Pathophysiology of cerebellar ataxia.
Identifieur interne : 004D39 ( PubMed/Corpus ); précédent : 004D38; suivant : 004D40Pathophysiology of cerebellar ataxia.
Auteurs : H C Diener ; J. DichgansSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1992.
English descriptors
- KwdEn :
- Cerebellar Ataxia (diagnosis), Cerebellar Ataxia (physiopathology), Cerebellum (physiopathology), Electromyography, Gait (physiology), Humans, Myoclonic Cerebellar Dyssynergia (diagnosis), Myoclonic Cerebellar Dyssynergia (physiopathology), Neurologic Examination, Posture (physiology), Tremor (diagnosis), Tremor (physiopathology).
- MESH :
- diagnosis : Cerebellar Ataxia, Myoclonic Cerebellar Dyssynergia, Tremor.
- physiology : Gait, Posture.
- physiopathology : Cerebellar Ataxia, Cerebellum, Myoclonic Cerebellar Dyssynergia, Tremor.
- Electromyography, Humans, Neurologic Examination.
Abstract
Human and animal experiments performed recently have resulted in a more detailed understanding of limb movement and body posture disorders associated with cerebellar dysfunction. The delay in movement initiation can be explained by a delay in onset of phasic motor cortex neural discharge owing to decreased input from the cerebellar hemispheres. Disorders of movement termination (dysmetria), which can occur for movements at proximal and distal joints, result from disturbances of the timing and intensity of antagonist electromyographic (EMG) activity necessary to break the movement. Disorders in velocity and acceleration of limb movements result from muscular activity that is smaller in amplitude and more prolonged. The cerebellum is important for control of constant force but not for generation of maximal force. Dysdiadochokinesia is explained by a combination of the above mentioned mechanisms. During complex movements in three-dimensional space, the cerebellum contributes to timing between single components of a movement, scales the size of muscular action, and coordinates the sequence of agonists and antagonists. The basic structure of motor programs is not generated in the cerebellum. Hypotonia can be observed only in acute cerebellar lesions. Cerebellar tremor appears to result from a central mechanism, but is modulated or provoked through increased long-loop EMG responses. The common assumption that cerebellar ataxia of stance does not improve with visual feedback is true only of vestibulocerebellar lesions, not for ataxia resulting from atrophy of the anterior lobe of the cerebellum.
DOI: 10.1002/mds.870070202
PubMed: 1584245
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Dichgans</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1992">1992</date><idno type="RBID">pubmed:1584245</idno><idno type="pmid">1584245</idno><idno type="doi">10.1002/mds.870070202</idno><idno type="wicri:Area/PubMed/Corpus">004D39</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Pathophysiology of cerebellar ataxia.</title><author><name sortKey="Diener, H C" sort="Diener, H C" uniqKey="Diener H" first="H C" last="Diener">H C Diener</name><affiliation><nlm:affiliation>Department of Neurology, University of Tübingen, F.R.G.</nlm:affiliation></affiliation></author><author><name sortKey="Dichgans, J" sort="Dichgans, J" uniqKey="Dichgans J" first="J" last="Dichgans">J. Dichgans</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="1992" type="published">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cerebellar Ataxia (diagnosis)</term><term>Cerebellar Ataxia (physiopathology)</term><term>Cerebellum (physiopathology)</term><term>Electromyography</term><term>Gait (physiology)</term><term>Humans</term><term>Myoclonic Cerebellar Dyssynergia (diagnosis)</term><term>Myoclonic Cerebellar Dyssynergia (physiopathology)</term><term>Neurologic Examination</term><term>Posture (physiology)</term><term>Tremor (diagnosis)</term><term>Tremor (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cerebellar Ataxia</term><term>Myoclonic Cerebellar Dyssynergia</term><term>Tremor</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gait</term><term>Posture</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebellar Ataxia</term><term>Cerebellum</term><term>Myoclonic Cerebellar Dyssynergia</term><term>Tremor</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Electromyography</term><term>Humans</term><term>Neurologic Examination</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Human and animal experiments performed recently have resulted in a more detailed understanding of limb movement and body posture disorders associated with cerebellar dysfunction. The delay in movement initiation can be explained by a delay in onset of phasic motor cortex neural discharge owing to decreased input from the cerebellar hemispheres. Disorders of movement termination (dysmetria), which can occur for movements at proximal and distal joints, result from disturbances of the timing and intensity of antagonist electromyographic (EMG) activity necessary to break the movement. Disorders in velocity and acceleration of limb movements result from muscular activity that is smaller in amplitude and more prolonged. The cerebellum is important for control of constant force but not for generation of maximal force. Dysdiadochokinesia is explained by a combination of the above mentioned mechanisms. During complex movements in three-dimensional space, the cerebellum contributes to timing between single components of a movement, scales the size of muscular action, and coordinates the sequence of agonists and antagonists. The basic structure of motor programs is not generated in the cerebellum. Hypotonia can be observed only in acute cerebellar lesions. Cerebellar tremor appears to result from a central mechanism, but is modulated or provoked through increased long-loop EMG responses. The common assumption that cerebellar ataxia of stance does not improve with visual feedback is true only of vestibulocerebellar lesions, not for ataxia resulting from atrophy of the anterior lobe of the cerebellum.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">1584245</PMID><DateCreated><Year>1992</Year><Month>06</Month><Day>12</Day></DateCreated><DateCompleted><Year>1992</Year><Month>06</Month><Day>12</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>7</Volume><Issue>2</Issue><PubDate><Year>1992</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Pathophysiology of cerebellar ataxia.</ArticleTitle><Pagination><MedlinePgn>95-109</MedlinePgn></Pagination><Abstract><AbstractText>Human and animal experiments performed recently have resulted in a more detailed understanding of limb movement and body posture disorders associated with cerebellar dysfunction. The delay in movement initiation can be explained by a delay in onset of phasic motor cortex neural discharge owing to decreased input from the cerebellar hemispheres. Disorders of movement termination (dysmetria), which can occur for movements at proximal and distal joints, result from disturbances of the timing and intensity of antagonist electromyographic (EMG) activity necessary to break the movement. Disorders in velocity and acceleration of limb movements result from muscular activity that is smaller in amplitude and more prolonged. The cerebellum is important for control of constant force but not for generation of maximal force. Dysdiadochokinesia is explained by a combination of the above mentioned mechanisms. During complex movements in three-dimensional space, the cerebellum contributes to timing between single components of a movement, scales the size of muscular action, and coordinates the sequence of agonists and antagonists. The basic structure of motor programs is not generated in the cerebellum. Hypotonia can be observed only in acute cerebellar lesions. Cerebellar tremor appears to result from a central mechanism, but is modulated or provoked through increased long-loop EMG responses. The common assumption that cerebellar ataxia of stance does not improve with visual feedback is true only of vestibulocerebellar lesions, not for ataxia resulting from atrophy of the anterior lobe of the cerebellum.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Diener</LastName><ForeName>H C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Department of Neurology, University of Tübingen, F.R.G.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dichgans</LastName><ForeName>J</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CitationSubset>S</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002524">Cerebellar Ataxia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002531">Cerebellum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004576">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005684">Gait</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002527">Myoclonic Cerebellar Dyssynergia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009460">Neurologic Examination</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011187">Posture</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014202">Tremor</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>86</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1584245</ArticleId><ArticleId IdType="doi">10.1002/mds.870070202</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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