Human optokinetic afternystagmus. Slow-phase characteristics and analysis of the decay of slow-phase velocity

Events following the extinction of lights after 1-minute exposures of naive, normal subjects to an optokinetic stimulus at 40 deg/sec have been closely examined and quantified. Mean eye displacement in each slow phase decreased from 10.12 +/- 1.61 deg during optokinetic nystagmus (OKN) to 3.36 +/- 2.32 deg during optokinetic afternystagmus (OKAN). Slow-phase duration increased from 0.26 +/- 0.03 sec during OKN to 0.45 +/- 0.195 sec during OKAN. Eye displacement per slow phase remained fairly constant during OKAN, suggesting a spatial reference for the resetting of gaze. OKAN decay is a two-component process which can be closely approximated by a sum of two exponentials, one with a short time constant of 1.15 sec and the other with a long time constant of 48.8 sec. OKAN decay commenced at a time after lights out which depended upon the presence and timing of an intervening fast phase. When a fast phase intervened, OKAN decay commenced about 230 msec after it, and about 460 msec after lights out. When lights out occurred during the fast phase, OKAN decay commenced about 340 msec later.     

Human optokinetic afternystagmus. Charging characteristics and stimulus exposure time dependence in the two-component model

The dependence of human optokinetic afternystagmus (OKAN) velocity storage (charging) and optokinetic nystagmus (OKN) characteristics on optokinetic (OK) stimulus exposure time was investigated, using the two-component double exponential model for OKAN decay. Results are compatible with our previously proposed concept of two velocity storage integrators, one responsible for the short time constant decay (pursuit-mediated) and the other for the long time constant decay (OK system-mediated). The dependence of the long time constant integrator of OKAN on stimulus exposure time was clearly demonstrated. The short time constant integrator appeared to be independent of stimulus exposure time within the range studied. We conclude that the charging time-course of each component is distinct from that of the other. The time constants of each component decay were found to be invariant. A left-right asymmetry observed in both OKN and OKAN responses suggests that the integrators are direction sensitive.     

Effect of body positions in human optokinetic nystagmus and optokinetic after nystagmus

We determined whether whole body tilt would shift the axis of optokinetic nystagmus (OKN) and optokinetic-after nystagmus (OKAN) induced by full-field rotation at 35 degrees/sec. Fifteen normal people were positioned upright or tilted 30 degrees, 60 degrees or 90 degrees to both sides. Stripes of 5 degrees were projected on a 10-foot dome around the subject's yaw axis. Each trial lasted 45 sec. The lights were then extinguished, and the subject remained in darkness for 30 sec, while after nystagmus (OKAN) was recorded. Horizontal and vertical eye movements were recorded by video-oculography at 60 Hz. Eye position and velocity data were stored on optic disk cartridge by use of the data acquisition system. A. OKAN: For the subject in the upright position, the OKN velocity vector was aligned with both gravity and the subject's yaw axis with two minor exceptions. When the subject was tilted, a vertical OKN component (VOKN) appeared in a majority of subjects. For all 15 subjects, the mean angle of the OKN velocity vector regravity (Vectorg) was 22.6 +/- 7.2 degrees at 30 degrees tilted position. The Vectorg were 48.5 +/- 10.3 degrees at 60 degrees tilted position, and 76.4 +/- 12.6 degrees at 90 degrees tilted position. This represented shifts of the OKN velocity vector from the body axis of 7.4 degrees, 11.5 degrees and 13.6 degrees, respectively. The horizontal OKN (HOKN) gain remained unchanged in different positions. B. OKAN: The duration of HOKAN and initial slow phase velocity (SPV) of HOKAN decreased as the body position increased from upright to 30 degrees, 60 degrees and 90 degrees tilted position, respectively. The incidence and initial SPV of VOKAN and Re-Body did not change as the body position increased from upright to 30 degrees, 60 degrees and 90 degrees tilted position, respectively. Thus, VOKN was observed during HOKN as subjects were tilted and tended to vector to gravity, but VOKAN was not always observed during horizontal OKAN when subjects were tilted.     

