We set out to test the hypothesis that the cerebellar fastigial nucleus acts as a functional bottleneck for programming sequences of saccades. Our prior study had raised this possibility when we observed that certain cerebellar patients (those with SCASI)2
would overshoot single target jumps but at times make less hypermetric initial saccades to double-step stimuli ().1
Our hypothesis, based on the concept of governance of the brainstem push–pull control of saccades by FOR,6,7,17
predicted that a critically timed and oppositely directed second target jump might terminate an ongoing initial saccade in SCASI patients, making it less hypermetric, and that this effect would be a function of the interstimulus interval. Conversely, patients with lesions involving the FOR would not be expected to show such a correlation between interstimulus interval and saccade amplitude, lacking any governance of saccadic burst neuron firing by the FOR. We also measured the latency of saccades to double-step stimuli to look for evidence of parallel processing.
We found that both patients and normal subjects showed lower gain values of the initial saccade to double-step stimuli compared with responses to single target jumps (). For both normal subjects and FOR patients, the smallest mean gain values tended to occur with the shorter interstimulus intervals.
Our second finding was that, using currently accepted methods,14,15
normal subjects showed evidence of parallel processing of saccades, but SCASI patients and patients with FOR lesions did not (). Taken together, these findings support our proposal that the cerebellar circuits, especially those involving the fastigial nucleus, are important for parallel processing of saccades. However, a different mechanism from the one we proposed must be invoked to account for why initial saccades are smaller when second targets are presented. One possibility is that this behavior was due to the superior colliculus, which sends projections to brainstem omnipause neurons18
that could then terminate a saccade by inhibiting brainstem burst neurons.19
Since omnipause neurons are silent during blinks as well as combined saccade–vergence movements,17
it might be possible to investigate further the mechanisms that terminate saccades in patients with lesions involving the fastigial nucleus.
Prior experiments have shown that parallel processing of saccades relies heavily on circuits between cerebral cortex and thalamic nuclei.20
Our study shows that such studies rest on the assumption that the cerebellar connections with the fastigial nucleus are functioning normally, which is usually the case. However, if there is coexistent cerebellar disease, then deductions about cortical processing of saccades may be confounded by the independent effects of the cerebellum on parallel processing.