The caudal part of the cerebellar fastigial nucleus (CFN) influences the horizontal component of saccades. Previous reports show that activity in the CFN contralateral to saccade direction aids saccade acceleration and that activity in the ipsilateral CFN aids saccade deceleration. Here we refine this description by characterizing how blocking CFN activity changes the distance that the eye rotates during each of 4 phases of saccades, the increasing and decreasing saccade acceleration (phases 1 & 2) and deceleration (3 and 4). We found that unilateral CFN inactivation increases total eye rotation to ~1.8X normal. This resulted from rotation increases in all four phases of ipsiversive saccades. Rotation during phases 1 and 2 increases slightly, more during phase 3, and most during phase 4, to ~4.4X normal. Thus, the ipsilateral CFN normally reduces eye rotation throughout a saccade but reduces it the most near saccade end. After unilateral CFN inactivation, rotation during contraversive saccades was ~0.8X normal. This resulted from decreased rotation during phases 1–3, to ~0.7X normal, and then normal rotation during phase 4. Thus the CFN contraversive to saccade direction normally increases eye rotation during acceleration and the first phase of deceleration. These data indicate that the influences of the CFNs on saccades overlap extensively and that there is a smooth shift from predominance of the contralateral CFN early in a saccade to the ipsilateral CFN later. The pathway from the CFN to contralateral IBNs and then to the abducens nucleus can account for these effects.

Background/Aims: Posterior fossa tumors are the most common brain tumors in children. Surgeons usually remove these tumors via a midline incision through the posterior vermis of the cerebellum. Though often effective, this surgery causes hypotonia, ataxia, oculomotor deficits, transient mutism, difficulty in swallowing and nausea. To date, there is no animal model that mimics these complications. We found that the rhesus macaque is a good model for the consequences of this surgery. Methods: We made a midline incision through the cerebellar vermis of one monkey to mimic the posterior fossa surgery. Then, we closely monitored the monkey for deficits following the surgery. Results: In the first few days, the monkey exhibited nausea, hypotonia, ataxia, difficulty in swallowing and an absence of vocalization. At 28 days, we recorded eye movements and found severe deficits in the accuracy of rapid eye movements and smooth pursuit of a target. Additionally, the animal had trouble fixating and a rightward-beating nystagmus. Oculomotor signs persisted until we sacrificed the animal 99 days after surgery, but the other effects resolved by 37 days. Conclusion: Our surgery in a monkey caused the same postsurgical signs observed in humans. We expect to use this model to improve the posterior fossa surgery methods.