Eye movements induced by off-vertical axis rotation (OVAR) at small angles of tilt

Summary Off-vertical rotation (OVAR) in darkness induced continuous horizontal nystagmus in humans at small tilts of the rotation axis (5 to 30 degrees). The horizontal slow eye velocity had two components: a mean velocity in the direction opposite to head rotation and a sinusoidal modulation around the mean. Mean velocity generally did not exceed 10 deg/s, and was less than or equal to the maximum velocity of optokinetic after-nystagmus (OKAN). Both the mean and modulation components of horizontal nystagmus increased with tilt angle and rotational velocity. Vertical slow eye velocity was also modulated sinusoidally, generally around zero. The amplitude of the vertical modulation increased with tilt angle, but not with rotational velocity. In addition to modulations in eye velocity, there were also modulations in horizontal and vertical eye positions. These would partially compensate for head position changes in the yaw and pitch planes during each cycle of OVAR. Modulations in vertical eye position were regular, increased with increases in tilt angle and were separated from eye velocity by 90 deg. These results are compatible with the interpretation that, during OVAR, mean slow velocity of horizontal nystagmus is produced by the velocity storage mechanism in the vestibular system. In addition, they indicate that the otolith organs induce compensatory eye position changes with regard to gravity for tilts in the pitch, yaw and probably also the roll planes. Such compensatory changes could be utilized to study the function of the otolith organs. A functional interpretation of these results is that nystagmus attempts to stabilize the image on the retina of one point of the surrounding world. Mean horizontal velocity would then be opposite to the estimate of head rotational velocity provided by the output of the velocity storage mechanism, as charged by an otolithic input during OVAR. In spite of the lack of actual translation, an estimate of head translational velocity could, in this condition, be constructed from the otolithic signal. The modulation in horizontal eye position would then be compensatory for the perceived head translation. Modulation of vertical eye velocity would compensate for actual changes in head orientation with respect to gravity.     

Neural basis for eye velocity generation in the vestibular nuclei of alert monkeys during off-vertical axis rotation

Summary Activity of vestibular only (VO) and vestibular plus saccade (VPS) units was recorded in the rostral part of the medial vestibular nucleus and caudal part of the superior vestibular nucleus of alert rhesus monkeys. By estimating the null axes of recorded units (n = 79), the optimal plane of activation was approximately the mean plane of reciprocal semicircular canals, i.e., lateral canals, left anterior-right posterior (LARP) canals or right anterior-left posterior (RALP) canals. All units were excited by rotation in a direction that excited a corresponding ipsilateral semicircular canal. Thus, they all displayed a type I response. With the animal upright, there were rapid changes in firing rates of both VO and VPS units in response to steps of angular velocity about a vertical axis. The units were bidirectionally activated during vestibular nystagmus (VN), horizontal optokinetic nystagmus (OKN), optokinetic afternystagmus (OKAN) and off-vertical axis rotation (OVAR). The rising and falling time constants of the responses to rotation indicated that they were closely linked to velocity storage. There were differences between VPS and VO neurons in that activity of VO units followed the expected time course in response to a stimulus even during periods of drowsiness, when eye volocity was reduced. Firing rates of VPS units, on the other hand, were significantly reduced in the drowsy state. Lateral canal-related units had average firing rates that were linearly related to the bias or steady state level of horizontal eye velocity during OVAR over a range of ±60 deg/s. These units could be further divided into two classes according to whether they were modulated during OVAR. Non-modulated units (n = 5) were VO types and all modulated units (n = 5) were VPS types. There was no significant difference between the bias level sensitivities relative to eye velocity of the units with and without modulation (P>0.05). The modulated units had no sustained change in firing rate in response to static head tilts and their phases relative to head position varied from unit to unit. The phase did not appear to be linked to the modulation of horizontal eye velocity during OVAR. The sensitivities of unit activity to eye velocity were similar during all stimulus modalities despite the different gains of eye velocity vs stimulus velocity during VN, OKN and OVAR. Therefore, VO and VPS units are likely to carry an eye velocity signal related to velocity storage. For example, when unit sensitivities were related to head or surround velocity, sensitivity relative to OVAR was less than for VN or OKN. Firing rates of both vertical canal-related VO and VPS units (n= 19) were strongly modulated during OVAR, although they did not show changes in discharge rate during static head tilts relative to the spatial vertical up to a maximal 25 deg. In some cases the amplitude of the modulation increased with increases in head velocity and eye velocity. Average activity of vertical canal-related units was linearly related to steady state horizontal eye velocity in the ipsilateral direction during OVAR. The mean sensitivities of RALP units were not significantly different from those of LARP neurons (P>0.05). Together, their mean sensitivity during OVAR about a subject yaw axis was 0.34 (imp/s)/(deg/s) relative to horizontal eye velocity. This could be explained as a contribution of the vertical canals to horizontal eye velocity due to their orientation in the head. During OVAR to the ipsilateral side, the bias level of neuronal activity decreased and saturated. For steps of rotation about a vertical axis with the animal upright, the firing rates of RALP and LARP units were linearly related to stimulus velocity and eye velocity. Contralateral rotation excited the units reflecting the orientation of the semicircular canals relative to the yaw axis of rotation. RALP and LARP units also responded during horizontal optokinetic stimulation producing both OKN and OKAN. All the vertical canal units had dynamic characteristics closely related to velocity storage. Their response characteristics were consistent with the model that they contribute to horizontal slow phase velocity as part of a three-dimensional system based on a semicircular canal frame of reference. Otolith-related units (n= 5) in the vestibular nuclei showed no evidence of velocity storage and were modulated in accordance with head position during OVAR. Mean amplitude of the modulation of activity during OVAR at a 20 deg tilt and 60 deg/s rotational velocity was 24 imp/s. The data indicate that the vestibular nuclei contain the requisite signals to generate horizontal eye velocity during OVAR. VO and VPS units probably contribute to the bias or velocity storage component while otolith units mainly contribute to the oscillations in eye velocity by generating gravity dependent eye position changes during OVAR. In addition to the velocity storage component of horizontal eye velocity, the vertical VO neurons also have oscillations in their discharge patterns probably related to the vertical component of eye movements generated by the velocity storage integrator.     

