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.     

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.     

Effect of alertness and visual attention on optokinetic nystagmus in humans

The effect of alertness and visual attention on optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) was studied in 20 volunteers. Electroencephalographic (EEG) activity was recorded over the occipital lobe. Exposure to sound and vibration caused a significant increase in the mean slow-phase velocity of OKN, whereas its maximum slow-phase velocity remained unaffected. Vibration tended to increase the mean slow-phase velocity of OKN more than sound did, though the difference was not statistically significant. Vibration also significantly increased the OKAN. When alpha rhythm appeared in the occipital EEG during OKN, the velocity of concurrent slow phases was reduced. However, the periods of alpha rhythm did not differ between the different stimulus conditions. The findings suggest that sound and vibration activate the subcortical optokinetic mechanism, thus causing an increase in the mean velocity of OKN. Abatement of visual attention is reflected in temporary reduction of OKN in conjunction with the appearance of alpha waves and is to be interpreted as transient quiescence of the cortical optokinetic mechanism.     

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.     

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.     

Effects of ketamine on ocular movements of the cat.

We studied the effects of ketamine, an antagonist of the N-methyl-D-aspartate receptors, on (1) the spontaneous saccades, (2) the vestibulo-ocular reflex (VOR), and (3) the optokinetic nystagmus (OKN) in 8 cats. Ketamine was given intramuscularly at four dosages (1, 2, 8, and 16 mg/kg). Eye movements were measured using the magnetic field-search coil technique. Ketamine did not prevent the occurrence of saccades, but each of them was followed by a centripetal postsaccadic drift. The time-constant of the drift induced by ketamine was 1.0 s when the given dosage was 1 mg/kg and 0.35 s when the given dosage was 16 mg/kg. Post-saccadic drift caused by a low dosage of ketamine may reflect only a mismatch between the pulse and the step commands that create saccades. The highest used dosages of ketamine aggravated the post-saccadic drift probably by disturbing the oculomotor neural integrator. To elicit the horizontal VOR, the head was submitted either to sinusoidal rotations (+/- 20 degrees; 0.05 to 1 Hz) or to a rotation at a constant velocity (100 degrees/s during 40 s). In darkness, the VOR step gain was reduced by ketamine in a dosage-dependent manner. VOR phase lead at 0.10 Hz oscillation in darkness increased from 4.0 degrees +/- 2.4 degrees to 51.6 degrees +/- 7.5 degrees after administration of ketamine at 16 mg/kg. This suggests that ketamine, at least at higher dosages, induces a failure of the neural integrator. Chemical blockade of the vestibular commissure by ketamine may also be responsible for the reduction of the VOR gain. Horizontal OKN was tested using a step stimulus (30 degrees/s during 40 s). When ketamine was given at 1 mg/kg, the average steady-state gain of the OKN diminished from 0.6 +/- 0.2 to 0.3 +/- 0.1. After administration of ketamine at 2 mg/kg, the OKN was abolished. The sensitivity of OKN to ketamine is explained at least partly by the fact that ketamine acts against the visual pathways in the retina, in the geniculate nucleus, and in the visual cortex. The time course of the optokinetic afternstagmus (OKAN) and that of the decrease of the prerotatory and postrotatory VOR were not reduced by ketamine administered at 1 or 2 mg/kg. This shows that ketamine does not affect the velocity-storage mechanism at these dosages.     

Restoration of 3D vestibular sensation in rhesus monkeys using a multichannel vestibular prosthesis

Profound bilateral loss of vestibular hair cell function can cause chronically disabling loss of balance and inability to maintain stable vision during head and body movements. We have previously shown that chinchillas rendered bilaterally vestibular-deficient via intratympanic administration of the ototoxic antibiotic gentamicin regain a more nearly normal 3-dimensional vestibulo-ocular reflex (3D VOR) when head motion information sensed by a head-mounted multichannel vestibular prosthesis (MVP) is encoded via rate-modulated pulsatile stimulation of vestibular nerve branches. Despite significant improvement versus the unaided condition, animals still exhibited some 3D VOR misalignment (i.e., the 3D axis of eye movement responses did not precisely align with the axis of head rotation), presumably due to current spread between a given ampullary nerve's stimulating electrode(s) and afferent fibers in non-targeted branches of the vestibular nerve. Assuming that effects of current spread depend on relative orientation and separation between nerve branches, anatomic differences between chinchilla and human labyrinths may limit the extent to which results in chinchillas accurately predict MVP performance in humans. In this report, we describe the MVP-evoked 3D VOR measured in alert rhesus monkeys, which have labyrinths that are larger than chinchillas and temporal bone anatomy more similar to humans. Electrodes were implanted in five monkeys treated with intratympanic gentamicin to bilaterally ablate vestibular hair cell mechanosensitivity. Eye movements mediated by the 3D VOR were recorded during passive sinusoidal (0.2-5?Hz, peak 50°/s) and acceleration-step (1000°/s(2) to 150°/s) whole-body rotations in darkness about each semicircular canal axis. During constant 100?pulse/s stimulation (i.e., MVP powered ON but set to stimulate each ampullary nerve at a constant mean baseline rate not modulated by head motion), 3D VOR responses to head rotation exhibited profoundly low gain [(mean eye velocity amplitude)/(mean head velocity amplitude)?相似文献   

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 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.     

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.     

Effect of alertness on the vestibulo-ocular reflex and on the slow rise in optokinetic nystagmus in rabbits

The effect of alertness on the time constant of the vestibulo-ocular reflex (VOR) and the time constant of the slow rise of the optokinetic nystagmus (OKN) was studied in nine pigmented rabbits. When the rabbits were alerted by vibration, the time constant of the VOR was prolonged, and that of the slow rise in OKN was shortened, whereas the gain of VOR and OKN remained largely unaffected. These findings agree with the suggestion that the state of alertness affects the vestibular system by way of the so-called velocity storage mechanism.     

Vestibular-optokinetic interactions in normal subjects and in patients with peripheral vestibular dysfunction.

The vestibulo-ocular reflex (VOR) during rotation, optokinetic nystagmus (OKN), and interactions between the vestibulo-ocular and optokinetic systems were studied quantitatively in 10 normal human subjects, 15 patients with unilateral horizontal semicircular canal paralysis (UP), and 11 patients with bilateral horizontal semicircular canal paralysis (BP). The OKN gain (eye velocity/drum velocity) was not significantly different between the normal subjects and the patient groups. During tests in which rotatory and visual stimuli were presented simultaneously, the contribution to the observed eye movements by the VOR was only one-fourth to one-third of its gain during rotation in the dark in the normal subjects and UP patients. These interactive tests did not differentiate UP patients from normal subjects but did separate BP patients from normal subjects.     

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.     

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.     

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 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     

A review of the effects of space flight on the asymmetry of vertical optokinetic and vestibulo-ocular reflexes

Prolonged microgravity during orbital flight is a unique way to modify the otolith inputs and to determine the extent of their contribution to the vertical vestibulo-ocular reflex (VOR) and optokinetic nystagmus (OKN). This paper reviews the data collected on 10 astronauts during several space missions and focuses on the changes in the up-down asymmetry. Both the OKN elicited by vertical visual stimulation and the active VOR elicited by voluntary pitch head movements showed an asymmetry before flight, with upward slow phase velocity higher than downward slow phase velocity. Early in-flight, this asymmetry was inverted, and a symmetry of both responses was later observed. An upward shift in the vertical mean eye position in both OKN and VOR suggests that these effects may be related to otolith-dependent changes in eye position which, in themselves, affect slow phase eye velocity.     

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.