Pathophysiology of cerebellar ataxia
作者:
H.‐C. Diener,
J. Dichgans,
期刊:
Movement Disorders
(WILEY Available online 1992)
卷期:
Volume 7,
issue 2
页码: 95-109
ISSN:0885-3185
年代: 1992
DOI:10.1002/mds.870070202
出版商: Wiley Subscription Services, Inc., A Wiley Company
关键词: Cerebellum;Ataxia;Cerebellar tremor;Dysmetria;Long‐loop responses
数据来源: WILEY
摘要:
AbstractHuman 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 abovementioned 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 cerebel
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