Spatial orientation of the vestibular system: dependence of optokinetic after-nystagmus on gravity.

1. Monkeys received optokinetic stimulation at 60 degrees/s about their yaw (animal vertical) and pitch (animal horizontal) axes, as well as about other head-centered axes in the coronal plane. The animals were upright or tilted in right-side-down positions with regard to gravity. The stimuli induced horizontal, vertical, and oblique optokinetic nystagmus (OKN). OKN was followed by optokinetic after-nystagmus (OKAN), which was recorded in darkness. 2. When monkeys were tilted, stimulation that generated horizontal or yaw axis eye velocity during OKN induced a vertical or pitch component of slow phase velocity during OKAN. This has been designated as "cross-coupling" of OKAN. Eigenvalues and eigenvectors associated with the system generating OKAN were found as a function of tilt. They were determined by use of the Levenberg-Marquardt algorithm to minimize the mean square error between the output of a model of OKAN and the data. 3. The eigenvector associated with yaw OKAN (yaw axis eigenvector) was maintained close to the spatial vertical regardless of the angle of tilt. The eigenvector associated with pitch OKAN (pitch axis eigenvector) was always aligned with the body axis. The data indicate that velocity storage can be modeled by a piecewise linear system, the structure of which is dependent on gravity and the yaw axis eigenvector, which tends to align with gravity. 4. Yaw axis eigenvectors were also determined by giving optokinetic stimulation about head-centered axes in the coronal plane with the animal in various angles of tilt. A technique using a spectral analysis of residuals was developed to estimate whether yaw and pitch OKAN slow phase velocities decayed concurrently at the same relative rate and over the same time course. The eigenvectors determined by this method were in agreement with those obtained by analyzing OKAN elicited by yaw OKN. 5. During yaw OKN with the animal in tilted positions, the mean vector of the ensuing nystagmus was closer to the body axis than to the spatial vertical. This suggests that there is suppression of the cross-coupled pitch component during OKN. The direction of the stimulus may be utilized to suppress components of velocity storage not coincident with the direction of stimulus motion. 6. There were similarities between the monkey eigenvectors and human perception of the spatial vertical, and the mean of eigenvectors for upward and downward eye velocities overlay human 1-g perceptual data.(ABSTRACT TRUNCATED AT 400 WORDS)     

Difference between horizontal and vertical optokinetic nystagmus in cats at upright position

The slow-phase velocity (SPV) of optokinetic nystagmus (OKN) and optokinetic after nystagmus (OKAN) in response to a velocity step of surround rotation in the horizontal direction is composed of the rapid and slow components in the cat: a rapid rise, a slow rise to a steady state, a rapid fall, and a slow decline to 0 deg/s. The rapid and slow components are attributed to the direct pathway and velocity storage neuronal mechanisms, respectively. The difference between horizontal and vertical OKN has been reported in the monkey at the upright position, but the slow and rapid components have not been distinguished. The present study compared horizontal OKN-OKAN with vertical OKN-OKAN in the cat at the upright position, distinguishing the rapid and slow components. Constant velocity rotation of a random dot pattern at a velocity of 5 to 160 deg/s was used for optokinetic stimulation. The results: First, the amplitude of the rapid rise was relatively small in all SPV directions and all stimulus velocities investigated, with a slight upward-SPV preference to the downward-SPV (maximum 6.4, 6.0, and 3.4 deg/s in horizontal, upward, and downward SPV directions, respectively). Second, the steady state velocity was large during horizontal OKN (maximum 69.0 deg/s), small during upward-SPV OKN (12.9 deg/s), and missing (SPV is negligibly small and irregular) during downward-SPV OKN, indicating a large directional difference of OKN. Third, the acceleration of the slow rise decreased with the stimulus velocity at higher stimulus velocities >20 deg/s during both horizontal and upward-SPV OKN, suggesting strong nonlinearity in the velocity charge system. Fourth, the decay time course of the OKAN was described by the time constant of the exponential function, and the time constant was longer during horizontal (mean, 8.3 s at a stimulus velocity of 20 deg/s) than during upward-SPV (5.4 s) OKAN, suggesting that the velocity discharge system is relatively linear compared with the velocity charge system. It is concluded that horizontal OKN-OKAN is much larger than vertical OKN-OKAN in the cat at the upright position, and this directional difference is caused mainly by the directional difference in the velocity storage mechanism, but not in the direct pathway mechanism.     

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 相似文献   

Otolith-semicircular canal interaction during postrotatory nystagmus in humans

The otolith-semicircular canal interaction during postrotatory nystagmus was studied in ten normal human subjects by applying fast, short-lasting, passive head and body tilts (15, 30, 45, or 90° in the roll or pitch plane) 2 s after sudden stop from a constant-velocity rotation (100°/s) about the earth-vertical axis in yaw. Eye movements were measured with three-dimensional magnetic search coils. Following the head tilt, activity in the semicircular canal primary afferents continues to reflect the postrotatory angular velocity vector in head-centered coordinates, whereas otolith primary afferents signal a different orientation of the head relative to gravity. Despite the change in head orientation relative to gravity, postrotatory eye velocity decayed closely along the axis of semicircular canal stimulation (horizontal in head coordinates) for large head tilts (90°) and also for small head tilts (15–45°) for reorientations in the pitch plane. Only for small head tilts (15–45°) in the roll plane was there a reorientation of the eye rotation axis toward the gravitational vector. This reorientation was approximately compensatory for 15° head tilts. For 30° and 45° head tilts the eye rotation axis tilted toward the gravitational vector by about the same amount as for 15° head tilts. These results suggest that, with the exception of small head tilts in the roll plane, there was no compelling data showing a relationship between the eye rotation axis and head tilt and that postrotatory nystagmus is largely organized in head-centered rather than gravity-centered coordinates in humans. This indicates a rudimentary, nonlinear, and direction-specific interaction of semicircular canal and otolith signals in the central vestibular system in humans.     

Spatial orientation of optokinetic nystagmus and ocular pursuit during orbital space flight

