Timothy C. Hain, MD. • See also OKN testing • Page last modified: August 1, 2022

Optokinetic afternystagmus (OKAN) describes the eye movements that occur after the lights are turned out for OKN, and the subject is in complete darkness. The darkness must be 100% -- small light leaks will obliterate OKAN.

OKAN is only elicited by large field stimuli. It simply is not elicited by the typical, small field stimulators used in clinical laboratories. If you are thinking about doing OKAN in your lab, don't bother unless you can somehow surround the person with a full field and have some method of blocking vision completely (either a very dark room or video goggles. Furthemore, OKAN is somewhat difficult to elicit now due to the adoption of video frenzel goggle systems for eye movement monitoring. Most of these allow viewing of the optokinetic stimulus through a small aperature in the goggle, reducing the potential full field stimulus to a small aperature. One would think that a better methodology would involve using a VR system, equipped with an eye movement monitor. More easily said than done.

An example of OKAN is shown below. Section 1 is the OKN, and section 2 is the OKAN. This is a rather strong one.

Optokinetic afternystagmus. The lights go out in section 2, but the nystagmus continues on. This response was elicited in a Micromedical Rotatory chair system, using a full-field surround.


OKAN can be quantified by using two parameters, the time constant and the gain (ratio of peak slow-phase velocity to stimulus)

Time constant of OKAN in normal subjects Peak slow-phase velocity of OKAN in normal subjects

The figures above show the distribution of normal values for OKAN time-constant and slow-phase velocity from Tijssen et al (1989). OKAN is a weak response in humans, generally decaying from an initial value of about 10 degrees/second to zero, over about 15 seconds. OKAN is characterized by three parameters, namely initial velocity, the time constant of decay. Another method is to compute the slow-cumulative eye position or SCEP. This is roughly equal to the product of the gain and time constant, but it can also be computed directly.

The major pitfall to be aware of when attempting to use OKAN for clinical diagnosis is that OKAN varies substantially in the same individual from trial to trial. Averaging can be used to overcome this problem but this is time consuming.

Conditions that may result in abnormal OKAN are listed in the table below. OKAN is more sensitive to diseases associated with dizziness than OKN, but it is variable in normal subjects, which greatly limits its usefulness.

Directional Preponderance (DP) of OKAN in normal subjects

While one might think that the DP of OKAN might be useful for diagnosis of unilateral vestibular loss, it is not very effective at this, and there are much better ways to go about this (e.g. VHIT, vibration, HSN).

Disorders of Optokinetic Afternystagmus (OKAN)

Optokinetic nystagmus disorders (mainly reduce it)
Peripheral vestibular lesions (reduce it or make it asymmetrical)
Central vestibular lesions (can do almost anything)
Mal de debarquement syndrome (reportedly makes it wrongly vectored)

Symmetrical Reduction of OKAN

There are three abnormal patterns to OKAN: complete loss, significant asymmetry, and hyperactive OKAN. Complete loss of OKAN, or bilateral reduction of the SCEP to less than 40 deg, occurs very commonly in patients with bilateral vestibular loss. Optokinetic afternystagmus can also be lost in central lesions that affect vestibular connections. There are far easier ways to diagnose these conditions than OKAN, and we do not recommend it for any of these purposes.

Asymmetrical Reduction of OKAN

Asymmetry of OKAN occurs in patients with unilateral vestibular loss. A stronger response is found for drum rotation towards the side of lesion. Asymmetrical OKAN also occurs in many subjects who are otherwise normal, for uncertain reasons. Because of this normal variability, a significant directional preponderance in OKAN occurs in only about half of patients with complete unilateral vestibular loss.

Hyperactive OKAN

Abnormally increased OKAN may be found in patients with "mal de debarquement", which is a condition in which the vestibular system is overactive, and causes a prolonged "land sickness" (Brown and Baloh, 1987; Hain et al, 1999). It may be that this simply reflects a propensity for people with motion sickness to have increased OKAN (see below).

Stimulants increase OKAN in guinea pigs (Marlinski et al, 1999). OKAN is generally increased in young women compared ot other populations (Tijssen et al, 1989). Young women also tend to have more motion sickness.

OKAN in malingering

OKN and OKAN have usefulness in detection of malingering, particularly in persons who are pretending to have bilateral vestibular loss in an attempt to obtain a legal result of some kind. Unfortunately, legal activity is common in cases of bilateral loss, because most are due to ototoxicity.

As noted above, OKN is difficult to stop and someone who has no OKN is probably (but not always) not cooperating. OKAN has utility in bilateral vestibular loss, as it should be absent. Thus the OKN/OKAN test can detect uncooperative subjects in two ways -- lack of OKN, and presence of OKAN are both suggestive of a person who is either uncooperative or who has substantial vestibular function.

OKAN in motion sickness

One would expect that larger amounts of OKAN, being a proxy for velocity storage, would be correlated with greater susceptibility to motion sickness (Dai et al, 2007). Guo et al (2017) stated that they found a correlation between scores on a motion sickness questionnaire (VIMS), and OKAN time constant, in 27 normal subjects. More research needs to be done on this question, but it does seem reasonable to expect that motion sickness susceptibility might be correlated with OKAN time constant. .

References about OKAN: