EFFECTS OF DOPAMINE ON POSTURAL CONTROL IN PARKINSONIAN SUBJECTS: SCALING, SET AND TONE. Horak, F.B., Frank, J. and Nutt, J. R.S. Dow Neurological Sciences Institute, 1120 N.W. 20th Avenue, Portland, OR, USA 97209, Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1, Department of Neurology, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Rd., Portland, OR, USA 97201.
APStracts 3:0006N, 1996.
1. This study investigates the effects of parkinsonism and of dopamine replacement therapy (levodopa) on scaling the magnitude of automatic postural responses based on sensory feedback and on predictive central set. Surface reactive torques and electromyographic (EMG) activity in response to backward surface translations were compared in patients with parkinsonism ON and OFF levodopa and in elderly control subjects. Correlations between the earliest postural responses (initial rate of change of torque and integrated EMG) and translation velocity provided a measure of postural magnitude scaling using somatosensory feedback. Correlations of responses with expected translation amplitude provided a measure of scaling dependent upon predictive central set because the responses preceded amplitude completion. 2. Parkinsonian EMG responses in six leg and trunk muscles were not later than in elderly control subjects. In fact, quadriceps antagonist latencies were earlier than normal resulting in coactivation at the knee not present in control subjects. EMG activation was fragmented with short burst durations and high tonic levels which often returned to baseline with multiple bursts. In addition, parkinsonian responses showed smaller than normal agonist extensor bursts and larger than normal activation in tibialis and rectus femorus antagonist flexors. 3. Although parkinsonian subjects scaled postural responses to both displacement velocities and amplitudes, their torque response were smaller than that of elderly controls, especially in response to the largest displacement amplitudes. The gain (slope) of postural response magnitude scaling to displacement velocity was similar for parkinsonian and control subjects although parkinsonian subjects had smaller torques. Parkinsonian subjects were also able to use prediction to scale responses to small expected displacement amplitudes, but many patients did not generate the larger plantarflexion torques required at larger displacement amplitudes. Reduced torque at large amplitudes was associated with less agonist gastrocnemius IEMG and increased tibialis antagonist burst response and increased tibialis tonic background activity . 4. Levodopa further reduced the already low magnitude of initial torque and IEMG responses to displacement velocities and amplitudes in parkinsonian patients. The ability to scale postural response to velocity feedback was not affected by Levodopa, but the ability to scale responses to large displacement amplitudes based on central set was worsened by Levodopa. Levodopa also significantly reduced the tonic, background levels of EMG, particularly the distal gastrocnemius and tibialis activity. 5. High baseline muscle tone was apparent in parkinsonian subjects from their high background EMG activity in quiet stance, especially in tibialis and quadriceps, and the slow initial velocity of center of mass falling in response to displacements. By reducing tone, levodopa reduced passive stiffness to perturbations without increasing EMG burst magnitudes resulting in less resistance to external displacements and thus, faster CoM displacements. 6. The biggest postural deficit in parkinsonian subjects was not in response latency, pattern, or in reactive or predictive scaling of response magnitude but in quickly generating an adequate level of postural force. Dopamine improved tonic background postural tone but further weakened automatic postural responses to external displacements. Thus, the basal ganglia may participate in postural control by regulating appropriate levels of background postural tone and by enabling adequate force generation for resisting external displacements.

Received 17 April 1995; accepted in final form 11 December 1995.
APS Manuscript Number J256-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96