On Earth, eye velocity of horizontal optokinetic nystagmus (OKN) orients to gravito-inertial acceleration (GIA), the sum of linear accelerations acting on the head and body. We determined whether adaptation to microgravity altered this orientation and whether ocular pursuit exhibited similar properties. Eye movements of four astronauts were recorded with three-dimensional video-oculography. Optokinetic stimuli were stripes moving horizontally, vertically, and obliquely at 30°/s. Ocular pursuit was produced by a spot moving horizontally or vertically at 20°/s. Subjects were either stationary or were centrifuged during OKN with 1 or 0.5 g of interaural or dorsoventral centripetal linear acceleration. Average eye position during OKN (the beating field) moved into the quick-phase direction by 10° during lateral and upward field movement in all conditions. The beating field did not shift up during downward OKN on Earth, but there was a strong upward movement of the beating field (9°) during downward OKN in the absence of gravity; this likely represents an adaptation to the lack of a vertical 1-g bias in-flight. The horizontal OKN velocity axis tilted 9° in the roll plane toward the GIA during interaural centrifugation, both on Earth and in space. During oblique OKN, the velocity vector tilted towards the GIA in the roll plane when there was a disparity between the direction of stripe motion and the GIA, but not when the two were aligned. In contrast, dorsoventral acceleration tilted the horizontal OKN velocity vector 6° in pitch away from the GIA. Roll tilts of the horizontal OKN velocity vector toward the GIA during interaural centrifugation are consistent with the orientation properties of velocity storage, but pitch tilts away from the GIA when centrifuged while supine are not. We speculate that visual suppression during OKN may have caused the velocity vector to tilt away from the GIA during dorsoventral centrifugation. Vertical OKN and ocular pursuit did not exhibit orientation toward the GIA in any condition. Static full-body roll tilts and centrifugation generating an equivalent interaural acceleration produced the same tilts in the horizontal OKN velocity before and after flight. Thus, the magnitude of tilt in OKN velocity was dependent on the magnitude of interaural linear acceleration, rather than the tilt of the GIA with regard to the head. These results favor a filter model of spatial orientation in which orienting eye movements are proportional to the magnitude of low frequency interaural linear acceleration, rather than models that postulate an internal representation of gravity as the basis for spatial orientation.Abbreviations A_g Acceleration of gravity - A_c Centripetal acceleration - CCW Counterclockwise - CW Clockwise - FD- X Flight day X - g Gravity - GIA Gravito-inertial acceleration - H Horizontal - LED Left-ear-down - LEO Left-ear-out - LOB Lying-on-back - L- X Launch minus X days - NCM No-chair-motion - ND Nose-down - NU Nose-up - OCR Ocular counter-colling - OKAN Optokinetic after-nystagmus - OKN Optokinetic nystagmus - OKS Optokinetic stimulus - pos Position - REO Right-ear-out - R+ X Recovery plus X days - T Torsional - V Vertical - vel Velocity     

Compensatory and orienting eye movements induced by off-vertical axis rotation (OVAR) in monkeys

Nystagmus induced by off-vertical axis rotation (OVAR) about a head yaw axis is composed of a yaw bias velocity and modulations in eye position and velocity as the head changes orientation relative to gravity. The bias velocity is dependent on the tilt of the rotational axis relative to gravity and angular head velocity. For axis tilts <15 degrees, bias velocities increased monotonically with increases in the magnitude of the projected gravity vector onto the horizontal plane of the head. For tilts of 15-90 degrees, bias velocity was independent of tilt angle, increasing linearly as a function of head velocity with gains of 0.7-0.8, up to the saturation level of velocity storage. Asymmetries in OVAR bias velocity and asymmetries in the dominant time constant of the angular vestibuloocular reflex (aVOR) covaried and both were reduced by administration of baclofen, a GABA(B) agonist. Modulations in pitch and roll eye positions were in phase with nose-down and side-down head positions, respectively. Changes in roll eye position were produced mainly by slow movements, whereas vertical eye position changes were characterized by slow eye movements and saccades. Oscillations in vertical and roll eye velocities led their respective position changes by approximately 90 degrees, close to an ideal differentiation, suggesting that these modulations were due to activation of the orienting component of the linear vestibuloocular reflex (lVOR). The beating field of the horizontal nystagmus shifted the eyes 6.3 degrees /g toward gravity in side down position, similar to the deviations observed during static roll tilt (7.0 degrees /g). This demonstrates that the eyes also orient to gravity in yaw. Phases of horizontal eye velocity clustered ~180 degrees relative to the modulation in beating field and were not simply differentiations of changes in eye position. Contributions of orientating and compensatory components of the lVOR to the modulation of eye position and velocity were modeled using three components: a novel direct otolith-oculomotor orientation, orientation-based velocity modulation, and changes in velocity storage time constants with head position re gravity. Time constants were obtained from optokinetic after-nystagmus, a direct representation of velocity storage. When the orienting lVOR was combined with models of the compensatory lVOR and velocity estimator from sequential otolith activation to generate the bias component, the model accurately predicted eye position and velocity in three dimensions. These data support the postulates that OVAR generates compensatory eye velocity through activation of velocity storage and that oscillatory components arise predominantly through lVOR orientation mechanisms.     

Role of irregular otolith afferents in the steady-state nystagmus during off-vertical axis rotation.

