Slow Phase Eye Velocity Research Articles

Optokinetic and pursuit system: A case report

Several studies have demonstrated the importance of the pretectal Nucleus of the Optic Tract (NOT) and the Dorsal Terminal Nucleus of the accessory optic system (DTN) for the generation of horizontal optokinetic nystagmus (OKN). Although single unit data from trained rhesus monkey NOT/DTN cells are available it is still unclear if there is a link between the pursuit and the optokinetic system at this level of motion analysis. In order to address the question whether the NOT/DTN is important for the optokinetic as well as the pursuit system an electrolytic lesion was placed where NOT/DTN activity was recorded previously. The monkey was tested on optokinetic and pursuit paradigms. Immediately following the lesion the monkey performed a spontaneous nystagmus with slow phases directed away from the lesioned side. This spontaneous nystagmus persisted even during optokinetic stimulation in the opposite direction. During the first week postlesion the spontaneous nystagmus disappeared and the monkey regained the ability to perform optokinetic nystagmus toward the lesioned side. The gain of the mean slow phase eye velocity was, however, largely reduced for this stimulus direction. The onset of OKN following the onset of optokinetic stimulation was not affected by the lesion. During smooth pursuit the mean eye velocity was more reduced for pursuit towards the lesioned side. The resulting position error was compensated by an increase in the number of catch-up saccades. In addition to the confirmation of the well-known directional deficits of the optokinetic system caused by a lesion of the pretectum, a directional deficit in the pursuit system was demonstrated.

Otolith responses in man during parabolic flight.

The influence of the varying gravito-inertial (Gz) force during parabolic flight on human otolith function was investigated experimentally. It was hypothesised that a varying Gz force profile initiates an otolith-ocular response that manifests itself in modulation of optokinetic nystagmus slow-phase eye velocity (OKN-SPV). Six subjects were seated in the ESA-Caravelle, facing perpendicular to the aircraft's longitudinal axis. The Gz profile was subsequently 1.8 Gz pull-up, 0 Gz microgravity, and 1.8 Gz recovery, each phase lasting about 20 s. Vertical eye movements were recorded with electro-nystagmography throughout the parabolic manoeuvre. Conditions were: (1) visual fixation, (2) darkness and (3) optokinetic stimulation of 50 deg/s in an upward or downward direction, projected on a cylindrical screen at 0.6 m viewing distance. No consistent nystagmus or gaze shift was measured in darkness. With optokinetic stimulation, however, ANOVA revealed downward enhancement of OKNSPV by 5 degrees/s in 1.8 Gz hypergravity, as compared with the 0 Gz condition and the 1 Gz condition. It is concluded that an otolith-ocular pathway modulates optokinetic eye movements in parabolic flight.

Effects of toluene, styrene, trichloroethylene, and trichloroethane on the vestibulo- and opto-oculo motor system in rats

The acute effects of inhalation of four solvents on the central vestibular system of rats were analyzed by recording eye movements upon different stimuli. The dose-response relationship was investigated. Optokinetic stimulation was obtained by placing the animals in front of a surrounding visual pattern, moving at different velocities. The slow-phase eye velocity (SPV) of nystagmus was calculated and divided by the stimulus velocity, giving the gain. All the solvents caused a decrease of the gain. Vestibular stimulation was performed on a turntable by an angular acceleration/deceleration in darkness. The SPV and the duration of the post-stimulatory nystagmus were calculated. The shape of the SPV dose-response curves differed among the four solvents. Toluene, styrene, and trichloroethylene prolonged the duration of nystagmus while trichloroethane did not. A conflicting vestibular and optokinetic stimulation was performed by an angular acceleration/deceleration with a surrounding visual pattern moving with the turntable. All solvents decreased the ability to cancel nystagmus, elicited by vestibular stimulation in conflict with a visual input. Quick movements of the eyes, saccades, were elicited by tactile stimulation. Toluene, styrene, and trichloroethylene changed the generation of the saccades while trichloroethane did not. Most of the findings indicate a common site of action in the central vestibular system, viz., the cerebellar-vestibular circuit. However, within this domain, there are evident differences in the effects among the solvents. This finding, together with previous results obtained in other experimental models of the central nervous system (CNS), suggest that different solvents should be considered as individual compounds. While the current results are consistent with the notion that solvents affect cerebellar-vestibular function, they also demonstrate differences on selected components of this system which may be of concern.

