Short and long latency afferent inhibition in Parkinson's disease.
Identifieur interne : 001421 ( PubMed/Curation ); précédent : 001420; suivant : 001422Short and long latency afferent inhibition in Parkinson's disease.
Auteurs : Alexandra Sailer [Canada] ; Gregory F. Molnar ; Guillermo Paradiso ; Carolyn A. Gunraj ; Anthony E. Lang ; Robert ChenSource :
- Brain : a journal of neurology [ 0006-8950 ] ; 2003.
English descriptors
- KwdEn :
- MESH :
- innervation : Fingers.
- methods : Electric Stimulation.
- physiopathology : Afferent Pathways, Median Nerve, Motor Cortex, Parkinson Disease.
- Adult, Aged, Female, Humans, Male, Middle Aged, Neural Inhibition, Reaction Time.
Abstract
Sensory abnormalities have been reported in Parkinson's disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of approximately 20 ms, and long latency afferent inhibition (LAI) at an ISI of approximately 200 ms. We studied SAI and LAI in 10 Parkinson's disease patients with the aim of assessing whether sensorimotor processing is altered in Parkinson's disease. Patients were studied on and off medication, and the findings were compared with 10 age-matched controls. Median nerve and middle finger stimulation were delivered 20-600 ms before TMS to the contralateral motor cortex. The motor evoked potentials were recorded from the relaxed first dorsal interosseous (FDI) muscle. SAI was normal in Parkinson's disease patients off dopaminergic medications, but it was reduced on the more affected side in Parkinson's disease patients on medication. LAI was reduced in Parkinson's disease patients compared with controls independent of their medication status. LAI reduced long interval intracortical inhibition in normal subjects but not in Parkinson's disease patients. The different results for SAI and LAI indicate that it is likely that separate mechanisms mediate these two forms of afferent inhibition. SAI probably represents the direct interaction of a sensory signal with the motor cortex. This pathway is unaffected by Parkinson's disease but is altered by dopaminergic medication in Parkinson's disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non-dopaminergic manifestation of Parkinson's disease.
DOI: 10.1093/brain/awg183
PubMed: 12805105
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Molnar</name></author><author><name sortKey="Paradiso, Guillermo" sort="Paradiso, Guillermo" uniqKey="Paradiso G" first="Guillermo" last="Paradiso">Guillermo Paradiso</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="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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12805105</idno><idno type="pmid">12805105</idno><idno type="doi">10.1093/brain/awg183</idno><idno type="wicri:Area/PubMed/Corpus">001421</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001421</idno><idno type="wicri:Area/PubMed/Curation">001421</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001421</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Short and long latency afferent inhibition in Parkinson's disease.</title><author><name sortKey="Sailer, Alexandra" sort="Sailer, Alexandra" uniqKey="Sailer A" first="Alexandra" last="Sailer">Alexandra Sailer</name><affiliation wicri:level="1"><nlm:affiliation>5W445 Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8.</nlm:affiliation><country>Canada</country><wicri:regionArea>5W445 Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Molnar, Gregory F" sort="Molnar, Gregory F" uniqKey="Molnar G" first="Gregory F" last="Molnar">Gregory F. Molnar</name></author><author><name sortKey="Paradiso, Guillermo" sort="Paradiso, Guillermo" uniqKey="Paradiso G" first="Guillermo" last="Paradiso">Guillermo Paradiso</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="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">Brain : a journal of neurology</title><idno type="ISSN">0006-8950</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Afferent Pathways (physiopathology)</term><term>Aged</term><term>Electric Stimulation (methods)</term><term>Female</term><term>Fingers (innervation)</term><term>Humans</term><term>Male</term><term>Median Nerve (physiopathology)</term><term>Middle Aged</term><term>Motor Cortex (physiopathology)</term><term>Neural Inhibition</term><term>Parkinson Disease (physiopathology)</term><term>Reaction Time</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Fingers</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electric Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Afferent Pathways</term><term>Median Nerve</term><term>Motor Cortex</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neural Inhibition</term><term>Reaction Time</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sensory abnormalities have been reported in Parkinson's disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of approximately 20 ms, and long latency afferent inhibition (LAI) at an ISI of approximately 200 ms. We studied SAI and LAI in 10 Parkinson's disease patients with the aim of assessing whether sensorimotor