Time Constant Of Optokinetic After-nystagmus Research Articles

Measuring optokinetic after-nystagmus: potential for detecting patients with signs of visual dependence following concussion

Concussed patients with chronic symptoms commonly report dizziness during exposure to environments with complex visual stimuli (e.g. supermarket aisles, busy crossroads). Such visual induced dizziness is well-known in patients with vestibular deficits, in whom it indicates an overreliance on visual cues in sensory integration. Considering that optokinetic after-nystagmus (OKAN) reflects the response of the central network integrating visual and vestibular self-motion signals (velocity storage network), we investigated OKAN in 71 patients [17 (23.9%) females, 30.36 ± 9.05 years old] who suffered from persistent symptoms after a concussion and presented clinical signs suggesting visual dependence. Data were retrospectively compared with 21 healthy individuals [13 (61.9%) females, 26.29 ± 10.00 years old]. The median values of the slow cumulative eye position and of the time constant of OKAN were significantly higher in patients than in healthy individuals (slow cumulative eye position: 124.15 ± 55.61° in patients and 77.87 ± 45.63° in healthy individuals—p = 0.012; time constant: 25.17 ± 10.27 s in patients and 13.95 ± 4.92 s in healthy individuals—p = 0.003). The receiving operating curve (ROC) estimated on the time constant had an overall area under the curve of 0.73. Analysis of the ROC suggests that a test measuring the OKAN time constant could obtain a sensitivity of 0.73 and specificity of 0.72 in determining the origin of the visual-related disturbances in those patients (threshold 16.6 s). In a subset of 43 patients who also performed the Sensory Organization Test (SOT), the proposed OKAN test was twice as sensitive as the SOT. This study suggests that concussed patients with persisting visual symptoms may have an underlying impairment of the velocity storage mechanism and that measuring the OKAN time constant can objectify such impairment.

Correlations between individual susceptibility to visually induced motion sickness and decaying time constant of after-nystagmus

This study examines the correlations between optokinetic after-nystagmus (OKAN) parameters and individual susceptibility to visually induced motion sickness (VIMS). Twenty-seven participants were exposed to vertical black-and-white stripes drifting along the yaw axis at 60° per second for 30 min to collect individual VIMS data (Phase 1). Two weeks after the exposure, OKANs were measured (Phase 2). 19 out of 27 participants (i.e., 70%) exhibited consistent OKAN patterns. Significant correlations between the time constants of OKAN and levels of VIMS experienced by the same viewers were found. Four months later, these 27 participants were invited back for a second OKAN measurement (Phase 3). Twenty-one participants came back. Their two OKAN measurements were significantly correlated (r = 0.69, p = 0.001). Rated levels of VIMS in phase 1 significantly correlated with the time constant of OKAN in both Phase 2 (r = 0.51, p = 0.044) and Phase 3 (r = 0.74, p = 0.006). The implications of the correlation results are discussed.

Asymmetry of visuo-vestibular mechanisms contributes to reversal of optokinetic after-nystagmus

When the visual background is moving while subject fixate a visual target, optokinetic eye movements (OKN) are suppressed and the after response, called optokinetic after nystagmus (OKAN), occurring at the stimuli offset is often inverted as compared to the situation when the OKN movements are allowed. In this study, we investigated whether this reversal of OKAN results from a perceptual or extra-retinal feedback in relation with the pursuit system and/or the vestibular indirect system. Optokinesis performance was studied in normal subjects in four experiments always using the same background motion (1) to characterize the OKN and OKAN performance elicited by the whole visual field motion while fixating or not a central visual target, (2) to investigate the 3D characteristics of the OKAN reversal by using different orientations of the visual stimulation, (3) to correlate the occurrence of an inverted OKAN with functional asymmetry of the visuo-vestibular system, by studying the effects of ocular fixation deviations and finally (4) to examine the effects of the depth plane of gaze fixation on the OKAN characteristics. In Experiments 1 and 2, we observed that the visual fixation during full-field motion induced either a dumping effect or an inversion of the OKAN response that could occur in the different planes of eye movements. The time constant was significantly increased in the inverted after-responses as compared to the not inverted ones. In Experiment 3, we found that the occurrence of an OKAN reversal after eye movement inhibition was significantly related to the presence of right/left asymmetrical OKAN responses. Moreover, the OKAN time constant was strikingly dependent on the eye fixation position during the visual stimulation and this time constant/eye position relation diverged between OKAN responses with and without inversion. Finally, Experiment 4 showed that the OKAN inversion tended to disappear when the visual target to fixate was in the near space as compared to the far space included in the background. These results argue in favor of an extraretinal influence in relation to the dynamics of the vestibulo-motor system, rather than for a perceptual influence on the inverted OKAN mechanisms. More precisely, we postulate that the reversal of OKAN could be linked to an inhibition issued from pursuit signals combined with an asymmetrical activity in the VSM vestibular complex.