Angular velocity detection by head movements orthogonal to the plane of rotation.

Sinusoidal oscillation of rhesus monkeys about a head-fixed, earth-horizontal axis while rotating at constant velocity about an earth-vertical axis generates a characteristic ocular nystagmus where the three-dimensional slow phase eye velocity is compensatory to the spatially and temporally changing head angular velocity vector. This includes the generation of a unidirectional nystagmus characterised by a "bias" slow phase velocity component, albeit of small gain (0.2-0.7), that persists for the duration of the combined two-axes stimulation and is compensatory to the constant velocity earth-vertical axis rotation. Specifically, there is a torsional bias velocity in supine position, a vertical bias velocity in ear down position and a horizontal bias velocity in upright position. Since the semicircular canals can not sense prolonged constant velocity rotation, the ocular bias velocity must be centrally constructed from canal afferent signals using head position information. Thus, optimal performance of the vestibular system as a three-dimensional rate sensor relies on afferent information from both the semicircular canals and the otolith organs.

OKN and OKAN induced by stripe and random dot patterns

The velocity storage mechanism in optokinetic nystagmus (OKN) was studied in 50 healthy adults. We used stepwise stimulations generated by projecting stripe and numerous random dot patterns on a screen at 20, 40, 60 and 80 deg/sec. The slow-phase OKN velocity followed stripe and random dot patterns almost immediately after the onset of the stimuli at 20 deg/sec. On the other hand, it tended to gradually increase after the onset of stimuli at 60 or 80 deg/sec. This gradual increase in slow-phase eye velocity has also been observed in several animal species, such as the monkey and cat. The slow-phase velocity of the first OKAN beat was higher with the random dot pattern than with the stripe pattern regardless of stimulation velocity. The above findings indicate that OKN in man is mediated through direct and also indirect pathways as observed in animals. With random dot pattern stimulation, particularly, the indirect pathway seems to perform an important role in generating OKN and OKAN.

Ｖｅｌｏｃｉｔｙ Ｓｔｏｒａｇｅの中枢メカニズムについて

The oculomotor system uses both vestibular and visual information to stabilize images on the retina. Together, they maintain the angle of gaze when either the individual or the visual surroundings are moving. By modelling consistent with experimental data, it has been suggested that several mathematical integrations are necessary to produce the adequate gaze signal in the CNS. The velocity storage integrator holds or stores activity related to slow phase eye velocity, which is utilized in generating OKN and OKAN, and it is also responsible for producing the dominant time constant of vestibular nystagmus. Recent studies have shown that the velocity storage system has a three-dimensional structure dependent on gravity (cross-coupling).The neural circuits, however, underlying the velocity storage are still unknown. Recently, we recorded single units in the vestibular nuclei (VN) and the nucleus prepositus hypoglossi (PPH) and stimulated these sites electrically to determine the location of the neural structures associated with the various integrators. Our data suggest that there are two different integrators in the rostral medulla. One is the velocity storage integrator, which appears to lie in the VN. The other is the velocity-to-position integrator, probably closely associated with the PPH.

