Flexion movements of the wrist were studied in a patient who showed signs of hemiballismus following a unilateral infarction, which damaged the region neighboring the subthalamic nucleus. The experiments were designed to test whether a lesion of this nature impairs load compensation and, specifically, whether antagonist activity can be appropriately suppressed when initiating a movement. The latency between movement onset and agonist EMG onset changed from the normal relationship where agonist onset precedes movement to one where agonist onset followed movement when an extensor load was placed on the affected limb. This was found to result from the inability to inhibit tonic activity in the antagonist and simultaneously activate the agonist muscle. The results suggest that the indirect pathway through the basal ganglia may be necessary to compensate for mechanical loads and to suppress antagonist activity when a movement is initiated.