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Timothy C. Hain, MD

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The tracking test measures the ability of subjects to match eye movement to visual target movement. Here we will discuss smooth pursuit and optokinetic nystagmus.

An example of a tracking test (a pursuit test) is shown below. Sinusoidal pursuit is processed with fourier fits and a Bode Plot is produced.  This figure hows normal pursuit, where only one eye was recorded.




Both the sinusoidal and the triangular wave pursuit stimuli are used for clinical testing. Sinusoidal stimuli are appropriate for detecting symmetrical disturbances of pursuit and triangular wave stimuli are used to detect pursuit which is better in one direction than the other. Pursuit gain, which is the ratio of eye velocity to target velocity, is affected by target velocity, acceleration and frequency. For the sinusoidal pursuit stimulus, these three stimulus parameters are mutually interdependent, as discussed in the preceding chapter. For the triangular wave pursuit stimulus, velocity is constant, and acceleration appears as periodic pulses. Accordingly, frequency and velocity can be varied independently of acceleration. Unfortunately, perfect tracking of the triangular wave stimulus is impossible because of the abrupt accelerations at turn-around time.

Registration of smooth pursuit is of minor diagnostic utility, because disturbances of pursuit are usually nonspecific. Pursuit performance is strongly affected by attention, and inattentive or uncooperative subjects can perform poorly without having any significant central lesion. Another source of difficulty is that the lack of a standard pursuit paradigm associated with a well defined normal data set. Simple sinusoidal pursuit paradigms can be characterized by pair of three variables (frequency, amplitude and peak velocity), and pursuit tracking performance is a function of all three variables. Most laboratories have used idiosyncratic combinations of paradigm variables, which has resulted in the generation of many small normal data sets which cannot be compared to others. There is considerable variability even when the paradigm variables are similar. This variability may be related to factors that are difficult to quantify such as the degree of alertness present in subjects, or the visibility of the pursuit target. Pursuit is easily disrupted by common centrally acting medications such as anticonvulsants, minor tranquilizers, and preparations used for sleep. Finally, it is also clear that pursuit performance declines with age (Zackon and Sharpe, 1987).


Normal Limits for Smooth Pursuit

Sinuosoidal smooth pursuit is strongly reduced by frequency, age and gender (women have poorer pursuit than men).


 Symmetrical Disturbances of Pursuit

Disorders of Smooth Pursuit

Symmetrical reduction of smooth pursuit is encountered frequently. Table 9 lists the most common causes of reduced pursuit gain. For the reasons advanced above, one should be conservative when diagnosing abnormalities of pursuit. Clinically, it is adequate to classify patients with symmetrical pursuit into those with perfect pursuit, those with moderately impaired pursuit, and those with no pursuit at all. This classification can usually be done by eye from the position trace, when one uses a reasonable sinusoidal stimulus (e.g. 0.5 Hz, +- 20 degree amplitude). Cerebellar lesions have significant but relatively minor effects on pursuit (Straube et al, 1997).

Those with perfect or near perfect pursuit, as judged from the lack of catch-up saccades, or from pursuit gains greater than 0.8, are normal. Persons with some, but not perfect pursuit, e.g. pursuit gains greater than 0.2 but less than 0.8 are in a grey zone. Such moderately impaired pursuit tracking might be related to inattention or medication, an underlying central nervous system disorder, or advanced age.

Persons with no pursuit at all, operationally defined as pursuit gain less than 0.2, are the most important ones to identify because they will nearly always have a central nervous system disturbance. Rarely, pursuit gain greater than 1.0 is noted. This is recognized by the occurrence of "backup" saccades, or in other words, saccades directed against target motion. If backup saccades are not present, one will inevitably find a technical error. Pursuit gain which is truly greater than 1.0 occurs most frequently in patients with a form of congenital nystagmus called "latent nystagmus", during triangular wave pursuit. Some normal subjects can also track with gains slightly greater than 1.0.