垂直半規管刺激性回転検査 正常耳での回転後眼振の観察

We developed a new type of rotatory chair system to examine vertical semicircular canal-stimulative postrotatory nystagmus in normal ears. The subjects sat on the rotatory chair with their heads and backs tilting backward 60 from the vertical line, and their heads at 30°, 45°, or 60°to the plane of rotation. The rotation was performed with an initial acceleration of 10°/sec 2 for 10 sec and a terminal acceleration of 100° or 180°/sec 2 following a period of constant velocity for 20 sec in each position with either clockwise or counter-clockwise rotation. In this position, we were able to examine isolated excitatory single canals for all four of the vertical semicircular canals. The postrotatory nystagmus was analyzed with an infrared video recording system. There were no remarkable differences in the maximum slow phase eye velocity and the duration of postrotatory nystagmus between terminal acceleration of 100°/sec 2 and that of 180°/sec 2. Moreover, there were no obvious differences in the balance of nystagmic reactions, after stimulative rotation for the anterior or posterior semicircular canal, between the left and the right sides.However, the degree of postrotatory nystagmic reaction in each posterior semicircular canal was usually much more than that in each anterior semicircular canal in most normal subjects.

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)

Characteristics of Nystagmus Evoked by Electrical Stimulation of The Uvular/Nodular Lobules of the Cerebellum in Monkey

Electrical stimulation in the monkey vestibulocerebellum has previously been shown to produce ocular nystagmus, but large stimulating current values were used. Using long duration (< or = 10-second) stimulus pulse trains and low current values (< 50 microA), we studied the nystagmus evoked by microstimulation in the uvular/nodular regions of the cerebellum. In doing this, we found quantitative differences in the nystagmus evoked from these two regions. Stimulation of the nodulus typically produced a vigorous nystagmus with a contralateral slow phase and a prolonged afternystagmus in the same direction. In contrast, stimulation of the uvula typically produced a regular ipsilateral nystagmus pattern with a very short, if any, afternystagmus in the same direction. In addition, at some stimulation sites in the uvula we observed an adaptation in the slow phase eye velocity during the time that the stimulation remained on. This effect could result in a secondary nystagmus, with a slow phase velocity direction opposite to that first evoked by the stimulation, followed by a prolonged afternystagmus in the direction of the secondary nystagmus at stimulus offset. The nystagmus evoked by these cerebellar stimulations differs from both natural nystagmus produced by large field visual motion and from the nystagmus produced by electrical stimulation of the nucleus of the optic tract. The nystagmus produced by uvular and nodular stimulation shows a shorter latency and a more rapid slow phase eye velocity buildup. The uvula stimulations also showed a much shorter afternystagmus. Also, the same nystagmus was evoked whether the animal was in a lighted or dark surround. These characteristics and recent single-unit recording studies in the uvula seem to suggest that the uvula acts not as a direct input to the velocity storage mechanism, but instead perhaps as part of an internal regulator for balance between the bilateral vestibular nuclei which are normally part of the nystagmus response. On the other hand, the nodulus, with its prolonged afternystagmus in the same direction as the evoked nystagmus, may be involved as a part of the velocity storage mechanism.

Uvula-nodulus and gravity direction (a study on vertical optokinetic-oculomotor functions)

Some characteristics of vertical optokinetic nystagmus and after-nystagmus, in particular, its up/down gain asymmetry, are known to be influenced by gravity direction, which is basically perceived by otolith organs. However, how such an information of gravity direction is processed within the central nervous system is not well understood, even though the role of cerebellar uvula and nodulus in vertical eye movements has been identified for some time. Accordingly, in this study, vertical optokinetic nystagmus and after-nystagmus were studied in squirrel monkeys both in the upright and side-lateral positions (different gravity direction to the head), before and after uvulonodulectomy. When the optokinetic stimulus was given, the slow phase eye velocity of optokinetic nystagmus was significantly higher in the side-lateral position than that obtained in the upright position. This difference disappeared after uvulonodulectomy. When the initial slow phase eye velocity of optokinetic after-nystagmus was compared, the one obtained in the side-lateral position was significantly higher than that acquired in the upright position. This difference also disappeared after the uvulonodular ablation. Thus, in this study of vertical optokinetic nystagmus and after-nystagmus, the role of uvula and nodulus in relaying the information of gravity direction was confirmed.

