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
Links to Exploration step
pubmed:1584245Le document en format XML
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<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>
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<author><name sortKey="Dichgans, J" sort="Dichgans, J" uniqKey="Dichgans J" first="J" last="Dichgans">J. Dichgans</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<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>
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<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>
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<keywords scheme="MESH" xml:lang="en"><term>Electromyography</term>
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<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>
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<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>
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<MeshHeading><DescriptorName MajorTopicYN="N" UI="D004576">Electromyography</DescriptorName>
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<MeshHeading><DescriptorName MajorTopicYN="N" UI="D002527">Myoclonic Cerebellar Dyssynergia</DescriptorName>
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