Rapid voluntary conjugate movements of the eyes to the opposite side are initiated in area 8 of the frontal lobe (see Fig. 21-2) and relayed to the pons. These quick movements, whose peak velocity may exceed 700 degrees per second, are termed saccades. Their purpose is to rapidly change ocular fixation and bring images of new objects of interest onto the foveae. Saccades are so rapid that there is no subjective awareness of movement during the change in eye position. Saccadic movements can be elicited by instructing an individual to look to the right or left (commanded saccades), or to move the eyes to a target (refixation saccades). These two movements are sometimes differently affected in neurologic disease. Saccades may also be elicited reflexively, as when a sudden sound or the appearance of an object in the peripheral field of vision attracts attention and triggers an automatic movement of the eyes in the direction of the stimulus. Saccadic latency, the interval between the appearance of a target and the initiation of a saccade, is approximately 200 ms.
The neurophysiologic pattern of pontine neurons that produces a saccade has been characterized as “pulse-step” in type. This refers to the sudden increase in neuronal firing (the pulse) that is necessary to overcome the inertia and viscous drag of the eyes and move them into their new position; it is followed by a return to a new baseline firing level (the step), which maintains the eyes in their new, eccentric position by tonic contraction of the extraocular muscles (gaze holding).
Saccades are distinguished from the slower and smoother pursuit movements, for which the major stimulus is a moving target. The function of pursuit movements is to stabilize the image of an object that is moving relative to the position of the head and eyes, thus maintaining a continuous clear image of the object on the fovea. Unlike saccades, pursuit movements to each side are generated in the ipsilateral parietooccipital cortex, with modulation by the ipsilateral cerebellum, especially the vestibulocerebellum (flocculus and nodulus).
When following a moving target, as the visual image slips off the foveae, the firing rate of the governing motor neurons increases in proportion to the speed of the target, so that eye velocity matches target velocity. If the eyes fall behind the target, supplementary catch-up saccades are required for refixation. In this situation, the pursuit movement is not smooth, but becomes jerky (“saccadic” pursuit). A lesion of one cerebral hemisphere may cause pursuit movements to that side to break up into saccades. Diseases of the basal ganglia also commonly disrupt pursuit into a ratchet-like saccadic pursuit in all directions.
If a series of visual targets enters the visual field, as when one is watching trees from a moving car or the stripes on a rotating drum, involuntary repeated quick saccades refocus the eyes centrally; the resulting cycles of pursuit and refixation are termed optokinetic nystagmus. This phenomenon is used as a bedside test, the main value of which is in revealing a lesion of the ipsilateral posterior parietal lobe. It may also be found that a frontal lobe lesion eliminates the quick nystagmoid refixation phase away from the side of the lesion, thereby causing the eyes to continue to follow the target until it is out of view. This optokinetic phenomenon is described more fully further on, in the section on nystagmus.