1. During constant velocity off-vertical axis rotations (OVAR) in the dark a compensatory ocular nystagmus is present throughout rotation despite the lack of a maintained signal from the semicircular canals. Lesion experiments and canal plugging have attributed the steady-state ocular nystagmus during OVAR to inputs from the otolith organs and have demonstrated that it depends on an intact velocity storage mechanism. 2. To test whether irregularly discharging otolith afferents play a crucial role in the generation of the steady-state eye nystagmus during OVAR, we have used anodal (inhibitory) currents bilaterally to selectively and reversibly block irregular vestibular afferent discharge. During delivery of DC anodal currents (100 microA) bilaterally to both ears, the slow phase eye velocity of the steady-state nystagmus during OVAR was reduced or completely abolished. The disruption of the steady-state nystagmus was transient and lasted only during the period of galvanic stimulation. 3. To distinguish a possible effect of ablation of the background discharge rates of irregular vestibular afferents on the velocity storage mechanism from specific contributions of the dynamic responses from irregular otolith afferents to the circuit responsible for the generation of the steady-state nystagmus, bilateral DC anodal galvanic stimulation was applied during optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN). No change in OKN and OKAN was observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Velocity storage in the vestibulo-ocular reflex arc (VOR)

Summary Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 °/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 °/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression).These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.     

Stimulation of the nodulus and uvula discharges velocity storage in the vestibulo-ocular reflex

The nodulus and sublobule d of the uvula of rhesus and cynomolgus monkeys were electrically stimulated with short trains of pulses to study changes in horizontal slow-phase eye velocity. Nodulus and uvula stimulation produced a rapid decline in horizontal slow phase velocity, one aspect of the spatial reorientation of the axis of eye rotation that occurs when the head is tilted with regard to gravity during per- and post-rotatory nystagmus and optokinetic after-nystagmus (OKAN). Nodulus and uvula stimulation also reproduced the reduction of the horizontal time constant of post-rotatory nystagmus and OKAN that occurs during visual suppression. The brief electric stimuli (4–5 s) induced little slow-phase velocity and had no effect on the initial jump in eye velocity at the onset or the end of angular rotation. Effects of stimulation were unilateral, suggesting specificity of the output pathways. Activation of more caudal sites in the uvula produced nystagmus with a rapid rise in eye velocity, but the effects did not outlast the stimulus and did not affect VOR or OKAN time constants. Thus, stimulation of caudal parts of the uvula did not affect eye velocity produced by velocity storage. We postulate that the nodulus and sublobule d of the uvula control the time constant of the yaw axis (horizontal) component of slow-phase eye velocity produced by velocity storage.     

Evaluation of the vestibulo-ocular reflex using sinusoidal off-vertical axis rotation in patients with acoustic neurinoma

The vestibulo-ocular reflex (VOR) was studied to examine the utility of off-vertical axis rotation (OVAR) in the diagnosis of acoustic neurinoma. Subjects were sinusoidally rotated with eyes open in complete darkness at frequencies of 0.4 and 0.8 Hz with a maximum angular velocity of 60°/s at either earth-vertical axis rotation (EVAR) or OVAR. Thirteen patients with acoustic neurinomas were investigated. Results showed that VOR gain during OVAR at 0.8 Hz and in a 30° nose-up position in patients with internal auditory canal tumors was significantly less than the gain measured during EVAR. The VOR gain measured from all patients (including those with tumors extending to the cerebellopontine angle) was not significantly different when the patients were subjected to EVAR and OVAR. These observations were possibly due to superior vestibular nerve dysfunction. We concluded that certain stimulating parameters—patient's nose tilted up 30°; sinusoidal OVAR at 0.8 Hz and 60°/s maximum angular head velocity—were useful for evaluating vestibular function in patients suffering from an acoustic neurinoma located within the internal auditory canal.     

Recovery of otolith function in patients with benign paroxysmal positional vertigo evaluated by sinusoidal off-vertical axis rotation

The vestibulo-ocular reflex (VOR) was studied via sinusoidal off-vertical axis rotation (OVAR) to evaluate otolith function in patients with benign paroxysmal positional vertigo (BPPV). Subjects were sinusoidally rotated with eyes open in complete darkness at frequencies of 0.4 and 0.8 Hz with a maximum angular velocity of 60 degrees /s in earth vertical axis rotation (EVAR) and OVAR. Ten patients with BPPV patients were investigated. We performed OVAR tests for all patients for the following different points and compared otolith function: (1) The point at which patients had typical nystagmus; we call this state 'Before', that is, before recovery. (2) The point when their nystagmus disappeared; we call this state 'After' that is, after nystagmus disappear. Results showed that VOR gain during OVAR at 0.8 Hz in a 30 degrees nose-up position in BPPV patients was significantly less than the gain during EVAR at the point Before. On the other hand, gain was not significantly different between EVAR and OVAR at the point After. VOR gain itself at 0.8 Hz nose-up OVAR showed a significant increase at the point After compared to Before. This increase of VOR gain might be caused by the recovery of the otolith function in patients with BPPV.     

Role of the flocculus and paraflocculus in optokinetic nystagmus and visual-vestibular interactions: Effects of lesions

Optokinetic nystagmus (OKN), optokinetic after-nystagmus (OKAN), vestibular nystagmus and visual-vestibular interactions were studied in monkeys after surgical ablation of the flocculus and paraflocculus. After bilateral flocculectomy the initial rapid rise in slow phase eye velocity of horizontal and vertical OKN was severely attenuated, and maximum velocities fell to the preoperative saturation level of OKAN. There is generally little or no upward OKAN in the normal monkey, and upward OKN was lost after bilateral lesions. Unilateral flocculectomy affected the rapid rise in horizontal velocity to both sides. Consistent with the absence of a rapid response to steps of surround velocity, animals were unable to follow acceleration of the visual field with eye accelerations faster than about 3-5 degrees/s2. The slow rise in OKN slow phase velocity to a steady state level was prolonged after operation. However, rates of rise were approximately equal for the same initial retinal slips before and after operation. The similarity in the time course of OKN when adjusted for initial retinal slip, and in the gain, saturation level and time course of OKAN before and after flocculectomy indicates that the lesions had not significantly altered the coupling of the visual system to the velocity storage integrator or its associated time constant. When animals were rotated in a subject-stationary visual surround after flocculectomy, they could not suppress the initial jump in eye velocity at the onset of the step. Despite this, they could readily suppress the subsequent nystagmus. The time constant of decline in the conflict situations was almost as short as in the normal monkey and was in the range of the peripheral vestibular time constant. This suggests that although the animals were unable to suppress rapid changes in eye velocity due to activation of direct vestibulo-oculomotor pathways, they had retained their ability to discharge activity from the velocity storage mechanism. Consistent with this, animals had no difficulty in suppressing OKAN after flocculectomy. Visual-vestibular interactions utilizing the velocity storage mechanism were normal after flocculectomy, as was nystagmus induced by rotation about a vertical axis or about axes tilted from the vertical. Also unaffected were the discharge of nystagmus caused by tilting the head out of the plane of the response and visual suppression of nystagmus induced by off-vertical axis rotation. The flocculus does not appear to play an important role in mediating these responses. The data before and after flocculectomy were simulated by a model which is homeomorphic to that presented previously.(ABSTRACT TRUNCATED AT 400 WORDS)     

Motion sickness induced by off-vertical axis rotation (OVAR)

We tested the hypothesis that motion sickness is produced by an integration of the disparity between eye velocity and the yaw-axis orientation vector of velocity storage. Disparity was defined as the magnitude of the cross product between these two vectors. OVAR, which is known to produce motion sickness, generates horizontal eye velocity with a bias level related to velocity storage, as well as cyclic modulations due to re-orientation of the head re gravity. On average, the orientation vector is close to the spatial vertical. Thus, disparity can be related to the bias and tilt angle. Motion sickness sensitivity was defined as a ratio of maximum motion sickness score to the number of revolutions, allowing disparity and motion sickness sensitivity to be correlated. Nine subjects were rotated around axes tilted 10°–30° from the spatial vertical at 30°/s–120°/s. Motion sickness sensitivity increased monotonically with increases in the disparity due to changes in rotational velocity and tilt angle. Maximal motion sickness sensitivity and bias (6.8°/s) occurred when rotating at 60°/s about an axis tilted 30°. Modulations in eye velocity during OVAR were unrelated to motion sickness sensitivity. The data were predicted by a model incorporating an estimate of head velocity from otolith activation, which activated velocity storage, followed by an orientation disparity comparator that activated a motion sickness integrator. These results suggest that the sensory-motor conflict that produces motion sickness involves coding of the spatial vertical by the otolith organs and body tilt receptors and processing of eye velocity through velocity storage.     