Optokinetic reflex dysfunction in multiple sclerosis.

The aim of this study was to further investigate optokinetic reflex function in multiple sclerosis. Gaze-holding in darkness, optokinetic nystagmus, optokinetic afternystagmus and latency to circularvection were measured using electro-oculography and a rotating optokinetic drum. Gaze-holding was not significantly different between the multiple sclerosis and control groups; however, four of 23 multiple sclerosis patients exhibited eccentric gaze-evoked nystagmus. There were no significant differences in either optokinetic nystagmus frequency or latency to circularvection. However, optokinetic nystagmus slow phase velocity during rise time and amplitude during beat time were significantly reduced in the multiple sclerosis group (p < 0.05 and p < 0.0001, respectively). The time constant of optokinetic afternystagmus was also significantly reduced in the multiple sclerosis group (p < 0.005). These results indicate that optokinetic nystagmus and optokinetic afternystagmus are significantly impaired multiple sclerosis.

Effects of tilt of the gravito-inertial acceleration vector on the angular vestibuloocular reflex during centrifugation.

Effects of tilt of the gravito-inertial acceleration vector on the angular vestibuloocular reflex during centrifugation. Interaction of the horizontal linear and angular vestibuloocular reflexes (lVOR and aVOR) was studied in rhesus and cynomolgus monkeys during centered rotation and off-center rotation at a constant velocity (centrifugation). During centered rotation, the eye velocity vector was aligned with the axis of rotation, which was coincident with the direction of gravity. Facing and back to motion centrifugation tilted the resultant of gravity and linear acceleration, gravito-inertial acceleration (GIA), inducing cross-coupled vertical components of eye velocity. These components were upward when facing motion and downward when back to motion and caused the axis of eye velocity to reorient from alignment with the body yaw axis toward the tilted GIA. A major finding was that horizontal time constants were asymmetric in each monkey, generally being longer when associated with downward than upward cross coupling. Because of these asymmetries, accurate estimates of the contribution of the horizontal lVOR could not be obtained by simply subtracting horizontal eye velocity profiles during facing and back to motion centrifugation. Instead, it was necessary to consider the effects of GIA tilts on velocity storage before attempting to estimate the horizontal lVOR. In each monkey, the horizontal time constant of optokinetic after-nystagmus (OKAN) was reduced as a function of increasing head tilt with respect to gravity. When variations in horizontal time constant as a function of GIA tilt were included in the aVOR model, the rising and falling phases of horizontal eye velocity during facing and back to motion centrifugation were closely predicted, and the estimated contribution of the compensatory lVOR was negligible. Beating fields of horizontal eye position were unaffected by the presence or magnitude of linear acceleration during centrifugation. These conclusions were evaluated in animals in which the low-frequency aVOR was abolished by canal plugging, isolating the contribution of the lVOR. Postoperatively, the animals had normal ocular counterrolling and horizontal eye velocity modulation during off-vertical axis rotation (OVAR), suggesting that the otoliths were intact. No measurable horizontal eye velocity was elicited by centrifugation with angular accelerations </=40 degrees /s2 and angular velocities </=400 degrees /s. We conclude that in rhesus and cynomolgus monkeys, differences between horizontal eye velocities recorded during facing and back to motion constant velocity centrifugation can be explained by orienting effects of the GIA tilt on the time constants of the horizontal aVOR and not by a superposed lVOR.

The effect of uvulonodular lesions on horizontal optokinetic nystagmus and optokinetic after-nystagmus in cats.

