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Brain, Vol. 117, No. 6, 1409-1422, 1994
© 1994 Guarantors of Brain

research-article

Acute effects of levodopa on wrist movement in Parkinson's disease

Kinematics, volitional EMG modulation and reflex amplitude modulation

M. T. V. Johnson2,, A. Mendez1, A. N. Kipnis4, P. Silverstein5, F. Zwiebel5 and T. J. Ebner1,3

1Department of Neurosurgery Minneapolis, Minnesota, USA 2Department of Neurology Minneapolis, Minnesota, USA 3Department of Physiology, University of Minnesota Minneapolis, Minnesota, USA 4EMPI Incorporated Minneapolis, Minnesota, USA 5Minneapolis Clinic of Neurology Minneapolis, Minnesota, USA

Correspondence to: Correspondence to: Michael T. V. Johnson/Timothy J. Ebner, Department of Neurosurgery, University of Minnesota, Lions Research Building, 2001 Sixth Street SE, Minneapolis, MN 55455, USA

Acute changes in motor performance due to levodopa were evaluated by a series of four motor tests unified by their focus on wrist flexion–extension movements. Subjects with idiopathic Parkinson's disease were evaluated with this battery of tests before (OFF) and after their usual morning dose of levodopa (ON). The test battery consisted of (i) repetitive self-paced movement in which velocity was to be maximized; (ii) visually guided tracking of a sinusoid and a square wave; and (Hi) an assay of stretch reflex modulation during volitional sinusoidal tracking. The maximal wrist joint velocity of self-paced reciprocating flexion and extension movements increased after levodopa (ON), without significant changes in the movement period or amplitude. In the two tracking tasks, some subjects improved as evident by a lower root mean square (rms) error, but in similar numbers of subjects the rms error increased. Overall, the rms error, peak velocity or peak movement amplitude did not change after levodopa in either tracking task. Significant and consistent changes did occur after levodopa in an assay of reflex modulation during error-constrained tracking (Johnson etai, Brain 1991; 114: 443–60). The amplitude of volitional EMG increased after levodopa, with a concurrent reduction in reflex EMG. These changes are consistent with the noted increase in movement velocity. These results show that the effects of levodopa on movement velocity were not consistently translated into increased accuracy. The changes in the long latency reflex gain argue for a central control of this reflex, mediated by structures sensitive to levodopa. Finally, the results show that the quantitative evaluation of levodopa therapy cannot be unidimensional, but requires a battery of motor tests as undertaken in this study.

Parkinson's disease; stretch reflex; human wrist; pursuit tracking

Received December 20, 1993. Revised May 17, 1994. Accepted June 13, 1994.


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