Static roll and the vestibulo-ocular reflex (VOR)

Summary We measured the effect of static lateral tilt (roll) on the gain and time constant of the vestibulo-ocular reflex (VOR) in five normal subjects by recording both the horizontal and vertical components of eye velocity in space for rotation about an earth vertical axis with the head either upright or rolled to either side. The time constant of the VOR in the upright position was 19.6 ±3.2s (mean ± standard deviation). The time constant of the horizontal component with respect to the head decreased to 15.7±4.0s for 30° roll and to 12.7±2.7s for 60° roll. The time constant of the vertical component with respect to the head was 11.0±1.4 s for 30° roll and 7.5±1.6 s for 60° roll. The gain of the horizontal VOR with respect to space did not vary significantly with roll angle but a small space-vertical component to the VOR appeared during all rotations when the head was rolled away from upright. This non-compensatory nystagmus built up to a maximum of 2–3°/s at 17.0±4.7s after the onset of rotation and then decayed. These data suggest that static otolith input modulates the central storage of semicircular canal signals, and that head-horizontal and head-vertical components of the VOR can decay at different rates.     

Optokinetic nystagmus and afternystagmus in human beings: relationship to nonlinear processing of information about retinal slip

Summary In four normal human subjects we measured eye movements during full-field optokinetic stimulation (10–220 deg/s) and determined the relationship among retinal-slip velocity (drum velocity minus slow-phase eye velocity), the slow-phase velocity of optokinetic nystagmus (OKN) and the initial value of the slow-phase velocity of optokinetic afternystagmus (OKAN) measured in darkness. OKN and OKAN were maximum (63–84 and 11–19 deg/s, respectively) when retinal slip ranged from 30–100 deg/s. For higher values of retinal slip, OKN and OKAN fell (in 3 subjects) or reached a plateau (in the fourth). The amplitude of OKAN in human beings was much less than that reported in monkeys. The shape, however, of the curve relating retinal slip to the amplitude of OKAN was similar to that of monkeys. Furthermore, in both cases the curve resembles that obtained by plotting the results of experimental recordings of neural discharge in the nucleus of the optic tract as a function of retinal slip. These results imply that the processing of visual information for generation of OKAN is similar in monkeys and human beings but that the gain of the system is much less in human beings. We also found that fixation of a small target during optokinetic stimulation nearly completely prevented the development of OKAN while fixation of a small target for short periods after optokinetic stimulation did not alter the pattern of decay of OKAN. Thus, fixation may actively prevent the coupling of visual information into the velocity-storage mechanism.     

Effects of midline medullary lesions on velocity storage and the vestibulo-ocular reflex

Summary 1. Crossing fibers were sectioned at the midline of the medulla caudal to the abducens nucleus in four cynomolgus monkeys. In two animals the lesions caused the time constant of horizontal and vertical per- and post-rotatory nystagmus to fall to 5–8 s. The slow rise in optokinetic nystagmus (OKN), as well as optokinetic after-nystagmus (OKAN) and cross-coupling of horizontal to vertical OKN and OKAN were abolished. Steady state velocities could not be maintained during off-vertical axis rotation (OVAR). Pitch and yaw nystagmus were affected similarly. We conclude that the ability to store activity related to slow phase eye velocity, i.e., velocity storage, was lost in these monkeys for nystagmus about any axis. Velocity storage was partially affected by a small midline lesion in the same region in a third animal. There was no effect of a more superficial midline section in a fourth monkey, and it served as a control. 2. The gain (eye velocity/head velocity) of the vestibuloocular reflex (VOR) was unaffected by the midline lesions. Saccades were normal, as was the ability to hold the eyes in eccentric gaze positions. The gain of the fast component of OKN increased in one monkey to compensate for the loss of the slow component. 3. One animal was tested for its ability to adapt the gain of the VOR due to visual-vestibular mismatch after lesion. Average changes in gain in response to wearing magnifying (2.2 x) and reducing (0.5 x) lenses, were + 35% and — 30%, respectively. This is within the range of normal monkeys. Thus, a midline lesion that abolished velocity storage did not alter that animal's ability to adapt the gain of the VOR. 4. Lesions that reduced or abolished velocity storage interrupted crossing fibers in the rostral medulla, caudal to the abducens nuclei. Cells that contributed axons to this portion of the crossing fibers are most likely located in central portions of the medial vestibular nucleus (MVN) and/or in rostral portion of the descending vestibular nucleus (DVN). The implication is that velocity storage arises from neurons in MVN and DVN whose axons cross the midline.Supported by NS-00294, SFB 220-D8 and Core Center Grant EY-01867     

