This project investigates the role of the basal ganglia in integrating somatic sensory information and motor commands for executing purposeful movements. This project tests the hypothesis that the basal ganglia use somatic sensory signals to calibrate voluntary muscle activity. Human subjects with two types of pathology-Parkinson's disease (ON and OFF dopaminergic medication) and focal putamen lesion-will be studied to test hypotheses that the basal ganglia: (1) calibrate muscle activity during changing exigencies of voluntary motor action; (2) use somatic sensory inputs for muscle activity calibration needed for voluntary muscle activity. (3) rely upon perception of limb position and muscular effort to calibrate voluntary muscle activity. Muscle activity, limb movements, limb dynamics, and perceptual decisions will be measured in human subjects during isometric and isotonic motor actions using the wrist or combined action of the elbow and shoulder. 1. Do the basal ganglia contribute to calibration of muscle activity during voluntary motor actions? We hypothesize that patients with Parkinson's disease or putamen lesion will not appropriately adjust motor strategy required for changes in intended motor action magnitude, direction, and speed. We predict that basal ganglia dysfunction will specifically disrupt adaptive adjustment of EMG patterns. 2. Do the basal ganglia use somatic sensory information to calibrate muscle activity? Errors in calibrating muscle activity may be related to errors in somatic sensory information to adapt motor output. Experiments will evaluate how basal ganglia dysfunction affects calibration of muscle activity following changes in somatic sensory inputs. We predict that the patients with basal ganglia dysfunction will not adapt their motor strategies when sensory input is modified by shifts in initial limb configuration. 3. Do the basal ganglia rely on perception of limb position and muscular output to calibrate muscle activity? Errors in adapting muscle activity to somatic sensory inputs may be related to disrupted use of perceived limb position or mismatching somatic sensory inputs with motor commands. These experiments will examine perception of limb position and muscular effort in Parkinson's disease and putamen lesion patients. We predict that basal ganglia dysfunction will impair perception of limb position and muscular effort. These studies will provide substantial information on how the basal ganglia use somatic sensory information to adjust motor strategies and to pathophysiological descriptions and analysis of the motor disorders in patients with Parkinson's disease and putamen lesion. The relationships between perceptual judgments and muscle activity could lead to strategies for rehabilitation treatment of basal ganglia disease.
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