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J Neurophysiol 80: 1911-1931, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 4 October 1998, pp. 1911-1931
Copyright ©1998 The American Physiological Society

Effects of Lesions of the Oculomotor Vermis on Eye Movements in Primate: Saccades

Mineo Takagi3, David S. Zee1, and Rafael J. Tamargo2

1 Department of Neurology and 2 Department of Neurosurgery, The Johns Hopkins Hospital, Baltimore, Maryland 21287; and 3 Department of Ophthalmology, Niigata University School of Medicine, Niigata 951, Japan

Takagi, Mineo, David S. Zee, and Rafael J. Tamargo. Effects of lesions of the oculomotor vermis on eye movements in primate: saccades. J. Neurophysiol. 80: 1911-1931, 1998. We studied the effects on saccades of ablation of the dorsal cerebellar vermis (lesions centered on lobules VI and VII) in three monkeys in which the deep cerebellar nuclei were spared. One animal, with a symmetrical lesion, showed bilateral hypometric horizontal saccades. Two animals, with asymmetrical lesions, showed hypometric ipsilateral saccades, and saccades to vertically positioned targets were misdirected, usually deviating away from the side to which horizontal saccades were hypometric. Postlesion, all animals showed an increase (2- to 5-fold) in trial-to-trial variability of saccade amplitude. They also showed a change in the ratio of the amplitudes of centripetal to centrifugal saccades (orbital-position effect); usually centrifugal saccades became smaller. In the two animals with asymmetrical lesions, for saccades in the hypometric direction, latencies were markedly increased (up to ~500 ms). There was also an absence of express and anticipatory saccades in the hypometric direction. When overall saccade latency was increased, centrifugal saccades became relatively more delayed than centripetal saccades. The dynamic characteristics of saccades were affected to some extent in all monkeys with changes in peak velocity, eye acceleration, and especially eye deceleration. There was relatively little effect of orbital position on saccade dynamics, however, with the exception of one animal that showed an orbital position effect for eye acceleration. In a double-step adaptation paradigm, animals showed an impaired ability to adaptively adjust saccade amplitude, though increased amplitude variability postlesion may have played a role in this deficit. During a single training session, however, the latency to corrective saccades---which had been increased postlesion---gradually decreased and so enabled the animal to reach the final position of the target more quickly. Overall, both in the early postlesion period and during recovery, changes in saccade amplitude and latency tended to vary together but not with changes in saccade dynamics or adaptive capability, both of which behaved relatively independently. These findings suggest that the cerebellum can adjust saccade amplitude and saccade dynamics independently. Our results implicate the cerebellar vermis directly in every aspect of the on-line control of saccades: initiation (latency), accuracy (amplitude and direction), and dynamics (velocity and acceleration) and also in the acquisition of adaptive ocular motor behavior.




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