Orientation of human optokinetic nystagmus to gravity: a model-based approach

Optokinetic nystagmus (OKN) was induced by having subjects watch a moving display in a binocular, head-fixed apparatus. The display was composed of 3.3° stripes moving at 35°/s for 45 s. It subtended 88° horizontally by 72° vertically of the central visual field and could be oriented to rotate about axes that were upright or tilted 45° or 90°. The head was held upright or was tilted 45° left or right on the body during stimulation. Head-horizontal (yaw axis) and head-vertical (pitch axis) components of OKN were recorded with electro-oculography (EOG). Slow phase velocity vectors were determined and compared with the axis of stimulation and the spatial vertical (gravity axis). With the head upright, the axis of eye rotation during yaw axis OKN was coincident with the stimulus axis and the spatial vertical. With the head tilted, a significant vertical component of eye velocity appeared during yaw axis stimulation. As a result the axis of eye rotation shifted from the stimulus axis toward the spatial vertical. Vertical components developed within 1–2 s of stimulus onset and persisted until the end of stimulation. In the six subjects there was a mean shift of the axis of eye rotation during yaw axis stimulation of 18° with the head tilted 45° on the body. Oblique optokinetic stimulation with the head upright was associated with a mean shift of the axis of eye rotation toward the spatial vertical of 9.2°. When the head was tilted and the same oblique stimulation was given, the axis of eye rotation rotated to the other side of the spatial vertical by 5.4°. This counterrotation of the axis of eye rotation is similar to the Müller (E) effect, in which the perception of the upright is counterrotated to the opposite side of the spatial vertical when subjects are tilted in darkness. The data were simulated by a model of OKN with a direct and indirect pathway. It was assumed that the direct visual pathway is oriented in a body, not a spatial frame of reference. Despite the short optokinetic after-nystagmus time constants, strong horizontal to vertical cross-coupling could be produced if the horizontal and vertical time constants were in proper ratio and there were no suppression of nystagmus in directions orthogonal to the stimulus direction. The model demonstrates that the spatial orientation of OKN can be achieved by restructuring the system matrix of velocity storage. We conclude that an important function of velocity storage is to orient slow-phase velocity toward the spatial vertical during movement in a terrestrial environment.     

The horizontal optokinetic nystagmus in the cat

Summary 1)Horizontal optokinetic eye nystagmus (OKN) and afternystagmus (OKAN) were recorded in the alert cat (head restrained) in response to velocity steps and sinusoidal optokinetic stimuli. 2)A strong dependency of OKN performance on stimulus pattern was found: responses were most regular and gain was high over a large range of stimulus velocities when the stimulus consisted of a high-contrast random dot pattern. 3) Following velocity steps, OKN showed a small amplitude fast rise in slow phase velocity (SPV) which was followed by a slow build-up to steady state. The amplitude of the initial jump in SPV increased with stimulus amplitude up to 30°/s and saturated afterwards. The plateau level of initial SPV ranged from 5 to 15°/s. 4) The slow build-up of SPV showed non-linearities, i.e. the time to steady state increased with stimulus amplitude and the slow rise of SPV was irregular. In most animals steady state SPV showed no signs of response saturation for step amplitudes up to 60–80°/s or more. The open-loop gain (steady state SPV/ retinal slip velocity) dependend on retinal slip velocity and decreased from 46 at 0.5°/s to 0.4 at about 60°/s. 5) OKAN I and II were consistently observed and occasionally OKAN III was noted. OKAN I durations (mean 13.8 +- 5.1 s) and OKAN II amplitudes were independent of stimulus magnitude. Initial SPV of OKAN I was typically the same as that of OKN, i.e. no fast fall was observed. Cessation of pattern rotation in light, however, produced a fast initial decay of SPV. 6) A least square fitting of OKAN time course was performed with various time functions. The SPV of OKAN I and II was best fitted with a damped sine wave, indicating that cat optokinetic system behaves like a second order underdamped system. 7) Sinusoidal stimuli produced strong response non-linearities. At a given frequency gain decreased with increasing stimulus amplitudes. Gain correlated best with stimulus acceleration. In addition, strong stimuli produced characteristic response distortions. 8) In the visual-vestibular conflict situation vectorial summation of VOR and OKN was observed only with small stimuli.Supported by grants nos. 3.505.79 and 3.403.83 from the Swiss National Science Foundation and Dr. Erik Slack-Gyr Foundation