The effect of uvulonodular lesions on horizontal optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) was investigated in alert cats. A lesion in each of 6 cats was made by suction-ablation under anesthesia. In the 3 cats with only a uvular lesion, both the initial slow phase velocity and the time constant of OKAN were unchanged. In the remaining 3 cats whose lesions included the nodulus as well as the uvula, the time constant of OKAN was markedly prolonged, but the initial slow phase velocity of OKAN was not affected. The postoperative average time constant of OKAN increased from the normal value of 9 s to about 40 s. In contrast, OKN parameters (the steady-state velocity and the rising time constant) were not affected by uvular or uvulonodular lesions. These results strongly suggest that the nodulus is involved in the velocity storage mechanism and might control the discharge characteristics of the velocity storage integrator.

ヒトの視運動性眼振に対する視連動訓練効果と機構の検討

We investigated the mechanism by which repetitive optic stimulation affects optokinetic responses. Eleven persons, physically healthy, took part in this study. The subjects were stimulated optokinetically to the right. The angular velocity of the Ohm type drum was 50 deg/sec, and the duration of the stimulation was 30 seconds. This stimulation was successively applied 5 times a day over a period of 3 weeks. Optokinetic nystagmus (OKN) was recorded with electronystagmography and analyzed with a computer. Before and during this trial, we did 2 tests every week. First, the drum was rotated with an angular acceleration of 2 deg/sec2, and optokinetic adaptation limit (OAL) was estimated. Next, the drum was rotated with an equal velocity of 40, 60 and 80 deg/sec. The initial rapid rise (IR), the maximum steady state slow phase velocity (SS) and the time constant of optokinetic afternystagmus (TC) were calculated. These items were evaluated with stimulation towards the right only in 5 subjects and with stimulation towards both the right and the left in 6 subjects.Optokinetic training produced the following results : OAL increased significantly on stimulation towards the right, but did not increase on stimulation towards the left. SS increased significantly at a velocity of 60 and 80 deg/sec in both directions. IR increased significantly on stimulation toards the right, and increased slightly on stimulation towards the left. TC decreased on stimulation towards the right. We conclude that the increase of the slow phase velocity of OKN was due mainly to the enhanced function of the pursuit system, but other factors also had a role in training effects.

Habituation and adaptation of the vestibuloocular reflex: a model of differential control by the vestibulocerebellum

We habituated the dominant time constant of the horizontal vestibuloocular reflex (VOR) of rhesus and cynomolgus monkeys by repeated testing with steps of velocity about a vertical axis and adapted the gain of the VOR by altering visual input with magnifying and reducing lenses. After baseline values were established, the nodulus and ventral uvula of the vestibulocerebellum were ablated in two monkeys, and the effects of nodulouvulectomy and flocculectomy on VOR gain adaptation and habituation were compared. The VOR time constant decreased with repeated testing, rapidly at first and more slowly thereafter. The gain of the VOR was unaffected. Massed trials were more effective than distributed trials in producing habituation. Regardless of the schedule of testing, the VOR time constant never fell below the time constant of the semicircular canals (approximately 5 s). This finding indicates that only the slow component of the vestibular response, the component produced by velocity storage, was habituated. In agreement with this, the time constant of optokinetic after-nystagmus (OKAN) was habituated concurrently with the VOR. Average values for VOR habituation were obtained on a per session basis for six animals. The VOR gain was adapted by natural head movements in partially habituated monkeys while they wore x 2.2 magnifying or x 0.5 reducing lenses. Adaptation occurred rapidly and reached about +/- 30%, similar to values obtained using forced rotation. VOR gain adaptation did not cause additional habituation of the time constant. When the VOR gain was reduced in animals with a long VOR time constant, there were overshoots in eye velocity that peaked at about 6-8 s after the onset or end of constant-velocity rotation. These overshoots occurred at times when the velocity storage integrator would have been maximally activated by semicircular canal input. Since the activity generated in the canals is not altered by visual adaptation, this finding indicates that the gain element that controls rapid changes in eye velocity in the VOR is separate from that which couples afferent input to velocity storage. Nodulouvulectomy caused a prompt and permanent loss of habituation, returning VOR time constants to initial values. VOR gain adaptation, which is lost after flocculectomy, was unaffected by nodulouvulectomy. Flocculectomy did not alter habituation of the VOR or of OKAN. Using a simplified model of the VOR, the decrease in the duration of vestibular nystagmus due to habituation was related to a decrement in the dominant time constant of the velocity storage integrator (1/h0).(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of Uvulonodular Lesions on Optokinetic Nystagmus and Optokinetic After-nystagmus in Cats

