Interhemispheric and ipsilateral connections in Parkinson's disease: relation to mirror movements.
Identifieur interne : 001047 ( PubMed/Checkpoint ); précédent : 001046; suivant : 001048Interhemispheric and ipsilateral connections in Parkinson's disease: relation to mirror movements.
Auteurs : Jie-Yuan Li [Canada] ; Alberto J. Espay ; Carolyn A. Gunraj ; Pramod K. Pal ; Danny I. Cunic ; Anthony E. Lang ; Robert ChenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- MESH :
- anatomy & histology : Corpus Callosum.
- physiology : Motor Activity.
- physiopathology : Brain, Corpus Callosum, Movement Disorders, Parkinson Disease.
- Electromyography, Female, Functional Laterality, Humans, Male, Middle Aged, Reference Values.
Abstract
Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.
DOI: 10.1002/mds.21386
PubMed: 17290459
Affiliations:
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Espay</name></author><author><name sortKey="Gunraj, Carolyn A" sort="Gunraj, Carolyn A" uniqKey="Gunraj C" first="Carolyn A" last="Gunraj">Carolyn A. Gunraj</name></author><author><name sortKey="Pal, Pramod K" sort="Pal, Pramod K" uniqKey="Pal P" first="Pramod K" last="Pal">Pramod K. Pal</name></author><author><name sortKey="Cunic, Danny I" sort="Cunic, Danny I" uniqKey="Cunic D" first="Danny I" last="Cunic">Danny I. Cunic</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. 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Espay</name></author><author><name sortKey="Gunraj, Carolyn A" sort="Gunraj, Carolyn A" uniqKey="Gunraj C" first="Carolyn A" last="Gunraj">Carolyn A. Gunraj</name></author><author><name sortKey="Pal, Pramod K" sort="Pal, Pramod K" uniqKey="Pal P" first="Pramod K" last="Pal">Pramod K. Pal</name></author><author><name sortKey="Cunic, Danny I" sort="Cunic, Danny I" uniqKey="Cunic D" first="Danny I" last="Cunic">Danny I. Cunic</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name></author><author><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (physiopathology)</term><term>Corpus Callosum (anatomy & histology)</term><term>Corpus Callosum (physiopathology)</term><term>Electromyography</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Motor Activity (physiology)</term><term>Movement Disorders (physiopathology)</term><term>Parkinson Disease (physiopathology)</term><term>Reference Values</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Corpus Callosum</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Corpus Callosum</term><term>Movement Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Electromyography</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17290459</PMID><DateCreated><Year>2007</Year><Month>05</Month><Day>01</Day></DateCreated><DateCompleted><Year>2007</Year><Month>07</Month><Day>12</Day></DateCompleted><DateRevised><Year>2007</Year><Month>05</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>22</Volume><Issue>6</Issue><PubDate><Year>2007</Year><Month>Apr</Month><Day>30</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Interhemispheric and ipsilateral connections in Parkinson's disease: relation to mirror movements.</ArticleTitle><Pagination><MedlinePgn>813-21</MedlinePgn></Pagination><Abstract><AbstractText>Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jie-Yuan</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Division of Neurology, Department of Medicine, Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Espay</LastName><ForeName>Alberto J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Gunraj</LastName><ForeName>Carolyn A</ForeName><Initials>CA</Initials></Author><Author ValidYN="Y"><LastName>Pal</LastName><ForeName>Pramod K</ForeName><Initials>PK</Initials></Author><Author ValidYN="Y"><LastName>Cunic</LastName><ForeName>Danny I</ForeName><Initials>DI</Initials></Author><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Anthony E</ForeName><Initials>AE</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Robert</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003337" MajorTopicYN="N">Corpus Callosum</DescriptorName><QualifierName UI="Q000033" MajorTopicYN="N">anatomy & histology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004576" MajorTopicYN="N">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007839" MajorTopicYN="N">Functional Laterality</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009043" MajorTopicYN="N">Motor Activity</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009069" MajorTopicYN="N">Movement Disorders</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012016" MajorTopicYN="N">Reference Values</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>2</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>7</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>2</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17290459</ArticleId><ArticleId IdType="doi">10.1002/mds.21386</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><noCountry><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name><name sortKey="Cunic, Danny I" sort="Cunic, Danny I" uniqKey="Cunic D" first="Danny I" last="Cunic">Danny I. Cunic</name><name sortKey="Espay, Alberto J" sort="Espay, Alberto J" uniqKey="Espay A" first="Alberto J" last="Espay">Alberto J. Espay</name><name sortKey="Gunraj, Carolyn A" sort="Gunraj, Carolyn A" uniqKey="Gunraj C" first="Carolyn A" last="Gunraj">Carolyn A. Gunraj</name><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name><name sortKey="Pal, Pramod K" sort="Pal, Pramod K" uniqKey="Pal P" first="Pramod K" last="Pal">Pramod K. Pal</name></noCountry><country name="Canada"><region name="Ontario"><name sortKey="Li, Jie Yuan" sort="Li, Jie Yuan" uniqKey="Li J" first="Jie-Yuan" last="Li">Jie-Yuan Li</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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