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

The effects of static tilts about the roll (anterior-posterior) axis on human horizontal optokinetic afternystagmus (HOKAN) were examined. Static tilts in roll, with subjects lying on their left side, produced significant tilt-dependent HOKAN suppression. Only the slow (indirect pathway) component time constant (1/D) of the double exponential model for human HOKAN decreased with angle of roll tilt. The effect was direction specific in that suppression occurred only following a leftward-going stimulus. These findings provide further support for the postulate that otolith-organ-mediated activity can couple to the horizontal velocity storage mechanism in humans. A slight trend towards a tilt-dependent reduction of coefficient A (initial slow phase velocity of fast component decay) was revealed, suggesting the possibility that otolith-organ-mediated activity could couple to direct (pursuit-mediated?) pathways as well. No horizontal-to-vertical cross-coupling occurred, indicating that this aspect of the 3-dimensional model for velocity storage proposed by Raphan & Cohen (1988) may not completely apply to humans.     

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.     

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.     

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.     

Human optokinetic afternystagmus. Effects of repeated stimulation

Normal human subjects were exposed to repeated optokinetic afternystagmus (OKAN) testing in either one direction or alternating directions of stripe movement. Sessions were conducted at intervals of either one week or several weeks. Repeated exposure to OKAN stimulation in one direction produced significant response decrements in cumulative displacement, short time constant, long time constant, and the coefficient of the long time constant component (C). The data suggest that the decrease in C and cumulative displacement occurred most noticeably between trials 3 and 4 of the first session. Retesting after 1 week, and up to 8 weeks later revealed no recovery. Repeated exposure to alternating leftward and rightward stimuli resulted in response decrement in both cumulative displacement and C. Responses to leftward stimuli were indistinguishable from responses to rightward stimuli.     

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.     

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.     

Reverse optokinetic after-nystagmus generated by gaze fixation during optokinetic stimulation

Gaze fixation during optokinetic stimulation generates an after-nystagmus with a slow component towards the reverse direction of the optokinetic stimulation. The duration and maximum slow component velocity (SCV) of this "reverse OKAN" were observed by changing the duration, velocity and direction of the optokinetic stimulation in nine normal volunteers. The duration of reverse OKAN increased with increasing stimulation time but was unaffected by changes in the stimulation velocity. The maximum SCV of reverse OKAN decreased with an increase in the stimulation velocity but was not significantly affected by changes in the optokinetic stimulation time. There was no directional difference among the horizontal, upwards and downwards reverse OKANs. The reverse OKAN was thought to be generated by a mechanism different from the velocity storage mechanism which produced optokinetic nystagmus and the first phase of OKAN. Retinal slip during the optokinetic stimulation was considered to be an input to the mechanism which generated the reverse OKAN. We hypothesize that the mechanism causing the reverse OKAN may be a generator of the second phase of OKAN, which was also intimately connected with self-motion sensation during the optokinetic stimulation.     

Reverse Optokinetic After-nystagmus Generated by Gaze Fixation During Optokinetic Stimulation

Gaze fixation during optokinetic stimulation generates an after-nystagmus with a slow component towards the reverse direction of the optokinetic stimulation. The duration and maximum slow component velocity (SCV) of this "reverse OKAN" were observed by changing the duration, velocity and direction of the optokinetic stimulation in nine normal volunteers. The duration of reverse OKAN increased with increasing stimulation time but was unaffected by changes in the stimulation velocity. The maximum SCV of reverse OKAN decreased with an increase in the stimulation velocity but was not significantly affected by changes in the optokinetic stimulation time. There was no directional difference among the horizontal, upwards and downwards reverse OKANs. The reverse OKAN was thought to be generated by a mechanism different from the velocity storage mechanism which produced optokinetic nystagmus and the first phase of OKAN. Retinal slip during the optokinetic stimulation was considered to be an input to the mechanism which generated the reverse OKAN. We hypothesize that the mechanism causing the reverse OKAN may be a generator of the second phase of OKAN, which was also intimately connected with self-motion sensation during the optokinetic stimulation.     

Human optokinetic afternystagmus. Stimulus velocity dependence of the two-component decay model and involvement of pursuit

The dependence of human OKAN characteristics on optokinetic (OK) stimulus velocity was examined using the two-component double exponential model for OKAN decay. Drum velocities studied were between 10 degrees and 70 degrees deg/sec over a constant exposure period of 60 sec. Results reveal two distinct types of response: a 'low'-level response at lower drum velocities (10 degrees, 20 degrees, 30 degrees/sec) and a 'high'-level response at higher drum velocities (40 degrees, 60 degrees, 70 degrees /sec). These findings support our previous proposal that OKAN decay is a two-component process, and extend it by demonstrating that these two components have differing stimulus velocity sensitivities, as would be predicted if it were assumed that they represented direct (pursuit) and indirect (non-pursuit) pathways respectively.     