Effects on the optokinetic system of midline lesions in the pretectum of monkeys

The nucleus of the optic tract (NOT), an important visuo-motor relay between the retina and preoculomotor structures, is responsible for mediating horizontal optokinetic nystagmus (OKN) in monkeys, cats, rabbits and rats. In addition to its projection to the vestibular nuclei, the NOT has a prominent projection to the contralateral NOT via the posterior commissure. In order to evaluate the role of the commissural fibers between the NOTs in OKN, we cut the posterior commissure in three Macaca fuscata. The animals viewed the OKN stripes under three conditions: right eye viewing, left eye viewing, and both eyes viewing. OKN was recorded in response to counter-clockwise and clockwise stimulation at stimulus velocities of 30 degrees/s, 60 degrees/s and 90 degrees/s. After control data were gathered, the posterior commissure was transected with an operating knife. Before the animal was sacrificed, biocytin, an anterograde tracer, was injected into the left NOT in order to confirm that all of the commissural fibers had been cut. Although the midline lesions decreased the initial rapid rise and steady state OKN slow-phase velocity in all three animals, there were no directional differences observed during monocular clockwise or counter-clockwise visual stimulation to either eye. In two of the three animals, there were no significant differences in the time-constants of optokinetic after nystagmus (OKAN) after the lesion. In the remaining animal, the time-constants decreased at stimulus velocities of 30 degrees/s and 60 degrees/s. In conclusion, gain reduction in the rapid rise and steady state slow-phase velocity of OKN can be explained by removal of an excitatory signal mediated by commissural fibers to inhibitory interneurons in the contralateral NOT. However, interrupting the commissural fibers had no effect on the velocity storage mechanism, because the time-constants of OKAN mostly remained largely unchanged by the lesion.     

Transfer of optokinetic activity to vestibular nystagmus

Transfer of activity generated by prior optokinetic (OK) stimuli of one minute's duration to nystagmus induced in darkness by a subsequent vestibular stimulus consisting of step velocities to and from 40 degrees/s-1 was studied in 10 normal subjects. Four types of OK stimuli were used: (a) full field 'passive'; (b) full field 'active'; (c) full field in the presence of optic fixation, and (d) small OK drum stimulation. Transfer (T) was evident under all conditions and resulted in an enhancement of the vestibulo-ocular (VO) response when activity from the two stimuli were in the same direction (S) and a suppression when in the opposite (O). Expressed by the equation: Formula See Text. the respective transfer values obtained for the above conditions were (a) 66%, (b) 58%, (c) 22%, and (d) 54%. In all tests, rightward OK drum movement was more effective than leftward. In respect of passive OKN the resultant response can be well represented as the algebraic summation of the expected optokinetic after-nystagmus (OKAN) and the VO response, though opposing OKAN is more effective than enhancing. Passive OKN is more effective than active and this can be accounted for by the small contribution made by retinal slip in the former (the indirect path). Surprisingly, the small drum proved almost as effective as active OKN in terms of transfer. Fixation in the presence of full-field OK stimuli induces a non-directionally specific depression of the subsequent VO response, implying that retinal slip could contribute to the mechanism of VO response suppression.     

Slow cumulative eye position to quantify optokinetic afternystagmus.

In 30 normal subjects we computed the slow cumulative eye position (SCEP) of optokinetic afternystagmus (OKAN) that followed 60 seconds of full-field optokinetic stimulation at 60 degrees/s. The mean SCEP was 112.8 degrees +/- 65.0 degrees. The lower and upper fifth percentile limits for directional preponderance of the SCEP were -38.8% and 44.3%, respectively. The time constant, which we calculated by dividing the SCEP by the initial velocity, was 12.0 +/- 7.4 seconds. This value is nearly identical to the time constant obtained from semilogarithmic regression of the decay of OKAN slow-phase velocity versus time. We conclude that the SCEP is a good measure of OKAN and that it reflects the substantial amount of variability and directional asymmetry observed in the optokinetic responses of normal subjects.     

Human optokinetic after-nystagmus: variability in serial test results.

Test-retest variability of values for directional asymmetry in primary and secondary horizontal optokinetic after-nystagmus (OKAN I and OKAN II, respectively) was studied in 16 apparently healthy subjects. OKAN was induced by 60 s of whole-field optokinetic stimulation at speeds of 60 degrees/s and 90 degrees/s in either direction (left and right), each subject being tested on the same respective weekday once a week for 4 consecutive weeks. Values for directional asymmetry were calculated as the relative side-difference between response to drum rotation toward the right and toward the left. The subjects manifested considerable variation in values for directional asymmetry in OKAN I. This suggests prediction of a given individual's true value for directional asymmetry in OKAN I to require several measurements. On the other hand, 15/16 subjects manifested no asymmetry in OKAN II (the 16th subject was a further investigation found to have significant asymmetric caloric responses). As both OKAN I and OKAN II are known to reflect asymmetric vestibular function it is suggested that studying OKAN II may require fewer measurements of directional asymmetry, compared with studying OKAN I, when assessing the course of peripheral vestibular asymmetry.     

