I ANATOMY            


II PHYSIOLOGY                 








Definition: Nystagmus induced by a moving full-field visual stimulus either during sustained self-rotation in the light or by the visual stimulus rotating around the subject. 
Slow phases are in the direction of visual motion and can be horizontal, vertical, or torsional depending on the stimulus1.

The rVOR (rotational or angular vestibulo-ocular reflex) cannot provide continuous stable gaze during persistent rotation, since the semicircular canals detect accleration, not constant velocity. For example, on a spinning amusement park ride, the initial acceleration of the ride is easily detected, but if the ride reaches a constant speed and occupant has their eyes are closed, with time the sense of motion becomes less and less, and then is  lost. Once constant velocity is reached, the endolymph fluid ceases to displace the hair bundles and a motion signal is no longer sent to the brain.

Consquently, in conditions such as running around in a circle or constant rotation in light, the requirement for image stabilization is provided by the visual system and not the vestibular system, by a process which generates optokinetic nystagmus (OKN).  The OKN builds up at approximately the same rate as the rVOR decays.  The OKN also maintains a stable image of the world on the retina, but rather than using the vestibular system as an input, it uses the motion of the visual image to initiate the eye movements. For example, the OKN is activated when a stationary observer watches a merry-go-round2. The brain normally interprets movement of the entire visual field as evidence for self-motion, as is shown by the sometimes overwhelming motion illusions experienced when watching IMAX movies, or when the train adjacent to an observer starts to move out of the station3. Note that determing direction of motion is not necessarily straightforward: vection (the sensation of movement produced by visual input) is dictated by the background, as is shown nicely in this little movie:

Video 1. Determining direction of motion

(vv)Chasing Dots.mp4(tt)

See: Chasing dots illusion

The optokinetic reflex is classically considered to be the reflexive response of the eyes to the motion of a large visual field, which stabilizes the eyes during tracking of a large moving visual scene and matches slow-phase eye velocity to the velocity of the visual surround. The OKN reflex therefore is therefore complementary to the rVOR, but acting at low-frequencies.  Therefore, despite the fact that, during constant-velocity rotation, eye velocity will decay to zero, the same rotation in the presence of a surrounding visual field results in a steady-state nystagmus pattern that is sustained indefinitely, as necessary to compensate for the applied stimulus. 

Figure 1. Rotatory chair and rotatory drum (with vertical stripes) 

From: Brandt T, Strupp M. General vestibular testing. Clin Neurophysiol. 2005;116(2):406-426. doi:10.1016/j.clinph.2004.08.009


In the laboratory, the OKN system is usually stimulated by rotating a large patterned drum around the stationary subject. Under these circumstances, the nystagmus pattern typically consists of a fast-velocity rise, followed by a slower increase in eye velocity to a steady-state level that is proportional to the rotational velocity of the drum; the eyes will track the full-field rotation of the patterned stripes on the drum with a nystagmus pattern of slow phases in the direction of drum rotation and quick phases in the opposite direction3.

Video 1. Full field OKN


(vv)Optokinetic To The Right For Projection 2.mp4(tt)


Slowly decaying optokinetic after-nystagmus (OKAN) in the dark occurs after visual stimulation has stoped, and shares the same velocity-storage mechanism with the VOR3. When head rotation (or drum rotation) is suddenly halted, OKAN cancels out the postrotatory vestibular nystagmus pattern, and eye velocity drops quickly to zero.

The slow component of OKN–OKAN appears designed to perfectly complement the rVOR. Despite the fact that during constant-velocity rotation eye velocity decays to zero, the same rotation in the presence of a visual surround elicits a steady-state nystagmus pattern that is sustained indefinitely, as necessary to compensate for the applied stimulus. This happens because the OKN builds up at approximately the same rate as the rVOR decays.

The smooth pursuit system also participates at the onset of the response to an optokinetic (full-field) stimulus bringing the eyes quickly to the maximum velocity. Accordingly, the cerebellar regions involved in generating both pursuit and the VOR contribute to the tracking response to an optokinetic stimulus.
These visual–vestibular interactions are impaired after lesions that also impair velocity storage4:  floccular Lesions affecting pursuit and OKN


Examination of eye movements with the optokinetic drum allows combined testing of smooth pursuit movements and saccades in horizontal and vertical directions. It is especially helpful with uncooperative or drowsy patients and with children.

It should be noted that although clinicians sometimes may try to elicit OKN using simpler devices such as the drum below, "this device, not even pretending to be a full field, is even more of a "pursuit" stimulus than the larger drum methods shown above. It can be useful in evoking convergence retraction nystagmus in persons with dorsal midbrain lesions, as well as asymmetrical tracking in persons with latent nystagmus5. Note that smooth pursuit is typically elicited voluntarity by the images of small objects being maintained on the fovea, all features which make the standard clinical OKN drum a useful method of testing pursuit3.

Figure 2. The Optokinetic Drum


Video 1. OKN in response to OKN drum rotation


(vv)Optokinetic Reflex.mp4(tt)


Video 2. Demonstration of OKN



One should look for asymmetries in the following clinical situations:

  1. Between right and left (indicates a unilateral cortical or pontine lesion)
  2. Vertical worse than horizontal (indicative of a vertical supranuclear gaze palsy due to a mesencephalic lesion)
  3. Dissociations of the two eyes (a sign of diminished adduction in INO)
  4. Reversal of pursuit (indicates congenital nystagmus)5

The best known example is that of parietal lobe lesions. With an infarction of right posterior cerebral cortex that affects secondary visual areas concerned with motion processing, the response will be reduced as the stripes move to the patient’s right (impaired ipsilateral smooth pursuit) and less corrective quick phases will be triggered. That is, there will be less nystagmus as the stripes move to the patient’s right compared with moving to the left6.





  1. Eggers SDZ, Bisdorff A, von Brevern M, et al. Classification of vestibular signs and examination techniques: Nystagmus and nystagmus-like movements. J Vestib Res. 2019;29(2-3):57-87. 
  2. Klier EM, Angelaki DE. Gaze Stabilization and the VOR. Encycl Behav Neurosci 2010; : 569–75.
  3. Wong, A. M. (2008). Eye movement disorders. Oxford: Oxford University Press.
  4. Kheradmand A, Zee DS. Cerebellum and ocular motor control. Front Neurol. 2011;2:53.
  5. Hain T.C. OKN/OKAN Testing. Retrieved from https://www.dizziness-and-balance.com/practice/nystagmus/okn.htm
  6. Serra A, Leigh RJ. Diagnostic value of nystagmus: spontaneous and induced ocular oscillations. J Neurol Neurosurg Psychiatry. 2002;73(6):615-8.