To investigate the effect of uvulonodular lesions on horizontal optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN), 6 cats were tested before and after lesions made by ablation under anesthesia. In the 3 cats with only uvular lesion, the initial slow phase velocity and the time constant of OKAN were unchanged. In the remaining three cats whose lesions included not only the uvula but also the nodulus, the time constant of OKAN was markedly prolonged, and the initial OKAN velocity was not affected. The postoperative average time constant of OKAN increased from normal value of 9 s to about 40 s. In contrast, OKN was unchanged in all of the 6 animals. These findings indicate that the nodulus may contribute to the discharge characteristics of the velocity storage integrator.

Influence of static head position on the horizontal nystagmus evoked by caloric, rotational and optokinetic stimulation in the squirrel monkey

We studied the influence of static head position on the horizontal nystagmus produced by caloric, rotational and optokinetic stimulation in alert squirrel monkeys. Caloric nystagmus is stronger for nose up (NU) than for nose down (ND) pitches; so, for example, slow-phase eye velocity is four times larger in supine than in prone positions. A similarly directed asymmetry occurs in the horizontal vestibulo-ocular (HVOR) responses to long-duration, constant angular-head accelerations, but not to midband (0.1 Hz) sinusoidal head rotations. Consistent with a first-order model of the HVOR, the low-frequency or acceleration gain of the reflex (GA) is equal to the product of the midband velocity gain (GV) and a time constant (TVOR). GV is proportional to the cosine of the angle between the horizontal-canal plane and the plane of rotation, from which it is concluded that signals from the horizontal, but not from the vertical canals contribute to the HVOR. TVOR can be as much as twice as large in NU than in ND positions. GA is proportional to TVOR and it, too, shows a NU-ND asymmetry. The time constant of optokinetic after nystagmus (TOKAN) was also studied. Since TVOR and TOKAN are modified in similar ways by static tilts, it is concluded that head position affects the time constants by way of velocity-storage mechanisms. Evidence is presented that the position-dependent modification of velocity storage is otolith-mediated. The results are used to analyze the mechanisms of caloric nystagmus. The caloric response consists of a convective component (CC), as originally envisioned by Bárány (1906), and a nonconvective component (NC). CC accounts for 75% of the caloric response in the conventional supine testing position. Both components can be affected by the position-dependent modification of TVOR or, equivalently, of GA. It has been suggested that two mechanisms might contribute to NC: 1) a direct thermal effect on hair cells or afferents; or 2) a thermal expansion of labyrinthine fluids that results in a cupular displacement. Both theoretical and experimental evidence indicates that only the first of these mechanisms could result in the steady-state caloric response that is observed in the absence of convection (e.g., in spaceflight and after canal plugging) and that contributes to the prone-supine asymmetry seen in caloric testing.

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.

