medical Research Council UK</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Charles Wolfson Charitable Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Oxford Biomedical Research Centre</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The pedunculopontine nucleus is composed of cholinergic and non‐cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post‐mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note><note xml:id="fn2"><p>This article is part of the journal's online CME program. The CME activity including form, can be found online at <url href="http://www.movementdisorders.org/education/journalcme/">http://www.movementdisorders.org/education/journalcme/</url></p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PPN Review</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus</title></titleInfo><name type="personal"><namePart type="given">Ned</namePart><namePart type="family">Jenkinson</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation><description>Correspondence: Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dipanker</namePart><namePart type="family">Nandi</namePart><namePart type="termsOfAddress">DPhil</namePart><affiliation>Imperial College London, Division of Neuroscience and Mental Health, Charing Cross Campus, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kalai</namePart><namePart type="family">Muthusamy</namePart><namePart type="termsOfAddress">MSurg</namePart><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicola J.</namePart><namePart type="family">Ray</namePart><namePart type="termsOfAddress">DPhil</namePart><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ralph</namePart><namePart type="family">Gregory</namePart><namePart type="termsOfAddress">FRCP</namePart><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John F.</namePart><namePart type="family">Stein</namePart><namePart type="termsOfAddress">FRCP</namePart><affiliation>Department of Physiology, Anatomy and Genetics, Parks Road, Oxford, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tipu Z.</namePart><namePart type="family">Aziz</namePart><namePart type="termsOfAddress">DMedSci</namePart><affiliation>Oxford Functional Neurosurgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><affiliation>Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">reviewArticle</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-02-15</dateIssued><dateCaptured encoding="w3cdtf">2008-05-06</dateCaptured><dateValid encoding="w3cdtf">2008-06-01</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="references">116</extent><extent unit="words">6914</extent></physicalDescription><abstract lang="en">The pedunculopontine nucleus is composed of cholinergic and non‐cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post‐mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man. © 2008 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="content">*This article is part of the journal's online CME program. The CME activity including form, can be found online at http://www.movementdisorders.org/education/journalcme/</note><note type="funding">Medical Research Council UK</note><note type="funding">Charles Wolfson Charitable Foundation</note><note type="funding">Oxford Biomedical Research Centre</note><subject lang="en"><genre>Keywords</genre><topic>PPN</topic><topic>pedunculopontine</topic><topic>Parkinson's disease</topic><topic>anatomy</topic><topic>physiology</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>319</start><end>328</end><total>10</total></extent></part></relatedItem><identifier type="istex">F8A804FC7A5031E670C1DF07EEB78B934B925243</identifier><identifier type="DOI">10.1002/mds.22189</identifier><identifier type="ArticleID">MDS22189</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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