Visual suppression of torsional vestibular nystagmus in rhesus monkeys

Juvenile rhesus monkeys, placed on a motorized turntable, were rotated at constant velocity and then decelerated about an Earth-vertical axis. The animals were implanted with dual search coils to measure eye movements in three dimensions. By changing the monkey's body position (upright, ear-down, supine), postrotatory nystagmus was elicited in the horizontal, vertical, or torsional direction. Peak slow phase eye velocity and time constant of velocity decay were compared between decelerations in the dark and in the light. In all nystagmus directions, illumination reduced the time constant ( T c) to values around 5 sec. Peak velocity ( V p) was markedly attenuated in the horizontal and vertical directions (around 50%), but the effect of light on V p in the torsional direction was small (< 20%). These findings were independent of the velocity step size. Our hypothesis is that the two dynamic components of optokinetic nystagmus, as they interact with postrotatory nystagmus during visual suppression, differ in their dimensionality: the early component (fast component, direct pathway, pursuit system) is mainly activated in the horizontal and vertical directions, while the late component (slow component, indirect pathway, optokinetic system) effectively operates in all three dimensions.

A "beat-to-beat" interval generator for optokinetic nystagmus.

An analysis of optokinetic responses was used to derive an iterative model that reproduces the duration of nystagmus slow phases and eye position control during optokinetic nystagmus. Optokinetic nystagmus was recorded with magnetic search coils from red-eared turtles (Pseudemys scripta elegans) during monocular, random dot pattern stimulation at constant velocities ranging from 0.25-63 degrees/s. The beat-to-beat behavior of slow phase durations was consistent with the existence of an underlying neural clock, termed the basic interval generator, that is based on an integrate-to-fire neuron model. This hypothetical basic interval generator produces an interval that is the product of the duration of the previous interval and a mean 1 truncated normal variate with variance sigma 2. Data analyses indicated that the initial value of the interval generator during a period of nystagmus, termed tau 0, is proportional to the inverse square root of slow phase eye velocity. Further, if the eye was deviated in the slow phase direction (re mean eye position) when the slow phase began, the slow phase duration was consistent with a single cycle of the basic interval generator. However, if the eye was deviated in the fast phase direction, the distribution of the durations of the ensuing slow phases indicated that a proportion of the slow phases were produced by more than one cycle of the basic interval generator. This phenomenon is termed "skipping a beat" and occurs with probability Ps. Finally, the amplitude of fast phases behaved as a linear function of eye position at the fast phase onset and the product of tau 0 and slow phase eye velocity. A computer simulation reproduced the observed distribution of slow phase durations, the proportion of fast phases in the fast phase and slow phase directions and the distribution of eye positions at the onset and end of fast phases. This novel model suggests that both timing and eye position information contribute to the alternation of nystagmus fast and slow phases.

Influence of gravitoinertial force level on vestibular and visual velocity storage in yaw and pitch

Velocity storage is an important aspect of sensory-motor control of body orientation. The effective decay rate and three-dimensional organization of velocity storage are dependent upon body orientation relative to gravity and also are influenced by gravitoinertial force (G) level. Several of the inputs to velocity storage including otolithic, somatosensory, proprioceptive, and possibly motor are highly dependent on G level. To see whether the G dependency of velocity storage is related to changes in the effective coupling of individual sensory inputs to the velocity storage mechanism or to alterations in the time constant of velocity storage per se, we have studied horizontal vestibular nystagmus, horizontal optokinetic afternystagmus (OKAN) and vertical vestibular nystagmus as a function of force level. Horizontal OKAN and vestibular nystagmus both showed no effect of G level on their initial or peak slow phase velocities but their decay rates were quicker in 0G and 1.8G than in IG. Vertical vestibular nystagmus also showed no effect of G level on peak velocity but decayed quicker in 0G relative to 1G. These findings indicate that the intrinsic decay rate of a common velocity storage mechanism is affected by the magnitude of G. A negligible amount of slow phase eye velocity was observed in planes outside the planes of stimulation, thus short-term changes in G across multiple body axes can change velocity storage, but the change is restricted to the axis common to the rotary stimulus and the G vector.

