Areas of cerebellar cortex related to saccadic eye movements were ablated in three Macaca mulatta monkeys trained to fixate visual targets. There followed a postoperative dysmetria of saccadic eye movements which appeared to be the result of an impairment specifically within the saccadic system. 2. Convergent evidence from two experimental paradigms indicated that the saccadic deficit was a function of the position of the eye in the orbit and did not involve retinal error processing. 3. The pattern of this position-dependent dysmetria suggests that the eye was no longer fully compensating for the elastic restoring forces imposed by the orbital medium and antagonist muscle(s). 4. The similarity of these data to saccadic eye movements of human cerebellar patients and arm movements of rhesus monkeys with cerebellar lesions indicates that the inability to compensate for the differential loads placed on motor systems by the mechanics of those systems may explain several cerebellar symptoms.