Cortical areas involved in OKN and VOR in cats: cortical lesions

Eye movements evoked by optokinetic and vestibular stimulation were measured by scleral search coil before and up to 8 weeks after unilateral cortical lesions in 11 cats. During both monocular and binocular viewing conditions, several deficits in the velocity-storage component of optokinetic nystagmus (OKN) were found. At low target velocities, the final steady-state slow-phase eye velocity and the peak value of optokinetic afternystagmus (OKAN) were reduced for slow phases towards the side of the lesion. At high target velocities OKN and OKAN were no longer elicited. The time constant of OKAN was also reduced for slow phases towards the side of the lesion. These deficits in OKN and OKAN were quantitatively similar in cats with large cortical (LC) lesions involving all known visual areas and in cats with suprasylvian (SS) lesions involving areas 21a, 21b, PMLS, and VLS. Ablation of areas 17 and 18 alone had no effect, but when combined with section of the corpus callosum (17/18+CC) resulted in a qualitatively similar but less severe deficit as the LC and SS lesions. By 3 weeks postoperatively, OKN recovered to near preoperative values in cats with SS lesions. Vestibular adaptive capabilities were impaired during the duration of the study in cats with LC, SS, and 17/18+CC lesions. Cats with these lesions could not normally increase VOR gain for slow phases directed ipsilateral to the lesion, and following vestibular adaptation most of these cats developed persistent asymmetries in VOR gain and VOR time constants. These results can be better conceptualized using a mathematical model of the vestibulo-ocular and optokinetic system adapted from Robinson (1977). This model contains a single positive-feedback velocity storage loop common to the VOR and OKN systems and a retinal-slip velocity nonlinearity. Our results suggest that SS cortex improves the retinal-slip nonlinearity feeding into the velocity-storage system by extending its range and increasing its gain. The SS cortex depends in part upon areas 17 and 18 either directly, or indirectly via the corpus callosum, for processing of high retinal-slip velocities. Cerebral cortex is also involved in increasing the gain of the velocity-storage loop during vestibular adaptation for ipsilaterally directed slow phases.

Nystagmus induced by stimulation of the nucleus of the optic tract in the monkey.

1. The nucleus of the optic tract (NOT) was electrically stimulated in alert rhesus monkeys. In darkness stimulation evoked horizontal nystagmus with ipsilateral slow phases, followed by after-nystagmus in the same direction. The rising time course of the slow phase velocity was similar to the slow rise in optokinetic nystagmus (OKN) and to the charge time of optokinetic after-nystagmus (OKAN). The maximum velocity of the steady state nystagmus was approximately the same as that of OKAN, and the falling time course of the after-nystagmus paralleled OKAN. 2. Increases in frequency and duration of stimulation caused the rising and falling time constants of the nystagmus and after-nystagmus to become shorter. Changes in the falling time constant of the after-nystagmus were similar to changes in the time constant of OKAN produced by increases in the velocity or duration of optokinetic stimulation. 3. Stimulus-induced nystagmus was combined with OKN, OKAN and per- and post-rotatory nystagmus. The slow component of OKN as well as OKAN could be prolonged or blocked by stimulation, leaving the rapid component of OKN unaffected. Activity induced by electrical stimulation could also sum with activity arising in the semicircular canals to reduce or abolish post-rotatory nystagmus. 4. Positive stimulus sites for inducing nystagmus were located in the posterolateral pretectum. This included portions of NOT that lie in and around the brachium of the superior colliculus and adjacent regions of the dorsal terminal nucleus (DTN). 5. The data indicate that NOT stimulation had elicited the component of OKN which is responsible for the slow rise in slow phase velocity and for OKAN. The functional implication is that NOT, and possibly DTN, are major sources of visual information related to retinal slip in the animal's yaw plane for semicircular canal-related neurons in the vestibular nuclei. Analyzed in terms of a model of OKN and OKAN (Cohen et al. 1977; Waespe et al. 1983), the indirect pathway, which excites the velocity storage mechanism in the vestibular system to produce the slow component of OKN and OKAN, lies in NOT in the monkey, as it probably also does in cat, rat and rabbit. Pathways carrying activity for the rapid rise in slow phase velocity during OKN or for ocular pursuit appear to lie outside NOT.

Baclofen and velocity storage: a model of the effects of the drug on the vestibulo-ocular reflex in the rhesus monkey.