Asymmetrical Pursuit

Causes of Asymmetrical Pursuit


Pursuit which is significantly worse in one direction than another is asymmetrical. While rare, asymmetrical pursuit is more often of clinical utility than is symmetrically reduced pursuit, because it is specific for a central nervous system disorder. One can easily detect pursuit asymmetry if a plot is available in which there is an indication of mean gain and the standard deviation in each direction. One must use a pursuit stimulus in which velocity is constant, such as the triangular wave paradigm, in order to be able to compare rightward and leftward gain.

There are several causes of asymmetrical pursuit, as listed in table 10. Patients with acute cortical lesions involving the parietal or frontal lobes, or a brainstem lesion involving the pontine nuclei may transiently exhibit better pursuit directed contralateral to their lesion. Pursuit asymmetry due to a cortical injury is rarely useful because it typically persists only for several weeks.

Unidirectional spontaneous nystagmus may be superimposed upon pursuit and cause asymmetry. Spontaneous nystagmus due to peripheral vestibular lesions, when weak, may not affect pursuit at all but when it is strong (e.g. 20 deg/sec in the dark), it may overwhelm the pursuit system. Spontaneous nystagmus due to central lesions may go uncorrected by the pursuit system, and result in a pronounced asymmetry pattern. These patients present with a spontaneous nystagmus, poorly suppressed by fixation, reduced and asymmetrical pursuit, and gaze-evoked nystagmus. An example is shown in figure 10. In these instances it is helpful to measure pursuit gain only around regions where the eye is crossing primary position, as in this way, the effects of gaze can be eliminated.

In patient with a form of congenital nystagmus called latent nystagmus, a pursuit asymmetry can be recorded which alternates direction according to the viewing eye. These patients usually have a history of amblyopia. As no pursuit asymmetry or nystagmus may be seen with both eyes viewing, this condition can cause confusion if the patient alternates fixation during the oculomotor battery.

Reversed Pursuit

In certain patients with congenital nystagmus, the eyes will make saccades in the direction of target motion and slow smooth movements against target motion. Some authors prefer avoid using the term "reversed pursuit" because eye velocity is not proportional to target velocity in these patients (Abadie and Dickenson, 1981).

Miscellaneous Pursuit Abnormalities.

In patients with poor peripheral vision, such as those with retinal pigmentary degenerations, from time to time the eyes may "get lost" during tracking, showing a characteristic pattern of searching saccades. However, because the patient can find the target intermittently, numerical figures for tracking may be normal. Figure 11 shows an example of such a case. The term "disorganized pursuit" is sometimes applied to severely abnormal pursuit falling into one of the categories mentioned above. Disconjugate eye movements may rarely occur during pursuit. In most cases it is not necessary to scrutinize the pursuit trace, because the same underlying disorders which cause disconjugate pursuit, also cause disconjugate saccades.



Normal Optokinetic Nystagmus and OKAN

Normal values for OKN gain are similar to those given for pursuit gain, or slightly greater, but OKN gain is less strongly reduced at high frequencies (27). While normal values are available for OKN phase, it is uncertain whether or not phase is affected by disease. Practically, OKN is best evaluated by comparing it to smooth pursuit, using the normal values developed for pursuit.

There are several pitfalls unique to optokinetic testing. While less sensitive to attention than pursuit, because OKN is disturbing to some patients, there may be an active attempt made to suppress it by fixating upon an object in the room which is not moving. This pattern is easily recognized because these persons are generally otherwise normal individuals, and because their initial responses are robust. Also, as discussed in the preceding chapter, many commercial "optokinetic simulators", are actually devices which elicit smooth pursuit. If one is using such a device, the diagnostic points listed below which depend on noticing differences between pursuit and optokinetic responses do not apply.

References related to normal values for OKN/OKAN.

