Optokinetic nystagmus is elicited by periodic visual stimuli drifting across the subject's visual field. The classical stimulus is a rotating drum provided with co-axial stripes. Drifting targets typically elicit pursuit eye movements in the direction of target movement, regularly alternating with resetting saccades in the opposite direction. In the absence of a drum, a computer-graphics OKN target may be useful. Right-click on the display to start or stop movement, left-click to switch the direction of movement. Whenever a change has been made, be sure to remove the cursor from the display area, otherwise the subject may fixate on the cursor, and fixation overrides optokinetic nystagmus. Incidentally, the fixation override phenomenon has been used in the past to try to estimate visual acuity, by so-called arrestovisography.
Note: technical limitations may prevent a perfectly smooth stripe movement.
The subject's task is simply to watch the display center. If nystagmus cannot be induced in any direction, it may be helpful to ask the subject to silently count the number of dark bars passing across the display center.
One way to view the subject's response is to place a small mirror below the screen and watch the subject's eyes in the mirror. Alternatively, the examiner can view the subject's eyes from behind the screen, looking over the screen frame. The examiner's task is to decide whether responses are symmetrical or not, between the eyes and between directions. An absence of nystagmus is not necessarily abnormal as long as the symmetry requirement is met.
Visual field defects do not cause an asymmetry of OKN. Asymmetric OKN is evidence of a motor lesion, not a sensory lesion.A horizontal asymmetry is most commonly due to a unilateral, posterior hemisphere lesion. The direction of target movement associated with a an absent or poor OKN points to the side of the lesion. Hence, if a poorer response is obtained on target movement to the right, the lesion resides on the right side. An exception to this rule occurs with recent frontal lobe lesions, which may cause a transient asymmetry of OKN. This asymmetry typically vanishes within a week or so, in contrast to posterior lesions, where repair is much more protracted.
Horizontal asymmetries may also occur with brainstem lesion but very rarely as an isolated finding. Brainstem lesions associated with OKN asymmetry typically generate a multitude of clinical signs that help differentiation from a hemisphere lesion, e g, diplopia and spontaneous nystagmus.
A horizontal asymmetry between the eyes, i e, a dissociated response, is most commonly encountered with internuclear ophthalmoplegia, INO. Indeed, a horizontally dissociated OKN may be the sole sign of a subtle lesion of a medial longitudinal fascicle.
As to vertical OKN, it is common to encounter some up/down asymmetry in normal subjects, so interpretation should be cautious. More important than looking for asymmetry is looking for convergence/retraction jerks. Downward moving stripes elicit upward saccades and the induction of upward saccades is the best way to elicit convergence/retraction nystagmus as a sign of upper brainstem disease. Convergence/retraction nystagmus usually appears at an earlier stage of disease than does upgaze palsy.End