Abnormal conduction in corticospinal pathways in Wilson's disease: investigation of nine cases with magnetic brain stimulation.
Identifieur interne : 004E56 ( PubMed/Curation ); précédent : 004E55; suivant : 004E57Abnormal conduction in corticospinal pathways in Wilson's disease: investigation of nine cases with magnetic brain stimulation.
Auteurs : B U Meyer [Allemagne] ; T C Britton ; C. Bischoff ; J. Machetanz ; R. Benecke ; B. ConradSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1991.
English descriptors
- KwdEn :
- Adult, Electromagnetic Fields, Electromyography, Follow-Up Studies, Hepatolenticular Degeneration (diagnosis), Hepatolenticular Degeneration (drug therapy), Hepatolenticular Degeneration (physiopathology), Humans, Motor Cortex (drug effects), Motor Cortex (physiopathology), Muscle Contraction (drug effects), Muscle Contraction (physiology), Muscles (innervation), Neurologic Examination, Penicillamine (therapeutic use), Pyramidal Tracts (drug effects), Pyramidal Tracts (physiopathology), Synaptic Transmission (drug effects), Synaptic Transmission (physiology).
- MESH :
- chemical , therapeutic use : Penicillamine.
- diagnosis : Hepatolenticular Degeneration.
- drug effects : Motor Cortex, Muscle Contraction, Pyramidal Tracts, Synaptic Transmission.
- drug therapy : Hepatolenticular Degeneration.
- innervation : Muscles.
- physiology : Muscle Contraction, Synaptic Transmission.
- physiopathology : Hepatolenticular Degeneration, Motor Cortex, Pyramidal Tracts.
- Adult, Electromagnetic Fields, Electromyography, Follow-Up Studies, Humans, Neurologic Examination.
Abstract
Electromyographic (EMG) responses evoked by transcranial magnetic brain stimulation were studied in nine patients with Wilson's disease (WD). Six of the nine patients had prolonged central motor latencies (CMLs), reduced amplitude, or absent responses in at least one of the examined muscles. In one patient, abnormal EMG responses normalized following treatment with penicillamine. Pathophysiologically abnormal EMG responses might result from a potentially reversible impairment of corticomotoneuronal pathways and/or a reduced excitability of motoneurons due to basal ganglia dysfunction. The possible pathophysiological mechanisms are discussed.
DOI: 10.1002/mds.870060409
PubMed: 1661845
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Machetanz</name></author><author><name sortKey="Benecke, R" sort="Benecke, R" uniqKey="Benecke R" first="R" last="Benecke">R. Benecke</name></author><author><name sortKey="Conrad, B" sort="Conrad, B" uniqKey="Conrad B" first="B" last="Conrad">B. 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Bischoff</name></author><author><name sortKey="Machetanz, J" sort="Machetanz, J" uniqKey="Machetanz J" first="J" last="Machetanz">J. Machetanz</name></author><author><name sortKey="Benecke, R" sort="Benecke, R" uniqKey="Benecke R" first="R" last="Benecke">R. Benecke</name></author><author><name sortKey="Conrad, B" sort="Conrad, B" uniqKey="Conrad B" first="B" last="Conrad">B. Conrad</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="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Electromagnetic Fields</term><term>Electromyography</term><term>Follow-Up Studies</term><term>Hepatolenticular Degeneration (diagnosis)</term><term>Hepatolenticular Degeneration (drug therapy)</term><term>Hepatolenticular Degeneration (physiopathology)</term><term>Humans</term><term>Motor Cortex (drug effects)</term><term>Motor Cortex (physiopathology)</term><term>Muscle Contraction (drug effects)</term><term>Muscle Contraction (physiology)</term><term>Muscles (innervation)</term><term>Neurologic Examination</term><term>Penicillamine (therapeutic use)</term><term>Pyramidal Tracts (drug effects)</term><term>Pyramidal Tracts (physiopathology)</term><term>Synaptic Transmission (drug effects)</term><term>Synaptic Transmission (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Penicillamine</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Cortex</term><term>Muscle Contraction</term><term>Pyramidal Tracts</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Hepatolenticular Degeneration</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Muscles</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Muscle Contraction</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hepatolenticular Degeneration</term><term>Motor Cortex</term><term>Pyramidal Tracts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Electromagnetic Fields</term><term>Electromyography</term><term>Follow-Up Studies</term><term>Humans</term><term>Neurologic Examination</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Electromyographic (EMG) responses evoked by transcranial magnetic brain stimulation were studied in nine patients with Wilson's disease (WD). Six of the nine patients had prolonged central motor latencies (CMLs), reduced amplitude, or absent responses in at least one of the examined muscles. In one patient, abnormal EMG responses normalized following treatment with penicillamine. Pathophysiologically abnormal EMG responses might result from a potentially reversible impairment of corticomotoneuronal pathways and/or a reduced excitability of motoneurons due to basal ganglia dysfunction. The possible pathophysiological mechanisms are discussed.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">1661845</PMID><DateCreated><Year>1992</Year><Month>02</Month><Day>05</Day></DateCreated><DateCompleted><Year>1992</Year><Month>02</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>6</Volume><Issue>4</Issue><PubDate><Year>1991</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Abnormal conduction in corticospinal pathways in Wilson's disease: investigation of nine cases with magnetic brain stimulation.</ArticleTitle><Pagination><MedlinePgn>320-3</MedlinePgn></Pagination><Abstract><AbstractText>Electromyographic (EMG) responses evoked by transcranial magnetic brain stimulation were studied in nine patients with Wilson's disease (WD). Six of the nine patients had prolonged central motor latencies (CMLs), reduced amplitude, or absent responses in at least one of the examined muscles. In one patient, abnormal EMG responses normalized following treatment with penicillamine. Pathophysiologically abnormal EMG responses might result from a potentially reversible impairment of corticomotoneuronal pathways and/or a reduced excitability of motoneurons due to basal ganglia dysfunction. The possible pathophysiological mechanisms are discussed.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meyer</LastName><ForeName>B U</ForeName><Initials>BU</Initials><AffiliationInfo><Affiliation>Department of Neurology, Technical University, Munich, F.R.G.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Britton</LastName><ForeName>T C</ForeName><Initials>TC</Initials></Author><Author ValidYN="Y"><LastName>Bischoff</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Machetanz</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Benecke</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Conrad</LastName><ForeName>B</ForeName><Initials>B</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><ChemicalList><Chemical><RegistryNumber>GNN1DV99GX</RegistryNumber><NameOfSubstance UI="D010396">Penicillamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004574">Electromagnetic Fields</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004576">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005500">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006527">Hepatolenticular Degeneration</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009044">Motor Cortex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009119">Muscle Contraction</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009132">Muscles</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000294">innervation</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009460">Neurologic Examination</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010396">Penicillamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011712">Pyramidal Tracts</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009435">Synaptic Transmission</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1991</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1991</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1991</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1661845</ArticleId><ArticleId IdType="doi">10.1002/mds.870060409</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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