1. Baclofen had a characteristic effect on vestibular and optokinetic nystagmus in rhesus monkeys. Each aspect of nystagmus that is dependent on the velocity-storage mechanism in the vestibulo-ocular reflex (v.o.r.) was altered by the drug: (a) Baclofen reduced the dominant time constant of the v.o.r. in a dose-dependent manner up to 5 mg/kg, the highest dosage used. The alteration in v.o.r. time constant began within 15 min of injection, was maximal between 1 and 4 h, and lasted for 14-18 h. This effect mirrors changes in plasma levels of baclofen after oral doses in humans (Faigle, Keberle & Agen, 1980). (b) Slow-phase velocities of steady-state nystagmus induced by rotation about axes tilted from the vertical (off-vertical axis rotation, o.v.a.r.) were reduced after baclofen and could not be maintained at previous levels. (c) There was a dose-dependent decline in the steady-state gain of optokinetic nystagmus (o.k.n.), and at the highest dosages little o.k.n. was induced. In parallel, the peak velocity and falling time constant of optokinetic after-nystagmus (o.k.a.n.) were reduced. Since baclofen is a GABA agonist, systems utilizing GABA and acting on GABAB receptors appear to produce inhibitory control of velocity storage. 2. The step gain of the v.o.r., measured at the beginning and end of constant-velocity rotation in darkness, was unaffected by baclofen, as were saccades, quick phases of nystagmus, and the ability to hold positions of fixation or to generate linear slow phases of nystagmus. This indicates that it is possible to use baclofen to manipulate the dominant time constant of the v.o.r. and of o.k.a.n. in relative isolation from effects on other oculomotor components. 3. Baclofen caused a dose-dependent reduction in the initial jump in eye velocity at the onset of o.k.n., suggesting that the initial jump is also under inhibitory control of GABAB receptors. However, there were still occasional slow phases with velocities up to 30-40 deg/s after baclofen, and animals were capable of visually suppressing the v.o.r. This indicates that pathways responsible for causing rapid changes in slowphase velocity were capable of functioning, at least intermittently, in the presence of the drug.(ABSTRACT TRUNCATED AT 400 WORDS)

The variable gain element of the vestibulo-ocular reflex is common to the optokinetic system of the cat

The gain (slow-phase eye velocity/head velocity) of the vestibulo-ocular reflex (VOR) of 6 alert cats was sequentially adapted to values between 0.2 and 1.66 by the chronic wearing of visual reversing or 2 X magnifying spectacles, combined with forced rotation in the light. Gain was measured during sinusoidal oscillation in darkness at 0.05 Hz at a peak velocity of about 30 degrees/s. In each state of VOR gain adaptation, optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN) were measured in a full-field optokinetic drum at velocities of 20-80 degrees/s. Steady-state, slow-phase, optokinetic eye velocity nearly equaled low drum velocities, but saturated at higher velocities and declined when drum velocity further increased. The saturation velocity varied in relation to VOR gain, ranging from 10-20 degrees/s at a VOR gain of 0.2-0.4, to 65 degrees/s at a VOR gain of 1.66. The means that the variable gain element of the VOR is shared by the optokinetic system (OKS). OKAN, measured in darkness, had a roughly exponential decay. The time constant of OKAN (Tokan) also varied with VOR gain, ranging form about 2 s at a VOR gain of 0.2, to 10 s at a VOR gain of 1.66. This is a novel finding which suggests that the velocity-storage mechanism was also affected by gain changes. A model is proposed in which a neural, variable-gain element is located in a positive-feedback, velocity-storage loop common to both the VOR and the OKS. Computer simulation showed that this hypothesis could account for most of the observed changes in OKN saturation and Tokan with changes in VOR gain. The model also predicts that low frequency VOR phase lead in darkness should increase with decreasing VOR gain. Experimental VOR phase lead at 0.05 Hz varied from about 10 degrees for VOR gains above 1.1 to about 50 degrees for VOR gains below 0.3. Such phase-lead data agree with the trend predicted by the model.

The effect of habituating vestibular and optokinetic nystagmus on each other

Currently, the vestibulo-ocular and optokinetic reflexes are both thought to require a velocity storage mechanism within their neural pathways. To test whether these storage mechanisms are shared by both reflexes, animals were given programs of stimulation known to change the status of the storage mechanism of one of the type of nystagmus. The other type of nystagmus was examined then to ascertain whether the characteristic of its velocity storage system had remained invariant. Horizontal eye movements of three macaque monkeys were recorded during post-rotatory nystagmus and optokinetic afternystagmus (OKAN) before and after 20 habituating exposures to either vestibular or optokinetic stimulation. Repetitive exposures to vestibular stimulation alone markedly reduced the time constant of post-rotatory nystagmus and this effect was accompanied only occasionally by a reduction in the time constant of OKAN. Repetitive exposure to optokinetic stimulation alone reliably reduced the time constant of OKAN but produced no reliable change in the time constant of post-rotatory nystagmus. These results suggest that the vestibulo-ocular and optokinetic reflexes do not share a single common velocity storage mechanism.