Effect of otolith end organ ablation on horizontal optokinetic nystagmus, and optokinetic afternystagmus in the squirrel monkey.

Horizontal optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN) (stimulus speed 0-200 degrees/sec with 1 degree/sec constant angular acceleration) were examined before and after utriculo-sacculectomy (bilateral, two-stage) in squirrel monkeys. OKN exhibited a slight decline only after bilateral otolith and organ ablations. OKAN showed a minimal decline after unilateral operation but no change after bilateral operations. Severe OKN reduction and disappearance of OKAN after bilateral labyrinthectomy in primates should basically reflect the elimination of inputs from the cristae ampullares, and not from the maculae.     

Suppression of optokinetic velocity storage in humans by static tilt in pitch.

The effects of static tilts about the pitch axis on human horizontal optokinetic after-nystagmus OKAN (HOKAN) were examined. Static tilts in pitch produced tilt-dependent HOKAN suppression. The slow decay (indirect pathway) component (coefficient C and long time constant 1/D) of the two-component model for OKAN was significantly reduced, while the short decay (direct pathway) component (coefficient A and short time constant 1/B) remained invariant as angle of tilt was increased. These results provide further evidence that otolith organ activity can couple to horizontal velocity storage in humans, in accordance with models proposed in the literature.     

The effects of intense click sounds on velocity storage in optokinetic after-nystagmus

Vestibular evoked myogenic potentials (VEMP) occurring after click stimulation in cervical muscles are thought to be a polysynaptic response of otolith-vestibular nerve origin. In optokinetic after-nystagmus (OKAN) the direction of after-nystagmus changes and slow-phase velocity decreases with head tilt. This phenomenon may be an otolith response to the direction of gravity. We assumed that intense clicks might have some influence on OKAN via the otolith-vestibular nerve. Twelve normal subjects who showed VEMP at 75 dB normal hearing level (nHL) clicks were examined. The OKAN was recorded under four conditions: right monaural, left monaural and binaural stimulation by 75 dB nHL clicks, and absence of click stimulation. Horizontal optokinetic stimulation was applied using stepwise increasing speeds from 30 deg/s to 90 deg/s. Two seconds before the stimulus ended, clicks were sounded. The slow-phase velocity of the recorded electro-nystagmography was manually measured. There was no effect on OKAN with unilateral stimulation but binaural stimulation suppressed it. These results suggest that a velocity storage integrator is influenced by intense clicks via the otolithic area. Received: 17 November 1999 / Accepted: 30 May 2000     

Experimental parameter estimation of a visuo-vestibular interaction model in humans

Visuo-vestibular interactions in monkeys can be accurately modelled using the classical Raphan and Cohen's model. This model is composed of direct vestibular and visual contributions to the vestibulo-ocular reflex (VOR) and of a velocity storage. We applied this model to humans and estimated its parameters in a series of experiments: yaw rotations at moderate (60°/s) and high velocities (240°/s), suppression of the VOR by a head-fixed wide-field visual stimulus, and optokinetic stimulation with measurements of optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN). We found the velocity storage time constant to be 13 s, which decreased to 8 s during visual suppression. OKAN initial velocity was 12% of the OKN stimulus velocity. The gain of the direct visual pathway was 0.75 during both visual suppression and OKN; however, the visual input to the velocity storage was higher during visual suppression than during OKN. We could not estimate the time constant of the semicircular canals accurately. Finally, we inferred from high-velocity rotations that the velocity storage saturates around 20-30°/s. Our results indicate that the dynamics of visuo-vestibular interactions in humans is similar as in monkeys. The central integration of visual cues, however, is weaker in humans.     

The velocity storage mechanism in human optokinetic nystagmus

The velocity storage mechanism was studied in 12 normal human subjects. For optokinetic stimulation, we principally used step stimuli of 80 deg/sec generated by an Ohm type optokinetic stimulation drum. The charge characteristics of the velocity storage mechanism in the human optokinetic nystagmus were closely approximated by the first-degree delay formula having an average time constant of 26.1 sec. This value was much longer than that reported in other animals. The OKN slow phase eye velocity reached nearly 100% of the stimulus velocity immediately after the onset of stimuli. Then, the velocity gradually decreased during first 30 seconds to approximately 70% of the stimulus velocity, and it increased again to velocity the initial during the next 50-60 seconds of the continuous stimuli. These findings, indicating the characteristics specific in the human OKN may be related to the long time constant in the charge characteristics in human OKN as compared to other animals.     