processing is altered in Parkinson's disease. Patients were studied on and off medication, and the findings were compared with 10 age-matched controls. Median nerve and middle finger stimulation were delivered 20-600 ms before TMS to the contralateral motor cortex. The motor evoked potentials were recorded from the relaxed first dorsal interosseous (FDI) muscle. SAI was normal in Parkinson's disease patients off dopaminergic medications, but it was reduced on the more affected side in Parkinson's disease patients on medication. LAI was reduced in Parkinson's disease patients compared with controls independent of their medication status. LAI reduced long interval intracortical inhibition in normal subjects but not in Parkinson's disease patients. The different results for SAI and LAI indicate that it is likely that separate mechanisms mediate these two forms of afferent inhibition. SAI probably represents the direct interaction of a sensory signal with the motor cortex. This pathway is unaffected by Parkinson's disease but is altered by dopaminergic medication in Parkinson's disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non-dopaminergic manifestation of Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12805105</PMID><DateCreated><Year>2003</Year><Month>07</Month><Day>15</Day></DateCreated><DateCompleted><Year>2003</Year><Month>09</Month><Day>16</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-8950</ISSN><JournalIssue CitedMedium="Print"><Volume>126</Volume><Issue>Pt 8</Issue><PubDate><Year>2003</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Short and long latency afferent inhibition in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1883-94</MedlinePgn></Pagination><Abstract><AbstractText>Sensory abnormalities have been reported in Parkinson's disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of approximately 20 ms, and long latency afferent inhibition (LAI) at an ISI of approximately 200 ms. We studied SAI and LAI in 10 Parkinson's disease patients with the aim of assessing whether sensorimotor processing is altered in Parkinson's disease. Patients were studied on and off medication, and the findings were compared with 10 age-matched controls. Median nerve and middle finger stimulation were delivered 20-600 ms before TMS to the contralateral motor cortex. The motor evoked potentials were recorded from the relaxed first dorsal interosseous (FDI) muscle. SAI was normal in Parkinson's disease patients off dopaminergic medications, but it was reduced on the more affected side in Parkinson's disease patients on medication. LAI was reduced in Parkinson's disease patients compared with controls independent of their medication status. LAI reduced long interval intracortical inhibition in normal subjects but not in Parkinson's disease patients. The different results for SAI and LAI indicate that it is likely that separate mechanisms mediate these two forms of afferent inhibition. SAI probably represents the direct interaction of a sensory signal with the motor cortex. This pathway is unaffected by Parkinson's disease but is altered by dopaminergic medication in Parkinson's disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non-dopaminergic manifestation of Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sailer</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>5W445 Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Molnar</LastName><ForeName>Gregory F</ForeName><Initials>GF</Initials></Author><Author ValidYN="Y"><LastName>Paradiso</LastName><ForeName>Guillermo</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Gunraj</LastName><ForeName>Carolyn A</ForeName><Initials>CA</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><ArticleDate DateType="Electronic"><Year>2003</Year><Month>06</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Brain. 2004 Apr;127(Pt 4):E8; author reply E9</RefSource><PMID Version="1">15044312</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000344" MajorTopicYN="N">Afferent Pathways</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005385" MajorTopicYN="N">Fingers</DescriptorName><QualifierName UI="Q000294" MajorTopicYN="N">innervation</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008475" MajorTopicYN="N">Median Nerve</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009044" MajorTopicYN="N">Motor Cortex</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009433" MajorTopicYN="Y">Neural Inhibition</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011930" MajorTopicYN="N">Reaction Time</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>6</Month><Day>14</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>9</Month><Day>17</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>6</Month><Day>14</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12805105</ArticleId><ArticleId IdType="doi">10.1093/brain/awg183</ArticleId><ArticleId IdType="pii">awg183</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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