Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor
Identifieur interne : 000294 ( Main/Corpus ); précédent : 000293; suivant : 000295Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor
Auteurs : Rick C. Helmich ; Marcel J. R. Janssen ; Wim J. G. Oyen ; Bastiaan R. Bloem ; Ivan ToniSource :
- Annals of Neurology [ 0364-5134 ] ; 2011-02.
Abstract
Objective:: Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor. Methods:: We studied 21 tremor‐dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor‐related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine‐123‐N‐omega‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl)tropane [[I‐123]FP‐CIT] single photon emission computed tomography. Results:: Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor‐dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex. Interpretation:: Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine‐depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor. Ann Neurol 2011
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DOI: 10.1002/ana.22361
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor</title><author><name sortKey="Helmich, Rick C" sort="Helmich, Rick C" uniqKey="Helmich R" first="Rick C." last="Helmich">Rick C. Helmich</name><affiliation><mods:affiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</mods:affiliation></affiliation></author><author><name sortKey="Janssen, Marcel J R" sort="Janssen, Marcel J R" uniqKey="Janssen M" first="Marcel J. R." last="Janssen">Marcel J. R. Janssen</name><affiliation><mods:affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Oyen, Wim J G" sort="Oyen, Wim J G" uniqKey="Oyen W" first="Wim J. G." last="Oyen">Wim J. G. Oyen</name><affiliation><mods:affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R." last="Bloem">Bastiaan R. 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Helmich</name><affiliation><mods:affiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</mods:affiliation></affiliation></author><author><name sortKey="Janssen, Marcel J R" sort="Janssen, Marcel J R" uniqKey="Janssen M" first="Marcel J. R." last="Janssen">Marcel J. R. Janssen</name><affiliation><mods:affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Oyen, Wim J G" sort="Oyen, Wim J G" uniqKey="Oyen W" first="Wim J. G." last="Oyen">Wim J. G. Oyen</name><affiliation><mods:affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R." last="Bloem">Bastiaan R. Bloem</name><affiliation><mods:affiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</mods:affiliation></affiliation></author><author><name sortKey="Toni, Ivan" sort="Toni, Ivan" uniqKey="Toni I" first="Ivan" last="Toni">Ivan Toni</name><affiliation><mods:affiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-02">2011-02</date><biblScope unit="volume">69</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="269">269</biblScope><biblScope unit="page" to="281">281</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">9F595A6461B040ECFCDEAE5E023542D89D2BDE76</idno><idno type="DOI">10.1002/ana.22361</idno><idno type="ArticleID">ANA22361</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective:: Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor. Methods:: We studied 21 tremor‐dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor‐related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine‐123‐N‐omega‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl)tropane [[I‐123]FP‐CIT] single photon emission computed tomography. Results:: Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor‐dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex. Interpretation:: Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine‐depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor. Ann Neurol 2011</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Rick C. Helmich MD</name><affiliations><json:string>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</json:string><json:string>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</json:string></affiliations></json:item><json:item><name>Marcel J. R. Janssen MD, PhD</name><affiliations><json:string>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</json:string></affiliations></json:item><json:item><name>Wim J. G. Oyen MD, PhD</name><affiliations><json:string>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</json:string></affiliations></json:item><json:item><name>Bastiaan R. Bloem MD, PhD</name><affiliations><json:string>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</json:string></affiliations></json:item><json:item><name>Ivan Toni PhD</name><affiliations><json:string>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</json:string></affiliations></json:item></author><articleId><json:string>ANA22361</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective:: Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor. Methods:: We studied 21 tremor‐dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor‐related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine‐123‐N‐omega‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl)tropane [[I‐123]FP‐CIT] single photon emission computed tomography. Results:: Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor‐dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex. Interpretation:: Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine‐depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor. 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R.</forename><surname>Janssen</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</affiliation></author><author><persName><forename type="first">Wim J. G.</forename><surname>Oyen</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</affiliation></author><author><persName><forename type="first">Bastiaan R.</forename><surname>Bloem</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</affiliation></author><author><persName><forename type="first">Ivan</forename><surname>Toni</surname></persName><roleName type="degree">PhD</roleName><affiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-02"></date><biblScope unit="volume">69</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="269">269</biblScope><biblScope unit="page" to="281">281</biblScope></imprint></monogr><idno type="istex">9F595A6461B040ECFCDEAE5E023542D89D2BDE76</idno><idno type="DOI">10.1002/ana.22361</idno><idno type="ArticleID">ANA22361</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective:: Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor. Methods:: We studied 21 tremor‐dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor‐related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine‐123‐N‐omega‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl)tropane [[I‐123]FP‐CIT] single photon emission computed tomography. Results:: Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor‐dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex. Interpretation:: Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine‐depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor. 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R.</givenNames><familyName>Janssen</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Wim J. G.</givenNames><familyName>Oyen</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Bastiaan R.</givenNames><familyName>Bloem</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ivan</givenNames><familyName>Toni</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="NL" type="organization"><unparsedAffiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="NL" type="organization"><unparsedAffiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</unparsedAffiliation></affiliation></affiliationGroup><supportingInformation><p> Additional supporting information can be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana22361:ANA_22361_sm_SuppMaterials"></mediaResource><caption>Supporting Information Materials.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Objective:</title><p>Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor.</p></section><section xml:id="abs1-2"><title type="main">Methods:</title><p>We studied 21 tremor‐dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor‐related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine‐123‐N‐omega‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl)tropane [[I‐123]FP‐CIT] single photon emission computed tomography.</p></section><section xml:id="abs1-3"><title type="main">Results:</title><p>Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor‐dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex.</p></section><section xml:id="abs1-4"><title type="main">Interpretation:</title><p>Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine‐depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor. Ann Neurol 2011</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Neural Mechanisms of PD Tremor</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor</title></titleInfo><name type="personal"><namePart type="given">Rick C.</namePart><namePart type="family">Helmich</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</affiliation><affiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</affiliation><description>Correspondence: Donders Centre for Brain, Cognition, and Behavior, Center for Neuroscience, Department of Neurology (HP 935), PO Box 9101, 6500 HB Nijmegen, the Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marcel J. R.</namePart><namePart type="family">Janssen</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wim J. G.</namePart><namePart type="family">Oyen</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Nuclear Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bastiaan R.</namePart><namePart type="family">Bloem</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology and Parkinson Center Nijmegen, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ivan</namePart><namePart type="family">Toni</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Donders Institute for Brain, Cognition, and Behavior, Center for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-02</dateIssued><dateCaptured encoding="w3cdtf">2010-07-30</dateCaptured><dateValid encoding="w3cdtf">2010-12-17</dateValid><copyrightDate encoding="w3cdtf">2011</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">4</extent><extent unit="tables">4</extent><extent unit="references">43</extent><extent unit="words">6519</extent></physicalDescription><abstract lang="en">Objective:: Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor. Methods:: We studied 21 tremor‐dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor‐related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine‐123‐N‐omega‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl)tropane [[I‐123]FP‐CIT] single photon emission computed tomography. Results:: Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor‐dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex. Interpretation:: Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine‐depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor. Ann Neurol 2011</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional supporting information can be found in the online version of this article.Supporting Info Item: Supporting Information Materials. - </note><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>69</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>269</start><end>281</end><total>13</total></extent></part></relatedItem><identifier type="istex">9F595A6461B040ECFCDEAE5E023542D89D2BDE76</identifier><identifier type="DOI">10.1002/ana.22361</identifier><identifier type="ArticleID">ANA22361</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 American Neurological Association</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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