Quantitative analysis of horizontal and vertical optokinetic nystagmus and optokinetic after-nystagmus in the cat

This study reported on the horizontal optokinetic nystagmus (OKN) and vertical OKN of cats under the same conditions with quantitative parameters. Using the search coil method, the horizontal and vertical OKN was investigated in 5 alert cats in an upright position. As the optokinetic stimulus, a stepped random dot pattern was used. We recorded the quantitative parameters in both the horizontal and vertical OKN (for the direct pathway parameters, initial fast rise and fast fall; for the indirect pathway parameters, steady state slow phase velocity [SPV] and the optokinetic after-nystagmus [OKAN] area) in cats. The SPV of the horizontal OKN increased with the stimulus amplitude up to 40-60 degrees/s but saturated thereafter (in some cats even more). Right and left OKN were almost symmetrical. The SPV of the downward OKN increased with the stimulus amplitude up to 20 degrees/s but saturated thereafter. This was lower than the horizontal OKN. On the other hand, the SPV of the upward OKN was weak and irregular. As for the OKAN, the right and left OKAN was also almost symmetrical. A downward OKAN was also observed but was weaker than the horizontal OKAN. A fast fall in the SPV of the OKAN was observed in the horizontal and downward OKN. On the other hand, there was little upward OKAN. OKN in cats was composed of both a direct pathway and an indirect pathway. This study suggested that directional differences of OKN were mainly responsible for the indirect pathway. Both the direct and indirect pathways of cats were smaller than those of monkeys. This suggested that the differences in OKN between cats and monkeys were mainly responsible for the direct pathway.     

Optokinetic afternystagmus in humans: normal values of amplitude, time constant, and asymmetry

It has been suggested that the appearance of directional asymmetry and/or a reduced time constant of optokinetic afternystagmus (OKAN) might be a clinical index of vestibular imbalance. However, we do not know the limits for OKAN parameters in normal humans. Accordingly, we studied OKAN in 30 normal subjects using a "sampling" method, in which a number of values of OKAN are obtained by turning out the lights periodically during optokinetic stimulation. We found that the initial velocity of OKAN has a large intrasubject variability. Accordingly, if precision is desired so as to obtain 95% confidence that the measured mean of the initial velocity of OKAN is within 25% of the true mean in an individual subject, at least eight measurements of the initial OKAN velocity must be taken. When 12 measurements are made, all subjects had a minimum value of 5 degrees/s initial OKAN, and there was little directional asymmetry (mean of -0.47 degree/s +/- 3.13 degrees/s). The intrasubject variability of the time constant of OKAN was similar to the variability of initial OKAN velocity. However, because it is not possible to obtain repeated measures of the time constant in a short period of time, the time constant of OKAN is less likely to be useful in clinical testing.     

Computerized analysis of voluntary eye movements. A clinical method for evaluation of smooth pursuit and saccades in oto-neurological diagnosis

To permit rapid and exact quantification of the oculomotor function in clinical practice, a computerized program has been designed for the recording and analysis of pursuit eye movements and voluntary saccades. In a pursuit sequence the subject tracks a moving target, projected onto a screen at a constant speed of 20 degrees/sec over a horizontal visual angle of 60 degrees. The pursuit sequence is followed by a refixation saccade when the subject rapidly shifts his gaze back to the starting point of the target. A complete test procedure consists of ten consecutive pursuit sequences and refixation saccades in each direction. The EOG signal is fed to a PDP11/23 computer for storage and analysis. The pursuit eye movements are quantified and arranged in five velocity intervals: less than 8, 8-16, 16-24, 24-32 and greater than 32 degrees/sec. The relative distribution of the velocity content is calculated for these intervals and presented in histogram form. Saccades superimposing on the smooth pursuit are identified and grouped according to amplitude and direction. The refixation saccades are quantified as mean peak velocities and also the highest and lowest velocities of the refixation saccades are determined. In a material of 70 healthy subjects, normative data and limits for pathological function were established. In the smooth pursuit, 69% of the velocity values were located within the 16-24 degrees/sec interval. Pathological limits were set for each velocity interval and impaired pursuit tracking ability was considered to be present when those limits were reached in at least three of the five intervals. Normal mean peak eye velocity of the refixation saccade was found to be 460 degrees/sec with a range of 354-575 degrees/sec. Application of the test procedure and method of analysis is described in two patients with impairment of the oculomotor function due to a disturbance in the cerebellar brain stem area.     