TORSIONAL NYSTAGMUS

Thirty-five patients with torsional nystagmus (TN) underwent vestibular and ocular motor assessment and magnetic resonance image (MRI) scanning of the head. Patients were divided into two groups according to whether TN was predominant and present in primary gaze (Group I, 23 patients) or elicited by head positioning or gaze deviation and less prominent than other concurrent nystagmus (Group II, 12 patients). The main aetiologies in both groups were demyelination, vascular disease and posterior fossa tumours. In Group I, a frequent pattern of findings, occurring in 30-50% of cases, was a caloric canal paresis contralateral to the direction of the fast phases ('beat') of the TN, whereas the duration of horizontal caloric/rotational nystagmus and the slow-phase eye velocity of pursuit and of optokinetic nystagmus were all reduced in the direction of beating. The TN was more frequently and consistently modulated by vertical canal stimuli (head oscillation in roll) than by otolith stimuli (static tilt). Statistical analysis of the MRI showed significant overlap of abnormal MRI signals in the area of the vestibular nuclei, on the side opposite to the beat direction of TN. These results suggest that TN originates in a central imbalance of vertical semicircular canal function, resulting from lesions involving the vestibular nuclei on the opposite side of the TN. Group II was heterogeneous with no consistent pattern of neuro-otological findings, although lesions ipsilateral to the TN were frequent occurrence; in these cases cerebellar system lesions may have produced ipsilateral vestibular nuclei disinhibition.

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

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 vestibulo-ocular 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 (2.2x) and reducing (0.5x) 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.

Off-line computing of slow-phase eye velocity profiles evoked by velocity steps or caloric stimulation

We describe a method to compute the slow-phase eye velocity profile without explicit removal of quick phases. It can be used for off-line analysis of eye movements evoked by angular head velocity steps or caloric stimulation. Zero-crossings of eye velocity from negative to positive values divide the velocity trace into intervals of different length. In each interval, the velocity data points are sorted in an ascending order. The value at the least slope (mode value) is taken as the representative slow-phase velocity for the processed interval. Spline interpolation between the representative points of all intervals results in an envelope that gives an accurate description of the slow-phase velocity over time and is used to determine parameters such as peak slow-phase velocity, time constant etc. The method can easily be implemented on a computer.

The horizontal vestibulo-ocular reflex during linear acceleration in the frontal plane of the cat

Horizontal and vertical eye movements were recorded in alert, restrained cats that were subjected to whole-body rotations with the horizontal semicircular canals in the plane of rotation and the body centered on the axis or 45 cm eccentric from the axis of rotation. Changes in the horizontal vestibulo-ocular reflex (HVOR) due to the resultant of the linear forces (i.e., gravity and linear acceleration) acting on the otolith organs were examined during off-axis rotation when there was a centripetal acceleration along the animal's interaural axis. The HVOR time constant was slightly shortened when the resultant otolith force was not parallel to the animal's vertical axis. This effect was independent of the direction of the otolith force relative to the direction of the slow phase eye velocity. No effect on the HVOR amplitude was observed. In addition to changes in the HVOR dynamics, a significant vertical component of eye velocity was observed during stimulation of the horizontal canals when the resultant otolith force was not parallel with the animal's vertical axis. The effect was greater for larger angles between the resultant otolith force and gravity. An upward or downward component was elicited, depending on the direction of the horizontal component of eye velocity and the direction of the resultant otolith force. The vertical component was always in the direction that would tend to align the eye velocity vector with the resultant otolith force and keep the eye movement in a plane that had been rotated by the angle between the resultant otolith force and gravity.

