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.     

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.     

Asymmetric optokinetic afterresponse in patients with vestibular neuritis.

The symmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 14 patients with vestibular neuritis, as well as in 50 normals. The patients were examined at onset of symptoms and at follow-up 3 and 12 months later. At onset, OKAN was found mainly to reflect the spontaneous nystagmus. Although the spontaneous nystagmus disappeared in all patients within 3 months, both OKAN I and OKAN II was asymmetric at the 3- and 12-month check-ups. OKAN beating toward the lesioned ear was weaker than the OKAN beating toward the healthy ear. Thus, the asymmetric vestibular function was reflected not only in the OKAN I, but also by an asymmetry in OKAN II. Between the 3- and 12-month check-ups, asymmetry in OKAN declined, even among those patients who showed no improvement in caloric response during that time. The decreasing asymmetry in OKAN with time after lesion was, however, related to the disappearance of a positional nystagmus. Hence, the results may be interpreted as suggesting OKAN not only to be affected by vestibular side-difference, but also to be modified by the process responsible for vestibular compensation following a peripheral vestibular lesion.     

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.     

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.     

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.     

Classification of optokinetic after-nystagmus and its topographical-diagnostic significance in man

The existence of optokinetic after-nystagmus (OKAN) has long been known, as far back as the age of Bárány. The term OKAN means nystagmus appearing after first inducing optokinetic nystagmus, and then the optokinetic stimulation is removed. It appears easily with the eyes open in a dark place. There have been various theories about the mechanism of the onset of OKAN. Sakata et al. previously classified the types of OKAN into the following 7 types: 1) The normal type, (2) the directional preponderance type, (3) the disinhibitory type, (4) the inversive type, (5) the inhibitory type, (6) the dysmetric type, (7) the clonic type. In the present study, the authors performed a vestibular equilibrium function inspection, including an OKAN inspection, on about 10,000 patients who visited the Department of Neuro-Otology with complaints of vertigo and equilibrium disturbance. The results of the inspection were classified in accordance with Sakata's method, and the diagnostic contribution of the OKAN inspection was examined. The diagnostic significance of the OKAN inspection is considered as follows: (1) This inspection can detect a very small difference between the left and right of nystagmus in the vestibular-optokinetic system, which difference cannot be detected with OKP inspection giving a rather strong stimulation or with the caloric test giving a non-physiological strong stimulation. (2) This can be a focal localization diagnostic method by the classification by type.     

Effect of vestibulo-cerebellar lesions on asymmetry of vertical optokinetic functions in the squirrel monkey

The role of the cerebellar uvula and nodulus in vertical optokinetic after-nystagmus (OKAN) was studied in 4 squirrel monkeys. Aspiration ablation of the uvula and nodulus resulted in no significant change in the initial or peak gain of vertical optokinetic nystagmus (OKN) during the 24-week post-operative observation. However, the asymmetry of vertical OKAN was significantly altered. Using a protracted upward OK stimulus, slow phase-down OKAN-II, which was not seen pre-operatively, was significantly increased. In contrast, a downward OK stimulus produced little change in slow phase-up OKAN-II. Thus, the asymmetric degree of vertical OKAN-II was decreased after uvulonodulectomy. In addition, there was a post-operative reduction in the vertical oculomotor stability. When slow-phase eye velocity of OKAN was plotted along the time scale, the amplitude and frequency of the sinusoidal pattern was increased. OKAN-III and OKAN-IV were found in 50% of the monkeys after uvulonodulectomy. It is therefore thought that inhibition and directional control from the uvula and nodulus influence the stability and asymmetrical behaviour of the leaky integrator in the second order output system.     

Mechanisms of vibration-induced nystagmus in normal subjects and patients with vestibular neuritis

It has been reported that vibration applied either on the mastoid or on the sternocleidomastoid (SCM) muscles induces nystagmus in normal subjects or patients after unilateral vestibular neuritis (VN). The aims of the study were to characterize vibration-induced nystagmus (VIN) in normal and patient groups and to propose the mechanism of VIN. We recorded eye movements during unilateral 100-Hz vibration on the mastoid bone and SCM muscles in 22 normal subjects and 19 patients with unilateral VN. In normal subjects, the direction of slow-phase velocity (SPV) tended to be toward the vibrated side. Vibration on the right/left SCM muscles induced mean SPV of 1.7 degrees/s, -1.9 degrees/s toward the stimulated side in all normal subjects. Vibration on the right/left mastoid bone induced mean SPV of 1.5 degrees/s, -0.4 degrees/s toward the stimulated side in most of the normal subjects. Positive value means SPV to the right side. This directional preponderance to the vibrated side was statistically significant. Among the patients with VN, the slow phase of the VIN was directed towards the lesioned side, irrespective of whether vibration was applied on the lesioned or intact side. Vibration on the right/left mastoid bone induced mean SPV of -10.4 degrees/s, -10.8 degrees/s toward the lesioned side. Vibration on the right/left SCM induced mean SPV of -7.9 degrees/s, -10.5 degrees/s toward the lesioned side. The amplitude of SPV showed a significant correlation with the unilateral weakness of caloric test. Our results suggest that the proprioceptive stimulation plays a major role in producing VIN in normal subjects, while VIN is generated mostly by the vestibular stimulation in patients with unilateral VN, which helps us localize the lesion side. Vibration tests on the SCM muscles as well as on the mastoid are recommended and our hypothetic mechanisms of VIN are presented.     