Galvanically induced asymmetric optokinetic after-nystagmus

The effect of an asymmetric vestibular input on the symmetry of horizontal optokinetic after-nystagmus (OKAN) was studied in twenty healthy subjects. Optokinetic nystagmus (OKN) was elicited by a whole-field optokinetic drug, rotating at 90 degrees/s, and eye-movements were recorded by a DC electro-oculographic technique (EOG). The ratio of OKAN following right and left-beating OKN respectively was computed. An asymmetric vestibular input was generated by a continuous bi-polar, bi-aural galvanic stimulus (1 mA) to the vestibular nerves during the optokinetic stimulation and the recording of the OKAN. During galvanic stimulation the relation between left and right-beating OKAN was asymmetric, compared with the OKAN found after optokinetic stimulation only. The galvanic stimulus caused a preponderance for OKAN with the fast phase beating toward the cathode. Thus, the small vestibular asymmetry induced by the galvanic stimulus, which was not strong enough to produce nystagmus by itself, caused an asymmetric OKAN. These findings suggest that examination of OKAN may be of value to detect small vestibular asymmetries in peripheral vestibular disorders in man.     

Asymmetry of vertical optokinetic after-nystagmus in squirrel monkeys

Asymmetry of vertical optokinetic after-nystagmus (OKAN) was studied in 6 squirrel monkeys. The slow-phase eye velocity (SPEV) of upward OKAN first-phase (OKAN-I) increased with increasing stimulus velocity, whereas the SPEV of downward OKAN-I diminished. The time constant of OKAN-I was shortened with the increase in stimulus speed in both directions. With a downward stimulus, the short stimulus duration failed to produce OKAN second-phase (OKAN-II) (upward slow-phase); however, with an increase in stimulus duration, the percentage appearance increased. There was no change in percentage appearance, regardless of the duration of upward stimulus. The asymmetry of OKAN-I and that of OKAN-II differed to a certain degree.     

The effect of saccular ablation on vertical optokinetic after-nystagmus in squirrel monkeys

Summary The effect of bilateral saccular ablation on the asymmetry of vertical optokinetic after-nystagmus (OKAN) was studied in squirrel monkeys. No significant changes occurred in the initial slow-phase eye velocity (SPEV) or the time constant of the upward or downward OKAN first phase (OKAN-I) under various stimulus conditions. However, with a protracted downward stimulus, the maximum SPEV and the number of beats of the slow-phase-up OKAN second phase (OKAN-II) significantly increased. This increase should be the result from enhancement of the downward optokinetic input. In contrast, there was only minimal change in the slow-phase-down OKAN-II. Thus, the asymmetrical dominance of the vertical OKAN (dominance upward) remained the same after saccular deafferentation. Offprint request to: M. Igarashi     

Die optokinetische Untersuchung mit Reizbeschleunigung im Vergleich zu konstanten Reizen

Summary Earlier investigations showed the optimal parameters for the optokinetic test with accelerated stimuli. The acceleration is 1.2 degrees/s² and the maximum stimulus velocity is 40 degrees/s.As we can show now, this test for patients is much more difficult than the tests with constant velocities. As a result we gain more pathologic results. We compared the accelerated tests with constant velocities of 20, 40, and 60 degrees/s.     

Cervical and vestibular afferent control of oculomotor response in man.

Oculomotor response in the absence of vision has been compared in a group of 12 normal humans in two experimental conditions testing (a) the vestibulocular reflex by whole-body oscillation on a turntable, and (b) the cervico-ocular reflex by oscillation of the body with the head held stationary. The stimulus was a sinusoidal oscillation (peak angular velocity +/- 50 degrees/sec) at frequencies between 0.2 and 1.3 Hz. The slow-phase eye movements of the vestibulo-ocular response were compensatory for head movement and showed a mean gain of 0.54--0.90, increasing with frequency. The cervicoocular response was found to be very variable. The slow-phase eye movements were of low velocity (mean gain 0.05) and did not generally compensate for body movement. During neck torsion, some subjects exhibited large overall eye deviations composed of both slow and fast phase eye movements.