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The Journal of Neurophysiology Vol. 83 No. 5 May 2000, pp. 3019-3030
Copyright ©2000 by the American Physiological Society
1Program in Physical Therapy, 2Department of Anatomy and Neurobiology, and 3Department of Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri 63108
Bastian, A. J.,
K. M. Zackowski, and
W. T. Thach.
Cerebellar Ataxia: Torque Deficiency or Torque Mismatch
Between Joints?. J. Neurophysiol. 83: 3019-3030, 2000. Prior work has shown that cerebellar subjects have difficulty
adjusting for interaction torques that occur during multi-jointed movements. The purpose of this study was to determine whether this
deficit is due to a general inability to generate sufficient levels of
phasic torque inability or due to an inability to generate muscle
torques that predict and compensate for interaction torques. A second
purpose was to determine whether reducing the number of moving joints
by external mechanical fixation could improve cerebellar subjects'
targeted limb movements. We studied control and cerebellar subjects
making elbow flexion movements to touch a target under two conditions:
1) a shoulder free condition, which required only
elbow flexion, although the shoulder joint was unconstrained and
2) a shoulder fixed condition, where the shoulder
joint was mechanically stabilized so it could not move. We measured
joint positions of the arm in the sagittal plane and electromyograms (EMGs) of shoulder and elbow muscles. Elbow and shoulder torques were
estimated using inverse dynamics equations. In the shoulder free
condition, cerebellar subjects made greater endpoint errors (primarily
overshoots) than did controls. Cerebellar subjects' overshoot errors
were largely due to unwanted flexion at the shoulder. The excessive
shoulder flexion resulted from a torque mismatch, where larger shoulder
muscle torques were produced at higher rates than would be appropriate
for a given elbow movement. In the shoulder fixed condition, endpoint
errors of cerebellar subjects and controls were comparable. The
improved accuracy of cerebellar subjects was accompanied by reduced
shoulder flexor muscle activity. Most of the correct cerebellar trials
in the shoulder fixed condition were movements made using only muscles
that flex the elbow. Our findings suggest that cerebellar subjects'
poor shoulder control is due to an inability to generate muscle torques
that predict and compensate for interaction torques, and not due to a
general inability to generate sufficient levels of phasic torque. In
addition, reducing the number of muscles to be controlled improved
cerebellar ataxia.
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