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     

The use of computer electronystagmography in the assessment of optokinetic nystagmic reactions

A novel technique of computer-assisted electronystagmography (CENG) has been used in 90 patients with vertigo. Two variants of optokinetic nystagmus (cortical and subcortical) were analysed. Registration of optokinetic nystagmus (OKN) was carried out using original devices for CENG. Right- and left-directed nystagmic reactions and their quantitation were performed according to specially devised registering and analysing programs. In one-sided vestibular disorders cases of cross-over OKN asymmetry prevailed in affection of the cerebellopontine angle (neurinoma of the VIII nerve) compared to labyrinthine disturbances (one-sided Meniere's disease). In 90% of patients with vertebrobasillar deficiency OKN asymmetry was found even in a straight position of the head. OKN asymmetry was less pronounced or disappeared in the OKN test performed with the head turned right or left by 90 degrees.     

Optokinetic nystagmus and after-nystagmus during a 6 hour bedrest study

CONCLUSIONS: A lengthy alteration of gravity direction produced different effects on the intrinsic horizontal and vertical optokinetic oculomotor systems. OBJECTIVE: To examine both optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) in a 6 h 6 degrees head-down bedrest study, in which the subjects were kept lying under simulated micro-gravity conditions. SUBJECTS AND METHODS: In six normal healthy adults, we repeatedly (five times) and comparatively studied OKN and OKAN evoked by horizontal and vertical stimuli. Stage 1 was an upright sitting position. During the 6 h bedrest condition, we studied OKN and OKAN in 90 degrees recumbent lateral positions (stages 2, 3, and 4). In stage 5 the subject returned to an upright position. RESULTS: We confirmed that the change in gravity direction had various effects on the condition of OKN and OKAN. Also, we found that it took more than 3 h to reach a desirable level of systemic adaptive modification to the unique environmental condition. We considered that the early change was basically due to the changes in sensory inputs through the otolith organs, and the latter changes represented the adaptive process of the spatial orientation system. During the tilt, the occurrence rates of both horizontal and vertical OKANs were decreased; however, the conditions of these changes were different.     

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.     

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.     

Modification of constant optokinetic nystagmus by vestibular stimuation.

Experiments were conducted to quantify the effect of a vestibular stimulation of known magnitude on a constant optokinetic nystagmus (OKN). Ten normal human subjects were tested with varying magnitudes of vestibular stimuli that were superimposed on a constant 30 degrees optokinetic stimulus. The gain of the vestibular system in the dark was 0.42 +/- 0.11, and the gain in the light during superimposition testing was 0.12 +/- 0.02. From these results, predictions were made that the degree of vestibular imbalance necessary to produce an asymmetric OKN would generate a spontaneous nystagmus in the dark, which would be equivalent to 20 to 30 degrees. Data from a large group of patients were used for corroboration of the results.     

Effect of head orientation on human postural stability following unilateral vestibular ablation.

Effective interpretation of vestibular inputs to postural control requires that orientation of head on body is known. Postural stability might deteriorate when vestibular information and neck information are not properly coupled, as might occur with vestibular pathology. Postural sway was assessed in unilateral vestibulopathic patients before and acutely, 1, 4, and 18+ months after unilateral vestibular ablation (UVA) as well as in normal subjects. Postural equilibrium with eyes closed was quantified as scaled pk-pk sway during 20 s trials in which the support surface was modulated proportionally with sway. Subjects were tested with the head upright and facing forward, turned 45 degrees right, and 45 degrees left. Equilibrium was uninfluenced by head orientation in normal subjects. In contrast, patients after UVA showed both a general reduction in stability and a right/left head orientation-dependent asymmetry. These abnormalities adaptively recovered with time. It is concluded that vestibular inputs to postural control are interpreted within a sensory-motor context of head-on-body orientation.     

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.     

Comparison of vertical and horizontal optokinetic nystagmus in the squirrel monkey.

Horizontal and vertical optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) of squirrel monkeys were compared with those of rabbits, cats and humans that were previously described. Squirrel monkeys showed similar findings to cats, in which vertical optokinetic nystagmus (VOKN) is not as well elicited as horizontal optokinetic nystagmus (HOKN) and down-pursuit OKN is poorer than up-pursuit OKN. As to the reasons that bring about different responses of OKN and OKAN (and vestibular nystagmus) in different planes, we speculated two possibilities: compensatory activation of horizontal eye movement for narrowed visual field accompanied by frontally positioned eyes, and the gravity that restricts and modifies posture and locomotion. Directional difference of VOKN may be caused by a physiological mechanism that makes visual fixation not susceptible to downward movement of the ground surface during forward locomotion.