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.     

Cross-coupling between horizontal and vertical eye movements during optokinetic nystagmus and optokinetic afternystagmus elicited in microgravity

The occurrence of horizontal jerks with larger amplitudes than on Earth was observed during vertical optokinetic nystagmus in astronauts tested throughout a 7-day spaceflight. During early exposure to microgravity, a horizontal spontaneous-like nystagmus was recorded in darkness following both vertical and horizontal optokinetic stimulation. In addition, the time constant of vertical OKAN with slow phase up was larger than on the ground. These effects disappeared on flight day 2. Then, the horizontal and vertical OKAN time constants decreased, and gradually returned to the preflight values, as previously observed with the gain of the vestibulo-ocular reflex. The early changes in microgravity are in agreement with those obtained on Earth in monkeys and humans during static tilt relative to gravity. Our findings suggest that the absence of otolithic input in microgravity may have an effect on the optokinetic system which could be mediated by the velocity storage mechanism.     

Changes in the perceived head transversal plane and the subjective visual horizontal induced by Coriolis stimulation during gondola centrifugation

For studying the influence of the vertical semicircular canals on spatial orientation in roll, the subjective visual horizontal (SVH) and the subjective transversal plane of the head (STP) were measured in a situation where the vertical canals sense a roll-velocity stimulus while the otolith organs persistently signal that the head is upright in roll. During gondola centrifugation (resultant gravitoinertial force vector 2.5 G, gondola inclination 66 degrees) subjects were exposed to controlled rotational head movements (angular speed 27 degrees/s, magnitude 40 degrees) about the yaw (body z-) axis, produced by means of a motor-driven helmet. This causes a roll-plane Coriolis stimulus to the canals, while the otoliths persistently sense upright head position in roll. The subjects reported intense sensations of rotation and tilt in the roll plane. This was reflected in tilts of both the SVH and STP. The initial tilt of the SVH was 13.0 +/- 9.7 degrees (mean +/- S.D., n=10). The STP was changed in the opposite direction. The initial tilt was 23.8 +/- 12.2 degrees (mean +/- S.D., n=5). The changes in the SVH and STP were not of equal magnitude. A few subjects who had almost no deviations in the SVH showed pronounced tilts of the STP. The time constant for exponential decay of the tilts of the SVH and STP was on average approximately 1 minute. These findings indicate that a difference in activity of the vertical canals in the right versus left ear may cause substantial tilts of the SVH even if there is no asymmetry in the activity of the otolith system. Further, the canal stimulus may induce a tilt of the fundamental egocentric frame of reference.     

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.     

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.     

Visual-vestibular interaction in humans during earth-horizontal axis rotation

Visual-vestibular interaction (VVI) using 60 degrees/s constant velocity earth horizontal axis (EHA) yaw rotation was measured in 7 human subjects. This so-called 'barbecue spit' rotation stimulated both the horizontal semicircular canals and the otolith organs. Subjects were tested with their eyes open in the dark (EOD), while fixating upon a target rotating with them (FIX), and while observing stationary optokinetic stripes (VVR). The resulting nystagmus slow component velocity (SCV) was analyzed. During EOD, subjects showed an exponentially decaying SCV response with a time constant of between 10 and 15 s that decayed to a non-zero baseline value (bias). Superimposed was a cyclic activity, modulation, whose period equalled the time for a complete revolution of the subject. During FIX, the average value of SCV was nearly zero indicating almost complete abolition of the exponential decay and bias components. The modulation component was reduced by half. During VVR, an exponential decay was observed in most subjects and the average value of the bias component nearly equalled that of the velocity of rotation. Modulation during VVR varied on a cycle-by-cycle basis. On average, the modulation component was nearly twice that for the EOD condition. We conclude that visual-vestibular interactions during EHA differ significantly from those during rotation about the vertical; specifically, there is a non-linear interaction between linear acceleration and optokinetic nystagmus.     

Asymmetric optokinetic afterresponse in patients with small acoustic neurinomas.

Directional asymmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 20 patients with small acoustic neurinomas (< or = 20 mm), and results were compared to those for 24 normal controls. The optokinetic afterresponse was induced by 60 s of horizontal whole-field optokinetic stimulation in both directions. Among patients, the optokinetic afterresponse was asymmetric, OKAN I and OKAN II beating toward the lesioned ear being significantly weaker than the OKAN I and OKAN II beating toward the healthy ear. Hence, in these patients with gradual deterioration of vestibular function, the vestibular side-difference was reflected both in OKAN I and OKAN II. Although asymmetry in OKAN I was frequently observed among controls, it was significantly more pronounced among the patients. Moreover, patients could be distinguished by the occurrence of OKAN II, as it did not occur at all among controls exposed to the same stimulation.     

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.     

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.