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Pursuit disorder and saccade dysmetria after caudal fastigial inactivation in the monkey

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The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccadic and pursuit eye movements. We investigated the consequences of unilateral inactivation on the pursuit eye movement made immediately after an interceptive saccade toward a centrifugal target. We describe here the effects when the target moved along the horizontal meridian with a 10 or 20°/s speed. After muscimol injection, the monkeys were unable to track the present location of the moving target. During contralesional tracking, the velocity of postsaccadic pursuit was reduced. This slowing was associated with a hypometria of interceptive saccades such that gaze direction always lagged behind the moving target. No correlation was found between the sizes of saccade undershoot and the decreases in pursuit speed. During ipsilesional tracking, the effects on postsaccadic pursuit were variable across the injection sessions, whereas the interceptive saccades were consistently hypermetric. Here also, the ipsilesional pursuit disorder was not correlated with the saccade hypermetria either. The lack of correlation between the sizes of saccade dysmetria and changes of postsaccadic pursuit speed suggests that cFN activity exerts independent influences on the neural processes generating the saccadic and slow eye movements. It also suggests that the cFN is one locus where the synergy between the two motor categories develops in the context of tracking a moving visual target. We explain how the different fastigial output channels can account for these oculomotor tracking disorders. NEW & NOTEWORTHY Inactivation of the caudal fastigial nucleus impairs the ability to track a moving target. The accuracy of interceptive saccades and the velocity of postsaccadic pursuit movements are both altered, but these changes are not correlated. This absence of correlation is not compatible with an impaired common command feeding the circuits producing saccadic and pursuit eye movements. However, it suggests an involvement of caudal fastigial nuclei in their synergy to accurately track a moving target.
Title: Pursuit disorder and saccade dysmetria after caudal fastigial inactivation in the monkey
Description:
The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccadic and pursuit eye movements.
We investigated the consequences of unilateral inactivation on the pursuit eye movement made immediately after an interceptive saccade toward a centrifugal target.
We describe here the effects when the target moved along the horizontal meridian with a 10 or 20°/s speed.
After muscimol injection, the monkeys were unable to track the present location of the moving target.
During contralesional tracking, the velocity of postsaccadic pursuit was reduced.
This slowing was associated with a hypometria of interceptive saccades such that gaze direction always lagged behind the moving target.
No correlation was found between the sizes of saccade undershoot and the decreases in pursuit speed.
During ipsilesional tracking, the effects on postsaccadic pursuit were variable across the injection sessions, whereas the interceptive saccades were consistently hypermetric.
Here also, the ipsilesional pursuit disorder was not correlated with the saccade hypermetria either.
The lack of correlation between the sizes of saccade dysmetria and changes of postsaccadic pursuit speed suggests that cFN activity exerts independent influences on the neural processes generating the saccadic and slow eye movements.
It also suggests that the cFN is one locus where the synergy between the two motor categories develops in the context of tracking a moving visual target.
We explain how the different fastigial output channels can account for these oculomotor tracking disorders.
NEW & NOTEWORTHY Inactivation of the caudal fastigial nucleus impairs the ability to track a moving target.
The accuracy of interceptive saccades and the velocity of postsaccadic pursuit movements are both altered, but these changes are not correlated.
This absence of correlation is not compatible with an impaired common command feeding the circuits producing saccadic and pursuit eye movements.
However, it suggests an involvement of caudal fastigial nuclei in their synergy to accurately track a moving target.

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