Disorders of Optokinetic Nystagmus

Optokinetic nystagmus (OKN), like pursuit, has only minor diagnostic utility. Although OKN is more specific than pursuit, as it is not as affected by inattention and medication as is pursuit, it is also less sensitive. Presumably the relative lack of sensitivity of OKN to ocular and central disorders is due to the fact that OKN is the sum of two tracking mechanisms, namely the smooth pursuit system, which uses foveal vision, and a separate tracking system, which uses both foveal and extrafoveal vision.

Causes of OKN disorders

Visual disorders
Pursuit system disorder (i.e. floccular lesion, medication)
Fast phase disorder (i.e. PSP)
Superimposed nystagmus
Congenital nystagmus

Symmetrically Reduced OKN Gain

There are several causes of OKN abnormalities. There are three specific patterns of abnormal OKN, the first of which is symmetrically reduced OKN gain. Reduced OKN occurs in visual disorders, in pursuit system disorders, and in disorders of fast phases. While smooth pursuit is most affected by visual acuity, which represents foveal vision, OKN is produced both by foveal and extrafoveal vision, and thus may persist even when visual acuity is poor. In disorders which selectively affect foveal vision, a slow build-up of OKN may occur to a constant velocity stimulus (7). In disorders which spare foveal vision but abolish peripheral vision, such as extremely severe retinal pigmentary degenerations, no buildup of OKN is seen. Another context in which pursuit is normal but OKN is symmetrically reduced are patients with fast phase disorders. The most common clinical disorder of this type is a degenerative disorder of the brainstem called progressive supranuclear palsy (PSP), in which saccades are slowed and difficult to initiate. Accordingly, patients with PSP may have normal pursuit to a sinusoid or triangular wave target, but poor OKN to a drum moving at constant velocity because their OKN "hangs up" in the orbit. In other words, the eyes deviate out to the orbital edge and just stay there, instead of undergoing periodic resetting quick phases which bring the eye back to the center. These patients show a similar disorder of vestibular fast-phases, and get hung up when rotated at constant velocity. In the later stages of PSP, both pursuit and OKN are lost.

Zee DS, Yee RD, Robinson DA. (1976a) Optokinetic responses in labyrinthine-defective human beings. Brain Res; 113:423-28.

Asymmetrical OKN Gain

Asymmetrical OKN is not as helpful for diagnosis of central nervous system disorders as asymmetrical pursuit, mainly because it occurs so infrequently. Presumably asymmetrical OKN is uncommon because it requires lesions in two tracking systems -- foveal and extrafoveal. Only a minor asymmetry of OKN appears following complete unilateral peripheral vestibular lesions. Asymmetrical OKN is present in patients with maldeveloped foveas and also appears briefly following unilateral parieto-occipital lesions.

Baloh RW, Yee RD, Honrubia V. (1980) Optokinetic asymmetry in patients with maldeveloped foveas. Brain Res 186: 211-216.


Reversed OKN

Reversed or inverted OKN occurs in patients with congenital nystagmus, which is discussed under the heading of fixation. In these patients, the nystagmus beats in the direction of stripe movement. However, the slow-phase velocity of the nystagmus does not scale with the stimulus speed.


Disorders of Optokinetic Afternystagmus (OKAN)

Optokinetic afternystagmus (OKN) is the nystagmus that follows a constant velocity optokinetic stimulation, after the lights have been turned off. It is a weak response in humans, generally decaying from an initial value of about 10 degrees/second to zero, over about 15 seconds. There is a good normal database for OKAN (36). OKAN is characterized by three parameters, namely initial velocity, the time constant of decay, and the slow-cumulative eye position or SCEP. The most useful of these parameters is the SCEP. The lower limit of normal for SCEP used in the author's laboratory is 40 deg. 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 (36). Averaging can be used to overcome this problem. Conditions that may result in abnormal OKAN are listed in table 12.

Table 12 - Causes of Abnormal Optokinetic Afternystagmus

Optokinetic nystagmus disorders
Peripheral vestibular lesions
Central vestibular lesions
Mal de debarquement syndrome

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 (8)

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). 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).

General References