brings new objects of interest onto the fovea
fast, steplike
saccades are too fast (900deg/s) to modify their course by visual feedback, so corrections are made in small saccades after the primary one
saccades are tonically inhibited by the inhibitory omnipause cells in the reticular formation
when these omnipause cells are inhibited, the saccades are controlled by the reticular formation#burst cells (see also extraocular motor neurons#pulse)
decisions to saccade are controlled by the higher cortical structures (frontal eye fields, supplementary eye fields, posterior parietal cortex), and controlled through the superior colliculus
like the vestibulo-ocular reflex, the saccadic system can adapt to changes in muscle function
e.g. weakness in one of the extraocular muscles (hypometric) - if the strong eye is patched, the system learns to compensate for the insufficient signal, and when the stronger eye is unpatched there is significant overshooting by the weaker one
may involve cerebellum - see saccades#clinical
you might still be able to saccade
(according to sara)
because the saccade signal can go directly from the frontal eye fields to the extraocular motor neurons
or it can come directly from the superior colliculus to the extraocular motor neurons
but you might not be able to suppress saccades (see supplementary eye fields#clinical)
damage to the cerebellum prevents adaptive changes
does this involve the cerebellar flocculus too???