Changes in the dynamics of the vertical vestibulo-ocular reflex due to linear acceleration in the frontal plane of the cat

The vertical and horizontal components of the vestibulo-ocular reflex (VOR) were recorded in alert, restrained cats who were placed on their sides and subjected to whole-body rotations in the horizontal plane. The head was either on the axis or 45 cm eccentric from the axis rotation. During off-axis rotation there was a change in the linear force acting on the otolith organs due to the presence of a centripetal acceleration along the animal's vertical axis. Otolith forces (defined to be opposite to the centripetal acceleration) directed ventrally with respect to the animal (negative) decreased both the amplitude and time constant of the first-order approximation to the slow phase eye velocity of the vertical vestibulo-ocular reflex (VVOR). Otolith forces directed dorsally (positive) increased the amplitude and time constant. The effects were greater for the up VOR. The asymmetry in the VVOR time constant also depended on the otolith forces, being less in the presence of negative otolith forces that caused the resultant otolith force to move ventrally, towards the direction along which gravity normally acts when the animal is in the upright position. The effects of otolith forces on the up VVOR were independent of whether the animals were tested in the dark or in the light with a stationary visual surround (i.e., during visual suppression). In contrast, the changes in the time constant of the down VVOR were smaller during visual suppression. Simulations of the eye velocity storage mechanism suggest that the gain of the feedback in the storage integrator was modified by the angle between the resultant otolith force and an animal-fixed reference. This could be the animal's vertical, i.e., the direction along which gravity normally acts. For larger angles the feedback was less and the amplitude and time constant of the VVOR increased. The transformation of the otolith input was the same for both the up and down VOR, even though the final effect on the eye velocity was asymmetric (larger for up VOR) due to a separate, asymmetric gain element in the velocity storage feedback pathway.

Influence of Repeated Unidirectional Rotatostimulation on Squirrel Monkey's Perrotatory Nystagmus

In this investigation of response decline (RD) phenomenon of the vestibulo-ocular reflex (VOR), five healthy squirrel monkeys were rotated repeatedly in a darkroom. First they were rotated clockwise for 5 sec at a constant angular acceleration of +20°/sec2, then decelerated slowly to the zero point by subliminal clockwise rotation of -0.4°/sec2. This rotation was repeated 20 times a day for 2 weeks. The constant angular acceleration test performed after repetition of the rotatostimulation showed directional preponderance (DP) to the left, which was caused by the RD phenomenon in the slow phase eye velocity (SEV) of right beating nystagmus. However, significant DP was not observed in other nystagmus parameters, such as duration, jerk number, and quick phase velocity.The DP of SEV tended to decrease during a rest of 24 hours after stimulation and disappeared completely after a rest of 2 weeks.

Evaluation of the Vestibulo-ocular Reflex by High-frequency Head Oscillation

Subjects were divided into three different groups. The normal group consisted of 10 normal adult volunteers aged 22 to 31 years (mean: 26). The unilateral lesioned group consisted of 35 patients aged 26 to 65 years (mean: 45) who had undergone surgery for acoustic neuroma by an extended middle cranial fossa approach (2) 2 weeks to 7 years prior to the examination. All patients showed no or little response upon ice water irrigation. In addition, we examined a 28-year-old male patient with dead labyrinths due to congenital inner ear anomalies. Subjects were asked to rotate their head smoothly while gazing at a target on the wall, starting from slow oscillations (about 0.5 Hz), then accelerating to faster ones (over 2.0 Hz). Head movements were recorded by a gyrosensor which was firmly fixed on the head. Eye movements were recorded by a DC electro-oculograph. Head and eye movements were electrically added to ascertain gaze movements in space. We obtained the gain by calculating the ratio of the maximum slow phase eye velocity to the corresponding head velocity. In normal subjects, the peak oscillation frequency was higher than 4 Hz. Unilateral and bilateral labyrinthine loss markedly decreased the maximum head frequency (Fig. 1). Mean values of the maximum frequency were 4.0 Hz in the normal group, 2.4 Hz in the unilateral lesioned group, and 1.7 Hz in the patient with bilateral labyrinthine loss. We suspect that patients with labyrinthine loss, whether unilateral or bilateral, may involuntarily restrict head movements to prevent gaze oscillation. Although daily head movements involve high-frequency components, their amplitude is relatively small in the case of to-and-fro movements like walking and running (3). Therefore, the head movements in this examination are unusual in daily life. This may explain why more than 50% of patients did not complain of oscillopsia after surgery for acoustic neuroma.